[ { "U_id": "MPX1009", "TAC": [ "MPX1009_synpic46283", "MPX1009_synpic46295" ], "MRI": [], "Case": { "Title": "Bladder Diverticulum", "History": "73-year-old male with hematuria and numerous white blood cells found on UA", "Exam": "N/A", "Findings": "Bladder with thickened wall and diverticulum on the right. Diverticulum is mostly likely secondary to chronic outflow obstruction.\n\nProstate enlargement.", "Differential Diagnosis": "Bladder Diverticulum", "Case Diagnosis": "Bladder Diverticulum", "Diagnosis By": "N/A" }, "Topic": { "Title": "Bladder Diverticulum", "Disease Discussion": "Bladder diverticula most often occur as a result of outlet obstruction. Occasionally, a congenital weakness in the bladder wall adjacent to the ureteral orifice results in a diverticulum. This is termed a \"Hutch\" diverticulum.\nIn children, outlet obstruction causing a diverticulum is rare and can be seen with urethral valves. In men, diverticula are associated with outlet obstruction from urethral stricture, prostatic hypertrophy, prostatic carcinoma etc. acquired diverticula are rare in women.\nDiverticula usually occur on the lateral bladder walls, rarely the dome. They are often multiple. Large diverticula often displace the bladder and or ureters. \ndiverticula can have wide or narrow necks. The wide necked variety empty urine readily. The narrow neck type are slow to empty and therefore are more likely to have urinary stasis.\nInfection, tumor and stone formation can occur as a result of urine stasis within a diverticulum. Tumor formation in a diverticulum is more likely to spread beyond the bladder because the diverticulum wall consists only of urothelium without muscle.\nBladder diverticula can be evaluated with excretory urography, ultrasound, CT and cystoscopy.\n\nRef:\nDunnick, R., McCallum, R., Sandler, C., Textbook of Uroradiology.", "ACR Code": "8.9", "Category": "Diverticulum" } }, { "U_id": "MPX1024", "TAC": [ "MPX1024_synpic40275", "MPX1024_synpic40277" ], "MRI": [], "Case": { "Title": "Left upper lobe collapse caused by an enlarging, obstructing small cell lung carcinoma.", "History": "60-year-old woman presents with chest pain and shortness of breath.", "Findings": "\u2022 PA chest radiograph demonstrates left lung volume loss, silhouetting of the left cardiac border, and Luftsichel sign.\n\n\u2022 Lateral chest radiograph shows anterior displacement of the major fissure and elevation of the left mainstem bronchus.\n\n\u2022 CT of the chest reveals an obstructing mass and resultant LUL collapse.", "Differential Diagnosis": "This combination of radiographic findings are consistent with LUL collapse and highly suspicious for an underlying endobronchial mass causing obstruction of the LUL bronchus.", "Case Diagnosis": "Left upper lobe collapse caused by an enlarging, obstructing small cell lung carcinoma.", "Diagnosis By": "Lung biopsy proven Small Cell Lung Cancer.", "Discussion": "This woman had known small cell lung carcinoma. The radiographic findings described above are diagnostic of left upper lobe collapse. Such a finding should raise suspicion for an underlying obstructing mass. In this case, the patient presents with a known diagnosis of small cell lung carcinoma. Thus CT is not required to confirm collapse or the cause of collapse." }, "Topic": { "Title": "Lung, lobar collapse (left upper lobe)", "Disease Discussion": "Total left upper lobe atelectasis is caused by obstruction of the left upper lobe bronchus. This may be due to pulmonary mass, mucous plugging or foreign bodies. In older individuals, a pulmonary mass is a common cause.\n\nPA films of left upper lobe atelectasis demonstrate opacification of the left upper lung field with obliteration of the left cardiac border. In addition, there is often a relative lucency adjacent to the aortic knob which represents an overinflated lower lobe. This lucency is referred to as the Luftsichel sign.\n\nThe lateral film demonstrates anterior displacement of the major fissure with increased anterior opacification.\n\nThis patient had a previously known left upper lobe mass with total left upper lobe atelectasis proven by CT scan.", "ACR Code": "64.749", "Category": "Obstruction or Stenosis", "Reference": "Fraser et al. Synopsis of Diseases of the Chest. 2nd ed. WB \n Saunders. Philadelphia. 1994." } }, { "U_id": "MPX1012", "TAC": [ "MPX1012_synpic22949", "MPX1012_synpic22950" ], "MRI": [], "Case": { "Title": "Ovarian torsion", "History": "24 hours of pelvic, RLQ pain.", "Exam": "Tender in the right adnexa and right lower quadrant. Negative pregnancy test.", "Findings": "CT: Large heterogeneous pelvic mass displacing the uterus anteriorly.\n\nUS: Enlarged right ovary with central cystic component. Absent blood flow.", "Differential Diagnosis": "Ovarian Torsion\nOvarian mass, benign vs. malignant\nHemorrhagic cyst\nEctopic pregnancy\nTOA", "Case Diagnosis": "Ovarian torsion", "Diagnosis By": "Laporoscopy" }, "Topic": { "Title": "Ovarian torsion", "Disease Discussion": "Ovarian torsion is caused by partial or complete rotation of the ovary on its mesenteric pedicle. This results first in compromise of the lymphatic and venous drainage, causing congestion and edema of the ovarian parenchyma and eventually leading to loss of the arterial perfusion and infarction. The condition is a surgical emergency much like a testicular torsion. Torsions may occur in normal or abnormal (ie ovarian cyst, dermoid) ovaries. This condition usually occurs in children and younger woman who have more mobile adnexa. \n\nThe imaging findings of ovarian torsion are variable. However, any abnormal ovary on ultrasound in the proper clinical setting should suggest the diagnosis. The sonographic findings depend on the degree of vascular compromise and whether an adnexal mass is present. The ovary is usually enlarged. Multiple enlarged cortical follicles in a big ovary with the proper history-acute lower quadrant pain (same side as the abnormal ovary), nausea, vomiting, mildly elevated WBC-is considered a specific sign. Color and spectral Doppler examination may show absent flow in the affected ovary. However this is neither a specific nor sensitive sign. Torsed ovaries may have Doppler flow, and normal ovaries may not show flow on Doppler interrogation. (Rumack, Diagnostic Ultrasound p.550)", "ACR Code": "8.2", "Category": "Infarction and/or Necrosis", "Reference": "Rumack, Diagnostic Ultrasound p. 550" } }, { "U_id": "MPX1016", "TAC": [ "MPX1016_synpic34317", "MPX1016_synpic34318" ], "MRI": [], "Case": { "Title": "Adenocarcinoma of the Lung", "History": "The patient is a 43-year-old female who presented with a 6-month history of progressively worsening shortness of breath with exertion during her 5-mile runs. The patient also complained of wheezing but denied having a cough, fevers, chills, or weight loss. This patient does not have a previous history of any chronic illnesses and does not have any history of tobacco use.", "Exam": "Physical Exam: \nNo abnormalities.\n\nLabs:\n- Fungal, acid-fast, and Gram stains showed no organisms. \n- Pleural fluid analysis was suspicious for malignancy.\n- Histopathologic analysis of tissue samples of all three right lung lobes including mediastinal lymph nodes revealed extensive lymphovascular invasion, focal areas of necrosis, and several areas with signet-ring cells.", "Findings": "Chest PA/LAT revealed increased interstitial markings in the right lower lobe.\n\nContrast enhanced chest CT revealed diffuse increased interstitial markings involving the right middle and lower lobes, pleural thickening/scarring of the posterior right lower lobe, and a small right-sided pleural effusion.", "Differential Diagnosis": "lymphangitic spread of malignancy\nprimary malignancy\nlymphoma\nSjogrens syndrome\nlymphangioleiomyomatosis\npneumonia (bacterial, atypical, viral)\ncollagen vascular disease (SLE, RA)\nhypersensitivity pneumonitis\nasbestosis\nedema (secondary to fluid overload, CHF, or nephrotic syndrome)", "Case Diagnosis": "Adenocarcinoma of the Lung", "Diagnosis By": "Biopsy histology", "Treatment & Follow Up": "The patient was initially treated for pneumonia based on her symptoms and the findings on chest x-ray. Further evaluation was completed after recurrence of symptoms within one month of therapy. VATS and mediastinoscopy were performed after bronchoalveolar lavage yielded cells suspicious for malignancy. A whole body PET scan and brain MRI were performed and did not reveal any evidence of distant metastases. Chemotherapy was initiated and the patient later underwent a right-sided pneumonectomy.", "Discussion": "Lung cancer must be ruled out in any patient with a nonresolving pneumonia. Lung cancer has surpassed breast cancer in becoming the leading cause of cancer death in women. Adenocarcinoma accounts for 30-40% of lung cancers and is the most common histologic type. It is also the most common type of lung cancer in non-smokers (an estimated 10-15% of patients diagnosed with lung cancer are non-smokers). The most common sites of distant metastases are the brain, bones (most commonly vertebrae), liver, adrenals, and skin. The American Thoracic Society recommends measurement of a CBC, serum electrolytes, calcium, alkaline phosphatase, albumin, AST, ALT, total bilirubin, and creatinine in all patients with lung cancer. Abnormal LFTs should be followed up with a contrast-enhanced CT of the liver, and an elevated alkaline phosphatase or calcium level should be followed up with a bone or PET scan to detect metastases (there is conflicting evidence as to which imaging modality has greater sensitivity). Stage IV disease is primarily managed with chemotherapy or with palliative measures for symptomatic relief, and the five year survival rate is less than 5%." }, "Topic": { "Title": "Adenocarcinoma of the Lung", "Disease Discussion": "Lung cancer has surpassed breast cancer in becoming the leading cause of cancer death in women. Adenocarcinoma accounts for 30-40% of lung cancers and is the most common histologic type. It is also the most common type of lung cancer in non-smokers (an estimated 10-15% of patients diagnosed with lung cancer are non-smokers). The most common sites of distant metastases are the brain, bones (most commonly vertebrae), liver, adrenals, and skin. The American Thoracic Society recommends measurement of a CBC, serum electrolytes, calcium, alkaline phosphatase, albumin, AST, ALT, total bilirubin, and creatinine in all patients with lung cancer. Abnormal LFTs should be followed up with a contrast-enhanced CT of the liver, and an elevated alkaline phosphatase or calcium level should be followed up with a bone or PET scan to detect metastases (there is conflicting evidence as to which imaging modality has greater sensitivity). With regard to monitoring response to therapy, one study reported that changes in FDG uptake on PET scan rather than changes in lesion size on CT more accurately correlates with response to therapy. Stage IV disease is primarily managed with chemotherapy or with palliative measures for symptomatic relief, and the five year survival rate is less than 5%.\n\nSystematic screening for lung cancer is not currently recommended by any major medical organizations. The USPSTF concluded that there is currently insufficient evidence to argue for or against screening asymptomatic individuals for lung cancer with either chest x-ray, low dose computerized tomography, sputum cytology, or a combination of these tests. Studies evaluating the benefits of screening have shown increased detection of early stage lung cancer in asymptomatic individuals but have not shown a reduction in mortality. The Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial is an ongoing trial evaluating the use of a single posterior-anterior CXR, and the Early Lung Cancer Action Project is currently evaluating the use of low-dose spiral CT for screening.", "ACR Code": "6.3", "Category": "Neoplasm, carcinoma", "Keywords": "adenocarcinomalungnon small cell lung cancer", "Reference": "1. The American Thoracic Society and The European Respiratory Society. Pretreatment evaluation of non-small-cell lung cancer. Am J Respir Crit Care Med 1997;156: 320-332. \n\n2. Cerfolio RJ, Bryant AS, Winokur TS, et al. Repeat FDG-PET after neoadjuvant therapy is a predictor of pathologic response in patients with non-small cell lung cancer. Ann Thorac Surg 2004; 78: 1903-1909.\n\n3. Henschke CI, Yankelevitz DF, Libby DM, et al. Early lung cancer action project: annual screening using single-slice helical CT. Ann N Y Acad Sci 2001; 952:124.\n\n4. Lobrano, MB. Partnerships in oncology and radiology: The role of radiology in the detection, staging, and follow-up of lung cancer. Oncologist 2006; 11: 774-779.\n\n5. Oken MM, Marcus PM, Hu P, et al. Baseline chest radiograph for lung cancer detection in the randomized Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial. J Natl Cancer Inst 2005; 97: 1832." } }, { "U_id": "MPX1035", "TAC": [ "MPX1035_synpic21867" ], "MRI": [], "Case": { "Title": "Occipital Condyle Fractures", "History": "22yo M transported to the emergency department after a motorcycle accident. The head CT showed multiple intraparenchymal bleeds and small subarachnoid bleed. No other fractures of the cervical spine identified. Patient was monitored non-operatively by a hard collar. He developed a right cranial VI nerve palsy two days after the accident due to hemorrhage related to the fracture.", "Exam": "R cranial nerve VI palsy", "Findings": "Axial and coronal CT of the head and cervical spine demonstrating a R Occipital condyle fracture.", "Differential Diagnosis": "Occipital condylar fracture Type I, II, or III", "Case Diagnosis": "Occipital Condyle Fractures", "Diagnosis By": "CT" }, "Topic": { "Title": "Occipital Condyle Fractures", "Disease Discussion": "The most common classification is by Anderson and Montesano that describes three basic types of occipital condylar fractures.\n\n\nType I is usually the result of an impaction type injury due to asymmetrical axial forces applied to the head and may be seen with other lateral mass fractures in the upper cervical spine. The result is a comminuted fracture of the occipital condyle at the insertion of the alar and apical ligament complex. It is considered a stable fracture.\n\n\n\nType II is often the result of distraction type forces applied through the apical and alar ligament complex. The result is a basilar skull fracture extending to and involving the occipital condyle with an intact alar and apical ligament complex. It is considered stable unless the fracture completely separates the occipital condyle from the occiput. \n\n\nType III is an avulsion type fracture of the occipital condyle. The appearance is a fracture of the distal tip of the occipital condyle resulting in a free condylar fragment that may be displaced into the foramen magnum toward the odontoid process. A type III fracture is considered unstable.", "ACR Code": "1.-1", "Category": "Miscellaneous", "Keywords": "Occipital Condyle FractureOccipital Fracture", "Reference": "Anderson PA, Montesano PX. Morphology and treatment of occipital condyle fractures. Spine 1988; 13:731-736" } }, { "U_id": "MPX1031", "TAC": [ "MPX1031_synpic20041" ], "MRI": [], "Case": { "Title": "COPD and chronic ILD secondary to leukemia with acute PAP", "History": "74 yo female with history of leukemia and COPD now with acute onset of shortness of breath.", "Exam": "rales and crackles at the bases, CBC with elev white count (lymphocytes and neutrophils) and immature forms, BAL is PAS+", "Findings": "Predominately basilar and peripheral interlobular septal thickening with scattered areas of ground glass opacity, consolidation, and fibrosis.", "Differential Diagnosis": "DDX is that of ILD (see FACTOID). \n*Pulmonary edema (CHF)\n*Bacterial pneumonia\n*Pulmonary alveolar proteinosis", "Case Diagnosis": "COPD and chronic ILD secondary to leukemia with acute PAP", "Diagnosis By": "Bronchoalveolar lavage PAP+" }, "Topic": { "Title": "Interstital Lung Disease", "Disease Discussion": "INTERSTITIAL LUNG DISEASE --- The lung interstitium is composed of three components: bronchoarterial (axial), peripheral and parenchymal (using the terminology of Fraser and Pare). The axial component consists of the bronchovascular couplets (bronchiole and accompanying pulmonary artery). The peripheral space is composed of pulmonary veins and paired lymphatics and run within the interlobular septa. The peripheral component is continuous with the pleura. Finally, the interstitial parenchyma consists of the gas exchanging components of the lung (i.e. the walls of the alveoli). An understanding of these components allows one to think logically of the disease categories which affect the lung interstitium. This is especially true is regard to the interpretation of HRCT.\n\nWhile there are numerous methods by which to categorize ILD none are completely satisfying for ILD consists of a broad array of processes that share similar histopathologic and radiographic manifestations. Broadly they may be categorized as follows: (1) interstitial pneumonias (UIP, DIP), (2) diffuse infiltrative processes characterized by granuloma formation [e.g. sarcoidosis], (3) lymphocytic interstitial pneumonia, (4) pneumoconioses, (5) ILD associated with cysts [LAM and EG], (6) disorders characterized by interlobular septal thickening (pulmonary edema, pulmonary alveolar proteinosis and primary lymphangitic carcinomatosis), (7) eosinophilic syndromes, (8) pulmonary hemorrhage syndromes and (9) vasculitis. The combination of radiographic, clinical and laboratory findings are usually necessary to make a diagnosis and biopsy may be necessary to be definitive. \n\nPULMONARY ALVEOLAR PROTEINOSIS ---- PAP was shown to complicate the underlying COPD in the case presented. As noted above, PAP is within the category of diseases associated with interlobular septal thickening. Populations at risk for development of PAP include the immunocompromised (e.g lymphopenia in children and leukemia in adults); humans exposed to high concentrations of silicon dioxide; those infected with a variety of microorganisms (especially Nocardia, Aspergillus and Cryptococcus).\n\nPATHOLOGIC FINDINGS IN PAP show the alveoli to be filled with fine granular material which stains positive with periodic acid-Schiff stain (PAS+). Further histopathologic findings which may be present include: air-spaces filled with cholesterol crystals as well as needle-shaped crystals and laminated bodies (probably cellular fragments) and degenerating macrophages. Rarely interstitial fibrosis is present. \n\nRADIOGRAPHICALLY PAP was first described in a group of 27 patients in 1958. All demonstrated perihilar vaguely nodular air-space consolidation on plain film. Less severe disease may manifest as ground-glass opacity only. In general, findings may range from ill defined nodular densities or patchy areas of confluence confined to the lower lung to diffuse consolidation throughout both lungs. On conventional CT PAP may manifest as ill defined consolidation, while on HRCT the characteristic \u201ccrazy-paving\u201d may be evident. This latter finding is secondary to a fine linear pattern forming (3-10mm) polygonal shapes superimposed on a background of GGO. Of special note is the fact that \u201ccrazy-paving\u201d is NOT pathognomonic of PAP. Differential considerations include BAC, lipid pneumonia, pulmonary hemorrhage, hydrostatic and permeability pulmonary edema, and bacterial pneumonia.", "ACR Code": "6.2", "Category": "Inflammatory, non-infectious", "Keywords": "pulmonary alveolar proteinosisPAPinterstitial lung disease", "Reference": "Fraser, R.S. and Pare, P.D.; DIAGNOSIS OF DISEASES OF THE CHEST, 4th ed Vol IV, pgs 2700-08.\nGotway, M.B.; \"Interstitial Lung Disease\", UCSF Resident Review Notes in Diagnostic Imaging, Feb. 2003." } }, { "U_id": "MPX1034", "TAC": [ "MPX1034_synpic39422", "MPX1034_synpic39539" ], "MRI": [], "Case": { "Title": "Congenital Cholesteatoma", "History": "4 year old male with presented with white mass behind the left tympanic membrane noted on routine physical exam. Pt has no hx of ear surgery, perforations or trauma.", "Exam": "Ear exam: White mass behind the tympanic membrane, with bilateral tympanostomy tubes.\n\nAudiometry: left sided airbone gap of 30dBs, left sided type B tympanogram, right sided type A tympanogram", "Findings": "- Cholesteatoma of the left mesotympanum and epitympanum\n- Extends medially toward the malleus and incus without clear erosion of the bones\n- No dehiscence of the facial nerve noted", "Differential Diagnosis": "Congenital Cholesteatoma\nAcquired Cholesteatoma\nGiant Cholesterol Cyst\nAcoustic Neuroma\nGlomus tumor\nSarcoma\nMeningioma", "Case Diagnosis": "Congenital Cholesteatoma", "Diagnosis By": "Appearance was consistant with cholesteatoma on specimen examination both grossly and histologically.", "Treatment & Follow Up": "Canal wall up tympanomastoidectomy with complete removal of the ossicle chain.\nPlanned reconstruction of the ossicle chain if no recurrence is noted." }, "Topic": { "Title": "Congenital Cholesteatoma", "Disease Discussion": "Congenital cholesteatoma\n\nCholesteatomas can be divided into two catagories, aquired cholesteatomas caused by traumatic, infectious or post surgical causes and congenital ectopic tissue rests.\n\nClinical criteria: pearly white mass medial to an intact tympanic membrane, a normal pars tensa and flaccida, and no history of otorrhea, perforation, or previous otologic procedure\n\nClinical presentation: Most common presentation is a white retrotympanic mass noted on routine otoscopy. Now typically noted around the age of 4-5 years old. If they go undetected other symptoms are determined by the middle ear structure they interfere with. Facial nerve paralysis, conductive or sensorineural hearing loss, vertigo and extension into the middle fossa are all possibilities. The most common complication is a conductive hearing loss due to fixation of the ossicles by the mass. However, some large cholesteatomas can allow for sound conduction through the cholesteatoma itself.\n\nLocation: Most commonly found in the anterior superior quadrant of the tympanic membrane when found early, but as they grow they tend to migrate to the posterior hypotympanum.\n\nPathophysiology: There are four theories on how a congenital cholesteatoma is formed, the most widely accepted is the epithelial rest theory\n- Epithelial rests: Teed-Michael theory, ectodermal implants have been found in the 10 week old fetus between the first branchial cleft and pouch which is distinct from the surrounding tissue. They have an unknown function and typically are resorbed at 33 weeks gestion. If they do not involute then they may form a chronic cholesteatoma. While there is histologic evidence of rests prior to 33 weeks there are now two documented histological cases such rests persisting after 33 weeks.\n- Invagination: This theory suggested that tissue from the external canal invaginates through the tympanic membrane due to a very small inflammatory injury near the neck of the malleus which causes adherence of squamous tissue to the malleus. This may occur in utero or during childhood. Another related theory is that there is no actual macroscopic perforation of the tympanic membrane, only microperforations of the basal layer. This allows for squamous epithelium to enter the middle ear space.\n- Implantation: This is actually a theory against the existence of congenital cholesteatomas and implies that they are actually formed by unrecognized perforations of the tympanic membrane.\n- Metaplasia: This theory explains that epithelial tissue in the middle ear is via metaplasia to keratinizing squamous epithelium, although this theory appears to be unlikely due to the fact that most congenital cholesteatomas occur in one quadrant of the middle ear.\nHistology: Stratified squamous epithelial lined cyst which is filled with keratinous debris, this histology of a congential cholesteatoma is exactly the same as an acquired cholesteatoma.\nRadiology: High resolution CT of the temporal bone is the ideal modality for imaging congenital cholesteatomas, especially since most patients are young and without other ear pathology found in patients with aquired cholesteatomas. On CT a cholesteatoma appears as a hypodense lesion with well defined margins which does not enhance with constrast.\nMR imaging of the temporal bone may also be used. This will show low signal on T1W with moderately high signal on T2W images. It does not enhance with gadolinium. MR imaging is useful for differentiating a cholesteatoma from other intracranial processes. \n\nTreatment: Surgical resection with either complete removal of the cholesteatoma matrix or permanent exteriorization is curative. Depending on the size and location of the cholesteatoma a transtympanic, transmastoid, middle cranial fossa approach or a transphenoidal approach may be used.", "ACR Code": "1.3", "Category": "Neoplasm, benign", "Keywords": "cholesteatomacongenitalear disease", "Reference": "Congenital cholesteatoma: theories, facts, and 53 patients. Bennett M - Otolaryngol Clin North Am - 01-DEC-2006; 39(6): 1081-94\n\nThe pathophysiology of cholesteatoma.\nSemaan MT - Otolaryngol Clin North Am - 01-DEC-2006; 39(6): 1143-59\n\nCummings: Otolaryngology Head and Neck Surgery 4th ed. Chapter 110, Deep Space Neck Infection, Robert M. Kellman, Mobsy, Inc. 2005." } }, { "U_id": "MPX1048", "TAC": [ "MPX1048_synpic17415" ], "MRI": [], "Case": { "Title": "Pericardial cyst", "History": "20 year old healthy male for re-commissioning physical exam. Patient also C/O worsening cough and congestion over last week", "Findings": "PA/LAT: smoothly marginated soft tissue opacity noted in Right cardiophrenic angle, otherwise normal. \n\nCT: homogenous fluid attenuating and smoothly marginated lesion abutting the right cardiac border with Hounsfield attenuation unit = 7; Measures 5 x 4.4 x 7 cm", "Differential Diagnosis": "\u2022 Pericardial cyst\n\u2022 Morgagni hernia\n\u2022 Cardiac (epicardial) fat pad\n\u2022 Adenopathy\n\u2022 Thymoma\n\u2022 Lymphoma", "Case Diagnosis": "Pericardial cyst", "Treatment & Follow Up": "This case may require puncture and drainage due to its increased size, but pericardial cysts rarely require surgical treatment. Usually they can be followed serially." }, "Topic": { "Title": "Pericardial cyst", "Disease Discussion": "Clinical importance lies in the need to differentiate pericardial cysts from other masses with a similar appearance. Pericardial cysts represent fluid-filled outpouchings of the parietal pericardium. They occur in 1/100,000 people. The cysts rarely calcify and do not communicate with the pericardial space. One-third of patients are symptomatic at presentation and complain of chest pain and dyspnea. Pericardial cysts are best diagnosed by CT, MRI, or echo as smoothly marginated fluid-filled structures adjacent to the Rt heart border, although 20% of pericardial cysts lie along the left heart border, sometimes mimicking a prominent left atrial appendage or left ventricular aneurysm.", "ACR Code": "55.1942", "Category": "Unsure", "Keywords": "pericardialcysts", "Reference": "Braunwald: Heart Disease: A Textbook of Cardiovascular Medicine, 6th ed\n\nGrainger & Allison\u2019s Diagnostic Radiology: A Textbook of Medical Imaging, 4th Ed.\n\nTekeda et al, Clinical Spectrum of Mediastinal Cyst. Chest Vol 124, Number 1, Jul 2003" } }, { "U_id": "MPX1038", "TAC": [ "MPX1038_synpic20727", "MPX1038_synpic20729", "MPX1038_synpic20730", "MPX1038_synpic20731" ], "MRI": [], "Case": { "Title": "Jefferson Fracture", "History": "27 year old female involved in high speed motor vehicle accident.", "Exam": "Patient presented to ED with GCS of 12, no focal neurologic findings, as well as multiple abrasions and minor lacerations on all extremeties and the face.", "Findings": "Selected axial CT images in bone window show multiple fractures of C1 including bilateral anteriolateral fractures with no displacement of left lateral mass and moderate displacement of the right lateral mass best visualized on the coronal reformatted images. There is also a comminuted fracture in the right posteriolateral portion of the c1 ring with a small, triangular fragment abutting, but not compromising the thecal sac.", "Differential Diagnosis": "Fracture", "Case Diagnosis": "Jefferson Fracture", "Diagnosis By": "NA", "Treatment & Follow Up": "Patient should be stabilized with Halo for three months.", "Discussion": "Multiple C1 ring fractures, otherwise known as Jefferson fractures,account for 10% of all cervical spine injuries and 25% of alantoaxial injuries and result from a significant axial force directed from vertex through occiput such as diving in shallow water or in this case a motor vehicle accident. The C1 ring much like the pelvic ring will not typically fracture in one place. Multiple fracture points allow displacement of the lateral masses usually seen on the AP open mouth view of the c-spine series. Although plain films are routinely used in evaluation of the trauma patient, anyone suspected to have disruption of the C1 or other cervical vertebrae should undergo CT evaulation. Plain film criteria for diagnosis of Jefferson fracture states that the C1 lateral masses must be displaced greater than 2mm and must extend beyond the margins of C2. CT is used to better define the fracture fragments and to determine any compromise of the spinal cord." }, "Topic": { "Title": "Brain Tumor and Cancer Protocols", "Disease Discussion": "You may search the NIH/NCI cancer treatment protocol database:\nhttp://clinicalstudies.info.nih.gov/\n\nAdult Brain tumors - http://www.cancer.gov/cancertopics/pdq/treatment/adultbrain/healthprofessional\n\nPediatric Brain tumors - http://www.cancer.gov/cancertopics/pdq/treatment/childbrain/HealthProfessional\n\nClinical Trials - http://bethesdatrials.cancer.gov/clinical-research/search-results.asp?Specific=31&TextSearch=&Search+for+Clinical+Trials=Search+for+Clinical+Trials\n--", "ACR Code": "1.3", "Category": "Neoplasm, malignant (NOS)", "Keywords": "protocolscancer treatmentglioblastoma", "External Links": "clinicalstudies.info.nih.gov/" } }, { "U_id": "MPX1045", "TAC": [ "MPX1045_synpic46886", "MPX1045_synpic46887" ], "MRI": [], "Case": { "Title": "Horseshoe kidney", "History": "78 year old man with new onset of painless hematuria. There is no significant past medical history.", "Exam": "UA - hematuria", "Findings": "\u2022 Parenchymal bridge (\"isthmus\") connecting the inferior poles of both kidneys = Horseshoe kidneys\n\u2022 Complete duplication of the right ureter. \n\u2022 a 0.7 x 0.3 cm fat containing lesion in the inferior pole of the left kidney. \n\u2022 Multiple tiny calcifications bilaterally.\n\u2022 1.3cm cyst in the anterior aspect of the left kidney, containing a small calcification on its edge.", "Differential Diagnosis": "\u2022 Horseshoe kidney\n\u2022 Right Ureter duplication\n\u2022 Angiomyolipoma\n\u2022 Nonobstructing stones\n\u2022 Renal Cyst", "Case Diagnosis": "Horseshoe kidney", "Diagnosis By": "Imaging configuration" }, "Topic": { "Title": "Horseshoe kidney", "Disease Discussion": "Horseshoe kidney is in a group of congenital kidney anomalies called fusion anomalies. The fusion occurs at the lower poles in 90% of the cases, while 10% are fused at the upper pole. This anomaly is found in approximately 1/500-100 people. It is thought that the abnormal fusion likely occurs when the kidneys are still in the pelvis and the renal capsule is not fully developed. During the kidneys ascent these fused kidneys are trapped by the inferior mesenteric artery as the isthmus is unable to pass. The kidneys ascend to their normal positions between the fourth and ninth weeks of gestation. Complications include: ureteropelvic junction obstruction, recurrent UTI (urine stasis and vesicoureteric reflux), recurrent stone formation, and increased risk of trauma (due to kidney positioning). Horseshoe kidney may occur as an isolated anomaly or associated with other anomalies. Associated anomalies may include: ureteral duplication, hypospadias, undescended testis, ectopic ureter, anorectal malformations, GI malrotation, Meckel\u2019s diverticulum, neural tube defects, clubfoot, congenital hip dislocation, and ventricular septal defect. Chromosomal abnormalities have also been associated with horseshoe kidney. Horseshoe kidney is often evaluated with intravenous urography, CT, and/or ultrasound. MRI and scintigraphy may also be useful.", "ACR Code": "8.1", "Category": "Congenital, malformation", "Keywords": "Horseshoe kidneyfused kidneys", "Reference": ") Irshad, A; Ackerman, S; Ravenel, J. Horseshoe Kidney. www.emedicine.com Feb 03\n 2) Gross, G. Crossed fused Renal Ectopia. www.emedicine.com Feb 02\n 3) Cotran, R S; Kumar, V; Collins, T. Robins Pathologic Basis of Disease. W.B. Saunders Company. 1999. p 937." } }, { "U_id": "MPX1056", "TAC": [ "MPX1056_synpic41083", "MPX1056_synpic41084" ], "MRI": [], "Case": { "Title": "Hepatic fatty infiltration with focal sparing", "History": "This is 51 year old woman with known history of nephrolithiasis and left renal cyst. She was being followed for stones and had long history of abdominal/pelvic CT\u2019s and KUB films.", "Exam": "Physical Exam - unremarkable\nLabs: CMP, amylase, Lipase pending", "Findings": "Selected Images \u2013 CT (contrast, arterial phase) of abdomen/pelvis\n1. Large, diffusely infiltrated fatty liver with accessory left lobe. Compare to density of spleen. Multiple areas of focal sparing in left lobe that appears nodular. \n2. Area of focal sparing near portal vein.\n3. Area focal sparing in left lobe. Renal cyst and renal calculi.", "Differential Diagnosis": "Hepatomegaly\n1.\tMetabolic/diffuse infiltration\n\u2022 \tFatty infiltration \u2013 EtOH, drugs, toxins, Guacher\u2019s\n\u2022 \tCarbohydrate \u2013 diabetes, glycogen storage disease\n\u2022 \tIron \u2013 hemochromatosis\n\u2022 \tAmyloid - amyloidosis\n2.\tTumor\n3.\tCysts\n4.\tInflammation/infection\n5.\tVascular congestion\n\nNodular appearance\n1.\tfocal fat infiltration/sparing\n2.\thepatocellular carcinoma\n3.\tmetastases", "Case Diagnosis": "Hepatic fatty infiltration with focal sparing", "Diagnosis By": "Radiographically", "Treatment & Follow Up": "No specific treatment at this time. Follow-up with liver function tests to determine if stable or continuing to rise.", "Discussion": "Previous non-contrast abdominal CT dating back approx 6 months showed evidence for diffuse fatty infiltration and hepatomegaly. Additionally, a non-contrast CT performed 1 month ago showed increased thickness of the pancreatic head. A pre- and post-contrast CT were obtained to evaluate for change.\n\nThis is a presumptive diagnosis of diffuse fatty liver disease. The causes for which are many, for instance, alcoholism, obesity, malnutrition, steroid therapy, and diabetes mellitus. Laboratory testing of liver function tests could aid in further diagnosis. CT imaging is consistent with this diagnosis as the liver appears less dense than the spleen. Given that the liver findings were discovered incidentally and the patient has been asymptomatic there is no need to aggressively pursue this with further imaging or biopsy. However, from a medical record review, the patient reported that her primary care manager requested that she be taken off acetaminophen because of high liver function tests. The results of this test were unavailable. So significant delay in diagnosis could lead to long-term liver damage. Furthermore, most cases of fatty liver disease will resolve if the etiology is discovered and the offending agent is removed.\n\nThe appearance of focal fatty sparing is concerning and could misinterpreted as liver tumor, primary of metastasis. In this case, the focal sparing is in a triangular shape near the portal vein which is consistent with fat sparing and not a mass. \n\nAccessory lobes of liver are normal variant and if asymptomatic require no intervention." }, "Topic": { "Title": "Hepatic fatty infiltration with focal sparing", "Disease Discussion": "Fatty metamorphosis is a common metabolic response of the liver to a variety of inciting agents and disease states. These agents and states include corticosteroids, chemotherapy, diabetes mellitus, hyperlipidemia, hepatotoxic drugs, obesity, severe hepatitis, chronic alcoholism, malnutrition / malabsorption, jejuno-ileal and jejunocolic bypass surgery, hyperalimentation, congestive heart failure, and blunt hepatic trauma. Despite these associations, the exact pathophysiologic mechanisms remain obscure. Possibly diminished portal venous perfusion has a significant effect on producing fatty change and altering hepatic density. A relative hepatocellular ischemia is proposed to result in decreased parenchymal glycogen and increased accumulations of fat. The fat content of the liver may rise as high as 40% - 50% of the weight, well above the normal value of approximately 5%.\nRegional variation in amount of liver-cell fat can produce entities called pseudolesions or pseudotumors, usually discovered during imaging. Focal fatty sparing in an otherwise fatty liver occurs in several typical locations: along the gallbladder fossa, along the falciform ligament, occasionally in the periphery of the liver and near the hilum which is perfused with low-insulin blood from a pyloric vein. Because focal fatty sparing can only occur in the presence of fatty liver disease, most of these patients have a history of one of the disease states or agent exposures mentioned above.\n\nClassic features that will help differentiate focally fatty sparing from a hypoechoic mass are that it occurs in these typical locations, often has a geographic (triangular or quadrangular) shape vice being round like most masses and focally fatty sparing, since it is not a mass, will not demonstrate mass effect on adjacent structures, particularly crossing vessels.", "ACR Code": "7.3", "Category": "Metabolic (see also Toxic)", "Keywords": "Hepatic fatty infiltration with focal sparingLiver fatty infiltrationfocal sparing", "Reference": "Wanless IR. Clinics in Liver Disease. Volume 6, Number 2, May 2002\n\nWhite EM. Focal Periportal Sparing in Hepatic Fatty Infiltration: A Cause of Hepatic Pseudomass on US. Radiology 1987; 162:57-9" } }, { "U_id": "MPX1033", "TAC": [ "MPX1033_synpic45450", "MPX1033_synpic45451" ], "MRI": [], "Case": { "Title": "Idiopathic Pulmonary Hemosiderosis", "History": "Patient with diagnosis of idiopathic pulmonary hemosiderosis per open lung biopsy 10/07 who has been relatively asymptomatic but with persistent presence of hemosiderin-laden macrophages in bronchoalveolar lavage and desaturation noted on exercise test in May 2008. \n\nHISTORY\nPatient was product of pregnancy complicated by pre-eclampsia. Patient was born at 27weeks after 2 days of antenatal steroids. Significant respiratory distress requiring intubation was noted immediately after birth. \n\nNeonatal course included multiple doses of surfactant. 68 days mechanical ventilation, and 3 months of NICU care. Complications included multiple episodes of pneumonia, presumed sepsis, NEC, anemia, and electrolyte abnormalities. \n\nThe patient was discharged home on O2 which she used until 9 months of age, as well as Fe, diuretics, steroids.\n\nAfter 1 year of age, patient began to have multiple episodes of pneumonia, bronchitis, and asthma requiring hospitalization. Anemia, requiring 2 transfusions, was noted in context of one episode of pneumonia. \n\nIn addition, the patient experienced failure to thrive, reaching less than 3% height/weight for her age.\n\nAt the present, the patient is at 25% height, 3% weight.\n\nParents otherwise deny recent URI, cough, wheeze.\n\nHospitalizations: \nafter birth x 3 mos\n2004-pna\n2005-pna and transfusion for anemia\n2006-pulmonary hemorrhage, respiratory failure\n2007-multifocal pna\n\nSurgeries:\nbronchoscopy 12/06, 12/07, 5/08\nopen lung bx 10/07\nport cath placement 12/07\n\nMeds: \nPrevacid 15 mg tablet QD\nMiralax, 17 gm QD\nIron oral solution75mg/0.6mL- 25 mg/mL\nHydroxychloroquine 25mg/mL- 6ml QD\nTums \u2013 1 tablet QD for calcium\nFlinstones MVT \nImmunizations: Up to date\nAllergies: Cow\u2019s Milk \n\nDevelopmental History: delayed fine motor skills per MOP; otherwise met all milestones. \n\nFamily History: non-contributory\n\nSocial History: lives with mother, father, older brother. No pets, no smoking", "Exam": "VS: T 98.4 HR BP RR O2 Sat 98% on RA Wt 15.2 kg Ht 44cm \nGen: Small for age; NORMAL ACTIVITY FOR AGE, ALERT AND RESPONSIVE,\nHEENT: left TM well visualized with good light reflex; right TM occluded by cerumen (unable to extract at this time); EOMI, PERRLA, no nasal discharge, oropharynx clear and w/o exudates or erythema, No LAD appreciated\nCV: reg rate and rhythm, no murmurs, rubs, or gallops appreciated\nResp: CTAB\nGI: normoactive bowel sounds, NTND, no HSM, no masses\nExt: FROM, no edema\nSkin: warm, dry, no lesions, no bruises\nNeuro: grossly intact\n\nLABS\nNormal: C3, IgG, IgA, IgM, IgE, Rheumatoid Factor, ESR, CH50, GBM ab, ACE, ANCA,\nLow Fe, elevated ferritin and TIBC", "Findings": "During acute bleeding episode, areas of increased opacity and decreased lung volume are seen throughout the lungs, especially in the bases.", "Differential Diagnosis": "DDX for diffuse alveolar hemorrhage: \n\nimmune related- anti-basement membrane antibody disease (Goodpasture's syndrome), vasculitis and collagen vascular disease (systemic lupus erythematosus, Wegener's granulomatosis, systemic necrotizing vasculitis, and others), and pulmonary capillaritis associated with idiopathic rapidly progressive glomerulonephritis. \n\nNonimmune-coagulopathy, necrotizing pulmonary infection, drugs (penicillamine), toxins (trimellitic anhydride), Heiner\u2019s Syndrome, and idiopathic pulmonary hemosiderosis", "Case Diagnosis": "Idiopathic Pulmonary Hemosiderosis", "Diagnosis By": "Open Lung Biopsy, 10/07 - reviewed by TAMC pathology, AFIP, Texas Children\u2019s Hospital\n\nCommon findings on diagnostic tests:\n\nCXR: \u201cbutterfly or batwing\u201d pattern \u2013 symmetrical alveolar infiltrates slanting upwards towards lateral chest wall\nCT: \u201cground glass appearance\u201d\nDx: \nBAL showing hemosiderin-laden macrophages\nLung biopsy \nintact or minimally fragmented erythrocytes in the distal airways and alveoli\nhaemosiderin-laden macrophages (siderophages) \n\u201cbland\u201d \u2013 no capillaritis, vasculitis, any focal or diffuse smooth muscle cell proliferations, vascular malformations, malignancy, pulmonary infarcts, granulomatous inflammation, or infectious agents.", "Treatment & Follow Up": "Patient is presently receiving monthly IVIG (2mg/kg) infusions with pretreatment of Tylenol 15mg/kg and concurrent steroid bursts (Solumedrol 30mg/kg). Will reassess with CT, PFTs every 6 months.\n\nLiterature review shows current recommendations as follows:\n\n* Systemic glucocorticoids - noted improvement during acute phase but unclear effects during resolution. Studies suggest fewer exacerbations and possible decrease in fibrogenesis. Oral >> inhaled. Generally starting dose recommended <1mg/kg/day\n* Immunosuppression as adjunct to steroid treatment (most supporting evidence for decreased excarebations): \n - Azathriopine \n - Cyclophosphamide\n* IVIG\n* Tranfusions for anemia" }, "Topic": { "Title": "Idiopathic Pulmonary Hemosiderosis", "Disease Discussion": "***IN PROGRESS****\n\n\nLesions/Condition: Idiopathic Pulmonary Hemosiderosis\n\nCell of Origin:\n\nWHO Grade(s):\n\nSynonyms:\n\nAssociations/Predisposing Factors: \n\nCommon Locations:\n\nDemographics:\n\nGross Morphology:\n\nHistology:\n\nSpecial Stains:\n\nGross Appearance:\n\nRadiology:\n\nPrognosis and Treatment:", "ACR Code": "6.9", "Category": "Idiopathic or Unknown", "Keywords": "pulmonary hemorrhagehemosiderosispediatric" } }, { "U_id": "MPX1058", "TAC": [ "MPX1058_synpic17148" ], "MRI": [], "Case": { "Title": "Pulmonary Embolism", "History": "Complains of several days of vague abdominal pain, general weakness and shortness of breath.", "Exam": "Decreased breath sounds to right lower lobe. \nElevated ESR.\nNormocytic anemia.", "Findings": "Bilateral pleural effusions, R>>L. Right basilar atelectasis. \nMain PA filling defect C/W saddle embolism.\nRight lower lobe branch of PA filling defect c/w thromboembolism.", "Differential Diagnosis": "Clot embolus\nIn situ thrombus\nTumor embolus", "Case Diagnosis": "Pulmonary Embolism", "Diagnosis By": "Imaging of clot" }, "Topic": { "Title": "Pulmonary Embolism", "Disease Discussion": "Pulmonary embolism (PE) can be associated with significant mortality if untreated. The clinical diagnosis of pulmonary embolism is unreliable. Symptoms of PE include tachypnea/dyspnea (most common), tachycardia, hypoxia, pleuritic chest pain, hemoptysis, syncope, and atrial fibrillation. Blood gas may be normal. \n\nThe D-dimer blood test is a screening tool for pulmonary embolism. A serum level less than 500 ng/L excludes pulmonary embolism with a 90% accuracy. A positive test is non-specific. Additionally, the test is unreliable in the presence of malignancy, sepsis, recent surgery, or trauma. \n\nThe source is most commonly from deep venous thrombosis in the lower extremity, however, about 10% arise from clot in the upper extremity. Risk factors are Immobilization, Recent Surgery, Underlying Malignancy, History of Deep Venous Thrombosis or Pulmonary Embolism, Estrogen use, or Pre-existing cardiac disease. A low percentage of cases of pulmonary embolism result in pulmonary infarction, due to the presence of the bronchial circulation. \n\nTreatment for PE most commonly consists of anticoagulation with heparin or coumadin. Anticoagulation prevents clot propagation and allows endogenous fibrinolytic activity to dissolve existing thrombiAnticoagulation decreases mortality form 30-60% to <5%. \nThrombolytic agents are not routinely used for the treatment of acute PE. Thrombolytic treatment is generally reserved for patients with massive pulmonary embolism producing circulatory shock (hypotension).\n\nFor patients that cannot be anticoagulated, an inferior vena caval filter can be placed in order to prevent life-threatening PE. Major complications occur in about 1% of cases. Complications include central migration of the filter, filter fracture, inferior vena caval perforation, and vena caval thrombosis.\nV/Q scanning has been the mainstay for screening symptomatic patients for the presence of pulmonary embolism. A negative V/Q scan essentially excludes PE, and a high probability study is associated with the presence of a PE in about 85% of cases at angiography. Confusion arises with low or intermediate probability examinations, and there is common disagreement among expert readers in the interpretation of scans in these categories. The problem with V/Q scanning is that it does not directly visualize thromboembolism, but rather its effects on perfusion and ventilation . This problem causes the need for probability criteria, which in turn causes confusing results. Nuclear medicine scanning for PE is probably most useful in previously healthy patients with a normal chest radiograph. As the complexity of the patients underlying cardiopulmonary disease increases, so does the likelihood that the scan will not be informative (intermediate probability). Using PIOPED criteria, intermediate probability V/Q scans occurred in 60% of patients with COPD, but in only 13% of patients with normal CXR's. However, a generalized abnormality on CXR such as diffuse pulmonary edema or reticulonodular disease may not cause the perfusion lung scan to be abnormal.\n\nThe CXR is abnormal in the majority of cases of PE. The PIOPED study showed that among patients with angiographically proven pulmonary embolism, only 12% had chest X-rays interpreted as normal. (24% of patients with PE in another study had normal CXR's ). Atelectasis and other focal pulmonary parenchymal abnormalities are the most common CXR findings in pulmonary embolism, occurring in up to 68% of patients with PE. Pleural effusions are also common but usually small and unilateral. Other palin film findings indicative of PE include regional oligemia (Westermark sign), a pleural-based wedge shaped area of increased opacity (Hampton's hump), and prominence of the central pulmonary artery with abrupt tapering (Knuckle sign).\n\nIn pulmonary angiography,an embolus classiclally produces a filling defect within the affected pulmonary artery. Non-occlusive emboli have a \"tram-track\" appearance. Although considered the gold standard, angiography may not always detect the presence of emboli. Some indirect angiographic evidence for the presence of emboli such as vascular pruning and delayed capillary blush are non-specific. Additionally, agreement among angiographers regarding the presence of subsegmental emboli is poor and can be as low as 15%. V/Q scans can provide a road map to angiography, but if the abnormally perfused segment on the V/Q scan appears normal at angiography, complete evaluation the remainder of the lungs for the presence of pulmonary emboli is warranted. One important point to remember is that a negative angiogram has been shown to be an excellent indicator of a good prognosis. \n\nHelical CT is able to identify main, lobar, and segmental emboli with a reported sensitivity over 90%. Although the detection of subsegmental emboli is worse, the clinical significance of these small emboli has not yet been establishished. Additionally, on angiography there is poor interobserver agreement for the presence of subsegmental emboli and the true incidence of isolated subsegmental emboli is difficult to determine. Helical CT has also been shown to have a significantly better sensitivity, specificity, positive, and negative predictive values compared to V/Q scanning . Helical CT permits a more confident diagnosis to be made in a greater number of cases when compared with V/Q scanning . \n\nIt has been suggested that helical or electron beam CT should be the initial imaging modality to screen patients suspected of having PE- particularly in patients with abnormal CXR's in whom there is a greater likelihood of inconclusive V/Q scan results. If emboli are detected, no further work-up is required. If this study is negative, a lower extremity US or CT DVT exam can be performed to assess for the presence of DVT. Again, a positive exam would lead to patient treatment. If both studies were negative, then a decision would be required regarding whether the patient should proceed to angiography or not. Another benefit of CT is the ability to suggest an alternative diagnosis.", "ACR Code": "5.6", "Category": "Vascular", "Keywords": "Pulmonay embolismv/q scanhelical ct", "Reference": "Pulmonary embolism revealed on helical CT angiography: comparison with ventilation-perfusion radionuclide lung scanning. Journal of Vascular Surgery. 33(1):206, January 2001. \nAJR 2000; Blachere H, et al\n\nHenteleff, Harry J.A.. Drover, John W.. Members of the CAGS Evidence Based Reviews in Surgery Group *. Canadian Association of General Surgeons Evidence Based Reviews in Surgery. 3. Helical computed tomography versus pulmonary arteriography in pulmonary embolism. Canadian Journal of Surgery. 45(5):373-375, October 2002.\n\nWorsley et al. Comprehensive Analysis of the Results of the PIOPED Study. Journal of Nuclear Medicine, vol 36, No 12 Dec 95\n\nScott C. Williams, www.auntminnie.com(reference section, thoracic imaging)", "External Links": "www.auntminnie.com" } }, { "U_id": "MPX1043", "TAC": [ "MPX1043_synpic47072" ], "MRI": [ "MPX1043_synpic47071", "MPX1043_synpic47074", "MPX1043_synpic47075", "MPX1043_synpic47076" ], "Case": { "Title": "Disseminated Coccidioidomycosis", "History": "The patient is a 23 year old man who presented with four weeks of persistent mid back pain. He received pain medications with minimal relief. His pain gradually worsened over three months to involve his left leg and hip. The patient had associated fevers, weight loss, night sweats, fatigue, and intermittent abdominal pain.", "Exam": "Pertinent physical exam findings included:\n\u00bb splenomegaly to 1 cm below the costal margin\n\u00bb mild tenderness to palpation in the left upper quadrant\n\u00bb 1-2 cm firm immobile nodule left midclavicular costovertebral margin\n\u00bb midline tenderness to T12 and L1\n\u00bb decreased range of motion in flexion secondary to pain.\nWBC: 9.39 Hgb:11.2 Hct:35.7 Plt:535 ESR:117", "Findings": "The frontal and lateral views of the thoracic spine demonstrate a mixed lucent/sclerotic appearance of the T12 vertebral body and the left pedicle. \n\nA sagittal view MRI with gadolinium of the thoracic spine and lumbar spine demonstrates enhancing lesions multiple vertebrae, including T12. Soft tissue enhancement is also present from T9-L2 paraspinal muscles. \n\nA sagittal nonconstrast CT obtained several weeks later demonstrates worsening expansile lytic lesions to T10, T11, and T12.\n\nMRI of the thoracic spine was obtained five months after the patient began treatment. Interval worsening present at multiple levels, including multiple compression deformities and enhancing mass with cortical disruption and contiguous anterior soft tissue mass lifting the anterior longitudinal ligament. Involvment of the posterior elements is present with narrowing of multiple neural foramina and spinal cord compression.", "Differential Diagnosis": "--Osteomyelitis, including mycobacterial and fungal.\n--Metastatic disease\n--Multiple myeloma", "Case Diagnosis": "Disseminated Coccidioidomycosis", "Diagnosis By": "A biopsy of the L3 vertebral body lesion demonstrates Coccidioides spores.", "Treatment & Follow Up": "The patient was placed on amphotericin B and fluconazole and was discharged from the hospital. However, he returned to the hospital one month later with worsening back pain. Imaging demonstrated progressive disease. He was placed on multiple antifungal therapies with no success. The patient was then placed on interferon gamma and posaconazole with noted improvement.", "Discussion": "Coccidioidomyocosis is a common fungal infection in the southwestern United States. It usually leads to a self limited pulmonary infection. However, in less than 5% of cases, the infection can disseminate to the soft tissue, meninges, and bone. Those who are most susceptible to dissemination include the immunocompromised, pregnant women, and certain ethnic groups, such as Latinos, Filipinos, and African Americans. The most common antifunals used to treat disseminated coccidioidomycosis includes amphotericin B and the azoles. The patient was initially placed on amphotericin B and fluconazole, but his disease progressed. He was placed on itraconazole and posaconazole with no improvement. He was then placed on interferon gamma because it was believed that his immune system was unable to recognize Coccidiodes. He was also placed on posaconazole, after which he improved. He was discharged from the hospital. He will require lifelong antifungal therapy." }, "Topic": { "Title": "Disseminated Coccidioidomycosis", "Disease Discussion": "Lesions/Condition: Disseminated Coccidioidomycosis\n\nCell of Origin: Dimorphic fungus\n\nSynonyms: Valley Fever\n\nAssociations/Predisposing Factors: Immunosuppressed or certain ethnic groups\n\nCommon Locations: Lungs, bone, meninges, skin\n\nDemographics: Filipinos, Latinos, Asians, African Americans, pregnant women, immunocompromised\n\nGross Appearance: Dimorphic fungus \n\nRadiology: Radiologic findings of coccidioidomycosis disseminated to the skeleton generally involves the axial skeleton. Lesions may be lytic or demonstrate permeative type bone destruction. Lesions on CT may have low attenuation. T1 MRI demonstrates decreased signal and T2 MRI shows increased signal. Lesions often enhance with gadolinium administration.\n\nPrognosis and Treatment: Patients with disseminated coccidioidomycosis are usually on lifelong antifungal therapy, particularly amphotericin B and the azoles.", "ACR Code": "3.6", "Category": "Infection, fungi", "Keywords": "InfectionFungal", "Reference": "Anstead GM, Corcoran G, Lewis J, Berg D, Grayhill JR. \"Refractory Coccidioidomycosis Treated with Posaconazole.\" Clinical Infectious Diseases 2005;40:1770-1776.\n\nBlair, J.E. \"State-of-the-Art Treatment of Coccidioidomycosis Skeletal Infections.\" Annals of the New York Academy of Sciences 2007; 1111: 422-433.\n\nJohnson RH, Einstein HE. \"Amphotericin B and Coccidioidomycosis.\" Annals of the New York Academy of Sciences 2007;1111:434-441.\n\nKirkland TN, Raz E, Datta SK. \"Molecular and cellular mechanisms of protective immunity to coccidioidomycosis.\" Vaccine 2006;24:495-500.\n\nKuberski TT, Servi RJ, Rubin PJ. \"Successful Treatment of a Critically Ill Patient with Disseminated Coccidioidomycosis, Using Adjunctive Interferon-gamma.\" Clinical Infectious Diseases 204;38:910-912.\n\nMagee DM, Cox RA. \"Roles of Gamma Interferon and Interleukin-4 in Genetically Determined Resistance to Coccidioides immitis.\" Infection and Immunity 1995;63:3514-3519. \n\nParish, J.M., Blair, J.E. \"Coccidioidomycosis.\" Mayo Clinic Proceedings 2008;83: 343-349.\n\nStevens DA, Rendon A, Gaona-Flores V, Catanzaro A, Anstead GM, Pedicone L, Graybill R. \"Posaconazole Therapy for Chronic Refractory Coccidioidomycosis.\" American College of Chest Physicians 2007;132:952-958.\n\nZeppa, Michael A., et al. \"Skeletal Coccidioidomycosis: imaging findings in 19 patients.\" Skeletal Radiology (1996) 25: 337-343." } }, { "U_id": "MPX1064", "TAC": [ "MPX1064_synpic41377", "MPX1064_synpic41378" ], "MRI": [ "MPX1064_synpic41380", "MPX1064_synpic41381" ], "Case": { "Title": "Chronic Fungal Sinusitis", "History": "Patient presented after a 9-month cruise - his parents did not recognize his face. His nose was bigger and his eyes were farther apart than they remembered. He complained of slight frontal headaches, but had no other symptoms.", "Exam": "Showed hypertelorism of the eyes.", "Findings": "\u2022 Image 1: Axial CT with expansion and opacification of frontal sinus, with marked thinning and disruption of bone comprising the inner table of the frontal bone\n\u2022 Image 2: Axial CT with expansion of ethmoid sinus, with disruption of bone comprising the left lamina papyracea\n\u2022 Image 3: Coronal CT with expansion of all paranasal sinuses, with extradural extension into the anterior cranial fossa and extraconal extension into the left orbit\n\u2022 Image 4: T1 MRI with heterogeneous signal in the frontal sinuses without changes to the frontal lobe of the brain\n\u2022 Image 5: T2 MRI with extradural expansion of heterogeneous mass into the anterior cranial fossa", "Differential Diagnosis": "\u2022 Sinus neoplasm\n\u2022 Chronic bacterial sinusitis\n\u2022 Allergic fungal sinusitis\n\u2022 Acute fungal sinusitis\n\u2022 Chronic fungal sinusitis\n\u2022 Granulomatous fungal sinusitis\n\u2022 Sinus mycetoma", "Case Diagnosis": "Chronic Fungal Sinusitis", "Diagnosis By": "Histopathology and culture", "Treatment & Follow Up": "Surgical exploration and resection\nIV amphotericin B\nLong-term itraconazole\n\nFollow-up is with otorhinolaryngology, with repeat culture of nasal discharge and radiologic studies", "Discussion": "The patient had not noticed the cosmetic effects on his face of the expanding sinonasal fungal ball; nor did his coworkers aboard the ship. It was only after he saw that his parents did not recognize him that anyone realized that his face had changed shape. This may be due to the slowly progressive changes.\n\nMore on Allergic Fungal Sinusitis - http://www.emedicine.com/ent/topic510.htm" }, "Topic": { "Title": "Chronic Fungal Sinusitis", "Disease Discussion": "Lesions/Condition: Nasal sinus aspergillosis\n\nSynonyms: Fungal sinusitis\n\nAssociations/Predisposing Factors: Immunocompromised (invasive fungal sinusitis), Anatomic abnormalities (mycetomas may occur after sinus surgery), Atopic patients (allergic fungal sinusitis)\n\nDemographics: \n\n -Mycetoma: Equal in race and gender, may occur at any age\n -Invasive Fungal Sinusitis: Typically immune compromised adults\n -Allergic fungal sinusitis: Most common in young adults. There is a slight male predominance.\n\nGross Pathology:\n -Mycetoma: Cheesy, semisolid mass\n -Invasive Fungal Sinusitis: Necrotic tissue\n -Allergic Fungal sinusitis: Brownish or green-black thick mucous with \"cottage cheese\" consistency\n\nHistology: \n -Mycetoma:Fungal hyphae that are tightly packed without allergic mucin. No tissue invasion. Calcification can be seen within.\n -Invasive fungal sinusitis: Invasion of mucosa and blood vessels by fungal hyphae. Mucormycosis is the other common organism.\n -Allergic fungal sinusitis: Non-invasive fungi along with eosinophils. Charcot-Leyden crystals are seen, which are needle-shaped crystalline structures that represent breakdown products of eosinophils. Other fungi that can also cause: Curvularia, Bipolaris, Fusarium, and Pseudallescheria.\n\nSpecial Stains: Gomori methenamine silver \n\n\n\nRadiology: \n\n-Invasive Fungal Sinusitis: In patients with invasive fungal sinusitis bone destruction and soft tissue invasion are seen (infiltration of periantral and retroantral fat). On CT bone erosion as well as complete or partial opacification of the affected sinus is seen. CT angiography may reveal vessel involvement (dissection, narrowing, occlusion). Variable signal is seen on T1 and T2. On post contrast imaging enhancement of the involved tissues is seen.\n\n-Allergic Fungal Sinusitis: On CT, allergic fungal sinusitis typically shows high density material within the sinuses. On MRI there is low T1 and T2 weighted signal in the sinuses. The peripheral inflamed mucosa will enhance on post contrast imaging.\n\n-Mycetoma: In patients who are otherwise healthy, occasionally a mycetoma may develop. This sometimes occurs afer the chang in the local sinus microenvironment, as can be seen after sinus surgery or radiation therapy. This involves one sinonasal cavity, and on CT is seen as a focal mass within the sinus lumen. It typically has areas of high density and may have calcification. The adjacent bone is thick and sclerotic as a result of chronic inflammation. After the administration of contrast, the inflamed mucosa at the periphery of the sinus may enhance. On MRI, a low signal mass on both T1 and T2 is seen within the sinus. Occasionally, on T2 the signal may be so low as to be mistaken for air.\n\nPrognosis and Treatment: \n-Mycetoma: Surgical excision curative\n-Invasive Fungal Sinusitis: Radical debridment, IV amphotericin B, with use of itraconazole as long-term suppressive treatment. Acute fungal sinusitis is life-threatening and can be lethal within a matter of hours. \n-Allergic Fungal Sinusitis: May be treated with topical and systemic antifungal agents along with topical steroids and saline irrigation. Also, may undergo surgical debridement.\n---------------------------------------------------------\neMedicine Topic - http://www.emedicine.com/ent/topic510.htm", "ACR Code": "2.7", "Category": "Infection, fungi", "Keywords": "sinusaspergillosisaspergilis", "Reference": "UpToDate: Fungal Sinusitis, by Dr. Gary Cox and Dr. John Perfect\n\nMukherji SK et al: Allergic fungal sinusitis: CT findings. Radiology. 207(2):417-22, 1998\n\nManning SC et al: Computed tomography and magnetic resonance diagnosis of allergic fungal sinusitis. Laryngoscope. 107(2): 170-6, 1997\n\nSiliverman CS et al: Periantral soft-tissue infiltration and its relevance to the early detection of invasive fungal sinusitis: CT and MR fingins. AJNR. 19(2):321-5, 1998.\n\nZinreich SJ et al: Fungal sinusits: Diagnosis with CT and MR imaging. Radiology. 169:439-44, 1988\n\nHarnsherger R et al. Diagnostic Imaging: Head and Neck. Amirsys.", "External Links": "www.utdol.com.gw3.lrc.usuhs.mil/utd/content/topic.do?topicKey=fung_inf/5646&selectedTitle=3~150&source=search_result" } }, { "U_id": "MPX1063", "TAC": [ "MPX1063_synpic22165", "MPX1063_synpic22166", "MPX1063_synpic22167" ], "MRI": [], "Case": { "Title": "thoracic aortic dissection", "History": "76 year-old woman with long history of hypertension, with acute-onset chest pain.", "Exam": "N/C", "Findings": "Multiple axial CT images of the chest with intravenous contrast material demonstrates a Stanford type A thoracic aortic dissection, with a clear intimal flap separating the true and false lumens of the ascending aorta. Additionally, the pericardium full of dense fluid, likely hemopericardium.", "Differential Diagnosis": "thoracic aortic dissection", "Case Diagnosis": "thoracic aortic dissection", "Diagnosis By": "confirmed during surgery", "Treatment & Follow Up": "Despite prompt surgical treatment, the patient did not survive the post-operative course. The patient passed away at post-operative day 3." }, "Topic": { "Title": "thoracic aortic dissection", "Disease Discussion": "Multidetector CT imaging, with faster acquisition of images and utilization of contrast-tracking/event-triggering protocols like CARE Bolus (Siemens) or SmartPrep (GE), is fast becoming the imaging modality of choice for many acute clinical settings such as trauma and the diagnoses of pulmonary embolism as well as aortic dissection. For the purposes of aortic dissection, the literature advocates at least a four-row CT scanner, with 150 ml dose of non-ionic contrast material intravenously at a rate of 3 ml/sec, with the region of interest for the event-triggering at the level of the thoracic descending aorta.\n\nAortic dissection is a life-threatening condition that is the most common cause of aortic emergency. Classification of aortic dissection can be via the DeBakey system, but a simpler Stanford system is now commonly used. Under the Stanford classification system, a dissection involving the ascending aorta is a type A and any dissection which is limited to the descending thoracic aorta (distal to the left subclavian artery origin) is a type B. Stanford type A dissections are treated surgically, as these have life-threatening complications such as hemopericardium, dissection which compromises the coronary artery ostia and subsequent massive myocardial infarcts, and severe acute aortic insufficiency causing heart failure and death. Stanford type B dissections, on the other hand, are typically more stable and can be treated medically with close surveillance.", "ACR Code": "9.9", "Category": "Vascular", "Keywords": "aortic dissection", "Reference": "1. Hatem Alkadhi, Simon Wildermuth, Lotus Desbiolles, Thomas Schertler, David Crook, Borut Marincek, and Thomas Boehm. Vascular Emergencies of the Thorax after Blunt and Iatrogenic Trauma: Multi\u2013Detector Row CT and Three-dimensional Imaging. RadioGraphics 2004; 24: 1239-1255. \n\n2. Eva Casta?er, Marta Andreu, Xavier Gallardo, Josep Maria Mata, Mar?a ?ngeles Cabezuelo, and Yolanda Pallard?. CT in Nontraumatic Acute Thoracic Aortic Disease: Typical and Atypical Features and Complications. RadioGraphics 2003; 23: 93-110." } }, { "U_id": "MPX1072", "TAC": [ "MPX1072_synpic34898", "MPX1072_synpic34899", "MPX1072_synpic34900" ], "MRI": [], "Case": { "Title": "Grave's Ophthalmopathy", "History": "45 year-old man with a past history of malignant testicular neoplasm and Hashimoto\u2019s thyroiditis, presents now with a several-month history of worsening eye swelling, dryness, and irritation, gradually progressing to lid retraction and intermittent blurry vision, prompting a referral to ophthalmology. He denies recent trauma, fever, chills, nausea, headaches.", "Exam": "PE: Bilateral proptosis, mild periorbital edema, sclera clear, PERRLA, EOMI, no discharge", "Findings": "\u2022 Bilateral proptosis and periorbital tissue edema\n\u2022 Enlarged inferior recti muscles\n\u2022 Increased periorbital fat distribution\n\u2022 Bellies of medial recti enlarged with normal tapering of tendons.\n\u2022 Enlarged superior, medial, inferior rectus muscles", "Differential Diagnosis": "\u2022 Periorbital / Orbital Cellulitis\n\u2022 Histiocytosis\n\u2022 Orbital Myositis / Orbital Pseudotumor\n\u2022 Grave\u2019s Orbitopathy\n\u2022 Lymphoma", "Case Diagnosis": "Grave's Ophthalmopathy", "Diagnosis By": "Clinical findings and CT images", "Treatment & Follow Up": "Treatment for Grave's ophthalmopathy depends on severity of symptoms. If present, treat hyperthyroidism with methimazole. For mild involvement including dry, irritated eyes, natural tears are helpful during the day and an eye lubricant (methycellulose) is appropriate at night. For moderate disease that can include conjunctival erythema, progressive proptosis, and diplopia, prednisone 30mg daily for 4 weeks should be initiated additionally. \n\nExternal radiation may be used in conjunction with prednisone if high dose is contraindicated or not tolerated in the case of persistent orbital edema. \n\nIn severe disease in which the patient presents with threatened loss or complete loss of vision, initial pulse therapy with intravenous methylprednisone or immediate intramuscular dexamethasone 4mg may be done before urgent orbital decompression surgery. Surgery is also indicated for refractory disease despite glucocorticoids or cosmetic correction of severe proptosis. \n\nThe orbit may be decompressed transantrally, which involves removal of medial wall and floor of the orbits. This procedure is preferred over others because it does not involve craniotomy or extensive scarring. \n \nFollow-up should include monthly clinic visits that may be progressively spaced out to 3 months, 6 months, or 12 months - depending on patient's clinical course and severity of disease. Regular follow-up with ophthalmology, endocrinology, and surgery as needed, particularly if patient has persistent or worsening symptoms, and especially if disease complications are anticipated.", "Discussion": "The patient has Grave\u2019s ophthalmopathy, but he does not have symptoms of hyperthyroidism such as heat intolerance, tachycardia, heart palpitations, tremors, anxiousness, and unintentional weight loss. Rather, he is clinically hypothyroid and requires synthroid treatment. With his past history of Hashimoto's thyroiditis and subsequent thyroid ablation therapy, the patient may have little functional thyroid tissue left for clinical manifestations of hyperthyroidism as a result of his Grave's disease. However, the thyroid stimulating hormone receptor (TSHR) autoantibodies are still circulating and affect other cell types with TSHR antigens such as fibroblasts, adipocytes, and T-cells contributing to tissue proliferation, inflammation and edema consistent with Grave's ophthalmopathy and pretibial myxedema." }, "Topic": { "Title": "Grave's Ophthalmopathy", "Disease Discussion": "Grave\u2019s ophthalmopathy (orbitopathy). Although rare, it can occur in 2% patients with a history of Hashimoto\u2019s thyroiditis. Grave\u2019s and Hashimoto\u2019s diseases are on opposite sides of the thyroid disease spectrum \u2014 manifesting hyperthyroid and hypothyroid symptoms, respectively. Both diseases can occur in the same person with variable temporal manifestations. However, the majority of ophthalmopathy cases correlate with Grave\u2019s disease.\n\nApproximately 10% of patients who have ophthalmopathy do not have clinical thyroid disease and are considered euthyroid, but do have elevated serum thyroid autoantibodies and thyroid-specific T-cells circulating. Within the remaining 90% who do have clinical thyroid disease, approximately 40% have ophthalmic presentation within 6 months after diagnosis of hyperthyroidism, 20% have concurrent clinical thyroid and ophthalmic disease presentation, and 20% have ophthalmic involvement prior to diagnosis of thyroid disease. Grave\u2019s orbitopathy affects about 16 women and 3 men in a population of 100,000 per year with men having greater severity of disease. \n\nRisk factors for development of Grave's ophthalmopathy are female, positive family history autoimmune diseases, smoking, age, and radioiodine therapy for Grave's hyperthyroidism (compared to surgery or antithyroid drugs). \n\nGrave\u2019s orbitopathy results in bilateral proptosis, lid retraction, chemosis, and vision changes in affected persons attributing to the increase in retroorbital connective tissue and extraocular muscle enlargement. Complications may involve corneal ulceration and infection due to loss of eye protection and lubrication.\n\nThe pathogenesis involves autoantibodies against thyroid stimulating hormone receptor (TSHR) antigens that can be found in the thyroid as well as in other tissues. It is unknown why retroorbital tissues are predominantly affected. Studies show that retroorbital fibroblasts and adipocytes express TSHR mRNA suggesting the mechanism of TSHR antibodies directly stimulating the fibroblasts and adipocytes resulting in increased production of glycosaminoglycans (GAGs) and fat tissue.\n\nAnother mechanism in the pathogenesis of Grave's ophthalmopathy involves T-cells that recognize self TSHR antigens as foreign. This autoimmune process stimulates T-cells to produce cytokines such as tumor necrosis factor (TNF) alpha and interferon gamma that recruit lymphocytes and create inflammation and edema within the orbit. Hence, there is lymphocytic infiltration of extraocular muscles and associated edema accounting for muscle belly enlargement. It is not known why the inferior recti are usually affected first, followed by the medial recti, then superior recti, and lastly the lateral recti, but this is a consistent finding.\n\nTreatment for Grave's ophthalmopathy depends on severity of symptoms. If present, treat hyperthyroidism with methimazole. For mild involvement including dry, irritated eyes, natural tears are helpful during the day and an eye lubricant (methycellulose) is appropriate at night. For moderate disease that can include conjunctival erythema, progressive proptosis, and diplopia, prednisone 30mg daily for 4 weeks should be initiated additionally. \n\nExternal radiation may be used in conjunction to prednisone if high dose is contraindicated or not tolerated in the case of persistent orbital edema. In severe disease in which the patient presents with threatened loss or complete loss of vision, initial pulse therapy with intravenous methylprednisone or immediate intramuscular dexamethasone 4mg may be done before urgent orbital decompression surgery. \n\nSurgery is also indicated for refractory disease despite glucocorticoids or cosmetic correction of severe proptosis. The orbit may be decompressed transantrally, which involves removal of medial wall and floor of the orbits. This procedure is preferred over others because it does not involve craniotomy or extensive scarring.", "ACR Code": "1.2", "Category": "Ophthalmology", "Keywords": "Graveorbitopathyophthalmopathy", "Reference": "Bahn RS; Heufelder AE. Pathogenesis of Graves' ophthalmopathy. N Engl J Med 1993 Nov 11;329(20):1468-75. \n\nBartley GB; et al. Chronology of Graves' ophthalmopathy in an incidence cohort. Am J Ophthalmol 1996 Apr;121(4):426-34. \n\nLyons CJ; Rootman J. Orbital decompression for disfiguring exophthalmos in thyroid orbitopathy. Ophthalmology 1994 Feb;101(2):223-30.\n\nMcGregor AM; et al. Effects of radioiodine on thyrotrophin binding inhibiting immunoglobulins in Graves' disease. Clin Endocrinol (Oxf) 1979 Oct;11(4):437-44.\n\nPerros P; et al. Age and gender influence the severity of thyroid-associated ophthalmopathy: a study of 101 patients attending a combined thyroid-eye clinic. Clin Endocrinol (Oxf) 1993 Apr;38(4):367-72. \n\nPrummel MF; Wiersinga WM. Smoking and risk of Graves' disease. JAMA 1993 Jan 27;269(4):479-82. \n\nShah, KJ; et al. Computed tomography of Grave\u2019s ophthalmopathy. Diagnosis, management, and posttherapeutic evaluation. Clin Imaging 1989 Mar;13(1):58-61.\n\nSpitzweg C; et al. Analysis of human thyrotropin receptor gene expression and immunoreactivity in human orbital tissue. Eur J Endocrinol 1997 Jun;136(6):599-607.\n\nStadlmayr W; et al. TSH receptor transcripts and TSH receptor-like immunoreactivity in orbital and pretibial fibroblasts of patients with Graves' ophthalmopathy and pretibial myxedema. Thyroid 1997 Feb;7(1):3-12." } }, { "U_id": "MPX1081", "TAC": [ "MPX1081_synpic24311" ], "MRI": [], "Case": { "Title": "Acute appendicitis", "History": "34 y/o WF w/ abdominal pain for past 30hrs. Pain started midepigastric and has moved slightly inferior and to the right. No radiation and no relief with oral meds. Has had nausea but no vomiting. Denies fevers, chills, melena, hematachezia, constipation, diarrhea. Anorexia for 30 hrs. No BM since pain began. LMP unknown.", "Exam": "Vitals: BP 130/75 P 95 T 99.9oF\nGen: well nourished and developed. MS: alert and oriented X3. Chest.Lungs: RRR no M/R/G CTA bil. AB: nondistended, TTP with guarding, no palpable masses, BS+. Ext: no cyanosis clubbing or edema.\nLabs: bHCG negative. WBC 13.2 H/H 14/40 plt 123 85%neutr. Amylase/lipase normal", "Findings": "CT scan abdomen: Positive \u201carrowhead sign\u201d in appendix. Presence of thickened appendix. Questionable appendicolith. Terminal ileum normal and seen with contrast, Good visualization of ileocecal juntion. Cecum normal size without evidence of edema.", "Differential Diagnosis": "Diff from History: Appendicitis, Ectopic pregnancy, Crohns Dz, Mesenteric adenitis\nDiff from viewing CT: Appendicitis from\u2026 lymphoprolifertation, apendicolith, cecal obstruction of proximal opening (cancer)", "Case Diagnosis": "Acute appendicitis", "Diagnosis By": "Surgery", "Treatment & Follow Up": "Emergent Laproscopic Appendectomy", "Discussion": "In the ED the patient clearly had a diffusely tender abdomen, with evidence of appendicitis. B-HCG was used to rule out ectopic preg and amylase and lipase were normal. Likely the patient clinical picture was not overtly obvious for appendicitis (while on paper it seems that way) or else a CT scan should not have been done. Her CT showed clear evidence of thickening in the appendix with fat stranding. In addition, there was a positive arrowhead sign, which is indicative of appendicitis. Finally, the terminal ileum was visible with contrast and showed no evidence of inflammation or changes. The most likely cause of appendicitis is lymphoproliferation (most common cause of appendicitis) or a fecolith. The path report is still pending." }, "Topic": { "Title": "Acute appendicitis", "Disease Discussion": "In the ED the patient clearly had a diffusely tender abdomen, with evidence of appendicitis. B-HCG was used to rule out ectopic preg and amylase and lipase were normal. Likely the patient clinical picture was not overtly obvious for appendicitis (while on paper it seems that way) or else a CT scan should not have been done. Her CT showed clear evidence of thickening in the appendix with fat stranding. In addition, there was a positive arrowhead sign, which is indicative of appendicitis. Finally, the terminal ileum was visible with contrast and showed no evidence of inflammation or changes. The most likely cause of appendicitis is lymphoproliferation (most common cause of appendicitis) or a fecolith. The path report is still pending.", "ACR Code": "7.2", "Category": "Clinical Exam Finding or Sign", "Keywords": "Acute appendicitisappendicitisfecolith", "Reference": "Way, Lawrence. Current Surgical Diagnosis and Treatment 11th Edition. McGraw Hill Co. 2003.\nKang, Peter MD. WRAMC Department of Radiology." } }, { "U_id": "MPX1075", "TAC": [ "MPX1075_synpic20513" ], "MRI": [], "Case": { "Title": "Typical Bronchial Carcinoid", "History": "66yo asymptomatic female with significant past smoking history and abnormal, incidental chest finding on routine EBCT.", "Exam": "Asymptomatic. Initial labs (CBC/Chem) WNL.", "Findings": "PA/Lat CXR: There is irregularity to the contour of the right hilum on the PA view. On the lateral view, there is a central, RML nodule which when going back to the PA, can barely be seen.\n\nAxial CT: Note the round, smooth nodule just anterior to the takeoff of the medial RML bronchus. There is no calcification, and no strong enhancement with intravenous contrast. The lesion does not appear to involve the bronchial lumen. \n\nCoronal CT reformation: Round nodule superior to the RML bronchus again demonstrated.", "Differential Diagnosis": "Hilar LAD\nPrimary Bronchial Neoplasm\nPrimary Lung Neoplasm\nMetastatic Disease", "Case Diagnosis": "Typical Bronchial Carcinoid", "Diagnosis By": "Confirmed by bronchoscopy and biopsy", "Treatment & Follow Up": "Patient is scheduled for lesion resection in August 2004.", "Discussion": "The location of this lesion is somewhat more peripheral than is usually seen with typical carcinoids. This carcinoid is also \"atypical\" in that it does not enhance, and is not calcified. The pathology, however, was consistent with a low-grade (typical) bronchial carcinoid. This patient fell into the 25% of patients who present asymptomatically with the lesion as an incidental finding on another study, which in this case was an EBCT." }, "Topic": { "Title": "Bronchial Carcinoid", "Disease Discussion": "Carcinoids are neuroendocrine neoplasms that are considered malignant based on potential for metastasis (15%)\u2014typically to the liver, bone, adrenals, and brain. While the vast majority of carcinoids arise in the GI tract (~90%), bronchial carcinoid accounts for 1-2% of all lung neoplasms. These lesions are classified from low grade (typical) to high grade (atypical). Both extremes have similar imaging features, with the majority of lesions being centrally located, well-defined, and round-to-ovoid in shape. Calcifications are common; there is no association with tobacco use. Typical age at presentation is wide, with a mean of 45 years, affecting males and females equally.\n\nApproximately 20% of bronchial carcinoids arise peripherally, distal to the segmental bronchi. The majority of these neoplasms are of the atypical subtype. Both typical and atypical subtypes can be associated with hilar and mediastinal lymphadenopathy; hyperplasia results from repeated post-obstructive infections or metastasis. Local nodal metastasis is more common in atypical carcinoids.\n\nGiven the majority of bronchial carcinoids arise within or adjacent to the central bronchi, the most common presenting symptoms are secondary to obstruction with resultant infection or air-trapping. The lesions tend to be vascular, and hemotypsis is the presenting symptom in ~50%. Up to 25% of patients are asymptomatic.\n\nPrognosis is dependent on the subtype, with typical carcinoids having 92% 5-year and 76% 15-year survival rates. Atypical lesions carry a somewhat more dismal 69% and 52% 5/15-year survival rate. Treatment is by surgical excision.", "ACR Code": "6.3", "Category": "Neoplasm, malignant (NOS)", "Keywords": "CarcinoidBronchi, NeoplasmBronchi, CT", "Reference": "Jeung MY, Gasser B, et al. Bronchial Carcinoid Tumors of the Thorax: Spectrum of Radiologic Findings. Radiographics 2002; 22:351-365." } }, { "U_id": "MPX1067", "TAC": [ "MPX1067_synpic16962" ], "MRI": [], "Case": { "Title": "Takayasu"s Arteritis", "History": "22 y.o. woman with hypertension.", "Findings": "ABDOMINAL AORTA: There is narrowing of the abdominal aorta, both above and below the renal arteries. The superior mesenteric artery is occluded at its origin, and not seen on the lateral view. There is a large Arc of Riolan from the IMA, which reconstitutes the SMA distribution. The celiac axis is patent, however, there is a 50% stenosis at the origin. There are single renal arteries bilaterally, both of which demonstrate stenoses. On the right, there is a long segment stenosis with approximately 50% narrowing. On the left, there is 60% to 70% stenosis at the origin of the vessel, extending to an early bifurcation, with an early upper pole branch. This is also stenotic at its origin.", "Differential Diagnosis": "\u2022 TAKAYASU\"S ARTERITIS\n\u2022 giant cell arteritis\n\u2022 syphilis, tuberculosis\n\u2022 SLE, rheumatoid arthritis\n\u2022 Buerger\u2019s disease\n\u2022 Kawasaki disease\n\u2022 Arteritis with spondyloarthropathies", "Case Diagnosis": "Takayasu\"s Arteritis", "Diagnosis By": "Imaging" }, "Topic": { "Title": "Takayasu's Arteritis", "Disease Discussion": "DEFINITION\nTakayasu\u2019s arteritis refers to a chronic systemic granulomatous vasculitis primarily affecting large arteries (aorta and its branches).\n\nSYNONYMS\nPulseless disease\nAortitis syndrome\nAortic arch arteritis\n\nEPIDEMIOLOGY & DEMOGRAPHICS\n\u2022 Most cases have been reported from Japan, China, India, and Mexico. \n\u2022 Exact incidence and prevalence is not known. \n\u2022 Incidence in the U.S. 2.6/1 million. \n\u2022 Females > males 9:1. \n\u2022 Seen predominantly in patients <30 yr old. \n\nWORKUP\nAny young patient with findings of absence pulses and loud bruits merits a workup for Takayasu\u2019s arteritis. The workup generally includes blood testing to look for signs of inflammation and imaging studies with the angiogram being the diagnostic gold standard.\n\nLABORATORY TESTS\n\u2022 CBC may reveal an elevated WBC count \n\u2022 ESR is elevated in active disease \nIMAGING STUDIES\n\u2022 Ultrasound: Carotid, thoracic, and abdominal ultrasound are useful adjunctive imaging studies in diagnosing occlusive disease resulting from Takayasu\u2019s arteritis ( Fig. 1-358 ). \n\u2022 Doppler and noninvasive upper and lower extremity studies are helpful in assessing blood flow and absent pulses. \n\u2022 CT scan is used to assess the thickness of the aorta. \n\u2022 Angiogram can show narrowing of the aorta and/or branches of the aorta, aneurysm formation, and poststenotic dilation. \n\n\nAngiographic findings are classified as four types: \nType I: Lesions involve only the aortic arch and its branches. \nType II: Lesions only involving the abdominal aorta and its branches. \nType III: Lesions involving the aorta above and below the diaphragm. \nType IV: Lesions involving the pulmonary artery. \n\n\nPEARLS & CONSIDERATIONS\nCOMMENTS\nOverall the long-term prognosis of treated patients with Takayasu\u2019s disease is good, with >90% of patients surviving more than 15 yr.", "ACR Code": "9.2", "Category": "Inflammatory, non-infectious", "Keywords": "takayasu's \r\ntakayasuarteritisvasculitis", "Reference": "Arend WP et al: American College of Rheumatology 1990 criteria for the classification of Takayasu\u2019s arteritis, Arthr Rheum 33:1129, 1990. \n\nIshikawa K, Maetani S: Long-term outcome for 120 Japanese patients with Takayasu\u2019s disease: clinical and statistical analyses of related prognostic factors, Circulation 90:1855, 1994. \n\nKerr GS et al: Takayasu arteritis, Ann Intern Med 120:919, 1994. \n\nMD consult: www.mdconsult.com" } }, { "U_id": "MPX1073", "TAC": [ "MPX1073_synpic16494", "MPX1073_synpic16495" ], "MRI": [], "Case": { "Title": "biliary leak, status post laparoscopic cholecystectomy", "History": "s/p recent laparoscopic cholecystectomy, now with fevers and abdominal pain", "Exam": "fever\nright upper quadrant abdominal tenderness", "Findings": "Axial CT with intravenous and oral contrast material demonstrates a large fluid collection predominantly within the porta hepatis around multiple surgical clips consistent with prior cholecystectomy. More fluid is seen around the right lobe of the liver and more inferiorly within the right paracolic gutter. Peritoneal fat around the fluid collection demonstrates stranding suggestive of inflammation.\n\nPlanar and SPECT images after the administration of Tc99m-disofenin IV demonstrates large amount of abnormal radiotracer accumulation within the area corresponding to the large fluid collection seen on the CT images, consistent with a biliary leak. Note that a tubular area of radiotracer uptake leading from the large collection apparently outside the body is the collection within the percutaneous drainage tube placed prior to the scintigraphic study.", "Differential Diagnosis": "biliary leak, status post laparoscopic cholecystectomy", "Case Diagnosis": "biliary leak, status post laparoscopic cholecystectomy" }, "Topic": { "Title": "biliary leak, status post laparoscopic cholecystectomy", "Disease Discussion": "Laparoscopic cholecystectomy (LC) has replaced open cholecystectomy for most routine treatment of gallbladder disease by cholecystectomy due to clear advantages associated with any laparoscopic procedures, namely shortened inpatient stays, smaller incisions yielding better cosmetic results and requiring smaller amounts of pain medication, better pulmonary toilet due to better pain control, and so on. (1, 2) Early days of LC demonstrated a higher incidence of bile duct injuries and biliary leak, and initially this phenomenon was attributed to the \"learning curve\", but there is increasing evidence that the \"learning curve\" may not be entirely the reason why this is so. (2)\n\nIn the literature, biliary leaks after LC occur in approximately 1% of patients. In a series of 64 patients with leaks addressed with endoscopic evaluation (ERCP), the vast majority of the leaks (50) were from the cystic duct. Other places of biliary leaks were the ducts of Luschka (4), common bile duct (6), and common hepatic duct (4). (5)\n\nScintigraphic evaluation of patients with potential biliary leaks after LC has been clearly established in the literature (3, 4). Other anatomic modalities such as US or CT can demonstrate a fluid collection, and a bile leak can be suggested from history, but it would be difficult to actually demonstrate a leak via purely anatomic studies alone. Scintigraphic evaluation with an agent such as Tc99m-disofenin, as in this case, will clearly demonstrate whether or not the fluid collection is indeed a leakage of bile from the biliary system.\n\nTreatment of biliary leaks in this setting can be done by percutaneous drainage, but the literature demonstrates increasing use of endoscopic evaluation, sphincterotomy, and possible stent placement. The rationale is that by decreasing the resistance of the normal flow through the common bile duct and into the duodenum, the biliary leak will, in time, close itself. Percutaneous drainage may be appropriate for patients with possible infection of the bile collection within the peritoneal cavity, which was suspected in this case. (1, 2, 5)", "ACR Code": "7.9", "Category": "Iatrogenic or Surgical (complications)", "Keywords": "laparoscopic cholecystectomybiliary leakbiliary scintigraphy", "Reference": "1. Rossi P, et al. Bile leak from the hepatic bed after laparoscopic cholecystectomy. Chir Ital. 2002 Jul-Aug;54(4): 507-9. (treatment with endoscopic sphincterectomy and stent placement)\n2. Slater K, et al. Iatrogenic bile duct injury: the scourge of laparoscopic cholecystectomy. ANZ J Surg. 2002 Feb;72(2)83-8.\n3. Estrada WN, et al. Scintigraphic evaluation of postoperative complications of laparoscopic cholecystectomy. J Nucl Med. 1991 Oct;32(10): 1910-1.\n4. Gentili A, et al. Scintigraphic detection of bile leaks after laparoscopic cholecystectomy. Clin Nucl Med. 1993 Jan;18(1): 1-6.\n5. De Palma GD, et al. Leaks from laparoscopic cholecystectomy. Hepatogastroenterology. 2002 Jul-Aug;49(46): 924-5." } }, { "U_id": "MPX1060", "TAC": [ "MPX1060_synpic19246" ], "MRI": [ "MPX1060_synpic19251" ], "Case": { "Title": "L parietal ischemic infarct", "History": "74 yo WF with Diabetes and HTN, S/P cystectomy, TAH/RSO and ventral hernia now with acute mental status changes 2 days post op. On first night postop, patient had a one-hour episode of hypotension (SBP 80-90)", "Exam": "Tachycardia, difficulty with word finding, ideomotor apraxia and confusion.", "Findings": "Noncontrast CT shows hypodensity in L parietal lobe with no visible compression of other structures. No hyperdens or hemorrhagic areas are noted.\n\nMRI DWI image shows hyperintense signal within same area demonstrating restricted diffusion of water molecules.", "Differential Diagnosis": "Ischemic infarction of L parietal lobe with no evidence of hemorrhagic nature.", "Case Diagnosis": "L parietal ischemic infarct", "Diagnosis By": "Radiologic diagnosis", "Treatment & Follow Up": "Transfusion with PBRC\u2019s, IVF, Aspirin 325 mg po qd, Carotid Doppler US, TTE, started heparin drip at 700 units/hr. Repeat CT in 48 hrs to rule out hemorrhagic conversion as patient is starting heparin drip. Speech therapy and swallow test to assure no possibility of aspiration. MRA can be used to visualize the vasculature and determine if nature of infarct was thrombotic or embolic." }, "Topic": { "Title": "Stroke, ischemic infarction", "Disease Discussion": "CT has been recognized as the standard of care for initial imaging of suspected strokes. It is able to discriminate between an ischemic vs a hemorrhagic cerebral infarct. However, it may be relatively less sensitive during the first 12 hours and is not consistently high until after 24 hrs.\n\nMRI may be needed - especially with Diffusion Weighted Imaging has been studied as a predictor of early edema due to cytoxicity to neural cells. If edema is present, a hyperintense signal will be present in the affected area due to restricted diffusion of water molecules. For the same reason, these areas will have correspondingly low signal on ADC (Apparent Diffusion Coefficient) images.", "ACR Code": "1.7", "Category": "Infarction and/or Necrosis", "Keywords": "ischemicinfarct", "Reference": "Chung et al; \u201cDiffusion-weighted MRI of intracerebral hemorrhage clinically undifferentiated from ischemic stroke\u201d; American Journal of Emergency Medicine; May 2003, 21(3) ." } }, { "U_id": "MPX1106", "TAC": [ "MPX1106_synpic45737" ], "MRI": [ "MPX1106_synpic45735", "MPX1106_synpic45736" ], "Case": { "Title": "Atypical Pulmonary Hamartoma", "History": "58 yo man presented with neck pain to his primary care physician. An MRI of the cervical spine was obtained revealing an abnormal finding.", "Findings": "T2 weighted axial MR image reveals a well-marginated mass with smooth borders in the left lung at the level of the aortic arch, which demonstrates multiple small foci of increased T2 signal intensity, giving the mass a speckled appearance.\n\nContrast enhanced axial CT image shows a homogeneous, well-marginated, solid mass with minimal contrast enhancement in the left upper lobe. No fat or calcification is evident.", "Differential Diagnosis": "\u2022 Tuberculoma\n\u2022 Metastatic Disease\n\u2022 Carcinoid Tumor\n\u2022 Adenocarcinoma\n\u2022 Small-cell carcinoma\n\u2022 Pulmonary hamartoma", "Case Diagnosis": "Atypical Pulmonary Hamartoma", "Diagnosis By": "Patient underwent biopsy, with histological evaluation.", "Discussion": "The biopsy demonstrated cartilage lobules without intervening stroma, and sparse cellularity. Additionally, respiratory epithelium was visualized lining the margin of the mass and invaginating into the mass forming multiple small cystic areas, with fat tissue intermixed within adjacent respiratory epithelium, consistent with chondromatous hamartoma." }, "Topic": { "Title": "Pulmonary Hamartoma", "Disease Discussion": "Lesions/Condition: Pulmonary Hamartoma\n\nPredisposing Factors:\n\nMost commonly occurs in the fourth to fifth decade. Most common chromosomal abnormality involves the q13-q15 region of chromosome 12.\n\nSymptoms:\n\nMost patients presenting with peripheral pulmonary hamartomas are asymptomatic. When symptomatic, hemoptysis is the most common presenting symptom.\n\nDiscussion: \n\nPulmonary hamartomas are benign neoplasm with 90% arising within the lung parenchyma, and are usually in a peripheral location. They comprise approximately 5% of all solitary pulmonary nodules. Pulmonary Hamartomas contain cartilage surrounded by fibrous connective tissue with variable amounts of fat, smooth muscle, and seromucous glands. Approximately 30% contain calcium in the form of multiple clumps (\u2018popcorn\u2019 calcification). \n\nGenerally, pulmonary hamartomas can be observed by CT alone. Indications for transthoracic biopsy or resection are rapid growth, a size greater than 2.5 cm, or new pulmonary symptoms. \n\nRadiology:\n\t\nChest Radiographs:\nWell-circumscribed, smoothly marginated solitary nodule without lobar predilection. Most pulmonary hamartomas are smaller than 4 cm in diameter. Calcification is visible in less than 10% of cases.\n\nCT:\nWell-circumscribed nodule with a smooth or lobulated border.\nComposed entirely of fat, a mixture of fat and soft tissue, or fat and calcification. Calcification when present is in the form of multiple clumps of calcium dispersed throughout the lesion (\u201cpopcorn\u201d calcification)", "ACR Code": "6.3", "Category": "Neoplasm, benign", "Keywords": "Pulmonary HamartomaBenign Neoplasm of the LungPopcorn Calcification", "Reference": "Brant W., Helms C. Fundamentals of Diagnostic Radiology. 2nd Edition. Lippincott Willliams & Wilkins. Philadelphia, PA 1999.\n\nFraser et al. Synopsis of Diseases of the Chest. Third Edition. Elsevier Saunders. Philadelphia, PA. 2005." } }, { "U_id": "MPX1086", "TAC": [ "MPX1086_synpic25218" ], "MRI": [ "MPX1086_synpic25219", "MPX1086_synpic25220", "MPX1086_synpic25221", "MPX1086_synpic25222", "MPX1086_synpic25224" ], "Case": { "Title": "Pilocytic astrocytoma", "History": "His mother provides a history of increasing headaches over past month, gait disturbances, and possible seizure activity.", "Exam": "No metabolic abnormality.", "Findings": "Large, solid mass in the left cerebellar hemisphere with ill-defined margins and significant surrounding T2 signal abnormality representing vasogenic edema. This exerts mass effect upon and displaces the 4th ventricle. Mild hydrocephalus. Diffuse, heterogeneous enhancement following IV gadolinium infusion. CT scan demonstrates a notably low attenuation mass, and inferior displacement of the cerebellar tonsils to the level of the foramen magnum.", "Differential Diagnosis": "\u2022 Astrocytoma (pilocytic or fibrillary)\n\u2022 Ependymoma\n\u2022 Medulloblastoma", "Case Diagnosis": "Pilocytic astrocytoma", "Diagnosis By": "Surgical resection and pathology", "Treatment & Follow Up": "Resection, if complete, is usually sufficient. It has not yet been decided if this patient will undergo additional Tx.", "Discussion": "The mass arises from the left cerebellar hemisphere and not the 4th ventricle, and is hypodense on CT. These findings make medulloblastoma far less likely. A mass entirely outside the ventricle makes ependyoma less likely. While pilocytic astrocytomas (PA) are usually cystic with an enhancing mural nodule, this case represents the less common solid variant. Approximately 85% of posterior fossa astrocytomas in childhood are pilocytic - the remainder are fibrillary-diffuse. Pilocytic astrocytomas are WHO Grade 1; whereas fibrillary may be Grade 2-4. Enhancement in PA is almost universal. Enhancement in diffuse astrocytoma is associated with vascular changes and a higher tumor grade - either Grade 3 or Grade 4.\n\nClick here to see other Pilocytic Astrocytomas:\nhttp://rad.usuhs.mil/medpix/medpix.html?mode=image_finder&action=search&srchstr=pilocytic%20astrocytoma&srch_type=all#top\n\nClick here to see Medulloblastoma:\nhttp://rad.usuhs.mil/medpix/medpix.html?mode=image_finder&action=search&srchstr=medulloblastoma&srch_type=all#top\n\nClick here to see Ependymoma:\nhttp://rad.usuhs.mil/medpix/medpix.html?mode=image_finder&action=search&srchstr=ependymoma&srch_type=all#top" }, "Topic": { "Title": "Cerebellar astrocytoma (pilocytic astrocytoma)", "Disease Discussion": "Cerebellar astrocytoma accounts for about 11 - 30% of primary CNS tumors in children, and has a post-resection survival of up to 94% at 10 years. This tumor makes up about one-third of childhood posterior fossa tumors, typically presenting late in the first decade or in the early second decade. These well-circumscribed masses are often completely resected surgically, with no other therapy required.\n\nCerebellar astrocytoma tends to involve the hemispheres, although extension into or origin within the vermis or even the fourth ventricle have been described infrequently. It may be predominantly cystic with a mural nodule (as shown in a different patient, Film .4), multicystic, or predominantly solid (diffuse) on CT or MR. Recognizable cysts occur in up to 80%. Histologically, most are juvenile pilocytic astrocytomas similar to those of the third ventricle region. Diffuse infiltrating fibrillary types occur in up to 15% of cerebellar astrocytomas and have a less favorable prognosis. Frank malignancy, leptomeningeal seeding, and spontaneous hemorrhage are distinctly unusual.\n\nRadiographically, cerebellar astrocytoma arises within the cerebellar hemisphere and less often in the vermis, and displaces the fourth ventricle without invading it. On CT, 10-25% contain foci of calcification. The mass is hypointense on T1-weighted and hyperintense on T2-weighted MR, with one or more cystic components. After contrast administration, the mural nodule and/or solid components enhance, rendering nonenhancing cysts more conspicuous.\n\nIn children, vermian or diffuse astrocytoma or those involving the fourth ventricle may mimic medulloblastoma or ependymoma. In older adolescents or adults, hemangioblastoma may present as a cystic mass indistinguishable from cerebellar astrocytoma. Metastasis is the most common posterior fossa neoplasm in adulthood. Rarely vascular malformation, abscess, or lymphoma might have a similar radiographic appearance.", "ACR Code": "1.3", "Category": "Neoplasm, glial" } }, { "U_id": "MPX1117", "TAC": [ "MPX1117_synpic15330" ], "MRI": [], "Case": { "Title": "Cerebral infarct, PCA territory, bilateral", "History": "Sudden onset of blindness in both eyes", "Exam": "Pupils react to light, but patient cannot see", "Findings": "Bilateral occipital lesions of abnormal decreased attenuation", "Case Diagnosis": "Cerebral infarct, PCA territory, bilateral" }, "Topic": { "Title": "Cerebral infarct", "Disease Discussion": "Thromboembolic disease is, by far, the most common cause of acute stroke accounting for 4 out of 5 patients who present with cerebral infarct. Cerebral hemorrhage is the next most common with almost 1 in 5 patients. Venous occlusive disease is the next, but much less frequent than the previous mentioned etiologies.\n\nThe two most common causes of thromboembolic disease are atherosclerosis and cardiac origin. Atherosclerosis follows a typical distribution of accumulation within the arterial distribution of the brain. The internal carotid artery is first, then the distal basilar artery, carotid siphon, and middle cerebral artery. The parts of the brain perfused by the middle cerebral artery and basilar artery are most vulnerable to infarct due both the region of atherosclerotic disease and flow patterns that cause more proximal sources of thrombus to favor those vessels.\n\nThe first patient\u2019s infarct is due to occlusion of penetrating vessels of the right middle cerebral artery. Likely the lenticulostriates which supply the lentiform nucleus, caudate capsule, and internal capsule, as well as the thalamoperferators were affected. These types of strokes, when smaller than 15mm, are called lacunar infarcts and they account for 20% of all strokes. Patients with lacunar infarcts can present with a pure motor hemiparesis like this patient or a pure hemisensory deficit, hemiparetic ataxia, dysarthria, or hand deficit.\n\nCT examination early in the course of an acute stroke can be negative and cannot exclude this diagnosis. Stroke in the emergent setting is more a clinical diagnosis and if suspected, imaging with MR is prudent. CT, CTA, MR, and diffusion-perfusion imaging can be useful in management decisions regarding thrombolysis.", "ACR Code": "1.9", "Category": "Hypoxic or Ischemic", "Keywords": "Cerebral ischemiainfarctthromboembolic disease", "Reference": "Osborn, AG. Diagnostic neuroradiology; 1994" } }, { "U_id": "MPX1108", "TAC": [ "MPX1108_synpic16234" ], "MRI": [ "MPX1108_synpic16232" ], "Case": { "Title": "vertebra plana", "History": "39 y/o non-smoking female presenting with back pain for two months. No history of fever or weight loss.", "Findings": "-CT/MRI: There is vertebra plana of L5, with edema and enhancement of the remaining marrow into the posterior elements. There is displacement of the thecal sac posteriorly by the extruded bony fragments.\n\n-RADIOGRAPH/CT:\nLeft upper lobe lung mass with numerous bilateral pulmonary nodules, consistent with metastatic disease.", "Differential Diagnosis": "-Multiple myeloma\n-Metastatic disease\n-Langerhans cell histiocytosis \n-Lymphoma, leukemia\n-Trauma\n-Infection", "Case Diagnosis": "vertebra plana" }, "Topic": { "Title": "vertebra plana", "Disease Discussion": "Marked flattening of a vertebral body is termed vertebra plana.\nLangerhans cell histiocytosis is the most common cause of vertebra plana. Other disease processes should be considered in the differential diagnosis if the clinical situation warrants. Other causes of vertebra plana include:\n\u2022 multiple myeloma\n\u2022 metastatic disease\n\u2022 Ewing sarcoma\n\u2022 lymphoma\n\u2022 leukemia\n\u2022 Gaucher disease\n\u2022 aneurysmal bone cyst\n\u2022 trauma\n\u2022 infection\n\nBecause most lesions spontaneously regress, vertebra plana is often treated conservatively. In young patients, vertebral height typically is partially restored with growth of the skeleton. Temporary bracing may help to relieve symptoms.\n\nRadiation may be indicated for treatment of mild neurologic signs. Surgical decompression and fusion with instrumentation is indicated for rapidly progressive neurologic signs or cord compression that is not responsive to radiation.", "ACR Code": "3.3", "Category": "Neoplasm, carcinoma", "Keywords": "VERTEBRAPLANA", "Reference": "Canale: Campbell's Operative Orthopaedics, 10th ed., Copyright \u00a9 2003 Mosby, Inc." } }, { "U_id": "MPX1109", "TAC": [ "MPX1109_synpic28526" ], "MRI": [], "Case": { "Title": "Achalasia", "History": "33 year-old woman with shortness of breath and dyspnea on exertion.", "Exam": "N/A", "Findings": "Frontal chest radiograph demonstrated a wideneded mediastinum on the right side, which on the lateral chest radiograph was a mass within the middle mediastinum superiorly and crossed into the posterior mediastinum inferiorly.\n\nNon-contrast CT examination of the chest demonstrates a diffusely dilated esophagus filled with mottled soft tissue consistent with ingested food material.\n\nImaged from an upper GI fluoroscopic examination demonstrates a dilated thoracic esophagus with a focal narrowing at the gastroesophageal junction. A complete lack of peristalsis was noted during the examination.", "Differential Diagnosis": "Primary achalasia\nSecondary achalasia\nObstructing gastric or distal esophageal mass\nEsophageal stricture", "Case Diagnosis": "Achalasia", "Diagnosis By": "Upper GI fluoroscopic examination.", "Treatment & Follow Up": "This patient subsequently underwent ballon dilations of the lower esophageal sphinter.", "Discussion": "Please see topic for discussion, and note that this patient is the same as that of ID# 8959 with additional images submitted in the interim." }, "Topic": { "Title": "Achalasia", "Disease Discussion": "Clinical symptoms include dysphagia, foul breath, regurgitation and/or aspiration. The condition is usually insidious, developing between age 30-50, and is likely due to a defect in esophageal innervation, with impairment or absence of ganglion cells in Auerbach's Plexus. \n Radiographically, abnormal peristalsis (often completely absent) and abnormal LES opening are seen with barium swallows. Barium remains above the LES until pressure (hydrostatic or nonperistaltic contractions) wedges the LES open. When this occurs, the barium column appears as an elongated \"V\" or \"bird beak\" yet latter term is not specific for achalasia.\n Upper endoscopy is necessary to rule out a benign or malignant stricture. Failure of LES relaxation is confirmed by esophageal manometry that also reveals complete absence of contractile activity, referred to as aperistalsis (\u201cclassic achalasia\u201d) or persistent spastic contractions (\u201cvigorous achalasia\u201d).\n Treatment options aim to relax the LES, and include medicines (smooth muscle relaxants), balloon dilation (70-80% success, often requires re-dilation, risk of perforation), or surgical myotomy of the LES (now often done laparascopically, and combined with antireflux surgery.)", "ACR Code": "7.0", "Category": "Physiology", "Keywords": "achalasiaLESesophagus", "Reference": "Alimentary Tract Radiology,Third Edition 1983 C.V. Mosby Co. Alexander Margulis, Joachim Burhenne\nRakel: Conn's Current Therapy 2002, 54th ed., W. B. Saunders Company" } }, { "U_id": "MPX1121", "TAC": [ "MPX1121_synpic41016" ], "MRI": [], "Case": { "Title": "Lung Metastasis", "History": "57yo F with 1 mo cough presents for f/u CXR. CXR 1 mo ago showed interstitial infiltrates and was prescribed abx. PMH includes colon cancer \u2013 dx 5y ago as stage 2 with hepatic metastases.", "Findings": "Numerous, scattered, small masses", "Differential Diagnosis": "Malignancy (primary, metastatic)\nInflammation/Granulomatous dz\nBenign neoplasm \nCongenital abn", "Case Diagnosis": "Lung Metastasis", "Discussion": "15-20% of colon cancer patients have distant metastases at time of presentation. Spread is via lymphatic or hematogenous dissemination, or continguous spread. Liver is the frequent site of metastases, as the portal vein is the primary drainage for the intestinal tract; other common sites of metastases include lungs, lymph nodes, peritoneum; more rare sites include brain and bone. 5yr survival 50-75% dependent upon stage at presentation." }, "Topic": { "Title": "Lung Metastasis", "Disease Discussion": "Cancers can metastasize to the lungs by several pathways. Most commonly, cancers spread to the lungs via pulmonary arteries or lymphatic channels. Less often, spread is by direct extension or endobronchial spread. Cancers that commonly metastasize to the lungs include: prostate, breast, renal, thyroid, testicle, gastrointestinal, melanoma, and sarcomas. \nRadiograpically metastases tend to be multiple (95%). They are more often in the lung periphery and bases. Typically they have sharp margins. They can cavitate, particularly squamous cell carcinomas. Some may have calcifications.", "ACR Code": "6.3", "Category": "Neoplasm, metastatic", "Keywords": "MetastasisBladder Cancer", "Reference": "Primer of Diagnostic Imaging" } }, { "U_id": "MPX1120", "TAC": [ "MPX1120_synpic24332" ], "MRI": [], "Case": { "Title": "Sialolithiasis resulting in Sialoadenitis", "History": "Hx not provided", "Exam": "Physical exam not provided", "Differential Diagnosis": "Sialolithiasis resulting in Sialoadenitis", "Case Diagnosis": "Sialolithiasis resulting in Sialoadenitis", "Treatment & Follow Up": "Augmentin, fluids and sour candies. Follow up in 7 days.", "Discussion": "Sialolithiasis is an accumulation of hardened deposits in the salivary ducts. The most common site of occurrence is in the submandibular (Warthon\u2019) duct which accounts for about 80% of all salivary duct stones.1 The large majority of cases occur in patients over 30 years of age with rare occurrences in children. The exact etiology of stone formation in the salivary ducts remains uncertain however it is believed to be the result from trauma, inflammation of the ductal epithelium or other processes which slow the movement of saliva down the salivary ducts resulting in stagnation. Patients typically present complaining of neck swelling and colicky pain, though this patient denied pain. Diagnosis is achieved through direct palpation of the stone and imaging which should include CT with contrast or ultrasound. Sialolithiasis often leads to Sialoadenitis, which is inflammation of salivary gland, caused by granulomatous processes or more typically in the case of Sialolithiasis infection caused by bacterial migration up the obstructed duct. Staphylococcus, Streptococcus viridans and S. pneumoniae are usually implicated in the infection. 2 Treatment is with broad spectrum antibiotics, sialogogues (sour candy to promote salivation), massage, manual removal of stones near the orifice. 1(p1239),2(p935) Failure of these treatments should prompt consideration of surgical intervention, which is not considered first line treatment due to the high incidence of post-operative stricture formation and resulting predisposition for chronic Sialoadenitis.1(p1240" }, "Topic": { "Title": "Sialolithiasis resulting in Sialoadenitis", "Disease Discussion": "Sialolithiasis is an accumulation of hardened deposits in the salivary ducts. The most common site of occurrence is in the submandibular (Warthon\u2019) duct which accounts for about 80% of all salivary duct stones.1 The large majority of cases occur in patients over 30 years of age with rare occurrences in children. The exact etiology of stone formation in the salivary ducts remains uncertain however it is believed to be the result from trauma, inflammation of the ductal epithelium or other processes which slow the movement of saliva down the salivary ducts resulting in stagnation. Patients typically present complaining of neck swelling and colicky pain, though this patient denied pain. Diagnosis is achieved through direct palpation of the stone and imaging which should include CT with contrast or ultrasound. Sialolithiasis often leads to Sialoadenitis, which is inflammation of salivary gland, caused by granulomatous processes or more typically in the case of Sialolithiasis infection caused by bacterial migration up the obstructed duct. Staphylococcus, Streptococcus viridans and S. pneumoniae are usually implicated in the infection. 2 Treatment is with broad spectrum antibiotics, sialogogues (sour candy to promote salivation), massage, manual removal of stones near the orifice. 1(p1239),2(p935) Failure of these treatments should prompt consideration of surgical intervention, which is not considered first line treatment due to the high incidence of post-operative stricture formation and resulting predisposition for chronic Sialoadenitis.1(p1240)", "ACR Code": "2.6", "Category": "Endocrine", "Keywords": "Sialolithiasischronic Sialoadenitissalivary ducts", "Reference": "1. Cummings: Otolaryngology: Head and Neck Surgery, 3rd ed, Copyright 1998 Mosby-Year Book Inc.; 1238-1240.\n2. Marx: Rosen\u2019s Emergency Medicine: Concepts and Clinical Practice, 5th ed., Copyright 2002 Mosby, Inc; 935." } }, { "U_id": "MPX1118", "TAC": [ "MPX1118_synpic17090" ], "MRI": [ "MPX1118_synpic17088", "MPX1118_synpic17089" ], "Case": { "Title": "Stress fracture Tarsal Navicular Bone", "History": "21 y.o. female long distance runner presents with a several week history of pain along the dorsum of the foot. The pain is exacerbated by running.", "Exam": "Tenderness to palpation along the dorsal aspect of the foot.", "Differential Diagnosis": "-Fracture\n-Stress fracture", "Case Diagnosis": "Stress fracture Tarsal Navicular Bone", "Treatment & Follow Up": "The stress fracture went on to completion and required internal fixation.", "Discussion": "This patient presented with the typical history of pain with running. The AP radiograph (not shown) does demonstrate a short first metatarsal and a long second metatarsal, which is a risk factor for this specific stress injury. CT and MRI were diagnostic of the tarsal navicular stress fracture." }, "Topic": { "Title": "Stress fracture Tarsal Navicular Bone", "Disease Discussion": "Stress fractures occur when normal bone is subjected to abnormal stress or repetitive stress, and they typically occur in athletes who have either recently changed their type of training or have increased their level of training. Bone is a very dynamimc tissue that continuously remodels as a result of altering stresses. Repetitive stress overload results in an imbalance of bone remodeling. The abnormal level of stress results in the bone resorption exceeding the rate of bone repalcement leading to a weakening of the bone. There is a continuum of injury beginning with weakening of the bone, fatigue, stress fracture and finally, complete fracture of the involved bone.\n\nStress injuries of bones are very common among athletes and can occur in nearly any bone, however, the vast majority of stress injuries occur in the bones of the lower extremity. Tarsal navicular stress fractures typically occur in elite athletes, including runners, basketball players, gymnasts, and football players. Those athletes that play on artificial turf seem to be at an increased risk for stress fractures of the tarsal navicular bone.\n\nThe diagnosis of tarsal navicular stress fracture is often delayed many weeks to months because the onset of symptoms are insidious and in addition, the diagnosis is often difficult to make on conventional radiographs. Patients usually present with pain along the dorsal aspect of the foot which is made worse by running or jumping. Tarsal navicular stress fractures are usually treated with casting and athletes typically return to full activity within 5 to 6 months. If a complete fracture occurs, the individual may require internal fixation, which can delay return to normal activity.\n\nMost tarsal navicular stress fractures occur in the middle third of the navicular bone, which is a relatively avascular portion of the bone. The fracture may be complete or incomplete, however the incomplete fractures tend to begin along the dorsal aspect of the bone adjacent to the talonavicular joint. Foot anomalies can be associated with stress fractures of the tarsal navicular. This injury is most often seen in individuals that have a short first metatarsal or long second metatarsal. This is thought to result in increased shear forces being transmitted along the second metatarsal through the middle cunieform and into the middle third of the navicular bone.\n\nEvaluation of a suspected stress injury of the tarsal navicular should begin with radiographs of the foot, however this area of the navicular is difficult to visualize on radiographs and MR or CT is often required to correctly establish the diagnosis.", "ACR Code": "4.4", "Category": "Sports Medicine", "Keywords": "stress fracturetarsal navicularfoot", "Reference": "Spitz DJ, Newberg AH. Imaging of stress fractures in the athlete. Magn Reson Imaging Clin N Am. 11(2003) 323-339." } }, { "U_id": "MPX1114", "TAC": [ "MPX1114_synpic19630", "MPX1114_synpic19631", "MPX1114_synpic19632" ], "MRI": [], "Case": { "Title": "Sarcoid", "History": "36 year-old Caucasian man with worsening shortness of breath, exercise intolerance and fatigue. Referred to pulmonary for evaluation.", "Findings": "CXR and CT demonstrate nodular interstitial lung disease with multiple superimposed pulmonary masses/nodules. Significant mediastinal and hilar lymphadenopathy are seen. Numerous splenic and renal nodules are also present.", "Differential Diagnosis": "Sarcoid\nLymphoma\nLymphangitic Carcinomatosis", "Case Diagnosis": "Sarcoid", "Diagnosis By": "Biopsy confirmed.", "Treatment & Follow Up": "Unavailable." }, "Topic": { "Title": "Sarcoid", "Disease Discussion": "Sarcoidosis is a multisystem granulomatous disorder of unknown etiology characterized by the presence of noncaseating granulomas in several affected organs. It is typically a disease of young adults, with a peak incidence in the third decade. The diagnosis is suggested by a combination of consistent clinical and radiological findings along with the presence of some nonspecific features such as depressed delayed-type hypersensitivity, abnormal immunoglobulins, hypercalcaemia, and elevated serum angiotensin-converting enzyme. It can be confirmed by biopsy evidence of widespread noncaseating granulomas. Pulmonary involvement accounts for most of the morbidity and mortality associated with sarcoidosis. The disease has a worse prognosis in blacks than whites, with a greater tendency for chronicity and multiorgan involvement.\n\nAbout 90% of patients will have an abnormal chest radiograph at some stage, showing lymphadenopathy, parenchymal opacities, or both. Other findings are uncommon and seldom occur in isolation. Sarcoidosis is traditionally staged according to its appearance on the chest radiograph: stage I, lymphadenopathy; stage II, lymphadenopathy with parenchymal opacity; stage III, parenchymal opacity alone. Low stages at presentation carry a better prognosis than high stages. \n\nLymphadenopathy is evident on the chest radiograph in about 70\u201380% of patients at some time during the course of the condition. Sarcoidosis is characterized by bilateral, symmetrical hilar and paratracheal lymphadenopathy. In 90% of patients with lymphadenopathy, nodal enlargement is maximal on the first radiograph and usually disappears within 6\u201312 months. In about 5%, however, large nodes persist more or less indefinitely, and these can be a source of confusion when found later with other incidental chest pathology. Recurrence of lymphadenopathy is virtually unrecorded. The lymph nodes may calcify, sometimes in a characteristic eggshell fashion. This latter feature is shared by only a few conditions. \n\nAbout 40% of patients presenting with nodal enlargement will develop parenchymal opacities, usually within a year, and of these, about one third will go on to have persistent (fibrotic) shadowing. Nodal enlargement does not develop after parenchymal opacities have appeared.\n\nParenchymal changes probably occur histologically in all patients but are only detected on the chest radiograph in 50\u201370% of cases. They may be classified as reversible, nonreversible (fibrotic), and mixed. Changes may resolve completely (two thirds of cases) or in part, leaving irreversible fibrosis. There are three major patterns of reversible opacity: irregular or rounded 2-4mm nodules, patchy airspace consolidation, or rarely 1-4cm irregular nodules. Characteristically they appear as the nodal enlargement is subsiding, in contrast to lymphoma in which these abnormalities tend to progress in unison. \n\nParenchymal opacities are well demonstrated on high-resolution CT. High-resolution CT is very sensitive and the findings are frequently highly specific for sarcoidosis. The principal abnormality is 1\u20135 mm nodules distributed in a perilymphatic fashion, predominantly along the bronchovascular bundles and subpleurally and, to a lesser extent, along interlobular septa.\n\nOther manifestations of sarcoidosis include pleural thickening and effusions. These are unusual though and do not occur in isolation. \n\nCor pulmonale, mycetoma formation and pneumothorax are all recognized complications of this fibrotic stage.", "ACR Code": "-1.-1", "Category": "Idiopathic or Unknown", "Keywords": "SarcoidHRCT", "Reference": "Grainger & Allison's Diagnostic Radiology: A Textbook of Medical Imaging, 4th Ed., 2001 Churchill Livingstone, Inc." } }, { "U_id": "MPX1115", "TAC": [ "MPX1115_synpic23840" ], "MRI": [], "Case": { "Title": "Stage IV Melanoma\r\nMigration of broken catheter", "History": "52 y/o woman with hx of resected skin lesion. Had latest PA and lateral done as part of a fever work up, with prior study in August 2004 and CT in November 2004. Past surgical history consists of placement of a port-a-cath.", "Exam": "Temp 100.8, BP 140/88, HR 70, RR 17. Remainder of physical exam and labs were unavailable.", "Findings": "Study from December demonstrates increase in size and quantity of masses over all lung fields as compared to previous study of August in the same year. Largest mass, measuring 3cm, is located peripherally in the left lung field. There is prominent lymphadenopathy in both hila. A 9.5 cm length of catheter is present in the left pulmonary artery and extends into the inferior branch.", "Differential Diagnosis": "Mass Lesion:\nGranulomatous disease\nInflammation\nBenign neoplasm\nMalignant primary\nMetastatic disease\nCongenital abnormality", "Case Diagnosis": "Stage IV Melanoma\nMigration of broken catheter", "Diagnosis By": "Biopsy and histology", "Treatment & Follow Up": "The prognosis for this patient is poor. Possible therapies are palliative chemotherapy and palliative radiotherapy. The pt was taken to the special procedures lab the day the chest film was read by a radiologist and the portion of the catheter was removed through an intravascular approach.", "Discussion": "Complication rates. Next to skin, subcutaneous tissue, and lymph nodes, the lungs are the most common sites of melanoma to metastasize. This is thought to be due to the capillary beds in the lung parenchyma. Once there is metastasis to the lungs or other distant sites, the disease is stage IV and has a 5-year survival of 8-10%. Placement of indwelling catheters is not without complications. At the time of insertion pneumothorax is a known complication. Once in place complications include infection, thrombosis with possible SVC syndrome, erosion of SVC, PE and breakage with migration as in this case. Migration of the catheter has its own complications to include pulmonary infarctions, PE, perforation and arrhythmias.\n\nUp To Date \u2013 Imagining Studies in Melanoma\nHarrison\u2019s Principals of Internal Medicine 15th ed." }, "Topic": { "Title": "Diagnosis: Stage IV Melanoma and migration of broken catheter", "Disease Discussion": "Discussion (include references): complication rates. Next to skin, subcutaneous tissue, and lymph nodes, the lungs are the most common sites of melanoma to metastasize. This is thought to be due to the capillary beds in the lung parenchyma. Once there is metastasis to the lungs or other distant sites, the disease is stage IV and has a 5-year survival of 8-10%. Placement of indwelling catheters is not without complications. At the time of insertion pneumothorax is a known complication. Once in place complications include infection, thrombosis with possible SVC syndrome, erosion of SVC, PE and breakage with migration as in this case. Migration of the catheter has its own complications to include pulmonary infarctions, PE, perforation and arrhythmias.\n\nUp To Date \u2013 Imagining Studies in Melanoma\nHarrison\u2019s Principals of Internal Medicine 15th ed", "ACR Code": "68.33", "Category": "Clinical Exam Finding or Sign", "Keywords": "Stage IV Melanoma and migration of broken catheterStage IV MelanomaMelanoma", "Reference": "Up To Date \u2013 Imagining Studies in Melanoma\nHarrison\u2019s Principals of Internal Medicine 15th ed" } }, { "U_id": "MPX1122", "TAC": [ "MPX1122_synpic20035" ], "MRI": [], "Case": { "Title": "Crohn's Disease", "History": "55 y/o WF with years of diarrhea and increasing diffuse crampy abdominal pain.", "Exam": "Distended abdomen with diffuse tenderness.\n\nLabs: no significant abnormality.", "Findings": "Multiple spot images and overhead views from a small bowel follow through demonstrate narrowing of the terminal ileum with proximal dilated loops of small bowel. Abdominal CT with contrast demonstrates stricture of theterminal ileum with mild fat stranding.", "Differential Diagnosis": "Crohn's disease, Ulcerative colitis with backwash ileitis, malignancy, adhesions, radiation fibrosis, infection.", "Case Diagnosis": "Crohn's Disease", "Diagnosis By": "Sugical resection with tissue pathology.", "Treatment & Follow Up": "Surgical resection and anastomosis with gastrointestinal follow up." }, "Topic": { "Title": "Crohn's Disease", "Disease Discussion": "Pathology: Crohn disease is a chronic inflammatory process of the bowel that can affect any part of the GI tract from the mouth to the anus. It is likely multifactoral including genetic influence, dysfunctional immune response, enteric normal flora bacteria, and other environmental factors. It is believed to be the result of an imbalance between inflammatory and anti-inflammatory mediators. Most cases involve the small bowel, particularly the terminal ileum. Crohn disease typically affects the bowel asymmetrically, involving the mesenteric side more severely than the antimesenteric border. Although any area of the GI system may be affected, the most common site of disease is the ileo-cecal region, followed by the colon. Microscopically, the initial lesion appears as a focal inflammatory infiltrate around the crypts, followed by ulceration of superficial mucosa, then by deeper invasion and non-caseating granulomas. Grossly, the early abnormality is hyperemia and edema of the involved mucosa. Later, superficial ulcers form, which become deep serpentine linear ulcers located both longitudinally and transversely giving the mucosa a \u201ccobblestone\u201d appearance. The lesions are often segmental; being separated by healthy areas, hence the term \u201cskip lesions\u201d. Transmural inflammation results in thickening of the bowel wall and narrowing of the lumen. As the disease progresses, it is complicated by obstruction, fistula formation, abscess formation, adhesions, and malabsorption.\n\nClinical: The characteristic presentation of Crohn disease is with abdominal pain and diarrhea, which may be complicated by intestinal fistula formation, obstruction, or both. Unpredictable flares and remissions with a long course characterize Crohn\u2019s. Treatment is generally medical including antidiarrheal, anti-inflammatory, and sometimes antibiotics. Chronic complications include fistulas, adhesions, and marked luminal narrowing with partial bowel obstruction which may require surgery.\n\nRadiographic findings:\nRadiological evaluation includes diagnosis, evaluation of distribution, and evaluation for complications. The distribution of small bowel Crohn\u2019s disease is best assessed by enteroclysis and CT. The terminal ileum is nearly always involved in small bowel disease and is the only site in up 30 % of patients.\n \nSmall bowel contrast studies: The sensitivity of enteroclysis is reported as very good in detecting Crohn\u2019s disease but often does not correlate well with disease activity. Superficial abnormalities include thickened folds due to mucosal edema, transverse and longitudinal ulcers, punctate collections of barium, and small nodules. Transmural abnormalities include deep fissures and penetrating ulcers. Cobblestoning results from intersecting longitudinal and transverse ulcers with intervening heaped-up edematous tissue. Deep ulcerations may result in fistulae. Thickened bowel may appear as separations of loops. Luminal narrowing is always present resulting from spasm and edema during the acute phase or fibrotic strictures in chronic disease. Ileitis can also manifest as a \u201csting sign\u201d on barium study secondary to spasm or fibrotic stricture fromation. The mesenteric aspect and adjacent mesentery are commonly affected more than the antimesenteric border. Extramural mesenteric inflammation and abscesses may induce compression and displacement of bowel loops.\n\nCross sectional imaging: Both CT and MR imaging are reported to have a sensitivity of over 95% for the detection of Crohn disease. At more advanced stages, CT and MR imaging can help identify and characterize pathologically altered bowel segments as well as extraluminal lesions including abscesses, fat stranding, and adenopathy. Cross sectional imaging can also clearly depict inflammatory lesions and conditions that require elective gastrointestinal surgery, aiding in treatment planning.", "ACR Code": "7.2", "Category": "Inflammatory, NOS", "Keywords": "CrohnInflammatory bowel diseasestring sign", "Reference": "1. Radiology of the Small Bowel. Michael Chen, MD. Igaku-Shoin publishers. 1992.\n2. Cross-sectional Imaging in Crohn Disease. Furukawa et al. Radiographics.2004; 24: 689-702. \n3. http://www.eurorad.org\n4. Crohn Disease.Senthil Nachimuthu, MD. E-medicine. 10 March 2004." } }, { "U_id": "MPX1087", "TAC": [ "MPX1087_synpic34297", "MPX1087_synpic34298", "MPX1087_synpic34299", "MPX1087_synpic34300", "MPX1087_synpic34301", "MPX1087_synpic34302", "MPX1087_synpic34303", "MPX1087_synpic34304" ], "MRI": [], "Case": { "Title": "Goldenhar Syndrome", "History": "14 year old boy with a known syndrome presents with right mandibular pain.", "Exam": "N/A", "Findings": "Contrast enhanced axial CT images of the neck demonstrate agenesis of the right pinna, external auditory canal and middle ear. The right inner ear appears intact with slight increased sclerosis about its osseous components. The right mastoid air cells are essentially absent.\n\nThe right zygomatic arch is hypoplastic and the right mandibular ramus and condyle are markedly hypoplastic and malformed. \n\nThe right mandible does not articulate at the TMJ. The globes appear symmetric bilaterally.", "Differential Diagnosis": "\u2022 Goldenhar Syndrome\n\u2022 Hemifacial Microsomia", "Case Diagnosis": "Goldenhar Syndrome", "Diagnosis By": "Known diagnosis with supporting imaging findings.", "Treatment & Follow Up": "Please see topic.", "Discussion": "This patient was being evaluated by the plastic surgery clinic for a planned mandibular surgery." }, "Topic": { "Title": "Goldenhar Syndrome", "Disease Discussion": "Goldenhar Syndrome comprises a spectrum of congenital facial, ocular and vertebral abnormalities. First described in 1952 by Dr. Goldenhar, this rare syndrome involves malformations of the ear (microtia), mandible, maxilla, eye, facial muscles and vertebral bodies. In the majority of cases, these malformations occur unilaterally, although bilaterality can occur. When these findings occur unilaterally, and without vertebral involvement, the disorder is often referred to as hemifacial microsomia. Additional involvement of the vertebral bodies is then referred to as Goldenhar syndrome. Overall these grouped malformations fall under the oculo-auriculo-vertebral spectrum (OAV spectrum). The heart, limbs and kidneys can also be affected within this spectrum.\n\n Goldenhar syndrome is believed to occur randomly without an any genetic cause, although research into a multifactoral inheritance pattern is ongoing. This disorder occurs more frequently in males (~70%), and is associated clinically with hearing, vision, and mastication problems. Affected patients typically enjoy normal life expectancies and normal intelligence (approximately 10% of patient display moderate learning disabilities). Cosmetic surgery consultation, orthodontic planning and speech and hearing therapy are important early interventions for patients with Goldenhar Syndrome.", "ACR Code": "2.6", "Category": "Congenital, malformation", "Keywords": "Goldenhar SyndromeHemifacial Microsomia", "Reference": "Batshaw ML. Children with Disabilities, 5th ed. 2002 Brookes, Baltimore.\nHay WH et al. Current Pediatric Diagnosis and Treatment, 16th ed. 2004 McGraw Hill, New York.", "External Links": "www.deafblind.com/goldenha.html" } }, { "U_id": "MPX1139", "TAC": [ "MPX1139_synpic18560", "MPX1139_synpic18561" ], "MRI": [], "Case": { "Title": "Incidental Malrotation and Acute Appendicitis", "History": "67 year old male presents to the ED with acute onset of lower abdominal pain associated with fever, nausea and vomiting.", "Exam": "Rebound tenderness with palpation of abdomen and associated guarding.\n\nFever 103 F\nWBC 17,000", "Findings": "Contrast enhanced axial CT images of the abdomen demonstrates the presence of a \"whirlpool sign\" - inversion of the superior mesenteric vessels - all of the small bowel loops on the right, left-sided colon, and inflamatory changes within the appendix consistent with phlegmon.", "Differential Diagnosis": "Malrotation\nDiverticulitis\nAcute Appendicitis\nMesenteric Adenitis\nInfectious Enteritis\nAtypical cholecystitis", "Case Diagnosis": "Incidental Malrotation and Acute Appendicitis", "Diagnosis By": "CT imaging and surgical removal of inflamed appendix.", "Treatment & Follow Up": "Patient underwent an uneventful appendectomy. A Ladd's procedure was not performed given symptoms were believed to be primarily the result of the acute appendicitis and not due to malrotation.", "Discussion": "This is a case of acute appendicitis in an adult with incidental malrotation of the midgut." }, "Topic": { "Title": "Incidental Malrotation and Acute Appendicitis", "Disease Discussion": "Intestinal malrotation is an error of normal rotation of the midgut around the superior mesenteric artery and the midgut\u2019s fixation in the peritoneal cavity. Although the true incidence is unknown, it occurs in approximately 1 in 500 live births. About sixty percent present in the first month of life, twenty percent present between one month and one year. Intestinal malrotation in adults is rare. Zissen suggests this anomaly should be sought in patients with a situs problem, inferior vena cava anomalies, polysplenia, or preduodenal portal vein. \n\nAcute appendicitis in adults, although less frequent than in adolescents, is much more common than adult malrotation. Both can present with obstructive symptoms in up to 50% of cases. Like a symptomatic malrotation, an acute appendicitis requires immediate surgery for repair. A symptomatic malrotation requires a Ladd\u2019s procedure. An acute appendicitis requires an appendectomy. \n\nZissen warns that intestinal malrotation in adults is usually an incidental finding on CT. Therefore, it is important to continue to look for the cause of any acute symptoms. Intestinal malrotation can be diagnosed on CT by the anatomic location of a right-sided small bowel, left-sided colon and an abnormal relationship of the superior mesenteric vessels. Acute appendicitis will show inflammatory changes of the appendix associated with fat stranding, bowel wall thickening, luminal expansion and occasionally frank phlegmon.", "ACR Code": "7.2", "Category": "Congenital, malformation", "Keywords": "MalrotationAcute Appendicitis", "Reference": "Kamal I, Defuising the intra-abdominal ticking bomb: intestinal malrotation in children. Canadian Medical Association Journal 2000; 162(9):1315-7.\n\nHalpert R, Feczko P, Gastrointestinal Radiology: The Requisites. 2nd Ed. Mosby, 1999. pages 92-93, 133-134, 285-286. \n\nZissin R, et al, Intestinal malrotation as an incidental finding on CT in adults. Abdominal Imaging. 1999 Nov-Dec;24(6):550-5.\n\nCotran, R, et al, Robbins: Pathologic Basis of Disease. 5th ed. W.B. Saunders Company, 1994. pages 823-824." } }, { "U_id": "MPX1135", "TAC": [ "MPX1135_synpic16704", "MPX1135_synpic16705", "MPX1135_synpic16706" ], "MRI": [], "Case": { "Title": "Pheochromocytoma", "History": "30 y/o male with no significant PMH presents with symptoms of headache and flushing. Was discovered to have BP 250/140.", "Exam": "Physical exam unremarkable. Thyroid normal. Lungs clear. Cardiac exam WNL. No abdominal masses. Lan: 24 hr VMA 107.6 (0-10.0), epinephrine 170 (. 5-20), norepinephrine 460 (15-18) total catecholamines 3196 (123-671 supine)", "Findings": "CT Chest Abd Pelvis with oral and IV contrast large soft tissue mass arising from left adrenal gland measuring 9.5 X 8.9 X 13cm in the oblique coronal, AP, and Craniocaudal dimensions. Loss of tissue plane between tail of pancreas, spleen, and bowel.", "Differential Diagnosis": "Hyperthyroidism, meduloblastoma, soft tissue sarcoma, incidentaloma, myeloolipoma, renal cell carcinoma, adrenal cortical carcinoma", "Case Diagnosis": "Pheochromocytoma", "Treatment & Follow Up": "prazosin 1mg po BID prior to surgery followed by surgical excision. Follow up with repeat VMA and metanephrines and imaging studies. If the pheochromocytoma is malignant, as evidenced by invasion and metastasis then treatment is primarily surgical with chemotherapy playing only a palliative role." }, "Topic": { "Title": "Pheochromocytoma", "Disease Discussion": "Pheochromocytoma is a rare cause of hypertension, accounting for about .2% of hypertension. The classic presentation involves the triad of episodic headache, sweating, and tachycardia. It is occasionally discovered incidentally on CT or MRI in 10% of patients. In fact, this tumor is often known as the 10% tumor because 10% are familial, 10% are bilateral, 10% occur in children, and 10% are malignant. It is associated with familial disorders such as multiple endocrine neoplasia (MEN) type II and in von Hippel-Lindau, therefore a family history and test for other associated abnormalities should be performed. The diagnosis is typically confirmed by measuring elevated plasma and urinary catecholamines and their metabolites and from radiographic tests. Treatment is primarily surgical with extirpation after the patient has been appropriately medically prepared, typically with a regimen of 10-14 days of alpha blockade. Beta blockade may be added after adequate alpha blockade. Hypertensive crises are typically treated with nitroprusside or phentolamine. Surgery has a high morbidity rate of 40% and a mortality rate of 1-2%. The tumor pathology often does not reveal if the tumor is malignant or benign. Metastasis are required to demonstrate malignancy. If the tumor is malignant then the primary treatment is surgical excision of metastasis with palliative chemotherapy.", "ACR Code": "8.3", "Category": "Neoplasm, NOS", "Keywords": "Pheochromocytoma", "Reference": "Young, W.F. and N. M Kaplan. Diagnosis and Treatment of Pheochromocytoma in Adults. Up to Date. 2002\n\n\"Pheochromocytoma\" Larsens: Williams Textbook of Endocrinology, 10th ED C 2003 MD Consult" } }, { "U_id": "MPX1136", "TAC": [ "MPX1136_synpic46363" ], "MRI": [], "Case": { "Title": "Situs Inversus Totalis", "History": "41 yo man has painless microscopic hematuria found on screening urinalysis with primary care manager. No prior Hx.", "Exam": "CV: RRR, mo m/r/g. Apical impulse located right of sternum in 5th intercostal space.\nLungs: CTAB\nAbd: soft, NT/ND, no rebound, guarding. Normal BS. Palpable liver edge in the LUQ.", "Findings": "\u2022 CXR - dextrocardia, bronchus intermedius on the left side of the chest\n\u2022 KUB- Liver edge on the left, gastric bubble on the right\n\u2022 Abd CT- complete mirror image of all abdominal organs. No evidence of nephrolithiasis on non-contrast CT", "Differential Diagnosis": "\u2022 Situs Inversus Totalis\n\u2022 Technical error\n\u2022 Imaging findings unrelated to clinical picture\n\u2022 Kartagener Syndrome", "Case Diagnosis": "Situs Inversus Totalis", "Diagnosis By": "imaging", "Treatment & Follow Up": "Pt was referred to Nephrology for follow up of hematuria.", "Discussion": "Companion Case: http://www.thoracic.org/clinical/ats-clinical-cases/pages/uncontrolled-asthma-recurrent-rhinosinusitis-and-infertility-in-a-young-woman.php\n\nSpectrum of Cilia Diseases: PMID: 21926397\n\nCilia in developmental disorders: PMID: 17021045" }, "Topic": { "Title": "Situs Inversus Totalis", "Disease Discussion": "There are three types of situs:\n\u00bb situs solitus (normal), \n\u00bb situs inversus (mirror image of normal), and \n\u00bb situs ambiguous (1). \n\nIn regards to situs inversus, the systemic atrium is on the left, with a left-sided trilobed lung, liver, gallbladder, and inferior vena cava. The pulmonary atrium is on the right with a right-sided bilobed lung, stomach, single spleen, and aorta. Additionally, the cardiac apex is on the right (situs inversus with dextrocardia or situs inversus totalis) (2, 3). Identified in about 0.01% of the population, situs inversus is recessively inherited, more common in males, and is associated with other congenital disorders such as polysplenia, asplenia, horseshoe kidney, diaphragmatic hernia, and annular pancreas (2, 4). \n\nKartagener syndrome is a type of primary ciliary dyskinesia (PCD) that includes: situs inversus, nasal polyposis with chronic sinusitis, and bronchiectasis. It is present in anywhere from 20%-25% of patients have situs inversus, however, only 50% of patients with immotile cilia syndrome have situs inversus. This 50/50 split relates to the role of cilia in creating chemical gradients in the embryo that organize Left-Right asymmetric development.\n\nImpaired mucociliary clearance leads to recurrent lung infections, bronchiectasis predominately affecting the lower lung fields, chronic sinusitis, and otitis media (1, 2, 3).", "ACR Code": "5.1", "Category": "Congenital, normal variant", "Keywords": "Kartagener SyndromeSitus Inversus TotalisPrimary Cilia Dyskinesia", "Reference": "1. Maldjian et al. AJR 2007;188:S39-S49.\n2. Applegate et al. RadioGraphics 1999:19:837-852.\n3. Wilhelm A. Situs Inversus. Emedicine Topic 639 Available from http://www.emedicine.com/radio/topic639.htm 2007. [cited 1 MAR 08].\n4. Hughes J, Feigin D. Situs Inversus MedPixTM Topic: 3681 Available from http://rad.usuhs.mil/medpix/radpix.html?mode=single&recnum=3681&table=&srchstr=&search=#References 2002 [cited 1 MAR 08]." } }, { "U_id": "MPX1123", "TAC": [ "MPX1123_synpic24317", "MPX1123_synpic24318" ], "MRI": [], "Case": { "Title": "Wilms\u2019 Tumor (nephroblastoma). Negative left renal involvement. Negative mesenteric lymph node pathology.", "History": "13 year old Caucasian female who presented to the ER following a two week history of right sided abdominal pain and one episode of hematuria (patient was not currently menstruating). Patient denies fever, weight loss, nausea, vomiting.", "Exam": "CBC: Normal\nSerum Chemistry panel: normal\nUA: Blood and RBCs noted, otherwise normal Back: No CVAT\nLungs: CTAB GU: Normal female external genitalia\nAbdominal Exam: Soft, obvious right sided mass, relatively non-tender. Extremities: All pulses 2+ palpable, equal", "Findings": "RUQ Ultrasound: A large mass is seen in the right upper quadrant in the expected placement of the right kidney. The mass appears heterogeneous with multiple cystic components. The mass appears somewhat well marginated. No hypervascularity is seen. A wedge of renal parenchyma can be seen at the interface of the tumor and the liver on slide #2.\nAbd. CT: A 14cm, heterogenous renal mass extending from the right kidney with surrounding rim of renal parenchyma. There are multiple low density collections within the mass. There is no evidence of fat within the mass or calcifications (suggesting against renal angiomyolipoma or rhabdoid tumor of the kidney respectively). Both kidneys demonstrate contrast enhancement and excretion. No obvious tumor extensions into the renal vein or inferior vena cava is noted. Mildly enlarged mesenteric lymph nodes adjacent to the kidney suggest possible malignant spread or may be reactive.", "Differential Diagnosis": "Renal cell carcinoma\nWilms\u2019 Tumor (nephroblastoma)\nAngiomyolipoma\nSoft-tissue sarcoma of the kidney\nClear cell sarcoma of the kidney\nNeuroblastoma", "Case Diagnosis": "Wilms\u2019 Tumor (nephroblastoma). Negative left renal involvement. Negative mesenteric lymph node pathology.", "Diagnosis By": "Surgical resection and pathologic confirmation", "Treatment & Follow Up": "Patient underwent right radical nephrectomy and exploration of left kidney. Uneventful hospital course. Discharged to home on POD #6 following first course of chemotherapy by pediatric oncology service.", "Discussion": "Wilms\u2019 tumor is a mixed embryonal neoplasm that is the most common intra-abdominal tumor and renal malignancy in childhood. It is the fourth most common pediatric cancer1,2. \nThe median age of sporadic Wilms\u2019 is 44 months, although teenage patients (as in this case presentation) may present with it. The incidence of bilateral tumours is between 8\u201312% and the gender ratio is fairly even at 1:1.2. The mass is usually smooth, fixed and firm, occasionally extending across the midline of the abdomen. Though usually asymptomatic, 20-30% of patients experience hematuria, abdominal pain, hypertension, and fever. Symptoms such as weight loss, cachexia, or bone pain are uncommon for Wilms\u2019 tumor3.\nWilms\u2019 tumor can spread locally through the tumor capsule or hematogenously to the lungs, liver, or the other kidney. It may progress into the inferior vena cava as far as the right atrium3. \nWilms\u2019 tumor, which is intra-renal in development, must be distinguished from neuroblastoma. Neuroblastoma typically arises in the adrenal glands and is the second most common childhood solid tumor. Neuroblastomas also tend to have calcifications, another difference from Wilms\u2019 tumors that may be discerned radiologically1, 4.\nPatients with chromosomal aberrations on 11p13 and 11p15 have been shown to be at increased risk of Wilms\u2019 tumor. Such patients may present with other conditions that include aniridia, mental retardation, macroglossia, organomegaly, or genitourinary anomalies3.\nThe first line of diagnostic studies for Wilms\u2019 tumor is ultra sound, providing a non-invasive means of evaluating tumor mass in the abdomen. It can be helpful in ruling out an extra-renal mass (neuroblastoma) or hydronephrosis5. CT becomes especially useful in detection of bilateral tumors and in evaluation of other abdominal structures, peritoneum, and lymph nodes. On CT Wilms\u2019 tumor appears as a heterogenous, enhancing mass with less than 10% showing calcification. A \u201cclaw sign\" of the displaced renal tissue may be seen2. On MRI the tumors are hypointense with T1, variable with T2, and enhance poorly with gadolinium. Gadolinium is given, however, to evaluate the other kidney for another Wilms\u2019 mass2.\nA chest xray is important when evaluating a patient preoperatively for lung metastasis. Most centers, however, prefer the use of chest CT. Though chest CT is a sensitive modality for Wilms tumor, it is susceptible to false positives for lung metastasis as well as inter-reader variability. Histological assessment may show the presence of nephrogenic rests, primordial precursor lesions in the kidney, common in the setting of Wilms\u2019 tumor6.\nNearly all patients undergo surgery as the primary treatment method. Chemotherapeutic regimens of vincristine, doxorubicin, and dactinomycin with or without radiation therapy (depending on the stage of the tumor) are used in treating Wilms\u2019 tumor. Bilateral renal involvement is considered Stage V disease3.\nRelapse rates are relatively low with 10-15% experiencing relapse in patients with favorable histologic findings. They increase up to 50% in patients with anaplastic findings3." }, "Topic": { "Title": "Wilms\u2019 Tumor (nephroblastoma)", "Disease Discussion": "Wilms\u2019 tumor is a mixed embryonal neoplasm that is the most common intra-abdominal tumor and renal malignancy in childhood. It is the fourth most common pediatric cancer1,2. \nThe median age of sporadic Wilms\u2019 is 44 months, although teenage patients (as in this case presentation) may present with it. The incidence of bilateral tumours is between 8\u201312% and the gender ratio is fairly even at 1:1.2. The mass is usually smooth, fixed and firm, occasionally extending across the midline of the abdomen. \nThough usually asymptomatic, 20-30% of patients experience hematuria, abdominal pain, hypertension, and fever. Symptoms such as weight loss, cachexia, or bone pain are uncommon for Wilms\u2019 tumor3.\nWilms\u2019 tumor can spread locally through the tumor capsule or hematogenously to the lungs, liver, or the other kidney. It may progress into the inferior vena cava as far as the right atrium3. \nWilms\u2019 tumor, which is intra-renal in development, must be distinguished from neuroblastoma. Neuroblastoma typically arises from the adrenal glands and is the second most common childhood solid tumor. Neuroblastomas also tend to have calcifications, another difference from Wilms\u2019 tumors that may be discerned radiologically1, 4.\nPatients with chromosomal aberrations on 11p13 and 11p15 have been shown to be at increased risk of Wilms\u2019 tumor. Such patients may present with other conditions that include aniridia, mental retardation, macroglossia, organomegaly, or genitourinary anomalies3.\nThe first line of diagnostic studies for Wilms\u2019 tumor is ultra sound, providing a non-invasive means of evaluating tumor mass in the abdomen. It can be helpful in ruling out an extra-renal mass (neuroblastoma) or hydronephrosis5. CT becomes especially useful in detection of bilateral tumors and in evaluation of other abdominal structures, peritoneum, and lymph nodes. On CT Wilms\u2019 tumor appears as a heterogenous, enhancing solid mass with less than 10% showing calcification. A \u201cclaw sign\" of the displaced renal tissue may be seen2. On MRI the tumors are hypointense with T1, variable with T2, and enhance poorly with gadolinium. Gadolinium is given, however, to evaluate the other kidney for another Wilms\u2019 mass2.\nA chest xray is important when evaluating a patient preoperatively for lung metastasis. Most centers, however, prefer the use of chest CT. Though chest CT is a sensitive modality for Wilms tumor, it is susceptible to false positives for lung metastasis as well as inter-reader variability. Histological assessment may show the presence of nephrogenic rests, premordial precursor lesions in the kidney, common in the setting of Wilms\u2019 tumor6.\nNearly all patients undergo surgery as the primary treatment method. Chemotherapeutic regimens of vincristine, doxorubicin, and dactinomycin with or without radiation therapy (depending on the stage of the tumor) are used in treating Wilms\u2019 tumor. Bilateral renal involvement is considered Stage V disease3.\nRelapse rates are relatively low with 10-15% experiencing relapse in patients with favorable histologic findings. They increase up to 50% in patients with anaplastic findings3.", "ACR Code": "8.3", "Category": "Neoplasm, embyronal", "Keywords": "Wilms\u2019 Tumor (nephroblastoma).nephroblastoma", "Reference": "1.\tBehrman: Nelson Textbook of Pediatrics, 17th ed., 2004 Elsevier \n2.\tGrainger & Allison's Diagnostic Radiology: A Textbook of Medical Imaging, 4th ed., 2001 Churchill Livingstone\n3.\tAbeloff: Clinical Oncology, 3rd ed., 2004 Elsevier\n4.\tKumar: Robbins and Cotran: Pathologic Basis of Disease, 7th ed., 2005 Elsevier\n5.\tEisenberg R. L., Diagnostic Imaging in Internal Medicine, McGraw Hill 1985\n6.\tBrenner & Rector's The Kidney, 7th ed., 2004 Elsevier" } }, { "U_id": "MPX1152", "TAC": [ "MPX1152_synpic20557" ], "MRI": [], "Case": { "Title": "Sarcoidosis.", "History": "34 year old female presents to the emergency room with abdominal pain.", "Exam": "PE: Mild bilateral flank pain.\nLabs: Elevated serum calcium.", "Findings": "1. Lungs with reticulonodular interstitial pattern.\n2. Nephrolithiasis.\n3. Diffuse lymphadenopathy.", "Differential Diagnosis": "Tuberculosis \n Lymphoma - almost never shows the striking symmetry \n Carcinoma (metastatic) \n Sarcoid\n Fungal disease", "Case Diagnosis": "Sarcoidosis.", "Diagnosis By": "Retroperitoneal lymph node CT-guided biopsy.", "Treatment & Follow Up": "To Follow.", "Discussion": "The patient presented with abdominal pain secondary to bilateral nephrolithiasis." }, "Topic": { "Title": "Sarcoidosis", "Disease Discussion": "Clinical: Sarcoidosis is a disease of non caseating granulomas. The specific etiology of sarcoidosis has not yet been identified, but it likely the combination of environmental and genetic factors. Events are triggered by an unknown factor with activation of pulmonary T cells and pulmonary alveolar macrophages. T cells proliferate in the lungs and release chemotactic factors which attract monocytes into the lungs, increasing the macrophage response which in turn leads to proliferation of fibroblasts with promotion of collagen synthesis and eventual fibrosis. Hypercalcemia and elevated serum angiotensin-converting enzyme are seen secondary to activation of pulmonary alveolar macrophages. Hypercalcemia can lead to nephrocalcinosis. T cell changes in the lungs are not seen in the peripheral circulation where there is lymphopenia. Manifestations are also seen in other organ systems. Bilateral hilar lymphadenopathy is present in about 80% cases and is often asymptotic but may be associated with dull ache, malaise and fever. Generalized lymphadenopathy may occur in about 10%. Nervous system involvement includes cranial nerve palsies and neuropathy. The eyes can be involved with uveitits and keratoconjuctivivits. Skeletal manifestations include phalangeal cysts and arthritis. The heart can be affected with cardiomyopathy and associated heart block. In the united stated, sarcoid is more common in blacks. In blacks, the skin, joints, and eyes are more often involved. Additionally, manifestation of the disease tends to be more florid in blacks. \n\nRadiographic findings: Plain film CXR abnormalities are found in over 90% of patients. Bilateral hilar adenopathy is most common, oftentimes with right paratracheal and AP window adenopathy. Subcarinal nodes are less common. Lymph nodes can calcify, usually in an amorphous, popcorn-like fashion. Nodal calcification is related to duration of disease. Sarcoid causes interstitial lung disease, which can have a variety of appearances: a reticulo-nodular pattern is the most common and is typically bilateral and symmetric. An alveolar pattern with small indistinct nodular opacities can be seen but is actually the result of interstitial lung disease.\nCT is more sensitive in the detection of adenopathy and parenchymal lung disease. HRCT is used to evaluate for parenchymal lung disease demonstrating nodular peribronchiovascular thickening. Similar changes may be noted along the fissures. Nodules greater than 1 cm in diameter are actually the result of coalescence of small nodules. Areas of ground glass attenuation can be seen resulting from microscopic interstitial granulomas. CT appearance does not correspond well to patient\u2019s pulmonary state. Sarcoid can lead to end stage fibrosis, which is indistinguishable from other causes. \nAbdominal involvement includes liver involvement which most commonly produces hepatomegaly, but can result in focal nodules. Additionally, hypodense splenic nodules can be found. Intra-abdominal adenopathy can be seen in nearly a 3rd of patients. Nephrolithiasis can be seen from hypercalcemia. Skeletal findings tend to involve the small bones of the hands with associated skin changes. Findings include a lace-like reticular pattern or cystic lesions. The bone lesions are hot on bone scan and FDG PET imaging. \nCardiac changes can include thinning of the myocardium seen on CT. On MRI, there can be areas of increased MRI T2 signal intensity and areas of T-1 contrast enhancement.\n\nStaging/prognosis: Staging is based upon the CXR findings. Stage 0- Normal CXR; Stage 1- Mediastinal/ Hilar adenopathy; Stage 2- Adenopathy plus parenchymal infiltrates; Stage 3- Lung infiltrates only; and Stage 4- Fibrosis/ Cystic changes. Prognosis is directly correlated with the patients staging. Sarcoid will resolve in over half of stage 1 patients. Overall, about 20% of affected patients will progress to pulmonary fibrosis with 5% mortality.\n\nTreatment: Usually no treatment is necessary. Spontaneous remission occurs in 90% of patients with stage 1 pulmonary disease and half of patients with stage 2. If chest x-rays showed persistent pulmonary infiltration with associated decreased serial lung functions oral steroids are used. In patients who are unresponsive to steroids, other medications such as azathioprine or cyclosporin may be useful. Chloroquine is used as a steroid sparing agent in patients with severe skin disease.", "ACR Code": "6.7", "Category": "Inflammatory, non-infectious", "Keywords": "SarcoidLymphadenopathygranuloma", "Reference": "1. Radiologic Manifestations of Sarcoidosis in Various Organs\nTakashi Koyama, Hiroyuki Ueda, Kaori Togashi, Shigeaki Umeoka, Masako Kataoka, and Sonoko Nagai. RadioGraphics 2004; 24: 87-104. \n2. www.gpnotebook.co.uk\n3. 3. www.auntminnie.com. References, thoracic radiology. Scott C. Williams, M.D." } }, { "U_id": "MPX1159", "TAC": [ "MPX1159_synpic47786" ], "MRI": [], "Case": { "Title": "Burkitt's Lymphoma", "History": "46 year old male presented to Gastroenterology clinic complaining of 2 weeks of abdominal fullness, early satiety, pale colored stools. Admits two days of nausea.", "Exam": "On physical exam, patient is visibly uncomfortable, moderately jaundiced, with abdominal distention and mild tenderness to palpation of RUQ.\nLabs reveal transaminitis.", "Findings": "\u2022 RUQ Ultrasound: a heterogenous mass in the region of the head of the pancreas with hepatic biliary ductal dilation.\n\u2022 CT Chest/Abd/Pelvis w/contrast: multiple ground glass opacities bilaterally in lungs, large mass about the pancreatic head which surrounds the periaortic tissues and celiac axis.\n\u2022 PET scan: focal increased uptake about the pancreatic head, scattered foci bilateral lungs L>R", "Differential Diagnosis": "\u2022 pancreatitis\n\u2022 pancreatic cancer\n\u2022 Lymphoma\n\u2022 soft tissue sarcoma\n\u2022 metastatic disease", "Case Diagnosis": "Burkitt's Lymphoma", "Diagnosis By": "CT guided biopsy", "Treatment & Follow Up": "\u2022 Immediately following imaging, a biliary stent was placed. 3 courses of chemotherapy with agressive tumor lysis syndrome prophylaxis were given and tolerated. \n\u2022 Recent PET study obtained showed no evidence of disease recurrence." }, "Topic": { "Title": "Burkitt's Lymphoma", "Disease Discussion": "Definition:\n\u2022 Burkitt lymphoma (BL) is a highly aggressive B-cell neoplasm characterized by the translocation and deregulation of the c-myc gene, which causes the tumor cells to remain in cycle. This makes the neoplasm morphologically homogenous, but also allows for its oftentimes quick response to chemotherapeutics; it grows quickly and dies quickly.\n\n\nPresentation:\n\u2022 Patients with BL present with rapidly growing tumor masses and often have evidence of tumor lysis with a very high serum lactate dehydrogenase (LDH) concentration and elevated uric acid levels. \n\n\u2022 Three distinct clinical forms of BL are recognized: sporadic, endemic, and immunodeficiency-associated. Although they are histologically identical and have similar clinical behavior, there are differences in epidemiology, clinical presentation, and genetic features between the three forms:\n\n\u00bb\u00bbThe nonendemic (sporadic) form usually has an abdominal presentation, most often with massive disease and ascites, involving the distal ileum, stomach, cecum and/or mesentery, kidney, testis, ovary, breast, bone marrow, or central nervous system. Presenting symptoms can include those related to bowel obstruction or gastrointestinal bleeding, often mimicking acute appendicitis or intussusception. \n\n\u00bb\u00bbThe endemic (African) form usually presents as a jaw or facial bone tumor that spreads to extranodal sites including the mesentery, ovary, testis, kidney, breast, and especially to the bone marrow and meninges.\n\n\u00bb\u00bbImmunodeficiency-related cases more often involve lymph nodes; both these and sporadic cases may present with blood involvement.\n\n\nRadiology: \n\u2022 For lymphomas, CT is usually the primary staging modality in the neck, chest, abdomen, and pelvis because of its generally superior spatial resolution.\n\n\u2022 CT is typically superior to MRI in the evaluation of subtle bone destruction, if present.\n\n\u2022 MRI has superior tissue resolution, often allowing it to distinguish a small focus of tumor from surrounding normal soft tissue far better than CT.\n\n\nTreatment:\n\u2022 The standard of care for BL has yet to be defined. Aggressive combination chemotherapy with central nervous system (CNS) prophylaxis is often used. As response to chemotherapy is rapid and disease is inevitably diffuse, there is no role for radiation therapy in BL, even in patients with localized disease. In addition, surgery is no longer employed in BL.", "ACR Code": "-1.3", "Category": "Neoplasm, hematopoietic", "Keywords": "Burkitt", "Reference": "1. Freedman, A., MD and Aster, J., MD, \"Clinical Manifestations, pathological features, and diagnosis of Burkitt's Lymphoma.\" UpToDate. Last review of literature: Oct 2008.\n\n2. Munn, S., MD, \"Imaging HIV/AIDS, Burkitt's Lymphoma.\" AIDS Patient Care and STD's, vol 16, number 8, 2002." } }, { "U_id": "MPX1154", "TAC": [ "MPX1154_synpic53544", "MPX1154_synpic53549" ], "MRI": [ "MPX1154_synpic53543" ], "Case": { "Title": "Cysticercosis", "History": "43 year old man presents with a new onset of seizures.", "Exam": "Normal between seizures.", "Findings": "\u2022 Solitary ring-enhancing lesion in the right temporal lobe.\n\u2022 Thin and smooth rim of enhancement\n\u2022 Small chunk of calcification in the lateral/peripheral rim", "Differential Diagnosis": "\u2022 Abscess - chronic (because of calcification)\n\u2022 Neoplasm (astrocytoma, oligodendroglioma)", "Case Diagnosis": "Cysticercosis", "Diagnosis By": "Pathology", "Treatment & Follow Up": "The lesion was resected completely" }, "Topic": { "Title": "Cysticercosis", "Disease Discussion": "Taeniasis (adult intestinal tapeworm) is from eating undercooked or raw \"measly\" pork. Definitive host (for the adult tapeworm) is man. Normally the adults shed eggs (proglottids) into human feces that are then eaten by the intermediate host (pig/cow). There, the ingested larvae (cystercerci) are liberated and released into the gut of the secondary host where they invade mucosa, spread via blood and lymphatics to the muscles of the secondary/intermediate host (pig/cow).\n\nCystercosis is an infection in man by the larval stage of the pork tapeworm Taenia solium. The oncospheres (larvae) spread hematogeneously and then encyst in the muscle and brain. (Moving larva can be seen in eye - yechh!) In 3-4 mon the larva has developed fully, by an invagination of the bladder (cyst) wall into itself. The larva is at the end of this invagination. The live larva is inocuous - dead and dying larva are irritating, and cyst capsule may expand by 5-20mm w/fluid. Slowly (2-3 yrs) the cyst will calcify, and ultimately die. Usually of fairly uniform size in the brain. The \"racemose\" multiloculated cysts occur in CSF cisterns.\n\nCysticercosis and CSF\n326/694 pts had \"inflammatory\" CSF\nCSF eosinophilia (1-12% of leukocytes) was present in 58% of 326 w/inflammatory CSF; complement fixation + in 84% of pts with \"inflammatory\" CSF\n===========================\n358/694 had \"noniflammatory\" CSF\n4.3% had eosinophilia of CSF\n22% had positive comp. fixation test", "ACR Code": "1.2", "Category": "Infection, parasite", "Keywords": "cysticercosistaeniasis" } }, { "U_id": "MPX1169", "TAC": [ "MPX1169_synpic20076" ], "MRI": [], "Case": { "Title": "PHEOCHROMOCYTOMA", "History": "Hypertension, occ palpations, heat intolerance", "Exam": "elevated urine vma", "Findings": "large left adrenal mass. Location within the adrenal gland excluded adenopathy. Contrast within bowel excluded bowel as an etiology.", "Differential Diagnosis": "Pheochromocytoma\nMets\nHemorrhage\nAdenoma", "Case Diagnosis": "PHEOCHROMOCYTOMA", "Diagnosis By": "Surgical biopsy", "Treatment & Follow Up": "The mass was surgically excised." }, "Topic": { "Title": "Pheochromocytoma, MIBG uptake", "Disease Discussion": "Meta-Iodobenzylguanidine (MIBG): Neuroblastoma, ganglioneuro(blasto)ma and pheochromocytoma are tumors derived from the tissues of the sympathetic nervous system. Structurally MIBG resembles norepinephrine and guanethidine (neurosecretory-depleting agent). MIBG is taken up into the storage granules of both normal and abnormal neural crest cells. The uptake is proportional to the number of neurosecretory granules within a tumor. MIBG uptake is blocked by many drugs. Catecholamine agonists (phenylephrine, pseudoephedrine), antipsychotics (phenothiazines), tricyclic antidepressants, calcium channel blockers, long acting beta blockers (labetalol), drugs that deplete catocholamine stores (reserpine, guanethidine) and cocaine are examples of drugs that interfere with MIBG uptake. Radiolabeling is done with I-123 and I-131 (I-123: half life 13.2 hrs, energy 159 KeV; I-131: half life 8.1 days, energy 364 KeV). \nI-123 MIBG is used in much larger administration activities because of its much lower absorbed radiation dose per mCi compared with I-131. In addition, current gamma camera detection crystals can more efficiently detect the 159 KeV photons. Collimation is easier at lower energy and I-123 has a higher photon flux at 24 hour imaging. For these reasons MIBG studies with \n\nI-123 is of considerably higher quality than with I-131. Normal distribution of MIBG includes salivary glands, myocardium, liver and urine. Amount in the GI tract is variable and related to excretion into the gut. A small percentage of patients show some activity in a blocked thyroid gland, normal adrenals, lung, and skeletal muscle. In normal subjects, activity should not be seen in bone, bone marrow or spleen. Utilizing SPECT MIBG can increase certainty of interpretation over planar imaging although it has not shown to increase the number of lesions detected.\nAlthough in this particuar case, the tumor was not identified on planar images but it was visualized on SPECT imaging. Overall, primary tumor, lymph node metastasis, bone and bone marrow metastasis are detected using MIBG.\n\nPheochromocytoma is a rare tumor of chromaffin cells most commonly arising from the adrenal medulla. An estimated 800 cases are diagnosed yearly in the U.S. The peak incidence is in the third to fifth decades of life. Bilateral disease is present in approximately 10% of patients. Bilaterality is much more common in familial pheochromocytoma, often found in association with the familial multiple endocrine neoplasia syndromes (MEN, types IIA and IIB). In patients with MEN type II syndromes, the risk of developing a contralateral tumor following unilateral adrenalectomy is approximately 50%. Other syndromes associated with pheochromocytoma include neurofibromatosis, von Hippel-Lindau disease, cerebellar hemangioblastoma, Sturge-Weber\\'s syndrome, and tuberous sclerosis. Therefore, all patients with pheochromocytomas should be screened for MEN-2 and von Hippel-Lindau disease to avert further morbidity and mortality in the patients and their families. Extra-adrenal pheochromocytoma or functional paraganglioma occurs in approximately 10% to 15% of cases and may arise from any extra-adrenal chromaffin tissue in the body associated with sympathetic ganglia. \n\nExtra-adrenal pheochromocytoma is most often located within the abdomen and may have greater malignant potential than adrenal pheochromocytoma. Extra-adrenal tumors usually have a poorer prognosis than adrenal tumors. Due to the production and release of catecholamines, pheochromocytomas cause hypertension. However, only 0.1% to 0.5% of all hypertension patients will be found to have a pheochromocytoma. The importance of the recognition of this disease is that over 90% of patients properly diagnosed and treated are curable.\n\nThe hypertension caused by pheochromocytoma may be sustained or paroxysmal and is often severe with occasional malignant features of encephalopathy, retinopathy and proteinuria. Less commonly, severe hypertensive reactions may occur during incidental surgery, following trauma, exercise, or micturition (in the setting of bladder pheochromocytoma) when the diagnosis is unsuspected. Other clinical features of pheochromocytoma include headache, sweating, palpitation, tachycardia and severe anxiety along with epigastric or chest pain. The diagnosis of pheochromocytoma is established by the demonstration of elevated 24-hour urinary excretion of free catecholamines (norepinephrine and epinephrine) or catecholamine metabolites (VMA and total metanephrines). The measurement of plasma catecholamines can also be of value in the diagnosis of pheochromocytoma. However, the measurement of plasma catecholamines has limited sensitivity and specificity. Plasma metanephrines have been reported to be more sensitive than plasma catecholamines. \n\nOnce the diagnosis is confirmed by biochemical determinations the localization and extent of disease should be determined. Ninety-seven percent are found in the abdomen, 2% to 3% in the thorax, and 1% in the neck. The initial studies should be a chest film and abdominal computed tomographic (CT) scan. \n\nI123meta-iodobenzylguanidine (MIBG) has been found to be useful as a scintigraphic localization agent. If the tumor is not adequately localized by these methods then magnetic resonance imaging (MRI), or rarely, vena cava catheterization with selective venous sampling for catecholamines may be indicated. CT and MRI scans are about equally sensitive (98%-100%), while MIBG scanning has a sensitivity of only 80%. However, MIBG scanning has a specificity of 100%, compared to specificity of 70% for CT and MRI. Surgical resection is the standard curative modality. If the primary tumor is localized to the adrenal gland and is benign, then survival is that of the normal age-matched population. In patients with unresectable, recurrent, or metastatic disease long-term survival is possible however, the overall 5-year survival is less than 50%. Pharmacologic treatment of the catecholamine excess is mandatory and surgery, radiation therapy, or chemotherapy may provide palliative benefit.", "ACR Code": "8.3", "Category": "Nuclear Medicine", "Keywords": "paragangliomaPheochromocytoma", "Reference": "Gelfand, MJ. Meta-Iodobenzylguanidine in Children. Semin Nucl Med. 1993 Jul;23(3):231-42. Review.\n\t\nGelfand MJ, Elgazzar AH, Kriss VM, Masters PR, Golsh GJ. Iodine-123-MIBG SPECT versus planar imaging in children with neural crest tumors. J Nucl Med. 1994 Nov;35(11):1753-7.\n\nNeumann HP, Berger DP, Sigmund G, et al.:Pheochromocytomas, multiple endocrine neoplasia type 2, and von Hippel-Lindau disease. N Engl J Med 329 (21): 1531-8, 1993. \n\nWilson JD, Foster DW, Kronenberg HM, et al., eds.: Williams Textbook of Endocrinology. 9th ed. Philadelphia, Pa: W.B. Saunders Company, 1998, pp 705-716. \n\nMcEwan AJ, Shapiro B, Sisson JC, et al.: Radio-iodobenzylguanidine for the scintigraphic location and therapy of adrenergic tumors. Semin Nucl Med 15 (2): 132-53, 1985." } }, { "U_id": "MPX1165", "TAC": [ "MPX1165_synpic16241", "MPX1165_synpic16243" ], "MRI": [], "Case": { "Title": "Juvenile Nasopharyngeal Angiofibroma (JNA)\r\nDiagnosis confirmed at histology after first resection.", "History": "This young Pacific Island teenager presents with a recurrent right face mass.", "Exam": "large right face mass", "Findings": "A large right nasopharyngeal mass has recurred in a benign, expansile remodeling format - disrupting the pterygoid plate from the sphenoid bone. This tumor is highly vascular, demonstrating marked enhancement at CT and MR, with flow voids on MR, and a characteristic dense tumor stain at angiography.", "Differential Diagnosis": "Juvenile Nasopharyngeal Angiofibroma (JNA)\nSarcoma\nMeningioma", "Case Diagnosis": "Juvenile Nasopharyngeal Angiofibroma (JNA)\nDiagnosis confirmed at histology after first resection.", "Treatment & Follow Up": "Treatment for this recurrence will first involve external beam radiation. After this, embolisation may be tried with or without subsequent surgical excision.", "Discussion": "This boy's JNA recurred after excision. Its impressive size now requires the stepwise treatment described above." }, "Topic": { "Title": "Juvenile Nasopharyngeal Angiofibroma (JNA)", "Disease Discussion": "Juvenile Nasopharyngeal Angiofibroma (JNA) is a beign, non-epithelial tumor that originates near the sphenopalatine foramen. This causes widening at this foramen and can remodel the posterior maxillary sinus wall. The tumor invades the pterygopalatine fossa and then generally deforms the posterior wall of the maxillary sinus. This case is a bit unusual since the bone is destroyed rather than remodeled, a sign of longstanding or aggressive JNA. This destruction causes detatchment of the pterygoid plate from the body of the sphenoid bone. Once the tumor gains access to the pterygopalatine fossa, it can then extend via the inferior and superior orbital fissure, into the orbit and from there into the middle cranial fossa via the supraorbital foramen.", "ACR Code": "2.3", "Category": "Neoplasm, benign", "Keywords": "juvenilenasopharyngealangiofibroma", "Reference": "Som, Head and Neck Imaging, Mosby, St. Louis, 1991, p. 903." } }, { "U_id": "MPX1172", "TAC": [ "MPX1172_synpic19490", "MPX1172_synpic19491", "MPX1172_synpic19493" ], "MRI": [], "Case": { "Title": "Small Bowel Volvulus", "History": "60 year old male with metastatic colorectal cancer and acute renal failure has acute onset abdominal pain and distension.", "Exam": "Patient is Afebrile\nAbdomen is diffusely tender and distended. \nCreatinine is 4.0.\nLactate Pending.", "Findings": "Flat and Upright Abdominal Films reveal multiple dilated loops of small bowel with prominent air fluid levels. \n\nAxial CT images from the upper abdomen show normal orientation of the Superior Mesenteric Artery and Vein proximally with twisting and malposition of the Superior Mesenteric Artery distally (SMA to the left of the SMV proximally and to the right of the SMV distally). \n\nAxial CT images from the mid-lower abdomen show the mesenteric whorl sign (twisting of the mesentery) and associated mesenteric vessel engorgement. Bowel wall thickening suggests ischemia.", "Differential Diagnosis": "Small Bowel Volvulus", "Case Diagnosis": "Small Bowel Volvulus", "Diagnosis By": "Surgically.", "Treatment & Follow Up": "Patient's Small Bowel Volvulus was corrected surgically.", "Discussion": "Small bowel obstruction is a common cause of abdominal pain inpatient and emergency room settings. Frequently plain flat and upright radiographs are the initial diagnostic study obtained to evaluate for obstruction. Radiographic signs of small bowel obstruction include small bowel dilatation (> 3 cm), differential (stair step pattern) air-fluid levels on upright films, and a paucity of distal bowel air. \n\nOnce a small bowel obstruction is suggested on abdominal plain films, CT of the Abdomen and Pelvis is frequently used to better differentiate between the vast array of possible etiologies. Adhesions, incarcerated hernias, intussusception, midgut volvulus, inflammatory disease (Crohn\u2019s Disease), and neoplasm (primary and metastasis) are all common mechanical causes of small bowel obstruction. By far the most common cause of mechanical small bowel obstruction is postoperative adhesion, accounting for nearly 75% of cases. \n\nSmall bowel volvulus is reported to account for 3.5% to 6.2% of small bowel obstruction in the Western world, with a higher percentage in Asia and Africa (increased incidence of parasitic infection and associated increase in gut motility). Common causes of small bowel volvulus in the western world include adhesive bands, Meckel's diverticulum, internal hernia, obstruction neoplasm, and pregnancy. \n\nWhile conventional radiographs frequently reveal signs of small bowel obstruction in the patient with volvulus, CT is an excellent means through which to make the diagnosis. Findings include, twisting of the superior mesenteric artery and vein from their normal orientation proximally to a reversed orientation distally and the \u201cmesenteric whorl sign\u201d of the rotated mesentery. Bowel ischemia is suggested by bowel wall thickening and/or pneumatosis. \n\nOnce diagnosed, treatment is surgical with bowel derotation, resection of infarcted bowel, and possibly bowel fixation. \n\nReferences:\n\n1. Iwuagwu O, Deans G.T. Small bowel volvulus: a review. \nJournal of the Royal College of Surgeons of Edinburgh. 1999: 44 (3) \n\n2. Friedberg B. Small-Bowel Obstruction.\nhttp://www.emedicine.com/ped/topic1203.htm. 2003\n\n3. http://chorus.rad.mcw.edu" }, "Topic": { "Title": "Small Bowel Volvulus", "Disease Discussion": "Volvulus - from the Latin \"volvere\" meaning \"to turn\"\n\nSmall bowel obstruction is a common cause of abdominal pain inpatient and emergency room settings. Frequently plain flat and upright radiographs are the initial diagnostic study obtained to evaluate for obstruction. Radiographic signs of small bowel obstruction include small bowel dilatation (> 3 cm), differential (stair step pattern) air-fluid levels on upright films, and a paucity of distal bowel air. \n\nOnce a small bowel obstruction is suggested on abdominal plain films, CT of the Abdomen and Pelvis is frequently used to better differentiate between the vast array of possible etiologies. Adhesions, incarcerated hernias, intussusception, midgut volvulus, inflammatory disease (Crohn\u2019s Disease), and neoplasm (primary and metastasis) are all common mechanical causes of small bowel obstruction. By far the most common cause of mechanical small bowel obstruction is postoperative adhesion, accounting for nearly 75% of cases. \n\nSmall bowel volvulus is reported to account for 3.5% to 6.2% of small bowel obstruction in the Western world, with a higher percentage in Asia and Africa (increased incidence of parasitic infection and associated increase in gut motility). Common causes of small bowel volvulus in the western world include adhesive bands, Meckel's diverticulum, internal hernia, obstruction neoplasm, and pregnancy. \n\nWhile conventional radiographs frequently reveal signs of small bowel obstruction in the patient with volvulus, CT is an excellent means through which to make the diagnosis. Findings include, twisting of the superior mesenteric artery and vein from their normal orientation proximally to a reversed orientation distally and the \u201cmesenteric whorl sign\u201d of the rotated mesentery. Bowel ischemia is suggested by bowel wall thickening and/or pneumatosis. \n\nOnce diagnosed, treatment is surgical with bowel derotation, resection of infarcted bowel, and possibly bowel fixation. \n\nReferences:\n\n1. Iwuagwu O, Deans G.T. Small bowel volvulus: a review. \nJournal of the Royal College of Surgeons of Edinburgh. 1999: 44 (3) \n\n2. Friedberg B. Small-Bowel Obstruction.\nhttp://www.emedicine.com/ped/topic1203.htm. 2003\n\n3. http://chorus.rad.mcw.edu", "ACR Code": "7.9", "Category": "Obstruction or Stenosis", "Keywords": "Small Bowel VolvulusSmall Bowel Obstructionischemia strangulation perforation", "Reference": "References:\n\n1. Iwuagwu O, Deans G.T. Small bowel volvulus: a review. \nJournal of the Royal College of Surgeons of Edinburgh. 1999: 44 (3) \n\n2. Friedberg B. Small-Bowel Obstruction.\nhttp://www.emedicine.com/ped/topic1203.htm. 2003\n\n3. http://chorus.rad.mcw.edu" } }, { "U_id": "MPX1151", "TAC": [ "MPX1151_synpic19448", "MPX1151_synpic19449", "MPX1151_synpic19450", "MPX1151_synpic19451", "MPX1151_synpic19452", "MPX1151_synpic19453" ], "MRI": [], "Case": { "Title": "Sub-acute thromboembolism of SMA", "History": "47 year old, with 12 day hx of steadily worsening, crampy abdominal pain. Pt reported experiencing sudden onset of pain on the morning of 01 Jan and worsening over the course of day. Pt presented to local ED and underwent CT and US (both negative), was diagnosed with viral vs bacterial gastroenteritits, and released. Pt and family returned to his geographical home, however the pain did not subside, and pt presented to the local hospital 2 days later (9 days prior to current presentation). Pt was seen in the family health clinic and was referred to GI for workup and treatment for gastric ulcer. He was started on prevacid and zantac, and sent home. H pylori test at that time was negative. The pain did not improve over the course of the next several days, and steadily worsened. He stated that eating made it worse, and that curling into a fetal position helped. On the morning of 13 Jan he presented to the ED again, stating that the pain peaked the night before, and the pain is as low as it has been in days. Negative nausea or vomiting. + fever and chills on initial presentation 01Jan, however currently afebrile.", "Exam": "Gen: 47 y/o healthy, caucasian male, in mild distress\nCV: Reg rhythm, slightly tachicardic, no rubs/murmurs/gallops\nPul: Clear to ascultation bilaterally\nABD: Slightly tender to palpation in R and L upper quadrant. +Bowl sounds; Non-distended; neg Murphy\u2019s; No guarding or rebound\nPulses: 2+ throughout\nExt: No clubbing/cyanosis/edema\nCBC: 10.7> 15.4/46.4 < 495", "Findings": "Abdominal CT (with contrast):1. Mild stranding focally in the lesser sac, medial to the second portion of the duodenum, anterior to the third portion of the duodenum, posterior to the pancreas and just inferior to the pancreatic head, with mild stranding adjacent to the SMA.2. Possible mild narrowing of the third portion of the duodenum between the SMA and aorta.Addendum: Small thrombus within the proximal portion of the SMA. Distal to this region the contrast is not as bright as the proximal SMA, with mild adjacent inflammatory changes adjacent to the SMA consistent with SMA Syndrome.", "Differential Diagnosis": "1. Thrombus of SMA\n2. Mild focal pancreatitis\n3. Small perforation of medial 2nd portion of duodenum", "Case Diagnosis": "Sub-acute thromboembolism of SMA", "Treatment & Follow Up": "Pt was referred to interventional radiology for definitive diagnosis and possible treatment. Interventional angiography confirmed presence of thrombus in the proximal superior mesenteric artery, involving most of the first 10cm of the artery. Urokinase was infused in an attempt to lyse the thrombus with minimal improvement noted. Pt was subsequently taken to the OR for exploratory laparoscopy, resulting in resection of approximately 20cm of small bowel, and re-vascularization of SMA. Pt tolerated procedure well, and was improving at time of writing." }, "Topic": { "Title": "Sub-acute thromboembolism of SMA", "Disease Discussion": "The superior mesenteric artery (SMA) arises approximately 1 cm below the celiac artery and runs inferiorly toward the cecum, terminating as the ileocolic artery. Along the way, it gives rise to the inferior pancreaticoduodenal artery, several jejunal and ileal branches, the middle colic artery, and the right colic artery. Complete or partial occlusion of the SMA leads to acute mesenteric ischemia, with a mortality rate of 60-70%. There are four major causes of acute mesenteric ischemia: 1) SMA embolism (50%); 2) SMA thrombosis (15-25%); 3) Mesenteric venous thrombosis (5%); 4) Nonocclusive ischemia (20 to 30 percent). , The SMA is particularly susceptible to embolic events of cardiac origin, due to it\u2019s relatively large caliber, and narrow take-off angle from the descending aorta. The embolus usually lodges 3 to 10 cm distal to the origin of the SMA, in a tapered segment distal to the take off of the middle colic artery. In general, the clinical presentation of acute mesenteric ischemia is limited to sudden onset of pain, pain out of proportion to physical findings, and possibly some nausea and/or vomiting. The laboratory findings are non-specific. Radiographically, mesenteric angiography remains the gold standard diagnostic study for mesenteric arterial ischemia. Plain fim radiography of the abdomen is non-specific, and in 25% of all cases, will be normal. The use of traditional CT (with contrast) for the detection of mesenteric ischemia is limited by the ability of the radiologist to distinguish areas of decreased opacity distal to site of obstruction. One small study demonstrated a sensitivity of 64% and specificity of 92%. MRA and Multi detector row CT (MDCT) hold promise as viable tools to evaluate mesenteric arteries, however no comparison studies are available for study. Angiography therefore remains the gold standard.Treatment of mesenteric arterial embolism, traditionally, has been early surgical laparotomy with embolectomy. Intra-operative palpation for SMA pulses is performed and the small bowel is carefully examined for areas of persistent ischemia, which are resected. A \"second look\" laparotomy within the next 24 to 48 hours may be necessary to resect additional ischemic or gangrenous bowel. A less well-established approach (which was used initially in this case) is local infusion of thrombolytic therapy, which has been successful in a number of reports. , , Thrombolytic therapy should only be considered in patients who can undergo angiography within eight hours of the onset of abdominal pain, and who do not have clinical evidence of bowel necrosis or other contraindications to thrombolytic therapy. Surgical exploration is mandatory in patients who do not demonstrate clot lysis within four hours or develop evidence of progressive ischemia. Despite success in case series, the long-term reocclusion rate after thrombolytic therapy has not been well studied. Long term treatment is aimed at limiting the chance of recurrence and usually requires the use of Warfarin.", "ACR Code": "-1.-1", "Category": "Unsure", "Keywords": "thromboembolism", "Reference": "McKinsey, JF, Gewertz, BL. Acute mesenteric ischemia. Surg Clin North Am 1997; 77:307\n Reinus, JF, Brandt, LJ, Boley, SJ. Ischemic diseases of the bowel. Gastroenterol Clin North Am 1990; 19:319\n Cappell, MS. Intestinal (mesenteric) vasculopathy. I. Acute superior mesenteric arteriopathy and venopathy. Gastroenterol Clin North Am 1998; 27:783.\n ibid\n McKinsey, JF, Gewertz, BL. Acute mesenteric ischemia. Surg Clin North Am 1997; 77:307\n Taourel, PG, Deneuville, M, Pradel, JA. Acute mesenteric ischemia: Diagnosis with contrast-enhanced CT. Radiology 1996; 199:632\n McBride, KD, Gaines, PA. Thrombolysis of a partially occluding superior mesenteric artery thromboembolus by infusion of streptokinase. Cardiovasc Intervent Radiol 1994; 17:164.\n Rivitz, SM, Geller, SC, Hahn, C, Waltman, AC. Treatment of acute mesenteric venous thrombosis with transjugular intramesenteric urokinase infusion. J Vasc Interv Radiol 1995; 6:219.\n Simo, G, Echenagusia, AJ, Camunez, F, et al. Superior mesenteric arterial embolism: Local fibrinolytic treatment with urokinase. Radiology 1997; 204:775." } }, { "U_id": "MPX1182", "TAC": [ "MPX1182_synpic20289" ], "MRI": [], "Case": { "Title": "Replaced Right Hepatic Artery", "History": "59 year-old female with abdominal pain. CT evaluation demonstated a mass in the head of the pancreas.", "Exam": "Mid-epigastic abdominal tenderness.", "Findings": "CT evaluation demonstrates a mass arising in the head of the pancreas. Incidental note was made of a vessel passing along the mass and through the portal-caval space with branches feeding the right hepatic lobe. Angiogram confirmed the presence of a replaced right hepatic artery.", "Differential Diagnosis": "Replaced Right Hepatic Artery", "Case Diagnosis": "Replaced Right Hepatic Artery", "Diagnosis By": "angiographically", "Treatment & Follow Up": "The portion of the replaced right hepatic artery involving in the tumor was resected and the artery transplanted to arise from the distal aorta by means of a venous graft." }, "Topic": { "Title": "Replaced Right Hepatic Artery", "Disease Discussion": "The vascular supply to the liver is widely varied with accessory and replaced arteries frequently demonstrated. To being with, the common hepatic artery usually arises from the celiac trunk (86%). Other sources include the superior mesenteric artery (2.9%), the aorta (1.1%), and rarely, the left gastric artery. \n\nWhen it originates from the celiac axis, the common hepatic artery runs horizontally along the upper border of the head of the pancreas. The gastroduodenal artery branches off the common hepatic artery posterior and superior to the duodenum. The common hepatic artery then continues as the proper hepatic artery and turns upward to ascend in the hepatoduodenal ligament, in front of the epiploic (Winslow's) foramen. Within the hepatoduodenal ligament, the proper hepatic artery lies to the left of the common bile duct and anterior to the portal vein. Within the ligament the proper hepatic artery divides into the right and left hepatic arteries. Arterial distribution to different functional segments is identical to the distribution of portal vein The right hepatic artery passes to the right behind (or occasionally in front of) the hepatic duct in front of the portal vein. Before entering the liver, the right hepatic artery gives off the cystic artery in the hepatocystic triangle located between the cystic duct and the common bile duct.\n\nAberrant hepatic arteries are found in about 45% of subjects. If the arteries arise entirely from some source other than the celiac arterial distribution, they are called replaced arteries and can supply an entire lobe of the liver or even the entire liver. Atypical hepatic arteries are commonly called accessory arteries if they arise from some aberrant source and are additive to lobar branches. Even so, it should be noted that they often provide the primary arterial supply to a specific portion of the liver and therefore are not accessory arteries. These aberrant hepatic arteries should be distinguished from segmental arteries arising outside the liver.\n \nThe most common occurrences of aberrant hepatic arteries involve , the left hepatic artery arising from the left gastric artery, which comprises 25-30% of instances. In about 17% of cases, the right hepatic artery branches from the superior mesenteric artery (as in this patient).", "ACR Code": "9.1", "Category": "Congenital, normal variant", "Keywords": "replaced right hepatic arteryaberrantvariant", "Reference": "Skandalakis JE, Skandalakis LJ, Skandalakis PN, Mirilas P. Hepatic Surgical Anatomy. Surg Clin N Am 2004;84(2)" } }, { "U_id": "MPX1164", "TAC": [ "MPX1164_synpic33081", "MPX1164_synpic33082", "MPX1164_synpic33084" ], "MRI": [], "Case": { "Title": "Bilateral Wilms Tumor", "History": "10 month old boy, previously healthy, brought to clinic after mom notices a bulge in his abdomen while bathing him.", "Findings": "Right-sided 5x5x8cm echogenic mass in renal fossa exerting mass effect on the right lobe of liver.\n\nOn CT, left kidney shows 3x2x2cm mass in the interpolar region. Involvement of right renal vein could no be excluded.", "Differential Diagnosis": "- Wilms Tumor\n- Neuroblastoma\n- Polycystic kidney disease\n- Sarcoma\n- Hydronephrosis", "Case Diagnosis": "Bilateral Wilms Tumor", "Diagnosis By": "Pathological/surgical specimen", "Treatment & Follow Up": "F/U Ultrasound q 3-6 months to assess for recurrence" }, "Topic": { "Title": "Bilateral Wilms Tumor", "Disease Discussion": "Wilms tumor or nephroblastoma is the most common childhood abdominal neoplasm; and, is often discovered as an asymptomatic palpable abdominal mass. This neoplasm accounts for 5% of all childhood malignancies. Additionally, 10% of patients with Wilms tumor have other associated congenital malformations, including Beckwith Wiedemann syndrome, hemihypertrophy, WAGR syndrome, and other genitourinary abnormalities. \n\nWith current multimodal therapy, over 90% of patients recover completely. Therefore, early detection and staging is essential. A set of chest and abdominal radiographs are usually obtained to look for mass effect, calcifications, and lung mets. Ultrasound is the initial study to evaluate the characteristics of the mass. It is also the preferred study for follow up of the abdominal mass during treatment and post-surgery. Finally CT with contrast is obtained in suspected Wilms tumor to evaluate extension into surrounding structures, like renal veins. \n\nOf paramount importance is to evaluate the contralateral kidney, since 5-10% of tumors are bilateral.", "ACR Code": "8.3", "Category": "Congenital, malformation", "Keywords": "WilmsNephroblastoma", "Reference": "1. Tanagho E, McAninch J., Smith's General Urology 16th ed. NY, 2004. p 358-362.\n2. Paulino A. Wilms Tumor, eMedicine May 23, 2006" } }, { "U_id": "MPX1186", "TAC": [ "MPX1186_synpic46969" ], "MRI": [], "Case": { "Title": "Intrinsic sclerotic bone dysplasia (likely Osteopetrosis) with fracture", "History": "Four year-old female presenting with right hip pain and inability to bear weight.", "Findings": "Increased sclerosis is noted throughout the osseous structures. A vertical oriented lucency in the medial femoral metaphysis is seen.", "Differential Diagnosis": "Differential Diagnosis for Dysplasias with Increased Bone Density:\nOsteopetrosis\nPyknodysostosis\nOsteosclerosis, Stanescu Type\nOsteomesopyknosis\nCentral Osteosclerosis with Ectodermal Dysplasia\nAxial Osteosclerosis with Bamboo Hair\nOsteopoikilosis\nMelorheostosis\nOsteopathia Striata\nRenal Osteodystrophy\nHyperparathyroidism\nOsteomalacia", "Case Diagnosis": "Intrinsic sclerotic bone dysplasia (likely Osteopetrosis) with fracture", "Diagnosis By": "Unconfirmed, differential case with a fracture." }, "Topic": { "Title": "Intrinsic sclerotic bone dysplasia (likely Osteopetrosis) with fracture", "Disease Discussion": "Osteopetrosis is a family of rare bone disorders caused by dysfunctional osteoclasts. \n\nFrequently, a spectrum of skeletal abnormalities are seen leading to at least four types (Precocious Type i.e. autosomal recessive, Delyaed Type i.e. autosomal dominant, Intermediate Recessive Type, and Tubular Acidosis Type), characterized by a generalized increase in the density of bone. Because of osteoclast dysfunction, bone remodeling is impaired and the primary calcified substantia spongiosa ossium is not reabsorbed. Eventually, the normal marrow spaces may become obliterated, resulting in pancytopenia.\n\nTwo modes of genetic transmission have been described: autosomal recessive and autosomal dominant. Autosomal recessive is associated with worse outcomes, as most patient\u2019s die from infection or bone marrow failure before adolescence. The autosomal dominant form is frequently discovered incidentally in adulthood with benign outcomes. \n\nClinical presentations for the autosomal recessive form include failure to thrive, hepatosplenomegaly, severe anemia, and cranial nerve dysfunction. Progressive loss of the normal marrow leads to pancytopenia and predisposes to recurrent infection. Other associations include renal tubular acidosis and neuronal storage diseases. \n\nVarious synonyms include: Albers-Schonberg disease, osteosclerosis, osteopetrosis generalisata, and marble bones disease. \n\nPrecocious Type: Radiographic findings are characterized by generalized osteosclerosis. Tubular bones demonstrate a failure of differentiation between the cortex and medullary cavity. A bone within bone appearance may be seen.\n\nDelayed Type: May be detected because of a pathologic fracture. The radiographic findings are similar to the autosomal recessive form. Bones are diffusely osteosclerotic, with defective tubulation and a thickened cortex. The vertebral endplates are accentuated, producing a \u201csandwich\u201d vertebra appearace in children, and a \u201crugger-jersey\u201d spine may be seen in adults. A bone within bone appearance is frequently seen.\n\nIntermediate Recessive Type: Short stature patients, with pathologic fractures, anemia, and hepatomegaly, characterized by diffuse bone sclerosis, bone within bone appearance, and retained primary and impaced permanent teeth. Ischemic necrosis of the femoral head has been reported.\n\nTubular Acidosis Type: \u201cMarble Brain\u201d or \u201cSly disease\u201d consists of osteopetrosis, renal tubular acidosis, and cerebral calcifications. Radiographic findings include osteosclerosis, loss of the medullary cavity, and pathologic fractures.", "ACR Code": "4.9", "Category": "Unknown, Not specified", "Keywords": "Intrinsic sclerotic bone dysplasiaOsteopetrosis", "Reference": "Elster et al. Autosomal Recessive Osteopetrosis: Bone Marrow Imaging. Radiology 1992;182:507-514.\nResnick. Diagnosis of Bone and Joint Disorders. 4th Ed. Saunders. Philadelphia, PA. 2002.\nKumar et al. The vertebral body: Radiographic Configurations in varios congenital and acquired disorders. RadioGraphics 1988;8(3):455-485." } }, { "U_id": "MPX1191", "TAC": [ "MPX1191_synpic17425", "MPX1191_synpic17426", "MPX1191_synpic17429" ], "MRI": [], "Case": { "Title": "Hepatocellular carcinoma with extension to the right atrium", "History": "Patient presented in this case is an 81 year old woman who was originally diagnosed with hepatocellular carcinoma in 2001. At that time she underwent radioablation. At the surveillance appointment in 2002, CT demonstrated a recurrence of tumor. Due to her comorbid conditions and metastatic lung disease, surgery options were not offered. In September of 2003, she experienced shortness of breath and chest pain and was seen in the emergency room. A CT pulmonary angiogram was perfomed to evaluate for a pulmonary embolism. She ruled out for a pulmonary embolism. However, selected images from that study are presented here and demonstrate a very large liver tumor with extension into the right atrium", "Exam": "AFP > 1000", "Findings": "There is a very large liver mass with heterogeneous enhacement that extends into hepatic veins, inferior vena cava and into the right atrium.", "Differential Diagnosis": "Vascular extension of the tumor is almost always a result of hepatocellular carcinoma. Without this finding a liver mass has its usual differential diagnosis, mets, adenoma, Focal nodular hyperplasia.", "Case Diagnosis": "Hepatocellular carcinoma with extension to the right atrium", "Treatment & Follow Up": "After initial diagnosis of hepatocellular carcinoma in 2001, this patient underwent radioablation. Unfortunately, tumor recurred in 2002. Further surgery was not offered because of comorbid conditions and metastatic lung disease. Patient current status is DNR.", "Discussion": "see factoid" }, "Topic": { "Title": "Hepatocellular carcinoma with extension to the right atrium", "Disease Discussion": "Hepatocellular carcinoma, or hepatoma, refers to a malignant lesion originating in the liver parenchymal cells. The most significant risk factors for development of HCC include cirrhosis and hepatitis B or C infection. Other less common risk factors include hemochromatosis, aflatoxin exposure and alpha-1-antiprotease deficiency.\n\nClinical presentation: Patients often present with cachexia, weakness, right upper quadrant pain, and weight loss. HCC should be suspected in previously stable cirrhosis patients who experience a sudden deterioration in their condition.\n\nPhysical examination: The physician may find an enlarged and tender liver, palpable mass, and bruit or friction rub.\n\nLaboratory: A sudden and sustained elevation in AFP is suggestive of HCC.\n\nRadiographic evaluation:\n\n\tCT: HCC can present as a solitary mass, multiple masses with a dominant lesion and satellites or as a diffusely infiltrating neoplasm. The masses can be characterized as areas of low attenuation. Ten percent of tumors will show calcification. Dual phase imaging in arterial and portal venous phases may be necessary to detect the tumor. These tumors commonly invade blood vessels such as portal and hepatic veins. Portal vein thrombosis appears as regional wedge-like shapes of low density that project peripherally. Tumor thrombus will enhance on arterial phase CT images.\n\n\tMRI: MRI findings depend on the amount of fibrosis and necrosis in the liver. HCC can be recognized as low-signal intensity on T1 with an increase in signal intensity on T2. MR demonstrates vascular involvement well.\n\n\tUS: HCC appears as mosaic pattern, peripheral sonolucency with lateral shadow due to fibrotic pseudocapsule, posterior acoustic enhancement. Along with AFP levels, ultrasound is used as a screening tool in patients with a history of cirrhosis.\n\n\nPatient presented in this case is an 81 year old woman who was originally diagnosed with hepatocellular carcinoma in 2001. At that time she underwent radioablation. At the surveillance appointment in 2002, CT demonstrated a recurrence of tumor. Due to her comorbid conditions and metastatic lung disease, surgery options were not offered. In September of 2003, she experienced shortness of breath and chest pain and was seen in the emergency room. A CT pulmonary angiogram was perfomed to evaluate for a pulmonary embolism. Selected images are presented from this study. There is a very large mass with heterogeneous enhacement that extends into hepatic veins, inferior vena cava and into the right atrium.\n\nApproved by Dr. Thomas Murphy, M.D. - staff radiologist, Tripler Hospital", "ACR Code": "7.3", "Category": "Neoplasm, carcinoma", "Keywords": "hepatocellular \r\ncarcinoma\r\nHCCvein \r\nthrombosis\r\nvascular \r\nextensionatrium", "Reference": "1. Halpert, R. and P. Feczko. Gastrointestinal Radiology. 1999.\n2. Kamel, I. and D. Bluemke. Imaging Evaluation of Hepatocellular Carcinoma. J. of Vascular and Interventional Radiology. Vol 13 (9,Part 2) Supplement. Sept. 02 pp. S173-S183.\n3. Tierney, L. (ed.) Current Diagnosis and Treatment 2003." } }, { "U_id": "MPX1193", "TAC": [ "MPX1193_synpic51666", "MPX1193_synpic51667", "MPX1193_synpic51669" ], "MRI": [], "Case": { "Title": "Thyroglossal Duct Cyst", "History": "65 year-old man with a firm neck mass for three months.", "Exam": "Palpable non-tender mass at the midline of the anterior neck.", "Findings": "Well-defined hypodense lesion along the right paramidline anterior neck at the level of the thyroid cartilage and imbedded within the strap muscles. It has internal fluid attenuation. No nodular focus or calcification is demonstrated. This lesion measures 2.8cm transverse by 2.2cm AP.", "Differential Diagnosis": "\u2022 Lingual or sublingual thyroid\n\u2022 Thyroid carcinoma\n\u2022 Dermoid or epidermoid of tongue\n\u2022 Submandibular of sublingual space abscess\n\u2022 Mixed laryngocele\n\u2022 Thyroglossal duct cyst", "Case Diagnosis": "Thyroglossal Duct Cyst", "Diagnosis By": "Characteristic imaging findings.", "Treatment & Follow Up": "Surgical resection.", "Discussion": "A thyroglossal duct cyst is a remnant of the thyroglossal duct found between the foramen cecum of the tongue base and the thyroid in the infrahyoid neck. Its formation is secondary to failure of involution of the thyroglossal duct and persistent secretion of epithelial cells lining the duct. They can occur anywhere along the route of descent of the thyroglossal duct. Thyroglossal duct cysts are the most common congenital neck lesion, being three times as common as branchial cleft cyst.\n\nThyroglossal duct cysts most commonly present at a doughy compressible painless neck mass along the midline or paramedian in a child or young adult. 90% present at less than 10 years of age. Other signs and symptoms include recurrent appearance of neck mass with upper respiratory tract infections or trauma. Often, the patient will have a history of multiple prior incision & drainage procedures for \u201cneck abcess\u201d. A rapidly enlarging mass suggests either infection of associated differentiated thyroid carcinoma. Any associated nodularity or chunky calcification suggests associated thyroid carcinoma.\n\nA thyroglossal duct cyst presents as a midline cystic neck mass imbedded within the infrahyoid strap muscles, \u201cclaw sign\u201d. 50% of the time they are found at the level of the hyoid bone, 25% on the infrahyoid neck and 25% timed at the suprahyoid neck. There usually to 2-4 cm in size and are round or ovoid. On contrast-enhanced CT it appears low density mass, occasionally with internal septations and a thin rim of peripheral enhancement. They are anechoic on ultrasound evaluation.\n\nREFERENCES: \n\nDedivitis RA, et al. Thyroglossal duct: A review of 55 cases. J Am Coll Surg. 194(3):274-7, 2002.\n\nReede DL, et al. CT of thyroglossal duct cysts. Radiology. 157(1):121-5, 1985.\n\nhttps://my.statdx.com." }, "Topic": { "Title": "thyroglossal duct cyst", "Disease Discussion": "The thyroglossal duct cyst (TDC) is the most common result of abnormal thyroid development. Because there is ectopic thyroid tissue embedded in the wall of these cysts, there is a small but finite risk of development of thyroid neoplasms associated with these cysts. At least 150 cases of cancer arising in TDC have been reported - most are papillary carcinomas. {UI:98242298- Vera-Sempere F, et atl} Irregular calcification of the papillary carcinoma within the TDC has also been reported. Squamous cell carcinomas have also been reported within a TDC. The presentation of a cancer developing within a TDC, is similar to that of a TDC alone: a palpable yet non-tender midline neck mass. The recommendations for cancer developing within a TDC include the Sistrunk procedure, with variable recommendations made for the use of radioiodine and/or removal of any normal thyroid tissue.", "ACR Code": "2.3", "Category": "Congenital, malformation" } }, { "U_id": "MPX1174", "TAC": [ "MPX1174_synpic18375", "MPX1174_synpic18376" ], "MRI": [], "Case": { "Title": "Malignant Melanoma", "History": "The patient is a 79-year-old woman who presented with a two-day history of left lower extremity weakness associated with loss of proprioception, and vomiting after falling and striking the back of her head. The patient's past medical history is significant for multiple medical problems, including recent seizures.", "Exam": "3/5 left lower extremity weakness.\nDiminished proprioception.\nLoss of vision in left eye.", "Findings": "Non-contrast CT images of the brain demonstrate a 1.3 x 1.2 cm mass within the left optic nerve with multiple additional diffuse hemorrhagic lesions with associated vasogenic edema and mass effect. The largest and most concerning mass is within the right frontal lobe. This mass measures approximately 2.9 cm in greatest dimension.\n\nA whole body bone scan demonstrates intense focal uptake at the left femoral head, and subtle intake within the mid right femoral diaphysis.", "Differential Diagnosis": "Metastatic carcinoma (breast, kidney, lung, thyroid)\nmelanoma, \nlymphoma\nsarcoma", "Case Diagnosis": "Malignant Melanoma", "Diagnosis By": "Biopsy/pathology of palpable lymphnode", "Treatment & Follow Up": "Supportive", "Discussion": "Radiologic Diagnosis: Patients with melanoma of 1 mm thickness will undergo chest radiography. Patients with advanced disease may undergo MR imaging of the head, as well as computed tomography of the chest, abdomen, and pelvis.\n\nHowever, single whole body positron emission tomography is quickly emerging as the study of choice to detect metastatic disease." }, "Topic": { "Title": "Malignant Melanoma", "Disease Discussion": "Cutaneous melanoma is readily curable-85% of diagnosed patients will enjoy survival following surgical excision. Unfortunately, this prognosis cannot be offered to those with metastatic disease. Overall, the median survival is six to nine months, but in the subset of patients with bone metastases, the survival is only four months. Bone metastasis is usually a late occurrence is the course of the disease. \n\nEtiology and Pathogenesis: \nMelanoma can be broadly divided into two categories: sporadic (90 %) and familial (10 %). As is true with most neoplasms the cause is multifactorial. A host of environmental and genetic factors combine in synergy to produce unregulated cell proliferation. In the case of sporadic melanoma, exposure to ultraviolet B (290 to 320 nm) and ultraviolet A (320 to 400 nm) is the most significant environmental factor. The most influential genetic component of this disease is a deletion or mutation in the p16INK4 gene. Normally, this protein regulates cell proliferation by inhibiting the assembly of cyclin D/CDK 4/6 complex. This genetic error occurs in 25 to 40 percent of sporadic melanomas. Other risk factors include, in decreasing order: past history of melanoma; family history of melanoma or dysplastic nevus; presence of large congenital nevi; presence of ten or greater dysplastic nevi; presence of 100 or greater common acquired nevi; fair skin; red hair; and high intermittent sun exposure. \n\nMalignant melanoma is the final lesion in a series of premalignant lesions that follow a predictable pattern of progression. First, a normal melanocyte escapes keratinocyte control and becomes a nevus cell. Next, the cell separates from the basement membrane and demonstrates cytologic atypia, thus becoming a dysplastic nevus cell. Subsequently, the cell exhibits a radial growth phase, followed by a vertical growth phase. The Breslow Depth (0.76 mm) is the most reliable predictor of the behavior of the primary lesion, so that the likelihood of metastatic transformation increases with the depth of vertical growth. The ability to spread to distant sites is a function of the b3 subunit of the vitronectin receptor.\n\nEpidemiology: \nLancaster is credited with discovering a relationship between melanoma incidence and latitude. As the distance to the equator decreases, the incidence and rate of melanoma mortality in whites increases. Interestingly, there are 30 cases per 100,000 people in Australia. Australia exhibits the highest melanoma incidence in the world because of its equatorial climate, fair-skinned population, and ozone depletion. In the United States, the incidence has increased from 1 per 100,000 in 1935 to 15 per 100,000 in 1996. In 1973, the mortality was 1.6 per 100,000 individuals; in 1996, the mortality rate was 2.3 per 100,000 individuals. At present, melanoma ranks as the sixth most common cancer in American men, and the seventh most common cancer among American women. The risk for developing melanoma among white Americans is 1 in 85.\n\nClinical Manifestations:\nCutaneous melanoma is distinguished by its asymmetry, diffuse borders, variegated color, diameter greater than 5 mm, and evolving morphology. Ten percent of lesions ulcerate and bleed. In a study of 84,000 with melanoma, 2.2% of all melanoma presented without signs of a primary lesion (Chang, Cancer 1998; 83: 1664). These patients are usually younger than other melanoma patients, and they tend to be male. The prognosis is similar to that of patients with known primary cutaneous melanoma. The most common sites for metastasis are skin, lungs, liver, brain, and bone.\t\nBrain metastases are present in 8% to 46% of melanoma patients.\n\nDiagnosis: \nLymph node core biopsy with subsequent immunohistochemical analysis provides a definitive diagnosis. Ninety percent of melanomas are positive for S-100 antigen. HMB-45 (Melanoma Associated Marker) is more specific for melanoma than S-100, but it is less sensitive. Melanoma cells do not exhibit cytokeratin, leukocyte common antigen, or desmin. \n\nTreatment:\nAt present, there is no cure for disseminated melanoma (Stage IV: M1). Because brain metastases cause symptoms via compression of neural parenchyma, all therapy is geared toward reducing intracranial pressure. This can be achieved via corticosteroids, gamma knife irradiation or conventional surgery (in the case of a solitary brain lesion), and/or whole brain radiotherapy (in the case of multiple lesions). The pain associated with bone metastases is successfully treated by radiotherapy.", "ACR Code": "1.3", "Category": "Neoplasm, metastatic", "Keywords": "melanomaHMB-45vitronectin receptor b3 subunit", "Reference": "1. Bakerman, S. et al. ABC's of Interpretive Laboratory Data, 3rd Edition. Myrtle Beach: Interpretive Laboratory Data, Inc., 1994.\n\n2. DeVita, V. et al. Cancer: Principles and Practice of Oncology, 6th Edition. Philadelphia: Lippincott, Williams, and Wilkins, 2001." } }, { "U_id": "MPX1194", "TAC": [ "MPX1194_synpic24336" ], "MRI": [], "Case": { "Title": "Stage IVB Non-Hodgkin\u2019s lymphoma (Pre B-cell variety) diagnosed by biopsy", "History": "15 year old male with two months of progressive swelling over left chest, under left axilla, and left neck. The patient has also had an unintentional 10 lb weight loss over the past six months. Denies F/C/NS", "Exam": "Chest: Diffuse solid tissue discrete from underlying muscle layer over left pectoralis muscle that continues under left axilla and over left shoulder and neck. There is no color change to the skin. The area is non-tender and non-mobile. \nLungs are CTAB \nExt: DTRs and distal pulses are normal and equal bilaterally in the UEs. Full ROM, strength normal and equal bilaterally in UEs\nCV: RRR with no M/R/Gs\nAbd: Soft NT/ND with +abs", "Findings": "On the contrast CT of the chest there is a large mass that is beneath and discrete from the pectoralis muscle layer of the chest that stretches from the left pectoralis muscle under the left axilla. It is not attached to any surrounding structures and has the density of surrounding soft tissue. The mass appears to be a conglomeration of multiple enlarged lymph nodes. These nodes are discrete from surrounding structures and do not appear to be invading any surrounding structure. There appears to be a mass effect that is compressing the chest wall\n\nThe contrast CT of the abdomen shows hepatosplenomegaly with multiple densities seen in the spleen and a large density also visible in the liver. There may also be enlarged para-aortic lymph nodes but it hard to determine from this image.", "Differential Diagnosis": "Infectious \u2013 TB, reactive lymphadenitis, fungal\nNeoplastic \u2013 Lymphoma, soft tissue tumor, liposarcoma, metastatic disease", "Case Diagnosis": "Stage IVB Non-Hodgkin\u2019s lymphoma (Pre B-cell variety) diagnosed by biopsy", "Diagnosis By": "Biopsy", "Treatment & Follow Up": "Infectious \u2013 TB, reactive lymphadenitis, fungal\nNeoplastic \u2013 Lymphoma, soft tissue tumor, liposarcoma, metastatic disease", "Discussion": "Lymphoma (Hodgkin\u2019s or Non-Hodgkin\u2019s) is a common form of cancer that presents in a bimodal age distribution with a peak between 20-30 years of age and then a peak again around age 60. Type is determined with histochemical testing of tumor cells. Staging is done with CT or MRI. Staging system is based on the Ann Arbor classification system and is I-IV with the A or B modifier. \nStage I \u2013 Single lymph node or organ Stage II \u2013 Two or more lymphoid organs on same side of diaphragm\nStage III - Involvement on both sides of diaphragm Stage IV \u2013 Involvement of extralymphoid organs\nNodal involvement is determined with CT or MRI and a node is considered positive if greater than 8mm. Tumors may be B-cell or T-cell in origin. Treatment is almost exclusively chemotherapeutic in nature and is aimed at specific tumor type. Specific type is determined by bone marrow aspiration and testing of cells." }, "Topic": { "Title": "Stage IVB Non-Hodgkin\u2019s lymphoma (Pre B-cell variety) diagnosed by biopsy", "Disease Discussion": "Lymphoma (Hodgkin\u2019s or Non-Hodgkin\u2019s) is a common form of cancer that presents in a bimodal age distribution with a peak between 20-30 years of age and then a peak again around age 60. Type is determined with histochemical testing of tumor cells. Staging is done with CT or MRI. Staging system is based on the Ann Arbor classification system and is I-IV with the A or B modifier. \nStage I \u2013 Single lymph node or organ Stage II \u2013 Two or more lymphoid organs on same side of diaphragm\nStage III - Involvement on both sides of diaphragm Stage IV \u2013 Involvement of extralymphoid organs\nNodal involvement is determined with CT or MRI and a node is considered positive if greater than 8mm. Tumors may be B-cell or T-cell in origin. Treatment is almost exclusively chemotherapeutic in nature and is aimed at specific tumor type. Specific type is determined by bone marrow aspiration and testing of cells.", "ACR Code": "99.34", "Category": "Clinical Exam Finding or Sign", "Keywords": "LymphomaHodgkin\u2019s or Non-Hodgkin\u2019s", "Reference": "Grainger & Allison's Diagnostic Radiology: A Textbook of Medical Imaging, 4th ed. 2001 Churchill Livingstone, Inc.\nHennessy, B., T. et al. Non-Hodgkin\u2019s Lymphoma: an update. The Lancet Oncology. 5:6 June 2004." } }, { "U_id": "MPX1195", "TAC": [ "MPX1195_synpic55737" ], "MRI": [ "MPX1195_synpic55738", "MPX1195_synpic55739" ], "Case": { "Title": "Diprosopus (conjoined) twins, Anencephaly", "History": "Young primigravida (G1P0) with uncomplicated pregnancy. Previous US (not known when) reported as \u201cno abnormalities\u201d. Returns to clinic, and now US fails to show heartbeat.", "Exam": "Stillborn baby", "Findings": "\u2022 Duplication of facial structures (eyes, teeth)\n\u2022 Cleft with partial duplication of vertebrae (\uf0e0L1)\n\u2022 Absence of spinal cord and brain\n\u2022 Enlarged liver, distorting abdominal and thoracic structures\n\u2022 Congenital diaphragmatic hernia (lack of normal lung tissue found on autopsy)", "Differential Diagnosis": "Conjoined Twins", "Case Diagnosis": "Diprosopus (conjoined) twins, Anencephaly", "Diagnosis By": "Autopsy", "Discussion": "For discussion, please read the [Topic]" }, "Topic": { "Title": "Diprosopus Twins (conjoined)", "Disease Discussion": "Diprosopus is a rare form of conjoined twinning characterized by a single body, one unusual head and two faces or a spectrum of duplication of the raniofacial structures. This is seen in less than 1% of cases of conjoined twins.\n\nEctoderm forms skin and neural plate\nNeural differentiation signal from mesoderm (notochord)\nNeural plate folds outwards during wk 3 gestation creating the neural groove\nBy end of wk 4 the neuropores close off\n\nIf folds fail to close, neural tissue is exposed to amniotic fluid - leading to necrosis and loss of tissue\n\nDiprosopus Twins (conjoned) is a very rare condition.\nSpinal cord and brain development are depended on a combination of many signal messengers and synchronized tissue migration\n\nOnce identified on fetal sonography, close monitoring is required.", "ACR Code": "1.1", "Category": "Congenital, malformation", "Keywords": "twinsstillbornanencephaly", "Reference": "Ekinci, Gazanfer et al. An anencephalic monocephalus diprosopus \u201cheaded twin\u201d: postmortem and CT findings with emphasis on the cranial bones. The Turkish Journal of Pediatrics. 2005; 47: 195-198.\n\nSadler, T.W. Langman\u2019s Medical Embryology. 10th ed. Baltimore: Lippincott Williams & Wilkins, 2006." } }, { "U_id": "MPX1197", "TAC": [ "MPX1197_synpic46446", "MPX1197_synpic46448", "MPX1197_synpic46449" ], "MRI": [], "Case": { "Title": "Pyopneumothorax", "History": "60 yo M brought in from outside facility after being on broad spectrum antibiotics x 5 days.\n\nThe patients presents with severe dyspnea, renal failure, and hypotension. Soon after admitance, the patient progressed to frank Acute Respiratory Distress Syndrome", "Exam": "Lungs: Decreased breath sounds throughout, more pronounced on the right side, with wheezing and rales in the left side.\n\nLabs: No organism identified from pleural drainage, which was serosanguinous and purulent.", "Findings": "An air-fluid level in the right hemithorax, with marked atelectasis of the right lung.", "Differential Diagnosis": "Hydropneumothorax\nHemopneumothorax\nPyopneumothorax", "Case Diagnosis": "Pyopneumothorax", "Diagnosis By": "CT and direct surgical visualization", "Treatment & Follow Up": "Surgical management of pyopneumo thorax with medical management of Acute Respiratory distress, Acute Renal Failure, and sepsis." }, "Topic": { "Title": "Pyopneumothorax", "Disease Discussion": "Condition: \nPyopneumothorax - pus and gas in the pleural space\n\nCauses:\nUsually a necrotizing infection causing a bronchopleural fistula. Also caused by esophageal perforation. The organisms responsible are anaerobes, tuberculosis, pyogenic or fungal. Coccidiodes is the most common fungal cause.\n\nGross Morphology:\nA hemithorax filled with fluid and gas causing the lung to collapse on itself\n\nHistology:\nSerosanguinous or purulent fluid\n\nSpecial Stains:\nTypically tested for acid fast bacilli, fungus, and anerobes.\n\nRadiology:\nOn imaging, an air fluid level observed in the thorax, outside of the lung parenchyma. Imaging findings can be identical to hydropneumothorax.\n\nPrognosis and Treatment:\nDepends on clinical picture. The patient generally presents with sepsis and sequela of the infection which exacerbate the respiratory issues", "ACR Code": "6.2", "Category": "Radiologic Sign or Finding", "Keywords": "empyemapneumothoraxhydropneumothorax", "Reference": "Harrison's Online\nMedcyclopedia" } }, { "U_id": "MPX1205", "TAC": [], "MRI": [ "MPX1205_synpic17592", "MPX1205_synpic17593", "MPX1205_synpic17594", "MPX1205_synpic17595" ], "Case": { "Title": "Left PICA Infarct confirmed with MRI. MR angiogram images and CT angiogram images demonstrated a patent vertebral system and patent left PICA. A focal stenosis was detected at the origin of the left posterior inferior cerebellar artery.", "History": "58 y/o female with past medical history of diabetes and hypertension presents with 4 day history of right sided numbness and tingling.", "Exam": "Physical exam was signficant to decreased sensation to pain and\ntemperature on right upper and lower extremity and right trunk.", "Findings": "Axial FLAIR images demonstrate multiple punctate foci of signal abnormality in the deep white matter. Axial and coronal diffusion images demonstrate a single focus of high signal within the left medulla consistent with recent infarct.", "Differential Diagnosis": "Left PICA infarct\nLeft Vertebral Dissection", "Case Diagnosis": "Left PICA Infarct confirmed with MRI. MR angiogram images and CT angiogram images demonstrated a patent vertebral system and patent left PICA. A focal stenosis was detected at the origin of the left posterior inferior cerebellar artery." }, "Topic": { "Title": "Medullary (PICA) Infarct", "Disease Discussion": "\u2022 Lateral medullary syndrome, otherwise known as Wallenberg's syndrome, occurs after a vertebral or posterior inferior cerebellar artery infarction. \n\n\u2022 Causes may be secondary to vertebral artery dissection, atherosclerotic disease or embolism. \n\n\u2022 Symptoms produced may vary depending upon the size of the infarct, but typically include loss of pain and temperature senses on the side of the body opposite to the lesion (spinothalamic tract) and face on the ipsilateral side of the body (descending trigeminothalamic tract). Other signs and symptoms include dysarthria, dysphagia, staggering gait, vertigo, nystagmus, and ipsilateral Horner's syndrome.", "ACR Code": "1.9", "Category": "Vascular", "Keywords": "PICAWallenbergLateral medullary syndrome", "Reference": "Goetz CG, Pappert EJ. Textbook of Clinical Neurology, 1st ed, WB Saunders, Philadelphia, 1999. p 210.\n\nGrossman RI, Yousem DM. Neuroradiology, The Requisites. Mosby. St. Louis, 1994. p 59-60.\n\nKim JS .Sensory symptoms in ipsilateral limbs/body due to lateral medullary infarction. Neurology 9-OCT-2001; 57(7): 1230-4" } }, { "U_id": "MPX1212", "TAC": [ "MPX1212_synpic29914" ], "MRI": [], "Case": { "Title": "Acute Subdural Hematoma with temporal bone fracture", "History": "An 18-year-old Hispanic man was brought by ambulance to the Emergency Department following a high-speed motor vehicle collision in which the patient was ejected from his vehicle.", "Exam": "He was lethargic on presentation, but without evidence of any focal neurological deficits. Physical examination in the trauma bay showed swelling over his left temporal region and scattered facial abrasions.", "Findings": "Figure 1: Axial CT without contrast\n\nThe noncontrast head CT revealed a small hyperdense subdural hematoma, consistent with the acute injury (Fig. 1a). There is pneumocephalus, seen as small bubbles of air within the left extraaxial parietal subdural collection as well as a single focus of air posteriorly at the left paramidline aspect of the extraaxial space shown (Fig. 1a). \n\nThese findings indicate that a fracture has occurred, allowing communication of outside air or a sinus cavity with the intracranial space. Indeed a complex adjacent temporal bone fracture was detected and is best appreciated using bone windows (Fig. 1b).", "Differential Diagnosis": "Epidural hematoma\nSubdural hygroma\nSubdural empyema", "Case Diagnosis": "Acute Subdural Hematoma with temporal bone fracture", "Diagnosis By": "Radiographic findings and clinical presentation", "Treatment & Follow Up": "Drainage via craniostomy has become the treatment of choice for acute subdural hematoma, but craniotomy may be required in certain cases." }, "Topic": { "Title": "1. Acute subdural hematomas (bilateral convexities, interhemispheric, tentorial leaf) 2. Transtentorial herniation 3. Traumatic subarachnoid hemorrhage.", "Disease Discussion": "The inner (or \"meningeal\") layer of dura contributes to the formation of the falx cerebri, tentorium, and falx cerebelli. SDHs are to be anticipated along these structures since there is a continuation of the potential subdural space along these dural reflections. Interhemispheric fissure and tentorial leaf SDHs are commonly seen in elderly trauma victims, especially if they are alcoholic. The enlarged subarachnoid spaces of these patients may contribute to an excessive mobility of the brain and greater susceptibility of the interhemispheric/tentorial veins to traumatic injury. \n\nAcute subdural hematomas can be classified as \"simple\" or \"complicated,\" depending on whether parenchymal brain injuries (contusions, intracerebral hematomas, diffuse axonal injury) are also present. Notably, intra-axial injuries are much more common with acute SDHs than with either EDHs or chronic SDHs. The majority of patients with acute SDHs, in fact, will have associated parenchymal brain injuries. Secondary forms of brain injury (anoxic/ischemic injury, trans-tentorial/subfalcine/tonsilar herniation, increased intracranial pressure) are also quite common in patients with acute SDHs. \n\nAcute SDHs still carry a significant risk of morbidity and mortality. The overall mortality of patients with acute SDHs is greater than that for any other traumatic intracranial mass lesion (ICH, EDH, focal contusion). Despite modern therapy, the mortality is over 35% in all large series and greater than 50% in most reports. A primary factor related to clinical outcome of patients with acute SDHs is the presence or absence of associated intraaxial lesions. In one series of patients, the mortality of \"simple\" SDHs was 22% as compared to over 50% for those with \"complicated\" SDHs. A second major factor significantly related to outcome is the presence and severity of mass effect. Mass effect from a SDH may be due to a combination of factors; the hematoma itself, underlying parenchymal injury, intracerebral hematoma, and diffuse cerebral edema/swelling from a loss of vasomotor autoregulation. The mass effect can produce injury to the brain through a generalized increase in intracranial pressure, global or localized impairment of blood flow, transtentorial/tonsilar herniation resulting in ischemic/pressure necrosis of the upper brain stem. Other factors directly related to a poor outcome are; greater age of the patient, low Glasgow Coma Scores at the time of operation, bilateral lesions, rapid rate of SDH accumulation, and delayed surgical evacuation (> 4 hours) of the SDH.", "ACR Code": "1.4", "Category": "Trauma" } }, { "U_id": "MPX1201", "TAC": [ "MPX1201_synpic30961", "MPX1201_synpic30962", "MPX1201_synpic30963", "MPX1201_synpic30964", "MPX1201_synpic30967" ], "MRI": [], "Case": { "Title": "Metastatic Adenocarcinoma of the Lung", "History": "Chief complaint:\n\n47 y/o male presented in Nov 2005 with pain in right anterior thigh. X-ray revealed a mass in the femur and adjacent soft tissue. Partial surgical resection of mass revealed adenocarcinoma. Subsequent PET scan indicated increased uptake at several locations in the right lung.\n\nPatient had a history of pulmonary nodules dating to 2003/2004. However a PET conducted in August of 2004 was negative except for minimal uptake in one pulmonary nodule. Serial X-rays showed no changes in these nodules through mid 2005.\n\nPatient was diagnosed with metastatic adenocarcinoma of the right lung and referred to oncology for radiation and chemotherapy.\n\nPMX:\n \u2022 Nephrolithiasis\n \u2022 Hyperlipidemia\n\nPSHX:\n \u2022 Right neck lymph node resection (benign) at 22 yo\n \u2022 Cholestectomy in 2004\n\nSocHx:\n \u2022 >1PPD for 20 years\n \u2022 No ETOH\n\nFMHX:\n \u2022 Sister (smoker) died of lung cancer in 1979\n \u2022 Sister (non-smoker) died of lunger cancer at 40 yo\n \u2022 Sister (non-smoker) died of lung cancer at 62 yo\n \u2022 Brother (smoker) diagnosed with head and neck cancer 2006\n\nMeds:\n \u2022 Percocet\n\nAllergies:\n \u2022 Aspirin - upset stomach", "Exam": "Not applicable", "Findings": "Chest and abdominal CT on 13 April 2006 revealed the following in comparison with an August 2004 chest and abdominal CT:\n \u2022 Progression of right hilar adenopathy and enlargement of the pleural-based soft tissue mass along the posteromedial aspect of the right lower lobe.\n \u2022 Pulmonary parenchyma demonstrates enlargement of multiple\nright lower lobe pulmonary nodules.\n \u2022 The pancreas, spleen, adrenal glands, and kidneys are normal. \n \u2022 Soft tissue in the bilateral gluteal regions are normal.\n\nChest and abdomal CT on 16 August 2006 after 4 months of chemotherapy and radiation revealed the following in comparison with the 13 April 2006 study:\n \u2022 Subcarinal lymphadenopathy is demonstrated and increased from previous study.\n \u2022 Associated rib destruction is demonstrated.\n \u2022 Associated endobronchial narrowing is demonstrated extending to the right lower lobe.\n \u2022 No pulmonary nodules are seen in the left lung.\n \u2022 Interval development of bilateral adrenal masses.\n \u2022 Soft tissue masses are demonstrated within the mesentery.\n \u2022 Interval development of right gluteal mass", "Differential Diagnosis": "Metastatic Adenocarcinoma of the Lung\nMetastatic Small Cell Cancer of the Lung\nMetastatic Squamous Cell Cancer of the Lung\nOther Metastatic Cancer", "Case Diagnosis": "Metastatic Adenocarcinoma of the Lung", "Diagnosis By": "Pathology", "Treatment & Follow Up": "Patient is unlikely to improve with continued chemotherapy and/or radition therapy. Hospice care with symptomatic therapy is recommended.", "Discussion": "Aggressive spread of adenocarcinoma of the lung to thoracic, abdominal and soft tissues." }, "Topic": { "Title": "Metastatic Adenocarcinoma of the Lung", "Disease Discussion": "Chief complaint:\n\n47 y/o male presented in Nov 2005 with pain in right anterior thigh. X-ray revealed a mass in the femur and adjacent soft tissue. Partial surgical resection of mass revealed adenocarcinoma. Subsequent PET scan indicated increased uptake at several locations in the right lung.\n\nPatient had a history of pulmonary nodules dating to 2003/2004. However a PET conducted in August of 2004 was negative except for minimal uptake in one pulmonary nodule. Serial X-rays showed no changes in these nodules through mid 2005.\n\nPatient was diagnosed with metastatic adenocarcinoma of the right lung and referred to oncology for radiation and chemotherapy.\n\nPMX:\n \u2022 Nephrolithiasis\n \u2022 Hyperlipidemia\n\nPSHX:\n \u2022 Right neck lymph node resection (benign) at 22 yo\n \u2022 Cholestectomy in 2004\n\nSocHx:\n \u2022 >1PPD for 20 years\n \u2022 No ETOH\n\nFMHX:\n \u2022 Sister (smoker) died of lung cancer in 1979\n \u2022 Sister (non-smoker) died of lunger cancer at 40 yo\n \u2022 Sister (non-smoker) died of lung cancer at 62 yo\n \u2022 Brother (smoker) diagnosed with head and neck cancer 2006\n\nMeds:\n \u2022 Percocet\n\nAllergies:\n \u2022 Aspirin - upset stomach\n\nChest and abdominal CT on 13 April 2006 revealed the following in comparison with an August 2004 chest and abdominal CT:\n \u2022 Progression of right hilar adenopathy and enlargement of the pleural-based soft tissue mass along the posteromedial aspect of the right lower lobe.\n \u2022 Pulmonary parenchyma demonstrates enlargement of multiple\nright lower lobe pulmonary nodules.\n \u2022 The pancreas, spleen, adrenal glands, and kidneys are normal. \n \u2022 Soft tissue in the bilateral gluteal regions are normal.\n\nChest and abdomal CT on 16 August 2006 after 4 months of chemotherapy and radiation revealed the following in comparison with the 13 April 2006 study:\n \u2022 Subcarinal lymphadenopathy is demonstrated and increased from previous study.\n \u2022 Associated rib destruction is demonstrated.\n \u2022 Associated endobronchial narrowing is demonstrated extending to the right lower lobe.\n \u2022 No pulmonary nodules are seen in the left lung.\n \u2022 Interval development of bilateral adrenal masses.\n \u2022 Soft tissue masses are demonstrated within the mesentery.\n \u2022 Interval development of right gluteal mass.\n\nConclusion:\nContinued agressive development and growth of metastases are demonstrated between April 2006 and August 2006 chest and abdominal CTs. This represents a failure of radiation and chemotherapy with future remission unlikely.", "ACR Code": "6.3", "Category": "Neoplasm, carcinoma", "Keywords": "Adenocarcinoma" } }, { "U_id": "MPX1170", "TAC": [ "MPX1170_synpic19419", "MPX1170_synpic19421", "MPX1170_synpic19422", "MPX1170_synpic19423", "MPX1170_synpic19424", "MPX1170_synpic19425", "MPX1170_synpic19426", "MPX1170_synpic19427", "MPX1170_synpic19428" ], "MRI": [], "Case": { "Title": "Intracerebral hemorrhage (likely related to chronic hypertension)", "History": "89 y/o with past medical history significant for dementia and hypertension, noted to have altered mental status at home.", "Exam": "Admission vitals included BP 165/105 and GCS=4. No evidence of external trauma. Pupils reactive to light but w/ slow response. Breath sounds clear bilat; normal S1 & S2, no m/r/g; abdomen s/nd/nt; radial pulses 2+ bilat; GCS-4 (verbal-1, eyes-1, motor-2)Na-145, K-4.0, Cl-106, CO2-30, BUN-28, Creat-0.8, GLU-109WBC-13.4, Hgb-14.1, Hct-43.1, Plt-383Alk phos-92, AST-32, ALT 35, TBili-0.9", "Findings": "Parenchymal hematoma, right occipital lobe\nSmall amount of ventricular blood", "Differential Diagnosis": "Vascular malformation\nHypertensive hemorrhage\nAmyloid angiopathy\nMetastatic disease (e.g. renal, lung etc.)\nOccult trauma", "Case Diagnosis": "Intracerebral hemorrhage (likely related to chronic hypertension)", "Diagnosis By": "By exclusion", "Treatment & Follow Up": "Patient had been admitted to another hospital one week prior and was diagnosed with acute occipital lobe hemorrhage. Right occipital blood collection noted on CT was unchanged from the previous admission. \n\nEvaluation for acute change of mental status revealed a urinary tract infection. After antibiotic treatment for UTI, patient\u2019s GCS improved to 10-12 (pt unable to speak x 3 years).\n\nHospice care was arranged for the patient.", "Discussion": "This patient presented with altered mental status prompting an evaluation for intracranial bleed. Her long history of hypertension is likely the main factor leading to the intracerebral hemorrhage (ICH) noted." }, "Topic": { "Title": "Intracerebral hemorrhage, chronic hypertension", "Disease Discussion": "Chronic hypertension causes fibrinoid necrosis in the penetrating and subcortical arteries, weakening of the arterial walls, and formation of small aneurysmal outpouchings, known as Charcot-Bouchard microaneurysms. These microaneurysms, predispose the patient to spontaneous ICH. Bleeding is limited by the resistance of tissue pressure in the surrounding brain structures. If the hematoma is large, distortion of structures and increased ICP may cause headache, vomiting, and decreased alertness. ICH accounts for 10 to 15 percent of all strokes in whites and about 30 percent in blacks and individuals of Asian origin.\n\nLocations of hypertensive ICHs are putamen (40%), lobar (22%), thalamus (15%), pons (8%), cerebellum (8%), and caudate (7%).\n\nThe differential diagnosis should include hypertension, bleeding diatheses (especially as a result of iatrogenic coumadin), trauma (subdural and epidural hematomas), and amyloid angiopathy as the most frequent causes. Rarely, brain tumors and abscesses can have a rapid onset mimicking ICH.\n\nIn young, normotensive patients, especially those with lobar and intraventricular hemorrhages, vascular malformations (AVM) are the most likely source of bleeding. \n\nSome primary and metastatic brain tumors, especially renal carcinoma and choriocarcinoma, can develop hemorrhages within the tumor. The initial evaluation, should include CBC, chemistries, coagulation studies (PT, PTT, bleeding time, and platelet count), arterial blood gas analysis, and toxicology screen.\n\nCT scan should be performed immediately in patients suspected of having an ICH. Follow-up CT should be performed to evaluate a change in clinical signs or mental status.\n\nPatients who have ICH after cocaine use have a high likelihood of vascular malformations and aneurysms and need angiography.Medical management involves reduction and maintenance of intracranial pressure. Commonly, patients are intubated if they are unable to protect their airway. Blood pressure swings may be controlled with IV labetolol (adequate intracranial perfusion pressure must be maintained). As an adjunct, patients may be placed in the reverse-Trendelenberg position to assist in relieving increased intracranial pressure.\n\nRecent studies of hematoma removal have shown promise for open surgical decompression, but only if accomplished early after the onset of symptoms. The best candidates for surgery may be patients with moderate to large hematomas who are still awake. Neuroimaging techniques have made it possible to drain hematomas percutaneously, using stereotactic surgery. Survival depends on the location, size, and rapidity of development of the hematoma. ICHs are at first soft and dissect along white matter fiber tracts.\n\nIf the patient survives the initial changes in ICP, blood is absorbed and a cavity or slit forms that may interrupt brain pathways. Patients with small hematomas located deep and near midline structures often develop secondary herniation and mass effect, and these patients have a high mortality rate. Survivors invariably have severe neurological deficits. In patients with medium-sized hematomas, the deficit varies with the location and size of the hematomas.", "ACR Code": "1.3", "Category": "Hemorrhage", "Keywords": "Intracerebralhemorrhage", "Reference": "1.\tGoetz CG, and Pappert EJ. Textbook of Clinical Neurology. Philadelphia: W.B. Saunders, 1999.\n\n2.\tJuhl JH, Crummy AB, and Kuhlman JE. Essentials of Radiologic Imaging. Philadelphia: Lippincott, 1998." } }, { "U_id": "MPX1229", "TAC": [ "MPX1229_synpic22020" ], "MRI": [], "Case": { "Title": "Annular Pancreas", "History": "6 yo girl with multiple year history of early satiety and borderline normal weight gain. History of 25lb weight loss after viral illness.", "Findings": "UGI demonstrated severe focal narrowing of the second portion of the duodenum with medial displacement of the second portion of the duodenum. \n\nCT retrospectively demonstrated a thin segment of pancreatic tissue encircling the second portion of the duodenum.", "Differential Diagnosis": "DDx for duodenal narrowing:\nAnnular pancreas\nDuodenal web\nPost-bulbar ulcer\nDuodenal adenocarcinoma\nLymphoma\nExtrinsic compression", "Case Diagnosis": "Annular Pancreas", "Diagnosis By": "Surgery", "Treatment & Follow Up": "Surgical excision of second portion of duodenum with duodenoduodenal anastomosis." }, "Topic": { "Title": "Annular Pancreas", "Disease Discussion": "An annular pancreas is pancreatic tissue that encircles the descending duodenum as a result of fusion of the bilobed ventral component with the dorsal component. Although overall uncommon, is the most common congenital anomaly of the pancreas. Given the varying degree of narrowing, patients present between the neonatal period up to adulthood. Symptoms usually include nausea, vomiting, abdominal pain, and occasional jaundice, and there is a high association with postbulbar peptic ulceration. Diagnostic tests include an upper GI (UGI) series, CT, and endoscopic retrograde cholangiopancreatography (ERCP). The UGI will demonstrate eccentric or concentric narrowing of the descending duodenum. CT demonstrates pancreatic tissue encircling the duodenum, and ERCP demonstrates the annular pancreatic duct encircling the duodenum.", "ACR Code": "7.1", "Category": "Congenital, malformation", "Keywords": "Annular Pancreas", "Reference": "Brant WE and Helms CA. Fundamentals of Diagnostic Radiology. 2nd ed. Philadelphia: Lippincott Williams and Wilkins, 1999." } }, { "U_id": "MPX1214", "TAC": [], "MRI": [ "MPX1214_synpic1100", "MPX1214_synpic1101" ], "Case": { "Title": "Endolymphatic Sac Tumor", "History": "A 54-year-old woman presented with chronic ear pain.", "Findings": "\"Bipolar\" mass involving the petrous bone and posterior fossa\nDestructive petrous (temporal bone) mass\n- posteromedial, near vestibular aqueduct\n- extends to middle ear\n- erosion includes right sigmoid area\n\n- heterogeneous mixed cystic and solid\n- hyperintense on both T1W and T2W \n- proteinaceous and/or hemorrhagic fluid", "Differential Diagnosis": "Endolymphatic sac tumor\n\t\"Heffner tumor\"\n\tcystic and papillary adenocarcinoma\nChondroid tumor\n\tChondroma/Chondrosarcoma\n\tChondromyxoid fibroma\nOther destructive petrous masses\n\tcholesterol granuloma\n\tepidermoid\n\tmetastasis", "Case Diagnosis": "Endolymphatic Sac Tumor", "Diagnosis By": "resection, pathology and histology", "Discussion": "DIAGNOSIS: Cystic and papillary neoplasm of endolymphatic sac origin (Heffner tumor).\n\nDISCUSSANT: Mahmood F. Mafee, MD \n\nDISCUSSION:\t\nThe membranous labyrinth or cavity consists of the cochlear aqueduct, the vestibular organ, the endolymphatic duct and sac, the round window membrane, and their associated vasculature. The bony labyrinth includes the vestibule, the semicircular canals, and the cochlea. The membranous labyrinth of the inner ear begins to form during the early months of gestation. By mid-term, the mesenchyme that surrounds the labyrinth has transformed into cartilage, and begins to ossify. The endolymphatic duct and sac are the only portions that grow after birth, and they continue to enlarge until sometime after puberty.\n\nThere is considerable controversy concerning the origin of these slowly growing, yet highly destructive lesions of the temporal bone. Several recent reports have emphasized that these tumors probably do arise from the epithelial elements lining the endolymphatic system (especially the sac). The most common presentation is hearing loss, facial nerve palsy, and vestibular dysfunction. \n\nThere appear to be at least 2 categories of this lesion, a slowly growing, relatively benign adenomatous tumor, and a more aggressive lesion with a capillary configuration. The papillary lesions probably arise within the posterior aspects of the petrous bone in the retrolabyrinthine region. The lesions may be hypervascular, supplied by branches of the external carotid artery, and may contain blood products that produce characteristic regions of hyperintensity on T1WI and hypointensity on T2WI. Intratumoral calcifications within these lesions may represent \"bone sequestra\" produced when the tumor infiltrates into the petrous bone. Because these lesions may be surrounded by a thin shell of reactive bone, it has been suggested that at least during some portion of their growth, they may expand relatively slowly. The lesions almost invariably show contrast enhancement. Some of the tumors have a speckled pattern of hyperintensity on T1WI, which can mimic the appearance of other vascular lesions of the petrous apex, including glomus tumors.\n\nThe papillary endolymphatic sac tumor has been associated with von Hippel-Lindau disease (VHL)and may present with bilateral papillary endolymphatic sac neoplasms. It is also interesting to remember that patients with VHL may develop cystadenomas in the testis and in relationship to the female pelvic adnexa. \n\nIn this patient, the differential diagnosis could include chondroid lesions (benign chondroma as well as low-grade chondrosarcoma, and chondromyxoid fibroma), cholesterol granuloma, metastatic disease, and possibly an aggressive epidermoid cyst.\n\nBecause the histology of this lesion may be confusing to surgical pathologists, an accurate preoperative localization by neuroimaging can assist in suggesting the correct diagnosis. The prognosis can be quite good after careful gross removal of the lesion. However, incomplete resection is associated with recurrence.\n\nSUGGESTED READINGS:\n\nBatsakis, J.G. and el-Naggar, A.K. Papillary neoplasms (Heffner's tumors) of the endolymphatic sac [see comments]. Ann Otol Rhinol Laryngol. 1993;102:648-651\n\nDelisle, M.B., Uro, E., Rouquette, I., Yardeni, E., and Rumeau, J.L. Papillary neoplasm of the endolymphatic sac in a patient with von Hippel-Lindau disease. J Clin.Pathol 1994;47:959-961. \n\nHeffner, D.K. Low-grade adenocarcinoma of probable endolymphatic sac origin A clinicopathologic study of 20 cases. Cancer 1989;64:2292-2302.\n\nMukherji, S.K. and Castillo, M. Adenocarcinoma of the endolymphatic sac: imaging features and preoperative embolization. Neuroradiol 1996;38:179-180,.\n\nMukherji, S.K., Albernaz, V.S., Lo, W.W., Gaffey, M.J., Mergerian, C.A., Feghali, J.G., Brook, A., Lewin, J.S., Lanzieri, C.F., Talbot, J.M., Meyer, J.R., Carmody, R.F., Weissman, J.L., Smirniotopoulos, J.G., Rao, V.M., Jinkins, J.R., and Castillo, M. Papillary endolymphatic sac tumours: CT, MR imaging, and angiographic findings in 20 patients. Radiology 1997;202(3):801-808.\n\nTibbs Jr., R.E., Bowles Jr., A.P., Raila, F.A., Fratkin, J.D., and Hutchins, J.B. Should Endolymphatic Sac Tumors Be Considered Part of the Von Hippel-Lindau Complex? Pathology Case Report. Neurosurg 1997;40(4):848-855" }, "Topic": { "Title": "Endolymphatic Sac Tumor", "Disease Discussion": "Cystic and papillary tumor of endolymphatic sac origin.", "ACR Code": "0.0", "Category": "Neoplasm, benign" } }, { "U_id": "MPX1227", "TAC": [ "MPX1227_synpic12941" ], "MRI": [ "MPX1227_synpic12942", "MPX1227_synpic12943" ], "Case": { "Title": "Parosteal Osteogenic Sarcoma", "History": "26 y/o male with a mass for past 18 months on lower leg. There is no history of trauma. The patient does not have any fever or chills, and he notes occasional pain at the site of the mass.", "Findings": "Radiographically it is a broad-based, juxtacortical, densely ossified mass, the periphery somewhat less dense that the base. CT scan is most useful and can demonstrate a radiolucent zone of periosteum and fibrous tissue trapped between the tumor and cortex. The lesion may consist of three layers: at the cortical surface it is dense and compact, it has a middle layer of amorphous dense bone, and the outer layer there are dense spicules extending into the periphery. These tumors typically have a low signal intensity on T1-weighted images and a high signal intensity on T2-weighted images. The lesion may eventually progress to cortical destruction and medullary invasion, MRI can be used to grade the extent of tumor extension and cortical disruption.", "Differential Diagnosis": "myositis ossificans\nosteochondroma \nperiosteal sarcoma", "Case Diagnosis": "Parosteal Osteogenic Sarcoma" }, "Topic": { "Title": "Parosteal Osteogenic Sarcoma", "Disease Discussion": "Parosteal Osteosarcoma (Juxtacortical Osteosarcoma) is an uncommon tumor that is found in a somewhat older age group than osteosarcoma, ranging from 15-50 years of age (median age of 27), and it is more commonly found in women. It accounts for 4% of all osteogenic sarcomas. The classic location for a parosteal osteosarcoma is the posterior distal metaphysis of the femur; however, it may also arise in the posterior metaphysis of the proximal tibia and the proximal metaphysis of the humerus, and rarely elsewhere. It is slow-growing but has a tendency to recur after inadequate excision, and it may metastasize. The lesion arises from the outer fibrous layer of periosteum. Common presenting symptoms are aching or limited range of motion due to interference with a joint. \n\nThe tumor merges with the cortex by a stalk early on in the disease process and has a broad base later on in the progression. The bone marrow of the bone does not extend into the base of the tumor. Although, there may be occasional medullary involvement by the tumor. Radiographically it is a broad-based, juxtacortical, densely ossified mass, the periphery somewhat less dense that the base. CT scan is most useful and can demonstrate a radiolucent zone of periosteum and fibrous tissue trapped between the tumor and cortex. The lesion may consist of three layers: at the cortical surface it is dense and compact, it has a middle layer of amorphous dense bone, and the outer layer there are dense spicules extending into the periphery. These tumors typically have a low signal intensity on T1-weighted images and a high signal intensity on T2-weighted images. The lesion may eventually progress to cortical destruction and medullary invasion, MRI can be used to grade the extent of tumor extension and cortical disruption.\n\nDifferential diagnosis should include; myositis ossificans, osteochondroma and periosteal sarcoma. Myositis ossificans is more densely calcified at its periphery and usually does not involve the adjacent cortex. With an osteochondroma the stalk of an exostosis is contiguous with the cortex of the bone from which it arises and the medullary bone within the stalk is also contiguous with that of the adjacent bone. Chondroid calcification within the cartilaginous cap may be present and is also distinctive.\n\nParosteal osteosarcoma has a relatively good prognosis compared to conventional osteosarcoma. Wide excision is the preferred treatment and there is normally no role for chemotherapy.", "ACR Code": "4.3", "Category": "Neoplasm, carcinoma", "Keywords": "osteosarcomaparosteal", "Reference": "1)Juhl: Paul and Juhl's Essentials of Radiologic Imaging, 7th ed., Copyright \u00a9 1998 Lippincott Williams & Wilkins.\n2)Dahlin DC: Bone tumors: General Aspects and Data on 8,542 cases, 4th ed. Springfield, Illinois, Charles C Thomas, 1986\n3)Levine E, Desmet AA, Huntrakoon M: Juxtacortical osteosarcoma: A radiologic and histologic spectrum.Skeletal Radiol 14:38, 1985 \n4)Pediatric Musculoskeletal Radiology, Volume 39 Number 4, July 2001, Copyright \u00a9 2001 W. B. Saunders Company." } }, { "U_id": "MPX1213", "TAC": [ "MPX1213_synpic10585", "MPX1213_synpic10586", "MPX1213_synpic10587", "MPX1213_synpic10589", "MPX1213_synpic10590", "MPX1213_synpic10591" ], "MRI": [], "Case": { "Title": "Diffuse cerebral edema - mimic of SAH", "History": "18 y.o. young woman \"found down\" - unconscious for an unknown time and for unknown cause.", "Exam": "Comatose", "Findings": "\u2022 The sulci and ventricles are not visible.\n\u2022 There is high attenuation on the surface of the brain.\n\u2022 The suprasellar cistern shows visible CSF - but high attenuation linear material", "Differential Diagnosis": "\u2022 Subarachnoid hemorrhage\n\u2022 Diffuse cerebral edema\n\u2022 Hyperemic brain swelling", "Case Diagnosis": "Diffuse cerebral edema - mimic of SAH", "Diagnosis By": "Imaging and death certificate (autopsy results not known)", "Treatment & Follow Up": "Despite vigorous resuscitation efforts she died." }, "Topic": { "Title": "Diffuse cerebral edema - mimic of SAH", "Disease Discussion": "Diffuse cerebral swelling (either from edema or hyperemia) cause profound increased intracranial pressure. This may eventually progress to a complete cessation of cerebral perfusion and subsequent brain death.\n\nA number of traumatic, toxic, metabolic, and vascular lesions may lead to diffuse cerebral swelling. In some situations, the brain may be edematous (lower than normal attenuation) except for the outer cortex and the pial vessels. In this situation, the appearance may mimic the high attenuation in the subarachnoid space that is more commonly caused by subarachnoid hemorrhage (SAH).\n\nReal Subarachnoid Hemorrhage:\nhttp://rad.usuhs.mil/medpix/radpix.html?mode=single&recnum=691", "ACR Code": "1.5", "Category": "Hypoxic or Ischemic", "External Links": "rad.usuhs.mil/medpix/radpix.html?mode=single&recnum=691" } }, { "U_id": "MPX1231", "TAC": [ "MPX1231_synpic27572" ], "MRI": [], "Case": { "Title": "Osteochondritis Dissecans", "History": "Chronic right ankle pain with occasional locking of the joint and a history a severe right ankle injury approximately six months earlier.", "Exam": "N/A", "Findings": "Radiographs of the right ankle demonstrate a cortical lucency at the superior and lateral aspect of the talar dome.\nNoncontrast CT images of the talus demonstrate a shallow, rounded cortical defect within the superior lateral talar dome and an adjacent fragment of bone within the ankle joint.", "Differential Diagnosis": "Osteochondritis dessicans, normal variant ossification abnormality, acute traumatic fracture fragment.", "Case Diagnosis": "Osteochondritis Dissecans", "Diagnosis By": "CT scan.", "Treatment & Follow Up": "Orthopaedic follow up.", "Discussion": "Please see factoid. Osteochondritis dissecans (OCD) is also called an osteochondral fracture. However, osteochondral lesion is the more current preferred term." }, "Topic": { "Title": "Osteochondritis Dissecans", "Disease Discussion": "Osteochondral defects are believed to be related to repeated microtrauma. They are a form of avascular necrosis that is smaller and more focal. The appearance is usually a concave subchondral fracture line containing an osseous body. It is frequently found in the knee, most commonly in the lateral portion of the medial femoral condyle. Alternatively, it is also seen in the dome of the talus and the capitellum. MRI examination can be performed to evaluate the stability of the osseous body and to check for effusion tracking along its borders in symptomatic patients. Evaluation with gadolinium show high signal intensity surrounding the fragment, this is felt to represent granulation tissue formation around an unstable fragment. Differential considerations include spontaneous osteonecrosis which usually affects older patients who complaint of severe pain and shows flattening of the weight bearing surface of the femoral condyle on radiographic examination.", "ACR Code": "4.4", "Category": "Trauma", "Keywords": "subchondralmicrotraumaavascular necrosis", "Reference": "Manaster, B.J. Musculoskelletal Imaging. The Requisites. 2nd edition. Mosby" } }, { "U_id": "MPX1239", "TAC": [ "MPX1239_synpic45229" ], "MRI": [], "Case": { "Title": "Ivory Vertebral Body", "History": "63 y.o. woman with a history of breast cancer", "Exam": "s/p left mastectomy", "Findings": "Uniformly dense (white) vertebra at T-7, with no abnormality of its contour or adjacent disks.", "Differential Diagnosis": "\u2022 Metastatic disease (osteoblastic)\n\u2022 Paget disease \n\u2022 Lymphoma (usually Hodgkins)", "Case Diagnosis": "Ivory Vertebral Body", "Diagnosis By": "N/A", "Treatment & Follow Up": "None for this sign of metastatic disease.", "Discussion": "There are numerous possible etiologies for the ivory vertebra sign. Ivory vertebrae can represent osteoblastic metastatic disease, commonly stemming from breast cancer (as in this case), or carcinoma of the prostate. This finding can also be associated with Paget disease, lymphoma, and less commonly with osteosarcoma and carcinoid. This finding is much less common in children and usually related to Hodgkin\u2019s lymphoma. \n\nIvory vertebra appears as a uniformly white vertebra with no abnormality of its contour or adjacent disks. The vertebra stands out against the adjacent normal, or darker, vertebral bodies. \n\nOsteoblastic metastases and lymphoma both result in the replacement of the vertebral body spongiosa with dense, confluent bony mass. This produces a homogenous sclerotic appearance. Paget disease often causes expansion of the vertebral body, disrupting the external contours. \n\nReferences:\n\nGraham TS. The Ivory Vertebra Sign. Radiology 2005; 235:614-615.\n\nhttp://www.gentili.net/signs/" }, "Topic": { "Title": "Ivory Vertebral Body", "Disease Discussion": "Sclerosis of one or more vertebral bodies in the elderly patient is most compatible with the diagnosis metastatic disease. However, the differential diagnosis for this finding includes lymphoma or treated lytic mets, and rarely, chordoma, plasmacytoma, or Paget disease. This appearance should be differentiated from the corduroy vertebral body (accentuated vertical striations) of an hemangioma, The rugger jersey vertebral body (radiodense stripes at the top and bottom of the vertebra) of renal osteodystrophy, the picture frame vertebral body (condensation of bone along the margins of the vertebral body) of Paget disease, and the sandwich vertebral body (extreme and uniform increase in radiodensity along the inferior and superior margins of the vertebral body) of osteopetrosis.\n\nPedicle involvement is one clue to the cause of a sclerotic vertebral body. Destruction of one or both pedicles is a well known result of metastatic disease that is rarely present in the case of plasmacytoma. Keep in mind, though, that this finding is typically a result of extension of the tumor deposit into the pedicle from the posterior vertebral body, rather than primary deposition into the pedicle. \n\nPreservation of disc space and vertebral body size are another important indicator of the nature of a sclerotic vertebral body. Indolent infection such as TB commonly produces end plate destruction, disc space narrowing, and paraspinal soft tissue mass.\n\nPaget disease of the vertebral body may be difficult to separate from neoplastic causes because it usually involves a single vertebral body. The classic appearance includes an expanded body with thickened cortex and coarsened trabeculation, with preservation of the disc space.", "ACR Code": "3.3", "Category": "Differential Diagnosis", "Reference": "Resnick,D. Bone and Joint Imaging, 2nd Ed, W.B. Saunders Co, 1996." } }, { "U_id": "MPX1237", "TAC": [ "MPX1237_synpic28520" ], "MRI": [], "Case": { "Title": "Findings consistent with Eagle Syndrome in the proper clinical setting.", "History": "32 year-old male, rule out sinusitis.", "Exam": "N/A", "Findings": "Ossification of the bilateral stylohyoid ligaments (right greater than left). No significant paranasal sinus disease.", "Differential Diagnosis": "Elongations of the styloid process bilaterally\nOssification of the bilateraly stylohyoid ligaments", "Case Diagnosis": "Findings consistent with Eagle Syndrome in the proper clinical setting.", "Diagnosis By": "Non-contrast CT of the paranasal sinuses.", "Treatment & Follow Up": "Treatment is based upon the presence of symptoms, and includes conservative medical management or surgical removal.", "Discussion": "Please see factoid." }, "Topic": { "Title": "Eagle Syndrome", "Disease Discussion": "Eagle Syndrome is either the overgrowth of the styloid process itself or the ossification of the stylohyoid ligament, first described by Watt Eagle, an otolaryngologist in Duke University in 1937. Eagle eventually described two distinct group of patients: the classic syndrome in post-tonsillectomy patients for whom the palpation of the styloid process/ossified stylohyoid ligament reproduced the symptoms (and he believed that the post-surgical changes caused incorporation of the glossopharyngeal nerve by the scar tissue/ossification), and patients with no history of prior tonsillectomy who complained of pain along the distribution of the carotid artery. (1)\n\nRadiologically, one would see either an elongated styloid process or an abnormal ossification in the anatomic distribution of the stylohyoid ligament (extending from the stylohyoid ligament to the hyoid bone). Lengths of greater than 2.5 cm has been thought to be significant, but at times the position and/or contour may be more significant in the cause of the patient\\'s symptomatology. (1)\n\nCase reports of surgical cure of patient\\'s symptoms from Eagle Syndrome describe first the infiltration of local anesthetic at the styloid process to see if the patient\\'s symptoms are relieved by this injection. If so, surgical excision of the styloid process/ossified stylohyoid ligament can be considered. (2,3)", "ACR Code": "2.1", "Category": "Unknown, Not specified", "Keywords": "Eagle Syndrome", "Reference": "1. Lorman JG, Biggs JR. The Eagle syndrome. AJR Am J Roentgenol. 1983 May;140(5):881-2.\n\n2. Slavin KV. Eagle syndrome: entrapment of the glossopharyngeal nerve? Case report and review of the literature. J Neurosurg. 2002 Jul;97(1):216-8.\n\n3. Kelly RJ, Jackson FE, DeLave DP, Dunn J. The Eagle syndrome. Hemicrania secondary to elongated styloid process. US Navy Med. 1975 Apr;65(4):11-6" } }, { "U_id": "MPX1235", "TAC": [ "MPX1235_synpic16212" ], "MRI": [], "Case": { "Title": "Partial Anomalous Pulmonary Venous Return", "History": "64 y/o male smoker with history of interstitial changes and ?RLL nodule on CT from outside institution in 1999 (not available). Referred for new chest CT to evaluate.", "Exam": "NA", "Findings": "5.0 mm contiguous axial CT images of the chest demonstrated normal parenchyma without nodule, effusion or infiltrate. Mild interstitial disease, left basilar fibronodular scarring and mild hyperinflation. No mediastinal, hilar or axillary adenopathy. Mild degenerative changes of the thoracic spine. Coronary artery calcifications. No acute cardiopulmonary abnormality.\n\tIncidental finding of aberrant vessel seen lateral to the aortic arch on the left. Following the vessel through many cuts demonstrated that the vessel was a left upper lobe pulmonary vein which drained into the left brachiocephalic. There was no other venous abnormalities seen.", "Differential Diagnosis": "DDX: PAPVR\n Persistent Left Sided Superior Vena Cava", "Case Diagnosis": "Partial Anomalous Pulmonary Venous Return", "Treatment & Follow Up": "No treatment indicated.", "Discussion": "See Factoid." }, "Topic": { "Title": "Partial Anomalous Pulmonary Venous Return", "Disease Discussion": "Partial Anomalous Pulmonary Venous Return (left upper lobe pulmonary vein)\n\nPartial anomalous venous return occurs when a pulmonary lobe drains into the right side of the circulation, usually a systemic vein. Anomalous venous drainage of the left upper lobe is usually an isolated congenital abnormality that has no clinical significance. Anomalous drainage of the right pulmonary vein to the inferior vena cava (scimitar syndrome) can present as a left to right shunt in patients with volume loss of the right hemithorax and a peculiar comma shaped density in the right lung base. Anomalous drainage of the right upper lobe is associated with a sinus venosus type of atrial septal defect. Left lower lobe pulmonary systemic drainage is associated with extralobar sequestration.\t\n\tWhen the left upper lobe vein drains into the left brachiocephalic vein, a vertical vein is seen coursing lateral to the aortic arch and the AP window. This appearance must be distinguished from a persistent left superior vena cava. The distinction comes from following the entire course of the vein to its drainage, and if you see two vessels in the left hilum or just one. One is consistent with PAPVR while two indicates persistent left SVC (one vessel is svc other is normal left upper lobe vein.\n\tA persistent left SVC occurs in about 0.3% of the normal population with a substantially higher incidence in patients with congenital heart disease. This anomaly results from embryologic failure of regression of part of the left common and anterior cardinal veins. It at least drains the left jugular and subclavian veins. On CT a persistent left SVC is positioned immediately lateral to the left common carotid artery and anterior to the left subclavian artery. The anomalous vessel descends lateral to the aortic arch, in approximately the same coronal plane as the normal right SVC. It passes lateral to the main pulmonary artery and anterior to the left hilum. It typically drains into a dilated coronary sinus posterior to the left ventricle.", "ACR Code": "9.1", "Category": "Congenital, malformation", "Keywords": "pulmonary vein variantsPAPVRpersistent left svc", "Reference": "Computed Body Tomography with MRI Correlation. 3rd edition, 1997. Lee J.K., Sagel S.S., Stanley R.J., CD rom version, chapter five. \n\nBody CT: A practical approach.1st edition, 2000. Slone R.M., Fisher A.J., Pickhardt P.J., pg 84." } }, { "U_id": "MPX1238", "TAC": [ "MPX1238_synpic27745" ], "MRI": [], "Case": { "Title": "Skull cap in anterior abdominal wall with underlying liquified hematoma.", "History": "26 yo man developed persistent GI symptoms after craniocerebral trauma.", "Exam": ">>tissue culture negative for bacteria", "Findings": "Skull cap within the left lower anterior abdominal wall. There is a 10x6x1.5 cm nonenhancing fluid collection just posterior to the skull cap.", "Differential Diagnosis": ">> Liquified Hematoma\n>> Abscess\n>> Proteinaceous Fluid Collection", "Case Diagnosis": "Skull cap in anterior abdominal wall with underlying liquified hematoma.", "Diagnosis By": "Surgical history and negative bacterial cultures", "Treatment & Follow Up": "Surgical removal of skull cap from abdomen and cranioplasty using prosthetic plastic material.", "Discussion": "Patient had a craniectomy for intracranial hypertension. The removed skull cap was placed subcutaneously in his abdominal wall for preservation. \n\nThere is a companion case:\nhttp://rad.usuhs.mil/medpix/medpix.html?mode=pt&pt_id=6414#top" }, "Topic": { "Title": "Skull Cap in Anterior Abdominal Wall", "Disease Discussion": "Decompressive craniectomy is a neurosurgical procedure aimed at relieving elevated intra-cranial pressure (ICP) by removing the patient\u2019s rigid skull1. Decompressive craniectomy is a surgical option for the treatment of ICP in cases where medical management fails and in acute severe traumatic brain injury. The surgery alone has been shown to reduce ICP by 15% and up to 70% if the surgeon opens the dura2. More than 40,000 cranial surgeries are performed in the United States each year. The most frequent principle diagnosis in patients receiving such surgeries is subdural hemorrhage3. \n Upon resolution of the intra-cranial hypertension, a cranioplasty is performed to close the hole in the skull. There are a number of suitable materials that can be used for this purpose and one of the more common materials is the patient\u2019s own bone flap (removed segment of skull). This option is cost-effective, strong, immunologically compatible with the host, and yields the best cosmetic result. \n Several techniques for preserving the bone flap exist to include freezing, placement in storage solutions, and placement in the subcutaneous tissue of the patient\u2019s abdominal wall. Placement in the patient\u2019s abdominal wall minimizes the risk of plate loss and maintains the sterility of the plate. Additionally, host bone contains osteoinductive factors which stimulate the maturation of chondroblasts and osteoblasts. Freezing, irradiation, and storage solutions inactivate these factors leading to bone resorption and impaired healing. Placing the bone flap in the abdominal wall allows these factors to remain active and eliminates bone resorption1.", "ACR Code": "1.1", "Category": "Iatrogenic or Surgical (complications)", "Keywords": "CranioplastyDecompressive CraniectomySkull Cap", "Reference": "1. Flanndry T; McConnell RS; Cranioplasty: why throw the bone flap out?, British Journal of Neurosurgery, 2001; 15(6): 518-520\n2. Jourdan C; Convert J; Mottolese C; Bachour E; Gharbi S; Artru F.; Evaluation of the clinical benefit of decompression hemicraniectomy in intracranial hypertension not controlled by medical treatment, Neurochirurgie 1993;39(5):304-10.\n3. Buczko W.; Cranial surgery among Medicare beneficiaries.\nThe Journal of Trauma. 2005 Jan;58(1):40-6." } }, { "U_id": "MPX1243", "TAC": [ "MPX1243_synpic24671", "MPX1243_synpic24673", "MPX1243_synpic24674" ], "MRI": [], "Case": { "Title": "Bizarre Parosteal Osteochondromatous Proliferation", "History": "24 year old male with history of blunt trauma to right thigh, presents with palpable soft tissue mass at site of injury.", "Exam": "Physical exam demonstrates firm soft tissue mass with poorly defined margins at the medial right thigh. No history of fevers, chills or unexplained weight loss. Normal neuromuscular examination.", "Findings": "Irregular soft tissue calcification is seen adjacent to the lateral aspect of the mid right femur, underlying site of known prior trauma and now-palpable soft tissue mass. Cortical contiguity is uncertain. Additionally, there is curvilinear extension of the posteromedial mid right femoral cortex consistent with a chronic tug lesion of the thigh adductors.", "Differential Diagnosis": "Bizarre Parosteal Osteochondromatous Proliferation / Myositis Ossificans\nFlorid Reactive Periostitis\nOsteochondroma\nParosteal Osteosarcoma \nEwings Sarcoma", "Case Diagnosis": "Bizarre Parosteal Osteochondromatous Proliferation", "Diagnosis By": "Combination of clinical and radiographic findings.", "Treatment & Follow Up": "None.", "Discussion": "Bizarre Parosteal Osteochondromatous Proliferation (BPOP) is a rare benign lesion in which heterotopic bone arises from otherwise normal periosteum. BPOP most commonly results after minor trauma to tubular and long bones which results in myositis ossificans in closely adjacent soft tissues being incorporated into the underlying periosteum. The theory of this continuum is supported by the report by Ly JQ et al. entitled \u201cRadiologic demonstration of temporal development of bizarre parosteal Osteochondromatous proliferation\u201d in which the natural course of a case of blunt trauma was followed from soft tissue edema through myositis ossificans to BPOP over the course of a year. There should be no periosteal reaction aside from the parosteal osteochondromatous proliferation and importantly no associated cortical or medullary involvement or associated soft tissue mass. Absence of cortical or permeative bone destruction excludes neoplastic etiologies while absence of medullary extension excludes the more common benign osteochondroma. \n\tSurgical resection may be sought in symptomatic patients; however, when surgery is contemplated, bone scan must be performed prior to surgery. Recurrence typically occurs in lesions that have increased uptake on nuclear medicine bone scan. \n\n\nReference:\n\nThe statements in the above discussion were taken largely from the following source:\n\nLy JQ, Bui-Mansfield LT, Taylor DC. Radiologic demonstration of temporal development of bizarre parosteal Osteochondromatous proliferation. Clin Im 2004:28;216-218." }, "Topic": { "Title": "Bizarre Parosteal Osteochondromatous Proliferation", "Disease Discussion": "Bizarre Parosteal Osteochondromatous Proliferation (BPOP) is a rare benign lesion in which heterotopic bone arises from otherwise normal periosteum. BPOP most commonly results after minor trauma to tubular and long bones which results in myositis ossificans in closely adjacent soft tissues being incorporated into the underlying periosteum. The theory of this continuum is supported by the report by Ly JQ et al. entitled \u201cRadiologic demonstration of temporal development of bizarre parosteal osteochondromatous proliferation\u201d in which the natural course of blunt trauma was followed from soft tissue edema through myositis ossificans to BPOP over the course of a year. There should be no periosteal reaction aside from the parosteal osteochondromatous proliferation and importantly no associated cortical or medullary involvement or associated soft tissue mass. Absence of cortical or permeative bone destruction excludes neoplastic etiologies while absence of medullary extension excludes the more common benign osteochondroma. \n\tSurgical resection may be sought in symptomatic patients; however, when surgery is contemplated, bone scan must be performed prior to surgery. Recurrence typically occurs in lesions that have increased uptake on nuclear medicine bone scan.", "ACR Code": "4.4", "Category": "Trauma", "Keywords": "Myositis OssificansBPOP", "Reference": "The statements in the above discussion were taken largely from the following source:\n\nLy JQ, Bui-Mansfield LT, Taylor DC. Radiologic demonstration of temporal development of bizarre parosteal Osteochondromatous proliferation. J Clin Im 2004:28;216-218." } }, { "U_id": "MPX1255", "TAC": [ "MPX1255_synpic18243" ], "MRI": [], "Case": { "Title": "Swyer-James Syndrome", "History": "9 y/o boy with dyspnea on exertion. Chest radiograph done a year later (patient at the time had a viral infection) was reported as normal.", "Exam": "Unrevealing.", "Findings": "CXR demonstrates a hyperlucent left hemithorax. Follow up CT reveals diminished left lung vasculature and associated decreased parenchymal density.", "Differential Diagnosis": "P Poland Syndrome\nO Obstruction (i.e. airway foreign body)\nE Embolus/Emphysema\nM Mastectomy (not applicable in this young male)\nS Swyer-James Syndrome", "Case Diagnosis": "Swyer-James Syndrome", "Diagnosis By": "Radiographically" }, "Topic": { "Title": "Swyer-James Syndrome", "Disease Discussion": "Swyer-James Syndrome is also called \"unilateral hyperlucent lung\". This a radiologic *classic* where one lung field is more radiolucent (darker) on chest films.\n\nEtiology: likely secondary to childhood adenoviral infection with subsequent acute obliterative bronchiolitis, bronchiectasis, and distal air-space destruction\n\nClinical Presentation: varies from asymptomatic to DOE, usually relates a history of recurrent childhood respiratory infections\n\nRadiographic Findings\n - increased lucency in affected lung (usually entire lung with lobar/subsegmental distribution having been reported)\n - small ipsilateral hemithorax with normal-to-decreased volume\n - small ipsilateral hilum\n - air trapping on expiratory films\n - V/Q scan classically shows decreased perfusion as well as diminished ventilation with delayed washout\n - angio will show a \u201cpruned tree\u201d appearance of affected side\u2019s pulmonary vasculature", "ACR Code": "6.2", "Category": "Infection, generalized", "Keywords": "adenovirushyperlucentSwyer-James", "Reference": "Dahnert W. Radiology Review Manual. 5th ed. 2002 Lippincott Williams and Wilkins" } }, { "U_id": "MPX1253", "TAC": [ "MPX1253_synpic21241" ], "MRI": [], "Case": { "Title": "Colorectal adenocarcinoma", "History": "58yo F asymptomatic seen for routine health maintenance.", "Exam": "Rectal mass", "Findings": "Eccentric nodular mass in the left side of the rectum, no local invasion, stranding, or lymphadenopathy. No metastases to liver.", "Differential Diagnosis": "Sessile Polyp\nStool\nChronic Diverticulitis\nStromal cell Tumor\nCarcinoid\nLymphoma", "Case Diagnosis": "Colorectal adenocarcinoma", "Diagnosis By": "Biopsy", "Treatment & Follow Up": "CT was performed for staging. Patient is a Dukes B1 stage and underwent successful resection of the tumor.", "Discussion": "None" }, "Topic": { "Title": "Colorectal adenocarcinoma with mets to liver", "Disease Discussion": "): Surveillance After Resection of Colorectal Cancer \nNearly fifteen percent of all cancer deaths in the United States are caused by colorectal adenocarcinomas, making it the third most common cause of cancer deaths in the country. Although surgery is curative in the majority of Dukes I lesions, patients with distant metastases (such as this patient with liver mets), the 5-year survival rate is less than 10%. The following recommendations are suggested by the American Society of Clinical Oncology and supported by the Gastroenterological Association and the American Cancer Society for patients with disease stages II-IV:\n1.\tHistory, physical, and rectal exam by regular physician every 3-6 months\n2.\tSerum CEA measurements every three months for the first two years following resection (controversial)\n3.\tComplete colonoscopy before resection and again several months after to exclude synchronous polyps and every 3 years thereafter to exclude new lesions\n4.\tFor low anterior resections, flexible proctosigmoidoscopy yearly for the first two years, with complete colonoscopy in the third year.\n5.\tAnnual CXR if respiratory symptoms or if CEA is elevated\nAbdominal CT to look for interaabdominal metastases if CEA is elevated or if patient complains of abdominal symptoms. PET may be useful in patients with elevated CEA but otherwise normal imaging studies.", "ACR Code": "-1.-1", "Category": "Neoplasm, carcinoma", "Keywords": "adenocarcinoma", "Reference": "1.\tDesch, CE, et al. Recommended colorectal cancer surveillance guidelines by the American Society of Clinical Oncology. J Clin Oncol 1999; 17:1312.\n2.\tRenehan, AG, et al. Impact on survival of intensive follow up after curative resection for colorectal cancer: systematic review and meta-analysis of randomised trials. BMJ 2002; 324:813\n3.\tJacobson, BC. Surveillance after colorectal cancer resection. UpToDate online. Updated December 12, 2002." } }, { "U_id": "MPX1254", "TAC": [ "MPX1254_synpic21658", "MPX1254_synpic21659" ], "MRI": [], "Case": { "Title": "Reactivation TB", "History": "shortness of breath", "Exam": "ppd +", "Findings": "strandy right apical scarring and tree-in-bud opacity with minimal cystic change. Tree-in-bud opacity within superior segment of right upper lobe. No pleural effusions and no significant lymphadenopathy", "Differential Diagnosis": "Reactivation TB\nOther prior infection etiology with residual apical scarring.", "Case Diagnosis": "Reactivation TB" }, "Topic": { "Title": "Reactivation TB", "Disease Discussion": "Organism(s):Mycobacterium tuberculosis\n\nRoute of Infection:Primary, airborne; Secondary: reactivation often with endobronchial spread.\n\nClinical: Patients with reactivation present with constitutional symptoms such as weight loss, night sweats, cough, chills.\n\nLaboratory: Confirmation with sputum/bronchial washings.\n\nPathology:Casseous necrosis\n\nImaging: Ill-defined patchy and nodular opacities, often with cavitation, the latter an important radiographic feature as it implies active and transmissable disease. Apical and posterior segments of the upper lobes as well as superior segments of lower lobes involved most frequently, due to realtively high oxygen tension and favorable V/Q ratios. Clustered nodules suggest endobronchial spread of infection.\n\nTreatment: Antituberculous agents\n\nComplications: Late complications include interstitial fibrosis with pulmonary insufficiency and secondary pulmonary hypertension. Hemoptysis due to bronchiectasis, mycetoma formation within a cystic cavity, or erosion of a broncholith into the bronchus. Rasmussen\\'s aneurysm is caused by erosion of the cystic cavity into a branch of the pulmonary artery and can also cause hemoptysis.\n\nOTHER:", "ACR Code": "6.2", "Category": "Infection, NOS", "Keywords": "tuberculosisinfection", "Reference": "Fundamentals of Diagnostic Radiology. Brant and Helms. 1999. pp 404-406." } }, { "U_id": "MPX1259", "TAC": [ "MPX1259_synpic52409" ], "MRI": [], "Case": { "Title": "Mesenteric carcinoid tumor", "History": "Right upper quadrant pain, hx of urolithiasis.", "Findings": "Mesenteric carcinoid tumor with areas of calcification.", "Differential Diagnosis": "Desmoid tumor\nPrimary mesenteric tumors\nSclerosing mesenteritis\nLipomas \nSchwannomas \nSmooth muscle tumors", "Case Diagnosis": "Mesenteric carcinoid tumor" }, "Topic": { "Title": "Carcinoid tumor", "Disease Discussion": "CARCINOID TUMORS\n\nINTRO:\nCarcinoid tumors are slow growing tumors of neuroendocrine origin. The are the most common type of neuroendocrine tumors with an estimated 1.5 clinical cases per 100,000. Autopsy case incidence is higher at 650 per 100,000. \n \nOver 2/3 of carcinoid tumors are in the GI tract, but can also occur in lungs, ovaries, testes, mediastinum, kidneys, etc. More than 95% of GI carcinoids originate in only 3 sites: appendix, ileum, and rectum. Carcinoids are most often benign, but those affecting the ileum and bronchus are frequently malignant. \n\nCLINICAL FEATURES: \nSigns and symptoms vary depending on size, location, and metastases. Most tumors are slow growing and asymptomatic until late disease. Metastatic disease can occur but is not common. Carcinoid tumors can be endocrinologically inert or secrete several hormones (serotonin, histamine, kallikrein, insulin, etc) which are responsible for carcinoid syndrome (cutaneous flushing, venous telangiectasia, diarrhea, bronchospasm, cardiac valvular lesions). \n\nDIAGNOSIS: \nMany carcinoid tumors are found incidentally on endoscopic or radiographic procedures. The most useful test for carcinoid syndrome is to measure 24-hour urinary excretion of 5-HIAA. Once the diagnosis has been confirmed, the tumor must be localized using abdominal CT and indium-111 octreotide imaging. If metastases are suspected, then use of CT or MRI is recommended to rule out liver metastases.\n\nCOMPLICATIONS:\nCarcinoid crisis - life threatening form of carcinoid syndrome that results from the release of extremely high amounts of biologically active compounds (catecholamines, etc) from the tumor. Symptoms include flushing, diarrhea, tachycardia, arrhythmias, blood pressure fluctuation, bronchospasm, and altered mental status.\n\nMANAGEMENT:\nLocalize tumor and metastases by CT and somatostatin receptor scintigraphy. Remove tumor if it has not metastasized. Control carcinoid symptoms (octreotide for flushing and/or diarrhea).", "ACR Code": "7.3", "Category": "Neoplasm, benign", "Keywords": "carcinoid tumorneuroendocrine tumorcarcinoid syndrome", "Reference": "UpToDate\nMerck Manual of Diagnosis\neMedicine.com" } }, { "U_id": "MPX1241", "TAC": [ "MPX1241_synpic40299", "MPX1241_synpic40300", "MPX1241_synpic40301", "MPX1241_synpic40302", "MPX1241_synpic40303" ], "MRI": [], "Case": { "Title": "Crohns Disease", "History": "19 year-old male with epigastric abdominal pain and hematochezia.", "Exam": "Diffuse TTP, Soft, non-distended, +BS, No HSM, No rebound tenderness.", "Findings": "CT demonstrates homogeneous density of thickened bowel wall with intestinal lumen surrounded by edematous mucosa. The distal jejunum and terminal ileum were involve. Intervening segments of bowel were unremarkable.\nSubsequent colonoscopy demonstrated nodularity within the terminal ileum.\nSmall bowel follow through revealed delayed transit time with persistent narrowing and thickening of the distal jejunum and terminal ileum.", "Differential Diagnosis": "Thickened small bowel folds are nonspecific and can be seen in a wide variety of condtions, including : Inflammatory bowel dieseae, other inflammatory conditions, ischemia, hemorrhage,infection (TB, celiac). neoplasm (lymphoma, carcniod, adenocarcinoma) and amyloidosis.\nDecreased Small Bowel transit time is possible in: Inflammatory bowel dieseae, Hypothyroidism, Diabetes, Scleroderma, Opiate use or Celiac disease.", "Case Diagnosis": "Crohns Disease", "Diagnosis By": "Imaging and colonoscopic findings in conjunction with patient history. Biopsy demonstrated inflammatory changes.", "Discussion": "Crohns disease is an idiopathic inflammatory process which can involve any part of the GI tract from the esophagus to rectum (small bowel-80%). This patient's findings are limited to the distal jejunum and terminal ileum. These findings constitue \"skip lesions\", or discontinous involvement of bowel segments, with normal intervening bowel.\nCrohns can be categorized into 3 phases: early, advanced and stenotic. This patient's presentation is most consistent with the early phase which includes nodular enlargement of lymphoid follices with obstructive lyphedema fist arising in the T.I.. Later, \"advanced\" findings may include coboblestoning and lumenal narrowing. The final or \"stenotic phase\" involve strictures with dilated proximal loops.\nCrohns Disease can exhibit many extraintestinal manifestations including hepatobiliary, GU, MSK findings. This young patient did not demonstrate any of these at this point." }, "Topic": { "Title": "Crohn's Disease", "Disease Discussion": "CROHN'S DISEASE\ndisease of unknown etiology with prolonged unpredictable course characterized by discontinuous asymmetric involvement of entire GI tract\n\nClinically:\nonset between 15 - 30 years; M:F = 1:1\n\u2022 recurrent episodes of diarrhea\n\u2022 colicky / steady abdominal pain\n\u2022 low-grade fever\n\u2022 weight loss, anorexia\n\u2022 occult blood + anemia\n\u2022 perianal abscess / fistula (40%)\n\u2022 malabsorption (30%)\nAssociated with: erythema nodosum, pyoderma gangrenosum\n\nImaging can show\n-homogeneous density of thickened bowel wall\n-\"double halo configuration\" = intestinal lumen surrounded by inner ring of low attenuation(= edematous mucosa) + outer ring of soft-tissue density (= thickened fibrotic muscularis + serosa)\n-luminal narrowing + proximal dilatation\n-skip areas of asymmetric bowel wall thickening \n-\"creeping fat\" = massive proliferation of mesenteric fat (40%) with mass effect separating small bowel loops\n-mesenteric adenopathy (18%)\n-abscess (DDx: postoperative blind loop)\n\nPrognosis: recurrence rate of up to 39% after resection (commonly at the site of the new terminal ileum, most frequently during first 2 years after resection); mortality rate of 7% at 5 years, 12% at 10 years after 1st resection", "ACR Code": "7.2", "Category": "Inflammatory, autoimmune", "Keywords": "Crohn's DiseaseInflamatory bowel disease", "Reference": "Dahnert's Electronic Radiology Review. 1988: William's and Wilkins." } }, { "U_id": "MPX1270", "TAC": [ "MPX1270_synpic21803" ], "MRI": [], "Case": { "Title": "Oligodendroglioma", "History": "45 year old male with history of persistent headaches.", "Findings": "Post operative noncontrasr CT of the head demonstrates a large mass with ill defined borders that involves the posterior temporal lobe. Chunky calcifications are present. MRI reveals vasogenic edema in the region of the lesion.", "Differential Diagnosis": "Differential diagnosis of temporal lobe lesions:\n>ganglioglioma\n>astrocytoma\n>oligodendroglioma", "Case Diagnosis": "Oligodendroglioma", "Diagnosis By": "Pathology" }, "Topic": { "Title": "Oligodendroglioma, Profile and WHO Grade", "Disease Discussion": "Neoplasm Name: oligodendroglioma\nICD-O code 9450/3\n\nSynonyms:\n\nCell of Origin: adult oligodendrocytes\n\nWHO Grade(s):\nGrade 2 for well differentiated\nGrade 3 for anaplastic oligodendroglioma\n\nGenetics and Associations:\nChromosome 1p and 19qassays may correlate with a more positive response to chemotherapy. {INO2001}{BURGER2001} {SASAKI2002} Whereas tumors with a 10q mutations are resistant\n\nDemographics (Age, Sex, Incidence):\n\nCommon Locations:\nfrontal > temporal > parietal\narise preferentially in the cortex\n\nGross Appearance:\nwell defined soft masses, some with gelatinous mucoid regions\ncalcification is common\nhemorrhage may occur\n\nRadiology:\nOften large, superficial, heterogeneous, CT shows thick/dense calcifications, often curvilinear in the cerebral cortex\n\nHistology:\nmonotonous with moderate cellularity, perinuclear halo (a fixation artifact) creates a \"fried egg\" appearance that goes well with the \"chicken wire\" vascularity\n\nSpecial Stains:\nusually GFAP +\n\nPrognosis and Treatment:\n\nCOMMENTS:", "ACR Code": "1.3", "Category": "Neoplasm, glial", "Keywords": "oligodendrogliomaanaplastic oligodendrogliomaWHO grading", "Reference": "Pathology and Genetics of Tumours of the Central Nervous System. Kleihues P, Cavenee WK Eds.\nIARC Press, Lyon, 2000, pgs. 56 - 64" } }, { "U_id": "MPX1278", "TAC": [ "MPX1278_synpic21143" ], "MRI": [], "Case": { "Title": "Bronchiectasis - Bronchial Artery Embolization.", "History": "65 year old German woman who has complained of a 5 year history of hemoptysis", "Exam": "Gen: A+0x3. Resting comfortabily.\nLungs: CTA.\nCV: WNL.\nHCT 39\nWBC 10", "Findings": "Selective catherization of a lingular bronchial artery reveals enlarged, tortuous, abnormal bronchial vessels.", "Differential Diagnosis": "Cystic fibrosis\nChronic infection\nChronic granulomatous disease\nBronchiectasis\nTumor", "Case Diagnosis": "Bronchiectasis - Bronchial Artery Embolization.", "Diagnosis By": "CT Chest and angiography", "Treatment & Follow Up": "Particle embolization of the bronchial artery. The patient's symptoms have resolved.", "Discussion": "There are several finer points to this case. \n\nFirst, the angiographer must take care to identify hazardous collaterals originating from the intercostal-bronchial trunk (ICBT), namely the anterior spinal artery. Filling the anterior spinal artery from ICBT injection is at least a relative contraindication to embolization. If the catheter cannot be positioned distal to the origin of the spinal artery, embolization should not be performed. \n\nSecond, coils should not be used for embolization. The hemostasis required is at the capillary level. Placing a large, proximal coil will not treat the abnormal vessels, which will recruit proximal supply via other ICBT collaterals." }, "Topic": { "Title": "Bronchiectasis - Bronchial Artery Embolization.", "Disease Discussion": "Clinical history. Hemoptysis.\n\nTechnique:\nRight femoral artery access.\nFlush descending aortogram to define anatomy.\nSelective catheterization of the offending artery.\nEmbolization with Gelfoam.\n\nRisks:\nNon target emoblization such as a lumbar artery which could cause paralysis.", "ACR Code": "6.2", "Category": "Infection, NOS", "Keywords": "Hemoptysis", "Reference": "Vascular and Interventional Radiology: Radiology Requisites Series\nJohn A. Kaufman, Michael J. Lee\n\nPrimer of Diagnostic Imaging\nRalph Weissleder, Jack Wittenberg, Mukesh G. Harisinghani" } }, { "U_id": "MPX1275", "TAC": [ "MPX1275_synpic54182" ], "MRI": [], "Case": { "Title": "Biloma, after cholecystectomy", "History": "This 56 y.o. man had a laparoscopic cholecystectomy for acute cholecystitis. Due to significant inflammatory changes, the procedure was converted to an open cholecystectomy. Nine days later, he presents with shortness of breath and abdominal pain.", "Findings": "\u2022 CT scan performed 9 days post cholecystectomy shows subcapsular fluid displacing the liver medially.\n\n\u2022 Hepatobiliary scan obtained one day after the above CT scan demonstrated progressive accumulation of radiotracer surrounding the right hepatic lobe and the dome of the liver. This corresponds to the large collection seen on the CT scan of the abdomen. The radiotracer flowed through a drain with a subsequent decrease in the activity surrounding the right hepatic lobe and the dome.\n\n\u2022 ERCP demonstrated extravasation of contrast originating from the cystic duct remnant. The surgical clips did not ligate the cystic duct remnant and is responsible for causing the bile leak.", "Differential Diagnosis": "\u2022 Hepatic Pseudocyst\n\u2022 Hepatic Subcapsular Hematoma\n\u2022 Biloma (bile collection)\n\u2022 Abscess", "Case Diagnosis": "Biloma, after cholecystectomy", "Diagnosis By": "ERCP confirmed extravasation of contrast from the cystic duct.", "Treatment & Follow Up": "A hepatobiliary scan revealed radiotracer uptake surrounding the liver consistent with a bile leak into a biloma with subsequent drainage through the right upper quadrant drain. \n\nAn ERCP confirmed extravasation of contrast from the cystic duct.\n\nDuring the ERCP, a biliary stent was placed. A follow-up CT performed 6 days after the ERCP showed near complete resolution of the subcapsular fluid.", "Discussion": "CT scans detect perihepatic fluid well, but they fail to accurately identify whether the fluid is bilious or, more importantly, if the fluid arose from a communication with the biliary tree. Tc-99m labeled hepatobiliary scanning is a well-known modality that provides excellent physiologic evaluation of bile leaks." }, "Topic": { "Title": "Biloma, post operative", "Disease Discussion": "Postcholecystectomy Biloma Assessment with Hepatobiliary Imaging\n\nBilomas are a well known and well documented complication of open cholecystectomies. CT scans detect perihepatic fluid well, but they fail to accurately identify whether the fluid is bilious or, more importantly, if the fluid arose from a communication with the biliary tree. Tc-99m labeled hepatobiliary scanning is a well-known modality that provides excellent physiologic evaluation of bile leaks.", "ACR Code": "7.3", "Category": "Nuclear Medicine", "Keywords": "Hepatobiliary ScanBilomaLaparoscopic Cholecystectomy", "Reference": "1. Rosenberg DJ, Brugge WR, Alavi A. Bile leak following an elective laparoscopic cholecystectomy: the role of hepatobiliary imaging in the diagnosis and management of bile leaks. J Nucl Med. 1991;32(9):1777-1781. \n2. Schirmer BD, Winters KL, Edlich RF. Cholelithiasis and cholecystitis. J Long Term Eff Med Implants. 2005;15(3):329-338. \n3. Morgenstern L, Berci G, Pasternak EH. Bile leakage after biliary tract surgery. A laparoscopic perspective. Surg Endosc. 1993;7(5):432-438. \n4. Walker AT, Shapiro AW, Brooks DC, Braver JM, Tumeh SS. Bile duct disruption and biloma after laparoscopic cholecystectomy: imaging evaluation. AJR Am J Roentgenol. 1992;158(4):785-789. \n5. Gilsdorf JR, Phillips M, McLeod MK, et al. Radionuclide evaluation of bile leakage and the use of subhepatic drains after cholecystectomy. Am J Surg. 1986;151(2):259-262. \n6. A prospective analysis of 1518 laparoscopic cholecystectomies. The Southern Surgeons Club. N Engl J Med. 1991;324(16):1073-1078. \n7. Peters JH, Ellison EC, Innes JT, et al. Safety and efficacy of laparoscopic cholecystectomy. A prospective analysis of 100 initial patients. Ann Surg. 1991;213(1):3-12. \n8. Weissmann HS, Byun KJ, Freeman LM. Role of Tc-99m IDA scintigraphy in the evaluation of hepatobiliary trauma. Semin Nucl Med. 1983;13(3):199-222." } }, { "U_id": "MPX1261", "TAC": [ "MPX1261_synpic15907", "MPX1261_synpic15908", "MPX1261_synpic15910", "MPX1261_synpic15911" ], "MRI": [], "Case": { "Title": "Horseshoe Kidney (midline renal fusion)", "History": "Editor's note: Although no history was provided by the author of this case file, in all likelyhood this patient presented with a history of recurrent urinary tract infection.\nUreterovesicular junction obstruction is commonly associated with this entity due to abnormal insertions of the ureters into the bladder. UPJ obstructions is also common and duplicated ureters may also be present. In this patient, note the double ureter on the right. Together, these abnormalities lead to hydronephrosis, recurrent infections and stone fomation.", "Exam": "No physical examination or labratory data was provided by the author of this file. One can safely assume however, that secondary to the degree of hydronephrosis seen bilaterally, the patient's creatinine level is elevated.\nSome patient's with horseshoe kidney's exhibit a physical finding called Rovsing sign which is nausea, vomiting, and abdominal pain with hyperextension of the spine. \nSome patients may have a palpable lump in their abdomen.", "Findings": "CT shows that the isthmus of the horseshoe kidney is thick and enhances to the same degree as the rest of the kidney, proving it to be functioning renal tissue rather than simply a fibrous band. Notice that the isthmus of the horseshoe kidney is constrained by the inferior mesenteric artery, the structure that prevented tis continued ascention within the abdomen. Note on conventional angiography that supernumary renal arteries are present bilaterally, a common finding associated with this entity.\nNote the severe bilateral hydronephrosis secondary, in all likelyhood, to severe vesicoureteric reflux. the IUP show a duplicated ureter on the right.", "Differential Diagnosis": "Spinal bifida can also cause severe bilateral hydronephrosis but the angiographic picture here is classic and this diagnosis is an \"Aunt Minnie\"", "Case Diagnosis": "Horseshoe Kidney (midline renal fusion)", "Diagnosis By": "Conventional angiography and CT", "Treatment & Follow Up": "Pyeloureteroplasty, ureterocalicostomy, or minimally invasive pyeloplasty, depending on the judgement of the consulting urologist.\n\nFollow-up scanning for survailance for renal tumor due to the greater incidence of tumors in patients with this entity. No specific guideline has been set, but yearly screening seems reasonable.", "Discussion": "Once a horseshoe kidney is diagnosed, a search for other developmental anomalies should be undertaken. About a third of cases are associated with another anomaly.\n\nTwo excellent review articles on this subject may be found on the emedicine website\n1) http://www.emedicine.com/radio/topic348.htm\n2) http://www.emedicine.com/med/topic2860.htm" }, "Topic": { "Title": "Horseshoe kidney", "Disease Discussion": "Horseshoe kidney is in a group of congenital kidney anomalies called fusion anomalies. The fusion occurs at the lower poles in 90% of the cases, while 10% are fused at the upper pole. This anomaly is found in approximately 1/500-100 people. It is thought that the abnormal fusion likely occurs when the kidneys are still in the pelvis and the renal capsule is not fully developed. During the kidneys ascent these fused kidneys are trapped by the inferior mesenteric artery as the isthmus is unable to pass. The kidneys ascend to their normal positions between the fourth and ninth weeks of gestation. Complications include: ureteropelvic junction obstruction, recurrent UTI (urine stasis and vesicoureteric reflux), recurrent stone formation, and increased risk of trauma (due to kidney positioning). Horseshoe kidney may occur as an isolated anomaly or associated with other anomalies. Associated anomalies may include: ureteral duplication, hypospadias, undescended testis, ectopic ureter, anorectal malformations, GI malrotation, Meckel\u2019s diverticulum, neural tube defects, clubfoot, congenital hip dislocation, and ventricular septal defect. Chromosomal abnormalities have also been associated with horseshoe kidney. Horseshoe kidney is often evaluated with intravenous urography, CT, and/or ultrasound. MRI and scintigraphy may also be useful.", "ACR Code": "8.1", "Category": "Congenital, malformation", "Keywords": "Horseshoe kidneyfused kidneys", "Reference": ") Irshad, A; Ackerman, S; Ravenel, J. Horseshoe Kidney. www.emedicine.com Feb 03\n 2) Gross, G. Crossed fused Renal Ectopia. www.emedicine.com Feb 02\n 3) Cotran, R S; Kumar, V; Collins, T. Robins Pathologic Basis of Disease. W.B. Saunders Company. 1999. p 937." } }, { "U_id": "MPX1272", "TAC": [ "MPX1272_synpic26877", "MPX1272_synpic26878", "MPX1272_synpic26879", "MPX1272_synpic26880", "MPX1272_synpic26881" ], "MRI": [], "Case": { "Title": "Adrenal Myelolipoma", "History": "83 year old male presents with hematuria \n\nPMHx: NIDDM, HTN, HLP, COPD, skin cancer, stroke, macular degeneration, and mycosis fungoides\n\nPSHx: Left hip replacement, appendectomy, laparotomy, intestinal blockade repair", "Findings": "Patient noted to have a 3X3cm right adrenal mass with with a large fatty component and small focal areas of calcification.", "Differential Diagnosis": "Adrenal Myelolipoma\nAdrenal Adenoma \nAdrenal Carcinoma \nAngiomyolipoma, Kidney \nLipoma/Liposarcoma, Soft Tissue", "Case Diagnosis": "Adrenal Myelolipoma", "Diagnosis By": "Appearance on CT scan", "Treatment & Follow Up": "Clinical montioring. Follow up if symptomatic.", "Discussion": "Lesion was found incidentally on this patient undergoing CT with stone protocol to determine the presence of a possible renal or ureteral mass. Stones were present on imaging in addition to adrenal myelipoma." }, "Topic": { "Title": "Adrenal Myelolipoma", "Disease Discussion": "Adrenal myelolipoma is a benign neoplasm composed of adipose tissue and hematopoietic elements that are usually small and asymptomatic. These tumors are generally discovered incidentally at autopsy or imaging studies performed for other reasons (0.08-0.2% at autopsy). Extra-adrenal sites include the pelvis, thorax and retroperitoneum. They are typically unilateral and variable in size from mm to 30cm. There is an equal incidence in males and females with slight predilection in the Caucasian population. These neoplasms typically occur in the fifth to seventh decades, and no death rate is reported in the literature due to the rarity of these tumors. \n\nCT is the imaging modality of choice for these lesions which can be diagnosed macroscopically by focal fatty density within the mass. Occasionally, discrete calcifications can be found in small amounts along with a thin rim of residual adrenal cortex. MRI can also accurately depict both microscopic and macroscopic fat through chemical shift imaging and explicit fat saturation technique. Ultrasound is typically not used for the characterization of adrenal neoplasms, but has been known to find them incidentally. \n\nIt is believed that these tumors might represent an extramedullary site of hematopoiesis or that they arise from metaplasia of the reticuloendothelial cells of capillaries in the adrenal gland in response to stimuli (ie. necrosis, infection, stress). \n\nThese lesions are usually asymptomatic but might result in complications such as rupture (rare-only 11 reported cases as of 2003), tumor necrosis and retroperitoneal hemorrhage, and mechanical compression from tumor bulk. Myelolipomas do not undergo malignant transformation and they are rarely associated with endocrine disorders. However, Conn\u2019s and Cushing\u2019s syndromes as well as congenital adrenal hyperplasia have been documented in the literature (25 cases reported by one study). \n\nSmall asymptomatic tumors are generally monitored clinically while symptomatic lesions are treated by adrenalectomy. Large asymptomatic tumors are occasionally removed surgically to prevent rupture, and transcatheter embolization is used prior to surgery to stop bleeding of ruptured tumors. As most adrenal myelolipomas are small, asymptomatic, and discovered incidentally, surgery is rarely required.", "ACR Code": "8.3", "Category": "Neoplasm, benign", "Keywords": "adrenal myelolipomaneoplasm, benignincidentaloma", "Reference": "Andreas Meyer and Matthias Behrend, \u201cPresentation and Therapy of Myelolipoma,\u201d International Journal of Urology, 12.3:239-243, 2005.\n\nEdward M. Schaeffer and Louis R. Kavoussi, \u201cAdrenal Myelolipoma,\u201d The Journal of Urology, 173.5:1760, May 2005.\n\nMasatoyo Nakajo et al., \u201cEmbolization for Spontaneous Retroperitoneal Hemorrhage from Adrenal Myelolipoma,\u201d Radiation Medicine, 21.5:214-219, 2003.\n\t\nJeff Wenzel and Ken L. Ford III, \u201cAunt Minnie\u2019s Corner,\u201d Journal of Computer Assisted Tomography, 23.3:485, May/June 1999.\n\nSaroja Adusumilli and Parvati Ramchandani, \u201cAdrenal Myelolipoma,\u201d eMedicine\u00ae, last updated 1/19/05, found 10/25/05 at: http://eMedicine.com." } }, { "U_id": "MPX1264", "TAC": [ "MPX1264_synpic32979", "MPX1264_synpic32981" ], "MRI": [], "Case": { "Title": "Large B cell lymphoma of the liver with malignant biliary obstruction", "History": "One month of abdominal pain, nausea, and vomiting.", "Exam": "The patinet is a cachectic, jaundiced, elderly asian female. Serum total bilirubin 14.9mg/Dl, Alkaline phosphatase 956 U/l.", "Findings": ">> CT Liver: infiltrative mass in right lobe of liver, intrahepatic biliary dilatation, lymphadenopathy.\n\n>> Percutaneous cholangiogram and external biliary drain placement: mildly dilated intrahepatic biliary ducts, mass effect displaces common hepatic duct.\n\n>> Percutaneous cholangiogram and endobiliary stent placement: Gore Viabil covered metallic stent allows internal drainage.", "Differential Diagnosis": ">> Hepatocellular carcinoma\n>> Cholangiocarcinoma", "Case Diagnosis": "Large B cell lymphoma of the liver with malignant biliary obstruction", "Diagnosis By": "core biopsy and cytology", "Treatment & Follow Up": ">> Treatment for advanced disease usually includes chemotherapy (traditionally CHOP although this is evolving and has changed significantly over the last 30 years). \n\n>> Other interventions are usually palliative, as in this case where percutaneous biliary drainage followed by endobiliary stenting with internal drainage was performed.", "Discussion": "Key facts for biliary stenting of malignant obstructive jaundice:\n>> It is palliative therapy.\n\n>> Metal stents demonstrate longer patency than plastic (polyethylene) stents for malignant biliary obstruction (median expected patency: 250 and 110 days respectively).\n\n>> This treatment provides significant palliation of patient symptoms due to biliary obstruction and is cost-effective in patients with longer than 6 months expected survival resulting in fewer hospital admissions.\n\n>> Covered endobiliary stents like the Gore Viabil used in this case have good patency rates in malignant biliary obstruction and allow endobiliary drainage into the small bowel which is desirable for outpatient management of these patients." }, "Topic": { "Title": "Malignant biliary obstruction due to B Cell Lymphoma", "Disease Discussion": "Tumor Name: Large B-cell Lymphoma \n\nCell of Origin: B lymphocytes \n\nSpecial Stains: Strong membranous staining for CD45, CD20, bcl-2 and bcl-6. Negative for pancytokeratin and synaptophysin. \n\nRadiology: \n>> CT Liver: infiltrative mass in right lobe of liver, intrahepatic biliary dilatation, lymphadenopathy. \n\n>> Ultrasound guided percutaneous biliary access with cholangiogram and external biliary drain placement: mildly dilated intrahepatic biliary ducts, mass effect displaces common hepatic duct. \n\n>> Percutaneous cholangiogram and biliary stent placement: Gore Viabil covered metallic stent allows internal drainage. \n\nPrognosis and Treatment: \n>> 5 yr survival 26-73%. Lower in this case due to age >60, elevated serum LDH, and extra nodal involvement (liver mass). \n\n>> Treatment for advanced disease usually includes chemotherapy (traditionally CHOP although this is evolving and has changed significantly over the last 30 years). \n\n>> Other interventions are usually palliative, as in this case where percutaneous biliary stenting and eventual internal drainage was performed. \n\n\nKey facts for biliary stenting of malignant obstructive jaundice: \n>> It is palliative therapy. \n\n>> Metal stents demonstrate longer patency than plastic (polyethylene) stents for malignant biliary obstruction (median expected patency: 250 and 110 days respectively). \n\n>> This treatment provides significant palliation of patient symptoms due to biliary obstruction and is cost-effective in patients with longer than 6 months expected survival resulting in fewer hospital admissions. \n\n>> Covered endobiliary stents like the Gore Viabil used in this case have good patency rates in malignant biliary obstruction and allow endobiliary drainage into the small bowel which is desirable for outpatient management of these patients.", "ACR Code": "7.3", "Category": "Obstruction or Stenosis", "Keywords": "Malignant biliary obstructionBiliary interventionLiver lymphoma", "Reference": ">> Rossi P, Bezzi M, Rossi M, et al: Metallic stents in malignant biliary obstruction: results of a multicenter European study of 240 patients. Journal of Vascular and Interventional Radiology 1994 Mar-Apr; 5: 279 -85.\n\n>> Hammarstrom LE: Endobiliary stents for palliation in patients with malignant obstructive jaundice. J Clin Gastroenterol 2005 May/Jun; 39(5): 413-21.\n\n>> Fisher RI, Gaynor ER, Dahlberg S, et al: Comparison of a standard regimen (CHOP) with three intensive chemotherapy regimens for advanced non-Hodgkin's lymphoma. N Engl J Med 1993 Apr 8; 328(14): 1002-6." } }, { "U_id": "MPX1268", "TAC": [ "MPX1268_synpic26628" ], "MRI": [], "Case": { "Title": "Adenocarcinoma", "History": "This is a case of an 82 year old man presenting with acute onset lower gastrointestinal bleeding.", "Exam": "Patient had bright red blood per rectum\n\nINR-1.2\nCr-1.2\nBUN-17\nHgb-13\nHCT-30", "Findings": "The tagged red cell scan showed activity in the left transverse colon and splenic flexure moving both proximally and distally with time.\n\nArteriography demonstrated an abnormal vascular blush in the arterial recta downstream from the ascending branch of the left colic artery and extravasation of contrast material into the bowel.\n\nFollowing embolization with microcoils, extravasation was no longer appreciated and the study was concluded.\n\nA CT study with bowel contrast only demonstrates an apple core filling defect adjacent to the microcoils.", "Differential Diagnosis": "Ddx of Lower Gastrointestinal Bleed:\n-Diverticulosis\n-Hemorrhoids\n-Neoplasm\n-Angiodysplasia/AVM\n-Vasculitis\n-Ischemic bowel", "Case Diagnosis": "Adenocarcinoma", "Diagnosis By": "Pathology", "Treatment & Follow Up": "Following microcoil embolization of the lower gastrointestinal bleed, the patient did well, had no further episodes of bleeding, and did not require further transfusion. The following day, colonoscopy was unable to move beyond the splenic flexure. A CT study with bowel contrast demonstrated an apple core lesion adjacent to the microcoils. Pathologic evaluation revealed adenocarcinoma.", "Discussion": "Lower gastrointestinal bleeding can be caused by several factors, including diverticulosis, neoplasm, angiodysplasia, and inflammatory bowel disease. This patient's lower GI bleed was caused by adenocarcinoma of the colon, as demonstrated by CT and confirmed by pathology. The patient proceeded to the OR for removal of the cancerous lesion. Had the bleeding vessel not been occluded by transcatheter embolization, this patient would have had to undergo two operations: one to resect the bowel and one to reanastomose his ostomy. Because this microcoil embolization procedure was successful, the patient received a bowel prep before his resection, which allowed him to undergo a single operation instead of two operations. Thus, in addition to stopping this patient's hemorrhage, this embolization procedure decreased this patient's risk of surgery- and anesthesia-related morbidity and mortality." }, "Topic": { "Title": "Microcoil Embolization of a Lower Gastrointestinal Bleed", "Disease Discussion": "A lower gastrointestinal bleed (LGIB) is hemorrhage distal to the ligament of Treitz and includes hemorrhage of the small bowel and colon. Common etiologies include diverticulosis, angiodysplasia, neoplasm, and inflammatory bowel disease (IBD) [1]. The most common etiology in patients over 50 is diverticulosis, while the most common etiology in young patients is IBD [1]. Infection is the most common etiology in immunocompromised hosts [1].\n\n Acute lower gastrointestinal (GI) hemorrhage is a potentially life threatening condition. Although most cases can be managed medically, 10-15% require intervention to control the hemorrhage [2]. Therapeutic options include surgery, vasopressin infusion, endoscopy, and transcatheter embolization. Surgery is associated with mortality rates as high as 15-30% in emergent operations, and vasopressin is associated with high rates of rebleeding and systemic side effects [2]. Although colonoscopy has become first line in the investigation and treatment of lower GI hemorrhage, endoscopy is limited in cases of massive hemorrhage because the presence of copious amounts of blood and stool in the bowel may prevent visualization of a bleeding source [2]. Given a positive dynamic bleeding scan, mesenteric angiography becomes important not only because it localizes active bleeding, but also because it provides a pathway for potential treatment [2]. Modern transcatheter embolotherapy has become an option in the the management of lower GI hemorrhage, and microcoils are the preferred embolic agent for many interventionalists [2].\n\n_______________________________________________________________________________________\nTable 1. Complications of LGI Embolization: Incidence of Postembolic Colonic Ischemia\n---------------------------------------------------------------------------------------------------------------------\nReference/Yr......#Patients........#Complications(%).....#Clinically Significant Complications(%)\n---------------------------------------------------------------------------------------------------------------------\n[3]/1996.....................9.....................2 (22.2).........................0 (0.0)*\n[4]/1997...................17.....................3 (17.6).........................1 (5.9)\n[5]/1998.....................7.....................0 (0.0)..........................0 (0.0)\n[6]/1998...................14.....................3 (21.4).........................0 (0.0)*\n[7]/1998...................21.....................1 (4.8)..........................0 (0.0)\n[8]/1999.....................4.....................1 (25.0).........................0 (0.0)*\n[9]/1999...................10.....................7 (70.0).........................0 (0.0)\n[10]/2000.................17.....................2 (11.8).........................0 (0.0)\n[11]/2000.................17.....................4 (23.5).........................1 (5.9)\n[2]/2001...................48.....................6 (12.5).........................0 (0.0)\n[12]/2001.................27.....................4 (14.8).........................1 (3.7)*\n[13]/2001.................10.....................0 (0.0)..........................0 (0.0)\n[14]/2001.................11.....................0 (0.0)..........................0 (0.0)\n________________________________________________________________________________________\n*Studies in which microcoils are the sole agents of embolization\n\t\t\n Table 1 reviews the literature from the past decade demonstrating the incidence of lower GI postembolization colonic infarction. Note the graph shows the total number of ischemic complications in each study, as well as the number of clinically significant complications, defined here as those necessitating surgical therapy or causing major morbidity or death. Numbers in parentheses are percentages. Asterisks indicate studies in which microcoils were the only agents of embolization. It is interesting to note that studies from the 1980s (not charted) demonstrate a 20% incidence of clinically significant postembolization infarction, whereas these later studies demonstrate no or few cases of postembolization infarction [2]. It is reasonable to suspect that this difference is a result of the advent of finer coaxial systems and microcoils, which have enabled more distal and selective catheterization and embolization.\n\n Embolization may not be possible in all patients in whom bleeding is identified at angiographic examination because of several factors. These factors include vessel spasm, spontaneous cessation of bleeding, and vessel tortuosity [7]. Technical failure caused by these factors occurs in approximately 20% of cases at Naval Medical Center San Diego, which is similar to rates reported in the literature [2],[7].", "ACR Code": "7.3", "Category": "Technique/Modality", "Keywords": "microcoilembolizationgastrointestinal bleed", "Reference": "1. Kaufman JA and MJ Lee. Vascular & Interventional Radiology: The Requisites. Mosby, Inc: 2004; 298-304.\n\n2. Bandi R, Shetty PC, Sharma RP, Burke TH, Burke MW, Kastan D. Superselective arterial embolization for the treatment of lower gastrointestinal hemorrhage. J Vasc Intervent Radiol 2001; 12: 1399-1405.\n\n3. Curzon IL, Nicholson AA Dyet JF, Hartley J. Transcatheter coil embolotherapy for major colonic hemorrhage. Cardiovasc Intervent Radiol 1996; 19 (suppl 2):S83.\n\n4. Gordon RL, Ahl KL, Kerlan RK, et al. Selective arterial embolization for the control of lower gastrointestinal bleeding. Am J Surg 1997; 174:24-28.\n\n5. Ledermann HP, Schoch E, Jost R, Decurtins M, Sollikofer CL. Superselective coil embolization in acute gastrointestinal hemorrhage: personal experience in 10 patients and review of the literature. J Vasc Interv Radiol 1998; 9:753-760.\n\n6. Nicholson AA, Ettles DF, Hartley JE, et al. Transcatheter coil embolotherapy: a safe and effective option for major colonic haemorrhage. Gut 1998; 43:79-84.\n\n7. Peck DJ, McLoughlin RF, Hughson MN, Rankin RN. Percutaneous embolotherapy of lower gastrointestinal hemorrhage. J Vasc Interv Radiol 1998; 9:747-751.\n\n8. Dobson CC, Nicholson AA. Treatment of rectal hemorrhage by coil embolization. Cardiovasc Intervent Radiol 1999; 22: 143-146.\n\n9. Bulakbasi N, Kurtaran K, Ustunsoz B, Somuncu I. Massive lower gastrointestinal hemorrhage from the surgical anastamosisin patients with multiorgan trauma: treatment by subselective embolization with polyvinyl alcohol particles. Cardiovasc Intervent Radiol 1999; 22: 461-467.\n\n10. Evangelista PT, Hallisey MJ, Transcatheter embolization for acute lower gastrointestinal hemorrhage. J Vasc Intervent Radiol 2000; 11:601-606.\n\n11. Luchtefeld MA, Senagore AJ, Szomstein M, Fedeston B, Van Erp J, Rupp S. Evaluation of transarterial embolization for lower gastrointestinal bleeding. Dis Colon Rectum 2000; 43:532-534.\n\n12. Funaki B, Kostelic JK, Lorenz J, Ha TV, Yip DL, Rosenblum JD, et al. Superselective microcoil embolization of colonic hemorrhage. AJR Am J Roentgenol 2001; 177:829-836.\n\n13. Patel TH, Cordts PR, Abcarian P Sawyer MA. Will transcatheter embolization replace surgery in treatment of gastrointestinal bleeding? Curr Surg 2001; 58:323-327.\n\n14. Defreyne L, Vanlangenhove P, De Vos M, et al. Embolization as a first approach with endoscopically unmanageable acute nonvariceal gastrointestinal hemorrhage. Radiology 2001; 218: 739-748." } }, { "U_id": "MPX1256", "TAC": [], "MRI": [ "MPX1256_synpic50758", "MPX1256_synpic50760", "MPX1256_synpic50761" ], "Case": { "Title": "Calvarial Hemangioma", "History": "53 y/o man with history of basal cell carcinoma presents with painful lump on right forehead. Pt had similar lesion 9 years ago that was operated on by plastic surgery, no records available. Lesion has been very slow growing over past year, becoming more painful on deep palpation recently.", "Exam": "PE: WDWN, NAD, 71\u201d/205#, Vitals WNL/Stable; Noncontributory physical exam except palpation of 2x3cm bony lesion at right frontotemporal region of skull that is TTP. No neurological deficits.\n\nLABS: CBC, CMP, LFTs, Chol PNL all WNL, PSA 2.4 (stable).", "Findings": "Skull Series: There is a small lesion adjacent to the right frontal sinus measuring 2.6 x 1.5 cm in size. This lesion has a partially sclerotic margin and no other significant osseous abnormality is seen.\n\nCT: There is an expansile intra-osseous lesion, measuring approximately 3.1 x 1.3 cm, in the right frontal bone, with a thin sclerotic rim with preservation of the trabeculae. There is an apparent disruption in the cortex anteriorly, which is well corticated and likely represents an enlarged\nfeeding vessel. There is no periosteal reaction.\n\nMRI: Expansile lesion of the frontal bone. Low in signal on T1, high signal on T2, and avid enhancement post contrast. Foci of high signal on T1 are noted, most likely representing fat.", "Differential Diagnosis": "\u2022 Calvarial Hemangioma\n\u2022 Eosinophilic Granuloma - wrong age group\n\u2022 Intraosseous Meningioma\n\u2022 Metastasis - unlikely since there is preservation of the trabeculae", "Case Diagnosis": "Calvarial Hemangioma", "Diagnosis By": "Patient history and radiologic correlation to previous history of lesion.", "Treatment & Follow Up": "The patient is being managed conservatively with serial observation of the lesion. Repeat resection of lesion will be considered at a later date if lesion continues to expand or becomes more symptomatic.", "Discussion": "Reports having more of the same lesions on L2 and right femur by history. No fevers, chills, weight changes, bowel changes. Had chronic neck pain, R arm parasthesias relieved with recent laminectomy. No other neurologic complaints.\n\n\n\nPMHx: HTN, BCC on face, chronic back pain, spondylolysis with myelopathy, congenital fusion of C6/7, B12 Deficiency\nMeds: B12, Methylprednisilone taper 3 months ago, Docusate Sodium, Methocarbamol, Percocet or Oxycontin for back pain\nPSHx: June 2009 C-spine Laminectomy/fusion, Remote excision of BCC, Remote Appendectomy\nFamHx: + Cancer in family (unknown type), +CVD\nSoc Hx: +Alcohol, socially, -Tob" }, "Topic": { "Title": "Calvarial Hemangioma", "Disease Discussion": "Lesions/Condition: Calvarial Hemangioma\n\nCell of Origin: Endothelium\n\nSynonyms: Hemangioma, bone\n\nAssociations/Predisposing Factors: None\n\nCommon Locations: Skull, other bone hemangiomas in Lumbar Vertebrae and Long Bones (1,2)\n\nDemographics: F:M, 3:1\n\n\nHistology: Multiple engorged single walled vessels interwoven in trabeculae (1)\n\n\n\nGross Appearance: Fleshy and vascular with scalloping of calvarium. (1)\n\nPrognosis and Treatment: Benign lesion, typically not treated. Surgical resection can be performed.", "ACR Code": "1.3", "Category": "Neoplasm, benign", "Keywords": "Hemangiomacalvarialskull", "Reference": "1. D Bastug, O Ortiz and SS Schochet. Hemangiomas in the calvaria: imaging findings, American Journal of Roentgenology, 1995, Vol 164, 683-687 \n\n2. Naama O, Gazzaz M, Akhaddar A, Belhachmi A, Asri A, Elmostarchid B, et al.\u00a0Cavernous hemangioma of the skull: 3 case reports.\u00a0Surg Neurol.\u00a0Jan 18\u00a02008" } }, { "U_id": "MPX1269", "TAC": [ "MPX1269_synpic48266", "MPX1269_synpic48267", "MPX1269_synpic48268" ], "MRI": [], "Case": { "Title": "Primary Epidermoid Splenic Cyst", "History": "31 y.o. woman with 6 weeks of cough.", "Exam": "Non-productive cough, otherwise normal physical exam.", "Findings": "PA and lateral chest radiograph: Vague airspace opacity within the left lung base, which partially silhouettes the left heart border near the apex, representing lingular pneumonia. Additionally, there is an ovoid soft-tissue density with peripheral calcifications seen occupying the left upper quadrant that measures 15.8cm X 12.4cm X 12.9cm, likely representing a calcified splenic cyst. \n \nCT abdomen/pelvis: Confirms a large cyst within in the spleen with a thin calcified rim. The spleen is enlarged secondary to cyst. The pancreas and stomach are displaced to the right. The colon is displaced inferiorly. The left kidney is slightly compressed.", "Differential Diagnosis": "\u2022 Post-traumatic \u201cFalse-cyst\u201d\n\u2022 True (epidermoid) cyst\n\u2022 Abscess (pyogenic or fungal)\n\u2022 Hydatid cyst\n\u2022 Infarction\n\u2022 Benign neoplastic (Hemangioma, lymphangioma)\n\u2022 Malignancy (lymphoma, metastasis)\n\u2022 Splenic peliosis", "Case Diagnosis": "Primary Epidermoid Splenic Cyst", "Diagnosis By": "Pathology following surgical intervention.", "Treatment & Follow Up": "Direct surgical intervention was performed. This patient recovered uneventfully from surgery. No follow-up is required after the post-operative recovery period.", "Discussion": "A splenic cyst (or multiple cysts) may be noted as an incidental finding on conventional imaging techniques, as in this case, or as a result of evaluation of a patient with left upper quadrant pain, left shoulder pain, abdominal enlargement, or splenomegaly. The differential considerations for a splenic cyst include post-traumatic, epidermoid cyst, abscess, hydatid cyst, infarction, splenic peliosis, and neoplasia, both benign and malignant. 80% of cases in North America are post-traumatic. Direct surgical intervention in this case yielded a diagnosis of epidermoid cyst, as defined by the presence of an inner endothelial lining.\n\nSplenic cysts can remain stable in size for many years, or enlarge slowly, occasionally to massive proportion (as was the case with this patient). The potential for rupture and hemorrhage increases with increasing size. There is also a risk for secondary infection. Optimal surgical management is not clearly defined, but a number of procedures are available for symptomatic or enlarging cysts. Available options for those with non-parasitic cysts include percutaneous procedures (eg, biopsy, aspiration, drainage), or more direct surgical interventions such as decapsulation/cyst wall unroofing, partial or total splenectomy. However, only splenectomy provides diagnostic certainty, which is rarely clinically justified. \n\nReferences:\n\nUrrutia M, Mergo PJ, Ros LH, et al. Cystic mass of the spleen: radiologic-pathologic correlation. Radiographics. 1996;16(1):107-29. \n\nWarshauer DM, Hall HL. Solitary splenic lesions. Seminars in Ultrasound, CT and MR. 2006;27:370.\n\nWeissleder, R, Wittenberg, J, Harisinghani, MG, et al. Primer of Diagnostic Imaging, 4th ed. Philadelphia, Mosby, 2007." }, "Topic": { "Title": "Congenital Splenic Cyst", "Disease Discussion": "Primary splenic cysts include epidermoid, mesothelial, and dermoid cysts. Nearly half of epidermoid splenic cysts involve children under 15 years of age, and very few have been reported in neonates. Two splenic cysts reported in neonates and operated upon were discovered to be epidermoid cysts.\n\nSecondary cysts are from trauma/hemorrhage, infarction or infection \u2013 all entities that would be highly unusual in the prenatal period. Additionally, they would likely have a different appearance than the epidermoid cyst with its thin wall, absence of internal echoes, and increased through-transmission.\n \nIn a review of asymptomatic splenic cyst-like lesions diagnosed in 7 fetuses and/or neonates, 3 completely disappeared (within a 3 year period), and the remaining lesions remained unchanged in size or appearance during follow-up (3 months n=2; 6 months n=1, and 3 years n=1). \n\nA conservative approach to such lesions is suggested, with follow-up and potential intervention only if the lesion substantially enlarges, exposing the spleen to rupture or hemorrhage.", "ACR Code": "9.1", "Category": "Congenital, malformation", "Keywords": "congenitalspleniccyst", "Reference": "C. Garel, M. Hassan, Pediatric Radiology (1995) 25:360-362" } }, { "U_id": "MPX1285", "TAC": [ "MPX1285_synpic20838", "MPX1285_synpic20840" ], "MRI": [], "Case": { "Title": "Fracture right mandibular condyle", "History": "Fell on jaw, mouth does not open and close right", "Exam": "Jaw uneven, rt TMJ not palpable", "Findings": "Rt mandibular condyle fractured, angulated and displaced", "Differential Diagnosis": "Fracture right mandibular condyle", "Case Diagnosis": "Fracture right mandibular condyle", "Diagnosis By": "CT, surgery", "Treatment & Follow Up": "Internal fixation" }, "Topic": { "Title": "Mandibular condyle", "Disease Discussion": "Posterior superior process of the mandibular ramus that articulates with the mandibular fossa of the temporal bone. (You can feel this while chewing, by putting your finger in your external ear canal.)\n\nFor image, see: http://rad.usuhs.mil/rad/radbrowser2/head/PlainFilm/hn015.html", "ACR Code": "2.1", "Category": "Glossary", "External Links": "rad.usuhs.mil/rad/radbrowser2/head/PlainFilm/hn015.html" } }, { "U_id": "MPX1282", "TAC": [ "MPX1282_synpic19929" ], "MRI": [], "Case": { "Title": "Ameloblastoma", "History": "20 year old male with left jaw pain.", "Exam": "Noncontributory", "Findings": "Noncontrast CT shows a well-marginated, radiolucent, multiloculated, expansile lesion at the left mandibular angle. The lesion abuts but does not destroy several posterior molar teeth.", "Differential Diagnosis": "Ameloblastoma\nOdontogentic Keratocyst\nCentral Giant Cell Granuloma\nResidual Cyst\nCemento-osseous Dysplasia\nFollicular Cyst\nMyxoma\nHemorrhagic/Traumatic Bone Cyst", "Case Diagnosis": "Ameloblastoma", "Diagnosis By": "Biopsy", "Treatment & Follow Up": "Exploration, enucleation, and curettage of biopsy-proven ameloblastoma in the left posterior mandible." }, "Topic": { "Title": "Ameloblastoma", "Disease Discussion": "Amelobastomas are rare, slow-growing, painless, expansile masses of odontogenic tissue origin, occuring in the jaw (in 75% of cases) and sinuses. Patients usually present between 30-50 years of ages. They are most commonly located in the posterior mandible and ramus. When they occur in the maxilla, these locally aggressive tumors can extend into the nasal cavity and skull base.\n\nClinically, ameloblastomas are the most aggressive of the odontogenic tumors and can cause large facial deformities. These lesions characteristically have a soap bubble appearance (multiloculated) with sharply-defined margins, although more aggressive features of cortical disruption and soft tissue extension are possible findings.\n\nAmeloblastomas can also have a unilocular appearance and may then be confused with odontogenic cysts. Most are not associated with tooth impaction, but can be associated with displacement or resorption of adjacent teeth.\n\nStandard treatment involves en bloc resection or curretage for mandibular lesions and resection for maxillary ameloblastomas. Rarely they may have malignant transformation and metastatic potential; and, the recurrence rate is relatively high after treatment (20%); patients are generally followed postoperatively for a period of 5 years.", "ACR Code": "2.3", "Category": "Neoplasm, NOS", "Keywords": "AmeloblastomaMandibleSoap Bubble", "Reference": "1. Torske, KR. Radiologic differential diagnosis of the jaws. Radiologic Pathology 2003-2004; Vol 2, p724; 2003: American Registry of Pathology; AFIP, Washington DC. \n\n2. http://webcenter.health.webmd.netscape.com/hw/cancer/nord908.asp\n\n3. http://oi.odont.ku.dk/lucas/amelobla.html", "External Links": "hardcore-porn-1.net/free_hardcore_porn_.com/" } }, { "U_id": "MPX1274", "TAC": [ "MPX1274_synpic35536" ], "MRI": [ "MPX1274_synpic35537", "MPX1274_synpic35546" ], "Case": { "Title": "Ganglioglioma", "History": "10 y.o. boy", "Exam": "Ganglioglioma", "Findings": "Ganglioglioma", "Differential Diagnosis": "Ganglioglioma", "Case Diagnosis": "Ganglioglioma", "Treatment & Follow Up": "Ganglioglioma", "Discussion": "Ganglioglioma" }, "Topic": { "Title": "Ganglioglioma", "Disease Discussion": "Ganglioglioma", "ACR Code": "1.3", "Category": "Neoplasm, glial", "Keywords": "Ganglioglioma" } }, { "U_id": "MPX1289", "TAC": [ "MPX1289_synpic50615", "MPX1289_synpic50618" ], "MRI": [], "Case": { "Title": "Persistent Ceco-Abdominal Fecal Fistula", "History": "10 year-old female presented with 3 days nausea, vomiting and periumbilical pain that progressed to RLQ. Appendiceal fecolith found on abdominal ultrasound. Patient underwent laparoscopic appendectomy. Post-operatively, patient developed fevers, recurrence of pain and elevated WBC to 24.7 on POD#6.", "Exam": "Diffuse abdominal pain on palpation.", "Findings": "Image 1: Lower abdominal fluid collection s/p appendectomy\nImage 2: Successful drain placement\nImage 3: Fistula from abscess pocket and drainage catheter tip to cecum\nImage 4: Persistent fistula from abscess pocket and drainage catheter tip to cecum", "Differential Diagnosis": "Persistence of fistula likely due to repeated flushing with saline and presence of catheter.", "Case Diagnosis": "Persistent Ceco-Abdominal Fecal Fistula", "Diagnosis By": "Fistula resolved with cessation of saline flushes", "Treatment & Follow Up": "Saline flushes were stopped, catheter tip was repositioned. Fistula showed evidence of resolving and decision was made to pull catheter on POD#16. Patient's WBC continued to decline and she remained afebrile with no pain.", "Discussion": "Post-operative appendectomy intra-abdominal abscess incidence has been found to be 5-20% (1). Options for treatment include open vs. percutaneous drainage, with the latter being preferred. After the initial drain placement the output in this patient was minimal (<5mL) and the fistula was likely kept open my the TID saline flushes (5mL not counted in output). On POD#13 the catheter tip was repositioned away from the fistula tract by rotating the catheter. Saline flushes were stopped at this time. On POD#16 the fistula was minimally patent (image not available) and the drainage catheter was removed. While there is a risk that the abscess may recur, the patient was asymptomatic and the WBC was normal. It was reasoned that the removal of the catheter would further promote closure of the space. \n\n1. Teich, S., Caniano, D., Reoperative Pediatric Surgery, Ch 14, New Jersey, 2008." }, "Topic": { "Title": "Persistent Ceco-Abdominal Fecal Fistula", "Disease Discussion": ".Post-operative complications\n.Interventional Radiology case", "ACR Code": "7.9", "Category": "Procedure or Intervention", "Keywords": "FistulaAppendectomyFecal", "Reference": "1. Teich, S., Caniano, D., Reoperative Pediatric Surgery, Ch 14, New Jersey, 2008." } }, { "U_id": "MPX1219", "TAC": [ "MPX1219_synpic14406", "MPX1219_synpic14407", "MPX1219_synpic14409", "MPX1219_synpic14410" ], "MRI": [], "Case": { "Title": "Pancoast\u2019s tumor of chest, Stage IV NSCLC (non-small cell lung cancer)", "History": "67 y/o male presents for further evaluation of an abnormal chest radiograph, discovered during a recent episode of both hepatic and left kidney abscesses.", "Exam": "Left apical chest tenderness, Dsypnea, and a chronic cough. \nTransbronchial Biopsy: Non-Small Cell Carcinoma", "Findings": "\u2022 CXR: \nLarge destructive left apical mass involving the chest wall. There is vertebral destruction, pleural metastasis, lymphadenopathy, and a contralateral lung nodules.\n\n\u2022 CT: \n1) Large left upper lobe mass with adjacent chest wall invasion with bony destruction and vertebral body destruction. Multiple left lingular segment masses\n2) Right upper lobe mass with adjacent air space disease\n3) Mediastinal and left hilar adenopathy\n4) Right liver lobe ductal dilatation\n5) Right adrenal mass enlargement\n6) Left kidney mass\n\n\u2022 PET:\n1) Malignant neoplasm extensively involving the apical posterior segment of the left upper lobe and extending locally into the mediastinum and the chest wall. No discontinuous foci within the mediastinum or cervical region specifically to suggest metastatic disease to the lymph nodes. Several satellite nodules in the left mid lung field and possible nodular metastases to left mid ribs.", "Differential Diagnosis": "\u2022 Metastatic Lung Cancer\n\u2022 Metastatic Kidney Cancer\n\u2022 Metastatic Liver cancer", "Case Diagnosis": "Pancoast\u2019s tumor of chest, Stage IV NSCLC (non-small cell lung cancer)", "Diagnosis By": "Surgery and Histology", "Treatment & Follow Up": "Patient has stage IV NSCLC. Patient will be offered both chemotherapy and radiation therapy concurrently. Chemotherapy has been shown to provide both pallative and survival benefits in patient\u2019s with stage IV disease.Radiation therapy has been shown to control hemoptysis in up to 80% of patient\u2019s, a cough in up to 60% of patient\u2019s, and can reduce tumor associated pain in up to 50% of patient\u2019s.Potential synergy with radiation therapy and paclitaxel has been shown. Paclitaxel stabilizes cells in the radiosensitive G2/M phase of the cell cycle.", "Discussion": "Patient underwent evaluation for metastatic cancer from an unknown primary source before the chest mass biopsy.\n\nRelated cases: http://rad.usuhs.edu/medpix/pod.html?mode=quiz&imid=58612&quiz=&th=&table=card&showall=#pic\n\nYouTube Video: http://www.youtube.com/watch?v=mjJIQzew8ec" }, "Topic": { "Title": "Pancoast tumor", "Disease Discussion": "Malignant neoplasm extensively involving the apical posterior segment of the left upper lobe and extending locally into the mediastinum and the chest wall. No discontinuous foci within the mediastinum or cervical region specifically to suggest metastatic disease to the lymph nodes. Several satellite nodules in the left mid lung field and possible nodular metastases to left mid ribs. \n\nUnderwent a chest x-ray and CT scan for pathological staging. Patient chest x-ray reveals invasion and destruction of bony structures in the chest. This classifies him as stage IV giving a 5 year survival of 1% with treatment. Because of his recent history of a liver abscess and kidney abscess a PET scan was done to determine the extent of the disease. The PET scan showed the extensive uptake of the left apical mass and showed extension into the chest wall and mediastinum. Additionally, their were a few satellite nodules in the left lung fields. However, within the kidneys appeared to only be physiologic and there abnormality to suggest metastatic disease to the left kidney or to the liver.\n\nYouTube Video - http://www.youtube.com/watch?v=mjJIQzew8ec", "ACR Code": "68.3222", "Category": "Unsure", "Keywords": "Pancoast tumorlung cancer", "Reference": "Lung Cancer: Team Approach to Therapy, Federal Forum Supplement to U. S. Medicine Vol. 36 No. 9, Department of Veterans Affairs" } }, { "U_id": "MPX1300", "TAC": [ "MPX1300_synpic24424" ], "MRI": [], "Case": { "Title": "Omental Torsion", "History": "36 year old female with left upper quadrant pain. A right upper quadrant ultrasound demonstrated a small gallstone, but no evidence of acute cholecystitis.", "Exam": "On exam, diffuse left upper quadrant tenderness was exhibited, however, there were no peritoneal signs, and a Murphy's sign was not present.", "Findings": "Contrast enhances axial CT demonstrates a 1.9 x 4.5cm, predominantly fat density mass anterior to the transverse colon. The fat in this region is mildly infiltrated, and there are multiple, concentric, streaky rings surrounding and within the lesion, as well as focal subjacent peritoneal thickening.", "Differential Diagnosis": "Omental infarct\nEpiploic appendagitis\nDiverticulitis", "Case Diagnosis": "Omental Torsion", "Diagnosis By": "The patient was treated conservatively and her symptoms resolved. A short-interval follow-up CT scan demonstrated improvement in the inflammatory changes." }, "Topic": { "Title": "Omental Torsion", "Disease Discussion": "Omental torsion is a rare diagnosis - only 250 cases have been reported. They may be thought of as primary or secondary. Primary factors that predispose a patient to this condition include an accessory omentum, bifid omentum, irregular accumulations of omental fat in the obese, and a narrowed omental pedicle. The higher incidence of right-sided torsion is thought to be due to the greater size and mobility of omentum on that side. Secondary torsion is more common, and is usually associated with cysts, tumors, foci of intraabdominal inflammation, postsurgical scarring, or hernia sacs.\n\nClinically, this is rarely diagnosed prior to surgery. It usually presents suddenly with signs of peritoneal irritation in the affected area of the abdomen. Patients may experience nausea, vomiting, or low-grade fever. Two thirds of patients have mild leukocytosis. Half of patients have a palpable mass. With these symptoms, it is not surprising that it is usually mistaken for appendicitis, acute cholecystitis, or adnexal pathology.", "ACR Code": "9.5", "Category": "Hypoxic or Ischemic", "Keywords": "omentumtorsionischemia", "Reference": "Saber A, LaRaja R. Omental Torsion. eMedicine, volume 2, number 2. December 5, 2001." } }, { "U_id": "MPX1301", "TAC": [ "MPX1301_synpic26169" ], "MRI": [], "Case": { "Title": "Metastatic breast cancer", "History": "39 year old female with lumbar back pain.", "Exam": "N/A", "Findings": "Lytic lesion within the left posterior elements of the L3 vertebra.", "Differential Diagnosis": "Lytic bone lesion: metastatic disease, myeloma, osteosarcoma, chondrosarcoma, fibrosarcoma, hemangioma, lymphoma, aneurysmal bone cyst, eosinophilic granuloma, Paget's disease, giant cell tumor.", "Case Diagnosis": "Metastatic breast cancer", "Diagnosis By": "Biopsy", "Treatment & Follow Up": "N/A", "Discussion": "See factoid" }, "Topic": { "Title": "Metastatic breast cancer", "Disease Discussion": "Breast cancer represents the most common cancer among women in the United States. Additionally it represents the second leading cause of cancer death amongst women (behind lung cancer), and the most common cause of death in women ages 45 to55. Breast cancer has a strong predilection for metastatic spread with bone being the most common target. Metastatic breast cancer to bone can be osteolytic, osteoblastic or mixed. Imaging plays a major role in detecting metastatic spread in breast cancer patients, but a consensus has yet to evolve on the ideal modality (plain film, scintigraphy, magnetic resonance, computed tomography, and positron emission tomography) for detection. Plain radiographs represent an early screening tool for patients with clinical suspicion (e.g. localized skeletal pain), as they are relatively inexpensive, widely available, and carry a relatively low ionizing radiation dose.", "ACR Code": "3.3", "Category": "Neoplasm, metastatic", "Keywords": "metastatic breast cancerlytic vertebral lesion", "Reference": "Brant WE Helms CA. Fundamentals of Diagnostic Radiology 2nd ed. Philadelphia: 1999 Lippincott, Williams and Wilkins.\n\nHamaoka T, et al. Bone Imaging in Metastatic Breast Cancer. Journal of Clinical Oncology, Vol 22, No 14 (July 15), 2004: pp. 2942-2953." } }, { "U_id": "MPX1298", "TAC": [ "MPX1298_synpic25021", "MPX1298_synpic25023", "MPX1298_synpic25024" ], "MRI": [], "Case": { "Title": "Ascending thoracic aortic aneurysm", "History": "51 y/o Caucasian male with sudden onset of chest and mid back pain. No prior history of acute chest syndrome, angina, or other heart disease. No other significant past medical history or family history. No history of alcohol or tobacco use. No medications.", "Exam": "General: Healthy appearing male in no acute distress.\nVS: stable\nLungs: clear \nHeart: RRR. \nAbdomen: Normal.\n\nEKG: Normal.\nNo pertinent labs.", "Findings": "PA and Lateral CXR demonstrates no mediastinal widening. Heart size is normal. The lungs are clear.\n\nContrast CT demonstrates a large ascendning aortic aneurysm beginning at the root and extending to the arch just proximal to the take off of the innominate artery.", "Differential Diagnosis": "None.", "Case Diagnosis": "Ascending thoracic aortic aneurysm", "Diagnosis By": "Contrast enhanced CT of the chest", "Treatment & Follow Up": "Surgery", "Discussion": "No apparent radiographic findings for a large ascending aortic aneurysm which in this case was concealed on plain films by superimposed mediastinal structures." }, "Topic": { "Title": "Ascending thoracic aortic aneurysm", "Disease Discussion": "RADIOLOGICAL FINDINGS: The visualized mediastinum is noteworthy for aneurysmal dilatation of the aortic root which appears to involve all three cusps. If the cusps are included in the measurement, this dilation measures approximately 6.8 cm in transverse dimensions x 5.7 cm in AP dimensions. If the cusps are not included in the measurement, the aortic root measures approximately 5.2 cm transverse x 5.8 cm in maximum AP dimension. Dilation of the cardiac silhouette is noted compatible with cardiomegaly\n\nDIAGNOSIS: 1. Aneurysmal dilation of the aortic root suspicious for sinus of Valsalva aneurysm as described above. 2.Cardiomegaly\n\nDIFERENTIAL DIAGNOSIS: Ascending Aortic Aneurysm secondary to syphilis, Dilation of the aortic root secondary to conective tissue diseases including Marfan\u2019s Syndrome and Ehlers-Danlos syndrome. Trauma, or Dissection.\n\nDISCUSSION: Aneurysms of the thoracic aorta are classified by location with the most common being the descending portion of the aorta. The ascending portion of the aorta is the second most common with aneurysms of the arch of the aorta being the most rare. \nCauses for thoracic aortic aneurysms usually consist of cystic medial necrosis. This may be a result of connective tissue disorders such as Marfan\u2019s syndrome or Ehlers-Danlos syndrome. Other causes can include athersclerotic vascular disease, syphilis, infectious aortitis, trauma, and dissection. \nThere are a wide range of signs and symptoms associated with thoracic aortic aneurysms. Most problems associated with this disease entity are cardio-vascular in nature. This includes congestive heart failure, continuous murmur, and thromboembolism. If the aneurysm is large enough superior vena cava syndrome may occur secondary to mass affect. It has been reported that up to forty percent of patients with aneurysms involving the thoracic aorta are asymptomatic at incidental diagnosis. \nThere are multiple diagnostic modalities that may be used in the diagnosis of thoracic aortic aneurysms. The gold standard is aortography. Contrast enhanced CT may be used as well. MRI and MRA have been particularly useful in defining vascular anatomy. Trans-thoracic echocardiography has limited accuracy in diagnosis of aneurysms, but trans-esophogeal echocardiography is quite accurate. \nTreatment consists of surgery and is recommended if the ascending thoracic aorta is 5.5 cm or greater. The Bentall procedure is usually performed. It consists of grafting in a Dacron tube with a prosthetic aortic valve. If surgery is not performed patients have a 32 to 68 percent chance of rupture. \n\nREFERENCES:\nBraunwald: Heart Disease: A Textbook of Cardiovascular Medicine, 6th ed., Copyright \u00a9 2001 W. B. Saunders Company \n\nJuhl: Paul and Juhl\\'s Essentials of Radiologic Imaging, 7th ed., Copyright \u00a9 1998 Lippincott Williams & Wilkins", "ACR Code": "562.731", "Category": "Aneurysm", "Keywords": "thoracicaorticaneurysm", "Reference": "Braunwald: Heart Disease: A Textbook of Cardiovascular Medicine, 6th ed., Copyright \u00a9 2001 W. B. Saunders Company \n\nJuhl: Paul and Juhl\\'s Essentials of Radiologic Imaging, 7th ed., Copyright \u00a9 1998 Lippincott Williams & Wilkins" } }, { "U_id": "MPX1309", "TAC": [ "MPX1309_synpic15871" ], "MRI": [], "Case": { "Title": "Juvenile Dermatomyositis", "History": "Steroid dependent child with systemic weakness and established diagnosis presents with abdominal pain. Later clinicians supplied additional history of hematuria.", "Findings": "Plain films of the extremities demonstrate diffuse calcinosis compatible with established diagnosis of juvenile dermatomyositis.\n\nCT scan performed to evaluate abdominal pain shows extensive pneumatosis of the right colon at the hepatic flexure. Free abdomenal air is noted.\n\nAssymetric perfusion of the kidneys was incidentally discovered and confirmed with repeat delayed scanning of the abdomen done to look for free abdominal air.", "Differential Diagnosis": "Bowel Ischemia\nInfection in immune compromised patient", "Case Diagnosis": "Juvenile Dermatomyositis", "Treatment & Follow Up": "Child was taken to the OR for hemicolectomy. Stress dose steroid replacement was provided.", "Discussion": "Vasculitis is associated with dermatomyositis and can cause both the bowel wall ischemia and the differential renal perfusion. Because the patient is on high dose steroids, the free abdomenal air may have been occult." }, "Topic": { "Title": "Juvenile Dermatomyositis", "Disease Discussion": "Although relatively rare, juvenile dermatomyositis (JDM) can be a catastrophic diagnosis. It is closely related to juvenile polymyositis (JPM) which does not present with a heliotrophic facial rash. JDM is an autoimmune disorder in which B lymphocytes and completment are noted in the perivascular areas of the soft tissue, while in JPM the CD8+ T lymphocytes predominate.\n\nJDM seems to have some genetic predisposition and has been shown to have a seasonal increase in the spring and summer months. It is associated with Coxsachie B antibodies in children. Another reported association occurs between echovirus and chronic polymyositis. \n\nSigns and symptoms of the disease include viral prodrome and a change in gait which suggests muscle weakness. Rash is a later finding in JDM. Radiographically, calcinosis of soft tissues is the hallmark although it occurs in only about 40% cases. Superfical plaque calcifications, deep tumoral calcifications and deposits in myofascial planes can be seen. Reticular skin calcifications are often quite extensive.\n\nIn contrast to the adult form of dermatomyositis, there is no increase in pulmonary disease and risk of malignancies with JDM.\n\nMRI is becoming the method of choice for surveying large muscle groups for evidence of inflammation. Spectroscopy can demonstrate an abnormal ratio of muscle phosphocreatine to inorganic phosphates.\n\nThe most difficult differential diagnosis is with muscular dystrophy; which in contrast occurs predeominantly in males and is accompanied by the presence of dystrophy.", "ACR Code": "4.2", "Category": "Inflammatory, autoimmune", "Keywords": "dermatomyositiscalcinosispneumatosis coli", "Reference": "UpToDate Online 11.1" } }, { "U_id": "MPX1279", "TAC": [ "MPX1279_synpic24372", "MPX1279_synpic24373", "MPX1279_synpic24375" ], "MRI": [], "Case": { "Title": "Wilms\u2019 tumor, Stage I (Stage III at biopsy) with favorable histology", "History": "This 2.5-year-old girl presented to her pediatrician in Italy after her parents noted a prominence in the right abdomen after bathing her in March 2004. The child had consistently been at the fifth percentile for growth up to that point. An ultrasound in Italy revealed a 7 x 8cm abdominal mass, and she was immediately air-evac\u2019d to WRAMC for further evaluation and treatment.", "Exam": "BP 137/90 Pulse 112 Resp 28 Wt 11kg Ht 80.6cm BMI 16.9 Temp 36.2\u02daC \nGen: Crying but consolable; child is small for age but proportionate. Height is < 5th percentile for age, weight just at 5th percentile for age. \nHEENT: Normal. Oropharynx is clear. Neck supple with no lymphadenopathy.\nLungs: CTAB\nCV: No murmurs, RRR\nAbd: Distended but nontender. +BS. Palpation c/w large firm mass filling right side of the abdomen and extending below the umbilicus. Lower edge of mass is palpable about the level of the anterior iliac spine. \nGU: Only superficial visual inspection of perineal region. Normal female genitalia with no labial edema or obvious rash. \nExt: No C/C/E\nNeuro: CN 2-12 intact, reflexes symmetric. Normal gait.\nSkin: No lesions or rashes. \nSOFT TISSUE, RIGHT RENAL MASS, BIOPSIES: Tissue suboptimal for definitive evaluation. Small round blue cell neoplasm. Unable to evaluate the architecture of the neoplasm. Immunostains for vimentin, LCA, synaptophysin and chromogranin all appear negative while keratin appears weakly positive. The differential diagnosis includes Wilms tumor, clear cell sarcoma, or other small round blue cell neoplasm, although the negative immunostains would seem to exclude neuroblastoma, lymphoma and Ewing's sarcoma.", "Findings": "CT in the axial plane demonstrates a heterogeneous mass in the right kidney, with considerable mass effect. The liver and IVC are markedly compressed with no obvious invasion. Initial measurements of this mass were 15.4 cm in the craniocaudal dimension, 12.3 cm in the AP dimension, and 7.7 cm in the lateral dimension. The left kidney is normal with no evidence of masses or hydronephrosis. \n\nCoronal and sagittal reconstruction views demonstrate a well-circumscribed mass that has most likely infiltrated the right renal capsule. Cystic regions within the mass are most notable on the sagittal view. The lateral image shows medial displacement of functioning right renal parenchyma (i.e., claw sign) with contrast excretion, and there is normal excretion from the left kidney. The right adrenal gland and right renal vein are not well visualized. \n\nFollowup CT after 5 weeks of preoperative chemotherapy shows considerable tumor shrinkage and more defined areas of margination. The tumor now measures 10.5 cm in the craniocaudal dimension, 8 cm in the AP dimension, and 5.2 cm in the lateral dimension. The right renal vein is not well visualized.\n\nSedated abdominal U/S demonstrates no right renal vein thrombus, although there is considerable mass effect and tortuosity of the right renal vein. The IVC is clearly visualized with no evidence of intraluminal thrombus. Flow is seen throughout the lumen.", "Differential Diagnosis": "Wilms\u2019 tumor\nClear cell sarcoma\nMesoblastic nephroma \nNephroblastomatosis\nNeuroblastoma\nComplex teratoma\nCystic renal dysplasia", "Case Diagnosis": "Wilms\u2019 tumor, Stage I (Stage III at biopsy) with favorable histology", "Diagnosis By": "Surgical resection and pathologic examination", "Treatment & Follow Up": "This patient was initially given captopril at a dose of 0.2mg/kg BID to keep her BP at a target range of 100-110/70. She was thought to have tumor-induced hypertension that would improve with chemotherapy.", "Discussion": "Wilms\u2019 tumor is the most common renal tumor of childhood, with a peak incidence at 3-4 years of age. It is thought to be due to abnormal proliferation of the metanephric blastema, without normal differentiation into tubules and glomeruli. Wilms\u2019 tumors are histologically heterogeneous, comprised of three cell types in varying distributions: blastemal cells, stromal cells, and epithelial cells. While each of these components is variable in its level of differentiation, anaplasia (either focal or diffuse) is associated with an unfavorable prognosis. Nephroblastomatosis is characterized by the presence of multiple nephrogenic rests, which are foci of abnormally present renal blastemal cells. It is thought to be a precursor of Wilms\u2019, as the presence of intralobular nephrogenic rests has been associated with the development of WT.\n\nGrossly, WT is an intrarenal mass with both solid and cystic components. Although it distorts the anatomy of the collecting ducts, it rarely grows into the renal pelvis, ureter, or bladder. If invasion of the collecting system occurs, a patient may present with hematuria and/or obstruction. The tumor is usually surrounded by a pseudocapsule. It may contain areas of necrosis, which lead to hemorrhage and the appearance of cystic structures. True cysts may also be seen. Extension of the tumor mass into the corresponding renal vein is seen in about 40% of cases, and is associated with a higher incidence of surgical complications. Extension into the IVC is associated with a 40% rate of surgical complications. Large tumors that involve vital structures are associated with a higher rate of surgical complications, most notably tumor rupture which could then lead to recurrence. They are considered inoperable without preoperative chemotherapy.\n\nRadiologically, WT may be confused with congenital mesoblastic nephroma, in the first year of life. A mesoblastic nephroma is a solitary hamartoma which consists of immature renal stromal cells. It lacks blastemal cells and neoplastic metanephric elements, making it easy to differentiate from WT pathologically. However, it is a unilateral, single, solid mass arising from the kidney that may appear heterogeneous with areas of necrosis and hemorrhage on ultrasound and/or CT. Unlike WT, mesoblastic nephroma tends to infiltrate the renal parenchyma and does not form a pseudocapsule. It is more prominent in neonates, with a peak age at diagnosis of 3.5 months; however, isolated cases of mesoblastic nephroma in childhood and adulthood have been documented. Radiation therapy and chemotherapy increase the chances for overall morbidity, while excision alone results in cure.\n\nThe National Wilms\u2019 Tumor Study Group (NWTSG) recommends surgical staging of every case with the following breakdown:\nStage I: The tumor is isolated to the kidney and has been excised completely.\nStage II: The tumor had extended beyond the kidney but is excised completely. Capsular penetration, renal vein involvement, and renal sinus involvement may be found. Biopsy of the tumor results in some local spill.\nStage III: There is residual non-hematogenous tumor s/p resection, but it is confined to the abdomen. The resected specimen may have histologically positive margins, or part of the tumor has infiltrated the abdominal cavity. Lymph node findings are positive and/or peritoneal implants are found. \nStage IV: Hematogenous or lymph node metastasis has occurred outside the abdomen or pelvis. \nStage V: There is bilateral renal involvement at the time of diagnosis. Each side is assigned a stage from I to III, and histology is based on biopsy findings. \nPostoperative chemotherapy and radiotherapy are based on surgical staging and follow the guidelines of the NWTSG:\nStage I with favorable or unfavorable histology OR Stage II with favorable histology:\n- Nephrectomy\n- Postoperative chemotherapy with vincristine and actinomycin D (18 week course)\nStage II with focal anaplasia OR Stage III with favorable histology or focal anaplasia:\n- Nephrectomy\n- Abdominal irradiation (1080 cGy)\n- Chemotherapy with vincristine, actinomycin D, and doxorubicin (24 week course)\nStage IV with favorable histology or focal anaplasia: \n- Nephrectomy\n- Abdominal irradiation according to local stage \n- Bilateral pulmonary irradiation and PCP prophylaxis \n- Chemotherapy with vincristine, actinomycin D, and doxorubicin (24 week course)\nStage II through Stage IV with diffuse anaplasia:\n- Nephrectomy\n- Abdominal irradiation\n- Whole lung irradiation \n- Chemotherapy with vincristine, doxorubicin, etoposide, and cyclophosphamide (24 week course)" }, "Topic": { "Title": "Wilms\u2019 tumor, Stage I (Stage III at biopsy) with favorable histology", "Disease Discussion": "Wilms\u2019 tumor is the most common renal tumor of childhood, with a peak incidence at 3-4 years of age. It is thought to be due to abnormal proliferation of the metanephric blastema, without normal differentiation into tubules and glomeruli. Wilms\u2019 tumors are histologically heterogeneous, comprised of three cell types in varying distributions: blastemal cells, stromal cells, and epithelial cells. While each of these components is variable in its level of differentiation, anaplasia (either focal or diffuse) is associated with an unfavorable prognosis. Nephroblastomatosis is characterized by the presence of multiple nephrogenic rests, which are foci of abnormally present renal blastemal cells. It is thought to be a precursor of Wilms\u2019, as the presence of intralobular nephrogenic rests has been associated with the development of WT.\n\nGrossly, WT is an intrarenal mass with both solid and cystic components. Although it distorts the anatomy of the collecting ducts, it rarely grows into the renal pelvis, ureter, or bladder. If invasion of the collecting system occurs, a patient may present with hematuria and/or obstruction. The tumor is usually surrounded by a pseudocapsule. It may contain areas of necrosis, which lead to hemorrhage and the appearance of cystic structures. True cysts may also be seen. Extension of the tumor mass into the corresponding renal vein is seen in about 40% of cases, and is associated with a higher incidence of surgical complications. Extension into the IVC is associated with a 40% rate of surgical complications. Large tumors that involve vital structures are associated with a higher rate of surgical complications, most notably tumor rupture which could then lead to recurrence. They are considered inoperable without preoperative chemotherapy.\n\nRadiologically, WT may be confused with congenital mesoblastic nephroma, in the first year of life. A mesoblastic nephroma is a solitary hamartoma which consists of immature renal stromal cells. It lacks blastemal cells and neoplastic metanephric elements, making it easy to differentiate from WT pathologically. However, it is a unilateral, single, solid mass arising from the kidney that may appear heterogeneous with areas of necrosis and hemorrhage on ultrasound and/or CT. Unlike WT, mesoblastic nephroma tends to infiltrate the renal parenchyma and does not form a pseudocapsule. It is more prominent in neonates, with a peak age at diagnosis of 3.5 months; however, isolated cases of mesoblastic nephroma in childhood and adulthood have been documented. Radiation therapy and chemotherapy increase the chances for overall morbidity, while excision alone results in cure.\n\nThe National Wilms\u2019 Tumor Study Group (NWTSG) recommends surgical staging of every case with the following breakdown:\nStage I: The tumor is isolated to the kidney and has been excised completely.\nStage II: The tumor had extended beyond the kidney but is excised completely. Capsular penetration, renal vein involvement, and renal sinus involvement may be found. Biopsy of the tumor results in some local spill.\nStage III: There is residual non-hematogenous tumor s/p resection, but it is confined to the abdomen. The resected specimen may have histologically positive margins, or part of the tumor has infiltrated the abdominal cavity. Lymph node findings are positive and/or peritoneal implants are found. \nStage IV: Hematogenous or lymph node metastasis has occurred outside the abdomen or pelvis. \nStage V: There is bilateral renal involvement at the time of diagnosis. Each side is assigned a stage from I to III, and histology is based on biopsy findings. \nPostoperative chemotherapy and radiotherapy are based on surgical staging and follow the guidelines of the NWTSG:\nStage I with favorable or unfavorable histology OR Stage II with favorable histology:\n- Nephrectomy\n- Postoperative chemotherapy with vincristine and actinomycin D (18 week course)\nStage II with focal anaplasia OR Stage III with favorable histology or focal anaplasia:\n- Nephrectomy\n- Abdominal irradiation (1080 cGy)\n- Chemotherapy with vincristine, actinomycin D, and doxorubicin (24 week course)\nStage IV with favorable histology or focal anaplasia: \n- Nephrectomy\n- Abdominal irradiation according to local stage \n- Bilateral pulmonary irradiation and PCP prophylaxis \n- Chemotherapy with vincristine, actinomycin D, and doxorubicin (24 week course)\nStage II through Stage IV with diffuse anaplasia:\n- Nephrectomy\n- Abdominal irradiation\n- Whole lung irradiation \n- Chemotherapy with vincristine, doxorubicin, etoposide, and cyclophosphamide (24 week course)\n\nTen percent of patients with Wilms\u2019 tumor have a recognizable phenotypic syndrome, such as WAGR syndrome, Beckwith-Wiedemann syndrome, or Denys-Drash syndrome. Only 1% of Wilms\u2019 tumors are thought to be familial in origin.", "ACR Code": "8.3", "Category": "Neoplasm, embyronal", "Keywords": "Wilms\u2019 tumor, Stage I (Stage III at biopsy) with favorable histology", "Reference": "Green DM. The treatment of Stages I-IV favorable histology Wilms\u2019 tumor. J Clin Onc. 2004, 22(8):1366-1372.\nNeulander EZ, Wajsman Z. Wilms tumor. August 22, 2001. \u00a92005, eMedicine.com, Inc.\nOzcan T, Bahado-Singh R. Prenatal diagnosis of fetal renal masses. August 7, 2001. \u00a92005, UpToDate.\nSchofield D, Cotran RS. Diseases of infancy and childhood. In: Cotran RS, Kumar V, Collins T, editors. Robbins Pathologic Basis of Disease.\n 6th ed. Philadelphia: W.B. Saunders Company, 1999. p. 459-491.\nShamberger RC, Guthrie KA, Ritchey ML, Haase GM, Takashima J, Beckwith JB, D\u2019Angio GJ, Green DM, Breslow NE. Surgery-related\n factors and local recurrence of Wilms tumor in National Wilms Tumor Study 4. Ann Surg. 1999, 229(2):292-297." } }, { "U_id": "MPX1297", "TAC": [ "MPX1297_synpic19924" ], "MRI": [], "Case": { "Title": "Killian-Jamieson Diverticulum", "History": "55 YO male with symptoms of dysphagia.", "Exam": "NC", "Findings": "CT of the neck demonstrates an air-filled lesion adjacent to the proximal esophagus with a questionable connection between the two lumens. Subsequent evaluation of the hypopharynx and upper esophagus demonstrates a large outpouching from the left side of the cervical esophogus originating just inferior to the cricopharyngeus muscle.", "Differential Diagnosis": "Killian-Jamieson diverticulum\nZenker's diverticulum", "Case Diagnosis": "Killian-Jamieson Diverticulum", "Diagnosis By": "radiographically", "Treatment & Follow Up": "none" }, "Topic": { "Title": "Killian-Jamieson Diverticulum", "Disease Discussion": "Killian-Jamieson diverticula (also termed \"proximal lateral cervical esophageal diverticula\" or \"lateral diverticula from the pharyngoesophageal junction area\") are outpouchings from the lateral wall of the proximal cervical esophagus. These diverticula protrude through a muscular gap in the anterolateral wall of the cervical esophagus below the cricopharyngeus muscle and lateral to the longitudinal muscle of the esophagus just below its insertion on the cricoid cartilage. This gap should be differentiated from the muscular gap in the posterior portion of the cricopharyngeus, the site of development of a Zenker's diverticulum. \n\nBoth Zenker's diverticulum and Killian-Jamieson diverticula occur at locations of anatomic weakness in the hypopharynx or cervical esophagus near the cricopharyngeus muscle. In contrast to the Killian-Jamieson diverticulum, a Zenker's diverticulum originates on the posterior wall of the pharyngoesophageal segment in a midline area of weakness just above the cricopharyngeus. On pharyngoesophagography, it is seen lying posterior to the cervical esophagus on lateral images and in the midline on frontal images. In contrast, the Killian-Jamieson diverticulum is seen lying lateral to the cervical esophagus on frontal images and overlapping the anterior wall of the cervical esophagus on lateral images. \n\nThe diagnosis of either type of diverticulum is based primarily on the radiographic findings rather than on endoscopy. While endoscopy may identify the opening of a either type of diverticulum, its location in relation to the cricopharyngeus muscle is best seen when passage of the barium bolus outlines the protruding cricopharyngeus. The size of the sac and the relationship of the sac to the cervical esophagus are also best evaluated on barium studies. Therefore, the two forms of diverticula can be differentiated on the based upon the radiographic findings. \n\nStudies indicate that Killian-Jamieson diverticula are less common and considerably smaller than Zenker's diverticulum. They are also less likely to cause symptoms or be associated with gastroesophageal reflux than are Zenker's diverticula.", "ACR Code": "7.1", "Category": "Diverticulum", "Keywords": "esophagusdiverticulumKillian-Jamieson", "Reference": "Rubesin SE, Levine MS. Killian-Jamieson diverticula: Radiographic findings in 16 patients. AJR 2001;177:85 - 89" } }, { "U_id": "MPX1317", "TAC": [ "MPX1317_synpic24308", "MPX1317_synpic24309" ], "MRI": [], "Case": { "Title": "Early appendicitis", "History": "42 y/o female with 6 hour history of bilateral 9/10 lower abdominal pain, nausea and vomiting. One loose bowel movement.", "Exam": "BP 133/61, P 80, R 18, T 97.0, Pox 98\nPatient in visible pain and moving her legs to distract herself. Abdominal: BS normal, no guarding, tenderness to palpation in the bilateral pelvic region worse on the right side. Labs: Neg HCG, CBC: 15.4>15.1/44.6<219", "Findings": "The appendix does not demonstrate filling of contrast. It measures between 8-9 mm in diameter. There is no surrounding fluid and no evidence of abscess or significant inflammatory change. There is no evidence of adnexal mass or inflammatory bowel disease.", "Differential Diagnosis": "Early appendicitis", "Case Diagnosis": "Early appendicitis", "Diagnosis By": "Surgery", "Treatment & Follow Up": "Patient received laparoscopic appendectomy that night. The surgery was uncomplicated and a large inflamed appendix was removed. No sign of perforation was present in the abdomen. The patient was admitted to the hospital overnight and had an uneventful stay. She still had mild surgical pain the morning but she returned home. A few days later the pathology results returned confirming she had acute appendicitis.", "Discussion": "): Appendicitis can often be difficult to diagnose especially at ages less than three and greater than 60, leading to a possible delay in diagnosis in these groups and perforation rates up to 80%. Furthermore, as the most common abdominal surgical emergency with an incidence of 233/100,000, physicians tend to approach potential cases aggressively. This leads to a high number of appendectomies with normal appendices: about 15% nationwide. This negative appendectomy rate has unfortunately remained constant in the last fifteen years despite increased use of CT and ultrasound1. CT has a fairly high sensitivity and specificity for appendicitis. In the literature the exact sensitivity and specificity varies significantly: 84-100% and 83-98% respectively2,3.\n\nOn a oral/IV contrast CT, looking for acute appendicitis several findings can be expected. Increased appendiceal diameter greater than 6 mm is usually seen in addition to circumferential and symmetric wall thickening. Periappendiceal inflammation is usually seen in the form of linear fat stranding, local fascial thickening and subtle clouding of the mesentery. The CT may also have focal cecal apical thickening and the \u201carrowhead sign\u201d or cecal contrast that funnels symmetrically at the cecal apex. If the appendix is perforated then pericecal phlegmon or an abscess may be present. Extraluminal air, ileocecal thickening, localized lymphadenopathy and small bowel obstruction may also be seen4." }, "Topic": { "Title": "Early appendicitis", "Disease Discussion": "): Appendicitis can often be difficult to diagnose especially at ages less than three and greater than 60, leading to a possible delay in diagnosis in these groups and perforation rates up to 80%. Furthermore, as the most common abdominal surgical emergency with an incidence of 233/100,000, physicians tend to approach potential cases aggressively. This leads to a high number of appendectomies with normal appendices: about 15% nationwide. This negative appendectomy rate has unfortunately remained constant in the last fifteen years despite increased use of CT and ultrasound1. CT has a fairly high sensitivity and specificity for appendicitis. In the literature the exact sensitivity and specificity varies significantly: 84-100% and 83-98% respectively2,3.\n\nOn a oral/IV contrast CT, looking for acute appendicitis several findings can be expected. Increased appendiceal diameter greater than 6 mm is usually seen in addition to circumferential and symmetric wall thickening. Periappendiceal inflammation is usually seen in the form of linear fat stranding, local fascial thickening and subtle clouding of the mesentery. The CT may also have focal cecal apical thickening and the \u201carrowhead sign\u201d or cecal contrast that funnels symmetrically at the cecal apex. If the appendix is perforated then pericecal phlegmon or an abscess may be present. Extraluminal air, ileocecal thickening, localized lymphadenopathy and small bowel obstruction may also be seen4.", "ACR Code": "7.2", "Category": "Clinical Exam Finding or Sign", "Keywords": "AppendicitisappendectomiesPeriappendiceal inflammation", "Reference": "1. Goldberg J, Hodin R. Appendicitis in adults. Up to Date Online.\n2. Siewert B, Raptopoulos V. CT of the acute abdomen: findings and impact on diagnosis and treatment. AJR Am J Roentgenol. 1994 Dec;163(6):1317-24.\n3. Sivit CJ, Applegate KE, Stallion A, Dudgeon DL, Salvator A, Schluchter M, Berlin SC, Myers MT, Borisa VJ, Weinert DM, Morrison SC, Grisoni ER. Imaging evaluation of suspected appendicitis in a pediatric population: effectiveness of sonography versus CT. AJR Am J Roentgenol. 2000 Oct;175(4):977-80.\n4. Birnbaum BA, Wilson SR. Appendicitis at the millennium. Radiology. 2000 May;215(2):337-48." } }, { "U_id": "MPX1322", "TAC": [ "MPX1322_synpic45731", "MPX1322_synpic45732", "MPX1322_synpic45734" ], "MRI": [], "Case": { "Title": "Pulmonary Embolus", "History": "76 yo female presents with respiratory distress.", "Findings": "Contrast enhanced CT images from a PE/DVT CT protocol reveal large intraluminal filling defects in the right and left main pulmonary arteries. Notice the enlarged main pulmonary artery.", "Case Diagnosis": "Pulmonary Embolus", "Diagnosis By": "Imaging findings are diagnostic.", "Treatment & Follow Up": "The patient was admitted to the hospital and continued to deteriorate clinically. A bedside echocardiogram demonstrated right-sided heart failure. Interventional radiology was consulted, and catheter directed thrombolysis was attempted. Shortly thereafter in the medical intensive care unit, the patient went into pulseless electrical activity (PEA) and shortly expired after unsuccessful cardiopulmonary resuscitation." }, "Topic": { "Title": "Pulmonary Embolus", "Disease Discussion": "Lesions/Condition: Pulmonary Embolus\n\nDiscussion: \n\nThe most important indication for Venitilation-Perfusion (V/Q) imaging is suspected pulmonary embolism (PE). Numerous clinical conditions predispose to PE, including recent surgery (within 3 months), immobilization, thrombophlebitis, and underlying malignancy or other causes of a hypercoagulable state. In women, pregnancy and use of estrogen are known risk factors.\n\nThe clinical presentation is often variable, and nonspecific, and dependent upon the size and number of emboli occluding the pulmonary circulation. The classic presenting triad of dyspnea, pleuritic chest pain, and hemoptysis is infrequently encountered. The majority of patients presenting with PE demonstrate tachypnea, dyspnea, chest pain, and cough. Patients may have a feeling of impending doom. Tachycardia is commonly present. Less commonly, patients may demonstrate wheezing, hypotension and syncope.\n\nThe D-dimer blood test is a screening tool for PE. If a serum level less than 500 ng/L, further evaluation with imaging is unnecessary since the post-test probability of PE is 5% or lower.\n\nThe radiographic findings are often nonspecific and depend on whether the pulmonary emboli are associated with infarction. Abnormalities seen include an increase in the size of the central pulmonary arteries because of the presence of a large embolus. Local oligemia may be present in the area distal to the PE. Westermark\u2019s sign is when oligemia involves an entire lung secondary to a proximal clot. A small pleural effusion may be evident. In severe cases acute cor pulmonale may be seen with cardiac enlargement and prominence of the superior vena cava and azygos vein. Other findings include an elevated hemidiaphragm on the affected side, small pleural effusions, atelectasis with linear opacities, and occasionally Hamptom\u2019s hump, which is a pleura-based , wedge-shaped density may be evident.\n\nThe source of PE is most commonly from deep venous thrombosis in the lower extremity. Treatment most commonly consists of anticoagulation, which prevents clot propagation and allows endogenous fibrinolytic activity to dissolve existing thrombi. Anticoagulation decreases mortality from 30-60% to less than 5%. \n\nPrior to the advent of CT angiography, V/Q studies had been the mainstay for screening symptomatic patients for the presence of pulmonary embolism. A normal perfusion scan excludes PE with a negative predictive value close to 100%. A low-probability V/Q scan combined with a low-probability clinical assessment results showed PE in only 4% of patients. A high-probability V/Q scan in a patient with high-probability clinical findings showed PE in 96% of patients. With other combinations, PE was present in 16%-88% of patients requiring further evaluation. \n\nThe V/Q scan is safe, widely available, and is an alternative chest imaging technique for patients who cannot undergo CT angiography. One problem with scintigraphy is that many patients do not have a definitive result, (high or low probability) and limited alternative diagnostic information is provided.", "ACR Code": "6.6", "Category": "Medicine", "Keywords": "High-Probability V/QPulmonary EmbolusV/Q scan", "Reference": "Thrall: Nuclear Medicine. The Requisites. 2nd Edition. St. Louis: \n Mosby, Inc. 2001. \t \nBrant: Fundamentals of Diagnostic Radiology. 2nd Edition. \n Philadelphia: Lippincott Williams & Wilkins. 1999. \nQaseem et al. Ann Fam Med. 2007; 5(1):57-62.\nRemy-Jardin et al. Radiology. 2007; 245(2):315-329.\nBook S, Dykes T. Pulmonary Embolism. MedPixTM Topic: 5100. Available from http://rad.usuhs.edu/medpix/parent.php3?mode=single&recnum=5100&table=card&srchstr=V/Q&search=V/Q#images 2003 [cited 2008 Feb 1]." } }, { "U_id": "MPX1312", "TAC": [ "MPX1312_synpic26478", "MPX1312_synpic26479", "MPX1312_synpic26480", "MPX1312_synpic26481", "MPX1312_synpic26482", "MPX1312_synpic26484" ], "MRI": [], "Case": { "Title": "Right aortic arch with aberrant left subclavian artery", "History": "58y/o white male with dyspnea received CT to rule out PE/DVT", "Exam": "Noncontributory", "Findings": "Right aortic arch with aberrant left subclavian artery", "Case Diagnosis": "Right aortic arch with aberrant left subclavian artery", "Diagnosis By": "CT imaging (PE/DVT protocol)" }, "Topic": { "Title": "Left aortic arch with aberrant right subclavian artery", "Disease Discussion": "This is the most common malformation of the aortic arch resulting in a complete vascular ring around the trachea and esophagus.The most common type of right aortic arch is right aortic arch with an aberrant left subclavian artery and it is 2-3 times more common than right arch with mirror image branching of the brachiocephalic vessels. Right arch and aberrant left subclavian artery has a 5-12% incidence of associated congenital heart disease while right arch with mirror branching of the brachiocephalic vessels has a 98% incidence of associated congenital heart disease.\n \n\nTwo types:\n1.Origin of the left subclavian artery from a posterior aortic diverticulum from which a ductus arteriosus extends to the left pulmonary artery. The retroesophageal part of the ring is large and compression is produced by the diverticulum (Diverticulum of Kummerell).\n\n2.Origin of the left subclavian artery from the descending aorta with a left ductus connecting the left subclavian artery to the left pulmonary artery. The retroesophageal part of the ring is small.\n \nIn both types of aberrant subclavian arteries, the vessel runs behind the esophagus.\n\nDefinitive diagnosis is now usually accomplished by CT or MRI. Both display the severity of airway narrowing and the retro-esophageal aberrant artery.Both demonstrate the large aortic diverticulum invariably at the site of airway compression with an aberrant left subclavian artery.", "ACR Code": "562.1532", "Category": "Congenital, malformation", "Keywords": "Right aortic archaberrant left subclavian arterydysphagia", "Reference": "http://www.amershamhealth.com/medcyclopaedia/Volume%20VII/AORTIC%20ARCH%20ANOMALIES.asp", "External Links": "www.amershamhealth.com/medcyclopaedia/Volume%20VII/AORTIC%20ARCH%20ANOMALIES.asp" } }, { "U_id": "MPX1334", "TAC": [ "MPX1334_synpic23516" ], "MRI": [], "Case": { "Title": "Large Bowel Obstruction Secondary to Sigmoid Stricture", "History": "92 year old female presented with abdominal distention, abdominal pain, nausea/vomiting, and anorexia.", "Case Diagnosis": "Large Bowel Obstruction Secondary to Sigmoid Stricture" }, "Topic": { "Title": "Large Bowel Obstruction Secondary to Sigmoid Stricture", "Disease Discussion": "The differential for segmental lesions of the colon with narrowing include carcinoma, diverticulitis, Crohn's disease, ischemic colitis, or extrinsic narrowing from adjacent neoplastic or inflammatory process. (Reeder) The focus here will be considerations in distinguishing diverticular disease versus carcinoma in the setting of large bowel obstruction. Diverticular disease has sigmoid involvement in 99% of the cases in industrialized Western countries. (Farrell) Colorectal adenocarcinoma is the most common malignancy of the GI tract and the second most common malignant tumor in the United States. (Beutow) Approximately 50% arise in the rectum and rectosigmoid area. Another 25% occur in the sigmoid colon, and the remaining 25% are evenly distributed throughout the remainder of the colon. (Beutow) The determination of benign versus malignant stricture in the sigmoid colon is very important because of the differences in the treatment. In addition, the implications for staging of cancer and determination of appropriate therapy are issues that make identifying the correct diagnosis vital. Further, large bowel obstruction secondary to sigmoid strictures is not uncommon. In fact, the most common cause of large bowel obstruction is primary colon cancer estimated at 53% while diverticular disease is the cause in approximately 12% of the cases. (Greenllee)\n\tThe barium enema and computed tomography (CT) are two modalities used often to evaluate the cause of a sigmoid stricture. There are general characteristics used to delineate benign versus malignant strictures with both. With the barium enema, a gradual zone of transition, preserved mucosal folds and presence of diverticula are considered benign features. In contrast , an abrupt transition at the site of obstruction, destruction of mucosa and apple core configuration are considered malignant features. (Blakeborough) It has been shown that in making the diagnosis of diverticulitis with CT, the most specific findings are pericolonic stranding and length of the involved segment of more than 10 cm. The presence of pericolonic edema also favors diverticulitis. For colon cancer, the most specific findings are the presence of pericolonic lymph nodes and luminal mass. (Chintapalli) In cases in which the patient presents with large bowel obstruction, both of these modalities may be helpful in evaluating the cause. An added advantage of barium enema is its benefit in aiding in the differentiation of mechanical versus pseudoobstruction.\n\tChapman et al reviewed 140 cases of LBO to determine the accuracy of water-soluble contrast enema in comparison with plain abdominal radiography. Findings at laparotomy and follow-up (for the nonoperative cases) were used as the reference. When reviewing the plain radiographs (being aware of the case history), the diagnosis of mechanical obstruction was made with a sensitivity and specificity of 84% and 72%, respectively, whereas contrast enema had a sensitivity and specificity of 96% and 98%, respectively. \n\n\n\n\n\nREFERENCES\n\n1. Reeder, M.M., Felson, B., Gamuts in Radiology, Audiovisual Radiology of Cincinnati, Inc., 1975, p. G-55.\n2. Farrell, R.J., Farrell, J.J., and Morrin, M.M., Diverticular Disease in the Elderly, Gastroenterology Clinics, Volume 30, Number 2, June 2001.\n3. Buetow P.C., et al, Colorectal adenocarcinoma: radiologic-pathologic correlation. RadioGraphics 1995, 15:127-146.\n4. Greenlee HB, Pienkos EJ, Vanderbilt PC, et al: Acute large bowel obstruction. Comparison of county, Veterans Administration, and community hospital populations. Arch Surg 108:470, 1974.\n5. Blakeborough, A., Chapman, A. H., Swift, S., Culpan, G., Wilson, D., Sheridan, M. B. (2001). Strictures of the Sigmoid Colon: Barium Enema Evaluation. Radiology 220: 343-348\n6. Chintapalli, Kedar N. et al. Diveriticulitis versus Colon Cancer: Differentiation with Helical CT Findings. Radiology. 210(2):429-35, 1999 Feb.\n7. Chapman AH, McNamara M, Porter G: The acute contrast enema in suspected large bowel obstruction: Value and technique. Clin Radiol 46:273, 1992", "ACR Code": "7.9", "Category": "Unsure", "Reference": "1. \tBlakeborough, A., et al, Strictures of the Sigmoid Colon: Barium Enema Evaluation, Radiology, August 2001, pp. 343-348.\n2. \tReeder, M.M., Felson, B., Gamuts in Radiology, Audiovisual Radiology of Cincinnati, Inc., 1975, p. G-55.\n3. \tFarrell, R.J., Farrell, J.J., and Morrin, M.M., Diverticular Disease in the Elderly, Gastroenterology Clinics, Volume 30, Number 2, June 2001.\n4. \tBoulos PB, Karamanolis DG, Salmon PR, et al: Is colonoscopy necessary in diverticular disease? Lancet 1:95-96, 1984 Abstract \n5. \tLopez-Kostner, F., Hool, G.R., and Lavery, I.C., Management and Causes of Acute Large Bowel Obstruction, Surgical Clinics of North America, Volume 77, Number 6, December 1997.\n6. \tBuetow P.C., et al, Colorectal adenocarcinoma: radiologic-pathologic correlation. RadioGraphics 1995, 15:127-146.\n7. \tSchrock TR: Colonoscopy versus barium enema in the diagnosis of colorectal cancer and polyps. Gastrointest Endosc Clin N Am 3:585, 1993. \n8. \tHogan WJ, Stewart ET, Geenen JE, et al: A prospective comparison of the accuracy of colonoscopy vs air-barium contrast exam for detection of colonic polypoid lesions. Gastrointest Endosc 23:230," } }, { "U_id": "MPX1321", "TAC": [ "MPX1321_synpic54278" ], "MRI": [], "Case": { "Title": "Coarctation of the Aorta", "History": "11 y.o. girl with systemic hypertension and a murmur.", "Exam": "\u2022 Blood pressure in right arm 140/90 and in right leg 118/66. \n\u2022 HEENT: Normocephalic, atraumatic, no scleral icterus\n\u2022 Cardiovascular: Regular rate and rhythm with normal S1 and S2 physiologic splitting, no S3 or S4. Murmur auscultated at anterior chest which is moderately harsh, low-pitched, grade 2/6 systolic ejection murmur that is best heard at the left upper sternal boarder. From the posterior, the murmur is more distinct and clear at the left parasternal area.\n\u2022 Lungs: Clear to auscultation bilaterally with no wheezes, rhonchi, rales\n\u2022 Abdomen: Soft, nontender, nondistended, normal auscultation\n\u2022 Extremities: No clubbing or edema noted\n\nPMH: Nephrology evaluation heard a systolic murmur. No murmur had ever been mentioned to the patient\u2019s mother in the past. She never had any cardiovascular symptoms during feeding as an infant; such as sweating, dyspnea, irritability, cyanosis, frequent pauses, etc. Her growth and development have been normal. She is active without cardiovascular symptoms during exercise.\n\u2022 Echocadiogram showed possible coarctation of the aorta and a cardiac gated CT was ordered for better demonstration of the anomaly.", "Findings": "The thoracic aorta is notable for high-grade coarctation with post-stenotic dilatation. The level of the stenosis is 2.5 cm distal to the take off of an otherwise enlarged left subclavian artery. Multiple enlarged collateral vessels are identified, including bilateral internal mammary, intercostal, and subphrenic arteries. The branch vessels are all patent.", "Differential Diagnosis": "\u2022 Aortic dissection\n\u2022 Coarctation of the aorta\n\u2022 Focal vasculitis\n\u2022 Extrinsic mass pressing on the aorta", "Case Diagnosis": "Coarctation of the Aorta", "Diagnosis By": "Cardiac gated CT with angiography of the heart and aorta", "Treatment & Follow Up": "The patient will undergo an interventional catheterization procedure for repair", "Discussion": "\u2022 The typical location for coarctation of the aorta is just distal to the left subclavian artery, which is the location of the patient's lesion in this case.\n\u2022 Though not a functional study, this patient is suspected to have a bicuspid aortic valve from this imaging. Bicuspid aortic valve is frequently associated with coarctation of the aorta (reported incidence of 30 to 40 percent).\n\u2022 The stenotic area of the proximal aorta had an area of 0.17 cm^2 while the proximal descending aorta 1 cm below the stenosis had an area of 2.65 cm^2\n\u2022 \tCoarctation of the aorta is a common malformation accounting for six to eight percent of all congenital heart defects. \n\u2022 \tGirls with Turner syndrome are at increased risk with a prevalence rate of greater than 10 percent. \n\u2022 \tThe classical clinical manifestations are hypertension in the upper extremities, diminished and/or delayed femoral pulses, and low or unattainable arterial blood pressure in the lower extremities. \n\u2022 \tClinical presentation varies in different age groups. Neonates may be asymptomatic if there is a PDA or if the coarctation is not severe. Neonates with severe disease may present in heart failure and/or shock. Older infants and children may be asymptomatic or present (especially with exertion) with chest pain, cold extremities, and claudication. Adults will present with hypertension and if the coarctation is severe may have headaches, epistaxis, heart failure or aortic rupture or dissection.\n\u2022 \tChest radiographic findings vary with age and severity of the coarctation. In infants with heart failure, the chest radiograph usually shows generalized cardiomegaly with increased pulmonary vascular markings due to pulmonary venous congestion. In older children and adults, the heart size may remain normal but other findings include rib notching and the 3 sign (indentation of the aortic wall at the site of coarctation with pre and post-coarctation dilatation). \n\u2022 \tTwo-dimensional and Doppler transthoracic echocardiography is indicated for initial evaluation to establish the diagnosis and detect associated cardiac defects. \n\u2022 \tMR or CT angiography is indicated to define the location of the obstruction and identify collateral vessels. \n\u2022 \tEchocardiography or MRI are also useful for post-repair follow-up. CT may be helpful if MRI is contraindicated." }, "Topic": { "Title": "Coarctation of the Aorta", "Disease Discussion": "Coarctation of the Aorta (CoA), also known as congenital aortic stenosis, is a narrowing of the lumen of the aorta, which produces a flow obstruction. The anomaly accounts for 5-10% of all congenital heart defects and shows predominance in males of roughly 1.3 to 2.1 times that of females. When CoA becomes clinically relevant, it can lead to systemic hypertension and secondary left ventricular hypertrophy with heart failure. If it is not treated, the patient\u2019s mean age of death is about 34 years.\n\nCoA can present with other anomalies, most frequently of which is a bicuspid aortic valve, accompanying up to 60-85% of aortic coarctations. Although the true etiology of CoA is still unknown, this high correlation leads to the hypothesis that these two anomalies stem from a common congenital malformation. Due to the relatively high prevalence in males and in patients with Turner\u2019s syndrome, it has also been suggested that a link exists between the X-chromosome and the anomalous aorta and valve.\n\nCoarctation can occur in various locations along the length of the aorta. Stenosis prior to the emergence of the left subclavian artery is infrequent, with most coarctations occurring just distal to the left subclavian artery. Narrowing that occurs in the descending thoracic or abdominal aorta is exceedingly rare. Clinical presentation and symptoms are less related to anatomical position and more related to the degree of stenosis and the presence of associated abnormalities.\n\nCommon symptoms associated with CoA include epistaxis, arterial hypertension, headache, and leg fatigue. In younger male patients CoA should always be considered in differential diagnosis if upper extremity hypertension exists with lower extremity hypotension and weak pulses.\n\nIf a pressure gradient >30 mm Hg is present across the stenosis, surgical treatment should be considered. Various surgical interventions have been performed throughout the years, including resection of the stenotic tract with end-to-end anastamosis, subclavian flap aortoplasty, percutaneous balloon angioplasty, and more recently, expandable endovascular stents.", "ACR Code": "5.1", "Category": "Radiologic Sign or Finding", "Keywords": "CoarctationAortic StenosisCoA", "Reference": "Secchi F, Iozzelli A, Papini GD, Aliprandi A, Di Leo G, Sardanelli F. MR imaging of aortic coarctation. Radiol Med. 2009 Jun;114(4):524-37. Epub 2009 May 14.\n\nTanous D, Benson LN, Horlick EM. Coarctation of the aorta: evaluation and management. Curr Opin Cardiol. 2009 Nov;24(6):509-15.\n\nAbbruzzese PA, Aidala E. Aortic coarctation: an overview. J Cardiovasc Med (Hagerstown). 2007 Feb;8(2):123-8.", "External Links": "mc.uky.edu/radiology" } }, { "U_id": "MPX1325", "TAC": [ "MPX1325_synpic22299" ], "MRI": [], "Case": { "Title": "Liver metastases, from bronchogenic carcinoma", "History": "69yo M presented to the emergency department with a 4 month history of dull right upper quadrant abdominal pain. He has had a 15 lb weight loss over the last year and admits to a 70 pack year smoking history. The chest CT demonstrated a 1.9 cm speculated mass in the right lower lobe that was the primary tumor.", "Exam": "No abdominal tenderness or jaundice.\nAST = 102, ALT= 116, ALP= 460, nl bilirubin and INR", "Findings": "Multiple target appearing masses that have a hyperechoic center with a hypoechoic rim in the left and right lobes of the liver\n\nThe ultrasound was followed by a CT that demonstrated multiple low density solid hepatic masses.", "Differential Diagnosis": "Regenerative nodules in cirrhosis, microabcesses, multiple bacterial abscesses, Histoplasmosis, lymphoma, Kaposi sarcoma, multnodular hepatocellular carcinoma, sarcoidosis", "Case Diagnosis": "Liver metastases, from bronchogenic carcinoma", "Diagnosis By": "Ultrasound and CT, patient declined biopsy" }, "Topic": { "Title": "Liver metastases, from bronchogenic carcinoma", "Disease Discussion": "This case demonstrates hepatic metastases not visualized on a liver sulfur colloid scan but seen vividly on a sonogram.\n\nThree major noninvasive imaging modalities are used to evaluate hepatic metastases: CT, ultrasound, and scintigraphy. CT has the best sensitivity and specificity if done both with and without intravenous contrast, with narrow window settings, and with 1-cm continuous sections. The disadvantages include expense, radiation, time, intravenous contrast, and poor visualization of lesions near the diaphragmatic dome.\n\nUltrasound is comparable to CT in sensitivity and specificity. It is usually less expensive, fast, has no radiation exposure, and allows excellent visualization of lesions near the diaphragms using longitudinal views. Disadvantages include difficulty with obese patients and those with excessive bowel gas, and a strong technical dependence (e.g., using the proper focal length or frequency of transducer). Both CT and ultrasound have the advantage of visualizing multiple organs in the search for a primary lesion.\n\nScintigraphy has the lowest specificity and sensitivity but is fast, relatively inexpensive, and has few technical dependencies. Disadvantages are a low specificity, visualization limited to the liver and spleen, poor visualization of small or deep lesions, and limited usefulness in the face of underlying hepatocellular disease.\n\nEach modality has specific advantages that can be applied to particular situations. For example, ultrasound is ideal for lesions in the left lobe or near the dome of the liver and at times can define small lesions not seen with other methods. Other lesions may be better seen with CT; however, this is usually not predictable in advance. In general, scintigraphy is the least informative of the three techniques.\n\nLiver function tests are used as the initial screening for hepatic metastases. They are nonspecific and also surprisingly insensitive for occult hepatic metastases. With occult hepatic metastases, the tests for serum enzymes have the following sensitivities: alkaline phosphatase 6%, SGOT 38%, and LDH 81% (the most sensitive). Once the hepatic metastases are palpable, all of these tests have sensitivities greater than 80%.", "ACR Code": "-1.-1", "Category": "Unsure" } }, { "U_id": "MPX1318", "TAC": [ "MPX1318_synpic41392" ], "MRI": [], "Case": { "Title": "Multiple Myeloma and secondary amyloidosis and history of sarcoidosis", "History": "46 year-old woman with history of sarcoidosis, anemia, hypertension, and carpal tunnel syndrome with complaint of intermittent bilateral conjunctival inflammation and hemorrhage for one year. She was initially seen by opthalmology who diagnosed and treated her for conjunctivitis associated with bilateral lacrimal gland enlargement demonstrated on numerous CT studies of the orbits. She was diagnosed with sarcoidosis thirteen years prior via bronchoscopy and maintains that she has remained asymptomatic. She also has bilateral upper extremity paresthesias that are diffuse but most notable in the ulnar nerve distribution of both the right and left hands and she has been diagnosed with bilateral carpal tunnel syndrome in the past year. She presents with no other complaints and review of systems is negative for constitutional, cardiopulmonary, gastrointestinal, genitourinary, or musculoskeletal complaints. Her most recent head CT was obtained during evaluation of URI symptoms and pain over the right maxillary sinus, for which she was diagnosed with sinusitis.", "Exam": "Physical exam: notable only for bilateral conjunctivitis and conjunctival hemorrhage and swelling \n\nLab:\nNo abnormal findings", "Findings": "Head CT: Bilateral Lacrimal gland enlargement with homogenous tissue attenuation. Multiple lucenies of the skull bilaterally, particularly posterior to the vertex ranging 5-9 mm in size. Diffuse soft tissue attenuation noted in right maxillary sinus consistent with sinusitis. \n\nSkeletal Survey: Left upper extremity-single round, punched-out appearing lucencies in the region of the radial tuberosity and proximal humerus; PA-chest-single, round, punched out appearing lucency in the lateral left clavicle; Skull-numerous, round, punched-out appearing lucencies over the parietal and frontal bones.", "Differential Diagnosis": "Multiple Myeloma\nOsteolytic Metastatic Carcinoma\nHyperparathyroidism", "Case Diagnosis": "Multiple Myeloma and secondary amyloidosis and history of sarcoidosis", "Diagnosis By": "Lacrimal gland biopsy demonstrating diffuse amyloid deposition. Serology demonstrates monoclonal gammopathy. Bone marrow biopsy pending pathologic analysis.", "Treatment & Follow Up": "The patient is currently being followed by hematology/oncology. Treatment plan currently pending further bone marrow biopsy confirmation of current diagnosis.", "Discussion": "This is a case of a 46 year-old black female with a history of sarcoidosis diagnosed at age 32 years, and bilateral carpal tunnel syndrome diagnosed within the past year now presenting with mulitple myeloma. Multiple myeloma (MM) is a monoclonal B-cell malignancy consisting of terminally differentiated plasma cells. In the United States, the incidence of disease is 3-4 newly diagnosed cases per 100,000 population per year, and represents 1% of all malignancies. Demographically, patients are commonly African-American, with males slightly outnumbering females by 1.4-1. Patients are typically elderly with a median age of 65 years at diagnosis, although cases in much younger patients have been reported.\n\nThe patient's presentation for MM is unusual given her relatively young age (46 years), lack of physical findings and history (i.e. fatigue, bone, recurrent infections), and laboratory abnormalities (i.e. hypercalcemia, elevated creatinine, elevated total protein) suggestive of MM. The bilateral lacrimal gland amyloidosis is a unusual initial presentation for MM. By comparison, lacrimal gland involvement in sarcoidosis is more common affecting 55-61% of patients at sometime during their disease course with similar findings on CT imaging. Therefore, her management was based on the conclusion her presentation was a manifestation of her sarcoidosis and not MM. The lack of response to therapy for the lacrimal gland enlargement ultimately prompted a biopsy of the gland six months from the time she sought medical attention, and one year since she reported initially having symptoms. \n\nThe lacrimal gland biopsy showed an inflamatory cell infiltrate, with nodules of pauci-cellular, eosinophillic staining material exhibiting apple-green birefringence on Congo Red staining. This is consistent with amyloidosis of the lacrimal gland. The lack of evidence of granulomatous disease present in the biopsy specimen strongly suggests that sarcoidosis is not the etiology of her lacrimal gland enlargement. \n\nBased on the above findings, the patient received further laboratory and radiological investigations for the diagnosis of MM. The diagnosis of MM is based on the demonstration of three components: 1) Serum or urine monoclonal protein identified by a characteristic monoclonal M protein spike on electrophoresis of urine and blood specimens; 2) >10% abnormal plasma cells on bone marrow biopsy; and 3) end-organ damage in the form of hypercalcemia, renal insufficiency, sequelae of amyloid deposition, and/or bone abnormalities on imaging. Most patients will demonstrate symptomatic sequelae of of end-organ damage. However, nearly 25% of patients with MM are discovered through incidental findings on laboratory studies and imaging. Indeed, radiographs provided the only significant finding suggestive of MM via a head CT that was obtained for the evaluation of URI symptoms of sinusitis in an emergency department several months prior to the lacrimal gland biopsy. \n\nThe characteristic radiological feature of MM is the presence of a single osteolytic lucency (plasmacytoma), or, as in this patient's case, multiple discrete osteolytic lucencies (myelomatous) that are subcortical and found predominantly in the axial and proximal appendicular skeleton. Lesions may also coalesce or take the form of diffuse osteopenia. Sclerosing myeloma has also been described, although it is rare. The osteolysis of MM is mediated by the secretion of chemokine factors by the malignant plasma cells that stimulate osteoclast proliferation, chemotaxis, maturation, and activity. \n\nPlain film radiograph skeletal survey is the preferred diagnostic modality for the detection of bony involvement in MM. Nearly 50% of the density of bone must be affected before the \"punched-out\" lesions are apparent, however, the presence of bone lesions is confirmed in 60-80% of all patients initially surveyed for MM with radiograph. Other useful imaging studies include MRI, which may be used for the precise determination of lesion size and location for bone marrow biopsy, targeted radiotherapy, and for characterization of the extent of disease. Imaging via CT is adjunctive to MRI for guided biopsy of lesions. Recently, PET scanning has shown promise for monitoring disease recurrence by detection of lesions not readily seen on conventional radiograph. \n\nDue to the osteolytic nature of MM, nuclear imaging via technec tium-99m (Tc-99m) bone scanning has no role in diagnosis or monitoring. The sensitivity of Tc-99m scanning is dependent on osteoblastic activity, and therefore, underestimates the extent of disease. Uptake of Tc-99m into radiographically abnormal regions is only 44% compared to conventional plain film. This uptake is secondary to osteoblastic activity from pathological fracture, calcification within a plasmacytoma, or amyloidosis in association with tumor. \n\nThe presence of osteolytic lesions is not pathognomonic of MM, as such findings may be present in a variety of conditions including other osteolytic metastases and occasionally lymphoma) and hyperparathyroidism Furthermore, bilateral lacrimal gland enlargement with homogenous soft tissue attenuation seen on CT is more suggestive of lacrimal gland sarcoidosis than other etiologies. Neoplastic and infectious processes tend to present with discrete lesions within the lacrimal gland and/or are likely unilateral. The chronicity of symptoms also would argue against a bilateral infection, as such a condition would be likely self-limiting. The apparent overlap of expected findings in sarcoidosis versus that of MM likely contributed to the lag between initial presentation and diagnosis." }, "Topic": { "Title": "46 yo female with chronic bilateral lacrimal gland enlargement of >6 mo duration.", "Disease Discussion": "HPI: 46 yo african american woman with a history of sarcoidosis presented with one year of intermittent conjunctiva inflammation and bleeding. She has been followed by opthalmology who initially treated her for conjunctivitis. The patient received numerous imaging studies of the orbits demonstrating bilateral lacrimal gland enlargement. A head CT obtained in a emergency department for conjunctivitis and sinusitis demonstrated numerous 5-9mm lucencies in the posterior vertex of the skull in addition to soft tissue density in the right maxillary sinus and lacrimal gland enlargement that were not initially clinically coordinated. A biopsy of the left lacrimal gland was performed and pathology showed non-granulomatous inflammation with nodules of paucicellular, esinophillic stroma. The tissue showed was positive for congo red staining demonstrating the presence of amyloid. She was then referred to hematology/oncology who subsequently confirmed the diagnosis of amyloidosis based on serology and demonstration of numerous bone lucencies demonstrated on plain-film skeletal survey consistent with multiple myeloma.", "ACR Code": "1.3", "Category": "Clinical Vignette or Pearl", "Keywords": "Multiple MyelomaLacrimal GlandBone lucencies", "Reference": "1.\tAngtuaco, E.J., et al., Multiple myeloma: clinical review and diagnostic imaging. Radiology, 2004. 231(1): p. 11-23.\n2.\tMavrikakis, I. and J. Rootman, Diverse clinical presentations of orbital sarcoid. Am J Ophthalmol, 2007. 144(5): p. 769-775.\n3.\tPettersson, T., et al., Sarcoidosis and multiple myeloma: an association. Br Med J (Clin Res Ed), 1987. 295(6604): p. 958.\n4.\tSen, F., K.P. Mann, and L.J. Medeiros, Multiple myeloma in association with sarcoidosis. Arch Pathol Lab Med, 2002. 126(3): p. 365-8.\n5.\tSirohi, B. and R. Powles, Multiple myeloma. Lancet, 2004. 363(9412): p. 875-87.\n6.\tUchiumi, H., et al., Does sarcoidosis induce multiple myeloma? Am J Hematol, 1993. 44(3): p. 220.\n7. Katzel, J. A., P. Hari, et al. (2007). Multiple myeloma: charging toward a bright future. CA Cancer J Clin 57(5): p. 301-18." } }, { "U_id": "MPX1333", "TAC": [ "MPX1333_synpic44967", "MPX1333_synpic44968", "MPX1333_synpic44969", "MPX1333_synpic44970", "MPX1333_synpic44971", "MPX1333_synpic44972", "MPX1333_synpic44973", "MPX1333_synpic44974" ], "MRI": [], "Case": { "Title": "Right MCA Infarction", "History": "Acute onset of left hemiparesis", "Exam": "Left hemiparesis", "Findings": "Effacement of right basal ganglia\nAbnormal hyperintensity of most of the right MCA territory\nOccluded Right Internal Carotid Artery", "Differential Diagnosis": "Dissection\nThrombosis\nCerebral Infarction", "Case Diagnosis": "Right MCA Infarction", "Discussion": "Some discussion" }, "Topic": { "Title": "Early cerebral infarction", "Disease Discussion": "Early signs of cerebral infarction\n\nIt can be difficult to visualize cerebral infarcts within the first 24 hours on routine noncontrast CT examinations. This is rapidly changing since our images have improved and can be augmented with contrast studies.\n\nSome early signs of infarction include:\n\u2022 basal ganglia obscuration (loss of gray-white demarcation)\n\u2022 hyperdense MCA / hyperintense MCA\n\u2022 the \"insular ribbon sign\"\n\u2022 Cortical gray white junction obscuration\n\nIn some cases, we may see hyperdense distal MCA vessels, demonstrating intraluminal thrombus. Whereas a repeat CT scan from the next day may not demonstrate these hyperdense areas.", "ACR Code": "1.7", "Category": "Vascular", "Keywords": "gray-white demarcation obscurationinfarctiondiagnosis" } }, { "U_id": "MPX1342", "TAC": [ "MPX1342_synpic16786" ], "MRI": [ "MPX1342_synpic16787" ], "Case": { "Title": "Rabdomyosarcoma, prostate. botryoid subtype", "History": "Urinary obstruction, hematuria. Afebrile w/o history of febrile illness.", "Findings": "Findings: US: lobulated mass at bladder trigone with color flow, with apparent involvement of bilateral ureteral orifices.Mild right pelvocaliectesis . \n\nCT: Irregular soft tissue mass posterior bladder wall outlined by contrast instilled through catheter\n\nMRI: T2WI shows enlargement of the prostate.", "Differential Diagnosis": "Rhabdomyosarcoma, hemangioma, neurofibroma, pheochromocytoma, leiomyoma, focal cystitis, inflammatory pseudotumor, RP abcess (unlikely given history), hematoma (unlikely w/ flow), TCC and Leimyosarcoma (rarely), benign tumors (rarely)", "Case Diagnosis": "Rabdomyosarcoma, prostate. botryoid subtype" }, "Topic": { "Title": "Rhabdomyosarcoma", "Disease Discussion": "Rhabdomyosarcoma accounts for 5-10% of all malignant tumors in patients under 15 years and is most common malignant tumor of the vagina, prostate, and bladder. Other sites of involvement include perineal region, head & neck, skeletal muscle/soft-tissue, protahepatis, peritoneal, \nMost neoplasms of the bladder in children are malignant, with Rhabdomyosarcoma most common. TCC and Leiomyosarcomsa are rarely seen. Clinically bladder tumors present with hematuria and retention and can cause flank pain secondary to hydronephrosis and constipation. \nRhabdomyosarcoma appears either as peduunculated soft-tissue mass with bunch of grapes appearance (Botryoid) or as focal or diffuse wall thickening. On CT assymmetry of fat planes or direct soft tissue into adjacent organs is usefull for assessing stage. Pelvic lymph nodes may be enlarged indicative of metastatic disease. Metastatic disease to the nodes, liver, bone, lung, brain.\nDistinguishing between localized benign and malignant tumors of the bladder may not be possible with CT. \nGU rhabdomyosarcoma is initially managed by chemo. Patients with operable tumors undergo surgery and radiation rendered for residual inoperable tumor. \nThree year survival rates are 70-80%.", "ACR Code": "8.3", "Category": "Neoplasm, sarcoma", "Keywords": "RhabdomyosarcomaProstatebladder", "Reference": "Pediatric Body CT. Marilyn J. Siegel. Lippincott Williams & Williams, 1999. 299-302" } }, { "U_id": "MPX1357", "TAC": [ "MPX1357_synpic17883" ], "MRI": [], "Case": { "Title": "Unilateral Coronal Synostosis\r\nHelical CT with 3-D reconstructions.", "History": "5 y/o former 24 wk prematue infant with 5 mo NICU with multiple medical problems including history of IVH, CP, MR, congenital cardiac defects including PDA and ASD, and 47 XXY. Patient's twin was stillborn. Patient presents with recent history of siezures and a progressively oddly shaped head.", "Exam": "Irregularly shaped head with prominant l frontal calvarium.", "Findings": "See Captions.\n\nSaggital suture is displaced laterally and obliquely angled. The labdoid suture is displaced left posteriorly. The right coronal suture is fused.\nThere is a white matter cleft in the right frontal lobe c/w schizencephaly.", "Differential Diagnosis": "Cranial Synostosis - isolated\nCranial Synostosis - syndromic\nMoulding.", "Case Diagnosis": "Unilateral Coronal Synostosis\nHelical CT with 3-D reconstructions.", "Treatment & Follow Up": "Pt. undergoing pre-op evaluation for surgical correction.", "Discussion": "This patient has multiple medical and genetic problems, but his cranial deformity is likely an isolated abnormality perhaps from prematurity and/or function of being a twin. Craniosynostosis is not noted in the literature as being associated with XXY genotypes." }, "Topic": { "Title": "Unilateral Coronal Synostosis", "Disease Discussion": "Synostosis is the premature closure of one or more of the calvarial sutures which limits the ability of the skull to expand in a direction perpendicular to the suture. The sutures are dynamic: as the brain grows, the sutures expand, adding new bone. An infant\u2019s brain grows rapidly, doubling in 6 months and again in 2 years. If the sutures are compressed, either mechanically or due to failure of underlying CNS expansion, the sutures may either resorb or fuse. Underlying brain growth causes increased growth parallel to the suture, resulting in characteristic head shapes. Synostoses can be primary (fusion of single suture as an isolated event) or secondary, often associated with several syndromes. The prevalence of primary synostosis is about 1/4000 to 1/1000 live births. An inherited tendency or family history has been reported in many cases in the literature, however, most cases of isolated craniosynostosis are usually sporadic in occurrence with no known etiology.\n\nTrue craniosynostosis will not improve with time and usually worsens with growth.\n\nDiagnosis is made on the basis of characteristic head shape, presence of ridges overlying fused sutures, and rotation of facial landmarks. Radiologic studies are discussed below.\n\nClinically, signs of increased intracranial pressure (ICP) may also be present (vomiting, lethargy). Some synostoses are diagnosed in the context of syndromes (discussed below). \nA quick basic anatomy review is helpful before naming the synostoses. The bones of the calvarium are divided by sutures The metopic suture divides the frontal bones. The frontal bones are separated from the parietal bones by the coronal suture, and the two parietal bones are separated from each other by the sagittal suture. The occipital bone is separated from the parietal bones by the lambdoidal sutures. The space where the metopic, coronal and sagittal sutures come together is the anterior fontanel, and the posterior fontanel is present where the lambdoidal and sagittal sutures meet.\n\nCranial synostoses definitions are as follows:\nSagittal craniosynostosis results in scaphocephaly (keel/boat skull).\nMetopic craniosynostosis results in trigonocephaly (triangular skull).\nLambdoidal synostosis results in plagiocephaly (asymmetric skull).\nCoronal synostosis results in brachycephaly (short skull) if bilateral and frontal plagiocephaly if unilateral with ipsilateral eyebrow elevation giving the classic \u201charlequin eye\u201d appearance.\nBetween 10-20% of synostoses are associated with syndromes. Most of these syndromes are sporadic in occurrence. However, if one parent and one sib are affected, subsequent siblings have about 50% risk of having the syndrome. The most common is Crouzon syndrome involving the sagittal and coronal sutures with shallow orbits, proptosis, hypertelorism and sometimes hydrocephalus. \n\nApert Syndrome involve the coronal, sagittal and lambdoidal sutures with facial dysmorpism, syndactyly and cardiac defects. Other rarer syndromes include Carpenter\u2019s, Pfeiffer\u2019s and Conrad\u2019s syndromes.\n\nRadiologic workup should center around CT. CT remains the most sensitive barometer of bony fusion. Plain films of the skull may appear normal. Bone windows and thin slices are necessary with conventional axial CT slices. 3-D CT has simplified the diagnosis and has been show in studies to increase sensitivity. Three-dimensional CT scan processing by shaded-surface reconstruction, volumetric, and depth-coded methods have been shown to be superior to conventional plain radiographs and CT scans in diagnosing craniosynostosis. The skull base and brain may show underlying abnormalities in the syndromic craniosynostoses. If the patient has increased intercranial pressure, calvarial table resorbtion has been seen with unknown clinical significance.\n\nMost patients with simple craniosynostosis have no neurological compromise, therefore corrective surgery is cosmetic. If the child is 18 months and the deformity is mild, it will not likely worsen and surgery can be avoided. Conservative therapy involves positional therapy (head position while sleeping and controversial helmet therapy).\n\nSurgical correction is often done for psychosocial reasons with good results. Timing of surgical reconstruction is also controversial with some advocating early intervention (3-4 mos) and others recommend waiting until 8-10mos for better long-term results with less morbidity. Most craniosynostoses today can be treated with a single surgery with excellent cosmetic results and minimal morbidity and nearly nonexistent mortality.", "ACR Code": "1.1", "Category": "Congenital, malformation", "Keywords": "Cranial Synostosiscranial Stenosisplagiocephaly", "Reference": "1. Keating. Cranyosynostosis: Diagnosis and Management in the New Millennium. Pediatric Annals 26:10/Oct 97.\n2. Vannier MW, Hildebolt CF, Marsh JL et. al. , Craniosynostosis: diagnostic value of 3-dimensional reconstruction. Radiology 1989;173:669-673\n3. American Journal of Neuroradiology 21:1951-1954 (11 2000)\nThree-dimensional CT Maximum Intensity Projections of the Calvaria: A New Approach for Diagnosis of Craniosynostosis and Fractures \nL. Santiago Medinaa,b", "External Links": "http://www.family.georgetown.edu/welchjj/netscut/neurology/synostosis.html" } }, { "U_id": "MPX1359", "TAC": [ "MPX1359_synpic29148", "MPX1359_synpic29149" ], "MRI": [], "Case": { "Title": "Toxic Megacolon", "History": "This 83 year-old African-American female with a past medical history of hypothyroidism, hypertension, and type II diabetes mellitus presented to the emergency room with one week of constipation. The patient had fallen 2 weeks prior to this presentation and by her report had been placed on acetaminophen/oxycodone for pain in her right knee. Shortly thereafter, the frequency of her stools decreased. At presentation, the patient had not passed stool in 5 days. Of note, the patient was admitted about one month prior for hyponatremia that was complicated by Clostridium difficile colitis. The patient was still receiving oral vancomycin for treatment. On arrival, she denied any abdominal pain, nausea or vomiting, recent diarrhea, abdominal distension, dark or bloody stools, or bright red blood per rectum. \n Evaluation by the emergency physician noted a heart rate >150 beats per minute. An electrocardiogram showed new onset atrial fibrillation with rapid ventricular response. The patient was admitted to the cardiac care unit for further evaluation of the new dysrhythmia. An acute abdominal series was obtained on admission for evaluation of constipation.\n Over the first night of admission, the dysrhythmia spontaneously converted to sinus tachycardia. The patient had two large solid bowel movements, but then developed severe diffuse abdominal pain and distension with altered mental status by morning. A surgical consult and further imaging were obtained.", "Exam": "Vitals: T 101.0F, HR 88 (with beta blockade), BP 113/50, RR 28, Sa 97% 2L NC\nExam: Generally ill-appearing, distended abdomen without bowel sounds, tympanitic and tender diffusely, peritoneal signs\nLabs: WBC: 8.8 (51% bands), Anion Gap: 16, ABG: 7.399/28.4/73/17.5/95%, Lactate 5.7", "Findings": "Supine Abdominal Film: There is a large amount of air and stool seen throughout the colon. The colon is diffusely dilated. The cecum is dilated to 11.5cm. The transverse colon is dilated to 9.5cm. There is air seen to the level of the rectum. \n\nCT, Abdomen/Pelvis with Intravenous and Enteric Contrast: There is diffuse dilation of the colon with air and fluid levels present. There is diffuse wall thickening and enhancement in the rectosigmoid colon. The descending, transverse, and ascending colon are dilated to as much as 8.5cm. The colonic wall enhances, but is not abnormally thickened. There is contrast within the small bowel. A small amount of air is seen within the small bowel and terminal ileum. There is no evidence of perforation or extraluminal process.", "Differential Diagnosis": "1. Toxic Megacolon\n2. Distal Colonic Obstruction\n3. Ileus\n4. Ogilvie syndrome\n5. Volvulus", "Case Diagnosis": "Toxic Megacolon", "Diagnosis By": "Computed Tomography demonstrating diffusely dilated colon with clinical evidence of toxicity.", "Treatment & Follow Up": "An emergent total colectomy with ileostomy placement was performed on hospital day two. The patient had a 10-day postoperative intensive care unit stay complicated by sepsis. She slowly recovered over a period of 21 days and was discharged to an inpatient rehabilitation facility.", "Discussion": "Simply put, toxic megacolon is diffuse colonic dilatation combined with clinical evidence of toxicity. This condition has multiple causes including inflammatory bowel disease, (traditionally ulcerative colitis), infectious colitis, (most notably Clostridium difficile in hospitalized patients), and malignancy. Frequently, an exacerbating factor is present in addition to the predisposing condition. These factors can include, but are not limited to, abrupt cessation of either steroids or smoking in ulcerative colitis patients, use of narcotics, use of anticholinergics, or electrolyte disturbances. \nPresenting symptoms range from bloody diarrhea to obstipation, with severe abdominal pain and distension. Physical examination will likely show an ill-appearing patient with absent bowel sounds, and a tympanitic abdomen. Signs of peritoneal inflammation may be present as well. In 1969, Jalan established criteria for clinical toxicity. These require that a patient present with any three of the following: fever >101.5\u00b0F (>38.6\u00b0C), heart rate >120 beats/min, white blood cell count >10.5, or anemia. Patients will likely also have evidence of dehydration, mental status changes, electrolyte disturbances, or hypotension. \nThe diagnosis of colonic dilatation can be made by plain radiograph, but patients may also undergo computed tomography (CT). Findings suggestive of toxic megacolon on plain film include dilatation of the transverse colon >6cm with or without small bowel distension. A CT scan may reveal colonic wall thickening, pericolic stranding, or evidence of perforation or abscess formation.\nMedical management begins with fluid resuscitation, colonic decompression with nasointestinal tube and/or rectal tube, broad-spectrum antibiotics, and frequent repositioning to prevent air collections in one area of colon. Abdominal radiographs should be repeated frequently. Surgical intervention is often required. Indications for total colectomy include perforation, and progressive toxicity or dilatation despite appropriate medical care." }, "Topic": { "Title": "Toxic Megacolon", "Disease Discussion": "Simply put, toxic megacolon is diffuse colonic dilatation combined with clinical evidence of toxicity. This condition has multiple causes including inflammatory bowel disease, (traditionally ulcerative colitis), infectious colitis, (most notably Clostridium difficile in hospitalized patients), and malignancy. Frequently, an exacerbating factor is present in addition to the predisposing condition. These factors can include, but are not limited to, abrupt cessation of either steroids or smoking in ulcerative colitis patients, use of narcotics, use of anticholinergics, or electrolyte disturbances. \n Presenting symptoms range from bloody diarrhea to obstipation, with severe abdominal pain and distension. Physical examination will likely show an ill-appearing patient with absent bowel sounds, and a tympanitic abdomen. Signs of peritoneal inflammation may be present as well. In 1969, Jalan established criteria for clinical toxicity. These require that a patient present with any three of the following: fever >101.5\u00b0F (>38.6\u00b0C), heart rate >120 beats/min, white blood cell count >10.5, or anemia. Patients will likely also have evidence of dehydration, mental status changes, electrolyte disturbances, or hypotension. \n The diagnosis of colonic dilatation can be made by plain radiograph, but patients may also undergo computed tomography (CT). Findings suggestive of toxic megacolon on plain film include dilatation of the transverse colon >6cm with or without small bowel distension. A CT scan may reveal colonic wall thickening, pericolic stranding, or evidence of perforation or abscess formation.\n Medical management begins with fluid resuscitation, colonic decompression with nasointestinal tube and/or rectal tube, broad-spectrum antibiotics, and frequent repositioning to prevent air collections in one area of colon. Abdominal radiographs should be repeated frequently. Surgical intervention is often required. Indications for total colectomy include perforation, and progressive toxicity or dilatation despite appropriate medical care.", "ACR Code": "7.5", "Category": "Clinical Vignette or Pearl", "Keywords": "Toxic MegacolonPseudomembranous ColitisColonic Dilatation", "Reference": "Aslam S, Hamill RJ, Musher DM. Treatment of Clostridium difficile-associated disease: old therapies and new strategies. Lancet Infect Dis. 2005 Sep;5(9):549-557.\n\nGan SI, Beck PL. A new look at toxic megacolon: an update and review of incidence, etiology, pathogenesis, and management. Am J Gastroenterol. 2003 Nov;98(11):2363-2371.\n\nPresent DH. Toxic megacolon. Med Clin North Am. 1993 Sep;77(5):1129-1148.\n\nScully RE, Mark EJ, McNeely WF, Ebeling SH, Phillips LD. Case records of the MGH. Case 36-1997. A 58-year-old man with bloody stools and fever. \nN Engl J Med. 1997 Nov 20;337(21):1532-1540." } }, { "U_id": "MPX1366", "TAC": [ "MPX1366_synpic22186", "MPX1366_synpic22188" ], "MRI": [ "MPX1366_synpic22189", "MPX1366_synpic22190", "MPX1366_synpic22191" ], "Case": { "Title": "Fibromuscular Dysplasia, Renal Infarct", "History": "38 year old healthy male with past medical history significant only for recent onset hypertension. Presented to the Emergency Department with acute onset of left flank pain.", "Exam": "Labs were normal except for a small amount of blood in the urine", "Findings": "CT KUB was performed to evaluate for suspected renal stones. CT evaluation demonstrated normal appearing kidneys, with no evidence of renal obstruction or urolithiasis. A recently passed stone was considered, and the patient discharged home.\n\nThe patient returned 4 days later with continued and worsening left flank pain. There was flank tenderness on physical exam. UA showed moderate blood. CBC was normal, including a normal white count. CT KUB was again performed. There was no urolithiasis or hydronephrosis, but there was interval development of significant perinephric stranding. Given lack of other clinical findings of pyelonephritis, a renal mass could not be excluded, and a contrast examination was ordered.\n\nContrast CT demonstrated a wedge shaped area of non-perfusion in the upper outer aspect of the left kidney. A renal infarct was felt to be the most likely etiology, though there was no history to suggest a source. Further evaluation included echocardiography, which was negative. Laboratory analysis for abnormal clotting factors was negative. As fibromuscular dysplasia and vasculitis were also considered, renal MRA performed. This again demonstrated the area of non-perfusion in the left kidney, but also showed irregular narrowing and dilation of both renal arteries, highly suggest of fibromuscular dysplasia.\n\nThe patient was treated for symptoms and placed on Plavix. Outpatient angiography was then performed, confirming findings of FMD previously seen on MR", "Differential Diagnosis": "Initial appearance of the kidney:\nPyelonephritis\nRenal infarct\nRenal neoplasm (RCC, AML), possibly with acute hemorrhage\n\nFor renal artery changes:\nAtherosclerotic disease\nFibromuscular dysplasia\nVasculitis\nTrauma", "Case Diagnosis": "Fibromuscular Dysplasia, Renal Infarct", "Diagnosis By": "Imaging to include CT, MR, and Angiography", "Treatment & Follow Up": "Although intervention with angioplasty was considered, it was felt that the risk for further renal injury outweighed any immediate benefits of PTA, given that hypertension is currently controlled with 2 medications. He will continue on Plavix indefinitely to prevent recurrence of renal infarction. Should the patient become symptomatic again (either infarct or hypertension), percutaneous intervention will be reconsidered.", "Discussion": "This patient\u2019s demographics and presentation where somewhat atypically, but demonstrate the need for proper differential diagnoses." }, "Topic": { "Title": "Fibromuscular Dysplasia, Renal Infarct", "Disease Discussion": "Fibromuscular dysplasia represents a group of related noninflammatory disorders, all sharing the characteristic of overgrowth of one or multiple layers of the vessels wall. Also affecting the carotid, external iliac, and rarely the mesenteric arteries, it most commonly affects the renal arteries. There are 6 types, with medial fibroplasias representing the most common by far (70%). This type is characterized by the classic \u201cstring of beads\u201d appearance. Other types have less characteristic findings, though all will have findings vessels narrowing, which may appear as irregular beaded narrowing, tubular smooth narrowing, or false channels. Most patients present with renovascular hypertension or progressive renal insufficiency. \n\nThe six types are:\nMedial fibroplasia\nPerimedial fibroplasias\nMedial hyperplasia\nMedial dissection\nIntimal fibroplasias\nPeriarterial fibroplasias\n\nThe majority of patients will be female (3:1 female to male) and less than 30-40 years old, including children. Most patients respond well to angioplasty, with stenting typically reserved only for complications (dissection).", "ACR Code": "9.6", "Category": "Vascular", "Keywords": "Fibromuscular DysplasiaFMDRenal Infarct", "Reference": "Vascular and Interventional Radiology by Karim Valji; 1999" } }, { "U_id": "MPX1386", "TAC": [ "MPX1386_synpic38159", "MPX1386_synpic38161" ], "MRI": [], "Case": { "Title": "Orbit \"blow-out\" fracture", "History": "51 y/o male with trauma to face.", "Exam": "Facial edema.", "Findings": "\u2022 inferior orbit fracture\n\u2022 soft tissue swelling\n\u2022 bleeding into maxillary sinus", "Differential Diagnosis": "Given the history, there is no other differential in this case. The soft tissue swelling, fluid in the maxillary sinus, and trap-door appearance of the inferior orbital wall are the classic appearance of an inferior orbital wall blow out fracture.\n\nOther etiologies of disruption of the inferior orbital wall would include neoplasm, resection, and aggressive infection.", "Case Diagnosis": "Orbit \"blow-out\" fracture", "Diagnosis By": "CT" }, "Topic": { "Title": "Blowout fracture of orbit", "Disease Discussion": "When an object of large diameter (greater than 4-5 cm) like a fist or a baseball, strikes the orbit, forces may be transmitted through increased intra-orbital pressure. When there is increased pressure in the orbit, the thinnest bones break first, and the orbital contents may herniate through the fracture. This is the so-called \"Blow-out Fracture\". Typically, the floor of the orbit, parts of the medial wall (lamina papyracea) and rarely the orbital roof may \"blowout\".\n\nClinical signs of entrapment (abnormal EOM's with restricted upward gaze) and enophthalmos (retraction of the eyeball) may occur.\n\nComplications of Blow-Out Fx:\nPneumo-orbita\nCellulitis and Abscess\nDiplopia and Restricted EOM's\n\nBlunt force trauma (e.g. Ball or fist) \nHydraulic (pressure) forces increased intra-orbital pressure \nFractures thin bones \n Floor (orbital process of maxilla) \n Medial (20-50%) (lacrimal and ethmoid) \nHerniation and entrapment of orbital fat & EOM (inf. Oblique)\n\nThe literature continues to emphasize this \"Hydraulic Theory\" over the alternative hypothesis of direct transmission of forces from the orbital rim and/or the globe itself.\nhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12020203&query_hl=4&itool=pubmed_docsum", "ACR Code": "221.414", "Category": "Trauma", "Keywords": "blow-out fractureblowout fracturehydraulic theory", "External Links": "www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Display&dopt=pubmed_pubmed&from_uid=12020203" } }, { "U_id": "MPX1387", "TAC": [ "MPX1387_synpic17040" ], "MRI": [ "MPX1387_synpic17042", "MPX1387_synpic17043", "MPX1387_synpic17044", "MPX1387_synpic17045", "MPX1387_synpic17046", "MPX1387_synpic17500", "MPX1387_synpic17501" ], "Case": { "Title": "RSNA-COTD Infected Dermoid Cyst", "History": "21 month old male with high fever, mental status changes and possible seizure.", "Exam": "On admission, the patient was febrile and irritable.Physical examination revealed a palpable soft tissue nodule over the occiput. CSF and laboratory examinations were consistent with bacterial meningitis.", "Findings": "Contrast head CT is significant for a multiloculated cystic posterior fossa midline mass that is adjacent to the torcula with a portion extending into the occipital calvarium. This mass is low in density with HU measuring 17. There is rim enhancement with several internal septations. There is distortion of the 4th. ventricle with associated dilatation of the temporal horns. Bone windows demonstrate smooth calvarial remodeling of the occiput with a small focal dehiscence within the bone that may represent a sinus tract. The overlying skin is unremarkable. \n\nBrain MRI again demonstrates this intra- extraaxial posterior fossa mass with homogeneous increased T2 , decreased T1 signal. DWI demonstrates marked restricted diffusion which darkens on the ADC map suggesting an abscess, epidermoid,dermoid or other process with restricted diffusion. Mass effect with hydrocephalus is again demonstated. Findings are consistent with a multiloculated intra and extraaxial posterior fossa mass most consistent with cerebritis/abscess. Given the bony remodeling and midline location, findings are most consistent with a congenital process such as dermoid which has become secondarily infected.", "Differential Diagnosis": "Epidermoid \nArachnoid Cyst\nHemangioblastoma\nCystic Astrocytoma", "Case Diagnosis": "RSNA-COTD Infected Dermoid Cyst", "Diagnosis By": "Pathology", "Treatment & Follow Up": "The patient underwent surgery with the posterior fossa mass removed by neurosurgery. The patient was placed on the appropriate pre and post antibiotic prophylaxis. The patient continued to improve during the postoperative period without complications.\n\nHistopathologic workup showed a portion of scalp with a dermal sinus tract. A benign squamous lined cyst with evidence of rupture were included. Additional specimen consisted of typical hair elements and pearly white soft tissue .", "Discussion": "In this particular case of a young child presenting with a cystic posterior fossa mass, imaging was helpful in narrowing the diagnosis. Evidence of bony remodeling and presence of a sinus tract indicated that this process was a chronic and possibly a congenital process. The midline location of this mass favors a dermoid rather than epidermoid which tends to occur more laterally. The presence of restricted diffusion on the DWI images suggested that this mass may represent an abscess or epidermoid. The presence of enhancement indicated infection which also fit the clinical picture.\n\nIn regards to cerebellar abscesses, treatment is dictated by the patient's clinical status, the size and location of the abscess and whether or not a capsule exists. Antibiotics with or without aspiration or complete excision may be performed.\n\nOther diagnostic possibilities for a cystic posterior fossa mass include a cystic astrocytoma, hemangioblastoma, arachnoid cyst, and an epidermoid cyst. The presence of fat helps diferentiate dermoids from these other lesions. Intracranial lipomas are homogeneous fatty lesions and should not be confused with a heterogeneous lesion such as a dermoid." }, "Topic": { "Title": "Dermoid Cyst", "Disease Discussion": "Intracranial dermoids are slow growing, congenital, cystic masses that contain not only squamous epithelium, as found in an epidermoid, but also sweat glands, hair, and sebaceous glands. Dermoid cysts(and epidermoid cysts) are not true neoplasms but are inclusions of ectoderm within the neural tube during its closure from the third to fifth week of embryonic development. \n\nIntracranial dermoids are rare. The posterior fossa is the most common location for intracranial dermoids, which can be found anywhere in the CNS. The lesions are most often midline and can have an intra- or extra-axial location. When in the posterior fossa dermoids often have a sinus tract to the skin(dermal sinus) along with a defect of the overlying skull. The dermal sinus can allow the dermoid to become infected by providing direct access to overlying bacteria on the skin.\n\nPresenting symptoms can include headache, seizures, and cranial nerve deficits. The most common presentation is meningitis. There can be a painless lump under the scalp. Dermoid cysts are usually discovered during the first three decades of life with posterior fossa lesions often presenting in infancy and early childhood. Infection or rupture of a dermoid will lead to acute presentation of symptoms.\n\nThe CT appearance of a dermoid cyst is a unilocular, low attenuation, usually hetergeneous, well circumscribed mass. Hounsfeld Units below 0 help comfirm the presence of lipid. A heterogeneous nodule within the mass may represent matted hair. On MR a dermoid will be a hetergeneous mass with multiple regions of high T1 signal due to the liquified fat. If the dermoid has ruptured the high T1 signal will be scattered within the subarachnoid space. \n\nTreatment consists of surgical excision.", "ACR Code": "1.3", "Category": "Neoplasm, benign", "Keywords": "dermoidsposterior fossa dermoid tumors", "Reference": "Smirniotopoulos JG, Teratomas,dermoids, and epidermoids of the head an neck. Radiographics 1995;1437-55.\n\nAkhaddar, A, Mohamed J. Cerebellar abscesss secondary to occipital dermoid cyst with dermal sinus: case report. Surg Neurol 2002;58:266-70.\n\nRuediger S, Terttu A. Ruptured intracranial dermoid cysts. Surg Neurol 2002;57:391-98." } }, { "U_id": "MPX1307", "TAC": [ "MPX1307_synpic20064" ], "MRI": [], "Case": { "Title": "Benign Metastasizing Leiomyoma", "History": "48 year old female presents for Computed Tomography after notifying her primary care provider that years earlier she was told she had a nodule in her lung on chest x-ray.\n\nSurgical History: \nCholecystectomy at age 35\nHysterectomy at age 43 (for fibroids)", "Exam": "Physical Examination: Normal\n\nLabs: None", "Findings": "Multiple bilateral well circumscribed pulmonary nodules, without spiculations or irregularities. No pathologic lymphadenopathy.", "Differential Diagnosis": "Metastatic Malignant Tumor\n\nFungal Infection\n\nGranulomatous Diseases\n\nMuch less likely: Metastatic Benign Tumor (Leiomyoma, Meningioma, Pleomorphic Adenoma, Giant Cell tumor)", "Case Diagnosis": "Benign Metastasizing Leiomyoma", "Diagnosis By": "CT Guided Biopsy", "Treatment & Follow Up": "N/A", "Discussion": "Benign Metastasizing Leiomyoma is an extremely rare disorder, occuring almost exclusively in women (20+ years of age), most of whom have a history of uterine leiomyoma resection or hysterecomy due to large leimyomata. Lesions which metastasize to the lung may be solitary or multiple, appear as well circumscribed rounded lesions, and cannot be distinguished from other causes of pulmonary nodules without tissue sampling. \n\nPatients are usually asymptomatic. Lesions behave as slow growing benign tumors but some reports refer to them as a low grade sarcoma, particularly when found in children. Lesions are generally quite hormone sensitive, though again less so in children. \n\n \nReference(s):\nArmstrong P. et al. Imaging of Diseases of the Chest 3rd Edition. Mosby 2000:351 \n\nGalvin JR. et al. Benign metastasizing leiomyoma. The International Thoracic Teaching Resource: Neoplastic Diseases.http://www.vh.org/adult/provider/radiology/ITTR/BenignMetaLeiomyoma/BngMetaLeiomyoma.html \n\nJoon Beom Seo. et al. Atypical Pulmonary Metastases: Spectrum of Radiologic Findings. Radiographics. 2001;21:403-417" }, "Topic": { "Title": "Benign Metastasizing Leiomyoma", "Disease Discussion": "Benign Metastasizing Leiomyoma is an extremely rare disorder, occuring almost exclusively in women (20+ years of age), most of whom have a history of uterine leiomyoma resection or hysterecomy due to large leimyomata. Lesions which metastasize to the lung may be solitary or multiple, appear as well circumscribed rounded lesions, and cannot be distinguished from other causes of pulmonary nodules without tissue sampling. \n\nPatients are usually asymptomatic. Lesions behave as slow growing benign tumors but some reports refer to them as a low grade sarcoma, particularly when found in children. Lesions are generally quite hormone sensitive, though again less so in children.", "ACR Code": "6.3", "Category": "Neoplasm, benign", "Keywords": "Multiple Pulmonary NodulesLeiomyoma", "Reference": "Armstrong P. et al. Imaging of Diseases of the Chest 3rd Edition. Mosby 2000:351\n\nGalvin JR. et al. Benign metastasizing leiomyoma. The International Thoracic Teaching Resource: Neoplastic Diseases.http://www.vh.org/adult/provider/radiology/ITTR/BenignMetaLeiomyoma/BngMetaLeiomyoma.html" } }, { "U_id": "MPX1375", "TAC": [ "MPX1375_synpic41148", "MPX1375_synpic41149", "MPX1375_synpic41151" ], "MRI": [], "Case": { "Title": "Cryptococcal Pneumonia", "History": "A 53-year-old woman presents to the ED with a three month history of a chronic dry cough, malaise, and increasing dyspnea on exertion. Significant medical history included a positive PPD in 1985 which was treated with 1 year of Isoniazid. Other medical history included hypertension and type II diabetes mellitus. She had immigrated to the United States from the Phillipines two decades ago. She denied any history of smoking or alcohol use. She had also visited the Philippines several months ago.", "Exam": "On examination the patient\u2019s lungs were clear to auscultation. Her heart rate was regular without murmurs, gallops or rubs. Neurologic examination was normal. Her room air resting SaO2 was 99% which quickly fell to 93% with ambulation. Following imaging, bronchioaveolar lavage was conducted revealing Cryptococcus neoformans on fluid culture. Cell count 1 revealed RBC 386, WBC 133, Neutrophils 9, Lymphocytes 24, and Macrophages 67. Cell count 2 revealed RBC 363, WBC 199, Neutrophils 41, Lymphocytes 24, Macrophages 33, and Eosinophils 2. Culture was negative to all else including aerobic cultures, acid fast bacilli, and fungal smears. Subsequent serum labs revealed a negative ANCA, IgE 64, LDH 586, Eosinophils 0, and negative HIV. Serum Cryptococcal antigen testing was also negative.", "Findings": "Chest x-ray demonstrated rounded lobular nodules in the left lower lobe. CT pulmonary angiogram revealed multiple enhancing left lower lobe masses, some with cavitation.", "Differential Diagnosis": "1) Malignancy\n- Metastatic disease: testicular, ovarian, renal, breast, melanoma and sarcoma\n- Lymphoma\n- Benign: hamartomas, papillomatosis, bronchogenic cysts, benign metastasizing leiomyomatosis \n\n2) Infectious\n- Multiple abscesses\n- Septic emboli\n- Granulomatous infections\n- Viral: varicella, measles\n- Parasitic: Paragonimus westermani \n\n3) Inflammatory\n- Wegener\u2019s granulomatosis\n- Sarcoidosis\n- Rheumatoid nodules", "Case Diagnosis": "Cryptococcal Pneumonia", "Diagnosis By": "Bronchioaveolar lavage with fluid culture.", "Treatment & Follow Up": "Due to the symptomatic nature of her disease, treatment was begun with Fluconazol 300 mg by mouth daily for 6 months. Her check-up 1 month later revealed markedly decreased nodular infiltrates on both chest x-ray and CT. The patient also reported resolution of her cough and overall malaise.", "Discussion": "The presentation of this patient along with her positive cultures solidifies the diagnosis of Cryptococcal pneumonia, a rare condition in an otherwise healthy female. Cryptococcus neoformans is a fungus usually acquired via inhalation of dehydrated yeast cells or basidiospores that has been shown in analysis of soils to be found with pigeon excreta. Inhalation of the spores is believed to be the primary means of acquisition. When considering the prevalence of the disease, serologic studies have demonstrated evidence of widespread subclinical infection in individuals without a history of symptomatic infection with most adults having a positive serum antibody to Cryptococcus neoformans. Thus, it appears that the subclinical primary infection is common and the vast majority of patients are asymptomatic. Despite strong serologic evidence, symptomatic Cryptococcus remains a very rare disease in individuals without impaired immunity. An active surveillance conducted in the early 90\u2019s in Alabama estimated the incidence of active Cryptococcus infections at 0.84 cases per 100,000 in non-HIV individuals. However, in patients with advanced HIV infections living in San Francisco and Atlanta in the early 90\u2019s, the incidence was higher and was estimated to be anywhere from 17 to 66 cases per 1000 individuals. Other patients who appear to be at increased risk include cancer patients and those individuals receiving organ transplants. Thus, the subsequent course of the infection (resolution vs. latent infection vs. acute infection with or without dissemination) appears to be primarily determined by the host\u2019s immune status." }, "Topic": { "Title": "Cryptococcal Pneumonia in an Immunocompetent Host", "Disease Discussion": "NOTE: Please EDIT the CATEGORY and LOCATION - Above\n\nYou may use the template below - or [Clear] for a blank page.\n\nLesions/Condition: Cryptococcal Pneumonia\n\nCell of Origin: Cyptococcal Fungal Spores\n\nWHO Grade(s): n/a\n\nSynonyms: Pulmonary Cryptococcosis \n\nAssociations/Predisposing Factors: Immunocompromised state\n\nCommon Locations: Lungs, CNS\n\nDemographics: Individuals immunocompromised with T-cell deficiencies, HIV, transplant history, DM2, chronic steroid use\n\nGross Morphology: Fibrocaseating Granulomata \n\nHistology: Cryptococcus Neoformans v. Grubii via bronchoscopy lavage/culture\n\nSpecial Stains: 1) Gomori's methenamine-silver nitrate stain, 2) Mucicarmine Stain \u2013 stains capsule\n\nGross Appearance: n/a\n\nRadiology: Multiple well defined pulmonary nodules\n\nPrognosis and Treatment: Good for immunocompetent patients as described in this case. Treatment consists of oral antifungal therapy (Flucanozole) for 6months.", "ACR Code": "6.9", "Category": "Infection, fungi", "Keywords": "Cryptococcal Pneumonia", "Reference": "-Chang W et al. Pulmonary Crytpococcosis. Chest 2006; 129:333-340\n\n-Ginsberg M et al. Pulmonary nodules resected at VATS. Radiology 1999; 213:277-282\n\n-Kidd SE et al. Cryptococcus gattii dispersal mechanisms, British Columbia, Canada. Emerg Infect Dis. 2007 Jan. \nhttp://www.cdc.gov/ncidod/EID/13/1/51.htm \n\n-Lindell R et al. Pulmonary Cryptococcosis: CT Findings in Immunocompetent Patients. Radiology 2005; 236:326-331.\n\n-Nadrous H et al. Pulmonary Cryptococcosis in Nonimmunocompromised Patients. Chest 2003; 124:2143-7.\n\n-Sagg M et al. Practice Guidelines for the Management of Cryptococcal Disease. CID 2000; 30:710-8.\n\nhttp://www.cdc.gov/ncidod/dbmd/diseaseinfo/cryptococcosis_t.tm\n\n-Perfect JR, Casadevall A. Cryptococcus. Infectious Disease Clinics of North America 2002;16:837-874. \n\n-Chen L-C, Goldman DL, Doering TL. Antibody response to Cryptococcus neoformans proteins in rodents and humans. Infect Immunol 1999;67:2218-24.\n\n-Thomas CJ, Lee JY, Conn LA. Surveillance of Cryptococcosis in Alabama, 1992-1993. Ann Epidemiol 1998;8:212-6.\n\n-Hajjman A, Conn LA, Stephens DS. Cryptococcosis: population-based multistate active surveillance and risk factors in human immunodeficiency virus-infected persons. Cryptococcal Active Surveillance Group. J Infect Dis 1999;179:449-54." } }, { "U_id": "MPX1398", "TAC": [ "MPX1398_synpic27375", "MPX1398_synpic27376", "MPX1398_synpic27377" ], "MRI": [], "Case": { "Title": "Pneumomediastinum from Blast Trauma", "History": "24 yo man with IED blast injury from OIF with penetrating brain injury. He underwent a decompressive right hemicraniectomy at the 10th CSH. CT chest showed bilateral pneumothoraces and pneumomediastinum, therefore bilateral chest tubes were placed. Patient was then transported to LRAMC, and finally NNMC for definitive care.", "Exam": "BP 158/65, P 91, intubation O2sats 100%\nGCS 3\nBilateral chest tubes and bilateral breath sounds on lung exam.", "Findings": "Pneumomediastinum with air in the anterior aspect tracking up to the thoracic inlet.\nSubcutaneous air noted adjacent to the chest tubes and running up into the axilla bilaterally.\nPneumothoraces bilaterally.\nLeft subclavian line, endotracheal tube, enteric tube, and bilateral chest tubes appropriately placed.", "Differential Diagnosis": "Barotrauma\nPenetrating injury to neck or chest\npositive pressure ventilation\nesophageal rupture\npostoperative mediastinitis", "Case Diagnosis": "Pneumomediastinum from Blast Trauma", "Diagnosis By": "CT with IV and enteric contrast", "Treatment & Follow Up": "Patient maintained in ICU with supportive care.\nPlan is to eventually transfer pt to WRAMC.", "Discussion": "A retrospective study of blast lung injury in Israel found that BLI is not commonly lethal if sufficiently treated, but a large majority (76%) require intubation and mechanical ventilation. Out of 29 patients who met the BLI inclusion criteria of hypoxia and pulmonary infiltrates on CXR, 3 patients had pneumomediastinum and 12 patients sustained pneumothorax. None of those patients had penetration injuries to the neck or chest. Blast lung injury is the second most common primary blast injury (ruptured tympanic membrane is first). The pressure wave from explosive devices causes a transient increase in intrathoracic pressure, leading to alveolar rupture and air dissecting into surrounding tissues.\nOn CXR, the pulmonary infiltrates found in those with BLI occur centrally (bat wing appearance), which can help differentiate from the pleural infiltrates of blunt trauma.\n\nAvidan, Vered et al. \"Blast Lung Injury: Clinical Manifestations, Treatment, and Outcome.\" American Journal of Surgery. 190:6. Dec 2005." }, "Topic": { "Title": "Pneumomediastinum", "Disease Discussion": "Pneumomediastinum refers to the presence of extraluminal gas within the mediastinum. This may result from alveolar rupture, perforation of the tracheobronchial tree or esophagus, or gas leaking into the thorax from the neck, chest wall, or abdomen.\n\nRadiographically, pneumomediastinum is characterized by lucent streaks in the mediastinal soft tissues. A number of radiographic signs of pneumomediastinum result from the gas outlining normal anatomic structures. \nThese signs include:\nthymic sail sign- elevation of the thymus\n\nNacleiros V sign - gas outlining the descending aorta laterally with extension laterally between the parietal pleura and medial hemi diaphragm\n\ndouble bronchial wall sign- gas next to a major bronchus, delineating the bronchial walls \n\ncontinuous diaphragm sign- gas extending posterior to the pericardium delineating the central portion of the diaphragm on the frontal projection \n\n\n\"ring around the artery\" sign- gas surrounding the right main pulmonary artery as seen on the lateral radiograph\n\ntubular artery sign- gas adjacent to the major branches of the aorta, delineating the walls medially, while aerated lung delineates the walls laterally\n\n\nextrapleural sign- gas from the mediastinum extending laterally between the parietal pleura and the diaphragm", "ACR Code": "6.735", "Category": "Trauma", "Keywords": "pneumomediastinum", "Reference": "Brant W, Helms C: Fundamentals of Diagnostic Radiology, 2nd ed, PA, 1999, Williams and Wilkins, 337-338\n\nZylak CM, Standen JR, Barnes GR, MD Zylak CJ: Pneumomediastinum Revisited, Radiographics. 2000;20:1043-1057" } }, { "U_id": "MPX1402", "TAC": [ "MPX1402_synpic16952" ], "MRI": [], "Case": { "Title": "Crohn\u2019s Disease complicated by partial small bowel obstruction", "History": "Teenage (14) boy with abdominal pain and diarrhea.", "Findings": "Scout: proximal partial bowel obstruction (dilated loops of small bowel with CT oral contrast in colon)\n\t-NGT\n\nCT: \tThickened segment of distal small bowel with luminal narrowing\n\t\t-Focal fatty proliferation \u201ccreeping fat\u201d", "Differential Diagnosis": "Small bowel obstruction in a young adult: adhesions, appendicitis, intussusception, incarcerated inguinal hernia, and malrotation.\n\nThickened segment of small bowel: Inflammatory Bowel Disease (IBD), infection, malignancy (lymphoma), and ischemia", "Case Diagnosis": "Crohn\u2019s Disease complicated by partial small bowel obstruction", "Discussion": "Crohn\u2019s disease is a transmural granulomatous inflammatory disease that can affect any part of the GI tract. The peak incidence is between 20 and 40 years of age but many cases present in childhood (especially the early teenage years). \n\t\nCommon presenting symptoms are abdominal pain and diarrhea but GI symptoms may be mild or absent. Weight loss, growth failure, delayed puberty, or fever of unknown origin may be presenting complaint. \n\nThe terminal ileum is involved in the majority of cases. Most children will have involvement of the distal ileum and the right colon. Children also can have isolated involvement of the small bowel with a normal terminal ileum or isolated colonic disease.\n\n\nCT is useful to demonstrate complications such as sinuses, fistulas, abscesses, and phlegmons. It is also able to demonstrate focal fat proliferation \u201ccreeping fat\u201d. CT is also effective at showing thickened bowel wall, luminal narrowing, proximal dilation, and identification of the level of bowel obstruction.\n\n\nThis patient responded well to conservative management." }, "Topic": { "Title": "Crohn's Disease", "Disease Discussion": "Crohn\u2019s disease is a transmural granulomatous inflammatory disease that can affect any part of the GI tract. The peak incidence is between 20 and 40 years of age but many cases present in childhood (especially the early teenage years). \n\t\n\tCommon presenting symptoms are abdominal pain and diarrhea but GI symptoms may be mild or absent. Weight loss, growth failure, delayed puberty, or fever of unknown origin may be presenting complaint", "ACR Code": "7.2", "Category": "Inflammatory, NOS", "Keywords": "IBD" } }, { "U_id": "MPX1349", "TAC": [ "MPX1349_synpic45566" ], "MRI": [], "Case": { "Title": "Sand Aspiration", "History": "A 34 year old man injured by a blast - he was facing the explosion when it went off.", "Exam": "He arrived with a Glasgow coma score of 15 and hypotensive. Physical exam on arrival revealed injuries consistent with the blast including multiple injuries to the face, left flank, back, left lower extremity, and an open distal tibia and fibula fracture with a retained foreign body. \n\nThe bronchoscopy was notable for mild mucosal inflammation and a finding of yellow \u201cmud\u201d adherent to both the tracheal wall and the upper bronchi.", "Findings": "The chest x-ray was \"negative\" and is not included in this report. \n\nChest CT imaging, obtained with the patient lying supine, revealed radiopaque material lining the dependant portions of the trachea as well as the main stem bronchi and bronchioles. \n\nNo particulate matter was noted within the sinuses.", "Differential Diagnosis": "\u2022 Sand Aspiration\n\u2022 Drowning\n\u2022 Blast Lung", "Case Diagnosis": "Sand Aspiration", "Diagnosis By": "Bronchoscopy", "Treatment & Follow Up": "The victim was facing the blast when it went off. The patient was evacuated to ??????. The patient was intubated in the emergency department for declining respiratory status, and taken to the operating room for external fixation and wound debridement. Following surgery, the patient was taken to the ICU and extubated. \n \nOn hospital day 2, copious thick fluid described as \u201cmuddy\u201d was suctioned from the respiratory tract, at which time a well tolerated bronchoscopy was performed and CT imaging of the chest was obtained.\n\nEmpiric antibiotic coverage with meropenim for actinobacter was started, as well as levoquin and cefazolin. The patient was transferred to the ward from ICU on hospital day 2 following improvement in his respiratory status. Over the next several days the patient was taken back to the operating room for revision and further repair of extremity injuries. He continued to recover, and was discharged on hospital day 14 with no further pulmonary complications.", "Discussion": "Sand aspiration has been previously associated with drowning, cave in, and accidental burial. It can be a fatal complication due to obstruction of the airway and subsequent anoxic death. However, to the authors knowledge, it has not previously been associated with blast injuries. \nThe patient described in this report suffered a blast injury, rather than submersion near-drowning or a variation of cave in. This different primary mechanism of injury necessitates consideration of pulmonary damage due to barotrama secondary to the blast itself. Further, the patient exhibited multiple additional wounds, consistent with close exposure to an explosive device. Blast lung, as the condition has been termed, is the second most common manifestation of primary organ damage in blast injuries and is due to the pressure differential across the alveolar-capillary interface. Pulmonary injury can be sustained without evidence of external thoracic injury when the pressure wave carries sufficient force to compress the chest wall posteriorly against the spine. The result is a transient elevation in intrathoracic pressure. The classic imaging finding in pulmonary barotrauma, not present in this case, is described as a bihilar \u201cbutterfly\u201d pattern consistent with pulmonary contusion. Additional findings may include pulmonary infiltrates, pneumothorax, and hemothorax among others." }, "Topic": { "Title": "Sand Aspiration", "Disease Discussion": "Lesions/Condition: Sand Aspiration\n\nSynonyms: Gravel Aspiration, Silt Aspiration\n\nAssociations/Predisposing Factors: Blast injury, Drowning, Near Drowning\n\nThe presentation of sand aspiration is highly variable. Certainly, sand visible within the oral cavity, oropharynx, or nasal passages can be indicative of sand aspiration in the correct clinical context. Clinical presentation can range from rapid death due to total occlusion of the airway and subsequent anoxic death to a spectrum of dyspnea, cough, and variable obstructive symptoms.1-4 \nIn the past, the focus of reported radiographic imaging in sand aspiration has been on chest x-ray. Findings on chest roentgenograms may be highly variable, however Bonilla-Santiago described a characteristic \u201csand bronchogram\u201d in two patients suffering from sand aspiration.2 Both of these patients exhibited particulate matter filling the bronchial tree as evidenced by radiodense material lining the central tracheobronchial tree in one case and linear radiodense opacities in the other. In reported cases of particulate aspiration following accidental burial or cave-in, similar classic sand bronchograms have been reported.3,4 Other findings on x-ray are highly variable, ranging from near normal imaging to pulmonary edema characterized by fluffy, confluent, nodular perihilar opacities.2,4 The general pattern is that of opacification of the airway involved in aspiration.\nMore recent reports have included CT imaging of sand aspiration, though it is not routinely obtained and reports specifically detailing CT findings are limited in number.4 In a recent retrospective examination of post-mortem CT, as opposed to conventional autopsy in the diagnosis of drowning victims, sand and sediment in the bronchial tree were visualized on nearly half of the drowning victims.5 This finding raises the possibility that sand aspiration has been historically under-recognized in drowning and near-drowning incidents. \t\nOn CT, it may be possible to appreciate sand bronchograms in the form of radiodense material filling the bronchial tree, similar to those previously described for plain chest films. These findings may be more apparent in CT imaging when relatively subtle on chest x-ray.4 Additionally, aspirated material may be visible in the trachea as radiodensities, as it was in this case\u2019s presentation. Findings of air fluid levels in the sinuses, while nonspecific and present in a wide variety of situations, can be suggestive of either drowning or aspirated material.5 Dunagan, et al reported findings of air-fluid-sand levels in the maxillary sinuses in one near drowning patient with sand aspiration. CT is not routinely recommended in drowings, however, the true utility of CT in these instances has not been determined.3,4 In the setting of conclusive plain film radiographic findings, CT may not be necessary. \nThere is increasing interest in the use of post-mortem CT in the evaluation of drowning patients which may in time be expanded to use in near-drowning and other causes of sand aspiration with equivocal chest x-ray findings. Post-mortem CT may be especially valuable in determining the course of events and progression of injury leading to death.", "ACR Code": "6.4", "Category": "Trauma", "Keywords": "sandaspirationblast", "Reference": "1) Hewer, C.L. Drowning. Lancet. 1962 1:636.\n2) Bonilla-Santiago J, Fill WL. Sand aspiration in drowning and near drowning. Radiology. 1978 Aug;128(2):301-2.\n3) Choy IO, Idowu O. Sand aspiration: a case report. J Pediatr Surg. 1996 Oct;31(10):1448-50.\n4) Dunagan DP, Cox JE, Chang MC, Haponik EF. Sand aspiration with near-drowning. Radiographic and bronchoscopic findings. Am J Respir Crit Care Med. 1997 Jul;156(1):292-5. \n5) Levy AD, Harcke HT, Getz JM, Mallak CT, Caruso JL, Pearse L, Frazier AA, Galvin JR. Virtual autopsy: two- and three-dimensional multidetector CT findings in drowning with autopsy comparison. Radiology. 2007 Jun;243(3):862-8." } }, { "U_id": "MPX1381", "TAC": [ "MPX1381_synpic17620", "MPX1381_synpic17621", "MPX1381_synpic17622", "MPX1381_synpic17623" ], "MRI": [], "Case": { "Title": "Cholangiocarcinoma - radiographic appearance and biopsy", "History": "84 year old white male with vague RUQ abdominal pain and elevated CA 19-9 marker.", "Exam": "RUQ Tenderness.\n\u2022 CA 19-9: 514 (0-36)\n\u2022 AST: 32\n\u2022 ALT: 53\n\u2022 Alk Phos: 118\n\u2022 Amylase: 56\n\u2022 Lipase: 129\n\u2022 AFP 6.6 (0-10)\n\u2022 DEA 3.0 (0-3.4)", "Findings": "4x4cm hepatic mass with necrotic center\nboth early and delayed enhancement\nassociated left portal vein thrombosis and left hepatic lobe atrophy.\n\nUltrasound images of biopsy of heterogeneous liver mass.", "Differential Diagnosis": "Cholangiocarcinoma\nHepatocellular carcinoma\nAbscess\nMetastatic neoplasm", "Case Diagnosis": "Cholangiocarcinoma - radiographic appearance and biopsy", "Treatment & Follow Up": "US guided biopsy reported as moderately differentiated adenocarcinoma.\n\nUnfortunately, this lesion is non-resectable due to other coexisting disease. The only chance for cure is complete resection.", "Discussion": "Non-resectable due to comorbidities.\n\nThe only chance for cure is complete resection. Palliative care consists of ERCP or PCT stenting to relieve obstruction, possible chemo with 5FU and radioablation. Pain control with possible celiac plexus block." }, "Topic": { "Title": "Cholangiocarcinoma", "Disease Discussion": "\u2022 Discussion: Cholangiocarcinomas are rare slow-growing malignancies of the biliary duct system, that may occur anywhere within the biliary system from the liver to the ampulla of Vater. Cholangiocarcinomas are encountered in 3 geographic regions: intrahepatic, extrahepatic (ie, perihilar), and distal extrahepatic. Perihilar tumors are the most common and intrahepatic tumors are the least common. Perihilar tumors also called Klatskin tumors occur at the bifurcation of right and left hepatic ducts. 95% of these tumors are ductal adenocarcinomas and the remainder are squamous cell tumors. Local extension occurs into the liver, porta hepatis, and regional lymph nodes of the celiac and pancreaticoduodenal chains. The etiology of most bile duct cancers remains undetermined. Long-standing inflammation, as with primary sclerosing cholangitis (PSC) or chronic parasitic infection, has been suggested as playing a role by inducing hyperplasia, cellular proliferation, and, ultimately, malignant transformation. Cholangiocarcinomas is slow growing and tends to invade locally dissecting along tissue planes. In Southeast Asia, chronic infection with liver flukes, Clonorchis sinensis has been causally related to cholangiocarcinomas. It also has an association with ulcerative colitis and primary sclerosing cholangitis. Increased incidence has been noted in exposure to Thortrast radiopaque medium and in rubber industries. Several congenital diseases also show a relationship, including choledochal cysts and Caroli\u2019s disease. \n\n\u2022 Clinical presentation:\nPatients often present with painless jaundice and many patients present with unresectable or metastatic disease. Pruritis and non-specific abdominal pain are other common complaints. Physical exam findings include hepatomegaly (tender/non-tender), a palpable non-tender gallbladder (Courvoisier sign) and splenomegaly secondary to portal hypertension. Lab findings include elevated LFT\u2019s. CEA and CA 19-9 tumor markers may be positive but cholangiocarcinomas does not produce alpha feto proteins (AFP).\n\n\u2022 Imaging:\nInitial evaluation should be with ultrasound and CT. The most common US finding is general ductal dilitation. Focal ductal dilitation, lobar atrophy, bile duct wall thickening and rarely a polypoid mass within the ducts may also be seen. CT demonstrates biliary dilation as well but can show thickening of the bile duct walls more accurately. In peripheral cholangiocarcinomas the CT scan is often nonspecific demonstrating minimal contrast enhancement with a poorly defined isoattenuating or hypoattenuating mass. Delayed enhancement (8-10 min) is useful in hilar tumors. The tumor itself is only identified in about 50% of cases. CT is good at showing lymphadenopathy and lobar atrophy. Cholangiography(ERCP or PTC) is very helpful in demonstrating ductal anatomy and has the added benefit of enabling stent placement for drainage. MRI Cholangiography is being used more frequently and may help define tumor extension into portal vessels.\n\n\u2022 Treatment:\nStenting is very useful in both palliative care to relieve obstruction and for symptomatic relief preop. The only possible cure is complete resection but imaging confirmation of complete resection is often impossible. Lesions are considered unresectable if tumor involves either both lobes of the liver or major portal veins or hepatic arteries. Overall resecatability is about 40%. Chemo and radiation therapy can be used for palliative treatment but show little benefit. Celiac-plexus block via regional injection of alcohol or other sclerosing agent can relieve pain in the mid-back associated with retroperitoneal tumor growth.", "ACR Code": "7.3", "Category": "Neoplasm, carcinoma", "Keywords": "cholangiocarcinomaklatskindilated bile ducts", "Reference": "Alimentary Tract Radiology 5th Edition, Vol 2." } }, { "U_id": "MPX1389", "TAC": [ "MPX1389_synpic42580", "MPX1389_synpic42582" ], "MRI": [], "Case": { "Title": "Os Acromiale", "History": "26 year old male with left shoulder pain.", "Findings": "Plain radiographs demonstrate a subtle lucency in the acromion. A CT ordered to rule out fracture clearly demonstrates a congentially unfused acromion.", "Differential Diagnosis": "Acromion fracture\nNormal unfused ossification center in patients under 25 years\nOs Acromiale", "Case Diagnosis": "Os Acromiale", "Diagnosis By": "CT findings and patient age", "Treatment & Follow Up": "Treatment choices in symptomatic patients include open acromioplasty or arthroscopic acromioplasty." }, "Topic": { "Title": "Os acromiale", "Disease Discussion": "The os acromiale is a persistent ossification center at the free end of the acromion that is present in up to 15% of the population. It forms a synchondrosis with the acromion and articulates with the clavicle. This ossification center typically fuses before 25 years of age. Bilateral os acromiale occur in one third of patients. \n\nFour types of Os acromiale have been described. The most common is non-union between a meso-acromion and a meta-acromian. Less common variations include nonunions at the pre-acromian and meso-acromion as well as meta-acromion and basi-acromion and variations of the three locations. See the second listed source for helpful images. \n\nOs acromiale may cause pain, shoulder impingement syndrome and rotator cuff tears. The appearance may simulate fracture of the acromion. Axillary conventional radiographs, CT, and MR imaging are good at detecting os acromiale.\n\nTreatment choices in symptomatic patients include open acromioplasty or arthroscopic acromioplasty.", "ACR Code": "4.1", "Category": "Anatomy, Normal Variant", "Keywords": "Osacromiale", "Reference": "Resnick, Donald. Diagnosis of Bone and Joint Disorders. \nSaunders; 4 edition. 2002. pages 4576-4577.\n\nPeter Habermeyer, Petra Magosch and Sven Lichtenberg. Classifications and Scores of the Shoulder. Springer Berlin Heidelberg. 2006." } }, { "U_id": "MPX1411", "TAC": [ "MPX1411_synpic23301" ], "MRI": [], "Case": { "Title": "Pathology consistent with leiomyosarcoma.", "History": "69 y/o African-American female with a history of chronic renal insufficiency and hypertension presented with a 2 month history of worsening low back pain.", "Exam": "Cr 2.4, BUN 5.5 (baseline Cr 1.6, BUN 29)\nUA- 26 WBCs/HPF, blood 25/ul, 2+ leukocyte esterase and many bacteria/HPF", "Findings": "Abdominal CT with IV contrast reveals a 5x7x8cm retroperitoneal mass at the level of the juxtarenal IVC and right hydronephrosis. Inferior vena caval venography reveals total IVC occlusion below the renal veins to the retrohepatic region with significant venous collateralization.", "Differential Diagnosis": "Angiosarcoma, leiomyosarcoma, leiomyomatosis, and neurogenic tumor such as paraganglioma", "Case Diagnosis": "Pathology consistent with leiomyosarcoma.", "Treatment & Follow Up": "The patient underwent an exploratory laparotomy with resection of the mass, juxtarenal IVC, right kidney, and right adrenal gland with graft revision of the juxtarenal IVC. She was discharged without complication on post-operative day 5 with scheduled follow-up.", "Discussion": "Inferior vena cava leiomyosarcoma is a rare tumor representing approximately 0.5% of all adult soft tissue sarcomas. Presenting symptoms, management, and prognosis are related to tumor location. Upper IVC leiomyosarcomas occur superior to the hepatic vein, present with Budd-Chiari syndrome, and are the least amenable to resection resulting in the worst prognosis. Middle IVC leiomyosarcomas occur between the hepatic and renal veins, may present with right upper quadrant pain or renovascular hypertension, and have improved survival. Lower IVC leiomyosarcomas occur inferior to the renal vein, may present with right lower quadrant, back, or flank pain or lower extremity edema, are the most amenable to complete resection, and have the best prognosis. 5 year survival among all patients has been reported to be 33-53%." }, "Topic": { "Title": "leiomyosarcoma.", "Disease Discussion": "Inferior vena cava leiomyosarcoma is a rare tumor representing approximately 0.5% of all adult soft tissue sarcomas. Presenting symptoms, management, and prognosis are related to tumor location. Upper IVC leiomyosarcomas occur superior to the hepatic vein, present with Budd-Chiari syndrome, and are the least amenable to resection resulting in the worst prognosis. Middle IVC leiomyosarcomas occur between the hepatic and renal veins, may present with right upper quadrant pain or renovascular hypertension, and have improved survival. Lower IVC leiomyosarcomas occur inferior to the renal vein, may present with right lower quadrant, back, or flank pain or lower extremity edema, are the most amenable to complete resection, and have the best prognosis. 5 year survival among all patients has been reported to be 33-53%.", "ACR Code": "9.3", "Category": "Anatomy, Normal and Measurements", "Keywords": "leiomyosarcomasarcoma", "Reference": "Hollenbeck, et.al. \u201cSurgical Treatment and Outcomes of Patients with Primary Inferior Vena Cava Leiomyosarcoma.\u201d Journal of the\n American College of Surgeons 2003; 197.\nGriffin, AS, Sterchi, JM. \u201cPrimary Leiomyosarcoma of the Inferior Vena Cava: a Case Report and Review of the Literature.\u201d Journal of \n Surgical Oncology 1987; 34: 53-60." } }, { "U_id": "MPX1371", "TAC": [ "MPX1371_synpic20119", "MPX1371_synpic20120", "MPX1371_synpic20122" ], "MRI": [], "Case": { "Title": "Pancreatic Carcinoma", "History": "Painless jaundice.", "Exam": "Elavated CA 19-9 = 185 (37 upper limits normal)", "Findings": "The images through the level of the liver and porta hepatis demonstrate extrahepatic and intrahepatic biliary ductal dilatation. Images through the level of the pancreas demonstrate a 3cm mass in the head of the pancreas. Pelvic images demonstrate thrombi within the right common iliac and left common femoral vein.", "Differential Diagnosis": "Pancreatic carcinoma\nMass due to chronic pancreatitis\nCholangiocarcinoma\nDuodenal/ampullary carcinoma", "Case Diagnosis": "Pancreatic Carcinoma", "Diagnosis By": "CT imaging characteristics, elevated CA 19-9, and clinical history highly suggests the diagnosis of pancreatic CA and make other etiologies far less likely. The finding of multiple DVTs also helps confirm the diagnosis (Trousseau's sign - strongly associated with pancreatic carcinoma). \n\nPatient underwent a Whipple's procedure. \n\nDefinitive diagnosis was made by post-operative tissue path examination:\n\nFINAL DIAGNOSIS:\n (A) PERITONEAL NODULE, BIOPSY:\n \u2022 LYMPH NODE IDENTIFIED (SEE COMMENT).\n \u2022 BENIGN FIBROADIPOSE TISSUE WITH FAT NECROSIS.\n\n (B) DISTAL STOMACH/DUODENUM/HEAD OF PANCREAS/COMMON BILE \n DUCT, WHIPPLE PROCEDURE:\n - MODERATELY TO POORLY DIFFERENTIATED \n PANCREATIC DUCTAL ADENOCARCINOMA.\n - TUMOR IS LOCATED WITHIN THE HEAD OF THE PANCREAS.\n - TUMOR IS 4 CM IN GREATEST DIMENSION.\n+ - IN SITU CARCINOMA IS ALSO PRESENT.\n TUMOR INVADES PERIPANCREATIC ADIPOSE TISSUE, COMMON \n BILE DUCT WALL,AND DUODENUM WALL AND MUCOSA.\n - METASTATIC CARCINOMA IS PRESENT IN FIFTEEN OUT OF \n TWENTY-TWO REGIONAL LYMPH NODES EXAMINED (15/22).\n - DEEP PANCREATIC MARGINS (ANTERIOR AND POSTERIOR \n RETROPERITONEAL MARGINS) ARE INVOLVED BY INVASIVE \n CARCINOMA.\n - DISTAL PANCREATIC, PANCREATIC DUCT, COMMON BILE \n DUCT, GASTRIC AND DUODENAL MARGINS ARE NOT INVOLVED \n BY INVASIVE CARCINOMA.\n - LYMPHOVASCULAR INVASION IS PRESENT.\n - PERINEURAL INVASION IS PRESENT.", "Treatment & Follow Up": "Whipple procedure +/- adjuvant radiation therapy and chemotherapy", "Discussion": "Classic CT imaging findings for pancreatic carcinoma are present in this case to include pancreatic head mass and extrahepatic and intrahepatic ductal dilatation. The finding of multiple DVTs is consistent with Trousseau's sign, a paraneoplastic migratory thrombophlebitis strongly associated with pancreatic and lung cancers." }, "Topic": { "Title": "Pancreatic Carcinoma", "Disease Discussion": "Pancreatic cancer is the 10th most common cancer in the United States and the 4th most common cause of cancer death. It is an aggressive and usually fatal tumor. Most pancreatic cancers occur in the pancreatic head (60%)and less commonly in the body (15%) or tail (5%). 20% diffusely involve the entire gland. The overall 5 year survival rate is less than 5%. The only realistic hope for cure is in early detection and aggressive surgery (Whipple procedure). Imaging modalities utilized in the detection and evaluation of pancreatic carcinoma include ultrasound, MRI, and CT.\n\nThe sensitivity and specificity of transabdominal ultrasound for the detection of pancreatic carcinoma approaches 90% in advanced cases, with much lower sensitivity and specificity in early stage disease. Small carcinomas (2 to 3cm) are solid, hypoechoic, and ill-defined. Larger tumors are more heterogeneous with well defined, lobulated, or irregular margins. Ultrasound may also detect calcifications, ductal dilatation and fluid collections. Pancreatic carcinoma may be surrounded by chronic pancreatitis and ultrasound is not very useful in differentiating the two.\n\nContrast enhanced CT is the most frequently performed study for the evaluation of pancreatic carcinoma. Characteristic findings include a minimally enhancing, hypodense mass that commonly produces the \"double-duct\" sign - a dilated common bile duct and pancreatic duct. The uncinate process often appears blunted. There may be stranding in the peripancreatic mesentery signaling peri-pancreatic invasion. Vascular encasement of the nearby superior mesenteric vessels, portal vein, hepatic artery, or celiac trunk renders the tumor inoperable. \n\nMRI can be used to correlate CT findings and for surgical staging. MRI has a similar sensitivity to CT for detecting peri-pancreatic and vascular invasion. On non-contrast MR imaging, pancreatic carcinomas are typically hypointense on T1 weighted images and hyperintense on T2 weighted images, With gadolium MRI, the most prominent enhancement of the lesion occurs 15 seconds after injection.", "ACR Code": "7.3", "Category": "Neoplasm, carcinoma", "Keywords": "PancreaticCarcinomaImaging", "Reference": "Nishiharu, Taiji, et al. Local Extension of Pancreatic Carcinoma: Assessment with Thin-Section Helical CT versus with Breath-hold Fast MR Imaging-ROC analysis. Radiology 1999; 212 (2): 445-452\n\nPulay, Istvan, et al. Pancreatic Head Mass: What Can Be Done. Journal of the Pancreas 2000; 1 (3 Suppl.): 85-90\n\nWebb WR, Brant WE, and Welms CA. Fundamentals of Body CT, 2nd ed. WB Saunders: St. Louis; 1991: 227-230.\n\nMortele KJ. CT and magnetic resonance imaging in pancreatic and biliary tract malignancies. Gastrointest Endosc 2002; 56(6 Suppl): S206-12\n\nBrant WE. The Core Curriculum - Ultrasound. Lippincot, Williams, and Wilkins: New York; 2001: 79- 80", "External Links": "www://lef.org/protocols/prtcls-txt/t-prtcl-113.html" } }, { "U_id": "MPX1408", "TAC": [ "MPX1408_synpic23222" ], "MRI": [], "Case": { "Title": "Medial deviation of internal carotid artery", "History": "Patient c/o night sweats and fevers.", "Exam": "Clinicians thought they felt multiple enlarged lymph nodes in the axillae and inguinal regions.", "Findings": "Axial CT image of the neck demonstrates medial deviation of the left internal carotid artery. Note that the left internal carotid artery is just below the pharyngeal mucosa in the retropharyngeal fat. \n\nCurved reconstruction of the axial images delineates the medially deviated course of the left internal carotid artery.\n\nIncidentally, the patient had no lymphadenopathy pathologic by size criteria throughout her neck, chest, abdomen, and pelvis study.", "Differential Diagnosis": "Medial deviation of internal carotid artery", "Case Diagnosis": "Medial deviation of internal carotid artery", "Diagnosis By": "Based on imaging", "Treatment & Follow Up": "No treatment required - but clinicians should recognize this abnormality - especially ENT surgeons." }, "Topic": { "Title": "medial deviation of internal carotid artery", "Disease Discussion": "Medial deviation of the internal carotid artery, also known as (aberrant) retropharyngeal internal carotid artery, is an important congenital variant that should be considered in the differential for a retropharyngeal mass. Once found, this finding should be reported to the clinicians so that the devastating consequences of biopsy or surgery is avoided.", "ACR Code": "2.1", "Category": "Congenital, normal variant", "Keywords": "medial deviation of internal carotid arteryretropharyngeal carotid artery", "Reference": "Som PM, et al. Head and Neck Imaging, 4/e. Mosby 2002." } }, { "U_id": "MPX1397", "TAC": [ "MPX1397_synpic31411" ], "MRI": [], "Case": { "Title": "subarachnoid hemorrhage secondary to aneurysm rupture", "History": "27 year old woman presenting to the emergency room with the worst headache of her life.", "Exam": "Nuchal rigidity, but no neurologic deficits.", "Findings": "Noncontrast CT scan of the head demonstrates dense subarachnoid collection in the suprasellar and basilar cisterns, as well as along the tentorium. Note the hydrocephalus demonstrated by the dilatation of the temporal horns and fourth ventricle.", "Differential Diagnosis": "Trauma\nAneurysm rupture \nnonaneurysmal perimesencephalic hemorrhage, arteriovenous malformations (AVM),\nhemorrhagid neoplasm\nhypertensive parenchymal hemorrhage with subarachnoid extension\nanticoagulant therapy", "Case Diagnosis": "subarachnoid hemorrhage secondary to aneurysm rupture", "Diagnosis By": "Angiogram", "Treatment & Follow Up": "After demonstration of the subarachnoid hemorrhage and left internal carotid artery aneurysm, the patient underwent emergent surgical clipping. Three days after surgery she experienced altered mental status, and a repeat angiogram demonstrated vasospasm which was treated with triple H therapy (hypertension, hypervolemia and hemodilution) and remained stable until post operative day eight when she became unresponsive. A CT scan demonstrated a large area of ischemia involving the majority of the left hemisphere. Serial clinical exams demonstrated absence of brain stem reflexes and apnea. Brain death was declared, and after discussion with her family, advanced life support was terminated." }, "Topic": { "Title": "Nontraumatic Subarachnoid Hemorrhage", "Disease Discussion": "The classic presentation of nontraumatic subarachnoid hemorrhage is the acute onset of a severe headache which reaches its maximum intensity within minutes, often referred to as the \u201cthunder clap\u201d headache. Many patients describe this as \"the worst headache of my life\". There may be associated neck stiffness, photophobia, nausea, vomiting, and possibly obtundation or coma.\n\nPhysical examination may show retinal hemorrhages, nuchal rigidity, or focal neurological signs. An altered level of consciousness is seen in approximately one third of patients while meningeal irritation signs are seen in up to 85% of patients and virtually all have nausea. Kernig sign is pain elicited by straightening the knee with the thigh flexed at the hip. Brudzinski sign is pain and/or ridgidity with simultaneous neck and knee/hip flexion. \n\nThe differential diagnosis of a thunder clap headache includes aneurysm thrombosis without rupture, \u201cleakage\u201d into an aneurysm wall, aneurysm rupture with subarachnoid hemorrhage, cerebral vein/dural venous sinus thrombosis, localized meningeal inflammation, nonaneurysmal perimesencephalic hemorrhage, first or worst migraine headache attack, benign exertional headache, and benign thunderclap headache [no associated subarachnoid hemorrhage]. Since early recognition and surgery may benefit patients with aneurysm rupture, all patients with thunderclap headache require evaluation for subarachnoid hemorrhage. In North America, 75% to 90% of nontraumatic subarachnoid hemorrhage is caused by aneurysm rupture. \n\nThe primary diagnostic modalities in the evaluation of subarachnoid hemorrhage include noncontrast computed tomography (CT) scan and, if negative, a lumbar puncture with cerebrospinal fluid (CSF) spectrophotometry. The probability of detecting subarachnoid hemorrhage of CT scans performed at various intervals after the ictus is: day 0, 95%; day 3, 74%; day 7, 50%; day 14, 30%; and day 21, almost zero. It is important to note that the sensitivity of CT in detecting subarachnoid hemorrhage decreases with time, and may miss up to 5% of cases even in the first 12 hours after symptom onset.\n\nMagnetic resonance (MR) imaging is not as sensitive in the detection of acute subarachnoid hemorrhage and does not usually play a role in the initial diagnostic evaluation. MR findings include alteration of CSF (reduced diffusion and bright CSF on DWI, bright on FLAIR). CT has greater availability, lower expense, and faster scanning times. \n\nAcute subarachnoid hemorrhage appears as high attenuation on noncontrast CT within the subarachnoid spaces. Blood will insinuate within the sulci over the cerebral convexities as it mixes with CSF. A focal cisternal or parenchymal hemorrhage may suggest the location of a ruptured aneurysm - although this localization is often postural. Focal anterior interhemispheric blood may be due to an anterior communicating artery aneurysm rupture. Blood in the sylvian fissure may be due to a middle cerebral artery, internal carotid artery terminus, or posterior communicating artery aneurysm rupture. Posterior communicating artery aneurysms may be associated with third cranial nerve palsies and often bleed into the temporal lobe. Posterior inferior cerebellar artery aneurysms often bleed into the fourth ventricle.\n\nNonthrombosed aneurysms may be seen as a well delineated, isodense to slightly hyperdense mass located somewhat eccentrically in the suprasellar cistern or sylvian fissure. \n\nAfter detection of subarachnoid hemorrhage by either CT or lumbar puncture the evaluation can proceed directly to a four vessel catheter angiogram. At some institutions, however, a CT angiogram (CTA) of the head is the preferred next step. Several studies have shown that CTA is excellent at detecting aneurysms larger than 3 mm. When a CTA adequately demonstrates an aneurysm, patients can proceed to definitive treatment without a catheter angiogram. In some institutions, catheter angiograms are preferred to CTA, and are always the next step for patients in whom no aneurysm is detected on CTA or in patients with aneurysms amenable to endovascular intervention by coils or balloon occlusion.\n\nApproximately 90% of all intracranial aneurysms arise from the anterior (carotid) cerebral circulation while 10% arise from the posterior (vertebrobasilar) circulation. The most common locations are the anterior communicating artery (35%), posterior communicating artery origin (30%), middle cerebral artery bifurcation or trifurcation (25%), basilar artery tip (5%), and the posterior inferior cerebellar artery and other sites distal to the circle of Willis (5%). Up to 30% of patients with aneurysmal subarachnoid hemorrhage have multiple intracranial aneurysms, that may present in \"mirror image\" locations. Patent aneurysms are seen as a contrast filled outpouching from the vessel wall on angiography. Ruptured aneurysms typically have an irregular or lobulated appearance. Localized vasospasm and subarachnoid hemorrhage are also helpful signs of aneurysm rupture, particularly in those patients with multiple aneurysms.\n\nRisk factors for development of intracranial aneurysms include numerous connective tissue disorders and account for approximately 5% of cases. Associated conditions include: autosomal dominant polycystic kidney disease, hypertension, aortic coarctation, alpha-1-antitrypsin deficiency, Ehlers-Danlos syndrome, and fibromuscular dysplasia. Other etiologies include drug abuse (cocaine), infection (mycotic aneurysms), neoplasm, or trauma. \n\nIn approximately 15-30% of patients with nontraumatic subarachnoid hemorrhage, no aneurysm is found despite a complete four vessel cerebral angiogram. These patients fall into two distinct subsets: a nonaneurysmal perimesencephalic hemorrhage pattern and an \u201caneurysmal\u201d pattern. In the first (perimesencephalic) subset, the hemorrhage is typically anterior to the brainstem and within the interpeduncular fossa or ambient cisterns and is thought to result from rupture of small pontine or perimesencephalic veins.\n\nIn the second subset of patients, subarachnoid hemorrhage fills the suprasellar cistern and extends into the sylvian or anterior interhemispheric fissures. Patients with an aneurysmal pattern of nontraumatic subarachnoid hemorrhage are at risk for rebleeding, cerebral ischemia, and neurological deficit Repeat four-vessel cerebral angiography demonstrates an aneurysm in 5% to 10% of these cases. Non-identification of the aneurysm on the first angiogram may be secondary to local vasospasm with incomplete filling of the aneurysm. \n\nAcute subarachnoid hemorrhage carries a mortality rate of 25% in the first 24 hours and 50% within three months. Causes of sudden death include a large intraparenchymal hematoma, destruction of brain tissue, acute hydrocephalus, increased intracranial pressure, myocardial ischemia, cardiac arrhythmias, and respiratory failure. Of the patients that reach a major medical center the leading causes of death are the sequelae of the initial hemorrhage, recurrent aneurysmal rupture and vasospasm with ischemic stroke. While the potential complications of subarachnoid hemorrhage are extensive, the primary goal of medical management is to address the leading causes of death by trying to prevent vasospasm and recurrent hemorrhage. \n\nVasospasm typically occurs seven days (5-10 days) after the subarachnoid hemorrhage, and is prevented predominantly via administration of a calcium channel blocker such as nimodipine, which decreases blood pressure but increases cerebral blood flow. Maintaining adequate hydration is also important. Transcranial Doppler evaluation is helpful in monitoring for the development of vasospasm by detecting elevated intracranial arterial velocities. This is seen most frequently in the distal internal carotid artery and the proximal portions of the anterior and middle cerebral arteries, regardless of the location of the aneurysm rupture. Once vasospasm occurs, medical therapy is aimed at increasing cerebral blood flow, predominantly with volume expansion and drug-induced hypertension. Transluminal angioplasty is extremely successful in dilating vasospastic arteries.\n\nThe prevention of recurrent hemorrhage, which is highest immediately after the initial subarachnoid hemorrhage, is through early surgical or endovascular treatment of the ruptured aneurysm. Endovascular therapy with platinum coils was introduced in 1990 as an alternative to surgical clipping. The International Subarachnoid Aneurysm Trial (ISAT) demonstrated a significant risk reduction with endovascular therapy over surgery for ruptured aneurysms amenable to either therapy. Endovascular treatment is particularly useful in posterior circulation aneurysms, such as a basilar tip aneurysm, in which the surgical approach is extremely difficult. With the exception of difficult access to posterior circulation aneurysms, surgical clipping is an effective and definitive treatment modality of ruptured aneurysms. Patients with subarachnoid hemorrhage should be evaluated in treatment centers that offer both neurosurgery and neuroendovascular treatment, allowing the neurosurgeons and interventional neuroradiologists to assess the advantages and disadvantages of clipping or coiling for each individual patient.\n\nIn summary, nontraumatic subarachnoid hemorrhage is the most common secondary cause of the worst headache of life and 75% to 90% of nontraumatic subarachnoid hemorrhage is caused by aneurysm rupture. Since early diagnosis and treatment of aneurysm rupture may improve the patient\u2019s outcome, all patients presenting with the worst headache of life require evaluation for subarachnoid hemorrhage with a noncontrast CT scan and a lumbar puncture if the CT scan is negative. Once subarachnoid hemorrhage is detected, either a CT angiogram or a catheter angiogram should be performed, preferably at a facility with both interventional neuroradiologists and neurosurgeons. This allows the patient to undergo aneurysm coiling or clipping and be appropriately managed for common complications such as vasospasm or recurrent hemorrhage.", "ACR Code": "1.7", "Category": "Hemorrhage", "Keywords": "subarachnoid hemorrhageaneurysmthunderclap", "Reference": "http://www.jem-journal.com/article/PIIS0736467905000673/related", "External Links": "http://www.jem-journal.com/article/PIIS0736467905000673/related" } }, { "U_id": "MPX1407", "TAC": [ "MPX1407_synpic16606", "MPX1407_synpic16607", "MPX1407_synpic16608" ], "MRI": [], "Case": { "Title": "Penetrating orbital trauma", "History": "27 y.o. man was in a combat firefight in Afghanistan.", "Exam": "\u2022 Hand-grenade fragments on face, to include right eye.\n\u2022 Minimal light sensitivity OD.\n\na CT was performed in Afghanistan to determine treatment and mobilization.", "Findings": "Radiopaque fragments in right orbit near expected location of the optic nerve", "Differential Diagnosis": "Optic nerve avulsion\nFragment missed optic nerve, or did not sever", "Case Diagnosis": "Penetrating orbital trauma", "Diagnosis By": "Surgery", "Treatment & Follow Up": "Surgical debridement.\nThe globe was intact, however the patient still lost vision.", "Discussion": "A grenade went off directly in front of him with fragments embedding into his face, to include his right eye.\n\nPatient was airlifted to medical center for surgery where optic nerve damage was verified." }, "Topic": { "Title": "Optic nerve", "Disease Discussion": "The second cranial nerve, responsible for the special sensation of sight, is the optic nerve. This is not really a \"nerve\", but is actually a post-synaptic\nwhite-matter tract that connects the retinal ganglion cells to the occipital (visual) cortex, via the chiasm, lateral geniculate body, and the optic radiations.\n\nThe optic nerve is clinically tested by looking for reactivity to light, followed by testing of the visual fields - either at the bedside or using test equipment.\n\nBoth pupils should react (constrict) when light is shone in either eye.\n\nMany diseases may affect the Optic nerve, including demyelination (Multiple Sclerosis), orbital inflammation (infection and non-infectious), and trauma.\n\n\nClinical Eye Exam Simulator:\nhttp://rad.usuhs.mil/rad/eye_simulator/eyesimulator.html\n\nLabled normal image: http://rad.usuhs.mil/rad/radbrowser2/head/CT/hn046.html", "ACR Code": "1.1", "Category": "Glossary", "Keywords": "optic nerve", "External Links": "rad.usuhs.mil/rad/radbrowser2/head/CT/hn046.html" } }, { "U_id": "MPX1355", "TAC": [ "MPX1355_synpic55466" ], "MRI": [], "Case": { "Title": "Nodular Sclerosing Hodgkin\u2019s Lymphoma", "History": "A previously healthy 23 y/o woman presents with a 4-month history of itchy skin, night sweats, and a 20-lb unintentional weight loss.", "Findings": "\u2022 Anterior (superior) mediastinal mass, surrounding the great vessels and aortic arch.", "Differential Diagnosis": "Mediastinal Mass:\n\u2022 Thymoma \n- Most common 1\u00b0 anterior mediastinal mass (20%)\n\u2022 Lymphoma\n\u2022 Germ Cell Tumors\n\u2022 Mediastinal Cysts\n\u2022 Pericardial, Bronchogenic, Enteric, Thymic\n\u2022 Aneurysm of Ascending Aorta\n\u2022 Thyroid/Parathyroid Tissue", "Case Diagnosis": "Nodular Sclerosing Hodgkin\u2019s Lymphoma", "Diagnosis By": "Pathology", "Treatment & Follow Up": "Standard treatment: ABVD w/XRT\nAdriamycin [doxorubicin], Bleomycin, Vinblastine, Dacarbazine\n\nPrognosis is good, especially for young pts with early-stage disease 5 year survival rate of 90%", "Discussion": "\u2022 Signs & Symptoms\nOften asymptomatic \nMost common = painless lymphadenopathy\n1/3 of pts present w/systemic symptoms\nFatigue, generalized pruritis, \u201cB\u201d symptoms [low-grade fever, night sweats, weight loss]\nMediastinal masses may also produce mass effects\n\n\u2022 Subtypes\nNodular Sclerosing\nMixed Cellularity \nLymphocyte-Depleted\nLymphocyte-Rich\nNodular Lymphocyte-Predominant\n\n\u2022 Nodular Sclerosing Subtype\nMost common subtype in the US\nAffects females > males\nMedian age of onset = mid-20\u2019s\n\n\u2022 Bimodal peak distribution of onset \nYoung adults (15-35) and late adulthood (>55)\nAssociated with EBV and HIV\n\nhttp://www.uptodate.com/contents/anterior-mediastinal-mass-lesions\nhttp://emedicine.medscape.com/article/201886-overview" }, "Topic": { "Title": "Nodular Sclerosing Hodgkin\u2019s Lymphoma", "Disease Discussion": "Discussion: \nThe right paratracheal stripe is usually 2mm wide, but may be up to 5mm wide. An enlarged paratracheal stripe (>5mm) is an important marker for otherwise subtle adenopathy, as well as tracheal tumor, mediastinal inflammation or hemorrhage, pleural thickening or pleural effusion. The margins of the paratracheal stripe are: \n1. distal end\u2014formed by the azygous vein\n2. medial margin\u2014the air-soft tissue interface along the right mucosal surface of the trachea\n3. outer margin\u2014begins around the medial end of the clavicle and is formed by the RUL plural surface\nThe stripe ends where the RUL bronchus goes under the azygous vein as it arches anteriorly to empty into the SVC.\nThe malignant lymphomas are divided into Hodgkin\u2019s and non-Hodgkin\u2019s groups. Sir Thomas Hodgkin was the first to describe Hodgkin\u2019s disease in 1932. Hodgkin\u2019s can present at any age, but it is more prevalent among adolescents and young adults. It typically presents as painless, rubbery lymphadenopathy involving the superficial lymph node groups. Cervical nodes are involved nearly 70% of the time. Approximately half of patients also have splenomegaly. Mediastinal involvement occurs in approximately 10% of patients, and mediastinal involvement is characteristic of the Nodular Sclerosing type (as in this patient). Cutaneous involvement can occur and is usually a late complication. Patients may also present with constitutional symptoms (night sweats, pruritis, fatigue, weight loss, etc) with widespread disease. \nThe diagnosis of Hodgkin\u2019s disease is made by lymph node biopsy (as was done in this patient). There are 4 histological types:\n1.\tNodular Sclerosing (>50%, most common; worst prognosis)\n2.\tMixed cellularity (25%)\n3.\tLymphocyte predominant (5%; best prognosis)\n4.\tLymphocyte depleted (5%)\nStaging of Hodgkin\u2019s disease is made by the use of CXR, BM biopsy, and CT imaging. There are 4 stages:\n1.\tStage I\u2014confined to one lymph node group (90% 5-yr survival rate)\n2.\tStage II\u2014confined to 2 or more lymph node groups on one side of the diaphragm\n3.\tStage III\u2014involving nodes on both sides of the diaphragm\n4.\tStage IV\u2014Extra-nodal disease (60% 5-yr survival rate) \nTreatment involves radiation therapy and/or chemotherapy. Patients with Stage I or Stage II Hodgkin\u2019s disease are usually treated by radiation therapy, while Stage III & IV disease is usually treated with radiation therapy and chemotherapy.\nReferences:\n1. Mendenhall, NP. \u201cThe role of radiation in the management of Hodgkin\u2019s disease: an update,\u201d Cancer Invest 1999; 17:47-55.\n2. Potter, R. \u201cPediatric Hodgkin\u2019s Disease,\u201d Eur J Cancer 1999; 35: 1466-1477.\n3. Wirth, A, et al, \u201cCurrent trends in the management of early stage Hodgkin\u2019s disease,\u201d Aust NZ J Med 1999; 29: 535-544\n4. http://www.surgical-tutor-org/tutorials/hodgkins.htm\n5. http://rad.usuhs.mil/rad/chest_review/mediasti/mediasti.html", "ACR Code": "68.342", "Category": "Neoplasm, hematopoietic", "Keywords": "Nodular Sclerosing Hodgkin\u2019s LymphomaHodgkin\u2019sLymphoma", "Reference": "References:\n1. Mendenhall, NP. \u201cThe role of radiation in the management of Hodgkin\u2019s disease: an update,\u201d Cancer Invest 1999; 17:47-55.\n2. Potter, R. \u201cPediatric Hodgkin\u2019s Disease,\u201d Eur J Cancer 1999; 35: 1466-1477.\n3. Wirth, A, et al, \u201cCurrent trends in the management of early stage Hodgkin\u2019s disease,\u201d Aust NZ J Med 1999; 29: 535-544\n4. http://www.surgical-tutor-org/tutorials/hodgkins.htm\n5. http://rad.usuhs.mil/rad/chest_review/mediasti/mediasti.html" } }, { "U_id": "MPX1426", "TAC": [ "MPX1426_synpic41470" ], "MRI": [], "Case": { "Title": "Adrenal Myelolipoma", "History": "68 yo male with history of gross hematuria with no other complaints", "Exam": "Vitals within normal range, normal labs", "Findings": "-solitary left adrenal mass measuring 2.8cm in diameter\n- focal areas of hypodensity within a circumscrimed higher attenuation mass. \n-no areas of calcification", "Differential Diagnosis": "Adrenal Adenoma\nAdrenal Carcinoma\nAngiomyolipoma\nLiposarcoma\nAdrenal Myelolipoma", "Case Diagnosis": "Adrenal Myelolipoma", "Diagnosis By": "Axial CT imaging revealing hypodense area within an adrenal mass is virtually diagnostic", "Treatment & Follow Up": "Majority of patients are asymptomatic and hence no further action is necessary. Larger lesion may require closer follow up as mass effect may cause various symptoms. In those cases, surgical resection may be considered.", "Discussion": "The etiology of this patient's episode of gross hematuria is unclear, and there is no indication that there may have been hemorrhage within the adrenal myelolipoma as there are no areas of acute bleeding or calcification present. Hence it is reasonable that the cause of hematuria be extra-adrenal. The size of this patient's adrenal mass does not appear to interrupt the architecture of other surrounding organs. Prognosis of this patient is good in terms of the adrenal mass as he has been asymptomatic with normal hormonal labs. Follow up imaging may be indicated to monitor the growth of the mass." }, "Topic": { "Title": "Adrenal Myelolipoma", "Disease Discussion": "Lesions/Condition: Adrenal Mass\n\nPathophysiology: There is no clear understanding of how these lesions originate, however one largely accepted theory explains it as metaplasia of reticuloendothelial cells of blood capillaries in the adrenal gland in response to various stimuli. \n\nAssociations/Predisposing Factors: rare potential of spontaneous rupture producing retroperitoneal hemorrhage. \n\nCommon Locations: Most myelolipomas occur within the adrenal gland but in rare cases are found extra-adrenal such as mediastinum, perirenal and pararenal retroperitoneum\n\nDemographics: Male to female ratio is 1:1, occurs mostly at 5th through 7th decades\n\nHistology: mature adipose tissue intermixed with hematopoietic elements to include megakaryocytes\n\nGross Appearance: size varies from several millimeters to 30cm\n\nRadiology:\nCT is the diagnostic modality of choice as evidence of macroscopic focal fat density, interspersed with the higher-attenuation myeloid tissue\n\nPrognosis and Treatment: Adrenal Myelolipomas are usually benign lesions and do not undergo malignant transformations. Most patients are asymptomatic. However some potential complications include spontaneous rupture resulting in retroperitoneal hemorrhage, which is noted to be rare.", "ACR Code": "8.3", "Category": "Neoplasm, benign", "Keywords": "Adrenal Mass", "Reference": "El-Mekresh MM, Abdel-Gawad M, El-Diasty T, et al. Clinical, radiological and histological features of adrenal myelolipoma: review and experience with a further eight cases. Br J Urol. Sep 1996;78(3):345-50.\n\nBhansali A, Dash RJ, Singh SK, et al. Adrenal Myelolipoma: Profile of Six Patients with a Brief Review of LIterature. International Journal of Endocrinology and Metabolism. March 2003; Vol1,No1." } }, { "U_id": "MPX1423", "TAC": [ "MPX1423_synpic16631" ], "MRI": [], "Case": { "Title": "Moderately differntiated adenocarcinoma of stomach (antrum). Tissue sampling during upper endoscopy.", "History": "History of early satiety and weight loss.", "Findings": "Upper GI study reveals markedly distended stomach with poorly opening pyloris and delayed passage of contrast through the pyloric channel into duodenum.\n\nCT images reveal markedly distended, debri filled stomach with focal narrowing of pyloris and decompressed duodenum.", "Differential Diagnosis": "Malignant tumor: primary gastric adenocarcinoma, metastatic disease\nPeptic ulcer disease\nInflammatory disoders: Crohn's, corrosive stricture, sarcoidosis, tuberculosis, syphilis, amyloidosis\nCongenital disorders: antral mucosal diaphragm, annular pancreas", "Case Diagnosis": "Moderately differntiated adenocarcinoma of stomach (antrum). Tissue sampling during upper endoscopy.", "Treatment & Follow Up": "Partial gastrectomy" }, "Topic": { "Title": "Gastric Outlet Obstruction", "Disease Discussion": "The second leading cause of gastric outlet obstruction (30 to 35% of cases) is malignant tumor. Most of these cases are due to advanced gastric carcinoma and less commonly related to metastatic cancer or invasion of adjacent malignancies such as bile duct cancer or gallbladder cancer. Malignant obstruction causes luminal narrowing due to an annular constricting lesion or diffuse mural infiltration by tumor. Approximately one-third of patient with malignancy have no pain, and most others have a history of pain of less than 1 year\u2019s duration. \n\nThe most common cause of gastric outlet obstruction in adults is peptic ulcer disease (60% to 65% of cases). The obstructing lesion is usually in the duodenum, occasionally in the pyloric channel or prepyloric gastric antrum, and rarely in the body of the stomach. Obstruction is from severe luminal narrowing resulting from spasm, acute inflammation and edema, muscular hypertrophy, or contraction of scar tissue. Distortion and scarring of the duodenal bulb make peptic ulcer disease the most likely cause of obstruction, while a radiographically normal bulb increases the likelihood of underlying malignant disease. These patients often have a long history of ulcer pain. \n\nInflammatory disorders which cause gastric outlet obstruction include Crohn\u2019s disease, sarcoidosis, syphyllis, tuberculosis, amyloidosis, corrosive stricture, pancreatitis, and cholecystitis. Congenital disorders such as antral mucosal diaphragm (antral web), gastric duplication and rarely annular pancreas can cause outlet obstruction. Other causes of outlet obstruction include gastric volvulus, bezoars, hypertrophic pyloric stenosis, and prolapsed antral mucosa.", "ACR Code": "7.3", "Category": "Differential Diagnosis", "Keywords": "GastricObstruction", "Reference": "Eisenberg RL. Clinical Imaging: An Atlas of Differential Diagnosis, 3rd ed. Philadelphia, PA: Lippincott, 1996." } }, { "U_id": "MPX1432", "TAC": [ "MPX1432_synpic21430" ], "MRI": [], "Case": { "Title": "Bilateral sacral fractures", "History": "History (can include gestational age, or age in days, weeks, months):77 y/o Caucasian female with past medical history significant for Stage IIa bladder cancer treated with radiation therapy complaining of progressive left leg and hip pain that occurs while standing. Onset of pain and difficulty ambulating began just after her treatment for bladder cancer a few months ago. Over the last three weeks, she has lost the ability to walk without experiencing pain. Pain radiates from her left buttock to her knee and relieved when sitting, lying down, or using a heating pad. Patient has had two recent physical therapy visits, which provided notable relief but most recent visit provided no such relief. Patient also notes prior history of pain in her buttocks while walking. She has a questionable history of a fall a few weeks ago for which she did not seek medical care.", "Exam": "Phsical examination is positive straight leg raising test on the left", "Findings": "A-P radiograph of the pelvis can not adequately evaluate the pelvis secondary to obscuration by contrast-enhanced bowel. No hip fracture is seen.Axial CT of sacrum with bone windows shows shows bilateral sacral insufficiency fractures. Coronal reformatted CT of sacrum confirms bilateral sacral fractures.", "Differential Diagnosis": "Differential Diagnosis for these findings in this case:1.\tInsufficiency fracture secondary to radiation therapy2.\tInsufficiency fracture secondary to osteoporosis3.\tFracture secondary to trauma", "Case Diagnosis": "Bilateral sacral fractures", "Treatment & Follow Up": "Sacral fractures can be treated non-operatively or operatively. Conservative treatment with non-operative modalities include protected weight bearing, bracing, and recumbent traction. These are applied to sacral fractures that are stable when patient is without neurologic compromise, patient can tolerate recumbency, and patient is without significant soft tissue defect.Surgical treatment is warranted if any of the above parameters is not met. This can be accomplished with anterior pelvic fixation methods, sacroiliac screws, lumbopelvic fixation, or retrograde sacral pinning.", "Discussion": "Sacral fractures, especially insufficiency fractures in which stresses of normal activity are greater than the resistance ability of bone, are not uncommon in elderly women. Sacral fractures may be caused by high impact trauma or metastatic cancer or secondary to radiation therapy, steroid therapy, or osteoporosis. Several risk factors are associated with sacral insufficiency fractures, the most common being osteoporosis. However, rheumatoid arthritis, corticosteroid therapy, osteomalacia, Paget\u2019s disease, osteogenesis, osteopetrosis, and fibrous dysplasia are also potential risk factors (1). Patients with sacral insufficiency fractures typically present with low back pain, buttock pain, groin pain, or hip pain. The most common site of sacral fractures is the sacral ala. The fractures typically course vertically parallel to the sacroiliac joints. Sacral insufficiency fractures are often times difficult to diagnose for several reasons. Findings on plainradiographs are subtle and may be overlooked due to obscuration of bony detail by bowel gas. Stress fractures are difficult to detect through cancellous bone in patients with osteoporosis. Another reason that this diagnosis is overlooked if the interpreter is not familiary with insufficiency fractures in the sacrum (2). The main radiographic evidence of such a fracture is sclerosis secondary to trabecular compression and callus formation. Additional studies may be performed to confirm the diagnosis. Computed tomography can accurately confirm diagnosis by demonstrating unilateral or bilateral fracture lines in the sacral ala parallel to the sacroiliac joints. With healing, the fracture lines become sclerotic. Magnetic resonance imaging demonstrates fracture lines as decreased areas of signal intensity on T1 weighted images. Bone scintigraphy commonly produces an H-pattern or butterfly pattern of increased signal uptake consistent with bilateral sacral fractures with vertical and horizontal fracture components (3)." }, "Topic": { "Title": "Bilateral sacral fractures", "Disease Discussion": "Sacral fractures, especially insufficiency fractures in which stresses of normal activity are greater than the resistance ability of bone, are not uncommon in elderly women. Sacral fractures may be caused by high impact trauma or metastatic cancer or secondary to radiation therapy, steroid therapy, or osteoporosis. Several risk factors are associated with sacral insufficiency fractures, the most common being osteoporosis. However, rheumatoid arthritis, corticosteroid therapy, osteomalacia, Paget\u2019s disease, osteogenesis, osteopetrosis, and fibrous dysplasia are also potential risk factors (1). Patients with sacral insufficiency fractures typically present with low back pain, buttock pain, groin pain, or hip pain. The most common site of sacral fractures is the sacral ala. The fractures typically course vertically parallel to the sacroiliac joints. Sacral insufficiency fractures are often times difficult to diagnose for several reasons. Findings on plainradiographs are subtle and may be overlooked due to obscuration of bony detail by bowel gas. Stress fractures are difficult to detect through cancellous bone in patients with osteoporosis. Another reason that this diagnosis is overlooked if the interpreter is not familiary with insufficiency fractures in the sacrum (2). The main radiographic evidence of such a fracture is sclerosis secondary to trabecular compression and callus formation. Additional studies may be performed to confirm the diagnosis. Computed tomography can accurately confirm diagnosis by demonstrating unilateral or bilateral fracture lines in the sacral ala parallel to the sacroiliac joints. With healing, the fracture lines become sclerotic. Magnetic resonance imaging demonstrates fracture lines as decreased areas of signal intensity on T1 weighted images. Bone scintigraphy commonly produces an H-pattern or butterfly pattern of increased signal uptake consistent with bilateral sacral fractures with vertical and horizontal fracture components (3).", "ACR Code": "4.9", "Category": "Trauma", "Keywords": "Bilateral sacral fracturessacral fracturesfractures", "Reference": "1.\tLin JT, Lane JM. \u201cSacral Stress Fractures,\u201d J Womens Health. 12(9): 879-88, 2003. 2.\tCooper KL, Beabout JW, Swee RG. \u201cInsufficiency Fractures of the Sacrum,\u201d Radiology. 156:15, 1985.3.\tResnick, Diagnosis of Bone and Joint Disorders, 4th Edition, Philadelphia, PA W.B. Saunders, 2002, pp. 2914-2915." } }, { "U_id": "MPX1416", "TAC": [ "MPX1416_synpic50980", "MPX1416_synpic50983", "MPX1416_synpic50984" ], "MRI": [], "Case": { "Title": "Idiopathic Constipation/Retained Stool", "History": "33 year old woman with constipation since childhood. She presented with abdominal distension and pain.", "Findings": "Plain Film: Mottled gas Pattern in the LUQ (large intestine).\n\nCT: Markedly abnormal study demonstrating stool-distended bowel extending from the distal transverse colon to the level of the rectum, with associated compression of several structures, most noticeably the distal right ureter with associated mild dilatation of the collecting system. There is also shift of the adnexal structures and uterus to the left. The largest dilatation of the bowel appears to be at the level of the sigmoid colon which measures approximately 11.6cm in short axis diameter.", "Differential Diagnosis": "DDX for Mottled Gas Pattern on Plain film:\n*Stool\n*Abscess\n*Sponge\n*Bezoar\n\nDDX for Constipation:\n*Poor Diet\n*Poor Bowel Habits\n*Hirschsprung's Disease\n*Medications: Iron, antacids, narcotic pain meds...\n*Laxative abuse\n*Anal Fissures", "Case Diagnosis": "Idiopathic Constipation/Retained Stool", "Diagnosis By": "Exclusion of Hirschprungs and Celiac Disease by negative Bx", "Treatment & Follow Up": "Patient has had biopsies to test for Hirschprungs and Celiac Disease - both of which were negative. She received treatment to clean out her bowel." }, "Topic": { "Title": "Constipation", "Disease Discussion": "Constipation affects about 2% of the population in the US. Women and the elderly are more commonly affected. Frequency of bowel movements can vary from person to person. Some people may go 3 times a day and others 1-2 times a week. When a patient goes longer than 3 days, the stool will begin to harden and will be more difficult to pass. \n\nConstipation can be caused by motility disorders, inadequate water or fiber intake, eating a lot of dairy, stress, resisting the urge to have a bowel movement, overuse of laxatives which can weaken the bowel muscles, hypothyroidism, medications, depression, colon cancer, and pregnancy, among others. Symptoms can include but are not limited to infrequent or difficulty having a bowel movement, distended abdomen, pain, and vomiting. \n\nIn most cases, extensive testing does not need to be performed. If constipation last for more than two weeks, blood tests can be obtained to detect hormonal imbalances or barium studies, colonoscopy or CT to detect obstruction. \n\nConstipation can be treated with a laxative, stool softener, and/or a well balanced diet, exercise, and drinking plenty of water.", "ACR Code": "7.1", "Category": "Idiopathic or Unknown", "Keywords": "constipationHirschsprungceliac disease" } }, { "U_id": "MPX1429", "TAC": [ "MPX1429_synpic46943" ], "MRI": [ "MPX1429_synpic46945", "MPX1429_synpic46946", "MPX1429_synpic46947" ], "Case": { "Title": "Glioblastoma multiforme", "History": "The patient is a 50 y/o caucasian female in otherwise good health that complains of frequent headaches over the last 3 months that wake her from sleep at night and are present when she wakes in the morning. Sometimes accompanied by nausea and vomiting", "Exam": "PE: all systems beside neuro have no abnormalities\nNeuro: CN II-XII intact\n-Sensation- pain, temp and light touch normal, neg Romberg\n-Strength- 5/5 on right side, some deficit on left with 3/5 strength noted in lower extremity\n-No cerebellar or gait deficits", "Findings": "* CT w/out contrast: mass effect evident with poorly defined isodense lesion with surrounding vasogenic edema\n*T1 image w/out contrast: mass effect with isodense, poorly defined lesion involving splenium of the corpus callosum\n* Flair: poorly demarcated, hyperintense mass adjacent to ventricles with mass effect, lesion appears to be crossing the corpus collosum and invading opposite hemisphere\n* DWI: hyperintense lesion adjacent to ventricles and crossing the corpus collosum\n*ADC: poorly defined hypointense mass demonstrating mass effect on ventricles", "Differential Diagnosis": "1) Lymphoma\n2) GBM\n3) metastatic disease\n4) CNS melanoma", "Case Diagnosis": "Glioblastoma multiforme", "Diagnosis By": "Brain biopsy with pathology demonstrating characteristics of Grade IV astrocytoma.", "Treatment & Follow Up": "PT underwent a brain biopsy to confirm the diagnosis. After the procedure, pt became obtunded and showed symptoms of herniation. She was taken to the OR and a temporal lobectomy was performed. By the time new imaging was obtained, the mass effect had filled the space created by the lobectomy. The pt regained her cognitive ability but developed left sided hemiparesis. She was discharged to hospice care and passed away 3 months later.", "Discussion": "This patients presentation and the rapidity of her deterioration is consistent with the general coarse associated with this diagnosis. However, the initial imaging findings suggested that the lesion was more likely to be a CNS lymphoma. These tumors also arise quickly, are highly cellular, grow rapidly, and often appear deep in the brain near the corpus collosum. They can also produce a \"butterfly\" appearance on imaging. There is usually less edema and mass effect present as compared to a GBM. They tend to be hyperintense to grey matter on DWI and hypointense on ADC map, as was the case with this patient. A GBM is generally hyperintense on both DWI and ADC, which was not the case here. Pathology confirmed that this lesion was a GBM and not a CNS lymphoma." }, "Topic": { "Title": "Glioblastoma multiforme (GBM, Astrocytoma Grade 4/IV)", "Disease Discussion": "Lesions/Condition: Gioblastoma multiforme\n\nCell of Origin: Astrocytes\n\nWHO Grade(s): The term glioblastoma multiforme is reserved for Grade IV gliomas. By definition, they meet at least 3 out of 4 of the following criteria: 1) nuclear atypia 2) mitosis 3) endothelial proliferation 4) necrosis\nGrading system for Gliomas\n*Grade I: none of above criteria\n*Grade II: at least one of above criteria is met\n*Grade III: at least 2 of above criteria met\n*Grade IV: at least 3 of above criteria\n\nSynonyms: Grade IV astrocytoma, Grade IV Glioma\n\nAssociations/Predisposing Factors: \n* Incidence slightly higher in caucasians than other ethnicities\n* More common in men than women (3:2)\n* More common with increasing age (40 years and older)\n\nCommon Locations: GBMs generally arise in the deep white matter but may also cross the corpus collosum and invade the opposite hemishpere producing a \"butterfly\" tumor.\n\nHistology: Variable- most often consists of poorly differentiated astrocytes with nulcear atypia and mitotic activity. Necrosis and microvascular proliferation may be significant, especially in high grade lesions such as a GBM.\n\nSpecial Stains: no special stains are required\n\nGross Appearance: Tumors appear large and amorphous with several infiltrating, finger-like extensions that can represent microscopic invasion beyond the obvious tumor sites.\n\nRadiology:\n* CT: tend to be irregularly shaped, hypodense lesions with peripheral ring-like enhancement surrounded by edema.\n* MRI with and without contrast- study of choice; on T1 = ring-enhancing lesions with hypodense core, has high-signal intensity on T2\n\nMolecular Biology:\n* IDH1 mutations are more common in secondary GBM - associated with a better prognosis\n* MGMT status may predict a better response to standard therapy with radiation and temozolomide chemotherapy\n\nPrognosis and Treatment: poor\n*Median survival without treatment ~ 3 months\n*With treatment, mean survival is 8-15 months\n* treatment is often palliative and consists of debulking surgery, external beam radiation and chemotherapy with temozolomide\n\nMost patients are eligible to volunteer for clinical trials.\n\nhttp://emedicine.medscape.com/article/283453-overview\nhttp://www.cancer.gov/cancertopics/pdq/treatment/adultbrain/HealthProfessional/page4\nhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3792931/", "ACR Code": "1.3", "Category": "Neoplasm, glial", "Keywords": "Glioblastoma GBManaplastic astrocytomaastrocytoma" } }, { "U_id": "MPX1419", "TAC": [ "MPX1419_synpic43433", "MPX1419_synpic43434", "MPX1419_synpic43435", "MPX1419_synpic43437" ], "MRI": [], "Case": { "Title": "Moderately Differentiated Adenocarcinoma (Hereditary Nonpolyposis Colon Cancer)", "History": "42 yo male with abdominal pain", "Findings": "Acute abdominal series demonstrates a normal PA chest radiograph without subdiaphragmatic free air. There are differential air fluid levels in the mid-abdomen, with dilated loops of small bowel. There is a paucity of bowel gas projecting over the rectum, and stool is noted in the RLQ.\n\nContrast enhanced axial CT images through the abdomen demonstrate a bulky, irregular heterogeneous cecal mass with pericolic inflammation and asymmetric wall thickening. Multiple dilated fluid filled loops of small bowel are noted, some of which contain air fluid levels. Additionally, there is fecalization of the terminal ileum. The appendix is normal.", "Differential Diagnosis": "Adenocarcinoma (Hereditary Nonpolyposis Colon Cancer)\nLymphoma\nMetastasis\nCarcinoid Tumor\nGIST\nDiverticulitis\nCrohn\u2019s Disease\nTyphlitis (Neutropenic Colitis)\nIschemic Necrosis of the Cecum (rare \u2013 patients with a history of cardiac failure and arrhythmia).\n\nReference:\nHoeffel et al. RadioGraphics 2006;26:1373-1390.", "Case Diagnosis": "Moderately Differentiated Adenocarcinoma (Hereditary Nonpolyposis Colon Cancer)", "Diagnosis By": "The patient underwent an exploratory laparotomy and subsequent subtotal colectomy. Pathologic evaluation of the surgical specimen demonstrated a 10.1 cm moderately differentiated adenocarcinoma involving the cecum. 0/24 lymph nodes were positive for metastasis, the appendix and ileal mucosa were normal." }, "Topic": { "Title": "Hereditary Nonpolyposis Colon Cancer", "Disease Discussion": "Hereditary nonpolyposis colon cancer (HNPCC) is also known as Lynch syndrome, of which, there are two types. Lynch I has no history of associated cancers. Lynch II often presents with other cancers most commonly of ovarian or uterine origin. Both types are predisposed to a higher frequency of proximal colonic tumors with advanced pathology compared to typical colon cancer. \n\nHNPCC typically presents during the fourth and fifth decades and characterized by adenomas that progress much more rapidly to carcinoma than typical. These are not as numerous as those in Familial adenomatous polyposis (FAP). It also has a more heterogenous genetic basis than FAP, with most cases linked to chromosomes 2,3, and 7. As such, the diagnosis is often based upon familial history of early colorectal cancer presentations (prior to 50 years of age).\n\nGenetic testing is often difficult secondary to multiple site mutations and is positive in approximately 80% of affected individuals. However, agressive surveillance of all first degree relatives of individuals clinically suspected to have the syndrome is warranted.\n\nScreening should begin at age 20 to 25 consist of colonoscopy every other year. Alternatively, genetically positive individuals should be considered for prophylactic colectomy. Affected females should consider early childbearing followed by prophylactic total abdominal hyterectomy and bilateral oophorectomy.\n\nImaging characteristics are those of the respective cancers. In the case of colon cancer, it often presents as an intraluminal filling defect with bowel wall thickening and adjacent inflammation (fat stranding). It is often focal and is frequently accompanied by adjacent lymphadenopathy. It can be difficult to differentiate this entity from diverticulitis which can also present with similar findings. However, the wall thickening and pericolonic inflammation are more likely to be focal in colon cancer, whereas it more likely to involve larger segments in diverticulitis (greater than 10 CM). Also, diverticulitis is much less likely to have associated lymphadenopathy and intaluminal mass.", "ACR Code": "7.3", "Category": "Neoplasm, carcinoma", "Keywords": "hereditary nonpolyposis colon cancerHNPCCLynch syndrome", "Reference": "Abeloff: Clinical Oncology, 2nd ed., copyright 2000, Churchill Livingstone, Inc.\n\nChintapalli,et al., Diverticulitis versus Colon Cancer: Differentiation with Helical CT findings., Radiology, 1999: 210; 429-435, RSNA, 1999." } }, { "U_id": "MPX1424", "TAC": [ "MPX1424_synpic17817", "MPX1424_synpic18483", "MPX1424_synpic18484", "MPX1424_synpic18486" ], "MRI": [], "Case": { "Title": "Intralobar Pulmonary Sequestration", "History": "This 12 year old girl has recurrent left lower lobe pneumonia. She is otherwise healthy. Other previous medical history is noncontributory.", "Exam": "Current physical exam nonrevealing.", "Findings": "CXR: The mediastinal structures and pulmonary vascularity are normal in appearance. Symmetric aeration is noted bilaterally. Slight increased parenchymal opacity is noted in the left lower lobe posteriorly. Overlying bony thorax is unremarkable.\n\nCT: There is an area of increased lucency in the inferior left lower lobe, with multiple dilated abnormal blood vessels. The area is supplied predominantly by a large artery arising from the aorta just above the aortic hiatus. Drainage is to the left inferior pulmonary vein (not shown).", "Differential Diagnosis": "Sequestration\nCystic Congenital Adenomatoid Malformation \nBronchiectasis\nTuberculosis", "Case Diagnosis": "Intralobar Pulmonary Sequestration", "Diagnosis By": "Systemic Arterial Supply (imaging)", "Treatment & Follow Up": "Treatment: Uncomplicated surgical resection. \n\nPathology: Lung, left lower lobe, partial lobe resection. Lung parenchyma and pleura with mucus-filled cyst like bronchi, lymphoid hyperplasia, numerous pulmonary macrophages, thick-walled vessels, and fibrosis consistent with clinical history of pulmonary sequestration.", "Discussion": "Multimedia movie showing origin of vessel from descending thoracic aorta:\nhttp://rad.usuhs.mil/medpix/include/multimedia/MV002.MPG" }, "Topic": { "Title": "Intralobar Pulmonary Sequestration", "Disease Discussion": "Pulmonary sequestration is a congenital anomaly of the bronchopulmonary foregut in which there is a nonfunctional segment of lung. The blood supply is anomalous, arising from the systemic circulation (ie. the aorta or bronchial arteries ). By definition, there is no typical communication with the bronchial tree or with the pulmonary arteries. Intralobar and extralobar discrimination is based primarily upon venous drainage, and the presence of an independent pleural lining (as in the extralobar type). The intralobar variant drains to the pulmonary veins or left atrium, the extralobar type to the systemic venous system (the inferior vena cava or the azygous system). Both gain blood supply from the systemic arterial circulation, frequently from below the diaphragm, and identification of this confirms the diagnosis (although failure to identify the arterial supply does not exclude it). \n\nIn comparison, intralobar sequestrations usually become manifest during adolescence or adulthood, whereas extralobar sequestrations present at birth or soon thereafter (or may be suspected based upon prenatal ultrasonography). Intralobar sequestrations are three times more common with a male predominance, and a much lower incidence of associated anomalies (10% with associated skeletal, foregut, or diaphragmatic anomalies). Extralobar sequestrations may have associated anomalies in up to 65% of patients, including diaphragmatic defects, pulmonary hypoplasia, bronchogenic cysts, and cardiac anomalies. Intralobar sequestrations present with recurrent pneumonias, chronic cough, or dyspnea, or may be completely asymptomatic. Other complications of intralobar sequestrations include hemoptysis, and intrathoracic hemorrhage, and where there is marked vascular shunting, cardiac decompensation. Extralobar sequestrations, presenting at birth or infancy, may manifest as cyanosis, respiratory distress, feeding difficulties, failure to thrive, and recurrent pneumonias. Both predominantly are located in the left base in 60-90%. Treatment of both is resection.\n\n==========================================\nAnimation showing origin of pulmonary vessel from descending thoracic aorta:\nhttp://rad.usuhs.mil/medpix/multimedia_files/mv002.mpg", "ACR Code": "6.1", "Category": "Congenital, malformation", "Keywords": "SequestrationPulmonaryIntralobar", "Reference": "Binnet EF, Kalla A: Lung intralobar and extralobar sequestration. In Radiology Resource and Review, 2000, CD-ROM, version 6.5, Medical College of Georgia and the American Roentgen Ray Society.\n\nBoiselle PM, McLoud TC: Case Review: Thoracic Imaging, Mosby, St. Louis, 2001, p 142. \n\nBramson RT, Blickman JG: Pediatric Imaging. In Primer of Diagnostic Imaging, Second edition, Mosby, St. Louis, 1997, p. 748.", "External Links": "rad.usuhs.mil/medpix/multimedia_files/mv002.mpg" } }, { "U_id": "MPX1457", "TAC": [ "MPX1457_synpic52424" ], "MRI": [], "Case": { "Title": "Burst Fracture of L1", "History": "Pt is a 58yo man presented with focal back pain. One day prior to presentation he fell from a ladder at a height of 6ft and landed on his feet.", "Exam": "No neurologic abnormalities. Focal 9/10 low back pain.", "Findings": "Radiograph of L-spine:\nCompression fracture involving the posterior aspect of L1 with posterior displacement of the fracture fragment--concern for burst fracture\n\nCT:\nL1 burst fracture\nKnown polycystic kidney disease incidentally imaged", "Differential Diagnosis": "Compression vs. Burst fracture", "Case Diagnosis": "Burst Fracture of L1", "Diagnosis By": "CT", "Treatment & Follow Up": "Surgical spinal fusion", "Discussion": "Important to note that this is a post-traumatic burst fracture rather than pathologic fracture. \n\nBurst fractures:\n-Typically occurs in cervical or lumbar vertebrae after axial loading (falling and landing on feet)\n-Mechanism: Nucleus pulposus of disk is forced into vertebral body, which, in turn, shatters\n-Fracture must involve all 3 columns of vertebra\n-All burst fx should be considered unstable since 42-58% of fx result in neurologic injury\n-Spinal cord injury usually caused by retropulsion of fragment of posterior aspect of vertebral body\n-These fractures are commonly associated with calcaneal fractures" }, "Topic": { "Title": "Burst Fracture of L1", "Disease Discussion": "Lesion/Condition Name: Burst Fracture of L1\n\nAssociations/Predisposing Factors: Commonly associated with calcaneal fractures after a fall and landing on feet\n\nCommon Locations: Cervical and lumbar vertebrae\n\nRadiology: Retropulsed fragment of the posterior aspect of the vertebral body. Fracture invovles all 3 of the vertebral columns\n\nPrognosis and Treatment: Spinal fusion surgery", "ACR Code": "3.4", "Category": "Trauma", "Keywords": "Burst Fracture" } }, { "U_id": "MPX1454", "TAC": [ "MPX1454_synpic24715" ], "MRI": [ "MPX1454_synpic24717", "MPX1454_synpic24718", "MPX1454_synpic24719" ], "Case": { "Title": "Von Meyenburg Complex - Multiple biliary hamartomas", "History": "45 yo female with multiple hepatic, non enhancing lesions seen on CTPA", "Exam": "Shortness of breath prompted CTPA. Normal labs (including LFTs)", "Findings": "CTPA shows multiple, non enhancing hepatic low density lesions, 4-10 mm.\nMR further characterizes these lesions as non enhancing, fluid signal lesions.", "Differential Diagnosis": "Numerous hepatic cysts\nPolycystic liver disease\nHepatic microabscesses\nMultiple metastases\nCholedochal cyst 4-5", "Case Diagnosis": "Von Meyenburg Complex - Multiple biliary hamartomas", "Diagnosis By": "Imaging characteristics suggest Von Meyenburg", "Treatment & Follow Up": "Recommend 3 month follow up to document stability vs tissue biopsy.", "Discussion": "Incidence: .15-2.8% of autopsies\nEtiology: failure of involution of embryonic bile ducts\nAssociations: polycystic liver disease\nSymptoms: asymptomatic\n\nBile duct hamartoma, aka von Meyenburg complex, is a benign tumor composed of disorganized bile ducts and ductules and fibrocollagenous stroma. Although bile duct hamartoma is benign, there have been reports of an association of cholangiocarcinoma with multiple bile duct hamartomas. \nBile duct hamartoma has a nonspecific imaging appearance and can simulate metastases or microabscesses. Therefore, histologic diagnosis is required." }, "Topic": { "Title": "Von Meyenburg Complex - Multiple biliary hamartomas", "Disease Discussion": "Incidence: .15-2.8% of autopsies\nEtiology: failure of involution of embryonic bile ducts\nAssociations: polycystic liver disease\nSymptoms: asymptomatic\n\nBile duct hamartoma, aka von Meyenburg complex, is a benign tumor composed of disorganized bile ducts and ductules and fibrocollagenous stroma. Although bile duct hamartoma is benign, there have been reports of an association of cholangiocarcinoma with multiple bile duct hamartomas. \nBile duct hamartoma has a nonspecific imaging appearance and can simulate metastases or microabscesses. Therefore, histologic diagnosis is required.", "ACR Code": "7.3", "Category": "Congenital, malformation", "Keywords": "Multiple bile duct hamartomaVon Meyenburg ComplexMultiple hepatic low density lesions", "Reference": "CT and MR Imaging of Benign Hepatic and Biliary Tumors. Karen M. Horton, MD, David A. Bluemke, MD, Ralph H. Hruban, MD, Philippe Soyer, MD, PhD and Elliot K. Fishman, MD Radiographics. 1999;19:431-451.\n\nRadiology Review Manua, 5th ed. Dahnert. p722." } }, { "U_id": "MPX1458", "TAC": [ "MPX1458_synpic13273" ], "MRI": [ "MPX1458_synpic13275", "MPX1458_synpic13276", "MPX1458_synpic13277" ], "Case": { "Title": "Necrotizing fasciitis", "History": "57 y/o diabetic male presents to ER with painful swollen right upper leg progressing over two days.", "Exam": "temp 102\nwbc 36,000 with 85% neutrophils and bandemia\nlungs: CTAB\nheart: regular; rate 100\nabdomen: soft, NT, ND, normal BS\nright leg: warm, tense, mottled skin, tender to palpate", "Findings": "Severe edema of the deep fascia of the proximal quadriceps muscle group is seen on CT extending posteriorly to its insertion on the linea aspera.\nFat sat T2 axial imaging shows extensive edema in the deep facia of several muscles, the soft tissues, and the vastus intermedius/lateralis, and the tensor fascia lata.\nSomewhat paradoxically, the fat sat gadolinium enhanced axial T1 images do not demonstrate enhancement of the fascia, perhaps do to its normal ligamentous character.", "Differential Diagnosis": "Necrotizing fasciitis\nCellulitis\nHemorrhage\nMyositis\nLarge DVT", "Case Diagnosis": "Necrotizing fasciitis", "Diagnosis By": "The constellation of physical and imaging findings, patient history, vital signs, and laboratory tests are enough to confirm the diagnosis.", "Treatment & Follow Up": "Editors Note: the author of this teaching file did not report on treatment and follow up. However, treatment involves extensive fasciotomy, debridement, multi-antibiotic therapy, and hyperbaric oxygen treatments." }, "Topic": { "Title": "Necrotizing fasciitis", "Disease Discussion": "Necrotizing fasciitis spreads suddenly and rapidly. The infection located in the deep fascia along which is spreads as it migrates into the surrounding softer tissues.\n\nInfections usually include multiple organisms which take advantage of conditions of local hypoxia acute tissue injury, or systemic immunosupression such as that seen in patients with diabetes or cancer.\n\nIf the causitive organisim is anaerobic subcutaneous air may be seen radiographically.\n\nNecrotizing fasciitis is almost always fatal without treatment. A combination of surgical debridement including fasciotomy, aggressive antibiotic therapy, and hyperbaric oxygen treatment combined are the best theraputic regimen for these patients.", "ACR Code": "4.2", "Category": "Infection, bacteria", "Keywords": "Necrotizingfasciitisinfection", "Reference": "http://www.emedicine.com/EMERG/topic332.htm\nhttp://www.emedicine.com/DERM/topic743.htm\nAtlas of Human Anatomy. Netter FH. Chiba, Summit, NJ" } }, { "U_id": "MPX1452", "TAC": [ "MPX1452_synpic58265" ], "MRI": [], "Case": { "Title": "Pulmonary valve stenosis", "History": "21 y.o. asymptomatic man with an incidental finding on a screening chest radiograph", "Exam": "IV/VI holosystolic murmur heard best at the right upper-sternal border", "Findings": "Chest radiograph findings:\n- Left mediastinal mass, a prominent pulmonary artery\n\nCardiac gated CT (with and without contrast) findings:\n- Enlarged main pulmonary artery measuring 4.4cm\n- Enlarged left pulmonary artery measuring 3.9cm\n- Normal right pulmonary artery measuring 2.2 cm\n- Pulmonary valve stenosis without subpulmonic membrane. Pulmonary valve is diffusely thickened. \n\nThere is incomplete coaptation of the valve in diastole with a regurgitant area of 0.16 cm2.\n- Enlarged inferior vena cava", "Differential Diagnosis": "\u2022 Pulmonary valve stenosis\n\u2022 Chronic pulmonary hypertension\n\u2022 Pulmonary artery aneurysm\n\u2022 Idiopathic pulmonary artery dilation", "Case Diagnosis": "Pulmonary valve stenosis", "Diagnosis By": "CT Measurement of Pulmonic valve", "Treatment & Follow Up": "CT measurement of the stenotic pulmonary valve with regurgitant cross-sectional area of 0.16cm2 and characteristic dilatation of main and left pulmonary arteries with normal right pulmonary artery. \n\nIn this patient with mild, asymptomatic, pulmonary valve stenosis with pressure gradiant >30mmHg is monitored with survelliance echocardiograhpy every 2-3 years, as per the 2008 ACC/AHA adult congenital heart disease guidelines.", "Discussion": "Please see the linked disease topic for general discussion of a dilated pulmonary artery." }, "Topic": { "Title": "Dilated Pulmonary Artery", "Disease Discussion": "Pulmonary artery dilation is most commonly an acquired sequela of chronic pulmonary hypertension, although rarely idiopathic dilation of the pulmonary trunk does occur, a diagnosis that can only be conferred after exclusion of underlying cardiac pathology and confirmatory measurements of normal right ventricular and pulmonary artery pressures. \n\nChronic pulmonary hypertension (resting mean pulmonary artery pressure > 25mm Hg or >30mm Hg with exercise) is most commonly the result of hypoxic lung disease such as obstructive lung disease or fibrosis. Less commonly, pulmonary hypertension may occur secondarily as the result of scleroderma, CREST syndrome, chronic pulmonary embolism or thrombotic disease, chronic left-to-right shunting, intravascular pulmonary metastases, or chronic parasitic infection. \n\nLess commonly, pulmonary artery dilation can be seen in the context of a congenitally stenotic pulmonary valve. The stenotic valve creates a high pressure jet of blood that results in post stenotic dilation of the main and left pulmonary artery. The right pulmonary artery is spared thanks to a sharp, 90 degree take-off from the main pulmonary artery that allows it to avoid the high pressure flow. \n\nAlternatively, a pulmonary artery aneurysm may be initially interpreted as concentric pulmonary artery dilation. Causes of pulmonary artery aneurysms included mycotic aneurysm, Marfan syndrome, Behcet's disease, or may be iatrogenic following an intravascular procedure. \n\nOn PA or AP chest xray, pulmonary artery dilation will appear as a left mediastinal bulge, and may be confused for a mediastinal mass between the aortic arch and border of the left ventricle. \n\nOn chest CT, the diameter of a dilated pulmonary artery may be directly measured as being greater than 29mm, a finding that is 87% sensitive and and 89% specific for pulmonary hypertension. Additional CT findings suggestive of pulmonary hypertension include a ratio of pulmonary artery diameter to aorta diameter greater than 1:1, as well as decreased caliber of peripheral pulmonary vessels due to vasoconstriction, mosaic lung attenuation, and right ventricular dilation.\n\nIn the setting of pulmonary valve stenosis, the main and left pulmonary arteries are dilated, the right pulmonary artery retains normal diameter, and the right ventricle may be dilated due increased resistance across the stenotic valve. \n\nManagement and follow up for dilated pulmonary artery is dictated by the underlying etiology.", "ACR Code": "5.9", "Category": "Vascular", "Keywords": "Pulmonary ArteryPulmonary HypertensionPulmonary Valve", "Reference": "1.Castaner E, Gallardo X, et al. Congenital and Acquired Pulmonary Artery Anomalies in the Adult: Radiologic Overview. RadioGraphics 2006(26): 349-371.\n\n2.Chen JJ, Manning MA, et al. CT Angiography of the Cardiac Valves: Normal, Diseased, and Postoperative Appearances. RadioGraphics 2009(29):1393-1412.\n\n3. Nguyen ET, Silva CIS, et al. Pulmonary Artery Aneurysm and Pseudoaneurysms in Adults: Findings at CT and Radiography. AJR February 2007(188): W126-W134." } }, { "U_id": "MPX1460", "TAC": [ "MPX1460_synpic27175", "MPX1460_synpic27176" ], "MRI": [], "Case": { "Title": "Mucus Plug", "History": "26 y/o man with traumatic brain injury had oxygen saturation decrease to mid 80\u2019s which would not correct with O2 by face mask.", "Exam": "Pt. with tachypnea and increased respirations.", "Findings": "There is a large loculated mucous plug within the right main stem bronchus, from the level of the carinaand extending into the bronchus intermedius and its branching airways within the right lower lobe to affect mostly the basal segment of the right lower lobe. There is consolidation in the medial basal and posterior basal segments of the right lower lobe with associated pleural fluid collection.", "Differential Diagnosis": "foreign body, mucus plug, infection [fungus, TB, pneumonia], bronchogenic carcinoma, carcinoid tumor, adenocystic carcinoma, endobronchial metastases, lymphoma.", "Case Diagnosis": "Mucus Plug", "Diagnosis By": "Radiologic and by aspiration" }, "Topic": { "Title": "Mucus Plug", "Disease Discussion": "Mucus plugs have numerous causes which include dysfunctional cilia, transport defects seen at the cellular level, pathology that causes airflow obstruction/edema/inflammation, and hypersecretion of the goblet cells. Some disease processes known to cause these problems include cystic fibrosis, pneumonia, COPD, bronchiectasis, bronchitis, asthma, Kartagener\u2019s syndrome, tuberculosis, aspergillous ect. \n \nThe exact mechanism of mucus plugging is not known. Mucus accumulation is governed by the rate of mucus secretion and clearance through epithelial reabsorption, evaporation, cough transport, and ciliary transport. A defect in any one of these systems can disrupt the balance and cause pathology. It is postulated in infammatory processes that the inflammation and edema impair the mucociliary transport system, and epithelial reabsorption causing an inability to effectively clear the mucus that is produced. Accummulation of mucus in lungs with mucosal edema and bronchoconstriction give optimal conditions for airway plugging. \n \nOther causes of increased mucosal production are decreased cilia motility include inhaled pollutants. The most notorious of these is cigarette smoke which is also one of the major risk factors for developing COPD. Under optimal conditions, mucus can be propelled by cilia at speeds up to 10mm/min with cilia beating at 20Hz. Normal functioning cilia can clear 50% of particulate matter introduced into the lung in approximately 30 minutes. However, this lung function can be dramatically reduced in acute and chronic lung processes leading to pulmonary dysfunction.\n \nThere are a variety of methods to control the accumulation of mucus in the pulmonary system. Proposed methods include inhibiting hypersecretion, stimulating ciliary clearance, and stimulating cough clearance. It was believed that mucolytic agents such as N-acetylcysteine help decrease the viscosity and elasticity of the mucus allowing for easier clearance. However, studies involving this medication have not shown a significant effect in the clearance of mucus. Chest physical therapy which moves mucus by gravity, vibration has been demonstrated to increase mucus clearance and is a commonly emplyed therapy. Bronchodilators are also often used to help open the airways. However, the best method for decreasing pathologic mucus in the pulmonary system is to treat and control the underlying disorder.", "ACR Code": "6.3", "Category": "Obstruction or Stenosis", "Keywords": "mucusplugatlectasis", "Reference": "Bronchial Mucology and Related diseases, edited by Luigi Allegra, Pier Carlo Baga, Raven Press, NY,NY, 1990\n\nAirway Secretion, Physiological Bases for the control of mucous hypersecretion, edited by Tamotsu Takishima, Sanae Shimura , Marcel Dekker INC, NY,NY 1994\n\nHarrison's Principles of Internal Medicine, Braunwald, Fauce, Kasper, Hauser, Longo, Jameson, Mcgraw Hill Companies, 2001" } }, { "U_id": "MPX1459", "TAC": [ "MPX1459_synpic43456", "MPX1459_synpic43457", "MPX1459_synpic43459" ], "MRI": [], "Case": { "Title": "Poorly Differentiated Non-Small Cell Lung Carcinoma", "History": "An 82-year-old female with productive cough and chest pain.", "Findings": "Dual-energy PA and subtraction soft-tissue-selective radiographs demonstrates nodular, irregular pleural thickening involving the right upper and mid peripheral lung fields. Blunting of the right costophrenic angle is noted. \n\nDual-energy PA subtraction bone-selective radiograph exhibits no areas of abnormal calcification within the region of pleural thickening.\n\nLateral chest radiograph demonstrates nodular pleural thickening involving the right upper lung margin, and a small pleural effusion is noted.\n\nWhen compared to the chest radiograph from 3.5 months prior, this area of nodular, irregular pleural thickening, and right pleural effusion is relatively new.\n\nContrast enhanced axial CT images through various levels of the chest demonstrate a unilateral right sided pleural effusion, with mildly enhancing circumferential, nodular, irregular thickened pleura, encasing the right hemithorax with a rindlike appearance. Additionally, there is focal nodularity of the mediastinal pleura. There is no significant adenopathy, nor evidence of a chest wall abnormality", "Differential Diagnosis": "Metastatic Adenocarcinoma: \nLung\nBreast\nOvarian\nStomach\nKidney\nMalignant Mesothelioma\nMesothelial Hyperplasia", "Case Diagnosis": "Poorly Differentiated Non-Small Cell Lung Carcinoma", "Diagnosis By": "A biopsy was performed.", "Discussion": "The biopsy specimen\u2019s immunoprofile was as follows:\n\nCytokeratin - Positive\nVimentin - Positive\nS-100 - Focally positive\nSmooth Muscle Actin - Negative\nCalretinin - Negative\n\nThis immunoprofile, along with the morphologic features seen on HE stained sections, are consistent with a poorly differentiated non-small cell lung carcinoma." }, "Topic": { "Title": "Poorly Differentiated Non-Small Cell Lung Carcinoma", "Disease Discussion": "Pleural effusion with nodular pleural thickening on chest radiographs or CT are an indication of malignancy. The pleural effusion may be secondary to metastatic adenocarcinoma, malignant mesothelioma, or less commonly invasive thymoma, or in a patient with AIDS, Kaposi sarcoma. Metastatic adenocarcinoma accounts for 95% of cases of pleural thickening with effusion, while mesothelioma is a relatively rare cause with approximately 5% of cases. Lung, and breast adenocarcinomas most frequently metastasize to the pleura. Other tumors, such as lymphoma, colon, pancreas, kidney, or ovarian are other diagnostic considerations. Until thoracocentesis or pleural biopsy is performed, mesothelioma or metastatic disease cannot be distinguished.\n\nCT is more advantageous over chest radiography in evaluating nodular pleural thickening. All pleural surfaces are evaluated for enhancing tumor implants, in addition to the presence of pleural effusions. Circumferential pleural thickening, including involvement of the mediastinal pleura is more often due to malignancy than benign pleural disease. CT also assesses for adjacent lung or chest wall involvement, adenopathy, or evidence of a primary tumor such as an occult lung cancer, breast mass, or thymoma.", "ACR Code": "6.3", "Category": "Neoplasm, metastatic", "Keywords": "Non-Small Cell Lung CarcinomaMalignant Pleural DiseaseNodular Pleural Thickening", "Reference": "Wang et al. RadioGraphics 2004; 24:105-119\nKuhlman et al. RadioGraphics 1997;17:63-79\nAisner J. Chest 1995;107:332-344\nFraser et al. Synopsis of Diseases of the Chest. Third Edition. Elsevier Saunders. Philadelphia, PA. 2005." } }, { "U_id": "MPX1433", "TAC": [ "MPX1433_synpic52647", "MPX1433_synpic52648" ], "MRI": [], "Case": { "Title": "Dacryocystocele with dacryocystitis and periorbital cellulitis", "History": "A 4 month-old boy presents with left eye swelling for about 48hours that started with dark discoloration on left lower lid. No history of trauma.", "Exam": "Afebrile. Left eye has periorbital swelling with palpable mass on medial canthus. No discharge.", "Findings": "A cystic mass located anteromedial to left globe", "Differential Diagnosis": "\u2022 \tDacryocystocele with or without dacryocystitis \n\u2022 \tPeriorbital cellulitis \n\u2022 \tOrbital cellulitis \n\u2022 \tMeningocele \n\u2022 \tEncephalomeningocele \n\u2022 \tHemangioma \n\u2022 \tDermoid cyst\n\u2022 \tGlioma", "Case Diagnosis": "Dacryocystocele with dacryocystitis and periorbital cellulitis", "Diagnosis By": "Head CT imaging", "Treatment & Follow Up": "Due to significant swelling around the eye, treatment for this patient included IV and topical antibiotics, probing, drainage and surgical marsupialization under general anesthesia.", "Discussion": "A dacryocystocele is a grey-blue cystic swelling often filled with mucoid material below the medial canthus. It is a rare complication of congenital nasolacrimal duct obstruction. It often results from incomplete canalization of the lower part of the nasolacrimal duct at the valve of Hasner (anatomical) and secondary obstruction proximally at the Rosenmuller valve from distension of the sac and compression of the canal system (functional).\n Incidence of imperforate NLD in full-term fetuses is 35-73% with spontaneous resolution in about 85-95% of patients by age 1. It is more common in females and often presents unilaterally. Complications include dacryocystitis, cellulitis, astigmatism, narrowing of lid fissure and respiratory difficulty from mass effect." }, "Topic": { "Title": "Dacryocystocele", "Disease Discussion": "A dacryocystocele is a grey-blue cystic swelling often filled with mucoid material below the medial canthus. It is a rare complication of congenital nasolacrimal duct obstruction. It often results from incomplete canalization of the lower part of the nasolacrimal duct at the valve of Hasner (anatomical) and secondary obstruction proximally at the Rosenmuller valve from distension of the sac and compression of the canal system (functional).\n Incidence of imperforate NLD in full-term fetuses is 35-73% with spontaneous resolution in about 85-95% of patients by age 1. It is more common in females and often presents unilaterally. Complications include dacryocystitis, cellulitis, astigmatism, narrowing of lid fissure and respiratory difficulty from mass effect.\n Noninvasive management initially includes massage and antibiotics. For persistent case like this, probing, drainage and surgical marsupialization under general anesthesia and administration of antibiotics (topical and oral or IV) are needed to prevent further complications.", "ACR Code": "2.2", "Category": "Cyst, benign", "Keywords": "DacryocystoceleNasolacrimal duct obstructionDacryocystitis", "Reference": "Cavaza S, Laffi GL, Tassinari G, Dall\u2019olio D. \u201cCongenital Dacryocystocele: Diagnosis and Treatment.\u201d Acta Otorhinolaryngologica Italica (2008) 28: 298-301." } }, { "U_id": "MPX1445", "TAC": [ "MPX1445_synpic22851" ], "MRI": [], "Case": { "Title": "MEDIASTINAL FIBROSIS", "History": "Thirty-eight year old male presents to primary care complaining of chronic cough and shortness of breath that has significantly progressed over several days.", "Exam": "unknown", "Findings": "Pulmonary perfusion scan showing complete lack of perfusion to the left lung.\nCT pulmonary angiogram showed near complete occlusion of the left main pulmonary artery.\n\nCT pulmonary angiogram showing calcified mediastinal adenopathy and near complete opacificaton of the left main pulmonary artery.", "Differential Diagnosis": "bronchogenic carcinoma, hyperlucent lung / Swyer-James syndrome, fibrosing mediastinitis, and post surgical change.", "Case Diagnosis": "MEDIASTINAL FIBROSIS", "Diagnosis By": "biopsy", "Treatment & Follow Up": "Patient is to be closely followed by both cardiothoracic surgery and pulmonology.", "Discussion": "see factoid" }, "Topic": { "Title": "MEDIASTINAL FIBROSIS", "Disease Discussion": "Unilateral pulmonary artery nonperfusion on a radionuclide scan is uncommon. Unilateral nonperfusion with a normally perfused contralateral lung is even less common. While pulmonary thromboembolism is the most common cause of a perfusion defect on perfusion imaging, it is a relatively uncommon cause of unilateral hypoperfusion (especially if the perfused lung shows little or no abnormalities). Because pulmonary emboli are usually multiple, a single large unilateral defect suggests other diagnoses. The differential diagnosis for the most common causes of unilateral nonperfusion with a normally perfused contralateral lung includes bronchogenic carcinoma (the most common cause), congenital heart disease, hyperlucent lung syndrome / Swyer-James syndrome, post surgical changes, and fibrosing mediastinitis. \n\nHistoplasmosis is the most common cause of fibrosing mediastinitis in the United States, several times more common than tuberculosis, the second leading cause. Fibrosing mediastinitis results from excessive scarring around the hilar and mediastinal lymph nodes, presumably resulting from reaction to antigens released from Histoplasma organisms. Typically this presents several years after the initial infection. Fibrosing mediastinitis represents a noninfectious complication of histoplasmosis rather than an active and progressive infection. The presence of calcification indicates that the initial infection occurred several years earlier. Also, failure to isolate Histoplasma capsulatum from surgical specimens supports the assumption that the infection is no longer active.", "ACR Code": "6.2", "Category": "Infection, fungi", "Keywords": "unilateral perfusionHistoplasmosisFibrosing mediastinitis", "Reference": "1. Hirsch AM, Moser KM, Auger WR, Channick RN, Fedullo PF. Unilateral pulmonary artery thrombotic occlusion: is distal arteriopathy a consequence?. Am J Respir Crit Care Med 1996; 154:491-496.[Abstract] \n\n2.Mallin, W., Silberstein, E. Fibrosing mediastinitis causing nonvisualization of one lung on pulmonary scintigraphy. Clin Nucl Med. 1993 Jul;18(7):594-6.\n\n3. Robbins, Ivan M. MD; Davis, Angela M. MD; Doyle, Thomas P. MD; Loyd, James E. MD Pulmonary Artery Stenosis and Fibrous Mediastinitis. Chest. 120(5):1750-1751, November 2001." } }, { "U_id": "MPX1463", "TAC": [ "MPX1463_synpic17575" ], "MRI": [ "MPX1463_synpic17576", "MPX1463_synpic17577", "MPX1463_synpic17578" ], "Case": { "Title": "Optic Neuritis (imaging and clinical findings combined to verify diagnosis)", "History": "A 6 YO female presented to the emergency department with a 3 day history of right eye pain and severe decreasing visual acuity.", "Exam": "Ocular exam demonstrated a swollen right optic nerve.", "Findings": "CT of the orbits shows asymmetry of the optic nerves with the right optic nerve enlarged when compared to the left. Subsequent MRI evaluation of the orbits demonstrates enlargement of the right optic nerve with associated abnormal increased T2 signal intensity and enhancement on post-gadolinium series extending from globe to just anterior to the optic chiasm. Enhancement of the intraorbital fat adjacent to the nerve is also present. The remainder of the optic pathways are normal (not shown).", "Differential Diagnosis": "Optic nerve glioma\nMeningioma\nGraves disease\nSarcoidosis", "Case Diagnosis": "Optic Neuritis (imaging and clinical findings combined to verify diagnosis)", "Treatment & Follow Up": "The Opthomology service was consulted and the patient underwent radiologic and laboratory evaluation for ebv, lyme disease, multiple sclerosis, meningitis, sarcoid, syphillis, and lupus with negative results for all etiologies. The patient was subsquently treated with steroids and had complete visual recovery." }, "Topic": { "Title": "Optic Neuritis", "Disease Discussion": "Optic neuritis is an inflammatory lesion of the optic nerve clinically associated with pain, decreased visual acuity, abnormal color vision, and afferent papillary defect. In acute cases, visual loss may progress rapidly in only a few days. The condition is bilateral in 30% of cases. While most incidents are idiopathic, about half of all patients presenting with optic neuritis will go on to develop multiple sclerosis with young adults having the greatest risk. Of all cases of MS, optic neuritis is the initial presenting symptom in 15-20%. Other less common diseases associated with optic neuritis include ischemia, sarcoid, systemic lupus erythematosus, syphilis, viral infection, toxoplasmosis, tuberculosis, and radiation therapy. MR is the best imaging modality for optic neuritis with thin slice axial and coronal images are preferred. T2-weighted images and short-tau inversion recovery (STIR) sequences show high signal intensity in the abnormal nerve with the nerve being frequently enlarged. Gadolinium is particularly useful, especially with fat saturation, with focal enhancement of the retrobulbar optic nerve sometimes being seen. Perivenous inflammation is responsible for the enhancement and can be seen in approximately 50% of patients with acute optic neuritis. Overall, MR sensitivity for optic neuritis is low, with much of the utility derived from its ability to exclude other causes of optic nerve compromise such as an orbital tumor.", "ACR Code": "2.2", "Category": "Inflammatory, NOS", "Keywords": "optic neuritisoptic nerve", "Reference": "Carmody RF. The orbit and visual system. In Orrison WW Jr, ed. Neuroimaging Philadelphia, Pa: W.B. Saunders, 2000; 1009-1069" } }, { "U_id": "MPX1442", "TAC": [ "MPX1442_synpic18717" ], "MRI": [], "Case": { "Title": "Wegener Granulomatosis", "History": "Patient presented with a 2 month history of increasing inspiratory and expiratory stridor which began after 2 separate sinus surgeries.\n\nPertinent history is that the patient experienced her first episode of epistaxis several years prior to surgery and had multiple subsequent clinical visits for sinusitis.\n\nShe also has a remote history of migratory arthralgias/joint effusions/fevers and ulcerative colitis (diagnosed by colonscopy).", "Exam": "Physical exam demonstrated a petite female (wt 45 kg) with a low pitched inspiratory and expiratory stridor audible across the room. She was afebrile but tachypneic. \nSpirometry demonstrated complete flattening of the inspiratory and expiratory loops. \nESR elevated at 82, HCT low at 29.4, RF elevated at 80, ANA neg, LFT's WNL, CHEM 7 WNL, proteinase 3AB c-ANCA elevated at 1.66.", "Findings": "Image 1: AP neck radiographic demonstrates subglottic narrowing and loss of subglottic shouldering.\nImage 2: Lateral neck radiograph demonstrates subglottic narrowing and posterior tracheal mucosal thickening and irregularity.\nImage 3: Same as 2 with arrows and explanation.\nImage 4: Axial CT demonstrates marked narrowing of the subglottic trachea with prominent paratracheal soft tissue thickening.\nImage 5: Axial CT slightly lower than image 4 demonstrates a blind fistulus tract arising anterior right aspect of the subglottic trachea just inferior to the level of the stenosis.\nImages 6,7: Demonstrate maxillary and ethmoidal sinus mucosal thickening.\nImages 8,9: virtual bronchoscopy images demonstrate laryngeal anatomy and the area of stenosis seen below the cords.\nImages 10,11: virtual bronchoscopy images slightly inferior than the prior images demonstrate the false cords, true cords, and stenotic segment.\nImages 12,13: Reverse virtual bronchoscopy images (looking from the trachea toward the larynx) at the exact level of the tracheal pathology demonstrate mucosal thickening and irregularity with the opening of a fistulus tract along the right anterior trachea.", "Differential Diagnosis": "Intubation trauma causing subglottic stenosis\nAcute bacterial tracheatis\nWegener's granulomatosis\nNeoplastic disease (lymphoma, etc)", "Case Diagnosis": "Wegener Granulomatosis", "Diagnosis By": "proteinase 3AB c-antineutrophil cytoplasmic antibody (c-ANCA) was elevated to 1.66 (normal less than 0.8) and is highly specific (99%) for Wegener granulomatosis", "Treatment & Follow Up": "Fiberoptic bronchoscopy demonstrated beefy red, erythematous, edematous subglottic trachea. Biospy was not attempted in order to protect the patients airway. Additional labs: proteinase 3AB c-antineutrophil cytoplasmic antibody\n(c-ANCA) was elevated to 1.66 (normal less than 0.8) and is highly specific (99%) for Wegener granulomatosis. The sinus surgery was performed at another institution and the pulmonologist is attempting to obtain the sinus specimens for re-evaluation to help confirm the diagnosis of Wegener.\n\nThe patient will receive corticosteroids and either cyclophosphamide or methotrexate. She will also receive antibiotic prophylaxis. Further interventions may include tracheal dilatation and/or direct injection of the stenotic region with steroids or mitomycin-C.\nTracheostomy may be required if her airway continues to stenose.", "Discussion": "Patient presented with a 2 month history of increasing inspiratory and expiratory stridor which began after 2 separate sinus surgeries within the past two months for chronic erosive sinusitis. During the first surgery, the patient was intubated with a cuffed 6.5mm endotracheal tube. During the second surgery, the anesthesiologist could only pass a 5mm uncuffed tube.After the surgeries she developed worsening inspiratory and expiratory stridor. \n\nPertinent past history is that the patient experienced her first episode of epistaxis several years prior to surgery and had multiple subsequent clinical visits for sinusitis. She was diagnosed with erosive chronic sinusitis, for which the surgeries were performed. She also has a remote history of migratory arthralgias/joint effusions/fevers and ulcerative colitis (diagnosed by colonscopy). \n\nIn regards to her acute presentation, she was referred to a pediatric pulmonologist for evaluation of her stridor.\n\n1. In retrospect, many if not all, of the patient's prior illnesses (migratory arthralgias, ulcerative colitis, and sinusits) were likely a manifestation of Wegener's.\n\n2. Virtual bronchoscopy is an expanding technical application of raw data obtained from CT examinations. Computer \"Navigator\" software converts the raw data into cine-3D images which can be used to simulate bronchoscopy. In this specific case, virtual bronchoscopy was very helpful to the pulmonologist who determined to limit his actual examination to the larynx due to the stenotic/edematous appearance of the subglottic region seen on virtual bronchoscopy. He did not want to risk further inflamation of the already critically stenotic airway. Video of the actual laryngoscopy confirmed anatomy and pathology seen with virtual images." }, "Topic": { "Title": "Wegener's Granulomatosis", "Disease Discussion": "WEGENER\u2019S GRANULOMATOSIS is a systemic vasculitis which most commonly involves the upper and lower respiratory tract and kidneys and less commonly the eyes, joints, skin, neurologic, cardiac and gastrointestinal tissues. The disease was first described in 1931 and 1936 by H. Klinger and F. Wegener, respectively. \n\nETIOLOGY: The cause of Wegener\u2019s granulomatosis is not yet known. Granuloma formation, altered immune reactivity, immune complex deposition, and altered cellular immune responses are believed to play significant roles. There may be a genetic predisposition. [1]\n\nINCIDENCE: In the United States, the disease frequency is approximately 1 in 30,000, with mean age of onset of 40, equal prevalence in men and women, and increased prevalence in whites. Old data indicated that the disease was rare in children and that children accounted for only 0.1% of cases, but the most recent NIH data demonstrates that children and adolescents account for approximately 15% of affected individuals. [2]\n\nPATHOLOGY: The classic histopathology in Wegener's granulomatosis is necrotizing granulomatous vasculitis involving small arteries and veins, most reliably found on biopsies of the lung. Upper respiratory tract biopsies, including the nasal septum, sinus, and trachea, most often show non-specific acute and chronic inflammation with or without giant cells and generally without true vasculitis. Renal biopsies typically show focal segmental glomerulonephritis, with crescent formation and necrosis in more severe forms. \n\nCLINICAL MANIFESTATIONS: The spectrum of clinical features and organ system involvement in Wegener's granulomatosis is broad. As a multisystem disorder predominantly involving the upper and lower respiratory tracts and the kidneys, clinical manifestations vary from \"classic,\" with sinusitis, serous otitis media, rhinitis with nasal ulcerations, cough, hemoptysis, and constitutional symptoms, to \"fulminant,\" with rapidly progressive renal failure and respiratory failure requiring intensive care unit management, to \"mild,\" with arthralgias, polymyalgia rheumatica-type symptoms, or inflammatory eye disease as examples. [1] \n\nSinusitis is present at initial presentation in about one half to two thirds of patients with Wegener's granulomatosis and is seen in 85 percent of cases during the entire course of disease. A computed tomographic scan of the sinuses is often anatomically more informative than are plain radiographs, especially in the setting of destructive and erosive bone changes. \n\nAlthough laryngotracheal disease in Wegener's granulomatosis may be asymptomatic, clinical presentations may range from subtle hoarseness to stridor and life-threatening upper airway obstruction. The most characteristic lesion is that of subglottic stenosis, which occurs in up to 16 percent of patients. In pediatric and adolescent patients with Wegener's granulomatosis, the frequency of subglottic stenosis is dramatically increased, reaching an alarming 48 percent. Direct laryngoscopy may reveal active erythematous, friable mucosa or bland scar. Tracheal tomograms, computed tomographic scans, and magnetic resonance imaging may be useful adjuncts in the diagnosis of subglottic stenosis. Only 20 percent of lesions diminish with immunosuppressivetherapy alone, whereas 80 percent are fixed or irreversible owing to chronic fibrosis. [2]\n\n\nDIAGNOSIS: in the past 15 years, c-ANCA and its relationship to Wegener's granulomatosis have been studied. Clearly, this test is helpful in Wegener's granulomatosis, particularly during active generalized disease, and may be confirmatory. Because reports of false positives are increasing and because sensitivity varies from 30 to 90% in a clinician's diagnosis of Wegener's granulomatosis, depending on the extent of disease and disease activity level, the test cannot be used as a sole diagnostic criterion for Wegener's granulomatosis. Radiologic imaging studies are helpful in diagnosing Wegener's granulomatosis, including chest and sinus radiographs and computed tomography. The differential diagnosis is quite broad and depends on the patient's signs and symptoms. When the classic triad of involvement occurs, with confirmatory tissue biopsy and a positive c-ANCA, the diagnosis is easy. When the process is early and/or limited to the upper airway or kidney, the diagnosis is clinically challenging. [1]\n\nRADIOGRAPHIC FINDINGS: Imaging studies of the paranasal sinuses may reveal characteristic findings in patients with Wegener's granulomatosis. Plain film findings include mucosal thickening, opacification, air-fluid levels, and bony sclerosis or frank obliteration . Computed tomographic findings include bilateral sinus opacification, orbital mass, bone erosion, septal perforation, and mucosal thickening [3]\n\nTracheobronchial involvement by Wegener\u2019s manifests on CT as mural thickening and narrowing of involved airways. 90% of inflammatory lesions are located in the subglottic region with circumferential tracheal involvement and narrowing occur with a length of involvement ranging from 5 to 45 mm. \n\nOn CT, the most common finding of pulmonary Wegener\u2019s is multiple irregularly marginated nodules, which can range from 2 to 20 in number and from 2 to 90 mm in size. Areas of opacification ranging from ground-glass attenuation to frank consolidation are the second most common CT pattern of pulmonary Wegener\u2019s and often represent findings of pulmonary hemorrhage . [4]\n\nTREATMENT: Treatment depends on the severity and location of the disease. A multidisciplinary approach is often needed. Glucocorticoids and cyclophoshamide are the primary medications used for treatment. Combination therapy with oral daily cyclophophamide and glucocorticoids is considered the standard therapy. Methotrexate at times is used as an alternative to cyclophosphamide. Surgical treatment is often required to treat sinus disease, tracheal disease, and less frequently to provide renal transplant. \n \nPROGNOSIS: Whereas Wegener's granulomatosis was once an invariably fatal disease, the combination of cyclophosphamide and prednisone has provided remission in 75% of all patients and improvement in 90%, as evidenced in the National Institutes of Health (NIH) series of long-term follow-up studies. However, relapses occur in at least 50% of those achieving remission at any time from several months to 15 to 20 years after stopping cytotoxic therapy. [2]", "ACR Code": "2.2", "Category": "Idiopathic or Unknown", "Keywords": "Wegener'sGranulomatosisVasculitides", "Reference": "1. Goldman: Cecil Textbook of Medicine, 21st ed. New York: W. B. Saunders Company, 2000. \n\n2. Ruddy: Kelley\\'s Textbook of Rheumatology, 6th ed. New York: W. B. Saunders Company, 2001.\n\n3. Gubbels SP, et al. Head and neck manifestations of Wegener\\'s granulomatosis. Otolaryngol Clin North Am 2003; 36(4): 685-705.\n\n4. Zinck SE, et al. CT of noninfectious granulomatous lung disease. Radiol Clin North Am 2001; 39(6): 1189-209." } }, { "U_id": "MPX1473", "TAC": [ "MPX1473_synpic17391", "MPX1473_synpic17392" ], "MRI": [], "Case": { "Title": "Usual Interstitial Pneumonia", "History": "55 year old white female with PMH of HTN, CHF, PE, Anti-phoshpolipid antibody syndrome, admitted for 3mo Hx of SOB, acutely worsening over past week, now with O2 saturation of 75% at rest.", "Exam": "Gen: Obese, Aox3, SOB HEENT: no JVD/HJR LUNGS: rhales B/L, wheezes B/L C/V: RRR no m/r/g ABD: soft nt/nd, NABS EXT: 2+ pulses, 2+ pitting tibial edema NEURO: wnl LYMPH: wnl", "Findings": "HRCT Chest: Peripheral/Basilar honeycombing, irregular Intralobular septal thickening, irregular Interlobular septal thickening, Patchy ground glass", "Differential Diagnosis": "Usual Interstitial Pneumonia, Non-specific Interstitial Pneumonia, Rheumatoid lung dz, Chronic Hypersensitivity Pneumonitis", "Case Diagnosis": "Usual Interstitial Pneumonia", "Treatment & Follow Up": "The pt spent one week on the general medicine wards, requiring 4L 100% O2 at rest. She underwent a VATS for lung biopsy. She had a difficult post-op course characterized by refractory hypotension and severe pulmonary hypertension. She spent several weeks in the ICU on pressor support and intubated, but eventually died from PEA." }, "Topic": { "Title": "Usual Interstitial Pneumonia", "Disease Discussion": "Idiopathic Pulmonary Fibrosis (IPF) is a type of Idiopathic Interstitial Pneumonia (IIP) that carries the histological title of Usual Interstitial Pneumonia (UIP). This is a restrictive lung disease characterized by decreased total lung volume and impaired gas exchange. IPF almost invariably follows a progressive and relentless course, but its progression can be slowed by immunosuppressive therapy. HRCT now has a very strong role in diagnosing IPF. Typical findings progress from scant and patchy ground glass to inter and intralobular septal thickening to peripheral and basilar honeycombing. The specific amount and location of these findings help narrow the ddx for this disease, determine the need for biopsy, and help determine the level of disease activity and extent. HRCT has a 90% accuracy in diagnosing IPF, but the disease remains undiagnosed in 1/3 of patients who eventually show UIP on biopsy. Therefore, biopsy is still recommended for definitive diagnosis.", "ACR Code": "68.792", "Category": "Unsure", "Keywords": "Idiopathic Pulmonary Fibrosis", "Reference": "References: Sullivan et al. Treatment of IPF with corticosteroids. UTD.COM: 2003, Stark. High Resolution Computed Tomography of the Lungs. UTD.COM: 2003, ATS Guidelines: IPF: Diagnosis ands Treatment. UTD.COM: 2003" } }, { "U_id": "MPX1472", "TAC": [ "MPX1472_synpic19581" ], "MRI": [], "Case": { "Title": "Odontogenic Keratocyst", "History": "26 year old female with a history of possible \"maxillary cyst\" that causes intermittent drainage into her posterior oral cavity. Prior oral surgery workup was negative by report.", "Exam": "N/A", "Findings": "Axial and coronal CT imgages demonstrate an expansile, cystic lesin within the left maxillary sinus. This lesion has areas of dense calcification (tooth-like) and soft tissue components. The lesion has caused bony remodeling of the sinus walls and has expanded into the osteomeatal unit, and protruding into the nasal cavity. Mucoperiosteal thickening is also present in the left ethmoid, sphenoid and left frontal sinuses.", "Differential Diagnosis": "Odontogenic cysts\n -Follicular cysts\n -Periodontal cysts\n -Odontogenic keratocysts\n -Calcifying odontogenic cysts\nFissural Cysts\nOdontogenic tumors\n -ameloblastoma\n -odontoma\n -fibromyxoma", "Case Diagnosis": "Odontogenic Keratocyst", "Discussion": "Odontogenic Keratocysts compose up to 17% of all jaw cysts and usually occur in the second to third decade. The mandible is the usual site of origin, however, when ivolving the maxilla, extension to the maxillary sinuses is common and can lead to obstructive symptoms. These lesions are associated with Marfan's syndrome and Basal cell nevus syndrome, and may have neoplastic potential. These cysts tend to be unilocular, and surgical resection results in low recurrence rated.\n\nSom, PM, Curtin, HD. Head and Neck Imaging. 3rd edition. Mosby, 1996." }, "Topic": { "Title": "Dentigerous cyst", "Disease Discussion": "Developmental cysts of the maxilla and mandible (i.e. jaw) may be subdivided into nonodontogenic and odontogenic types. Nonodontogenic cysts lie in the jaw but do not contain tooth derivatives. A fissural cyst is a type of nonodontogenic cysts arising along lines of fusion of embryonic structures.\n\nIn contradistinction, odontogenic cysts are derived from embedded remnants of odontogenic (tooth forming) epithelium. The most common type of odontogenic cyst is the radicular cyst which occurs after the eruption of the involved tooth and surrounds the root of the tooth. \n\nThe second most common type of odontogenic cyst - the dentigerous cyst - is associated with an unerupted tooth. The dentigerous cysts are unilocular, as opposed to the odontogenic cysts that are multilocular - ameloblastoma and keratocysts \u2014 and also surrounds an unerupted tooth. They are more often found in the mandible (70%) as compared to the maxilla. Dentigerous cysts have a non-keratinizing epithelium.\n\nThe odontogenic keratocyst is similar, but has a keratinizing epithelium and may be multilocular.\n\nhttp://www.usc.edu/hsc/dental/opath/Chapters/Chapter10_Main.html", "ACR Code": "2.3", "Category": "Cyst, benign", "Keywords": "dentigerousodontogenicradicular", "Reference": "Grossman and Yousem, Neuroradiology The Requisites,p. 288-90 \nHasso, et. al., ACR Head and Neck Syllabus #34, p. 607-10", "External Links": "www.usc.edu/hsc/dental/opath/Chapters/Chapter10_Main.html" } }, { "U_id": "MPX1475", "TAC": [ "MPX1475_synpic40014", "MPX1475_synpic40015" ], "MRI": [], "Case": { "Title": "Primary Pulmonary Tuberculosis", "History": "16 month asymptomatic male and 3 year old asymptomatic sister with exposure to uncle from India.", "Exam": "+PPD.", "Findings": "16 month male: Chest radiographs demonstrates focal air space opacity in the right lower lobe, and right hilar fullness. Contrast enhanced CT of the chest shows consolidation in the superior segment of the right lower lobe. Additionally, there is a heterogeneous mass in the right paratracheal region with foci of central hypodensity, and minimal peripheral enhancement, suggestive of necrotic lymphadenopathy. In the subcarinal region, there is contined area of central hypodenisty that is contiguous with the consolidated lung.\n\n3 year old female: Chest radiographs demonstrate unilateral right sided hilar adenopathy. Repeat chest radiographs two weeks later demonstrate new right middle lobe opacity.", "Differential Diagnosis": "Differential Diagnosis for Tuberculous Adenopathy.\n\nMetastases\nHistoplasmosis in endemic areas.", "Case Diagnosis": "Primary Pulmonary Tuberculosis", "Diagnosis By": "+AFB" }, "Topic": { "Title": "Primary Pulmonary Tuberculosis", "Disease Discussion": "Lesions/Condition: Primary Pulmonary Tuberculosis\n\nClinical Manifestations: The majority of patients with primary pulmonary tuberculosis are asymptomatic. Cough and fever are the most prominent symptoms, followed by weight loss, hemoptysis, and sweating.\n\nDiscussion: \n\nPrimary pulmonary tuberculosis traditionally has been thought to occur predominately in children, with the incidence steadily increasing especially in edemic areas such as India, Southeast Asia, and sub-Saharan Africa.\n\nThe presenting radiologic manifestation may be air space consolidation within any lobe, typically affecting the areas of greatest ventilation; the most common sites are the middle lobe, lower lobes, and the anterior segments of the upper lobes. Additionally, approximately 90% to 95% of children with primary tuberculosis will demonstrate lymph node enlargement on the chest radiograph. The majority of cases have right-sided hilar involvement, and/or right paratracheal region disease. Atelectasis may also be a presenting manifestion, secondary to bronchial compression by enlarged lymph nodes, occuring more often in a right-sided lobar distribution. Pleural effusion in association with parechymal abnormalities have also been reported in 5% to 10% of children. Rarely, cavitation or military disease may develop in about 2% to 5% of cases of primary parenchymal disease.\n\nOn CT, there is dense, homogeneous, well-defined air-space consolidation. Approximately 50% of affected nodes have central low attenuation with Hounsfield units measuring less than 30, and the remaining nodes demonstrate soft tissue density. After the administration of IV contrast material, approximately 60% of affected lymph nodes demonstrate low attenuation of the central region as well as peripheral enhancement.\n\nIn summary, when lung consolidation with associated unilateral hilar lymphadenopathy is identified, primary pulmonary tuberculosis should be highly suspected.", "ACR Code": "6.2", "Category": "Infection, generalized", "Keywords": "Primary Pulmonary Tuberculosis", "Reference": "Brant: Fundamentals of Diagnostic Radiology. 2nd Edition. Philadelphia: \n Lippincott Williams & Wilkins. 1999. \nDonnelly. Fundamentals of Pediatric Radiology. Philadelphia. Elsevier \n Saunders. 2001.\nFraser et al. Synopsis of Diseases of the Chest. 3rd Edition. Philadelphia: \n Elsevier Saunders. 2005.\nHarisinghani et al. RadioGraphics 2000; 20:449-470." } }, { "U_id": "MPX1427", "TAC": [ "MPX1427_synpic17014" ], "MRI": [], "Case": { "Title": "Choledocholithiasis", "History": "82 year old female examined for vague abdominal pain.", "Findings": "There is focal areas of increased density in the gallbladder and common bile duct. There is dilation of the pancreatic duct, intra and extrahepatic biliary ducts.", "Differential Diagnosis": "choledocolithiasis", "Case Diagnosis": "Choledocholithiasis" }, "Topic": { "Title": "Choledocholithiasis", "Disease Discussion": "Biliary stone disease (cholelithiasis) is a common etiology of abdominal pain in the United States. Although choledocholithiasis (bile duct stones) represents a diagnostic possibility in almost any setting of biliary stone disease, certain risk factors should be elicited from the patient to develop a diagnostic perspective.\n\nIn the setting of jaundice, elevated serum bilirubin, and pancreatitis, a dilated common bile duct is should lead to a careful search for distal obstructing stones. Up to 15% of patients having cholelithiasis, also have choledocholithiasis. The size of the extrahepatic bile duct is the most sensitive means of determining obstruction (whether seen or unseen). Furthermore, although there are some special cases, CBD should measure less than or equal to 4mm + 1mm per decade after 40.\n\n\nUltrasound remains up to 95% sensitive in the detection of cholelithiasis. However, detection of common duct stones remains at approximately 80%. Certain maneuvers (drinking water, using compression with the US probe) and certain positions (RPO, R lateral decubitus) can assist with detection. Sometimes the overlying bowel & gas can obscure imaging by ultrasound. A level and cause of the obstruction needs to be obtained to guide the need for further tests, diagnostic and therapeutic procedures. Options include MR cholangiogram, CT, and endoscopic procedures.\n\nAbout 90% of biliary obstructions and subsequent biliary ductal dilatation occur distally and are caused by 3 entities:\n1) pancreatic carcinoma\n2) choledocholithiasis\n3) chronic pancreatitis with stricture formation\n\nIf the diagnosis is uncertain then further diagnostic studies should be undertaken to better delineate these etiologies. \n\nComplications of choledocholithiasis include strictures, complicatiosn of operative procedures, and cholangitis. \n\nAlthough the clinical setting will dictate\u2014especially in the presence of infection\u2014stones < 6mm typically can pass on their own. Until that time every effort is made to make the patient most comfortable. For larger stones surgical management remains the mainstay of therapy.", "ACR Code": "7.5", "Category": "Systemic, Generalized" } }, { "U_id": "MPX1478", "TAC": [ "MPX1478_synpic17566" ], "MRI": [], "Case": { "Title": "Emphysematous Cystitis", "History": "47 yo female with persistent N/V, epigastric pain;", "Exam": "Pt presented in DKA (diabetic ketoacidosis). LFTs and amylase/lipase normal.", "Findings": "intramural bladder gas", "Differential Diagnosis": "infectious emphysematous cystitis\nbladder instrumentation or surgery\ntrauma\nenteric fistula (colo-vesicle)", "Case Diagnosis": "Emphysematous Cystitis", "Treatment & Follow Up": "The diagnosis is confirmed by the unique imaging appearance.\n\nTreatment of emphysematous cystitis involves early broad spectrum antibiotics, drainage of the bladder, and management of hyperglycemia if present. \n\nPrognosis in patients diagnosed and treated early in the disease process is usually good.The development of emphysematous ureteritis, nephritis, or adrenalitis portends a poor prognosis.", "Discussion": "Emphysematous cystitis is a rare entity (in 2001, a researcher reported his was only the 166th case in medical literature). Typical patients are immunocompromised or elderly and debilitated, and 50% of cases are seen in diabetics. \n\nPatients may present with anything from no symptoms to an acute abdomen. Pneumaturia is rare, since the gas is within the bladder wall. Prevalence in females is twice that in males. Often associated with urinary stasis, and growth of gas forming organisms (most commonly E. coli, but others include Enterobacter aerogenes, Proteus mirabilis, Staphylococcus aureus, streptococci. Clostridium perfrigens, and Candida albicans).\n\nPlain abdominal radiographs are generally sufficient to confirm the diagnosis. \n\nThis disease is often not suspected until discovered on the abdominal radiograph. Findings include curvilinear gas lucencies throughout the bladder, often described as a \"cobblestone\" or \"beaded necklace\" appearance.\n\nIntraluminal gas may ascend the ureters and create an air pyelogram. In rare cases where plain images are negative despite high clinical suspicion, CT may show intramural bladder gas (as in this case)." }, "Topic": { "Title": "Emphysematous Cystitis", "Disease Discussion": "Emphysematous cystitis is a rare entity (in 2001, a researcher reported his was only the 166th case in medical literature). Typical patients are immunocompromised or elderly and debilitated, and 50% of cases are seen in diabetics. Patients may present with anything from no symptoms to an apparent acute abdomen. Pneumaturia is rare. Prevalence in females is twice that in males. Often associated with urinary stasis, and growth of gas forming organisms (most commonly E. coli, but others include Enterobacter aerogenes, Proteus mirabilis, Staphylococcus aureus, streptococci. Clostridium perfrigens, and Candida albicans).\n\nPlain abdominal radiographs are generally suffiecient to confirm the diagnosis. This disease is often not suspected until discovered on the abdominal radiograph. Findings include curvilinear gas lucencies throughout the bladder, often described as a \"cobblestone\" or \"beaded necklace\" appearance. Gas may ascend the ureters and reveal an air pyelogram. In rare cases where plain images are negative despite high clinical suspicion, CT may show intramural bladder gas (as in this case).\n\nThis appearance differs from that of bladder gas introduced by trauma, instrumentation, or vesicocolic fistula, where gas is confined to the bladder lumen, and does not exhibit the curvilinear appearance.\n\nTreatment of emphysematous cystitis involves early broad spectrum antibiotics, drainage of the bladder, and management of hyperglycemia if present. \n\nPrognosis in patients diagnosed and treated early in the disease process is usually good.The development of emphysematous ureteritis, nephritis, or adrenalitis portends a poor prognosis.", "ACR Code": "8.2", "Category": "Infection, generalized", "Keywords": "emphysematous cystitispyelonephritisdiabetic", "Reference": "1. Grainger & Allison's Diagnostic Radiology: A Textbook of Medical Imaging, 4th Ed., Copyright 2001 Churchill Livingstone, Inc. p. 1000, p1552\n(MDConsult)\n\n2. O'Connor LA, American Journal of Emergency Medicine\nVolume 19 \u2022 Number 3 \u2022 May 2001\nCopyright \u00a9 2001 W. B. Saunders Company (MDConsult)" } }, { "U_id": "MPX1481", "TAC": [ "MPX1481_synpic30242", "MPX1481_synpic30243", "MPX1481_synpic30244", "MPX1481_synpic30246", "MPX1481_synpic30247", "MPX1481_synpic30248" ], "MRI": [], "Case": { "Title": "Aberrant Right Subclavian Artery", "History": "54 year-old female with acute onset chest pain.", "Exam": "N/A", "Findings": "CT examination of the chest performed with IV contrast according to a PE/DVT protocol demonstrated an aberrant right subclavian artery. The mediastinum was otherwise unremarkable. There was no pulmonary embolism detected.", "Differential Diagnosis": "Aberrant right subclavian artery", "Case Diagnosis": "Aberrant Right Subclavian Artery", "Diagnosis By": "Characteristic appearance on a Contrast enhanced CT of the chest", "Treatment & Follow Up": "None needed.", "Discussion": "None." }, "Topic": { "Title": "Aberrant Right Subclavian Artery (ARSA)", "Disease Discussion": "\u2022 most common congenital vascular anomaly of the aortic arch\n\u2022 with the anterior aorta, the ARSA creates a vascular ring around the mediastinal structures, including the trachea and esophagus\n\u2022 most often asymptomatic\n\u2022 may cause wheezy or stridorous breathing; usually picked-up by 2 years\n\u2022 dysphagia (\"dysphagia lusoria\"), particularly in patients with a wide based take-off of the aberrant vessel ('Diverticulum of Kommerell').\n\u2022 widened mediastinum silhouette on plain PA/AP chest films\n\u2022 posterior notch on barium swallow/esophagogram \n\u2022 associated with many types of congenital heart disease, Down's, VCFS (Velo-Cardio-Facial), DiGeorge's, Dubowitz's, and Edward's syndromes", "ACR Code": "562.1521", "Category": "Congenital, malformation", "Keywords": "vascular ringaberrantgreat vessel", "Reference": "Practical Pediatric Imaging Diagnostic Radiology of Infants and Children, 3rd Edition, D.R. Kirks (Ed.),Lippincott-Raven Publishers, Philadelphia, 1998" } }, { "U_id": "MPX1487", "TAC": [ "MPX1487_synpic24425" ], "MRI": [], "Case": { "Title": "Lipomas of the small bowel", "History": "Sixty-three year-old man with upper abdominal discomfort.", "Findings": "Multiple intraluminal small bowel collections of fat,\nconsistent with lipomas, are demonstrated. The largest measures approximately 3.1 x 1.7 cm, and is located in the third portion of the duodenum.", "Differential Diagnosis": "Gastrointestinal lipomas", "Case Diagnosis": "Lipomas of the small bowel", "Diagnosis By": "CT attenuation measurements", "Treatment & Follow Up": "Esophago gastro duodenoscopy (EGD) demonstrated numerous polypoid masses in the duodenum.", "Discussion": "Several gastric lipomas were also identified." }, "Topic": { "Title": "Probability of lipoma of the small bowel", "Disease Discussion": "Solitary, smooth surface tumors that protrude into the bowel lumen include a carcinoid, leiomyoma, lipoma, adenoma, very rarely an inflammatory fibroid polyp or a neurogenic tumor. Of these only the lipoma would be soft enough to be flattened by abdominal compression. The absence of an associated exoenteric mass would be against the diagnosis of carcinoid, a more frequently found small bowel tumor. Lack of ulceration together with the softness of the tumor would be against a leiomyoma, a slightly more frequent small bowel tumor than a lipoma. The benign character of this tumor is supported by the long history and its smoothly round surface appearance.\n\nThe benign character of the tumor would have been rendered definite if lack of significant growth could have been shown by a further examination one or two years later. This could be demonstrated in another case included here to underline this point. Film .3 is a small bowel meal study done at another hospital in a patient who complained of intermittent pain. Arrows outline an oval shaped, smooth intraluminal tumor. The patient's symptoms continued and a small bowel enema was done two years later. Film .4 demonstrates the same elongated intraluminal lesion which had not appreciably increased in size during the two years; a lipoma was removed at surgery.\n\nAll benign small bowel tumors are rare, leiomyoma and lipoma being the least infrequent. Though lipomas arise in submucosal fat, their slow growth is deflected by the muscularis and directed into the bowel lumen to make them present like a mucosal polyp. They will occasionally ulcerate and bleed. More frequently, they will transiently intussuscept to give rise to crampy abdominal pain, the symptoms of the first patient in this case. The diagnosis of lipoma can be supported by CT when it would show an attenuation number compatible with fat.\n\nFURTHER CASE EXAMPLE: A 50-year-old man complained of crampy abdominal pain of sudden onset; stools were heme positive; a small bowel enema (Film .5) outlined an almost 2-cm rounded, intraluminal filling defect with slight surface irregularity (arrow) seen at the top of the film; in the course of the barium study (Film .6) the lesion was seen to intussuscept and advance about 4 cm (arrows indicate the narrow passage through the intussusception). The differential diagnosis included lipoma, lymphoma (very rare as a single polypoid lesion), carcinoid (they virtually never intussuscept) and inflammatory fibroid polyp (very rare). The patient later came to laparotomy and a very rare adenoma was resected.", "ACR Code": "7.3", "Category": "Mnemonic" } }, { "U_id": "MPX1489", "TAC": [ "MPX1489_synpic38833", "MPX1489_synpic38836", "MPX1489_synpic38837", "MPX1489_synpic38838", "MPX1489_synpic38839" ], "MRI": [], "Case": { "Title": "Duplicated Inferior Vena Cava", "History": "55 yo male with gross hematuria.", "Exam": "Within Normal Limits.", "Findings": "The left inferior vena cava extends cephalad as a continuation of the left common iliac vein adjacent to the left side of the aorta, ending in the left renal vein. The normal right IVC extends from the right common iliac vein, following its normal course through the abdomen.", "Case Diagnosis": "Duplicated Inferior Vena Cava", "Diagnosis By": "Cross Sectional Imaging" }, "Topic": { "Title": "Duplicated Inferior Vena Cava", "Disease Discussion": "Lesions/Condition: Duplicated Inferior Vena Cava (IVC)\n\nDiscussion: \n\nA duplicated IVC is commonly identified as an incidental finding during routine abdominal CT examinations, and is present in 3% of the population. It is derived from a persistence of both right and left supracardinal veins. \n\nTypically, the left IVC is a direct continuation of the left common iliac vein, ascending to the left of the abdominal aorta, crossing midline anterior to the aorta to join the right IVC via the left renal vein. \n\nKnowledge of a duplicated IVC is important in the planning of vascular procedures, both surgical and radiologic.", "ACR Code": "9.1", "Category": "Congenital, normal variant", "Keywords": "Duplicated Inferior Vena CavaLeft sided Inferior Vena Cava", "Reference": "Webb: Fundamentals of Body CT. 3rd Edition. Philadelphia: Saunders\n 2006. \nBrant: Fundamentals of Diagnostic Radiology. 2nd Edition. Philadelphia: \n Lippincott Williams & Wilkins. 1999. \nKellman et al. RadioGraphics 1988; 8(3):533-556." } }, { "U_id": "MPX1496", "TAC": [ "MPX1496_synpic18546" ], "MRI": [], "Case": { "Title": "Fibrous Dysplasia of the Clivus", "History": "41 year old female with increasing headaches and a family history of aneurysms. A head CT performed at another institution was reportedly unremarkable. MRI/MR angiography of the Circle of Willis was performed at our institution to evaluate for possible aneurysm.", "Exam": "Noncontributory", "Findings": "The MRI/MRA study showed no vascular pathology, but incidentally it was noted that there was a heterogeneous and mildly expanded clivus.\n\nWhole body skeletal scintigraphy showed nonspecific increased uptake in the clivus region.\n\nRepeat CT of the sinus was performed, revealing a \u201cground glass appearance\u201d, containing a smaller circumscribed area, which has the appearance of a cystic lesion. Overall the process appeared nonaggressive and was stable on 5 month follow-up CT.", "Differential Diagnosis": "\u2022 Chordoma*\n\u2022 Chondrosarcoma*\n\u2022 Plasmacystoma\n\u2022 Lymphoma\n\u2022 GCT*\n\u2022 Cavernous hemangioma*\n\u2022 Carcinomas (adenocystic or nasopharyngeal)\n\u2022 Mets*\n\u2022 Paget\u2019s\n\n* should have low T1, high T2 signal", "Case Diagnosis": "Fibrous Dysplasia of the Clivus", "Diagnosis By": "Presumptive based on characteristic imaging findings.", "Treatment & Follow Up": "Pending Biopsy/Resection", "Discussion": "None" }, "Topic": { "Title": "Fibrous Dysplasia", "Disease Discussion": "\u2022 1st described by Lichtenstein 1938\n\u2022 Benign, presents in 1st two decades\n\u2022 Etiology unknown\n\u2022 Marrow replaced by fibro-osseous connective tissue replacing mature bone with structurally weak, immature woven bone\n\u2022 Classified into 3 subtypes:\n\u2013Monostotic (long bones of extremities, ribs, vertebrae, craniofacial bone) 70%\n\u2013Polyostotic 30%\n\u2013McCune-Albright syndrome: one-sided involvement of multiple bones, skin hyperpigmentation, endocrine dysfunction (hyperthyroid, precocious puberty/menstruation in females)\n\u2022 Craniofacial bones commonly involved - frontal, sphenoid, ethmoid, maxillary, mandible \n\u2022 Clivus involvement in monostotic form is rare\n\u2022 Presentation: asymptomatic, headache\n\nIMAGING:\n\u2022 XR - cystic, sclerotic, mixed forms (Leeds et al)\n\u2022 CT - amorphous \u201cground glass\u201d or \u201csmudgy\u201d appearance\n\u2022 MR - thinning of cortical bone, ballooning of affected area\n\u2013Heterogeneous-homogenous, low to intermediate T1 and low to high T2 signal\n\u2013Contrast enhancement with variable signal\n\u2013Signal reflects overall cellularity, varying collagen content, extent of bone trabeculae, cyst formation\n\u2013Cystic components will follow fluid signal\n\u2013Sclerotic\u2014low T1 and T2 signal\n\u2013Low signal may also be seen with fibrous tissue\n\u2013Intermediate T2 signal \u2013 high metabolic activity (Utz et al.)\n\n\u2022 Pathology:\n\u2013Fibrous connective tissue with trabeculae of immature bone without surrounding osteoblasts\n\u2013Termination of active phase = increasing ossification\n\u2013Histologic: degree of acitivity closely corresponds to radiologic findings (Ameli et al)\n\u2022 Disease ceases to progress or evolves slowly after bone maturation\n\n\u2022 Treatment:\n\u2013Generally nonsurgical \n\u2013But does depend on activity level, symptoms/cranial nerve compromise, location in skull\n\u2013If active phase, total excision recommended (Ameli et al)\n\u2013Generally good prognosis but risk of malignant change/aggressive behavior\n\n\u2022 Prognosis:\nMonostotic craniofacial lesions have 0.05% malignant transformation\n\u2013Osteosarcoma, fibrosarcoma, chondrosarcoma", "ACR Code": "1.3", "Category": "Neoplasm, NOS", "Keywords": "McCune-Albrightenlarged boneground glass", "Reference": "Leeds at al. Fibrous dysplasia of the skull and its differential diagnosis. Radiology 1962;78:570-582.\n\nUtz et al. MR appearance of fibrous dysplasia. J Comput Assist Tomogr 1989;13:845-851\n\nAmeli NO, et al. Monostotic fibrous dysplasia of the cranial bones. Report of fourteen cases. Neurosurg Rev 1981;4:71-77." } }, { "U_id": "MPX1495", "TAC": [ "MPX1495_synpic23460", "MPX1495_synpic23462", "MPX1495_synpic23463" ], "MRI": [], "Case": { "Title": "Non-Hodgkins Lymphoma (Large B-cell) of the proximal small bowel", "History": "Active duty soldier with three week history of nausea, vomiting, and epigastric abdominal pain while deployed in Iraq.", "Exam": "No significant physical exam findings.", "Findings": "Focal wall thickening (11mm) of a segment of jejunum in the left upper quadrant. This segment of jejunum is also dilated with a maximum diameter of 5.3 cm with retained contrast and an air-fluid level. Also noted is surrounding lymphadenopathy and peritoneal fat stranding, the largest mesenteric lymphnode measuring 1.3cm in its shortest diameter.", "Differential Diagnosis": "Lymphoma\nAdenocarcinoma\nCarcinoid tumor\nMetastases", "Case Diagnosis": "Non-Hodgkins Lymphoma (Large B-cell) of the proximal small bowel", "Diagnosis By": "Excisional biopsy proven diagnosis, B-cell Non-Hodgkin Lymphoma of the small bowel", "Treatment & Follow Up": "Surgical resection and started on chemotherapy", "Discussion": "Non-Hodgkin lymphoma is the most common malignancy of the small bowel, representing 20% of small bowel malignancies. It most often occurs in males between 50 to 60 years old and occurs most often in the distal ileum. Prognosis is worse for younger patients and females. Immunocompromised patients have an increased frequency of Non-Hodgkin\u2019s lymphoma of the small bowel.\n\nThe radiographic appearance of small bowel varies to include fold thickening or effacement, luminal narrowing, diffuse nodularity, extrinsic compression by mesenteric masses, and most often marked luminal dilatation. Lymphoma of the small intestine may also present as an ulcerating mass. Diagnosis of primary small bowel lymphoma is made by the presence of an isolated small bowel lesion and regional lymphadenopathy without splenic, hematologic, or hepatic involvment. \n\nThe differential diagnosis of Non-Hodgkin includes adenocarcinoma, carcinoid tumor, gastrointestinal stromal tumor, lipoma, metastases, and Peutz-Jeghers syndrome. Imaging modalities include fluoroscopy, CT, and MRI.\n\nThe diagnosis can be suggested with imaging when focal thickening of a bowel loop associated with \"aneurysmal dilatation\" of the segment and regional lymphadenopathy is seen, as on this case." }, "Topic": { "Title": "Non-Hodgkins Lymphoma of the Small Bowel", "Disease Discussion": "A CT-guided biopsy of the mass was performed which revealed a Non-Hodgkins diffuse mixed B-cell lymphoma. Lymphomas of the GI tract are the most common site for extra-nodal lymphomas, and since other small bowel malignancies are rare, lymphomas of the small intestines make up 20-40 % of all small bowel malignancies. However, lymphomas of the small bowel make up only 2 % of GI malignancies. Interestingly, in Western societies GI lymphomas are predominately in the stomach (50-60 %) with only 20-30% in the small bowel, where in the middle east these values are reversed. B cell lymphomas account for 2/3 of GI lymphomas and have a 2:1 male predominance. T cell lymphomas account for the other 1/3 and have an occur equally between males and females. \nThe usual presenting symptoms in small bowel lymphomas are abdominal pain, weight loss anorexia, and Lymphomas of the small bowel are staged using CT and respond well to various chemotherapeutic regimens. Surgical excision is usually not performed, and is used mainly for debulking when radiation therapy is used as the primary therapeutic modality. Low grade B cell lymphomas of the small intestine have a 50 percent 5 year survival where high grade (high nuclear to cytoplasmic ratio) fare a little worse with a 35-40 percent 5 year survival.", "ACR Code": "74.343", "Category": "Neoplasm, non-CNS" } }, { "U_id": "MPX1506", "TAC": [ "MPX1506_synpic37594" ], "MRI": [], "Case": { "Title": "Fracture dislocation at thoraco-lumbar junction, resulting in spinal cord transection.", "History": "8 year old boy in MVA. Patient was in back seat wearing seatbelt.", "Exam": "\u2022 Paraplegia\n\u2022 Multiple extremity injuries", "Findings": "\u2022 CT:\n- Fracture dislocation of spine at T12/L1\n\n\u2022 MRI:\n- (Post-reduction) Spinal cord transection with intraaxial hemorrhage and spinal cord edema", "Differential Diagnosis": "None", "Case Diagnosis": "Fracture dislocation at thoraco-lumbar junction, resulting in spinal cord transection.", "Diagnosis By": "CT and MRI", "Treatment & Follow Up": "Open reduction with fusion of spine", "Discussion": "This young boy was wearing a seatbelt across his lap without using the shoulder component." }, "Topic": { "Title": "Fracture dislocaton at thoraco-lumbar junction, resulting in spinal cord transection.", "Disease Discussion": "Diagnostic imaging of acute spinal trauma has and will continue to rely upon plain film and CT examination (1). However, none of these modalities can assess the cord directly and its relationship to the surrounding structures. The introduction of MR compatible hardware for spine stabilization and modification of life support devices for use in MR scanning has made imaging of the acutely injured spine possible. Cord edema and hemorrhage are frequently seen in the acutely traumatized spinal cord. Cord edema can cause focal enlargement of the cord, but more frequently elongates T1/T2 due to the water content. This is usually best seen on T2-weighted images as an area of increased signal. Clinically, it may be important to distinguish an edematous cord from a hemorrhagic contusion (3). Cord hemorrhages evolve similarly to intracerebral hemorrhage, and therefore acute hemorrhages tend to have low T1 and T2 signal characteristics. On the T2-weighted sequences, the hemorrhagic low signal portion is often surrounded by a ring of high signal intensity edema. Finally, cord maceration and transection represent the most severe form of cord injury. This is usually seen as a loss of cord signal or marked inhomogenity of signal where the cord should be. In this particular case, the thoracolumbar junction acts as a fulcrum, tending to produce flexion-compression (i.e., burst) fractures, with motion instability and a tendency to produce retropulsion of the fracture fragment.", "ACR Code": "3.4", "Category": "Trauma", "Keywords": "spine translationspinal cord injury", "Reference": "http://www.neurosurgery.org/sections/section.aspx?Section=PD&Page=ped_spine.asp", "External Links": "http://www.neurosurgery.org/sections/section.aspx?Section=PD&Page=ped_spine.asp" } }, { "U_id": "MPX1507", "TAC": [ "MPX1507_synpic16282", "MPX1507_synpic16283", "MPX1507_synpic16284" ], "MRI": [], "Case": { "Title": "Prenatal Cytomegalovirus Infection", "History": "Infant with developmental delay.", "Findings": "Noncontrast CT of the head demonstrated periventricular calcifications consistant with congenital cytomegalovirus infection.", "Differential Diagnosis": "Toxoplasmosis", "Case Diagnosis": "Prenatal Cytomegalovirus Infection" }, "Topic": { "Title": "Prenatal Cytomegalovirus Infection", "Disease Discussion": "Cytomegalovirus (CMV) is a perinatally aquired infection that belongs to the TORCH group (toxoplasmosis, other-varicella, rubella, cytomegalovirus, herpes simplex and HIV) Most of these viral infections are aquired transplacentally.\n\nCMV infection is the most common of the TORCH infections. Symptomatic patients have hepatosplenomegaly, cerebral involvement, chorioretinits and deafness. The intracranial manifestations are dependent on when during gestation the infection occured. When infection occurs during the first trimester necrosis of the germinal matrix can occur resulting in migration abnormalities. Patients who are affected later in gestation may have a delay in myelination, periventricular white matter lesions, and ventriculomegaly. The classic radiologic presentation is periventricular calcifications. There are usually no basal ganglia nor cortical calcifications, which helps differentiate it from toxoplasmosis.", "ACR Code": "1.9", "Category": "Infection, viral", "Keywords": "cytomegalovirusTORCHPeriventricular calcifications", "Reference": "Barkovich, AJ: Pediatric neuroimaging 2nd ed. Raven Press 1995: pp571-572.\nBrant W and Helms C: Fundamentals of Diagnostic Radiology, 2nd ed Lippincott, Philadelphia 1999, pp 155-156." } }, { "U_id": "MPX1513", "TAC": [ "MPX1513_synpic24287" ], "MRI": [], "Case": { "Title": "Abdominal aortic aneurysm", "History": "81 year old male with a one month history of positional back pain.", "Exam": "VSS: stable\nMarked lordosis, no vertebral tenderness, no pulsatile abdominal masses, neuro. exam non focal", "Findings": "L-spine: Lower lumbar hyperlordosis with marked degenerative changes involving multiple levels of the lower thoracic and lower lumbar spine. 6 cm abdominal aortic aneurysm with extensive aortoiliac calcification.\nAbdominal CT: Infrarenal abdominal aortic aneurysm with a maximum AP dimension of 5.4 cm and transverse dimension of 4.9 cm. The aneurysm is 1 cm below the left renal artery ostium and ends 3 cm above the aortic bifurcation. There is extensive calcification in the aorta, SMA, bilateral renal arteries, iliac arteries, and common iliac arteries. All the vessels are patent.", "Differential Diagnosis": "Abdominal aortic aneurysm\nOther causes of back pain: musculoskeletal back pain, malignancy, vertebral infection, nephrolithiasis, herniated disc, degenerative disease", "Case Diagnosis": "Abdominal aortic aneurysm", "Treatment & Follow Up": "Patient was seen in the medicine clinic and a lumbar spine was ordered for a one month history of positional back pain. The abdominal aortic aneurysm was an incidental finding. Due to the size of the aneurysm, vascular surgery was consulted. The aneurysm was determined to be well calcified and in no immediate danger of rupture. The patient is scheduled for aortic endograft repair this month. An endograft will be placed in the lumen of the aneurysm to exclude the aneurysm from flow through the aorta and reduce the risk of rupture.", "Discussion": "Patient was seen in the medicine clinic and a lumbar spine was ordered for a one month history of positional back pain. The abdominal aortic aneurysm was an incidental finding. Due to the size of the aneurysm, vascular surgery was consulted. The aneurysm was determined to be well calcified and in no immediate danger of rupture. The patient is scheduled for aortic endograft repair this month. An endograft will be placed in the lumen of the aneurysm to exclude the aneurysm from flow through the aorta and reduce the risk of rupture." }, "Topic": { "Title": "Abdominal aortic aneurysm", "Disease Discussion": "An aneurysm is defined as a focal dilation of the aorta involving an increase in diameter of at least 50 percent as compared with the expected normal diameter. The normal size diameter of the aorta in this area is 2 cm. The pathogenesis of abdominal aortic aneurysms is multifactorial. Familial clustering, genetic predisposition, and hemodynamic factors all play a role in the formation of abdominal aortic aneurysms. The overall incidence of abdominal aortic aneurysm is 15 to 37 cases per 100,000 patient years. \n\nMuch of the research has focused on the relationship of aneurysm size to the risk of rupture. Studies using CT and ultrasound have recorded average expansion rates of 0.4 cm per year. Risk factors for rupture include elevated blood pressure, smoking, atherosclerotic disease, and the presence of COPD. Smoking is the major risk factor for aneurysm formation. Aneurysms can also occur as part of certain disease such as Marfans or Ehler-Danlos syndrome. The risk of rupture for aneurysms less than 4.0 cm is 2 percent. For aneurysm greater than 5.0 cm the risk is between 25 to 41 percent. The risk of rupture for aneurysms between 4 to 5 cm is between 3 to 12 percent. Immediate repair vs. surveillance for aneurysms less than 5.5 cm has not improved survival. \n\nAbdominal ultrasound can be used as screening tool for abdominal aortic aneurysm. Ultrasound has sensitivity of 100 percent. Both the longitudinal and transverse aortic diameters can be measured and there is no need for IV contrast. Ultrasound can measure aneurysm within a range of 0.6 cm. Ultrasound is limited in its use for surgical planning because it cannot document the proximal or distal extent of the aneurysm. \n\nCT is highly sensitive and specific for identification of abdominal aortic aneurysms and is more accurate in determining the size of the aneurysm. CT is also valuable in surgical planning because it provides information on the anatomical relationship of the visceral and renal vessels. Disadvantages to CT include the need for IV contrast and exposure to radiation.\n\nThe mortality of a ruptured abdominal aortic aneurysm is over 90 percent, but for those who make it to a hospital alive 50 percent survive. The classic triad of hypotension, back pain, and a pulsatile abdominal mass is only present half of patients. Diagnostic tests such as CT or ultrasound should not delay immediate operation.", "ACR Code": "5.7", "Category": "Aneurysm", "Keywords": "abdominal aortic aneurysm.aortic aneurysmaneurysm", "Reference": "1.\tErnst, Calvin. Abdominal Aortic Aneurysm. NEJM 1993; 328:1167-1172\n2.\tLederle et al. Immediate Repair Compared with Surveillance of Small Aortic Aneurysms. NEJM; 346:1437-1444.\n3.\tTownsend: Sabiston Textbook of Surgery, 17th ed. Abdominal Aortic Aneurysm p. 1969." } }, { "U_id": "MPX1509", "TAC": [ "MPX1509_synpic52774", "MPX1509_synpic52775", "MPX1509_synpic52776" ], "MRI": [], "Case": { "Title": "Septic Pulmonary Emboli", "History": "49-year-old male with PMH significant for end stage renal disease s/p external arteriovenous shunt placement for home dialysis presents with complaint of 3 days of fevers, chills, nausea, vomiting, anorexia, cough and pleuritic chest pain. Patient had similar signs and symptoms 1 year, was found to have MSSA bacteremia with septic pulmonary emboli. Following shunt replacement and antimicrobial therapy he demonstrated improvement. Denies tobacco, alcohol or illicit drug use. No family history of pulmonary disease or cancer", "Exam": "PE:\nVital signs\n101.9 130/90 98 22 97RA\nGeneral\nIll appearing morbidly obese male sitting on side of bed in mild\nrespiratory distress \nCardiovascular\nMild tachycardia. No murmurs rubs or gallops\nPulmonary\nMild tachypnea with decreased breath sounds at base R>L\nAbdominal \nSoft, nontender, nondistended with normal active bowel sounds\nLabs:\nWBC 15.8, H/H 9.7/29.1, Plt 256 G 91%\nESR 105, CRP 19.407\nBUN/Cr 71/12.2\nBlood Cx MSSA", "Findings": "Rads:\nAP CXR demonstrates patchy alveolar infiltrates in bilateral lower lung zones. Representing loculated pleural effusions \nChest CT demonstrates bilateral effusions with R>L. Multiple bilateral peripherally distributed nodular opacities with cavitations and feeding vessels leading to the peripheral lung lesions", "Differential Diagnosis": "C- Carcinoma - Squamous is most common \nA- Autoimmune - Wegener's granulomatosis, Rheumatoid nodules \nV- Vascular - Emboli (septic emboli or bland emboli) \nI- Infection - Lung abscess, Bacterial pneumonia, Fungal pneumonia, Tuberculosis, Pneumatocele \nT- Trauma - Pulmonary laceration \nY- Young (congenital) - Congenital cystic adenomatoid malformation, Pulmonary sequestration, Bronchogenic cyst", "Case Diagnosis": "Septic Pulmonary Emboli", "Diagnosis By": "Based on patients clinical presentation, persistent MSSA bacteremia, typical radiographic findings of septic pulmonary emboli and history of diagnosis.", "Treatment & Follow Up": "shunt replacement, exahastive search for other sources and appropriate antimicrobial therapy", "Discussion": "Septic pulmonary embolism occur when an infected thrombus fragments and an emboli colonized with bacteria or fungi lodges in the pulmonary arterial circulation. Common sources septic thrombi include vegetative endocarditis and septic thrombophlebitis. Other less common sources include infected transvenous pacemakers, catheters, or shunts. \n\nOrganisms most commonly associated with septic pulmonary embolism include, Staphylococcus aureus and group A Streptococcus. However many patients, especially Intravenous drug abusers may harbor polymicrobial emboli, including anaerobic and gram-negative organisms. Blood cultures may be falsely negative, particularly early in the disease process.\n\nPatients with septic pulmonary emboli have varied presentations depending upon the organism and the underlying disease. A high level of clinical suspicion is necessary given most often only non specific signs and symptoms including fevers, chills, nausea, vomiting, anorexia, cough, dyspnea or pluritic chest pain are obvious. \n\nThe classic plain film findings of septic pulmonary emboli include multiple pulmonary nodules of variable size with or without cavitation, located predominantly in the periphery and bases. However, most radiographs reveal only ill-defined infiltrates and effusions. \n\nCT is the preferred imaging technique for septic pulmonary emboli. The presence of cavitating nodules with associated feeding vessels in highly specific for septic pulmonary emboli." }, "Topic": { "Title": "Septic Pulmonary Embolism", "Disease Discussion": "Septic Pulmonary Emboli", "ACR Code": "6.9", "Category": "Miscellaneous", "Keywords": "Septic Pulmonary Emboli", "Reference": "Cook RJ, Rendell AW. Septic Pulmonar Embolism: Presenting Features and Clinical Course of 14 Patients. Chest 2005;128;162-166\n\nKuhlman JE, Elliot FK. Pulmonary septic Emboli: Diagnosis with CT. Radiology 1990;174;211-213\n\nhttp://www.medicalmnemonics.com/" } }, { "U_id": "MPX1520", "TAC": [ "MPX1520_synpic19417" ], "MRI": [], "Case": { "Title": "Mucinous Cystadenoma", "History": "53 year old male noted to have a 2 cm cecal mass on screening colonoscopy.", "Exam": "Asymptomatic", "Findings": "Well circumscribed 3 cm low attenuation mass in cecum originating from the appendiceal orifice.", "Differential Diagnosis": "Chronic appendicits; Mucinous cystadenoma; Mucinous Cystadenocarcinoma", "Case Diagnosis": "Mucinous Cystadenoma", "Treatment & Follow Up": "Mucin accumulation within the appendix is most commonly secondary to a mucin secreting neoplasm, mucinous cystadenoma or cystadenocarcinoma. Rarely, chronic appendiceal obstruction may result in mucin accumulation." }, "Topic": { "Title": "Mucocele of the appendix", "Disease Discussion": "The term \"mucocele of the appendix\" refers to an accumulation of mucus within an abnormally distended appendiceal lumen, regardless of its cause. Most mucoceles are, however, probably neoplastic in nature, and thought to be the result of a pathologic spectrum consisting of hyperplasia, mucinous cystadenoma and mucinous cystadenocarcinoma. Many patients are asymptomatic, and the mass is only discovered incidentally at laparotomy.\n\nAt barium enema, a smooth globular mass indenting the cecum may be seen, associated with non-filling of the appendix. The combination of appendiceal non-filling and deformity of the inferomedial aspect of the cecum should always suggest the possibility of appendiceal disease, whether this be due to appendicitis (as is usually the case), appendiceal neoplasm or a mucocele. Occasionally, an inverted appendiceal stump following appendectomy may be sufficiently large (indicated by arrow in Film .3) that it simulates a neoplasm.\n\nOn CT, an appendiceal mucocele typically is seen as a near-water-density rounded mass adjacent to the cecum, with or without peripheral calcification.\n\nRupture of an appendiceal mucocele may give rise to pseudomyxoma peritonei, in which the peritoneal cavity becomes filled with the gelatinous material either in the form of circumscribed collections or lying free. If this condition is discovered incidentally at laparotomy, a careful search should be made for an underlying tumor which is most commonly ovarian or appendiceal in origin. CT sometimes shows a characteristic appearance in pseudomyxoma peritonei, with septated fluid-density material in the peritoneal cavity and/or marked deformity and scalloping of the liver by the mucinous material (Films .4 and .5).", "ACR Code": "7.3", "Category": "Obstruction or Stenosis", "Keywords": "appendicitismucoceleappendix" } }, { "U_id": "MPX1523", "TAC": [ "MPX1523_synpic23556", "MPX1523_synpic23557" ], "MRI": [], "Case": { "Title": "Renal infarct", "History": "65 year old male presented with flank pain.\nHe had stones several years ago that uneventfully passed.", "Exam": "Initial evaluation for stones was negative. CT through the kidneys was obtain with IV contrast.", "Findings": "CT of the kidneys with IV contrast demonstrates large segmental area of non enhancement in the anterior left kidney. There is a very thin rim of enhancement in the outer most cortex which has blood supply from the capsular vascular branches.", "Differential Diagnosis": "Infarct\nInfection", "Case Diagnosis": "Renal infarct", "Treatment & Follow Up": "No follow up is available for this patient." }, "Topic": { "Title": "Renal infarct", "Disease Discussion": "Renal infarct is the formation of a necrotic area in a kidney that results from renal blood vessel occlusion. The size and location of the infarct depends on the site of vascular occlusion. Occlusion can be either thrombotic or embolic in nature. Thrombotic events are more likely to occlude large renal arteries or its branches. Emboli, on the other hand, can cause more distal occlusions resulting in smaller defects and/or multiple ones. Residual renal function after infarction depends on the extent of the damage.\n\nCause: Most common caused - renal artery embolism secondary to mitral stenosis. Other causes include infective endocarditis, atrial fibrillation, microthrombus in the left ventricle, rheumatic valvular disease, or recent myocardial infarction.\nMay also be caused by atherosclerosis with or without thrombus formation, thrombus from flank trauma, sickle cell anemia.\n\nPatients may present with acute or chonic abdominal pain, generalized or localized to affected flank. Occlusive events may also be clinically silent.\n\nOn IVP study, the infarcted portion of the kidney does not excrete contrast and is seen as a defect in a renal contour. CT through the kidneys after administration of intravenous contrast demonstrates an area of non perfusion. There may be a rim of enhancement along the cortex. This occurs when there is enough blood flow from the renal capsular vessels that penetrate into the outer most cortex.\nInfarcted part of the kidney may be revascularized either through collateral, resolution of the thrombus, or by intervention. If imaged during revascularization phase, the areas of infarct may have heterogenous enhancement. In the absence of a baseline study, this may cause confusion and difficulty in making the correct diagnosis.\n\nDifferential diagnosis of a non enhancing kidney (part or whole) includes infection, tumor and ischemia. Secondary signs such as rim enhancement and clinical picture help to offer the right diagnosis.", "ACR Code": "8.9", "Category": "Vascular", "Keywords": "renal infarctischemiacortical rim sign" } }, { "U_id": "MPX1514", "TAC": [ "MPX1514_synpic26852" ], "MRI": [ "MPX1514_synpic26853", "MPX1514_synpic26854", "MPX1514_synpic26855", "MPX1514_synpic26856" ], "Case": { "Title": "oropharyngeal (tongue) cancer, squamous cell carcinoma (SCC)", "History": "HPI: Presented with a 6 month hisotry of an asymptomatic left neck mass s/p failed course of abx therapy and two non-diagnostic FNAs.\n\nPMH: Denies any h/o CA, XRT, chemo. Denies any h/o heart dz, lung dz, DM, SLE, scleroderma, or IBD.\n\nPSH: T&A at 6; BTL at 41; Right foot surgery at 51.\n\nFHX: mom h/o uterine and colon CA; 3 sisters h/o breast CA; sister h/o uterine CA; sister h/o breast and kidney CA, died at 52; brother died of lung CA at 52\n\nAllergies: NKDA\n\nMeds: Tylenol\n\nSHx: G4P4, postmenopausal; lifetime non-smoker, non-drinker; no significant travel or occupational exposure history\n\nROS: Pos for globus sensation. Denies weight loss, pain, hoarseness, dysphagia, constitutional symptoms.", "Exam": "Notable only for 3x3.5cm firm nodule in level 2 region. Nasopharyngoscope exam was benign.", "Findings": "Neck CT: Mass adjacent to left parotid and medial to digastric measuring 2.8 (AP)x 1.6 (trans)x 4.5cm(cc). Soft tissue asymmetry superior to left vallecula - mass cannot be excluded.\n\nNeck MRI: Enhancing plaque-like mass measuring 0.9 x 2.2 x 3.4 cm at base of the tongue. A second enhancing mucosal plaque-like lesion at same level of tongue base to the right of midline measuring 1.5cm (trans) x 2.9cm (CC) x 6mm thick. Masses do not appear to extend into musculature of tongue. Hemorrhagic and necrotic lymph node in level 1 left side just inferior to mandible and deep portion of parotid lateral to carotids measuring 3 x 1.8 x 3.8cm. Second necrotic node above previous measuring 1.1 x 1.3 x 1.6cm.", "Differential Diagnosis": "\u00bb Neoplasm - primary vs metastatic\n\u00bb Infection\n\u00bb Connective Tissue Disorder\n\u00bb Vasculitis\n\u00bb Other autoimmune disease\n\u00bb Other inflammatory process", "Case Diagnosis": "oropharyngeal (tongue) cancer, squamous cell carcinoma (SCC)", "Diagnosis By": "Bx of mass at tongue base revealed squamous cell carcinoma.\nFNA of lymph node revealed squamous cell carcinoma.", "Treatment & Follow Up": "This patient has T2N2aM0 or Stage IVa disease. Surgical excision or combined chemoradiation are the accepted treatment options. Given liklihood of severe morbidity post-surgery, patient chose chemoradiation. However, left neck dissection is still a possibility. Patient will have IMRT M-F for about 8 weeks and opted for amifostine for parotid sparing. Patient will have lifetime follow-up to monitor for recurrent and new primary disease.", "Discussion": "This patient is unique given a lack of any classic risk factors for oropharyngeal cancer. However, her extensive family history of cancer raises the question of a familial risk factor. Although oropharyngeal squamous cell carcinoma is not classically related to any of the other cancers her mother and siblings sufferred from, the same overexpression or underexpression of cell cycle regulators and tumor suppressors implicated in the pathogenesis of those cancers are being studied as playing a role in oropharyngeal carcinogenesis as well." }, "Topic": { "Title": "Oropharyngeal cancer", "Disease Discussion": "Oropharyngeal cancer is usually a squamous cell carcinoma (SCC).\n\nEpidemiology:\n- Fifth most common cancer worldwide\n- 2.8% of cancer in US\n- 39,250 cases in US per year; 11,090 deaths in US per year\n- M:F ratio 2:1 to 4:1\n- Higher incidence and mortality in African-American males\n\nRisk Factors:\n- smoking\n- alcohol (combined with smoking, accounts for 80% of cases)\n- viruses (EBV, HSV, HPV, HIV)\n- occupational exposure\n- prior XRT\n- diet \n- genetics (p16, p53, HER-2/neu, Bcl-2)\n\nPresentation:\n- Multistep carcinogenesis progressing from hyperplasia through dysplasia and carcinoma in situ; and, finally to invasive carcinoma.\n- Symptoms are location dependent and include LAD, pain, dysphagia, hoarseness, fixed tongue, and globus sensation.\n\nDiagnosis:\n- Primary, secondary, and metastatic sites are visualized by imaging (CT or MRI)and panendoscopy.\n- Risk factors cause global damage so secondary sites are very common and often missed.\n- Tissue diagnosis made by biopsy.\n\nStaging:\n- TNM classification\n\nPrognosis:\n- Dependent on site and genetic abnormalities\n- Stage I and II: \n \u2022 30-40% of cases\n \u2022 60-98% 5-year survival\n \u2022 curative intent to treatment\n- Resectable Stage III, IV (M0)\n \u2022 >50% of cases\n \u2022 30% 5-year survival\n- Unresectable Stage III, IV (M0)\n \u2022 10-30% 5-year survival\n \u2022 Recurrent - palliative treatment\n- Metastatic disease (usually lung, liver, bone)\n \u2022 5-10% of cases\n \u2022 palliative treatment\n\nTreatment:\n- Dependent on location and stage\n- Usually combination of surgery, radiation therapy, and concommitant chemotherapy.\n- Rehabilitation and prosthetics are often needed due to disfiguring nature of surgery.\n\nFollow-up:\n- High recurrance rate.\n- Lifetime follow-up.\n- Risk factor modification.", "ACR Code": "2.3", "Category": "Neoplasm, carcinoma", "Keywords": "oropharyngeal cancerhead and neck cancersquamous cell carcinoma", "Reference": "1)Jemal, A, Murray, T, Ward, W, et al. Cancer statistics, 2005. CA Cancer J Clin 2005; 55:10. \n2)Sankaranarayanan, R, Masuyer, E, Swaminathan, R, et al. Head and neck cancer: A global perspective on epidemiology and prognosis. Anticancer Res 1998; 18:4779. \n3)Spitz, MR. Epidemiology and risk factors for head and neck cancer. Semin Oncol 1994; 21:281. \n4)Vokes, EE, Athanasiadis, I. Chemotherapy of squamous cell carcinoma of head and neck: The future is now. Ann Oncol 1996; 7:15. \n5)Vokes, EE, Weichselbaum, RR, Lippman, SM, Hong, WK. Head and neck cancer [see comments]. N Engl J Med 1993; 328:184." } }, { "U_id": "MPX1504", "TAC": [ "MPX1504_synpic49211" ], "MRI": [], "Case": { "Title": "Lipohemarthrosis (s/p BKA for IED & shrapnel injury)", "History": "26 year old man with with a swollen knee after falling. Past history of a below the knee amputation (BKA) five years ago.", "Findings": "AP radiograph of the right knee shows cortical irregularity at the superior aspect of the medial femoral condyle, and lateral aspect of the lateral femoral condyle. The patient is post BKA, with prior surgical changes noted in the proximal tibia and diffuse osteopenia. Heterotopic ossification and shrapnel are seen in the soft tissues.\n\nLateral radiograph of the right knee shows a complex fracture of the distal femur, with cortical disruption of the medial femoral condyle and a 6 mm gap involving the lateral femoral condyle. A joint effusion is noted. The patient is post BKA, with prior surgical changes noted in the proximal tibia and diffuse osteopenia. Heterotopic ossification and shrapnel are seen in the soft tissues.\n\nNonenhanced axial CT image in bone windows through the level of the femoral condyles, shows the complex fracture with an associated joint effusion with three distinct layers: an anterior fat density layer, an intermediate fluid density layer, and a posterior hyperdense layer.\n\nNonenhanced axial CT image in soft tissue windows through the level of the femoral condyles, shows the complex fracture with an associated joint effusion with three distinct layers: an anterior fat density layer, an intermediate fluid density layer, and a posterior hyperdense layer.\n\nX-table lateral radiograph of the right knee shows interval placement of a partially imaged trans-tibial pin and reduction of the complex distal femoral fracture. The joint effusion again demonstrates three distinct layers: an anterior fat density layer, an intermediate fluid density layer, and a posterior hyperdense layer.", "Case Diagnosis": "Lipohemarthrosis (s/p BKA for IED & shrapnel injury)", "Diagnosis By": "Imaging findings are characteristic" }, "Topic": { "Title": "Lipohemarthrosis", "Disease Discussion": "Lipohemarthrosis is the result of extruded bone marrow fat and blood into joint space following an intraarticular fracture [1]. First described in 1929 by Kling, Holmgren demonstrated the \u201cfat-fluid\u201d level radiographically in 1939 [1,2]. In 1942, Pierce et al. described a fat-fluid level, which had a fluid-fluid component and suggested that this phenomenon was the result of separation of blood into serum and cellular elements [2]. In 1996, Lugo-Olivieri et al. performed a retrospective review of 41 patients with tibial plateau fractures and found that joint effusions with fluid levels resulted from blood separating into cellular elements and supernatant serum, confirmed with CT or MR imaging. Lugo-Olivieri concluded that a single fluid-fluid level on radiographs in a post-traumatic knee did not necessarily reflect lipohemarthrosis, as hemarthrosis could appear similarly. They suggested that a double fluid-fluid level is a more specific finding for intraarticular fat and an underlying fracture.\n\nLipohemarthrosis is more common in fractures about the knee, but has been described in the shoulder, elbow, and hip fractures [1]. CT and MRI are more specific than radiography in evaluating the composition of the effusion, but sonography may also have a role [1]. The anterior layer on ultrasound will appear hyperechogenic because of the fat. On CT, this area will be fat-density, and will follow fat signal on all MR pulse sequences [1,2]. The supernatant layer will be anechoic on US, fluid density on CT, and follow simple fluid signal on all MR sequences [1,2]. The hemorrhagic cellular layer will appear hypoechogenic on sonography, hyperdense (50 \u2013 70 HU) on CT, and produce intermediate signal on T1 and hypointense signal on T2-weighted images [1,2].", "ACR Code": "-1.-1", "Category": "Trauma", "Keywords": "Lipohemarthrosis", "Reference": "1. Costa DN, Cavalcanti CF, Sernik RA. Sonographic and CT Findings in Lipohemarthrosis. AJR Am J Roentgenol. 2007 Apr;188(4):W389.\n\n2. Lugo-Olivieri CH, Scott WW Jr, Zerhouni EA. Fluid-fluid levels in injured knees: do they always represent lipohemarthrosis? Radiology 1996;198 : 499-502" } }, { "U_id": "MPX1528", "TAC": [ "MPX1528_synpic16718" ], "MRI": [], "Case": { "Title": "Gastric Rupture - iatrogenic", "History": "84 yo male with severe abdominal pain several hours s/p Schatzki ring dilation. One episode of emesis with a bloody streak.", "Exam": "Generally well appearing but in moderate distress, awake, A+O X 3, HEENT normal, Lungs CTAB, Heart tachycardic with normal s1s2 and no MRG. Pulses 2+ and equal. Abd soft, diffusely tender to palpation, esp over LUQ which was tender to percussion with rebound. NABS. Labs: 138/5.4/109/23/19/1.0, CBC: 7.1>14.5/40.5<130, Amy/Lip: 61/101, Coags: 14.3/1.2/27.4", "Findings": "Acute Abd: Rigler\u2019s Sign = Air on both sides of the bowel wall indicating free air and perforated viscus.\n\nCT: Free air in the abdomenUpper GI: Gastrograffin leak indicating gastric rupture near the esophagogastric junction", "Differential Diagnosis": "Esophagus Rupture: iatrogenic, Mallory Weiss, Boerhaave\u2019s\n\nGastric Rupture: iatrogenic, perforated ulcer", "Case Diagnosis": "Gastric Rupture - iatrogenic", "Treatment & Follow Up": "Exploratory laparotomy and repair of gastric wall. Patient taken to ICU where he did not clinically improve. Second ex-lap revealed hepatic and mesenteric bleeds which were also repaired. Upon return to ICU, patient entered into PEA and subsequently expired." }, "Topic": { "Title": "Gastric Rupture - iatrogenic", "Disease Discussion": "The major complication of esophageal dilation is perforation. Incidence of this outcome is related to etiology of stricture, technique, operator experience and equipment used. Overall incidence is estimated at 0.1%. Perforation may be cervical esophagus, intrathoracic or gastric (as in this case). Clinical features are dependent on location of rupture, but include dysphonia, hoarseness, subcutaneous emphysema, and/or pain exacerbated with inspiration or swallowing.Appropriate initial studies when perforation is suspected include cervical and thoracic radiographs and gastrograffin swallow (which may be falsely negative in up to 10% of cases). When clinical suspicion remains high, despite negative swallow, the study may be repeated with barium which has much higher sensitivity, but is extremely irritating to pulmonary tissue. When both swallows are negative and concern for perforation remains, CT should be performed.Management is usually surgical but, in select cases of early diagnosis without evidence of intrapleural or intraperitoneal extravastion of contrast in a stable patient, medical management may be adequate. This includes 10-14 days NPO with parenteral nutritional support, antibiotics and drainage of fluid pockets. Prognosis for patients with perforation due to instrumentation tends to be better than in those occurring spontaneously. However, in those cases of delayed diagnosis or very elderly patients (such as the one in this case) mortality may be up to 50%.", "ACR Code": "7.4", "Category": "Iatrogenic or Surgical (complications)", "Keywords": "Gastric Rupture", "Reference": "1. Gueirud, Moises MD. \u201cComplications of Esophageal Stricture Dilation.\u201d UpToDate: 2003.\n\n2. Farrell, James J MD and Lawrence S. Friedman MD. \u201cGastrointestinal Disorders in the Elderly: Gastrointestinal Bleeding in the Elderly.\u201d Gastroenterology Clinics V 30 N 2, June 2000: W.B. Saunders Company." } }, { "U_id": "MPX1531", "TAC": [ "MPX1531_synpic16441" ], "MRI": [], "Case": { "Title": "Liposclerosing Myxofibrous Tumor of Bone (LSMFT)", "History": "40 y/o male with hip pain.", "Exam": "NA", "Findings": "AP radiographs of the left hip show a geographic lesion with a thin, well-defined sclerotic margin in the intertrochanteric region of the femur. There is globular amorphous mineralized matrix in the middle lower portion of the lesion, with more extensively mineralized globular matrix in the upper aspect.\n\nAxial CT scan through the middle portion of the lesion shows the mineralized matrix. The attenuation of the lesion is greater than that of marrow fat and less than that of skeletal muscle.", "Differential Diagnosis": "1. Fibrous dysplasia\n2. Fibroxanthoma \n3. Myxofibroma\n4. Lipoma\n5. Cyst\n6. Bone infarct\n7. Paget's disease\n8. Chondroma", "Case Diagnosis": "Liposclerosing Myxofibrous Tumor of Bone (LSMFT)", "Treatment & Follow Up": "NA", "Discussion": "LSMFT has a predilection for the proximal femur at the intertrochanteric region - as was seen in this case. More than 90% of these femoral lesions occur here.\n\nRadiographs showed a well-defined, sclerotic margin. The bone contour showed mild expansile remodeling. Mineralization within the lesion was apparent. Findings at computed tomography reflected those at radiography." }, "Topic": { "Title": "Liposclerosing Myxofibrous Tumor of Bone (LSMFT)", "Disease Discussion": "Liposclerosing myxofibrous tumor (LSMFT) of bone is a benign fibro-osseous lesion that is characterized by a complex mixture of histologic elements, which may include lipoma, fibroxanthoma, myxoma, myxofibroma, fibrous dysplasia\u2013like features, cyst formation, fat necrosis, ischemic ossification, and, rarely, cartilage. Despite its histologic complexity, LSMFT has a relatively characteristic radiologic appearance and skeletal distribution [1]. \n\nLSMFT is usually an incidental finding. According to Gilkey [2], they have a broad adult age range, but quite likely have their inception in childhood and slowly alter their appearance over a lifetime. In the majority of instances asymptomatic discovery, lack of distortion of bone outline, and sclerotic borders are indications of stability over many years. Other lesions gradually enlarge, predisposing to pathologic fracture. \n\nThe designation of \"sclerosing\" refers to the intralesional bone formed or mineralized within altered fat. The term \"myxofibrous\" refers to the fibrous or myxofibrous areas. \n\nThe radiologic appearance of LSMFT is often quite characteristic. LSMFT has a striking predilection for the femur: In a study by Kransdorf, et al, approximately 85% of the lesions were at this site, and 91% of the femoral lesions were in the intertrochanteric region. Radiographs typically showed a geographic lesion with a well-defined, often extensively sclerotic margin. The bone contour was normal or showed mild expansile remodeling. Mineralization within the lesion was not uncommon. \n\nLSMFT can be readily distinguished from intraosseous lipoma on CT scans or MR images by the identification of fat within a lipoma. Intraosseous lipomas do occur in the proximal femur, and the differentiation between LSMFT and intraosseous lipoma with involutional change may not be possible on imaging studies. Similarly, in some cases, differentiation between infarct and myxoma may not be possible. \n\nMalignant transformation in lipomatous lesions has been well documented. The prevalence of malignant transformation in LSMFT has been previously reported to be 10%\u201316%. The increased propensity of LSMFT for malignant transformation is likely to be secondary to its extensive involutional and ischemic change, with the associated sarcoma arising from areas of ischemic ossification within the lesion or from progressive in situ atypism of the altered lipomatous elements. \n\nIn summary, LSMFT of bone is a lesion characterized by a complex admixture of histologic patterns. Although LSMFT is not unique in terms of histogenesis, it is distinctive in terms of its morphologic and characteristic radiologic appearances and skeletal distribution. The apparent increased risk of malignant transformation associated with LSMFT underscores the need for close observation of this condition.", "ACR Code": "4.3", "Category": "Neoplasm, benign", "Keywords": "liposclerosing; myxofibrous; tumor; bone; lipo; sclerosing; myxo; fibrous; LSMFT", "Reference": "1. Kransdorf MJ, Murphey MD, Sweet DE. Liposclerosing myxofibrous tumor: a radiologic-pathologic-distinct fibro-osseous lesion of bone with a marked predilection for the intertrochanteric region of the femur. Radiology. 1999 Sep;212(3):693-8. \n2. Gilkey FW. Liposclerosing myxofibrous tumor of bone.\nHum Pathol. 1993 Nov;24(11):1264." } }, { "U_id": "MPX1548", "TAC": [ "MPX1548_synpic17636", "MPX1548_synpic17637" ], "MRI": [], "Case": { "Title": "Iliac vein compression sydrome", "History": "77 y/o man with right lower quadrant pain", "Exam": "Spongy mass in soft tissue over right lower quadrant", "Findings": "Dimunuitive right common iliac vein with large collateral vessles. No evidence for cirrhosis.", "Differential Diagnosis": "Iliac vein compression\nDVT\nMass effect\nIatrogenic\nRadiation", "Case Diagnosis": "Iliac vein compression sydrome", "Treatment & Follow Up": "Long standing collaterals are present relieving congestion. Anticoagulation.", "Discussion": "May-Thurner occurs in left common iliac. This case differs because of compression of right common iliac between a large osteophyte and right iliac artery." }, "Topic": { "Title": "Iliac vein compression sydrome", "Disease Discussion": "Clinically significant stenoses of lower extremity veins is uncommon. Multiple causes include: surgery, mass, radiation, chronic DVT, trauma, pregnancy, compression between artery and spine, or venospasm. The most common cause is compression of upper left common iliac vein as it passes between right common iliac artery and the spine (May-Thurner syndrome). Symptoms are typically leg swelling and pain. Diagnosis can be suggested by US but usually femoral or MR venography is needed for the diagnosis. Collaterals and thrombotic occlusion are common. Treatments include angioplasty and stents with short term anticoagulation therapy or surgery for refractory cases.", "ACR Code": "9.9", "Category": "Obstruction or Stenosis", "Keywords": "May ThurnerIliac venous thrombosisDVT", "Reference": "Valji K., Vascular and Interventional Radiology, W.B. Saunders, Philidelphia, 1999, pp 295-6." } }, { "U_id": "MPX1547", "TAC": [ "MPX1547_synpic21028" ], "MRI": [], "Case": { "Title": "Pancreatic adenocarinoma, well-to-moderately differentiated.", "History": "60yo female with history of abdominal lymphoma presents to the ER with abdominal pain.", "Exam": "No physical exam or laboratory findings available.", "Findings": "US Findings: The common bile duct measures 14mm with this pancreatic parenchymal tissue and pancreatic duct dilatation, measuring 5mm in diameter. These findings were concerning for mucinous duct ecstatic pancreatic carcinoma vs. pancreatic head neoplasm.\n\nCT findings: A 23 x 21 mm heterogeneous mass is visualized within the head of the pancreas with moderate dilatation of the pancreatic duct as well as marked extra- and moderate intra-hepatic ductal dilatation. The SMA and SMV fat planes appear preserved.", "Differential Diagnosis": "Pancreatic adenocarcinoma\nMucinous duct ectatic pancreatic carcinoma\nLymphoma\nCholecystitis", "Case Diagnosis": "Pancreatic adenocarinoma, well-to-moderately differentiated.", "Diagnosis By": "Surgical resection with pathology reported as well-to-moderately differentiated adenocarinoma.", "Treatment & Follow Up": "The patient was treated with a Whipple procedure.", "Discussion": "Pancreatic adenocarcinoma accounts for 3% of all cancers and is commonly unresectable at time of presentation giving an average survival time of 5-8 months. When assessing the lesion radiographically, care must be taken to determine respectability, as surgery (i.e. Whipple procedure) is the only hope of cure. \n\nSonographically, adenocarcinoma appears as a hypoechoic mass or just a subtle alteration of echotexture of the pancreas. Biliary and pancreatic ductal dilatation can easily be identified and may be the only abnormality identified. Characteristically, the dilated ducts will terminate into a hypoechoic mass. If the portal vein, superior mesenteric artery, superior mesenteric vein, hepatic artery or celiac trunk are seen to be encased in tumor or involved with direct tumor invasion, the lesion is determined to be non-resectable. Also, if liver or peritoneal metastases are identified, the lesion is not resectable. \n\nOn CT, pancreatic adenocarcinoma appears as a hypodense mass distorting the contour of the pancreas with common bile duct and pancreatic duct dilatation and possible atrophy of the remaining pancreatic tissue. Criteria for non-resectability on CT include extension of the tumor beyond the margins of the pancreas, tumor involvement of adjacent organs, enlarged regional lymph nodes (>15mm), encasement or involvement of peripancreatic vessels, metastases in the liver, or peritoneal carcinomatosis." }, "Topic": { "Title": "Pancreatic Adenocarcinoma", "Disease Discussion": "Pancreatic adenocarcinoma accounts for 3% of all cancers and is commonly unresectable at time of presentation giving an average survival time of 5-8 months. When assessing the lesion radiographically, care must be taken to determine respectability, as surgery (i.e. Whipple procedure) is the only hope of cure. \n\nSonographically, adenocarcinoma appears as a hypoechoic mass or just a subtle alteration of echotexture of the pancreas. Biliary and pancreatic ductal dilatation can easily be identified and may be the only abnormality identified. Characteristically, the dilated ducts will terminate into a hypoechoic mass. If the portal vein, superior mesenteric artery, superior mesenteric vein, hepatic artery or celiac trunk are seen to be encased in tumor or involved with direct tumor invasion, the lesion is determined to be non-resectable. Also, if liver or peritoneal metastases are identified, the lesion is not resectable. \n\nOn CT, pancreatic adenocarcinoma appears as a hypodense mass distorting the contour of the pancreas with common bile duct and pancreatic duct dilatation and possible atrophy of the remaining pancreatic tissue. Criteria for non-resectability on CT include extension of the tumor beyond the margins of the pancreas, tumor involvement of adjacent organs, enlarged regional lymph nodes (>15mm), encasement or involvement of peripancreatic vessels, metastases in the liver, or peritoneal carcinomatosis.", "ACR Code": "7.3", "Category": "Neoplasm, carcinoma", "Keywords": "PancreasAdenocarcinoma", "Reference": "Brant, WE. Ultrasound. Philadelphia: Lippincott Williams and Wilkins. 2001. \n\nBrant, WE and Helms, CA. Fundamentals of Diagnostic Radiology, second edition. Philadelphia: Lippincott Williams and Wilkins. 1999." } }, { "U_id": "MPX1538", "TAC": [ "MPX1538_synpic41609", "MPX1538_synpic41611", "MPX1538_synpic41612" ], "MRI": [], "Case": { "Title": "Pneumocystis jiroveci (P. carinii) Pneumonia", "History": "39 year old male who is HIV positive, with a CD4 count of 71 cells/mm3, and complaint of dyspnea on exertion.", "Exam": "WBC: 5.2 K/UL\nLDH: 541 (100-225) U/L", "Findings": "Chest Radiography: Biapical air space opacities are noted with stranding toward the hila. No pleural effusions or adenopathy is evident.\n\nContrast Enhanced CT: Both patchy and confluent air space opacities are evident in a central bilateral upper lobe distribution, with sparing of the lower lung zones. No significant adenopathy is noted.", "Differential Diagnosis": "M. tuberculosis\nBacterial Pneumonia\nPneumocystis jiroveci (carinii)\nM. avium-intracellulare\nFungal organisms", "Case Diagnosis": "Pneumocystis jiroveci (P. carinii) Pneumonia", "Diagnosis By": "BAL was positive for pneumocystis jiroveci.", "Discussion": "This case demonstrates atypical radiographic findings of PCP, as the salient abnormalities are air space opacities occurring in a predominately upper lobe distribution. These findings are in stark contrast to the symmetric perihilar and bilateral lower lobe reticular opacities frequently identified in PCP." }, "Topic": { "Title": "Pneumocystis jiroveci (P. carinii) Pneumonia", "Disease Discussion": "Condition: Pneumocystis jiroveci (P. carinii) Pneumonia\n\nDiscussion: \n\nPneumocystis jiroveci (P. carinii) originally thought to be protozoan, now classified as a fungal element, results in clinically significant pneumonia, and is an AIDS defining illness that occurs when the CD4 count drops to below 200 cells/mm3. Additionally, any immunocompromised patient may be affected; organ recipients on immunosuppressive treatment, oncologic and hematologic patients, the elderly, severely malnourished children, and patients requiring prolonged corticosteroid therapy.\n\nThe most common radiographic finding in patients with PCP consists of diffuse, bilateral symmetric ground-glass reticulonodular, or finely granular opacities occurring in a perihilar, or lower lung zone distribution. Less commonly, PCP will occur with upper lobe predominance. If untreated, these opacities may manifest as diffuse air space consolidation. As the disease progresses, interstitial disease will become more pronounced, and air cysts may be noticed in 5% to 35% of patients. Occasionally, single or multiple nodules, miliary nodules, cavitation, hilar or mediastinal adenopathy, and pleural effusion will be identified. CT typically demonstrates symmetric bilateral ground-glass opacities, which may be diffuse, or have a mosaic pattern with sharp transitions between normal and abnormal lung giving a \u201ccrazy-paving\u201d pattern. Spontaneous pneumothorax may be identified in 5% to 10% of patients, and is more common when cysts are present. Pneumomediastinum may also be evident occurring by itself or in concert with pneumothorax.\n\nMost patients have characteristic radiographic findings of PCP, eliminating the need for CT. However, in patients with symptoms and atypical radiographic findings, CT may show ground-glass opacities, that when correlated with the CD4+ count and other clinical markers may allow the correct diagnosis of PCP to be made. Other causes of ground-glass opacities in patients with AIDS include CMV pneumonia and lymphocytic interstitial pneumonia.\n\nClinically, patients with PCP demonstrate nonspecific complaints. Fever, cough, progressive dyspnea on exertion, weight loss, night sweats, and chest pain are all common symptoms. Lactate dehydrogenase (LDH) levels are frequently elevated, and patients demonstrate restrictive patterns on pulmonary function tests, with hypoxemia when exercising. Clinicians may employ induced sputums, or use bronchoscopy with BAL to clinch the diagnosis. BAL which has close to 100% sensitivity and 89% specificity in diagnosing PCP, is useful when positive, however when results are negative, transbronchial or open lung biopsy may be pursued when the clinical findings suggest a high probability of PCP. Patients will often begin empirical therapy in the absence of definitive diagnosis to avoid potential complications.\n\nSummary: Perihilar and bilateral lower lobe reticular opacities on chest radiography in a patient with a CD4 count less than 200 cells/mm3 suggests PCP.", "ACR Code": "6.2", "Category": "Infection, fungi", "Keywords": "Pneumocystis jiroveci PneumoniaPCPAIDS defining illness", "Reference": "Shah et al. RadioGraphics 1997;17:47-58\nSider et al. RadioGraphics 1993; 13:771-784\nFraser et al. Synopsis of Diseases of the Chest. Third Edition. Elsevier Saunders. Philadelphia, PA. 2005. \nPope T. Aunt Minnie\u2019s Atlas and Imaging-Specific Diagnosis. 2nd Ed. Lippincott Williams & Wilkins. Philadelphia, PA. 2003." } }, { "U_id": "MPX1544", "TAC": [ "MPX1544_synpic54563" ], "MRI": [ "MPX1544_synpic54565", "MPX1544_synpic54566" ], "Case": { "Title": "Non communicating hydrocephalus due to aqueductal stenosis", "History": "21 yr old pregnant female at 11 wks of gestation presents with two weeks history of severe headache. She reports recent MVC one week prior to presentation to the ED. Subsequently, she noted a remote history of salmonella meningitis as a child.", "Exam": "Non-contributory. Non-focal neuro exam.", "Findings": "CT imaging without contrast showed ventricular enlargement of lateral and third ventricles with a normal fourth ventricle. Subsequent MRI confirmed the CT findings without evidence of transependymal flow of CSF. High resolution MRI demonstrated multiple thin septations in the aqueduct of Sylvius.\n\nMR imaging with CINE CSF flow study (not depicted) showed no significant CSF flow through the cerebral aqueduct.", "Differential Diagnosis": "Communicating vs. Non-communicating Hydrocephalus", "Case Diagnosis": "Non communicating hydrocephalus due to aqueductal stenosis", "Diagnosis By": "The diagnosis was confirmed by the imaging studies.", "Treatment & Follow Up": "Neurosurgery was consulted and patient underwent surgery with ventriculo-peritoneal shunt placement to alleviate pressure and to prevent any further complications. \n\nEndoscopic ventriculostomy is an alternative to the shunt surgery.", "Discussion": "Hydrocephalus is defined as an active distension of the ventricular system due to inadequate passage of CSF from its point of production within the ventricular system to its point of absorption into the systemic circulation (2). The incidence of hydrocephalus is equal in men and women. However, there are a few exceptions such as an X-linked hydrocephalus and normal pressure hydrocephalus that is predominant in male patients.\n\nThis 21 yr old woman presented with headache and was diagnosed with aqueductal stenosis. Headache is the most common clinical manifestation of an adult with aqueductal stenosis. The signs and symptoms of hydrocephalus vary with age and disease progression. A symptomatic adult patient could have additional neurological symptoms such as nausea, vomiting, blurred and double vision, gait impairment, drowsiness and cognitive deterioration. Possible physical exam findings include those due to increased intracranial pressure such as papilledema, failure of upward gaze and accommodation, enlarged head, and gait instability(1). \n\nBased on the imaging findings, the patient suffered from chronic hydrocephalus because there was no significant transependymal flow of CSF or sulcal effacement . Chronic hydrocephalus are typically due to congenital causes or longstanding processes, and this patient\u2019s aqueductal septations are likely associated with post-inflammatory changes and sequelae of her childhood case of salmonella meningitis. The incidence of chronic hydrocephalus increases with increasing age and clinical symptoms appear when hydrocephalus decompensates due to late onset of aqueductal stenosis (3,4). \n\nIn order to relieve the pressure and improve patient\u2019s clinical manifestation, this patient underwent VP shunt placement. Currently, there are two forms of surgical treatment for aqueductal stenosis: shunt placement and endoscopic third ventriculostomy. Shunt surgery remains the standard of care due to its effectiveness, but ETV experience is growing with improving patency rates and avoids shunt malfunction complications. After obstruction is resolved, a patient\u2019s gait, postural function, cognitive functions may improve (1). This patient had complete resolution of headache.\n\nReferences:\n1.\tTisell, M, Tullberg, M, Hellstrom, P, Blomsterwall, E, Wikkelso, C. Neurological symptoms and signs in adult aqueductal stenosis. Acta Neurologica Scandinavica. 2003;107(5):311-317.\n2.\tRekate, HL. A contemporary definition and classification of hydrocephalus. Seminars in Pediatric Neurology. 2009; 16(1):9-15.\n3.\tPartington MD. Congenital hydrocephalus. Neurosurg Clin N Am. 2001;12(4):737-42. \n4.\tEdwards, RJ, Dombrowski, SM, Luciano, MG, Pople, IK. Chronic hydrocephalus in adults. Brain Pathol. 2004;14(3)325-36.\n5.\tTisell, M. How should primary aqueductal stenosis in adults be treated? A review. Acta Neurologica Scandinavica. 2005;111(3):145-153." }, "Topic": { "Title": "Hydrocephalus", "Disease Discussion": "Hydrocephalus can be categorized in a variety of ways. By etiology, both congenital and acquired entities can result in hydrocephalus. Congenital abnormalities such as Arnold Chiari and Dandy Walker malformation and acquired diseases such as tumors, infections, and trauma and result in hydrocephalus. \n\nHydrocephalus can also be divided into communicating and non-communicating hydrocephalus. In communicating hydrocephalus, the CSF flow is blocked after it exits the ventricles. It is most commonly due to defective absorption of CSF, venous drainage insufficiency, and overproduction. In non-communicating hydrocephalus, the CSF flow is blocked along one or more of the narrow passages connecting the ventricles. The most common cause is Aqueductal Stenosis. The symptoms vary with patient age and degree of disease progression. Treatment options include placement of ventriculoperitoneal shunt system and endoscopic third ventriculostomy.", "ACR Code": "1.9", "Category": "Obstruction or Stenosis", "Keywords": "HydrocephalusAqueductal stenosis", "Reference": "1.Tisell, M, Tullberg, M, Hellstrom, P, Blomsterwall, E, Wikkelso, C. Neurological symptoms and signs in adult aqueductal stenosis. Acta Neurologica Scandinavica. 2003;107(5):311-317.\n2.Rekate, HL. A contemporary definition and classification of hydrocephalus. Seminars in Pediatric Neurology. 2009; 16(1):9-15.\n3.Partington MD. Congenital hydrocephalus. Neurosurg Clin N Am. 2001;12(4):737-42. \n4.Edwards, RJ, Dombrowski, SM, Luciano, MG, Pople, IK. Chronic hydrocephalus in adults. Brain Pathol. 2004;14(3)325-36.\n5.Tisell, M. How should primary aqueductal stenosis in adults be treated? A review. Acta Neurologica Scandinavica. 2005;111(3):145-153." } }, { "U_id": "MPX1549", "TAC": [ "MPX1549_synpic24681", "MPX1549_synpic24682", "MPX1549_synpic24683" ], "MRI": [], "Case": { "Title": "Craniosynostosis of the metopic suture", "History": "3.5 month-old baby girl with an abnormally shaped, large head, and prominent scalp veins.", "Exam": "Head circumference: 41cm. Hypotelorism. Normal newborn metabolic screening labs.", "Findings": "Trigonocephaly\nHypotelorism (eyes too close together)\nMild macrocephaly (by skull circumference)\nPremature closure of the anterior and posterior fontanels", "Differential Diagnosis": "Skull molding\nCraniosynostosis", "Case Diagnosis": "Craniosynostosis of the metopic suture", "Diagnosis By": "Characteristic imaging and surgery", "Treatment & Follow Up": "Treatment of craniosynostosis is primarily surgical. These infants are usually operated on early in their life. Patients with metopic craniosynostosis are treated prior to sixth months of age.\n\nFactors that may necessitate earlier treatment are increasing intracranial pressure and corneal exposure secondary to exorbitism.\n\nThe procedure to correct symmetric craniosynostosis (as in this case) involves fracturing the bone parallel to the affected suture. A synthetic material graft is placed between the bone and the new \u201csuture\u201d that helps delay fusion.", "Discussion": "Craniosynostosis is the early fusion of one or more of the cranial sutures. In this case, the patient\u2019s metopic suture has fused early, resulting in trigonocephaly.\n\nThe incidence of craniosynostosis in newborns is approximately .4 per 1000 and less than 10% of these involve the metopic suture.\n\nMetopic craniosynostosis usually only has cosmetic consequences, and the patients usually have normal intellectual development.\n\nThis condition is usually idiopathic, but there are other varieties of craniosynostosis that are components of syndromes." }, "Topic": { "Title": "Craniosynostosis of the metopic suture", "Disease Discussion": "Craniosynostosis is the early fusion of one or more of the cranial sutures. The incidence of craniosynostosis in newborns is approximately .4 per 1000; and, less than 10% involve the metopic suture. Metopic craniosynostosis usually only has cosmetic consequences, and the patients usually have normal intellectual development. This condition is usually idiopathic, but there are other varieties of craniosynostosis that are components of syndromes.", "ACR Code": "1.1", "Category": "Congenital, malformation", "Keywords": "CraniosynostosistrigonocephalyMetopic craniosynostosis", "Reference": "Not provided" } }, { "U_id": "MPX1539", "TAC": [ "MPX1539_synpic19063", "MPX1539_synpic19064", "MPX1539_synpic19065", "MPX1539_synpic19066", "MPX1539_synpic19067", "MPX1539_synpic19068", "MPX1539_synpic19070" ], "MRI": [], "Case": { "Title": "Suspected meningioma", "History": "Middle aged white male status post motor vehicle accident after passing out at the wheel in stable and lucid condition. Patient is a civilian trauma who is ineligible for care follow-up and definitive care at our military institution.", "Exam": "N/A", "Findings": "A large hyperdense extraaxial mass with hypodense cystic regions fills the right middle cranial fossa in the area of the sphenoid ridge. The mass involves the skull base and indents the right frontotemporal parenchyma with local mass-effect and edema with protrusion into the right lateral ventricle and compression of the upper aspect of the right midbrain. Basal cisterns and lateral ventricles remain open. There has been bony remodeling and scalloping of the skull base. Calcification and hyperostosis are also present. There is no evidence of acute intracranial hemorrhage.", "Differential Diagnosis": "Meningioma, malignant meningioma, metastasis.", "Case Diagnosis": "Suspected meningioma", "Diagnosis By": "Unable to confirm.", "Treatment & Follow Up": "MRI was recommended anticipating subsequent surgical resection.", "Discussion": "Unfortunately, this patient was not eligible for care at a military institution and a non-contrast enhanced axial CT scan of the head was the only study performed. It is thought that this slow growing tumor (suspected meningioma) was responsible for this patient's loss of consciousness and subsequent motor vehicle accident." }, "Topic": { "Title": "Suspected meningioma", "Disease Discussion": "Meningiomas originate from arachnoid cap cells and are the most common extraaxial neoplasms of the brain, representing 15-20% of all brain tumors. Although it is hormonally sensitive and is three times more common in women, meningioma represents a significant proportion of the extraaxial neoplasms in men and in adults of all age groups. Most patients present between the ages of 40 and 60 years of age. Meningiomas are uncommon in children without associated neurofibromatosis type-2. The most common locations for meningiomas (in descending order) are the parasagital dura, convexities, sphenoid wing, juxtasellar, cerebellopontine angle cistern, olfactory groove, posterior fossa clivus, planum sphenoidale, and tentorium. Uncommon locations are the ventricles (pediatric patients), with a distinct propensity for the left lateral ventricle, and the optic nerve sheath (adult females). 2-3% occur in the spine. Less than one percent of meningiomas are extradural and result from embryologic arachnoid rests outside the CNS. These extradural menigiomas have been found in the interdiploic space, outer table of skull, skin, paranasal sinuses, parotid gland, and parapharyngeal space. Multiple lesions occur in 1-2% of patients increasing to 30% with a previous history of radiation therapy.\n\nMeningiomas often incite a variable amount of intracranial edema with lesions adjacent to the cerebral cortex tending to cause greater edema than those along the basal cisterns or planum. However, edema is absent in 40% of cases because of slow growth. The lesions themselves demonstrate calcifications in 20% of cases while cystic areas are seen 15% of the time. Meningiomas can sometimes demonstrate intraosseous extension or grow through the bone or into the dura. Hyperostosis or osteolysis occur in 20% to 46% of cases. Hyperostosis is particularly common when the tumor is at the skull base or anterior cranial fossa where it may resemble fibrous dysplasia or Paget\u2019s disease. The skull base is the one region where meningiomas can become unresectable because of collateral damage to vital structures. Occasionally, meningiomas may have necrotic centers. Thrombosis and, rarely, osteblastic, chondromatous, or fatty degeneration occurs. Meningiomas may encase and narrow adjacent vessels. Meningiomas often parasitize pial vessels. As such, these lesions have both a dural and a pial blood supply. In the typical convexity or sphenoid wing meningioma, the middle meningeal artery is enlarged.\n\nAtypical meningiomas make up 2.4% of all meningiomas and are classified as WHO grade II. Atypical lesions must exhibit increased mitotic rates, small cells with high nucleus/cytoplasmic ratio, prominent nucleoli, sheet like growth, and foci of necrosis causing nonhomogenous enhancement. They look like benign meningiomas radiographically, but recur more frequently. Hemorrhage is common as are peripheral low density zones from trapped CSF in arachnoid cysts.\n\nMelignant meningiomas are classified as WHO grade III, are uncommon and are usually diagnosed when intraparenchymal invasion, markedly rapid growth, or sarcomatous degeneration has taken place, most likely arising from benign tumors gone awry. The papillary variety of meningioma undergoes malignant differentiation more commonly than the rest. Higher grade is associated with a higher rate of recurrence. Survival varies with the site, size, grade, and extent of surgical removal of tumor.\n\nRadiation therapy induces five times more meningiomas than it does schwannomas or sarcomas. Diagnosis of radiation induced meningioma is made if the meningioma arises in the radiation field, appears after a latency period (of years), was not the primary tumor irradiated, and is not seen in a patient with neurofibromatosis. Low dose radiation treatment for tinea capitis has been associated with meningiomas following a latency period of about 35 years. Recurrence rates are higher in radiation-induced meningiomas than in non-radiation induced tumors.\n\nOn unenhanced CT scan, 75% of meningiomas are slightly hyperdense while 25% are isodense to normal brain parenchyma. Strong, homogenous enhancement is a hallmark (90%). Signal intensity is similar to normal falx on enhanced and nonenhanced CT. Calcifications are seen in 20% of lesions and cystic areas are present in 15% of tumors. The tumors appear round and unilobulated with sharp margins. A lobulated, extraaxial, parasagittal mass with a dural tail is a typical finding on CT scan. Rarely, they may appear en plaque, with pancake-like spread along the dura. Extension of tumor or dural reaction along a dural surface is not uncommon and is known as a \u201cdural tail\u201d which is suggestive, but not specific for meningioma. Bony erosions are rare, but are more common with malignant meningiomas, where as hyperostosis is more common and more often associated with benign nature.\n\nTumors are typically isointense to gray matter on MRI with strong gadolinium enhancement. MRI is the best technique for detecting the dural tail. Increased vascular flow voids within and around the lesion are characteristic.\n\nAngiographic characteristics include a spoke-wheel appearance with dense venous filling, a persistent tumor blush (\u201ccomes early and stays late\u201d) with well demarcated margins and a dural vascular supply. The middle meningeal artery may be enlarged.", "ACR Code": "1.3", "Category": "Neoplasm, non-glial", "Keywords": "meningiomaextraaxialneoplastic", "Reference": "Fundamentals of Diagnostic Radiology / (edited by) William E. Brant, Clyde A. Helms.\u20142nd ed., Lippincott Williams & Wilkins, 1999\n\nNeuroradiology: The Requisites / Robert I. Grossman, David M. Yousem.\u20142nd ed., Mosby, 2003\n\nPrimer of Diagnostic Imaging / (edited by) Janice M. Gaillard\u20143rd ed., Mosby Inc., 2003" } }, { "U_id": "MPX1519", "TAC": [ "MPX1519_synpic31538", "MPX1519_synpic31539", "MPX1519_synpic31540", "MPX1519_synpic31547", "MPX1519_synpic31548", "MPX1519_synpic31550" ], "MRI": [], "Case": { "Title": "Bilateral pleural effusions, bilateral pelvic hematomas, fracture/tract of left iliac, Left 5th rib fracture, thickening of gastric wall - non-specific changes, and post surgical changes to left upper quadrent status post splenectomy.", "History": "25 y/o man with 3 GSW to chest, abdomen, and Left buttock. Pt was resuscitated and had an ex-lap performed before transfer to WRAMC.", "Exam": "HR 116/65, P 85, RR 16, T 97.6. AOx3, equal BS with no rales, rhonchi, or wheezes. 3 cm chest wall wound tracking under subcutaneous tissue inferiorly. Abdomen is soft, NT, ND. Midline incision with staples, no erythema, purulence, or tenderness. LLQ end colostomy with stoma in place. Less than 1 cm entrance wound on the left buttock with no signs of purulence or erythema. No neurological deficits noted.", "Findings": "Chest film: Blunting of CP angles especially on left. Air bronchograms and atelectatic lungs. Positive spine sign.\n\nCT: Bilateral pleural effusions with compressive attelectasis L>R. Multiple prominent axillary lymph nodes are identified meeting pathologic criteria in number but not in size. A hypodense band is seen in the upper pole of the left kidney representing laceration. Post surgical changes are noted in the L upper abdomen with 2 metallic clips seen and an absent spleen. Clip is in the L hemidiaphragm status post diaphragmatic rupture. Colostomy is seen on left with descending colon attached. The stomach reveals a thickened and irregular wall with out evidence of a filling defect or focal mass. Two fluid collections are seen in the pelvis, one in the left hemipelvis anterior to the iliac and the second in the right hemipelvis consistent with hematomas. Air can be seen in the left gluteus maximus and in the left lateral wall representing bullet tract. In the bony structures there is a complete fracture through the wing of the left ilia with several bone fragments in the pelvis consistent with the ballistic tract. A fracture is also noted in the middle portion of the left 5th rib from another bullet.", "Differential Diagnosis": "PolyTrauma from multiple ballistics", "Case Diagnosis": "Bilateral pleural effusions, bilateral pelvic hematomas, fracture/tract of left iliac, Left 5th rib fracture, thickening of gastric wall - non-specific changes, and post surgical changes to left upper quadrent status post splenectomy.", "Diagnosis By": "Imaging, Findings from previous exploratory laparotomy", "Treatment & Follow Up": "Pt underwent theraputic thoracentesis for pleural effusions.", "Discussion": "This patient illustrates the challenges of caring for patients en-route. In the United States, many patients with significant trauma are evaluated at a trauma center, resuscitated at that same center and receive definitive care all within one hospital. In the military this is different as they may pass through many different facilities on their way back to the US for definitive care in a relatively short time. A complete set of images may not always be available and the Radiologist must try to look at repeat scans to figure out what interventions may have been done prior to the patient\u2019s arrival and what are the remaining complications. Often the patients may not be aware of what surgeries they have had because they were unconscious and are unable to provide accurate histories.\n\nThis is illustrated in trying to follow the even number rule of GSW\u2019s. For each entrance wound, it is important to see either an exit wound or a bullet. If we do not see a paired wound or bullet with an entrance wound it is important to keep searching because the bullet may have embolized or we are missing the exit wound. In patients who have received care en-route it is possible to have a violation of this rule because the bullets may have been removed during previous surgeries at different facilities.\n\nThis patient had a repaired diaphragm laceration before reaching our facility which is evidence by 2 clips in the left hemi-diaphragm. Penetrating diaphragm injuries tend to be smaller (length 1-2cm) and more subtle than blunt diaphragm injuries. The signs used for detecting blunt diaphragm injury are not as useful in assessing penetrating diaphragm injuries. One early and specific sign of PDI is herniation of abdominal fat through the injury into the thorax. If a wound tract is seen on both sides of the diaphragm the specificity of this sign is reportedly 100% (sensitivity 36%). The diaphragm can also be abnormally thickened when being compared to the contralateral hemidiaphragm due to hematoma, edema, or muscle retraction. One must have a high index of suspicion when evaluation for penetrating diaphragm injuries." }, "Topic": { "Title": "Penetrating Diaphragm Injury After Trauma", "Disease Discussion": "Typically, penetrating diaphragm injury is difficult to diagnose without a high index of suspicion. Penetrating diaphragm injuries (PDI) tend to be smaller than blunt diaphragm injuries. PDI\u2019s typically are \u22641-2 cm in length. Diaphragm injuries are most easily diagnosed at laparotomy but not all patients have indications for an initial laparotomy.\n\nIn trauma, a chest radiograph is typically the first imaging modality employed. This can be helpful in the initial evaluation for inspecting the integrity of the hemi-diaphragms but patient positioning and the quality of portable films can limit their usefulness. Many patients with trauma ultimately undergo a CT study. Multiplanar reconstructed images have been reported by some to be helpful in detecting diaphragm injuries. There are fewer studies on the use of CT with PDI, one small study by Larici, et al. reported a sensitivity of 86% and a specificity of 79% of detecting PDI\u2019s with helical CT. \n\nHerniation of abdominal fat into the thorax is one sign that is commonly used to detect blunt diaphragm rupture can still be used when looking for PDI. The most specific sign of PDI is a wound tract that is found on both sides of the diaphragm. This has a reported specificity of 100% and a sensitivity of 36%. A hemothorax or wound tract near the diaphragm should heighten the radiologist\u2019s suspicion for a diaphragm injury.", "ACR Code": "4.4", "Category": "Trauma", "Keywords": "traumadiaphragm", "Reference": "Sliker CW. Imaging of diaphragm injuries. Radiol Clin N Am. 2006; 44:199-211.\n\nLarici AR, Gotway MB, Litt HI, et al. Helical CT with sagittal and coronal reconstructions: accuracy for detection of diaphragmatic injury. Am J Roentgeol. 2002;179:451-7.\n\nShackleton KL, Stewart ET, Taylor AJ. Traumatic diaphragm injuries: spectrum of radiographic findings. Radiographics. 1998; 18(1):49-59." } }, { "U_id": "MPX1556", "TAC": [ "MPX1556_synpic45716", "MPX1556_synpic45717", "MPX1556_synpic45718", "MPX1556_synpic45719", "MPX1556_synpic45721" ], "MRI": [], "Case": { "Title": "Metastatic Pancreatic Adenocarcinoma", "History": "52 yo male with RUQ pain and abnormal liver associated enzymes.", "Exam": "AST: 52 (H) U/L\nALT: 49 (30-65) U/L\nAPhos: 236 (H) U/L\nTBili: 0.7 mg/dL\nDBili: 0.1 mg/dL", "Findings": "Contrast enhanced images through the liver, obtained during the hepatic arterial phase and viewed with liver windows, shows multiple nodular hypodensities throughout the liver parenchyma, with surrounding peripheral rim enhancement and associated wedge-shaped high-attenuation areas.\n\nContrast enhanced image through the pancreas shows a hypodense mass in the body. Note the attenuation difference between the tumor and the avidly enhancing normal pancreas.", "Differential Diagnosis": "Differential Diagnosis for Transient Hepatic Attenuation Difference (THAD):\n\nHepatocellular carcinoma is the most common primary hepatic tumor associated with THAD. In regards to cholangiocarcinoma, THAD is an important indirect sign of vascular invasion. Metastatic hypervascular lesions from islet cell tumors, carcinoids, renal cell carcinoma, and breast carcinoma may also have this imaging appearance. Hemangiomas, focal nodular hyperplasia, pyogenic abscess, and focal eosinophilic necrosis are additional differential considerations. Finally, hepatic hemodynamic alterations caused by liver cirrhosis, portal or hepatic vein thrombosis, and arterioportal shunts may result in THAD.", "Case Diagnosis": "Metastatic Pancreatic Adenocarcinoma", "Diagnosis By": "Biopsy confirmed pancreatic adenocarcinoma." }, "Topic": { "Title": "Transient hepatic attenuation difference", "Disease Discussion": "Discussion:\n\nTransient hepatic attenuation difference (THAD) is an attenuation difference of the liver visible during the hepatic arterial phase of CT imaging, caused by the liver\u2019s dual hepatic blood supply. Generally, THAD is associated with malignant tumors, however, this finding may also be seen with hemangiomas, focal nodular hyperplasia, pyogenic abscesses, focal eosinophilic necrosis, long-standing biliary obstruction, trauma, and hepatic hemodynamic alterations caused by liver cirrhosis, portal or hepatic vein thrombosis, arterioportal shunts, or an aberrant hepatic blood supply. The visualized high-attenuation areas are the result of increased arterial flow and decreased portal venous flow from disruption in normal hepatic homeostasis. An MR imaging correlate is Transient Hepatic Intensity Difference (THID).", "ACR Code": "7.3", "Category": "Radiologic Sign or Finding", "Keywords": "Transient hepatic attenuation differenceTHAD", "Reference": "Foley, D. Multidetector CT: Abdominal Visceral Imaging. RadioGraphics 2002;2701-719.\n\nColagrande et al. AJR 2007; 188:154-159\n\nKim et al. AJR 2005;184:83-90" } }, { "U_id": "MPX1560", "TAC": [ "MPX1560_synpic52005", "MPX1560_synpic52010" ], "MRI": [], "Case": { "Title": "Laryngeal Papillomatosis with malignant transformation", "History": "This 51yo man has a history of progressive recurrent stridor and hoarseness. He has been admitted multiple times for respiratory distress. He has known laryngeal papillomatosis with +HPV.", "Exam": "On physical exam, patient has marked inspiratory stridor, with resultant prolonged inspiratory phase. His voice is very soft, and markedly hoarse. Lung fields are clear to auscultation bilaterally aside from referred upper airway stridor.", "Findings": "Within the subglottic region there is an ill-defined and heterogeneous mass with postcontrast enhancement that measures 5.1 cm (CC) x\n3.0 cm (AP) x 2.4 cm (trans) mass. This is within the tracheal lumen and is precluding the airway. In addition, this is compressing the upper esophagus. There is no evidence of bony erosion at the adjacent hyoid bone. There is no evidence of additional mass lesions within the nasal or oral pharynx. There is no evidence of lesions within the distal trachea or mainstem bronchi. A tracheostomy tube is seen that enters the trachea just distal to this mass lesion. There is no evidence of adenopathy.", "Differential Diagnosis": "Differential considerations include respiratory papillomatosis given the patient's history. Primary malignancy cannot be entirely excluded on this study, though there is no evidence of local invasion or adenopathy.", "Case Diagnosis": "Laryngeal Papillomatosis with malignant transformation", "Diagnosis By": "Surgical excision and biopsy", "Treatment & Follow Up": "Patient received a tracheostomy for airway protection. He will likely undergo more extensive surgical resection and neck dissection. He will also likely receive radiation therapy." }, "Topic": { "Title": "Laryngeal Papillomatosis with malignant degeneration", "Disease Discussion": "Lesion/Condition Name: Laryngeal papillomatosis secondary to HPV infection with malignant degeneration to Papillary Squamous Cell Carcinoma\n\nCell of Origin: Respiratory squamous epithelium\n\nAssociations/Predisposing Factors: HPV infection, male gender, age greater than 60 years, alcohol and/or tobacco usage\n\nCommon Locations: glottic and subglottic airway icluding the vocal cords themselves, may extend into trachea and mainstem bronchi\n\nHistology: \nExophytic and papillary squamous cell carcinomas (SCCs) are uncommon variants of SCC. It is marked by atypical epithelium, often with loss of orientation, loss of polarity, increased nuclear to cytoplasmic ratio, dyskeratosis, paradoxical keratinization, and increased number of mitotic figures, including atypical forms. This may be associated with inflammatory infiltrate and/or focal desmoplastic stroma. Invasion into the stroma is common, and may be associated with paradoxical keratinization. By convention, papillary and exophytic squamous cell carcinomas are by \t\ndefinition invasive lesions. \n\nRadiology: Laryngeal papillomas are usually benign and non-invasive unless they undergo malignant degeneration which is uncommon. They occur moost often in children, and are usually multiple. Involvement of the trachea and bronchial tree is common. Etiology is thought to be viral seconary to HPV. When they occur in adults, the lesions are more likley to be singular. Lesions are exophytic, and diagnosis is usually made via bronchoscopy. CT or MR imaging may however be used to evaluate extent of disease. Pulmonary involvement is generally evaluated by Chest plain film, which appears as small cavitating nodules.\n\nGlottic Narrowing DDx: \n-Congenital: laryngeal atresia, stenosis, webs\n-Neoplastic: papilloma, squamous cell carcinoma, hemangiomas, lipomas, chondromas\n-Neurogenic: vocal cord paralysis\n-Traumatic: Foreign body, hematoma, vocal cord nodules (reactive)\n\nPrognosis and Treatment: Treatment generally consists of surgery \n(excisional biopsy, vocal cord stripping, and/or laryngectomy), often in conjunction with radiation therapy. Although recurrences do occur, prognosis for exophytic and papillary squamous cell carcinoma tend to have better prognosis than traditional SCC. 5-year survival rates for T1 lesions are 88% for exophytic type, and 100% for papillary type. Whether the tumor is glottic vs. subglottic, transglottic, or supraglottic has no effect on mortality in contrast to traditional SCC in which glottic tumors pend a better prognosis.", "ACR Code": "2.3", "Category": "Neoplasm, carcinoma", "Keywords": "PapillomaCarcinomaAirway", "Reference": "Thompson, Lester DR, Wenig, Bruce M., Heffner, Dennis K., Gnepp, Douglass R. Exophytic and papillary squamous cell carcinomas of the larynx: A clinicopathologic series of 104 cases. Otolaryngol Head Neck Surg 1999 May;120(S):718-24.\n\nSom, Peter M., and Hugh D. Curtin. Head and Neck Imaging. 4th Edition. 2. Philadelphia, PA: Elsevier, 2003. 1647-51. Print." } }, { "U_id": "MPX1563", "TAC": [ "MPX1563_synpic51033" ], "MRI": [ "MPX1563_synpic51034", "MPX1563_synpic51035" ], "Case": { "Title": "Left frontal cavernous malformation with DVA.", "History": "76 y.o. woman who fell; LOC; no trauma to head; twisted ankle", "Exam": "Bruise on left ankle. No cranial nerve deficits or other neurological deficits.", "Findings": "1.\tOutside head CT reported small 1cm homogenously round hyperdense lesion in left frontal lobe as an intraparenchymal hemorrhage (IPH).\n2.\tHead CT in our hospital 5 hours later: stable 1 cm homogenously round hyperdense lesion, suspicious for cavernoma, suggest MRI for confirmation.\n 3. Brain MRI later shows classic \u201cpopcorn\u201d appearance on T2-weighted image with low T2 signal in the periphery of the lesion consistent with cavernoma. In addition, small deep frontal vessels, draining towards the left ventricle, are noted on the post-contrast T1W image, consistent with a developmental venous anomaly (DVA).", "Differential Diagnosis": "1.\tIPH (intra-parenchymal hemorrhage)\n2.\tOther vascular lesions such as AVM, AVF, or aneurysm.\n3.\tHypercellular neoplasm, either primary or metastatic.", "Case Diagnosis": "Left frontal cavernous malformation with DVA.", "Diagnosis By": "MRI", "Treatment & Follow Up": "1.\tNo treatment if no symptoms. Can follow up over time.\n2.\tIf symptomatic, stereotactic radiosurgery or surgery depending on individual cases.", "Discussion": "Cavernomas are often associated with DVAs. Limited role of CT due to lack of specificity. MRI including T2 and GRE sequences are preferred.\n\u2022 \tIde C, De Coene B, Baudrez V. MR features of cavernous angioma. JBR-BTR. Dec 2000;83(6):320. \n\u2022 \tSage MR, Blumbergs PC. Cavernous haemangiomas (angiomas) of the brain. Australas Radiol. May 2001;45(2):247-56. \n\u2022 \tGrossman RI, Yousem DM. Vascular diseases of the brain. In: Neuroradiology: The Requisites. St Louis: Mosby-Year Book;. 1994: 121-6, 141-2. \n\u2022 \tHallam DK, Russell EJ. Imaging of angiographically occult cerebral vascular malformations. Neuroimaging Clin N Am. May 1998;8(2):323-47." }, "Topic": { "Title": "Cavernous Malformation (Cavernous Angioma)", "Disease Discussion": "Cavernous Angiomas make up approximately 10-15% of vascular malformations of the brain. They consist of large sinusoidal vascular spaces which lack normal endothelial tight juctions. As a result, bleeding is frequent. The majority of bleeds from these lesions, however, are subclinical with nearly 100% demonstrating hemosiderin staining of the adjacent parenchyma at diagnosis. There is a 0.5-1% incidence of symptomatic hemmorhage/year. The most common clinical presentation as a result of hemmorhage is the development of seizures or progressive neurologic deficits, with a seizure disorder being the presenting symptom in approximately 50% of patients with cavernous angiomas. The degree to which a lesion is symptomatic is,like most CNS abnormalities, dependent on location. Brainstem lesions tend to present earlier with neurologic deficits.\n\nCavernous angiomas may occur anywhere within the CNS with roughly 3/4 occurring supratentorially, 1/4 within the posterior fossa and brainstem, and occasional lesions within the spinal cord. While the occurrence may be sporadic, there is a strong familial association identified where close to 80% of members of affected families may demonstrate lesions. In about 50% of patients the lesions will be multiple. Whenever more than one cavernous malformation is identified in the CNS, there is probably an autosomal dominant inheritence. This should prompt an evaluation of all first-degree relatives.\n\nImaging findings are related to the degree of prior hemmorhage of the lesions. On CT, these lesions may be heavily calcified. MR often demonstrates blood products of various ages centrally and a rim of hemosiderin peripherally. Gradient-echo images may be helpful in identification of small lesions secondary to the gradient suseptibility or characteristic \"blooming\" artifact produced by hemosiderin. Following contrast administration, on either CT or MR, variable enhancement may occur.", "ACR Code": "1.3", "Category": "Vascular", "Keywords": "cavernous angiomacavernoma", "External Links": "rad.usuhs.mil/rad/home/vascmalf/malf0.html" } }, { "U_id": "MPX1568", "TAC": [ "MPX1568_synpic21206", "MPX1568_synpic21208" ], "MRI": [], "Case": { "Title": "Sarcoidosis, Abdomen and Liver", "History": "Patient with history of thoracic sarcoid presenting with increasing LFTs and pruritis.", "Exam": "Evidence of hepatomegaly on physical examination but no palpable focal abdominal mass. Labs notable for nonspecifically and mildly elevated LFTs.", "Findings": "Enlarged liver with nodular and heterogeneous pattern of enhancement. Periportal and retroperitoneal lymphadenopathy. These findings are consistent with abdominal sarcoid in this clinical setting.", "Differential Diagnosis": "Metastatic Disease (colon, stonach, pancreas, breast, lung)\nLymphoma\nOther Infiltrative Liver Processes", "Case Diagnosis": "Sarcoidosis, Abdomen and Liver", "Diagnosis By": "Biopsy proven" }, "Topic": { "Title": "HEPATIC/ABDOMINAL SARCOID", "Disease Discussion": "Sarcoidosis is a granulomatous disease of unclear etiology, most commonly recognized by its thoracic manifestations of interstitial lung disease and hilar and mediastinal adenopathy. Sarcoidosis is a multisystem disease, with histologic evidence of sarcoid involvement of the liver and spleen seen in 50-80% of all surgical specimens, although most cases do not result in organ dysfunction. Cross-sectional imaging abnormal findings are uncommon and include mild organomegaly and the identification of MR hypointense or CT hypodense nodules, which represent coalescent granulomas. These imaging findings are not specific for sarcoidosis however, and metastatic disease and lymphoma cannot be excluded, although involvement of both the spleen and liver favors sarcoidosis and lymphoma as differential possibilities. Evaluation of the laboratory data, to include tumor markers, can be helpful in determining the presence of malignancy. In the absence of other evidence of sarcoidosis, liver biopsy is advised. Isolated hepatosplenic disease in asymptomatic patients does not usually require specific treatment.", "ACR Code": "7.6", "Category": "Idiopathic or Unknown", "Keywords": "SarcoidosisLiverAbdominal", "Reference": "Koyama T, Ueda H, Togashi K et al. Radiologic manifestations of sarcoidosis in various organs. RadioGraphics 2004;24:87-104.\n\nScott GC. Berman JM, Higgins JL Jr. CT patterns of nodular hepatic and splenic sarcoidosis: a review of the literature. JCAT 1997;21:369-372.", "External Links": "http://hotmature50.com/2091/" } }, { "U_id": "MPX1578", "TAC": [ "MPX1578_synpic18360" ], "MRI": [ "MPX1578_synpic18361", "MPX1578_synpic18362" ], "Case": { "Title": "Cavernous Angioma", "History": "Adult female with history of headaches after hitting head one day prior to presentation.", "Case Diagnosis": "Cavernous Angioma" }, "Topic": { "Title": "Cavernous Malformation (Cavernous Angioma)", "Disease Discussion": "Cavernous Angiomas make up approximately 10-15% of vascular malformations of the brain. They consist of large sinusoidal vascular spaces which lack normal endothelial tight juctions. As a result, bleeding is frequent. The majority of bleeds from these lesions, however, are subclinical with nearly 100% demonstrating hemosiderin staining of the adjacent parenchyma at diagnosis. There is a 0.5-1% incidence of symptomatic hemmorhage/year. The most common clinical presentation as a result of hemmorhage is the development of seizures or progressive neurologic deficits, with a seizure disorder being the presenting symptom in approximately 50% of patients with cavernous angiomas. The degree to which a lesion is symptomatic is,like most CNS abnormalities, dependent on location. Brainstem lesions tend to present earlier with neurologic deficits.\n\nCavernous angiomas may occur anywhere within the CNS with roughly 3/4 occurring supratentorially, 1/4 within the posterior fossa and brainstem, and occasional lesions within the spinal cord. While the occurrence may be sporadic, there is a strong familial association identified where close to 80% of members of affected families may demonstrate lesions. In about 50% of patients the lesions will be multiple. Whenever more than one cavernous malformation is identified in the CNS, there is probably an autosomal dominant inheritence. This should prompt an evaluation of all first-degree relatives.\n\nImaging findings are related to the degree of prior hemmorhage of the lesions. On CT, these lesions may be heavily calcified. MR often demonstrates blood products of various ages centrally and a rim of hemosiderin peripherally. Gradient-echo images may be helpful in identification of small lesions secondary to the gradient suseptibility or characteristic \"blooming\" artifact produced by hemosiderin. Following contrast administration, on either CT or MR, variable enhancement may occur.", "ACR Code": "1.3", "Category": "Vascular", "Keywords": "cavernous angiomacavernoma", "External Links": "rad.usuhs.mil/rad/home/vascmalf/malf0.html" } }, { "U_id": "MPX1575", "TAC": [ "MPX1575_synpic39398" ], "MRI": [], "Case": { "Title": "Metastatic Squamous Cell Lung Cancer with Underlying Idiopathic Pulmonary Fibrosis", "History": "86 y/o male with PMHX of HTN, Afib, hypothyroidism, idiopathic pulmonary fibrosis, dementia, and depression transferred by his assisted living facility for 3 week hx of decreased PO intake, dry cough, increased confusion, and more recently hypotension. Admitted to the hospital for treatment of bilateral pneumonia and malnutrition.", "Exam": "86 y/o well developed, but poorly nourished, demented male, who is a poor historian. Does not appear to be in distress, however c/o of cough and poor apetite. \n\nPulm: Bilateral rales, and ronchi. No wheezing, or stridor.\nCV: Irregular Rate and rythm, no rubs, or gallops, equal pulses X4. \nSkin: Pale, warm and dry.\nAbd: NT/ND, + BS throughout.\nExtremeties: No edema noted, DTRs equal, strength and sensation equal and WNL.\n\nLabs: WBC 17.7, HGB 13.4, HCT 40.7, Plt 417.\nChem: Na 144, K 3.9, CL 106, CO2 27, BUN 17, Cr1.35, Gluc 92, Alb 2.8\nBC X2 Negative for organisms.\nResp Cx: Candida \nBronchoscopy: Cells consistent with metastatic Squamous Cell Non-small Cell Lung Cancer.", "Findings": "CXR: Diffuse opacities throughout bilateral lungs indicative of a fibrotic process. Multiple pulmonary nodules found throughout bilateral lung fields.\n\nCT: Multifocal nodular opacities throughout the bilateral lungs concerning for diffuse metastatic disease. Fibrotic changes with a lower lobe predominance at the representing idiopathic pulmonary fibrosis.", "Differential Diagnosis": "1. Metastatic Non-small Cell lung cancer. \n\n2. Metastatic small cell lung cancer. \n\n3. Idiopathic pulmonary fibrosis\n\n4. Pneumoconiosis (such as asbestosis, silicosis etc) this would depend on his exposure.\n\n5. Infection", "Case Diagnosis": "Metastatic Squamous Cell Lung Cancer with Underlying Idiopathic Pulmonary Fibrosis", "Diagnosis By": "bronchoscopy and tissue biopsy.", "Treatment & Follow Up": "Pt was determined to be inoperable, and not a good candidate for chemotherapy. Pt was returned to Nursing Home as per family's wishes.", "Discussion": "On both CT slices there are good representative images of honeycombing with its characteristic peripheral location, no more than 3 cm into the lung parenchyma and with thick walled air filled cysts that are no more than 1-3cm in diameter. This specific pattern suggests extensive lung fibrosis with alveolar destruction and will often result in a cystic appearance in pathology." }, "Topic": { "Title": "Metastatic Squamous Cell Lung Cancer with Underlying Idiopathic Pulmonary Fibrosis", "Disease Discussion": "Lesions/Condition: Multiple bilateral pulmonary nodules too many too count. Underlying idiopathic pulmonary fibrosis.\n\nCell of Origin: Squamous Cell.\n\nWHO Grade(s): Stage IIIB (T2N3M0)\n\nSynonyms: Non-Small Cell Lung Cancer\n\nAssociations/Predisposing Factors: Smoker.\n\nCommon Locations: Lung\n\nDemographics: 86 y/o white male.\n\nRadiology: A-P Chest, Chest/Abd/Pelvis CT.\n\nPrognosis and Treatment: Poor, non surgical candidate", "ACR Code": "6.3", "Category": "Neoplasm, metastatic", "Keywords": "non small cell lung cancersquamous cell lung canceridiopathic pulmonary fibrosis", "Reference": "Up to Date: Mandel, J. Thomas, K. Weinberger, S. 18 SEP 2007: Overview of non small cell lung cancer staging." } }, { "U_id": "MPX1583", "TAC": [ "MPX1583_synpic24105", "MPX1583_synpic24107" ], "MRI": [ "MPX1583_synpic24109", "MPX1583_synpic24110", "MPX1583_synpic24111" ], "Case": { "Title": "CAVERNOUS HEMANGIOMA", "History": "41-year-old female bulging eye", "Exam": "Eyes:\n OD: 20/40, full visual fields to confrontation. Slight proptosis.\n OS: WNL", "Findings": "A well-circumscribed mass of heterogeneous attenuation (soft tissue attenuation as well as bone attenuation) is present within the intraconal region of the right orbit lateral to the optic nerve. This lesion has the following dimensions: 2.1 cm AP by 1.9 cm transverse by 2.1 cm craniocaudal. The surrounding soft tissues, including the extraocular muscles, are within normal limits. Post-contrast images demonstrate heterogeneous enhancement of this lesion. Exophthalmos is noted with the right globe.", "Differential Diagnosis": "Orbital Dermoid, Orbital Tumors, Cavernous Hemangioma, Metastasis, Lymphoma", "Case Diagnosis": "CAVERNOUS HEMANGIOMA", "Diagnosis By": "Surgical Resection", "Treatment & Follow Up": "Surgical excision is the best treatment for this individual with a symptomatic cavernous hemangioma (Scheuerle 2004). After the surgery she should be followed-up with semi annual ophthalmologic exams that should include fudoscopic and visual field examinations.\n\nTissue excisional biopsy: RIGHT ORBITAL TUMOR consists of a 1.7 x 1.6 x 1.2 cm well circumscribed, grey/blue nodule. The specimen is unoriented. The surgical margins are inked in black. Serial sectioning reveals a dense, red/brown, clot-like interior. Specimen is consistent with cavernous hemangioma", "Discussion": "Cavernous hemangiomas are the most common intraorbital tumors in adults (Kim 2002). As far as the distribution between men and women is concerned, Henderson (1984) reported an almost equal ratio of 8:7 in women and men, while Harris and Jakobiec (1978) found a 7:3 occurrence ratio of women to men. The lesions themselves are benign vascular lesions that are slow growing and can manifest as a painless, progressively proptotic eye. Most of these tumefactions are unilateral and bilateral cases have rarely been reported. Orbital cavernous angiomas cause proptosis by increasing the intraorbital volume with a resultant mass effect. Although cavernous hemangiomas are histologically benign, they can encroach on intraorbital or nearby structures and can be considered anatomically malignant. Therefore surgical excision is merited in most cases for definitive treatment." }, "Topic": { "Title": "CAVERNOUS HEMANGIOMA", "Disease Discussion": "Cavernous hemangiomas are the most common intraorbital tumors in adults (Kim 2002). As far as the distribution between men and women is concerned, Henderson (1984) reported an almost equal ratio of 8:7 in women and men, while Harris and Jakobiec (1978) found a 7:3 occurrence ratio of women to men. The lesions themselves are benign vascular lesions that are slow growing and can manifest as a painless, progressively proptotic eye. Most of these tumefactions are unilateral and bilateral cases have rarely been reported. Orbital cavernous angiomas cause proptosis by increasing the intraorbital volume with a resultant mass effect. Although cavernous hemangiomas are histologically benign, they can encroach on intraorbital or nearby structures and can be considered anatomically malignant. Therefore surgical excision is merited in most cases for definitive treatment.", "ACR Code": "2.3", "Category": "Vascular", "Keywords": "CAVERNOUS HEMANGIOMAHEMANGIOMA", "Reference": "Harris GJ, Jakobiec FA: Cavernous hemangioma of the orbit: A clinicopathologic analysis of sixty-six cases. In: Jakobiec, ed. Ocular and Adnexal Tumors. Birmingham, Ala; 1978: 741-81. \nHenderson GW: Vascular hamartomas, hyperplasias, and neoplasms. In: Henderson, ed. Orbital Tumors. New York: Raven Press; \n 1994: 94-100. \nKim YH; Baek SH; Choi WC: The transconjunctival approach to a large retrobulbar cavernous hemangioma of the orbit. Korean \n J Ophthalmol - 01-JUN-2002; 16(1): 37-42\nScheuerle AF et. al.: Treatment and long-term outcome of patients with orbital cavernomas. Am J Ophthalmol - 01-AUG-2004; \n 138(2): 237-44" } }, { "U_id": "MPX1576", "TAC": [ "MPX1576_synpic46365", "MPX1576_synpic46366" ], "MRI": [ "MPX1576_synpic46367", "MPX1576_synpic46368", "MPX1576_synpic46369", "MPX1576_synpic46370", "MPX1576_synpic46371", "MPX1576_synpic46372", "MPX1576_synpic46373" ], "Case": { "Title": "Berry Aneurysm", "History": "68 y.o. woman with 6 months of daily frontal headaches.", "Exam": "Non-focal neurological exam.", "Findings": "CT: There is a berry aneurysm arising from the supraclinoid portion of the left internal carotid artery, measuring 16 mm AP x 13.5 mm CC x12 mm LAT with a 5-mm neck. The aneurysm projects medially and inferiorly from its origin and encroaches on the optic chiasm and pituitary fossa. The pituitary infundibulum may be displaced posteriorly. \n\nMR: The ventricles are the upper limits of normal in size. There is a mixed but primarily hypointense signal foci in the parasellar region to the left of midline superimposed over the sella. On T2WI this has a hypointense signal similar to the signal void of the vesicle. MR (T1W-Gd) shows enhancement.\n \nMRA of the circle of Willis shows a flow void component and a central heterogeneous hyperintense signal component.", "Differential Diagnosis": "\u2022 Congenital berry aneurysm\n\u2022 Atherosclerotic fusiform aneurysm\n\u2022 Mycotic aneurysm", "Case Diagnosis": "Berry Aneurysm", "Diagnosis By": "Angiography at coiling.", "Treatment & Follow Up": "This aneurysm was coiled soon after discovery. Interval imaging since coiling has confirmed resolution for the past three years.", "Discussion": "Saccular (berry) aneurysms are rounded outpouchings that arise from arterial bifurcation points. They most commonly arise secondary to abnormal hemodynamic shear stresses, and are not congenital as previously believed. Berry aneurysms can also be associated with trauma, infection, tumor, drug abuse, AVM, and AVF. \n\n15-20% of cases are multiple. They are found in the COW / MCA bifurcation 90% of the time. Most berry aneurysms become symptomatic between 40 and 60 years of age, commonly presenting with subarachnoid hemorrhage, with an associated high mortality and morbidity rate. The risk of rupture is 1-2% annually. There is a 20-50% rebleed risk. Larger size correlates with increased rupture risk, but there is no critical size that can be used to predict risk for bleed. When a berry aneurysm is discovered, aneurysm obliteration is necessary, because of the poor prognosis for subarachnoid hemorrhage.\n\nCT: In the case of a patent aneurysm, a well-delineated iso/hyperdense lesion that exhibits uniform intense enhancement is demonstrated. In the case of a thrombosed aneurysm, the residual lumen and outer rim may enhance strongly. No enhancement is seen in complete thrombosis.\n\nMR: Appearance can be highly variable, secondary to varied flow characteristics. Patent aneurysms can demonstrate a hyper or hypointense signal depending on flow. Wall enhancement may occur. Thrombosed aneurysms demonstrate flow void signal surrounded by concentric layers of clot. \n\nReferences:\n\nCebral JR, et al. Characterization of cerebral aneurysms for assessing risk of rupture by using patient-specific computational hemodynamics models. Am J Neuroradiol. 2005; 26(10):2550-9.\n\nFoutrakis GN, Yonas H, Sclabassi RJ. Saccular aneurysm formation in curved and bifurcating arteries. Am J Neuroradiol. 1999; 20(7):1309-17.\n\nOsborn AG. Diagnostic Neuroradiology. Mosby, St Louis, 1994. pp 248-281." }, "Topic": { "Title": "Aneurysm", "Disease Discussion": "The dilation of the wall of an artery, vein, or the heart, that forms a sac-like structure. \n\nFor image, see: http://rad.usuhs.mil/rad/radbrowser2/head/PlainFilm/zzsaneur.html", "ACR Code": "9.6", "Category": "Glossary", "External Links": "rad.usuhs.mil/rad/radbrowser2/head/PlainFilm/zzsaneur.html" } }, { "U_id": "MPX1582", "TAC": [ "MPX1582_synpic39368", "MPX1582_synpic39369", "MPX1582_synpic39370", "MPX1582_synpic39371", "MPX1582_synpic39372", "MPX1582_synpic39373", "MPX1582_synpic39374", "MPX1582_synpic39375", "MPX1582_synpic39376", "MPX1582_synpic39377" ], "MRI": [], "Case": { "Title": "Renal Cell Carcinoma (clear cell)", "History": "72 year old female with gross hematuria", "Exam": "N/A", "Findings": "Axial CT images after intravenous contrast material administration demonstrate an aggressive enhancing heterogenous exophytic mass arising from the upper pole of the left kidney and extending into the left renal vein. The inferior vena cava remains patent. A small ventral hernia is also noted.", "Differential Diagnosis": "Renal cell carcinoma\nOncocytoma\nMetastatic disease", "Case Diagnosis": "Renal Cell Carcinoma (clear cell)", "Diagnosis By": "Histology", "Treatment & Follow Up": "The patient subsequently underwent left total nephrectomy.", "Discussion": "Please see factoid." }, "Topic": { "Title": "Renal Cell Carcinoma", "Disease Discussion": "Renal cell carcinoma (RCC) is also known as renal adenocarcinoma, hypernephroma, clear cell carcinoma, and malignant nephroma. It is responsible for approximately 2% of adult malignancies. Male-female ration is 1.5:1. Age at presentation ranges from 50 to 70 years, with a median age at diagnosis of 57 years. Risk factors for RCC inclued tobacco use, long-term phenacetin use, Von Hippel-Lindau disease (VHLD), chronic dialysis, and family history.\n\nBilateral RCC commonly develops in patients with VHLD, tuberous sclerosis, acquired cystic kidney disease and familial RCC. Bilateral neoplasms occur in less than 2% of patients with sporadic RCC. This tumor may spread via local extension, hematogenously, or by the lymphatic system. \n\nROBSON CLASSIFICATION FOR STAGING OF RCC:\n I - Tumor confined to renal capsule\n II - Tumor extends throught renal capsule but is confined \n to renal fascia. Ipsilateral adrenal may be involved\n in this stage\n IIIA - Tumor involves renal vein, IVC, or both\n IIIB - Tumor involves regional lymph nodes\n IIIC - Tumor involves regional nodes and renal venous structure\n IVA - Direct extension of tumor through renal fascia to \n involve adjacent organs besides ipsilateral adrenal\n IVB - Distant metastases\n\nTreatment options include surgery (radical or partial nephrectomy), angioinfarction (arterial tumor embolization), hormonal therapy (e.g. progestins, antiestrogens, and androgens), chemotherapy, immunotherapy (Interferons), and radiation therapy. Tumor embolization may be used to minimize blood loss during surgery or to produce palliation. Objective tumor regression after treatment with hormonal agents is achieved in less than 6% of patients. Immunotherapy is mainly used in patients with metastatic RCC after resection of primary tumors with successful results in about 20% to 30% of patients with 5% to 10% complete responses. RCC is relatively radioresistant tumor. The role of radiation therapy is primarily in preoperative reduction in the size and fixation of tumors.\n\nCT FINDINGS IN RENAL CELL CARCINOMA\n - Most occur in the renal cortex and demonstrate an exophytic growth pattern. They distort the renal contour and larger tumors involve both the renal cortex and medulla. Solid tumors may be hyperdense, hypodense, or hyperdense on non-enhanced CT. Some lesions may appear heterogenous on non-enhanced scans because of hemorrhage and necrosis. Tumor calcification occurs in approximately 30% of cases. They may also rarely demonstrate small amounts of adipose tissue. A combination of fat and calcification shoud suggest RCC because fat-containing AMLs do not usually calcify. Solid RCCs usually demonstrates heterogenous enhancement(>10 HU). 2% to 5% of RCCs are predominantly cystic. Filling defects (clots, tumor thrombus) in the collecting sytem and renal veins may be seen.", "ACR Code": "811.419", "Category": "Neoplasm, carcinoma", "Keywords": "renal cell carcinoma", "Reference": "Pollack, M. Howard et al. Clinical Urography, 2nd ed. vol 2\n W.B. Saunders Company: Philadelphia, 2000 \n\nWeissleder, Ralph et al. Primer of DiagnosticImaging, \n 2nd ed. Mosby: Philadelphia, 1997" } }, { "U_id": "MPX1594", "TAC": [ "MPX1594_synpic41187" ], "MRI": [], "Case": { "Title": "Renal Angiomyolipoma", "History": "59 yo woman referred for renal ultrasound.", "Exam": "Noncontributory", "Findings": "Gray-scale sonographic images of the right kidney demonstrate a well circumscribed 1 cm hyperechoic lesion in the lower pole that is isoechoic with the renal sinus.\n\nUnenhanced CT of the kidneys was obtained demonstrating a tiny focal area of fat density in the lower pole of the right kidney, confirming the diagnosis of renal angiomyolipoma.", "Differential Diagnosis": "Differential diagnosis for a hyperechoic, apparently solid renal lesion on ultasound:\n\nRenal Angiomyolipoma\n\nRenal Cell Carcinoma (RCC)\n\nOther renal neoplasms (eg, oncocytoma)\n\nComplex renal cysts\n\nRenal hematoma or abscess", "Case Diagnosis": "Renal Angiomyolipoma", "Diagnosis By": "Confirmatory unenhanced CT of the kidneys was obtained demonstrating a tiny focal area of fat density in the lower pole of the right kidney, correlating with the sonographic findings of a AML.", "Treatment & Follow Up": "Renal AMLs may safely be followed at this size.", "Discussion": "Renal angiomyolipomas are typically circumscribed and hyperechoic on ultrasound, but these finding are not entirely specific. The presence of macroscopic fat on CT or MR is virtually pathognomonic for the diagnosis of AML.\n\n\nRenal Cell Carcinoma (RCC) may also appear hyperechoic on ultrasound. To distinguish a RCC from an AML, the presence of a peripheral hypoechoic rim surrounding an echogenic solid lesion, as well as demonstrable cystic elements strongly suggests a RCC. Additionally, RCC typically lacks an acoustic shadow, whereas 20%-30% of AMLs have a varied degree of posterior shadowing.\n\nOncocytoma is classically hypo- to iso- echoic, but may have a hyperechoic central scar.\n\nDeep Cortical Scar:\nDeep Cortical Scars are filled with crystals and perinephric fat, producing a color Doppler ring down artifact not seen with AML.\n\nRenal cysts complicated by hemmorrhage or proteinaceous debris may be hyperechoic, but often demonstrate enhanced through transmission.\n\nBlood products and the contents of abscesses may also be hyperechoic, but typically these lesions are not as sharply defined. They may also assume a subcapsular configuration.\n\nRenal Hemangioma:\nRenal Hemangioma demonstrates variable echogenecity. In some cases, renal hemangiomas are hyperechoic, similar to liver hemangiomas, or they may appear isoechoic to renal parenchyma." }, "Topic": { "Title": "Renal Angiomyolipoma", "Disease Discussion": "Angiomyolipoma (AML) is the most common benign renal tumor composed of blood vessels, smooth muscle, and adipose tissue. AML is identified most frequently in middle-aged women, and may be seen in patients diagnosed with tuberous sclerosis. In patients without tuberous sclerosis, AML is most often unilateral in location, whereas patients with tuberous sclerosis frequently demonstrate multiple, small, bilateral AMLs.\n\nPatients with AML smaller than 4 cm are generally asymptomatic. If an AML is found to be larger than 4 cm, the presenting signs or symptoms are typically hematuria and or flank pain, and the tumor is resected secondary to an increased risk of hemorrhage. Additionally, if the tumor size is 1 cm or larger, thin section CT should be performed to evaluate for the presence of fat. If fat is not identified on CT, then the diagnosis of Renal Cell Carcinoma should be entertained. Small, asymptomatic AMLs should be followed for evidence of growth.\n\n\n\u2022 Ultrasound \n\nAngiomyolipoma (AML) may have a varied acoustic pattern as the amount of adipose tissue, smooth muscle, and blood vessels vary from lesion to lesion. Generally, AML is a homogenous well defined hyperechoic cortical neoplasm arising from the renal parenchyma, with echogenecity similar to that of the renal sinus. Occasionally, AML may appear as a hypoechoic focus when smooth muscle, blood vessels, or hemorrhage constitute the majority of the lesion. Color flow Doppler imaging is helpful in cases of hemorrhagic AML. \n\nRenal Cell Carcinoma (RCC) may also appear hyperechoic on ultrasound. To distinguish a RCC from an AML, the presence of a peripheral hypoechoic rim surrounding an echogenic solid lesion, as well as demonstrable cystic elements strongly suggests a RCC. Additionally, RCC typically lacks an acoustic shadow, whereas 20%-30% of AMLs have a varied degree of posterior shadowing.", "ACR Code": "8.3", "Category": "Neoplasm, NOS", "Keywords": "AngiomyolipomaAMLSonographic AML", "Reference": "Rumack, Carol. Diagnostic Ultrasound. Third Edition. Elsevier Mosby, Inc. \n Mosby. St. Louis, Missouri 2005.\nMiddleton, William. Ultrasound. The Requisites. Second Edition. Mosby. \n St. Louis, Missouri 2004.\nPrasad et al. RadioGraphics 2005; 25:321\u2013331.\nNuman et al. Clin Imaging 1993;17:106-108.\nLee et al. Korean J Radiol 2000;1:60-63." } }, { "U_id": "MPX1596", "TAC": [ "MPX1596_synpic20748" ], "MRI": [], "Case": { "Title": "Meningioma", "History": "26 y.o. man complains of headache", "Exam": "No abnormal findings", "Findings": "6 cm extra axial left parietal mass with vasogenic edema", "Differential Diagnosis": "\u2022 meninigioma if extra-axial\n\u2022 astrocytoma, oligo-dendroglioma if intra-axial", "Case Diagnosis": "Meningioma", "Diagnosis By": "Surgical excision with pathologic confirmation", "Treatment & Follow Up": "Resection and re-imaging to insure no recurrence or residual tumor", "Discussion": "This extra axial mass demonstrates a large number of arterial feeders, typical for meningioma.\n\nAngiographically, a large stain of contrast is seen with a central focus. This capillary tumor blush arrives early in the arterial phase and stays late into the venous phase. Previously coined the \"mother-in-law\" phenomenon, since it comes early, stays late, and usually is very dense." }, "Topic": { "Title": "Meningioma", "Disease Discussion": "Epidemiology and Location\nMeningiomas comprise approximately 20% of adult intracranial tumors, have a female predominance, and occur most often during middle and older ages. They may be found in intracranial and intraspinal compartments. In the head, meningiomas are most commonly located in frontal, parasagittal, and parietal convexities (50% of cases). Less than 10% of tumors are infratentorial; multiple meningiomas occur less than 10% of the time. Clinical presentation is varied, depending on particular structures compressed by the mass. Headache and visual changes are frequently reported. A large number of patients with meningiomas are asymptomatic.\n\nOrigins, Growth, and Histology\nThe majority of meningiomas are histologically benign tumors, arising from the cap cells of the arachnoid layer. In many cases, serial imaging studies have revealed a cessation of growth after the time of initial tumor detection. These tumors project inward from the dura, and can cause clinically significant effects due to compression of surrounding neurological structures. A variety of classification systems based on cytology and histopathology are used with meningiomas. While the overwhelming majority of meningiomas are histologically benign, the malignant type may result in rapid, widespread infiltration with small (microscopic) \"finger\" projections into adjacent cortex. In patients with malignant meningiomas, marked deficits in physical and mental status may culminate in death.\n\nRadiological Findings\nPlain films may reveal hyperostosis, erosion, or calcification adjacent to tumor site. Noncontrast CT's of meningiomas often reveal sharply demarcated, rounded, homogenous masses with slightly increased density when compared to surrounding cortex. Up to 10% of meningiomas may appear isodense with respect to surrounding brain. CT may reveal focal cerebral atrophy, edema, or widening of subarachnoid spaces, direct effects of tumor compression of surrounding structures. Contrast enhanced CT most often reveals homogenous enhancement in approximately 85% of cases.\n\nOn MRI, T1 images are often hypo- or isointense; T2 images often reveal isointense or slightly hyperintense masses. Gadolinium increases signal intensity of meningiomas. A \"dural tail\" consisting of tissue tapering into the dura may be appreciated. Imaging studies may reveal extension of mass into cortical structures, or invasion of the calvarium. Angiography often reveals a homogenous, hypervascular pattern.\n\n\nTreatment Options\nA variety of clinical and experimental treatment options exist, including surgery, radiotherapy, stereotactic radiosurgery, brachytherapy, chemotherapy, and hormonal therapy. Resection is the most widely utilized treatment option, although advanced age, concern about loss of neurological function due to surgery, advanced age, and being a poor surgical candidate preclude some from surgical options. Tumor embolization may be employed 3-5 days prior to surgery in an attempt to decrease blood supply to the meningioma. Recurrence of tumor is a possibility after resection. Complete removal of initial tumor and all affected bone results in recurrence rates of less than 10%.\n\nRadiotherapy is often employed during the presurgical period. Likewise radiotherapy after incomplete resection of a meningioma may be of considerable benefit to patients. Stereotactic radiosurgery with a \"gamma knife\" has shown decrease in tumor size in approximately 50% of cases. Since this technology is relatively new, long term outcome of gamma knife therapy is not known. Brachytherapy with iodine-125 has been described in the literature; long term outcomes have yet to be determined. Medical treatment options include recommendations of anticonvulsant prophylaxis in patients with supratentorial masses; corticosteroids to reduce brain swelling may also be warranted. The use of traditional antineoplastic agents in treating meningiomas has not been met with great success. Hormonal manipulation may have a beneficial effect on stopping tumor growth; research this area continues.", "ACR Code": "1.3", "Category": "Neoplasm, non-glial", "Reference": "Akeyson et al. Management of benign and aggressive intracranial meningiomas. Oncology 1996. 10 (5): 747-759.\n\nBraunstein et al. Meningiomas: the decision not to operate. Neurology 1997. 48 (5). \n\nGo et al. The natural history of asymptomatic meningiomas\u2026 Neurology 1998. 51 (6).\n\nHaaga, John et al. Computed Tomography and Magnetic Resonance Imaging of the Whole Body. Vol. 1 Mosby. New York. 1994. pp.198-202." } }, { "U_id": "MPX1592", "TAC": [ "MPX1592_synpic40521" ], "MRI": [], "Case": { "Title": "Hepatic Congestion secondary to Congestive Heart Failure", "History": "71 yo female with elevated liver-associated enzymes, and concern for cholelithiasis.", "Exam": "Laboratory:\n\nAlkaline Phosphatase: 689 \nGGT: 369 \nAST: 60\nALT: 62\n\nBNP: 218 H", "Findings": "Sonographic evaluation of the gallbladder demonstrates diffuse gallbladder wall thickening. There is no evidence of cholelithiasis, or biliary sludge. The common bile duct measured 6 mm, which is acceptable for this patient's age.\n\nDuplex Doppler sonogram of portal vein shows highly pulsatile blood flow. Color Doppler shows both blue and red, indicating flow reversal.\n\nDuplex Doppler waveforms of the inferior vena cava (IVC), and hepatic vein demonstrate normal triphasic flow with abnormally high amplitude retrograde flow in the IVC and hepatic vein, caused by high right heart pressures during the cardiac cycle.\n\nPA chest radiograph demonstrates cardiomegaly, a small right-sided pleural effusion and increased interstitial markings.\n\nUnenhanced axial CT image through the level of the heart demonstrates small bilateral pleural effusions.", "Differential Diagnosis": "Cholecystitis\nHepatic congestion secondary to Tricupsid Regurgitation\nHepatitis\nAcute pancreatitis\nBudd-Chiari Syndrome", "Case Diagnosis": "Hepatic Congestion secondary to Congestive Heart Failure", "Diagnosis By": "Diagnosis was confirmed clinically, radiographically, and laboratory results revealed an elevated BNP." }, "Topic": { "Title": "Hepatic Congestion secondary to Congestive Heart Failure", "Disease Discussion": "Lesions/Condition: Hepatic Congestion secondary to Congestive Heart Failure\n\n\nDiscussion: \n\nPassive hepatic congestion is caused by stasis of blood within the liver parenchyma due to the compromise of hepatic venous drainage. It is a common complication of congestive heart failure and constrictive pericarditis, wherein elevated central venous pressure is directly transmitted from the right atrium to the hepatic veins because of the their close anatomic relationship. The liver becomes tensely swollen as the hepatic sinusoids dilate and engorge to accommodate the back flow of blood. Liver dysfunction arises from a combination of decreased hepatic blood flow, elevated hepatic venous pressure, and diminished arterial oxygen content, resulting in hepatocellular hypoxia.\n\nHepatic changes are manifested as hepatomegaly, ascites, jaundice, and abdominal pain caused by stretching of the liver capsule. Transient abnormalities of the liver-associated enzymes include elevations of serum bilirubin, transaminases, alkaline phosphatase, and prothrombin time. The transaminase levels are typically elevated 20-fold but normalize rapidly over several days. Passive hepatic congestion typically occurs in elderly individuals with right-sided congestive heart failure and low cardiac output. Precipitating factors include cardiac ischemia, dysrhythmias, cardiac or extracardiac infection, valvular heart disease, cardiomyopathies, noncompliance with medical therapy, and dietary indiscretion, to name a few. Symptoms include weakness, shortness of breath, and right upper quadrant pain. \n\nLaboratory:\n\nIn right-sided heart failure, hyperbilirubinemia may be evident, and the transaminases are moderately elevated. Occasionally, there is isolated elevation of cholestatic enzymes. In left sided failure, there is a more marked elevation of serum bilirubin and of transaminases, which rapidly return to normal when congestive heart failure is treated.\n\n\nSonographic Evaluation:\n\nPatients normally demonstrate inferior vena caval and hepatic venous triphasic flow patterns. The first two peaks are toward the heart and are reflections of right atrial and ventricular diastole. The third peak is a short period of reversed blood flow, accompanied by atrial systole. As central venous pressure rises, the inferior vena cava and hepatic veins dilate because the failing right atrium cannot accommodate the venous return. Clinically, this is manifested by a hepatojugular reflux on physical examination.\n\nWith elevated central venous pressure, the hepatic veins lose their triphasic pattern. In long-standing disease, a unidirectional, low-velocity, continuous flow pattern may be seen. Mixed flow patterns can also be seen on color flow Doppler sonograms. \n\nNormal portal venous flow is steady and continuous except for a mild increase during expiration. In patients with passive hepatic congestion, the energy of the elevated pressure from the right atrium and hepatic veins is transmitted directly via the dilated hepatic sinusoids into the portal vein. The result is that portal venous blood flow becomes pulsatile, because the liver no longer prevents changes in central venous pressure from reaching the portal circulation.\n\nAdditionally, sonographic evaluation of the gallbladder may demonstrate diffuse gallbladder wall thickening, which is a nonspecific finding, found in a variety of conditions unrelated to intrinsic gallbladder disease. Edema of the gallbladder wall, as seen in congestive heart failure, is likely secondary to elevated portal venous pressure, elevated systemic venous pressure, and decreased intravascular osmotic pressure. However, passive edema of the gallbladder wall may be difficult to differentiate from other causes of gallbladder wall thickening such as an acute inflammatory process in the right upper quadrant, acute pancreatitis, perforated duodenal ulcer, hepatitis, right-sided diverticulitis, and acute right-sided pyelonephritis. \n\nWhen the above findings are considered with other ancillary findings of congestive heart failure to include cardiomegaly, pleural effusions, pericardial effusions, hepatomegaly, and ascites, one should have little difficulty in arriving at the proper diagnosis of passive hepatic congestion secondary to congestive heart failure.", "ACR Code": "7.6", "Category": "Systemic, Generalized", "Keywords": "Hepatic Congestion secondary to Congestive Heart FailureHepatic Congestion", "Reference": "Hanbidge et al. RadioGraphics 2004;24:1117-1135.\nEbert EC. Mayo Clin Proc. 2006;81(9):1232-6.\nSeeto et al. Am J Med. 2000;109(2):109-13.\nMyers et al. J Clin Invest 27:620-627.\nCohen et al. Gastroenterology 1974;74:583-587.\nKubo et al. Arch Int Med 1987;147:1227-1230.\nDe La Monte et al. Gastroenterology 1984;86:627-631\nMoulton et al. AJR 1988;151(5):939-942.\nVan Breda Vriesman et al. AJR 2007;188(2):495-501.\nGore et al. AJR 1994;162(1):71-75." } }, { "U_id": "MPX1601", "TAC": [ "MPX1601_synpic39455" ], "MRI": [ "MPX1601_synpic39456", "MPX1601_synpic39457", "MPX1601_synpic39458", "MPX1601_synpic39459", "MPX1601_synpic39460", "MPX1601_synpic39461", "MPX1601_synpic39462", "MPX1601_synpic39463", "MPX1601_synpic39464", "MPX1601_synpic39465", "MPX1601_synpic39466" ], "Case": { "Title": "Herpes Encephalitis HSV-1", "History": "21 yo male presenting with fever, new onset of aphasia, and one episode of loss of consciousness.", "Exam": "PCR of CSF:\nHSV 1 DNA\u2026..Detected\nHSV 2 DNA\u2026..Not Detected\n\nCSF:\nGLUCOSE . . . . . . . 115.0 H (40-70) mg/dL\nPROTEIN CSF . . . . . 150 H (12-60) mg/dL\nCOLOR. . . . . . COLORLESS \nAPPEAR . . . . . . . CLEAR \nWBC. . . . . . . . 259 H (0.0-5.0) cu/mm\nRBC . . . . . . . . . 133 H (0-1) cu/mm\nLYMPH.. . . . . . . . 99 H (40-80) %\nMONO . . . . . . . . 1 %\n \nSerum WBC: 11.2", "Findings": "Non-contrast CT: Hypoattenuation in the left temporal and inferior frontal lobes. Mild mass effect is also seen with effacement of the Sylvian cistern, and Ambient cistern.\n\nContrast enhanced CT: Patchy peripheral enhancement in the bilateral temporal lobes, and insula. There are also foci of circumscribed low density within the left insula, and evidence of subtle mass effect.\n\nMRI:\n\nDWI: T2 signal hyperintensity with restricted diffusion, in the left temporal lobe, and bilateral insula.\n\nT2WI: Increased signal intensity and swelling of the gray matter of the left temporal lobe with mild mass effect, evidenced by effacement of the Ambient cistern at the left medial temporal lobe and midbrain. Additionally, there is mild increased signal intensity of the right medial temporal lobe. Also, there is increased signal intensity in the left greater than right insular gray matter.\n\nCoronal T2-weighted FLAIR MR shows bilateral asymmetric involvement of the medial temporal lobes and insula.\n \nT1WI: Low signal intensity in the left greater than right insula secondary to surrounding edema, with no evidence of hyperintensity to suggest the presence of subacute blood products. \n\nPost-gadolinium T1WI demonstrates patchy peripheral enhancement in the left temporal lobe, and left greater than right insula.", "Differential Diagnosis": "HSV Encephalitis\nIschemia\nInfiltrating Neoplasm\nStatus Epilepticus\nAbscess\nOther Encephalitides (Neurosyphilis)", "Case Diagnosis": "Herpes Encephalitis HSV-1", "Diagnosis By": "Polymerase Chain Reaction detected HSV-1 antigen in the CSF.", "Treatment & Follow Up": "Intravenous acyclovir.", "Discussion": "The prognosis of this patient is very poor, as he presented with aphasia, and one episode of loss of consciousness before receiving intravenous acyclovir." }, "Topic": { "Title": "HSV Encephalitis", "Disease Discussion": "Lesions/Condition: HSV Encephalitis\n\nDiscussion: \n\nHerpes Encephalitis occurs at any age, with the highest incidence in adolescents and young adults, affecting men and women equally. HSV-1 accounts for 95% of all herpetic encephalitis, and is the most common cause of viral encephalitis in the United States. \n\nThe presenting symptoms are multiple and often originate with fever, headache, seizures, confusion, stupor, and coma. Patients may also demonstrate the gradual onset of olfactory hallucinations, anosmia, personality change, psychotic behavior, delirium, aphasia, and hemiparesis. These symptoms are directly related to the involvement of the temporal lobes, insular cortex, and orbital surface of the frontal lobes by this disease.\n\nAfter initial contact through infected secretions in the oronasopharnyx, HSV-1 travels via the lingual portion of the trigeminal nerve, to the gasserian ganglia where the virus remains dormant. Upon reactivation from the influences of local trauma, immunosuppression, or stress, or the result of primary infection, the virus spreads in a retrograde fashion along the fibers that innervate the leptomeninges of the anterior and middle fossa.\n\nEarly diagnosis and rapid therapy is essential, as herpes encephalitis progresses rapidly. The mortality rate ranges from 50% to 70%, with those surviving left with significant neurological impairment to include amnesia, dementia, seizures, and aphasia. Both the patient\u2019s age and level of consciousness at the time of initiation of intravenous acyclovir dictate outcomes. If the patient is unconscious prior to beginning therapy, the outcome is poor. If the patient is awake, and treatment is begun within 4 days of onset of the illness, survival is greater than 90 percent. \n\nLaboratory:\n\nCSF demonstrates increased pressure and a pleocytosis with lymphocyte predominance. \nRed cells, and xanthochromia are identified in a minority of cases, secondary to hemorrhage. Protein content is increased, and CSF glucose may rarely be lower than 40 mg/dL.\n\nPolymerase Chain Reaction may be employed to identify HSV antigen in the CSF while the virus is replicating in the first few days of the illness.\n\nPathology:\n\nGross Pathologic Features: \n\nHemorrhagic and necrotizing encephalitis of gray and white matter, with severe edema and tissue necrosis localized to the inferior frontal, temporal lobes, and insular cortex. \n\nMicroscopically:\n\nFocal necrotizing vasculitis with perivascular inflammatory infiltrates, with eosinophilic Cowdry intranuclear inclusion bodies located in neurons, and glial cells.\n\nHerpes viruses include HSV-1, HSV-2, Epstein-Barr virus, cytomegalovirus, varicella-zoster virus, B virus, HSV-6, and HSV-7.\n\n\nRadiology:\n\nThe imaging findings of HSV encephalitis on CT may be initially normal or subtly abnormal. Generally, abnormalities are not identified until 3-5 days after the onset of significant symptoms. Common initial findings are low attenuation in the medial temporal lobes and insula, with mild mass effect. Hemorrhage may occasionally be identified and is a late finding that is highly suggestive of herpes encephalitis. On contrast enhanced CT, there is ill-defined patchy enhancement, with gyriform enhancement being a late finding. \n\nMRI is more sensitive than CT in detecting early changes, and demonstrates signal changes in almost all sequences. T1 weighted images demonstrate areas of low signal intensity with surrounding edema localized to the temporal lobes, insular cortex, subfrontal area, and cingulate gyri. Loss of the gray-white matter differentiation, and evidence of mass effect is frequently encountered. Additionally, in cases of hemorrhage, there may be foci of increased signal in the inferior parts of the frontal and temporal lobes. T2 weighted images demonstrate asymmetric bilateral high signal intensity in gray, and subcortical white matter of the temporal lobes, extending into the insular cortex, secondary to edema. The basal ganglia are usually spared. Findings are initially unilateral, followed by less severe contralateral temporal lobe signal abnormalities.\n\nProton density sequences demonstrate increased signal intensity in affected areas. T2 weighted Fluid Attenuated Inversion Recovery (FLAIR) sequences demonstrate hyperintense signal with edematous cortex and subcortical white matter. T2 gradient recalled echo sequences show hypointensity if there is hemorrhage within the edematous brain parenchyma. \n\nDiffusion weighted images demonstrate marked hyperintense restricted diffusion, and reduced ADC values. It is important to distinguish these findings from ischemic stroke, hemorrhage, abscess, lymphoma, Creutzfeldt-Jakob disease, glioma, and metastatic disease, for the determination of appropriate treatment. HSV encephalitis can be differentiated from other high signal intensity DW MR images, and low ADC values based on the clinical presentation of the patient, distribution of the imaging findings, and results of the polymerase chain reaction test.\n\nT1 weighted gadolinium enhanced images demonstrate asymmetric mild patchy enhancement indicating abnormalities of the blood-brain barrier. Gyriform enhancement may be seen one week after initial symptoms. Meningeal enhancement is an early finding, with parenchymal enhancement being a late finding, or evidence of hemorrhage.\n\nMR spectroscopy may be utilized demonstrating elevated peaks of lactate, choline, and myoinositol, and reduced N-acetylaspartate signal. \n\nFollow-up imaging demonstrates progressive abnormalities with worsening involvement of the contralateral temporal lobe, insula, and cingulate gyri. Encephalomalacia, atrophy, and dystrophic calcification are commonly seen as sequelae of HSV encephalitis.", "ACR Code": "1.9", "Category": "Infection, viral", "Keywords": "HSV EncephalitisHerpetic EncephalitisHSV-1 Encephalitis", "Reference": "Brant: Fundamentals of Diagnostic Radiology. 2nd Edition. Philadelphia: Lippincott Williams & Wilkins. 1999. \nAdams and Victor\u2019s Principles of Neurology. 7th Edition. New York. McGrw-Hill. 793-795. 2001.\nFriedman, D. RadioGraphics 1998; 18:246-250.\nOsborn, Anne. Diagnostic Neuroradiology. Mosby. St. Louis, Missouri. 1994.\nAl-Okaili, R. RadioGraphics 2006;26:S173-S189.\nStadnik. Radiographics.2003;23:e7-e7.\nOsborn, Anne. Diagnostic Imaging Brain. Amirsys. Salt Lake City, Utah. 2004." } }, { "U_id": "MPX1610", "TAC": [ "MPX1610_synpic51798", "MPX1610_synpic51799", "MPX1610_synpic51801" ], "MRI": [], "Case": { "Title": "Intralobar Pulmonary Sequestration", "History": "22-year-old woman with history of recurrent pulmonary infections presents with cough for 2.5 weeks, fever, intermittent sputum production, but no hemoptysis", "Exam": "Egophony was heard on the right lower/mid lung field. Labs within normal limits, no leukocytosis.", "Findings": "1st Image: PA and lateral radiographs of the chest demonstrate patchy air space density involving the right lower lobe. There is a cavitary lesion with an air-fluid level worrisome for abscess formation. The remainder of the lung parenchyma is clear and evenly aerated without additional regions of consolidation identified. There is focal extroconvex curvature involving the thoracic spine, unchanged. \n\nNext 3 images: Within the right lung base there is a large area of consolidation with accompanying bronchiectasis as well as a cavitary lesion with an air fluid level. Several additional areas of patchy opacity are present likely representing accompanying atelectasis. There is no evidence of pneumothorax or pleural effusion. No enlarged lymph nodes are identified.\n\nLast image: There is a cluster of well-defined thin-walled cysts in the right lung base, some of which are confluent. The previously noted marked soft tissue thickening around them has resolved during the study interval as has the air-fluid level. No soft tissue thickening persists in this region. The lungs are otherwise clear.", "Differential Diagnosis": "Congenital lesions- Intralobar pulmonary sequestration\nblebs\nbullae\npneumatoceles\ntraumatic lesions\ncoccidioidomycosis\nPneumocystis jiroveci pneumonia\nhydatid disease\nmetastatic malignant lesions\nbronchogenic carcinomas\nlymphomas\ninfections and abscesses (bacterial, fungal)\nWegener granulomatosis\nrheumatoid nodule\npulmonary infarct\nseptic embolism\nprogressive massive fibrosis with pneumoconiosis lymphocytic interstitial pneumonia\nbronchiectasis\ncongenital lesions\npulmonary lymphangioleiomyomatosis\npulmonary Langerhans cell histiocytosis\nhoneycomb lung associated with advanced fibrosis", "Case Diagnosis": "Intralobar Pulmonary Sequestration", "Diagnosis By": "Surgical removal of sequestered lung tissue", "Treatment & Follow Up": "Patient was treated with 21 day course of oral clindamycin with resolution of infection but with remaining cystic lesions on chest CT. Based on patient history of recurrent lung infections and radiographic findings, patient was suspected of having an intralobar pulmonary sequestration. Thoracic surgery resected the affected lung segment, confirming the diagnosis.", "Discussion": "This patient's history is typical for patients with intralobar pulmonary sequestration. She has had recurrent RLL pneumonia - one episode was 4 years ago while in boot camp; and, a second documented RLL pneumonia one year ago as well. She also describes a long history of periodic episodes of severe fatigue and subjective fevers that were most likely undiagnosed pulmonary infections." }, "Topic": { "Title": "Intralobar Pulmonary Sequestration", "Disease Discussion": "Pulmonary sequestration is a developmental thoracic anomaly. A sequestration is an abnormal congenital mass of lung lacking a normal communication with the tracheobronchial tree and is supplied by abnormal vessels from the descending aorta. It is NONFUNCTIONING lung. \n\nPulmonary sequestrations are divided into extralobar (covered by their own pleura, venous return via systemic veins) or intralobar (covered by pleura of the adjacent normal lung, venous return via pulmonary veins). Most appear as a triangular or oval-shaped mass in the medial and basal portion of a lung and more are commonly left (extralobar 90%, intralobar 60%). Extralobar sequestrations are always airless. Intralobar sequestrations are mostly airless though there may be \"collateral air drift\" via the pores of Kohn. Most are clinically silent until they become infected and can present as recurrent pneumonias. Extralobar sequestrations often present in neonatal life and intralobar in older children and adults.\n\nAlso included in the category of thoracic anomalies are: pulmonary agenesis (pulmonary artery and lung bud are absent), pulmonary aplasia (pulmonary artery and lung parenchyma are absent but a blind-ending bronchial stump exists), unilateral pulmonary hypoplasia/scimitar syndrome with aberrant pulmonary venous return* (small RIGHT pulmonary artery with hypoplasia of all or part of RIGHT lung AND partial anomalous drainage of the pulmonary veins - subdiaphragmatic into IVC, hepatic or portal veins), unilateral pulmonary hypoplasia secondary to congenital diaphragmatic hernia, bilateral pulmonary hypoplasia (incompatible with life), congenital lobar emphysema (isolated and progressive hyperinflation of a single lobe likely secondary to dysplasia, hypoplasia, or immaturity of bronchial cartilage in involved lobe), CCAM or Congenital Cystic Adenomatoid Malformation (abnormal proliferation of terminal respiratory structures lacking mature alveoli resulting in a cystic mass structure, usually unilobar), bronchogenic cysts (bronchopulmonary foregut malformation likely secondary to an ectopic bronchial bud which communicates with the tracheobronchial tree), esophageal duplication cyst (bronchopulmonary foregut malformation usually of distal esophageal wall), and neurenteric cyst (failed separation of pulmonary and notochordal elements in 3rd gestational week). Note ^. \n\n* cardiac abnormalities \n^ Acquired unilateral pulmonary hypoplasia (Swyer-James or MacLeod syndrome) is post-infectious.", "ACR Code": "6.9", "Category": "Congenital, malformation", "Keywords": "Congenital anomaly - pulmonaryintralobarsequestration", "Reference": "1) Armstrong P, Wilson AG, Dee P, Hansell DM. Imaging of Diseases of the Chest, 2nd ed. St. Louis: Mosby-Year Book; 1995." } }, { "U_id": "MPX1609", "TAC": [ "MPX1609_synpic19713", "MPX1609_synpic19714" ], "MRI": [ "MPX1609_synpic19716", "MPX1609_synpic19717", "MPX1609_synpic19718", "MPX1609_synpic19719", "MPX1609_synpic19720" ], "Case": { "Title": "Cysticercosis", "History": "A 35 year-old Hispanic female with no significant past medical history presented with new onset of seizures.", "Exam": "Hemodynamically stable.\n\nNo focal neurological abnormalities.\n\nCBC, Chem7, LFTs, serum etOH and drug screen negative.", "Findings": "CT and MR evaluation of the brain demonstrated multiple well-defined cystic lesions in the brain parenchyma and subarachnoid spaces. All lesions were approximately 1cm in size and several appeared to have a small internal nodule. Only one of the lesions (an intra-axial cyst in the frontal lobe) demonstrated any surrounding edema.", "Differential Diagnosis": "Septic Emboli\nMetastatic Disease\nInfection\nMultifocal GBM", "Case Diagnosis": "Cysticercosis", "Diagnosis By": "Radiologically confirmed.", "Treatment & Follow Up": "Patient was started on antihelminthic therapy - albendazole, in addition to steroids and antiseizure Rx." }, "Topic": { "Title": "Neurocysticercosis", "Disease Discussion": "Cysticercosis is a parasitic infection caused by Taenia solium, the pork tapeworm, which is endemic to Central and South America, southern Africa, and Asia. The prevalence is often higher in rural areas, particularly where pigs are raised and poor sanitary conditions prevail. Humans develop cysticercosis by ingestion of foods contaminated with the parasites eggs (typically fruits & vegetables), not from eating pork infected with the parasite itself as is popularly believed. Thus, individuals who have never eaten pork can still acquire cysticercosis.\n \nOnce eggs are ingested by humans, the embryos are released in the small intestine and invade the bowel wall. They then disseminate hematogenously and develop into cysticerci over a period of 3-8 weeks. Cysticerci are liquid-filled vesicles consisting of a membranous wall and a nodule containing the invaginated scolex. The scolex has a head armed with suckers and hooks and a rudimentary body. Humans with cysticercosis are incidental dead end hosts.\n \nThe most prominent manifestations of cystircercosis infection involve the CNS, a syndrome referred to as neurocysticercosis (NCC) and it is thought to be the most common parasitic infection of the brain. Clinical syndromes of cysticercosis are therefore often divided into neurocysticercosis and extraneural manifestations.\n \n80% of neurocysticercal infections are asymptomatic. Consequently, many cases are found accidentally during imaging procedures or at autopsy. When symptoms due occur, they may be due to mass effect, an inflammatory response, or obstruction of foramina and ventricular system of the brain.\n \nCysticerci that enter the CSF do not initially cause much inflammation. The host develops immune tolerance to the parasite, and cysticerci can remain in this stage for years without eliciting symptoms. Clinical manifestations frequently develop when an inflammatory response develops secondary to a degenerating cysticercus. It is not known what triggers this degeneration, but after a number of years the cyst loses its ability inhibit the host immune response. Peak presentation with NCC is estimated to occur 3-5 years after infection. After a variable period of degeneration, cysts become calcified and inactive. Once inactive, they may cease to cause symptoms or may serve as a focus for epileptic activity.\n \nActive parenchymal disease is the most common form of NCC and is present in >60 percent of patients. Cysticerci tend to lodge in the cerebral cortex or basal ganglia. The cysts are usually <1 cm. Patients with parenchymal NCC frequently present with seizures, occurring in 50-80% of patients. In many endemic countries, NCC is the most common cause of adult-onset epilepsy. Because of NCC, the prevalence of epilepsy is almost twice as high in developing countries as it is in the Western world.\n \nNeurologic examinations are usually normal, but focal neurologic signs or headache may be present. Patients rarely have fever or signs of meningeal irritation. If a patient has massive numbers of cysts in the brain parenchyma, an intense immune reaction can occur, resulting in encephalitis. This reaction can occur spontaneously or it can be provoked by therapy. This presentation is most common in children and young females for unknown reasons. \n \nCysticerci that lodge in the subarachnoid space may grow to 10 cm or more since they are not limited by pressure from the brain parenchyma. Cysticerci can also develop in the ventricles of the brain, either floating freely in the ventricular cavity or attached to the choroid plexus, and is seen in only 10-20% of cases. Mobile cysts in the forth ventricle can occasionally cause intermittent obstruction, leading to episodes of sudden loss of consciousness related to head movements (Bruns' syndrome). Involvement of the spinal cord occurs in approximately 1-3% of cases of NCC. Spinal cysticerci can be intramedullary or located in the subarachnoid space. \n \nExtraneural cysticercosis typically involves the eye, muscle, or subcutaneous tissue. Patients with ocular involvement may have parasites located in the subretinal space or vitreous humor. These are often asymptomatic, but inflammation around degenerating cysticerci can threaten vision by causing chorioretinitis, retinal detachment or vasculitis and therefore this entity should be excluded before initiating therapy. Cysticerci also have a predilection for muscle or subcutaneous tissues, however, cysticerci at these sites are usually asymptomatic. \n \nCalcified cysticercal lesions in muscle or subcutaneous tissue may be seen on routine skeletal radiographs or intracranial calcifications may be seen on skull x-rays. Any case of suspected NCC needs to be evaluated with a CT scan or MR imaging. The appearance depends upon the location and stage of the lesions and upon the host immune response. In parenchymal NCC, viable cysts are seen as nonenhancing hypodense lesions. Degenerating cysts may enhance with contrast and may have variable degrees of surrounding inflammation. Old cysts often appear as calcified lesions. MRI is preferred over CT scanning, since MRI is more sensitive in detecting small lesions, brainstem or intraventricular lesions, and is better at visualizing the scolex. MRI is also more useful in evaluating degenerative changes in the parasite. However, CT scanning is better at detecting small areas of calcification.\n \nA number of different serologic tests have been developed to aid in the diagnosis of cysticercosis. Some tests detect anticysticercal antibodies, and others identify cysticercal antigens. Some can only be performed on blood, while others can done on other fluids, such as CSF or saliva. As with all serologic tests, results need to be interpreted with caution in individuals from highly endemic areas where a positive serology may be due to past infection and may not prove current active disease.", "ACR Code": "1.6", "Category": "Infection, parasite", "Keywords": "neurocystircercosiscystircercosisparasite", "Reference": "Leder K, Weller PF. Epidemiology; clinical features and diagnosis of cystircercosis. UpToDate 12.1. Dec2003." } }, { "U_id": "MPX1616", "TAC": [ "MPX1616_synpic29137" ], "MRI": [], "Case": { "Title": "Adenocarcinoma", "History": "2 week h/o of dysphagia to solids and hematemesis\nPMH: HTN\nPSH: none\nMeds: Atenolol\nALL: Carbamazepine\nSH: no tobacco or EtOH use", "Exam": "H/H: 13.1/39.5 (low)\nChem Panel normal\nLFTs normal\nAmylase/Lipase normal", "Findings": "IV contrast CT of chest, abd, pelvis:\nA 6.1x4.5cm mass that extended into the proximal portion of the stomach was noted at the gatroesophageal junction. There does not appear to be any obstruction of fluids as contrast has advanced through the lesion and into the distal bowel. \nThere is a 1.9cm rounded lesion near the tail of the pancreas and a 1.0cm enlarged lymph node adjacent to the portal vein that is concerning for metastatic disease and should be further evaluated by a PET scan. \nThere are multiple hypodensities in the liver and left kidney that are too small to characterize but should be further evaluated.", "Differential Diagnosis": "Lymphoma\nMetastatic Disease", "Case Diagnosis": "Adenocarcinoma", "Diagnosis By": "Pathology/Biopsy", "Treatment & Follow Up": "Patient received an EGD which demonstrated a large, fungating mass in the lower third of the esophagus. The mass was partially obstructing and circumferential involving two thirds of the lumen. This mass appeared to extend to the gastric cardia. Multiple biopsies were obtained. \nA malignant esophageal tumor was suspected and patient subsequently received an IV-contrast enhanced CT of the chest, abdomen, and pelvis to evaluate for any metastatic disease. A PET scan obtained after the CT test did not show evidence of lymphatic or hematogenous metastases", "Discussion": "Esophageal cancer is the 10th leading cause of deaths due to cancer in the United States and continues to be the 19th among cancers in incidence. The two main types are squamous cell carcinoma and adenocarcinoma. Although squamous cell constitutes 95% of esophageal cancers worldwide, adenocarcinoma has steadily increased to be the major histological type in the US since the 1970s.\n\nAdenocarcinoma affects white males in the 6th or 7th decade and is most commonly located in the distal esophagus. Risk factors include gastroesophageal reflux disease and Barrett\u2019s esophagus where there is replacement of normal squamous lining with intestinal-type columnar epithelium. Interestingly, these histological changes were found in patients without reflux symptoms. In a Swedish population-based study, 40% of patients with cancer did not have symptoms at least weekly. In comparison, squamous cell cancer of esophagus is located in proximal-mid esophagus, affects black males, and is commonly associated with tobacco and alcohol consumption. \n\nCommon presenting symptoms of esophageal cancer are dysphagia, weight loss, GERD odynophagia, and dyspnea. These symptoms, especially any evidence of mechanical obstruction, should prompt an upper endoscopy where biopsies can be obtained. The primary tumor can then be imaged suing CT and endoscopic ultrasound. CT provides a general overview of the cancer and demonstrates adjacent organ involvement, although esophageal wall layers are not easily distinguished. EUS is gaining popularity due to its strength in visualizing the wall layers. Its drawbacks include operator skill and viewing \u201chard to reach\u201d tumors. \n\nOnce the diagnosis of the tumor is made, imaging to rule out metastatic disease should be performed. Intravenous-contrast enhanced CT of the chest, abdomen, and pelvis remains the gold standard although sensitivity is dependent on the size of the lesion. MRI and US modalities can be used to further characterize metastatic lesions. Positron Emission Tomography is a new tool that visualizes the higher rate of glucose uptake by malignant tissue versus normal, thus, providing more information about metastatic disease. \n\nAppropriate imaging allows clinicians to properly stage the tumor, which directly affects the treatment options and prognosis. Well localized tumors can be resected and have the best 5-year survival of 65-85%. More invasive tumors and those with distant metastses are not surgical candidates and are treated with combined chemotherapy and radiation therapy for palliation. The overall 5yr survival of esophageal cancer is 12-15%.\n\n\n\nReferences\n\nElton, Eric. \u201cEsophageal Cancer,\u201d Disease-A-Mouth, V51, N12 (2005) 664-684.\n\nKorst, R and Altorki,N. \u201cImaging for Esophageal Tumors,\u201d Radiologic Clinics of North America 43(2005) 611-619.\n\nPatel, A and Buenaventura, P. \u201cCurrent Staging of Esophageal Carcinoma,\u201d Surgical Clinics of North America 85 (2005) 555-567." }, "Topic": { "Title": "Adenocarcinoma of the gastroesophageal junction", "Disease Discussion": "Adenocarcinoma of the gastroesophageal (GE) junction is notable in that its incidence that increased more than any other malignancy in the western world. The reasons for such an increase are unknown. (1) There are three classifications of this type of cancer: Type I mainly involves the distal esophagus, Type II is primarily located at the GE junction, and Type II mainly involves the subcardial/proximal stomach region. (3) GE junction adenocarcinoma can either arise from the esophagus or proximal gastric area. It is very difficult to determine the primary cancer site. (1) Risk factors for gastric adenocarcinoma include familial adenomatous polyposis, gastric adenomas/ dysplasia, chronic atrophic gastritis, gastric metaplasia, diet high in nitrates, and Helicobacter pylori infection. Risk factors for esophageal adenocarcinoma include smoking, obesity, and Barrett\u2019s esophagus- patients affected with Barrett\u2019s esophagus have a 30-40% higher chance of developing cancer. (4) \n\nRadiological evaluation of GE adenocarcinoma should be able to determine tumor spread and response to chemotherapy. The sensitivity of CT for detection of distant metastases ranges between 50% to 90%. Of those shown to have only local disease with CT, FDG-PET detected metastatic disease in approximately 20% more cases. In addition, esophageal ultrasound (EUS) can differentiate between stages T1/T2 and stages T3/T4 with an accuracy > 90%. Assessment of tumor response to chemotherapy by FDG-PET correlates with tumor regression proven by histology and can predict patient outcome as early as 2 weeks after initiation of therapy. (5)", "ACR Code": "7.3", "Category": "Neoplasm, carcinoma", "Keywords": "Adenocarcinomacarcinoma", "Reference": "1. Hashem B. \u201cThe epidemic of esophageal adenocarcinoma.\u201d Gastroenterology Clinics of North America 31(2):421\u2013440, 2002.\n2. Macdonald JS; Smalley SR; Benedetti J; Hundahl SA; Estes NC; Stemmermann GN; Haller DG; Ajani JA; Gunderson LL; Jessup JM; Martenson JA. \u201cChemoradiotherapy after surgery compared with surgery alone for adenocarcinoma of the stomach or gastroesophageal junction.\u201d N Engl J Med 345(10): 725-30, 2001.\n3. M?nig SP; Schr?der W; Beckurts KT; H?lscher AH. \u201cClassification, diagnosis and surgical treatment of carcinomas of the gastroesophageal junction.\u201d Hepatogastroenterology 48(41): 1231-7, 2001.\n\n4. Kumar V, Collins T, Robbins SL. Robbins Pathologic Basis of Disease. W.B. Saunders Company, Philadelphia, 1999, pgs 784-802.\n\n5. Weber WA, Ott K. \u201cImaging of esophageal and gastric cancer.\u201d Semin Oncol. 31(4):530-41, 2004." } }, { "U_id": "MPX1617", "TAC": [ "MPX1617_synpic35941" ], "MRI": [], "Case": { "Title": "Absence of IVC", "History": "64 y.o. man with a Hx of HTN, HLD, DM2, CAD, with recent intermittent angina. Angioplasty 3 days ago showed 60% obstruction of left main coronary artery. Pt scheduled in 1 week for for 2 vessel CABG, LIMA to LAD and SVG to Ramus Intermedius.", "Exam": "Non-contributory", "Findings": "Axial and coronal images of abdominal and chest CT significant for absence of IVC below liver. Enlarged azygous/hemiazygous systems present. Drainage from right renal vein into azygous vein and left renal vein into hemiazygous vein. Hemiazygous vein drains into azygous vein near level of diaphragm. Lateral Chest radiograph shows absence of IVC.", "Differential Diagnosis": "Normal anatomic variant.", "Case Diagnosis": "Absence of IVC", "Diagnosis By": "Abdominal and Chest CT scan", "Treatment & Follow Up": "None required.", "Discussion": "PATIENT WAS ASYMPTOMATIC AND THIS FINDING WAS INCIDENTAL. OTHER SIMILAR CASES OF INTERRUPTED IVC SUGGEST THAT THE WELL-DEVELOPED AZYGOUS SYSTEM IS MORE OFTEN FOUND IN PATIENTS THAT ARE ASYMPTOMATIC WHILE WHEN POORLY DEVELOPED, PATIENTS MORE OFTEN PRESENT WITH SYMPTOMS SUCH AS DVT, LEG SWELLING, AND LEG PAIN. \n\nADDITIONAL CONSIDERATIONS IN THIS PATIENT INCLUDE IVC FILTER PLACEMENT AND PLACEMENT OF PERIPHERAL LINES SUCH AS FEMORAL VENOUS ACCESS WHICH MAY REQUIRE VENOGRAM PRIOR TO PLACEMENT" }, "Topic": { "Title": "Absence of IVC", "Disease Discussion": "ABSENCE OF IVC", "ACR Code": "5.1", "Category": "Anatomy, Normal Variant", "Keywords": "IVC" } }, { "U_id": "MPX1625", "TAC": [ "MPX1625_synpic55661" ], "MRI": [], "Case": { "Title": "Amiodarone Liver, increased attenuation (density) on CT", "History": "54 y.o. woman with a long history of cardiac problems. Currently an inpatient after an elective cardiac procedure. CT scan ordered because of decreasing hemoglobin and hematocrit after cardiac procedure.", "Findings": "\u2022 No evidence of large intra-abdominal or thoracic hemorrhage.\n\n\u2022 Postsurgical changes in the left chest wall compatible with recent placement of AICD (implanted cardiac defibrillator).\n\n\u2022 Unchanged cardiomegaly.\n\n\u2022 and, \u2026 a hyperdense liver!", "Differential Diagnosis": "\u2022 Iron deposition\n\u00bb Multiple blood transfusions, increased iron oral intake, ineffective erythropoiesis, primary hemochromatosis (congenital hemochromatosis)\n\u2022 Glycogen storage diseases (Types I and IV)\n\u2022 Gold therapy\n\u2022 Wilson\u2019s disease\n\u2022 Thoratrast (contrast agent 1920s-1950s)\n\u2022 Amiodarone therapy", "Case Diagnosis": "Amiodarone Liver, increased attenuation (density) on CT", "Diagnosis By": "CT and history", "Treatment & Follow Up": "None required - continued followup of liver function", "Discussion": "Normal liver attenuation, precontrast, is similar to spleen, but often slightly greater (+10 HU) - reported to be about 55 (PMID: 10789806) to 63 HU (PMID: 1389665). http://www.ajronline.org/cgi/reprint/174/5/1417\n\nAmiodarone is an antiarrhythmic medication -which this patient was taking. Primary hepatic metabolism of amiodarone - and it is slowly excreted into bile by the liver. Chronic amiodarone therapy increases hepatic parenchymal attenuation - even at normal/typical dosage without toxicity. Normalization of liver attenuation takes weeks to months after discontinuation of the drug.\n\nhttp://www.youtube.com/watch?v=t2Kb7QwGv40&\n\nMore information on AICD - implanted defibrillators: http://www.heartonline.org/defibrillator.htm" }, "Topic": { "Title": "Liver, increased attenuation (density) on CT", "Disease Discussion": "Normal liver attenuation, precontrast, is similar to spleen, but often slightly greater (+10 HU) - reported to be about 55 (PMID: 10789806) to 63 HU (PMID: 1389665). http://www.ajronline.org/cgi/reprint/174/5/1417 \n\nHomogeneous increased attenuation (density) of the liver may result from a variety of causes to include drug toxicity. Hemochromatosis, hemosiderosis and cirrhosis may all result in increased density of the liver. Pharmaceuticals which have been implicated include thorotrast, thallium, gold, and amiodarone.\n\nAmiodarone is an antidysrhythmic drug which contains 40% iodine by weight. Iodine deposits within the liver and causes homogeneous increased attenuation of the liver. Increased liver density may occur with therapeutic levels of the drug and this appearance does not necessarily correlate with amiodarone toxicity.\n\nThe liver attenuation may return to near normal after several months of drug withdrawl.\n\nMedPix Video - http://www.youtube.com/watch?v=t2Kb7QwGv40&", "ACR Code": "7.1", "Category": "Imaging Finding or Artifact", "Keywords": "amiodarone, hemochromatosisfatty liverhyperdensity hyperattenuation", "Reference": "Margulis et al. Alimentary Tract Radiology. 3rd ed, vol 2. C.V. Mosby; St. Louis. 1983.\n\nHalper et al. Gastrointestinal Radiology, The Requisites. 2nd Ed. Mosby; St. Louis. 1999." } }, { "U_id": "MPX1628", "TAC": [ "MPX1628_synpic41584", "MPX1628_synpic41585", "MPX1628_synpic41586", "MPX1628_synpic41588", "MPX1628_synpic41589" ], "MRI": [], "Case": { "Title": "Situs Inversus Totalis", "History": "87 year old man with complaint of a cough.", "Findings": "Chest radiography demonstrates dextrocardia with the cardiac apex pointing to the right. There is a right-sided aortic arch, associated with slight deviation of the distal trachea to the left. A loop of bowel projects in the right upper quadrant of the abdomen. The minor fissure is on the left side. There is no evidence of bronchiectasis. \n\nContrast enhanced CT at the level of the origin of the great vessels demonstrates mirror-image branching of the great vessels; a left-sided superior vena cava; and a contrast filled esophagus posterior to the trachea.\n\nContrast enhanced CT at the level of the diaphragm demonstrates reversal of the normal cardiac anatomy. Note that the cardiac apex and descending aorta are on the right, and the inferior vena cava is on the left side.\n\nContrast enhanced CT of the upper abdomen show mirror-image anatomy of the viscera. The liver, gallbladder, and inferior vena cava are all left-sided. The stomach, spleen, and aorta are right-sided structures. \n\nContrast enhanced CT at the level of the iliac crests demonstrates a left-sided inferior vena cava, and a right-sided abdominal aorta.\n\nMaximal Intensity Projection demonstrates the right-sided aortic arch, left-sided superior vena cava, dextrocardia, right-sided contrast filled stomach, and left sided liver, and gallbladder.\n\nContrast enhanced CT with lung windowing and leveling, demonstrates normal lung parenchyma without evidence of bronchiectasis. Additionally, mirror-image anatomy is evident with a left-sided minor fissure, the pulmonary outflow tract and aortic root are in reversed position, and the left pulmonary artery is seen crossing the mediastinum anterior to the esophagus and left main bronchi.", "Differential Diagnosis": "\u2022 False-positive on Radiography: Technologists or radiologist\u2019s inattention to labeling of the radiograph. The technologist prepares for a PA radiograph, labels the image, but images the patient in an AP projection.\n\n\u2022 False-Positive on CT: Depending on how the patient is positioned into the CT scanner, head first or feet first, supine or prone, and if incorrectly marked by the technologist, the left-right orientation will be displayed erroneously suggesting situs inversus.\n\n\u2022 Situs Inversus\n\u2022 Situs Inversus totalis\n\u2022 Dextrocardia\n\u2022 Situs ambiguous or heterotaxy\n\u2022 Kartagener Syndrome", "Case Diagnosis": "Situs Inversus Totalis", "Diagnosis By": "Imaging findings are diagnostic situs" }, "Topic": { "Title": "Situs Inversus Totalis", "Disease Discussion": "There are three types of situs:\n\u00bb situs solitus (normal), \n\u00bb situs inversus (mirror image of normal), and \n\u00bb situs ambiguous (1). \n\nIn regards to situs inversus, the systemic atrium is on the left, with a left-sided trilobed lung, liver, gallbladder, and inferior vena cava. The pulmonary atrium is on the right with a right-sided bilobed lung, stomach, single spleen, and aorta. Additionally, the cardiac apex is on the right (situs inversus with dextrocardia or situs inversus totalis) (2, 3). Identified in about 0.01% of the population, situs inversus is recessively inherited, more common in males, and is associated with other congenital disorders such as polysplenia, asplenia, horseshoe kidney, diaphragmatic hernia, and annular pancreas (2, 4). \n\nKartagener syndrome is a type of primary ciliary dyskinesia (PCD) that includes: situs inversus, nasal polyposis with chronic sinusitis, and bronchiectasis. It is present in anywhere from 20%-25% of patients have situs inversus, however, only 50% of patients with immotile cilia syndrome have situs inversus. This 50/50 split relates to the role of cilia in creating chemical gradients in the embryo that organize Left-Right asymmetric development.\n\nImpaired mucociliary clearance leads to recurrent lung infections, bronchiectasis predominately affecting the lower lung fields, chronic sinusitis, and otitis media (1, 2, 3).", "ACR Code": "5.1", "Category": "Congenital, normal variant", "Keywords": "Kartagener SyndromeSitus Inversus TotalisPrimary Cilia Dyskinesia", "Reference": "1. Maldjian et al. AJR 2007;188:S39-S49.\n2. Applegate et al. RadioGraphics 1999:19:837-852.\n3. Wilhelm A. Situs Inversus. Emedicine Topic 639 Available from http://www.emedicine.com/radio/topic639.htm 2007. [cited 1 MAR 08].\n4. Hughes J, Feigin D. Situs Inversus MedPixTM Topic: 3681 Available from http://rad.usuhs.mil/medpix/radpix.html?mode=single&recnum=3681&table=&srchstr=&search=#References 2002 [cited 1 MAR 08]." } }, { "U_id": "MPX1643", "TAC": [ "MPX1643_synpic23455" ], "MRI": [ "MPX1643_synpic23456", "MPX1643_synpic23457", "MPX1643_synpic23458", "MPX1643_synpic23459", "MPX1643_synpic24557" ], "Case": { "Title": "Optic nerve sheath meningioma.", "History": "70 year old female for follow up follow up tumor.", "Exam": "N/A", "Findings": "Film #1: Nonenhanced axial CT image of the head shows a bilobed circumscribed hyperdense lesion centered on the left optic nerve that extends to the orbital apex. No evidence of extension is seen outside the bony orbit. \n\nFilm #2 and 3: Axial T1 and T2 weighted images, respectively, shows a bilobed T1 hypointense and T2 heterogenously hyperintense mass arising from the left optic nerve sheath with mildly associated proptosis. There is a clear demarcation present between the mass and optic nerve. \n\nFilm #4: Axial T1 postgadolinium with fat saturation shows the mass to enhance intensely and is only slightly inhomogeneous.", "Differential Diagnosis": "1. Optic nerve sheath meningioma.\n2. Neurofibroma.\n3. Cavernous hemangioma.\n4. Intraconal hematoma.", "Case Diagnosis": "Optic nerve sheath meningioma.", "Diagnosis By": "MR", "Treatment & Follow Up": "N/A" }, "Topic": { "Title": "Meningioma", "Disease Discussion": "Menigioma is the most common extra-axial neoplasm and the second most common intracranial neoplasm. It is typically seen in middle-aged women and it is the most common tumor induced by radiation treatment. There are many histologic varieties and subtypes. Pediatric menigiomas are more aggressive and found in atypical or multiple locations. Multicentric types are uncommon (1-10%) but are frequently found in association with neurofibromatosis 2 (50% of all multicentric disease). Metastases and sarcomatous transformation are rare. \n\t Location: Supratentorial 90%\n ( 1) parasagittal dura \n (2) convexities \n (3) sphenoid wing \n (4) CPA cistern. \n Ventricles or bone. \n Spine \u2013 25 to 30% of all spinal tumors \u2013 the most common spinal tumor\n\t \n\t Imaging: \n CT - Usually slightly hyperdense. \n Calcifications (20%). \n Avid enhancement.\n\t Bony reaction or hyperostosis\n\n MRI: Iso-to slightly hypointense to gray\n matter on T1W, isointense to \n hyperintense on T2W. \n Dural tail is non-specific sign -\n possible benign fibrous reaction\n Encases and narrows vessels, \n especially in the sella region.\n Flow voids in enlarged feeding\n vessels. \n Allows better distinction of cystic\n and fatty change, full extent \n of tumor, bony changes or\n thrombosis. \n \t\t Hemorrhage (rarely)\n\n Angiography: Vascular, supplied by meningeal and\n falcine arteries. \n\t Prolonged \u201csunburst\u201d blush", "ACR Code": "1.3", "Category": "Neoplasm, NOS", "Keywords": "MeningiomaExtra-axial", "Reference": "Grossman RI, Yousem DM: Neuroradiology. The Requisites, St. Louis, Mosby, 1994, 68-73.\n\nOsborn AG, Tong KA: Handbook of Neuroradiology: Brain and Skull, second edition, Mosby, St. Louis, 1996, 289-295." } }, { "U_id": "MPX1646", "TAC": [ "MPX1646_synpic17395", "MPX1646_synpic17397", "MPX1646_synpic17398" ], "MRI": [], "Case": { "Title": "Surgical storage of craniotomy fragment pending definitive management", "History": "GSW from global war on terrorism. Evacuated to CONUS for definitive management after stabilization in Germany.", "Findings": "Bilateral medial frontal lobe lesions.\nBone in anterior abdominal wall.", "Differential Diagnosis": "ACA ischemia\n\n-\tSurgical\n-\tHeterotopic ossification\n-\tMyositis ossificans", "Case Diagnosis": "Surgical storage of craniotomy fragment pending definitive management", "Diagnosis By": "Surgical history", "Treatment & Follow Up": "Surgical storage of craniotomy fragment pending definitive management", "Discussion": "The ACA territory infarcts may be the result of subfalcial herniation causing compression of the artery against the free margin of the falx. The herniation could have occurred from the bullet shock-wave and/or subsequent brain swelling." }, "Topic": { "Title": "Surgical storage of craniotomy fragment pending definitive management", "Disease Discussion": "The calvarial bone is being *stored* inside the patient's own body for later use in reconstructing the skull.", "ACR Code": "1.4", "Category": "Trauma", "Keywords": "craniotomy", "Reference": "Wilkins et al, Neurosurgery V2, 1990, Mcgraw Hill, p 2792" } }, { "U_id": "MPX1648", "TAC": [ "MPX1648_synpic20206" ], "MRI": [], "Case": { "Title": "Acute appendicitis with an appendicolith", "History": "9 yo male with history of abdominal pain for 3 days that is localized to the RLQ. Please assess for possible appendicitis.", "Findings": "Appendicitis is the most frequent abdominal process requiring surgery in the pediatric population. Although the diagnosis can be clinically evident in 80% of patients, imaging using mostly plain film, ultrasound and CT can aid in the diagnosis. Findings can include appendiceal calculus, appendiceal abscess, periappendiceal soft tissue mass, small and/or large bowel obstruction, ileus, intraperitoneal fluid, obliteration of the psoas shadow, splinting of the lumbosacral spine, and a dilated blind-ending tubular structure measuring more than 6mm on sonographic examination", "Case Diagnosis": "Acute appendicitis with an appendicolith", "Treatment & Follow Up": "Infectious enteritis, colitis, intussusception, appendicitis" }, "Topic": { "Title": "Acute appendicitis with an appendicolith", "Disease Discussion": "The term appendicolith is preferred over the less specific terms, coprolith and fecolith. Approximately 10% of patients with acute appendicitis have a radiographically visible appendicolith. One third of surgically removed appendices, however, contain an appendicolith. The calcification may form around any type of nidus, including a piece of vegetable matter, swallowed foreign body, or even barium. The appendicolith tends to be round or oval, smooth, and laminated (Film .2Z). The size varies, but stones in the l-2 cm range are common with stones up to 4 cm in size having been reported. The location is usually in the right lower quadrant, but the pelvis, right upper quadrant in the case of retrocecal appendix, and even the left upper quadrant may be the site. \n\nThe differential diagnosis includes the following:\n\n\ta) Phlebolith - these rounded calcifications tend to occur in clusters, are usually lower in the pelvis, and frequently contain a central lucency.\n\tb) Calcified lymph node - these tend to be amorphous, irregular, \"popcorn\" calcifications.\n\tc) Ureteral calcifications - this calcification should conform to the course of the ureter and tends to be smaller and less often laminated.\n\td) Benign bone island in the iliac wing - this density will not move with changes in position of the patient, maintaining a constant location within the iliac bone.\n\nThe presence of an appendicolith is significant clinically since patients with this radiograph finding are more likely to have appendicitis complicated with perforation or abscess. This is especially true in children. \n\nThe plain film diagnosis of acute appendicitis in the absence of an appendicolith can be difficult with the plain film demonstrating abnormalities in approximately one half of patients. The following radiographic findings have been described, but no one of these is as helpful as an appendicolith. \n\n\t1) Abnormal bowel gas pattern. The bowel gas pattern in acute appendicitis can be anywhere from normal to consistent with a complete small bowel obstruction. A local ileus in the right lower quadrant with air fluid levels can be seen. Occasionally fluid-filled right lower quadrant small bowel loops may present as a soft tissue mass. A dilated transverse colon in pediatric patients with a perforated appendix has also been described. \n\t2) Abnormal cecum and ascending colon. Local inflammation and edema may cause thickening of the colon wall and widen the haustra. A cecal air fluid level may be present. \n\t3) Extraluminal soft tissue mass. This finding can be seen in up to one third of patients with perforation. A combination of edema, fluid, and fluid-filled loops of small bowel produce the effect. A mottled gas collection within the soft tissue mass is highly suggestive of an abscess. \n\t4) Obliteration of normal fat planes. Sufficient inflammation from appendicitis may alter the water density of the surrounding fat and obscure the right properitoneal flank stripe, psoas muscle, or obturator muscle. \n\t5) A small amount of free intraperitoneal or retroperitoneal air may rarely be present.\n\nThe use of the barium enema, ultrasound, and CT in diagnosing acute appendicitis will be discussed in a separate section.", "ACR Code": "7.2", "Category": "Infection, NOS" } }, { "U_id": "MPX1654", "TAC": [ "MPX1654_synpic26198" ], "MRI": [], "Case": { "Title": "landmine", "History": "Was near a soldier who stepped on a landmine. The soldier who stepped on the landmine died shortly after arriving at the combat support hospital emergency department.", "Exam": "Multiple penetrating wounds to the extremities, pelvis, and abdomen.", "Findings": "Multiple ball baring-like projectiles in the superficial soft tissues, with some penetrating into the abdominal cavity, and into the pelvis.", "Case Diagnosis": "landmine", "Diagnosis By": "Surgery" }, "Topic": { "Title": "landmine", "Disease Discussion": "Landmines are still used today as an antipersonnel weapon. They vary in type and can cause devastating injuries and death.", "ACR Code": "4.4", "Category": "Trauma", "Keywords": "landmine" } }, { "U_id": "MPX1657", "TAC": [ "MPX1657_synpic24451" ], "MRI": [], "Case": { "Title": "Medullary Nephrocalcinosis.", "History": "A 39 year old female patient presented with a history of cloudy urine and dysuria. She also reported 6/10 bilateral flank pain. A renal-stone protocol abdominal CT was ordered to assess for nephrolithiasis.", "Exam": "Urinalysis was positive for microscopic hematuria.\nUrine pH was normal.", "Findings": "An unenhanced renal-stone protocol CT scan demonstrates calcifications in the renal medullary pyramids bilaterally, consistent with medullary nephrocalcinosis.", "Differential Diagnosis": "Medullary nephrocalcinosis.", "Case Diagnosis": "Medullary Nephrocalcinosis.", "Diagnosis By": "Medullary nephrocalcinosis was confirmed by imaging.", "Treatment & Follow Up": "Not known.", "Discussion": "Please refer to the accompanying TOPIC discussion." }, "Topic": { "Title": "Medullary Nephrocalcinosis", "Disease Discussion": "Medullary nephrocalcinosis (95% of all nephrocalcinoses) is usually associated with hypercalciuria and often with hypercalcemia. Approximately 40% of cases of medullary nephrocalcicosis are attributable to primary hyperparathyroidism, another 20% to renal tubular acidosis, and the remaining 40% divided among many other causes. Most of the conditions that cause nephrocalcinosis can also result in nephrolithiasis. Their coexistence helps establish the etiology and may significantly impact patient management. The appearance of medullary nephrocalcinosis equates to calcifications involving the distal convoluted tubules in the loops of Henle.\n \nHYPERCALCIURIA, in general, is due to to dissolution of the bone, excessive ingestion or absorption of calcium from the gastrointestinal tract, or faulty renal reabsorption of calcium. Hyperparathyroidism is the most common single cause. Medullary nephrocalcicosis is seen in 5% of those with primary hyperparathyroidism (parathyroid adenoma), and nephrolithiasis is seen in 50-80% of these patients. Secondary hyperparathyroidism (usually due to renal disease) is a much less likely cause.\n\nRENAL TUBULAR ACIDOSIS is characterized by abnormal renal tubular function that results in chronic systemic acidosis and a persistent alkali urine. There are two types of RTA. Type II RTA consists of proximal abnormalities, in which there is a greater than normal loss of bicarbonate, and renal calculi are not formed. Distal tubular dysfunction (type I RTA) interferes with hydrogen ion transfer into the urine, and may result in stone formation. 30% of infants and 70% of adults with type I RTA develop medullary nephrocalcicosis or nephrolithiasis. RTA may cause delayed skeletal maturation and osteomalacia. Primary RTA results from an inherited enzymatic defect. Diseases known to cause secondary RTA include Wilson\u2019s disease, Fanconi\u2019s syndrome, hyperglobinemias, nephrotoxic drugs (outdated tetracycline, amphotericine B), and acetazolamide administration. These processes (primary or secondary causes of RTA) result in an inability to acidify urine. Since calcium ions are much more soluble in acidic urine crystalline calcium salts precipitate.\n\nRENAL TUBULAR ECTASIA, or medullary sponge kidney, is a disease in which the terminal nephrons and ducts of Bellini are dilated. Calculi form in about half the cases owing to stasis of urine in these dilated ducts. Approximately 15% of these patients develop calcifications, which may be present in both kidneys, one kidney, or even a single collecting system.\n\nMedullary nephrocalcicosis and urolithiasis occur in a variety of other conditions, including but not limited to sarcoidosis, Cushing syndrome diabetes insipidus, hyperthyroidism, milk-alkali syndrome (excess calcium + alkali = milk + antacids), and hypervitaminosis D.", "ACR Code": "8.5", "Category": "Metabolic (see also Toxic)", "Reference": "Putman CE, Ravin CE: Textbook of Diagnostic Imaging, 2nd ed. Saunders 1994, pp1157-8.\n\nSlone MS, Fisher AJ, Pickhardt PJ, Gutierrez FR, Baalfe DM. Body CT: A Practical Approach, McGraw-Hill 2000, pp191-2." } }, { "U_id": "MPX1663", "TAC": [ "MPX1663_synpic51009", "MPX1663_synpic51013", "MPX1663_synpic51015" ], "MRI": [], "Case": { "Title": "Left atrial appendage thrombus", "History": "80 year-old man with a known history of rate-controlled atrial fibrillation and aortic stenosis presented one week prior to study with facial droop.", "Exam": "Left sided facial droop with noted drooling.\n\nINR 1.3", "Findings": "\u2022 There is a low-attenuating mass in the left atrial appendage. This is most suggestive of a thrombus. \n\u2022 The trileaflet aortic valve is calcified and stenotic, with a systolic valve area of 1.4-1.7cm^2.\n\u2022 There are no infective vegetations present on either the aortic or mitral valves.", "Differential Diagnosis": "Infective endocarditis\nLeft atrial myxoma\nPapillary fibroelastoma\nMetastatic disease", "Case Diagnosis": "Left atrial appendage thrombus", "Treatment & Follow Up": "The patient was anticoagulated, then continued on long-term warfarin therapy with goal INR of 3.0.", "Discussion": "The initial brain MRI showed scattered lesions consistent with thromboembolic phenomena.\n\nThis patient had suspected thromboembolic disease with a cardiac origin. In a patient of this age and with his history of atrial fibrillation and aortic stenosis, left atrial thrombus and infective endocarditis were high on the differential for the embolic source.\n\nThe patient underwent two transthoracic echocardiograms (TTEs) evaluating for possible endocarditis. Both TTEs were negative for atrial thrombus, and neither could effectively image the aortic valve due to the high level of valvular calcification present. It should be noted that TTE has a relatively low sensitivity (high false negative rate) for visualizing left atrial appendage thrombi compared to TEE and cardiac-gated CT.\n\nA transesophageal echocardiogram was bypassed after the patient was deemed not to be a good surgical candidate (based on age and comorbidities); this cardiac-gated CT scan was later performed instead to evaluate for the embolic source. The CT scan showed no evidence of infective endocarditis, but did reveal a filling defect within the left atrial appendage. Of note, single-phase contrast imaging with cardiac-gated CT can have a falsely positive filling defect in the left atrial appendage, especially in cases of atrial fibrillation when the atria may be dilated and/or there is little contractility to allow adequate contrast mixing within the appendage. Key to this study is the late-phase imaging, which showed contrast filling the atrial appendage and highlighting the presence of a thrombus. This finding was pathognomonic. \n\nCardiac tumors, including atrial myxomas and papillary fibroelastomas (as well as metastatic disease), are other possibilities, but are considerably more rare; thus, they remain low on the differential diagnosis." }, "Topic": { "Title": "Left atrial appendage thrombus", "Disease Discussion": "The three classic mechanisms for thrombus formation include blood flow stasis, blood vessel wall damage, and a hypercoagulable state. All three of these are thought to contribute to the development of thrombi in patients with atrial fibrillation. This has considerable clinical relevance, with atrial fibrillation being a major cause of thromboembolic disease leading to serious morbidity and mortality.\n\nWhile thrombus formation is possible anywhere within the heart depending on variations in anatomy and function of the atria, ventricles and valves, the left atrial appendage is of particular interest. Low blood velocities in the atrial appendage result in high incidences of thrombus formation compared to elsewhere in the heart. Roughly 90% of thrombi in patients with non-valvular atrial fibrillation arise in, or associated with, the left atrial appendage. It is thought that the anatomy of the appendage, with its relatively small communication to the left atrium and the presence of trabeculations, predisposes the area to low blood flow. In patients with atrial fibrillation, atrial contractile function decreases significantly, and there is relative blood stasis in the appendage leading to thrombus formation.\n\nTraditionally, the left atrial appendage has been best evaluated by transesophageal echocardiography (TEE); while more invasive than transthoracic echocardiography (TTE), TEE was found to be much more effective at visualizing thrombi in the atria and the left atrial appendage. More recently, cardiac-gated computed tomography (CT) angiography has been shown to have thrombus detection values very similar to that of TEE (sensitivity and specificity values near 100%). Cardiac-gated CT may become the preferred modality for evaluation of suspected thromboembolic disease from a cardiac source in cases where TEE is not tolerated or non-diagnostic.\n\nThrombus formation in patients with atrial fibrillation is counteracted in the majority of moderate to high risk patients with warfarin therapy. However, a sizable proportion of patients are unable to take oral anticoagulation therapy due to contraindications or are non-compliant. For this reason, there are techniques used to close the left atrial appendage, either in an open approach during surgery (for valve replacement, for example) or, more recently, with percutaneous devices. Long term outcome studies are still pending, however, left atrial appendage occlusion may become a viable method for stroke prevention in patients unable to take oral anticoagulants.", "ACR Code": "5.7", "Category": "Vascular", "Keywords": "atrial appendagethromboembolismatrial fibrillation", "Reference": "Donal E, Yamada H, Leclercq C, Herpin D. The left atrial appendage, a small, blind-ended structure: a review of its echocardiographic evaluation and its clinical role. Chest. 2005 Sep;128(3):1853-62. Review.\n\nAl-Saady, NM, Obel, OA, Camm, AJ. Left atrial appendage: structure, function, and role in thromboembolism. Heart 1999; 82:547.\n\nHur J, Kim YJ, Lee HJ, Ha JW, et al. Left atrial appendage thrombi in stroke patients: detection with two-phase cardiac CT angiography versus transesophageal echocardiography. \nRadiology. 2009 Jun;251(3):683-90.\n\nOnalan O, Crystal E. Left atrial appendage exclusion for stroke prevention in patients with nonrheumatic atrial fibrillation. Stroke. 2007 Feb;38(2 Suppl):624-30. Review." } }, { "U_id": "MPX1660", "TAC": [ "MPX1660_synpic16988" ], "MRI": [ "MPX1660_synpic16991" ], "Case": { "Title": "Vertebral metastasis on Indium-111 tagged WBC scanning", "History": "74 year old male presenting with persistent low grade fevers. Previous history of cystoprostatectomy and right nephroureterectomy for transitional cell carcinoma of the bladder and right renal collecting system respectively.", "Exam": "Examination revealed a chronically ill appearing elderly male. Abdominal exam was negative save evidence of prior surgery to include a ileal conduit stoma in the right lower quadrant. Laboratory evaluation revealed mild leukocytosis. Urine culture revealed Klebsiella pneumoniae.", "Findings": "CT scan (without contrast due to renal insufficiency) revealed no evidence of intra-abdominal abscess, however the liver was found to harbor multiple lesions, biopsy of which revealed metastatic transitional cell carcinoma (figure 1). Additonally, a lytic lesion was found of the L2 vertebral body (figure 2). Because of the recurring fevers an Indium-111 tagged WBC study was requested (figures 3 and 4). After reviewing the indium scan results, the primary service relayed that the patient was also complaining of back pain. The differential diagnosis of the findings from the CT and Indium scan included possible discitis/vertebral osteomyelitis, and metastatic disease. \n\nSubsequent MR (figure 5) of the lumbar spine demonstrates collapse of the L2 vertebral body, as well as heterogeneous marrow replacement. There was no surrounding fluid component. The discs did not demonstrate involvement with the process. There was marked gadolinium enhancement of the lesions within the vertebral body.", "Differential Diagnosis": "Photopenic lesion of the spine with In-111/WBC: osteomyelitis\ninfarction (late)\nmetastasis\noverlying hardware or bone resection\nradiation effects\nmyelofibrosis\nPaget\u2019s disease (lytic phase)", "Case Diagnosis": "Vertebral metastasis on Indium-111 tagged WBC scanning", "Discussion": "see factoid" }, "Topic": { "Title": "Vertebral metastasis on Indium-111 tagged WBC scanning", "Disease Discussion": "Indium-111 oxine tagged WBC scanning is of utility in localizing an occult site of infection, particularly in the abdomen where uptake of Ga-67 citrate may be masked by bowel activity. However, for suspected osteomyelitis of the spine Ga-67 is superior to indium-WBC. The false negative rate of In-111 tagged WBCs in the diagnosis of spinal osteomyelitis is up to 40%. However, in this case the complaint of back pain in this patient with fever was actually elicited only after the In-111/WBC scan findings were known. In the case of a photopenic lesion of the spine with In-111/WBC the differential diagnosis is: osteomyelitis, infarction (late), metastasis, overlying hardware or bone resection, radiation effects, myelofibrosis, and Paget\u2019s disease (lytic phase). In-111/WBC has a high accuracy in the diagnosis of osteomyelitis except for within the spine. Ga-67 uptake, while more sensitive for spinal osteomyelitis is less specific, being seen in any situation where there is bone turn over, to include fracture or osteomyelitis. In this case, MR was obtained to evaluate the photopenic lesion seen on the In-111/WBC scan. MR findings of osteomyelitis would include decreased SI in the marrow on T1, variable SI on T2 and enhancement with gadolinium, all of which are seen in this case. However, findings that argue in favor of metastatic disease are the involvement of the pedicles, and sparing of the adjacent discs and surrounding tissues.", "ACR Code": "3.3", "Category": "Neoplasm, metastatic", "Keywords": "vertebral metastasesosteomyelitis/discitisIndium-111 tagged WBC", "Reference": "Thrall JH, Ziessman HA: Nuclear Medicine: The Requisites. Mosby, St. Louis, 2001, p 189.\n\nKaplan PA, Helms CA, Dussalt R, et al: Musculoskeletal MRI. WB Saunders, Philadelphia, 2001, pp. 37-40." } }, { "U_id": "MPX1665", "TAC": [ "MPX1665_synpic54372", "MPX1665_synpic54373", "MPX1665_synpic54374" ], "MRI": [], "Case": { "Title": "Pancreatic Mucinous Cystic Neoplasm (Mucinous Cystadenoma)", "History": "A 57 yo F with recent gastric bypass surgery developed shortness of breath and tachycardia several days after surgery.", "Exam": "Tachycardia\nElevated D dimer test\nOtherwise normal physical exam findings and BMP", "Findings": "On CT imaging an incidental 3.6cm mass was seen in the tail of the pancreas. Follow up contrast enhanced CT demonstrated a macrocystic mass in the tail of the pancreas with a coarse calcification. No pancreatic ductal dilation was seen.", "Differential Diagnosis": "1. Mucinous cystic neoplasm (macrocystic cystadenoma)\n2. Intraductal papillary mucinous neoplasm\n3. Pseudocyst\n4. Adenocarcinoma\n5. Oligocystic variant of a microcystic serous cystadenoma", "Case Diagnosis": "Pancreatic Mucinous Cystic Neoplasm (Mucinous Cystadenoma)", "Diagnosis By": "Pathology confirmed diagnosis", "Treatment & Follow Up": "Surgical resection was performed because of malignant potential of neoplasm.", "Discussion": "During the patient's gastric bypass surgery the surgeon noted that the pancreas \"looked funny\". Her pancreatic neoplasm was then later incidentally discovered on CT scan." }, "Topic": { "Title": "Pancreatic Mucinous Cystadenoma", "Disease Discussion": "Lesion/Condition Name: Pancreatic Mucinous Cystadenoma.\n\nWhat is it? Neoplasm - cystic adenoma of the pancreas. Often benign but has malignant potential.\n\nCell of Origin: Columnar epithelial cells.\n\nSynonyms: Mucinous cystic neoplasm.\n\nCommon Locations: Body or tail of pancreas.\n\nDescription: Mucinous cystadenomas are the most common cystic pancreatic neoplasms accounting for approximately 10% of pancreatic cysts. Cystic neoplasms make up less than 1% of all pancreatic neoplasms, most being adenocarcinomas. \nMucinous cystadenomas occur most often in middle age women. Mean age 50 years old. 50% occur between 40-60 years of age. M:F 1:19.\n\nGross Morphology: Macrocystic mass, can have thick irregular walls and septa. Peripheral or septal calcifications.\n\nGross Appearance: Multiloculated cysts filled with thick mucinous material.\n\nHistology: Columnar mucinous epithelium, dense stroma.\n\nRadiology: CT shows unilocular or multilocular macrocystic appearance. They can have peripheral or septal calcification in 20% of cases. Mucinous cystadenoma's typically show contrast enhancement.\n\nPrognosis and Treatment: Mucinous cystadenomas can be benign or malignant and can undergo \nmalignant transformation. Histopathology is necessary for definitive diagnosis. Prognosis \nis generally good if there is no evidence of distant metastasis. Treatment is surgical \nresection. 5 year survival is 74-90%.", "ACR Code": "7.3", "Category": "Neoplasm, non-CNS", "Keywords": "mucinous cystadenomacystic pancreatic neoplasmscystic adenoma of pancreas", "Reference": "D?hnert, W. F. (2003). Radiology Review Manual (5 ed.). Philadelphia, PA: Lippincott Williams & Wilkins.\n\nHutchins, G. F., & Draganov, P. V. (2009). Cystic neoplasms of the pancreas: a diagnostic challenge. World J Gastroenterol, 15(1), 48-54.\n\nSahani, D. V., Kadavigere, R., Saokar, A., Fernandez-del Castillo, C., Brugge, W. R., & Hahn, P. F. (2005). Cystic pancreatic lesions: a simple imaging-based classification system for guiding management. Radiographics, 25(6), 1471-1484." } }, { "U_id": "MPX1671", "TAC": [ "MPX1671_synpic52966" ], "MRI": [], "Case": { "Title": "Arteriovenous Malformation (AVM)", "History": "27 year old active duty man with acute onset or deep, non-radiating, chest pain", "Exam": "Uncomfortable, tall, thin man; dyspnea noted;\nChest clear to auscultation bilaterally", "Findings": "left pulmonary AVM", "Differential Diagnosis": "\u2022 AVM\n\u2022 Pulmonary nodule", "Case Diagnosis": "Arteriovenous Malformation (AVM)", "Diagnosis By": "Pulmonary Angiography", "Treatment & Follow Up": "Embolization of AVM" }, "Topic": { "Title": "Arteriovenous Malformation (AVM)", "Disease Discussion": "ARTERIOVENOUS MALFORMATION (AVM)\n\nClinical Features: AVMs are the most common symptomatic congenital vascular malformations. The peak age at presentation is between 20 and 40. Approximately 50% of patients with AVMs present with symptoms caused by hemorrhage (25% present with seizures). The overall risk of hemorrhage from an AVM is estimated at 2% to 4% per year, cumulative. 98% of AVMs are solitary. Multiple AVMs outside the setting of vascular neurocutaneous disorders such as Rendu-Osler-Weber and Wyburn-Mason syndromes are extremely uncommon.\n\nPathology: AVMs are complex networks of abnormal vascular channels that consist of dilated arterial feeder(s) and draining veins, without intervening capillaries. These vessels often demonstrate flow-induced angiopathic changes secondary to endothelial hyperplasia (flow-related\u201d aneurysms in 10 - 20%). AVMs may contain gliotic brain and hemorrhagic residua. Atrophy of otherwise normal adjacent brain results from chronic regional arterial hypoperfusion and venous hypertension, as the AVMs steal vascular supply from adjacent brain tissue.\n\nImaging: Intracranial AVMs are subdivided into parenchymal (pial or within the brain), and dural (outside the brain). A mixed type occurs when a parenchymal AVM recruits dural vascular supply. 85% of AVMs are supratentorial. On cerebral angiography an AVM appears as a tightly packed mass of enlarged feeding arteries that supply a central nidus, a plexiform web of small vessels. One or more dilated veins drain the AVM nidus. The main goals of the diagnostic imaging workup are to delineate the size of the AVM, the eloquence of adjacent brain, and the pattern of venous drainage. These 3 characteristics are used to determine the long-term risk of an untreated AVM, as the table below explains.\n\nTable 1. Spetzler AVM Grading System\nGraded feature\t Points assigned\n Size\n Small (<3 cm)\t\t\t\t1\n Medium (3-6 cm)\t\t\t2\n Large (>6cm)\t\t\t\t3\n\nEloquence of adjacent brain\n Noneloquent \t\t0\n Eloquent\t\t\t\t\t1\n\nVenous drainage\n Superficial only\t\t\t 0\n Deep\t\t\t\t\t 1\n\n========================================\n \nSpetzler grades range from 1 to 5. A separate grade 6 is reserved for inoperable lesions. Prospective studies have confirmed the accuracy and utility of the Spetzler grade in guiding patient management and estimating postoperative neurologic complications.", "ACR Code": "1.3", "Category": "Congenital, malformation", "Keywords": "AVMvascular malformationcongenital", "Reference": "Osborn. Diagnostic Neuroradiology. 1994. Mosby.\nOsborn. Diagnostic Cerebral Angiography. 2nd Ed, 1999. LW&W." } }, { "U_id": "MPX1673", "TAC": [ "MPX1673_synpic23299" ], "MRI": [], "Case": { "Title": "Subarachnoid hemorrhage, aneurysm", "History": "64 y.o. male medivac\u2019ed. Per daughter, pt had a hx of sudden severe HA one month ago. Seven days ago, pt had LOC. Ventricular catheter on right frontal placed at outside hospital.", "Exam": "Per CIS notes, upon arrival, pt moved only upper extremities, did not open eyes, pupils were small, and did not follow commands. No further PE found.", "Findings": "On non-contrast CT of head, fluid-fluid level with tracking into ventricles noted. Ventricular catheter on R frontal noted. Scattered aneurismal subarachnoid hemorrhage seen in sulci.", "Differential Diagnosis": "Rupture of saccular aneurysm, AVM, angioma, neoplasm\nMeningitis, TIA, ischemic stroke, hemorrhagic stroke", "Case Diagnosis": "Subarachnoid hemorrhage, aneurysm", "Diagnosis By": "Radiologic", "Treatment & Follow Up": "Address ABCs with intubation if patient is obtunded\nTransport to nearest facility with CT scan and neurosurgery backup\nNon-contrast CT of head\nDiagnostic cerebral angiogram (if no lesion found then MRI)\nPossible ventricular catheter placement, endovascular aneurysm coiling, open microsurgical clipping, or hemicraniectomy", "Discussion": "In the U.S., annual incidence of aneurismal non-traumatic SAH 6-25 per 100,000. About 10-15% of pts die before they reach the hospital. Mortality as high as 40% within first week. Better/prompt management decreases mortality rates, although 1/3 have neurologic deficits. Pt usu. experience severe HA and about half presents with LOC. Most importantly, addressing ABC is crucial at the beginning and transferring the pt to hospital with appropriate facility. Non-contrast CT is initial study of choice. Once dx is made, cerebral angiography used to assess vascular anatomy, current bleeding site, and present of other aneurysms. It also helps with operative planning mentioned above.\nReferences: eMedicine, 2004 UpToDate" }, "Topic": { "Title": "Subarachnoid hemorrhage, aneurysm", "Disease Discussion": "In the U.S., annual incidence of aneurysmal non-traumatic SAH is about 6-25 per 100,000. About 10-15% of pts die before they reach the hospital. Mortality as high as 40% within first week. Better/prompt management decreases mortality rates, although 1/3 have neurologic deficits. Pt usu. experience severe HA and about half presents with LOC. Most importantly, addressing ABC is crucial at the beginning and transferring the pt to hospital with appropriate radiolgic capabilities.\n\nNon-contrast CT is initial study of choice. Once dx is made, cerebral angiography used to assess vascular anatomy, current bleeding site, and present of other aneurysms. It also helps with operative planning mentioned above.\n\nMany aneurysms may be treated with endovascular therapy, using coils or balloons to occlude the aneurysm neck - obviating the need for a craniotomy. These interventional procedures can be performed at the time of diagnostic angiography.\n\nReferences: eMedicine, 2004 UpToDate", "ACR Code": "1.6", "Category": "Aneurysm", "Keywords": "Subarachnoid hemorrhageaneurysmbleeding", "Reference": "References: eMedicine, 2004 UpToDate" } }, { "U_id": "MPX1670", "TAC": [ "MPX1670_synpic39560", "MPX1670_synpic39561" ], "MRI": [], "Case": { "Title": "Pulmonary Hamartoma", "History": "40 year old male presents for screening chest radiograph for an over 40 physical examination.", "Exam": "Within Normal Limits", "Findings": "PA chest radiograph demonstrate a well circumscribed opacity within the LUL. The lateral view demonstrates a well circumscribed opacity within the LUL, obscuring the trachea.\n\nAxial contrast enhanced CT demonstrates a well circumscribed nodule in the LUL, with a lobulated border, and multiple clumps of calcium or \u2018popcorn\u2019 calcifications, as well as discrete areas of fat dispersed throughout the lesion.", "Differential Diagnosis": "Differential Diagnosis for a Solitary Pulmonary Nodule or Mass:\n\nNeoplasm:\tBronchogenic carcinoma\n\t\tHamartoma\n\t\tBronchial adenoma\n\t\tGranular Cell myoblastoma\n\t\tMesenchymal neoplasms\n\t\t\tLeiomyoma/Leiomyosarcoma\n\t\t\tFibroma\n\t\t\tNeurofibroma\n\t\t\tLipoma\n\t\tLymphoma\n\t\tSolitary metastasis\n\t\t\tColon carcinoma\n\nInfection:\tSeptic embolus\n\t\t\tStaphylococcus\n\t\tRound pneumonia\n\t\t\tPneumococcus\n\t\t\tLegionella\n\t\t\tNocardia\n\t\t\tFungi\n\t\tLung Abscess\n\t\tInfectious granuloma\n\t\t\tTuberculosis\n\t\t\tHistoplasmosis\n\t\t\tCoccidiomycosis\n\t\t\tCryptoccoccosis\n\t\tParasitic\n\t\t\tEchinococcal Cyst\n\t\t\tAmebic Abscess\n\nCollagen Vascular Disease: Necrobiotic Nodule \n (rheumatoid lung)\n\t\t\t Wegener\u2019s granulomatosis\n\nVascular:\tInfarct\n\t\tAVM\n\t\tPulmonary Artery Aneurysm\n\t\tHematoma\n\nAirways:\tCongenital foregut malformations\n\t\tBronchogenic cyst\n\t\tSequestration\n\t\tMucocele\n\t\tInfected Bulla\n\nMiscellaneous: Amyloidoma\n\t\tRound Atelectasis", "Case Diagnosis": "Pulmonary Hamartoma", "Diagnosis By": "Characteristic imaging appearance" }, "Topic": { "Title": "Pulmonary Hamartoma", "Disease Discussion": "Lesions/Condition: Pulmonary Hamartoma\n\nPredisposing Factors:\n\nMost commonly occurs in the fourth to fifth decade. Most common chromosomal abnormality involves the q13-q15 region of chromosome 12.\n\nSymptoms:\n\nMost patients presenting with peripheral pulmonary hamartomas are asymptomatic. When symptomatic, hemoptysis is the most common presenting symptom.\n\nDiscussion: \n\nPulmonary hamartomas are benign neoplasm with 90% arising within the lung parenchyma, and are usually in a peripheral location. They comprise approximately 5% of all solitary pulmonary nodules. Pulmonary Hamartomas contain cartilage surrounded by fibrous connective tissue with variable amounts of fat, smooth muscle, and seromucous glands. Approximately 30% contain calcium in the form of multiple clumps (\u2018popcorn\u2019 calcification). \n\nGenerally, pulmonary hamartomas can be observed by CT alone. Indications for transthoracic biopsy or resection are rapid growth, a size greater than 2.5 cm, or new pulmonary symptoms. \n\nRadiology:\n\t\nChest Radiographs:\nWell-circumscribed, smoothly marginated solitary nodule without lobar predilection. Most pulmonary hamartomas are smaller than 4 cm in diameter. Calcification is visible in less than 10% of cases.\n\nCT:\nWell-circumscribed nodule with a smooth or lobulated border.\nComposed entirely of fat, a mixture of fat and soft tissue, or fat and calcification. Calcification when present is in the form of multiple clumps of calcium dispersed throughout the lesion (\u201cpopcorn\u201d calcification)", "ACR Code": "6.3", "Category": "Neoplasm, benign", "Keywords": "Pulmonary HamartomaBenign Neoplasm of the LungPopcorn Calcification", "Reference": "Brant W., Helms C. Fundamentals of Diagnostic Radiology. 2nd Edition. Lippincott Willliams & Wilkins. Philadelphia, PA 1999.\n\nFraser et al. Synopsis of Diseases of the Chest. Third Edition. Elsevier Saunders. Philadelphia, PA. 2005." } }, { "U_id": "MPX1672", "TAC": [ "MPX1672_synpic24428", "MPX1672_synpic4070", "MPX1672_synpic4072" ], "MRI": [ "MPX1672_synpic24429", "MPX1672_synpic24440" ], "Case": { "Title": "Acute Stroke, Hemorrhage in Basal Ganglia", "History": "36 year old male with long standing history of poorly controlled hypertension. Patient reported to medical attention with right upper and lower extremity weakness and expressive aphasia.", "Exam": "Right upper and lower extremity weakness, expressive aphasia. Blood pressure 200/160.", "Findings": "Hemorrhage of the putamen with local edema and mass effect.", "Differential Diagnosis": "Hypertensive hemorrhage of the putamen\nBleeding mass lesion\nBleeding vascular malformation", "Case Diagnosis": "Acute Stroke, Hemorrhage in Basal Ganglia", "Diagnosis By": "By imaging", "Treatment & Follow Up": "Patient has been treated with supportive therapy. He is doing well.", "Discussion": "The putamen is the most common location for hypertensive hemorrhage." }, "Topic": { "Title": "Hemorrhage in Basal Ganglia, Hypertensive, Acute Stroke", "Disease Discussion": "The history of a sudden onset unilateral motor and.or sensory changes in a patient are strongly suggestive of stroke, which can be generally classified as either ischemic or hemorrhagic. Although this patient had no known history of hypertension, her CT and MRI both demonstrate evidence of chronic small vessel ischemia secondary to longstanding hypertension. The differential diagnosis for a hemorrhagic lesion in the putamen/posterior capsule includes lacunar infarct, hypertensive hemorrhage, vascular malformation, and neoplasm.\n\nLacunar infarcts represent 15-20% of all strokes, and appear as small cavitary lesions in subcortical regions. They result from the thrombosis of a small penetrating artery, often as a result of a chronic hypertensive change known as lipohyalinosis. Characteristic locations for lacunar infarcts include the following: putamen (37%), pons (16%), thalamus (14%), caudate (10%), and internal capsule (10%). Posterior limb lacunes are the most important clinically because of their potential for severe motor and sensory deficits. Anterior limb lacunes are often clincally silent.\nThese \"perforating\" arteries (lenticulostriate aa., thalamogeniculate aa., and anterior choroidal branch of ICA) are common sites for both lacunar infarcts and hypertensive hemorrhage, and both types of lesions can result from a process known as lipohyalinosis. This is the impregnation of hyaline-lipid material into the walls of small arteries in the setting of hypertension combined with atherosclerosis. Lipohyalinosis predisposes the artery to thrombosis and may also weaken the vessel wall, resulting in small dissecting \"Charcot-Bouchard\" aneurysms.\n\nHypertensive hemorrhages are slightly less common than lacunar infarcts, representing 10-15% of all strokes. Two-thirds of hypertensive hemorrhages occur in the putamen, but most cases occur in the presence of systolic blood pressures much higher than 170. Active bleeding usually lasts less than one hour, while edema progresses over the next few days. Complications of hypertensive hemorrhage include brain herniation and hydrocephalus.", "ACR Code": "1.6", "Category": "Vascular", "Keywords": "hypertensive hemorrhagebasal ganglia", "Reference": "1. Brant, W. E., and Helms, C. A., Fundamentals of Diagnostic Radiology, 2nd ed., 1999, pp. 96-98, 107.\n2. Adams, R. D., and Victor, M., Principles of Neurology, 5th ed., 1993, pp. 692-697, 718.\n3. Fischbein, N. J., et al, Teaching Atlas of Brain Imaging, 1st ed., 2000, pp. 264-266." } }, { "U_id": "MPX1674", "TAC": [ "MPX1674_synpic34452", "MPX1674_synpic34453" ], "MRI": [], "Case": { "Title": "Bronchopleural Fistula", "History": "26 y.o. returning from Operation Iraqi Freedom s/p GSW to right chest three weeks ago - now presenting with fevers, chills, night-sweats, and painful, non-productive cough overnight.", "Exam": "Physical exam was significant for the following:\n-Lungs: Symmetric chest expansion with decreased breath sounds throughout right lung fields and faint crackles in the right lung base.\n-Cardiac: Tachycardic; no murmurs/rubs/gallops\n\nLab findings were significant for the following: \nWBC count of 19.1 and rising.", "Findings": "\u2022 CXR1: At the right lung apex, there is a prominent air-fluid level with post-traumatic changes. There is subcutaneous air within the right neck. Shrapnel overlies the midline and surgical clips are noted at the right lung apex. These findings are consistent with right hydropnemothorax. Also, with noted subcutaneous air over the right neck, these findings altogether make this concerning for bronchopleural fistulous formation between the right pleural space and the subcutaneous tissues of the right neck.\n\n\u2022 CXR2: There is a moderate sized right apical pneumothorax with air fluid level within the mid portion of the right hemithorax consistent with a hydropneumothorax. There is opacification along the right lateral thoracic wall with additional right basilar opacification. Again, there is a large subcutaneous collection of air along the soft tissues overlying the right apex. Also noted are multiple riht apical posterior rib fractures unchanged from previous films. Persistent opacification along the lateral aspect of the right lower lung and along the right lung base is consistent with tracking pleural fluid and adjacent atelectasis. \n\n\u2022 CT scans: Within the right hemithorax, there is a persistent moderate sized pleural effusion with a focal area of fluid at the right lung apex with an internal air fluid level consistent with loculated hydropneumothorax. Along the anterior aspect of this focal fluid collection there is soft tissue density material with internal air bronchograms as well as heterogeneous low density material which may represent an infarcted portion of the right upper lobe. A prior chest tube tract is appreciated along the anterior lateral aspect of the right thorax. Interval increase in size of the patient\u2019s right apical subcutaneous emphysema as well as increased size of the patient\u2019s right hydropneumothorax consistent with bronchopleural fistula with continued communication to the subcutaneous tissues likely via the posterior apical comminuted rib fractures. Findings also suggestive of lung infarction involving the posterior aspect of the right upper lobe.", "Differential Diagnosis": "Bronchopleural fistula\nHydropneumothorax with subcutaneous emphysema", "Case Diagnosis": "Bronchopleural Fistula", "Diagnosis By": "Video-Assisted Thoracic Surgery (VATS)", "Treatment & Follow Up": "1. Medical Therapy\n A. Flexible Bronchoscopy\n 1. Direct visualization, glues, coils, and sealants\n 2. Direct administration of abx\n B. Chest tubes for drainage and pressure relief\n C. Aggressive parenteral abx for infection \n2. Surgical procedures\n A. Surgical closure has success of 80-95%\n 1. Chronic open drainage, direct stump closure with intercostal muscle reinforcement, omental flap, transsternal bronchial closure, and thoracoplasty +/- extrathoracic chest wall muscle transposition.\n 2. Video-Assisted Thoracic Surgery (VATS)", "Discussion": "Bronchopleural Fistulas (BPFs) are communications between the pleural space and the bronchial tree. They are relatively rare but a feared complication of several pulmonary conditions. They have a high morbidity and mortality rate, associated with a prolonged hospital stay, and result in high resource utilization. The incidence of BPF has been reported from 1.5 to 28% after pulmonary resection. This patient\u2019s BPF is a result of penetrating trauma that over time caused necrotizing lung to form a fistula. As a result, the patient\u2019s subcutaneous emphysema was able to increase in size rather quickly. Additionally, tracking pleural fluid is able to accumulate as well. After the chest x-ray and CT scan of the chest, the patient was started on broad-spectrum antibiotics and had a right chest tube placed. Later that morning, the patient was taken for Video-Assisted Thoracic Surgery for drainage and surgical closure of the fistula. The patient did not have any intraoperative complications and is currently recovering." }, "Topic": { "Title": "Bronchopleural Fistula", "Disease Discussion": "Bronchopleural Fistula\n\nBronchopleural Fistulas (BPFs) are communications between the pleural space and the bronchial tree. They are relatively rare but a feared complication of several pulmonary conditions. They have a high morbidity and mortality rate, associated with a prolonged hospital stay, and result in high resource utilization. The incidence of BPF has been reported from 1.5 to 28% after pulmonary resection. This patient\u2019s BPF is a result of penetrating trauma that over time caused necrotizing lung to form a fistula. As a result, the patient\u2019s subcutaneous emphysema was able to increase in size rather quickly. Additionally, tracking pleural fluid is able to accumulate as well. After the chest x-ray and CT scan of the chest, the patient was started on broad-spectrum antibiotics and had a right chest tube placed. Later that morning, the patient was taken for Video-Assisted Thoracic Surgery for drainage and surgical closure of the fistula. The patient did not have any intraoperative complications and is currently recovering.", "ACR Code": "6.4", "Category": "Trauma", "Keywords": "Bronchopleural FistulaFistula" } }, { "U_id": "MPX1683", "TAC": [ "MPX1683_synpic16676", "MPX1683_synpic16677", "MPX1683_synpic16678" ], "MRI": [], "Case": { "Title": "Pheochromocytoma with metastases to the left celiac lymph node", "History": "30 yo with no past medical history who felt dehydrated in Iraq in May. BP measurement was 250/140 and he was evacuated to Landstuhl for stabilization. He noted a prior history of headaches, flushing, shortness of breath, arrhythmias, fainting and dyspnea upon closer questioning, but no nausea, vomiting, chest pain or palpitations. He was started on labetolol initially, and then switched to prazosin after CT and labs diagnosed pheochromocytoma. He was eventually transferred to WRAMC surgical oncology for adrenalectomy and pheochromocytoma excision.", "Exam": "24hr VMA 107.6 (0-10 normal), epinephrine 170 (.5-20), norepinephrine 460 (15-80).", "Findings": "Abdominal CT demonstrates a mass adjacent to the left kidney with distinct borders. There is no indication of a \u201cclaw\u201d sign. In-111 octreotide uptake fusion study demonstrates an area of increased uptake corresponding to the pararenal mass, and another area of increased uptake corresponding to a celiac lymph node.", "Differential Diagnosis": "\u2022 Adenoma (50%\u201380%)\u201390% Nonfunctioning\u2013 10% Functioning (Cushing syndrome or aldosteronoma)\u2022 Cyst and pseudocysts (5%\u201320%)\n\u2022 Pheochromocytoma (5%\u201315%)\n\u2022 Adrenocortical carcinoma (2%\u201310%)\n\u2022 Metastatic (0%\u201310%)\n\u2022 Adrenal hyperplasia (5%\u201310%)\n\u2022 Myelolipoma and lipoma (5%\u201315%)\n\u2022 Ganglioneuroma (0%\u20135%)\n\u2022 Hematoma, infection (Histo), lymphoma, neuroblastoma, granuloma (rare)", "Case Diagnosis": "Pheochromocytoma with metastases to the left celiac lymph node", "Treatment & Follow Up": "L. adrenalectomy, pheochromocytoma removal" }, "Topic": { "Title": "Pheochromocytoma with metastases to the left celiac lymph node", "Disease Discussion": "Adrenal masses are found on CT both when evaluating for a specific disease and also incidentally (the \u201cincidentaloma\u201d) while evaluating for another non-specific complaint. The incidence of incidentalomas has been estimated to be as high as 1.4% to 10% based on autopsies, but in actual practice occur at a frequency of .35% to 5%. \n\n Amongst the various imaging modalities available to the clinical/surgical team, CT is the most useful for evaluating adrenal masses. Utilizing 5 mm collimations, tumors as small as 10 mm may be detected. Although not accepted in clinical practice, multiple studies indicate that low HU masses are more likely to be benign than malignant. One series indicates that masses less than 18 HU are benign (85% sensitivity, 100% specificity). Another set of studies states that those less than 10 HU are benign (73% sensitivity, 96% specificity). Another factor to consider in evaluation for malignancy is the size of the lesion. The greater the size of the lesion, the greater the likelihood of adrenal carcinoma versus adenoma. Lesions less than 3 cm on CT are unlikely to be malignant, whereas lesions greater than 6 cm are usually carcinomas. In addition metastases tend to be less then 4 cm in size.\n Plain films, ultrasound, and tomograms are not as sensitive, whereas angiography, and scintigraphy are too invasive. MRI is indicated if malignancy or a pheochromocytoma is suspected. On T1 or T2 weighted MRI, a benign adrenal adenoma will have the same signal intensity as the surrounding adrenal tissue. On the other hand, a pheochromocytoma will have a very high signal intensity relative to the surrounding tissue on T2 weighted MRI. An adrenal carcinoma will be hyperintense relative to the liver, but less so than a pheochromocytoma; and metastatic lesions will similarly have a high signal intensity but not as high as a pheochromocytoma. Dynamic gadolinium enhanced MRI has been demonstrated to have over 90% specificity and sensitivity in differentiating benign from malignant adrenal masses.\n Fine needle aspiration is very fine for differentiating metastatic versus primary adrenal tumor with 80-100% sensitivity. However, it is not quite as good at differentiating benign versus malignant primary tumors (54-86% sensitivity). However, this is countered by the fact that primary adrenal tumors are usually greater than 6 cm, whereas metastatases are usually less than 4 cm.\n Other imaging modalities include nuclear scintigraphy with cholesterol radiotracers (I 19-iodocholesterol and selenomethylnorcholesterol [scintiadren]). Non hypersecrecting adenomas and tumors secreting cortisol, aldosterone and androgen demonstrate increased uptake. \n One other powerful and exciting imaging modality is positron emission tomography scanning, particularly when fused with CT scans. PET has proven to be 100% sensitive and specific in differentiating benign and metastatic lesions. 18-F-fluorodeoxyglucose imaging and 131-I MIBG imaging have been used for pheochromocytomas. 111-In octreotide imaging is also used.\n 85-90% of pheochromocytomas originate from the chromaffin cells of the adrenal medulla. The other 10% are extramedullary in origin and more properly termed paragangliomas. The vast majority are benign with just 10% of them being malignant. While we are tossing tens around, 10% of pheochromocytomas are found in childhood, 10% are familial, meaning that they are found in certain syndromes.\n Pheochromocytomas cause paroxysmal or persistent hypertension due to excess epinephrine/normetanephrine production. However, only .1-.3% of hypertensive patients have this as cause of hypertension. Less than half of the patients with pheochromocytoma present with paroxysmal hypertension. The majority have chronic hypertension, or chronic hypertension with overlying lability. Paroxysms can be triggered by stress, exercise, posture change, palpation, smoking, and even urination. Other symptoms include tachycardia, palpitations, headache, sweating, tremor, anxiety and a sense of impending doom. Less frequent symptoms include abdominal or chest pain, nausea and vomiting. Hypertension can lead to CHF, pulmonary edema, MI, ventricular fibrillation and CVAs. Catecholamine cardiomyopathy describes the damage to the heart due to pheochromocytoma: the process of cardiac ischemic damage secondary to catecholamine induced vasomotor constriction of myocardial circulation or direct toxicity from catecholamines.\n Occasionally, pheochromocytomas elaborate other steroids or peptides, leading to syndromes such as Cushing\u2019s. Classically, however, catecholamine secreting pheochromocytoma is diagnosed by increased urinary excretion of catecholamines, their metabolites (VMA), and metanephrines, and the imaging modalities described above. Certain medications may confound diagnosis by falsely elevating catecholamines. These include TCAs, BZDs, amphetamines; labetalol, L-dopa, methyldopa, clonidine, and alcohol.\n Pheochromocytomas occasionally (10%) occur in familial, mainly autosomal dominant syndrome including : MEN II a or II b, tuberous sclerosis, von Hippel-Lindau, von Recklinghausen and Sturge-Weber syndrome. Familial forms occur mainly in childhood with a male preponderance. Non-familial forms typically occur between 40-60 years of age with a slight female preponderance.\n After diagnosis, pheochromocytomas must be localized with the use of CT, MRI, MIBG, and PET scans. 98% are found in the abdominal cavity, but pheochromocytomas can be found anywhere from the base of the skull to the pelvis, in a para-aortic or para-vertebral location. Occult pheochromocytomas are classically found in the bladder, or in the organ of Zuckerkandl (which is located superior to the branching of the inferior mesenteric artery, anterior to the aorta).\n Pheochromocytomas must be removed surgically. It is absolutely essential to modulate catecholamine release pre-operatively by administering alpha blockers (usu phenoxybenzamine 40-160 mg QD divided) in sufficient dose to cause nasal stuffiness or borderline hypotension. Beta blockade with propanolol to control excess beta stimulation (tachycardia/cardiac arrhythmia) is doen AFTER alpha blockade. Otherwise peripheral perfusion may be compromised. Volume replace for adequate circulating volume if necessary. Utilize a midline or transverse incision to explore the adrenals bilaterally and explore the paraaortic and paracaval retroperitoneum from diaphragm to pelvis. Laparoscopic adrenalectomy utilizing a flank, retroperitoneal or transabdominal approach is a newer technique which offers lower morbidity, and decreased hospital stay. However, the surgeon must be sure to localize all tumors in advance via imaging studies.", "ACR Code": "-1.-1", "Category": "Unsure", "Keywords": "pheochromocytoma", "Reference": "Delbeke D, Martin W. \u201cPositron Emission Tomography Imaging in Oncology\u201d. Radiologic Clinics of North America. 39:5. September 2001.\n\nGay SB and Woodcock RJ. Radiology Recall. Lippincott, Williams and Wilkins. 2000.\n\nHiggins JC. \u201cDiagnosis of Renal and Adrenal Incidentalomas\u201d Clinics in Family Practice 4:3, Sept 2002.\n\nLawrence P. Essentials of General Surgery. Third edition. Lippincott, Williams and Wilkins, 2000.\n\nRobbins. Pathology. Sixth edition.\n\nUdelsman R and Fishman E. \u201cEndocrine Incidentalomas: Radiology of the Adrenal\u201d Endocrinology and Metabolism Clinics. 29:1. March 2000." } }, { "U_id": "MPX1689", "TAC": [ "MPX1689_synpic48730", "MPX1689_synpic48731" ], "MRI": [], "Case": { "Title": "Ureterolithiasis", "History": "51 y/o male presented to the ER with acute sharp left flank pain and blood in urine.", "Exam": "Vital Signs WNL\nPatient had left flank pain to tenderness\nUA: Large blood in urine, otherise normal\nNo other focal findings or labs", "Findings": "Non contrast CT of the abdomen demonstrates perinephric stranding of the left kidney and mild hydronephrosis. Two distal left ureteroliths are present, associated with obstruction and both measuring about 6 mm. Also fatty replacement of the left psoas muscle from a previous myositis.", "Differential Diagnosis": "Ureterolithasis with obstruction\nNeoplasm (TCC)\nPeripelvic cysts\nPreexisting perinephric fat stranding\nAtherosclerotic calcifications\nPhleboliths", "Case Diagnosis": "Ureterolithiasis", "Diagnosis By": "CT and stone analysis", "Treatment & Follow Up": "Pain management with NSAID and allow the ureteroliths to pass on their own. Specialist referral to urology for further work up or intervention if stones continue or recur.", "Discussion": "This patient had a long history of nephrolithasis and recent hematuria and left flank pain. CT demonstrated two left distal ureteral stones both measuring 6 mm in size. The patient passed the stones without instrumentation. Specialist referral was made and the stones were determined to be calcium oxalate. \n\nReference:\nBrant W, Helms C. \u201cFundamentals of Diagnostic \n Radiology\u201d Lippincott Williams & Wilkins, \n Philadelphia, PA 2007." }, "Topic": { "Title": "Ureterolithiasis", "Disease Discussion": "Ureterolithiasis is the formation or presence of a calculus or calculi in one or both ureters. Typically the stones form in the renal pelvis and travel along the ureter and may become enlarged. Hydronephrosis, obstruction, and/or pyonephrosis may result from a stone trapped in the ureters. Often patients have pain and hematuria. There are typically four different kinds of stones that may form in the kidney or ureter and can become impacted or have a slow transit through the ureter including the most common calcium oxalate or phosphate, struvite , cystine, and uric acid stones.", "ACR Code": "8.9", "Category": "Physiology", "Keywords": "ureterolithiasisureterstone", "Reference": "Brant W, Helms C. \u201cFundamentals of Diagnostic Radiology\u201d \n Lippincott Williams & Wilkins, Philadelphia, PA 2007." } }, { "U_id": "MPX1690", "TAC": [ "MPX1690_synpic55882" ], "MRI": [ "MPX1690_synpic55883", "MPX1690_synpic55888", "MPX1690_synpic55889" ], "Case": { "Title": "Vertebral Artery Dissection", "History": "33 year old woman with 2 weeks of posterior headache and neck pain, nausea, and intermittent dizziness. This has been worsening over the last 2 days. She reports subjective paresthesias of both hands as well as left upper extremity weakness.", "Exam": "No objective weakness on exam. Neurologically intact.", "Findings": "On the right, there is a long segment vertebral artery dissection spanning approximately from C1-C6. Brain imaging was did not show any restricted diffusion to suggest secondary ischemia.", "Differential Diagnosis": "Differential diagnosis based on clinical presentation:\n\nSub-arachnoid hemorrhage\nTension headache\nTIA/Stroke\nArterial dissection", "Case Diagnosis": "Vertebral Artery Dissection", "Diagnosis By": "CTA and MRA", "Treatment & Follow Up": "The patient was placed on antiplatelet therapy with full dose aspirin administered daily. At 1 week, she had progression of neurologic symptoms but imaging revealed no progression of the dissection or infarct. She was subsequently treated with coumadin for anti-coagulation.", "Discussion": "This patient is near the average age for vertebral artery dissection, which occurs most typically between 30 and 45 years of age. \n\nCommonly a history of trauma or external neck manipulation is elicited. Although the patient did not initially report trauma, she did note significant wretching with her nausea and vomiting (presumed gastroenteritis). This may have been resulted in enough mechanical force to cause her vertebral artery dissection." }, "Topic": { "Title": "Vertebral Artery Dissection", "Disease Discussion": "Vertebral artery dissections may occur after head and neck trauma or spontaneously. Cervical artery dissections, including vertebral and carotid arteries, are the leading cause of stroke in patients under 45. In adults, there is no predominance between men and women. \n\nCommon clinical features associated with vertebral artery dissection include neck pain, headache (often posterior/occipital), Horner syndrome, tinnitus, audible bruits, or symptoms of TIA/stroke.\nA dissection of the artery can occur between the media and adventitia, between the intima and media, or a combination of both. The dissection can result with stenosis, occlusion, aneurysmal dilation, intraluminal thrombus formation, or extravascular hemorrhage.\n\nRadiographic evaluation for vertebral artery dissection can be complicated by false negatives and false positives. The most common radiographic techniques used for evaluation include CT and MR. Common causes of false positives include turbulent flow simulating stenosis or adjacent structures that mimic hematoma, or patient body habitus. False negatives are often related to lack of inclusion of the affected area in the study field. Often times, evaluation of headache which may be secondary to dissection results in imaging of the head without inclusion of the neck, although the majority of vertebral dissections occur in the cervical neck. \n\nTreatment for vertebral artery dissection often involves antiplatelet or anticoagulation therapy. The highest risk of ischemia secondary to dissection is in the first several days after the dissection occurs. Repeat imaging to confirm stability and/or revascularization is recommended prior to discontinuing treatment.", "ACR Code": "2.0", "Category": "Ischemia, Ischemic Infarction", "Keywords": "Vertebral artery dissectioncervical artery dissectioncerebral ischemia", "Reference": "Daniel D. Federman, M.D., Elizabeth G. Nabel, MD, eds. 2011. ACP Medicine. Hamilton, Ontario & Philadelphia, PA. Decker Publishing Inc. ISSN 1547-1659. STAT!Ref Online Electronic Medical Library. http://online.statref.com.proxy.lib.umich.edu/document.aspx?fxid=48&docid=1886. 6/22/2011 12:35:16 PM CDT (UTC -05:00).\n\nFusco, Matthew R MD; Harrigan, Mark R MD. Cerebrovascular Dissections\u2014A Review Part I: Spontaneous Dissections. Neurosurgery. 2011;68(1):242-257\n\nProvenzale JM, Sarikaya B, Hacein-Bey L, Wintermark M. Causes of misinterpretation of cross-sectional imaging studies for dissection of the craniocervical arteries. AJR Am J Roentgenol. 2011 Jan;196(1):45-52." } }, { "U_id": "MPX1692", "TAC": [ "MPX1692_synpic22147", "MPX1692_synpic22148", "MPX1692_synpic22150", "MPX1692_synpic22151", "MPX1692_synpic22152" ], "MRI": [], "Case": { "Title": "epiploic appendagitis", "History": "27 year old female with acute onset left lower quadrant pain, r/o diverticulitis or appendicitis.", "Exam": "beta-HCG negative\notherwise N/C", "Findings": "A small round fatty lesion adjacent to the proximal sigmoid colon outlined by a ring of soft tissue attenuation, plus surrounding stranding of mesenteric fat. There is also a small focal thickening of the adjacent sigmoid colonic wall. No diverticula were noted in the entirity of the sigmoid colon (not shown).", "Differential Diagnosis": "epiploic appendagitis", "Case Diagnosis": "epiploic appendagitis" }, "Topic": { "Title": "epiploic appendagitis", "Disease Discussion": "Epiploic appendages are lobulated masses of fat attached to the serosal surface of the colon, and because of its fatty density, normally they cannot be distinguished from the mesenteric fat. Only with ascites or perhaps with gross free air would one be able to distinguish a normal epiploic appendage. \n\nHyperattenuating ring sign has been described in the literature as a rather characteristic finding of epiploic appendagitis. These epiploic appendages can torse at its attachment to the serosal surface of the colon and become infarcted and inflammated due to compromise of the vascular supply. In this case, the inflammed peritoneum surrounding the epiploic appendage becomes thickened and evident on CT, drawing an apparent ring around the epiploic appendage.\n\nPrimary epiploic appendagitis has been reported in 2.5-7.1% of patients who are suspected clinically of having diverticulitis, and approximately in 1.0% of patients suspected of having appendicitis.", "ACR Code": "7.2", "Category": "Inflammatory, NOS", "Keywords": "epiploic appendagitiscolon, CTappendix epiploica", "Reference": "1. Adriaan C. van Breda Vriesman. The Hyperattenuating Ring Sign. Radiology 2003; 226: 556-557.\n2. Jose M. Pereira, Claude B. Sirlin, Pedro S. Pinto, R. Brooke Jeffrey, Damien L. Stella, and Giovanna Casola. Disproportionate Fat Stranding: A Helpful CT Sign in Patients with Acute Abdominal Pain. RadioGraphics 2004; 24: 703-715.\n3. Patrick M. Rao and Robert A. Novelline. Case 6: Primary Epiploic Appendagitis. Radiology 1999; 210: 145-148." } }, { "U_id": "MPX1695", "TAC": [ "MPX1695_synpic21567" ], "MRI": [], "Case": { "Title": "Tuberous Sclerosis", "History": "test case for TS", "Findings": "muliple parenchymal calcifications", "Differential Diagnosis": "TS\ncystcercosis", "Case Diagnosis": "Tuberous Sclerosis", "Treatment & Follow Up": "annual monitor for SEGA" }, "Topic": { "Title": "Tuberous Sclerosis", "Disease Discussion": "Clinical Presentation:\nTuberous sclerosis, or Bourneville's disease, can either be spontaneous (60%) or inherited through a mutation on chromosome 9 or 11 (40%). 1 in 10,000 to 150,000 individuals are diagnosed with the disease. Adenoma sebaceum, mental retardation and seizures are commonly seen. The disease affects the whole body with retinal hamartomas, shagreen patches, ungual fibromas, rhabdomyomas of the heart, angiomyolipomas of the kidney, cystic skeletal lesions, and intracranial manifestations also seen.\n\nPathology/Imaging:\n95% of patients show hamartomas, including periventricular subependymal nodules, cortical and subcortical peripheral tubers, white matter lesions, and subependymal giant cell astrocytomas. Periventricular subependymal nodules appear calcified and rarely enhance. The tubers and white matter lesions are commonly located in the frontal lobes. The tubers show high intensity on T2WI while the white matter lesions do not typically enhance. These lesions appear as curvilinear or straight, thin bands extending from the ventricles. Subependymal giant cell astrocytomas arise from the degeneration of the subependymal nodules. They enhance moderately, show high signal intensity on T2WI, and are located at the foramina of Monroe. These astrocytomas typically cause hydrocephalus and show a low rate of calcification. However, these astrocytomas only occur in 1.7 to 15% of cases. \n\nDifferential Diagnosis:\nDifferential diagnosis of giant cell astrocytoma is central neurocytoma, ependymoma, subependymoma, and a colloid cyst.\n \nTreatment:\nResection of the GCA or shunting to treat hydrocephlaus.", "ACR Code": "1.3", "Category": "Congenital, genetic" } }, { "U_id": "MPX1697", "TAC": [ "MPX1697_synpic24667" ], "MRI": [], "Case": { "Title": "Hodgkin's Lymphoma", "History": "32 year old active duty soldier who presents with increasing shortness of breath and low grade fever.", "Exam": "Physical Exam: Vitals are normal.\nGen: Thin white male. Non toxic appearing. \nChest/Heent: Axillary adenopathy. Lungs are clear.\n\nLabs: Chem 7/UA normal. CBC shows Lymphocytosis with Reed Sternberg cells.", "Findings": "Anterior mediastinal mass.", "Differential Diagnosis": "Hodgkin's Lymphoma\nNon Hodgkin's Lymphoma\nThymoma\nThymolipoma\nBenign thymic hyperplasia\nThyroid Masses\nGerm Cell Tumors.", "Case Diagnosis": "Hodgkin's Lymphoma", "Diagnosis By": "Lab data.", "Treatment & Follow Up": "Radiation and chemotherapy", "Discussion": "The cell of orgin is the antigen presenting interdigitating cells in the paracortical regions of the lymph node. The pathological diagnosis is based on the presence of Reed Sternberg cells. Approximately 90% originate in the lymph nodes and 10% originate in extranodal lymphoid tissue or parenchymal organs. \n\nTypes of Hodgkins's Lymphoma/Prognosis best to worst. Lymphocyte predominant > Nodular Sclerosiing > Mixed Cellularity > Lymphocyte Depleted. The most common type is Nodular Sclerosing. \n\nIncidence is 1:50,000. Bimodal age distribution with peaks in 30's and 70's years of age. \n\nRadiographic Features. \n-Superior and anterior mediastinal nodal involvement- 95%. \n-Contiguous progression from one lymph node group to the next. \n-Lung involvement - 15% \n-Pleural effusions - 15%" }, "Topic": { "Title": "Hodgkin's Lymphoma", "Disease Discussion": "Hodgkin's Lymphoma.\n\nThe cell of orgin is the antigen presenting interdigitating cells in the paracortical regions of the lymph node. The pathological diagnosis is based on the presence of Reed Sternberg cells. Approximately 90% originate in the lymph nodes and 10% originate in extranodal lymphoid tissue or parenchymal organs. \n\nTypes of Hodgkins's Lymphoma/Prognosis best to worst. Lymphocyte predominant > Nodular Sclerosing > Mixed Cellularity > Lymphocyte Depleted. The most common type is Nodular Sclerosing.\n\nIncidence is 1:50,000. Bimodal age distribution with peaks in 30's and 70's years of age.\n\nRadiographic Features.\n-Superior and anterior mediastinal nodal involvement - 95%.\n-Contiguous progression from one lymph node group to the next.\n-Lung involvement - 15%\n-Pleural effusions - 15%", "ACR Code": "6.3", "Category": "Neoplasm, hematopoietic", "Keywords": "HodgkinLymphoma", "Reference": "Primer of Diagnostic Imaging. Ralph Weissleder, Jack Wittenberg, Mukesh G. Harisinghani. Paperback - 3RD edition. Pub. Date: November 2002" } }, { "U_id": "MPX1696", "TAC": [ "MPX1696_synpic51558" ], "MRI": [], "Case": { "Title": "Fibrous Dysplasia", "History": "54 year old woman with headache and syncope", "Exam": "\u2022 Unremarkable physical exam\n\u2022 Laboratory studies within normal limits", "Findings": "CT Head without contrast: Expansile ground glass lesion involving the ethmoid bone and crista galli with extension into the sphenoid sinuses with mass effect on the medial right orbit favored to represent fibrous dysplasia.\n\nFollow-up CT of the orbits and sinuses: The known fibrous dysplasia is again seen involving the crista galli and ethmoid bone with extension into the sphenoid sinuses. Minimal interval expansion of the fibrous dysplastic lesion of the ethmoid bone and crista galli into the medial right orbit. \n\nBone Scan: Moderately intense tracer activity in the region of the previously described ground-glass, expansile lesion centered on the ethmoid air cells, involving the crista galli and extending into the sphenoid sinuses", "Differential Diagnosis": "\u2022 Enchondroma and Enchondromatosis\n\u2022 Eosinophilic Granuloma (Skeletal)\n\u2022 Fibrous Cortical Defect and Nonossifying Fibroma\n\u2022 Giant Cell Tumor\n\u2022 Bone Hemangioma\n\u2022 Primary Hyperparathyroidism\n\u2022 Neurofibromatosis Type I\n\u2022 Paget Disease\n\u2022 Metastases", "Case Diagnosis": "Fibrous Dysplasia", "Diagnosis By": "-Characteristic radiographic features (expansile ground glass bone lesion) and Bone Scan (increased tracer uptake corresponding to involved areas noted on CT scan)", "Treatment & Follow Up": "\u2022 Long-term observation with interval imaging to assess for progression of the lesion\n\u2022 Medical management of symptoms (i.e. pain control)\n\u2022 Bisphosphonates have been shown to reduce bone pain\n\u2022 Surgery may be considered for complicated lesions with mass effect and/or resulting fractures", "Discussion": "Fibrous dysplasia is a skeletal developmental anomaly of the bone-forming mesenchyme resulting from abnormal osteoblast function. Fibrous dysplasia is a nonheritable disease related to a sporadic mutation in the gene that encodes the subunit of a stimulatory G protein on chromosome 20. As a result, osteoblasts abnormally produce fibrous tissue within the bone marrow. Fracture is the most common complication of fibrous dysplasia. Malignant transformation occurs less than 0.5% of cases. \n\nFibrous dysplasia represents approximately 5% of all benign bone tumors. Any bone can be affected. 70% of cases are the monostotic form whereas 30% are of the polystotic form. The incidence rates are equal in males and females. However the true incidence is unknown since many patients are asymptomatic. Fibrous dysplasia usually presents in persons aged 3-15. Most cases manifest themselves before the age of 30. Clinically patients present with pain and deformity or with a pathologic fracture. Long bones are commonly affected. The femur is the most common long bone affected. Other common areas include the tibia, facial bones and skull. \n\nThe diagnosis is typically made with plain radiography. Characteristic radiographic findings include a relatively homogenous lucent lesion with or without bone expansion commonly described as a ground-glass appearance. Additionally the lucent lesion has a thick sclerotic border that is called the rind sign. There should be an absence of periosteal reaction. CT is commonly used to assess complex areas such as the spine, pelvis, chest and craniofacial bones. CT is very useful in evaluating the extent of disease in these complex areas. Nuclear imaging may also be used in conjunction with other imaging modalities to assist with the diagnosis of fibrous dysplasia. However nuclear imaging is not specific for fibrous dysplasia. Needle biopsy can be used to confirm the diagnosis if there is uncertainty.\n\nAsymptomatic patients do not require treatment. Bisphosphonates have been shown to be helpful treating chronic bone pain associated with fibrous dysplasia. Surgical treatment is indicated for the treatment and prevention of pathologic fractures. Surgery may also be utilized for the treatment of severe deformity.\n\nReferences:\nAnand MKN. Fibrous Dysplasia. Accessed 01Nov2009.\nGrossman RI and Yousem DM. Neuroradiology: The requisites 2nd edition. Mosby 2003. \nVargas B, and Clayer M. Fibrous Dysplasia. Accessed 01Nov2009." }, "Topic": { "Title": "Fibrous Dysplasia", "Disease Discussion": "Fibrous dysplasia is a skeletal developmental anomaly of the bone-forming mesenchyme resulting from abnormal osteoblast function. Fibrous dysplasia is a nonheritable disease related to a sporadic mutation in the gene that encodes the subunit of a stimulatory G protein on chromosome 20. As a result, osteoblasts abnormally produce fibrous tissue within the bone marrow. Fracture is the most common complication of fibrous dysplasia. Malignant transformation occurs less than 0.5% of cases. \n\nFibrous dysplasia represents approximately 5% of all benign bone tumors. Any bone can be affected. 70% of cases are the monostotic form whereas 30% are of the polystotic form. The incidence rates are equal in males and females. However the true incidence is unknown since many patients are asymptomatic. Fibrous dysplasia usually presents in persons aged 3-15. Most cases manifest themselves before the age of 30. Clinically patients present with pain and deformity or with a pathologic fracture. Long bones are commonly affected. The femur is the most common long bone affected. Other common areas include the tibia, facial bones and skull. \n\nThe diagnosis is typically made with plain radiography. Characteristic radiographic findings include a relatively homogenous lucent lesion with or without bone expansion commonly described as a ground-glass appearance. Additionally the lucent lesion has a thick sclerotic border that is called the rind sign. There should be an absence of periosteal reaction. CT is commonly used to assess complex areas such as the spine, pelvis, chest and craniofacial bones. CT is very useful in evaluating the extent of disease in these complex areas. Nuclear imaging may also be used in conjunction with other imaging modalities to assist with the diagnosis of fibrous dysplasia. However nuclear imaging is not specific for fibrous dysplasia. Needle biopsy can be used to confirm the diagnosis if there is uncertainty.\n\nAsymptomatic patients do not require treatment. Bisphosphonates have been shown to be helpful treating chronic bone pain associated with fibrous dysplasia. Surgical treatment is indicated for the treatment and prevention of pathologic fractures. Surgery may also be utilized for the treatment of severe deformity.", "ACR Code": "2.3", "Category": "Radiologic Sign or Finding", "Keywords": "Fibrous dysplasiaMonostoticGround glass", "Reference": "Anand MKN. Fibrous Dysplasia. Accessed 01Nov2009.\n\nGrossman RI and Yousem DM. Neuroradiology: The requisites 2nd edition. Mosby 2003. \n\nVargas B, and Clayer M. Fibrous Dysplasia. Accessed 01Nov2009." } }, { "U_id": "MPX1702", "TAC": [ "MPX1702_synpic25371", "MPX1702_synpic25373" ], "MRI": [], "Case": { "Title": "HCC", "History": "65 yo male with h/o hemochromatosis", "Exam": "PE \u2013 noncontributory\n Labs \u2013 PT 14.1 PTT 34.5 INR 1.1 CBC 6.6/15.2/44/180\n A-1-fetoprotein 1.9 AST/ALT 37/33 Alk phos 78 Alb 4.6 Tprotein 7.9\n Tbili 1.1 Dbili 0 Iron 98 TIBC 393 Fe sat 24.9%", "Findings": "2.9 cm mass in R lobe of liver, L liver lobe atrophy", "Differential Diagnosis": "Hepatocellular carcinoma\n Focal Nodular Hyperplasia\n Metastatic disease", "Case Diagnosis": "HCC", "Treatment & Follow Up": "Unknown at this time\u2026resection vs. transplantation. Other options include chemotherapy and radioablation.", "Discussion": "HCC occurs in 19-24% of pts with hemochromatosis, which is a 20 to 200 fold increased risk compared with the general population (similar to that of pts with cirrhosis secondary to viral hepatitis). Risk factors include advancing age (>50), male sex, and the presence of cirrhosis. LFT\u2019s are often normal as the pathophysiology is not an inflammatory process. HCC is the leading cause of death in pts with hemochromatosis (approximately 30%). Other causes include cardiac failure resulting from iron deposition in the heart tissue and hepatic failure. \nFNH is almost always seen in women of childbearing age (90%) and is frequently associated with oral contraceptive use.\nThe remainder of the abdominal pelvic CT was neg for malignancy and pts unremarkable physical exam (non-cachectic) makes mets unlikely." }, "Topic": { "Title": "Hemochromatosis, Hepatocellular Carcinoma, HCC", "Disease Discussion": "Hepatocellular Carcinoma (HCC) occurs in 19-24% of pts with hemochromatosis, which is a 20 to 200 fold increased risk compared with the general population (similar to that of pts with cirrhosis secondary to viral hepatitis). \n\nRisk factors include advancing age (>50), male sex, and the presence of cirrhosis. LFT\u2019s are often normal as the pathophysiology is not an inflammatory process. HCC is the leading cause of death in pts with hemochromatosis (approximately 30%). Other causes include cardiac failure resulting from iron deposition in the heart tissue and hepatic failure.\n\nFNH is almost always seen in women of childbearing age (90%) and is frequently associated with oral contraceptive use.\nThe remainder of the abdominal pelvic CT was neg for malignancy and pts unremarkable physical exam (non-cachectic) makes mets unlikely.", "ACR Code": "9.7", "Category": "Clinical Exam Finding or Sign", "Keywords": "HCChemochromatosishepatic failure", "Reference": "Grainger & Allison's Diagnostic Radiology: A Textbook of Medical Imaging, 4th ed., Copyright \u00a9 2001 Churchill Livingstone, Inc.\n -Harrison\u2019s Principles of Internal Medicine, 15th ed., Copyright \u00a9 2001 McGraw-Hill.\n -Relation of hemochromatosis with hepatocellular carcinoma: epidemiology, natural history, pathophysiology, screening, treatment, and prevention. Harrison, S. & Bacon, B. Medical Clinics of North America 89(2): 391-409.\n -Uptodate, online 13.1., Copyright \u00a9 December 2004" } }, { "U_id": "MPX1699", "TAC": [ "MPX1699_synpic53462" ], "MRI": [ "MPX1699_synpic53463", "MPX1699_synpic53464", "MPX1699_synpic53465" ], "Case": { "Title": "Metastatic Squamous Cell Carcinoma", "History": "52 yo woman presented with headaches and mental status changes. Hx of L breast SCCa three years ago treated at that time with lumpectomy & chemoradiotherapy.", "Exam": "N/A", "Findings": "Bilobed \"cystic\" appearing right hemispheric mass, with a thin peripheral rim of enhancement.", "Differential Diagnosis": "\u2022 Abscess\n\u2022 Parasitic disease\n\u2022 Ganglioglioma, Pleomorphic Xanthoastrocytoma (PXA)\n\u2022 Metastasis (unusual appearance)", "Case Diagnosis": "Metastatic Squamous Cell Carcinoma", "Diagnosis By": "Biopsy and Histology", "Discussion": "Squamous cell carcinoma is an uncommon form of breast cancer. In addition, SCCa from any source is an infrequent CNS metastasis. However, metastatic SCCa often forms large necrotic deposits in lung and elsewhere." }, "Topic": { "Title": "Breast Cancer, Metastatic", "Disease Discussion": "Breast cancer remains the leading cause of death in women in the 40-44 age group. Breast metastases to bone are generally blastic, but can be lytic or mixed lytic/blastic. Patients with skeletal mets most commonly present with bone pain (70%), followed by the vague constellation of symptoms due to hypercalcemia (fatigue, depression, confusion, anorexia, nausea, constipation, renal tubule defects, polyuria, or short QT interval). Breast cancer is the second-most common neoplasm to cause release of PTHrp (following non-small cell lung cancer); hence, breast metastases do not uncommonly cause hypercalcemia, and usually NOT from local osteolysis. Of patients with metastatic disease to the skeleton and hypercalcemia, 80% of the cases of hypercalcemia are due to PTHrP but only 20% due to local osteolysis.\n\nIf a patient with skeletal metastases presents with acute neurologic impairment, a vertebral body lesion compressing the spinal cord may be found - 'spinal syndrome'; this is an indication for IMMEDIATE local irradiation (even in the middle of the night) and massive intravenous steroid therapy.\n\nNote that 30-50% of bone has to be removed by a lytic lesion prior to becoming a conspicuous lucency on plain films!!!", "ACR Code": "4.3", "Category": "Neoplasm, carcinoma", "Keywords": "breast cancer metastaticskeletal metastasesbone metastases" } }, { "U_id": "MPX1705", "TAC": [ "MPX1705_synpic23363" ], "MRI": [], "Case": { "Title": "Pheochromocytoma (Path proven)", "History": "Hypertension and episodic headaches, palpitations, and diaphoresis.", "Exam": "24 hour urine lab values\n METANEPHRINE. . . . . 4764 ug/L\n METANEPHRIN 24H . . . 7146 (45-290) ug/24hr\n NORMETANEPHRINE . . . 3052 ug/L\n NORMETA 24H . . . . . 4578 (82-500) ug/24hr\n METANEPH TOT 24 . . 11724 (120-700) ug/24hr\n EPINEPHRINE 24H . . . 407 (0.5-20.0) ug/24 Hr\n NOREPINEPHRINE. . . . 422 ug/L\n NOREPI 24H. . . . . . 633 (15-80) ug/24 Hr\n CORTSL PT CHA . . . . . 36.2 H (5.0-18.0) ug/dL", "Findings": "CT demonstrates a large left adrenal mass without calcification on the non-contrast CT. The tumor has heterogenous enhancement with central necrotic area.", "Differential Diagnosis": "Pheochromocytoma\nAdrenocortical Carcinoma\nMetastasis\nLipid-poor adenoma [on the unenhanced CT (27HU)]", "Case Diagnosis": "Pheochromocytoma (Path proven)", "Diagnosis By": "Elevated urine metanephrines and surgical specimen", "Treatment & Follow Up": "Surgical resection of mass" }, "Topic": { "Title": "Pheochromocytoma", "Disease Discussion": "Pheochromocytoma is a rare tumor that causes symptoms by excessive secretion of catecholamines. The majority (>90%) of pheochromocytomas are found in the adrenal glands. A 10% rule for pheochromocytomas says that 10% are malignant, 10% are bilateral and 10% are extra-adrenal. They occur with equal frequency in males and females and can occur at any age. The classic symptoms include episodes of headaches, palpitations, diaphoresis and severe hypertension. 24 hour urine tests for catecholamines, metanephrines and VMA are helpful for diagnosis. A new plasma free metanephrines assay has higher sensitivity of 99% compared to 63% for VMA and 83% to 85% for urinary or plasma catecholamines. \n \n Extra-adrenal pheochromocytomas can occur anywhere that sympathetic nervous tissue exists. Two common locations are the organ of Zuckerkandl and the bladder wall. CT and MRI have high sensitivity for detection of pheochromocytomas. CT is faster, less expensive and generally more available than MRI, but is less specific for distinguishing adrenal pheochromocytoma from other masses. MRI is more specific for pheochromocytoma, but not as well tolerated as CT. A nuclear medicine scan with I-131 meta-iodobenzylguanidine is more specific and is particularly useful in cases where pheochromocytoma is stronly suspected clinically but not visualized anatomically by CT or MRI as it can screen the entire body for a focus of uptake. The false-negative rate of MIBG scintigraphy is 10%. \nCT typically demonstrates a large adrenal mass without calcification on the non-contrast CT. If contrast is given the tumor may have heterogenous enhancement. Contrast is not essential for detection and usually is not given if pheochromocytoma is suspected due to reported cases in which iodinated contrast caused precipitation of hypertensive crisis. CT is reported to be more than 93% sensitive and 95 % specific for the diagnosis of pheochromocytomas. \n \n The differential diagnosis for large necrotic adrenal masses include adrenal cortical carcinomas and metastases, but in the context of confirmatory laboratory values the diagnosis can be made with near 100% accuracy.\n \n \n RadioGraphics 2004;24:S87-S99\n \n >>Pheochromocytomas are often clinically silent, and the diagnosis can sometimes be first made at imaging. Although an incidental adrenal nodule is unlikely to represent a pheochromocytoma, additional endocrine investigation is warranted if there is any clinical suspicion for this tumor. As with every imaging interpretation, radiologists should be cognizant of the individual patient\u2019s clinical history and, in particular, of his or her blood pressure status. Despite the fact that most pheochromocytomas have high signal intensity on T2-weighted MR images, more than 30% have low signal intensity on these images. Although pheochromocytomas usually show increased uptake on FDG PET scans, results at conventional radionuclide imaging can also be inconsistent. However, new PET radioisotopes may allow more consistently accurate tests in the future, and these tests may soon play a larger role in the imaging evaluation of both incidental adrenal masses and suspected pheochromocytomas. Pheochromocytoma currently remains a true imaging chameleon, and its diagnosis should always be considered in the imaging evaluation of a patient with an adrenal mass, hypertension, or characteristic symptoms.\n\n Most pheochromocytomas have an attenuation higher than 10 HU; rarely do they contain sufficient intracellular fat to have an attenuation of less than 10 HU. Still, some pheochromocytomas could be incorrectly categorized as adenomas. Pheochromocytomas and paragangliomas with macroscopic fat may also be seen. Conversely, some pheochromocytomas may demonstrate very high attenuation due to hemorrhage. << RadioGraphics 2004;24:S87-S99", "ACR Code": "8.3", "Category": "Neoplasm, NOS", "Keywords": "pheochromocytomaAdrenal", "Reference": ".http://www.pheochromocytoma.org\n\n.Pheochromocytoma January 14, 2002 Author: Ann T Sweeney, MD\nhttp://www.emedicine.com/med/topic1816.htm\n\n.Pheochromocytoma May 3, 2002 Anant Krishnan, MD\nhttp://www.emedicine.com/radio/topic552.htm\n\n.Pheochromocytoma: An Imaging Chameleon\n RadioGraphics 2004;24:S87-S99", "External Links": "www.emedicine.com/radio/topic552.htm" } }, { "U_id": "MPX1708", "TAC": [ "MPX1708_synpic18841" ], "MRI": [], "Case": { "Title": "Patent ductus arteriosus", "History": "20 year old female referred to cardiology clinic following a syncople episode while on active duty. Echocardiogram demonstrated a possible patent ductus arteriosis and a CT angiogram was ordered to confirm.", "Exam": "Physical exam was normal\nLaboratory studies were normal\nEchocardiogram- LVEF 60%, color flow was observed into the pulmonary artery from the aorta but the study was otherwise normal.", "Findings": "A CT angiogram image was submitted demonstrating contrast in a patent ductus arteriosis communicating the aorta to the left main pulmonary artery.", "Differential Diagnosis": "Patent ductus arteriorsus", "Case Diagnosis": "Patent ductus arteriosus", "Diagnosis By": "Echocardiogram and contrast enhanced CT scan.", "Treatment & Follow Up": "The PDA is non-clinical and was not treated. The syncopal episode was felt to be secondary to dehydration, and not the PDA.\nShe requires prophalaxis prior to dental work." }, "Topic": { "Title": "Patent ductus arteriosus", "Disease Discussion": "Patent ductus arteriosus is a common malformation that accounts for approximately 10-12% of congenital heart disease. Patients commonly present in infancy with acyanotic congestive heart failure, with a left to right shunt. Embryologically, the ductus arises from the left VI aortic arch, connecting the proximal descending aorta to the left pulmonary artery. This structure typically closes in the first 24 hours of life. Persistence of the ductus is not well understood, but is related to prostagladins. \n\nPatients with PDA often have other associated structural abnormalities such as VSD, aortic stenosis, pulmonic stenosis, and aortic coartcation. PDA is more prevalent in patients with trisomy 18 and 21. Other common causes of left to right shunt include VSD, ASD, and endocardial cushion defect.", "ACR Code": "5.1", "Category": "Congenital, malformation", "Keywords": "CongenitalCardiacMRI", "Reference": "1) Tonkin, ILD: Pediatric cardiovascular imaging, WB Saunders, 1992. pp1-45.\n\n2) Higgins, CB: Essentials of cardiac radiology and imaging, JB Lippincott, 1992. pp 283-330." } }, { "U_id": "MPX1706", "TAC": [ "MPX1706_synpic30077", "MPX1706_synpic30080" ], "MRI": [], "Case": { "Title": "Schistosomiasis Japonicum", "History": "A 51-year-old woman presents with chronic left flank and pelvic pain. Her past medical history is remarkable for a remote liver biopsy. She reports prior travel to several Asian countries. Surgical history is notable for a prior cesarean section.", "Exam": "The physical examination shows a nondistended abdomen and nonspecific lower abdominal pain and was otherwise noncontributory. Abdominal radiography and CT of the abdomen and pelvis were obtained.", "Findings": "Abdominal radiography showed subtle curvilinear densities overlying in the left lower quadrant and central within the pelvis. This was confirmed on intravenous contrast-enhanced abdominopelvic CT to be the caused by thin mucosal surface calcifications within the descending and sigmoid colons. Incidental note is made of thin right hepatic lobe capsule calcifications.", "Differential Diagnosis": "\u2022 Schistosomiasis Japonicum\n\u2022 Tuberculosis (TB)\n\u2022 Alkaline encrustation cystitis\n\u2022 Primary amyloidosis\n\u2022 Radiation", "Case Diagnosis": "Schistosomiasis Japonicum", "Diagnosis By": "Liver Biopsy", "Treatment & Follow Up": "The primary treatment of schistosomiasis is the use of drug therapy, namely praziquantel, oxamniquine, and metrifonate. Early treatment can lead to rapid clinical improvement. Extensive fibrosis is associated with irreversible disease. Bleeding esophageal varices can be managed by sclerotherapy or surgery. As of yet, there remains no vaccination for this disease; however, research is currently being conducted towards producing a safe and effective protective vaccine as a long-term solution to this significant health problem.", "Discussion": "Bladder calcifciation was not present on remainder of pelvis CT (images not included). These colonic and hepatic calcifications are characteristic of Schistosomiasis infection of the gastrointestinal tract. Liver biopsy confirmed Schistosomiasis japonicum infection.\n\nImaging is useful for showing the extent of involvement and identifying complications of disease. Definitive diagnosis is achieved with serologic testing or tissue biopsy. Drug therapy is the primary form of treatment and can lead to rapid clinical improvement. \n\n\nMore images of Schistosomiasis:\nhttp://images.google.com/images?q=schistosomiasis+usuhs&btnG=Search&svnum=10&hl=en&lr=" }, "Topic": { "Title": "Schistosomiasis Japonicum", "Disease Discussion": "Organism(s): Schistosomiasis Japonicum \n\nSchistosomiasis (aka bilharzias or \u201csnail fever\u201d), is a chronic parasitic illness that, although rare in the United States, affects between 200 to 300 million people across the world, with another 600 million people at risk of contracting the infection. This disease is endemic to 74 countries to include Central and South America, Egypt and other African nations, the Middle East, Asia (particularly rural areas in China), and India. The infection is brought to the United States by immigrants and travelers returning from endemic areas. \n\nThe main species of blood flukes or Schistosomes to infect humans are S. mansoni, S. japonicum, S. mekongi, and S. haematobium. The first three species characteristically affect the gastrointestinal tract (inhabiting the portal veins) and the latter typically affects the urinary tract (inhabit veins of bladder) and is the most common cause of bladder calcification in the world. The incidence in males is nine times greater than in females. Risk factors include but are not limited to extreme poverty, lack of public health facilities, and poor sanitary conditions. Infection most commonly occurs in adults who live in rural areas and/or who work in either the agricultural or freshwater fishing fields.\n\nRoute of Infection: Schistosomiasis is a chronic infection caused by parasitic trematode worms that currently affects 200 million people in subtropical and tropical environments and is not an insignificant threat to deployed military members. Schistosomiasis infection in humans begins with cercariae penetration of the skin or buccal mucosal from a contaminated water source. Schistosome ova are subsequently deposited within the liver, gastrointestinal tract, and genitourinary tract and a granulomatous and fibrotic reaction ensues, resulting in a multisystemic and often nonspecific clinical manifestations. Schistosomiasis is major cause of portal hypertension worldwide and can potentially result in permanent gastrointestinal and urinary system damage if not appropriately treated. \n\nClinical: Clinical manifestations can be separated into three different phases: acute, chronic, and severe. Also known as Katayama fever, the acute phase is usually found in children or young adults who have not had any prior exposure to Schistosomes. Believed to be the result of high antigen exposure, this early phase is more commonly associated with S. japonicum infections. Clinical manifestations of this early phase include: dermatitis, bronchospasm, fever, malaise, diarrhea, lymphadenopathy, and arthralgia; amongst other nonspecific complaints. The chronic phase, which is usually subclinical, is characterized clinically by diarrhea and fevers. There may be related growth rate depression, hepato- and/or splenomegaly, and complications of hepatic fibrosis (i.e. portal hypertension, hepatosplenomegaly, ascites, varices of the esophagus and related hemetemesis). \n\nThe most frequent cause of death in hepatosplenic schistosomiasis is gastrointestinal bleeding. Bladder fibrosis may contribute to ureteral obstruction, pyelonephritis, and hydronephrosis which can lead to renal failure. Bladder infection has been linked with the development of bladder carcinoma. The severe phase of disease, unlike the chronic phase, is typically symptomatic. \n\nThe Schistosome has a complex life cycle: humans are infected through contact with contaminated fresh water. The pathophysiology of gastrointestinal calcification is related to the Schistosome fluke eggs deposited in tissues and not caused by the flukes themselves. Following deposition of these Schistoma fluke eggs within the venules of the urinary tract (most commonly the bladder and distal ureters), and gastrointestinal tract lumen, there is development of a hypersensitivity or granulomatous reaction and fibrosis around the Schistosome eggs. The severity or degree of calcification correlates with the number of eggs deposited. Many of the eggs are swept back into the liver, where they become lodged within the parenchyma and result in hepatic calcification, fibrosis and associated portal hypertension. \n\nClinical manifestations can be separated into three different phases: acute, chronic, and severe. Also known as Katayama fever, the acute phase is usually found in children or young adults who have not had any prior exposure to Schistosomes. Believed to be the result of high antigen exposure, this early phase is more commonly associated with S. japonicum infections. Clinical manifestations of this early phase include: dermatitis, bronchospasm, fever, malaise, diarrhea, lymphadenopathy, and arthralgia; amongst other nonspecific complaints. The chronic phase, which is usually subclinical, is characterized clinically by diarrhea and fevers. There may be related growth rate depression, hepato- and/or splenomegaly, and complications of hepatic fibrosis (i.e. portal hypertension, hepatosplenomegaly, ascites, varices of the esophagus and related hemetemesis). \n\nThe most frequent cause of death in hepatosplenic schistosomiasis is gastrointestinal bleeding. Bladder fibrosis may contribute to ureteral obstruction, pyelonephritis, and hydronephrosis which can lead to renal failure. Bladder infection has been linked with the development of bladder carcinoma. The severe phase of disease, unlike the chronic phase, is typically symptomatic. \n\nThe diagnosis can be readily made through the identification of eggs in stool in S. japonicum and S. mansoni infection or by detecting eggs in urine in S. haematobium infection. Other more aggressive means of definitive diagnosis include liver, rectal, or bladder biopsy. Additonal nonaggressive yet relatively sensitive diagnostic tests include oval precipitaiton testing and an intradermal immunological skin test for the Schistosome antigen. \n\nImaging can play a role in demonstrating the extent of organ involvement and complications of Schistosomiasis infection. Conventional radiography may be the initial means of detecting calcification of the bladder or distal ureters (parallel linear radiodense appearance). Intravenous pyleogram (IVP) or cystography in particular are very good studies for demonstrating ureteritis cystica, ureteral stricture (or dilation), hydronephrosis, mucosal irregularity, urolithiasis, decreased bladder capacity, bladder tumor, and inflammatory pseudoployps. CT is useful and more sensitive than radiography for the detection and characterization of urolithiasis and pyelonephritis. \n\nNodular hepatic lesions have been demonstrated sonographically and by CT in acute Schistosomiasis. In the colon, extensive curvilinear or tram-track calcifications have been identified in patients with schistosomiasis japonica. Another study involving intravenous contrast-enhanced CT in Schistosomiasis japonica hepatic infection, showed septal, amorphous, and capsular contrast enhancement patterns. This study concluded that septal enhancement may suggest the diagnosis of hepatic schistosomiasis japonica, particularly when calcification is not identified on noncontrast CT study. The most reliable diagnostic techniques for detecting chronic bladder disease are cystoscopy, serology, CT and to a lesser extent urography. Urinalysis in chronic disease may result in missed detection of disease that would otherwise be identified during the early phase of disease. \n\nhttp://tmcr.usuhs.mil/tmcr/chapter2/intro.htm", "ACR Code": "7.2", "Category": "Infection, parasite", "Keywords": "SchistosomiasisJaponicumParasites", "Reference": "1. Iarotski LS, Davis A. The schistosomiasis problem in the world: results of a WHO questionnaire survey. Bull World Health Organ. 1981;59:115-127.\n2. Da Silva LC, Carrilho FJ. Hepatosplenic schistosomiasis. Pathophysiology and treatment. Gastroenterol Clin North Am. 1992;21:163-77.\n3. Cesmeli E, Vogelaers D, Voet D, Duyck P, Peleman R, Kunnen M, Afschrift M. Ultrasound and CT changes of liver parenchyma in acute schistosomiasis. Br J Radiol. 1997;70:758-60.\n4. Lee RC, Chiang JH, Chou YH, Rubesin SE, Wu HP, Jeng WC, Hsu CC, Tiu CM, Chang T. Intestinal schistosomiasis japonica: CT-pathologic correlation. Radiology. 1994;193:539-42.\n5. Monzawa S, Uchiyama G, Ohtomo K, Araki T. Schistosomiasis japonica of the liver: contrast-enhanced CT findings in 113 patients. AJR Am J Roentgenol. 1993;161:323-7.\n6. Patil KP, Ibrahim AI, Shetty SD, el Tahir MI, Anandan N. Specific investigations in chronic urinary bilharziasis. Urology. 1992;40:117-9.\n7. Pearce EJ. Progress towards a vaccine for schistosomiasis. Acta Trop. 2003;86:309- 13.", "External Links": "tmcr.usuhs.mil/tmcr/chapter2/intro.htm" } }, { "U_id": "MPX1711", "TAC": [ "MPX1711_synpic18538", "MPX1711_synpic18539", "MPX1711_synpic18541", "MPX1711_synpic18542", "MPX1711_synpic18543" ], "MRI": [], "Case": { "Title": "Portal Vein Thrombosis", "History": "71 year-old male three months post radio frequency ablation of liver malignancy.", "Findings": "Near occlusive thrombosis is seen in the main portal vein with complete occlusion of the right portal vein, but trace contrast to the left portal vein. There is no evidence of enhancement within the thrombus. These findings suggest a bland thrombus.", "Differential Diagnosis": "Idiopathic, portal vein invasion or compression by tumor, post operative (splenectomy, transplant), blood dyscrasias, coagulopathies, sepsis, pylephlebitis, pancreatitis, cholangitis, suppurative lymphadenitis, cirrhosis, and portal hypertention.", "Case Diagnosis": "Portal Vein Thrombosis", "Diagnosis By": "CT scan", "Treatment & Follow Up": "Arterial or venous thrombolysis, thrombectomy, or surgical decompression and shunt placement." }, "Topic": { "Title": "Portal Vein Thrombosis", "Disease Discussion": "Although portal vein thrombosis (PVT) is due to hematologic conditions associated with thrombogenic tendencies, the cause of PVT is evident in less than 50 percent of cases. PVT occurs in 10 percent of patients with cirrhosis and frequently accompanies hepatocellular carcinoma. PVT may be associated with systemic or local infection or mesenteric inflammation. PVT can complicate pregnancy, especially eclampsia, and conditions causing portal venous stasis such as hepatic venous obstruction, chronic heart failure, and constrictive pericarditis. Encasement of the portal vein by pancreatic, gastric, and other malignancies can also lead to PVT.\n\nSigns and symptoms of PVT depend on the location and extent of the thrombus, how rapidly PVT develops, and the nature of any underlying liver disease. PVT may lead to segmental atrophy and infarction. It can be acutely fatal when associated with mesenteric vein thrombosis. Collateral channels form and the portal vein recanalizes (cavernous transformation) in 1/3 of patients in whom PVT develops slowly (subacute or chronic). Portal vein thrombosis can cause or exacerbate portal hypertension.\n\nAs in this case, the predominant clinical feature is often the underlying disease. However, bleeding from esophageal varices is a frequent presentation. The presence of splenomegaly and absence of ascities are common findings.\n\nCT findings may include (1) increased size of the portal vein, (2) hyperdense thrombus on noncontrast CT or low density, nonenhancing intraluminal thrombus on contrast enhanced CT, (3) low density filling defect on contrast CT/lack of contrast medium enhancement of the portal vein, (4) failure to visualize the portal vein, (5) canvernous transformation (nest of collateral veins in the porta hepatis), and (6) calcification within the thrombus. T1WI reveals hperintense portal vein thrombus and numerous portal flow voids (collaterals). Ultrasound is the best screening imaging modality. Thrombus appears echogenic and collaterals and varices are often seen.", "ACR Code": "9.3", "Category": "Obstruction or Stenosis", "Keywords": "coagulopathythrombogenicportal hypertension", "Reference": "Fundamental of Body CT / (edited by) W. Richard Webb, William E. Brant, Clyde A. Helms.\u20142nd ed., W. B. Saunders Co, 1998.\n\nFundamentals of Diagnostic Radiology / (edited by) William E. Brant, Clyde A. Helms.\u20142nd ed., Lippincott Williams & Wilkins, 1999\n\nPrimer of Diagnostic Imaging / (edited by) Janice M. Gaillard\u20143rd ed., Mosby Inc., 2003\n\nThe Merck Manual of Diagnosis and Therapy/ (edited by)( Mark H. Beers and Robert Berkow\u201417th ed., Merck Research Laboratories, 1999." } }, { "U_id": "MPX1713", "TAC": [ "MPX1713_synpic30211", "MPX1713_synpic30213" ], "MRI": [], "Case": { "Title": "Pulmonary Sarcoidosis", "History": "36 year old African-American male presents with shortness of breath and a persistent cough.", "Exam": "N/A", "Findings": "Chest radiographs (PA and lateral) reveal bilateral hilar fullness as well as a thin linear opacity at the lower left lateral lung field.\n\nNoncontrast CT examination of of the chest demonstrates bilateral hilar adenopathy as well as mediastinal adenopathy. Within the lung parenchyma, a small linear opacity is seen within the left lower lobe consistent with atelectasis versus scarring. Otherwise the pulmonary parenchyma was unremarkable.", "Differential Diagnosis": "Considerations for mediastinal adenopathy include: infection (e.g. TB or fungal infection), inflammation (e.g. sarcoidosis), neoplasm (e.g. lymphoma), and idiopathic (e.g. Castleman's Disease).", "Case Diagnosis": "Pulmonary Sarcoidosis", "Diagnosis By": "Subcarinal lymph node biopsy during bronchoscopy.", "Treatment & Follow Up": "Pulmonay referral and follow up.", "Discussion": "This diagnosis was new for this individual." }, "Topic": { "Title": "Pulmonary Sarcoidosis", "Disease Discussion": "Incidence rates for sarcoidosis vary greatly from country to country and depend, among other factors, on race, the sophistication of medical care, and the use of screening programs. Quoted figures are in the order of 1 to 10 cases per 100,00 population per year, but this is almost certainly an underestimate as many cases remain subclinical. Sarcoidosis occurs with about 10 times greater frequency in blacks than in whites. \n\nPresentation is most common between 20 and 40 years of age. The mode of presentation varies among series, depending on racial mix and the use of screening radiography. In white-dominated series, presentation as an incidental radiographic finding is common and may occur in 40-50% of cases. Respiratory illness, erythema nodosum, ocular symptoms, and other skin lesions represent the other common presentations. In predominantly black series, respiratory and systemic symptoms like fatigue, malaise, weakness, weight loss, and fever are most common.\n\nA firm diagnosis for sarcoidosis can be made with consistent clinicoradiologic findings and histologic evidence of widespread non-caseating granulomas in more than one organ or a positive Kveim skin test. In clinical practice the organs most commonly sampled are lymph nodes, liver, and lung. \n\nLaboratory investigations also show elevated serum angiotensin-converting enzyme (ACE) levels. Serum ACE levels correlate with degree of total body granuloma burden and the activity of clinical disease as a whole but not convincingly with the degree of and activity of pulmonary disease. \n\nSarcoidosis can be managed conservatively. If treatment is indicated then steroids are the agents of choice. Indications for treating chest disease are not firmly established but most patients with symptomatic or progressive stage II or III disease will be on treatment. There is no doubt in the short-term efficacy of steroids but the long-term value is less clear. The majority of deaths from sarcoidosis are related to pulmonary or cardiac disease. \n\nSarcoidosis is commonly staged according to its appearance on the chest radiograph:\n\nStage 0 \u2013 clear\nStage I \u2013 node enlargement only\nStage II \u2013 node enlargement and parenchymal shadowing\nStage III \u2013 parenchymal shadowing only\nStage IV \u2013 Fibrosis with distortion and bullae\n\nThe stage at presentation is generally considered to correlate with prognosis.\n\nLymphadenopathy is the most common intrathoracic manifestation of sarcoidosis. Symmetric, bilateral hilar adenopathy with some form of paratracheal adenopathy is the classic pattern. Fluctuation in nodal enlargement during intermittent steroid treatment is well recognized. Sarcoid nodes may calcify.\n\nParenchymal shadowing is seen at the time of presentation in a little under a half of the patients with sarcoidosis. A practical division is that between reversible and irreversible opacities. \n\nReversible changes consist of three patterns: reticulonodular opacities, ill-defined opacities with characteristics of consolidation (alveolar), and large nodules. These patterns can occur alone or in varying combinations. They may resolve partially or completely, or they may progress to a irreversible, fibrotic pattern. Such fibrosis ranges from minor and radiologically undetectable, to gross with scar-like shadowing and distortion on the chest radiograph.\n\nOn HRCT, sarcoidosis is characterized by mid-upper zone peribronchovascular thickening and irregularity with small nodules distributed in a perilymphatic fashion: along bronchovascular margins, along interlobular septa, and subpleurally (including fissures). The most common and almost universal finding is small, 1 to 5 mm nodules, usually with irregular but sharp borders. \n\nFocal opacities larger than 1cm in diameter maybe cause by localized areas of consolidation \u2013 alveolar sarcoid \u2013 characterized by ill-defined margins and an air bronchogram. \n\nGround glass opacity is seen in about 40% of patients. It is patchy and may have a lobular distribution. Ground glass opacity is usually produced by multiple granulomas rather than alveolitis.\n\nScarring causes a number of signs: lobular distortion, traction bronchiolectasis, honeycombing, and cyst or bullae formation. Nodules, consolidation, ground-glass opacity, and septal lines are potentially reversible. On the contrary irregular course lines, cysts, honeycombing, bronchiolectasis, and distortion are permanent.", "ACR Code": "6.2", "Category": "Idiopathic or Unknown", "Keywords": "Sarcoidosis", "Reference": "1. Peter Armstrong et al. IMAGING OF DISEASES OF THE CHEST, 3rd ed.\n2. Fraser et al. DIAGNOSIS OF DISEASES OF THE CHEST, 3rd ed." } }, { "U_id": "MPX1716", "TAC": [ "MPX1716_synpic54798" ], "MRI": [], "Case": { "Title": "Patent Ductus Arteriosus", "History": "56 y.o. man, a commercial airline pilot, presented with with acute onset of severe chest pain, radiating to the back. \nPMH: HTN, HLP, Type B (descending aorta) thoracic aortic dissection\nFamHx: noncontributory\nMeds: Metoprolol, Amlodipine, HCTZ, Atorvastatin, Omeprazole\nAllergies: NKDA", "Exam": "Vital signs: 127/85 61bpm 68\u201d 206lb BMI 31.32\n\nCV: RRR, normal S1/S2. No murmurs. No carotid bruit. Normal peripheral pulses. No peripheral edema. \n\nEKG: Sinus bradycardia at 57bpm, otherwise normal.", "Findings": "Cardiac-gated CTA images in multiple planes demonstrate a patent ductus arteriosus, shown by a small contrast-enhanced vessel connecting the descending aorta to the pulmonary artery. Patency of vessel is demonstrated by a jet of contrast spilling into the pulmonary artery at its connection with the ductus arteriosus. \nOf note, you can see changes in the proximal descending aortic wall indicative of this patient's stable aneurysm/dissection.", "Differential Diagnosis": "Patent ductus arteriosus\nIntraarterial fistula", "Case Diagnosis": "Patent Ductus Arteriosus", "Diagnosis By": "CTA imaging is diagnostic.", "Treatment & Follow Up": "The plan for this patient is to follow his aortic dissection with cardiac-gated CT imaging at regular intervals. He is currently being managed with medication for blood pressure control, and the dissection has been stable over the intial 6 months since onset.\n\nRegarding the PDA, since it is long-standing and has at this point only caused mild dilation of the pulmonary artery, there is no plan to correct it. The patient has no symptoms from his PDA, either at rest or with exertion, and indeed no murmur is appreciable on exam.", "Discussion": "Currently, this incidental finding of PDA is of little clinical consequence, as the patient does not have symptoms at this time. However, if he were to develop symptoms such as exercise intolerance or differential cyanosis, it would become important to evaluate the shunt fraction with a functional study or transthoracic echocardiogram." }, "Topic": { "Title": "Patent Ductus Arteriosus", "Disease Discussion": "Patent Ductus Arteriosus\nPatent Ductus Arteriosus (PDA) results when the ductus arteriosus fails to close during the early postnatal period (starting within hours of birth, complete by 2-3 weeks). In utero, the ductus arteriosus (DA) serves as a shunt between the pulmonary artery and the descending aorta, allowing fetal blood to bypass the high-pressure vascular system of the lungs, which are filled with fluid and not serving to oxygenate blood. \nShortly after birth, the lungs fill with air and the pressure within the pulmonary vasculature drops, reversing the shunt through the DA. The DA begins to close at this time, and eventually fibroses and becomes the ligamentum arteriosum, and there is no more shunt. \nIn some people, the DA does not close, so that a left-to-right shunt persists from the aorta to the pulmonary artery. The diameter and length of the PDA, and thus the amount of arterial blood being shunted to the lungs, determines whether or not the PDA causes symptoms or eventual complications. In general, there are three categories (small, moderate, large) based on the pulmonary to systemic flow ratio of blood through the PDA.\nA small PDA may never be detected, because the amount of higher-pressure arterial blood being shunted to the pulmonary artery is not enough to cause pulmonary hypertension or exercise intolerance, as may be seen in larger shunts. The astute clinician may detect a continuous flow murmur during cardiac auscultation, but this is not always present. \nA moderate size PDA may cause exercise intolerance when lower extremity demand for oxygen is not met by left ventricular output, because some of the blood is being shunted back into the pulmonary circulation before it circulates systemically. The upper extremities may not be affected to the same degree, because the DA arises distal to the Left Subclavian Artery, and thus the upper extremities receive blood before it is shunted back into the pulmonary system. Also, as a result of this shunting, the left heart receives a larger volume of blood and, over time, this can result in left ventricular dilation and eventual dysfunction. These patients will likely have an audible flow murmur. \nA large PDA causes a significant shunt and overloading of the left ventricle because it must pump a larger amount of blood. This can result in dilation and LV failure. In addition, the higher systemic blood pressure is transmitted through the PDA to the normally-low pressure pulmonary vascular bed. Over time, this will result in pulmonary hypertension, which may become severe enough to overcome the systemic pressure and result in a reversal of the shunt (Eisenmenger Syndrome). Now deoxygenated blood passes from the pulmonary artery through the PDA into the systemic circulation and mixes with arterial blood. This can cause cyanosis, which may be more pronounced in the lower extremities.", "ACR Code": "5.1", "Category": "Medicine", "Keywords": "patent ductus arteriosuscongenitalheart", "Reference": "Doyle, Thomas, MD; Ann Kavanaugh-McHugh, MD; Thomas P. Graham, Jr, MD. Clinical Manifestations and Diagnosis of Patent Ductus Arteriosus. www.UpToDate.com. Last update 31JUL2009.", "External Links": "www.uptodate.com/online/content/topic.do?topicKey=cong_adu/6089&selectedTitle=1%7E150&source=search_result" } }, { "U_id": "MPX1723", "TAC": [ "MPX1723_synpic34926" ], "MRI": [ "MPX1723_synpic34923", "MPX1723_synpic34924", "MPX1723_synpic34928" ], "Case": { "Title": "Ischemic stoke in right temporal-parietal lobes secondary to emboli from carotid bulb atheroma", "History": "-87 year old woman\n-Left upper extremity weakness and numbness for past couple days\n-Son says her left face is \u201cdroopy\u201d\n-No documented medical history\n-On no medications", "Exam": "Left upper extremity weakness and numbness for past couple days", "Findings": "23 Jan: NON-CONTRAST Head CT (from emergency dept)\n-regional hypoattenuation in right temporal lobe, extending from cerebral cortex into white matter\n-loss of gray/white matter differentiation\n-sulcal effacement of right temporal-parietal lobes (may represent ischemia and resultant edema)\n-some chronic microvascular ischemic disease of periventricular white matter\n-ventricles and cisterns preserved, no intracranial hemorrhage or mass\n-likely represents infarct of unknown time course (subacute vs. acute)\n-MRI recommended\n\n24 Jan: Brain MRI (from emergency dept)\n-axial DWI\u2014increased signal in right posterior parietal lobe=restricted diffusion\n-ADC map--corresponding decreased signal\n-consistent with acute stroke in right posterior parietal lobe\n\n24 Jan: CAROTID US\n-echogenic calcified plaque in right carotid bulb and proximal internal carotid artery with 50-69% stenosis with elevated velocities in internal carotid\n-hemodynamically insignificant stenosis in left carotid bulb\n\n24 Jan: TRANSTHORACIC ECHO (no images shown)\n-normal left and right ventricular size and function\n-negative bubble study\n\n25 Jan: CT ANGIOGRAPHY W/ CONTRAST (sagittal view)\n-large calcified plaque in right carotid bifurcation and proximal ICA \n-hemodynamically significant stenosis of 64%\n\n26 Jan: NON-CONTRAST Head CT (following worsening left sided weakness and sensory loss)\n-hypodensity of right temporal lobe\n-two new foci of calcification within the right sylvian fissure, not present on previous exams, likely represent further acute thromboemboli\n-more prominent ventricles and cisterns\n-no intracranial hemorrhage or mass effect\n\n28 Jan: Brain MRI (following worsening left sided weakness and sensory loss)\n-DWI\u2014interval increase in size of signal in right temporal-parietal region\n-ADC map\u2014corresponding decrease in signal", "Differential Diagnosis": "Ischemic stroke (embolus, thrombus, arterial dissection)\nHemorrhagic stroke\nMalignancy", "Case Diagnosis": "Ischemic stoke in right temporal-parietal lobes secondary to emboli from carotid bulb atheroma", "Diagnosis By": "Head CT, MRI (DWI and ADC map), CT angiography", "Treatment & Follow Up": "Treatment: ASA, heparin if no bleed and large vessel atherothrombosis, thrombolytic (t-PA) if within 3 hours of symptom onset\nDisposition: Often long term inpatient stroke rehabilitation", "Discussion": "Etiology of ischemic stroke:\n-cardioemboli\n-carotid occlusion\n-arterial dissection\n-local arterial thrombosis\n\nMiddle cerebral artery most common destination with\ncontralateral hand, arm and face weakness and sensory deficits, and spatial neglect--especially if the infarct is in the right parietal lobe resulting in left sided neglect as seen in this patient\n\nImaging in ischemic stroke patients:\n-Noncontrast CT to rule out hemorrhage/mass, some early signs of infarction, yet relatively insensitive to acute infarction\n-MRI (DWI/ADC map): DWI can detect infarction within minutes of symptom onset with high sens/spec\n-CT angiography, magnetic resonance angiography, transthoracic echocardiogram to evaluate vascular integrity" }, "Topic": { "Title": "Parietal lobe", "Disease Discussion": "The upper central portion of the cerebral hemisphere, posterior to the central sulcus, and anterior to the parietooccipital notch\n(medial hemisphere). \n\nFor image, see: http://rad.usuhs.mil/rad/radbrowser2/head/MRI/hn030.html\n\nDamage to the non-dominant (usually right) parietal lobe may produce Gerstmann Syndrome:\n\u2022 agraphia or dysgraphia (a writing disability) \n\u2022 acalculia or dyscalculia (can't calculate)\n\u2022 inability to distinguish right from left\n\u2022 finger agnosia (inability to identify fingers\n\nhttp://www.ninds.nih.gov/disorders/gerstmanns/gerstmanns.htm", "ACR Code": "1.1", "Category": "Glossary", "Keywords": "Gerstmann SyndromeParietal Syndromeagraphia", "External Links": "rad.usuhs.mil/rad/radbrowser2/head/MRI/hn030.html" } }, { "U_id": "MPX1731", "TAC": [ "MPX1731_synpic35276", "MPX1731_synpic35277", "MPX1731_synpic35278" ], "MRI": [], "Case": { "Title": "Meckel's Diverticulum", "History": "42 year old female with a 10 day history of lower abdominal/pelvic pain and dysuria despite antibiotic therapy for presumed cystitis", "Exam": "General: No acute distress, alert and oriented\nPulmonary: Clear to auscultation bilaterally\nCardiovascular: Regular\nAbdomen: Soft, tenderness to palpation in the suprapubic region\nPelvic: Mild posterior vaginal tenderness\nRectal: Normal with no gross blood", "Findings": "\u2022 Within the pelvis, just posterior to the uterus and just to the right of the midline, there is a 1.9 cm round mass with an internal air-fluid level and some enteric contrast material present within. \n\u2022 The density of the enteric contrast material within the lesion is somewhat less than that of the surrounding small bowel. \n\u2022 There is no mesenteric inflammatory change surround this lesion. \n\u2022 The appendix is not definitely identified on this examination. No secondary signs of appendiceal inflammation are noted. \n\u2022 The bowel loops otherwise demonstrate normal attenuation and configuration throughout. \n\u2022 There is no evidence of bowel obstruction.", "Differential Diagnosis": "\u2022 Meckel's Diverticulum\n\u2022 Duplication Cyst\n\u2022 Appendicitis", "Case Diagnosis": "Meckel's Diverticulum", "Diagnosis By": "Pathology", "Treatment & Follow Up": "Pt was admitted for diagnositic laporoscopy with resection of obstructed diverticulum that was confirmed by pathology. Pt recovered well from the operation and was discharged shortly.", "Discussion": "While Meckel's Diverticulum is most common in children, it can present at any time. When it presents in females it can mimic many gastroinestinal or genitourinary problems that may be difficult to differentiate clinically. A Meckel's Scan is not very sensitive or specific in the adult population and an abdominal CT Scan is the imaging of choice to evaluate a patient with a possible Meckel's Diverticulum in an adult." }, "Topic": { "Title": "Meckel Diverticulum", "Disease Discussion": "A Meckel Diverticulum is a remnant of the vitelline duct, which is a persistent embryologic connection between the small bowel (usually distal ileum) and the umbilicus. It most commonly presents in children, about 1/2 by the age of 2. In children a Meckel Scan is 85% sensitive and 95% specific for a Meckel Diverticulum. It is performed using 99m-Tc pertechnetate, which is preferentially taken up by mucous secreting cells of gastric mucosa or ectopic gastric tissue (i.e. Meckel Diverticulum).\n\nThe classic presentation of a Meckel Diverticulum is a male younger than 5 who presents with massive painless bleeding. However, it may also cause intestinal obstruction as a lead point for a volvulus or commonly mimics appendicitis. In 80-85% of cases, a Meckel Diverticulum is ectopic gastric mucosa. It can also be ectopic pancreatic, duodenal, or colonic tissue. The pancreatic tissue secretes digestive enzymes, which can cause an ulcer in the small bowel distal to the Meckel Diverticulum. This ulceration may cause the bleeding seen at presentation.\n\nMeckel Diverticulum is known for the \"Rule of Two's.\" In general it is present in only 2% of the population, but will only become symptomatic in 2% of that population. It is usually 2 cm wide and 2 cm long and located 2 feet from the ileocecal valve.", "ACR Code": "7.9", "Category": "Differential Diagnosis", "Keywords": "MeckelDiverticulum", "Reference": "Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed. 2006. Mosby Inc.\nFeldman: Sleisenger and Fordham's Gastrointestinal and Liver Disease, 8th ed. 2006. Saunders, An Imprint of Elsevier.\nBehrman: Nelson Textbook of Pediatrics, 17th ed. 2004. Saunders, An Imprint of Elsevier." } }, { "U_id": "MPX1735", "TAC": [ "MPX1735_synpic16735", "MPX1735_synpic16737", "MPX1735_synpic16738", "MPX1735_synpic16739" ], "MRI": [], "Case": { "Title": "1. Myasthenia Gravis\r\n2. Chronic immunosuppression\r\n3. S/P Total Thymectomy via median sternotomy", "History": "This is a 22 y/o AD WF at NNMC where she has been followed by Neurology for one year for myasthenia gravis, treated with prednisone and cyclosporin. She has good strength. Chest CT in July 2002 shows residual thymus, and no mass. Now s/p total thymectomy via median sternotomy. Path specimen revealed thymic hyperplasia without malignancy.", "Exam": "Physical exam finding significant for left ptosis and bilateral sluggish papillary reflexes.Path Specimen: Thymic Hyperplasia", "Findings": "Residual Thymus", "Differential Diagnosis": "Thymic Hyperplasia vs. Thymic atrophy\nThymoma\nMalignancy", "Case Diagnosis": "1. Myasthenia Gravis\n2. Chronic immunosuppression\n3. S/P Total Thymectomy via median sternotomy", "Treatment & Follow Up": "1.\tLong-term immunosuppression with prednisone and cyclosprorin\n2.\tTotal thymectomy\n3.\tRecommend pneumonia vaccine \n4.\tMay consider adding pyridostigmine for worsening symptoms\n5.\tLong-term outpatient care with neurology\n6.\tProvide patient education; ensure that she knows danger signs of her disease" }, "Topic": { "Title": "Residual Thymus in Myasthenia Gravis", "Disease Discussion": "Discussion : Myasthenia gravis is an autoimmune disorder resulting in weakness of skeletal muscles, due to autoantibodies directed against acetylcholine receptors at neuromuscular junctions.Clinical Features:Myasthenia presents in women between the ages of 20 \u2013 30, and in men over the age of sixty. The symptoms worsen with exertion. Cranial muscles are affected in 85% cases (lids, extraocular muscles, facial weakness, nasal or slurred speech, dysphagia). These may be the only muscles affected, especially in the elderly. As the disease becomes generalized, the limb muscles (often proximal and asymmetric) become involved. Reflexes and sensation should be normal. Primary complications are aspiration pneumonia (weak bulbar muscles) and respiratory failure (weak chest wall muscles).Pathophysiology:Specific anti-AchR antibodies reduce the number of AchRs at the NMJ. With repeated muscle contraction, there is a decrease in the amount of acetylcholine released per impulse. This results in pathologic fatigue. The thymus is abnormal in 75% of patients with myasthenia (65% hyperplasia and 10% thymomas). The reason for this compelling association remains unknown, but it is theorized that because the thymus contains a small number of myoid cells (which are distinguished by muscle striations and AcH receptors on their surface) along with the B-cells and T-cells, the thymus may play a role in myasthenia gravis by acting as an antigenic peptide sequence on the surface of antigen presenting cells. Evaluation:\nOther autoimmune disorders may also be associated with myasthenia gravis (thyroiditis, Graves\u2019 Disease, rheumatoid arthritis, SLE, and pure red cell aplasia) and should be evaluated for in the newly diagnosed patient with myasthenia.\n\nEvaluation:\n1.\tAchR antibodies \u2013 positive antibodies are diagnostic but not correlated with disease severity\n2.\tTensilon (edrophonium) test \u2013 short-acting anticholinesterase\n3.\tEMG \u2013 low frequency (2-4Hz) repetitive stimulation produces decreased amplitude\n4.\tChest CT/MRI \u2013 search for thymic abnormalities\n5.\tOther associated autoimmune disorders\n\nMedical Management:\n1.\tOcular only \u2013 pyridostigmine\n2.\tGeneralized \u2013 pyridostigmine, and immunosuppression (while steroids are the mainstay of treatment, the addition of cyclosporin may allow a decrease in the steroid dose)\n3.\tCrisis \u2013 Intensive care (intubate, fluids), plasmapheresis or IVIg\n\nSurgical Management:\n1.\tEvaluate for thymectomy (improves the likelihood of long-term remission in the adult).\n\nThe efficacy and use of thymectomy in the absence of thymoma is still controversial. A review of literature shows that thymectomy was associated with disease remission and improvement with a rate of medication free remission of 2.1 and an improvement rate of 1.7. However, there are other studies that reveal no statistical difference between thymectomy in the absence of thymoma and medical management only. Still, for several reasons most neurologists and CT surgeons still recommend that total thymectomy be done. First, you cannot tell the difference between thymic hyperplasia and thymic atrophy on imaging studies. A residual thymus as in this case, may represent thymic hyperplasia with potential to become a thymoma or be simple residual tissue. Also, if a thymoma is present there is always a chance of malignancy. Lastly, because it is theorized that the thymus acts as an APC for auto-antibodies, it is widely believed that a total thymectomy will improve the likelihood of long-term remission.", "ACR Code": "673.3155", "Category": "Unsure", "Keywords": "myasthenia gravisthymoma", "Reference": "1. Gronseth GS, Barohn RJ. Practice parameter. Thymectomy for autoimmune myasthenia gravis (an evidence-based review). Neurology:55(1) 2000.\n\n2.Salgia R. Clinical presentation and management of thymoma. UpToDate:Online 11.2.\n\n3. Allan W. Pathogenesis and treatment of myasthenia gravis. UpToDate:Online 11.2.\n\n4.\tBraunwald E, Faues AS, Kasper DL, Hauser SL, Longo DL, Jameson JL. Harrison\u2019s principles of internal medicine. 15th ed. New York:McGraw Hill, 2001." } }, { "U_id": "MPX1746", "TAC": [ "MPX1746_synpic51005" ], "MRI": [], "Case": { "Title": "Echinococcal cyst (hydatid disease) of the liver", "History": "Injured in motor vehicle accident with comminuted tibial plateau fracture. Abdomen/pelvis CT imaging included in trauma work-up.", "Exam": "Unremarkable abdominal exam.", "Findings": "Incidentally found on CT are two well-defined cysts with thin calcified rim in the posterior right hepatic lobe. Serpentine calcifications are noted within the matrix of one of the cysts.", "Differential Diagnosis": "Metastatic Carcinoma\nHepatic cystadenoma and cystadenocarcinoma\nPrimary Hepatic Tumor\nEchinococcal Cyst\nLiver Abscess", "Case Diagnosis": "Echinococcal cyst (hydatid disease) of the liver", "Treatment & Follow Up": "None Indicated", "Discussion": "The patient's CT findings were consistent with Type V cysts due to the presence of calcifications. In turn, no treatment was indicated because these cysts are considered inactive." }, "Topic": { "Title": "Echinococcal cyst (hydatid disease) of the liver", "Disease Discussion": "Hydatid disease or Echinococcal cysts are caused by the parasite Echinococcus Granulosus or Echinococcus Multiloculoris. These are carried by dogs, sheep and cattle. The disease is rare in the United States, with only about 200 cases a year reported, mostly in the southwest and Alaska. The disease is acquired as a child, with a latent period of 5 to 20 years before signs or symptoms are noted. The cysts continue to grow, eventually causing mechanical compression which leads to most symptoms. Sixty percent of all these cysts are found in the liver, 25% in the lung, and 15% in the peritoneum, kidney, spleen, and retroperitoneum combined. If the cysts of E. Granulosus rupture, they can cause an anaphylactoid reaction. Theoretically, therefore, these masses should not be drained percutaneously. In practice, however, some have been inadvertently punctured without complications.\n\nHydatid disease presents in four basic ultrasound patterns. The first and most common is the cystic pattern, a round, anechoic, well-defined mass with smooth walls and posterior acoustic enhancement. In 60% of cases, there is more than one parent cyst. Some cysts may have septa dividing the cyst into numerous sections. Occasionally the cysts may become infected. With age, the cyst may collapse away from the edge of the cavity and may even fold in upon itself, forming what has been called the matrix. This type of cyst cannot be differentiated from congenital cysts, traumatic cysts, or a cavitating tumor. A second pattern, the racemose pattern, has the parent cyst with daughter cysts (the pattern seen in this case). The daughter cysts can be any number and appear round until they are so numerous that they become irregular and flat. A third pattern consists of a solid mass that can be hypoechoic, hyperechoic, or isoechoic. A fourth pattern presents with calcified walls. Due to acoustic shadowing, a complete examination is often difficult. However, by using different planes of section and varying the frequency and gain, the interior can usually be examined. The interior is usually anechoic but may also be calcified.", "ACR Code": "7.2", "Category": "Infection, parasite", "Keywords": "liverechinococcosiscyst" } }, { "U_id": "MPX1744", "TAC": [ "MPX1744_synpic24676", "MPX1744_synpic24677" ], "MRI": [], "Case": { "Title": "Extravasation of blood from R common femoral artery and vein.", "History": "58yo F, PMH significant for DVTx3 on coumadin therapy at home, currently on Lovenox window, POD #1 s/p normal cardiac catheterization, continued hypotension s/p cath, had an episode of lightheadedness with fall.", "Exam": "ABD: obese, soft, TTP suprapubic area, ND, BS present, no peritoneal signs\nSKIN: 4cm R groin hematoma, several areas of resolving hematomas on abdomen, large hematoma on L flank\nH/H: initially 13/38, POD#1 7.8/22.7", "Findings": "Fluid seen around R common femoral vein and artery that is moving posterior to rectus abdominis muscles, ending in a large fluid collection anterior to the bladder. Well-circumscribed 10.5cm x 7.5cm x 9.5cm fluid collection within the Space of Retzius", "Differential Diagnosis": "Hematoma, Urine, Abscess", "Case Diagnosis": "Extravasation of blood from R common femoral artery and vein.", "Treatment & Follow Up": "POD#2 CT cystogram (not shown) showed the fluid collection increased to 16cm x 16cm x 18cm, with no contrast extravasation from the bladder. H/H continued to drop, taken to OR where a defect in the R femoral vein was repaired. Post-op, BP responded to IVF and blood transfusions", "Discussion": "Bleeding s/p cardiac catheterization has been reported in the range of 2-14%, retroperitoneal bleeding reported in 0.12-0.3% of cases. Risk factors for vascular complications s/p cath include age>70, female, BSA <1.6, CHF, COPD, LE vascular disease, MI, bleeding disorder, shock, and Plavix use. Furthermore, Enoxaparin given on the day of the cath doubled the patient\u2019s risk of bleeding." }, "Topic": { "Title": "Angiographic complication, extravasation of blood from common femoral artery and vein", "Disease Discussion": "Bleeding after cardiac catheterization has been reported in the range of 2-14%, retroperitoneal bleeding reported in 0.12-0.3% of cases. Risk factors for vascular complications s/p cath include age>70, female, BSA <1.6, CHF, COPD, LE vascular disease, MI, bleeding disorder, shock, and Plavix use. Furthermore, Enoxaparin given on the day of the cath doubled the patient\u2019s risk of bleeding.", "ACR Code": "9.4", "Category": "Iatrogenic or Surgical (complications)", "Keywords": "Extravasationcomplicationangiography", "Reference": "1. Kinnaird, et al. \u201cIncidence, Predictors, and Prognostic Implications of Bleeding and Blood Transfusion Following Percutaneous Coronary Interventions\u201d The American Journal of Cardiology vol. 92, Oct 15, 2003. 2. Lubavin, Boris V., M.D. \u201cRetroperitoneal Hematoma as a Complication of Coronary Angiography and Stenting\u201d American Journal of Emergency Medicine vol.22, number 3, May 2004. 3. Piper, Winthrop D., MS, et al. \u201cPredicting Vascular Complications in Percutaneous Coronary Interventions\u201d American Heart Journal vol. 145, number 6, June 2003." } }, { "U_id": "MPX1750", "TAC": [ "MPX1750_synpic18372", "MPX1750_synpic18487", "MPX1750_synpic18488", "MPX1750_synpic18490" ], "MRI": [], "Case": { "Title": "Eosinophilic granuloma", "History": "23 y/o female with 6-week history of right sided chest pain. No history of trauma.", "Exam": "Right-sided chest discomfort to palpation.", "Findings": "PA image of the chest demonstrates increased density in soft tissure and subtle bony lytic lesion on right seventh rib. Upon further evaluation, CT images of the chest demonstrate bony destruction of the posterior/lateral aspect of the right seventh rib, with an associated soft tissue mass, which extends into the right lower lobe.", "Differential Diagnosis": "Healing fracture\nLymphoma/leukemia\nPlasmacytoma\nAneurismal bone cyst\nEwing sarcoma\nHemangioma\nInfection/osteomyelitis/abscess\nChondorblastoma", "Case Diagnosis": "Eosinophilic granuloma", "Diagnosis By": "Biopsy/pathology", "Discussion": "-Radiologic findings:\n Plain radiography is the mainstay in the diagnosis of EG, although a specific diagnosis cannot always be made without bone biopsy because children and adolescents are not spared skeletal neoplasms. Radionuclide study; CT; MRI; and, occasionally, angiography are complementary examinations. Any or all may be used to arrive at a diagnosis. The ribs show lytic expansile lesions, which may be associated with pathologic fractures. Lesions are lytic, round or oval, and expansile, with ill-defined or sclerotic margins. The medullary cavity may be expanded and associated with cortical thinning, intracortical tunneling, and erosion of the cortex and an adjacent soft-tissue mass. Laminated periosteal new bone formation is common around the involved segment of bone.\n\t CT scans may be particularly useful in osseous lesions in areas with complex anatomy, such as the mastoids, atlantoaxial joints, and posterior elements of the vertebral bodies. Also, soft tissue components are better depicted on CT scans than on other images. The destruction of the mastoid, petrous ridge, tegmen tympani, and lateral sinus plate and the destruction of the inner and external ear are depicted elegantly on CT scans. CT may demonstrate an isoattenuating and homogeneously enhancing mass in the hypothalamus/pituitary gland. CT is considerably better than plain radiography and conventional tomography in depicting an intracranial extension of EG. CT appearances of EG are nonspecific, and a variety of inflammatory and neoplastic processes may mimic EG.\n\tOn spin-echo MRIs, osseous lesions of EG reveal decreased signal intensity on T1-weighted and high signal intensity on T2-weighted sequences. The lesion may enhance after the administration of a gadolinium-based contrast agent. The value of using MRI to image patients with EG lies in the sensitivity of MRI because its specificity is low. However, the cost of the procedure and the procedural problems encountered in imaging young children confer no advantages over plain radiography. The soft tissue component around the osseous lesion has poor definition and shows signal inhomogeneity, which may mimic that of a malignant tumor, infection, or stress fracture." }, "Topic": { "Title": "Eosinophilic granuloma", "Disease Discussion": "-Factoid Discussion:\n\n The hallmark of Langerhans cell histiocytosis (LCH) in most patients is an osseous lesion. When the bone is the only organ involved, the disease is referred to as eosinophilic granuloma. EG is the benign form of the 3 clinical variants of Langerhans cell histiocytosis, which include Litterer-Siwe disease, Hand Schuller-Christian disease, and EG (formerly termed histiocytosis X). When more organs are affected, causing cranial lesions, diabetes insipidus, and exophthalmos, it is refered to a Hand-Schuller-Christian disease. The disseminated form of LCH, called Litterer-Siwe disease, is more often seen in infants and children who are less than 3 years old and is characterized by wasting, hepatosplenomegally, generalized lymphadenopathy, skin rash, generalized multiple lesions, and sometimes pancytopenia.\nEG is characterized by a single or multiple skeletal lesions, and it predominantly affects children, adolescents, or young adults. Solitary lesions are more common that multiple lesions. When multiple lesions occur, the new osseous lesions appear within 1-2 years. Any bone and be involved, but the most common sites include the skull, mandible, spine, ribs, and long bones.\n\n-Etiology and Pathogenesis: \n\n EG is a benign disorder that affects children and young adults, particularly males. The solitary bone lesion may be asymptomatic, or it may cause bone pain because of expansion of the medullary bone. Pathologic fractures may ensue. The pathogenesis of LCH is unknown. An ongoing debate exists over whether this is a reactive or neoplastic process. Arguments supporting the reactive nature of this disorder include the occurrence of spontaneous remissions, the failure to detect aneuploidy, metaphase or karyotypic abnormalities, and the good survival rate in patients without organ dysfunction. On the other hand, the infiltration of organs by aberrant cells, a possible lethal evolution, and the cancer-based modalities of successful treatment are all consistent with a neoplastic process. In addition, the demonstration of LCH as a monoclonal proliferation by X chromosome-linked DNA probes supports a neoplastic origin for this proliferation; however, the presence of this finding in distinct subtypes with different evolutions demands further investigations to evaluate its significance. \nThere is evidence for a role of immune dysfunction in the pathogenesis of LCH by the creation of a permissive immunosurveillance system. Abnormalities of suppressor cell number and function have been documented in several reports. Increased levels of messenger RNA for macrophage colony stimulating factor and platelet derived growth factor have been detected in cells from a pulmonary LCH lesion.\n\n-Epidemiology:\n LCH is a rare disease. Estimated annual incidence ranges from 0.5-5.4 per million persons per year. Approximately 1200 new cases per year are reported in the United States. More than half of the patients younger than 2 years, with disseminated LCH and organ dysfunction die of the disease; whereas, unifocal LCH and the majority of cases of congenital self-healing histiocytosis, are self-limited. Multifocal chronic LCH is self-limited in most cases, though increased mortality has been observed among infants with pulmonary involvement. Prevalence of LCH seems to be higher among whites. Incidence of LCH is greater in males than in females (male-to-female ratio 2:1). LCH affects patients from neonates to adults. Age of onset varies according to the variety of LCH. Letterer-Siwe disease occurs predominantly in children younger than 2 years. The chronic multifocal form, including the Hand-Schuller-Christian syndrome, has a peak of onset between 2-10 years of age. Localized eosinophilic granuloma occurs mostly frequently in those aged 5-15 years.\n\n-Clinical Manifestations:\n Most patients have no symptoms, and the diagnosis is usually based on radiographic demonstration of a destructive bone lesion arising from the marrow cavity and on characteristic morphologic findings. Localized bone pain and focal tenderness may occur as a result of bone erosion and, rarely, a pathologic fracture. A swelling or mass may be palpable at the site of osseous involvement. Rarely, children may present with fever and leukocytosis. Involvement of the mastoid process involvement may appear with intractable otitis media with a chronic discharge. Mandibular involvement may present with gingival and continuous soft-tissue swelling.\n\n- Diagnosis:\n Definite diagnosis is based on biopsy. Because of the absence of distinctive morphologic characteristics of the LCH cell, special studies are used to identify the cell. The Birbeck granule is the distinctive ultrastructural hallmark of the LC. It consists of an intracytoplasmic membranous body, 33 nm wide and 190-360 nm long, possessing a short, rodlike shape with a dotted line down the midline of the space between the membranes (resembling a zipper) and a terminal expansion in the form of a vesicle giving a \"racquet\" appearance. Although these granules are resistant to destruction by formalin fixation and paraffin embedding, the sensitivity of detection in such specimens is slightly decreased. Birbeck granules are rarely detected in lesions of the liver, gastrointestinal tract, and spleen. Langerhans cells also contain laminated substructures of lysosomes, tuboreticular structures, and trilaminar membranous loops. \nThe Writing Group of the Histiocyte Society (1987) has proposed 3 levels of certainty in the diagnosis of LCH based on the clinical features, histopathology, and special immunohistochemical techniques. A presumptive diagnosis is based on a typical clinical presentation and light microscopic findings. A designated diagnosis includes light microscopy in combination with positive S-100 and PNA staining studies. To make a definitive diagnosis, identification of Birbeck granules and CD1a antigens is required.\n\n-Treatment:\n Solitary bone lesions are treated locally with curettage or excision. Painful bone lesions may require intralesional steroid injection (triamcinolone acetonide). Polyostotic bone lesions are best treated with indomethacin or a short course of systemic steroids. Rarely, lesions that are unusually large and painful occur in inaccessible sites or involve vital structures. They require radiation (3-6 Gy [300-600 rads]).", "ACR Code": "471.663", "Category": "Neoplasm, benign", "Keywords": "EGLangerhans cell histiocytosishistiocytosis X", "Reference": "1. Khan, Ali Nawaz, MBBS. Eosinophilic Granuloma, Skeletal. E-medicine, instant access to the minds of medicine. Internet source. Feb 28, 2003.\n\n2. Selim, Angelica M., MD. Langerhans Cell Histiocytosis. E-medicine, instant access to the minds of medicine. Internet source. Feb 28, 2002.\n\n3. Ghanem, Ismat MD. Langerhans Cell Histiocytosis of Bone in Children and Adolescents. Journal of Pediatric Orthopedics Vol 23, pp124-130 2003." } }, { "U_id": "MPX1756", "TAC": [ "MPX1756_synpic41199" ], "MRI": [], "Case": { "Title": "Nephrolithiasis with \"twinkle\" artifact on color Dopler ultrasound", "History": "59 yo woman referred for renal ultrasound.", "Findings": "Transverse gray-scale view of the lower pole of the right kidney demonstrates a small bright echogenic focus with possible shadowing suggestive of a nonobstructing renal stone. Color Doppler imaging shows a \u201ctwinkle\u201d artifact confirming this echogenic focus is a renal calculi.\n\nUnenhanced axial CT from the same patient obtained a few months later, demonstrates the non-obstructing renal calculi in the lower pole of the right kidney.", "Differential Diagnosis": "\u2022 Nephrolithiasis\n\u2022 Intrarenal gas\n\u2022 Renal artery calcification\n\u2022 Calcified sloughed papilla\n\u2022 Calcified transitional cell tumor", "Case Diagnosis": "Nephrolithiasis with \"twinkle\" artifact on color Dopler ultrasound", "Diagnosis By": "Characteristic Imaging Findings", "Discussion": "Using color Doppler imaging, the twinkle artifact, which appears as a colored ring-down artifact behind a strong acoustic interface, is able to help identify small non-shadowing calculi. When sound reflects off the acoustic interface and returns to the transducer, the returning pulse may be robust enough that the energy is reflected off the transducer and directed back into the body so that the pulse can interact with the same near field interface a second time, or even multiple times, producing an additional set of echoes that are registered as arising deep to the original reflector. By placing the focal zone at or slightly below the area of interest, one is able to identify this characteristic rapidly fluctuating mixture of Doppler signals. \n\nIn this particular case, the demonstration of the twinkle artifact is helpful because the non-obstructing renal calculi was diagnosed, sparing the patient further diagnostic tests or interventions. \n\nA few months later, the same patient underwent a abdominal CT which confirmed the presence of renal calculi." }, "Topic": { "Title": "Nephrolithiasis", "Disease Discussion": "Lesions/Condition: Nephrolithiasis\n\nAssociations/Predisposing Factors: \n\nDietary: High content of animal protein. Low Fluid Intake.\nMetabolic: Hypercalciuria is the most commonly noted metabolic \n abnormality. \n Decreased levels of magnesium and citrate. \nObstruction: Urinary stasis from ureteropelvic junction obstruction.\nAutosomal dominant polycystic kidney disease\nCaliceal diverticula\n\nSymptoms:\n\nNonobstructing caliceal stones are generally asymptomatic, although pain or hematuria is not an uncommon finding. Renal stones that result in obstruction frequently produce significant pain and may result in infection.\n\nDiscussion: \n\nRenal Calculi is a common entity affecting approximately 12% of the population. White males with advancing age are frequently more affected, and in general males are three more times likely to develop renal stones than females. \n\nThe most common type of renal stone is composed of either calcium oxalate or calcium phosphate (80 % - 85%). Uric acid stones comprise about 5% to 10% of all renal calculi, and have been associated with gout, and Crohn\u2019s disease. Struvite stones formed by urea-splitting bacteria such as Proteus, Pseudomonas, Staphylococcus aureus, and Klebsiella encompass about 10% of renal stones, and may develop into staghorn calculi. Rarely, cistine stones may occur related to the metabolic disorder cistinuria. \n\nSonographically: \n\t\nUltrasound has been described as having as high as 96% sensitivity for renal stone detection, with increasing sensitivity for larger calculi. Sonographically, the appearance of a renal stone is dependent on the size of the stone, and not the chemical composition. Large stones demonstrate an echogenic focus with an associated acoustic shadow. Stones smaller than 5 mm may also appear as an echogenic focus, however, often lack an acoustic shadow creating difficulty in differentiating the stone from the echogenic renal sinus. To further characterize small renal calculi, use of a high-frequency transducer may be of value. Additionally, color Doppler imaging may demonstrate the twinkling artifact, appearing as a colored ring-down artifact.", "ACR Code": "8.1", "Category": "Radiologic Sign or Finding", "Keywords": "NephrolithiasisRenal CalculiTwinkle Artifact", "Reference": "Rumack, Carol. Diagnostic Ultrasound. Third Edition. Elsevier Mosby, Inc.\n Mosby. St. Louis, Missouri 2005.\nMiddleton, William. Ultrasound. The Requisites. Second Edition. Mosby. St. \n Louis, Missouri 2004.\nCampbell et al. RadioGraphics 2004; 24:497\u2013506." } }, { "U_id": "MPX1738", "TAC": [ "MPX1738_synpic19950" ], "MRI": [], "Case": { "Title": "Pancoast Tumor (poorly differentiated adenocarcinoma)", "History": "38-year-old longstanding female smoker presented with right upper extremity radicular symptoms.", "Exam": "Noncontributory", "Findings": "Chest Radiograph-PA image from a two view study (lateral not shown) shows an irregular apical pleural thickening and a heterogeneous and predominantly lucent process at the right apex with 2nd and 3rd rib posterior rib destruction.\n\nContrast-enhanced CT chest showed a lobular hypodense and minimally enhancing lesion arising from the region of the posterior right lung apex with extension into the adjacent posterior chest wall with extension to involve several levels of C-spine neuroforamina and likely involves the brachial plexus and intercostals nerves at that level.", "Differential Diagnosis": "Mesothelioma\nLymphoma\nPlasmacytoma\nMetastatic malignancies (thyroid, larynx)\nLymphomatoid granulomatosis\nCervical rib syndrome\nTuberculosis\nFungal infections", "Case Diagnosis": "Pancoast Tumor (poorly differentiated adenocarcinoma)", "Diagnosis By": "CT-guided biopsy" }, "Topic": { "Title": "Pancoast Tumor", "Disease Discussion": "\u00bb This syndrome is named after Henry Pancoast, 1932 http://www.whonamedit.com/doctor.cfm/2505.html\n\n\u00bb malignancy of pulmonary origin/superior sulcus \n\n\u00bb direct extension lower trunks of brachial plexus, intercostal nerves, stellate (sympathetic) ganglion, adjacent ribs, and vertebrae\n\n\u00bb lung cancer is leading cause of death in males and females; 2:1 m:f \n\n\u00bb incidence increases with age; peak incidence in 50-70\n\n\u00bb smoking = major risk factor, 15-30 X greater risk than nonsmoker\n\n> 95% are non\u2013small cell carcinomas, most commonly squamous cell (53%) > adenocarcinomas and large cell carcinomas\n\n< 1-5% of primary lung malignancies \n\n\u00bb located @ extreme-pleuropulmonary groove or superior sulcus near subclavian vessels; invades upper ribs, intercostal nerves, brachial plexus, vertebral bodies posteriorly\n\n\u00bb minimum, T3N0M0 (T3 for chest wall invasion); T4--if brachial plexus, mediastinal structures, or vertebral bodies involved \n \n\u00bb Clinical Findings: \nshoulder or scapular pain (most common initial presentation is pain localized to shoulder), weakness, atrophy, and paresthesias of upper extremity; compression of cord and paraplegia when tumor extends into intervertebral foramina; Horner\u2019s syndrome (ptosis, miosis, anhidrosis, enopthalmus) due to invasion of paravertebral sympathetic chain/stellate ganglion; SVC syndrome, phrenic / recurrent laryngeal neuropathy; pulmonary symptoms are rare\n\n\u00bb Imaging: \n\n\u2022 Radiography-apical mass (up to 75%) or unilateral apical pleural thickening > 5mm (up to 50%)\n\n\u2022 MRI ideal for determining soft tissue extent/involvement particularly brachial plexus and subclavian vessel involvement; MRI is most accurate for detecting chest wall invasion; brain imaging for staging highly recommended; PET prior to surgery should be considered\n\n\u00bb Histologic Dx:\n percutaneous transthoracic needle biopsy using imaging guidance \n\n\u00bb Treatment:\nStage IIIa: preoperative irradiation, then lobectomy and chest wall resection\nStage IIIb/IV: palliative radiation---<10% 5 year survival", "ACR Code": "6.3", "Category": "Neoplasm, carcinoma", "Keywords": "Pancoast tumor superior sulcus tumorlung cancersquamous cell carcinoma", "Reference": "Armstrong, Peter, et al., Imaging of Diseases of the Chest, Mosby, 2000, pp 323-5.\n\nHttp://www.emedicine.com/radio/topic515.htm. Guerrero M et al. Pancoast tumor.\n\nFraser, R.S. et al., \"Pulmonary Carcinoma,\" in Diagnosis of Diseases of the Chest, Fourth Edition, Saunders, 1999, pp. 1069-1202" } }, { "U_id": "MPX1754", "TAC": [ "MPX1754_synpic51421" ], "MRI": [ "MPX1754_synpic51422", "MPX1754_synpic51423", "MPX1754_synpic51426" ], "Case": { "Title": "Hypertensive Intracerebral Hemorrhage", "History": "75 y.o. man with CAD and chronic HTN presents with sudden onset right-sided weakness and sensory deficit.", "Exam": "Expressive aphasia, right-sided weakness, slight right-sided facial drooping", "Findings": "There is acute hemorrhage within the left thalamus and basal ganglia measuring up to 3 cm in greatest dimension. There is extension of this hemorrhage into the third and lateral ventricles. There is mild midline shift measuring on the order of 2 mm. There is mild heterogeneity of the hemorrhage. No underlying mass is identified. No other parenchymal hemorrhage or mass is seen.", "Differential Diagnosis": "Hemorrhagic infarction\n Hemorrhagic neoplasm \n Septic embolism\n AV malformation\n Amyloid angiopathy \n Blood dyscrasia\n Anticoagulants/Thrombolytic therapy\n CNS infection (eg, herpes simplex encephalitis)\n Mycotic aneurysm\n Vasculitis\n Drugs (cocaine, amphetamines)", "Case Diagnosis": "Hypertensive Intracerebral Hemorrhage", "Diagnosis By": "Clinical presentation and CT/MR Imaging studies", "Treatment & Follow Up": "Labs:\nCBC\nPlatelet count, Bleeding time\nPT/PTT\nLiver function tests\n\nImaging:\nAngiography of the head\n\nManagement:\n- ABCs\n- Maintain MAP < 110 mm Hg or BP < 160/90\n- Treat elevated ICP with analgesia and sedation, osmotic diuretics, CSF drainage. Maintain CPP 60-80 mm Hg.\n- Consider seizure prophylaxis\n- Maintain normothermia\n- Clinical monitoring for neurologic worsening for the initial 24 hours w/ sequential imaging as indicated\n- Ventriculostomy and/or surgical evacuation if there is continued deterioration in status or continued expansion of hematoma", "Discussion": "Watch the video-\nhttp://www.youtube.com/watch?v=p3sjh8bN6lU" }, "Topic": { "Title": "Hypertensive Intracerebral Hemorrhage", "Disease Discussion": "Epidemiology:\n- Incidence of intracerebral hemorrhage (ICH) is estimated\u00a0to be\u00a09 per 100,000\n- ICH accounts for 10-15% of stroke\n- 5-20% higher incidence in men\n- 70-90%\u00a0have hypertension\n\nPathophysiology:\n- Blood vessels adapt to chronic HTN via lipidosis and hyalinization leading to focal necrosis and ultimately a pseudoaneurysm that is susceptible to rupture.\n- The vessels involved are small penetrating arteries that originate from major cerebral arteries.\n\nHemorrhage Location:\n- thalamus (thalamostriate penetrators off the posterior cerebral arteries)\n- putamen and caudate (lenticulostriate penetrators off the middle cerebral artery)\n- pons and midbrain (penetrators off the basilar artery)\n- cerebellar hemisphere\n\nMechanisms of Brain Injury:\n- Ischemia\n- Increased intracranial pressure secondary to hydrocephalus or edema\n- Herniation secondary to mass effect of hematoma\n\nAssociated Risk Factors:\n- High alcohol intake \n- Black ethnicity \n- Lower cholesterol and lower LDL cholesterol \n- Lower triglycerides\n- Blood and bleeding disorders\n- Cerebral amyloid or brain tumors\n- Liver disease\n- Use of aspirin or blood thinners\n\nNeurological Findings:\n- Large hematoma \u2013 headache, nausea, vomiting, and a decreased level of consciousness\n- Small hematoma \u2013 no headache, maintained alertness, gradually progressing stroke symptoms\n- Neurologic signs related to the bleeding site (coma, pinpoint pupils, eye deviation, sensorimotor disturbance, hemianopia, seizure)\n\nIMAGING:\nCT\n- hematoma appears as areas of high density with sharply defined borders\n- the mass effect and the surrounding extruded serum/edema are hypodense\n- the hematoma changes from high density to isodense and finally to hypodense relative to the brain density overtime\n- several weeks after the bleed, the appearance may transiently simulate a tumor or abscess\n\nMR\nIntracerebral hematomas have a very dynamic appearance on MRI\n- acute blood, in the form the oxyhemogloblin, is isointense with the brain giving this appearance on T1\n- within hours, the oxyhemoglobin within the hematoma is converted to deoxyhemoglobin which gives the dark appearance on T2. \n- after a couple of days, the deoxyhemoglobin is progressively converted to methemoglobin which changes the appearance on T1 from isointense to bright while T2 remains dark.\n- over the next weeks, the methemoglobin is slowly broken down into hemichromes which results in bright appearance on T1 and T2. \n- beyond 2 weeks, there is conversion of the iron moiety to hemosiderin which gives a dark appearance on both T1 and T2.\n- a good mnemonic is \"I Be ID BD BaBy DooDoo\"\n\nDifferential Diagnosis:\n Hemorrhagic infarction (including venous sinus thrombosis)\n Hemorrhagic neoplasm \n Septic embolism (from bacterial endocarditis)\n AV malformation\n Amyloid angiopathy \n Blood dyscrasia\n Anticoagulants/Thrombolytic therapy\n CNS infection (eg, herpes simplex encephalitis)\n Mycotic aneurysm\n Vasculitis\n Drugs (cocaine, amphetamines)\n\nLabs:\nCBC\nPlatelet count, Bleeding time\nPT/PTT\nLiver function tests\nAngiography of the head\n\nImaging:\nHead CT/MR\nHead Angiography\n\nManagement:\n- ABC's\n- Maintain MAP < 110 mm Hg or BP < 160/90\n- Treat elevated ICP with analgesia and sedation, osmotic diuretics, CSF drainage. Maintain CPP 60-80 mm Hg.\n- Consider seizure prophylaxis\n- Maintain normothermia\n- Clinical monitoring for neurologic worsening for the initial 24 hours w/ sequential imaging as indicated\n- Ventriculostomy and/or surgical evacuation if there is continued deterioration in status or continued expansion of hematoma", "ACR Code": "1.0", "Category": "Hemorrhage", "Keywords": "HypertensiveIntracerebralHemorrhage", "Reference": "Chapter 45 Stroke and Other Neurovascular Disorders. Goetz: Textbook of Clinical Neurology, 3rd ed. 2007\n\nChapter 45 Stroke and Other Neurovascular Disorders. Goetz: Textbook of Clinical Neurology, 3rd ed. 2007\n\nChapter 432 Hemorrhagic Cerebrovascular Disease. Goldman: Cecil Medicine, 23rd ed. 2007\n\nChapter 226 Intracerebral Hemorrhage. Rakel & Bope: Conn's Current Therapy, 1st ed. 2008", "External Links": "emedicine.medscape.com/article/338055-overview" } }, { "U_id": "MPX1755", "TAC": [ "MPX1755_synpic17666", "MPX1755_synpic17667" ], "MRI": [], "Case": { "Title": "Calcified pericardium", "History": "68 year-old man with increased dyspnea on exertion and orthopnea.", "Exam": "Echocardiography and cardiac catheterization show evidence of constrictive physiology.", "Findings": "PA and lateral chest x-rays demonstrate normal heart size with anterior and inferior pericardial calcifications and question of mild pulmonary venous engorgement. On non-contrast CT scan, the calcifications are described as eggshell-type calcifications which do not significantly involve the AV grooves. There is no pericardial effusion, evidence of right heart enlargement or failure, or vena cava and hepatic vein distention. Accessory splenules, old fractures of the spine and inferior sternum at the level of the pericardial calcifications are also seen. Echocardiography revealed mild dilatation of the inferior vena cava. Doppler of the mitral valve was suggestive of abnormal respiratory variation which can be seen in constrictive physiology.", "Differential Diagnosis": "Calcific constrictive pericarditis vs. calcified pericardium from remote Post-traumatic hemopericardium. Underlying etiologies of constrictive pericardial disease include previous pericardiotomy or hemopericardium, radiation, virus, TB, chronic renal failure, rheumatoid arthritis, neoplastic involvement, and idiopathic.", "Case Diagnosis": "Calcified pericardium", "Diagnosis By": "Radiologic - confirmed by CT scan.", "Treatment & Follow Up": "Constrictive pericarditis work-up. Patients with constrictive pericarditis may benefit from pericardial stripping." }, "Topic": { "Title": "Constrictive pericarditis, calcified pericardium", "Disease Discussion": "Elevated filling pressures in the presence of calcification of the pericardium is consistent with constrictive pericarditis. Fibrous or calcific thickening of the pericardium may lead to constrictive pericardial disease due to restriction of cardiac motion which chronically compromises ventricular filling. Onset of constrictive pericarditis is usually between the ages of 30-50 years and prevalence is three times greater in males than in females. An associated protein losing enteropathy may be present. The most common cause of constrictive pericardial disease is postpericardiotomy and hemopericardium for any reason. The second most common cause is radiation therapy, but Coxsackie B virus, TB, uremia, connective tissue disease, neoplasm, and idiopathic etiologies may be seen. \n\nPatients with constrictive pericarditis commonly present with symptoms of heart failure to include dyspnea, orthopnea, and fatigability. They may occasionally present with liver enlargement, ascites and later on with cirrhosis (\"cardiac cirrhosis\")secondary to chronic hepatic congestion.\n\nNormal pericardial thickness is less than 2mm. When greater than 4mm and accompanied by clinical findings of heart failure, constrictive pericarditis is highly likely. It is essential to realize, however, that neither pericardial thickening nor calcification is pathognomonic of constrictive pericarditis unless the patient also has concomitant symptoms of physiologic constriction. However, 50% of patients with pericardial calcifications have constrictive pericarditis. Pericardial thickening may be global or limited to the right side of the heart or to the right AV groove.\n\nCalcifications are seen on plain film radiography in up to 50% of patients. Ascites and plural effusions are common. Normal to mild enlargement of the cardiac silhouette is commonly seen along with small atria, dilated superior and inferior vena cava and azygos vein, and flat or straitened right heart border.\n\nEchocardiography may show thickened pericardium, abnormal septal motion, and increased left ventricular ejection fraction with a small end-diastolic volume. \n\nCT and MR imaging are excellent in depicting the pericardium, and in aiding the diagnosis of constrictive pericarditis, especially in difficult cases. CT is particularly good for demonstrating pericardial thickening and calcification. Reflux of contrast into the coronary sinus, a bowed interventricular septum, flattening of the right ventricle, ascites, and pleural effusions, may all be seen. Both CT and MR show pericardial thickening, dilatation of the right atrium, inferior vena cava and hepatic veins along with a sigmoid septal shift (or prominent leftward septal convexity) and narrowing/reduced volume of the right ventricle. MR may demonstrate abnormal flow mechanics in the vena cava and atria.\n\nFrom the clinical standpoint it is important to differentiate constrictive pericarditis from other restrictive myocardial diseases ( Myocarditis)since both entities have identical pathophysiologic findings on echocardiography or card cath. Myocarditis is difficult to treat and the only treatment is medical therapy. Constrictive pericarditis is treated surgically with pericardial stripping.", "ACR Code": "5.4", "Category": "Pathology", "Keywords": "PericardiumCalcificationConstrictive", "Reference": "Fundamentals of Diagnostic Radiology / (edited by) William E. Brant, Clyde A. Helms.\u20142nd ed., Lippincott Williams & Wilkins, 1999\n\nPrimer of Diagnostic Imaging / (edited by) Janice M. Gaillard\u20143rd ed., Mosby Inc., 2003\n\nWang et al. CT and MR Imaging of Pericardial Disease. Radiographics; 23:S167-S180; 2003" } }, { "U_id": "MPX1763", "TAC": [ "MPX1763_synpic253" ], "MRI": [], "Case": { "Title": "Spleen Maximum Dimensions", "Case Diagnosis": "Spleen Maximum Dimensions" }, "Topic": { "Title": "Spleen Maximum Dimensions", "Disease Discussion": "Maximum Dimensions of Spleen : \" 4711 \"\n(4711 is a well known German brand of cologne water.)\n \nIntercostal (vertical) Length < 11.0 cm \nWidth < 7.0 cm\nDepth < 4.0 cm (between Splenic Hilum and surface)", "ACR Code": "7.1", "Category": "Mnemonic" } }, { "U_id": "MPX1769", "TAC": [ "MPX1769_synpic15560" ], "MRI": [], "Case": { "Title": "Calyceal Diverticulum", "History": "27 year old female who presented to the Internal Medicine clinic with a complaint of chronic right flank pain and a history of multiple urinary tract infections. Routine Labs revealed microhematuria. Request was made for a Abdominal CT.", "Exam": "Microhematuria", "Findings": "Axial CT images with contrast demonstrate a 2 cm hypodensity in the inferior pole of the right kidney. The mass contains 2 dependent calcifications. On the delayed phase of imaging, The hypdense mass fills with excreted contrast confirming the diagnosis of calyceal diverticulum.", "Differential Diagnosis": "Renal sinus cyst.\nObstructed Hydrocalyx.", "Case Diagnosis": "Calyceal Diverticulum" }, "Topic": { "Title": "Calyceal Diverticulum", "Disease Discussion": "A calyceal diverticulum is a lesion that results from an out pouching of a portion of the collecting system that protrudes into the corticomedullary region. They can arise in any part of the collecting system from a fornix to the renal pelvis. Size varies anywhere from a few millimeters to several centimeters in diameter. They are uroepithelial-lined cavities that communicate via a narrow channel to a nearby calyx. They may be congenital, or acquired lesions.\n\nIt is not uncommon to see calcified stones characteristically layering in the dependent portion of the diverticulum. The stones that form within the diverticulum may pass and cause symptomatic renal colic but they are typically confined to the diverticulum due to its narrow neck connection to the distal collecting system.. \n\nThey are regions of urinary stasis and the dependent sediment that eventually develops in a calyceal diverticulum is referred to as \u201cmilk of calcium.\u201d Larger stones may form that are confined to the diverticulum and may be a source of chronic pain.\n\nOn CT, the diagnosis is made with delayed imaging showing the diverticulum fill with contrast. Alternatively if stones are present, the patient can be rescanned in the opposite position. If the stones settle dependently, and are confined to the lesion, the diagnosis can be made in the absence of delayed imaging.\n\nManagement of symptomatic stone disease associated with Calyceal diverticula has changed from an open surgical approach to include ESWL, percutaneous, laproscopic or ureteroscopic techniques. The choice of therapy depends largely on the anatomic location of the diverticulum.", "ACR Code": "8.9", "Category": "Diverticulum", "Keywords": "CalycealDiverticulum", "Reference": "1.Dunnick NR. Textbook of Uroradiology. 3rd Edition. Philadelphia: Williams & Wilkins, 2001. p.303-304.\n\n2.Brant WE. Fundamentals of Diagnostic Radiology 2nd Edition. Baltimore: Williams & Wilkins 1999. p.801.\n\n3.Canales B et al. Surgical Management of the Calyceal Diverticulum. Curr Opin Urol 2003 May:13(3):255-60." } }, { "U_id": "MPX1748", "TAC": [ "MPX1748_synpic53121", "MPX1748_synpic53123", "MPX1748_synpic53124", "MPX1748_synpic53125" ], "MRI": [], "Case": { "Title": "Mixed Germ Cell Testicular Tumor", "History": "20 y.o. man with trauma to the groin 4 days ago, presents with increasing pain and swelling of his left testicle for two days.", "Exam": "\u00bb \"Rock hard\" left testicle.\n\n\u00bb Lab values -\nAlpha-Fetoprotein: 10314 ng/mL \nBeta HCG: 89937 mIU/mL \nLDH: 580 U/L", "Findings": "Testicle Ultrasound\n\u2022 Well-circumscribed, heterogeneously hypoechoic mass with mixed solid and cystic components, arising from the left testicle and confined within the tunica albuginea.\n\nAbdominal CT\n\u2022 Bulky retroperitoneal and para-aortic lymphadenopathy. \n\nChest Film and CT\n\u2022 Supraclavicular and subcarinal adenopathy and multiple lung nodules. \n\nAll of these findings suggest a metastatic testicular cancer", "Differential Diagnosis": "\u2022 Germ cell tumor (likely non-seminomatous)\n\u2022 Stromal tumor\n\u2022 Lymphoma", "Case Diagnosis": "Mixed Germ Cell Testicular Tumor", "Diagnosis By": "Pathology examination showing: Teratoma (50%); Choriocarcinoma, Biphasic (30%); Embryonal Carcinoma (15%); Yolk Sac Tumor (5%)", "Treatment & Follow Up": "T2N2M1bS3 \tAJCC Stage IIIC (poor risk, but ~70% respond to initial chemo, with 10-15% eligible for salvage therapy).\n\nScreening abdomen and chest studies show dissemination - but there are no brain metastases.\n\n\nOrchiectomy with retroperitoneal lymph node dissection, was followed by chemotherapy.", "Discussion": "Lymph node drainage from the testicle follows the path of embryonic develoment back to the renal hilus and para-aortic lymph nodes. Staging of testicular cancers includes imaging of the abdomen and chest. Metastatic spread usually follows this cascade: local lymph nodes/veins > renal and para-aortic nodes/veins > lung > system spread. The lung is usually involved before there can be spread to the CNS - unless there is right-to-left shunt." }, "Topic": { "Title": "Mixed Germ Cell Testicular Tumor", "Disease Discussion": "Of all malignant intratesticular neoplams, mixed germ cell tumors are the second most common. Of these the majority are at least a portion of embryonal cell carcinoma which constitute 20-25% of all primary germ cell malignancies. Unfortunately this subtype of germ cell tumor tend to be more aggressive and will invade the tunica albuginea and/or cause visceral metastases. Although embryonal cell carcinomas have three sub-types: adult, infantile and endodermal sinus tumor, embryonal cell carcinomas tend to be less radio and chemosensitive than seminomatous tumors. Infantile and endodermal sinus types are associated with elevated alpha-fetoprotein which can be used to monitor therapy/recurrence. \nTeratomas are a second type of germ cell tumor. Teratoma also has three subtypes: mature, immature, and with malignant transformation. Teratomas must have three germinal layers: endoderm, mesoderm, ectoderm. They constitute 5% of all primary testicular neoplasms. Although approximately 30% will metastasize, the reported 5-year survival is 70%. \nAlthough not seen in this case the other type of non-seminomatous germ cell tumor type is choriocarcinoma which is the rarest and least favorable of the three basic types. Although it rarely occurs in its pure form, it represents 23% of mixed germ cell tumors. These leisons are highly vascular and metastasize early.", "ACR Code": "8.3", "Category": "Neoplasm, malignant (NOS)", "Keywords": "Nonseminomatous", "Reference": "Diagnostic Ultrasound. Rumack, C.et al. 2nd Edition. Mosby Publishing. 1998." } }, { "U_id": "MPX1770", "TAC": [ "MPX1770_synpic23443" ], "MRI": [], "Case": { "Title": "Battered child syndrome. Chronic bilateral subdural hematomas.", "History": "5 month old female brought to ER with lethargy. Imaging request stated \"hypoglycemia.\"", "Findings": "Non-contrast CT demonstrated bilateral subdural fluid collections", "Differential Diagnosis": "Non-accidental trauma", "Case Diagnosis": "Battered child syndrome. Chronic bilateral subdural hematomas." }, "Topic": { "Title": "Battered child syndrome. Chronic bilateral subdural hematomas. Multifocal areas of acute/chronic cerebral contusions/edema/encephalomalacia.", "Disease Discussion": "The spectrum of intracranial injuries in physically abused children includes: acute subdural hematoma, chronic subdural hematoma, acute epidural hematoma, cerebral contusion, focal/multifocal/diffuse cerebral edema, and atrophy. Acute and/or chronic subdural hematomas and cerebral contusion are common in child abuse. Intracerebral hematomas and epidural hematomas are uncommon.\n\nUntreated acute subdural hematomas undergo a series of predictable pathologic changes. Soon after the acute hemorrhage, the blood collection becomes surrounded by endothelial cells and there is invasion by granulation tissue. Progressive liquefaction of the hematoma results in its conversion to a serous fluid. These serous subdural collections are referred to as chronic subdural hematomas or subdural hygromas. Chronic subdural hematomas, related to prior trauma, are most often located adjacent to one or both cerebral convexities but may also extend into the interhemispheric fissure.\n\nThe CT appearance of a subdural hematoma varies according to the time period since the injury. The initial hemorrhage is visualized as a high-attenuation fluid collection on CT. The attenuation values of the lesion progressively decrease over the next weeks to months. Chronic subdural hematomas usually contain serous fluid and produce attenuation values slightly greater than those of CSF. It is not uncommon for an abused child to have suffered multiple episodes of trauma, resulting in intracranial hematomas in different stages of evolution.\n\nAt times, chronic subdural hematomas are difficult to differentiate from enlargement of the subarachnoid spaces. In many cases, a distinct transition is visible between the subdural fluid collection and the slightly lower attenuation CSF of the subarachnoid space. A membrane of variable thickness separating the two spaces may be identifiable. The brain adjacent to a chronic subdural hematoma is often displaced, and the sulci may be compressed and effaced. In contradistinction, enlarged subarachnoid spaces are associated with interdigitation of the fluid into the cerebral sulci.\n\nThe differential diagnosis of isolated chronic subdural fluid collections in infants includes bacterial meningitis, remote trauma, rickets, and Menke's syndrome. In the absence of a clear-cut, suitable clinical history of other forms of trauma, the CT demonstration of coexistent acute and chronic subdural hematomas is highly suggestive of child abuse.", "ACR Code": "1.-1", "Category": "Trauma" } }, { "U_id": "MPX1771", "TAC": [ "MPX1771_synpic16984" ], "MRI": [], "Case": { "Title": "Crohn's Disease on PET and Tc-99m HMPAO tagged WBC Scanning", "History": "Two patients with the same diagnosis, the request for the studies read \"assess disease status\".", "Findings": "Figure 1. Patient A. Tc-99m HMPAO tagged WBC study demonstrates normal biodistribution of the radiopharmaceutical as well as a focal region of linear uptake in the right lower quadrant of the abdomen.\n\nFigure 2. Patient A. Contrast enhanced CT through the pelvis demonstrates a loop of small bowel with wall thickening abutting the right pelvic sidewall. \n\nFigure 3. Patient B. F-18 FDG PET axial image through pelvis demonstrates focal linear FDG avidity.\n\nFigure 4. Patient B. Non-contrast CT of pelvis demonstrates a loop of small bowel with wall thickening. There is mild surrounding mesenteric edema as well as prominence of the surrounding fat. \n\nFigure 5. Patient B. PET image fused with the CT image (studies were obtained simultaneously). Correlation of FDG avidity to thickened small bowel loop.\n\nFigure 6. Patient A. Selected image from a small bowel follow-through concentrating on the right lower quadrant. Demonstration of narrowing of the terminal ileum (a \u201cstring\u201d sign), surrounding mass effect and effacement of the cecum. Study was obtained several months after the previously shown Tc-99m HMPAO/WBC study.", "Differential Diagnosis": "Crohn's Disease (Known diagnosis)", "Case Diagnosis": "Crohn's Disease on PET and Tc-99m HMPAO tagged WBC Scanning", "Discussion": "See factoid." }, "Topic": { "Title": "Crohn's Disease on PET and Tc-99m HMPAO tagged WBC Scanning", "Disease Discussion": "Crohn\u2019s disease, (aka \u201cgranulomatous\u201d colitis, regional enteritis, granulomatous ileitis) is a transmural inflammatory bowel disease of unknown etiology, affecting the terminal ileum in the vast majority of affected patients. Skip lesions may also occur, with eventual involvement of the colon in 70%. Initial presentation is in the teens or early twenties, with males and females equally affected. Onset may be insidious, with initial symptoms ranging from mild diarrhea and low grade fever, to more acute symptoms resembling appendicitis. The earliest macroscopic manifestation is apthoid ulceration of the gut mucosa with eventual enlargement of the ulcers and confluence thereof. Microscopically small granulomas resembling sarcoid granulomas are found, containing multinucleated giant cells of Langhans\u2019 type. Interestingly, such granulomas are more frequently found in the lymph nodes draining the diseased segment, and less so in the segment itself. Ultimate complete loss of mucosa, fibrosis and narrowing of the lumen is a common outcome. Associated inflammation leads to mass effect displacing or effacing structures in the right lower quadrant. Due to the transmural ulceration fistulization between adjacent loops of small bowel and the colon may be seen, as well as fistulization between the bladder, vagina, ureter, and skin. The proximal small bowel, stomach, and esophagus may also be affected, in that decreasing order of frequency. Such proximal involvement, however, rarely occurs independent of terminal ileal involvement. \n\n\nPrevious studies of nuclear medicine inflammatory bowel imaging demonstrate good correlation between locale of uptake on In-111/WBC scanning and region of bowel affected, however Tc-99m HMPAO/WBC scanning has been shown to demonstrate better localization properties. Additionally, Tc-99m provides a lesser radiation dose to the spleen by virtue of its shorter half life (6hrs vs 67 hrs); thus it is preferred in the pediatric population. Finally, Tc-99mHMPAO/WBC results may be obtained as rapidly as within one hour after injection of the radiopharmaceutical. Should In-111/WBC scanning be done, however, initial imaging should be done at 4 hours rather than the typical 24 hour delay. This is because there will be shedding of leukocytes from the inflamed bowel and peristalsis will carry the labeled leukocytes distally, possibly resulting in inaccuracy in determining site of inflammation. \n\nUse of F-18 FDG PET scanning in the evaluation of inflammatory bowel disease is promising. In a study of 86 patients with suspected inflammatory bowel disease undergoing PET scanning followed by endoscopic confirmation PET was found to have a sensitivity of 98%, specificity of 83%, positive predictive value of 93%, and negative predictive value of 95%.", "ACR Code": "7.2", "Category": "Nuclear Medicine", "Keywords": "Crohn's DiseasePositron Emission TomographyTechnitium 99m HMPAO WBC", "Reference": "Chen MYM, Zagoria RJ, Ott DJ, Gelfand DW: Radiology of the Small Bowel. Igaku-Shoin, New York, 1992, pp. 161-182.\n\nMernagh J, Sommers S: A New Way to Look at Inflammatory Bowel Disease. Canadian Medical Association Journal, November 2, 1999; 161 (9).\n\nThrall JH, Zeissman HA: Nuclear Medicine: The Requisites. Mosby, St. Louis, 2001, pp. 189-190." } }, { "U_id": "MPX1774", "TAC": [ "MPX1774_synpic24333" ], "MRI": [], "Case": { "Title": "Bone metastasis from prostate cancer.", "History": "Patient is a 60 y/o WM with history of prostate CA, s/p radical prostatectomy with regional lymph node resection. Patient subsequently underwent 2 courses of chemotherapy treatments with response. With 3 months the patient developed bone metastases from his prostatic carcinoma. He is currently enrolled in a trial therapy, which requires interval follow-up diagnostic imaging study to evaluate response to therapy.", "Exam": "PSA levels: Increasing levels of PSA from 15.81 to 96.91 during a six month period of time", "Findings": "Multiple sclerotic lesions involving the vertebrae and the iliac bones consistent with metastases from prostate cancer", "Differential Diagnosis": "Bone metastases most commonly from prostate\nSclerotic Paget's- less likely\nInfection, such as tuberculosis, unusual without joint space involvement", "Case Diagnosis": "Bone metastasis from prostate cancer.", "Treatment & Follow Up": "-Analgesics for treatment of bone pain\n-Antineoplastic therapy with androgen deprivation.\n-Radiation therapy", "Discussion": "Metastatic prostate cancer is usually spread hematogenously;. Metastases to bone are the most common metastasis with prostate cancer. The proposed hypothesis for this pattern of spread of metastasis is retrograde spread to the axial skeleton (pelvis and vertebrae) via Batson\u2019s venous plexus, which is a valveless venous plexus of the spine and paraspinal region with communication between the pelvic and vertebral venous systems, femoral and iliac veins, inferior and superior vena cava, and other veins. This system may be important for hematogenous spread of either metastases or of microorganisms in spinal infection. Prostatic metastases are usually osteoblastic as shown on radiographs and on CT images. However, scintigraphy (bone scans) are useful for detecting early metastases several weeks or months before the radiographs become abnormal. \n \nThe increase in public awareness of prostate cancer and in the use of PSA to screen for the disease has led to early diagnosis and treatment of prostate cancer.Prior to 1991, greater than 30% of patients developed distant metastases Currently approximately 6% have metastases." }, "Topic": { "Title": "Bone metastasis, secondary to prostate cancer.", "Disease Discussion": "Video for this Topic = http://youtu.be/T2KtPKMpCrM\n\nMetastatic prostate cancer is usually spread hematogenously;. Metastases to bone are the most common metastasis with prostate cancer. The proposed hypothesis for this pattern of spread of metastasis is retrograde spread to the axial skeleton (pelvis and vertebrae) via Batson\u2019s venous plexus, which is a valveless venous plexus of the spine and paraspinal region with communication between the pelvic and vertebral venous systems, femoral and iliac veins, inferior and superior vena cava, and other veins. This system may be important for hematogenous spread of either metastases or of microorganisms in spinal infection. Prostatic metastases are usually osteoblastic as shown on radiographs and on CT images. However, scintigraphy (bone scans) are useful for detecting early metastases several weeks or months before the radiographs become abnormal. \n \nThe increase in public awareness of prostate cancer and in the use of PSA to screen for the disease has led to early diagnosis and treatment of prostate cancer.Prior to 1991, greater than 30% of patients developed distant metastases Currently approximately 6% have metastases.", "ACR Code": "4.3", "Category": "Neoplasm, metastatic", "Keywords": "Blastic Bone metastasisProstate cancer Batson plexus valveless veins", "Reference": "Walsh: Campbell's Urology, 8th ed.\nKirby, Roger MD. An Illustrated Pocketbook of Prostatic Diseases. New York, NY 2002" } }, { "U_id": "MPX1779", "TAC": [ "MPX1779_synpic18321" ], "MRI": [], "Case": { "Title": "1. Metastatic breast cancer to lungs \r\n2. Right side vocal cord paralysis \r\n3. Anemia, thrombocytopenia \r\n4. Transamnitis", "History": "48 y/o AAF with h/o of metastatic infiltrating ductal breast CA and pulmonary nodules presents with SOB and progressive vocal loss. Pt had lumpectomy and XRT in 1998. In March 2000, a sternal lesion and R breast lesion were discovered, biopsied and found to be metastases. Right upper lobe lung mass first found in 3/01. Jan 2002, RUL wedge resection/matastectomy was performed. Pt has undergone numerous chemo regimens, XRT and autologous BMT. Pt was recently hospitalized for mucositis complicated by neutropenia.", "Exam": "Gen: Cachetic\nChest/Lung: Equal BS, no rales, rhochi, wheezes or rubs; decreased breath sounds\nEdema present in the lower extremity bilaterally\nVATS, Lung Bx Jan 2002-confirmed metastatic breast cancer to the RUL \nCA 27-29 on 01 Oct 2003 was 58\nBasic Labs at admission on 09 Oct 20033.7 \\10.9 /46 135/2.9/101/36/9/0.8/98 Alk phos 128, AST 147, ALT 53 TBILI 1.7 32.7", "Findings": "Chest x-ray: multiple pulmonary nodules which are too numerous to count, increased size and number in comparison to the last one from 04 Dec 02. A left arm catheter is present with the tip projecting over the level of the right superior cavoatrial junction. Evidence of prior right breast surgery. No infiltrates or effusion.CT-No PE/DVT. No bone or liver mets. Increase in mediastinal adenopathy in the aortopulmonary window and subcarinal region. Evidence of right masectomy within the soft tissues. Overall progression of lung parenchymal disease.", "Differential Diagnosis": "1.\tMetastatic breast Cancer to the lung\n2.\tMultiple abscesses\n3.\tSeptic emboli\n4.\tFungal infection\n5.\tNon-Hodgkin\u2019s lymphoma\n6.\tKaposi\u2019s sarcoma\n7.\tWegener\u2019s granulomatosis", "Case Diagnosis": "1. Metastatic breast cancer to lungs \n2. Right side vocal cord paralysis \n3. Anemia, thrombocytopenia \n4. Transamnitis", "Treatment & Follow Up": "2001-chemo(busulphan/melphalan/thiotepa)Pt has been treated with XRT, adriamycin, Taxetere, Gimca and Zolita. SOB was determined to be due likely to decreased lung volume from mass effect. Laryngoscopy was performed and showed paralysis of right sided vocal chords likely due to metastatic impingement of recurrent laryngeal nerve. Heme-Onc consult determined that the pt had reached the endpoint for chemotherapy. Pt was not a candidate for Rad-Onc therapy either. During this hospital course, pt was anemic, thrombocytopenic with elevated LFT\u2019s and eventually neutropenic. Pt was discharged when on HD#5, WBC, HCT, platelets, and LFT\u2019s showed upward trend, and pt reported mild improvement of SOB with greatly improved voice. Pt was advised to seek hospice care." }, "Topic": { "Title": "Metastatic breast cancer to lungs - nodules", "Disease Discussion": "Metastatic solid organ malignancies represent about 80 percent of multiple pulmonary nodules discovered in imaging studies. (1) Helical CT is generally recommended to detect and radiographically characterize multiple pulmonary nodules. Helical CT detects up to 40 percent more nodules than conventional CT. (2) Not all lesions that appear after a diagnosis of breast cancer represent metastases. A biopsy should be done even in women with a prior history of breast cancer. Up to 50 percent of solitary pulmonary nodules represent new primary lung cancers (2). The biopsy can also further delineate the hormonal characteristics of the metastases. One study showed that up to 20 percent of estrogen receptor measurements might be different between the primary and metastatic lesions (3). Fewer than 10 percent of women present with metastatic disease at the time of diagnosis. With metastases, a complete remission is rare. 5 to 10 percent of patients with metastatic breast cancer may survive five or more years (4).", "ACR Code": "68.333", "Category": "Neoplasm, metastatic", "Keywords": "Metastaticcancer", "Reference": "1.\tHarrison\u2019s Principles of Internal Medicine 15 th Edition\n\n2.\tRemy-Jardin, M, Remy, J, Giraud, F, Marquette, CH. Pulmonary nodules: Detection with thick-section spiral CT versus conventional CT. Radiology 1993; 187:513\n\n3.\tHull DF, 3d, Clark, GM, Osborne, CK, et al. Multiple estrogen receptor assays in human breast cancer. Cancer Res 1983; 43:413\n \n4. Greenberg, PA, Hortobagyi, GN, Smith, TL, et al. Long-term follow-up of patients with complete remission following combination chemotherapy for metastatic breast cancer. J Clin Oncol 1996; 14: 2197" } }, { "U_id": "MPX1787", "TAC": [ "MPX1787_synpic25265", "MPX1787_synpic25266" ], "MRI": [], "Case": { "Title": "Endobronchial Tumors", "History": "23 yo male with recurrent hemoptysis.", "Exam": "No findings", "Findings": "PA and lateral chest films were unremarkable. \nLingular bronchial lesion. No associated calcifications. Post obstructive air trapping in lingula.", "Differential Diagnosis": "Neoplasm (benign or malignant. Unlikley mucous plug or foreign body given symptomatology.", "Case Diagnosis": "Endobronchial Tumors", "Diagnosis By": "Carcinoid diagnosed by bronchoscopy guided biopsy/ resection and histology.", "Treatment & Follow Up": "Lesion resected.", "Discussion": "Endobronchial lesions: \n - Tumors 80%, Inflammatory 20%\n - Less than 10% of tumors are benign\n \nBenign: Squamous cell papilloma - most common\n Hamartomas \n Pleomorphic adenoma\n\nMalignant: Squamous cell carcinoma - most common\n Adenoid cystic carcinoma\n Mucoepidermoid carinoma\n Carccinoma\n\nBall valve phenomenon can generate distal air trapping. During exhalation the bronchial caliber decreases. This combined with endobronchial lesion can partially or completely occlude the bronchial lumen generating peripheral air trapping." }, "Topic": { "Title": "Endobronchial Tumors", "Disease Discussion": "Endobronchial tumors: \n - Tumors 80%, Inflammatory 20%\n - Less than 10% of tumors are benign\n \nBenign: Squamous cell papilloma\n Hamartomas \n Pleomorphic adenoma\n\nMalignant: Neuroendocrine (typical/atypical carcinoid)\n Squamous Cell Carcinoma\n Mucoepidermoid Carcinoma\n Adenoid Cystic Carcinoma", "ACR Code": "6.3", "Category": "Neoplasm, NOS", "Keywords": "Endobronchial lesionBronchial tumor", "Reference": "Cardiopulmonary Imaging, Kazerooni and Gross. Lippincott, Williams, Wilkins. 2004." } }, { "U_id": "MPX1792", "TAC": [ "MPX1792_synpic24221" ], "MRI": [], "Case": { "Title": "Congenital Adrenal Hyperplasia", "History": "Patient presents to her primary care provider with non-specific abdominal and pelvic complaints for the last several months. No fever.", "Exam": "Thin hirsuite hispanic female in no apparent distress. Pelvic exam demonstrates vulvar irregularities and questionable clitoralmegaly. Bi-manual exam is normal.\n\nLabs show increased levels of 17 hydroxy progesterone in blood and elevated 17-ketosteroids in urine.", "Findings": "Contrast enhanced CT image through the adrenals shows marked symmetric enlargement of the adrenals and no other significant abnormality.", "Differential Diagnosis": "Congenital Adrenal Hyperplasia\nCushing's Syndrome\nConn's Syndrome\nPrimary bilateral Adrenocortial Neoplasms\nDiffuse lymphoma or metastatic disease", "Case Diagnosis": "Congenital Adrenal Hyperplasia", "Diagnosis By": "By physical exam, blood and urine labs.", "Treatment & Follow Up": "Patient was put on hormone therapy and instructed to follow up with endocrinology after genetic counseling.", "Discussion": "This case represents an uncommon diagnosis in an adult with bilateral adrenal hyperplasia. In most circumstances, Cushings would be far more likely. In this case, the imaging, physical exam and labs corroborate perfectly with the diagnosis." }, "Topic": { "Title": "Congenital Adrenal Hyperplasia", "Disease Discussion": "Congenital adrenal hyperplasia represents a spectrum of rare disorders that cause an inability to produce certain corticosteroids and an overproduction of androgen. It is an autosomal recessive disease that can affect both men and women and is seen in about 1 in 18,000 children. The disease causes a spectrum of abnormalities ranging from rapidly fatal salt wasting effects in newborns to mild chronic virilization varieties of the female genitalia caught in later life on incidental studies.\n\n In boys, the disease is manifested by early muscle development and maturation of the genitals. Girls may be born with ambiguous external genitalia but the internal structures are normal. Later in life, females develop excessive hair growth, failure to menstruate, and a deep voice. \n\n Diagnostic studies are usually blood and urine elevations of 17-ketosterioids and serum elevations in DHEA. CT, US, or MR of the adrenals can show unspecific though marked symmetric enlargement of the adrenals.\n\n Other differential diagnosis for CT findings of symmetrically enlarged adrenal glands includes: \n Cushing\u2019s syndrome \u2013 usually from excessive ACTH \n production in a pituitary adenoma.\n Conn\u2019s syndrome \u2013 usually from excessive aldosteronism\n via adrenal adenomas.\n Hyperandrogenism \u2013 from adrenocortial neoplasms.\n And less commonly symmetric bilateral pheochromocytomas,\n diffuse lymphoma or metastatic disease.", "ACR Code": "8.6", "Category": "Congenital, genetic", "Keywords": "AdrenalCongenitalHyperplasia", "Reference": "Stewart, Douglas R. MedlinePlus Medical Encyclopedia: Congenital Adrenal Hyperplasia at http://www.nlm.nih.gov/medlineplus/ency/article/000411.htm.\n\nElsayes, KM, Mukundan G, et al. Adrenal Masses: MR Imaging Features with Pathologic Correlation. RadioGraphics 2004; 24 S73-S86.\n\nMayo-Smith WW, Boland GW, et al. From the RSNA Refresher Courses: State-of-the- Art Adrenal Imaging. RadioGraphics 2001; 21:995-1012.\n\nAgrons GA, Lonegran GJ, et al. From the Archives of the AFIP: Adrenocortical Neoplasms in Children: Radiologic-Pathologic Correlation. Radiographics 1999; 19:989-1008." } }, { "U_id": "MPX1809", "TAC": [ "MPX1809_synpic17628" ], "MRI": [], "Case": { "Title": "Cervical cancer with bilateral hydronephrosis", "History": "29 y/o G6P5051 female arrived on airevac from micronesia island with history of post-coital bleeding.", "Findings": "-6 x 6 cm cervical mass with infiltrated surrounding fat, consistent with cervical cancer. \n-There are several prominent asymmetric pelvic lymph nodes on the left side. These are not pathologic by size criteria, however, in the presence of nearby malignancy these may represent metastatic disease. \n-There is mild bilateral hydronephrosis from the cervical mass compressing both ureters. Additionally, the image through the kidneys demonstrates delayed nephrogram of the right kidney secondary to higher back pressure of the right hydronephrosis compared with the left.", "Differential Diagnosis": "cervical cancer", "Case Diagnosis": "Cervical cancer with bilateral hydronephrosis", "Discussion": "Bilateral hydronephrosis should always cause concern for cervical cancer in a female patient." }, "Topic": { "Title": "Cervical cancer with bilateral hydronephrosis", "Disease Discussion": "Cervical carcinoma is ordinarily diagnosed by pap smear and physical exam. The diagnosis is confirmed by tissue biopsy. CT Scans are useful to evaluate the primary tumor and to stage the spread of the carcinoma. CT Scan is also useful in evaluation of hydronephrosis and presence of pelvic and para-aortic lymph nodes. It may also be used to evaluate patients who are difficult to examine. Secondary obstruction of the endocervical canal can result in endometrial distention & hydrometra visible on CT.\n\n-Etiology and Pathogenesis:\nRisk factors include prior infection with HPV, lower socioeconomic status, \nmultiple sexual partners, and age <20 at time of first coitus. Young age at first pregnancy and high parity are also risk factors.\n\n-Epidemiology:\n2nd most common gynecologic malignancy in American women age 45-55 (after Endometrial CA). 16,000 new cases diagnosed each year, 7,000 deaths per year (6th on list of cancer mortality). Most common malignancy in women younger than 50 years of age. \n\nThe majority (90%) are SCCA; 8% are adenocarcinoma (in offspring of women who used DES during pregnancy). The remainder are either sarcomas or lymphomas.\n\nStaging:\n\t0-Carcinoma in situ\n\tI-Carcinoma confined to the cervix\n\tII-Carcinoma extends beyond cervix, but not to pelvic wall\n\t\tA-No parametrial involvement\n\t\tB-Parametrial involvement\n\tIII-Carcinoma extends beyond cervix\n\t\tA-To, but not into, pelvic wall\n\t\tB-Onto pelvic wall, ureter involved\n\tIV-Carcinoma extends beyond true pelvis or invades bladder/rectum\n\n-Clinical Manifestations: \nEarly, non-invasive disease is typically asymptomatic. Invasive disease presents with abnormal vaginal bleeding in 80% of patients. A palpable mass may be evident on physical exam, and dysplastic epithelium appears white under colposcope after surface application of acetic acid. \n\t\nApproved by Dr. Thomas Murphy, M.D. - Chief of abdominal section, Tripler AMC", "ACR Code": "8.3", "Category": "Neoplasm, non-CNS", "Keywords": "cervixcancerneoplasmhydronephrosis", "Reference": "1. Patricial Lipford Abbitt, Imaging in Obstetrics and Gynecology.\n2. Ronald Zagoria, Genitourinary Radiology: The Requisites.\n3. Juan Taveras & Joseph Ferrucci, Radiology: Diagnosis, Imaging, Intervention." } }, { "U_id": "MPX1793", "TAC": [ "MPX1793_synpic41476", "MPX1793_synpic41478" ], "MRI": [], "Case": { "Title": "Granuloma", "History": "10 y.o. girl with \"chronic congestion\" presented to clinic with new onset of cough and sore throat. The patient also had complained of 6 months of intermittent headaches. The patient denied any sputum production or fevers.", "Exam": "Head: cloudy nasal discharge\nLungs: scattered rhonchi, no crackles, no wheezing\nLymph: No cervical lymphadenopathy\n\nLABS: \nPPD negative\nHistoplasma negative\nESR \u2013 12\nWBC 9.3 (w/ NL distribution)", "Findings": "There is a left upper lobe pulmonary nodule which measures approximately 1.1 cm in diameter. There is central calcification within this lesion, which has become slightly more dense over the year in between CT. The borders are well demarcated.", "Differential Diagnosis": "Granuloma\n -TB\n -Histoplasmosis\nHamartoma\nInfectious\n - Pneumocystis carinii \n -Aspergilloma\nPulmonary metastatic disease \nPrimary pulmonary malignancy", "Case Diagnosis": "Granuloma", "Diagnosis By": "Stability of lesion on follow up", "Treatment & Follow Up": "No further work up is necessary. It is important for the mother to convey these findings to future physicians when a chest xray or CT is performed and to relay the current dimensions.", "Discussion": "There are many algorithms for the evaluation of the \"solitary pulmonary nodule\". In a young child, metastatic disease is very uncommon - and thus this girl was followed with repeat imaging that documented a stable lesion size - now, most likely a healed granuloma." }, "Topic": { "Title": "Solitary Pulmonary Nodule - Calcified Granuloma", "Disease Discussion": "One of the most common tasks in the daily life of a radiologist is assessing new solitary pulmonary nodules. By definition, a solitary pulmonary nodule is an opacity, 3 cm or less in diameter, without associated mediastinal lymphadenopathy or atelectasis. Lesions larger than 3 cm in diameter usually are defined as masses. Most of these represent bronchogenic carcinomas. But even a smaller nodular opacity may represent a relatively early and potentially curable primary bronchogenic carcinoma. The task of the radiologist is to distinguish such a lesion from common benign causes of a pulmonary nodule, especially a granuloma or hamartoma. Proper evaluation is important so that expeditious surgical removal of a potentially curable bronchogenic carcinoma can be accomplished, while concomitantly avoiding unnecessary invasive procedures for the benign conditions. In some surgical series, <50% of resected nodules are due to a malignant neoplasm. \nThe initial evaluation of the suspicious nodule should begin with a comparison of any obtainable previous chest radiographs. Absence of growth for two years generally is indicative of a benign lesion. \n\nLesion calcium and contour are important clues to the nature of a solitary pulmonary nodule. Calcium is easy to recognize when it is deposited in a distinctive pattern\u2014such as a central nidus, in concentric rings, or in a popcorn-like configuration\u2014because of the contrast difference with noncalcified areas of the nodule. But it is much more difficult to ascertain when the calcium is distributed diffusely throughout the lesion in a homogeneous fashion. Since density on a radiographic film is an imprecise parameter, the determination of the calcium content of a nodule that appears homogeneous on standard radiography is often quite subjective. \n\nIn most situations when the plain chest radiograph demonstrates a suspicious nodule, CT should be used because it is the most effective, objective, and widely available radiologic technique to further assess the nature (shape, borders, and density) of a presumed solitary pulmonary nodule. Furthermore, simultaneous assessment of the mediastinum and chest wall is achieved, along with comprehensive evaluation of both lungs. Not infrequently, other pulmonary nodules are detected in the patient suspected to have a single lesion on chest radiography. The alternatives generally available besides CT are surgical resection via thoracotomy or thoracoscopic wedge resection, needle biopsy, or the much less desirable approach of obtaining frequent serial radiographs to monitor possible growth of the lesion.\n\nThe basic assumption underlying the use of CT densitometry is that the presence of calcification in a well-circumscribed pulmonary nodule is a strong indicator of a benign lesion because granulomas contain greater amounts of calcium much more frequently than malignant neoplasms. Obviously, CT would not be warranted in an attempt to distinguish a benign granuloma from a metastasis in a patient who has had a primary osseous or soft-tissue sarcoma (e.g., osteosarcoma or chondrosarcoma) or a mucin-producing adenocarcinoma (e.g., colon, ovary, or breast) that might calcify. Also, metastases that have a propensity to bleed (e.g., choriocarcinoma or melanoma) may have higher CT numbers than soft tissue because of fresh hemorrhage or calcification induced by prior bleeding, but such lesions almost always have irregular margins. \nOccasionally, other features are detected that permit confident diagnosis of a benign lesion, such as lucent areas of fat within the nodule consistent with a hamartoma. Adjacent small satellite nodules suggest a benign etiology, most typically granulomatous infection. Lesions that are not truly nodular on CT, but rather linear or ovoid, also are usually benign. \n\nWhile there are no pathognomonic radiologic features of a malignant pulmonary lesion, thin section CT may strongly suggest that a small peripheral nodule represents a primary lung carcinoma. An outer margin that has a spiculated interface with lung or is hazy and less dense than centrally due to lepidic growth favors a malignant neoplasm. An endobronchial component, convergence with a peripheral pulmonary vein, or focal pleural retraction toward the lesion are additional signs suggesting a malignant lesion. A heterogeneous internal composition, especially with small areas of necrosis, supports the diagnosis of a carcinoma. Small air bronchograms, or focal bubble lucencies (air bronchiolograms), in a poorly marginated pulmonary nodule are more common in a malignant lesion, especially bronchioloalveolar cell carcinoma, and sometimes lymphoma; however, these findings may also occur in benign inflammatory masses. If the lesion is probably malignant, a subsequent or preceding standard post-contrast-enhanced CT examination of the thorax and upper abdomen should be obtained for comprehensive staging, including a search for additional lung lesions.\n \nThe margins of the lesion must be relatively smooth in order to confidently diagnose a benign lesion, since a small percentage of primary bronchogenic carcinomas may contain foci of dystrophic calcification. Such calcification, usually eccentric and stippled, is most typically found in larger lesions that almost always have markedly irregular margins. Relatively large and central carcinoid tumors also may contain foci of calcification; a clue to the proper etiology is their central location immediately adjacent to a secondary bronchus. Most calcified granulomas are in the periphery of the lung. Hamartomas, which also may be peripherally located, can contain calcification. It is sometimes characteristically popcorn or chondroid-like, and at times may be detected in conjunction with fat in the lesion.\n\nBecause thinly collimated scans are noisier and subject to greater statistical variation and it is known that malignant neoplasms may contain calcification, it is generally judicious to obtain follow-up chest radiographic study in 3 to 6 months to corroborate that the calcified nodule depicted on CT has a stable growth pattern. \n\nThe presence or absence of enhancement after intravenous contrast administration may contribute further data in predicting the etiology of a well-circumscribed homogeneous nodule that remains indeterminate. Similarly, FDG PET imaging, which assesses metabolic activity, may have equivalent or superior efficacy in separating a benign from a malignant nodule.", "ACR Code": "65.2811", "Category": "Differential Diagnosis", "Keywords": "granuloma", "Reference": "Lee and Sagel, Computed Body Tomography with MRI Correlation, 3rd ed., Lippincott Williams & Wilkins, 1998, pp393-401." } }, { "U_id": "MPX1803", "TAC": [ "MPX1803_synpic28579", "MPX1803_synpic28581", "MPX1803_synpic28584" ], "MRI": [], "Case": { "Title": "Urothelial Cancer", "History": "82 yo man with 2-month history of painless gross hematuria", "Exam": "Normal physical exam. Urinalysis was consistent with gross hematuria, no crystals were visualized, WBC's were within normal limits.", "Findings": "- Bilateral extrarenal pelves.\n- No evidence of obstructing stones or stones in the bladder. \n- Abnormal layering of contrast material within the posterior aspect of the bladder concerning for clot vs mural mass.\n- Metastatic disease with spread to bilateral hilar and mediastinal lymph nodes.\n- Metastatic disease with spread to left lower lung lobe.", "Differential Diagnosis": "Bladder Cancer - mainly urothelial (transitional cell) cancer\nBPH\nRenal Stones\nCystitis", "Case Diagnosis": "Urothelial Cancer", "Diagnosis By": "Cytology of bladder washings were consistent with high grade urothelial cancer.", "Treatment & Follow Up": "Transurethral Resection of Bladder Tumor, TURBT, with biopsy of remaining bladder and prostatic urethra is normally sufficient for low-grade urothelial cancer. Adjuvant intravesicular therapy may be included for cases of high-grade urothelial cancer. BCG is most commonly used due to its favorable toxicity profile and its efficacy. Six months of BCG therapy is usually required to qualify as BCG resistant tumors. Alternatives for these tumors include adding mitomycin C, anthracyclines, and interferon.\n\nHigh grade tumors are most likely to be muscle-invasive. MVAC is considered first line multi-agent chemotherapy.\n\nFollow-up includes screening cystography for recurrence of disease which is not uncommon.", "Discussion": "This man had metastasis to his right acetabulum and right femur, right lower lung, and caudate lobe of the liver, with large infiltration of mediastinal and perihilar lymph nodes. Up to 45% of new urothelial cancers are high grade and half of those are already invasive. Metastases most commonly travel to lung and liver.\n\nThis patient's initial non-contrast CT did not clearly show the mural mass as it is shown here. His enlarged prostate produced a mass effect indenting the contour of the posterior bladder wall. This highlights the need for careful evaluation of the bladder wall when it is opposed by the prostate and having a properly distended bladder to evaluate thickening of the trabeculated bladder wall.\n\nThis patient's hilar and mediastinal lymphadenopathy with mass effect on the pulmonary vessels aggravated this man's congestive heart failure with frequent admissions for exacerbations to rule out pulmonary embolisms." }, "Topic": { "Title": "Transitional Cell Carcinoma", "Disease Discussion": "Transitional Cell Carcinoma(TCC) is the commonest malignancy of the urinary tract. TCC along with squamous cell carcinoma and adenocarcinoma make up the group of epithelial derived malignancies of the bladder, which together, are responsible for over 90% of the malignancies of the bladder. \n Appropriate screening modalities include urinalysis, IVP, and cystoscopy. These lesions can appear as a papillary or sessile filling defect in the bladder wall on IVP. Differential diagnostic considerations would include multiple non-epithelial primary neoplasms (leiomyoma,fibroma,lymphoma,etc), metastatic disease, inflammatory etiologies, and infectious etiologies.\n If the tumor is superficial (70%), transurethral resection and multiple biopsies are sufficient for both diagnosis and cure. If the tumor is invasive, anatomic staging with CT or MR and sometimes US is indicated. The most common staging sytem used is the TNM classification. Treatment for invasive malignancies include segmental cystectomy, pelvic lymphadenectomy, radical cystectomy, pelvic radiation, and systemic chemotherapy depending on the specific TNM classification.", "ACR Code": "8.3", "Category": "Neoplasm, carcinoma", "Keywords": "TransitionalCellCarcinoma", "Reference": "Bladder Tumors, Encyclopoedia of Medical Imaging, vol. IV:2, Hricak,Hedvig, Amersham (online), 2003." } }, { "U_id": "MPX1807", "TAC": [ "MPX1807_synpic21706" ], "MRI": [], "Case": { "Title": "Ovarian Torsion", "History": "10 year old girl with intermittent lower abdominal pain for approximately one month now presents with severe lower abdominal pain, anorexia and some vomitting. No fever.\n\nThe patient was premenarchal and not sexually active.", "Exam": "Vital signs normal.\nLower abdominal and pelvic tenderness with guarding. No mass palpable.\nWBC 12.5 (4.5-13.5) with 10% PMNs (1.8-8)\nUA >80 ketones otherwise negative\nChem 7 normal except for mild hyperglycemia. \nHCG negative\nAFP tumor marker negative", "Findings": "Contrast enhanced abdominal/pelvic CT with oral and rectal contrast performed first: Approximately 8 cm hetergeneous but predominantly low attenuation midline pelvic mass with multiple peripheral peripherally enhancing cysts or follicles. Anterior and rightward uterine deviation.\nNormal left ovary. Normal appendix.\n\nLimited transabdominal pelvic ultrasound performed next: Large midline hyperechoic pelvic mass with peripherally located cysts/follicles. Venous and arterial Doppler waveforms absent.", "Differential Diagnosis": "CT: ovarian torsion, ovarian/adnexal mass with or without torsion.\n\nUltrasound: ovarian torsion", "Case Diagnosis": "Ovarian Torsion", "Diagnosis By": "Surgical pathology revealed hemorrhagic necrosis of the right ovary. Normal right fallopian tube.", "Treatment & Follow Up": "Over the course of the month, prior to the most current presentation, the patient was treated for constipation a few times as well as a UTI (based on an earlier U/A). Once the diagnosis was established with the current presentation the patient underwent right salpingo-oophorectomy, did well and was discharged home a few days after the surgery.", "Discussion": "This patient was likely experiencing intermittent torsion over the course of a month and experiencing intermittent nonspecific symptoms until the diagnosis was established at her most recent presentation when the CT was performed to evaluate for appendicitis." }, "Topic": { "Title": "Ovarian Torsion", "Disease Discussion": "Ovarian torsion results from rotation of the ovary (with or without the fallopian tube) on its axis resulting in arterial, venous and lymphatic congestion. Pathologically enlarged ovaries from cysts, tumors or paraovarian cysts are at risk for torsion. The most common ovarian neoplasm involved is the benign cystic teratoma. Ovarian torsion may also occur in a normal ovary with a hypermobile adnexa, which may be seen in prepubertal girls and pregnancy, or an excessively long mesosalpinx. Ovarian torsion usually affects young women and more commonly prepubertal girls. There is also an increased risk during pregnancy. \n\nThe patient presentation may be nonspecific and therefore the patients may undergo extensive evaluation before establishing a diagnosis. Patients typically present with sudden onset or gradual severe lower abdominal or pelvic pain with or without nausea, vomiting and fever. Approximately half of patients with ovarian torsion will have a palpable mass. Initially the torsed ovary undergoes venous stasis and if prolonged, congestion and edema progress with arterial stasis resulting in hemorrhagic necrosis and gangrene. Torsion involves the right ovary more than the left and this is thought due to a potential protective effect of the sigmoid mesentery. \n\nRadiologic evaluation of patients with ovarian torsion is optimally performed with ultrasound but often these patients undergo other imaging modalities due to their nonspecific presentation. Ultrasound findings include a markedly enlarged hypo or hyperechoic midline mass with multiple peripheral cysts/follicles measuring 8-12 mm in diameter. There is often good sound transmission due to edema from vascular engorgement. Cul-de-sac free pelvic fluid may be seen in approximately one third. Absence of ovarian arterial and venous Doppler waveforms is helpful to establish the diagnosis but not always reliable due to the dual blood supply by the uterine and ovarian arteries. Also helpful but not always visible is the \u201cwhirlpool\u201d sign from the twisted ovarian pedicle. A complex mass may be identified if there is a cyst or tumor as a lead point. \n\nComputed tomography may be performed as the initial imaging modality. Findings of ovarian torsion on CT include a large adenxal or ovarian mass with smooth wall thickening and no enhancing solid component. Peripherally located follicles may or may not be visible. Other associated findings include thickening of the involved fallopian tube or visualizing the torsed vascular pedicle as a whorled structure adjacent to the ovarian mass. Attenuation greater than 50 on a nonenhanced CT suggests hemorrhagic infarction.\n\nTreatment is immediate surgery. However, most ovaries are not salvageable.", "ACR Code": "8.7", "Category": "Differential Diagnosis", "Keywords": "ovariantorsionultrasound", "Reference": "Dahner, W, Radiology Review Manual, 5th ed, Lippincott, Williams and Wilkins, 2003.\nBlanda, M, Ovarian Torsion, emedicine, April 2002\nMiddleton, W, Ultrasound, The Requisites, 2nd ed, Mosby Inc. 2004." } }, { "U_id": "MPX1815", "TAC": [ "MPX1815_synpic21774" ], "MRI": [], "Case": { "Title": "Lymphangioleiomyomatosis (LAM)", "History": "dyspnea", "Findings": "multiple thin walled cystic structures are seen throughout the lungs on high resolution CT scanning. These are slightly more prominent in the upper lobes. No fibrosis, nodularity, or interstitial thickening is noted. Increased volumes are seen on CXR.", "Differential Diagnosis": "The differential is extremely limited. LAM (lymphangiomamyomatosis) is essentially the only diagnosis. Langerhans histiocytosis can have cystic structures but these are typically more irregular and often times there are assoicated small nodules. Centrilobular emphysema will have cysts with inperceptible walls (LAM has perceptible, thin walls) more concenetrated towards the apices.", "Case Diagnosis": "Lymphangioleiomyomatosis (LAM)", "Diagnosis By": "based on HRCT combined with patient presentation, gender and age", "Discussion": "No angiomyolipomas were visible in the kidneys. The patient has a prior history of pneumothorax." }, "Topic": { "Title": "Lymphangioleiomyomatosis", "Disease Discussion": "Lymphangioleiomyomatosis (LAM) is a rare disease that usually affects women only. It often occurs during the reproductive years with a mean age of onset in the early 30's. Because of the relationship of this disease in women during their reproductive years, many have postulated that estrogen may somehow be related. In the lungs, the pathologic characteristics of LAM are diffuse cystic changes associated with the proliferation of atypical smooth muscle cells. The most common presenting symptoms of LAM are dyspnea, pneumothorax, and cough. It is interesting to note that cabin pressure changes that occur during air travel may increase the risk of pneumothorax in these individuals necessitating chest radiographs upon landing. \n\nRenal angiomyolipomas are often seen in patients with LAM. Renal angiomyolipomas are rare hamartomatous tumors of the kidneys that are composed of smooth muscle, blood vessels, and adipose tissue. These tumors usually do not cause any symptoms, however, they may be associated with flank pain, hematuria, or a palpable mass.", "ACR Code": "68.829", "Category": "Idiopathic or Unknown", "Reference": "Eugene J. Sullivan MD, FCCP. Lymphangioleiomyomatosis: A Review. Chest; December 1998; Volume 114.\n\nElizabeth M. Brunt MD. Benign Tumors of the liver. Clinics in Liver Disease; February 2001; Volume 5, No. 1." } }, { "U_id": "MPX1817", "TAC": [ "MPX1817_synpic52486", "MPX1817_synpic52487", "MPX1817_synpic52488", "MPX1817_synpic52489", "MPX1817_synpic52490" ], "MRI": [], "Case": { "Title": "Combined-type Intraductal Papillary Mucinous Neoplasm", "History": "79 y/o white male, preoperative evaluation pending CABG. History of hypertension, hyperlipidemia and diabetes. Recent 50 lb weight loss.", "Exam": "Slender, elderly male. No abdominal pain, no localized symptoms.", "Findings": "Lobulated multicystic lesion which involves the pancreatic head and uncinate process, predominantly. The main pancreatic duct is dilated to 10mm and there is also branch duct involvement within the pancreatic body. No mural nodules or solid masses are identified.", "Differential Diagnosis": "\u2022 Chronic pancreatitis\n\u2022 Pancreatic pseudocyst\n\u2022 Mucinous cystic neoplasm\n\u2022 Serous cystadenoma", "Case Diagnosis": "Combined-type Intraductal Papillary Mucinous Neoplasm", "Diagnosis By": "Pathological proven with tissue biopsy", "Treatment & Follow Up": "In this older patient with multiple comorbidities and surgical risk factors, periodic monitoring is currently planned.", "Discussion": "Intraductal papillary mucinous neoplasm (IPMN), also referred to in previous literature as intraductal papillary mucinous tumor (IPMT) is a low-grade malignancy that arises from the epithelial lining of the main or branch pancreatic ducts, and is characterized by excessive mucin production. IPMN is classified into three types: branch pancreatic duct type, main pancreatic duct type, and combined type. Combined type is the most common.\n\nIPMN presents clinically with diarrhea, pain, weight loss, acute pancreatitis and diabetes. Typical age of onset is 60-80 y/o, more commonly in males.\n\nCT findings for branch pancreatic duct type include a thin, irregular and peripheral lobulated multicystic lesion (\u201cgrape-like\u201d clusters).The main pancreatic duct type appears as a markedly dilated and tortuous main pancreatic duct. Polypoid lesions may be seen lining the main duct. The combined type appears as a multicystic lesion (commonly within the uncinate process) which is contiguous with a markedly dilated and tortuous main pancreatic duct. MRCP will show communication between the dilated duct and cystic lesions.\n\nThe differential diagnosis for IPMN includes chronic pancreatitis, pancreatic pseudocyst, mucinous cystic neoplasm and serous cystadenoma. This patient had no history of pancreatitis. \n\nImaging features of IPMN with invasive carcinoma may include mural nodularity or solid mass measuring 3-10 mm, diffuse or multifocal main duct involvement, main or combined duct types, main pancreatic duct measuring > 10-15 mm, branch duct type measuring > 3 cm or mural nodularity, common bile duct > 15 mm, or evidence of metastases. Generally, main duct and combined duct types are resected in good surgical candidates. Branch duct type IPMN without suggestion of invasive carcinoma may be monitored. Although all IPMNs are felt to have malignant potential.\n\nReferences:\n\nLim JH, et al. Radiologic spectrum of intraductal papillary mucinous tumor of the pancreas. Radiographics. 2001. 21(2):323-40.\n\nPrasad SR, et al. Intraductal papillary tumors of the pancreas. Abdom Imaging. 2003. 28(3):357-65.\n\nTaouli B, et al. Intraductal papillary mucinous tumors of the pancreas: features with multimodality imaging. J Comput Assist Tomogr. 2002. 26(2):223-31." }, "Topic": { "Title": "Intraductal Papillary Mucinous Neoplasm", "Disease Discussion": "Lesion/Condition Name: Intraductal Papillary Mucinous Neoplasm\n\nCell of Origin: Epithelial cells of the pancreas\n\nSynonyms: IPMT, IPMN\n\nICD-0 code: 157.0\n\nAssociations/Predisposing Factors: Diabetes, Pancreatitis\n\nCommon Locations: Pancreas\n\nDemographics: M>F, 60-80y/o.\n\nRadiology: Multiloculated cystic lesion within the pancreas.\n\nPrognosis and Treatment: Generally slow-growing. Surgical intervention if fast growing, or younger patients.", "ACR Code": "7.3", "Category": "Neoplasm, malignant (NOS)", "Keywords": "IntraductalPapillaryPancreas", "Reference": "Lim JH, et al. Radiologic spectrum of intraductal papillary mucinous tumor of the pancreas. Radiographics. 2001. 21(2):323-40.\n\nPrasad SR, et al. Intraductal papillary tumors of the pancreas. Abdom Imaging. 2003. 28(3):357-65.\n\nTaouli B, et al. Intraductal papillary mucinous tumors of the pancreas: features with multimodality imaging. J Comput Assist Tomogr. 2002. 26(2):223-31." } }, { "U_id": "MPX1832", "TAC": [ "MPX1832_synpic21084" ], "MRI": [ "MPX1832_synpic21083" ], "Case": { "Title": "Pancreatic Divisum", "History": "45 year old male with recurrent pancreatitis. No history of alcohol use or gallstones.", "Exam": "amylase - 648", "Findings": "CT abdomen: parallel pancreatic ducts\n\nMRCP: Dorsal duct of Santorini tranversely crossing the bile duct to enter the minor papilla.", "Differential Diagnosis": "Persistent duct of Santorini", "Case Diagnosis": "Pancreatic Divisum", "Diagnosis By": "ERCP" }, "Topic": { "Title": "Pancreatic Divisum", "Disease Discussion": "Pancreatic divisum is an embryologic malformation of the pancreatic ductal system and the most common congenital anomaly of the human pancreas. The normal embryology of the pancreas is the pancreas forms from a ventral anlage that forms the inferior pancreatic head and a dorsal anlage that forms the superior pancreatic head and the body and tail of the pancreas. At approximately 7 weeks gestation, the two anlages fuse, and in over 90% of individuals their ducts fuse. The normal anatomy is the duct draining the dorsal anlage joins the duct draining the ventral anlage to enter the major ampulla; thus the major route of pancreatic drainage is established through the duct of Wirsung at the major ampulla. In 5-7% of individuals, there is failure of fusion of the dorsal and ventral anlage, resulting in pancreatic divisum. The predominant drainage (body/tail) is performed by dorsal duct of Santorini through the minor papilla, the head is drained by ventral duct of Wirsung through the major papilla.Many of the patients present with acute idiopathic pancreatitis.", "ACR Code": "7.1", "Category": "Congenital, malformation", "Keywords": "Pancreatic divisumidiopathic pancreatitis", "Reference": "1.Fulcher AS, Turner MA. MR Pancreatography: A useful tool for evaluating pancreatic disorders. Radiographics 1999; 19:5-24.\n2.Agha FP, Williams KD. Pancreas Divisum: incidence, detection, and clinical significance. Am J Gastroenterol. 1987; Apr;82(4):315-20.", "External Links": "http://www.surgery.usc.edu" } }, { "U_id": "MPX1834", "TAC": [ "MPX1834_synpic40778", "MPX1834_synpic40780", "MPX1834_synpic40781" ], "MRI": [], "Case": { "Title": "Pseudomembranous Colitis", "History": "22 year old male OIF patient s/p blast injury and several weeks of antibiotic therapy.", "Exam": "Fever, leukocytosis and diarrhea.\nAbdominal exam limited.", "Findings": "Abdominal CT demonstrates diffuse colonic wall thickening and a shaggy endoluminal contour. Mucosal and submucosal edema results in \"accordian pattern\" or \"target sign.\"", "Differential Diagnosis": "Pseudomembranous Colitis\nInflammatory bowel disease\nTyphlitis\nIschemic Colitis\nRadiation Colitis\nOther Infectious Colitis", "Case Diagnosis": "Pseudomembranous Colitis", "Diagnosis By": "Fecal culture positive for Clostridium Difficile.", "Treatment & Follow Up": "N/A", "Discussion": "CT findings in this patient were consistent with a diagnosis of Pesudomembranous Colitis. While the \"accordian sign\", produced by diffuse bowel wall thickening from mucosal and submucosal edema, is not pathgnomonic for pseudo membranous colitis, it is highly suggestive of the diagnosis. In this case, imaging findings were confirmed with fecal cultures." }, "Topic": { "Title": "Pseudomembranous Colitis", "Disease Discussion": "Many of the findings of colonic inflammation are fairly characteristic of the specific type of colitis that is present. CT findings used to differentiate one form of colitis from another include:\n\nDegree of mural thickening\nExtent to which the layers of the thickened colonic wall are visible\nPresence of fistulae or abscesses\nAnatomic distribution of the CT abnormalities in the large and small intestine\n\n \nUlcerative colitis involves the rectum in virtually all patients. It extends proximally in one continuous segment to involve the remainder of the colon to a variable extent. Computed tomography shows mild-to-moderate, concentric, mural thickening. The mucosa, the low-density, thickened submucosa, and the serosa are usually visible as three distinct layers. These abnormalities sometimes give the rectum a target-like appearance. In most patients, there is loss of the normal haustral contour and the colon is shortened. Fistulae and pericolonic abscesses are rare. Proliferation of the perirectal fat is also commonly seen.\n\nIn patients with Crohn disease (granulomatous colitis), the entire colon and distal small bowel may be involved; the most common sites are the terminal ileum, right colon, and rectum. Normal intervening segments, so-called skip areas, often separate affected segments of bowel. The colonic wall tends to be thicker than in patients with ulcerative colitis. The layers of the affected bowel wall may be similar in CT attenuation, giving the wall a homogeneous appearance, but this is not always the case. Typically, there is inflammation of the pericolonic fat, which appears as a diffuse, hazy increase in its CT attenuation, reflecting the transmural nature of this disease. As in patients with ulcerative colitis, carcinoma can occasionally develop. In this setting, adenocarcinoma is sometimes scirrhous in type and its CT appearance can mimic that of a benign inflammatory stricture. Fistulae are common in patients with granulomatous colitis, particularly in the perirectal area. Abdominal abscesses also may develop adjacent to severely affected segments of bowel.\n\nPseudomembranous colitis is caused by toxins produced by Clostridium difficile, a gram-positive bacterium that colonizes the gastrointestinal tract in some patients receiving antibiotic therapy. CT shows characteristic marked thickening of the colonic wall and interhaustral folds, which are sometimes so severe as to nearly obliterate the colonic lumen. The entire colon is usually involved, but involvement confined to the right colon is not unusual. Strand-like pattern of edema in the pericolonic fat is present in nearly half of cases. Fifteen percent of patients have ascites.\n\nCytomegalovirus colitis is seen in the setting of an immunocompromised patient. Findings mimic those of C. difficile disease, with profound thickening of the colonic wall and haustra and pericolonic edema. In both conditions, the mural thickening is largely the result of an edematous submucosal layer that has a low CT attenuation value. \n\nDisseminated histoplasmosis is being seen with increasing frequency because of the susceptibility of patients with AIDS to this disease, especially in endemic areas. Colonic lesions often have an \u201capple-core\u201d appearance on barium enema, which appear on CT as one or more focal areas of mural thickening with adjacent adenopathy of mixed attenuation. Usually, tissue diagnosis is required to separate these lesions from adenocarcinoma.\n\nColitis due to Schistosoma japonicum presents as left colon mild mural thickening with obliteration of the normal haustral pattern. Frequently, there is a peculiar pattern of curvilinear calcification in the colonic wall. Since dense radioopaque contrast can obscure these calcifications, water should be considered as a colonic contrast agent when schistosomiasis is considered a possible etiology. \n\nBeh?et disease most commonly involves the ileocecal region and ascending, but abnormalities may occur anywhere in the colon. Marked focal thickening of the colonic wall surrounds isolated large cecal ulcers. This appearance may easily be confused with the ileocecal mural thickening of tuberculosis, which may be distinguished based on associated with low-density caseating lymph nodes in the mesentery. In the setting of neutropenia, typhlitis may present with low-attenuation cecal mural thickening, with or without mural gas.\n\nFinally, a noninflammatory etiology that must be considered is ischemia. This classically involves the descending colon and may involve the spenic flexure and sigmoid region. Expect to see a segmental area of mural thickening which may be severe enough to narrow the lumen.", "ACR Code": "7.2", "Category": "Infection, bacteria", "Reference": "Lee JK, Sagel SS, Stanley RJ, Heiken JP, ed. Computed Body Tomography with MRI Correlation, 3rd ed. Lippincott Williams & Wilkins, 1998, pp759-61." } }, { "U_id": "MPX1825", "TAC": [ "MPX1825_synpic24340" ], "MRI": [], "Case": { "Title": "Parosteal osteosarcoma", "History": "24 y/o male with right posterior knee mass", "Exam": "Firm, tender mass of the posterior right knee.\nNormal CBC, Metabolic Panel, and liver enzymes.", "Findings": "Radiographs: Large mass with well defined margins emanating from posterior cortex of the distal right femur. Radiolucent line, visible on the lateral radiograph separates tumor from cortex .\n\nMRI: Posterior cortical surface distal femoral diaphysis mass, 7.3cm x 6.7cm x 8.3cm, with heterogeneous signal intensity. On T1-weighted MR image shows a heterogenously low signal intensity mass signal. T2-weighted MR image shows a well-defined parosteal mass juxtaposed to the cortex with heterogenous high signal intensity mass posterior to it. T2 post gadolinium study shows low signal intensity in posterior mass correlating with high signal intensity region on T2 image consistent with necrosis. Ossification center at base of mass adjacent to cortical bone. No popliteal vessel invasion, no adjacent soft tissue invasion. No femoral distant metastasis.", "Differential Diagnosis": "Parosteal osteosarcoma, juxtacortical myositis ossificans, sessile osteochondroma, periosteal osteosarcoma", "Case Diagnosis": "Parosteal osteosarcoma", "Diagnosis By": "Confirmed by biopsy", "Treatment & Follow Up": "Mass was surgically resected with no further evidence of metastasis on follow-up studies.", "Discussion": "Parosteal osteosarcomas are uncommon malignant bone tumors that account for approximately 3% of osteosarcomas. They occur in adults between the 2nd and 5th decades and affect both males and females equally. They typically present with insidious onset of symptoms of pain, swelling, and a palpable mass. The large size of many of these tumors on presentation is due to a delay in the patient consulting a physician because of the slow onset of symptoms. Parosteal osteosarcomas occur nearly exclusively in long tubular bones, most commonly in the femur, which accounts for 65% of cases. in this bone, they typically arise on the posterior surface of the distal femur in the metaphyseal region.\n\nOn plain radiographs, parosteal osteosarcomas appear as a large radiodense, oval or spheroid mass with smooth lobulated or irregular margins, attached in a sessile manner to a possibly thickened external cortex. A thin radiolucent line or cleavage plane separates the tumor from the underlying bone and is caused by a 2-3mm fibrous membrane. As the lesion grows in size, the radiolucent line is obscured by the tumor growing circumferentially around the bone.\n\nOssification of the tumor extends from the base of the lesion to its periphery in contrast to myositis ossificans, which, when mature, shows a zonal pattern with peripheral ossification.\n\nOn CT images, foci of radiolucencies in the superficial parts of the tumor may represent low-grade malignant cartilaginous, fibrous tissue, or entrapped fat and trabeculae, whereas, more central radiolucencies may correlate with high-grade dedifferentiated tumor.\n\nMRI should be done to evaluate the extent of the tumor. \n\nAt imaging studies, parosteal sarcoma should be differentiated from myositis ossificans, sessile osteochondroma, periosteal osteosarcoma, and ossifying soft tissue tumors arising from the cortical bone surface.\n\nMyositis ossificans may present with a history of trauma followed by rapid development of a soft tissue mass, which ossifies at the periphery initially as opposed to the base.\n\nSessile osteochondroma should show a continuity between both the cortex and spongiosa of the underlying normal bone. \n\nPeriosteal osteosarcoma is smaller and has a distinctive spiculated periosteal reaction. \n\nOther ossifying masses from the cortex such as chondrosarcomas, high-grade osteosarcomas and osteoma should be differentiated by their combined imaging, clinical and histologic findings. \n\nThe treatment of parosteal sarcoma is surgical resection without adjuvant chemotherapy.\n\nParosteal osteosarcomas are uncommon malignant bone tumors that account for approximately 3% of osteosarcomas. They occur in adults between the 2nd and 5th decades and affect both males and females equally. They typically present with insidious onset of symptoms of pain, swelling, and a palpable mass. The large size of many of these tumors on presentation is due to a delay in the patient consulting a physician because of the slow onset of symptoms. Parosteal osteosarcomas occur nearly exclusively in long tubular bones, most commonly in the femur, which accounts for 65% of cases. in this bone, they typically arise on the posterior surface of the distal femur in the metaphyseal region.\n\nOn plain radiographs, parosteal osteosarcomas appear as a large radiodense, oval or spheroid mass with smooth lobulated or irregular margins, attached in a sessile manner to a possibly thickened external cortex. A thin radiolucent line or cleavage plane separates the tumor from the underlying bone and is caused by a 2-3mm fibrous membrane. As the lesion grows in size, the radiolucent line is obscured by the tumor growing circumferentially around the bone.\n\nOssification of the tumor extends from the base of the lesion to its periphery in contrast to myositis ossificans, which, when mature, shows a zonal pattern with peripheral ossification.\n\nOn CT images, foci of radiolucencies in the superficial parts of the tumor may represent low-grade malignant cartilaginous, fibrous tissue, or entrapped fat and trabeculae, whereas, more central radiolucencies may correlate with high-grade dedifferentiated tumor.\n\nMRI should be done to evaluate the extent of the tumor. \n\nAt imaging studies, parosteal sarcoma should be differentiated from myositis ossificans, sessile osteochondroma, periosteal osteosarcoma, and ossifying soft tissue tumors arising from the cortical bone surface.\n\nMyositis ossificans may present with a history of trauma followed by rapid development of a soft tissue mass, which ossifies at the periphery initially as opposed to the base.\n\nSessile osteochondroma should show a continuity between both the cortex and spongiosa of the underlying normal bone. \n\nPeriosteal osteosarcoma is smaller and has a distinctive spiculated periosteal reaction. \n\nOther ossifying masses from the cortex such as chondrosarcomas, high-grade osteosarcomas and osteoma should be differentiated by their combined imaging, clinical and histologic findings. \n\nThe treatment of parosteal sarcoma is surgical resection without adjuvant chemotherapy.\n\nThe major prognostic factors are the grade of the lesion and presence of intramedullary involvement. Low-grade lesions have a better prognosis than high-grade lesions. Intramedulary invasion has a poor prognosis. It is extremely rare for distant metastasis to occur without intramedulary involvement.\n\nAnother poor prognostic factor is progressive dedifferentiation from low-grade to high-grade osteosarcoma. This has been reported to develop with recurrence after surgical resection or with undetected conventional parosteal osteosarcoma over a long period of time. The incidence of dedifferentiation of parosteal osteosarcomas is reported can be as frequent as 20-25% of patients. The posterior aspect of the femur is the usual site for dedifferentiated osteosarcoma.\n\nAs mentioned earlier, parosteal osteosarcoma is the most favorable osteosarcoma variant. Patients with conventional parosteal osteosarcoma typically do well after resection with a long-term survival rate of 80-90%." }, "Topic": { "Title": "Parosteal osteosarcoma", "Disease Discussion": "Parosteal osteosarcomas are uncommon malignant bone tumors that account for approximately 3% of osteosarcomas. They occur in adults between the 2nd and 5th decades and affect both males and females equally. They typically present with insidious onset of symptoms of pain, swelling, and a palpable mass. The large size of many of these tumors on presentation is due to a delay in the patient consulting a physician because of the slow onset of symptoms. Parosteal osteosarcomas occur nearly exclusively in long tubular bones, most commonly in the femur, which accounts for 65% of cases. in this bone, they typically arise on the posterior surface of the distal femur in the metaphyseal region.\n\nOn plain radiographs, parosteal osteosarcomas appear as a large radiodense, oval or spheroid mass with smooth lobulated or irregular margins, attached in a sessile manner to a possibly thickened external cortex. A thin radiolucent line or cleavage plane separates the tumor from the underlying bone and is caused by a 2-3mm fibrous membrane. As the lesion grows in size, the radiolucent line is obscured by the tumor growing circumferentially around the bone.\n\nOssification of the tumor extends from the base of the lesion to its periphery in contrast to myositis ossificans, which, when mature, shows a zonal pattern with peripheral ossification.\n\nOn CT images, foci of radiolucencies in the superficial parts of the tumor may represent low-grade malignant cartilaginous, fibrous tissue, or entrapped fat and trabeculae, whereas, more central radiolucencies may correlate with high-grade dedifferentiated tumor.\n\nMRI should be done to evaluate the extent of the tumor. \n\nAt imaging studies, parosteal sarcoma should be differentiated from myositis ossificans, sessile osteochondroma, periosteal osteosarcoma, and ossifying soft tissue tumors arising from the cortical bone surface.\n\nMyositis ossificans may present with a history of trauma followed by rapid development of a soft tissue mass, which ossifies at the periphery initially as opposed to the base.\n\nSessile osteochondroma should show a continuity between both the cortex and spongiosa of the underlying normal bone. \n\nPeriosteal osteosarcoma is smaller and has a distinctive spiculated periosteal reaction. \n\nOther ossifying masses from the cortex such as chondrosarcomas, high-grade osteosarcomas and osteoma should be differentiated by their combined imaging, clinical and histologic findings. \n\nThe treatment of parosteal sarcoma is surgical resection without adjuvant chemotherapy.\n\nParosteal osteosarcomas are uncommon malignant bone tumors that account for approximately 3% of osteosarcomas. They occur in adults between the 2nd and 5th decades and affect both males and females equally. They typically present with insidious onset of symptoms of pain, swelling, and a palpable mass. The large size of many of these tumors on presentation is due to a delay in the patient consulting a physician because of the slow onset of symptoms. Parosteal osteosarcomas occur nearly exclusively in long tubular bones, most commonly in the femur, which accounts for 65% of cases. in this bone, they typically arise on the posterior surface of the distal femur in the metaphyseal region.\n\nOn plain radiographs, parosteal osteosarcomas appear as a large radiodense, oval or spheroid mass with smooth lobulated or irregular margins, attached in a sessile manner to a possibly thickened external cortex. A thin radiolucent line or cleavage plane separates the tumor from the underlying bone and is caused by a 2-3mm fibrous membrane. As the lesion grows in size, the radiolucent line is obscured by the tumor growing circumferentially around the bone.\n\nOssification of the tumor extends from the base of the lesion to its periphery in contrast to myositis ossificans, which, when mature, shows a zonal pattern with peripheral ossification.\n\nOn CT images, foci of radiolucencies in the superficial parts of the tumor may represent low-grade malignant cartilaginous, fibrous tissue, or entrapped fat and trabeculae, whereas, more central radiolucencies may correlate with high-grade dedifferentiated tumor.\n\nMRI should be done to evaluate the extent of the tumor. \n\nAt imaging studies, parosteal sarcoma should be differentiated from myositis ossificans, sessile osteochondroma, periosteal osteosarcoma, and ossifying soft tissue tumors arising from the cortical bone surface.\n\nMyositis ossificans may present with a history of trauma followed by rapid development of a soft tissue mass, which ossifies at the periphery initially as opposed to the base.\n\nSessile osteochondroma should show a continuity between both the cortex and spongiosa of the underlying normal bone. \n\nPeriosteal osteosarcoma is smaller and has a distinctive spiculated periosteal reaction. \n\nOther ossifying masses from the cortex such as chondrosarcomas, high-grade osteosarcomas and osteoma should be differentiated by their combined imaging, clinical and histologic findings. \n\nThe treatment of parosteal sarcoma is surgical resection without adjuvant chemotherapy.\n\nThe major prognostic factors are the grade of the lesion and presence of intramedullary involvement. Low-grade lesions have a better prognosis than high-grade lesions. Intramedulary invasion has a poor prognosis. It is extremely rare for distant metastasis to occur without intramedulary involvement.\n\nAnother poor prognostic factor is progressive dedifferentiation from low-grade to high-grade osteosarcoma. This has been reported to develop with recurrence after surgical resection or with undetected conventional parosteal osteosarcoma over a long period of time. The incidence of dedifferentiation of parosteal osteosarcomas is reported can be as frequent as 20-25% of patients. The posterior aspect of the femur is the usual site for dedifferentiated osteosarcoma.\n\nAs mentioned earlier, parosteal osteosarcoma is the most favorable osteosarcoma variant. Patients with conventional parosteal osteosarcoma typically do well after resection with a long-term survival rate of 80%.", "ACR Code": "4.3", "Category": "Neoplasm, sarcoma", "Keywords": "Osteosarcoma, parostealBone tumor, malignant", "Reference": "Resnick D, Kyriakos M, Greenway G. Tumors and Tumor-like lesions of Bone: Imaging and Pathology of Specific Lesions. In Resnick D, ed. Diagnosis of Bone and Joint Disorders 4th ed., 2002; 3825-29.\nKricun, M. Tumors of Long Bones. In Kricun M, ed. Imaging of Bone Tumors, 1993; 132-34.\nSheth DS, Yasko AW, Raymond AK, et al. Conventional and dedifferentiated parosteal osteosarcoma: Diagnosis, treatment, and outcome. Cancer 1996; 78:2136-45.\nStoker DJ, Saifuddin A. Bone Tumors: Malignant Lesions. In Grainger R, ed. Grainger and Allison\u2019s Diagnostic Radiology: A Textbook of Medical Imaging, 4th ed, 2001; pp. 1885-6." } }, { "U_id": "MPX1844", "TAC": [ "MPX1844_synpic20208" ], "MRI": [], "Case": { "Title": "Splenic laceration without coil embolization", "History": "20 yo male mountain biking accident victim with a chief complain of abdominal pain.", "Findings": "CT demonstrates parenchymal splenic injuries and may demonstrate active extravasation of contrast if active hemorrhage is present. Fluid densities within the dependent portions of the peritoneal cavity are often seen.\n\nAngiography may demonstrate active hemorrhage and or mass effect secondary to adjacent hematoma causing compression. Active hemorrhage would warrant proximal coil embolization to improve hemodynamic status.", "Differential Diagnosis": "Splenic laceration with or without frank hemorrhage, other visceral trauma with subsequent peritoneal fluid collections.", "Case Diagnosis": "Splenic laceration without coil embolization", "Diagnosis By": "Imaging", "Treatment & Follow Up": "Due to the spleen\u2019s key immunologic function in the fighting of infections with encapsulated organisms, splenectomy is a last resort with conservative therapy currently advocated. As a result, arteriography with the option of embolization therapy is indicated after lacerations are evident on CT imaging of hemodynamically stable patient. The goal of embolization is essentially to reduce the main arterial pressure head via the placement of coils proximally within the splenic artery. Infarctions are thus prevented due to sufficient blood flow around the occlusive coils via collateral areteries already present.", "Discussion": "The spleen is the most frequently injured abdominal organ in blunt trauma accounting for approximately a quarter of all blunt injuries to the abdominal viscera. Although peritoneal lavage can be diagnostic, CT has superceded its usage; although, some studies have demonstrated that this modality can underestimate the degree of splenic injury. CT classification of splenic injuries has been proposed as follows:\n\nClass I Capsular disruption and/or subcapsular hematoma without significant parenchymal injury.\n\nClass II Single or multiple capsular and parenchymal defects that do not extend into the hilum or involve major vessels.\n\nClass III Deep lacerations extending into the hilum and involving major vessels.\n\nClass IV Shattered spleen.\n\nAlthough only 30 to 40% of patients present with hypotension, hemodynamic instability can be a presenting symptom that requires immediate intervention. Abdominal pain often localized to the left upper quadrant can be present. Left shoulder pain also known as Kehr\u2019s sign may be exhibited upon supine or Trendelenburg positioning. Balance\u2019s sign represents free peritoneal fluid with dullness to percussion overlying the paracolic gutters, which disappears with positional changes." }, "Topic": { "Title": "Splenic laceration with coil embolization", "Disease Discussion": "The spleen is the most frequently injured intraperitoneal organ in blunt abdominal trauma. Clinically, patients present with an appropriate history as well as the possible presence of upper abdominal, left upper quadrant, flank, or referred left shoulder pain. Plain film findings of splenic injury can be subtle and include medial displacement of the stomach, downward or medial displacement of the splenic flexure, elevation of the left hemidiaphragm, scoliosis of the spine with leftward concavity, sentinel loops over the left upper quadrant, pleural effusions or atelectasis at the left lung base, and associated rib fractures. CT is greater than 95% sensitive in the detection of splenic trauma but is not reliable with respect to determining the need for surgical intervention. Types of splenic injury include intrasplenic laceration, splenic fracture, subcapsular hematoma, perisplenic hematoma, and delayed splenic rupture. Coil embolization of the spleen is performed by placing coils proximally within the splenic artery (possible because of the spleen\u2019s rich collateral network).", "ACR Code": "7.4", "Category": "Trauma", "Keywords": "TraumaSplenic lacerationEmbolization", "Reference": "1. Dahnert W. Radiology Review Manual, 4th ed. Williams & Wilkins: 662.\n2. Swischuk LE. Emergency Imaging of the Acutely Ill or Injured Child, 4th ed. Lippincott Williams & Wilkins: 245-247." } }, { "U_id": "MPX1852", "TAC": [ "MPX1852_synpic29134" ], "MRI": [], "Case": { "Title": "Interstitial Lung Disease", "History": "63 yo male with hx of dermatomyositis c/o increased SOB", "Exam": "Pulmonary - Bilbasilar rhonci, increased SOB\n\nCBC - 5.2/13.8/40.9/241\nBMP - 145/3.4/104/31/13/1.0/87\nCK - 104", "Findings": "Pulmonary fibrosis in a bibasilar pattern. Characterisitc honeycomb pattern commonly seen in interstitial lung disease.", "Differential Diagnosis": "Dermatomyositis \nOther Connective Tissue Disease\nAsbestos\nRadiation\nMedication Side Effect", "Case Diagnosis": "Interstitial Lung Disease", "Diagnosis By": "Radiographically", "Treatment & Follow Up": "High dose prednisone 1 mg/kg\nMethotrexate", "Discussion": "Interstitial lung disease is seen in approximately 10% of cases of dermatomyositis." }, "Topic": { "Title": "Interstitial Lung Disease", "Disease Discussion": "Discussion - Interstitial lung disease is characterized by diffuse parenchymal lung involvement, primarily affecting the tissue between the alveoli. It is known to be caused by over 200 conditions with asbestos, radiation, aspiration pneumonia, connective tissue disease, chemotherapy drugs, and amyloidosis being some of the most common causes. Interstitial lung disease is believed to result from inflammation and secondary fibrosis. Patients often present with progressive exertional dyspnea or non productive cough. Hemoptysis, chest pain, and wheezing may also be present. Dermatomyositis is an inflammatory myopathy that results in interstitial lung disease in approximately 10% of patients with the disease. It causes skeletal muscle weakness, affects both children and adults, and tends to affect women more than men. A characteristic rash often accompanies or more often precedes the disease helping differentiate it clinically from polymyositis. The rash is often heliotrope (blue-purple discoloration) and tends to affect the upper eyelids with associated edema. A flat red rash on the face and upper trunk, as well as erythema of the knuckles with raised violaceous scaly eruption (Gottron Rash) may also be present. Diagnosis is confirmed by examining serum muscle enzymes, EMG findings, and muscle biopsy. Treatment options include high dose prednisone 1mg/kg, azathioprine or methotrexate, or IVIG. This patient's PA/Lateral CXR shows diffuse bilateral reticular and nodular opacities consistent with interstitial lung disease. Chest CT scan w/ contrast shows pulmonary fibrosis in a bibasilar distribution and characteristic honeycombing pattern.", "ACR Code": "6.0", "Category": "Systemic, Generalized", "Keywords": "Interstitial Lung DiseaseDermatomyositisHoneycomb Lung", "Reference": "Braunwald, Fauci, et al. Harrison\u2019s Principles of Internal Medicine. United States of America: McGraw Hill, 2001." } }, { "U_id": "MPX1853", "TAC": [ "MPX1853_synpic17932" ], "MRI": [], "Case": { "Title": "orbital osteoid osteoma", "History": "35 year old male with lumbar pain of unclear etiology.", "Exam": "Normal lumbar spine.", "Findings": "Normal spine, with incidentally noted intense focal uptake at the superolateral left orbit.", "Differential Diagnosis": "metastatic disease\nBrodie's abcess\nosteoid osteoma", "Case Diagnosis": "orbital osteoid osteoma", "Diagnosis By": "Surgical excisional biopsy", "Treatment & Follow Up": "UPON REVIEWING THE BONE SCAN WITH HIS PHYSICIAN, THE PATIENT REPORTED INTENSE LEFT FRONTAL HEADACHE AND LEFT FACIAL NEURALGIA IN THE V1/V2 DISTRIBUTION.", "Discussion": "SEE FACTOID" }, "Topic": { "Title": "orbital osteoid osteoma", "Disease Discussion": "Osteoid osteoma is a benign osteoid nidus with a center that may be radiographically sclerotic or lucent, and a surrounding zone of reactive bone formation. The lesion is typically subcentimeter, unifocal, and causes pain that is worst at night and relieved within 20-25 minutes of taking aspirin. It can occur virtually anywhere in the skeleton, but most commonly appears in the femoral neck, tibial midshaft, and diaphysis of other long bones. Rarely, osteoid osteomas occur in the bones of the face. Patients are usually between 10 and 35 years old.\n\nConventional radiography and CT imaging typically reveal a benign-appearing, cortical, medullary, or subperiosteal radiolucency surrounded by a well-defined zone of sclerosis. Often, a radiodense nidus is seen centrally. 90% of osteoid osteomas show intense focal uptake on bone scan. CT is becoming the diagnostic modality of choice, as its capacity for excellent bony detail easily demonstrates the characteristic sclerotic nidus within the sclerotic-rimmed lucency, and allows precise location of the lesion. MRI may define a nidus that remains unapparent on CT or scintigraphy, but is not generally employed.\n\nDifferential diagnosis includes stress fracture, cortical abcess, and intracortical osteosarcoma in cortical lesions; Brodie's abcess, bone island, and osteoblastoma in medullary lesions. The characteristic appearance of osteoid osteoma often is enough to confirm the diagnosis. Osteoid osteomas lack the lucent lines of stress fractures, the lucent tracts of abcesses, the bulging cortical disruptions of osteosarcoma, the periosteal reaction of osteoblastoma, and the normal bone scan and \u201cbrush\u201d trabecular borders of bone islands. Intense focal uptake on bone scan may confirm the diagnosis. \n\nThese lesions are treated by either curettage or percutaneous radiofrequency ablation, often with CT or gamma camera guidance. Anything less than total resection or ablation of the central nidus risks a high rate of recurrence.", "ACR Code": "2.3", "Category": "Neoplasm, benign", "Keywords": "osteoid osteomaorbitneuralgia", "Reference": "1.\tOrthopedic Radiology A Practical Approach. Greenspan, A. 550-561. Lippincott Williams and Wilkins, 2000.\n\n2.\tIs osteoid osteoma an iodophilic lesion?: pathologically proved osteoid osteoma of nasal bone first seen on whole-body iodine-131 scan.\nRachinsky I - Clin Nucl Med - 01-AUG-2003; 28(8): 696-8\nFrom NIH/NLM MEDLINE\n\n3.\tOsteoid osteoma in the mandible.\nIda M - Dentomaxillofac Radiol - 01-NOV-2002; 31(6): 385-7\nFrom NIH/NLM MEDLINE" } }, { "U_id": "MPX1856", "TAC": [ "MPX1856_synpic21474", "MPX1856_synpic21475" ], "MRI": [], "Case": { "Title": "Ameloblastoma", "History": "A 22 yo military basic trainee had routine screening dental evaluation - no symptoms reported.", "Exam": "Firm mandibular lesion. Nonmobile. Nontender to palpation.", "Findings": "Radiographic evaluation of the mandible demonstrated a multilocular cystic lesion of the right mandible arising along the crown of a tooth at the ramus of the mandible. There is significant expansion of the bone with cortical disruption medially.", "Differential Diagnosis": "Odontogenic keratocyst\nDentigerous cyst\nAmeloblastoma\nCemento-osseous dysplasia", "Case Diagnosis": "Ameloblastoma", "Diagnosis By": "Pathologically proven resection", "Treatment & Follow Up": "The lesion was treated by enbloc resection of the lesion and surrounding mandible." }, "Topic": { "Title": "Ameloblastoma", "Disease Discussion": "Ameloblastoma is a benign neoplasm originating from odontogenic epithelium and represent approximately 10% of odontogenic tumors. They occur predominantly in the 3rd through 5th decades of life, but are seen in a wide age range of patients and demonstrate no gender or racial predilection. Most ameloblastomas occur in the ramus and posterior body of the mandible (80% of cases) and patients usually present with a slow-growing, painless mass. Although usually considered benign, ameloblastoma can demonstrate locally aggressive behavior.\n\nAmeloblastoma is typically expansile with an osseous shell that represents the involved bone. They can perforate the lingual cortex of the mandible and extend into the adjacent soft tissues. Ameloblastomas can vary in radiographic appearance. Some appear as well-defined, unilocular, well-corticated, lucent lesions that are often associated with the crowns of impacted or unerupted teeth. \n\nAs a result, a unilocular ameloblastoma may be radiographically indistinguishable from odontogenic keratocysts and dentigerous cysts. Other ameloblastomas are multilocular with internal septa and a honeycomb or soap bubble appearance and are often similar in appearance to large odontogenic keratocysts. Definitively diagnosis is by histological evaluation. \n\nTreatment of ameloblastoma depends on the extent of tumor infiltration through the cyst wall and into surrounding bone. Excision of a relatively contained ameloblastoma could involve localized removal of the lesion with wide margins; if the lesion is highly infiltrative and extensive, en bloc resection would be performed. Recurrent ameloblastomas may be more widespread and destructive than the original lesion. \n\n\nPMID: 17102048\nPMID: 10489168", "ACR Code": "2.3", "Category": "Neoplasm, benign", "Keywords": "wisdom teeth toothodontogenic keratocystmandible maxilla", "Reference": "Scholl RJ, Kellett HM, Neumann DP, Lurie AG. Cysts and cystic lesions of the mandible: Clinical and radiologic-histopathologic review. Radiographics 1999;19:1107-1124 PMID: 10489168", "External Links": "http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&DbFrom=pubmed&Cmd=Link&LinkName=pubmed_pubmed&LinkReadableName=Related%20Articles&IdsFromResult=17102048&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstractPlus" } }, { "U_id": "MPX1860", "TAC": [ "MPX1860_synpic46093" ], "MRI": [], "Case": { "Title": "Osteopoikilosis", "History": "Patient 1: 25 yo female with right lower quadrant pain.\n\nPatient 2: 35 yo female with left lower quadrant pain.", "Findings": "Patient 1: AP radiograph of the abdomen reveals multiple 2 \u2013 3mm punctate ovoid sclerotic foci in the femurs and pelvis, clustered in a periarticular distribution.\n\nPatient 2: CT of pelvis demonstrates multiple punctate, oblong sclerotic foci symmetrically distributed throughout the proximal feumurs and pelvis, clustered in a periarticular distribution. No aggressive features are noted.", "Differential Diagnosis": "\u2022 Osteopoikilosis\n\u2022 Osteoblastic metastases\n\u2022 Mastocytosis\n\u2022 Tuberous sclerosis", "Case Diagnosis": "Osteopoikilosis", "Diagnosis By": "Imaging findings are characteristic." }, "Topic": { "Title": "Osteopoikilosis", "Disease Discussion": "Osteopoikilosis originally described by Albers-Schonberg and Ledoux-Lebard in the early 20th century is an asymptomatic osteosclerotic dysplasia. Seen in both men and women, it is not typically seen in patients younger than three years old, and may be more common than previously thought. Osteopoikilosis displays an autosomal dominant mode of transmission.\n\nClinical manifestations are absent or mild. In approximately 25% of cases, osteopoikilosis is associated with a specific syndrome such as mixed sclerosing bone dysplasia (coexistence of two or more of melorheostosis, osteopoikilosis, and osteopathia striata), Buschke-Ollendorf syndrome (osteopoikilosis and connective tissue nevi -dermatofibrosis lenticularis disseminata), and Gunal-Seber-Basaran syndrome (osteopoikilosis and dacrocystitis). Additionally, dwarfism, dystocia, and spinal stenosis are other associations.\n\nRadiographic findings are diagnostic. Numerous, small, well-defined, homogeneous ovoid or circular foci of increased density are clustered in a symmetric distribution in the epiphyses of long bones in a periarticular distribution or throughout smaller bones, such as the carpal and tarsal bones. The sclerotic foci can also occur throughout the pelvis and vertebrae, and may increase in size with age until skeletal maturity is reached. Complete disappearance of sclerotic foci has been observed.\n\nDifferential considerations include osteoblastic metastases, mastocytosis, and tuberous sclerosis. The symmetric distribution, the predilection for the epiphyses and metaphyses, and the uniform size of the sclerotic foci suggest osteopoikilosis. Bone scintigraphy is useful in differentiating osteopoikilosis from bony metastases, as sclerotic foci of osteopoikilosis do not accumulate radiotracer in bone scans, unlike osteoblastic metastasis. Positive bone scans are possible in children, and occur rarely in adults.\n\nHistologically, each sclerotic lesion represents a focus of lamellar bone containing haversian systems, and is identical to enostosis.", "ACR Code": "4.-1", "Category": "Miscellaneous", "Keywords": "Osteopoikilos", "Reference": "1. Resnick D. Diagnosis of Bone and Joint Disorders. 4th Ed. Philadelphia: Elsevier Saunders, 2002.\n\n2. Nissman D, Conway WF. Osteopoikilosis. ACR Case in Point. Thursday, June 29, 2006. Available from http://caseinpoint.acr.org/edactic/QMachine.ASP?UID=1P40P23P&PageId=1&Sess=127972980 Accessed 5 October 2008.\n\n3. Alymlahi E, Chami I, Boujida N, Bacadi D. Osteopoikilosis. Applied Radiology Volume 36 Number 3 March 2007. Available from http://www.appliedradiology.com/case/case.asp?Id=649&IssueID=172&CatID=29&SubCatID=290&ThreadID=&Quiz= Accessed 5 October 2008." } }, { "U_id": "MPX1862", "TAC": [ "MPX1862_synpic19661", "MPX1862_synpic19662", "MPX1862_synpic19663" ], "MRI": [], "Case": { "Title": "Hypertensive Encephalopathy in an eclamptic / hypertensive patient.", "History": "22 year-old female presents to ER with seizure and mental status changes", "Exam": "Physical Exam - BP 170/100\nNeuro Exam: Consistent with post-ictal state. Fundoscopic exam not performed.\n\nLabs WNL\n\n\nUpon further questioning, she is 3 days post-partum.", "Findings": "Within the bilateral posterior, temporal, occipital and parietal lobes, there are several small foci of \nlow density, with cytoxic and vasogenic edema patterns.", "Differential Diagnosis": "hypertensive encephalopathy\nIschemic infarct \nIntraaxial neoplasm (i.e. astrocytoma)\nEmbolic infarcts\nMets", "Case Diagnosis": "Hypertensive Encephalopathy in an eclamptic / hypertensive patient.", "Diagnosis By": "Further history yielded the fact that she was three days post-partum and hypertensive.", "Treatment & Follow Up": "ICU monitoring and nitroprusside to control BP\nMagnesium sulfate is used in pregnancy but this pt has already delivered." }, "Topic": { "Title": "Hypertensive Encephalopathy", "Disease Discussion": "Hypertensive encephalopathy occurs in the setting of increase systemic blood pressures with an inability of the normal autoregulation of cerebral vasculature to compensate. \n\n-Etiology and Pathogenesis: It is thought that there is a breakthrough of the autoregulatory mechanism of the cerebral vasculature. This leads to chronic vascular dilatation and increased pressure within the vessels. This leads to extravasion of proteins through the wall with associated fluid shift leading to edema.\n\n-Radiologic findings: Areas of increased signal are seen on T2 weighted MRI images, most commonly seen in the occipital or parietal regions bilaterally. In addition, there may be focal areas of petechial hemorrhage associated with the lesion.\n\n-Epidemiology: Occurs in the setting of increased systemic blood pressure with no other known predisposing factors\n\n-Clinical Manifestations: patients usually present with visual symptoms, seizures, or other neurological manifestations.\n\n-Differential Diagnosis: \nEmbolic infarct with a focal petechial hemorrhage \nNeoplasm, such as a cortical tumor or astrocytoma\n\n-Treatment: Resolves with the reduction in systemic blood \npressure", "ACR Code": "1.9", "Category": "Vascular", "Keywords": "hypertensive encephalopathyPRES" } }, { "U_id": "MPX1865", "TAC": [ "MPX1865_synpic41613", "MPX1865_synpic41615", "MPX1865_synpic41616" ], "MRI": [], "Case": { "Title": "Esophageal Lipomatosis", "History": "62 yo male with history of lung carcinoma.", "Findings": "Unenhanced axial CT image demonstrates the smooth double ring appearance of the proximal esophagus. The lower attenuating central band is in the range of fat attenuation.", "Differential Diagnosis": "Lipoma\nLiposarcoma", "Case Diagnosis": "Esophageal Lipomatosis", "Diagnosis By": "Imaging findings are characteristic." }, "Topic": { "Title": "Esophageal Lipomatosis", "Disease Discussion": "Esophageal lipomatosis is a benign condition of the esophagus that seems not well recognized by radiologists. In fact, until the 2002 article cited below, benign deposition of fat within the esophagus had never been decribed in the American radiology literature - rather only in European radiology literature. \n\nThe appearance is known as the \"double ring esophageal sign.\" The double ring consists of a low-attenuation ring between two higher-density bands. The low attenuation ring shows negative Hounsfield unit measurements as with subcutaneous fat. The fat ring is smooth and ranges in thickness from 1 mm to 3 mm. \n\nThis typical CT feature is consistent with esophageal lipomatosis and should be differentiated from other fatty lesions of the esophagus , e.g, lipoma and liposarcoma. Lipomas and liposarcomas are masses often surrounded by a single ring of the normal esophageal wall. Esophageal lipomatosis, on the other hand, has the double ring previously described - and that can be seen in the associated images in this case.\n\nA potential etiology of esophageal lipomatosis includes steroid use, which is known to induce atrophy or fatty infiltration of striated muscles. Esophageal lipomatosis is most often seen in the proximal esophagus, where striated muscle predominates in the esophagus.\n\nIncidence is difficult to accurately measure, but the article below found esophageal lipomatosis present in 7 of 1555 CT exams reviewed - equal to 0.45%.\n\nPMID: 12218824\nPMID: 10997425", "ACR Code": "7.1", "Category": "Miscellaneous", "Keywords": "esophageallipomatosisdouble ring sign", "Reference": "Marom ED, Goodman PC. Double-Ring Esophageal Sign: Pathognomonic for Esophageal Lipomatosis. Journal of Computer Assisted Tomography 2002; 26(4): 584-6. PMID: 12218824", "External Links": "www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&DbFrom=pubmed&Cmd=Link&LinkName=pubmed_pubmed&LinkReadableName=Related%20Articles&IdsFromResult=12218824&ordinalpos=3&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstractPlusDrugs2" } }, { "U_id": "MPX1873", "TAC": [ "MPX1873_synpic28988", "MPX1873_synpic28989", "MPX1873_synpic28991", "MPX1873_synpic28992" ], "MRI": [], "Case": { "Title": "Coarctation of the Aorta", "History": "14 year old male with chronic shortness of breath", "Exam": "Unknown", "Findings": "PA view of the chest demonstrates an abnormal contour to the aortic knob, with a focal indentation, with prominence of the descending aorta distal to this region.\n\nAxial contrast-enhanced CT examination of the chest demonstrates a focal narrowing of the aorta just distal to the ostium of the left subclavian artery with post-stenotic dilation of the descending thoracic aorta, consistent with coarctation of the aorta. Note also the enlarged collateral vessels in the internal mammary and subcostal distributions.", "Differential Diagnosis": "Coarctation of the aorta", "Case Diagnosis": "Coarctation of the Aorta", "Diagnosis By": "By CT, as described in the images." }, "Topic": { "Title": "Coarctation of the Aorta", "Disease Discussion": "Coarctation of the aorta commonly results from an abnormality of the aortic media (1). A discrete infolding of the posterolateral wall of the aorta in the region of the ligamentum or ductus is typically noted. This abnormality can occur in either the preductal or postductal location which modulates the age and severity of presentation.\n\nCoarctation proximal to the ductus presents shortly after birth and is usually associated with hypoplasia of the arch between the left subclavian artery and the ductus (2). The preductal location limits the blood volume load needed for normal aortic development.\n\nPostductal coarctation is more common than the preductal form and often is not symptomatic in the neonatal period.\n\nTypically, there is dilatation of the descending aorta distal to the coarctation with collateralization of vessels into the aorta primarilly via the intercostal arteries (2). This finding can result in rib notching. An abberant right subclavian artery that originates distal to the coarctation can serve as a major collateral to the right and rib notching occurs only on the left. If the left subclavian artery arises distal to the coarctation, then the rib notching is unilateral on the right (3).\n\n\nBalloon Angioplasty - http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1767490", "ACR Code": "5.6", "Category": "Vascular", "Keywords": "coarctationrib notchingpseudocoarctation", "Reference": "1. Freedom, R.M., Culham, J.G.and Moes, C.A., Angiocardiography of Congenital Heart Disrease. New York, Macmillan, Inc. 1984.\n2. Link, K.M., Szczesniak, D.M., Lesko, N.M., Imaging of the Great Valves and Great Vessels. InCardiac Imaging, Skorton, Ed; W.B. Saunders, Philadelphia, 1996 pp 698-700.\n3. Gomes, A.S., Lois, J.F., George, B., et al., Congenital Abnormalities of the Aortic Arch: MR Imaging. Radiology 165:691, 1987." } }, { "U_id": "MPX1875", "TAC": [ "MPX1875_synpic23054" ], "MRI": [], "Case": { "Title": "Non-small Cell Lung Cancer\r\n(Large-cell/clear-cell variant)", "History": "\u2022 Smoker\n\u2022 Cough\n\u2022 Shortness of breath", "Exam": "\u2022 Cachectic\n\u2022 Normal vital signs", "Findings": "\u2022 CXR shows an ill defined mass in the RUL\n\u2022 CT shows a lobulated 4 cm mass with spiculation in the RUL\n\u2022 Histology shows abundant cytoplasm and prominent nucleoli", "Differential Diagnosis": "\u2022 Small cell lung cancer\n\u2022 non-small cell lung cancer\n\u2022 focus of pneumonia, metastatic disease\n\u2022 fungal infection\n\u2022 benign neoplasm", "Case Diagnosis": "Non-small Cell Lung Cancer\n(Large-cell/clear-cell variant)", "Diagnosis By": "Biopsy", "Treatment & Follow Up": "Surgical excision", "Discussion": "15% of lung cancers are large cell type. Smoking is a major risk factor and five year survival is 10-15%." }, "Topic": { "Title": "Non-small Cell Lung Cancer", "Disease Discussion": "For practical puroses, lung carcinoma is classified into two types, small cell and non-small cell (NSCLC). Non-small cell includes squamous or epidermoid, adenocarcinoma, and large cell carcinoma. Small cell lung cancer is diagnosed in approximately 20% of lung cancer. It is generally treated with chemotherapy, with or without radiation treatment. Non small cell is diagnosed in approximately 75% or patients with lung cancer. Majority of NSCLC are not surgically respectable at the time of diagnosis. Adenocarcinoma most often arises as a peripheral lung nodule. Small cell and squamous are mostly central in location. \n \nFor NSCLC, approximately 12-20% are asymptomatic at the time of diagnosis. Peripheral tumors are clinically silent for a longer period and are more likely to be discovered incidentally on a routine chest radiograph. Symptoms include cough, wheezing, hemoptysis, recurrent pneumonia, and paraneoplastic syndromes. Invasion often causes hoarseness, chest wall pain, brachial plexus neuropathy, Horner\u2019s syndrome, phrenic nerve paralysis, superior vena caval obstruction, dysphagia, plural effusion, or pericardial tamponade. Hilar and mediastinal node involvement and distant metastases to the brain and adrenal glands are frequent at or after initial presentation. \n\nStaging for non-small cell is largely based on the TNM system. The most frequently used imaging modalities are plain chest radiograph and CT. Staging of the tumor influences the management options and prognosis.", "ACR Code": "63.321", "Category": "Neoplasm, carcinoma", "Keywords": "Non-small cellAdenosquamous" } }, { "U_id": "MPX1880", "TAC": [ "MPX1880_synpic34284", "MPX1880_synpic34286", "MPX1880_synpic34287", "MPX1880_synpic34288", "MPX1880_synpic34289" ], "MRI": [], "Case": { "Title": "medial deviation of internal carotid artery", "History": "84 year old male referred to otolaryngology clinic for a right tonsillar \"mass.\"", "Exam": "On physical exam the patient had assymetric fullness of the right posterior oropharynx.", "Findings": "Contrast enhanced axial CT images of the neck demonstrate a marked tortuosity of the right internal carotid artery just distal to the carotid bulb. There is medial deviation of the internal carotid with mass effect on the adjacent retropharyngeal soft tissues of the neck. This correlates with the patient's \"mass\" alluded to in the clinical history. Incidentally noted are calcified atherosclerotic plaques.\n\nA thick section multi-planar reformatted image demonstrates the tortuosity of this vessel well.\n\nAlso in the patient's prior studies was a carotid dopler ultrasound examination which again demonstrated the tortuosity of this vessel.", "Differential Diagnosis": "Medial deviation of the internal carotid artery (aka retropharyngeal internal carotid)", "Case Diagnosis": "medial deviation of internal carotid artery", "Diagnosis By": "Contrast enhanced neck CT", "Treatment & Follow Up": "No treatment is necessary beyond notification of the ordering physician so as to avoid any attempted biopsy and for pre-operative planning if intervention in the region is required for some other reason.", "Discussion": "The referring physician was contacted by telephone at the time of intrepretation of the examination." }, "Topic": { "Title": "medial deviation of internal carotid artery", "Disease Discussion": "Medial deviation of the internal carotid artery, also known as (aberrant) retropharyngeal internal carotid artery, is an important congenital variant that should be considered in the differential for a retropharyngeal mass. Once found, this finding should be reported to the clinicians so that the devastating consequences of biopsy or surgery is avoided.", "ACR Code": "2.1", "Category": "Congenital, normal variant", "Keywords": "medial deviation of internal carotid arteryretropharyngeal carotid artery", "Reference": "Som PM, et al. Head and Neck Imaging, 4/e. Mosby 2002." } }, { "U_id": "MPX1886", "TAC": [ "MPX1886_synpic15650", "MPX1886_synpic15651" ], "MRI": [], "Case": { "Title": "Thyroid Ophthalmopathy", "History": "70 year old male referred for imaging due to noticeable bulging of both eyes.", "Exam": "Marked exopthalmos, and drying of eyes.", "Findings": "CECT demonstrates prominence of retro bulbar fat as well as prominence of extraocular musculature. No enlargement is noted at the tendonous insertion on the globes.", "Differential Diagnosis": "Thyroid Ophthalmopathy, Orbital pseudotumor", "Case Diagnosis": "Thyroid Ophthalmopathy" }, "Topic": { "Title": "Thyroid Ophthalmopathy", "Disease Discussion": "The most common cause of unilateral or bilateral proptosis in the adult, thyroid ophthalmopathy results from deposition of mucopolysaccharides in the retro bulbar fat and extaocular musculature. While the majority of patients have signs and symptoms of hyperthyroidism, 10-15% of patients with thyroid ophthalmopathy are clinically and serologically euthyroid. Clinically patients have painless proptosis. The definition of proptosis is protrusion of the globe more than 21 mm beyond the interzygomatic line at the level of the mid lens. Eighty-five percent of patients have bilateral involvement, 5% unilateral. The most common pattern is enlargement of all the muscles most profoundly the inferior and medial rectus muscles (especially apparent on coronal images). If the lateral rectus is the only muscle enlarged an alternative diagnosis should be considered. Unlike orbital pseudotumor, a granulomatous disease of unknown etiology (but may be related to sarcoidosis), there is not involvement of the muscular insertions on the globes in thyroid ophthalmopathy. \n\tWhile 90% of patients experience complete resolution of symptoms over several months, 5-10% can develop optic neuropathy due to ischemia to the optic nerve at the orbital apex. Indicators of patients at risk are those that have intracranial prolapse of fat into the supraorbital fissure, with more than 50% crowding of the perineural fat about the nerve.", "ACR Code": "2.5", "Category": "Endocrine", "Keywords": "Extraocular muscleThyroidopthalmopathy", "Reference": "Grossman RI, Yousem DM: Neuroradiology: The Requisites. Mosby, St. Louis, 1994, pp. 296-297.\n\nHarnsberger, HR: Handbook of head and neck imaging. Mosby, St. Louis, 1995, pp. 330-331.\n\nDahnert W: Radiology Review Manual. Lippincott Williams and Wilkins,Philadelphia, 2000, p. 288." } }, { "U_id": "MPX1892", "TAC": [ "MPX1892_synpic23311", "MPX1892_synpic23313", "MPX1892_synpic23314", "MPX1892_synpic23315", "MPX1892_synpic23316", "MPX1892_synpic23317", "MPX1892_synpic23318", "MPX1892_synpic23322" ], "MRI": [], "Case": { "Title": "Sarcoidosis", "History": "History (can include gestational age, or age in days, weeks, months):\n70 y/o female for follow up CT scan to monitor for any pulmonary changes due to a recent 15lb weight loss, otherwise asymptomatic.", "Exam": "Na, K, Cl, CO2, Glucose, BUN, Creatinine, CA, drawn on the same day the CT scan was taken were all normal.", "Findings": "1. The parenchyma of the lung demonstrates bilateral upper lobe predominant fibrotic changes with interlobular septal thickening. 2. Numerous 1 cm nodular densities with in the periphery.\n3. As well as dominant fibrotic masses at the end of the bronchovascular bundle on the right side seen best on image #16 measuring 3.6 cm x 1.7 cm and on the left upper lobe seen best on image #10 measuring 2.4 cm X 1.8 cm with associated traction bronchiectasis, as well as some sparse areas of effected regions within the superior segments of the lower lobes bilaterally as well as the right middle lobe, which appears to have not changed significantly in comparison with the prior CT scan performed on 27 Feb 2002.\n4. No evidence of pleural effusion or pneumothorax.\n5. Mediastinum demonstrates no evidence of lymphadenopathy pathologic by size criteria. \n6. No evidence of axillary lymphadenopathy pathologic by size criteria.", "Differential Diagnosis": "Nodular Interstitial Pattern: Granulomatous diseases both infectious (TB, Fungal, Bacteria, Atypical mycobacterium) and non- infectious (Sarcoidosis, Vasculitis-granulomatosis diseases, Histiocytosis) Hematogenous spread of malignancy, and, Pneumoconiosis.", "Case Diagnosis": "Sarcoidosis", "Diagnosis By": "Biopsy", "Treatment & Follow Up": "Pt is currently not receiving treatment but is being worked up followed with serial CT scans due to unexplained weight loss.", "Discussion": "Sarcoidosis is a granulomatous disorder of unknown etiology that can affect multiple systems; the presence of noncaseating granulomas in the involved organs is what characterizes it pathologically. Sarcoidosis is estimated to have a prevalence of 10-20 per 100,000 and is 3-4 times more common in African Americans than Caucasians. The most common target of sarcoidosis is the lungs, around 90% of all patients with sarcoidosis have lung involvement, resulting in the main symptoms including cough, dyspnea, chest pain, and the less common features include fatigue, weakness, malaise, fever, and weight loss. Sarcoidosis, when in its extrapulmonary form, can result in a plethora of other complaints depending on the organ system affected. But approximately 50% of those with sarcoidosis are asymptomatic at the time it is discovered. The treatment for sarcoidosis is not straightforward. It is typically agreed upon that treatment should begin if the patient is symptomatic, if lung function is deteriorating, or the radiological findings associated with sarcoidosis are worsening. The current primary treatment is with daily oral corticosteroids. The best dose is not known so a dose must be chosen by balancing the risk of adverse effects versus the benefits of therapy. Treatment typically lasts between 6 to 12 months." }, "Topic": { "Title": "Sarcoidosis", "Disease Discussion": "Sarcoidosis is a granulomatous disorder of unknown etiology that can affect multiple systems; the presence of noncaseating granulomas in the involved organs is what characterizes it pathologically. Sarcoidosis is estimated to have a prevalence of 10-20 per 100,000 and is 3-4 times more common in African Americans than Caucasians. The most common target of sarcoidosis is the lungs, around 90% of all patients with sarcoidosis have lung involvement, resulting in the main symptoms including cough, dyspnea, chest pain, and the less common features include fatigue, weakness, malaise, fever, and weight loss. Sarcoidosis, when in its extrapulmonary form, can result in a plethora of other complaints depending on the organ system affected. But approximately 50% of those with sarcoidosis are asymptomatic at the time it is discovered. The treatment for sarcoidosis is not straightforward. It is typically agreed upon that treatment should begin if the patient is symptomatic, if lung function is deteriorating, or the radiological findings associated with sarcoidosis are worsening. The current primary treatment is with daily oral corticosteroids. The best dose is not known so a dose must be chosen by balancing the risk of adverse effects versus the benefits of therapy. Treatment typically lasts between 6 to 12 months.", "ACR Code": "68.22", "Category": "Differential Diagnosis", "Keywords": "Sarcoidosislung involvementdyspnea", "Reference": "Paramothayan, Shanthi. \u201cCorticosteroid Therapy in Pulmonary Sarcoidosis\u201d, JAMA. 2002:287(10): 1301-1307\nKing, Talmadge. \u201cOverview of sarcoidosis\u201d, UpToDate: www.uptodate.com, 5 Aug 2004" } }, { "U_id": "MPX1904", "TAC": [ "MPX1904_synpic16150" ], "MRI": [], "Case": { "Title": "Fibrous tumor of the pleura", "History": "71 yo male with a 100 pack yr smoking history with chest mass found on routine physical exam.", "Exam": "Negative broncho-alveolar lavage", "Findings": "Plain Radiographs of the chest demonstrate a large pleural based mass.\n\nSingle axial CT image demonstrates a large pleural based mass.", "Differential Diagnosis": "Loculated effusion or Empyema\nLipoma\nFibrous Tumors\nOther Neoplasm:\n Peripheral Bronchogenic Carinoma\n Mesothelioma\n Liposarcoma\n Pleural Metastasis (Breast carcinoma, lymphoma", "Case Diagnosis": "Fibrous tumor of the pleura", "Treatment & Follow Up": "None at this time." }, "Topic": { "Title": "Fibrous tumor of the pleura", "Disease Discussion": "Localized fibrous tumors of the pleura are known by various names, including pleural fibroma, fibrous mesothelioma, and localized pleural mesothelioma. These tumors arise from mesenchymal cells rather than epithelial cells and range from benign to malignant.\n\nTypically, patients range in age from 45-65 years of age and there is no association with asbestos exposure. Histologically the tumor is composed of spindle shaped cells interspersed within a collagen matrix. Grossly the lesions appear as pleural based masses. Occasionally they may be surrounded entirely by lung. Seventy five percent arise from the visceral pleura while the remaining twenty five percent arise from the parietal pleura. The mass is pedunclated in fifty percent of the tumors; this form has the greatest association with benignity. Histologically malignant tumors often invade the chest wall and mediastinum.\n\nClinically the patients are usually asymptomatic and the tumors are found as an incidental finding. The tumors are slow growing and, when symptomatic, the patient presents with cough, pleuritic chest pain, and dyspnea. Hypertrophic osteoarthropathy is seen in 4%-12% of the cases and is more common in larger tumors (> 7cm). Episodic hypoglycemia is reported in up to 6% of patients.\n\nChest radiographs demonstrate an ovoid homogenous mass in contact with the pleural surface which may invaginate or arise from a fissure. Tumors range is size from 1 to 30 cm. The pleural origin of the mass may be difficult to determine in extremely large masses. The angle of the mass with the chest wall may be obtuse or acute, and peduculated lesions may change position within the chest on subsequent images (and with stages of respiration). Malignant tumors can invade the chest wall and cause destruction of bone. \n\nCT images usually will show well marginated pleural based lesions growing outward from a narrow base forming acute angles with the chest wall (75% of cases). Small tumors show soft tissue attenuation and larger lesions may demonstrate central necrosis. The mass shows homogenous enhancement. Again, lesions may appear to arise from fissures and pedunculated lesions may appear mobile. Pleural effusions are rare and calcification has been reported to occur in 10% of cases.", "ACR Code": "66.317", "Category": "Neoplasm, benign", "Keywords": "benignpleuralfibrous tumor", "Reference": "Imaging of the Diseases of the Chest; Armstrong P. et al, 3rd ED" } }, { "U_id": "MPX1900", "TAC": [ "MPX1900_synpic45738", "MPX1900_synpic45739" ], "MRI": [], "Case": { "Title": "Renal Angiomyolipoma", "History": "76 y.o. woman with right flank pain.", "Findings": "Contrast enhanced axial CT images reveal a large enhancing mass involving the upper pole of the right kidney. The mass has multiple foci of fat density.\n\nCatheter angiogram demonstrates a single right renal artery, with a defect in the upper pole corresponding to the angiomyolipoma. There is minimal blood supply to this lesion although it arises from a single upper pole branch. The artery supplying this mass was subselected with a microcatheter and then embolized to obtain arterial stasis using 300 to 500 micron bead block. \n\nPost-embolization image shows absent flow to the mass.", "Differential Diagnosis": "\u2022 Angiomyolipoma\n\u2022 Renal Cell Carcinoma", "Case Diagnosis": "Renal Angiomyolipoma", "Diagnosis By": "Imaging findings are diagnostic.", "Treatment & Follow Up": "Due to an interval increase in size of the mass from 4.5 x 4.1 cm to 5.3 x 4.2 cm, and the increased risk of hemorrage, treatment was indicated. The patient underwent selective catheter based embolization, as embolization is an effective, minimally invasive treatment. The technical success rate is near 100%, with a rare incidence of recurrence in sporadic AMLs.\n\nKothary N, Soulen MC, Clark TW, et al. Renal Angiomyolipoma: Long-term Results after Arterial Embolization. J Vasc Interv Radiol. 2005; 16:45-50." }, "Topic": { "Title": "Renal Angiomyolipoma", "Disease Discussion": "Angiomyolipoma (AML) is the most common benign renal tumor composed of blood vessels, smooth muscle, and adipose tissue. AML is identified most frequently in middle-aged women, and may be seen in patients diagnosed with tuberous sclerosis. In patients without tuberous sclerosis, AML is most often unilateral in location, whereas patients with tuberous sclerosis frequently demonstrate multiple, small, bilateral AMLs.\n\nPatients with AML smaller than 4 cm are generally asymptomatic. If an AML is found to be larger than 4 cm, the presenting signs or symptoms are typically hematuria and or flank pain, and the tumor is resected secondary to an increased risk of hemorrhage. Additionally, if the tumor size is 1 cm or larger, thin section CT should be performed to evaluate for the presence of fat. If fat is not identified on CT, then the diagnosis of Renal Cell Carcinoma should be entertained. Small, asymptomatic AMLs should be followed for evidence of growth.\n\n\n\u2022 Ultrasound \n\nAngiomyolipoma (AML) may have a varied acoustic pattern as the amount of adipose tissue, smooth muscle, and blood vessels vary from lesion to lesion. Generally, AML is a homogenous well defined hyperechoic cortical neoplasm arising from the renal parenchyma, with echogenecity similar to that of the renal sinus. Occasionally, AML may appear as a hypoechoic focus when smooth muscle, blood vessels, or hemorrhage constitute the majority of the lesion. Color flow Doppler imaging is helpful in cases of hemorrhagic AML. \n\nRenal Cell Carcinoma (RCC) may also appear hyperechoic on ultrasound. To distinguish a RCC from an AML, the presence of a peripheral hypoechoic rim surrounding an echogenic solid lesion, as well as demonstrable cystic elements strongly suggests a RCC. Additionally, RCC typically lacks an acoustic shadow, whereas 20%-30% of AMLs have a varied degree of posterior shadowing.", "ACR Code": "8.3", "Category": "Neoplasm, NOS", "Keywords": "AngiomyolipomaAMLSonographic AML", "Reference": "Rumack, Carol. Diagnostic Ultrasound. Third Edition. Elsevier Mosby, Inc. \n Mosby. St. Louis, Missouri 2005.\nMiddleton, William. Ultrasound. The Requisites. Second Edition. Mosby. \n St. Louis, Missouri 2004.\nPrasad et al. RadioGraphics 2005; 25:321\u2013331.\nNuman et al. Clin Imaging 1993;17:106-108.\nLee et al. Korean J Radiol 2000;1:60-63." } }, { "U_id": "MPX1905", "TAC": [ "MPX1905_synpic28196" ], "MRI": [], "Case": { "Title": "Heterotopic ossification", "History": "A 39 year-old man was injured in a gunfight. The patient suffered a GSW to the right buttock that exited the scrotum. The patient underwent an exploratory laparotomy, found to be negative, and a transscrotal exploration that found injury to the bladder and urethra. A probing of the right hip wound revealed that the injury went posterior to the femur and did not invade the capsule. Approximately four months post-injury, the patient reported a progressive limiting of his hip range of motion and inability to perform activities of daily living.", "Exam": "The patient was found to have an antalgic gait. He had no neurologic symptoms and had limited mobility secondary to a mass on his right hip. His right hip range of motion was from 90 degrees of flexion to 7 degrees of flexion. His external rotation was approximately 15 degrees, and internal rotation was 30 degrees.", "Findings": "Both CT and x-ray show a calcified mass posterior to the acetabulum and femur.", "Differential Diagnosis": "Heterotopic ossification\nSoft-tissue neoplasm\nBone neoplasm", "Case Diagnosis": "Heterotopic ossification", "Diagnosis By": "Surgery", "Treatment & Follow Up": "Surgery to remove the HO was conducted six months from the time of injury. The eight centimeter by eight centimeter mass was found to lay superficial to the external short external rotators. Upon removal of the mass, the patient\u2019s hip range of motion was from 120 degrees of hip flexion and to 20 degrees of extension. His external rotation improved to approximately 50 degrees, with an internal rotation of 30 degrees. Six months post-surgery, the patient has regained his mobility and the ability to run without significant difficulty.", "Discussion": "Cases of HO have been reported after lateral hip soft tissue trauma, with ectopic/heterotopic ossification found in areas of hematoma or where soft tissue surgical trauma has occurred.(3-5) A plausible explanation for this unusual case of HO involving a gunshot wound is likely the same as occurs in any soft tissue trauma. The localized trauma induces metaplastic change of multipotent connective tissue cells into osteogenic cells which then lay down stroma and calcify.(9)" }, "Topic": { "Title": "Heterotopic ossification", "Disease Discussion": "Heterotopic ossification (HO) is the pathological formation of new bone in soft tissues. HO has been extensively studied and reported as a complication that develops following brain trauma, spinal cord injury, thermal injury, local joint trauma, acetabular fracture, lateral hip soft tissue hematoma, and total hip arthroplasty.(1-4) Post- traumatic ectopic calcification following a direct blow to muscle (particularly in the anterior thigh) has been described as well.(5) All forms of HO, however, are histologically identical.(4) \n\nThe incidence of such HO has been described as occurring from 5% to 90% of the time with the various traumas/surgeries.(3) Most cases of heterotopic ossification are asymptomatic, but 2% to 10% of HO can be extensive.(4) \n\nThe most common clinical manifestations of hip HO are decreased range of motion, pain around the joint, and difficulty walking.(3, 6-7) Prophylaxis recommended for HO includes nonsteroidal anti-inflammatory drugs and low dose local radiation.(8) \n\nOnce HO becomes established and extensive with joint movement restriction, the only effective treatment is surgical resection.(4)", "ACR Code": "4.9", "Category": "Trauma", "Keywords": "heterotopic ossificationheterotopic bone formationgunshot and shrapnel wounds", "Reference": "1 Pape HC, Lehman U, van Griensven M, Gansslen A, von Glinski S, Krettek C. Heterotopic ossifications in patients after severe blunt trauma with and without head trauma: incidence and patterns of distribution. Journal of Orthopaedic Trauma. 2001 May; 15(4); 229-237.\n2 Evans EB. Heterotopic bone formation in thermal burns. Clinical Orthopaedics and Related Research. 1991 February; (263); 94-101.\n3 Ebinger T, Roesch M, Kiefer H, Kinzl L, Schulte M. Influence of etiology in heterotopic bone formation of the hip. Journal of Trauma. 2000 June; 48(6); 1058-1062.\n4 Evans BG. Late complications and their management: Total hip arthroplasty and heterotopic ossification. The Adult Hip. 1998; 1149-1161.\n5 King JB. Post-traumatic ectopic calcification in the muscles of athletes: A review. British Journal of Sports Medicine. 1998; (32); 287-290.\n6 Heindl UT, Laub MC. Outcome of persistent vegetative state following hypoxic or traumatic brain injury in children and adolescents. Neuroorthopediatrics. 1996; (27); 94-100.\n7 Rosendahl S, Christoffersen JK, Norgaard M. Para-articular ossification following hip replacement: 70 arthoplasties ad modum Moore using McFarland\u2019s approach. Acta Orthopedics Scandinavia. 1977; (48); 400-404.\n8 Zagaja GP, Cromie WJ. Heterotopic bone formation in association with pelvic fracture and urethral disruption. The Journal of Urology. 1999 June; 161(6); 1950-1953.\n9 Morash MD, Shoup M, Marshall WJ, Maull KI. Journal of Accidents and Emergency Medicine. 1996 May; 13(3); 227-229." } }, { "U_id": "MPX1902", "TAC": [ "MPX1902_synpic35488" ], "MRI": [], "Case": { "Title": "Colloid cyst", "History": "Adult patient with headaches", "Case Diagnosis": "Colloid cyst", "Diagnosis By": "Pathology" }, "Topic": { "Title": "Colloid cyst, neuroepithelial cyst", "Disease Discussion": "Colloid cysts are uncommon benign cysts of the anterior superior third ventricle, which are thought to arise from embryologic tissues of the paraphysis, ependyma, or choroid plexus. These lesions typically present in young adults in the 2nd to 5th decade with complaints referable to acute or chronic hydrocephalus. Other symptoms include ataxia, memory disturbances, and gait disorders. The cyst contents include secretory and breakdown products of the epithelial lining tissue, including hemorrhage, lipid (cholesterol), hemosiderin, and CSF. \n\nOn T1-weighted MR images, these cysts vary widely from hypo- to hyperintense in comparison to normal brain. Although they may be bright on T2-weighted images, moderate to marked hypointensity is common and has been attributed to a very short T1 relaxation time or to magnetic susceptibility effect from paramagnetic substances in the cyst. On noncontrast MR, these lesions occasionally are indistinguishable by intensity from neoplasia; however, the absence of enhancement, classic location, and relative hypointensity on T2-weighted studies should suggest this diagnosis. Treatment is variable, including ventricular shunting alone, stereotactic cyst drainage, or surgical resection. \n\nOn noncontrast CT, colloid cysts are solitary, round to oval, usually hyperdense masses at the foramen of Monro with associated enlargement of one or both lateral ventricles (Film .3). Minimal or absent contrast enhancement is typical. Moderate enhancement with contrast suggests a different etiology, such as glioma, craniopharyngioma, choroid plexus papilloma, or remotely meningioma. Other cystic masses such as arachnoid or ependymal cysts will mimic CSF in density and intensity.\n\nVideo - http://www.youtube.com/watch?v=9NbKjXChneo&", "ACR Code": "1.3", "Category": "Cyst, benign", "Keywords": "Colloid cystshydrocephalusBrun syndrome", "External Links": "rad.usuhs.edu/medpix/medpix.html?mode=single&recnum=1437&table=card&srchstr=colloid%20cyst&search=colloid%20cyst#top" } }, { "U_id": "MPX1908", "TAC": [ "MPX1908_synpic57616" ], "MRI": [ "MPX1908_synpic57617", "MPX1908_synpic57619", "MPX1908_synpic57744", "MPX1908_synpic57746", "MPX1908_synpic57747" ], "Case": { "Title": "Chiari I malformation", "History": "21 y/o woman who presented to the ER with gradual onset headache for the past 2 weeks.", "Exam": "Negative neurological exam.", "Findings": "Low lying cerebellar tonsils with cervical cord syringohydromyelia.", "Differential Diagnosis": "Cerebellar tonsillar herniation differential includes: space occupying lesions or mass effect within the posterior fossa and Chiarir II malformation.\n\nSyrinx differential includes cord masses.", "Case Diagnosis": "Chiari I malformation", "Diagnosis By": "CT and MR (including CSF flow studies)", "Treatment & Follow Up": "Neurosurgery consultation for evaluation and possible decompression.", "Discussion": "Twenty five percent of all Chiari I malformations present with cervical syringohydromyelia. It is important to evaluate the cord upon recognition of low lying or herniated cerebellar tonsils." }, "Topic": { "Title": "Chiari I with cervical spine syrinx.", "Disease Discussion": "The Chiari I formation (sometimes termed congenital tonsillar ectopia) that presents in adult patients is herniation of the cerebellar tonsils over 5mm below the line connecting the basion with the opisthion (the foramen magnum). Several proposed causes are a small posterior fossa, disproportionate CSF absorption from subarachnoid spinal space, and cerebellar overgrowth. It is commonly associated with syringohydromyelia 30-60% and hydrocephalus 20-25%. Other associated defects include basilar invagination (25-50%), Klippel-Feil (5-10%), and atlantooccipital assimilation (1-5%). Unlike the Chiari II formation, Chiari I formations are not associated with myelomeningoceles.\n\nThe diagnosis is based on the amount of herniation of the cerebellar tonsils into the foramen magnum and the patient\u2019s age. Up to age 10, at least 6mm is required for the diagnosis, at least 5mm for 10-30 years, and 4mm for greater than 30 years of age.", "ACR Code": "1.1", "Category": "Congenital, malformation", "Keywords": "chiari Ichiari malformation", "Reference": "Osborn, A.G. M.D., F.A.C.R., Diagnostic Neuroradiology, Mosby, St.Louis, 1994.", "External Links": "www.medscape.com/viewarticle/405725_6" } }, { "U_id": "MPX1920", "TAC": [ "MPX1920_synpic18742" ], "MRI": [], "Case": { "Title": "Boerhaave's syndrome", "History": "85 year old woman reported vomiting several times after eating, probably secondary to food poisoning. While retching she experienced sudden severe pain in her mid chest and began to vomit blood.", "Findings": "CXR shows left-sided pleural effusion. CT confirms left sided pleural effusion and also shows \u201cbubbly\u201d pneumomediastinum. UGI shows small perforation on left side of distal esophagus near the GE junction. There is spasm of the esophagus probably as a result of the perforation. There is also a large amount of aspirated contrast material.", "Differential Diagnosis": "Esophageal perforation from ingested foreign object, infection, neoplasm, or instrumentation.", "Case Diagnosis": "Boerhaave's syndrome", "Diagnosis By": "The diagnosis was confirmed by surgical repair of the esophageal perforation." }, "Topic": { "Title": "Boerhaave's syndrome", "Disease Discussion": "Boerhaave's syndrome is defined as spontaneous rupture of the esophagus with transmural perforation. The perforation is thought to result from a dramatic increase in intra-esophageal pressure caused by such activities as coughing, retching, heavy lifting or even parturition. The perforation usually occurs in the left posterior aspect of the lower esophagus near the gastro-esophageal junction. Patient presentation includes severe chest pain after straining in up to 95% of cases and hematemesis in up to 30%. It occurs 5 times more commonly in males. Chest X-ray classically shows pneumomediastinum and pleural effusion. The effusion tends to be greater on the left. Chest radiographs are said to be abnormal in up to 90% of cases of esophageal perforation although abnormalities \nmay be non-specific and may not be evident immediately after the perforation occurs. Other radiographic findings that may result from esophageal perforation include subcutaneous emphysema, mediastinal air-fluid levels, mediastinal widening, pneumothorax, hydrothorax, or pulmonary infiltrates. CT allows more sensitive evaluation for mediastinal fluid and air in addition to pleural effusion. Radiographic \ncontrast study of the esophagus may show the site of perforation although the false negative rate has been reported as high as 10%. The study can be done with water-soluble contrast and/or thin barium depending on the preference of the cardiovascular surgeon. The risk of using water-soluble contrast is pulmonary edema if patient aspirates, \nand the risk of using barium is reportedly barium mediastinitis if barium leaks into the medistinum through a large perforation. \nOf the various causes of esophageal perforation, postemetic spontanous perforation is considered the most morbid secondary to massive contamination and frequently delayed diagnosis. This is in contrast to iatrogenic injuries which are frequently diagnosed at the time of injury. The reported mortality with early primary repair varies widely ranging from 43% (even if the condition is diagnosed and treated less than 24 hours after perforation) to as low as 5% in some reports. The most important factor in regards to morbidity is the length of time between perforation and repair. On occasion with very small contained perforations the cardiovascular surgeon may elect conservative management, but in the majority of cases immediate surgical repair is necessary. Conservative management is associated with a 22 to 38% mortality. The difficulty with nonoperative management is prospective determination of which perforation will remain contained and which will cause continued contamination with subsequent uncontrolled infection. Sepsis, shock, pneumothorax, pneumoperitoneum, mediastinal emphysema, and respiratory failure are all absolute indications for rapid surgical interventions.", "ACR Code": "7.4", "Category": "Hemorrhage", "Keywords": "Esophageal perforationBoerhaave's SyndromeHematemesis", "Reference": "Grainger & Allison's Diagnostic Radiology: A Textbook of Medical Imaging, 4th Ed., pp 1032-1033\nFeldman: Sleisenger & Fordtran's Gastrointestinal and Liver Disease, 7th ed. pp 637-640 \nTownsend: Sabiston Textbook of Surgery, 16th ed. p 724", "External Links": "www.amershamhealth.com/medcyclopaedia/Volume%20IV%201/ BOERHAAVES%20SYNDROME.asp" } }, { "U_id": "MPX1922", "TAC": [ "MPX1922_synpic24915" ], "MRI": [], "Case": { "Title": "Stage IIIB Adenocarcinoma", "History": "56 yo Female presents for screening x-ray. She is aymptomatic except for a mild cough and slight fatigue for about one month.", "Exam": "Resp: R side CTA, L side with decreased BS and egophany over lower ? of lung.\nCVS: RRR without r/g/m Extr: no c/c/e \n\nWBC 11.4, H/H 11.1/34, Plt 548\n136/4.8/98/27/12/0.6/106 Ca 8.4 Alb 2.7 Mg 2.2", "Findings": "LUL mass, Tracheal Deviation\nL sided pleural effusion\nFissure present as an edge on lateral CXR\nSpine Sign on Lateral CXR\nIndistinct LV heart border on lateral CXR\nMass on CT abutting mediastinum", "Differential Diagnosis": "Lung cancer\nGranulomatous Disease\nBenign Mass\nOther Inflammation (Pneumonia)\nCongenital Abnormality", "Case Diagnosis": "Stage IIIB Adenocarcinoma", "Diagnosis By": "Biopsy", "Treatment & Follow Up": "Likely treatment will consist of chemotherapy and radiation. There was and currently is discussion of performing VATS in this case for further staging and potential treatment.", "Discussion": "Adenocarcinoma is the most common form of lung cancer in the US. It is associated with smoking although this less strongly than other types of lung cancer. Adenocarcinomas typically are well-defined masses that occur in a peripheral location. This type of lung cancer is more common in women, usually occurring in current or former smokers although occasionally occurring in non-smokers. Staging involves the TMN system with this patient at Stage IIIB based on a T4NoMo lesion (5 cm in size with mediastinal invasion). Surgery is the treatment of choice for stage I and II lung adenocarcinoma. Stage III and IV adenocarcinoma is usually treated with chemotherapy and radiation although there select stage III and IV cancers may be amenable to surgical treatment. Median survival for stage IIIB lung cancer is 12 months and 5-year surival is less than 5%." }, "Topic": { "Title": "Lung, Stage IIIB Adenocarcinoma", "Disease Discussion": "Adenocarcinoma is the most common form of lung cancer in the US. It is associated with smoking although this less strongly than other types of lung cancer. Adenocarcinomas typically are well-defined masses that occur in a peripheral location. This type of lung cancer is more common in women, usually occurring in current or former smokers although occasionally occurring in non-smokers. Staging involves the TMN system with this patient at Stage IIIB based on a T4NoMo lesion (5 cm in size with mediastinal invasion). Surgery is the treatment of choice for stage I and II lung adenocarcinoma. Stage III and IV adenocarcinoma is usually treated with chemotherapy and radiation although there select stage III and IV cancers may be amenable to surgical treatment. Median survival for stage IIIB lung cancer is 12 months and 5-year surival is less than 5%.", "ACR Code": "68.321", "Category": "Neoplasm, carcinoma", "Keywords": "Adenocarcinomalung cancerstage IIIB lung cancer", "Reference": "\u2022 Hanley, Michael E and Welsh, Carolyn H. Diagnosis and Treatment in Pulmonary Medicine. 2003.\n\u2022 UpToDate online. Search title: \u2018Management of stage III non-small cell lung cancer.\u2019\n\u2022 Weitberg, Alan B., and Klastersk, Jean. Cancer of the Lung: From Molecular Biology to Treatment Guidelines. Humana Press. 2002.\n\u2022 Cancer Medicine. 6th Edition. Ch. 28 Neoplasms of the Thorax" } }, { "U_id": "MPX1923", "TAC": [ "MPX1923_synpic23831" ], "MRI": [], "Case": { "Title": "Diagnosis: Thinning and irregularity of the anterior talofibular ligament consistent with previous inversion injury.", "History": "History (can include gestational age, or age in days, weeks, months):\n 25 year-old male with multiple right- sided inversion injuries over past ten years. Currently complains of subluxing peroneal tendons.", "Exam": "Physical Exam and Laboratory: \nWell-developed, white man who has no swelling, erythema, scars or point tenderness of the right ankle. He has full and equal range of motion bilaterally. He is able to sublux his peroneal tendons. Negative anterior drawer sign. No subtalar instability onphyscial examination.", "Findings": "Image Findings: Axial fat-saturated T1-weighted MR image of the right ankle shows a thinned and irregular anterior talofibular ligament and fluid communicating between the joint space and the peroneal tendon sheath. No other ligamentous or tendinous abnormality, fracture or soft tissue swelling is present.", "Differential Diagnosis": "Differential Diagnosis for these findings in this case:\nChronic injury to anterior talofibular ligament.", "Case Diagnosis": "Diagnosis: Thinning and irregularity of the anterior talofibular ligament consistent with previous inversion injury.", "Treatment & Follow Up": "Treatment and Follow-up When the anterior talofibular ligament (ATFL) is acutely injured, the patient receives conservative treatment with rest, ice, compression and elevation and provided with crutches for ambulation. Nonsteroidal anti-inflammatory medications are given as needed for pain and to minimize swelling. A soft compress such as an ankle sleeve or ace wrap may also help to provide symptomatic relief. If the injury to the ATFL is not acute, appropriate shoe wear is recommended for activity; also proprioceptive exercises may be instituted to decrease likelihood of further sprains. If symptomatic with complete rupture of anterior talofibular ligament, surgery may include transfer of extensor digitorum brevis to improve stability.", "Discussion": "Discussion (include references): \n Inversion injuries are very common in the young active population. This injury may result in a fracture, ligamentous injury, or both. The initial evaluation of a patient with inversion injuries requires a good history and physical examination as well as plain radiographs to assess for any fractures. Stress views of the both ankles should show similar tibiotalar tilt (less than 5 degrees difference between the affected and normal ankle). MRI is the best imaging for evaluating the ligamentous structures of the lateral ankle. \n The lateral ankle is supported by three ligaments, the anterior talofibular, the calcaneofibular, and the posterior talofibular ligaments. In this case the patient had thinning of the anterior talofibular ligament. This is often the first ligament damaged in an inversion injury and is seen in approximately 40% of these injuries. With increasing force the next ligament injured in an inversion injury is the calcaneofibular ligament. The final ligament injured is often the posterior talofibular ligament. Following injury as many as 20% may experience symptomatic ankle instability. \n The best visualization of the ATFL and PTFL occurs on the axial image at the talar neck, while evaluation of the calcaneofibular ligament may require an oblique view. A complete interruption of the low intensity ligament is seen in a rupture of the ligament. In this case there is thinning and irregularity of the ligament.\nReference: 1) Physical Examination of the Spine and Extremities; Stanley Hoppenfeld, pp222, Prentice Hall NJ 1976\n 2) Netter\u2019s Concise Atlas of Orthopaedic Anatomy; Jon C. Thompson MD, pp 254\n 3) Wheeless\u2019 Textbook of Orthopaedics Online; www.wheelessonline.com\n 4) Ahmad, M.A. \u201cMagnetic Resonance Imaging of the normal and injured lateral collateral ligaments of the ankle\u201d Ann Chir Gynaecol 1998; 87(4):311-6\n 5)Colville, M.R., \u201cSurgical Treatment of the Unstable Ankle\u201d, JAAOS Vol 6, No.6" }, "Topic": { "Title": "Diagnosis: Thinning and irregularity of the anterior talofibular ligament consistent with previous inversion injury.", "Disease Discussion": "Discussion (include references): \n Inversion injuries are very common in the young active population. This injury may result in a fracture, ligamentous injury, or both. The initial evaluation of a patient with inversion injuries requires a good history and physical examination as well as plain radiographs to assess for any fractures. Stress views of the both ankles should show similar tibiotalar tilt (less than 5 degrees difference between the affected and normal ankle). Finally MRI has been shown as a good modality for evaluating the ligamentous structures of the lateral ankle. \n The lateral ankle is supported by three ligaments, the anterior talofibular, the calcaneofibular, and the posterior talofibular ligaments. In this case the patient had thinning of the anterior talofibular ligament. This is often the first ligament damaged in an inversion injury and is seen in approximately 40% of these injuries. With increasing force the next ligament injured in an inversion injury is the calcaneofibular ligament. The final ligament injured is often the posterior talofibular ligament. Following injury as many as 20% may experience symptomatic ankle instability. \n The best visualization of the ATFL and PTFL occurs on the axial image at the talar neck, while evaluation of the calcaneofibular ligament may require an oblique view. A complete interruption of the low intensity ligament is seen in a rupture of the ligament. In this case there is thinning and irregularity of the ligament.\nReference: 1) Physical Examination of the Spine and Extremities; Stanley Hoppenfeld, pp222, Prentice Hall NJ 1976\n 2) Netter\u2019s Concise Atlas of Orthopaedic Anatomy; Jon C. Thompson MD, pp 254\n 3) Wheeless\u2019 Textbook of Orthopaedics Online; www.wheelessonline.com\n 4) Ahmad, M.A. \u201cMagnetic Resonance Imaging of the normal and injured lateral collateral ligaments of the ankle\u201d Ann Chir Gynaecol 1998; 87(4):311-6\n 5)Colville, M.R., \u201cSurgical Treatment of the Unstable Ankle\u201d, JAAOS Vol 6, No.6", "ACR Code": "4.4", "Category": "Trauma", "Keywords": "anterior talofibular ligament injuryligament injury", "Reference": "Reference: 1) Physical Examination of the Spine and Extremities; Stanley Hoppenfeld, pp222, Prentice Hall NJ 1976\n 2) Netter\u2019s Concise Atlas of Orthopaedic Anatomy; Jon C. Thompson MD, pp 254\n 3) Wheeless\u2019 Textbook of Orthopaedics Online; www.wheelessonline.com\n 4) Ahmad, M.A. \u201cMagnetic Resonance Imaging of the normal and injured lateral collateral ligaments of the ankle\u201d Ann Chir Gynaecol 1998; 87(4):311-6\n 5)Colville, M.R., \u201cSurgical Treatment of the Unstable Ankle\u201d, JAAOS Vol 6, No.6" } }, { "U_id": "MPX1924", "TAC": [ "MPX1924_synpic19604", "MPX1924_synpic19605", "MPX1924_synpic19606" ], "MRI": [], "Case": { "Title": "Mucinous Cystic Neoplasm of the Pancreas", "History": "Patient recently had surgical repair of left inguinal hernia. Pathology on the sac and surrounding soft tissue came back as \"metastatic adenocarcinoma \". Patient is otherwise healthy and asymptomatic. CT was performed in a search for primary malignancy.", "Exam": "CA19-9: 1164 (0-36) U/mL \nAFP: 1.7 (0.0-15.0) ng/mL \nCEA 7.9 (0.0-4.6) ng/mL", "Findings": "Hypodense lesion in the tail of the pancreas, with cystic and soft tissue components. Minimal pancreatic duct dilatation. There were no hepatic lesions, and all mesenteric and retroperiteoneal nodes were sub-centimeter.", "Differential Diagnosis": "Mucinous Cystadenoma/Cystadenocarcinoma\nIntraductal Papillary Tumor\nAtypical pseudocyst", "Case Diagnosis": "Mucinous Cystic Neoplasm of the Pancreas", "Diagnosis By": "CA 19-9.", "Treatment & Follow Up": "Imaging guided biopsy of the lesion was considered, and declined secondary to inaccessibility. Patient will decide whether to undergo laproscopy.", "Discussion": "Finding of such markedly increased CA 19-9, along with pathologic evidence of metastatic disease nearly seal the diagnosis. The mucinous cystic pancreas tumors favor the tail. Ductal neoplasms tend to favor the head and body, and contain more soft tissue component. Imaging features in this case are highly suggestive of the diagnosis. There is no surrounding inflammation to suggest pseudocyst." }, "Topic": { "Title": "Mucinous Cystic Neoplasm of the Pancreas", "Disease Discussion": "Mucinous Csytic Neoplasm of the Pancreas; AKA-macrocystic adenoma, mucinous cystadenoma, cystadenocarcinoma.\n\nFrequency- 10% of pancreatic cysts, 1% of pancreatic neoplasms\n\nMean Age- 50 years ( 20-95 ), 50% between 40-60 years old\n M:F 1:19\n\nPathology: Large smooth round/lobulated multiloculated cystic mass encapsulated by a layer of fibrous connective tissue\n\nHistology: similar to biliary and ovarian mucinous tumors; cysts lined by tall columnar, mucin-producing cells subtended by a densely cellular mesenchymal stroma (reminiscent of ovarian stroma), often in papillary arrangement\n\nLocation: often in the tail (90%), body, infrequently in head\n\n-well-demarcated thick-walled mass, mean 10-12 cm\n-multi/unilocular large cyss >2 cm with thin septa <2 mm\n* a tumor with <6 cysts of >2 cm in diameter is in 93-95% a mucinous cystic neoplasm\n-amorphous discontinuous peripheral mural calcifications (10-15%)\n-solid papillary excresences protrude into the interior of the tumor\n-hypovascular mass with sparse neovascularity\n-great propensity for invasion of adjacent organs\nU/S: -cysts may contain low level echoes; echogenic mural calcifications if present\nCT: -internal septations may not be seen without contrast enhancement; cysts with HU of water, different cysts with different HU's; enhance of cyst walls\nMRI: -high T2 from mucinous component\nAngio: -predominantly avascular mass, small area of blush in cyst wall and solid components, mass effect on adjacent arteries and veins by cysts\nMets: -round thick walled cystic lesions in the liver\nPrognosis: -invariable transformation into cystadenocarcinoma\nRx: -complete surgical excision, 5 yr survival is 74-90%\nDDx: pseudocyst, lymphangioma/hemangioma, variants of ductal adenocarcinoma, solid and cystic papillary epithelioid neoplasm, cystic islet cell tumor, cystic met, atypical serous cystadenoma, sarcoma, infection (amebiasis, echinococcus0", "ACR Code": "7.-1", "Category": "Neoplasm, malignant (NOS)", "Keywords": "neoplasmmucinouspancreas", "Reference": "Radiology Review Manual, Dahnert, W., MD, 4th Edition, Lippincott, Williams and Wilkins, Philadelphia.\nMagnetic Resonance Imaging, Stark, D., and Bradley, W., 3rd Edition," } }, { "U_id": "MPX1928", "TAC": [ "MPX1928_synpic17867" ], "MRI": [], "Case": { "Title": "Peritoneal Metastasis", "History": "62-year-old African American female presents with diffuse abdominal pain and bloating. bHCG was negative.", "Exam": "She was afebrile with stable vital signs and a normal white blood count. Exam showed a diffusely distended nonacute abdomen and enlarged uterus by palpation. There was clinical concern for bowel obstruction. Contrast-enhanced CT of the abdomen/pelvis was obtained as the initial imaging study and was followed with a pelvic US.", "Findings": "CT FINDINGS: There is a significant amount of ascites within the abdomen extending down into the pelvis where a heterogeneous and calcified mass is identified. This is in the area near the uterus and probably represents a fibroid uterus, although there is a lot of streaking artifact limiting visualization of the structures in the pelvis. There is fluid surrounding this calcified heterogeneous mass without definite identification of the ovaries; ovarian mass cannot be excluded. Within the upper abdomen, there is the appearance of omental caking concerning for metastatic process, seeding the greater omentum; ovarian malignancy is most common cause of this finding and is suspected in this older female patient. \n\nUS FINDINGS: The uterus is enlarged measuring 9.97 x 6.65 x 8.96 cm and has a heterogeneous appearance consist with a fibroid uterus, which was suspected on recent CT. There is a 4.9 x 4.1 x 6.3 cm anterior myometrial fibroid identified. There is a marked amount of free-fluid noted within the pelvis. The left adnexa /ovary is not well seen. Within the right adnexal region, the right ovary is visualized and is enlarged measuring 4.75 x 3.65 x 4.2 cm, and contains a complex cystic mass measuring 2.6 x 2.5 x 3.3 cm. This mass contains numerous septations some of which are irregular and thickened. There is no significant blood flow within the mass. The right ovary itself demonstrates normal arterial and venous blood flow and spectral Doppler analysis.", "Differential Diagnosis": "Ovary\nColon\nStomach\nPancreas", "Case Diagnosis": "Peritoneal Metastasis", "Treatment & Follow Up": "GYN service was consulted on the evening the patient presented. The patient is currently being considered for further management by the GYN Oncology service at another institution.", "Discussion": "SEE FACTOID. No specific discussion pertaining to this case." }, "Topic": { "Title": "Peritoneal Metastasis", "Disease Discussion": "Perintoneal Metastasis\n\n-aka peritoneal carcinomatosis\n-c/w intraabdominal/peritoneal spread of malignancy\n-common: ovary (#1), stomach, colon\n-less common: pancreas, uterus, bladder\n-COPS differential: Colon, Ovary, Pancreas, Stomach\n-can be a/w massive ascites\nCT findings: \n-loculated peritoneal fluid collections \n-adnexal / ovarian cystic or soft tissue mass (Krukenberg\u2019s tumor)\n-thickening of mesenteric vessels\n-\u201comental caking\u201d=thickening of greater omentum, secondary to tumor-cell implantation, is followed by serosal invasion and proliferation within omental fat. Omental fat eventually replaced by tumor=soft tissue mass appearance\n-\u201cperitoneal studding\u201d=small soft tissue nodular densities on peritoneal surface\n-calcified peritoneal implants are seen with serous cystadenocarcinoma of ovary (up to 40% with late stage disease)\n-\u201cpseudomyxoma peritonei\u201d-gelatinous material within peritoneum due to spread of mucin-secreting malignancy", "ACR Code": "7.3", "Category": "Neoplasm, NOS", "Keywords": "omental cakingperitoneal metastasisovarian neoplasm", "Reference": "1. Dahnert W. Radiology Review Manual. Williams and Wilkins, Baltimore 1996:620.\n2. Weissleder R, et al. Primer of Diagnostic Imaging. Mosby, Philadelphia 2003:344." } }, { "U_id": "MPX1936", "TAC": [ "MPX1936_synpic18349", "MPX1936_synpic18351" ], "MRI": [], "Case": { "Title": "Osteochondritis Dissecans of the Tarsal Navicular", "History": "40 year old female with chronic right dorsal mid foot pain. Patient\u2019s symptoms were relieved with therapeutic injection of the talonavicular joint.", "Exam": "N / A", "Findings": "Axial CT with sagittal reformats through the ankle reveals cortical disruption at the proximal articular surface of the tarsal navicular bone. Multiloculated subchondral cyst adjacent to the cortical defect is noted.", "Differential Diagnosis": "Stress fracture (Expect to see partial or complete sagittal fracture line through navicular)\nOsteonecrosis (Usually see sclerosis and/or collapse of the navicular)", "Case Diagnosis": "Osteochondritis Dissecans of the Tarsal Navicular", "Diagnosis By": "Clinical Course / Symptoms Recovery", "Treatment & Follow Up": "Patient\u2019s symptoms were relieved with therapeutic injection of the talonavicular joint.", "Discussion": "Osteochondritis dissecans is the traditional term used to describe osteochondral fracture. The osteochondral fragment may remain in situ or partially or completely detached from its origin, forming a loose body. Osteochondritis dissecans has been described in a variety of bones. The ankle accounts for 4% of all cases of OCD and the tarsal navicular bone is rarely involved. Most commonly, ankle OCD\u2019s are seen in the talar dome. \n\nRadiographically, osteochondritis dissecans is often seen best on a lateral view as a lucent lesion disrupting the articular rim of the involved bone. CT demonstrates the navicular lesions well in both sagittal and coronal reformats, frequently as cortical depressions with a rim of sclerosis. MRI shows osteochondral lesions with low signal intensity on T1 and high signal intensity on T2 sequences (secondary to adjacent edema). Nuclear medicine bone scan typically shows mild to marked focal uptake in the region of the osteochondral defect. \n\nThe pathogenesis of the process is unknown but believed to be related to repetitive trauma, particularly from forces transmitted through the metatarsal rays on plantar flexion of the foot. Treatment is conservative with non-weight bearing activity and analgesia. Only patients with completely detached osteochondral fragments need consider undergo surgery to remove a symptomatic loose body. \n\n\nReferences:\n\nBui-Mansfield LT, Lenchick L, Rogers LF, Chew FS, Boles CA, and Kline M. Osteochondritis dissecans of the tarsal navicular bone: Imaging findings in four patients. Journal of Computer Assisted Tomography 24(5): 744-747\n\nWalther-Lansen S, Larsen E. Bilateral osteochondritis dissecans of the tarsal navicular. Ugeskr Laeger 1985;147:3816." }, "Topic": { "Title": "Osteochondritis Dissecans of the Tarsal Navicular", "Disease Discussion": "Osteochondritis dissecans is the traditional term used to describe osteochondral fracture. The osteochondral fragment may remain in situ or partially or completely detached from its origin, forming a loose body. Osteochondritis dissecans has been described in a variety of bones. The ankle accounts for 4% of all cases of OCD and the tarsal navicular bone is rarely involved. Most commonly, ankle OCD\u2019s are seen in the talar dome.", "ACR Code": "-1.-1", "Category": "Trauma", "Keywords": "OsteochondritisDissecansOsteochondral", "Reference": "Bui-Mansfield LT, Lenchick L, Rogers LF, Chew FS, Boles CA, and Kline M. Osteochondritis dissecans of the tarsal navicular bone: Imaging findings in four patients. Journal of Computer Assisted Tomography 24(5): 744-747\n\nWalther-Lansen S, Larsen E. Bilateral osteochondritis dissecans of the tarsal navicular. Ugeskr Laeger 1985;147:3816." } }, { "U_id": "MPX1937", "TAC": [ "MPX1937_synpic17376" ], "MRI": [], "Case": { "Title": "Orbital granular cell tumor", "History": "This 31 year old man presented with intermittent diplopia and slight exophthalmus of the right eye. Examination showed restricted lateral movement of the right eye. CT showed a mass involving the medial rectus muscle.", "Findings": "Fig 1. Non-contrasted axial CT showing mass involving medial aspect of right orbit.\n\nFig 2. Contrasted coronal CT showing mass involving medial aspect of right orbit including medial rectus muscle.\n\nFig 3. Histological section showing the neoplasm to be composed of lobules of uniform cells with eosinophilic granular cytoplasm and small oval vesicular to pycnotic nuclei.\n\nFig 4. The neoplastic cells are stained red with the periodic acid Schiff (PAS) reaction.\n\nFig 5. The neoplastic cells are stained by an immunoperoxidase technique for S-100.", "Differential Diagnosis": "\u2022 Metastasis\n\u2022 Thyroid opthalmopathy\n\u2022 Lymphoma", "Case Diagnosis": "Orbital granular cell tumor" }, "Topic": { "Title": "Orbital granular cell tumor", "Disease Discussion": "Granular cell tumors are most frequently found in the skin and subcutaneous tissues. They are infrequently encountered within the orbit. Currently, most authors consider granular cell tumors to be of neural derivation. This is supported by the immunostaining reaction for S-100. Ultrastructurally, the neoplastic cells contain abundant phagolysosomes. This accounts for the granular appearance by light microscopy and the the staining with the PAS reaction. The histological appearance of the orbital granular cell tumor is somewhat similar to an oncocytoma of the lacrimal gland from which it is distinguished by location and staining with the S-100 reaction.", "ACR Code": "1.3", "Category": "Neoplasm, NOS", "Keywords": "granular cell tumor" } }, { "U_id": "MPX1938", "TAC": [ "MPX1938_synpic22899", "MPX1938_synpic22900", "MPX1938_synpic22901", "MPX1938_synpic22902" ], "MRI": [], "Case": { "Title": "Nonspecific Interstitial Pneumonitis", "History": "Worsening chronic cough and mild dyspnea.", "Exam": "mild crackles bilateral lung bases", "Findings": "Initial chest radiographs interpreted as normal. Subsequent chest radiographs 3 months later showed bibasilar interstitial opacities. \nHigh resolution chest CT revealed predominantly mid and lower lung zone ground-glass opacities and prominent but not enlarged mediastinal lymph nodes.", "Differential Diagnosis": "Interstitial pneumonitis to include nonspecific interstitial pneumonitis.\npneumocytis carinii pneumonia\nnon tuberculous mycobacterial infection\npulmonary alveolar proteinosis", "Case Diagnosis": "Nonspecific Interstitial Pneumonitis", "Diagnosis By": "Lung biopsy", "Treatment & Follow Up": "Steroids and azathioprine therapy just initiated. No follow-up as of yet.", "Discussion": "No underlying etiology for this patient's interstitial lung disease was identified. A subclinical collagen vascular disease is speculated." }, "Topic": { "Title": "Nonspecific Interstitial Pneumonitis", "Disease Discussion": "This is a case of nonspecific interstitial pneumonitis; one of the idiopathic interstitial pneumonias.\n\nIdiopathic interstitial pneumonia refers to a group of disorders that are characterized by inflammation and/or fibrosis affecting the interstitium to a greater extent than the airways or alveoli. This group of disorders is a distinct subset of interstitial lung disease in that a known etiology is not identified. The idiopathic interstitial pneumonias are classified into groups with similar pathology, disease progression, treatment response and prognosis. The groups include (in decreasing order of incidence): Usual interstitial pneumia (UIP), nonspecific interstitial pneumonitis (NSIP), bronchioloitis obliterans-organizing pneumonia (BOOP), respiratory bronchiolitis-interstitial lung disease (RB-ILD), desquamative interstitial pneumonitis (DIP), lymphocytic interstitial pneumonitis (LIP) and acute interstitial pneumonitis. \n\nNonspecific interstitial pneumonits (NSIP) is nonclassifiable; meaining it cannot be classified as the other idiopathic interstitial pneumonias. The patients are typically middle-aged to elderly but tend to be younger than UIP and older than RB-ILD and DIP. NSIP affects females more commonly than males. Presenting symptoms include chronic dry cough, shortness of breath, low-grade fever and malaise. Chest radiographs may be normal or demonstrate irregular interstitial opacities with or without consolidation. Lung volumes may be normal to slightly decreased. CT reveals scattered bilateral ground-glass opacities in all patients. Other potential findings include airspace consolidation, linear opacities, bronchial dilatation and mediastinal lymphadenopathy. A unique feature of NSIP is the lack of honeycombing.\n\nOn biopsy there is typically a uniform appearance of interstitial inflammation. Inflammation only and no fibrosis are seen in the majority (48%) with inflammation and fibrosis (38%) and fibrosis only (14%) less common findings. \n\nNSIP has been related to underlying collagen vascular disease, inhalational exposure, severe pneumonia and ARDS. Therapy is based on immunosuppression including steroids and cytotoxic agents. Clinical and radiographic improvement is seen in 50-86% of patients with an 11% overall mortality.", "ACR Code": "6.2", "Category": "Idiopathic or Unknown", "Keywords": "Interstitial lung diseasenonspecific interstitial pneumonitis", "Reference": "Chapman, J: Disease Management Project; Interstitial Lung Disease. 13 Aug 2002\nDahnert, W. Radiology Review Manual 5th ed. Lipincott, Williams & Wilkins." } }, { "U_id": "MPX1942", "TAC": [ "MPX1942_synpic4378", "MPX1942_synpic4380", "MPX1942_synpic4381", "MPX1942_synpic4382", "MPX1942_synpic4383" ], "MRI": [], "Case": { "Title": "Diffuse Cerebral Edema from cardiac arrest", "History": "35 year old man presented to the emergency department with complaints of epigastric pain. He is diaphoretic, but otherwise appears in good health. During initial ER presentation patient became pulseless and was resuscitated for one hour, until a stable rhythm was established.", "Exam": "12-lead EKG demonstrated marked ST elevations c/w an acute infarct.", "Findings": "Noncontrast CT images demonstrate effacement of the the sulci. There is diffuse graying of the cerebral hemispheres with blurring and loss of normal gray-white differentiation and interface. The ventricles are small. Note that the cerebellum and brainstem are well preserved and have a normal appearance.\nAlso note pansinusitis with air-fluid level in sphenoids.", "Differential Diagnosis": "Any anoxic or hypoxic events - to include drowning, strangulation\nClosed Head Injury\n(These findings can be normal in premature infants)", "Case Diagnosis": "Diffuse Cerebral Edema from cardiac arrest", "Diagnosis By": "Clinical and Radiologic", "Treatment & Follow Up": "During initial ER presentation patient became pulseless and was resuscitated for one hour, when a stable rhythm was established.", "Discussion": "Patient is currently in poor condition in the ICU with deteriorating neurologic exam." }, "Topic": { "Title": "Diffuse Cerebral Edema, Swelling", "Disease Discussion": "Diffuse cerebral edema is among the most life-threatening of all cerebral insults with a mortality approaching 50%. Imaging findings may occur within hours after onset, but recognizable abnormalities may be delayed by 24 to 48 hours.\n\n\u2022 Imaging:\nThe most reliable early sign is effacement of the cerebral (surface) sulci, suprasellar and perimesencephalic cisterns. The ventricles appear small or compressed.\n\n\u2022 CT shows homogeneously decreased attenuation with loss of the gray-white differentiation. The cerebellum may appear relatively hyperdense compared to the the cerebral hemispheres - the \"white cerebellum\" sign. This is due to vascular (autoregulatory) events.\n\n\u2022 The \"reversal sign\" is similar, with the cerebellum, thalamus, and brainstem retaining their normal density appearance in comparison to the darker edematous cerebral cortex.\n\nUnilateral or bilateral cerebral edema may lead to brain displacement, accompanied by signs of herniation that are discussed on other topics at this site.", "ACR Code": "1.2", "Category": "Hypotension or Shock", "Keywords": "subarachnoid hemorrage mimicCNSbrain swelling", "Reference": "Osborn, A.G. (1994). Diagnostic Neuroradiology. St. Louis : Mosby.\n\nhttp://www.ajnr.org/cgi/content/full/24/2/254" } }, { "U_id": "MPX1941", "TAC": [ "MPX1941_synpic24519", "MPX1941_synpic24520", "MPX1941_synpic24522", "MPX1941_synpic24523" ], "MRI": [], "Case": { "Title": "Carotid Cavernous Fistula and ICA Aneurysm", "History": "20 y/o male inside HUM-V when hit with an RPG (rocket propelled grenade).", "Findings": "CT with contrast shows an enlarged R parasellar region consistent with an ICA aneurysm, and abnormal vasculature filling with contrast in the R posterior fossa. The R Carotid angiogram shows a large, cavernous ICA aneurysm. The angiogram also shows that this aneurysm is draining into the cavernous sinus. The R superior opthalmic vein is engorged, and visible in the arterial phase. The carotid cavernous fistula is also draining posteriorly into the transverse and sigmoid sinuses (likely through the superior petrosal and inferior petrosal sinuses)which are also visible in the arterial phase of the angiogram.", "Differential Diagnosis": "Trauma", "Case Diagnosis": "Carotid Cavernous Fistula and ICA Aneurysm", "Diagnosis By": "Angiographic", "Treatment & Follow Up": "Patient was treated endovascularly. ICA aneurysm was coiled." }, "Topic": { "Title": "Carotid Cavernous Fistula", "Disease Discussion": "This is a traumatic carotid cavernous fistula as a result of a HUM-V explosion in IRAQ.", "ACR Code": "1.4", "Category": "Vascular", "Keywords": "CarotidAneurysmFistula" } }, { "U_id": "MPX1948", "TAC": [ "MPX1948_synpic46440" ], "MRI": [], "Case": { "Title": "Centrilobular Emphysema", "History": "66 y.o. man with a 25 pack/year smoking history", "Findings": "Apical predominant parenchymal architectural distortion. Pulmonary vessels and bronchioles can be seen in the middle of the lucent bullae, indicating a centrilobular pattern.", "Differential Diagnosis": "Centrilobular Emphysema\nPanacinar Emphysema\nToxic Chemical Exposure\nLangerhans' cell histiocytosis\nlymphangioleiomyomatosis\ncystic bronchiectasis", "Case Diagnosis": "Centrilobular Emphysema", "Diagnosis By": "CT", "Discussion": "http://pathhsw5m54.ucsf.edu/ctpath/ctpath33.html" }, "Topic": { "Title": "Emphysema", "Disease Discussion": "Emphysema, a form of chronic obstructive lung disease is a debilitating chronic condition of lung destruction. Occurring at the level of the alveolus (distal to terminal bronchiole) there is destruction of the alveolar wall and subsequent enlargement of the air space without associated fibrosis. Although there are three types, centriacinar(lobular) is the most common. The other two types being paraseptal (thought to represent the basic lesion of bullous lung disease) and panacinar (the most widespread and most severe and is associated with alpha-1-antitrypsin deficiency). Chest x-ray findings include large lung volumes, flattening of the hemidiaphragms, increased retrosternal clear space, increased AP diameter, and distortion of the pulmonary vasculature which usually occur late in the disease. CT is important in the assessment of emphysema since it can asses the severity and distribution of the disease and reliably differentiate types in patients with mild to moderate forms of the disease. Unfortunately treatment for emphysema remains limited to removing the offending substance (often cigarette smoke) and supplemental oxygen.", "ACR Code": "68.751", "Category": "Idiopathic or Unknown", "Keywords": "EmphysemaCOPD", "Reference": "Armstrong, P. Imaging Diseases of the Chest. Mosby 2000. pp 924-31." } }, { "U_id": "MPX1950", "TAC": [ "MPX1950_synpic27241", "MPX1950_synpic27243" ], "MRI": [], "Case": { "Title": "Duplicated Renal Collecting System", "History": "36 year old female with a liver mass.", "Exam": "N/A", "Findings": "Triple phase IV contrast study of the abdomen demonstrates a liver hemangioma, and incidental note is made of a left-sided bifid ureter.", "Differential Diagnosis": "N/A", "Case Diagnosis": "Duplicated Renal Collecting System", "Diagnosis By": "CT scan", "Treatment & Follow Up": "N/A", "Discussion": "See Factoid" }, "Topic": { "Title": "Duplicated Renal Collecting System", "Disease Discussion": "Duplicated renal collecting systems represent renal units with two distinct pyelocalyceal systems associated with either a single or double ureter. In the case of two distinct ureters, the ureters either join together along their course and form a single ureter, or they both insert individually on the bladder. This anomaly presents either unilaterally or bilaterally, and is estimated to occur in up to fifteen percent of the population. Most individuals with a duplicated renal collecting system remain asymptomatic with their anomaly being found incidentally on imaging studies. Those patients who become symptomatic with their duplicated collecting system generally have two distinct and complete urters, and are prone to developing obstruction, reflux, and infection.\n A duplicated renal collecing system forms by one of two ways. The first results from the embryologic bifurcation of a single ureteral bud prior to the bifurcation of the ampulla, and produces either a bifid ureteral pelvis or a bifid ureter which joins distally prior to bladder insertion. The second results when two distinct embryologic ureteral buds arise from the Wolffian duct, giving rise to two complete and separate ureters which insert separately into the bladder. In this second case, with two separate ureters, the upper pole ureter drains below and medial to the lower pole ureter at its insertion. According to the Weigert-Meyer rule, the upper pole ureter is prone to obstruction and hydronephrosis as well as ureterocele formation, while the lower pole ureter is prone to refulx and at is risk for pyleonephritis. Additionally, this upper pole ureter may insert ectopically inferior to the bladder (e.g. urethera, or vagina), causing continual leakage of urine in females (not the case in males as the ectopic insertion is proximal to the external uretheral sphinter).", "ACR Code": "8.1", "Category": "Unsure", "Keywords": "renal collecting system duplicationcollecting system anomalyWiegert-Meyer rule", "Reference": "Brant, W. E., & Helms, C. A. (Eds.) Fundamentals of Diagnostic Radiology, 2nd edition. Baltimore: Williams \nand Wilkins 1999.", "External Links": "www.emedicine.com/radio/topic226.htm" } }, { "U_id": "MPX1953", "TAC": [ "MPX1953_synpic22194", "MPX1953_synpic22195" ], "MRI": [], "Case": { "Title": "Renal Tubular Acidosis, Medullary Nephrocalcinosis", "History": "35 year old white male with flank pain. Patient has history of frequent stone passage, sometimes as frequently as every other day", "Exam": "Mild flank pain. Microhematuria, with creatinine of 2.0. Remaining labs normal.", "Findings": "Severe bilateral medullary nephrocalcinosis", "Differential Diagnosis": "The primary differential covering the majority of cases:\n1.\tHyperparathyroidism\n2.\tRenal tubular acidosis\n3.\tMedullary sponge kidney\n\nAn exhaustive differential includes\u2026.\nHypercalciuria: Hyperparathyroidism\n\tParaneoplastic syndrome of lung and renal primaries\n\tCushings syndrome\n\tDiabetes insipidis\n\tHyper or hypothyroidism\nAlimentary: Mild-alkali syndrome\n\tHypervitaminosis D\n\tBeryllium poisoning\nOsseous: Osseous mets, multiple myeloma\n\tPorlonged immobilization\n\tProgessive senile osteoporosis\nRenal:\tMedullary sponge kidney\n\tRenal tubular acidosis\n\tBarter syndrome\nDrugs:\tFurosemide in infants\n\tProlonged ACTH therapy\n\tExcess vitamin E, D or calcium\n\tNephrotoxic drugs such as amphotericin B\nMiscellaneous\n\tSarcoidosis\n\tIdiopathic hypercalciuria or hypercalcemia", "Case Diagnosis": "Renal Tubular Acidosis, Medullary Nephrocalcinosis", "Diagnosis By": "Nephrology workup; laboratory analysis.", "Treatment & Follow Up": "Treated with a mixture of sodium and potassium bicarbonate, constant hydration.", "Discussion": "With treatment, the patient noted a decrease in the number of stones he would pass, from 2-3 a day, down to 1 every week or two." }, "Topic": { "Title": "Renal Tubular Acidosis, Medullary Nephrocalcinosis", "Disease Discussion": "Discussion: Distal renal tubular acidosis arises from the inability to adequately secrete hydrogen ions in distal renal tubule; functionally this means a person is unable to acidify their urine. This causes a number of problems, to include\na. Hypovolemia \u2013 the patient develops hyperchloremia, due to constant loss of serum sodium bicarbonate without concommitant loss of chloride ions. This retention of sodium chloride leads to loss of the normal extracellular fluid, and to compensate the patient must constantly hydrate.\nb. Bone pain from osteomalacia, as there is constant mobilization of calcium phosphate from bones due to metabolic acidosis.\nc. Nephrocalcinosis and nephrolithiasis due to underlying hypercalciuria combines with elevated urine pH and reduced urinary secretion of citrate.\nd. Hypokalemia and muscle weakness due to potassium wasting\n\nTreatement: Patients are treated with a mixture of sodium and potassium bicarbonate, constant hydration, and supplimenting their diet with substances rich in citric acid (such as lemonade).", "ACR Code": "8.5", "Category": "Metabolic (see also Toxic)", "Keywords": "Renal Tubular AcidosisRTAMedullary Nephrocalcinosis" } }, { "U_id": "MPX1954", "TAC": [ "MPX1954_synpic27245", "MPX1954_synpic27246" ], "MRI": [], "Case": { "Title": "Abdominal wall hematoma following the initiation of therapeutic anticoagultion.", "History": "56 year old female patient in the intensive care unit found to have a sudden drop in her hemoglobin and hematocrit following the recent initiation of anticoagulation therapy for a pulmonary embolus.", "Exam": "Drop in the patient's hemoglobin and hematocrit from 9.1/26.7 to 5.9/17.4 within a 24 hour period and the development of a palpable left sided tender adbominal mass. Just prior to her CT scan, while receiving heparin, the patient's PT was 18.3 (nml 11-13.8), PTT was 133.7 (23.8-35.5), PT ratio 1.5, INR 2.0.", "Findings": "Non contrast CT of the abdomen and the pelvis demonstrates a large hyperdense heterogeneous mass at the left lateral abdominal wall, not present on a prior CT of the abdomen from less than a week prior.", "Differential Diagnosis": "Acute hemorrhage/hematoma\nAbscess\nSoft tissue neoplasm", "Case Diagnosis": "Abdominal wall hematoma following the initiation of therapeutic anticoagultion.", "Diagnosis By": "This diagnosis was confirmed by the fact that the patient did not have an elevated white blood count or fever at the time of the scan, nor was the hyperdense mass present on the most recent prior examination, additionally, her acute drop in hemoglobin and hematocrit supports the diagnosis of acute hemorrhage/hematoma.", "Treatment & Follow Up": "Temporary withdrawal of anticoagulation.", "Discussion": "This patient was being started on anticoagulation therapy for a recent pulmonary embolism with intravenous heparin. Her PTT was elevated at 133.7, which falls beyond the goal of 70-90 (by this institution's laboratory) for a patient starting anticoagulation. Unfortunately patients starting herparin therapy often overshoot their goal PTT values during their initial titration." }, "Topic": { "Title": "Anticoagulation, complication, Abdominal wall hematoma", "Disease Discussion": "Medical anticoagulation represents an important therapeutic option for both treatment of and prophylaxis against thromboembolic disease. Typically heparing and warfarin are the agents employed. Unfractionated heparin acts primarily as an indirect thrombin inhibitor, and to a lesser extent as a factor Xa inhibitor. It has the advantage of fast activity, but presents difficulty with dosing (requiring intravenous administration) and monitoring of the patient's PTT. Dosing normally follows a nomogram and varies from institution to institution depending upon laboratory ranges. The introduction of low molecular weight heparin, a factor Xa inhibitor, as an alternative to unfractionated heparin allows easier administration with standard dosing, subcutaneous administration, and no laboratory monitoring. Alternatively, warfarin, an inhibitor of vitamin K-dependant coagulation factors, is typically used for long term out patient anticoagulation needs owing to its oral administration. Warfarin is monitored therapeutically on a weekly basis with the patient's PT and INR (standard INR goal 2.0-3.0).\n\nAs is the case with nearly all medical interventions, anticoagulation does not come without potential side-effects. The most significant of these centers around hemorrhage. Patients undergoing anticoagulation are at increased risk for bleeding, both following trauma and sponaneously. Abdominal wall hematomas represent a real and potentially fatal side effect of therapeutic anticoagulation. Several cases of abdominal wall hemorrhage have been reported in the literature following the initiation of anticoagulation therapy. In the majority of these cases, bleeding occured spontaneuosly.", "ACR Code": "4.9", "Category": "Iatrogenic or Surgical (complications)", "Keywords": "abdominal wall hematomaanticoagulation", "Reference": "Sharafuddin MJ, et al. Spontaneous extraperitoneal hemorrhage with hemodynamic collapse in patients undergoing anticoagulation: management with selective arterial embolization. J Vasc Interv Radiol. 2001 Oct;12(10):1231-4.\nBrant, WE, Helms, CA, Fundamentals of Diagnostic Radiology, 2nd ed, Williams & Wilkins, Baltimore, MD, 1999." } }, { "U_id": "MPX1959", "TAC": [ "MPX1959_synpic20918" ], "MRI": [], "Case": { "Title": "Psoas abscess", "History": "Patient presented to the ER in Jan2003 with 2 day history of fever, night sweats, groin pain, anorexia, nausea, and fatigue. Approximately 2 weeks prior to presentation the patient was seen by PCP for low-grade fevers and mild groin pain that radiated to her hip and back. She was diagnosed with groin strain and prescribed Flexeril. The patient continued to experience intermittent fevers and progressively worsening pain in her hip and groin despite frequent use of Flexeril. The pain was noted to be particularly bad while climbing stairs that would improve with sitting and rest. There were otherwise no changes in her bowel habits or stool quality (2-3 loose stools/day), no urinary symptoms, chest pain, dispnea, hemoptysis, or musculoskeletal trauma. The patient also denied a history of chronic gastrointestinal disease. She had an appendectomy 10 years ago. Past medical history also significant for a right sided nephrectomy in 2002 for an angiolipoma. Post-operative course complicated by a septic hematoma in the right kidney fossa, pneumonia and deep venous thromboses (DVTs). In 2003 an IVC Greenfield filter was placed for recurrent DVTs unresponsive to anticoagulation therapy. Medications Flexeril, Aygestin (for Menorrhagia), Progestin and Coumadin.", "Exam": "Patient was normotensive, tachycardic, and febrile. The abdomen was without rashes, distention, tenderness, masses, hepatosplenomegaly, guarding or rebound, and bowel sounds were present throughout. The right groin area was tender to mild palpation. The patient had tenderness with passive extension of right thigh (a positive psoas sign) and no tenderness with passive internal rotation of flexed thigh (negative obdurator sign). The physical exam was otherwise unremarkable.\nLabs: CBC: 20>12.1/36.5<350; basic metabolic panel: wnl; urinalysis abnormal for high amount of blood; stool guaiac negative", "Findings": "Frontal view of the abdomen shows an abnormal psoas shadow (i.e. blurring of the right psoas muscle edge).\nAxial images from CECT (IV and oral) of the abdomen and pelvis at L2 or L3 shows a rim enhanced low-attenuation mass in the right posterior abdomen in close proximity to the cecum laterally, extending medially into the psoas muscle. Additional axial images shows that the mass is fusiform and extends from approximately T12 into the pelvis along the psoas muscle.", "Differential Diagnosis": "Abdominal plain film: retroperitoneal inflammatory process resulting in fluid or pus accumulation, retroperitoneal malignancy (primary or metastatic), hematoma\nCT with IV and oral contrast: Abscess (ruptured appendix/diverticulum, Crohn\u2019s disease with fistula formation, chronic pyelonephritis, spreading infection from the spine), Neoplastic (locally invasive colon cancer/ renal cell carcinoma, metastatic cancer, lymphoma)", "Case Diagnosis": "Psoas abscess", "Treatment & Follow Up": "Following an unsuccessful attempted CT guided percutaneous aspiration of the abscess under local anesthetic, the abscess was surgically incised and drained of approximately 150 milliliters of purulent material containing gram positive cocci (cultures revealed Group A Streptococcus) The patient was then placed on triple antibiotic therapy until the end of her hospital stay", "Discussion": "Psoas abscess is an uncommon and potentially deadly disease usually following a protracted and insidious course. Classically a patient with a psoas abscess presents with a triad of complaints of flank pain, a prolonged fever, and a limitation in hip movement, however, other symptoms include a pain or mass in the thigh,loin or flank, malaise, weight loss, and a flexion contracture of the hip joint. When the cause of the infection is not identifiable the psoas abscess is considered \u201cprimary\u201d, otherwise, it is \u201csecondary\u201d. In the US 60% of psoas abscess cases are primary, 88% of which are caused by Staphylococcus aureus. For cases involving a secondary psoas abscess the most significant cause is Crohn\u2019s disease; local infectious processes involving the gastrointestinal tract, urinary tract, and bones are also significant causes. In this patient the psoas abscess was located on the same side that a heminephrectomy was performed a year prior to presentation suggesting a possible link. There are a few reported cases of psoas abscess formation following nephrectomy.\n\nBecause of the insidious nature and variation in clinical presentation of this disease the diagnosis is often delayed. Plainfilm, ultrasound and computed tomography (CT) have proven useful in the diagnosis. On plainfilm a psoas abscess may appear as a mass or blur the ipsilateral psoas muscle edge. Ultrasound (US) is a rapid screening method for identifying a retroperitoneal abscess which appears as an hypoechoic mass. However, US cannot identify the cause of the abscess and requires an experienced technician. CT has the highest sensitivity for diagnosing psoas abscess and remains the method of choice for describing the structure of the lesion and identifying the underlying cause.\n\nTreatment of the abscess typically begins with a CT guided biopsy followed by drainage and antibiotic therapy. If at all possible the abscess should be drained via the less invasive method of radiological guided percutaneous needle aspiration; however, if this fails, open surgical drainage should be performed." }, "Topic": { "Title": "Psoas abscess", "Disease Discussion": "Psoas abscess is an uncommon and potentially deadly disease usually following a protracted and insidious course. Classically a patient with a psoas abscess presents with a triad of complaints of flank pain, a prolonged fever, and a limitation in hip movement, however, other symptoms include a pain or mass in the thigh,loin or flank, malaise, weight loss, and a flexion contracture of the hip joint. When the cause of the infection is not identifiable the psoas abscess is considered \u201cprimary\u201d, otherwise, it is \u201csecondary\u201d. In the US 60% of psoas abscess cases are primary, 88% of which are caused by Staphylococcus aureus. For cases involving a secondary psoas abscess the most significant cause is Crohn\u2019s disease; local infectious processes involving the gastrointestinal tract, urinary tract, and bones are also significant causes. In this patient the psoas abscess was located on the same side that a heminephrectomy was performed a year prior to presentation suggesting a possible link. There are a few reported cases of psoas abscess formation following nephrectomy.\n\nBecause of the insidious nature and variation in clinical presentation of this disease the diagnosis is often delayed. Plainfilm, ultrasound and computed tomography (CT) have proven useful in the diagnosis. On plainfilm a psoas abscess may appear as a mass or blur the ipsilateral psoas muscle edge. Ultrasound (US) is a rapid screening method for identifying a retroperitoneal abscess which appears as an hypoechoic mass. However, US cannot identify the cause of the abscess and requires an experienced technician. CT has the highest sensitivity for diagnosing psoas abscess and remains the method of choice for describing the structure of the lesion and identifying the underlying cause.\n\nTreatment of the abscess typically begins with a CT guided biopsy followed by drainage and antibiotic therapy. If at all possible the abscess should be drained via the less invasive method of radiological guided percutaneous needle aspiration; however, if this fails, open surgical drainage should be performed.", "ACR Code": "4.2", "Category": "Differential Diagnosis", "Keywords": "PsoasAbscess", "Reference": "References: \nAgrawal SN, Dwivedi AJ, Khan M.Primary psoas abscess. 2002. Digestive Diseases and Sciences. 47(9):2103-5. \n\nCantasdemir M, Kara B, Cebi D, Selcuk ND, Numan F. 2003. Computed tomography-guided percutaneous catheter drainage of primary and secondary iliopsoas abscesses. Clinical Radiology. 58(10):811-5.\n\nChern Chii-Hwa, Sheng-Chuan Hu, Wei-Fong Kao, Jeffrey Tsai, David Yen, Chen-Hsen Lee. 1997. Psoas abscess: making an early diagnosis in the ED. American Journal of Emergency Medicine. 15(1):83-8. \n\nTez S, Dilmen G, Unsal A, Koktener A, Cimentepe E, Saglam R. 2002. Psoas abscess twenty-one years after ipsilateral nephrectomy. International Urology and Nephrology. 34(3):311-3" } }, { "U_id": "MPX1960", "TAC": [ "MPX1960_synpic23964", "MPX1960_synpic23965" ], "MRI": [ "MPX1960_synpic23968", "MPX1960_synpic23970" ], "Case": { "Title": "Congenital partial absence of the pericardium.", "History": "Chronic cough.", "Exam": "Non contributory.", "Findings": "Scout view from CT demontrates left sided heart deviation.\nAxial CT images demonstrate left sided cardiac deviation with rotational component and absence of left sided pericardium with interpostion of lung between aorta and left main pulmonary artery.\nMultiplane MRI images demonstrate absent left and posterior pericardial fat and pericardium.", "Differential Diagnosis": "For leftward deviation of heart on plain radiograph:\n\n\u2022 Chest wall deformities: pectus excavatum\n\u2022 Post surgical: volume loss\n\u2022 Congenital heart disease with right vent hypertrophy\n\u2022 Surgical or congenital abscence of the pericardium", "Case Diagnosis": "Congenital partial absence of the pericardium.", "Diagnosis By": "CT and MRI", "Treatment & Follow Up": "Surgical consult." }, "Topic": { "Title": "Congenital absence of pericardium", "Disease Discussion": "Congenital absence of the pericardium is a rare anomaly which usually (67%) occurs on the left side. A complete form exists and is usually diagnosed incidentally. Normally, the aortopulmonary window is covered by pericardium and contains some fat. Left sided pericardial absence absence allows interposition of lung between the aorta and and the main segment of the pulmonary artery. The defect usually causes the heart to rotate to the left. Sometimes, the left atrial appendage can bulge through the defect. Associated congenital heart defects include atrial septal defect, patent ductus arteriosus, mitral valve stenosis, or tetralogy of Fallot.\n\nClinical: \nPatients are often asymptomatic and the defect is found incidentally. The defect may cause herniation and strangulation of parts of the left heart. Symptoms can include syncope, chest pain or arrhythmias. Death may be caused by torsion of the great arteries, constriction of a coronary artery or herniation and/or incarceration of the left atrial appendage.\n\nImaging:\nChest x-ray shows left-sided displacement and posterior bulging of the heart. Herniation of the left atrial appendage resembles enlargement of the pulmonary artery. On echocardiography excessive cardiac motion and enlargement of the left atrial appendage may be seen. Definitive diagnosis can by obtained with MRI and CT. Interposition of lung between the aorta and left pulmonary artery is diagnostic.\n\nTreatment:\nThe defect can be enlarged or patched surgically to alleviate herniation.", "ACR Code": "5.2", "Category": "Congenital, malformation", "Keywords": "pericardiumcardiac deviation", "Reference": "1. CT and MR Imaging of Pericardial Disease1 Wang et al Radiographics. 2003;23:S167-S180.\n2.http://public2.bcm.tmc.edu/radiology/cases/pediatric Texas Children's Hospital, Houston, Texas. Texas Heart Institute. Edward B. Singleton" } }, { "U_id": "MPX1957", "TAC": [ "MPX1957_synpic41668", "MPX1957_synpic41669", "MPX1957_synpic41670", "MPX1957_synpic41671", "MPX1957_synpic41676", "MPX1957_synpic41677" ], "MRI": [], "Case": { "Title": "Pneumocystis jiroveci (P. carinii) Pneumonia", "History": "60 year old male with tachypnea and tachycardia with high clinical concern for pulmonary embolus.", "Exam": "Initial Laboratory Data:\nWBC: 5.4, HGB: 11.0, HCT: 33.6, PLTS: 309.\n\nFurther in the Hospitalization:\nLDH: 506 U/L\nGram Stain: Few RBCs, No organisms noted.\nAFB: Negative\nPneumocystis Direct Fluorescent Antibody (DFA): Negative \nC. Neoformans: Negative\nLegionella: Negative\nS. Pneumonia: Negative\n\nHIV: Positive\nCD4/CD8 ratio: 0.55 L (0.79-4.39)\nABS CD3/CD4: 144 L (414-1293 cell/uL)\nABS CD3: 413 L (690-2540 cell/uL)\nABS CD19+: 51 L (90-660 cell/uL)", "Findings": "Admission radiography: PA chest radiograph reveals a right subclavian central venous catheter with hypoinflated lung volumes and increased bibasilar ground glass opacities.\n\nContrast enhanced CT on admission: Diffuse multilobar ground-glass opacities with sharp transitions between normal and abnormal lung, with interstitial thickening in a predominately lower-lobe distribution.\n\nHospital Day 2: AP chest radiograph demonstrates a stable right subclavian venous catheter, with bibasilar reticulonodular ground glass opacities.\n\nHospital Day 6: AP chest radiograph from hospital day 6, reveals that the patient has been intubated, and has developed a spontaneous pneumomediastinum with extensive subcutaneous emphysema surrounding the neck. There is no pneumothorax. There are continued bibasilar reticulonodular ground glass opacities.\n\nAP chest radiograph from hospital day 6, obtained later in the day secondary to new respiratory distress, reveals that the patient has developed a significant left sided pneumothorax, with persistent pneumomediastinum, bibasilar ground-glass reticulonodular opacities, and subcutaneous emphysema surrounding the base of the neck. The patient\u2019s support devices are stable when compared to the prior studies.\n\nOn hospital day 10 the patient experienced worsening respiratory distress, and an unenhanced CT of the chest was performed.\n\nAn axial image at the level of the aortic arch demonstrates continued pneumomediastinum, and a left-sided pneumothorax. There is a small right-sided pleural effusion, with persistent ground-glass opacities.\n\nAn axial image at the level of the hila demonstrates continued pneumomediastinum, and a left-sided pneumothorax. There are persistent ground-glass opacities with focal areas of consolidation.\n\nAn axial image at the level of the right hemidiaphragm demonstrates continued pneumomediastinum, and a left-sided pneumothorax. There are persistent ground-glass opacities with focal areas of consolidation, and a small right-sided pleural effusion.", "Differential Diagnosis": "\u2022 Pneumocystis jiroveci pneumonia.\n\u2022 CMV pneumonia\n\u2022 Lymphocytic interstitial pneumonia.", "Case Diagnosis": "Pneumocystis jiroveci (P. carinii) Pneumonia", "Diagnosis By": "Lung Biopsy", "Treatment & Follow Up": "The lingular biopsy specimen demonstrated diffuse alveolar damage, with an organizing fibrosing pattern. The anterior segment of the left upper lobe specimen revealed marked interstitial fibrosis, focal type II pneumocyte hyperplasia, squamous metaplasia, and scattered residual alveoli consistent with organizing to fibrosing pattern of diffuse alveolar damage. The typical histologic findings of PCP consist of proliferation of type II pneumocytes, diffuse alveolar damage, granulomatous inflammation, and cyst formation.\n\nOpen lung biopsy demonstrated the histologic findings of pneumocystis jiroveci, and the GMS stain was positive, confirming the suspected diagnosis of pneumocystis jiiroveci pneumonia.", "Discussion": "This case demonstrates typical radiographic findings of PCP, with symmetric bilateral lower lobe reticulonodular opacities, complicated by pneumomediastinum followed by the development of pneumothorax. Additionally, the BAL was negative, necessitating open lung biopsy to confirm the diagnosis." }, "Topic": { "Title": "Pneumocystis jiroveci (P. carinii) Pneumonia", "Disease Discussion": "Lesions/Condition: Pneumocystis jiroveci (P. carinii)\n\nDiscussion: \n\nPneumocystis jiroveci (P. carinii) originally thought to be protozoan, now classified as a fungal element, results in clinically significant pneumonia, and is an AIDS defining illness that occurs when the CD4 count drops to below 200 cells/mm3. Additionally, any immunocompromised patient may be affected; organ recipients on immunosuppressive treatment, oncologic and hematologic patients, the elderly, severely malnourished children, and patients requiring prolonged corticosteroid therapy.\n\nThe most common radiographic finding in patients with PCP consists of diffuse, bilateral symmetric ground-glass reticulonodular, or finely granular opacities occurring in a perihilar, or lower lung zone distribution. Less commonly, PCP will occur with upper lobe predominance. If untreated, these opacities may manifest as diffuse air space consolidation. As the disease progresses, interstitial disease will become more pronounced, and air cysts may be noticed in 5% to 35% of patients. Occasionally, single or multiple nodules, miliary nodules, cavitation, hilar or mediastinal adenopathy, and pleural effusion will be identified. CT typically demonstrates symmetric bilateral ground-glass opacities, which may be diffuse, or have a mosaic pattern with sharp transitions between normal and abnormal lung giving a \u201ccrazy-paving\u201d pattern. Spontaneous pneumothorax may be identified in 5% to 10% of patients, and is more common when cysts are present. Pneumomediastinum may also be evident occurring by itself or in concert with pneumothorax.\n\nMost patients have characteristic radiographic findings of PCP, eliminating the need for CT. However, in patients with symptoms and atypical radiographic findings, CT may show ground-glass opacities, that when correlated with the CD4+ count and other clinical markers may allow the correct diagnosis of PCP to be made. Other causes of ground-glass opacities in patients with AIDS include CMV pneumonia and lymphocytic interstitial pneumonia.\n\nClinically, patients with PCP demonstrate nonspecific complaints. Fever, cough, progressive dyspnea on exertion, weight loss, night sweats, and chest pain are all common symptoms. Lactate dehydrogenase (LDH) levels are frequently elevated, and patients demonstrate restrictive patterns on pulmonary function tests, with hypoxemia when exercising. Clinicians may employ induced sputums, or use bronchoscopy with BAL to clinch the diagnosis. BAL which has close to 100% sensitivity and 89% specificity in diagnosing PCP, is useful when positive, however when results are negative, transbronchial or open lung biopsy may be pursued when the clinical findings suggest a high probability of PCP. Patients will often begin empirical therapy in the absence of definitive diagnosis to avoid potential complications.\n\nSummary: Perihilar and bilateral lower lobe reticular opacities on chest radiography in a patient with a CD4 count less than 200 cells/mm3 suggests PCP.", "ACR Code": "6.2", "Category": "Infection, fungi", "Keywords": "Pneumocystis jiroveci PneumoniaPCPAIDS defining illness", "Reference": "Shah et al. RadioGraphics 1997;17:47-58\nSider et al. RadioGraphics 1993; 13:771-784\nFraser et al. Synopsis of Diseases of the Chest. Third Edition. Elsevier Saunders. Philadelphia, PA. 2005. \nPope T. Aunt Minnie\u2019s Atlas and Imaging-Specific Diagnosis. 2nd Ed. Lippincott Williams & Wilkins. Philadelphia, PA. 2003." } }, { "U_id": "MPX1965", "TAC": [ "MPX1965_synpic30982" ], "MRI": [], "Case": { "Title": "Classical Hodgkin's Lymphoma, nodular sclerosing type", "History": "21 year old man with a 2 month history of abdominal pain, weight loss, fevers, and chills.", "Exam": "N/A", "Findings": "\u2022 Increased densities in the anterior and posterior mediastinum\n\u2022 Enlarged prevascular lymph node, 1.7cm\n\u2022 Enlarged Peritracheal lymph node, 1.6cm\n\u2022 Moderate pericardial effusion", "Differential Diagnosis": "\u2022 Thymic tumors\n\u2022 Pericardial tumors\n\u2022 Mediastinal carcinoids\n\u2022 Cystic mediastinal lesions\n\u2022 Thoracic fungal infections\n\u2022 Other causes of lymphadenopathy", "Case Diagnosis": "Classical Hodgkin's Lymphoma, nodular sclerosing type", "Diagnosis By": "biopsy and histology", "Treatment & Follow Up": "The Pt will receive combination radiation and chemotherapy. The overall 5 year survival for Hodgkin's disease with treatment is 82%. PET scans are a useful means of staging and followup to determine relapse. This Pt has received a PET scan which will be entered and updated soon.", "Discussion": "\u2022 Lymphomas are divided into Hodgkin\u2019s and non-Hodgkin\u2019s.\n\u2022 Hodgkin\u2019s lymphoma is characterized by Reed-Sternberg cells, with 4 subtypes.\n\u2022 In the thorax, nodular sclerosing is the most common subtype with a predilection for the mediastinum.\n\u2022 Nodular sclerosing accounts for >50% of Hodgkin\u2019s lymphomas.\n\u2022 Frequency - In the US, 7400 estimated new cases in 2001\n\u2022 Bimodal distribution - 15-40 years old, >55 years old\n\u2022 Treatment consists of radiation and/or chemotherapy\n\u2022 Survival rates, 1yr-93%, 5yr-82%, 10yr-72%, 15yr-63%" }, "Topic": { "Title": "Classical Hodgkins Lymphoma, nodular sclerosis subtype", "Disease Discussion": "Lymphoma", "ACR Code": "6.3", "Category": "Neoplasm, NOS", "Keywords": "hodgkinslymphomanodular", "Reference": "Bradley AJ, Carrington BM, Lawrance JA, et al: Assessment and significance of mediastinal bulk in Hodgkin\u2019s disease: comparison between computed tomography and chest radiography. J Clin Oncol 1999 Aug: 17(8): 2493-8.\n\nCastellino RA, Blank N, Hoppe RT, Cho C: Hodgkin disease: contributions of chest CT in the initial staging evaluation. Radiology 1986 Sep; 160(3): 604-5.\n\nSchomberg PJ, Evans RG, O\u2019Connell MJ, et al: Prognostic significance of mediastinal mass in adult Hodgkin\u2019s disease. Cancer 1984 Jan 15; 53(2): 324-8.\n\nLichtenstein AK, Levine A, Taylor CR, et al: Primary mediastinal lymphoma in adults. Am J Med 1990 Apr; 68(4): 509-14." } }, { "U_id": "MPX1956", "TAC": [ "MPX1956_synpic54992", "MPX1956_synpic54993", "MPX1956_synpic54994", "MPX1956_synpic54995" ], "MRI": [ "MPX1956_synpic54997", "MPX1956_synpic54998", "MPX1956_synpic54999", "MPX1956_synpic55000", "MPX1956_synpic55001", "MPX1956_synpic55003", "MPX1956_synpic55004", "MPX1956_synpic55005" ], "Case": { "Title": "Nonketotic Hyperglycemic Hemichorea/Hemiballismus", "History": "This previously healthy 50 y.o. woman presents with the acute onset of left sided hemichorea.", "Exam": "Spontaneous choreiform movements of the left arm.\n\u2022 BP 220/104 mm Hg\n\u2022 Glu 421 mg/dl\n\u2022 Ketones (-)\n\u2022 Hgb A1C - 17.7%\n\nVideo of hemichorea(different pt) - http://en.wikipedia.org/wiki/File:Hemichorea_and_dystonia.ogv", "Findings": "\u00bb CT (acute)\n\u2022 abnormal hyper-attenuation in the right basal ganglia\n (putamen and caudate head)\n\u2022 old left basal ganglia lacunar infarct\n\u2022 bilateral cerebellar wedge lesions\n\n\u00bb MRI (subacute - 3 days)\n\u2022 T1W hyperintensity in the same region as hyper-attenuation on CT\n (putamen and caudate head)\n\u2022 T2W hypointensity in basal ganglia - putamen and caudate head", "Differential Diagnosis": "\u2022 Cerebral infarction\n\u2022 Reperfusion contrast enhancement\n\u2022 Hemorrhagic stroke\n\u2022 Hypertensive hemorrhage\n\u2022 Angioinvasive mycotic hemorrhage", "Case Diagnosis": "Nonketotic Hyperglycemic Hemichorea/Hemiballismus", "Diagnosis By": "Clinical, autopsy, and pathology", "Treatment & Follow Up": "During her hospitalization she developed acute respiratory failure and died 36 days after admission. Her autopsy showed a \"mummified\" appearance to the Right basal ganglia infarct, with \"mineralization and scattered hemosiderin\". There were \"focal microhemorrhages\" and \"calcification-mineralization of the infarcted tissue. Mineralized neurons are seen.\"", "Discussion": "Hyperglycemia is associated with damage to the basal ganglia (BG). Proposed mechanisms include selective vulnerability, altered BG metabolism, breakdown of the blood brain barrier, hyper-viscosity of blood, and underlying small vessel disease.\n\nThe appearance of a hyperdense infarction on CT is often related to re-perfusion. This may be seen following thrombolysis, especially after a contrast injection. In this patient, without a contrast injection, there must be another explanation for the high attenuation. On the non-contrast CT, the hyper attenuation could be due to microscopic extravasated RBCs - but it is not confluent like a hematoma. \n\nThe subacute (3 days) MRI findings might also be explained by intact RBCs, extravasated - with intracellular met-hemoglobin. Intracellular methemoglobin is bright on T1W and dark on T2W - just as shown in this case. Lysed RBCs, with extracellular methemoglobin, is bright on both T1 and T2.\n\nThere are, however, other explanations for T1W bright/T2 dark putamen in non-ketotic hyperglycemic hemichorea/hemiballismus - including reactive astrogliosis with manganese accumulation. You may read the linked topics for more discussion." }, "Topic": { "Title": "Nonketotic hyperglycemic hemichorea hemiballismus", "Disease Discussion": "Hyperglycemic hemichorea/hemiballismus is a recognized entity, seen most often in older patients, women more often than men, Type 2 diabetes mellitus (DM), presenting with a blood glucose > 400 mg/dl - and usually without ketosis. It has been reported more often in Asian women. \n\nThis may be the patient's first presentation with DM. The \"classic\" MR findings include unilateral or bilateral signal changes in the basal ganglia (putamen >> caudate) on MR and CT. \n\nMost characteristic is T1 hyperintensity in the putamen; and, corresponding T2 hypointensity. CT scans may show hyperattenuation in the putamen.\n\nIn most patients, both the clinical and the imaging findings are reversible with control of blood sugar.\n\nREFS for hyperintense basal ganglia - http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=link&linkname=pubmed_pubmed&uid=7677016\nPMID: 7677016\n\nPossible explanations for the imaging features (hyperattenuation on CT, Dark Bright T1, Dark T2) include blood-brain-barrier breakdown (BBB), deposition of calcium and mineralization, microhemorrhages, myelin destruction, and manganese associated with reactive astrogliosis. Some of these would be acute (contrast and hemorrhage), and others more likely to be subacute or chronic (mineralization and astrogliosis).\n\nReferences below courtesy of \nMichael H Lev, MD, FAHA\nDirector, Emergency Neuroradiology and Neurovascular Lab\nMassachusetts General Hospital\nAssociate Professor of Radiology\nHarvard Medical School\n---------------------------------------------------------------\nWintermark M, Fischbein NJ, Mukherjee P, Yuh EL, Dillon WP. Unilateral putaminal CT, MR, and diffusion abnormalities secondary to nonketotic hyperglycemia in the setting of acute neurologic symptoms mimicking stroke.\nAJNR Am J Neuroradiol. 2004 Jun-Jul;25(6):975-6.\nPMID: 15205134\n\n\nAbstract\nA 75-year-old Asian man presented with two episodes of chorea associated with nonketotic hyperglycemia. His chorea rapidly resolved after restitution of a normal serum glucose level, although an MR image obtained at the time of acute symptoms demonstrated high signal intensity on T1-weighted images, low signal intensity on T2-weighted images, and restricted diffusion, all involving the left putamen. A CT scan obtained 1 month later demonstrated faint hyperattenuation of the involved putamen. The reported pathophysiologic considerations for these imaging features are reviewed, and an original explanation is proposed.\n\nComments\nAJNR Am J Neuroradiol. 2005 Jan;26(1):194; author reply 194-5. PMID: 15661727\n \n----------------------------------------------------------------------\nLai PH, Tien RD, Chang MH, Teng MM, Yang CF, Pan HB, Chen C, Lirng JF, Kong KW. Chorea-ballismus with nonketotic hyperglycemia in primary diabetes mellitus.\nAJNR Am J Neuroradiol. 1996 Jun-Jul;17(6):1057-64.\n\nAbstract\nPURPOSE: To describe the neuroimaging (Ct, MR, and single-photon emission CT [SPECT]) findings in a series of patients with chorea-ballismus associated with nonketotic hyperglycemia in primary diabetes mellitus and to correlate the imaging findings with the clinical presentation.\n\nMETHODS: The neuroimaging and clinical data from 10 patients with chorea-ballismus associated with nonketotic hyperglycemia in primary diabetes mellitus were evaluated. Family and drug histories, as well as other causes of chorea, were excluded. All 10 patients had CT, 5 also had MR imaging, and 3 had SPECT examinations. Three had follow-up CT and MR imaging studies, and MR findings were correlated with CT findings in 5 cases. Two experienced neuroradiologists, aware of the diagnosis but blinded to the clinical status of the patients, evaluated all images and reached a consensus as to the final\ninterpretation.\n\nRESULTS: CT studies in 9 of 10 patients showed a hyperdense putamen and/or caudate nucleus; in 1, the CT findings were normal. T1-weighted MR images in all 5 patients who had MR imaging (including the patient with a normal CT study) showed hyperintense lesions without significant T2 signal alternation at the basal ganglia. In all 3 of the patients who had SPECT studies of the brain, the scans revealed hypoperfusion at corresponding areas. All 3 follow-up studies depicted resolution of the lesions in the abnormal basal ganglia. Increased hypointensity on T2-weighted and gradient-echo T2*-weighted images was also\nobserved in the sequential MR images. In all patients, the initial side of involvement correlated well with the neuroimaging findings. The chorea resolved within 2 days after treatment of the hyperglycemia in 9 patients.\n\nCONCLUSION: In patients with chorea-ballismus associated with nonketotic hyperglycemia in primary diabetes mellitus, CT and T1-weighted MR images show unilateral or bilateral lesions of the putamen and/or caudate. SPECT scans show hypoperfusion. These findings may be related to petechial hemorrhage and/or myelin destruction. Early recognition of these imaging characteristics may facilitate diagnosis of primary diabetes mellitus with hyperglycemia and prompt appropriate therapy.\n\nPMID: 8791916", "ACR Code": "1.5", "Category": "Metabolic (see also Toxic)", "Keywords": "diabetes basal ganglia (putamen)hemiballismus hemichoreaCT hyperdense, T1W hyperintense T2W hypointense", "External Links": "www.ncbi.nlm.nih.gov/pubmed?term=nonketotic%20hyperglycemia%20stroke&itool=QuerySuggestion" } }, { "U_id": "MPX1971", "TAC": [ "MPX1971_synpic16543" ], "MRI": [], "Case": { "Title": "Primary adenocarcinoma of small bowel", "History": "N/A", "Exam": "Unknown", "Findings": "Mass involving the small bowel wall (probably jejunum) and extending into the mesentery. Mild thickening of adjacent small bowel wall. No frank obstruction.", "Differential Diagnosis": "Small bowel adenocarcinoma, carcinoid, lymphoma, sarcoma or metastasis.", "Case Diagnosis": "Primary adenocarcinoma of small bowel", "Treatment & Follow Up": "Unknown", "Discussion": "Unknown" }, "Topic": { "Title": "Primary adenocarcinoma of small bowel", "Disease Discussion": "Small bowel cancer in uncommon with about 4,600 cases reported annually in the United States (total incidence of 1.4 per 100,000 patients). Types of small bowel cancer include adenocarcinoma, carcinoid, lymphoma and sarcoma. \nPrimary adenocarcinoma of the small bowel is a rare entity accounting for less than 1% of all primary GI malignant tumors. The small bowel contains more than 75 percent of the length and about 90 percent of the mucosal surface area of the gastrointestinal tract but is the least common site of primary cancer within the GI tract. It is much more uncommon than colorectal cancer, gastric or esophageal cancer. Conditions with higher incidence of small bowel adenocarcinoma include familial polyposis, AIDS, Peutz-Jeghers, Lynch II syndrome, celiac disease and Crohns disease. \nMalignant small bowel tumors tend to be symptomatic; whereas, benign tumors are often found incidentally. Symptoms initially are vague including abdominal pain, weight loss, occult fecal blood (50%) and jaundice (33% of duodenal tumors). 1/2 to 2/3 of cases are discovered late in their course at emergency laparotomy for obstructive symptoms. The most common location for adenocarcinoma to occur is in the duodenum. \nBarium studies and CT can both be helpful for detecting small bowel adenocarcinoma. Small bowel follow-through sensitivity is 50-80 percent. Enteroclysis has higher sensitivity, but requires greater technical skill.\nOn CT the tumor typically appears as focal bowel wall nodular thickening and may have a soft tissue mass extending into the mesentery. CT can be helpful for evaluating the extent of extraluminal disease, including local extension, lymph nodes and distant metastasis. \n5-year survival after diagnosis of adenocarcinoma of the small bowel is 20-30%.", "ACR Code": "7.3", "Category": "Neoplasm, carcinoma", "Keywords": "small boweladenocarcinoma", "Reference": "Medcyclopaedia, Amersham Health\nhttp://www.amershamhealth.com/medcyclopaedia\n\nAbeloff: Clinical Oncology, 2nd ed., Small bowel neoplasms by David M. Mahvi, James Stone, pp 1589-1594", "External Links": "www.amershamhealth.com/medcyclopaedia" } }, { "U_id": "MPX1986", "TAC": [ "MPX1986_synpic26293" ], "MRI": [], "Case": { "Title": "Nephrolithiasis", "History": "Right upper quadrant pain.", "Exam": "N/A", "Findings": "Ultrasound of the RUQ demonstrated a normal liver, common duct, and gall bladder. The right kidney deomstrated mild hydronephrosis, hyperemia, mild perinephric fluid, and an enlarged dilated ureter.", "Differential Diagnosis": "Nephrolithiasis with obstructing stone\nPyelonephritis\nDistal ureter obstruction secondary to a mass", "Case Diagnosis": "Nephrolithiasis", "Diagnosis By": "Non-contrast CT of the abdomen/pelvis demonstrating a right-sided stone at the UVJ.", "Discussion": "See Factoid" }, "Topic": { "Title": "Nephrolithiasis", "Disease Discussion": "Nephrolithiasis classically presents with renal colic and hematuria. Stones within the renal collecting system typically obstruct at one of three locations: the ureteropelvic junction, the pelvic brim, or the ureterovessicular junction. Occasionally obstructing stones may also lodge at the bladder outlet. When acute in onset, many patients with obstructing stone disease will present to the emergency department with acute flank pain. The differential diagnosis consideration for such presentations can often include appendicitis, pyelonephritis, pelvic inflammatory disease, ectopic pregnancy, tubo-ovarian abscess, and inflammatory bowel disease. For this reason imaging typically plays an important role in diagnosis. A study from Radiology in 2000 looking at the detection of ureteral calculi in emergency room patients determined that the sensitivity for stone detection by CT was 96%, and by ultrasound was 61% (both with specificities of 100%).\n\nIt is estimated that somewhere between 3 and 12 percent of individuals in the United States will experience symptomatic renal stones at some point in their lives. The majority of stones (eighty percent) are composed of calcium (typically calcium oxalate and less often calcium phosphate). The main other types include include uric acid, struvite (magnesium ammonium phosphate), and cystine stones. Generalized risk factors for forming stones include low water intake, high protein intake, family history, urinary tract infection with a urease splitting organism (e.g. Proteus or Klebsiella), and disease states resulting in hypercalciuria, hyperuricosuria, or hypocitriuria. Treatment of ureteral stones in the acute setting begins with adequate pain control. Once an obstructing stone has been identified within the collecting system, location and size of the stone plays a major role in determining management with stone size of 5mm typically representing the threshold for intervention\u2014with stones smaller than 5mm being managed conservatively (pain control, oral hydration, and urine straining for spontaneous passage), and stones greater than or equal to 5mm being managed with some sort of intervention (e.g. lithotripsy, cystoscopy, etc).", "ACR Code": "8.2", "Category": "Obstruction or Stenosis", "Keywords": "kidney stonesnephrolithiasisflank pain", "Reference": "Shaefor DH, Hertzberg BS, Freed KS et al. Nonenhanced Helical CT and US in the Emergency Evaluation of Patients with Renal Colic: Prospective Comparison. Radiology 2000; 217:792-797.", "External Links": "www.fpnotebook.com/URO116.htm" } }, { "U_id": "MPX1984", "TAC": [ "MPX1984_synpic34420", "MPX1984_synpic34421", "MPX1984_synpic34423", "MPX1984_synpic34426" ], "MRI": [], "Case": { "Title": "Pleural Plaques consistent with asbestos exposure", "History": "56 y.o. man presents for follow up after initial evaluation of rib pain from a bicycle tumble.\n\nDenies any pulmonary symptoms", "Exam": "Normal Exam & Labs", "Findings": "\u2022 Lung parenchyma - no masses or airspace disease.\n\n\u2022 Bilaterally, numerous calcified pleural plaques along thoracic cage and diaphragmatic surfaces.\n\n\u2022 Small rectangular scattered non-calcified pleural thickenings are also observed. \n\n\u2022 There is no mediastinal, hilar or axillary lymphadenopathy.", "Differential Diagnosis": "\u2022 Asbestos exposure\n\u2022 Pleural TB\n\u2022 Pleural metastasis", "Case Diagnosis": "Pleural Plaques consistent with asbestos exposure", "Treatment & Follow Up": "Semi-annual monitoring CT scan to evaluate for progression of disease. If plaques remain stable, will conduct annual follow-up evaluations.", "Discussion": "Pleural plaques are circumscribed areas of pleural thickening, often diffuse or multifocal. These may frequently be calcified, and are characteristically found along the lower thorax and diaphragmatic pleura. The lesions are only rarely found in the costophrenic sulci and lung apices most often avoiding these areas. Calcified diaphragmatic pleural plaques are essentially pathognomonic for asbestos exposure, and may develop as much as 20 years after initial exposure. \n\nAsbestosis is a pneumoconiosis resulting from the inhalation of asbestos fibers and leads to a slowly progressive diffuse pulmonary fibrosis. The primary complications are respiratory failure and malignancy (asbestos expsore may increase the risk of malignant mesothelioma by 300 fold compared to non-exposed individuals)." }, "Topic": { "Title": "Pleural Plaques", "Disease Discussion": "Pleural plaques are circumscribed areas of pleural thickening, often diffuse or multifocal. These may frequently be calcified, and are characteristically found along the lower thorax and diaphragmatic pleura. The lesions are only rarely found in the costophrenic sulci and lung apices most often avoiding these areas. Pleural plaques are essentially pathognomonic for asbestos exposure, and may develop as much as 20 years after initial exposure. Asbestosis is a pneumoconiosis resulting from the inhalation of asbestos fibers and leads to a slowly progressive diffuse pulmonary fibrosis. The primary complications are respiratory failure and malignancy (asbestos expsore may increase the risk of malignant mesothelioma by 300 fold compared to non-exposed individuals).", "ACR Code": "6.5", "Category": "Toxic (see also Metabolic)", "Keywords": "pleural plaquesasbestosis", "Reference": "Verschakelen, J.A., The chest wall, pleura and diaphragm. In: Grainger & Allison\u2019s Diagnositc Radiology: A Textbook of Medical Imaging, 4th ed. Churchill Livingstone, 2001.\n\nKing, T.E. Asbestosis. www.UpToDate.com, last changed January 18, 2005." } }, { "U_id": "MPX1980", "TAC": [ "MPX1980_synpic34840", "MPX1980_synpic34950" ], "MRI": [ "MPX1980_synpic34841", "MPX1980_synpic34842", "MPX1980_synpic34843", "MPX1980_synpic34844" ], "Case": { "Title": "Chondroblastoma with secondary aneurysmal bone cyst", "History": "24 yo man with right-sided lower posterior chest/rib pain for 4-6 months, increases with deep inspiration. He denies history of trauma.", "Exam": "Tenderness to palpation approximately at posterior rib 11", "Findings": "\u2022 right paraspinal chest wall mass\n\u2022 measures 6.9x4.7x4.6 cm\n\u2022 located at levels T8 - T10\n\u2022 mass erodes into T9 & T10 vertebral bodies, T9 pedicle, rib 9\n\u2022 does not appear to disrupt thecal sac, though neural foramina is eroded\n\u2022 mild enhancement with gadolinium on T1 MR\n\u2022 sclerotic margins present in surrounding eroded structures\n\u2022 multiple fluid-fluid levels on T2\n\u2022 no pathologic lymphadenopathy\n\u2022 no other abnormal findings are noted", "Differential Diagnosis": "\u00bb Benign Primary Bone Tumors\n\u2022 fibrous dysplasia\n\u2022 chondroblastoma\n\u2022 chondromyxoid fibroma\n\u2022 osteochondroma\n\u2022 giant cell tumor\n\u2022 enchondroma\n\n\u00bb Malignant Primary Bone Tumors\n\u2022 chondrosarcoma\n\u2022 osteoblastoma, aggressive variant\n\u2022 osteosarcoma\n\n\u00bb Other\n\u2022 aneurysmal bone cyst\n\u2022 neurogenic tumors", "Case Diagnosis": "Chondroblastoma with secondary aneurysmal bone cyst", "Diagnosis By": "Core biopsy and pathology", "Treatment & Follow Up": "After CT-guided core biopsies were obtained, the patient was scheduled for metastatic work-up with whole body bone scan, PET, and brain MR. As of submission date, the patient continues to be in the diagnostic stages of medical care and planning. \n\nSurgery is likely to be planned, as most of these primary bone tumors must be removed by en bloc resection. Despite their benign taxonomy, a majority of these benign lesions tend to recur, therefore making wide excision standard regardless of malignant potential.", "Discussion": "Paraspinal masses can invoke an enormous list of differential diagnoses: lymphoma, metastatic disease, nerve sheath tumors, primary bone tumors, myeloma, meningocele, cysts, abscesses, and beyond. Based on location and radiographic appearance, this particular patient's findings suggested a neoplastic process, which directed him to biopsy. Indeed biopsy results initially indicated that a primary bone neoplasm was probable, based on presence of osteoblasts and cartilage.\n\nPrimary bone tumors are relatively rare, with an incidence of approximately 10,000 cases a year in the US. Using the patient's demographics as well as radiographic features can narrow the differential significantly. The suspected neoplasms, with the exception of chondrosarcoma, fit this patient\u2019s age group, as all frequently present in the second and third decades (chondrosarcoma has a peak incidence in the 5th and 6th decades of life). Using mass location to assign a probably diagnosis, an osteoblastoma becomes likely as it is often found in the spinal elements. By histology, of the differentials listed, the primary bone neoplasms seem most probable as those tumors are associated with chondro-osseous derivatives. More distinctively, the radiographic features suggest that there is a cystic component to the tumor, likely aneurysmal bone cysts. Because only a small fraction of the tumor contains these structures, they are likely to be secondary versus a primary aneurysmal bone cyst.\n\nWhen considering primary bone tumors with secondary aneurysmal bone cyst components, the differential is further pointed. Only 5 types of primary bone tumors typically display this pattern: giant cell tumor of bone, osteoblastoma, chondroblastoma, fibrous dysplasia, and telangiectatic osteosarcoma.\n\nFinal pathology reading of the core biopsy revealed the tumor was a chondroblastoma. This is a very rare tumor, and even rarer is the location of the tumor in this patient. Chondroblastomas account for less than 1% of all bone tumors; this corresponds to approximately 100 cases a year, considering the scarcity of primary bone tumors in general. Additionally, nearly 75% of the cases occur in the long bones of the lower extremity - distal femur and proximal tibia/fibula. Another 20% of chondroblastomas occur in the humerus, while a small fraction has also been reported in the small bones of the hand and feet. Case reports have described these tumors occurring in the skull, mandible, maxilla, vertebra, ribs, scapula, patella, and sternum.\n\nThis patient fits the expected demographics of the majority of primary bone tumors: second decade in age, male, black, history of chronic pain. What is so profound regarding this case remains the specific type of primary bone tumor, given its rarity by statistical incidence, and its unusual location originating from the ninth rib.\n\n\n\n\nREFERENCES:\n\nBullough, Peter. Orthopaedic Pathologv (third edition). Times Mirror International Publishers Limited: London, 1997.\n\nFines, Bonnie and Stacey, Gregory. Chondroblastoma, Radiology, Musculoskeletal. EMedicine Online. Last updated July 19, 2006. Accessed on March 2, 2007.\n\nGitelis, S. et al. Benign Bone Tumors. Instructional Course Lectures, 45:p. 426-46, 1991. Accessed via EMedicine on 2/26/07.\n\nMorgan, Hannah and Damron, Timothy. Chondroblastoma, Surgery, Orthopedic. EMedicine Online. Last updated March 15, 2005. Accessed information March 2, 2007.\n\nMurphey, Mark D. Fundamental Concepts of Musculoskeletal Neoplasm: Radiographs. Lecture given at USUHS. 2/28/07.\n\nPrimary Bone Tumors. Journal of Cancer Control. Vol. 13, No. 4. Moffitt Cancer Center. Accessed via Medscape on 2/25/2007." }, "Topic": { "Title": "primary bone neoplasm, chondro-osseous variants", "Disease Discussion": "The following list describes some familiar features tumors of the chondro-osseous origin, with mean age of presentation, most common anatomic location, likely radiographic findings, and histologic correlation given for each tumor.\n\nchondroblastoma\n\u2022 20's\n\u2022 long bones, femur\n\u2022 lobulated mass, scalloped cortical margins, calcifications, cysts\n\u2022 chondroid matrix\n\nchondromyxoid fibroma\n\u2022 20's & 30's\n\u2022 metaphysis of tibula/fibula\n\u2022 eccentric lytic lesion, decreased signal on T1\n\u2022 chondroid matrix with cytologic features of anaplastic processes\n\nosteochondroma\n\u2022 teens & 20's\n\u2022 long bones, around knee\n\u2022 can be exophytic, but generally subperiosteal\n\u2022 osteoid and cartilage\n\ngiant cell\n\u2022 25-40\n\u2022 long bones\n\u2022 solitary, locally aggressive, highly expansile\n\u2022 giant cells\n\nenchondroma\n\u2022 30's\n\u2022 long bones\n\u2022 oval, lytic, scalloped cortex\n\u2022 cartilage with layer of smooth, thin bone surrounding\n\nchondrosarcoma\n\u2022 50's & 60's\n\u2022 femur, humerus, ribs, pelvis\n\u2022 luceny, calcifications, scalloped edges, and extension into soft tissues\n\u2022 cartilage with anaplasia\n\nosteoblastoma, aggressive variant\n\u2022 20's\n\u2022 spine - vertebra and posterior elements\n\u2022 varies - lucent to sclerotic, can be expansile, adjacent bone thinning\n\u2022 osteoid, osteoblasts, spindle cells, cartilage (rare)\n\nosteosarcoma\n\u2022 teens - 30's\n\u2022 long bones (knee)\n\u2022 vary - lytic, sclerotic, mixed\n\u2022 osteoblasts, chondroblasts, fibroblasts", "ACR Code": "4.3", "Category": "Neoplasm, non-CNS", "Keywords": "boneosseouscartilage", "Reference": "Bullough, Peter. Orthopaedic Pathologv (third edition). Times Mirror International Publishers Limited: London, 1997.\n\nGitelis, S. et al. Benign Bone Tumors. Instructional Course Lectures, 45:p. 426-46, 1991. Accessed via EMedicine on 2/26/07.\n\nMurphey, Mark D. Fundamental Concepts of Musculoskeletal Neoplasm: Radiographs. Lecture given at USUHS. 2/28/07.\n\nPrimary Bone Tumors. Journal of Cancer Control. Vol. 13, No. 4. Moffitt Cancer Center. Accessed via Medscape on 2/25/2007." } }, { "U_id": "MPX1993", "TAC": [ "MPX1993_synpic23559" ], "MRI": [], "Case": { "Title": "Small bowel obstruction from inguinal hernia", "History": "75 year old man presented to emergency room with abdominal pain.", "Exam": "WBC normal\nPhysical exam of the groin area suggested the diagnosis of an inquinal hernia.", "Findings": "Plain film: \nSeveral dilated stacked loops of small bowel.\n\nCT scan of the abdomen and pelvis was performed and demonstrates bowel in the inguinal canal - consistent with hernia.", "Case Diagnosis": "Small bowel obstruction from inguinal hernia", "Diagnosis By": "Physical exam and radiological study", "Treatment & Follow Up": "The hernia was manually reduced in the emergency room.\nLaparoscopic hernia repair was the performed. \nThere was no ischemia of the involved bowel loop." }, "Topic": { "Title": "Small bowel obstruction secondary to adhesions", "Disease Discussion": "The plain film findings of a small bowel obstruction will vary according to the duration of symptoms, the site of obstruction and the type of obstructing lesion. Once an obstruction has occurred, gastric, pancreatic, biliary and small bowel fluid as well as swallowed air will begin to collect proximal to the obstruction dilating the small bowel and causing colicky symptoms. Distal to the obstruction the bowel contents will empty. The eventual radiographic picture is that of dilated small bowel with air fluid levels and a preponderance of fluid with little if any gas distal in the small intestine or colon. If the bowel dilates with air it assumes a step ladder configuration. Differential air fluid levels within the same intestinal loop can be seen in either an adynamic ileus or a bowel obstruction and are not helpful in distinguishing the two. The presence of a large amount of fluid is more suggestive of an obstruction. If small amounts of air are trapped in between the plicae circulares, a line of small round air collections, the \"string of pearls,\" (Film .2Z) can be seen, as in this case. This finding is indicative of large amounts of fluid and is more suggestive of an obstruction than an adynamic ileus. The extent of small bowel gas may be a clue as to the site of the obstruction. Proximal obstructions may result in a fairly benign appearing radiograph. One third of patients will present with a history and plain film findings sufficiently characteristic that further radiographic work-up is unnecessary. If a contrast study is performed, barium is the agent of choice because water soluble contrast material becomes too dilute to pin-point a site of obstruction. Administering the barium through an already indwelling long arm tube or radiographically placed duodenal catheter may be a more expeditious way of pin-pointing the site of a partial obstruction. With a complete obstruction it is difficult to get the barium column to reach the site of a distal obstruction using any technique without causing the patient either increased discomfort or emesis of the barium. Many surgeons are content with supportive plain films and clinical history to justify a surgical approach. \n\nApproximately 60% of mechanical small bowel obstructions occur because of adhesions. Approximately 20% of obstructions are from hernias, the vast majority of which are external hernias. Included in this group are inguinal, femoral, umbilical and incisional hernias. The diagnosis of an incisional hernia can be very difficult and requires oblique views of the abdomen. Obstructing inguinal hernias in adults are usually symptomatic and readily apparent. In the neonate, however, an obstructing inguinal hernia may be difficult to diagnose clinically. A close search for air below the pubic ramus should always be made when a small bowel obstruction is present. Internal hernias account for less than 5% of obstructing hernias and rarely have a specific enough plain film picture to allow for diagnosis. \n\nA rounded soft tissue density associated with an obstructed small bowel pattern should always raise the possibility of a closed loop obstruction, representing a twisted or adhesed isolated loop of intestine blocked at both ends. Other causes of small bowel obstruction include benign or malignant primary tumors, large gallstones, intussusceptions, Crohn's disease, and perforated appendix with abscess formation.\n\nIt should be remembered that the plain film diagnosis of a small bowel obstruction should be made with correlation with the patient's clinical picture. A single series of films is frequently insufficient and sequential films may be necessary.", "ACR Code": "7.7", "Category": "Obstruction or Stenosis", "Keywords": "inguinal hernia" } }, { "U_id": "MPX1997", "TAC": [ "MPX1997_synpic21435" ], "MRI": [ "MPX1997_synpic21436", "MPX1997_synpic21437" ], "Case": { "Title": "Arteriovenous Malformation (AVM)", "History": "26 yo female who had sudden loss of consciousness followed by the worst headach of life. She was previously healthy with no history of trauma.", "Exam": "General decreased level of consiousness\nSensitivity to light\nNo focal neurologic deficits", "Findings": "CT: left frontal mass with associated serpiginous areas of decreased density.\n\nMRI: Mass of tangled flow voids with a large central nidus.", "Differential Diagnosis": "findings are pathoneumonic", "Case Diagnosis": "Arteriovenous Malformation (AVM)", "Diagnosis By": "Angiography with AVM glueing followed by surgery", "Treatment & Follow Up": "Patient was treated with three sessions of angiography with glueing of the feeding arteries. The patient was then taken to the OR for surgical resection." }, "Topic": { "Title": "Arteriovenous Malformation (AVM)", "Disease Discussion": "ARTERIOVENOUS MALFORMATION (AVM)\n\nClinical Features: AVMs are the most common symptomatic congenital vascular malformations. The peak age at presentation is between 20 and 40. Approximately 50% of patients with AVMs present with symptoms caused by hemorrhage (25% present with seizures). The overall risk of hemorrhage from an AVM is estimated at 2% to 4% per year, cumulative. 98% of AVMs are solitary. Multiple AVMs outside the setting of vascular neurocutaneous disorders such as Rendu-Osler-Weber and Wyburn-Mason syndromes are extremely uncommon.\n\nPathology: AVMs are complex networks of abnormal vascular channels that consist of dilated arterial feeder(s) and draining veins, without intervening capillaries. These vessels often demonstrate flow-induced angiopathic changes secondary to endothelial hyperplasia (flow-related\u201d aneurysms in 10 - 20%). AVMs may contain gliotic brain and hemorrhagic residua. Atrophy of otherwise normal adjacent brain results from chronic regional arterial hypoperfusion and venous hypertension, as the AVMs steal vascular supply from adjacent brain tissue.\n\nImaging: Intracranial AVMs are subdivided into parenchymal (pial or within the brain), and dural (outside the brain). A mixed type occurs when a parenchymal AVM recruits dural vascular supply. 85% of AVMs are supratentorial. On cerebral angiography an AVM appears as a tightly packed mass of enlarged feeding arteries that supply a central nidus, a plexiform web of small vessels. One or more dilated veins drain the AVM nidus. The main goals of the diagnostic imaging workup are to delineate the size of the AVM, the eloquence of adjacent brain, and the pattern of venous drainage. These 3 characteristics are used to determine the long-term risk of an untreated AVM, as the table below explains.\n\nTable 1. Spetzler AVM Grading System\nGraded feature\t Points assigned\n Size\n Small (<3 cm)\t\t\t\t1\n Medium (3-6 cm)\t\t\t2\n Large (>6cm)\t\t\t\t3\n\nEloquence of adjacent brain\n Noneloquent \t\t0\n Eloquent\t\t\t\t\t1\n\nVenous drainage\n Superficial only\t\t\t 0\n Deep\t\t\t\t\t 1\n\n========================================\n \nSpetzler grades range from 1 to 5. A separate grade 6 is reserved for inoperable lesions. Prospective studies have confirmed the accuracy and utility of the Spetzler grade in guiding patient management and estimating postoperative neurologic complications.", "ACR Code": "1.3", "Category": "Congenital, malformation", "Keywords": "AVMvascular malformationcongenital", "Reference": "Osborn. Diagnostic Neuroradiology. 1994. Mosby.\nOsborn. Diagnostic Cerebral Angiography. 2nd Ed, 1999. LW&W." } }, { "U_id": "MPX2001", "TAC": [ "MPX2001_synpic23578", "MPX2001_synpic23580" ], "MRI": [ "MPX2001_synpic23576", "MPX2001_synpic23577" ], "Case": { "Title": "Recurrent pyogenic cholangitis (a.k.a. oriental cholangitis or oriental cholangiohepatitis)", "History": "41 year old samoan woman presented with recurrent bouts of pancreatitis.", "Exam": "Not provided by author.", "Findings": "Both CT and MRI demonstrate dilated intrahepatic biliary ducts in the posterior right lobe of the liver. Within the dilated system are several calculi that were formed secondary to chronic infection.", "Differential Diagnosis": "Biliary Cystadenoma or Cystadenocarcinoma \nCaroli Disease \nCholangiocarcinoma \nPrimary Sclerosing Cholangitis\nAIDS Cholangitis\nCholedochal Cyst \nCholelithiasis \nMetastases", "Case Diagnosis": "Recurrent pyogenic cholangitis (a.k.a. oriental cholangitis or oriental cholangiohepatitis)", "Diagnosis By": "Radiographically and surgically.", "Treatment & Follow Up": "Cholecystectomy and choledocojejunostomy", "Discussion": "The most common location for recurrent pyogenic cholangitis is the left lateral lobe. The second most common portion of the liver involved is the right posterior lobe as in this case. It is interesting in this case that the dilated ducts are peripheral in location; Most case involve dilation of the secondary ducts leading to a \"pruned tree\" appearance to the biliary system." }, "Topic": { "Title": "Recurrent pyrogenic cholangitis", "Disease Discussion": "An unusual form of recurrent pyogenic cholangitis occurs in Orientals and asian immigrants and is characterized by an extreme propensity for intraductal stone formation. The bile ducts become filled with stones (usually pigment stones), pus and sludge-like material. The intra- and extrahepatic ducts become focally and irregularly dilated secondary to multiple strictures. Distal obstruction is not usually present. Biliary cirrhosis from longstanding obstruction may ultimately develop. The disease seems to involve the left ductal system more severely.\n\nYoung adults are most commonly affected. Clinical symptoms include fever, chills, RUQ pain and jaundice. Septic shock and liver abscess may develop.\n\nThe etiology of this condition is debated. Multiple pathogenic factors are proposed, including repeated infections with enteric organisms, malnutrition, parasitic infestation and portal bacteremia. It is postulated that enteric bacteria deconjugate bilirubin and predispose to pigment calculi formation. Parasitic infection with Clonorchis sinensis or Fasciola hepatica commonly coexist and may contribute to the pathogenesis. However the most common organism culture from the bile in patients with RPC is E. coli\n\nThe diagnosis is often suggested on CT or US by asymmetric or patchy intrahepatic ductal dilatation and intra- and extrahepatic duct calculi. The disease most commonly effects the lateral left lobe. Calculi are multiple, vary in size, consistency and color and are frequently non-calcified. Air in the bile ducts (with no previous surgery), contrast enhancement of the ductal walls, and parenchymal changes of segmental atrophy, fatty change and hepatic abscesses may also be identified on CT. CT should be done without oral or IV contrast initially. Intrahepatic calculi are more easily detected on non-enhanced scans, and oral contrast refluxing through an anastomosis may obscure calculi.\n\nOn sonography, the biliary sludge and amorphous intrahepatic calculi can be missed, appearing as soft tissue density without an acoustic shadow and obscuring visibility of dilated intrahepatic ducts. Pneumobilia may be mistaken for intrahepatic calculi. Biliary Direct cholangiography with PTC or ERCP is used to delineate specific details but must be done carefully with prophylactic antibiotics.\n\nThere is a high recurrence rate in this disease. Medical therapy is ineffective. Percutaneous or endoscopic drainage, stone removal and stricture dilatation are useful in management. Resection of the affect portion of the liver and choledocojejunostomy may be performed to improve biliary drainage and protect the unaffected portions of the liver. Some surgeons elect to create a stoma from the afferent loop of jejunum to the skin to allow easy access to the biliary system if further intervention is necessary.", "ACR Code": "7.-1", "Category": "Obstruction or Stenosis", "Keywords": "cholangitischolangiogramhepatobiliary", "Reference": "http://www.emedicine.com/radio/topic156.htm" } }, { "U_id": "MPX2002", "TAC": [ "MPX2002_synpic57895" ], "MRI": [], "Case": { "Title": "Partial Anomalous Pulmonary Venous Return", "History": "Healthy 5 y.o. girl with a normal birth history", "Exam": "Harsh systolic ejection murmur at left upper sternal border.", "Findings": "Cardiac gated CT: Left sided supracardiac partial anomalous pulmonary venous return with all left pulmonary veins draining into the left innominate vein via a persistent left vertical cardinal vein. The vertical vein is intimate with the left atrial appendage. Right atrium and right ventricle are mild to moderately enlarged.", "Differential Diagnosis": "\u2022 Partial anomalous pulmonary venous return (PAPVR)\n\u2022 Persistent left sided SVC\n\u2022 Left superior intercostal vein", "Case Diagnosis": "Partial Anomalous Pulmonary Venous Return", "Diagnosis By": "Cardiac gated CT correlated with echocardiogram", "Treatment & Follow Up": "Patient offered elective surgical repair" }, "Topic": { "Title": "Partial Anomalous Pulmonary Venous Return (PAPVR)", "Disease Discussion": "Partial anomalous pulmonary venous connection (PAPVC) is a rare congenital cardiac defect. As the name suggests, in PAPVC, the blood flow from a few of the pulmonary veins return to the right atrium instead of the left atrium. Usually, a single pulmonary vein is anomalous. Rarely, all the veins from one lung are anomalous. Thus, some of the pulmonary venous flow enters the systemic venous circulation. PAPVC from the right lung is twice as common as PAPVC from the left lung. \n\nThe main differential for a vertically oriented vessel lateral and to the left of the aortic arch is PAPVR and Left Sided SVC. A quick way to differentiate PAPVR from Persistent Left Sided Superior Vena Cava is to look at the size of the coronary sinus. In persistent left sided SVC venous return is to the coronary sinus and the coronary sinus will be enlarged while it is not in PAPVR. PAPVR may have feeding intraparenchymal pulmonary veins not seen in left SVC. MR phase contrast can show cephalad flow in PAPVR and caudal flow in left sided SVC.", "ACR Code": "5.9", "Category": "Congenital, malformation", "Keywords": "AnomalousPulmonaryConnection" } }, { "U_id": "MPX2006", "TAC": [ "MPX2006_synpic21120", "MPX2006_synpic21155" ], "MRI": [], "Case": { "Title": "Ischemic colitis", "History": "57 yo female with rectal bleeding and hypotension", "Findings": "Multiple CT images demonstrate difuse, smooth distal colonic thickening from the splenic flexure to the proximal sigmoid colon. There is surrounding pericolonic inflammation. There is no pneumatosis or abnormal dilation.", "Differential Diagnosis": "ischemic colitis associated with IMA hypoperfusion.", "Case Diagnosis": "Ischemic colitis", "Discussion": "Multiple CT images through the abdomen demonstrate symmetric, smooth thickening of the colon from the level of the splenic flexure to the proximal rectum. The small bowel, ascending-to-mid-transverse colon and distal rectum are spared. The differential for thickened, nondilated loops of bowel includes ischemia, edema, hemorrhage and infiltrative processes such as lymphoma and amyloidosis. \nSeveral features of this case are suggestive of ischemic colitis in the distribution of the inferior mesenteric artery (IMA). The clinical history of abrupt onset of lower abdominal pain and rectal bleeding associated with hypotension is classic for IMA hypoperfusion. The segmental involvement from the Griffith point (transition point from superior mesenteric artery to IMA vascular territories) to the point of Sudeck (transition from (IMA to hypogastric vascular territories) is also characteristic of IMA hypoperfusion. Other supporting features include symmetric, lobulated colon wall thickening and pericolic edema. \nFeatures not present in this case but which suggest infarction and impending perforation include intramural gas and portal or mesenteric venous air. \n\nDahnert, W. Radiology Review Manual, 5th Edition. Lippincott, Williams and Wilkins, Philadelphia, 2003. Pages 837-838." }, "Topic": { "Title": "Ischemic colitis", "Disease Discussion": "Ischemic colitis is an acute inflammatory process secondary to arterial thrombosis (most commonly) or venous thrombosis. It usually occurs in older patients. It is usually treated conservatively. On CT, there is typically mild to moderate wall thickening. Involvement of the splenic flexure and descending colon is a characteristic distribution. Pneumatosis and portal venous gas are ominous signs (obviously), signifying a more severe course that usually requires surgery. Stricture formation can occur after the acute inlammation has resolved.", "ACR Code": "7.6", "Category": "Hypoxic or Ischemic", "Keywords": "Colitis", "Reference": "Slone RM, Fisher AJ, Pickhardt PJ, et al. Body CT: a practical approach. McGraw-Hill: New York. 2000." } }, { "U_id": "MPX2009", "TAC": [ "MPX2009_synpic16272" ], "MRI": [], "Case": { "Title": "Angiomyolipomas in tuberous sclerosis", "History": "Follow-up for known history of tuberous sclerosis.", "Exam": "Unremarkable", "Findings": "multiple bilateral solid renal masses. Many of the masses contain macroscopic fat.", "Differential Diagnosis": "Multiple angiomyolipomas, renal cysts, renal cell carcinoma.", "Case Diagnosis": "Angiomyolipomas in tuberous sclerosis" }, "Topic": { "Title": "Angiomyolipomas in tuberous sclerosis", "Disease Discussion": "Tuberous sclerosis is a neuroectodermal syndrome characterized by formation of hamartomatous tumors in the skin, brain and viscera, including most commonly lungs and kidneys. Incidence of tuberous sclerosis has been reported be as rare as 1 in 150,000 and as common as 1 in 10,000. It has significant morbidity and mortality with 75% of patients dying by the age of 20 - either from CNS, cardia, or renal complications. The mean age of presentation of renal lesions is about 9 years. \n\nThe most common renal lesion is the angiomyolipoma (AML) which is present in about 80% of cases. The 2nd most common renal lesion is renal cysts. Ultrasound, CT and MRI can all be used for evaluation of renal tuberous sclerosis. CT is the most sensitive and specific imaging modality for evaluating renal tuberous sclerosis. The finding of multiple, less than 3cm , often bilateral cysts with fat-containing tumors is highly suggestive of tuberous sclerosis. AML's of tuberous sclerosis are not prone to malignant degeneration and so no yearly follow-up is needed. However, AML's of tuberous sclerosis can grow very large and are prone to hemorrhage. Therapy for very large AML's can include prophylactic arterial embolization or tumors.", "ACR Code": "8.3", "Category": "Congenital, genetic", "Keywords": "Tuberous sclerosisneuroectodermal syndromeangiomyolipoma", "Reference": "The Encyclopaedia of Medical Imaging, Volume IV:2\nTuberous sclerosis, renal involvement\nhttp://www.amershamhealth.com/medcyclopaedia\n\nTuberous sclerosis complex: renal imaging findings. \nCasper KA - Radiology - 01-Nov-2002; 225(2): 451-6\n\nAngiomyolipomas in Tuberous Sclerosis\nLogue - Radiographics, 2003; 23:241-246", "External Links": "www.amershamhealth.com/medcyclopaedia" } }, { "U_id": "MPX2007", "TAC": [ "MPX2007_synpic18261" ], "MRI": [], "Case": { "Title": "Gorlin Syndrome", "History": "51 yo female injured right index finger.\n\nReview of prior studies and labs revealed diagnosis.", "Exam": "Multiple skin biopsies diagnosed as Basal Cell Carcinoma", "Findings": "Hands: Multiple well circumscribed elongated (flame shaped) cortical lucencies throughout both hands. Nondisplaced fracture at the base of the right second proximal phalanx.\nFoot: Healed fractures of the second/third metatarsals. Multiple lucencies of hindfoot and distal tibia/fibula. \nBone Scan: Multiple areas of focal increased and decreased uptake. Increased uptake along the falx cerebri. \nHead CT: Calcifications along the falx and tentorium.", "Differential Diagnosis": "Differential Diagnosis of Multiple Lytic Lesions: Fibrous Dysplasia, Metastases, Myeloma, Osteoporosis, Disseminated Osteomyelitis, Hyperparathyroidism, Gorlin Syndrome.", "Case Diagnosis": "Gorlin Syndrome", "Diagnosis By": "Multiple biopsies diagnosed as Basal Cell Carcinoma \nAlso meets several of the major and minor diagnostic criteria. (See Factoid)", "Treatment & Follow Up": "Excision of suspicious lesions and limited exposure to U.V. and ionizing radiation." }, "Topic": { "Title": "Gorlin Syndrome", "Disease Discussion": "Gorlin syndrome (basal cell nevus syndrome, nevoid basal cell carcinoma syndrome) is an autosomal dominant syndrome on chromosome 9q. However, up to 40% of cases are spontaneous mutations. It has a multitude of abnormalities with the most common (90%) being multiple basal cell carcinomas at an early age. Proposed diagnostic criteria include 2 major criteria features or 1 major and 2 minor features. (1)\n\nMajor criteria \n\u2022 \tTwo or more basal cell carcinomas in persons younger than 20 years \n\u2022 \tOdontogenic keratocysts of the jaw \n\u2022 \tThree or more palmar or plantar pits \n\u2022 \tBilamellar calcification of the falx cerebri and tentorium. \n\u2022 \tBifid, fused, or markedly splayed ribs \n\u2022 \tFirst-degree relative with Gorlin syndrome\n\nMinor criteria \n\u2022 \tMacrocephaly \n\u2022 \tCongenital malformations (eg, cleft lip or palate, frontal bossing, \"coarse face,\" hypertelorism) \n\u2022 \tOther skeletal abnormalities, such as Sprengel deformity, marked pectus deformity, or syndactyly of the digits \n\u2022 \tRadiological abnormalities such as bridging of the sella turcica, vertebral anomalies such as hemivertebrae or fusion or elongation of the vertebral bodies, modeling defects of the hands and feet, or flame-shaped lucencies of the hands or feet \n\u2022 \tOvarian fibroma \n\u2022 \tMedulloblastoma\n\nSpecial Note(4): Radiation therapy in patients with Gorlin syndrome has been shown to increase the number of basal cell carcinoma. Therefore, all ionizing radiation should be limited. Gorlin syndrome patients with medulloblastoma are routinely not treated with radiation.", "ACR Code": "4.6", "Category": "Congenital, genetic", "Keywords": "Gorlinbasal cell nevus", "Reference": "1. Kimonis VE, Goldstein AM, Pastakia B, et al: Clinical manifestations in 105 persons with nevoid basal cell carcinoma syndrome. Am J Med Genet 1997 Mar 31; 69(1): 299-308\n\n\n2. Taybi H, Lachman R. Radiology of Syndromes, Metabolic Disorders, and Skeletal Dysplasias, 4th ed. Mosby, St. Louis 1995: 204-205.\n\n3. Resnick, Donald. Diagnosis of Bone and Joint Disorders, 4th ed. WB Saunders :4683-4685\n\n4. Walter, Andrew W. \u201cGorlin Syndrome\u201d, eMedicine, 20Sep2002. www.emedicine.com/ped/topic890.htm" } }, { "U_id": "MPX2012", "TAC": [ "MPX2012_synpic45729", "MPX2012_synpic45730" ], "MRI": [], "Case": { "Title": "Staghorn Calculus", "History": "62 yo male with left flank pain and urinary tract infections.", "Findings": "Coronal MIP noncontrast CT images reveal a staghorn calculus, which forms a cast of nearly the entire left renal collecting system.", "Differential Diagnosis": "Calcifications from granulomatous disease\nCalcified tumor\nStaghorn Calculus", "Case Diagnosis": "Staghorn Calculus", "Diagnosis By": "Imaging findings are diagnostic.", "Treatment & Follow Up": "Treatment options for staghorn calculi include percutaneous stone removal, open surgery, or a combination of percutaneous debulking and extracorporeal shockwave lithotripsy (ESWL)." }, "Topic": { "Title": "Staghorn Calculus", "Disease Discussion": "\u201cStaghorn calculi\u201d is like a cast of the renal collecting system, and resembles the antlers of a stag.\n\nComposition: Struvite >> cystine or uric acid.\n\nUsually associated with recurrent urinary tract infections from bacterial pathogens that produce alkaline urine (thus, F>M cases).\n\nStaghorn can be disrupted if infection complicates obstruction related to the stone. Renal enlargement from pyonephrosis or xanthogranulomatous pyelonephritis may produce a fragmented staghorn.\n\nClassic excretory urographic triad of xanthogranulomatous pyelonephritis:\n1.\tObstructing stone\n2.\tRenal enlargement \n3.\tNonexcretion of contrast material from the involved kidney", "ACR Code": "8.5", "Category": "Metabolic (see also Toxic)", "Keywords": "staghorncalculusnephrolithiasis", "Reference": "Dyer, R. et.al. \u201cClassic Signs in Uroradiology\u201d\nRadioGraphics 2004;24:S247-S280" } }, { "U_id": "MPX2016", "TAC": [ "MPX2016_synpic24560" ], "MRI": [], "Case": { "Title": "Pulmonary manifestations of Neurofibromatosis 1. However, pulmonary fibrosis with bullous formation from smoking related pulmonary diseases can\u2019t be ruled out.", "History": "66 y.o. female with NF1, vomiting, 25 pack year smoking history, No history of COPD. CXR obtained initially and Chest CT later obtained for further evaluation of CXR findings.", "Exam": "N/A", "Findings": "CXR: Ill-defined density in upper lateral peri-hilar region on PA view, not definitively seen on lateral projection, but possibly more anterior.\n\nCT, chest w/contrast: Multiple soft tissue attenuated skin nodules noted on anterior chest. No pulmonary nodules or masses seen. Pulmonary fibrosis with honey-combing predominately occurring in the upper lobes. Bullous changes are seen adjacent to mediastinum near azygoesophageal recess. Pulmonary scaring and honey-combing extends to right lower lung.", "Differential Diagnosis": "Emphysema\nIdiopathic Pulmonary Fibrosis (IPF)\nAutoimmune disorders (Sarcoidosis, RA)\nCollagen-vascular diseases with fibrosising aveolitits", "Case Diagnosis": "Pulmonary manifestations of Neurofibromatosis 1. However, pulmonary fibrosis with bullous formation from smoking related pulmonary diseases can\u2019t be ruled out.", "Treatment & Follow Up": "Treatment/Management: No known effective cure/treatment. Steroids have not been proven to change course of disease once fibrosis has begun. Stopping smoking may slow progression. Neurofibromatosis 1 has soft tissue neoplastic tendencies that should be monitored periodically for interval changes if there is suspicision for malignancy or if the patient is symptomatic.", "Discussion": "Dx: Pulmonary fibrosis with bullous formation consistent with pulmonary manifestations of Neurofibromatosis 1, however, smoking related pulmonary diseases can\u2019t be ruled out.\n\nDisease Discussion: Neurofibromatosis 1 (von Reckinghausen\u2019s disease, or NF1), is a autosomal dominant disorder involving Chromosome 17 of probable neural crest origin affecting all 3 germinal layers. Considered the most common neurocutanous disorder, both neuroectodermal and mesenchymal derivatives. Typically NF1 is recognized on clinical exam (85% of patients) with cutanous neurofibromas. NF1 can manifest in any organ in the body. Projection of neurofibromas over the thorax on frontal and lateral radiographs may be misinterpreted as a pulmonary nodule (as demonstrated on above CXR), so it is important to use CT to help differentiate.\n\nPulmonary involvement occurs in 10-20% of all NF1 patients. Occurring usually not until adult hood. The lung parenchyma can progress to developing interstitial fibrosis with associated severe thin-walled bullous formations reported to typically occur in the upper lobes and apical segments of the lower lobes bilaterally and symmetrically. Honey-combing, also described as subpleural small-blister-like changes, is reportedly seen in the bibasilar regions of the lungs. These findings may be coincidental with other lung diseases, however, the noted mesenchymal abnormalities caused by NF1 may affect lung parenchyma. The pathology of the lung parenchyma shows alveolar wall thickening progressing to fibrosis and lung destruction. Pulmonary function tests show either an obstructive or a restrictive process." }, "Topic": { "Title": "Neurofibromatosis NF1, Pulmonary disease", "Disease Discussion": "Neurofibromatosis 1 (von Reckinghausen\u2019s disease, or NF1), is a autosomal dominant disorder involving Chromosome 17 of probable neural crest origin affecting all 3 germinal layers. Considered the most common neurocutanous disorder, both neuroectodermal and mesenchymal derivatives. Typically NF1 is recognized on clinical exam (85% of patients) with cutanous neurofibromas. NF1 can manifest in any organ in the body. Projection of neurofibromas over the thorax on frontal and lateral radiographs may be misinterpreted as a pulmonary nodule (as demonstrated on above CXR), so it is important to use CT to help differentiate.\n\nPulmonary involvement occurs in 10-20% of all NF1 patients. Occurring usually not until adult hood. The lung parenchyma can progress to developing interstitial fibrosis with associated severe thin-walled bullous formations reported to typically occur in the upper lobes and apical segments of the lower lobes bilaterally and symmetrically. Honey-combing, also described as subpleural small-blister-like changes, is reportedly seen in the bibasilar regions of the lungs. These findings may be coincidental with other lung diseases, however, the noted mesenchymal abnormalities caused by NF1 may affect lung parenchyma. The pathology of the lung parenchyma shows alveolar wall thickening progressing to fibrosis and lung destruction. Pulmonary function tests show either an obstructive or a restrictive process.\n\n\n========================================\nHx: 66 y.o. female with NF1, vomiting, 25 pack year smoking history, No history of COPD. CXR obtained initially and Chest CT later obtained for further evaluation of CXR findings. \n\nDx: Pulmonary fibrosis with bullous formation consistent with pulmonary manifestations of Neurofibromatosis 1, however, smoking related pulmonary diseases can\u2019t be ruled out.", "ACR Code": "6.6", "Category": "Congenital, genetic", "Keywords": "Honey-comb lungpulmonary fibrosislung manifestations of NF1", "Reference": "Bukhalter, JL. Diffuse interstitial lung disease in neurofibromatosis. [Abstract] South Med J. 1986 Aug ; 79 (8): 944-6\nRossi, Santiago. Thoracic manifestations of neurofibromatosis-1. AJR1999 Dec;173:1631-1638\nKhan, Ali, MBBS, FRCP,FRCR, Turnbull, Ian. Neurofibromatosis type 1. www.eMedicine.com: last updated 10 Feb 04\nWebb WR, Goodman PC. Fibrosising alveolitis in patients with neurofibromatosis. Radiology 1977 Feb; 122 (2): 289-93" } }, { "U_id": "MPX2015", "TAC": [ "MPX2015_synpic50876" ], "MRI": [], "Case": { "Title": "Hiatal Hernia", "History": "83 y.o. woman with shortness of breath.", "Findings": "PA and lateral radiographs of the chest. \nFINDINGS:\n-There is near complete opacification of the left hemidiaphragm. There is consolidation and/or atelectasis with accompanying effusion present on the \nleft. Small right basilar opacities are present with a small right effusion. There is no evidence of pneumothorax. The cardiac silhouette is stable. A \nlarge hiatal hernia is present. Calcifications are seen within the thoracic aorta. The remainder of the visualized bones and soft tissues are remarkable \nfor degenerative changes to the acromioclavicular joint and spine. \n \nIMPRESSION: \n1. LEFT LUNG BASE CONSOLIDATION AND/OR ATELECTASIS WITH ACCOMPANYING EFFUSION WITH SMALLER BASILAR RIGHT OPACITY AND EFFUSION. \n2. LARGE HIATAL HERNIA. \n\n\nCT chest PE protocol. \nFINDINGS: \n-The study is somewhat limited by motion artifact. The mediastinal, hilar and pulmonary parenchyma vasculature appear widely patent and normal in\ncourse, caliber and contour without evidence of filling defects. There is a large hiatal hernia. Otherwise, there are no mediastinal or hilar masses\nidentified, and no adenopathy is evident. Atherosclerotic calcific changes of the aorta and coronary arteries are present. There is no evidence of\naneurysmal dilation. \n \nLeft greater than right-sided simple-appearing pleural effusions are present with underlying compressive atelectasis. The lungs are otherwise clear and \nevenly aerated without evidence of mass, calcification or pulmonary parenchymal disease. The airways appear normal, and no thickening is evident. \n \nMultilevel degenerative changes of the thoracic spine are seen. The visualized upper abdomen as well as the remainder of the visualized soft tissues and osseous structures are unremarkable. \nIMPRESSION: \n1. NO COMPUTED TOMOGRAPHIC EVIDENCE OF PULMONARY EMBOLISM. \n2. LEFT GREATER THAN RIGHT-SIDED SIMPLE-APPEARING PLEURAL EFFUSIONS WITH SUBJACENT COMPRESSIVE ATELECTASIS. \n3. LARGE HIATAL HERNIA.", "Differential Diagnosis": "DDx for atelectasis:\nasbestosis\npneumonia\npulmonary embolism\nrespiratory failure\ncarcinoma\nblunt chest trauma\ndiaphragmatic paralysis\n\nDDx hiatal hernia\nmass lesion in central chest\ncongenital diaphragmatic hernia", "Case Diagnosis": "Hiatal Hernia", "Diagnosis By": "Barium swallow", "Treatment & Follow Up": "Unknown, however as previously stated repair of an isolated, asymptomatic type I hiatal hernia is rarely indicated. If symptoms of GERD occur in association with a large hiatus hernia, either medical or surgical treatment is indicated to control the reflux.\nIn contrast, the enlarging types II, III, and IV hernias pose a constant risk of serious complications and should be treated surgically even in the absence of symptoms." }, "Topic": { "Title": "Hiatal Hernia", "Disease Discussion": "A hiatal hernia is a protrusion of the upper part of the stomach into the thorax through a tear or weakness in the diaphragm.\n\nTYPES OF HIATAL HERNIA \u2014 4 Types\nType I: Sliding hernia \u2014 accounts for more than 95 percent of cases.\n-Characterized by a widening of the muscular hiatal tunnel and circumferential laxity of the phrenoesophageal membrane, allowing a portion of the gastric cardia to herniate upward. \n-In terms of diagnosis, those larger than 2 cm can be diagnosed by barium swallow. However, in order to detect small hiatal hernias, one must use high-resolution manometry.\n-Etiology-trauma, congenital malformation, and iatrogenic factors. \n-Prognosis-Most small hiatal hernias are asymptomatic. With larger type I hernias, the main clinical implication is the propensity to develop gastroesophageal reflux disease (GERD). \n\nType II, III, and IV: Paraesophageal hernias \u2014 account for up to 5 percent of all hiatal hernias. \nEtiology: usually unclear, but a recognized complication of surgical dissection of the hiatus as occurs during antireflux procedures, esophagomyotomy, or partial gastrectomy.\n-Description: As the hernia enlarges, the greater curvature of the stomach rolls up into the thorax. Because the stomach is fixed at the gastroesophageal junction, the herniated stomach tends to rotate around its longitudinal axis, resulting in an organoaxial volvulus. \n-Diagnosis: barium swallow or endoscopy. If the hernia involves organs other than just the stomach, a definitive diagnosis is established with CT or MRI.\n\nTypes III and IV hiatal hernias are variants of the type II hernia:\n-Type III -with progressive enlargement of the hernia through the hiatus, the phrenoesophageal membrane stretches, displacing the gastroesophageal junction above the diaphragm. \n-Type IV hiatus hernia is associated with a large defect in the phrenoesophageal membrane, allowing other organs, such as the colon, spleen, pancreas, and small intestine, to enter the hernia sac. \n\nSYMPTOMS \u2014 usually discovered as a finding on upper gastrointestinal studies or endoscopy. \nType II-vague, intermittent symptoms, epigastric or substernal pain, postprandial fullness, substernal fullness, nausea, and retching. An upright radiograph of the thorax may be diagnostic, revealing a retrocardiac air-fluid level within a paraesophageal hernia or intrathoracic stomach. \n\nTREATMENT \u2014 Repair of an isolated, asymptomatic type I hiatal hernia is rarely indicated. If symptoms of GERD occur in association with a large hiatus hernia, either medical or surgical treatment is indicated to control the reflux.\nIn contrast, the enlarging types II, III, and IV hernias pose a constant risk of serious complications. These hernias never regress and progressively enlarge. If left untreated, the paraesophageal hernia eventually reaches the stage of the giant intrathoracic stomach, at which point the prognosis is poor and the complication rate is high. Thus, once a paraesophageal hernia is identified, it should be treated surgically even in the absence of symptoms.", "ACR Code": "7.9", "Category": "Unsure", "Keywords": "Hiatal herniaParaesophageal herniaGastroesophageal junction", "Reference": "Kahrilas PJ; Kim HC; Pandolfino JE. Approaches to the diagnosis and grading of hiatal hernia. Best Pract Res Clin Gastroenterol. 2008;22(4):601-16.\n\nPouderoux P; Lin S; Kahrilas PJ. Timing, propagation, coordination, and effect of esophageal shortening during peristalsis. Gastroenterology 1997 Apr;112(4):1147-54. \n\nKahrilas P. Hiatus hernia. UpToDate Online." } }, { "U_id": "MPX2018", "TAC": [ "MPX2018_synpic16378" ], "MRI": [ "MPX2018_synpic16377" ], "Case": { "Title": "Osseous hemangioma - The CT correlation with recent MRI showing serpiginous contrast enhancement within the cortically based lesion and the constellation of CT findings is most consistent with a cortically based osseous hemangioma.", "History": "55 y/o white female with persistent lower extremity pain.", "Exam": "NA", "Findings": "Plain film: film shows anatomic alignment without fracture. Ill-defined sclerosis is seen in the lateral aspect of the metadiaphysis of the proximal tibia. Osteophytosis is seen in the medial femoral condyle and patella.\n\nNM scan (25.3 mCi of Tc-99m MDP IV): There is moderate, focal uptake in the region of the plain film abnormality. No other areas of abnormal radiopharmaceutical uptake.\n\nMR: Lesion within the lateral proximal tibia in a metadiaphyseal location measures 8 cm in greatest dimension. Ill-defined borders. Lateral cortex appears intact and may or may not be involved with the lesion. Some new bone formation may be present. Lesion has low T1, low T1 fat-sat, high T2 and some enhancement heterogeneously in the lesion.\n\nCT: There is an anterolateral, cortically based sclerotic lesion extending into the anteromedial medullary space, with whispy margins and note\nof serpiginous lucencies running through it. There is no evidence of cortical destruction or fracture or fibular involvement or soft tissue involvement. There is no significant periosteal change. This\nlesion involves the anterolateral metaphysis and proximal diaphysis of the left tibia.", "Differential Diagnosis": "fibrous dysplasia\nmetastatic carcinoma\ninfection\nchondroid tumors\neosinophilic granuloma", "Case Diagnosis": "Osseous hemangioma - The CT correlation with recent MRI showing serpiginous contrast enhancement within the cortically based lesion and the constellation of CT findings is most consistent with a cortically based osseous hemangioma.", "Treatment & Follow Up": "Orthopedic consultation was recommended.", "Discussion": "see factoid." }, "Topic": { "Title": "Osseous Hemangioma", "Disease Discussion": "The majority of hemangiomas that involve bone are discovered incidentally in asymptomatic patients. Men are affected twice as often as women, and lesions are usually discovered in the 4th 5th decades of life. Soft-tissue components may also be associated with these lesions. Osseous hemangioma is particularly common in the spine and calvaria and less frequently affects long bones such as the tibia, femur, and humerus. \n\nOsseous hemangiomas may have radiating trabecular thickening on radiographs. Another common pattern is a bubbly bone lysis that creates a honeycomb, latticelike, or \"hole-within-hole\" appearance. These lytic areas are invariably multifocal and usually metaphyseal or epiphyseal. Bone lysis can have linear and circular components on radiographs, suggestive of a vascular lesion, with linear and circular elements representing vascular channels seen longitudinally and en face, respectively. However, these serpentine vascular channels are recognized more easily with CT and MR imaging. Characteristically, these channels have low signal intensity on T1-weighted images and very high signal intensity on T2-weighted images because of slow blood flow. In arteriovenous lesions with faster blood flow, low signal intensity may persist with all MR imaging pulse sequences. The appearance of osseous hemangiomas at bone and red blood cell labeled scintigraphy is variable, from photopenia to moderate increased activity. \n\nPeriosteal or cortical hemangiomas occur most frequently in the anterior tibial diaphysis. These lytic cortical lesions may also show the characteristic multifocal vascular channels or be seen as a larger, nonspecific region of bone destruction. Cortical hemangiomas may predispose the bone to fracture, and periosteal reaction may accompany these lesions.", "ACR Code": "4.3", "Category": "Neoplasm, benign", "Keywords": "osseous; hemangioma", "Reference": "Archives of the AFIP. RadioGraphics 1995; 15:893-917" } }, { "U_id": "MPX2022", "TAC": [ "MPX2022_synpic51766", "MPX2022_synpic51767", "MPX2022_synpic51768", "MPX2022_synpic51769", "MPX2022_synpic51770", "MPX2022_synpic51772" ], "MRI": [], "Case": { "Title": "Wilms Tumor", "History": "30 month old girl with right-sided abdominal mass.", "Exam": "Asymptomatic right-sided abdominal mass.", "Findings": "\u2022 Initial study:\n- Large right-sided renal mass (12.2cm AP x 10.6cm Trans x 14.1cm CC). Predominantly hypodense w/ areas of heterogeneity. Possible cystic degeneration along superior border.\n- Classic \u201cclaw sign\u201d demonstrating renal origination.\n- Significant mass effect on liver, pancreas, and inferior vena cava.\n- Non-opacification of right renal vein and mass effect on IVC limit evaluation for tumor thrombosis.\n- Right lower lobe ground glass opacity (3mm x 5mm). DDX includes metastatic, atelectasis, or infection.\n\n\u2022 After 6 weeks Doxorubicin (DD4A) therapy:\n- Decrease in right renal mass size (7.3cm AP x 8.4cm Trans x 11.7cm CC).\n- Increased calcification and heterogenicity of mass.\n- Continued mass effect on liver, adjacent IVC, and right renal vein.\n- IVC and right renal vein grossly patent.\n- Resolution of previously noted right lower lobe lung mass.\n- Internal reproductive organs within normal limits for age.", "Differential Diagnosis": "\u2022 Wilms Tumor\n\u2022 Neuroblastoma\n\u2022 Multilocular Cystic Nephroma\n\u2022 Mesoblastic nephroma\n\u2022 Renal cell carcinoma", "Case Diagnosis": "Wilms Tumor", "Diagnosis By": "Tissue pathology", "Treatment & Follow Up": "6 weeks of neoadjuvant chemotherapy comprised of Vincristine, Dactinomycin, Doxorubicin (DD4A) followed by right nephrectomy.", "Discussion": "This case demonstrates the classic \"claw sign\" expected for tumor originating from the kidney. Also demonstrated the significant mass effect that Wilms tumors can have on intra-abdominal organs and vessels. Finally, benefits on neoadjuvant therapy was appreciated with decreased tumor burden prior to tumor removal." }, "Topic": { "Title": "Wilms Tumor", "Disease Discussion": "Wilms tumor (nephroblastoma) is the most common renal malignancy in children and the 4th most common pediatric malignancy in the U.S. Diagnosis is usually between 2 and 5 years of age with a peak at around 3 years. 5 to 10 percent involve both kidneys with a median onset about 10 months earlier than unilateral involvement.\n\nWilms tumor most commonly presents as an asymptomatic abdominal mass but may present with abdominal pain, particularly if there is intratumoral hemorrhage.\n\nImaging considerations when evaluating suspected Wilms tumor:\n- Usually appears as large well-defined mass on CT or MRI\n- Tumors commonly appear solid, however, larger lesions may have areas of heterogeneity or cystic components due to previous hemorrhage or necrosis\n- Tumor arises from the Kidney producing classic \u201cclaw sign\u201d with renal parenchyma surrounding a portion of the more hypodense mass.\n- Tends to have spherical growth displacing vessels\n- It is also important to document and evaluate for the following features:\no Lymph node involvement\no Lung metastases\no Contralateral kidney involvement\no Renal vein and IVC involvement\no Path ureters in relation to mass if visualized\no Other anomalies, i.e. gonadal, they may raise suspicion of a syndrome. See below.\n\nAn increase risk of Wilms tumor has been associated with several syndromes. Although syndrome association accounts for less than 10 percent of tumors, syndrome possibility should be considered when evaluating for Wilms. Syndromes include:\n\n1. WAGR syndrome (wilms, aniridia, genital anomalies, mental retardation).\n- 33% chance in developing Wilms tumor.\n- Studies on WAGR patients led to identification of first Wilms tumor associated gene (WT1). Tumors manifestation is thought to follow the \u201c Two hit\u201d theory with the syndrome producing the first hit.\n2. Denys-Drash syndrome (gonadal dysgenesis, gonadoblastoma, early onset renal failure).\n- 90% develop Wilms tumor.\n- Bi-allelic inactivation of WT1.\n3. Beckwith-Wiedemann syndrome (organomegaly, macroglossia, hemihypertorphy, adrenal cytomegaly)\n- 5% chance of developing Wilms tumor\n- Thought to involve second locus (WT2).\n\nThe primary differential in evaluating a possible Wilms tumor is to distinguish it from a neuroblastoma (the most common extracranial solid tumor of childhood). Specifically, by determining if the mass arises from the kidney and therefore most likely a Wilms tumor or whether it arises from the suprarenal region and more likely a neuroblastoma. The table below outlines differentiating features between the two. Tissue pathology, however, is usually obtained to definitively distinguish between the two and rule out more rare renal pathology in this age group such as renal cell carcinoma.\n\n\nFeature\t Neuroblastoma\t Wilms Tumor\nAge\t Most common <2yrs Peak at 3 yrs\nGrowth Surrounds/engulfs Grows like ball \n vessels displacing vessels\nRelation to kidney\tInferiorly displaces Arises from kidney\n \"claw sign\"\nLung metastasis\tUncommon\t More common (20%)\nVascular invasion\tDoes not occur\t Invasion of renal vein/IVC \n is common\nCalcification\tCommon (85% on CT)\tLess common (15%)\nAdapted from Donnelly, 2008.\n\nThere are two predominate schools of thought in regards to staging and treatment of Wilms tumor. The Nation Wilms Tumor Study Group (NWTSG) advocates for a surgery up-front approach allowing for a more accurate histologic and tumor extent assessment. The International Society of Pediatric Oncology (SIOP) advocates for chemotherapy first which reduces tumor volume and likely the possibility of tumor spillage during removal. Both stratagies use their own somewhat complicated staging system but generally follow the more simplistic outline below. \n\nI.\tConfined to kidney\nII.\tExtension into perinephric spaces\nIII.\tLymphnode involvement\nIV.\tMets to liver/lung\nV.\tBilateral kidney involvement\n\nIt is important to note that due to the differences in surgical timing and variations in criteria a \u201cstage to stage\u201d comparison of the two staging systems is confounded. It is also important to note the histologic characteristics are felt to be a more powerful prognostic indicator for Wilms.\n\nThe prognosis for Wilms tumor is generally good with excellent results obtained with a combination of nephrectomy and chemotherapy in most cases. Survival rates are reported as high as 90% which includes tumors that have spread beyond the kidney. Tumors with diffuse anaplasia have a less favorable outcome and reinforce the importance of correctly identifying the histologic pattern.", "ACR Code": "8.3", "Category": "Neoplasm, NOS", "Keywords": "WilmsNephroblastoma", "Reference": "1. Kumar V, Abbas AK, Fausto N, Robbins SL, Cotran RS. Robbins and Cotran pathologic basis of disease. 7th ed ed. Philadelphia: Elsevier Saunders; 2005.\n2. Metzger ML, Dome JS. Current therapy for Wilms' tumor. Oncologist. 2005;10:815-826.\n3. Donnelly LF. Pediatric imaging: the fundamentals. WB Saunders Co; 2008." } }, { "U_id": "MPX2031", "TAC": [ "MPX2031_synpic38140", "MPX2031_synpic38141", "MPX2031_synpic38142", "MPX2031_synpic38144" ], "MRI": [], "Case": { "Title": "Pneumatosis Intestinalis/Portal Venous Gas", "History": "76 yo man presents with 1.5 day history of increasing nausea, vomiting, and abdominal distention.", "Exam": "Large, distended abdomen, mental status changes", "Findings": "Multiple linear and curvilinear lucencies are noted on the scout images throughout the liver, as well as multiple dilated air filled loops of small and large bowel. On the axial CT images, air was noted within the bowel wall completely surrounding the lumen throughout multiple loops of small bowel, as well as air within the mesenteric vasculature, and within the portal venous system peripherally to the edges of the liver.", "Differential Diagnosis": "\u2022 Mesenteric ischemia\n\u2022 Trauma \n\u2022 Small/Large Bowel obstruction\n\u2022 Infectious enterocolitis\n\u2022 Inflammatory enterocolitis\n\u2022 Post-operative\n\u2022 Medications, i.e. steroids, chemotherapy, immunosuppresants\n\u2022 Necrotizing enterocolitis (pediatric cases)", "Case Diagnosis": "Pneumatosis Intestinalis/Portal Venous Gas", "Diagnosis By": "Radiographically, surgically (ischemic bowel)" }, "Topic": { "Title": "Pneumatosis Intestinalis and Portal Venous Gas", "Disease Discussion": "Portal venous gas is usually due to an extension of air within the mesenteric venous system and associated bowel, or pneumatosis intestinalis. Pneumatosis intestinalis occurs in two distinct forms, primary (15%) and secondary (85%). Primary penumatosis occurs as an idiopathic entity secondary to formation of thin walled cysts within the submucosa of the bowel wall. Secondary pneumatosis is generally related to disease of the bowel wall, or may occur secondary to pulmonary disease. \n\nDisruption of the normal mucosa by infection, trauma, ischemia/necrosis, surgery, or secondary to medication allows air to move into the submucosal spaces, where it tracks peripherally around the bowel wall. If enough air is collected within the bowel wall, it eventually spills into the mesenteric venous system, and then will begin to track superiorly and fill the portal venous system. \n\nRadiographically, pneumatosis appears as multiple thin, curvilinear lucencies surrounding the bowel lumen within the bowel wall. It will be seen within the dependant and non-dependant portions of the bowel, often outlined by adjacent fluid filling the bowel lumen. On CT, gas may be noted to fill the mesenteric vasculature, collecting and eventually spreading to the portal venous system more centrally. If enough gas is present, air may fill the portal venous vasculature of the liver and will appear as thin linear streaks branching out towards the periphery of the liver from a central location. Differentiating portal venous from biliary gas may be difficult on plain films, however usually portal venous gas will be seen to within 2cm of the peripheral edge of the liver, while biliary gas generally appears more centrally. On CT, air may be followed centrally within the liver and its location determined after observing collections within the main portal vein or common bile ducts. \n\nRadiographs will demonstrate pneumatosis and portal venous gas in approximately 2/3 of patients, however the underlying cause can often not be determine with plain films. CT will more definitively demonstrate the extent of pneumatosis/portal venous gas, and will additionally give further clues as to the source of the problem, i.e bowel ischemia, obstruction, inflammation, etc. Once the source is identified, prompt surgical or medical treatment should be started in order to treat the underlying pathological process.", "ACR Code": "7.5", "Category": "Hypoxic or Ischemic", "Keywords": "Pneumatosis IntestinalisPortal Venous Gasliver air", "Reference": "1. Fundamentals of Diagnostic Radiology, William Brant and Clyde Helms, 2006, 3rd Ed.\n\n2. Fundamentals of Body CT, Richard Webb, 2005, 3rd ED" } }, { "U_id": "MPX2028", "TAC": [ "MPX2028_synpic34049", "MPX2028_synpic34050", "MPX2028_synpic34052", "MPX2028_synpic34053", "MPX2028_synpic34054", "MPX2028_synpic34055" ], "MRI": [], "Case": { "Title": "Acute appendicitis", "History": "17 year old female presented to the emergency room with a 12 hour history of abdominal pain that began in her periumbilical region and progressed to the right mid abdomen.", "Exam": "Focally tender over the mid right anterior abdominal wall.\nTemperature 100.6 F\nWBC 14k", "Findings": "Axial CT images from the mid abdomen following oral and intravenous contrast material administration demonstrate a blind-ending loop of bowel arising from the cecum directed superiorly with the tip just inferior to the inferior margin of the liver. The bowel loop is not filled with contrast and measures 1.3 cm from outer wall to outer wall in diameter. There is some associated inflammatory infiltration of the mesentary and a small amount of perinephric fluid anterior to the right kidney. There is no free air or abnormal fluid collections to suggest abscess formation.", "Differential Diagnosis": "Acute appendicitis", "Case Diagnosis": "Acute appendicitis", "Diagnosis By": "Pathology", "Treatment & Follow Up": "The patient underwent emergent appendectomy.", "Discussion": "Note the location of the appendix in this case (directed anteriorly in the right abdomen), which might explain why this patient's pain was not at the \"classical\" location for acute appendicitis (McBurney's Point)." }, "Topic": { "Title": "Acute appendicitis", "Disease Discussion": "Appendicitis occurs most frequently in the 2nd to 3rd decade of life, less commonly in the extremes of age. Pain is usually the initial presenting complaint and often starts in the peri-umbilical region before migrating to the right lower quadrant with maximal tenders often located at McBurney\u2019s point. This typical sequence is absent in more than 1/3 of older children. Often pain is worse with movement, coughing (cough sign) driving over bump (cat\\'s eye sign), or standing on toes and dropping heels to ground (heel drop sign) (Rothrock). Vomiting occurs in the majority of school-aged children and may precede or begin concurrent with pain. Physical exam often reveals an elevated temperature and tenderness to palpation in the right lower quadrant. However, tenderness may involve the entire lower abdomen, or may be diffuse, especially with a perforation. Compared with those with non-perforated appendicitis, children with perforated appendicitis are significantly younger, have a longer duration of symptoms before diagnosis, have more physician visits before correct diagnosis, have higher temperatures, and are more likely to exhibit vomiting, diffuse abdominal tenderness, and peritoneal signs (Rothrock). Perforation generally occurs 36 to 48 hours after the onset of symptoms. Plain abdominal radiographs have been recommended as potentially useful for evaluating children with suspected appendicitis. Radiographic findings believed to be suggestive of appendicitis include rightward scoliosis, soft tissue masses, localized ileus, bowel obstruction, calcified fecolith, and free peritoneal fluid. Of these features, the most specific for appendicitis is a calcified fecolith (appendicolith) found in up to 13% to 22% with appendicitis and in only 1% to 2% of those without (Rothrock). While often recommended, these films rarely altered a patient\\'s diagnosis or management. Ultrasonography is appropriate in patients in which the diagnosis is unclear by history and physical examination, especially in pediatric and female patients. A normal appendix must be identified to rule out appendicitis. An inflamed appendix usually measures greater than 6 mm in diameter, is non-compressible and tender with focal compression (Hardin). Numerous other right lower quadrant conditions such as inflammatory bowel disease, cecal diverticulitis, Meckel\\'s diverticulum, endometriosis and pelvic inflammatory disease can cause false-positive ultrasonography results (Hardin). Appendiceal CT is more accurate than ultrasound and consists of a focused, helical CT after a Gastrografin-saline enema. It can be performed and interpreted usually within an hour. The accuracy of CT is due in part to its ability to identify a normal appendix better than ultrasound. If appendiceal CT is not available, standard abdominal/pelvic CT with contrast remains useful and may still be more accurate than ultrasound (Hardin). The standard for management of appendicitis remains appendectomy. The procedure may be performed by laparotomy (usually through a small right lower quadrant incision) or laparoscopy. While laparoscopic intervention is advantageous in adults due to decreased postoperative pain, earlier return to normal activity and better cosmetic results, an open appendectomy remains the primary approach to treatment in children due to their smaller size (Rothrock).\n\nhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=15155894", "ACR Code": "7.2", "Category": "Infection, bacteria", "Keywords": "appendicitis", "Reference": "Contran, et al. Robbins: Pathologic Basis of Disease, 6th ed. 1999, W.B Saunders Co.\n\nHardin DM Jr: Acute appendicitis: review and update. American Family Physician. 1-Nov-1999; 60(7): 2027-34\n\nRothrock SG: Acute appendicitis in children: emergency department diagnosis and management. Annals of Emergency Medicine. 01-Jul-2000; 36(1): 39-51", "External Links": "www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=15155894" } }, { "U_id": "MPX2027", "TAC": [ "MPX2027_synpic46451", "MPX2027_synpic46452", "MPX2027_synpic46453", "MPX2027_synpic46455", "MPX2027_synpic46456", "MPX2027_synpic46457", "MPX2027_synpic46459", "MPX2027_synpic46460", "MPX2027_synpic46461", "MPX2027_synpic46462", "MPX2027_synpic46463", "MPX2027_synpic46464", "MPX2027_synpic46465" ], "MRI": [], "Case": { "Title": "Right preseptal cellulitis and Choroidal Melanoma.", "History": "58 yo woman with orbital cellulitis preceded by open lesion inferior to right eye.", "Findings": "Contrast enhanced axial and coronal CT images reveal abnormal infiltration and thickening of the right preseptal soft tissues, extending into the right medial canthus. No postseptal extension is noted. No peripheral enhancing fluid collections are seen. Additionally, images demonstrate an enhancing lentiform mass along the superoposterior aspect of the right globe.", "Differential Diagnosis": "\u2022 Right preseptal cellulitis with\n\n\u00bb Choroidal Melanoma\n\u00bb Metastases (Breast, Lung)\n\u00bb Lymphoma\n\u00bb Leukemia\n\u00bb Choroidal hemangioma\n\u00bb Coat\u2019s Disease\n\u00bb Toxocara Canis Infection\n\u00bb Retrolental Fibroplasia", "Case Diagnosis": "Right preseptal cellulitis and Choroidal Melanoma.", "Diagnosis By": "Histologic evaluation confirmed choroidal melanoma.", "Discussion": "Clinically, the abnormality at the superoposterior aspect of the right globe was thought to represent a nevus." }, "Topic": { "Title": "Uveal Melanoma", "Disease Discussion": "Choroidal melanomas are the most common primary intraocular tumors in adults, and the most commonly occurring uveal melanoma. The uvea is subdivided into the iris, the ciliary body, and the choroids. Most choroidal melanomas are believed to develop from preexisting melaanocytic nevi. The estimated prevalence is five to seven cases per 1 million adults, occurring most commonly in people of northern European descent. Sixty-five percent of melanomas occur in those older than 50 years. Patients may be asymptomatic with lesions discovered during a routine ophthalmologic examination. Other patients may notice vision loss, photopsia, and visual field deficits. \n\nMelanomas primarily metastasize to the liver, as well as to the lung, bone, kidney, and brain. Treatment is dependent on site of origin, size, location of the primary lesion, and on the presence of extraocular extension, recurrence, or metastases. Melanomas greater than 1 cm in thickness are managed with enucleation. Medium sized lesions (3 mm to 1 cm) may be managed with enucleation, plaque brachytherapy and external-beam radiation. Small tumors (<3 mm in thickness) are monitored every 3-6 months with US. \n\nUveal melanomas are usually assessed by ophthalmologic examination, fluorescein angiography, US, CT or MR imaging. On unenhanced CT, these lesions appear elevated, hyperdense, are sharply marginated, and following contrast administration avidly enhance. At MR imaging, most melanomas appear as well-defined solid masses that are hyperintense on T1-weighted images, and hypointense on T2-weighted images secondary to the paramagnetic effects of melanin. Contrast enhanced fat-suppressed MR images are useful to demonstrate scleral invasion, tumor extension to the optic disc, and extraocular invasion.", "ACR Code": "1.3", "Category": "Neoplasm, malignant (NOS)", "Keywords": "Uveal MelanomaIntraocular MelanomaChoroidal Melanoma", "Reference": "Smoker W. et al. Vascular Lesions of the Orbit: More than Meets the Eye. RadioGraphics 2008; 28:185-204.\n\nEscott EJ. A Variety of Appearances of Malignant Melanoma in the Head: A Review. RadioGraphics 2001; 21:625-639\n\nSmall Choroidal Melanoma. Intraocular Melanoma Treatment (PDQ). National Cancer Institute. Accessed 8 Nov 2008.\nhttp://www.cancer.gov/cancertopics/pdq/treatment/intraocularmelanoma/HealthProfessional/page7" } }, { "U_id": "MPX2039", "TAC": [ "MPX2039_synpic18750", "MPX2039_synpic18752", "MPX2039_synpic18753" ], "MRI": [], "Case": { "Title": "PRIMARY CHOLESTEATOMA", "History": "14 y/o male with intermittent otorrhea of right ear and right TM perforation.", "Exam": "Right TM perforation", "Findings": "Soft tissue opacity is present in the right middle ear within the epi- and mesotympanum, extending into the mastoid air cells. The right TM is perforated. The ossicles and tegmen are intact. However, the scutum is blunted.", "Differential Diagnosis": "Otitis Media\nCholesterol Granuloma\nCongenital Cholesteatoma", "Case Diagnosis": "PRIMARY CHOLESTEATOMA", "Diagnosis By": "Surgery", "Treatment & Follow Up": "Right mastoidectomy and tympanoplasty" }, "Topic": { "Title": "PRIMARY CHOLESTEATOMA", "Disease Discussion": "Introduction: The term cholesteatoma is a misnomer coined by Johannes Muller in 1838. Initially described as a layered pearly tumor of fat containing biliary fat or cholestrin interspersed among sheets of polyhedral cells. Cholesteatomas actually do not contain fat but are composed of an outer matrix which surrounds layers of desquamated epithelium. The matrix is comprised of differentiated keratinized squamous epithelium in a collagen matrix.\nIncidence: The incidence of cholesteatomas is unknown, but it is a relatively common reason for otologic surgery. Death from intracranial complications of a cholesteatoma is uncommon, due to early recognition, timely surgical intervention, and supportive antibiotic therapy. Cholesteatomas remain a relatively common cause of permanent, moderate conductive hearing loss in children and adults. \nTypes: Cholesteatoma may be classified according to presumed etiology into two general categories: congenital and acquired. Acquired cholesteatomas can be further divided into primary and secondary acquired. \nCongenital: (2%) Congenital cholesteatomas are believed to arise from embryonal inclusions or rests of epithelial cells in the middle ear, mastoid, or petrous bone. Applies only to cholesteatomas in patients with the following criteria: an intact tympanic membrane, no continuity with the external ear canal, and lack of etiological factor, i.e. tympanic membrane perforation, history of ear infections or Eustachian tube dysfunction.\nAcquired: 98%\n1.\tPrimary Acquired: most common type; arises from retraction of the superior pars flaccida (Prussak's space) of the tympanic membrane which results in the formation of an epithelial pocket. \n2.\tSecondary Acquired: due to chronic infection and perforation of the pars tensa which results in trapping of epithelial cells within the middle ear. \n\nPathogenesis: Several pathogenic mechanisms have been produced to explain the development of acquired cholesteatomas, however, in all types the keratinizing squamous epithelium has spread beyond its normal location.\n\tThe pathogenesis of primary cholesteatoma is poorly understood. \tIt is believed that infection/inflammation, TM or Eustachian tube dysfunction, leads to retraction of the tympanic membrane, usually in the region of the superior pars flaccida in Prussak's space. This retraction results in an epithelial-lined pocket that becomes sealed and subsequently expands b/c of progressive accumulation of epithelial debris, extending posteriorly through the aditus and antrum to the mastoid air cells. Extension also occurs along the posterior tympanic recesses and petrous apex.\n\tSecondary acquired cholesteatoma is believed to occur via implantation of squamous epithelium into the middle ear as a result of TM perforation (iatrogenic vs traumatic). Another mechanism is via metaplasia of the cuboidal epithelium of the middle ear to keratinized stratified squamous epithelium due to chronic or recurrent otitis media. \n\nPathophysiology:\n\tCholesteatomas enlarge with fairly typical patterns of growth. The most common locations from which cholesteatoma arise are the posterior epitympanum, the posterior mesotympanum and the anterior epitympanum. Cholesteatomas are channeled along characteristic pathways by surrounding mucosal folds, the middle ear ossicles, and their suspensory ligaments. \n\tCholesteatomas may grow and cause primarily bony erosion of the following:\n\t\tScutum\n\t\tOssicles\n\t\tMastoid air cells\n\t\tTegmen\n\t\tSigmoid sinus plate\n\t\tFacial nerve canal\n\t\tLateral semicircular canal wall\n\n\tExtensive disease may result in: meningitis, abscess, venous sinus thrombosis, CSF rhinorrhea, labrynthine fistula.\n\tCholesteatoma in children is considered to be more aggressive than in the adult population. Extensive disease is found more frequently in children compared to adults. Also, higher rates of residual and recurrent disease have been documented in the pediatric population. However, the incidence of complications is directly related to the duration of disease, which is longer in adult patients. Therefore, complication rates are higher in adults. \n Clinical Manifestations: Most cholesteatomas are asymptomatic in their early development; children may come to medical attention with otorrhea and rarely complain of decreased hearing. The most common presenting symptoms are hearing loss, otorrhea, otalgia, nasal obstruction, tinnitus and vertigo. A previous history of middle ear disease, such as chronic otitis media and/or tympanic membrane perforation may be evident. Progressive unilateral hearing loss with a chronic foul smelling otorrhea should raise suspicion.\nPhysical exam: white mass behind the posterior half of the tympanic membrane, A retraction pocket may be seen, often in the attic or posterosuperior quadrant of the TM. facial nerve palsy, vertigo When extensive, a polyp may protrude through an attic defect.\n\nRadiologic Findings: Classic finding on CT is a soft tissue density in Prussak's space (superior recess of the TM) with subtle erosion of the scutum and neck of malleus and medial displacement of the remaining ossicles.\n\nCT: nondependent homogenous mass with well-or ill-defined borders; TM bulging with displacement of ossicles, +/- erosion of the scutum and ossicles; expansion of the attic. Mastoid air cells are usually underpneumatized and sclerotic\n\t\n \t \nMR: isoitense on T1 and moderate intensity on T2; enhancement of the otic capsule or facial nerve canal\n\nDx: Usually made otoscopically; Computerized tomography may be used to delineate the extent of disease, check the aeration of the mastoid and to help rule out intratemporal and /or intracranial complications. \n\nDDx: \n\tOtitis media\n\tCholesterol Granuloma\n\tCongenital Cholesteatoma\n\nTx: Tympanomastoidectomy\n\tThe primary surgical goal is to removing disease while preserving anatomy. Success rates of first surgery ranges from 40-80%, therefore, the need for a second procedure is fairly common.", "ACR Code": "1.2", "Category": "Inflammatory, non-infectious", "Keywords": "cholesteatoma" } }, { "U_id": "MPX2040", "TAC": [ "MPX2040_synpic27362", "MPX2040_synpic27363", "MPX2040_synpic27364" ], "MRI": [], "Case": { "Title": "Celiac Artery Aneurysm", "History": "72 yo man with celiac aneurysm noted on screening virtual colonography.", "Exam": "Patient without symptoms.", "Findings": "A 4.5cm x 2cm fusiform aneurysm of the celiac artery located 1cm from the origin with extensive mural thrombus just distal to the aneurysm.", "Differential Diagnosis": "celiac artery aneurysm\ninfected/inflammatory celiac artery aneurysm\nfistula formation between celiac artery and other lumens", "Case Diagnosis": "Celiac Artery Aneurysm", "Diagnosis By": "CT w/contrast", "Treatment & Follow Up": "Patient seen in vascular surgery for preop assessment, where best surgical approach (open vs. endovascular) will be decided.", "Discussion": "This patient's imaging shows no sign of inflammatory aneurysm, an encasement of the aneurysm by inflammation that often results in chronic abdominal pain, elevated ESR, and dense adherence of the surrounding viscera. Radiographic findings that increase the suspicion of an infected aneurysm are saccular shape (94% of infected aneurysms), lobulated contour, stranding or fluid around the vessel, and rapid progression on sequential imaging. Associated mural thrombus also increases the risk for an infected aneurysm. \nCeliac artery aneurysms are rare (4-6% of visceral aneurysms), and 2 cm is often the size at which intervention will be recommended. While open reconstructive aneurysmectomy has had a longer history of success, newer endovascular techniques have been gaining ground in recent years.\n\nD'Ayala, Marcus et al. \"Giant Celiac Artery Aneurysm with Associated Visceral Occlusive Disease.\" Vascular. 2004; 12(6):390-393.\nMacedo, Thanila et al. \"Infected Aortic Aneurysms: Imaging Findings.\" Radiology. 2004; 231: 250-257." }, "Topic": { "Title": "Celiac Artery Aneurysm", "Disease Discussion": "Celiac artery aneurysms are usually caused by atherosclerosis. Infection and trauma are also reported etiologies. While these aneurysms are considered quite rare, they may present with vague abdominal pain, as in this case, or merely as an incidental finding. In most cases surgery is the desired treatment to avoid rupture or thrombosis.", "ACR Code": "9.9", "Category": "Aneurysm", "Keywords": "Celiac ArteryCeliac Aneurysm", "Reference": "Valji K. Vascular and Interventional Radiology. WB Saunders, 1999: 199-200." } }, { "U_id": "MPX2046", "TAC": [], "MRI": [ "MPX2046_synpic42117", "MPX2046_synpic42118", "MPX2046_synpic42119", "MPX2046_synpic42120" ], "Case": { "Title": "Citrobacter koseri osteomyelitis/discitis", "History": "52 y/o AA male recently deployed soldier who was medically evacuated due to chronic back pain that interfered with his duties as a truckdriver. While being evaluated stateside his pain worsened and he developed altered mental status, prompting a lumbar puncture which revealed signs consistent with a potential infection. An MRI was then obtained for further evalutaion.", "Exam": "Back: Mild tenderness to palpation over lower thoracic/upper lumbar spine. \n\nCSF: LP opening pressure: 18 cm H2O, wbc=32,rbc=2, glc=53, prtn=92 76%lymphs. Gram stain: pmns present. no organisms. \n\nCBC: 5.68>10.6/31.6<443 \n\nCMP: 140/4.4/99/29/11/0.5<95, Ca 9.6, PO4 4.8, Mg 1.6", "Findings": "-Plain radiograph one week later showed decreased disk space between T10-T11 \n\n-On fat-suppressed MRI (STIR and FSE T2-weighted with fat sat MRI), high-signal -ntensity mass anterior to thoracic vertebrae, high signal intensity in the disc space and in the thoracic vertebrae at this level are consistent with infection. These areas enhance after contrast on the contrast-enhanced fat-saturated T1-weighted MR images.", "Differential Diagnosis": "1. Discitis/osteomyelitis \n2. Pott's Disease \n3. DJD \n4. Metastatic cancer", "Case Diagnosis": "Citrobacter koseri osteomyelitis/discitis", "Diagnosis By": "CT guided needle biopsy", "Treatment & Follow Up": "Pt started on 6 week course of florquinalone antibiotic therapy and discharged to outpatient care with a back brace.", "Discussion": "The specific cause or underlying condition leading to the development of discitis in this patient is unclear. Most cases of discitis show increased signal intensity on T2WI MRI within 48 hours of presentation and the course of infection typically moves anterior to posterior as seen with this patient, ultimately moving posterior until the spinal cord was involved.\n\nThe diagnosis of Pott's Disease was considered in the differential diagnosis; however, the unremarable CT obtained one month prior suggests against a tuberculosis infection due to the historically slower progression of disease seen with Pott's. \n\nMetastatic bone lesions were also considered; however, were less likely due to the rare incidence of intramedullary involvement and the involvement of the disc space.\n\nMRI is considered the best method for diagnosing disc space infection with a sensitivity of 96% and a specificity of 94%." }, "Topic": { "Title": "Citrobacter koseri osteomyelitis/discitis", "Disease Discussion": "NOTE: Please EDIT the CATEGORY and LOCATION - Above\n\nYou may use the template below - or [Clear] for a blank page.\n\nLesions/Condition:\n\nCell of Origin:\n\nWHO Grade(s):\n\nSynonyms:\n\nAssociations/Predisposing Factors:\n\nCommon Locations:\n\nDemographics:\n\nGross Morphology:\n\nHistology:\n\nSpecial Stains:\n\nGross Appearance:\n\nRadiology:\n\nPrognosis and Treatment:", "ACR Code": "3.2", "Category": "Infection, bacteria", "Keywords": "DiscitisOsteomyelitis", "Reference": "Spinal Imaging, Part7 and 9, Pgs 461-474, 521-541, Springer, 2007.\nSchindler, O.S. \"MRI Changes in infectious discitis: report on two cases.\" European Spine Journal, 4:360-361, 1995." } }, { "U_id": "MPX2051", "TAC": [ "MPX2051_synpic26329", "MPX2051_synpic26330" ], "MRI": [], "Case": { "Title": "Liver metastases from breast cancer", "History": "46 yo woman with a 15 year history of breast cancer referred to radiology for followup evaluation.", "Exam": "Not entered", "Findings": "Suspicious metastases in the liver, lungs, and bone. Biopsy from liver.\n\n(#56) 3.3 x 3.2 cm heterogeneous mass seen in posterior right lobe of liver. \n(#59) Additional 3.3 x 2.7 cm heterogeneous mass seen in posterior right lobe of liver.\n(#66) Additional 1.6 cm diameter heterogeneous mass seen in posterior right lobe of liver close to parenchymal edge.\n(#23, #28, #35) Numerous lung nodules on bilateral lung fields.\n(#98) well defined lucencies noted within right iliac in proximity to sacroiliac joint.", "Differential Diagnosis": "Metastatic disease\nPrimary neoplasm\nCystic Mass", "Case Diagnosis": "Liver metastases from breast cancer", "Diagnosis By": "Pathology (Malignant cells derived from adenocarcinoma, favoring metastatic breast carcinoma.)", "Treatment & Follow Up": "She was referred to radiology for followup evaluation and subsequent CT-guided biopsy of the liver lesion.", "Discussion": "Liver metastases from breast cancer is usually a late finding and as this case indicates, possible other metastases have already occurred to other organ systems1,2. It is therefore essential to have diligent follow up of treated primary breast cancer patients. Thorough history and physical (review of system for systemic recurrence, and complete physical looking for locoregional recurrence) is recommended every 3-6 months for the first 3 years post primary therapy and then every 6-12 months for 2 years and then annually3. Mammography should be taken every 6 months after radiation treatment if the patient had breast conserving surgical treatment. Yearly mammography should be taken for those that did not have breast conserving surgery3. Patients should also conduct monthly breast examinations3. Pelvic examination should be conducted regularly, but could be extended if patient has had total hysterectomy and oophorectomy3. If the patient had isolated and single liver metastases then the patient may be a good candidate for surgical resection. However, due to possibility of extrahepatic lesions and numerous liver metastases, the patient in the case is not a good surgical candidate1,2." }, "Topic": { "Title": "Liver metastases from breast cancer. (Path) Malignant cells derived from adenocarcinoma, favoring metastatic breast carcinoma.", "Disease Discussion": "Liver metastases from breast cancer is usually a late finding and as this case indicates, possible other metastases have already occurred to other organ systems1,2. It is therefore essential to have diligent follow up of treated primary breast cancer patients. Thorough history and physical (review of system for systemic recurrence, and complete physical looking for locoregional recurrence) is recommended every 3-6 months for the first 3 years post primary therapy and then every 6-12 months for 2 years and then annually3. Mammography should be taken every 6 months after radiation treatment if the patient had breast conserving surgical treatment. Yearly mammography should be taken for those that did not have breast conserving surgery3. Patients should also conduct monthly breast examinations3. Pelvic examination should be conducted regularly, but could be extended if patient has had total hysterectomy and oophorectomy3. If the patient had isolated and single liver metastases then the patient may be a good candidate for surgical resection. However, due to possibility of extrahepatic lesions and numerous liver metastases, the patient in the case is not a good surgical candidate1,2.", "ACR Code": "6.3", "Category": "Clinical Exam Finding or Sign", "Keywords": "Liver metastases from breast cancerMalignant cells derived from adenocarcinoma", "Reference": "1. Sakamoto Y, et al. Hepatic resection for metastatic breast cancer: prognostic analysis of 34 patients. World Journal of Surgery. 29(4):524-7, 2005 Apr.\n\n2. Elias D, et al. An attempt to clarify indications for hepatectomy for liver metastases from breast cancer. American Journal of Surgery. 185(2):158-64, 2003 Feb.\n\n3. Saverese D, Hayes D. Overview of Treatment For Locally Advanced and Metastatic Breast Cancer. UpToDate Online 13.1" } }, { "U_id": "MPX2050", "TAC": [ "MPX2050_synpic19947" ], "MRI": [], "Case": { "Title": "Eosinophilic granuloma of the calvarium", "History": "Skull pain", "Exam": "Noncontributory", "Findings": "Mutliple well-defined lytic lesions that coalesce and in an overall geographic appearance. \nLocation is predominatly posterior half of calvarium. \n\"Beveled-edge\" appearance can be seen radiographically.\nCT show greater destruction of the inner table compared to the outer.", "Differential Diagnosis": "Metastatic disease\nOsteomyelitis\nLymphoma\nEwing's sarcoma\nEosiniphilic granuloma", "Case Diagnosis": "Eosinophilic granuloma of the calvarium", "Diagnosis By": "Biopsy", "Treatment & Follow Up": "N/A", "Discussion": "Note the atypical greater destruction of inner table relative to outer table, yet still resulting in the classic \"beveled edge\" appearance" }, "Topic": { "Title": "Eosinophilic granuloma of the calvarium", "Disease Discussion": "Eosinophilic granuloma (EG) comprises 75% of a disease complex known as Langerhans Cell Histiocytosis (LCH), which is characterized by proliferation of the Langerhans cell histiocyte. EG is essentially LCH that is limited to the skeleton.\n\nAge: 6-10 yrs\nIncidence M:F = 2:1\nClinical: pain, fever\n\nMost commonly monostotic\nMultifocal 10-20%\nSkeletal sites (flat bones 70%): calvarium (25%), ribs (14%), femur (14%), pelvis (10%). Less common: mandible, spine, humerus.\nSpinal involvement can result in scoliosis.\n\nImaging appearance:\n-\"punched out\" (rounded lytic lesion with USUALLY nonsclerotic margins with sharp or thin zone of transition) on radiography\n-\"vertebra plana\" in spine very suggestive finding of this diagnosis\n-long bones (metadiaphyseal) show permeative/lytic lesions; appearance can be variable and can mimic osteomylitis\n-\"floating tooth\" appearance with lytic lesion in mandible\n-CT and MR useful in imaging workup; skelelal scintigraphy not as helpful as only 60% of cases will show uptake\n-can be very aggressive and extend into the soft tissues; MR best for demonstrating and characterizing soft tissue involvement\n\nOther characteritics of calvarial lesions:\n-\"hole within a hole\" appearance due to \"beveled edge\" which is caused by greater involvement of outer than inner bone\n-best appreciated on CT\n-multiple lesions may coalesce to produce geographic appearance\n-sclerotic margins can appear in healing phase\n\nDDX: metastasis, Ewing sarcoma, lymphoma, osteomyelitis\n\nIn most cases EG is self-limiting and associated with an excellent prognosis", "ACR Code": "1.3", "Category": "Neoplasm, NOS", "Keywords": "eosinophilic granulomalangerhans cell histiocytosis", "Reference": "1. Blickman H, ed. Pediatric Radiology: The Requisites. 2nd ed. 1998. Mosby: St. Louis. pp 221-222. \n2. Weissleder, Ralph; Wittenberg, Jack; Harisinghani, Mukesh G. Primer of Diagnostic Imaging. Philadelphia: Mosby International, 2002. \n3. Dahnert, Wolfgang. Radiology Review Manual. Baltimore: Williams and Wilkins, 1996." } }, { "U_id": "MPX2062", "TAC": [ "MPX2062_synpic34418" ], "MRI": [], "Case": { "Title": "Infectious cavitary abcess", "History": "Patient seen for shortness of breath at rest at the begining of December. In the work up a right lower lobe mass was discovered. Patient has a history of breast cancer and colon cancer 3 and 5 years ago respectively. Bronchoscopy was performed and the BAL showed cells suspicious for malignancy but a biopsy was negative. Patient was discharged on antibiotic therapy that was soon modified to include multiple antibiotic medications none of which provided improvement. She was referred for repeat bronchoscopy and lung biopsy to exclude carcinoma. Multiple anaerobes were cultured from the cavity fluid. The biopsy was negative for malignant cells. An endobronchial drain was placed to facilitate healing.", "Findings": "Opacity in RLL field. Well circumscribed, thick walled with a with an air fluid level that has organized in comparison with previous frontal CXR one month prior. On CT the opacity appears to have an air passageway that extends into the abnormality. On fluroscopy a guide wire can be seen in the abnormality and in another fluro image a pigtail catheter can be seen in the lesion.", "Differential Diagnosis": "DDx for cavitary mass in lung fields includes:\n-Malignancy- either primary, secondary,\n-Granulomatous dz- infx or non-infx and can be active or inactive, this includes vasculitis such as Wegener's granulomatosis\n-Infection(non-granulomatous) such as PNA and abcess, including septic emboli, especially if multiple \n-Congenital abnormality", "Case Diagnosis": "Infectious cavitary abcess", "Diagnosis By": "With the insertion of the pigtail catheter during the bronchoscopy fluid was drained that grew enterococcus faecalis, Klebsiella, and enterobacter cloacae.", "Treatment & Follow Up": "PICC line placed for Imipenem 500mg IV q6h and serial scans to follow abcess resolution.", "Discussion": "All three bacteria showed sensitivity to Imipenem. There was some discussion about the possibility of direct infusion of abx into the abcess though the pigtail catheter but in a recent paper ( Herth et al. Chest 2005) patients did just as well with systemic abx and leaving the pigtail for drainage purposes.\nPlacement of a catheter for lung abscess treatment is not common. In this case the drain was placed because the patient had shown no improvement despite aggressive antibiotic therapy, and because the abscess was easily accessible through the tracts created by earlier biopsies." }, "Topic": { "Title": "Lung abscess (solitary)", "Disease Discussion": "A lung abscess is a collection of purulent material within a destroyed portion of the lung. The incidence is much lower than earlier days, secondary to improved antibiotic coverage and earlier treatment. \n\nThe most common bacteria to form a lung abscess are anaerobes, Staph aureus, gram-negatives (Klebsiella, Proteus, Pseudomonas,others). Streptococcus pneumoniae/pyogenes and few others are less common. Lung abscess formation usually involves the normal oral flora (nearly all cases involving anaerobics). Staph and gram-negative infections are often nosocomial in origin. \n\nPathogenesis usually involves aspiration as the mechanism to access the lung. Periodontal disease often coexists. Loss of consciousness/gag reflex (alcoholism, drug addiction, general anesthesia, seizure, sedatives, neurological d/o) and esophageal d/o's increase aspiration risk. Also a nasogastric tube, tracheostomy, throat and dental surgeries increase the risk.\n\nInitially, there is an area of pneumonitis or aspiration pneumonia that follows gravity. Aspiration in the supine position more likely lead to pneumonia in the posterior segments of upper lobes or superior segments of lower lobes - often on the right. Aspiration in the upright/semi-upright position leads to basal segmental lower lobe involvement.\n\nSymptoms of an abscess are similar to pneumonia with fever, malaise, cough, pleuritic chest pain and sputum production. Anaerobic abscess often have a more indolent course. Those caused by Staph or Gram-negatives often have a more fulminant course. Typically it takes 7-14 days from aspiration to form an abscess cavity that is seen on CXR.", "ACR Code": "63.216", "Category": "Infection, bacteria", "Keywords": "lung abscess anaerobic bacteriacavitary lung lesionaspiration pneumonia", "Reference": "1. Groskin SA: Bacterial Lung Abscess. A review of 50 cases. J. Thorac Imaging 6:62-67, 1991.\n2. Armstrong P: Imaging of Diseases of the Chest. 99-112, 2000." } }, { "U_id": "MPX2065", "TAC": [ "MPX2065_synpic46278" ], "MRI": [ "MPX2065_synpic46279", "MPX2065_synpic46280", "MPX2065_synpic46281", "MPX2065_synpic46282", "MPX2065_synpic46300", "MPX2065_synpic46301" ], "Case": { "Title": "Arteriovenous Malformation (AVM)", "History": "26 year-old man with increasing right-sided parietal and occipital headaches", "Exam": "N/A", "Findings": "\u2022 Right occipital lesion\n\u2022 Serpentine hypointensities with surrounding edema\n\u2022 Enlarged feeding vessels from both PCA and MCA supply\n\u2022 Small feeder from the ACA\n\u2022 Enlarged draining veins - varix -drains into superior sagittal sinus", "Differential Diagnosis": "\u2022 Arteriovenous Malformation\n\u2022 Aneurysm \n\u2022 Spontaneous intracerebral hemorrhage \n\u2022 Stroke \n\u2022 Intracranial neoplasm", "Case Diagnosis": "Arteriovenous Malformation (AVM)", "Diagnosis By": "MRI/MRA", "Discussion": "Spetzler-Martin grade 4 arteriovenous malformation within the right occipital lobe that extends into the right posterior aspect of the parietal lobe. There is evidence of surrounding edematous changes which may suggest impairment of venous drainage. Arterial supply is predominantly from the right PCA. There is also supply from the posterior division of the right MCA as well as minimal supply from the right ACA. There is a large associated venous varix which drains to the posterior superior sagittal sinus." }, "Topic": { "Title": "Arteriovenous Malformation (AVM)", "Disease Discussion": "ARTERIOVENOUS MALFORMATION (AVM)\n\nClinical Features: AVMs are the most common symptomatic congenital vascular malformations. The peak age at presentation is between 20 and 40. Approximately 50% of patients with AVMs present with symptoms caused by hemorrhage (25% present with seizures). The overall risk of hemorrhage from an AVM is estimated at 2% to 4% per year, cumulative. 98% of AVMs are solitary. Multiple AVMs outside the setting of vascular neurocutaneous disorders such as Rendu-Osler-Weber and Wyburn-Mason syndromes are extremely uncommon.\n\nPathology: AVMs are complex networks of abnormal vascular channels that consist of dilated arterial feeder(s) and draining veins, without intervening capillaries. These vessels often demonstrate flow-induced angiopathic changes secondary to endothelial hyperplasia (flow-related\u201d aneurysms in 10 - 20%). AVMs may contain gliotic brain and hemorrhagic residua. Atrophy of otherwise normal adjacent brain results from chronic regional arterial hypoperfusion and venous hypertension, as the AVMs steal vascular supply from adjacent brain tissue.\n\nImaging: Intracranial AVMs are subdivided into parenchymal (pial or within the brain), and dural (outside the brain). A mixed type occurs when a parenchymal AVM recruits dural vascular supply. 85% of AVMs are supratentorial. On cerebral angiography an AVM appears as a tightly packed mass of enlarged feeding arteries that supply a central nidus, a plexiform web of small vessels. One or more dilated veins drain the AVM nidus. The main goals of the diagnostic imaging workup are to delineate the size of the AVM, the eloquence of adjacent brain, and the pattern of venous drainage. These 3 characteristics are used to determine the long-term risk of an untreated AVM, as the table below explains.\n\nTable 1. Spetzler AVM Grading System\nGraded feature\t Points assigned\n Size\n Small (<3 cm)\t\t\t\t1\n Medium (3-6 cm)\t\t\t2\n Large (>6cm)\t\t\t\t3\n\nEloquence of adjacent brain\n Noneloquent \t\t0\n Eloquent\t\t\t\t\t1\n\nVenous drainage\n Superficial only\t\t\t 0\n Deep\t\t\t\t\t 1\n\n========================================\n \nSpetzler grades range from 1 to 5. A separate grade 6 is reserved for inoperable lesions. Prospective studies have confirmed the accuracy and utility of the Spetzler grade in guiding patient management and estimating postoperative neurologic complications.", "ACR Code": "1.3", "Category": "Congenital, malformation", "Keywords": "AVMvascular malformationcongenital", "Reference": "Osborn. Diagnostic Neuroradiology. 1994. Mosby.\nOsborn. Diagnostic Cerebral Angiography. 2nd Ed, 1999. LW&W." } }, { "U_id": "MPX2055", "TAC": [ "MPX2055_synpic35457" ], "MRI": [], "Case": { "Title": "Ependymoma", "Case Diagnosis": "Ependymoma", "Diagnosis By": "Pathology and Histology" }, "Topic": { "Title": "Ependymoma", "Disease Discussion": "Ependymoma \n\nCell of Origin: \nEpendymal cells lining the ventricle and central canal of the cord \n\nWHO Grade(s): \nEpendymoma - Gr 2 \nAnaplastic Ependymoma - Gr 3 \nMyxopapillary - Gr 1 \nSubependymoma - Gr 1 \n\nSynonyms: \n\nAssociations/Predisposing Factors: \nNeurofibromatosis Type 2 \n\nCommon Locations: \n70% in fourth ventricle \n\nDemographics: \n70% under the age of 20 \n\nGross Morphology: \nsoft intracavitary mass \n\nHistology: \nsharply demarcated, perivascular pseudorosettes, ependymal rosettes (canals), \n\nSpecial Stains: \n\nGross Appearance: \nsoft grayish sharply marginated, rarely invade brain \nin spinal cord - sharply demarcated central masses \n\nRadiology: \nheterogeneous intraventricular mass \nsmall chunks of calcification \nsmall 'cystic' areas \nintraspinal are sharply demarcated, often with a hemosiderin 'cap' \n\nPrognosis and Treatment: \n50% or more at 5 years", "ACR Code": "1.3", "Category": "Neoplasm, glial", "Keywords": "EpendymomaEpendymoma - Gr 2Anaplastic Ependymoma - Gr 3", "External Links": "http://rad.usuhs.edu/medpix/medpix.html?mode=single&recnum=4836&table=card&srchstr=ependymoma&search=ependymoma#top" } }, { "U_id": "MPX2058", "TAC": [ "MPX2058_synpic33788" ], "MRI": [], "Case": { "Title": "Cervical Cancer - Stage IIIB with ureteral obstruction", "History": "Patient is a 42 y/o G5 P4014 woman who had not had cervical cancer screening for several years. Patient developed right sided pelvic pain and presented to a local Emergency Department, where she was initially felt to have an enlarged uterus and symptomatic fibroids. \nShe was referred to a local primary care physician for a Pap Smear.", "Exam": "Physical exam showed an irritated cervical os, and Pap smear results returned High-grade SIL. \nPatient was then referred to OB/GYN.", "Findings": "Normal pelvic ultrasound.\n\nPET/CT - right hydronephrosis with abnormal pelvic uptake in region of uterus. No pathologic up-take seen in region of local lymph nodes.\n\nFluoroscopic images obtained during a right percutaneous nephrostomy tube placement showed right sided hydronephrosis and high-grade stricture of distal right ureter. Stricture was dilated using balloon angioplasty technique, and a nephroureteral stent (NUS) was placed.", "Differential Diagnosis": "Transitional cell carcinoma.\nEndometrial carcinoma.\nDrop Metastasis", "Case Diagnosis": "Cervical Cancer - Stage IIIB with ureteral obstruction", "Diagnosis By": "PET and Pap Smear", "Treatment & Follow Up": "Patient returned to IR 4 weks later for removal of NUS and placement of antegrade ureteral stent. From this point on, the stent can be exchanged through the bladder by Urology service.", "Discussion": "In the management of cervical cancer, surgical candidacy is in part based on an assessment of parametrial tumor extension by physical examination. \nRadical hysterectomy is usually reserved for medically-fit patients with tumor confined to the cervix (stage I) or with minimal extension to the proximal vagina (stage IIA). Radiation therapy is the treatment of choice for tumor that has spread to the parametria or beyond (stage IIB or greater). Several previous studies have demonstrated that computed tomography has a disappointing accuracy (of only approximately 50%) in evaluating parametrial extension of cervix cancer. CT alone usually cannot accurately differentiate stage lB from IIB lesions and thus usually does not play a significant role in deciding surgical vs. nonsurgical treatment. In this particular case, the right sided hydronephrosis makes parametrial extension more obvious. The PET scan findings further help with staging and management in this patient." }, "Topic": { "Title": "Cervical Cancer", "Disease Discussion": "In the management of cervical cancer, surgical candidacy is in part based on an assessment of parametrial tumor extension by physical examination. \nRadical hysterectomy is usually reserved for medically-fit patients with tumor confined to the cervix (stage I) or with minimal extension to the proximal vagina (stage IIA). Radiation therapy is the treatment of choice for tumor that has spread to the parametria or beyond (stage IIB or greater). Several previous studies have demonstrated that computed tomography has a disappointing accuracy (of only approximately 50%) in evaluating parametrial extension of cervix cancer. CT alone usually cannot accurately differentiate stage lB from IIB lesions and thus usually does not play a significant role in deciding surgical vs. nonsurgical treatment. In this particular case, the right sided hydronephrosis makes parametrial extension more obvious. The PET scan findings further help with staging and management in this patient.", "ACR Code": "8.3", "Category": "Neoplasm, carcinoma", "Keywords": "Cervical Cancerextension into the parametriahydronephrosis", "Reference": "1. Hricak H, Yu KK. Radiology in invasive cervical\ncancer. AJR Am J Roentgenol 1996; 167:1101\u2013\n1108.\n2. Eifel PJ, Berek JS, Thigpen JT. Cancer of the cervix,\nvagina, and vulva. In: DeVita VT, Hellman S,\nRosenberg SA, eds. Cancer: principles and practice\nof oncology. Philadelphia, Pa: Lippincott,\n1997; 1433\u20131475.\n3. Subak LL, Hricak H, Powell CB, Azizi L, Stern\nJL. Cervical carcinoma: computed tomography\nand magnetic resonance imaging for preoperative\nstaging. Obstet Gynecol 1995; 86:43\u201350." } }, { "U_id": "MPX2056", "TAC": [ "MPX2056_synpic35393" ], "MRI": [], "Case": { "Title": "Pilocytic Astrocytoma", "Case Diagnosis": "Pilocytic Astrocytoma", "Diagnosis By": "Pathology and Histology" }, "Topic": { "Title": "Pilocytic Astrocytoma", "Disease Discussion": "Neoplasm Name: Pilocytic Astrocytoma \n\nSynonyms: Juvenile pilocytic, spongioblastoma \n\nICD-O code: \n\nCell of Origin: Astrocyte \n\nWHO Grade(s): Grade 1 \n\nGenetics and Associations: Occures in the optic nerve in NF-1 \n\nDemographics (Age, Sex, Incidence): Most common in childhood, with a peak incidence 9 - 15 years. Slight female predilection (13:9 F>M). Accounts for approximately 1/3 of pediatric posterior fossa neoplastic masses. \n\nCommon Locations: Cerebellum >> hypothalamus > brainstem, cerebral hemisphere, spinal cord \n\nGross Appearance: Circumscribed with very narrow zone of infiltration, mural nodule and fluid collection (\\\"cyst\\\") \n\nHistology: biphasic with dense and loose areas, microcysts, Rosenthal fibers \n\nSpecial Stains: \n\nRadiology: \\\"cyst with nodule\\\" showing intense enhancement of nodule on MR and CT. Largely hypovascular or avascular on angiography \n\nProgression: Does not progress \n\nPrognosis and Treatment: Surgical resection is often curative \n\nCOMMENTS: Most benign of astrocytoma types, most common subtype of astrocytoma in posterior fossa in children, most common type of hypothalamic glioma", "ACR Code": "1.3", "Category": "Clinical Exam Finding or Sign", "Keywords": "Pilocytic AstrocytomaAstrocytoma", "External Links": "rad.usuhs.edu/medpix/topic_display.html?recnum=6596#top" } }, { "U_id": "MPX2077", "TAC": [ "MPX2077_synpic51017", "MPX2077_synpic51018", "MPX2077_synpic51019", "MPX2077_synpic51020" ], "MRI": [ "MPX2077_synpic51021", "MPX2077_synpic51022", "MPX2077_synpic51023", "MPX2077_synpic51024", "MPX2077_synpic51025", "MPX2077_synpic51026", "MPX2077_synpic51027" ], "Case": { "Title": "Choroid Plexus Carcinoma", "History": "15 month old girl fell off a chair. The following day, she was acting more somnolent. Head CT was abnormal.", "Exam": "Physical exam was normal for age. No neurological deficits", "Findings": "CT: High density mass in the trigone of the right lateral ventricle. Mass effect.\n\nMRI: Right lateral ventriclular mass with separate enhancing mass in left temporal horn, suggesting carcinoma. Mass effect with midline shift. Acute hemorrhage, right temporal horn, best seen on GRE images. Trapping of right temporal horn", "Differential Diagnosis": "Choroid plexus carcinoma\nChoroid plexus papilloma\nPNET\nMedulloepithelioma (infants)\nTeratoma\nMetastatic Adenocarcinoma (adults)", "Case Diagnosis": "Choroid Plexus Carcinoma", "Diagnosis By": "Biopsy", "Treatment & Follow Up": "Surgical excision with follow-up CT and MRI", "Discussion": "Wesley Ferley, MD wrote:\nChoroid plexus carcinoma is an aggressive intraventricular tumor derived from choroid plexus epithelium. It corresponds to WHO grade III glioma. It accounts for 30-60 of all choroid plexus tumors in children. 50% occur in the lateral ventricles. The most common presentation is obstructive hydrocephalus (vomiting, vision changes, headache, balance problems, mental status changes). \nOn CT, these lesions are seen arising from the choroid plexus and are often hyperdense on non-contrast images. They have a grape-like or cauliflower appearance and avidly enhance. They often cause ventricular obstruction. Central necrosis and hemorrhage may occur. The differential diagnosis includes choriod plexus pappiloma, medulloepithelioma (infants), teratoma, and metastasic adenocarcinoma (adults). The 5-year survival is 40%.\nReferences\n1. \"http://wiki.cns.org/wiki/index.php/Choroid_Plexus_Carcinoma\" Site accessed on 02/07/08. Site was lasted revised 07/23/08.\n2. \u201cUncommon Brain Tumors\u201d http:www.uptodate.com. Chenda, Kesari, Chen. Copyright 2008." }, "Topic": { "Title": "Choroid Plexus Neoplasm, Papilloma, Carcinoma", "Disease Discussion": "Choroid Plexus Papilloma (WHO Grade I)\nChoroid Plexus Carcinoma (WHO Grade III-IV)\nCell of Origin: Choroid plexus epithelium\n\nCommon Locations:\nAdults - Fourth ventricle\nChildren - Lateral ventricle\n\nDemographics: Children > Adults. 40-50% papillomas seen in first year of life, 85% < 5 yrs. May be a congenital. Carcinomas usually seen only in pediatric age group.\n\nClinical Presentation: Hydrocephalus with headaches\n\nHistology: Papillomas have characteristic lobulated gross appearance. Most are well-differentiated and may resemble normal choroid plexus, however, anaplastic transformation may occur. Parenchymal invasion suggests carcinoma, but can be seen with benign tumors as well.\n\nTransformation of papilloma into carcinoma has been reported.\n\nSpecial Stains: Cytokeratin distinguishes CPP from ependymoma; Prealbumin (transthyretin) may be helpful (although choroid metastases may also stain positive)\nProgression: CSF seeding may occur in both papillomas and carcinomas.\n\nRadiology: Well-demarcated intraventricular (or cerebellopontine angle) mass with hydrocephalus. Calcification especially frequent in fourth ventricular tumors. In adult patients the fourth ventricle is more common. The tumor is attached to the choroid plexus.\n\nComments: Hydrocephalus may reflect multiple factors, including CSF over-production, ventricular obstruction, and impaired CSF reabsorption. Can present as a congenital brain tumor or neoplasm.\n\n===================================================\n[REF 1]\n\"Choroid plexus tumours are rare epithelial brain tumours and limited information is available regarding their biology and the best treatment. A meta-analysis was done to determine prognostic factors and the influence of various treatment modalities. A thorough review of the medical literature (1966-1998) revealed 566 well-documented choroid plexus tumours. These were entered into a database, which was analysed to determine prognostic factors and treatment modalities. Most patients with a supratentorial tumour\n were children, while the most common sites in adults were the fourth ventricle and the cerebellar pontine angle. Cerebellar pontine angle tumours were more frequently benign. Histology was the most important prognostic factor, as one, five, and 10-year projected survival rates were 90, 81, and 77% in choroid plexus-papilloma (n=353) compared to only 71, 41, and 35% in choroid plexus-carcinoma respectively (P<0.0005). Surgery was prognostically relevant for both choroid plexus-papilloma (P=0.0005) and choroid plexus-carcinoma (P=0.0001). Radiotherapy was associated with significantly better survival in choroid plexus-carcinomas.\n\nEight of 22 documented choroid plexus-carcinomas responded to chemotherapy. Relapse after primary treatment was a poor prognostic factor in choroid plexus-carcinoma patients but not in choroid plexus-papilloma patients. Treatment of choroid plexus tumours should start with radical surgical resection. This should be followed by adjuvant treatment in case of choroid plexus-carcinoma, and a \"wait and see\" approach in choroid plexus-papilloma. Copyright 2002 Cancer Research UK\"", "ACR Code": "1.3", "Category": "Neoplasm, glial", "Keywords": "choroid plexuspapillomacarcinoma", "Reference": "1)Wolff JE, Sajedi M, Brant R, Coppes MJ, Egeler RM: Choroid plexus tumours. Br J Cancer 2002 Nov 4;87(10):1086-91.", "External Links": "WWW.UAB.EDU/pedradpath/case31a.html" } }, { "U_id": "MPX2060", "TAC": [ "MPX2060_synpic27725", "MPX2060_synpic27727" ], "MRI": [], "Case": { "Title": "Bullet to the clivus.", "History": "A male soldier was shot in the right shoulder while on security detail in Iraq.", "Exam": "Entrance and exit wound in right shoulder. Also entrance wound in Right EAM. Not able to hear out of right ear.", "Findings": "Metallic fragments from projectile in right temporal bone demonstrating ballistic tract. The bullet entered the external auditory canal, penetrated the petrous portion of the temporal bone, and stopped in the clivus. \n\nThe bullet appears to have tumbled from when it entered the EAM to lodging into the clivus.", "Differential Diagnosis": "Bullet to the clivus.", "Case Diagnosis": "Bullet to the clivus.", "Diagnosis By": "CT only, bullet was left in.", "Treatment & Follow Up": "Since the patient was stable without clinically evident manifestations of the injury, it was decided to leave the bullet in the clivus and closely follow the individual.", "Discussion": "Several points of interest this case demonstrates are the following: the even number rule (see factoid), tumbling bullet, projectile in unexpected location (shot in shoulder, however, bullet ended up in clivus), and the size of the round (thought to be AK-47, however, not determined in this case).\n\nWhen a bullet has more mass at its proximal end due to distal tapering, there is a tendency for tumbling 180\u00b0. This tendency frequently results in bullets seen on radiographs pointing toward their direction of travel and entrance wound.\n\n\nThis case demonstrates an unusual path bringing up another unintuitive situation called bullet embolism, which is a rare but well documented phenomenon. With bullet embolism, the bullet travels through vascular channels; however, in our patient, the bullet traveled through both an air-filled channel (the external auditory canal) and a vascular channel (the petrous carotid canal). Although this case does not represent bullet embolism by definition, its unusual path brings up another reason to use the even number rule (see factoid)." }, "Topic": { "Title": "Ballistic Trauma: Even # Rule and Bullet Embolism", "Disease Discussion": "In ballistic trauma it is important to account for all bullets, whether lodged in the patient\u2019s body or exited through a wound. The even # rule, as discussed below, is a useful tool to quickly account for all foreign bodies that have entered a patient. Even # rule deviation should prompt the physician to initiate further investigation to locate the discordant bullet(s) or come up with another explanation (i.e. shared exit wound).\n\nEVEN # RULE\n\u2022 Entrance + exit + bullet = even # (all bullets accounted for)\n Any of the following may occur:\n \u2013 all bullets exited\n \u2013 all bullets lodged in body tissue\n \u2013 all bullets exited or lodged in body tissue\n\n\u2022 If entrance + exit + bullet = an odd # then not all bullets are accounted for, hence further imaging or explanation necessary\n\n \u2013 shared exit wound\n \u2013 bullet embolization\n\nBULLET EMBOLISM\nBullet embolism is a rare complication of vascular trauma. When a firearm missile enters a vascular structure, the projectile can pass through both walls of the vessel or settle within the wall or lumen. If the latter occurs, the missile may be carried by the flow of blood to a new site resulting in an embolism (1,2,3).\nSymptomatic arterial emboli may result in peripheral ischemia and should be removed quickly to avoid tissue or neurologic damage. Asymptomatic, cerebral, pulmonary, and pelvic arterial emboli may remain in place, especially if removal is technically difficult (3). Possible adverse effects of this decision, however, may lead to further embolization or migration, thrombosis, potential delayed arterial insufficiency, and subsequent pseudoaneurysm. \n\nThe Lodox Statscan\u2122 (see related links) allows for total body imaging in a short period of time for quantifying multiple projectiles.", "ACR Code": "9.4", "Category": "Trauma", "Keywords": "EvenBulletEmbolism", "Reference": "1. Ikonomidis et al. \u201cParadoxical Embolism of a Shotgun Pellet\u201d. Annals of Thoracic Surgery 1998;66:562-4.\n2. Khanna, A and Drugas, GT. \u201cAir gun Pellet Embolization to the Right Heart: Case Report and Review of the Literature.\u201d The Journal of Trauma Injury, Infection, and Critical Care 2003;54:1239-1241.\n3. Yoshioka et al. \u201cShotgun Wounds and Pellet Emboli: Case Reports and Review of the Literature.\u201d The Journal of Trauma Injury, Infection, and Critical Care 1995;39(3):596-601.\n4. Wilson AJ. Gunshot injuries: what does a radiologist need to know? Radiographics 1999; 19:1358-1368.\n5. Brogdon BG. Forensic radiology. Boca Raton: CRC Press, 1998.", "External Links": "rad.usuhs.mil/medpix/medpix.html?mode=single&recnum=6955&table=card&srchstr=lodox&search=lodox#top" } }, { "U_id": "MPX2067", "TAC": [ "MPX2067_synpic11184", "MPX2067_synpic11185" ], "MRI": [], "Case": { "Title": "Pseudomyxoma Peritonei", "History": "28 y.o. woman with onset of crampy abdominal pain.", "Exam": "Physical exam reveal a protuberant abdomen with decreased bowel sounds.", "Findings": "An acute abdominal series suggest early small bowel obstruction, with a dilated loop of small bowel and paucity of large bowel gas. The abdomen is protuberant, with centralization of bowel loops suggesting ascites. This is best demonstrated on follow up CT Scanogram obtained at a latter date.\n\nCT images demonstrate ascites that causes mass effect on abdominal viscera, demostrated by scalloping of the liver margins.", "Differential Diagnosis": "Ascities\nPseudomyxoma peritonei\nAbscesses", "Case Diagnosis": "Pseudomyxoma Peritonei", "Diagnosis By": "Surgery and Pathology", "Treatment & Follow Up": "Removal of source of possible tumor origin required bilateral salpingo-oophorectomy and appendectomy. Surgical debulking (performed on a number of occasions) of mucinous ascities was performed for relief of symptoms. The patient has also received multiple rounds of chemotherapy with Taxol/Carboplatin.", "Discussion": "Her diagnosis was confirmed by CT imaging and pathologic examination after the surgical debulking, hysterectomy and salpingo-oophorectomy and appendectomy. Pseudomyxoma peritonei is a complication of intraperitoneal seeding of mucinous producing cells from a number of neoplastic processes, leading to mucinous ascites. The majority of true examples (diffuse form) are due to appendiceal mucoceles from mucinous adenocarcinoma. Mucinous neoplasms of the ovary and colon can give a similar appreance. Some suggest that even some suspected ovarian sources originated from the appendix, with secondary spread to both the ovaries and peritoneum.\n\nSeeding may occur from rupture of the primary tumor, or from accidental rupture during surgical exploration and/or excision. The majority (~95%) of the peritoneal material is acellular mucin, which is produced by the neoplastic cells implanted within the peritoneal cavity. \n\nFindings on CT include loculated ascites with scalloping of the abdominal organs and septations - with or without calcification. The Peritoneal surface may also contain punctate calcifications. The mucinous ascities is usually loculated, and a key finding is mass effect on the solid viscera, such as scalloping of the liver and displacement of hollow viscera (bowel). This is in contrast to typical non-neoplastic ascites, which will surround organs, but may not alter their normal contours.\n\nAlthough the primary process may be benign or malignant, some authorities believe the unrelenting diffuse form is only from malignant disease.\n\nTreatment often consists of removal of the primary tumor, omentectomy, and debulking of the mucoid material but recurrences are common. There is progressive distention of the peritoneum and compression of abdominal viscera. Repeated surgical debridement of mucoid material from the abdomen carries the risks of surgical complications, which is often the eventual cause of death. Patients also often experience progressive wasting, and can suffer from repeated bowel obstruction." }, "Topic": { "Title": "Pseudomyxoma Peritonei", "Disease Discussion": "Pseudomyxoma peritonei is a complication of intraperitoneal seeding by mucin producing cells from a number of different neoplastic processes, leading to mucinous ascites. The majority of true examples (diffuse form) are due to appendiceal mucoceles from mucinous adenocarcinoma. Mucinous neoplasms of the ovary and colon can give a similar appreance. It has been suggested that even some of the suspected ovarian sources actually originated from the appendix, with secondary spread to both the ovaries and peritoneum.\n\nSeeding may occur from rupture of the primary tumor, or from accidental spillage during surgical exploration and/or excision. The majority (~95%) of the peritoneal material is acellular mucin, which is produced by neoplastic cells implanted within the peritoneal cavity. \n\nFindings on CT include loculated ascites with scalloping of the margins of the abdominal organs, septations of the fluid collecions, with or without calcification. The peritoneal surface may also contain punctate calcifications. The mucinous ascities is usually loculated, and a key findings is mass effect on the viscera, such as scalloping of the liver and displacement of bowel loops. This is in contrast to typical ascites which will surround organs, but usually do not alter normal contours.\n\nAlthough the primary neoplasm may be either benign or malignant, some authorities believe the the unrelenting diffuse form is only associated with malignant disease\n\nTreatment often consists of removal of the primary tumor, omentectomy, and debulking of the mucoid material. However, recurrences are common. There is progressive distention of the peritoneal cavity and compression of abdominal viscera. Repeated surgical debridement of mucoid material from the abdomen carries the risks of surgical complications, which are often the eventual cause of death. Patients also often experience progressive wasting, and can suffer from repeated bowel obstruction.", "ACR Code": "7.3", "Category": "Neoplasm, metastatic", "Keywords": "pseudomyxoma peritoneiappendiceal mucoceleadenocarcinoma", "Reference": "Fundamentals of Diagnostic Radiology, 2cd Edition; Brant & Helms, 1999" } }, { "U_id": "MPX2057", "TAC": [ "MPX2057_synpic50105" ], "MRI": [], "Case": { "Title": "Embolized Central Venous Catheter", "History": "3 y/o boy with neuroblastoma s/p treatment with Cytoxan, Vincristine, Cisplatin, Etoposide, and Doxorubicin requiring an off-therapy scan.", "Exam": "Port-A-Cath hub palpated in left upper chest; rest of exam and labs unremarkable.", "Findings": "\u2022 Image 1: Port-A-Cath hub with catheter dislodged with proximal catheter tip in proximal subclavian vein. Notice the access needle (Huber needle) in the hub with contrast in the surrounding soft tissue.\n\n\u2022 Image 2: Proximal tip of catheter in main pulmonary artery with distal end extending into the right pulmonary artery.", "Differential Diagnosis": "\u2022 failure of Port-A-Cath device with catheter in pulmonary artery \n\n\u2022 other tubular foreign body", "Case Diagnosis": "Embolized Central Venous Catheter", "Diagnosis By": "CT with contrast", "Treatment & Follow Up": "Patient was referred to interventional radiology and underwent a successful catheter retrieval procedure via the femoral vein. The Port-A-Cath hub was also removed successfully from the upper chest. The patient tolerated the procedure well and was discharged home after spending the night in the hospital for observation.", "Discussion": "A common mechanism for catheter embolization is \u201cpinch-off\u201d syndrome, which may or may not be evident on chest x-ray. This condition occurs in catheters placed via the subclavian vein. The catheter lumen passes between the clavicle and first rib before entering the subclavian vein lumen, usually observed when the skin incision for the port is made medial to the mid-clavicular line. Repeated trauma to the catheter during shoulder adduction weakens the catheter\u2019s structural integrity, eventually leading to fracture and subsequent embolization. \n\nOptimal placement of a Port-A-Cath is via the right internal jugular vein.\n\nJensen, M. Anatomical Basis of Central Venous Catheter Facture. Clinical Anatomy 2008 21:106-110." }, "Topic": { "Title": "Embolized Central Venous Catheter", "Disease Discussion": "Central venous catheter embolisms are rare. They tend to occur with a forced injection, or are due to a large positive pressure in the catheter, causing it to break or rupture. They are most often found in the pulmonary arteries.\n\nThey require removal since they may cause arrythmias or cardiac irritation. This may be done with snares through venous access.", "ACR Code": "67.4613", "Category": "Iatrogenic or Surgical (complications)", "Reference": "Rosen, Emergency medicine and Concepts, 0 Ed. 1998, p 1849?1852." } }, { "U_id": "MPX2075", "TAC": [ "MPX2075_synpic33087", "MPX2075_synpic33089" ], "MRI": [], "Case": { "Title": "Metastatic Colon Cancer", "History": "69 year old male with remote history of Colon Cancer status post total colectomy 9 years ago presents with unintentional weight loss and vague abdominal pain. Patient Currently smokes 1/2 pack/day.\n\nPast Medical history notable for:\nDiabetes Mellitus Type 2,\nHypertension,\nAtrial Fibrillation", "Exam": "Scars on Abdomen from Previous Surgeries. Physical exam is otherwise unremarkable.", "Findings": "The first image shows a 1 x 1 cm area of hypoattnuation in the left lobe of the liver. This was the image taken when the patient presented with his abdominal complaints. His symptoms resolved and he failed to follow up. The second and third images are from a year later. They show a left hepatic lobe mass that has diminished attenuation and heterogeneous enhancement. The mass measures approximately 4 x 4cm and there is intrahepatic ductal dilatation distal to the mass lesion", "Differential Diagnosis": "1. Metastatic Colon Cancer\n2. Primary Cholangiocarcinoma, or Hepatocellular Carcinoma\n3. Benign Hepatoma", "Case Diagnosis": "Metastatic Colon Cancer", "Diagnosis By": "Diagnosis was confirmed by Ex-Lap Biopsy", "Treatment & Follow Up": "Patient Treated with Xelox [Capecitabine plus Oxiliplatin]Chemotherapy. Repeat imaging has showed modest decrease in the size of his hepatic lesion. Typically patients with metastases this advanced have very poor prognosis.", "Discussion": "This case brings to light the utility of CT in the post operative period as a method of surveillance for recurrence and or metastases of a primary colon cancer. In 2005, the American Society of Clinical Oncology [ASCA] updated their post resection surveillance recommendations to include yearly CT for patients who had stage II or worse disease. They had previously recommended against CT monitoring but unanimously changed their recommendation after 3 meta-analyses all showed significant decrease in mortality when post op CT surveillance was done. The decrease was due to early identification of resectable hepatic metastases!\n\nASCA recommended a surveillance period of 3 years based on the average length of the meta-analyses. Given that our patient was 9 years post resection, these guidelines would not have affected his outcome." }, "Topic": { "Title": "Metastatic Disease- Liver", "Disease Discussion": "Surveillance of Post Colectomy Cancer Patients", "ACR Code": "7.3", "Category": "Neoplasm, metastatic", "Keywords": "ColonLiverNeoplasm", "Reference": "Desch, et al. Colorectal Cancer Surveilance: 2005 Update of an American Society of Clinical Oncology Practice Guideline. J Clin Oncol. 2005; 23:8512\n\nSadahiro et al. Prophylactic Hepatic Arterial Infusion Chemotherapy for the Prevention of Liver Metastasis in Patients with Colon Carcinoma. Cancer. 2004:100:590-597\n\nLeonarou et al. Screening of Post Colectomy Patients: Virtual Colonography. Abdom Imaging. 2006 Sep 22" } }, { "U_id": "MPX2078", "TAC": [ "MPX2078_synpic35704", "MPX2078_synpic35705", "MPX2078_synpic35706" ], "MRI": [], "Case": { "Title": "Rapunzel Syndrome, Gastric trichobezoar", "History": "A 9 year old girl presents with abdominal pain and feeding intolerance", "Findings": "\u2022 Plain film shows LUQ mass displacing bowel loops\n\u2022 CT shows concentric rings of air and soft-tissue density within the stomach and extending into the proximal small bowel (duodenum)", "Differential Diagnosis": "\u2022 Abscess\n\u2022 Emphysematous gastritis\n\u2022 Gastric phlegmon\n\u2022 Bezoar", "Case Diagnosis": "Rapunzel Syndrome, Gastric trichobezoar", "Diagnosis By": "Surgery and Pathology", "Treatment & Follow Up": "The bezoar was surgically excised. \n\nFollow-up Care: From now on she will only play with the Rehab Edition of the Brittany Spears dolls.", "Discussion": "Watch the video - http://www.youtube.com/watch?v=4aQJ9LYCtHY\n\nThis young girl has a a long history of chewing on her dolls\u2019 hair. The long \"tail\" of this trichobezoar, extending through three segments of the duodenum, qualifies as a \"Rapunzel Syndrome\".\n\nTrichobezoars are most common in young females, 13-20 years old, and may be associated with psychiatric problems - especially trichotillomania and trichophagia (eating hair). Patients may eat their own hair, doll hair, wigs, and occasionally the hair of pets.\n\nNOTE: Compulsive hair pulling is \"trichotillomania\"." }, "Topic": { "Title": "Gastric trichobezoar (hairball), Rapunzel Syndrome", "Disease Discussion": "Watch the video - http://www.youtube.com/watch?v=4aQJ9LYCtHY\n\nA bezoar is mass of impacted matter trapped in the stomach. There are many types of gastric bezoars. The most common is composed of fibrous plant matter. These are called phytobezoars, and are usually assymptomatic. Trichobezoars are composed of hair, and are less common, but can be larger. Bezoars are generally asymptomatic, but occasionally may produce gastric outlet obstruction, or in the case of trichobezoars can be abrasive, causing mucosal ulcerations. Bezoars of all types can produce early satiety. Patients who have had gastric surgery or delayed gastric emptying are at increased risk of developing all types of bezoars.\n\nWest WM, Duncan ND. CT appearances of the Rapunzel syndrome: an unusual form of bezoar and gastrointestinal obstruction. Pediatr Radiol. 1998 May;28(5):315-6. PMID: 9569269 \n\nHoover K, Piotrowski J, St Pierre K, Katz A, Goldstein AM. Simultaneous gastric and small intestinal trichobezoars--a hairy problem. J Pediatr Surg. 2006 Aug;41(8):1495-7. PMID: 16863865 \n\nQuraishi AH, Kamath BS. Rapunzel syndrome.\nGastrointest Endosc. 2005 Oct;62(4):611. PMID: 16185980\n\nRapunzel Syndrome - Rapunzel's syndrome: gastric bezoars and endoscopic management.\nGastrointest Endosc Clin N Am. 2006 PMID:16546027\n \nRapunzel syndrome with a long tail.\nIndian J Pediatr. 2001 PMID:11669043\n \nThe Rapunzel syndrome: a case report and review of the literature. Eur J Pediatr Surg. 1993 PMID:8353119\n \nGiant gastric trichobezoar.Int J Clin Pract. 2002 PMID:12137451\nhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Search&db=PubMed&term=bezoar+rapunzel+syndrome&tool=QuerySuggestion\nhttp://www.blackwell-synergy.com/doi/pdf/10.1111/j.1651-2227.2007.00012.x\nhttp://ajp.psychiatryonline.org/cgi/content/full/162/2/242", "ACR Code": "7.5", "Category": "Foreign Body", "Keywords": "bezoarforeign bodytrichobezoar, phytobezoar, Rapunzel Syndrome, hairball", "Reference": "Gastrointestinal Radiology, The Requisites. Robert Halpert. 1999, Mosby Press\n\nHoover K, Piotrowski J, St Pierre K, Katz A, Goldstein AM. Simultaneous gastric and small intestinal trichobezoars--a hairy problem.\nJ Pediatr Surg. 2006 Aug;41(8):1495-7.\nPMID: 16863865 [PubMed - indexed for MEDLINE]", "External Links": "www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=pubmed_Abstract&db=pubmed&cmd=Display&dopt=pubmed_pubmed&from_uid=7941500" } }, { "U_id": "MPX2049", "TAC": [ "MPX2049_synpic20940" ], "MRI": [], "Case": { "Title": "Gastric pull through", "History": "46-year-old Caucasian male with a history of squamous cell carcinoma of the middle third of the esophagus in 2001. Pt is s/p transhiatal esophagectomy and chemoradiation and neoadjuvant chemotherapy. Here for follow-up and screening for recurrence.", "Exam": "No recent physical exam on record\n24Jun2004: biopsy of esophagus \u2013 no metaplasia present\n25June2005: all values of basic metabolic panel are within normal limits", "Findings": "Chest PA: Descending aorta shadow obscured by retrocardiac opacity. \nChest Lat: Abnormal soft tissue density in a retrocardiac position obscuring the posterior border of left ventricle. \n\nCT: Dilated esophagus with air contrast level extending from the thoracic inlet to the diaphragm. Lower images show surgical clips.", "Differential Diagnosis": "(Lower Middle Mediastinal Mass)\nEsophageal processes: achalasia, esophageal mass (leiomyoma), hiatal hernia, or gastric pull through\nTracheal or Esophageal Duplication Cysts\nAortic Ectasia or Aneurysm", "Case Diagnosis": "Gastric pull through", "Diagnosis By": "Surgical history", "Treatment & Follow Up": "Patient has had stable postoperative films since 2001. Continue with annual biopsies and CT and plain films twice a year for at least five years.", "Discussion": "Malignant epithelial tumors of the esophagus are almost always primary carcinomas. Worldwide, squamous cell carcinoma (SCCA) is the most common type and ranks fifth in mortality rate among tumor sites. Genetic predisposition, dietary habits, environmental exposures, and alcohol and tobacco use have all been implicated as causative factors for the disease. 1\n\nClinically, patients with esophageal cancer present with dysphagia (90%) and/or odynophagia (50%). By the time they seek treatment upwards of 75% have experienced anorexia and weight loss and report considerably altered diets due to luminal compromise. Generally there are no specific physical findings with SCCA. Patients with symptoms of esophageal cancer are often worked up in the following manner. PA and lateral chest radiographs are obtained in those with chronic cough or abnormal findings on chest auscultation to demonstrate metastases or infiltrates suggestive of aspiration or esophagorespiratory fistula. Findings may include lateral deviation of the mediastinal contents, widening of the mediastinum, and esophageal air-fluid levels. Contrast esophagography using barium is usually indicated to rule out other disorders with similar presentations such as achalasia. Barium swallows in patients with SCAA can demonstrate high-grade stenosis, complete obstruction, and fistulas. Flexible endoscopy is also generally indicated since it allows direct visualization of the esophagus as well as the opportunity to obtain tissue samples. Obtaining at least six biopsy samples yields a diagnosis with an accuracy approaching 100%. Endoscopy aids in accurate characterization of the tumor\u2019s configuration, length, and localization. It also aids in initial relief of dysphagia because dilation can be performed at the same time. 1\n\nEsophageal cancer is considered a treatable disease, but one that is rarely curable. The overall five-year survival rate in patients that are amenable to surgery ranges from 5-20%. Radiation or chemoradiotherapy alone are considered suboptimal primary treatment modalities because of locally persistent or recurrent disease. Current studies suggest combined modality therapy with preoperative chemoradiotherapy followed by surgery is acceptable management for patients with stage II and III cancer. Optimal treatment for patients with earlier stage disease is less clear and surgery alone is considered reasonable. 2 \n\n1. Feldman: Sleisenger and Fordtran\u2019s Gastrointestinal and Liver Disease, 7th ed., Chapter 35 \u2013 Esophageal Tumors, Copyright 2002 Elsevier\n2. Radiation therapy, chemoradiotherapy, and neoadjuvant approaches for localized esophageal cancer. By: Forastiere, A, et al. UpToDate" }, "Topic": { "Title": "Lower Middle Mediastinal Mass/gastric pull through", "Disease Discussion": "Discussion (include references): Malignant epithelial tumors of the esophagus are almost always primary carcinomas. Worldwide, squamous cell carcinoma (SCCA) is the most common type and ranks fifth in mortality rate among tumor sites. Genetic predisposition, dietary habits, environmental exposures, and alcohol and tobacco use have all been implicated as causative factors for the disease. 1Clinically, patients with esophageal cancer present with dysphagia (90%) and/or odynophagia (50%). By the time they seek treatment upwards of 75% have experienced anorexia and weight loss and report considerably altered diets due to luminal compromise. Generally there are no specific physical findings with SCCA. Patients with symptoms of esophageal cancer are often worked up in the following manner. PA and lateral chest radiographs are obtained in those with chronic cough or abnormal findings on chest auscultation to demonstrate metastases or infiltrates suggestive of aspiration or esophagorespiratory fistula. Findings may include lateral deviation of the mediastinal contents, widening of the mediastinum, and esophageal air-fluid levels. Contrast esophagography using barium is usually indicated to rule out other disorders with similar presentations such as achalasia. Barium swallows in patients with SCAA can demonstrate high-grade stenosis, complete obstruction, and fistulas. Flexible endoscopy is also generally indicated since it allows direct visualization of the esophagus as well as the opportunity to obtain tissue samples. Obtaining at least six biopsy samples yields a diagnosis with an accuracy approaching 100%. Endoscopy aids in accurate characterization of the tumor\u2019s configuration, length, and localization. It also aids in initial relief of dysphagia because dilation can be performed at the same time. 1Esophageal cancer is considered a treatable disease, but one that is rarely curable. The overall five-year survival rate in patients that are amenable to surgery ranges from 5-20%. Radiation or chemoradiotherapy alone are considered suboptimal primary treatment modalities because of locally persistent or recurrent disease. Current studies suggest combined modality therapy with preoperative chemoradiotherapy followed by surgery is acceptable management for patients with stage II and III cancer. Optimal treatment for patients with earlier stage disease is less clear and surgery alone is considered reasonable. 2", "ACR Code": "67.45", "Category": "Anatomy, Normal and Measurements", "Keywords": "Mediastinal Massgastric pull through", "Reference": "1. Feldman: Sleisenger and Fordtran\u2019s Gastrointestinal and Liver Disease, 7th ed., Chapter 35 \u2013 Esophageal Tumors, Copyright 2002 Elsevier2. Radiation therapy, chemoradiotherapy, and neoadjuvant approaches for localized esophageal cancer. By: Forastiere, A, et al. UpToDate" } }, { "U_id": "MPX2071", "TAC": [ "MPX2071_synpic16474", "MPX2071_synpic16475" ], "MRI": [], "Case": { "Title": "Bronchogenic Carcinoma with Metastasis to the Liver. \r\nDiagnosis confirmed by US guided needle biopsy of the liver lesion and cytopathologic study of the recovered tissue.", "History": "76 year old man with known primary lung cancer referred to radiology for 3 phase contrast enhanced abdominal CT to clarify liver lesion noted on prior study.", "Findings": "CECT demonstrates:\n1. Two masses in left lower lobe. The larger mass is approx. 4cm in diameter, with a lobulated and spiculated margin. \n2. 3.7 cm mass in the right posterior lobe of the liver with a vaguely enhancing margin and hypodense necrotic center. \n\nUltra-sound guided needle biopsy of the liver lesion images demonstrate a complex mass in the right posterior lobe of the liver, superior to the right kidney. One of the images demonstrates the biopsy needle in place at the periphery of the lesion.", "Differential Diagnosis": "Differential for the liver lesion (on ultrasound)\n\n\u2022 Metastatic lung cancer\n\u2022 Cavernous hemangioma\n\u2022 Pyogenic abscess\n\u2022 Hepatocellular carcinoma\n\u2022 Fibrolamellar carcinoma\n\u2022 Hepatic adenoma", "Case Diagnosis": "Bronchogenic Carcinoma with Metastasis to the Liver. \nDiagnosis confirmed by US guided needle biopsy of the liver lesion and cytopathologic study of the recovered tissue.", "Treatment & Follow Up": "The liver metastasis confirms the cancer as a Stage IV non-resectable cancer. Palliative chemotherapy and radiation therapy may be considered." }, "Topic": { "Title": "Bronchogenic Carcinoma of the Lung with Metastasis to the Liver", "Disease Discussion": "Neoplasm : Bronchogenic carcinoma of the lung\n\nSynonyms: Lung cancer\n\nCell of Origin: Non-small cell carcinoma\n\nGenetics and Associations: Cigarette smoking (total pack years) is the most significant risk factor. Other associations include radiation exposure, asbestos exposure, occupational inhaled substances (especially nickel, chromates, and arsenic), genetically dominant oncogenes, and loss of tumor suppressor genes.\n\nDemographics (Age, Sex, Incidence): Cancer of the lung occurs most often between the ages of 40 and 70, with a peak incidence in the 6th or 7th decade. It is the leading cause of cancer deaths in both sexes and the male:female death ratio is about 3:1. The annual death rate for lung cancer is about 70/100,000 for males and 19/100,000 for females.\n\nCommon Locations: Bronchogenic cancers arise most often as a hilar mass but may also present as a large peripheral mass.\n\nGross Appearance: The neoplastic tissue is typically gray-white and firm to hard. Bulky tumors often have areas of necrosis that appear yellow-white and mottling. \n\nHistology: Histology varies depending on the subtype: adenocarcinoma is the most common subtype and features include gland formation, mucin production, and often an adjacent desmoplastic response. Other subtypes include squamous cell carcinomas, small cell carcinomas, and large cell carcinomas.\n\nSpecial Stains: Mucicarmine, Cytokeratin 7, Cytokeratin 20, and TTF -1.\n\nRadiology: Plain chest films may show single or multiple nodules, well defined or poorly defined masses in the hilar or peripheral regions or no findings. Mediastinal enlargement may be evident due to primary tumor or metastatic lymphadenopathy. CT may show an irregular or spiculated edge due to fibrosis surrounding the tumor, a lobulated contour, air bronchograms within the nodule, or cavitation. 95% of lung nodules exceeding 2 cm are cancers. \nOf particular significance for this case is the radiologic appearance of lung cancer metastases to the liver. A liver met will typically appear as a well-defined, low-density, solid mass with vague peripheral enhancement. The mass will often appear hypodense centrally due to tumor necrosis. Calcifications may be present. Multiple masses or diffusely infiltrating metastases may also occur. \n\nProgression: Bronchogenic CA spreads by direct invasion or via the hematogeneous or lympahngitic routes. Mediastinal nodes are commonly involved, and distal mets to the liver, brain, bone, and adrenals are common.\n\nPrognosis and Treatment: Overall prognosis is approximately 9% 5 year survival. Small-cell carcinoma has a median survival rate of 12-18 months and is treated with chemotherapy and radiation therapy. Non-small cell cancers are treated surgically if disease is limited. Chemotherapy and radiation may be used in advanced disease.", "ACR Code": "7.3", "Category": "Neoplasm, carcinoma", "Keywords": "Lung CA" } }, { "U_id": "MPX2073", "TAC": [ "MPX2073_synpic12218" ], "MRI": [ "MPX2073_synpic12212", "MPX2073_synpic12214", "MPX2073_synpic12215", "MPX2073_synpic12216" ], "Case": { "Title": "Ewing Sarcoma", "History": "22 year-old Caucasian man with 6-month history of right hip pain", "Findings": "A-P radiograph of the pelvis shows mottled, osteolytic lesion of the right iliac wing with suggestion of soft tissue mass.\nThe lytic lesion of the right femoral head, which was shown on the subsequent CT and MRI, is not defined.\nCT\nContrast-enhanced axial CT (bone windows) shows a large heterogeneously enhancing soft tissue mass originating in the right iliac wing and extending into the adjacent muscles both anteriorly and posteriorly. Spiculated periosteal reaction of the iliac wing is present. At the level of the hips, axial contrast-enhanced CT shows a lytic mass of the right femoral head.\nMRI\nAxial and coronal FSE T2-weighted MR images show a heterogeneously high-signal-intensity mass originating from the right iliac wing and extending into the adjacent muscles. The coronal MR image also shows a heterogeneously high-signal-intensity mass in the right femoral head.\nAxial and coronal contrast-enhanced T1-weighted MR images show heterogeneous enhancement of the right iliac wing mass and soft tissue extension with a large nonenhancing region posterior to the iliac wing consistent with necrosis. The coronal MR also shows a heterogeneously enhancing mass in the right femoral head.\n\nP-A radiograph of the chest shows development of bilateral lower lobe pulmonary nodules consistent with metastases.", "Differential Diagnosis": "Ewing Sarcoma, lymphoma, osteolytic osteosarcoma", "Case Diagnosis": "Ewing Sarcoma", "Treatment & Follow Up": "Treatment of primary lesions is wide excision, when feasible, and chemotherapy and adjunctive radiation therapy when indicated." }, "Topic": { "Title": "Ewing Sarcoma", "Disease Discussion": "Ewing Sarcoma (ES), a small malignant round cell tumor, is the second most common primary bone tumor in children after osteosarcoma (1). ES occurs usually in individuals less than 25 years of age but rarely before the age of 5 years. There is a slight male predominance. Osseous Ewing sarcoma is usually medullary but rarely can be periosteal in location (2). Ewing sarcoma of the bones is most frequently found in the axial skeleton and proximal extremities. On radiographs, ES shows a osteolytic (permeative/moth eaten type of bone destruction) pattern usually with associated large soft tissue mass. Aggressive periosteal response manifests as an onion-skin or \u2018sunburst\u2019 appearance. The overall disease-free 5-year survival in patients presenting with nonmetastatitic disease is 54-95% for Ewing sarcoma (3). Prognosis is worse for larger central lesions (e.g.retroperitoneal) as compared to distal ones with the best prognosis with periosteal or subperiosteal tumors. The addition of chemotherapy to wide exision and/or radiation therapy has improved the prognosis in these patients (3).", "ACR Code": "4.3", "Category": "Neoplasm, sarcoma", "Keywords": "Ewing\u2019s Sarcoma", "Reference": "Greenspan, A. Orthopedic Radiology: A Practical Approach, 3rd ed. Lippincott Williams & Wilkins 2000, pp. 690-694.Putman, C., Ravin, C. Textbook of Diagnostic Imaging, 2nd ed. W.B. Saunders Co. 1994. pp 1531-1532.\nShapeero LG, Vanel D, Sundaram M, et al. Periosteal Ewing sarcoma. Radiology 1994;191:825-831\nShapeero LG, Vanel D. Imaging evaluation of the response of high-grade osteosarcoma and Ewing sarcoma to chemotherapy with emphasis on dynamic contrast-enhanced magnetic resonance imaging. Sem Musculoskel Rad 2000;4;137-146" } }, { "U_id": "MPX2064", "TAC": [ "MPX2064_synpic53130", "MPX2064_synpic53230", "MPX2064_synpic53231", "MPX2064_synpic53232", "MPX2064_synpic53233", "MPX2064_synpic53234", "MPX2064_synpic53235", "MPX2064_synpic53236", "MPX2064_synpic53238", "MPX2064_synpic53239" ], "MRI": [], "Case": { "Title": "Pneumopericardium", "History": "22 y.o. man with a history of polytrauma, gun shot wound to chest, 2 weeks ago, status post multiple right thoracostomy tube placements.", "Exam": "Tracheotomy. Heart sounds slightly diminished.", "Findings": "Thin rim of lucency surrounding the cardiac shadow. Previous Chest CT showed a small amount of pericardial air at the apex.", "Differential Diagnosis": "\u2022 Pneumopericardium\n\u2022 Pneumomediastinum\n\u2022 Pneumothorax", "Case Diagnosis": "Pneumopericardium", "Diagnosis By": "Diagnosis confirmed by re-interpretation of prior CT Chest.", "Treatment & Follow Up": "Change to pressure-control ventilation. \nClose in-patient clinical and serial radiographic exams." }, "Topic": { "Title": "Pneumopericardium", "Disease Discussion": "Pneumopericardium is defined as air with the pericardial sac. It is an uncommon finding and the exact mechanism is still not well understood although it is an associated complication of existing pneumothorax or pneumomediastinum. It may occur in patients with barotrauma seondary to a blast injury or from valsalva maneuver. It can also be idiopathic and should be considered as a potential source of chest pain, especially if no trauma is present. It is important to recognize because it can result in cardiac tamponade for which the treatment is either surgical with needle drainage or close observation because they can spontaneously resolve.", "ACR Code": "-1.9", "Category": "Iatrogenic or Surgical (complications)", "Keywords": "Pneumopericardium", "Reference": "Images in clinical medicine: Pneumomediastinum. N Engl J Med 2006 Mar 16;354(11)1177." } }, { "U_id": "MPX2066", "TAC": [ "MPX2066_synpic26219" ], "MRI": [ "MPX2066_synpic26220", "MPX2066_synpic26221", "MPX2066_synpic26222" ], "Case": { "Title": "Calcaneal Stress Fracture", "History": "18 y/o male undergoing military boot camp who complains of right ankle pain upon jumping out of bed (approximately 6 ft high fall) and landing on ankle.", "Exam": "Patient complained of point tenderness upon palpation of ankle. Rest of physical noncontributory.", "Findings": "Plain Films: No acute findings\n\nMRI: Nondisplaced, compression type fracture of posterior calcaneus with extensive bone marrow and surrounding soft tissue edema.", "Differential Diagnosis": "-Ankle Sprain\n-Stress Fracture\n-Arthritis\n-Tenosynovitis", "Case Diagnosis": "Calcaneal Stress Fracture", "Diagnosis By": "Radiographically" }, "Topic": { "Title": "Calcaneal Stress Fracture", "Disease Discussion": "Stress fractures are classified into either fatigue or insufficiency type fractures. Fatigue type fractures result from the application of unusual force/torque onto a normal bone, this is common among athletes (especially long distance runners or ballet dancers) or in military members (especially recruits in basic training or undergoing parachute training). Insufficiency type fractures results from the application of normal stress on an abnormal bone. The underlying abnormality of the bone arises from a diverse array of causes, including osteoporosis, Paget's disease, osteomalacia, hyperparathyroidism, renal osteodystrophy, rheumatoid arthritis, fibrous dysplasia, irradiation, and so forth. \n\nClinically the patient complains of activity-related pain that is relieved by rest. There also may be a localized soft tissue swelling or tenderness, though the specific site and activity being engaged in influences these variables.\n\nThe most common site of fatigue-type stress fractues is the metatarsals (march fracture) with the second most frequent location being the calcaneus. These calcaneal stress fractures are usually found with a vertical or oblique orientation in the posterior or posterosuperior portion of calcaneus. Radiographs are often normal initially though MR and bone scan offer increased sensitivity and can be used with a high index of clinical suspsion even if the plain radiograph is normal.", "ACR Code": "4.4", "Category": "Trauma", "Keywords": "CalcaneusStress FractureT", "Reference": "1. \"Traumatic Diseases.\" Bone and Joint Imaging. Resnick D and Kransdorf MJ, ed. 3rd Edition. Philadelphia: Elsevier Saunders, 2005. Pg 796-799.\n\n2. \"Osseous Trauma.\" Musculoskeletal MRI. Kaplan PA, ed. Philadelphia: WB Saunders Company, 2001. Pg 157-161." } }, { "U_id": "MPX2096", "TAC": [ "MPX2096_synpic28571", "MPX2096_synpic28598", "MPX2096_synpic28599" ], "MRI": [], "Case": { "Title": "Grade 2 anterior spondylolisthesis at the level of L4/L5.", "History": "51 year-old Caucasian female with progressive low back pain.", "Findings": "Lateral radiograph shows grade 2 anterior spondylolisthesis at the level of L4/L5 and osteoarthritic changes at the level of L5/S1 and L4/L5. Sagittal CT shows grade 2 anterior spondylolisthesis at L4/L5. Coronal CT show levo scoliosis of lumbosacral spine. Axial CT shows vacuum disc phenomenon and osteoarthritic changes of the apophyseal joints and rotatory component.", "Differential Diagnosis": "Grade 2 spondylolisthesis with apophyseal joint degenerative changes", "Case Diagnosis": "Grade 2 anterior spondylolisthesis at the level of L4/L5.", "Diagnosis By": "Lateral radiograph and CT with bone windows.", "Discussion": "This 51-year-old female who had back pain and the radiographs and CT showed significant levoscoliosis and grade 2 anterior spondylolisthesis at L4/L5 with degenerative changes secondary to apophyseal joint disease. It is difficult to determine definitively the grade of displacement on the radiograph due to the rotatory component. ACR Codes: 4.9\nThe term spondylolisthesis originated in the 18th century. In 1882, Franz Ludwig Neubebauer described spondylolisthesis in women who had died during labor due to difficulties resulting from narrow birth canals. The word is of Greek origin, spondylo meaning spine and listhesis meaning slippage or slip. \nSpondylolisthesis is defined as a displacement of a superior vertebra in relation to the inferior one. The most common type of spondylolisthesis occurs due to fracture of the pars interarticularis, with L5/S1 being the most frequent level. A grading system that is commonly used describes a grade 1 as displacement of 25% or less of the involved vertebra, grade 2 is displacement greater than 25% and up to 50%, grade 3 is displacement greater than 50% and up to 75% and grade 4 is greater than 75% displacement and up to 100% displacement. \nBecause spondylolisthesis typically occurs at levels below the spinal cord, the condition is rarely fatal. However, besides low back pain, nerve root involvement is common, especially because of compression from the inferior articular process. Other common presentations besides musculoskeletal pain and radiculopathy are related to degenerative disc disease and spinal stenosis when present. \nAs mentioned previously, there are different etiologies of spondylolisthesis. The most common, occurring nearly 80% of the time, is type II, or spondylolytic spondylolisthesis (also known as isthmic). This commonly follows spondylolysis, often as a result of athletic activity (common athletics include diving, gymnastics, and wrestling). Type I is congenital, or dysplastic, and is a defect involving the facet joint that allows displacement. Type III is due to degenerative changes and is common in older patients. Type IV is traumatic and can be included in Type 2, but also includes trauma that causes displacement but that does not involve the pars interarticularis. Lastly, type V is pathologic spondylolisthesis, such as displacement following a fracture due to a neoplasm. \nLateral radiographs are often excellent for diagnosing and grading sponylolisthesis, especially when the displacement is anterior/posterior. Oblique views are also helpful to view the pars interarticularis, which is often described as a \u201cScotty dog\u201d (the eye is the pedicle, the ear is the superior articular process, and a fracture of the par interarticularis is described as the collar and appears as a lucency). CT imaging is often used to confirm the diagnosis as well as to better define bony defects, whether it be a fracture of the pars interarticularis, fractures elsewhere allowing displacement, or other bony anomalies. MR imaging is used to image soft tissue, such as nerve root involvement, spinal stenosis, and disc disorders. \nSpondylolisthesis is common; 5% of adults have a degree of displacement. Spondylolysis involvement is twice as common in men compared to women, and etiologies such as dysplastic and degenerative are more common in women. Eskimos have an incidence as high as 50% in adults for reasons unknown. \nTreatments are typically performed by orthopedic surgeons or neurosurgeons when symptoms and disability are determined severe enough. Treatment includes fixation with hardware and fusion of the involved vertebra. There are no interventional radiological treatments yet." }, "Topic": { "Title": "Spondylolisthesis", "Disease Discussion": "The term spondylolisthesis originated in the 18th century. In 1882, Franz Ludwig Neubebauer described spondylolisthesis in women who had died during labor due to difficulties resulting from narrow birth canals. The word is of Greek origin, spondylo meaning spine and listhesis meaning slippage or slip. \nSpondylolisthesis is defined as a displacement of a superior vertebra in relation to the inferior one. The most common type of spondylolisthesis occurs due to fracture of the pars interarticularis, with L5/S1 being the most frequent level. A grading system that is commonly used describes a grade 1 as displacement of 25% or less of the involved vertebra, grade 2 is displacement greater than 25% and up to 50%, grade 3 is displacement greater than 50% and up to 75% and grade 4 is greater than 75% displacement and up to 100% displacement. \nBecause spondylolisthesis typically occurs at levels below the spinal cord, the condition is rarely fatal. However, besides low back pain, nerve root involvement is common, especially because of compression from the inferior articular process. Other common presentations besides musculoskeletal pain and radiculopathy are related to degenerative disc disease and spinal stenosis when present.\nAs mentioned previously, there are different etiologies of spondylolisthesis. The most common, occurring nearly 80% of the time, is type II, or spondylolytic spondylolisthesis (also known as isthmic). This commonly follows spondylolysis, often as a result of athletic activity (common athletics include diving, gymnastics, and wrestling). Type I is congenital, or dysplastic, and is a defect involving the facet joint that allows displacement. Type III is due to degenerative changes and is common in older patients. Type IV is traumatic and can be included in Type 2, but also includes trauma that causes displacement but that does not involve the pars interarticularis. Lastly, type V is pathologic spondylolisthesis, such as displacement following a fracture due to a neoplasm.\nLateral radiographs are often excellent for diagnosing and grading sponylolisthesis, especially when the displacement is anterior/posterior. Oblique views are also helpful to view the pars interarticularis, which is often described as a \u201cScotty dog\u201d (the eye is the pedicle, the ear is the superior articular process, and a fracture of the par interarticularis is described as the collar and appears as a lucency). CT imaging is often used to confirm the diagnosis as well as to better define bony defects, whether it be a fracture of the pars interarticularis, fractures elsewhere allowing displacement, or other bony anomalies. MR imaging is used to image soft tissue, such as nerve root involvement, spinal stenosis, and disc disorders.\nSpondylolisthesis is common; 5% of adults have a degree of displacement. Spondylolysis involvement is twice as common in men compared to women, and etiologies such as dysplastic and degenerative are more common in women. Eskimos have an incidence as high as 50% in adults for reasons unknown.\nTreatments are typically performed by orthopedic surgeons or neurosurgeons when symptoms and disability are determined severe enough. Treatment includes fixation with hardware and fusion of the involved vertebra. There are no interventional radiological treatments yet.", "ACR Code": "4.9", "Category": "Degenerative Disease", "Keywords": "pars interarticularisspondylolyticdegenerative", "Reference": "Zubin, Irani. Spondylolisthesis. Department of Radiology, Dotter Interventional Institute, Oregon Health & Science University. Peer Reviewed Article. http://www.emedicine.com/radio/topic651.htmMay 2004 \n\nResnick, Donald. Diagnosis of Bone and Joint Disorders, 3rd Edition. W.B. Saunders Company 1995, Philidelphia, PA. Volume 3 pp. 1409-1415.\n\nResnick, Donald. Diagnosis of Bone and Joint Disorders, 3rd Edition. W.B. Saunders Company 1995, Philidelphia, PA. Volume 5 pp 2886-2890. \n\nRang, Mercer. The Story of Orthopaedics. W.B. Saunders Company 2000 Philidelphia, PA. p. 180." } }, { "U_id": "MPX2094", "TAC": [ "MPX2094_synpic31715", "MPX2094_synpic31716", "MPX2094_synpic31718", "MPX2094_synpic31719", "MPX2094_synpic31720", "MPX2094_synpic31721", "MPX2094_synpic31722", "MPX2094_synpic31723", "MPX2094_synpic31724" ], "MRI": [], "Case": { "Title": "Azygous Lobe", "History": "45 year old male with recent diagnosis of gastric carcinoma undergoing staging CT.", "Exam": "N/A", "Findings": "Contrast enhanced axial images (in lung windows) of the upper lungs demonstrates a pleural invagination from the right apex investing the azygous vein.", "Differential Diagnosis": "Azygous lobe\nFocal atelectasis or pleural scarring.", "Case Diagnosis": "Azygous Lobe", "Diagnosis By": "Contrast enhanced CT.", "Treatment & Follow Up": "None required.", "Discussion": "See factoid." }, "Topic": { "Title": "Azygous Lobe", "Disease Discussion": "The azygous fissure is a common variant, occurring in about 1% of the population. It occurs from the failure of normal migration of the azygous vein from the chest wall to its usual location. The resulting fissure is caused by the invagination of both the visceral and parietal pleura. There is still normal architecture, vascular, and bronchial supply to this region of lung.", "ACR Code": "6.1", "Category": "Anatomy, Normal Variant", "Keywords": "azygous lobe", "Reference": "Hansell, et al. Imaging of Diseases of the Chest, 4th Ed. 2005." } }, { "U_id": "MPX2114", "TAC": [ "MPX2114_synpic29550", "MPX2114_synpic29569" ], "MRI": [], "Case": { "Title": "Renal Cell Carcinoma.", "History": "Patient is a 21 year old male who presented with a 5 month history of painless hematuria. The hematuria was more pronounced after vigourous exercise. Otherwise patient has been in good health.", "Exam": "Normal exam and normal laboratory values.", "Findings": "Horseshoe kidney with large mass in the left kidney. Patient also had a stone in the left sided collecting system. \n\nCoronal images demonstrate extravasation of contrast representing urinoma after partial nephrectomy to remove renal mass. \n\nFluroscopic images demonstrate placement of nephrostomy tube and abscess drainage tube.", "Differential Diagnosis": "Mass in the Left kidney could represent:\n- Renal Cell Carcinoma\n- Oncocytoma\n- Adenoma\n- Metastasis\n- Wilms' tumor.", "Case Diagnosis": "Renal Cell Carcinoma.", "Diagnosis By": "Pathology gross speciman.", "Treatment & Follow Up": "The patient underwent a partial nephrectomy to remove the tumor which was complicated by a post operative urinoma. This required a percutaneous nephrostomy tube placement for urinary diversion. In addition, during the interventional procedure a collection of complicated fluid was identified at the lower aspect of the urinoma which also required percutaneous drainage.", "Discussion": "Horseshoe kidney is a relatively common renal anomaly, occuring in 1 in 400 births. It is more common in males, 2 to 1. The abnormality is thought to occur because of an abnormal position of the umbilical artery which inhibits normal cephalad migration of the fetal kidneys. The metanephric blastema is pushed together and fuses, usually at the lower pole. \n\nThe central isthmus can either contain parenchymal tissue or it can be a simply fibrous band. The parenchymal isthmus is more common. The isthmus is normally anterior to the aorta and IVC, but posterior to the inferior mesenteric artery. \n\nPatients with horseshoe kidney can remain assymptomatic throughout their lives. However patients with horseshoe kidney are at increased risk for developing a variety of abnormalities including:\n- ureteropelvic junction obstruction (30%).\n- infection.\n- renal calculus.\n- carcinoma.\n- increased risk from traumatic injury especially when the isthmus has normal paranchyma." }, "Topic": { "Title": "USUHS Faculty Senate, Education Committee, 2010-2011", "Disease Discussion": "USU Education Day 2011:\nWebsite - http://www.lrc.usuhs.mil/educationday/\nSchedule - http://www.lrc.usuhs.mil/educationday/index.php?Page=Schedule\n\nUSU Faculty Senate Education Committee - our monthly meetings are open to all USU Faculty, and are held the same day as the Faculty Senate meeting, but will begin after the full Senate meeting, at roughly 1730 (5:30 pm) - in a nearby room.\nSchedule - http://www.usuhs.mil/faculty/senate/fscalofevents.html\n\nSignificant responsibilities include:\n\u2022 Organizing USUHS Education Day\n\u2022 Selection of the annual winners for the \"Innovation in Education\" award\nWEBSITE - http://www.lrc.usuhs.mil/Innovation/TeachingAwardMain.php\n\u2022 Review and Approval of the budget for spending the award\n\u2022 Interface with Curriculum Reform group (impact on Faculty)\n\nFaculty Senate Education Day\n0800 - 1630 \n16 June 2011\nSanford Auditorium\n\nCommittee Membership:\n\u2022 Chair, James Smirniotopoulos (RAD)\n\u2022 Patrick Malone (PMB)\n\u2022 Eric Marks (MED)\n\u2022 Steve Rothwell (APG)\n\u2022 Joe Lopreiato (PED)\n\u2022 Donna Burge, replacing Michaela Shafer (GSN)\n\u2022 Tonie Hooper (PMB)\n\u2022 Debra Malone (SUR) debra.malone@???.navy.???\n\u2022 Mike Ellis (MED)\n\u2022 Brian Hemann (MED)\n\u2022 Johnan Kaleeba (MIC)\n\nEx-Officio\n\u2022 Ildy Katona (PED)\n\u2022 Rich Conran (PATH)\n\u2022 Stephen G Waller (PMB)\n\n<======================================>\nPer Faculty Senate President, Gary Wind, M.D.:\n\ti coordination with curriculum reform (impact on faculty)\n\tii basic and clinical innovation in teaching awards\n\tiii Education day\n\n\n<======================================>\nMeeting Minutes - November\nThe meeting was called to order on 18 November, 2010 at 1735 and was concluded at 1835\n\nPresent:\nArtino\nHooper\nLopreiato\nKatona\nMarks\nWaller\nRothwell\nKaleeba\nHemann\nSchiltz\nWind\nSmirniotopoulos, Chair\n\n1) Curriculum reform:\nIt was agreed that we need more information from the planners and more feedback from the faculty on the proposed curriculum reform.\n\nAction: Gary will invite representation from the Curriculum committee to brief the Senate at each meeting and provide updates\n\n2) Education Day:\nThere was agreement that the 2011 Faculty Senate Education day - Thursday 16 June 2011 - should be focused on Faculty Development. Breifly, we agreed that the day should begin \nwith a lecture from an invited outside speaker - an educator of some fame/notoriety - who should speak on the \"art\" of the lecture.\nThis will be followed by the Award Ceremony for the Faculty Senate Innovation Award.\nThe two winners will have 20 minutes to present their work as well as outline how they will use the award funds.\nThe remainder of the day - roughly 10:15 am through 4:00 pm will be devoted to a series of Faculty Development lectures and workshops.\nThe general template for the day is attached.\n\nAction: Joe will provide addition information on topics, faculty, etc and Liaison between the Senate Education committee and Brian Reamy and the Dean's office regarding the choice of lectures and workshops for Education Day.\n\nAction: Jim S and Tony Artino will work on a process for nomination and selection of the Innovation Award winners\n\n<======================================>\nMeeting minutes, 7 March 2011\nMembers Present: Toni Hooper, Joe Lopreiato, Rich Conran, Jim Smirniotopoulos, Tony Artino, Donna Burge\n\nThe overall plan for Education Day, and the for nomination of the Innovation Awards was reviewed and approved.\n\n<======================================>\nApril Meeting - by Email April 2011\nAdded a new breakout session: \"Tools and Techniques for Teaching\" by Dina Kurzweil (USU ETI)\n\n<======================================>", "ACR Code": "-1.-1", "Category": "Procedure or Intervention", "Keywords": "Education DayTeaching Innovation Awardcurriculum reform" } }, { "U_id": "MPX2119", "TAC": [ "MPX2119_synpic56350", "MPX2119_synpic56367" ], "MRI": [], "Case": { "Title": "Superior Vena Cava Syndrome secondary to lung cancer", "History": "59 year-old woman presents with facial swelling and discomfort in her breasts. These symptoms are worse in the morning, and are exacerbated when lying flat. The patient also endorses worsening orthopnea.", "Exam": "VS:BP 115/75, HR 106, RR 18, O2 90% on 2-4 LNC\nGen: Alert and oriented, in no acute distress. \nHEENT: Extensive JVD while upright. \nHeart: Normal S1, S2. No murmurs, rubs, gallops.\nChest: Coarse breath sounds bilaterally. Both breasts were enlarged.\nAbd: Unremarkable\nNeuro: no focal deficits", "Findings": "\u2022 CXR: bilateral breast enlargement, blunting of the costophrenic sulci, bilateral pleural effusions, consolidation of the right upper lobe\n\n\u2022 CT: bilateral breast enlargement, right sided pleural effusion, elevation of the right hemidiaphragm, right upper lobe mass causing occlusion of the right brachiocephalic vein, extensive venous collateral formation", "Differential Diagnosis": "SVC syndrome\n-malignancy related\n-secondary to thrombosis\n-fibrosing mediastinitis\n-post-radiation fibrosis\n-sarcoidosis\nInflammatory breast cancer\nPulmonary HTN", "Case Diagnosis": "Superior Vena Cava Syndrome secondary to lung cancer", "Diagnosis By": "Previous biopsy\nCT", "Treatment & Follow Up": "This woman has a past medical history of non-small cell lung cancer, status post external beam radiotherapy and chemotherapy. She was treated palliatively with venous stent placement to relieve the venous obstruction.", "Discussion": "This patient's lung cancer was refractory to radiation and chemotherapy. Therefore, when she started to experience swelling in her face and chest, SVC syndrome would have been at the top of the differential since it is a fairly common complication of this type of malignancy. Her lung cancer was most likely related to her smoking history. The patient could very well have a component of post radiation fibrosis contributing to the occlusion of the SVC, but the malignancy was the main contributor. Surgery was not an option for this patient, due to the overwhelming tumor burden." }, "Topic": { "Title": "Superior Vena Cava Syndrome", "Disease Discussion": "Superior vena cava (SVC) syndrome occurs when there is compression of the SVC vessel wall that results in obstruction of blood flow returning to the heart. Common symptoms include dyspnea, jugular venous distention, and edema of the face and upper extremities. The most common cause is malignancy. In cases of SVC syndrome secondary to malignancy, 90% are caused by either bronchogenic carcinoma or non-Hodgkin's lymphoma. Around 2-4% of all lung cancer patients will develop SVC syndrome at some point during their disease course. While Hodgkin's lymphoma is known for mediastinal lymphadenopathy, it rarely causes SVC syndrome.\n\nThere are multiple other non-malignant etiologies. Patients with indwelling intravascular catheters can develop thrombosis resulting in obstruction of the vessel. Fibrosing mediastinitis can result in an excessive fibrotic reaction in the mediastinum that can affect multiple structures within this compartment, to include the SVC. Excessive radiation can cause a similar response, with fibrosis of the vessels resulting in SVC syndrome. \n\nThe severity of symptoms can vary based on the rate of occlusion. A rapid SVC occlusion may not allow enough time for systemic compensation with collateral vein formation, thus increasing the severity of symptoms. \n\nPrognosis and treatment varies greatly but is often based on the etiology of disease. Benign causes of SVC syndrome that can resolve completely if the underlying benign disease is treated. In other cases, such as advanced malignancy, the goal of therapy is palliation, such as use of radiation therapy or vascular stent placement. In general, surgical care is not the best option. \n\nAs most cases of SVC syndrome are due to malignancy, a key question is how advanced the disease as progressed. If tumor is infiltrating the SVC (and mediastinum), resection will not provide a cure. In cases of advanced malignancy, the goal of therapy is palliation, such as use of radiation therapyto shrink tumor burden or vascular stent placement for symptom relief. In general, surgical care is not the best option in these cases. Steroids have been used for temporary relief of symptoms, but chronic steroid use can cause systemic fluid retention, which often exacerbates this condition.", "ACR Code": "6.3", "Category": "Neoplasm, carcinoma", "Keywords": "SVC syndromelung cancervenous congestion", "Reference": "Up to date (Online)\n\nWan JF, Bezjak A. \u201cSuperior Vena Cava Syndrome\u201d Hematology/Oncology Clinics of North America. 2010 Jun;24(3):501-13." } }, { "U_id": "MPX2127", "TAC": [ "MPX2127_synpic19438" ], "MRI": [ "MPX2127_synpic19439", "MPX2127_synpic19440", "MPX2127_synpic19441" ], "Case": { "Title": "Empty sella syndrome", "History": "53 yo male with acute onset of severe headache", "Exam": "Unremarkable", "Findings": "Focal cyst like collection of fluid at the sella turcica which minimally displaces the pituitary tissue inferiorly and the surrounds the pituitary infundibulum, but does not displace it. The sella is minimally expanded to 1.6 cm in diameter.", "Differential Diagnosis": "Arachnoid cyst\nRathke\u2019s cleft cyst\npartially empty sella turcica", "Case Diagnosis": "Empty sella syndrome", "Diagnosis By": "Radiologic diagnosis", "Treatment & Follow Up": "No treatment necessary. See discussion below. Follow-up with primary care physician to evaluate other etiologies of headache." }, "Topic": { "Title": "Empty sella syndrome", "Disease Discussion": "An empty sella turcica results from arachnoid herniation through an incomplete diaphragma sellae. This syndrome may occur in the absence of a recognized pituitary tumor and is either primary, resulting from a congenital diaphragmatic defect which is thought to allow CSF pressure to enlarge the sella, or secondary, resulting from an injury to the diaphragm by pituitary surgery, radiation, or infarction.\n\nPrimary empty sella syndrome usually occurs in obese, multiparous, hypertensive women who experience headaches but have no underlying neurologic disorders. Pituitary function is usually normal, but occasionally the PRL level is increased and GH reserve is reduced.\n\nSecondary empty sella syndrome is observed in patients with otherwise benign cerebrospinal fluid hypertension and in patients with a loss of pituitary function from apoplexy or surgical therapy. Abnormal GH, PRL, or ACTH secretion may persist in such patients.\n\nThe diagnosis is confirmed with MRI or CT. No treatment is necessary for the primary condition, whereas correction of the underlying cause is necessary for the secondary form.\n\n=================================================\nhttp://www.ohiohealth.com/healthreference/reference/images/image_popup/ans7_pituitary_gland.jpg\n\n=================================================\nhttp://www.roentgenpraxis-paderborn.de/fallsammlung/kopf/empty_sella.htm\n\n=================================================\nhttp://www.ohiohealth.com/healthreference/reference/4942AF41-96A2-4882-AE691797FB10B6C4.htm?category=questions\n\n=================================================", "ACR Code": "1.3", "Category": "Idiopathic or Unknown", "Keywords": "Empty sella syndromesella", "Reference": "Townsend: Sabiston Textbook of Surgery, 16th ed., Copyright \u00a9 2001 W. B. Saunders Company\n\nGoldman: Cecil Textbook of Medicine, 21st ed., Copyright \u00a9 2000 W. B. Saunders Company\n\nSage MR, Blumbergs PC: Primary empty sella turcica: A radiological anatomical correlation.\nAustralasian Radiology 2000; 44: 341-348." } }, { "U_id": "MPX2131", "TAC": [ "MPX2131_synpic27159" ], "MRI": [], "Case": { "Title": "Acute calculous cholecystitis", "History": "77 year-old man with right upper quadrant pain and microhematuria.", "Exam": "Physical exam and labs were normal.showed right sided abdominal pain. CBC was normal. Urinalysis showed microhematuria.", "Findings": "Non-contrast axial CT shows enlarged gall bladder with heterogenous attenuation. Contrast CT shows multiple septations within the body of the gall bladder. Right upper quadrant ultrasound shows thickened gall bladder wall with a shadowing stone.", "Differential Diagnosis": "For CT findings:\n\nAcute calculous cholecystitis\nAcute acalculous cholecystitis\nChronic cholecystitis (cholesteroloses)\nGall bladder carcinoma", "Case Diagnosis": "Acute calculous cholecystitis", "Diagnosis By": "Ultrasound", "Treatment & Follow Up": "Cholecystectomy is the treatment of choice for cholecystitis.", "Discussion": "Because this patient was a poor surgical candidate due to comorbid conditions, he was taken to the Interventional Radiology suite where a percutaneous cholecystostomy was performed. This is a recurring problem for him, he underwent the same procedure 10 months before this admission with a good outcome" }, "Topic": { "Title": "Acute calculous cholecystitis", "Disease Discussion": "Acute calculous cholecystitis is an acute inflammation of the gallbladder mucosal lining secondary to inflammation, distention and subsequent mucosal ischemia secondary to an impacted stone in the gallbladder neck. A secondary bacterial infection may ensue. \n Diagnosis is most often made with a right upper quadrant ultrasound, and can be confirmed with a nuclear medicine hepatobiliary scan. Diffuse gallbladder wall thickening (>3mm), pericholecystic fluid and gallstones all in the presence of a sonographic Murphy's sign is virtually diagnostic for acute cholecystitis. Diagnosis with computed tomography is most of the time incidentally made when the CT is ordered looking for other causes of abdominal pain. With CT the diagnosis is suggested when gallbladder distention, visible stones (rarely visible), cystic duct dilatation, contrast enhancement of the gall bladder wall, and edema or abscess in surrounding tissues is observed.\n Treatment is cholecystectomy and/or medical management. Many patients are managed medically with bowel rest, non-steroidal anti-inflammatory drugs and antibiotics, when indicated. Surgery is reserved for urgent cases or elective resections after cholecystitis.\n Because cholecystectomy in the emergency setting can be associated with 4%-7% mortality, an alternative treatment is percutaneous cholecystostomy with a pigtailcatheter in order to continuously drain bile from the gall bladder.", "ACR Code": "7.2", "Category": "Inflammatory, non-infectious", "Keywords": "Acute calculous cholecystitis", "Reference": "Braunwald E, et al. Harrison\u2019s Principles of Internal Medicine, 15th Ed, McGraw-Hill, 2001, 1781-2.\nGreenbaum, E. Radiology of the Emergency Patient: An Atlas Approach. John Wiley & Sons Inc, 1982\nMettler, F; Essential of Radiology, 2nd edition, Elsevier Saunders, 2005. pp 193-4.\nRamakrishnan K, Menon S, Mathew A, Mohan M (2003) Percutaneous Cholecystostomy - An alternative to surgery in a high-risk patient with Acalculus Cholecystitis. Ind J Radiol Imag 13:3:307-310." } }, { "U_id": "MPX2102", "TAC": [ "MPX2102_synpic51448", "MPX2102_synpic51449", "MPX2102_synpic51450", "MPX2102_synpic51452", "MPX2102_synpic51453", "MPX2102_synpic51462" ], "MRI": [], "Case": { "Title": "VACTERL Syndrome", "History": "56 d/o male in NICU with history of imperforate anus, malrotation, tracheal and esophageal atresia, s/p multiple bowel surgeries and gastrostomy tube placement who presents with decreased lung sounds throughout the R lung and collapsed RMSB on bronchoscopy.", "Exam": "CVS/Resp: Decreased lung sounds throughout R lung fields, most notable in the base. RRR, NS1S2. \nAbd: Gastrostomy tube visible, site clean. Bowel sounds present throughout. Anal surgery site clean.", "Findings": "CXR DOL 0: Endotracheal tube with distal tip over the top of the carina. Enteric tube with the distal tip lying over the clavicular heads in the setting of known esophageal atresia.\n\nCT CHEST W/ & W/O CONTRAST DOL 56:\n1. R-SIDED AORTA W/ RMSB INTERPOSED BETWEEN THE DESCENDING AORTA AND R PULM ARTERY RESULTING IN CONSOLIDATION AND ATELECTASIS IN R LUNG BASE.\n2. DISTAL TRACHEAL ATRESIA AND BRONCHIAL ATRESIA.\n3. ESOPHAGEAL ATRESIA W/ BLIND ENDING POUCH ENDING JUST ABOVE THE AORTIC ARCH.\n4. LIVER IS ENLARGED W/ LIKELY 2CM ABSCESS IN R HEPATIC LOBE. SPLEEN ENLARGED MEASURING 7.4 CM CRANIOCAUDALLY.\n5. MIDLINE FUSION OF INFERIOR POLES SUGGESTIVE OF HORSESHOE KIDNEY.", "Differential Diagnosis": "\u2022 PHAVER Syndrome\n\u2022 Patau Syndrome (T13)\n\u2022 Edward's Syndrome (T18)\n\u2022 Tracheoesophageal Fistula\n\u2022 VACTERL Syndrome", "Case Diagnosis": "VACTERL Syndrome", "Diagnosis By": "Clinical Examination, Multiple Congenital Abnormalities (5 categories) on CT CHEST", "Treatment & Follow Up": "At time of print, patient remains in NICU w/ multisystem support including: \n-ET Tube\n-PICC line\n-Enteric Tube" }, "Topic": { "Title": "VACTERL Syndrome", "Disease Discussion": "VACTERL syndrome presents as an array of findings involving various systems: Vertebral/Vascular, Anal/Auricular, Cardiac, TracheoEsophageal, Renal/Radial, and Limb/Liver. At least three of these systems (72% of patients) must be involved for the diagnosis of VACTERL to be made (although 8% of patients with the syndrome have at least 5 abnormalities). This syndrome should be suspected if a pediatric patient is found to have the combination of vertebral plus one other associated anomaly during infantile years. Since the findings span throughout the body, a wide modality of radiographic techniques may be used to make the diagnosis.\n\nCertain organ systems and their abnormalities arise more often than others and are listed in order of prevalence: Cardiac, Renal, Anal, Radial, Tracheoesophageal, Vertebral. The most common combination of abnormalities are as follows:\n3 abnormalities: Cardiac-renal-limb or Cardiac-Anal-Renal \n5 abnormalities: Cardiac-Anal-TEF-Renal-Limb.\n\nThe MC abnormalities in each organ system (and often seen on imaging) are as follows:\n\nVertebral: Hemi/cleft vertebrae, kyphosis/scoliosis, caudal regression, Branchial Arch/Cleft Abnormalities\n\nCardiac: VSD (30%), PDA, ASD\n\nTracheoEsophageal: TEF (25% TEF pts have VACTERL), Esophageal Atresia, Tracheal Atresia, Horseshoe Lung, Ectopic Bronchus\n\nRenal/ GU: Renal Agenesis, Horseshoe Kidney, Cryptoorchidism, Vaginal Atresia\n\nLimb: Radial ray abnormalities, Absent / Hypoplastic Extremity Bones/Vessels, Polydactyly\n\n\nRISK FACTORS / EPIDEMIOLOGY\n\nVACTERL syndrome has been associated with maternal diabetes and prenatal lead exposure causing abnormal mesodermal development before 35 days of gestation. \n\nVACTERL synrome has also been linked to the inhibition of cholesterol synthesis and down-regulation of the cholesterol-dependent sonic-hedgehog morphogenic pathway.\n\nDIFFERENTIAL DIAGNOSIS:\n\nPHAVER syndrome: Limb Pterygia, Congenital Heart, Vertebral Defects, Ear Anomalies,Radial Defects\n\nTrisomy 13 (Patau Syndrome): Cranial/Brain Defects, Microopthalmia, Polydactyly \n\nTrisomy 18 (Edwards Syndrome): Clenched Fist, Microcephaly, Micrognathia, Rocker-Bottom Feet\n\nOTHER CONSIDERATIONS:\n\nHolt-Oram Syndrome\nPseudothalidomide Syndrome\nJarcho-Levin Syndrome\n\n \n\nIMAGING\n\nVarious imaging modalities may be used but are not limited to the following:\n\n-Prenatal Ultrasound: Polyhydramnios may suggest possible TEF. Oligohydramnios may suggest renal abnormalities.\n\n-Angiography: For diagnosis of radial artery hypoplasia or cardiac abnormalities.\n\n-Plain Films, CT, and MRI can aid in diagnosis of core organ system and musculoskeletal abnormalities. \n\n \n\nPROGNOSIS / TREATMENT\n\nMortality is 12% intrapartum, 28% during the neonatal period, and 48% during the first year of life. 1/3 of all patients with VACTERL are born prematurely. If VACTERL syndrome is suspected on prenatal ultrasound, it is suggested that the fetus be delivered at a tertiary care facility to ensure best postpartum care for the baby.", "ACR Code": "-1.-1", "Category": "Congenital, malformation", "Keywords": "Tracheoesophageal FistulaCongenitalMultisystem", "Reference": "https://my.statdx.com/vacterl\nhttp://www.utdol.com/online/content/topic.do?topicKey=pedipulm/7763&selectedTitle=1~50&source=search_result\nhttp://www.medterms.com/script/main/art.asp?articlekey=31930" } }, { "U_id": "MPX2133", "TAC": [ "MPX2133_synpic21405" ], "MRI": [], "Case": { "Title": "Adenocarcinoma of the gastroesophageal junction, no evidence of Barrett esophagus found - Stage: T3N0M0", "History": "The patient is a 39 year old female with a chief complaint of worsening solid and liquid dysphagia over a >6 months duration.", "Exam": "Physical exam unremarkable.Laboratory significant for Hct of 21. Endoscopy revealed a 2-3 cm ulcerated mass at the gatroesophageal junction", "Findings": "CT of chest, abdomen, and pelvis with contrast- lobular thickening of the lower esophageal wall and luminal wall at the GE junction; no adenopathyPET- no abnormal findingsEsophageal US-T2/T3", "Differential Diagnosis": "Malignancy, leiomyoma or benign tumor, Irritation, Inflammation", "Case Diagnosis": "Adenocarcinoma of the gastroesophageal junction, no evidence of Barrett esophagus found - Stage: T3N0M0", "Diagnosis By": "Bx Pathology", "Treatment & Follow Up": "This patient will initially receive adjuvant chemotherapy (5- fluorouracil ) and radiotherapy. She will then undergo surgical resection of her tumor followed by additional adjuvant chemotherapy and radiotherapy to prevent recurrence." }, "Topic": { "Title": "Adenocarcinoma of the gastroesophageal junction", "Disease Discussion": "Adenocarcinoma of the gastroesophageal (GE) junction is notable in that its incidence that increased more than any other malignancy in the western world. The reasons for such an increase are unknown. (1) There are three classifications of this type of cancer: Type I mainly involves the distal esophagus, Type II is primarily located at the GE junction, and Type II mainly involves the subcardial/proximal stomach region. (3) GE junction adenocarcinoma can either arise from the esophagus or proximal gastric area. It is very difficult to determine the primary cancer site. (1) Risk factors for gastric adenocarcinoma include familial adenomatous polyposis, gastric adenomas/ dysplasia, chronic atrophic gastritis, gastric metaplasia, diet high in nitrates, and Helicobacter pylori infection. Risk factors for esophageal adenocarcinoma include smoking, obesity, and Barrett\u2019s esophagus- patients affected with Barrett\u2019s esophagus have a 30-40% higher chance of developing cancer. (4) \n\nRadiological evaluation of GE adenocarcinoma should be able to determine tumor spread and response to chemotherapy. The sensitivity of CT for detection of distant metastases ranges between 50% to 90%. Of those shown to have only local disease with CT, FDG-PET detected metastatic disease in approximately 20% more cases. In addition, esophageal ultrasound (EUS) can differentiate between stages T1/T2 and stages T3/T4 with an accuracy > 90%. Assessment of tumor response to chemotherapy by FDG-PET correlates with tumor regression proven by histology and can predict patient outcome as early as 2 weeks after initiation of therapy. (5)", "ACR Code": "7.3", "Category": "Neoplasm, carcinoma", "Keywords": "Adenocarcinomacarcinoma", "Reference": "1. Hashem B. \u201cThe epidemic of esophageal adenocarcinoma.\u201d Gastroenterology Clinics of North America 31(2):421\u2013440, 2002.\n2. Macdonald JS; Smalley SR; Benedetti J; Hundahl SA; Estes NC; Stemmermann GN; Haller DG; Ajani JA; Gunderson LL; Jessup JM; Martenson JA. \u201cChemoradiotherapy after surgery compared with surgery alone for adenocarcinoma of the stomach or gastroesophageal junction.\u201d N Engl J Med 345(10): 725-30, 2001.\n3. M?nig SP; Schr?der W; Beckurts KT; H?lscher AH. \u201cClassification, diagnosis and surgical treatment of carcinomas of the gastroesophageal junction.\u201d Hepatogastroenterology 48(41): 1231-7, 2001.\n\n4. Kumar V, Collins T, Robbins SL. Robbins Pathologic Basis of Disease. W.B. Saunders Company, Philadelphia, 1999, pgs 784-802.\n\n5. Weber WA, Ott K. \u201cImaging of esophageal and gastric cancer.\u201d Semin Oncol. 31(4):530-41, 2004." } }, { "U_id": "MPX2134", "TAC": [ "MPX2134_synpic57586" ], "MRI": [ "MPX2134_synpic57588", "MPX2134_synpic57589" ], "Case": { "Title": "OPLL - Ossification of the Posterior Longitudinal Ligament", "History": "57 yo man with type 2 diabetes presents with 4-5 mo of posterior neck and shoulder pain accompanied by severe \u201cshock like\u201d pain down neck w/flexion. In addition, he c/o walking \u201clike a drunken sailor\u201d and loss of fine motor skills, such as difficulty buttoning shirt.", "Exam": "Physical exam remarkable for 2-3 beats of ankle clonus bilaterally.", "Findings": "\u2022 Plain Films, CT, and MR demonstrate Ossification of the Posterior Longitudinal Ligament (OPLL) with subsequent marked narrowing of the spinal canal. \n\n\u2022 Also notice the associated syringohydromyelia, below the narrowing", "Differential Diagnosis": "None (pathognomonic)", "Case Diagnosis": "OPLL - Ossification of the Posterior Longitudinal Ligament", "Diagnosis By": "Imaging", "Treatment & Follow Up": "Posterior cervical laminectomy (C1-6) pending with Neurosurgery.", "Discussion": "In addition to aforementioned bullet points, pt has hx of DM2, which has also been found to be associated with OPLL." }, "Topic": { "Title": "OPLL", "Disease Discussion": "\u2022 \t2:1 M:F, 5th-7th decade\n\u2022 \tJapanese > Non-Japanese, Diabetes Mellitus (DM) > Non-DM patients\n\u2022 \tMost frequently seen: C3-5, also T4-7, L1-2\n\u2022 \tAssociated with: DISH, Ossification of the Ligamentum Flavum (OLF), \n\u2022 \tMechanism: not precisely known\n\u2022 \tTypes:\no\tContinuous: vertebral + disc involvement\no\tSegmental : no disc involvement\no\tMixed: components of both\no\tLocalized\n\u2022 \tSurgery\no\tANT: corpectomy (discectomy + vertebral body removal +PLL removal + fusion) w/iliac strut graft reconstruction\no\tPOST: laminoplasty/laminectomy", "ACR Code": "3.9", "Category": "Symptom or Sign", "Keywords": "OPLL", "Reference": "1)\tResnick, et al. Chapter 32: Calcification and Ossification of the Posterior Spinal Ligaments and Tissues. Bone and Joint Imaging. pp 438-443\n2)\tSmith, Z et al. \u201cOssification of the Posterior Longitudinal Ligament: Pathogenesis, Management, and Current Surgical Approaches\u201d Journal of Neurosurgery, Vol. 30 (3): E10 (2011) \n3)\tYamashita et al. \\\"Spinal cord compression due to ossification of ligaments: MR imaging\\\" Radiology 175 (3): 843. (1990)" } }, { "U_id": "MPX2144", "TAC": [ "MPX2144_synpic36252", "MPX2144_synpic36254" ], "MRI": [], "Case": { "Title": "Medial Migration of PE (tympanostomy) Tube", "History": "17 year old girl with history of chronic otitis media resulting in multiple ear surgeries including bilateral PE (pressure equalization) tubes (2 yrs. ago), tympanoplasties, and canalplasty/meatoplasty> She returns for routine follow up exam of external ear canals. She had no complaints, and reported stable hearing. She wears a hearing aid in right ear from previously diagnosed mild sensorineural hearing loss.", "Exam": "The left tympanic membrane was intact and within normal limits s/p tympanoplasty. \n\nOn the right, a blue-green hue was noted behind the posterior inferior tympanic membrane.", "Findings": "CT showed round hollow structure in inferior portion of middle ear consistent with size and shape of PE tube.", "Differential Diagnosis": "Other foreign object", "Case Diagnosis": "Medial Migration of PE (tympanostomy) Tube", "Diagnosis By": "Surgical removal had not been carried out at time of submission, so a positive confirmation is not available.", "Treatment & Follow Up": "The patient was sent for CT to rule out medialized PE tube in left middle ear; and, that was confirmed by imaging.\n\nThere are no clear guidelines regarding treatment of medial displaced PE tubes. Leaving them in place and surgical removal both carry risks that must be considered. If left in place, possibilities include a foreign body reaction, nidus for infection, and physical obstruction of the Eustachian tube or ossicles. Surgical removal carries some risk of hearing loss and infection. Either course of action should be regularly followed for complications.", "Discussion": "Since the patient was asymptomatic and already had mild hearing loss in her right ear, the risk of hearing loss from surgery in the left ear had to be carefully considered. She and her parents were given the option of surgical removal of the PE tube, or continuing regular follow up with observation. Eventually, the patient and her parents decided that surgery was the better option, and plan to follow through before the end of the year." }, "Topic": { "Title": "Medial Migration of Tympanostomy Tube", "Disease Discussion": "Medial migration of tympanostomy tubes into the middle ear space is a rare complication of a common procedure. Clear guidelines on treatment are not available. In many cases, medial displaced tubes are removed surgically, especially if there is concern for hearing loss or other complication. However, some medialized tubes have been left in place if hearing is not impaired and the patient is asymptomatic.", "ACR Code": "1.9", "Category": "Foreign Body", "Keywords": "ear tubesmiddle ear" } }, { "U_id": "MPX2147", "TAC": [ "MPX2147_synpic20509" ], "MRI": [], "Case": { "Title": "Left Lower Lobe Collapse", "History": "Soldier in ICU s/p closed head trauma. On ventilator via tracheostomy. Waxing & waning oxygen desaturation and fever.", "Exam": "Decreased breath sounds on left.", "Findings": "The AP radiograph demonstrates obscuration of the left heart border, retrocardiac decending aorta, and hemidiahpram. Note the presence of a Kattan's Triangle -- the shift of the anterior junction line towards the side of volume loss. The left main bronchus is depressed, and there is shift of the heart to the left. \nThe two axial CT images demonstrate clearly the leftward displacement of the anterior junction line (causing the Kattan's Triangle) and the completely collapsed left lower lobe.", "Differential Diagnosis": "Left Lower Lobe Collapse\nLeft Lower Lobe Mass", "Case Diagnosis": "Left Lower Lobe Collapse", "Diagnosis By": "CT images are confirmatory.", "Treatment & Follow Up": "Patient was bronchoscoped and suctioned to remove mucous plug. Follow up CSR demonstrated marked improvement.", "Discussion": "This case serves to correlate the plain film and CT findings of classic left lower lobe collapse. Of particular note are the secondary findings of left lower lobe volume loss -- the Kattan's Triangle, depression of the left bronchus and the shift of structures to the side of volume loss abnormality." }, "Topic": { "Title": "LEFT LOWER LOBE COLLAPSE", "Disease Discussion": "Lower lobe collapse may involve the whole lobe, however the superior segment is frequently spared. With collapse the major fissure rotates posterior and medially and the upper half of the fissure deviates inferiorly. Consequently the collapsed lobe lies posteromedially in the thoracic cavity adjacent to the diaphragm and mediastinum. If the inferior pulmonary ligament does not attach to the diaphragm, the lobe is positioned against the mediastinum with little if any contact with the diaphragm. \n\nFrontal radiographs frequently demonstrate left retrocardiac triangular density. If the superior segment remains aerated, the upper half of the major fissure is commonly seen as a horizontal line contacting the spine on frontal radiographs. In such cases the major fissure may be confused with the minor fissure, however this can be avoided by recalling that the minor fissure does not cross medial to the hilum.\n\nOn the lateral view mild partial volume loss may be difficult to recognize. With more significant volume loss, however, there is an ill-defined triangular opacity in the lower posterior quadrant of the chest, often with loss of the outline of the posterior half of the diaphragm. With very severe collapse the posterior half of the hemidiaphragm may become visible secondary to compensatory expansion of the upper and middle lobes, which contact the previously effaced diaphragm. In contrast to normal, in lower lobe collapse the lower vertebrae appear denser than those located more superiorly. Posterior displacement of the main bronchus can also be recognized on lateral radiographs in lower lobe collapse, however is subtle and requires confident knowledge of the normal.\n\nThe distal lobar and segmental divisions of the pulmonary artery are invisible with severe lower lobe collapse because they course through an opaque lobe. In such cases one must be careful not to mistake displaced middle and upper lobe trunks as lower lobe arteries. \n\nThe outline of the top of the aortic knob may be obliterated in severe left lower lobe collapse. The flat waist sign may also occur with severe collapse and is secondary to leftward displacement and rotation of the heart. This is seen as flattening of the contours of the aortic knob and adjacent pulmonary artery.", "ACR Code": "65.74", "Category": "Unsure", "Keywords": "AtelectasisCollapse", "Reference": "Armstrong, Peter et al. Imaging of Diseases of the Chest, 3rd edition. Baltimore: Mosby" } }, { "U_id": "MPX2150", "TAC": [ "MPX2150_synpic30984", "MPX2150_synpic30985", "MPX2150_synpic30986" ], "MRI": [], "Case": { "Title": "Angiomyolipoma", "History": "68-year-old female with a 30-pack-year smoking history, presents with cough and nose bleed. CXR reveals a nodular density, which further evaluated with chest CT. Chest CT has incidental finding of possible hepatic vascular malformation. Abdominal ultrasound is recommended to evaluate liver findings. During abdominal ultrasound, four echogenic masses are noted in the right kidney. Further evaluation of renal masses with abdominal CT is then recommended.", "Exam": "Chem 7 reveals no electrolyte abnormalities and normal renal function.", "Findings": "Axial CT of the abdomen demonstrates solitary 1cm mass in right kidney, with an attenuation of -20 Hounsfield units.", "Differential Diagnosis": "Renal cell carcinoma, Teratoma, Oncocytoma, Xanthogranulomatous pyelonephritis, Wilms tumor, Liposarcoma, Angiomyolipoma. (1)", "Case Diagnosis": "Angiomyolipoma", "Diagnosis By": "The demonstration of fat by CT (-10 to -100 Hounsfield units) and ultrasound (echogenicity) is virtually diagnostic of angiomyolipoma. On rare occasions fat may be seen in other renal tumors, including RCC. (2)", "Treatment & Follow Up": "For asymptomatic patients with small (<4cm), single/few masses, no further follow-up required. For questionable or symptomatic masses, follow-up with US or tumor resection may be prudent. A few patients who present with hemorrhage may be a surgical emergency (1). If the diagnosis of tuberous sclerosis is considered (present at younger age, multiple/large/bilateral tumors, symptomatic), may need to further screen with skin, opthalmologic, neurologic examinations, and brain MRI (2).", "Discussion": "Benign tumors. Majority are small and single. Composed of fat, vascular and smooth muscle tissues. Majority of cases are asymptomatic, but may present with flank pain, palpable mass, hematuria, altered renal function, or spontaneous hemorrhage. Incidence in the US between 0.3-3%. More common in females (4:1). 80% of cases involve the right kidney. Associated with tuberous sclerosis in 20% of cases (lesions are usually multiple, larger, and bilateral). 80% of patients with tuberous sclerosis have angiomyolipomas. (2)" }, "Topic": { "Title": "Angiomyolipoma", "Disease Discussion": "Findings: Axial CT of the abdomen demonstrates solitary 1cm mass in right kidney, with an attenuation of -20 Hounsfield units. \n\nDifferential Diagnosis for Renal Mass: Renal cell carcinoma, Teratoma, Oncocytoma, Xanthogranulomatous pyelonephritis, Wilms tumor, Liposarcoma, Angiomyolipoma. (1)\n\nAnalysis: The demonstration of fat by CT (-10 to -100 Hounsfield units) and ultrasound (echogenicity) is virtually diagnostic of angiomyolipoma. On rare occasions fat may be seen in other renal tumors. (2)\n\nDiscussion: Benign tumors. Majority are small and single. Composed of fat, vascular and smooth muscle tissues. Majority of cases are asymptomatic, but may present with flank pain, palpable mass, hematuria, altered renal function, or spontaneous hemorrhage. Incidence in the US between 0.3-3%. More common in females (4:1). 80% of cases involve the right kidney. Associated with tuberous sclerosis in 20% of cases (lesions are usually multiple, larger, and bilateral). 80% of patients with tuberous sclerosis have angiomyolipomas. (2)\n\nTreatment Plan: For asymptomatic patients with small (<4cm), single/few masses, no further follow-up required. For questionable or symptomatic masses, follow-up with US or tumor resection may be prudent. A few patients who present with hemorrhage may be a surgical emergency (1). If the diagnosis of tuberous sclerosis is considered (present at younger age, multiple/large/bilateral tumors, symptomatic), may need to further screen with skin, opthalmologic, neurologic examinations, and brain MRI. (2)", "ACR Code": "8.3", "Category": "Neoplasm, benign", "Keywords": "Angiomyolipoma", "Reference": "1. \u201cAngiomyolipoma, Kidney.\u201d Ali Nawaz Khan. Emedicine. Last updated July 28, 2005.\n\n2. \u201cRenal manifestations of tuberous sclerosis and renal angiomyolipoma.\u201d Burton D. Rose, MD and William M. Bennet, MD. UpToDate. Accessed Aug. 25, 2006." } }, { "U_id": "MPX2155", "TAC": [ "MPX2155_synpic22532", "MPX2155_synpic22533" ], "MRI": [], "Case": { "Title": "PANCREATIC DUCTAL ADENOCARCINOMA", "History": "56 year old male with severe upper abdominal pain, left greater than right, for 1 week.", "Exam": "N/A", "Findings": "Film #1: Non-enhanced CT image shows a slightly decreased attenuating focal mass in the pancreatic body with diffuse atrophic changes. Several enlarged peripancreatic lymph nodes are present with the largest measuring 13 mm on short axis diameter.\n\nFilm #2: Dynamic contrast-enhanced CT image shows a 2.5 x 4.3 cm unenhancing, hypodense mass in the pancreatic body. No metastases were seen in the liver. \n\nFilm #3: Dynamic contrast-enhanced CT image (on liver window) shows a 7 mm obstructed pancreatic duct (arrow) surrounded by contrast-enhanced pancreatic parenchyma seen distal to the pancreatic mass.", "Differential Diagnosis": "1.)Most exocrine pancreatic tumors; 2.)Lymphoma; 3.)Pancreatic endocrine tumors (mostly non-functional).", "Case Diagnosis": "PANCREATIC DUCTAL ADENOCARCINOMA", "Diagnosis By": "Pathologic specimen", "Treatment & Follow Up": "Surgical resection", "Discussion": "A majority of non-endocrine pancreatic carcinomas, up to 75-85%, are ductal cell adenocarcinomas[1,2]. The tumor is highly lethal and is usually unresectable at presentation. The average survival time of a patient with this disease is only 8 months or less. These tumors usually occur in the seventh decade of life. \n\nCurrently, computed tomography (CT) is the most commonly used imaging method in the assessment of pancreatic tumors. The sensitivity of CT detection of pancreatic tumors is reported to be more than 90% when direct or indirect signs are used for diagnosis[1]. However, the potential to differentiate exocrine (non-endocrine) tumors of the pancreas is limited. \n\nOn non-enhanced CT imaging, there is often a slightly decreased attenuating pancreatic mass seen. Following rapid bolus of contrast injection, the tumor usually appears as a hypodense mass with ill-defined borders. Calcification is almost never present within the mass. Indirect signs of a pancreatic mass include abrupt obstruction of the common bile and/or pancreatic duct and atrophy of pancreatic tissue beyond the tumor. The typical distribution of ductal cell adenocarcinoma is as follows: 60\u201370% at the pancreatic head, 10% the body, 5% the tail, 5% both head and body, and about 10% body and tail [1]. \n\nThose who present with a pancreatic head mass often have symptoms earlier than in those with pancreatic tail masses, mainly due to symptomatic obstruction of the biliary or pancreatic duct. Radiographic assessment of resectability is critical because surgical resection offers the only hope of cure[2]. However, the surgery itself carries a high morbidity. Resectable patients may live 1-2 years. Signs of potential resectability include an isolated pancreatic mass with or without dilation of the bile or pancreatic ducts or combined dilation of both the bile and pancreatic ducts without an identifiable pancreatic head mass." }, "Topic": { "Title": "PANCREATIC DUCTAL ADENOCARCINOMA", "Disease Discussion": "Ductal adenocarcinoma of the pancreas is second only to colorectal cancer as the most common digestive tract malignancy.\n\nAdenocarcinomas make up 95% of pancreatic malignancies. 65% of pancreatic adenocarcinomas occur in the pancreatic head. Because of this location, classic signs include obstructive jaundice (secondary to common bile duct obstruction) and Courvoisier's sign (an enlarged nontender palpable gall bladder). Weight loss and/or back pain are also presentations for pancreatic adenocarcinoma. Pancreatic adenocarcinomas are lethal tumors, usually unresectable at presentation with average survival time estimated to be 5-8 months. \n\nRadiographic assessment of resectability is critical because surgical resection offers the only hope of cure. Thin-slice contrast-enhanced CT is generally more sensitive than ultrasound for radiographic characterization. Tumors appear hypodense on CT. Other pertinent associated CT findings include obstruction of the common bile and pancreatic ducts, pancreatic atrophy beyond the tumor, and regional spread (nodes, liver, peritoneal cavity). Signs of resectability include isolated pancreatic mass (+/- ductal dilitation) or no identifiable pancreatic mass but combined ductal dilitation. Signs of unresectability include tumor extension beyond pancreas. Only 10-15% of patients have potentially resectable tumors. \n\nMRCP and ERCP are adjunctive modalities for selectively imaging the pancreatic duct and biliary tree. Specifically, ERCP is important in obtaining tissue and/or in performing palliative interventions (i.e. stent placements for decompression).", "ACR Code": "7.3", "Category": "Neoplasm, carcinoma", "Keywords": "PANCREATIC CARCINOMAPANCREATIC ADENOCARCINOMAGASTROINTESTINAL NEOPLASM", "Reference": "1) WEBB WR, BRANT WE, HELMS CA, EDS. FUNDAMENTALS OF BODY CT. 2ND ED. PHILADELPHIA: WB SAUNDERS CO, 1998: 223-233." } }, { "U_id": "MPX2160", "TAC": [ "MPX2160_synpic47787", "MPX2160_synpic47795" ], "MRI": [], "Case": { "Title": "Aortic dissection.", "History": "A previously healthy 22-year-old active duty male presented with intermittent left upper quadrant/epigastric abdominal pain for two and a half weeks.", "Exam": "Physical exam was nonspecific.", "Findings": "An acute abdominal series/chest xray demonstrated widening of the mediastinum with a dilated aortic knob and apparent aneurysmal dilatation of the descending thoracic aorta.", "Differential Diagnosis": "Traumatic aortic dissection\nAortic aneurysm\nNon Traumatic aortic dissection\nMediastinal tumors", "Case Diagnosis": "Aortic dissection.", "Diagnosis By": "Gated contrast imaging of the chest and abdomen.", "Treatment & Follow Up": "Emergent aortic valve replacement and thoracic aortic graft. Abdominal aorta graft placement will be performed in the future.", "Discussion": "Dissections involving the ascending aorta can induce one or more of the following: aortic insufficiency, heart failure, acute myocardial ischemia/MI, cardiac tamponade and sudden death (rupture of the aorta into the pericardial space), variation (>20 mmHg) in systolic blood pressure between the arms, neurologic deficits, Horner syndrome (compression of the superior cervical sympathetic ganglion), vocal cord paralysis and hoarseness (compression of the left recurrent laryngeal nerve). \n\nDissection involving the descending aorta can lead to: splanchnic ischemia, renal insufficiency, lower extremity ischemia, or focal neurologic deficits due to spinal artery involvement and spinal cord ischemia." }, "Topic": { "Title": "Aortic Dissection, Aortic Tear", "Disease Discussion": "Aortic dissection represents a spectrum of processes in which blood enters the media layer of the aortic wall and splits it in a longitudinal fashion. Most dissections are spontaneous and occur in the setting of acquired or inherited degeneration of the aortic media, medial necrosis. This occurs most commonly as an acquired lesion in mid-old age hypertensive patients. Spontaneous dissections almost exclusively originate in the thoracic aorta and secondarily involve the abdominal aorta by extension from above. Aortic dissection results in the separation of two lumens by an intimal flap. The false lumen represents the space created by the splitting of the aortic wall; the true lumen represents the native aortic lumen. In chronic dissections the false channel may become aneurysmal. \n\n\u2022 Clinical findings:\n-chest or back pain, 80-90%\n-aortic insufficiency\n-blood pressure discrepancies between extremities\n-neurologic deficits\n-ischemic extremity\n-pulse deficits\n\n\u2022 Associated conditions/diseases:\n-hypertension (most common)\n-collagen disorders, ex. Marfan\u2019s, Ehlers-Danlos\n-congenital, ex. Aortic coarctation, bicuspid or unicuspid valve\n-pregnancy\n-collagen vascular disease\n\n\u2022 Classification:\n-Stanford:\n\tType A: involves at least ascending aorta; surgical treatment, 60%\n\tType B: limited to descending aorta; medical treatment, 40%\n-DeBakey:\n\tType I: ascending and descending; surgical treatment, 50%\n\tType II: ascending only; surgical treatment, 10%\n\tType III: descending only; medical treatment, 40%\n\n< ================================= >\nCT for diagnosis of Acute Chest Pain - http://radiology.rsna.org/content/252/2/332.full\n< ================================= >\nMideast Envoy Richard Holbrook died from an aortic dissection in December of 2010. \n\u2022 http://en.wikipedia.org/wiki/Richard_Holbrooke\n\u2022 http://www.cnn.com/2010/US/12/11/richard.holbrooke.obit/\n\u2022 http://www.foxnews.com/topics/politics/obama-administration/richard-holbrooke.htm", "ACR Code": "562.74", "Category": "Aneurysm", "Keywords": "aortic aneurysmbleeding aortadissecting aortic aneurysm", "Reference": "Armstrong, P., et. al., Imaging of Diseases of the Chest. 3rd ed., Mosby, Edinburgh, 2003.", "External Links": "radiology.rsna.org/content/252/2/332.full" } }, { "U_id": "MPX2158", "TAC": [ "MPX2158_synpic19196" ], "MRI": [ "MPX2158_synpic19197", "MPX2158_synpic19198", "MPX2158_synpic19199", "MPX2158_synpic19200", "MPX2158_synpic19201", "MPX2158_synpic19202", "MPX2158_synpic19203" ], "Case": { "Title": "High-grade chondroid neoplasm", "History": "45 y/o white male initially presented with five week hx of left buttock burning pain and numbness extending into lower thigh. Initially treated with NSAIDS and physical therapy, symptoms continued to worsen. Presented to WRAMC with numbness and tingling extending into left testicle and penis. Patient denies bowel or bladder incontinence, weight loss, or other constitutional symptoms. Denies any numbness, pain, or abnormal sensations on right side.\nPMHx: HTN, hyperlipidemia\nPSHx: remote tonsillectomy/ bilateral herniorrhaphy\nMEDS: Ramipril 5 mg PO qd, HCTZ 12.5 mg PO qd, Amitryptyline 25 mg PO qd, Zocor 10 mg PO qd", "Exam": "normal sphincter tone, guaiac negative, diminished light touch and temperature sensation along left penis and scrotum, otherwise normal exam", "Findings": "1) Plain films- normal SI joints, ill defined lucent area over lower left sacrum, two sacral neural foramina on left widened with erosions of borders\n2) CT- mass left side of sacrum, left side of S1 encroaching on left side neural foramen, normal vertebral bodies\n3) MRI- infiltrating lesion with high T2 signal intensity within body of sacrum infiltrating into the epidural space", "Differential Diagnosis": "metastatic disease, primary bone tumor, lymphoma, multiple myeloma, giant cell tumor, and chondroma", "Case Diagnosis": "High-grade chondroid neoplasm", "Treatment & Follow Up": "Chondrosarcoma is managed similarly to osteosarcoma, with radical surgery being the treatment of choice. When only excision is employed, 90% of tumors recur locally. The overall 10 year survival rate following surgery is approximately 65%. Radiation therapy as the primary modality for chondrosarcoma is limited. Pulmonary metastasis occur, but the value of chemotherapy is not well established. Doxorubicin yields a response rate of only 17% for metastatic chondrosarcoma." }, "Topic": { "Title": "High-grade chondroid neoplasm", "Disease Discussion": "Chondrosarcoma encompasses 20-25% of all bone sarcomas and is the second most frequent malignant bone tumor of the spine after chordoma (3-12% arise in the spine). The average age of onset is in the adult between the ages of 40- 60 with a greater predisposition for men. The distribution is more common in the flat bones, especially the shoulder and pelvis. The presentation is most commonly of the exostotic type, as a large calcified mass in a vertebral body developing into the paraspinal tissue. The center of the tumor is often calcified with stippling and mottling with underlying bone distruction with a thick cap of sarcomatous cartilage surrounding the calcified mass. The causes include de novo appearance, malignant transformation of an enchondroma, or development from the cartilaginous cap of an osteochondroma. The clinical hx is often one of an indolent pain, swelling, with a progressive increase in size to the point of compression of neighboring organs, nerve root, or spinal cord compression. The cartilage emits a high T2 signal on MRI. Treatment is radical surgical resection due to the fact that the tumor is very refractory to chemotherapy. Incidently, most tumors are discovered late in presentation forcing a piecemeal resection and increased recurrence post-op. The dedifferentiated chondrosarcoma a low-grade tumor often transforms into osteosarcoma or malignant fibrous histiocytoma and becomes responsive to chemotherapy. Prognosis is that a low-grade lesion has a 90% 10-year survival, while high-grade have 20-40% 10-year survival. Follow-up with plain films to screen for recurrence.", "ACR Code": "-1.-1", "Category": "Unsure", "Keywords": "chondroid neoplasm", "Reference": "1)\tLaredo, J, El Quessar, A, Bossard, P. \u201cImaging of Low Back Pain 2: Vertebral Tumors and Pseudotumors\u201d. Radiologic Clincis of North America. Volume 39, Number 1, January 2001\n\n2)\tCanale. Campbell\u2019s Operative Orthopaedics, 10th ed., 2003" } }, { "U_id": "MPX2166", "TAC": [ "MPX2166_synpic16314" ], "MRI": [], "Case": { "Title": "Suprasellar epidermoid cyst", "History": "This 47 year old man had a history of organic brain syndrome and blindness in the left eye for one year. He presented to the emergency department following the new onset of a seizure. He had headaches, weakness or sensory abnormalities.", "Exam": "Physical examination disclosed the patient to be alert but oriented only to person. There was a Marcus Gunn pupil on the left while the right pupil was normally reactive. The left eye was blind and there was a visual field cut on the right. There was no papilledema. The patient had anosmia. Cranial nerves 3 through 12 were intact. Strength was 5/5 throughout. The sensory examination to light touch was intact. The deep tendon reflexes were 2+ and the toes were down going.", "Findings": "Extensive lobulated suprasellar mass, largely homogeneous and of nearly water attenuation.", "Differential Diagnosis": "\u2022 Craniopharynioma\n\u2022 Epidermoid inclusion cyst\n\u2022 Rathke cleft cyst\n\u2022 Dermoid inclusion cyst", "Case Diagnosis": "Suprasellar epidermoid cyst" }, "Topic": { "Title": "Suprasellar epidermoid cyst", "Disease Discussion": "Dermoid cysts and epidermoid cysts are postulated to be derived from ectodermal cells that are displaced during neural tube closure. The wall of an epidermoid cyst is composed of stratified squamous epithelium and is devoid of hair follicles or sebaceous glands. The cyst is filled with thin desquamated epithelial squames that do not harbor nuclear remnants and are designated as \"dry keratin\". Grossly the contents may have a pearly white appearance.", "ACR Code": "1.3", "Category": "Cyst, benign", "Keywords": "epidermoid cysts" } }, { "U_id": "MPX2169", "TAC": [ "MPX2169_synpic50697" ], "MRI": [], "Case": { "Title": "Transient adult jejunojejunal intussusception secondary to IBD (Crohn disease).", "History": "23 y/o female smoker w/ history of inflammatory bowel disease (IBD) type disease s/p partial colectomy with intermittent abdominal symptoms.", "Exam": "Unremarkable except for an enterocutaneous fistula intermittently draining yellow fluid in the vicinity of a surgical scar.", "Findings": "Contrast enhanced axial CT of the abdomen demonstrates extraluminal mesenteric fat located around a proximal jejununal segment (intussusceptum) telescoping into the lumen of an adjacent and more distal jejunal segment (intussuscipiens).", "Differential Diagnosis": "\u2022 Transient enteroenteric intussusception (adult)\n - IBD-associated\n - Idiopathic\n - Other inflammatory or malabsorption syndromes\n - Giardiasis\n - HIV-associated (infectious, inflammatory)\n\u2022 Lead point enteroenteric intussusception (adult)\n - Benign tumors\n - Malignant tumors (metastases, primary)\n - Meckel diverticulum \n - HIV or AIDS-associated (tumor)", "Case Diagnosis": "Transient adult jejunojejunal intussusception secondary to IBD (Crohn disease).", "Diagnosis By": "Diagnosis was confirmed with Promethius IBD Serology 7", "Treatment & Follow Up": "Evidence suggests transient adult enteroenteric intussusception may be more common than originally thought. Many of these intussusceptions are more readily identified now with the increased use of multidetector CT. In patients that are asymptomatic or minimally symptomatic, many of these may be managed conservatively. Proximal small bowel intussusceptions with a target appearance and without a lead point or obstruction that measure less than 3.5 cm in length, will likely be self-limiting. Intussusceptions measuring greater than 3.5 cm without lead point or obstruction should probably be further evaluated with additional imaging (eg. small bowel series, enteroclysis, CT enteroclysis, CT or MR enterography). However, cases demonstrating ischemia, obstruction, or a lead point, require surgical exploration.", "Discussion": "Adult intussusception has traditionally been regarded as rare and usually associated with an identifiable cause such as a tumor functioning as a lead point. However, with recent advancements and increased use of CT technology, transient enteroenteric intussusceptions are being identified; many of which are in asymptomatic or minimally symptomatic patients.\n An intussusception is a medical condition in which a part of the intestine invaginates into another section of intestine, similar to a collapsible telescope. The part that prolapses into the other is called the intussusceptum, and the part that receives it is called the intussuscipiens. Usually the intussusception occurs in an antegrade fashion following the direction of peristalsis. The peristaltic tightening of smooth muscle in the intussuscipiens around the intussusceptum can lead to obstruction, ischemia and necrosis. \n Presenting symptoms can vary depending on the underlying condition. Although, ultrasound is generally considered the imaging modality of choice in a young child, CT is more frequently the imaging study by which adult intussusceptions are identified.\n The three CT patterns of intussusception are the target appearance, reniform pattern, and sausage-shaped pattern. The target appearance is felt to correspond to an early intussusception without ischemia. \n Proximal transient enteroenteric intussusceptions without an identifiable lead point that measure less than 3.5 cm in length are likely to be self limiting not requiring surgical intervention. Intussusceptions measuring greater than 3.5 cm without lead point or obstruction should probably be further evaluated with additional imaging (eg. small bowel series, enteroclysis, CT enteroclysis, CT or MR enterography). However, cases demonstrating ischemia, obstruction, or a lead point, require surgical exploration.\n\nHorton KM, Fishman EK. MDCT and 3D imaging in transient enteroenteric intussusception: clinical observations and review of the literature. AJR Am J Roentgenol. 2008 Sep;191(3):736-42.\n\nIBD Serology 7\t\t\nSaccharomyces cerevisiae Ab IgA-15.3Ehrlich Units/ml (0.0-19.9)\nSaccharomyces cerevisiae Ab IgG-33.2Ehrlich Units/mL(0.0-39.9)\nOmpC Ab IgA-13.4\tEhrlich Units/mL(0.0-16.4)\t\nCbir1 Flagellin Ab-26.6(H)Ehrlich Units/mL(0.0-20.9)\t\nNeutrophil Spec Nuclear Ab-\t<12.1Ehrlich Units/mL(<12.1)\nNeutrophil Spec Nuclear Ab Perinuc Pattern-Detected (H) \nNeutrophil Speci Nuclear Ab Dnase Sens-DNAse Sensitive \nIBD Autoab Profile\t >>>>>\tIBD/Crohn Disease Predicted" }, "Topic": { "Title": "Adult Enteroenteric Intussusception", "Disease Discussion": "Adult intussusception has traditionally been regarded as rare and usually associated with an identifiable cause such as a tumor functioning as a lead point. However, with recent advancements and increased use of CT technology, transient enteroenteric intussusceptions are being identified; many of which are in asymptomatic or minimally symptomatic patients.\n\nAn intussusception is a medical condition in which a part of the intestine invaginates into another section of intestine, similar to a collapsible telescope. The part that prolapses into the other is called the intussusceptum, and the part that receives it is called the intussuscipiens. Usually the intussusception occurs in an antegrade fashion following the direction of peristalsis. The peristaltic tightening of smooth muscle in the intussuscipiens around the intussusceptum can lead to obstruction, ischemia and necrosis. \n\nPresenting symptoms can vary depending on the underlying condition. Although, ultrasound is generally considered the imaging modality of choice in a young child, CT is more frequently the imaging study by which adult intussusceptions are identified.\n\nThe three CT patterns of intussusception are the target appearance, reniform pattern, and sausage-shaped pattern. The target appearance is felt to correspond to an early intussusception without ischemia. \n\nProximal transient enteroenteric intussusceptions without an identifiable lead point that measure less than 3.5 cm in length are likely to be self limiting not requiring surgical intervention. Intussusceptions measuring greater than 3.5 cm without lead point or obstruction should probably be further evaluated with additional imaging (eg. small bowel series, enteroclysis, CT enteroclysis, CT or MR enterography). However, cases demonstrating ischemia, obstruction, or a lead point, require surgical exploration.\n\nHorton KM, Fishman EK. MDCT and 3D imaging in transient enteroenteric intussusception: clinical observations and review of the literature. AJR Am J Roentgenol. 2008 Sep;191(3):736-42.", "ACR Code": "7.2", "Category": "Inflammatory, NOS", "Keywords": "inflammatory bowel disease" } }, { "U_id": "MPX2171", "TAC": [ "MPX2171_synpic20416" ], "MRI": [], "Case": { "Title": "Pericardial Effusion", "History": "Patient is a 19 year-old female, 24 weeks pregnant, with history of systemic lupus erythematosus. Pt now presents with pleuritic chest pain. Pt denies SOB.", "Findings": "A very large pericardial effusion is seen which does not enhance with contrast, and which is hypodense when compared to adjacent heart. Additionally, there is a left pleural effusion with area of compressive atelectasis in left lower lobe.", "Differential Diagnosis": "Of pericardial effusion: None.\nOf cardiac tamponade: Constrictive pericarditis, restrictive cardiomyopathy.", "Case Diagnosis": "Pericardial Effusion", "Treatment & Follow Up": "Treatment: If pericardial effusion is small (0.5-1.0 cm on CT/MRI), follow with serial echocardiograms. If greater than 1.0-2.0 cm and/or if patient is symptomatic, treatment is pericardiocentesis or pericardial window.", "Discussion": "Excess pericardial fluid may be present in all forms of pericardial disease, including percarditis secondary to SLE and other collagen vascular diseases.\n\nPericardial effusion in the setting of pericarditis may be found incidentally, as was in this patient, upon imaging studies in patients complaining of pleuritic chest pain.\n\nIf the collection of fluid is rapid, a small amount, (100-200 ml of pericardial fluid), can result in cardiac tamponade. Conversely, if accumulation of fluid is more insipid, larger amounts (up to 1500 ml) can accumulate within the pericardium without tamponade physiology." }, "Topic": { "Title": "Pericardial Effusion with Tamponade", "Disease Discussion": "The response of normal pericardium to injury is cellular proliferation and/or the production of fluid (pericardial effusion). Inflammation of the pericardium (i.e. pericarditis) can be the result of many different etiologies. The most common of these etiologies include infectious (viral, bacterial, fungal and TB), post-MI, association with malignancy (breast, lung, lymphoproliferative and melanoma), association with systemic disease (uremia, hypothyroidism and connective tissue disorders) and post-chest radiation exposure (Primack 1998). \n\nThe most common result of acute pericarditis is the formation of a pericardial effusion, which can be transudative or exudative depending on the underlying pathology. Clinical signs of effusion include pericardial friction rub, chest pain, increased dullness over precordium and pulsus paradoxus. Plain film diagnosis of pericardial disease is based on the observation of the changes in the contours of the heart borders contained by the pericardium (Rozenshtein 1999). Radiographic signs of pericardial effusion include a smooth generalized increase in size of the cardiac silhouette without specific chamber enlargement, \"water-bottle\" or \"globular\" cardiac configuration and an anterior pericardial stripe thicker than 2 mm in the lateral view (Rozenshtein 1999). \n\nPericardial effusion can progress to the point where diastolic filling of the ventricles is severely impeded and the patient becomes hemodynamically unstable. This condition is termed cardiac tamponade and is heralded clinically by Beck's triad, which includes muffled heart sounds, distended neck veins and hypotension. Pulsus paradoxus is another clinical sign frequently seen in tamponade. Because acute tamponade is possible with small effusions, plain films are not a sensitive technique for detecting clinically significant pericardial enlargement. Subtle changes in cardiac contour may only be evident through comparison to prior films. If there is cardiac enlargement with decreased pulmonary vasculature or if the azygous and SVC are dilated, one should have a high index of suspicion for tamponade (Rozenshtein 1999).", "ACR Code": "55.821", "Category": "Infection, viral", "Reference": "1. Rozenshtein A, Boxt LM: Plain-Film Diagnosis of Pericardial Disease. Sem Roent 34(8): 195-204, 1999\n2. Primack SL, Muller NL: Thoracic Manifestations of the Systemic Autoimmune Diseases. Clin Chest Med 19(4): 573-86, 1998" } }, { "U_id": "MPX2174", "TAC": [ "MPX2174_synpic43" ], "MRI": [], "Case": { "Title": "Tuberous Sclerosis", "History": "Seizures since age two. Mild mental handicap.", "Exam": "Numerous reddish papular lesions on both cheeks.", "Findings": "Multiple periventricular calcifications.", "Differential Diagnosis": "Tuberous Sclerosis Complex.", "Case Diagnosis": "Tuberous Sclerosis" }, "Topic": { "Title": "Tuberous Sclerosis", "Disease Discussion": "Tuberous Sclerosis is an autosomal dominant disorder producing systemic lesions. Two genes are associated: TSC1 (9q) and TSC2 (16p). TSC1 codes for a protein \"hamartin\" of 130 kD, expressed in brain, kidney and heart. TSC2 codes for \"tuberin\".\n\nThe most commonly affected organ systems include:\nSkin - angiofibroma, ash leaf macule\nBrain - cortical tubers, subependymal nodules\nKidney - angiomyolipoma, cysts, rarely renal cell Ca\nBone - bone islands, cystic lucencies\nHeart - rhabdomyoma\nLung - lymphangioleiomyomatosis\n\nRemember PRINGLE's Snack can:\nMild (inconstant) mental retardation\nFacial angiofibroma (Pringle's Rash)\nSeizures (shake the can)\nTubers (hard potatoes ground into potato flour)\n\nMore about AML:\nhttp://www.rsna.org/REG/publications/rg/afip/privateM/1997/0017/0001/0155/1.htm#topAnchor", "ACR Code": "1.6", "Category": "Congenital, genetic", "Reference": "; Accepted by jsmirnio", "External Links": "rad.usuhs.mil/rad/handouts/tuberous.html" } }, { "U_id": "MPX2173", "TAC": [ "MPX2173_synpic24935", "MPX2173_synpic24936" ], "MRI": [ "MPX2173_synpic24937", "MPX2173_synpic24938" ], "Case": { "Title": "Inflammatory Breast Cancer, Metastatic to thoracic spine (Stage IV)", "History": "55 y/o woman seen as an outpatient for possible mastitis.", "Exam": "Patient with darkened, thickened, warm skin over right breast. Skin dimpling present. Adenopathy present in right axilla.\n\nLeft breast and axilla normal. Exam otherwise unremarkable.", "Findings": "CT of chest shows skin thickening over right breast, significant enlargement of right breast compared to left. Fat streaking within the right breast.\nMRI of thoracic spine shows abnormal signal intensity at T4 and T7 consistent with metastases.", "Differential Diagnosis": "Inflammatory Breast Cancer Metastatic -Stage IV\nInflammatory Breast Cancer, locally advanced-Stage III\nAcute Mastitis and/or cellulitis\nDiffuse inflammation by lymphoma \nAdvanced non-inflammatory breast cancer", "Case Diagnosis": "Inflammatory Breast Cancer, Metastatic to thoracic spine (Stage IV)", "Diagnosis By": "Biopsy and pathology", "Treatment & Follow Up": "This patient was treated with antibiotics and failed to improve with therapy.\n\nA biopsy was done when the patient returned without resolution of disease.\n\nPathology: Biopsy showed dermal lymphatic invasion by tumor cells, atypical mitotic figures and pleomorphic tumor cells consistent with inflammatory breast cancer. \n\nThe patient was then referred for an NIH treatment protocol.\n\nNeoadjuvant Chemotherapy protocol followed by mastectomy and local radiation therapy.", "Discussion": "In 2004, approximately 217,440 women were diagnosed with breast cancer and approximately 40,580 died from it. Breast cancer is the leading cause of death in women in the U.S. ages 45-55.\n\nInflammatory breast cancer is rare, consisting of 1-5% of invasive breast cancers. It is rapidly progressive and the most lethal form of locally advanced breast cancer. It is characterized by early metastatic spread. In fact, up to 1/3 of patients have distant metastases at the time of diagnosis.\n\nWhile biopsy tends to show characteristic dermal lymphatic invasion by tumor cells, which create tumor emboli that facilitate in the early metastatic spread, diagnosis is basically clinical. The hallmark of inflammatory breast cancer is the classic peau d\u2019orange skin changes. The classic definition is \u201cdiffuse brawny induration of the skin of the breast with an erysipeloid edge, usually without underlying palpable mass.\u201d1 As in this case, patients are frequently misdiagnosed with acute mastitis or a breast abscess, especially if lactating, when they first present. \n\nWhile bilateral mammograms are recommended for all patients with breast cancer, in these patients CT and MRI and performed to look for distant metastases to differentiate between stage III and stage IV cancers." }, "Topic": { "Title": "Inflammatory Breast Cancer", "Disease Discussion": "In 2004, approximately 217,440 women were diagnosed with breast cancer and approximately 40,580 died from it. Breast cancer is the leading cause of death in women in the U.S. ages 45-55. Inflammatory breast cancer is rare, consisting of 1-5% of invasive breast cancers. It is rapidly progressive and the most lethal form of locally advanced breast cancer. It is characterized by early metastatic spread. In fact, up to 1/3 of patients have distant metastases at the time of diagnosis. While biopsy tends to show characteristic dermal lymphatic invasion by tumor cells, which create tumor emboli that facilitate in the early metastatic spread, diagnosis is basically clinical. The hallmark of inflammatory breast cancer is the classic peau d\u2019orange skin changes. The classic definition is \u201cdiffuse brawny induration of the skin of the breast with an erysipeloid edge, usually without underlying palpable mass.\u201d1 Patients are frequently misdiagnosed with acute mastitis or a breast abscess, especially if lactating, when they first present. While mammogram is recommended for all patients with breast cancer, in these patients CT and MRI are performed to look for distant metastases to differentiate between stage III and stage IV cancers.", "ACR Code": "0.3", "Category": "Neoplasm, carcinoma", "Keywords": "Inflammatory Breast Cancer, Metastatic to thoracic spine (Stage IV)Metastatic to thoracic spine (Stage IV)", "Reference": "AJCC Cancer Staging Manual, 6th ed, Green, FL, Page, DL, Flemming, ED, et al (eds), Springer-Verlag, NewYork, 2002, p. 223.\nEsserman, Jaura J, MD, MBA and Paul C Stomper, MD. Diagnostic evaluation and initial staging work-up of women with suspected breast\n cancer. From UpToDate. Accessed 4/19/05.\nMerajver, Sofia D, MD, PhD. Pathology and molecular pathogenesis of inflammatory breast cancer. From UpToDate. Accessed 4/19/05.\nSavarese, Diane MF, MD and Daniel F Hayes, MD. Overview of treatment for locally advanced and metastatic breast cancer. \n From UpToDate. Accessed 4/19/05.\nTaghian, Alphonse, MD, PhD, Moataz El-Ghamry, MB, BCH and Sofia Merajver, MD, PhD. Management of locally advanced and \n inflammatory breast cancer. From UpToDate. Accessed 4/19/05." } }, { "U_id": "MPX2176", "TAC": [ "MPX2176_synpic34064", "MPX2176_synpic34065", "MPX2176_synpic34067", "MPX2176_synpic34068", "MPX2176_synpic34069", "MPX2176_synpic34070", "MPX2176_synpic34071" ], "MRI": [], "Case": { "Title": "Adenocarcinoma of the gastroesophageal junction", "History": "79 year old male presents with dysphagia.", "Exam": "N/A", "Findings": "Axial CT images through the lower thorax and upper abdomen following the administration of oral and IV contrast material demonstrate a segment of significant circumferential wall thickening and lumenal narrowing involving the distal third of the esophagus and the proximal aspect of the stomach. There is associated lymphadenopathy.\n\nPET/CT fusion images in axial, sagital and coronal planes deomstrate focal increased FDG-18 metabolism in the region of wall thickening identified on the CT scan with a maximum SUV of 11.6.", "Differential Diagnosis": "Adenocarcinoma in a Barrett esophagus\nGastric Adenocarcinoma with extension into the distal esophagus\nMetastatic disease", "Case Diagnosis": "Adenocarcinoma of the gastroesophageal junction", "Diagnosis By": "Pathology", "Treatment & Follow Up": "The patient first underwent EGD for biopsy and then underwent surgical resection of the mass. The patient expired approximately nine months after detection of the cancer.", "Discussion": "Please see factoid." }, "Topic": { "Title": "Adenocarcinoma of the gastroesophageal junction", "Disease Discussion": "Adenocarcinoma of the gastroesophageal (GE) junction is notable in that its incidence that increased more than any other malignancy in the western world. The reasons for such an increase are unknown. (1) There are three classifications of this type of cancer: Type I mainly involves the distal esophagus, Type II is primarily located at the GE junction, and Type II mainly involves the subcardial/proximal stomach region. (3) GE junction adenocarcinoma can either arise from the esophagus or proximal gastric area. It is very difficult to determine the primary cancer site. (1) Risk factors for gastric adenocarcinoma include familial adenomatous polyposis, gastric adenomas/ dysplasia, chronic atrophic gastritis, gastric metaplasia, diet high in nitrates, and Helicobacter pylori infection. Risk factors for esophageal adenocarcinoma include smoking, obesity, and Barrett\u2019s esophagus- patients affected with Barrett\u2019s esophagus have a 30-40% higher chance of developing cancer. (4) \n\nRadiological evaluation of GE adenocarcinoma should be able to determine tumor spread and response to chemotherapy. The sensitivity of CT for detection of distant metastases ranges between 50% to 90%. Of those shown to have only local disease with CT, FDG-PET detected metastatic disease in approximately 20% more cases. In addition, esophageal ultrasound (EUS) can differentiate between stages T1/T2 and stages T3/T4 with an accuracy > 90%. Assessment of tumor response to chemotherapy by FDG-PET correlates with tumor regression proven by histology and can predict patient outcome as early as 2 weeks after initiation of therapy. (5)", "ACR Code": "7.3", "Category": "Neoplasm, carcinoma", "Keywords": "Adenocarcinomacarcinoma", "Reference": "1. Hashem B. \u201cThe epidemic of esophageal adenocarcinoma.\u201d Gastroenterology Clinics of North America 31(2):421\u2013440, 2002.\n2. Macdonald JS; Smalley SR; Benedetti J; Hundahl SA; Estes NC; Stemmermann GN; Haller DG; Ajani JA; Gunderson LL; Jessup JM; Martenson JA. \u201cChemoradiotherapy after surgery compared with surgery alone for adenocarcinoma of the stomach or gastroesophageal junction.\u201d N Engl J Med 345(10): 725-30, 2001.\n3. M?nig SP; Schr?der W; Beckurts KT; H?lscher AH. \u201cClassification, diagnosis and surgical treatment of carcinomas of the gastroesophageal junction.\u201d Hepatogastroenterology 48(41): 1231-7, 2001.\n\n4. Kumar V, Collins T, Robbins SL. Robbins Pathologic Basis of Disease. W.B. Saunders Company, Philadelphia, 1999, pgs 784-802.\n\n5. Weber WA, Ott K. \u201cImaging of esophageal and gastric cancer.\u201d Semin Oncol. 31(4):530-41, 2004." } }, { "U_id": "MPX2175", "TAC": [ "MPX2175_synpic59056", "MPX2175_synpic59057", "MPX2175_synpic59058", "MPX2175_synpic59059", "MPX2175_synpic59060", "MPX2175_synpic59061", "MPX2175_synpic59062", "MPX2175_synpic59063", "MPX2175_synpic59064", "MPX2175_synpic59065", "MPX2175_synpic59066", "MPX2175_synpic59067", "MPX2175_synpic59068", "MPX2175_synpic59070", "MPX2175_synpic59071", "MPX2175_synpic59072", "MPX2175_synpic59073", "MPX2175_synpic59074" ], "MRI": [ "MPX2175_synpic59075", "MPX2175_synpic59076", "MPX2175_synpic59077", "MPX2175_synpic59078", "MPX2175_synpic59079", "MPX2175_synpic59080", "MPX2175_synpic59081", "MPX2175_synpic59082", "MPX2175_synpic59083", "MPX2175_synpic59084", "MPX2175_synpic59085", "MPX2175_synpic59086", "MPX2175_synpic59087" ], "Case": { "Title": "Venous thrombosis of the vein of Galen, straight sinus, and dominant left transverse venous dural sinus.", "History": "17 yo girl presents with left sided facial weakness and numbness and the worst headache of her life that is rated 10/10. The headache has been progressive for about 24 hours. She has a history of migraine, but the patient states that her current headache does not feel like her typical migraine headache.", "Exam": "She is obese and has a history of polycystic ovarian syndrome (PCOS) and currently on oral contraceptive pills (OCPs) for symptom control. Exam is significant for her degree of discomfort and for confirming facial numbness. The facial strength is intact bilaterally.", "Findings": "The vein of Galen, straight sinus, and dominant left transverse venous dural sinus are particularly hyperattenuating, and apparently prominent in caliber.\n \nThe superior sagittal sinus is notably less hyperattenuating and is normal in appearance. The right transverse dural venous sinus is hypoplastic.\n \nGray/white matter discrimination is preserved. There is no evidence for infarction or intracranial hemorrhage. There are no brain masses or mass effect. There is no hydrocephalus.\n \nThe skull is intact. The partially imaged aerated portions of the skull base are free of significant effusions..\n\nImpression: The vein of Galen, straight sinus, and dominant left transverse venous dural sinus are all particularly hyperattenuating and apparently prominent in caliber, all very concerning for thrombosis.", "Differential Diagnosis": "Venous sinus thrombosis\nSevere dehydration\nPolycythemia", "Case Diagnosis": "Venous thrombosis of the vein of Galen, straight sinus, and dominant left transverse venous dural sinus.", "Diagnosis By": "MRV (MR venography)", "Treatment & Follow Up": "Admission and heparin drip anticoagulation.", "Discussion": "Venous thrombosis is a medical emergency. Complications include cerebral infarct and intracerbral hemorrhage. Patients may present with headache, seizure, and focal neurologic deficits. The neurologic findings can wax and wane. Risk factors include the typical thrombosis risk factors such as pregnancy, OCP use, smoking, dehydration, and the hypercoaguable disorders. \n\nRadiographic findings include hyperdense venous structures. One should be aware of a few diagnostic pitfalls, such as normally dense venous structures. These structures can be more dense with dehydration or elevated hematocrit, but the density is concerning when the venous structures are more dense than arteries on non-contrast CT scans. Other findings, such as infarct and hemorrhage, if present, can also help confirm a diagnosis of a venous sinus thrombosis. CT angiography and MR venography (MRV) can be used to verify findings. One common variant that can confuse the diagnostic picture is an aberrant or hypoplastic transverse sinus." }, "Topic": { "Title": "Dural sinus thrombosis", "Disease Discussion": "Venous sinus thrombosis is caused by thrombus formation in the dural venous sinuses or cerebral veins. It is an uncommon disorder (2-7 per million) which can have serious complications. Causal factors include local (regional infection, trauma, neoplasm) and systemic (dehydration, hypercoagulable states, pregnancy, oral contraceptives). Clinical presentation includes headache, neurologic deficits or seizures. The superior sagittal sinus is most commonly affected, followed by the transverse and sigmoid sinuses. Complications include venous infarcts, intracerebral hemorrhage and intracranial hypertension.\n\nOn noncontrast CT, the thombosed sinus is usually hyperdense. This is nonspecific as dehydrated patients, adjacent subdural or subarachnoid hemorrhage or elevated hematocrit can cause increased sinus attenuation. On contrast enhanced CT, the empty delta sign is a central defect from thrombus surrounded by contrast enhanced blood. On MRI, absence of a flow void or abnormal signal within the sinus is seen. \n\nMR venography with two-dimensional time-of-flight is used due to high sensitivity for slow flow compared to 3D TOF. Contrast enhanced MRV improves visualization of small vessels. CT venography is a rapid and accurate method for evaluating the venous sinuses. Disadvantages include ionizing radiation exposure and need for iodinated contrast material.", "ACR Code": "1.9", "Category": "Vascular", "Keywords": "dural sinusthrombosisBlood Clot between brain and skull", "Reference": "Leach JL, Fortuna RB, et al. Imaging of Cerebral Venous Thrombosis: Current Techniques, Spectrum of Findings, and Diagnostic Pitfalls. Radiographics. 2006; 26:S19-43.\n\nPatel MR. Brain, Venous Sinus Thrombosis. eMedicine. July 2005.", "External Links": "www.emedicine.com/radio/topic105.htm" } }, { "U_id": "MPX2190", "TAC": [ "MPX2190_synpic57896" ], "MRI": [], "Case": { "Title": "Angioinvasive aspergillosis", "History": "68 year old man with a past medical history of AML, HTN, Type 2 DM, and CHF s/p FLAG chemotherapy for recurrent AML. He was admitted to the ICU because of severe neutropenia.", "Findings": "CT Chest with and without contrast: \nPulmonary nodule noted with surrounding \"ground glass opacification\" with 2.9cm mass within the right middle lobe with central cavitation.", "Differential Diagnosis": "\u2022 Invasive aspergillosis\n\u2022 Hemorrhagic metastasis\n\u2022 Mucormycosis\n\u2022 Vasculitis (e.g. Wegeners)", "Case Diagnosis": "Angioinvasive aspergillosis", "Diagnosis By": "Serologically" }, "Topic": { "Title": "CT Halo Sign", "Disease Discussion": "The computed tomographic (CT) halo sign, also known as the halo sign, refers to a zone of ground-glass attenuation surrounding a pulmonary nodule or mass on CT images.\nThe presence of a halo of ground-glass attenuation is usually associated with hemorrhagic nodules . This CT appearance was described by Kuhlman et al(1) in patients with invasive aspergillosis. In severely neutropenic patients, the CT halo sign is highly suggestive of infection by an angioinvasive fungus, most commonly Aspergillus. Vascular invasion by this fungus results in thrombosis of small- to medium-sized vessels, which causes ischemic necrosis. At pathologic examination, the nodules represent foci of infarction, and the halo of ground-glass attenuation results from alveolar hemorrhage. Although it is less common, the halo sign may also be observed in nonhemorrhagic nodules, in which case either tumor cells or inflammatory infiltrate account for the halo of ground-glass attenuation. Nonetheless, in the appropriate clinical setting, the halo sign is considered early evidence of pulmonary aspergillosis even before serologic tests become positive, and it warrants the administration of systemic antifungal therapy(2).\n\nEarly recognition of this complication is critical because this disease is associated with a high mortality rate that ranges from 50% to 90%. The frequency of the halo sign in patients with invasive aspergillosis is relatively high in the early stages of the disease, but alters with time and becomes progressively less frequent. In a group of 25 patients with invasive pulmonary aspergillosis studied by using serial CT scans, the frequency of this sign ranged from 96% at day 0 to 19% at day 14(1).", "ACR Code": "6.9", "Category": "Radiologic Sign or Finding", "Keywords": "CTHaloSign", "Reference": "1.\tKuhlman JE, Fishman EK, Siegelman SS. Invasive pulmonary aspergillosis in acute leukemia: characteristic findings on CT, the CT halo sign, and the role of CT in early diagnosis. Radiology 1985; 157:611-614.\n2.\tPedro S. Pinto, The CT Halo Sign; Jan 2004 Radiology, 230, 109-110" } }, { "U_id": "MPX2183", "TAC": [ "MPX2183_synpic43438", "MPX2183_synpic43439", "MPX2183_synpic43440", "MPX2183_synpic43441", "MPX2183_synpic43442", "MPX2183_synpic43443", "MPX2183_synpic43444", "MPX2183_synpic43446", "MPX2183_synpic43447" ], "MRI": [], "Case": { "Title": "Rectovaginal Fistula", "History": "71 year old female, status post hysterectomy presenting with feces per the vagina.", "Findings": "Initial axial CT images through the pelvis demonstrate a paucity of contrast in the rectum. There is no contrast material in the vagina. The patient is status post hysterectomy. Delayed axial CT images through the pelvis, obtained 6 hours after the initial scan reveal contrast within the bladder and rectum. No contrast material is noted within the vagina. Rectal contrast was administered, with subsequent axial CT images through the pelvis with rectal tube and balloon in place, demonstrating contrast material within the vagina. A fistula tract is not visualized. The rectal tube was removed, and the patient was reimaged. Contrast material is again noted within the vagina. Additionally, there is soft tissue stranding posterior to the vagina, and anterior to the rectum, which may represent the fistula tract. Fluoroscopic images from a barium enema demonstrate a rectovaginal fistula. Although a fistula tract is not clearly visualized, contrast is noted to pass from the anterior rectum to the vagina.", "Differential Diagnosis": "Rectovaginal Fistula\nColovaginal (Sigmoidovaginal) Fistula\nEnterovaginal Fistula\nEnterovesical Fistula", "Case Diagnosis": "Rectovaginal Fistula", "Diagnosis By": "Imaging findings correlated with the patient's clinical presentation are diagnostic." }, "Topic": { "Title": "Rectovaginal Fistula", "Disease Discussion": "Colovaginal fistula, which is an abnormal communication between the colon and vagina is most frequently caused by diverticular disease. The sigmoid colon is most commonly affected, and most women who develop a sigmoidovaginal fistula have a history of a hysterectomy. Other causes included neoplasms, inflammatory bowel disease, radiation, infection, and trauma. \n\nRectovaginal fistulas represent a small portion of all anorectal fistulas, and are frequently secondary to obstetric complications, perineal infections, neoplasms such as colorectal adenocarcinoma or cervical cancer, radiation, trauma, and inflammatory bowel disease (ulcerative colitis). Diverticular disease, which is typically absent in the rectum, is not a factor. \n\nPatients with colovaginal fistulas may present with feces, flatus, or mucus discharge from the vagina. Anal incontinence may also be present secondary to anal sphincter compromise. \n\nAlthough the clinical symptoms, particularly the passage of feces through the vagina, indicate the presence of a fistula, its detection is often difficult unless a large communication is present. Vaginography and barium enema in conjunction with physical examination have traditionally been used for diagnosis. CT, MR imaging, and endorectal US are alternative imaging modalities.\n\nColovaginal fistulas are managed surgically, by takedown of the fistula with colon resection and primary anastomosis. Conservative management may be attempted in poor surgical candidates.", "ACR Code": "7.7", "Category": "Fistula or Shunt", "Keywords": "Rectovaginal FistulaColovaginal Fistula", "Reference": "Yu et al. RadioGraphics 2004;24:1331-1352\nPickhardt et al. Radiology 2002;224:9-23" } }, { "U_id": "MPX2195", "TAC": [ "MPX2195_synpic4099", "MPX2195_synpic4100", "MPX2195_synpic4101" ], "MRI": [ "MPX2195_synpic4103", "MPX2195_synpic4104", "MPX2195_synpic4105", "MPX2195_synpic4106" ], "Case": { "Title": "cerebellar AVM with PICA aneurysm", "History": "38 y/o man presents to ER with history of headache after being choked during a basketball game.", "Findings": "NCHCT demonstrates hemorrhage in the lateral ventricles and the fourth ventricle with intraparenchymal hemorrhage adjacent to this in the right cerebellum. MRI demonstrates multiple flow voids in the right cerebellum which enhance on post gadolinium images. Angiography demonstrates right PICA aneurysm with a cerebellar AVM.", "Case Diagnosis": "cerebellar AVM with PICA aneurysm", "Diagnosis By": "Classic angiographic findings" }, "Topic": { "Title": "Arteriovenous Malformation (AVM)", "Disease Discussion": "ARTERIOVENOUS MALFORMATION (AVM)\n\nClinical Features: AVMs are the most common symptomatic congenital vascular malformations. The peak age at presentation is between 20 and 40. Approximately 50% of patients with AVMs present with symptoms caused by hemorrhage (25% present with seizures). The overall risk of hemorrhage from an AVM is estimated at 2% to 4% per year, cumulative. 98% of AVMs are solitary. Multiple AVMs outside the setting of vascular neurocutaneous disorders such as Rendu-Osler-Weber and Wyburn-Mason syndromes are extremely uncommon.\n\nPathology: AVMs are complex networks of abnormal vascular channels that consist of dilated arterial feeder(s) and draining veins, without intervening capillaries. These vessels often demonstrate flow-induced angiopathic changes secondary to endothelial hyperplasia (flow-related\u201d aneurysms in 10 - 20%). AVMs may contain gliotic brain and hemorrhagic residua. Atrophy of otherwise normal adjacent brain results from chronic regional arterial hypoperfusion and venous hypertension, as the AVMs steal vascular supply from adjacent brain tissue.\n\nImaging: Intracranial AVMs are subdivided into parenchymal (pial or within the brain), and dural (outside the brain). A mixed type occurs when a parenchymal AVM recruits dural vascular supply. 85% of AVMs are supratentorial. On cerebral angiography an AVM appears as a tightly packed mass of enlarged feeding arteries that supply a central nidus, a plexiform web of small vessels. One or more dilated veins drain the AVM nidus. The main goals of the diagnostic imaging workup are to delineate the size of the AVM, the eloquence of adjacent brain, and the pattern of venous drainage. These 3 characteristics are used to determine the long-term risk of an untreated AVM, as the table below explains.\n\nTable 1. Spetzler AVM Grading System\nGraded feature\t Points assigned\n Size\n Small (<3 cm)\t\t\t\t1\n Medium (3-6 cm)\t\t\t2\n Large (>6cm)\t\t\t\t3\n\nEloquence of adjacent brain\n Noneloquent \t\t0\n Eloquent\t\t\t\t\t1\n\nVenous drainage\n Superficial only\t\t\t 0\n Deep\t\t\t\t\t 1\n\n========================================\n \nSpetzler grades range from 1 to 5. A separate grade 6 is reserved for inoperable lesions. Prospective studies have confirmed the accuracy and utility of the Spetzler grade in guiding patient management and estimating postoperative neurologic complications.", "ACR Code": "1.3", "Category": "Congenital, malformation", "Keywords": "AVMvascular malformationcongenital", "Reference": "Osborn. Diagnostic Neuroradiology. 1994. Mosby.\nOsborn. Diagnostic Cerebral Angiography. 2nd Ed, 1999. LW&W." } }, { "U_id": "MPX2201", "TAC": [ "MPX2201_synpic39416", "MPX2201_synpic39417" ], "MRI": [], "Case": { "Title": "Enostosis", "History": "24 year old male with ulnar sided left elbow pain.", "Exam": "N/A", "Findings": "Frontal and lateral radiographs of the left elbow demonstrate normal alignment and joint spaces. Negative for fracture. At the intracondylar portion of the distal humeral metaphysis there is a non-aggressive sub-1 cm sclerotic focus within the medullary cavity. There is no osseous expansion, periosteal reaction or associated soft tissue mass. Multiplanar non-contrast CT images of the distal humerus show that the sclerotic focus has tiny spicules projecting outward to the surrounding medullary cavity.", "Differential Diagnosis": "Enostosis\nSclerotic metastatic focus", "Case Diagnosis": "Enostosis", "Diagnosis By": "Classic imaging characteristic", "Treatment & Follow Up": "None required", "Discussion": "Please see factiod." }, "Topic": { "Title": "Enostosis", "Disease Discussion": "Etiology of enostosis is unknown. Usually it is an asymptomatic lesion that is incidentally found but may become dynamic and change (ie. appear, disappear, grow, diminish in size). In its dynamic phase, it can produce increased uptake of radionuclide on bone scan. It may occur in any bone but the most frequently in the pelvic bones, the proximal femur, and the ribs. Histologic examination shows circumscribed foci of compact bone in the spongiosa.\n\nRadiologic findings: 1. single or multiple intraosseous sclerotic areas 2. alignment along the long axis of the trabecular architecture 3. homogeneous 4. usually negative bone scan (see above)\n\nClinical Manifestations: Usually asymptomatic\n\nDifferential Diagnosis: 1. enostosis, bone island 2. osteoblastic bone metastasis (should show uptake on bone scan; often multiple lesions) 3. fibrous dysplasia 4. liposclerosing myxofibrous tumor (a benign lesion, frequently located at the femoral neck) 5. sclerosing hemangioma of bone\n\nTreatment: \tno treatment necessary", "ACR Code": "4.9", "Category": "Anatomy, Normal Variant", "Keywords": "enostisbone islandprostatic cancer", "Reference": "Diagnosis of Bone and Joint Disorders by Resnick and Niwayama, 1988", "External Links": "TAMC, Internet tumor board" } }, { "U_id": "MPX2209", "TAC": [ "MPX2209_synpic18368" ], "MRI": [], "Case": { "Title": "Pancreatic Pseudocyst", "History": "18 year-old male with history of T cell lymphoma, common bile duct dysfunction, MRSA, and candida albicans sepsis, and recent distributive shock clinical picture presents with acute pancreatitis possibly secondary to L-asparaginase therapy.", "Exam": "Physical exam demonstrated increasing abdominal circumfrence and tenderness over a period of 1 week.", "Findings": "Upright abdominal plain film showing displacement of stomac and course of the Dobhoff feeding tube by a large, left paracentral, abdominal mass.\n\nAn axial CT image of upper abdomen without contrast demonstrates a fluid collection in the Lesser sac. note the dense, thin rim in the periphery representing the fibrous capsule. These findings are consistent with a pancreatic pseudocyst.", "Differential Diagnosis": "Pancreatic pseudocyst\nPancreatic abscess\nPancreatic necrosis with or without infection; \nPancreatic hemorrhage\nCystic Pancreatic Neoplasm", "Case Diagnosis": "Pancreatic Pseudocyst", "Diagnosis By": "Imaging findings and percutaneous catheter drainage", "Treatment & Follow Up": "In studies with sonography, pseudocysts were seen to resolve in 25 to 40% of patients. Pseudocysts that are greater than 5 cm in diameter and that persist for longer than 6 weeks should be considered for drainage. Recent natural history studies have suggested that noninterventional, expectant management is the best course in selected patients with minimal symptoms and no evidence of active alcohol use in whom the pseudocyst appears mature by radiography and does not resemble a cystic neoplasm. A significant number of these pseudocysts resolve spontaneously more than 6 weeks after their formation. Also, these studies demonstrate that large pseudocyst size is not an absolute indication for interventional therapy and that many peripancreatic fluid collections detected on CT in cases of acute pancreatitis resolve spontaneously. In patients who are stable and free of complications, and in whom serial ultrasound studies show that the pseudocyst is shrinking, conservative therapy is indicated. Conversely, if the pseudocyst is expanding and is complicated by rupture, hemorrhage, or abscess, the patient should be operated on. With ultrasound or CT guidance, sterile chronic pseudocysts can be treated safely with single or repeated needle aspiration or more prolonged catheter drainage with a success rate of 45 to 75%. The success rate of these techniques for infected pseudocysts is considerably less (40 to 50%). Patients who do not respond to drainage require surgical therapy for internal or external drainage of the cyst.", "Discussion": "On CT, pseudocysts are round or oval in shape, and have a relatively thin (1-2mm) symmetrical capsule and a fluidly content of <15 HU. They can vary significantly in size. Their circumferential capsule can later calcify, and they can dissect fascial planes traveling sometimes at great distances from the mediastinum to the lower pelvis. The detection of a cystic lesion with an even thick capsule containing peripheral or lumenal soft tissue nodules or septations is less consistent with a pseudocyst and more indicative of a neoplastic process with associated necrosis. When the attenuation values of the pseudocyst are slightly elevated, associated necrotic tissue or secondary infection should be suspected. Higher attenuation values of >40 to 50 HU are indicative of intracystic hemorrhage." }, "Topic": { "Title": "Pancreatic Pseudocyst", "Disease Discussion": "Pancreatic pseudocysts are non-epithelial lined cystic fluid collections that arise from disruption of a pancreatic duct, with leakage of amylase-rich pancreatic juice into the surrounding peripancreatic tissues. Pancreatic pseudocysts are one of four cystic lesions of the pancreas but accounts for 75% of all pancreatic cysts. The other three lesions include 1) benign and malignant cystic neoplasms (10%), 2) congenital cysts (5%), and 3) retention cysts (10%). Although pancreatic pseudocysts are the most common cystic lesion, neoplastic cysts must always be considered, particularly when contemplating nonsurgical treatment of a pancreatic cyst, since no diagnostic test or method is definitive or sensitive enough to distinguish the two.\n\n-Etiology and Pathogenesis: \nPseudocysts form after rupture of a pancreatic duct with extravasation of amylase-rich fluid and failure of reabsorption of this secretion. The extravasated fluid forms an encapsulated collection that is bound by surrounding viscera, that is, the stomach, spleen, liver, and transverse mesocolon. The fluid collections initially communicate with the ruptured pancreatic duct. Endoscopic studies have shown that pancreatic pseudocysts communicate with the pancreatic duct in 80% of cases. Pseudocysts are preceded by pancreatitis in 90% of cases and by trauma in 10%. Approximately 85% are located in the body or tail of the pancreas and 15% in the head. Some patients have two or more pseudocysts. Abdominal pain, with or without radiation to the back, is the usual presenting complaint. A palpable, tender mass may be found in the middle or left upper abdomen. The serum amylase level is elevated in 75% of patients at some point during their illness and may fluctuate markedly\n\n-Epidemiology: \nAxial imaging in acute pancreatitis has demonstrated peripancreatic fluid collections in as many as 80% of studies. Pseudocysts occur less frequently than do acute fluid collections and require more time to form with prevalence ranging from 5% to 70% depending on the severity of the attack and the depth of investigation. There is no gender preference. \n\n-Clinical Manifestations: \nPseudocysts usually require at least 4 or more weeks to evolve, following an episode of acute pancreatitis. However, the natural history and clinical relevance of pancreatic pseudocysts have been challenging due to lack of unified methods of dectection. Cysts have indeterminate age and most are stable on follow-up examinations. Symptomatic cysts may manifest as persistent abdominal pain with or without radiating to back, abdominal mass, gastric outlet obstruction, and biliary obstruction. Infection is suspected in septic patients and, unless air bubbles produced gas-forming bacteria are present, the diagnosis should be confirmed with FNA. A pseudocyst that does not resolve spontaneously may lead to serious complications, such as (1) pain caused by expansion of the lesion and pressure on other viscera, (2) rupture, (3) hemorrhage, and (4) abscess. Rupture of a pancreatic pseudocyst is a particularly serious complication. Shock almost always supervenes. Mortality rates range from 14%, if the rupture is not associated with hemorrhage, to over 60% if hemorrhage has occurred. Rupture and hemorrhage are the prime causes of death from pancreatic pseudocyst. A triad of findings: (1) increase in the size of the mass, (2) a localized bruit over the mass, and (3) a sudden decrease in hemoglobin level and hematocrit without obvious external blood loss, should alert one to the possibility of hemorrhage from a pseudocyst.\n\n-Treatment: \nIn studies with sonography, pseudocysts were seen to resolve in 25 to 40% of patients. Pseudocysts that are greater than 5 cm in diameter and that persist for longer than 6 weeks should be considered for drainage. Recent natural history studies have suggested that noninterventional, expectant management is the best course in selected patients with minimal symptoms and no evidence of active alcohol use in whom the pseudocyst appears mature by radiography and does not resemble a cystic neoplasm. A significant number of these pseudocysts resolve spontaneously more than 6 weeks after their formation. Also, these studies demonstrate that large pseudocyst size is not an absolute indication for interventional therapy and that many peripancreatic fluid collections detected on CT in cases of acute pancreatitis resolve spontaneously. In patients who are stable and free of complications, and in whom serial ultrasound studies show that the pseudocyst is shrinking, conservative therapy is indicated. Conversely, if the pseudocyst is expanding and is complicated by rupture, hemorrhage, or abscess, the patient should be operated on. With ultrasound or CT guidance, sterile chronic pseudocysts can be treated safely with single or repeated needle aspiration or more prolonged catheter drainage with a success rate of 45 to 75%. The success rate of these techniques for infected pseudocysts is considerably less (40 to 50%). Patients who do not respond to drainage require surgical therapy for internal or external drainage of the cyst.", "ACR Code": "7.2", "Category": "Inflammatory, NOS", "Keywords": "Pancreatic pseudocystsPeripancreatic fluid collection", "Reference": "1. Avram M. Cooperman. An overview of Pancreatic Pseudocysts. Surgical Clinics of North America, volume 81, number 2, April 2001\n2. Balthazar, Emil J. Complications of acute pancreatitis: clinical and CT evaluation. Radiologic Clinics of North America, volume 40, number 6, December 2002\n3. Harrison's Principles of Internal Medicine, 15th edition" } }, { "U_id": "MPX2216", "TAC": [ "MPX2216_synpic34291", "MPX2216_synpic34292", "MPX2216_synpic34293", "MPX2216_synpic34295" ], "MRI": [], "Case": { "Title": "Thyroid Ophthalmopathy", "History": "45 year old male with known Graves' disease referred to ophthamology for proptosis.", "Exam": "N/A", "Findings": "Non-enhanced axial CT image of the orbits demonstrates bilateral proptosis with enlargement of the medial rectus muscle bellies with sparing of the tendonous insertions. Coronal reformatted images demonstrate symmetric bilateral enlargement of the inferior, medial, superior, and to a lesser extent, lateral retus muscles. The retrobulbar fat and globes are unremarkable.", "Differential Diagnosis": "Graves' Ophthalmopathy\nPseudotumor\nLymphoma", "Case Diagnosis": "Thyroid Ophthalmopathy", "Diagnosis By": "Imaging characterisitcs (involvement of the muscle belly with sparing of the tendinous insertion, bilaterally symmetric) and correlation with the patient's known Graves' disease.", "Treatment & Follow Up": "Treatment depends upon severity of involvement. When indicated, medical management with steroids and artificial tears to maintain corneal moisture is typically employed.", "Discussion": "Please see factoid." }, "Topic": { "Title": "Thyroid Ophthalmopathy", "Disease Discussion": "Clinical: Proptosis secondary to swelling of extraocular muscles. A mild form is seen in young females and is associated with thyrotoxicosis. A severe form is seen in middle-aged women and men with Graves disease, demonstrating severe proptosis and ophthalmoplegia. \n\nPathology: \nInfiltration of muscles by lymphocytes, plasma cells, mast cells; deposition of mucopolysaccharides. \n\nImaging: \nhttp://www.smw.ch/docs/PdfContent/smw-12741.pdf\nCT and MR: Classically shows enlargement of extraocular muscles with sparing of tendinous attachments to the globe. Classic patterns include involvement of the inferior rectus and medial rectus muscles, followed by the lateral and superior rectus.\n\nhttp://bjr.birjournals.org/content/72/860/757.full.pdf\n\nIn 80% of patients, there is bilateral muscle involvement. In 10%, involvement of one isolated muscle is seen. There may be increased amount of retroglobar fat. Enhanced images will show moderate to marked enhancement of muscle bodies.", "ACR Code": "2.5", "Category": "Ophthalmology", "Keywords": "Graves diseasethyrotoxicosis", "Reference": "Harsnberger, Ric. Handbook of Head and Neck Imaging. St. Louis: Mosby, 1995.\n\nSmirniotopoulos, James. MedPix Topic Factoid Card 60.", "External Links": "www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001398/" } }, { "U_id": "MPX2215", "TAC": [ "MPX2215_synpic48402", "MPX2215_synpic48403" ], "MRI": [], "Case": { "Title": "Congenitally Corrected Transposition of the Great Vessels", "History": "A 63 year old lady is being evaluated for cirrhosis.", "Exam": "Non-contributory", "Findings": "CT Scout radiograph demonstrated mild enlargement of the cardiac silouhette with mild increase in pulmonary vascularity. There are calcification in the aorta.\n\nThe CT images reveal cardiac enlargement. The positions of the aorta and main pulmonary artery are transposed, with the aorta lying anterior and to the left of the main pulmonary artery. \n\nThe positions of the ventricles are also reversed, with the anatomic left ventricle lying directly behind the sternum and the trabeculated right ventricle posterior, forming the left heart border. \n\nThese findings are consistent with a congenitally corrected transposition of the great arteries.", "Differential Diagnosis": "\u2022 Congenitally corrected Transposition of Great Arteries\n\u2022 Ventricular noncompaction\n\u2022 Some other congenital heart disease", "Case Diagnosis": "Congenitally Corrected Transposition of the Great Vessels", "Diagnosis By": "Cardiology evaluation with echocardiography and cardiac MRI", "Treatment & Follow Up": "Surgery is recommended only for treatment of symptomatic lesions and only when significant hemodynamic benefit is expected. This woman has lived for six decades without significant cardiac symptoms." }, "Topic": { "Title": "Congenitally Corrected Transposition of the Great Vessels", "Disease Discussion": "Congenitally-corrected (Levo) transposition of the great vessels (TVG) is a complex abnormality comprising less than 1% of congential heart defects. It can be thought of as two anomalies that cancel each other out -- transposed great vessels and transposed ventricles.\n\nIn the more common (Dextro) variant of TGV, there is separation of systemic and pulmonary circulations, with the aorta arising from the right ventricle (RV) and the pulmonary trunk arising from the left ventricle (LV). An ASD or VSD is usually seen in association. \n\nIn congentially corrected TGV, the ventricles are transposed such that the right atrium connects to the left ventricle, and the left atrium to the right ventricle. The aorta arises from a morphologically appearing right ventricle (acting as a left ventricle) and carries oxygenated blood through the body. The pulmonary artery arises from a morphologically appearing left ventricle (acting as the right ventricle)and carries deoxygenated blood to the lungs.\n\nPeople affected with congenitally corrected TVG may be asymptomatic throughout life but most develop symptoms from associated conditions, including other morphological and conduction abnormalities that require intervention (such as VSD, LV outflow obstruction to the lungs, tricuspid valve regurgitation [valve is exposed to systemic pressures], and complete heart block.)", "ACR Code": "5.9", "Category": "Congenital, malformation", "Keywords": "TranspositionCorrectedVentricular Inversion", "Reference": "Lundstrom U, Bull C, Wyse RK, Somerville J. The natural and \"unnatural\" history of congenitally corrected transposition. Am J Cardiol. May 15 1990;65(18):1222-9.\n\nConnelly MS, Liu PP, Williams WG, et al. Congenitally corrected transposition of the great arteries in the adult: functional status and complications. J Am Coll Cardiol. Apr 1996;27(5):1238-43.\n\nhttp://emedicine.medscape.com/article/904528-overview", "External Links": "www.mayoclinic.org/corrected-transposition-great-arteries/about.html" } }, { "U_id": "MPX2224", "TAC": [ "MPX2224_synpic36031", "MPX2224_synpic36032" ], "MRI": [], "Case": { "Title": "Bipartite Patella", "History": "18 y/o man fell down the stairs. Now with right knee pain, localized to the patella. Pain is reported as constant and throbbing, increasing to 8-9/10 pain with weight bearing.", "Exam": "Right knee with mild-moderate edema compared to left. Significant tenderness to palpation over entire knee, worse lateral to patella. Pt able to bear weight on right leg with difficulty.", "Findings": "\u2022 Rounded bony fragment at superolateral aspect.\n\u2022 Wide well-defined radiolucent line.\n\u2022 Smooth, well-corticated, opposing margins.\n\u2022 No sharp fracture fragments or intra-articular loose bodies.\n\u2022 No evidence of suprapatellar effusion.", "Differential Diagnosis": "\u2022 Bipartite patella, incidental\n\u2022 Bipartite patella, symptomatic\n\u2022 Patellar fracture\n\u2022 Dorsal defect of the patella", "Case Diagnosis": "Bipartite Patella", "Diagnosis By": "Imaging", "Treatment & Follow Up": "No treatment or follow-up required.", "Discussion": "Bipartite patella (BP) is typically an incidental finding, with only 2% being symptomatic. Symptomatic BP is usually associated with chronic stress injury, although there are reported cases of symptomatic BP following injury. If the patient continues to have clinical tenderness over his superolateral pole for >3 months, surgery should be considered." }, "Topic": { "Title": "Multipartite Patella", "Disease Discussion": "Name: Multipartite Patella\n\nSubclassifications: Tripartite, Bipartite\n\nDemographics: 2% incidence. 9:1 Male-to-female ratio. Unilateral in 57%.\n\nCommon Locations: 75% superolateral (Saupe classification type 3)\n\nRadiology: Well-defined radiolucent line coursing across typically superolateral corner with smooth, well-corticated margins.\n\n99mTc bone scan would show increased uptake.\nBut high scintigraphic uptake is a frequent finding in both symptomatic and asymptomatic bipartite patella.\n\nComments: Typically asymptomatic, incidental finding. Should not be confused with a patellar fracture.\n\nOssification occurs between ages 2-6 years.\n23% of children have >1 ossification center.\nTypically merge, but un-united in 2% of people.", "ACR Code": "4.1", "Category": "Anatomy, Normal Variant", "Keywords": "MultipartiteBipartitePatella, kneecap", "Reference": "Elias DA, White LM. Imaging of patellofemoral disorders. Clin Radiol. 2004 Jul;59(7):543-57." } }, { "U_id": "MPX2230", "TAC": [ "MPX2230_synpic18503" ], "MRI": [], "Case": { "Title": "Juvenile Angiofibroma, Nasal", "History": "14-year-old American Samoan male who presents with a history of epistaxis and expansile right facial mass.", "Exam": "Nasal exam: A mass completely occludes the right naris and is apparent in the right nasal vestibule. Fiberoptic endoscopy of the left naris reveals that the lesion also extends into the posterior left nasal passage. The septum is also mildly deviated to the left. The nasopharyngoscope was unable to be manipulated posterior to this lesion. The mass appears extremely hypervascular in nature. Oral exam reveals no loose dentition. There is firmness noted within the right buccal space. There is also noted some mild fullness in the soft palate with poor palatal elevation. The gag reflex is intact, however. The remaining intraoral mucosa appears normal. Palpation over the right cheek reveals a soft, fluctuant mass extending through the maxillary sinus wall and over the ramus of the mandible. The skin is intact. The lesion is nontender to palpation.", "Findings": "1. Large hypervascular mass, measuring 9 cm in its greatest\nlongitudinal dimension, which is situated in the region of the right\nmaxillary sinus, with extensive extension to surrounding regions, to include\nbony destruction of the right pterygoid, tumor extension to the lateral\naspect of the right mandible, via the right infratemporal fossa, bony\ndestructive changes of the right base of the skull, to involve the foramen\novale and rotundum, with intracranial extension on the right into the right\ncavernous sinus. \n 2. Enlarged right cervical chain lymph nodes at both levels I and II\nmay represent inflammatory enlargement or metastatic disease. There is tumor\nextension to involve the right cavernous carotid, cranial nerves VII and III,\nas well as expansion of the vidian canal, with likely involvement of the\ngreater petrousal nerve. \n 3. Bony destruction of the right maxilla and skull base, are also\npresent.\n 4. The most likely etiology of this tumor is a juvenile nasal\nangiofibroma. Other considerations would include a sarcoma or possibly a\nmeningioma.", "Differential Diagnosis": "-Juvenile nasal angiofibroma\n-Sarcoma\n-Meningioma", "Case Diagnosis": "Juvenile Angiofibroma, Nasal" }, "Topic": { "Title": "Juvenile Angiofibroma, Nasal", "Disease Discussion": "Juvenile Angiofibroma, vascular, unencapsulated, polypoid, locally aggressive yet histologically benign, almost exclusively males [\"women\" should have a chromosomal analysis], 10-18 yo, epistaxis, nasal obstruction, \nPTERYGOPALATINE FOSSA in 89% of cases, anterior bowing of posterior maxillary antral wall AND 99% of cases of ant. antral bowing are caused by angiofibromas, sphenoid involved in 61% (through roof of nasopharynx), 35% involve ethmoid, 5-20% extend intracranial usu middle fossa. (also sphenopalatine)\n\nHighly vascular, fed by internal max or ascending pharyngeal\n\nTREATMENT by embo, resection, 30-35 Gy radiation produces 78% control\n\nMale w/nasal mass, epistaxis, benign, from post/lat nasal wall near SPHENOPALATINE FORAMEN (SPF). Usually extends through the SPF into the PTERYGOPALATINE Fossa, then into PTERYGOPALATINE FORAMEN, nasopharynx, vidian canal and f. rotundum into middle fossa, laterally through PTERYGOMAIXLLARY FISSURE into INFRATEMPORAL FOSSA (masticator space)\nMR - multiple flow voids", "ACR Code": "2.3", "Category": "Neoplasm, non-CNS", "Keywords": "angiofibromapterygopalatine" } }, { "U_id": "MPX2228", "TAC": [ "MPX2228_synpic15174" ], "MRI": [], "Case": { "Title": "Pulmonary Embolism", "History": "42 y/o AAM with hx/of LLE DVT, presents to ER with acute shortness of breath and chest pain", "Exam": "VS: BP-140/90 HR-103 RR-22 SpO2-94% Tc-98.7F Gen- middle aged obese male, in mild distress; Cardiac- tachycardic, no appreciable m/r/g; Pulm- tachypnic, slightly diminished breath sounds bilaterally with bibasilar coarse breath sounds; Abd- non-distended, mild TTP LLQ, NABS; Extr- (+) LLE mild edema with thigh pain, pulses intact throughout", "Findings": "CXR- bilateral small pleural effusions,no Westermark\u2019s sign or Hampton\u2019s hump. There may be slight evidence of acute PAH with enlarged PA's on lateral view.\n\nSpiral Chest CT demonstrating bilateral filling defects found in the right and left pulmonary arteries.\n\nUS of L common femoral vein and artery show decreased compressibility of vein with highly diminished blood flow.", "Differential Diagnosis": "Pulmonary Embolism\nOld PE with other pulmonary or cardiac etiologies of the patient\u2019s pain: MI, Pericarditis, Esophageal rupture, Pneumonia, Pneumothorax, Asthma, COPD\nHowever, these other possibilities on the differential were not supported by ECG, CT, or the patient\u2019s clinical presentation/history", "Case Diagnosis": "Pulmonary Embolism", "Treatment & Follow Up": "The pt had supplemental oxygen and 2 large bore IVs started. He was admitted to the hospital and started on anticoagulation with heparin. Even though the clots were rather large, t-PA was not started secondary to the patient being hemodynamically stable after initial resuscitation and without any signs of right heart strain. Due to the pt\u2019s history of the LLE DVT and the current bilateral PEs, in spite of therapeutic coumadin levels, a Greenfield filter was placed in the IVC." }, "Topic": { "Title": "Pulmonary Embolism", "Disease Discussion": "The diagnostic approach and treatment for pulmonary embolism continues to be an evolving and controversial area in medicine. Current recommendations are based on numerous studies, such as the PIOPED study. Imaging modalities vary and can be situation or institution dependent. The initial work-up for a pt suspected of having a pulmonary embolism involves a CXR in order to rule out other pulmonary or cardiac findings, such as a pneumothorax, pneumonia, or rib fracture. If the CXR is non diagnostic, other imaging modalities include V/Q scan, helical CT with PE protocol, pulmonary angiography, echocardiography, or venous US of the lower extremities. The gold standard is generally thought to be pulmonary angiography. There are advantages and disadvantages to each modality. CXR is rarely diagnostic of PE, nor does it often show the classic findings (Hampton\u2019s hump, Westermark\u2019s sign). However, it can be useful for ruling out other pathology. The most common findings on CXR in pt\u2019s with PE include atelectasis, pleural effusions, infiltrates, and elevation of the hemidaphragm. V/Q scans also are rarely diagnostic. The scans can be difficult to interpret and often meaningless if there is other underlying pulmonary pathology. Additionally, the diagnosis of PE was highly dependent on the clinical suspicion of the physician. More recently, helical CT has been used to aid in diagnosing PE. Disadvantages include poor visualization of the periphery of the lungs at the subsegmental level. The main advantage is the relative ease of the procedure and the decreased variable of reader interpretation (when compared to V/Q scans). As previously stated, pulmonary angiography continues to be the gold standard for diagnosing pulmonary emboli. However, these studies are slightly more invasive than other modalities and can carry up to a 0.5% risk of mortality.", "ACR Code": "68.721", "Category": "Unsure", "Keywords": "PulmonaryEmbolism", "Reference": "Pulmonary Thromboembolism, Samuel Z. Goldhaber, Harrison\u2019s Principles of Internal Medicine, 14th edition, 1998, 1469-72. Plantz, Scott H., Emergency Medicine, Williams & Wilkins, 1998, 118-122. \n\nUpToDate, ATS Guidelines: The diagnostic approach to acute venous thrombembolism" } }, { "U_id": "MPX2233", "TAC": [ "MPX2233_synpic17324" ], "MRI": [], "Case": { "Title": "Congenital Lobar Emphysema- Radiographic findings", "History": "2wk old male with respiratory distress", "Exam": "Progressive respiratory distress/tachypnea/ cyanosis/ wheezing/ decreased breath sounds on left", "Findings": "Hyperlucent lobe(s)- with oligemia\nIncreased lobar opacity (rare) in newborn due to retained fetal lung fluid \nCompression atelectasis of adjacent parenchyma \nContralateral mediastinal shift", "Differential Diagnosis": "Pneumothorax \nAtelectasis with compensatory hyperinflation \nPneumatocele \nCyst \nDiaphragmatic hernia \nCystic adenomatoid malformation \nForeign body", "Case Diagnosis": "Congenital Lobar Emphysema- Radiographic findings", "Treatment & Follow Up": "The appropriate treatment of CLE in newborns with respiratory distress is surgical resection of the affected lobe. Conservative management is reasonable in infants who have no or minimal symptoms.\nThis case was treated with surgical resection." }, "Topic": { "Title": "Congenital Lobar Emphysema", "Disease Discussion": "Congenital lobar emphysema (CLE) is a developmental anomaly of the lower respiratory tract that is characterized by hyperinflation of one or more of the pulmonary lobes. CLE is a rare congenital malformation. It was diagnosed in 10 of 70 patients with congenital malformations of the lung seen from 1970 to 1995 at Children's National Medical Center in Washington, DC. Depending upon the pattern of referrals, other tertiary medical centers may treat one or two cases per year. Males appear to be affected more than females, in a ratio of 3:1. The reason for the male predominance is unknown. Progressive lobar hyperinflation is likely the final common pathway that results from a variety of disruptions in bronchopulmonary development. These result from abnormal interactions between embryonic endodermal and mesodermal components of the lung. Disturbances may lead to changes in the number of airways or alveoli or alveolar size. However, a definitive causative agent cannot be identified in approximately 50 percent of cases. The most frequently identified cause of CLE is obstruction of the developing airway, which occurs in 25 percent of cases. Airway obstruction can be intrinsic or extrinsic, with the former more common. This leads to the creation of a \"ball-valve\" mechanism in which a greater volume of air enters the affected lobe during inspiration than leaves during expiration, producing air trapping.\nIntrinsic obstruction often is caused by defects in the bronchial wall, such as deficiency of bronchial cartilage. This results in airway collapse during expiration. Intraluminal obstruction caused by meconium or mucous plugs, granulomas, or mucosal folds can cause partial obstruction of a lower airway. Extrinsic compression may be caused by vascular anomalies, such as a pulmonary artery sling or anomalous pulmonary venous return, or intrathoracic masses, such as foregut cysts and teratomas. CLE is characterized by overdistention of one or more lobes of the lung. This leads to compression of the remaining lung tissue and herniation of the affected lobe across the anterior mediastinum into the opposite chest, causing displacement of the mediastinum. The different pulmonary lobes are variably affected by CLE. The left upper lobe is affected most often (40 to 50 percent of cases). The distribution in right middle, right upper, and lower lobes is 25 to 35, 20, and 2 to 10 percent, respectively. CLE affecting multiple lobes is rare.", "ACR Code": "6.1", "Category": "Congenital, malformation", "Keywords": "congenitallobaremphysema", "Reference": "www.uptodate.com\nGrainger & Allison's Diagnostic Radiology: A Textbook of Medical Imaging, 4th Ed., Copyright \u00a9 2001 Churchill Livingstone, Inc." } }, { "U_id": "MPX2229", "TAC": [ "MPX2229_synpic28529", "MPX2229_synpic28530", "MPX2229_synpic28531", "MPX2229_synpic28532", "MPX2229_synpic28533", "MPX2229_synpic28534", "MPX2229_synpic28536" ], "MRI": [], "Case": { "Title": "Pulmonary Sequestration", "History": "54 year old male with a right lower lobe mass seen on virtual colonoscopy.", "Exam": "N/A", "Findings": "Non-enhanced virtual colonoscopy images demonstrate a soft tissue density mass within the right lower lobe.\n\nIntravenous contrast enhanced CT of the chest demonstrates a well-defined mass within the right lower lobe with an arterial supply arising from the abdominal aorta. Lung window images demonstrate no air-filled bronchi within the mass.\n\n3D reconstructed image from the Vitrea workstation demonstrates the mass within the right lower lobe adjacent to the right hemi-diaphragm.", "Differential Diagnosis": "Pulmonary sequestration \nNecrotizing pneumonia \nBronchogenic cyst \nDiaphragmatic hernia \nRounded atelectasis \nNeurogenic tumor", "Case Diagnosis": "Pulmonary Sequestration", "Diagnosis By": "Contrast enhanced CT of the chest with multiplanar reformatation showing the arterial supply from the abdominal aorta", "Treatment & Follow Up": "As the patient was asymptomatic, no treatment was indicated.", "Discussion": "Please see factoid." }, "Topic": { "Title": "Pulmonary Sequestration", "Disease Discussion": "Pulmonary sequestrations are masses of pulmonary parenchyma which do not communicate with the central airways through a normal bronchial connection, if at all. In addition, their blood supply is from the systemic circulation. Demonstrating the feeding systemic arterial vessels is the key point in differentiating sequestrations from bronchogenic cysts, lobar atelectasis or other abnormalities. \n\nExtralobar sequestrations are congenital in origin and contain their own pleural covering. Most (over 90%) are left-sided and associated congenital anomalies, such as congenital diaphragmatic hernias and congenital heart disease, are frequent. The venous return is through the systemic circulation. These may not only be seen adjacent to the mediastinum, but also in the mediastinum, pericardium, diaphragm, and retroperitoneum. Rarely is a connection with the bronchial tree present and rarely are they symptomatic. A majority of these are noticed incidentally.\n\nIntralobar sequestrations are located within the lung and have no separate pleural coverings. Although their arterial supply is systemic, their venous return is through pulmonary veins. Compared to the extralobar form, intralobar sequestrations are likely acquired lesions, possibly due to chronic bronchial obstruction or postobstructive pneumonia. Connection to the bronchial tree may be present. This variety may produce symptoms as a result of infections.", "ACR Code": "6.9", "Category": "Congenital, malformation", "Keywords": "pulmonary sequestration", "Reference": "Hansell, D., et al. Imaging of Diseases of the Chest, 4th Ed. Mosby 2005." } }, { "U_id": "MPX2235", "TAC": [ "MPX2235_synpic20144" ], "MRI": [], "Case": { "Title": "Retroperitoneal Fibrosis", "History": "69 y/o man with abdominal pain, rule out stone.", "Findings": "Bilateral ureteral dilation. Soft tissue thickening anterior to the sacrum.", "Differential Diagnosis": "Retroperitoneal fibrosis\nRadiation fibrosis\nLymphoma\nSarcoma", "Case Diagnosis": "Retroperitoneal Fibrosis" }, "Topic": { "Title": "Retroperitoneal Fibrosis", "Disease Discussion": "Retroperitoneal fibrosis is a fibrotic process of the retroperitoneum which can lead to ureteral narrowing and obstruction. Between 50 and 70 of the time there is no identifiable cause (Idiopathic retroperitoneal fibrosis of Ormond's disease). Other causes include inflammation from adjacent organs (diverticulitis, appendicitis), aortic aneurysm, retroperitoneal metastases, abscesses, radiation, or drugs (methylsergide, hydralazine, ergotamines). Idiopathic retroperitoneal fibrosis is often associated with inflammatory bowel disease, sclerosing cholangitis, or fibrosing mediastinitis.\n\nRadiographically retroperitoneal fibrosis can appear as a soft tissue mass around the aorta and/or the inferior vena cava. It can cause extrensic compression and medial deviation of the ureters. Typically it will affect the left ureter before it affects the right ureter. It can occur any where from the bladder to the UPJ, but most often occurs at L3-L5 level. Late findings include functional ureteral obstruction, and compression of the inferior vena cava or aorta.", "ACR Code": "8.2", "Category": "Idiopathic or Unknown", "Keywords": "Retroperitonal Fibrosis", "Reference": "Genitourinary Radiology, The Requisites. Ronald Zagoria.\nPrime of Diagnostic Imaging. Ralph Weissleder." } }, { "U_id": "MPX2242", "TAC": [ "MPX2242_synpic38162", "MPX2242_synpic38163", "MPX2242_synpic38165", "MPX2242_synpic38166" ], "MRI": [], "Case": { "Title": "Pulmonary embolism", "History": "86 y/o woman with shortness of breath", "Exam": "Tachypnea and tachycardia", "Findings": "Multiple filling defects in the right and left pulmonary arteries (lower lobes) consistent with pulmonary embolism.", "Differential Diagnosis": "\u2022 Thromboemboli\n\u2022 Tumor emboli\n\u2022 Septic emboli", "Case Diagnosis": "Pulmonary embolism", "Diagnosis By": "CT angiography" }, "Topic": { "Title": "Pulmonary embolism", "Disease Discussion": "Pulmonary Embolism: \n\nClinical presentation for pulmonary embolism is variable and symptoms/signs are overall nonspecific. Symptoms include dyspnea, pleuritic chest pain, tachypnea, tachycardia, hemoptysis, cough. \n\nEKG, pO2, A-a gradient abnormalities are also nonspecific. D-dimer (if negative) is useful in low clinical probability patients to exclude PE. A positive D-dimer is nonspecific and has many causes (surgery, pregnancy, cancer, etc). \n\nCXR can be normal in setting of PE. Abnormalities, however, are common and include atelectasis, parenchymal infiltrate, pleural effusion, or diaphragm elevation. Westermark\u2019s sign (oligemia) and Hamptom\u2019s hump (infarct) are uncommonly seen. In addition, a CXR can exclude other potential etiologies of patient's symptoms: like pneumonia, pneumothorax, CHF or rib fracture. Also, it is essential for correlation to the V/Q scan. \n\nRisk factors for pulmonary embolism include: recent surgery or prolonged immobilization, cancer, pelvis/lower extremity trauma or surgery, pregnancy, estrogens, coagulopathy, others. \n\nWith improvement in technology, CT angiography is now the standard evaluation tool for the diagnosis of pulmonary embolism. However, to date Ventilation/Perfusion scintigraphy still has a role in the evaluation of PE. (although it has been limited by advances/improvements of CT angiography)", "ACR Code": "6.7", "Category": "Vascular", "Keywords": "pulmonary embolismpulmonary thromboembolismPE", "Reference": "1. Muller NL, Fraser RS, Colman NC, Par PD. Radiologic diagnosis of diseases of the chest, 1st ed. Philadelphia, Sauders, 2001;378-409. \n\n2. Garg K. CT of pulmonary thromboembolic disease. Radiol Clinic North Am 2002;40:111-122." } }, { "U_id": "MPX2246", "TAC": [ "MPX2246_synpic48550" ], "MRI": [], "Case": { "Title": "Acute ischemic stroke", "History": "82-year-old woman with history of significant coronary and peripheral artery disease with sudden onset of headache and left-sided weakness during a peripheral arterial interventional procedure in the cardiology catheterization lab.", "Exam": "Patient presented with acute onset of headache and left-sided weakness.", "Findings": "Stroke protocol consisted of noncontrast head CT, CT perfusion mapping, and CTA of the head and neck.\n\nInitial noncontrast head CT scan demonstrated no evidence of intracranial hemorrhage. No dense middle cerebral artery sign or evidence of loss of gray and white matter differentiation. There was subtle asymmetry of right parietal sulci compared to left.\n\nCT perfusion demonstrated abnormally prolonged MTT (mean transit time), in a wedge-shaped configuration, involving the distal M3 distribution of the right MCA in the right posterior parietal lobe and posterior frontal lobe. \n\nCerebral blow flow (rCBF) in these two regions was also mildly diminished. \n\nCerebral blood volume (rCBV) in these two regions was relatively normal; however, within the centers of the two wedge-shaped areas of abnormal perfusion there were small areas of decreased blood volume. The summary tissue at risk map indicates a small region of core infarct with a larger region of penumbra. \n\nCT angiogram of the neck and head demonstrated no proximal occlusion to the anterior or posterior circulation. \n\nMRI performed 6 days later demonstrates subacute infarct in the region of ischemia noted acutely with increased flair and diffusion-weighted signal in the area of interest.", "Differential Diagnosis": "Ischemic stroke\nVasculitis", "Case Diagnosis": "Acute ischemic stroke", "Diagnosis By": "CT perfusion imaging coupled with history", "Treatment & Follow Up": "Due to the peripheral position of the perfusion defects and absence of a proximal occlusion on CTA (not shown), it was elected to treat with intravenous tPA rather than intraarterial intervention. Additional considerations included patient\u2019s multiple comorbidities and multiple recent arteriotomies with complicated access.\n\nAt the time of her second head CT her symptoms consisted of left facial droop, left hemineglect and left pronator drift. Her neurologic symptoms neither improved nor worsened with IV tPA." }, "Topic": { "Title": "Acute ischemic stroke, CT perfusion imaging", "Disease Discussion": "Neuroimaging continues to be an important aspect of acute stroke management as it guides appropriate treatment decisions. Noncontrast CT scan rules out hemorrhagic stroke immediately, but CT has poor sensitivity for demonstrating acute ischemic strokes. However, more advanced neuroimaging, to include MRI with diffusion weighting has been used to better identify acute infarct. Additionally, CT and MR perfusion imaging are able to detect early hemodynamic changes associated with ischemia and infarction. Perfusion imaging can be useful to differentiate between potential salvageable ischemic tissue and tissue infarction. This has many treatment implications, to include identification of patients amenable to catheter-directed therapies such as intraarterial thrombolysis and mechanical thrombectomy, even if the patient is outside the accepted 3-hour time window for IV thrombolysis.\n Measurements for brain perfusion include mean transit time (MTT), cerebral blood volume (CBV), and cerebral blood flow (CBF). For CT Perfusion, a tissue-at-risk map can be generated from these perfusion maps based on minimum threshold values for CBV and CBF to maintain brain viability. Regions of increased MTT and mildly decreased CBF represent the penumbra and therefore are at risk for infarction. Due to autoregulation and collateralization, CBV is usually last to be affected by ischemic events and the CBV is maintained as normal or slightly increased. However, infarction is characterized by increased MTT coupled with significantly decreased CBF and CBV. Identifying the penumbra is important as this area is potentially salvageable with prompt therapeutic intervention.", "ACR Code": "1.7", "Category": "Infarction and/or Necrosis", "Keywords": "CT cerebral perfusion" } }, { "U_id": "MPX2244", "TAC": [ "MPX2244_synpic21443", "MPX2244_synpic21446" ], "MRI": [], "Case": { "Title": "Pyogenic liver abscess (subcapsular)", "History": "40 year old man airevaced from micronesia island to Tripler Medical Center with fevers and abdominal pain lasting for approximately three weeks.", "Exam": "Leukocytosis", "Findings": "Axial CT images throught the liver demonstrate low density region within the liver which subcapsular in location. One of the images has a small pocket of air differentiated this fluid collection from a simple hematoma.\nThere are bilateral pleural effusions seconary to diaphragmatic irritation.", "Differential Diagnosis": "Pyogenic abscess\nAmoebic abscess\nHematoma", "Case Diagnosis": "Pyogenic liver abscess (subcapsular)", "Diagnosis By": "Cultures obtained during percutaneous drainage", "Treatment & Follow Up": "The patient was placed on broad spectrum antibiotics. the abscess was percutanously drained. Patient recovered over the coarse of several weeks on IV antibiotcs without complications." }, "Topic": { "Title": "Pyogenic liver abscess", "Disease Discussion": "Infections of the biliary tract are the most common identifiable source of liver abscess. Infection of the liver may occur via the bile duct, along a penetrating vessel, or from an adjacent septic focus. Less commonly, liver abscess is a complication of bacteremia arising from underlying abdominal disease, such as diverticulitis, perforated or penetrating peptic ulcer, gastrointestinal malignancy, inflammatory bowel disease, or peritonitis, or rarely from bacterial endocarditis. Occasionally, a pyogenic liver abscess may be the presentation of a hepatocellular or gallbladder carcinoma or a complication of chemoembolization of a hepatic neoplasm. In approximately 40% of cases, no obvious source of infection can be identified. The most frequently isolated organisms are Escherichia coli and Klebsiella, Proteus, Pseudomonas, and Streptococcus species, particularly Streptococcus milleri. Most are polymicrobial. With improved culture methods and earlier diagnosis, the number of cases identified as being caused by anaerobic organisms has also increased. In the past, patients typically presented with acute spiking fevers, right upper quadrant pain, and often shock. Since the introduction of antibiotics, the presentation has become less acute, and is often insidious. The presentation is characterized by malaise, low-grade fever, weight loss, and dull abdominal pain that may increase with movement. Symptoms may be present for 1 month or more before a diagnosis is made. Multiple abscesses are typical when biliary disease is the source and are associated with a more acute systemic presentation, often with sepsis and shock. Solitary abscesses tend to present more insidiously. When an abscess is situated near the dome of the liver, pain may be referred to the right shoulder, or a cough may be present resulting from diaphragmatic irritation or atelectasis.", "ACR Code": "-1.-1", "Category": "Unsure", "Keywords": "abscess", "Reference": "1. Chung RT, Friedman LS. \u201cLiver Abscess and Bacterial, Parasitic, Fungal, and Granulomatous Liver Disease\u201d Chapter 69 from Feldman: Sleisenger & Fordtran\u2019s Gastrointestinal and Liver Disease, 7th ed. Elsevier: 2002, pg 1343-1346.\n\n2. Meyers WC, Kim RD. \u201cPyogenic and Amebic Liver Abscess\u201d from Townsend: Sabiston Textbook of Surgery, 16th ed., W. B. Saunders Company: 2001. pg. 1044-1052.\n\n3. Alvarez P?rez JA. \u201cClinical course, treatment, and multivariate analysis of risk factors for pyogenic liver abscess\u201d Am J Surg. 01-FEB-2001; 181(2): pg. 177-186." } }, { "U_id": "MPX2255", "TAC": [ "MPX2255_synpic19025" ], "MRI": [], "Case": { "Title": "Celiac Artery Aneurysm", "History": "65 year old male presents to the primary care clinic with several weeks of vague abdominal pain, sometimes felt to increase with meals.", "Exam": "Labs: Within Normal Limits.\nExam: Normal abdominal exam. No significant tenderness to palpation despite patient report of persistent symptoms. Stool is heme negative.", "Findings": "Axial and reconstructed sagittal contrast enhanced CT of the abdomen demonstrates focal proximal fusiform dilatation of the celiac artery with partially occluding soft tissue density intraluminal thrombus.", "Differential Diagnosis": "Celiac Artery Aneurysm\n- Atherosclerotic\n- Traumatic\n- Mycotic / Infectious\n- Inflammatory", "Case Diagnosis": "Celiac Artery Aneurysm", "Diagnosis By": "With no history of trauma or evidence of infection, atherosclerotic etiology is felt to be most likely.", "Treatment & Follow Up": "Patient was referred for same day Vascular Surgery consultation.", "Discussion": "Celiac artery aneurysms are usually caused by atherosclerosis. Infection and trauma are also reported etiologies. While these aneurysms are considered quite rare, they may present with vague abdominal pain, as in this case, or merely as an incidental finding. In most cases surgery is the desired treatment to avoid rupture or thrombosis. \n\nReference: \nValji K. Vascular and Interventional Radiology. WB Saunders, 1999: 199-200." }, "Topic": { "Title": "Celiac Artery Aneurysm", "Disease Discussion": "Celiac artery aneurysms are usually caused by atherosclerosis. Infection and trauma are also reported etiologies. While these aneurysms are considered quite rare, they may present with vague abdominal pain, as in this case, or merely as an incidental finding. In most cases surgery is the desired treatment to avoid rupture or thrombosis.", "ACR Code": "9.9", "Category": "Aneurysm", "Keywords": "Celiac ArteryCeliac Aneurysm", "Reference": "Valji K. Vascular and Interventional Radiology. WB Saunders, 1999: 199-200." } }, { "U_id": "MPX2258", "TAC": [ "MPX2258_synpic42061" ], "MRI": [], "Case": { "Title": "Atlas fracture", "History": "20 y/o male ejected from a vehicle during a rollover crash. The patient reports a brief loss of consciousness.", "Exam": "His Glasgow Coma Score (GCS) was 15 when initially evaluated. Exam notable for multiple facial abrasions and contusions. There were no focal neurologic deficits.", "Findings": "Minimally displaced fracture of the Right lateral mass of the Atlas (first cervical vertabra).", "Differential Diagnosis": "\u2022 Atlas fracture\n\u2022 Transverse ligament injury", "Case Diagnosis": "Atlas fracture", "Diagnosis By": "computed tomography", "Treatment & Follow Up": "The patient was placed in a cervical spine orthos and scheduled for follow-up imaging in six weeks.", "Discussion": "Given the stability of the fracture and the lack of neurologic findings, conservative management was appropriate." }, "Topic": { "Title": "Atlas fracture", "Disease Discussion": "Synonyms: Jefferson fracture, burst fracture\n\nAssociations/Predisposing Factors: motor vehicle crashes, sports injury (e.g. football), falls, violence\n\nCommon Locations: posterior arch, lateral mass, bilateral anterior and posterior arches (burst or Jefferson fracture).\n\nDemographics: The majority of spinal fractures and dislocations occur in the cervical spine due to its mobility. The incidence is 25,000. Atlas fractures represent 10% or cervical spine injuries and 2% or all spine injuries. Most cervical spine injuries occur in males age 15-24. \n\nRadiology: Atlas pathology can be detected by plain film images, especially with the odontoid, or open-mouth, view where lateral displacement of greater than 6.9mm is indicative of a fracture. However, this modality has low sensitivity so diagnosis is facilitated by computed tomography(CT). Magnetic resonance imagine (MRI) is indicated for investigating soft tissue injury, such as when ligamentous disruption is suspected or when there are neurologic deficits. Arteriography may be necessary to evaluate vascular injury.\n\nPrognosis and Treatment: Isolated posterior arch and non- or minimally-displaced Jefferson fractures are considered stable. Treatment is a rigid cervical collar for 8-12 weeks with follow-up imaging to re-evaluate stability. The patient is expected to resume normal activity once the fracture has healed. Any fracture where the lateral mass is displaced 7mm or more is considered unstable. This requires halo traction for 3-6 weeks followed by further immobilization with a halo vest until stability is confirmed. Even with an unstable fracture, the prognosis is favorable provided that there are no other associated injures (such as neurologic insults).", "ACR Code": "3.4", "Category": "Trauma", "Keywords": "AtlasJeffersonburst", "Reference": "1) Campbell\u2019s Operative Orthopaedics, 10th ed. \n2) Waseem, M. A 4-year-old who fell from the slide; J Urgent Care Med; Feb 2008. \n3) Jefferson, G. Fracture of the atlas vertebra: report and four cases, and a review of those previously recorded. British J of Surg, London, 1920, 7:407-2.\n4) Braddom\u2019s Physical Medicine & Rehabilitation, 3rd ed.\n5) Vaccaro et al. Diagnosis and Management of Sacral Spines Fractures. J of Bone and Joint Surg. 2004:86(1) 166-75.\n6) eMedicine.com: C-1 fractures, Cervical Spine Acute Boney Injury" } }, { "U_id": "MPX2257", "TAC": [ "MPX2257_synpic25203", "MPX2257_synpic25204" ], "MRI": [ "MPX2257_synpic25199", "MPX2257_synpic25200", "MPX2257_synpic25201", "MPX2257_synpic25202" ], "Case": { "Title": "jugular foramen mass (unknown; patient underwent surgery and we are awaiting the results of pathologic evaluation)", "History": "26 year-old man, detailed history withheld", "Exam": "N/C", "Findings": "Multiple MR images demonstrate a dumb-bell-shaped mass at the level of the left jugular foramen, fairly isointense to brain on both T1 and T2 weighted images, which demonstrate homogeneous enhancement on T1-weighted images obtained after the IV administration of gadolinium-DTPA contrast material. It has mass effect on the underlying medulla. It also has thickened, enhancing, \"dural tail.\"\n\nNon-contrast CT images demonstrate fairly diffuse calcification throughout the mass.", "Differential Diagnosis": "meningioma\nnerve sheath tumor (schwannoma)\nless likely:\nparaganglioma\nmetastatic disease\nlymphoma", "Case Diagnosis": "jugular foramen mass (unknown; patient underwent surgery and we are awaiting the results of pathologic evaluation)", "Diagnosis By": "surgical resection" }, "Topic": { "Title": "jugular foramen mass", "Disease Discussion": "Differential diagnosis of a mass at the level of the jugular foramen includes:\nNon-neoplastic processes such as:\n Large jugular bulb, which is a normal variant\n Jugular vein thrombosis\n Osteomyelitis\n Malignant external otitis\nNeoplasms such as:\n Paraganglioma\n Metastasis\n Lymphoma\n Meningioma\n Schwannoma\n Neurofibroma\n Epidermoid tumor\nAs one can see, there's some overlap with the tumor diagnosis with the standard differential diagnosis for cerebellopontine angle masses. (1)\n\nThis case most likely represents a meningioma. It has MR signal characteristics similar to that of brain parenchyma, enhances homogeneously (with a dural tail, which is non-specific but has been associated with meningiomas), and has evidence of calcifications on non-contrast CT. (3) It could also potentially be a schwannoma/nerve sheath tumor. (2) It does not have the characteristic flow-related signal void of a paraganglioma, which tends to be very vascular. This patient's young age, with no significant past medical history, makes metastatic disease and lymphoma very remote possibilities.", "ACR Code": "1.3", "Category": "Neoplasm, NOS", "Keywords": "jugular foramen massmeningioma", "Reference": "1. Osborn AG. Diagnostic Neuroradiology. Mosby, Inc. 1994.\n\n2. Eldevik OP, Gabrielsen TO, Jacobsen EA. Imaging findings in schwannomas of the jugular foramen. AJNR Am J Neuroradiol. 2000 Jun-Jul;21(6):1139-44.\n \n3. Macdonald AJ, Salzman KL, Harnsberger HR, Gilbert E, Shelton C. Primary jugular foramen meningioma: imaging appearance and differentiating features. AJR Am J Roentgenol. 2004 Feb;182(2):373-7." } }, { "U_id": "MPX2263", "TAC": [ "MPX2263_synpic20905", "MPX2263_synpic20906" ], "MRI": [], "Case": { "Title": "Empyema", "History": "19 y/o male s/p facial and upper body burns without inhalation injury, history of intubation, mechanical ventilation, and multi-organism pneumonia with recurrent left-sided effusions requiring drainage with chest tubes. Extubated, chest tubes removed, and transferred to Ward after initial clinical improvement. Patient complained of being short of breath with exertion after a few days on the Ward. PA and lateral chest radiographs were obtained.", "Exam": "Vitals: T 98.9 F, P 112, BP 112/68, RR 20, POx >95% on room air.\n\nPhysical exam significant for decreased breath sounds on left side.\n\nLabs significant for WBC 19.3 with 78% segs. Chem 7, total protein, and albumin all WNL.", "Findings": "PA and lateral chest radiographs significant for an air-fluid level in the left mid-posterior chest (heart and mediastinal outlines preserved on PA, clearly posterior on lateral), silhouetting of the left hemidiaphram, and LLL/lingula air space disease. Axial CT of the chest with IV contrast significant for a loculated, rim-enhancing fluid collection with multiple pockets of air, consistent with a bronchopleural fistula vs. infection with a gas-forming organism, in the left posterior-lateral chest. The split-pleura sign is also present. CT findings also significant for air space consolidation with air bronchograms in the LLL and lingula.", "Differential Diagnosis": "The air fluid level on the PA and lateral chest radiographs could represent:\n\u2022 an empyema with a bronchopleural fistula vs. infection with gas-producing organism\n\u2022 an abscess in the lung parenchyma with a bronchopleural fistula vs. infection with gas-producing organism\n\u2022 loculated pleural effusion and pneumothorax\n\u2022 a pneumatocele with bronchopleural fistula\n\u2022 post-traumatic hemothorax with bronchopleural fistula\n\nThe axial CT of the chest findings are classic and pathognomonic for a thoracic empyema.", "Case Diagnosis": "Empyema", "Diagnosis By": "Gram stain and culture of the pleural fluid, surgical exploration.", "Treatment & Follow Up": "Patient was initially treated with placement of a left-sided chest tube placed at the bedside, which immediately returned 400 cc of creamy, purulent material. A CT of the chest with IV contrast was obtained to confirm the diagnosis of empyema and further characterize the lesion. The patient was then taken to the OR where a left video assisted thoracoscopy (VATS) was performed followed by a thoracotomy and decortication. Operative findings significant for an organized inflammatory rind with entrapment of the entire lung, including the lingula. Two intra-operative chest tubes were placed for persistent air leaks secondary to small parenchymal injuries. There were no significant complications and the patient tolerated the procedure well.\n\nCultures of the fluid obtained during the initial chest tube placement were significant for growth of pan-sensitive enterococcus faecalis, Streptococcus Group G, and Bacillus. Previously obtained sputum cultures were significant for Acinetobacter baumannii sensitive only to imipenem/cilastatin.", "Discussion": "The main differential in this clinical scenario is between a primary lung abscess and an empyema. Features suggestive of an empyema included:\n\n\u2022 a lenticular, non-spherical shape with unequal air-fluid level lengths on orthogonal projections as opposed to a usually spherical shape with abscesses;\n\n\u2022 split-pleura sign on axial CT demonstrating filling of the pleural space instead of a rim-enhance cavity within the lung parenchyma;\n\n\u2022 extension into the costophrenic angle and silhouetting of the posterior aspect of the left hemidiaphram.\n\nThe diagnosis of empyema was likely in this patient with a history of persistent pneumonia, recurrent effusions, and instrumentation to the affected area (left-sided chest tubes). The gas within the empyema was likely due to a bronchopleural fistula, secondary to either trauma from chest tube insertion or via necrosis of lung tissue. Alternatively, the gas may have come from one of the anaerobic microorganisms cultured from the purulent pleural fluid." }, "Topic": { "Title": "Empyema", "Disease Discussion": "A parapneumonic effusion is any pleural effusion associated with suppurative parenchymal lung disease. Simple parapneumonic effusions are uninfected, free-flowing fluid collections. Complicated parapneumonic effusions are early infected fluid collections prone to develop loculations by fibrinous septations. Empyema is a collection of frank pus within the pleural space. An effusion is termed complex when it develops loculations. The natural evolution of untreated simple and complicated parapneumonic effusions is to become complex and to progress to frank empyema with development of a residual cavity or entrapment of the lung by a fibrous peel or cortex.\n\nPneumonia results in parapneumonic effusion in approximately 45% of cases, although less than 5% of these progress to an empyema. Other common causes include mediastinal or pulmonary surgery and trauma. Less frequently, empyema may result from spread of infection from adjacent structures. Mortality from empyema ranges from 1% to 20%. \n\nClinical manifestations vary, depending on the underlying pulmonary process, the responsible organism, the quantity of bacteria and fluid in the pleural space, the stage of the disease, and the host defense mechanisms. The clinical presentation can range from an absence of symptoms to a severe febrile illness with toxemia and shock. In general, it is difficult to distinguish patients with infected pleural effusions from those with sterile parapneumonic effusions on the basis of history and physical examination alone. Clinical manifestations include fever, dyspnea, chest pain, and cough with mucopurulent sputum. Physical examination often reveals decreased breath sounds, dull percussion, and restricted respiratory excursions. \n\nWith the introduction of antibiotics in the mid-1940s, a significant shift occurred in the microbiology of pleural space infections. Anaerobic organisms are now the most common bacteria isolated from infected pleural effusions, being identified in up to 75% of cases, either alone (35%) or in combination with aerobic organisms (40%). Up to 35% of established empyemas have negative Gram stain evaluations and many patients with complicated parapneumonic effusions have negative culture results. Staphylococcus aureus is a relatively common cause of empyema in otherwise healthy adults, children and in patients who have had chest trauma or prior surgery, whereas alcoholic males are particularly susceptible to infection with Klebsiella pneumoniae. \n\nThoracentesis plays a critical role in the management of pleural effusions and in 90% of adult cases yields useful information. Fluid is removed and samples obtained for measurement of pH, glucose, LDH, protein, and differential cell count. An exudate is defined by: (1) a ratio of pleural fluid to serum protein greater than 0.5, (2) a ratio of pleural fluid LDH to serum LDH greater than 0.6, or (3) a pleural fluid LDH more than two-thirds of the upper normal limit for serum or >200 IU [3] . A transudate does not meet any of the above three criteria. \n\nIf the patient has a transudative effusion, no further laboratory tests on the pleural fluid are indicated. If the patient has an exudative pleural effusion, the remaining pleural fluid is sent for WBC and differential, cytologic examination, Gram's stain and cultures for aerobic and anaerobic bacteria, and mycobacteria and fungi if clinically indicated. The aspiration of frank pus confirms the presence of empyema and establishes an absolute indication for urgent drainage of the pleural space. In this instance, Gram's stain and culture are the only laboratory studies necessary to guide initial therapy. Pleural fluid Gram's stains can identify pathogens in 55% to 65% of patients with established empyemas. \nThe posterior-anterior and lateral chest radiographs are the best initial diagnostic modalities. When the patient is upright, free pleural fluid first accumulates in the lowest part of the hemithorax\u2014the posterior costophrenic angles. Lateral decubitus views allow detection of 50 to 100 ml of fluid and the presence of loculations if the fluid fails to layer out along the dependent chest. In the view with the involved side superior, the free fluid layers against the mediastinum and one can assess how much of the radiodensity is due to the fluid and how much is due to a parenchymal infiltrate. In the view with the involved side dependent, the amount of free pleural fluid can be semi-quantitated by measuring the distance from the chest wall to the outside of the lung. If the thickness of fluid exceeds 10 mm, a diagnostic thoracentesis is indicated. However, it is not necessary to tap all parapneumonic effusions, especially if the volume of fluid remains small, the patient is doing well, the fluid moves freely, or serial roentgenograms show improvement. \n\nCT is of great value in the overall evaluation of parapneumonic effusions and should be done early in the assessment of patients with complex parapneumonic effusion or empyema. CT is helpful in (1) differentiating pleural fluid from peripheral parenchymal infiltrates or pleural thickening, (2) evaluating the parenchymal disease, (3) determining the presence of loculations, (4) characterizing the pleural surfaces, and (5) guiding and assessing therapy. Complicated effusions and empyemas are frequently associated with nearby pulmonary consolidation and can be mistaken for a lung abscess. A lung abscess usually presents as a poorly defined, roughly spherical mass surrounded by consolidated but non compressed lung. An empyema is usually elongated, conforms to the shape of the chest wall, and compresses the adjacent lung. Its wall is thin and uniform and the interface angle with the chest wall is obtuse. The margins of the empyema cavity are composed of inflamed visceral and parietal pleura that enhance after administration of intravenous contrast. The visceral and parietal layers are separated by the interposed empyema fluid, giving rise to the \u201csplit pleura sign\u201d.\n\nUS is widely available, provides guidance for thoracentesis or pleural catheter placement, and can be transported to the bedside. US is particularly useful for sampling fluid that does not layer freely on decubitus films, and can distinguish solid from liquid pleural abnormalities better than chest roentgenography. The presence of discrete pleural septations has prognostic importance because loculated collections require drainage for their resolution. Computed tomography, however, gives additional information not obtained by US.\n\nThe sine qua non of empyema management is early, adequate, and dependent drainage. The therapeutic armamentarium for parapneumonic effusion or empyema consists of antibiotic therapy, thoracentesis, chest tube drainage, image-guided percutaneous catheter drainage, intrapleural fibrinolytic agents, and a variety of surgical drainage procedures, including video-assisted thoracic surgery (VATS) and open thoracotomy.", "ACR Code": "6.2", "Category": "Infection, generalized", "Keywords": "empyemaeffusionthoracentesis", "Reference": "DeHoyos A, Sundaresan S. Thoracic empyema. Surg Clin N Am\n2002;82(3)" } }, { "U_id": "MPX2269", "TAC": [ "MPX2269_synpic17845", "MPX2269_synpic17846" ], "MRI": [], "Case": { "Title": "Single Kidney - Renal Agenesis", "History": "51 year old female with a history of left breast carcinoma presents for bone scan to evaluate for metastatic disease.", "Exam": "Status post left mastectomy.\nUnremarkable blood chemistry and CBC.", "Findings": "Bone scan demonstrates no osteoblastic metastatic disease. The right kidney is not visualized. A CT scan demonstrates absence of the right kidney, but the right adrenal gland is intact and normal in appearance. The patient reports no history of right nephrectomy.", "Differential Diagnosis": "Renal agenesis", "Case Diagnosis": "Single Kidney - Renal Agenesis" }, "Topic": { "Title": "Renal Anomalies\r\nRenal Agenesis/Supernumerary Kidney", "Disease Discussion": "Renal Agenesis: True renal agenesis is defined as the complete congenital absence of renal tissue. Acquired forms of agenesis are characterized by the development of renal tissue which atrophies either during development or during childhood.\n\nIncidence: between 1:500 and 1:1500 births\n\nEtiology: Failure of formation of the ureteral bud or because of an inherent deficiency of the metanephric blastema [in this case, partial development of the ureter may be present].\n\nImaging studies: In true agenesis, a hemitrigone is found in the bladder on cystoscopy. No renal artery is present. The colon occupies the renal fossa on the affected side, and this may suggest the diagnosis on plain films or barium enema.\n\nAssociated anomalies: The ipsilateral adrenal gland is absent in \n8-10% of cases. Some investigators report a twofold increase in the incidence of congenital anomalies of the contralateral kidney. Associated genital abnormalities in males may include cysts of the ipsilateral seminal vesicle, absence of the ipsilateral vas deferens, hypoplasia or agenesis of the testicle, and hypospadias. In females, unicornuate or bicornuate uterus, absence or hypoplasia of the uterus, and absence or aplasia of the vagina (Rokitansky-Kuster-Hauser syndrome) may be present.\n\nBilateral renal agenesis: This is extremely rare and is incompatible with life. Males are affected in three-fourths of cases. Infants demonstrate characteristic features of Potter's syndrome including low-set ears and a prominent palpebral fold.\n\nSupernumerary kidney: Extremely rare. Cleavage of the metanephric blastema has been suggested as the cause. Most supernumerary kidneys are caudally placed and are hypoplastic. A separate collecting system is generally present.", "ACR Code": "8.1", "Category": "Congenital, malformation", "Keywords": "renal agenesissupernumerary kidneyrenal anomalies", "Reference": "N. Reed Dunnick, Textbook of Uroradiology" } }, { "U_id": "MPX2266", "TAC": [ "MPX2266_synpic21019", "MPX2266_synpic21020", "MPX2266_synpic21021", "MPX2266_synpic21024" ], "MRI": [ "MPX2266_synpic21022" ], "Case": { "Title": "Glioblastoma Multiforme", "History": "61 year old white male with 2 weeks of difficulty concentrating and remembering, slower movements. High blood pressure, otherwise healthy, though wife has noticed subtle changes in mentation over last 6 months", "Exam": "N/A", "Findings": "CT: Low attenuation focus in the post left parietal lobe, with surrounding vasogenic edema. Second lesion in the left temporal lobe, with irregular central high attenuation consistent with hemorrhage. There is not a clear connection between the two discrete lesions. The cerebral sulci and left lateral ventricle are effaced, and there is mild midline shift.\n\nMR: Left posterior parietal and left temporal lesions with peripheral enhancement, and surrounding vasogenic edema. The temporal lesion has very low central signal on T2 weighted images. Mass effect as seen on CT.", "Differential Diagnosis": "DDx: The primary differential for most brain lesions is metastatic disease vs. primary malignancy vs infection (abscess). A mnemonic for ring enhancing lesions is MAGICAL DR:\n\nMetastatic Disease \u2013 may favor due to multiplicity and \n hemorrhage\nAbscess/Cerebritis \u2013 hemorrhage would be atypical,and \n not febrile\nGBM \u2013 multicentric GBM also common, and can hemorrhage\nIschemic: Hemorrhagic stroke \u2013 despite known \n hypertension, unlikely to have defined enhancing \n tissue\nContusion \u2013 no history of trauma, and unlikely with \n enhancing soft tissue mass\nAIDs: Toxo \u2013 no history to suggest\nLymphoma \u2013 would be atypical in an otherwise healthy \n individual\nDemylinating Disease \u2013 hemorrhage would be \n uncharateristic, and not comon\nRadiation Necrosis \u2013 no history of radiation therapy", "Case Diagnosis": "Glioblastoma Multiforme", "Diagnosis By": "Biopsy", "Treatment & Follow Up": "Patient is currently undergoing radiation therapy.", "Discussion": "This gentleman\u2019s acute presentation is likely due to acute hemorrhage.\n\nGBMs are the most malignant of all gliomas (WHO Grade IV). They are the most common primary brain tumor, occuring in all ages with peak at 65-75 years of age. The are more common in men (men > women 3:2), and more common in whites. They can be associated with certain conditions, to included Turcot syndrome, neurofibromatosis type-1 and Li-Faumeni syndrome. GBMs prefer the hemispheric white matter, frontal more than temporal. \n\nGBMs are most commonly a solitary lesion, but they can be multifocal in 2-5% of cases. 5% of lesions will present with hemorrhage; they rarely calcify. They can also present as a \u201cbutterfly glioma,\u201d crossing the midline, usually across the corpus callosum. They can present as a primary leptomeningeal tumor, or metastasize by meningeal or subependymal routes." }, "Topic": { "Title": "Glioblastoma Multiforme", "Disease Discussion": "This gentleman\u2019s acute presentation is likely due to acute hemorrhage.\n\nGBMs are the most malignant of all gliomas (WHO Grade IV). They are the most common primary brain tumor, occuring in all ages with peak at 65-75 years of age. The are more common in men (men > women 3:2), and more common in whites. They can be associated with certain conditions, to included Turcot syndrome, neurofibromatosis type-1 and Li-Faumeni syndrome. GBMs prefer the hemispheric white matter, frontal more than temporal.\n \nGBMs are most commonly a solitary lesion, but they can be multifocal in 2-5% of cases. 5% of lesions will present with hemorrhage; they rarely calcify. They can also present as a \u201cbutterfly glioma,\u201d crossing the midline, usually across the corpus callosum. They can present as a primary leptomeningeal tumor, or metastasize by meningeal or subependymal routes.", "ACR Code": "1.3", "Category": "Neoplasm, glial", "Keywords": "glioblastoma multiformeGBM" } }, { "U_id": "MPX2270", "TAC": [ "MPX2270_synpic55620" ], "MRI": [], "Case": { "Title": "Lemierre\u2019s Syndrome", "History": "20 y.o. active duty man walks in to the ER c/o nagging neck pain of about 1 month duration. He crashes and codes en route to an ER bed.", "Exam": "\u2022 Septic Shock w/ MODS 2/2 severe CAP diagnosed, pt resuscitated, extubated HD 2, fevers persisted despite empiric abx.\n\u2022 48h Bcx positive for ANA non-spore-forming GNR\n\u2022 Diagnostic Imaging was performed\u2026", "Findings": "\u2022 L IJV Thrombophlebitis \n\u2022 Mult septic emboli of upper lungs bilat\n\u2022 Bilat Pleural effusions R > L \n\u2022 Myositis of L Lateral Pterygoid \n\n\nA 1.23 cm x 0.5 cm x 0.5 cm filling defect seen involving the L IJV at the level of C5, likely septic thrombophlebitis according to history. Distal to the clot a 2.42cm narrowing vessel, possible spasm or elongation of clot. Mild right paratracheal adenopathy. \nBiapical & RUL nodular densities with ill-defined margins suggestive of septic emboli. Cannot exclude additional nodules in the atelectatic portions of the lungs. \nLarge right pleural fluid collection w/ associated atelectasis of right lower/middle lobes & partial atelectasis right upper lobe.\nSmall left pleural fluid collection and left basilar atelectasis.", "Differential Diagnosis": "\u2022 Lemierre\u2019s Syndrome\n\u2022 SBE\n\u2022 Severe Pneumonia\n\u2022 EBV mononucleosis", "Case Diagnosis": "Lemierre\u2019s Syndrome", "Diagnosis By": "Blood cultures for Fusobacterium necrophorum", "Treatment & Follow Up": "Pt was transferred out for excision of IJV.\n2/2 confusion at accepting facility, Flagyl was D/Cd. Pt\u2019s condition deteriorated requiring re-intubation, bilateral chest tubes and prolonged ICU stay. \nAntibiotics were restarted with improvement.\nPt was discharged home w/ PICC in place. \nPt currently doing well." }, "Topic": { "Title": "Lemierre\u2019s Syndrome", "Disease Discussion": "Initially described by Andre Lemierre in 1936 with a series of 20 cases w/ mortality rate of 90%. With the advent of Penicillin, incidence dropped precipitously. Dubbed the \u201cforgotten disease\u201d in a case series published in 1994. \n\n\u00bb DEMOGRAPHICS\n\u2022 Incidence 0.8 cases per million\n\u2022 Significant increase in cases over last decade.\n\u2022 Male to Female ratio 1:1\n\u2022 Mainly affects previously healthy young adults, median age 22 yo.\n\u2022 Mortality rate 5% (with antibiotic therapy).\n\n\u00bb CLINICAL COURSE\nDisease progresses in a stepwise fashion;\n\u2022 Pharyngitis\n\u2022 Local invasion of lateral pharyngeal space \n\u2022 IJV (internal jugular vein) septic thrombophlebitis\n\u2022 Metastatic infections\n\n\u00bb ETIOLOGY\nEtiologic agent is usually normal oropharyngeal flora. \n\u2022 Most commonly Fusobacterium necrophorum (82%).\n\u2022 Occasionally polymicrobial in origin.\n\nOther etiologic agents reported:\n\u2022 Bacteroides, Peptostreptococcus, Streptococcus, Staphylococcus, Enterococcus, Proteus, Eikinella, Lactobacilli, and Candida.\n\n\u00bb SIGNS AND SYMPTOMS\nMost common presenting signs & symptoms:\nsore throat & fever, neck pain/mass, pleuritic chest pain, dyspnea.\n\nHowever, most patients progress to severe pneumonia & sepsis prior to diagnosis.\n\n\u00bb DIAGNOSIS:\nRequires high clinical suspicion:\nantecedent pharyngitis, septic pulmonary emboli & persistant fever despite antimicrobial therapy.\n\n\u00bb Diagnosis confirmed with laboratory & radiologic correlation.\n\n\u00bb Microbiologic diagnosis made based on culture \n\n\u00bb Radiographic diagnosis most commonly confirmed by HRCT with contrast.\n\n\u00bb TREATMENT:\nProlonged antibiotic therapy.\nEmpiric regimens should include a B-Lactamase resistant B-lactam (amp/sul, pip/tazo, tic/clav). Therapy tailored to Culture and Sensitivity is essential.\n3-6 weeks IV doses required 2/2 endovascular nature of the disease.\n\nAnticoagulation remains controversial ... ligation/excision of IJV may be required w/ uncontrolled sepsis or persistent shedding of septic emboli.", "ACR Code": "2.2", "Category": "Infection, bacteria", "Keywords": "fusobacterium necrophorumjugular septic thrombophlebitis" } }, { "U_id": "MPX2276", "TAC": [ "MPX2276_synpic35908" ], "MRI": [], "Case": { "Title": "Fibrous dysplasia", "History": "50 year old male with incidental left femoral neck lesion noted on routine virtual colonoscopy. No history of limp, hip pain, or affected gait. No unintended weight loss or night sweat.", "Findings": "Anteroposterior radiograph of the pelvis and of the left hip and CT of the femoral heads in bone windows show a lesion with sclerotic margins in the proximal metadiaphysis of the left femur with narrow transition zone; no evidence of bony expansion, no cortical break-through, no periosteal reaction.", "Differential Diagnosis": "Fibrous dysplasia", "Case Diagnosis": "Fibrous dysplasia", "Diagnosis By": "Diagnostic by radiograph; no biopsy necessary.", "Treatment & Follow Up": "No treatment necessary unless patient experiences bone pain or pathological fracture." }, "Topic": { "Title": "Fibrous Dysplasia", "Disease Discussion": "Tumor Name: Fibrous Dysplasia\n\nCell of Origin: osteoblast\n\nCommon Locations for monostotic fibrous dysplasia: ribs, femur, tibia, craniofacial bones, calvarium and humerus in decreasing order of frequency\n\nDemographics: age range 10-70 years, with highest prevalence in 10-30 years of age. No ethnicity or gender predilection.\n\nHistology: Collagenous/fibrous matrix and randomly oriented trabeculae formed by spindle stromal cells, and immature-appearing bone spicules not lined by osteoblasts.\n\nSpecial Stains: None\n\nGross Appearance: grey-whitish lesion with gritty texture\n\nRadiology: On plain radiographs, in the extremities, fibrous dysplasia appears as as a well-defined lucent lesion, with \"ground glass\" appearance with narrow zone of transition with or without calcifications or ossifications. Periosteal reaction is uncommon; stress fractures and pathological fractures can occur.\n\nPrognosis and Treatment: Lesions are often stable, but in the prepubertal patient, some lesions can be vascular; occasionally aggressive particularly in the maxillary sinus. Treatment of lesions in the extremity is usually not indicated unless patient experiences bone pain or pathological fracture, at which case, orthopedic consultation for stabilization may be required.", "ACR Code": "4.3", "Category": "Congenital, genetic", "Keywords": "Fibrous dysplasiafemoral neck", "Reference": "Grainger & Allison's Diagnostic Radiology: A Textbook of Medical Imaging, 4th ed. 2001. Dysplasia. Clin Nucl Med. 2007 May;32(5):409-410.\nSaglik Y, Atalar H, Yildiz Y, Basarir K, Erekul S. Management of fibrous dysplasia. A report on 36 cases. Acta Orthop Belg. 2007 Feb;73(1):96-101. \nShapeero LG, Vanel D, Ackerman LV, et al. Aggressive fibrous dysplasia of the maxillary sinus. Skeletal Radiol 1993; 22:63-568" } }, { "U_id": "MPX2275", "TAC": [ "MPX2275_synpic24623" ], "MRI": [], "Case": { "Title": "Neurofibroma, likely neurofibromatosis type I.", "History": "80 year old female with history of low grade lymphoma (ocular MALToma) and meningioma admitted for Left inguinal hernia repair. Found to have abnormal mass on CXR during pre-op evaluation.", "Exam": "Gen- Well nourished, Well developed, Awake, Responsive, Oriented x3\nHEENT- Normocephalic, supple neck without masses or LAD, PERRLA, Hearing grossly intact, Poor oral hygiene\nLungs- Equal BS bilaterally, no rales, rhonchi, wheezes or rubs\nHeart- RRR, No M/G/R\nAbd- NABS, Soft, non-distended, TTP in periumbilical area and LLQ \nExtremities- no clubbing, cyanosis or edema, peripheral pulses palpable and equal. \nSkin- No lesions, petechiae or decubiti \nCBC- 6.5 > 12.6 / 38.2 < 220\nLytes- 140 / 4.1 101 / 28 13 / 0.6 < 135 Ca-9.5", "Findings": "CXR- Normal aeration of the lungs. Multiple sub cm nodular opacities throughout the lungs which correspond to pleural-based nodules on CT. There is a 3.7 x 3.0 cm right paraspinal mass adjacent to the T3-4 vertebral body. No focal airspace consolidation, pneumothorax or effusion. The cardiac silhouette and pulmonary vessels are within normal limits. The aorta is ecstatic, with atherosclerotic calcification. Hiatal hernia noted. Senescent changes are noted in the thoracolumbar spine and bilateral AC joints. \n\nCT Chest W/O Contrast- Significant amount of calcification involving the coronary vessels, aorta, and splenic artery. The heart, great vessels, esophagus, large airways and other mediastinal structures are otherwise unremarkable. Small mediastinal lymph nodes are seen which are thought to be within normal limits. Of note, there are multiple sub-clinical axillary nodes present along with a single 1.2cm right axillary lymph node which is at the upper limits of normal. There is a 2.4 x 3.4 cm soft tissue density mass-like lesion seen in the right paraspinous space with apparent extension into the T3-4 intervertebral neural foramina. There is also a 1cm soft tissue nodule seen at the T11-12 paraspinous space on the right side (not seen in the CT slice provided).", "Differential Diagnosis": "Neurofibroma vs. Schwannoma vs. Meningioma vs. Sarcoma (bone, cartilage, muscle) vs. Glioma (Ependymoma, astrocytoma, oligodendroglioma) vs. vertebral/spinal cord metastases of Breast, Lung Cancer or recurrent lymphoma (MALToma).", "Case Diagnosis": "Neurofibroma, likely neurofibromatosis type I.", "Diagnosis By": "Biopsy", "Treatment & Follow Up": "Due to the slow-growing nature of these tumors, the relative lack of neurologic symptoms and the age of the patient, close follow up with serial CT or MRI looking for interval size change would likely represent the most appropriate management for this patient. (MRI produces exquisite detail of the spinal cord. Most tumors are isointense or slightly hypointense compared to the normal cord signal. Contrast-enhanced MRI is very sensitive for tumors and may disclose minute lesions). This patient should be followed by neurology on a routine basis. Any new onset in local or radiating pain, progressive weakness in the arms or legs, loss of balance and impaired bowel or bladder function should initiate a complete neurologic workup. Examination may reveal a combination of upper and lower motor neuron signs. Lower motor signs may be at the level of the lesion and may aid in localization. Other signs upon physical examination may include spine tenderness, stiffening of gait, trophic changes of extremities or sensory loss. If the patient becomes symptomatic the benefits of surgical removal of the tumor(s) should be weighed against the intrinsic risk of surgery in this patient. Absolute contraindications to surgical intervention include uncorrected coagulopathy and systemic infection. Relative contraindications to surgical intervention include complete neurologic deficit over 24 hours and short life expectancy (which should be considered in this patient). Additionally, although tumors that give rise to symptoms or those that become malignant are generally excised, if the tumor is on a vital nerve, excision may be impossible . Radiation therapy prior to surgery may be of benefit. \nNo laboratory tests are specific or sensitive to tumors arising from the spinal cord. Genetic testing may benefit patient\u2019s children.", "Discussion": "Spinal tumors can be divided into extradural, intradural extramedullary, and intradural intramedullary. (each subset is briefly described below). The location of the soft tissue mass-like lesion in this patient is representative of an intradural-extramedullary tumor (ie. neurofibroma, meningioma or schwannoma)." }, "Topic": { "Title": "Neurofibroma, likely neurofibromatosis type I.", "Disease Discussion": "Spinal tumors can be divided into extradural, intradural extramedullary, and intradural intramedullary. (each subset is briefly described below). The location of the soft tissue mass-like lesion in this patient is representative of an intradural-extramedullary tumor (ie. neurofibroma, meningioma or schwannoma- see discussion below).\n\nExtradural tumors: usually metastatic and most often arise in the vertebral bodies. Metastatic lesions can cause spinal cord compression either by intradural invasion or, more commonly, by epidural growth that results in extrinsic spinal cord or cauda equina compression. \n\nIntradural-extramedullaryTumors: arise within the dura, but outside the actual spinal cord. They are usually nerve sheath tumors or meningiomas. \n\nIntramedullary Tumors: arise within the spinal cord itself. The majority are gliomas, either astrocytomas or ependymomas, although metastases are recognized with increasing frequency. Although most spinal tumors are extradural, most primary spinal malignancies are intradural. The thoracic, lumbosacral, and cervical spinal canal is involved in 50, 30, and 20 percent of cases, respectively. \n\nIntradural-extramedullary Tumors:\nMeningiomas can arise from arachnoidal cells anywhere along the neuraxis and are occasionally found in association with neurofibromatosis. Approximately 90 percent of the tumors occur within the cranial fossa and the majority of spinal meningiomas occur within the thoracic spine (of note: this patient has a prior hx of intracranial meningioma). The tumors are frequently adherent to the spinal dura, requiring dural resection for complete removal, and also grow along intradural and extradural components of the nerve roots. Spinal meningiomas are typically slowly growing invasive lesions and often erode bone. Rarely, the tumors may be considered malignant or aggressive if they demonstrate a proclivity to recur. The usual treatment for spinal meningiomas is resection; complete resection can often be achieved. The dural origin is generally cauterized and occasionally resected. Thoracic spinal roots may be sacrificed as necessary to obtain a complete resection; however, cervical and lumbar roots are preserved whenever possible. Subtotally resected lesions are generally followed expectantly for regrowth. Symptomatic recurrences are generally treated with further surgery.\nSchwannomas are generally benign lesions that arise from schwann cells that normally produce the myelin coverings of nerve roots. These lesions are slow growing and cause compression of nerve roots and other neural elements. The tumors can be intradural or extradural in location and are often dumbbell-shaped. Their biologic behavior is similar to neurofibromas (see below) but they do not, as a rule, invade the nerve. Schwannomas are generally encapsulated and may have both an extradural and intradural component and cause widening the neural foramina. Treatment consists of tumor resection, though sacrificing the nerve to ensure complete removal may be required. Additionally, complete resection may require removal of the facet joints and reconstruction of the spine may be necessary. \nNeurofibromas are biologically similar to schwannomas but the incidence is lower, except in patients with neurofibromatosis (see below). The tumors usually develop along peripheral or cranial nerves and are a central feature of neurofibromatosis 1, where they may occur intracranially or involve several spinal roots. Involvement of peripheral nerves is manifest as firm, rubbery, subcutaneous lesions. Tumors found in association with the spinal nerve roots (as seen in this patient) are grossly similar in appearance to schwannomas. Nerve dysfunction may be caused by fusiform enlargement of the nerve with encasement of the axons by fibrous strands. Neurofibromas can be identified easily with MR imaging. The lesions are ovoid in appearance and increase in intensity with the administration of contrast material. CT myelography may demonstrate focal epidural compression at the involved site, and further delineate the tumor extent. The treatment for symptomatic neurofibromas is surgical resection. However, because there is usually no clear plane between the tumor and the nerve it is impossible to remove the tumor without sacrificing the involved nerve. The prognosis is good for the removal of a single neurofibroma. In cases of neurofibromatosis, the prognosis is poorer because of the multiplicity of lesions and the possibility that one of the lesions will undergo malignant transformation. \nNeurofibromatosis is an inherited disorder and is divided into two types. Neurofibromatosis 1 (von Recklinghausen\u2019s disease) is characterized cutaneous neurofibromas, pigmented lesions of the skin called caf? au lait spots, freckling in non-sun exposed areas such as the axilla, hamartomas of the iris termed Lisch nodules, and pseudoarthrosis of the tibia. It is associated with a mutation of a tumor suppressor gene on chromosome 17 that codes for the protein, rofibromin, which modulates signal transduction through the ras GTPase pathway. Patients with NF1 are at increased risk of developing nervous system gliomas, ependymomas, meningiomas, astrocytomas and pheochromocytomas. Neurofibromas may undergoe secondary malignant degeneration and become sarcomas. Neurofibromatosis 2 is sometimes called central neurofibromatosis. It is caused by a gene on chromosome 22. Bilateral schwannomas of the acoustic nerve and multiple meningiomas are characteristic.", "ACR Code": "68.316", "Category": "Clinical Exam Finding or Sign", "Keywords": "Neurofibroma, likely neurofibromatosis type I.neurofibromatosis type I", "Reference": "1.\tKleihues, P, Burger, PC, Collins, VP, et al. Glioblastoma. In: Kleihues, P, Cavenee, WK. Pathology of the nervous system: World Health Organization classification of tumors. IARC (International Agency for Research on Cancer), Lyon, France 2000. p.29.\n\n2.\tBraunwald, E, Fauci, A, Kasper, D, Hauser, S, Longo, D, Jameson, J. Harrison\u2019s Principles of Internal Medicine, 15th edition. McGraw-Hill Medical Publishing Division. Copyright 2001. Pg. 2448\n\n3.\tPollack, IF, Colak, A, Fitz, C, et al. Surgical management of spinal cord compression from plexiform neurofibromas in patients with neurofibromatosis 1. Neurosurgery 1998; 43:248.\n\n4.\tMcCormick, PC. Surgical management of dumbbell and paraspinal tumors of the thoracic and lumbar spine. Neurosurgery 1996; 38:67.\n\n5.\tCreange, A, Zeller, J, Rostaing-Rigattieri, S, et al. Neurological complications of neurofibromatosis type 1 in adulthood. Brain 1999; 122 ( Pt 3):473.\n\n6.\tUp To Date \u201cSpinal Cord Tumors\u201d" } }, { "U_id": "MPX2278", "TAC": [ "MPX2278_synpic32998" ], "MRI": [], "Case": { "Title": "Anterior mediastinal nonseminomatous germ cell tumor", "History": "19 yo white male who was previously healthy until he developed a chronic dry cough, DOE, and dyspnea x 2 months after returning from a trip from Cancun, Mexico. Pt was diagnosed with walking pneumonia after being seen at a civilian pediatric clinic. Pt's symptoms did not get any better and was eventually seen by his PMD. Pt had a 30 lb intentional weight loss since Nov 2005 (~ 8 months before symptoms, but a 10 lb unintentional wt loss since returning from Mexico.", "Exam": "Pt had a insignificant physical exam. Pt's labs were significant for AFP-6188, B-HCG-110, LDH-3101.", "Findings": "CXR- PA/LAT- showed Large anterior mediastinal mass\nCT Chest- Confirmation of large anterior mediastinal mass with mixed attenuation. The mass exerts considerable mass effect on other mediastinal structures.", "Differential Diagnosis": "Thymoma\nTerrible Lymphoma\nThyroid carcinoma\nGerm Cell tumor (Teratoma, SGCT, NSGCT)", "Case Diagnosis": "Anterior mediastinal nonseminomatous germ cell tumor", "Diagnosis By": "CXR-PA/LAT, Elevated AFP, HCG, LDH, Biopsy- pending", "Treatment & Follow Up": "Pt had 4 cycles of BEP chemotherapy tx with reduction in size of mass and normalizing tumor markers. Pt most recently underwent median sternotomy to resect residual mass" }, "Topic": { "Title": "Anterior mediastinal germ cell tumor, nonseminomatous", "Disease Discussion": "Nonseminomatous germ cell tumors include choriocarcinomas, emryonal carcinoma, endodermal sinus tumor, and mixed germ cell tumors. These are not pure seminomas or benign teratomas. They are commonly grouped together because of therapeutic and prognostic similarities. They are six times more common in males than females. Serologic tumor markers are very important in the evaluation, therapy, and diagnosis of patients with nonseminomatous germ cell tumors. The most common tumor marker is an elevated serum level of alpha feto protein (AFP), which is elevated in ~ 80% of patients. Elevation of AFP is consistent with presence of endodermal sinus tumor or embryonal carcinoma. Serum HCG is elevated in 30% and serum LDH is elevated in 60 % of patients with nonseminomatous germ cell tumors. The therapy of choice is a combination of chemotherapy with bleomycin, etoposide, and cisplatin followed by surgical resection of any residual masses.", "ACR Code": "6.3", "Category": "Neoplasm, embyronal", "Keywords": "extragonadal germ cell tumoranterior mediastinal mass", "Reference": "Moran, Cesar A., Maj, USAF, MC, Rosado-de-Christenson, Melissa L., Lt Col, USAF, MC, Templeton, Philip A. MD, Mediastinal Germ Cell Tumors: Radiologic and Pathologic Correlation. Radiographic 1992; 12: 1013-1030" } }, { "U_id": "MPX2281", "TAC": [ "MPX2281_synpic37388", "MPX2281_synpic37390", "MPX2281_synpic37555" ], "MRI": [], "Case": { "Title": "Classic Bosniak Class III complex renal cyst", "History": "61 year old woman complains of non-specific abdominal pain.", "Exam": "Patient had non-specific abdominal pain for the last 3 months. Patient did not have any signs of infection and the physical exam was normal except for some diffuse abdominal tenderness.", "Findings": "CT scan with contrast showed an incidental finding of a complex renal cyst. This was evaluated as a Bosniak Class 3 renal cyst.", "Differential Diagnosis": "\u2022 Renal cell carcinoma\n\u2022 Benign complex cyst\n\u2022 Oncocytoma (usually solid)\n\u2022 Abscess\n\u2022 Multilocular Cystic Nephroma (MLCN)", "Case Diagnosis": "Classic Bosniak Class III complex renal cyst", "Diagnosis By": "Imaging using Bosniak criteria", "Treatment & Follow Up": "Surgical follow up was recommended with referral to a urologist for consultation.", "Discussion": "Within most of the literature discussing Bosniak classification of complex renal cysts, Class 3 cysts have been consistently diagnosed post-surgery as renal cell carcinoma or other cancer. So all diagnosed class 3 cysts should be referred for surgical evaluation." }, "Topic": { "Title": "Classic Bosniak Class III complex renal cyst", "Disease Discussion": "The Bosniak classification of renal cysts has been a has been a relatively consistent way of distinguishing benign renal cystic disease from renal cell carcinoma (or other cancers) since 1986. This system uses radiologic findings from CT or ultrasound to classify renal \"cysts\" into four categories.\nIsrael & Bosniak - http://radiology.rsnajnls.org/cgi/content/full/236/2/441\nTable of Classes - http://radiology.rsnajnls.org/cgi/content-nw/full/236/2/441/T1\n\u2022 Class 1:\n\u00bb Homogeneous water attenuation\n\u00bb No internal architecture\n\u00bb No enhancement\nThe first category includes only simple cysts that are homogeneous, have well defined margins, are -10 to +20 Hounsfield units in density (like that of water), do not contain septa, calcifications, nor solid components; and, they do not enhance with contrast. This is the most common category, occurring in at least 50% of the population over 50 years of age. This is also the most benign category and requires little if any follow-up.\n\n\u2022 Class 2:\nThe second category includes simple cysts that may have additional radiologic findings. Findings that will increase the classification from Class 1 to Class 2 include:\n\u00bb the presence of thin hyaline septa\n\u00bb mild calcification in the cyst wall or in the thin septa\n\u00bb uniform hyperdensity\n\nThese have < 5% chance of malignancy and often are not provided follow up.\n\nThere has been much controversy in the literature about inter-observer variability when it comes to the distinguishing between class 2 and class 3 cysts. This forced the classification system to give rise to a new category so as to more accurately describe the range between Class 2 and Class 3 cysts. \n \n\u2022 Class 2F (meaning \"needs follow-up\"): \n\u00bb multiple thin septa that may have mild or moderate nodular calcification\n\u00bb mild thickening of the wall or septa\n\u00bb minimal \"perceived enhancement\" of cyst wall or septa\n\u00bb non-enhancing hyperdense intrarenal cysts > 3cm\n\nClass 2F cysts may require 6 month follow-up exams over 24 months.\n\nAll Class 2 and 2F cysts may NOT have \"measurable enhancement\" with contrast and should be generally well marginated.\n\n\u2022 Class 3:\nThe third category includes complex cysts that have irregular, thickened walls and/or septa. These cysts may have extensive calcification and will enhance with contrast. However, these cysts should be relatively homogeneous in density and should not contain solid components.\n\nThese masses need surgical intervention in most cases, because they may be:\n\u00bb MLCN - Multiloculated Cystic Nephroma\n\u00bb Hemorrhagic cysts\n\u00bb Infected cysts\n\n\u2022 Class 4:\nThe fourth and last Bosniak category can include all of the previously stated components - but show definite enhancing soft-tissue regions, appear heterogeneous in density, and have various solid or hypercalcified inclusions - indicating possible necrosis. In previous studies, this class has always been shown to indicate cancer on follow-up pathological report - and they should be removed. \n \nMany small retrospective studies have shown the Bosniak classification system to be quite useful in making a clinical decision between choosing surgical therapy versus clinical follow-up with serial CT scans. \n\nIts only criticism comes from individuals who feel that the radiologic inter-observer variability is too large and is a major diagnostic concern.\n\neMedicine - http://www.emedicine.com/med/topic3189.htm\n\nCTISUS - http://www.ctisus.org/cta_web/8_05/Fielding/AR_08-05_CTA_Fielding.htm\n\nRadiology - http://radiology.rsnajnls.org/cgi/content/abstract/231/2/365\n\nAJR - http://www.ajronline.org/cgi/content/full/181/5/1425", "ACR Code": "8.3", "Category": "Radiologic Sign or Finding", "Keywords": "Bosniakcyst classificationrenal cell carcinoma", "Reference": "Warren KS, McFarlane J. The Bosniak classification of renal cystic masses. BJU International 2005:95, 939-942\n\nIsrael GM, Bosniak MA. Follow-up CT of moderately complex cystic lesions of the kidney (Bosniak Category IIF). Am J Roentgenol 2003: 181, 627-633\n\nKoga S, Nishikido M, Inuzuka S, et al. An evaluation of Bosniak's radiological classification of cystic renal masses. BJU International 2000: 86, 607-609", "External Links": "www.ajronline.org/cgi/content/full/181/5/1425" } }, { "U_id": "MPX2282", "TAC": [ "MPX2282_synpic35350", "MPX2282_synpic35352" ], "MRI": [], "Case": { "Title": "Pulomary Embolism", "History": "61 years-old man with known stage II pancreatic cancer. Underwent contrast CT of the chest, abdomen and pelvis for pre-operative evaluation.", "Exam": "N/A", "Findings": "There are multiple area of hypoattenuation and filling defect within the right and left pulmonary arteries. There is a comet shaped area of hypoattenuation extending from the left pulmonary artery nearly to the branch point of the main pulmonry artery.", "Differential Diagnosis": "Pulmonary embolism\nVenous thromboembolism\nPrimary thrombus\nSeptic emboli\nTumor emboli", "Case Diagnosis": "Pulomary Embolism", "Diagnosis By": "Clinically", "Treatment & Follow Up": "Unknown.", "Discussion": "Venous thromboembolic disease, especially resulting in pulmonary embolism represents a significant disease burden in terms of morbidity and mortality in hospitalized and non-hospitalized patients1. Thrombus, or clot, often forms in the proximal, deep leg veins and only may only become clinically evident once a thrombus segment has embolized[1, 2]. Upon embolization from a vein (in the proximal leg or elsewhere) the first bed of vessels of decreasing diameter is usually the lungs, where the embolus may lodge occluding blood flow and creating clinically significant or insignificant (based on size) ventilation-perfusion mismatches[1, 3]. The progression from thrombus formation in the legs to pulmonary embolism is believed to account for up to 10% of hospital deaths[1]. Tragically, acute pulmonary embolism is among the leading causes of preventable hospital deaths in the United States[4].\n\tDetection and therapy for acute pulmonary embolism, once it has become clinically apparent is difficult and often without optimum result. The best method of preventing pulmonary embolism is to prevent primary thrombus formation[1, 4]. Extensive clinical trials have resulted in revised clinical guidelines in 2007 for the prevention and management of venous thrombosis and venous thromboembolic disease[2, 5]. These new recommendations state that (1) low molecular weight heparins are preferable to unfractionated heparins in inpatient populations; (2) low molecular weight heparins are safe and cost effective for treating deep venous thrombosis and pulmonary embolism in selected outpatients; (3) compression stocking should be utilized to prevent postthrombotic syndrome within one month of diagnosis and used for a minimum of one year; (4) there is inadequate evidence to recommend specific types of anticoagulation in pregnant women; (5) recommendations on length of treatment; and (6) low molecular weight heparin is safe and efficacious for long term treatment on venous thromboembolism in selected patients, such as those with cancer[2, 5]. For additional information on this complex and everchanging topic, the reader is directed to the references below and the references\u2019 references." }, "Topic": { "Title": "Pulomary Embolism", "Disease Discussion": "Venous thromboembolic disease, especially resulting in pulmonary embolism represents a significant disease burden in terms of morbidity and mortality in hospitalized and non-hospitalized patients1. Thrombus, or clot, often forms in the proximal, deep leg veins and only may only become clinically evident once a thrombus segment has embolized[1, 2]. Upon embolization from a vein (in the proximal leg or elsewhere) the first bed of vessels of decreasing diameter is usually the lungs, where the embolus may lodge occluding blood flow and creating clinically significant or insignificant (based on size) ventilation-perfusion mismatches[1, 3]. The progression from thrombus formation in the legs to pulmonary embolism is believed to account for up to 10% of hospital deaths[1]. Tragically, acute pulmonary embolism is among the leading causes of preventable hospital deaths in the United States[4].\n\tDetection and therapy for acute pulmonary embolism, once it has become clinically apparent is difficult and often without optimum result. The best method of preventing pulmonary embolism is to prevent primary thrombus formation[1, 4]. Extensive clinical trials have resulted in revised clinical guidelines in 2007 for the prevention and management of venous thrombosis and venous thromboembolic disease[2, 5]. These new recommendations state that (1) low molecular weight heparins are preferable to unfractionated heparins in inpatient populations; (2) low molecular weight heparins are safe and cost effective for treating deep venous thrombosis and pulmonary embolism in selected outpatients; (3) compression stocking should be utilized to prevent postthrombotic syndrome within one month of diagnosis and used for a minimum of one year; (4) there is inadequate evidence to recommend specific types of anticoagulation in pregnant women; (5) recommendations on length of treatment; and (6) low molecular weight heparin is safe and efficacious for long term treatment on venous thromboembolism in selected patients, such as those with cancer[2, 5]. For additional information on this complex and everchanging topic, the reader is directed to the references below and the references\u2019 references.", "ACR Code": "5.9", "Category": "Medicine", "Keywords": "pulmonary embolismvenous thromboembolismdeep vein thrombosis", "Reference": "1. Marino P. The ICU Book. 3rd ed. Philadelphia, PA: Lippincott, Williams, & Wilkins; 2007.\n2. Segal JB, Streiff MB, Hofmann LV, Thornton K, Bass EB. Management of Venous Thromboembolism: A Systematic Review for a Practice Guideline. Ann Intern Med 2007;146(3):211-22.\n3. Fedullo PF, Tapson VF. The Evaluation of Suspected Pulmonary Embolism. N Engl J Med 2003;349(13):1247-56.\n4. Geerts WH, Pineo GF, Heit JA, et al. Prevention of Venous Thromboembolism: The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest 2004;126(3_suppl):338S-400.\n5. Snow V, Qaseem A, Barry P, et al. Management of Venous Thromboembolism: A Clinical Practice Guideline from the American College of Physicians and the American Academy of Family Physicians. Ann Intern Med 2007;146(3):204-10." } }, { "U_id": "MPX2284", "TAC": [ "MPX2284_synpic23330", "MPX2284_synpic23331" ], "MRI": [], "Case": { "Title": "Craniosynostosis; Idiopathic Scaphocephaly", "History": "9 month old male with premature closure of anterior fontanelle.", "Exam": "Frontal bossing. Subtle ridge palpated at midline skull.", "Findings": "Hull shaped skull with increased anterior-posterior length relative to width. Bony ridge at sagittal suture. Bifrontal bossing with bitemporal narrowing.", "Differential Diagnosis": "\u2022 Idiopathic Scaphocephaly\n\u2022 Hyperthyroidism \n\u2022 Rickets \n\u2022 Hyperparathyroidism \n\u2022 Underlying genetic disorder (Apert's Syndrome, Crouzon's Syndrome, Pfeiffer's Syndrome)", "Case Diagnosis": "Craniosynostosis; Idiopathic Scaphocephaly", "Diagnosis By": "Clinically / Radiographically", "Treatment & Follow Up": "See discussion." }, "Topic": { "Title": "Craniosynostosis; Scaphocephaly", "Disease Discussion": "Scaphocephaly, also known as boat or hull shaped skull, is the most common form of craniosynostosis, accounting for approximately 50 percent of cases. Scaphocephaly results from sagittal suture synostosis. The cranium has reduced width and compensatory elongation in the anteroposterior or sagittal axis.\n\nThe major complications associated with craniosynostosis are inhibition of brain growth and increased intracranial pressure. Brain growth is inhibited by prolonged uncorrected restriction of cranial growth. Compression of underlying brain is more likely when multiple sutures are affected. \n\nThe mechanism of synostosis is unknown. One mechanism proposes an intrinsic abnormality in the cranial base that causes early fusion. This theory is supported by laboratory studies of osteoblasts from craniosynostotic sutures. Craniosynostosis also has been associated with endocrine abnormalities, such as hyperthyroidism, and use of warfarin during pregnancy.\n\nThe diagnosis of craniofacial deformities is based primarily upon physical examination. Historically, pattern recognition has been the basis for clinical diagnosis. Radiographic studies including plain radiographs and CT may be used to help confirm or exclude the diagnosis of craniosynostosis.\n\nScaphocephaly is treated by a strip craniectomy performed at three or four months of age. A limitation of this technique is that reossification and growth arrest can occur prior to completion of remodeling. In children six months to one year of age, a Pi or T craniectomy can be utilized to improve the cephalic contour. If the deformity is severe, barrel-stave osteotomies with rearrangement of cranial segments is required to achieve the desired contour.", "ACR Code": "4.9", "Category": "Idiopathic or Unknown", "Keywords": "CraniosynostosisSagittal suture synostosis", "Reference": "1. Shillito, J Jr, Matson, DD. Craniostenosis: a review of 519 surgical patients. Pediatrics 1968; 41:829.\n2. Fragale A, Tartaglia M, Bernardini S, et al. Decreased proliferation and altered differentiation in osteoblasts from genetically and clinically distinct craniosynostotic disorders.\nAm J Pathol. 1999 May;154(5):1465-77 \n3. Marchac, D, Renier, D. Craniofacial Surgery for Craniosynostosis. Little, Brown Company, Boston 1982" } }, { "U_id": "MPX2286", "TAC": [ "MPX2286_synpic28890" ], "MRI": [], "Case": { "Title": "Aneurysmal Bone Cyst", "History": "11y/o female with h/o trauma now with persistent pain.", "Findings": "AP, lateral and oblique radiographic views of the right foot show a well-defined radiolucent medullary mass of the cuboid bone that expands the cortex but does not cause cortical disruption. There is a narrow zone of transition. Follow-up radiographs after curettage show the cement placement in the region of curettage without recurrence of the aneurysmal bone cyst.\n\nAxial CT of the right foot with bone windows show a lytic mass expanding the cuboid bone and measuring 3 cm x 2.6 cm in greatest dimension with multiple fluid-fluid levels. The cortex is thinned. Soft tissue windows suggest fluid-fluid levels. No matrix calcifications are seen. These findings are consistent with an aneurysmal bone cyst.", "Differential Diagnosis": "Simple bone cyst\nGiant cell tumor\nEosinohilic granuloma\nOsteoblastoma\nChondroblastoma\nInfection (Brodie\u2019s abscess)", "Case Diagnosis": "Aneurysmal Bone Cyst", "Diagnosis By": "Aneurysmal Bone Cyst (ABC) without associated tumor was confirmed by histologic evaluation of curettage material.", "Treatment & Follow Up": "Usually when symptomatic, biopsy and curettage are the main treatment options. The patient had a curettage of the cuboid with placement of bone graft material to help structurally support her foot. \n\nFollow-up included additional imaging to ensure proper healing as well as evaluating for recurrence of the aneurysmal bone cyst. Radiographs showed the cement in the region of the curettage and no recurrence of lucency.", "Discussion": "Aneurysmal bone cysts (ABC) are described as a benign \u201cvascular reactive lesion.\u201d They usually present as lytic expansile masses found most commonly in the metaphysis of the tibia and femur and posterior portions of the vertebrae. They usually are non-aggressive in appearance and do not disrupt the cortex. The mass may have a thin rim of cortex remaining giving it an \u201cegg-shell\u201d appearance. The lytic portion of the mass has also been described as having a \u201csoap-bubble\u201d appearance. \n\tCT is also helpful in the evaluation of this lesion since it may show more clearly that the matrix has no calcifications and show preservation of the cortex. CT can sometimes show the fluid-fluid levels which represent blood products in heterogeneous stages of breakdown on histological examination.\n\tMRI confirms the contours and shows the fluid-fluid levels, while also demonstrating the surrounding soft tissues more clearly than CT. This is because of the improved contrast seen on the MR images. It is also the modality of choice for identifying nodularity within the wall of the cyst, which may direct future biopsy.\n\tAneurysmal bone cysts are accompanied by associated tumor approximately 20-30% of the time. These associated tumors include, most commonly giant cell tumors, but may also include fibrous dysplasia, chondroblastoma, osteoblastoma, osteosarcma, and chondrosarcoma. \n\tTreatment of ABC\u2019s generally treated surgically, although they may also be observed for growth rate and further involvement. If there are questions regarding the exact diagnosis and there appears to be an associated lesion, then biopsy should be performed. If a malignancy is found, the patient has a wide resection of the tumor. If the ABC is symptomatic and no malignancy is seen, curettage is the treatment of choice. Selective embolization, intralesional injection, irradiation, and en bloc resection have also been described. Recurrence rates are not uncommon with these bone cysts, occurring approximately 0-30%." }, "Topic": { "Title": "Aneurysmal Bone Cyst", "Disease Discussion": "Aneurysmal bone cysts (ABC) are described as a benign \u201cvascular reactive lesion.\u201d They usually present as lytic expansile masses found most commonly in the metaphysis of the tibia and femur and posterior portions of the vertebrae. They usually are non-aggressive in appearance and do not disrupt the cortex. The mass may have a thin rim of cortex remaining giving it an \u201cegg-shell\u201d appearance. The lytic portion of the mass has also been described as having a \u201csoap-bubble\u201d appearance. \n\tCT is also helpful in the evaluation of this lesion since it may show more clearly that the matrix has no calcifications and show preservation of the cortex. CT can sometimes show the fluid-fluid levels which represent blood products in heterogeneous stages of breakdown on histological examination.\n\tMRI confirms the contours and shows the fluid-fluid levels, while also demonstrating the surrounding soft tissues more clearly than CT. This is because of the improved contrast seen on the MR images. It is also the modality of choice for identifying nodularity within the wall of the cyst, which may direct future biopsy.\n\tAneurysmal bone cysts are accompanied by associated tumor approximately 20-30% of the time. These associated tumors include, most commonly giant cell tumors, but may also include fibrous dysplasia, chondroblastoma, osteoblastoma, osteosarcoma, and chondrosarcoma. \n\tTreatment of ABC\u2019s generally treated surgically, although they may also be observed for growth rate and further involvement. If there are questions regarding the exact diagnosis and there appears to be an associated lesion, then biopsy should be performed. If a malignancy is found, the patient has a wide resection of the tumor. If the ABC is symptomatic and no malignancy is seen, curettage is the treatment of choice. Selective embolization, intralesional injection, irradiation, and en bloc resection have also been described. Recurrence rates are not uncommon with these bone cysts, occurring approximately 0-30%.", "ACR Code": "4.1", "Category": "Cyst, benign", "Keywords": "aneurysmal bone cystbenign cyst", "Reference": "Grainger and Allison. Diagnostic Radiology: A Textbook of Medical Imaging, 4th ed., London, 2001: pp1854-1855, 2102-2103.\n\nCanale. Campbell\u2019s Operative Orthopaedics, 10th ed., St Louis, 2003; pp.798-799.\n\nMcCarthy and Frassica. Pathology of Bone and Joint Disorders: with Clinical and Radiographic Correlation, 1st ed., Philadelphia, 1998; pp 279-284." } }, { "U_id": "MPX2288", "TAC": [ "MPX2288_synpic18787" ], "MRI": [ "MPX2288_synpic18788", "MPX2288_synpic18789", "MPX2288_synpic18790" ], "Case": { "Title": "Intraosseous Lipoma", "History": "A 45-year-old female with no significant past medical history presented to the emergency department with a painful knee following a fall from standing height.", "Exam": "Tender to palpation over patella.", "Findings": "CR, CT, and MR demonstrate a well-defined lytic lesion in the distal femur with mixed fluid and fat attenuation and scattered calcification.", "Differential Diagnosis": "Fibrous Dysplasia, ABC, Hemangioma, Bone Infarct, Chondroid Tumor, Intraosseous Lipoma", "Case Diagnosis": "Intraosseous Lipoma", "Diagnosis By": "radiographically", "Treatment & Follow Up": "none" }, "Topic": { "Title": "Intraosseous Lipoma", "Disease Discussion": "Intraosseous lipomas is an uncommon benign bone lesion that accounts for approximately 0.1% of bone tumors. Common sites of occurrence include the femoral neck and calcaneus. They can also occur in the flat bones, the pelvis, and other locations. \nHistopathologically, intraosseous lipomas are categorized into three types: stage 1, solid tumor composed of viable lipocytes; stage 2, transitional cases with partial fat necrosis and focal calcification intermixed with regions of viable lipocytes; and stage 3, advanced cases in which fat cells have died with variable degree of cyst formation, calcification, and reactive new bone formation. The progression from stage 1 to stage 3 is caused by ischemia and infarction within the lesion and is thought to be related to the rigid structure of bone opposing the lesion\u2019s fat cell expansion and multiplication. These lesions may also cause resorption and expansion of bone, whereas bone infarcts do not cause expansion of the bone.\n The radiographic features of intraosseous lipomas are based upon the histologic stage of the lesion. The stage 1 lesions are lucent and represent viable fat with resorption of bony trabeculae. Stage 2 lesions have lucent areas, which consist of viable fat and radiodense areas that consist of fat necrosis and dystrophic calcification. Stage 2 lesions can be expansile. Stage 3 lesions reflect resorption of normal bone, but they are more radiodense than stage 1 or 2 lesions. The radiodensity is a result of calcification and extensive fat necrosis. Stage 3 lesions also have thick sclerotic borders, presumably related to involution of these lesions. Radiologically, the differential diagnosis of intraosseous lipomas includes fibrous dysplasia, aneurysmal bone cysts, simple bone cysts, bone infarcts, chondroid tumors, and liposclerosing myxofibrous tumors. \n On CT, stage 1 intraosseous lipomas exhibit resorption of bone trabeculae in the lesion and bone expansion. The area of lucency seen on the radiograph corresponds to fat attenuation visible on CT. Stage 2 lesions have areas of fat attenuation and patchy areas of increased density corresponding to calcification and fat necrosis. Stage 3 intraosseous lipomas are the most difficult to diagnose because of the reactive ossification, calcification, fat necrosis, and cyst formation caused by necrosis of the fat component. If the lesion has a peripheral rim of discernible fat, it will help to eliminate other conditions generally considered in the differential diagnosis. Lesions that exhibit resorption of trabecular bone and predominantly central calcification instead of peripheral calcification are more likely to be stage 3 intraosseous lipomas than bone infarcts; the latter are non-expansile lesions that have a peripheral serpentine thin rim of sclerosis and are not associated with trabecular resorption. \n MR imaging reveals viable fat in stage 1 intraosseous lipomas. The fat is isointense to subcutaneous fat on T1-weighted sequences and exhibits low signal intensity with fat suppression on T2-weighted images. A thin circumferential rim of low signal intensity on T1- and T2- weighted sequences is typically present demarcating the margin of the fatty lesion consistent with reactive sclerosis surrounding the lesion. In stage 2 lesions, one can again identify fat and the circumferential rim of decreased signal on T1- and T2-weighted images. Low-signal-intensity areas within the central portion of the lesion on T1- and T2-weighted images are consistent with calcifications. Stage 3 lesions show a thin peripheral rim of fat, which can be identified on MR imaging. They also have central calcification and a thick rim of surrounding sclerosis, which have low signal intensity on T1- and T2-weighted sequences. Areas of fat necrosis have a variable signal on T1-weighted and increased signal on T2-weighted images.", "ACR Code": "4.3", "Category": "Neoplasm, benign", "Keywords": "lipomaintraosseousbenign bone tumor", "Reference": "Propeck T, Bullard MA, Lin J, Doi K, Martel W. Radiologic-pathologic correlation of intraosseous lipomas. AJR Am J Roentgenol 2000;175:673-678." } }, { "U_id": "MPX2291", "TAC": [ "MPX2291_synpic15150", "MPX2291_synpic15151" ], "MRI": [], "Case": { "Title": "Bochdalek hernia", "History": "Known congenital right diaphragmatic hernia and occasional episodes of SOB, but normal PF tests. Request for assessment with UGI and SBFT was made to evaluate for evidence of malrotation and to determine the extent of herniated bowel within the thoracic cavity.", "Exam": "Clinical Manifestations: Patients' with Bochdalek hernias typically present in infancy with pulmonary insufficiency. In the neonate, Bochdalek's hernia is one of the leading causes of respiratory distress and is one of the most common congenital anomalies of the thorax. Affected adults typically have no symptoms and are diagnosed incidentally on imaging studies.", "Findings": "Radiologic findings: \nBochdalek's hernia is seen as a posterolateral diaphragmatic interruption with the finding of fat herniating through the interruption above the diaphragm. Other intraperitoneal and/or retroperitoneal structures can also be seen herniating through the diaphragmatic interruption. Axial CT scan (with sagittal and/or coronal reformations occasionally) of the abdomen is commonly accepted as the best diagnostic test to evaluate for diaphragmatic hernias. Fluoroscopic Upper GI/SBF studies are helpful in defining the extent of intestinal herniation if present, and to evaluate for possible malrotation or strangulation.", "Differential Diagnosis": "Differential Diagnosis: Congenital diaphragmatic hernia: Bochdalek, Morgagni, Paraesophageal hernia through esophageal hiatus. Traumatic diaphragmatic hernia. Diaphragmatic eventration.", "Case Diagnosis": "Bochdalek hernia", "Treatment & Follow Up": "-Treatment: Neonate: Surgical repair\nAdult: Usually none.", "Discussion": "-Factoid Discussion: Hernias through the foramen of Bochdalek are developmental defects in the posterior part of the diaphragm which contain omental fat and tissues, and additionally, often contain intraperitoneal and/or retroperitoneal structures. Patients' with Bochdalek hernias typically present in infancy with pulmonary insufficiency.\n\n-Etiology and Pathogenesis: Congenital diapharagmatic hernias result from developmental failure of posterolateral diaphragmatic foramina to fuse properly. Bochdalek hernias occur much more frequently on the left than on the right, presumably because the presence of the liver on the right prevents many Bochdalek hernias from occurring on that side." }, "Topic": { "Title": "Bochdalek hernia", "Disease Discussion": "Factoid Discussion: Hernias through the foramen of Bochdalek are developmental defects in the posterior part of the diaphragm which contain omental fat and tissues, and additionally, often contain intraperitoneal and/or retroperitoneal structures. Patients' with Bochdalek hernias typically present in infancy with pulmonary insufficiency. These hernias are usually posterior (\"Bochdalek= Back\")and located on the left side 70% of the time.", "ACR Code": "7.9", "Category": "Congenital, malformation", "Keywords": "bochdalekherniacongenital", "Reference": "Scott C. Gaerte, Cristopher A. Meyer, Helen T. Winer-Muram, Robert D. Tarver, and Dewey J. Conces, Jr Fat-containing Lesions of the Chest. RadioGraphics 2002 22: 61S-78S.\n\nGale ME. Bochdalek hernia: prevalence and CT characteristics. Radiology 1985;156:449 -452\n\nMullins ME, Stein J, Saini SS, Mueller PR. Prevalence of incidental Bochdalek's hernia in a large adult population. AJR Am J Roentgenol 2001;177:363-366." } }, { "U_id": "MPX2289", "TAC": [ "MPX2289_synpic15889" ], "MRI": [], "Case": { "Title": "Right aortic arch with aberrant left subclavian artery", "History": "3 year old male with history of drooling.", "Exam": "vital signs unremarkable\nphysical exam normal", "Findings": "CXR: right-sided aortic arch\n\nBarium swallow: posterior impression upon the esophagus at level of T-5 vertebral body\n\nEnhanced chest CT: right aortic arch with aberrant origin of left subclavian artery", "Differential Diagnosis": "right aortic arch with aberrant left subclavian artery", "Case Diagnosis": "Right aortic arch with aberrant left subclavian artery", "Treatment & Follow Up": "none", "Discussion": "http://www.quintemri.com/casestudies_AorticArch.html\nhttp://www.visn1.med.va.gov/boston/radiology/radcases/case2p2.htm\nhttp://www.med.umn.edu/radiology/cvrad/chd/chd.html" }, "Topic": { "Title": "Left aortic arch with aberrant right subclavian artery", "Disease Discussion": "This is the most common malformation of the aortic arch resulting in a complete vascular ring around the trachea and esophagus.The most common type of right aortic arch is right aortic arch with an aberrant left subclavian artery and it is 2-3 times more common than right arch with mirror image branching of the brachiocephalic vessels. Right arch and aberrant left subclavian artery has a 5-12% incidence of associated congenital heart disease while right arch with mirror branching of the brachiocephalic vessels has a 98% incidence of associated congenital heart disease.\n \n\nTwo types:\n1.Origin of the left subclavian artery from a posterior aortic diverticulum from which a ductus arteriosus extends to the left pulmonary artery. The retroesophageal part of the ring is large and compression is produced by the diverticulum (Diverticulum of Kummerell).\n\n2.Origin of the left subclavian artery from the descending aorta with a left ductus connecting the left subclavian artery to the left pulmonary artery. The retroesophageal part of the ring is small.\n \nIn both types of aberrant subclavian arteries, the vessel runs behind the esophagus.\n\nDefinitive diagnosis is now usually accomplished by CT or MRI. Both display the severity of airway narrowing and the retro-esophageal aberrant artery.Both demonstrate the large aortic diverticulum invariably at the site of airway compression with an aberrant left subclavian artery.", "ACR Code": "562.1532", "Category": "Congenital, malformation", "Keywords": "Right aortic archaberrant left subclavian arterydysphagia", "Reference": "http://www.amershamhealth.com/medcyclopaedia/Volume%20VII/AORTIC%20ARCH%20ANOMALIES.asp", "External Links": "www.amershamhealth.com/medcyclopaedia/Volume%20VII/AORTIC%20ARCH%20ANOMALIES.asp" } }, { "U_id": "MPX2294", "TAC": [ "MPX2294_synpic16805" ], "MRI": [ "MPX2294_synpic16809" ], "Case": { "Title": "Thromboembolic Stroke", "History": "The patient is a resident of an assisted living center who presents to the ED with \"global aphasia\" of unspecified duration. She has a history of chronic atrial fibrillation and a recent interruption of her prophylactic anticoagulant therapy. A CT scan is obtained which reveals subacute L MCA and L PCA strokes, felt to be secondary to left atrial emboli. She is admitted for supportive treatment. Two days later, during her inpatient stay, she is discovered unresponsive with intact pupils. A repeat CT scan and MRI are immediately obtained.", "Findings": "Image 1, is a non-contrast CT obtained immediately following her altered mental status on hospital day 3. It reveals hypodensities in the cortical and subjacent white matter regions of the left MCA and left PCA. These findings had been present on HD1 and were felt to represent subacute embolic strokes from cardiac emboli due to a lapse of anticoagulant therapy for her chronic A-fib. \nImage 2, a diffusion weighted MRI, is obtained shortly after the CT in image 1. It reveals the subacute L MCA stroke, but also reveals an extensive acute R MCA stroke which is not evident on the CT image. This additional stroke is responsible for her acute mental status decline on HD3.", "Differential Diagnosis": "Embolic Infarction\nThrombotic Infarction\nVasculitic Infarction", "Case Diagnosis": "Thromboembolic Stroke", "Treatment & Follow Up": "She was not felt to be a candidate for thrombolytic therapy and treatment was conservative.", "Discussion": "Diffusion weighted MRI (DWI) scans are more sensitive for the detection of the acute phase of stroke than CT scans. DWI reveals diffusion restricted regions of cytotoxic edema as hyperintense signal." }, "Topic": { "Title": "Thromboembolic Stroke", "Disease Discussion": "Brain embolism usually presents abruptly with clinical abnormalities. Fluctuations or worsening symptoms and sudden improvements are common during the first 24 to 48 hours, probably because of emboli passing distally. Usually embolic infarcts are large, and deficits are more severe in patients with emboli than with in situ occlusions. Single or infrequent but longer lasting TIAs may precede embolic infarctions. Embolic events often occur during activity or sudden straining, coughing, or sneezing. Infarcts may involve multiple vascular territories and are mixed in age. Early angiographic or TCD studies may show the presence of distal intra-arterial emboli. Hemorrhagic conversion of infarcted areas is commonly noted on CT and MRI scans. Infarcts are often wedge-shaped and involve the cerebral cortical surface.(1)\n\nAtrial fibrillation is the underlying cause of 30,000 to 40,000 embolic strokes per year in the United States. The precentage of AF caused strokes increases with age, rising from 1.5 percent in patients aged 50 to 59 years to 23.5 percent in patients aged 80 to 89 years. Although co-morbid conditions such as hypertension and vascular disease are factors, the predominant cause of strokes in patients with atrial fibrillation is embolization of a clot from the left atrium.\n\nWhen evaluated using transesophageal echocardiography, up to 30 percent of patients with atrial fibrillation and embolic stroke are found to have atrial thrombi within 72 hours of the stroke. Risk factors for stroke in patients with atrial fibrillation include a history of transient ischemic attack or stroke, age greater than 65 years, a history of hypertension, the presence of a prosthetic heart valve (mechanical or tissue), rheumatic heart disease, left ventricular systolic dysfunction, or diabetes.(2)", "ACR Code": "1.9", "Category": "Hypoxic or Ischemic", "Keywords": "cerebral infarction ischemiaEmbolismatrial fibrillation", "Reference": "1. Goetz: Textbook of Clinical Neurology, 1st ed., Copyright \u00a9 1999 W. B. Saunders Company:916.\n2. Acute management of atrial fibrillation: Part II. Prevention of thromboembolic complications.\nKing DE - Am Fam Physician - 15-JUL-2002; 66(2): 261-4" } }, { "U_id": "MPX2297", "TAC": [ "MPX2297_synpic19052" ], "MRI": [], "Case": { "Title": "Transmesenteric Internal Hernia", "History": "Abdominal pain. No known history of surgeries.", "Exam": "N/A", "Differential Diagnosis": "Malrotation with partial volvulus\nOmental hernia\nPartial sbo from adhensions", "Case Diagnosis": "Transmesenteric Internal Hernia", "Diagnosis By": "no surgery yet", "Discussion": "Most transmeseteric hernias are felt to be complications from surgery causing a defect in the mesentery. Interestingly, this patient has no known history of surgery." }, "Topic": { "Title": "Transmesenteric Internal Hernia", "Disease Discussion": "Internal hernia is an uncommon cause of small-bowel obstruction, which is often missed (preopereative diagnosis rare), can be intermittent, and possibly increasing in incidence. Usually small bowel herniates through a normal or abnormal aperture within the peritoneal cavity. Paraduodenal hernia has traditionally been considered the most common type (50%), however recent publication shows transmesenteric hernia (TMH) are probably more common secondary to increased frequency of Roux-en-Y surgeries which predisposes to this type of internal hernia. Other types of internal hernia, including supra and perivesical, intersigmoid, foramen of Winslow, and omental hernia are rare .\nComplications include volvulus and resulting ischemia.\n\nReliable CT signs of TMH are as follows:\n1. engorgement of the mesenteric vessels\n2. crowding and stretching of the mesenteric vessels\n3. medial displacement of the descending colon with herniated bowel loops, usually adjacent to the abdominal wall\n4. right and left displacement of the main mesenteric trunk\n5. dilatation of the small bowel\n6. presence of a transition point between dilated and nondilated small bowel\n7. and presence of small-bowel obstruction.\n\nClustering of SB loops had poor interobserver variability in the referenced study.\n\nSigns complications such as Volvulus (whirl sign/abnormal position of mesenteric vessels) and Ischemia secondary to strangulation should be sought when a internal hernia is suspected.\n\n\nParaduodenal hernia (most common on the left) manifest as a cluster of bowel loops encased in a peritoneal sac, located between the pancreas body and/or tail and the stomach. Signs include:\n1. saclike mass\n2. encapsulation of small bowel\n3. mass effect on the posterior wall of the stomach\n4. left displacement of the main mesenteric trunk\n5. mesenteric vessel abnormalities\n6. inferior displacement of duodenal-jejunal junction (often difficult to asses on CT.", "ACR Code": "7.9", "Category": "Hernia/herniation", "Keywords": "Internal hernaiTransmesenteric herniaSmall bowel obstruction", "Reference": "Arye Blachar, Michael P. Federle, Giuseppe Brancatelli, Mark S. Peterson, James H. Oliver, and Wei Li. Radiologist Performance in the Diagnosis of Internal Hernia by Using Specific CT Findings with Emphasis on Transmesenteric Hernia\nRadiology 2001 221: 422-428" } }, { "U_id": "MPX2292", "TAC": [ "MPX2292_synpic43610", "MPX2292_synpic43611", "MPX2292_synpic43612", "MPX2292_synpic43613", "MPX2292_synpic43614" ], "MRI": [], "Case": { "Title": "Acute Appendicitis in Cystic Fibrosis Patient", "History": "10 y.o. girl with known cystic fibrosis presents with acute onset of right lower quadrant pain, fever, and leukocytosis.", "Exam": "+tnderness to palpation over McBurney's point.\nIncreased WBC count\nFever to 102 F", "Findings": "Ultrasound demonstrates a dilated, blind-ended tubular structure with surrounding fluid.\nCT confirms a massively dilated appendix with surrounding inflammatory changes.", "Differential Diagnosis": "Prior to imaging, the most important diagnostic consideration is to rule out appendicitis. Additional entities which patients with Cystic Fibrosis are predisposed to include intussusception, Crohn Disease, fibrosing colonopahty and bowel wall edema secondary to hypoproteinemia.", "Case Diagnosis": "Acute Appendicitis in Cystic Fibrosis Patient", "Diagnosis By": "Pathology from appendectomy", "Treatment & Follow Up": "Treatment is surgical.", "Discussion": "Although the pulmonary manifestations of Cystic Fibrosis are prominent, significant morbidity secondary to gastrointestinal disease is also seen. Concerning bowel, CF patients are at a higher risk for the development of meconium ileus, meconium ileus equivelent, intussusception, GERD, Crohn Disease, fibrosing colonopahty and bowel wall edema (from hyproteinemia).\nWith respect to appendicitis, however, the incidence is actually lower in patients with CF. This is important to remember when imaging a patient with CF for appendicitis as the appendix may be dilated to 6mm without obstruction or inflammation." }, "Topic": { "Title": "Ultrasound Imaging of Acute Appendicitis", "Disease Discussion": "Acute appendicitis constitutes the most common abdominal surgical emergency, affecting approximately 1 in 14 americans at some point in theirs lives, and 0.1% of the US population per year. Approximately 250,000 appendectomies are performed each year, of which approximately 20% disclose a normal appendix. Ultrasound has recently received considerable attention as a means of diagnosing appendicitis. In skilled hands, it has a sensitivity over 90% and an even higher specificity. The examination is performed by gradually pressing the transducer down on the skin of the right lower quadrant, thereby displacing gas filled bowel loops and minimizing the distance between the transducer and the appendix. The diagnosis is made when the diseased appendix is identified as a tubular, noncompressible structure measuring 6mm or more in diameter and demonstrating no peristalsis. Confidence is further increased when a appendicolith, an echogenic focus with posterior shadowing seen in approximately one-third of patients, is identified. Difficulties with the ultrasongraphic approach include a retrocecal appendix and obese or uncooperative patients. Moreover, the examination is highly operator dependent.", "ACR Code": "7.2", "Category": "Infection, NOS", "Reference": "Gunderman, Richard B : Essential Radiology:clinical presentation/pathophysiology/imaging. 1998." } }, { "U_id": "MPX2295", "TAC": [ "MPX2295_synpic25562", "MPX2295_synpic25568" ], "MRI": [], "Case": { "Title": "Angiomyolipoma (sporadic), Cholelithiasis", "History": "68 y.o. woman with DM type 2, on metformin; with proteinuria.", "Exam": "Urine protein 100mg/dL\nUrine Creatine 56.2mg/dL\nUrine Glucose 500mg/dL\nSerum Glucose 313mg/dL\nSerum Creatine 2.9mg/dL", "Findings": "On ultrasound, there is a well-circumscribed, partially exophytic, uniformly hyperechoic mass measuring approximately 1.8cm. There is no visualized internal blood flow on the doppler image.\n\nOn CT, this well-circumscribed mass is hetergenously hypodense with respect to renal parenchyma. There is macroscopic fat and mildly enhancing internal soft tissue components. No calcification.", "Differential Diagnosis": "Angiomyolipoma\nRenal cell carcinoma (especially clear-cell variant)\nRenal lipoma\nMetastatic disease", "Case Diagnosis": "Angiomyolipoma (sporadic), Cholelithiasis", "Diagnosis By": "Imaging - macroscopic fat and low attenuation ~-60HU on plain CT", "Treatment & Follow Up": "Patient will undergo survellience imaging to follow lesion size. Imaging will include ultrasound, as she is in chronic renal insufficiency from her DM and actually went into acute renal failure following the current CT exam with contrast.", "Discussion": "Although the given lesion has a morphology and density characteristics diagnostic of AML, there are case reports in the literature of cystic/clear cell renal carcinomas having a similar appearance. Further reassuring is the lack of calcification. These lesions should be followed, as they can hemorrhage when large. The AML is a hamartomatous lesion, considered ostensibly benign although sarcomatous degeneration has rarely been known to occur. In the vast majority of cases, however, a renal lesion (partially exophytic 25% of the time) containing macroscopic fat, HU < -60, and internal soft tissue components is an AML until proven otherwise. There is a 15% association with Tuberous Sclerosis." }, "Topic": { "Title": "Angiomyolipoma", "Disease Discussion": "An angiomyolipoma (AML) is a hamartomatous lesion containing fat, smooth muscle, and blood vessels. AMLs are felt to represent a subset of familial neoplasms derived from perivascular epithelioid cells. Most are asymptomatic, and one source (Eble) reports an incidence of 13 per 10,000 adults.\n\nThe typical imaging finding is fat in a renal lesion, thought by many to be virtually diagnostic of AML. Rarely, however, renal cell cancers and oncocytomas can also contain fat. Hence, these lesions should also be considered in the differential.\n\nSmall lesions generally receive no treatment, with resection or embolization being reserved for larger or symptomatic lesions. The primary complication associated with this lesion is spontaneous hemorrhage. Other possible complications include extension into the inferior vena cava and spread to local lymph nodes without progression to malignancy. It should be noted, however, that one subtype of AML, the epithelioid angiomyolipoma, does have malignant potential.\n\nAMLs, in particular bilateral AMLs, are associated with tuberous sclerosis. In tuberous sclerosis, concurrent cysts and, occasionally, renal cell carcinoma may be present.\n\nHormones may stimulate the growth of these lesions as evidenced by the observations that (1) they are generally diagnosed only after puberty in patients with tuberous sclerosis, (2) large AMLs are more common in women than in men, and (3) AMLs sometimes demonstrate significant growth during pregnancy.", "ACR Code": "8.3", "Category": "Neoplasm, benign", "Keywords": "Renal neoplasmAngiomyolipomatuberous sclerosis", "Reference": "1. Eble JN. Angiomyolipoma of kidney. Abstract, Semin Diagn Pathol 1998 Feb;15(1):21-40." } }, { "U_id": "MPX2301", "TAC": [], "MRI": [ "MPX2301_synpic45657", "MPX2301_synpic45808", "MPX2301_synpic45809" ], "Case": { "Title": "Spinal stenosis", "History": "57 year old man with 4 weeks of gradually progressive right lower extremity weakness and gait instability, now acutely worsening.", "Exam": "Diffuse RLE weakness with spasticity noted in both arms and legs (R>L). Additionally, 7-8 beats of sustained clonus on RLE ankle jerk and mildly ataxic gait secondary to instability.", "Findings": "\u2022 MR Brain - Sagittal T1 image w/o contrast demonstrates normal brain parenchyma with apparent tapering of the spinal cord at the C3-C4 level.\n\u2022 MR c-spine - Sagittal T2 FRFSE image w/o contrast demonstrates diffuse disk desiccation at all levels with posterior projecting disk material at C3-C4 level causing cord impingement and severe central canal narrowing.\n\u2022 MR c-spine - Axial T2 FRFSE image w/o contrast at the C3-C4 level demonstrates posterior disk bulge, eccentric to the right with superimposed uncovertebral spurring causing mass impression and effacement of the ventral thecal sac and cord, resulting in severe central canal stenosis.", "Differential Diagnosis": "\u2022 Disk Herniation w/mass effect\nPrior to imaging, considerations also included transverse myelitis, acute inflammatory demyelinating polyneuropathy, and peripheral nerve trauma.", "Case Diagnosis": "Spinal stenosis", "Diagnosis By": "Surgery", "Treatment & Follow Up": "C3-C4 Laminectomy with subsequent physical and occupational therapy" }, "Topic": { "Title": "Spine, spinal stenosis", "Disease Discussion": "Spinal stenosis is a narrowing of the spinal canal. There are many causes, including both congenital and acquired conditions.\n\nCauses:\ncongenital\nshort pedicles\nfacet joint arthritis/hypertrophy\nligament hypertrophy\ndisc bulge and herniation\n\nPresentation: Back and limb pain, neurogenic claudication (*), + straight-leg-raising test and + extension signs, abnormal reflex and sensory examination, weakness.\n\nDiagnosis:\nA meta-analysis boy Vroomen et al (PMID: 10552236)\nStraight leg-raising sens 0.85 spec 0.52\nCrossed straing leg-rasing sens 0.30 spec 0.84\n\nImaging:\nThere continues be controversy about the diagnosis. In symptomatic patients the front-to-back (antero-posterior or sagittal diameter)is often less than 12-20 mm. The side-to-side dimension (lateral narrowing) is usually less than 20-30 mm. The posterior lamina (that form the roof of the spinal canal) are connected to the body of the vertebra by the pedicles. Some patients with short pedicles have symptoms of spinal stenosis.\n\nPneumaticos et al (PMID: 10992311) reported:\ndural sac (AP)10.2mm at L3-4, L4-5, or L5-S1 was 74% sensitive and 74% specific for leg pain (sciatica)\n\nHurri et al (PMID: 9588466) reported:\nsevere stenosis - AP < 7.0 mm\nmoderate stenosis - AP 7.0 - 10.5 mm", "ACR Code": "3.4", "Category": "Systemic, Generalized", "Reference": "; Accepted by jsmirnio", "External Links": "www.nmis.com/onm/html/spconf_stenosis.htm" } }, { "U_id": "MPX2305", "TAC": [ "MPX2305_synpic45395" ], "MRI": [ "MPX2305_synpic45393", "MPX2305_synpic45394", "MPX2305_synpic45396", "MPX2305_synpic45398" ], "Case": { "Title": "Pseudohypoparathyroidism", "History": "25 y.o. woman", "Case Diagnosis": "Pseudohypoparathyroidism" }, "Topic": { "Title": "Hypoparathyroidism", "Disease Discussion": "In 1939, Drake et al. established the following criteria for the diagnosis of hypoparathyroidism: 1) low serum calcium; b) high serum inorganic phosphorus level; c) the absence of renal insufficiency, steatorrhea, chronic diarrhea, and alkalosis; d) exclusion of rickets and osteomalacia.\n\nThe disease may result from a deficiency in parathyroid hormone production or an end organ resistance to the action of the hormone. Pseudohypoparathyroidism (PHP) was first described by Albright et al. in 1942. It is a congenital hereditary abnormality that appears to be transmitted as an X-linked dominant trait characterized by hypocalcemia, hyperphosphatemia, basal ganglion and soft tissue calcification.\n\nIn PHP, there is a defect in the parathyroid hormone receptor-adenylate cyclase system which accounts for end organ resistance.\n\nIn most patients with classic PHP, there is a deficiency of guanyl nucleotide regulatory protein (G-unit) that normally couples receptor activity to adenylate cyclase activity. As a result, the kidney and, less commonly, the bones are unable to respond to parathyroid hormone. There may also be renal inability to hydroxylase 25-hydroxyvitamin D to 1,25 hydroxyvitamin D, the active form.\n\nPseudopseudohypoparathyroidism (PPHP) was the name selected by Albright and Reifenstein to describe a syndrome in short-statured patients with rounded faces, whose roentgen features simulated exactly those of PHP, the difference being the absence of blood chemical changes.\n\nOsteosclerosis, which may be generalized or localized, is the most common skeletal abnormality of hypoparathyroidism. Typically, radiographic findings include increased radiodensity of the skeleton, calvarial thickening and hypoplastic dentition. Subcutaneous calcification may be seen, especially in the area of the hips and shoulders.\n\nParticularly suggestive of hypoparathyroidism are intracranial calcifications of the basal ganglia that may later coalesce into homogeneous masses. Occasionally, these calcifications develop in the cerebellum.\n\nThe clinical syndrome of pseudotumor cerebri in association with hypoparathyroidism was reported as early as 1959 by Palmer et al.\n\nDIFFERENTIAL DIAGNOSIS: Skeletal osteosclerosis is also seen in certain other disorders such as osteoblastic metastasis, myelofibrosis, Paget's disease, fluorosis, renal osteodystrophy, sickle cell anemia, and mastocytosis. In these and other diseases, other radiographic findings are usually apparent, allowing accurate diagnosis. In hypoparathyroidism and PHP, calvarial thickening and hypoplastic dentition are helpful clues, although Paget's disease, sickle cell anemia, and even metastasis may produce increased thickening and sclerosis of the calvarial vault.\n\nBasal ganglion calcification is particularly characteristic of hypoparathyroidism and PHP. It is also seen without known cause in infectious disorders such as toxoplasmosis and cytomegalic inclusion disease, following radiation therapy, and following exposure to toxic substances such as carbon monoxide.\n\nSubcutaneous calcifications are also seen in collagen vascular disease, hypervitaminosis D, milk alkali syndrome, and renal osteodystrophy. Hypoplastic dentition is also seen in cleidocranial dysostosis and pyknodysostosis, hypopituitarism, and hypothyroidism.\n\nSclerosis of the metaphyseal region of long bones seen in some patients with hypoparathyroidism is not specific. It may be seen in children with systemic illness leading to growth arrest lines, leukemia during treatment, heavy metal poisoning, hypothyroidism, healing scurvy, and hypervitaminosis.", "ACR Code": "1.5", "Category": "Endocrine" } }, { "U_id": "MPX2307", "TAC": [ "MPX2307_synpic19895", "MPX2307_synpic19896", "MPX2307_synpic19900" ], "MRI": [], "Case": { "Title": "Sialadenitits", "History": "30 year old male complains of neck soreness and dysphagia with fever.", "Exam": "Elevated WBC, PMN's.\nNegative blood culture.", "Findings": "Enlargement and enhancement of left parotid, submandibular and sublingual glands with inflammatory stranding. No stones or masses. Reactive cervical adenotpathy seen.", "Differential Diagnosis": "Bacterial or viral infection.\nInflammatory disease by stones or radiation\nAutoimmune diseases including Sj?gren disease, lupus\nGranulomatous diseases: Tuberculosis, tularemia, sarcoidosis, catscratch disease, actinomycosis\nDrug-related \nBenign neoplasms\nMalignant neoplasms.\nEndocrine causes including hypothyroidism and diabetes mellitus\nMetabolic causes icluding vitamin deficiency, bulimia, malabsorption", "Case Diagnosis": "Sialadenitits", "Diagnosis By": "Not confirmed. Resolved with antibiotic therapy.", "Treatment & Follow Up": "Failed oral antibiotics. Admitted and treated with IV antibiotics.", "Discussion": "Unilateral envolvement of all 3 sets of glands." }, "Topic": { "Title": "Sialadenitits", "Disease Discussion": "Acute bacterial infections of the salivary glands are uncommon but are usually due to Staphylococcus aureus, Streptococcus, and Haemophillus influenza. Predisposing factors include decreased flow, dehydration, post radiation, chemotherapy, imunosuppression, and recent dental work. TB and cat scratch fever can cause granulomatous sialadenitis. Acute infectious sialadenitis is most commonly viral. The most common viral cause is mumps (a myxovirus) which usually involves only the parotid glands bilaterally. Other viral causes include HIV, coxsackie, and influenza. \n\nClinical findings:\nSigns and symptoms include erythema, pain, tenderness, and swelling which may increase with eating. Frank pus may drain from the ducts, especially with massage of the glands. Adenopathy may be associated. \n \nComplications:\nInfection of the submandibular gland can lead to abscess and Ludwig\u2019s Angina, which is a life-threatening infection of the sublingual and submental spaces. Other complications include stricture of the ducts and chronic sialadenitis.\n\nRadiographic imaging:\nWith infectious indications, CT should be the mainstay of imaging. Noncontrast imaging is useful to identify sialolythiasis and contrast imaging to identify abscesses, cysts, adenopathy and possible neoplasms. If infection is less likely and there is a strong suspicion of neoplasm, fat-saturated MR is the study of choice. Sialography is reserved for the evaluation of chronic sialadenitis without stones. Conventional sialography may be replaced by thin section MR sialography.\n\nTreatment:\nOral antibiotics and hydration are usually sufficient. Palliative methods to decrease inflammation include warm compresses and massage and/or sialogogues to promote drainage. Small abscesses can be treated conservatively as well. Abscesses that do not respond to antibiotic treatment may require surgical drainage.", "ACR Code": "2.2", "Category": "Infection, bacteria", "Keywords": "sialadenitissalivary glandludwig angina", "Reference": "1. Major Salivary Gland Imaging avid M. Yousem, MD, Michael A. Kraut, MD, PhD and Ara A. Chalian, MD Radiology. 2000;216:19-29.)\n\n2. Baylor college of Medicine, http://www.bcm.tmc.edu/oto/studs/saliv.html Core Curriculum SyllabusSALIVARY GLAND DISORDERS, Bobby R. Alford department of otorhinolanyngolgy and Communicative Sciences.\n\n3. Submandibular Sialadenitis/Sialadenosis, Adi Yoskovitch, MD, MSc, Consulting Staff, Department of Otolaryngology - Head and Neck Surgery, Sir Mortimer B Davis Jewish General Hospital. http://www.emedicine.com/ent/topic598.htm" } }, { "U_id": "MPX2308", "TAC": [ "MPX2308_synpic24663" ], "MRI": [], "Case": { "Title": "Non-small cell (squamous cell) carcinoma of the lung (RLL); T3N2M0, corresponding to stage III-A", "History": "74 y/o male (retired O-8 physician) c hx of COPD and s/p CABG and MV replacement presents c SOB and productive cough. (Note: Further H&P records unavailable)", "Exam": "PE: Pt was noted to be hypoxemic. (Note: Further H&P records unavailable)\nLabs: \nCBC \u2013 10.0/16.1/48.6/201; CMP \u2013 BUN 29 (o/w ~wnl)\nAFB culture \u2013 negative p 6 wks; Mycology \u2013 no fungal growth p 6 wks; Bacteriology (bronchial washing) \u2013 few gm neg rods\nHistology \u2013 squamous cell CA and squamous cell CA in-situ", "Findings": "CXR \u2013 increased opacity over lower T-spine on lateral film\nCT \u2013 spiculated mass (~2cm) in RLL c reticular stranding in contact c pleura; no chest wall invasion\nPET \u2013 increased radiotracer uptake along posterior aspect of R mediastinum in region of R atrium", "Differential Diagnosis": "Based upon radiographic demonstration of pulmonary mass:\nMalignancy (primary versus metastatic)\nBenign neoplasm\nGranulomatous disease (e.g., TB, fungal, sarcoidosis)\nOther inflammation (e.g., pneumonia, abscess)\nCongenital abnormality\nMay also consider foreign body or mucus plug", "Case Diagnosis": "Non-small cell (squamous cell) carcinoma of the lung (RLL); T3N2M0, corresponding to stage III-A", "Diagnosis By": "Biopsy", "Treatment & Follow Up": "Radiation therapy\n Chemotherapy (Carboplatin, Taxol)\n Bronchoscopy repeated with radiologic follow-up (Pt most recently c enlarging nodules at site of treated \n malignancy.)", "Discussion": "Based upon the radiographic findings for this patient, the diagnostic possibilities included the differential diagnosis for a pulmonary mass (as above). The definitive diagnosis was made with bronchoscopy and histologic examination, which was consistent with squamous cell carcinoma of the lung.\n\n The American Cancer Society estimated over 160,000 deaths in the United States from lung cancer in 2004, and 87% of all deaths from lung cancer are attributed to tobacco use1. Lung cancer is generally categorized histologically into one of four major types of carcinoma: adenocarcinoma, squamous cell, large cell, and small cell. The former three are distinguished from the latter as non-small cell tumors, in contradistinction to small cell carcinoma, which is generally faster growing and will more likely respond to chemotherapy. Small cell carcinoma only accounts for about 20% of all lung cancers, while the remaining 80% are mostly non-small cell tumors. The type of non-small cell carcinoma seen in this patient, squamous cell, accounts for 20-30% of all lung cancers. It can be distinguished histologically based upon keratin production and the presence of intercellular bridges as seen on light microscopy. \n\n In terms of clinical presentation, cough is present in 45-75% of patients with lung cancer2, and is the most common associated symptom. Squamous cell carcinoma in particular may be associated with elevated serum calcium levels (not noted in this patient) secondary to production of a parathyroid-like hormone, although hypercalcemia may also be the result of metastatic bone disease. Initial workup includes a chest x-ray with two views. While most lesions, even those less than 3 cm in diameter (i.e., T1 lesions) can be identified with radiographs, CT is, of course, more sensitive. \n\n Imaging is also a necessary tool in terms of staging. CT is helpful for identifying the most common sites of metastases from bronchogenic carcinoma\u2014specifically, metastatic liver or adrenal disease, and these organs are generally assessed regardless of whether or not the patient is symptomatic. Other imaging studies for staging are generally reserved for patients whose presentation may suggest involvement of other organs3, such as the brain or the bones. PET may be useful in finding metastatic disease, and according to one source, \u201cCurrently, the accuracy of PET in the detection of M stage is 96%\u201d.4 This patient\u2019s PET scan revealed an area of increased radiotracer uptake consistent with malignancy in the lower lobe of the right lung, and was otherwise normal.\n\n Treatment options and prognosis for non-small cell carcinoma of the lung vary depending on the type of tumor, the degree of differentiation, and the stage of disease. This patient was found to be a T3N2M0, which equates to a stage III-A, signifying locally advanced disease. While stage III-A is technically operable, the role of surgery in stage III disease is somewhat controversial. Additionally, among patients with non-small cell carcinoma undergoing surgical resection, there is a 50% relapse rate. Treatment options other than surgery include radiation and chemotherapy. Radiation therapy, while palliative, does not improve survival over the long-term for most patients with stage III non-small cell lung cancer.5 Following radiation therapy, this patient underwent chemotherapy with carboplatin and Taxol. Overall, the 5-year survival rate associated with stage III-A N2 disease is 10-15%." }, "Topic": { "Title": "Non-small cell (squamous cell) carcinoma of the lung (RLL); T3N2M0, corresponding to stage III-A", "Disease Discussion": "The American Cancer Society estimated over 160,000 deaths in the United States from lung cancer in 2004, and 87% of all deaths from lung cancer are attributed to tobacco use1. Lung cancer is generally categorized histologically into one of four major types of carcinoma: adenocarcinoma, squamous cell, large cell, and small cell. The former three are distinguished from the latter as non-small cell tumors, in contradistinction to small cell carcinoma, which is generally faster growing and will more likely respond to chemotherapy. Small cell carcinoma only accounts for about 20% of all lung cancers, while the remaining 80% are mostly non-small cell tumors. The type of non-small cell carcinoma seen in this patient, squamous cell, accounts for 20-30% of all lung cancers. It can be distinguished histologically based upon keratin production and the presence of intercellular bridges as seen on light microscopy. \n\n In terms of clinical presentation, cough is present in 45-75% of patients with lung cancer2, and is the most common associated symptom. Squamous cell carcinoma in particular may be associated with elevated serum calcium levels (not noted in this patient) secondary to production of a parathyroid-like hormone, although hypercalcemia may also be the result of metastatic bone disease. Initial workup includes a chest x-ray with two views. While most lesions, even those less than 3 cm in diameter (i.e., T1 lesions) can be identified with radiographs, CT is, of course, more sensitive. \n\n Imaging is also a necessary tool in terms of staging. CT is helpful for identifying the most common sites of metastases from bronchogenic carcinoma\u2014specifically, metastatic liver or adrenal disease, and these organs are generally assessed regardless of whether or not the patient is symptomatic. Other imaging studies for staging are generally reserved for patients whose presentation may suggest involvement of other organs3, such as the brain or the bones. PET may be useful in finding metastatic disease, and according to one source, \u201cCurrently, the accuracy of PET in the detection of M stage is 96%\u201d.4 This patient\u2019s PET scan revealed an area of increased radiotracer uptake consistent with malignancy in the lower lobe of the right lung, and was otherwise normal.\n\n Treatment options and prognosis for non-small cell carcinoma of the lung vary depending on the type of tumor, the degree of differentiation, and the stage of disease. This patient was found to be a T3N2M0, which equates to a stage III-A, signifying locally advanced disease. While stage III-A is technically operable, the role of surgery in stage III disease is somewhat controversial. Additionally, among patients with non-small cell carcinoma undergoing surgical resection, there is a 50% relapse rate. Treatment options other than surgery include radiation and chemotherapy. Radiation therapy, while palliative, does not improve survival over the long-term for most patients with stage III non-small cell lung cancer.5 Following radiation therapy, this patient underwent chemotherapy with carboplatin and Taxol. Overall, the 5-year survival rate associated with stage III-A N2 disease is 10-15%.", "ACR Code": "6.321", "Category": "Clinical Exam Finding or Sign", "Keywords": "Non-small cell (squamous cell) carcinoma of the lungsquamous cellcarcinoma", "Reference": "1. Website for the American Cancer Society (www.cancer.org)\n2. Midthun, DE, Jett, JR. Clinical presentation of lung cancer. In: Pass, HI, et al (Eds), Lung Cancer: Principles and Practice, Lippincott-Raven, Philadelphia 1996. p.421.\n3. Pretreatment evaluation of non-small-cell lung cancer. The American Thoracic Society and The European Respiratory Society. Am J Respir Crit Care Med 1997; 156:320.\n4. Bury, T, Dowlati, A, Paulus, P, et al. Whole-body (18)FDG positron emission tomography in the staging of non-small cell lung cancer. Eur Respir J 1997; 10:2529.\n5. Strauss, GM, Langer, MP, Elias, AD, et al. Multi-modality treatment of stage IIIA non-small cell carcinoma of the lung: a critical review of the literature and strategies for future research. J Clin Oncol 1992; 10:829.\n6. Website for the National Cancer Institute (www.cancernet.nci.nih.gov" } }, { "U_id": "MPX2314", "TAC": [ "MPX2314_synpic20230", "MPX2314_synpic20231" ], "MRI": [], "Case": { "Title": "Malignant Embryonal Rhabdomyosarcoma", "History": "26-year old shortness-of-breath walking one flight of stairs for roughly twenty yards. 5 years ago she was diagnosed with a bulky embryonal rhabdomyosarcoma of her right hand. She received 5400 cGy to the area and hoping to gain local control. She did have local recurrence and required amputation in 2001 when the locally recurrent tumor became bulking and had uncontrolled bleeding.", "Exam": "Non-contributory.", "Findings": "CT without----There is a 12 x 9 x 10cm mass in the base of the right lung. There is some mass effect on the mediastinal structures, shifting them to the left. The mediastinal structures are poorly visualized, however, on this non-contrast study. The cardiac fat plane appears to be intact. There is no significant mediastinal lymphadenopathy demonstrated. There is a moderate-sized right pleural effusion. \nCT with----Axial images were obtained through the thorax demonstrating a large highly vascular right lower thoracic mass. The mass causes mild left shift with mediastinal structures and has enlarged slightly compared to the prior CT. It is unclear whether the mass originates from the parenchyma or from the chest wall. There is complete collapse of the right lower lobe and right middle lobe, with a right pleural effusion. There is no mediastinal adenopathy or additional pulmonary lesions.)", "Differential Diagnosis": "Primary Lung CA, Infection, Lymphoma, Pleuropulmonary Blastoma, Malignant Fibrous Histiocytoma, Neuroblastoma, Synovial Sarcoma, Extraskeletal Myxoid Chondrosarcoma , Pseudomesotheliomatous Angiosarcoma", "Case Diagnosis": "Malignant Embryonal Rhabdomyosarcoma", "Diagnosis By": "Unknown.", "Treatment & Follow Up": "Unknown.", "Discussion": "No spicific discussion for this case." }, "Topic": { "Title": "Malignant Embryonal Rhabdomyosarcoma", "Disease Discussion": "Rhabdomyosarcomas describe sarcomas of skeletal muscle. Rhabdomyosarcoma has two forms, embryonal and alveolar. Embryonal is the most common form of this tumor in children and young adolescents, and occurs in head, neck, retroperitoneum, genitourinary system, and rarely in the extremities. Metastasis is frequent and prognosis is poor. Alveolar rhabdomyosarcoma tends to occur in older children and adolescents and metastasis is common. Without recurrent metastasis, survival may be 80% or higher. Treatment includes surgery, chemotherapy, radiation therapy, bone marrow transplant, and clinical trials.", "ACR Code": "6.3", "Category": "Neoplasm, malignant (NOS)", "Keywords": "EmbryonalRhabdomyosarcomaMalignant", "Reference": "Cotran RS, Kumar V, Robbins SL: Robbins Pathologic Basis of Disease, 5th Ed. Philadelphia, W.B. Saunders, 1994, pp. 727-728.\nP. Tabrizi MD, Childhood Rhabdomyosarcoma of the trunk and extremities. The American Journal of Orthopaedics. Aug. 1999. Pg 440.\nWijnaendts LCD van der Linden JC et al. Histopathological features and grading in rhabdomyosarcomas of childhood. Histopathogy. 1994; 24: 303-309." } }, { "U_id": "MPX2315", "TAC": [ "MPX2315_synpic16520" ], "MRI": [ "MPX2315_synpic16521", "MPX2315_synpic16522", "MPX2315_synpic16523", "MPX2315_synpic16524" ], "Case": { "Title": "Cerebral Infarction encompassing the left MCA and ACA territories with occlusion of the left ICA.", "History": "Acute onset right sided neurological collapse two hours prior to presentation.", "Exam": "None.", "Findings": "Non-Enhanced CT - Subtle left sided \"insular ribbon sign\" with loss of normal gray-white differenciation and overlying sulcal effacement. \n\nMRI - Diffusion weighted images demonstrate marked intensity over the entire left ACA and MCA territories. Corresponding ADC hypointensity seen in this case confirms that there has been an acute infarct. The displayed FLAIR image further reveals the hyperintensity involving these same regions. Note the sparing of the PCA territory on the affected side. Selected MRA image of the bilateral carotid arteries demonstrates occlusion of the left ICA shortly after the bifurcation. Note the vertebrobasilar system is intact, supplying the PCA territories.", "Differential Diagnosis": "Left Internal Carotid Artery Occlusion", "Case Diagnosis": "Cerebral Infarction encompassing the left MCA and ACA territories with occlusion of the left ICA.", "Treatment & Follow Up": "None.", "Discussion": "The term \"stroke\" encompasses a wide array of pathological causes of cerebral ischemia. The clinical manifestations which lead to the diagnosis of \"stroke\" may be a result of cerebral infarction, primary intracranial hemorrhage, subarachnoid hemorrhage, or venous occlusion. Of these, cerebral infarction is found to account for patient symptoms 80% of the time. More specifically large vessel infarcts (ICA, MCA, and PCA) account for up to 50% of all clinical strokes. \n\nNECT of the Head is frequently used as an initial study in patients presenting with stroke symptoms because of its relative speed and efficiency in stratifying patients into \"bleed\" and \"infarct\" groups for treatment purposes. While NECT may be fairly effective at ruling out hemorrhage, ruling in infarction in the acute setting is more problematic. Up to 60% of NECT scans will be completely negative within the first few hours of a cerebral infarction. Even when NECT findings are found in the first 24 hrs, they can be quite subtle. \n\nSomewhere between 6 to 24 hours after an acute infarct NECT may begin to reveal the \"dense MCA sign,\" the \"insular ribbon sign,\" and early cerebral hypodensity with associated sulcal effacement indicating evolving edema. The dense MCA sign is seen as hyperattenuation of the MCA usually at the base of the brain on the affected side (the MCA is responsible for up to 40-50% of acute cerebral stokes). The insular ribbon sign is seen as loss of the normally distinct gray-white matter differentiation in the insular cortex along the sylvian fissure. \n\nIn cases where the NECT is non-specific or negative in the setting of clinical stroke, MRI has proven to be particularly helpful. Specific MRI sequences reveal acute infraction immediately following an event. The sensitivity is therefore far greater than NECT in the first few minutes to hours. Early MR findings include the loss of normal flow voids in occluded vessels, signal abnormalities consistent with edema in the affected regions, and most notably diffusion abnormalities seen on diffusion weighted images (DWI). In an acute stroke, hyperintensity on the DWI will correspond to hypointensity on the ADC maps. Further explanation of the physics behind these imaging sequences is beyond the scope of this discussion but can be easily found in any comprehensive Neuroradiology or MRI Physics text.\n\nIn this case, you should notice that the initial NECT of the Head demonstrates some early findings concerning for left sided ACA and MCA infarction. The follow up MRI with DWI, ADC, and MRA sequences reveal much more dramatically the extent and severity of this patient's condition.\n\nReference:\n1. Osborn AG: Diagnostic Neuroradiology, pp341-355, Mosby, St. Louis 1994." }, "Topic": { "Title": "Cerebral Vascular Accident", "Disease Discussion": "The term \"stroke\" encompasses a wide array of pathological causes of cerebral ischemia. The clinical manifestations which lead to the diagnosis of \"stroke\" may be a result of cerebral infarction, primary intracranial hemorrhage, subarachnoid hemorrhage, or venous occlusion. Of these, cerebral infarction is found to account for patient symptoms 80% of the time. More specifically large vessel infarcts (ICA, MCA, and PCA) account for up to 50% of all clinical strokes. \n\nNECT of the Head is frequently used as an initial study in patients presenting with stroke symptoms because of its relative speed and efficiency in stratifying patients into \"bleed\" and \"infarct\" groups for treatment purposes. While NECT may be fairly effective at ruling out hemorrhage, ruling in infarction in the acute setting is more problematic. Up to 60% of NECT scans will be completely negative within the first few hours of a cerebral infarction. Even when NECT findings are found in the first 24 hrs, they can be quite subtle. \n\nSomewhere between 6 to 24 hours after an acute infarct NECT may begin to reveal the \"dense MCA sign,\" the \"insular ribbon sign,\" and early cerebral hypodensities with associated sulcal effacement indicating evolving edema. The dense MCA sign is seen as hyperattenuation of the MCA in usually at the base of the brain on the affected side (the MCA is responsible for up to 40-50% of acute cerebral stokes). The insular ribbon sign is seen as loss of the normally distinct gray-white matter differentiation in the insular cortex along the sylvian fissure. \n\nIn cases where the NECT is non-specific or negative in the setting of clinical stroke, MRI has proven to be particularly helpful. Specific MRI sequences reveal acute infraction immediately following an event. The sensitivity is therefore far greater than NECT in the first few minutes to hours. Early MR findings include the loss of normal flow voids in occluded vessels, signal abnormalities consistent with edema in the affected regions, and most notably diffusion abnormalities seen on diffusion weighted images (DWI). In an acute stroke, hyperintensity on the DWI will correspond to hypointensity on the ADC maps. Further explanation of the physics behind these imaging sequences is beyond the scope of this discussion but can be easily found in any comprehensive Neuroradiology or MRI Physics text.\n\nIn this case, you should notice that the initial NECT of the Head demonstrates some early findings concerning for left sided ACA and MCA infarction. The follow up MRI with DWI, ADC, and MRA sequences reveal much more dramatically the extent and severity of this patient's condition.", "ACR Code": "1.9", "Category": "Infarction and/or Necrosis", "Keywords": "InfarctionStroke", "Reference": "1. Osborn AG: Diagnostic Neuroradiology, pp341-355, Mosby, St. Louis 1994." } }, { "U_id": "MPX2324", "TAC": [ "MPX2324_synpic56946", "MPX2324_synpic56948", "MPX2324_synpic56949" ], "MRI": [], "Case": { "Title": "Infected 4th branchial cleft sinus.", "History": "23 y/o female presents to ER with difficulty breathing and swollen base of neck.", "Exam": "Swollen base of neck on physical exam.", "Findings": "There is a rim enhancing fluid and gas collection originating from the left pyriform sinus and extending inferiorly to the left thyroid lobe.", "Differential Diagnosis": "Deep space neck abscess\nNecrotic lymph node\nInfrahyoid thyroglossal duct cyst\nThyroid abscess\nSquamous cell carcinoma\nThyroid carcinoma with local spread", "Case Diagnosis": "Infected 4th branchial cleft sinus.", "Diagnosis By": "Surgically.", "Treatment & Follow Up": "Surgery confirmed sinus tract extending from pyriform sinus to thyroid consistent with infected 4th branchial cleft sinus. The left thyroid lobe was resected due to suppurative thyroiditis and left thyroid lobe abscess." }, "Topic": { "Title": "Fourth Branchial Cleft Cyst", "Disease Discussion": "The branchial apparatus serves as an embryological precursor to the tissues of the neck. It consists of four branchial arches, clefts and pouches. The branchial arches form musculoskeletal and vascular structures of the head and neck while the pouches form the middle ear, tonsils, thymus and parathyroid gland. The first branchial clefts give rise to the external ear but the other three branchial clefts involute during normal development. Failure of the other branchial clefts to involute forms a branchial cleft cyst. Rarely, when a residual branchial cleft connects with a pouch structure, a complete sinus tract from the pharynx to a blind pouch cyst will form.\n\nBranchial cleft anomalies differ in clinical presentation depending on the specific cleft that fails to involute. Classically, branchial cleft cysts present as a well demarcated mass along the anterior upper third along the sternocleidomastoid muscle. This presentation is consistent with a second branchial cleft cyst which accounts for 95% of branchial cleft anomalies. Fourth branchial cleft anomalies are the rarest developmental defect of the branchial apparatus. These defects commonly form a fistula extending from the apex of the pyriform sinus to end as a blind pouch near the superior pole of the thyroid gland. \n\nFourth branchial anomalies are often not appreciated on physical exam until they become secondarily infected. Typical presentation is that of an inflammatory neck mass, often involving the thyroid gland. These lesions most commonly occur on the left side of the neck. Common sources of secondary infection include oropharyngeal pathogens that inoculate the sinus tract, usually after an upper respiratory infection or surgical manipulation of the oral cavity. Infections can present as generalized erythema and cellulitis along the sinus tract or as supprative thyroditis. Recurrent supprative thyroiditis is highly suggestive of a fourth branchial cleft sinus.\n\nThe initial imaging test of choice is a contrast enhanced CT scan of the neck to detect the location and extent of the lesion. Finding air within a left-sided neck infection in close relation to the thyroid gland is thought to be almost pathognomonic for a fourth branchial cleft sinus tract. A barium study of the pharynx is often utilized to further localize the path of the sinus tract. Ultimately, definitive diagnosis occurs by direct pharyngoscopy to identify the origin of the sinus tract within the pyriform sinus.\n\nInitial management consists of antibiotic therapy. The antibiotic regimen will vary depending on culture results if a biopsy is performed or the clinician\u2019s judgment if not performed. Definitive treatment is surgical excision. Incision and drainage is a poor therapeutic option given the high rate of recurrence without obliteration of the sinus tract. An isolated cyst that has become secondarily infection can be excised once antibiotics have controlled local inflammation. With fourth branchial cleft sinus tracts, optimal therapy consists of closure of the sinus opening. Surgical options for closure include endoscopic assisted monopolar diathermy, abrasion with Tisseel surgical sealant closure of the sinus or another variation of the same theme. Depending on the level of thyroid involvement, an ispilateral hemithyroidectomy may be required.", "ACR Code": "2.1", "Category": "Congenital, malformation", "Keywords": "Fourth Branchial Cleft Sinus TractFusobacteriumActinomycosis", "Reference": "Bajaj, Y., et al. \u201cBranchial anomalies in children.\u201d International Journal of Pediatric Otorhinolaryngology, v. 75 issue 8, 2011, p. 1020-3.\n\nKalwani, A.K. (2004). Current diagnosis & treatment in otolaryngology - head & neck surgery. New York: McGraw-Hill Lange .\n\nLeboulanger, N., et al. \u201cNeonatal vs delayed-onset fourth branchial pouch anomalies: therapeutic implications.\u201d Archives of Otolaryngology - Head & Neck Surgery, v. 136 issue 9, 2010, p. 885-90.\n\nLucente, F.E., & Har-El, G. (2004). Essentials of otolaryngology. Philadelphia: Lippincott Williams & Wilkins.\n\nMisawa, K., et al. \u201cA right-sided fourth branchial cleft cyst: a case report.\u201d International Journal of Pediatric Otorhinolaryngology, v. 75 issue 3, 2011, p. 438-40.\n\nThomas, B., et al. \u201cRevisiting imaging features and the embryologic basis of third and fourth branchial anomalies.\u201d American Journal of Neuroradiology, v. 31 issue 4, 2010, p. 755-60." } }, { "U_id": "MPX2325", "TAC": [ "MPX2325_synpic50880", "MPX2325_synpic50881" ], "MRI": [], "Case": { "Title": "Situs Inversus with Dextrocardia", "History": "64 y.o. woman with symptoms of pulmonary embolism.", "Findings": "Two-view chest x-ray: \nFINDINGS: Frontal and lateral radiographic views of the chest demonstrate stable appearance of complete situs inversus. Left atrial and ventricular enlargement is again noted, grossly stable from prior examination. The lungs are grossly clear. Median sternotomy wires remain intact. Degenerative changes are visualized throughout the bony structures. \n \nIMPRESSION: \n1. Stable appearance of left atrial and ventricular enlargement in the setting of dextrocardia.\n\n\nPA PROTOCOL CHEST CT: \nFINDINGS: There are sternotomy wires surrounded by bone, suggesting surgery at a young age. There is mirror image anatomy of the heart and upper abdominal organs, findings consistent with the patient\"s known situs inversus. The patient has a left-sided aortic arch with mirror image branching vessels.\n \nThe right side of the heart is enlarged, as is the main pulmonary artery, which demonstrates some possible focal narrowing just distal to the pulmonic valve.\n \nThere is no evidence of pulmonary embolism. There is focal band-like attenuation in the lower lungs, likely representing bibasilar atelectasis. No bronchiectasis is seen.\n\nIMPRESSION:\n1. Findings consistent with situs inversus with a left aortic arch and mirror image branching vessels.\n2. No evidence of pulmonary embolism. \n \n\nCT HEMATURIA PROTOCOL (ABDOMEN/PELVIS): \nFINDINGS: Situs inversus is noted.", "Differential Diagnosis": "-Asplenia/Polysplenia\n-Congenital Coronary Abnormalities\n-Sinusitis\n-Ventricular Septal Defect\n-The most common cause of false-positive results is the technologist\"s or radiologist\"s inattention to proper labeling. \n-Kartagener Syndrome", "Case Diagnosis": "Situs Inversus with Dextrocardia", "Diagnosis By": "Imaging", "Treatment & Follow Up": "No treatment required", "Discussion": "Situs abnormalities may be recognized first by using radiography or ultrasonography. However, CT is the preferred examination for the definitive diagnosis of situs inversus with dextrocardia.\n\nPatients with situs inversus usually have a normal life expectancy. In the rare instances of cardiac anomalies, life expectancy is reduced, depending on the severity of the defect. Patients with Kartagener syndrome have a normal life expectancy if the bronchiectasis is treated adequately." }, "Topic": { "Title": "Situs Inversus", "Disease Discussion": "In situs inversus, the morphologic right atrium is on the left, and the morphologic left atrium is on the right. The normal pulmonary anatomy is also reversed so that the left lung has 3 lobes and the right lung has 2 lobes. Additionally, the liver and gallbladder are located on the left, whereas the spleen and stomach are located on the right. The remaining internal structures are also a mirror image of the normal. Situs inversus is present in 0.01% of the United States\u2019 population with no racial or male to female predilection.\n\nFurther classification is independent of the cardiac apical position, indicating only the direction of the cardiac apex at birth: \nSitus inversus with levocardia: base-to-apex axis points to the left.\nSitus inversus with dextrocardia: base-to-apex points to the right.\n\nSitus inversus occurs more commonly with dextrocardia with only 3-5% of these patients having associated congenital heart disease. In patients with situs inversus with levocardia, there is almost always an association with congenital heart disease. \n\nSitus inversus totalis that is associated with primary ciliary dyskinesia is known as Kartagener syndrome. Kartagener Syndrome is a rare autosomal recessive disorder consisting of triad of sinusitis, bronchiectasis predominantly affecting the lower lobes, and situs inversus with dextrocardia. In addition to this triad, some patients present with nasal polyps, an impaired sense of smell, reduced fertility (females) and/or infertility (males).\n\nPatients with situs inversus usually have a normal life expectancy. In the rare instances of cardiac anomalies, life expectancy is reduced, depending on the severity of the defect. Patients with Kartagener syndrome have a normal life expectancy if the bronchiectasis is treated adequately.", "ACR Code": "5.0", "Category": "Procedure or Intervention", "Keywords": "Situs InversusKartagener syndromeDextrocardia", "Reference": "Kinney TB, DeLuca SA. Kartagener's syndrome. Am Fam Physician. Jul 1991;44(1):133-4.\n\nBohun CM, Potts JE, Casey BM, Sandor GG. A population-based study of cardiac malformations and outcomes associated with dextrocardia. Am J Cardiol. Jul 15 2007;100(2):305-9.\n\nWilhelm, A. Situs Inversus. Emedicine.com. Feb 24, 2009.\n\nBergstrom, S. Primary ciliary dyskinesia (immotile-cilia syndrome). UpToDate.com. May 2009." } }, { "U_id": "MPX2319", "TAC": [ "MPX2319_synpic22061", "MPX2319_synpic22062", "MPX2319_synpic22063", "MPX2319_synpic22064", "MPX2319_synpic22065", "MPX2319_synpic22066", "MPX2319_synpic22067", "MPX2319_synpic22068", "MPX2319_synpic22069", "MPX2319_synpic22071", "MPX2319_synpic22072", "MPX2319_synpic22073" ], "MRI": [], "Case": { "Title": "leiomyosarcoma of the inferior vena cava", "History": "Patient is s/p placement of right ureteral stent for extrinsic obstruction of the right ureter due to a \"mass\" demonstrated on previous non-contrast renal stone protocol CT.", "Exam": "Unknown, but a patient with this lesion might present with lower extremity edema.", "Findings": "CT with intravenous and oral contrast material demonstrates a large retroperitoneal mass with central dystrophic calcifications. This mass is completely separate from the right kidney, which other than the hydronephrosis and the presence of the ureteral stent, is otherwise unremarkable. The liver was also normal.\n\nSuperior images demonstrate a \"beak sign\" with the inferior vena cava and the left renal vein, strongly suggestive of the vascular origin of this tumor.\n\nNote the presence of the ureteral stent, and the image demonstrating that the mass has extrinsic mass effect on the course of the ureter, causing the original clinical problem for which this patient was treated.", "Differential Diagnosis": "leiomyosarcoma\nmetastatic disease with tumor thrombus\nangiosarcoma\nhigh-grade liposarcoma", "Case Diagnosis": "leiomyosarcoma of the inferior vena cava", "Diagnosis By": "surgical excision" }, "Topic": { "Title": "leiomyosarcoma of the inferior vena cava", "Disease Discussion": "Leiomyosarcoma is the second most common primary retroperitoneal tumor in adults, and it is the most common venous neoplasm. This entity shows three growth patterns: 1) extravascular (62%), 2 intravascular (5%), and 3) both (33%). The clinical manifestations are: 1) large abdominal mass; symptoms consistent with venous thrombosis/Budd Chiari syndrome. The most common radiologic feature is a large, partially necrotic soft-tissue mass in the retroperitoneum with or without extension into the inferior vena cava. Computed tomography and magnetic resonance imaging typically show a nonfatty, necrotic retroperitoneal mass and a vascular component when it is present. \n\nIn this case, the tumor exhibited both extravascular and intravascular growth patterns, with a couple of images demonstrating a \"beak sign\" with both the IVC and the left renal vein strongly suggesting the origin as being from the IVC itself.\n\nTreatment of choice is surgical excision. Long-term prognosis is usually poor.", "ACR Code": "9.3", "Category": "Neoplasm, sarcoma", "Keywords": "leiomyosarcomainferior vena cava", "Reference": "1. DS Hartman, WS Hayes, PL Choyke and GP Tibbetts. From the archives of the AFIP. Leiomyosarcoma of the retroperitoneum and inferior vena cava: radiologic-pathologic correlation. RadioGraphics, Vol 12, 1203-1220.\n\n2. Mizuki Nishino, MD, Katsumi Hayakawa, MD, Manabu Minami, MD, Akira Yamamoto, MD, Hiroyuki Ueda, MD and Kosho Takasu, MD. Primary Retroperitoneal Neoplasms: CT and MR Imaging Findings with Anatomic and Pathologic Diagnostic Clues. Radiographics. 2003;23:45-57." } }, { "U_id": "MPX2326", "TAC": [ "MPX2326_synpic52459" ], "MRI": [], "Case": { "Title": "Cortical nephrocalcinosis due to acute renal cortical necrosis", "History": "50 yo woman with history of retroperitoneal paraganglioma, s/p resection. Patient developed gross hematuria one week post-op. CT for hematuria revealed an incidental finding.", "Findings": "Abnormal Study With Development Of Thin Cortical Calcifications, Which Extend Into The Medullary Spaces Along The Columns Of Bertin, As Well As Heterogeneous Enhancement Of The Kidneys And Minimal Delayed Excretion.\n\nThe Overall Pattern Is Compatible With Acute Cortical Necrosis.", "Differential Diagnosis": "Acute renal cortical necrosis\nPrimary/secondary oxalosis\nChronic glomerulonephritis\nAlports syndrome (glomerulonephritis, endstage kidney disease, and hearing loss) \nIntrarenal infection in HIV+\nAmphotericin B\nAcute/chronic renal allograft rejection\nAutosomal recessive polycystic disease", "Case Diagnosis": "Cortical nephrocalcinosis due to acute renal cortical necrosis", "Diagnosis By": "Imaging and clinical correlation", "Treatment & Follow Up": "No follow-up apparent. Hematuria symptoms resolved.", "Discussion": "Patient had episode of hypotension during paraganglioma resection. Hypotension hypothesized to have induced acute renal cortical necrosis." }, "Topic": { "Title": "Cortical nephrocalcinosis", "Disease Discussion": "* 95% of cases of nephrocalcinosis are commonly medullary. Cortical nephrocalcinosis accounts for ~5% of cases. \n\n* Causes of cortical nephrocalcinosis:\n\n1. Acute renal cortical necrosis\n-- Usually caused by significantly diminished renal arterial perfusion secondary to vascular spasm, microvascular injury, or intravascular coagulation\n-- Presumed initiating factor is intense vasospasm of the small vessels \n\n2. Primary/secondary oxalosis\n\n3. Chronic glomerulonephritis\n\n4. Alports syndrome \n-- Combination of glomerulonephritis, endstage kidney disease, and hearing loss\n\n5. Intrarenal infection in HIV+\n\n6. Amphotericin B\n\n7. Acute/chronic renal allograft rejection\n\n8. Autosomal recessive polycystic disease\n\n\n* Diagnosis by Ultrasound or CT includes one of the following radiographic patterns:\n1. Thin peripheral band of calcifications\n2. Two thin parallel calcified tracks\n3. Multiple punctate calcifications w/ random distribution", "ACR Code": "8.9", "Category": "Imaging Finding or Artifact", "Keywords": "renalnephrocalcinosis" } }, { "U_id": "MPX2328", "TAC": [ "MPX2328_synpic34951" ], "MRI": [ "MPX2328_synpic34919", "MPX2328_synpic34920" ], "Case": { "Title": "Metastatic ductal carcinoma (breast)", "History": "60 year old woman with PMH of T1bN0M0 breast CA and melanoma, both 9 years ago. S/P lumpectomy, XRT, Tamoxifen, local excision. Presents with 3 months of early satiety and nausea. Additional complaint of blurred vision when looking to her left while driving for 1 week.", "Exam": "Liver edge palpable to 4 cm below ribcage on exam.", "Findings": "Multiple liver lesions replacing approximately 80% of liver volume. Multiple lesions of brain parenchyma in bilateral parietooccipital regions with diffuse enhancement of overlying skull and dura.", "Differential Diagnosis": "Metastatic disease - Melanoma\nMetastatic disease - Ductal Breast CA", "Case Diagnosis": "Metastatic ductal carcinoma (breast)", "Diagnosis By": "Pathology on US guided liver biopsy consistent with Ductal carcinoma. 100% of nuclei stained positive for Estrogen Receptor and 95% positive for Progesterone Receptor.", "Treatment & Follow Up": "Although the patient had used Tamoxifen in the past, she was considered to be chemotherapy naive. Due to systemic dissemination of disease it was decided to attempt chemotherapy first and reserve radiation therapy as a palliative option.", "Discussion": "This is a rather unfortunate case of a woman who was concurrently diagnosed with stage I breast cancer and melanoma 8 years ago. Neither disease demonstrated pathologic lymph node involvement at time of initial diagnosis / treatment. Sadly she now demonstrates diffuse metastasis of pathologically proven ductal carcinoma involving approximately 80% of her liver, her parietooccipital brain parenchyma and overlying skull and meninges, as well as the body of her L4 vertebrae." }, "Topic": { "Title": "Metastatic ductal carcinoma (breast)", "Disease Discussion": "Metastatic ductal carcinoma", "ACR Code": "7.3", "Category": "Neoplasm, carcinoma", "Keywords": "metastaticductalcarcinoma" } }, { "U_id": "MPX2330", "TAC": [ "MPX2330_synpic15177", "MPX2330_synpic15178", "MPX2330_synpic15179", "MPX2330_synpic15180", "MPX2330_synpic15181", "MPX2330_synpic15183" ], "MRI": [], "Case": { "Title": "Retropharyngeal abscess", "History": "Patient reported 1 ? weeks of sore neck and mild throat pain that became acutely severe the night prior to initial presentation. Patient complained of inability to move neck secondary to pain and mother noticed left sided neck fullness and reported intermittent fevers. On presentation, a lateral X-ray showed increased retropharyngeal space width and CT demonstrated phlegmon vs. abscess. Patient was I/D\u2019d 2 days prior to this study with no pus drainage and no clinical improvement. Patient was started on IV clindamycin on admission.", "Exam": "Left sided neck fullness with tenderness to palpation. Positive throat erythema/edema. Otherwise unremarkable. \n \\16/\n9.9-------245 \n /46\\", "Findings": "The is an irregularly margined fluid collection in left lateral retropharyngeal space measuring 1.3 x 2.7 cm at its level of greatest area in the axial plane. Although the slice thickness is not noted the lesion extends from the nasopharynx to the oropharynax and in all likelyhood inferiorly in the retropharyngeal space. There is only minimal enchancement of the margin of the lesion.", "Differential Diagnosis": "Retropharyengeal abscess, \ncellulitis, \nnecrotic liquifactive lymph nodes\nbranchial cleft cyst.", "Case Diagnosis": "Retropharyngeal abscess", "Diagnosis By": "Incision and drainage", "Treatment & Follow Up": "Abscess was incised and drained with ~3 mls serosanguinous/pus fluid removed. Patient was started on clindamycin 150 mg q8hrs for 14 days. Patient was markedly improved clinically immediately following I/D. Cultures were positive for gram positive cocci in singles and pairs consistent with Group A Beta Hemolytic Streptococci. Patient was discharged POD#3." }, "Topic": { "Title": "Retropharyngeal abscess", "Disease Discussion": "Retropharyngeal abscess (RPA) is a disease most commonly seen in children. It is typically associated with viral upper respiratory infections, pharyngitis, and otitis media. These conditions commonly result in adenopathy and RPA is theorized to stem from suppuration of the retropharyngeal lymph nodes. The most common organisms grown from these abscesses are Group A Beta-hemolytic streptococci, Staphylococcus aureus, and Hemophilus influenza. RPA is seen in adults but is often associated with an underlying illness, oral trauma, or dental work. The diagnosis of RPA is based on clinical as well as radiological findings. The presence of soft tissue swelling in the retropharyngeal space on a lateral X-ray (>7 mm @ C2 and >22 mm @ C6) combined with clinical symptoms of pharyngitis, throat erythema, edema is highly suggestive of RPA. Likewise, any abnormal fluid collection in the retropharyngeal space seen on CT combined with physical symptoms is likely RPA. The primary danger of RPA is the spreading of the infection into the area of the carotid sheaths or into a potential space found between the alar and prevertebral fascia which extends into the mediastinum. Treatment typically includes surgical incision and drainage coupled with broad spectrum antibiotic coverage.", "ACR Code": "-1.-1", "Category": "Infection, generalized", "Keywords": "Retropharyngealabscessmediastinum", "Reference": "Morrison JE, et al. Retropharyngeal abscess in children: a 10 year review. Ped Emerg Care 1988; 4: 9-11\nTannebaum, R.D. Adult retropharyngeal abscess: A case report and review. J Emer Medic. 1996;147-158\nWholey MH, et al. The lateral roentenogram of the neck. Radiology. 1958; 71:350-6." } }, { "U_id": "MPX2332", "TAC": [ "MPX2332_synpic48217", "MPX2332_synpic48218" ], "MRI": [], "Case": { "Title": "PCP pneumonia (Pneumocystis jiroveci pneumonia)", "History": "31y/o black female who is HIV positive, with slow onset of fatigue, low grade fever and dyspnea over the past several weeks.", "Exam": "Hypoxic, tachypneic, fatigued black female with diffuse crackles. CD4 count of 6.", "Findings": "Summary of Image Findings: \nCXR: \n\nUnremarkable chest radiograph obtained at admission.\n\nFrontal chest radiograph taken 48 hours after admission demonstrating ill-defined ground glass opacities within the bilateral suprahilar regions. There is also a retrocardiac opacity. Atypical or viral infectious process. A CT was recommended. The admission chest x-ray was unremarkable. \n\nFrontal chest radiograph taken at 72hrs demonstrates interval placement of endotracheal tube and right-sided central venous catheter. New right-sided subcutaneous air. Hypoinflation and mils increased interstitial markings of the lungs. \n\nPortable chest radiograph demonstrates interval development of moderate right-sided pneumothorax\n\nCT:\nChest CT demonstrating diffuse patchy bilateral upper and lower lobe groundglass opacities. Differential considerations include PCP and CMV pneumonia as well as other opportunistic infection. This could represent hypersensitivity pneumonitis.", "Differential Diagnosis": "Non-Cardiogenic Edema\nCytomegalovirus Pneumonitis\nDiffuse Pulmonary Hemorrhage Syndromes\nHypersensitivity Pneumonitis\nPulmonary Alveolar Proteinosis", "Case Diagnosis": "PCP pneumonia (Pneumocystis jiroveci pneumonia)", "Diagnosis By": "Positive pneumocystis DFA (sample obtained from bronchial wall)", "Treatment & Follow Up": "The patient\u2019s respiratory status continued to worsen during her first 48 hours of admission. She subsequently required intubation for 5 days. Her inpatient course was complicated by a moderate right-sided pneumothorax. Her respiratory symptoms eventually improved and she was discharged to home.", "Discussion": "Pneumocystis pneumonia (PCP) is a potentially life-threatening infection that occurs primarily in immunocompromised individuals. The nomenclature for the species of Pneumocystis that infects humans has been changed from Pneumocystis carinii to Pneumocystis jirovecii. Typical immunocompromised states include AIDS patients with CD4 counts<200, long term corticosteroid therapy, organ transplants, and chemotherapy patients. \n\nIn immunocompetent patients presenting symptoms develop rapidly (over 4-10 days); and include hypoxia, dry cough, and fever. A less specific, indolent pattern (over 2-6 weeks) is more common in immunocompromised patients; including fever, malaise, and dyspnea. \n\nClinical suspicion should be high in a hypoxic, immunocompromised patient with ground-glass opacities on plain film or high-resolution CT.\n\nCXR: Perihilar or diffuse ground-glass opacities early, which can advance to a consolidative appearance if untreated. There is a slight upper lobe predominance, which may be associated with prophylaxis with aerosolized pentamidine. Upper lobe thin-walled cysts can develop in 30% of AIDS patients, which can result in pneumothorax. \n\nUncommon plain film findings include multiple pulmonary nodules (some of which may cavitate), a miliary pattern, reticular opacities, and asymmetric consolidation.\n\nPleural effusions and enlarged lymph nodes are associated rarely.\n\nCT: Ground glass opacities on HRCT are the predominant finding. Superimposed smooth intralobular and interlobular septal thickening can also be seen (\u201ccrazy-paving\u201d). Upper lobe cysts can be demonstrated more frequently on CT. The tree-in-bud pattern is not seen in association with pneumocystis pneumonia. \n\nReferences:\n\nBollee, G, Sarfati, C, Thiery, G, et al. Clinical picture of Pneumocystis jirovecii pneumonia in cancer patients. Chest 2007; 132:1305.\n\nGurney, JW. Diagnostic Imaging: Chest. Salt Lake: Amirsus, 2006..\n\nThomas, CF, Jr., Limper, AH. Pneumocystis pneumonia. N Engl J Med 2004; 350:2487." }, "Topic": { "Title": "PCP pneumonia (Pneumocystis jiroveci pneumonia)", "Disease Discussion": "Pneumocystis pneumonia (PCP) is a form of pneumonia caused by the yeast-like fungal microorganism Pneumocystis jirovecii. The causal agent was originally described as a protozoan and spelled P. jiroveci and prior to then was formerly classified as a form of Pneumocystis carinii, a name still in common usage. As a result, Pneumocystis pneumonia (PCP) has also been known as Pneumocystis jiroveci pneumonia and as Pneumocystis carinii pneumonia.\n\nIt is relatively rare in people with normal immune systems but common among people with weakened immune systems, such as premature or severely malnourished children, the elderly, and especially AIDS patients, in whom it is most commonly observed today. PCP can also develop in patients who are taking immunosuppressant medications (e.g., patients who have undergone solid organ transplantation) and in patients who have undergone bone marrow transplantation.\n\nThe organism is distributed worldwide.\n\nPMID 12194762", "ACR Code": "6.2", "Category": "Infection, fungi", "Keywords": "PCPPneumocystisGMS", "Reference": "1. Stringer JR, Beard CB, Miller RF, Wakefield AE (2002). \"A new name (Pneumocystis jiroveci) for Pneumocystis from humans\". Emerg Infect Dis 8 (9): 891-6. PMID: 12194762 \n\n2. Redhead SA, Cushion MT, Frenkel JK, Stringer JR (2006). \"Pneumocystis and Trypanosoma cruzi: nomenclature and typifications\". J Eukaryot Microbiol 53 (1): 2\u201311. PMID: 16441572 \n\n3. Cushion MT . (1998). \"Chapter 34. Pneumocystis carinii. In: Collier, L., Balows, A. & Sussman, M. (ed.), Topley and Wilson's Microbiology and Microbial Infections 9th ed. Arnold and Oxford Press, New York.\": 645\u2013683. \n\n4. Ryan KJ; Ray CG (editors) (2004). Sherris Medical Microbiology, 4th ed., McGraw Hill. ISBN 083858", "External Links": "en.wikipedia.org/wiki/Pneumocystis" } }, { "U_id": "MPX2335", "TAC": [ "MPX2335_synpic38840", "MPX2335_synpic38842" ], "MRI": [], "Case": { "Title": "Benign Adrenal Adenoma", "History": "53 yo asymptomatic female with known adrenal mass.", "Exam": "Within Normal Limits.", "Findings": "Non-contrast axial CT image demonstrates a well-circumscribed smoothly marginated, heterogeneous 3.5 x 3.2 cm mass arising from the left adrenal gland. There are areas within the mass that are low density and measure 5 HU. 50 seconds postcontrast axial CT image demonstrates the lesion to enhance heterogeneously, with areas within the mass measuring 113 HU. 15-minute delay postcontrast axial CT image demonstrates the lesion to enhance heterogeneously, with areas within the mass measuring 35 HU. The percentage enhancement washout was determined to be 72% consistent with a benign adrenal adenoma.", "Differential Diagnosis": "Metastases:\n (Lung, Breast, Melanoma, Gastrointestinal, and Renal Cell \n Carcinoma )\nAdrenal Myelolipoma\nBenign Nonfunctional Adrenal Adenoma\nHyperfunctioning Adrenal Neoplasms with associated endocrine\n syndromes:\n (Cushing\u2019s Syndrome, Conn\u2019s Syndrome, Adrenogenital syndrome in\n newborns and infants.)\n Pheochromocytoma\nInfectious Etiologies:\n Tuberculosis\n Histoplasmosis \nPrimary Adrenal Carcinoma", "Case Diagnosis": "Benign Adrenal Adenoma", "Diagnosis By": "Cross sectional CT imaging." }, "Topic": { "Title": "Benign Adrenal Adenoma", "Disease Discussion": "Lesions/Condition: Benign Adrenal Adenoma\n\nSymptoms: \n\nPatients with benign, nonhyperfunctioning adrenal adenomas typically are asymptomatic, with normal adrenal hormone levels.\n\n\nDiscussion: \n\n\nAdrenal masses are common, occurring as incidental findings in as much as 9% of the population. In patients with either a known malignancy or no known malignancy, benign adrenal masses are more common than adrenal gland metastases. It is important to be able to differentiate between a benign and malignant adrenal mass as the distinction ultimately affects treatment decisions and overall prognosis for oncology patients. \n\nBenign adrenal adenomas contain increased intracytoplasmic lipid content resulting in low attenuating lesions (less than 10 HU) on noncontrast CT scans. Typically, adrenal adenomas are smaller than 4 cm, appearing as smoothly marginated, homogeneous, round masses. In contrast, metastatic lesions to the adrenal gland are large, heterogeneous, lobulated masses with poorly defined margins, and contain very little intracellular fat.\n\nAn attenuation value of less than 10 HU on noncontrast CT scans is diagnostic of an adrenal adenoma. However it is important to note that an attenuation value greater than 10 HU is not necessarily diagnostic of a metastatic lesion. Approximately 30% of benign adenomas will yield attenuation values greater than 10 HU. Thus, contrast enhanced CT can be employed to further characterize a adrenal lesion.\n\nAfter the administration of intravenous contrast material, benign adrenal adenomas avidly enhance, and the washout of contrast material is more rapid than with metastases. Comparing noncontrast scans, with immediate postcontrast scans, and following with delayed postcontrast scans (15 minutes after contrast administration) the percentage enhancement washout of a adrenal lesion can be calculated, and determined as benign or malignant. \n\nPercentage enhancement washout is calculated as the immediate enhancement attenuation minus the delayed enhancement attenuation divided by the immediate enhancement attenuation minus the nonenhanced attenuation multiplied by 100%. If the percentage enhancement washout is greater than 60%, then the adrenal lesion can be characterized as a benign adrenal adenoma. Additionally, if the nonenhanced attenuation is unavailable, the relative percentage enhancement washout can be calculated similarly as the immediate enhancement attenuation minus the delayed enhancement attenuation divided by the immediate enhancement attenuation multiplied by 100%. If the relative percentage enhancement washout is greater than 50%, then the adrenal lesion can be classified as a benign adrenal adenoma. Values of less than either 60% or 50% for the appropriate calculation are indicative of either a metastases or an atypical adenoma.\n\nIf an adrenal lesion cannot be adequately characterized on contrast enhanced CT, chemical shift MR imaging can be used exploiting the knowledge that adrenal adenomas contain intracellular lipid. Chemical shift MR is the difference in behavior of lipid and water protons in a magnetic field. Within an imaged voxel, gradient echo image sequences are performed to separate fat and water protons. Using the spleen as an internal standard, demonstrating loss of signal within an adrenal mass on the T1-weighted out-of-phase image when compared to a corresponding T1-weighted in-phase image, confirms the presence of intracellular lipid, which characterizes a benign adrenal adenoma. A metastatic lesion will not demonstrate a loss of signal intensity on the T1-weighted out-of-phase image, secondary to its poor intracytoplasmic lipid composition.\n\nOf note, chemical shift imaging and nonenhanced CT are not complimentary, since both modalities will most likely characterize the same subset of lipid-rich adenomas.\n\n\nFollow-up:\n\nFollowing the change in a lesion\u2019s size is a useful indicator in predicting malignancy. Adrenal adenomas are slow growing, remaining stable in size and appearance on follow-up examinations.", "ACR Code": "-1.3", "Category": "Neoplasm, benign", "Keywords": "Benign Adrenal AdenomaPercentage enhancement washoutChemical shift MR imaging and adrenal adenoma", "Reference": "Webb: Fundamentals of Body CT. 3rd Edition. Philadelphia: Saunders.\n 2006. \nBrant: Fundamentals of Diagnostic Radiology. 2nd Edition. Philadelphia: \n Lippincott Williams & Wilkins. 1999.\nSiegelman. Body MRI. Philadelphia: Elsevier Saunders 2005.\nMayo-Smith et al. RadioGraphics 2001; 21:995-1012." } }, { "U_id": "MPX2336", "TAC": [ "MPX2336_synpic49838" ], "MRI": [ "MPX2336_synpic49839", "MPX2336_synpic49840", "MPX2336_synpic49841" ], "Case": { "Title": "Cerebellar hemangioblastoma", "History": "33 y/o man with complaints of nonspecific headaches, without focal neurological finding.", "Exam": "Subjective headaches, without focal neurological finding on examination.", "Findings": "\u2022 CT: Well-marginated low-density cystic appearing cerebellar mass with a mural nodule. \n\n\u2022 MRI: T1 hypointense / T2 Hyperintense cystic cerebellar lesion with isointense mural nodule.", "Differential Diagnosis": "\u2022 Hemangioblastoma\n\u2022 Pilocytic Astrocytoma\n\u2022 Metastatic disease\n\u2022 Astrocytoma\n\u2022 Cavernous malformation\n\u2022 Ependymoma", "Case Diagnosis": "Cerebellar hemangioblastoma", "Diagnosis By": "Post-surgical tissue analysis.", "Treatment & Follow Up": "Surgical resection with uneventful postoperative course.", "Discussion": "Hemangioblastomas are uncommon vascular tumors of the central nervous system that occur mainly in the cerebellum and spinal cord. They are benign neoplasms of endothelial origin; most commonly seen in young and middle aged adults. They are the most common primary cerebellar neoplasm in adults 40-60 years old. Among patients with hemangioblastoma, 25 percent occur in those with von Hippel-Lindau disease. On the other hand, hemangioblastomas are the most common lesions associated with VHL disease, eventually affecting 44 to 80 percent of patients. Sporadic hemangioblastoma are usually solitary; multiple tumors within the neuraxis should raise suspicion for VHL disease.\nHemangioblastomas cause neurologic deficits, both by direct compression or tumor-associated hemorrhage. The specific deficit from direct compression depends upon tumor location, and may include cerebellar ataxia, oculomotor nerve dysfunction, motor weakness, or sensory deficits. Patients with spinal hemangioblastomas frequently present with pain. Secondary to this associated risk of hemorrhage, surgical treatment is indicated, as in this patient.\n\nThe diagnostic procedure of choice is gadolinium-enhanced magnetic resonance imaging (MRI). The classic appearance is a well-defined cystic mass with an intensely enhancing mural nodule (60% of cases). Because the tumor nodule receives it\u2019s blood supply from the pia mater, the nodule, which represents the tumor itself, is almost always superficial. Up to 40% are entirely solid. In these cases, the margins can be ill-defined and occasionally can see hemorrhage. Surrounding edema may be present. Flow voids within the nodule may be present.\n\nAn acute hemorrhage secondary to hemangioblastoma can be catastrophic. Intracerebral bleeding from a cerebellar hemangioblastoma may cause rapid obstructive hydrocephalus, cerebellar tonsillar herniation, brainstem compression, or uncal herniation. Bleeding from a spinal hemangioblastoma may result in acute quadriplegia or paraplegia from hemorrhage into the spinal cord. Headache, back pain, or radiculopathy can result from subarachnoid hemorrhage. In these situations, emergency neurosurgical intervention is indicated.\n\nReferences:\nBrant WE, Helms CA. Fundamentals of Diagnostic Radiology. Lippincott, Williams & Wilkins. Philadelphia. 2007.\n\nNeumann, HP, Eggert, HR, Weigel, K, Friedburg, H. Hemangioblastomas of the central nervous system. A 10-year study with special reference to von Hippel-Lindau syndrome. Journal of Neurosurgery 1989; 70:24.\n\nOsborn AG. Diagnostic Neuroradiology. Mosby. St Louis. 1994.\n\nSlater A, Moore NR, Hudson SM. The natural history of cerebellar hemangioblastomas in von Hippel-Lindau disease. American Journal of Neuroradiology. 2003; 24(8):1570-4." }, "Topic": { "Title": "Cerebellar hemangioblastoma", "Disease Discussion": "Cerebellar hemangioblastomas are benign neoplasms of vascular origin. They are not malformations. They account for less than 3% of all intracranial neoplasms (1). These tumors are most common in young and middle-aged adults, where the incidence in males exceeds that of females (2). The cerebellar hemisphere is the most common location, although they may be located in the spinal cord, brain stem, or cerebral hemispheres. Ten percent of hemangioblastomas occur as part of the von Hippel-Lindau disease.\n\nSixty percent of these tumors are cystic, as in this case. The enhancing mural nodule is a common finding in hemangioblastoma. At CT, the cystic portion of the tumor appears low density and does not enhance, while the mural nodule enhances homogeneously and intensely. The MR findings, as seen in this case, include a predominantly cystic tumor with long T1 and long T2 relaxation times, and intense enhancement of the peripheral nodule following gadolinium administration. If the vascular nodule has bled or is proteinaceous, it may be hyperintense on short TR precontrast sequences. More than one enhancing tumor nodule may be seen. Forty percent of hemangioblastomas are solid and display variable degrees of contrast enhancement.\n\nLateral projections of a left vertebral artery subtraction angiogram (arterial and venous phases) in another patient with hemangioblastoma are shown in Films .6 and .7. The angiographic findings are characteristic for a hemangioblastoma. Notice the focal enhancing nodule fed predominantly by the superior cerebellar artery and seen densely enhancing in the arterial phase. Because of significant artifact in the posterior fossa on CT, a small peripheral nodule may be missed and angiography is felt to be more sensitive than contrast CT scan for detecting nodules. MRI with Gd-DTPA may replace angiography for evaluation of patients with suspected hemangioblastoma.\n\nvon Hippel-Lindau disease is an autosomal dominant disorder with incomplete and variable penetrance (3). The incidence is equal in males and females. Multiple lesions have been reported in this syndrome, but the most important lesions which cause significant morbidity include retinal angiomatosis, cerebellar or spinal cord hemangioblastoma, renal cell carcinoma, and pheochromocytoma. Over 50% of patients with this syndrome have hemangioblastomas of the retina, which may present with acute or chronic retinal detachment. Ophthalmoscopic examination reveals these lesions, and radiographic evaluation plays a small role.\n\nThirty-six to sixty percent of patients with von Hippel-Lindau disease have cerebellar hemangioblastoma. Signs and symptoms due to this tumor are the most common cause for patients to present with the syndrome.\n\nAlthough the reported occurrence of spinal cord hemangioblastoma is 5%, autopsy data and MRI suggest the incidence may be higher (4,5). Signs and symptoms of a cerebellar hemangioblastoma may be dramatic, and neurologic deficit from a spinal cord lesion may be overlooked. Typical MR findings in a spinal cord hemangioblastoma include syringomyelia, enhancing nodule, and enlarged feeding and draining vessels. \n\nTwenty-five to thirty-eight percent of patients with von Hippel-Lindau disease will develop renal cell carcinoma, which may be multiple and bilateral. Pheochromocytoma is found in 10% of patients with this disease.\n\nOther lesions in von Hippel-Lindau disease include angiomas of the liver and kidney and cysts of the pancreas, liver, kidney and epididymis. \n\nRoutine screening of family members of a patient with von Hippel-Lindau disease has been recommended. MRI with Gd-DTPA is the procedure of choice to screen for CNS involvement.\n\nIn the adult, the differential diagnosis for a cystic mass in the posterior fossa includes a simple arachnoid cyst or a cerebellar astrocytoma. A simple arachnoid cyst is extra- axial and will not demonstrate an enhancing nodule, although such a nodule may be seen in a cerebellar astrocytoma. Since 40% of cerebellar hemangioblastomas may be solid, this lesion should be included in the differential of a solid or partially solid mass in the posterior fossa in the adult. These lesions are uncommon in children, and medulloblastoma, ependymoma, or astrocytoma are more likely than a cerebellar hemangioblastoma when a posterior fossa mass is seen in a child.", "ACR Code": "1.3", "Category": "Neoplasm, non-glial", "Keywords": "hemangioblastoma" } }, { "U_id": "MPX2327", "TAC": [ "MPX2327_synpic59966", "MPX2327_synpic59967" ], "MRI": [ "MPX2327_synpic59969", "MPX2327_synpic59970", "MPX2327_synpic59971", "MPX2327_synpic59972", "MPX2327_synpic59973", "MPX2327_synpic59974", "MPX2327_synpic59975" ], "Case": { "Title": "Subacute infarction, Broca's area & arcuate fasciculus", "History": "79 y.o. man\u00a0had 2 episodes (approx. 2 months apart) of sudden expressive aphasia (word finding difficulty) lasting 30 - 45 minutes - each with complete resolution. The first episode was in early four months ago; and, the most recent was three months ago. He was labeled with a TIA diagnosis; and, had negative carotid US and negative echocardiograms (for thrombus) - but with a <50% carotid stenosis.\n\nPMH - He has atrial fibrillation and has always been appropriately anticoagulated with warfarin. He does not drink EtOH or smoke, he has medication-controlled hypertension.", "Exam": "No focal neurological deficits.", "Findings": "Small lesion in left thalamus (dark CT, bright T2) \nSubcortical lesion (dark CT, bright T2) in the inferior right frontal lobe", "Differential Diagnosis": "Low grade glioma (astrocytoma Gr 2)\nLacunar infarction\nSubcortical white matter infarct\nCortical MCA infarction", "Case Diagnosis": "Subacute infarction, Broca's area & arcuate fasciculus", "Diagnosis By": "Imaging and Clinical history", "Treatment & Follow Up": "Supportive, with continued control of hypertension and monitoring of INR for warfarin treatment.", "Discussion": "Many patients with resolving neurologic deficits (\"TIAs\") actually have permanent imaging findings - as shown here in this case. The subcortical infarction (old) is in the location of the frontal lobe and arcuate fasciculus, which may be the related to his two episodes of \"word finding\" problems. http://brain.oxfordjournals.org/content/136/11/3451.full.pdf+html http://en.wikipedia.org/wiki/Arcuate_fasciculus\n------------------- Additional History ---------------\nThere was also one episode 18 months ago where he had transient blurry vision in one eye (can't remember which one) that lasted 3 - 4 hours with a negative exam by an ophthalmologist during the symptomatic phase. No recurrence of the ocular/vision issue.\u000b\u000b\n\nThe last piece of history is he was in a horrendous MVA (head-on collision, on the way to the beach) where someone crossed the double yellow in the opposite direction while turning on to the two lane road. This occurred several months after the one-time ocular event. He sustained a neck injury and Fx ribs - but without any loss of consciousness nor any CNS effects. Despite being fully anticoagulated, he did not have any bleeding. His residual effects are decreased range of motion in his cervical spine, primarily unable to completely turn his head to the right. His wife had multiple fractures as well. Both were cut out of their vehicle and airlifted to the hospital." }, "Topic": { "Title": "Speech lateralization, Wada Test, Stroke", "Disease Discussion": "We have all heard of \"left brain - right brain\" - a general concept that each cerebral hemisphere has specific duties, responsibilities, and talents. One of the most important of these is \"lateralization\" of speech functions to the \"dominant\" cerebral hemisphere.\n\nThe \"gold standard\" for lateralization of motor speech function is the \"Wada test\". This is performed by an injection into the carotid artery of sodium amobarbital - if speech functions are depressed, you have injected the \"speech dominant\" hemisphere. \n\nThis procedure was first documented by Dr. Juhn Atsushi Wada, a Japanese-Canadian Neurosurgeon born in 1924; and, it is named for him - the Wada Test.\nSources - http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11624159&dopt=Abstract, http://www.whonamedit.com/doctor.cfm/3132.html, http://www.epilepsy.com/epilepsy/surgery_wada.html\n\nLesions of the speech-dominant hemisphere may produce combinations of\"\n\u2022 Broca Expressive (motor) aphasia - http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=pubmed_Abstract&db=pubmed&cmd=Display&dopt=pubmed_pubmed&from_uid=16881250\n\u2022 Wernicke Receptive (sensory) aphasia - http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Search&db=PubMed&term=wernicke+sensory+aphasia&tool=QuerySuggestion\n\nMany researchers are trying using fMRI to replace the arterial injection used for the Wada test. Source - http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=321227\n\nThe Wada test may be inconclusive, since some patients need and use both hemispheres for speech function. In addition, there are differences in the lateralization of speech function for languages learned later in life. Source - http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=pubmed_DocSum&db=pubmed&cmd=Display&dopt=pubmed_pubmed&from_uid=2917285, http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=pubmed_Abstract&db=pubmed&cmd=Display&dopt=pubmed_pubmed&from_uid=1944849", "ACR Code": "1.1", "Category": "Differential Diagnosis", "Keywords": "speechBroca motor aphasiaWernicke receptive aphasia", "External Links": "www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=pubmed_ExternalLink&db=pubmed&cmd=Display&dopt=pubmed_pubmed&from_uid=15346156" } }, { "U_id": "MPX2338", "TAC": [ "MPX2338_synpic19911" ], "MRI": [], "Case": { "Title": "Pulmonary Arteriovenous Malformation", "History": "Cough.", "Exam": "N/A", "Findings": "Chest X-Ray:\nSolitary Left Pulmonary Nodule.\n\nNoncontrast CT:\nWell defined, lobular left pulmonary nodule with apparent feeding / draining vessel.\n\nContrast Enhanced CT: \nPrompt pulmonary arterial phase enhancement of well defined, lobular left pulmonary nodule with enhancing feeding and draining vessels.", "Differential Diagnosis": "Pulmonary Arteriovenous Malformation", "Case Diagnosis": "Pulmonary Arteriovenous Malformation", "Diagnosis By": "Imaging", "Treatment & Follow Up": "Patient was referred to pulmonary medicine and eventually to Interventional Radiology to discuss emobolization. Feeding vessel diameter measured 3 mm and total lesions size was 1 cm. Shunt fraction determined to be 8%. Patient was offered embolization but opted for follow up in 6 months.", "Discussion": "Pulmonary arteriovenous malformations are abnormal direct connections between the pulmonary arterial and venous systems forming a right to left shunt. Lesions may be single or multiple and are frequently discovered as solitary pulmonary nodules on chest x-ray. Many are associated with Rendu-Osler-Weber syndrome and autosomal dominant disorder. Most often lesions are asymptomatic but they may present with symptoms related to arteriovenous shunting. Symptoms may include hypoxia, dyspnea, hemoptysis, and possibly from embolic events. \n\nOn chest x-ray finding is usually a pulmonary nodule, possibly with a visible feeding vessel extending from the hilum. On CT, lesions appear somewhat lobulated and well defined, also with feeding and draining vessels emanating from and to the hilum. The vascular nature of these lesions is well defined with characteristic intravenous contrast enhancement. Similar findings can also be seen on pulmonary angiography. \n\nImportant radiographic criteria include feeding vessel thickness, overall size, and shunt fraction. Lesions are typically recommended for treatment with the feeding vessel is > 3 mm, the lesion is > 2 cm in size, or the shunt fraction is > 12-15 %. Treatment may be surgical or endovascular. \n\nTreatment is intended to reduce right to left shunting and subsequently to reduce the risk of venous to arterial embolization.\n\n\n\nReferences:\n\n1. Armstrong P. et al. Imaging of Diseases of the Chest. 3rd Edition. Mosby 2000:708-711\n2. http://www.amersham-health.com/" }, "Topic": { "Title": "Pulmonary Arteriovenous Malformation", "Disease Discussion": "Pulmonary arteriovenous malformations are abnormal direct connections between the pulmonary arterial and venous systems forming a right to left shunt. Lesions may be single or multiple and are frequently discovered as solitary pulmonary nodules on chest x-ray. Many are associated with Rendu-Osler-Weber syndrome and autosomal dominant disorder. Most often lesions are asymptomatic but they may present with symptoms related to arteriovenous shunting. Symptoms may include hypoxia, dyspnea, hemoptysis, and possibly from embolic events. \n\nOn chest x-ray finding is usually a pulmonary nodule, possibly with a visible feeding vessel extending from the hilum. On CT, lesions appear somewhat lobulated and well defined, also with feeding and draining vessels emanating from and to the hilum. The vascular nature of these lesions is well defined with characteristic intravenous contrast enhancement. Similar findings can also be seen on pulmonary angiography. \n\nImportant radiographic criteria include feeding vessel thickness, overall size, and shunt fraction. Lesions are typically recommended for treatment with the feeding vessel is > 3 mm, the lesion is > 2 cm in size, or the shunt fraction is > 12-15 %. Treatment may be surgical or endovascular. \n\nTreatment is intended to reduce right to left shunting and subsequently to reduce the risk of venous to arterial embolization.\n\n\n\nReferences:\n\n1. Armstrong P. et al. Imaging of Diseases of the Chest. 3rd Edition. Mosby 2000:708-711\n2. http://www.amersham-health.com/", "ACR Code": "6.9", "Category": "Congenital, malformation", "Keywords": "AVMPulmonary Arteriovenous Malformation" } }, { "U_id": "MPX2345", "TAC": [ "MPX2345_synpic36477" ], "MRI": [], "Case": { "Title": "Thoracic Neuroblastoma", "History": "4-month-old baby boy presents with persistent cough.", "Exam": "Vital signs are normal. Lungs are clear bilaterally and heart demonstrates a regular rate and rhythm. The remainder of the physical exam is unremarkable. Laboratory studies including CBC and CMP are within normal limits.", "Findings": "\u2022 Frontal view of the chest shows a large right paraspinal mass with splaying of the 3rd and 4th posterior ribs.\n\n\u2022 Non-contrast CT image of the chest below the carina shows a soft-tissue paraspinal mass with calcification medially. \n\n\u2022 Contrast-enhanced CT image above the carina shows epidural extension. Ovoid region of enhancement; and, anteriorly is atelectatic lung.\n\n\u2022 Pre- and post-contrast T1-weighted MR images show the mass to be of intermediate intensity with heterogeneous enhancement. The mass abuts the trachea and epidural extension is clearly seen. \n\n\u2022 Sagittal T2-weighted MR image shows extension of the mass into the right neural foramina from T2-T4.", "Differential Diagnosis": "\u2022 Neuroblastoma\n\u2022 Ganglioneuroblastoma\n\u2022 Ganglioneuroma\n\u2022 Neurofibroma\n\u2022 Schwannoma\n\u2022 Rhabdomyosarcoma", "Case Diagnosis": "Thoracic Neuroblastoma", "Diagnosis By": "Biopsy and Pathology", "Treatment & Follow Up": "The patient underwent complete surgical resection with greater than 95% of the tumor removed. Adjuvant chemotherapy was also initiated. The patient will be followed clinically and with follow-up MRIs.", "Discussion": "Posterior mediastinal masses in children are most commonly neurogenic in origin (30-40%). These lesions are divided into those arising from: sympathetic ganglia (neuroblastoma, ganglioneuroma, ganglioneuroblastoma), peripheral nerves (neurofibroma, Schwannoma), and paraganglion cells (very rare in children). \n\nA posterior mediastinal mass found in a young child should be considered neuroblastoma until proved otherwise. This patient presented with only persistent cough despite evidence of intraspinal extension. This is not unexpected given that about one half of cases are discovered incidentally on chest films.\n\nClassic radiologic findings of thoracic neuroblastoma are demonstrated. These lesions can be mistaken for pneumonia, atelectasis, or prominent thymus. Splaying of the ribs is a clue to the diagnosis of neuroblastoma in this case. \n\nPlain films are sensitive in suggesting the diagnosis, while MRI is the best modality for evaluating extent of disease. Biopsy is necessary to confirm the diagnosis. Complete surgical resection is the treatment of choice." }, "Topic": { "Title": "Thoracic Neuroblastoma", "Disease Discussion": "Thoracic neuroblastoma is a neoplasm arising from sympathetic ganglia and accounts for approximately 16% of all neuroblastomas. These typically present as a posterior mediastinal mass at a median age of 0.9 years. Other tumors arising from sympathetic ganglia include ganglioneuroblastoma and ganglioneuroma, which more commonly occur in older children.\n\nThe clinical presentation of thoracic neuroblastoma is characterized by a variety of symptoms and signs, including fever, malaise, back pain, anemia, and respiratory symptoms such as cough and shortness of breath. Apical lesions may produce Horner's syndrome, and spinal canal involvement may cause lower limb weakness. Rarely, patients may present with the opsoclonus cerebellar ataxia syndrome. That being said, approximately 50% of thoracic neuroblastomas are found incidentally on chest films. \n\nChest radiographs demonstrate a posterior mediastinal mass, which may be mistaken for pneumonia, atelectasis, or normal thymus. Rib erosion and costal separation may be evident. Calcification is often present and metastatic tumors are most often bilateral, paravertebral, and in the lower posterior mediastinum. Computed tomography typically shows an inhomogeneously enhancing paraspinal mass. Approximately 40% of lesions show calcification, and extradural extension occurs in approximately 20%. MRI is valuable in determining intraspinal extension, marrow involvement, and chest wall and lymph node involvement.\n\nDiagnosis is made with biopsy of the lesion, and complete surgical resection is the treatment of choice. Compared to abdominal neuroblastoma, thoracic neuroblastoma presents at an earlier age and stage, and is associated with a more favorable 4-year survival rate (58% versus 48%).", "ACR Code": "6.3", "Category": "Neoplasm, malignant (NOS)", "Keywords": "NeuroblastomaPosterior mediastinal mass", "Reference": "1. Kuhn JP, Slovis TL, Haller JO. Caffey's Pediatric Diagnostic Imaging. 10th ed. Vol.1. 2004. pp 1210-1214\n2. Slovis TL et al (1997) Thoracic Neuroblastoma: What is the best imaging modality for evaluating extent of disease? Pediatr Radiol 27: 273-275" } }, { "U_id": "MPX2344", "TAC": [ "MPX2344_synpic39231" ], "MRI": [], "Case": { "Title": "Medulloblastoma", "History": "8yo African American female who presents with morning vomiting, wide-based gait, headache, and blurred vision\n\nHer complaints began four to six weeks ago, and her pediatrician attributed her symptoms to a \"viral syndrome\", prescribing rest, fluids and Tylenol. Her vomiting is projective in nature, without associated nausea. It started only occasionally, but progressed to daily over the course of 3-4 weeks. Her headache is described as pancephalic, worse in the morning as well and not relieved by aspirin. She describes the blackboard at school as being \"fuzzy\". Her pre-natal course and delivery were unremarkable, and she has been in the 85th percentile on her growth curve. Developmental milestones wore reached at appropriate ages. She has done very well in school with an 89 average, but notes she does less well in gym class lately. There is a positive family history for cancer in her paternal grandmother and aunt, location and type unknown. Review of systems also reveals photophobia of three weeks duration. No meds, NKDA.", "Exam": "Pulse 105, BP 90/60 R 20. T 99.0 Pertinent findings include 3+ bilateral papillary edema, EOMI, PERRLA with complaints of brightness of light. VA 20/50 O.D., 20/60 O.S., CN II-XII grossly intact, neck supple, heart, lungs and abdominal exam normal, motor and sensory exam normal, cerebellar exam remarkable for wide-based gait, inability to tandem walk, and decreased finger to nose, heel to shin and rapid alternating movements with dysmetria and dysdiadochokinesis.\n\nLab studies: CBC normal, chemistries normal, urinanalysis normal", "Findings": "Contrast and Non-contrast study of the head: Turning attention to the non-contrast study first, the most striking finding is the extent of hydrocephalus, with dilatation of both lateral ventricles and third ventricle. Looking at images three and four, there is an obvious hyperdense mass in the posterior fossa in the midline, obliterating the fourth ventricle. There seems to be hypodense regions in the center of the mass, suggesting central necrosis or cyst. Compression of the brainstem anteriorly is also evident There is no evidence of calcification, and both internal auditory canals are normal, and there are no cortex lesions. The contrast exam shows enhancement of the mass in a uniform manner. Vascularity is otherwise normal.", "Differential Diagnosis": "Cerebellar astrocytoma, Medulloblastoma, Ependymoma,\nHemangioblastoma, Dermoid tumor, Choroid plexus papilloma, Colloid cyst, Meningioma, and secondary metastases are neoplasms which occur in the posterior fossa", "Case Diagnosis": "Medulloblastoma", "Discussion": "1) Medolloblastoma- occurs 2:1 males versus females, most common in the first and second decades of life, arise in the region or the medullary velum, therefore midline and often obliterate the fourth ventricle. The large majority of lesions are rounded or lobulated, denser than surrounding brain and generally homogenous with occasional cystic regions or central necrosis. Also a probable choice in this case due to the presence of the above characteristics.\n\n2) Ependymoma- a relatively uncommon tumor arising within the fourth ventricle, which is therefore obliterated, resembles a medulloblastoma in that it is hyperdense and homogenous. Calcification suggests ependymoma and hydrocephalus is usually marked. Possible here as all of the findings of ependymoma are present except for calcification.\n\n3) Cerebellar astrocytomas- most common type of primary intracranial al tumor found in the posterior fossa, usually show low attenuation lying in one cerebellar hemisphere, but midline position is not uncommon. Not likely here due to the high attenuation relative to surrounding brain.\n\n4) Meningioma- occur in the cerebello-pontine angle and may be confused wish acoustic neuromas, grow over the cerebellar convexity, particularly at its lateral angle. They enhance markedly. Also unlikely here due to the midline position of to lesion, the obstructive hydrocephalus, and the anterior shift of the brain stem with fourth ventricle obliteration.\n\n5) Hemangioblastoma - may be solitary or multiple. less commonly as part of the von Hippel-Lindau syndrome with eye, brain and cord involvement, usually in the cerebellar hemispheres, hypodense on non-contrast study with marked enhancement with contrast. Unlikely here as well since the lesion was hyperdense before enhancement.\n\n6) Dermoid tumor - heterogeneous tumor with mixed soft tissue and bone density, uncommon in the posterior fossa- unlikely due to relative homogeneity of the lesion.\n\n7) Colloid cyst - existence of which is debated in the fourth ventricle, (usually present in the third ventricle at the posterior margin of the foramen of Monroe), present as hypodense lesions, not likely with this hyperdense lesion, far too big.\n\n8) Metastases- form the most common type of cerebellar tumor seen in adults, usually in the hemispheres, with mild hydrocephalus Unlikely here due to the patient's age, prior excellent health, location of the tumor and the severe hydrocephalus.\n\n9) Choroid plexus papilloma- exceedingly rare, and the choroid is normal on contrast study." }, "Topic": { "Title": "Medulloblastoma", "Disease Discussion": "Definition: A malignant, invasive embryonal tumor of the cerebellum with preferential manifestation in children, predominantly neuronal differentiation, and an inherent tendency to metastasize via CSF pathways.", "ACR Code": "1.3", "Category": "Neoplasm, glial", "Reference": "WHO Classification of Tumors: Tumors of the Nervous System, 2001." } }, { "U_id": "MPX2352", "TAC": [ "MPX2352_synpic17766" ], "MRI": [], "Case": { "Title": "Congenital Bronchial Atresia", "History": "65 year old female, afebrile with cough.", "Exam": "Afebrile. Lungs Clear Bilaterally.", "Findings": "Hyperlucent/Hyperinflated basilar left lower lobe with central tubular opacity.", "Differential Diagnosis": "Congenital Bronchial Atresia\nCongenital Lobar Emphysema\nForeign Body Aspiration w/ Air Trapping\nEndobronchial Tumor w/ Air Trapping", "Case Diagnosis": "Congenital Bronchial Atresia", "Treatment & Follow Up": "None.", "Discussion": "Congenital bronchial atresia is felt to be the result of an in-utero vascular insult after the 15th week of gestation which results in focal obliteration of a lobar or segmental bronchial airway while the distal structures remain intact. Most commonly in the LUL, any lobe can be affected. Typically, mucous plugging affects the atretic and distal segment secondary to inadequate clearing past the focal occlusion. Collateral air filling through pores of Kohn and channels of Lambert results in a hyperlucent hyperinflated lobe distal to the atretic segment. The mucous impacted bronchus distal to the atresia appears as a tubular / ovoid opacity near the center of the hyperlucent lobe. Hyperinflation of the affected lobe may result in secondary findings such as diaphragmatic flattening, mediastinal shift, or displacement of normal fissures. \n\nReferences:\nMcLoud TC. Thoracic Radiology, The Requisites. Mosby 1998:72" }, "Topic": { "Title": "Congenital Bronchial Atresia", "Disease Discussion": "Congenital bronchial atresia is felt to be the result of an in-utero vascular insult after the 15th week of gestation which results in focal obliteration of a lobar or segmental bronchial airway while the distal structures remain intact. Most commonly in the LUL, any lobe can be affected. Typically, mucous plugging affects the atretic and distal segment secondary to inadequate clearing past the focal occlusion. Collateral air filling through pores of Kohn and channels of Lambert results in a hyperlucent hyperinflated lobe distal to the atretic segment. The mucous impacted bronchus distal to the atresia appears as a tubular / ovoid opacity near the center of the hyperlucent lobe. Hyperinflation of the affected lobe may result in secondary findings such as diaphragmatic flattening, mediastinal shift, or displacement of normal fissures.", "ACR Code": "6.-1", "Category": "Congenital, malformation", "Keywords": "Bronchial AtresiaCongenital", "Reference": "References:\nMcLoud TC. Thoracic Radiology, The Requisites. Mosby 1998:72" } }, { "U_id": "MPX2350", "TAC": [ "MPX2350_synpic30202", "MPX2350_synpic30204" ], "MRI": [], "Case": { "Title": "Crohn's Disease - with ileo-rectal fistualization", "History": "67 year-old woman with long standing history of Crohn's disease and multiple prior abdominal surgeries who is status post colectomy with rectal stump and diverting ileostomy and complaints of rectal discharge over the past 2-3 months.", "Exam": "N/A", "Findings": "CT examination from four months prior to the fluoroscopic study demonstrating an ill-definied soft tissue density within the left hemiabdomen adjacent to multiple loops of small bowel consistent with a phlegmon. Additionally the superior aspect of the patient's remnant rectum is visualized.\n\nSingle contrast water-soluable (gastrograffin) enema was performed to assess for any fistulous connections between the rectal stump and the aformentioned phlegmon. Fluoroscopic images demonstrate a thin column of contrast coursing superiorly and anteriorly into the left hemiabdomen into the region of the phlegmon. There was no cutaneous extension of the contrast material. No contrast material was present within the dependant regions of the abdomen to suggest free spillage into the abdomen.", "Differential Diagnosis": "Ileo-rectal fistua", "Case Diagnosis": "Crohn's Disease - with ileo-rectal fistualization", "Diagnosis By": "Fluoroscopic evaluation", "Treatment & Follow Up": "Increased steroid dosing regiment.", "Discussion": "The patient tolerated the fluoroscopic examination without any difficulty. Water soluable contrast material was utilized in case there was leakage into the peritoneum and in the event that she would require immediate surgical intervention." }, "Topic": { "Title": "Crohn's Disease", "Disease Discussion": "Pathology: Crohn disease is a chronic inflammatory process of the bowel that can affect any part of the GI tract from the mouth to the anus. It is likely multifactoral including genetic influence, dysfunctional immune response, enteric normal flora bacteria, and other environmental factors. It is believed to be the result of an imbalance between inflammatory and anti-inflammatory mediators. Most cases involve the small bowel, particularly the terminal ileum. Crohn disease typically affects the bowel asymmetrically, involving the mesenteric side more severely than the antimesenteric border. Although any area of the GI system may be affected, the most common site of disease is the ileo-cecal region, followed by the colon. Microscopically, the initial lesion appears as a focal inflammatory infiltrate around the crypts, followed by ulceration of superficial mucosa, then by deeper invasion and non-caseating granulomas. Grossly, the early abnormality is hyperemia and edema of the involved mucosa. Later, superficial ulcers form, which become deep serpentine linear ulcers located both longitudinally and transversely giving the mucosa a \u201ccobblestone\u201d appearance. The lesions are often segmental; being separated by healthy areas, hence the term \u201cskip lesions\u201d. Transmural inflammation results in thickening of the bowel wall and narrowing of the lumen. As the disease progresses, it is complicated by obstruction, fistula formation, abscess formation, adhesions, and malabsorption.\n\nClinical: The characteristic presentation of Crohn disease is with abdominal pain and diarrhea, which may be complicated by intestinal fistula formation, obstruction, or both. Unpredictable flares and remissions with a long course characterize Crohn\u2019s. Treatment is generally medical including antidiarrheal, anti-inflammatory, and sometimes antibiotics. Chronic complications include fistulas, adhesions, and marked luminal narrowing with partial bowel obstruction which may require surgery.\n\nRadiographic findings:\nRadiological evaluation includes diagnosis, evaluation of distribution, and evaluation for complications. The distribution of small bowel Crohn\u2019s disease is best assessed by enteroclysis and CT. The terminal ileum is nearly always involved in small bowel disease and is the only site in up 30 % of patients.\n \nSmall bowel contrast studies: The sensitivity of enteroclysis is reported as very good in detecting Crohn\u2019s disease but often does not correlate well with disease activity. Superficial abnormalities include thickened folds due to mucosal edema, transverse and longitudinal ulcers, punctate collections of barium, and small nodules. Transmural abnormalities include deep fissures and penetrating ulcers. Cobblestoning results from intersecting longitudinal and transverse ulcers with intervening heaped-up edematous tissue. Deep ulcerations may result in fistulae. Thickened bowel may appear as separations of loops. Luminal narrowing is always present resulting from spasm and edema during the acute phase or fibrotic strictures in chronic disease. Ileitis can also manifest as a \u201csting sign\u201d on barium study secondary to spasm or fibrotic stricture fromation. The mesenteric aspect and adjacent mesentery are commonly affected more than the antimesenteric border. Extramural mesenteric inflammation and abscesses may induce compression and displacement of bowel loops.\n\nCross sectional imaging: Both CT and MR imaging are reported to have a sensitivity of over 95% for the detection of Crohn disease. At more advanced stages, CT and MR imaging can help identify and characterize pathologically altered bowel segments as well as extraluminal lesions including abscesses, fat stranding, and adenopathy. Cross sectional imaging can also clearly depict inflammatory lesions and conditions that require elective gastrointestinal surgery, aiding in treatment planning.", "ACR Code": "7.2", "Category": "Inflammatory, NOS", "Keywords": "CrohnInflammatory bowel diseasestring sign", "Reference": "1. Radiology of the Small Bowel. Michael Chen, MD. Igaku-Shoin publishers. 1992.\n2. Cross-sectional Imaging in Crohn Disease. Furukawa et al. Radiographics.2004; 24: 689-702. \n3. http://www.eurorad.org\n4. Crohn Disease.Senthil Nachimuthu, MD. E-medicine. 10 March 2004." } }, { "U_id": "MPX2354", "TAC": [ "MPX2354_synpic20936", "MPX2354_synpic20937" ], "MRI": [], "Case": { "Title": "Diagnosis: L1 Burst Fracture.", "History": "History: 34 y/o active duty white male with 2/10 lower back pain after a fall. The fall occurred while exiting a helicopter at an unknown height by \u201cfast-roping:\u201d sliding down a rope suspended from the helicopter using only hands and feet to control speed of descent. Initially he landed on his feet, but then he fell onto his sacrum. The onset of pain was immediate and localized to his lower back. Since the date of injury, the patient denies change in quality or radiation of pain, lower extremity numbness or weakness, loss of bladder or bowel control, erectile dysfunction.", "Exam": "Physical Exam and Laboratory: Pertinent physical exam findings: Lower extremities were neurovascularly intact distally with brisk capillary refill and no edema. Patellar and Achilles deep tendon reflexes were 2+ and symmetric. Babinksi sign was negative. Strength was 5/5 in bilateral iliopsoas, quadriceps, hamstrings, tibialis anterior, gastrocnemius, extensor hallicus longus. Cranial nerves II \u2013 XII were intact. Sensation and proprioception were normal and symmetric in both upper and lower extremities. There was no tenderness to palpation on the patients back or costovertebral angle tenderness. Gait was normal.", "Findings": "Imaging Findings: \nL-Spine: Lateral view shows anterior wedging of the L1 vertebral body. The superior end-plate of L1 is displaced posteriorly approximately 1 cm relative to the inferior end plate of T12. The inferior end-plate of L1 is displaced posteriorly approximately 0.5 cm relative to the superior end-plate of L2.\nCT: Fracture of the L1 vertebral body with posterior displacement of the central fragment, right lateral displacement of the right fragment.", "Differential Diagnosis": "Differential Diagnosis for these findings in this case: L1 Burst Fracture", "Case Diagnosis": "Diagnosis: L1 Burst Fracture.", "Treatment & Follow Up": "Treatment and Follow-up: Surgical stabilization of the L1 vertebral body spine to prevent compression of the spinal cord was done. An L1 corpectomy and T12 to L2 fixation posteriorly with pedicle screws and rods and laterally with a single parallel rod was performed. An intervertebral cage with bone graft was inserted into the body of L1. Follow up was scheduled at 3 and 6 months to ensure that L1 remained stable without encroaching into the spinal canal and that the patient remained free of neurological deficits.", "Discussion": "Discussion (include references): Burst fractures of the lumbar spine occur when the anterior (anterior longitudinal ligament, anterior half of the vertebral body, and anterior portion of the annulus fibrosis) and middle (posterior longitudinal ligament, posterior half of the veterbral body, and posterior portion of the annulus fibrosis) columns of the spine fail under a compressive load. This forces the intervertebral disc into the vertebral end-plate, causing the vertebral body to burst with outward displacement of its fragments. (Canale: Campbell\u2019s Operative Orthopaedics, 10th ed., 2003. pp1643-4)\n Patients should first be evaluated with radiographs. To determine the position and extent of fracture fragments, CT should be performed. If patients have symptoms of spinal cord compression, MRI should be performed.\n Although conservative treatment of a burst fracture can be attempted using a brace, surgical correction is indicated if a posteriorly displaced fragment may cause neurological symptoms. Pedicle screws with rods can be used to fix the vertebral bodies cephalad and caudal to the burst vertebra. Titanium cages with bone graft can be left in place after corpectomy of the fractured body to promote fusion and rotational stability. (Mariotti AJ, Diwan AD, Current concepts in anterior surgery for thoracolumbar trauma. Ortho Clin North Am 2002;33(2):403-12)\n Plain film radiographs and CT can be used to assess postoperative hardware stability. Physical exam will also ensure that neurological symptoms have not developed." }, "Topic": { "Title": "Burst Fracture", "Disease Discussion": "Burst fractures of the lumbar spine occur when the anterior (anterior longitudinal ligament, anterior half of the vertebral body, and anterior portion of the annulus fibrosis) and middle (posterior longitudinal ligament, posterior half of the veterbral body, and posterior portion of the annulus fibrosis) columns of the spine fail under a compressive load. This forces the intervertebral disc into the vertebral end-plate, causing the vertebral body to burst - with outward displacement of its fragments. (Canale: Campbell\u2019s Operative Orthopaedics, 10th ed., 2003. pp1643-4)\n\nPatients should first be evaluated with radiographs. To determine the position and extent of fracture fragments, CT should be performed. If patients have symptoms of spinal cord compression, MRI should be performed.\n\nAlthough conservative treatment of a burst fracture can be attempted using a brace, surgical correction is indicated if a posteriorly displaced fragment may cause neurological symptoms. Pedicle screws with rods can be used to fix the vertebral bodies cephalad and caudal to the burst vertebra. Titanium cages with bone graft can be left in place after corpectomy of the fractured body to promote fusion and rotational stability. (Mariotti AJ, Diwan AD, Current concepts in anterior surgery for thoracolumbar trauma. Ortho Clin North Am 2002;33(2):403-12)\n\nPlain film radiographs and CT can be used to assess postoperative hardware stability. Physical exam will also ensure that neurological symptoms have not developed.", "ACR Code": "3.4", "Category": "Trauma", "Keywords": "L1 Burst FractureBurst FractureFracture", "Reference": "(Mariotti AJ, Diwan AD, Current concepts in anterior surgery for thoracolumbar trauma. Ortho Clin North Am 2002;33(2):403-12)" } }, { "U_id": "MPX2358", "TAC": [ "MPX2358_synpic16279" ], "MRI": [], "Case": { "Title": "MYELOLIPOMA", "History": "89 year old woman with CHF who had questionable pulmonary nodule on chest radiograph which prompted a CT exam.", "Exam": "NA", "Findings": "The lungs were negative for pulmonary nodule or any acute cardiopulmonary abnormality (CHF was successfully treated prior to scan). Incidental finding of a well circumscribed, heterogeneous mass seen in the right adrenal fossa. This measured 5.0 x 4.0 x 5.5 cm. There is macroscopic fat (HU= - 50 ) seen through most of this mass with some areas of soft tissue density. No calcification is identified. There is a normal left adrenal gland. Also identified are multiple hepatic cysts demonstrating fluid attenuation (HU= 11 ), imperceptible walls and no lesion enhancement, indicating simple cysts.", "Differential Diagnosis": "Myelolipoma \nMyelolipoma\nMyelolipoma\nAdrenal Adenoma (not likely given appearance)\nLiposarcoma (very rare)", "Case Diagnosis": "MYELOLIPOMA", "Treatment & Follow Up": "No treatment reguired unless becomes symptomatic or bleeds.", "Discussion": "See Factoid." }, "Topic": { "Title": "MYELOLIPOMA", "Disease Discussion": "Myelolipoma is an uncommon, benign, nonfunctioning neoplasm of the adrenal, found in less than 1% of population based on autopsy series. It is composed of variable amounts of fat and hematopoietic tissue, including myeloid and erythroid cells and megakaryocytes. The imaging appearance is based on the fat content of this lesion. Thus they appear echogenic on US, low attenuation on CT and hyperintense on T1 weighted in phase MR images. The etiology is unclear, but myelolipoma may be a result of metaplasia of cells in the adrenal, possibly myeloid cells misplaced during embryogenesis. It affects men and women equally. Although this is a nonfunctioning tumor, in 10% it is associated with endocrine disorders, including Cushing syndrome, congenital adrenal hyperplasia, and Conn syndrome. Most myelolipomas (80%) are asymptomatic and are of no clinical significance. Some (10%) become large and cause vague symptoms or pain. Large myelolipomas may hemorrhage, which can be the cause of pain. Size ranges from 1 to 15 cm, with a mean of about 4 cm. \n\nOn CT, most myelolipomas are well-circumscribed masses. Nearly all contain some definite fat density (<-20 HU). However, the amount of fat is widely variable, ranging from nearly all fat, to more than half fat (50%), to only a few tiny foci of fat in a soft-tissue mass (10%). Occasionally, the mass has an attenuation value between that of fat and water because the fat and myeloid elements are diffusely mixed. Calcification is seen in 30%, often punctate. With hemorrhage, high density areas can be seen. Bilateral myelolipomas occur in about 10%. \n\nThe presence of fat in an adrenal mass is the key to the diagnosis of myelolipoma, because virtually no other adrenal lesion contains fat. Teratoma and liposarcoma of the adrenals are extraordinarily rare. Macroscopic fat on CT (HU= -30 to -110), usually obviates the need for biopsy, but if necessary (i.e. extra-adrenal location which may then mimic a liposarcoma), diagnosis can be confirmed by percutaneous needle sampling. A definite diagnosis is important because surgical resection is not indicated unless there has been significant hemorrhage. In nearly all cases, a diagnosis of adrenal myelolipoma can be made confidently based on CT findings alone.", "ACR Code": "8.3", "Category": "Neoplasm, benign", "Keywords": "adrenal glandmyelolipomabenign neoplasm", "Reference": "Computed Body Tomography with MRI Correlation. 3rd edition, 1997. Lee J.K., Sagel S.S., Stanley R.J., CD rom version, chapter 19. \n\nState of the Art Adrenal Imaging-RSNA Refressher Course. Mao-Smith W.W., Boland G.W., Noto R.B., Lee M.J. Radiographics 2001; 21:995-1012.\n\nBody CT: A practical approach.1st edition, 2000. Slone R.M., Fisher A.J., Pickhardt P.J., pg 184-185." } }, { "U_id": "MPX2347", "TAC": [ "MPX2347_synpic39279" ], "MRI": [ "MPX2347_synpic39275", "MPX2347_synpic39276", "MPX2347_synpic39277", "MPX2347_synpic39714", "MPX2347_synpic39715", "MPX2347_synpic39716", "MPX2347_synpic39717", "MPX2347_synpic39718", "MPX2347_synpic39719", "MPX2347_synpic39720" ], "Case": { "Title": "Vein of Galen Malformation, Onyx embolization; and, embolization into branches of the Pulmonary arteries.", "History": "8 yo girl for follow-up of after embolization of Vein of Galen Aneurysm with Onyx. A Chest X-ray was ordered to confirm endotracheal tube placement following an uneventful post-operative course.", "Exam": "Physical exam and vitals normal. No respiratory complaints.", "Findings": "Chest radiograph demonstrates branching opacity in a bronchovascular distribution in the right middle lobe.\nReview of prior imaging demonstrates presence of a Vein of Galen Malformation (VOM) with recent embolization treatment with Onyx. Multiple serpentine flow voids seen on MRI. Angiogram confirms shunting from multiple feeders into a dilated Vein of Galen, draining into an enlarged straight sinus.", "Differential Diagnosis": "Without the provided history, this radiographic finding is concerning for aspiration of contrast or other radio-opaque material.", "Case Diagnosis": "Vein of Galen Malformation, Onyx embolization; and, embolization into branches of the Pulmonary arteries.", "Diagnosis By": "Based upon surgical history.", "Treatment & Follow Up": "The patient denied pulmonary symptoms. The patient did complain of persistent headaches in the days following the embolization procedure.", "Discussion": "This radiographic finding was noted immediately following embolization of the patient's Vein of Galen (VOG) malformation using the liquid embolic agent, Onyx. Onyx is a relatively new material composed of an ethylene-vinyl alcohol copolymer, DMSO, and tantalum. Tantalum provides the radio-opaque property for intraoperative visualization and accounts for the appearance on this patients chest radiograph.\n\nRelatively little formal analysis of the efficacy and safety of the use of Onyx in the treatment intracerebral AVM's has been conducted. A study by Van Rooij et al, revealed an average of 75% reduction in the volume of AVM's with a complication rate of 13.6%. Jahan et al reported similar numbers of 63% and 26%, respectively. While post-embolization headaches were reported, the majority of collected and reported problems involved hemorrhagic complications. Such complications are postulated to be secondary to physiologic changes in the regional cerebral blood flow surrounding the perinidal tissues. Proposed solutions to such complications include possible staged emobolization procedures such to produce less-drastic changes in flow dynamics.\n\nWhile no instances of symptomatic pulmonary embolism(PE) were reported in these investigations, symptomatic pulmonary embolism is a serious potential consequence of accidental peripheral emobolization. As in this patient\u2019s case, the risk of symptomatic PE is likely lower if only small volumes of the embolic agent migrate to the pulmonary vasculature. This is a risk that may be mitigated with careful technique and intraoperative observation.\n\nReferences\nVan Rooij et al, Brain AVM Embolization with Onyx.\nAmerican Journal of Neuroradiology. 28:172-177, January 2007\n\nJahan et al, Embolization of Arteriovenous Malformations with Onyx: Clinicopathological Experience in 23 Patients.\nNeurosurgery. 48(5):984-997, May 2001" }, "Topic": { "Title": "Vein of Galen Malformation", "Disease Discussion": "The vein of Galen is a short but large diameter vein that drains the paired internal cerebral veins and the two basal veins of Rosenthal into the straight sinus. It is just posterior to the pineal gland, in the quadrigeminal plate cistern. This vein probably arises from remnants of the posterior median prosencephalic vein of Markowski.\n\nBy tradition, an aneurysmal enlargement of a midline venous structure in this location has been called a \"Vein of Galen Aneurysm\". However, the true origin of this dilated vascular structure is probably persistence of the anterior portion of the median prosencephalic vein (ProsV) of Markowski. In many patients with this malformation, there is no \"classic\" vein of Galen; and, often, there is no straight sinus. Instead, the dilated remnant of the ProsV drains into upward directed \"falcine sinus\".\n\nThese lesions most often result from vascular shunts developing between the early choroidal arteries and the deep or midline veins, during the 6th to 11th week of gestation. At this time in development, the brain is primarily supplied by multiple choroidal arteries, then - later - the circle of Willis.\n\nThese AV shunts persist, preventing involution of the anterior prosencephalic vein. A persistent falcine vein is often present, that drains the ProsV into the straight sinus or superior sagittal sinus.\n\nVein Of Galen Malformation Symptoms, Signs\n\u2022 Childhood\n\u00bb High Output Failure\n\u00bb Persistent Ductus \n\u00bb Hydrocephalus\n\u00bb Cranial Bruit/Thrill\n\u2022 Adult\n\u00bb Asymptomatic \n\u00bb Pineal Symptoms\n \n \n\u2022 Vein Of Galen Malformation Types/Causes\n\u00bb Parenchymal AVM (Shunt)\n\u00bb Direct Fistulae To VOG\n\u00bb Dural Fistula Draining into VOG\n\u00bb Sinus Thrombosis (Intrauterine)\n\u00bb Hypoplastic Straight Sinus\n \n \n\u2022 Hydrocephalus is very common in childhood\n\u00bb Mechanical\n - Aqueductal Obstruction from compression of tectum\n\u00bb Impaired CSF Resorption\n - Venous Hypertension\n \n\nUoR Teaching File - http://www.urmc.rochester.edu/smd/Rad/neurocases/Neurocase06.htm", "ACR Code": "1.3", "Category": "Vascular", "Keywords": "pineal regionmedian prosencephalic vein of Markowskivein of Galen Aneurysm", "Reference": "http://www.ajnr.org/cgi/content/abstract/27/2/317\nhttp://www.nature.com/jp/journal/v25/n8/fig_tab/7211349ft.html\nhttp://www.urmc.rochester.edu/SMD/rad/neurocases/Neurocase06.htm\nhttp://www.esnr.com/www/case_studies/vien_of_galen_malformations.htm\nhttp://www.radpod.org/2007/07/24/vein-of-galen-malformation/", "External Links": "www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&DbFrom=PubMed&Cmd=Link&LinkName=pubmed_pubmed&LinkReadableName=Related%20Articles&IdsFromResult=16015373&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstract" } }, { "U_id": "MPX2355", "TAC": [ "MPX2355_synpic52990", "MPX2355_synpic52992", "MPX2355_synpic52993" ], "MRI": [], "Case": { "Title": "Cowden's Syndrome", "History": "48y/o female with history of bilateral breast cancer s/p bilateral mastectomy who is currently hospitalized after obtaining bronchoscopy to evaluate multiple pulmonary nodules.", "Exam": "Physical exam shows thyroid enlargement with prominent left sided nodules as well as bilateral mastectomy.", "Findings": "CXR: hypoinflation of lungs, increased pulmonary vascular markings throughout bilateral lung fields, multiple pulmonary nodules with the most prominent in the right lower lobe, mild cardiomegaly, lack of breast shadows bilaterally, fluid withing the right major and minor fissure. \n\nCT of Chest/ABD/Pelvis: Diffuse thyroid enlargement with nodule present in the left lobe, multiple large (>5mm) pulmonary nodules throughout both lungs, bilateral myelolipomas with L larger than R.", "Differential Diagnosis": "Cowden's Syndrome\nLi-Fraumeni Syndrome\nPeutz-Jeghers Syndrome\nBRCA1/2\nAtaxia-Telangiectasia Syndrome", "Case Diagnosis": "Cowden's Syndrome", "Diagnosis By": "Genetic Testing", "Discussion": "Patient had bilateral mastectomy prior to age of 50 indicating a likely genetic disorder contributing to early onset breast cancer vs. prophylactic mastectomy's. The patient's thyroid abnormalities make Cowden's syndrome the most likely genetic abnormality. The multiple pulmonary nodules as well as myelolipomas are also consistent with this diagnosis" }, "Topic": { "Title": "Early Onset Breast Cancer", "Disease Discussion": "Differential diagnosis for genetic disorders that cause early onset breast cancer\n\nBRCA1/2 - most common genetic cause of breast cancer. \n - Other Associated cancers include:\n 1. Ovarian cancer - usually with BRCA1\n 2. Fallopian tube and primary peritoneal cancer\n 3. Prostate cancer - usually with BRCA2\n 4. Pancreatic, Melanoma, Uterine, Cervical, Colon, and Gastric\n\nLi-Fraumeni Syndrome \u2013 p53 mutation\n - Associated cancers include\n 1. Soft tissue sarcomas\n 2. Osteosarcomas\n 3. Leukemias\n 4. Brain tumors\n 5. Adrenocortical malignancies\n 6. Early onset breast cancer in 22% of affected individuals \n\nAtaxia-Telangiectasia \u2013 mutation in the ATM gene\n - Associated cancers include\n 1. Lymphomas and leukemias in homozygotes\n 2. Solid tumors that occur at younger age in heterozygotes.\n 3. Breast cancer occurs 2 times more often in heterozygotes.\n\nCowden Syndrome \u2013 mutation in PTEN gene (tumor suppressor)\n - Associated cancers/tumors\n 1. multiple hamartomatous lesions in the skin, mucosa, breast \n and intestine\n 2. early onset breast cancer as well as increased frequency of \n benign breast lesions - breast cancer is usually ductal and \n usually bilateral\n 3. early onset thyroid cancer\n 4. Benign thyroid abnormalities\n 5. Endometrial cancer\n 6. Renal cancer\n 7. Increased prevalence of lipomas and adenomas\n\nPeut-Jeghers syndrome \u2013 mutation in STK11\n - Associated cancers/tumors\n 1. Hamartomatous polyps in GI tract\n 2. Mucocutaneous melanin deposits in buccal mucosa, lips, \n fingers and toes\n 3. Gastrointestinal cancers\n 4. Pancreatic cancer\n 5. 55% risk of developing breast cancer\n 6. 20% risk of ovarian cancer\n 7. Increased risk of uterine cancer", "ACR Code": "0.3", "Category": "Congenital, genetic", "Keywords": "Breast CancerCowdenMultiple Hamartoma syndrome", "Reference": "Peshkin, BN, Isaacs, C. Risk assessment and clinical characteristics of women with a family history of breast and/or ovarian cancer. UpToDate Online version 18.1. 15 Oct, 2009.", "External Links": "www.utdol.com.gw3.lrc.usuhs.mil/online/content/topic.do?topicKey=breastcn/7619&selectedTitle=1%7E14&source=search_result" } }, { "U_id": "MPX2359", "TAC": [ "MPX2359_synpic17942" ], "MRI": [], "Case": { "Title": "Aortic Dissection", "History": "76 year old gentleman with abdominal pain scheduled for a CT of the abdomen and pelvis to delineate cause.", "Exam": "PE: BP 160/93. Other vitals unremarkable.\nLabs: CBC, CHEM 7, AMYLASE/LIPASE, LFTs - WNL.", "Findings": "- Infrarenal abdominal aorta (normal size) with a contrast-filled false lumen and displacement of intimal calcifications, between true and false lumens.", "Differential Diagnosis": "- Aortic wall hematoma\n- Penetrating aortic ulcer\n- Chronic dissection", "Case Diagnosis": "Aortic Dissection", "Treatment & Follow Up": "- When confined to the descending aorta (Stanford Type B) as this is, medical treatment is standard (control of HTN). Surgery is indicated if a Type B dissection is complicated by 1) an ischemic extremity, 2) mesenteric ischemia, 3) renal artery compromise, 4) rupture or 5) aneurysmal enlargement of false lumen." }, "Topic": { "Title": "Aortic Dissection", "Disease Discussion": "Def: blood within the medial of the aortic wall resulting from\u2026\n(1)\tintimal tear (VAST MAJORITY/95+% of cases)\n(2)\tintramural hematoma (vasa vasorum)\n\nCONTRIBUTING FACTORS (3):\n*medial degeneration\n*wall stress from persistent aortic motion\n*HTN?hydrodynamic forces\n\nClassifications Schemes (2)\n\nI. DeBakey (memory aid: \u201cthe world\u2019s #1 surgeon!\u201d, and this classification system uses numbers) \n\tType I (29-34%): involves ascending and descending aorta\n\tType II (12-21%): involves ascending aorta only\n\tType III (50%!!!): IIIA and IIIB (B = \u201cBelow diaphragm\u201d)\n\nMemory aid: \u201cI = II + III\u201d (Jack H, 2002)\n\nII. Stanford:\n\tType A (70%)\n\tType B (30%)\n\nIncidence:\n\n\t3/1,000\n\n\t1/205 autopsies\n\n\tapproximately 2,000 cases/year in the U.S.\n\n\tM:F = 3:1\n\nPredisposing factors: cystic medial necrosis/aortic wall disease\n\nPEARLS:\n*28% start in fusiform aortic aneurysms (>5 cm in diameter)\n*when in females, 50% occur during pregnancy\n*re-entry into the aortic lumen occurs in a minority (10%)\n*important associations: HTN (in 60-90% of cases), Marfan\u2019s (16%), ED, Relapsying Polychondritis, Valvular AS, Turner\u2019s, Behcet\u2019s, Coarctations, Bicuspid Aortic Valves, s/p Prosthetic Valves, Traumatic (rare), s/p Catheterization, Pregnancy, Aortitis (e.g., SLE), Cocaine abuse\n\nSigns & Symptoms: \n*tearing, sharp chest pain (ddx includes acute MI)\n*asymmetric or absent peripheral pulses\n*shock (in 25%)\n*neurologic deficits (in 25%), including anterior spinal artery syndrome\n*persistent oliguria\n*signs of tamponade\n\nClinical classification:\n\tACUTE: if present < 2 weeks\n\tCHRONIC: > 2 weeks old\n\nHelical Flow Pattern:\n\n*Ascending aorta: anterior/right lateral wall\n*Arch: superior and posterior wall\n*Proximal/thoracic descending aorta: posterior and left lateral wall\n*Abdominal aorta:\n(1)\tusually terminates in the left iliac artery (80%)\n(2)\tinvolves the left renal artery in 50%\n\nRADIOLOGIC FINDINGS:\n*CXR-->compare to priors\n\t-normal in 20-25% of cases\n\t-displace intimal calcifications in descending aorta\n\t-increased aortic diameter\n\t-widened mediastinum (>8cm)?from hemorrhage\n\t-enlargement of the cardiac silhouette (LVH,hemopericardium)\n\t-L-sided pleural effusion (27%)\n\t-Rightward deviation of the trachea, endotracheal tube\n\t-left apical pleural cap\n\n*ECHO: TEE > TTE in sensitivity (99%) and specificity (77-97%); intravascular ECHO may also be performed\n\t-intimal flap\n\n*ANGIO: 1st choice for final confirmation and staging; use a percutaneous right (not left) femoral artery approach; ensure the rapid washout of contrast material during the test injection (especially if a false lumen is present)\n\t-esp. good for demarcating entry and re-entry pints\n\t-detecting branch vessel involvement\n\t-AI\n\t-false negatives: if complete thrombosis of false lumen is \n present or if intimal flap is not tangential to the x-ray \n beam\n\nContrast-enhanced CT:\n\t-crescentic high attenuation clot within the false lumen\n\t-internally displaced intimal calcifications\n\t-intimal flap separating 2 aortic channels may be seen \n without contrast in anemic patients\n\t-FALSE NEGATIVES:\n\t\t*inadequate contrast opacification\n\t\t*misinterpreted as aortic aneurysm with mural \n thrombus\n\t-FALSE POSITIVES:\n\t\t*streak artifact secondary to cardiac/aortic \n motion-->can mimic the intimal flap\n\t\t*opacifiec normal sinus of Valsalva\n\t\t*normal pericardial recess mistaken form thrombus\n\t-CT protocol: AORTA\n\t\tContrast: precontrast images prn, then 150 ml IV \n contrast @ 2-3 ml/sec with 20 sec delay\n\t\tCoverage: top of arch through iliac bifurcation in \n suspended inspiration\n\t\tParameters: 5 mm collimationat 5 mm intervals with \n pitch of 1.5\n\t\t\t\n\nMR (95-100% sensitive and specific)\n\t-white blood GE sequences and phase reconstruction \n techniques can help identify slowing flowing blood in the \n false channel\n\t-limitation = resolution of the arch vessels\n\t-\u201dblack blood\u201d images (SE)\n\t-phase image reconstructions!\n\t-get GE cine study\n\nTreatment\n(1)\tDeBakey Type III/Stanford Type B: medical management to \n maintain blood pressures <120/70 mmHg\n(2)\tDeBakey Types I & II/Stanford Type A: immediate surgical \n graft re-inforcement of aortic wall?prevents both \n rupture and progressive AI\n-surgical procedure: 80% retain opacification of both lumens after \n surgery\n\t*Bentall Prodecure\n\nWithout treatment\u2026\n*death immediately (2%)\n*death within one day (20-30%)\n*death within one week (50%)\n*death within three weeks (60%)\n*death within one month (75%)\n*death within three months (80%)\n*death within one year (80-95%).\n\nWith treatment\u2026\n*5-10% mortality rate following timely surgery.\n*40% 10-year survival once out of the hospital.", "ACR Code": "5.4", "Category": "Vascular", "Keywords": "Aortic dissectionDissectionDeBakey", "Reference": "Dahnert W. Radiology Review Manual, Fourth Edition. \nLippincott Williams & Wilkins: Philadelphia, 2000.\n\nMiller SW. Cardiac Radiology, The Requisites. Mosby Inc.: \nSt. Louis, 1996: pp. 391-400.\n\nSlone RM, et. Al. Body CT, A Practical Approach. McGraw- Hill: New York, 2000, pp. 1-3, 86-87." } }, { "U_id": "MPX2361", "TAC": [ "MPX2361_synpic8322" ], "MRI": [], "Case": { "Title": "Renal cell carcinoma", "History": "Request CT Abdomen with contrast. \n 60 yo male had a large left perinephric hematoma after mild blunt trauma. Unable to evaluate left kidney on prior study. Please evaluate.", "Findings": "RADIOLOGIC FINDINGS: axial CT of abd w/contrast \n 4 cm rounded solid mass in upper left kidney with extracapsular spread. Likely renal cell carcinoma. No\n evidence of regional lymphadenopathy or renal vein involvement. Evidence of left perirenal hematoma -\n resolving. Liver and lungs normal. \n Multiple bilateral renal cysts, 6.5 by 5cm on right.", "Differential Diagnosis": "primary tumors: \n -oncocytoma - indistinguishable from renal cell ca preoperatively. \n -Angiomyolipoma - usually have fat density on CT \n -Transitional cell ca -usually in renal pelvis and collecting system \n -Adrenal tumors \n -simple cyst -smooth, thin wall on CT, sharply demarcated, no contrast uptake \n\n secondary tumors: \n -metastatic disease - lung, breast, stomach ca \n -lymphoma", "Case Diagnosis": "Renal cell carcinoma", "Discussion": "Renal cell ca is relatively rare, comprising 2.3% of all adult cancers. It affects males twice as often as females and incidence peaks in the sixth decade of life. Renal tumors are being detected more commonly as incidental findings with the increased use of CT. Symptomatic patients may present with flank pain, hematuria, and/or abdominal mass. This tumor invades perinephric tissue but has not metastasized to regional nodes or to distant sites. The stage is thus T3aN0M0. \n The treatment for renal cell ca is radical nephrectomy. Patients with tumors extending beyond the renal capsule have a 50% disease-free survival 5 yrs postoperatively. The cysts seen bilaterally are benign and have no association with the malignancy. \n This case emphasizes the importance of follow-up studies, since the patient's initial CT showed a perirenal hematoma obscuring the left kidney." }, "Topic": { "Title": "Renal malignancy", "Disease Discussion": "HISTORY: Request CT Abdomen with contrast.\n60 yo male had a large left perinephric hematoma after mild\nblunt trauma. Unable to evaluate left kidney on prior study. Please evaluate.\n\nRADIOLOGICAL FINDINGS: \n4 cm rounded solid mass in upper left kidney with extracapsular spread. Likely renal cell carcinoma. No evidence of regional lymphadenopathy or renal vein involvement. Evidence of left perirenal hematoma - resolving. Liver and lungs normal.\nMultiple bilateral renal cysts, 6.5 by 5cm on right. \n\nDIAGNOSIS: renal cell carcinoma\n\nDIFERENTIAL DIAGNOSIS: \nprimary tumors:\noncocytoma - indistinguishable from renal cell ca preoperatively.\nAngiomyolipoma - usually have fat density on CT\nTransitional cell ca -usually in renal pelvis and collecting system\nAdrenal tumors\nsimple cyst -smooth, thin wall on CT, sharply demarcated, no contrast uptake\n\nsecondary tumors:\nmetastatic disease - lung, breast, stomach ca\nlymphoma\n\nDISCUSSION: \nRenal cell ca is relatively rare, comprising 2.3% of all adult cancers. It affects males twice as often as females and incidence peaks in the sixth decade of life. Renal tumors are being detected more commonly as incidental findings with the increased use of CT. Symptomatic patients may present with flank pain, hematuria, and/or abdominal mass. \n\nThis tumor invades perinephric tissue but has not metastasized to regional nodes or to distant sites. The stage is thus T3aN0M0.\nThe treatment for renal cell ca is radical nephrectomy. Patients with tumors extending beyond the renal capsule have a 50% disease-free survival 5 yrs postoperatively. The cysts seen bilaterally are benign and have no association with the malignancy.\n\nThis case emphasizes the importance of follow-up studies, since the patient's initial CT showed a perirenal hematoma obscuring the left kidney.", "ACR Code": "8.3", "Category": "Neoplasm, carcinoma", "Keywords": "renal cell carcinoma", "Reference": "Guinan, PD. Renal cell carcinoma:Tumor size, stage, and survival. J Urol 1995;153:901", "External Links": "cancernet.nci.nih.gov" } }, { "U_id": "MPX2374", "TAC": [ "MPX2374_synpic21447" ], "MRI": [], "Case": { "Title": "Pulmonary artery pseudoaneurysm secondary to erosion of tumor into the wall of the middle lobar branches of the right pulomary artery and obstruction of superior lobar branches of the right pulmonary artery due to mass effect from the tumor.", "History": "59 year old male with recent diagnosis of right lung non-small cell lung cancer presents with severe hemoptysis.", "Exam": "Severe cachexia, hemodynamic instability, respiratory distress, and a falling hematocrit.", "Findings": "A contrast enhanced axial CT image demonstrates a pseudoaneurysm arising from a middle lobar branch of the rightpulmonary artery just proximal to the right inferior lobar artery (often incorrectly called the interlobar artery or artery intermedius). There is complete obstruction of the superior lobar branches of the right pulmonary artery. There is high density consolidation surrounding the lesion representing hemorrhage into the surrounding parenchyma of the lung. The window of the CT image provided does not allow for differentiation of tumor from hemorrhagic consolidation and a comparision image from a prior study would be helpful. \n\nAfter coiling the pseudo were placed no flow is noted in the aneurysm.", "Differential Diagnosis": "Pulmonary artery pseudoaneurysm (much more likely to bleed)\n\u2022 infection (especially tuberulosis = Rasmussen\u2019s aneurysm)\n\u2022 tumor invasion\n\u2022 trauma ( especially iatrogenic)\nPulmonary artery aneurysm\n\u2022 pulmonary hypertension\n\u2022 pulmonic valve stenosis\n\u2022 Behcet's disease\n\u2022 Takayasu's arteritis\n\u2022 congenital\n\u2022 Hugh Stoven disease\nPulmonary artery aneurysm mimic\n\u2022 arterio-venous fistulas", "Case Diagnosis": "Pulmonary artery pseudoaneurysm secondary to erosion of tumor into the wall of the middle lobar branches of the right pulomary artery and obstruction of superior lobar branches of the right pulmonary artery due to mass effect from the tumor.", "Diagnosis By": "CT pulmonary angiogram", "Treatment & Follow Up": "Conventional pulmonary arteriography and coiling.", "Discussion": "Although not performed in this case, selective angiograms of the bronchial arteries and other arteries which can subserve lung masses (intercostals, thyrocervical trunk, internal mammary, lateral thoracic, long thoracic) should be considered in this type of case. The source of massive hemorrhage might not have been from the pulmonary artery pseudoaneuysm solely or at all." }, "Topic": { "Title": "Right pulmonary artery", "Disease Discussion": "The right pulmonary artery originates from the pulmonary trunk and passes posterior to the SVC horizontally and inferior to the right mainstem bronchus. It branches into the superior, medial and inferior lobar branches of the lung.\n\nThe inferior lobar branches usually share a common trunk which is often termed the interlobar artery (an misnomer from the perspective of an anatomist) or the artery intermedius.\n\nFor image, see: http://rad.usuhs.mil/rad/radbrowser2/chest/Mediastinum/GreatVessels/PulmonaryArteriogram/c004.html", "ACR Code": "9.1", "Category": "Glossary", "Keywords": "pulmonaryarteryanatomy", "Reference": "1)FCAT:Terminologia Anatomica. Thieme, London\n2)Williams et. al:Gray's Anatomy, Thirty-Seventh British Edition. Churchill Livingston, London", "External Links": "rad.usuhs.mil/rad/radbrowser2/chest/Mediastinum/GreatVessels/PulmonaryArteriogram/c004.html" } }, { "U_id": "MPX2379", "TAC": [ "MPX2379_synpic34083" ], "MRI": [], "Case": { "Title": "Round atelectasis", "History": "46 year old male presents with a cough.", "Exam": "N/A", "Findings": "AP and lateral chest radiographs demonstrate an opacity within the right lower lobe at the posterior costophrenic angle that appears somewhat mass-like and a chest CT was recommended.\n\nAxial chest CT images following intravenous contrast administration (in both soft tissue and lung windows) demonstrate a focal area of pleural thickening with moderate sized adjacent linear parenchymal opacification and a drawing in of the bronchovascular bundles toward to pleural thickening in a comet tail pattern. There is also some associated volume loss within the right lower lobe.", "Differential Diagnosis": "Round atelectasis\nNeoplasm", "Case Diagnosis": "Round atelectasis", "Diagnosis By": "The patient had a prior chest CT from four years earlier that demonstrated no significant change in the appearance of the lesion.", "Treatment & Follow Up": "None needed in this case. In cases that are equivocal, follow up or even biopsy is needed to confirm the diagnosis.", "Discussion": "Please see factoid." }, "Topic": { "Title": "Round atelectasis", "Disease Discussion": "Round atelectasis is a form of chronic atelectasis that can appear as a mass. In the past this condition has been frequently associated with asbestos exposure. However, our institution has seen this condition more often in the post heart bypass patient. The mechanism for round atelectasis is not certain. It is thought to occur with plueral invagination due to acute atelectasis or effusion. Then there is a fibrinous adhesion of the adjacent pleural surfaces. The lung then folds in on itself as the acute inciting event resolves. Signs of round atelectasis are plureal thickening, a pulmonary mass, and bronchi and blood vessels leading a curvilinear path from the hilum to the mass (\u201ccomet tail sign\u201d). CT will often show air bronchograms and enhancement.", "ACR Code": "6.749", "Category": "Miscellaneous", "Keywords": "round atelectasis", "Reference": "Armstrong P, Wilson AG, Dee P, Hansell DM, Imaging Diseases of the Chest, third edition, 2000, 97-8." } }, { "U_id": "MPX2376", "TAC": [ "MPX2376_synpic33072", "MPX2376_synpic33073", "MPX2376_synpic33075", "MPX2376_synpic33076", "MPX2376_synpic33077" ], "MRI": [ "MPX2376_synpic33071" ], "Case": { "Title": "Chance Fracture", "History": "21 year old man with back pain after a motor vehicle accident.", "Findings": "T11 Fracture of vertebral body, posterior elements, and widened interspinous space\nT11 abnormal Hyperintense signal and compression on T1 MRI", "Differential Diagnosis": "Wedge Fracture\nChance Fracture\nCompression Fracture", "Case Diagnosis": "Chance Fracture", "Diagnosis By": "CT / MRI" }, "Topic": { "Title": "Chance Fracture", "Disease Discussion": "Chance fractures, first described by G.Q. Chance in 1948, are horizontal vertebral fractures that extend through the vertebral body, pedicles and to the spinous process or lamina. The plain films are characteristic of wedge compression fractures while the posterior components are displaced to varying degrees. The posterior displacements are often better visualized on MRI and more specifically CT. CT with sagittal reconstructions are recommended. \n\nChance fractures commonly occur at the thoracic/lumbar junction where the spine transitions from a rigid to a more flexible segment. The etiology of these fractures is most often hyperflexion of the back. With the increasing use of lap seat belts in the 1950s-70s these fractures became known as \u201cseat belt\u201d fractures as vehicle accidents would cause sudden flexion of the waist at the thoracic/lumbar junction inducing significant stress on the posterior column. With the addition of shoulder belts these injuries have become significantly less common. Most Chance fractures seen today are a result of falls or crush type injuries where the spine is acutely hyperflexed. Intraabdominal injuries are likely in approximately 50% of chance fractures so vigilance should be given to a thorough evaluation involving a CT of the abdomen. \n\nMost Chance Fractures are managed with immobilization. Instability is frequently associated with a kyphosis of 20\u00b0 or more and a kyphosis of 30\u00b0 or more usually requires internal stabilization. Main treatment for unstable fractures is surgical fixation with spinal canal decompression.", "ACR Code": "3.4", "Category": "Trauma", "Keywords": "Chance FractureSpinetrauma", "Reference": "Groves, Clare J; Casser, Victor N. \u201cChance-Type Flexion-Distraction Injuries in the Thoracolumbar Spine: MR Imaging Characteristics. Radiology. 2005. Pgs 601-608.\nKaplan, Helmes, Dussault, Anderson, Major. Musculoskeletal MRI. W.B. Saunders Company. 2001. \nKeats, Theodore; Sistron, Christopher. Atlas of Radiology Measurement 7th Edition. Mosby 2001. Pgs 127-176\nLee F. Rogers. Radiology of Skeletal Trauma 3rd Edition Vol. 1. Churchill Livingston. 2002.\nStoller, Tirman. Diagnostic Imaging. Amirsys Publishing Company. 2004." } }, { "U_id": "MPX2384", "TAC": [ "MPX2384_synpic60015" ], "MRI": [ "MPX2384_synpic60013", "MPX2384_synpic60014" ], "Case": { "Title": "Methanol intoxication, putamen infarction", "History": "42 y.o. alcoholic man who works as a carpenter, found down in his workshop on Monday morning.", "Exam": "Profound metabolic acidosis, depressed mental status, and bilateral (\"cortical\") blindness.", "Findings": "Bilateral abnormal hyperintensity in the lateral lenticular nuclei (putamen).", "Differential Diagnosis": "Bilateral symmetric BG lesions suggest aToxic-metabolic insult:\npoisoning\norganic alcohol (methanol, ethylene glycol, etc.)\nhypoxia\nhypoglycemia\nnon-ketotic hyperglycemia", "Case Diagnosis": "Methanol intoxication, putamen infarction", "Diagnosis By": "Blood MeOH levels", "Treatment & Follow Up": "Methanol toxicity is related to its metabolism by alcohol dehydrogenase, producing formic acid and formaldehyde. The patient was treated with IV Ethanol and dialysis. Ethanol is a metabolic competitor for alcohol dehydrogenase in the liver and may slow the formation of the toxic products. \nNOTE: This patient was treated prior to the availability of fomepizole (Antizol\u00ae). \nhttp://www.nejm.org/doi/full/10.1056/NEJMct0806112\nhttp://emedicine.medscape.com/article/1174890-overview\nhttp://mdpoison.com/healthcareprofessionals/antidote%20facts/fomepizole%20antidote%20facts.pdf\nhttp://en.wikipedia.org/wiki/Fomepizole", "Discussion": "As a carpenter, this unfortunate patient might have ingested methanol - which is a common (but toxic) solvent used to dilute shellac for finishing wood cabinets. The mechanism of blindness is usually attributed to primary damage to the optic nerve and retina.\n\nhttp://www.ncbi.nlm.nih.gov/pubmed/6889696/\nhttp://www.ncbi.nlm.nih.gov/pubmed/10894122" }, "Topic": { "Title": "Methanol Toxicity, Basal Ganglia, Putamen", "Disease Discussion": "Each year, more than 2000 people in the US have methanol toxicity. Methanol is found in Winter Windshield Washer fluid, as a solvent (for shellac, etc.), and in some household cleaners. Also called \"wood alcohol\", as little as 30 - 100 ml may cause toxicity. Yet there are survivors of ingestions of up to 500 ml .\n\n\nMethanol Toxicity may be due to metabolism of MeOH into formates (e.g. formaldehyde and formic acid).\n\nMeOH causes direct retinal toxicity and ocular (not cortical) blindness.\n\nMeOH may also causes hemorrhagic necrosis of the lateral lenticular nucleus (putamen).\n\nTx: IV Ethanol, fomepizole (alcohol dehydrogenase inhibitor), dialysis\n\nPMID: 11145199 PMID: 10911425 PMID: 10738494 PMID: 8418579\nhttp://content.nejm.org/cgi/content/short/344/6/424\n\nhttp://www.embbs.com/cr/alc/alc6.html", "ACR Code": "1.5", "Category": "Toxic (see also Metabolic)", "Keywords": "methanol poisoning organic alcohol antifreezeretinal formic acid formaldehyde blindnessalcohol dehydrogenase", "Reference": "1: Pediatrics 2001 Oct;108(4):E77 \n\nChildhood methanol ingestion treated with fomepizole and hemodialysis.\n\nBrown MJ, Shannon MW, Woolf A, Boyer EW.\n\nChildren's Hospital, Harvard Medical School, Boston, Massachusetts, USA.\n\nFomepizole (4-methylpyrazole; Antizol) is used increasingly in the treatment of\nmethanol toxicity in adults. Little experience exists with this drug in the\npediatric population, however. We present a case of methanol poisoning in a\nchild in whom the use of fomepizole averted intravenous ethanol infusion and the\nattendant side effects of this therapy.\n\nPMID: 11581485 [PubMed - indexed for MEDLINE]\n\n\n\n2: Brain Pathol 2001 Jan;11(1):121-2, 125 \n\nAugust 2000: Two cases with necrosis and hemorrhage in the putamen and white\nmatter.\n\nFeany MB, Anthony DC, Frosch MP, Zane W, De Girolami U.\n\nDepartment of Pathology, Brigham and Women's Hospital and Children's Hospital,\nBoston, MA, USA.\n\nThe August COM: Acute methanol poisoning is an uncommon, but well-recognized,\ncause of central nervous system injury. We present two autopsy cases showing the\nclassic neuropathologic injuries in acute methanol poisoning: putamen and white\nmatter necrosis and hemorrhage. In Case 1, putamen hemorrhages were striking;\nwhite matter pathology predominated in Case 2. The precise mechanism of methanol\ntoxicity is unclear. Direct toxicity of metabolites, particularly formic acid,\nas well as ischemic injury and acidosis likely play a role. Methanol is readily\navailable in many commercial products, and may be ingested accidentally or\nintentionally.\n\nPMID: 11145199 [PubMed - indexed for MEDLINE]\n\n\n\n3: Harefuah 1998 Apr 15;134(8):613-5, 671 \n\n[Toxic optic neuropathy caused by methanol poisoning]\n\n[Article in Hebrew]\n\nReisin R, Liebovitz E, Levartovsky S.\n\nDept. of Ophthalmology, Barzilai Medical Center, Ashkelon.\n\nA 40-year-old woman attempted suicide by drinking methanol. Her visual acuity\nbegan to deteriorate 36 hours later and was found to be 6/60 in her right eye\nwith no light perception in the left. No systemic manifestations other than the\neye symptoms were found. In the following months visual acuity improved without\nspecific therapy. 2 months following the methanol, visual acuity was 6/6 in the\nright eye and finger-counting at 1 meter in the left eye. There was pronounced\noptic atrophy in the left eye, as well as a central defect in the left visual\nfield due to the methanol toxicity.\n\nPMID: 10911425 [PubMed - indexed for MEDLINE]\n\n\n\n4: N Z Med J 2000 Jan 28;113(1102):11-3 \n\nMethanol poisoning.\n\nMeyer RJ, Beard ME, Ardagh MW, Henderson S.\n\nChristchurch Hospital.\n\nAIMS: This study examines clinical experience with methanol poisoning during a\none-year period. METHODS: All admissions with the diagnosis of suspected\nmethanol toxicity were analysed and the current guidelines for the management of\nthis problem were reviewed. RESULTS: Twenty-four subjects were identified. Most\nhad a history of chronic use of methylated spirits. Four died before admission\nto hospital and the other 20 patients had 26 admissions to hospital and form the\nbasis for this report. Four patients died in the Intensive Care Unit. In total\n11 patients were admitted to the Intensive Care Unit. Seven patients received\nhaemodialysis. There was no correlation between the methanol level and the\noutcome. The strongest predictor of death or a poor outcome was a blood pH <\n7.0. Some patients, in spite of potentially lethal methanol levels of up to 160\nmmol/L, did not develop signs of toxicity. CONCLUSIONS: The overall mortality\nwas high and ethanol was given to most of the patients for up to several days.\nSome patients did not show any toxicity and some of those were not given\nethanol. It is recommended that chronic meths drinkers, who are not acidaemic\nand are generally well, do not require ethanol treatment. Only the complete\nremoval of methanol from methylated spirits will reduce the morbidity of this\ncondition.\n\nPMID: 10738494 [PubMed - indexed for MEDLINE]\n\n\n\n5: Vet Hum Toxicol 1998 Apr;40(2):95-8 \n\nPutaminal infarct in methanol intoxication: case report and role of brain\nimaging studies.\n\nRoberge RJ, Srinivasa NS, Frank LR, Scorza L, Krenzelok EP.\n\nDepartment of Emergency Medicine, Western Pennsylvania Hospital, Pittsburgh\n15224, USA.\n\nMethanol toxicity can cause severe central nervous system insult in which a\ncharacteristic pattern of bilateral putaminal injury is noted on brain imaging\nstudies. We present a fatal case of subacute methanol toxicity with associated\ndiffuse brain involvement, including bilateral putaminal necrosis and cerebral\nedema with ventricular compression. Theoretical basal ganglia toxicologic\nmechanisms of methanol poisoning are reviewed, and the role of brain imaging\nstudies will regard to diagnosis, prognosis and impact on management is\ndiscussed.\n\nPMID: 9554064 [PubMed - indexed for MEDLINE]\n\n\n\n6: Aust N Z J Ophthalmol 1997 Aug;25(3):225-30 \n\nAcute ocular methanol toxicity: clinical and electrophysiological features.\n\nMcKellar MJ, Hidajat RR, Elder MJ.\n\nDepartment of Ophthalmology, Christchurch Hospital, New Zealand.\n\nPURPOSE: The present report describes previously undocumented changes in the\nelectroretinogram (ERG) and visual-evoked response (VER) following acute\nmethanol ingestion and highlights the ocular effects of methanol poisoning.\nMETHODS: Two cases of acute ocular damage following methanol ingestion are\npresented. One patient underwent extensive electrophysiological and\npsychophysical testing. RESULTS: Both patients reported transient visual\ndisturbances. In each patient vision was 6/6 in both eyes at presentation but\nsubsequently improved to 6/4. Colour vision (Ishihara plates) and pupillary\nreactions were normal. The optic discs were hyperaemic and swollen and retinal\noedema extended along the major vascular arcades. There was cystoid macular\noedema and 'pseudo cherry red spots' were observed. Automated field analysis\nrevealed a generalized depression of retinal sensitivity, an enlargement of one\nblind spot and paracentral scotomas. The scotopic ERG was subnormal with\ndiminished a- and b-waveforms and the cone response to flicker was reduced. The\npattern VER P2 waveform was normal in latency but decreased in amplitude.\nCONCLUSIONS: Acute methanol ingestion can cause characteristic ocular damage,\ntogether with widespread electrophysiological dysfunction. The data presented\nsuggest that methanol affects the photoreceptors, Muller cells and the\nretrolaminar portion of the optic nerve.\n\nPublication Types:\nReview\nReview of Reported Cases\n\nPMID: 9296298 [PubMed - indexed for MEDLINE]\n\n\n\n7: Toxicol Lett 1995 Dec;82-83:707-11 \n\nRecent developments in methanol toxicity.\n\nMedinsky MA, Dorman DC.\n\nChemical Industry Institute of Toxicology, Research Triangle Park, NC\n27709-1237, USA.\n\nThe disposition of methanol and its putative toxic metabolite formate has been\nstudied in humans, non-human primates, and rodents after exposure to high,\nneurotoxic doses. The rate at which rodents detoxify formate is more rapid than\nthat of primates. Formate, an endogenous biological substrate, is detoxified by\nmetabolism to CO2 via a tetrahydrofolate-(THF) dependent pathway. Species with\nhigh hepatic THF levels, such as rodents, are less sensitive to the neurotoxic\neffects of large methanol doses compared with species with low THF levels, such\nas primates. Data on the capacity of primates to detoxify formate derived from\ninhalation of low levels of methanol are critical for assessing human risk from\nmethanol fuels. Female cynomolgus monkeys exposed to low concentrations of\n[14C]methanol (10-200 ppm) for 2 h have blood levels of methanol-derived formate\nthat are 100- to 1000-fold lower than endogenous levels of formate. Healthy\nhuman volunteers exposed at rest or during exercise to 200 ppm methanol for 6 h\nor exposed to 20 mg/kg orally have elevated blood levels of methanol, but blood\nformate concentrations are not significantly increased above endogenous\nconcentrations. Deficiencies in THF may prolong blood levels of formate and\nincrease the likelihood of toxic effects. Limited studies in non-human primates\nwith low THF levels exposed to 900 ppm methanol for 2 h have shown that\nconcentrations of methanol-derived formate in blood remain below endogenous\nlevels. Thus human populations may not be at added risk of neurotoxic effects\nresulting from exposure to low levels of methanol.\n\nPublication Types:\nReview\nReview, Tutorial\n\nPMID: 8597130 [PubMed - indexed for MEDLINE]\n\n\n\n8: J Toxicol Environ Health 1994 Jan;41(1):71-82 \n\nAnimal model for the study of methanol toxicity: comparison of folate-reduced\nrat responses with published monkey data.\n\nLee EW, Garner CD, Terzo TS.\n\nBiomedical Science Department, General Motors North American Operations, Warren,\nMichigan 48090-9055.\n\nWe attempted to develop a rodent model that exhibits characteristics of human\nmethanol toxicities such as acidosis and visual dysfunction, which are\ncorrelated with an accumulation of formate, a toxic metabolite of methanol.\nInitially three groups of Long-Evans rats with different levels of liver folate\nwere prepared and examined for formate accumulation after methanol\nadministration (3.5 g/kg). The folate-reduced (FR) rats prepared by feeding a\nfolate-deficient diet with 1% succinylsulfathiazole yielded blood formate levels\nequivalent to those found in methanol-intoxicated humans and developed signs of\nthe visual system toxicity (a manuscript on the latter aspect is in\npreparation). Responses of FR rats to a variety of methanol exposure scenarios\nwere then investigated, and the results were compared with those reported in the\nliterature for monkeys. Formate accumulation and/or lethality were used as toxic\nparameters for this comparative evaluation. In FR rats dosed orally with 3 g/kg,\nthe blood formate concentration was 9.2 mmol/L at 24 h postadministration and\nincreased to 15.6 mmol/L at 48 h. The same dose given to monkeys yielded a\nplateau of 7.4 mmol/L at 12 h after methanol administration, and stayed at this\nlevel for an additional 12 h. The area under the concentration vs. time curve\nfor blood formate in FR rats was 2.5-fold greater than that in monkeys when 2.0\ng/kg methanol was administered. After a 6-h exposure to 1200 ppm and 2000 ppm\nmethanol, the blood formate concentrations in FR rats were increased by 370% and\n636% above the endogenous level, respectively. However, blood formate did not\naccumulate above the endogenous level when monkeys were exposed to methanol up\nto 2000 ppm for 6 h. Under acute inhalation exposure conditions, FR rats exposed\nto 3000 ppm methanol, 20 h/d, could not survive more than 4 d. On the other\nhand, monkeys exposed to 3000 ppm, 21 h/d, out-lived 20 d. Moreover, monkeys\nsurvived for more than 4 d even after an exposure to 10,000 ppm. Thus, these\nresults indicate that FR rats are more sensitive to methanol challenges than\nmonkeys, and suggest that the FR rat could be a congruous animal model for\nevaluating the health effects of methanol in humans.\n\nPMID: 8277527 [PubMed - indexed for MEDLINE]\n\n\n\n9: Am Fam Physician 1993 Jan;47(1):163-71 \n\nComment in:\n Am Fam Physician. 1993 Oct;48(5):731.\n\nMethanol toxicity. Agency for Toxic Substances and Disease Registry.\n\nMethanol is used in a variety of commercial and consumer products. Increased use\nof methanol as a motor fuel may lead to higher ambient air levels and a greater\npotential for ingestion from siphoning accidents. Methanol toxicity initially is\nnot characterized by severe toxic manifestations. Pathophysiologically, methanol\ntoxicity represents a classic example of \"lethal synthesis,\" in which toxic\nmetabolites can cause fatality after a characteristic latent period. Methanol is\nwell absorbed following inhalation, ingestion or cutaneous exposure. It is\noxidized in the liver to formaldehyde, then to formic acid, which contributes to\nthe profound metabolic acidosis occurring in acute methanol poisoning. The\nmetabolic products of methanol can produce a syndrome of delayed-onset acidosis,\nobtundation, visual disturbance and death. Intravenous sodium bicarbonate\ntherapy should be considered if the patient's blood pH is below 7.2. Symptoms\nand history determine whether intravenous ethanol therapy and hemodialysis\nshould be instituted.\n\nPublication Types:\nReview\nReview, Tutorial\n\nPMID: 8418579 [PubMed - indexed for MEDLINE]\n\n\n\n10: Aust N Z J Ophthalmol 1992 Feb;20(1):57-64 \n\nPartly reversible visual failure with methanol toxicity.\n\nStelmach MZ, O'Day J.\n\nSt Vincent's Hospital, Fitzroy, Victoria, Australia.\n\nMethanol is a highly toxic substance which is used as an industrial solvent and\nin automotive antifreeze. If accidentally ingested blindness or death may\nresult. The case of a young woman who developed sudden onset of visual failure\nfollowing ingestion of a methanol-fortified beverage is presented. Although she\nfailed to seek immediate medical help visual function improved. Acute changes of\nbilateral optic disc hyperaemia and venous engorgement were present at initial\nexamination. She subsequently developed optic disc atrophy together with\nglaucomatous-like cupping of the optic discs. The aetiology of visual failure in\nmethanol poisoning is discussed, as are the current therapeutic guidelines in\nthe management of acute cases.\n\nPMID: 1599670 [PubMed - indexed for MEDLINE]\n\n\n\n11: Arch Ophthalmol 1991 Jul;109(7):1012-6 \n\nMethanol poisoning. A rodent model with structural and functional evidence for\nretinal involvement.\n\nMurray TG, Burton TC, Rajani C, Lewandowski MF, Burke JM, Eells JT.\n\nDepartment of Ophthalmology, Medical College of Wisconsin, Milwaukee 53226.\n\nMethanol ingestion can lead to visual impairment, central nervous system\ndysfunction, or death. The extent of ocular involvement has been difficult to\ndetermine because the toxicity is restricted to humans and nonhuman primates due\nto species differences in methanol metabolism. A rodent model of methanol\ntoxicity recently developed by us was used to evaluate retinal dysfunction in\nmethanol poisoning. Formic acidemia and visual toxic reactions developed in\nmethanol-intoxicated rats. Electroretinographic analysis indicated a significant\nearly deficit in b-wave amplitude followed by a temporally delayed, lesser\nreduction in a-wave amplitude. Histologic evaluation of the eyes 60 hours after\nmethanol administration revealed generalized retinal edema and vacuolation in\nthe photoreceptors and retinal pigment epithelium. Ultrastructural examination\nshowed swelling and disruption of the mitochondria in photoreceptor inner\nsegments, optic nerve, and the retinal pigment epithelium. These studies\ndocument direct retinal involvement in this nonprimate model of methanol\ntoxicity.\n\nPMID: 2064555 [PubMed - indexed for MEDLINE]\n\n\n\n12: Life Sci 1991;48(11):1031-41 \n\nThe toxicity of methanol.\n\nTephly TR.\n\nDepartment of Pharmacology, University of Iowa, Iowa City 52242.\n\nMethanol toxicity in humans and monkeys is characterized by a latent period of\nmany hours followed by a metabolic acidosis and ocular toxicity. This is not\nobserved in most lower animals. The metabolic acidosis and blindness is\napparently due to formic acid accumulation in humans and monkeys, a feature not\nseen in lower animals. The accumulation of formate is due to a deficiency in\nformate metabolism which is, in turn, related, in part, to low hepatic\ntetrahydrofolate (H4 folate). An excellent correlation between hepatic H4 folate\nand formate oxidation rates has been shown within and across species. Thus,\nhumans and monkeys possess low hepatic H4 folate levels, low rates of formate\noxidation and accumulation of formate after methanol. Formate, itself, produces\nblindness in monkeys in the absence of metabolic acidosis. In addition to low\nhepatic H4 folate concentrations, monkeys and humans also have low hepatic\n10-formyl H4 folate dehydrogenase levels, the enzyme which is the ultimate\ncatalyst for conversion of formate to carbon dioxide. This review presents the\nbasis for the role of folic acid-dependent reactions in the regulation of\nmethanol toxicity.\n\nPublication Types:\nReview\nReview, Academic\n\nPMID: 1997785 [PubMed - indexed for MEDLINE]\n\n\n\n13: Med Toxicol 1986 Sep-Oct;1(5):309-34 \n\nMethanol and ethylene glycol poisonings. Mechanism of toxicity, clinical course,\ndiagnosis and treatment.\n\nJacobsen D, McMartin KE.\n\nMethanol and ethylene glycol poisonings share many characteristics both\nclinically and biochemically. Both alcohols are metabolised via alcohol\ndehydrogenase to their toxic metabolites. Methanol is slowly metabolised to\nformaldehyde which is rapidly metabolised to formate, the metabolite mainly\nresponsible for methanol toxicity. Formate metabolism depends upon the folate\npool which is small in primates compared with other animals. Therefore, formate\naccumulates in primates during methanol intoxication and is mainly responsible\nfor the metabolic acidosis in the early stage of intoxication. In late stages\nlactate may also accumulate, mainly due to formate inhibition of the respiratory\nchain. This tissue hypoxia caused by formate may explain the ocular as well as\nthe general toxicity. Ethylene glycol is metabolised more rapidly than methanol,\nvia alcohol dehydrogenase to glycolaldehyde which is rapidly metabolised to\nglycolate, the metabolite mainly responsible for the metabolic acidosis in\nethylene glycol poisoning. Glycolate is metabolised by various pathways,\nincluding one to oxalate which rapidly precipitates with calcium in various\ntissues and in the urine. Ethylene glycol toxicity is complex and not fully\nunderstood, but is mainly due to the severe metabolic acidosis caused by\nglycolate and to the calcium oxalate precipitation. The clinical course in both\npoisonings is initially characterised by the development of metabolic acidosis\nfollowing a latent period, which is more pronounced in methanol poisoning and is\nthe time taken for both alcohols to be metabolised to their toxic metabolites.\nIn methanol poisoning there are usually visual symptoms progressing to visual\nimpairment, whereas ethylene glycol victims develop renal and cardiopulmonary\nfailure. Prognosis is excellent in both poisonings provided that there is early\ntreatment with alkali to combat acidosis, ethanol as an antimetabolite, and\nhaemodialysis to remove the alcohols and their toxic metabolites. Ethanol is\nalso metabolised by alcohol dehydrogenase, but has a much higher affinity for\nthis enzyme than methanol and ethylene glycol. Presence of ethanol will\ntherefore inhibit formation of toxic metabolites from methanol and ethylene\nglycol. Due to competition for the enzyme, the therapeutic ethanol concentration\ndepends on the concentration of the other two alcohols, but a therapeutic\nethanol concentration around 22 mmol/L (100 mg/dl) is generally recommended.\nMost patients are, however, admitted at a late stage to hospitals not capable of\nperforming analyses of these alcohols or their specific metabolites on a 24-hour\nbasis.(ABSTRACT TRUNCATED AT 400 WORDS)\n\nPublication Types:\nReview\n\nPMID: 3537623 [PubMed - indexed for MEDLINE]\n\n\n\n14: J Emerg Med 1983;1(1):51-8 \n\nMethanol poisoning.\n\nBecker CE.\n\nMethanol poisoning is an uncommon but an extremely hazardous intoxication. Since\nmethanol is a versatile fuel and is having increasing usage in an\nenergy-conscious society, a high index of suspicion and swift laboratory\nconfirmation is essential in managing this poisoning. Methanol poisoning may\noccur in sporadic or epidemic circumstances. Chronic exposure may occur in the\noccupational setting. Man is uniquely susceptible to methanol toxicity, perhaps\ndependent upon folate metabolism. Classic symptoms of methanol toxicity can only\noccur in laboratory animals who are rendered folate deficient. Folate may be\nuseful in humans enhancing removal of the toxic products of methanol poisoning.\nThe enzyme responsible for metabolism of methanol is alcohol dehydrogenase.\nEthanol has a higher affinity for this enzyme and is preferentially metabolized.\nSimultaneous ethanol and methanol administration may confuse the onset of the\nintoxication. Pyrazoles may also be used to inhibit alcohol dehydrogenase thus\npreventing the intoxication. The most important initial symptom of methanol\npoisoning is visual disturbance. The symptoms may be delayed up to 24 hours\nafter ingestion due to simultaneous alcohol administration and metabolic\nprocesses. Laboratory evidence of severe metabolic acidosis with increased anion\nand osmolar gaps strongly suggest the clinical diagnosis. There may be an\nimportant association between mean corpuscular volume which is significantly\nhigher in cases of severe methanol poisoning than in mild cases.(ABSTRACT\nTRUNCATED AT 250 WORDS)\n\nPublication Types:\nReview\n\nPMID: 6386968 [PubMed - indexed for MEDLINE]\n\n\n\n15: Am J Med 1980 Mar;68(3):414-8 \n\nMethanol poisoning in human subjects. Role for formic acid accumulation in the\nmetabolic acidosis.\n\nMcMartin KE, Ambre JJ, Tephly TR.\n\nWhereas a great deal of information is available on the etiology of methanol\npoisoning in the monkey, very little study has been made in human subjects. The\nrole of formic acid in methanol toxicity in human subjects has not been\nestablished. Two patients have been studied who have presented with the\ncharacteristics of methanol poisoning--metabolic acidosis and ocular toxicity.\nThis has made possible a confirmation of the role of formate in the toxic\nsyndrome. Acidosis was very severe in both cases with arterial pH values of\nabout 6.9 and plasma bicarbonate concentrations of 3 meq/liter. A sensitive and\nspecific assay was used to measure formic acid levels in blood and other fluids.\nFormate accumulation was marked with initial blood levels ranging from 11.1 to\n26.0 meq/liter. Decreases in blood bicarbonate concentrations of similar\nmagnitude coincided with the increase in formate. Thus, accumulation of formic\nacid plays a major part in the acidosis observed in human subjects poisoned with\nmethanol, as has been demonstrated in monkeys. Treatment involving bicarbonate\nadministration, ethanol infusion and hemodialysis, rapidly decreased formate\nlevels in the blood to control values. Methanol concentrations were reduced but\nto lesser extent than that of formate. Despite the reduction in formate and\nmethanol concentrations in both cases, the treatment was successful in only one\nof the two patients.\n\nPMID: 7361809 [PubMed - indexed for MEDLINE]", "External Links": "www.emedicine.com/neuro/topic217.htm" } }, { "U_id": "MPX2387", "TAC": [ "MPX2387_synpic26379" ], "MRI": [], "Case": { "Title": "Synovial sarcoma-biphasic", "Exam": "palpable midline mass", "Findings": "Axial and reformatted sagittal CT scans of the abdomen after oral and intraveous contrast show a large extraluminal mass with areas of low-attenuation mass with nodularity and large areas of necrosis and hemorrhage. On some images, the mass is adherent to the stomach and displaces surrounding viscera.", "Differential Diagnosis": "Synovial sarcoma, leiomyosarcoma,metastatic disease, malignant fibrous histiocytoma sarcoma, rhabdomyosarcoma, liposarcoma, Burkitt lymphoma", "Case Diagnosis": "Synovial sarcoma-biphasic", "Diagnosis By": "Biopsy: \nImmunohistology-biphasic spindle cells admixed with epithelioid cells.\nMolecular studies-t(X:18) translocation", "Treatment & Follow Up": "Marginal excision, radiotherapy, and chemotherpay (doxyrubicin and cyclophosphamide)\n\nPatient developed metastases to the liver within 2 years of primary treatment.", "Discussion": "Unfortunately this patient developed an uncommon soft tissue neoplasm in an atypical location, which progressed despite optimal surgical and medical management." }, "Topic": { "Title": "Synovial sarcoma", "Disease Discussion": "Synovial sarcoma is an uncommon variant of the soft tissue sarcomas, occuring in less than 10% of adult cases. Although the typical clinical presentation is a young adult with a painless rapidly growing extremity mass (80-95%of patients), there is a wide age variation with most common age group being the 15-35 year age group. Besides the extremities, primary synovial sarcomas have been described throughout the body to include the heart, brain, and abdomen.\n\nSarcomas are classified according to the tissue they most closely resemble, as such, synovial sarcoma is classically described as a having a biphasic fibrous spindle cell population admixed with an epitheliod component. They likely originate from genetic mutations in totipotent mesenchymal cells, which may explain variations in histologic and anatomic presentation as well as the clinical course of the neoplasm. The translocation t(X:18) is present in greater than 90% of synovial sarcomas.\n\nRadiographs of these patients may be nomral in one-half of patients. Thirty percent of masses shows calcification or less commonly ossification. In 11-20% of patients, bony erosion of the adjacent bone can be seen. Both CT and MRI can show areas of necrotic or hemoorhage that appear as aresa of low attenuation on CT images and high attenuation on T2-weighted MR images. Both modalities can demonstrate a multilobulated lesion with septation. Fluid-fluid levels may be seen in areas of hemorrhage. For staging of tumors, MRI is the best modality. The histologic and chromosomal findings described above are often the key to diagnosis.\n\nTreatment for all synovial sarcomas is resection. According to a retrospective study performed by Ferrari et al, primary synovial sarcoma with clear margins and no evidence of metastases carries a 5-year overall survival of greater than 70%(1). That rate decreases to less than 40% with locally advanced disease. Unfortunately, nearly 60% of those with macroscopically resected disease developed metastases within 5 years (primarily to the lungs and liver). Nearly 40% of patients also receiving chemotherapy (doxyrubicin, cyclophosphamide, and occasionally cisplatin) developed metastases within 5 years (1).", "ACR Code": "7.3", "Category": "Neoplasm, sarcoma", "Keywords": "synovial sarcoma", "Reference": "1. Ferrari, Andrea. et al. Synovial Sarcoma: A Retrospective Analysis of 271 Patients of All Ages Treated at a Single Institution. Cancer, Volume 101, Issue 3, 2004(p 627-634)\n\n2.DeLaney, Thomas F. Savarese, Diane. Overview of soft tissue sarcoma. Up To Date. 2005\n\n3.SCHAAL, Carlos H., Navarro, F?bio C. and Moraes Neto, Francisco A. Primary renal sarcoma with morphologic and immunohistochemical aspects compatible with synovial sarcoma. Int. braz j urol. [online]. May/June 2004, vol.30, no.3 \n\n4.Przkora, Rene, et al. Synovial sarcoma -unusual presentation with cerebral hemorrhage. Arch Orthop Trauma Surg (2003) 123: 376-378" } }, { "U_id": "MPX2385", "TAC": [ "MPX2385_synpic27520", "MPX2385_synpic27521", "MPX2385_synpic27522", "MPX2385_synpic27524", "MPX2385_synpic27525", "MPX2385_synpic27526" ], "MRI": [], "Case": { "Title": "mucus plug", "History": "ICU patient who, after extubation, developed acute onset dyspnea and hypoxia.", "Exam": "N/C", "Findings": "Multiple axial CT images obtained according to the CT pulmonary angiography protocol demonstrates mixed-density (including air density) endoluminal lesion within the bronchus intermedius extending from just past the carina and down, with large areas of atelectasis in the right lower lobe. The air densities strongly suggest that this is a large mucus plug.\n\nOblique coronal reconstructed image shows the extent of this large mucus plug.", "Differential Diagnosis": "mucus plug", "Case Diagnosis": "mucus plug", "Diagnosis By": "bronchoscopy and aspiration" }, "Topic": { "Title": "mucus plug", "Disease Discussion": "At least in our institutional experience, CT pulmonary angiography has effectively replaced the V/Q scan and conventional catheter pulmonary angiography as the modality of choice for diagnosing pulmonary embolism. Probably one of the greatest advantage of CTPA is the ability to show other disease processes which can explain the patient's clinical symptoms.\n\nIn this case, the large mucus plug was the cause of the patient's dyspnea and hypoxia. Mucus plug can be a potential cause of a false positive study as well. The mucus plug surrounded by the bronchial wall, which can enhance due to inflammation, can definitely mimic an acute pulmonary embolism. The key to diagnosing a mucus plug is to see the abnormality tracking within the airway, rather than the pulmonary artery.", "ACR Code": "6.9", "Category": "Obstruction or Stenosis", "Keywords": "mucus plugpulmonary embolismcomputed tomography", "Reference": "Conrad Wittram, Michael M. Maher, Albert J. Yoo, Mannudeep K. Kalra, Jo-Anne O. Shepard, and Theresa C. McLoud. CT Angiography of Pulmonary Embolism: Diagnostic Criteria and Causes of Misdiagnosis. RadioGraphics 2004; 24: 1219-1238." } }, { "U_id": "MPX2386", "TAC": [ "MPX2386_synpic23826" ], "MRI": [], "Case": { "Title": "Diagnosis: 64 y.o. female with recurrent breast cancer with metastasis to lymph nodes and lungs. Liver mass biopsy reveals adenocarcinoma, with histology consistent with breast tissue.", "History": "History (can include gestational age, or age in days, weeks, months):\n64 y.o. WF with hx of Breast CA (1996), s/p lumpectomy and XRT, admitted for workup of fatigue, 15-20 lb weight loss in 8 months, and increased abdominal girth in the setting of imaging studies, which show ascites (with peritoneal fluid negative for malignant cells), liver lesions, and multiple lung masses. Prior workup demonstrated elevated LFTs, Elevated CEA, CA 19-9, CA 125, and negative viral hepatitis panels.", "Exam": "Physical Exam and Laboratory: \nPertinent Physical Findings: Abdomen--distended, non-tender, ascites present, no organomegaly detected. Exam otherwise benign.\nLab Findings: Chem7\u2014141/5.0/105/31/12/0.6/112; CBC\u20148.7/11.0/34.0/181; Coag PT 12.8/PTT 27.8; \nLFTs\u2014AlkPhos 1052/AST 233/ ALT 91/ Tbili 2.7 \nTumor markers: CA 27-29 1371 (normal 0-37), CA 15-3 1464 (normal 0-31), CA 125 196 (normal 0-34), AFP normal\nHistology of Breast Bx: Infiltrating Ductal CA T3N2M2\nHistology of Liver Bx: Adenocarcinoma; Special stains include cytokeratin 7: positive, cytokeratin 20: negative, progesterone/estrogen: positive, CEA: focally positive, Thyroid transcription factor 1: negative.", "Findings": "Image Findings: \n1.\tPET scan\u20142 hypermetabolic foci in Left breast; Focal hypermetabolic uptake in inferior Right liver lobe and Left liver lobe with diffuse/heterogeneous uptake in Right lobe; diffuse bone uptake in axial/appendicular skeleton that is nonspecific: malignant vs liver failure.\n2.\tMRCP/MRI abdomen\u2014liver cirrhosis and portal HTN leading to splenomegaly and ascites; no pancreatic ductal dilatation; liver lesions are peripheral with capsular retraction\n3.\tCT chest\u2014too numerous to count non-calcified nodules in lungs; Left breast lesion and axillary lymph node\n4.\tBreast U/S (image not available for MedPix) used for core Bx\u20141.2cm lesion in Left upper outer breast; BIRADS category 5", "Differential Diagnosis": "Differential Diagnosis for these findings in this case:\n1.\tLiver lesions and ascites: Periportal fibrosis, cirrhosis leading to HCC, regenerating nodules, inflammation, neoplastic infiltration in interstitium\n2.\tLung nodules: metastasis, infectious, granulomatous, TB, mycobacterial\n3.\tBreast lesions: primary lesion, metastasis", "Case Diagnosis": "Diagnosis: 64 y.o. female with recurrent breast cancer with metastasis to lymph nodes and lungs. Liver mass biopsy reveals adenocarcinoma, with histology consistent with breast tissue.", "Treatment & Follow Up": "Treatment and Follow-up: \nPlan to have pt follow-up with pulmonology for assessment of lung function and work-up of lung nodules. Also, pt to have colonoscopy. Consult general surgery placed for evaluation of left breast mass. This patient insisted that she be discharged after the diagnostic imaging took place to attend an important family event. Thus, she was discharged on hospital day six, with the aforementioned follow-up appointments made.", "Discussion": "Discussion (include references): \nThe lung nodules are likely adenocarcinoma, which is the most common type of lung cancer in most recently reported series, and is the most frequent histologic type in women and nonsmokers of either sex. This patient has a 40 pack year hx of smoking. Metastasis is the most common neoplasm in an adult liver, and the liver is the second most common site for metastatic spread, after the lymph nodes. The patient also has recurrent breast cancer. Infiltrating ductal carcinoma is the most common type of invasive breast cancer, accounting for 70 to 80 percent of invasive lesions. The final pathology report indicates that the liver mass is adenocarcinoma, with the special stains being consistent with breast tissue. The TTF1 stain is 70-80% specific for lung metastasis, and it is negative in this case. The recurrent breast cancer stage is T3N2M2 with metastasis to the liver and presumably lung." }, "Topic": { "Title": "Metastatic Breast Cancer", "Disease Discussion": "The lung nodules are likely adenocarcinoma, which is the most common type of lung cancer in most recently reported series, and is the most frequent histologic type in women and nonsmokers of either sex.\n\nThis patient has a 40 pack year hx of smoking. Metastasis is the most common neoplasm in an adult liver, and the liver is the second most common site for metastatic spread, after the lymph nodes. The patient also has recurrent breast cancer. Infiltrating ductal carcinoma is the most common type of invasive breast cancer, accounting for 70 to 80 percent of invasive lesions.\n\nThe final pathology report indicates that the liver mass is adenocarcinoma, with the special stains being consistent with breast tissue. The TTF1 stain is 70-80% specific for lung metastasis, and it is negative in this case. The recurrent breast cancer stage is T3N2M2 with metastasis to the liver and presumably lung.", "ACR Code": "9.5", "Category": "Staging of Cancer, etc.", "Keywords": "adenocarcinomacarcinoma", "Reference": "www.uptodate.com\nwww.eMedicine.com" } }, { "U_id": "MPX2389", "TAC": [ "MPX2389_synpic29628", "MPX2389_synpic30345" ], "MRI": [], "Case": { "Title": "Intestinal Malrotation", "History": "This 44 yo man was referred to Radiology for virtual colonoscopy. He has a remote family history of colon cancer. He denies melena, hematochezia, constipation, diarrhea, and abdominal pain.\n\nMedical Hx: asthma, hypertension, chronic lower back pain.\nSurgical Hx: none\nFamily Hx: Colon cancer - remote.\nSocial Hx: (-)tobacco, (-)alcohol", "Exam": "VS: BP 126/83, HR 86, afebrile. \nGen: Awake, alert, oriented to person, place, time. No apparent distress. \nAbdomen: Mildly protuberant abdomen. Soft, non-tender, no organomegaly.", "Findings": "All of the small bowel loops are confined to right hemi-abdomen. \nThe Cecum is in a normal RLQ anatomical position. \nThe Colon is mostly in left hemi-abdomen, and the ascending colon deviates to the left.", "Differential Diagnosis": "\u2022 Intestinal malrotation\n\u2022 Intestinal non-rotation", "Case Diagnosis": "Intestinal Malrotation", "Diagnosis By": "Pathognomonic Imaging", "Treatment & Follow Up": "The patient was offered and scheduled for prophylactic Ladd procedure. He later withdrew consent for the procedure and has been lost to follow-up.", "Discussion": "The management of asymptomatic adults with intestinal malrotation should involve a discussion of the benefits and risks of surgical intervention versus the risk of developing instestinal volvulus or obstruction. As virtual colonoscopy becomes more available, the discovery of intestinal malrotation as an incidental finding is likely to become more frequent using this imaging modality." }, "Topic": { "Title": "Intestinal Malrotation", "Disease Discussion": "Malrotation is a congenital anomaly of midgut development. In the fifth week of normal embryonic development the midgut rapidly elongates, forming the primary intestinal loop. The vascular supply to the midgut, the superior mesenteric artery (SMA), serves as the axis for the primary intestinal loop. The primary intestinal loop elongates so rapidly that the abdominal cavity cannot contain the developing midgut; and, as a result, the primary intestinal loop herniates into the umbilical cord. During this herniation, the developing loop rotates 90 degrees counterclockwise about its axis. In the tenth week of development, the intestinal loop returns to the abdominal cavity, rotating an additional 180 degrees counterclockwise. \n\nThe cephalic limb of the primary loop forms the distal duodenum, the jejunum, and the proximal ileum. The caudal limb forms the distal ileum, the cecum, ascending colon, and most of the transverse colon. \n\nThe proximal or pre-arterial midgut returns to the abdominal cavity first and begins to occupy the right side of the abdominal cavity. The proximal midgut becomes fixed to the posterior abdominal wall at the ligament of Treitz.\n\nAs the distal or post-arterial midgut returns to the abdomen, the counterclockwise rotation causes the cecum to initially occupy the right upper quadrant. The rotation is completed as the cecum migrates to the right iliac fossa in the right lower quadrant (RLQ). \n\nThe ascending colon gradually becomes fixed to the posterior abdominal wall, losing its free mesentery. Normal counterclockwise rotation of the midgut results in a wide-based mesentery. In malrotation, the proximal midgut returns to the abdominal cavity with normal rotation, but the distal midgut fails to rotate completely. As a result, the cecum will become fixed to the posterior abdominal wall in the upper abdomen. This position results in a mesentery with a narrow base that is prone to volvulus and midgut ischemia. \n\nPeritoneal bands of fibrosis that fix the cecum to the right lateral abdominal wall (Ladd\u2019s bands) run anterior to the duodenum and may cause compression and obstruction of the duodenum.\n\nSymptomatic malrotation typically presents in infancy or childhood. The acute symptomatic presentation is usually related to duodenal obstruction or midgut ischemia. Although it is less common, intestinal malrotation may first become symptomatic in adolescence or adulthood. The later onset of symptoms ranges from chronic abdominal pain to acute mesenteric ischemia. Occasionally, malrotation is discovered as an incidental radiographic finding. \n\nThe management of asymptomatic malrotation is controversial. Some authors have suggested that all asymptomatic patients with malrotation should undergo an open or laparoscopic Ladd\u2019s procedure (transaction of Ladd\u2019s bands, counterclockwise reduction of malrotation, and appendectomy). Others have proposed that prophylactic surgical intervention is only indicated in children with asymptomatic malrotation. \n\nThe prevalence of asymptomatic malrotation is unknown. As the use of of computed tomography increases and new abdominal imaging modalities emerge, it is likely that the diagnosis of intestinal malrotation as an incidental finding will become more frequent.", "ACR Code": "7.1", "Category": "Congenital, malformation", "Keywords": "MalrotationVolvulusLadd", "Reference": "Behrman RE, Kliegman RM, Jenson HB. Nelson Textbook of Pediatrics, 17th Ed. Philadelphia: Saunders, 2004.\n\nGamblin TC, Stephens RE, Johnson RK, Rothwell M. Adult malrotation: a case report and review of the literature. Curr Surg 2003:60;517-20. \n\nMalek MM, Burd RS. Surgical treatment of malrotation after infancy: a population based study. J Pediatr Surg 2005:40;285-89. \n\nMalek MM, Burd RS. The optimal management of malrotation diagnosed after infancy: a decision analysis. Am J Surg 2006:191;45-51\n\nPickhardt PJ, Bhalla S. Intestinal malrotation in adolescents and adults: spectrum of clinical and imaging features. Am J Roentgenol 2002;179:1429-35.\n\nSadler TW. Langman's Medical Embryology, Ninth Ed. Philadelphia: Lippincott Williams & Wilkins, 2004." } }, { "U_id": "MPX2388", "TAC": [ "MPX2388_synpic34942", "MPX2388_synpic34943", "MPX2388_synpic34945" ], "MRI": [ "MPX2388_synpic34946", "MPX2388_synpic34948", "MPX2388_synpic34949" ], "Case": { "Title": "Cerebellar PICA Infarction", "History": "47 yo man with 6 month Hx of headaches - now reports experiencing \u201cworst headache of his life\u201d accompanied by nausea, vomiting, and dizziness. Pt notes waking up with a mild headache on the day of admission, unrelieved by caffeine consumption, that progressively worsened. The pain was sharp, but throbbing and located behind his left eye and radiating posteriorly.", "Exam": "Initial vital signs demonstrated afebrile pt with BP 159/77, HR 82, RR 22. Initial exam wnl, including neurologic exam. HD#5, mild gait disturbance noted with deviation to the left, and deficits in high level and dynamic gait activity.\n\nLabs: SPEP, Protein C, Protein S, Antithrombin III, Hypercoag panel, ANA, ENA, RF, B12, Folate, MMA, CoagII, ESR, CRP, Homocysteine, cardiolipin panel, RPR, Lipid panel all wnl. \nAn LP was performed and wnl.\nTTE and TEE both showed no abnormalities or clots.", "Findings": "\u2022 CT on HD#1 demonstrated no evidence of infarction, inflammation, or bleeding.\n\u2022 CT on HD#3 showed a change in density in areas of the left cerebellum\n\u2022 MRI/MRA of the head and brain on HD#4 demonstrated subacute L PICA territory infarcts and normal intracranial MRA.\n\u2022 MRI/MRA of the neck on HD#5 demonstrated no dissection, aneurysm or focal stenosis of the vertebral arteries.", "Differential Diagnosis": "\u2022 Cerebellar embolic Infarction\n\u2022 Vertebral artery dissection", "Case Diagnosis": "Cerebellar PICA Infarction", "Diagnosis By": "Confirmed by MRI with matching DWI and ADC abnormalities.", "Treatment & Follow Up": "This pt is being transitioned from Effexor to Zoloft, his HTN is being addressed with HCTZ, and he will receive rehabilitative treatment from PM&R and physical therapy. \n\nHis medical conditions will continue to be followed by psychiatry, medicine, and neurology.", "Discussion": "This patient had an atypical presentation for stroke, without any of the classic risk factors. While it is true that headaches are sometimes seen with stroke, this patient had no focal neurologic findings at the time of his presentation, which confused the picture. His headache presentation was most consistent with migraine, if one assumes a primary headache. If one looks further for causes of secondary headache, the differential includes subarachnoid hemorrhage (SAH), aneurysm, acute ischemic cerebrovascular disorder, arteritis, artery dissection, hypertension(HTN), pseudotumor cerebri, infection, and substance use or withdrawal. \n\tIn this case, the team did a CT for bleeding including SAH and mass effect, which was negative, blood work to rule out arteritis and infection, and (later) an MRA to examine the arteries, which was also normal everywhere but the L PICA. Physical exam and lumbar puncture ruled out pseudotumor cerebri in this case. That leaves HTN, ischemia/infarct, and substance or drug use or withdrawal.\n\tThe patient's systolic blood pressure was elevated on presentation, and with further digging, continued to remain elevated during his hospital course (with diastolic also elevated most of the time). It is possible that his blood pressure had been elevated for quite some time, leading to an occult risk factor. If his headache was a caused by a hypertensive crisis, one would expect his blood pressure to be further elevated on presentation. \n\tThe patient was taking Effexor (venlafaxine), which is a Selective Serotonin/ Norepinephrine Reuptake Inhibitor(SNRI), and has both HTN and headaches as possible side effects. Stroke is not listed as a known side effect. However, there is one case study in the literature that describes a patient having a \"migraine-like\" stroke while having a serotonin syndrome. Serotonin syndrome is caused by too much serotonin in the brain, usually secondary to patients taking SSRIs/ SNRIs and then taking a second serotonin promoter. It does sometimes occur when patients are taking elevated doses of medication. It is unknown how long this patient was taking Effexor before his headaches began or if he experienced any of the other symptoms of serotonin syndrome, including acute mental status changes, involuntary movements, altered muscle tone, and autonomic instability. Even if the patient did not have serotonin syndrome on presentation, it is worth noting that he received sumatriptan while in the hospital, while also receiving his venlafaxine. Could this combination have precipitated a serotonin syndrome? Certainly, however, the patient did not report an increase in symptoms after receiving the drug, so the possibility is very slim.\n\tCocaine is also associated with stroke in the younger population. It is associated with vasoconstriction, and has been known to cause slow flow in the vertebrobasilar system (which supplies the PICA), among other cerebral infarcts, and HTN. While this patient does not report any cocaine use, it is a possibility to be entertained.\n\tThe actual cause of this patient\u2019s infarct may never be known, in part because we do not know when the actual infarct occurred. CT best demonstrates signs of cerebral infarct at least 24 hours after the event. There are cases of CT being used to identify infarcts earlier, but this is generally by identifying secondary signs (like a clot in the MCA) and in the cerebrum rather than the cerebellum. The differential for headaches is very broad, but stroke must be kept in mind especially when no other obvious cause presents itself, as it can often be reversed if found early enough.\nReferences:\nClinch,CR. Evaluation of Acute Headaches in Adults. Amer Fam Physician. 2001 Feb15;63(4):685-92.\nMolaie, M. Serotonin Syndrome Presenting with Migrainelike Stroke. Headache. 1997 Sep;37(8):519-21.\nNanda A, Vannemreddy P, Willis B, Kelley R. Stroke in the young: relationship of active cocaine use with stroke mechanism and outcome. Acta Neurochir Suppl. 2006;96:91-6.\nWardlaw JM, Mielke O. Early signs of brain infarction at CT: observer reliability and outcome after thrombolytic treatment--systematic review. Radiology 2005 May;235(2):444-53. Clinch,CR. Evaluation of Acute Headaches in Adults. Amer Fam Physician. 2001 Feb15;63(4):685-92.\nCaplan LR. Posterior Circulation Cerebrovascular Syndromes. www.uptodate.com. Last updated 21Nov2006. \nOliveira-Filho J, Koroshetz WJ. Neuroimaging of acute ischemic stroke. www.uptodate.com. Last updated May 2006.\n\n=====================================================\nPt notes waking up with a mild headache on the day of admission, unrelieved by caffeine consumption, that progressively worsened. The pain was sharp, but throbbing and located behind his left eye and radiating posteriorly. The nausea and vomiting began just after lunch, and shortly after the patient took a motrin for his headache. He denied any fevers, chills, night sweats, recent ill contacts, or diarrhea. The patient was given ativan, morphine, phenergan, zofran and benadryl along with a 1L bolus of NS. CT was performed and determined to be negative for acute pathology. On day 2, the headache had resolved in the AM, but IV phenergan was required for nausea, and the dizziness persisted. The patient reported a headache in the afternoon, unresolved with 2 separate doses of Imitrex (sumatriptan), but partially alleviated with Tylenol. The patient continued to experience pain the following day, so a repeat CT was done, which showed a \u201cprobable left cerebellar infarct\u201d.\nPMHx: Hypertriglyceridemia, psoriasis, anxiety, G6PD, Crohns\nMeds: Lopid (gemfibrozil), Effexor (venlafaxine)\nAllergies: Iodine, Primaquin" }, "Topic": { "Title": "Posterior Inferior Cerebellar Artery Infarct", "Disease Discussion": "Posterior Inferior Cerebellar Artery Infarction\n\nThe posterior inferior cerebellar artery (PICA) territory includes all of the posteroinferior cerebellum, the ipsilateral cerebellar tonsil, and the ipsilateral inferior vermis. The PICA also frequently supplies the posterolateral medulla and infarction in this location results in the lateral medullary syndrome or the so-called Wallenberg syndrome. The clinical manifestations and structures affected in Wallenberg's syndrome include:\n\nIpsilaterally:\n-preganglionic Horner syndrome (descending reticulospinal tracts to cord sympathetics)\n-ataxia (cerebellum, inferior peduncle)\n-facial pain, numbness, impaired sensation (CN V nucleus, spinal tract)\n-dysphagia, hoarseness, diminished gag reflex (CN's IX and X)\n-diminished taste (CN IX nucleus and solitary tract)\n-vertigo, nausea, vomiting (vestibular nuclei and connections)\n-nystagmus, diplopia, oscillopsia (restiform body, inferior and medial vestibular nuclei)\n-hiccups\n\nContralaterally:\n-numbness, decreased pain and temperature in trunk and extremities (spinothalamic tract)\n\nThe variability in vascular supply of the cerebellum and medulla is reflected by PICA infarcts. Sometimes a PICA infarct produces the classic Wallenberg syndrome described above while others may spare the medulla. Single PICA branch occlusions can affect a very small area.", "ACR Code": "1.9", "Category": "Hypoxic or Ischemic", "Keywords": "infarct", "Reference": "Osborn AG. Diagnostic Neuroradiology. St. Louis, Mosby-Year Book, Inc. 1994. pp 364-370.", "External Links": "www.ninds.nih.gov/health_and_medical/disorders/wallenbergs.htm" } }, { "U_id": "MPX2391", "TAC": [ "MPX2391_synpic17893" ], "MRI": [], "Case": { "Title": "Pneumothorax", "History": "Patient admitted originally for hemoptysis. She has a history of chronic lung disease and bronchiectasis. During the course of hospitalization, she required the introduction of a pacemaker.", "Findings": "Image 1 shows the pre-pacer portable cxr with evidence of chronic lung disease and scarring in both bases. Images 2,3, and 4 demonstrate the left medial pneumothorax which occurred during pacemaker placement. Image 5 demonstrates reduction of the pneumothorax by a small lumen anterioly placed chest catheter. Image 6 and 7 demonstrates acute left hemothorax which occurred immediately after removal of the chest catheter. Her left internal thoracic artery had been lacerated but tamponaded during chest tube insertion. Removal of the chest tube released the tamponade resulting in acute hemorrhage. Image 8 demonstrates successful embolization of the hemorrhage and introduction of a pigtail chest tube catheter to drain the hemothorax.", "Differential Diagnosis": "Pneumopericardium\nPneumomediastinum\nPneumoperitoneum\nLarge Bullae", "Case Diagnosis": "Pneumothorax", "Diagnosis By": "Diagnosed with right lateral decubitus view and CT", "Treatment & Follow Up": "A series of iatrogenic complications resulted that ultimately required interventional radiology. Treatment of the pneumothorax was introduction of a small lumen chest catheter through the anterior chest wall just lateral to the sternum.\nTreatment of the hemothorax was deployment of embolization coils to the lacerated left internal thoracic artery, performed by the interventional radiologists. A pigtail chest tube catheter was also introduced anteriorly to drain the pneumothorax.", "Discussion": "Iatrogenic pneumothorax occurs in approximately 1.5% of pacemaker insertions. Iatrogenic hemothorax is an infrequent, but known complication of anterior chest tube insertion. ICU patients are frequently the recipients of multiple invasive procedures and the radiologist viewing portable ICU films must maintain continuous vigilance for complications, which often are subtle in presentation." }, "Topic": { "Title": "Pneumothorax: Atypical Signs", "Disease Discussion": "Atypical signs of Pneumothorax\n\nThese arise when the patient is supine or the pleural space partly obliterated. In the supine position, pleural air rises and collects anteriorly, particularly medially and basally, and may not extend far enough posteriorly to separate lung from the chest wall at the apex or laterally. Signs that suggest a pneumothorax under these conditions are: \n\n1. an ipsilateral transradiancy, either generalized or hypochondrial \n2. a deep, finger-like costophrenic sulcus laterally\n3. a visible anterior costophrenic recess seen as an oblique line or interface in the hypochondrium; when the recess is manifest as an interface it mimics the adjacent diaphragm (\u2018double diaphragm sign\u2019)\n4. a transradiant band parallel to the diaphragm and/or mediastinum with undue clarity of the mediastinal border \n5. visualization of the undersurface of the heart, and of the cardiac fat pads as rounded opacities suggesting masses \n6. diaphragm depression. \n\nIn a patient who cannot stand, the presence of a pneumothorax can be confirmed with a lateral decubitus view or a supine decubitus projection with the cassette placed dorsolaterally at 45\u00b0 and the X-ray tube angled perpendicular to the cassette.\nWhen the pleural space is partly obliterated a pneumothorax may be loculated, and must be differentiated from other localized transradiancies. These include cysts, bullae, pneumatoceles, pneumomediastinum, and local emphysema. These cannot always be differentiated by plain radiographs, but can be by CT.", "ACR Code": "6.9", "Category": "Iatrogenic or Surgical (complications)", "Keywords": "pneumothorax", "Reference": "Grainger & Allison\\'s Diagnostic Radiology: A Textbook of Medical Imaging, 4th Ed., Copyright \u00a9 2001 Churchill Livingstone, Inc. pp 336-337" } }, { "U_id": "MPX2403", "TAC": [ "MPX2403_synpic53336" ], "MRI": [], "Case": { "Title": "Tuberculosis Pott's Disease", "History": "56 y.o. woman with a history of tuberculosis as a child that was incompletely treated. She presents with low back pain and dry cough x 6 months.", "Findings": "There is a moderate amount of peritoneal fluid. Complete destruction of the L2 vertebral body and superior portion of the L3 vertebral body. There is retropulsion of a bony fragment into the\nspinal canal with severe spinal canal stenosis.\n\nBilateral multiloculated psoas fluid collections are seen with rim enhancement.\n\nFor the left psoas fluid collection, the largest pocket now measures 2.1 x 4.2 cm and is found at the level of L3-4.\n \nThe right psoas fluid collection is again seen, measuring 4 x 1.8 cm in\nlargest dimension, found at the L1-2 level.", "Differential Diagnosis": "Trauma\nNeoplasm\nPyogenic Osteitis of the spine", "Case Diagnosis": "Tuberculosis Pott's Disease", "Diagnosis By": "Acid Fast Culture", "Treatment & Follow Up": "Patient was treated with RIPE therapy for the tuberculosis and drain placement for the abscesses", "Discussion": "Drainage of the abscesses continues to be a challenge. She continues to have daily fevers but overall is improving s/p drain placement and commencement of RIPE therapy." }, "Topic": { "Title": "Pott's Disease", "Disease Discussion": "Lesion/Condition Name: Pott's Disease\n\nSynonyms: tuberculous spondylitis\n\nAssociations/Predisposing Factors: \nEndemic tuberculosis.\nPoor socio-economic conditions.\nHIV infection.\n\nCommon Locations: Lower thoracic and upper lumbar vertebrae. Usually more than one vertebra is involved. The area most affected is the anterior part of the vertebral body adjacent to the subchondral plate. Tuberculosis may spread from that area to adjacent intervertebral discs.\n\nDemographics: The disease affects males more than females in a ratio of between 1.5 and 2:1. In the USA it affects mostly adults but in the countries where it is commonest it affects mostly children.\n\nSpecial Stains: Acid Fast Stain\n\nRadiology:\n-Spinal X-ray may be normal in early disease as 50% of the bone mass must be lost for changes to be visible on X-ray. Plain X-ray can show vertebral destruction and narrowed disc space.\n-MRI scanning may demonstrate the extent of spinal compression and can show changes at an early stage. Bone elements visible within the swelling, or abscesses, are strongly suggestive of Pott\\'s disease rather than malignancy. \n-CT scans and nuclear bone scans can also be used but MRI is best to assess risk to the spinal cord.\n\nPrognosis and Treatment:\nPrognosis is better if caught early but diagnosis is difficult and often late.", "ACR Code": "3.-1", "Category": "Infection, bacteria", "Keywords": "Pott's Disease" } }, { "U_id": "MPX2407", "TAC": [ "MPX2407_synpic48714" ], "MRI": [ "MPX2407_synpic48720", "MPX2407_synpic48721", "MPX2407_synpic48722", "MPX2407_synpic48723", "MPX2407_synpic48725", "MPX2407_synpic48727" ], "Case": { "Title": "Postpartum Cerebral Angiopathy", "History": "34-year-old African American G1P1 female with no significant medical history presents to the ER four days postpartum complaining of the \u201cworst headache of her life\u201d on the right-sided of her head.", "Exam": "BP: 111/63, HR: 98, RR: 18, T: 97.6 \u00b0F, HT: 63 in, WT: 158 lbs, BMI: 27.99.\nNo focal neurological findings found on exam\nCSF: large amount of RBC with xanthochromia\nESR: 56 mm/hour\nNo proteinuria on UA\nOtherwise Normal exam and labs", "Findings": "CT: Axial Noncontrast CT of the Brain showed an acute SAH in the right frontal lobe brain. \n\nCerebral angiogram: Lateral projection of the right cerebral angiogram demonstrated irregular variable caliber in cortical vessels in the right MCA distribution. \n\nMRI/MRA: Diffusion weight image, Apparent Diffusion Coefficient MRI, and T2-weighted images of brain demonstrate an acute infarct in the right mid-posterior cerebellar in the superior cerebellar vascular territory. \n\nAxial FLAIR MRI of the brain showed multiple nonspecific small foci of increased FLAIR signal within the anterior aspects of the external capsule bilaterally. \n\n3D time of flight MRA of the cerebral arteries demonstrated MCA cortical vessel caliber variation.", "Differential Diagnosis": "Postpartum Cerebral Angiopathy \nPreeclampsia \nPseudoanyeurysm \nPrimary Cerebral Vasculitis \nOther secondary Cerebral Vasculitis: \n\u2022 Polyarteritis nodosa \n\u2022 Giant cell arteritis \n\u2022 Takayasu\u2019s arteritis \n\u2022 Wegener\u2019s granulomatosis \n\u2022 SLE \n\u2022 RA \n\u2022 Behcet\u2019s syndrome \n\u2022 Lyme Disease \n\u2022 Illicit drugs \n \uf0a7\tcocaine \n \uf0a7\theroin \n \uf0a7\tamphetamines \n\u2022 Sarcoidosis", "Case Diagnosis": "Postpartum Cerebral Angiopathy", "Diagnosis By": "Contrast Catheter Cerebral Angiography & MRI/MRA", "Treatment & Follow Up": "Cerebral vasculitis is a highly treatable condition; there currently is no standard management that has been established, but most authors agree that acute-phase treatment includes cessation of vasoconstrictors, treatment of associated conditions, vasospasm treatment (calcium channel antagonists), corticosteroids, headache relief, blood pressure control, and stroke, cerebral edema, and seizure treatment as needed. A high dose intravenous steroids \u2013 probably best as intravenous methyl prednisolone 1 gram daily for 3 days. Other treatments including azathioprine (2 mg/kg/day) for 10 months, methotrexate 10\u201325 mg on a weekly basis, intravenous immunoglobulin (0.4 mg/kg/day for 5 days), plasmapheresis, and Campath-1H may be used depending upon the etiology. \n\nReferences:\n\u2022 Calado S, Viana-Baptista M. \u201cBenign cerebral angiopathy; postpartum cerebral angiopathy: characteristics and treatment\u201d. Curr Treat Options Cardiovasc Med. 2006 May;8(3):201-12.\n\u2022 Joseph F, Scolding N. \u201cCerebral Vasculitis a practical approach\u201d Practical Neurology 2002, 2, 80\u201393. pn.bmj.com/cgi/reprint/2/2/80.pdf", "Discussion": "Postpartum cerebral angiopathy is a rare ailment that affects females who are otherwise healthy and recently had a normal pregnancy and uncomplicated delivery. Like primary and other secondary cerebral vasculitis, postpartum cerebral angiopathy may cause ischemic or hemorrhagic stroke, and neurological deficits. More commonly, secondary cerebral angiopathy occurs in the setting of other medical conditions such as infections, systemic vasculitis (Wegener\u2019s granulomatosis & polyarteritis), connective tissue diseases (systemic lupus erythematosus & rheumatoid arthritis), medications, illicit drugs, carcinomas (lymphoma & leukemia), and Behcet\u2019s disease. Other conditions, therefore, need to be ruled out before a diagnosis of postpartum cerebral angiopathy can be made including preeclampsia /eclampsia. \n\n Contrast catheter angiography and magnetic resonance imaging/angiography (MRI/MRA) are the typical imaging modalities used to help with the diagnosis of cerebral vasculitis although, single photon emission computed tomography (SPECT) and Indium-labelled white cell nuclear scanning may provide some benefit. Definitive diagnosis of cerebral vasculitis is typically made by biopsy of brain. \n\n In this patient she presented to the ER with the \u201cworse headache of her life\u201d on the right side 4 days postpartum. Noncontrast computed tomography (CT) showed subarachnoid hemorrhage (SAH) with the right sylvian fissure and the sulci of the right frontal lobe. Further vascular studies including a CT angiogram (CTA), contrast angiography, and MRA showed no evidence of an intracerebral aneurysm. The patient had no history of hypertension and was not hypertensive during the headache. She was tested several times throughout pregnancy with no evidence of elevated blood pressure, proteinuria, or headaches looking for preeclampsia. The patient had an elevated erythrocyte sedimentation rate (ESR) of 56 mm/hour. \n\nUpon further investigation the patient had a contrast enhanced angiogram which showed irregular variable caliber vessels with \u201csausage linked\u201d appearance in the cortical branches of both the middle cerebral arteries with a more prominence on the right side as opposed to the left. The MRI also showed and acute 5 mm left cerebellar infarct located within a superior cerebellar artery vascular territory and multiple nonspecific small foci of increased FLAIR signal within the anterior aspects of the external capsule bilaterally. \n\nThis patient had several classic imaging findings of cerebral vasculopathy of small vessel ischemic disease, SAH, and cortical enhancement. She had no known significant past medical history including autoimmune disorders, systemic vasculitis, or connective tissue disorders. She had a normal uncomplicated pregnancy and developed her first symptoms 4 days postpartum fitting the description of postpartum cerebral angiopathy. \n\nThe patient was treated with oral prednisolone and was felt that a brain biopsy was not necessary in this case to make the definitive diagnosis.\n\nReferences:\n\u2022 Brant W, Helms C. \u201cFundamentals of Diagnostic Radiology\u201d Lippincott Williams & Wilkins, Philadelphia, PA 2007.\n\u2022 Singhal A, Bernstein R. \u201cPostpartum angiopathy and other cerebral vasoconstriction syndromes\u201d. Neurocrit Care. 2005;3(1):91-7.\n\u2022 Wilhelm K. \u201cImaging of cerebral vasculitis\u201d \u201cInternational Journal of Stroke\u201d Vol 2(3), 184 \u2013190.\n\u2022 Amos P. Postpartum cerebral angiopathy: a case study. J Neurosci Nurs. 2007 Feb;39(1):9-12.\n\u2022 Joseph F, Scolding N. \u201cCerebral Vasculitis a practical approach\u201d Practical Neurology 2002, 2, 80\u201393. pn.bmj.com/cgi/reprint/2/2/80.pdf" }, "Topic": { "Title": "Postpartum Cerebral Angiopathy", "Disease Discussion": "Postpartum cerebral angiopathy is a rare ailment that affects females who are otherwise healthy and recently had a normal pregnancy and uncomplicated delivery. Like primary and other secondary cerebral vasculitis, postpartum cerebral angiopathy may cause ischemic or hemorrhagic stroke, and neurological deficits. More commonly, secondary cerebral angiopathy occurs in the setting of other medical conditions such as infections, systemic vasculitis (Wegener\u2019s granulomatosis & polyarteritis), connective tissue diseases (systemic lupus erythematosus & rheumatoid arthritis), medications, illicit drugs, carcinomas (lymphoma & leukemia), and Behcet\u2019s disease. Other conditions, therefore, need to be ruled out before a diagnosis of postpartum cerebral angiopathy can be made including preeclampsia /eclampsia. \n\nContrast catheter angiography and magnetic resonance imaging/angiography (MRI/MRA) are the typical imaging modalities used to help with the diagnosis of cerebral vasculitis although, single photon emission computed tomography (SPECT) and Indium-labelled white cell nuclear scanning may provide some benefit. Definitive diagnosis of cerebral vasculitis is typically made by biopsy of brain. \n\nIn this patient she presented to the ER with the \u201cworst headache of her life\u201d on the right side 4 days postpartum. Noncontrast computed tomography (CT) showed subarachnoid hemorrhage (SAH) with the right sylvian fissure and the sulci of the right frontal lobe. Further vascular studies including a CT angiogram (CTA), contrast angiography, and MRA showed no evidence of an intracerebral aneurysm. The patient had no history of hypertension and was not hypertensive during the headache. She was tested several times throughout pregnancy with no evidence of elevated blood pressure, proteinuria, or headaches looking for preeclampsia. The patient had an elevated erythrocyte sedimentation rate (ESR) of 56 mm/hour. \n\nUpon further investigation the patient had a contrast enhanced angiogram which showed irregular variable caliber vessels with \u201ca sausage link\u201d appearance in the cortical branches of both the middle cerebral arteries, more prominent on the right side as opposed to the left. The MRI also showed an acute 5 mm left cerebellar infarct located within a superior cerebellar artery vascular territory and multiple nonspecific small foci of increased FLAIR signal within the anterior aspects of the external capsule bilaterally. \n\nThis patient had several classic imaging findings of cerebral vasculopathy of small vessel ischemic disease, SAH, and cortical enhancement. She had no known significant past medical history including autoimmune disorders, systemic vasculitis, or connective tissue disorders. She had a normal uncomplicated pregnancy and developed her first symptoms 4 days postpartum fitting the description of postpartum cerebral angiopathy. \n\nThe patient was treated with oral prednisolone and was felt that a brain biopsy was not necessary in this case to make the definitive diagnosis.", "ACR Code": "1.2", "Category": "Vascular", "Keywords": "Postpartum Cerebral AngiopathyCerebral VasculitisAngiopathy", "Reference": "\u2022 Brant W, Helms C. \u201cFundamentals of Diagnostic Radiology\u201d Lippincott Williams & Wilkins, Philadelphia, PA 2007. \n\u2022 Singhal A, Bernstein R. \u201cPostpartum angiopathy and other cerebral vasoconstriction syndromes\u201d. Neurocrit Care. 2005;3(1):91-7. \n\u2022 Wilhelm K. \u201cImaging of cerebral vasculitis\u201d \u201cInternational Journal of Stroke\u201d Vol 2(3), 184 \u2013190. \n\u2022 Amos P. Postpartum cerebral angiopathy: a case study. J Neurosci Nurs. 2007 Feb;39(1):9-12. \n\u2022 Joseph F, Scolding N. \u201cCerebral Vasculitis a practical approach\u201d Practical Neurology 2002, 2, 80\u201393. pn.bmj.com/cgi/reprint/2/2/80.pdf" } }, { "U_id": "MPX2421", "TAC": [ "MPX2421_synpic27129" ], "MRI": [], "Case": { "Title": "Tuberous Sclerosis Complex (TSC)", "History": "13 y/o girl with Hx of seizures since childhood", "Exam": "Physical exam not available at time of imaging", "Findings": "- Calcified subependymal nodules in lateral ventricles\n- Low density cortical tubers\n- Pulmonary \"honeycomb\" pattern suggestive of Lymphangiomyomatosis (LAM)", "Differential Diagnosis": "Tuberous sclerosis complex (TSC) (with this constellation of features). Subependymal gray matter heterotopia does not calcify like this; and, other causes of periventricular Ca++ cause volume loss and do not protrude into ventricle.", "Case Diagnosis": "Tuberous Sclerosis Complex (TSC)", "Diagnosis By": "Classic imaging findings with clinical correlation", "Discussion": "This specific case is interesting for the fact that the patient also had pulmonary lymphangiomyomatosis. Lymphangiomyomatosis is a pulmonary condition in which there is infiltration of smooth muscle in the interstitium that leads to cystic changes throughout the lung parenchyma. One source suggests that this process occurs in less than 10% of all TSC patients (2). Treatment goals are geared toward preserving lung tissue. Patients usually undergo serial CT scans to monitor the disease process." }, "Topic": { "Title": "Tuberous Sclerosis Complex (TSC)", "Disease Discussion": "Tuberous Sclerosis Complex (TSC), also known as \u201cBourneville\u2019s disease\u201d, is a multi-organ disorder that can present in a variety of ways. It is inherited as an autosomal-dominant trait. Its incidence is approximately 1:10,000 to 1:50,000 (1). The clinical presentation of tuberous sclerosis is dependent on the age of the patient, the organ systems involved, and the severity of their involvement. Classically, however, tuberous sclerosis presents with Vogt\u2019s triad: adenoma sebaceum (Pringle\u2019s disease), mental retardation, and seizures. Adenoma sebaceum are angiofibromas that usually develop between the ages of 1 and 4 years. They are usually pink or red papules that form on the face in a malar distribution, similar to the butterfly rash of SLE. They occur in approximately 75% of tuberous sclerosis patients. \n\nAnother common physical exam finding in tuberous sclerosis is hypopigmented macules on the trunk and extremities. These lesions are commonly present at birth and become more noticeable as the patient ages. At least three types of hypopigmented macules have been documented in TSC: polygonal (most frequent), ash-leaf shaped, and confetti-shaped (multiple 1-3 mm macules) . These hypopigmented lesions can sometimes be better seen with a Wood\u2019s lamp. \n\nAlthough the above two physical findings are classic for TSC, there are many other physical features that are suggestive of the diagnosis (see table below).\n\nTable 1: Major and Minor Diagnostic Features of Tuberous Sclerosis Complex (2)\n\n\u2022 \tMajor features\n\u2022 \tFacial angiofibromas or forehead plaque \n\u2022 \tNontraumatic ungual or periungual fibrom \n\u2022 \tHypomelatonic macules (three or more) \n\u2022 \tShagreen patch (connective-tissue nevus) \n\u2022 \tMultiple retinal nodular hamartomas \n\u2022 \tCortical tubera \n\u2022 \tSubependymal nodule \n\u2022 \tSubependymal giant-cell astrocytoma \n\u2022 \tCardiac rhabdomyoma, single or multiple \n\u2022 \tLymphangiomyomatosis \n\u2022 \tRenal angiomyolipoma \n\u2022 \tMinor features\n\u2022 \tMultiple, randomly distributed pits in dental enamel \n\u2022 \tHamarromatous rectal polyps \n\u2022 \tBone cysts \n\u2022 \tCerebral white matter radial migration lines \n\u2022 \tGingival fibromas \n\u2022 \tNonrenal hamartoma \n\u2022 \tRetinal achromic patch \n\u2022 \t'Confetti' skin lesions \n\u2022 \tMultiple renal cysts \n\n\u2022 \tDefinite tuberous sclerosis complex\n\u2022 \tEither two major features or one major feature plus two minor features \n\u2022 \tProbable tuberous sclerosis complex\n\u2022 \tOne major plus one minor feature \n\u2022 \tPossible tuberous sclerosis complex\n\u2022 \tEither one major feature or two or more minor features \n\u2013\tWhen cerebral cortical dysplasia and cerebral white matter migration tracts occur together, they should be counted as one rather than two features of tuberous sclerosis. \n\u2013\tWhen both lympangiomyomatosis and renal angiomyolipomas are present, other features of tuberous sclerosis should be present before a definite diagnosis is assigned. \n\u2013\tHistologic confirmation is suggested. \n\u2013\tRadiographic confirmation is sufficient. \n\u2013\tOne panel member felt strongly that three or more radial migration lines should constitute a major sign.", "ACR Code": "1.3", "Category": "Congenital, genetic", "Keywords": "Tuberous SclerosisTuberous Sclerosis ComplexLymphangiomyomatosis", "Reference": "1) Goldman, L. and Ausello, D. Cecil Textbook of Medicine, 22nd Ed. pp. 2362-2363. \n2) Roach ES, et al. Tuberous sclerosis consensus conference: revised clinical diagnostic criteria. J Child Neurol 1998; 13: 624\n3) Dambro, MR. Griffith's 5 Minute Clinical Consult 2004. Electronic Book. Search Topic: Tuberous Sclerosis. \n\nBibliography\nSwaiman, KF and Ashwal, S. Pediatric Neurology - Principles and Practices. 3rd Ed. Chapter 29. pg. 533-537." } }, { "U_id": "MPX2423", "TAC": [ "MPX2423_synpic20203" ], "MRI": [], "Case": { "Title": "Hepatic laceration with biloma.", "History": "29 y/o male s/p liver laceration with repair three weeks ago.", "Findings": "Findings include a fluid density on CT within the right upper quadrant adjacent to the liver. Loculations and septations may be present as well. An adjacent hepatic parenchymal defect is often present. As they mature, bilomas usually appear round with a thin surrounding capsule. Free intra-peritoneal fluid collections can indicate biloma rupture. \n\nOnly biliary scintigraphy, can definitively demonstrate a communication between the biliary tree and the biloma contents.", "Differential Diagnosis": "Biloma, hematoma, seroma, abscess", "Case Diagnosis": "Hepatic laceration with biloma.", "Diagnosis By": "Biliary scintigraphy." }, "Topic": { "Title": "Hepatic laceration", "Disease Discussion": "Hepatic injuries occur in roughly 5-10% of patients with blunt abdominal trauma; other associated visceral injuries are very common. Capsular disruption and intraperitoneal hemorrhage is often present. The mortality, which is relatively high (10-25%), is usually due to either an associated injury or an uncontrollable hemorrhage from a laceration or a central burst that involves the major hepatic veins and/or the intrahepatic or retrohepatic inferior vena cava. These latter patients rarely come to CT because of instability. Contrast-enhanced CT is the procedure of choice for evaluating hepatic injuries in stable patients. It can define the extent of injury, detect associated injuries and roughly quantitate the amount of hemoperitoneum. The amount of hemoperitoneum does not always correlate with clinical stability and the need for immediate surgery. Fairly large hepatic injuries may be missed without intravenous contrast enhancement. Conversely, small hematomas may be visible as densities on a non-contrast scan (and obscured by contrast-enhanced parenchyma). These are usually not clinically significant and preliminary non-contrast CT may be safely omitted when you are pressed for time. If non-operative management is chosen, CT or sonography can be used for follow-up. The liver injuries likely to be encountered on CT include contusions, subcapsular and parenchymal hematomas, lacerations and fractures. Contusions are ill-defined intraparenchymal lucencies. Subcapsular hematomas are lenticular lucent peripheral collections that indent the liver contour. Intraparenchymal hematomas are rounded or slightly irregular lucent collections. Fresh and clotted blood is hyperdense on non-contrast scans as opposed to its hypodense appearance after contrast. Lacerations are linear, sometimes branching radiolucencies, referred to as burst injuries when complex and extensive. When a laceration avulses a segment or lobe it is called a fracture. \n\nPotential complications that should be sought during follow-up of a conservatively treated hepatic trauma patient or a postoperative patient include: arterial pseudoaneurysm (angiography and Doppler sonography are helpful additional studies), intra- or perihepatic abscess, biloma or biliary fistula. Radionuclide hepatobiliary scintigraphy is a sometimes helpful noninvasive adjunctive study for the latter two conditions.", "ACR Code": "7.-1", "Category": "Trauma" } }, { "U_id": "MPX2427", "TAC": [ "MPX2427_synpic4861", "MPX2427_synpic4862" ], "MRI": [], "Case": { "Title": "Epidural Hematoma of middle fossa (temporal bone)", "History": "5 year old male S/P fall from shopping cart. Now presents with lethargy and headache.", "Findings": "Rt temporal-occipital epidural hematoma with mild mass effect on right lateral ventricle.", "Case Diagnosis": "Epidural Hematoma of middle fossa (temporal bone)", "Treatment & Follow Up": "Patient being followed conservatively." }, "Topic": { "Title": "Epidural Hematoma, Talk and Die Syndrome, Lucid Interval", "Disease Discussion": "Watch Video - http://youtu.be/30XPVg0DWH4\nAn epidural hematoma (EDH) is an accumulation of blood between the outer (periosteal) layer of the dura mater (literally \"tough mother\") and the naked bone of the inner table of the skull. Most patients will have an acute clinical presentation. The blood will, therefore, be hyperdense (white) on a plain CT scan. The most common source of bleeding is a laceration or tear in one of the meningeal arteries that feed the dura itself. Posterior or occipital epidurals may develop from lacerations of the dural transverse sinus.\n\nMore than 90% of patients with an EDH will have a skull fracture (and associated scalp trauma) in addition to the EDH. The temporal bone and the underlying middle cranial fossa are the most commonly affected areas. Because of the firm fixation of the dura to the suture, the hematoma only rarely crosses a cranial suture.\n\nSome patients are knocked unconscious by the initial head impact (a \"concussion\") - but then wake up and may appear normal. This is often described as the \"lucid interval\" and occurs in about 40% of patients with epidural hematoma.\n\nDr. Paul Cooper, in his book \"Head Injury\", reports these five patterns of the clinical EDH:(U=unconscious; L=lucid; C=conscious)\n\n1. U-->L-->U: 11 to 67%\n2. U throughout: 19 to 56%\n3. U-->C: 16 to 26%\n4. C-->U: 7 to 21%\n5. C throughout: 9 to 25%\n6. unknown or unstated: 5%\n\nNOTE: A significant number of patients do not even have a transient loss of consciousness. (Data courtesy of Vern Armbrustmacher).\n\nAs the blood accumulates from bleeding meningeal arteries, it forms a bi-convex or lens shaped mass that pushes the brain inward and downward - causing brain herniation.\n\nThe acute formation of the EDH often causes secondary downward transtentorial brain herniation. This, in turn, may cause neurologic signs,including oculomotor nerve (CNN-3) dysfunction and a \"blown pupil\" (fixed and dilated).\n\nMany patients have the injury, but appear to be alright afterwards. As the blood accumulates and the brain begins to shift, they may slip into a coma. This is \"lucid interval\" is also sometimes described as \"Talk and Die\". Sadly, this is not rare, and in 2009 Tony Award winning actress Natasha Richardson died from an epidural hematoma. She had a lucid interval after falling while skiing, not wearing a helmet.\n\u2022 http://www.sciam.com/article.cfm?id=talk-and-die-richardson\n\u2022 http://abcnews.go.com/Entertainment/Movies/story?id=7119825&page=1'>http://abcnews.go.com/Entertainment/Movies/story?id=7119825&page=1\n\u2022 http://www.cnn.com/2009/HEALTH/03/18/brain.injury/index.html?iref=mpstoryview\n\u2022 http://www.washingtonpost.com/wp-dyn/content/article/2009/03/19/AR2009031902515.html\n\u2022 http://www.baltimoresun.com/news/health/bal-epidural-hematoma-0318,0,7024060.story\n\u2022 http://abcnews.go.com/Entertainment/Movies/story?id=7119825&page=1\n\nFor more on Intracranial Hemorrhage: http://rad.usuhs.mil/rad/handouts/jsmirnio/Intracranial_Hemorrhage_%20RSNA_2008_HO.pdf\nhttps://www.youtube.com/watch?v=30XPVg0DWH4\nhttps://www.youtube.com/watch?v=jiscvATspCA", "ACR Code": "1.4", "Category": "Trauma", "Keywords": "TBI Traumatic Brain Injurylucid interval", "Reference": "; Accepted by jsmirnio; Accepted by jsmirnio; Accepted by jsmirnio", "External Links": "rad.usuhs.edu/rad/handouts/jsmirnio/Traumatic_Brain_Injury_Epidural_Hematoma.pdf" } }, { "U_id": "MPX2435", "TAC": [ "MPX2435_synpic24449" ], "MRI": [], "Case": { "Title": "Acute on chronic bilateral subdural hematomas.", "History": "Recent onset gait disturbance and history of 2 falls in the past 6 weeks.", "Findings": "Non-contrast CT of the brain demonstrates bilateral frontal subdural hemorrhages of varying chronicity. The right collection contains some prominent areas of high density, consistent with acute on-chronic hemorrhage. The left collection also contains a small amount of high density that may also represent acute blood. Overall, these collections are roughly symmetric in size and cause no midline shift. There is no hydrocephaplus; the ventricular systems are smaller than expected for age, perhaps secondary to\ncompression by the extraaxial fluid collections.", "Differential Diagnosis": "Acute on chronic bilateral subdural hematomas.", "Case Diagnosis": "Acute on chronic bilateral subdural hematomas.", "Diagnosis By": "Diagnosis confirmed by imaging.", "Treatment & Follow Up": "The bilateral collections were surgically evacuated." }, "Topic": { "Title": "subdural hematoma", "Disease Discussion": "Subdural hematomas are usually from the venous vasculature, and are often specifically as a result of tearing the cortical veins that bridge the subdural space en route to the dural sinuses. Because the inner dural layer and the arachnoid are not firmly attached the bleeding can spread over a large area and can form a distinctive crescent shape.\n\nThese extra-axial bleeds are often the result of blunt trauma that causes the brain to shift rapidly within the skull. Typically, it is the older population where these are most common, because cerebral atrophy can lead to more room for the brain to move, and more stress placed upon the bridging veins. Another unique characteristics of subdural hematomas is that they will not cross the dural reflections formed by the falx cerebri and tentorim (they will cross sutural margins which helps differentiate subdual from epidural bleeds). Also, a subdual bleed can be chronic with episodes of rebleeding which leads to a layering of blood as new bleeding occurs and old blood is being absorbed called a hematocrit effect.", "ACR Code": "9.4", "Category": "Vascular", "Keywords": "subdural hematomabridging veins", "Reference": "1.\tBrant, WE. Helms, CA. Fundamentals of Diagnostic Radiology. 2nd ED., Williams & Wilkins 1999.\n2.\tSawauchi S, Beaumont A, Signoretti S, Tomita Y, Marmarou C, Marmarou A. Diffuse brain injury complicated by acute subdural hematoma in the rodents: the effect of early or delayed surgical evacuation. Acta Neurochir Suppl. 2002;81:243-4.\n3.\tNakamizo A, Inamura T, Inoha S, Kuba H, Amano T, Sasaki M, Fukui M. Occurrence of subdural hematoma and resolution of gait disturbance in a patient treated with shunting for normal pressurehydrocephalus. Clin Neurol Neurosurg. 2002 Sep;104(4):315-7.\n4.\tShiomi N, Hashimoto N, Takeuchi H, Yamanaka T, Nakagawa N, Mineura K. Endoscopic findings in chronic subdural hematoma. No Shinkei Geka. 2002 Jul;30(7):717-22." } }, { "U_id": "MPX2439", "TAC": [ "MPX2439_synpic32188" ], "MRI": [], "Case": { "Title": "Epidural brain abscess, CNS", "History": "9 year old boy presented to the Emergency Department with a head ache and \"swollen eyes\". The patient had been treated for a sinus infection for 14 days but his head ache and eye swelling were getting worse despite finishing his course of antibiotics.", "Exam": "WBC 13,000\nH/H 14/40\nTemp 102.2 F", "Findings": "Non contrast CT demonstrated an isodense to grey matter-extraaxial, intracranial fluid collection that followed the convexity of the frontal cranium. It did not enhance after contrast - but showed rim enhancement of the displaced dura. There were numerous foci of air within it. Additionally, there was extensive paranasal sinus opacification with air fluid levels, most prominent in the left maxillary sinus and in frontal and ethmoid sinuses bilaterally. There are bilateral inflammatory changes seen in the preseptal orbital tissues that extended over the zygomatic arches bilaterally.\n\nMR imaging shows an epidural fluid collection with these signal characteristics: Iso to grey matter on T1, Hyperintense to grey matter on T2, FLAIR and DWI with low signal on ADC mapping. The child could not remain still enough for contrast enhanced MR images.", "Differential Diagnosis": "Subdural hematoma\nSubdural abscess\nEpidural hematoma\nEpidural abscess", "Case Diagnosis": "Epidural brain abscess, CNS", "Diagnosis By": "Surgery", "Treatment & Follow Up": "The patient underwent emergent surgery which required cranialization of the frontal sinuses with drainage of the epidural abcess.", "Discussion": "There was no bone breakdown. Transvenous thrombophlebitis may allow spread of sinus infection, while the bone remainas, apparently, intact. Another consideration would be microerosions of bone with direct spread from the contiguous frontal sinuses. \n\nThe distinction between pre- vs post-septal orbital cellutitis was important in this case, as it would have changed operative approach. Venous thrombosis would not have changed the surgical approach; however it would portend a poor prognosis." }, "Topic": { "Title": "Brain abscess, Central Nervous System", "Disease Discussion": "The most common source of CNS infections is hematogenous spread from an extracranial site. Infection can occur from direct extension from retrograde thrombophlebitis as in sinus infections. The infectious organisms may be pyogenic bacteria; and, in more than 33 percent more than one organism is involved.\n\nThe corticomedullary junction is the most common location and involves the frontal and parietal lobes most frequently. Less than 15% occur in the posterior fossa.\n\nComplications of abscesses include daughter abscesses, ventriculitis, choroid plexitis and purulent leptomeningitis.\n\nFour pathologic stages of cerebritis to abscess are described:\n\u2022 early cerebritis(3-5 days),\n\u2022 late cerebritis (4-5 days to 10-14 days)\n\u2022 early capsule formation (2 weeks)\n\u2022 late capsule (weeks to months).\n\nEarly cerebritis findings are poorly marginated, hypointense or isointense mass on T1WI, ill defined hyperintense mass on T2WI, and patchy enhancement on post contrast T1WI.\n\nLate cerebritis demonstrates a hypointense center with isointense to mildly hyperintense rib on T1WI, hyperintense center and hypointense rim with hyperintense edema on T2WI and intense but irregular rim on post contrast T1WI.\n\nEarly capsule stage shows an isointense to hyperintense rim with a hyperintense center on T1WI, hypointense rim and hyperintense center on T2WI and thickened capule of rim enhancement on post contrast T1WI.\n\nLate capsule stage includes decreased edema and mass effect on T2WI, collapse of the cavity and thickened capsular enhancement on post contrast T1WI.\n\nDiffusion weighted imaging shows increased signal intensity; and, the Apparent Diffusion Coefficient maps show a decreased signal within the abscess.", "ACR Code": "1.2", "Category": "Infection, bacteria", "Keywords": "abscesscerebritismeningitis", "Reference": "Osborn, Anne. \"Abscess\". Diagnostic Imaging: Brain. 2004.\n\nOsborn, Anne. \"Infections of the Brain and Its Linings\". Diagnostic Neuroradiology. 1994.", "External Links": "spinwarp.ucsd.edu/NeuroWeb/Text/br-200.htm" } }, { "U_id": "MPX2433", "TAC": [ "MPX2433_synpic48293", "MPX2433_synpic48294", "MPX2433_synpic48295", "MPX2433_synpic48296", "MPX2433_synpic48297", "MPX2433_synpic48298", "MPX2433_synpic48299" ], "MRI": [], "Case": { "Title": "Benign Orbital Calcifications", "History": "Patient 1: 72 year old man with remote history of right zygomatic arch fracture and chronic blindness.\n\nPatients 2 and 3: 24 and 32 year old patients with concern for papilledema and visual field deficits.", "Findings": "\u2022 Patient 1: Scleral plaques and phthisis bulbi (\"wood eye\")\n\u00bb Axial NECT shows calcified scleral plaques in the left globe at the insertion sites of the medial and lateral rectus muscles. The right globe is calcified and shrunken, indicative of phthisis bulbi.\n\n\u2022 Patients 2 and 3: Optic Drusen\n\u00bb Axial NECT shows a punctate calcification near the optic discs.", "Differential Diagnosis": "\u2022 Benign globe calcification\n\u2022 Retinoblastoma\n\u2022 Radiation therapy (e.g. for pituitary, other skull base tumor)\n\u2022 Retinal astrocytic hamartoma (Tuberous Sclerosis)\n\u2022 Toxocara canii or other parasitic infection", "Case Diagnosis": "Benign Orbital Calcifications", "Diagnosis By": "Imaging findings are characteristic.", "Treatment & Follow Up": "None required" }, "Topic": { "Title": "Benign Orbital Calcifications", "Disease Discussion": "Orbital calcifications are common incidental findings, occurring in characteristic locations. Commonly encountered calcifications include trochlear calcifcations, optic drusen, scleral plaques, and phthisis bulbi.\n\nTrochlear calcifcations occur in adults as normal age-related variants or in young patients with diabetes mellitus. These calcifications are typically in a superomedial location within the orbit.\n\nOptic drusen are a cause of benign pseudopapilledema, and are commonly seen in patients with age-related macular degeneration, although, they may also be found in young patients. On CT, optic drusen are recognized as punctate calcifications located at the junction of the head of the optic nerve and globe, involving the optic disc.\n\nScleral plaques are commonly seen in the elderly, and are calcifications located at the insertion sites of the medial and lateral rectus muscles. Other causes include systemic hypercalcemic states such as hyperparathyroidism, hypervitaminosis D, sarcoidosis, chronic renal disease.\n\nPhthisis bulbi is the sequela of infection, inflammation, trauma, or autoimmune disease with a resultant nonfunctioning globe. CT imaging reveals a shrunken globe with ocular calcification or ossification.", "ACR Code": "1.9", "Category": "Idiopathic or Unknown", "Keywords": "Orbital CalcifcationOptic DrusenPhthisis Bulbi", "Reference": "LeBedis CA. Sakai O. Nontraumatic Orbital Conditions: Diagnosis with CT and MR Imaging in the Emergent Setting. RadioGrapics 2008;28:1741-1753.\n\nGrossman R. Yousem D. Neuroradiology The Requisites. Mosby, NY. 1994.\n\nPeyster RG, Hoover ED, Hershey BL, Haskin ME. High-Resolution CT of Lesions of the Optic Nerve. AJR 1982;140(5):869-874." } }, { "U_id": "MPX2444", "TAC": [ "MPX2444_synpic17399", "MPX2444_synpic17400" ], "MRI": [], "Case": { "Title": "Autosomal Dominant (Adult) Polycystic Kidney Disease (ADPKD)", "History": "26 year of African American male", "Findings": "Multiple bilateral renal cysts consistent with the diagnosis of Adult Polycystic Kidney Disease", "Differential Diagnosis": "Adult Polycystic Kidney Disesase\nCystic Renal Dysplasia\nNephronophthisis\nAcquired Cystic Kidney Disease", "Case Diagnosis": "Autosomal Dominant (Adult) Polycystic Kidney Disease (ADPKD)", "Treatment & Follow Up": "First-line therapy for patients with ADPKD typically involves controlling hypertension. Treating hypertension appears to serve two functions. The first is to slow the rate of loss of renal function. The second is with controlled hypertension the risk of a rupturing a cerebral aneurysm (which these patients are predisposed to) is decreased. ACE Inhibitors are currently the anti-hypertensive medication of choice. Patients that develop end-stage renal disease will ultimately need dialysis or kidney transplant." }, "Topic": { "Title": "Autosomal Dominant (Adult) Polycystic Kidney Disease (ADPKD)", "Disease Discussion": "Adult polycystic kidney disease is a hereditary condition that affects approximately 1 in 400-1000 births. It is characterized by many cysts in both kidneys that expand over time and cause renal failure as a result of parenchymal destruction. The inheritance pattern is autosomal dominant with penetrance estimated to be 90% by age 90. End-stage renal disease occurs in up to 70% of patients by the age of 65. Although the disease itself has no predilection for a particular gender of race, it has been observed that the progression of the disease is accelerated in males and African Americans. Clinically, patients often initially present with hematuria. Physical exam may be remarkable for enlarged palpable kidneys. As the disease progresses hypertension, polyuria, and proteinuria may develop.A number of extrarenal anomalies are associated with Adult polycystic kidney disease. Approximately 40% of patients have polycystic liver disease and about 25% have mitral valve prolapse. Both of these conditions are usually asymptomatic in these patients. By far, the most clinically relevant extrarenal anomaly is the presence of intracranial berry aneurysms located in the Circle of Willis.", "ACR Code": "8.3", "Category": "Congenital, genetic", "Keywords": "polycystic kidneyADPKD", "Reference": "Robbins: Pathologic Basis of DiseaseUpToDate: Course and treatment of polycystic kidney disease" } }, { "U_id": "MPX2425", "TAC": [ "MPX2425_synpic50903", "MPX2425_synpic50904", "MPX2425_synpic50905" ], "MRI": [ "MPX2425_synpic50895", "MPX2425_synpic50896", "MPX2425_synpic50897", "MPX2425_synpic50898", "MPX2425_synpic50899", "MPX2425_synpic50900", "MPX2425_synpic50901", "MPX2425_synpic50902" ], "Case": { "Title": "Cerebellar hemangioblastoma", "History": "33 year old male with increasing headaches and dizziness.", "Exam": "None available.", "Findings": "CT: Large cystic mass in the right cerebellar hemisphere with rounded mural soft tissue nodule.\nMR: Cystic right cerebellar hemisphere mass with enhancing mural nodule.", "Differential Diagnosis": "DDx for cyst with mural nodule:\nHemangioblastoma (cerebellar hemisphere)\nJuvenile Pilocytic astrocytoma (pediatric)\nPilocystic Xanthoastrocytoma", "Case Diagnosis": "Cerebellar hemangioblastoma", "Diagnosis By": "Pathology.", "Treatment & Follow Up": "The patient underwent a suboccipital craniectomy and mass excision.", "Discussion": "Classic imaging findings for cerebellar hemangioblastoma of a cyst with enchancing mural nodule. Imaging findings of hemangioblastoma however, may range from primarily cystic to mostly solid." }, "Topic": { "Title": "Cerebellar hemangioblastoma", "Disease Discussion": "Cerebellar hemangioblastomas are benign neoplasms of vascular origin. They are not malformations. They account for less than 3% of all intracranial neoplasms (1). These tumors are most common in young and middle-aged adults, where the incidence in males exceeds that of females (2). The cerebellar hemisphere is the most common location, although they may be located in the spinal cord, brain stem, or cerebral hemispheres. Ten percent of hemangioblastomas occur as part of the von Hippel-Lindau disease.\n\nSixty percent of these tumors are cystic, as in this case. The enhancing mural nodule is a common finding in hemangioblastoma. At CT, the cystic portion of the tumor appears low density and does not enhance, while the mural nodule enhances homogeneously and intensely. The MR findings, as seen in this case, include a predominantly cystic tumor with long T1 and long T2 relaxation times, and intense enhancement of the peripheral nodule following gadolinium administration. If the vascular nodule has bled or is proteinaceous, it may be hyperintense on short TR precontrast sequences. More than one enhancing tumor nodule may be seen. Forty percent of hemangioblastomas are solid and display variable degrees of contrast enhancement.\n\nLateral projections of a left vertebral artery subtraction angiogram (arterial and venous phases) in another patient with hemangioblastoma are shown in Films .6 and .7. The angiographic findings are characteristic for a hemangioblastoma. Notice the focal enhancing nodule fed predominantly by the superior cerebellar artery and seen densely enhancing in the arterial phase. Because of significant artifact in the posterior fossa on CT, a small peripheral nodule may be missed and angiography is felt to be more sensitive than contrast CT scan for detecting nodules. MRI with Gd-DTPA may replace angiography for evaluation of patients with suspected hemangioblastoma.\n\nvon Hippel-Lindau disease is an autosomal dominant disorder with incomplete and variable penetrance (3). The incidence is equal in males and females. Multiple lesions have been reported in this syndrome, but the most important lesions which cause significant morbidity include retinal angiomatosis, cerebellar or spinal cord hemangioblastoma, renal cell carcinoma, and pheochromocytoma. Over 50% of patients with this syndrome have hemangioblastomas of the retina, which may present with acute or chronic retinal detachment. Ophthalmoscopic examination reveals these lesions, and radiographic evaluation plays a small role.\n\nThirty-six to sixty percent of patients with von Hippel-Lindau disease have cerebellar hemangioblastoma. Signs and symptoms due to this tumor are the most common cause for patients to present with the syndrome.\n\nAlthough the reported occurrence of spinal cord hemangioblastoma is 5%, autopsy data and MRI suggest the incidence may be higher (4,5). Signs and symptoms of a cerebellar hemangioblastoma may be dramatic, and neurologic deficit from a spinal cord lesion may be overlooked. Typical MR findings in a spinal cord hemangioblastoma include syringomyelia, enhancing nodule, and enlarged feeding and draining vessels. \n\nTwenty-five to thirty-eight percent of patients with von Hippel-Lindau disease will develop renal cell carcinoma, which may be multiple and bilateral. Pheochromocytoma is found in 10% of patients with this disease.\n\nOther lesions in von Hippel-Lindau disease include angiomas of the liver and kidney and cysts of the pancreas, liver, kidney and epididymis. \n\nRoutine screening of family members of a patient with von Hippel-Lindau disease has been recommended. MRI with Gd-DTPA is the procedure of choice to screen for CNS involvement.\n\nIn the adult, the differential diagnosis for a cystic mass in the posterior fossa includes a simple arachnoid cyst or a cerebellar astrocytoma. A simple arachnoid cyst is extra- axial and will not demonstrate an enhancing nodule, although such a nodule may be seen in a cerebellar astrocytoma. Since 40% of cerebellar hemangioblastomas may be solid, this lesion should be included in the differential of a solid or partially solid mass in the posterior fossa in the adult. These lesions are uncommon in children, and medulloblastoma, ependymoma, or astrocytoma are more likely than a cerebellar hemangioblastoma when a posterior fossa mass is seen in a child.", "ACR Code": "1.3", "Category": "Neoplasm, non-glial", "Keywords": "hemangioblastoma" } }, { "U_id": "MPX2446", "TAC": [ "MPX2446_synpic4182" ], "MRI": [], "Case": { "Title": "Colloid cyst (syn. neuroepithelial cyst)", "History": "49 y/o man presents with headaches.", "Findings": "Noncontrast head CT demonstrates a rounded sharply defined mass in the 3rd ventricle adjacent to the foramen of Monro.", "Differential Diagnosis": "Colloid Cyst\nCysticercosis\nCraniopharyngioma", "Case Diagnosis": "Colloid cyst (syn. neuroepithelial cyst)" }, "Topic": { "Title": "Colloid cyst, neuroepithelial cyst, endodermal cyst", "Disease Discussion": "\u00bb Colloid cyst is the number one mass lesion of the third ventricle. In a review of 262 cases, they represented 55% of third ventricular masses. (Neurochirurgie 2000 Jun;46(3):211-38) PMID: 10854981\nhttp://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10854981&dopt=Abstract\n\n\u00bb A true cyst, lined by an epithelium, of uncertain origin. Colloid cyst is a congenital lesion, that takes 15 to 25 years to become 15-25 mm in diameter. By the original description, colloid cysts are always found in third ventricle. Usually anterior, and usually attached to the roof of the third ventricle (the tela choroidea or velum interpositum). In this location they may obstruct the F. of Monro and cause obstructive hydrocephalus.\n\n\n\u00bb The center may be \"dry\" and dark on T2, with the rim \"wet\" and bright.\nJ Comput Assist Tomogr 1998 Jul-Aug;22(4):524-7\n\n\u00bb Colloid cysts histology supports an endodermal rather than neuroepithelial origin.\nJ Neurosurg 1993 Jan;78(1):101-11 and Acta Neuropathol. 1992;83(6):605-12. PMID: 1636378\n\nNote: Although the colloid cyst is a \"mass\" it is not really a neoplasm.\n\n\u00bb Conservative management (serial follow-up w/o surgery) may be appropriate for asymptomatic colloid cysts. PMID: 10470808 (J Neurosurg 1999 Sep;91(3):364-9) \n\n\u00bb Four factors are associated with cyst symptoms PMID: 10807239 (Neurosurgery. 2001 Mar;48(3):701-2.)\n\u2022 younger age (44 vs 57, P <0.001)\n\u2022 larger cyst (13 mm vs 8 mm, P <0.001)\n\u2022 ventricular enlargement (83% vs 31%, P < 0.001)\n\u2022 bright on T1W MR (44% vs 8%, P=0.001)\n\n\n\u00bb Liquid consistency, allowing stereotactic aspiration, may be predicted by the characteristics of:\n\u2022 isodense on CT\n\u2022 hypointense on T1W MR\n\u2022 hyperintense on T2W MR\n(Neurochirurgie 2000 Jun;46:296-319) PMID: 10854987\nhttp://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10854987&dopt=Abstract\n\nModern neurosurgical techniques include endoscopic (ventriculoscope) resection, that is not deterred by inspissated (hyperdense/hypointense) cyst contents.", "ACR Code": "1.3", "Category": "Cyst, benign", "Keywords": "inspissated black hole cystsprognosisimaging", "Reference": "1) Neurochirurgie 2000 Jun;46(3):211-38\n2) J Neurosurg 1993 Jan;78(1):101-11\n3) J Comput Assist Tomogr 1998 Jul-Aug;22(4):524-7\n4) J Neurosurg 1999 Sep;91(3):364-9\n5) Neurochirurgie 2000 Jun;46:296-319", "External Links": "www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10854987&dopt=Abstract" } }, { "U_id": "MPX2453", "TAC": [ "MPX2453_synpic23426" ], "MRI": [ "MPX2453_synpic23428", "MPX2453_synpic23429" ], "Case": { "Title": "Cerebellopontine angle meningioma", "History": "31 year old female with chronic headaches.", "Findings": "On non-contrast CT of the head a hyperdense mass was seen in the left CPA angle. On MRI the mass was confirmed to be extraaxial and enhanced avidly.", "Differential Diagnosis": "\u2022 Menigioma\n\u2022 Acoustic neuroma\n\u2022 Epidermoid\n\u2022 Arachnoid cyst\n\u2022 Metastasis", "Case Diagnosis": "Cerebellopontine angle meningioma" }, "Topic": { "Title": "Cerebellopontine angle meningioma", "Disease Discussion": "The CPA is the extra-axial space triangulated by the pons, cerebellum, and petrous temporal bone. Located within it are meningeal layers, cranial nerves 5, 7, and 8, CSF and the flocculus of the cerebellum. \n\nMeningiomas arise from the arachnoid granulation cells within the meningeal layers. Other lesions in the CPA, from which they must be differentiated, include acoustic schwannoma, epidermoid, trigeminal schwannoma, exophytic brain stem glioma, metastasis, cholesteatoma (acquired), cholesterol granuloma, arachnoid cyst, aneurysm, and vertebrobasilar dolichoectasia.\n\nAcoustic schwannomas are the most common CPA masses and usually arise from the vestibular division of the 8th cranial nerve within the internal auditory canal. They present as a mass within the internal auditory canal and often widen the canal. Meningiomas, on the other hand, are extrinsic to the internal auditory canal although they may compress the 7th-8th nerve complex (see Film 2). Classically, meningiomas are hyperdense compared to gray matter on noncontrast CT and enhance intensely, whereas acoustic neuromas are isodense or hypodense and also enhance. It may be difficult to visualize small acoustic neuromas or meningiomas on CT because of artifacts from the adjacent petrous temporal bone. When present, changes in the temporal bone can be quite helpful. Acoustic neuroma will widen or erode the internal auditory canal in up to 90% of cases, although small intracanalicular lesions are increasingly recognized with Gd-DTPA MR prior to development of internal auditory canal abnormalities. Meningiomas may demonstrate hyperostosis of the adjacent temporal bone. MRI, without bone artifact, surpasses CT for mass localization relative to the internal auditory canal, especially with the use of Gd-DTPA. Acoustic schwannomas are isointense to gray matter on T1-weighted images and enhance homogeneously after Gd-DTPA. Meningiomas are iso- to hypointense on T1-weighted images and also enhance homogeneously, but are located outside of the internal auditory canal. On T2-weighted imaging, meningioma has a variable signal while acoustic schwannoma is usually increased in intensity. \n\nAngiographically, meningiomas classically have a persistent, homogeneous blush lasting through the venous phase, which is not typical of schwannoma or the other more common CPA lesions. CPA masses, if large, enough, can be detected angiographically by characteristic displacement of the adjacent vascular structures. Such masses may elevate and posteriorly displace the anterior inferior cerebellar artery, elevate the superior cerebellar artery, displace the basilar artery if the mass extends medially, or elevate and compress the petrosal vein. \n\nThe other lesions within the differential diagnosis are less common. Epidermoid tumors result from epidermal tissue that is included within the neural tube during embryonic development. They may be markedly hypointense to cortex on T1-weighted MRI images (there are some reports of hyperintense epidermoids on T1 imaging) and are hyperintense compared to CSF on T2 imaging with no enhancement following Gd - DTPA. CT demonstrates a hypodense (density slightly greater than CSF) mass without enhancement; thus, differentiation from meningioma is not difficult. Trigeminal neuroma is radiographically similar to acoustic neuroma except the course follows that of the 5th cranial nerve and the IAC and 7th/8th nerve complex are normal. Exophytic brain stem glioma will have both intra- and extra-axial components by multiplanar MR imaging. Arachnoid cysts have imaging characteristics paralleling CSF. Vascular abnormalities can usually be detected by MRI demonstrating flow void and/or clot. The flocculus of the cerebellum should not be mistaken for a lesion based on its known anatomic location and signal characteristics. Metastatic disease may be difficult to distinguish from benign lesions because of the varied appearance, unless one sees multiple lesions or there is obvious bone destruction, which may require CT demonstration. Acquired cholesteatomas may also require CT evaluation of the temporal bone to demonstrate the characteristic pattern of involvement of the middle ear which is necessary to differentiate these lesions from the bony destruction caused by metastatic disease.", "ACR Code": "1.3", "Category": "Neoplasm, non-glial" } }, { "U_id": "MPX2449", "TAC": [ "MPX2449_synpic48161" ], "MRI": [], "Case": { "Title": "Bronchial Carcinoid", "History": "67-year-old Irish woman who presents with cough and worsening shortness of breath.", "Exam": "Physical exam shows decreased breath sounds at right lung base.", "Findings": "CXRs show an opacity in the right lower lobe. Chest CT revealed that the right lower lobe is fluid filled and enhancement of the interstitium of the lung is noted. The appearance is consistent with a \"drowned\" right lower lobe, usually seen from endobronchial obstruction.", "Differential Diagnosis": "Lung cancer\nEndobronchial carcinoid tumor\nForeign body\nMetastatic disease (eg. RCC, Melanoma, Colon cancer)\nBroncholith\nBronchial stenosis", "Case Diagnosis": "Bronchial Carcinoid", "Diagnosis By": "Bronchoscopic visualization and subsequent surgical resection.", "Treatment & Follow Up": "The lesion was removed." }, "Topic": { "Title": "Bronchial Carcinoid", "Disease Discussion": "Bronchial carcinoid tumors are neuroectoderm carcinomas that can occur in a wide age range, from the 2nd decade of life to old age. They account for only 5% of all pulmonary tumors. The most aggressive form of pulmonary neuroectoderm carcinomas is the small cell lung cancer. Then, in order of decreasing aggressiveness are atypical bronchial carcinoid tumors and typical carcinoid tumors. Atypical type occurs in just 10-15% of bronchial carcinoid tumors with typical bronchial carcinoid tumors occurring 85-90% of the time. Bronchial carcinoid tumors, in general, are slow growing and have a relatively good prognosis after surgical resection, even with metastatic spread to hilar and ipsilateral lymph nodes. These highly vascular tumors can secrete ACTH and cause Cushing\u2019s syndrome. \nSymptoms occur from mechanical obstruction of the bronchus by the tumor and present as a cough or wheezing. Carcinoid syndrome can occur with rare hepatic metastatic disease. \nThese tumors are visible 25% of the time, if the lesion is central. CT imaging will typically reveal a well-circumscribed central lesion with soft-tissue attenuation. It can be difficult to distinguish this from lung carcinoma. However, the presence of calcification within the tumor, which occurs often, will favor carcinoid over carcinoma. Octreotide is 96% sensitive for detection of bronchial carcinoid tumors. PET/CT will not accurately detect carcinoid tumors due to their low metabolic activity.", "ACR Code": "65.3111", "Category": "Neoplasm, carcinoma", "Keywords": "BronchialCarcinoid", "Reference": "Armstrong P, Wilson AG, Dee P, Hansell DM, Imaging of Diseases of the Chest, 2000, 339-43." } }, { "U_id": "MPX2442", "TAC": [ "MPX2442_synpic45439", "MPX2442_synpic45442", "MPX2442_synpic45443", "MPX2442_synpic45444", "MPX2442_synpic45445", "MPX2442_synpic45446", "MPX2442_synpic45447" ], "MRI": [], "Case": { "Title": "Celiac, Abdominal Aorta, & Common Iliac Aneurysms", "History": "A 75-year-old white man with a history of smoking and mid-abdomen pain.", "Exam": "Mid-abdomen pulsatile mass with deep palpitation.", "Findings": "The axial CT image demonstrates a 2.4-cm fusiform aneurysm of the celiac artery. The origin of this aneurysm is patent. Also seen within the celiac aneurysm is an extensive mural thrombosis in the distal half of the aneurysm. The splenic and\ngastroduodenal arteries are patent. \n\nThere also is a fusiform infrarenal aortic aneurysm identified measuring 4 cm. There is also an intimal flap along the abdominal aortic vasculature. The aorta returns to normal diameter of 2 cm just prior to the bifurcation of the common iliac arteries. \n \nIn addition there is also a distal left common iliac artery dilation with a diameter of 1.5 cm.", "Differential Diagnosis": "\u2022 Celiac, Abdominal Aortic, Common Iliac Aneurysms:\n- Atherosclerotic \n- Inflammatory \n- Mycotic / Infectious\n- Arteriovenous Malformation\n- Traumatic", "Case Diagnosis": "Celiac, Abdominal Aorta, & Common Iliac Aneurysms", "Diagnosis By": "CT with contrast - Imaging", "Treatment & Follow Up": "Treatment of abdominal aneurysm includes vascular surgical options such as vascular repair and/or stent placement. If aneurysms remain stable overtime close observation may also be an effective management strategy. \n\nAltering risk factors that can aggravate aneurysms such as cessation of smoking, maintaining adequately managing hyperlipidemia & hypertension to help control atherosclerosis.", "Discussion": "An aneurysm is a focal dilation of a arterial vasculature with regard to the primary or adjacent artery. In the abdomen the most typical aneurysm is an abdominal aortic aneurysm (AAA) which is defined as an aortic diameter that should have a normal value at the level of the renal arteries of ranging from 1.4 to 3.0 cm with the average typically being 2.0cm. (1,2). Iliac aneurysms may be associated with AAA about 16% of the time (3) and most of the time it involves the common iliac artery. However, celiac artery aneurysms are one of the more uncommon forms of splanchnic artery aneurysm. The celiac trunk gives rise to the left gastric, common hepatic, and splenic arteries.\n\nAs in this case, AAA most often occur in the segment of aorta between the renal and inferior mesenteric arteries. Typically, unlike dissecting thoracic \"aneurysms,\" abdominal aortic aneurysms involve all layers of the aorta and do not usually create an intimal flap or false lumen as in this case. Mural thrombus may also develop due to poor blood flow/movement through the aneurysm as seen in the celiac artery aneurysm in this case.\n\nThe most common risk factors for developing abdominal aneurysms include age (>60), smoking, sex (>males), race (2x more common in whites as opposed to blacks), atherosclerosis, hypertension, and family history. The USPSTF recommends that men ages 65 \u2013 75 who smoke should get a one time screen for AAA via the preferred modality of real-time ultrasonography (4). CT and MRI are alternative imaging modalities that may also be used." }, "Topic": { "Title": "Celiac, Abdominal Aorta, & Common Iliac Aneurysms", "Disease Discussion": "Celiac trunk, abdominal aorta, & the iliac arteries are all prone to get aneurysms and may all develop over time together.\n\nAn aneurysm is a focal dilation of a arterial vasculature with regard to the primary or adjacent artery. In the abdomen the most typical aneurysm is an abdominal aortic aneurysm (AAA) which is defined as an aortic diameter that should have a normal value at the level of the renal arteries of ranging from 1.4 to 3.0 cm with the average typically being 2.0cm. (1,2). Iliac aneurysms may be associated with AAA about 16% of the time (3) and most of the time it involves the common iliac artery. However, celiac artery aneurysms are one of the more uncommon forms of splanchnic artery aneurysm (4). The celiac trunk gives rise to the left gastric, common hepatic, and splenic arteries.\n\nAs in this case, AAA most often occur in the segment of aorta between the renal and inferior mesenteric arteries. Typically, unlike dissecting thoracic \"aneurysms,\" abdominal aortic aneurysms involve all layers of the aorta and do not usually create an intimal flap or false lumen as in this case. Mural thrombus may also develop due to poor blood flow/movement through the aneurysm as seen in the celiac artery aneurysm in this case.\n\nThe most common risk factors for developing abdominal aneurysms include age (>60), smoking, sex (>males), race (2x more common in whites as opposed to blacks), atherosclerosis, hypertension, and family history. The USPSTF recommends that men ages 65 \u2013 75 who smoke should get a one time screen for AAA via the preferred modality of real-time ultrasonography (5). CT and MRI are alternative imaging modalities that may also be used.", "ACR Code": "9.9", "Category": "Vascular", "Keywords": "celiacabdominal aortacommon iliac", "Reference": "1. Hirsch, AT, Haskal, ZJ, Hertzer, NR, et al. ACC/AHA 2005 Practice Guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): a collaborative report from the American Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Peripheral Arterial Disease): endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation; National Heart, Lung, and Blood Institute; Society for Vascular Nursing; TransAtlantic Inter-Society Consensus; and Vascular Disease Foundation. Circulation 2006; 113:e463. \n\n2. Ouriel, K, Green, RM, Donayre, C, et al. An evaluation of new methods of expressing aortic aneurysm size: Relationship to rupture. J Vasc Surg 1992; 15:12.\n\n3. LearningRadiology.com, \"Abdominal Aortic Aneurysm,\" Dahnert Radiology Review Manual 2002 http://www.learningradiology.com/notes/cardiacnotes/aaapage.htm\n \n4. D. Michael McMullan, MD, Michael McBride, MD, et al. \u201cCeliac Artery Aneurysm: A Case Report,\u201d Tex Heart Inst J. 2006; 33(2): 235\u2013240, 2006.\n\n5. LaRoy, LL, Cormier, PJ, Matalon, TA, et al. Imaging of abdominal aortic aneurysms. AJR Am J Roentgenol 1989; 152:785." } }, { "U_id": "MPX2455", "TAC": [ "MPX2455_synpic55402" ], "MRI": [], "Case": { "Title": "Osteochondroma", "History": "23 yo male who initially presented to the emergency department with epigastric pain. Abdominal plain films were obtained wich showed an incidental finding of a bony mass arising from the left iliac wing. \n\nOn questioning he endorses a several year history of atraumatic left posterior buttocks pain. This pain is worsened by bending or strenuous running.", "Exam": "Tenderness to palpation over left posteriour ilium, with no mass noted. No spinal or paraspinal tenderness. \n\n5/5 strength and normal sensation to light touch throughout both lower extremities. \n2+ reflexes to bilateral knees and ankles. No Babinski.", "Findings": "Circumscribed multilobulated bony exostosis arising from the lateral aspect of the upper left ilium. This lesion appears to have cortical and medullary contiguity with the ilium.", "Differential Diagnosis": "- Osteochonrdoma\n- Enchondroma\n- Post-traumatic change", "Case Diagnosis": "Osteochondroma", "Diagnosis By": "Imaging and subsequent excisional biopsy", "Treatment & Follow Up": "The patient underwent surgical excision of the mass which was uncomplicated.", "Discussion": "This patient's presentation is fairly typical for a deep osterochondroma. He fits the typical demographic of a male with the tumor arising in the second decade of life. The fact that it was found incidentally is not surprising given the tumor's deep location. It was not palpable on exam even with its location known. Had it been more superficial, painful or disabling it is likely the patient would have presented earlier.\n\nThough observation without treatment is a perfectly acceptable option, surgical management is recommended for symptomatic lesions." }, "Topic": { "Title": "Osteochondroma", "Disease Discussion": "The characteristic radiographic findings of these tumors are a pedunculated or sessile mass projecting from and continuous with the metaphysis of long bones, most frequently the tibia, femur, or humerus. Typically, these masses point toward the diaphysis and away from the joint. On the radiographs, the cartilaginous cap has stippled calcifications, typical of a cartilaginous tumor. MR imaging confirms the tumor\u2019s continuity with medullary and cortical bone and shows the high-signal-intensity cartilaginous cap surrounded by low-signal-intensity perichondrium. Osteochondromas are found among all ages, although most commonly found in males less than 20 years of age. Most are asymptomatic and found as an incidental finding. \n Malignant transformation occurs in approximately 1% of single osteochondromas, although in multiple osteochondromas, malignant change may develop in 2 to 27% of patients (particularly the femur, humerus, tibia, and innominate bone). Most malignant transformation is to chondrosarcoma although unusual cases of osteosarcoma or malignant fibrous histiocytoma have been reported. Besides bursal inflammation, pathologic fracture, and malignant transformation, osteochondromas may cause vascular and neurological complications and osseous deformities because of displacement or compression of adjacent structures. At times in children and adolescents, the osteochondromas may spontaneously disappear or be resorbed, or be integrated into the metaphysis.", "ACR Code": "4.3", "Category": "Neoplasm, benign", "Keywords": "osteochondromaBenign bone tumorsCartilaginous tumor", "Reference": "1. Greenspan, A. Benign tumors and tumor-Like Lesions II: Lesions of cartilaginous origin: Osteochondroma. Orthopaedic Radiology: A Practical Approach, 3rd ed. Philadelphia: 2000. Pgs. 580-588.\n\n2. Resnick D. Tumors and tumor-like lesions of the bone: Imaging and pathology of specific lesions: Osteochondroma. Bone and Joint Disorders, 4ed. Vol 4. Philadelphia: 2002. pp. 3870-86." } }, { "U_id": "MPX2448", "TAC": [ "MPX2448_synpic26310", "MPX2448_synpic26311" ], "MRI": [], "Case": { "Title": "Acute on chronic osteomyelitis\r\nPost-traumatic changes with deformity after trauma", "History": "82 y/o female with significant left knee pain for four days; the patient is asplenic and has a prior history of osteomyelitis in the same knee.", "Exam": "The patient had significant pain to palpation of the left knee and on weightbearing. She had an elevated WBC with a left shift and eleveated ESR and C-reactive protein. A joint aspirate of the left knee revealed polymorphonucleated and mononucleated white blood cells.", "Findings": "1) Anteroposterior radiograph of the left knee demonstrates areas of osteolysis in the distal metaphysis of the femur.\n2) Lateral radiograph of the left knee demonstrates extensive cortical thickening with foci of osteolysis in the visualized distal femur and some deformity of the femur most marked in the distal metadiaphysis and the medial femoral condyle\n3) 3-phase methylene diphosphonate (MDP) 99-m bone scintigraphy demonstrates increased radiopharmaceutical uptake in the distal left femur. The 20-hour delayed fused images (99m Tc-MDP with 111-In-WBC) showed concordant dual tracer accumulation in the distal left femur consistent with osteomyelitis.\n4) Axial CT of the left knee with bone windows demonstrates sclerotic medullary and cortical changes of the left mid and distal femur with cortical lucencies and acute nonfatty medullary inflammatory changes. An osseous sequestrum is present in the distal posterior femur. At the level of the condyles, the medullary canal communicates through a cortical defect into the soft tissues.", "Differential Diagnosis": "Acute on chronic osteomyelitis\nPost-traumatic changes with deformity after trauma", "Case Diagnosis": "Acute on chronic osteomyelitis\nPost-traumatic changes with deformity after trauma", "Treatment & Follow Up": "Systemic antibiotics (vancomycin) and surgical debridement", "Discussion": "Osteomyelitis, an infectious process that produces bony destruction, can be limited to a single area of bone or can involve multiple areas, including the marrow, cortex, periosteum, and surrounding soft tissue. Osteomyelitis may spread by a hematogenous route, from a contiguous contaminated source (e.g. following trauma, bone surgery, or joint replacement), or be a complication of vascular insufficiency (predominantly in diabetic patients). Staphylococcus aureus is by far the common pathogen causing osteomyelitis. The infection may be acute or chronic; acute infections tend to evolve over several days to weeks. Acute infection may resolve with appropriate treatment. Osteomyelitis that is untreated or insufficiently treated may give rise to a chronic infection which may be characterized by a sequestrum (necrotic bone, bacteria, and granulation that have been walled off by new reactive bone or fibrous tissue). Chronic osteomyelitis is also characterized by the persistence of microorganisms, low-grade inflammation, and fistulous tracts. Recurrent osteomyelitis in the same area along with the presence of fever is indicative of a chronic infection. The diagnosis of osteomyelitis is based on clinical, laboratory, and imaging findings, and when possible, identification of the offending organism by blood culture or direct bone biopsy.\n\nPlain radiographs should be the first imaging modality for evaluating osteomyelitis. Initially they may be normal or only show periosteal reaction and soft tissue swelling. Bone destruction (osteolytic foci on the radiographs) may not be visible until 10-21 days after the infection has begun. With chronicity, reactive osteosclerosis as well as areas of osteolysis and sequestra and involucra may occur. Differentiation of acute osteomyelitis from inactive chronic osteomyelitis can be difficult, but certain indications on the radiograph aid in distinguishing between the two, including a change from a previous radiograph, poorly defined areas of osteolysis, and thin and linear periostitis. Although CT is useful for evaluating cortical destruction, sequestration, cloacae, and bone and soft tissue abscesses, MR imaging (T1-weighted, T2-weighted with fat sat and post contrast sequences) is the best modality for evaluating osteomyelitis, cellulitis and areas of necrosis for debridement. Tc 99m \u2013bone scintigraphy may also be useful for diagnosing osteomyelitis but does not have the resolution of MRI. Dual isotope bone-granulocyte scintigraphy (Tc 99m MDPbone and white blood cells labeled with Indium-111) has a high sensitivity (84%) and specificity (71%) in detecting areas of acute infection. However, MRI has increased sensitivity and accuracy in the detection of osteomyelitis as compared to three-phase bone scintigraphy. In cases of acute osteomyelitis, the process is identified as area(s) of low signal intensity on T1-weighted images and high signal intensity images in the medullary canal on fat-saturated T2-weighted MR images or STIR (short tau inversion recovery) MR images. Cellulitis shows similar findings (low-signal-intensity foci on T1-weighted images and high-signal-intensity foci on fat-saturated T2-weighted or STIR MR images). Contrast-enhanced T1-weighted MR imaging shows not only the enhancement of areas of osteomyelitis and cellulitis, but also shows non-enhancing areas of necrosis important for debridement. Active and inactive phases of osteomyelitis may be differentiated by in the acute phase the presence of periosteal bone formation with subperiosteal fluid and areas of high signal intensity areas on T2-weighted and STIR MR images that enhance after contrast media. Bone sclerosis is low signal intensity on MR sequences. Abscesses and tracts can also be demonstrated on MRI. For definitive histologic diagnosis, fluoroscopy and/or CT is used to biopsy appendicular and axial lesions and fluoroscopy can be sometimes use for biopsying appendicular lesions. Deep abscesses can be drained with CT guidance and superficial abscesses with sonographic or CT guidance." }, "Topic": { "Title": "Acute on chronic osteomyelitis\r\nPost-traumatic changes with deformity after trauma", "Disease Discussion": "Osteomyelitis, an infectious process that produces bony destruction, can be limited to a single area of bone or can involve multiple areas, including the marrow, cortex, periosteum, and surrounding soft tissue. Osteomyelitis may spread by a hematogenous route, from a contiguous contaminated source (e.g. following trauma, bone surgery, or joint replacement), or be a complication of vascular insufficiency (predominantly in diabetic patients). Staphylococcus aureus is by far the common pathogen causing osteomyelitis. The infection may be acute or chronic; acute infections tend to evolve over several days to weeks. Acute infection may resolve with appropriate treatment. Osteomyelitis that is untreated or insufficiently treated may give rise to a chronic infection which may be characterized by a sequestrum (necrotic bone, bacteria, and granulation tissue that have been walled off by new reactive bone or fibrous tissue). Chronic osteomyelitis is also characterized by the persistence of microorganisms, low-grade inflammation, and fistulous tracts. Recurrent osteomyelitis in the same area along with the presence of fever is indicative of a chronic infection. The diagnosis of osteomyelitis is based on clinical, laboratory, and imaging findings, and when possible, identification of the offending organism by blood culture or direct bone biopsy.\n\nPlain radiographs should be the first imaging modality for evaluating osteomyelitis. Initially they may be normal or only show periosteal reaction and soft tissue swelling. Bone destruction (osteolytic foci on the radiographs) may not be visible until 10-21 days after the infection has begun. With chronicity, reactive osteosclerosis as well as areas of osteolysis and sequestra and involucra may occur. Differentiation of acute osteomyelitis from inactive chronic osteomyelitis can be difficult, but certain indications on the radiograph aid in distinguishing between the two, including a change from a previous radiograph, poorly defined areas of osteolysis, and thin and linear periostitis. Although CT is useful for evaluating cortical destruction, sequestration, cloacae, and bone and soft tissue abscesses, MR imaging (T1-weighted, T2-weighted with fat sat and post contrast sequences) is the best modality for evaluating osteomyelitis, cellulitis and areas of necrosis for debridement. Tc 99m \u2013bone scintigraphy may also be useful for diagnosing osteomyelitis but does not have the resolution of MRI. Dual isotope bone-granulocyte scintigraphy (Tc 99m MDP)bone and white blood cells labeled with Indium-111) has a high sensitivity (84%) and specificity (71%) in detecting areas of acute infection. However, MRI has increased sensitivity and accuracy in the detection of osteomyelitis as compared to three-phase bone scintigraphy. In cases of acute osteomyelitis, the process is identified as area(s) of low signal intensity on T1-weighted images and high signal intensity images in the medullary canal on fat-saturated T2-weighted MR images or STIR (short tau inversion recovery) MR images. Cellulitis shows similar findings (low-signal-intensity foci on T1-weighted MR images and high-signal-intensity foci on fat-saturated T2-weighted or STIR MR images). Contrast-enhanced T1-weighted MR imaging shows not only the enhancement of areas of osteomyelitis and cellulitis, but also shows non-enhancing areas of necrosis important for debridement. Active and inactive phases of osteomyelitis may be differentiated by periosteal bone formation with subperiosteal fluid and by areas of high signal intensity areas on T2-weighted and STIR MR images that enhance after contrast media. Bone sclerosis is low signal intensity on MR sequences. Abscesses and tracts can also be demonstrated on MRI. For definitive histologic diagnosis, fluoroscopy and/or CT is used to biopsy appendicular and axial lesions and fluoroscopy can be sometimes use for biopsying appendicular lesions. Deep abscesses can be drained with CT guidance and superficial abscesses with sonographic or CT guidance.", "ACR Code": "4.4", "Category": "Clinical Exam Finding or Sign", "Keywords": "Acute on chronic osteomyelitisPost-traumatic changes with deformity after trauma", "Reference": "(1)\tLew, DP, Waldvogel, FA. Osteomyelitis. Lancet 2004; 364:369-79\n(2)\tResnick, D. Osteomyelitis, Septic Arthritis, and Soft Tissue Infection: Mechanisms and Situations. Diagnosis of Bone and Joint Disorders. WB Saunders, Philadelphia 2002. pp 2377-2480.\n(3)\tBuhl, T, Stentzer, K, Hede, A, Kjaer, A, Hesse, B. Bone infection in patients suspected of complicating osteomyelitis: the diagnostic value of dual isotope bone-granulocyte scintigraphy. Clin Physiol Funct Imaging 2005; 25:20-26." } }, { "U_id": "MPX2450", "TAC": [ "MPX2450_synpic55685" ], "MRI": [ "MPX2450_synpic55646", "MPX2450_synpic55647", "MPX2450_synpic55648", "MPX2450_synpic55649", "MPX2450_synpic55650", "MPX2450_synpic55651" ], "Case": { "Title": "Sarcoidosis", "History": "32 year old woman with a 2 year history of slowly growing lump on neck along and progressive shortness of breath. No history of fevers, weight loss or recent illness. Patient had recently undergone dental procedure around time the lump was first noted.", "Exam": "Sub-mandibular and cervical regions of neck enlarged bilateraly, with left greater than right. Masses were firm, mobile and non-tender. No changes in the skin overlying the masses. Ears/Eyes/Nose/Oropharynx normal. Lungs clear bilateraly. Cardiovascular exam was normal.", "Findings": "Significant bilateral neck adenopathy. Confluent left parotid and periparotid nodal mass with largest single node measuring 2.7cm x 1.9cm. Numerous other left level II and III nodes with largest measuring 3.6cm x 2.1cm. Mediastinal and bihilar adenopathy.", "Differential Diagnosis": "\u2022 Sarcoidosis\n\u2022 Lymphoma\n\u2022 Reactive lymphadenopathy (fungal, etc.)\n\u2022 Catscratch disease\n\u2022 Metastatic carcinoma", "Case Diagnosis": "Sarcoidosis", "Diagnosis By": "Pathology from neck dissection revealing noncaseating granulomas and radiographic findings of adenopathy.", "Treatment & Follow Up": "Left neck dissection for debulking of mass. PO steroids for respiratory symptoms.", "Discussion": "Sarciodosis is a systemic multisystem granulomatous disease characterized by a variable clinical presentation and course. Cutaneous lesions are present in about one fourth of patients. Although any organ can be affected, 90% of patients demonstrate thoracic involvement with decreased diffusion capacity being the most common abnormality found on pulmonary function testing. There is a strong association between subcutaneous sarciodosis and bilateral hilar lymphadenopathy (72.7%). Sarciodosis is a diagnosis of exclusion supported by three elements: 1. Compatible clinical and radiologic findings, 2. Tissue biopsy specimen that reveals noncaseating epithelioid granulomas, and 3. Absence of known granulomagenic agents. \n\nEtiology\nA large multi centered study called A Case Control Etiologic Study of Sarciodosis (ACCESS) showed that environmental factors such as mold, mildew, must odors and pesticides were associated with a modestly increased risk (OR~1.5) of developing sarciodosis. Genetics and host factors also are involved in the pathogenesis of sarciodosis. In the US, blacks are more frequently affected and the ACCESS trial showed that affected patients were five times more likely than controls to report a sibling with the disease. Further, recent studies have identified specific genes associated with sarciodosis. A single-nucleotide polymorphism on the BTNL2 gene may influence T-lymphocyte activation and regulation and make people carrying this polymorphism more susceptible to sarciodosis. A second gene associated with sarciodosis is Annexin A11 on chromosome 10q22.3 responsible for calcium signaling, cell division and apoptosis. \n\n\n\nDeficits of this gene have been associated with sarciodosis. Further, HLA haplotypes and T-cell receptor expression play an intricate role in the development of the disease.\n\nBiomarker screening\nIn an attempt to aid in diagnosis of sarciodosis, investigators continue to search for potential biomarkers in disease activity. Chitotriosidase is an enzyme expressed by activated macrophages and Bargagli et al. found elevated levels of this enzyme in patients with sarciodosis, with >90% exhibiting elevated levels of the marker. A second marker IL-2, a cytokine that induces T-cell proliferation and activation is elevated in serum of patients with sarciodosis and may have prognostic value. \n\nDiagnosis\nDiagnosis of sarciodosis is best supported by a combination of radiographic evidence of lymphadenopathy and tissue specimens that show noncaseating granulomas. Endobronchial ultrasound guided transbronchial needle aspiration when compared to non-guided transbronchial needle aspiration had a diagnosis yield of 83.3% compared to 53.8%. \n\nTreatment\nTherapy for patients with chronic sarciodosis requires prolonged treatment often with steroids which cause systemic side effects. TNF inhibitors have been investigated for the treatment, but a study by Utz et al, found treatment failure in nearly 65% of participants. A new TNF-alpha antagonist Ustekinumab, approved for dosing in patients with RA, psoriatic arthritis, and ankylosing spondylitis; is currently being tested for its efficacy in treatment of sarciodosis with completion of the study anticipated in July 2011. Surgical indication for patients with sarciodosis remains controversial. Surgery has potential to reduce symptoms and decrease need for oral steroids, but does not eradicate or prevent recurrence of disease. Corticosteroids remain the cornerstone for treatment, but care must be taken to assess for potential adverse effects." }, "Topic": { "Title": "Sarcoidosis", "Disease Discussion": "Sarcoidosis is a systemic and multisystem granulomatous disease characterized by a variable clinical presentation and course. Cutaneous lesions are present in about one fourth of patients. Although any organ can be affected, 90% of patients demonstrate thoracic involvement with decreased diffusion capacity being the most common abnormality found on pulmonary function testing. There is a strong association between subcutaneous sarcoidosis and bilateral hilar lymphadenopathy (72.7%). Sarcoidosis is a diagnosis of exclusion supported by three elements: 1. Compatible clinical and radiologic findings, 2. Tissue biopsy specimen that reveals noncaseating epithelioid granulomas, and 3. Absence of known granulomagenic agents. \n\nEtiology:\nA large multi centered study called A Case Control Etiologic Study of Sarcoidosis (ACCESS) showed that environmental factors such as mold, mildew, must odors and pesticides were associated with a modestly increased risk (OR~1.5) of developing sarcoidosis. Genetics and host factors also are involved in the pathogenesis of sarcoidosis. In the US, blacks are more frequently affected and the ACCESS trial showed that affected patients were five times more likely than controls to report a sibling with the disease. Further, recent studies have identified specific genes associated with sarcoidosis. A single-nucleotide polymorphism on the BTNL2 gene may influence T-lymphocyte activation and regulation and make people carrying this polymorphism more susceptible to sarcoidosis. A second gene associated with sarcoidosis is Annexin A11 on chromosome 10q22.3 responsible for calcium signaling, cell division and apoptosis. \n\n\nDeficits of this gene have been associated with sarcoidosis. Further, HLA haplotypes and T-cell receptor expression play an intricate role in the development of the disease.\n\nBiomarker screening:\nIn an attempt to aid in diagnosis of sarcoidosis, investigators continue to search for potential biomarkers in disease activity. Chitotriosidase is an enzyme expressed by activated macrophages and Bargagli et al. found elevated levels of this enzyme in patients with sarcoidosis, with >90% exhibiting elevated levels of the marker. A second marker IL-2, a cytokine that induces T-cell proliferation and activation is elevated in serum of patients with sarcoidosis and may have prognostic value. \n\nDiagnosis:\nDiagnosis of sarcoidosis is best supported by a combination of radiographic evidence of lymphadenopathy and tissue specimens that show noncaseating granulomas. Endobronchial ultrasound guided transbronchial needle aspiration when compared to non-guided transbronchial needle aspiration had a diagnosis yield of 83.3% compared to 53.8%. \n\nTreatment:\nTherapy for patients with chronic sarcoidosis requires prolonged treatment often with steroids which cause systemic side effects. TNF inhibitors have been investigated for the treatment, but a study by Utz et al, found treatment failure in nearly 65% of participants. A new TNF-alpha antagonist Ustekinumab, approved for dosing in patients with RA, psoriatic arthritis, and ankylosing spondylitis; is currently being tested for its efficacy in treatment of sarcoidosis with completion of the study anticipated in July 2011. Surgical indication for patients with sarcoidosis remains controversial. Surgery has potential to reduce symptoms and decrease need for oral steroids, but does not eradicate or prevent recurrence of disease. Corticosteroids remain the cornerstone for treatment, but care must be taken to assess for potential adverse effects.", "ACR Code": "2.2", "Category": "Inflammatory, autoimmune", "Keywords": "adenopathynon-caseating granulomasneck dissection", "Reference": "1.\t Morganthau, Adam. Recent Advances in Sarciodosis. Chest. January 2011. Vol. 139 no. 1 174-182.\n2.\tVedove, Camilla. Subcutaneous sarciodosis: Report of two cases and review of the literature. Clinical Rheumatology 7 March 2011. 1731-4." } }, { "U_id": "MPX2461", "TAC": [ "MPX2461_synpic37573" ], "MRI": [], "Case": { "Title": "Pneumoscrotum", "History": "55 year man status-post a 10 foot fall", "Exam": "Scrotal crepitance", "Findings": "Pnsuemoscrotum (air in scrotal sac) is present, as well as diffuse subcutaneous emphysema extending along the patient's entire left side. Numerous left-sided rib fractures, left-sided pneumothorax and chest tube are present (not shown).", "Differential Diagnosis": "Pneumoscrotum as a result of:\n\u2022 Trauma\n\u2022 Pneumothorax\n\u2022 Chest tube insertion\n\u2022 Fournier's gangrene\n\u2022 Recent Surgery", "Case Diagnosis": "Pneumoscrotum", "Diagnosis By": "imaging", "Discussion": "Trauma patient with extensive subcutaneous emphysema, likely the result from 6 broken ribs on the left with a left pneumothorax and chest tube.\n\nFournier Gangrene at eMedicine - http://www.emedicine.com/emerg/topic929.htm" }, "Topic": { "Title": "Pneumoscrotum", "Disease Discussion": "\u2022 Pneumoscrotum may occur for a variety of iatrogenic or procedural reasons, including: various endoscopies (colonoscopy, etc), pacemaker placement, tracheal intubation, CPR, chest drain insertion, and open gastrostomy. \n\n\u2022 Pathologic etiologies also exist, including: pneumothorax, pneuomediastinum, scrotal trauma, gas-producing infections, and visceral perforations. \n\n\u2022 Management is usual supportive with intervation directed at the etiology.", "ACR Code": "8.4", "Category": "Trauma", "Keywords": "pneumoscrotum", "Reference": "Casey, RG, et al. Chest drain insertion may result in the acute scrotum. Scandinavian Journal of Urology and Nephrology, 2006; 40: 78-9." } }, { "U_id": "MPX2458", "TAC": [ "MPX2458_synpic24148" ], "MRI": [], "Case": { "Title": "Small Bowel Lymphoma - diffuse large B cell", "History": "48 year old male presents with LUQ pain and nausea for the past 4 months.", "Exam": "nl physical exam and nl labs", "Findings": "Digital Fluroscopic images demonstrate persistent separation of small bowel loops in the LUQ that are only minimally mobile with compression.\n\nCT of the abdomen demonstrates sig mesenteric adenopathy in a bed of fatty mesenteric panniculus and aneurismal dilitation of the small bowel\n\nCT/PET scan of the abd and pelvis demonstrates sig increase in uptake in the small bowel and mesentery indicating diffuse involvement. Rounded areas of sparing corresponsing to low density on CT are likely areas of necrosis.", "Differential Diagnosis": "Infection\nIschemia\nEdema\nNeoplasm\n - lymphoma\n - adenocarcinoma\n - metastatic disease", "Case Diagnosis": "Small Bowel Lymphoma - diffuse large B cell", "Diagnosis By": "Tissue biopsy", "Treatment & Follow Up": "Patient was treated with CHOP+Rituxan and is awaiting bone marrow transplant.", "Discussion": "This case represents a good example of small bowel lymphoma and the modalities used to explore this disease." }, "Topic": { "Title": "Small Bowel Lymphoma", "Disease Discussion": "Primary gastrointestinal lymphoma represents nearly 20% of all malignant soft bowel wall tumors in otherwise previously healthy patients. Secondary involvement of the bowel by lymphoma is present in more that 50% of all cases. Most cases are of the non-Hodgkin\u2019s variety. The usual age at presentation is in 5th and 6th decades of life. Symptoms can vary depending on the degree of mass effect on the small bowel. Fatigue, weight loss and emesis is a common presentation. \n\nRadiographic imaging is not entirely specific. Real time evaluation of the small bowel with digital fluoroscopic exams using barium may show thickened and adherent bowel loops with loss of normal barium transit or frank obstruction. CT imaging often shows diffuse mesenteric adenopathy, and multiple round enhancing homogenous masses. The tumor often encases the bowel and causes both aneurismal dilatation and eventual stenosis as the tumor enlarges becomes more lobulated and necrotic. PET imaging is helpful initially in determining disease extension and perhaps later for chemotherapy and radiation treatment response. Definitive diagnosis is by percutaneous biopsy.\n\nThe prognosis of the patient depends on the degree of involvement and co-morbid factors. Younger patients with HIV tend to have high grade and diffuse aggressive disease at presentation and fair much worse than healthy individuals who often present with low-grade malignancy. Treatment is chemotherapy and radiation. 10 year survival and relapse-free survival for patients with low-grade disease are estimated at 80% and 60%. 10 year survival and relapse-free survival for patients with mid to high-graded disease is estimated at 50% and 50%.", "ACR Code": "7.3", "Category": "Neoplasm, hematopoietic", "Keywords": "Small BowelLymphomaNon Hodgekin", "Reference": "Weissleder R, Wittenberg J and Harisinghani MG. Primer of Diagnostic Imaging 3rd Ed. Mosby 2003, page 183.\n\nChang, Tony. Small Bowel Lymphoma. LearningRadiology.com http://www.learningradiology.com/notes/ginotes/smallbowellymphomapage.htm\n\nSheth S, Horton KM, et al. Mesenteric Neoplasms: CT Appearances of Primary and Secondary Tumors and Differential Diagnosis. RadioGraphics 2003; 23:457-473.\n\nHa CS, Cho MJ, et al. Primary Non-Hodgkin Lymphoma or the Small Bowel. Radiation Oncology 1999; 211:183-187." } }, { "U_id": "MPX2463", "TAC": [ "MPX2463_synpic17001", "MPX2463_synpic17003" ], "MRI": [], "Case": { "Title": "Probable metastatic rhabdomyosarcoma", "History": "Remote Hx of Bladder Rhabdomyosarcoma. Now with 2months Of Pelvic Pain , Possible Tumor Recurrence s/p Chemo & Xrt 5 Yrs Ago", "Exam": "Proteinuria", "Findings": "CT: enlargement of the left internal pelvic musculature w/ mild sclerosis of the adjacent acetabulum", "Differential Diagnosis": "\u2022 Metastatic rhabdomyosarcoma\n\u2022 Other sarcoma, ie Ewings\n\u2022 hematoma", "Case Diagnosis": "Probable metastatic rhabdomyosarcoma", "Discussion": "Metastatic/Recurrent rhabdomyosarcoma is by far the most likely diagnosis in this patient with a history of bladder rhabdomyosarcoma. Less likely considerations would include primary Ewings sarcoma." }, "Topic": { "Title": "Rhabdomyosarcoma", "Disease Discussion": "Rhabdomyosarcoma accounts for 5-10% of all malignant tumors in patients under 15 years and is most common malignant tumor of the vagina, prostate, and bladder. Other sites of involvement include perineal region, head & neck, skeletal muscle/soft-tissue, protahepatis, peritoneal, \nMost neoplasms of the bladder in children are malignant, with Rhabdomyosarcoma most common. TCC and Leiomyosarcomsa are rarely seen. Clinically bladder tumors present with hematuria and retention and can cause flank pain secondary to hydronephrosis and constipation. \nRhabdomyosarcoma appears either as peduunculated soft-tissue mass with bunch of grapes appearance (Botryoid) or as focal or diffuse wall thickening. On CT assymmetry of fat planes or direct soft tissue into adjacent organs is usefull for assessing stage. Pelvic lymph nodes may be enlarged indicative of metastatic disease. Metastatic disease to the nodes, liver, bone, lung, brain.\nDistinguishing between localized benign and malignant tumors of the bladder may not be possible with CT. \nGU rhabdomyosarcoma is initially managed by chemo. Patients with operable tumors undergo surgery and radiation rendered for residual inoperable tumor. \nThree year survival rates are 70-80%.", "ACR Code": "8.3", "Category": "Neoplasm, sarcoma", "Keywords": "RhabdomyosarcomaProstatebladder", "Reference": "Pediatric Body CT. Marilyn J. Siegel. Lippincott Williams & Williams, 1999. 299-302" } }, { "U_id": "MPX2466", "TAC": [ "MPX2466_synpic24693" ], "MRI": [], "Case": { "Title": "Pulmonary arteriovenous malformations in hereditary hemorrhagic telangiectasia.", "History": "81 year old man with facial telangiectasias, daily epistaxis and decreased blood oxygenation is found to have pulmonary arteriovenous malformation on CT.", "Findings": "Pulmonary AVM with single feeding artery and single feeding vein", "Case Diagnosis": "Pulmonary arteriovenous malformations in hereditary hemorrhagic telangiectasia.", "Treatment & Follow Up": "Patient was treated with coil embolization of the feeding artery to the AVM." }, "Topic": { "Title": "Pulmonary arteriovenous malformations, Hereditary hemorrhagic telangiectasia", "Disease Discussion": "Pulmonary arteriovenous malformations (PAVM's) are relatively rare in the general population, but are seen more commonly in patients with hereditary hemorrhagic telangiectasia (HHT), also called Osler-Weber-Rendu disease.\n \nHHT is an inherited autosomal dominant disorder that primarily consists of multiple small and large abnormal arteriovenous communications involving the skin, mucous membranes, lungs, gastrointestinal tract, and central nervous system. The most common presenting symptom is recurrent epistaxis due to telangiectasias in the nasal mucosa.\n \nA pulmonary AVM is an abnormal communication between pulmonary arteries and veins without normal intervening capillaries. About 70% of patients with pulmonary AVM's also have HHT. Up to 50% of patients with HHT have at least one PAVM. Multiple PAVM's are common in patients with HHT.\n \nPAVM's can cause symptoms from the right-to-left shunts causing deoxygenation, hemoptysis, hemothorax, and paradoxical embolization. Patients frequently compensate for the chronic blood deoxygenation.\n\nThe most catastrophic complications are caused by paradoxical embolization to the brain causing stroke, brain abscess, TIAs and pulmonary hemorrhage.\n\nHigh resolution CT is a sensitive screening method for detecting pulmonary AVMs. Pulmonary angiography remains the gold standard for confirming the diagnosis of pulmonary AVM's and is necessary for endovascular treatment with embolization.\n\nIt is recommended that PAVM's with a feeding artery 3 mm or larger should be treated, due to the risk of stroke in these patients. The most common method of treatment is endovascular deployment of metallic coils into the feeding artery or arteries of the AVM. Surgery is usually reserved for difficult cases that fail embolization.", "ACR Code": "9.3", "Category": "Vascular", "Keywords": "Pulmonary arteriovenous malforationhereditary hemorrhagic telangiectasiaOsler-Weber-Rendu", "Reference": "Embolization of Pulmonary Arteriovenous Malformations, Swischuk J L \u2013 Seminars In Interventional Radiology \u2013 17(2): 171-183" } }, { "U_id": "MPX2468", "TAC": [ "MPX2468_synpic23781", "MPX2468_synpic23782" ], "MRI": [], "Case": { "Title": "Diffuse Rhabdomyosarcoma", "History": "History (can include gestational age, or age in days, weeks, months):\nPreviously healthy 13 y/o female with shortness of breath on exertion.", "Exam": "Physical Exam and Laboratory: \nNo pertinent findings", "Findings": "Image Findings: \nCXR (AP Portable): mediastinal mass, left pleural effusion\nChest CT: large mediastinal mass spanning the anterior, middle, and posterior mediastinum and descending into abdomen and \n encircling the aorta, large left and right pleural effusions\nAbdomen and Pelvis CT: large mass descending from mediastinum into the retroperitoneal space and into the pelvis compressing \n the Inferior Vena Cava, Hydronephrosis of the Left kidney", "Differential Diagnosis": "Differential Diagnosis for these findings in this case:\nBased on CXR: Malignancy, Granulomatous disease, Other inflammation (abscess/pneumonia), Benign neoplasm, and Congenital \n anomaly\nBased on CT: Lymphoma, Other malignancy (most likely soft tissue in origin), Metastatic disease", "Case Diagnosis": "Diffuse Rhabdomyosarcoma", "Diagnosis By": "Biopsy", "Treatment & Follow Up": "Treatment and Follow-up: \n-Diuresis for pleural effusions initially which decreased the patient\u2019s symptom of dyspnea on exertion\n-Placement of ureteral stents due to compression of Left ureter causing Hydronephrosis\n-Chemotherapy started at diagnosis and continued for greater than one year\n-Patient succumbed to her disease approximately 15 months following her diagnosis", "Discussion": "Discussion (include references): \nRhabdomyosarcoma is the most common soft tissue sarcoma of childhood and adolescence, usually arising before age 20. It is classified into three histological subtypes: Embryonal, the most common subtype often with the best prognosis; Alveolar, the most common subtype in adolescents and this patient\u2019s final diagnosis; and Pleomorphic, the least common of the three subtypes. Overall, in children, 65% of patients diagnosed with Rhabdomyosarcoma are cured with treatment consisting of chemotherapy, surgery, and occasionally radiation. \n\nInformation from Robbins Pathologic Basis of Disease. 6th ed. 1999." }, "Topic": { "Title": "Diffuse Rhabdomyosarcoma", "Disease Discussion": "Discussion (include references): \nRhabdomyosarcoma is the most common soft tissue sarcoma of childhood and adolescence, usually arising before age 20. It is classified into three histological subtypes: Embryonal, the most common subtype often with the best prognosis; Alveolar, the most common subtype in adolescents and this patient\u2019s final diagnosis; and Pleomorphic, the least common of the three subtypes. Overall, in children, 65% of patients diagnosed with Rhabdomyosarcoma are cured with treatment consisting of chemotherapy, surgery, and occasionally radiation. \n\nInformation from Robbins Pathologic Basis of Disease. 6th ed. 1999.", "ACR Code": "67.325", "Category": "Clinical Exam Finding or Sign", "Keywords": "Diffuse RhabdomyosarcomaRhabdomyosarcomasarcoma", "Reference": "Information from Robbins Pathologic Basis of Disease. 6th ed. 1999" } }, { "U_id": "MPX2471", "TAC": [ "MPX2471_synpic4188" ], "MRI": [], "Case": { "Title": "Astrocytoma, low-grade, supratentorial", "History": "43 y/o male who presents with chronic headaches but recently worsened.", "Findings": "Noncontrast head CT demonstrates a large intraaxial mass which appears based in the right parietal lobe then extends into the right lateral ventricle. Some calcification is present. Pathology from a brain biopsy came back as a grade 2 astrocytoma.", "Case Diagnosis": "Astrocytoma, low-grade, supratentorial" }, "Topic": { "Title": "Astrocytoma, low-grade (WHO 2), supratentorial", "Disease Discussion": "Astrocytomas are graded on an ascending scale of agression, from WHO Gr 1 to Gr 4. Circumscribed astrocytoma - like pilocytic and subependymal giant cell - are Gr 1.\n\nNon-enhancing low-grade diffuse astrocytoma are Gr2, while anaplastic are Gr 3, and glioblastoma is Gr 4.\n\nWHO Gr 2 - most simply called just \"astrocytoma\" - have a relatively good prognosis. They should not have prominent enhancement. In fact, some literature indicates they should not enhance at all, and they should not have increased perfusion. Sometimes they may have reduced perfusion. They should not show increased metabolism.\n\nPrognosis and survival are relatively good.\n\nIn a review of 179 adult supratentorial low-grade astrocytomas (over 10 years). 80% alive at 5yrs after \"total removal\". 50% alive at 5yrs after incomplete removal, 45% alive at 5yrs after biopsy. \"Among the entire population, the influence of radiotherapy was not obvious: 65% of patients were alive at 5 years without radiotherapy compared to 55% with radiotherapy.\"\nNeurosurgery. 1993 Apr;32(4):554-9. PMID: 8474646", "ACR Code": "1.3", "Category": "Neoplasm, glial", "Keywords": "astrocytoma", "External Links": "www.ncbi.nlm.nih.gov/pubmed/8474646" } }, { "U_id": "MPX2477", "TAC": [ "MPX2477_synpic21251" ], "MRI": [], "Case": { "Title": "Pneumatosis intestinalis (PI)", "History": "76 yo male with PMH of metastatic colon CA with chief complaint of abdominal pain.PMH: metastatic colon CA, HTN, MI, Renal insuffiency, emphysema.PSH: Partial colon resection, kidney stone removal, nephrostomy tubes placedSH: nonsmoker, nondrinker", "Exam": "Abd: soft, nondistendend, mildly tender to palpation in LLQ, no rebound, no guarding", "Findings": "KUB (image 1)- pneumatosis intestinalis of large bowel; dilated loops of small bowel, no air-fluid levelsNon-contrast CT (image 2)- pneumatosis intestinalis from splenic flexure to the sigmoid colon, no free intraperitoneal air; known ventral hernia containing small portion of transverse colon; no obstruction.", "Differential Diagnosis": "Primarily ischemia vs infection. Other consideratins for pneumatosis include intestinal trauma, obstruction, inflammatory bowel disease, COPD", "Case Diagnosis": "Pneumatosis intestinalis (PI)", "Discussion": "Pneumatosis intestinalis (PI) is the presence of gas within the wall of the small or large intestine. Radiologic findings for PI on plain radiographs (positive in approximately two-thirds of affected patients) reveal intramural gas that can be linear, curvilinear, or circular in form. In images 1, the PI is seen as tiny radiolucent bubbles projecting obliquely across the left lower abdomen and hemipelvis. CT is more sensitive than plain films and shows circumpherential collections of air adjacent to lumen of bowel that run parallel with bowel wall, as seen in image 2. In contrast to air in the lumen, PI lacks the characteristic air-fluid/air-contrast levels seen in intraluminal air. Also contrast studies of the intestines can be confirmatory, revealing filling defects within the lumen corresponding to the protruding gas cysts.PI can be associated with a wide variety of gastrointestinal (eg. ischemia, infection, intestinal trauma, obstruction, inflammatory bowel disease) and nongastrointestinal causes (COPD). Assesment of the patient\u2019s clinical status is critical to determine treatment. Urgent surgery is commonly required for patients with PI and clinical evidence of bowel obstruction or ischemia, while asymptomatic patients without metabolic acidosis may be safely observed/medically managed." }, "Topic": { "Title": "Pneumatosis intestinalis (PI)", "Disease Discussion": "Pneumatosis intestinalis (PI) is the presence of gas within the wall of the small or large intestine. Radiologic findings for PI on plain radiographs (positive in approximately two-thirds of affected patients) reveal intramural gas that can be linear, curvilinear, or circular in form. \n\nIn images 1, the PI is seen as tiny radiolucent bubbles projecting obliquely across the left lower abdomen and hemipelvis. \n\nCT is more sensitive than plain films and shows circumpherential collections of air adjacent to lumen of bowel that run parallel with bowel wall, as seen in image 2. In contrast to air in the lumen, PI lacks the characteristic air-fluid/air-contrast levels seen in intraluminal air. Also contrast studies of the intestines can be confirmatory, revealing filling defects within the lumen corresponding to the protruding gas cysts.\n\nPI can be associated with a wide variety of gastrointestinal (eg. ischemia, infection, intestinal trauma, obstruction, inflammatory bowel disease) and nongastrointestinal causes (COPD). Assesment of the patient\u2019s clinical status is critical to determine treatment. Urgent surgery is commonly required for patients with PI and clinical evidence of bowel obstruction or ischemia, while asymptomatic patients without metabolic acidosis may be safely observed/medically managed.", "ACR Code": "7.9", "Category": "Differential Diagnosis", "Keywords": "Pneumatosis intestinalisPIIschemic bowel", "Reference": "1.Goldberg, E, Lamont, JT. Pnuematosis intestintialis. In: UpToDate, Rose, BD (Ed), UpToDate, Wellesley, MA, 2004.2. Sachse, RE, Burke GW, 3rd, Jonas, M, et al. Benign pneumatosis intestinalis with subcutaneous emphysema in a liver transplant recipient. Am J Gastroenterol 1990; 85:876.3. Knechtle, SJ, Davidoff, AM, Rice, RP. Pneumatosis intestinalis. Surgical management and clinical outcome. Ann Surg 1990; 212:160." } }, { "U_id": "MPX2478", "TAC": [ "MPX2478_synpic18340", "MPX2478_synpic18342" ], "MRI": [], "Case": { "Title": "Adenocarcinoma (poorly differentiated)", "History": "55 yo WM presented with a 3 week hx of fatigue, fever, SOB, and myalgias. The patient has no significant past medical or surgical hx. He has an 80-pack year smoking hx and his mother died of lung ca.", "Exam": "Physical exam was significant for coarse breath sounds bilaterally (R=L). The patient also had a diffuse maculopapular rash at presentation. \n \\10.5/ 130|94|24 33------600 ------------ 103 / 32 \\ 4.9 |31|.8, \nAST 60, ALT 66, Tbili .3, PT 14.7, PTT 33", "Findings": "AP chest radiograph: right upper lobe mass, right hilar mass, right pleural thickening with several right masses along the junction of the pleura and lung.", "Differential Diagnosis": "Mass differential includes: malignancy, granulomatous disease, inflammation, benign neoplasm, and congenital abnormality", "Case Diagnosis": "Adenocarcinoma (poorly differentiated)", "Diagnosis By": "Pathology diagnosis was Adenocarcinoma (poorly differentiated)", "Treatment & Follow Up": "The primary team is currently considering palliative care plan as this patient has stage IV disease." }, "Topic": { "Title": "Adenocarcinoma (poorly differentiated)", "Disease Discussion": "Adenocarcinoma of the lung is currently the most frequent lung cancer in all individuals. There is still a slightly higher frequency of squamous cell in men. Adenocarcinoma is also the most frequently diagnosed lung cancer in women and nonsmokers. The malignancy is often identified (in 75% of cases) in the peripheral lung and often involves the pleura. Other malignancies such as small cell and squamous cell are most often centrally located within the lung. Once the tissue diagnosis is confirmed, the patient is staged using the TNM system. This patient has mediastinal node involvement (on CT) which automatically makes him an M1 (stage IV). The 5-year survival for all stage four non-small cell lung malignancies is 1%. This patient\u2019s 5-year survival may even be worse as he has the poorly differentiated form of adenocarcinoma which leads to a poorer prognosis. One interesting characteristic of lung adenocarcinoma is that studies have not shown a clear link between this malignancy and tobacco.", "ACR Code": "61.321", "Category": "Neoplasm, carcinoma", "Keywords": "Adenocarcinoma", "Reference": "Strauss GM, MD., Clinical and pathologic prognostic factors in non-small cell lung cancer. \u00a92003 UpToDate\u00ae \n\nhttp://www.utdonline.com/application/topic.asp?file=lung_ca/2968&type=A&selectedTitle=3~6" } }, { "U_id": "MPX2479", "TAC": [ "MPX2479_synpic24743", "MPX2479_synpic24745", "MPX2479_synpic24748", "MPX2479_synpic24749", "MPX2479_synpic24750" ], "MRI": [], "Case": { "Title": "Bronchiectasis", "History": "15 year old boy, air evacuated from Japan with a history of recurrent productive cough.", "Exam": "NA", "Findings": "\u2022 Chest radiograph demonstrates opacity in LLL. Thin slice CT with IV contrast in arterial phase demonstrates no abnormal vessels extending to this consolidation to indicate that this may be a sequestration.\n\n\u2022 A repeat chest radiograph and a CT after 10 day antibiotic therapy demonstrates partial resolution of retrocardiac opacity. CT shows segmental bronchiectasis most likely resulting from numerous prior infections.", "Differential Diagnosis": "\u2022 Bronchiectasis\n\u2022 CCAM (this case demonstrates dilated bronchi and not cysts as in CCAM)\n\u2022 Pulmonary Sequestration - (no abnormal blood supply in this case)", "Case Diagnosis": "Bronchiectasis", "Diagnosis By": "Response to treatment (no pathology) and Imaging characteristics", "Treatment & Follow Up": "This segment of lung will probably be resected. However, no definite therapy has been done yet. Update will follow", "Discussion": "Companion cases -\n\u2022 Pulmonary Sequestration:\nhttp://rad.usuhs.mil/medpix/medpix.html?mode=tsearch2&srchstr=sequestration&srch_type=any#top\n\u2022 Congenital Cystic Adenomatoid Malformation (CCAM):\nhttp://rad.usuhs.mil/medpix/medpix.html?mode=tsearch2&srchstr=adenomatoid%20malformation&srch_type=all#top" }, "Topic": { "Title": "Bronchiectasis", "Disease Discussion": "Bronchiectasis is defined as irreversible local dilatation of the bronchial tree with associated bronchial wall thickening. Clinically most patients present with cough (usually chronic), recurrent infections and hemoptysis. Although not a single disease process, bronchiectasis remains a descriptive final common pathway for several distinct disease processes. Etiologies include:\nPost-infectious: Measles, whooping cough, TB and allergic\nbronchopulmonary aspergillosis)\nInflammatory: Association with Crohn\u2019s & Ulcerative Colitis\nCongenital: Bronchial atresia, Williams-Campbell syndrome, Cystic Fibrosis\nObstruction: Primary neoplasm, Foreign body, Enlarged lymph nodes\nImpaired Clearance: Kartagener\u2019s syndrome (Dysmotile cilia syndrome + situs)\nImmunodeficiencies: Hypogammaglobulinemia, alpha-1 antitrypsin deficiency\nPulmonary Fibrosis: Traction bronchiectasis \n\nAlthough findings consistent with bronchiectasis can be observed on routine chest radiographs and moreso on chest CT, dedicated high-resolution CT (HRCT) remains the modality of choice for the evaluation of bronchiectasis. Although some authors report up to 7% normal chest radiographs in patients with bronchiectasis, even conventional CT may not delineate the etiology in a small percentage of patients. Therefore, not only does HRCT delineate the location of the lesions in the lung, but remains the most sensitive and specific examination available. \n\nFindings on HRCT include:\n-Lack of bronchial tapering -wall thickening \n- bronchial dilatation -mucoid filling \n-\u201csignet ring\u201d sign with adjacent pulm artery as stone and bronchi as ring ie: relative enlargement of the bronchial \n-\u201ctram lines\u201d sign \n\nThree classifications have been adopted as standard which include: \n1. Cylindrical: bronchi have fusiform dilation and lack of tapering and presence of abrupt termination.-ABPA\n2. Varicose: usually has a more dilated bronchi than cylindrical, however will have bronchial constrictions that produce an irregular outline to the bronchi. \u2013 Cystic Fibrosis\n3. Cystic: thick-walled saccular dilatations that can have air-fluid levels secondary to retained secretions-Bronchial stenosis\n\nAlthough various disease processes have some regularity, there is some overlap and variablity of the type and location of the involved bronchi. \n\n\nTreatment:\n\tAntibiotics and respiratory therapy are the mainstays of conservative therapy. Surgical resection is an option of last resort for advanced disease. Episodes of massive hemoptysis have been known to occur requiring emergent embolization of involved bronchial artery. In the case of bronchiectasis in the setting of inflammatory bowel disease however the mainstay of therapy remains steroids as they lesions can undergo striking resolution once proper therapy is initiated.", "ACR Code": "6.26", "Category": "Infection, NOS", "Keywords": "bronchitis" } }, { "U_id": "MPX2480", "TAC": [ "MPX2480_synpic21360" ], "MRI": [], "Case": { "Title": "Giant Cell Tumor", "History": "24 year-old male with back pain.", "Exam": "tenderness lower thoracic spine", "Findings": "Plain film and CT: 6.1 x 2.2 cm expansile lytic lesion involving the left T11 vertebral body, pedicle, lamina and transverse process narrowing the spinal canal without associated soft tissue mass.\nBone scan: intense radiopharmaceutical uptake in the left T11 vertebral body and posterior elements correlating to the CT abnormality.", "Differential Diagnosis": "Osteoblastoma\nAneurysmal bone cyst\nGiant Cell tumor\nExpansile metastasis", "Case Diagnosis": "Giant Cell Tumor", "Diagnosis By": "Resection", "Treatment & Follow Up": "The patient underwent resection, grafting and fusion. No early evidence of recurrence.", "Discussion": "Unusual location and presentation for a giant cell tumor." }, "Topic": { "Title": "Giant Cell Tumor", "Disease Discussion": "Giant cell tumor (GCT) is a primary bone tumor affecting women more commonly than men (2:1) and associated with an Asian ancestry. The usual age of presentation is 20-40 years of age after the growth plate has been obliterated. Patients usually present with tenderness and swelling over the primary site and rarely pathologic fracture. GCTs comprise 5-9% of all primary bone tumors, 25% of benign bone tumors and are the 6th most common primary bone neoplasm. The majority of GCTs are benign with approximately 5-10% malignant, which are indistinguishable radiographically. 60% occur in the long bones and almost all GCTs involve the articular end of the bone with the following most common sites: proximal tibia, distal femur, distal radius and proximal humerus. \n\nInitial evaluation is usually with radiography, which often reveals a geographic, well-defined lucent lesion usually lacking sclerotic margins or periosteal reaction. The lesion is usually in an eccentric location and usually extends to the articular surface. Further evaluation requires CT or MRI, which can demonstrate associated soft tissue mass and full extent of the lesion. MRI is useful in defining the full extent of the tumor in preparation for surgical resection and may occasionally reveal fluid/fluid levels or subchondral breakthrough or joint involvement. \n\nTreatment consists of surgical curettage with bone grafting or orthopedic cement or wide resection with secondary implantation of an allograft endoprosthesis. Pathologic evaluation reveals vascular tissue with mononuclear stromal cells and multinucleated giant cells of osteoclast type. Recurrence is frequent (approximately 50%) and usually due to inadequate surgical resection. Recurrence is often manifested radiographically by resorption of the bone graft and appearance of new lucenies. Malignant degeneration may occur especially following radiation therapy. Even histologically benign tumors may metastasize to lung.", "ACR Code": "4.3", "Category": "Neoplasm, benign", "Keywords": "Giant cell tumor", "Reference": "1) Miller SL, Hoffer FA: Malignant and Benign Bone Tumors, Radiology Clinics of North America. 01 Jul 01; 39 (4): 673-699\n\n2) Greenspan, A: Orthopedic Radiology, 3rd ed. Lippincott Williams & Wilkins Philadelphia, PA 2000" } }, { "U_id": "MPX2481", "TAC": [ "MPX2481_synpic23898", "MPX2481_synpic23899", "MPX2481_synpic23904", "MPX2481_synpic23927" ], "MRI": [], "Case": { "Title": "Transmesenteric internal hernia, small bowel volvulus", "History": "27 y/o woman with sudden onset of periumbilical abdominal pain relieved only by \"bending forward\". Previous surgery - gastric bypass 2 years ago.", "Exam": "Severe periumbilical pain, peritoneal signs. Unable to tolerate oral contrast.", "Findings": "Early studies demonstrate an internal transmesenteric small bowel hernia without volvulus or ischemia.\n\nRecent study demonstrate the \"whirl\" sign - indicating twisting of the bowel and, hence, volvulus. No evidence of intestinal ischemia or necrosis on CT (no submucosal enhancement, bowel wall thickening, free fluid or pneumatosis intestinalis).", "Differential Diagnosis": "Clinical difeerential diagnosis:\n\n\u2022 Acute appendicitis\n\u2022 Acute cholecystitis\n\u2022 Mesenteric ischemia\n\u2022 Volvulus\n\nImaging findings are diagnostic.", "Case Diagnosis": "Transmesenteric internal hernia, small bowel volvulus", "Diagnosis By": "Surgery", "Treatment & Follow Up": "Procedure - Exploratory laparotomy with detorsion of small intestine, lysis of adhesions and closure of mesenteric defect. Surgical findings included: large mesenteric defect at root of mesentery with volvulus of small bowel around SMA axis. Some mesenteric venous congestion but bowel pink and healthy after detorsed. No evidence of congenital malrotation.", "Discussion": "Whirl sign - uncommonly seen - indicates twisting of the mesenteric vessels, or twisting of the bowel itself, that is diagnostic of volvulus." }, "Topic": { "Title": "Transmesenteric hernia (internal hernia), small bowel volvulus", "Disease Discussion": "Internal hernia is an uncommon cause of small bowel obstruction that may be increasing in frequency. Because the clinical diagnosis of internal hernia is difficult, imaging studies such as computed tomography (CT) and small bowel follow through play an important role. Transmesenteric hernia is the most common type and is usually related to prior abdominal surgery, especially with creation of a Roux-en-Y anastomosis (eg, liver transplantation, gastric bypass). CT may allow confident diagnosis in most cases.\n\nWhen the small bowel herniates through a defect in the mesentery or omentum, the herniated bowel is compressed against the abdominal wall, with no overlying omental fat in most cases and at most levels of anatomic section through the herniated bowel. The herniated bowel tends to appear clustered and lies outside the colon, a reversal of the normal anatomic arrangement. As a result, the adjacent colon is displaced centrally (eg, transverse colon displaced dorsally, ascending colon displaced medially). There will be some degree of compression, crowding, displacement, and obstruction of both the bowel and blood vessels.\n\nThe herniated bowel may also twist within the hernia sac, which results in volvulus and a predisposition to bowel ischemia. Twisting of the mesenteric vessels, or the whirl sign, or twisting of the bowel itself is diagnostic of volvulus, and engorged blood vessels, mesenteric ascites, and bowel wall thickening suggest bowel ischemia.\n\nCT signs most suggestive of transmesenteric hernia are those that depict the abnormal cluster of bowel loops along the periphery of the peritoneal cavity and lack of omental fat covering the clustered small bowel.", "ACR Code": "7.9", "Category": "Hernia/herniation", "Keywords": "transmesenteric herniasmall bowel volvulusintestinal ischemia", "Reference": "1. Blachar A, Federle MP. Internal hernia: an increasingly common cause of small bowel obstruction.Semin Ultrasound CT MR. 2002 Apr;23(2):174-83. \n\n2. Blachar A, Federle MP, Dodson SF. Internal hernia: clinical and imaging findings in 17 patients with emphasis on CT criteria.Radiology. 2001 Jan;218(1):68-74." } }, { "U_id": "MPX2483", "TAC": [ "MPX2483_synpic27408" ], "MRI": [ "MPX2483_synpic27405" ], "Case": { "Title": "Ventriculoperitoneal Shunt Failure secondary to tubing disconnection.", "History": "17 year-old-male with new onset headaches and a history of a VP shunt.", "Exam": "N/A", "Findings": "Axial T2 MRI from 3 months prior to presentation demonstrating baseline lateral ventricular size.\nLateral radiograph of the skull on presentation (as part of a VP shunt evaluation series) demonstrating a disconnection at a branch point of the shunt system external to the skull at the right temporal region.\nNon-contrast CT of the head demonstrating enlarged lateral ventricles.\nPost shunt revision non-contrast CT of the head demonstrating mild decrease in the size of the lateral ventricle as well as the post revision head CT scout image demonstrating shunt disconnection repair.", "Differential Diagnosis": "Shunt disconnection--diagnostic images.", "Case Diagnosis": "Ventriculoperitoneal Shunt Failure secondary to tubing disconnection.", "Diagnosis By": "Pre and post shunt revision imaging.", "Treatment & Follow Up": "Shunt revision.", "Discussion": "Please see factoid." }, "Topic": { "Title": "Ventriculoperitoneal Shunt Failure", "Disease Discussion": "Patients with hydrocephalus have a disturbance in the formation, flow, or absorption of their cerebrospinal fluid (CSF), leading to an increased volume occupied by this fluid within the central nervous system. CSF is made primarily by the choroid plexus within the ventricular system, and is normally produced at a rate of 0.2-0.35 mL/min. The capacity of the lateral and third ventricles in a healthy adult is approximately 20 mL, with a total CSF volume of approximately 120 mL. CSF is absorbed through arachnoid granulations back into the systemic venous system. An imbalance between CSF production and resorption results in an increase in intracranial pressure.\n The majority of hydrocephalus results from obstructive causes--either intraventricular or extraventricular. Treatment options for these patients include a variety of surgical options: choroid plexectomy, opening of a stenotic auqaduct, tumor removal (in cases where tumor mass is causing obstruction), fenestration of the floor of the third ventricle, and shunting. Of these, shunting represents the most common and successful procedure. Essentially shunts provide a conduit for CSF to drain from the ventricles or subarachnoid space to another compartment of the body. A variety of options exist, but the preffered route is the ventriculoperitoneal shunt. Shunts require routine follow up, and in children, revisions on a scheduled basis according to growth rates. Potential complications include: infection, obstruction, and hardware disconnection, and warrant swift clinical attention with imaging studies to assess the patients intracranial status as well as the shunt hardware.", "ACR Code": "1.9", "Category": "Unsure", "Keywords": "VP shunthydrocephalus", "Reference": "Brant, WE, Helms, CA, Fundamentals of Diagnostic Radiology, 2nd ed, Williams & Wilkins, Baltimore, MD, 1999.", "External Links": "www.emedicine.com/NEURO/topic161.htm" } }, { "U_id": "MPX2488", "TAC": [ "MPX2488_synpic24858", "MPX2488_synpic24859", "MPX2488_synpic24860" ], "MRI": [], "Case": { "Title": "Silent Sinus Syndrome", "History": "13 year old with chronic sinusitis, worse for last 3 weeks.", "Exam": "unremarkable", "Findings": "Opacified atelectatic left maxillary sinus with infundibular occlusion. Associated nasal septal deviation, enlargement of left middle meatus, retraction of left anterior maxillary sinus wall, and mild retraction of inferior orbital wall.", "Differential Diagnosis": "Chronic sinusitis\nCongenital opacification\nSilent Sinus\nPost traumatic deformity", "Case Diagnosis": "Silent Sinus Syndrome", "Diagnosis By": "CT imaging", "Treatment & Follow Up": "ENT consult, antibiotic therapy and possible surgery." }, "Topic": { "Title": "Silent Sinus Syndrome", "Disease Discussion": "Silent sinus syndrome is characterized by painless enophthalmos associated with chronic maxillary sinus atelectasis from chronic infundibular obstruction. This results in negative sinus pressure and collapse over time. This syndrome has primarily been described in the otolaryngology and ophthalmology literature. The patient is typically an adult who presents to an ophthalmologist or an ENT specialist with a chronic history of painless facial asymmetry (one eye lower and sunken), diplopia, or both. The patient may have symptoms of sinusitis but may be asymptomatic. \n\nThe diagnosis is made clinically and confirmed radiologically. Physical exam reveals a combination of enophthalmos, hypoglobus, upper-lid retraction, deepened upper-lid sulcus, and malar depression.\n\nRadiologic evaluation is primarily by CT. The imaging findings of the silent sinus syndrome a fully developed and opacified maxillary sinus with occluded infundibulum. Occlusion is usually caused by lateral retraction of the uncinate process with apposition of the uncinate process against the inferomedial aspect of the orbital wall. There is resultant enlargement of the adjacent middle meatus with associated lateral retraction of the middle turbinate. The feature most characteristic is inward retraction of the sinus walls (medial wall, posterolateral wall, and orbital floor) with associated decrease in sinus volume. The downward retraction of the orbital floor into the maxillary sinus creates the eye or facial asymmetry.\n\nTreatment is surgical involving making an outlet for mucous drainage from the obstructed sinus. A nasal antral window or a maxillary antrostomy is performed endoscopically. The post surgical sinus deformity may remain unchanged, improve slightly, or be restored to a near-normal configuration over time. Additional corrective surgery of the orbital floor may be accomplished.\n\n============================\nhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=94203633\nhttp://www.ajronline.org/cgi/content/figsonly/178/2/503\nhttp://www.laryngoscope.com/pt/re/laryngoscope/abstract.00005537-200106000-00008.htm;jsessionid=CFN5meDK83rOWfejtjGhVdI9eNOhOeY6WnvGHqPCy2fdePgnNvQU!583875742!-949856031!9001!-1\nhttp://www.laryngoscope.com/pt/re/laryngoscope/abstract.00020840-199902000-00009.htm;jsessionid=CFN58WbqxkzTMJuHWoh1quFdWgPKXuCwImn5HUmV2wdjisErBWqc!583875742!-949856031!9001!-1", "ACR Code": "1.2", "Category": "Infection, NOS", "Keywords": "silent sinus syndromesinsus atelectasisopacified sinus", "Reference": "The Silent Sinus Syndrome, Clinical and Radiographic Findings.Anna Illner, et al. AJR 2002; 178:503-506.", "External Links": "http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Search&db=PubMed&term=silent+sinus+syndrome&tool=QuerySuggestion" } }, { "U_id": "MPX2494", "TAC": [ "MPX2494_synpic20417" ], "MRI": [], "Case": { "Title": "Pulmonary Embolism", "History": "37-year-old woman with a chief complaint of chest pain, fever of 103, and left flank pain. She had a questionable left lower lobe infiltrate on plain film. The patient was sent for a CT-pulmonary angiogram for a suspected pulmonary embolus (PE).", "Findings": "An acute pulmonary embolism can be seen beyond the bifurcation of the left pulmonary artery as a filling defect with the contrast media. Incidental left saline breast implant.", "Differential Diagnosis": "none", "Case Diagnosis": "Pulmonary Embolism", "Diagnosis By": "CT pulmonary angiogram", "Treatment & Follow Up": "Most cases of acute PE are treated with anticoagulation therapy and supportive care, and the embolism undergoes autothrombolysis. In the cases of hemodynamic instability, patients receive thrombolytic therapy. When long-term anticoagulation therapy is contraindicated, an IVC filter can be placed." }, "Topic": { "Title": "Pulmonary Embolism", "Disease Discussion": "Although numerous studies utilizing new imaging modalities such as helical CT scans have been performed to improve the diagnosis of pulmonary embolism (PE), ventilation/perfusion (V/Q) scans remain the screening tool of choice. This test is a nuclear medicine study that compares images of inhaled radionuclide material to pulmonary perfusion images of intravenously injected radiolabeled protein. These images must be closely compared to a chest X-ray taken at or near the time of the V/Q scan. This is done to ensure defects on the V/Q images are not accounted for by findings on the chest X-ray. A high probability scan, defined as two or more moderate or large segmental mismatched perfusion defects, in the presence of high clinical suspicion was found to be accurate 96% of the time in the PIOPED study. The same study also found that a low probability scan in the presence of low clinical suspicion was only falsely negative in 6% of the patients. However, this leaves a large number of cases in which there is either a moderate clinical suspicion, an intermediate scan, or a discrepancy between pre-test clinical suspicion and final test results. Therefore, more invasive tests such as pulmonary angiography must often be used for a definitive diagnosis. \n\nThe chest X-ray is also an important tool in the evaluation a patient with a suspected PE. In addition to being used in the interpretation of the V/Q scan as mentioned above, chest x-rays are often useful in determining that the cause of the patient's signs and symptoms is due to a condition other than PE. For example, a fractured rib or cavitary lung lesion may present in a manner similar to PE. In relatively uncommon situations, radiologic findings on chest X-ray such as decreased vascular markings distal to engorged arteries (Westermark's sign) or a wedge-shaped pleural based infiltrate (Hampton's hump) may lead to the diagnosis of PE.", "ACR Code": "6.7", "Category": "Vascular", "Keywords": "pulmonary embolism", "Reference": "1. PIOPED Investigators. Value of the ventilation/perfusion scan in acute pulmonary embolism: results of the prospective investigation of pulmonary embolism diagnosis (PIOPED). JAMA 1990; 263:2753-2759.\n2. Maki DD, Gefter WB, Alavi A. Global theme issue: emerging technology in clinical medicine. Chest 1999; 119:1388-1401.\n3. Baker WF. Diagnosis of deep venous thrombosis and pulmonary embolism. Med Clin N Am 1998; 82:459-474.\n4. Tintinalli JE, Kelen GD, Stapczynski JS. Emergency medicine: a comprehensive study guide, fifth ed McGraw-Hill. 2000.\n5. Murray IP, Ell PJ. Nuclear medicine in clinical diagnosis and treatment, second ed Churchill Livingstone. 1998.", "External Links": "www.vh.org/Providers/Textbooks/ElectricPE/ElectricPE.html" } }, { "U_id": "MPX2487", "TAC": [ "MPX2487_synpic35909", "MPX2487_synpic35911", "MPX2487_synpic35913", "MPX2487_synpic35914" ], "MRI": [], "Case": { "Title": "Intestinal Malrotation", "History": "77 yo female presents to emergency department for worsening abdominal pain", "Findings": "Axial CT images with contrast show the entire small bowel in Right side of abdomen, and large bowel in Left side of abdomen. There is inversion of SMV-SMA relationship with the SMV located to the Left of the SMA.", "Differential Diagnosis": "Intestinal Malrotation\nIntestinal non-rotation\nIntestinal Malrotation with midgut volulus", "Case Diagnosis": "Intestinal Malrotation", "Diagnosis By": "CT Scan", "Treatment & Follow Up": "The patient was admitted for observation. Surgery was not performed.", "Discussion": "Intestinal malrotation is a congenital anomaly which usually presents in infancy, with bilious vomiting in the first month of life. It is rare for malrotation to present in adulthood. Symptomatic adults usually present with acutely or chronic bowel obstruction, chronic vague abdominal pain, or intestinal ischemia with midgut volulus. \n\nCT scan findings of Intestinal malrotation include right-side small bowel, left-sided colon; inversion of SMV-SMA complex with SMV either vertical or left sided SMV. The direction of the jejunal vessels can also be determined going in a rightward direction.\n\nThe ascending colon gradually becomes fixed to the posterior abdominal wall, losing its free mesentery. Peritoneal bands of fibrosis that fix the cecum to the right lateral abdominal wall (Ladd\u2019s bands) run anterior to the duodenum and may cause compression and obstruction of the duodenum.\n\nLadd\u2019s procedure is performed to correct the intestinal malrotation. In the Ladd\u2019s procedure there is division of ladd\u2019s bands, mobilization of right colon and duodenum, division of adhesions around the SMA and appendectomy may be performed. \n\nLadd\u2019s procedure is recommended for all children with diagnosed malrotation and symptomatic adults may also have the surgery for resolution of pain. It is controversial if an asymptomatic adult with malrotation should have the surgery." }, "Topic": { "Title": "Intestinal Malrotation", "Disease Discussion": "Common Locations: Abdomen\n\nDemographics: Infants and children\n\nRadiology: \nDiagnosis can be made by upper GI series, barium enema, and CT scan\n\nPrognosis and Treatment: \nLadd\u2019s procedure is performed to correct the intestinal malrotation. In the Ladd\u2019s procedure there is division of ladd\u2019s bands, mobilization of right colon and duodenum, division of adhesions around the SMA and appendectomy may be performed.", "ACR Code": "7.1", "Category": "Congenital, malformation", "Keywords": "Intestinal malrotation" } }, { "U_id": "MPX2492", "TAC": [ "MPX2492_synpic31013" ], "MRI": [], "Case": { "Title": "Clinically insignificant hiatal hernia.", "History": "75 yo smoker presents for CT follow-up of pulmonary nodules", "Exam": "No pertinent exam or laboratory information", "Findings": "Small Type 1 hiatal hernia (aka axial or sliding hiatal hernia)", "Differential Diagnosis": "Hiatal Hernia\nParaesophageal Hernia", "Case Diagnosis": "Clinically insignificant hiatal hernia.", "Diagnosis By": "N/A", "Treatment & Follow Up": "Treatment not indicated at this time as there are no clinically significant symptoms or complications", "Discussion": "One study has shown that up to 7% of patients scanned with CT for Virtual Colonoscopy were found incidentally to have hiatal hernias. (Hellstrom et al 2004)" }, "Topic": { "Title": "Hiatal Hernia", "Disease Discussion": "In the United States and Canada, a large proportion of adults undergoing upper gastrointestinal barium radiographs are found to have a small hiatal hernia. About 90% to 95% of hiatal hernias found by radiograph are sliding hernias, and the rest are paraesophageal or mixed. Most sliding hiatal hernias are small and of little clinical significance. Patients with symptomatic paraesophageal hernias are most often middle-aged to elderly. Many patients with small, simple sliding hiatal hernias are asymptomatic. The main clinical significance of the sliding hiatal hernia is its contribution to gastroesophageal reflux . In addition to heartburn and regurgitation, patients with large sliding hiatal hernias may complain of dysphagia or discomfort in the chest or upper abdomen. In a prospective, population-based study the risk of iron-deficiency anemia was found to be increased in adults with hiatal hernia. On chest radiograph a hiatal hernia may be noted as a soft tissue density in the retrocardiac area. Hiatal hernias are most often diagnosed on upper gastrointestinal barium radiographic studies. At endoscopy the gastroesophageal junction is noted to be proximal to the impression of the diaphragm. [1]\n\nPatients with paraesophageal and mixed hiatal hernias are rarely completely asymptomatic if closely questioned. About half of patients with paraesophageal hernias have gastroesophageal reflux. Other symptoms include dysphagia, chest pain, vague postprandial discomfort, and shortness of breath. A substantial number of patients have chronic gastrointestinal blood loss. If the hernia is complicated by gastric volvulus, acute abdominal pain and retching will occur, often progressing rapidly to a surgical emergency. A paraesophageal or mixed hiatal hernia may be seen on chest radiograph as an abnormal soft tissue density (often with a gas bubble) in the mediastinum. Upper gastrointestinal radiograph is the best diagnostic study. [1]\n\nHiatal hernias are occasionally complicated by volvulus. The stomach is normally fixed in position by ligamentous attachments to the duodenum, spleen, liver, and diaphragm. Laxity of these ligaments, elevation of the left hemidiaphragm, adhesions, gastric tumor, or masses in adjacent organs may predispose to volvulus. In about one third of cases the volvulus occurs below the diaphragm. In the other two thirds of cases volvulus occurs above the diaphragm in association with a diaphragmatic hernia. Sliding hiatal hernias are not associated with gastric volvulus. Gastric volvulus may be mesenteroaxial or organoaxial. In about 60% of cases gastric volvulus is organoaxial: the stomach twists along its long axis. This axis usually passes through the gastroesophageal and gastropyloric junctions. The antrum rotates anteriorly and superiorly, the fundus posteriorly and inferiorly, twisting the greater curvature at some point along its length. This type of volvulus is commonly associated with a diaphragmatic hernia. Organoaxial volvulus is usually an acute event. Vascular compromise and gastric infarction may occur. The other major type of gastric volvulus is mesenteroaxial, in which the stomach folds on its short axis running across from the lesser curvature to the greater curvature, and the antrum twists anteriorly and superiorly. [1]\n\nSimple sliding hiatal hernias do not require treatment. Patients with symptomatic giant sliding hiatal hernias, paraesophageal, and mixed hernias should be offered surgery. Many experts suggest that surgery should be offered to patients with asymptomatic paraesophageal hernias, because about 30% of these patients will develop complications if left untreated. Many surgeons routinely perform a fundoplication on all repairs, both to prevent postoperative reflux esophagitis and to fix the stomach in the abdomen. Less commonly a gastrostomy is used to fix the stomach in position. Patients with sliding hiatal or paraesophageal hernias may have shortening of the esophagus. This makes it difficult to restore the gastroesophageal junction below the diaphragm without tension. In such cases an extra length of neoesophagus can be constructed from the proximal stomach (Colles-Nissen procedure). Paraesophageal and mixed hernias can be repaired through the chest or abdomen, with open or laparoscopic techniques. Compared with open repair, laparoscopic repair is associated with less blood loss, fewer overall complications, shorter hospital stay, and quicker return to normal activities. Long-term results are probably equal with either approach. Potential surgical complications include esophageal and gastric perforation, pneumothorax, and liver laceration. Potential long-term complications may include dysphagia if the wrap is too tight or gastroesophageal reflux if the fundoplication breaks down or migrates into the chest. Recurrence rates are about 10 [1]\n \n\n1. Feldman: Sleisenger & Fordtran's Gastrointestinal and Liver Disease, 7th ed., Copyright \u00a9 2002 Elsevier: MD Consult Online Core Collection Textbook: pp 369-374", "ACR Code": "7.9", "Category": "Hernia/herniation", "Keywords": "hiatal herniagastric volvulusdiaphragmatic hernia", "Reference": "1. Feldman: Sleisenger & Fordtran\\'s Gastrointestinal and Liver Disease, 7th ed., Copyright \u00a9 2002 Elsevier: MD Consult Online Core Collection Textbook: pp 369-374" } }, { "U_id": "MPX2500", "TAC": [ "MPX2500_synpic23570", "MPX2500_synpic23571", "MPX2500_synpic23573" ], "MRI": [], "Case": { "Title": "Acute Appendicitis", "History": "59 year old male \nRecent onset of right lower quadrant pain", "Exam": "Evevated tempurature\nRight lower quadrant tenderness and guarding\nElevated white blood cell count", "Findings": "The appendix is strikingly enlarged. An oval appendicolith is seen obstructing the proximal aspect of the appendix. High density debris is seen in the distal appendix as well. Small bubbles of air are seen anterior to the lumen of the appendix may be intramural or intraperitoneal. Minimal fat stranding is seen in the surrounding fat. The walls of the cecum and terminal ileum are significantly thickened.\n\nImpression:\nRuptured acute appendicitis with associated appendicolith.", "Differential Diagnosis": "Acute Appendicitis\nMucinous tumor of the appendix", "Case Diagnosis": "Acute Appendicitis", "Diagnosis By": "At surgery", "Treatment & Follow Up": "Appendectomy" }, "Topic": { "Title": "Acute appendicitis", "Disease Discussion": "Appendicitis occurs most frequently in the 2nd to 3rd decade of life, less commonly in the extremes of age. Pain is usually the initial presenting complaint and often starts in the peri-umbilical region before migrating to the right lower quadrant with maximal tenders often located at McBurney\u2019s point. This typical sequence is absent in more than 1/3 of older children. Often pain is worse with movement, coughing (cough sign) driving over bump (cat\\'s eye sign), or standing on toes and dropping heels to ground (heel drop sign) (Rothrock). Vomiting occurs in the majority of school-aged children and may precede or begin concurrent with pain. Physical exam often reveals an elevated temperature and tenderness to palpation in the right lower quadrant. However, tenderness may involve the entire lower abdomen, or may be diffuse, especially with a perforation. Compared with those with non-perforated appendicitis, children with perforated appendicitis are significantly younger, have a longer duration of symptoms before diagnosis, have more physician visits before correct diagnosis, have higher temperatures, and are more likely to exhibit vomiting, diffuse abdominal tenderness, and peritoneal signs (Rothrock). Perforation generally occurs 36 to 48 hours after the onset of symptoms. Plain abdominal radiographs have been recommended as potentially useful for evaluating children with suspected appendicitis. Radiographic findings believed to be suggestive of appendicitis include rightward scoliosis, soft tissue masses, localized ileus, bowel obstruction, calcified fecolith, and free peritoneal fluid. Of these features, the most specific for appendicitis is a calcified fecolith (appendicolith) found in up to 13% to 22% with appendicitis and in only 1% to 2% of those without (Rothrock). While often recommended, these films rarely altered a patient\\'s diagnosis or management. Ultrasonography is appropriate in patients in which the diagnosis is unclear by history and physical examination, especially in pediatric and female patients. A normal appendix must be identified to rule out appendicitis. An inflamed appendix usually measures greater than 6 mm in diameter, is non-compressible and tender with focal compression (Hardin). Numerous other right lower quadrant conditions such as inflammatory bowel disease, cecal diverticulitis, Meckel\\'s diverticulum, endometriosis and pelvic inflammatory disease can cause false-positive ultrasonography results (Hardin). Appendiceal CT is more accurate than ultrasound and consists of a focused, helical CT after a Gastrografin-saline enema. It can be performed and interpreted usually within an hour. The accuracy of CT is due in part to its ability to identify a normal appendix better than ultrasound. If appendiceal CT is not available, standard abdominal/pelvic CT with contrast remains useful and may still be more accurate than ultrasound (Hardin). The standard for management of appendicitis remains appendectomy. The procedure may be performed by laparotomy (usually through a small right lower quadrant incision) or laparoscopy. While laparoscopic intervention is advantageous in adults due to decreased postoperative pain, earlier return to normal activity and better cosmetic results, an open appendectomy remains the primary approach to treatment in children due to their smaller size (Rothrock).\n\nhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=15155894", "ACR Code": "7.2", "Category": "Infection, bacteria", "Keywords": "appendicitis", "Reference": "Contran, et al. Robbins: Pathologic Basis of Disease, 6th ed. 1999, W.B Saunders Co.\n\nHardin DM Jr: Acute appendicitis: review and update. American Family Physician. 1-Nov-1999; 60(7): 2027-34\n\nRothrock SG: Acute appendicitis in children: emergency department diagnosis and management. Annals of Emergency Medicine. 01-Jul-2000; 36(1): 39-51", "External Links": "www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=15155894" } }, { "U_id": "MPX2498", "TAC": [ "MPX2498_synpic24417", "MPX2498_synpic24418", "MPX2498_synpic24419", "MPX2498_synpic24420", "MPX2498_synpic24421", "MPX2498_synpic24423" ], "MRI": [], "Case": { "Title": "Right aortic arch with aberrant left subclavian artery", "History": "Vomiting 4 days prior, now with cough and chest pain.", "Exam": "N/A", "Findings": "Initial PA/Lateral images of the chest show a right sided aortic arch without other focal abnormality. CT confirms a right sided arch with aberrant left subclavian artery. Of note is a very prominent diverticulum at the origin of the aberrant left SCA.", "Differential Diagnosis": "Right arch versus Double aortic arch. Mirror image branching vs. aberrant left subclavian artery.", "Case Diagnosis": "Right aortic arch with aberrant left subclavian artery", "Diagnosis By": "CT scan", "Treatment & Follow Up": "None", "Discussion": "Asymptomatic patient with relatively common anomaly of aortic arch. No further follow up needed." }, "Topic": { "Title": "Left aortic arch with aberrant right subclavian artery", "Disease Discussion": "This is the most common malformation of the aortic arch resulting in a complete vascular ring around the trachea and esophagus.The most common type of right aortic arch is right aortic arch with an aberrant left subclavian artery and it is 2-3 times more common than right arch with mirror image branching of the brachiocephalic vessels. Right arch and aberrant left subclavian artery has a 5-12% incidence of associated congenital heart disease while right arch with mirror branching of the brachiocephalic vessels has a 98% incidence of associated congenital heart disease.\n \n\nTwo types:\n1.Origin of the left subclavian artery from a posterior aortic diverticulum from which a ductus arteriosus extends to the left pulmonary artery. The retroesophageal part of the ring is large and compression is produced by the diverticulum (Diverticulum of Kummerell).\n\n2.Origin of the left subclavian artery from the descending aorta with a left ductus connecting the left subclavian artery to the left pulmonary artery. The retroesophageal part of the ring is small.\n \nIn both types of aberrant subclavian arteries, the vessel runs behind the esophagus.\n\nDefinitive diagnosis is now usually accomplished by CT or MRI. Both display the severity of airway narrowing and the retro-esophageal aberrant artery.Both demonstrate the large aortic diverticulum invariably at the site of airway compression with an aberrant left subclavian artery.", "ACR Code": "562.1532", "Category": "Congenital, malformation", "Keywords": "Right aortic archaberrant left subclavian arterydysphagia", "Reference": "http://www.amershamhealth.com/medcyclopaedia/Volume%20VII/AORTIC%20ARCH%20ANOMALIES.asp", "External Links": "www.amershamhealth.com/medcyclopaedia/Volume%20VII/AORTIC%20ARCH%20ANOMALIES.asp" } }, { "U_id": "MPX2506", "TAC": [ "MPX2506_synpic21439" ], "MRI": [], "Case": { "Title": "Pancreatic adenocarcinoma", "History": "55 year old male presented to his primary care doctor with weight loss and abdominal discompfort.", "Findings": "Axial CT images after administration of intravenous contrast demonstrate a mass in the head of the pancreas with dilated pancreatic ducts. A more superior image through the liver shows dilated intrahepatic biliary tree secondary to obstruction of the common bile duct by pancreatic mass", "Differential Diagnosis": "Pancreatic malignancy\nAcute pancreatitis", "Case Diagnosis": "Pancreatic adenocarcinoma", "Diagnosis By": "Surgical resection", "Treatment & Follow Up": "No follow up available for this case." }, "Topic": { "Title": "Pancreatic adenocarcinoma", "Disease Discussion": "Pancreatic adenocarcinoma is associated with a dismal prognosis, with 5 year survival rates of only 3%. About 10-15% of patients have resectable disease, with resection being the only hope of long-term cure/survival. On CT, findings include a predominantly hypodense mass which only minimally enhances compared to the normal pancreatic parenchyma, loss of the expected lobulated marginal surface of the normal pancreas, blunting of the uncinate process, dilatation of the pancreatic and biliary ducts, and associated pancreatitis. Resectable lesions often show a single focal mass without ductal dilatation or ductal dilatation without an identifiable mass lesion. Unresectable tumors show extension, invasion of adjacent organs or vascular structures, associated adenopathy, liver metastases, and ascites. One mimic of a pancreatic mass is focal pancreatitis. Biopsy is sometimes performed to confirm that a lesion represents carcinoma and not pancreatitis (1).", "ACR Code": "7.3", "Category": "Neoplasm, carcinoma", "Keywords": "PancreasPancreatic massPancreatic cancer", "Reference": "1. Webb WR, Brant WE, and Helms CA. Fundamentals of Body CT, 2nd ed. WB Saunders: St. Louis; 1991: 227-230." } }, { "U_id": "MPX2508", "TAC": [ "MPX2508_synpic17381" ], "MRI": [], "Case": { "Title": "Arteriovenous Fistula (angiographically confirmed)", "History": "54 YO male with hx of CAD with PCTA x2 presented to the emergency department with abdominal pain. Contrast-enhanced CT was obtained which was unremarkable, but had an incidental finding noted in the most proximal portion of the imaged RLE.", "Exam": "Non-contributory.", "Findings": "CECT of the pelvis demonstrated an incidental finding of abnormal contrast concentration within the right femoral vein during the arterial phase of enhancement. Subsequent angiogram demonstrated abnormal early opacification of the IVC during flush aortagram as well as abnormal communication between the right profunda femoris artery and femoral vein.", "Differential Diagnosis": "AVF", "Case Diagnosis": "Arteriovenous Fistula (angiographically confirmed)", "Treatment & Follow Up": "Patient was referred to vascular surgery for further evaluation and management." }, "Topic": { "Title": "Arteriovenous Fistula", "Disease Discussion": "Arteriovenous fistulas (AVFs) are abnormal connections between arteries and veins that bypass the normal anatomic capillary beds. AVFs of the lower extremity can be divided into congenital and acquired causes. Iatrogenic causes, primarily occurring during cardiac catheterization, are the most common etiology. These may ensue when a needle tract crosses both femoral the artery and vein, and is then dilated during catheterization, creating a communication between the vessels after catheter removal. In three large series from experienced cardiac catheterization centers, the incidence of AVF was 0.1-0.2%. Similar values have been noted with the use of arterial closure devices. Other femoral arterial complications include pseudoaneurysm formation, hematoma, groin hemorrhage that may require transfusion, and arterial occlusion. Risk factors for AVF formation during catheterization include low femoral arterial puncture, large arterial sheath size, older age, and prolonged anticoagulation or fibrinolytic therapy. The incidence is higher in therapeutic compared to diagnostic catheterization (0.9 versus 0.2% in one report).\n\nAlmost all AVFs are clinically silent early in the postcatheterization period. If untreated, the time of onset of clinical presentation ranges from two days to several months after catheterization. Clinical complications include lower extremity edema, varicose veins, nerve compression, the development of or worsening of intermittent claudication, and rest pain secondary to distal ischemia. The most significant complication is the development of high-output heart failure which, in an older report, was estimated to occur after 0.01 to 0.02 percent of cardiac catheterizations.\n\nEarly diagnosis is dependent upon careful examination of the groin area, with evaluation for a femoral bruit, large hematoma, decreased or absent lower extremity pulses, or a groin pulsatile mass. Any of these findings is suggestive of a vascular complication and needs to be investigated further. Prior to the development and widespread use of ultrasound-Doppler technology, AVFs were suspected on clinical findings and diagnosed with an arteriogram. However, Doppler ultrasound is the current diagnostic test of choice in evaluating patients with suspected AVFs. The ultrasound image appears as a blush in the extremity and the connecting artery and vein can often be identified.\n\nBecause of greater awareness and ease of diagnosis, AVFs come to attention and, if necessary, are treated early. On the other hand, small AVFs are often monitored with ultrasound imaging. Indications for intervention are lack of spontaneous closure, increase in fistula size, and/or the development of symptoms. Surgical repair is the most common approach for fistulas that need closure, but other modalities have been evaluated. These nonsurgical alternatives may be particularly important in patients treated with aggressive antiplatelet therapy. One method is ultrasound-guided compression repair or closure (UGCR). This technique involves placing the ultrasound probe on the skin over the AVF and then compressing the area (usually for ten minute periods) with a sufficient force to abolish flow through the fistula without sacrificing distal perfusion of the leg. Compression results in stasis of blood in the fistula and secondary thrombosis. UGCR has been used successfully in pseudoaneurysms after cardiac catheterization, but only limited data are available for AVFs with variable success.\n\nPreliminary data suggest that percutaneous approaches also may prove to have a role. One report evaluated 53 patients, 21 with an AV fistula and most of the remainder with a pseudoaneurysm, who failed repeated attempts at UGCR. The patients were primarily treated with either implantation of a covered stent or coil embolization. The procedure was successful in 47 (89 percent). Follow-up documented closure of all lesions, but four late stent occlusions occurred at three to six months. This study and other early investigations are suggestive that percutaneous interventions such as stent placement or embolization may be effective measures to avoid surgical repair when UGCR fails to result in obliteration of the AVF.", "ACR Code": "9.4", "Category": "Vascular", "Keywords": "AVFcatherizationiatrogenic", "Reference": "Kesseler J, Mohler ER. Arteriovenous fistulas of the lower extremity. UpToDate Version 11.2:April,2003." } }, { "U_id": "MPX2512", "TAC": [ "MPX2512_synpic19965" ], "MRI": [], "Case": { "Title": "Bilateral jumped locked facets", "History": "33 year old woman was sitting on the trampoline while another person was bouncing on it. She was thrown into the air about 1 foot and was hyperflexed on landing.", "Findings": "More than 50% anterior subluxation of C5 on C6 with bilateral locked facets.", "Case Diagnosis": "Bilateral jumped locked facets", "Diagnosis By": "Radiologic Dx", "Treatment & Follow Up": "Bilateral locked facets of C5/6 resulted in almost complete quadriplegia with only minimal motor residual to left arm. The sensory loss was from T2 down. It is very unlikely that the patient will recover any motor or sensory deficits.\n\nLocked facets were almost completely reduced by applying cervical traction. The patient was then taken to surgery for vertebral fusion with bone graft (from pelvis).\n\nAfter recovery from surgery, patient was transferred to a rehabilitation center.", "Discussion": "It is important to consider the neurologic status and evaluate the spinal cord with MR if there are signs of cord compression." }, "Topic": { "Title": "Hyperflexion Injuries of the Cervical Spine", "Disease Discussion": "Hyperflexion injuries are a common mechanism of injury of the cervical spine, accounting for up to 46% of cervical spinal injuries, and include a spectrum of radiographic abnormalities. The mechanism of the hyperflexion injury is usually a significant force directed against the occiput, forcing the face towards the chest, and resulting primarily in distraction of the posterior structures, with a lesser force vector resulting in compression of the anterior column. The spectrum of injuries ranges from the relatively stable \u201chyperflexion sprain\u201d to the unstable flexion injuries (flexion teardrop fractures and bilateral locked/jumped facets). \n\nThe \u201chyperflexion sprain\u201d is a ligamentous injury associated with varying degrees of disruption of the posterior ligaments (progressively involving the supraspinous ligaments, interspinous ligaments, facet joint capsules, and posterior longitudinal ligament, respectively), usually without associated fractures. These patients present with persistent pain, muscle spasms and, occasionally, mild reversible neurologic defects. Radiographic abnormalities, when they are present, include widening of the interspinous distance or posterior aspect of the apophyseal joints, and/or localized kyphotic angulation of the cervical spine. \n\nOccasionally, a pure hyperflexion injury of the cervical spine completely spares the posterior ligaments and results only in osseous disruption of the anterior column, manifesting as either avulsion of the anterior portion of the superior vertebral ring (in the immature skeleton) or simple compression fractures of one or more vertebrae (in adults).\n\nAnother stable hyperflexion injury of the C-spine is the clay-shoveler\u2019s fracture, an oblique fracture of one or more of the spinous processes of the sixth cervical through third thoracic vertebrae, from avulsion by the supraspinous ligament.\n\n============== UNSTABLE INJURY ================\nAs previously mentioned, bilateral locked/jumped facets are one example of an unstable hyperflexion injury and result from rupture of the posterior portion of the annulus fibrosus, the posterior longitudinal ligament, and the capsular, interspinous, and supraspinous ligaments. Destabilization of the ligamentous support-structure of the spine allows such severe anterolisthesis of the cephalad portion of the cervical spinal column that facet locking occurs, with resultant severe narrowing of both the spinal canal and intervertebral neural foramina. Consequently, this injury pattern is invariably associated with neurologic deficits (75 percent of cases). The radiographic hallmark of bilateral jumped/locked facets is greater than 50% (half the width of the vertebral body) of anterior displacement of the superior vertebra, as demonstrated on the lateral radiograph. Associated osseous injuries include avulsion fractures of the spinous process above the locked level, and triangular fractures of the anterosuperior corner of the inferior vertebral body.\n\nA second type of unstable hyperflexion C-spine injury is the flexion teardrop fracture, which typically results from the combination of flexion and axial loading. This injury manifests radiographically as an anteroinferior (teardrop) fracture fragment of a lower cervical vertebra (most commonly C5). The teardrop fragment may be large and frequently retains anatomic alignment with the adjacent inferior vertebral body or shows minimal anterior and downward displacement, while the larger posterior fragment shows posterior displacement relative to the vertebra below. Frequently, concomitant sagittal fractures through the vertebral body and laminae (associated with axial loading) are also present.\n \n=============== ADDITIONAL PEARLS: \n\nIf the flexion force is associated with a rotational component, either a unilateral perched facet or a unilateral locked facet may result.. This category of C-spine injuries accounts for approximately 12% of the total.\n\nThe other C-spine hyperflexion injuries are: anterior subluxation, vertebral compression, flexion teardrop fracture, and spinous process (clay shoveler\u2019s) fracture.", "ACR Code": "3.4", "Category": "Trauma", "Keywords": "flexion injuriesjumped facetslocked facets", "Reference": "McCort JJ, ed. Trauma Radiology. New Youk, Churchill Livingstone, Inc, 1990; pp. 31-74.\n\nResnick D. Bone and Joint Imaging, Second Edition. Philadelphia, W.B. Saunders Company, 1996; pp. 805-808." } }, { "U_id": "MPX2501", "TAC": [ "MPX2501_synpic43616", "MPX2501_synpic43617", "MPX2501_synpic43618", "MPX2501_synpic43619", "MPX2501_synpic43621", "MPX2501_synpic43622", "MPX2501_synpic43623", "MPX2501_synpic43624", "MPX2501_synpic43625", "MPX2501_synpic43626", "MPX2501_synpic43627", "MPX2501_synpic43628" ], "MRI": [], "Case": { "Title": "Crossed fused ectopia", "History": "72 Y/O MALE with hematuria.", "Exam": "RBC's noted on UA.", "Findings": "There is a lobular contour to the single right kidney with separate collecting systems which fuse proximally with congenital megaureter present distally.", "Differential Diagnosis": "N/A.", "Case Diagnosis": "Crossed fused ectopia", "Diagnosis By": "CT", "Treatment & Follow Up": "Congenital variant.", "Discussion": "Crossed fused renal ectopia is a congenital anomaly which is normally asymptomatic. It does however, place the patient at greater risk in the event of injury to the single kidney. In this case, the CT demonstrates the anomaly but does not reveal the etiology of the patient's hematuria." }, "Topic": { "Title": "Crossed fused ectopia", "Disease Discussion": "Crossed Fused Ectopia (CFE) is seen in 1/1000 to 1/1500 autopsies. In 85-90% of patients with ectopic kidney will be fused. CFE is believed to occur when either there is a failure of nephrogenic cells to separate or fusion of 2 blastemas during abdominal ascent. Typically the lower kidney is malrotated and both pelves point toward midline. The ureter of the ectopic kidney crosses midline and enters the bladder on the contralateral side. There are no known congenital anomalies associated with CFE.\n\nTypically CFE is asymptomatic and is an incidental finding. There can be an higher risk of injury the the ectopic kidney if it overlies the spine.", "ACR Code": "8.9", "Category": "Congenital, malformation", "Keywords": "ectopicfused", "Reference": "Rumack, C., Diagnostic Ultrasound, 2nd Ed, pp 336-337.\nKurtz, A, Ultrasound, 1996, pp 75-76." } }, { "U_id": "MPX2507", "TAC": [ "MPX2507_synpic50867", "MPX2507_synpic50868", "MPX2507_synpic50869", "MPX2507_synpic50870" ], "MRI": [ "MPX2507_synpic50871", "MPX2507_synpic50872", "MPX2507_synpic50873", "MPX2507_synpic50874" ], "Case": { "Title": "Hepatic adenoma", "History": "28 y/o woman with no significant medical hx only taking OCP presented with dysuria, polyuria, & left flank pain.", "Exam": "Physical exam left costovertebral pain upon palpation\n \nUA Trace Leuko Est, Large Blood, 30mg/dl of protein, & WBC of 13.\nUA Culture positive for multiple bacterial growth \n\nLDH 377 U/L\nAST 36 U/L\nALT 29 U/L\nAFP 0.7 U/L", "Findings": "CT findings consistent with acute pyelonephritis involving left kidney. A large solid heterogeneously enhancing mass 14.1 x 9.9 x 14.6 cm is seen in the left upper quadrant which is associated with the left lobe of the liver displacing the spleen infra-medially. Some lower attenuating areas near the center of this lesion may represent necrosis. No calcification or cystic components. Prominent vessels are seen at the periphery of the lesion near the left lobe of the liver. The remainder of the liver demonstrates multiple round hypoattenuating foci of varying sizes, many of which are too small to characterize. \n \nMRI shows multiple lesions in the liver with the largest in the left lobe with similar imaging appearances as in the CT.", "Differential Diagnosis": "Hepatocellular Adenoma (HA)\nFocal Nodular Hyperplasia (FNH)\nHemangioma\nHepatocellular Carcinoma (HCC)\nFibrolamellar Carcinoma\nHepatic Metastases\nCholangiocarcinoma\nLiver Abscess", "Case Diagnosis": "Hepatic adenoma", "Diagnosis By": "Surgical Resection and pathologic examination", "Treatment & Follow Up": "The pt's pyelonephritis was treated with antibiotics successfully.\n\nHowever, the incidental finding of the left lobe hepatic mass was ultrasound guided biopsied that was indeterminate for hepatic adenoma, HCC, or FNH the pt was sent to surgery for surgical resection of the mass. Pt improved s/p surgery and is doing well.", "Discussion": "Hepatocellular adenomas (HA) are usually large, fatty, well circumscribed, nonlobulated, encapsulated tumors. HA are typically solitary in nature, but ~20% are multiple. They typically do not have bile ducts or portal vein areas. They are typically rows of heapatocytes. HA can develop central necrosis and hemorrhage because the vascular supply is often restricted to the outer surface of the tumor. Typically in young woman using oral contraceptives pills (OCP) HA is one of the more common hepatic neoplasm as in this patient. Also, individuals with hemochromatosis , glycogen storage disease, acromegaly, and anabolic steroids users with a hepatic mass are likely to be HA as well. Some believe that the OCP & anabolic steroids lead to generalized vascular ectasia of the liver leading to the development of HA. 80% of adenomas are solitary and 20% are multiple.\n\nComputed Tomography (CT) in triple phase liver dedicated study demonstrate most HA as a lesion with homogeneous enhancement in the late arterial phase, that will stay isodense to the liver in later phases. However, these findings in the late arterial phase are not specific to adenomas, since hepatocellular carcinoma (HCC), hemangiomas, hypervascular metastases, & focal nodular hyperplasia (FNH) can show similar enhancement in the arterial phase. The finding of hemorrhage as an area of high attenuation can be seen in as many as 40% of adenomas. Fat deposition within adenomas is often difficult to identify on CT and is better visualized on magnetic resonance imaging (MRI).\n\nDue to the risk of intraperitoneal hemorrhage of the HA & the rare occurrence of malignant transformation to HCC, surgical resection has been advocated as the best solution for patients with presumed HA as was done in this case. Percutaneous fine needle biopsy of a mass suspicious for HA is controversial because of a significant risk hemorrhage & difficult to distinguish from FNH histologically (FNH does not require surgical resection), however, was still performed in this case, but diagnosis could not be made from biopsy. Also, HA may also decrease in size if not disappear after OCPs have been stopped, in this pt the lesion was felt to be too large to pursue this treatment. \n\nReference:\nRichard Baron. \u201cLiver : Masses Part II : common liver tumors\u201d. Radiology department of Univ of Chicago. http://www.radiologyassistant.nl/en/448eef3083354." }, "Topic": { "Title": "Hepatic adenoma", "Disease Discussion": "Hepatic adenoma is a rare benign liver tumor that occurs in patients that take oral contraceptives, anabolic steroids or have glycogen storage disease. These tumors are usually 5-10 cm in size, have a capsule and are made up of benign hepatocytes. \n\nOn CT, hepatic adenomas usually are well defined and hypoattenuating. They demonstrate early enhancement. On MRI, hepatic adenomas can be hyperintense, hypointense or isointense on T1. On T2 they are isointense to hyperintense. Early arterial enhancement is seen with the lesion appearing isointense on delayed images.\n\nDifferential diagnosis includes focal nodular hyperplasia, fibrolamellar hepatocellular carcinoma and hypervascular metastatic disease. Focal nodular hyperplasia is typically isointense on T1 and T2 images. There is also early enhacment seen. However, a central scar is usually seen in FNH and not in hepatic adenomas. Fibrolamellar HCC is usually large, heterogeneous, and contains calcificaltions. Lymphadenopathy is seen in majority of patients. In metastatic disease, there are usually multiple lesions that are T1 hypointense, T2 markedly hyperintense. Fat and hemorrhage is common in adenomas but rare in metastases.\n\nTreatment of hepatic adenomas is controversial. It usually involves cesation of oral contraceptives. Some literature advocates removal of the lesion due to risk of hemorrhage and malignant transformation.", "ACR Code": "7.3", "Category": "Neoplasm, benign", "Keywords": "Hepatic adenoma", "Reference": "1. Webb WR, Brant WE, Major NM. Fundamentals of body CT. Saunders. 3rd edition. 2006.\n2. Grazioli L, Federle MP, Brancatelli G, et al. Hepatic adenomas: imaging and pathologic findings. Radiographics 2001;21:877-894.\n3. Horton KM, Bluemke DA, Hruban RH et al. CT and MR imaging of benign hepatic and biliary tumors. Radiographics 1999;19:431-451." } }, { "U_id": "MPX2515", "TAC": [ "MPX2515_synpic28376", "MPX2515_synpic28377" ], "MRI": [], "Case": { "Title": "Ruptured Appendicitis", "History": "18yo man presents to the ER c/o 5d of RLQ abdominal pain and nausea. The patient states that his siblings have had flu-like illnesses recently with nausea and vomiting, so he initially attributed his symptoms to a virus. However, over the last 5 days the pain has progressively worsened. Pain is described as intermittent, stabbing, improved with Tylenol, and aggravated by movement. The patient has never had pain like this before. \n\nROS: significant for RLQ abdominal pain, nausea, 1 episode of non bloody, non bilious vomiting 2 days prior to admission, and subjective chills. Denies fevers, diarrhea, hematochezia, or dysuria.", "Exam": "Vitals: Temp: 103.1, BP 132/71, HR 88, RR 30, O2 sat 995 on RA\n\nGeneral: Thin appearing male laying still on exam table, in tears due to pain\nHeart: No murmurs\nLungs: Clear to auscultation BL, no wheezes or rhonchi\nAbdomen: No discoloration, no distension. + bowel sounds. Tender to percussion and palpation over McBurney\u2019s point. No rebound tenderness. + Rovsing\u2019s sign.\nGenitalia: Normal ext male genitalia, testes descended\nRectal: Normal tone, no masses, tender with pressure aimed towards RLQ, no masses.\n\nCBC: 12.1 > 15.5/45.6 < 166\nCMP: 139/4.4/102/30/17/1.0/100\nCa: 9.2 AST: 13 ALT: 29 AP: 84\nUA: Yellow, clear, SG 1.026, Ph 6.0, neg prot, ket, gluc, bili, nitrite, LE. \n1-3 WBC, Mod Blood, 4-10 RBC, squam 1-2/HPF", "Findings": "Supine and upright abdominal radiographs: No evidence of free air. Evidence of free fluid within the pelvis with indistinctness of the fat planes. Two calcifications are seen within the right pelvis, one measuring approximately 12mm and one measuring approximately 5 mm in size. Bowel gas pattern unremarkable, no air fluid levels\n\nAbdominal CT: The appendix is markedly enlarged and edematous. There is a\nlarge inflammatory mass surrounding the appendix. There is enhancement of\nthe wall of the appendix. There are two appendicoliths within the appendix,\none measuring 12 mm in greatest diameter and a smaller 6 mm appendicolith. \nThere is a moderate amount of free fluid within the pelvis. The appendix is\ndilated to a maximum diameter of 12.5 mm. There is no evidence of free air.", "Differential Diagnosis": "Appendicitis\nRuptured Appendicitis\nMesenteric Adenitis\nPsoas abscess\nUreteral Calculus", "Case Diagnosis": "Ruptured Appendicitis", "Diagnosis By": "CT of abdomen and open surgical removal of ruptured appendix with subsequent pathologic tissue examination.", "Treatment & Follow Up": "The patient was admitted and taken to the OR the evening of admission where he underwent an open appendectomy. The patient tolerated the procedure well, and was transferred to the surgical ward post op. On post op day 4 the patient had a normal white count, was tolerating a regular diet, and was transitioned to oral abx, oral pain medicine, and d/c to home.", "Discussion": "Since the first description of acute appendicitis in 1886 by Reginald Fitz, it has been recognized as one of the most common causes of the acute abdomen worldwide; with 250,000 cases yearly in the United States. Sixty five percent of patients that have symptoms of acute appendicitis for longer than 48 hours present with perforation of the appendix due to significant inflammation and necrosis. Perforation of the appendix can cause widespread intraperitoneal contamination or a sealed-off abscess, and can be lethal if not promptly recognized. The size of the perforation, the virulence of bacterial infection, and the ability of the infection to be contained will determine the extent of the inflammatory response. Abscesses are variable in size, have low attenuation numbers (10 to 30 Hounsfield units) and may display an identifiable capsule which signals chronicity. If the abscess is due to gas-forming bacteria or fistulization to bowel occurs, bubbles of air or air-fluid levels may be observed. Abscesses may be found in locations distant from the cecum due to variable position of the appendix and the patterns of fluid migration in the peritoneal cavity. Most abscesses are located inferior, medial, or posterior to the cecum or in the right paracolic gutter. \n\nIt has been suggested that imaging is not necessary if a patient presents with history and physical exam strongly suggestive of acute appendicitis. However, imaging is advisable for the patients with atypical symptoms, infants, small children, and young women\n\nRadiographs demonstrate some abnormality in up to 80% of patients with acute appendicitis. Appendicoliths are the most specific radiographic sign, but are only found in 10% of patients with acute appendicitis. However, when an appendicolith is present, the incidence of perforation is nearly 50%. Appendicoliths can be differentiated from bone islands, ureteral stones and pheleboliths by their calcified rims. In cases of retrocecal appendicitis, the appendicolith may be located in the right upper quadrant. Other radiographic findings suggestive of acute appendicitis are: cecal ileus, right lower quadrant fluid levels, paucity of right lower quadrant gas, distortion of flank stripe, loss of psoas margin, loss of properitoneal flank stripe, thickening of cecal wall, scoliosis, mottled gas collection in right lower quadrant, and pneumoperitoneum\n\nHigh resolution or helical CT techniques have been shown to be superior to radiographs in establishing the diagnosis of acute appendicitis due to high accuracy and sensitivity. CT scans have accuracy of 96% to 98%, sensitivity of 96% to 100%, specificity 95% to 97%, a PPV of 97% to 99%, and a NPV of 88% to 100%\nThe diagnosis of appendicitis can be made with confidence when an abnormal appendix is identified or when an appendicolith associated with a phlegmon or abscess is detected in the right lower quadrant. The abnormal appendix appears slightly distended, fluid filled structure about 0.5 to 2cm in diameter. In almost all cases of acute appendicitis, the appendiceal wall may display circumferential and asymmetrical thickening. Periappendicieal inflammation is another hallmark of acute appendicitis. The inflammatory response is variable and may show the following: Slightly increased hazy density of the mesenteric fat, linear strands, fluid containing abscesses, or heterogeneous ill defined soft tissue densities representing a phelgmon. A summary of findings of acute appendicitis seen on CT scan are listed below:\n\nCircumferential mural thickening of appendix \nMural contrast enhancement\nAppendicolith\nHazy, streaked periappendiceal densities\nPericecal soft tissue mass (phlegmon)\nPericecal fluid collection (abscess)\nMural thickening of adjacent cecum and terminal ileum \u201cArrowhead sign\u201d\nCecal bar\nFocal cecal apical thickening\nEnlarged lymph nodes\nPneumoperitoneum\n\nIn patients without acute appendicitis CT is also useful as it is able to diagnose other intra abdominal conditions. Using CT in patients with equivocal clinical presentations leads to a substantial decrease in the expected negative appendectomy rate. (4% compared to an expected 20% negative laparotomy rate based on clinical evaluation.)" }, "Topic": { "Title": "Ruptured Appendicitis", "Disease Discussion": "Ruptured Appendicitis", "ACR Code": "7.2", "Category": "Surgery, NOS", "Keywords": "AppendicitisRuptured", "Reference": "Gore, R., Levine, M. Textbook of Gastrointestinal Radiology, 2nd edition. WB Saunders. 2000, p 1125-37.\nFitz, RH. Perforating inflammation of the vermiform appendix with special reference to its early diagnosis and treatment. Am J Med Sci 1886; 92:321.\nAddiss, DG, Shaffer, N, Fowler, BS, Tauxe, RV. The epidemiology of appendicitis and appendectomy in the United States. Am J Epidemiol 1990; 132:910.\nHale, DA, Jaques, DP, Molloy, M, et al. Appendectomy. Improving care through quality improvement. Arch Surg 1997; 132:153.\nSchuler, JG, Shortsleeve, MJ, Goldenson, RS, et al. Is there a role for abdominal computed tomographic scans in appendicitis? Arch Surg 1998; 133:373." } }, { "U_id": "MPX2519", "TAC": [ "MPX2519_synpic34369", "MPX2519_synpic34370" ], "MRI": [], "Case": { "Title": "Massive Pulmonary Embolism", "History": "42 year old active duty female required resuscitation, intubation after an episode of unresponsiveness with no evidence of trauma.", "Exam": "EKG: Right ventricular heart strain\n\n>>Hypotension", "Findings": "Filling defects in both right and left main pulmonary arteries with defects continuing into small arterial branches in peripheral lung fields. Also present is a small right pleural effusion.", "Differential Diagnosis": "N/A", "Case Diagnosis": "Massive Pulmonary Embolism", "Treatment & Follow Up": "Patient was successfully anticoagulated with warfarin." }, "Topic": { "Title": "Massive Pulmonary Embolism", "Disease Discussion": "When a Pulmonary embolism is associated with a systolic pressure of less than 90 or a drop of 40 systolic pressure for more than 15 minutes, it is termed a massive PE. If the embolus is large enough, the patient may present in acute right ventricular heart failure and/or hypotension. In a patient with high clinical suspicion for PE a CT should be preformed as plain radiographs are almost always normal.", "ACR Code": "5.-1", "Category": "Vascular", "Keywords": "pumonary embolism", "Reference": "Hales CA, Thompson BT. Overview of acute pulmonary embolism (2006) www.uptodate.com" } }, { "U_id": "MPX2518", "TAC": [ "MPX2518_synpic39508" ], "MRI": [ "MPX2518_synpic39509", "MPX2518_synpic39510", "MPX2518_synpic39511", "MPX2518_synpic39512", "MPX2518_synpic39513" ], "Case": { "Title": "HSV Encephalitis", "History": "21 y/o soldier deployed to Iraq. Found down in barracks three days after being treated for non-specific viral illness.", "Exam": "Mental status changes, aphasia.", "Findings": "Bilateral temporal lobe involvement (L>R) with low attenuation on non-contrast CT, enhancement with gadolinium on T1, T2 hyper-intensity and restricted diffusion consistent with edema.", "Differential Diagnosis": "HSV encephalitis\nVZV encephalitis\nHHV-6 encephalitis\nEBV encephalitis\nvasculitis\nsyphilis\ntuberculous meningitis\nWNV", "Case Diagnosis": "HSV Encephalitis", "Diagnosis By": "PCR for HSV on CSF sample", "Treatment & Follow Up": "The patient received a 14 day course of iv acyclovir. He remained aphasic but otherwise responded well." }, "Topic": { "Title": "HSV Encephalitis", "Disease Discussion": "Lesions/Condition: HSV Encephalitis\n\nAssociations/Predisposing Factors: Prior HSV infection, primarily HSV-2 in neonates and HSV-1 after the neonatal period.\n\nCommon Locations: The limbic region is most freqently involved - temporal lobes, insula, subfrontal, and cingulate gyri. Involvlement is usually bilateral, but asymmetric. In infants and children, the imaging findings may be atypical, with predominant involvement of the cerebral hemispheres.\n\nDemographics: All ages can be affected, however, the highest incidence is in adolescents and young adults.\n\nHistology: May demonstrate mononuclear inflammation, perivascular cuffing, focal inflammatory infiltrates, microglial nodules, necrosis, macrophage infiltration.\n\nGross Appearance: Areas of hemorrhagic necrosis may be present.\n\nRadiology: Temporal lobe involvement is the most common finding, and there may be resultant mass effect. On CT, hypoattenuation may be seen in the temporal lobe, but MRI is the best imaging modality if herpes encephalitis is suspected. \n\nT1 weighted imaging may reveal mass efect and loss of grey white differentiation. Subacute hemorrhage may be seen, and if present will \"bloom\" on T2* GRE. T2 weighted imaging demonstrates increased signal in the involved regions, which is frequently bilateral but assymetric. There may be restricted diffusion on DWI. On post contrast imaging mild, patchy enhancement may be seen in the early phases. Meningeal enhancement is occasionally seen, and gyriform enhancement is usually seen 1 week after symptom onset.\n\nPrognosis and Treatment: 70% mortality if untreated. Even with treatment approximately 50% will have neurological deficit. Standard treatment consists of acyclovir iv 10 mg/kg three times daily for 14-21 days. Treatment should begin as soon as diagnosis suspected, and not delayed for imaging or laboratory confirmation.", "ACR Code": "1.2", "Category": "Infection, viral", "Keywords": "HSVEncephalitis", "Reference": "Osborne A. Diagnostic imaging: brain.Amirsys 2005. ppI8: 34-36.\nSmirniotopoulos JG et al.From the Archives of the AFIP: Patterns of Contrast Enhancement in the Brain and Meninges.\nRadioGraphics 2007; 27: 525-551." } }, { "U_id": "MPX2524", "TAC": [ "MPX2524_synpic17734", "MPX2524_synpic17736", "MPX2524_synpic17737" ], "MRI": [], "Case": { "Title": "Mature Cystic Teratoma", "History": "18 y.o. girl with distension of abdomen for 3 years, abdominal discomfort and reflux symptoms for 1-2 years.", "Exam": "Firm distension of upper abdomen.", "Findings": "Frontal abdominal radiographs demonstrated a well formed calcification in the left upper quadrant. A follow up CT scan revealed a 23x16x27cm cystic mass in the abdomen containing a focus of calcification and adjacent fat. The mass appeared to arise from the right ovary, ascending from the pelvis and pulling the right broad ligament, in turn causing rightward deviation of the uterus. A smaller left ovarian teratoma, measuring 4.0x3.7cm was seen to contain a larger fat content. All other abdominopelvic organs were displaced, but normal.", "Differential Diagnosis": "Dermoid, cystadenocarcinoma, abscess, endometriosis, any germ cell or other ovarian solid or cystic tumor.", "Case Diagnosis": "Mature Cystic Teratoma", "Diagnosis By": "Surgery, Histology", "Treatment & Follow Up": "Surgical removal", "Discussion": "Frontal abdominal radiographs were initially obtained which revealed a well-formed calcification overlying the left psoas stripe adjacent to L3. A subsequent CT scan was obtained which revealed bilateral mature cystic teratomas arising from both of the ovaries." }, "Topic": { "Title": "Mature Cystic Teratoma", "Disease Discussion": "Teratomas are germ cell tumors that typically present as large, benign (80%) or malignant (20%), mass lesions - usually containing variable amounts of fat, soft tissue, and fluid-filled cystic areas. Thirty percent contain calcifications. They vary from an almost entirely cystic mass to a predominately solid mass with internal cystic components.\n\nBenign (mature) cystic teratomas, often incorrectly termed \"dermoid cysts\", are usually found in female patients 10-30 years old - very common in the reproductive years. Teratoma is the most common ovarian tumor in children, adolescents, and young women (<30 years) with the majority presenting in adolescents. Fifteen to 25% of cases are bilateral. Most authors differentiate Dermoid cysts from Dermoids which are predominately cystic, but the presence of heterogeneous and varied tissue elements give them a complex and varied imaging appearance. \n\nTrue dermoids - unlike mature cystic teratomas - originate from ectoderm only and may contain hair, teeth, and sebaceous glands, whereas teratomas originate from multipotential germ cells that may and may contain any tissue element: ectoderm, mesoderm, and endoderm .\n\nTeratomas may also be found in the mediastinum, intracranially, or anywhere rests of multipotential germ cells were left during embryogenesis. In fact, teratomas are the most common congenital intracranial tumor. Additionally, teratomas are the most common benign mediastinal germ cell neoplasm and may be cystic or solid. The cystic teratomas are usually more mature and more common than the solid type which is usually malignant. \n\nBenign teratomas have a slight female predominance; and, malignant teratomas are seen almost exclusively in men. Malignant abdominopelvic teratomas may be accompanied by ascites, intraperitoneal spread, and metastasis to the liver. \n\nMalignant degeneration of a mature cystic teratoma is rare - but may occurs in 1-2% of cases. \n\nCommon complications of ovarian teratomas include torsion (ovarian) and hemorrhage.\n\nThe initial imaging modality is usually a sonographic study, as many patients present with abdominal pain. The mixture of sebum and hair within a mature teratoma is highly echogenic with acoustic shadowing that may totally obscure the back wall of a large mass, a finding known as the \u201ctip of the iceberg\u201d sign. However, calcification may not be easily detected on ultrasound and plain radiographs may be diagnostic of benign cystic teratomas by demonstrating well formed teeth or bone. A recognizable tooth within the mass is an almost pathognomonic finding. Plain film may also reveal a subtle well-defined mass of fat density. \n\nCT scan confirms the cystic, fatty, and calcified components and demonstrates a well circumscribed cystic mass lesion with fluid, fat, and calcification. \n\nCharacterization by MRI depends on demonstration of fat by chemical shift artifact or fat suppression imaging. Fat or sebaceous material within the cyst follows the signal of subcutaneous fat on all imaging sequences. Fat-fluid levels, layering of debris, dermoid plugs (mural nodules), and calcifications are additional findings. A small percentage of cystic teratomas contain simple fluid showing low signal on T1WI and high signal on T2WI which may be diagnosed as teratomas by demonstration of small deposits of fat in the walls.", "ACR Code": "8.3", "Category": "Neoplasm, benign", "Keywords": "dermoid cystcystic teratomagerm cell tumor", "Reference": "http://education.auntminnie.com/AuntMinnie/QMachine.ASP?UID=0GG0ZIWG&PageId=5&Sess=3775141\n\nFundamentals of Diagnostic Radiology / (edited by) William E. Brant, Clyde A. Helms.\u20142nd ed., Lippincott Williams & Wilkins, 1999\n\nPrimer of Diagnostic Imaging / (edited by) Janice M. Gaillard\u20143rd ed., Mosby Inc., 2003" } }, { "U_id": "MPX2531", "TAC": [ "MPX2531_synpic41981", "MPX2531_synpic41983" ], "MRI": [ "MPX2531_synpic41986" ], "Case": { "Title": "Citrobacter koseri osteomyelitis/discitis", "History": "52 y/o AA male recently deployed soldier who was medically evacuated due to chronic back pain that interfered with his duties as a truckdriver. While being evaluated stateside, his pain worsened and he had a lumbar puncture which revealed signs consistent with a potential infection. An MRI was then obtained for further evalutaion.", "Exam": "Back: Mild tenderness to palpation over lower thoracic/upper lumbar spine.\n\nCSF: LP opening pressure: 18 cm H2O, wbc=32,rbc=2, glc=53, prtn=92 76%lymphs. Gram stain: pmns present. no organisms.\n\nCBC: 5.68>10.6/31.6<443\n\nCMP: 140/4.4/99/29/11/0.5<95, Ca 9.6, PO4 4.8, Mg 1.6", "Findings": "Initial plain radiograph showed narrowed disk space between T10-T11 and left paraspinal mass\n\n-MRI showed paraspinal mass in the anterior paraspinal soft\ntissues at T10-T11. T10-and T11 and intervertebral disc space show low signal intensity on T1 that becomes high signal intensity on T2 and enhanced after contrast consistent with vertebral osteomyelitis and discitis with paraspinal mass.", "Differential Diagnosis": "1. Discitis/osteomyelitis\n2. Pott's Disease", "Case Diagnosis": "Citrobacter koseri osteomyelitis/discitis", "Diagnosis By": "CT guided needle biopsy", "Treatment & Follow Up": "Pt underwent antibiotics treatment both as an inpatient and outpatient with improvement. However, follow-up MRI revealed no direct cord compression despite remaining inflammatory changes and parapinal inflammation. The T10-T11 disc space showed near complete obliteration.", "Discussion": "Culture of the CT-guided biopsy material from the this patient yielded Citrobacter koseri. This organism is a rare cause of vertebral osteomyelitis. Vertebral osteomyelitis due to Citrobacter koseri has been reported in the literature only in association with preceding infections such as a pneumonia or bacteremia, endocarditis in a pacemaker lead, or in the postoperative period following transurethral prosatectomy. This organism is relatively non-virulent. Citrobacter infections are usually nosocomial and are acquired as a result of instrumental seeding from the commonly colonized gastrointestinal and genitourinary tract. In adults, Citrobacter infections most frequently involve the urinary and gastrointestinal tracts, soft tissue wounds, and occasionally bone. That the current patient had no history of bacteremia, invasive procedure, abdominal or pelvic infection, or soft tissue wound, which is atypical history for this particular pathogen." }, "Topic": { "Title": "Vertebral Osteomyelitis/Discitis", "Disease Discussion": "Vertebral osteomyelitis is a rare disease that can occur at any age, but primarily in patients of middle age. Spread of infection is mainly hematogenous, however vertebral osteomyelitis can result from non-hematogenous sources such as direct inoculation from spinal surgery and penetrating trauma. Blood-borne bacteria can seed the vertebral bodies via the spinal arteries. The primary venous route for extension from the pelvis to the spine is Batson\u2019s vertebral venous plexus. This plexus contains no valves and is of variable direction, depending on the intra-abdominal pressure. Vertebral body endplates are well vascularized, and it is within the large venous sinusoids that the multidirectional blood flow allows the infection to spread throughout the vertebral bodies. Once the vertebral body endplates are infected, the pathogen can break through these endplates into the intervertebral space with resultant discitis. Most patients with vertebral osteomyelitis result from a remote site of infection, most frequently the urinary tract by hematogenous seeding. Less commonly, affected patients have history of skin, respiratory, gastrointestinal or pelvic infections, or an episode of penetrating or non-penetrating trauma prior to the onset of vertebral osteomyelitis. ent:", "ACR Code": "3.2", "Category": "Infection, bacteria", "Keywords": "OsteomyelitisBack Painabscess", "Reference": "References\n1. Mylona E, Samarkos M, Kakalou E, Fanourgiakis P, and Skoutelis A. Pyogenic vertebral osteomyelitis: A systematic review of clinical characteristics. Semin Arthritis Rheum 2008 June 10 [Epub ahead of print]. \n2. Batson OV. The function of the vertebral veins and their role in the spread of metastasis. Ann Surg. 1940; 112: 138-49. \n3. 9.\tAn HS, Seldomridge JA. Spinal infections: diagnostic tests and imaging studies. Clin Orthop Rel Res 2006; 444: 27-33." } }, { "U_id": "MPX2536", "TAC": [ "MPX2536_synpic24348" ], "MRI": [], "Case": { "Title": "Neurofibromatosis type 1 (NF1), right orbital plexiform neurofibroma, sphenoid wing hypoplasia, possible optic nerve glioma.", "History": "21 month old girl with proptosis", "Exam": "Right eye proptosis", "Findings": "\u2022 \tA soft tissue mass noted laterally to the lateral rectus muscle in the pre and post septal portions of the right orbit \n\u2022 \tAsymmetry of the CSF-containing spaces in the middle cranial fossa, larger on the right without mass effect on the temporal lobe.\n\u2022 \tRight sphenoid wing hypoplasia causing deformity of the right orbit, which is widened and flattened posteriorly rather than conical.\n\u2022 \tRight optic nerve has a globular appearance near the orbital fissure\n\n\u2022 \tUnenhanced brain parenchyma demonstrates no abnormality. \n\u2022 \tGlobes are symmetrical in size and appearance\n\u2022 \tLeft optic nerve is unremarkable", "Differential Diagnosis": "Soft tissue mass\n\u2022 \tPlexiform neurofibroma of the orbit\n\u2022 \tDermoid cyst\n\u2022 \tInfectious (lacrimal gland, orbital cellulitis)\n\u2022 \tOther sarcoma (i.e. rhabdomyosarcoma, lipoma)\n\u2022 \tLymphoma\n\nRight Middle Fossa Fluid\n\u2022 \tEpidermoid cyst\n\u2022 \tArachnoid cyst\n\nSphenoid wing hypoplasia\n\u2022 \tBone dysplasia secondary to plexiform neurofibroma\n\u2022 \tCongenital bony malformation\n\u2022 \tTrauma\n\nRight optic nerve globular appearance\n\u2022 \tOptic nerve glioma\n\u2022 \tSuprasellar germinoma\n\u2022 \tCraniopharyngioma\n\u2022 \tInfiltrative disorders such as sarcoidosis, lymphoma, and Langerhans histiocytosis.", "Case Diagnosis": "Neurofibromatosis type 1 (NF1), right orbital plexiform neurofibroma, sphenoid wing hypoplasia, possible optic nerve glioma.", "Diagnosis By": "Imaging findings", "Treatment & Follow Up": "Children with NF1 should be monitored for developmental progress and should be seen yearly for neurological exams. More about general treatment for NF1 patients will be discussed in the discussion. As for her specific findings on this CT study, treatment and follow-up are as follows:\n\nPlexiform neurofibroma: Lesions usually involve multiple nerve fascicles with significant vascularity. Thus, surgical excision is generally difficult and frustrating, with excessive bleeding and a poor cosmetic result. Repeated debulking may be necessary for severe symptoms, and orbital evisceration for extensive cases. Radiotherapy offers no benefit. However, farnesyl transferase inhibitors, which inhibit growth of these tumors in animals, are a possible treatment in the future and are currently undergoing clinical trials. Of concern, there is a small risk of malignant transformation of these tumors. They may occasionally erode into the anterior cranial fossa, which results in death.\n\nOptic nerve glioma: The radiologist of this case recommended further evaluation with MRI of the brain and orbits. If the MRI is positive for an optic nerve glioma, MRI and an ophthalmic exam are repeated every 3-6 months. Otherwise, if vision is ok, observation is the treatment. If the tumor progresses, the child should be referred to neurooncology for evaluation. Surgical excision is offered if a tumor approaches the chiasm. Surgery also is indicated for pain or disfiguring proptosis. The role of radiotherapy remains controversial; it may be associated with CNS complications. More recently, chemotherapy has shown promising results.", "Discussion": "Our patient has been given the definitive diagnosis of NF1 because of the plexiform neurofibroma and sphenoid hypoplasia. It is a likely assumption that the optic nerve mass is an optic nerve glioma given this patient\u2019s diagnosis of NF1. Follow-up MRI should reveal a hypotense to isotense T1 signal and variable intensity compared to muscle on T2 weighted imaging. Enhancement with gadolinium is also variable. Typically, the lesion appears as a fusiform enlargement of the optic nerve, possibly involving the optic chiasm. The nerve may appear kinked with cystic spaces.\n\nIf no potential problem develops, this 2 year old needs yearly medical visits to include physical exam, ophthalmologic exam, growth measurements, assessment for precocious puberty, developmental assessment, and review of educational progress. Also, as previously mentioned, because of her tumors, she would need a follow-up MRI every 3-6 months. Obviously, this management involves a multidisciplinary team involving genetics, neurology, ophthalmology, dermatology, neurosurgery, and plastic surgery." }, "Topic": { "Title": "Neurofibromatosis type 1, NF-1", "Disease Discussion": "NF1 also known as von Recklinghausen\u2019s disease is a common neurocutaneous disorder and the most common type of neurofibromatosis. It is an autosomal dominant disorder with an incidence of 1 in 3000. It involves chromosome 17, which encodes for the protein neurofibromin, which is expressed in many tissues including brain, kidney, spleen, and thymus. Mutations leading to loss of function of this protein results in a wide spectrum of clinical findings.\n\nDiagnostic criteria were developed in 1987 by the NIH Consensus Conference (updated in 1997) and are based on clinical features. Two of the following must be present to diagnose as NF1: 6 or more caf?-au-lait macules (>5mm-prepuberty or >15mm-postpuberty), 2 or more neurofibromas of any type or 1 plexiform neurofibroma, freckling in the axillary or inguinal regions, optic glioma, 2 or more Lisch nodules, distinctive bony lesion (i.e. sphenoid dysplasia, thinning of long bone cortex with or without pseudoarthrosis), a first degree relative diagnosed with NF1.\n\nOptic nerve glioma is a pilocytic astrocytoma that primarily affects children. The lesion may be bilateral in NF1 (29% of optic gliomas are associated with NF1). Clinical findings include gradual loss of vision, optic atrophy or edema, and exophthalmos. Eighty percent of patients experience an initial decrease in vision which then stabilizes. Hypothalamic signs, to include precocious or delayed puberty, may be seen in 22% of cases. Prognosis for vision is poor. Lesions initially confined to the optic nerve have a mortality of 10%. Lesions involving the chiasm have a mortality of 20%. With midbrain and hypothalamus involvement, the prognosis is poor, with mortality greater than 55%.\n\nPlexiform neurofibroma is the most common benign peripheral nerve tumor in the eyelid and orbit. The tumor grows along the nerve, is not encapsulated, and is invasive. Children in the first decade of life are most commonly affected. The tumor tends to grow along sensory nerves, but also may involve motor, parasympathetic, and sympathetic nerves. Thirty one percent of plexiform neurofibromas occur in the eyelids. The clinical description of this tumor is as a palpable \u201cbag of worms,\u201d with thickened overlying skin and an S-shaped eyelid. On MRI the T1 is hypointense and the T2 hyperintense to muscle.", "ACR Code": "1.3", "Category": "Congenital, genetic", "Keywords": "neurofibromasphenoid wing hypoplasiaoptic nerve glioma", "Reference": "Yanoff. Ophthalmology, 2nd ed. Ch. 95 Sec. 3, Mosby, Inc., 2004Packer R, et al. Plexiform neurofibromas in NF1. Neurology. Vol. 58 No. 10. May 2002.\n\nLynch T and Gutmann D. Neurofibromatosis 1. Neurol Clin N Am. Vol 20. 2002.\n\nPlon S and Blazo M. Neurofibromatosis type 1 (von Recklinghausen\u2019s disease). Uptodate.com, Dec 2004.\n\nHabif T. Clinical Dermatology: A Color Guide To Diagnosis And Therapy, 4th ed. St. Louis: Mosby, 2004." } }, { "U_id": "MPX2533", "TAC": [ "MPX2533_synpic35402" ], "MRI": [], "Case": { "Title": "glioblastoma", "Findings": "Radiology: Glioblastoma is usually seen as a grossly heterogeneous mass. Ring enhancement surrounding a necrotic \ncenter is the most common presentation, but there may be multiple rings. Surrounding vasogenic edema can be \nimpressive, and adds significantly to the mass effect. Signs of recent (methemoglobin) and remote (hemosiderin) \nhemorrhage are common. Despite it\u2019s apparent demarcation on enhanced scans, the lesion may diffusely infiltrate into \nthe brain, crossing the corpus callosum in 50-75% of cases", "Case Diagnosis": "glioblastoma", "Discussion": "Radiology: Glioblastoma is usually seen as a grossly heterogeneous mass. Ring enhancement surrounding a necrotic \ncenter is the most common presentation, but there may be multiple rings. Surrounding vasogenic edema can be \nimpressive, and adds significantly to the mass effect. Signs of recent (methemoglobin) and remote (hemosiderin) \nhemorrhage are common. Despite it\u2019s apparent demarcation on enhanced scans, the lesion may diffusely infiltrate into \nthe brain, crossing the corpus callosum in 50-75% of cases" }, "Topic": { "Title": "Glioblastoma multiforme (WHO Grade 4 astrocytoma)", "Disease Discussion": "Synonyms: GBM, glioblastoma multiforme, spongioblastoma multiforme \n\nCommon Locations: cerebral hemispheres, occasionally elsewhere (brainstem, cerebellum, cord) \n\nDemographics: peak from 45-60 years \n\nHistology: grossly heterogeneous, degeneration, necrosis and hemorrhage are common with mitoses and prominent neovascularity\n\nSpecial Stains: GFAP varies, often present in areas of better differentiation \n\nProgression : Can't get any worse histologically with a median survival of 8-12 months. \n\nRadiology: Glioblastoma is usually seen as a grossly heterogeneous mass. Ring enhancement surrounding a necrotic center is the most common presentation, but there may be multiple rings. Surrounding vasogenic edema can be impressive, and adds significantly to the mass effect. TWithin the area of vasogenic edema, there may be angiogenesis and microscopic tumor infiltration. Signs of recent (methemoglobin) and remote (hemosiderin) hemorrhage are common.\n\nDespite it\u2019s apparent demarcation on enhanced scans, the lesion may diffusely infiltrate into the brain, crossing the corpus callosum in 50-75% of cases.", "ACR Code": "1.3", "Category": "Neoplasm, glial", "Keywords": "GBMglioblastoma multiformespongioblastoma multiforme", "External Links": "rad.usuhs.edu/medpix/medpix.html?mode=single&recnum=719&table=card&srchstr=glioblastoma&search=glioblastoma#top" } }, { "U_id": "MPX2540", "TAC": [ "MPX2540_synpic18531", "MPX2540_synpic18533", "MPX2540_synpic18534" ], "MRI": [], "Case": { "Title": "Midgut malrotation with appendicitis", "History": "Several week history of poorly localized abdominal pain.", "Exam": "Diffuse lower abdominal pain without rebound or guarding.", "Findings": "Midgut malrotation with duodenum failing to cross midline and small bowel in right abdomen. Cecum in lower mid-right abdomen. Abnormal position of SMV/SMA. Inflammatory changes surrounding cecum and area of appendix with fluid collection.", "Differential Diagnosis": "Malrotation\nAppendicitis with rupture\nAbscess\nPerforated diverticula", "Case Diagnosis": "Midgut malrotation with appendicitis", "Diagnosis By": "radiographic diagnosis", "Treatment & Follow Up": "pending", "Discussion": "Incidental malrotaion. See factoid." }, "Topic": { "Title": "Midgut malrotation", "Disease Discussion": "Embryology: The alimentary tract initially develops as a pouchlike extension of the yolk sac. At 6 weeks gestation, the intestinal tract is a continuous, tubular structure that is divided into the foregut (supplied by the celiac artery), midgut (supplied by the superior mesenteric artery), and hindgut (supplied mainly by the inferior mesenteric artery). During embryonic development, the bowel introduces itself into the abdomen and both the duodenojejunal and ileocolic segments of the primitive digestive tube rotate 270\u00b0 counterclockwise about the omphalomesenteric vessels (ie, the future superior mesenteric artery and superior mesenteric vein) to reach their final normal positions. Before 6 weeks gestation, the duodenum initially rotates 90\u00b0 counterclockwise so that it lies to the right of the superior mesenteric artery. Similarly, the cecum rotates 90\u00b0 counterclockwise so that it lies to the left of the superior mesenteric artery. During the 6th week of gestation, the duodenum rotates another 90\u00b0 counterclockwise so that it lies posterior to the superior mesenteric artery. By the 10th to 12th weeks of gestation, the intestine slides back into the peritoneal cavity, where the final 90\u00b0 rotation of the duodenum and 180\u00b0 rotation of the cecum occur. The right colon is the last portion of the gastrointestinal tract to rotate completely, allowing the cecum to descend into the right lower quadrant. This rotation is followed in the last stage by peritoneal fixation of the bowel. The small bowel mesentery is normally broad based, with its attachment extending from the ligament of Trietz to the ileocecal valve. This wide base prevents the small intestine from twisting around the superior mesenteric artery. Malrotation most commonly is caused by incomplete rotation (<270\u00b0 of counterclockwise rotation occurring in weeks 5-12).\n\nThis group of disorders can be divided into 3 different categories:1) Nonrotation (0\u00b0 to <90\u00b0 of counterclockwise rotation occurring before 6 weeks), 2) Reverse rotation (abnormal rotation >90\u00b0 and <180\u00b0 causing obstruction or reversal of the normal duodenal/SMA relationship, occurring in weeks 6-10), and 3) Malrotation most often associated with malfixation (>180\u00b0 and <270\u00b0 of counterclockwise rotation, occurring after 10 weeks). Nonrotation is often an incidental finding in older children and adults during routine examination, but volvulus as a result of local clockwise rotation may accompany this anomaly.\n\nClinical: Incidence is unknown, as many are asymptomatic. No racial or gender predilection is seen. In approximately 60% of patients, malrotation presents by age 1 month with bilious vomiting and high intestinal obstruction. Another 20-30% of patients present at age 1-12 months. Older children with malrotation may show failure to thrive, chronic recurrent abdominal pain, malabsorption, or other vague presentations. The older the child, the less readily identifiable the clinical presentation. Nonrotation of the intestine may be asymptomatic, thus is an incidental finding on UGI performed for other reasons. \n\nRadiographic findings: \nPlain films: In midgut volvulus, the classic radiographic finding is a partial duodenal obstruction (dilation of both the stomach and proximal duodenum, with paucity of bowel gas distally). \nUGI: The preferred diagnostic test for malrotation with midgut volvulus. Duodenal-jejunal junction (DJJ) displaced downward and to the right on the frontal view An abnormal position of the jejunum (lying on right side of abdomen) should alert one to the possibility of a malrotation but should not be relied upon to either make or exclude the diagnosis. Corkscrew of small bowel around SMA.\nUS: The \"whirlpool sign\" on color Doppler shows mesentery and flow within the SMV wrapping around the SMA (in a clockwise direction), indicating malrotation with volvulus \nCT: The DJJ is low and to the right of the normal location. The duodenum doesn\u2019t cross midline. The proximal jejunum is in the right upper quadrant. The cecum is in the upper and/or left abdomen. The large bowel is in the left abdomen. Abnormal relationship of the superior mesenteric vein (SMV) to the superior mesenteric artery (SMA). The SMV should lie to the right of the SMA. \n\nTreatment: Silent malrotation requires no treatment. Symptomatic malrotation in an infant requires surgical correction and midgut volvulus is a surgical emergency.", "ACR Code": "7.1", "Category": "Congenital, malformation", "Keywords": "malrotationvolvuluscorkscrew", "Reference": "1. Carlos J. Sivit et al , \nEvaluation of Suspected Appendicitis in Children and Young Adults: Helical CT\nRadiology 2000; 216: 430-433. \n2. Yuriko Okino, et al \nRoot of the Small-Bowel Mesentery: Correlative Anatomy and CT Features of Pathologic Conditions\nRadioGraphics 2001; 21: 1475-1490. \n3. Teresa Berrocal et al, Congenital Anomalies of the Small Intestine, Colon, and Rectum\nRadioGraphics 1999; 19: 1219-1236. \n4. JM Zerin and MA DiPietro\nMesenteric vascular anatomy at CT: normal and abnormal appearances\nRadiology 1991; 179: 739-742. \n5. http://www.emedicine.com/radio/topic450.htm Midgut volvulus, Author: Janet R Reid, MD, FRCPC, Associate Professor, Department of Radiology, Section of Pediatric Radiology, Cleveland Clinic Children's Hospital", "External Links": "www.emedicine.com/radio/topic450.htm" } }, { "U_id": "MPX2539", "TAC": [ "MPX2539_synpic60243" ], "MRI": [], "Case": { "Title": "Linitis Plastica (gastric cancer)", "History": "This 26 y.o. man presents with a three week history of early satiety and postprandial nausea and vomiting.", "Exam": "N/A", "Findings": "Frontal fluoroscopic images from a solid column barium enema and subsequent upper GI study demontrate concentric annular long segment luminal narrowing of the gastric antrum which extends into the pyloric channel. Also, these images demonstrate a concentric annular long segment narrowing of the lumen of the transverse colon from gastrocolic extension. Axial CT images of the abdomen demonstrate gastric wall thickening and concentric narrowing of the gastric antrum and pylorus. Axial CT images also demonstrate long segment narrowing of the transverse colon. These findings are compatible with the patient\"s history of gastric adenocarcinoma with spread via the gastrocolic ligament to the transverse colon.", "Differential Diagnosis": "Malignant neoplasms\n\tGastric adenocarcinoma\n\tLymphoma (especially Hodgkin disease)\n\tMetastases (hematogenous - esp. breast)\nGranulomatous infiltration\n\tCrohn\u2019s disease\n\tSarcoidosis\n\tSyphilis\n\tTuberculosis\n\tHistoplasmosis\n\tActinomycosis\nEosinophilic gastritis\nVasculitis\nCorrosive agents\nGastric irradiation\t\nGastric freezing\nIron intoxication\nHepatic arterial infusion if chemotherapy\nStenosing antral gastritis \t\nAmyloidosis", "Case Diagnosis": "Linitis Plastica (gastric cancer)", "Diagnosis By": "Imaging", "Treatment & Follow Up": "Gastric adenocarcinoma, linitis plastica, spread to transverse colon via gastrocolic ligament.\n\nAt the time of case compilation, the patient was undergoing evaluation for palliative resection of his tumor burden vs. other therapeutic options to include chemotherapy.", "Discussion": "Please refer to the topic for this case:\nhttp://rad.usuhs.edu/medpix/topic.html?mode=kiosk_topic&recnum=2772&pt_id=3975&imageid=8930" }, "Topic": { "Title": "Linitis plastica", "Disease Discussion": "Linitis plastica is most often caused by infiltration of the gastric wall by scirrhous gastric adenocarcinoma. This is a condition marked by thickening and fibrosis of the gastric wall with subsequent luminal narrowing, gastric wall rigidity, nondistensibility, and hypoperistalsis. The most common site of gastric adenocarcinoma occurrence is the antral and pyloric regions (with variable spread proximally toward the gastric body). The fundus is least often involved.\n\nCT is the imaging study of choice to demonstrate tumor spread, either locally by direct extension or distant metastases to lymph nodes, liver, ovary, adrenals, kidneys, and/or peritoneum. Other causes of linitis plastica are listed in the differential diagnosis section for this case, but certain etiologies will be briefly mentioned.\n\nNon-hodgkin lymphoma commonly involves the stomach by submucosal spread but rarely results in a true linitis plastica pattern. Gastric Hodgkin lymphoma is much less common but will more often result in linitis plastica. Hematogenous metastatic disease, most often from breast cancer, is another cause of linitis plastica. Rare benign causes of linitis plastica include Crohn?s disease, sarcoidosis, atyplical infection (e.g., syphilis and tuberculosis), eosinophilic gastritis, vasculitis, corrosive agents, gastric irradiation, amyloidosis, iron intoxication, and hepatic arterial infusion chemotherapy.\n\nhttp://www.orpha.net/consor/cgi-bin/OC_Exp.php?Lng=GB&Expert=36273", "ACR Code": "7.3", "Category": "Neoplasm, carcinoma", "Keywords": "Gastric lymphoma M\u00e9n\u00e9trier's scirrhous carcinomamesenteric peritoneal metastasesLeather bottle stomach", "Reference": "1. Cotran, RS, Kumar V, and Robbins SL. Pathologic Basis of Disease, 5th ed. WB Saunders, Philadelphia: 1994, p. 781.\n\n2. Eisenberg, Ronald L. Gastrointestinal Radiology: A Pattern Approach, 2nd ed. J.B. Lippincott, Philadelphia: 1990, pp. 205-222." } }, { "U_id": "MPX2548", "TAC": [ "MPX2548_synpic24222" ], "MRI": [], "Case": { "Title": "Radicular cyst", "History": "23 y/o man with chronic sinus disease.", "Exam": "Unknown.", "Findings": "A 6 mm unilocular lytic lesion surrounding the root of the right incisor.", "Differential Diagnosis": "Radicular (periapical) cyst--this appearance is fairly characteristic for a radicular cyst, however other considerations include a dentigerous cyst and less likely keratocyst or ameloblastoma.", "Case Diagnosis": "Radicular cyst", "Diagnosis By": "Radiographically", "Treatment & Follow Up": "Unknown.", "Discussion": "See Topic" }, "Topic": { "Title": "Odontogenic Cysts", "Disease Discussion": "Radicular cysts (also known as periapical or apical cysts) are the most common benign lytic dental lesions and are seen in the mandible or maxilla with an associated infected tooth. They are seen as a unilocular lucent lesion at the apex of an erupted tooth with loss of lamina dura with sclerotic borders. The patient typically presents with a tender, carious, non vital tooth. \n\nThe second most common benign odontogenic cyst is a dentigerous cyst which is associated with an unerupted tooth, usually within the mandible around the posterior molars. Radiographically, these are unilocular, lucent, expansile lesions adjacent to an unerupted tooth which spares the cortex and has sclerotic margins. The patient typically presents with an asymptomatic unerupted third molar or canine tooth.\n\nThe two most common aggressive odontogenic cysts are the keratocyst and ameloblastoma. These lesions are benign, but aggressive and tend to recur. The keratocyst is also called the primordial cyst Keratocysts are multi-locular, expansile lucent lesions that erode the cortex but does not perforate it. They usually affect the mandible. Patients typically present with recurrent posterior mandibular lesions with thin walls. Keratocysts are associated with basal cell nevus (Gorlin\u2019s) syndrome where patients have proliferative falcian calcification, multiple basal cell carcinomas of the skin, scoliosis, ribbon-shaped ribs, CNS tumors and keratocyts of the mandible.\n\nThe ameloblastoma is a multiloculated cyst that arises from the mandible in 81% of the cases. The molar region is affected in 70% of cases. Radiographically, the lesion demonstrates scalloped margins, multiloculation, and expanded cortical surfaces. The cortex is seen to be eroded or penetrated. Patients typically present with a painless, expanded jaw unless superinfected. There is male predominance.", "ACR Code": "2.3", "Category": "Cyst, benign", "Keywords": "Odontogenicradicularkeratocyst", "Reference": "Grossman RI and Yousem DM. The Requisites: Neuroradiology. Second edition. Philadelphia: Mosby, 2003.", "External Links": "http://ddmfr.ath.cx/dentalexpertbi/main/default.htm" } }, { "U_id": "MPX2544", "TAC": [ "MPX2544_synpic55624" ], "MRI": [ "MPX2544_synpic55621", "MPX2544_synpic55622" ], "Case": { "Title": "Left Ventricular Non Compaction", "History": "A 38 year old female presented to clinic with symptoms of new onset fatigue and dyspnea on exertion. The patient\u2019s family history was significant for a brother with known history of cardiomyopathy and sudden cardiac death of the patient\u2019s mother in her 40s.", "Exam": "Vital signs:\n\u2022 Blood pressure-- Elevated diastolic BP. RR was normal. \n\nCardiovascular system:\nNo Jugular Venous Distention\nNormal Heart Rate And Rhythm\nNo murmurs were heard.", "Findings": "Abnormal left ventricular dilatation with noncompacted myocardium of the inferior and lateral walls of the mid ventricle as well as apex. The ratio of non compacted to compacted myocardium was measured at 2.4 in the short axis view of the left ventricle at the end of diastole. The patient was also noted to have a small ASD, and there were no noted abnormalities of the coronary vasculature.", "Differential Diagnosis": "--Physiologic trabeculations\n--Left Ventricular Noncompaction\n--Dilated cardiomyopathy\n--Hypertrophic Cardiomyopathy", "Case Diagnosis": "Left Ventricular Non Compaction", "Diagnosis By": "MRI", "Treatment & Follow Up": "ICD Implantation\nNeurohumoral blockade with coreg and lisinopril\nVolume regulation with lasix\nRegular Cardiology Follow Up", "Discussion": "This case illustrates the importance of screening patients with early onset of CHF symptoms and a family history of cardiomyopathy. Although left ventricular noncompaction is typically more common in males, this patient demonstrated common presenting symptoms, with dyspnea on exertion and fatigue. Patients with left ventricular noncompaction often exhibit symptoms of congestive failure. \n\nIn this case, MDCT findings correlated well with with MR findings and could be used to establish the diagnosis independent of other modalities." }, "Topic": { "Title": "Left Ventricular Non Compaction", "Disease Discussion": "Left ventricular noncompaction (LVNC) is a congenital cardiomyopathy associated with loose trabeculations in the middle and apical segments of the left ventricle. It is thought to result from\nfailure of compaction of the myocardium during development. Patients have variable age at presentation from birth to the 4th decade of life, with earlier presentations portending a worse prognosis. There has been no predilection for race or sex elucidated to this point. Both familial and sporadic cases have been documented, demonstrating isolated LVNC and presentations associated with other\ncardiac anomalies. The patient in this case has a history which points to a familial form; however, no formal testing exists as research into potential mutations is ongoing.\n\nDiagnostic parameters with echocardiography have been used as the gold standard since being described by Chin et al.(1) and later by Jenni et al.(2). However, more recent advances in MR and CT imaging now allow for comparable if not superior imaging(3) of left\nventricular trabeculations characteristic of the disease, especially in the apical region.\n\nLVNC is underdiagnosed as a result of lack of knowledge about the disease and screening of relatives of those presenting with LVNC (4). Though echocardiography has historically been the diagnostic test of choice, MR and more recently CT have been shown to be complimentary or superior in detecting the characteristic, 2-layered myocardium (5). MR offers high quality images, preventing misdiagnosis of the characteristic trabeculations as apical hypertrophic cardiomyopathy or other cardiac pathology. It allows for acquisition of images in any plane without limitations of acoustic windows and has been utilized to diagnose cases that went undetected by echocardiographic exam.\n\nMR has been found to be diagnostic of LVNC at a ratio of noncompacted to compacted myocardium > 2.3 at the end of diastole, with sensitivities and specificities of 84 and 99% (6). Furthermore, MR delayed hyperenhancement correlates with degree of wall motion abnormality and has been found to be a positive independent predictor of ejection fraction and disease severity (7). Others have used the ratio of 2.3 as the basis for CT diagnosis of LVNC (8-10), finding a good correlation to MR results. CT is advantageous over other modalities in its ability to exclude anomalies of the coronary vasculature which have been described with LVNC (11). This modality further demonstrates a high spatial and temporal resolution with quick acquisition of images as compared to MR (12).", "ACR Code": "5.7", "Category": "Cardiac & Renal", "Keywords": "NoncompactionTrabeculationsEKG Gated CT", "Reference": "1 Chin TK, et al. Isolated Noncompaction of the Left Ventricular Myocardium: A Study of Eight Cases.\nCirculation 1990; 82:507-513.\n2 Jenni, R et al. Echocardiographic and Pathoanatomical Characteristics of Isolated Left Ventricular\nNoncompaction: A Step Towards Classification as a Distinct Cardiomyopathy. Heart 2001;86:666-671.\n3 Hamamichi, Y et al. Isolated Noncompaction of the Ventricular Myocardium: Ultrafast Computed\nTomography and Magnetic Resonance Imaging. International Journal of Cardiovascular Imaging\n2001;17:305-314.\n4 Goo HW and Park IS. Left Ventricular noncompaction in an infant: use of non-ECG-gated cardiac CT.\nPediatric Radiology 2007;37:217-220.\n5 Amir, O et al . The Value of Cardiac Magnetic Resonance Imaging in the Diagnosis of Isolated Non-\nCompaction of the Left Ventricle. Israel Medical Association Journal 2009;11:313-314.\n6 Peterson SE et al. Left Ventricular Noncompaction: Insights from Cardiovascular Magnetic Resonance\nImaging. Journal of the American College of Cardiology 2005;46:101-105.\n7 Dodd, JD et al. Quantification of Left Ventricular Noncompaction and Trabecular Delayed\nHyperenhancementwith Cardiac MRI: Correlation with Clinical Severity. American Journal of\nRoentgenology 2007;189:974-980.\n8 Conces, Jr., DJ et al. Noncompation of the Ventricular Myocardium: CT Appearance. American Journal of\nRoentgenology 1991;156:717-718.\n9 Goo HW, and Park IS. Left Ventricular Noncompaction in an Infant: Use of non-ECG-Gated Cardiac CT.\nPediatr Radiol 2007;37:217-220.\n10 Bladt O et al. Isolated Noncompaction of Ventricular Myocardium. Diagnosis with Multidetector Computed\nTomography. Journal Belge de Radiologie - Belgisch Tijdschrift voor Radiologi 2008;91:153-154.\n11 Hamamichi, Y et al. \u201cIsolated noncompaction of the ventricular myocardium: Ultrafast computed\ntomography and magntic resonance imaging.\u201d The International Journal of Cardiovascular Imaging\n(2001) 17: 305-314.\n12 Ito H and Dajani KA. A case with noncompactionof the left ventricular myocardium detected by 64-slice\nmultidetector computed tomography.\u201d Journal of Thoracic Imaging (2009) 24:38-40." } }, { "U_id": "MPX2550", "TAC": [ "MPX2550_synpic18049" ], "MRI": [], "Case": { "Title": "Ovarian Cancer metastasis", "History": "53 year old white woman reports with clincal history of ovarian cancer and shortness of breath.", "Exam": "Muffled heart sounds and no breath sounds on the right side of the chest.\n\nNull mutation in p53 gene.", "Findings": "Chest X-Ray (PA and LAT) shows right side volume loss with complete opacification of right lung. There is cardiomegally and calcified nodular opacities at the right cardiophrenic border. \n\nAxial CT of the chest shows soft tissue mass surounding heart and complete drowning of the right lung.", "Differential Diagnosis": "Calcium producing Metastatic Tumor vs. New Malignancy\n- Bone Tumors: osteosarcoma, chondrosarcoma\n- Mucinous Tumors: colon cancer, thyroid cancer,\n pancreatic cancer, stomach cancer, ovarian cancer\nInfection", "Case Diagnosis": "Ovarian Cancer metastasis", "Treatment & Follow Up": "Palliative care.", "Discussion": "Ovarian cancers in women with a null mutation in the p53 gene have been associated with distant mets more than 8 times more frequently. More than 85 percent of the time, ovarian cancer remains in the peritoneum throughout its course. Metastasis to the pericardium, as in this case, is extremely rare and has been reported infrequently." }, "Topic": { "Title": "Ovarian Cancer", "Disease Discussion": "Cancer of the ovary is the second most frequent gynecological malignancy in the United States. It is, however, more deadly than all the other genital cancers combined. More than three-fourths of patients already have extragonadal spread of the tumor to the pelvis or abdomen at the time of diagnosis. It is most common between the ages of 40 and 60 and rare in those under 35. By the time the carcinoma reaches 10-15 cm it often has already spread beyond the ovary and seeded the peritoneum.\n\nDistant metastasis, however, is unusual at presentation. In fact, eighty-five percent of the time the disease remains confined to the peritoneal cavity throughout its course. When it does metastasize, it tends to develop in the liver, lung or brain. Metastasis to the pericardium, as in this case, is extremely rare. \n\nWhile some contend that improving chemotheraputic treatments, particularly with drugs like cisplatin, has changed the pattern of metastasis by prolonging the disease, others report tumor behavior, and metastatic potential, is due to a specific molecular abnormality at the onset. Perhaps there is some truth in both these schools of thought. \n\nAs it is reported, aggressive ovarian cancers that tend to have distant metastasis are more frequently associated with having a null mutation of p53. Sood et al. reports distant metastasis is nearly eight fold more frequent in tumors with this mutation than with any other. His study also demonstrated that patients who had ovarian cancers with wild-type p53 or missense mutations did not present with distant metastasis. \n\nAs radiologists, it is important for us to be careful when considering the likelihood of distant ovarian metastasis. In light of a genetic work up suggesting distant metastasis potential, and corresponding radiological findings, regional versus systemic treatment modalities might improve quality and perhaps quantity of life.", "ACR Code": "6.3", "Category": "Neoplasm, metastatic", "Keywords": "Ovarian CancerPericardial Metastasisp53", "Reference": "Rubin, E. and Farber, JL. Pathology, 2nd Ed. Lippincott, Philadelphia, 1994, pages 950-951. \n\nSood, AK. et al. Distant Metastasis in Ovarian Cancer: Association with p53 Mutations. Clinical Cancer Research, Vol. 5, 2485-2490, September 1990.\n\nJain, H. et al. Cardiac tamponade: A rare initial presentation of metastatic ovarian cancer. Proc Am Soc Clin Oncol. 22: page 470, 2003 (abstr 1890).\n\nReed, E. et al. Analysis of autopsy evaluations of ovarian cancer patients treated at the National Cancer Institute, 1972-1988. Am J Clin Oncol. Apr: 23(2): 107-16." } }, { "U_id": "MPX2547", "TAC": [ "MPX2547_synpic23806", "MPX2547_synpic23810", "MPX2547_synpic23814", "MPX2547_synpic23815", "MPX2547_synpic23816", "MPX2547_synpic23818", "MPX2547_synpic23819", "MPX2547_synpic23820", "MPX2547_synpic23822" ], "MRI": [], "Case": { "Title": "Classic Nodular Sclerosing Hodgkin\u2019s Lymphoma (Stage II)", "History": "27 yr old woman with c/o lymphadenopathy and fatigue for several months", "Exam": "PE significant for mild, non-tender cervical lymphadenopathy\nLaboratory unremarkable", "Findings": "\u2022 CXR: Enlargement of the right paratracheal stripe (8mm).\n\u2022 CT, neck: 2.4 x 2.4 cm mediastinal mass (enlarged lymph node)", "Differential Diagnosis": "\u2022 Malignancy\n\u00bb Hodgkin\u2019s disease\n\u00bb Non-Hodgkin\u2019s lymphoma\n\u00bb Mediastinal malignancy\n\u2022 Benign neoplasm\n\u2022 Granulomatous disease\n\u2022 Other inflammation (abscess)\n\u2022 Congenital abnormality", "Case Diagnosis": "Classic Nodular Sclerosing Hodgkin\u2019s Lymphoma (Stage II)", "Diagnosis By": "Biopsy", "Treatment & Follow Up": "Patient was recently diagnosed and is undergoing radiation therapy at this time.", "Discussion": "The right paratracheal stripe is usually 2mm wide, but may be up to 5mm wide. An enlarged paratracheal stripe (>5mm) is an important marker for otherwise subtle adenopathy, as well as tracheal tumor, mediastinal inflammation or hemorrhage, pleural thickening or pleural effusion. The margins of the paratracheal stripe are: \n1. distal end\u2014formed by the azygous vein\n2. medial margin\u2014the air-soft tissue interface along the right mucosal surface of the trachea\n3. outer margin\u2014begins around the medial end of the clavicle and is formed by the RUL plural surface\nThe stripe ends where the RUL bronchus goes under the azygous vein as it arches anteriorly to empty into the SVC.\nThe malignant lymphomas are divided into Hodgkin\u2019s and non-Hodgkin\u2019s groups. Sir Thomas Hodgkin was the first to describe Hodgkin\u2019s disease in 1932. Hodgkin\u2019s can present at any age, but it is more prevalent among adolescents and young adults. It typically presents as painless, rubbery lymphadenopathy involving the superficial lymph node groups. Cervical nodes are involved nearly 70% of the time. Approximately half of patients also have splenomegaly. Mediastinal involvement occurs in approximately 10% of patients, and mediastinal involvement is characteristic of the Nodular Sclerosing type (as in this patient). Cutaneous involvement can occur and is usually a late complication. Patients may also present with constitutional symptoms (night sweats, pruritis, fatigue, weight loss, etc) with widespread disease. \nThe diagnosis of Hodgkin\u2019s disease is made by lymph node biopsy (as was done in this patient). There are 4 histological types:\n1.\tNodular Sclerosing (>50%, most common; worst prognosis)\n2.\tMixed cellularity (25%)\n3.\tLymphocyte predominant (5%; best prognosis)\n4.\tLymphocyte depleted (5%)\nStaging of Hodgkin\u2019s disease is made by the use of CXR, BM biopsy, and CT imaging. There are 4 stages:\n1.\tStage I\u2014confined to one lymph node group (90% 5-yr survival rate)\n2.\tStage II\u2014confined to 2 or more lymph node groups on one side of the diaphragm\n3.\tStage III\u2014involving nodes on both sides of the diaphragm\n4.\tStage IV\u2014Extra-nodal disease (60% 5-yr survival rate) \nTreatment involves radiation therapy and/or chemotherapy. Patients with Stage I or Stage II Hodgkin\u2019s disease are usually treated by radiation therapy, while Stage III & IV disease is usually treated with radiation therapy and chemotherapy.\nReferences:\n1. Mendenhall, NP. \u201cThe role of radiation in the management of Hodgkin\u2019s disease: an update,\u201d Cancer Invest 1999; 17:47-55.\n2. Potter, R. \u201cPediatric Hodgkin\u2019s Disease,\u201d Eur J Cancer 1999; 35: 1466-1477.\n3. Wirth, A, et al, \u201cCurrent trends in the management of early stage Hodgkin\u2019s disease,\u201d Aust NZ J Med 1999; 29: 535-544\n4. http://www.surgical-tutor-org/tutorials/hodgkins.htm\n5. http://rad.usuhs.mil/rad/chest_review/mediasti/mediasti.html" }, "Topic": { "Title": "Nodular Sclerosing Hodgkin\u2019s Lymphoma", "Disease Discussion": "Discussion: \nThe right paratracheal stripe is usually 2mm wide, but may be up to 5mm wide. An enlarged paratracheal stripe (>5mm) is an important marker for otherwise subtle adenopathy, as well as tracheal tumor, mediastinal inflammation or hemorrhage, pleural thickening or pleural effusion. The margins of the paratracheal stripe are: \n1. distal end\u2014formed by the azygous vein\n2. medial margin\u2014the air-soft tissue interface along the right mucosal surface of the trachea\n3. outer margin\u2014begins around the medial end of the clavicle and is formed by the RUL plural surface\nThe stripe ends where the RUL bronchus goes under the azygous vein as it arches anteriorly to empty into the SVC.\nThe malignant lymphomas are divided into Hodgkin\u2019s and non-Hodgkin\u2019s groups. Sir Thomas Hodgkin was the first to describe Hodgkin\u2019s disease in 1932. Hodgkin\u2019s can present at any age, but it is more prevalent among adolescents and young adults. It typically presents as painless, rubbery lymphadenopathy involving the superficial lymph node groups. Cervical nodes are involved nearly 70% of the time. Approximately half of patients also have splenomegaly. Mediastinal involvement occurs in approximately 10% of patients, and mediastinal involvement is characteristic of the Nodular Sclerosing type (as in this patient). Cutaneous involvement can occur and is usually a late complication. Patients may also present with constitutional symptoms (night sweats, pruritis, fatigue, weight loss, etc) with widespread disease. \nThe diagnosis of Hodgkin\u2019s disease is made by lymph node biopsy (as was done in this patient). There are 4 histological types:\n1.\tNodular Sclerosing (>50%, most common; worst prognosis)\n2.\tMixed cellularity (25%)\n3.\tLymphocyte predominant (5%; best prognosis)\n4.\tLymphocyte depleted (5%)\nStaging of Hodgkin\u2019s disease is made by the use of CXR, BM biopsy, and CT imaging. There are 4 stages:\n1.\tStage I\u2014confined to one lymph node group (90% 5-yr survival rate)\n2.\tStage II\u2014confined to 2 or more lymph node groups on one side of the diaphragm\n3.\tStage III\u2014involving nodes on both sides of the diaphragm\n4.\tStage IV\u2014Extra-nodal disease (60% 5-yr survival rate) \nTreatment involves radiation therapy and/or chemotherapy. Patients with Stage I or Stage II Hodgkin\u2019s disease are usually treated by radiation therapy, while Stage III & IV disease is usually treated with radiation therapy and chemotherapy.\nReferences:\n1. Mendenhall, NP. \u201cThe role of radiation in the management of Hodgkin\u2019s disease: an update,\u201d Cancer Invest 1999; 17:47-55.\n2. Potter, R. \u201cPediatric Hodgkin\u2019s Disease,\u201d Eur J Cancer 1999; 35: 1466-1477.\n3. Wirth, A, et al, \u201cCurrent trends in the management of early stage Hodgkin\u2019s disease,\u201d Aust NZ J Med 1999; 29: 535-544\n4. http://www.surgical-tutor-org/tutorials/hodgkins.htm\n5. http://rad.usuhs.mil/rad/chest_review/mediasti/mediasti.html", "ACR Code": "68.342", "Category": "Neoplasm, hematopoietic", "Keywords": "Nodular Sclerosing Hodgkin\u2019s LymphomaHodgkin\u2019sLymphoma", "Reference": "References:\n1. Mendenhall, NP. \u201cThe role of radiation in the management of Hodgkin\u2019s disease: an update,\u201d Cancer Invest 1999; 17:47-55.\n2. Potter, R. \u201cPediatric Hodgkin\u2019s Disease,\u201d Eur J Cancer 1999; 35: 1466-1477.\n3. Wirth, A, et al, \u201cCurrent trends in the management of early stage Hodgkin\u2019s disease,\u201d Aust NZ J Med 1999; 29: 535-544\n4. http://www.surgical-tutor-org/tutorials/hodgkins.htm\n5. http://rad.usuhs.mil/rad/chest_review/mediasti/mediasti.html" } }, { "U_id": "MPX2555", "TAC": [ "MPX2555_synpic14611" ], "MRI": [], "Case": { "Title": "Multiple C1 fractures", "History": "21 yo WM was entering the surf when a wave crashed directly on top of him. Patient was violently toppled over and struck his head on the sandy shore. Patient denies loss of consciousness or aspiration. He immediately felt bilateral paracervical neck pain upon impact on his head onto the shore. Patient emerged from the ocean under own strength and without any other complaints. He was promptly taken to the ED in ambulance without cervical spine precautions.", "Exam": "Tender to palpation over C1-C3, no neurological deficits. No other significant findings", "Findings": "C-spine CT- multiple fractures on C1, bilateral posterior ring, right anterior ring. Fragmentation on right side of C1 into spinal canal, spinal cord intact. All other cervical vertebrae intact and without compromise.", "Differential Diagnosis": "Multiple C1 fractures", "Case Diagnosis": "Multiple C1 fractures", "Treatment & Follow Up": "The essential priority in initial care of patients with potential spinal cord injury is to maintain strict immobilization of the entire spine. This immobilization is most often initiated in the field, which was not implemented in this patient. As soon as practical, and often before extrication is complete, the neck should be immobilized in a cervical collar, and the patient secured to a full-length backboard. The head is maintained in neutral position in the midline. Before transportation, the patient's body is securely strapped at all major joints, the head is taped to the board, and sandbags may be applied alongside the head. On arrival in the emergency department, the protective cocoon must be partially removed to allow assessment of the patient, but it is critical that the immobilization of the spine be maintained until an unstable injury has been ruled out both by radiologic and clinical examination. In the cervical spine, it is essential for the radiographs to include all seven cervical vertebrae, down to and including the articulation between C7 and T1. The lower portion of the cervical spine is often difficult to visualize well on lateral views, especially in large patients. If the region of C7 to T1 is not visualized, there is potential for dramatic missed injury. Under these circumstances, or if findings on plain films are equivocal, CT is a useful adjunct." }, "Topic": { "Title": "Multiple C1 fractures", "Disease Discussion": "The need for surgical intervention for injury to the spinal column itself is dictated by the degree of deformity and the perceived stability of the injury. Displaced fractures of the cervical spine are usually treated with careful application of traction, using a halo or Gardner-Wells tongs. Weight is gradually added to the traction apparatus until the spine is realigned. The rule of thumb is that a weight of approximately 5 pounds per cervical level is required for reduction. The neurologic examination must be followed very closely as weight is added to the traction. Serial radiographs are used to determine when adequate reduction has been obtained. Inability to obtain adequate reduction is usually an indication for surgical intervention.Those injuries thought to be relatively stable or with instability in only one column can be managed with immobilization only. For significant fractures this involves the use of a halo brace in the cervical spine, and an orthosis, usually a molded jacket, in the thoracic and lumbar spine. Unstable injuries usually require surgical stabilization. Stabilization can be achieved by placement of hardware posteriorly, by use of hardware and bone grafting anteriorly, or in some cases using both techniques simultaneously. The anterior approach allows better access to the vertebral body and better decompression of the spinal canal. Three-column injuries generally require both anterior and posterior stabilization.The benefits of early spinal stabilization in patients with complete injury are primarily related to the prevention of complications of long-term immobilization. Data show fewer complications in patients whose spinal injuries are fixed early, although there are no compelling survival differences. Therefore, spinal column injuries should be fixed as early as practical, once the patient is physiologically stable and no longer at risk to suffer deterioration of neurologic function, either from exacerbation of brain injury or as a result of manipulation of the spinal cord.", "ACR Code": "-1.-1", "Category": "Trauma", "Keywords": "fracturespine", "Reference": "No references were submitted by author." } }, { "U_id": "MPX2558", "TAC": [ "MPX2558_synpic20826", "MPX2558_synpic20827", "MPX2558_synpic20828", "MPX2558_synpic20829", "MPX2558_synpic20830", "MPX2558_synpic20831", "MPX2558_synpic20832" ], "MRI": [], "Case": { "Title": "Mondini deformity, incomplete partition type I.", "History": "9 year old male with left-sided sensorineural hearing loss.", "Exam": "NA.", "Findings": "High-resolution CT through the petrous bone in axial section shows a cystic cochleovestibular malformation of both ears. The bilateral cochlear turns are incomplete with a small appearance of the apex (last cochlear turn). The bilateral semicircular canals are abnormal with dilatation of the posterior and lateral semicircular canals. The vesibule is dilated on both sides. The vestibular aqueduct appears normal.\nThe findings are bilateral although more pronounced on the right.", "Differential Diagnosis": "Mondini Deformity.\nLarge vestibular aqueduct syndrome (can be isolated only to vestibular aqueduct or can be associated with cochlear and vestibular dysplasia)\nCochlear hypoplasia (associated with one large cavity between coclea and vestibule)\nMichel's Aplasia (complete lack of formation. Cock's Deformity).\nPendred syndrome.", "Case Diagnosis": "Mondini deformity, incomplete partition type I.", "Diagnosis By": "Radiographically.", "Treatment & Follow Up": "NA.", "Discussion": "These CT results were reviewd as Mondini deformity, incomplete partition type I (IP-I). Incomplete partition type I is defined as a malformation in which the cochlea lacks the entire modiolus and interscalar septa, resulting in a cystic appearance and there is an accompanying grossly dilated vestibule. \n\nAt first glance, the overall cochlea in this anomaly shows no significant difference from normal findings. Close inspection demonstrates the small size of the superior aspect or final turn of the cochlea. Only the internal architecture is different. Inspection of the semicircular canals is important since the can also be abnormally dilated (as in this case)." }, "Topic": { "Title": "Mondini Deformity.", "Disease Discussion": "In the original scientific report written in Latin by Carlo Mondini in 1791, titled The Anatomic Section of a Boy Born Deaf, translated to English by Gordon J. Hartley in the American Journal of Otology, the inner ear anomaly described by Mondini consisted of:\n\n1) a cochlea of one-and-one-half turns instead of the normal two-and-one-half turns, comprising a normal basal turn and a cystic apex in place of the distal one-and-one-half turns; \n2) an enlarged vestibule with normal semicircular canals; and \n3) an enlarged vestibular aqueduct containing a dilated endolymphatic sac. \n\nThus, the cochlear anomaly was relatively mild, and would correspond to incomplete partition in the spectrum of congenital cochlear malformation because of an arrest of embryogenesis. Arrests at earlier stages in the spectrum include cochlear hypoplasia and common cavity and cochlear aplasia. Even earlier arrests result in otocyst and complete labyrinthine aplasia (Michel's anomaly).\n\nThe most common of the congenital cochlear deformities is Mondini's defect, which occurs late in auditory embryologic development, usually at 7 to 8 weeks. The scala separations of the lumen of the cochlea are not developed completely at this point. Essentially, Mondini's defect is incomplete development of the two-and-a-half turns of the cochlea. The basal turn is relatively well formed, but the middle and apical turns are malformed. Variations in the number of remaining turns in the cochlea comprise various types of otic dysplasia. Enlargement of the vestibule is not an uncommon finding with cochlear abnormalities. Enlargement of the endolymphatic sac in association with a large vestibular aqueduct is present in about 20% of Mondini malformations. \n\nRadiologically, the anomaly was recognized on polytomography by Jensen as early as 1969. Subsequently, he also described a more severe type of deformity consisting of an amorphous cochlear sac continuous with a dilated vestibule, for which he suggested the term \"dysplasia\". Unfortunately, the term \"Mondini dysplasia\" has come to mean virtually any congenital malformation of the osseous labyrinth detectable on radiographic examination.\n\nA recent retrospective review of temporal bone high-resolution CT findings was performed because it was realized that the term Mondini deformity was being used to describe two different types of incomplete partition of the cochlea. By taking inner ear measurements on radiologic findings they confirmed the presence of two different types of incomplete partition: IP-I (unpartitioned cochlea, cystic cochleovestibular malformation) and IP-II (incompletely partitioned cochlea, the classic Mondini deformity).\n\nIncomplete partition type I (unpartitioned cochlea, cystic cochleovestibular malformation) is defined as a malformation in which the cochlea lacks the entire modiolus and interscalar septa, resulting in a cystic appearance and there is an accompanying grossly dilated vestibule. Cochlear measurements show no significant difference from normal.\n\nThe type I malformation is less differentiated than the type II malformation. Classic Mondini deformity has three components (a cystic apex, dilated vestibule, and large vestibular aqueduct), whereas type I malformation has an empty, unpartitioned cochlea and dilated vestibule without an enlarged vestibular aqueduct. Classic Mondini deformity represents a later malformation, so the degree of dysplasia is milder than that in type I.", "ACR Code": "1.1", "Category": "Congenital, malformation", "Keywords": "Mondinicochleavestibular", "Reference": "1. Sennaroglu L, Saatci I. Unpartitioned Versus Incompletely Partitioned Cochleae: Radiologic Differentiation. Otol Neurotol. 2004 Jul;25(4):520-529. \n2. William WML. What is a \u2018Mondini\u2019 and What Difference Does a Name Make? American Journal of Neuroradiology 20:1442-1444 (9 1999).\n3. Grossman RI, Yousem DM. Neuroradiology: The Requisites, 2nd ed.,. Copyright 2003, 1994, Elsevier Inc." } }, { "U_id": "MPX2562", "TAC": [ "MPX2562_synpic16800", "MPX2562_synpic16801", "MPX2562_synpic16803" ], "MRI": [], "Case": { "Title": "Perinephric/Subcapsular Hematoma", "History": "22 year old male with nephrotic syndrome of undetermined etiology undergoing ultrasound guided percutaneous renal biopsy.", "Exam": "N/A", "Findings": "Ultrasound initially demonstrates the normal sonographic appearance of the left kidney prior to percutaneous biopsy. Note the normal cortical and medullary differentiation as well as the intact perinephric hyperechoic cortical-capsular interface. \n\nUltrasound image selected during the second pass core biopsy (using a spring loaded biopsy needle) demonstrates the course of the biopsy needle.\n\nUltrasound image captured following the cessation of core biopsy attempts demonstrates complete loss of the previously seen hyperechoic cortical-capsular interface. A wide and slightly irregular perinephric hypoechogenic fluid collection is seen posteriorly (patient prone) most likely representing hematoma. \n\nSelected axial non-contrast CT slices through the level of the kidneys (taken minutes after the post-biopsy ultrasound) demonstrates left posterior-lateral and inferior perinephric hyperattenuation consistent with acute hemorrhage. The slightly irregular margin of the abnormality suggests this lesion is both subcapsular and perinephric.", "Differential Diagnosis": "Perinephric Hematoma\nSubcapsular Hematoma\nRenal Laceration", "Case Diagnosis": "Perinephric/Subcapsular Hematoma", "Treatment & Follow Up": "In this case, real time ultrasound imaging guiding the biopsy provided the first images suggesting an injury had occurred soon after the initial core sample had been obtained. \n\nAs a result, the injury was quickly recognized and the patient was promptly transported to CT for a non-contrast enhanced study of the kidneys to better delineate the full extent of his injury. During this time, the patient complained in mild to moderate ipsilateral back pain but remained hemodynamically stable. \n \nThe patient was admitted to the inpatient ward for close observation. He remained hemodynamically stable and was discharged home the next day with no untoward effects.", "Discussion": "Ultrasound-guided percutaneous renal biopsy using a spring loaded biopsy device is one of the most common methods used for renal biopsy (3). In a review of 1090 normotensive patients without coagulopathy who underwent the procedure between 1993 and 1997 the risk of post-biopsy minor hematoma formation was found to be 2.2% (3). More severe injuries such as loss of a kidney, life threatening hemorrhage, or persisting AV fistula have been reported but are considered exceedingly rare and did not occur in the study cited here. \n\nRenal injuries are typically classified in one of four radiologic categories (2):\n\nCategory I \u2013 Cortical Contusion; Subcapsular Hematoma; Minor Laceration with Mild Perinephric Hematoma; or Small Cortical Infarct (2).\n\nCategory II \u2013 Major Laceration with medullary involvement; Segmental Infarct (2). \n\nCategory III- Multiple Renal Lacerations; Vascular Pedicle Injury (2).\n\nCategory IV- UPJ Injury (2)\n\nIn evaluating a suspected renal injury, CT is the primary modality relied upon to detect and characterize a lesion (2). Using contrast enhanced CT, a renal injury such as a hematoma or laceration can be evaluated and the presence of active hemorrhage or urinary extravasation can frequently be documented (2).\n\nSubcapsular hematomas appear on CT imaging as a crescenteric enlargement surrounding all or a portion of the renal cortex (1). The density of these lesions varies depending upon injury maturity; hyperattenuating in earlier stages and becoming more hypoattenuating with time (1). Slight mass affect on the adjacent renal cortex may also be recognized (1). When the renal capsule is injured whether by blunt trauma or penetrating injury (as in this case by means of a biopsy needle), hematoma can enter the perinephric space (1). Hemorrhage in the perinephric space, when limited, appears similar to the subcapsular hematoma but demonstrates more ragged and heterogeneous margins. \n\nMost subcapsular hematomas are managed conservatively (1). Only life threatening hemorrhage and impending circulatory collapse will prompt surgical exploration (1). \n\nThis patient was admitted to the hospital over night for close observation, following which he was discharged home with no untoward effects. \n\n\nReferences:\n\n1. Harris AC, Zwirewich CV, Lyburn ID, Torreggiani WC, Marchinkow LO. CT Findings in Blunt Renal Trauma. Radiographics 2001; 21:S201-214.\n\n2. Kawashima A, Sandler CM, Corl FM, West OC, Tamm EP, Fishman EK, Goldman SM. Imaging of Renal Trauma: A Comprehensive Review. Radiographics 2001; 21:557-574.\n\n3. Hergesell O, Felten H, Andrassy K, Kuhn K. Ritz E. Safety of ultrasound-guided percutaneous renal biopsy-retrospective analysis of 1090 consecutive cases. Nephrology Dialysis Transplantation 1998. 13(4):975-977." }, "Topic": { "Title": "Renal Injury", "Disease Discussion": "Renal injuries are either secondary to accidental trauma (blunt or sharp abdominal injuries) or iatrogenic (post renal biopsy).\n \n They are typically classified in one of five radiologic categories :\n\n\u2022 Class I\t- Renal contusion or contained subcapsular haematoma \n\u2022 Class II - Cortical laceration without urinary extravasation \n\u2022 Class III - Parenchymal lesion extending more than 1 cm into renal substance \n\u2022 Class IV - Laceration extending across cortico-medullary junction \n\u2022 Class V - Renal fragmentation or reno-vascular pedicle injury \n\n In evaluating a suspected renal injury, CT is the primary modality relied upon to detect and characterize a lesion (2). Using contrast enhanced CT, a renal injury such as a hematoma or laceration can be evaluated and the presence of active hemorrhage can be seen. Urinary extravasation, either from the kidney, ureter or bladder can frequently be documented with delayed imaging during the excretory urogram phase. \n\n \u2022 This classification is important because minor injuries -85 % of all injuries- (Class I-II and even III) will be treated conservatively. \n \u2022 The management of urine leaks or a laceration communicating with the collecting system is controversial.This is considered a moderate injury -10% of all injuries - but eventually 15-50% will require surgery. \n \u2022 Major injuries such as a macerated kidney, pedicle avulsion injury or vascular thrombosis -15% of all injuries- are treated surgically.", "ACR Code": "8.4", "Category": "Hemorrhage", "Keywords": "PerinephricSubcapsularHematoma", "Reference": "1. Harris AC, Zwirewich CV, Lyburn ID, Torreggiani WC, Marchinkow LO. CT Findings in Blunt Renal Trauma. Radiographics 2001; 21:S201-214.\n\n\n2. Kawashima A, Sandler CM, Corl FM, West OC, Tamm EP, Fishman EK, Goldman SM. Imaging of Renal Trauma: A Comprehensive Review. Radiographics 2001; 21:557-574.\n\n3. Hergesell O, Felten H, Andrassy K, Kuhn K. Ritz E. Safety of ultrasound-guided percutaneous renal biopsy-retrospective analysis of 1090 consecutive cases. Nephrology Dialysis Transplantation 1998. 13(4):975-977." } }, { "U_id": "MPX2567", "TAC": [ "MPX2567_synpic25984", "MPX2567_synpic25985", "MPX2567_synpic25986", "MPX2567_synpic25987", "MPX2567_synpic25988" ], "MRI": [], "Case": { "Title": "Sjogren's Syndrome with concomitant lymphoma", "History": "74 y/o female with h/o Sjogren's syndrome with left parotid mass and incidental note of upper mediastinal lymph nodes on CT of the neck.", "Exam": "Overall within normal limits without palpable lymphadenopathy. Patient is status-post parotidectomy at this time.", "Findings": "Bulky mediastinal and hilar lymphadenopathy including the pre-vascular space, AP window, and pretracheal, subcarinal, and bilateral perihilar regions.", "Differential Diagnosis": "Lymphoma (highly likely)\nInfection (less likely)\nSarcoidosis (much less likely)", "Case Diagnosis": "Sjogren's Syndrome with concomitant lymphoma", "Diagnosis By": "PET and histology pending" }, "Topic": { "Title": "Sjogren's Syndrome", "Disease Discussion": "Sjogren\u2019s syndrome is an autoimmune disorder characterized by infiltration of lymphocytes into the lacrimal, salivary, and mucous glands causing keratoconjuntivitis sicca (dry eyes), xerostomia (dry mouth), and xerorhinia (dry nose). Typically, the disease affects middle aged women and many of the patients have associated manifestations of other collagen vascular disorders (e.g. rheumatoid arthritis, scleroderma, or SLE). \n\nPulmonary involvement of Sjogren\u2019s disease occurs in approximately one-third of patients with or without collagen vascular disease. Most commonly this manifests as interstitial fibrosis. Thickened sputum with associated mucous plugging and recurrent atelectasis, pneumonia, bronchitis or bronchiectasis is also seen. Sjogren\u2019s patients are also at increased risk for developing non-Hodgkin\u2019s lymphoma and lymphocytic interstitial pneumonitis. \n\nLymphoma occurs in approximately 5-10% of Sjogren\u2019s patients. These lymphomas are mucosa-associated lymphoid tissue (MALT) lymphoma. Generally, there are no correlations with the severity or duration of Sjogren\u2019s and development of lymphoma. Lymphoma should be suspected in patients with nodular or alveolar opacities and mediastinal lymph node involement. \n\nLymphocytic interstitial pneumonitis or diffuse lymphoid hyperplasia is infiltration of the pulmonary interstitium by mature lymphocytes. A lower lobe reticulonodular and linear pattern of disease is seen. Often, air-space opacification will also be seen.", "ACR Code": "9.3", "Category": "Inflammatory, autoimmune", "Keywords": "Sjogren'sLymphoma", "Reference": "Brant WE and Helms CA. Fundamentals of Diagnostic Radiology. Second edition. Philadelphia: Lippincott, Williams and Wilkins, 1999.\n\nTonami H, Matoba M, Kuginuki Y, Yokota H, Higashi K, Yamamoto I, Sugai S. \"Clinical and imaging findings of lymphoma in patients with Sjogren syndrome.\" J Comput Assist Tomogr. 2003 Jul-Aug:27(4):517-24.\n\nPalacios E, Larusso G, Rojas R, and Ramirez G. \"Lymphoma of the parotid gland in Sjogren's syndrom.\" Ear, Nose, and Throat Journal. March, 2004." } }, { "U_id": "MPX2570", "TAC": [ "MPX2570_synpic18865", "MPX2570_synpic18867" ], "MRI": [], "Case": { "Title": "Spigelian hernia", "History": "54 y/o female with acute abdominal pain and a history of remote abdominal surgery, evaluate for adhesion/obstruction.\nPlain abdominal film showed possible obstruction", "Findings": "Axial, coronal MIP, sagittal, and adjusted coronal plane images reveal bowel herniation through a right lateral abdominal wall defect, near the level of the iliac spines. Oral contrast opacifies minimally dilated bowel to the point of prolapse, beyond which the prolapsed segment and remaining distal bowel are unopacified. There is prolapsed omental fat as well, with mild inflammatory stranding.", "Differential Diagnosis": "Spigelian hernia, congenital or acquired", "Case Diagnosis": "Spigelian hernia", "Discussion": "see factoid" }, "Topic": { "Title": "spigelian hernia", "Disease Discussion": "Spigelian hernia occurs in an area of transition from muscle to aponeurosis in the transverses abdominis. Spigelian hernias account for 2% of abdominal wall hernias. It is often missed or misdiagnosed and presents emergently with incarceration or strangulation in up to 25% of cases. There is no gender difference and the mean age at diagnosis is 50.\nSpigelian hernias can be congenital or acquired. Previous operations are found in 50% of all cases. Other factors mentioned are alterations in the tension of the abdominal wall aponeurosis produced by morbid obesity, multiple pregnancies, prostatic enlargement, or chronic pulmonary disease. Equally important seems to be rapid weight loss in obese patients.\nAlthough an SH can occur at any point along the semilunar line, 90% of them are found where the Spigelian fascia is broad and weak. This region, called the \u201cSpigelian belt\u201d (S belt), is a 6-cm horizontal transverse zone located within a plane between the umbilicus and a line joining both anterior iliac spines. \nDiagnosis will be virtually impossible unless the entity is previously considered. Most patients present with unilateral abdominal pain and sensation of an abdominal wall mass. Physical exam is of limited utility. At the bedside, diagnosis and reduction with ultrasound guidance is sometimes attempted. However, CT remains the study of choice for identification of the hernia and the bowel obstruction that often accompanies it. CT typically shows a short segment of bowel and/or omentum herniated through the typical location and sandwiched between the internal and external abdominal oblique muscles.\n\nManagement consists of bedside reduction when possible, often followed by surgical mesh or plug repair of the defect.", "ACR Code": "4.7", "Category": "Obstruction or Stenosis", "Keywords": "spigelianherniaabdominal wall", "Reference": "1. Irma Sanchez Montes, MD, MBA, FACS\nMaximo Deysine, MD, FACS, Spigelian and other uncommon hernia repairs, Surgical Clinics of North America Volume 83 \u2022 Number 5 \u2022 October 2003\n2. Michael Blaivas MD, RDMS, Ultrasound-guided reduction of a Spigelian hernia in a difficult case: An unusual use of bedside emergency ultrasonography, American Journal of Emergency MedicineVolume 20 \u2022 Number 1 \u2022 January 2002", "External Links": "www.mdconsult.com" } }, { "U_id": "MPX2572", "TAC": [ "MPX2572_synpic17801", "MPX2572_synpic17802" ], "MRI": [], "Case": { "Title": "Osteoid Osteoma confirmed by radiographic appearance and clinical history", "History": "15 year old white male presents with three month history of right upper leg pain that is unrelieved by rest. Pain reportedly is worse at night and is somewhat relieved by NSAIDs. There is no history of trauma or potential for overuse injury.", "Exam": "Well developed, well nourished adolescent male in no acute distress. Can bear full weight with both lower extremities despite visible pain. Palpation and manipulation does not localized pain in right upper leg on exam.\n\nNo labs.", "Findings": "Plain film x-rays demonstrate an oval area of lucency within the right femoral cortex surrounded by an increased periosteal reaction.\n\nCT of the right lower extremity demonstrates a cortically based oval lucency (nidus) surrounded by sclerotic bone.", "Differential Diagnosis": "Osteoid Osteoma \nSclerosing Osteomyelitis\nBrodie abscess\nEosinophilic Granuloma", "Case Diagnosis": "Osteoid Osteoma confirmed by radiographic appearance and clinical history", "Treatment & Follow Up": "In most instances pain is the only adverse effect of the tumor. Aspirin and NSAIDs can be used if surgery is not an option. Rarely is there are secondary pathologic consequences in young children with spine or joint oriented tumors. But, because the pain itself can be disabling and spontaneous regression over years is unpredictable, operative treatment is often recommended. Most recently radiofrequency ablation (RFA) has gained acceptance as the treatment of choice for this condition. It has replaced open surgery because it has far fewer complications and a much shorter recovery period. \n\nGenerally this procedure is performed under spinal or local anesthetic and the lesion is identified under CT guidance. Once the electrode is introduced into the lesion it is heated up to 85-90 degrees Celsius for 6 minutes and then withdrawn. Patients treated with RFA are usually pain free within 2-3 days and are advised to avoid running or jumping for 3 months.", "Discussion": "This patient underwent radiofrquency ablation of this lesion with complete symptomatic relief." }, "Topic": { "Title": "Osteoid Osteoma", "Disease Discussion": "The exact etiology of an osteoid osteoma is largely unknown. It is a relatively common benign bone-forming tumor first described in 1935 that occurs almost exclusively in patients under the age of 30, males predominantly. It is almost always painful, and classically presents with night pain that is relieved by aspirin and gets worse with alcohol intake. This lesion can occur in any part of any bone, but typically in the legs and femur with the following distribution: Metadiaphysis and metaphysis of long bones \u2013 73%; Spine \u2013 14%; Hands and feet \u2013 12%.\n\nRadiographically, an osteoid osteoma typically has a cortically based lucent nidus with a thickened sclerotic cortex that can be seen well both on pain film and CT. There is perinidal bone marrow edema and soft tissue inflammation if evaluated on MRI; but, in the right clinical setting, this modality is often unnecessary. A nuclear medicine study will help differentiate this lesion from osteomyelitis \u2013 both an osteoid osteoma and osteomyelitis can look identical on plain films and CT. A bone scan of an osteoid osteoma will demonstrate a \u201cdouble density\u201d sign due to the excessive vascular supply of the nidus. In contrast, osteomyelitis will be photopenic in the area corresponding to the plain film lucency representing pus and an avascular focus.\n\nIn most instances pain is the only adverse effect of the tumor. Rarely is there are secondary pathologic consequences in young children with spine or joint oriented tumors. Because the pain itself can be disabling and spontaneous regression over years is unpredictable, operative treatment is often recommended. Most recently radiofrequency ablation (RFA) has gained acceptance as the treatment of choice for this condition. It has replaced open surgery because it has far fewer complications and a much shorter recovery period. \n\nGenerally this procedure is performed under spinal or local anesthetic and the lesion is identified under CT guidance. Once the electrode is introduced into the lesion it is heated up to 85-90 degrees Celsius for 6 minutes and then withdrawn. Patients treated with RFA are usually pain free within 2-3 days and are advised to avoid running or jumping for 3 months.", "ACR Code": "4.3", "Category": "Neoplasm, benign", "Keywords": "Osteoid Osteomapainful tumorsrelived by aspirin or NSAIDs", "Reference": "1. Helms C. A., Fundamentals of Skeletal Radiology, 2nd Ed. 1995; pages 166-168.\n2. Rubin E., Farber J. Pathology, 2nd Ed. 1994; pages 1316-1317.\n3. MGH Department of Radiology website. http://www.massgeneralimaging.org/Osteoid_Osteoma_Site" } }, { "U_id": "MPX2576", "TAC": [ "MPX2576_synpic24358", "MPX2576_synpic24359", "MPX2576_synpic24360" ], "MRI": [], "Case": { "Title": "CT guided biopsy of liver revealed pt has cirrhosis with corresponding portal hypertension. The biopsy of the liver mass was consistent with focal fat deposit, but inconclusive, and will be re-biopsied for definitive diagnosis", "History": "49 y/o white male with a history of heavy EtOH use (3-4 hard dinks per day over past 35 years) complains of persistent bruising after two recent falls in which he did not lose consciousness. Pt reports yellowing of his skin and eyes, and a bloated abdomen over past five days. He has had several no bleeds in the past two days, and two black and tarry foul smelling stools. No episodes of hemoptysis", "Exam": "Overweight jaundiced male with severe scleral icterus. He has a distended abd with a palpable liver edge 4cm below the costal margin. There is also shifting dullness to percussion. Pt also has mild bilateral edema in the lower extremities.\nElectrolytes- 139/2.9/101/26/11/0.8/122 Mg-1.6 Ca-7.4 CBC- 4.4/9/7/27.8/40 PT/PTT- 18.7/37.1 \nAlk Phos- 198 AST/ALT- 422/109 Tbili- 20.8 ConjBili- 16.8 LDH- 1066 Amylase- 201 Lipase-4353 AFP-5.6", "Findings": "Ultrasound: Liver is echogenic with coarsened architecture and fatty infiltrate. There is a small mass in the left lobe.\nTriple phase contrast CT: Acites along the liver and pericolic gutter bilateral. Liver appears diffusely fatty. Evidence of portal hypertension such as cannulated umbilical artery, and esophageal varices. A hypoattenuated mass in the left lobe along the gallbladder fossa, which measures 6.1 x 4.5 cm. The region has decreased uptake, which is consistent with focal fat deposit.", "Differential Diagnosis": "With this patient\u2019s history, clinical findings, and radiographic images, the differential is alcoholic hepatitis versus cirrhosis. Mass in the patient\u2019s liver highly likely to be a hepatocellular carcinoma, but has a differential diagnosis of malignancy to include metastatic disease, and cholangiocarcinoma. A benign mass has the differential of a cyst, hemangioma, hepatic angioma, focal nodular hyperplasia, or an abcess.", "Case Diagnosis": "CT guided biopsy of liver revealed pt has cirrhosis with corresponding portal hypertension. The biopsy of the liver mass was consistent with focal fat deposit, but inconclusive, and will be re-biopsied for definitive diagnosis", "Treatment & Follow Up": "Pt treated for alcohol withdrawal and watched closely for life threatening complications of portal hypertension. He was given a Beta-blocker for control of BP in attempt to prevent rupture of gastric varices. He was also placed on spironalactone for treatment of acites. Liver nodule is awaiting biopsy and evaluation for removal will follow if malignancy is present. The pts cirrhosis could mildly regress with alcohol cessation, but the only definitive treatment is a liver transplant, which he is not eligible for at this time due to his current alcohol use. Pt will be placed in extended nursing facility for further evaluation, alcohol cessation, and observation of current portal hypertension.", "Discussion": "This pt has a strong PMH and social history with regards to alcoholic liver disease. His current episode could have been due to either an alcoholic hepatitis or cirrhosis. Unfortunately his biopsy, lab values (increased PT, elevated alk phos), and jaundice all suggest that his alcoholic liver disease has progressed to cirrhosis. Radiographic evaluation of a patient with cirrhosis begins with ultrasound, in which the liver may appear small and nodular. Echogenicities on US may also reveal a fatty pattern to the liver. A strong clinical history, lab values and US are sufficient to clinically diagnosis cirrhosis, but the gold standard for diagnosis is US. A CT cannot diagnose cirrhosis, but can be used to evaluate for symptoms of portal hypertension, and to further investigate the presence of masses found on US as seen in this patient. CT guided biopsy is also used to further evaluate liver masses in pt with cirrhosis. The greatest risk for primary hepatocellular carcinoma is seen in pts with cirrhosis and viral hepatitis." }, "Topic": { "Title": "Liver, cirrhosis, portal hypertension", "Disease Discussion": "This pt has a strong PMH and social history with regards to alcoholic liver disease. His current episode could have been due to either an alcoholic hepatitis or cirrhosis. Unfortunately his biopsy, lab values (increased PT, elevated alk phos), and jaundice all suggest that his alcoholic liver disease has progressed to cirrhosis. Radiographic evaluation of a patient with cirrhosis begins with ultrasound, in which the liver may appear small and nodular. Echogenicities on US may also reveal a fatty pattern to the liver. A strong clinical history, lab values and US are sufficient to clinically diagnosis cirrhosis, but the gold standard for diagnosis is US. A CT cannot diagnose cirrhosis, but can be used to evaluate for symptoms of portal hypertension, and to further investigate the presence of masses found on US as seen in this patient. CT guided biopsy is also used to further evaluate liver masses in pt with cirrhosis. The greatest risk for primary hepatocellular carcinoma is seen in pts with cirrhosis and viral hepatitis.\n\nCT guided biopsy of liver revealed pt has cirrhosis with corresponding portal hypertension. The biopsy of the liver mass was consistent with focal fat deposit, but inconclusive, and will be re-biopsied for definitive diagnosis", "ACR Code": "9.5", "Category": "Toxic (see also Metabolic)", "Keywords": "cirrhosisportal hypertension", "Reference": "Not provided" } }, { "U_id": "MPX2579", "TAC": [ "MPX2579_synpic12892" ], "MRI": [ "MPX2579_synpic12895", "MPX2579_synpic12896", "MPX2579_synpic12897" ], "Case": { "Title": "Frontonasal Encephalocele", "History": "8-week-old baby boy with a glabellar area mass.", "Exam": "Soft, fluctuant, non-tender midline mass, just above the nose. Exam otherwise unremarkable.", "Findings": "CT: Non-contrast CT demonstrates an extranasal soft tissue mass, contiguous with the frontal lobe, extending through an anterior cranial midline defect just above the nasal bones (fonticulus nasofrontalis).\n\nMR: There is an extranasal soft tissue mass is continuous with the frontal lobe, iso-intense to normal brain parenchyma on T1WI, slightly higher in signal compared with normal brain parenchyma on T2WI. There is no enhancement with gadolinium.", "Differential Diagnosis": "Encephalocele\nNasal Glioma\nDermoid Cyst\nSinus Tract", "Case Diagnosis": "Frontonasal Encephalocele", "Diagnosis By": "CT and MR imaging, Surgery", "Treatment & Follow Up": "Surgical reduction of the tissue, with placement of a dural patch over the defect (it is not excised!).", "Discussion": "Congenital lesions of the sinonasal cavity represent anomalies of invagination of the neural plate. In both encephaloceles and nasal gliomas, brain tissue becomes \u201ctrapped\u201d by closing bony growth plates (more precisely, it is a failure of adequate regression of the dermal connection). Encephaloceles maintain a CSF connection to the brain. They are categorized as extranasal (frontonasal) if they extend through the fonticulus nasofrontalis, and intranasal if they extend through the ethmoidal plate (nasoethmoidal). The isolated non-functional neuronal matter is isointense to brain on CT. On MR it is iso- to hypointense on T1 weighted images and hyperintense on T2 weighted images secondary to gliosis, but lacks contrast enhancement. Encephaloceles are associated with other craniofacial abnormalities and anomalies of the corpus callosum.\n\nNasal gliomas are not true glial tumors. They are similar to encephaloceles in that they represent isolated neuronal matter to due failures in regression during development, but the connection to the intracranial contents is limited to a fibrous band. They too are classified as intra- or extranasal. Interestingly, extranasal gliomas are neither truly nasal nor truly gliomas.\n\nDermoid cysts represent trapped ecto- and mesoderm. The patient often has a pit in the middle of the nose. An intracranial connection is maintained in 25% of lesions, placing the patient at risk for osteomyelitis, meningitis and cerebral abscess should they become infected. Sinus tracts maintain a connection to a dermoid cyst, and uncommonly to the brain. \n\nThis case represents a frontonasal encephalocele. The bony defect (fonticulus nasofrontalis) is best visualized on CT. MR confirms a connection to the brain parenchyma, with typical findings of gliosis but not enhancement in the non-functioning neuronal tissue." }, "Topic": { "Title": "Congenital lesions of the sinonasal cavity.", "Disease Discussion": "Congenital lesions of the sinonasal cavity represent anomalies of invagination of the neural plate. In both encephaloceles and nasal gliomas, brain tissue becomes \u201ctrapped\u201d by closing bony growth plates (more precisely, it is a failure of adequate regression of the dermal connection). Encephaloceles maintain a CSF connection to the brain. They are categorized as extranasal (frontonasal) if they extend through the fonticulus nasofrontalis, and intranasal if they extend through the ethmoidal plate (nasoethmoidal). The isolated non-functional neuronal matter is isointense to brain on CT. On MR it is iso- to hypointense on T1 weighted images and hyperintense on T2 weighted images secondary to gliosis, but lacks contrast enhancement. Encephaloceles are associated with other craniofacial abnormalities and anomalies of the corpus callosum.\n\nNasal gliomas are not true glial tumors. They are similar to encephaloceles in that they represent isolated neuronal matter to due failures in regression during development, but the connection to the intracranial contents is limited to a fibrous band. They too are classified as intra- or extranasal. Interestingly, extranasal gliomas are neither truly nasal nor truly gliomas.\n\nDermoid cysts represent trapped ecto- and mesoderm. The patient often has a pit in the middle of the nose. An intracranial connection is maintained in 25% of lesions, placing the patient at risk for osteomyelitis, meningitis and cerebral abscess should they become infected. Sinus tracts maintain a connection to a dermoid cyst, and uncommonly to the brain. \n\nThis case represents a frontonasal encephalocele. The bony defect (fonticulus nasofrontalis) is best visualized on CT. MR confirms a connection to the brain parenchyma, with typical findings of gliosis but not enhancement in the non-functioning neuronal tissue. Treatment involves surgical reduction of the tissue, with placement of a dural patch over the defect; it is not excised.", "ACR Code": "1.1", "Category": "Congenital, malformation", "Keywords": "EncephaloceleCongenital Sinonasal LesionNasal Glioma", "Reference": "Brandt WE, Helms CA. Fundamentals of Diagnostic Radiology, 2cd Ed.Lippincott William & Wilkins, 1999.\nGrossman RI, Yousem DM. Neuroradiology: The Requisites. Mosby, 1994." } }, { "U_id": "MPX2584", "TAC": [ "MPX2584_synpic19853", "MPX2584_synpic19854", "MPX2584_synpic19855", "MPX2584_synpic19856" ], "MRI": [], "Case": { "Title": "Stage V bilateral Wilms' Tumor", "History": "5 year female with a single episode of painless hematuria which rapidly progressed to clots of blood over two days. She initially presented to the emergency room. She was instructed to follow up the next day to her primary care provider. She returned to the emergency room the next morning with right upper quadrant pain and vomiting and was found to have a right abdominal mass. A CT scan was performed at that time demonstrating bilateral renal masses as described in the images.", "Exam": "Right abdominal mass that did not cross the midline.\nUA- 2+ proteinuria, gross hematuria", "Findings": "Bilateral heterogeneously enhancing renal masses with tumor thrombus extending into the right renal vein, IVC, and the right atrium. Bilateral neuroblastomatosis is demonstrated.", "Differential Diagnosis": "Bilateral Wilms tumor, nephroblastomatosis", "Case Diagnosis": "Stage V bilateral Wilms' Tumor", "Diagnosis By": "Bilateral renal biopsies, both showing favorable histology Wilm's tumor. No nuclear anaplasia was seen.", "Treatment & Follow Up": "After initial chemotherapy decreased the size, but did not eliminate the right atrial tumor thrombus, the pt. underwent thoracotomy to remove it. Later she underwent right nephrectomy when the largest right renal mass grew despite initial reponse to chemotherapy. Chemotherapy and radiation therapy continue to treat residual disease on the left." }, "Topic": { "Title": "Bilateral Wilms' Tumor", "Disease Discussion": "Wilms' tumor is the most common primary renal malignancy and intra-abdominal tumor of childhood. Ninety per cent occur in children less than 7 years of age, with a median age of 3-1/2 years. The children are usually asymptomatic, most often presenting with clinical suspicion of an abdominal mass (approximately 70%). Other symptoms include abdominal pain (30%), hematuria (15 to 20%), and less commonly with moderately severe hypertension and nonspecific constitutional symptoms (fever, malaise, gastrointestinal complaints). There is a higher incidence of Wilms' tumor in patients with certain congenital abnormalities such as aniridia, hemi-hypertrophy, Beckwith-Wiedemann syndrome, nephroblastomatosis, and various genitourinary abnormalities (hypoplasia, fusion, ectopia, duplicated collecting systems, hypospadias, and cryptorchidism).\n\nWilms' tumor is secondary to proliferation of metanephric blastema. It is typically bulky and usually extends within the renal parenchyma, displacing and distorting the pelvocalyceal system. However, the mass may be exophytic or may, although rarely, be extrarenal. The outcome following multimodal therapy depends on the initial stage and whether or not the tumor has favorable or unfavorable histology for response to treatment. The unfavorable types include anaplastic, sarcomatous, and rhabdoid types.\n\nThe following stages have been described for Wilms' tumor:\n\nI: Tumor limited to kidney and completely resected, negative margins, intact renal capsule, not rupture.\n\nII: Tumor extends beyond kidney, but completely excised, negative margins, regional infiltration, spillage.\n\nIII: Residual nonhematogenous tumor, confined to abdomen including lymph nodes, peritoneal implants, incomplete excision.\n\nIV: Hematogenous metastases beyond stage III, i.e., lung, liver, bone, brain.\n\nV: Bilateral renal involvement, at time of diagnosis.\n\nWilms' tumor is bilateral (Stage V) in 5 to 10% at time of initial diagnosis. In a patient with unilateral Wilms', a contralateral tumor may develop 5 to 10 years later, although the majority occur within 2 years. The work-up should include a plain abdominal supine radiograph, not only to look for mass affect but also to look for calcifications, skeletal abnormalities, and paravertebral masses which may help in differentiating Wilms' tumor from neuroblastoma. \n\nThe next imaging study should be abdominal and pelvic sonography to determine the organ of origin, the size and extent of the mass, the characteristics of the mass (solid, cystic, complex calcifications), the presence of regional lymphadenopathy, liver metastases, tumor thrombus in the renal vein, inferior vena cava, and/or right atrium, and to look for bilaterality of the mass. One should also look for any evidence of nephroblastomatosis which appears sonographically as hypoechoic masses in the periphery of the kidney, thickening of the renal capsule, or as nodularity or lobulation of the kidney. This entity, which may be an anlage for Wilms' tumor, is much more easily seen with contrast- enhanced CT. Duplex and/or color Doppler imaging are particularly helpful in the evaluation of the venous vasculature structures that may be involved with Wilms' tumor. Wilms' tumor is most often a solid mass, although cystic spaces may often be seen within the mass due to internal hemorrhage and/or necrosis. We have noted that some of the cystic spaces within Wilms' tumor are large venous channels due to arteriovenous shunting.\n\nDepending upon the sophistication of the ultrasound, one may choose to also obtain a baseline CT, unless nephroblastomatosis is suspected. Certainly a baseline chest CT is recommended prior to surgery to look for pulmonary metastases. During and after their treatment, sonography is an excellent noninvasive means of following the children.", "ACR Code": "8.3", "Category": "Neoplasm, NOS" } }, { "U_id": "MPX2589", "TAC": [ "MPX2589_synpic16318" ], "MRI": [], "Case": { "Title": "Microcystic meningioma", "History": "This 59 year old woman complained of mild left arm and leg weakness poor concentration and difficulty findings words. On the day of admission, she had \"blacked out\" for 6 to 8 minutes.", "Exam": "On admission, she was awake and attentive. Her pupils were normally reactive to light and accommodation. She had a flattened left naso-labial fold and bilateral decreased hearing. The remainder of the cranial nerves were apparently normal. Strength in the left arm was graded as 4/5 and left hand grip was graded as 2/5. Reflexes were normal. Radiologic studies and subsequent surgery were performed.", "Findings": "Round enhancing mass with intraaxial vasogenic edema", "Differential Diagnosis": "\u2022 Metastasis\n\u2022 Anaplastic Astrocytoma\n\u2022 Anaplastic Oligodendroglioma\n\nIf extraaxial - Meningioma", "Case Diagnosis": "Microcystic meningioma" }, "Topic": { "Title": "Microcystic meningioma", "Disease Discussion": "Microcystic meningiomas have occasionally been designated as \"humid\" meningiomas because of the soft, moist appearing cut surface. Microscopically they contain myriads of intracellular and intercellular spaces that are filled with fluid having a low protein content. Their behavior is similar to other benign meningiomas; however, the unusual histological appearance can lead to confusion with glial neoplasms. The meningeal nature of these tumors can be confirmed with immunostaining for epithelial membrane antigen. Vessels in these neoplasms may be markedly thickened.", "ACR Code": "1.3", "Category": "Neoplasm, non-glial", "Keywords": "meningiomas" } }, { "U_id": "MPX2580", "TAC": [ "MPX2580_synpic39472" ], "MRI": [ "MPX2580_synpic39474", "MPX2580_synpic39475", "MPX2580_synpic39476", "MPX2580_synpic39477", "MPX2580_synpic39478", "MPX2580_synpic39479", "MPX2580_synpic39480", "MPX2580_synpic39481", "MPX2580_synpic39482", "MPX2580_synpic39483", "MPX2580_synpic39484", "MPX2580_synpic39486", "MPX2580_synpic39487", "MPX2580_synpic39490" ], "Case": { "Title": "Epidermoid Tumor", "History": "52 yo female with complaint of hearing loss.", "Findings": "Noncontrast CT: The patient is status post right suboccipital craniotomy. There is a subtle area of hypoattenuation off-midline to the right, anterior and lateral to the pons.\n\nContrast enhanced CT demonstrates a subtle area of nonenhancing hypoattenuation off-midline to the right, anterior and lateral to the medulla.\n\nMRI:\n\nSagittal T1-weighted FLAIR demonstrates expansion of the prepontine cistern, and enlargement of the CSF space anterior to the proximal cervical spinal cord and medulla, with displacement of the medulla posteriorly. This space contains an extra-axial mass, demonstrating heterogeneous signal intensity.\n\nCoronal T2-weighted FLAIR demonstrates heterogeneous signal intensity in the prepontine cistern.\n\nAxial T1 weighted images demonstrates the prepontine cistern extra-axial mass that is near CSF signal intensity with enlargement of the pre-medullary cistern.\n\nAxial T2 weighted images demonstrates the lamellated mass, which is heterogenous in signal intensity posterior to the hypophsial fossa and anterior to the basilar artery.\n\nAxial T1-weighted image with gadolinium demonstrates no significant enhancement of the extra-axial mass.\n\nAxial Diffusion Weighted image demonstrate restricted diffusion.\n\nSagittal 3D FIESTA demonstrates low signal in the prepontine cistern, and enlargement of the CSF space anterior to the proximal cervical spinal cord and medulla.\n\nAxial 3D FIESTA image demonstrates low signal intensity in the prepontine cistern, medial to cranial nerve V, and adjacent to the right cranial nerve VII and VIII complex.", "Differential Diagnosis": "Epidermoid Tumor\nArachnoid Cyst", "Case Diagnosis": "Epidermoid Tumor", "Diagnosis By": "Pathology", "Treatment & Follow Up": "The patient underwent resection, with follow-up imaging demonstrating no evidence of reoccurence. However, as the patients symptoms continued, and clinical concern for reoccurence mounted, further MR imaging with the use of 3D Fast Imaging Employing STeady-state Acquisition (FIESTA) clearly demonstrates the epidermoid tumor, which may have been present all along." }, "Topic": { "Title": "Epidermoid Tumor", "Disease Discussion": "Lesions/Condition: Epidermoid Tumor\n\nDiscussion:\n\nEpidermoid tumors typically occur between the ages of 20 and 60, with the peak incidence in the fourth decade, affecting both men and women equally.\n\nIntracranial epidermoid tumors are congenital inclusion cysts that comprise 1% of primary intracranial neoplasms. They are thought to arise from the enclosure of ectodermal elements when the neural tube closes at 3-5 weeks gestation. Additionally, acquired epidermoid tumors may occur as the result of trauma, although this is relatively uncommon in the brain. Epidermoids are composed of an outer capsule of connective tissue that surrounds a layer of keratinized stratified squamous epithelium and inner cystic fluid that includes debris, keratin, water, and cholesterol. As the epithelial layer desquamates, the cells accumulate and form a cholesterol-rich layer that gives the tumor its characteristic pearly white appearance. Epidermoids subtly grow within the CSF spaces, surrounding and encasing adjacent neurovascular structures. The tumor has an irregular and lobulated cauliflower-like outer surface that shines like a \u201cmother of pearl.\u201d\n\nThe majority of intracranial epidermoid tumors are intradural lesions, in the basal subarachnoid spaces occurring off-midline. Between 40%-50% of cases are found in the cerebellopontine angle cistern. After schwannoma and meningioma, epidermoid tumors are the third most common cerebellopontine angle mass. Epidermoid tumors also occur in the sellar and parasellar regions. Less commonly, epidermoid tumors have been reported in the cerebral hemispheres, brain stem, and rarely in the lateral ventricles. Approximately ten percent of epidermoid tumors are extradural, occurring in the skull or spine.\n\nEpidermoid tumors are benign slow-growing tumors, and malignant degeneration is extremely rare. \n\nClinical Features:\n\nClinical features of epidermoid tumors are usually secondary to the mass effect of the tumor on adjacent structures. Gait disturbance, cranial neuropathies, and occasionally seizures are presenting symptoms. Hydrocephalus is not commonly seen with intracranial epidermoid tumors. Additionally, symptoms related to chemical meningitis caused by leakage of tumor contents into the subarachnoid space may be seen.\n\nRadiology:\n\nEpidermoid tumors on CT are well-circumscribed, homogenous lobulated extra-axial masses, that are nonenhancing, and hypoattenuating, and are similar to CSF, secondary to the presence of solid cholesterol and/or loculated CSF within the tumor, and rarely demonstrate calcification.\n\nMR imaging is the best modality for evaluating these tumors. Typically, epidermoid tumors demonstrate a lamellated appearance on MR imaging, secondary to the desquamated squamous epithelium. Most epidermoid tumors have signal intensities that are near CSF signal, low to intermediate on T1 weighted images, and slightly hyperintense on T2 weighted images. The main differential diagnostic consideration is that of an arachnoid cyst, with arachnoid cyst following the signal intensity patterns of CSF with all MR pulse sequences, whereas epidermoid tumors are not hypointense on FLAIR images and demonstrate areas of hyperintense signal relative to CSF. Furthermore, on DW images, epidermoid tumors demonstrate restricted diffusion, which is not characteristic of arachnoid cysts. Additionally, approximately 25% of epidermoid tumors will demonstrate a thin rim of peripheral enhancement following the administration of contrast material. Furthermore, employing the use of a high resolution gradient-echo T2 sequence, such as 3D Fast Imaging Employing STeady-state Acquisition (FIESTA) the lamellated epidermoid tumor is clearly depicted as low signal intensity as it is contrasted against a hyperintense CSF background, achieving a precise preoperative assessment of surgical anatomy.\n\nFinally, the signal characteristics of epidermoid tumors vary depending on its composition. Rarely, epidermoids will appear hyperattenuated on CT, secondary to elevated protein content, with reversal of signal characteristics on MR imaging, high signal intensity on T1WI, and low signal intensity on T2WI. \n\nTreatment: \n\nSubtotal resection is usually performed to alleviate compression of adjacent structures, and to avoid damaging vital structures. The reported rate of recurrence of epidermoid tumors is highly variable.", "ACR Code": "1.3", "Category": "Neoplasm, benign", "Keywords": "Epidermoid TumorCPA MassFIESTA", "Reference": "Brant: Fundamentals of Diagnostic Radiology. 2nd Edition. Philadelphia: Lippincott Williams & Wilkins. 1999. \nOsborn, Anne. Diagnostic Neuroradiology. Mosby. St. Louis, Missouri. 1994.\nForghani. RadioGraphics 2007; 27:1489-1494.\nSmirniotopoulos et al. RadioGraphics 1993; 13:1131-1147\nMikami et al. Neurosurg Rev. 2005 Oct;28(4):261-6." } }, { "U_id": "MPX2583", "TAC": [ "MPX2583_synpic35300", "MPX2583_synpic35301", "MPX2583_synpic35302", "MPX2583_synpic35303", "MPX2583_synpic35304", "MPX2583_synpic35306", "MPX2583_synpic35307" ], "MRI": [], "Case": { "Title": "Hiatal Hernia", "History": "74 year old female with dyspnea on exertion.", "Exam": "N/A", "Findings": "Frontal and lateral chest radiographs demonstrate no acute cardiopulmonary disease (clear lungs) as well as senescent change within the aorta and spine. Additionally a soft tissue density mass is present within the middle mediastinum with an internal air fluid level behind the heart disrupting the azygoesophageal edge.\n\nAxial CT images with oral and intravenous contrast material demonstrate a sliding hiatal hernia with the gastroesophageal junction and a portion of the proximal stomach superior to the diaphragm. An MPR obliqued image further demonstrates this superior migration of the gastroesophageal junction into the thorax.", "Differential Diagnosis": "Based upon the radiographs:\nHiatial hernia (sliding versus paraesophageal versus mixed)\nForegut duplication cyst\nAbscess\nNecrotic lymph node with cavitation\n\nDiagnosis of a sliding hiatal hernia is confirmed with CT.", "Case Diagnosis": "Hiatal Hernia", "Diagnosis By": "Contrast enhanced CT", "Treatment & Follow Up": "Non surgical symptomatic medical management", "Discussion": "Please see factoid" }, "Topic": { "Title": "Hiatal Hernia", "Disease Discussion": "In the United States and Canada, a large proportion of adults undergoing upper gastrointestinal barium radiographs are found to have a small hiatal hernia. About 90% to 95% of hiatal hernias found by radiograph are sliding hernias, and the rest are paraesophageal or mixed. Most sliding hiatal hernias are small and of little clinical significance. Patients with symptomatic paraesophageal hernias are most often middle-aged to elderly. Many patients with small, simple sliding hiatal hernias are asymptomatic. The main clinical significance of the sliding hiatal hernia is its contribution to gastroesophageal reflux . In addition to heartburn and regurgitation, patients with large sliding hiatal hernias may complain of dysphagia or discomfort in the chest or upper abdomen. In a prospective, population-based study the risk of iron-deficiency anemia was found to be increased in adults with hiatal hernia. On chest radiograph a hiatal hernia may be noted as a soft tissue density in the retrocardiac area. Hiatal hernias are most often diagnosed on upper gastrointestinal barium radiographic studies. At endoscopy the gastroesophageal junction is noted to be proximal to the impression of the diaphragm. [1]\n\nPatients with paraesophageal and mixed hiatal hernias are rarely completely asymptomatic if closely questioned. About half of patients with paraesophageal hernias have gastroesophageal reflux. Other symptoms include dysphagia, chest pain, vague postprandial discomfort, and shortness of breath. A substantial number of patients have chronic gastrointestinal blood loss. If the hernia is complicated by gastric volvulus, acute abdominal pain and retching will occur, often progressing rapidly to a surgical emergency. A paraesophageal or mixed hiatal hernia may be seen on chest radiograph as an abnormal soft tissue density (often with a gas bubble) in the mediastinum. Upper gastrointestinal radiograph is the best diagnostic study. [1]\n\nHiatal hernias are occasionally complicated by volvulus. The stomach is normally fixed in position by ligamentous attachments to the duodenum, spleen, liver, and diaphragm. Laxity of these ligaments, elevation of the left hemidiaphragm, adhesions, gastric tumor, or masses in adjacent organs may predispose to volvulus. In about one third of cases the volvulus occurs below the diaphragm. In the other two thirds of cases volvulus occurs above the diaphragm in association with a diaphragmatic hernia. Sliding hiatal hernias are not associated with gastric volvulus. Gastric volvulus may be mesenteroaxial or organoaxial. In about 60% of cases gastric volvulus is organoaxial: the stomach twists along its long axis. This axis usually passes through the gastroesophageal and gastropyloric junctions. The antrum rotates anteriorly and superiorly, the fundus posteriorly and inferiorly, twisting the greater curvature at some point along its length. This type of volvulus is commonly associated with a diaphragmatic hernia. Organoaxial volvulus is usually an acute event. Vascular compromise and gastric infarction may occur. The other major type of gastric volvulus is mesenteroaxial, in which the stomach folds on its short axis running across from the lesser curvature to the greater curvature, and the antrum twists anteriorly and superiorly. [1]\n\nSimple sliding hiatal hernias do not require treatment. Patients with symptomatic giant sliding hiatal hernias, paraesophageal, and mixed hernias should be offered surgery. Many experts suggest that surgery should be offered to patients with asymptomatic paraesophageal hernias, because about 30% of these patients will develop complications if left untreated. Many surgeons routinely perform a fundoplication on all repairs, both to prevent postoperative reflux esophagitis and to fix the stomach in the abdomen. Less commonly a gastrostomy is used to fix the stomach in position. Patients with sliding hiatal or paraesophageal hernias may have shortening of the esophagus. This makes it difficult to restore the gastroesophageal junction below the diaphragm without tension. In such cases an extra length of neoesophagus can be constructed from the proximal stomach (Colles-Nissen procedure). Paraesophageal and mixed hernias can be repaired through the chest or abdomen, with open or laparoscopic techniques. Compared with open repair, laparoscopic repair is associated with less blood loss, fewer overall complications, shorter hospital stay, and quicker return to normal activities. Long-term results are probably equal with either approach. Potential surgical complications include esophageal and gastric perforation, pneumothorax, and liver laceration. Potential long-term complications may include dysphagia if the wrap is too tight or gastroesophageal reflux if the fundoplication breaks down or migrates into the chest. Recurrence rates are about 10 [1]\n \n\n1. Feldman: Sleisenger & Fordtran's Gastrointestinal and Liver Disease, 7th ed., Copyright \u00a9 2002 Elsevier: MD Consult Online Core Collection Textbook: pp 369-374", "ACR Code": "7.9", "Category": "Hernia/herniation", "Keywords": "hiatal herniagastric volvulusdiaphragmatic hernia", "Reference": "1. Feldman: Sleisenger & Fordtran\\'s Gastrointestinal and Liver Disease, 7th ed., Copyright \u00a9 2002 Elsevier: MD Consult Online Core Collection Textbook: pp 369-374" } }, { "U_id": "MPX2592", "TAC": [ "MPX2592_synpic41579", "MPX2592_synpic41581", "MPX2592_synpic41582" ], "MRI": [], "Case": { "Title": "Left-sided Aortic Arch with an Aberrant Right Subclavian Artery", "History": "60 year old male with complaint of tachypnea and tachycardia with high clinical concern for pulmonary embolus.", "Findings": "Chest Radiography: : \n\nLateral chest radiograph demonstrates soft tissue density superior to the aortic arch causing anterior displacement of the trachea.\n\nContrast Enhanced CT: \n\nThe origin of the anomalous artery is evident arising from the posterior superior aortic arch as the last branching vessel of a left-sided aortic arch passing posteriorly to the esophagus in the retrotracheal space. At a level 1 cm superior to the aortic arch, the aberrant right subclavian artery is located ascending posteriorly in the right superior mediastinum. \n\nMaximal intensity projection demonstrates the aberrant right subclavian artery arising from the medial wall of the aorta as the last branching vessel, passing posterior to the esophagus, and ascending anterolaterally to the spine into the thoracic inlet.", "Case Diagnosis": "Left-sided Aortic Arch with an Aberrant Right Subclavian Artery", "Diagnosis By": "Imaging findings are characteristic." }, "Topic": { "Title": "Left-sided Aortic Arch with an Aberrant Right Subclavian Artery", "Disease Discussion": "Condition: Left-sided Aortic Arch with an Aberrant Right Subclavian Artery\n\nDiscussion: \n\nA left-sided aortic arch with an aberrant right subclavian artery is a relatively common finding, affecting approximately 1/100 people, and may be an isolated anomaly or occur with associated congenital heart disease. The aberrant right subclavian artery forms secondary to the involution of a segment of the embryonic right 4th aortic arch, between the right subclavian and right common carotid arteries. Thus, the right subclavian artery arises from the posterior medial wall of the aorta arch as the last branching vessel, crosses the retrotracheal space posterior to the esophagus, and lays anterolateral to the spine ascending on the right towards the thoracic inlet. \n\nThis anomaly may go undetected on chest radiographs, and is incidentally detected on CT scans obtained for other reasons. On the lateral chest radiograph, findings may be normal, or the anomalous artery will be visualized as an area of increased density in the retrotracheal space, with a focal impression upon the posterior wall of the trachea. The posteroanterior chest radiograph will demonstrate an area of increased soft-tissue density in the right paratracheal region.\n\nAdditionally, at the point of origin the artery may arise from an aortic diverticulum (Kommerell diverticulum) potentially causing compression of the esophagus and inducing symptoms of dysphagia (\u201cdysphagia lusoria\u201d or \u201cdysphagia by freak of nature\u201d as described by Dr. David Bayford in 1794), most often in the elderly.", "ACR Code": "9.1", "Category": "Vascular", "Keywords": "Left-sided Aortic Arch with an Aberrant Right Subclavian ArteryAberrant Right Subclavian Artery", "Reference": "Webb et al. Fundamentals of Body CT. 3rd Edition. Philadelphia: Elsevier. 2006.\nFranquet et al. RadioGraphics 2002;22:S231-246.\nCarrizo et al. Tex Heart Inst J. 2004;31(2):168-171." } }, { "U_id": "MPX2595", "TAC": [ "MPX2595_synpic51006", "MPX2595_synpic51007" ], "MRI": [], "Case": { "Title": "Renal Duplicity (duplication)", "History": "History of blunt trauma to abdomen during motor vehicle accident.", "Exam": "Unremarkable exam.", "Findings": "Absence of left kidney sinus incidentally noted on CT abdomen.", "Differential Diagnosis": "Intrarenal mass (transitional cell carcinoma)\nHypertrophied Column of Bertin", "Case Diagnosis": "Renal Duplicity (duplication)", "Treatment & Follow Up": "None indicated.", "Discussion": "The patient's CT findings were incidental, and the patient had no related symptoms or complaints. In turn, no further work-up or treatment was indicated." }, "Topic": { "Title": "\"Faceless Kidney\"", "Disease Discussion": "The term \u201cfaceless kidney\u201d most often refers to the presence of a duplicated renal collecting system; however, this term has also been used to describe anything which obliterates the renal sinus on imaging. Most patients with duplex collecting systems are asymptomatic (abnormalities are usually noted incidentally), but it is important to note that duplex systems are more likely to be associated with ureteropelvic obstruction, reflux, and infections. \n\nVarious imaging modalities may be useful in suggesting duplication, but CT is the superior modality for diagnosis. Plain films will usually exhibit a duplex kidney which is longer than the nonduplex kidney (1-3 cm longer), but this is nonspecific. Excretory urography may further characterize the renal anatomy and delineate anomalies, but may also prove difficult in discerning obstruction versus renal mass. The use of ultrasound may show the presence of two collecting systems with intervening parenchyma, but does not rule out an intrarenal mass. CT, however, is useful in detecting obstruction and further characterizing the renal parenchyma. It may also be valuable in illustrating partial versus complete duplication of ureters and ureter insertion points in the bladder. On transverse CT sections, scans of the upper and lower poles will exhibit normal morphology but will not show the presence of both renal pelvices. It\u2019s at the junction of the fused poles that one can appreciate the \u201cfaceless kidney\u201d due to the absence of vascular and collecting system elements.", "ACR Code": "8.1", "Category": "Radiologic Sign or Finding", "Keywords": "renal duplicationanomalieskidney", "Reference": "1. Dyer, R. B., Chen, M. Y., Zagoria, R. J. (2004). Classic Signs in Uroradiology. RadioGraphics, 24, S247-S280.\n2. Hulnick, D. H. and Bosniak, M. A. (1986). \"Faceless Kidney\": CT Sign of Renal Duplicity. Journal of Computer Assisted Tomography, 10 (5), 771-772.\n3. Zissin, R., Apter, S., Yaffe, D. Kots, E., Gayer, G., Nissenkorn, I., Hertz, M. (2001). Renal Duplication with Associated Complications in Adults: CT Findings in 26 Cases. Clinical Radiology, 56, 58-63." } }, { "U_id": "MPX2603", "TAC": [ "MPX2603_synpic15933" ], "MRI": [], "Case": { "Title": "Bicornuate Uterus", "History": "28 year old woman with right lower quadrant abdominal pain.", "Findings": "Endometrial fluid, with fluid pattern suggestive of an arcuate uterus, or less likely, partial bicornuate uterus. Small amount of free fluid in the pelvis. Prominent ovaries, with numerous enlarged follicles.", "Differential Diagnosis": "Partial Bicornuate Uterus\nArcuate Uterus", "Case Diagnosis": "Bicornuate Uterus", "Discussion": "Findings in this case are more consistent with arcuate uterus than bicornuate uterus." }, "Topic": { "Title": "Arcuate Uterus", "Disease Discussion": "Nine percent (9%) of women seen for infertility have anomalies of the genital tract. Congenital female reproductive organ abnormalities result from arrested or incomplete development of the mullerian ducts which normally fuse to form the cranial 1/3 of the vagina, cervix, uterus and fallopian tubes. Between 20-50% of these patients will also have urinary tract abnormalities. MRI and Hysterosalpingograms are commonly used for diagnosis. \n\nArrested mullerian duct development will result in uterine aplasia or unicornuate uterus. 5-20% of unicornuates will have ipsilateral renal agenesis.\n\nFailure of complete fusion of the mullerian ducts results in duplication of varying degrees:\n\n\u2022 Didelphys: 2 uterine horns, bicollis, 2 vaginal canals.\n\u2022 Septate: Midline septum within the uterus with normal contour of uterine fundus. These patients are at much higher risk for spontaneous abortion.\n\u2022 Bicornuate: 2 uterine horns as described above with single cervix and double vagina or single vagina and bicollis.\n\u2022 Arcuate: Most common anomaly not associated with reproductive failure. Has a normal fundal contour with smooth indentation of the fundal endometrial canal and no division of uterine horns.", "ACR Code": "8.1", "Category": "Congenital, malformation", "Keywords": "uterusbicornuatearcuate" } }, { "U_id": "MPX2604", "TAC": [ "MPX2604_synpic49129" ], "MRI": [], "Case": { "Title": "Renal Cell Carcinoma", "History": "A 55-year-old man complains of blood in his urine.", "Exam": "PE reveals a palpable abdominal mass.", "Findings": "Figure 1. Axial image from a contrast enhanced CT scan shows a heterogenous solid mass within the right kidney.\n\nFigure 2. Nephrectomy specimen demonstrates a well-circumscribed mass in the upper pole of the kidney.\n\nFigure 3. Histological examination of the mass demonstrates cuboidal cellls intermixed with foam cells in a papillary configuration.", "Differential Diagnosis": "\u2022 Renal Cell Adenoma\n\u2022 Renal Cell Carcinoma\n\u2022 Angiomyolipoma", "Case Diagnosis": "Renal Cell Carcinoma", "Diagnosis By": "Pathological examination of nephrectomy specimen", "Treatment & Follow Up": "Radical nephrectomy", "Discussion": "Computed tomography (Figure 1) confirms a solid mass in the upper pole of the right kidney. Radical nephrectomy was performed and the kidney sent to pathology (Figures 2 and 3)." }, "Topic": { "Title": "Renal Cell Carcinoma", "Disease Discussion": "Renal cancer is the seventh leading malignant condition affecting men and the twelfth among women.(1) Renal cell carcinoma (RCC) arises from the renal tubular epithelium, and accounts for approximately eighty-five percent of renal cancers. The classic triad presentation of RCC includes flank pain, hematuria and a palpable abdominal mass. These three findings are only seen in approximately ten percent of cases, and currently most cases are detected incidentally on imaging studies. Gross or microscopic hematuria is the most reliable symptom, but may be intermittent indicating the neoplasm may remain silent until it attains a particular size. Therefore, imaging studies of the genitourinary tract should be performed on any patient older than forty years of age with hematuria.\n\nTraditionally, RCC has been classified based on histology. In the past two decades, molecular genetic investigations of RCC have led to recurring chromosomal abnormalities occurring with specific RCC histological subtypes. Therefore, in 2004, the World Health Organization (WHO) integrated these consistent genetic abnormalities into the previous classification of renal neoplasms. Moreover, observations have indicated associated inherited cancer syndromes, which were reflected in the new WHO classification system. Of these subtypes, the most relevant subtypes include: Clear Cell (conventional), Papillary and Chromophobe, accounting for approximately seventy percent, fifteen to twenty percent, and five to ten percent of renal neoplasms, respectively.(1) The remaining subtypes are extremely less common.\n\nClear cell renal carcinoma (Figure 4), usually occurs as a solitary unilateral lesion from the proximal tubular epithelium. The growth pattern can be varied, but ranges from solid, trabecular or tubular. Histologically, the cells can have a rounded or polygonal shape, with clear or granular cytoplasm. The neoplastic cells have intracytoplasmic glycogen and lipids, which are dissolved during the preparation of the biopsy, giving the cells their clear appearance seen microscopically. The lipid containing cells in this subtype give the neoplasm its classic golden/yellow color on gross observation.(2)\n\nPapillary carcinoma (Figure 3) is characterized by a papillary growth pattern, with the papillary projections having a fibrovascular core consisting of foamy macrophages. There are two subtypes of papillary carcinoma recognized and differentiated by histomorphological characteristics. Type I neoplasms have a monolayer of cells with little cytoplasm. Type II neoplasms have an abundant eosinophilic cytoplasm and typically distinct nucleoli.(3)\n\nChromophobe renal carcinoma (Figure 5) is usually situated around blood vessels arranged in sheets. This neoplasm is composed of pale eosinophilic cells, often with a perinuclear halo. Abrahams et al found accentuated cell borders and a combination of hyperchromatic wrinkled nuclei, and perinuclear halos were the three most often associated histological features associated with this subtype.(4)\tCollecting duct renal carcinoma (CDC), or Bellini duct carcinoma, is an extremely rare entity, accounting for less than one percent of renal neoplasms. The neoplasm is located centrally with a gray appearance. Its borders are irregular and infiltrative with a so-called hobnail pattern. This subtype has been shown to have various histological patterns within a single neoplasm ranging from duct-like to papillary architecture, and therefore has been known to be misdiagnosed. This disease usually is diagnosed in advanced stage, and with its high rate of metastasis has a dismal prognosis.(5)\n\nRenal medullary carcinoma (RMC) is an extremely rare entity and associated with the sickle cell trait. Histologically, the neoplasm resembles CDC and grossly resembles urothelial carcinoma by its location, pattern and grade. RMC can be arranged in solid sheets, but usually in a reticular pattern with yolk sac-like areas. Furthermore, this neoplasm is typically found in the age range between ten to forty years with a male predominance.(1,2)", "ACR Code": "8.3", "Category": "Pathology", "Keywords": "nypernephromaNeoplasmKidney" } }, { "U_id": "MPX2606", "TAC": [ "MPX2606_synpic25192", "MPX2606_synpic25193", "MPX2606_synpic25195" ], "MRI": [ "MPX2606_synpic25197", "MPX2606_synpic25198" ], "Case": { "Title": "acute infarct", "History": "36 year-old woman with sudden-onset left-sided hemiparesis. PMH is significant for a history of SLE.", "Exam": "N/C", "Findings": "Non-contrast CT images of the head with \"stroke window\" settings demonstrate a wedge-shaped focal area of decreased density and loss of gray-white matter differentiation at the leve of the right frontal lobe, just anterior to the central sulcus.\n\nDiffusion weighted and associated ADC map axial MR images show a corresponding focus of restricted diffusion, consistent with an acute infarct.", "Differential Diagnosis": "acute infarct", "Case Diagnosis": "acute infarct" }, "Topic": { "Title": "acute infarct detection with non-contrast CT", "Disease Discussion": "Non-contrast CT of the head is still the initial tool of evaluation of patients suspected of having a stroke. It is used mainly to rule out hemorrhage (important in considering utilizing thrombolytic therapy) and/or mass effect. CT can sometimes show signs of acute infarct, although it is important to realize that the role of non-contrast CT is not to rule-out infarction, necessarily. (1)\n\nSince the widespread use of PACS workstation rather than printed films, it has been shown that varying the window settings can increase the sensitivity of acute infarction. Lev et al has shown in 1999 that utilizing the window and level settings of 32 and 8, respectively (which a lot of radiologist call \\\"the stroke window setting\\\") increased the sensitivity of non-contrast CT for detecting acute stroke from 57% to 71%. (2) This setting should be a part of every radiologist\\'s default setting on the PACS account, and radiologists should routinely examine every non-contrast head CT with the \\\"stroke window\\\" setting.", "ACR Code": "1.9", "Category": "Infarction and/or Necrosis", "Keywords": "acute infarctstrokenon-contrast computed tomography", "Reference": "1. Provenzale JM, Jahan R, Naidich TP, Fox AJ. Assessment of the patient with hyperacute stroke: imaging and therapy. Radiology. 2003 Nov;229(2):347-59.\n2. Lev MH, Farkas J, Gemmete JJ, Hossain ST, Hunter GJ, Koroshetz WJ, Gonzalez RG. Acute stroke: improved nonenhanced CT detection--benefits of soft-copy interpretation by using variable window width and center level settings. Radiology. 1999 Oct;213(1):150-5." } }, { "U_id": "MPX2608", "TAC": [ "MPX2608_synpic20532" ], "MRI": [], "Case": { "Title": "Empyema", "History": "60 YO female with a history of emphysema presented for follow-up care after completing a 2-week course of oral antibiotics for a community acquired pneumonia. The patient claimed to have worsening fatigue, myalgias, chills and fevers, and continued productive cough.", "Exam": "Bibasilar rales with decreased breath sounds over the lower left lung field.", "Findings": "When compared to the patient's original imaging studies, the follow-up CXR and subsequent chest CT demonstrated worsening air-space disease with a new large left sided effusion.", "Differential Diagnosis": "Parapneumonic effusion\nEmpyema\nPulmonary Abscess", "Case Diagnosis": "Empyema", "Diagnosis By": "US/Fluoroscopic guided drainage.", "Treatment & Follow Up": "The patient underwent image guided drainage and chest tube placement by interventional radiology. 600cc of purulent exudate was aspirated. Following 3 days of drainage and IV antibiotics, the patient underwent thoracotomy and decortication." }, "Topic": { "Title": "Empyema", "Disease Discussion": "A parapneumonic effusion is any pleural effusion associated with suppurative parenchymal lung disease. Simple parapneumonic effusions are uninfected, free-flowing fluid collections. Complicated parapneumonic effusions are early infected fluid collections prone to develop loculations by fibrinous septations. Empyema is a collection of frank pus within the pleural space. An effusion is termed complex when it develops loculations. The natural evolution of untreated simple and complicated parapneumonic effusions is to become complex and to progress to frank empyema with development of a residual cavity or entrapment of the lung by a fibrous peel or cortex.\n\nPneumonia results in parapneumonic effusion in approximately 45% of cases, although less than 5% of these progress to an empyema. Other common causes include mediastinal or pulmonary surgery and trauma. Less frequently, empyema may result from spread of infection from adjacent structures. Mortality from empyema ranges from 1% to 20%. \n\nClinical manifestations vary, depending on the underlying pulmonary process, the responsible organism, the quantity of bacteria and fluid in the pleural space, the stage of the disease, and the host defense mechanisms. The clinical presentation can range from an absence of symptoms to a severe febrile illness with toxemia and shock. In general, it is difficult to distinguish patients with infected pleural effusions from those with sterile parapneumonic effusions on the basis of history and physical examination alone. Clinical manifestations include fever, dyspnea, chest pain, and cough with mucopurulent sputum. Physical examination often reveals decreased breath sounds, dull percussion, and restricted respiratory excursions. \n\nWith the introduction of antibiotics in the mid-1940s, a significant shift occurred in the microbiology of pleural space infections. Anaerobic organisms are now the most common bacteria isolated from infected pleural effusions, being identified in up to 75% of cases, either alone (35%) or in combination with aerobic organisms (40%). Up to 35% of established empyemas have negative Gram stain evaluations and many patients with complicated parapneumonic effusions have negative culture results. Staphylococcus aureus is a relatively common cause of empyema in otherwise healthy adults, children and in patients who have had chest trauma or prior surgery, whereas alcoholic males are particularly susceptible to infection with Klebsiella pneumoniae. \n\nThoracentesis plays a critical role in the management of pleural effusions and in 90% of adult cases yields useful information. Fluid is removed and samples obtained for measurement of pH, glucose, LDH, protein, and differential cell count. An exudate is defined by: (1) a ratio of pleural fluid to serum protein greater than 0.5, (2) a ratio of pleural fluid LDH to serum LDH greater than 0.6, or (3) a pleural fluid LDH more than two-thirds of the upper normal limit for serum or >200 IU [3] . A transudate does not meet any of the above three criteria. \n\nIf the patient has a transudative effusion, no further laboratory tests on the pleural fluid are indicated. If the patient has an exudative pleural effusion, the remaining pleural fluid is sent for WBC and differential, cytologic examination, Gram's stain and cultures for aerobic and anaerobic bacteria, and mycobacteria and fungi if clinically indicated. The aspiration of frank pus confirms the presence of empyema and establishes an absolute indication for urgent drainage of the pleural space. In this instance, Gram's stain and culture are the only laboratory studies necessary to guide initial therapy. Pleural fluid Gram's stains can identify pathogens in 55% to 65% of patients with established empyemas. \nThe posterior-anterior and lateral chest radiographs are the best initial diagnostic modalities. When the patient is upright, free pleural fluid first accumulates in the lowest part of the hemithorax\u2014the posterior costophrenic angles. Lateral decubitus views allow detection of 50 to 100 ml of fluid and the presence of loculations if the fluid fails to layer out along the dependent chest. In the view with the involved side superior, the free fluid layers against the mediastinum and one can assess how much of the radiodensity is due to the fluid and how much is due to a parenchymal infiltrate. In the view with the involved side dependent, the amount of free pleural fluid can be semi-quantitated by measuring the distance from the chest wall to the outside of the lung. If the thickness of fluid exceeds 10 mm, a diagnostic thoracentesis is indicated. However, it is not necessary to tap all parapneumonic effusions, especially if the volume of fluid remains small, the patient is doing well, the fluid moves freely, or serial roentgenograms show improvement. \n\nCT is of great value in the overall evaluation of parapneumonic effusions and should be done early in the assessment of patients with complex parapneumonic effusion or empyema. CT is helpful in (1) differentiating pleural fluid from peripheral parenchymal infiltrates or pleural thickening, (2) evaluating the parenchymal disease, (3) determining the presence of loculations, (4) characterizing the pleural surfaces, and (5) guiding and assessing therapy. Complicated effusions and empyemas are frequently associated with nearby pulmonary consolidation and can be mistaken for a lung abscess. A lung abscess usually presents as a poorly defined, roughly spherical mass surrounded by consolidated but non compressed lung. An empyema is usually elongated, conforms to the shape of the chest wall, and compresses the adjacent lung. Its wall is thin and uniform and the interface angle with the chest wall is obtuse. The margins of the empyema cavity are composed of inflamed visceral and parietal pleura that enhance after administration of intravenous contrast. The visceral and parietal layers are separated by the interposed empyema fluid, giving rise to the \u201csplit pleura sign\u201d.\n\nUS is widely available, provides guidance for thoracentesis or pleural catheter placement, and can be transported to the bedside. US is particularly useful for sampling fluid that does not layer freely on decubitus films, and can distinguish solid from liquid pleural abnormalities better than chest roentgenography. The presence of discrete pleural septations has prognostic importance because loculated collections require drainage for their resolution. Computed tomography, however, gives additional information not obtained by US.\n\nThe sine qua non of empyema management is early, adequate, and dependent drainage. The therapeutic armamentarium for parapneumonic effusion or empyema consists of antibiotic therapy, thoracentesis, chest tube drainage, image-guided percutaneous catheter drainage, intrapleural fibrinolytic agents, and a variety of surgical drainage procedures, including video-assisted thoracic surgery (VATS) and open thoracotomy.", "ACR Code": "6.2", "Category": "Infection, generalized", "Keywords": "empyemaeffusionthoracentesis", "Reference": "DeHoyos A, Sundaresan S. Thoracic empyema. Surg Clin N Am\n2002;82(3)" } }, { "U_id": "MPX2610", "TAC": [ "MPX2610_synpic45673", "MPX2610_synpic45858" ], "MRI": [], "Case": { "Title": "Renal Cell Carcinoma.", "History": "History of right upper quadrant pain for the past two weeks.", "Exam": "No significant physical exam and laboratory findings.", "Findings": "Exophytic mass off inferior pole of left kidney. The solid, heterogenous mass measures 2.7 cm in diameter and disturbs the renal contour. The remainder of the left and right kidneys is normal. No renal vein or inferior vena cava thromboses are present. There is no adenopathy.", "Differential Diagnosis": "1. Renal Cell Carcinoma\n2. Renal metastasis\n3. Renal adenoma\n4. Oncocytoma\n5. Renal lymphoma\n6. Renal angiomyolipoma\n7. Acute focal pyelonephritis", "Case Diagnosis": "Renal Cell Carcinoma.", "Diagnosis By": "Although imaging can suggest differentiation between several benign and malignant renal masses, no imaging features are pathognomonic for malignancy. The patient was therefore referred to urology for management of this incidental renal mass. Tissue diagnosis was obtained during partial nephrectomy.", "Treatment & Follow Up": "Laparoscopic left partial nephrectomy preformed along with follow-up imaging.", "Discussion": "Renal cell carcinoma, the most common primary tumor of the kidney, is found incidentally in many patients with the widespread use of cross-sectional imaging. In fact, as many as one-half of renal cell carcinomas are discovered incidentally at early stages when they are asymptomatic. CT has also played an essential role in staging renal cell carcinoma in order to guide prognosis and surgical planning. The patient in this case underwent partial nephrectomy for his renal cell carcinoma. As a result, this case generates several interesting questions. What is the standard protocol for staging renal cell carcinoma with CT? What staging systems exist for renal cell carcinoma and what are their differences? Finally, what factors determine the use of radical nephrectomy versus nephron-sparing surgical techniques?\n\t\nOnce a renal cell carcinoma is suspected incidentally, there is a standard protocol for work-up using CT. First, an unenhanced CT is preformed to use as a baseline once intravenous contrast material is administered. Due to a significant vascular supply, renal cell carcinomas enhance following administration of contrast. 12 HU of enhancement suggest possible malignancy. Following the administration of contrast, images are obtained during the corticomedullary phase, nephrographic phase, and excretory phase. \n \nThe corticomedullary phase occurs between 25 and 70 seconds after injection and primarily enhances the renal cortex. While not perfect for detecting small lesions, this phase can aid in diagnosing venous extension of the tumor. The nephrographic phase, which occurs between 80 and 180 seconds following injection, is best for detecting renal masses and analyzing indeterminate lesions. Finally, the excretory phase begins 180 seconds following injection and helps evaluate the collecting system, as well as the calices and renal pelvis. \n \n Renal cell carcinoma has two potential staging systems: the Robson classification and the TMN classification. CT is reported to be 91% accurate in staging renal cell carcinoma. The TMN classification is considered more precise because of its clear definition of the anatomic extent of the tumor. With respect to the TMN classification, T1 is reserved for tumors less than 7 cm and T2 for tumors greater than 7 cm. T3 is broken down into three groups based on tumor position. T3a indicates spread to the perinephric fat. T3b indicates that the tumor is present in the renal vein only. T3c describes a tumor in the infradiaphragmatic IVC. T4a and T4b describe tumors with direct invasion of adjacent organs and presence in the supradiaphragmatic IVC, respectively. N1-3 are reserved for regional lymph node metastases and M1a-d for distant metastases. \n \nThe Robson classification is staged I-IV. I is given to a tumor confined within the renal capsule. II indicates spread to the perinephric fat. IIIA describes the presence of a venous thrombus, whereas IIIB describes regional lymph node metastases. IVA indicates direct invasion of adjacent organs and IVB indicates distant metastases. An important downfall of the Robson classification is that it uses stage III to describe both patients with venous extension alone and patients with regional lymph node metastases. The treatment for these two groups of patients varies significantly. Venous extension of the tumor can be treated surgically, whereas lymph node metastases indicate a need for palliative therapy. \n \nDue to the rapid increase in incidental discovery of renal cell carcinoma, many tumors are small in size and early-stage. Therefore, nephron-sparing surgery is often an option. The procedure consists of excision of the renal tumor and obtaining 0.5 cm margins of normal renal tissue and preserving the largest amount of functioning renal parenchyma. This procedure is particularly desirable when radical nephrectomy would lead to dialysis. Therefore, it is indicated in patients with a solitary functioning kidney, compromised renal function, or bilateral tumors. In addition, data indicates that small <4 cm in diameter lesions, which are polar, cortical, and a safe distance away from the renal hilum and collecting systems, have similar survival rates for the nephron-sparing procedure and radical nephrectomy. The size and position of the patient\u2019s tumor in this case made him a good candidate for the nephron-sparing procedure." }, "Topic": { "Title": "Renal Cell Carcinoma", "Disease Discussion": "Renal cell carcinoma is the most common primary tumor of the kidney and accounts for 2.6 percent of all adult cancers. While the cause is unknown, cigarette smoking has been identified as an environmental risk factor. Sporadic tumors are most common, but familial settings, such as von Hippel-Lindau syndrome, have been identified. The carcinoma develops from the proximal tubule cells of the kidney. Clear cell, papillary, chromophobe, collecting duct, and sarcomatoid are the different histologic types. These different patterns do not affect treatment. \n\nRenal cell carcinoma has two potential staging systems: the Robson classification and the TMN classification. CT is reported to be 91% accurate in staging renal cell carcinoma. The TMN classification is considered more precise because of its clear definition of the anatomic extent of the tumor. With respect to the TMN classification, T1 is reserved for tumors less than 7 cm and T2 for tumors greater than 7 cm. T3 is broken down into three groups based on tumor position. T3a indicates spread to the perinephric fat. T3b indicates that the tumor is present in the renal vein only. T3c describes a tumor in the infradiaphragmatic IVC. T4a and T4b describe tumors with direct invasion of adjacent organs and presence in the supradiaphragmatic IVC, respectively. N1-3 are reserved for regional lymph node metastases and M1a-d for distant metastases. \n\nThe Robson classification is staged I-IV. I is given to a tumor confined within the renal capsule. II indicates spread to the perinephric fat. IIIA describes the presence of a venous thrombus, whereas IIIB describes regional lymph node metastases. IVA indicates direct invasion of adjacent organs and IVB indicates distant metastases. \n\nThe common presentation of renal cell carcinoma includes gross or microscopic hematuria, flank pain or pass, systemic symptoms, or a solid renal mass on imaging. \n\nMany renal cell carcinomas are found incidentally on imaging. CT is the most valuable imaging modality. It can confirm the nature of the mass and stage the tumor by providing visualization of the lymph nodes, renal vein, and hepatic involvement. The contralateral kidney and other body organs can also be examined. \n\nTreatment for renal cell carcinoma varies based on the patient. Radical nephrectomy is common for a localized renal cell carcinoma. The indications for partial nephrectomy are reviewed in the discussion. Radiofrequency and cryosurgical ablation are new techniques being studied. Chemotherapy is not effective in treatment of metastatic renal cell carcinoma. Cryoreductive nephrectomy is recommended for patients who are in good status and have metastatic primary disease. Disease-free five-year survival is 90-100 percent for patients with tumors confined by the renal capsule. Tumors extending beyond the capsule have a 50-60 percent rate of disease-free five-year survival. The five-year disease-free survival drops to 0-15 percent for node-positive tumors.", "ACR Code": "8.3", "Category": "Neoplasm, carcinoma", "Keywords": "Renal cell carcinomapartial nephrectomy", "Reference": "Rugo Hope S, \"Oncology\" (Chapter). McPhee SJ, Papadakis MA, Tierney LM, Jr.: CURRENT Medical Diagnosis & Treatment 2008: http://0-www.accessmedicine.com.crusher.neoucom.edu:80/content.aspx?aID=21374.\n\nSheth, Sheila et al. \u201cCurrent Concepts in the Diagnosis and Management of Renal Cell Carcinoma: Role of Multidector CT and Three-dimensional CT.\u201d RadioGraphics 2001; 21: S237- S254.\n\nOlder, Robert and Resnick, Martin. Diagnosis of Genitourinary Disease. Thieme: 1997." } }, { "U_id": "MPX2601", "TAC": [ "MPX2601_synpic47404", "MPX2601_synpic47405", "MPX2601_synpic47406", "MPX2601_synpic47407", "MPX2601_synpic47408", "MPX2601_synpic47409", "MPX2601_synpic47410", "MPX2601_synpic47411", "MPX2601_synpic47412", "MPX2601_synpic47413", "MPX2601_synpic47418", "MPX2601_synpic47419", "MPX2601_synpic47420", "MPX2601_synpic47421", "MPX2601_synpic47423", "MPX2601_synpic47424" ], "MRI": [], "Case": { "Title": "Lipomatous hypertrophy of the interatrial septum", "History": "Shortness fo breath with concern for pulmonary embolism.", "Exam": "N/A", "Findings": "Axial CT images with intravenous contrast material demonstrate mild smooth thickening of the interatrial septum with diffuse fat attenuation. No pulmonary embolims was present. Note the large amount of subcutaneous fat circumferentially compatible with a large body mass index.", "Differential Diagnosis": "Lipomatous hypertrophy of the interatrial septum\nCardiac lipoma\nLiposarcoma", "Case Diagnosis": "Lipomatous hypertrophy of the interatrial septum", "Diagnosis By": "CT", "Treatment & Follow Up": "No specific treatment necessary.", "Discussion": "Please see factoid." }, "Topic": { "Title": "Lipomatous hypertrophy of the interatrial septum", "Disease Discussion": "Lipomatous hypertrophy of the interatrial septum (LHAS) is a benign process characterized by accumulation of fat within the interatrial septum. The incidence of LHAS is 1% in autopsy series and increases with increasing age and obesity. This lesion is of little clinical significance; patients with LHAS have slightly higher risk of supraventricular tachycardia, and several cases of hemodynamically significant SVC obstruction have been reported. Otherwise, LHAS tends to be an incidental finding.\n\tAt imaging, LHAS demonstrates fat attenuation and follows the signal intensity of fat on MR sequences. Narrowing of the lesion around the fossa ovalis lends the lesion a dumbbell-shaped contour. \n\tThe presence of fat in a cardiac mass excludes lesions such as myxomas, fibromas, and fibroelastosis. Cardiac lipomas are uncommon lesions and tend to be subendocardial or subpericaridal in location, and generally a capsule can be found at imaging. Cardiac liposarcomas are extremely rare, often presenting with metastases or cardiac constrictive symptoms.", "ACR Code": "5.3", "Category": "Hyperplasia", "Keywords": "lipomatous hypertrophy of th interatrial septumcardiac tumors", "Reference": "1.\tGaerte SC et al, Fat Containing Lesions of the Chest. Radiographics 2002; 22: S61-78\n2.\tMeaney JFM et al, CT Appearance of Lipomatous Hypertrophy of the Interatrial Septum. AJR 1997 April; 168: 1081-84 \n3.\tBreuer M et al, Lipomatous Hypertrophy of the Interatrial Septum and Upper Right Atrial Inflow Obstruction. European Journal of Cardio thoracic Surgery 22 (2002) 1023-1025." } }, { "U_id": "MPX2607", "TAC": [ "MPX2607_synpic52587" ], "MRI": [ "MPX2607_synpic52588", "MPX2607_synpic52590" ], "Case": { "Title": "Subependymoma, lateral ventricle", "History": "44 yo man with headaches", "Findings": "There is a mass in the frontal horn of the right lateral ventricle. The lesion appears attached to medial, rather than the lateral wall.\n\nThis lesion does not enhance after Gadolinium injection.", "Differential Diagnosis": "\u2022 Ependymoma\n\u2022 Subpendymoma\n\u2022 Central Neurocytoma\n\u2022 Choroid plexus neoplasm\n\u2022 Choroid meningioma\n\u2022 Choroid metastasis", "Case Diagnosis": "Subependymoma, lateral ventricle", "Diagnosis By": "Resection and histology", "Discussion": "Subpendymomas are uncommon low-grade tumors, thought (perhaps) to arise from subependymal cells called \"tanycytes\". These lesions occur most often either as asymptomatic masses in the 4th ventricle - or as symptomatic masses in the lateral ventricles.\n\nMost 4th ventricular ependymomas show some contrast enhancement; whereas most in the lateral ventricle do not enhance." }, "Topic": { "Title": "Subependymoma, lateral ventricle", "Disease Discussion": "Subependymoma is a relatively rare, slow-growing, benign glial tumor arising from cells just under the ependymal lining of the ventricles. They are most often found in the lateral and fourth ventricles and typically protrude into the ventricle lumen. They are usually asymptomatic but may cause hydrocephalus if they are sufficently large or strategically located. Their classic microscopic appearence includes scattered ependyma-appearing nuclei in a dense, fine, glial fibrillar background [1].\n\nA small study of 21 pts published in the J of Neurosurgery in 1991 showed an average age of onset for subependymomas of 48.5 yrs w/ 2/3 of the tumors arising in the lateral ventricles. Radiologic features include an isodense appearence with minimal enhancement on CT, frequent dystrophic calcification, and isointensity on T1-weighted or slight hyperintensity on T2-weighted MR images. Pathological features included a minor ependymoma content to in less than 1/3 of cases. The authors suggested that treatment should consist of surgical resection with postoperative irradiation only for those patients with symptomatic residual or recurrent tumors [2, 3].", "ACR Code": "1.3", "Category": "Neoplasm, glial", "Keywords": "stroke\r\nhemorrhagic\r\ninfarctsubependymoma\r\nlateral\r\nventricle\r\nependymoma", "Reference": "1. Robbins Pathologic Basis of Disease, 6th ed. Cotran, Ramzi S., MD, et. al., eds. W. B. Saunders Co, Philadelphia, 1999.\n\n2. Low-grade glioma. Recht, Lawrence, D. UpToDate, http://www.uptodate.com/\n\n3. Symptomatic subependymoma: a clinicopathological and flow cytometric study. Scheithauer, Lombardi D., et. al. J Neurosurg Oct 75(4):583-8, 1991.", "External Links": "rad.usuhs.mil/rad/home/locate/locate.html" } }, { "U_id": "MPX1020", "TAC": [], "MRI": [ "MPX1020_synpic17477", "MPX1020_synpic17478" ], "Case": { "Title": "Neuroblastoma with intraspinal extension", "History": "One-year-old boy was walking, but now only crawls.", "Exam": "N/A", "Findings": "Image 1: Fat-saturated Coronal T2 MRI of the abdomen / spine demonstrates a large mass over the right kidney. There is also increase T2 signal in several vertebral bodies. Increased T2 signal is present in both iliac wings, and some expansile remodeling is seen in the left iliac wing.\n\nImage 2: Fat-saturated Sagital T2 MRI of the spine shows a soft-tissue appearing mass that has invaded and insinuated itself within the epidural space - compressing the spinal cord.", "Differential Diagnosis": "If intraspinal extension were the only manifestation and the lesion were sharply marginated, spherical, or fusiform, then more benign nerve root tumors such as neurofibroma or schwannoma would be considered. Ganglioneuroma and ganglioneuroblastoma are also possible.\n\nHowever, given the large adrenal mass and the bone metastases, neuroblastoma becomes the primary consideration.", "Case Diagnosis": "Neuroblastoma with intraspinal extension", "Treatment & Follow Up": "Dependent on stage, but pre- and postoperative chemotherapy and sometimes radiation for local recurrence.", "Discussion": "This case of neuroblastoma with spinal invasion is especially intriguing in the that the mass has compressed the spinal cord to the extent that the infant who once walked will only now crawl. This was in fact what brought the child to medical attention." }, "Topic": { "Title": "Neuroblastoma, with intraspinal extension", "Disease Discussion": "Paraspinal masses typically originate from either the sympathetic ganglia (neurblastoma, ganglioglioma, or ganglioneuromas) or nerve roots (neurofibromas or schwannomas.) Ganglion tumors tend to be variably malignant. \n\nNeuroblastoma is a malignancy of primitive neural crest cells that form both the adrenal medulla and the paraspinal sympathetic ganglia.\n\nNeural tumors are typically of soft tissue density and calcifications are more common in neuroblstoma. Though myelography/CT has been used, MRI is especially well - suited for determining intraspinal extension of neurogenic tumors.\n\nNeuroblastoma is second to brain tumors as the most common solid childhood malignancy. One - third of patients are less than one-year-old. This malignancy accounts for 15% of childhood deaths from malignancy each year.\n\nThe tumor often presents as a firm, non-tender abdominal mass, can cause hypertension if it encases the renal vessels, can lead to respiratory distress when thoracic structures are compromised, or even causes symptoms related its effect upon the spinal cord as in this case.", "ACR Code": "3.3", "Category": "Neoplasm, embyronal", "Keywords": "neuroblastomasympathetic gangliaadrenal", "Reference": "Cohen, Magnetic Resonance Imaging of Children, B.C. Decker, Inc., Philadelphia, 1990, pp 598-600." } }, { "U_id": "MPX1007", "TAC": [], "MRI": [ "MPX1007_synpic46719", "MPX1007_synpic46720", "MPX1007_synpic46721", "MPX1007_synpic46722" ], "Case": { "Title": "Posterior Cerebral Artery Infarction", "History": "Elderly (>89 y.o.) man with 15 year history of HTN and atrial fibrillation presents with decreased alertness and responsiveness x 3 hours, which has resolved on presentation. \n\nPt had several episodes of L sided lower extremity weakness and facial drooping lasting from minutes to hours over the past several months. After one of these episodes, he was admitted with concern over his ability to manage his own medications. His Coumadin was discontinued and he was and placed on antiplatelet medication alone, due to the potential for falls and subsequent bleeds.", "Exam": "Mental status exam confounded by difficulty hearing and following directions. Vision unable to be assessed due to severe cataracts. Left corner of mouth drooping, left eye ptosis. MS: LUE flaccid, finger flexors +clonus, +Hoffmann's sign. LLE w/some spontaneous movement, unable to lift to gravity. DTRs 2+ throughout biceps, brachioradialis, knee, patellar. Babinski's upgoing bilaterally.\n\nINR 1.2", "Findings": "A new large area of restricted diffusion in the right posterior cerebral artery territory involving the parasagittal right parietal and right occipital regions. Numerous areas of periventricular and deep white matter intensities on the DWI are not present on the ADC map. This represents probable T2 shine-through corresponding to diffuse chronic microvascular\nischemic changes.", "Differential Diagnosis": "\u2022 Ischemia (with or without infarction in the PCA distribution)\n\u2022 Hyperemia with Migraine\n\u2022 Hyperemia after seizure\n\u2022 Encephalitis (HSV or other)\n\u2022 Meningitis\n\u2022 Hypertensive Encephalopathy", "Case Diagnosis": "Posterior Cerebral Artery Infarction", "Diagnosis By": "Imaging, PMH of atrial fibrillation, and subtherapeutic INR.", "Treatment & Follow Up": "Treatment consisted of reaching therapeutic level of anticoagulation with an INR of 3.0 and movement to a skilled nursing facility for an unknown duration. If patient able to regain ability to ambulate and the cognitive deficits do not persist, then he may be able to return home with some amount of home health care.", "Discussion": "This case demonstrates the importance of carefully weighing the risk/benefit ratio of anticoagulating patients with atrial fibulation. Also, it illustrates the importance and relevance of comparing DWI and ADC map images in the assessment of acute cerebral infarction." }, "Topic": { "Title": "Posterior Cerebral Artery Infarction", "Disease Discussion": "Patients who have sustained PCA strokes present with an interesting and diverse spectrum of neurologic symptoms. The most common long-term sequelae of PCA strokes are visual and sensory deficits. In general, patients with PCA distribution strokes exhibit less overall chronic disability than those with anterior cerebral, middle cerebral, or basilar artery infarctions.\n\nIschemic strokes occur when blood cannot flow to cerebral structures. Neuron metabolism tolerates a brief period of interrupted oxygen and glucose delivery. Cell death is imminent after approximately 6 minutes of halted blood circulation. Large cortical neurons are especially sensitive to ischemia. Infarcts include a central area, or umbra, of highly concentrated cell death, surrounded by a penumbra of tissue containing stunned cells that may recover, assuming circulation is reestablished or produced through nearby collaterals.\n\nThe right and left PCA vessels are formed from bifurcation of the basilar artery near the junction of the pons and midbrain over the ventral aspect of the brainstem and each PCA is divided into four segments (P1-P4)\nP1: extends from origin of the PCA to the posterior communicating artery (PCOM)\nP2: includes from junction with PCOM to its major branch, the lateral posterior choroidal artery, which supplies the posterior thalamus\nP3/P4: distal segments of the PCA whose branches circulate blood to cortical regions, most importantly the undersurface of the temporal lobe, the posterior 1/3 of the interhemispheric surface, occipital pole, visual cortex, and splenium of the corpus callosum.\n\nAnatomic localization of the point of vascular occlusion in the PCA infarcts may be simplified into (1) DEEP or PROXIMAL PCA strokes, causing ischemia in the thalamus and/or midbrain (regions supplied by P1 and P2), as well as in the cortex (regions supplied by P3 and P4); and (2) SUPERFICIAL or DISTAL PCA strokes, involving only cortical structures (P3,P4 branch areas)\n\nPatients with PCA infarcts present with symtptoms such as:\n- acute vision loss\n- confusion\n- new onset posterior cranium headache\n- paresthesias\n- limb weakness\n- dizziness\n- nausea\n- memory loss\n- language dysfunction\n\nThe most common examination finding is a homonymous visual field cut, usually a complete hemianopia, caused by a lesion in the contralateral occipital lobe.\n\nDeep or proximal PCA infarcts involve portions of the thalamus and midbrain. Thalamic lesions result in contralateral face and limb sensory loss. The midbrain cerebral peduncle carries corticospinal tract fibers that decussate caudally in the brainstem. A peduncle lesion is associated with contralateral motor weakness. Large or bilateral PCA infarcts that involve thalamus, temporal, and/or parietal-occipital lobes often result in a spectrum of possible findings (neuropsychologic deterioration and memory, language, or visual-cognitive dysfunction)\n\nMajor etiologies of PCA infarction include cardiac embolism, vertebrobasilar disease, and PCA atherothrombosis.\n\nhttp://rad.usuhs.mil/medpix/medpix.html?mode=single&recnum=3748&table=card&search=vascular+map#top\nhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Display&dopt=pubmed_pubmed&from_uid=10773642", "ACR Code": "1.4", "Category": "Infarction and/or Necrosis", "Keywords": "strokeinfarct", "Reference": "1) Hasso AN, Stringer WA, Brown KD: Cerebral Ischemia and Infarction. Neuroimaging Clin N Am 1994 Nov; 4(4): 733-752.\n\n2) Luzzio CC et al. Posterior Cerebral Artery Stroke. www.emedicine.com 2003 August.\n\n3) Brant and Helms. Fundamentals of Diagnostic Radiology. pp 94-95.", "External Links": "www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Display&dopt=pubmed_pubmed&from_uid=10773642" } }, { "U_id": "MPX1022", "TAC": [], "MRI": [ "MPX1022_synpic17356", "MPX1022_synpic17357" ], "Case": { "Title": "intraosseous lipoma of the distal femur confirmed by MRI", "History": "50 year-old female with bilateral knee pain.", "Findings": "A geographic, lobulated, well marginated, radiolucent, expansile, medulary lesion with a thin rim of sclerosis and central calcific densities is seen on plain radiograph in the posterior aspect of the metadiaphysis of the distal right femur without cortical destruction. T1 and T2 weighted magnetic resonance images show the lesion to have signal isointense to fat and a sclerotic rim.", "Differential Diagnosis": "Aneurysmal bone cyst, fibrous dysplasia, simple bone cyst, enchondroma, and bone infarct.", "Case Diagnosis": "intraosseous lipoma of the distal femur confirmed by MRI", "Treatment & Follow Up": "None; curettage and bone grafting if the structural stability of the affected bone is compromised." }, "Topic": { "Title": "intraosseous lipoma of the distal femur", "Disease Discussion": "Intraosseous lipomas are benign bone lesions that are histologically identical to extraosseous lipomas. They are comprised of mature adipose cells separated into lobules by fibrovascular septations. Patients may present with or without localized pain of variable duration and a variable amount of soft tissue swelling. Many of these lesions are discovered incidentally. Intraosseous lipomas may be seen in patients of all ages, with a predilection for young to middle age adults. They are most commonly detected in the metaphysis or epiphysis of the long bones of the lower extremity with 50% involving the femur, tibia, and fibula. These tumors may also be found in other long bones, the skull and jaws, ribs, pelvis, and frequently (15%) in the calcaneus, which is the most common tarsal bone involved.\n\nThe typical plain film appearance of intraosseous lipomas is a geographic, well marginated, osteolytic lesion with a thin sclerotic rim. Lobulations at the margins or internal osseous ridges are common as is a central nidus of dystrophic calcification, which is nearly pathognomonic for this tumor. This central calcification is secondary to fat necrosis. Osseous expansion may be evident, especially in bones of small caliber. Computed tomography demonstrates attenuation similar to subcutaneous fat with regions of cystic changes. The differential diagnosis includes simple bone cyst (unicameral), fibrous dysplasia, and when calcified, enchondroma and clear cell chondrosarcoma. Bone infarct is also a diagnostic consideration. If the lesion is in the calcaneous, normal trabecular variation (pseudocyst) secondary to the absence of stress and resulting atrophy of bony trabeculation should be considered. \n\nMRI findings are pathognomonic. Lesions include regions of fat with high signal intensity on T1 weighted sequences and low signal intensity on T2 weighted fat suppressed and STIR sequences. This may be combined with internal areas of low signal calcification and peripheral thick or thin rims of low signal sclerosis. On T1 weighted MR images, the homogenous high signal intensity of the lipoma is demarcated from the fat in the bone marrow by a sharp margined rim of low signal intensity. A dark, central focus is commonly seen and corresponds to dystrophic calcification.", "ACR Code": "4.3", "Category": "Neoplasm, benign", "Keywords": "benignneoplasmbone", "Reference": "Diagnosis of Bone and Joint Disorders (4th Ed)/edited by) Donald Resnick\u2014W.B. Saunders Co., 2002.\n\nFundamentals or diagnostic radiology / (edited by) William E. Brant, Clyde A. Helms.\u20142nd ed., Lippincott Williams & Wilkins, 1999\n\nMusculoskeletal Imaging: Case Review Series/ (edited by) Joseph Yu\u2014Mosby Inc., 2001.\n\nThe Core Curriculum: Musculoskeletal Imaging/ (edited by) Felix S. Chew\u2014Lippincott Williams & Wilkins, 2003." } }, { "U_id": "MPX1014", "TAC": [], "MRI": [ "MPX1014_synpic41745", "MPX1014_synpic41746", "MPX1014_synpic41747", "MPX1014_synpic41748" ], "Case": { "Title": "Wernicke encephalopathy", "History": "52 year old woman with a history of breast cancer, on chemotherapy. Poor oral intake and now stuporous.", "Findings": "\u2022 T2 hyperintensity within the both thalami\n\u2022 T2 hyperintensity of the periaqueductal grey matter\n\u2022 Enhancement of both mamillary bodies\n\u2022 Enhancement of the periaqueductal grey matter", "Differential Diagnosis": "\u2022 bilateral thalamic glioma\n\u2022 metabolic/toxic processes (Wernicke encephalopathy, Leigh disease, Wilson disease)\n\u2022 infectious agents (Japanese and West Nile encephalitis, Creutzfeldt-Jakob disease)\n\u2022 vascular lesions(deep venous thrombosis, top of the basilar syndrome, infarction of the artery of Percheron)", "Case Diagnosis": "Wernicke encephalopathy", "Diagnosis By": "Pathology, laboratory, and imaging", "Treatment & Follow Up": "Patient was given thiamine, but expired", "Discussion": "Limited differential diagnosis - MR imaging is the modality of choice Differential diagnosis can be narrowed by the imaging appearance in combination with the presence or absence of other regions of involvement, & the patient\u2019s history. The differential includes primary neoplastic processes (bilateral thalamic glioma), metabolic/toxic processes (Wernicke encephalopathy, Leigh disease, Wilson disease), infectious agents (Japanese and West Nile encephalitis, Creutzfeldt-Jakob disease), & vascular lesions(deep venous thrombosis, top of the basilar syndrome, infarction of the artery of Percheron)" }, "Topic": { "Title": "Wernicke encephalopathy", "Disease Discussion": "Severe neurologic disorder resulting from dietary vitamin B1 (thiamine) deficiency - frequently associated with chronic alcohol abuse. Thiamine is an essential coenzyme in intermediate carbohydrate metabolism, and is also an osmotic gradient regulator. Deficiency may cause swelling of the intracellular space along with a local disruption of the blood-brain barrier. Wernicke encephalopathy is associated with chronic alcohol abuse, but can be caused by other disorders such as: gastroplasty for obesity, psychogenic refusal of food, hyperemesis gravidarum, anorexia nervosa, voluntary food starvation, and parenteral therapy. The healthy body has a reserve of thiamine sufficient for up to 18 days, so any condition resulting in thiamine deficiency lasting 2 to 3 weeks may be an etiology\n\nIt is a medical emergency treated by intravenous administration of thiamine.Clinical triad of alteration in consciousness, ataxia, & ocular dysfunction\n\nImaging findings demonstrate symmetric T2 hyperintensity within the mamillary bodies, medial thalami , tectal plate, & periaqueductal grey.\n\nPost contrast enhancement may or may not be seen. Thiamine is an osmotic gradient regulator, & deficiency may result in disruption of the blood brain barrier - leading to enhancement.Reduced diffusion on DWI may be seen. This may be related to ischemic-like changes occurring within the thalami.", "ACR Code": "1.5", "Category": "Toxic (see also Metabolic)", "Keywords": "Wernicke encephalopathyMamillary bodyThiamine", "Reference": "American Journal of Neuroradiology 29:164-169, January 2008" } }, { "U_id": "MPX1028", "TAC": [], "MRI": [ "MPX1028_synpic24627", "MPX1028_synpic24628", "MPX1028_synpic24629", "MPX1028_synpic24630", "MPX1028_synpic24631", "MPX1028_synpic24632", "MPX1028_synpic24633", "MPX1028_synpic24634", "MPX1028_synpic24635", "MPX1028_synpic24641" ], "Case": { "Title": "Neurofibromatosis Type 1 (NF1) with optic glioma, dural ectasia, thoracic syrinx.", "History": "10 yo girl with known disease for routine followup", "Exam": "None Provided", "Findings": "\u2022 NF Spots in R posterior internal capsule. \n\u2022 L optic glioma. \n\u2022 Scoliosis with Severe Kyphosis of Cervical Spine.\n\u2022 Posterior Cervical fusion mass.\n\u2022 Dural ectasia. Widened spinal canal. Posterior vertebral body scalloping. \n\u2022 Syrinx. \n\u2022 Plexiform neurofibroma of L apex.", "Differential Diagnosis": "\u2022 Neurofibromatosis 1", "Case Diagnosis": "Neurofibromatosis Type 1 (NF1) with optic glioma, dural ectasia, thoracic syrinx.", "Diagnosis By": "Imaging and clinical findings", "Treatment & Follow Up": "Annual screening by multidisciplinary team to include physical exam, ophthalmology exam, growth measurements, developmental assessment and review of school progress.", "Discussion": "NF1 or von Recklinghausen disease is an autosomal dominant disorder, from a mutation on chromosome 17. It is found in approximately 1 in 3000 individuals. Common findings include caf?-au-lait spots, axillary or inguinal freckling, neurofibromas, optic gliomas, Lisch nodules, a variety of bony lesions, including dural ectasia with associated scalloping of the posterior vertebral bodies, pseudoarthrosis, CNS and soft tissue tumors, cognitive deficits, learning disabilities, seizures and macrocephaly." }, "Topic": { "Title": "Neurofibromatosis Type 1, diagnostic criteria", "Disease Discussion": "Diagnosis of Neurofibromatosis Type 1\n(Two Required for Dx)\n\n * Six or more caf? au lait macules over 5 mm in greatest diameter in prepubertal individuals and over 15 mm in greatest diameter in postpubertal individuals\n * Two or more neurofibromas of any type or one plexiform neurofibroma\n * Freckling in the axillary or inguinal regions\n * Optic glioma\n * Two or more Lisch nodules (iris harmartomas)\n * A distinctive osseous lesion such as sphenoid dysplasia or thinning of long bone cortex with or without pseudoarthrosis\n * A first-degree relative (parent, sibling, or offspring) with NF1 by the above criteria \n\nDiagnosis of Neurofibromatosis Type 2\n(Either #1 or #2)\n 1. Bilateral masses of the eighth cranial nerve seen with appropriate imaging techniques (e.g., CT or MRI)\n 2. A first-degree with NF2 and either A or B:\n A. Unilaterial mass of the eighth cranial nerve, or\n B. Two of the following:\n * Neurofibroma\n * Meningioma\n * Glioma\n * Schwannoma\n * Juvenile posterior subcapsular lenticular opacity\n=====================\nhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Search&db=pubmed&term=neurofibromatosis+diagnosis+criteria&tool=fuzzy\nhttp://odp.od.nih.gov/consensus/cons/064/064_statement.htm\nhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&list_uids=12473765&dopt=Abstract\nhttp://neurosurgery.mgh.harvard.edu/NFclinic/NFlinks.htm", "ACR Code": "1.1", "Category": "Differential Diagnosis", "Keywords": "neurofibromatosisneurofibromatosesdiagnostic criteria", "Reference": "D.A. Stumpf, J.F. Alksne, J.F. Annegers, et al. Neurofibromatosis. Arch Neurol 1988;45:575-578.", "External Links": "odp.od.nih.gov/consensus/cons/064/064_statement.htm" } }, { "U_id": "MPX1053", "TAC": [], "MRI": [ "MPX1053_synpic38935", "MPX1053_synpic38936", "MPX1053_synpic39272" ], "Case": { "Title": "Radiation Necrosis", "History": "The patient is a 25 year old man who initially presented s/p snow mobile accident with multiple hemorrhagic contusions. On initial evaluation, the patient was incidentally noted to have a left temporal Arteriovenous Malformation. This AVM was subsequently treated with Gamma Knife therapy. The patient now presents 12 months later with no complaints for routine follow up.", "Findings": "\u2022 12 months following gamma knife therapy, follow up imaging revealed a rim-enhancing mass in the left temporal lobe adjacent to the posterior horn of the left ventricle. Surrounding this lesion is extensive T2-high signal, likely representing edema.\n\u2022 Initial MR images show malacic changes in the frontal lobes with an incidental prominent vascular structures suggestive of a developmental venous anomaly. \n\u2022 Arteriogram also performed to therapy confirmed the presence of an AVM, predominantly fed by left lateral posterior choroidal artery.", "Differential Diagnosis": "\u2022 Radiation Necrosis\n\u2022 New Primary Brain neoplasm\n\u2022 Metastatic disease \n\u2022 Infectious process", "Case Diagnosis": "Radiation Necrosis", "Diagnosis By": "\u2022 Biopsy revealed necrotic tissue consistent with radiation necrosis.\n\u2022 MR spectroscopy", "Treatment & Follow Up": "The lesion was biopsied to definitively exclude a neoplastic process.", "Discussion": "The diagnostic dilemma in the evaluation of a suspected region of radiation necrosis often lies in the exclusion of recurrent tumor. In this case, without a prior history of neoplasm, the likelihood of a de novo tumor in the same location of radiation treatment is very low. Still, given the ambiguity of MRI findings coupled with equivocal results of MR spectroscopy imaging, the decision was made to biopsy the lesion." }, "Topic": { "Title": "Radiation Necrosis", "Disease Discussion": "Radiation necrosis is a strongly dose-dependent phenomenon which can occur from weeks to years following radiation therapy. Its effects can be progressive and fatal. Frank radiation necrosis is more likely with ablative gamma knife therapy.\n\nThe diagnostic dilemma in the evaluation of a suspected region of radiation necrosis often lies in the exclusion of recurrent tumor. Radiation necrosis and primary brain tumors may demonstrate identical signal characteristics on MRI, namely ring enhancement, surrounding edema, mass effect and growth over time. Useful tools in differentiating these two diagnostic considerations are PET and MR spectroscopy. \n\nPET scanning utilizes glucose uptake within tissue to demonstrate metabolic activity (in tumor) versus inactivity (necrotic tissue). \n\nMR spectroscopy evaluates characteristic metabolic profiles of major brain metabolites to help make this differentiation. Necrotic tissue normally reveals a profile of elevated lactate and lipids with diminished choline, creatine, and N-acetylaspartate.", "ACR Code": "1.3", "Category": "Radiation Injury", "Keywords": "Gamma KnifeSterotactic Radiation" } }, { "U_id": "MPX1049", "TAC": [], "MRI": [ "MPX1049_synpic55185", "MPX1049_synpic55186", "MPX1049_synpic55187", "MPX1049_synpic55188", "MPX1049_synpic55189", "MPX1049_synpic55190", "MPX1049_synpic55191", "MPX1049_synpic55192" ], "Case": { "Title": "Capillary Hemangioma", "History": "15 month old baby girl with enlarging right supraclavicular / shoulder mass.", "Exam": "Supraclavicular vascular mass with prominent superficial veins.", "Findings": "Lobulated, intensely enhancing mass lesion with high flow intralesional vessels.", "Differential Diagnosis": "\u2022 Capillary (Infantile) Hemangioma\n\u2022 Venous Malformation\n\u2022 Sarcoma (Rhabdomyosarcoma, Extraosseous Ewings, Undifferentiated Sarcoma)\n\u2022 Plexiform Neurofibroma\n\u2022 Arteriovenous Malformation", "Case Diagnosis": "Capillary Hemangioma", "Diagnosis By": "Characteristic imaging findings.", "Treatment & Follow Up": "This patient was treated with a short course of propranolol with marked interval decrease in the size of the lesion.", "Discussion": "Infantile hemangiomas are benign neoplasms of endothelial cells. They are the most common childhood tumor, occurring in 12% of children. They are more common in females, whites, premature infants, and twins. \n\nAt birth these lesions can be small and inconspicuous, with 60% absent at birth. The natural history is a two stage process of proliferation and regression. The typical hemangioma will begin to involute by 10 months of age, with half of all lesions having resolved by 5 years.\n\nClinically, hemangiomas appear as erythematous or blanching macules, or appear as a small telangiectasia. The clinical appearance depends upon the degree of dermal involvement and lesion depth. Lesions involving the skin have a more characteristic strawberry appearance. Deeper lesions demonstrate a blue appearance. \n\nMost hemangiomas are generally treated conservatively. Corticosteroids are the first line of treatment for problematic infantile capillary hemangiomas. Other options include interferon alpha and vincristine. Propranolol has also been observed to inhibit growth. While the mechanism of action is unclear, potential explanations include vasoconstriction; down-regulation of the RAF-mitogen-activated protein kinase pathway; and the triggering of apoptosis of capillary endothelial cells. \n\nCapillary hemangiomas can develop life threatening complications, such as consumptive coagulopathy, compression of vital structures, and bleeding secondary to fissure or ulcer formation." }, "Topic": { "Title": "Capillary Hemangioma", "Disease Discussion": "Overall, hemangiomas are present in 10-12% of Caucasian children - mostly as cutaneous lesions, often called \"strawberry marks\". \n\nIntra orbital vascular lesions account for 5-20% of all orbital masses in children. Some of these are neoplastic (capillary hemangioma) while others are malformations including venous varices and cavernous hemangioma. Capillary hemangiomas are composed of variably sized vascular spaces that are lined by proliferating endothelial cells. Capillary hemangiomas have been reported as the most common vascular tumor of the orbit, representing 5-12% of pediatric orbital lesions. \n\nMultiple synonyms have been used for these lesions, including infantile hemangioma, benign hemangioendothelioma, and hemangioblastoma. However, these terms are neither distinctive nor accurate and the most commonly used term is \u201ccapillary hemangioma\u201d \u2013 to allow distinction from the \u201ccavernous hemangioma\u201d (AKA \u201ccavernoma\u201d, cavernous malformation). The cavernous hemangioma is one of the most common orbital masses in the adult patient. The latter process is malformative and not neoplastic. [Mulliken 1982 PMID: 7063565] \n\nOrbital hemangiomas have been reported in association with PHACES (Posterior fossa malformations, Hemangiomas, Arterial anomalies, Cardiac defects and coarctation of the Aorta, Eye abnormalities, and Sternal abnormalities or ventral developmental defects); and also with blue rubber bleb nevus syndrome. [McCannel 1996 PMID: 8643250]\n\nOrbital capillary hemangiomas (OCH) may be supplied either by branches of the internal (e.g. ophthalmic) or external carotid artery, and may extend intracranially through the superior orbital fissure or optic canal.\n\n\u2022 Clinical\nOrbital capillary hemangioma (from now on just \u201chemangioma\u201d) present as sporadic lesions in childhood, with approximately 1/3 as congenital lesions noted at birth. The majority will present during the first decade. Almost half of them may enlarge during a Valsalva maneuver or with crying. There is a slight female predilection of 3:2 over males vs. up to 3:1 for cutaneous hemangioma. These endothelial vascular neoplasms typically proliferate in the first few months after presentation; and, then most stabilize \u2013 often at an alarming size. The natural history in most patients is for the lesions to stabilize for a period of years, and then begin spontaneous involution in adolescence, typically from 4-8 years of age. Some cases have been followed for up to 18 years, with eventual spontaneous but slow involution. [Henderson JW Ophthalmology 1990 - PMID: 2342808]\n\nIn addition to the obvious facial discoloration and mass, capillary hemangiomas may interfere with vision, cause proptosis, diplopia or amblyopia, and even optic atrophy. [Yap EY 1998 - PMID: 9703301]\n\n\u2022 Gross Pathology\nThese lesions are usually ruby-red soft, rounded and occasionally lobulated masses. Lesions with skin or subcutaneous involvement are often called \u201cstrawberry\u201d lesions due to their red color.\n\n\n\u2022 Histology\nThese lesions are usually well demarcated from surrounding tissues. The histology varies with the phase of the lesion. In younger patients, while the lesions are \u201cactive\u201d or growing, histology shows mitotic activity from plump proliferating endothelial cells that surround small irregular vascular spaces. Mast cells may be increased within the lesion. Classically, involution begins within the center of the mass, and the advances outward. Fatty and fibrous tissue surround the vascular space; and, the fibro-fatty tissue eventually replaced the vascular stroma. These features allow distinction from cavernous hemangiomas, that have larger vascular spaces that are lined by flattened endothelial cells.\n\n\n\u2022 Imaging\n\u00bb US\nUltrasound may play a dual role in capillary hemangioma \u2013 demonstrating the lesions as well as documenting their vascularity. [Verity DH EYE 2006 - PMID: 17019424] US shows great variability in lesion appearance, but can well document high-velocity flow in (100-1000 times normal) in feeding vessels. [Verity2006] Lesion involution is often preceded by stabilization in the rate of flow increase. Although US can be used to follow the progression-regression sequence in these tumors, MR provides the best evaluation in the diagnostic phase. \n\n\u00bb CT\nThe appearance of orbital capillary hemangiomas varies over time. Most commonly during the growing phase, they will appear as intensely enhancing lesions, that may be either well demarcated or poorly marginated. Lesions may be more dense than brain (50-60 HU) due to the blood filled vascular spaces. In the involution phase, the attenuation of the lesion will decrease, as fibro-fatty tissue replaces the vascularity.\n\n\u00bb MR\nThese lesions are usually well demarcated discrete lobulated masses with internal septations. They are usually dark on T1W and become hyperintense with T2-weighting. Bright contrast enhancement after Gadolinium is almost universal in these lesions. As these lesions involute, fatty and fibrous tissue may replace the tumor and the lesion may show areas of T1 shortening.\n\n\u00bb Treatment and Prognosis\nThe majority of these lesions will undergo spontaneous regression as the child ages. About one-half will show involution by age 5, and the overwhelming majority will show clear signs of involution by seven or eight years. Lesions that present at younger ages may also regress earlier in the life of the child. Both oral and parenteral steroids, interferon therapy, and surgery may be used when vision is threatened by periocular lesions. Fractionated stereotactic radiation may have potential benefit in some cases that do not regress or are not amenable to surgery. [Tsao MN J. Neurosurgery 2003 - PMID: 12546367]", "ACR Code": "2.3", "Category": "Neoplasm, benign", "Keywords": "capillary hemangiomaPHACESstrawberry mark" } }, { "U_id": "MPX1039", "TAC": [], "MRI": [ "MPX1039_synpic34347", "MPX1039_synpic34349", "MPX1039_synpic34350", "MPX1039_synpic34353" ], "Case": { "Title": "Multiple Sclerosis", "History": "21 y.o. woman with 5-7d h/o cervical neck pain associated intermittent shooting and tingling pains in both arms (L>R). \nNegative Medical history, Family history, or Social History. No medications.", "Exam": "Physical exam, including CN I-XII, within normal limits. CSF positive for two oligoclonal bands.", "Findings": "The cervical spine demonstrates T2 hyperintensity within the cord at C3 and C4 with mild expansion of the cord. \n\nEnhancement in the right side of the brain and enhancement adjacent to the posterior horn of the left lateral ventricle are well visualized on axial T1 post gadolinium MRI.\n\n\n\nThese high signal lesions are consistent with demylination.", "Differential Diagnosis": "\u2022 CNS infection (Lyme disease, syphilis, HIV infection, human T-lymphotrophic virus type I)\n\n\u2022 CNS inflammatory condition (sarcoidosis, SLE, Sj?gren's syndrome)\n\n\u2022 CNS microvascular disease (HTN, DM, vasculitis)\n\n\u2022 Genetic disorder (leukodystrophy, hereditary myelopathy, mitochondrial disease)\n\n\u2022 Structural or compressive condition of the brain and spinal cord\n\n\u2022 Vitamin B12 deficiency\n\n\u2022 Multiple sclerosis", "Case Diagnosis": "Multiple Sclerosis", "Diagnosis By": "Symptoms, MRI findings, and positive CSF oligoclonal bands.", "Treatment & Follow Up": "Patient admitted and recieved solumedrol x 5 days. Then discharged to home with followup in three months after repeat MRI brain and C-spine. In the event of an another episode, immunomodulating therapy to be initiated.", "Discussion": "Physical symptoms, MRI findings, and positive CSF oligoclonal bands are strongly indicative multiple sclerosis. The presence of CNS lesions that are disseminated in time and space with no better explanation for the disease process will confirm the diagnosis." }, "Topic": { "Title": "Multiple Sclerosis", "Disease Discussion": "Multiple Sclerosis\n\u2022 Idiopathic inflammatory disease of CNS\n\u2022 Pathologic demyelination and susbsequent axonal degeneration\n\u2022 Typically presents at 20-45 years of age\n\u2022 Females affected 2X more than males\n\u2022 Onset variable: insidious or sudden\n\nCommon Presenting Sx:\n\u2022 Paresthesias\n\u2022 Weakness\n\u2022 Impaired coordination\n\u2022 Optic neuritis (monocular visual impairment)\n\nAdditional signs/sx:\n\u2022 Bladder urgency/retention, constipation, sexual dysfunction, fatigue, depression, diplopia, gait and limb ataxia, and Lhermitte's sign (electrical sensation down the spine on neck flexion) \n\u2022 Frequently overlooked/mis-diagnosed because initial Sx may resolve spontaneously\n\n\u2022 Relapses occur within months or years\n\n\u2022 Some patients may have a primary progressive course from onset\n\n\u2022 Diagnosis of MS is \u201c based on the presence of central nervous system (CNS) lesions that are disseminated in time and space with no better explanation for the disease process \u201c", "ACR Code": "1.2", "Category": "Inflammatory, autoimmune", "Keywords": "Multiple Sclerosis", "Reference": "Calabresi, PA. Diagnosis and Management of Multiple Sclerosis. American Family Physician 2004; 70:1935-1943.\n\nCampbell, WW and RM Pridgeon. Practical Primer of Clinical Neurology 2002: 306-309.\n\nTaveras, JM. Neuroradiology. Baltimore: Williams and Wilkins, 1996." } }, { "U_id": "MPX1074", "TAC": [], "MRI": [ "MPX1074_synpic24653", "MPX1074_synpic24655" ], "Case": { "Title": "Gluteus minimus partial tear", "History": "Pt c/o pain in right hip, over greater for several months following uneventful SVD (single vaginal delivery). Exacerbated by weight bearing and lifting.", "Exam": "Pain is reproducible with palpation of anterior greater trochanter.", "Findings": "Axial T2-weighted MR image and STIR coronal MR image show an area of high signal intensity at anterior tubercle of the right greater trochanter. The right gluteus medius tendon is thickened, with high signal intensity on these fat suppressed MR images. Mild asymmetric increased signal is present on the fat-suppressed MR images, adjacent to the greater trochanter within the soft tissues.", "Differential Diagnosis": "Trochanteric bursitis\nGluteus minimus tear, avulsion\nMetastatic disease\nInfection", "Case Diagnosis": "Gluteus minimus partial tear", "Treatment & Follow Up": "Partial thickness tear can be treated with an injection of local anesthetic and corticosteroid. Ultrasound guidance is appropriate to locate area of tear, and injection itself should reproduce pain symptoms (both diagnostic and therapeutic in many cases). Gluteus medius injury and trochanteric bursitis can be treated with same methods. \nNSAIDs are a useful adjunct, to help reduce local inflammation and swelling. Physical therapy is recommended to combat any atrophy that may have developed, and prevent future recurrence.\nFull thickness tear, or retracted tear, is best treated with surgery to repair the deficit.", "Discussion": "Greater trochanteric pain syndrome (GTPS) is characterized by local tenderness over the greater trochanter. The pain is exacerbated by standing, lifting, descending stairs, lying on the affected side and crossing the legs. The pain can radiate down the lateral length of the leg, and cause tenderness along the length of the ilio-tibial tract. The differential diagnosis of these physical findings include hip fracture, avascular necrosis, osteoarthritis, ilio-tibial band syndrome, infection of the joint and/or soft tissues of the hip, metastatic disease, and lumbosacral radiculopathy \n\nTraditionally, the term GTPS was considered synonymous with trochanteric bursitis, and was treated with rest, injection and NSAIDs. More recently, several studies have identified pathology in the gluteus medius and minimus (the abductor tendons) as alternate causes of this pain, as identified on MRI and correlated with surgical findings. Findings include complete tears to mild tendonitis of the muscles at their insertion onto the greater trochanter. Studies have suggested that the bursitis may be secondary to abductor tendon pathology, prompting investigators to question the current treatment of the pain syndrome. Surgical intervention is recommended in the setting of a complete tear with retraction, while physical therapy and local injection at the affected tendon may be more appropriate for smaller tears and strains.\n\nWhile local trauma has been identified as a cause of GTPS, there have been no cases in the literature describing a tear occurring during childbirth. Because this syndrome is currently undergoing some change in thought and approach to cause and treatment, perhaps it will be more readily identified as a cause of post-partum hip pain in the future." }, "Topic": { "Title": "Gluteus minimus partial tear", "Disease Discussion": "Greater trochanteric pain syndrome (GTPS) is characterized by local tenderness over the greater trochanter. The pain is exacerbated by standing, lifting, descending stairs, lying on the affected side and crossing the legs. The pain can radiate down the lateral length of the leg, and cause tenderness along the length of the ilio-tibial tract. The differential diagnosis of these physical findings include hip fracture, avascular necrosis, osteoarthritis, ilio-tibial band syndrome, infection of the joint and/or soft tissues of the hip, metastatic disease, and lumbosacral radiculopathy \n\nTraditionally, the term GTPS was considered synonymous with trochanteric bursitis, and was treated with rest, injection and NSAIDs. More recently, several studies have identified pathology in the gluteus medius and minimus (the abductor tendons) as alternate causes of this pain, as identified on MRI and correlated with surgical findings. Findings include complete tears to mild tendonitis of the muscles at their insertion onto the greater trochanter. Studies have suggested that the bursitis may be secondary to abductor tendon pathology, prompting investigators to question the current treatment of the pain syndrome. Surgical intervention is recommended in the setting of a complete tear with retraction, while physical therapy and local injection at the affected tendon may be more appropriate for smaller tears and strains.\n\nWhile local trauma has been identified as a cause of GTPS, there have been no cases in the literature describing a tear occurring during childbirth. Because this syndrome is currently undergoing some change in thought and approach to cause and treatment, perhaps it will be more readily identified as a cause of post-partum hip pain in the future.", "ACR Code": "4.4", "Category": "Trauma", "Keywords": "Gluteus minimus partial tear", "Reference": "Bird PA, Oakley SP, Shnier R, Kirkham BW. Prospective evaluation of magnetic resonance imaging and physical examination findings in patients with greater trochanteric pain syndrome. Arthritis Rheum. 2001;44(9):2138-45.\nCvitanic O, Henzie G, Skezas N, et al. MRI diagnosis of tears of the hip abductor tendons (gluteus medius and gluteus minimus). AJR 2004;182:137-143.\nFoye PM. Trochanteric Bursitis. emedicine.com; Dec 16, 2004.\nKingzett-Taylor A, Tirman PF, Frll J, et al. Tendinosis and tears of gluteus medius and minimus tendons as a cause of hip pain: MRI findings. AJR 1999;173:1123-1126." } }, { "U_id": "MPX1084", "TAC": [], "MRI": [ "MPX1084_synpic21716", "MPX1084_synpic21717", "MPX1084_synpic21720", "MPX1084_synpic21722" ], "Case": { "Title": "Uveal (Choroidal)Melanoma of the left globe with extension of tumor into the retro-ocular tissues", "History": "Decreased vision left eye", "Exam": "N/A", "Findings": "Axial T1W images demonstrate ill-defined increased signal in posterior tissues of left globe and left retro-ocular tissues\nAxial contrast-enhanced fat saturated T1W images demonstrate\nenhancement and thickening of the posterior wall of the left globe and left retro-ocular tissues\nAxial T2W images demonstrate a low intensity mass involving the posterior aspect of the left globe and retro-ocular tissues.", "Differential Diagnosis": "Uveal melanoma\nChoroidal hemangioma\nOcular metastatic lesion\nHemorrhage", "Case Diagnosis": "Uveal (Choroidal)Melanoma of the left globe with extension of tumor into the retro-ocular tissues", "Diagnosis By": "Tissue pathologic examination", "Treatment & Follow Up": "Enucleation and radiation therapy", "Discussion": "Melanoma involving the eye has atypical MRI signal characteristics for a tumor in that the lesion is bright on T1W weighted images and dark on T2W images, which opposite from most tumors. The paramagnetic properties of the melanin content of the tumor are responsible for this signal characteristic." }, "Topic": { "Title": "Uveal Melanoma", "Disease Discussion": "Melanoma of the uveal tract is the most common primary intraocular malignancy in adults. The age range of presentation is typically 50 to 70 years old and unilateral ocular symptoms is the most common presentation. The diagnosis can be made with high sensitivity with combined ophthalmoscopic examination and ocular ultrasound. CT or MRI are used to supplement this evaluation if ocular clouding prevents a clear view of the lesion and may be used to follow response to treatment or progression of the tumor.\n\nThe tumor is unilateral and 85% of lesions arise from the choroidal portion of the uvea, with 9% arising from the ciliary body and 6% arising from the iris. Congenital melanosis, ocular melancytosis, oculodermal melanocytosis, and uveal nevi are predisposing conditions. The lesion may cause a retinal detachment and hemorrhage.\n\nCT features of the tumor demonstrate a soft tissue mass which is high density on noncontrast images, which enhances with contrast. The mass arises from the layer of tissue just deep to the external tissue of the globe and usually bulges inward toward the vitreous. The lesion may be small and flat in its early stages but may grow into a mushroom shaped intraocular tumor. CT or MRI may also demonstrate extraocular invasion which is associated with a poorer prognosis. \n\nThe lesion has unique MRI features in that the tumor is typically hyperintense on T1W sequences and hypointense on T2W sequences due to melanin content. The lesion is usually sharply circumscribed on MRI images. \n\nDifferential diagnosis of a unilateral ocular lesion include ocular metastases, choroidal hemangioma, retinal detachment with hemorrhage, and fat. \n\nTherapeutic options include enucleation, eye-sparing tumor excision, and radiation therapy.", "ACR Code": "2.3", "Category": "Neoplasm, malignant (NOS)", "Keywords": "uvealmelanomachorioidal", "Reference": "1. Harnsberger HR. Handbook of Head and Neck Imaging, 2nd ed. St. Louis, MO: Mosby, 1995: 323-324\n\n2. Grossman RI, Yousem DM. The Requisites: Neuroradiology, 2nd ed. Philadelphia, PA: Mosby, 2003: 483-484", "External Links": "www.moffitt.usf.edu/pubs/ccj/v5n4/ article1.html" } }, { "U_id": "MPX1089", "TAC": [], "MRI": [ "MPX1089_synpic52785", "MPX1089_synpic52786" ], "Case": { "Title": "Sacrococcygeal teratoma", "History": "The patient is a 20 year-old G1P0 woman with no significant past medical history noted to have an abnormality on routine ultrasound at 20 weeks gestational age. The patient now presents for follow-up fetal MRI.", "Exam": "Physical exam was not given.\nFetal HR on ultrasound exam: 134\nMost recent laboratory values were:\nWBC: 8.5\nHGB: 12.6\nHCT: 36.7\nGC/Chlamydia: neg\nRPR: Non-reactive\nNegative screen for neural tube defects, down syndrome, and trisomy 18\nNormal amniotic fluid volume on ultrasound\nChromosomal panel and AFP: pending", "Findings": "Large sacral mass with mixture of cystic and solid components with no apparent involvement of the spine.", "Differential Diagnosis": "\u2022 sacrococcygeal teratoma\n\u2022 meningocele, myelomeningocele\n\u2022 epidermoid or dermoid cyst\n\u2022 rhabdomyosarcoma", "Case Diagnosis": "Sacrococcygeal teratoma", "Treatment & Follow Up": "Close observation. Amniotic fluid levels will likely be closely monitored. Primary concern is nonimmune hydrops. Doppler ultrasound can evaluate the vascularity of the mass to further evaluate risk of high output CHF. Fetal surgery has been done in cases of hydrops, but is still largely experimental. If fetus is delivered at term, surgical resection of teratoma is likely course. Close follow-up even after surgical removal is necessary." }, "Topic": { "Title": "Sacrococcygeal teratoma", "Disease Discussion": "This is an unusual case of a cystic sacrococcygeal teratoma. Sacrococcygeal teratoma occurs in approximately 1 in 35,000 births but is reportedly the most common tumor encountered among neonates. The prenatal diagnosis of sacrococcygeal teratoma carries a very low rate of malignancy. However, the size and extension of the tumor is more important than the histology in prenatal studies. It may be mainly exterior with only a minimal presacral component, predominantly external with a significant intrapelvic component, predominantly internal with intra-abdominal extension, or entirely internal with no external component. The majority of sacrococcygeal teratomas are solid or mixed cystic and solid; only 15% are entirely cystic (as in this case). An intra-abdominal component often displaces the urinary bladder anteriorly and may obstruct the ureters.\n\nThe differential diagnosis depends on whether the mass is predominantly solid or cystic and external or internal. Other solid or complex masses in the sacrococcygeal region include chordoma, neurogenic tumor, lipoma, rhabdomyosarcoma, hemangioma, malignant melanoma, and meconium pseudocyst extending into the solid tissues. A predominantly or entirely cystic mass may resemble a myelomeningocele, which must be excluded by demonstrating intact posterior spinal elements. However, the teratoma may extend into the lumbosacral canal, and sacrococcygeal teratoma may occur with associated vertebral anomalies which make this distinction very difficult. The differential diagnosis for an entirely intra-abdominal sacrococcygeal teratoma includes ovarian cyst, meconium pseudocyst, enteric duplication cyst, or other bowel-related abnormality.\n\nApproximately 25% of fetuses with sacrococcygeal teratoma develop hydrops, probably secondary to the vascularity of the tumor. Because of the risk of dystocia and traumatic hemorrhage into the tumor, Cesarean delivery has been recommended for tumors larger than 5 cm. A predominantly cystic mass may undergo in utero aspiration immediately prior to vaginal delivery, as was accomplished in this case.", "ACR Code": "-1.-1", "Category": "Unsure" } }, { "U_id": "MPX1094", "TAC": [], "MRI": [ "MPX1094_synpic19922", "MPX1094_synpic19923", "MPX1094_synpic21793" ], "Case": { "Title": "Fronto-nasal encephalocele", "History": "8 year old female from the Pacific Islands with an encephalocele", "Findings": "There is an encephalocele in the frontal region, extending into the nasion.\nThere is a small fluid collection (syringohydromyelia) in the thoracic spinal cord.", "Case Diagnosis": "Fronto-nasal encephalocele", "Diagnosis By": "Imaging findings" }, "Topic": { "Title": "Fronto-nasal encephalocele", "Disease Discussion": "The term cephalocele refers to a defect in the skull and dura with extracranial extension of intracranial structures. The term encephalocele refers to herniation of both brain tissue and meninges through the skull defect, whereas the term meningocele refers to herniation of the meninges only. Both the skull defect and herniation are more common in the midline. \n\nMost encephaloceles are easily recognized by the clinician. On initial examination, the patient has a large midline extracranial mass that is soft to palpation. In patients with obvious masses such as these, the imaging study is obtained to look for associated brain anomalies that may alter the child's prognosis. An example of such an associated anomaly is shown in Films .3 - .6. This patient with a large frontal encephalocele also has agenesis of the corpus callosum and multiple gray matter heterotopias in the subependymal region. The absence of the corpus callosum can be detected on both the sagittal images by the absence of the corpus on the midline image and on the axial images by the characteristic shape of the frontal horns and the parallel lateral ventricles.\n\nAnother reason to obtain imaging studies in patients with encephaloceles is to look for the location of the major vascular structures of the brain. Particularly, because most encephaloceles are in the midline, the torcula and the superior sagittal sinus are crucial structures that must be located. In Films .7 - .9, a parietal encephalocele is shown. This case has two very important findings. The first is the deformity of the brain in the region of the encephalocele. Notice how the midbrain and cerebellum are stretched toward the calvarial defect. This stretching results from the pulsations of the brain causing it to be pushed out of the calvarial defect. The immature brain (before myelination) is very soft and easily deformed. Therefore it can be molded into just about any shape. It is common to see this sort of stretching of brain toward the skull defect in patients with encephaloceles. The other important feature of this case is the position of the superior sagittal sinus. On sequential coronal films, going from front to back, the sagittal sinus can be visualized in its entirety in relation to the encephalocele. Arrows point to the sinus as it courses within the most inferior and lateral aspect of the sac on the right. Notice that the sinus would be outside of the calvarium if the calvarium were present. More posteriorly, the torcula is high and the straight sinuses are seen to course steeply inferiorly within the walls of the tentorium cerebellum (arrows). The steep leaves of the tentorium probably result from the same process that causes herniation of the midbrain and cerebellum into the calvarial defect. \n\nSpecial mention should be made of sphenoidal and fronto-nasal encephaloceles because they are often clinically occult at birth. A high index of suspicion is necessary to make the diagnosis of encephalocele in adolescents and young adults who present with nasal or nasopharyngeal masses.", "ACR Code": "1.1", "Category": "Congenital, malformation" } }, { "U_id": "MPX1095", "TAC": [], "MRI": [ "MPX1095_synpic18844", "MPX1095_synpic19689", "MPX1095_synpic19690", "MPX1095_synpic19691" ], "Case": { "Title": "Pontine Glioma probably astrocytoma", "History": "Headache and CNN palsy", "Exam": "I wish I could say papilledema, but we could not get a good fundoscopic.", "Findings": "expansile lesion of the pons, without contrast enhancement", "Differential Diagnosis": "Pontine Astrocytoma:\nDiffuse type, WHO Grade 2,3, or 4\nPilocytic type, WHO Grade 1", "Case Diagnosis": "Pontine Glioma probably astrocytoma", "Diagnosis By": "Imaging appearance - no histology yet" }, "Topic": { "Title": "Brain stem astrocytoma", "Disease Discussion": "Brain stem neoplasms are uncommon, accounting for 10-15% of CNS tumors in children, with a peak age at presentation of less than 14 years. Most are gliomas, including slow-growing fibrillary or pilocytic astrocytoma, malignant astrocytoma, and glioblastoma multiforme. These tumors may initially infiltrate the brain stem pathways without tissue destruction, and few deficits may be present, in spite of extensive disease at the time of diagnosis. Presenting complaints include cranial nerve deficits, disturbances of motor or sensory pathways, ataxia, abnormal eye movements, somnolence, or hyperactivity. Hydrocephalus is characteristically a late finding, with the exception of those tumors arising in immediate proximity to the aqueduct. \n\nOn CT, these tumors infiltrate and enlarge the brain stem and secondarily displace the fourth ventricle. They commonly are hypodense but occasionally are of increased density compared to normal brain as seen on Film .3 in a different child. Calcification and cyst formation are infrequent (12%), and approximately half demonstrate enhancement after contrast (Film .4). When present, enhancement patterns are variable, with diffuse, nodular, or ring enhancement seen. A small number of these tumors may demonstrate exophytic growth into the posterior fossa cisterns, particularly the cerebellopontine angle cistern. These tumors tend to enhance with contrast administration. \n\nBecause of Hounsfield artifact in the posterior fossa, a small percentage of brain stem gliomas will be overlooked on initial CT scans. The superior imaging capability of MRI for brain stem and posterior fossa pathology allows recognition and characterization of lesions that are poorly delineated by CT, such as isodense or nonenhancing tumors. \n\nBrain stem gliomas, particularly those arising in the pons, have a relentlessly progressive course with little improvement in spite of radiation therapy. A subgroup of brain stem glioma consisting of localized small masses at the cervicomedullary junction have a more benign course and may potentially benefit from surgical resection. Attempts at surgical resection otherwise have not proven beneficial. Differential diagnosis includes non- neoplastic diseases of the brain stem such as demyelinating diseases (multiple sclerosis), encephalitis, and infarction. Exophytic and enhancing masses occasionally mimic medulloblastoma or ependymoma.", "ACR Code": "1.3", "Category": "Neoplasm, glial" } }, { "U_id": "MPX1102", "TAC": [], "MRI": [ "MPX1102_synpic21890" ], "Case": { "Title": "Primary sclerosing cholangitis", "History": "recurrent pruritis, hyperbilirubinemia and jaundice", "Exam": "jaundice\nelevated bilirubin", "Findings": "ERCP spot radiograph demonstrates dilatation and stricturing of portions of the extrahepatic and intrahepatic biliary tree.\nMRCP similarly demonstrates irregularity of the biliary tree. The intrahepatic involvement is primarily limited to the left lobe.", "Differential Diagnosis": "Primary sclerosing cholangitis\nAscending cholangitis\nCholangiocarcinoma\nPrimary biliary cirrhosis", "Case Diagnosis": "Primary sclerosing cholangitis", "Diagnosis By": "Tissue biopsy by ERCP pathologically confirmed primary sclerosing cholangitis", "Treatment & Follow Up": "Sphincterotomy and stent placement", "Discussion": "PSC is most often associated with inflammatory bowel disease. Although this patient had not been diagnosed with IBD at the time of the biliary findings, a colonoscopy and biopsy were performed to further investigate. Direct visualization and biopsy of the colon demonstrated ulcerative colitis." }, "Topic": { "Title": "Primary sclerosing cholangitis", "Disease Discussion": "Primary sclerosing cholangitis (PSC) is an inflammatory process which may involve all or segments of the intrahepatic and extrahepatic biliary ductal system. It is an idiopathic disease most often associated with inflammatory bowel disease, particularly ulcerative colitis and less often Crohn\u2019s disease. It less frequently associated with Reidel\u2019s thyroiditis, retroperitoneal fibrosis, or mediastinal fibrosis. The disease is more common in males than females with a 3:1 incidence ratio. The estimated prevalence in Western countries is 6 to 8 cases per 100,000 persons.\n\nSeveral mechanisms have been proposed to explain the pathogenesis of PSC, however, it is remains an idiopathic disease. Bile duct walls become progressively inflamed and thickened and the degree of severity may vary segmentally. There is typically alternating dilatation and stricturing of the involved ducts. The disease usually involves both the intrahepatic and extrahepatic biliary tree. It is characterized by progressive destruction of bile ducts, which may result in the development of biliary cirrhosis. It was previously thought to be a rare disorder, however, now PSC is one of the more common indications for liver transplantation.\n\nThe main symptoms of PSC include pruritis, jaundice, abdominal pain, and fatigue. However, as many as 44% of patients may be asymptomatic at presentation. Patients may also experience repeated episodes of bacterial cholangitis and have an increased tendency to develop pigmented biliary stones. Steatorrhea and malabsorption of fat-soluble vitamins may occur. Cholangiocarcinoma may occur in up to 30% of PSC patients. 2% of patient\u2019s may also develop hepatocellular carcinoma. \n\nThe diagnosis of PSC is based on characteristic ERCP findings in combination with laboratory, histologic, and clinical findings. It is important to exclude secondary causes of sclerosing cholangitis, such as prior surgeries, choledocolithiasis, chronic bacterial cholangitis and biliary neoplasms. The typical ERCP findings of PSC include multifocal strictures and dilatations that have a beaded appearance. Biliary diverticulae may also be present. The intrahepatic and extrahepatic bile ducts are usually involved, but either alone may be affected. Magnetic resonance cholangiopancreatography (MRCP) also shows promise as a valuable technique in the diagnosis and follow-up of patients with PSC and MRCP may be superior to ERCP for the demonstration of intrahepatic ductal findings. CT and ultrasonography play a more limited role in the diagnosis or followup of PSC and demonstrate nonspecific findings. \n\nMany modalities have been investigated for the treatment of PSC in an attempt to delay disease progression. Immunosupressants, corticosteroids, antifibrogenic agents, endoscopic management and limited surgical management are used with limited success. Liver transplantation is the only form of therapy that positively affects survival and up to 80% of patient\u2019s will experience significant quality of life improvement after liver transplant.", "ACR Code": "7.2", "Category": "Idiopathic or Unknown", "Keywords": "primarysclerosingcholangitis", "Reference": "Halpert RD, Feczko PJ. The Requisites: Gastrointestinal Radiology, 2nd ed. St. Louis, MO: Mobsy, Inc, 1999: 202-203\n\nMendes F. Primary sclerosing cholangitis. Clin Liver Dis 2004 Feb;8(1);195-199" } }, { "U_id": "MPX1110", "TAC": [], "MRI": [ "MPX1110_synpic16488", "MPX1110_synpic16489", "MPX1110_synpic16490", "MPX1110_synpic16491" ], "Case": { "Title": "Recurrence of paraganglioma", "History": "Patient with prior history of left paraganglioma at the carotid bifurcation, with recent MR suggestive of recurrence.", "Exam": "N/C", "Findings": "Multiple MR sequences of the neck demonstrate a lobulated mass at the prior surgical site with intermediate T1 signal, high T2 signal, and enhancement. Is this recurrence or changes induced by surgery and/or radiation?\n\nCoregistered SPECT/CT images after the administration of In-111-octreotide demonstrates a focus of increased radiotracer uptake at the left neck corresponding to the area in question demonstrated on MR. This is a recurrence of patient's known paraganglioma.", "Differential Diagnosis": "Recurrence of paraganglioma\nRadiation/surgical changes", "Case Diagnosis": "Recurrence of paraganglioma" }, "Topic": { "Title": "somatostatin receptor scintigraphy", "Disease Discussion": "Somatostatin membrane receptors are found on many cells and tumors of neuroendocrine origin (e.g. pheochromocytomas, neuroblastomas, ganglioneuro[blast]omas, paragangliomas, small cell lung cancers, pancreatic islet cells) and other cells not of neuroendrocrine origin such as activated lymphocytes, lymphomas, and breast cancer. [In-111-DTPA-D-Phe]octreotide (or just In-111-octreotide), a radiolabeled polypeptide which binds to somatostatin receptors, allows detection of such tumors in patients.\n\nThose tumors known to be positive on in vivo scintigraphy with In-111-octreotide include: TSH-producing pituitary tumor, gastrinoma, glucogonoma, paraganglioma, carcinoid, both small cell and non-small cell lung cancer, and meningiomas. Rheumatoid arthritis, sarcoidosis, and tuberculosis, all non-neoplastic systemic inflammator processes, may also demonstrate positivity on in vivo scintigraphy. \n\nThe advantage of scintigraphy in the setting of paragangliomas (and other tumor types with somatostatin receptors) is that unexpected additional paraganglioma sites not detected with anatomic imaging techniques were found in 33% of patients with known paragangliomas. This is especially important in the setting of paragangliomas, which demonstrate multicentricity and distant metastases in 10% of the cases.", "ACR Code": "2.3", "Category": "Endocrine", "Keywords": "octreotidesomatostatin receptorparaganglioma", "Reference": "Murray IPC, et al. Nuclear Medicine in Clinical Diagnosis and Treatment. Churchill Livingstone, 1994." } }, { "U_id": "MPX1134", "TAC": [], "MRI": [ "MPX1134_synpic16730", "MPX1134_synpic16731", "MPX1134_synpic16732" ], "Case": { "Title": "Brain biopsy confirmed patient has glioblastoma multiforme.", "History": "Patient presented with right-sided weakness and tonic-clonic activity in his right upper and lower extremity.", "Exam": "Patient was alert and oriented. Physical exam was significant for 4/5 strength in Right UE and 2/5 strength in Right LE. No other neurologic deficits were noted. HIV test was negative. TEE demonstrated no vegetations. Coagulation panel was within normal limits. Extensive laboratory work up failed to identify any abnormalities.", "Findings": "Patient has multiple ring-enhancing lesions with increased T2 signal within the deep cerebral white matter involving both hemispheres. Three of the lesions are centered on the periventricular area. A fourth lesion is present on the superior portion of the corpus collosum and a fifth cystic lesion in the posterior parieto-occiptial area. No deviation of the midline is appreciated.", "Differential Diagnosis": "Lymphoma, Glioblastoma multiforme, tumefactive multiple sclerosis, toxoplasmosis, neurocystercercosis, cryptococcus", "Case Diagnosis": "Brain biopsy confirmed patient has glioblastoma multiforme.", "Treatment & Follow Up": "Patient was treated with whole brain XRT, but could not tolerate the side effects. He was discharged to home for palliative care.", "Discussion": "Glioblastome multiforme (GBM) is the most common type of primary brain tumor in adult patients. It has an equal distribution among men and women with a peak incidence in the fifth decade of life. It is the most aggressive type of astrocytoma and has a poor prognosis. The average survival after diagnosis is eight months.\n\nSome patients (like this one) have multicentric GBM which is an uncommon and often more aggressive form of this disease, occurring in less than 1 - 15% of patients with GBM. It is characterized in this patient by its presence in both cerebral hemispheres.\n\nThe two most common presenting symptoms are headache and seizure. Hemiparesis was the most common neurologic deficit at presentation occurring in up to 83% of patients. This patient denied headaches, but did have seizures and hemiparesis. The imaging finding of ring-enhancing lesions is not specific enough to be diagnostic. Ultimately, a biopsy of the lesions was required for definitive diagnosis.CT or MRI can be used to image patients with suspected brain lesions. However, MRI is more sensitive and CT can miss lesions in the posterior fossa. In a small study looking at imaging in patients with multifocal glioblastoma multiforme, it was found that the lesions were always hypointense or isodense on CT and hyperintense on T-2 weighted MRI. Ring-like enhancement was also a common finding." }, "Topic": { "Title": "Glioblastoma multiforme (GBM)", "Disease Discussion": "WHO Grade IV\n\nCell of Origin: ASTROCYTE\n\nSynonyms: GBM, glioblastoma multiforme, spongioblastoma multiforme\n\nCommon Locations: cerebral hemispheres, occasionally elsewhere (brainstem, cerebellum, cord)\n\nDemographics: peak from 45-60 years\n\nHistology: grossly heterogeneous, degeneration, necrosis and hemorrhage are common\n\nSpecial Stains: GFAP varies, often present in areas of better differentiation\n\nProgression : Can't get any worse.\n\nRadiology: Glioblastoma is usually seen as a grossly heterogeneous mass. Ring enhancement surrounding a necrotic\ncenter is the most common presentation, but there may be multiple rings. Surrounding vasogenic edema can be\nimpressive, and adds significantly to the mass effect. Signs of recent (methemoglobin) and remote (hemosiderin)\nhemorrhage are common. Despite it\u2019s apparent demarcation on enhanced scans, the lesion may diffusely infiltrate into\nthe brain, crossing the corpus callosum in 50-75% of cases.\n\nCOMMENTS:", "ACR Code": "1.3", "Category": "Neoplasm, glial", "Keywords": "gliomaastrocytomaglioblastoma", "Reference": "; Accepted by jsmirnio", "External Links": "rad.usuhs.mil/rad/who/GBM.html" } }, { "U_id": "MPX1132", "TAC": [], "MRI": [ "MPX1132_synpic23654", "MPX1132_synpic23661", "MPX1132_synpic23663" ], "Case": { "Title": "Adenomyosis", "History": "36 yo female presents with intermenstrual bleeding for several month. The bleeding is now increased in the amount with cramping.", "Findings": "Ultrasound demonstrated heterogenous uterus. There were no fibroids. MRI of the pelvis confirmed suspicion of adenomyosis. T2 sequence demonstrates thickening of junctional zone and increased focal signal through out the myometrium.", "Case Diagnosis": "Adenomyosis", "Treatment & Follow Up": "Patient underwent transvaginal hysterectomy", "Discussion": "see factoid" }, "Topic": { "Title": "Adenomyosis", "Disease Discussion": "Adenomyosis is a common, benign gynecologic disorder of premenopausal, multiparous women usually greater than 30 years old. It frequently co-exists with other pelvic diseases. It represents focal or diffuse invasion of the basal endometrium into the myometrium causing a reactive hyperplasia amidst small foci of entrapped glandular elements and hemorrhage. Basal endometria is not responsive to menstrual cycle hormonal fluctuations and thus the thickness of the endometrial layer does not vary with the menstrual cycle. The disease is sometimes referred to as \u201cendometriosis interna\u201d.\n\nWomen with adenomysis present with the nonspecific symptoms of menorrhagia and dysmenorrhea. The prevalence of the disease is 8.8 \u2013 30% and is found in about 30% of hysterectomy specimens. Between 60 \u2013 80% of patients have other pelvic disorders such as leiomyoma (35-55%) and endometriosis (36-40%).\n\nMagnetic resonance imaging and transvaginal ultrasound are the best modalities with which to study adenomyosis. MRI has the advantage of better contrast resolution, larger field of view and superior sensitivity (88 \u2013 93%) and specificity (66 \u2013 91), but at a substantially greater financial cost. The MR image will show loss of the normal uterine junctional zone. It is instead expanded and replaced with focal or diffuse low T1 and T2 tissue signal, the thickness of which correlates well with the severity of adenomyosis. A junctional zone thickness of between 10 \u2013 12 mm is a commonly accepted criterion for diagnosis. A requirement for greater thickness provides increased specificity. The low T2 signal is due to the proliferation of reactive smooth muscle elements in response to the endometrial invasion and a generally decreased vascularity of these areas. Linear striations of high T2 signal radiating from the endometrium are specific for adenomyosis. One may also see small foci of increased T2 signal. These are thought to represent small endometrial cysts, hemorrhage or endometrial tissue. This finding adds specificity to the imaging study.\n\nContrast enhanced sequences are not typically necessary. T1 weighted sequences may be helpful in identifying small hemorrhagic foci but otherwise add little to the study", "ACR Code": "8.3", "Category": "Neoplasm, benign", "Keywords": "Adenomyosisendometriosisuterus", "Reference": "Byun JY, Kim SE, Cho BO, et al. Diffuse and Focal Adenomyosis: MR Imaging Findings. Radiographics 1999. 19:S161-S170.\n\nJha RC, Takahama J, Imaoka I, et al. Adenomyosis: MRI of the Uterus Treated with Uterine Artery Embolization. AJR 2003, 181:851-856.\n\nReinhold C, Tafazoli F, Mehio A. Uterine Adenomyosis: Endovaginal US and MR Imaging Features with Histopathologic Correlation. Radiographics 1999: 19:514-516.\n\nSiskin GP, Tublin ME, Stainken BF, et al. Uterine Artery Embolization for the Treatment of Adenomyosis: Clinical Response and Evaluation with MR Imaging. AJR 2001; 177:297-302." } }, { "U_id": "MPX1130", "TAC": [], "MRI": [ "MPX1130_synpic41020", "MPX1130_synpic41021", "MPX1130_synpic41022", "MPX1130_synpic41023", "MPX1130_synpic41024", "MPX1130_synpic41025", "MPX1130_synpic41026", "MPX1130_synpic41027", "MPX1130_synpic41028", "MPX1130_synpic41029", "MPX1130_synpic41030", "MPX1130_synpic41031", "MPX1130_synpic41032" ], "Case": { "Title": "Bicornuate Uterus", "History": "G1P0A1L0 with 6-7 episodes abnormal menstrual bleeding, FMH included Pt's mother took DES", "Findings": "Bicornuate uterus with uterine tissue between horns", "Differential Diagnosis": "complete bicornuate, incomplete bicornuate, infertility", "Case Diagnosis": "Bicornuate Uterus", "Diagnosis By": "imaging", "Discussion": "Pt was cleared of renal anomolies via MRI" }, "Topic": { "Title": "Bicornuate Uterus", "Disease Discussion": "Defects in mullerian duct development, fusion, or resorption occur in approximately 1% of women. There are 7 classifications of these congenital uterine anomalies. Some of these are associated with renal anomalies and/or infertility. Class I is partial or complete absence of the uterus and/or cervix. Class II is a unicornuate uterus which results from agenesis of one of the mullerian ducts. This is associated with the absence of the ipsilateral kidney. Class III is a fusion anomaly in which there us 2 separate uterus horns, cervices, and vaginas. Bicornuate uterus (class IV) is characterized by 2 uterine horns but one cervix and vagina. It is caused by incomplete resorption of the uterine septum. However, the septum is composed of myometrium and often doesn't extend the entire length of the uterine cavity. These features distinguish it from a septate uterus in which there is a fibrous septum. These patients are typically asymptomatic and no treatment is typically necessary. Most of these women maintain their fertility. However, there is an association between bicornuate uterus and incompetent cervix. Class V and VI are septate uterus (high incidence of infertility) and T-shaped uterus (results from diethylstilbestrol exposure inutero), respectively.\n\nHysterosalpingography is often used to evaluate the uterine cavity, while US is the typical screening exam for uterine wall abnormalities. MR is the best imaging modality to more definitively define the anatomy. It is often able to characterize a uterine anomaly that was unclear on one of the other imaging modalities.", "ACR Code": "8.9", "Category": "Congenital, genetic", "Keywords": "bicornuateuterusmullerian", "Reference": "Grainger & Allison's Diagnostic Radiology: A Textbook of Medical Imaging, 4th ed., 2001, Churchill and Livingston \n\nThurmond AS, MR Imaging of the Female Pelvis, Radiology Clinics of North America, 01-Jan-2003; 41(4): 757-67. NIH/Medline." } }, { "U_id": "MPX1129", "TAC": [], "MRI": [ "MPX1129_synpic31042", "MPX1129_synpic31043", "MPX1129_synpic31044" ], "Case": { "Title": "Brodie\u2019s abscess", "History": "14 year old boy presented initially for a sprained right ankle. No abnormalities were found at that time. The patient returned to clinic after 15 months due to increased swelling and pain in the right ankle over a 6 month period.", "Exam": "Physical exam at follow-up visit revealed swelling, erythema, and tenderness to palpation at the medial ankle.", "Findings": "Figure 1: Initial anteroposterior (A-P) radiograph of the right distal tibia and fibula 15 months prior to the current presentation showed no evidence of fracture and mild soft tissue swelling around the lateral malleolus. Incidentally, a lucent lesion with a well defined cortical margin was found along the lateral distal tibia, consistent with a nonossifying fibroma.\n\nFigure 2: Follow-up A-P radiograph of the right distal tibia and fibula 15 months after the initial injury shows a bilocular lytic lesion of the metaphysis and a unilocular lytic lesion of the epiphysis at the medial aspect of the tibia. The lesions are surrounded by a well defined sclerotic border with benign-appearing periosteal reaction and mild soft tissue swelling medially. The metaphyseal lesions extend across the physis into the epiphysis. There are no fracture lucencies and the joint spaces are maintained. The nonossifying fibroma of the lateral distal tibia is unchanged.\n\nFigure 3: A Tc-99m HDP bone scan demonstrates increased radiotracer uptake at the distal tibial meta-epiphysis, most marked on the medial aspect of the epiphysis.\n\nFigure 4: Axial T1-weighted MR image of right leg reveals multiple well defined low signal intensity masses surrounded by a thick medium intensity rim with a low signal intensity periphery. The tibial metaphyseal component measures 2.1cm longitudinal x 1.6cm transverse x 2.1cm AP. The epiphyseal component measures 2 cm longitudinal x 2.3cm transverse x 3cm AP. The inflammatory process extends posteromedially through the cortex of the tibial epiphysis to involve the adjacent soft tissues. \n\nFigure 5: On axial T2-weighted fat saturated MR image of the right leg, masses become high-signal intensity surrounded by low-signal intensity rims. The high signal-intensity inflammation extends into the adjacent soft tissues. There is a low signal intensity thickening of the soft tissues medially which extends anteriorly to the anterior aspect of the anterior-tibial tendon and posteriorly to the lateral aspect of the tibial tendon, flexor digitorum longus tendon and hallucis longus tendon. There are non-enhancing foci within the soft tissue consistent with extensive inflammation.\n\nFigure 6: Axial T1-weighted MR image after contrast demonstrates well defined masses with non-enhancing centers, enhancing thick rim, and non-enhancing periphery. The non-enhancing central lesions correspond to the low signal intensity centers seen on T1-weighted MR and high signal intensity centers seen on T2-weighted MR, which together is consistent with necrosis. The epiphyseal lesion expands through the anteromedial border of the tibia with extension of the abscess into the adjacent soft tissues. High-signal-intensity bone marrow edema extends 5.5cm proximally into the distal tibial diaphysis from the site of the lesions.", "Differential Diagnosis": "Brodie\u2019s abscess\nEosinophilic granuloma.", "Case Diagnosis": "Brodie\u2019s abscess", "Diagnosis By": "Histology and cultures grew Staphylococcus aureus", "Treatment & Follow Up": "Treatment for Brodie\u2019s abscess includes surgical debridement and antibiotic therapy.\n\nHistopathologic evaluation showed granulation tissue, acute and chronic inflammation, dense fibroconnective tissue, and bone fragments.\n\nCultures grew Staphylococcus aureus.", "Discussion": "In the 1830\u2019s, Sir Benjamin Collins Brodie recognized a chronic inflammatory process in the tibia with no acute symptoms or known precipitating infection. This rare lesion, known today as a Brodie\u2019s abscess, is a localized type of subacute or chronic pyogenic osteomyelitis. Pathogenesis is due to an insidious bacteremia with septic emboli to a normal or minimally traumatized long bone, often from an infection with Staphylococcus aureus. The lesion is predominant in young males with unfused epiphyseal plates, typically presenting during the second decade of life. Brodie\u2019s abscess is described as a small, eccentric, localized, lytic lesion with surrounding reactive sclerosis. It is characteristically found in the metaphyseal region of long bones of the lower extremity, most commonly in the tibia. The usual presenting complaint is recurrent pain and localized swelling; systemic symptoms are typically absent.\n\nRadiographs of a Brodie\u2019s abscess often demonstrate a localized area of radiolucency with surrounding sclerosis. The lucent region is commonly located in the metaphysis where it may extend to the growth plate by a tortuous channel. Detection of this focal metaphyseal abscess with involvement of the growth plate is diagnostic for osteomyelitis. Conventional radiographs should be the initial imaging study for evaluating osteomyelitis although, in early osteomyelitis they are usually normal or may show soft tissue swelling or benign periosteal reaction.\n\nBone scans are more sensitive than conventional x-rays for the early detection of osteomyelitis although not as sensitive as MR imaging. A focal area of radiopharmaceutical uptake at the site of suspected infection would suggest a Brodie\u2019s abscess. Both Brodie\u2019s abscesses and eosinophilic granulomas show radiopharmaceutical uptake and therefore this cannot be used as a distinguishing feature.\n\nMagnetic resonance (MR) imaging provides a greater accuracy in delineating the extent of disease, a more rapid evaluation. Furthermore, MR imaging possesses a high sensitivity in the detection of bone infection. On T1-weighted MR images, subacute osteomyelitis with Brodie\u2019s abscess presents as a low-intensity signal mass with low-signal-intensity rim that becomes a high-intensity signal mass with a thick, low-intensity rim on T2 weighted MR images. The abscess may rarely extend into the cortex and into soft tissues. In addition, the infection may rarely traverse the open growth plate, to involve the epiphysis. Other findings of chronic osteomyelitis include cortical bone thickening, sequestra, sinus tracts to the adjacent soft tissues. Post-contrast MR images show a non-enhancing mass with enhancing periphery.\n\nOn the imaging studies, our patient showed findings consistent with a Brodie\u2019s abscess with additional more unusual findings of extension across the growth plate into the epiphysis and cortical invasion into adjacent soft tissues. Alternate diagnoses in the differential can be excluded by the absence of a lesion 15 months prior to detection in this skeletally immature youth. Histopathologic confirmation with and positive cultures for Staphylococcus aureus, however, provide definitive diagnosis of a Brodie\u2019s abscess.\n\nTreatment for Brodie\u2019s abscess includes surgical debridement and antibiotic therapy. A sterile abscess may be treated without antibiotics only if there is symptomatic improvement and radiographic regression of the lesion. More aggressive treatment, such debridement followed by bone grafting, may be needed for abscesses that form slightly before or after bone maturation and do not resolve with surgical treatment." }, "Topic": { "Title": "Multi organism osteomyelitis", "Disease Discussion": "Osteomyelitis may result from open injury to bone and surrounding soft tissue, from hematogenous and local spread from adjacent tissues and as a postoperative complication(1). The specific organism isolated in bacterial osteomyelitis is often associated with the age of the patient or a common clinical scenario (i. e., trauma or recent surgery). Staphylococcus aureus is implicated in most patients with acute hematogenous osteomyelitis. Staphylococcus epidermidis, S. aureus, Pseudomonas aeruginosa, Serratia marcescens and Escherichia coli are commonly isolated in patients with chronic osteomyelitis. \n\nTreatment generally involves clinical evaluation, imaging evaluation for disease extent, laboratory determination of microbial etiology and susceptibilities, antimicrobial therapy and, if necessary, debridement, dead-space management and stabilization of bone. Localized bone pain, erythema and drainage around the affected area may be present. The cardinal signs of subacute and chronic osteomyelitis include draining sinus tracts, deformity, instability and local signs of impaired vascularity, range of motion and neurologic status. \n\nWhen there is clinical suspicion for osteomyelitis after physical examination and history, baseline radiographs should be performed followed by magnetic resonance imaging when available to define the extent of osteomyelitis and cellulitis. When MRI is not available, bone scans are useful for determining the extent of the infection. Laboratory tests may show leukocytosis (especially in the acute presentation) and elevations in the erythrocyte sedimentation rate and C-reactive protein level may be noted. Blood cultures are positive in as high as one-half of children with acute osteomyelitis. \n\nIn acute osteomyelitis, the radiographs may be negative or may show only soft tissue swelling and periosteal reaction. Evidence of medullary destruction may not appear until approximately two weeks after the onset of infection. Positive radiographic findings, when present include osteolysis, periosteal reaction and sequestra (segments of necrotic bone separated from living bone by granulation tissue). \n\nA bone abscess found during the subacute or chronic stage of hematogenous osteomyelitis is known as a Brodie's abscess. Magnetic resonance imaging (MRI) is the most sensitive test for evaluating osteomyelitis and the areas of osteomyelitis and cellulitis show high signal intensity on T2-weighted MR images enhancement on postcontrast T1-weighted MR images.", "ACR Code": "4.2", "Category": "Unsure", "Keywords": "osteomyelitis", "Reference": "1. Resnick D, Niwayama G. Osteomyelitis, septic arthritis, soft tissue infection: Mechanisms and situations. In Resnick D, ed. Diagnosis of Bone and Joint Disorders. W. B. Saunders, Philadelphia, 1995, pp.2325-2418.\n2. Waldvogel FA, Medoff G, Swartz MN. Osteomyelitis: a review of clinical features, therapeutic considerations and unusual aspects (first of three parts). N Engl J Med 1970;282:198-206. \n3. Waldvogel FA, Medoff G, Swartz MN. Osteomyelitis: a review of clinical features, therapeutic considerations and unusual aspects (second of three parts). N Engl J Med 1970;282:260-6. \n4. Waldvogel FA, Medoff G, Swartz MN. Osteomyelitis: a review of clinical features, therapeutic considerations and unusual aspects (third of three parts). N Engl J Med 1970;282:316-22." } }, { "U_id": "MPX1141", "TAC": [], "MRI": [ "MPX1141_synpic60798", "MPX1141_synpic60799" ], "Case": { "Title": "Desmoplastic infantile Astrocytoma", "History": "9 mo old girl with a history of trauma. A screening CT scan revealed a possible left hemisphere bleed. MRI and skeletal survey were ordered.", "Exam": "Non contributory", "Findings": "CT- Mixed density lesion within the posterior temporal and parietal lobes.\n\nMRI-Exophytic appearing lesion which has an intra axial component and enhances homogeneously.", "Differential Diagnosis": "Meningioma\nPXA\nMetastatic disease\nAVM", "Case Diagnosis": "Desmoplastic infantile Astrocytoma", "Diagnosis By": "Surgery and Pathologic examination", "Treatment & Follow Up": "Surgery only" }, "Topic": { "Title": "Pilomyxoid Astrocytoma (PMA), WHO Grade 2", "Disease Discussion": "WHO Grade 2 Neoplasm of astrocytes.\n\nPilomyxoid astrocytoma (PMA) is a newly described variant. Previously, this tumor may have been included under the diagnosis of pilocytic astrocytoma. Pilomyxoid astrocytoma has a shorter time to recurrence, is more likely to recur; and/or cause CNS metastasis.\n\nRelated to pilocytic astrocytoma with bipolar cells arranged around vessles, in a mucoid matrix. Does not have Rosenthal fibers - which are common in pilocytics.\n\nPilomyxoid astrocytoma is most commonly a solid enhancing mass in the hypothalamus, and the mean age is younger (10-15 months) than for pilocytic astrocytoma(58 - 108 months).\n\nMost common in the hypothalamus and chiasm. May occur anywhere, like pilocytic, including thalamus, brainstem, cerebellum, and spinal cord.\n\nhttp://www.medscape.com/viewarticle/493014_Tables#Table%201'>http://www.medscape.com/viewarticle/493014_Tables#Table%201\n\nhttp://www.aans.org/education/journal/neurosurgical/June05/18-6a-7.pdf\n\nThese tumors were first described in the hypothalamus, and have imaging characteristics that mimic pilocytic astrocytoma.\n\nhttp://www.medscape.com/viewarticle/493014\n\nCME Article on pilomyxoid astrocytoma:\nhttp://www.medscape.com/viewprogram/3582_pnt", "ACR Code": "1.3", "Category": "Neoplasm, glial", "Keywords": "pilocytic astrocytomaPilomyxoid Astrocytomahypothalamic glioma", "External Links": "www.aans.org/education/journal/neurosurgical/June05/18-6a-7.pdf" } }, { "U_id": "MPX1160", "TAC": [], "MRI": [ "MPX1160_synpic15204", "MPX1160_synpic15206", "MPX1160_synpic15208", "MPX1160_synpic15209" ], "Case": { "Title": "Tear of the Achilles tendon- almost complete (Grade II tear)", "History": "50 y/o WM with left posterior lower leg pain x 2months, made worse with walking/standing.", "Exam": "Decreased strength with plantar flexion, + Achilles TTP, Normal previous plain x-ray.", "Differential Diagnosis": "1.Almost complete rupture Achilles tendon- Grade II tear\n\n2.Almost complete rupture of Achilles tendon (Grade II tear) with interstitial tear and/or tendinopathy of the proximal Achilles tendon", "Case Diagnosis": "Tear of the Achilles tendon- almost complete (Grade II tear)", "Treatment & Follow Up": "1.\tOrtho Consult\n2.\tImmobilization\n3.\tNSAIDS\n4.\tPhysical Therapy" }, "Topic": { "Title": "Grade 2 Achilles Tendon Rupture", "Disease Discussion": "Achilles tendon rupture usually presents as abrupt onset of pain with loss of strength and range of motion following sudden, forceful contraction of the calf muscle. The patient may feel or hear an audible snap. Physical exam may reveal decreased strength, with a positive Thompson test. Poorly conditioned men over the age of 30 are typically affected. Fluoroquinolone use and chronic corticosteroid use are predisposing factors particularly in patients over 60 years of age. Partial rupture may not have a well-defined onset and may involve gradual worsening of symptoms. The degree of rupture is defined as follows:Tendon Grading SystemGrade 1: Minimal Disruption; Grade 2: Greater than 50% Fiber Disruption; Grade 3: Complete Tear. With partial ruptures, the clinical picture may not be as clear, the and imaging can play a crucial role. A complete tear shows discontinuity of fibers while a partial tear shows tendon thickening and increased signal on T2-weighted images. The patient described above has pain over 2 months with no specific inciting event. Treatment was immobilization. His decreased use of that limb had already resulted in soleus muscle wasting as shown by fatty replacement in that muscle. Therefore, he will also require physical therapy to assist in strengthening the lower leg.", "ACR Code": "-1.-1", "Category": "Unsure", "Keywords": "Achilles Tendon", "Reference": "Leffler, Susan and Disler, David. MRI imaging of tendon, ligament, and osseous abnormalities of the ankle and hindfoot. Radiological Clinics of North America. Sep 2002: 40(5).\n\nSheon, Robert. Tendon Injuries and Inflammation Around the Ankle. Up to Date." } }, { "U_id": "MPX1147", "TAC": [], "MRI": [ "MPX1147_synpic27148", "MPX1147_synpic27149", "MPX1147_synpic27150", "MPX1147_synpic27151", "MPX1147_synpic27152", "MPX1147_synpic27153" ], "Case": { "Title": "Vestibular (Acoustic) Schwannoma", "History": "Patient is a 34 year old man who presented with a 2 year history of increasing hearing loss, tinnitus and occasional vertigo. In the last few months he has developed L. facial numbness in the V1-V2 distribution.", "Exam": "Physical exam: \nVSS, afeb, patient in NAD. AOx4.\nThe physical exam revealed decreased hearing in the left ear consistent with a sensorineuronal process. Sensation to light touch and pin prick was also diminished in the V1-V2 distribution of the left side of his face. The patients exam, to include coordination and gait testing was otherwise completely normal.\n\nLabs: Thyroid, liver, renal panels as well as Chem 7 and calcium were all normal. CBC w/ diff was normal. Audiometry was not performed as hearing was grossly decreased in the left ear.", "Findings": "The MRI reveals an \"ice-cream cone\" shaped lesion originating from the L. IAC, with extension into the CPA, extending rostrally to compress the left CN V. It is not invading the brain stem but is compressing it. On T1, the mass is hypointense with adjacent brain parenchyma and hyperintense on T2 imaging. There is avid post-gadolinium enhancement on T1 imaging in a slightly heterogenous manner throughout the mass.", "Differential Diagnosis": "Vestibular (Acoustic) Schwannoma\nMeningioma", "Case Diagnosis": "Vestibular (Acoustic) Schwannoma", "Diagnosis By": "Intraoperative frozen section and final pathology report consistent with Schwannoma.", "Treatment & Follow Up": "The mass was resected surgically via retrosigmoid craniectomy. Pt. is currently being followed.", "Discussion": "The patient presented with symptoms classic of a vestibular schwannoma (see factoid). At 34, though on the young end, he still fit within the epidemiologic classification of most patients presenting between 30-50 years of age.\n\nInterestingly, in addition to his acoustic nerve symptoms, which are present in some degree in 95% of vestibular schwannoma patients, trigeminal nerve symptoms were pronounced and facial nerve symptoms were absent (despite the close proximity of CN VII to CN VIII). This has been noted in other cases as well. His vestibular symptoms were transient in nature.\n\nOther CPA masses such as eidermoid includion cysts (IEC's) that don't enhance, Lipomas (T1 doesn't show fat), and Hemangiomas (hyperintense on T1 and T2, often with flow voids present as well) though in the original differential were not in the final differential as the enhancement characteristics of the MRI (as well as morphology) was essentially able to eliminate them from further consideration. Though the mass looked morphologically like a schwannoma, there still was the possibility, though very slight, that it could be a meningioma as enhancement characteristics can be similar between meningiomas and schwannomas. \n\nThe pathological sample however, confirmed the very strong suspicion that it was a schwannoma." }, "Topic": { "Title": "Vestibular (Acoustic) Schwannoma", "Disease Discussion": "Vestibular schwannomas, also known as acoustic Schwannomas, acoustic neuromas, acoustic neurinomas, and vestibular neurilemomas are benign neoplasms derived from Schwann cells encompassing the vestibular (as opposed to cochlear) portion of CN VIII. They are the most common cerebropontine angle (CPA) mass, making up approximately 80% of all CPA tumors and approximately 8% of all intracranial tumors in adults.\n\nPatients with vestibular schwannomas typically present between 30-50 years of age with the overall incidence of symptomatic vestibular schwannomas at 1/100,000 person-years, though asymptomatic lesions may be more common. Most lesions are unilateral. However, as many as 10% of patients with vestibular schwannomas have Neurofibromatosis type 2 (NF2) with more than 75% of affected NF2 patients having bilateral vestibular schwannomas. \n\nMost patients present with complaints of hearing loss and/or tinnitus. Many also complain of difficulties with balance/and or gait. In a case series of 1000 acoustic Schwannomas, at time of diagnosis, 95% of patients had cochlear nerve symptoms, 61% had vestibular symptoms, 9% had trigeminal symptoms (most often sensory) and 6% had facial nerve complaints. (Note that more patients had trigeminal symptoms than facial nerve symptoms, despite the close proximity of CN VII to CN VIII!) \n\nAs most patients do have hearing loss from the affected nerve, audiometry is the most sensitive initial clinical screening test for a vestibular schwannoma. However, HRCT or MRI (MRI with gadolinium contrast being preferable to HRCT) is needed for more definitive diagnosis. \n \nAcoustic schwannomas typically originate at the entrance of the internal auditory canal (IAC) and extend out into the CPA, resembling an \u201cice-cream cone,\u201d often causing mass affect on other structures as they enlarge. This origin and appearance, evident with MRI and/or HRCT, helps distinguish them from other CPA masses such as meningiomas (the 2nd most common CPA mass), epidermoid inclusion cysts (EIC\u2019s, 3d most common CPA mass), lipomas, angiomas, arachnoid cysts, mets, etc. \n\nIn addition to the morphology and location/origin of vestibular schwannomas, they also have enhancing characteristics that aid in distinguishing them from other CPA masses. On T1-weighted images, schwannomas are hypointense compared to surrounding brain parenchyma, and enhance markedly with IV gadolinium. T2-weighted images show hyperintense signal. \n\nMeningiomas are typically isointense rather than hypointense on T1 but may be hyperintense with T2 imaging and also enhance brightly with gadolinium. With the enhancement however, meningiomas are often more homogeneous in appearance than the more heterogeneous Schwannomas that is sometimes due to benign cystic degeneration. Similar to Schwannomas, EIC\u2019s are hypointense with T1 images and are hyperintense with T2. However, EIC\u2019s don\u2019t enhance with gadolinium (other than occasionally a thin ring of enhancement around their periphery).\n\nWhen observation is not appropriate, treatment of vestibular schwannomas is usually surgical, though radiation therapy (stereotactic or \"Gamma Knife\" is also being used with success. Chemotherapy has not been proven beneficial.", "ACR Code": "1.3", "Category": "Neoplasm, benign", "Keywords": "Acoustic SchwannomaVestibular SchwannomaCPA Mass", "Reference": "Briggs, R; Gadre, A; Quinn, F; et. al. Differential Diagnosis of Temporal Bone and Skull Base Lesions. Grand Rounds Presentation, UTMB, Dept. of Otolaryngology, December 19, 2001. http://www.utmb.edu/otoref/Grnds/Skull-Base-Lesions-2001-12/Skull-Base-Lesions-2001-12.htm \n\nMatthies, C; Sammi, M. Management of 1000 vestibular schwannomas (acoustic neuromas): clinical presentations. Neurosurgery 1997; 40:1.\n\nPark, J; Black, P; Vernick, D. Acoustic Neuroma. UpToDate 2005. www..uptodate.com\n\nPirraglia, P; Ng, J. Acoustic Neuroma. Ferri: Ferri\u2019s Clinical Advisor: instant diagnosis and treatment, 2006 ed. pp 23-24. \n\nSmirniotopoulos, J. Posterior fossa masses: differential diagnosis and radiologic-pathologic correlation. USUHS and The Armed Forces Institute of Pathology, Washington D.C. http://rad.usuhs.mil/rad/home/postfoss/postfossa2w.html", "External Links": "rad.usuhs.mil/rad/home/postfoss/postfossa2w.html" } }, { "U_id": "MPX1171", "TAC": [], "MRI": [ "MPX1171_synpic26485", "MPX1171_synpic26486", "MPX1171_synpic26487", "MPX1171_synpic26497", "MPX1171_synpic26498" ], "Case": { "Title": "1) Fronto-nasal encephalocele\r\n2) Colpocephaly", "History": "2 day old female infant with midline mass above the nose.", "Exam": "Soft midline mass noted above the patient's nose.", "Findings": "T1 sagital view showing enlarged posterior lateral ventricles. The image shows a midline opening of the skull above the bridge of the nose with protrusion of brain parenchyma through the skull defect.\n\nT2 axial views show bilateral asymmetrically enlarged lateral ventricles (right>left). Brain parenchyma protruding from a midline skull defect at the level of the eyes with CSF communication into the mass. Parenchymal volume loss noted in parietal, occipital and frontal lobes.", "Differential Diagnosis": "Encephalocele\nMeningocele\nGlioma\nHemangioma\nNasal Dermoid", "Case Diagnosis": "1) Fronto-nasal encephalocele\n2) Colpocephaly", "Diagnosis By": "MRI - protrusion of brain parenchyma and CSF through a midline skull defect is pathognomonic for encephalocele.", "Treatment & Follow Up": "Treatment typically involves a frontal craniotomy with excision of the protruding and non-functional brain parenchyma. This requires immediate neurosurgical consultation. This particular patient is scheduled to undergo surgery.", "Discussion": "The open skull defect with protruding mass narrows the ddx to encephalocele and meningocele. Since both CSF and brain parenchyma are noted protruding from the skull defect, the dx is encephalocele." }, "Topic": { "Title": "Fronto-nasal encephalocele", "Disease Discussion": "The term cephalocele refers to a defect in the skull and dura with extracranial extension of intracranial structures. The term encephalocele refers to herniation of both brain tissue and meninges through the skull defect, whereas the term meningocele refers to herniation of the meninges only. Both the skull defect and herniation are more common in the midline. \n\nMost encephaloceles are easily recognized by the clinician. On initial examination, the patient has a large midline extracranial mass that is soft to palpation. In patients with obvious masses such as these, the imaging study is obtained to look for associated brain anomalies that may alter the child's prognosis. An example of such an associated anomaly is shown in Films .3 - .6. This patient with a large frontal encephalocele also has agenesis of the corpus callosum and multiple gray matter heterotopias in the subependymal region. The absence of the corpus callosum can be detected on both the sagittal images by the absence of the corpus on the midline image and on the axial images by the characteristic shape of the frontal horns and the parallel lateral ventricles.\n\nAnother reason to obtain imaging studies in patients with encephaloceles is to look for the location of the major vascular structures of the brain. Particularly, because most encephaloceles are in the midline, the torcula and the superior sagittal sinus are crucial structures that must be located. In Films .7 - .9, a parietal encephalocele is shown. This case has two very important findings. The first is the deformity of the brain in the region of the encephalocele. Notice how the midbrain and cerebellum are stretched toward the calvarial defect. This stretching results from the pulsations of the brain causing it to be pushed out of the calvarial defect. The immature brain (before myelination) is very soft and easily deformed. Therefore it can be molded into just about any shape. It is common to see this sort of stretching of brain toward the skull defect in patients with encephaloceles. The other important feature of this case is the position of the superior sagittal sinus. On sequential coronal films, going from front to back, the sagittal sinus can be visualized in its entirety in relation to the encephalocele. Arrows point to the sinus as it courses within the most inferior and lateral aspect of the sac on the right. Notice that the sinus would be outside of the calvarium if the calvarium were present. More posteriorly, the torcula is high and the straight sinuses are seen to course steeply inferiorly within the walls of the tentorium cerebellum (arrows). The steep leaves of the tentorium probably result from the same process that causes herniation of the midbrain and cerebellum into the calvarial defect. \n\nSpecial mention should be made of sphenoidal and fronto-nasal encephaloceles because they are often clinically occult at birth. A high index of suspicion is necessary to make the diagnosis of encephalocele in adolescents and young adults who present with nasal or nasopharyngeal masses.", "ACR Code": "1.1", "Category": "Congenital, malformation" } }, { "U_id": "MPX1188", "TAC": [], "MRI": [ "MPX1188_synpic18994", "MPX1188_synpic18995" ], "Case": { "Title": "Endometrioma", "History": "Young woman with chronic cyclical pelvic pain", "Findings": "Ultrasound shows a mass replacing the right ovary with diffuse homogenous low-level echoes. MRI demonstrates this mass to be high intensity on T1 weighted images and heterogenous low signal intensity on T2 weighted images.", "Differential Diagnosis": "Ultrasound differential diagnosis: hemorrhagic cyst, dermoid cyst and mucinous cystadenoma or cystadenocarcinoma of the ovary, or other ovarian neoplasm.", "Case Diagnosis": "Endometrioma" }, "Topic": { "Title": "Endometrioma", "Disease Discussion": "Endometriomas are caused by endometriosis which is endometrial tissue present outside of the uterine cavity. Typical locations include on the ovaries (76%), anterior and posterior cul-de-sac (69%), posterior broad ligament (47%), uterosacral ligament (36%), uterus (11%), colon (4%) and small bowel (0.5%). Women of childbearing age are affected and the mean age of diagnosis is 25-29. The overall prevalence of endometriosis in woman is estimated to be 5-10%. Clinical manifestations include dysmenorrhea, dyspareunia, abdominal pain, dysfunctional uterine bleeding and infertility. Small implants and adhesions are not well evaluated radiologically; therefore, laparoscopy remains the standard of reference for diagnosis and staging. \n\nAn endometrioma may be defined as an area of endometriosis, usually in the ovary, that has enlarged sufficiently to be classified as a tumor or cyst. It develops secondary to a deep endometriotic implant that undergoes repeated hemorrhage. It can completely replace normal ovarian tissue. If large enough to see by ultrasound the mass typically has homogenous low-level echoes -- a non-specific appearance which can also be seen with entities such as hemorrhagic cysts and malignancy. A recent study (Patel et al) noted that 95% of endometriomas in their study exhibited this typical appearance on ultrasound. Although endometriomas frequently contain septations, the absence of wall nodularity and presence of diffuse low level echoes favors endometrioma over malignancy. The appearance of endometriomas can mimic neoplasm including wall thickening, septations, wall nodularity and echogenic wall foci. Detection of endometriosis implants and adhesions by ultrasound is not practical due to their small size and large variety of appearances. Differential diagnosis includes hemorrhagic cysts, dermoid cysts and cystic neoplasms. Resolution of a cystic lesion on a follow-up ultrasound effectively rules out endometrioma. Because of the wide variability of ultrasound appearance of endometriomas pelvic MRI can be very helpful. \n\nThe appearance of endometriomas on MRI is more specific than other non-invasive imaging methods. Imaging planes can include all three standard projections (axial, sagittal, and coronal), with the sagittal plane being particularly useful for evaluating the cul-de-sac and rectum. Endometriomas appear hyperintense on T1-weighted images. On T2 weighted images they display heterogenous \u201cshading\u201d or loss of signal intensity compared with T1 weighted images which is due to the chronic cyclical nature of its blood products and helps differentiate it from other lesions with more acute hemorrhage. The findings on T2 weighted sequence are variable and depend on the concentration of blood products. Fat suppression increases the conspicuity of endometriomas and allows more detailed evaluation of their architecture. This is especially helpful in differentiating endometriomas from fat-containing lesions such as dermoid cysts. Gadolinium iv contrast enhancement is not particularly useful for differentiating endometriomas from other lesions as endometriomas have non-specific variable enhancement. Dermoids can be recognized and differentiated from endometriomas by the presence of chemical shift artifact and signal drop-out on the fat-suppression images. Mucinous lesions can have increased signal intensity on T1-weighted but their signal is considerably less intense than that of fat or blood. Hemorrhagic cysts can have similar T1 characteristics, but will not demonstrate T2 \u201cshading\u201d and can be differentiated from endometriomas when they resolve over time. Visualization of solid components, septations, and a size larger than expected for an endometrioma are features suggestive of malignancy.", "ACR Code": "8.3", "Category": "Cyst, benign", "Keywords": "EndometriomaOvaryEndometriosis", "Reference": "Grainger & Allison's Diagnostic Radiology: A Textbook of Medical Imaging, 4th Ed. p 2116\n\nRyan: Kistner's Gynecology & Women's Health, 7th ed., p 492\n\nMD Patel, VA Feldstein, DC Chen, SD Lipson, and RA Filly \nEndometriomas: diagnostic performance of US \nRadiology 1999 210: 739 \n\nP. J. Woodward, R. Sohaey, and T. P. Mezzetti Jr\nEndometriosis: Radiologic-Pathologic Correlation\nRadioGraphics, January 1, 2001; 21(1): 193 - 216." } }, { "U_id": "MPX1185", "TAC": [], "MRI": [ "MPX1185_synpic17343", "MPX1185_synpic17344" ], "Case": { "Title": "Lhermitte Duclos disease, Cowden disease", "History": "This 56 year old woman had breast carcinoma for which she had bilateral mastectomies six years apart. She also had a thyroidectomy in her twenties. Six years after the second mastectomy, she developed gait unsteadiness that progressed to the point that she was unable to walk.", "Findings": "Fig 1. Axial T1 weighted MRI shows coarse striations resulting from irregular, abnormally thickened cerebellar folia.\n\nFig 2. Axial T2 weighted MRI also showing the same coarse striations resulting from abnormally thick cerebellar folia. \n\nFig 3. Gross appearance of a portion of the surgical specimen showing the coarse widened folia.\n\nFig 4. Low magnification histological section showing subpial of myelinated fibers overlying a band of large neurons that replace the Purkinje cells and outer portion of the internal granular cell layer. \n\nFig 5. Higher magnification of the abnormal large neurons.", "Differential Diagnosis": "Cerebellar mass\n\u2022 Astrocytoma\n\u2022 Medulloblastoma (usually < 35 yo)\n\u2022 Cerebellar infarction\n\u2022 Lhermitte Duclos", "Case Diagnosis": "Lhermitte Duclos disease, Cowden disease", "Treatment & Follow Up": "An MRI showed a large right cerebellar mass with effacement of the fourth ventricle and hydrocephalus. Subtotal resection of the mass was performed.", "Discussion": "The associated breast cancer and thyroid disease form the constellation of findings known as Cowden disease - an autosomal dominant phakomatosis." }, "Topic": { "Title": "Lhermitte Duclos disease", "Disease Discussion": "Lhermitte Duclos disease is also know by a wide variety of terms including ganglioneuroma of the cerebellum, gangliocytoma dysplasticum and Purkinjioma. The lesion is variously regarded as a malformation or a true neoplasm similar to gangliocytomas elsewhere in the nervous system. The lesion is thought to result from aberrant migration of the internal granular cells. Very few of the large cells are thought to be derived from Purkinje cells. \n\nLhermitte Duclos disease may occur as an isolated lesion or in association with Cowden\u2019s syndrome. The latter is a phakomatosis that variablly includes breast carcinoma, thyroid carcinoma, intestinal polyps and oral mucosal lesions. Cowden\u2019s syndrome may be inherited as an autosomal dominant trait.", "ACR Code": "1.3", "Category": "Congenital, genetic", "Keywords": "Lhermitte DuclosganglioneuromaPurkinjioma" } }, { "U_id": "MPX1124", "TAC": [], "MRI": [ "MPX1124_synpic50738", "MPX1124_synpic50739", "MPX1124_synpic50740", "MPX1124_synpic50741", "MPX1124_synpic50742", "MPX1124_synpic50743", "MPX1124_synpic50744", "MPX1124_synpic50745", "MPX1124_synpic50746", "MPX1124_synpic50747", "MPX1124_synpic50748", "MPX1124_synpic50749", "MPX1124_synpic50750" ], "Case": { "Title": "Multiple Sclerosis, Quadrantanopsia", "History": "42 y.o. combat fighter pilot c/o \"blind spot\" - sudden onset six days ago and lasted about four hours. Previous Hx of a similar episode several years ago.", "Exam": "Right inferior quadrantanopsia on formal visual field testing\nG6PD deficiency", "Findings": "\u2022 Lateral geniculate body - abnormal signal and enhancement\n\u2022 Additional periventricular lesions", "Differential Diagnosis": "\u2022 Multiple sclerosis\n\u2022 Lyme disease\n\u2022 ADEM (Acute Disseminated Encephalomyelitis)\n\u2022 Sarcoidosis\n\u2022 Vasculitis (SLE, etc.)", "Case Diagnosis": "Multiple Sclerosis, Quadrantanopsia", "Diagnosis By": "Clinical Hx and response to steroid therapy", "Treatment & Follow Up": "This patient had an extensive workup. Lyme titers were negative. CSF did not show oligoclonal bands nor pleocytosis.", "Discussion": "Quadrantanopsia usually affects the optic radiations posterior (distal) to the lateral geniculate nucleus (body) - where the fibers from the superior retina diverge deep into the temporal lobe as Myer's loop. The separation of the superior and inferior axons allows a lesion to produce a scotoma (field cut) affecting a quadrant.\n\nThe lateral geniculate body is supplied by the both the lateral posterior choroidal artery and the anterior Choroidal Artery (AChA); and, ischemia could produce a hemianopsia usually in association with hemiplegia and hemianesthesia. PMID: 3790969 PMID: 10601806 PMID: 9556927 PMID: 8091255 PMID: 7922468" }, "Topic": { "Title": "Visual Fields, Differential Diagnosis", "Disease Discussion": "Monocular Blindness - Optic nerve proximal to Chiasm\n\u2022 Retinal Detachment\n\u2022 Central Retinal Artery/Vein Occlusion\n\u2022 Optic Neuritis\n\u2022 Trauma\n\u2022 Tumor\n\nBitemporal Hemianopsia - Suprasellar lesion behind chiasm\n\u2022 Pituitary Adenoma\n\nHomonymous Hemianoposia - Distal to Chiasm:\n\u2022 40% Occipital, 25% Temporal, 5% optic tract and LGB\n\u2022 70% infarcts, 15% neoplasms, 5% hemorrhage, ??% trauma\n>>>PCA infarct\n>>>MCA infarct\n>>>AChA infarct (Eur Neurol 2000;43(1):35-8)\n>>>Watershed Infarcts (Acta Med Scand 1984;216(4):417-22)\n>>>Carotid Dissection (J Neuroophthalmol 1999 Jun;19(2):136-9)\n>>>Chiropractic Manipulation (Am J Ophthalmol 1997 Jun;123(6):851-2)\n\u2022 Lateral Geniculate Body (LGB)\n\u2022 Occipital Infarct\n>>>Unilateral progressing to Bilateral (J Neurol Neurosurg Psychiatry 1983 Jan;46(1):78-80)\n\nQuandrantanopsia - Optic Radiations distal to LGB (Lateral Geniculate Body) Lesions in Myer's loop cause a superior quadrantanopsia. \n\nTest yourself:\nhttp://www.thinkingmedicine.com/elearning/vfield/\nhttp://www.thebarrow.org/Education_And_Resources/Barrow_Quarterly/205263\nhttp://en.wikipedia.org/wiki/Lateral_geniculate_nucleus\nhttp://en.wikipedia.org/wiki/File:ERP_-_optic_cabling.jpg\nhttp://www.ihrfoundation.org/intracranial/hypertension/info/C68/\nhttp://www.osnsupersite.com/view.aspx?rid=29843\nhttp://www.reingoldeyecenter.com/glaucoma.aspx", "ACR Code": "1.1", "Category": "Differential Diagnosis", "Keywords": "scotoma anopia anopsia quadrantanopsia hemianopsianeuroophthalmologyblindness blind spot", "Reference": "J Neurol Neurosurg Psychiatry 1983 Jan;46(1):78-80\nActa Med Scand 1984;216(4):417-22\nBr J Ophthalmol 1997;81:324-328 ( April )\nAm J Ophthalmol 1997 Jun;123(6):851-2\nJ Neuroophthalmol 1999 Jun;19(2):136-9\nEur Neurol 2000;43(1):35-8\nAJNR Am J Neuroradiol 2001 Jun-Jul;22(6):1043-9", "External Links": "bjo.bmjjournals.com/cgi/content/full/81/4/324" } }, { "U_id": "MPX1184", "TAC": [], "MRI": [ "MPX1184_synpic17446", "MPX1184_synpic17447", "MPX1184_synpic17448", "MPX1184_synpic17449", "MPX1184_synpic17450" ], "Case": { "Title": "Brain biopsy confirmed glioblastoma multiforme.", "History": "This patient presented with 3 weeks of progressive weakness in right upper and lower extremities.", "Exam": "Patient fully alert and oriented. His neurological exam revealed a right sided hemiparesis with strengths of 2/5 in his right lower extremity and 3/5 in the right upper extremity. He was hyperreflexic right greater than left, had right sided spasticity, and a right babinski present with clonus in the ankle. He also had decreased sensation to light touch throughout his right side including his face.", "Findings": "Solitary deep lesion with mild midline shift and patchy enhancement. Abnormal white matter signal in the right hemisphere suggesting tumor extension across the corpus callosum.", "Differential Diagnosis": "\u2022 Astrocytoma - Anaplastic (usually does not show 'cystic' or necrotic area)\n\u2022 Glioblastoma Multiforme (usually brighter enhancement)\n\u2022 Primary CNS Lymphoma (usually lower signal on T2W)\n\u2022 Tumefactive Demyelination (usually does not show edema like this)", "Case Diagnosis": "Brain biopsy confirmed glioblastoma multiforme.", "Treatment & Follow Up": "This patient received a six week course or radiation and will start a phase 2 clinical chemotherapy trial at the NIH. He was also started on seizure prophylaxis and pain medication.", "Discussion": "Gliomas are graded on the most aggressive histology. A small region of GBM may arise or coexist within larger areas of Anaplastic Astrocytoma. GBM usually presents in older patients (typically >40 yrs.)" }, "Topic": { "Title": "Glioblastoma multiforme", "Disease Discussion": "Glioblastoma Multiforme (GBM) is a WHO grade IV astrocytoma - with high mitotic activity and either endothelial proliferation or necrosis. They are the most common primary intracranial neoplasm and have the worst prognosis. They are typically seen in adults greater than 40 with lower grade astrocytomas occurring more often in younger adults and children. They present most commonly with headaches or seizures, but can also present with hemiparesis or signs of increased intracranial pressure. These symptoms usually present in a short time frame, on the order of weeks to months. \n\nRadiologically, they are usually show a heterogeneous signal on MR and commonly have extensive surrounding \"vasogenic edema\". Tumor necrosis is a hallmark of GBM and typically appears on MRI as an area of non-enhancing T-1 hypointensity. This area is frequently surrounded by an enhancing region. Invasion of white matter tracts is common with spread of the neoplasm to the opposite hemisphere through the corpus callosum in up to 75% of cases. The regions of \"vasogenic edema\" usually include white-matter that is infiltrated by neoplastic cells. Neoplastic infiltration often extends beyond any region of signal abnormality noted on imaging, and even into areas that are \"normal\" by both gross and microscopic pathology. \n\nRadiological features generally correlate with tumor grade but are not specific. Histological grading is the most reliable means of assessing this neoplasm. \n\nhttp://www.nabtt.org/overview.htm", "ACR Code": "1.3", "Category": "Unsure", "Keywords": "Glioblastoma Multiformeastrocytoma", "Reference": "Batchelor, T, \u201cClinical manifestations and diagnosis of high grade malignant astrocytoma,\u201d www.UpToDate.com, 18 Mar 2003.\n\nGrainger & Allison\u2019s Diagnostic Radiology: Textbook of Medical Imaging, 4th Edition, Churchhill Livingstone, 2001, p. 2330.", "External Links": "www.nabtt.org/" } }, { "U_id": "MPX1202", "TAC": [], "MRI": [ "MPX1202_synpic34351", "MPX1202_synpic34354", "MPX1202_synpic34374", "MPX1202_synpic34375", "MPX1202_synpic34376" ], "Case": { "Title": "Stroke", "History": "44yo RHD M with sudden onset of difficulty speaking, L facial droop and drooling. Pt had difficulty forming words, slurred speech, and numbness in L face and arm. Most of the reported symptoms resolved within 10 minutes, with slight numbess and tingling in the L corner of the mouth still present after 30-45 minutes.", "Exam": "BP: 222/141 HR 108\nCN: VII- L side of mouth hangs\n Vibration mildly decreased equally throughout distal fingers and toes\n Strength and motor intact\n Reflexes and coordiantion intact\n Normal Gait\n\nLabs: BUN 28 Cr 3.1", "Findings": "Multiplanar, multi-sequence MRI of brain without IV contrast. Time-of-flight and contrast enhanced MRA of neck and intracranial vasculature with 3D reconstructions.\n - several small areas of restricted diffusion, two in the right temporal lobe and two in right posterior frontal lobe. Areas have a small amount of associated T2 hyperintensity, most consistent with acute to subacute infarctions. Right frontal lobe lesions are gyroform.\n\nDWI shows area of hyperintensity in right cerebral hemisphere\n\nNo evidence of hemodynamically significant stenosis in the common carotids.", "Differential Diagnosis": "Transient Ischemic Attack\nFocal infection\nMeningo-encephalitis", "Case Diagnosis": "Stroke", "Diagnosis By": "MRI of the Brain, MRA of the brain, DWI", "Treatment & Follow Up": "Mean Arterial Pressure goal 100-130\nStart Aspirin 325mg PO qday\nStart Lisinopril 10mg PO qday", "Discussion": "The patient had a history of stage IV CKD and uncontrolled HTN and HLD which increased his risk for a stroke. The patient presented with left sided symptoms, with radiological evidence of areas of ischemia in the right posterior frontal and temporal lobes, which are consistent with the patient's presentation. Although the patient's symptoms were resolving after 45 minutes, there were findings on DWI consistent with infarction and therfore the diagnosis of stroke was made. The patient's symptoms and radiological findings indicate involvement of middle cerebral artery." }, "Topic": { "Title": "Stroke", "Disease Discussion": "Ischemic Stroke\n* Abrupt interruption of focal cerebral blood flow\n* 750,000 cases per year in United States\n* more than 150,000 deaths annually\n* 3rd leading cause of death US\n* #1 cause of disability in US", "ACR Code": "-1.-1", "Category": "Hypoxic or Ischemic", "Keywords": "ischemia", "Reference": "Taveras, JM. Neuroradiology 3rd Ed. Williams and \tWilkins:1996.pp 420-425.\n\nSolenski NJ. Transient ischemic attacks: Part I. diagnosis and evaluation. Am Fam Physician 2004; 69: 1655-74, 1679-80.\n\nLefkowitz D. Hyperacute ischemic stroke missed by diffusion-weighted imaging. Am J Neuororadiol 1999; 20: 18712-1875. \n\nBrott T, Bogousslavsky J. Treatment of acute ischemic stroke. N Engl J Med 2000; 343: 710-722." } }, { "U_id": "MPX1199", "TAC": [], "MRI": [ "MPX1199_synpic33608", "MPX1199_synpic33610" ], "Case": { "Title": "Carbon Monoxide Poisoning", "History": "23 year old man with headache and lethargy after an ice storm. Because of a power outage, he has been running a generator in his garage.", "Exam": "Bilateral \"cherry red macula\"", "Findings": "Bilateral symmetric lesions of abnormal signal intensity in the medial lenticular nuclei (globus pallidus)", "Differential Diagnosis": "\u2022 Carbon Monoxide Poisoning\n\u2022 Methanol intoxication\n\u2022 Hypotension", "Case Diagnosis": "Carbon Monoxide Poisoning", "Diagnosis By": "History and Imaging findings", "Discussion": "CO binds to Hgb 240X stronger than O2 making carboxyhemoglobin\nTypical Sx: HA, Lethargy, weakness, dizziness, nausea, and SOB \nTX is to displace CO with O2 \nT1/2 is 320 min on room air, 80 min on 100% O2, 23 min at 3atm 100% O2\n\nCarbon Monoxide - https://www.youtube.com/watch?v=f3VYQsUGJ00\nhttp://bmj.bmjjournals.com/cgi/content/full/319/7217/1082\nhttp://www.wfubmc.edu/AirCare/co.htm\nhttp://jama.ama-assn.org/cgi/content/full/294/12/1482\nhttp://www.diseasesdatabase.com/result.asp?glngUserChoice=2364&bytRel=2&blnBW=False&strBB=RL&blnClassSort=True" }, "Topic": { "Title": "Carbon monoxide poisoning", "Disease Discussion": "Carbon monoxide (CO) is a tasteless odorless gas produced by combustion of hydrocarbons. Common sources include automobile, truck, and bus engines; fireplaces; charcoal grills; and generators.\n\nIncidence: The CDC reports > 15,000 non-fire related CO exposure/poisoning cases each year resulting in 480 deaths. December and January are the peak months for these events.\nhttp://www.cdc.gov/od/oc/media/pressrel/fs050120.htm\n\n\nCO poisoning in the home is very common after power failures - especially in cold climates - when generators are used indoors. Even a home generator in a garage can kill, when combustion fumes enter through a parially open door. Space heaters may also release CO into a room or tent.\n\nSymptoms of CO poisoning include headache, nausea, lethargy, confusion, shortness of breath, and coma.\n\nCarbon monoxide is both cardiotoxic and neurotoxic. Lesions in the brain show a \"selective vulnerability\" for the medial lenticular nucleus (globus pallidus).[http://onlinelibrary.wiley.com/doi/10.1111/jon199993175/full]\n[http://www.tandfonline.com/doi/pdf/10.1080/02699050500488181?needAccess=true]\n\nSome sources suggest that the vulnerability of the globus pallidus is also related to reduced perfusion - which may occur from a variety of conditions. [https://www.ncbi.nlm.nih.gov/pubmed/26258901] \n[https://www.ncbi.nlm.nih.gov/pubmed/6650136]\n\nTreatment includes removal from the site/source of the exposure, oxygen, and hyperbaric therapy.\n\nCarbon Monoxide - https://www.youtube.com/watch?v=f3VYQsUGJ00\n\u2022 CDC - http://www.cdc.gov/co/ & http://www.bt.cdc.gov/agent/carbonmonoxide/casedef.asp\n\u2022 Detection of CO by Breathalyzer - http://www.ispub.com/ostia/index.php?xmlFilePath=journals/ijeicm/vol5n2/co.xml\n\u2022 CO Poisoning detection in the ER - http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=16798147&dopt=Abstract\n\u2022 Mass Poisoning by CO - http://emj.bmj.com/cgi/content/full/17/1/38\n\u2022 EPA - http://www.epa.gov/iaq/pubs/coftsht.html", "ACR Code": "1.5", "Category": "Toxic (see also Metabolic)", "Keywords": "carbon monoxideheadachebreathalyzer", "Reference": "[http://onlinelibrary.wiley.com/doi/10.1111/jon199993175/full]\n[http://www.tandfonline.com/doi/pdf/10.1080/02699050500488181?needAccess=true]\n[https://www.ncbi.nlm.nih.gov/pubmed/26258901] \n[https://www.ncbi.nlm.nih.gov/pubmed/6650136]", "External Links": "www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=16798147&dopt=Abstract" } }, { "U_id": "MPX1236", "TAC": [], "MRI": [ "MPX1236_synpic26278", "MPX1236_synpic26279", "MPX1236_synpic26280" ], "Case": { "Title": "Agenesis of the Corpus Callosum", "History": "This 60 year old man presents with a 4 month history of left side numbness, decreased sensation, and pain in the V2/V3 distribution of his face. There is no prior history of any neurologic problem.", "Exam": "Neurologically intact.", "Findings": "Sagittal T1, axial T2 and proton density-weighted images do not visualize the corpus callosum; and, there is associated colpocephaly. There is absence of the cingulate gyrus and a radial pattern of sulci and gyri along the medial surface of the cerebral hemisphere. \n\nProbst bundles are not well demonstrated on these images and would be best seen in the coronal plane. \n\nThe lateral ventricles demonstrate their classic wide and straight appearance.\n\nOf note, there is also a large incidental subarachnoid cyst in the occipital region posterior to the cerebellum.", "Differential Diagnosis": "Broadly - including the colpocephaly:\n1.Corpus Callosum Agenesis/dysgenesis\n2.Hydrocephalus\n3.Arnold Chiari malformation\n4.Dandy Walker malformation", "Case Diagnosis": "Agenesis of the Corpus Callosum", "Diagnosis By": "Classic imaging appearance", "Treatment & Follow Up": "No treatment is needed for uncomplicated congenital absence of the corpus callosum. If there was obstructive hydrocephalus, seizures, or other neurologic complications, treatment might be necessary", "Discussion": "In this patient, the congenital absence of the corpus callosum was an unexpected finding.\n\nCompanion cases:\nhttp://rad.usuhs.mil/medpix/medpix.html?mode=pt_finder&srchstr=agenesis%20corpus%20callosum#top\n\n\nMore on agenesis of the corpus callosum:\nhttp://rad.usuhs.mil/medpix/medpix.html?mode=tsearch2&srchstr=agenesis%20corpus%20callosum&srch_type=all#top" }, "Topic": { "Title": "Agenesis of the Corpus Callosum", "Disease Discussion": "Agenesis/dysgenesis of the corpus callosum can occur either as a primary congenital defect or secondary to an insult during embryological development early in life such as an infection, hemorrhage, or other malforming defect of the brain. The condition can be manifested shortly after birth, or it can remain asymptomatic for the life of the individual and be found subsequently on postmortem exam. Due to this large variation in presentation, this defect presents itself along a wide spectrum, making it difficult to diagnose unless imaging of the brain is preformed. \n\n\tOccurrence of corpus callosal defects is said to occur in roughly 0.7-5.3% of the US population, with a suggested similar worldwide occurrence . The condition is noted to be hereditary in some cases, being passed down either as an X-linked recessive or autosomal dominant depending on the associated disease. It has also been known to occur often with one of the many different trisomies, most often to include 8, 13, 18, and 21 . Conditions which often coincide with this defect include Chiari II malformations, encephalocele, schizencephaly, lissencephaly, and many syndromes such as Aicardi\u2019s, CRASH and fetal alcohol syndrome.\n\t\n\tThe congenital form of callosal agenesis usually occurs due to a defect in embryological development during the 7-20th gestational week . Normal development of the corpus callosum begins with formation from the commissural plate of the telencephalon . The genu and the body are formed first, followed in time by the development of the rostrum and splenium. From this, white matter axons develop which form projections into the bilateral cerebral cortices. An embryological defect in any of the stages can cause either complete or partial agenesis of the callosum, if occurring later in development a defect in the posterior section is generally observed. Finally, if the genu and body are dysgenic, one can assume that a secondary cause is manifesting such as infection or hemorrhage due to the embryologic sequence of formation previously mentioned. \n\n\tPresentation usually occurs secondary to an associated congenital defect, mental retardation, seizures, or as an incidental finding on an MRI. Diagnosis is best performed by MRI, which demonstrates much finer detail of the lesion and any surrounding neuronal disturbances. Findings often noted in addition to an agenic/dysgenic corpus callosum include a high riding third ventricle, enlarged occipital horns of the lateral ventricles (colpocephaly), longitudinal straightening of the lateral ventricles, and parallel white matter bands along the midline where the corpus would normally develop termed \u201cProbst bundles.\u201d In addition, the absence of the cingulate gyrus results in the sulci of the inner aspect of the cerebrum to be found to radiate outwards from the third ventricle instead of their normal appearance surrounding the corpus. Imaging is usually performed by midline sagittal MRI in order to fully demonstrate the extent of callosal dysgenesis, coronal views to best visualize Probst bundles if present, and axial views which demonstrate colpocephaly. T1, T2, FLAIR, and proton density enhanced scans can all be used in conjunction with each other to best visualize the anatomy of the lesion and its surrounding parts.\n\nTherapy for this condition depends completely upon the clinical presentation of the disease, along with any associated syndromes. Due to the wide range of presenting factors, some individuals may go their entire life unaware of their lesion, while others may present at birth. Due to this fact and the varying degree of callosal absence, treatment must be directed at the specific clinical symptoms and not towards the lesion itself.", "ACR Code": "1.1", "Category": "Congenital, malformation", "Keywords": "corpus callosumagenesis", "Reference": "-Manohar Aribandi, MD. Corpus Callosum, Agenesis. www.emedicine.com, March 11, 2004\n\n-Marszal, Elzbieta MD. Et al. Agenesis of Corpus Callosum: Clinical Description and Etiology. Journal of Child Neurology. 2000; 15(6):401-405\n\n-Grainger, Ronald MD, Allison, David MD. Grainger & Allison\u2019s Diagnostic Radiology: A Textbook of Medical Imaging, 4th Ed. 2001, 2492-2493, Churchill Livingstone Inc. London, England.\n\n-Behrman, Richard MD. Nelson Textbook of Pediatrics, 17th ed. 2004. 1987-1988, Elsevier, Philadelphia, PA.\n\n-Goetz, Christopher MD. Textbook of Clinical Neurology, 2nd ed. 2003. 563-564, Elsevier, Philadelphia, PA." } }, { "U_id": "MPX1233", "TAC": [], "MRI": [ "MPX1233_synpic51028", "MPX1233_synpic51029", "MPX1233_synpic51030", "MPX1233_synpic51032" ], "Case": { "Title": "Osmotic Myelinolysis, Central Pontine Myelinolysis", "History": "50 y.o. man with EtOH abuse presenting with intoxication and hypernatremia. Complains of progressive upper and lower extremity weakness on Day 5 of admission", "Exam": "Neurologic exam: Slurred speech. Oriented only to year and name. Poor concentration. Bilateral nystagmus. Positive for weakness 2/5 in proximal muscles of upper and lower extremity. Decreased vibratory sensation in feet and ankles. Bilateral upgoing toes. Unable to stand on own. \n\nLabs: Sodium on admission was 171 mEq/L with glucose 105mg/dL. 6 hours later Na++ =169mEq/L; 24 hours later Na++ =164 mEq/L; 48 hours later Na++ =138 mEq/L.", "Findings": "Central pontine MRI signal abnormalities with sparing of the peripheral pontine fibers. T1 signal hypointense, T2 and FLAIR signal hyperintense. Mild diffusion restriction with corresponding low ADC.", "Differential Diagnosis": "Pontine ischemia, demyelinating disease or metabolic disease.", "Case Diagnosis": "Osmotic Myelinolysis, Central Pontine Myelinolysis", "Diagnosis By": "Classic radiographic findings.", "Treatment & Follow Up": "Sodium has been maintained at normal levels. Patient is working with physical therapy", "Discussion": "Formerly known as central pontine myelinolysis, osmotic demyelination syndrome is classically seen in association of rapid correction of hyponatremia but can occasionally be seen on cases of rapid correction of hypernatremia, as seen in this case. Chronic hypernatremia should be corrected slowly due to the risk of brain edema which may lead to brain herniation, permanent neurologic deficits and lysis of myelin. In this case, the time course of the hypernatremia was unknown. Typical presentation is usually neurologic deterioration 48-72 hours after the sodium level has been corrected. Pseudobulbar palsy and spastic quadriplegia are two of the physical findings often associated with the syndrome. There is a large spectrum of outcomes ranging from complete recovery to a total \u201clocked in\u201d state which may progress to coma and even death. \n\n\nReferences:\n1.\tDiagnostic imaging: Brain. Osborn, et al. 2004. \n2.\tCentral Pontine Myelinolysis. Luzzio, C. e-Medicine online. http://www.emedicine.com/NEURO/topic50.htm\n3.\tHypernatremia. Pham, T. e-Medicine online. http://www.emedicine.com/med/topic1089.htm" }, "Topic": { "Title": "Osmotic Myelinolysis, Central Pontine Myelinolysis", "Disease Discussion": "CT and MR have allowed the earlier and more frequent recognition of central pontine myelinolysis (CPM) - more properly called \"Osmotic Myelinolysis\". This may be seen in patients with alcohol abuse, liver disease, burns, cancer, sepsis, and anorexia. Patients may present with spastic quadriparesis and cranial nerve paresis. The level of consciousness may range from normal to coma. \n\nUsually blamed on \"osmotic stress\" - the rapid correction of hyponatremia appears to play an important role with some descriptions of the disease portraying it as an osmotic demyelination syndrome. However, there are cases which have had relatively normal sodium values. PMID: 17462902\n\nRecovery may be variable. CPM may be more common than previously recognized with mild, clinically undetected cases found at autopsy.\n\nDifferential considerations for the central pontine lesions include: pontine glioma (astrocytoma), hemangioblastoma, ischemic changes, herniation syndromes, multiple sclerosis, and central pontine myelinolysis. Without mass effect the first two choices are less likely. An acute clinical history and an absent normal basilar artery flow void would suggest pontine infarction. Multiple sclerosis will usually exhibit additional characteristic lesions - typically in the cerebral hemispheric white matter, especially along the margins of the lateral ventricles.", "ACR Code": "1.5", "Category": "Metabolic (see also Toxic)", "Keywords": "sodiumhyponatremiaiatrogenic", "Reference": "http://www.emedicine.com/NEURO/topic50.htm\nPMID: 17462902\nPMID: 11148672\nhttp://content.nejm.org/cgi/content/extract/333/19/1259", "External Links": "www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&DbFrom=pubmed&Cmd=Link&LinkName=pubmed_pubmed&LinkReadableName=Related%20Articles&IdsFromResult=17462902&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum" } }, { "U_id": "MPX1220", "TAC": [], "MRI": [ "MPX1220_synpic29028", "MPX1220_synpic29029", "MPX1220_synpic29030", "MPX1220_synpic29031", "MPX1220_synpic29032", "MPX1220_synpic29033", "MPX1220_synpic29034" ], "Case": { "Title": "Hemangioblastoma (WHO Grade I)", "History": "26 year-old male with a history of a right posterior fossa mass.", "Exam": "N/A", "Findings": "Aggressive cystic mass lesion in the right aspect of the posterior fossa measuring 4.8 cm by 3.1 cm by 2.3 cm with a solid enhancing mural nodule measuring approximately 2.1 cm in diameter. There is mild to moderate surrounding edema and flow voids are present within the mural nodule.", "Differential Diagnosis": "Hemangioblastoma\nAstrocytoma\nMetastasis\nAbscess", "Case Diagnosis": "Hemangioblastoma (WHO Grade I)", "Diagnosis By": "Pathology proven.", "Treatment & Follow Up": "Surgical resection.", "Discussion": "Please see factoid." }, "Topic": { "Title": "Hemangioblastoma", "Disease Discussion": "Hemangioblastomas represent approximately 1-2% of all primary brain tumors. They are strongly associated with von Hippel-Lindau (VHL) syndrome. 10-20% of hemangioblastomas occur with VHL syndrome and approximately 45% of patients with VHL syndrome eventually develop a hemangioblastoma. 95% of hemangioblastomas occur in the posterior fossa (fewer than 100 case reports exist of supratentorial locations), and overall they account for 7-12% of all posterior fossa tumors in adults (including primary and metastatic tumors). \n\nPathologically, hemangioblastomas are highly vascular tumors comprised primarily of capillaries and pericytes (aka \u201cstromal\u201d cells). While their World Health Organization classification remains under tumors of uncertain histogenesis, hemangioblastomas may arise from embryonic plexus epithelium based upon their expression of transthyretin and transferrin. They are typically well circumscribed, with 60% being cystic with a mural nodule and 40% being solid. Their solid/nodular component is composed of tightly packed blood vessels varying in size from capillaries to cavernous, with the nidus of the tumor abutting the pial surface. Hemangioblastomas do not have a capsule, and when cystic, their wall is composed of compressed neural glial cells. The associated cystic fluid is xanthochromic, with a concentration of amino acids, alkaline phosphates, and mucoproteins similar to that of blood, suggesting origination from diffusion from the solid vascular component of the tumor.\n\nHemangioblastomas are rare in children and typically present during the third to fifth decade. They typically grow slowly and clinical presentation depends upon the tumor size and location. Posterior fossa tumors can present with minor neurological symptoms for months followed by an acute exacerbation. The most common symptoms include: headache, vomiting, and ataxia. A distinguishing clinical presentation of hemangioblastomas is their potential to present with polycythemia secondary to tumoral production of erythropoietin. This occurs in approximately 20% of posterior fossa tumors, and is more commonly seen in solid hemangioblastomas. Surgical resection is considered standard of care, however recurrence is seen in approximately 25% of cases, most frequently in association with VHL syndrome.\n\nCT evaluation of hemangioblastomas classically demonstrates a large, low density, cystic-appearing cerebellar mass. The addition of intravenous contrast material greatly increases the ability to identify a strongly enhancing mural nodule adjacent to the pial surface. Solid tumors enhance strongly and uniformly. During angiography, the common pattern is a large avascular posterior fossa mass with a small, highly vascular mural nodule. A prolonged vascular stain is typical. MR imaging reveals the cystic component with a low signal on T1-weighted sequences and a high signal on T2-weighted sequences. The solid/nodular component is variable in its signal characteristics, and typically is heterogeneously isointense on T1-weighted sequences and hyperintense on T2-weighted sequences. Intense enhancement following gadolinium is typical. Prominent serpentine \u201cflow voids\u201d can often be seen as well within the mass.", "ACR Code": "1.3", "Category": "Neoplasm, malignant (NOS)", "Keywords": "Hemangioblastomaring enhancing lesionflow void", "Reference": "Bleistein M, Geiger K, Franz K, et al: Transthyretin and transferrin in hemangioblastoma stromal cells. Pathol Res Pract 2000; 196(10): 675-81\nHo VB, Smirniotopoulos JG, Murphy FM, Rushing EJ: Radiologic-pathologic correlation: hemangioblastoma. AJNR Am J Neuroradiol 1992 Sep-Oct; 13(5): 1343-52\nOsbourne AG: Diagnostic Neuroradiology. Mosby, 1994" } }, { "U_id": "MPX1247", "TAC": [], "MRI": [ "MPX1247_synpic24621" ], "Case": { "Title": "Thrombosis of the right superior anastomotic vein (vein of Trolard)", "History": "31 year old G1 P2002 at 7 days post partum after spontaneous vaginal delivery complicated by late pre-eclampsia presents with new onset left sided weakness and headache.", "Exam": "VITALS\n- BP 110/70, HR 80, Resp 12, Temp 97.6\nPHYSICAL EXAM\n- Alert, Awake and Oriented\n- CN I-XII intact\n- 3/5 upper and lower extremity on both flexion and extention on left. normal right.\n- nl sensation to hot,cold,light touch and pin prick in all extremities.\nLABS\n- normal Electrolytes, Hgb/Hct, and WBCs.", "Findings": "MRI/MRV of the brain demonstrates a filling defect in a large cortical draining vein, likely the vein of Trolard, on the right corresponding to territorial high signal abnormalities on FLAIR and diffusion weighted images and low signal abnormalities on ADC images.", "Differential Diagnosis": "None.", "Case Diagnosis": "Thrombosis of the right superior anastomotic vein (vein of Trolard)", "Diagnosis By": "MRI/MRV", "Treatment & Follow Up": "This patient was treate with unfractionated heparin and fully recovered.", "Discussion": "This patient initially had a completely negative non contrast CT of the head. Had the workup stoped here, a diagnosis would never have been made. This case illustrates the advantate MRI/MRV of the brain has over conventional CT in the workup of neurologic abnormalities in a patient with a high risk for a cerebral venous thrombotic event." }, "Topic": { "Title": "Thrombosis of the Cortical Cerebral Venous System", "Disease Discussion": "Thrombosis of the cortical cerebral venous system resulting in stroke is a well known complication of prothrombotic states caused by pregnancy. Other reasons for this complication include hematological or systemic diseases such as polycythemia, lupus, various malignancies, severe dehydration or certain chemotheraputic agents. Virtually anything that slows down blood flow or causes direct inflammation can cause this potentially life-threatening complication. Fortunately, the mortality rate, which was once as high as 10-30% has now decreased to less than 10% because of improved early detection and more adequate therapy.\n\n The clinical presentation is often vague. A high index of clinical suspicion is often warranted if one is to make a timely diagnosis. Early symptoms can start off with headache that then progresses to focal neurological deficits. Reports of lethargy, confusion, nausea, drowsiness, nystagmus and hearing loss complicate the neurological exam. A high degree of clinical suspicion is helpful if evaluating an at risk population. Too often the thrombosis develops well before the symptoms manifest themselves and the symptoms are the result of the affected territories. \n\n The diffusion findings in human cerebral venous infarction are controversial though most recent studies describe high signal intensity on diffusion images that correspond to low signal intensity on ADC images. These signal findings have been attributed to cytotoxic edema. In direct contrast, some studies showed decreased to no increase in signal on diffusion images and increased to slightly decreased signal on ADC map. It is believed these findings represent early vasogenic edema perhaps in combination with early cytotoxic edema. The truth is likely to represent spectrum signal variation in both diffusion and ADC images that evolves over the course of the pathologic insult. \n \n Treatment of this condition often involves heparin and/or coumadin depending on the current condition of the patient and pregnancy status. In some patients who continue to deteriorate, aggressive micro catheter directed dural venous sinus thrombolysis with urokinase or other thrombolytic agents has shown clinical benefit. The use of mechanical thrombolysis is usually reserved for patients who have poor response to local infusions of urokinase and rapid neurological decline and/or contraindications to thrombolytics.", "ACR Code": "9.6", "Category": "Obstruction or Stenosis", "Keywords": "ThrombosisCortical Venous SystemDural Sinus", "Reference": "Lee, Emil J. The Empty Delta Sign. Radiology 2002; 224: 788-789.\n\nManzione J, Newman GC, et al. Diffusion- and Perfusion-Weighted MR Imaging of Dural Sinus Thrombus. AJNR 2000; 21: 68-73.\n\nMullens, ME, Grant PE, et al. Parenchymal Abnormalities Associated with Cerebral Venous Sinus Thrombosis: Assessment with Diffusion-Weighted MR Imaging. AJNR 2004; 25: 1666-1675.\n\nPeeters, E, Stadnik, T, et al. Diffusion-Weighted MR Imaging of an Acute Venous Stroke: Case Report. AJNR 2001; 22: 1949-1952\n\nStadnik, TW, Demaerel P, et al. Imaging Tutorial: Differrential Diagnosis of Bright Lesions on Diffusion-weighted MR Images. RadioGraphics (online) 2003; 23: e7-e7." } }, { "U_id": "MPX1260", "TAC": [], "MRI": [ "MPX1260_synpic43421", "MPX1260_synpic43422", "MPX1260_synpic43423" ], "Case": { "Title": "Disruption and tears of the patella tendons bilaterally.", "History": "This 42 y/o active duty man jumped from his vehicle and felt a pop. He then tried to hop on the other leg to the aid station and felt a pop in the good leg. The rest is history with him lying in the dirt unable to walk, asking for help, crawling on his belly, etc.", "Exam": "Swelling of patellar tendons and high riding patella bilaterally.", "Findings": "Plain lateral x-rays of bilateral knees showed patella alta, a high riding patella. Joint effusion was noted. On MRI, disrupted patellar tendons were noted bilaterally.", "Differential Diagnosis": "\u2022 Trauma due to extreme combat conditions (body armor, heat, stress). \n\u2022 Systemic lupus erythematosus \n\u2022 Rheumatoid arthritis\n\u2022 Steroid use/ abuse", "Case Diagnosis": "Disruption and tears of the patella tendons bilaterally.", "Diagnosis By": "Plain CR and MRI", "Treatment & Follow Up": "PT, surgery", "Discussion": "This unusual case may represent how the \"fog of war\" may increase incidence of otherwise systemic based injuries." }, "Topic": { "Title": "Partial avulsion of the patella tendon.", "Disease Discussion": "Avulsion injuries of the patella tendon are associated with tendonopathy or \u201cjumper\u2019s knee.\u201d Patella tendonopathy is an overuse syndrome that comes from a variety of exercises to include jumping, kicking, or running. Histologically, patella tendonopathy is not an inflammatory response, but a mechanical failure of the patella tendon fibers with resultant mucoid degeneration and fibrinoid necrosis. The tendon will thicken near its insertion at the inferior pole of the patella. The is the predisposing factor to tendon disruption. \nPartial avulsions of the patella tendon typically involve proximal fibers. Associated findings include, tendon thickening, soft tissue edema, and involvement of Hoffa\u2019s fat pad. Treatment is conservative for a partial rupture of the patella tendon with physical rehabilitation. Surgery is indicated if there is a complete rupture.", "ACR Code": "4.4", "Category": "Trauma", "Keywords": "Patellatendon", "Reference": "Stoller DW, Magnetic resonance imaging in orthopaedics & sports medicine, 1997, 376-9." } }, { "U_id": "MPX1276", "TAC": [], "MRI": [ "MPX1276_synpic54950" ], "Case": { "Title": "Fibrous Dysplasia", "History": "38 y.o. woman, presents now with headache. No known endocrinological abnormalities.", "Findings": "\u2022 Dramatic widening of the occipital bone diploic space and abnormal signal\n\u2022 Expansion of the clivus and abnormal signal\n\u2022 Thickening of the left petrous bone and abnormal signal\n\u2022 Maxillary, Ethmoid, and Sphenoid sinus mucoperiosteal thickening", "Differential Diagnosis": "\u2022 Fibrous dysplasia\n\u2022 Paget disease of Bone\n\u2022 Marrow hyperplasia (chronic anemia)", "Case Diagnosis": "Fibrous Dysplasia", "Diagnosis By": "Classic imaging appearance", "Treatment & Follow Up": "As needed, based on progression of bone thickening.", "Discussion": "This woman has a known diagnosis of fibrous dysplasia, since she was sixteen years old.\n\nMore cases of Fibrous Dysplasia:\nhttp://rad.usuhs.edu/medpix/master.php3?mode=topic_images&recnum=3890" }, "Topic": { "Title": "Fibrous dysplasia", "Disease Discussion": "The name fibrous dysplasia was coined by Lichtenstein in 1938 to describe a disorder of expanding fibro-osseous lesions that had been referred to as fibrous osteodystrophy, osteodystrophia fibrosa and osteitis fibrosa disseminata. Its etiology is unknown; however, the most widely accepted theory is that it is a developmental abnormality of mesenchyme in which osteoblasts fail to undergo normal morphologic differentiation and maturation. The medullary cavity is filled with fibrous tissue in which trabeculae of poorly calcified primitive new bone are developed by osseous metaplasia. Both sexes are equally affected. It begins early in life, often in infancy, but being frequently asymptomatic it usually remains unrecognized until adulthood.\n\nFibrous dysplasia is not hereditary, and it may involve one or many bones. The polyostotic variety and rarely the monostotic type when associated with endocrine dysfunction, typically manifested by precocious female sexual development and cutaneous pigmentation, is known as the McCune-Albright syndrome.\n\nFibrous dysplasia may be associated with either solitary or multiple lesions, in one or more bones. Approximately 70-80% of cases are monostotic, 20-30% are polyostotic, and 2-3% are associated with endocrinopathies. Abnormal cutaneous pigmentation, which is the most common extraskeletal manifestation of fibrous dysplasia, is evident in more than half of patients with polyostotic disease and is almost always present in those with both multiple bone lesions and endocrine dysfunction. However, it is quite infrequently seen with monostotic lesions. Monostotic fibrous dysplasia is most frequently encountered in a rib, femur, tibia, calvarium and humerus in order of decreasing frequency, however, polyostotic fibrous dysplasia more frequently involves the skull and facial bones, pelvis, spine and shoulder girdle.\n\nInvolvement of the skull and the facial bones is noted in approximately 10-25% of patients with monostotic fibrous dysplasia and in 50% of those with polyostotic involvement. Common areas of involvement in the skull include the frontal, sphenoid, maxillary and ethmoid bones; the occipital and temporal bones are affected less commonly.\n\nRoutine radiographs commonly reveal single or multiple, symmetric or asymmetric radiolucent or sclerotic lesions in the skull and facial bones or both. Profound and often extensive sclerosis tends to predominate in the skull and particularly affects its base and the sphenoid wings.\n\nHazy radiolucent lesions which are usually the most common manifestation of fibrous dysplasia are often associated with widened diploic spaces and expansion in the skull and facial bones. The osseous expansion is focal or widespread and is almost always in an outward direction. The outer table of the vault is invariably convex, whereas both tables remain essentially intact rather than destroyed as is the case frequently with Paget's disease. Another manifestation in the cranial vault represents variable sized, localized, relatively radiolucent zones which when surrounded by a sclerotic rim may have a doughnut shape. Due to the occasional marked hypervascularity of fibrous dysplasia in the skull, spontaneous recurrent hemorrhages do occur and complicate the picture.", "ACR Code": "1.3", "Category": "Neoplasm, benign" } }, { "U_id": "MPX1251", "TAC": [], "MRI": [ "MPX1251_synpic27552", "MPX1251_synpic27553", "MPX1251_synpic27554", "MPX1251_synpic27555", "MPX1251_synpic27556", "MPX1251_synpic27557", "MPX1251_synpic27558", "MPX1251_synpic27559", "MPX1251_synpic27560", "MPX1251_synpic27561" ], "Case": { "Title": "Chondrosarcoma of the skull base", "History": "37 year old woman who presented with headaches.", "Findings": "Homogeneous mass centered in the right petro-clival fissure. Low signal on T1, high on T2, with marked homogeneous enhancement. There is also extension of the tumor through the skull base into the right nasopharynx, anterior to the longus colli muscle and compressing it. The lesion is also producing mass effect in the region of the fossa of Rosenmueller.", "Differential Diagnosis": "Chondrosarcoma\nChordoma (same MRI signal pattern but usually midline)\nMetastatic disease\nPlasmacytoma (usually low T2 on MRI)\nLymphoma (usually lower signal on T2 and bright DWI)\nAdenoid Cystic Carcinoma (ACC) from nasopharynx", "Case Diagnosis": "Chondrosarcoma of the skull base", "Diagnosis By": "Biopsy", "Treatment & Follow Up": "Subtotal surgical resection.\nRadiation therapy was withheld at this point secondary to the low grade pathology.", "Discussion": "In this case, 37 year old woman present for routine MRI evaluation for symptoms of headache. Abnormal lesion was found at the base of the skull which was then worked up with a dedicated MRI for skull base.\n\nHeadaches are one of the more common clinical presentations for chondrosarcoma.\n\nOther symptoms include cranial nerve palsies, espcially CN6 because of its proximity to the most common location of the tumor. Other CN that could be involved are 3, 5, 6, and 8." }, "Topic": { "Title": "Chondrosarcoma of the skull base", "Disease Discussion": "There are a few diagnoses that must be considered when presented with a mass lesion at the base of the skull in the clival/petrous region. The classic differential diagnosis of the more common entities in this location includes:\n\u00bb chordoma\n\u00bb chondrosarcoma\n\u00bb metastatic disease (predominantly due to direct spread from nasopharynx)\n\u00bb multiple myeloma (plasmacytoma when solitary lesion)\n\u00bb cholesteatoma\n\n\n\u00bb Chordoma - is more likely to be midline centered in clivus (low T1, high T2, enhancing)\n\u00bb Chondrosarcoma - is more likely to be off midline centered in the petro-occipital fissure that harbors chondroid cells along its cartilagenous surface. (low T1, high T2, may have hypointense foci representing chondroid matrix, enhancing)\n\u00bb Metastatic tumor - destructive lesion, either direct extension from a nasopharynx or known remote primary tumor. (MRI variable depending on a primary, enhancing)\n\u00bb Plasmacytoma - clival or peri-clival, over 50% of patient have additional lesions and carry diagnosis of multiple myeloma (low T1 and T2, enhancing)\n\u00bb Cholesteatoma - usually smooth petrous apex lesion without enhancement.", "ACR Code": "1.3", "Category": "Neoplasm, sarcoma", "Keywords": "skull basepetro-occipital fissurechondrosarcoma, chordoma, plasmacytoma", "Reference": "H. Ric Harnsberger, Diagnostic Imaging: Head and Neck, Amirsys, 1st ed, 2004." } }, { "U_id": "MPX1249", "TAC": [], "MRI": [ "MPX1249_synpic24701" ], "Case": { "Title": "Intramuscular Hemangioma", "History": "43 year old woman with nontender left upper arm mass, present for >3 years.", "Exam": "Non-tender mobile mass in area of left triceps.", "Findings": "An intramuscular lesion is seen in the medial head of the triceps with intermediate signal intensity with slightly higher than muscle signal on T1 sequences with very high signal on T2 sequences with central areas of low signal consistent with flow voids. Post gadolinium sequences demonstrate serpentine vascular pattern. Images of the shoulder demonstate a similar lesion in the subcutaneous fat over the rotator cuff.", "Differential Diagnosis": "Hemangioma\nAngiosarcoma\nRhabdosarcoma", "Case Diagnosis": "Intramuscular Hemangioma", "Diagnosis By": "Radiographically", "Treatment & Follow Up": "No treatment.", "Discussion": "Multiple soft tissue hemangiomas suggest hemagiomatosis whih is rare in a patient of this age. Presenting this late, this is not likely syndromic." }, "Topic": { "Title": "Intramuscular Hemangioma", "Disease Discussion": "A hemangioma is an abnormal proliferation of blood vessels that may occur in any vascularized tissue including skin, subcutaneous tissue, viscera, muscle, synovium, and bone, but they do not spread to avascular tissue such as cartilage. Some believe that hemangiomas are neoplasms while others consider them hamartomas. Abnormal angiogenesis involving cytokines, such as basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) is suspected. They most often occur in the skin or subcutaneous tissues. Visceral hemangiomas are much less common but may result in organ dysfunction. They also occur in deep soft tissues and bones. Other diseases are associated with hemangiomas. Gorham disease is a process of massive osteolysis, which is believed to be within the spectrum of hemangiomatous disease. Hemangiomas occurring with multiple enchondromas exist in Maffucci syndrome.\n\nSkeletal muscle is the most common site for hemangioma of the deep soft tissue. Intramuscular hemangiomas are often asymptomatic or painless and found as an incidental finding. They may become symptomatic causing pain and swelling. Intramuscular hemangiomas are most commonly found in young people, virtually equal in males and females. The most common location is the thigh. The symptoms of pain and swelling due to increased blood flow through the hemangioma are often exacerbated by exercise, which results in vascular dilation. Rarely, large intramuscular hemangiomas may be associated with significant shunting of blood flow even leading to heart murmurs and/or congestive heart failure similar to that of an arteriovenous fistula. \n\nImaging: Plain film radiography of soft tissue hemangiomas may demonstrate soft tissue density without or with phleboliths. They may cause benign-appearing periosteal reaction or chronic cortical thickening and remodeling in adjacent bone. Cortical changes may include erosions, thickening, tunneling, and osteopenia. Phleboliths within the soft tissue mass are diagnostic but uncommon. MRI is the imaging modality of choice in concert with plain films. Hemangiomas show increased signal on both T1 and T2 weighted images, frequently with areas of signal void, which may represent fibrous tissue, phleboliths, thrombi or high flow. These signal characteristics with a serpentine pattern of vessels and interspersed fat are diagnostic. Gadolinium enhancement is also noted. Features separating hemangiomas from malignant soft tissue tumors include frequency of lobulation, septation, and central low-intensity dots on T2-weighted images. Hemangiomas tend to enhance markedly compared with malignant soft-tissue tumors. Angiography demonstrates a highly vascular lesion with parallel oriented vessels. \n\nTreatment: The natural course of intramuscular hemangiomas is usually fatty replacement with gradual involution. Therefore, conservative observation is appropriate if symptoms are absent or mild. If symptoms dictate treatment, embolization may be used to provide symptomatic relief of intramuscular hemangiomas. When surgical excision is required, embolization may be used preoperatively to decrease blood loss and recurrence. Excision can provide permanent relief. However, it is usually restricted to hemangiomas contained within a single muscle. If complete resection is not possible they nearly always recur. Radiation has been used as a non-surgical therapy. Chemotherapy has been used for extensive hemangiomatosis. Steroids have been used for some of the syndromic versions.", "ACR Code": "4.4", "Category": "Vascular", "Keywords": "Intramuscular hemangiomahemangiomatosis", "Reference": "1. Hemangioma from Head to Toe: MR Imaging with Pathologic Correlation. Joan C. Vilanova et al. RadioGraphics 2004; 24: 367-385. \n2. Osseous Change Adjacent to Soft-Tissue Hemangiomas of the Extremities: Correlation with Lesion Size and Proximity to Bone. Justin Q. Ly et al AJR 2003; 180:1695-1700\n3. Emedicine, Hemangioama. Daneille A. Katz, MD, Department of Orthopedic Surgery, State University of New York Upstate Medical University\n4. MR Imaging Differentiation of Soft-Tissue Hemangiomas from Malignant Soft-Tissue Masses Eu-Leong H. J. Teo, AJR 2000; 174:1623-1628" } }, { "U_id": "MPX1295", "TAC": [], "MRI": [ "MPX1295_synpic17964", "MPX1295_synpic17965", "MPX1295_synpic17966", "MPX1295_synpic17967", "MPX1295_synpic17968" ], "Case": { "Title": "B-cell Lymphoma", "History": "The patient was diagnosed with pseudotumor cerebri 3 yrs ago and presented for follow up with opthalmology with no complaints or specific symptoms. He did report a 10 lb weight loss over past 18 mos.", "Exam": "Patient is a well developed, well nourished. Bilateral optic nerve head edema noted. Normal visual acuity, EOMI, PERRLA, and all other cranial nerves showed no abnormality.", "Findings": "MRI: Extraconal mass along the roof of the left orbit, 8mm CC x 3.8cm AP x 3.4cm transverse, indistinct from lacrimal gland. Right lacrimal gland also enlarged or surrounded by mass.", "Differential Diagnosis": "Metastatic tumors (carcinomas of lung, prostate, GI, renal, skin, (breast in female)); lacrimal gland lesions (infiltrative processes and epithelial neoplasms); mesenchymal tumors (fibroma, fibrosarcoma, leiomyosarcoma, fibrous histiocytoma, and rhabdomyosarcoma (most common orbit tumor in children)); neurogenic tumors (neurofibroma, Schwannoma, and gliomas and meningiomas of the optic nerve); inflammations; structural lesions (dermoid cysts and mucoceles); vascular neoplastic lesions; lymphoproliferative lesions.", "Case Diagnosis": "B-cell Lymphoma", "Treatment & Follow Up": "Also noted on MRI was occipital bone marrow replacement and enhancement on undersurface along with lymphadenopathy on CT making diagnosis of lymphoma likely. Biopsy of axial lymph nodes and extraconal mass showed presence of B cell SLL/CLL and WBC was 47 with differential consistent with this diagnosis.\n\nDue to slow growth and lack of symptoms at this time, the patient may elect to not pursue treatment at this time. Radiation therapy could be given to orbits to prevent visual problems from continued growth of masses. It would be given to the complete orbits at dose of 20-25 Gy in 2 Gy fractions. This will invariably lead to cataracts, but retinal damage and xerophthalmia would be unlikely at this dose. Chemotherapy can also be considered for systemic treatment." }, "Topic": { "Title": "Lacrimal fossa orbital mass, B-cell Lymphoma", "Disease Discussion": "The differential diagnosis of this orbital mass can be narrowed by considering both epidemiology and typical morphology to illustrate features that are not common with this patient's lesions. \n\nLacrimal gland lesions tend to be well-circumscribed and round to oval, except adenoid cystic CA which often has bone destruction. Mesenchymal tumors are more often well-circumscribed and more common in pediatrics. \n\nCentral neurogenic tumors such as gliomas and meningiomas of the optic nerve are less likely since this mass is peripheral. \n\nNeurofibromas and Schwannomas tend to be well defined having round to oval or fusiform (AP) shapes respectively. \n\nDermoid cysts and mucoceles tend to be round or well-defined and have enhancing rim and fluid filled centers. \n\nInfections and inflammations tend to present with different clinical picture including pain (cellulitis) and often have diffuse enlargement of extraocular muscles (myositis, Grave's). Lymphoproliferative lesions can present with many variations in morphology, including as seen in this case. \n\nMalignant lymphomas tend to mold to surround adjacent structures and most lie anterior, superior in orbit. They frequently involve lacrimal gland and have insidious and painless presentation.", "ACR Code": "2.3", "Category": "Neoplasm, hematopoietic", "Keywords": "lymphomalacrimal fossa", "Reference": "Yanoff: Ophthalmology, 1st ed., Copyright \u00a9 1999 Mosby International Ltd.\n\nNoble: Textbook of Primary Care Medicine, 3rd ed., Copyright \u00a9 2001 Mosby, Inc.\n\nGrainger & Allison's Diagnostic Radiology: A Textbook of Medical Imaging, 4th Ed., Copyright \u00a9 2001 Churchill Livingstone, Inc." } }, { "U_id": "MPX1320", "TAC": [], "MRI": [ "MPX1320_synpic39575", "MPX1320_synpic40714", "MPX1320_synpic40715" ], "Case": { "Title": "Bilateral Optic Gliomas", "History": "The patient presented with a history of slowly progressive decreased visual acuity.", "Findings": "Increased signal intensity and widening of the optic nerves as they track posteriorly.\nThere is a well circumscribed 1.5X1cm mass of high signal intensity located at the location of the optic chiasm. The lesion is suprasellar.", "Differential Diagnosis": "Meningioma \nOptic glioma \nSarcoid\nOptic neuritis\nMetastasis\nLymphoma/leukemia", "Case Diagnosis": "Bilateral Optic Gliomas", "Diagnosis By": "Biopsy", "Discussion": "This case is unique in that it is a novel presentation of a lesion overwhelmingly found in children." }, "Topic": { "Title": "Bilateral Optic Gliomas", "Disease Discussion": "Lesions/Condition: Optic Glioma\n\nCell of Origin: Glial cells of varying differentiation\n\nAssociations/Predisposing Factors: Neurofibromatosis I in children. The adult form has no association with neurofibromatosis.\n\nCommon Locations: Anterior \u2013 orbital, infracannalicular, intracranial\nPosterior \u2013 chiasmal, hypothalamic, anterior third ventricle\n\nDemographics: most commonly in children (90% before 20, 75% before 10)\n\nRadiology: MRI - A tubular thickening of the optic nerve and chiasm \nA suprasellar tumor with contiguous optic nerve expansion \nA suprasellar tumor with optic tract involvement\n\nPrognosis and Treatment: Children have a good prognosis, worse in patients with chiasmal lesions.\nSpontaneous regression reported in some children with NF1.\nAdults have poorer prognosis, these lesions are either anaplastic astrocytoma or glioblastoma multiforme and are locally aggressive.\nTreatment is often chemotherapy initially with subsequent surgical resection.\nRadiation is effective, but neurologic sequelae prevents widespread use.", "ACR Code": "1.3", "Category": "Neoplasm, glial", "Keywords": "Optic gliomaastrocytomaneurofibromatosis", "Reference": "Alvord, EC Jr, Lofton, S. Gliomas of the optic nerve or chiasm. Outcome by patients' age, tumor site, and treatment. J Neurosurg 1988; 68:85. \nBenes, V, Julisova, I, Julis, I. Our treatment philosophy of gliomas of the anterior visual pathways. Childs Nerv Syst 1990; 6:75. \nHabiby, R, Silverman, B, Listernick, R, Charrow, J. Precocious puberty in children with neurofibromatosis type 1. J Pediatr 1995; 126:364. \nImes, RK, Hoyt, WF. Magnetic resonance imaging signs of optic nerve gliomas in neurofibromatosis 1. Am J Ophthalmol 1991; 111:729." } }, { "U_id": "MPX1303", "TAC": [], "MRI": [ "MPX1303_synpic24511", "MPX1303_synpic24512", "MPX1303_synpic24513" ], "Case": { "Title": "Metastatic Carcinoma, unknown primary", "History": "Patient presented with progressive worsening of headaches with no other signs or symptoms.", "Findings": "Large pineal region mass.", "Differential Diagnosis": "Germinoma\nPineocytoma\nPineoblastoma\nMeningioma\nMetastasis", "Case Diagnosis": "Metastatic Carcinoma, unknown primary", "Diagnosis By": "Pathology, final pathology unknown" }, "Topic": { "Title": "Metastatic Carcinoma unknown primary", "Disease Discussion": "This patient has a rare presentation of metastatic carcinoma to the pineal region.", "ACR Code": "1.3", "Category": "Neoplasm, metastatic", "Keywords": "carcinomametastatic" } }, { "U_id": "MPX1284", "TAC": [], "MRI": [ "MPX1284_synpic35420", "MPX1284_synpic35434" ], "Case": { "Title": "Pilocytic Astrocytoma", "Findings": "Neoplasm Name: Pilocytic Astrocytoma \n\nSynonyms: Juvenile pilocytic, spongioblastoma \n\nICD-O code: \n\nCell of Origin: Astrocyte \n\nWHO Grade(s): Grade 1 \n\nGenetics and Associations: Occures in the optic nerve in NF-1 \n\nDemographics (Age, Sex, Incidence): Most common in childhood, with a peak incidence 9 - 15 years. Slight female predilection (13:9 F>M). Accounts for approximately 1/3 of pediatric posterior fossa neoplastic masses. \n\nCommon Locations: Cerebellum >> hypothalamus > brainstem, cerebral hemisphere, spinal cord \n\nGross Appearance: Circumscribed with very narrow zone of infiltration, mural nodule and fluid collection (\"cyst\") \n\nHistology: biphasic with dense and loose areas, microcysts, Rosenthal fibers \n\nSpecial Stains: \n\nRadiology: \"cyst with nodule\" showing intense enhancement of nodule on MR and CT. Largely hypovascular or avascular on angiography \n\nProgression: Does not progress \n\nPrognosis and Treatment: Surgical resection is often curative \n\nCOMMENTS: Most benign of astrocytoma types, most common subtype of astrocytoma in posterior fossa in children, most common type of hypothalamic glioma", "Differential Diagnosis": "Neoplasm Name: Pilocytic Astrocytoma \n\nSynonyms: Juvenile pilocytic, spongioblastoma \n\nICD-O code: \n\nCell of Origin: Astrocyte \n\nWHO Grade(s): Grade 1 \n\nGenetics and Associations: Occures in the optic nerve in NF-1 \n\nDemographics (Age, Sex, Incidence): Most common in childhood, with a peak incidence 9 - 15 years. Slight female predilection (13:9 F>M). Accounts for approximately 1/3 of pediatric posterior fossa neoplastic masses. \n\nCommon Locations: Cerebellum >> hypothalamus > brainstem, cerebral hemisphere, spinal cord \n\nGross Appearance: Circumscribed with very narrow zone of infiltration, mural nodule and fluid collection (\"cyst\") \n\nHistology: biphasic with dense and loose areas, microcysts, Rosenthal fibers \n\nSpecial Stains: \n\nRadiology: \"cyst with nodule\" showing intense enhancement of nodule on MR and CT. Largely hypovascular or avascular on angiography \n\nProgression: Does not progress \n\nPrognosis and Treatment: Surgical resection is often curative \n\nCOMMENTS: Most benign of astrocytoma types, most common subtype of astrocytoma in posterior fossa in children, most common type of hypothalamic glioma", "Case Diagnosis": "Pilocytic Astrocytoma", "Discussion": "Neoplasm Name: Pilocytic Astrocytoma \n\nSynonyms: Juvenile pilocytic, spongioblastoma \n\nICD-O code: \n\nCell of Origin: Astrocyte \n\nWHO Grade(s): Grade 1 \n\nGenetics and Associations: Occures in the optic nerve in NF-1 \n\nDemographics (Age, Sex, Incidence): Most common in childhood, with a peak incidence 9 - 15 years. Slight female predilection (13:9 F>M). Accounts for approximately 1/3 of pediatric posterior fossa neoplastic masses. \n\nCommon Locations: Cerebellum >> hypothalamus > brainstem, cerebral hemisphere, spinal cord \n\nGross Appearance: Circumscribed with very narrow zone of infiltration, mural nodule and fluid collection (\"cyst\") \n\nHistology: biphasic with dense and loose areas, microcysts, Rosenthal fibers \n\nSpecial Stains: \n\nRadiology: \"cyst with nodule\" showing intense enhancement of nodule on MR and CT. Largely hypovascular or avascular on angiography \n\nProgression: Does not progress \n\nPrognosis and Treatment: Surgical resection is often curative \n\nCOMMENTS: Most benign of astrocytoma types, most common subtype of astrocytoma in posterior fossa in children, most common type of hypothalamic glioma" }, "Topic": { "Title": "Pilocytic Astrocytoma", "Disease Discussion": "Neoplasm Name: Pilocytic Astrocytoma \n\nSynonyms: Juvenile pilocytic, spongioblastoma \n\nICD-O code: \n\nCell of Origin: Astrocyte \n\nWHO Grade(s): Grade 1 \n\nGenetics and Associations: Occures in the optic nerve in NF-1 \n\nDemographics (Age, Sex, Incidence): Most common in childhood, with a peak incidence 9 - 15 years. Slight female predilection (13:9 F>M). Accounts for approximately 1/3 of pediatric posterior fossa neoplastic masses. \n\nCommon Locations: Cerebellum >> hypothalamus > brainstem, cerebral hemisphere, spinal cord \n\nGross Appearance: Circumscribed with very narrow zone of infiltration, mural nodule and fluid collection (\"cyst\") \n\nHistology: biphasic with dense and loose areas, microcysts, Rosenthal fibers \n\nSpecial Stains: \n\nRadiology: \"cyst with nodule\" showing intense enhancement of nodule on MR and CT. Largely hypovascular or avascular on angiography \n\nProgression: Does not progress \n\nPrognosis and Treatment: Surgical resection is often curative \n\nCOMMENTS: Most benign of astrocytoma types, most common subtype of astrocytoma in posterior fossa in children, most common type of hypothalamic glioma", "ACR Code": "1.3", "Category": "Neoplasm, glial", "Keywords": "Pilocytic AstrocytomaJuvenile pilocyticspongioblastoma", "External Links": "http://rad.usuhs.edu/medpix/topic_display.html?recnum=6596#top" } }, { "U_id": "MPX1335", "TAC": [], "MRI": [ "MPX1335_synpic16275", "MPX1335_synpic16276" ], "Case": { "Title": "Acromegaly from pituitary macroadenoma", "History": "30 year old man with changing glove and shoe size.", "Findings": "\u2022 Sellar enlargement can be seen on plain radiographs.\n\u2022 CT demonstrates sellar expansion with osseous erosion and remodeling.\n\u2022 MRI demonstrates an isointese lesion on T1 and T2 images, which expands the sella.", "Differential Diagnosis": "Pituitary adenoma\nCraniopharyngioma\nRathke cleft cyst\nPituitary metastasis", "Case Diagnosis": "Acromegaly from pituitary macroadenoma", "Treatment & Follow Up": "Surgical resection." }, "Topic": { "Title": "Pituitary macroadenoma", "Disease Discussion": "Pituitary adenomas are the most common intrasellar masses.\n\nMicroadenomas are those that are less than or equal to 10 mm in size, and macroadenomas are those that are greater than 10mm. Seventy-five percent of adenomas are microadenomas.\n\nProlactin and ACTH secreting tumors are more common, even in males. \nMicroadenomas are discovered while they are small due to endocrine symptoms.\n\nMacroadenomas most commonly present secondary to mass effect, with symptoms related to optic nerve/chiasm compression, hydrocephalus, cranial nerve palsies, or occasionally anterior pituitary dysfunction.\n\nClivus or cavernous sinus invasion generally precludes complete surgical resection.", "ACR Code": "1.3", "Category": "Neoplasm, non-glial", "Keywords": "macroadenomasellar massacromegaly", "Reference": "Grossman, RI and Yousem DM: Neuroradiology- The Requisites, St. Loyus 1994, Mosby pp 313-314" } }, { "U_id": "MPX1324", "TAC": [], "MRI": [ "MPX1324_synpic26181", "MPX1324_synpic26182" ], "Case": { "Title": "Infiltrating Ductal Carcinoma", "History": "32 year-old female, asymptomatic with respect to the breasts. Patient has a mother and sister with breast cancer before age 45. She is 10 months postpartum, is no longer lactating, but is trying to get pregnant.", "Exam": "Negative clinical breast exam by experienced surgeon, negative screening mammography. Genetics testing revealed BRCA-1 positivity.", "Findings": "Initial screening two view mammogram was negative for suspicious calcifications or mass. The brest tissue was heterogenously dense.\n\nPatient underwent routine screeing breast MR which demonstrates a small enhancing mass within the mid right breast, 12:00 position. There is minimal associated T2 hyperintensity, but this involves more the periphery of the lesion, rather than the substance of the lesion itslef. No other discordant foci of abnormal enhancement were present within either breast.\n\nThe patient was recalled for subsequent right breast ultrasound. This demonstrates an angulated, hypoechoic 5mm mass in at the 12:00 position, zone 1a.\n\nSubsequent ultrasound-guided 14ga core biopsy was performed.", "Differential Diagnosis": "Atypical fibroadenoma\nDuctal carcinoma in situ\nInfiltrating carcinoma\nAtypical lymph node\nAtypical papilloma\nGranular cell tumor", "Case Diagnosis": "Infiltrating Ductal Carcinoma", "Diagnosis By": "Core Biopsy", "Treatment & Follow Up": "Patient will undergo lymphoscintigraphy for sentinal node biopsy. If no metastases, she will likely opt for breast conservation therapy to include lumpectomy and radiation. She is considering the option of bilateral mastectomy. She will require continued close monitoring for development of additional disease.", "Discussion": "The issue of screening high risk patients with breast MR has been discussed for several years. It has taken some time for vendors to develop the software necessary to accurately and efficiently use existing MR technology for a screening population. MR utility has been extensively used for problem-solving and for evaluation of the patient with impants. \n\nThe exquisite contrast sensitivity of MR is balanced in the high-risk patient by somewhat decreased specificity; many things other than cancer enhance, but benign entities often have an intrinsic high T2 signal whereas breast cancer does not.\n\nSensitivity has been greatly improved with the use of dynamic contrast-enhancement, and the addition of software tools allowing the creation of a graphical depiction of contrast kinetics within a specified region of interest. Given that the region is selected appropriately, breast cancer tissue will typically exhibit an early wash-in, and a rapid wash-out of contrast enhancement. In contradistinction, beningn tissue will demonstrate a progressive increase in enhancement or alternatively a plateau. \n\nSoftware refinements continue to be made in order to hopefully better define the specific region of interest and therefore yield the best curve.\n\nAt the time this case was performed, the combination fo software and hardware technology necessary to perform adequate screening MR had only been available for approximately 2 months. This patient's cancer was only detectable initially through this modality. The mammogram was, even retrospectively, negative, and there was no palpable abnormality for which to justify an ultrasound (although the lesion was in fact visible under ultrasound). This cancer almost certainly would have not been found until it was at a much more advanced state, and this patient's life may have just been saved-- a feat that would have likely not been possible just a few months ago." }, "Topic": { "Title": "Infiltrating ductal carcinoma", "Disease Discussion": "The majority of invasive breast cancers are nonspecific forms of carcinoma that orginate in the ductal epithelium, likely in the terminal duct at its juncton with the lobule. The better differentiated forms of invasive ductal carcinoma create specfic patterns that have been subclassified but the majority of ductal malignancies fall into the general category of undifferentiated cancers. When a cancer does not fit into any of the defined subtypes it is termed not otherwise specified (NOS). The relative frequency of these lesion appears to remain fairly constant regardless of age. In general, infiltrating ductal carcinoma NOS elicits a vigorous desmosplastic response with fibrosis. \n\nSometimes, these cancers are found first by the woman herself. In general, these are firm lesions that may tether to the skin or the chest wall. Vascular and lymphatic spread result, and if left untreated, carcinoma may eventually erode through the skin, producing an ulcerated mass. Dermal lymphatic involvement with tumor can occur early in the course early in the course of the disease, signaling the poor prognosis associated with inflammatory carcinoma. \n\nPathologist have subclassified infiltrating ductal carcinoma into low-grade (I) fairly uniform cell types that show some differentiation (mucin or tubule) to high grade (III) in which anaplastic, pleomorphic cell predominate. Collagen production is prominent feature of many breast cancers, and calcium deposition is common within the tumor. These are responsible for the characteristic firm gritty nature of these malignancies.\n\nThe mammographic appearance of breast cancer is varied. The diagnosis is high suggestive when an irregular mass with spiculated margins is present. Lobulated shapes are fairly common, and the more undulating the border, the more suspicious the lesion. Some ductal cancers reveal their presence early by the deposition of calcium which is due to either direct cellular secretion or cell necrosis. The fibrosis, desmoplasia and cicatrization that accompany many ductal cancers may produce distortion of surrounding architecture with or without an apparent tumor mass, and this may lead to skin/nipple retraction. Breast cancer usually produces an ill-defined shadow, but even \u201cgarden variety\u201d infiltrating ductal carcinoma may produce a sharply circumscribed mass that is indistinguishable from a benign lesion. The generally greater x-ray attenutation relative to its volume often distinguishes the malignant lesion.\n\nSome cancers infiltrate without distorting the normal breast architecture and without calcium deposition. If the normal parenchymal abutting the tumor is the same radiographic density, the tumor may be undectable by mammography. Occasionally, the only indication of the presence of cancer nonspecific asymmetric density.\n\nJust as there is spectrum of mammographic presentations, the ultrasound appearance of breast cancer is extremely variable. The classic description of breast cancer is an irregularly shaped hypoechoic structure that frequently has a triangular anterior margin and attenuates and scatters sound, producing shadowing. This appearance is characteristic of a spiculated scirrhous lesion. Cancers are almost always irregular, frequently lobulated and hypoechoic. Breast cancers tend to be more vertically oriented relative to the skin surface but there are always exceptions. Ultrasound should be only used to differentiate cystic breast lesions from solid ones and to guide needle positioning for interventional procedure.", "ACR Code": "0.3", "Category": "Neoplasm, carcinoma", "Keywords": "infiltrating ductal carcinomainvasive ductal carcinoma", "Reference": "Kopans DB. Breast Imaging. 2nd ed. 1998. Lippincott Williams & Wilkins. Philadelphia." } }, { "U_id": "MPX1338", "TAC": [], "MRI": [ "MPX1338_synpic27420", "MPX1338_synpic27421" ], "Case": { "Title": "Bow Hunter's syndrome", "History": "58 year old male with one year history of feeling dizzy when turning his head to the right. His symptoms resolve each time once he returns his head to neutral position. No symptoms when the head is turned to the left or hyperextended.", "Findings": "Diagnostic angiogram:\n1. Head in neutral position. Angiogram demonstrates normal caliber of the left vertebral artery.\n2. Head in rotated position to the right (patient supine on the table with a small pad under his head). Angiogram demonstrates slight irregularity of the vessel distal to exit from f. transversarium at C1-2 level.\n3. Head is hyperextended and rotated to the right to a greater degree than in #2. Angiogram demonstrates significant narrowing of the vertebral artery at C1-2 level with slowing of contrast passage.\n\nMRI/MRA demonstrates occlusion of the right vertebral artery.", "Case Diagnosis": "Bow Hunter's syndrome", "Diagnosis By": "Dynamic angiogram", "Treatment & Follow Up": "Patient is scheduled for surgery to release soft tissues around left vertebral artery at C1-2 level", "Discussion": "In our case, patient presented with history of dizziness once he turns his head to the right. MRA demonstrated severely stenotic right verterbral artery. Diagnostic arterigram of the left artery was performed in several positions until patients symptoms were reproduced. Since the patient was placed supine on the table, his head had to be hyperextended and significantly rotated to the right. He experienced dizziness and the angiogram demonstrated narrowing of both horizontal segments of the loop of the left vertebral just distal to foramen transversarium at the C1-2 level. His symptoms promptly resolved once his head was returned to a neutral position." }, "Topic": { "Title": "Bow Hunter's syndrome (vertebral artery compression)", "Disease Discussion": "The name of this syndrome comes from the position of bow hunters who turn their heads significantly to one side for shooting and arrow. Typically, it is the contralateral vertebral artery (VA) that is compressed by the head rotation. If the compressed VA is dominant, or if the ipsilateral VA is stenosed , the patient may have symptoms of posterior fossa ischemia.\n\nPatients with this syndrome have classic symptoms that correlate with slow or lack of blood flow to the posterior fossa structures that are supplied by the vertebrobasilar arterial system. Patient's often experience pre-syncopal symptoms of dizziness or even syncopal episodes when they turn their head to one of the sides. This usually occurs when one of the vertebral arteries is occluded or severely stenosed secondary to any of the vascular occlusive diseases or congenitally diminutive caliver. \n\nBy turning the head towards the side of occluded vertebral artery, a contralateral vertebral artery may get stretched or occluded. This is a mechanical problem at C1-2 level just distal to the vertebral artery exiting the foramen transversarium. There may be redundant soft tissue or ligaments that press against the artery when there is rotation of the head or stretching of the vessel.\n\nOnce the head is turned, patients start feeling dizzy and may experience syncopy if the head is not promptly returned to a neutral position - where the flow throught the patent vertebral artery is restored.\n\nOnce the proper history has been established to suspect Bow Hunter's syndrome, a diagnostic angiogram could be performed. This is done in muliple projections and in neutral and with provocative manueuvers, that reproducethe patient's symptoms. Treatment usually involves releasing the soft tissues around the vertebral artery at C1-2 level.\n\nThe name comes from a head position of bow hunters who turn their heads significantly to one of the sides for shooting.", "ACR Code": "2.9", "Category": "Vascular", "Keywords": "bow huntervertebral artery occlusion stenosis compressiondizziness", "Reference": "Horowitz M, Jovin T, Balzar J, Welch W, Kassam A: Bow hunter's syndrome in the setting of contralateral vertebral artery stenosis: evaluation and treatment options.\nSpine. 2002 Dec 1;27(23):E495-8.", "External Links": "www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12461405&query_hl=1" } }, { "U_id": "MPX1190", "TAC": [], "MRI": [ "MPX1190_synpic38358" ], "Case": { "Title": "Multiple cranial neuropathies", "History": "This 36 y.o. woman has multiple cranial nerve palsies, affecting all twelve nerves - but not at the same time.", "Exam": "CN 1-12 are NOT intact", "Case Diagnosis": "Multiple cranial neuropathies", "Discussion": "This is actually a teaching scenario to link together all of the images for the Cranial Nerve Atlas." }, "Topic": { "Title": "Cranial Nerve Anatomy and Atlas", "Disease Discussion": "Cranial Nerve Diagrams! http://rad.usuhs.edu/medpix/parent.php3?mode=quiz&imid=37901&quiz=#pic\n\n\nCranial Nerve Name\n 1 Olfactory http://rad.usuhs.mil/medpix/parent.php3?mode=single&recnum=8344#top\n\n 2 Optic http://rad.usuhs.mil/medpix/parent.php3?mode=single&recnum=8345#top\n\n 3 Oculomotor http://rad.usuhs.mil/medpix/parent.php3?mode=single&recnum=8346#top\n\n 4 Trochlear http://rad.usuhs.mil/medpix/parent.php3?mode=single&recnum=8347#top\n\n 5 Trigeminal http://rad.usuhs.mil/medpix/parent.php3?mode=single&recnum=8348#top\n\n 6 Abducens http://rad.usuhs.mil/medpix/parent.php3?mode=single&recnum=8349#top\n\n 7 Facial http://rad.usuhs.mil/medpix/parent.php3?mode=single&recnum=8350#top\n\n 8 Vestibulocochlear http://rad.usuhs.mil/medpix/parent.php3?mode=single&recnum=8351#top\n\n 9 Glossopharyngeal http://rad.usuhs.mil/medpix/parent.php3?mode=single&recnum=8352#top\n\n 10 Vagus http://rad.usuhs.mil/medpix/parent.php3?mode=single&recnum=8353#top\n\n 11 Spinal Accessory http://rad.usuhs.mil/medpix/parent.php3?mode=single&recnum=8354#top\n\n 12 Hypoglossal http://rad.usuhs.mil/medpix/parent.php3?mode=single&recnum=8355#top", "ACR Code": "1.1", "Category": "Anatomy, Normal and Measurements", "Keywords": "cranial nerve atlascranial nerve anatomycranial neuropathy" } }, { "U_id": "MPX1363", "TAC": [], "MRI": [ "MPX1363_synpic43239" ], "Case": { "Title": "Alzheimer disease", "History": "An 84-year-old man presents with a 3-year history of progressive memory loss, dementia, and difficulty communicating as noted by his family. An MRI was performed.", "Case Diagnosis": "Alzheimer disease", "Diagnosis By": "Brain biopsy" }, "Topic": { "Title": "Alzheimer disease", "Disease Discussion": "1) An MRI of this patient revealed generalized cerebral atrophy with narrowed gyri and widened sulci, suggesting a diagnosis of Alzheimer disease (AD) (Figure 1). AD, the most common cause of dementia, is a frequent occurrence among the elderly population. Approximately 4.9 million people over the age of 65 are living with the diagnosis of AD.[1] The disease provides a great burden to family members and has a wide impact on Medicare spending. Although many advances have been made in providing clinical, radiographic, and biomarker evidence for AD diagnosis, the disease is only definitively diagnosed by brain biopsy or at autopsy. \n\nGross pathologic exam of the AD patient at autopsy reveals diffuse cerebral atrophy (Figure 2), most prominently in the medial temporal lobes. Histological exam reveals senile plaques composed of an amyloid \u03b2 (A\u03b2) core (Figure 3). A\u03b2 is also seen deposited in cerebral vessel walls of AD patients. Histological evaluation at autopsy additionally reveals neurofibrillary tangles (Figure 4) within the cerebral parenchyma, composed of hyperphosphorylated tau proteins.[2]\n\nAD is also associated with degeneration in the basal forebrain and a resulting loss of the neurotransmitter acetylcholine. This loss of acetylcholine is closely related to memory deficits.[3] As such, the major class of pharmacologic therapy for AD focuses on inhibitors of acetylcholinesterase such as donepezil, rivastigmine, and galantamine. While some relief from AD symptoms is seen with the use of this class of medication, the long-term progression of the disease does not appear to be altered.\n\nPatients with AD have been distinguished from age-matched controls by a significant bilateral reduction in blood flow or metabolism in the temporoparietal cortex using functional neuroimaging.[4] Additionally, perfusion and diffusion-weighted MR imaging illustrate a bilateral reduction in perfusion in the sensorimotor regions in patients with AD.[4] The radiographic evidence of hypoperfusion in these regions is consistent with the clinical presentation of AD, namely impairment of recent memory formation, language deficits, and difficulty executing previously learned motor processes.\n\nVarious radiographic measurement techniques have been attempted for relative certainty in early diagnosis of AD. Bastos-Leite et al identified that hippocampal atrophy could be measured by T1-weighted MR imaging of hippocampal sulcus width.[5] Furthermore, gross pathologic examination of patients with AD reveals significant bilateral atrophy of the cerebral parenchyma with widened sulci, most notably in the frontal, temporal, and parietal lobes.\n\nAtrophy in the frontal and temporal lobe pars orbitalis is suggestive of Pick disease (PD).[6] PD and AD may present clinically with similar features. PD typically presents with personality changes and frontotemporal lobe atrophy, and is characterized by greater atrophy of the anterior brain than is seen in AD.[6] A well-circumscribed lesion with a mass effect on noncontrast CT would indicate a hemorrhage or hematoma. Multiple oval lesions seen on MRI are found in multiple sclerosis and are frequently found in the periventricular white matter.[7] Structural changes in the substantia nigra pars compacta are characteristic of Parkinson disease. Parkinson disease structural changes can be detected through MR imaging while positron emission tomography can be used to measure dopa uptake into the striatum.[8]\n\n2. Central to the degeneration seen in AD is an accumulation of A\u03b2 peptides, derived from amyloid \u03b2 precursor protein (A?PP).[9] These peptides have been found deposited throughout the extracellular space of AD plaques and have thus been used as an important pathological marker for AD.[9] While a correlation between A? and AD has been identified, A? is not strictly localized to the central nervous system and is seen in many other organs including lung, liver, heart, and spleen.[9] The accumulation of A? in cerebral parenchyma has been shown to be neurotoxic [10,11] and likely contributes to spectrum of clinical features observed in AD.\n\nLewy bodies are aggregates of \u03b1-synuclein most commonly found in Parkinson disease. Astroglia are supportive cells of the central nervous system and an abundance of these cells would be associated with an astrocytoma. Sphingolipid accumulation is seen in Niemann-Pick disease. N-acetyl aspartate is used as a marker of neurons and a decrease is associated with neurodegenerative disorders such as AD.\n\n3. Apolipoprotein E (APOE) is a protein that is involved in the metabolism of cholesterol and is synthesized by astrocytes. The gene is located on chromosome 19 and is thought to play a role in the repair of injured nerves.[12] Of the four APOE alleles, the one with the closest association to AD is \u03b54. Many studies have suggested a correlation between APOE \u03b54 and AD memory impairment, most significantly in older adults.[12] APOE encodes a protein that, within the extracellular space, binds cholesterol and becomes incorporated into myelin and cell membranes. As such, this protein is believed to be involved in the generation of neural synapses.[12]\n\nSynaptic degradation resulting from the mutated apoE \u03b54 allele and defective synaptogenesis may play a role in the atrophy of the corpus collosum in AD.[13] The degeneration of the corpus collosum and cingulate gyrus in AD is reflected in the apparent deficits in intrahemispheric connection.[13] The role of an APOE \u03b54 mutation has been associated with AD as a significant risk factor for developing sporadic AD as well as earlier age of onset of the disease. Although these associations have been established, the role of APOE \u03b54 as a biomarker is still in question as not all patients with the \u03b54 allele develop AD. Similarly, patients lacking the \u03b54 allele are not excluded from developing sporadic AD.[14]\n\nA mutation in the sphingomyelin phosphodiesterase 1 (SMPD1) gene is seen in Niemann-Pick disease. The superoxide dismutase (SOD1) gene is associated with amyotrophic lateral sclerosis. Kinesin family member 1B (KIF1B) mutations have been linked to the peripheral nerve disorder Charcot-Marie-Tooth disease. \u03b2-Hexosaminidase A, \u03b1 subunit (HEXA) mutations are seen in association with Tay-Sachs disease.\n\n4. Patients suffering from AD exhibit pathological changes in the brain including a diffuse loss of neurons in the neocortex and hippocampus.[15] This neurological degradation leads to clinical memory loss and dementia. The hippocampus functions in memory formation and a loss of neurons leads to difficulty forming new memories. The loss of neurons in these regions correlates to the pathologic and neuroradiological findings of cerebral atrophy. As noted above, cerebral atrophy is prominent in the brain of a patient with AD at autopsy, particularly in the medial temporal lobes.[5] Loss of neurons in alternate brain regions, including hypothalamus, cerebellum, and mammillary bodies are not associated with AD pathology. \n\n5. The major histological diagnostic findings at autopsy of a patient with AD are senile plaques and neurofibrillary tangles. Two cerebrospinal fluid (CSF) biomarkers, A\u03b2 and tau, have been validated in association with AD and can be used to distinguish AD from other neurodegenerative disorders, such as Parkinson disease.[16] An elevation in neurotoxic A\u03b2 leads to the deposition of A\u03b2 plaques in the cerebral parenchyma (leading to the accumulation of senile plaques) as well as in the walls of cerebral blood vessels.[2] The neurofibrillary tangle (Figure 3), another pathologic finding in AD, consists of an aggregation of hyperphosphorylated tau proteins.[2]\n\nAmyloid precursor protein is normally cleaved by \u03b1-secretase to yield multiple fragments that are chiefly eliminated from the brain. Abnormal cleavage results from a mutation in the amyloid precursor protein, resulting in cleavage by both \u03b2-secretase and \u03b3-secretase, leading to aggregations of abnormally cleaved A\u03b2 with other proteins such as tau, apoE, and presenilin 1 and 2. These aggregates form the basis for senile plaques (Figure 3) in AD pathology.[17]\n\nAmyloid association with AD has been further established through the exploration of early AD development in adults with Down syndrome. Down syndrome (trisomy 21) patients living into adulthood have been found to develop senile plaques with A\u03b2 and neurofibrillary tangles in the cerebral cortex at a significantly younger age than individuals without Down syndrome. The findings of early development of plaques and tangles in association with a duplicate chromosome 21 lead to further linkage studies that proposed an association between the chromosome and AD pathology. These studies found that mutations in a region of the 21st chromosome, near the gene encoding \u03b2-amyloid and duplicated in trisomy 21, have been associated with familial early-onset AD.[17]\n\nThe presence of biomarkers in the CSF other than amyloid \u03b2 and tau have not been found in association with AD. Cystatin C is more closely associated with renal function than with neurodegeneration. \u03b1-synuclein is related to Lewy bodies found in patients with Parkinson disease and not a known AD biomarker. Fibrillin-1 is a gene associated with the connective tissue disorder Marfan syndrome. Secreted amyloid precursor protein alpha (sAPP-\u03b1) is related to the response of microglia to chronic inflammation and found in AD, yet has not been established as a significant biomarker.[18]", "ACR Code": "1.9", "Category": "Degenerative Disease", "Keywords": "AlzheimerNeurodegenerativeatrophy", "Reference": "1.\tFeng Z, Zhao G, Yu L. Neural Stem Cells and Alzheimer\u2019s Disease: Challenges and Hope. Am J Alzheimers Dis Other Demen 2009: 24; 52-57.\n\n2.\tVan der Zee J, Sleegers K, Van Broeckhoven C. The Alzheimer disease \u2013 frontotemporal lobar degeneration spectrum. Neurology 2008: 71; 1191-1197.\n\n3.\tMayeux R, Sano M. Treatment of Alzheimer\u2019s Disease. N Engl J Med 2000: 341; 1670-1679.\n\n4.\tBozzao A, Floris R, Baviera ME, et al. Diffusion and Perfusion MR Imaging in Cases of Alzheimer\u2019s Disease: Correlations with Cortical Atrophy and Lesion Load. Am J Neuroradiol 2001: 22; 1030-1036.\n\n5.\tBastos-Leite AJ, van Waesberghe JH, Oen AL, et al. Hippocampal Sulcus Width and Cavities: Comparison Between Patients with Alzheimer Disease and Nondemented Elderly Subjects. Am J Neuroradiol 2006: 27; 2141-2145.\n\n6.\tKizu O, Yamada K, Nishimura T. Proton Chemical Shift Imaging in Pick Complex. Am J Neuroradiol 2002: 23; 1387-1392.\n\n7.\tGe Y. Multiple Sclerosis: The Role of MR Imaging. Am J Neuroradiol 2006: 27; 1165-1176.\n\n8.\tHutchinson M, Raff U. Structural Changes of the Substantia Nigra in Parkinson\u2019s Disease as Revealed by MR Imaging. Am J Neuroradiol 2000: 21; 697-701.\n\n9.\tRoher AE, Esh CL, Kokjohn TA, et al. Amyloid beta peptides in human plasma and tissues and their significance for Alzheimer\u2019s disease. Alzheimer\u2019s & Dementia 2009: 5; 18-29.\n\n10.\tRevuelta GJ, Rosso A, Lippa CF. Association Between Progranulin and ?-Amyloid in Dementia With Lewy Bodies. Am J Alzheimers Dis Other Demen 2008: 23; 488.\n\n11.\tYan SD, Fu J, Soto C, et al. An intracellular protein that binds amyloid-\u03b2 peptide and mediates neurotoxicity in Alzheimer\u2019s disease. Nature 1997: 389; 689-695.\n\n12.\tHan SD, Bondi MW. Revision of the apolipoprotein E compensatory mechanism recruitment hypothesis. Alzheimer\u2019s & Dementia 2008: 4; 251-254.\n\n13.\tMurray C, Viehman A, Lippa C. The corpus callosum in Pick\u2019s disease, Alzheimer\u2019s disease, and amyotrophic lateral sclerosis: Gliosis implies possible clinical consequences. Am J Alzheimers Dis Other Demen 2006: 21; 37-43.\n\n14.\tSchipper H. The role of biologic markers in the diagnosis of Alzheimer\u2019s disease. Alzheimer\u2019s & Dementia 2007: 3; 325-332.\n\n15.\tSt George-Hyslop PH, Westaway DA. Antibody clears senile plaques. Nature 1999: 400; 116-117.\n\n16.\tZhang J, Sokal I, Peskind ER, et al. CSF Multianalyte Profile Distinguishes Alzheimer and Parkinson Diseases. Am J Clin Pathol 2008: 129; 526-529.\n\n17.\tMartin, J. Molecular Basis of the Neurodegenerative Disorders. N Engl J Med 1999: 340; 1970-1980.\n\n18.\tBarger S, Basile A. Activation of microglia by secreted amyloid precursor protein evokes release of glutamate by cystine exchange and attenuates synaptic function. J Neurochem 2008: 76; 846-854." } }, { "U_id": "MPX1319", "TAC": [], "MRI": [ "MPX1319_synpic46246", "MPX1319_synpic47475", "MPX1319_synpic47476", "MPX1319_synpic47477" ], "Case": { "Title": "Osteochondroma", "History": "Twisting injury. Rule out meniscal tear.", "Exam": "N/A", "Findings": "No evidence of arthrosis, fracture, avascular necrosis, or bone marrow edema. There is a bony exostosis in the posteromedial aspect of the posterior distal femoral metaphysis with contiguous marrow. The exophytic mass is well defined and measures 2-3mm. It has increased T2 singal. The image and history is consistant with osteochondroma. \n\nThere is no evidence of meniscal or ligament tears.", "Differential Diagnosis": "osteochrondroma\nosteosarcoma", "Case Diagnosis": "Osteochondroma" }, "Topic": { "Title": "Osteochondroma", "Disease Discussion": "\u2022 Lesions/Condition: Osteochondroma\n\nTumor Growth: Lesions grow by enchondral ossification of proliferating cartilage cells in its cap. The tumor will continue to enlarge during skeletal growth, but typically becomes latent at skeletal maturity. \n\n\u2022 Synonyms: Osteocartilaginous Exostosis\n\n\u2022 Common Locations: The most common site of origin for an osteochondroma is the metaphysis at bony sites of tendon and ligamentous attachments. Common sites include distal femur, proximal humerus, proximal tibia but also may occur less frequently in the pelvis, scapula, spine or any bone preformed in cartilage.\n\n\u2022 Demographics: Typically occur in first to third decades with prevalence greater in males than in females. It is the most common skeletal tumor in children with an occurrence of 1 in 200. They may be solitary or multiple and they may arise spontaneously.\n\n\u2022 Gross Morphology: Osteochondromas vary in size. The average lesion arising from tubular bones is approximately 4cm. Osteochondromas arising from flat bones tend to be larger with a higher likelihood of malignant transformation.\n\n\u2022 Histology: Pathologic sections show osteochondromas to have a cartilaginous cap. Histologically, the cartilaginous cap is identical to the physeal growth plate. During active growth, the cap is composed of hyaline cartilage. The thickness of the cap is correlated with the age of the patient, and the cap decreases in size as patient\u2019s age. In children and adolescents, the cap may be as thick as 3cm, whereas in older patients, it may be thin. A thick cartilaginous cap (>1cm) in an adult should raise the possibility of malignant transformation (usually chondrosarcomas)\n\n\u2022 Radiology: Plain radiographic appearances of an osteochondroma are those of a pedunculated or sessile bony excrescence with well-defined margins. In adults, the cartilage cap often contains flecks of calcification. Continuity of the osteochondroma with the medullary canal is a characteristic finding, particularly obvious in long bones. MR imaging is able to detect continuity of the cortical and medullary bone in the outgrowth with that of the parent bone. This finding is diagnostic of an osteochondroma. Of greatest utility in the functionality of the MR is the ability to precisely identify and measure the cartilaginous cap of an osteochondroma using T2 weighted spin echo images. These measurements can be used to supply information regarding the likelihood of malignant changes.\n\n\u2022 Prognosis and Treatment: Most solitary osteochondromas are discovered in children and adolescents and are painless, slow-growing masses and require no treatment. Significant symptoms may occur as a result of complications such as fracture, bony deformity, mechanical joint problems, and vascular or neurologic compromise. Appreciable morbidity is related to resection of osteochondromas and corrective surgery on the osseous deformity. Resections are typically only performed on mature bone due to the risk of damage to the epiphyseal growth plate resulting in severe growth deformity in the affected bone. Serial radiographs are performed to monitor for malignant transformation which is estimated at 1% for solitary osteochondromas. The most common resulting malignant tumor is a chondrosarcoma.", "ACR Code": "4.3", "Category": "Neoplasm, benign", "Keywords": "Osteochondromapediatric neoplasmbony neoplasm", "Reference": "1. Wheeless Textbook of Orthopedics\n2. Fritsch & Thompson, Radiologist, Diagnostic Radiology of Houston, TX Emedicine\n3. Diagnosis of Bone and Joint Disorders 3rd ed. Donald Resnick MD; W.B. Saunders Company 1995." } }, { "U_id": "MPX1379", "TAC": [], "MRI": [ "MPX1379_synpic17759", "MPX1379_synpic17760", "MPX1379_synpic17761", "MPX1379_synpic17762", "MPX1379_synpic17763", "MPX1379_synpic17764" ], "Case": { "Title": "Arteriovenous Malformation", "History": "History: 21y.o. male s/p resection of upper back melanoma with clear margins, work up for possible metastatic melanoma to the brain prior to selection for an NIH study for melanoma vaccine. No symptomatic complaints. This young individual underwent a brain MRI with contrast to determine possible melanoma metastatic lesions to the brain. An incidental arteriovenous malformation was discovered on imaging.", "Findings": "Right posterior parietal lobe arteriovenous malformation measuring\n2.1 x 1.5 x 1.7cm with no obvious deep drainage noted and no eloquent brain\nparenchyma involved. As an MRA was not obtained, a aneurysm cannot be\nentirely excluded.", "Differential Diagnosis": "dural Arteriovenous fistula", "Case Diagnosis": "Arteriovenous Malformation" }, "Topic": { "Title": "Arteriovenous Malformation", "Disease Discussion": "Arteriovenous Malformation:\nArteriovenous malformations consist of feeding arteries that are dilated with a cluster of entangled vascular loops. Blood flows preferentially through the AVM therefore depriving other areas of the brain of blood flow. This steal phenomenon can produce neurological symptoms, seizures, and parenchymal loss. This increase in blood flow also can produce aneurysms. The location of the AVMs is 80-85% in the cerebral hemispheres and 10-15% in the posterior fossa.\n\nClinical Presentation:\nArteriovenous malformations are usually congenital developmental anomalies, but are frequently asymptomatic until 30 to 40 years of age. Approximately 25% of these patients hemorrhage by age 15 and 80-90% of the patients are symptomatic by age 50. Symptoms include seizure and headaches.\n\nPathology:\nArteriovenous malformations consist of feeding arteries that are dilated with a cluster of entangled vascular loops. Blood flows preferentially through the AVM therefore depriving other areas of the brain of blood flow. This steal phenomenon can produce neurological symptoms, seizures, and parenchymal loss. This increase in blood flow also can produce aneurysms. The location of the AVMs is 80-85% in the cerebral hemispheres and 10-15% in the posterior fossa. \n\nImage Findings:\nCT scans typically show tangled vessels in the parenchyma that are high density contrast. These vessels are noted to have a serpentine configuration. Curvilinear or speckled calcification may also be present. MR scans show curvilinear flow voids secondary to fast flow seen on pulse sequences and dilated feeding arteries. The appearance of the arteries vary due to flow rate, direction, pulse sequence, and the presence and age of the hemorrhage. Gliosis and hemorrhages also appear on the MR images. Often MRA images are used to diagnose the disease. MR is more sensitive to the feeding arteries, the core or nidus, and the enlarged draining veins.\n\nDifferential Diagnosis:\nDifferential diagnosis includes vascular malformations. If normal blood flow is present, capillary telangiectasis and developmental venous anomalies are commonly confused with AVM. Capillary telangiectasis are lesions measuring approximately 3 cm in diameter and are typically found in the pons. The majority of the lesions do not hemorrhage and are observed as nodular enhancements after contrast on T1WI. Developmental venous anomalies are the most common cerebral vascular malformation. These malformations rarely hemorrhage. If hemorrhage is noted, it is most likely due to a coexisting cavernous angioma. If the malformation is isolated, they appear to be composed of dilated medullary veins that form a large channel draining into cortical veins or subependymal veins. If there is high blood flow, AV fistula shares similar characteristics with AVM. AV fistula is an arterial dissection or laceration that spontaneously communicates with an adjacent vein or dural sinus. These fistulas are commonly seen in the cavernous sinus, below the petrous temporal bone, and foramen magnum.\n\nTreatment:\nDepending on the size and location of the AVM, the treatment may include embolization, surgery, or radiation therapy.", "ACR Code": "1.-1", "Category": "Vascular" } }, { "U_id": "MPX1394", "TAC": [], "MRI": [ "MPX1394_synpic22908", "MPX1394_synpic22909" ], "Case": { "Title": "Partial Achilles Tendon tear", "History": "Left ankle/leg pain and weakness", "Exam": "Weakness on plantar flexion", "Findings": "Plain radiographs demonstrate thickening of the Achilles tendon, convex impression of Achilles tendon on the posterior margin of Kager's fat pad, and a lower limits normal Toygar's angle. \n\nMR findings demonstrates focal thickening of the Achilles tendon increased T2W signal within the tendon and overlying subcutaneous tissues", "Differential Diagnosis": "Partial Achilles rupture\nComplete Achilles rupture", "Case Diagnosis": "Partial Achilles Tendon tear", "Diagnosis By": "Imaging findings were confirmatory", "Treatment & Follow Up": "Conservative treatment, immobilization, followed by physical therapy" }, "Topic": { "Title": "Achilles Tendon Rupture", "Disease Discussion": "Spontaneous Achilles tendon rupture or partial tears typically occur in otherwise healthy, relatively young patients, with no history of heel or calf pathology. Most studies find that the majority of individuals who sustain Achilles tendon injury are men in their third to fifth decade of life, who are participating in sports activities. The injury most commonly occurs secondary to overloading of the musculotendinous unit in a poorly conditioned individual rather than secondary to an underlying tendinopathy. The mechanical cause of the injury is most commonly active, forceful plantarflexion, usually associated with pushing off athletic movements. Less commonly, Achilles rupture is caused by violent unexpected dorsiflexion of a plantarflexed foot, such as when a person steps in hole or falls from a height.(1)\n\n The diagnsosis can often be made by physical examination. Findings may include a palpable depression over the area of tendon rupture, weakness of plantarflexion, and positive Thompson test. A positive Thompson test is failure of the foot to plantarflex when the calf muscles are squeezed.(1)\n\n However, up to 25% of patients with partial or complete Achilles tear may be misdiagnosed based on physical exam findings alone. Radiographic findings can assist with the diagnsosis. When the Achilles tendon is ruptured, the sharp posterior contour of Kager's fat pad triangle will become serrated and indistinct. The Achilles tendon will appear thickened (> 8mm). Toygar's angle, which is the angle of the posterior skin surface overlying the distal Achilles and posterior calcaneal surfaces will decrease and is considered abnormal if less than 150 degrees. Positive Arner's sign, in which the anterior contour of the Achilles tendon at the insertion curves away from the superior-posterior aspect of the calcaneus, may be positive.(2)\n\n MR imaging findings may confirm the diagnosis. Partial Achilles tendon tears demonstrate heterogeneous signal intensity and thickening of the injured tendon without complete interruption. Edema manifested as increased T2 signal will usually be present within the tendon, subcutaneous tissues, and in Kager's fat pad. Hemorrhage signal may also be present in those structures and signal characteristics will vary according to the age of the injury. Complete Achilles rupture manifests as discontinuity of the tendon with fraying and retraction of the torn edges. In acute ruptures, the gap between the rupture will have intermediate T1 signal and high T2 signal due to edema and acute hemorrhage. In chronic ruptures, scar or fat signal will ususally predominate.(3)\n\n Treatment of Achilles rupture is controversial and there are advantages and disadvantages to conservative nonsurgical treatment versus surgical treatment. Nonsurgical treatment avoids surgical morbidity and cost, but rerupture rates are as high as 39%. Surgical treatment has higher cost and morbidity, but lower rerupture rates.(1)", "ACR Code": "4.4", "Category": "Trauma", "Keywords": "Achillesrupturetear", "Reference": "1. Delee: Delee and Drez's Orthopedics Sports Medicine. 2nd ed. Philedelphia: Elsevier, 2003: 2433-2435.\n\n2. Cetti R, Anderson I. Roentgenographic diagnoses of ruptured Achilles tendons. Clin Orthop, 1993; 286:215-221\n\n3. Goldberg et al. MR imaging of the ankle and foot. Radiographics, 2000; 20:S153-S179" } }, { "U_id": "MPX1384", "TAC": [], "MRI": [ "MPX1384_synpic49843", "MPX1384_synpic49844", "MPX1384_synpic49845", "MPX1384_synpic49846", "MPX1384_synpic49847", "MPX1384_synpic49848" ], "Case": { "Title": "Multiple Myeloma", "History": "61 y.o. woman with a \"lump\" on left side of head.", "Exam": "Non-tender superficial mass at the left superior frontal region of the skull. No focal neurological deficits.", "Findings": "Plain radiograph (skull): Multiple \u201cpunched-out\u201d lytic lesions are seen throughout the calvarium. \nA large lytic lesion at the vertex disrupts both the inner and outer table.\n\nT1 Sag: Large expansile mass lesion which is hypointense to bone marrow extending intracranially from the frontal clavarium.\n\nT1 Cor: Large expansile mass lesion which is hypointense to bone marrow extending intracranially from the frontal clavarium.\n\nT1 Ax +C: Enhancing expansile mass lesion extending intracranially and superficially from the calvarium.\n\nT1 Cor +C: Enhancing expansile mass lesion extending intracranially and superficially from the calvarium.\n\nT2 Ax: Expansile mass which is isointense to bone marrow extending both intracranially and superficially from the calvarium.", "Differential Diagnosis": "\u2022 Surgical defect\n\u2022 Lytic metastasis\n\u2022 Hemangioma\n\u2022 Brown Tumor\n\u2022 Hemangiopericytoma\n\u2022 Meningioma (multiple or Meningiomatosis)\n\u2022 Multiple myeloma", "Case Diagnosis": "Multiple Myeloma", "Diagnosis By": "Prior bone marrow biopsy & characteristic lytic lesions", "Treatment & Follow Up": "This woman was known to have multiple myeloma and a history of lytic lesions. This evaluation for interval change led to treatment with focused radiotherapy.", "Discussion": "Multiple myeloma is characterized by the neoplastic proliferation of a single line of plasma cells producing a monoclonal immunoglobulin. This proliferation replaces normal bone marrow and often results in extensive skeletal destruction with osteolytic lesions, osteopenia, and/or pathologic fractures. \n\nThe etiology of multiple myeloma is unknown. It is more common in the elderly and there is a slight increased risk among children and siblings of multiple myeloma patients. There is also an increased incidence amongst petroleum, leather, and cosmetology workers. Additionally, exposure to radiation (greater than 50 rad), hebricides, insecticides, heavy metals, plastics, and asbestos also increases risk. \n\n\u201cPunched-out\u201d lytic lesions are a common finding on plain film. An osteolytic skull lesion is the best diagnostic clue on imaging. The appearance can vary on T1-weighted MRI, ranging from focal hyperintensity in 53% of cases to a focal hypointensity in 25% of cases. Marked lesional enhancement is seen following gadolinium administration. On T2 weighted imaging, an iso- to hyperintense lesion can be seen. Intracranial myeloma, as in this patient, is a rare finding.\n\n\nReferences: \n\nAngtuaco EJ, et al. Multiple myeloma: clinical review and diagnostic imaging. Radiology. 2004; 231(1):11-23.\n\nBrant WE, Helms CA. Fundamentals of Diagnostic Radiology. Lippincott, Williams & Wilkins. Philadelphia. 2007\n\nOsborn AG. Diagnostic Neuroradiology. Mosby. St Louis. 1994. \n\nSmith, A, Wisloff, F, Samson, D. Guidelines on the diagnosis and management of multiple myeloma 2005. British Journal of Haematology. 2006; 132:410." }, "Topic": { "Title": "Multiple Myeloma", "Disease Discussion": "Multiple myeloma is a plasma cell neoplasm that is characterized by involvement of the skeletal system in multiple sites. It accounts for 1% of all malignancies and is most prevalent in the 70-80 year old range. Symptoms include bone pain, anemia, fever, weight loss, and weakness, as well as neurologic symptoms.\nLaboratory findings include elevated ESR, anemia, hypercalcemia and hyperuricemia. Elevated globin levels are present, usually involving IgG, but any of the immunoglobulins may be produced. The plasma cell burden will eventually displace and erode the bony trabeculae and give rise to the musculoskeletal symptoms.\n\nClassically, multiple myeloma will appear as osteolytic lesions. These arise predominantly in the verterbral bodies, ribs, skull, pelvis and femur. However, diffuse skeletal osteopenia may be observed without focal lytic lesions. Pathologic fractures are common.\n\nBoth plain films and MDP scintigraphy have a significant false negative problem: Plain film false negative 9-25%; and, MDP false negative 40-60%. http://www.med.harvard.edu/JPNM/TF94_95/Jan17/WriteUpJan17.html\n\nHowever, FDG PET may be useful, with a sensitivity of 85% and specificity of 92% reported. PMID: 15788594", "ACR Code": "4.3", "Category": "Neoplasm, NOS", "Keywords": "multiple myeloma", "Reference": "Resnick and Kransdorf. Bone and Joint Imaging, 3rd Edition. 2005." } }, { "U_id": "MPX1401", "TAC": [], "MRI": [ "MPX1401_synpic16223" ], "Case": { "Title": "Biceps tendon dislocation; posterior to subscapularis.", "History": "54 y/o man with right shoulder pain.", "Findings": "Bicipital groove is empty. Long head of biceps tendon is medial to lesser tuberosity and posterior to subscapularis tendon. Associated LHBT tear and full-thickness supraspinatus tear are seen.", "Differential Diagnosis": "Empty bicipital groove:\n-Long head of biceps tendon rupture\n-Long head of biceps tendon dislocation", "Case Diagnosis": "Biceps tendon dislocation; posterior to subscapularis.", "Discussion": "Note that the LHBT is posterior to subscapularis tendon and residual fibers of subscapularis tendon(transverse humeral ligament) still insert upon the greater tuberosity. Recent research by Sanders TG, et al, Wilford Hall Medical Center show that the fibers of the transverse humeral ligament are really an extension of the subscapularis tendon. The biceps tendon may dislocate in two ways; anterior to subscapularis tendon (rare) or posterior to subscapularis tendon (more common)." }, "Topic": { "Title": "Biceps tendon dislocation", "Disease Discussion": "The long head of the biceps tendon (LHBT) arises from the superior glenoid tubercle of the scapula. After traversing the joint deep to the coracohumeral ligament, it enters the bicipital groove and is covered by fibers of the transverse humeral ligament. LHBT dislocations are commonly associated with other abnormalities, particullary rotator cuff tears (RCT) (1). In one series, patients with anterior rotator cuff (subscapularis tendon) tears also had LHBT dislocations 78% of the time (2).", "ACR Code": "4.4", "Category": "Trauma", "Keywords": "Biceps Tendondislocationrotator cuff", "Reference": "1. Chan TW, Dalinka MK, Kneeland JB, et al. Biceps Tendon Dislocation: Evaluation with MR Imaging. Radiology 1991; 179:649-652.\n2. Pattern RM. Tears of the Anterior Portion of the Rotator Cuff: MR findings. AJR 1994;162:351-354." } }, { "U_id": "MPX1390", "TAC": [], "MRI": [ "MPX1390_synpic29157", "MPX1390_synpic29158", "MPX1390_synpic29159", "MPX1390_synpic29160", "MPX1390_synpic29161", "MPX1390_synpic29163" ], "Case": { "Title": "\u2022 Osteomyelitis of the head of the left, first metatarsal\r\n\u2022 Osteomyelitis of the medial sesamoid bone\r\n\u2022 Myositis of the plantar muscles of the foot\r\n\u2022 Cellulitis of the plantar aspect of the foot", "History": "The patient is an 83-year-old, African-American woman with a history of diabetes mellitus, hypertension, hyperlipidemia, hepatitis C, and neurosyphilis, who was admitted to the hospital for worsening of a chronic, nonhealing, left-foot ulcer that had been followed closely by the Podiatry service with repeated debridements and courses of oral antibiotics. On the current admission, the patient denied having had any fevers, chills, or feelings of malaise, but stated that her glycemic control had been poor.", "Exam": "Physical examination revealed a 2x2-cm ulceration superficial to the medial aspect of the head of the left, first metatarsal.\n\nHemoglobin A1c taken one month prior to admission was 10% (normal range 4.5% - 5.7%)", "Findings": "Anteroposterior and oblique radiographs of the left foot show severe osteopenia of the bones of the foot and ankle, as well as extensive calcifications of the visualized arteries of the foot. There is erosion of the medial aspect of the head of the first metatarsal and thickening of the adjacent medial soft tissues. Additionally, there is ulceration (1.2 cm in length) in the superficial soft tissues medial to the head of the first metatarsal. Also radiographs showed incidental findings of metatarsus primus varus with hallux valgus deformities.\n\nT1-weighted, axial MR images of the left foot show extensive areas of low-signal intensity around the head of the first metatarsal and the medial soft tissues.\n\nFast spin echo (FSE), T2-weighted with fat saturation, axial MR images of the left foot and short tau inversion recovery (STIR) sagittal MR images show that areas of low-signal intensity on T1-weighted MR images (the soft tissues) become areas of high-signal intensity. There are also areas of high-signal intensity in the head of the first metatarsal and the distal metaphysis and in the tibial (medial) sesamoid bone. These fat-suppressed MR images also show areas of high-signal intensity in the plantar muscles.\n\nPost-contrast T1-weighted with fat saturation MR images of the left foot in both the axial (not shown) and sagittal planes show enhancement of the head of the first metatarsal, the tibial sesamoid, and surrounding soft tissues. On post-contrast MR images, no necrosis in muscles or soft tissues, manifested by nonenhancing areas, are found.\n\nThese combined findings on fat-suppressed and contrast-enhanced MR images are consistent with myositis and cellulitis of the soft tissues and osteomyelitis of the head of the first metatarsal and tibial sesamoid. The tendons of the tarsus and foot are normal.", "Differential Diagnosis": "The image findings of these studies are definitive for osteomyelitis with cellulitis and myositis.", "Case Diagnosis": "\u2022 Osteomyelitis of the head of the left, first metatarsal\n\u2022 Osteomyelitis of the medial sesamoid bone\n\u2022 Myositis of the plantar muscles of the foot\n\u2022 Cellulitis of the plantar aspect of the foot", "Diagnosis By": "The diagnoses were confirmed by the imaging coupled with the patient\u2019s history, clinical presentation, and physical examination findings.", "Treatment & Follow Up": "The patient was discharged from the hospital after four days and placed on a 14-day course of antibiotics (clindamycin 300mg qid and ciprofloxacin 500mg bid) and acetaminophen (650mg q6h prn) for pain. Prior to discharge from the hospital, the Orthopaedic team discussed various treatment options with the patient, to include a left-foot-transmetatarsal amputation, left-foot-first-ray amputation, left-below-the-knee amputation, and continued antibiotics with dressing changes. The patient had follow-up appointments scheduled with the Vascular-Surgery Service (tissue oxygen pressure evaluation and wound monitoring) and with the Orthopaedic-Surgery Service (wound care and monitoring, and further discussion of surgical options).", "Discussion": "A prevalent sequela of diabetic foot ulcers is osteomyelitis.1 In fact, almost all diabetic foot infections originate from an ulcer (> 85%), making prompt diagnosis and aggressive management essential in preventing later amputation.2 A diabetic\u2019s peripheral neuropathy causes \u201cdecreased pedal sensation that leads to undetected mechanical and thermal injuries; excessive and repetitive pressure on plantar bony prominences, especially the metatarsal heads; gait disturbances and foot deformities that increase focal pressure; and autonomic neuropathy that leads to decreased sweating and dry, cracked skin.\u201d1 This coupled with a diabetic\u2019s peripheral vascular disease, peripheral motor neuropathy, dysfunctional immune system, and poor wound healing, increases the likelihood of an organism gaining a foothold in and causing an infection of the underlying bone.1\n\nWhile osteomyelitis in an otherwise normal patient would present with fever, chills, and local signs of infection (i.e., purulent drainage, erythema, warmth, and tenderness), the diabetic patient with osteomyelitis of the foot may be devoid of any or all of these symptoms.1 Often, \u201crecalcitrant hyperglycemia is the only systemic sign\u201d of osteomyelitis of the foot, and fever and chills are absent in up to 67% of infected patients.1 In short, the clinical diagnosis of osteomyelitis in this setting is poor.1 Therefore, clinicians must either resort to a bone biopsy or use diagnostic imaging. A bone biopsy is a surgical procedure, is time consuming and not without risk, and is expensive, whereas imaging is essentially noninvasive, provides rapid results with very little risk to the patient, and relative to surgery is inexpensive. Therefore, it is the modality used to make a diagnosis in these patients, although biopsy is occasionally needed for confirmation, particularly when patients have neuropathic joints and osteomyelitis.\n\nRadiographs of the foot are the easiest and least expensive imaging studies.1 However, \u201cthe sensitivity and specificity for the diagnosis of osteomyelitis of the diabetic foot are 60% and 66% respectively.\u201d1 Unfortunately, osteomyelitis must be present for 10 to 21 days before the infection is detectable on plain radiographs and a patient with severe neuropathic bone disease will have a similar appearing study.1 However, radiographs should be the initial imaging study, not only due to its ease and economy, but also as a baseline.\n\nMagnetic resonance imaging (MRI) is the best test for diagnosing osteomyelitis with a sensitivity and specificity of 99% and 83% respectively and demonstrates excellent contrast between the soft tissues and bones and pathological conditions such as osteomyelitis, myositis, and cellulitis.1 The main drawback of MRI in this role is cost.1 On T1-weighted MR images of the bone marrow, osteomyelitis causes a decreased signal intensity, but T2-weighted MR images with fat saturation and short tau inversion recovery (STIR) MR images of involved bone marrow will show an increased signal intensity.1,3 On contrast-enhanced T1-weighted MR images with fat saturation, areas of osteomyelitis will enhance. MRI can also detect the diabetic ulceration, and sometimes the sinus tract from osteomyelitis to ulcer. The addition of contrast-enhanced MRI allows the detection of nonenhancing necrosis, which is important to recognize for debridement.\n\n1. Schinabeck MK, Johnson JL. Osteomyelitis in diabetic foot ulcers. Postgrad Med 2005;118(1):11-15.\n\n2. Ledermann HP, Morrison WB. Differential diagnosis of pedal osteomyelitis and diabetic neuroarthropathy: MR Imaging. Semin Musculoskelet Radiol 2005;9(3):272-283.\n\n3. Chatha DS, Cunningham PM, Schweitzer ME. MR Imaging of the Diabetic Foot: Diagnostic Challenges. Radiol Clin N Am 2005;43:747-759." }, "Topic": { "Title": "Osteomyelitis", "Disease Discussion": "Osteomyelitis is infection of bone, usually bacterial in origin. Microbes can reach bone by three mechanisms: hematogenous spread, extension from a contiguous site of infection, and direct introduction of organisms into bone by trauma and surgery. \n\nAcute hematogenous osteomyelitis involves bone with red marrow. In children, most commonly affected are the long bones with relatively slow flow in metaphyseal sinusoidal veins and a paucity of phagocytes. Infection is often secondary to staphylococcal skin infections. In adults, acute osteo rarely involves the long bones because adipose tissue has replaced red marrow. Instead, it most commonly occurs in vertebral bodies, where the marrow is cellular and has abundant vascular supply. Septicemia is usually the inciting event.\n\nExtension from a contiguous site of infection is a common cause for osteomyelitis. Infection following trauma, radiation therapy, burns or pressure sores. In patients with vascular insufficiency, organisms can enter the soft tissues through a cutaneous ulcer, often in the foot, and cause cellulitis, then osteomyelitis.\n\nDirect introduction of organisms into the bone may occur during open fractures, open surgical reduction of closed fractures, or penetrating trauma by foreign bodies such as bullets. May also arise from perioperative contamination of bone during laminectomy, diskectomy, or joint prosthesis. The causitive organism is typically normal flora, such as Staph Epidermidis.", "ACR Code": "4.2", "Category": "Infection, bacteria", "Keywords": "osteomyelitisbone scanindium", "Reference": "Nuclear Medicine, The Requisites Copyright 2001, Mosby, Inc." } }, { "U_id": "MPX1346", "TAC": [], "MRI": [ "MPX1346_synpic22506", "MPX1346_synpic22507" ], "Case": { "Title": "Intraductal Papillary Mucinous Tumor - Branch Type", "History": "60 YO male. Asymptomatic", "Exam": "WNL", "Findings": "Small cystic foci in the inferior aspect of the pancreatic uncinate process. Cysts seen to communicate with main pancreatic duct on MRCP and ERCP. No evidence of main pancreatic ductal dilitation", "Differential Diagnosis": "Pseudocyst, Serous cystadenoma, Mucinous cystadenoma/ cystadenocarcinoma, IPMT - Branch Type", "Case Diagnosis": "Intraductal Papillary Mucinous Tumor - Branch Type", "Diagnosis By": "ERCP", "Treatment & Follow Up": "Partial Pancreatectomy vs close serial CT monitoring to detect stability in size vs growth (indication for resection).", "Discussion": "IPMT - Branch Type are relatively rare. 70% occur in the uncinate process, less frequently in the tail and body. These occur with equal frequency in males and females and the median age of discovery is 60. These tumors usually contain malignant cells, but their slow growth has created 2 camps of management: one advocating partial pancreatectomy, the other close monitoring with CTs at 3-6 month intervals. The key to diagnosis is to show via ERCP or MRCP that there is connection between the main pancreatic duct with the dilated side branches. The serous and mucinous neoplasms do not show this connection. Aspiration of thick mucinous ductal fluid also supports this diagnosis." }, "Topic": { "Title": "Cystic pancreatic neoplasms", "Disease Discussion": "Cystic Pancreatic Neoplasms: Serous adenoma (microcystic), mucinous adenoma/ adenocarcinoma (macrocystic), Intraductal papillary mucinous tumors (IPMT). \n - IPMT often are lower grade cystic pancreatic neoplasms than the mucinous cystadenocarcinomas. \n - Main and Branch Duct types\n - Main typically has greater malignant potential.\n - Both found at median age of 60, M:F = 1:1\n - Both Main and Branch can have pancreatic side duct distension which fill on ERCP and show communication with the main duct on MRCP", "ACR Code": "7.3", "Category": "Neoplasm, malignant (NOS)", "Keywords": "Cystic NeoplasmPancreas", "Reference": "Radiology Review Manual, Dahnert \nPrimer of Diagnostic Imaging, Weissleder et al." } }, { "U_id": "MPX1412", "TAC": [], "MRI": [ "MPX1412_synpic22157", "MPX1412_synpic22158", "MPX1412_synpic22159", "MPX1412_synpic22160" ], "Case": { "Title": "Vertebral Artery Dissection", "History": "65 year old white male presents with several year history of vertigo.", "Findings": "The left vertebral artery at the level of the foramen magnum is normal to increased in size with an absent flow void when compared to the right. The left vertebral artery then narrows for a two centimeter segment prior to reaching the basilar artery.", "Differential Diagnosis": "Vertebral artery dissection.", "Case Diagnosis": "Vertebral Artery Dissection", "Discussion": "The patient was clinically reevaluated after these findings were discussed with the ordering provider. The patient stated his vertigo had been chronic and stable for several years and he had no new symptoms of vertebral artery distribution ischemia. The clinical scenario coupled with longus capitis muscle atrophy (not shown) indicate that this is a chronic condition." }, "Topic": { "Title": "Vertebral Artery Thrombosis", "Disease Discussion": "Vertebral artery dissection comprises 20% of cervicocephalic arterial dissection and is responsible for up to 15% of strokes in young adults. Dissection related thromboembolism is implicated as the cause of these infarctions, underscoring the need for early diagnosis and anticoagulation. Cerebral infarction complicates up to 95% of spontaneous vertebral artery dissections, but prognosis is good with 90% of affected patients approaching full recovery. Traumatic vertebral artery injury associated with cervical spine fractures is common (40%) but remains largely asymptomatic even with complete vessel occlusion. \nSymptoms of vertebral artery dissection include headache and neck pain, with either abrupt or evolving gait, ocular or vestibular disturbances. Vertebral artery dissection is commonly spontaneous or due to mild trauma such as sneezing or head turning which can stretch the artery over the lateral mass of C2. Hyperextension may also stretch the vertebral artery at C1-2 where it exits the transverse foramen. Conditions which predispose to arterial dissection include fibromuscular displasia, cystic medial necrosis, Marfan\u2019s Syndrome and homocysteinuria. \nWhile clinicians may place great emphasis on MR angiography for evaluation of the cervical arteries, standard spin-echo MRI has much greater sensitivity than MRA for dissection in the vertebral arteries (60% vs. 20%). Findings include an enlarged vessel with associated pseudoaneurysm and an absent flow void. Distal narrowing may be present. MR appearance of the intramural hematoma will vary with the state of the blood products.", "ACR Code": "9.9", "Category": "Vascular", "Keywords": "vertebral arterydissection", "Reference": "Stark, DG, Bradley WG, Magnetic Resonance Imaging, 3rd Edition, Volume 2. Mosby 1999, St. Louis. Pages 1268, 1294, 1356-1358.\nDahnert, W. Radiology Review Manual, 5th Edition. Lippincott, Williams and Wilkins, Philadelphia, 2003. Pages 837-838." } }, { "U_id": "MPX1417", "TAC": [], "MRI": [ "MPX1417_synpic24443", "MPX1417_synpic24444", "MPX1417_synpic24445", "MPX1417_synpic24446" ], "Case": { "Title": "Hemorrhage in Basal Ganglia, Hypertensive, Acute Stroke", "History": "76 year-old hypertensive male with altered mental status, presenting to the emergency department via EMS.", "Exam": "Hypertension", "Findings": "CT demonstrates focal high density in the region of the left putamen. Contrast was administered due to apparent vasogenic edema on the preceding non-contrast examination. A follow-up MRI performed 3 months later demonstrates evidence of residual blood products in the same region. Note the decrease in mass effect on the follow-up study.", "Differential Diagnosis": "Hypertensive hemorrhage\nAmyloid angiopathy \nHemorrhagic primary or metastatic malignancy", "Case Diagnosis": "Hemorrhage in Basal Ganglia, Hypertensive, Acute Stroke", "Diagnosis By": "Clinical information supported the diagnosis of hypertensive hemorrhage.", "Treatment & Follow Up": "Medical control of blood pressure." }, "Topic": { "Title": "Hemorrhage in Basal Ganglia, Hypertensive, Acute Stroke", "Disease Discussion": "The history of a sudden onset unilateral motor and.or sensory changes in a patient are strongly suggestive of stroke, which can be generally classified as either ischemic or hemorrhagic. Although this patient had no known history of hypertension, her CT and MRI both demonstrate evidence of chronic small vessel ischemia secondary to longstanding hypertension. The differential diagnosis for a hemorrhagic lesion in the putamen/posterior capsule includes lacunar infarct, hypertensive hemorrhage, vascular malformation, and neoplasm.\n\nLacunar infarcts represent 15-20% of all strokes, and appear as small cavitary lesions in subcortical regions. They result from the thrombosis of a small penetrating artery, often as a result of a chronic hypertensive change known as lipohyalinosis. Characteristic locations for lacunar infarcts include the following: putamen (37%), pons (16%), thalamus (14%), caudate (10%), and internal capsule (10%). Posterior limb lacunes are the most important clinically because of their potential for severe motor and sensory deficits. Anterior limb lacunes are often clincally silent.\nThese \"perforating\" arteries (lenticulostriate aa., thalamogeniculate aa., and anterior choroidal branch of ICA) are common sites for both lacunar infarcts and hypertensive hemorrhage, and both types of lesions can result from a process known as lipohyalinosis. This is the impregnation of hyaline-lipid material into the walls of small arteries in the setting of hypertension combined with atherosclerosis. Lipohyalinosis predisposes the artery to thrombosis and may also weaken the vessel wall, resulting in small dissecting \"Charcot-Bouchard\" aneurysms.\n\nHypertensive hemorrhages are slightly less common than lacunar infarcts, representing 10-15% of all strokes. Two-thirds of hypertensive hemorrhages occur in the putamen, but most cases occur in the presence of systolic blood pressures much higher than 170. Active bleeding usually lasts less than one hour, while edema progresses over the next few days. Complications of hypertensive hemorrhage include brain herniation and hydrocephalus.", "ACR Code": "1.6", "Category": "Vascular", "Keywords": "hypertensive hemorrhagebasal ganglia", "Reference": "1. Brant, W. E., and Helms, C. A., Fundamentals of Diagnostic Radiology, 2nd ed., 1999, pp. 96-98, 107.\n2. Adams, R. D., and Victor, M., Principles of Neurology, 5th ed., 1993, pp. 692-697, 718.\n3. Fischbein, N. J., et al, Teaching Atlas of Brain Imaging, 1st ed., 2000, pp. 264-266." } }, { "U_id": "MPX1435", "TAC": [], "MRI": [ "MPX1435_synpic25189", "MPX1435_synpic25190" ], "Case": { "Title": "Developmental Venous Anomaly (Venous Angioma)", "History": "Right facial pain.", "Exam": "Noncontributory", "Findings": "Large left-sided venous vascular anomaly with the roentgen classic \"head of snakes (i.e., Medusa Head)\" configuration. There is a minimal amount of surrounding gliosis.", "Differential Diagnosis": "Venous Angioma\nArteriovenous Malformation", "Case Diagnosis": "Developmental Venous Anomaly (Venous Angioma)", "Diagnosis By": "Roentgen classic MR diagnosis.", "Treatment & Follow Up": "None", "Discussion": "This MR finding represents the classic \"Medusa Head\" configuration. These lesions are typically asymptomatic, and the patient's symptoms are likely unrelated." }, "Topic": { "Title": "Developmental Venous Anomaly (Venous Angioma)", "Disease Discussion": "There are four major types of vascular malformation: \u00bb arteriovenous malformation\n\u00bb cavernous malformation (cavernous hemangioma)\n\u00bb capillary telangectasia\n\u00bb developmental venous anomaly (venous angioma)\n\nThey are composed of radially arranged, dilated anomalous veins that converge into a \"collector vein\" - an enlarged transcortical or subependymal draining vein. \n\nMicroscopically they consist of dilated, thin walled venous channels separated by normal brain tissue. The precise etiology is unknown but they likely represent extreme anatomic variants and not true vascular malformations.\n\nThey are located in the deep cerebral or cerebellar white matter, most often near the margin of an adjacent ventricle. The most common site is adjacent to the frontal horn of the lateral ventricle.\n\nThey can occur at any age and often are asymptomatic and therefore may be incidental findings on imaging studies. \n\nThey are the most common vascular \u201cmalformation\u201d found at autopsy. Most are solitary, but multiple lesions can occur in the rubber bleb nevus syndrome.\n\nImaging:\nCT- Non enhanced CT scans are typically normal or show an ill-defined slightly hyperdense area. Following contrast administration, an enhancing tuft of rounded or linear vessels near the angle of a ventricle is identified. These enlarged medullary veins become continuous, with a dilated transcortical draining vein that in turn empties into an adjacent dural sinus, cortical or subependymal vein. Edema and mass effect are typically absent.\n\nMR- On magnetic resonance scans a stellate tangle of venous tributaries drains into a larger, sharply delineated vein that often shows high-velocity signal void. Flow-related enhancement can occasionally be seen. After contrast administration, the enlarged medullary tributaries and the transcerebral or subependymal draining veins are typically well seen. Evidence of gliosis or hemorrhage is present in 10-15% of cases.", "ACR Code": "1.1", "Category": "Vascular", "Keywords": "Developmental Venous AnomalyVenous Angioma", "Reference": "Osborn, Anne G. Diagnostic Neuroradiology. 1994. Mosby. Pgs 314-19." } }, { "U_id": "MPX1420", "TAC": [], "MRI": [ "MPX1420_synpic19078", "MPX1420_synpic19079", "MPX1420_synpic19080", "MPX1420_synpic19081" ], "Case": { "Title": "Ependymoma", "History": "A 32 year-old male presented to his primary care provider with unremitting neck pain. He denied any history of trauma. The patient was unresponsive to conservative therapy and plain-film radiographic evaluation was negative. Patient was subsequently referred for a cervical spine MR for further evaluation.", "Exam": "Diffuse posterior neck pain w/o any focal tenderness on exam. Patient was neurologically intact.", "Findings": "MRI of the cervical spine and with subsequent CE brain MR demonstrate a lobulated mass within the posterior fossa. The lesion appears to originate in the fourth ventricle and is centered on the midline. The tumor is isointense to gray matter on T1 and mixed iso/hypointense on T2 weighted images. There are scant areas of T1&T2 hypodensity seen which are representative of calcifications or flow voids. There is scattered enhancement with contrast administration.", "Differential Diagnosis": "Ependymoma\nChoroid Plexus Tumor\nPNET\nMetastasis", "Case Diagnosis": "Ependymoma", "Diagnosis By": "Surgically confirmed.", "Treatment & Follow Up": "The lesion was surgically resected and referred to Radiation-Oncology for XRT therapy." }, "Topic": { "Title": "Ependymoma", "Disease Discussion": "Ependymomas are an uncommon group of glial tumors. They account for less than 10 percent of central nervous system (CNS) lesions and 25 percent of spinal cord tumors. The incidence of these tumors is approximately equal between males and females. The median age at diagnosis is five years of age with 25-40% of patients being less than two years old. Ependymomas typically arise within or adjacent to the ependymal lining of the ventricular system; they occasionally occur within the brain parenchyma, and rarely outside the CNS. In children, approximately 90 percent of ependymomas are intracranial (60 percent in the posterior fossa); the remainder arise within the spinal cord. In adults, approximately 75 percent arise within the spinal canal. The fourth ventricle is the most common infratentorial site and extension into the subarachnoid space occurs frequently. Supratentorial lesions can be either intraventricular (most commonly in the lateral ventricles) or parenchymal. The biology and natural history of ependymomas resemble those of low-grade gliomas; as a result, local growth is predominant and less than 5 percent present with metastatic disease.\n\nEpendymomas are usually well demarcated with frequent areas of calcification, hemorrhage, and cysts. Ependymomas span a histologic appearance from low grade (WHO grade II) differentiated lesions (ependymoma or myxopapillary ependymoma) to anaplastic (WHO grade III) tumors. Rarer subtypes of ependymoma include cellular, papillary, and clear cell variants. Myxopapillary ependymoma is composed of morphologically distinct cells from nonmyxopapillary or regular ependymoma. It arises within the region of the conus medullaris and filum terminale and appears much less malignant than does regular ependymoma. These lesions are classified as grade I, or low grade.\n\nThe clinical presentation of ependymoma is dependent upon tumor location. Most patients with posterior fossa lesions have evidence of increased intracranial pressure. As a result, headache, nausea and vomiting, ataxia, vertigo, and papilledema are common at presentation. Cranial nerve palsies are very common, especially involving cranial nerves VI to X. Brain stem invasion may occur. Seizures or focal neurologic deficits are most prominent when the tumors arise in the supratentorial compartment. Tumors involving the spinal cord present with deficits related to involvement of ascending or descending nerve tracts, or exiting peripheral nerves, that are specific to the level of the tumor.\n\nThe differential diagnosis for tumors that present in the posterior fossa includes medulloblastoma, astrocytoma, and brain stem or choroid plexus tumors. In the supratentorial location, glial tumors, PNETs, and choroid plexus carcinoma or papilloma should be considered. The CT appearance is often hyperdense with homogeneous enhancement; cysts and calcifications are common. The presence of calcifications within a tumor located in the fourth ventricle is highly suggestive but not diagnostic of ependymoma. On MRI, these tumors have a hypointense appearance on T1, and are hyperintense on T2 or proton density images; gadolinium enhancement is usually prominent. A subependymoma should be suspected in adults who present with a long clinical history and evidence of a non-enhancing, well-demarcated, nodular intraventricular tumor that is isodense on CT, and isointense in T1 and hyperintense in T2-weighted images on MRI. Stereotactic biopsy or surgical resection are necessary for the diagnosis of ependymoma. All patients should have spinal imaging of the entire neuraxis by MRI to exclude metastatic disease, since up to 10 percent of patients have evidence of spinal seeding.\n\nStandard therapy for ependymoma consists of resection, usually followed by adjuvant radiotherapy. Chemotherapy does not appear to play an important role in the management of these tumors in adults but does in children. \n\nIt is difficult to estimate prognosis precisely in patients with ependymoma. In addition to tumor location, the extent of surgical resection and grade of malignancy have been identified as important factors in some studies. Approximately 90 percent of recurrences are local, underscoring the importance of local therapy to outcome. Supratentorial tumors appear to have a better prognosis than those located infratentorially. The risk of recurrence with myxopapillary and subependymoma is low and the prognosis is generally excellent for patients with these low grade tumors. High grade ependymomas are associated with poor outcome in most studies. In children, better performance status and older age are also associated with better prognosis. Compared to older children, infants may do less well partly because they have a higher incidence of infratentorial tumors, and partly because they tend not to receive timely adjuvant radiotherapy due to toxic effects on brain development.", "ACR Code": "1.3", "Category": "Neoplasm, glial", "Keywords": "ependymomaCNS", "Reference": "Kieran M. Ependymoma. UpToDate version 11.3 September 2003." } }, { "U_id": "MPX1434", "TAC": [], "MRI": [ "MPX1434_synpic49495", "MPX1434_synpic49496", "MPX1434_synpic49497" ], "Case": { "Title": "Chordoid Glioma", "History": "46 y.o. woman with progressive headache over several months.", "Findings": "Relatively homogeneous mass in the region of third ventricle and hypothalamus", "Differential Diagnosis": "\u2022 Hypothalamic glioma (astrocytoma)\n\u2022 Langerhan Histiocytosis\n\u2022 Germ Cell Neoplasm\n\u2022 Hypothalamic hamartoma\n\u2022 Chordoid Glioma", "Case Diagnosis": "Chordoid Glioma", "Diagnosis By": "Pathology" }, "Topic": { "Title": "Chordoid Glioma", "Disease Discussion": "Recently described neoplasm \u2013 WHO Grade 2\nRare\nOccurs in region of anterior 3rd ventricle & hypothalamus\nSx: Headaches, hydrocephalus, hypothalamic dysfunction & homonymous hemianopsia\nMean age 46 years\nChordoma-like histology\nCell of origin unknown\n\nCT: Well circumscribed, hyperdense, enhance\nMRI: Isointense to gray matter on T1, avidly enhance, slightly hyperintense on T2\n\nMean age reported as 46 but so uncommon demographics are hard to come by \u2013 slight female predilection noted\n\nHistology of Lesion and Host Response\nLow grade neoplasm given the name of choroid glioma because of it histologic appearance, which resembles a chordoma and stains avidly with the glial cell marker glial fibrillary acidic protein. The stroma is mucin rich. Vacuolization within the stroma may resemble physaliferous cells. The prognosis tends to be poor due to location and difficulty of obtaining a complete surgical resection.\n\nComputed Tomography : On imaging these lesions are well circumscribed, oval masses in the region of the anterior third ventricle and hypothalamus. CT imaging demonstrates a hyperdense lesion.\nMRI: They are isointense to gray matter on T1 and enhance homogeneously after contrast administration. On T2, they are slightly hyperintense.", "ACR Code": "1.3", "Category": "Neoplasm, glial", "Keywords": "hypothalamusoptic gliomahypothalamic hamartoma" } }, { "U_id": "MPX1410", "TAC": [], "MRI": [ "MPX1410_synpic19204", "MPX1410_synpic19205", "MPX1410_synpic19223", "MPX1410_synpic19224", "MPX1410_synpic19225", "MPX1410_synpic19226", "MPX1410_synpic27472" ], "Case": { "Title": "Obstructive Hydrocephalus (at level of Sylvian aqueduct)", "History": "Pt is a 10 y/o bright male with a h/o developmental tremor and some degree of gait asymmetry/ right toe flat walking with a short h/o new onset severe headache with associated loss of balance leading to fall, no LOC. Previous hx unknown.", "Exam": "GEN: WNWD. \nMental Status: awake, responsive, alert and oriented X 3. \nHead/Neck: normocephalic, supple without masses.\nEyes: See neuro exam. \nEars Clear TM\u2019s, normal canals. \nNose/Sinuses: Normal. \nThroat/Mouth/Teeth: Normal. \nChest/Lungs: Equal BS, no rales, ronchi, wheezes or rubs. \nHeart: No gallops, rubs or murmurs. \nAbdomen: Soft, nontender, normal BS, no organomegaly. \nMale genitalia: Normal phallus, bilaterally descended testes with normal size, position, and consistency, no inguinal hernia. \nBack: Nornal. \nNeuro: Bright, articulate, inquisitive, fluent speech, excellent math and recall Reflexes symmetric, no pathologic reflexes EOMI, PERRL, bilat papilladema, ou 20/20, face symmetry, gag symmetry, corneal reflex intact Mild hypesthesia in right face. No pronator drift, symmetric strength Bilat UE intention tremor, dysmetria, and dysdiadochokinesis Bilat LE normal gait, no dysmetria, normal tandem walk\nExtremeties: no clubbing, cyanosis or edema. \nSkin: No lesions, no petechiae, no decubiti", "Findings": "Symmetric severe dilation of the third and lateral ventricles. Fourth ventricle is of normal size and contour. There is obliteration of Sylvian aqueduct by an enlarged and convex portion of the superior tectal plate. There is no reliable evidence of parenchymal enhancement here or otherwise. There is a linear increased FLAIR signal noted around the lateral ventricles suggestive of transependymal pressure or CSF flow. The orbits, skull base and pituitary fossa are all WNL. Normal intracranial flow void seen", "Differential Diagnosis": "Obstructive hydrocephalus resulting from stenosis at the aqueduct of Sylvius. Although the stenosis may be congenital the images suggest a low grade neoplasm of the tectal plate.", "Case Diagnosis": "Obstructive Hydrocephalus (at level of Sylvian aqueduct)", "Diagnosis By": "Imaging diagnosis", "Treatment & Follow Up": "Ventricular catheter placed in OR. New symptoms resolved after placement of catheter. Subsequent studies have demonstrated significant decrease in ventricular size since catheter placement. Other follow-up unknown." }, "Topic": { "Title": "Obstructive Hydrocephalus (at level of Sylvian aqueduct)", "Disease Discussion": "Hydrocephalus: increased CSF volume as a result of imbalance between production and resorption of CSF which may lead to dilatation of one or several of the CNS ventricles. Typically described as either communicating or obstructive.\n\nIn communicating hydrocephalus, there is normal CSF flow through the foramen of Monroe and the foramina of Megendie and Luschka in the ventricular system implying that the cause is either overproduction of CSF or underabsorption of CSF in the arachnoid villi.\n\nObstructive hydrocephalus occurs when there is no longer free flow of CSF throughout the ventricles leading to gross dilatation of one or more ventricles. \n\nTypically these cases are treated with ventricular shunts which allow one way flow of CSF from the high pressure ventricules to an area where it may be reabsorbed. Shunts may be routed to places such as the right atrium but are more commonly placed in the peritoneum due to decreased complications. Failure of such shunts is typically mechanical and approaches 40% within the first year of placement.", "ACR Code": "1.1", "Category": "Obstruction or Stenosis", "Keywords": "Hydrocephalusshunttectum", "Reference": "Arch Dis Child Fetal Neonatal Ed 2001; 85:F149.\nNeurosurgery 1998 Aug;43(2):294-303; discussion 303-5." } }, { "U_id": "MPX1464", "TAC": [], "MRI": [ "MPX1464_synpic35497" ], "Case": { "Title": "oligodendroglioma", "History": "Adult with seizures", "Case Diagnosis": "oligodendroglioma", "Diagnosis By": "Pathology" }, "Topic": { "Title": "oligodendroglioma", "Disease Discussion": "Neoplasm Name: oligodendroglioma \nICD-O code 9450/3 \n\nSynonyms: \n\nCell of Origin: adult oligodendrocytes \n\nWHO Grade(s): \nGrade 2 for well differentiated \nGrade 3 for anaplastic oligodendroglioma \n\nGenetics and Associations: \nChromosome 1p and 19qassays may correlate with a more positive response to chemotherapy. {INO2001}{BURGER2001} {SASAKI2002} Whereas tumors with a 10q mutations are resistant \n\nDemographics (Age, Sex, Incidence): \n\nCommon Locations: \nfrontal > temporal > parietal \narise preferentially in the cortex \n\nGross Appearance: \nwell defined soft masses, some with gelatinous mucoid regions \ncalcification is common \nhemorrhage may occur \n\nRadiology: \nOften large, superficial, heterogeneous, CT shows thick/dense calcifications, often curvilinear in the cerebral cortex \n\nHistology: \nmonotonous with moderate cellularity, perinuclear halo (a fixation artifact) creates a \\\"fried egg\\\" appearance that goes well with the \\\"chicken wire\\\" vascularity \n\nSpecial Stains: \nusually GFAP +", "ACR Code": "1.3", "Category": "Neoplasm, glial", "Keywords": "oligodendrogliomaadult oligodendrocytesanaplastic oligodendroglioma", "External Links": "rad.usuhs.edu/medpix/medpix.html?mode=single&recnum=4914&table=card&srchstr=oligodendroglioma&search=oligodendroglioma#top" } }, { "U_id": "MPX1468", "TAC": [], "MRI": [ "MPX1468_synpic41396", "MPX1468_synpic41428", "MPX1468_synpic41429" ], "Case": { "Title": "Synovial Cyst", "History": "6 months of continuous, worsening back pain\nRadiates to Right KNEE and down to Right MEDIAL ANKLE\n\u201cKnee and ankle feel funny sometimes when I walk\u201d\nPain is not affected by time of day or activity\nDenies Hx of Trauma\nPain is minimally improved by stretching and OTC pain meds", "Exam": "VSS, afebrile. \nMinimal tenderness to palpation in back and leg. \nRight Patellar Reflex diminished relative to Left side. \nAll other reflexes equal bilaterally. \nNo decreased ROM. \nWeakness on inversion of R foot. \nCBC, CMP, ESR, CRP all normal.", "Findings": "Low T1 signal round lesion adjacent to the postero-lateral aspect of the thecal sac.\nRim is iso-signal on T1 and low signal on T2. \nBright on T2-weighted images.\nCommunication with the facet joint. \nHeterogeneity of cyst likely due to proteinaceous fluid or hemorrhage within the cyst.", "Differential Diagnosis": "extruded disk fragments\nganglion cysts\nnerve sheath tumors\nseptic facet arthritis\nasymmetric ligamentum flavum hypertrophy\nsynovial cyst", "Case Diagnosis": "Synovial Cyst", "Diagnosis By": "MRI and surgical excision.", "Treatment & Follow Up": "Surgical Resection with return of full function.", "Discussion": "Conservative Management is more common as the cyst may spontaneously regress. Additional conservative treatments include facet injection with steroids and percutaneous aspiration of the cyst material under CT guidance." }, "Topic": { "Title": "Synovial Cyst", "Disease Discussion": "Synovial cysts and synovial diverticula of the lumbar spine are associated with degenerative disease involving the facet joint. They are most frequent at the L4-5 level. The cysts have thick walls, whereas the diverticula are outpouchings of the synovial membrane, and have thinner walls. Both cysts and diverticula can cause sciatica if located in the superior articular recess, and can result in low back pain if located in the inferior articular recess. Hemorrhage into the cysts may cause acute symptoms.\n\n CT can diagnose the cysts, however, they are typically more conspicuous on MRI. On CT the cysts appear as low attenuation lesions adjacent to the facet joint. In 30 percent of cases they may show wall calcification. They may also demonstrate internal vacuum phenomenon. On T1W images they are typical low to intermediate signal intensity and on T2W images the cyst wall appears as a hypointense line and the fluid has high signal intensity. \n\n These cysts can be treated surgically, however, most of the patients are elderly, and are at increased risk from surgery. Steroid injections and cyst rupture are nonsurgical forms of treatment.", "ACR Code": "3.4", "Category": "Degenerative Disease", "Keywords": "synovialdegenerative", "Reference": "Sarazin, S et al. Lumbar Facet Joint Arthrography With the Posterior Approach. Radiographics 1999 19: 93-104.\nParlier-Cuau, C et al. Symptomatic Lumbar Facet Joint Synovial Cysts: Clinical Assessment of Facet Joint Steroid Injection After 1 and 6 months and Long-term Follow-up in 30 Patients. Radiology 1999 210:509-513.\nBureau, N et al. Lumbar Facet Joint Synovial Cysts: Percutaneous Treatment with Steroid Injections and Distention - Clinical and Imaging Follow-up in 12 Patients. Radiology 2001 221: 179-185." } }, { "U_id": "MPX1467", "TAC": [], "MRI": [ "MPX1467_synpic21881", "MPX1467_synpic21882", "MPX1467_synpic21883", "MPX1467_synpic21884", "MPX1467_synpic21885" ], "Case": { "Title": "Heterotopic gray matter", "History": "54yo female with life long history of epilepsy and seizures.", "Exam": "Focal EEG with left hemispheric slowing.", "Findings": "Broad strip of soft tissue which follows gray matter on all pulse sequences, extending off the left anterior ventricle and into the high left frontal gray matter. Focal thickening of the cortical gray matter and volume loss is associated.", "Differential Diagnosis": "Heterotopia\nNeoplasm", "Case Diagnosis": "Heterotopic gray matter", "Diagnosis By": "NA", "Treatment & Follow Up": "Neurology consult.", "Discussion": "Secondary to premature arrest of neuronal migration from the germinal matrix to the cortex, islands of gray matter are disorganized within white matter, causing clinical symptoms such as siezures, weakness, spasticity, hyperreflexia, and/or developmental delay. Heterotopias are classically divided into two main types: Band and nodular. Nodular types tend to be associated with less morbidity, while Band types show severe developmental delay with an earlier onset of seizures. This process is best described on MRI where soft tissue that follows gray matter on all sequences is found within in the deep white matter." }, "Topic": { "Title": "Heterotopic gray matter in the subependymal region of the lateral ventricles. (Supependymal gray matter heterotopia)", "Disease Discussion": "Gray matter heterotopias are collections of normal neurons in abnormal locations. They result from an arrest of the normal outward radial migration of neurons. Therefore, one could say that all neuronal migration anomalies are heterotopias. However, the term heterotopia is restricted in its use to neurons that lie either in the subependymal region or within the cerebral hemispheric white matter.\n\nSymptomatic patients with gray matter heterotopias almost always present with a seizure disorder. Developmental delay may be present if the arrest of neuronal migration has been extremely severe or if associated anomalies are present. MR is extremely sensitive to the presence of heterotopias; therefore, incidental heterotopias are now occasionally identified in patients who are minimally symptomatic or asymptomatic.\n\nThree major forms of heterotopic gray matter have been described: subependymal nodules (Films .1 and .2); deep white matter nodules (Films .3 and .4); and deep bands of gray matter (band heterotopia) embedded in the white matter. Films .5 and .6 show a band heterotopia in which a circumferential band of ectopic neurons sits within the cerebral hemisphere. Normal white matter tracts separate this band from the lateral ventricles and from the overlying cortex. Because they are very symmetric, band heterotopias are often overlooked by inexperienced imagers. A high index of suspicion is necessary to make the diagnosis.", "ACR Code": "1.9", "Category": "Congenital, malformation", "Keywords": "heterotopiasubependymal" } }, { "U_id": "MPX1500", "TAC": [], "MRI": [ "MPX1500_synpic19061", "MPX1500_synpic19062" ], "Case": { "Title": "ACL Tear with lateral femoral notch sign", "History": "18 y/o female with history of chronic pain with exercise. No history of specific trauma.", "Exam": "Noncontributory", "Findings": "Figure 1: Lateral radiograph in an 18 year old female with chronic pain during exercise. \nFigure 2: Sagital PD shows a \u201clow lying\u201d ACL consistent with tear. \nFigure 3: Sagital PD with FS shows an ostoeochondral defect of the lateral femoral condyle corresponding to the radiographic deep lateral femoral notch.", "Differential Diagnosis": "Normal Variant\nOsteochondral defect, nontraumatic vs traumatic", "Case Diagnosis": "ACL Tear with lateral femoral notch sign", "Diagnosis By": "MRI" }, "Topic": { "Title": "Lateral Femoral Notch Sign", "Disease Discussion": "The lateral femoral notch (lateral condylopatellar sulcus) is normally a shallow groove in the mid lateral femoral condyle. The groove is formed by the junction of the tibiofemoral and patellofemoral curvature. The sulcus is typically less than 2mm in depth and is more conspicuous than the medial sulcus due to its parallel alignment with the x-ray. The depth of the lateral sulcus can be measured by drawing a line tangential to the sulcus on the articular surface. The \u201clateral femoral notch sign\u201d is a result of anterior subluxation of the tibia with impaction of the lateral femoral condyle on the posterolateral tibial plateau. This pattern of injury is described as \u201ckissing contusions\u201d. \n\nThe finding of a deep lateral femoral notch has been associated with anterior cruciate ligament tears. Cobby et al found that a sulcus 1.5mm or deeper is a reliable indirect sign of a torn ACL. However, this sign was only present in 12% of patients with ACL tear. Garth et al also found a statistically significant association with lateral meniscus tears as well, in particular the anterior horn. \n\nWhile the lateral femoral notch sign occurs infrequently with ACL tears, careful attention to this area on the lateral radiograph of the knee can be a reliable indicator of internal deraingement of the knee.", "ACR Code": "4.4", "Category": "Trauma", "Keywords": "Lateral Femoral NotchACL TearKnee", "Reference": "1)\tCobby MJ, Schweitzer ME, Resnick D. The Deep Lateral Femoral Notch: An Indirect Sign of a Torn Anterior Cruciate Ligament. Radiology. 1992 Sep;184(3):855-8. \n2)\tDelzell PB, Schils JP, Recht MP. Subtle Fractures About the Knee: Innocuous-Appearing yet Indicative of Significant Internal Derangement. AJR Am J Roentgenol. 1996 Sep;167(3):699-703.\n3)\tGarth WP, Greco J, House MA. The Lateral Notch Sign Associated with Acute Anterior Cruciate Ligament Disruption. Am J Sports Med. 2000 Jan-Feb;28(1):68-73.\n4)\tPao DG. The lateral Femoral Notch Sign. Radiology. 2001 Jun;219(3):800-1." } }, { "U_id": "MPX1503", "TAC": [], "MRI": [ "MPX1503_synpic29643", "MPX1503_synpic29644", "MPX1503_synpic29645" ], "Case": { "Title": "Osteoid osteoma", "History": "29-year-old man with 3 year history of gradually worsening right medial thigh pain, eventually requiring the use of crutches for ambulation. Pain was worse at night, but never woke him from sleep. NSAIDs provided temporary relief of symptoms.", "Exam": "Physical exam revealed moderate tenderness to palpation over the right medial mid-thigh, and a 2-3 cm deep, firm, non-mobile mass palpable in the same region. The patient demonstrated full range of motion of his right lower extremity, however, pain was exacerbated by forced extension of the right knee.", "Findings": "AP and lateral (lateral not shown) radiographs of the right femur demonstrated a zone of cortical thickening with a smooth contour along the medial aspect of the distal right femoral metadiaphysis (Fig 1). A central lucency measuring 2.5 cm craniocaudal can be seen with a small component of associated cortical penetration. No surrounding soft tissue abnormalities were evident. \n\nMR T1 coronal image (Fig. 2) demonstrates the wide cortical thickening with associated cortical penetration. \n\nFollow-up MR imaging validated the cortical thickening as low signal intensity. On T2-weighted images a nidus in the mid femoral shaft was noted with high signal intensity and enhancement following administration of intravenous gadolinium (Figs. 3&4). There is marked bone production medially, with adjacent bone marrow edema involving the mid femoral shaft.\n\nNuclear medicine bone scan (Fig. 5)reveals intense focal uptake eccentrically in the right distal third of the femur.", "Differential Diagnosis": "Stress fracture\nFibrous dysplasia\nChronic osteomyelitis\nOsteosarcoma \nBrodie's abscess \nBone island\nOsteoblastoma", "Case Diagnosis": "Osteoid osteoma", "Diagnosis By": "Radiogaphic findings and clinical presentation", "Treatment & Follow Up": "Treatment usually follows one of three methods: surgical, medical, and percutaneous. Traditional surgical treatment has a limited success rate of 60% due to complications identifying lesions intraoperatively, leading to incomplete removal and possible recurrence. Medical management relies on NSAIDs while awaiting spontaneous regression under observation. The time to regression is unpredictable. CT-guided percutaneous radiofrequency ablation has become the treatment of choice for most osteoid osteomas located in the appendicular skeleton and pelvis, and a success rate of 91% has been demonstrated. After needle biopsy, the radiofrequency electrode is introduced under CT guidance and the tip is heated to 90?C and maintained for 3-6 minutes. This technique is limited because the electrode must be positioned at least 1 cm away from major nerves. Therefore, lesions in some locations such as the hand or vertebral column make poor candidates." }, "Topic": { "Title": "Osteoid osteoma", "Disease Discussion": "Osteoid osteoma is a benign tumor of the bone, which accounts for approximately 12% 2of all benign skeletal tumors. Over 50% of the time this tumor occurs in the proximal femur and tibia with another 13% occurring in the vertebral columns, especially the posterior elements.1 Generally, these lesions occur in the intracortical and diaphyseal portions of the long bones, although they can occur in the metaphysis of the bone as well.2 The typical history associated with an osteoid osteoma is that of a person in his or her teens to twenties with nocturnal pain which responds well to aspirin.2,3 The radiologic findings of this tumor classically consist of a small (usually less than 1.5 to 2 cm) sclerotic lesion with a cortically based radiolucency (nidus).2 Surrounding the sclerosis is cortical thickening which is secondary to an extensive surrounding inflammatory response.2 While this appearance may be evident on plain film, often a CT or MRI is necessary to identify these characteristic changes, however, MRI should be used with the understanding that this method of imaging can make the appearance of an osteoid osteoma confusing. MRI will show the sometimes extensive bone marrow reactions (which correlate with replacement of normal marrow with fibrous tissue, inflammatory cells, and hypervascularity) and soft tissue inflammation which are associated with an osteoid osteoma and the calcified nidus is often not seen with this imaging modality. Instead, MRI can suggest that a more aggressive process is occurring, such as malignancy, infection, or fracture.2 Intra-articular osteoid osteomas create problems not seen with the typical diaphyseal lesion. These can cause joint effusion and lymhoproliferative synovitis, and may suggest an arthritic condition. Indeed, this may lead to osteoarthritis in up to half of these patients.2 In the diagnosis of osteoid osteoma, the classic appearance on plain film or CT in addition to the classic history which appears in this case generally makes the diagnosis for the radiologist and the clinician. However there are several important other processes which are necessary to rule out. The most important of these processes is an osteosarcoma. This condition typically will not have the central nidus of calcification, but more importantly it will not respect the boundaries which an osteoid osteoma respects and stay in the cortex of the bone. While the pain may occur more strongly at night, the patient will typically not obtain strong relief from aspirin or other NSAIDs, as he or she will with an osteoid osteoma.Of the conditions which do respect the boundaries of the bone and are localized to the cortex, there are only three possibilities: osteiod osteoma, Langerhan\u2019s cell histiocytosis, and Brodie\u2019s abscess.2 Langerhan\u2019s cell histiocytosis typically occurs in the skull and spine, with typical lesions being lytic with well defined margins. Skull lesions have sharply defined punched out boarders (giving rise to \u201cgeographic skull\u201d); spine lesions lead to variable compression of the vertebral bodies.2 Brodie\u2019s abscess is a subacute osteomyelitis that commonly occurs as a well defined osteolytic metaphyseal lesion. It has a sclerotic margin that fades peripherally, creating a \u201cfuzzy\u201d appearance. There is no central nidus. Occasionally Brodie\u2019s abscess occurs as a serpiginous lucency in the metaphysis of the long bone. These findings are often pathognomonic on plain fims. The most common causative organism is S. aureus. 4", "ACR Code": "4.3", "Category": "Neoplasm, benign", "Keywords": "Osteoid osteoma", "Reference": "1. Luedtke LM, Flynn JM, Ganley TJ, Hosalkar HS, Pill SG, Dormans JP: Pediatric Musculoskeletal Radiology. Rad Clin of North America; July 2001; 39:4.\n2. Nomikos GC, Murphey MD, Kransdorf MJ, Kancroft LW, Peterson JJ: Primary bone tumors of the lower extremities. Rad Clin of North America; Sep 2002; 40:5.\n3. Nigrovic PA, Wilking AP: Overview of hip pain in childhood. Www.UpToDate.com. Aug 2002.\n4. Tehranzadeh J, Wong E, Wang F, Sadighpour M: Imaging of Musculoskeletal and Spinal Infections. Rad Clin of North America; Mar 2001; 39:2." } }, { "U_id": "MPX1515", "TAC": [], "MRI": [ "MPX1515_synpic16277", "MPX1515_synpic16278" ], "Case": { "Title": "Spinal meningioma", "History": "50 year old woman with neck pain", "Findings": "Axial post-gadolinium T1W images of the cervical spine demonstrated a homogenously enhancing mass that displaces the spinal cord to the right. T2W images of the cervical spine demonstrated an extramedullary-intradural ovoid, isointense mass.", "Differential Diagnosis": "MANDELINS: M(meningioma, mets), A (arachnoid cyst), N (neurofibroma), D (dermoid cyst), E (epidermoid, ependymoma), L (lipoma), IN (infection), S (schwannoma)", "Case Diagnosis": "Spinal meningioma" }, "Topic": { "Title": "Spinal meningioma", "Disease Discussion": "Meningiomas account for approximately 25% of spinal canal lesions. They can occur at any location throughout the spine, but predominate in the thoracic region (probably because this is the largest segment). \n\nThe usual location is extramedullary-intradural, however, an extradural component may exist. \n\nThere is a female preponderance of 4:1, and the average age is 45 years.\n\nMultiple meningiomas raise the possibility of neurofibromatosis type 2. \n\nTreatment consists of complete excision if possible. Radiation therapy is used if the meningioma is malignant or surgically inaccessable.\n\nOn T1W MR meningiomas are hypointense. The lesions enhance, and often a dural tail is seen. They may contain calcium.", "ACR Code": "3.3", "Category": "Neoplasm, non-glial", "Keywords": "meningiomaintradural-extramedullary", "Reference": "Grossman RI and Yousem DM: Neuroradiology-The Requisites, St Louis, Mosby 1994, p489\nBrant W and Helms C: Fundamentals of Diagnostic Radiology, 2nd ed Lippincott, Philadelphia 1999, pp 255-256." } }, { "U_id": "MPX1502", "TAC": [], "MRI": [ "MPX1502_synpic40651", "MPX1502_synpic40652", "MPX1502_synpic40653", "MPX1502_synpic40654", "MPX1502_synpic40655", "MPX1502_synpic40656" ], "Case": { "Title": "Clival chordoma", "History": "20 year-old female with a history of diplopia presents to the emergency department.", "Exam": "N/A", "Findings": "Multiple representative MR images are demonstrated. A sagital T1 pre-contrast shows a predominantly low signal intensity midline extra-axial clival mass with some mass effect on the pons. An axial diffusion weighted image demonstrates no restricted diffusion. Coronal FLAIR and axial T2 images demonstrate that the mass is predominantly high in signal intensity. Post gadolinium sagital and axial (fat sat) T1 images deomstrate enhancement within the mass.", "Differential Diagnosis": "Chordoma\nMetastatic disease\nMultiple myeloma\nChondrosarcoma\nCholestatoma", "Case Diagnosis": "Clival chordoma", "Diagnosis By": "Pathology", "Treatment & Follow Up": "The patient underwent surgical resection of the mass and follow-up MR examinations have demonstrated no evidence of residual disease or recurrence.", "Discussion": "Please see factoid." }, "Topic": { "Title": "Clival Chordoma", "Disease Discussion": "Chordomas are rare, histologically benign but aggressive tumors arising from remnants of the embryonic notochord. They usually lie in the sacrococcygeal area (50%) or the clivus (35%). These tumors most often affect patients greater than 30 years of age.\n\nClival chordomas comprise less that 2% of intracranial tumors. They typically arise within the bone and are therefore extradural. They also invade the surrounding bone and may extend to compress adjacent structures such as cranial nerves and the brain stem.\n\nClival chordomas are usually of a gelatinous consistency and may have secondary hemorrhage and necrosis. These changes can be present throughout the tumor. \n\nMicroscopically, physaliphorus cells are seen, that contain large cytoplasmic vacuoles rich in glycogen and mucin. These are separated into nests by fibrous sheets. \n\nImmunohistochemistry reveals positive staining for cytokeratin and epithelial membrane antigen. Chondroid chordomas, a more benign subtype, typically contains hyaline cartilage.\n\nBoth CT and MR are used to diagnose and delineate the extent of clival chordomas. On CT, adjacent bone destruction is seen, and areas of low attenuation in the mass may represent the gelatinous matrix. Calcification is occasionally seen inside the mass.\n\nOn MR, high signal intensity is seen on T2-weighted images. These tumors are usually iso or hypo-intense on T1-weighted imaging with areas of occasional high signal intensity, representing blood or mucin.\n\nAfter administration of gadolinium contrast, these tumors typically demonstrate heterogenous enhancement, and typically have a \u201choneycomb\u201d appearance, due their lobular organization.\n\nMR also is useful to characterize possible internal carotid or vertebrobasilar encasement.\n\nTreatment for clival chordomas usually consists of a dual approach: surgical removal and radiation. Depending upon direction of growth of the chordoma, a transphenoidal, transmaxillary, transbasal, cranioorbitozygomatic, or transcondylar approach may be used. Occasionally, subtotal resection of the mass is performed, due to high risk of injury to adjacent neurovascular structures. Potential complications include stroke, cranial nerve palsy, CSF leak, and meningitis.\n\nProton beam therapy has been the mainstay of radiation treatment for clival chordomas. Any form of radiation is given postoperatively, and in most cases, traditional forms of treatment are avoided to limit the amount of injury to vital surrounding structures. A study performed by Pearlman and Friedman showed an 80% local control rate with a minimum of 80 Gy and only 20% control rate with 40 to 60 Gy.\n\nAlthough histologically benign, clival chordomas have a high rate of recurrence, which may be related to sub-total resection. Distant metastases are uncommon. Survival rate approaches 50% at five years and 30% at ten years. Greater extent of resection is correlated with improved survival.", "ACR Code": "1.3", "Category": "Neoplasm, non-glial", "Keywords": "chordomaclivusskull base", "Reference": "DeMonte F, Diaz, E, Callender D, Suk I. Transmandibular, circumglossal, retropharyngeal approach for chordomas of the clivus and upper cervical spine. Neurosurg Focus. 10 (3): article 10, 2001.\nAl-Mefty O, Borba L. Skull base chordomas: A management challenge. J Neurosurg 86:182-189, 1997.\nKaplan M, Fischbein N, Harsh G. Anterior skull base surgery. Otolaryng Clinics N America. 38:107-131, 2005." } }, { "U_id": "MPX1529", "TAC": [], "MRI": [ "MPX1529_synpic39418", "MPX1529_synpic39419", "MPX1529_synpic39420" ], "Case": { "Title": "Maple syrup urine disease", "History": "1 week old baby boy with poor feeding, now developing increasing vomiting. His mother reports a strange odor to his urine.", "Exam": "Evaluation of plasma amino acids revealed elevation of branched chain amino acids, including alloisoleucine.", "Findings": "\u2022 Axial T2 weighted images reveal T2 prolongation, consistent with edema, in the deep cerebellar white matter, dorsal brainstem, cerebral peduncles, and posterior limb of the internal capsule.\n\u2022 MR spectroscopy reveals a broad peak at 0.9 ppm representing branched chain amino acids and branched chain alpha ketoacids. An abnormal peak is also present at 1.33 ppm consistent with lactate.", "Differential Diagnosis": "\u2022 Maple syrup urine disease\n\u2022 Other aminoacidopathies presenting in the first week of life", "Case Diagnosis": "Maple syrup urine disease", "Diagnosis By": "Laboratory values revealing elevation of branched-chain amino acids.", "Treatment & Follow Up": "Treatment of the acute metabolic decompensation, and dietary restriction of branched chain amino acids." }, "Topic": { "Title": "Aminoaciduria", "Disease Discussion": "Phenylketonuria, tyrosinemia, maple syrup urine, citrullinemia, ornithine, argininemia, homocystinuria, methioninemia, lactic acidemia, demonstrate foci of edematous white matter on CT and MR imaging.", "ACR Code": "1.5", "Category": "Congenital, genetic", "Keywords": "Maple Syrup Urine Diseasephenylketonuriahomocystinuria" } }, { "U_id": "MPX1537", "TAC": [], "MRI": [ "MPX1537_synpic39394", "MPX1537_synpic39395", "MPX1537_synpic39396" ], "Case": { "Title": "Salter-Harris Fracture", "History": "10 year old boy status post lateral blow while playing football.", "Exam": "N/A", "Findings": "PA and lateral radiographs of the left knee demonstrate an abnormal linear thin sclerotic line at the medial aspect of the intertorchanteric portion of the left femur as well as a joint effusion. Sagital and coronal T2 fat suppressed images demonstrate diffuse high T2 signal in the bone marrow consistent with edema in the distal femoral metaphysis and proximal tibial plateau. Additionally on the coronal T1 sequences there is an abnormal linear region of low signal extending from the joint space to the epiphysis at the intertrochanteric region of the femur. Additionally there is slight assymetric widening of the physis medially. These findings are consistent with a Salter Harris type III fracture of the distal femur.", "Differential Diagnosis": "Salter Harris type III fracture", "Case Diagnosis": "Salter-Harris Fracture", "Diagnosis By": "MRI", "Treatment & Follow Up": "Conservative management with orthopaedic follow up.", "Discussion": "Please see factoid." }, "Topic": { "Title": "Salter-Harris Fracture", "Disease Discussion": "In pediatric patients, fractures through the physis represent a serious clinical concern as they can lead to potentially poor outcomes if they are not accurately diagnosed and treated appropriately. The Salter Harris radiologic classification system of physeal fractures is the most commonly utilized method of describing these fractures. This system divides fractures into five types depending upon the involvement of the physis, epiphysis, or metaphysis.\n\nType I fractures are transverse through the hypertrophic zone of the physis and results in widening of the physis. In these injuries, the growing zone of the physis is typically not disturbed and overall growth disturbance is uncommon.\n\nType II fractures traverse the metaphysis and physis, but do not involve the epiphysis. This represents the most common type of physeal fracture, accounting for up to 75% of injuries. While these may result in mild limb foreshortening, functional limitations are rare.\n\nType III fractures traverse the physis and the epiphysis, but spare the metaphysis. These represent a more serious clinical issue, as they tend to involve the articular cartilage and have a greater predisposition for growth arrest.\n\nType IV fractures involve the epiphysis, physis, and metaphysis. Like the type III injury, these fractures have a greater predisposition for growth arrest.\n\nType V fractures result from a crush injury to all or part of the physis. Initial diagnosis may be dificult radiographically without specific clinical data. Often the diagnosis is made in follow up, after partial or complete boney fusion across the physeal plate has ensued.\n\nWhile it has been estimated that nearly 30% of these fractures result in growth plate disturbance, only 2% result in significant functional disability.", "ACR Code": "4.4", "Category": "Trauma", "Keywords": "Salter-HarrisPediatric traumaepiphysis", "Reference": "Donnelly, LF. Fundamentals of Pediatric Radiology. WB Saunders, Philadelphia 2001.", "External Links": "www.emedicine.com/radio/topic613.htm" } }, { "U_id": "MPX1550", "TAC": [], "MRI": [ "MPX1550_synpic17339" ], "Case": { "Title": "Adamantinomatous craniopharyngioma", "History": "This 70 year old man had progressive visual loss over 3 to 5 years. He denied headache, nausea or vomiting. Examination revealed no light perception in either eye. The remainder of his cranial nerves were intact as were his motor and sensory examinations.", "Findings": "Fig 1. Contrast enhanced axial MRI showing a partially cystic suprasellar mass.\n\nFig 2. Contrast enhanced coronal MRI showing the partially cystic suprasellar mass. \n\nFig 3. Histological section of the resected tumor showing irregular expanses of squamous epithelium in which basal cells and stellate cells can be seen. Also present are bands of eosinophilic fibrous tissue.\n\nFig 4. In other areas, there were large masses of \u201cwet\u201d keratin in which ill-defined remnants of nuclei can be seen.", "Differential Diagnosis": "\u2022 pituitary adenoma\n\u2022 craniopharyngioma\n\u2022 chordoma\n\u2022 hypothalamic glioma", "Case Diagnosis": "Adamantinomatous craniopharyngioma", "Discussion": "This is somewhate unusual, since the adamantinomatous craniopharyngioma is more common in childhood. The adult squamous and papillary craniopharyngioma is usually a solid mass without calcification." }, "Topic": { "Title": "Adamantinomatous craniopharyngioma", "Disease Discussion": "Craniopharyngiomas are thought to arise from ectopic nests of stomadeal epithelium left during the embryonic development of the adenohypophysis. Craniopharyngiomas are often designated as \u201cadamantinomatous\u201d when stellate cells and keratin pearls are prominent. Although craniopharyngiomas are commonly considered as childhood tumors, they may be encountered at any age as in this elderly man.", "ACR Code": "-1.-1", "Category": "Unsure", "Keywords": "Craniopharyngiomas" } }, { "U_id": "MPX1551", "TAC": [], "MRI": [ "MPX1551_synpic35369", "MPX1551_synpic35370", "MPX1551_synpic35371", "MPX1551_synpic35372", "MPX1551_synpic35373" ], "Case": { "Title": "Nonossifying fibroma", "History": "16 year old boy presents after inversion ankle injury.", "Exam": "N/A", "Findings": "Frontal and lateral radiographs of the left ankle demonstrate a small longitudinal well circumscribed cortically based lytic lesion at the lateral aspect of the distal tibial metaphysis. The lesion has sclerotic borders, somewhat scalloped inferiorly and medially, no periosteal reaction, and it has no appreciable associated soft tissue abnormality. There is no fracture or dislocation.\n\nSelected MRI images demonstrate the lesion is isointense to muscle on both T1 and T2 weighted images, does not demonstrate fat supression. It shows mild uniform enhancement with gadolinium.\n\nThe soft tissues and remainder of the osseous structures are unremarkable.", "Differential Diagnosis": "\u2022 Non-ossifying fibroma (strongly favored)\n\u2022 Eosinophilic granuloma\n\u2022 Osteoid osteoma\n\u2022 Infection", "Case Diagnosis": "Nonossifying fibroma", "Diagnosis By": "Radiographic appearance and patient age, as well as typical MRI findings.", "Treatment & Follow Up": "None needed.", "Discussion": "Please see topic." }, "Topic": { "Title": "Nonossifying fibroma", "Disease Discussion": "Nonossifying fibroma (NOF), also known as fibroxanthoma, is a benign proliferation of fibroblasts with unknown etiology. \n\nDemographics: NOFs are very common and routinely found in asymptomatic children over age 2. Peak occurrence in between ages 10-15 years. They are rarely found in patients over 25 years of age.\n\nDisease course: The most frequent presentation is a child with an unrelated injury whose NOF is found on plain radiographs. However, a child can sometime present with an NOF as the etiology for a primary complaint when the NOF causes noticeable deformity or pain. Rarely, an NOF presents as pathologic fracture, usually when the lesion occupies more than 50% of the bone diameter. NOFs of all presentations may increase or decrease in size before spontaneously resolving.\n\nDx: The diagnosis of NOF is usually made as an incidental finding on a radiograph obtained for other reasons. The diagnosis can be made on radiographs alone due to its characteristic appearance; a lucent, lobulated lesion that is well defined with an eccentric epicenter and defined, often sclerotic margin.\n\nDifferential Dx: \n*Fibrous cortical defect (defined as 0-2 cm and confined to cortex)\n*Osteoblastoma (suggested by ossification and calcification)\n*Adamantinoma (suggested by medullary invasion)\n*Osteoid osteoma (usually has a central nidus and is painful) \n\nTreatment: Unless symptomatic, these lesions are managed conservatively and no work-up is indicated. If a malignant process is suspected, biopsy will yield the definitive diagnosis. In the case of larger lesions where pathologic fracture has occurred or because of the size of the NOF, the patient may be prone to pathologic fracture, curettage with bone graft is performed. Such intervention is usually reserved for cases in which the lesion occupies more than 50% of the diameter of a weight-bearing bone, or the lesion is greater than 33 mm in diameter.", "ACR Code": "4.3", "Category": "Neoplasm, benign", "Keywords": "nonossifying fibromafibrous cortical defect", "Reference": "Levine SM. Cortical Lesions of the Tibia: Characteristic Appearances on Conventional Radiography. RadioGraphics 2003; 23: 157. \n\nResnick D. Diagnosis of bone and joint disorders. Saunders, New York, 2002, pp. 3767-73." } }, { "U_id": "MPX1561", "TAC": [], "MRI": [ "MPX1561_synpic26918", "MPX1561_synpic26919" ], "Case": { "Title": "Scheuermann Disease with Kyphosis", "History": "27 year old man with back pain.", "Exam": "N/A", "Findings": "Anterior wedge deformity of multiple contiguous thoracic vertebral bodies.", "Differential Diagnosis": "Scheuermann kyphosis, insufficiency fractures, and pathologic fractures.", "Case Diagnosis": "Scheuermann Disease with Kyphosis", "Diagnosis By": "Plain film and MRI", "Treatment & Follow Up": "N/A", "Discussion": "Please see factoid for discussion." }, "Topic": { "Title": "Scheuermann Kyphosis", "Disease Discussion": "Scheurmann first described the clinical findings of a rigid kyphosis associated with wedging of the vertebral bodies in 1920. In 1964, Sorensen defined the radiographic criteria associted with Scheuermann kyphosis as anterior wedging of at least 5 degrees in at least three adjacent vertebral bodies. \n\nTraditionally this disorder is described in the thoracic spine. Additional radiographic characteristics of Scheuermann kyphosis include endplate irregularities and Schmorl's nodes.\n\nScheuermann kyphosis is estimated to affect approximately 4 to 8 percent of the general population, with a slightly higher incidence reported in males when compared to females. \n\nClinical presentation typically occurs in early adolescence with parents noticing the deformity, or with children complaining of back pain. Pain associated with this deformity is characteristically located just distal to the apex of the deformity and radiates laterally in a paraspinal pattern. \n\nThe etiology of this disorder remains unclear, although most investigators agree that mechanical factors involving axial loading play some role in the pathogenesis.\n\nTreatment options for Scheuermann kyphosis depend upon the degree of deformity and its associated symptoms. The typical approach includes conservative management with non-steroidal pain medications, physical therapy, and bracing, and more aggressive treatment with surgical correction.", "ACR Code": "3.9", "Category": "Idiopathic or Unknown", "Keywords": "scoliosiswedge deformitythoracic kyphosis", "Reference": "Wegner DR, Frick SL. Scheuermann Kyphosis. Spine 1999; 24(24):2630-2646", "External Links": "www.emedicine.com/orthoped/topic555.htm" } }, { "U_id": "MPX1559", "TAC": [], "MRI": [ "MPX1559_synpic34909", "MPX1559_synpic34910" ], "Case": { "Title": "Non-displaced transverse fracture of right femoral neck.", "History": "A 76-year-old woman presents to her primary care manager with right hip pain. No known history of trauma.", "Exam": "Physical exam information is not available.", "Findings": "Anterior-posterior radiograph of the pelvis, and frog-leg radiograph of the right hip show diffusely diminished bone density of the pelvis and right hip. No periosteal reaction or fracture is seen.\n\nCoronal T1-weighted MR image of the pelvis demonstrates linear low-signal-intensity area extending from the medial cortex of the right femoral neck into the medullary canal and is consistent with fracture. On the T2-weighted fat-saturated coronal MR image, more extensive area of high-signal-intensity is present consistent with a combination of the fracture and post-traumatic edema and inflammation.", "Differential Diagnosis": "Non-displaced transverse fracture of right femoral neck\n\u2022 Stress fracture (abnormal stress to normal bone) \n vs. \n\u2022 Insufficiency fracture (normal stress to abnormal bone)", "Case Diagnosis": "Non-displaced transverse fracture of right femoral neck.", "Diagnosis By": "Confirmed by MRI.", "Treatment & Follow Up": "The patient underwent open reduction and internal fixation of the fracture.", "Discussion": "Hip fractures are very common, and, in the United States, =occur in more than 300,000 people annually. The incidence of hip fractures is rising in parallel with the rising age of our population, leading to increased disability and medical cost. Advancing age is the greatest risk factor for hip fractures; other risk factors include being Caucasian and female, having a maternal history of hip fracture, having decreased bone density, visual impairment or dementia, a sedentary lifestyle, smoking, a history of glucocorticoid, benzodiazepine or anticonvulsant use, or a history of hyperthyroidism. \n\nHip fractures often have a significant impact on the life of the person affected. Between 15-20% of elderly patients with a hip fracture die within one year of the injury. Half of the patients with a hip fractures who had previously lived independently are unable to do so following the fracture. In addition to the significant mortality, patients with hip fractures and their surgical correction are at risk for deep venous thrombosis and pulmonary embolism, pressure sores, delirium, and global deterioration of functionality. \n\nPatients with hip fractures often have a history of a fall followed by pain in the hip, groin, buttocks or back. They may have difficulty walking or bearing weight after the fall. On physical exam, there may be shortening and external rotation of the affected lower extremity. A history of trauma is not necessary, however, and patients with risk factors who present with hip pain or difficulty bearing weight should be evaluated thoroughly for an occult hip fracture and for osteoporosis that is often found in the elderly age group.\n\nTo evaluate for possible femoral fractures, radiographs should be done first. However, in patients with negative radiographs but a high clinical suspicion for fracture, MR imaging is the best imaging test to diagnose a fracture missed on plain radiographs. Early diagnosis is important in order that the hip fractures can be surgically corrected, preferably within 2-3 days of injury in order to reduce hospitalization and morbidity. \n\nIngari et al showed that low-signal-intensity on T1-weighted MR images were correlative with non-displaced fractures induced in cadavers. In contrast, the high-signal-intensity that is seen on the T2-weighted MR image may represent the fracture and secondary post-traumatic edema and inflammation and may appear more extensive than the actual fracture. MR should therefore be acquired without delay if plain radiographs are negative but clinical suspicion remains high.\n\nIf MR imaging is not available, bone scans of the hip can be useful for identifying proximal femoral fractures. However, bone scans demonstrate fracture because of the increased metabolic activity surrounding the injury; in the elderly, the bone scans may not be positive until 3 days after injury. This delay can have a negative impact on the patient\u2019s ultimate recovery. Therefore if MR imaging is available, it is the imaging test of choice in the patient with suspected hip fracture but with negative radiographs.\n\nHip fractures in the elderly have a significant rate of morbidity and mortality. Fractures of the femoral neck can lead to avascular necrosis of the femoral head due to disrupted blood supply from the lateral circumflex femoral artery. Fractures can also lead to malunion or nonunion between fragments as well as degenerative changes in the hip joint. Also, as mentioned previously, people who suffer a hip fracture are at significant risk for developing deep venous thrombosis or pulmonary embolism, pressure sores, delirium, infections, and decreased conditioning and functionality. Extended periods of hospitalization and limited mobility combine to create a major obstacle to the elderly person who may never be able to recover fully.\n\nPreventive measures are important in preventing hip fractures in the elderly. The USPSTF recommends routine bone mineral density screening for women after age 65 years, and after age 60 years in high risk women. Treatment of those with decreased bone density with bisphosphonates has been shown to reduce fracture risk. High-dose oral vitamin D supplementation has also been shown to reduce the risk of fractures. Modifiable lifestyle factors include smoking cessation and weight-bearing exercise. \n\nIn patients with hip fractures, early diagnosis and surgical fixation have been shown to reduce hospitalization and adverse events. Aggressive physical therapy is also very important in returning a patient to a functional level as close to baseline as possible. Plain radiographs are the first diagnostic imaging study for evaluating for hip fracture. However, if these are negative but clinical suspicion remains high for a fracture, MR imaging should be done for definitive diagnosis. \n\nReferences:\n\nBeaupre L, Jones A, Saunders D, Johnston W, Buckingham J, Majumdar S. Best practices for elderly hip fracture patients: a systematic overview of the evidence. J Gen Intern Med 2005; 20:1019\u20131025.\n\nBischoff-Ferrari H, Willett W, Wong J, Giovannucci E, Dietrich T, Dawson-Hughes B. Fracture prevention with vitamin D supplementation. JAMA 2005; 293: 2257-2264.\n\nBrunner L and Eschilian-Oates, L. Hip fractures in adults. Am Fam Physician 2003:67:537-42.\n\nCummings SR, Nevitt MC, Browner WS, Stone K, Fox KM, Ensrud KE, et\nal. Risk factors for hip fracture in white women. Risk factors for hip fracture in white women. N Engl J Med 1995;332:767-73.\n\nFrihagen F, Nordsletten L, Tariq R, Madsen J E. MRI diagnosis of occult hip fractures. Acta Orthopaedica 2005; 76 (4): 524\u2013530.\n\nIngari J V, Smith D K, Aufdemorte T B, Yaszemski M J. Anatomic significance of magnetic resonance imaging findings in hip fracture. Clin Orthop 1996; (332): 209-\n14.\n\nRao, S and Cherukuri M. Management of hip fracture: the family physician\u2019s role. Am Fam Physician 2006;73:2195-200, 2201-2." }, "Topic": { "Title": "Right femoral neck fracture", "Disease Discussion": "Patient had complete fracture of the R femoral neck with posterior rotation of the femoral head. Should have heightened suspicion in any elderly patient with hip pain even when there are negative radiographs. MRI or bone scan can be done to look for occult femoral neck fractures when suspicion is high. MRI is most sensitive at time of presentation. Age related bone loss is believed to be the most important factor in determining the incidence of femoral neck fractures. Fractures of the femoral neck occur primarily from low-energy injuries in the elderly and high-energy injuries in younger patients.", "ACR Code": "4.4", "Category": "Trauma", "Keywords": "femoral neck fracture", "Reference": "Rudman N, McIlmail D: Emergency Department Evaluation and Treatment of Hip and Thigh Injuries. Emergency Medicine Clinics of North America Vol 18 Number 1 February 2000.\n\nMarx: Rosen\u2019s Emergency Medicine: Concepts and Clinical practice, 5th ed. 2002." } }, { "U_id": "MPX1570", "TAC": [], "MRI": [ "MPX1570_synpic49446", "MPX1570_synpic49447", "MPX1570_synpic49448", "MPX1570_synpic49449", "MPX1570_synpic49450" ], "Case": { "Title": "Parsonage-Turner Syndrome", "History": "33 y.o. man with right shoulder pain and decreased range of motion. No history of trauma or overuse.", "Exam": "Right sided shoulder weakness", "Findings": "\u2022 On T1 weighted imaging, moderate muscular body atrophy and fatty replacement within a single or multiple rotator cuff or shoulder muscles. \u2022 Abnormal increased increased T2 or STIR signal will also be seen in these affected muscles.", "Differential Diagnosis": "\u2022 Traumatic neuropraxia\n\u2022 Neuropathy secondary to C-spine DJD\n\u2022 Non-specific myositis\n\u2022 Muscle belly trauma\n\u2022 Nerve compression\n\u2022 Rotator cuff tear", "Case Diagnosis": "Parsonage-Turner Syndrome", "Diagnosis By": "Characteristic imaging findings.", "Treatment & Follow Up": "OTC analgesics can be used to control any associated pain in the acute setting. Otherwise, no directed therapy is indicated.", "Discussion": "Parsonage-Turner syndrome (PTS), also known as acute brachial neuritis and neuralgic amyotrophy, defines a set of symptoms resulting from inflammation of the brachial plexus. \n\nPTS is idiopathic in etiology, but thought to be post viral and may follow illness, surgery, or immunization. Up to 50% report viral illness or vaccination that occurred days to weeks prior to onset of symptoms.\n\nParsonage Turner syndrome presents as the acute onset of severe shoulder pain followed shortly thereafter by weakness of at least one shoulder muscle. Bilateral involvement has been reported for as many as one third of patients. It can be confused clinically with cervical spondylosis, rotator cuff tear, shoulder impingement syndrome, and acute calcific tendonitis. Failure to identify PTS may result in inappropriate treatment or potnentially unnecessary surgery.\n\nPTS may involve single or multiple nerves originating from the brachial plexus. The suprascapular is the most commonly affected (97% of cases), followed by the axillary (50% of cases) and far less commonly the subscapular and long thoracic. In cases involving the suprascapular nerve, the supraspinatous and infraspinatous muscles are affected. Inflammation of the subscapular nerve affects the subscapularis muscle. The serratous anterior muscle is affected when the long thoracic nerve is involved, and the teres minor and deltoid muscles are affected in cases involving an axillary nerve distribution.\n\nThe MR finding most typical of PTS is that of diffuse high T2 signal involving one or more muscles innervated by the brachial plexus. T1-weighted images may also show atrophy of the affected muscle(s). The pattern of muscular involvement should match the distribution(s) of one or more peripheral nerves originating from the brachial plexus\n\nNo test can be used to diagnose PTS specifically. Both electromyograms and MR images must be interpreted with consideration of the clinical history. The disorder is self-limited, but can take up to a year to resolve. Residual denervation can be seen in 10-20% of cases after 2 years.\n\n\nReferences:\n\nGaskins CM, Helms CA. Parsonage-Turner syndrome: MR imaging findings and clinical information of 27 patients. Radiology. 2006. August; 240(2): 501-7.\n\nManaster BJ, May DA, Disler DG.Musculoskeletal Imaging, The Requisites. 3rd Ed. Philadelphia: Mosby, 2007.\n\nScalf RE, Wenger DE, Frick MA, Mandrekar JN, Adkins MC. AJR Am J Roentgenol. 2007 July; 189(1):W39-44." }, "Topic": { "Title": "Parsonage-Turner Syndrome", "Disease Discussion": "Parsonage-Turner syndrome is an immune mediated reaction against lower motor neurons of the brachial plexus. It affects approximately 1% of the general population. It causes denervation change seen as high signal on fluid sensitive sequences in the early and subacute phases. This progresses to fatty atrophy in the chronic phase.\n \nIt affects all age groups save neonatal. It is more prevalent in men. It commonly presents with acute pain following illness injury or trauma.", "ACR Code": "4.2", "Category": "Inflammatory, NOS", "Keywords": "brachialneuritisParsonage Turner", "Reference": "Stoller, DW; Tirman, PF; Bredella, MA; DIAGNOSTIC IMAGING ORTHOPEDICS 1st Edition pp.(34-37) 2004." } }, { "U_id": "MPX1574", "TAC": [], "MRI": [ "MPX1574_synpic16361", "MPX1574_synpic16370", "MPX1574_synpic16371" ], "Case": { "Title": "SLAP Lesion of the Glenoid Labrum", "History": "Soft-ball player who complains of several months of right shoulder pain, aggravated by throwing the ball. No history of an acute injury.", "Exam": "No findings of shoulder instability on physical exam.", "Findings": "T1-weighted axial and coronal images with fat-saturation of the shoulder following intra-articular administration of gadolinium. The coronal image demonstrates an irregular collection of contrast extending into the normally dark triangular appearing superior labrum. Axial image demonstrates an irregular collection of contrast between the frayed appearing posterior superior labrum and the posterior glenoid. The Biceps anchor appears normal.", "Differential Diagnosis": "SLAP lesion\nSublabral foramen\nSublabral recess", "Case Diagnosis": "SLAP Lesion of the Glenoid Labrum", "Treatment & Follow Up": "Surgical repair of the torn superior labrum.", "Discussion": "The administration of intra-articular gadolinium can be helpful in clearly demonstrating a SLAP lesion on MR imaging. On the coronal images, the superior labrum normally appears as a black triangle extending off of the superior glenoid. Any signal extending into the substance of the triangle is abnormal and represents a SLAP lesion. This can be differentiated from the normal variant sublabral recess, because in a sublabral recess the contrast collection appears smooth and tapering and extends toward the base of the triangle, rather than into the substance of the triangle, as in this SLAP lesion. A sublaral foramen can be differentiated from a SLAP lesion, because a sublabral foramen occurs in the anterior quadrant rather than posterior quadrant and as in the sublabral recess, the contrast collection is smooth and tapering in appearance rather than irregular as demonstrated in this SLAP tear.\nWhen describing a SLAP lesion, it is important to describe the extent of the lesion from front to back, as well as to describe whether there is involvement of the biceps anchor. When using direct MR arthrography, the biceps anchor is usually best evaluated on the axial and sagittal images." }, "Topic": { "Title": "SLAP Lesion of the Glenoid Labrum", "Disease Discussion": "SLAP stands for Superior Labrum from Anterior-to-Posterior, (relative to the biceps tendon anchor).\n\nThere are four types of SLAP tears. In type I lesions consist of a frayed and degenerative superior labrum with a normal biceps tendon anchor. Type II lesions demonstrate detachment of the superior labrum and biceps anchor and may also be associated with anterior glenohumeral joint dislocation and anterior instability. SLAP types I and II may be difficult to separate on MRI, depending on the technique used for diagnosis. Type III lesions involve a bucket-handle tear of the superior labrum (a vertical tear through a meniscoid-like superior labrum) without extension into the biceps tendon. The biceps anchor is stable and the remaining labrum is intact. Type IV lesions also involve a bucket-handle tear associated with a meniscoid-type superior labrum, but in this case with extension into the biceps tendon. The biceps anchor and the superior labrum are well attached. A partially torn biceps tendon may displace the superior labral flap into the joint. A complex SLAP lesion may consist of a combination of two or more types, usually type II and type IV.\n\nPossible mechanisms of injury include a fall on the outstretched abducted arm with associated superior joint compression and a proximal subluxation force or a sudden contraction of the biceps tendon, which avulses the superior labrum. Repetitive stress acting through the biceps tendon or instability of the glenohumeral joint may also produce SLAP lesions. \n\nTreatment of SLAP lesions is based on the type of labral lesion present. A type I SLAP lesion is treated with arthroscopic debridement of the degenerative labrum. Treatment of a type II SLAP lesion (which involves detachment of the superior labrum and biceps anchor) addresses the avulsed labrum and reattachment of the detached biceps anchor to the superior glenoid. A suture anchor technique, for example, may be used for a type II SLAP tear.", "ACR Code": "4.4", "Category": "Trauma", "Keywords": "SLAPShoulderLabrum", "Reference": "Stoller, David W., Magnetic Resonance Imaging in Orthopaedics & Sports Medicine, Second edition, 1996, Lippincott-Raven, CD ROM" } }, { "U_id": "MPX1581", "TAC": [], "MRI": [ "MPX1581_synpic20988", "MPX1581_synpic20989", "MPX1581_synpic20990", "MPX1581_synpic21016", "MPX1581_synpic21017", "MPX1581_synpic21018" ], "Case": { "Title": "Colloid cyst.", "History": "29 year old female with worsening headaches.", "Exam": "non-focal neurologic examination.", "Findings": "11 x 11 x 13 mm nonenhancing well-circumscribed mildly T1 hyperintense and markedly T2 hypointense round mass in the anterior-superior third ventricle without ventricular enlargement.", "Differential Diagnosis": "Colloid cyst.\nAlthough other lesions can occur in this region such as ependymoma, subependymoma, giant cell astrocytoma and central neurocytoma,the imaging findings are characteristic for a colloid cyst.", "Case Diagnosis": "Colloid cyst.", "Diagnosis By": "Imaging characteristics.", "Treatment & Follow Up": "No treatment. Being followed by neurosurgery with serial examinations.", "Discussion": "The diagnosis of colloid cyst was made based on the imaging characteristics. The patient and neurosurgeon have elected conservative management at this time as her headaches have resolved and she has no evidence of ventricular obstruction currently." }, "Topic": { "Title": "Colloid (neuroepithelial) cyst of the third ventricle", "Disease Discussion": "Colloid cysts are uncommon benign cysts of the anterior superior third ventricle, which are thought to arise from embryologic tissues of the paraphysis, ependyma, or choroid plexus. These lesions typically present in young adults in the 2nd to 5th decade with complaints referable to acute or chronic hydrocephalus. Other symptoms include ataxia, memory disturbances, and gait disorders. The cyst contents include secretory and breakdown products of the epithelial lining tissue, including hemorrhage, lipid (cholesterol), hemosiderin, and CSF. \n\nOn T1-weighted MR images, these cysts vary widely from hypo- to hyperintense in comparison to normal brain. Although they may be bright on T2-weighted images, moderate to marked hypointensity is common and has been attributed to a very short T1 relaxation time or to magnetic susceptibility effect from paramagnetic substances in the cyst. On noncontrast MR, these lesions occasionally are indistinguishable by intensity from neoplasia; however, the absence of enhancement, classic location, and relative hypointensity on T2-weighted studies should suggest this diagnosis. Treatment is variable, including ventricular shunting alone, stereotactic cyst drainage, or surgical resection.\n\nOn noncontrast CT, colloid cysts are solitary, round to oval, usually hyperdense masses at the foramen of Monro with associated enlargement of one or both lateral ventricles (Film .3). Minimal or absent contrast enhancement is typical. Moderate enhancement with contrast suggests a different etiology, such as glioma, craniopharyngioma, choroid plexus papilloma, or remotely meningioma. Other cystic masses such as arachnoid or ependymal cysts will mimic CSF in density and intensity.", "ACR Code": "1.3", "Category": "Cyst, benign", "Reference": "J Neurosurg 1999 Sep;91(3):364-9\nJ Comput Assist Tomogr 1998 Jul-Aug;22(4):524-7" } }, { "U_id": "MPX1604", "TAC": [], "MRI": [ "MPX1604_synpic53489" ], "Case": { "Title": "Budd-Chiari Syndrome", "History": "Ascites of uncertain etiology.", "Findings": "MRI w/ Contrast of liver shows peripheral lack of enhancement with increased central enhancement, enlargement of the caudate lobe, and decreased signal in the hepatic vein consistent with thrombosis.\n\nDoppler ultrasound of the right upper quadrant: Intrahepatic portion of the inferior vena cava, as well as the hepatic veins, are diminutive. There is also pulsatile hepatopetal flow in the portal vein, and ascites surrounding the liver.", "Differential Diagnosis": "1. Primary sclerosing cholangitis.\n2. Hepatic cirrhosis.", "Case Diagnosis": "Budd-Chiari Syndrome", "Diagnosis By": "Confirmed via clinical presentation and characteristic radiograohic findings.", "Treatment & Follow Up": "This patient received Lovenox with significant improvement.", "Discussion": "This case highlights Budd-Chiari syndrome as a cause of postpartum ascites." }, "Topic": { "Title": "Budd-Chiari Syndrome", "Disease Discussion": "NOTE: Please EDIT the CATEGORY and LOCATION - Above\n\nYou may use the template below - or [Erase] for a blank page.\n\nLesion/Condition Name: Budd-Chiari Syndrome\n\nCell of Origin:\n\nWHO Grade(s):\n\nSynonyms:\n\nICD-0 code: \n\nAssociations/Predisposing Factors:Myeloproliferative disorders, pregnancy, malignancy, infection.\n\nCommon Locations:Hepatic veins, Inferior Vena Cava.\n\nDemographics:More common in women. Usually presents in third to fourth decade.\n\nGross Morphology: Hepatomegaly, caudate lobe enlargement.\n\nGross Appearance:Hepatomegaly, caudate lobe enlargement, ascites, inability to visualize hepatic veins and/or inferior vena cava.\n\nHistology:Sinusoidal dilation, perivenular hemorrhage, hepatocyte necrosis, fibrosis, cirrhosis.\n\nSpecial Stains:\n\nRadiology:Doppler ultrasonography, MRI, CT, venography.\n\nPrognosis and Treatment:\n\nPrognosis:\nWhen the vein remains completely blocked, most people, if untreated, die of liver failure within 3 years. When the blockage is incomplete, life expectancy is longer but varies.\n\nTreatment:\nAnticoagulation with low-molecular weight heparin and/or warfarin.\nTIPS procedure\nSurgical intervention (portosystemic shunt).\nLiver transplantation.", "ACR Code": "7.-1", "Category": "Vascular", "Keywords": "Budd-Chiari", "Reference": "Mahmoud AE, Mendoza A, Meshikhes AN, Olliff S, West R, Neuberger J, Buckels J, Wilde J, Elias E. Clinical Spectrums, investigations, and treatment of Budd-Chiari Syndrome.QJM. 1996 Jan;89(1):37-43.\n\nMenon KVN, Shah V, Kamath PS. The Budd-Chiari Syndrome. NEJM 350:578, February 5, 2004.\n\nUptoDate.com" } }, { "U_id": "MPX1608", "TAC": [], "MRI": [ "MPX1608_synpic24721" ], "Case": { "Title": "Dilated Virchow Robin Space", "History": "Headache.", "Exam": "Non contributory.", "Findings": "Small cystic lesion in the medial left temporal lobe with signal that follows CSF on all sequences.", "Differential Diagnosis": "Dilated Virchow Robin Space", "Case Diagnosis": "Dilated Virchow Robin Space", "Diagnosis By": "Imaging only.", "Treatment & Follow Up": "None.", "Discussion": "See factoid." }, "Topic": { "Title": "Dilated perivascular spaces (etat crible)", "Disease Discussion": "Small foci of increased signal are frequently identified in the basal ganglia in the elderly. They may be caused by lacunar infarctions, gliosis, dilated perivascular spaces (DPS), demyelination, nonspecific protein depositions, cysts, and ventricular diverticuli.\n\nDilated perivascular spaces (etat crible) are dilated Virchow-Robin spaces which are extensions of the subarachnoid spaces that surround vessel walls as they traverse through the brain parenchyma. There may or may not be associated changes in the adjacent brain parenchyma. They may occur in the basal ganglia or the white matter (see Case 622).\n\nRadiographically, the DPS are generally smaller in size than lacunar infarctions and isointense to CSF on all sequences. They are identified, most commonly, in the basal ganglia along the course of the anterior commissure. There is an association with hypertension, but DPS are also seen in patients without a history of hypertension.", "ACR Code": "1.1", "Category": "Vascular", "Keywords": "etat cribleVirchow-Robin spaces" } }, { "U_id": "MPX1613", "TAC": [], "MRI": [ "MPX1613_synpic45595", "MPX1613_synpic45596", "MPX1613_synpic45597" ], "Case": { "Title": "Alexander Disease, Rosenthal Fiber Encephalopathy", "History": "Six month old baby boy with intermittent vomiting for 7 weeks Now listless. Parents say his head is too big.", "Exam": "Head circumference greater than 95%.", "Findings": "\u2022 Low T1 Signal involving the periventricular white matter and high T1 signal involving the periventricular rim.\n\u2022 Increased T2 signal int the involved white matter and the basal ganglia\n\u2022 On post-contrast imaging there is intense enhancement of the basal ganglia", "Differential Diagnosis": "\u2022 Canavan disease: Diffuse involvement of the brain, with the subcortical U fibers involved early\n\u2022 Megaloencephalic leukoencephalopathy with subcortical cysts: Diffuse white matter involvment (including subcortical U fibers), but spares the basal ganglia\n\u2022 Mucopolysaccharidoses: Prominent Virchow Robin spaces, and patchy, periventricular white matter signal abnormality\n\u2022 Alexander's Disease", "Case Diagnosis": "Alexander Disease, Rosenthal Fiber Encephalopathy", "Diagnosis By": "Imaging and Autopsy", "Treatment & Follow Up": "Supportive" }, "Topic": { "Title": "Alexander Disease, Rosenthal Fiber Encephalopathy", "Disease Discussion": "Alexander's disease (AD), also called \"Rosenthal Fiber Encephalopathy\" and \"fibrinoid leukodystrophy\" is an uncommon neurodegenerative disease. Both childhood and adult types have been described. It is caused by a mutation in the GFAP gene (Glial Fibrillary Acidic Protein). PMID: 16505300http://www.neurology.org/cgi/content/abstract/66/4/494\n\nEarly presentation (first weeks of age), macrocephaly, failure to achieve milestones, progressive spastic quadriparesis, intellectual failure, early death (infancy, childhood), low density in frontal white matter => extends posteriorly and into internal capsule, enhancement of tips of frontal horns, prolonged T1 and T2 in frontal regions => progresses posteriorly to parietal and the internal and external capsules, frankly cystic changes occur late with marked atrophy of the corpus callosum.\n\nThe adult-onset disease (AOAD) also affects the medulla oblongata and the upper cervical spinal cord.\n\n=====================================================\nCan MRI diagnose adult-onset Alexander Disease?\n\"Atrophy and changes in signal intensity in the medulla oblongata and upper cervical spinal cord were present in 11 of 11 cases and were the diagnostic features.\" PMID: 18388212 http://www.ajnr.org/cgi/content/abstract/29/6/1190\n\nhttp://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&DbFrom=pubmed&Cmd=Link&LinkName=pubmed_pubmed&LinkReadableName=Related%20Articles&IdsFromResult=18388212&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstract\n\n=====================================================\nhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Display&dopt=pubmed_pubmed&from_uid=9492095&tool=ExternalSearch'>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Display&dopt=pubmed_pubmed&from_uid=9492095&tool=ExternalSearch\n\n=====================================================\nhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&\nhttp://www.vetpathology.org/cgi/content/full/43/6/1025", "ACR Code": "1.6", "Category": "Congenital, genetic", "Keywords": "myelopathyleukodystrophymacrocephaly", "Reference": "http://archopht.ama-assn.org/cgi/content/full/117/2/265?ck=nck\nhttp://www.ninds.nih.gov/disorders/alexander_disease/alexander_disease.htm\nhttp://brain.oxfordjournals.org/cgi/content/short/131/9/2321\nhttp://www.ajnr.org/cgi/content/abstract/29/6/1190", "External Links": "www.waisman.wisc.edu/alexander/bib-date.html" } }, { "U_id": "MPX1631", "TAC": [], "MRI": [ "MPX1631_synpic51876", "MPX1631_synpic51877", "MPX1631_synpic51878", "MPX1631_synpic51879", "MPX1631_synpic51880", "MPX1631_synpic51881" ], "Case": { "Title": "Crohn Disease", "History": "54 year-old male with recurrent abdominal pain and diarrhea.", "Exam": "Slender male, currently asymptomatic.", "Findings": "Several regions of discontinuous and asymmetric bowel wall thickening with alternating regions of dilation. No fistulas were identified in this patient\u2019s case. Enhancement localized to the regions of mural thickening was demonstrated following the administration of intravenous gadolinium DTPA.", "Differential Diagnosis": "\uf06e\tUlcerative colitis (\u201cBackwash ileitis\u201d)\n\uf06e\tInfection\n\uf06e\tIschemia\n\uf06e\tRadiation enteritis\n\uf06e\tMetastases / lymphoma", "Case Diagnosis": "Crohn Disease", "Diagnosis By": "Biopsy", "Treatment & Follow Up": "Thus far, this patient has been received medical therapy only. Interval clinical and radiologic reevaluation is planned, with the reevaluation interval to be determined based on symptoms and disease progression.", "Discussion": "The exact etiology of Crohn\u2019s disease is unknown. There is a familial disposition. Most common age of presentation is 15-25 years, with an equal distribution between the sexes. There is a four-fold increase in incidence amongst smokers. The most common presenting symptoms include diarrhea, pain, melena, weight loss and fever. \n\nAssociated abnormalities include arthritis, cholelithiasis, sclerosing cholangitis, uveitis and ankylosing spondylitis. Based on pathology, there are three stages of Crohn\u2019s disease. The early stage includes hyperplasia of lymphoid tissue and shallow mucosal erosions (aphthoid ulcers). The intermediate stage is defined by transmural extension within the mucosa and subserosa with marked fold thickening. The advanced stage includes transmural extension to and through the serosa and deep ulcerations and fissures.\n\nLesions can occur anywhere along the entire length of the gut, from the mouth to the anus. The terminal ileum and proximal colon are the most common sites of involvement. Skip lesions more commonly involve the distal ileum.\n\n10-20% of patients lead symptom-free lives. Medical treatment includes steroids, azathioprine, mesalamine, and antibiotics. Surgical treatment involves resection of the affected bowel. 30-53% recur after surgical resection.\n\nReferences:\n\nGore RM, et al. CT features of ulcerative colitis and Crohn\u2019s disease. Am J Roentgenl. 167(1):3-15, 1996.\n\nHizawa K, et al. Crohn disease: early recognition and progress of aphthous lesions. Radiology. 190(2):451-4, 1994." }, "Topic": { "Title": "Crohn Disease", "Disease Discussion": "Crohn Disease, also known as Regional Enteritis, is a prolonged inflammatory bowel disease of unknown etiology and upredictable course. The disease may affect the entire GI tract and does so in a characteristic discontinuous and asymmetric pattern. Males and females are affected equally and usually present between ages 15 and 30. Symptoms vary but most commonly include abdominal pain with diarrhea, which may be bloody. Other symptoms include low-grade fever, anorexia and weight loss, anemia, perianal abscess/fistula and malabsorption. \n\nThe small bowel is most frequently involved followed by the colon. The terminal ileum alone or in combination with other sites is involved in 95% of cases. Typical findings on small bowel follow-through include fold thickening with nodularity, aphthous ulcers and cobblestone mucosa and ulceration. Crohn or granulomatous colitis occurs most frequently on the right side with sparing of the rectosigmoid. Often small nodular filling defects are seen with aphthous ulcers. Discontinuous involvement or \"skip lesions\" throughout the bowel are characteristic. Complications include fistulae, sinus tracts, abscesses, perforation, toxic megacolon and increased risk for bowel lymphoma and adenocarcinoma. \n\nFindings on CT include thickened bowel wall potentially with skip areas, \"creeping fat\" due to mesenteric fat proliferation, vascular dilation and tortuosity, mesenteric adenopathy, fistula, stricture or abscess. Although complications may be treated surgically, primary therapy is medical as recurrence rate after resection is up to 39%. \n\nThere are many extraintestinal manifestations including gallstones, urolithiasis, uveitis and arthritis. Also, Crohn Disease is associated with pyoderma gangrenosum and erythema nodosum.", "ACR Code": "7.2", "Category": "Inflammatory, NOS", "Keywords": "Crohn disease", "Reference": "Dahnert, W Radiology Review Manual 5th ed Lippincott Williams & Wilkins 2003." } }, { "U_id": "MPX1652", "TAC": [], "MRI": [ "MPX1652_synpic43724", "MPX1652_synpic43725" ], "Case": { "Title": "Neurofibroma", "History": "52 year-old-male presents with medial elbow pain.", "Exam": "Palpable mass in the medial elbow.", "Findings": "Radiographic examination demonstrates a rounded soft tissue mass in the medial aspect of the elbow.\nMRI findings include a T2 hyperintense fusiform tumor. On T1 weighted imaging, the mass is homogenous and isointense to muscle. The tumor strongly enhances follwing Gadolinium administration. Note that this infiltrating mass is contiguous with the nerve.", "Differential Diagnosis": "Neurofibroma vs Schwannoma (neurilemmoma). \nCat scratch disease may have similar plain film findings.", "Case Diagnosis": "Neurofibroma", "Diagnosis By": "Biopsy demonstrates a tumor composed of nerve fibers, fibroblasts, Schwann Cells and collagen.", "Treatment & Follow Up": "Treatment is usually surgical excision.", "Discussion": "While neurofibromas are a hallmark of NF Type I, only 10% of patient's with neurofibromas actually have Von Recklinghausen's disease. To meet diagnostic criteria for NF I, a patient must exhibit two of the following:\n6 or more caf?-au-lait macules (>5mm-prepuberty or >15mm-postpuberty), 2 or more neurofibromas of any type or 1 plexiform neurofibroma, freckling in the axillary or inguinal regions, optic glioma, 2 or more Lisch nodules, distinctive bony lesion (i.e. sphenoid dysplasia, thinning of long bone cortex with or without pseudoarthrosis), a first degree relative diagnosed with NF1. \nWhile malignant transformation is rare, this would present with indistinct margins, a sudden incrase in size and internal areas of hemorrhage and necrosis.\nLesions usually affect young adults 20-30 years without sex predilection.\nUnlike schwannomas, neurofibromas are intimately intermixed and are inseparable from the normal nerve tissue." }, "Topic": { "Title": "Neurofibromatosis Type 1 (NF-1, von Recklinghausen's Disease)", "Disease Discussion": "NF-1 is a congenital disease causing benign tumors of peripheral nerves. These tumors are formed by hyperproliferation of the nerve sheath cells. Although they can occasionally undergo malignant transformation, invade CNS spaces, or cause mental retardation, significant morbidity can result from hundreds of disfiguring neurofibromas and pedunculated molluscum fibrosum visible from a long distance. The psychological impact and physical inconvenience of such lesions cannot be overstated. \n\tNF-1 is disease whose gene with autosomal dominant inheritance involving an NF-1 gene on chromosome 17. However, as many as half of cases occur by spontaneous genetic defect with no known parental disease. This genetic defect is found in nearly 1 per 3000 births with varying expression. There is no increased incidence by sex or race.\n\tThe diagnosis is generally made in childhood or adolescence due to the appearance of caf?-au-lait macules. The disfiguring cutaneous neurfibromas and molluscum fibrosum generally appear a few years later, but the number of cutaneous lesions may grow into the hundreds. Diagnosis using the National Institutes of Health (NIH) Consensus Development Conference Criteria can be made with two of the following: six or more caf?-au-lait macules; two or more neurofibromas of any type or one plexiform neurofibroma; axillary or inguinal freckles; bilateral optic glioma; two Lisch nodules (iris hematomas); osseous dysplasia (sphenoid wing, occipital, or tibial pseudoarthrosis); or first degree relative with NF-1. Scoliosis is also not uncommon.\n\tRadiologic studies are not typically required for diagnosis of NF-1, but may be needed to assess lesion growth around critical nerve structures, particularly when focal neurological dysfunction is present. Furthermore, there is an increased incidence of certain tumors (including optic gliomas, acoustic neuromas, pheochromocytomas, astrocytomas, meningiomas, ependymomas, etc.) in NF-1 patients, so there is generally a low threshold for imaging studies in symptomatic patients. However, there is no protocol for periodic imaging unless indicated by clinical exam or for follow-up of previously identified lesions. The T2-weighted MRI is generally the best study for imaging neurofibromas due to a large amount of water in the neurofibroma lesions. \n\tTreatment of NF-1 is primarly limited to surgical resection of symptomatic lesions, such as one at the waist line that generates pain with clothing wear. In addition, neurofibromas which create neurological symptoms are debulked if possible. There are some experimental medical oncologic protocols, but no cure or remission agent yet.", "ACR Code": "38.1831", "Category": "Unsure", "Reference": "Alcorn, Deborah M., \"Phacomatoses for the General Ophthalmologist,\" Ophthalmology Clinics of North America, June 1999 (12:2), 243-245. \n\nEichenfield, LF, et al, \"Guidelines of Care for Neurofibromatosis type 1,\" Journal of the American Academy of Dermatology, October 1997 (37:4), 625-630.\n\nFauci, AS, Ed., Harrison's Principles of Internal Medicine, 14th ed., New York: McGraw-Hill, 1998, 2404.\n\nGoetz, CG and EJ Pappert, Textbook of Clinical Neurology, Philadelphia: W.B. Saunders Company, 1999, 619-622, 946-947.\n\nKirks, Donald R., Ed., Practical Pediatric Imaging: Diagnostic Radiology of Infants and Children, 3rd ed., Philadelphia: Lippincott-Raven, 1998, 174-178, 252, 360-362.\n\nMenkes, JH and HB Sarnat, Eds., Child Neurology, 6th ed., Philadelphia: Lippincott Williams & Wilkins, 2000, 859-864.\n\nTonsgard, JH, et al, \"CT Imaging in Adults with Neurofibromatosis-1,\" Neurology, June 1998 (50:6), 1755." } }, { "U_id": "MPX1675", "TAC": [], "MRI": [ "MPX1675_synpic21667", "MPX1675_synpic21668", "MPX1675_synpic21669" ], "Case": { "Title": "Atrial Septal Defect (ASD).Ostium primum.", "History": "25 year old asymptomtic womam presents for a cardiac MRI after a murmur was detected by her cardiologist.", "Exam": "Right Ventricular heave \nS2 Heart Sound with fixed wide split \nSystolic ejection murmur \nGrade II of VI \nHeard best at left upper sternal border \nMid-Diastolic Murmur \nFlow rumble in the tricuspid valve region", "Findings": "Radiographic findings:\nSelected axial ECG gated white blood MR imgaes of the heart demonstrate a mild to moderately enlarged right atrium with a suggestion of a jet of low signal across the inter atrial septum. A defect is identified at the inferior aspect of the inter atrial septum. No significant shunt vascularity is appreciated. The remaining heart is normal.", "Differential Diagnosis": "-Atrial Septal Defect.\n-Patent foramen Ovale\n-Endocardial cushion defect (no other shunt or defect is present)", "Case Diagnosis": "Atrial Septal Defect (ASD).Ostium primum.", "Diagnosis By": "Using Cardiac MRI", "Treatment & Follow Up": "Wait and see: \n-Spontaneous closure is possible however, it is less common than with a VSD, and unusual outside of childhood.\n\nSurgery Indications: \n-Large left to right shunt \n-Congestive Heart Failure \n-Pulmonary congestion", "Discussion": "It is a commmon congenital cardiac anomaly, present in 3.8 of 10,000 live births. There is a 3:2 female predominance.\n\nTypes: \nOstium Primum \n-Congenital opening in septum near AV valves \n-Associated with endocardial cushion defects. \nOstium Secundum \n-Congenital defect at the fossa ovalis \nSinus Venosus \n-Defect posterior to fossa ovalis \n-Associated with partial anomalous pulmonary return \n\nIn additon, ASD's can be associated with Holt - Oram syndrome, Lutembacher syndrome, and Down syndrome. They are more common in women then men.\n\nImaging should demonstrate a large RA, RV, and PA. There should not be LA enlargment. MR can show a jet of blood across the defect. The absence of signal in the inter atrial septum is not always reliable because the septum is typically thin and is not always seen." }, "Topic": { "Title": "Atrial Septal Defect (ASD)", "Disease Discussion": "ASD - Atrial Septal Defect.\n \nASD is a common congenital cardiac anomaly, seen in 3.8 per 10,000 live births. 3 different types exist.\n - Ostium secundum accounts for approximately 60% of the ASD's. \n - Ostium primun accounts for 35% of the ASD's.\n - Sinus venous defect is the least common.\n\nOstium primum ASD is seen as a part of ECD syndrome.\n\nSinus venosus ASD is seen at the junction with the SVC and is always associated with partial anomalous pulmonary venous return.\n\nThis causes a left to right shunt. The right atrium and ventricle may be enlarged with increased vascular flow.\n\nPatients may be asymptomatic for decades due to low atrial pressure. Women are affected more commonly then men. If symptomatic, patients may present with pulmonary artery hypertension.\n\nIt is associated with: \n - Holt Oram Syndrome. Ostium secundum defect.\n - Lutembacher syndrome. ASD and mitral stenosis.\n - Down syndrome. Ostium primum defect.\n\nhttp://www.tmc.edu/thi/aseptal.html\nhttp://www.nlm.nih.gov/medlineplus/congenitalheartdisease.html\nhttp://www.vh.org/pediatric/provider/radiology/PAP/CVDiseases/ASD.html", "ACR Code": "514.141", "Category": "Congenital, malformation", "Keywords": "ASDatrial septumcongenital heart", "Reference": "Primer of Diagnostic Imaging, 3rd Edition \nBy Ralph Weissleder, MD, PhD, Jack Wittenberg, MD and Mukesh G Harisinghani, MD. Copyright 2003", "External Links": "www.vh.org/pediatric/provider/radiology/PAP/CVDiseases/ASD.html" } }, { "U_id": "MPX1677", "TAC": [], "MRI": [ "MPX1677_synpic21841", "MPX1677_synpic21842", "MPX1677_synpic21843", "MPX1677_synpic21844", "MPX1677_synpic21845", "MPX1677_synpic21866", "MPX1677_synpic22032" ], "Case": { "Title": "COARCTATION", "History": "This case is based on a 3 year old female who at the age of 18 months underwent surgical resection with end-to-end repair of a mild preductal coarctation of the aorta just proximal to the left subclavian artery take-off.", "Exam": "Physical exam reveals a murmur that is difficult to localize in location and difficult to locate in the cardiac cycle. A difference in blood pressure between the upper and lower extremities was also found.", "Findings": "The study revealed a standard three-vessel arch with the brachiocephalic artery being the first great vessel, the left common carotid being the second vessel, and the left subclavian artery being the third vessel. Just proximal to the takeoff of the left subclavian artery is a significant web across the lumen of the aortic. This aortic web is seen to cause significant obstruction of flow through the aorta. A momentary delay was seen before blood flow was seen distal to the obstruction. A central post-stenotic jet was seen traveling through the thoracic aorta to below the level of the diaphragm. No obvious collateral blood vessels are noted throughout the thoracic aorta. No other cardiac abnormalities were identified.", "Differential Diagnosis": "Recurrent coarctation / restenosis at the site of the procedure.", "Case Diagnosis": "COARCTATION", "Diagnosis By": "MRA", "Treatment & Follow Up": "Balloon angioplasty of the area of stenosis.", "Discussion": "The patent underwent a balloon angioplasty procedure in hopes of relieving the obstruction before significant post-stenotic dilatation could occur and avoid repeat surgery which carries a significant chance of both morbidity and mortality." }, "Topic": { "Title": "aortic coarctation", "Disease Discussion": "The term coarctation is derived from the Latin word coarctation, meaning a drawing or pressing together. In medical terminology, coarctation refers to a localized narrowing of the lumen of a vessel producing an obstruction to flow. Coarctation of the aorta typically occurs in the \"juxta-ductal\" part of the aorta, or the part near where the ductus arteriosus attaches near the aortic isthmus. Depending on the exact location of the constriction of the aorta, it can be classified as either preductal / isthmic (infantile) coarctation or postductal / juxtaductal (adult type) coarctation. The most frequently encountered type is the postductal / juxtaductal variety. In the postductal type, the area of the coarctation is located at, or just distal to, the level of the left subclavian artery and ductus arteriosus and usually is short and discrete. In the rarer second type, (preductal, isthmic, or infantile) the area of narrowing usually lies proximal to the ductus arteriosus, somewhere between the left subclavian artery and the left carotid artery. Preductal coarctation is associated with an increased incidence of cardiac defects, and as preductal coarctations do not significantly alter normal fetal blood flow patterns, no collaterals form in utero hence they are typically not seen later in life. Several surgical methods of repair are employed, including end-to-end reanastomosis, subclavian flap aortoplasty, prosthetic patch onlay grafts, and interposition grafts. Usually, the presence of coarctation alone is indication for an operation. Several techniques are currently used to repair coarctation of the aorta and the method of repair employed is usually tailored specifically to each patient. Follow-up for these patients depends upon the clinical response to the intervention. The most common complications after coarctation repair are late restenosis and aneurysm formation at the repair site. One of the most common methods of repair of coarctation of the aorta is resection of the involved segment with end-to-end reanastomosis. Some of the benefits of this particular technique include avoidance of prosthetic materials, excision of ductal tissue, preservation of the left subclavian artery, and relief of left ventricular outflow obstruction. The current trend in management is to attempt a corrective surgery in neonates and to try transcatheter balloon dilation before surgery in older children and adults. Recently, treatment of aortic coarctation by percutatious catheter interventions has become more widespread, using both balloon dilation and primary stent implantation techniques. These techniques were first regarded mainly as a procedure for the treatment of recurrent coarctation. However, they have gained more widespread acceptance as a procedure for both the unoperated lesions and the recurrent coarctation / restenosis at the site of the procedure. Restenosis is a common complication and is often associated with post stenotic aneurismal dilatation. Follow-up imaging to assess for post surgical success and assessment of potential late complications can be accomplished using various modalities. Adequate visualization of the entire arch is needed. Angiography remain the gold standard, however noninvasive imaging with magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) is becoming more popular.", "ACR Code": "5.-1", "Category": "Congenital, malformation", "Keywords": "coarctation", "Reference": "1. Maziarz, David M. MD, Theodore C. Koutlas MD. Coarctation of the Aorta and Interrupted Aortic Arch: Surgical Perspective. Emedicine: May 16, 2003.\n\n2. McCrindle, Brian W. MD, MPH Coarctation of the aorta. Current Opinion in Cardiology. 14(5):448, September 1999.\n\n3. Celermajer, D S; Greaves, K. Survivors of coarctation repair: fixed but not cured. Heart. 88(2):113-114, August 2002." } }, { "U_id": "MPX1694", "TAC": [], "MRI": [ "MPX1694_synpic18249", "MPX1694_synpic18251" ], "Case": { "Title": "Recurrent high-grade astrocytoma", "History": "38 y.o. man with previously diagnosed high-grade glioma in the left parietal lobe, s/p radiation treatment.", "Exam": "N/C", "Findings": "Initial multiple MR images demonstrate a ring-enhancing lesion in the site of glioma, previously treated with radiation therapy, with some areas of nodular changes. \n\nMR spectroscopy of normal site, TE = 144 msec, which demonstrates prominent N-acetylaspartate (NAA) peak at the 2.0 ppm, which is the normal neuronal marker. Creatine peak at 3.0 ppm and choline peak at 3.2 ppm are also demonstrated, showing normal relationships.\n\nMR spectroscopy of the abnormal site, TE = 144 msec, which demonstrates elevation of the choline peak, and the suppression of the NAA peak, along with an inverted peak at the 1.0-1.2 ppm, which is the lactate peak (which characteristically inverts at TE = 144 msec). These findings suggest tumor recurrence with some areas of necrosis, rather than radiation-induced changes.", "Differential Diagnosis": "\u2022 Residual tumor\n\u2022 Recurrent tumor\n\u2022 Radiation effect\n\u2022 Normal brain\n\u2022 Post-operative changes", "Case Diagnosis": "Recurrent high-grade astrocytoma", "Diagnosis By": "MR Spectroscopy", "Media": "Diffuse Gliomas 2020 (narration).mp4\n\n\n\n Intraaxial Primary Neoplasms - Diffuse Gliomas 2020 (narration).mp4\n \n\n\n\n\n\n\u00d7\nDiffuse Gliomas 2020 (narration).mp4\n\n\n\n\nTo view this video please enable JavaScript, and consider upgrading to a web browser that supports HTML5 video" }, "Topic": { "Title": "MR spectroscopy, Neoplasm vs. Radiation", "Disease Discussion": "Approximately 20% of patients who undergo radiation treatment for cerebral glioma develop side effects from the treatment that mimic recurrent tumor, both clinically and radiologically. Anatomic changes seen on both CT and MR images are insufficient to discriminate radiation-induced changes from tumor recurrence. MR spectroscopy, PET, and SPECT imaging modalities have been proposed as possible tools for such differentiation. Of these, MR spectroscopy holds much promise due to its inherent advantages: high-energy radiation is not used, and radio-labeled tracers are not required. \n\nOn normal tissue, the most prominent peak is at around the 2.0 ppm (parts per million), the peak of N-acetylaspartate (NAA), which in past literature regarding MR spectroscopy is used as the normal neuronal marker, which is decreased in areas involved with tumor. Both lipid and lactate peaks are seen around 1.0-1.5 ppm, if they are present. The peak at the 3.0 ppm mark is the creatine (Cr), and the peak at the 3.2 ppm is the choline (Cho), which is usually elevated in areas involved with tumor.\n\nA study by Rabinov et al showed that in 16 of 17 biopsy locations in patients who has been previously treated with radiation therapy, they could be prospectively classified as either being predominantly tumor-involved or predominantly radiation effect based on a single criteria, that of the ratio of the peak area of choline at the biopsy site to that of the creatine at the corresponding normal site. When this ratio was greater than 1.3, the biopsy site were all tumor-involved.", "ACR Code": "1.3", "Category": "Neoplasm, glial", "Keywords": "MR spectroscopygliomaradiation induced changes", "Reference": "Rabinov, et al. In Vivo 3-T MR Spectroscopy in the Distinction of Recurrent Glioma versus Radiation Effects: Initial Experience. Radiology 2002; 225:871-879." } }, { "U_id": "MPX1686", "TAC": [], "MRI": [ "MPX1686_synpic41850", "MPX1686_synpic41851", "MPX1686_synpic41852", "MPX1686_synpic41853", "MPX1686_synpic41854", "MPX1686_synpic41855", "MPX1686_synpic41856", "MPX1686_synpic41857", "MPX1686_synpic41858", "MPX1686_synpic41860", "MPX1686_synpic41866" ], "Case": { "Title": "Complex Malformation", "History": "Full-term neonate with abnormal prenatal ultrasound.", "Findings": "This patient has agenesis of the corpus callosum. The posterior fossa is small, with a normally formed cerebellum, which is compressed inferiorly, and the 4th ventricle and cerebral aqueduct are patent. The globes maintain cross-midline symmetry, and hypotelorism is noted. The optic tracts are normally formed. The thalami are fused, and there is partial interhemispheric fusion of the insular parenchyma, and a suggestion of anterior frontal lobe fusion. There is a partially formed posterior falx cerebri, and anterior interhemispheric fissure. There is a probable large monoventricle with a dorsal interhemispheric cyst, abutting dysplastic cerebral tissue. There is an apparent hypoplastic left internal jugular vein. A cephalocele at the vertex is also noted.", "Differential Diagnosis": "Alobar Holoprosencephaly\nSemilobar Holoprosencephaly\nLobar Holoprosencephaly\nSeptooptic Dysplasia\nScizencephaly", "Case Diagnosis": "Complex Malformation", "Discussion": "In semi-lobar holoprosencephaly, the craniofacial anomalies are variable. There are rudimentary occipital and temporal horns, with a partially formed falx cerebri and interhemispheric fissure. There is fusion of the thalami and basal ganglia. Facial anomalies are either absent or milder than those seen with alobar holoprosencephaly. Facial anomalies seen include hypotelorism, as well as median and lateral cleft lip." }, "Topic": { "Title": "Lobar Holoprosencephaly", "Disease Discussion": "Holoprosencephaly is a congenital abnormality categorized as a disorder of diverticulation and cleavage. The cerebrum (prosencephalon) does not form separate hemispheres and lobes. One possible explanation is the interruption of lateral ventricular growth during the gestational 5th or 6th week. This results in a continuum of findings that range from minor to severe. \n\nThe hallmark of the disorder is absence of the septum pellucidum. With lobar holoprosencephaly, the mildest form, the interhemispheric fissure is formed except anteriorly where the grey and white matter are fused across the midline at the frontal lobe bases, the frontal horns are present but unseparated. Also, the splenium, 3rd ventricle, occipital horns, and cerebral vasculature are normal.\n\n The most severe form is alobar holoprosencephaly where there is a large mono-ventricle emptying into the aqueduct of Sylvius, thalami are fused, and there is absence of the interhemispheric fissure, frontal horns, splenium, 3rd ventricle, and occipital horns. The alobar type is associated with facial deformities. \n\nBetween the two extremes of holoprosencephaly lies semi-lobar holoprosencephaly.\n\nHoloprosencephaly is the only syndrome where the splenium and posterior corpus callosum may form with absence of the anterior corpus callosum (except for the rostrum). \n\nDisorders associated with holoprosencephaly are caudal agenesis, DiGeorge syndrome, fetal alcohol syndrome, Kallmann syndrome, maternal diabetes, and trisomies (13, 15, 18).\n\nSeptooptic dysplasia is considered in the spectrum of holoprosencephaly , albeit a milder form, and must be differentiated from lobar holoprosencephaly. Septooptic dysplasia presents with the septum pellucidum absent or partially absent in association with small hypoplastic optic nerves and a small optic chiasm. This results in dysplastic visual pathways.", "ACR Code": "1.9", "Category": "Congenital, malformation", "Keywords": "holoprosencephalyseptooptic dysplasia", "Reference": "Neuroradiology: The requisites 2nd Edition; Grossman, R.; Mosby 2003*" } }, { "U_id": "MPX1701", "TAC": [], "MRI": [ "MPX1701_synpic20166", "MPX1701_synpic20167", "MPX1701_synpic20168" ], "Case": { "Title": "Plantaris Tendon Tear", "History": "42 year old radiologist complains of sudden onset pain after experiencing a popping sensation in the right calf while playing tennis.", "Exam": "Tenderness to palpation and fullness in the right calf.\n\nNormal neurological and motor examination of the bilateral lower extremities.", "Findings": "Figure 1\nAxial T1 image shows curvilinear isointense signal between the medial head of the gastrocnemius and the soleus. \n\nFigure 2\nAxial T2 Fat Suppressed image shows the high intensity signal between the medial head of the gastrocnemius and the soleus as well as edema within the medial head of gastrocnemius muscle. \n\nFigure 3\nCoronal T2 image at a level between the gastrocnemius and the soleus muscles again shows the extent of this fluid collection between the two muscles.", "Differential Diagnosis": "Plantaris Tendon Tear", "Case Diagnosis": "Plantaris Tendon Tear", "Diagnosis By": "MRI", "Treatment & Follow Up": "Treatment is usually conservative with analgesics and 4-8 weeks of decreased activity and potentially with splinting.", "Discussion": "The plantaris muscle, absent in 7-10% of the population, arises from the lateral supracondylar line of the distal femur just superior to the attachment of the lateral head of the gastrocnemius. The long thin muscle body lies just deep to the lateral head of the gastrocnemius coursing inferiorly a few inches before terminating in the plantaris tendon. The Plantaris tendon is unusually long and thin, coursing medially between the medial head of the gastrocnemius and the soleus, inserting on the calcaneus anterior and medial to the Achilles tendon insertion. The tendon may also insert into the distal Achilles tendon. \n\nThe plantaris muscle and tendon (as well as the gastrocnemius) is more prone to injury than the soleus muscle likely because it traverses two joints rather than just one. Injury is felt to be related to dorsiflexion under tension, frequently a problem for runners, cyclists, and tennis players. \n\nPlantaris muscle injuries have been described with anterior cruciate ligament and posterolateral corner knee injuries. Plantaris injury can be diagnosed confidently with MRI. Findings include, increased T2 signal within the plantaris muscle or myotendinous junction, proximal retraction of the plantaris muscle body, fluid between the medial head of the gastrocnemius and soleus muscles, as well as associated injuries to other structures in the posterolateral compartment of the knee. \n\nTreatment is usually conservative with analgesics and 4-8 weeks of decreased activity and potentially with splinting. \n\n\nReference(s): \nBencardino JT, et al. Traumatic Musculotendinous Injuries of the Knee: Diagnosis with MR Imaging. Radiographics 2000; 20:S103-S120\n\nHelms CA, Fritz RC, Garvin GJ. Plantaris muscle injury: evaluation with MR imaging. Radiology 1995 Apr; 195(1):201-3" }, "Topic": { "Title": "Plantaris Tendon Tear", "Disease Discussion": "The plantaris muscle, absent in 7-10% of the population, arises from the lateral supracondylar line of the distal femur just superior to the attachment of the lateral head of the gastrocnemius. The long thin muscle body lies just deep to the lateral head of the gastrocnemius coursing inferiorly a few inches before terminating in the plantaris tendon. The Plantaris tendon is unusually long and thin, coursing medially between the medial head of the gastrocnemius and the soleus, inserting on the calcaneus anterior and medial to the Achilles tendon insertion. The tendon may also insert into the distal Achilles tendon. \n\nThe plantaris muscle and tendon (as well as the gastrocnemius) is more prone to injury than the soleus muscle likely because it traverses two joints rather than just one. Injury is felt to be related to dorsiflexion under tension, frequently a problem for runners, cyclists, and tennis players. \n\nPlantaris muscle injuries have been described with anterior cruciate ligament and posterolateral corner knee injuries. Plantaris injury can be diagnosed confidently with MRI. Findings include, increased T2 signal within the plantaris muscle or myotendinous junction, proximal retraction of the plantaris muscle body, fluid between the medial head of the gastrocnemius and soleus muscles, as well as associated injuries to other structures in the posterolateral compartment of the knee. \n\nTreatment is usually conservative with analgesics and 4-8 weeks of decreased activity and potentially with splinting.", "ACR Code": "4.4", "Category": "Sports Medicine", "Keywords": "Plantaris Tendon TearPlantaris Tendon RupturePlantaris Muscle", "Reference": "Reference(s): \nBencardino JT, et al. Traumatic Musculotendinous Injuries of the Knee: Diagnosis with MR Imaging. Radiographics 2000; 20:S103-S120\n\nHelms CA, Fritz RC, Garvin GJ. Plantaris muscle injury: evaluation with MR imaging. Radiology 1995 Apr; 195(1):201-3" } }, { "U_id": "MPX1710", "TAC": [], "MRI": [ "MPX1710_synpic50458", "MPX1710_synpic50481", "MPX1710_synpic50503", "MPX1710_synpic50525" ], "Case": { "Title": "Tophaceous gout", "History": "40 year old male with history of gout presents with chronic knee pain for 5 months.", "Exam": "Right knee findings:\n\nMinimal warmth noted. \nNo erythema.\nNo subcutaneous nodules. \nMinimally tender to palpation along joint line. \nFull range with both active and passive motion. \nNegative anterior/posterior drawer sign.", "Findings": "There is no evidence of bone marrow abnormality. A small joint\neffusion is present. A large nodular mass is seen adjacent to the lateral superior patella with isointense signal on T1 and heterogeneous signal on T2 measuring approximately 5.2 x 1.8 x 6 cm. Smaller similar masses are present at the femoropopliteal insertion site, within the femoral notch and at the base of the Hoffa's fat pad just anterior to the anteromedial tibia.\n \nThe PCL appears thickened but intact. The ACL, menisci, and collateral\nligament complexes are unremarkable. Full thickness fissuring is present in the medial trochlea cartilage.", "Differential Diagnosis": ">> Gout\n>> Pigmented villonodular synovitis\n>> Pseudogout\n>> Tumor\n>> Uric acid nephropathy\n>> Rheumatoid arthritis\n>> Sarcoidosis\n>> Amyloidosis", "Case Diagnosis": "Tophaceous gout", "Diagnosis By": "Needle biopsy", "Treatment & Follow Up": "The issue of ongoing urate deposition should be addressed with uricosuric medication. Probenecid (Benemid) is the most frequently used medication. Probenecid works at the level of the proximal tubule by blocking reabsorption of filtered uric acid. This action is inhibited by low-dose salicylates; this fact accounts for a significant number of \"treatment failures.\" Allopurinol (Zyloprim) can also be used and is currently the only readily available inhibitor of uric acid synthesis.\n\nTophi should not be surgically removed unless they are in a critical location or drain chronically.", "Discussion": "MRI is not used routinely in the evaluation of gout. However, when gouty tophi present as soft-tissue masses in the absence of articular disease, the tophi may be confused with a neoplastic process. In this instance, MRI evaluation is necessary. Tophaceous deposition should be considered in the differential diagnosis when a mass displays heterogeneous low to intermediate signal intensity on T1 and T2 weighting and a variable enhancement pattern, especially if multiple foci exist around the knee joint such as in this individual. Remarkably, the adjacent bone to these particular tophi did not show typical erosive changes, which is an unexpected finding in a patient with a chronic history of gout and knee pain. As such, needle biopsy was necessary to rule out a neoplastic and chronic infectious etiology." }, "Topic": { "Title": "Tophaceous gout", "Disease Discussion": "Associations/Predisposing Factors: Nonmodifiable risk factors include age and sex. Gout prevalence increases in direct association with age; the increased longevity of populations in industrialized nations may contribute to a higher prevalence of gout through the disorder's association with aging-related diseases such as metabolic syndrome and hypertension, and treatments for these diseases such as thiazide diuretics for hypertension. Modifiable risk factors for gout include obesity, the use of certain medications, high purine intake, and consumption of purine-rich alcoholic beverages.\n\nCommon Locations: acute gout is most often seen in the great toe; more rarely in the heel, ankle or instep. Tophi are chalky deposits of sodium urate that are large enough to be seen on radiographs and may occur at virtually any site. The most common sites include the joints of the hands or feet.\n\nRadiology: MR imaging is not routinely used for evaluation of tophaceous gout. However, gout may present clinically in an atypical or confusing manner. A gouty tophus occasionally mimics an infectious or neoplastic process and MR imaging may be helpful under these circumstances. On magnetic resonance imaging, tophi usually have low signal intensity on both TI- and T2-weighted images and a variable enhancement pattern.\n\nPrognosis and Treatment: Gout affects everyone differently. Some people have one episode and never have further progression of disease. Others have several episodes along with chronic pain and progressive joint damage. There is no cure for gout, but it can be controlled with medication. Proper treatment can help avoid attacks and long-term joint damage.", "ACR Code": "4.2", "Category": "Metabolic (see also Toxic)", "Keywords": "gouttophi" } }, { "U_id": "MPX1709", "TAC": [], "MRI": [ "MPX1709_synpic34687", "MPX1709_synpic34688" ], "Case": { "Title": "Periosteal Chondroma", "History": "This 41 y.o. woman presented to the Orthopedic clinic with a two month history of a painful mass on her left middle finger. The patient stated that the pain interfered with her work activity; she denied any trauma. \n\nThe patient was referred to a hand specialist for definitive treatment.\tExamination 1 month later revealed decreased grip strength in addition to the findings of the initial visit.", "Exam": "On physical exam, she was noted to have a 1 cm firm, fixed, tender mass on the volar aspect of the proximal phalanx with a full range of motion.\nSensory examination was within normal limits.", "Findings": "Plain film examination revealed a 9mm x 5mm focal ossific lesion with a chondroid matrix. The mass was adjacent to the cortical surface of the proximal phalanx and demonstrated saucerization of the underlying bone.\n\nMRI revealed a well demarcated lesion with a predominantly hypointense signal on both T1 and T2 weighted images, relative to skeletal muscle. A central, linear focus of hyperintense signal was also present on T2 weighted images. The lesion did not communicate with the underlying bone or surrounding soft tissue.", "Differential Diagnosis": "\u2022 Periosteal chondroma \n\u2022 Periosteal chondrosarcoma\n\u2022 Periosteal osteosarcoma \n\u2022 Bizarre parosteal osteochondromatous proliferation", "Case Diagnosis": "Periosteal Chondroma", "Diagnosis By": "Resection and Histopathologic evaluation", "Treatment & Follow Up": "After consideration of the treatment options, the patient elected to proceed with surgical excision. Surgery revealed a discreet, firm, osteocartilaginous lesion on the surface of the proximal phalanx that did not communicate with the medullary canal. There was a shallow depression in the underlying cortex, correlating with the radiographic findings. Histological evaluation revealed a lobulated fibrocartilaginous matrix with diffuse foci of ossification. The vast majority of chondrocytes were of normal appearance; an occasional binucleate cell was found. No mitotic figures were appreciated. The histopathologic examination, supported by radiographic imaging and historical data, supported the diagnosis of periosteal chondroma." }, "Topic": { "Title": "Periosteal Chondroma", "Disease Discussion": "Periosteal chondroma was first reported in the literature by Lichtenstein in 1952(1), although earlier descriptions of similar lesions have been found(2). It is a benign bone lesion, seen most commonly in the second and third decades, with a male to female predilection of approximately 2 to 1(3,4). Of all the chondromas, periosteal chondroma accounts for less than 2% of cases(5). The most common locations for this lesion are the metaphysis or diaphysis of the proximal humerus and distal femur(2-4).\nPeriosteal chondroma presents as a well demarcated, ossific mass in a juxtacortical position, with or without sclerotic borders and not continuous with the medullary cavity(2,4). Periosteal chondroma exhibits a characteristic saucerization of the underlying cortex(3). T1 weighted MRI imaging typically reveals a hypointense signal, and T2 weighted imaging shows a hyperintense signal. In addition, MR imaging reveals that this lesion does not show soft tissue involvement or continuity with the medullary cavity(6). \nHistologically, periosteal chondroma appears as a lobulated fibrocartilaginous matrix on low power. Higher power reveals lobules of chondrocytes, sometimes showing atypia such as binucleation (2,4,7). Ossification and calcification may also be present. \nSurgical excision is the treatment of choice(2,4,7), primarily due to the similarity to malignant lesions like osteosarcoma and chondrosarcoma. In addition, it may cause symptoms in the hand such as restricted range of motion or local pain and tenderness. Periosteal chondroma typically has a low rate of recurrence, particularly when excising the underlying periosteal tissue and any suspicious appearing cortex(2,3,8).", "ACR Code": "4.3", "Category": "Neoplasm, benign", "Keywords": "periostealchondroma", "Reference": "1. Lichtenstein L, Hall JE. Periosteal chondroma; a distinctive benign cartilage tumor. J Bone Joint Surg Am 1952; 24-A-3(691-697.\n2. Lewis MM, Kenan S, Yabut SM, Norman A, Steiner G. Periosteal chondroma. A report of ten cases and review of the literature. Clin Orthop Relat Res 1990; 256): 185-192.\n3. Bauer TW, Dorfman HD, Latham JT, Jr. Periosteal chondroma. A clinicopathologic study of 23 cases. Am J Surg Pathol 1982; 6(7): 631-637.\n4. Boriani S, Bacchini P, Bertoni F, Campanacci M. Periosteal chondroma. A review of twenty cases. J Bone Joint Surg Am 1983; 65(2): 205-212.\n5. Karabakhtsian R, Heller D, Hameed M, Bethel C. Periosteal chondroma of the rib--report of a case and literature review. J Pediatr Surg 2005; 40(9): 1505-1507.\n6. Woertler K, Blasius S, Brinkschmidt C, Hillmann A, Link TM, Heindel W. Periosteal chondroma: MR characteristics. J Comput Assist Tomogr 2001; 25(3): 425-430.\n7. Mora R, Guerreschi F, Fedeli A, Alfarano M, Angi V. Two cases of periosteal chondroma. Acta Orthop Scand 1988; 59(6): 723-727.\n8. Lorente Molto F, Bonete Lluch DJ, Marti Perales V. Childhood periosteal chondroma. Arch Orthop Trauma Surg 2000; 120(10): 605-608." } }, { "U_id": "MPX1714", "TAC": [], "MRI": [ "MPX1714_synpic20232", "MPX1714_synpic20233" ], "Case": { "Title": "Lateral epicondylitis", "History": "37 y/o male with elbow pain of unknown origin.", "Exam": "Most of the time the patient cannot pinpoint any distinct trauma, but relates a recent increase in training or new equipment to the onset of symptoms. The athlete complains of pain over the lateral elbow, which usually is worse during the activity and slowly improves after cessation of activity.\n\tWhen asked to pinpoint the pain, patients often point the area just distal to the lateral epicondyle. A frequent complaint is the \u201ccoffee cup sign.\u201d This is when the patient states that gripping their coffee cup or other object exacerbates the pain. Another frequent complaint is pain at the lateral epicondyle when shaking someone else\u2019s hand.", "Findings": ": Recent histologic studies have shown that angiofibroblastic tendinosis with a lack of inflammation in the surgical specimens of patients with lateral epicondylitis which suggests that the abnormal signal seen on MR images is secondary to tendon degeneration and repair rather than tendinitis. \n MR imaging is useful in assessing the degree of tendon damage in 4-10% of the cases that are resistant to conservative therapy. Tendon degeneration is manifested by normal to increased tendon thickness with increased signal intensity in T1-weighted images that does not further increase in signal intensity on the T2-weighted images. Complete tears may be diagnosed on MR imaging by identifying a fluid filled gap separating the tendon from its adjacent bony attachment site.\nMagnetic resonance imaging is useful in identifying high grade partial tears and complete tears that are unlikely to improve with rest and repeated steroid injections. The lack of a significant abnormality involving the common extensor tendon on MR imaging may prompt consideration of an alternate diagnosis such as radial nerve entrapment which may mimic or accompany lateral epicondylitis.\nCoronal, STIR image of the elbow demonstrates high T2 signal within and surrounding the common extensor tendons consistent with lateral epicondylitis.", "Differential Diagnosis": "Radial neuropathy, radial tunnel syndrome, lateral elbow instability, humeral fracture, radial head fracture, rotary instability of the elbow, posterior pinch syndrome/plica of the elbow, degenerative joint disease of the elbow, loose body, osteochondritis dissecans of the capitellum.", "Case Diagnosis": "Lateral epicondylitis", "Diagnosis By": "Radiographically and clinically.", "Treatment & Follow Up": "N/A", "Discussion": ": Lateral epicondylitis or tennis elbow is caused by degeneration and/or tearing of the common extensor tendons. The muscle groups that make up common extensor tendons that attach to the lateral epicondyle are the extensor carpi radialis brevis (ECRB), extensor digitorum communis, extensor carpi radialis longus, extensor carpi ulnaris, as well as the supinator muscle. many proposed pathophysiologic causes including inflammatory processes of the radial humoral bursa, synovium, periostium, and the annular ligament. \n\tIn 1979, Nirchl and Petronne attributed the pathology of lateral epicondylitis to angiofibroblastic hyperplasia which is microscopic tearing with formation of reparative tissue. This condition of microscopic tearing and repair response can lead to macroscopic tearing and structural failure of the origin of the ECRB muscle.\n\tThere can be numerous conditions that may lead to the above pathophysiology. Conditions such as weak rotator cuff muscles leading to poor shoulder mechanics which can cause overuse of wrist extensors in a back swing motion. Poor overall conditioning can also lead to improper wrist extension movements on long tennis or racquet ball matches. Improperly sized equipment and improper training technique can also attribute the condition.\n Intra-articular lesions such as loose bodies, synovitis, ulnohumoral osteophytes, and chondral lesions have been visualized during elbow arthroscopy in patients with lateral epicondylitis" }, "Topic": { "Title": "Lateral epicondylitis", "Disease Discussion": "Lateral epicondylitis, or tennis elbow, is the most common overuse syndrome of the elbow. A bit of controversy exists about not only the treatment of this condition, but also the exact pathophsiology, which is likely due to degeneration and/or tearing of the common extensor tendons. Lateral epicondylitis is reported more often in the industrial athlete and can be quite dedilitating. Because of the current controversy in regards to the pathophysiology, some debate exists on the proper treatment, which usually consists of a rehabilitation program, medical therapy, and surgical intervention, in combination or independently.", "ACR Code": "4.2", "Category": "Inflammatory, NOS", "Keywords": "lateral epicondylitistennis elbowangiofibroblastic hyperplasia", "Reference": "Disabella, Vincent N. D.O., Lateral Epicondylitis. E-medicine online. July 25, 2002.\nOwens, Brett D. M.D., Lateral Epicondylitis. E-medicine online. December 4, 2002.\nJin-Yang Ko, M.D., Treatment of Lateral Epicondylitis of the Elbow with Shock Waves. Clinical Orthopaedics and Related Research. Number 387, pp 60-67. June 2001.\nRussel, Fritz, M.D., Magnetic Resonance Imaging of the Musculoskeletal System: Part 3. The Elbow. Clinical Orthopaedics and related research. Volume 324, pp 321-339. March 1996." } }, { "U_id": "MPX1722", "TAC": [], "MRI": [ "MPX1722_synpic23304" ], "Case": { "Title": "Avascular Necrosis of Hip", "History": "History (can include gestational age, or age in days, weeks, months): 18 year old male with a 1 year history of pre B-cell acute lymphocytic leukemia currently on chemotherapy protocol that includes treatment with vincristine, methotrexate, prednisone/dexamethasone surges, and 6-MP. Patient complains of recent onset of bilateral hip pain.", "Exam": "Physical Exam and Laboratory: \nNormal physical exam except for bilateral decreased range of motion of the hips and atalgic gait secondary to hip pain. Laboratory studies showed mild macrocytic anemia and leukopenia.", "Findings": "Imaging Findings: Anteroposterior (AP) radiograph of the hips at presentation was normal and showed normal mineralization with no evidence of subluxation, dislocation, fractures, or osteoblastic/osteolytic changes. Magnetic resonance (MR) imaging of both the right and left hips demonstrated subchondral low signal intensity of the femoral head on coronal T1 imaging, best seen on the left, that becomes high signal intensity on a coronal STIR (fat suppressed) image. There was also increased signal intensity of the femoral neck, particularly the lateral margin, on STIR imaging. A subsequent AP hip radiograph 2 months after presentation shows new subchondral fracture lucencies in the right and left femoral heads and mild flattening of the left superior head along with bilateral preserved joint space. A year after presentation, an AP hip radiograph showed an increase in collapse of the left femoral head and bilateral early degenerative change of the hips.", "Differential Diagnosis": "Differential Diagnosis for these findings in this case:\nAvascular necrosis secondary to steroid therapy", "Case Diagnosis": "Avascular Necrosis of Hip", "Diagnosis By": "Imaging", "Treatment & Follow Up": "Treatment and Follow-up: The patient is currently receiving chemotherapy via the POG 9906 protocol, currently a phase III randomized study of multidrug antimetabolite therapy in children recently diagnosed with acute lymphoblastic leukemia designated as high risk. The protocol specifies a number of short bursts of steroids over the course of the 130-week regimen, which has been halted in this patient.", "Discussion": "Discussion (include references): Avascular necrosis of the hip may be a difficult diagnosis to make when a patient first presents with hip pain or mild gait abnormalities. Initial radiographs of the hips may no show no changes, as in this case. Therefore, clinical suspicion should be high for this disorder in a patient whose history suggests the diagnosis. Avascular necrosis is caused by a number of etiologies including femoral neck fracture, alcohol use, sickle cell disease, systemic lupus erythematosus, radiation treatment, and prolonged corticosteroid administration, as in this patient. Steroids have been implicated in about 20 to 35 percent of cases. The occurrence also appears to be directly related to the dosage level and duration of the medication. In decreasing order of frequency, the most common locations of steroid-induced avasular osteonecrosis are the femoral head, humeral head, the distal end of the femur, and the proximal part of the tibia. \n\nThe pathogenesis of steroid-induced osteonecrosis is unclear. However several mechanisms have been proposed and include both mechanical and vascular etiologies. Osteoporosis resulting in microfractures and later bone collapse is one mechanical theory. Vascular compromise due to hyperviscosity, vasculitis, fat embolization, and compression from marrow accumulation of relatively inelastic fat cells are also other possible causes.\n \nThe most common presenting symptom of avascular necrosis is pain. Groin pain and less commonly thigh and buttock pain are seen in patients with femoral head involvement. Patients may also complain of pain upon weight bearing. Thirty to fifty percent have bilateral involvement. Physical exam usually is nonspecific and may demonstrate limited range of motion particularly in abduction and internal rotation.\n\nRadiographic evaluation of a patient with suspected osteonecrosis includes an AP and frog-leg radiograph of both hips. As mentioned above, the initial radiographs may not show any evidence of disease. Subsequently, radiographic findings show sclerosis, indistinctive trabecular pattern, and patchy osteoporosis. Progressive radiograph findings include a crescentic subchondral line indicative of subchondral collapse, segmental flattening of the femoral head, and ultimately joint space narrowing, acetabular degenerative changes, and collapse of the femoral head.\n\nMR imaging is the most sensitive test for detecting avascular necrosis. As with this patient, MR imaging showed evidence of osteonecrosis prior to the radiographs. T1-weighted images typically show a line of low signal intensity, which corresponds to the presence of granulation tissue and sclerotic bone. T2-weighted images typically demonstrate a double line sign, which consists of a narrower line of low signal intensity that corresponds to bone sclerosis and an inner zone of high signal intensity that corresponds to granulation tissue. \n\nReferences\nLaPorte et al. \u201cMultifocal Osteonecrosis.\u201d Journal of Rheumatology. 25(10), Oct 1998, pp 1968-74. \nDonald Resnick. Diagnosis of Bone and Joint Disorders. Philadelphia: W.B. Saunders Co. 2002. pp. 3599-3637" }, "Topic": { "Title": "Avascular Necrosis of the Hips", "Disease Discussion": "Avascular necrosis of the hip may be a difficult diagnosis to make when a patient first presents with hip pain or mild gait abnormalities. Initial radiographs of the hips may not show any changes, as in this case. Therefore, clinical suspicion should be high for this disorder in a patient whose history suggests the diagnosis. Avascular necrosis is caused by a number of etiologies including femoral neck fracture, alcohol use, sickle cell disease, systemic lupus erythematosus, radiation treatment, and prolonged corticosteroid administration, as in this patient. Steroids have been implicated in about 20 to 35 percent of cases. The occurrence also appears to be directly related to the dosage level and duration of the medication. In decreasing order of frequency, the most common locations of steroid-induced avasular osteonecrosis are the femoral head, humeral head, the distal end of the femur, and the proximal part of the tibia. \n\nThe pathogenesis of steroid-induced osteonecrosis is unclear. However several mechanisms have been proposed and include both mechanical and vascular etiologies. Osteoporosis resulting in microfractures and later bone collapse is one mechanical theory. Vascular compromise due to hyperviscosity, vasculitis, fat embolization, and compression from marrow accumulation of relatively inelastic fat cells are also other possible causes.\n \nThe most common presenting symptom of avascular necrosis is pain. Groin pain and less commonly thigh and buttock pain are seen in patients with femoral head involvement. Patients may also complain of pain upon weight bearing. Thirty to fifty percent have bilateral involvement. Physical exam usually is nonspecific and may demonstrate limited range of motion particularly in abduction and internal rotation.\n\nRadiographic evaluation of a patient with suspected osteonecrosis includes an AP and frog-leg radiograph of both hips. As mentioned above, the initial radiographs may not show any evidence of disease. Subsequently, radiographic findings show sclerosis, indistinctive trabecular pattern, and patchy osteoporosis. Progressive radiograph findings include a crescentic subchondral line indicative of subchondral collapse, segmental flattening of the femoral head, and ultimately joint space narrowing, acetabular degenerative changes, and collapse of the femoral head.\n\nMR imaging is the most sensitive test for detecting avascular necrosis. As with this patient, MR imaging showed evidence of osteonecrosis prior to the radiographs. T1-weighted images typically show a line of low signal intensity, which corresponds to the presence of granulation tissue and sclerotic bone. T2-weighted images typically demonstrate a double line sign, which consists of a narrower line of low signal intensity that corresponds to bone sclerosis and an inner zone of high signal intensity that corresponds to granulation tissue. \n\nReferences\nLaPorte et al. \u201cMultifocal Osteonecrosis.\u201d Journal of Rheumatology. 25(10), Oct 1998, pp 1968-74. \nDonald Resnick. Diagnosis of Bone and Joint Disorders. Philadelphia: W.B. Saunders Co. 2002. pp. 3599-3637", "ACR Code": "4.9", "Category": "Differential Diagnosis", "Keywords": "osteoblastic/osteolytic changessubluxationsubchondral fracture lucencies", "Reference": "LaPorte et al. Multifocal Osteonecrosis J Rheumatol 1998; 25: 1968-74 \nResnick D. Diagnosis of Bone and Joint Disorders. Philadelphia: W.B. Saunders Co. 2002. pp. 3599-3637" } }, { "U_id": "MPX1725", "TAC": [], "MRI": [ "MPX1725_synpic24164", "MPX1725_synpic24165", "MPX1725_synpic24172" ], "Case": { "Title": "Cerebral infarct (L MCA territory)", "History": "36 y.o. African-American female with sickle cell anemia", "Exam": "Right facial numbness and slurring of speech", "Findings": "MRI\u2013brain: Diffusion-weighted images \u2013 Increased signal intensity involving L insular cortex and adjacent operculum. FLAIR and T2-weighted images \u2013 Increased signal intensity throughout L corona radiate w/ volume loss of the L frontal and parietal lobes. Large wedge-shaped region of encephalomalacia in the lateral R frontal lobe possibly secondary to prior infarct. \nMRA-brain: Severe near occlusion of ICAs bilaterally, normal appearance of vertebral and basilar arteries. \nDopper U/S-Carotids: R ICA completely occluded within a centimeter past bifurcation, L ICA \u2013 Very high resistance, abnormal flow at origin, possibly due to clot or very, very slow flow just above bifurcation", "Differential Diagnosis": "Cerebral infarct (L MCA territory), TIA, Common neurologic deficits after (old) stroke", "Case Diagnosis": "Cerebral infarct (L MCA territory)", "Treatment & Follow Up": "The primary medications used post-stroke are aspirin, coumadin, and clopidogrel for stroke prophylaxis. Depending on the severity and origin of the stroke, carotid endartarectomy, angioplasty and intralumenal stents, or extracranial-intracranial bypass may be considered.", "Discussion": "Cerebral infarcts (strokes) are either ischemic or hemorrhagic in origin. Ischemia is responsible for two-thirds of strokes, while hemorrhage causes about one-third. CT or MRI provide a more definitive diagnosis than simply the history or clinical symptoms. \n Ischemic strokes can be caused by thrombosis or embolism. Thrombosis more commonly occludes larger cerebral arteries, such as the ICAs, MCA or basilar artery, or the venous system. These are generally preceded by TIAs, which give warning of an impending stroke and its affected territory. The symptoms generally progress over minutes to hours. Embolism usually occurs when thrombi pass to distal cerebral arteries from larger vessels such as the heart, aorta, or large cerebral arteries. The symptoms at presentation usually do not progress further. Hemorrhagic strokes can result in destruction or compression of brain tissue or vessels that then cause neurologic symptoms. Some common causes are intracerebral hemorrhage, subarachnoid hemorrhage, or subdural or epidural hemorrhage. \n A patient who suffers from a cerebral infarct often has co-morbid conditions, broadly broken down into vascular, cardiac and hematologic disorders. Common vascular disorders are atherosclerosis, inflammatory disorders (e.g., SLE, temporal arteritis) and migraines. Arrhythmias, endocarditis, and rheumatic heart disease can lead to strokes. Like this patient, sickle cell disease and hypercoagulable states can also result in strokes.\n The middle cerebral artery is the most commonly occluded vessel in an ischemic stroke. A stroke of the superior division will result in contralateral hemiparesis affecting the upper body (but not the legs), contralateral hemisensory deficit and if the dominant hemisphere is involved, Broca\u2019s aphasia. An inferior division stroke may result in cortical sensory function impairment such as contralateral graphesthesia and stereognosis and disorders of spatial thought. In the dominant hemisphere, Wernicke\u2019s aphasia may occur. A stroke at the bifurcation or trifurcation will have superior and inferior divisional symptoms, plus homonymous hemianopia and global aphasia. Finally, an occlusion of the stem of the MCA will logically be the most devastating, as it can cause hemiparesis of the entire contralateral side." }, "Topic": { "Title": "Cerebral infarct (L MCA territory)", "Disease Discussion": "Cerebral infarcts (strokes) are either ischemic or hemorrhagic in origin. Ischemia is responsible for two-thirds of strokes, while hemorrhage causes about one-third. CT or MRI provide a more definitive diagnosis than simply the history or clinical symptoms. \n\nIschemic strokes can be caused by thrombosis or embolism. Thrombosis more commonly occludes larger cerebral arteries, such as the ICAs, MCA or basilar artery, or the venous system. These are generally preceded by TIAs, which give warning of an impending stroke and its affected territory. The symptoms generally progress over minutes to hours. Embolism usually occurs when thrombi pass to distal cerebral arteries from larger vessels such as the heart, aorta, or large cerebral arteries. The symptoms at presentation usually do not progress further. Hemorrhagic strokes can result in destruction or compression of brain tissue or vessels that then cause neurologic symptoms. Some common causes are intracerebral hemorrhage, subarachnoid hemorrhage, or subdural or epidural hemorrhage. \n\nA patient who suffers from a cerebral infarct often has co-morbid conditions, broadly broken down into vascular, cardiac and hematologic disorders. Common vascular disorders are atherosclerosis, inflammatory disorders (e.g., SLE, temporal arteritis) and migraines. Arrhythmias, endocarditis, and rheumatic heart disease can lead to strokes. Like this patient, sickle cell disease and hypercoagulable states can also result in strokes.\n\nThe middle cerebral artery is the most commonly occluded vessel in an ischemic stroke. A stroke of the superior division will result in contralateral hemiparesis affecting the upper body (but not the legs), contralateral hemisensory deficit and if the dominant hemisphere is involved, Broca\u2019s aphasia. An inferior division stroke may result in cortical sensory function impairment such as contralateral graphesthesia and stereognosis and disorders of spatial thought. In the dominant hemisphere, Wernicke\u2019s aphasia may occur. A stroke at the bifurcation or trifurcation will have superior and inferior divisional symptoms, plus homonymous hemianopia and global aphasia. Finally, an occlusion of the stem of the MCA will logically be the most devastating, as it can cause hemiparesis of the entire contralateral side.", "ACR Code": "9.6", "Category": "Hypoxic or Ischemic", "Keywords": "Cerebral infarct (L MCA territory)Cerebralinfarct", "Reference": "Clinical Neurology, 5th Edition, Chapter 9, 2002." } }, { "U_id": "MPX1733", "TAC": [], "MRI": [ "MPX1733_synpic55195", "MPX1733_synpic55196" ], "Case": { "Title": "Vestibular Schwannoma", "History": "24 y/o woman with hearing loss and ringing in the left ear", "Findings": "4x4x5mm soft tissue mass lesion located in the left internal auditory canal.", "Differential Diagnosis": "\u2022 Acoustic neuroma (vestibular Schwannoma)\n\u2022 Meningioma\n\u2022 Epidermoid inclusion cyst\n\u2022 Lipoma", "Case Diagnosis": "Vestibular Schwannoma", "Diagnosis By": "Clinical presentation and radiological interpretation", "Treatment & Follow Up": "She rec'vd gamma knife irradiation. However, since gamma-knife radiation was ineffective, surgery to remove the extra-axial mass would be the next option." }, "Topic": { "Title": "Vestibular Schwannoma", "Disease Discussion": "The differential diagnosis for an extrinsic intracranial mass in the cerebellopontine angle includes the vestibular Schwannoma, meningioma, and primary cholesteatoma (epidermoid inclusion cyst). Vestibular Schwannomas comprise 8-10% of cranial tumors and occur at a rate of 0.78-1.15/100,000 in the United States. They usually arise from the Obersteiner-Redlich transitional zone or line of the superior division of the vestibular nerve. This line occurs 8-12 mm distal to the brain, is the site where Schwann and connective cells give way to glia (oligodendrocytes), and marks the true boundary between the central and peripheral nervous system. They occur unilaterally in >95% of cases; bilateral masses are found in patients with neurofibromatosis Type 2, found on chromosome 22.\n\nThis mass is unusual in that one would expect extension of the mass to/from the IAC. Therefore, CPA meningioma was originally thought to be a strong possibility. However, the mass was confirmed by frozen section to exhibit pathology consistent with that of a vestibular Schwannoma. \n\nThin slice gadolinium-enhanced MRI is the study of choice with 98% sensitivity and a false-positive rate of ~0%. Computed tomography with intravenous contrast is the second line study.", "ACR Code": "25.3641", "Category": "Neoplasm, non-glial", "Keywords": "vestibularschwannomaneurofibromatosis", "Reference": "Fischbein, NJ et al. Teaching Atlas of Brain Imaging. Thieme: New York, 2000. \n\nGreenberg, MS. Handbook of Neurosurgery, 5th ed. Greenberg: Lakeland, 2001." } }, { "U_id": "MPX1751", "TAC": [], "MRI": [ "MPX1751_synpic24225" ], "Case": { "Title": "Osteochondritis Dissecans Stage IV", "History": "Hx: 22 y.o. male no chief complaint or physical exam available.", "Findings": "MRI: Intraarticular osseous fragment within the lateral aspect of medial femoral condyle with fluid seen surrounding the lesion and disruption of the articular cartilage, and slight posterior diplacement of the osseous fragment", "Differential Diagnosis": "DDx:Osteochondral fracture, chondral injuries, osteonecrosis, accessory ossicle", "Case Diagnosis": "Osteochondritis Dissecans Stage IV", "Treatment & Follow Up": "Non-operative management is based on lesion size and patient maturity. The smaller the lesion and acquiring the lesion prior to growth plate closure provides good prognostic indicators for favorable healing. Typically, with period of immobilization and gradual weight-bearing lesions heal. MRI can assess healing.\nOperative management is considered when lesions are detached or unstable and in patients approaching physeal closure and/or non-operative treatment has failed. There are many techniques from drilling into OCD lesion to create revascularization and heal with fibrocartilage (typically in 4-5mths) , to staples, and arthotomy with bone graph and K-wire fixation, in addition using autologous chondrocyte implantation.", "Discussion": "OCD has pathologic mechanism that continues to be unclear. A multitude of theories have developed to explain etiology, from repetitive microtrauma, and stress fractures to avascular necrosis. The most common site is in the knee. 85% of knee OCD lesions are located in medial condyle which is theorized to be caused by possible enlargement of tibial spines in combination with unusual stress against these surfaces.\n MRI has utility for OCD lesions. It accurately measures lesion size. Provides cartilage/subchondral bone status. The higher signal on T2 weighted sequences can show marrow changes consistent with bony edema. Interestingly, unstable OCD lesions that fail non-operative managment are most often lesions that have a high T2 signal linearity behind the OCD lesion and underlying bone. In addition, the high signal line maybe consistent with a disruption of the articular cartilage seen on T1 sequences.\n OCD lesion staging classification on MRI:\nStage I: small change of signal without clear margins of fragment.\t\nStage II: Osteochondral fragment with clear margins without fluid between fragment and underlying bone.\nStage III: Fluid is partially visible between fragment and underlying bone. \nStage IV: Fluid completely surrounds the fragment but the fragment is in situ.\nStage V: Fragment is completely detached and displaced (loose body)." }, "Topic": { "Title": "Osteochondritis Dissecans", "Disease Discussion": "OCD's pathologic mechanism is uncertain, so there remains no one clear etiology. A multitude of theories have developed to explain etiology, from repetitive microtrauma, and stress fractures to avascular necrosis. The most common site is in the knee. 85% of knee OCD lesions are located in medial condyle which is theorized to be caused by possible enlargement of tibial spines in combination with unusual stress against these surfaces.\n MRI has utility for detecting and characterizing OCD lesions. It accurately measures lesion size and provides cartilage/subchondral bone status. The higher signal on T2 weighted sequences can show marrow changes consistent with bony edema. Interestingly, unstable OCD lesions that fail non-operative managment are most often lesions that have a high T2 signal linearity behind the OCD lesion and underlying bone. In addition, the high signal line may be consistent with a disruption of the articular cartilage seen on T1 sequences.\n OCD lesion staging classification on MRI:\t\nStage I: small change of signal without clear margins of fragment.\nStage II: Osteochondral fragment with clear margins without fluid between fragment and underlying bone.\nStage III: Fluid is partially visible between fragment and underlying bone. \nStage IV: Fluid completely surrounds the fragment but the fragment is in situ.\nStage V: Fragment is completely detached and displaced (loose body).\nTreatment/Management: \nNon-operative management is based on lesion size and patient maturity. The smaller the lesion and acquiring the lesion prior to growth plate closure provides good prognostic indicators for favorable healing. Typically, with a period of immobilization and gradual weight-bearing, lesions heal. MRI can assess healing.\nOperative management is considered when lesions are detached or unstable and in patients approaching physeal closure and/or non-operative treatment has failed. There are many techniques from drilling into the OCD lesion to create revascularization and healing with fibrocartilage (typically in 4-5mths), to staples, and arthrotomy with bone graph and K-wire fixation, in addition using autologous chondrocyte implantation.", "ACR Code": "4.4", "Category": "Trauma", "Keywords": "MRI classsificationOsseous fragments", "Reference": "Flynn. Osteochondritis Dissecans. J Pediatric Orthop. 2004; July/Aug, 24 (4): 434-443\nSchenck, Jr. Robert, MD. Osteochrondritis Dissecans. J Bone and J Surg Am; 1996 Mar: 78-A(3): 439-456\nYochum, Terry. Essentials of Skeletal Radiology. 1996,Vol 2:1295-1301" } }, { "U_id": "MPX1737", "TAC": [], "MRI": [ "MPX1737_synpic52862", "MPX1737_synpic52863", "MPX1737_synpic52864", "MPX1737_synpic52865", "MPX1737_synpic52866", "MPX1737_synpic52867" ], "Case": { "Title": "Quadriceps tendon rupture", "History": "52 y/o male with swollen painful knee and weakness in extension s/p fall", "Exam": "Marked swelling superior aspect of joint. Mildly ballotable patella. 3/5 quad strength in extension.", "Findings": "Xray remarkable for effusion.\nMRI reveals complete quadriceps tendon discontinuity medially, with retraction. Some intact deep fibers laterally. Effusion and edema. Superior patellar enthesophyte. No patella alta.", "Differential Diagnosis": "Quadriceps tendon rupture", "Case Diagnosis": "Quadriceps tendon rupture", "Diagnosis By": "Patient taken to surgery for repair", "Treatment & Follow Up": "Patient taken to surgery for repair within 48 hrs of diagnosis.", "Discussion": "Risk factors included age, DJD and patellar enthesophyte (risk factor for tendon rupture vs quad muscle tear).\n\nOther risk factors not present: steroid Tx, obesity, HyperPTH, RA, leukemia, DM, SLE, gout, infection" }, "Topic": { "Title": "Quadriceps tendon rupture", "Disease Discussion": "Quadriceps tendon ruptures usually result from a rapid, strong eccentric contraction of the quadriceps muscle with the knee partially flexed, typically during a fall. This injury may also be seen after a direct blow to the quadriceps tendon. Ruptures are also known to occur spontaneously or after relatively trivial trauma, particulary in those with chronic conditions such as diabetes, chonic renal disease, rheumatoid arthritis, or any condition requiring the use of long-term steroids. These tears most commonly occur at the tendinous insertion of the quadriceps to superior pole of the patella. \n\nPatients usually present with knee pain, swelling and difficulty ambulating. Physical exam with complete tears classically demonstrates suprapatellar swelling, a palpable defect in the suprapatellar region with tenderness, a low-riding patella, and decreased active range of motion and strength of knee extension. Partial tears are often much more difficult to discern clinically and as such may be easily misdiagnosed as a \"knee sprain.\"\n\nImaging modalites such as plain radiography and MRI are often used to support the clinical findings. Findings that suggest quadriceps tear on plain radiographs include suprapatellar soft tissue swelling and distortion of the typical fat planes, and patella baja (inferiorly positioned patella). Due to the fact the injury commonly occurs at the tendinous insertion site at the patella, avulsion fractures of the patella may also be seen. MRI demonstrates disruption of the normal low intensity quadriceps tendon on T2 weighted images, which is replaced by high intensity fluid signal secondary to inflammatory response and edema. Ultrasound is another modality that may be used to demonstrate quadriceps tendon tears. However, unlike MRI, ultrasound will not demonstrate secondary associated findings often seen in traumatic injuries to the knee such as ligamentous and osteochondral insults, and as such is used much less frequently.\n\nPartial tears are treated conservatively, typically with a 1-2 month peroid of immobilization in full knee extesion, followed by a course of physical therapy to restore range of motion and strength. Complete tears are usually treated with early surgical intervention which again is followed by a course of immobilization and physical therapy.", "ACR Code": "4.4", "Category": "Trauma", "Keywords": "quadricepstearrupture", "Reference": "Rogers L. Radiology of Skeletal Trauma (2nd ed). Churchill Livingstone, New York., 1992\n\nResnick D. Diagnosis of Bone and Joint Disorders (3rd ed). W. B. Saunders, Philadelphia, 1995\n\nLyle, James, and Lynn A. Crosby. \"Quadriceps Tendon Rupture.\" 18 Mar. 2005. 3 Jan. 2006 http://www.emedicine.com" } }, { "U_id": "MPX1775", "TAC": [], "MRI": [ "MPX1775_synpic21376", "MPX1775_synpic21377", "MPX1775_synpic21378" ], "Case": { "Title": "Juvenile pilocytic astrocytoma", "History": "This patient originally presented at the age of 3 with right facial palsy, worsening over a six month period, now undergoing routine surveillance post-resection and chemotherapy for a CNS tumor.", "Exam": "Physical examination and laboratory data were noncontributory", "Findings": "Diffuse encephalomalacic changes are seen in the right cerebellum secondary to a right suboccipital craniectomy. A heterogeneous cystic and solid lesion is seen at the right cerebellopontine angle with heterogeneous contrast enhancement of a mural nodule.", "Differential Diagnosis": "Pilocytic astrocytoma\nMedulloblastoma \nHemangioblastoma\nEpendymoma", "Case Diagnosis": "Juvenile pilocytic astrocytoma", "Treatment & Follow Up": "Complete resection is often curative, but will recur if incomplete. Chemotherapy is used in cases of recurrence.", "Discussion": "Tumors of the posterior fossa are the most common brain tumor in children. They often present with symptoms of hydrocephalus (e.g. headache, vomiting and vertigo), cranial nerve or cerebellar symptoms (e.g. ataxia). Obstruction of the fourth ventricle leading to hydrocephalus is not uncommon. Cerebellar signs may be unilateral or axial depending on involvement of the vermis or a single hemisphere. Astrocytomas and medulloblastomas are the most common posterior fossa tumors in children and present with similar frequency. Ependymomas and hemangioblastomas are also commonly seen.\n\nAstrocytomas are common in children but are not uncommon in adults. The incidence is similar between male and female, with perhaps a slight female predominance. Pilocytic astrocytomas are, by definition, low-grade (WHO grade I) tumors. They are well circumscribed lesions and may be cystic, solid or both. The cystic form is seen in greater than 75% of lesions and has a classic appearance of a mural nodule in a cyst. With MRI, the mural tumor appears iso- or hypointense on T1-weighted images and iso- to hyperintense on T2-weight images. The cyst wall does not consist of tumor cells and thus will not enhance on CT or MRI. Complete resection is often curative, however solid tumors may not be as amenable to resection if the fourth ventricle is involved.\n\nMedulloblastoma, a primitive neuroectodermal tumor, is rare in adulthood, most commonly occurring between ages 5 and 15 with a 2:1 male predominance. These highly malignant tumors usually arise in the midline in the posterior fossa (85%). Medulloblastoma appears hypointense on T1, hyperintense on T2 and enhances with contrast. It may appear well-circumscribed but is often found to be invasive at the margins on histology, often invades the fourth ventricle and will seed the subarachnoid space \u2013 necessitating surveillance of the spinal cord. Death usually comes within months if not treated. Resection, chemotherapy and radiation can extend life, with 60-75% survival at five years.\n\nHemangioblastomas are benign, low-grade (WHO grade I) tumors that are associated with von Hippel-Lindau disease, but also occur in isolation. They have a very similar appearance on MRI to astrocytomas, consisting of a cyst with mural module, but may also be solid or multiple with von Hippel-Lindau. The mural nodule enhances and has classic flow and enhancement features on angiography. As with pilocytic astrocytoma complete resection is often curative, however recurrence is not uncommon.\n\nEpendymomas most commonly arise in the floor of the fourth ventricle. This is a malignant tumor that can spread throughout the ventricular system. This mass can be differentiated from the others discussed here as it often has calcifications on CT. Complete resection is rarely achievable, but these are usually radiosensitive. On MRI, ependymomas may appear as multiple small cysts that enhance with contrast.\n\nMRI is the leading diagnostic and surveillance modality for posterior fossa tumors. It provides greater detail of the lesion and has been shown to be more sensitive and specific than CT. Although pediatric patients are more frequently sedated for MRI studies, there is no radiation and no iodinated contrast as with CT" }, "Topic": { "Title": "Juvenile pilocytic astrocytoma", "Disease Discussion": "Tumors of the posterior fossa are the most common brain tumor in children between 2 and 15 yrs. They often present with symptoms of hydrocephalus (e.g. headache, vomiting and vertigo), cranial nerve or cerebellar symptoms (e.g. ataxia). Obstruction of the fourth ventricle leading to hydrocephalus is not uncommon.\n\nCerebellar signs may be unilateral or axial depending on involvement of the vermis or a single hemisphere. Astrocytomas and medulloblastomas are the most common posterior fossa tumors in children and present with similar frequency. Ependymomas and hemangioblastomas (adults) are also commonly seen in the posterior fossa.\n\nAstrocytomas are the most common intraaxial neoplasms. Pilocytic astrocytomas are, by definition, low-grade (WHO grade I) tumors. They are well circumscribed lesions and may be cystic, solid or both. The cystic form is seen in greater than 75% of lesions and has a classic appearance of a mural nodule in a cyst.\n\nWith MRI, the mural tumor nodule appears iso- or hypointense on T1-weighted images and iso- to hyperintense on T2-weight images. The cyst wall does not consist of tumor cells and thus will not enhance on CT or MRI. Complete resection is often curative, however solid tumors may not be as amenable to resection if the fourth ventricle is involved.", "ACR Code": "1.3", "Category": "Neoplasm, glial", "Keywords": "Juvenile pilocytic astrocytomapilocytic astrocytomaastrocytoma", "Reference": "1. Simon, R. Clinical Neurology, Fourth Edition, Appleton and Lange, 1999.\n2. Taveras J. Neuroradiology, Third Edition, Williams and Wilkins, 1996.\n3. Sutton D. Textbook of Radiology and Imaging, Seventh Edition, Churchill Livingstone, 2003.\n4. Medina LS, Kuntz KM, Pomeroy S. Children with headache suspected of having a brain tumor: a cost-effectiveness analysis of diagnostic strategies. Pediatrics. 2001 Aug;108:255-63" } }, { "U_id": "MPX1782", "TAC": [], "MRI": [ "MPX1782_synpic50939", "MPX1782_synpic50978" ], "Case": { "Title": "Pseudotumor cerebri", "History": "39 y/o woman with worsening headaches and blurry vision x 6 weeks.", "Exam": "Obese woman\nVA:20/125 right eye, 20/125 left eye\nIshihara color plate 3/11 right eye, 3/11 left eye\nExtraocular movements intact\nNo Relative afferent pupillary defect \nHumphrey visual field (30-2): constricted to approx 10 degree OU\nModerate optic disk edema 360 degrees OU", "Findings": "\u2022 Increased fluid within the optic nerve sheaths\n\u2022 Partially empty sella \n\u2022 Slight flattening of the posterior aspect of the left globe at the optic nerve insertion", "Differential Diagnosis": "\u2022 Idiopathic intracranial hypertension\n\u2022 Obstructive hydrocephalus\n\u2022 Intracranial mass lesion", "Case Diagnosis": "Pseudotumor cerebri", "Diagnosis By": "Lumbar puncture", "Treatment & Follow Up": "Bilateral optic nerve sheath fenestration. Visual acuity improved to 20/40 left eye and 20/40 right eye and color vision returned to 11/11 left eye and 11/11 right eye on ishihara color plates on post-op day 1." }, "Topic": { "Title": "Pseudotumor cerebri (\"benign\" idiopathic intracranial hypertension)", "Disease Discussion": "Idiopathic intracranial hypertension (IIH) - i.e. not produced by an expansile intracranial mass lesion - is often called \"pseudotumor cerebri\". Reported by Heinrich Quincke in 1893 and by Max Nonne in 1904, it was originally called \"serous meningitis\". It is most common in overweight women 20-50 years old. The clinical presentation usually includes headaches or visual problems.\n\n\u00bb Reported causes include:\n\u2022 Hypervitaminosis A\n - by increasing interstitial water?\nPMID: 4593602 - http://jn.nutrition.org/cgi/content/abstract/104/4/478\n\u2022 Dural sinus thrombosis/stenosis\n - increasing intracranial venous pressure\n - by deceasing CSF absorption\n\u2022 Pregnancy\n - increased venous pressure\n\u2022 Obesity\n - increased venous pressure\n\n\u00bb The diagnostic criteria include:\n\u2022 secondary features of increased pressure (e.g. papilledema)\n\u2022 elevated CSF pressure (>250 mm H2O) by LP in lateral decubitus position\n\u2022 normal cerebrospinal fluid chemistry and cells\n\u2022 normal cerebral anatomy by CT/MR imaging\n\n\u00bb LP Results in psedudotumor cerebri:\n\u2022 http://www.aafp.org/afp/20030915/1103.html\n\u2022 http://www.fpnotebook.com/Neuro/Lab/CrbrspnlFldExmntn.htm\n\u2022 http://www.ncbi.nlm.nih.gov/pubmed/19515130'>http://www.ncbi.nlm.nih.gov/pubmed/19515130\n\n\u00bb The physiology may be related to:\n\u2022 cerebral brain interstitial edema\n\u2022 hyperemic brain swelling - vasocongestion\n\u2022 imbalance between CSF production and resorption\n\u2022 venous hypertension\n\u2022 dural sinus thrombosis or stenosis (including bilateral transverse sinus stenosis) - PMID: 19515130 http://www.ncbi.nlm.nih.gov/pubmed/19515130\n\n\u00bb Recent literature has demonstrated that the transverse sinus stenosis may be secondary to increased intracranial pressure - and can be reversed with CSF shunting alone - no vascular intervention. It may also recur when intracranial pressure rises PMID: 17416816 - http://www.ajnr.org/cgi/reprint/28/4/656\nPMID: 21680652 - http://www.ajnr.org/content/32/11/1986.long\n\n\n\u00bb Thus, we have a classic \"chicken and egg\" problem: Is pseudo tumor caused by sinus stenosis or is it causing the stenosis?\n\n\u00bb Hypervitaminosis A may cause IIH. This was described in arctic explorer who ate polar bear liver, as well as acne patients treated with retinoic acid.\n\n\u00bb Patients with IIH may have elevation of both CSF and serum Vitamin A, w/o exogenous sources.\nhttp://www.neurology.org/cgi/content/full/64/11/1827\nPMID: 10496276 - http://www.neurology.org/cgi/content/abstract/53/5/1114\n\u2022 Treatment options\n\u00bb Reduce \n\nhttp://www.ninds.nih.gov/disorders/pseudotumorcerebri/pseudotumorcerebri.htm\nhttp://www.mayoclinic.com/health/pseudotumor-cerebri/DS00851\nhttp://www.webmd.com/brain/pseudotumor-cerebri-10678\nhttp://emedicine.medscape.com/article/1143167-overview\nhttp://www.revoptom.com/HANDBOOK/SECT53a.HTM\nhttp://en.wikipedia.org/wiki/Idiopathic_intracranial_hypertension", "ACR Code": "1.3", "Category": "Clinical Exam Finding or Sign", "Keywords": "CSF homeostasispapilledemadural sinus stenosis thrombosis", "External Links": "www.ncbi.nlm.nih.gov/pubmed/19515130" } }, { "U_id": "MPX1791", "TAC": [], "MRI": [ "MPX1791_synpic21757", "MPX1791_synpic21758", "MPX1791_synpic21759" ], "Case": { "Title": "Lipoma Arborescens", "History": "presents with atraumatic knee swelling", "Exam": "swollen knee", "Findings": "There are numerous villous-like projections within the joint space of the knee on MR imaging. These are fatty in signal intensity. There is an associated effusion.", "Differential Diagnosis": "essentially none.\nOther synovial processes; such as PVNS, synovial hemangioma and synovial osteochondromatosis; would not present with an arborizing fatty mass.", "Case Diagnosis": "Lipoma Arborescens", "Diagnosis By": "pathognomonic", "Treatment & Follow Up": "surgical excision", "Discussion": "This uncommon diagnosis has an \"Aunt Minnie\" appearance. The villous-like fatty synovial mass can only be lipoma arborescens" }, "Topic": { "Title": "Lipoma Arborescens", "Disease Discussion": "Lipoma Arborescens is a tumor-like non-neoplastic process that affects the synovium. Typically there is a villous-like hypertrophy of fat within the joint. It produces a very characteristic arborizing (tree-like) pattern on MR imaging with typical fat signal within the lesion. The knee is most commonly affected and the process is typically monoarticular. Typically there is an associated effusion. Patients present with slowly progressive joint swelling and pain. Treatment: surgical excision.", "ACR Code": "4.3", "Category": "Neoplasm, benign", "Keywords": "lipomaarborescnessynovium", "Reference": "Musculoskeletal Imaging--A Teaching File, Chew F. etal\nLippincott 1999" } }, { "U_id": "MPX1796", "TAC": [], "MRI": [ "MPX1796_synpic42084", "MPX1796_synpic42085", "MPX1796_synpic42086", "MPX1796_synpic42087", "MPX1796_synpic42088" ], "Case": { "Title": "Intracranial Epidermoid Tumor", "History": "This 78 year old man came to the hospital for recent seizure like activity. Past medical history is significant for seizures.", "Exam": "N/A", "Findings": "Irregularly shaped, well demarcated mass in the left cerebellopontine angle that is slightly hyperintense on axial T1 MRI before contrast, hypointense on axial T1 MRI after contrast, hyperintense on axial T2 MRI, hypointense on axial FLAIR, and hyperintense on axial DWI MRI.", "Differential Diagnosis": "\u2022 Epidermoid tumor\n\u2022 Arachnoid cyst\n\u2022 Dermoid tumor\n\u2022 Acoustic neuroma (Vestibular Schwannoma)\n\u2022 Malignancy", "Case Diagnosis": "Intracranial Epidermoid Tumor", "Diagnosis By": "MRI images", "Treatment & Follow Up": "See description of intracranial epidermoid tumor." }, "Topic": { "Title": "Intracranial Epidermoid Tumor", "Disease Discussion": "Epidermoids, or cholesteatomas, are the most common congentital or embryonal CNS tumor. Some sources state that they account for as little as 0.3% to as much as 1.8% of tumors. During the third and fifth week of fetal development during the closure of the neural tube, epidermoids derive from the ectopic inclusions of epithelial cells. If the cells have less cell differentiation, they result in dermoid tumors instead of epidermoid tumors. The epithelial lesions grow at a rate similar to skin cells, and as a result, cause a very slow symptomatic onset. \n\nThey usually arise in the suprasellar region, the skull base, brainstem, or cerebellopontine angle. Recent literature suggests that epidermoid tumors have mostly been found at the cerebellopontine angle (37.3%) and in the parasellar region (30%), growing by spreading in the subarachnoid space of the basal cisterns. They rarely develop into malignant processes.\n\nEpidermoids have a pearly appearance and are well circumscribed and encapsulated. The epidermoids that are hypodense on CT may contain a soft, waxy material that consists of cholesterol crystals. The hyperintense epidermoids on the other hand are mostly cystic and contain fluid of various colors. Other sources suggest that the inner material is due to the progressive desquamation and breakdown of keratin.\n\nSymptoms associated with epidermoids usually appear after the second decade of life. These symptoms are caused by displacement of adjacent vascular and neural structures. The most frequent presenting symptom is trigeminal neuralgia. Other symptoms that can occur are similar to those caused by acoustic neuroma like vertigo, asymmetric hearing loss, and unilateral tinnitus. If the lesion gets very large, symptoms like headache, nausea, vomiting, diplopia, and ataxia, or symptoms of increased intracranial pressure and hydrocephalus can develop. \n\nOn imaging, most epidermoid tumors show a distinctive MRI appearance. They are usually hypointense on T1 MRI and hyperintense on T2 MRI. On T1, they can also show a characteristically marbled inner pattern. Diffussion-weighted imaging can provide additional information by showing a clear, hyperintense signal. On CT, an epidermoid can appear as a well-defined lobulated hypodense mass.\n\nTreatment is surgical resection with radical removal of the tumor capsule.", "ACR Code": "1.3", "Category": "Neoplasm, benign", "Keywords": "EpidermoidCerebellopontineMRI", "Reference": "Dechambre S, Duprez T, Lecouvet F, Raftopoulos C, Gosnard G: Diffusion-weighted MRI postoperative assessment of an epidermoid tumour in the cerebellopontine angle. Neuroradiology 41: 829-831, 1999.\n\nGao P, Osborn AG, Smirniotopoulos JG, Hannis CP: Radiologic pathologic correlation: Epidermoid tumor of the cerebellopontine angle. American Journal of Neuroradiology 13:863-872, 1992.\n\nIaconetta G, Carvalho GA, Vorkapic P, Samii M. Intracerebral epidermoid tumor: A case report and review of the literature. Surgical Neurology 2001;55:218 \u201322.\n\nMerritt\u2019s Neurology 11th edition, 2005\n\nOchi M, Hayashi K, Hayashi T, Morikawa M, Ogino A, Hashmi R, Iwanaga M, Yasunaga A, Shibata S. Unusual CT and MR Appearance of an Epidermoid Tumor of the Cerebellopontine Angle. American Journal of Neuroradiology 1998; 19:1113-1115" } }, { "U_id": "MPX1788", "TAC": [], "MRI": [ "MPX1788_synpic27142", "MPX1788_synpic27143", "MPX1788_synpic27144", "MPX1788_synpic27145", "MPX1788_synpic27146" ], "Case": { "Title": "Creutzfeldt-Jakob Disease", "History": "63 y/o male with history of NHL, and three weeks of decreasing visual acuity, gait ataxia, and poor coordination of left arm, that is worse in AM and improving during the course of day. New onset of personality changes and mood lability.", "Exam": "Alert and Oriented X 3. Left homonymous hemianopsia with macular sparing, horizontal and vertical nystagmus, Normal DTRs bilat, severe upper extremity dysmetria on right, abnormal Romberg. Unable to do tandem gait, and bumps into objects on left. LP: Positive 14-3-3 protein, increased protein, RBCs, and polysegs. Elevated AST/ALT. Elevated thyroid auto-antibodies", "Findings": "DWI Abnormalities in right occipital lobe/post temporal cortex w/o corresponding T2 changes. \n\nPET: abnormal hypometabolism R cerebrum and R cerebellum.", "Differential Diagnosis": "Alzheimer disease, frontal and temporal dementia, HIV and HSV encephalitis, hydrocephalus, metabolic disorders, multi-infarct dementia, diffuse Lewey body disease, Hashimoto encephalopathy.", "Case Diagnosis": "Creutzfeldt-Jakob Disease", "Diagnosis By": "Brain Biopsy", "Treatment & Follow Up": "Pt was admitted to the neurology ward, and a full neurological work-up was started. Paraneoplastic/neoplastic etiologies were excluded due to rapid progression and as a result of test results. Pt\u2019s mental status continued to decline, and he was started on high dose steroids course for possible Hashimoto\u2019s encephalopathy, after labs showed increased auto-antibodies to the thyroid. Transitioned to Prednisone 80mg QD, and started on Serroquel and Geodon for agitation and sundowning. Condition continued to worsen with difficulty protecting airway and he was intubated and transferred to MICU. Pt was placed on ventilator and found to have a retroperitoneal bleed. Pt had brain biopsy that confirmed CJD. After consultation with the family he was extubated and moved to a General Medicine ward. He expired the following week.", "Discussion": "Creutzfeldt-Jacob disease (CJD) is a transmissible neurodegenerative spongiform encephalopathy, that is progressive and ultimately fatal, with no effective treatment at the present time. It is classified as a prion disease, which is an abnormal conformation of a host glycoprotein, that replicates in a self-perpetuating cycle of abnormal proteins and amyloid plaques. CJD has a long incubation period, with most cases presenting in the sixth or seventh decade of life. CJD has a mean onset of 62 years, with reports of cases ranging from 17 to 83 years of age. The incidence is approximately 1 case per million internationally and in the United States, with some Libyan Jewish populations and a few populations in rural areas of Slovakia, having 60-100 times this rate of familial CJD. \n\nThere are three classifications of CJD: sporadic (spontaneous mutation), variant (infectious), and familial. Familial CJD accounts for about 10% of all cases, and is inherited in an autosomal dominant pattern. The mean duration after symptoms present is 8 months for the sporadic form, 16 months for variant, and 26 months for familial form. \n\nCJD is characterized by a rapidly progressive cognitive imparement, behavorial abnormalities, myoclonic jerks, higher cortical dysfunction and visual cortical abnormalities, cerebellar dysfunction, and pyramidal and extrapyramidal signs. These signs and symptoms steadily increase, with death primarily occurring secondary to bronchopneumonia, due to overall disability and a bed-ridden state.\n\nTesting for CJD is difficult at best, and in its early stages can present like many different disease processes, with a definitive diagnosis being accomplished only after a biopsy of brain tissue. Sixty percent of patients show characteristic EEG changes of periodic sharp wave complexes (PSWCs) on a slow and low-voltage background. However, EEG has a low specificity and a sensitivity of only 50.0%. Testing for brain specific proteins such as the 14-3-3 protein and the neuron-specific enolase also supports a diagnoses of CJD, but even though they are more specific than EEG, they have a sensitivity of 84.0% and\n73.3% respectfully.\n\nPET scanning may show regional hypometabolism of glucose.\n\nThe most sensitive test to date is the MRI diffusion weighted images (DWI), which has a sensitivity and specificity of 92.3% and 93.8 respectfully. DWI is more sensitive than both T2I and FLAIR. DWI shows symmetrical high intensity lesions in the striatum (caudate and putamen), the dorsomedial thalamic nuclei, and cerebral cortical lesions. These findings were identifiable before PSWC\u2019s on EEG , and before the final stages of the disease, which results in brain atrophy. \n\nTreatment at this time is symptomatic and palliative, but a number of experimental interventions are being tested, such as antimalarial quinacrine, chlorpromazine, and pentosan polysulphate, which prevent prion conversion and production, and an immunization that reduces the cerebral amyloid accumulation. \n\nFinally, as seen with this patient, CJD must always be in a differential for rapid dementia or for patients experiencing changes in mood, ataxia, and visual disturbances.\n\nToday, we can only ease the suffering of CJD, but on the horizon a treatment may be near, and someday we can offer a real cure and a way to stop this deadly prion disease." }, "Topic": { "Title": "Creutzfeldt-Jakob Disease", "Disease Discussion": "Creutzfeldt-Jacob disease (CJD) is a neurodegenerative spongiform encephalopathy, that is progressive, transmissible, and ultimately fatal, with no effective treatment at the present time. It is classified as a prion disease, which is an abnormal conformation of a host glycoprotein, that replicates in a self-perpetuating cycle of abnormal proteins and amyloid plaques. CJD has a long incubation period, with most cases presenting in the sixth or seventh decade of life. CJD has a mean onset of 62 years, with reports of cases ranging from 17 to 83 years of age. \n\nThe incidence is approximately 1 case per million internationally and in the United States, with some Libyan Jewish populations and a few populations in rural areas of Slovakia, having 60-100 times the rate of familial CJD.\n\nThere are three classifications of CJD: sporadic (spontaneous mutation), variant (infectious), and familial. Familial CJD accounts for about 10% of all cases, and inherited in an autosomal dominant pattern. The mean duration after symptoms present is 8 months for the sporadic form, 16 months for variant, and 26 months for familial form. \n\nCJD is characterized by a rapidly progressive cognitive imparement, behavorial abnormalities, myoclonic jerks, higher cortical and cortical visual abnormalities, cerebellar dysfunction, and pyramidal and extrapyramidal signs. These signs and symptoms steadily increase, with death primarily occurring due to bronchopneumonia, due to a bed-ridden state.\n\nTesting for CJD is difficult at best, and in its early stages can present like many different disease processes, with a definitive diagnosis being accomplished only after a biopsy of brain tissue. Sixty percent of patients show characteristic EEG changes of periodic sharp wave complexes (PSWCs) on a slow and low-voltage background, but EEG has a low specificity and a sensitivity of only 50.0%. Testing for brain specific proteins such as the 14-3-3 protein and the neuron-specific enolase also supports a diagnoses of CJD, but even though they are more specific than EEG, only have a sensitivity of 84.0% and 73.3% respectfully. \n\nPET scanning may show regional hypometabolism of glucose. \n\nThe most sensitive test to date is the MRI diffusion weighted images (DWI), which has a sensitivity and specificity of 92.3% and 93.8 respectfully. DWI is more sensitive than both T2I and FLAIR. DWI shows symmetrical high intensity lesions in the striatum (caudate and putamen), the dorsomedial thalamic nuclei, and cerebral cortical lesions. These findings were identifiable before PSWC\u2019s on EEG , and before the final stages of the disease, which results in brain atrophy. \n\nTreatment at this time is symptomatic and palliative, but a number of experimental interventions are being tested, such as antimalarial quinacrine, chlorpromazine, and pentosan polysulphate, which prevent prion conversion and production, and an immunization that reduces the cerebral amyloid accumulation. \n\nFinally, as seen with this patient, CJD must always be in a differential for rapid dementia or for patients experiencing changes in mood, ataxia, and visual disturbances. Today, we can only ease the suffering of CJD, but on the horizon a treatment may be near, and someday we can offer a real cure and a way to stop this deadly prion disease.", "ACR Code": "1.2", "Category": "Pathology", "Keywords": "prion diseasedementia", "Reference": "1. Belay ED. Variant Creutzfeldt-Jakob Disease and Bovine Spongiform Encephalopathy. Clin Lab Med 2002; 22: 849-862\n2. Rao C. Variant Creutzfeldt-Jacob Disease and Bovine Spongiform Encephalopathy. EMedicine. August 8, 2005.\n3. Shiga Y. Diffusion-Weighted MRI Abnormalities as an early Daignostic Marker for Creutzfeldt-Jacob Disease. Neurology 2004; 63: 443-449.\n4. Wisniewski T. Prion-Related Diseases. Emedicine. October 4, 2004." } }, { "U_id": "MPX1781", "TAC": [], "MRI": [ "MPX1781_synpic50581", "MPX1781_synpic50633", "MPX1781_synpic50634", "MPX1781_synpic50635", "MPX1781_synpic50636", "MPX1781_synpic50637" ], "Case": { "Title": "Monostotic Fibrous Dysplasia", "History": "A 29-year-old man with injury to right shoulder while lifting weights. Clinically diagnosed with rotator cuff biceps tendinitis.", "Exam": "Rotator cuff biceps tendinitis.\nIncidental note of mid proximal humerus endosteal scalloping on plain film evaluation - Now, referred for evaluation of the right shoulder with MRI.", "Findings": "\u2022 Plain film RUE - Endjavascript:void(null);osteal scalloping and lucency within the mid to proximal shaft of the right humerus.\n\n\u2022 Plain MR of the right shoulder - Multiloculated cystic lesion of proximal humerous with some solid component and associated endosteal remodeling without evidence of cortical breakthru. \n\n\u2022 MRI of the right humerus w/ contrast - \nMultifocal, predominantly cystic multiloculated circumscribed bony lesions spare the humeral epiphyses, the largest proximal metaphyseal lesion measuring approximately 5.2 cm in its maximum diameter. The lesions exhibit predominantly peripheral enhancement and a mild increase in central T1 intensity suggesting a proteinaceous/fibrous matrix. No overlying cortical disruption is seen in the setting of grossly stable associated endosteal scalloping. No circumferential soft tissue abnormality is identified.", "Differential Diagnosis": "\u2022 polyostotic fibrous dysplasia\n\u2022 enchondroma\n\u2022 Other differential diagnoses include:\nEosinophilic Granuloma, Fibrous Cortical Defect, Nonossifying Fibroma, Giant Cell Tumor, Neurofibromatosis Type 1, Paget Disease, Hemangioma, Hyperparathyroidism, Metastasis", "Case Diagnosis": "Monostotic Fibrous Dysplasia", "Diagnosis By": "Characteristic imaging features", "Treatment & Follow Up": "No treatment is required if bone lesions are stable and do not incur pathological fracture. If so stabilization surgery is required.\nBone scan for evaluation of other bone involvement.\nFollow-up imaging is recommended to document stabilty and monitor for malignant degeneration.", "Discussion": "Plain radiographs are highly specific when characteristic features are present in a lesion. MRI findings complement plain radiographs. On T1-weighted MRIs, fibrous dysplasia has a low-to-intermediate signal intensity rougly equal to that of muscle." }, "Topic": { "Title": "Monostotic Fibrous Dysplasia", "Disease Discussion": "Fibrous dysplasia is a skeletal developmental anomaly of the bone-forming mesenchyme that manifests as a defect in osteoblastic differentiation and maturation. It is a nonhereditary disorder of unknown cause. \n\nIn fibrous dysplasia, the medullary bone is replaced by fibrous tissue, which appears radiolucent on radiographs, with the classically described ground-glass appearance. Trabeculae of woven bone contain fluid-filled cysts that are embedded largely in collagenous fibrous matrix, which contributes to the generalized hazy appearance of the bone. Fibrous dysplasia was found to affect males and females equally, but it was 50% more prevalent in the maxilla. \n\nThe following 4 disease patterns are recognized: Monostotic form, Polyostotic form, Craniofacial form and Cherubism\n\nMonostotic Fibrous Dysplasia. Approximately 70-80% of fibrous dysplasias are monostotic. This form most frequently occurs in the rib (28%), femur (23%), tibia or craniofacial bones (10-25%), humerus, and vertebrae, in decreasing order of frequency.\n\nThis form may present with pain or a pathologic fracture in patients aged 10-70 years, but this form most frequently occurs in those aged 10-30 years. The degree of bone deformity of the monostotic form is relatively less severe than that of the polyostotic type. No clearly documented evidence supports conversion of the monostotic form to the polyostotic form.\n\nFibrous dysplasia may be associated with endocrinopathies in 2-3% of cases; these include precocious puberty in girls, hyperthyroidism, hyperparathyroidism, acromegaly, diabetes mellitus, and Cushing syndrome. McCune-Albright syndrome may be associated with hyperthyroidism and, hence, exophthalmos.\n\nRadiological findings:\nThe usual appearance of fibrous dysplasia includes a lucent lesion in the diaphysis or metaphysis, with endosteal scalloping and with or without bone expansion and the absence of periosteal reaction. Usually, the matrix of the lucency is smooth and relatively homogeneous; classically, this finding is described as a ground-glass appearance. Irregular areas of sclerosis may be present with or without calcification. The lucent lesion has a thick sclerotic border and is called the rind sign.\n\nFollow-up:\nMalignant degeneration, Estimated frequency is 0.4-1%.\nThe interval from the diagnosis of fibrous dysplasia to the development of malignancy varies and is usually years or decades.\nMost often, skull and facial bones undergo malignant change in monostotic disease, whereas femoral and facial bones undergo malignant change in polyostotic disease.\nOsteosarcoma and fibrosarcoma are the most common tumors. Chondrosarcomas occur less frequently.\nRadiographic features suggestive of malignant degeneration include a rapid increase in the size of the lesion and a change from a previously mineralized bony lesion to a lytic lesion. Clinical findings of increasing pain and an enlarging soft-tissue mass suggest malignant change.\n\nMetabolic changes, Hypophosphatemic rickets and osteomalacia have been noted in patients with fibrous dysplasia. \nOne hypothesis to explain the associated metabolic disorder suggests that lesions such as fibrous dysplasia synthesize phosphaturic hormone.", "ACR Code": "4.3", "Category": "Radiologic Sign or Finding", "Keywords": "Polyostotic Fibrous DysplasiaFibrous DysplasiaRind Sign", "Reference": "Kumar Neelala Anand, Mahesh. Fibrous Dysplasia. eMedicine. Updated: Jul 29, 2009.", "External Links": "emedicine.medscape.com/article/389714-overview" } }, { "U_id": "MPX1810", "TAC": [], "MRI": [ "MPX1810_synpic42071", "MPX1810_synpic42072" ], "Case": { "Title": "Avascular Necrosis of femoral heads bilaterally with associated osteoarthritic changes.", "History": "Patient is a 49 year old African American male with a history of sarcoidosis, sinusitis with intermittent steroid treatment that presents with several years of bilateral hip pain.", "Exam": "Physical Exam: Bilateral hip pain upon standing and walking. Pt is TTP along hip joints bilaterally. Pt has longstanding pain with worsening in his hip pain recently.", "Findings": "Frontal and frog leg films of both hip joints revealed extensive degenerative changes on the bilateral femoral heads and acetabula. Acetabula demonstrate sclerosis and associated osteophyte and subchondral cyst formation. The bilateral femoral heads demonstrate extensive osteoarthritic changes with sclerosis, cyst formation, bilateral ring osteophytes and some mild flattening of the femoral heads. \n\nCoronal T1 and T2 MRI: T1 and T2 MRI revealed extensive degenerative changes on the bilateral femoral heads and acetabula. There is high signal intensity degenerative edema of the femoral heads on T2. Superior acetabula demonstrate low signal intensity on T1 and associated osteophyte and subchondral cyst formation. The bilateral femoral heads demonstrate extensive osteoarthritic changes with sclerosis, cyst formation, bilateral ring osteophytes and some mild flattening of the femoral heads. There are small areas of abnormal signal to suggest avascular necrosis.", "Differential Diagnosis": "Secondary Osteoarthritis from avascular necrosis\nPrimary Osteoarthritis", "Case Diagnosis": "Avascular Necrosis of femoral heads bilaterally with associated osteoarthritic changes.", "Diagnosis By": "Frontal and frog leg plain films. MRI", "Treatment & Follow Up": "Treatment options for avascular necrosis of the femoral heads include conservative management, total hip replacement, core decomprssion with or without bone grafting and osteotomy. \n\nThis patient received a total right hip arthroplasty with potential replacement of left hip in future.", "Discussion": "AVN most often occurs during the fourth or fifth decade of life and is bilateral in 55% of cases. The etiology for AVN of the femoral heads is vast and includes trauma, hemoglobinopathies, Caisson disease, local infiltrative diseases such as Gaucher disease, hypercortisolism, alcohol, pancreatitis, renal failure, cigarteet smoking, collagen vascular diseasese, congenital diseases such as SCFE and Legg-CalveP-Perthe, Fabry, giant cell arteritis, gout, hemodialysis, HLD, hyperparathyroidism, pregnancy, SLE, and idiopathic. The most common cause of bilateral AVN is steroid use, even for short periods. Our patient had a history of stage I sarcoid disease that was untreated. The etiology of this patient's bilateral AVN of the femoral head is unclear. There is no case report of a link between sarcoid and AVN. The patient did however have chronic recurrent bouts of sinusitis that required steroids. He received both fluticasone and oral prednisone for short periods during these recurrent attacks of sinusitis. This appears to be one possible etiology of his AVN." }, "Topic": { "Title": "Avascular Necrosis", "Disease Discussion": "Avascular Necrosis Etiology Mnemonic - ASEPTIC\n\nA- Alcoholism\nS- Sickle Cell Anemia, Steroids, Systemic lupus erythematosis\nE- Ehrlenmeyer flask (marrow packing disorders e.g.Gaucher's)\nP- Pancreatitis\nT- Trauma (Hip, Scaphoid, Talus)\nI- Idiopathic, Infection\nC- Caisson's disease (dysbaric osteonecrosis)\n\nSubmitted by Don Flemming, M.D. National Naval Medical Center, Bethesda, MD\n\nMore About Sickle Cell Disease:\nhttp://rad.usuhs.mil/sickle/index.html\n======================================\nAlso called 'aseptic necrosis'", "ACR Code": "4.5", "Category": "Idiopathic or Unknown", "Keywords": "AVNOstenecrosissickle cell", "External Links": "rad.usuhs.mil/rad/home/cases/sickle.html" } }, { "U_id": "MPX1828", "TAC": [], "MRI": [ "MPX1828_synpic41446", "MPX1828_synpic41447" ], "Case": { "Title": "Uterine Leiomyoma", "History": "Patient referred by OB-Gyn for pelvic MRI. No symptoms noted.", "Exam": "No specific findings noted. Possibly enlarged and irregular uterus on bimanual exam.", "Findings": "Numerous areas of discrete low signal intensity in the muscle of the uterus and below the serosa. Uterus is irregularly enlarged.", "Differential Diagnosis": "-Adenomyosis\n-Leiomyosarcoma\n-Endometrial polyps\n-Endometrial cancer", "Case Diagnosis": "Uterine Leiomyoma", "Diagnosis By": "Findings on MRI", "Treatment & Follow Up": "Depending on the patient's symptoms, surgical options may be discussed.", "Discussion": "Lesions/Condition: Uterine Leiomyoma \n\nCell of Origin: Smooth muscle cells of uterus \n\nSynonyms: Fibroids \n\nAssociations/Predisposing Factors: Increase estrogen states, pregnancy, african american, obesity, perimenopausal \n\nCommon Locations: Uterus; submucosal, intramural, subserosal \n\nDemographics: About 25% of American women and about 40% of African American women by age 40. \n\nGross Morphology: Smooth muscle tissue \n\nHistology: Smooth muscle tissue with a pseudocapsule \n\nRadiology: Ultrasound shows areas of hyperechogenicity and an enlarged uterus. MRI shows discrete areas of low signal intensity and an irregularly enlarged uterus. \n\nTreatment: Usually expectant management. If symptomatic, treated with medications to decrease estrogen (Provera, danazol, GnRH agonists), uterine artery embolization, myomectomy, endometrial ablation, or hysterectomy." }, "Topic": { "Title": "Uterine Leiomyoma", "Disease Discussion": "NOTE: Please EDIT the CATEGORY and LOCATION - Above\n\nYou may use the template below - or [Clear] for a blank page.\n\nLesions/Condition: Uterine Leiomyoma\n\nCell of Origin: Smooth muscle cells of uterus\n\nSynonyms: Fibroids\n\nAssociations/Predisposing Factors: Increase estrogen states, pregnancy, african american, obesity, perimenopausal\n\nCommon Locations: Uterus; submucosal, intramural, subserosal\n\nDemographics: About 25% of American women and about 40% of African American women by age 40.\n\nGross Morphology: Smooth muscle tissue\n\nHistology: Smooth muscle tissue with a pseudocapsule\n\nRadiology: Ultrasound shows areas of hyperechogenicity and an enlarged uterus. MRI shows discrete areas of low signal intensity and an irregularly enlarged uterus.\n\nTreatment: Usually expectant management. If symptomatic, treated with medications to decrease estrogen (Provera, danazol, GnRH agonists), uterine artery embolization, myomectomy, endometrial ablation, or hysterectomy.", "ACR Code": "8.-1", "Category": "Neoplasm, benign", "Keywords": "LeiomyomaFibroidsBenign tumors", "Reference": "-www.Uptodate.com\n-Beckmann et.al. Obstetrics and Gynecology. Fourth Edition. Lippincott Williams and Wilkins. 2002.\n-Hacker et.al. Essentials of Obstetrics and Gynecology. Fourth Edition. Elsevier Saunders. 2004." } }, { "U_id": "MPX1836", "TAC": [], "MRI": [ "MPX1836_synpic18218", "MPX1836_synpic18219", "MPX1836_synpic18220", "MPX1836_synpic18221" ], "Case": { "Title": "Optic neuritis (NOS)", "History": "49 y.o. white man who had an acute onset of bilateral decreased visual acuity.", "Exam": "bilateral papilledema, left greater than right", "Findings": "Multiple axial MR images demonstrate enlarged optic nerves bilaterally, with stranding of intraconal fat, with avid enhancement of the optic nerves and the surrounding intraconal fat bilaterally on the post-contrast T1-weighted images with fat-suppression, without fusiform enlargement of the nerves or tram-track-like enhancement seen in optic glioma or optic nerve meningioma, respectively. \n\nMR images of the brain (not shown) demonstrated no other abnormalities.", "Differential Diagnosis": "optic neuritis, bilateral:\n- multiple sclerosis (initial presentation)\n- acute disseminated encephalomyelitis\n- orbital pseudotumor\n- NMO-SD (Neuromyelitis Optica Spectrum Disorder) includes Devic disease (NMO) and anti-MOG (myelin oligodrocyte glycoprotein)", "Case Diagnosis": "Optic neuritis (NOS)", "Diagnosis By": "abnormal enhancement and enlargement on MR", "Discussion": "For this particular patient, his male gender, the fact that the MRI of the brain yielded no other lesions typical for MS, and the bilateral nature of the optic neuritis, all suggest Neuro-Myelitis-Optica Spectrum Disorder (NMO-SD) as a possible etiology for his disease. Anti-Aquaporin 4 disease (Devic Disease, common NMO, often has recurrences and affects the medulla (e.g. intractable hiccups) and spinal cord. In contrast, anti-MOG (Myelin Oligodendrocyte Glycoprotein) is often a single episode that may affect any part of the spinal cord, including the conus medullaris (weakness, impotence, incontinence) which is less common in NMO. Anti-MOG is more likely to cause bilateral optic neuritis (like this case) as well as \"dirty fat\" (also like this case). This patient was not tested for NMO antibodies to AQP4 (aquaporin 4) nor for anti-MOG (myelin oligodendrocyte glycoprotein) antibodies.\n\nFront Neurol. 2018; 9: 217. Published online 2018 Apr 4. doi: 10.3389/fneur.2018.00217\nPMCID: PMC5893792 PMID: 29670575\n\nTher Adv Neurol Disord 2018, Vol. 11: 1\u201315\nhttps://doi.org/10.1177/1756286418762083\n\nInt J Mol Sci.\u00a02016 Mar 2;17(3):273. PMID:26950113 PMCID:PMC4813137" }, "Topic": { "Title": "optic neuritis", "Disease Discussion": "Optic neuritis is an acute inflammatory optic neuropathy. It is the most common type of optic neuropathy which causes acute visual loss in young to middle-aged adults. Usual symptoms are acute reduction of visual acuity, pain (especially with eye movements), and papilledema. (1)\n\nIn a ten-year study of 388 patients who experienced acute optic neuritis, it was noted that the ten-year risk of developing multiple sclerosis was 38%. Patients who had one or more typical lesions for MS on the MRI of the brain had 56% risk, and those without such lesions had 22% risk. Among the patients with no typical MS lesions on the MRI of the brain, male gender, optic disc swelling, perpapillary hemorrhages, and retinal exudates were associated with a lower risk of developing MS. (2)\n\nAnother major cause of optic neuritis is acute disseminated encephalomyelitis (ADEM). ADEM is a post-infectious inflammatory process, mediated by auto-reactive immune cells or antibodies. It has been noted that bilateral optic neuritis and transverse myelitis are particularly suggestive of ADEM. (3)", "ACR Code": "2.2", "Category": "Inflammatory, non-infectious", "Keywords": "optic neuritismultiple sclerosisacute disseminated encephalomyelitis", "Reference": "1. Chan JW. Optic neuritis in multiple sclerosis.\nOcul Immunol Inflamm. 2002 Sep;10(3):161-86.\n\n2. Beck RW, et al. High- and low-risk profiles for the development of multiple sclerosis within 10 years after optic neuritis: experience of the optic neuritis treatment trial. Arch Ophthalmol. 2003 Jul;121(7):944-9.\t \n\n3. Dale RC. Acute disseminated encephalomyelitis. Semin Pediatr Infect Dis. 2003 Apr;14(2):90-5." } }, { "U_id": "MPX1838", "TAC": [], "MRI": [ "MPX1838_synpic19186", "MPX1838_synpic19187", "MPX1838_synpic19188" ], "Case": { "Title": "Herpes Encephalitis (HSV 1)", "History": "34 yo man from Guantanamo Bay presents with confusion. On day of presentation, he was discovered by roommates to be confused and drooling, oriented only to person. Following treatment at ED in Cuba, he was evacuated stateside for further care.", "Exam": "Rectal temp at time of ED presentation was 102.8. \n\nLP performed at ED in Cuba revealed CSF white count of 98, RBC 600, Protein 40, Gram Stain significant for Gram Positive Cocci. \n\nPE stateside revealed an obtunded WNWD male, responsive only to noxious stimuli, with asymmetric pupils, L larger than R. \nHSV 1 CSF titer HIGH, HSV II negative.", "Findings": "MRI revealed increased T2 signal intensity in R frontotemporal region, as well as insular gyri, right worse than left. R cingulate gyrus noted to have increased signal intensity compared to L side. Mild effacement of right lateral ventricle is also seen.", "Differential Diagnosis": "A. Vascular \u2013 \n 1. ischemia \n 2. infarction\n\nB. Inflammatory \u2013 \n 1. encephalitis \n 2. meningitis \n 3. meningoencephalitis", "Case Diagnosis": "Herpes Encephalitis (HSV 1)", "Diagnosis By": "HSV-1 CSF Viral Titers", "Treatment & Follow Up": "IV acyclovir, supportive care" }, "Topic": { "Title": "Herpes Encephalitis, (HSV 1)", "Disease Discussion": "HSV encephalitis is the most common cause of fatal encephalitis in the United States. Patients will usually present with altered consciousness, mentation, focal CN deficits, seizures, and other neurologic deficits, along with fever. T2 weighted MRI will usually reveal a unilateral increase in signal intensity in the temporal region, with cingulate and insulate gyri often involved. In fact this combination of findings, cingulate & temporal region edema, is the discriminatory factor which makes this appearance classic for HSV encephalitis. The involvement of two different blood supplies, the ACA supplying the cingulate gyrus, and the MCA supplying the frontotemporal region, makes a vascular etiology less likely, leaving an inflammatory etiology to be the most likely cause. Most literature regarding HSV encephalitis cite the common findings listed above in most MRI studies: unilateral gyral swelling of the cingulate, insula, and temporal lobe.", "ACR Code": "1.2", "Category": "Infection, viral", "Keywords": "encephalitisHerpesHSV 1", "Reference": "Ishida S, Moriguchi A, Sakane S, Furukawa K, Nakajima H. Herpes simplex encephalitis with expanded cerebral cortex lesions on T1-weighted MRI after clinical improvement: a case report. Rinsho Shinkeigaku. 2002 Jun;42(6):536-9.\n\nLee JW, Kim IO, Kim WS, Yeon KM, Lee HJ, Hwang YS. Herpes simplex encephalitis: MRI findings in two cases confirmed by polymerase chain reaction assay. Pediatr Radiol. 2001 Sep;31(9):619-23.\n\nDomingues RB, Fink MC, Tsanaclis AM, de Castro CC, Cerri GG, Mayo MS, Lakeman FD. Diagnosis of herpes simplex encephalitis by magnetic resonance imaging and polymerase chain reaction assay of cerebrospinal fluid. J Neurol Sci. 1998 May 7;157(2):148-53." } }, { "U_id": "MPX1851", "TAC": [], "MRI": [ "MPX1851_synpic27497", "MPX1851_synpic27498", "MPX1851_synpic27499" ], "Case": { "Title": "Renal Oncocytoma", "History": "The patient was a 39 y/o female admitted for a laproscopic BSO. On the night of surgery the patient became anuric and was noted to have an increasing BUN and creatinine.", "Exam": "PE was unchanged from pre-op\nLabs: BUN 21, Cr 2.9", "Findings": "Ultrasound of the L kidney shows mild hydronephrosis and a 7.5 by 5.5 cm mass located in the lower pole of the kidney.\n\nMRI: T1 axial image shows a low-intensity, homogenous mass within the L kidney that enhances with contrast and reveals a well-defined capsule. T2 coronal section shows a high-intensity homogenous mass in the lower pole of the L kidney", "Differential Diagnosis": "Renal Oncocytoma\nRenal Cell Carcinoma\nAngiomyolipoma", "Case Diagnosis": "Renal Oncocytoma", "Diagnosis By": "Pathology", "Treatment & Follow Up": "The patient underwent a total nephrectomy of the L kidney and reimplantation of the R ureter into the bladder.", "Discussion": "Renal oncocytomas are very difficult to distinguish from renal cell carcinomas. This patient had images that showed some features indicative of oncocytoma, but these cases are often considered renal cell carcinoma until proven otherwise. As a result the treatment was resection of the tumor with diagnosed confirmed by tissue pathology." }, "Topic": { "Title": "Renal Oncocytoma", "Disease Discussion": "The first report of Renal Oncocytoma occured in 1942, but it wasn't until 1976 that it was established as a clinical entity. Between 3% and 7% of renal masses are oncocytomas. Oncocytomas, much like renal cell carcinomas, are often found incidentally with no symptoms being present at the time of diagnosis. This tumor is classified as benign, but clinically and radiologically is very difficult to differentiate from renal cell carcinoma. Grossly the tumor is brown or tan and appears encapsulated. Often there is a central scar, but there is an absence of hemorrhage and necrosis.\n\nRadiologically these tumors are evaluated the same way as renal cell. On ultrasound the oncocytoma is indistinguishable from renal cell. Typical features on CT include a central, stellate pattern with low attentuation. Additionally the tumor appears very homogenous. With angiography oncocytomas have four typical signs: lucent rim, homogenous capillary nephrogram phase, absence of neoplastic vessels, and feeding arteries with a spoked wheel appearance. While these have been used as predictors of oncocytoma, they have shown poor predictive value in differentiating oncocytoms from renal cell. MRI is currently being evaluated for its ability to diagnose oncocytoma. Characteristics indicative of this tumor on MR include low intensity homogenous mass on T1 that shows increased intensity on T2 with a capsule, central scar or stellate pattern and no hemorrhage or necrosis. \n\nOncocytomas are very difficult to differentiate from renal cell carcinoma both clincally and radiologically and the use of renal biposy is not recommended due to the similar histological appearance of the two entities in certain situations. As a result they are treated surgically. Whether this is done with a partial or complete nephrectomy is often determined by the patient's clinical picture.", "ACR Code": "8.3", "Category": "Neoplasm, benign", "Keywords": "Renal Oncocytoma", "Reference": "Harmon, W. et al. Renal Oncocytoma: Magnetic Resonance Imaging Characteristics. The Journal of Urology 155(3): 863-867, 1996.\nWalsh: Campbell's Urology, 8th Edition. St. Louis, W.B. Saunders Company, 2002." } }, { "U_id": "MPX1861", "TAC": [], "MRI": [ "MPX1861_synpic20765", "MPX1861_synpic20766" ], "Case": { "Title": "Patellar Tendinosis (Jumper's Knee) with probable partial tear of the patellar tendon.", "History": "23 year old male with acute onset left knee pain, worse with full extension.", "Exam": "No obvious external deformity.\nTender to Palpation over the Patella.\nRelatively Weak Left Knee Extension.", "Findings": "Increased signal intensity and thickening within the patellar enthesis of the patellar tendon on Proton Density and T2 weighted sequences.", "Differential Diagnosis": "Patellar Tendinosis (Jumper's Knee)\nPatellar Tendon Rupture", "Case Diagnosis": "Patellar Tendinosis (Jumper's Knee) with probable partial tear of the patellar tendon.", "Diagnosis By": "MRI", "Treatment & Follow Up": "Conservative.", "Discussion": "Patellar tendinosis, also known as Jumper's Knee, is the result of micro and partial macro-tearing of patellar tendon fibers, usually due to repetitive running and/or jumping (Basketball, Football, and Volleyball). Either the patellar or tibial enthesis may be involved; however the condition is most often associated with patellar attachment involvement. Treatment is generally conservative. \n\n\nReferences:\n\nFerretti A. Epidemiology of Jumper\u2019s Knee. Sports Med 1986;3(4):289-95.\n\nStevens MA, El-Khoury GY, Kathol MH, et al. Imaging Features of Avulsion Injuries. Radiographics 1999;19:655-672.\n\nhttp://uwmsk.org:8080/UWR/stories/storyReader$764\nJohn Hunter's MSK Teaching File. Interesting MRI Cases from University of Washington Department of Radiology: Case 59b\n\nhttp://www.duke.edu/~ps4/patellar.html\nPatellar Tendinosis - from a tennis player's perspective." }, "Topic": { "Title": "Patellar Tendinosis (Jumper's Knee)", "Disease Discussion": "Patellar tendinosis, also known as Jumper's Knee, is the result of micro and partial macro-tearing of patellar tendon fibers, usually due to repetitive running and/or jumping (Basketball, Football, and Volleyball). Either the patellar or tibial enthesis may be involved; however the condition is most often associated with patellar attachment involvement. Treatment is generally conservative.", "ACR Code": "4.4", "Category": "Trauma", "Keywords": "Patellar Tendon InjuryPatellar TendinosisJumper's Knee", "Reference": "Ferretti A. Epidemiology of Jumper\u2019s Knee. Sports Med 1986;3(4):289-95. \n\nStevens MA, El-Khoury GY, Kathol MH, et al. Imaging Features of Avulsion Injuries. Radiographics 1999;19:655-672. \n\nhttp://uwmsk.org:8080/UWR/stories/storyReader$764 \nJohn Hunter's MSK Teaching File. Interesting MRI Cases from University of Washington Department of Radiology: Case 59b \n\nhttp://www.duke.edu/~ps4/patellar.html \nPatellar Tendinosis - from a tennis player's perspective." } }, { "U_id": "MPX1884", "TAC": [], "MRI": [ "MPX1884_synpic21850", "MPX1884_synpic21851", "MPX1884_synpic21852", "MPX1884_synpic21853", "MPX1884_synpic21854" ], "Case": { "Title": "Breast implant, rupture, extracapsular silicone", "History": "55 Y/O female with bilateral silicone iplants. Has right breast mass to 3-4o'clock", "Exam": "Right breast mass at 3 o'clock position of the right breast.", "Findings": "Ultrasound findings- classic linguini sign consisting of hyperechoic linear objects coursing through the implant. Hyperechoic shadowing of all structures, typical of silicon infiltrating into tissues surrounding the implant capsule.\n\nMRI- Linguini sign with high signal on h20 saturation in the soft tissue surrounding the implant.", "Differential Diagnosis": "silicone implant rupture", "Case Diagnosis": "Breast implant, rupture, extracapsular silicone", "Diagnosis By": "US, MRI", "Treatment & Follow Up": "Pt was referred back to the primary provider, for eventual referral to plastic surgery for possible revision.", "Discussion": "The findings of this case are classic for bilateral implant rupture, with extravasation of silicone to the tissues adjacent to the capsule. A silicone granuloma has formed." }, "Topic": { "Title": "Breast implant, rupture, extracapsular silicone", "Disease Discussion": "Breast implants may leak or rupture, and the material may be confined or dispersed.\n\nVariable degrees of cross-linking are present within the silicone elastomer shell surrounding the silicone or saline in a breast implant. \"Gel-bleed\" occurs as silicone or saline diffuses through the shell as a result of its semi-permeable nature. The immune system of women with intact implants is exposed to variable amounts of silicone soon after augmentation. Saline is resorbed into the lymphatics and is undetectable.\n\nImplants are foreign bodies which become walled off by the formation of a fibrous capsule. Such a capsule (bands of fibrous tissue) forms in all women with implants. The capsule may remain soft or harden and contract around the implant. As encapsulation occurs, the implants may become hard and immobile. Mammographic displaced implant views may be difficult to obtain. Encapsulation becomes apparent mammographically as the implants become round on MLO views. \n\nIntracapsular rupture occurs when the implant ruptures and the silicone is free within the fibrous capsule surrounding the implant. Intracapsular rupture is difficult to identify mammographically. \u201cLinguini sign\u201d describes the MRI findings of the low T2 signal redundant implant shell with high T2 fluid signal within and surroundng the shell, contained within the fibrous capsule.\n\nExtracapsular rupture occurs when silicone is free and found outside the implant and capsule. Silicone can often be seen migrating to the axillary lymph nodes. No definitive proof of a relationship between silicone and autoimmune disorders or cancer has been identified. \n\nWhen a saline implant ruptures, the saline is resorbed into the lymphatics resulting in decreased breast size. Intra- vs extracapsular rupture is difficult to distinguish as all extra-implant saline is resorbed. The implant shell becomes redundant, best seen on MRI imaging when compared to the opposite implant.", "ACR Code": "0.7", "Category": "Foreign Body", "Keywords": "breast implantextracapsular rupturesilicone", "Reference": "Breast Imaging Companion, Cardenosa, Gilda, Copyright 1997, by J.B.Lippincott Company (Lippincott Williams & Wilkins, Philadelphia, PA)\n\nBreast Disease (Third Series) Test and Syllabus, Basset, Lawrence W., etal, Copyright 2000, American College of Radiology, Reston, VA" } }, { "U_id": "MPX1879", "TAC": [], "MRI": [ "MPX1879_synpic48739", "MPX1879_synpic48740", "MPX1879_synpic48741", "MPX1879_synpic48742", "MPX1879_synpic48743", "MPX1879_synpic48744", "MPX1879_synpic48745", "MPX1879_synpic48746", "MPX1879_synpic48747", "MPX1879_synpic48748", "MPX1879_synpic48749", "MPX1879_synpic48750", "MPX1879_synpic48751", "MPX1879_synpic48752", "MPX1879_synpic48753", "MPX1879_synpic48754", "MPX1879_synpic48755", "MPX1879_synpic48756", "MPX1879_synpic48757", "MPX1879_synpic48758" ], "Case": { "Title": "Meningioma, Falx", "History": "21 y.o. man with a new onset seizure and severe headaches.", "Exam": "Physical exam normal when not seizing.", "Findings": "Large homogeneously enhancing lesion based in the dura of the falx, and pressing on the anterior cerebral hemisphere. There is rightward mass effect on the falx as well as inferior displacement of the body of the corpus callosum with partial effacement of the third ventricle. The mass looks extraaxial, but has intraaxial vasogengenic edema in frontal lobes surrounding the mass.", "Differential Diagnosis": "meningioma, lymphoma, hemangioparacytoma, metastatic carcinoma, inflammatory lesions such as sarcoidosis and Wegener's granulomatosis, and infections such as tuberculosis", "Case Diagnosis": "Meningioma, Falx", "Diagnosis By": "MRI and Surgical excision", "Treatment & Follow Up": "Surgical excision." }, "Topic": { "Title": "Meningioma", "Disease Discussion": "The most common extraaxial neoplasm of the brain, meningiomas, often affect middle-aged women. They account for 15-20% of all primary brain tumors. They are most commonly found in the parasagittal dura, convexities, sphenoid wing, cerebellopontine angle cistern, and olfactory groove. Up to 90% are supratentorial, and 1% occur outside the CNS (presumably due to arachnoid rests). Less than 10% cause symptoms, with the majority discovered incidentally or at autopsy or on brain imaging.\n\nOn CT, they are typically hyperdense, with up to 20% demonstrating calcification. On MR, they are typically well-circumscribed and iso- to hypointense on T1, iso- to hyperintense on T2, and strongly enhancing. A dural tail is seen in up to 72%, which is thought to represent a neoplastic infiltration or a reactive fibrovascular proliferation of the meninges. This finding is suggestive but not specific, however. Similarly, a distinct cleft of arachnoid with trapped CSF and vessels is common. Meningiomas typically take one of two forms, either \u201cglobose\u201d (spherical) or \u201cen plaque\u201d (flat).\n\nMeningiomas may encase and narrow vessels, and incite a varying amount of edema, depending on location (cerebral cortical lesions have more edema, basal cisterns \u2013 less). Bony changes may be hyperostotic or osteolytic, mimicking Paget\u2019s or fibrous dysplasia. On angiography, the \u201cin-law\u201d sign has been described (coming early and staying late) with an early blush and delayed washout. Due to their vascularity, preoperative embolization can be performed (particularly at the skull base, where the lesions may be unresectable).\n\nMalignant meningiomas, a rare variant, demonstrate rapid growth or intraparenchymal invasion. These are associated with a higher rate of recurrence \u2013 75%, versus a recurrence rate of 3-7% for benign meningiomas.", "ACR Code": "1.3", "Category": "Neoplasm, non-glial", "Keywords": "meningiomabrain tumor", "Reference": "\u201cMeningiomas.\u201d Neuroradiology: The Requisites. Philadelphia: Mosby, 2003. Pgs. 98-105.\n\n\u201cMeningioma.\u201d Diagnostic Neuroradiology. Anne Osborn. St. Louis: Mosby, 1994. Pgs. 584-601." } }, { "U_id": "MPX1891", "TAC": [], "MRI": [ "MPX1891_synpic24276", "MPX1891_synpic24277" ], "Case": { "Title": "cholecystitis", "History": "24 y/o female patient with history of abdominal pain and recurrent pancreatitis presents with hepatic panel lab values suggestive of obstructive pattern.", "Exam": "ALB 2.6 ALK PHOS 202 AST 572 ALT 757 TBILI 0.9 AMYLASE 505 LIPASE 2585 Normal Hepatitis panel and CBC", "Findings": "US: Contracted gallbladder with gallstones suggestive of cholecystitis\n MRCP: Multiple gallstones within gallbladder, small amt. of fluid around gallbladder, and thickening of gallbladder wall. No evidence of intrahepatic or extrahepatic ductal dilatations or of luminal stone within the common bile duct", "Differential Diagnosis": "cholecystitis, choledocholithiasis, cholangitis, acute pancreatitis", "Case Diagnosis": "cholecystitis", "Treatment & Follow Up": "Patient received laparoscopic cholecystectomy. Symptoms improved and patient was discharged.", "Discussion": "Acute cholecystitis typically presents with right upper quadrant or periumbilical abdominal pain that may radiate to the back or shoulder, fever, and leukocytosis. The gallbladder becomes inflamed due to blockage of the cystic duct--not all gallstones produce enough irritation to produce inflammation. Many people with gallstones are asymptomatic, some have episodes of biliary colic, and others develop cholecystitis.\n The diagnosis is most commonly made via ultrasound, which may show presence of gallstones, gallbladder wall thickening, and/or pericholic fluid. Studies have shown that US is fairly sensitive in >80% of cases. One study reported by M.T. Keogan suggested that MRCP with half-Fourier RARE sequence has a sensitivity of 91% and specificity of 79% for acute cholecystitis though other studies suggest lower sensitivity (70%). For detection of stones in the cystic duct, however, MRCP is indisputably more reliable than ultrasound; with reported sensitivity and specificity of 95 and 97 percent. ERCP has, in the past, been commonly used for visualization of the ductal system and is useful for concurrent stone extraction, stent insertion, or biopsy. But MRCP has become useful because it is less invasive and does not require addition of contrast--hence decreasing procedure morbidity.\n Left untreated, cholecystitis may resolve. But due to the various complications which can occur such as gallbladder gangrene, perforated gallbladder, or cholecystoenteric fistula leading to gallstone ileus, removal of the gallbladder is the preferred method of treatment and is commonly performed via laparoscopic method converted to open cholecystectomy as needed." }, "Topic": { "Title": "cholecystitis", "Disease Discussion": "Acute cholecystitis typically presents with right upper quadrant or periumbilical abdominal pain that may radiate to the back or shoulder, fever, and leukocytosis. The gallbladder becomes inflamed due to blockage of the cystic duct--not all gallstones produce enough irritation to produce inflammation. Many people with gallstones are asymptomatic, some have episodes of biliary colic, and others develop cholecystitis.\n The diagnosis is most commonly made via ultrasound, which may show presence of gallstones, gallbladder wall thickening, and/or pericholic fluid. Studies have shown that US is fairly sensitive in >80% of cases. One study reported by M.T. Keogan suggested that MRCP with half-Fourier RARE sequence has a sensitivity of 91% and specificity of 79% for acute cholecystitis though other studies suggest lower sensitivity (70%). For detection of stones in the cystic duct, however, MRCP is indisputably more reliable than ultrasound; with reported sensitivity and specificity of 95 and 97 percent. ERCP has, in the past, been commonly used for visualization of the ductal system and is useful for concurrent stone extraction, stent insertion, or biopsy. But MRCP has become useful because it is less invasive and does not require addition of contrast--hence decreasing procedure morbidity.\n Left untreated, cholecystitis may resolve. But due to the various complications which can occur such as gallbladder gangrene, perforated gallbladder, or cholecystoenteric fistula leading to gallstone ileus, removal of the gallbladder is the preferred method of treatment and is commonly performed via laparoscopic method converted to open cholecystectomy as needed.", "ACR Code": "-1.-1", "Category": "Clinical Exam Finding or Sign", "Keywords": "cholecystitisperforated gallbladder", "Reference": "Indar, Adran A. \"Acute Cholecystitis,\" BMJ 2002:325:639-643 (21 Sept).\nKeogan, Mary T and Edelman, Robert R. \"Technologic Advances in Abdominal MR Imaging,\" Radiology. 2001:220:310-320." } }, { "U_id": "MPX1909", "TAC": [], "MRI": [ "MPX1909_synpic16186", "MPX1909_synpic16187", "MPX1909_synpic16188", "MPX1909_synpic16189" ], "Case": { "Title": "meniscal tear", "History": "26 y.o. male injuried in weekend football game", "Exam": "N/A", "Findings": "Multiple sagittal MR sequence images demonstrate a tear of the medial meniscus with a displaced fragment in the intercondylar notch, in the classic \"double PCL\" sign, suggestive of a bucket handle tear.", "Differential Diagnosis": "bucket handle tear of medial meniscus", "Case Diagnosis": "meniscal tear" }, "Topic": { "Title": "meniscal tear", "Disease Discussion": "Vertical longitudinal tears or bucket-handle tears make up 10% of all meniscal tears. MR imaging characteristics include: 1) \"absent bowtie sign\", where only one instead of the normal two body segments present on the outermost sagittal images; 2) \"double PCL sign\", where the displaced fragment of the tear is found in the intercondylar notch just anterior to the posterior cruciate ligament; 3) \"anterior flipped meniscus sign\", where the tear fragment flip over the anterior horn of the affected meniscus. (1)\n\nMenisci in the knee are C-shaped, fibrocartilagenous structures with thick periphery and thin central portions. Vascularity of the meniscus is greatest near the periphery (near its attachment to the joint capsule) and is almost non-existent near the free edge. (1)\n\nAccording to current orthopedic surgery literature, meniscus tears known to be suitable for repair with high expectation for success are traumatic lesions within the vascular zone in which the peripheral circumferential fibers remain intact and there is minimal damage to the meniscus body. Tears should generally be greater than 8mm, as shorter tears are more likely to heal spontaneously and even if they persist are likely to be asymptomatic. The most common tear types that fit these criteria: peripheral or near peripheral, vertical, or longitudinal tears. Those tears that are questionable in terms of being surgical candidates are those which are in avascular portion of the meniscus or when vascularity is in question, complete radial tears at the meniscosynovial junction, and tears that result in extensive damage to the body. (2)", "ACR Code": "4.4", "Category": "Trauma", "Keywords": "meniscal tearbucket handle tear", "Reference": "1. Kaplan PA, et al. Musculoskeletal MRI, 1/e. W.B. Saunders Co.:2001.\n2. DeHaven KE. Meniscus Repair. American Journal of Sports Medicine. Volume 27 \u2022 Number 2 \u2022 March - April 1999." } }, { "U_id": "MPX1911", "TAC": [], "MRI": [ "MPX1911_synpic23324", "MPX1911_synpic23325", "MPX1911_synpic23326", "MPX1911_synpic23327", "MPX1911_synpic23328" ], "Case": { "Title": "Ductal Carcinoma in Situ (DCIS)", "History": "History (can include gestational age, or age in days, weeks, months): 59 y/o female with focal left breast pain x 2-3 months with increased risk by the Gail model. Mammogram was normal. Breast ultrasound was normal without any evidence of mass or cystic structure.", "Exam": "Physical Exam and Laboratory: Left breast tenderness on palpation. No masses, nodules or changes in the skin.", "Findings": "Image Findings: Breast MRI showed spiculated enhancing mass in anterior 1/3 of Left breast.", "Differential Diagnosis": "Differential Diagnosis for these findings in this case: \nMalignant neoplasm\u2014ductal carcinoma, lobular carcinoma, inflammatory carcinoma\nFibroadenoma\nAbscess", "Case Diagnosis": "Ductal Carcinoma in Situ (DCIS)", "Diagnosis By": "Needle placement for biopsy using MRI guidance", "Treatment & Follow Up": "Treatment and Follow-up: Pt had MRI guided placement of a wire. Breast was reimaged with mammogram after the wire placement to help the surgeon better locate the mass. A 6 mm focus of DCIS was excised.", "Discussion": "Discussion (include references): Given the increased use of mammographic screening over the past few decades, the DCIS is the most rapidly growing subgroup of breast cancer. DCIS was newly diagnosed over 55,000 times in 2003. As a direct precursor to invasive breast cancer, diagnosing DCIS is important to preventing widespread disease. For a pt such as this, where mammography and US showed no abnormalities, but she was still having pain, MRI is a logical next step. Almost all invasive cancers will enhance with gadolinium on MRI (95-100% sensitivity); it is less for DCIS. However, in this pt it did enhance. Also of note, MRI can be helpful in determining the extent of disease spread posteriorly (chest wall, muscle, etc.) However, the routine use of breast MRI is being studied and compared with that of mammagraphy. MRI is often much more expensive, less available, and may have a higher false positive rate for enhancing benign lesions." }, "Topic": { "Title": "Breast, Ductal Carcinoma in Situ (DCIS)", "Disease Discussion": "Discussion (include references): Given the increased use of mammographic screening over the past few decades, DCIS is the most rapidly growing subgroup of breast cancer. DCIS was newly diagnosed over 55,000 times in 2003. As a direct precursor to invasive breast cancer, diagnosing DCIS is important to preventing widespread disease. For a patient such as this, where mammography and US showed no abnormalities, but she was still having pain, MRI is a logical next step. Almost all invasive cancers will enhance with gadolinium on MRI (95-100% sensitivity); it is less for DCIS. However, in this patient, there was no enhancement. Also of note, MRI can be helpful in determining the extent of disease spread posteriorly (chest wall, muscle, etc.) However, the routine use of breast MRI is being studied and compared with that of mammagraphy. MRI is often much more expensive, less available, and may have a higher false positive rate for enhancing benign lesions.", "ACR Code": "0.3", "Category": "Neoplasm, carcinoma", "Keywords": "Ductal Carcinoma in Situ (DCIS)Ductal CarcinomaDCIS", "Reference": "No references provided" } }, { "U_id": "MPX1915", "TAC": [], "MRI": [ "MPX1915_synpic18650" ], "Case": { "Title": "Subependymal Giant Cell Astrocytoma", "Case Diagnosis": "Subependymal Giant Cell Astrocytoma" }, "Topic": { "Title": "Subependymal Giant Cell Astrocytoma", "Disease Discussion": "WHO Grade I\n\nCell of Origin:\n\nSynonyms: Ventricular tumor of Tuberous Sclerosis\n\nCommon Locations: Lateral ventricle, attached to caudate head.\nAssociations: Most patients have Tuberous sclerosis, of those with TS, 6-16% will develop this tumor\n\nDemographics: children, young adults (first two decades)\n\nHistology: Large cells that variously resemble astrocytes, although may express neuronal markers\n\nSpecial Stains: GFAP variable (usually present), S100 neuronal markers +/-\n\nProgression : May grow, does not change histology\n\nTreatment: Everolimus ( Afinitor, Novartis) has shown one-third (35%) of patients had a 50% or more reduction in tumor volume. http://www.thelancet.com/journals/lancet/article/PIIS0140-6736%2812%2961134-9/fulltext\n\nRadiology: Usually seen with other features of Tuberous Sclerosis (cortical tubers, calcified subependymal nodules, white matter streaks). May obstruct f. of Monro and cause hydrocephalus. Enhancement and calcification are both common.", "ACR Code": "1.3", "Category": "Neoplasm, glial", "Keywords": "everolimus tacrolimus rapamycintuberous sclerosissubependymal giant cell", "External Links": "rad.usuhs.mil/rad/who/rsnawho2.html#contents" } }, { "U_id": "MPX1916", "TAC": [], "MRI": [ "MPX1916_synpic18600", "MPX1916_synpic18601", "MPX1916_synpic18602", "MPX1916_synpic18603", "MPX1916_synpic18604" ], "Case": { "Title": "meniscal ossicle", "History": "39 year-old male with chronic history of left lateral knee pain and locking.", "Exam": "N/A", "Findings": "Within the substance of the posterior horn of the medial meniscus, there are two small lesions which demonstrate a low T1 and T2 signal rim with homogeneous high T1 signal equal to that of marrow fat which demonstrates decrease in signal on fat-saturation images.", "Differential Diagnosis": "meniscal ossicle", "Case Diagnosis": "meniscal ossicle", "Treatment & Follow Up": "pending" }, "Topic": { "Title": "Meniscal ossicle", "Disease Discussion": "Meniscal ossicles are a rare lesion which, on plain radiographs, can be difficult to distinguish from a loose osseous intraarticular body. It was found in 2 out of 1,287 patients (0.15%) in one series in a single institution who underwent MR imaging of the knee. Prior to MR imaging, fluoroscopy was used to help distinguish between the two. Arthrotomy or arthroscopy is confirmatory, and it remains the gold standard test.\n\nMeniscal ossicles have been shown to be more prevalent in young male patients. They have also been associated with meniscal tears, and some believe them to be a factor in causing meniscal tears. Clinically, patients can be asymptomatic or have symptoms similar to that of meniscal tears (pain, clicking, or locking). At MR imaging, meniscal ossicles characteristically are located in the posterior horns of the medial menisci. Signal characteristics are that of bone: low T1/T2 signal rim equal to that of cortical bone with marrow signal (high on T1 and T2 fast-spin echo sequences) within, which appropriately decreases in signal on fat-saturation images like marrow fat. Pathologically, the ossicles consist of bone marrow and cancellous bone contained by cortex covered with cartilage.\n\nOrigin or etiology of meniscal ossicles in humans are unknown. They have been found in other species such as rats and other rodents as a normal finding. Two hypotheses exist, one considering these as a congenital/developmental entities, and the other believing that these are post-traumatic lesions.\n\nExcision of the ossicle at arthroscopic examination is indicated for symptomatic patients.", "ACR Code": "4.1", "Category": "Unknown, Not specified", "Keywords": "meniscal ossicle", "Reference": "Schnarkowski P, et al. Meniscal Ossicle: radiographic and MR imaging findings. Radiology 1995; 196:47-50." } }, { "U_id": "MPX1935", "TAC": [], "MRI": [ "MPX1935_synpic34504", "MPX1935_synpic34505" ], "Case": { "Title": "Pigmented villonodular synovitis", "History": "A 36 y/o Caucasian woman presented with a chief complaint of pain & swelling in her left knee for three months. She denied history of trauma or exercise. Her past medical history was non-contributory. Review of systems is negative for fever, fatigue, adenopathy, weight loss, morning stiffness, or night pain.", "Exam": "Physical exam revealed decreased range of motion in the left knee greater on flexion & a moderate effusion without erythema or warmth. There was a tender mass palpable at the anterior medial and lateral joint lines. Arthrocentesis of the joint revealed gross blood but fluid analysis proved otherwise unremarkable. Erythrocyte sedimentation rate, c-reactive protein, prothrombin time, & activated partial thromboplastin time were all within normal limits.", "Findings": "Radiographs: Bilateral weight-bearing anterior-posterior and lateral radiographs showed an increased density within the soft tissues of the left knee joint. The bones were well mineralized with smooth borders and no erosions.\n\nMRI :T2 weighted with fat saturation MR images of the left knee showed multiple low-signal-intensity masses in the anterior and posterior knee. There was a large high-signal-intensity effusion present on axial & sagittal T2 sequences. The presence of hemosiderin within the mass demonstrated a low-signal intensity rim and \u201cblooming\u201d artifact on gradient-recalled echo and was better delineated than on the T2 weighted images. There was no evidence of erosion or osseous infiltration on any sequence.", "Differential Diagnosis": "Pigmented villonodular synovitis \nSynovial sarcoma \nLipoma Arborescens\nSynovial chrondromatosis\nHypertrophic synovitis", "Case Diagnosis": "Pigmented villonodular synovitis", "Diagnosis By": "Tissue biopsy", "Treatment & Follow Up": "Surgical resection with post operative MR monitoring." }, "Topic": { "Title": "Pigmented villonodular synovitis (PVNS)", "Disease Discussion": "Pigmented villonodular synovitis (PVNS) was first described by Jaffe in 1941(1). The etiology of the disease is not well defined. Some investigators favor an inflammatory pathogenesis while others consider PVNS a form of benign neoplasm. Other etiologies-metabolic, traumatic, and genetic-have also been considered. Although both polyclonal & monoclonal lineages of synovial cells have been demonstrated, current opinion favors a neoplastic process (2). \n\nA 1980 epidemiologic study of 166 patients reported the incidence of this tumor as 1.8-2 per million per year (3). There appears to be no sex predilection. The most common sites of involvement are the knee, hip, ankle, shoulder, & elbow in decreasing order of frequency (4). \n\nWhen the knee is involved symptoms are typically non-specific with pain, effusion, & warmth being the most frequently reported. Range of motion becomes limited as the mass occupies more space. Studies are generally normal with the exception of gross blood upon aspiration of the joint space (4).\n\nMR imaging is the primary modality for evaluating PVNS. Radiographs are used in the initial evaluation and are helpful in delineating osseous erosions. Synovial chondromatosis and PVNS are the two main differentials to consider when radiographs show well mineralized bones and focal sites of erosion. Absence of calcifications and characteristic MR imaging findings, however, are more suggestive of PVNS. On MR imaging PVNS appears as an intra-articular soft tissue mass (or masses) and can exhibit variable signal intensity depending on the amount of hemosiderin deposition, lipid filled macrophages, & fibrosis (4). Villous or cystic low-signal-intensity masses combined with a \u201cblooming\u201d artifact on the gradient-recalled echo sequence are nearly pathognomonic for PVNS. After contrast, PVNS will enhance. In the absence of typical MR findings, CT-guided biopsy should be considered. At histology, the presence of mononuclear cells, multinucleated giant cells, and hemosiderin deposition are consistent with the diagnosis of PVNS (4). \n\nThe traditional treatment of PVNS is total synovectomy (5). Post-surgical adjuvant radiation, either external beam or by intra-articular injection, has shown promise in some small case series (6,7). The ultimate goal of treatment is to remove the mass and prevent recurrence while preserving maximum joint function. Severe progression of the disease can lead to joint destruction and a need for arthrodesis.", "ACR Code": "4.3", "Category": "Neoplasm, benign", "Keywords": "Pigmented villonodular synovitisPVNSBenign neoplasm", "Reference": "1. Jaffe HL, Litchtenstein L, Sutro C. Pigmented villonodular synovitis: bursitis and tenosynovitis. Arch Pathol 194; 31: 731\u201465.\n\n2. Ray RA, Morton CC, Lipinski KK, et al. Cytogenetic evidence of clonality in a case of pigmented villonodular synovitis. Cancer 1991; 67:121 \u2013125.\n\n3. Myers BW, Masi AT. Pigmented villonodular synovitis and tenosynovitis: A clinical epidemiologic study of 166 cases and literature review. Medicine 1980; 59: 223\u2013238.\n\n4. Al-Nakshabandi NA, et al. Pigmented villonodular synovitis. Clin Radiol. 2004 May;59:414-20.\n\n5. Byers PD, Cotton RE, Deacon OW. The diagnosis and treatment of pigmented villonodular synovitis. J Bone Joint Surg Br 1968;50:290\u2013305.\n\n6. S. Shabat, Y. Kollender and O. Merimsky et al., The use of surgery and yttrium 90 in the management of extensive and diffuse pigmented villonodular synovitis of large joints, Rheumatolog 2002; 41: 1113\u20131118.\n\n7. Berger B, Ganswindt U, Bamberg M, Hehr T. External beam radiotherapy as postoperative treatment of diffuse pigmented villonodular synovitis. Int J Radiat Oncol Biol Phys 2006." } }, { "U_id": "MPX1930", "TAC": [], "MRI": [ "MPX1930_synpic40643", "MPX1930_synpic40644", "MPX1930_synpic40645", "MPX1930_synpic40646", "MPX1930_synpic40647", "MPX1930_synpic40648", "MPX1930_synpic40649", "MPX1930_synpic40650" ], "Case": { "Title": "Septo-Optic Dysplasia", "History": "10 year-old male with a known dignosis of septo-optic dysplasia.", "Exam": "N/A", "Findings": "An axial T2 image through the mid brain demonstrates absence of the septum pellucidum. Coronal T2 images also demonstrate absence of the septum pellucidum as well as hypoplasia of the optic tracts, chiasm and optic nerves. No other abnormalities were present.", "Differential Diagnosis": "Septo-optic dysplasia", "Case Diagnosis": "Septo-Optic Dysplasia", "Diagnosis By": "Brain MRI", "Treatment & Follow Up": "N/A", "Discussion": "Please see factoid." }, "Topic": { "Title": "Septo-Optic Dysplasia (DeMorsier syndrome)", "Disease Discussion": "Septo-optic dysplasia (SOD) (de Morsier syndrome) is a congenital malformation syndrome manifested by hypoplasia (underdevelopment) of the optic nerve, hypopituitarism, and absence of the septum pellucidum (a midline part of the brain). In a severe case, this results in pituitary hormone deficiencies, blindness, and mental retardation. However, there are milder degrees of each of the three problems, and some children only have one or two of the three.\n\nNeuroradiologically, intracranial malformations associated with septo-optic dysplasia include agenesis of the corpus callosum, schizencephaly, and lobar holoprosencephaly.\n\nThe optic nerve hypoplasia is generally manifested by nystagmus (involuntary eye movements, often side-to-side) and a smaller-than-usual optic disk. The degree of visual impairment is variable, and ranges from normal vision to complete blindness. When nystagmus develops, it typically appears by 1-4 months of age, and usually indicates that there will be a significant degree of visual impairment, but the severity is difficult to predict in infancy. Although there are many measures to compensate for visual impairment, no treatment is available to induce normal optic nerve function.\n\nThe degree of pituitary deficiency is also variable, and ranges from normal function, to deficiency of a single hormone, to deficiency of both anterior and posterior hormones (termed panhypopituitarism", "ACR Code": "1.4", "Category": "Ophthalmology", "Keywords": "OpthalmologyDysplasia", "External Links": "en.wikipedia.org/wiki/Septo-optic_dysplasia" } }, { "U_id": "MPX1947", "TAC": [], "MRI": [ "MPX1947_synpic16344" ], "Case": { "Title": "Dermoid cyst", "History": "This 3 1/2 year old girl had a midline subcutaneous lumbar mass. The patient complained of tenderness over the lesion but had no problems with bowel or bladder function, or walking.", "Exam": "The patient was described as having intact cranial nerves, normal strength and normal sensation.", "Findings": "1) Oblate spheroid mass in subcutaneous fat of lumbosacral region - distinct from neural structures\n\n2)probable tethered cord", "Case Diagnosis": "Dermoid cyst", "Discussion": "MRI, CT and myelogram showed that the lumbar lesion was not in continuity with the thecal sac. The patient was also thought to have a tethered cord." }, "Topic": { "Title": "Dermoid cyst", "Disease Discussion": "Dermoid and epidermoid cysts arise from ectodermal tissue displaced internally at the time of neural tube closure. Dermoid cysts are more likely to be encountered in the midline than epidermoid cysts. Dermoid cysts are distinguished from epidermoid cysts by the presence of cutaneous adnexal structures including hair follices and sebaceous glands.\n\n=========================================================\nHistology of true epithelial cysts:\nhttp://rad.usuhs.mil/medpix/epithelial_cyst_table00.html", "ACR Code": "3.3", "Category": "Cyst, benign", "Keywords": "Dermoidcyst" } }, { "U_id": "MPX1952", "TAC": [], "MRI": [ "MPX1952_synpic21351", "MPX1952_synpic21352", "MPX1952_synpic21353", "MPX1952_synpic21354", "MPX1952_synpic21355" ], "Case": { "Title": "Multiple Sclerosis", "History": "25 y/o woman has left UE weakness and chorea; with sensory loss to her left arm. Rapidly worsening of spasm in the wrist and hand.", "Exam": "Physical exam: not available\nLaboratory:-- 3 oligoclonal bands seen in CSF; no oligoclonal bands present in serum-- serum cardiolipin IgG, IgM, IgA negative-- ds DNA AB positive (28 IU/mL)-- ENA negative-- Lyme AB Total borderline; B. burgdorferi IgG, IgM negative", "Findings": "There are multifocal areas of predominately white matter abnormal signal intensity Several lesions are in the corpus callosum, the largest seen in the body of the corpus callosum; with periventricular and periatrial predominance. \n\nSeveral lesions are oriented perpendicular to the corpus callosum (Dawson\u2019s fingers). \n\nSimilar hyperintense lesions are also seen in the brain stem and spinal cord, best seen on the sagittal images.", "Differential Diagnosis": "1. Cerebral autosomal dominant arteriopathy with subcortical infarct (CADASIL)\n2. Lyme disease\n3. Central nervous system vasculitis\n4. Multiple Sclerosis\n5. ADEM (Acute Disseminated Encephalomyelitis", "Case Diagnosis": "Multiple Sclerosis", "Discussion": "Multiple sclerosis (MS) is a multifocal disease with a complex pathogenesis that includes inflammation and potentially disabling focal lesions that disseminate throughout the central nervous system. It is the most common primary myelin disorder, with an estimated patient prevalence of 250,000 to 350,000 in the United States. Eighty percent of patients have relapsing-remitting MS, and the minority of patients has primary progressive MS. This subtype of MS usually begins in the second or third decade of life and has a female predominance of approximately 2:1. The prevalence is highest in northern Europe, however, the occurrence of rapid shifts in the incidence of MS have been reported in recent studies.\nThe pathogenesis of MS remains unclear today. However, a multifactorial pathogenetic mechanism has been postulated given the heterogeneity of clinical, genetic, and radiological studies of MS. The pathological hallmark of chronic MS is the demyelinated plaque, which consisted of a well-demarcated hypocellular area characterized by the loss of myelin, relative preservation of axons, and the formation of astrocytic scars. Lesions have a predilection for the optic nerves, periventreicular white matter, brain stem, cerebellum, and spinal cord white matter. Lesions are usually round or ovoid, thought they may also have finger-like extensions along the path of small or medium-sized blood vessels (Dawson\u2019s fingers).\n \tThe diagnosis of multiple sclerosis is based on established clinical, laboratory and radiological findings. Patients with the relapsing forms of multiple sclerosis usually present with sensory disturbances, unilateral optic neuritis, diplopia, limb weakness, gait ataxia, and neurogenic bladder and bowel. Prominent cortical signs and extrapyamidal phenomena can also present but are rarely predominant features of the clinical presentation. Laboratory workup typically includes a cerebrospinal fluid analysis, which often shows increased intrathecal synthesis of immunoglobulins of restricted specificity (oligoclonal bands of IgG) with moderate lymphocytic pleocytosis. Cole and colleagues have suggested that the presence of oligoclonal bands in cerebrospinal fluid slightly increases the risk of recurrent disease.\n \tMRI is the preferred imaging modality to study suspected MS as it depicts the frequency, shape, and location of the characteristic MS lesions. These lesions have discrete foci with well-defined margins that are commonly located in a periventricular location, in the deep white matter, adjacent to the atria, occipital horns, and the body of the lateral ventricles. T2-weighted images reflect a broad spectrum of pathological changes, including inflammation, edema, demyelination, gliosis, and axonal loss. Many of the hyperintense T2-weighted lesions have little clinical significance, as they are more likely to be chronic MS lesions. Hence, there is no correlation with the number of brain lesions detected with a T2-weighted sequence and the patient\u2019s level of functional disability. Studies have shown that fluid-attenuated inversion recovery (FLAIR) sequences are superior to T2-weighted images for detecting MS brain lesions as it can detect many cortical and juxtacortial lesions in MS, which may present in secondary progressive disease and often missed by other sequences. Furthermore, gadolinium-DTPA injection, a paramagnetic contrast agent that crosses only disrupted blood-brain-barrier, may demonstrate foci of demyelination." }, "Topic": { "Title": "Multiple Sclerosis", "Disease Discussion": "Multiple sclerosis (MS) is a multifocal disease with a complex pathogenesis that includes inflammation and potentially disabling focal lesions that disseminate throughout the central nervous system. It is the most common primary myelin disorder, with an estimated patient prevalence of 250,000 to 350,000 in the United States. Eighty percent of patients have relapsing-remitting MS, and the minority of patients has primary progressive MS. This subtype of MS usually begins in the second or third decade of life and has a female predominance of approximately 2:1. The prevalence is highest in northern Europe, however, the occurrence of rapid shifts in the incidence of MS have been reported in recent studies.\n\nThe pathogenesis of MS remains unclear today. However, a multifactorial pathogenetic mechanism has been postulated given the heterogeneity of clinical, genetic, and radiological studies of MS. The pathological hallmark of chronic MS is the demyelinated plaque, which consisted of a well-demarcated hypocellular area characterized by the loss of myelin, relative preservation of axons, and the formation of astrocytic scars. Lesions have a predilection for the optic nerves, periventreicular white matter, brain stem, cerebellum, and spinal cord white matter. Lesions are usually round or ovoid, thought they may also have finger-like extensions along the path of small or medium-sized blood vessels (Dawson\u2019s fingers).\n\nThe diagnosis of multiple sclerosis is based on established clinical, laboratory and radiological findings. Patients with the relapsing forms of multiple sclerosis usually present with sensory disturbances, unilateral optic neuritis, diplopia, limb weakness, gait ataxia, and neurogenic bladder and bowel. Prominent cortical signs and extrapyamidal phenomena can also present but are rarely predominant features of the clinical presentation. Laboratory workup typically includes a cerebrospinal fluid analysis, which often shows increased intrathecal synthesis of immunoglobulins of restricted specificity (oligoclonal bands of IgG) with moderate lymphocytic pleocytosis. Cole and colleagues have suggested that the presence of oligoclonal bands in cerebrospinal fluid slightly increases the risk of recurrent disease.\n\nMRI is the preferred imaging modality to study suspected MS as it depicts the frequency, shape, and location of the characteristic MS lesions. These lesions have discrete foci with well-defined margins that are commonly located in a periventricular location, in the deep white matter, adjacent to the atria, occipital horns, and the body of the lateral ventricles. T2-weighted images reflect a broad spectrum of pathological changes, including inflammation, edema, demyelination, gliosis, and axonal loss. Many of the hyperintense T2-weighted lesions have little clinical significance, as they are more likely to be chronic MS lesions. Hence, there is no correlation with the number of brain lesions detected with a T2-weighted sequence and the patient\u2019s level of functional disability. Studies have shown that fluid-attenuated inversion recovery (FLAIR) sequences are superior to T2-weighted images for detecting MS brain lesions as it can detect many cortical and juxtacortial lesions in MS, which may present in secondary progressive disease and often missed by other sequences. Furthermore, gadolinium-DTPA injection, a paramagnetic contrast agent that crosses only disrupted blood-brain-barrier, may demonstrate foci of demyelination.", "ACR Code": "1.2", "Category": "Inflammatory, autoimmune", "Keywords": "Multiple SclerosisSclerosisMS", "Reference": "1. Bakshi R, Ariyaratana S, Benedict RB, Jacobs, L. Fluid-Attenuated Inversion Recovery Magnetic Resonance Imaging detects cortical and juxtacortical multiple sclerosis lesions. Archive Neurology 2001; 58: 742 \u2013 748.\n2. Bot JCJ, Barkhof F, et al. Differentiation of multiple sclerosis from other inflammatory disorders and cerebrovascular disease: value of spinal MR imaging. Radiology 2002; 223 (1): 46 \u2013 56. \n3. Cole SR, Beck RW, Moke PS, Kaufman DI, Tourtellotte WW. The predictive value of CSF oligoclonal banding for MS 5 years after optic neuritis. Neurology 1998; 51: 885 - 887.\n4. Noseworthy JH, Lucchinetti C, Rodriguez M, and Weinshenker BG. Multiple Sclerosis. The New England Journal of Medicine 2000; 343 (13): 938 - 952" } }, { "U_id": "MPX1962", "TAC": [], "MRI": [ "MPX1962_synpic25756", "MPX1962_synpic25757" ], "Case": { "Title": "Bilateral avascular necrosis (AVN) of the femoral heads", "History": "Inability to bear weight on right hip with constant, severe, non-radiating pain of abrupt onset. Patient fell yesterday.", "Exam": "Decreased range of motion of right hip secondary to pain.\n\nLabs normal.", "Findings": "X-ray: Serpntine sclerotic densities in the both femoral heads\n\nNuclear Scan: Focal areas of photopenia in the femoral heads with surrounding mild-to-moderate increased uptake in the subcapital areas and acetabuli. \n\nMRI: Serpentine areas of hypointensity seen in the bilateral femoral heads on T2 images. Increased T2 signal seen in the remaining marrow and femoral necks.", "Differential Diagnosis": "AVN (Avascular necrosis)\nFracture secondary to fall\nOsteoarthritis", "Case Diagnosis": "Bilateral avascular necrosis (AVN) of the femoral heads", "Diagnosis By": "MRI image findings", "Treatment & Follow Up": "Hip replacement is the best treatment, however this patient was a poor surgical candidate and was treated with oral pain meds and facet blocks.", "Discussion": "Male to female ratio for AVN is 8 to 1. Etiologies are numerous, however, in non-taumatic cases the etiology is poorly understood. Glucocorticoid steroid use and excessive alcohol intake are reported to account for more than 90 percent of cases.\n\nOne possible mechanism of steroid-induced osteonecrosis involves alterations in circulating lipids with resultant microemboli in the arteries supplying bone. A newer theory proposes that steroids induce changes in venous endothelial cells, leading to stasis, increased intraosseous pressure, and eventual necrosis. Excessive alcohol use and the development of osteonecrosis have been linked for decades; fat emboli, venous stasis, and increased cortisol levels have all been implicated as etiologic factors. \n\nPatients with SLE who have taken glucocorticoids are at greatest risk, although occasional cases have been noted in the absence of steroid therapy. In addition to their role in patients with SLE, antiphospholipid antibodies may be associated with an increased risk of osteonecrosis in other individuals. Fracture or dislocation may cause damage to the extraosseous blood vessels supplying the affected region. \n\nOsteonecrosis is common in patients with homozygous sickle cell disease. Approximately 50 percent of affected patients develop osteonecrosis by the age of 35. Gaucher Disease results in the accumulation of cerebroside-filled cells within the bone marrow. This process may lead to compression of the vasculature and subsequent osteonecrosis. Osteonecrosis can occur following renal transplantation, but usually multifocal. Ther is increased prevalence with thrombophillic disorders such as the factor V Leiden mutation. HIV may confer an increased risk of developing osteonecrosis of the femoral head as well as individuals undergoing radiation therapy. \n\nThere are two types of osteonecrosis limited to children: idiopathic osteonecrosis of the femoral head (Legg-Calv?-Perthes disease); and osteonecrosis occurring in children, usually adolescents, with a slipped capital femoral epiphysis." }, "Topic": { "Title": "Right hip pain", "Disease Discussion": "Male to female ratio of femoral head avascular necrosis is 8 to 1. Etiologies are numerous, however in non-traumatic cases the etiology is poorly understood. Glucocorticoid use and excessive alcohol intake are reported to account for more than 90 percent of cases. One possible mechanism of steroid-induced osteonecrosis involves alterations in circulating lipids with resultant microemboli in the arteries supplying bone. A newer theory proposes that steroids induce changes in venous endothelial cells, leading to stasis, increased intraosseous pressure, and eventual necrosis. Excessive alcohol use and the development of osteonecrosis have been linked for decades; fat emboli, venous stasis, and increased cortisol levels have all been implicated as etiologic factors. Patients with SLE who have taken glucocorticoids are at greatest risk, although occasional cases have been noted in the absence of steroid therapy. In addition to their role in patients with SLE, antiphospholipid antibodies may be associated with an increased risk of osteonecrosis in other individuals. Fracture or dislocation may cause damage to the extraosseous blood vessels supplying the affected region. Osteonecrosis is common in patients with homozygous sickle cell disease. Approximately 50 percent of affected patients develop osteonecrosis by the age of 35. Gaucher disease results in the accumulation of cerebroside-filled cells within the bone marrow. This process may lead to compression of the vasculature and subsequent osteonecrosis. Osteonecrosis can occur following renal transplant, but usually multifocal. There is increased prevalence with thrombophillic disorders such as the factor V Leiden mutation. HIV may confer an increased risk of developing osteonecrosis of the femoral head as well as individuals undergoing radiation therapy. There are two types of osteonecrosis limited to children: idiopathic osteonecrosis of the femoral head (Legg-Calv?-Perthes disease); and osteonecrosis occurring in children, usually adolescents, with a slipped capital femoral epiphysis.", "ACR Code": "4.9", "Category": "Nuclear Medicine", "Keywords": "AVNmusculoskelatal diseaseosteonecrosis", "Reference": "see web address", "External Links": "www.utdol.com:443/application/topic.asp?file=othrheum/7387&type=A&selectedTitle=1~48" } }, { "U_id": "MPX1967", "TAC": [], "MRI": [ "MPX1967_synpic15352", "MPX1967_synpic15590", "MPX1967_synpic15591", "MPX1967_synpic15592", "MPX1967_synpic15593" ], "Case": { "Title": "Synovial Cyst", "History": "back pain and left radicular sx", "Findings": "non enhancing cystic lesion, hypointense signal on T1 and hyperintense on T2 adjacent to a degenerative facet", "Differential Diagnosis": "free fragment\nsynovial cyst", "Case Diagnosis": "Synovial Cyst" }, "Topic": { "Title": "Synovial Cyst", "Disease Discussion": "Synovial cysts and synovial diverticula of the lumbar spine are associated with degenerative disease involving the facet joint. They are most frequent at the L4-5 level. The cysts have thick walls, whereas the diverticula are outpouchings of the synovial membrane, and have thinner walls. Both cysts and diverticula can cause sciatica if located in the superior articular recess, and can result in low back pain if located in the inferior articular recess. Hemorrhage into the cysts may cause acute symptoms.\n\n CT can diagnose the cysts, however, they are typically more conspicuous on MRI. On CT the cysts appear as low attenuation lesions adjacent to the facet joint. In 30 percent of cases they may show wall calcification. They may also demonstrate internal vacuum phenomenon. On T1W images they are typical low to intermediate signal intensity and on T2W images the cyst wall appears as a hypointense line and the fluid has high signal intensity. \n\n These cysts can be treated surgically, however, most of the patients are elderly, and are at increased risk from surgery. Steroid injections and cyst rupture are nonsurgical forms of treatment.", "ACR Code": "3.4", "Category": "Degenerative Disease", "Keywords": "synovialdegenerative", "Reference": "Sarazin, S et al. Lumbar Facet Joint Arthrography With the Posterior Approach. Radiographics 1999 19: 93-104.\nParlier-Cuau, C et al. Symptomatic Lumbar Facet Joint Synovial Cysts: Clinical Assessment of Facet Joint Steroid Injection After 1 and 6 months and Long-term Follow-up in 30 Patients. Radiology 1999 210:509-513.\nBureau, N et al. Lumbar Facet Joint Synovial Cysts: Percutaneous Treatment with Steroid Injections and Distention - Clinical and Imaging Follow-up in 12 Patients. Radiology 2001 221: 179-185." } }, { "U_id": "MPX1998", "TAC": [], "MRI": [ "MPX1998_synpic20791", "MPX1998_synpic20792", "MPX1998_synpic20793" ], "Case": { "Title": "Tuberous Sclerosis", "History": "8 month old male with sibling with tuberous sclerosis.", "Findings": "Numerous subcortical intensities with thinning of the overlying cortex, and subependymal nodules.", "Case Diagnosis": "Tuberous Sclerosis" }, "Topic": { "Title": "Tuberous Sclerosis", "Disease Discussion": "Tuberus Sclerosis is a multisystemic neuroectodermal disorder. It's incidence is between 1 in 6000 and 1 in 30,000. This disorder has a wide variety of expressions with a variable prognosis. There are numerous major and minor features and diagnosis depends on 2 major features or 1 major and 2 minor features. Approximately half of the cases are inherited in an autosomal dominant pattern, and the other half are sporadic. Classically, the clinical presentation \"zits, fits, nit-wits\"--adenoma sebacum, seizures and mental retardation.\n \nThis systemic disorder affects many systems. In the brain, it causes hamartomas in subependymal and subcortical (the Tubers) locations. The tubers may calcify, and may have enhancement on MRI. The subependymal hamartomas are most commonly located near the Foramen of Monroe. Additionally these patients are predisposed to Subependymal giant cell astrocytoma.\n\nAbout half of these patients will have renal angiomyolipomas (fatty containg masses). These are usually bilateral and multiple. 50% will have numerous bone islands, periosteal thickening and or bone cysts. Less common associations are lymphangioleiomyomatosis, chylothorax, and cardiac rhabdomyomas.", "ACR Code": "1.3", "Category": "Congenital, genetic", "Keywords": "Tuberous Sclerosis", "Reference": "Primer of Diagnostic Imaging\nEmedicine" } }, { "U_id": "MPX1996", "TAC": [], "MRI": [ "MPX1996_synpic16444", "MPX1996_synpic16445", "MPX1996_synpic16446" ], "Case": { "Title": "Autosomal Dominant \"Adult\" Polycystic Kidney Disease (ADPKD). \r\n\r\nFamily Hx revealed PT's father with history of HTN, RF, and subarachnoid hemmorhage.", "History": "41 y/o black male presented to the ER with atypical chest pain.", "Exam": "Vitals demonstrates hypertension (>190/>110) without laboratory evidence of end-organ damage (i.e., hypertensive urgency).\n\nPE is normal with non-focal neurologic exam.\nBUN - 17\nCreatinine - 1.2", "Findings": "Multiple, bilateral, cystic lesions are present on non-contrast MR. Cysts do not enhance with contrast on MR. 3D MRA demonstrates the distribution of cysts. There are no cystic lesions in the surrounding tissues or organs.", "Differential Diagnosis": "1. Renal cysts\n2. Acquired polycystic disease \n3. Autosomal recessive polycystic kidney disease \n4. Medullary kidney disorders \n -medullary sponge kidney\n -medullary cystic kidney", "Case Diagnosis": "Autosomal Dominant \"Adult\" Polycystic Kidney Disease (ADPKD). \n\nFamily Hx revealed PT's father with history of HTN, RF, and subarachnoid hemmorhage.", "Treatment & Follow Up": "The most significant therapy for those with symptomatic ADPKD involves the management of hypertension and associated sequelae. Screening for MCA berry aneurysms.", "Discussion": "With routine screening of blood pressure, hypertension has become the leading initial presenting symptom of autosomal dominant polycystic kidney disease." }, "Topic": { "Title": "Autosomal Dominant \"Adult\" Polycystic Kidney Disease (ADPKD)", "Disease Discussion": "BACKGROUND: \nThe autosomal dominant form of polycystic kidney disease (ADPKD) is an important cause of renal failure, accounting for 10% to 15% of patients who receive hemodialysis. Its incidence is approximately 1 in 500 to 1000, and approximately 500,000 Americans have been diagnosed with the disease. \n\nTwo genes for ADPKD have been localized, PKD1 on chromosome 16 and PKD2 on chromosome 4. A third but rare genetic locus, PKD3, is thought to exist but has not yet been identified. The trait theoretically has a 100% penetrance, and on average, because it is transmitted in an autosomal dominant fashion, 50% of an affected individual\u2019s offspring will likewise be affected. Ninety-six percent of affected persons will manifest the disease clinically by age 90 years.\n\nETIOLOGY:\nOne theory suggests that a defect in the basement membrane of the tubules accounts for cyst development. A 2nd theory holds that epithelial hyperplasia is an integral part of cyst formation. A 3rd theory postulates a defect in one of the proteins of the supportive extracellular connective tissue matrix. A 4th theory involves the location of Na+ -K+ -ATPase in the cystic epitheliumEach theory has supportive findings. However, it appears that tubular epithelial cell hyperplasia is the major component of cyst development.\n\nGENETICS: \nTwo genes have been identified as the culprits for ADPKD: the polycystic kidney disease (PKD1) gene localized on the short arm of chromosome 16, which accounts for approximately 85% to 90% of cases, and the PKD2 gene localized to chromosome 4, which accounts for approximately 5% to 10% of cases. The presence of a third locus (PKD3) is now accepted as the cause of disease in a very small percentage of patients. Those with the PKD2 defect usually typically have a later onset of clinical symptoms and a slower progression of disease. In addition, Bear, et al, suggested that the disease in general is more severe and manifests earlier when it is inherited from the mother rather than from the father.\n\nCLINICAL FEATURES:\nTypically, symptoms or signs first occur between the ages of 30 and 50 years. These include microscopic and gross hematuria, flank pain, gastrointestinal symptoms, and renal colic secondary either to clots or stone and hypertension. Microscopic or gross hematuria is seen in 50% of patients, and in 19% to 35% it is the presenting symptom. However, as blood pressure screening has become more widespread, hypertension more than hematuria has become the principal form of presentation. In children who present after 1 year of age, the principal signs and symptoms are related to hypertension, proteinuria, and/or hematuria. Neonates present mostly on the basis of renomegaly. When the disease is severe, stillbirth or significant respiratory distress can occur.\n\nApproximately 10% to 40% of patients have berry aneurysms, and approximately 9% of these patients die because of subarachnoid hemorrhages.\n\nOther abnormalities associated with ADPKD are mitral valve prolapse and colonic diverticulosis.\n\nHISTOPATHOLOGY:\nThe renal cysts range from a few millimeters to a few centimeters in diameter and appear diffusely throughout the cortex and medulla with communications at various points along the nephron. Epithelial hyperplasia or even adenoma formation in the cyst wall is common, and the basement membrane of the wall is thickened. Arteriosclerosis is present in more than 70% of patients with preterminal or terminal renal failure, and interstitial fibrosis, with or without infiltrates, is common. This fibrosis may be secondary to infection or to an inflammatory reaction set off by spontaneously rupturing cysts.\n\nASSOCIATION WITH RENAL CELL CARCINOMA (RCC):\nThe incidence of RCC in patients with ADPKD is no higher than that in the general population.\n\nEVALUATION:\nTo make the diagnosis, it is important to have a history of the patient\u2019s family spanning at least three generations. When there is no family history to support a diagnosis of ADPKD, a presumptive diagnosis can be made if bilateral renal cysts are present and two or more of the following symptoms are present as well: bilateral renal enlargement; three or more hepatic cysts; cerebral artery aneurysm; and a solitary cyst of the arachnoid, pineal gland, pancreas, or spleen.\n\nIn adults, intravenous urography usually reveals bilateral renal enlargement, calyceal distortion, and a bubble or Swiss cheese appearance in the nephrogram phase. A CT scan or MRI may is superior to sonography for detecting cysts in organs other than the kidney. CT is helpful in making the diagnosis of hemorrhage within a cyst. More acute hemorrhage has a higher density (50 to 90 Hounsfield units [HU]) than old hemorrhage. MRI also may be helpful, particularly in patients with compromised renal function, because no contrast agent is needed\n\nEXAMINATION OF FAMILY MEMBERS AND GENETIC COUNSELING\nBecause ADPKD is an autosomal dominant condition, 50% of the children of affected adults will also be affected. Therefore, when the disease is diagnosed, the patient\u2019s children should be examined by ultrasound. Before 1970, diagnosis of ADPKD before the age of 25 years was rare. With ultrasound, the possibility of making the diagnosis in affected individuals before this age is at least 85%. When genetic studies are used, the diagnostic accuracy approaches 100%.\n\nTREATMENT AND PROGNOSIS\nMore than 60% of patients with ADPKD who do not yet have renal impairment have hypertension, which can worsen renal function, cause cardiac disease, and predispose the patient to intracranial hemorrhage. The complications of ADPKD can be reduced significantly by controlling the blood pressure.\n\nAcute pain may be secondary to infection or hemorrhage into a cyst or to subcapsular bleeding. Chronic loin pain requiring narcotics is probably related to distention of cysts and the renal capsule. Some have proposed an operation that involves unroofing the cysts to relieve the pain. \n\nThe rate of renal deterioration seems to correlate with the rate of cyst growth. Churchill, et al, calculated that patients with sonographically identifiable ADPKD have a 2% chance of developing end-stage renal failure by age 40 years, a 23% chance by age 50, and a 48% chance by age 73.\n\nEMERGING THERAPEUTICS:\nBecause polycystic kidney disease entities represents hyperplastic cystic conditions, Grantham suggested that it is time to treat polycystic kidney diseases like the neoplastic disorders they are. One such method would be to block the action of growth factors or their receptors. Another would be to consider chemotherapeutic agents.", "ACR Code": "8.3", "Category": "Neoplasm, benign", "Keywords": "ADPKD; autosomal; dominant; polycystic; kidney; disease;", "Reference": "1. Walsh: Campbell's Urology, 8th ed., Copyright \u00a9 2002 Elsevier" } }, { "U_id": "MPX2004", "TAC": [], "MRI": [ "MPX2004_synpic24599", "MPX2004_synpic24600", "MPX2004_synpic24601", "MPX2004_synpic24602", "MPX2004_synpic24603", "MPX2004_synpic24604" ], "Case": { "Title": "Meningioma, WHO Grade 1", "History": "This is a 67yo white man with Hx of HTN, CM, and MI X 3\nreports of right-sided weakness, facial droop, dizziness leading to a fall. He reports no loss of consciousness, no post-ictal period. No loss of bowel or bladder function.\n\nThe patient reports some generalized weakness over the last month as well as headaches.", "Findings": "Dural based mass in anterior-medial portion of middle cranial fossa on the right. Roughly hemispheric in shape with a broad dural base and enhancement of the adjacent dura and cavernous sinus. There very extensive vasogenic edema.", "Differential Diagnosis": "\u2022 Meningioma\n\u2022 Atypical meningioma\n\u2022 Anaplastic meningioma\n\u2022 Hemangiopericytoma", "Case Diagnosis": "Meningioma, WHO Grade 1", "Diagnosis By": "Surgical resection and histology", "Treatment & Follow Up": "Surgical resection.", "Discussion": "This case demonstrates an unusually large amount of intraaxial vasogenic edema and the patient is male. Both of these factors may suggest an aggressive diagnosis such as hemangiopericytoma, anaplastic, or atypical meningioma. However, as was seen in this case, even typical WHO Grade 1 meningiomas may have surprisingly large amounts of edema." }, "Topic": { "Title": "Meningioma", "Disease Discussion": "Meningiomas account for up to 26% of primary intracrainal tumors. Annual incidence is about 6 per 100,000. Most are sporadic. Chromosome 22 (NF2 , 22q12) has mutations in almost all meningiomas. Other loci with mutations have been noted as well. A positive correlation has been noted with breast carcinoma. Peak incidence is in the fifth to seventh decades. Most meningiomas arise from arachnoid caps cells in the arachnoid granulations. A lesser number arise from dural fibroblasts.\n\nMeningiomas may be completely asymptomatic (>90%) or may present with hydrocephalus, seizures, focal neurological deficits, headaches, and neuropathies. Symptoms usually depend on the location of the lesion. 90% are supratentorial. Common locations include the parasagital region, cerebral convexities and sphenoid ridge. Others include the olfactory groove and the parasellar region.\n\nMeningiomas enhance uniformly on CT and are usually slightly hyperdense compared to surrounding brain on NCECT. About one-quarter calcify. With MRI, meningiomas are usually isointense on T1 and hyperintense on T2, but can vary. Homogeneous enhacement after gadolinium occurs as well. Edema-like changes in the surrounding whate matter can occur and may persist for some time after removal of the mass. The \u201cdural tail\u201d is found in a number of meningiomas (60-72%), but is not sensitive or specific enough to be a definitive sign. \n\nClassifications of meningiomas is based on histologic grading. WHO grade I are benign \u2013 typical meningioma (90%). WHO grade II are atypical meningiomas (5-7%). Anaplastic variants are WHO grade III (1-3%). Subtypes of each grade are recognized. \n\nManagement includes clinical follow-up only, endovascular treatment, surgical excision, or radiotherapy.", "ACR Code": "1.-1", "Category": "Neoplasm, non-glial", "Keywords": "meningioma", "Reference": "Wallace, E. The Dural Tail Sign. Radiology 2004; 233 (1).\n\nWhittle, I, et al. Meningiomas. Lancet 2004; 363: 1535-43.\n\nOsborn, A. Diagnostic Neuroradiology. Mosby. 1994." } }, { "U_id": "MPX2000", "TAC": [], "MRI": [ "MPX2000_synpic35440" ], "Case": { "Title": "Myxopapillary Ependymomas", "History": "Low back pain", "Findings": "Well defined centrally located mass within the spinal cord and or the conus medullaris.", "Case Diagnosis": "Myxopapillary Ependymomas" }, "Topic": { "Title": "Myxopapillary Ependymomas", "Disease Discussion": "Definition: Myxopapillary Ependymomas are slowly growing gliomas with preferential manifestation in young adults and are almost exclusively located in the conus medullaris, cauda equina, filum terminale region of the spinal cord. They are histologically characterized by tumor cells arranged in a papillary manner around vascularized mucoid stromal cores.", "ACR Code": "1.3", "Category": "Neoplasm, glial", "Keywords": "Myxopapillary EpendymomasMyxopapillaryEpendymomas", "External Links": "http://rad.usuhs.edu/medpix/medpix.html?mode=single&recnum=2271#top" } }, { "U_id": "MPX2008", "TAC": [], "MRI": [ "MPX2008_synpic27563", "MPX2008_synpic27564" ], "Case": { "Title": "Avascular Necrosis of the Femoral Heads", "History": "History of progressive bilateral hip pain.", "Exam": "N/A", "Findings": "Frontal radiograph of the pelvis demonstrates central sclerosis of the femoral heads and subtle serpiginous subchondral lucencies.\nMR images demonstrate low T1 and high T2 signal in a linear subchondral pattern.", "Differential Diagnosis": "Avascular necrosis of the femoral heads.", "Case Diagnosis": "Avascular Necrosis of the Femoral Heads", "Diagnosis By": "Characteristic Radiographic and MR imaging.", "Treatment & Follow Up": "The patient was later treated with intra-articular steroid injections and subsequent surgical core decompression.", "Discussion": "Please see factoid." }, "Topic": { "Title": "Avascular Necrosis of the Hips", "Disease Discussion": "Avascular necrosis of the hip may be a difficult diagnosis to make when a patient first presents with hip pain or mild gait abnormalities. Initial radiographs of the hips may not show any changes, as in this case. Therefore, clinical suspicion should be high for this disorder in a patient whose history suggests the diagnosis. Avascular necrosis is caused by a number of etiologies including femoral neck fracture, alcohol use, sickle cell disease, systemic lupus erythematosus, radiation treatment, and prolonged corticosteroid administration, as in this patient. Steroids have been implicated in about 20 to 35 percent of cases. The occurrence also appears to be directly related to the dosage level and duration of the medication. In decreasing order of frequency, the most common locations of steroid-induced avasular osteonecrosis are the femoral head, humeral head, the distal end of the femur, and the proximal part of the tibia. \n\nThe pathogenesis of steroid-induced osteonecrosis is unclear. However several mechanisms have been proposed and include both mechanical and vascular etiologies. Osteoporosis resulting in microfractures and later bone collapse is one mechanical theory. Vascular compromise due to hyperviscosity, vasculitis, fat embolization, and compression from marrow accumulation of relatively inelastic fat cells are also other possible causes.\n \nThe most common presenting symptom of avascular necrosis is pain. Groin pain and less commonly thigh and buttock pain are seen in patients with femoral head involvement. Patients may also complain of pain upon weight bearing. Thirty to fifty percent have bilateral involvement. Physical exam usually is nonspecific and may demonstrate limited range of motion particularly in abduction and internal rotation.\n\nRadiographic evaluation of a patient with suspected osteonecrosis includes an AP and frog-leg radiograph of both hips. As mentioned above, the initial radiographs may not show any evidence of disease. Subsequently, radiographic findings show sclerosis, indistinctive trabecular pattern, and patchy osteoporosis. Progressive radiograph findings include a crescentic subchondral line indicative of subchondral collapse, segmental flattening of the femoral head, and ultimately joint space narrowing, acetabular degenerative changes, and collapse of the femoral head.\n\nMR imaging is the most sensitive test for detecting avascular necrosis. As with this patient, MR imaging showed evidence of osteonecrosis prior to the radiographs. T1-weighted images typically show a line of low signal intensity, which corresponds to the presence of granulation tissue and sclerotic bone. T2-weighted images typically demonstrate a double line sign, which consists of a narrower line of low signal intensity that corresponds to bone sclerosis and an inner zone of high signal intensity that corresponds to granulation tissue. \n\nReferences\nLaPorte et al. \u201cMultifocal Osteonecrosis.\u201d Journal of Rheumatology. 25(10), Oct 1998, pp 1968-74. \nDonald Resnick. Diagnosis of Bone and Joint Disorders. Philadelphia: W.B. Saunders Co. 2002. pp. 3599-3637", "ACR Code": "4.9", "Category": "Differential Diagnosis", "Keywords": "osteoblastic/osteolytic changessubluxationsubchondral fracture lucencies", "Reference": "LaPorte et al. Multifocal Osteonecrosis J Rheumatol 1998; 25: 1968-74 \nResnick D. Diagnosis of Bone and Joint Disorders. Philadelphia: W.B. Saunders Co. 2002. pp. 3599-3637" } }, { "U_id": "MPX2019", "TAC": [], "MRI": [ "MPX2019_synpic42575", "MPX2019_synpic42576", "MPX2019_synpic42577", "MPX2019_synpic42578" ], "Case": { "Title": "Spontaneous osteonecrosis of the knee", "History": "72 year old female with knee pain.", "Findings": "Radiographs demonstrate an area of subchondral collapse with subchondral sclerosis in the weight bearing surface of the left lateral femoral condyle. MRI further illustrates osteonecrotic focus (low T1 and low T2 signal) with surrounding edema. Early in the disease process, some degree of T2 and PD hyperintensity can be seen. Also, surrounding edema can sometimes mask areas of subchondral sclerosis.", "Differential Diagnosis": "\u2022 Spontaneous Osteonecrosis of the knee\n\u2022 Osteochondritis dissecans\n\u2022 Meniscal Tear\n\u2022 Stress fracture", "Case Diagnosis": "Spontaneous osteonecrosis of the knee", "Diagnosis By": "MRI imagning", "Treatment & Follow Up": "\u2022 Initially, protected weight bearing\n\u2022 Advanced- surgical intervention (arthoscopic debridement, core decompression, high tibial osteotomy, drilling with or without bone grafting, osteochondral allografts, total knee arthroplasty)", "Discussion": "Imaging features, as above, are consistent with advanced Spontaneous Osteonecrosis of the Knee (SONK). There was no history of steroid use, SLE, renal transplantation, alcoholism or hemoglobinopathy. Classically, the weight bearing surface of the medial femoral condyle is involved. In this case, the lateral femoral condyle is affected." }, "Topic": { "Title": "Spontaneous osteonecrosis of the knee", "Disease Discussion": "Spontaneous osteonecrosis of the knee (SONK) is an idiopathic cause of knee pain commonly seen in osteoporotic women older than 50. This entity should not be confused with osteonecrosis secondary to steroid use, alcoholism, etc. SONK occurs spontaneously, but likely is the result of microtrauma and/or vascular comprimise.\n\nThe clinical presentation is very similar to more common entities such as degenerative joint disease or meniscal degeneration. Patients commonly present with acute medial joint pain.\n\nSONK typically involves the medial femoral condyle, but can affect the lateral femoral condyle or the tibial plateaus. SONK of the tibial plateau may be associated with meniscal injury.\n\nPlain radiographs often are normal, but may demonstrate a spectrum of findings such as flattening of the articular surface, subchondral lucency, an/or sclerosis. SONK shows increased uptake on nuclear bone scan. MR findings consist of long T2 signal associated with edema and necrosis. The overlying articular cartilage may also be abnormal.\n\nTreatment options range from conservative to surgical. Surgical treatments include core decompression, drilling, and total knee arthroplasty.\n\n\n\n*****Reviewed by MAJ Alex Freitas MC, Chief of Musculoskeletal Radiology, TAMC", "ACR Code": "4.9", "Category": "Idiopathic or Unknown", "Keywords": "OsteonecrosisKnee", "Reference": "1. Stoller, DW., Magnetic Resonance Imaging in Orthopaedics & Sports Medicine. 2nd edition., Lippincott- Raven, 1997: p411-413.\n2. Lotke PA, Ecker ML. Osteonecrosis of the Knee. Journal of bone and joint surgery. Vol 70-A. 1988. p470-473." } }, { "U_id": "MPX2021", "TAC": [], "MRI": [ "MPX2021_synpic19649", "MPX2021_synpic19650", "MPX2021_synpic19651", "MPX2021_synpic19656" ], "Case": { "Title": "Tethered spinal cord with terminal spinal lipoma.", "History": "17 Year old who at age 10 underwent surgery fo a tethered cord.", "Exam": "Well healed incision. No symptoms of tetherd cord.", "Findings": "Lipoma at level L2 and Filum terminale.\nCord rotated with fibrous band posteriorly at L2-3.", "Differential Diagnosis": "Expected post surgical change versus retethering.\nAlso, atypical dermoid is less likely given the history.", "Case Diagnosis": "Tethered spinal cord with terminal spinal lipoma.", "Diagnosis By": "surgicall / clinically", "Treatment & Follow Up": "Surgical, if symptomatic.", "Discussion": "Repositioning the patient prone and supine with breath hold technique on MRI may be considered to distinguish retethering from post-surgical change." }, "Topic": { "Title": "Tethered spinal cord with terminal spinal lipoma.", "Disease Discussion": "Early in embryogenesis, the spinal cord extends to the caudal end of the spinal canal. At that time, each neural segment is at the exact same level as the corresponding segment of the spinal canal. Each nerve root extends directly laterally to its neural foramen. As the embryo matures, the most distal portion of the cord undergoes a process known as retrogressive differentiation. In this process, the most distal fibers degenerate and elongate. At the same time, the vertebral bodies are growing more quickly than the cord. This combination of factors results in a relative ascent of the spinal cord within the spinal canal. The precise level of the conus medullaris within the spinal canal at the time of birth is debated. However, it has been established that the conus is usually positioned at the L1-L2 level by the age of 3 months. The conus is generally considered abnormal if it extends below the bottom of L2.\n\nIn some patients, the process of retrogressive differentiation goes awry. In these patients the conus medullaris remains below the bottom of L2. As a consequence, the distal spinal cord is stretched and does not function normally. \n\nPatients with tethered spinal cords can present at any age. All patients tend to suffer from difficulty with locomotion, ranging from muscle stiffness to actual weakness. All patients have abnormal lower extremity reflexes. The patients can also exhibit bladder dysfunction, sensory changes, and orthopedic deformities of the lower extremities (most commonly club foot). Back pain and radiculopathy are also common complaints; in fact, most adults with tethered cords present with radiculopathy.\n\nThe diagnosis of a tethered spinal cord is easily made with MR. The major findings are the conus medullaris ending below the bottom of L2 and a thickened filum terminale. The normal filum terminale measures less than or equal to 2 mm in diameter at the L5- S1 level. A word of caution should be issued concerning identification of the level of the conus medullaris. On sagittal images, it is sometimes difficult to differentiate the bottom of the spinal cord from the proximal cauda equina. Therefore, it is advisable to obtain axial, T1-weighted images if there is any question whatsoever about the level of the conus. It should be noted that approximately 25% of patients with tethering of the spinal cord will have a mild dilatation of the central canal of the distal cord. This mild dilatation does not represent frank syringohydromyelia and does not need to be directly treated. Often, this mild dilatation will go away after treatment of the tethered cord.", "ACR Code": "3.3", "Category": "Congenital, malformation", "Keywords": "dysraphismlipomyelomeningocelespina bifida" } }, { "U_id": "MPX2030", "TAC": [], "MRI": [ "MPX2030_synpic49047" ], "Case": { "Title": "Hyperostosis Frontalis Interna", "History": "Nasal stuffiness", "Findings": "There is thickening of the frontal bone - with widening of the diploic space.", "Case Diagnosis": "Hyperostosis Frontalis Interna" }, "Topic": { "Title": "Hyperostosis Frontalis Interna", "Disease Discussion": "Hyperostosis Frontalis Interna (HOFI) is a benign thickening of the skull, usually involving the inner table and diploic space of the frontal bone. I is seen virtually exclusively in women, usually middle-aged and nearing menopause. It has been associated with hirsutism and obesity - and endocrine changes may be a result rather than a cause. \n\nHOFI may be the result of a primary problem with bone metabolism, similar to osteopetrosis.\n\nSynonyms include Morgagni-Stewart-Morell syndrome.\n\nhttp://medical-dictionary.thefreedictionary.com/hyperostosis+frontalis+interna\nhttp://radiopaedia.org/articles/hyperostosis_frontalis_interna\nhttp://www.urmc.rochester.edu/smd/rad/neurocases/Neurocase206.htm\nhttp://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2163933\nhttp://www.learningradiology.com/archives2008/COW%20333-Hyperostosis%20frontalis%20interna/hyperostosiscorrect.htm", "ACR Code": "1.1", "Category": "Anatomy, Normal Variant", "Keywords": "fibrous dysplasiameningioma hyperostosis" } }, { "U_id": "MPX2033", "TAC": [], "MRI": [ "MPX2033_synpic47278", "MPX2033_synpic47279", "MPX2033_synpic47280", "MPX2033_synpic47281", "MPX2033_synpic47282", "MPX2033_synpic47283", "MPX2033_synpic47284", "MPX2033_synpic47285", "MPX2033_synpic47286", "MPX2033_synpic47287", "MPX2033_synpic47288", "MPX2033_synpic47289", "MPX2033_synpic47290", "MPX2033_synpic47291", "MPX2033_synpic47292" ], "Case": { "Title": "Parasellar Meningioma and arachnoid cyst", "History": "42 y.o. woman with elevated prolactin. Please evaluate for evidence of pituitary adenoma", "Exam": "Labs demonstrate an elevated Prolactin level.", "Findings": "Avidly enhancing suprasellar mass distinct from the pituitary measuring approximately 3.3 x 2.5 x 3.5 cm. The mass surrounds the left cavernous internal carotid artery extending into the medial aspect of the right cavernous sinus. \n\nThe tumor extends anteriorly to the left orbital apex. There is suprasellar and pontine cistern extension also coursing along the posterior margin of the majority of the clivus. There is posterior extension of the mass surrounding the left 5th cranial nerve involving Meckel's cave as well as surrounding the cisternal portion of the 5th cranial nerve. The mass extends to but not definitely within the left foramen ovale involving the left foramen rotundum as well. The mass abuts the left margin of the basilar artery and the left anterior margin of the mid brain. It extends into the posterior-superior aspect of the sphenoid sinus as well.\n\nA fluid intensity, non-enhancing structure is seen along the posterior margin of the above described mass filling the superior pontine cistern with extension into the left suprasellar cistern measuring 2.3x1.5x1.2 cm.", "Differential Diagnosis": "Meningioma with adjacent arachnoid cyst\nCystic Meningioma\nInvasive pituitary adenoma\nMetastasis\nSchwannoma", "Case Diagnosis": "Parasellar Meningioma and arachnoid cyst", "Diagnosis By": "Imaging characteristics", "Treatment & Follow Up": "Patient referred to neurosurgery for consultation.", "Discussion": "Although a common lesion, meningiomas may present with unusual imaging features such as large meningeal cysts, ring enhancement, and various metaplastic changes. The term \"cystic meningioma\" has been used to describe meningiomas with either intratumoral cavities or extratumoral arachnoid cysts. It has been postulated that this is a result of tumor necrosis or by direct secretion of fluid by tumor cells." }, "Topic": { "Title": "Meningioma with adjacent arachnoid cyst", "Disease Discussion": "Meningiomas are the most common extra-axial tumor and the most common non-glial intracranial tumor. They are normally solid, well-marginated benign lesions originating from the meninges accounting for 15- 20% of adult brain tumors. The most common locations include the bilateral convexities, parasagittal regions, parafalcine, sphenoid wing, olfactory groove, and suprasellar region. The typical appearance of a meningioma is a homogeneous solid tumor. Nonenhanced computed tomography demonstrates a homogeneous mass that is isodense to intracranial parenchyma. Contrast enhanced scans demonstrate diffusely homogeneous enhancement. MRI is typically isointense to relatively hypointense on T1 weighted images. T2 weighted images generally demonstrate slightly increased signal intensity in relationship to the contiguous gray matter. Gadolinium enhanced MR images demonstrate intense uniform enhancement. Although meningiomas are histologically benign, they may invade surrounding structures including the dura and bony structures. On rare occasions, the meningioma may completely penetrate the calvarium to invade the scalp. Meningiomas may occasionally present atypical imaging features such as those seen in cystic, lipoblastic, or angioblastic meningiomas. Peritumoral edema and ring enhancement may also be seen.", "ACR Code": "1.3", "Category": "Neoplasm, NOS", "Keywords": "Meningioma", "Reference": "Buetow MP, Buetow PC, Smirniotopoulos JG. Typical, atypical, and misleading features in meningioma. Radiographics 11 (6): 1087\u2013106.\n\nOsborn,Ann G. Diagnostic Radiology. 1994, Mosby." } }, { "U_id": "MPX2041", "TAC": [], "MRI": [ "MPX2041_synpic21981", "MPX2041_synpic21982", "MPX2041_synpic21983" ], "Case": { "Title": "Plantar Fibromatosis (Ledderhose Disease)", "History": "Enlarging mass on medial plantar aspect of his foot, becomming increasingly sypmpomatic over last 2 weeks.", "Exam": "Palpable, mildly tender subcutaneous mass on the plantar aspect of the foot, at the base of the first MTP joint. Mild overlying erythema. Otherwise healthy male. No recallable history of antecedent trauma.", "Findings": "2cm x 3cm well-circumscribed fusiform mass arising from the plantar fascia on the medial aspect of the foot proximal to the 1st MTP. Lesion is homogenously iso-intense to muscle on T1 sequences, and hetrogenslightly hyperintense on fat-saturated T2 sequences. Marked, homogeneous enhancement following administration of gadolinium DTPA. No surrounding soft tissue or bone marrow edema.", "Differential Diagnosis": "Plantar Fibromatosis\nNodular (Pesudosarcomatous)Fasciitis\nAggressive Fibromatosis", "Case Diagnosis": "Plantar Fibromatosis (Ledderhose Disease)", "Diagnosis By": "Diagnosis is presumed based on classic findings and location.", "Treatment & Follow Up": "Treatment consists of wide excision; some advocate post surgical radiation to help prevent recurrence.", "Discussion": "Location and imaging characteristics are classic for this entity of superficial fibromatosis. Nodular fasciitis is a differential consideration, but only involves the feet in ~15% of cases, being mostly found in the upper body and trunk. About 50% of plantar fibromas are painful. Lesions are not related to trauma and are of uncertain etiology. Lesions can be bilateral in up to 50% and can also involve the palmar fascia (Dupuytren's Contracture). Treatment with excision must include the entire lesion, and similiar to other fibromatoses, lesions tend to recurr. Not locally destructive as the deep (aggressive) fibromatoses(desmoid)." }, "Topic": { "Title": "Plantar fibromatosis", "Disease Discussion": "Plantar fibromatosis ( also known as Ledderhose disease) is a form of superficial fibromatoses. The musculoskeletal fibromatoses are a diverse group of diseases with a common histopathologic appearance being composed of spindle-shaped fibrous cells separated by abundant collagen material with few mitoses whose behavior varies between benign fibrous lesions and fibrosarcoma. The fibromatoses are separated into superficial - (palmar \u2013 aka Dupuytren disease, plantar, juvenile aponeurotic fibroma, infantile digital fibromatosis) which are usually small, slow growing lesions which arise from fascia/aponeuroses and deep-(infantile myofibromatosis, fibromatosis colli, extraabdominal desmoid tumor, and aggressive infantile fibromatosis) which arise from the deeper musculoaponeuroses and are larger and may grow rapidly. Both forms have a tendency to recur following excision.\n\tPlantar fibromatosis, like all fibromatoses, are three to four times more common in males. It occurs between the ages of 30 \u2013 50 and is seen bilaterally in 20-50% of cases. It is associated with palmar fibromatosis 10-65% of the time. The fibromas are most commonly seen on the medial aspect of the plantar aponeurosis. The lesions are often asymptomatic. Surgery is performed utilizing large margins. Post-surgical radiation treatment may decrease recurrence.\n\tThe typical appearance of plantar fibromatosis on MR is a poorly defined, infiltrative mass in the aponeurosis next to the plantar muscles. They are typically heterogeneously low signal when compared to muscle on both T1 and T2. Lesions which have an increased T2 signal have more cellularity and are more likely to recur, therefore, some surgeons may postpone resection until the lesion is more fibrous (ie. Low T2 signal). Enhancement following gadolinium administration is variable.", "ACR Code": "4.3", "Category": "Neoplasm, benign", "Keywords": "fibromatosisplantar", "Reference": "Robbin MR, Murphey MD. Imaging of Musculoskeletal Fibromatosis. Radiographics, May-June, 2001, 21:585-600." } }, { "U_id": "MPX2043", "TAC": [], "MRI": [ "MPX2043_synpic17061", "MPX2043_synpic17062", "MPX2043_synpic17064" ], "Case": { "Title": "HILL-SACHS DEFORMITY WITH ASSOCIATED BANKART LESION", "History": "H/O THREE ANTERIOR SHOULDER DISLOCATIONS SINCE AGE 21, ALL PLAYING RUGBY.", "Exam": "JOINT LAXITY ASSOCIATED WITH OVERHEAD AND CROSS-ARM MOVEMENT DIFFICULTY. OCCASIONAL LOCKING SYMPTOMS.", "Findings": "A-P RADIOGRAPHS: SUBCHONDRAL SCLEROSIS IN THE REGION OF THE GLENOID TUBERCLE WITH DEPRESSION OF POSTERO-LATERAL HUMERAL HEAD ON EXTERNAL ROTATION. REMAINDER OF BONES NORMAL; NO BANKART LESION APPRECIATED.\n\nTWO FSE PROTON DENSITY W/ FAT SAT. AXIAL MR IMAGES OF RIGHT SHOULDER SHOW:\n1.\tMORE SUPERIOR IMAGE, AT LEVEL OF SUPERIOR GLENOID, FLATTENING OF POSTERIOR-LATERAL ASPECT CONSISTENT WITH HILL-SACHS DEFORMITY. HIGH SIGNAL INTENSITY AROUND HUMERAL HEAD REPRESENTS CARTILAGINOUS/OSSEOUS TISSUE WITH EDEMA/CONTUSION.\n2.\tHIGH SIGNAL INTENSITY IN REGION OF POSTEROLATERAL MARGIN OF HUMERAL HEAD IS MORE EVIDENT, AND IN THE CARTILAGINOUS AND SUBJACENT HUMERUS IS CONSISTENT WITH EDEMA/CONTUSION, CONSISTENT WITH HILL-SACHS DEFORMITY.\n\nFSE PROTON DENSITY W/ FAT SAT. CORONAL OBLIQUE MR IMAGE OF RIGHT SHOULDER SHOWS HIGH SIGNAL INTENSITY SEPARATING ANTERIOR LABRUM FROM BONY LABRUM CONSISTENT WITH BANKART LESION.", "Differential Diagnosis": "FINDINGS DIAGNOSTIC OF HILL-SACHS DEFORMITY AND BANKART LESION, CORRELATIVE WITH THE PATIENT HISTORY OF RECURRENT ANTERIOR DISLOCATIONS.", "Case Diagnosis": "HILL-SACHS DEFORMITY WITH ASSOCIATED BANKART LESION", "Treatment & Follow Up": "Patients who have anterior dislocation for the first time undergo reduction and treatment for pain and physical therapy. If adequate trials of physical therapy fail, indicated by continued anterior instability and pain, or if multiple dislocations occur, more invasive procedures are performed. Various surgical procedures have been developed for treatment of recurrent anterior dislocations of the humeral head. Treatment can be either by arthroscopy or open anterior shoulder repair (axillary approach or the Bankart lesion fixation procedure); other procedures include the Bristow Helfet procedure, Magnuson Stack procedure, Eden Hybinette procedure, Oudard procedure and Trillat procedure. The Bankart procedure is the gold standard, with success rates of 90-95%. In associated Hill-Sachs lesions, the glenoid can be augmented with a tricortical iliac crest graft.Traditionally, arthroscopic techniques have had a failure rate of about 20% at 3.5 years, whereas the newer Bankart fixation techniques have brought this down to 10% or less. Support is gathering for earlier surgical intervention in patients with recurrent dislocations." }, "Topic": { "Title": "Hill-Sachs Deformity With Associated Bankart Lesion", "Disease Discussion": "Anterior dislocations are produced by complex forces acting on the humerus, including abduction and external rotation. The Hill-Sachs fracture results from this anterior dislocation (97% vs. 3%) with compression of posterolateral aspect of the humeral head by the inferior glenoid labrum. Hill-Sachs deformities occur in 35-40% of anterior dislocations and up to 80 % of recurrent dislocations. Hill-Sachs fractures can occur with subluxations, or single or multiple dislocations. The dislocation may also cause a Bankart fracture at the impact site on the glenoid. This is a fracture of the anterior aspect of the inferior rim of the glenoid caused by the anterior movement of the humeral head and is best seen on the anteroposterior projection with the arm in the neutral position. If radiographs at presentation show no dislocation, the presence of either Hill-Sachs deformities or Bankart\u2019s fractures are indicative of a prior dislocation. MRI is the best imaging modality for identifying cartilaginous and osseous Hill-Sachs deformities and associated tears of the anterior glenoid labrum. The contour defect of both cartilage and bone at the superior aspect of the humeral head posterolaterally represents the Hill-Sachs deformity and the high signal intensity separating the cartilaginous labrum from the bony labrum represents the tear \u2013 the Bankart lesion.\nThe younger the patient when the first dislocation occurs, the greater is the probability that dislocation will recur. Thus, patients 20 years old or younger have a 80-90% chance of lifetime recurrence, those 30 or younger have a 60% recurrence rate, and of those 40 and older at time of first dislocation, have a 10-15% probability of recurrence.", "ACR Code": "4.4", "Category": "Trauma", "Keywords": "Hill-SachsBankartshoulder dislocation", "Reference": "Stoller, David W. Magnetic Resonance Imaging in Orthopaedics & Sports Medicine. Lippincott, 1993.\nRogers, Lee. Radiology of Skeletal Trauma. 2nd ed.\nWheeless Textbook of Orthopaedics. \u201cAnterior Instability of the Shoulder\u201d. 1996.\n\nBurkhart, Stephen S. \u201cThe Arthroscopic treatment of Traumatic Anterior Instability\u201d. http://www.isakos.com/innovations/antinst.html" } }, { "U_id": "MPX2069", "TAC": [], "MRI": [ "MPX2069_synpic24284", "MPX2069_synpic24285", "MPX2069_synpic24286" ], "Case": { "Title": "Osteochondritis dissecans.", "History": "Patient is a 35-year-old man with a history of a left distal fibular fracture in January 2003. He now presents with repeated episodes of pain and swelling around the left lateral malleolus after playing basketball.", "Exam": "Physical exam was unremarkable. Complete blood count and basic metabolic panel were within normal limits.", "Findings": "AP and mortise radiographs of the left ankle shows a lucency in the medial talar dome.\n\nT1-weighted sagittal MR image of the left ankle shows a focus of low signal intensity in the talar dome.\n\nCoronal proton-density MR image with fat saturation and sagittal STIR MR image shows a focal high-signal-intensity osteochondral lesion of the medial talar dome with associated edema in the talus", "Differential Diagnosis": "1.Osteochondral fracture \n2. Osteochondritis dissecans", "Case Diagnosis": "Osteochondritis dissecans.", "Treatment & Follow Up": "Healing and revascularization of the lesion is dependent upon fragment stability and the degree of articular cartilage disruption. The Berndt and Harty classification system (1959) assigns lesions to one of four stages: small area of compressed subchondral bone (stage 1), partially detached fragment or flap (stage 2), completely detached fragment that remains in its crater (stage 3), and a loose body (stage 4). Stage 1 and 2 lesions are considered stable and are followed by close clinical evaluation. Stage 3 and 4 lesions are considered unstable loose fragments and are surgically removed or fixated. MRI has been found most valuable in surgical decision-making. Nelson et al. completed a small study of 12 patients with OCD of the talus and knee in 1990 that revealed a 91.7% correlation between MRI staging and arthroscopic staging.", "Discussion": "Osteochondritis dissecans (OCD) is a painful, usually unilateral condition commonly affecting 20-40 year olds (men more frequently than women) whereby a segment of articular cartilage and attached subchondral bone becomes partially or completely separated from the underlying parent bone. Etiology is thought to be secondary to trauma. Medial talar dome injury may be related to plantar flexion of the foot with accompanying inversion, followed by rotation of the tibia on the talus.\n The use of MR imaging in the evaluation of OCD is credited in large part to the studies of De Smet. Specifically, he focused on the correlation between signal intensity and fragment stability. High signal intensity at the junction between the fragment and the parent bone on a T2 weighted image strongly suggests an unstable lesion." }, "Topic": { "Title": "Osteochondral defect (OCD) secondary to trauma, specifically osteochondritis dissecans.", "Disease Discussion": "Osteochondritis dissecans (OCD) is a painful, usually unilateral condition commonly affecting individuals in the 20 to year old age group (men more frequently than women). In this lesion, a segment of articular cartilage and attached subchondral bone becomes partially or completely separated from the underlying parent bone. Etiology is thought to be secondary to trauma. Medial talar dome injury may be related to plantar flexion of the foot with accompanying inversion, followed by rotation of the tibia on the talus.\n The use of MR imaging in the evaluation of OCD is credited in large part to the studies of De Smet. Specifically, he focused on the correlation between signal intensity and fragment stability. High signal intensity at the junction between the fragment and the parent bone on a T2 weighted image was a strong predictor of an unstable lesion.", "ACR Code": "4.4", "Category": "Trauma", "Keywords": "Osteochondritis dissecans (OCD)osteochondral defecttalar dome", "Reference": "1.\tDe Smet AA, Fisher DR, Burnstein MI, et al. Value of MR imaging in staging osteochondral lesions of the talus (osteochondritis dissecans): Results in 14 patients. AJR 1990; 154: 555.\n2.\tNelson DW, DiPaola J, Colville M, et al. Osteochondritis dissecans of the talus and knee: Prospective comparison of MR and arthroscopic classifications. J Computer Assisted Tomography 14: 804, 1990.\n3.\tResnick D. Diagnosis of Bone and Joint Disorders, Vol. 3, Philadelphia, 2002, pp.2689-2692 and 2701-2704." } }, { "U_id": "MPX2084", "TAC": [], "MRI": [ "MPX2084_synpic40680", "MPX2084_synpic40681", "MPX2084_synpic40682" ], "Case": { "Title": "Chondrosarcoma metastatic to Brain", "History": "55 yo woman with history of a resected left lower extremity chondrosarcoma. Known to have lung metastases, she presents now with right upper and lower extremity weakness.", "Exam": "Weakness in both upper and lower extremities, right greater than left.", "Findings": "Multiple lesions within the brain. The most prominent were in the left frontal and parietal region. The lesions were very hyperintense on T2, and demonstrated only peripheral enhancement", "Differential Diagnosis": "Given the marked hyperintensity on T2 and history of chondrosarcoma, this is the most likely diagnosis. Metastases from other locations could also be in the differential.", "Case Diagnosis": "Chondrosarcoma metastatic to Brain", "Diagnosis By": "Biopsy and Histology" }, "Topic": { "Title": "Chondrosarcoma metastatic to Brain", "Disease Discussion": "Brain metastases from musculoskeletal sarcomas are uncommon. However, in patients with both advanced disease and systemic metastasis - over 10% will develop metastases to the brain. There is some thought that the systemic chemotherapy, which has prolonged the survival of sarcoma patients, may also be associated with an increased incidence of intracranial metastases. This may be due to the poor penetration of these chemotherapeutic agents across the blood-brain barrier. Thus, the deposits in the brain do not receive the same concentration of drug that controls the extra-CNS disease.\n\nThe chondroid matrix produced by the tumor has a water-like signal on both CT and MRI.", "ACR Code": "1.3", "Category": "Neoplasm, sarcoma", "Keywords": "ChondrosarcomaBrain metastaseslarge ugly things in brain", "Reference": "\u2022 Wronski M, Arbit E, Burt M, Perino G, Galicich JH, Brennan MF. Resection of brain metastases from sarcoma. Ann Surg Oncol 1995;2:392-9.\n\n\u2022 Salvati M, Cervoni L, Caruso R, Gagliardi FM, Delfini R. Sarcoma metastatic to the brain: a series of 15 cases. Surg Neurol 1998;49 :441-4. \n\n\u2022 Ogose A et al. Brain metastases in musculoskeletal sarcomas. Jpn J Clin Oncol. 1999 May;29(5):245-7\n\n\u2022 Marina NM, Pratt CB, Shema SJ, Brooks T, Rao B, Meyer WH. Brain metastases in osteosarcoma. Cancer 1993;71:3656-60." } }, { "U_id": "MPX2087", "TAC": [], "MRI": [ "MPX2087_synpic16289", "MPX2087_synpic16290" ], "Case": { "Title": "Metastatic Disease (Presumed Breast)", "History": "History of breast cancer, recently diagnosed. Now c/o progressive left knee pain.", "Findings": "Plain films of the knee demonstrate an ill-defined area of sclerosis along the posterior lateral aspect of the femur, superior to the patella.\n\nMRI of the tibia demonstrate focal decreased T1 signal and increased signal on IR corresponding to the area of plain film abnormality.", "Differential Diagnosis": "-Metastatic Disease\n-Primary marrow malignancy", "Case Diagnosis": "Metastatic Disease (Presumed Breast)", "Treatment & Follow Up": "Patient is awaiting formal bone marrow biopsy for confirmation, and will undergo chemotherapy for known breast cancer.", "Discussion": "This young woman had a suspicious lump in her left breast. After FNA and a later core biopsy, this was determined to be infiltrating ductal carcinoma. She has not yet undergone mastectomy. If it were not for the breast cancer diagnosis, her presentation with knee pain and the vague plain-film finding might normally not have raised such a high level of concern to warrant an MRI." }, "Topic": { "Title": "Metastatic disease", "Disease Discussion": "Metastatic disease, or more simply \"metastasis\" (single) or \"mestastases\" (pleural) occur when a neoplasm (tumor) spreads from one part of the body to another. There are three primary modes of spread:\n\nlocal invasion or infiltration\nblood-borne (hematogenous) dissemination\nlymphatic spread\n\nHematogenous dissemination is the most common and usually the most serious type of tumor spread. Most solid tumors larger than 4-5 milimeters in size grow their own blood vessels. [See Angiogenesis - http://rad.medpix.net/medpix/radpix.html?mode=single&recnum=2733 ] The tumor has \"angiogenic\" factors that stimulate blood vessels. Many of these same tumors also have angioinvasive factors that allow the tumor to penetrate through vessel walls. Therefore, the tumor is richly vascularized - giving it a path to the systemic circulation; and, once the tumor \"embolizes\" the small tumor fragments are able to erode through the vessel and implant into the surrounding tissue. Thus creating a metastatic deposit.\n\nThere is a \"cascade\" theory for tumor embolization and metastasis. Blood from the gut is \"filtered\" in the liver, and gastrointestinal metastases usually begin in the liver before they spread to other organs. The lung filters all of the systemic blood as it passes through, and metastatic disease here is common from all tumor sources. Brain and bone metastases usually occur after the lung has been affected - at least in theory. Some solid organs are affected more than others merely because they filter more blood - like the kidney, adrenal gland, and brain.", "ACR Code": "1.3", "Category": "Neoplasm, metastatic" } }, { "U_id": "MPX2083", "TAC": [], "MRI": [ "MPX2083_synpic52355", "MPX2083_synpic52356", "MPX2083_synpic52357", "MPX2083_synpic52358", "MPX2083_synpic52359" ], "Case": { "Title": "Cervical Cord hemangioblastoma", "History": "43 y/o man evacuated from Africa with 1 month history of symptoms \u2013 electric shock down the spine into the limbs with neck movement.", "Exam": "Lhermitte\u2019s sign (Barber chair phenomenon \u2013 electric shock down the spine into the limbs with neck flex/ext)", "Findings": "Focal, well-defined enhancing lesion in the posterior aspect of the cord at C2-C3, which replaces rather than displaces cord tissue. Increased T2 signal within and thickening of the spinal cord from C1 to C5, consistent with surrounding edema. No involvement of adjacent bone or dura.", "Differential Diagnosis": "\u2022 AVM\n\u2022 Cavernous malformation\n\u2022 Ependymoma\n\u2022 Astrocytoma\n\u2022 Hemangioblastoma\n\u2022 Metastatic vascular tumor (in particular RCC)\n\u2022 extramedullary/intradural tumor.", "Case Diagnosis": "Cervical Cord hemangioblastoma", "Diagnosis By": "Pathological tissue examination." }, "Topic": { "Title": "Cervical hemangioblastoma", "Disease Discussion": "Hemangioblastomas account for 2% of all primary cord tumors. Most occur in the dorsal portion of the cord, with 60% intramedullary and 40% intradural/extramedullary. They are frequently solitary (80%), with the most common location thoracic (50%), with 40% occurring in the cervical region. These tumors manifest in the fourth decade and 1/3 of patients have von Hippel-Lindau disease. They often present as intramedullary cysts with one or more vascular nodules and dilated, tortuous veins usually on the dorsal surface of the cord, seen on angiography. About 40% of all hemangioblastomas and 60% of intramedullary hemangioblastomas are associated with a syrinx.\n\nMR findings typically show an enlarged, sometimes irregular widening of the cord that is predominately hypointense on T1WI and becomes hyperintense on T2WI. This is due to the cystic component, which is also indistinguishable from the surrounding edema on T2WI. The tumor nidus may sometimes be seen as isointense (to cord), nodular on T1- weighted sequence within the intramedullary or intradural cystic cavity, but becoming hyperintense on T2WI (usually indistinguishable from the cystic cavity or surrounding edema). An associated syrinx may be quite extensive, extending over multiple levels above and below the tumor. Reports have shown that the tumor nidus rapidly and intensely enhances on T1WI following the administration of gadopentetate dimeglumine, helping to demarcate the tumor from the surrounding edema, thus providing valuable preoperative localization. Additionally, focal areas of signal void on both T1- and T2WI may be seen, depicting the flow in dilated feeding/draining vessels. Initial experience suggests that a densely enhancing solid tumor nodule within a large \"syrinx\" cavity and associated \"feeding\" vessels is highly suggestive, if not diagnostic, of a hemangioblastoma.", "ACR Code": "3.3", "Category": "Neoplasm, non-glial" } }, { "U_id": "MPX2093", "TAC": [], "MRI": [ "MPX2093_synpic26837" ], "Case": { "Title": "Kohler's Disease", "History": "Otherwise healthy 6 year old boy presents to primary care with 2-week history of discomfort in left foot. Mother reports that the boy had been acting normally until two weeks ago when he began to complain of left foot pain. There was no history of trauma, recent or in the past. His mother noted that over the last week the patient has been favoring the left foot and walked with a limp.", "Exam": "Well-appearing boy in no acute distress. Patient walked with a slight limp favoring his left foot. No swelling or erythema was present. The patient had normal sensation, range of motion and strength. Patient has tenderness to palpation localized to the medial side of the left mid-foot.", "Findings": "Oblique and Lateral radiographs demonstrate sclerosis and decreased A-P diameter of the navicular bone.\nFSE T2-weighted with fat sat sagittal MR image of the left foot shows high-signal-intensity necrosis and edema in the tarsal navicular bone and low-signal-intensity sclerosis of this bone.", "Differential Diagnosis": "Differential DX of imaging findings\n-Trauma\n-Avascular Necrosis\n\nDifferential Dx of Causes of Osteonecrosis\n-Vascular Insufficiency\n-Idiopathic\n-Trauma\n-Sickle Cell Disease\n-Hemoglobinopathies\n-abnormal order of bone ossification", "Case Diagnosis": "Kohler's Disease", "Diagnosis By": "Imaging characteristics and clinical", "Treatment & Follow Up": "Treatment is symptomatic. Patients are instructed to rest and decrease physical activity. Shoe inserts and walking casts can be used for patients with moderate discomfort.\nThis disease is self-limiting and resolves spontaneously. Within 2-4 years patients will become asymptomatic and radiographic studies will return to normal." }, "Topic": { "Title": "Kohler's Disease", "Disease Discussion": "\u00bb Definition:\nKohler's Disease is osteonecrosis of the navicular bone. Demographics:\nOsteonecrosis of the tarsal navicular bone usually occurs in patients ages 3-7 yrs. It is more common in males than females with a ratio of 5:1. It is unilateral in 75-80% of cases.\n\n\u00bb Etiology:\nThe underlying cause is typically idiopathic - meaning \"we don't know\". There is a documented history of trauma in only 35% of cases. \n\n\u00bb Clinical:\nThe disease usually presents as mild pain in the midfoot, local tenderness and decreased range of motion.\n\n\u00bb Treatment:\nTreatment is entirely symptomatic with rest, shoe inserts and walking casts when needed.\n\n\u00bb Prognosis is excellent and over a period of 2-4 yrs many patients recover entirely and the bone regains normal size.\n\n=========================================\nWho Named It:\nhttp://www.whonamedit.com/synd.cfm/2676.html", "ACR Code": "4.9", "Category": "Idiopathic or Unknown", "Keywords": "KohlerOsteonecrosis", "Reference": "Resnick D. ed. Diagnosis of Bone & Joint Disorders. 4th ed. WB. Saunders Company, Philadelphia. 2002. pp 3669-3711.\nTsirikos, A., Riddle, E. and R. Kruse. Bilateral Kohler\u2019s disease in identical twins. Clin Orthop and Rel Res 2003, 409:195-198." } }, { "U_id": "MPX2128", "TAC": [], "MRI": [ "MPX2128_synpic28895", "MPX2128_synpic28896", "MPX2128_synpic28897", "MPX2128_synpic28898" ], "Case": { "Title": "Enchondroma", "History": "The patient is a 31 year old AAF who, after twisting her knee while running, initially presented with a one month history of focal pain and stiffness to the medial aspect of the left knee. During workup, an enchondroma was identified on MRI.", "Exam": "Physical exam was remarkable for mild erythema of the medial aspect of the left knee, tenderness to palpation at the medial joint space, pain on flexion and extension, no locking. Pt is able to ambulate.", "Findings": "Radiographic images demonstrated normal anatomy.\nMRI demonstrated a left MCL injury\nIncidental finding on MRI demonstrated a 13x18mm mass located centrally in the left distal femoral metaphysis. It had distinct borders, did not extend to cortical bone, and was well circumscribed. There were no calcifications noted.", "Differential Diagnosis": "bone infarct\nenchondroma", "Case Diagnosis": "Enchondroma", "Diagnosis By": "Confirmed with findings on MRI", "Treatment & Follow Up": "Pt will be observed for changes suggestive of malignancy.", "Discussion": "A benign neoplasm composed of ectopic cartilage rests that have migrated into bones\u2019 metaphysis from the growth plate. Unless the patient has an enchondromatosis syndrome, these tumors rarely progress to chondrosarcoma. Occasionally, the tumor will cause a pathologic fracture which necessitates curretage of tumor in order to restore structural integrity of the bone. In cases without pathologic fracture, or melignant transformation, the treatment of choice is observation." }, "Topic": { "Title": "Enchondroma", "Disease Discussion": "A benign neoplasm composed of ectopic cartilage rests that have migrated into bones\u2019 metaphysis from the growth plate. Enchondromas are usually singular, but multiple lesions may occur in enchondromatosis syndromes such as Ollier\u2019s, Maffucci\u2019s and metachondromatosis. Enchondromas are a benign finding seen incidentally on plain radiographs MRI, and/or CT while investigating other pathology.\n\nTypically, patients are 20-40 years old when the tumor is identified. The patient with any of the enchondromatosis syndromes is typically younger when the first lesion is identified. There is no gender or racial predilection.\n\nIn the United States, enchondromas account for 12-14% of benign bone neoplasms and 3-10% of osseous neoplasms in general. They are most commonly found in the diaphyses of the hands and feet, and less commonly in the femur, humerus, or tibia. Enchondromas present as small (<5 cm) lytic masses which have a pattern of lobulated arcs and rings indicative of their chondroid matrix. When found in the larger bones, they are usually metaphyseal, centrally located and can have a sclerotic margin.\n\nFrequently plain radiographs are adequate to identify and diagnose enchondromas. Occasionally, further imaging such as CT or MRI may be required to offer a more complete picture of the bone surrounding the tumor. Bone scans are usually ineffective in the diagnosis of enchondromas as typical findings of mildly increased uptake are non-specific.\n\nEnchondromas are benign but can cause pathologic fractures or can rarely progress to chondrosarcoma. This malignant transformation is of concern due to the destructive changes which occur in high grade tumors as well as the 5 year survival rate which is as low as 15% in high grade tumors. \n\nTumors found in the hands and feet have a virtually negligible transformation rate while those seen in the long and flat bones should be monitored more closely for transformation. Transformation to malignancy occurs much more frequently in patients with enchondromatosis. \n\nThe following radiographic changes are suggestive of this transformation to chondrosarcoma:\n\u2022 \tScalloping of the inner surface of the bone\n\u2022 \tThickening of the bone cortex\n\u2022 \tReactive bone growth on the outer surface of the bone\n\u2022 \tErosion surrounded by reactive bone\n\u2022 \tNoticeable growth in the bony erosion\n\u2022 \tMRI may identify cortical extension and extension to the soft tissue mass.\n\nWith the exception of enlarged digits when hands and feet are involved, physical exam of the patient with an enchondroma is usually unremarkable. Pain found on exam is attributable to either adjacent but non-related pathology, pathologic fracture resulting from the enchondroma, or should raise the clinical suspicion for progression to chondrosarcoma.\n\nDifferential diagnosis varies depending on whether calcifications are present. In cases in which they are, bone infarct which may exhibit a serpiginous lining and low grade chondrosarcoma must be considered. If the lesion is purely lytic, however, non-ossifying fibroma, simple bone cyst, fibrous dysplasia, eosinophilic granuloma, and clear cell chondrosarcoma should be considered. \nWhen considering these diagnoses, the following factors are each used to rule out the diagnosis in question:\n\u2022 \tNon-ossifying fibroma \u2013 usually cortically based, enchondromas are medullary based\n\u2022 \tSimple bone cyst \u2013 usually seen before age 20\n\u2022 \tEosinophilic granuloma \u2013 also seen commonly in patients before age 20\n\u2022 \tFibrous dysplasia \u2013 has a ground glass appearance on imaging\n\u2022 \tClear cell chondrosarcoma \u2013 epiphyseally based, with extension into the metaphysis usually seen on MR\n\nWhen asymptomatic, treatment of enchondromas consists of observation. In the patient in whom a pathologic fracture has occurred, the fracture is usually allowed to heal, followed by curettage and filling of the cavity with bone fragments or cement.", "ACR Code": "4.3", "Category": "Neoplasm, benign", "Keywords": "enchodromaollier maffucci metachondromatosisbenign cartilaginous neoplasm tumor", "Reference": "Resnick DR, Diagnosis of Bone and Joint Disorders, 4th edition v4, WB Saunders Company, Philadelphia, PA 2002, pp 3833-3843 \n\nMurphey MD, Flemming DJ, Boyea SR, et al. Enchondroma vs chondrosarcoma in the appendicular skeleton: differentiating features, Radiographics, 1998 Sep-Oct 18(5): pp1213-1237\n\nRobbin MR, Murphey MD, Benign chondroid neoplasms of bone, Semin Musculoskelet Radiol. 2000; 4(1): 45-58" } }, { "U_id": "MPX2112", "TAC": [], "MRI": [ "MPX2112_synpic23367", "MPX2112_synpic23368" ], "Case": { "Title": "Hydroxyapatite deposition disease", "History": "65 y/o with longstanding right knee pain", "Findings": "AP radiograph and Proton Density Fat Saturation (PD FS) knee MR from 2002 showing calcific deposits within the lateral collateral ligament (LCL). More recent imaging from 2005 showed resolution of calcium deposits.", "Differential Diagnosis": "Hydroxyapatite deposition disease\nCalcium pyrophosphate deposition disease", "Case Diagnosis": "Hydroxyapatite deposition disease", "Diagnosis By": "Resolution confirms diagnosis" }, "Topic": { "Title": "Hydroxyapatite deposition disease", "Disease Discussion": "Hydroxyapatite deposition disease (HADD, Calcific Tendonitis) can be asymptomatic or be painful. Sometimes the pain can be accompanied by fever, swelling and erythema. In some cases, the inflammation can progress to severe bony and joint destruction. On the other hand, cases can also resolve spontaneously or with treatment with NSAIDs. In most cases the disease is self limiting. Several causes for deposition of calcium hydroxyapatite in tendons have been proposed, but thus far none is confirmed. \n\nThe calcific deposits occur most commonly at humerus or femur. They occur within tendons and ligaments. These can rupture into adjacent bursa, joint, or bone. When they rupture into bone, they can cause bone marrow edema that may mimic tumor or infection. If calcium hydroxyapatite is ruptured into a joint, it may cause joint destruction. \n\nResolution can occur with NSAIDs, ultrasound, joint injections, or spontaneously.", "ACR Code": "4.3", "Category": "Inflammatory, non-infectious", "Keywords": "Calcific tendonitishydroxyapatite deposition diseasetendon", "Reference": "Flemming DJ, Murphy MD, Shekita KM, Temple HT, Jelinek JJ, Kransdorf MJ. Osseous Involvement in Calcific Tendinitis: A Retropective Review of 50 Cases. AJR 2003; 181:965-972. \nBui-Mansfield LT, Moak M. Magnetic Resonance Appearance of Bone Marrow Edema Associated With Hydroxyapatite Deposition Disease Without Cortical Erosion. J Comput Assist Tomogr. 2005;29:103-107." } }, { "U_id": "MPX2097", "TAC": [], "MRI": [ "MPX2097_synpic19228", "MPX2097_synpic19229", "MPX2097_synpic19230", "MPX2097_synpic19231" ], "Case": { "Title": "1. Mid-substance anterior cruciate ligament tear.\r\n2. Lateral capsular avulsion consistent with Segond fracture.\r\n3. Partial thickness tear of medial collateral ligament.", "History": "47 y/o female status/post-skiing accident in which the patient\u2019s right knee was clipped by a snowboarder while her leg was planted and internally rotated.", "Exam": "Tenderness and swelling of the right knee, + Lachman/anterior drawer, + valgus stress test. No laboratory test results were available.", "Findings": "1. A-P radiograph of the knee taken at referring facility shows a Segond fracture.\n2.\tFSE proton density with fat saturation sagittal oblique MR image shows a mid-substance anterior cruciate ligament tear with increased obliquity of the ACL and a joint effusion. Edema of posterior tibial plateau correlative with the Segond fracture is also seen.\n3. More lateral FSE proton density with fat saturation sagittal oblique MR image shows both the high-signal-intensity edema of the Segond fracture and edema of the lateral femoral condyle, injuries seen with ACL tear.\n4.\tT1-weighted coronal MR image shows indistinctness of the medial collateral ligament at the joint line and low-signal- intensity edema of the lateral tibial plateau and defect of the Segond fracture.\n5.\tFSE T2-weighted with fat saturation coronal MR image shows the increased signal intensity within the medial collateral ligament consistent with a partial thickness tear. The Segond fracture is seen as a lateral capsule avulsion with a focal osseous deficit at the lateral proximal tibia. Associated with this is high-signal-intensity edema/contusion of the lateral tibial plateau and lateral femoral condyle.", "Differential Diagnosis": "Combined findings are characteristic for ACL, MCL tears and Segond fracture", "Case Diagnosis": "1. Mid-substance anterior cruciate ligament tear.\n2. Lateral capsular avulsion consistent with Segond fracture.\n3. Partial thickness tear of medial collateral ligament.", "Treatment & Follow Up": "Surgical repair of ACL with patellar tendon autograft followed by rehabilitation stretching and exercise." }, "Topic": { "Title": "1. Mid-substance ACL tear.\r\n2. Lateral capsular avulsion consistent with Segond fracture", "Disease Discussion": "A Segond fracture is a cortical avulsion of the tibia at the site of insertion of the lateral capsular ligament. This fracture results from excessive internal rotation and varus stress of the knee. Segond fractures are frequently associated with other internal knee derangements including ACL tear (75-100%), meniscal tears - particularly medial meniscus (66-75%), and other avulsion fractures of the fibular head or intercondylar eminence. Therefore, a patient with a Segond fracture, which is usually best seen on A/P radiographs, should be further evaluated by MRI for anterior cruciate ligament and other associated bone, ligamentous, and meniscal injuries. Sagittal T2W MRI with fat saturation is 95% sensitive and 98% specific for showing ACL tears. Treatment for Segond fracture is generally conservative for non-displaced/non-inverted fractures. Treatment for ACL tear is surgical for the athletic individual who wishes to return to his or her level of activity. Best results are usually achieved with a patellar tendon autograft.", "ACR Code": "4.4", "Category": "Trauma", "Keywords": "anterior cruciate ligamentavulsionmedial collateral ligament", "Reference": "1. Hess T, Rupp S, Hopf T, Gleitz M, Leibler J. Lateral tibial avulsion fracture and disruptions to the anterior cruciate ligament. A clinical study of their incidence and correlation. Orthopadische Universitatsklinik Homburg/Saar, Germany. Clin Orthop 1994; 303:193-197.\u00b7\t\n\n2. Kaplan PA, Musculoskeletal MRI, 1st ed. W.B. Saunders: Philadelphia, P. 376-378.\t\n\n3. Murphy BJ, Smith RL, Uribe JW, et al. Bone signal abnormalities in the posterolateral tibia and lateral femoral condyle in complete tears of the anterior cruciate ligament: a specific sign? Radiology. 1992 Jan:182:221-4." } }, { "U_id": "MPX2141", "TAC": [], "MRI": [ "MPX2141_synpic24031", "MPX2141_synpic24032" ], "Case": { "Title": "Epidural Lipomatosis", "History": "76 y.o. man presents with back pain and hyperreflexia in the lower extremities. MRI of brain showed no focal abnormalities.", "Exam": "+3 hyperreflexia of the lower extremities", "Findings": "MRI of the spine demonstrates proliferation of the dorsal epidural fat associated with complete effacement of the dorsal sub arachnoid space from the T3 - T9 levels which results in moderate central canal stenosis mild ventral cord flattening at the T6-7 level. There is also multilevel disk disease.", "Differential Diagnosis": "\u2022 epidural lipomatosis\n\u2022 epidural spread of liposarcoma\n\u2022 extradural lipoma", "Case Diagnosis": "Epidural Lipomatosis", "Diagnosis By": "MRI imaging", "Treatment & Follow Up": "Patient is currently being treated conservatively with pain meds as needed.", "Discussion": "The cause for this specific case of epidural lipomatosis is currently unknown. This man is not obease nor does he currently have a diagnosed endocrinopathy. Additionally, he does not take steriods for some underlying condition." }, "Topic": { "Title": "Epidural Lipomatosis", "Disease Discussion": "Epidural spinal lipomatosis is a rare disease occurring more often in men than in women that usually presents with peripheral neurologic deficits and clinical features not unlike disc disease. There is an increase in unencapsulated fat tissue within the epidural space of the spinal canal which subsequently leads to effacement of the sub arachnoid space, cord compression, and eventual cord atrophy. \n\nThe pathogenesis of this disorder ranges from excessive steroid use to frank obesity. This disease has been observed in people with Cushing\u2019s disease, hypothyroidism, and pituitary prolactinomas. A number of cases have been completely idiopathic. Most reported cases were associated with moderate to high steroid use. Thoracic involvement is most common followed by lumbar involvement next. No cases of cervical involvement have ever been reported.\n\nMR imaging has replaced CT as the study of choice for diagnosis of this disease. Classically there is bright fat signal on T1 weighted sequences where dark CSF signal is expected. Intermediate signal consistent with fat is seen on T2 weighted images were high CSF signal is expected. Fat suppression and gadolinium is helpful but not entirely necessary. \n\nTreatment options include surgical laminectomy to decompress the cord in cases of extreme compression. If steroids are implicated, reduction of medication has shown benefit. Finally, weight loss through increased physical activity has been successful in those capable.", "ACR Code": "3.3", "Category": "Hyperplasia", "Keywords": "epiduralspinallipomatosis", "Reference": "Fasset D and Schmidt M. Spinal epidural lipomatosis: a review of its causes and recommendations for treatment. Neurosurgery Focus 16(4): 1-3, 2004.\n\nWalchi B and Benini A. Spinal epidural lipomatosis. Swiss Med Weekly 131: 359, 2001.\n\nDar S. and Daoud S. Epidural lipomatosis Causing Spinal Cord Compression. NEJM 349: 14, 2003. \n\nPiefro L, Carlo D. et al. Cauda Equina Syndrome Secondary to Idiopathic Spinal Epidural Lipomatosis. Spine. 26(3): 307-309, 2001." } }, { "U_id": "MPX2142", "TAC": [], "MRI": [ "MPX2142_synpic20378", "MPX2142_synpic20379", "MPX2142_synpic20380", "MPX2142_synpic20381" ], "Case": { "Title": "Meningioma of planum sphenoidale", "History": "39 year-old woman with several month history of bilateral hemianopsia, worse in the morning", "Exam": "several month history of bilateral hemianopsia", "Findings": "Large cicrumscribed midline mass overlying the planum sphenoidale causing \"cortical buckling\" of adjacent brain parenchyma. Postcontrast images demonstrate enhancement of the periperipheral portion of the tumor, with a central non-enhancing region.", "Differential Diagnosis": "metastasis\nglioma\nlymphoma\nmeningioma", "Case Diagnosis": "Meningioma of planum sphenoidale", "Diagnosis By": "surgical resection" }, "Topic": { "Title": "Meningioma", "Disease Discussion": "Epidemiology and Location\nMeningiomas comprise approximately 20% of adult intracranial tumors, have a female predominance, and occur most often during middle and older ages. They may be found in intracranial and intraspinal compartments. In the head, meningiomas are most commonly located in frontal, parasagittal, and parietal convexities (50% of cases). Less than 10% of tumors are infratentorial; multiple meningiomas occur less than 10% of the time. Clinical presentation is varied, depending on particular structures compressed by the mass. Headache and visual changes are frequently reported. A large number of patients with meningiomas are asymptomatic.\n\nOrigins, Growth, and Histology\nThe majority of meningiomas are histologically benign tumors, arising from the cap cells of the arachnoid layer. In many cases, serial imaging studies have revealed a cessation of growth after the time of initial tumor detection. These tumors project inward from the dura, and can cause clinically significant effects due to compression of surrounding neurological structures. A variety of classification systems based on cytology and histopathology are used with meningiomas. While the overwhelming majority of meningiomas are histologically benign, the malignant type may result in rapid, widespread infiltration with small (microscopic) \"finger\" projections into adjacent cortex. In patients with malignant meningiomas, marked deficits in physical and mental status may culminate in death.\n\nRadiological Findings\nPlain films may reveal hyperostosis, erosion, or calcification adjacent to tumor site. Noncontrast CT's of meningiomas often reveal sharply demarcated, rounded, homogenous masses with slightly increased density when compared to surrounding cortex. Up to 10% of meningiomas may appear isodense with respect to surrounding brain. CT may reveal focal cerebral atrophy, edema, or widening of subarachnoid spaces, direct effects of tumor compression of surrounding structures. Contrast enhanced CT most often reveals homogenous enhancement in approximately 85% of cases.\n\nOn MRI, T1 images are often hypo- or isointense; T2 images often reveal isointense or slightly hyperintense masses. Gadolinium increases signal intensity of meningiomas. A \"dural tail\" consisting of tissue tapering into the dura may be appreciated. Imaging studies may reveal extension of mass into cortical structures, or invasion of the calvarium. Angiography often reveals a homogenous, hypervascular pattern.\n\n\nTreatment Options\nA variety of clinical and experimental treatment options exist, including surgery, radiotherapy, stereotactic radiosurgery, brachytherapy, chemotherapy, and hormonal therapy. Resection is the most widely utilized treatment option, although advanced age, concern about loss of neurological function due to surgery, advanced age, and being a poor surgical candidate preclude some from surgical options. Tumor embolization may be employed 3-5 days prior to surgery in an attempt to decrease blood supply to the meningioma. Recurrence of tumor is a possibility after resection. Complete removal of initial tumor and all affected bone results in recurrence rates of less than 10%.\n\nRadiotherapy is often employed during the presurgical period. Likewise radiotherapy after incomplete resection of a meningioma may be of considerable benefit to patients. Stereotactic radiosurgery with a \"gamma knife\" has shown decrease in tumor size in approximately 50% of cases. Since this technology is relatively new, long term outcome of gamma knife therapy is not known. Brachytherapy with iodine-125 has been described in the literature; long term outcomes have yet to be determined. Medical treatment options include recommendations of anticonvulsant prophylaxis in patients with supratentorial masses; corticosteroids to reduce brain swelling may also be warranted. The use of traditional antineoplastic agents in treating meningiomas has not been met with great success. Hormonal manipulation may have a beneficial effect on stopping tumor growth; research this area continues.", "ACR Code": "1.3", "Category": "Neoplasm, non-glial", "Reference": "Akeyson et al. Management of benign and aggressive intracranial meningiomas. Oncology 1996. 10 (5): 747-759.\n\nBraunstein et al. Meningiomas: the decision not to operate. Neurology 1997. 48 (5). \n\nGo et al. The natural history of asymptomatic meningiomas\u2026 Neurology 1998. 51 (6).\n\nHaaga, John et al. Computed Tomography and Magnetic Resonance Imaging of the Whole Body. Vol. 1 Mosby. New York. 1994. pp.198-202." } }, { "U_id": "MPX2139", "TAC": [], "MRI": [ "MPX2139_synpic29035", "MPX2139_synpic29036", "MPX2139_synpic29037", "MPX2139_synpic29038" ], "Case": { "Title": "Myxopapillary ependymoma.", "History": "19 year-old male with a six-month history of back pain and right leg weakness", "Exam": "N/A", "Findings": "In the spinal canal, from approximately the mid body of T11 through the sacrum, is a large expansile intradural mass which is isointense to the cord on T1, hyperintense to the cord on T2 and avidly enhances with gadolinium albeit eterogeneously. Marked scalloping of the posterior vertebral bodies is noted most marked in the sacrum. \n\n\tThis mass in the lumbar region extends into the neural foramina at all levels and expands the neural foramina at the lower segments with extension out of the right neural foramina at L5-S1. \n\tAt the level of L4, there is a focal T2 bright lesion which may represent a small fatty element or small region of hemorrhage.", "Differential Diagnosis": "Myxopapillary ependymoma\nLarge nerve sheath tumor\nChordoma\nGaint cell tumor\nAneurysmal bone cyst", "Case Diagnosis": "Myxopapillary ependymoma.", "Diagnosis By": "Imaging characteristics and location - confirmed by pathology", "Treatment & Follow Up": "Surgical resection and post operative radiation planned.", "Discussion": "Please see factoid." }, "Topic": { "Title": "Myxopapillary ependymoma.", "Disease Discussion": "Spinal ependymomas are the most common spinal cord tumor overall. They arise from ependymal cells lining the central canal or its remnants and from the cells in the filum terminale. Of these tumors, there are two subsets: intramedullary ependymomas (cellular ependymomas), and ependymomas occurring nearly exclusively in the conus medullaris and filum terminale (myxopapillary ependymomas). \nMyxopapillary ependymomas represent 10-15% of all ependymomas, and account for 90% of the primary tumors in the filum terminale and cauda equina. These tumors are fleshy, sausage-shaped, reddish to purple in color and moderately vascular on gross examination. Myxopapillary ependymomas tend to grow slowly and to large sizes (often spanning 2-4 vertebral segments), often expanding adjacent bone of the lumbosacral canal and neural foramina. They commonly hemorrhage which can lead to nonaneurysmal subarachnoid hemorrhage, and superficial siderosis, as well as complex internal signal characteristics and calcification. \nComputed tomography of myxopapillary ependymomas typically demonstrates an isodense intradural mass, with possible bony expansion, and strong, uniform contrast enhancement. Magnetic resonance imaging of these tumors demonstrates an intradural mass that is typically isointense to the spinal cord on T1-weighted images, hyperintense to the spinal cord on T2-weighted sequences, and demonstrated strong homogenous enhancement following contrast administration. Myxopapillary ependymomas with a hemorrhagic component may demonstrate heterogeneity on T1-weighted sequences, and a low signal-intensity hemosiderin rim on T2-weighted sequences.\nClinically myxopapillary ependymomas most often present with low back, leg or sacral pain. Leg weakness and sphincter dysfunction are only seen in 20-25% of patients. Due to their indolent growth, delay in diagnosis is common with these tumors, with an average of 2.4 years of symptoms before a correct diagnosis is established. Myxopapillary ependymomas tend to occur in males more often than females (2:1), with a peak age of diagnosis within the 3rd to 4th decades of life. Complete surgical resection is generally curative, although local recurrence is possible if resection is incomplete. Adjuvant radiation therapy is used for multifocal lesions. Certain aggressive sacral and presacral tumors may spread locally to lymph nodes and rarely to distant sites (e.g. lungs and bone).", "ACR Code": "3.3", "Category": "Neoplasm, malignant (NOS)", "Keywords": "EpendymomaFilum terminale massAstorcytoma", "Reference": "Wiestler OD et al: Myxopapillary ependymoma. In Kleihues P, Cavenee WK (eds): Tumors of the Central Nervous System, 78-9. IARC Press, 2000.\nWippold FJ II et al: MR imaging of myxopapillary ependymoma, Am J Roentgenol 165: 1263-7, 1995.\nOsbourne AG: Diagnostic Neuroradiology. Mosby, 1994." } }, { "U_id": "MPX2146", "TAC": [], "MRI": [ "MPX2146_synpic24431", "MPX2146_synpic24432" ], "Case": { "Title": "Chiari II Malformation", "History": "26 y.o. man with history of previous myelomeningocele repair. MRI requested to reassess anatomy.", "Exam": "Non-contributory.", "Findings": "Sagittal T1 MRI of the brain demonstrates multiple typical findings of an Arnold Chiari II malformation, including cerebellar tonsillar herniation, dysgensis of the corpus callosum, a beaked tectum, towering cerebellum, small posterior fossa, and hyperplastic massa intermedia.\n\nAxial FLAIR MRI demonstrates tonsillar herniation.", "Differential Diagnosis": "Chiari II malformation.", "Case Diagnosis": "Chiari II Malformation", "Treatment & Follow Up": "The patient was already status-post VP shunting for hydrocephalus and myelomeningocele repair." }, "Topic": { "Title": "Chiari II Malformation", "Disease Discussion": "Clinical Presentation:\nChiari II malformations occur in 0.02% of births and affects females twice the rate of incidence. The malformation is caused by the incomplete closing of the fetal neural tube, which allows CSF to leak through the dehiscent tube. Therefore, Chiari II is always associated with myelomeningocele.\nPathology/Imaging:\nThe malformation affects the skull, dura, brain, spine, and spinal cord. The skull and dura abnormalities include a lacunar skull, small posterior fossa, low-lying transverse sinuses, fenestrated falx, heart-shaped cerebellum, gaping foramen magnum, and concave clivus. Typically, the cerebellar tonsils, vermis, fourth ventricle, and brain stem are herniated through the foramen magnum. Abnormalities with the brain include an inferiorly displaced vermis and choroid plexus, tectal beaking, \"creeping\" cerebellum, \"towering\" vermis, callosal dysgenesis, medullary kink, and gyral anomalies including the stenogyria and interdigitating gyri. Hydrocephalus is common along with an elongated fourth ventricle, a large massa intermedia in the third ventricle, and enlarged occipital horns of the lateral ventricles. Spinal cord anomalies include myelomeningocele, syringohydromyelia, and diastematomyelia.\nTreatment:\nShunting to treat hydrocephalus or surgical closure of neural tube defect.", "ACR Code": "1.-1", "Category": "Congenital, malformation" } }, { "U_id": "MPX2185", "TAC": [], "MRI": [ "MPX2185_synpic16672" ], "Case": { "Title": "Anaplastic astrocytoma - WHO Grade 3", "History": "28 yo c/o right leg weakness. He denies headaches, nausea, vomiting, or vision changes. Currently complains of right leg weakness, slight sensory decrease and, and possible difficulty talking.", "Exam": "vitals: HR 67, BP 139/82, RR 16, Temp 97.6 140| 104| 13 <118 15.1>15.9/47<240gen: wn, wd, alert and oriented x3 3.8| 25 | 0.9 heent: normocephalic, supple w/o masses, perlapulm: equal breath sounds, no rales, rhonchi, wheezes Mg 1.9, PT 14.7, PTT 28heart: RRR, no murmurs, rubs, or gallopsabd: soft, nt, nd, normal BS, no organomegalyneuro: AAOx3, CN 2-12 intact, motor: R 4/5 in delt, biceps, triceps, quad; 2/5 in extensor hallucis longus, Achilles, and gluteus L 5/5 throughout sensory: slight decrease in light touch in right lower extremity throughout reflex: 3+ R Achilles, R patella, 5 beat clonus, up toe 2+ L Achilles, L patella, no clonus, down toe cerebellar: intact with finger-to-noseext: right shin with multiple abrasions, no clubbing, cyanosis, or edema; good pulses throughout", "Findings": "MRI w/ contrast: Within the L cerebral hemisphere, in the frontoparietal region, there is marked increased white matter signal throughout, with a mild amount of midline shift of the falx. Posteriorly in this region there is a cystic lesion that does not enhance. The largest single cyst measures approximately 6mm, with the overall largest size of the cluster of cysts measuring 10mm. There is also an extensive amount of edema, and at the area of midline shift of the falx, there is some increased white matter signal in the right hemisphere which may represent tumoral extension across the corpus colosum. There is some edema and effacement of the cerebral sulci on the left at the level of the lesion. The remaining soft tissues are unremarkable.", "Differential Diagnosis": "High-grade astrocytoma, oligodendroglial tumor, mixed glioma, ependymal tumor, infarction, or metastasis", "Case Diagnosis": "Anaplastic astrocytoma - WHO Grade 3", "Treatment & Follow Up": "Management of high-grade astrocytomas is a multi-step process, including treatment with glucocorticoids, surgery, radiation therapy, and chemotherapy. Administration of dexamethasone is usually initiated at the time of diagnosis and tapered to the lowest tolerated dose when radiation therapy is completed. Due to the invasive nature of high-grade astrocytomas, complete surgical resection is not possible. Therefore, surgery is only indicated to obtain tissue for pathologic diagnosis and control mass effects. In patients younger than 65, the extent of tumor resection correlates with survival, so accessible tumors are resected aggressively in this population if the patient is otherwise healthy. Following surgery, radiation therapy is administered. Focal radiation has been shown to be as effective and less toxic in this patient population, and is administered to the tumor mass, plus a 3-4-cm margin. A total dose of 5000 to 7000 cGy is administered in 25-35 equal fractions, 5 days per week. Finally, chemotherapy is initiated. This is only marginally effective, but is usually added as an adjuvant, following surgery and radiation therapy. The most effective available agents are nitrosoureas, such as carmustine (BCNU) and lomustine (CCNU).", "Discussion": "CT showed left frontal-parietal lesion w/ edema and minimal shift. Patient was transferred to NNMC for further w/u." }, "Topic": { "Title": "Anaplastic Astrocytoma, WHO Grade 3", "Disease Discussion": "Astrocytic tumors are the most common primary intracranial neoplasms. The WHO has devised a four-tiered grading system. Grade I and II are considered low-grade astrocytomas and are more common in children. The majority of astrocytomas occurring in adults are high-grade, grade III and IV. They are usually supratentorial and have poorly defined margins. Tumor cells migrate away from the main tumor mass and invade adjacent tissue, often traveling along white matter pathways. Therefore, imaging studies do not usually reveal the full extent of the tumor.\n\nAlthough all of these tumors are eventually fatal, longer survival has been associated with younger age, better clinical performance status, and greater extent of surgical resection. Mean survival for high grade glioma patients younger than 65, treated aggressively, is 11 to 13 months.", "ACR Code": "1.3", "Category": "Neoplasm, glial", "Keywords": "anaplastic astrocytoma", "Reference": "Braunwald, et al., Harrison\u2019s Principles of Internal Medicine, pp 2444-2445, McGraw-Hill, (Philadelphia, 1997)." } }, { "U_id": "MPX2199", "TAC": [], "MRI": [ "MPX2199_synpic15700" ], "Case": { "Title": "Takayasu Arteritis", "History": "55 year old Asian female with history of polymyalgia rheumatica, presenting with pulseless upper extremities.", "Exam": "Diffusely absent or very weak bilateral upper extremity pulses", "Findings": "Conventional and MR angiography showed multifocal stenosis of the great vessels and branch vessels.", "Differential Diagnosis": "atherosclerotic disease, giant cell arteritis, fibromuscular dysplasia, idiopathic carotid dissection", "Case Diagnosis": "Takayasu Arteritis", "Treatment & Follow Up": "N/A", "Discussion": "SEE FACTOID" }, "Topic": { "Title": "Takayasu Arteritis", "Disease Discussion": "Synonyms: pulseless disease, aortitis syndrome, aortic arch syndrome\n\nChronic inflammatory arteriopathy; typically disease of young Asian women\n\nAge-15-41 yrs; m:f 1:8\n\nUnknown etiology characterized by stenosis, occlusion, dilatation, and/or aneurysm formation of aorta, its major branches, pulmonary arteries\n\nClassified according to extent: Type I - involvement of aortic arch and branches; Type II - involvement of descending thoracic and abdominal aorta and branches; Type III - combination of Types I and II. Type IV-pulmonary arteries\n\nHistopathologically, characterized by inflammatory changes with marked tissue destruction and connective tissue proliferation initiated at jxn of media and adventitia or outer layer media; onion-skin type fibrosis in vasa vasorum, involvement limited to elastic arteries that possess vasa vasorum (aorta, proximal branches, pulmonary arteries) \n\nCXR: widened supracardiac shadow > 3 cm; irregular contour of aorta and/or great vessels and aortic calcification (15%)-arch and descending aorta; focal decrease in pulmonary vascularity\n\nAngiography/Aortography: stenosis, occlusion, dilatation, skip lesions, and/or aneurysm formation of aorta, its major branches, pulmonary arteries; collateralization; ectasia 10-15%\n\nMRA: pulmonary arterial lesions specific; 19% show dilation of pulmonary trunk, 66% show \u201cpruned tree\u201d appearance of pulmonary arteries\n\nDDX: atherosclerotic disease, giant cell arteritis, fibromuscular dysplasia\n\nComplications: ischemic injury, CVA, heart failure due to aortic regurgitation\n\nTX: steroids; PTA definitive tx for pts with htn due to renal artery stenosis, but not performed in pts with chronic active arterial inflammation or elevated ESR or C-reactive protein because of high rate of restenosis; PTA recently employed in variety of vessels to tx ischemic symptoms with relatively good success", "ACR Code": "562.625", "Category": "Inflammatory, NOS", "Keywords": "takayasupulseless diseasearteritis", "Reference": "1. Neuroradiology Learning File - \u00a9 ACR (ACR Learning File\u00ae)\n2. Weissleder, Ralph; Wittenberg, Jack; Harisinghani, Mukesh G. Primer of Diagnostic Imaging. Philadelphia: Mosby International, 2002.\n3. Dahnert, Wolfgang. Radiology Review Manual. Baltimore: Williams and Wilkins, 1996." } }, { "U_id": "MPX2193", "TAC": [], "MRI": [ "MPX2193_synpic42191", "MPX2193_synpic42192", "MPX2193_synpic42193", "MPX2193_synpic42194", "MPX2193_synpic42195", "MPX2193_synpic42196", "MPX2193_synpic42197" ], "Case": { "Title": "Tendon Xanthomas in Familial Hypercholesterolemia", "History": "51 yo male with soft-tissue ankle mass.", "Findings": "AP and lateral radiographs of the right ankle, reveal a soft-tissue mass without internal calcifications overlying the lateral malleolus. Additionally, there is fusiform thickening of the Achilles Tendon.\n\nMRI of the Right Ankle: There is a multilobulated mass, measuring 2.6 x 2.5 x 1.4 cm at the anterior aspect of the fibula, that is isointense on T1, hypointense on T2, and isointense to the Achilles tendon on T2 weighted sequences. There is no associated bony erosion. Additionally, there is marked thickening of the Achilles tendon without hyperintense signal to suggest tear. Also noted is convex curvature to the normally flat or concave anterior aspect of Achilles tendon.\n\nMRI of the Left Ankle: There is marked thickening of the Achilles tendon without hyperintense signal to suggest tear. Also noted is convex curvature to the normally flat or concave anterior aspect of Achilles tendon. Thickening of the tendinous portion of the medial plantar fascia is also noted.", "Differential Diagnosis": "Achilles Tendonitis\nPartial Achilles tendon tear\nGout\nNeoplasms of the Achilles tendon.\nAchilles\u2019-Tendon Xanthoma", "Case Diagnosis": "Tendon Xanthomas in Familial Hypercholesterolemia", "Diagnosis By": "Findings of bilateral symmetric diffuse thickening of the Achilles tendon without abnormal T2 signal, coupled with a similar focal mass with similar signal characteristics to the Achilles tendons, located adjacent to the right fibula, strongly suggests these are xanthomas related to familial hypercholesterolemia.", "Treatment & Follow Up": "The patient underwent surgery for removal of the mass overlying his lateral malleolus, which was symptomatic in terms of allowing his shoe to properly fit. At surgery, the mass was tightly adherent to the periosteum. Pathology confirmed a xanthoma.", "Discussion": "Further history obtained reveals the patient has a past medical history significant for hypercholesterolemia." }, "Topic": { "Title": "Achilles\u2019-Tendon Xanthoma in Familial Hypercholesterolemia", "Disease Discussion": "Achilles\u2019-Tendon Xanthoma in Familial Hypercholesterolemia\n\nDiscussion:\n\nAchilles tendon xanthomas are painless nodular masses, occurring most frequently in the distal third of the tendon in a bilateral symmetric distribution, and are strongly associated with heterozygous familial hypercholesterolemia. Interestingly, Achilles tendon xanthomas occur in less than 50% of patients with familial hypercholesterolemia, and may be imaged using US or MRI. Other common locations of tendon xanthomas involve the finger extensors on the dorsal aspect of the hands, as well as the plantar fascia, and less commonly the extensor tendons of the toes.\n\nOn radiographs, xanthomas appear as soft-tissue masses without calcification. Typical sonographic findings include an AP thickness greater than 7 mm in men, and 6 mm in women, as well as the presence of single or multiple hypoechoic foci, which alter the normal appearance of the tendon. \n\nMRI also demonstrates thickening of the AP diameter, and a speckled appearance to the tendon on both the axial and sagittal views may be noted, but this is not always visualized. The infiltration of tendon by histiocytes, is responsible for this pattern. Additionally, the normal concave or flat anterior surface of the Achilles tendon becomes convex in appearance. MRI is useful in excluding other causes of focal masses in the Achilles tendon such as tendinopathy, tear, infection, gout, or neoplasm.\n\nTendon xanthomas can decrease in size with appropriate treatment of the serum cholesterol levels.", "ACR Code": "4.6", "Category": "Systemic, Generalized", "Keywords": "XanthomaAchilles\u2019-Tendon XanthomaAchilles\u2019-Tendon Xanthoma in Familial Hypercholesterolemia", "Reference": "Njuguna,Njogu. Achilles tendon xanthomas, primary familial hypercholesterolemia. ACR Case in Point [database online]. Reston, VA: American College of Radiology January 18, 2008 Available at: http://caseinpoint.acr.org/ Accessed April 27, 2008.\nKaplan et al. Musculoskeletal MRI. Saunders, Philadelphia, PA. 2001.\nNarvaez et al. RadioGraphics 2000; 20:333-352.\nVan den Bosch et al. N Engl J Med. 1998;338:1591." } }, { "U_id": "MPX2204", "TAC": [], "MRI": [ "MPX2204_synpic23796", "MPX2204_synpic23797", "MPX2204_synpic23798", "MPX2204_synpic23799", "MPX2204_synpic23800", "MPX2204_synpic23801" ], "Case": { "Title": "Quadriceps tendon rupture, Medial retinacular tear", "History": "48 y/o male presents with pain in anterior aspect of distal right thigh, superior to right knee and increased pain in right knee. The patient has had knee pain for two years that limited his ability to run.", "Exam": "Physical Exam and Laboratory: \nPhysical examination shows a large deep palpable defect in the soft tissues in the anterior aspect of right thigh, superior to the patella. The patient was unable to extend his right leg. No laboratory data are available.", "Findings": "Lateral radiograph of the knee shows patella baja.\n\nProton-density and gradient-recalled echo sagittal oblique MR images show a complete tear of the quadriceps tendon with high-signal-intensity hemorrhage/edema filling the gap. Separation of the tibial tuberosity without associated edema suggest old Osgood-Schlatter\u2019s disease.\n\nT2-weighted fat sat axial images from the level of the distal femoral diaphysis to the femoral condyle show the quadriceps tendon tear with high signal intensity, the tear of the medial retinaculum at its attachment site to the patella with medial and posterior displacement of torn fibers and extensive high-signal-intensity edema/hemorrhage in the soft tissues particularly laterally. A post traumatic chondral defect with subchondral edema was also seen within the medial patellar facet (image not included).", "Differential Diagnosis": "Quadriceps tendon rupture\nMedial retinacular tear", "Case Diagnosis": "Quadriceps tendon rupture, Medial retinacular tear", "Diagnosis By": "At surgery.", "Treatment & Follow Up": "When identified, the quadriceps rupture should be treated expeditiously. When the injury is complete as in this case, direct end to end repair is done with immobilization of the knee in extension. The repair shows the best results when done within two months of the injury. With delay in treatment, proximal migration and scarring of the quadriceps occurs and surgery more difficult, sometimes requiring the quadriceps lengthening procedures, a muscle or tendon transplant or both.", "Discussion": "The mechanism of injury that causes quadriceps rupture is trauma, although this injury can also occur spontaneously. In the setting of trauma, it can either be direct or indirect. Direct trauma results from a direct blow to the quadriceps muscle, causing it to tear. An indirect injury is caused by a rapid and severe contraction of the quadriceps while the knee is in flexion. Both of these mechanisms can cause complete or partial tears. Spontaneous injury usually occurs in the elderly and is often associated with chronic diseases (although it can happen in healthy individuals) such as diabetes mellitus, renal failure, systemic lupus erythematosus, rheumatoid arthritis, or gout. It has also been associated with corticosteroid therapy. Most tears will occur at the quadriceps enthesis and distal quadriceps tendon near its insertion side into the patella. Medial and lateral retinacular tears occur when there is valgus or varus angulation while the quadriceps is contracted.\n\nOn physical exam a partial tear can be difficult to discern. The findings will include decreased extension strength that is often only evident only when done against resistance. Complete tears are much easier to observe. Examination will illicit inability to extend the knee, soft tissue hematoma, or a palpable/visible gap in the soft tissue superior to the patella. Studies that are done to support the physical findings should include radiographs followed by sonography when patellar subluxation is not present, and magnetic resonance imaging (MRI). \n\nOn routine radiograph, findings that are associated with a complete tear are soft tissue swelling, inferior positioning of the patella (also known as patella baja), distortion of the soft tissue planes above the patella, and avulsed patellar fragments. If there is no other injury suspected other than the quadriceps tendon rupture and no subluxation of the patella, sonography, sonography is a useful and inexpensive test to confirm the radiological findings. However, sonography does not allow an adequate evaluation of the osseous and cartilaginous structures and other ligaments such as retinacula and collateral ligaments. When other abnormalities are suspected. MRI should be performed after the plain radiographs. On MR images, a complete tear will appear as disruption of the low-signal-intensity tendon with high-signal-intensity hematoma/ post-traumatic inflammation filling the gap of the torn tendon. MRI also confirms the patella baja. The tear should be evaluated in three planes for its full extent. MRI also demonstrates associated injuries such as medial retinacular tear, with the disruption of the retinaculum usually at its patellar insertion and an infolding of the retinaculum medially and even posterior to the tendon. Hematomas of the soft tissue and patellar avulsions and contusions, and osteochondral trauma can also be shown.\n\nWhen identified, the quadriceps rupture should be treated expeditiously. When the injury is complete as in this case, direct end to end repair is done with immobilization of the knee in extension. The repair shows the best results when done within two months of the injury. With delay in treatment, proximal migration and scarring of the quadriceps occurs and surgery more difficult, sometimes requiring the quadriceps lengthening procedures, a muscle or tendon transplant or both. \n1. Skinner, H. Current Diagnosis and Treatment in Orthopedics (3rd edition). McGraw-Hill, 2003 STAT!Ref Ch. 4 Knee tendon injury\n2. Stoller, D. Magnetic Resonance Imaging in Orthopaedics and Sports Medicine, J. B. Lippincott, 1993 pp. 306, 310f\n3. El-Dieb A. et al, Pathologic conditions of the ligaments and tendons of the knee. Rad Clin North Am 2002; 40:1061-79\n4. Resnick D. Diagnosis of Bone and Joint Disorders (3rd edition,) W. B. Saunders, Philadelphia, 1995, pp. 3108-3109\t\n5. Rogers L. Radiology of Skeletal Trauma (2nd edition). Churchill Livingstone, New York., 1992, pp. 1269-1270" }, "Topic": { "Title": "Quadriceps tendon rupture; Medial retinacular tear", "Disease Discussion": "Discussion (include references): The mechanism of injury that causes quadriceps rupture is trauma, although this injury can also occur spontaneously. In the setting of trauma, it can either be direct or indirect. Direct trauma results from a direct blow to the quadriceps muscle, causing it to tear. An indirect injury is caused by a rapid and severe contraction of the quadriceps while the knee is in flexion. Both of these mechanisms can cause complete or partial tears. Spontaneous injury usually occurs in the elderly and is often associated with chronic diseases (although it can happen in healthy individuals) such as diabetes mellitus, renal failure, systemic lupus erythematosus, rheumatoid arthritis, or gout. It has also been associated with corticosteroid therapy. Most tears will occur at the quadriceps enthesis and distal quadriceps tendon near its insertion side into the patella. Medial and lateral retinacular tears occur when there is valgus or varus angulation while the quadriceps is contracted.\n\nOn physical exam a partial tear can be difficult to discern. The findings will include decreased extension strength that is often only evident only when done against resistance. Complete tears are much easier to observe. Examination will elicit inability to extend the knee, soft tissue hematoma, or a palpable/visible gap in the soft tissue superior to the patella. Studies that are done to support the physical findings should include radiographs followed by sonography when patellar subluxation is not present, and magnetic resonance imaging (MRI). \n\nOn routine radiograph, findings that are associated with a complete tear are soft tissue swelling, inferior positioning of the patella (also known as patella baja), distortion of the soft tissue planes above the patella, and avulsed patellar fragments. If there is no other injury suspected other than the quadriceps tendon rupture and no subluxation of the patella, sonography, sonography is a useful and inexpensive test to confirm the radiological findings. However, sonography does not allow an adequate evaluation of the osseous and cartilaginous structures and other ligaments such as retinacula and collateral ligaments. When other abnormalities are suspected,. MRI should be performed after the plain radiographs. On MR images, a complete tear will appear as disruption of the low-signal-intensity tendon with high-signal-intensity hematoma/ post-traumatic inflammation filling the gap of the torn tendon. MRI also confirms the patella baja. The tear should be evaluated in three planes for its full extent. MRI also demonstrates associated injuries such as medial retinacular tear, with the disruption of the retinaculum usually at its patellar insertion and an infolding of the retinaculum medially and even posterior to the tendon. Hematomas of the soft tissue and patellar avulsions and contusions, and osteochondral trauma can also be shown.\n\nWhen identified, the quadriceps rupture should be treated expeditiously. When the injury is complete as in this case, direct end to end repair is done with immobilization of the knee in extension. The repair shows the best results when done within two months of the injury. With delay in treatment, proximal migration and scarring of the quadriceps occurs and surgery more difficult, sometimes requiring the quadriceps lengthening procedures, a muscle or tendon transplant or both.", "ACR Code": "4.4", "Category": "Trauma", "Keywords": "Quadriceps tendon rupturequadriceps ruptureMedial retinacular tear", "Reference": "1. Skinner, H. Current Diagnosis and Treatment in Orthopedics (3rd edition). McGraw-Hill, 2003 STAT!Ref Ch. 4 Knee tendon injury\n2. Stoller, D. Magnetic Resonance Imaging in Orthopaedics and Sports Medicine, J. B. Lippincott, 1993 pp. 306, 310f\n3. El-Dieb A. et al, Pathologic conditions of the ligaments and tendons of the knee. Rad Clin North Am 2002; 40:1061-79\n4. Resnick D. Diagnosis of Bone and Joint Disorders (3rd edition,) W. B. Saunders, Philadelphia, 1995, pp. 3108-3109\t\n5. Rogers L. Radiology of Skeletal Trauma (2nd edition). Churchill Livingstone, New York., 1992, pp. 1269-1270" } }, { "U_id": "MPX2218", "TAC": [], "MRI": [ "MPX2218_synpic30796", "MPX2218_synpic30797", "MPX2218_synpic30800", "MPX2218_synpic30801", "MPX2218_synpic30802" ], "Case": { "Title": "Bicuspid Aortic Valve with Aortic Stenosis and Aortic Dilatation.", "History": "38-year-old man with heart murmur on physical exam.", "Exam": "Electrocardiogram (ECG)-gated MR of the chest was performed and included axial (Figure A) and sagittal (Figure B) black blood double inversion recovery fast spin echo (DIR FSE) and axial (Figure C) and sagittal (Figure D) bright blood fast steady state free precession images. Oblique sagittal cine bright blood fast gradient echo images (Figure E, select systolic images) were performed parallel to the long axis of the aortic root. Oblique axial bright blood cine phase contrast images (Figure F, select serial systolic images) through the base of the heart through the aortic valve plane were also performed.", "Findings": "On axial (Figure A) and sagittal (Figure B) black blood DIR FSE images, the patient is noted to have a dilated ascending aorta, which measures approximately 48 mm in diameter. Steady state free precession is a relatively newer MR pulse sequence that provides good homogeneity of the bright blood pool signal and confirms the aortic dilatation noted on black blood images (Figures C and D). On cine bright blood MR using fast gradient echo imaging, a distinctive systolic flow jet (Figure E, arrow) is noted which arises from the posterior aortic valve into the ascending aorta. This moderate to large jet is consistent with moderate to severe aortic stenosis. No diastolic jet to suggest aortic insufficiency was seen (not shown). On cine bright blood phase contrast imaging at the level of the aortic valve, the aortic valve orifice is noted to be lens shaped (Figure F, arrowheads). Contrast-enhanced three-dimensional MRA (Figure G) confirmed the dilated ascending aortic root and absence of an aortic dissection or coarctation.", "Differential Diagnosis": "Ascending Aortic Dilatation:\n1) Atheroscloerosis\n2) Aortic valvular disease (stenosis and/or insufficiency\n3) Collagen vascular disease (e.g. Marfan syndrome)\n4) Mycotic aneurysm\n5) Aortic dissection", "Case Diagnosis": "Bicuspid Aortic Valve with Aortic Stenosis and Aortic Dilatation.", "Diagnosis By": "MRI", "Treatment & Follow Up": "None", "Discussion": "This case has been published:\nCooney JR and HO VB: Bicuspid Aortic Valve\nRadiology Corner Case #3\nMilitary Medicine 2006; 171:iv-v." }, "Topic": { "Title": "Bicuspid aortic valve", "Disease Discussion": "Bicuspid aortic valve (BAV) is a common congenital heart defect occurring in 1-2% of the population, with a male predominance [1]. Patients with BAV are at increased risk for a variety of complications that includes aortic valvular disease, endocarditis, ascending aortic aneurysm and aortic dissection [1-4]. There is also an association of BAV with coarctation of the aorta [5,6]. While this BAV-coarctation relationship is widely known to exist in patients with Turner syndrome, this is also seen in non-syndromic individuals. \n\nThe detection of a bicuspid aortic valve is often incidental, but once found requires routine surveillance for its associated complications. Echocardiography remains the initial study of choice for most patients. However, MRI, capable of functional evaluation using cine bright blood techniques and of aortography using MRA, is well suited for further evaluation of patients with BAV for associated valvular and aortic conditions.\n\nFunctional impairment of the aortic valve\u2014namely aortic stenosis and aortic regurgitation\u2014is the most common complication (in up to 68-85% of patients [1,3]) seen in patients with BAV. Aortic stenosis may manifest as a systolic ejection murmur, best heard in the second right intercostal space. Aortic insufficiency, on the other hand, is characterized by a decrescendo diastolic murmur, best heard at the left sternal border. On echocardiography, of course, the severity of the valvular stenosis or insufficiency and co-existence of a BAV is typically evident. \n\nPatients with BAV also have an increased incidence of aortic disease [7-11]. While it is well known that aortic valvular dysfunction is associated with increased risk for aortic aneurysm, patients with BAV appear to have additional risks for aortic disease. Nistri et al. [12] reported significant aortic root enlargement in healthy patients with normally functioning BAV when compared to healthy subjects with normally functioning tricuspid aortic valves. Similarly, Hahn et al. [2] report significantly larger aortic root sizes in patients with BAV at all grades of valvular dysfunction when compared to subjects with tricuspid aortic valves matched for age, gender and grade of valvular disease. These studies suggest that the predisposition for aortic disease in patients with BAV is due to factors other than, or in addition to, traditional hemodynamic considerations. \n\nDe Sa et al. [8] and others [7,9,11] have reported severe degenerative changes, such as cystic medial necrosis, elastic fragmentation and alterations of smooth muscle orientation, in the media of the ascending aorta of patients with BAV. Moreover, de Sa et al [8] found more severe degenerative changes not only in the media of the ascending aorta but also in the pulmonary arteries of patients with BAV, compared to that of patients with tricuspid aortic valves. These studies suggest that the association of BAV with aortic disease results from a common developmental error and not only hemodynamic forces. \n\nIn patients with aortic dilatation and BAV, the risk for aortic rupture and aortic dissection are considerably higher [13]. The risk for aortic dissection, in particular, has been reported to be increased 5 to 9 fold in patients with BAV [10,14]. For this reason, some surgeons have advocated more aggressive and earlier elective surgical repair in patients with BAV, aortic valvular dysfunction and aortic dilation [13]. \n\nThe clinical presentation of patients with BAV varies and depends on the presence and severity of its associated complications. Often the finding is incidental, such as being found during a routine echocardiogram for evaluation of suspected aortic stenosis or aortic insufficiency. On occasion, it is identified during the evaluation of a dilated aorta as in this case. Alegret et al. [15] reported BAV in 20 percent of their patients with aortic root dilatation. Echocardiography will continue to be the initial study of choice in most instances. However, with the increased use of MRI in the evaluation of aortic pathology, the evaluation of the aortic valve should be considered during an MRI study especially in instances of aortic dilatation or in cases where there is suspicion or known aortic valvular dysfunction. \n\nOn MRI, aortic caliber is best evaluated using ECG-gated black blood pulse sequences (Figures A-D). Note that these images are typically performed during diastole and measurements may not necessarily correlate exactly with echocardiographic measurements. The aortic valve, on the other hand, is best seen using cine bright blood acquisitions, notably steady state free precession (SSFP; also known as TrueFISP, FIESTA and balanced FFE). To evaluate valvular function, cine images should be performed perpendicular to the left ventricular outflow track (Figure E). To evaluate the number of valve leaflets, imaging using cine SSFP (or cine phase contrast, Figure F) images should be performed parallel to the aortic valve plane. The determination of BAV is made by the configuration of blood flow across the actual aortic valve. In patients with BAV, the aortic valve orifice is shaped like a lens (Figure F); in patients with a tricuspid aortic valve, like a triangle. \n\nMRI is well suited for the determination of aortic caliber and valvular pathology, but can also reliably detect aortic dissection [16]. This can be performed using a combination of black and bright blood pulse sequences. However, contrast-enhanced three-dimensional MRA (Figure G) can particularly improve the diagnostic confidence for the diagnosis or exclusion of an intimal tear and or aortic coarctation [17].", "ACR Code": "5.1", "Category": "Anatomy, Normal Variant", "Keywords": "bicuspid aortic valvecardiac MR", "Reference": "1. Roberts WC. The congenitally bicuspid aortic valve: a study of 85 autopsy cases. Am J Cardiol 1970; 26:72-83.\n2. Hahn RT, Roman MJ, Mogtader AH, Devereux RB. Association of aortic dilation with regurgitant, stenotic and functionally normal bicuspid aortic valves. J Am Coll Cardiol 1992; 19(2):283-288.\n3. Fenoglio JJ, McAllister HA, DeCastro CM, Davia JE, Cheitlin MD. Congenital bicuspid aortic valve after age 20. Am J Cardiol 1977; 39:164-169.\n4. Ward C. Clinical significance of the bicuspid aortic valve. Heart 2000; 83:81-85.\n5. Becker AE, Becker MJ, Edwards JE. Anomalies associated with coarctation of aorta: particular reference to infancy. Circulation 1970; 41:1067-1075.\n6. Mazanti L, Cacciari E. Congenital heart disease in patients with Turner\u2019s syndrome. Italian study group for Turner syndrome (ISGTS). J Pediatr 1998; 133:688-692.\n7. Schmid FX, Bielenberg K, Schneider A, Haussler A, Keyser A, Birnhaum D. Ascending aortic aneurysm associated with bicuspid and tricuspid aortic valve: involvement and clinical relevance of smooth muscle cell apoptosis and expression of cell death-initiating proteins. Eur J Cardiothorac Surg 2003; 23(4):537-543.\n8. De Sa M, Moshkovitz Y, Butany J, David TE. Histologic abnormalities of the ascending aorta and pulmonary trunk in patients with bicuspid aortic valve disease: clinical relevance to the Ross procedure. J Thorac Cardiovasc Surg 1999; 118:588-596\n9. Bonderman D, Gharehbaghi-Schnell E, Wollenek G, Maurer G, Baumgartner H, Lang IM. Mechanisms underlying aortic dilatation in congenital aortic valve malformation. Circulation 1999; 99(16):2138-2143.\n10. Roberts CS, Roberts WC. Dissection of the aorta associated with congenital malformation of the aortic valve. J Am Coll Cardiol 1991; 17:712-716.\n11. Edwards WD, Leaf DS, Edwards JE. Dissecting aortic aneurysm associated with congenital bicuspid aortic valve. Circulation 1978; 57:1022-1025.\n12. Nistri S, Sorbo MD, Marin M, Palisi M, Scognamiglio R, Thiene G. Aortic root dilatation in young men with normally functioning bicuspid aortic valves. Heart 1999; 82:19-22.\n13. Ergin MA, Spielvogel D, Apaydin A, Lansman SL, McCullough JN, Galla JD, Griepp RB. Surgical treatment of the dilated ascending aorta: when and how? Ann Thorac Surg 1999; 67:1834-1839.\n14. Larson EW, Edwards WD. Risk factors for aortic dissection: a necropsy study of 161 cases. Am J Cardiol 1884; 53:849-855.\n15. Alegret JM, Duran I, Palaz?n O, Vernis JM, Ameijide A, Rabassa A, Masana L. Prevalence of and predictors of bicuspid aortic valves in patients with dilated aortic roots. Am J Cardiol 2003; 91:619-622.\n16. Nienaber CA, von Kodolitsch Y, Nicolas V, Siglow V, Piepho A, Brockhoff C, Koschyk DH, Spielmann RP. The diagnosis of thoracic aortic dissection by noninvasive imaging procedures. N Engl J Med1993; 328:1-9.\n17. Ho VB, Prince MR. Thoracic MR aortography: Imaging techniques and strategies. Radiographics 1998; 18:287-309." } }, { "U_id": "MPX2225", "TAC": [], "MRI": [ "MPX2225_synpic17072" ], "Case": { "Title": "Osteochondritis Dissecans, juvenile-type", "History": "12y/o female complaining of right medial knee pain for 3 years without a history of trauma", "Exam": "N/A", "Findings": "A/P Radiograph: Area of varied lucency on the lateral aspect of the medial femoral condyle of the right knee; just inferior to this lesion, there is an area of opacity into the knee joint, suggesting chondral or osseous tissue. Both lesions c/w OCD. O/w there is normal mineralization/alignment.MRI (T1W): Area of low signal intensity on the lateral aspect of the medial femoral condyle; surrounding this area within the femur is an area of very low signal intensity c/w fluid; there is also evidence of edema within the lesion, which may suggest an unstable fragment. There is evidence of mild cartilage thinning over the fragment but no tearing. The OCD is therefore nondisplaced.", "Differential Diagnosis": "Findings diagnostic of Osteochondritis Dissecans, likely juvenile-type.", "Case Diagnosis": "Osteochondritis Dissecans, juvenile-type", "Treatment & Follow Up": "A trial of conservative non-operative management is the first choice in a young growing patient with the goal to prevent further damage to the underlying bone and prevent total chondral collapse, which may lead to severe osteoarthritis later in the patient\u2019s life. Management may include activity modification, protected weight-bearing, and/or immobilization of the joint. Surgical options remain for older patients (with less healing potential) or for persistently symptomatic joints in younger patients; the goal being to stimulate healing and bone growth while maintaining the stability of the bone and joint. For intact lesions (typically younger patients), drilling, either retrograde or antegrade, is commonly performed with fairly high success rates. Very painful hinged lesions (flap of chondral tissue) require pegs, screws, or pins for security and provide rapid pain relief. Full-thickness lesions, where both bone and cartilage have eroded, are repaired using arthroscopic drilling, abrasion with a high-speed burr, or microfracturing using a pick. All three techniques for full-thickeness tears recruit marrow elements to stimulate bone growth, but in so doing create a weak area that requires very limited activity for up to 12 months after the surgery." }, "Topic": { "Title": "Osteochondritis Dissecans, juvenile-type", "Disease Discussion": "Osteochondritis Dissecans is of uncertain etiology. Possible causations include persistent microtrauma (or one incident of significant magnitude), ischemia, genetic and endocrine factors, and anomalies of ossification. The leading theory suggests that after repetitive microtrauma to the subchondral bone, focal areas of ischemia and/or alterations in bone growth causes the bone to break down. The overlying articular cartilage may weaken and either cave in forming an empty cavity or tear apart leading to a detached or nearly detached articular fragment within the joint space. Two types of OCD, juvenile and adult, are based primarily on growth potential of the bone. Juvenile OCD (5-15 years old at presentation) typically has a better healing potential and better prognosis; detachment of cartilage is rare in children. Adult OCD (16-50 years old at presentation) has a much higher risk for developing moderate to severe osteoarthritis later in life on the affected joint. The knee (usually the medial femoral condyle) is most affected comprising as high as 85% of all lesions. Other affected joints include the talus, capitellum, and wrist. Males are affected more than females, 3 to 1. Typically patients complain of a gradually increasing pain associated with activity. They may also complain that the knee swells, \u201cgives out,\u201d or locks. Physical exam may reveal poorly localized tenderness on the affected side along with crepitus and/or an effusion. In one-third of cases, the knees present bilaterally; therefore, the opposite knee should also be viewed on radiograph. Radiographic findings are as described above; however, three views (frontal, lateral, and tunnel) are usually required to identify all possible lesions. MRI is necessary not for diagnostic purposes, but to evaluate the cartilage overlying the lesion. Identifying the degree of cartilage damage, if any at all, is necessary for proper management of the disease, as discussed above.", "ACR Code": "4.4", "Category": "Unsure", "Keywords": "Osteochondritis Dissecans", "Reference": "Canale. Campbell\u2019s Operative Orthopedics, 10th ed. Mosby, Inc., 2003: pp. 2305-2310.\n\nOzonoff, M. B. Pediatric Orthopedic Radiology, 2nd ed. W. B. Saunders Co., 1992: pp. 358-363.\n\nPill, S. G. \u201cOsteochondritis Dissecans of the Knee: Experiences at The Children\u2019s Hospital of Philadelphia and a Review of Literature.\u201d University of Pennsylvania Orthopedic Journal. Spring 2001; 14: 25-34." } }, { "U_id": "MPX2234", "TAC": [], "MRI": [ "MPX2234_synpic18505" ], "Case": { "Title": "Chiari I Malformation", "History": "The patient is a 24 year old female who presents with paroxysmal episodes of loss of fine motor control of all of her extremities. The episodes last several hours and involve slurred speech and difficulty walking. She presented to the hospital for evaluation.", "Case Diagnosis": "Chiari I Malformation" }, "Topic": { "Title": "Chiari I Malformation", "Disease Discussion": "Chiari I malformations consist of cerebellar tonsillar ectopia. The cerebellar tonsils typically ascend with age with the normal position in the first 10 years of life allowing upto 6 mm of extension below the foramen magnum and decreasing to 5 mm in the second - third decades and 4 mm between the fourth to eighth. When ectopic, the cerebellar tonsils may be elongated and take on a pointed appearance inferiorly discribed as \"peg-like\". When there is extension of the tonsils greater than 12mm below the foramen magnum, symptoms are generally associated. While other brain anomalies are not usually associated with Chiari I malformations, a variety of spine and skull base abnormalities may be seen, including Klippel-Feil, C2-3 fusions, Basilar invagination and atlantooccipital assimilation. These associated skull base and spine abnormalites are present in approximately one-quarter of patients with Chiari I malformations. Also associated is the development of syringohydromyelia (or syrinx) which is present in approximately 30% of asymptomatic and 60-90% of symptomatic patients. While the syrinx usually occurs in the cerical spinal cord but can involve the entire length of the spinal cord or rarely occur as an isolated finding in the thoracic cord. The syrinx represents either a dilation of the central canal of the spinal cord (hydromyelia) or extension of the fluid through the ependyma of the central canal into the adjacent cord parenchyma (syringomyelia). The two are combined into a single term for MR purposes as they can not be distinguished from each other on imaging studies. The formation of the syrinx is theorize to occur as a result of altered fluid flow from the central canal at the obex secondary to compression of the brainstem in the foramen magnum region by the ectopic cerebellar tonsils. Symptoms that may be associated to the syrinx include upper extremity weakness/ sensory deficits which can lead to the formation of Charcot changes in the glenohumeral joints.", "ACR Code": "1.1", "Category": "Congenital, malformation", "Reference": "Magnetic resonance imaging of the brain and spine, 2nd ed. S. W. Atlas, editor. Lippincott-Raven publishing. Philadelphia. 1996. Pgs. 183 \u2013 188.\n\nMagnetic resonance imaging of the central nervous system. M. Brant-Zawadzki and D. Norman, editors. Raven Press. New York. 1987. Pgs. 145 \u2013 148.\n\nDiagnostic neuroradiology. A. G. Osborn. Mosby publishing. St. Louis. 1994. Pgs. 15 \u2013 18." } }, { "U_id": "MPX2236", "TAC": [], "MRI": [ "MPX2236_synpic18692", "MPX2236_synpic18695" ], "Case": { "Title": "Spongioform Encephalopathy, Presumed variant Creutzfeldt-Jacob Disease", "History": "25 Y/O with new onset progrssive dementia, myclonus, EEG abnormalities, history of eating raw sheep's brain approximately 2 years ago.", "Exam": "Left frontal lobe biopsy: Spongioform encephalopathy consistent with Creutzfeldt-Jacob disease.", "Findings": "Brain MRI scans approximately 6 months apart show progressive diffuse cortical atrophy, T2/FLAIR and Diffusion increased signal within the Basal Ganglia. Mild increased diffusion signal is seen in the posterior Thalamus (Pulvinar)\nCorrespoding relatively decreased ADC map basal ganglia signal.\n\nMR Spectroscopy demonstrated a decrease in NAA peak.", "Differential Diagnosis": "Cruetzfeldt-Jacob Disease\nVariant Creutzfeldt-Jacob Disease\nOther transmissible spongioform encephalopathies\nDiffuse ischemic insult\n\nLess likely:\nMethanol - putamen\nCarbon Monoxide - globus pallidus \nDeposition of iron or copper\nNeoplastic infiltration\u2014particularly of lymphoma or glioma.", "Case Diagnosis": "Spongioform Encephalopathy, Presumed variant Creutzfeldt-Jacob Disease", "Diagnosis By": "Frontal Lobe Biopsy" }, "Topic": { "Title": "Spongioform Encephalopathy, Presumed variant Creutzfeldt-Jakob Disease", "Disease Discussion": "Creutzfeldt-Jacob Disease and variant CJD are in a group of transmissible spongiform encephalopathies (TSEs), also known as prion diseases. The hallmark of a TSE disease is misshapen protein molecules that clump together and accumulate in brain tissue. Misshapen prion proteins have the ability to change their shape and cause other proteins of the same type malform. \nOther TSEs include Kuru, fatal familial insomnia, bovine spongiform encephalopathy in cattle ,scrapie in sheep and goats, and chronic wasting disease in deer and elk. \n\nCreutzfeldt-Jakob disease (CJD) is a rare fatal dementing illness caused by a prion agent. Antemortem diagnosis remains problematic because of variation in clinical presentation and lack of definitive clinical findings (classic triad of dementia, myoclonic jerks, and EEG abnormalities).\n\nT2WI, FLAIR and Diffusion imaging may show abnormalities in the basal ganglia (caudate and putamen), thalamus and cerebral cortex. Up to 21% of sporatdic CJD may have a normal MRI. MR Spectroscopy may show nonspecific depression of N-acetylaspartate (NAA).\n\nDiffusion imaging may show increased signal with ribbon-like signal abnormalities in cerebral cortex and/or diffuse hyperintensities in basal ganglia, or even thalamus (particularly the pulvinar [posterior thalamus] in variant CJD. Both increased and decreased ADC signal has been seen. Diffusion imaging is more sensitive than T2/FLAIR with abnormalities reported as early as 1 month after onset of symptoms. Abnormal DW imaging changes may be present in patients with CJD who have normal EEGs and normal CSF studies. The reason for the increased T2 and diffusion abnormalities are not well understood and it is unclear wheather these findings are specific for CJD or of the prion diseases in general.", "ACR Code": "1.2", "Category": "Infection, NOS", "Keywords": "Prion diseaseCreutzfeldt-JacobSpongioform encephalopathy", "Reference": "1. Yang MD, et.al Emerging Patterns of Diffusion-Weighted MR Imaging in Creutzfeldt-Jakob Disease: Case Report and Review of the Literature. AJNR; 2002 23: 550-556.\n\n2. National Institute of neurological disorders and stroke. http://www.ninds.nih.gov/health_and_medical/disorders/tse.htm" } }, { "U_id": "MPX2239", "TAC": [], "MRI": [ "MPX2239_synpic41018", "MPX2239_synpic41019" ], "Case": { "Title": "Choroid Plexus Papilloma", "History": "46 year old woman with history of new onset headaches.", "Exam": "No neurological deficits or seizures.", "Findings": "T1W gray matter isointense mass in fourth ventricle on T1 MRI.", "Differential Diagnosis": "\u2022 choroid plexus papilloma\n\u2022 ependymoma\n\u2022 subependymoma\n\u2022 metastasis to choroid plexus", "Case Diagnosis": "Choroid Plexus Papilloma", "Diagnosis By": "Resection and pathology confirmation", "Treatment & Follow Up": "Resection with no recurrence of disease.", "Discussion": "Choroid plexus papillomas are most commonly found in the fourth ventricle in adults. This patient's tumor location is classic. Hydrocephalus is not seen here but is a common complication of this benign tumor." }, "Topic": { "Title": "Choroid Plexus Papilloma", "Disease Discussion": "Lesions/Condition: Choroid Plexus Papilloma\n\nDerived from choroid plexus epithelium\n\nWHO Grade: I\n\nThe most common symptoms are headache, bulging fontenelle, vomiting, ataxia, and enlarging head circumference. The etiology of the hydrocephalus seen in these patients is not completely understood - it may be in part due to overproduction of CSF by the CPP, blockage of the arachnoid granulations by hemorrhage, or mechanical obstruction.\n\nCommon Locations: In children, CPPs more often occur in the lateral ventricles, while fourth ventricle CPPs are more common in adults. 50% occur in the atrium of the lateral ventricles, and 40% occur in the 4th ventricle.\n\nDemographics: Most common clinical profile is a child in the first 2 years of life. Lateral ventricle CPPs occur with equal frequency in males and females, whereas fourth ventricle CPPs are more common in males (3:2). CPP make up 2-4% of pediatric brain tumors, but only 0.5% of adult brain tumors.\n\nGross Morphology: Cauliflower-like mass.\n\nHistology: Normal choroid plexus tissue without atypia.\n\nRadiology: \nCT: CPPs are often calcified and ehnace with contrast.\nMRI: T1 hypo to isointense with characteristic hyperintensity on T2. The lesions enhance avidly on post contrast imaging. On GRE there may be low signal due to calcification or hemorrhage.\nMRA: can reveal enlarged choroid plexus vasculature\nBy imaging it is difficult to differentiate CPP from choroid plexus carcinomas. Both of these lesions may seed the CSF pathways.\n\nDifferential Diagnosis: Choroid plexus carcinoma, ependymoma, meningioma, metastasis\n\nPrognosis and Treatment: Resection. Without surgery, the patient is at risk for hydrocephalus from CSF outflow obstruction. Recurrence is rare, and although choroid plexus papillomas have premalignant potential, most have a benign course.", "ACR Code": "1.3", "Category": "Neoplasm, benign", "Keywords": "choroid plexusventricle", "Reference": "Up To Date- Uncommon Brain Tumors" } }, { "U_id": "MPX2260", "TAC": [], "MRI": [ "MPX2260_synpic46207", "MPX2260_synpic46208" ], "Case": { "Title": "Cerebral Cavernous Malformation", "History": "32 year-old man with the recent onset of seizures.", "Exam": "Non-focal neurological examination.", "Findings": "\u2022 Heterogeneous signal lesion - mixed iso and hyperintense on T1WI \n\u2022 Hyperintense on T2WI - in the region of the right lenticular nucleus, anterior limb of the right internal capsule, and external capsule\n\u2022 Hypointense rim on T1WI that \u201cblooms\u201d on T2WI\n\u2022 No mass effect\n\u2022 Minimal enhancement seen post-gadolinium", "Differential Diagnosis": "\u2022 Cavernous malformation\n\u2022 Hemorrhagic neoplasm\n\u2022 AVM\n\u2022 Capillary telangiectasia", "Case Diagnosis": "Cerebral Cavernous Malformation", "Diagnosis By": "Pathognomonic radiological features", "Treatment & Follow Up": "Surgical intervention pending.", "Discussion": "Cavernous angiomas are the most commonly identified brain vascular malformation. They are discrete multilobulated berry-like lesions, containing various stages of hemorrhage. There is no neural tissue seen within the lesion. Cavernous angiomas can be seen throughout the parenchyma, more commonly at the frontal and temporal lobes. 80% are supratentorial, often seen within the deep white matter, corticomedullary junction, and basal ganglia. They can also be seen within the spinal cord. Within the posterior fossa, the pons and cerebellar hemispheres are preferred locations. Multiple lesions are seen 50% of the time.\n\nThe most common age of presentation is 20 to 40 years of age, presenting with headache, seizure, or focal neurological deficit. Associated occult hemorrhage is common.\n\nOn CT, cavernous angiomas appear iso to hyperdense. Varied enhancement is seen following contrast administration, and calcifications are commonly seen. \n\nOn MR, a characteristic \u201cpopcorn-like\u201d appearance is seen. This pattern results from multiple mixed signal intensities secondary to varying stages of hemorrhage. A low signal rim that \u201cblooms\u201d on T2-weighted and gradient imaging is secondary to hemosiderin and is typical of cavernous angioma. \n\nReferences:\nBrant WE, Helms CA. Fundamentals of Diagnostic Radiology, 2nd Ed. Lippincott Williams and Wilkins, Philadelphia, 1994. p 108.\n\nHagiwara N, Yahikozawa H. Multiple cavernous haemangioma showing marked calcification on cranial radiography. Journal of Neurology Neurosurgery and Psychiatry 2002;72:410\n\nOsborn AG. Diagnostic Neuroradiology. Mosby, St Louis, 1994. pp311-313.\nStein BM, Mohr JP. Vascular malformations of the brain. N Engl J Med. 1988; 319(6):368\u2013370.\n\nStein BM, Mohr JP. Vascular malformations of the brain. N Engl J Med. 1988; 319(6):368\u2013370." }, "Topic": { "Title": "Cavernous hemangioma", "Disease Discussion": "Cerebral cavernous malformations (CCM) are also called angioma, cavernous angioma, and cavernous hemangioma. They are developmental vascular malformations - not a neoplasm - consisting of variably sized sinusoidal spaces closely grouped and without intervening brain tissue. Often described as a \"blood sponge\". They are associated with developmental venous anomaly (DVA) and may develop after radiation therapy.\n\nPresentation: Incidental or with Seizures\n\nInheritence: May be sporadic or autosomal dominant (KRIT1 gene)\n\nLocation: subcortical; often asymptomatic, but may present with seizures and rarely with hemorrhage.\n\nPreviously considered as the rarest form of vascular malformation because they are usually \"invisible\" on angiography. However, they are more frequently seen on MR and CT - often as unsuspected and asymptomatic (incidental) findings. \n\nApproximately 30% will calcify.\n\nAngiography may be unremarkable, or may rarely show an abnormal capillary blush. They are slow flow lesions, without shunting, and they do not cause enlargement of the feeding arteries. Watch for associated DVA malformation.\n\nCT may show partially calcified mass, typically without mass effect or edema, and homogenous enhancement of the non-thrombosed paten portions.\n\nMR demonstrates mixed signal intensity on T1 and T2 (subacute blood), and a hypointense rim (hemosiderin).\n\nNOTE: Multiple CCM indicate the autosomal dominant heritable form and first-degree relatives should be evaluated.", "ACR Code": "1.3", "Category": "Vascular", "Keywords": "cavernous angiomavascular malformationblood sponge", "External Links": "rad.usuhs.mil/rad/home/vascmalf/malf0.html" } }, { "U_id": "MPX2261", "TAC": [], "MRI": [ "MPX2261_synpic13155" ], "Case": { "Title": "Multiple Myeloma\r\nDiagnosis was confirmed by biopsy of humeral lesion and bone marrow aspirate.", "History": "60 year old male presents to ortho for evaluation of right upper extremity pain.", "Findings": "The images submitted are all from the same patient within a several month period. These demonstrate the various sensitivies of the imaging modality however are all nonspecific. All confirm a presence of a polyostotic intramedullary process with altered/increased bone metabolism.", "Differential Diagnosis": "Multiple Myeloma\nMetastatic disease\nLymphoma\nOsteomyelitis", "Case Diagnosis": "Multiple Myeloma\nDiagnosis was confirmed by biopsy of humeral lesion and bone marrow aspirate.", "Treatment & Follow Up": "Patient subsequently fractured the proximal humerus which was stabilized with internal fixation." }, "Topic": { "Title": "Multiple Myeloma", "Disease Discussion": "Multiple Myeloma\n\nMultiple myeloma is the most common primary malignant disease to involve bone. This abnormal proliferation of cells involves the marrow space and has a varity of imaging findings, which vary per modality. Imaging with plain film, CT, MRI, Bone Scan and recently PET can all play a complimentary role.\nPlain films can show lytic lesions however may only show osteopenia. Given that individuals, who at greastest risk are elderly, this may be confused with senile osteoporosis.\n\nCT has greater sensitivity to endosteal erosions however is often limited to aa single body part and has risk of increased exposure to ionizing radiation.\n\nMRI is an excellent modality for marrow space involvement but again is limited by field of view.\nBone scan findings are nonspecific however range from normal, to increased activity with associated fracture, or the difficult \"cold\" lesion.\n\nRecently PET has shown promise as an imaging technique. While not approved for multiple myeloma, entire/whole body imaging can be performed and may have increased sensitivity.\n\nNote: additional findings are addressed in other factoids on this site.", "ACR Code": "4.3", "Category": "Neoplasm, hematopoietic", "Keywords": "myeloproliferative disordermyeloma" } }, { "U_id": "MPX2272", "TAC": [], "MRI": [ "MPX2272_synpic148" ], "Case": { "Title": "Epidermoid Inclusion Cyst", "History": "Facial pain, progressively worse over 6 years", "Exam": "Numbness over her right face", "Differential Diagnosis": "\u2022 Vestibular Schwannoma\n\u2022 Meningioma\n\u2022 Epidermoid inclusion cyst\n\u2022 Arachnoid cyst\n\u2022 Ependymoma", "Case Diagnosis": "Epidermoid Inclusion Cyst", "Diagnosis By": "Pathology" }, "Topic": { "Title": "Vestibular schwannoma", "Disease Discussion": "The vestibular schwannoma (VS) is the most common neoplastic mass of the cerebellopontine angle (CPA). Over 95% of these masses are solitary and sporadic neoplasms. The remaining 4-5% are part of NF2, and in that disease are bilateral in at least 2/3 of patients. VS almost invariably enhances. Small lesions are homogeneous, larger lesions are heterogeneous due to benign cystic degeneration, and some lesions create a secondary \"arachnoid cyst\". \n\nThe second most common CPA mass is the meningioma, an enhancing hemispheric lesion with a broad base of dural attachment.\n\nThe third most common mass in the CPA is the epidermoid inclusion cyst. \n\nMRI: Often isointense or slightly hypointense to brain on T1W images, they may become heterogeneously bright on T2 - usually explained by the loose or myxoid (watery) \"Antoni B\" areas seen histologically.\n\nhttp://library.med.utah.edu/WebPath/CNSHTML/CNS187.html\nhttp://www.uhrad.com/mriarc/mri018.htm\n\nSurgical approach:\n\u00bb Translabyrinthine approach - removes the inner ear cochlea, causing hearing loss - but provides excellent visualization to preserve facial nerve\n\n\u00bb Middle Fossa approach - the inner ear is preserved, but 60-70% hearing loss\n\n\u00bb Retrosigmoid approach - 30-50% hearing loss\n\nhttp://www.umm.edu/otolaryngology/acoustic_neuromas.htm", "ACR Code": "1.3", "Category": "Neoplasm, non-glial", "Keywords": "Antoni A Antoni bacoustic neuromacerebellopontine angle cistern", "External Links": "http://clinicaltrials.gov/ct2/results?term=schwannoma" } }, { "U_id": "MPX2300", "TAC": [], "MRI": [ "MPX2300_synpic31225", "MPX2300_synpic31226", "MPX2300_synpic31227" ], "Case": { "Title": "Anterior Cruciate Ligament Disruption", "History": "The patient was a 21-year man, who twisted his knee while playing in a softball game. Following the injury, he complained of difficulty running, pain in the posterolateral aspect of the knee and joint swelling.", "Exam": "Initial physical examination of the knee revealed a small joint effusion, but no deformity. The knee demonstrated full range of motion and there was no documentation of instability.", "Findings": "Lateral radiograph of the knee demonstrates a deep, irregular appearing lateral femoral sulcus, and a small joint effusion, but is otherwise normal (Fig 1). Follow up MR imaging demonstrates marrow edema in the lateral femoral condyle and in the posterior tibial plateau. The lateral femoral sulcus appears deepened and irregular in contour. T2-weighted sagittal image through the region of the intercondylar notch demonstrates complete disruption of the anterior cruciate ligament (Fig 2).", "Differential Diagnosis": "Anterior Cruciate Ligament Disruption", "Case Diagnosis": "Anterior Cruciate Ligament Disruption", "Diagnosis By": "Follow up MRI confirmed the complete disruption of the anterior cruciate ligament.", "Discussion": "The \u201cdeep lateral femoral notch\u201d sign refers to an osteochondral impaction injury of the lateral femoral condyle that is associated with disruption of the anterior cruciate ligament (ACL). At the time of injury, the tibia translates anteriorly relative to the femur resulting in an impaction injury of the lateral femoral condyle against the posterior tibial plateau. Identification of the \u201cdeep\u201d sulcus on the lateral radiograph of the knee is a clear indicator of significant trauma and has a high association with ACL disruption." }, "Topic": { "Title": "The Deep Lateral Femoral Notch: A Sign of Anterior Cruciate Ligament Disruption", "Disease Discussion": "Several apparently minor osseous abnormalities of the knee have been described on conventional radiographs that are associated with more serious but radiographically occult soft tissue injuries. These include avulsion fracture of the anterior tibial spine and avulsion fracture of the lateral tibial plateau (Segond fracture), both associated with ACL disruption and avulsion fracture of the posterior intercondylar insertion of the posterior cruciate ligament (2-4). The deep femoral sulcus sign, however, is the most common radiographic sign associated with ligamentous injury of the knee. Because it is an impaction injury rather than an avulsion injury, it can be a subtle finding on radiographs, and one that is often overlooked.\n\nA normal lateral radiograph of the knee demonstrates a normal shallow groove along the lateral femoral condyle that is formed by the junction of the tibiofemoral and patellofemoral curvatures. This notch is referred to as the lateral condylopatellar sulcus and it is normally smooth and symmetric in appearance measuring less than 1.5 mm in depth (5). During the pivot shift mechanism of injury, the knee while in slight flexion undergoes a twisting injury and valgus stress that leads to disruption of the ACL thus allowing anterior translation of the tibia relative to the femur. As the tibia and femur return to their normal position, the lateral femoral condyle impacts the posterolateral tibial plateau resulting in an osteochondral impaction fracture of the lateral femoral condyle.\n\nThe radiograph will demonstrate an irregular asymmetric appearing notch that is greater than 2 mm in depth. This is referred to as the \u201cdeep lateral femoral sulcus\u201d sign. The depth of the notch is measured by drawing a line tangential to the sulcus along the articular surface of the lateral femoral condyle and then by measuring the distance from the line to the depth of the sulcus (Fig 5). The presence of a deep lateral femoral sulcus is nearly always associated with ACL disruption but lacks sensitivity; the absence of the sign therefore does not exclude the presence of an ACL tear (5).\n\nMR imaging also demonstrates an irregular appearing deep lateral femoral sulcus and in addition it will demonstrate marrow edema within the lateral femoral condyle and the posterior tibial plateau secondary to the impaction injury (6). This pattern of marrow edema has been referred to as the \u201cpivot shift\u201d marrow edema pattern and is also highly specific for ACL injury. See figures 2, 3 and 4 for examples in our case. MR imaging will demonstrate the ACL disruption along with associated injuries of internal derangement to include meniscal tear, chondral injury and collateral ligament tear.\n\nThe \u201cdeep lateral femoral sulcus\u201d sign is a subtle radiographic finding that when present on a plain film can provide an important clue that an ACL injury has occurred. It results from an impaction of the lateral femoral condyle against the posterior tibial plateau at the time of ACL disruption. Identification of this finding on radiographs of the knee should prompt further evaluation of the knee with MR imaging.", "ACR Code": "4.4", "Category": "Trauma", "Keywords": "Anterior cruciate ligament disruptionDeep lateral femoral notch", "Reference": "1. Cobby MJ, Schweitzer ME, Resnick D: The deep lateral femoral sulcus notch: an indirect sign of a torn anterior cruciate ligament. Radiology 1992; 184(3): 855-8.\n\n2. Eady JL, Cardenas CD, Sopa D. Avulsion of the femoral attachment of the anterior cruciate ligament in a seven-year-old child. J Bone Joint Surg [Am] 1982; 64-1376.\n\n3. Woods GW, Stanely RF, Tullos HS. Lateral capsular sign: X-ray clue to a significant knee instability. Am J Sports Med 1979; 7:27.\n\n4. Pauly T, VanEnde R. Avulsion fracture. Arch Orthop Trauma Surg 1989; 108:325. \n\n5. Delzell PB, Schils JP, Recht MP. Subtle fractures about the knee: Innocuous-appearing yet indicative of significant internal derangement. AJR Am J Roentgenol 1996; 167(3): 699-703.\n\n6. Gentili A, Seeger LL, Yao L, Do HM. Anterior cruciate ligament tear: indirect signs at MR imaging. Radiology 1994; 193(3): 835-40." } }, { "U_id": "MPX2312", "TAC": [], "MRI": [ "MPX2312_synpic26117" ], "Case": { "Title": "Septo-Optic Dysplasia", "History": "CC: I can\u2019t see on my right side and have been bumping into things for the last 1.5 years. \n\nReferred by optometry for a \u201cvisual field defect\u201d and optic nerve abnormality not noted prior\n\nNo decline in central vision\nNot progressive since detected by the patient\nNo records (no baseline VA ,VF, motility, photos)\n\nPOH:\tAmblyopia/patching,\n\t\tstrabismus surgery at age 19\nPMH:\tNarcolepsy, fibromyalgia, chronic lower\n\t\tback pain, TMJ\nFHx:\tNo history of visual or CNS\n\t\tdisease", "Exam": "BCVA: \tOD: 20/70-1, OS: 20/20\n V A Near:\tOD: 20/60-2, OS: 20/20\n TA: \t\t20, 19 mm Hg OU\n Pupils:\t2+ APD OD \n Stereo: \t(-)Fly\n PIP:\tOD: 9/14, OS 13/14\n MB: \t8 PD ET at distance and near\n\t\t\tNormal pursuits and saccades\n Neuro:\tNo other cranial nerve deficits and otherwise\n\t\t\tneurologically intact\n External:\tNo ptosis or exophthalmos\n Rest of exam WNL, except . . .", "Findings": "Absent septum pellucidum\natrophy of left optic nerve", "Differential Diagnosis": "Congenital maldevelopment/malformation\nAtypical compression (tumor or vascular lesions) of the optic nerve, chiasm or optic tract\nSequela of hydrocephalus\nPerinatal hypoxia\nVasculitis\nAtypical optic neuritis\nNon-organic\n\n*Initially thought she might have CVD*", "Case Diagnosis": "Septo-Optic Dysplasia", "Diagnosis By": "Imaging and clinical examination", "Discussion": "Septo-Optic Dysplasia,(de Morsier syndrome),Radiographic Features:\nDisorder of midline prosencephalic cleavage\nIncomplete development (or absence) of the septum pellucidum\nUni/bilateral Optic nerve, chiasm, optic tract dysplasia\n+/- Malformation of the corpus callosum and fornix, large chiasmatic cistern, schizencephaly\n\n*******When characteristic facial dysmorphism, open anterior fontanel, and other features are present along with septo-optic dysplasia, the term De Morsier syndrome is used, although in common parlance this term is used interchangably with septo-optic dysplasia, whether or not other features are present.\n\n\n\nClinical Features:\nPendular nystagmus\nVisual disturbance\nMental retardation \nHemiparesis (especially if associated with schizencephaly)\nQuadriparesis\nHypopituitarism in 15-60% \n\nTriad of a small anterior pituitary gland, an attenuated pituitary stalk, and an ectopic posterior pituitary enhancement (\u201cbright spot\u201d) on MRI \nEndocrine defects range from panhypopituitarism to isolated deficiencies of ACTH, GH, TSH, ADH or gonadotropins (delayed puberty)\nMay have isolated hyperprolactinemia or precocious puberty \nNeonatal hypoglycemia and seizures are important presenting signs in affected infants\n\n****Evaluation of the hypothalamic\u2013pituitary axis\u2014pot\u2019l life-threatening in infancy****\nElevation of prolactin with lack of hypothalamic inhibition\nPrecocious puberty with imbalance of pituitary precursor cells\n\n\nEtiology: \nSporadic\nMutation in the HESX1 homeobox gene\nYoung maternal age\nPregnancy risk factors:\nDiabetes\nAnticonvulsants\nPhencyclidine\nCocaine \nAlcohol" }, "Topic": { "Title": "Septo-Optic Dysplasia (DeMorsier syndrome)", "Disease Discussion": "Septo-optic dysplasia (SOD) (de Morsier syndrome) is a congenital malformation syndrome manifested by hypoplasia (underdevelopment) of the optic nerve, hypopituitarism, and absence of the septum pellucidum (a midline part of the brain). In a severe case, this results in pituitary hormone deficiencies, blindness, and mental retardation. However, there are milder degrees of each of the three problems, and some children only have one or two of the three.\n\nNeuroradiologically, intracranial malformations associated with septo-optic dysplasia include agenesis of the corpus callosum, schizencephaly, and lobar holoprosencephaly.\n\nThe optic nerve hypoplasia is generally manifested by nystagmus (involuntary eye movements, often side-to-side) and a smaller-than-usual optic disk. The degree of visual impairment is variable, and ranges from normal vision to complete blindness. When nystagmus develops, it typically appears by 1-4 months of age, and usually indicates that there will be a significant degree of visual impairment, but the severity is difficult to predict in infancy. Although there are many measures to compensate for visual impairment, no treatment is available to induce normal optic nerve function.\n\nThe degree of pituitary deficiency is also variable, and ranges from normal function, to deficiency of a single hormone, to deficiency of both anterior and posterior hormones (termed panhypopituitarism", "ACR Code": "1.4", "Category": "Ophthalmology", "Keywords": "OpthalmologyDysplasia", "External Links": "en.wikipedia.org/wiki/Septo-optic_dysplasia" } }, { "U_id": "MPX2316", "TAC": [], "MRI": [ "MPX2316_synpic12143", "MPX2316_synpic12144" ], "Case": { "Title": "Meniscal Tear (radiologic and athroscopic confirmation)", "History": "30 y.o. man with chronic left knee pain after an injury", "Exam": "No exam or lab findings available", "Findings": "1) This is a T2 weighted coronal image of the Left knee with fat saturation showing abnormal signal in the medial meniscus which clearly contacts the articular surface. This is consistent with a meniscal tear. Also note edema surrounding the lateral collateral ligament (sprain).\n\n2) This Sagittal proton density image of the left knee reveals linear abnormal signal in the posterior horn of the medial meniscus", "Differential Diagnosis": "Knee, medial meniscus tear", "Case Diagnosis": "Meniscal Tear (radiologic and athroscopic confirmation)", "Diagnosis By": "Imaging and arthroscopic surgery", "Treatment & Follow Up": "This patient was treated with a partial meniscectomy via arthroscopy", "Discussion": "Meniscal tears are common injuries in both the sport and non-sport population with acutely torn menisci cases numbering at 61 per 100,000. (1) The medial meniscus is the more commonly torn than the lateral meniscus in sports injuries where the mechanism for injury \u201cis a compressive, rotational, and shearing force.\u201d (1) \n MRI is reported to have a 95% accuracy of detection rate for meniscal tears, but studies note that this number also depands on magnetic field strength of the scanners. (1)\n The key to diagnosing meniscal tears on MRI is by noting abnormal signal in the meniscus. Nevertheless, the abnormal signal must clearly touch the inferior or superior articular surface to call a tear on MRI. Note that a normal meniscus can have some signal within it. Tears that have minimal symptoms can be left without treatment, but oftentimes tears are treated at the time of arthroscopy with shaving or debridement.\n\nReferences:\n\n1) Ruddy, Kelley's Textbook of Rheumatology, 6th ed., Copyright 2001 W. B. Saunders Company, pp. 447-448" }, "Topic": { "Title": "Meniscal Tear", "Disease Discussion": "Meniscal tears are common injuries in both the sport and non-sport population with acutely torn menisci cases numbering at 61 per 100,000. (1) The medial meniscus is the more commonly torn than the lateral meniscus in sports injuries where the mechanism for injury \u201cis a compressive, rotational, and shearing force.\u201d (1) \n\nMRI is reported to have a 95% accuracy of detection rate for meniscal tears, but studies note that this number also depends on magnetic field strength of the scanners. (1) \n\nThe key to diagnosing meniscal tears on MRI is by noting abnormal signal in the meniscus. Nevertheless, the abnormal signal must clearly touch the inferior or superior articular surface to call a tear on MRI. Note that a normal meniscus can have some signal within it. Tears that have minimal symptoms can be left without treatment, but oftentimes tears are treated at the time of arthroscopy with shaving or debridement.", "ACR Code": "-1.-1", "Category": "Trauma", "Keywords": "MeniscusMeniscaltear", "Reference": "1) Ruddy, Kelley's Textbook of Rheumatology, 6th ed., Copyright 2001 W. B. Saunders Company, pp. 447-448" } }, { "U_id": "MPX2322", "TAC": [], "MRI": [ "MPX2322_synpic28575", "MPX2322_synpic28576", "MPX2322_synpic28577", "MPX2322_synpic28578" ], "Case": { "Title": "Arachnoid Cyst", "History": "27 year old man with bilateral hearing loss after surgical removal of a PE tube stuck behind his left TM. He underwent an MRI of the internal auditory canals for further follow up.", "Exam": "HEENT: Bilateral hearing loss, AS>AD.\nNeurologic: No other focal deficits or abnormal findings.\nRest of exam was noncontributory.", "Findings": "MRI for Internal Auditory Canal\n1. Incidentally noted anterior left temporal fossa arachnoid cyst. \n2. No evidence of retrocochlear or temporal bone-based pathology.\n3. Sinusitis within both maxillary sinuses as well as fluid within the left mastoid air cells.", "Differential Diagnosis": "Arachnoid cyst\nEpidermoid cyst \nDermoid cyst \nParasitic cyst\nCystic glioma\nChronic Hematoma", "Case Diagnosis": "Arachnoid Cyst", "Diagnosis By": "MRI", "Treatment & Follow Up": "-None if asymptomatic\n-Diuretic therapy\n-Surgical drainage - Indicated when disability occurs due to compression or obstruction. This can be done open or image-guided by CT or open MRI. Outcomes are good, with concomitant risk of mild focal deficits and seizure disorders.", "Discussion": "Arachnoid cysts are histologically benign, intracranial fluid collections, usually congenital in origin. They account for 1% of intracranial masses, and has been reported as high as 5 per 1000 on autopsy. The male to female ratio is 4 to 1. Symptomatic cysts may present at any age. Arachnoid cysts can be diagnosed on fetal ultrasound, and can be seen as early as during the early second trimester. Most fetal diagnoses, however, are made later in pregnancy.\n\nArachnoid cysts usually occur from a congenital abnormality, arising from arachnoid clefts or arachnoid duplications. They are not associated with chromosomal aneuploidy, but can be associated with brain malformations such as agenesis of the corpus callosum, absent cava, deficient cerebellar lobulation, and Arnold-Chiari type I malformation. Acquired arachnoid cysts may develop due to CSF entrapment in arachnoid adhesions due to surgery, trauma, subarachnoid hemorrhage, neonatal infections, or neoplasm. They may or may not be connected to the ventricular system. They can occur in both the cranium and the spinal canal. They often indent a cerebral hemisphere or invaginate into fissures, however severe compression is rare. Slow growth may occur with accumulation of fluid.\n\nArachnoid cysts are usually asymptomatic and found incidentally on imaging. If symptoms do occur, they may include headache, calvarial bulging, seizures, and less commonly focal neurologic signs. Symptoms may occur due to cerebral cortical irritation, brain compression, or obstruction of CSF flow. Diagnosis is made through imaging.\n\nDiagnostic imaging characteristics of arachnoid cysts on CT and MRI include having a smooth-surface, being non-enhancing with contrast, approximating CSF, and being homogeneous. The consistency of the fluid in the cyst should approximate the CSF. It should be homogeneous throughout, although simple septa within the cyst can occur. The cysts usually occur near the cerebral fissures, with 50-60% in the middle cranial fossa. They occur more commonly on the left side.\nSpecifically on MRI, these cysts are isointense or hypointense to brain on T1, and hyperintense to brain on T2. MRI is superior to CT for detecting complicated cysts.\n\nFetal diagnosis of arachnoid cysts can be made by ultrasound. Characteristics on ultrasound include seeing an anechoic cystic mass and thin smooth walls\nadjacent to the cerebral hemispheres, cerebellum, or brain stem.\n\nThis patient's arachnoid cyst is asymptomatic, and is likely not the cause of his hearing loss. Further treatment of this cyst is not needed unless symptoms arise in the future." }, "Topic": { "Title": "Arachnoid Cyst", "Disease Discussion": "True cysts of the CNS are named by their lining. Arachnoid cysts - sometimes called \"intra-arachnoid cysts\" - are fluid filled spaces (containing CSF). They may be congenital or acquired. The most common location is in the middle cranial fossa. \n\nSo-called \"secondary\" or \"acquired\" arachnoid cysts may develop in relation to slowly growing extraaxial neoplasms, like meningioma and Schwannoma.\n\nArachnoid cysts are common and many if not most are discovered as asymptomatic incidental findings. A large study of almost 12,000 children (under nineteen) found a prevalence of 2.6% (309/11,738 pts.). They were more common in boys.\n\nA subset of 111 were followed for a mean of 3.5 years:\n11/111 increased in size (all these pts. < 4 yrs old)\n13/111 decreased\n87/111 did not change\n\nPMID: 20515330", "ACR Code": "1.9", "Category": "Cyst, benign", "Keywords": "CystArachnoidchildren prevalence", "Reference": "-Arachnoid cyst. Taken from: Kotagal S, Bicknese A, Eswara M, Fenton G, Geller T, Grange D, Martin D, Nigro M, Pittman T. Atlas of Clinical Neurology. Edited by Roger N. Rosenberg. Current Medicine, Inc., 2002. Available on www.images.md.\n-Brackmann DE, Arriaga MA. Extra-axial neoplasm of the posterior fossa. In Cummings CW, ed.: Otolaryngology: Head & Neck Surgery, 4th ed. Mosby, Inc., 2005, p. 3817. On MDConsult.com.\n-Gandy SE, Heier LA. Clinical and magnetic resonance features of primary intracranial arachnoid cysts. Ann Neurol. 1987 Apr;21(4):342-8.\n-Khan, AN. Arachnoid Cysts. In Levy LM, Coombs, BD, Salamon, GM, Krasny, RM, Smirnatopolis, JG, eds., WebMD, 2005. Available on eMedicine.com.\n-Kollias SS, Bernays RL. Interactive magnetic resonance imaging-guided management of intracranial cystic lesions by using an open magnetic resonance imaging system. J Neurosurg. 2001 Jul;95(1):15-23. \n-Melmed S. Disorders of the anterior pituitary and hypothalamus. In Braunwald E, Fauci AS, Kasper DL, Hauser SL, Longo DL, Jameson JL, eds., Harrison\u2019s Principles of Internal Medicine, 15th Ed. The McGraw-Hill Companies, Inc., 2001. p. 2035." } }, { "U_id": "MPX2317", "TAC": [], "MRI": [ "MPX2317_synpic27514", "MPX2317_synpic27515", "MPX2317_synpic27516", "MPX2317_synpic27517", "MPX2317_synpic27518", "MPX2317_synpic27519" ], "Case": { "Title": "benign cystic teratoma", "History": "Patient found incidental right adnexal mass during a non-related MR imaging study.", "Exam": "N/C", "Findings": "Ultrasound of the pelvis demonstrates a large right adnexal mass with predominantly hyperechoic echotexture. \n\nMRI demonstrates a right ovarian cystic mass with predominantly expected homogeneously high T2 signal, with a rind of high T1/T2 signal in the anterior surface which becomes dark on fat-saturation images. This clearly demonstrates the fatty component of what is most likely a benign cystic teratoma.", "Differential Diagnosis": "benign cystic teratoma", "Case Diagnosis": "benign cystic teratoma" }, "Topic": { "Title": "benign cystic teratoma", "Disease Discussion": "Germ cell tumors make up 25% of all ovarian tumors. Of these, the most common germ cell tumor of the ovaries is the benign cystic teratoma or the dermoid cyst. These usually occur in younger women. They are bilateral in about 15% of the time. They have a variegated appearance on ultrasound, but predominantly appear as a complex cyst. They can have a large area of shadowing due to the presence of tooth-like calcifications. Demonstration of fat in either CT or MR strongly suggests the diagnosis. Rarely these tumors undergo malignant degeneration into squamous cell carcinoma. (7)\n\nCurrently, the elective treatment of choice is laparoscopic excision. Series of articles in the literature has shown that laparoscopic excision compared to laparotomy is safe, with decreased hospital stay and less post-operative pain. (1, 2, 4, 5) Some techniques have advocated aspirating the cyst before the removal (so that the cyst can be removed from the abdominal cavity through a smaller incision), with a slightly increased incident of post-operative fever (presumably from a reaction to the cyst fluid) but without any significant increased incidence of adhesions or peritonitis. (6) There is the mention of the vaginal route of excision in the literature, with the article mentioning faster patient recovery and reduced spillage compared that to laparoscopic approaches. (3)", "ACR Code": "8.3", "Category": "Neoplasm, benign", "Keywords": "benign cystic teratomaovarian dermoidgerm cell tumor", "Reference": "1. Milingos S, Protopapas A, Drakakis P, Liapi A, Loutradis D, Rodolakis A, Milingos D, Michalas S. Laparoscopic treatment of ovarian dermoid cysts: eleven years' experience. J Am Assoc Gynecol Laparosc. 2004 Nov;11(4):478-85.\n\n2. Campo S, Garcea N. Laparoscopic conservative excision of ovarian dermoid cysts with and without an endobag. J Am Assoc Gynecol Laparosc. 1998 May;5(2):165-70.\n\n3. Sheth SS. Management of ovarian dermoids without laparoscopy or laparotomy. Eur J Obstet Gynecol Reprod Biol. 2001 Nov;99(1):106-8.\n\n4. Nezhat CR, Kalyoncu S, Nezhat CH, Johnson E, Berlanda N, Nezhat F. Laparoscopic management of ovarian dermoid cysts: ten years' experience. JSLS. 1999 Jul-Sep;3(3):179-84.\n\n5. Morgante G, Ditto A, la Marca A, Trotta V, De Leo V. Surgical treatment of ovarian dermoid cysts. Eur J Obstet Gynecol Reprod Biol. 1998 Oct;81(1):47-50.\n\n6. Zanetta G, Ferrari L, Mignini-Renzini M, Vignali M, Fadini R. Laparoscopic excision of ovarian dermoid cysts with controlled intraoperative spillage. Safety and effectiveness. J Reprod Med. 1999 Sep;44(9):815-20. \n\n7. Zagoria, Ronald J. Genitourinary Radiology: The Requisites. Mosby, 2004." } }, { "U_id": "MPX2351", "TAC": [], "MRI": [ "MPX2351_synpic45942", "MPX2351_synpic45943", "MPX2351_synpic45944" ], "Case": { "Title": "Osteochondritis dissecans", "History": "35 year old active duty Air Force male nordic skiier (National Ski Patrol European Division) who was training for advanced mountaineering expeditions on the Concordia Glacier presents with ankle pain.", "Exam": "The patient has point tenderness on the talus and has 12 degrees of pronation bilaterally. He has a history of multiple fractures of the left foot to include a Jones fracture and a navicular fracture. He has disregarded medical advice for post-trauma care in the past. For example, he began water skiing only three weeks after two fractures of the foot with refusal of a cast.", "Findings": "AP and lateral radiographs of left ankle are negative. T1-weighted MR image shows focal area of low signal intensity in the medial aspect of the left talus. FSE T2-weighted MR image with fat saturation shows focal area of high signal intensity in the anteromedial aspect of the left talus.", "Differential Diagnosis": "Osteochondritis dissecans\nOsteochondral fracture\nAcute stress fracture", "Case Diagnosis": "Osteochondritis dissecans", "Diagnosis By": "Diagnosis confirmed by radiographic findings and patient history of repetitive trauma.", "Treatment & Follow Up": "His pain was relieved with form fitted orthodics at Landstuhl Army Medical Center, Germany, to neutralize the pronation. At 10 year follow-up: He is still sking alpine, nordic, diagonal stride, and races cross county skate skiing with little pain. Surgery was not attempted to repair the OCD.", "Discussion": "Please see Osteochondritis dissecans topic." }, "Topic": { "Title": "Osteochondritis dissecans", "Disease Discussion": "Osteochondritis dissecans (OCD) is believed to result from repetitive microtrauma. The initial trauma is an acute osteochondral fracture. The knee is involved in 75% of all patient presentations. It is most common in young male athletes, with a male:female ratio of 2-3:1. It is rarely seen in patients younger than 10 years of age or older than 50 years. There are two forms of OCD, the juvenile form affects children with open physes between the ages of 5 to 15 years. The adult form is present in patients with closed physes. \n With OCD of the talus, patients present with complaints of ankle \"catching\" with active motion or walking. They may have swelling or pain depending of the stage of lesion. On physical examination, patients may have diffuse or well-defined tenderness with a joint effusion, pain with tibiotalar joint compression, and/or crepitus with dorsiflexion or plantar flexion.The cartilaginous and subchrondral bone lesions are usually on the posteromedial or the anterolateral talar aspect. \n OCD of the talus is likely due to trauma causing tibiotalar subluxation with subsequent impingement of the talus on the tibia or fibula. Berndt and Harty observed in cadavers that impaction of the talus on the fibula in inversion with the ankle positioned in dorsiflexion results in anterolateral talar lesions. Posteromedial lesions could be created after inversion with a plantar-flexed ankle with resulting talus impaction and twisting on the posterior aspect of tibia.\n Radiographs may be adequate for diagnosis but they may also show no findings. Radiographs should always be obtained, but if negative, an MRI should be done for confirming the suspected clinical diagnosis when necessary. AP, lateral, and mortise radiographs are the standard radiologic images. Berndt and Harty's radiographic classification of OCD of the talus is used for determining the type of treatment and the prognosis. Stage I is a small area of compression of subchondral bone. Stage II is a partially detached osteochondral fragment. Stage III is a completely detached fragment that remains in underlying bone depression. Stage IV is a completely detached fragment with displacement from the subchondral bone depression.\n Canale and Belding recommend the following for all Berndt and Harty talar lesions:\nStage I and II - conservative treatment and protected weight-bearing\nStage III anterolateral \u2013 operative debridement and curettage\nStage III posteromedial \u2013immobilize limb in cast or brace and no weight-bearing for six months\nStage IV - operative debridement and curettage", "ACR Code": "4.4", "Category": "Trauma", "Keywords": "Talar osteochondritis dissecansOsteochondritisTalar trauma", "Reference": "Resnik, Donald. Diagnosis of bone and joint disorders. 4th ed. Saunders: Philadelphia, 2002. Vol III. \n\nSchenck, R., Goodnight, J. Current Concept Review - Osteochondritis Dissecans. The Journal of Bone and Joint Surgery 78:439-56 (1996) \u00a9 1996 The Journal of Bone and Joint Surgery, Inc. http://www.ejbjs.org/cgi/content/full/78/3/439#R163\n\nZehava S. Rosenberg, MD, Javier Beltran, MD and Jenny T. Bencardino, MD. MR Imaging of the Ankle and Foot. Radiographics. 2000;20:S153-S179.\u00a9 RSNA, 2000 \n\nAA De Smet, DR Fisher, MI Burnstein, BK Graf and RH Lange. Value of MR imaging in staging osteochondral lesions of the talus (osteochondritis dissecans): results in 14 patients. American Journal of Roentgenology, Vol 154, 555-558, Copyright \u00a9 1990 by American Roentgen Ray Society http://www.ajronline.org/cgi/content/abstract/154/3/555?ijkey=5671977b87ea61bdd1ef70a9572fad64f02b818d\n\nBui-Mansfield, L. Osteochondritis Dissecans. Emedicine. 08JAN2008: http://www.emedicine.com/radio/topic495.htm" } }, { "U_id": "MPX2349", "TAC": [], "MRI": [ "MPX2349_synpic26324", "MPX2349_synpic26325", "MPX2349_synpic26326", "MPX2349_synpic26327", "MPX2349_synpic26328" ], "Case": { "Title": "Optic Nerve Glioma", "History": "2 y.o. noted to have right sided proptosis", "Exam": "Right sided proptosis, otherwise WNL", "Findings": "Right sided intraconal solid spherical mass continuous with the optic nerve. Meninges appear to be intact around mass with CSF surrounding mass. Mass appears to be confined within orbit and does not involve the optic chiasm. The signal intensity of the mass in T1W images is similar to the signal intensity of the optic nerves and brain matter. On T2W images, the mass again has similar intensity to the optic nerves and brain matter and has a higher intensity than the musculature. On T1W images, post-gadolinium, the mass shows fairly uniform contrast enhancement", "Differential Diagnosis": "Most Common Orbital Malignancies of Children:\nRhabdomyosarcoma (Primary)\nNeuroblastoma (usually metastatic)\nRetinoblastoma (intraocular)\nMost Common Orbital Masses:\nBenign cysts (Teratoma, dermoid, epidermoid, congenital cystic eye)\nVascular lesions (capillary hemangioma, cavernous hemangioma, AVM, lymphangioma)\nNeurogenic Orbital Masses of Children:\nOptic nerve glioma\nOptic sheath meningioma\nSphenoid wing meningioma\nSchwannoma\nNeurofibroma\nLess Common Considerations:\nLangerhans\u2019 Cell Histiocytosis\nLacrimal gland lesions (cysts, tumors)\nInflammatory process or infection", "Case Diagnosis": "Optic Nerve Glioma", "Treatment & Follow Up": "This patient has been treated with chemotherapy since August 2004 due to the proptosis caused by the mass. Chemotherapy agents include carboplatin and vincristine. Thus far the mass has had a minimal decrease in size.", "Discussion": "The pediatric patient presenting with proptosis should always make the clinician think of rhabdomyosarcoma. Although this tumor accounts for only about 10% of all orbital tumors, it is the most common primary malignancy of the orbit and is rapidly progressive and destructive. For this reason, children with proptosis, decreased vision, or ptosis should promptly be imaged with either CT or MRI (CT is better to evaluate for bony invasion of rhabdomyosarcoma) to evaluate for a mass suspicious for rhabdomyosarcoma. Other masses in the differential include orbital cysts (which are the most common orbital mass and generally benign), vascular lesions, neurogenic tumors as listed above, and metastatic disease (of which, neuroblastoma is the most common malignancy to metastasize to the orbit). Cysts of the orbit are by far the most common, with dermoid and epidermoid cysts accounting for about 30-46% of all orbital masses; vascular lesions account for about 15%; neurogenic tumors and metastatic tumors both account for about 2-3% each.\n\nThis patient had an MRI series of the orbits done, revealing a retrobulbar mass and the findings listed above. With the mass continuous with the optic nerve and encapsulated by the optic nerve sheath, it makes the diagnosis of an optic nerve tumor much more likely than the other possible diagnoses in the differential. As the mass has meninges smoothly lining it and there is CSF visualized between the mass and the dura, the mass is most likely a part of the optic nerve\u2014leading to the diagnosis of optic nerve glioma.\n\nAn optic nerve glioma is actually a juvenile pilocytic astrocytoma of the optic nerve, which is a benign and usually slow growing tumor. ONG accounts for about 20% of neurogenic tumors in the orbit, there is possibly a mild predilection for females, and it usually presents by 8 years of age. The presenting signs and symptoms are typically slow progressing painless proptosis, visual loss, nystagmus, strabismus, and optic atrophy or edema. About 29% of cases are associated with Neurofibromatosis Type I\u2014typically presenting with bilateral optic nerve gliomas. At the time of diagnosis, about 25-30% of gliomas involve only the intraorbital optic nerve, about 60-70% of gliomas involve the chiasm, of which about 40% have invaded surrounding structures. \n\nManagement of optic nerve gliomas is typically conservative, involving regular interval physical exams and MRI imaging to evaluate for changes in size (physical exam every 6 months and MRI every 1 year). This is because ONGs are benign, slow growing tumors, and in up to 80% of cases, vision does decline some but then remains stable. Surgical and radiologic intervention result in loss of vision and are usually only offered if vision loss or proptosis progresses, or the tumor begins invading the chiasm or hypothalamus. Chemotherapy is also available and is becoming a more popular form of treatment, as it can avoid the possible complete loss of vision and neurotoxic effects of surgery and radiation. Chemotherapy drugs being used include carboplatin and vincristine, and several studies have recommended that chemotherapy with these drugs be first-line treatment for optic nerve gliomas that involve the chiasm and/or hypothalamus." }, "Topic": { "Title": "Proptosis and Orbital Masses in Children, Optic Nerve Glioma", "Disease Discussion": "The pediatric patient presenting with proptosis should always make the clinician think of rhabdomyosarcoma. Although this tumor accounts for only about 10% of all orbital tumors, it is the most common primary malignancy of the orbit and is rapidly progressive and destructive. For this reason, children with proptosis, decreased vision, or ptosis should promptly be imaged with either CT or MRI (CT is better to evaluate for bony invasion of rhabdomyosarcoma) to evaluate for a mass suspicious for rhabdomyosarcoma. \n\nOther masses in the differential include orbital cysts (which are the most common orbital mass and generally benign), vascular lesions, neurogenic tumors as listed above, and metastatic disease (of which, neuroblastoma is the most common malignancy to metastasize to the orbit). Cysts of the orbit are by far the most common, with dermoid and epidermoid cysts accounting for about 30-46% of all orbital masses; vascular lesions account for about 15%; neurogenic tumors and metastatic tumors both account for about 2-3% each.\n\nThis patient had an MRI series of the orbits done, revealing a retrobulbar mass and the findings listed above. With the mass continuous with the optic nerve and encapsulated by the optic nerve sheath, it makes the diagnosis of an optic nerve tumor much more likely than the other possible diagnoses in the differential. As the mass has meninges smoothly lining it and there is CSF visualized between the mass and the dura, the mass is most likely a part of the optic nerve\u2014leading to the diagnosis of optic nerve glioma.\n\nAn optic nerve glioma is often a juvenile pilocytic astrocytoma of the optic nerve, which is a benign and usually slow growing tumor. ONG accounts for about 20% of neurogenic tumors in the orbit, there is possibly a mild predilection for females, and it usually presents by 8 years of age. The presenting signs and symptoms are typically slow progressing painless proptosis, visual loss, nystagmus, strabismus, and optic atrophy or edema. About 29% of cases are associated with Neurofibromatosis Type I\u2014typically presenting with bilateral optic nerve gliomas. At the time of diagnosis, about 25-30% of gliomas involve only the intraorbital optic nerve, about 60-70% of gliomas involve the chiasm, of which about 40% have invaded surrounding structures. \n\nManagement of optic nerve gliomas is typically conservative, involving regular interval physical exams and MRI imaging to evaluate for changes in size (physical exam every 6 months and MRI every 1 year). This is because ONGs are benign, slow growing tumors, and in up to 80% of cases, vision does decline some but then remains stable. Surgical and radiologic intervention result in loss of vision and are usually only offered if vision loss or proptosis progresses, or the tumor begins invading the chiasm or hypothalamus. Chemotherapy is also available and is becoming a more popular form of treatment, as it can avoid the possible complete loss of vision and neurotoxic effects of surgery and radiation. Chemotherapy drugs being used include carboplatin and vincristine, and several studies have recommended that chemotherapy with these drugs be first-line treatment for optic nerve gliomas that involve the chiasm and/or hypothalamus.\n\nPrognosis for these patients depends on extent of tumor\u2014for patients with ONG confined to the optic nerve, 20-year mortality is about 10%, if the chiasm is involved the mortality rate climbs to about 20%, and if the tumor extends into the hypothalamus, the 10-year mortality rate is greater than 55%.", "ACR Code": "2.3", "Category": "Differential Diagnosis", "Keywords": "Optic Nerve GliomaGliomaproptosis", "Reference": "Abeloff, MD, et al. Clinical Oncology, 3rd Ed. Elsevier, Philadelphia, 2004. pp 1465-1469.\n\nCastillo, BV and Kaufman, L. \u201cPediatric Tumors of the Eye and Orbit,\u201d Pediatric Clinics of North America 50(1):149-172, 2003.\n\nLacaze, E, et al. \u201cNeuropsychological Outcome in Children with Optic Pathway Tumors when First-Line Treatment is Chemotherapy,\u201d British Journal of Cancer 89(11):2038-2044, 2003\n\nSilva, MM, et al. \u201cOptic Pathway Hypothalamic Gliomas in Children Under Three Years of Age: the Role of Chemotherapy,\u201d Pediatric Neurosurgery 33(3):151-158, 2000.\n\nYanoff, Myron, et al. Ophthalmology, 2nd Ed. Mosby, Inc. St. Louis, 2004. pp 729-742." } }, { "U_id": "MPX2367", "TAC": [], "MRI": [ "MPX2367_synpic24362", "MPX2367_synpic24363", "MPX2367_synpic24364", "MPX2367_synpic24365" ], "Case": { "Title": "Hill-Sach\u2019s lesion with underlying subcortical bone contusion and subchondral cyst formation consistent with chronicity.", "History": "42 yo man presents with onset of right shoulder pain for two years, combined with right upper extremity numbness and tingling.", "Exam": "On physical exam there is no obvious deformity of right upper extremity and the shoulder girdles are symmetrical with normal contours. Pain in right upper extremity, with palpation internal and external rotation, and with passive and active range of motion. Special tests: Negative sulcus sign, positive apprehension test. No neurological deficits noted.", "Findings": "A-P radiograph of the right shoulder in internal rotation shows a grooved defect in the posterolateral humeral head. Axial proton-density with fat saturation MR image shows an area of high signal intensity of the posterolateral humeral head and overlying cartilage consistent with a Hill-Sachs lesion. Proton-density and the T2-weighted with fat sat coronal oblique MR images show the Hill-Sach\u2019s lesion of the humeral head with fractured cortex. T2-weighted with fat sat sagittal oblique MR image shows the high signal intensity edema and subchondral cyst formation in humeral head beneath the Hill-Sach\u2019s fracture. There is no evidence of bony Bankart lesion on the plain radiographs or bony or cartilaginous Bankart lesion on the MR images.", "Differential Diagnosis": "The findings are typical for Hill-Sach\u2019s lesion.", "Case Diagnosis": "Hill-Sach\u2019s lesion with underlying subcortical bone contusion and subchondral cyst formation consistent with chronicity.", "Treatment & Follow Up": "For a simple Hill-Sach\u2019s lesion, appropriate reduction should be done as soon as possible, followed by immobilization for approximately four to six weeks (although this remains controversial), and rehabilitation of shoulder to include increasing range of motion, increasing strength, and restoring neuromuscular control (if deficit present). If a Hill-Sach\u2019s lesion is coupled with a Bankart lesion, surgical intervention and repair may be required. Surgical repair may be conducted via arthroscopy or in an open procedure, with advantages and disadvantages to each approach. Some of the benefits of the arthroscopic approach are less morbidity such as less risk for injury to the axillary and musculocutaneous nerves and subcutaneous tissue, quicker recovery time, improved shoulder stability, and more effective response to physical therapy. The disadvantages of arthroscopic surgery include higher failure rates (7-17% will redislocate). The advantages of open surgery include less than 10% failure rate and more accurate repair. Disadvantages of open repair are significant loss of external rotation (approximately 12%) and abduction, extensive dissection and greater capsular scarring.", "Discussion": "A Hill-Sach\u2019s lesion occurs when the humeral head is dislocated anterolaterally and impacts against the anterior glenoid bony labrum. This lesion can be seen in approximately 30-40% of patients who have first-time anterior dislocations and approximately 80% of patients with repeat dislocations. A Bankart lesion, which is defined as an avulsion of the anterior inferior glenoid labrum at its attachment to the inferior glenohumeral ligament complex, can accompany the Hill-Sach\u2019s lesion. For patients with a Bankart lesion, 75% will also sustain a Hill Sach\u2019s lesion. The probability of a recurrence is related to the age of the patient at time of injury. Recurrence of dislocations develops in 90% of patients under age 20 years, 60% of patients between 20 and 40 years, and 10% in patients over 40 years. The type of sporting activity (i.e. contact versus individual) and the level of sport participation (i.e. recreational versus professional) is also related to recurrence. For both lesions males are affected much more often than females, especially active adolescents and adults who are younger than age 25. However, as young women become more involved with athletics, the incidence of dislocations may change. Ethnicity of the patient is not a predisposing factor for dislocations. Although plain radiographs should always be the first study done to evaluate patients with any shoulder pain, MR imaging is the procedure of choice to diagnose and define the extent of the lesion. In fact, MR imaging resulted in a sensitivity of 97%, a specificity of 91%, and an accuracy of 94% in the detection of Hill-Sach\u2019s lesions. T2-weighted MR images will show high signal intensity at the site of impaction of the humeral head. T2-weighted MR images may also show subcortical bone high signal intensity that represents an area of contusion or subchondral cyst formation when chronicity is present." }, "Topic": { "Title": "Hill-Sach\u2019s lesion", "Disease Discussion": "A Hill-Sach\u2019s lesion occurs when the humeral head is dislocated anterolaterally and impacts against the anterior glenoid bony labrum. This lesion can be seen in approximately 30-40% of patients who have first-time anterior dislocations and approximately 80% of patients with repeat dislocations. A Bankart lesion, which is defined as an avulsion of the anterior inferior glenoid labrum at its attachment to the inferior glenohumeral ligament complex, can accompany the Hill-Sach\u2019s lesion. For patients with a Bankart lesion, 75% will also sustain a Hill Sach\u2019s lesion. The probability of a recurrence is related to the age of the patient at time of injury. Recurrence of dislocations develops in 90% of patients under age 20 years, 60% of patients between 20 and 40 years, and 10% in patients over 40 years. The type of sporting activity (i.e. contact versus individual) and the level of sport participation (i.e. recreational versus professional) is also related to recurrence. For both lesions males are affected much more often than females, especially active adolescents and adults who are younger than age 25. However, as young women become more involved with athletics, the incidence of dislocations may change. Ethnicity of the patient is not a predisposing factor for dislocations. Although plain radiographs should always be the first study done to evaluate patients with any shoulder pain, MR imaging is the procedure of choice to diagnose and define the extent of the lesion. In fact, MR imaging resulted in a sensitivity of 97%, a specificity of 91%, and an accuracy of 94% in the detection of Hill-Sach\u2019s lesions. T2-weighted MR images will show high signal intensity at the site of impaction of the humeral head. T2-weighted MR images may also show subcortical bone high signal intensity that represents an area of contusion or subchondral cyst formation when chronicity is present.", "ACR Code": "4.4", "Category": "Trauma", "Keywords": "Hill-Sach\u2019s lesionssubcortical bone high signal intensitysubchondral cyst formation", "Reference": "http://www.ori.org.au/bonejoint/shoulder/surgery.htm'>http://www.ori.org.au/bonejoint/shoulder/surgery.htm\n\n http://www.ori.org.au/bonejoint/shoulder/surgery.htm\n\n http://www.wheelessonline.com/o6/76.htm\n Tuite MJ, Blankenbaker DG, Seifert M, Ziegert AJ, Orwin JF. Sublabral foramen and Buford complex: inferior extent of the unattached or absent labrum in 50 patients. Radiology 2002;223: 137-142.\n\n S. Terry Canale Campbell's Operative Orthopaedics, 10th ed. (St Louis, Mosby, 2003), pp 2399-2416.\n\n Habermeyer , Jund D, Ebert T. Treatment strategy in first traumatic anterior dislocation of the shoulder. Plea for a multi-stage concept of preventive initial management. Unfallchirurg 1998; 101: 328-41.\n\n Park, M., Blaine, T., Levine W. Shoulder dislocation in young athletes: Current concepts in management. The Physician and Sportsmedicine. Online 2002;30:30. \n Workman TL, Burkhard TK, Resnick D, Goff WB Jr, Balsara ZN, Davis DJ, Lapoint JM. Hill-Sachs lesion: Comparison of detection with MR imaging, radiography, and arthroscopy. Radiology 1992;185: 847-852.\n\n Sartoris, David J. Principles of Shoulder Imaging. New York: McGraw Hill, Inc., 1995; pp.297-302." } }, { "U_id": "MPX2372", "TAC": [], "MRI": [ "MPX2372_synpic52849", "MPX2372_synpic52850", "MPX2372_synpic52851" ], "Case": { "Title": "Giant Cell Tumor", "History": "23 y/o man with pain out of proportion to his apparently minor injury.", "Exam": "Patient unable to cooperate with ROM exam secondary to pain. Tenderness to palpation over the proximal right arm/shoulder. No overt swelling or erythema. Neurovascularity intact distally.", "Findings": "Expansile lytic lesion centered on the proximal humeral metaphysis with subarticular extension. It is geographic, and there is no significant marginal sclerosis. No periosteal reaction. The overlying cortex is thinned, and there is a pathologic fracture of the humeral neck.", "Differential Diagnosis": "\u2022 Giant cell tumor\n\u2022 Aneurysmal bone cyst - usually skeletally immature patient, should have no solid components on MRI \n\u2022 Intraosseus ganglion - usually older patient and has sclerotic margin, no solid components on MRI\n\u2022 Chondroblastoma - usually skeletally immature patient, smaller and centered on epiphysis, usually has a sclerotic margin and often contains calcifications\n\u2022 Chondromyxoid fibroma - more rare, typically metaphyseal location but without subarticular extension, usually sclerotic margin", "Case Diagnosis": "Giant Cell Tumor", "Diagnosis By": "Pathology examination", "Treatment & Follow Up": "Surgical curettage, with subsequent hardware fixation of the fracture.", "Discussion": "http://orthoinfo.aaos.org/topic.cfm?topic=A00080\nhttp://emedicine.medscape.com/article/389833-overview\nhttp://en.wikipedia.org/wiki/Giant_cell_tumor_of_bone\nhttp://www.bonetumor.org/tumors/pages/page106.html\nhttp://www.wheelessonline.com/ortho/giant_cell_tumor_of_bone" }, "Topic": { "Title": "Giant Cell Tumor", "Disease Discussion": "HISTORY: 27-year-old male with a one-year history of mass of the distal right clavicle, slowly increasing in size. The patient has tenderness with activity and at rest.\n\nFINDINGS: Plain films: Bilateral shoulder and acromioclavicular joints are remarkable for a geographic expansile lytic lesion of the distal right clavicle, with with intact cortex, no matrix formation, and no obvious soft tissue mass.\n\nMRI: There is a destructive, lytic, expansile mass lesion of the distal right clavicle extending into the acromioclavicular joint, with associated soft tissue mass. The expansile component is seen at its superior aspect, and the inferior distal clavicular cortex is intact. There are multiple lobulations to this mass, with both high and low intralesional signal intensity components on the T2-weighted images, suggestive of intralesional\nnecrosis and/or hemorrhage. Patchy enhancement is seen within the lesion and in the soft tissues surrounding it following the intravenous administration of gadolinium. Edematous changes of the adjacent and surrounding soft tissues are present.\n\nDIFFERENTIAL DIAGNOSIS: Giant cell tumor, Ewings Sarcoma, lymphoma, and osteosarcoma. In an older patient metastisis and multiple myeloma should also be considered.\n\nDIAGNOSIS: Giant Cell Tumor. \n\nGiant cell tumor is a frequent benign osseous neoplasm seen in young adults; it has\na predilection for the end of the long bones, more often around the knee. In the foot and ankle region, it is seen more often in the distal tibia, talus, and calcaneus. A multicentric propensity has been seen in these locations. \n\nRadiographically, giant cell tumors are well-circumscribed, expansile, lytic, geographical lesions without rims of sclerosis, and they extend to the subchondral bone. On MRI, they demonstrate expansile contours, often with a rim of low signal intensity, which does not correlate with a rim of sclerosis on plain films. Internally, these tumors often demonstrate heterogeneous signal intensity as a result of the repeated episodes of internal hemorrhage and the formation of cysts and internal septations. Internal hemorrhage may lead to the presence of fluid-fluid levels, simulating an ABC. Sometimes, a giant cell tumor with ABC transformation can be found. MRI can be used to evaluate the articular and soft tissue extension of the tumor", "ACR Code": "4.3", "Category": "Neoplasm, NOS", "Reference": "Stark, S. Bradley, W. Magnetic Resonance Imaging CD, 3rd Edition. Mosby, 1999. Chapter 39." } }, { "U_id": "MPX2390", "TAC": [], "MRI": [ "MPX2390_synpic36479", "MPX2390_synpic36480", "MPX2390_synpic36481", "MPX2390_synpic36482", "MPX2390_synpic36483" ], "Case": { "Title": "Leukoaraiosis", "History": "69 y/o woman with hypertension presents to inpatient service with \"left-sided weakness.\" Yesterday morning she noted that she began dragging her left side. A few hours later the weakness was more obvious and involved her left hand. She had a CT scan that was nonspecifically abnormal because of \"cerebral atrophy\", but no stroke was seen. She was admitted with a provisional diagnosis of stroke vs. transient ischemic attack. \n\nHer right side was not involved. There was no visual loss. There was no facial weakness. She noted that left sided sensations were diminished as compared to the right. She denied a history of strokes.\n\nSince that time, she has regained strength in her left leg, however today she noticed a slight slurring of her speech and was unable to lift her arm off the bed.\n\nPMH:\n1. Hypertension\n2. Hyperlipidemia\n3. Asthma, mild intermittent\n4. Depression\n5. Allergic Rhinitis\n6. Arthritis\n\nMEDS:\n1. ASA 81 mg qd\n2. Zoloft 100 mg qd\n3. Zetia 10 mg qd\n4. Zocor 40 mg qd\n5. Hyzaar 100/25 mg qd\n6. Claritin 10 mg qd\n7. Albuterol MDI PRN\n\nSocial Hx: denies use of tobacco and alcohol\nFamily Hx: unknown", "Exam": "Her blood pressure in the ER was 170/101.\nVitals: Tm 98.8, BP 134/74, Pulse 66, rr 18\n\nGEN: WDWN AAF in NAD, AAOx3\nHEENT: Speech is fluent. No dysartri. Visual acuity, visual fields, and fundi are normal. Pupils and extraocular movements are normal. Mild drooping on left side of face. \nCardio: RRR, no clicks, rubs, or murmurs\nLungs: CTA b/l, no wheezes, rhales, or rhonchi\nAbd: Soft, non-tender, non-distended, bowel sounds x4 quadrants, no guarding or rebound.\nNeuro: Facial sensation on left side are diminished compared to right. No cerebellar findings.\nMotro: 5/5 Right extremities. 2/5 left arm, 4/5 left leg.\nReflexes: 2+ right bicep, tricep, patella, achilles. 3+ left bicep, tricep, patella, achilles, with positive left Babinski\nGait: she is dragging her left foot and is unable to walk without aid of the wall\nFolstein Mini-Mental Status Exam: 30/30\n\nLABS:\nCBC: WNL\nChem7: BUN 24, Creatinine 1.3, otherwise WNL\nUA: WNL", "Findings": "\u2022 MRI Brain:\n\"There is mild, age-appropriate volume loss. There is periventricular and deep white matter symmetric signal abnormality. There is no intracranial hemorrhage, mass, or mass effect. The brain parenchyma, CSF-containing spaces, posterior fossa, limited views of the internal auditory canals and orbits, overlying skull, and soft tissues are unremarkable.\"\n\n\u2022 MRA Head w/o contrast:\n\"The circle of Willis is intact. There is no evidence of aneurysm. There is no evidence of vessel occlusion.\"", "Differential Diagnosis": "\u2022 Chronic Ischemic Changes\n\u2022 Transient Ischemic Attack\n\u2022 Leukoaraiosis", "Case Diagnosis": "Leukoaraiosis", "Diagnosis By": "Imaging and clinical correlation", "Treatment & Follow Up": "Leukoaraiosis is by definition a characteristic radiologic finding that is sometimes synonymous with cerebral small vessel disease, and is a diagnosis of exclusion. As the symptoms did not fully recover in 24 hours, a TIA is ruled out. As there are no other findings of pathology, Leukoaraiosis is the most likely diagnosis.The patient's care was transferred to a Medicare-approved Physical Rehabilitation Unit where she is scheduled to continue PT, OT, and Speech Therapy for at least 3 hours a day during the week for the next 6 weeks. While she is trated at this facility, her PCM becomes the physician working there. Care will be transferred back once she completes her rehabillitation and is discharged home. The patient will schedule a follow-up appointment upon discharge.", "Discussion": "In this case, physical rehabilitation plays an important role in the care of the patient. Under the 75/25 rule, 75% of patient's discharged from a Medicare-approved physical rehabilitation unit must meet a certain diagnosis, and 'stroke' is one of them. She does not qualify for a skilled nursing facility, although she is not ready to resume her ADLs and IADLs at this time, which makes a rehabilitation unit an attractive choice. What is important to realize is that her PCM will change to the physicians at the rehabilitation unit while she is there, and thus her Tricare-appointed physician will need to keep in touch with that person in order to stay updated about her health. The physician should also realize that vascular dementia is much more likely in patient's with Leukoaraiosis." }, "Topic": { "Title": "Leukoaraiosis", "Disease Discussion": "Leukoaraiosis is a radiologic finding of diffuse white matter changes in the brain, with bilateral patchy or diffuse areas of hyperintensity of the cerebral white matter on FLAIR and T2-weighted MRI This imaging finding is associated with cerebral small vessel disease. \n\nKey points are:\n\n\u2022 patients who present with stroke-like symptoms and found to have leukoaraiosis on imaging are not to be given thrombolysis treatment, as this is associated with intracerebral hemorrhage.\n\n\u2022 patients with incidental finding of leukoaraiosis are at increased risk for decline in cognitive functioning compared to age-matched controls\n\n\u2022 leukoaraiosis will eventually progress to a vascular dementia\n\n\u2022 there is an association between hyperhomocysteinemia and leukoaraiosis; some will consider treating homocysteinemia with folic acid but meta analysis shows no difference in outcome in use of folic acid vs. controls", "ACR Code": "1.6", "Category": "Vascular", "Keywords": "vascular hemorrhagecerebral small vessel diseasehypertensive change", "Reference": "Palumbo V, Boulanger JM, Hill MD, Inzitari D, Buchan AM: \"Leukoaraiosis and intracerebral hemorrhage after thrombolysis in acute stroke.\" Neurology. 2007 Mar 27;68(13):1020-4.\n\nInzitari D, Simoni M, Pracucci G, Poggesi A, et al: \"Risk of rapid global functional decline in elderly patients with severe cerebral age-related white matter changes: the LADIS study.\" Arch Intern Med. 2007 Jan 8;167(1):81-8.\n\nBrown WR, Moody DM, Thore CR, Challa VR, Anstrom JA: \"Vascular dementia in leukoaraiosis may be a consequence of capillary loss not only in the lesions, but in normal-appearing white matter and cortex as well.\" J Neurol Sci. 2007 Jun 15;257(1-2):62-6. Epub 2007 Feb 23.\n\nNaka H, Nomura E, Takahashi T, Wakabayashi S, et al: \"Plasma total homocysteine levels are associated with advanced leukoaraiosis but not with asymptomatic microbleeds on T2*-weighted MRI in patients with stroke.\" Eur J Neurol. 2006 Mar;13(3):261-5.Links\n\nBazzano LA, Reynolds K, Holder KN, He J: \"Effect of folic acid supplementation on risk of cardiovascular diseases: a meta-analysis of randomized controlled trials.\" JAMA. 2006 Dec 13;296(22):2720-6", "External Links": "rad.usuhs.edu/medpix/medpix.html?mode=single&recnum=4140&table=card&srchstr=leuko&search=leuko#top" } }, { "U_id": "MPX2399", "TAC": [], "MRI": [ "MPX2399_synpic55890", "MPX2399_synpic55891", "MPX2399_synpic55892" ], "Case": { "Title": "PANK 2 (Hallervorden-Spatz) PKAN (Pantothenate Kinase Associated Neurodegeneration)", "History": "5 y.o. girl with a history of gait problems presents with progressive dystonia and dysarthria, mild rigidity, and choreoathetosis. No Hx of seizures, infection, etc.", "Exam": "Neurologic exam shows spasticity, very brisk reflexes, and up-going toes. An MRI examination of the brain was ordered, to include a T2* image sequence.", "Findings": "\u2022 Abnormal T2 hypointensity in the globus pallidus\n\u2022 Abnormal T2 hyperintensity in the center creating an \"eye of the tiger\" sign appearance", "Differential Diagnosis": "\u2022 NBIA 1 - PKAN (\"Hallervorden-Spatz\" w/PANK2)\n\u2022 NBIA 1 - PKAN (\"Hallervorden-Spatz\" w/o PANK2)\n\u2022 NBIA 2 - Ferritin light-chain disease\n\u2022 INAD- infantile neuroaxonal dystrophy\n\u2022 Aceruloplasminemia", "Case Diagnosis": "PANK 2 (Hallervorden-Spatz) PKAN (Pantothenate Kinase Associated Neurodegeneration)", "Diagnosis By": "Clinical and Imaging findings", "Discussion": "We made up this history, based on the typical and common features of the PANK2 mutation positive or PKAN neurodegeneration with brain iron accumulation - NBIA type 1 disease - formerly known as Hallervorden-Spatz disease. The specific mutation (PANK2) is strongly linked to the specific MR appearance of the \"eye of the tiger\"." }, "Topic": { "Title": "Neurodegeneration with Brain Iron Accumulation (NBIA)", "Disease Discussion": "Neurodegeneration with Brain Iron Accumulation (NBIA) is a group of genetic disorders characterized by abnormal iron metabolism and deposition in the central nervous system. Progressive iron deposition is toxic to neurons. There are at least four known subtypes that may be distinguished genetically, biochemically, and also by MR imaging. PMID: 21286947 PMID: 21480873 PMID: 21496576 PMID: 18981035 PMID: 18443312 PMID: 17569231 PMID: 16416393\n\u2022 Hallervordin-Spatz (PKAN or MBIA-1, MIM 234200) familial or sporadic, is a mutation in panthothenate kinase 2 (PANK2) usually causing a childhood presentation with progressive extrapyramidal dysfunction and dementia.\n\n\u2022 Infantile neuroaxonal dystrophy (INAD, MIM 256600) is autosomal recessive, a mutation in PLA2G6.\n\n\u2022 Neuroferritinopathy (FLT, NBIA-2, MIM 606159) is caused by a mutation in the gene (FTL1) coding for the light chain of ferritin, is autosomal dominant with an adult presentation.\n\n\u2022 Aceruloplasminemia (MIM 604290) is an autosomal recessive deficiency of ceruloplasmin, causing Fe deposition in the brain (movement disorder) and reticuloendothelial system (diabetes).\n\nOn T2* imaging (e.g. GRE or gradient sequences) these disorders may all cause hypointensity in the globus pallidus from abnormal iron accumulation. However, they may often be distinguished by their patterns of associated lesions:\n\n\u2022 Hypointense globus pallidus (GP)\n\u00bb IAND does not have other lesions\n\n\u00bb PKAN (PANK2) causes the \"eye of the tiger\" - a T2* dark globus pallidus (Fe) surrounding a T2 bright center in the medial globus pallidus PMID: 16775270\n\n\u00bb Neuroferritinopathy may also cause \"eye of the tiger\", but usually also causes T2* shortening of the dentate, substantia nigra, and 1 or more of the following: putamen, caudate, thalamus. Dengeration may lead to confluent increased signal (cavitation) in the GO and putamen\n\n\u00bb Acerulplasminemia adds T2* shortening of the dentate, substantia nigra, and all three of putament, caudate, and thalmus W/O cavitation", "ACR Code": "1.5", "Category": "Congenital, genetic", "Keywords": "Hallervordin-Spatz (PKAN)neuroferritinopathy, aceruloplasminemiainfantile neuroaxonal dystrophy (INAD)", "Reference": "http://www.rarediseases.org/rare-disease-information/rare-diseases/byID/179/viewAbstract\nhttp://www.ajnr.org/cgi/reprint/27/6/1230" } }, { "U_id": "MPX2402", "TAC": [], "MRI": [ "MPX2402_synpic21796", "MPX2402_synpic21797", "MPX2402_synpic21798" ], "Case": { "Title": "Myxopapillary Ependymoma", "History": "36 year old female with a history of low back pain and mild radicular symptoms.", "Exam": "Noncontributory", "Findings": "Routine MRI imaging demonstrated and extramedullary intradural ovoid lesion at the L2 level.", "Differential Diagnosis": "Extramedually Intradural lesions (MANDELInS)\nM: Menigioma/metastatic\nA: Arachnoid cyst\nN: Neurofibroma\nD: Dermoid\nE: Epidermoid/Ependymoma\nL: Lipoma\nIn: Infection (TB, cysticercosis)\nS: Schwannoma", "Case Diagnosis": "Myxopapillary Ependymoma", "Diagnosis By": "Pathology.", "Treatment & Follow Up": "Surgical resection." }, "Topic": { "Title": "Myxopapillary Ependymoma", "Disease Discussion": "Definition: Myxopapillary Ependymomas are slowly growing gliomas with preferential manifestation in young adults and are almost exclusively located in the conus medullaris, cauda equina, filum terminale region of the spinal cord. They are histologically characterized by tumor cells arranged in a papillary manner around vascularized mucoid stromal cores.", "ACR Code": "3.3", "Category": "Neoplasm, glial", "Keywords": "Myxopapillary Ependymoma", "Reference": "WHO Classification of Tumours: Tumours of the Nervous System, 2001." } }, { "U_id": "MPX2441", "TAC": [], "MRI": [ "MPX2441_synpic24605", "MPX2441_synpic24606", "MPX2441_synpic24607" ], "Case": { "Title": "Sturge-Weber Syndrome", "History": "11 mo female with known syndrome and a recent diagnosis of glaucoma. No history of developmental delays or seizure activity. Procedure: Baseline MRI of brain with gadolinium for evaluation of disease progression in future.", "Exam": "No information provided", "Findings": "Focal cortical hypoplasia of the left occipital lobe seen with decreased T2 signal of deep white matter, along with increased enhancement of overlying leptomeninges in comparison with right. Increased signal intensity and size of choroidal plexus noted in occipital horn of left ventricle in comparison with right. Increased pial enhancement of left parietal lobe in comparison with right.\nLeft globe enlargement in comparison with right globe (measured at 2.5 cm vs 2.0 cm AP).", "Differential Diagnosis": "Findings consistent with known Sturge-Weber Syndrome\nMay consider: Wyburn-Mason Syndrome, Other phakomatoses", "Case Diagnosis": "Sturge-Weber Syndrome", "Diagnosis By": "Imaging findings and clinical examination", "Treatment & Follow Up": "Skin: Laser tx for cosmesis\nGlaucoma: Close follow-up with ophthalmology with goal to preserve vision and control IOP via medications and/or surgery.\nFollow up imaging to track disease progression in presence of new onset of Sx, seizures, etc..", "Discussion": "Sturge-Weber Syndrome (SWS) or encephalotrigeminal angiomatosis is a non-heritable congenital neurocutaneous disorder associated with vascular malformations of the leptomeninges, choroid of the eye, and skin of the face with a trigeminal distribution. Findings are ipsilateral in the overwhelming majority of patients, but can also be bilateral.1 Pathogenesis is theorized to be associated with inappropriate control of normal vascular maturation and a resultant persistence of the primitive vascular plexus2. Diagnosis is based on demonstration of port-wine stain in a trigeminal distribution (not pathognomonic) and leptomeningeal angiomas, although variants also occur with an absence of one of these findings in the presence of ocular angiomas.3 \n\nThe predominant ocular feature is glaucoma, with a congenital presentation seen in 50% of patients. Early presentation in the newborn begins as bupthalmos, or enlargement of the globe. Other ocular findings include choroidal angiomas, heterochromia of the iris, or visual field defects, such as homonymous hemianopsia, secondary to occipital cortex atrophy4.\n\nNeurologic features are progressive and include seizures, focal deficits, and mental retardation, although it is possible to be spared neurologic abnormalities. Typically children will have no developmental delay for several months after birth, but may begin to slow in their cognitive development as the disease progresses. Mechanism for this progression is suggested to be secondary to hypoxic ischemia in tissues that failed to vascularize appropriately adjacent to the leptomeningeal angiomas.4 Seizures are often the presenting symptom. Their frequency, age at onset, and response to treatment affect prognosis4.\n\nMRI reveals the angioma as a hyperintense enhancement of the leptomeninges on T2-weighted images frequently occipital or posterior temporoparietal, with atrophy of adjacent lobe. Choroidal angiomas enhance on fat suppressed T1 imaging.3" }, "Topic": { "Title": "Sturge-Weber Syndrome", "Disease Discussion": "Sturge-Weber Syndrome (SWS) or encephalotrigeminal angiomatosis is a non-heritable congenital neurocutaneous disorder associated with vascular malformations of the leptomeninges, choroid of the eye, and skin of the face with a trigeminal distribution. Intracranial findings are ipsilateral to the facial lesion in the overwhelming majority of patients, but can also be bilateral.[1] \n\nPathogenesis is theorized to be associated with inappropriate control of normal vascular maturation and a resultant persistence of the primitive vascular plexus.[2] \n\nDiagnosis is based on demonstration of port-wine stain in a trigeminal distribution (not pathognomonic) and leptomeningeal angiomas, although variants also occur with an absence of one of these findings in the presence of ocular angiomas.[3] \n\nThe predominant ocular feature is glaucoma, with a congenital presentation seen in 50% of patients. Early presentation in the newborn begins as buphthalmos, or enlargement of the globe. Other ocular findings include choroidal angiomas, heterochromia of the iris, or visual field defects, such as homonymous hemianopsia, secondary to occipital cortex atrophy.[4]\n\nNeurologic features are progressive and include seizures, focal deficits, and mental retardation, although it is possible to be spared neurologic abnormalities. Typically children will have no developmental delay for several months after birth, but may begin to slow in their cognitive development as the disease progresses. Mechanism for this progression is suggested to be secondary to hypoxic ischemia in tissues that failed to vascularize appropriately, adjacent to the leptomeningeal angiomas.[4] Seizures are often the presenting symptom. Their frequency, age at onset, and response to treatment affect prognosis4.\n\nMRI reveals the angioma as a hyperintense enhancement of the leptomeninges on T2-weighted images frequently occipital or posterior temporoparietal, with atrophy of adjacent lobe. Choroidal angiomas enhance on fat suppressed T1 imaging.[3]\n\n========================================\n\nTreatment of Sturge-Weber:\nProphylatic Anti Epileptic Tx - Ville D, Enjolras O, Chiron C, Dulac O.: Prophylactic antiepileptic treatment in Sturge-Weber disease. Seizure. 2002 Apr;11(3):145-50.\nPMID: 12018956\n\nHemispherectomy:\nKossoff EH, Buck C, Freeman JM.: Outcomes of 32 hemispherectomies for Sturge-Weber syndrome worldwide.\nNeurology. 2002 Dec 10;59(11):1735-8.\nPMID: 12473761", "ACR Code": "1.3", "Category": "Congenital, malformation", "Keywords": "Sturge-Weber Syndromecerebral hemisphereFocal cortical atrophy", "Reference": "1. Bodensteiner, JB, Roach, ES. Sturge-Weber syndrome: Introduction and overview. In: Sturge-Weber Syndrome, Bodensteiner, JB, Roach, ES (Eds), Sturge-Weber Foundation, Mt. Freedom, NJ 1999. p.1. \n2.\tBodensteiner, JB. Sturge-Weber Syndrome. In: Vascular Birthmarks of the Head and Neck, Hochman, M (Ed), Facial Plastic Surgery Clinics of North America 2001.\n3.\tRiviello, James J. Sturge Weber Syndrome. Emedicine.com, October 12, 2001.\n4.\tBodensteiner, JB. Sturge-Weber syndrome. Up to Date.com, January 6, 2003." } }, { "U_id": "MPX2454", "TAC": [], "MRI": [ "MPX2454_synpic39850" ], "Case": { "Title": "Chance Fracture T11", "History": "23 y.o. man after a high fall", "Exam": "Multiple trauma", "Findings": "AP/LAT T-SPINE: Anterior compression fracture of T11 with loss of approximately 50% of height. AP view demonstrates abnormal pedicles with linear fractures and widening bilaterally. Posterior elements not well seen on lateral secondary to spine board.\nCT (Sag recon): Horizontal fracture of T11 vertebral body extending horizontally throught posterior elements\nMRI (Sag ): No cord compression or abnormal signal", "Differential Diagnosis": "The differential diagnosis initially after plain films alone include (compression, burst, chance and fracture dislocation). The abnormal appearance of the pedicles with horizontal lucent fractures and widening rules-out compression fracture alone. The involvement of the posterior elements and non-comminution of body fracture rules-out a burst fracture. The fact that there are no associated dislocations rules-out fracture dislocation.", "Case Diagnosis": "Chance Fracture T11", "Diagnosis By": "CT sagittal reconstruction", "Treatment & Follow Up": "This fracture is horizontal through the posterior/middle/anterior vertebrae with minimal displacement (no dislocation) other than the distraction of the posterior elements. These features make this able to be managed non-operatively. Patients are placed in a TLSO (Thoracolumbosacral orthosis) or hyperextension cast.\nPatients will usually wear these for few months and then undergo an extensive rehab.\nIf unstable fracture or body habitus (precludes casting), surgical management is performed.", "Discussion": "The mechanism of Chance fractures is flexion of the thorax on the abdoman, at their junction. They are often associated with seat-belts and more than half the patients may have associated intra-abdominal injuries - especially in childhood.\n\nCT (especially sagittal reconstruction) is especially useful to define the exent and type of fracture well.\n\nMRI is useful in determining cord injury and impingement.\n\nThere is a high incidence of associated intra-abdominal injury (liver and/or splenic laceration, bowel perforation) especially with lap belt etiology. However, in this patient, these complications were not present." }, "Topic": { "Title": "Chance-type fracture", "Disease Discussion": "There are 4 types of thoracolumbar fractures often described. These include compression, burst, Chance (\"seatbelt\"), and fracture-dislocation. \n\nCompression fractures show anterior column compression (anterior vertebral body) with usually no middle or post column involvement. Burst fractures produce anterior and middle column compression (vertebral body and anterior neural arch). Fracture-dislocations involve all three (anterior, middle, and posterior) columns which results in intervertebral subluxation or dislocation.\n\nChance or Chance-type fractures involve the posterior, middle, and occasionally the anterior columns. The injury results from a severe flexion of the spine with the fulcrum not being the the anterior vertebral body as in compression fractures. Instead, the anterior abdominal wall (i.e. where the lap seatbelt fits) is the fulcrum area with hyperflexion at thoraco-lumbar junction (e.g. L1). This creates a distraction force on the posterior and middle columns of the vertebra, creating a horizontal fracture extending posterior to middle. This fracture may then extend anteriorly throught vertebral body (with an assoc compression of anterior body).\n\nChance fracture is an \u201ceponym\u201d, named after G.Q. Chance who described this injury in 1948 as anterior wedging, compression, and a frature through the body, lamina, and spinous process. Because of the mechanisms of injury (flexion over a seat belt) about \u00bd are associated with intra-abdominal trauma.\n\nBurst and fracture dislocations have a high incidence of instability. Chance fractures also have potential for instability although not as likely as the former two. Since radiographs may not clearly demonstrate the exact plane and extent of this fracture, CT (with sagital reconstruction is quite useful). Axial spine CT alone often won't delineate the fracture well due the fracture's horizontal (axial) nature. MRI can help determine cord compression and injury.", "ACR Code": "4.4", "Category": "Trauma", "Keywords": "Chance seat belt hyperflexion spine vertebra", "Reference": "Resnick,D: BONE AND JOINT IMAGING, 2nd Ed. pp 810-813.\nEismont,FJ: Flexion-Distraction Injuries of the Thoracic and Lumbar Spine, SPINE TRAUMA 1998; 402-414." } }, { "U_id": "MPX2428", "TAC": [], "MRI": [ "MPX2428_synpic46470", "MPX2428_synpic46471", "MPX2428_synpic46472", "MPX2428_synpic46473", "MPX2428_synpic46474", "MPX2428_synpic46475", "MPX2428_synpic46476", "MPX2428_synpic46477", "MPX2428_synpic46478", "MPX2428_synpic46479", "MPX2428_synpic46480", "MPX2428_synpic46481" ], "Case": { "Title": "Intradural Extramedullary Meningioma.", "History": "56 yo male with 24 month history of gradually worsening upper back pain.", "Findings": "An intradural extramedullary mass is seen at the T2 level measuring 1.2 cm AP x 1.1 cm transverse x 1.7 cm craniocaudad. This mass causes mild compression and leftward shift of the spinal cord. Subtle hyperintense T2 signal abnormality is noted within the mass, and uniformly enhances following gadolinium DTPA. There is a no dural tail. The spinal cord is normal in signal. No neural foraminal extension is seen.", "Differential Diagnosis": "Intradural Extramedullary Neoplasms:\n\nSchwannoma\nNeurofibroma\nGanglioneuroma\nMeningioma\nEpidermoid\nDermoid\nMetastasis", "Case Diagnosis": "Intradural Extramedullary Meningioma.", "Diagnosis By": "Histologic evaluation confirmed an intradural extramedullary meningioma." }, "Topic": { "Title": "Intradural Extramedullary Meningioma.", "Disease Discussion": "Meningiomas account for approximately of 25% of all spinal tumors. The peak incidence is in the fifth and sixth decades, with more than 80% occurring in women. Ninety percent of spinal meningiomas are intradural, whereas 5% are extradural lesions. The majority occur in the thoracic spine (80%), followed by cervical spine (15%). The lumbar spine is an uncommon location. Most occur lateral to the spinal cord.\n\nSpinal meningiomas are slow-growing neoplasms, and complete tumor removal is achieved in the vast majority of patients. Less than 10% experience tumor recurrence. Aggressive tumors and malignant degeneration are rare. \n\nMR scans clearly depict meningioma extension and relationship to the spinal cord. Most meningiomas are isointense with the spinal cord on T1 weighted images, and may have a slightly higher signal intensity on T2 weighted sequences. Moderate homogeneous enhancement is visualized following contrast administration. Most spinal meningiomas have a broad-based dural attachment, and a dural \u201ctail\u201d is sometimes seen. Occasionally, densely calcified meningiomas are hypointense and show minimal contrast enhancement.", "ACR Code": "3.3", "Category": "Neoplasm, benign", "Keywords": "Spinal MeningiomaIntradural Extramedullary Meningioma", "Reference": "Parsa et al. Spinal cord and intradural-extraparenchymal spinal tumors: current best care practices and strategies. J Neurooncol 2004;69:291.\n\nParizel et al. Gd-DTPA-Enhanced MR Imaging of Spinal Tumors. AJR 1989;152(5):1087.\n\nOsborn, Anne. Diagnostic Neuroradiology. Mosby. St. Louis, Missouri. 1994.\n\nKaplan, Phoebe. Muscculoskeletal MRI. Saunders. Philadelphia, PA. 2001" } }, { "U_id": "MPX2456", "TAC": [], "MRI": [ "MPX2456_synpic54567", "MPX2456_synpic54568", "MPX2456_synpic54570", "MPX2456_synpic54587", "MPX2456_synpic54588", "MPX2456_synpic54589" ], "Case": { "Title": "Enchondroma", "History": "67 year old asymptomatic woman presented for screening chest radiograph.", "Exam": "No physical exam findings", "Findings": "\u2022 Intramedullary \"popcorn-like\" calcifications in the left humeral shaft on the chest radiograph. NOTE: Metallic \"nipple marker\" beads\n\u2022 Followup MRI shows a well-defined intramedullary mass within the proximal left humerus diaphysis. T2 hyperintense matrix with predominantly T1 isointense to slightly hypointense signal. \n\u2022 There is diffuse robust enhancement present. Minimal endosteal scalloping is seen. There is no cortical breakthrough or periosteal reaction to suggest an aggressive lesion. Nor is there surrounding soft tissue component.", "Differential Diagnosis": "\u2022 Enchondroma\n\u2022 Chondrosarcoma\n\u2022 Bone Infarct\n\u2022 Simple bone cyst\n\u2022 Fibrous dysplasia", "Case Diagnosis": "Enchondroma", "Diagnosis By": "Characteristic imaging features and absence of symptoms.", "Treatment & Follow Up": "An enchondroma is a benign lesion. Occasionally, it can be difficult to distinguish between enchondroma and low-grade chondrosarcoma. However, in the absence of pain or other symptoms; and, with characteristic imaging findings - conservative management with observation is appropriate.", "Discussion": "Humeral shaft is a typical location of presentation, although enchondromas most commonly occur in tubular bones of the hands and feet. Imaging features of this lesion are typical, correlating with radiographic pattern of lobulated arcs and rings. Patient presentation is also typical, as these lesions are frequently discovered incidentally on plain radiographs, MRI, and CT scans as was the case with this patient.\n\nThis patient is older than the typical presentation, as these lesions are most commonly seen in patients who are 20-40 years of age. However, they can be seen at any age, and there is no gender or racial predilection. \n\nTypical symptoms include pathologic fracture or bone pain both of which our patient did not have. Often times, patients are asymptomatic. Prognosis is usually benign and cases are managed conservatively. Malignant transformation is extremely rare (<1%) but signs include bone scalloping, cortical thickening, periosteal reaction, bony erosion all of which can be seen on imaging." }, "Topic": { "Title": "Enchondroma", "Disease Discussion": "A benign neoplasm composed of ectopic cartilage rests that have migrated into bones\u2019 metaphysis from the growth plate. Enchondromas are usually singular, but multiple lesions may occur in enchondromatosis syndromes such as Ollier\u2019s, Maffucci\u2019s and metachondromatosis. Enchondromas are a benign finding seen incidentally on plain radiographs MRI, and/or CT while investigating other pathology.\n\nTypically, patients are 20-40 years old when the tumor is identified. The patient with any of the enchondromatosis syndromes is typically younger when the first lesion is identified. There is no gender or racial predilection.\n\nIn the United States, enchondromas account for 12-14% of benign bone neoplasms and 3-10% of osseous neoplasms in general. They are most commonly found in the diaphyses of the hands and feet, and less commonly in the femur, humerus, or tibia. Enchondromas present as small (<5 cm) lytic masses which have a pattern of lobulated arcs and rings indicative of their chondroid matrix. When found in the larger bones, they are usually metaphyseal, centrally located and can have a sclerotic margin.\n\nFrequently plain radiographs are adequate to identify and diagnose enchondromas. Occasionally, further imaging such as CT or MRI may be required to offer a more complete picture of the bone surrounding the tumor. Bone scans are usually ineffective in the diagnosis of enchondromas as typical findings of mildly increased uptake are non-specific.\n\nEnchondromas are benign but can cause pathologic fractures or can rarely progress to chondrosarcoma. This malignant transformation is of concern due to the destructive changes which occur in high grade tumors as well as the 5 year survival rate which is as low as 15% in high grade tumors. \n\nTumors found in the hands and feet have a virtually negligible transformation rate while those seen in the long and flat bones should be monitored more closely for transformation. Transformation to malignancy occurs much more frequently in patients with enchondromatosis. \n\nThe following radiographic changes are suggestive of this transformation to chondrosarcoma:\n\u2022 \tScalloping of the inner surface of the bone\n\u2022 \tThickening of the bone cortex\n\u2022 \tReactive bone growth on the outer surface of the bone\n\u2022 \tErosion surrounded by reactive bone\n\u2022 \tNoticeable growth in the bony erosion\n\u2022 \tMRI may identify cortical extension and extension to the soft tissue mass.\n\nWith the exception of enlarged digits when hands and feet are involved, physical exam of the patient with an enchondroma is usually unremarkable. Pain found on exam is attributable to either adjacent but non-related pathology, pathologic fracture resulting from the enchondroma, or should raise the clinical suspicion for progression to chondrosarcoma.\n\nDifferential diagnosis varies depending on whether calcifications are present. In cases in which they are, bone infarct which may exhibit a serpiginous lining and low grade chondrosarcoma must be considered. If the lesion is purely lytic, however, non-ossifying fibroma, simple bone cyst, fibrous dysplasia, eosinophilic granuloma, and clear cell chondrosarcoma should be considered. \nWhen considering these diagnoses, the following factors are each used to rule out the diagnosis in question:\n\u2022 \tNon-ossifying fibroma \u2013 usually cortically based, enchondromas are medullary based\n\u2022 \tSimple bone cyst \u2013 usually seen before age 20\n\u2022 \tEosinophilic granuloma \u2013 also seen commonly in patients before age 20\n\u2022 \tFibrous dysplasia \u2013 has a ground glass appearance on imaging\n\u2022 \tClear cell chondrosarcoma \u2013 epiphyseally based, with extension into the metaphysis usually seen on MR\n\nWhen asymptomatic, treatment of enchondromas consists of observation. In the patient in whom a pathologic fracture has occurred, the fracture is usually allowed to heal, followed by curettage and filling of the cavity with bone fragments or cement.", "ACR Code": "4.3", "Category": "Neoplasm, benign", "Keywords": "enchodromaollier maffucci metachondromatosisbenign cartilaginous neoplasm tumor", "Reference": "Resnick DR, Diagnosis of Bone and Joint Disorders, 4th edition v4, WB Saunders Company, Philadelphia, PA 2002, pp 3833-3843 \n\nMurphey MD, Flemming DJ, Boyea SR, et al. Enchondroma vs chondrosarcoma in the appendicular skeleton: differentiating features, Radiographics, 1998 Sep-Oct 18(5): pp1213-1237\n\nRobbin MR, Murphey MD, Benign chondroid neoplasms of bone, Semin Musculoskelet Radiol. 2000; 4(1): 45-58" } }, { "U_id": "MPX2460", "TAC": [], "MRI": [ "MPX2460_synpic17266" ], "Case": { "Title": "Sparsely granulated growth hormone adenoma", "History": "This 50 year old woman had a several year history of enlarging hands and decreased visual acuity in her right eye.", "Exam": "She was noted to have coarse facial features with prognathism, skin thickening and very large hands.\n\nVisual field examination disclosed a right nasal quadrantanopsia. The neurological examination was otherwise normal.\n\nEndocrine studies revealed an elevated baseline growth hormone level and normal prolactin.", "Findings": "Fig 1. Coronal CT showing the intrasellar tumor with suprasellar extension. \n\nFig 2. Intraoperative smear prepared from the neoplasm showing sparsely granulated cytoplasm. Also note the occasional intracytoplasmic eosinophilic fibrous bodies, best seen in the very center of the picture.\n\nFig 3. Histological section of the resected neoplasm showing the relatively uniform, sparsely granulated cells. \n\nFig 4. Electron micrograph showing a typical intracytoplasmic body, characteristic of the sparsely granulated growth hormone secreting adenoma.", "Differential Diagnosis": "Sella and suprasellar mass:\n\u2022 pituitary adenoma\n\u2022 pituitary carcinoma or metastasis\n\u2022 craniopharyngioma", "Case Diagnosis": "Sparsely granulated growth hormone adenoma", "Treatment & Follow Up": "CT disclosed a large intrasellar tumor with suprasellar extension more on the left than the right. Surgery was performed." }, "Topic": { "Title": "Sparsely granulated growth hormone adenoma", "Disease Discussion": "About 10 to 20% of pituitary adenomas produce growth hormone and virtually all are functional and produce acromegaly in the adult. Histologically, the tumors may be either heavily or sparsely granulated. The sparsely granulated growth hormone producing adenomas are further characterized by the presence of intracytoplasmic fibrous bodies. These are composed of a compact mass of tangled intermediate filaments that will stain for cytokeratin. The fibrous bodies are virtually diagnostic of the sparsely granulated growth hormone adenomas.", "ACR Code": "-1.-1", "Category": "Unsure", "Keywords": "adenoma" } }, { "U_id": "MPX2469", "TAC": [], "MRI": [ "MPX2469_synpic37216", "MPX2469_synpic37217" ], "Case": { "Title": "Retinal lymphoma, large B-cell type", "History": "62 y.o. man c/o progressive visual problem in his left eye", "Exam": "Visual symptoms:\nDecreased vision in his left eye to hand motions \nNormal vision, right eye\n\nOphthalmic examination:\nLarge yellow choroidal lesions and vitreous cells, left eye", "Findings": "\u2022 T2W MR shows bilateral frontal lobe involvement from a \"butterfly\" lesion in the genu of the corpus callosum\n\n\u2022 Enucleated eye - after vitrectomy w/silicone oil replacement - shows thickening of the posterior retina w/small round blue cells", "Differential Diagnosis": "\u2022 \"Butterfly Lesions\" - Astrocytoma, primary CNS lymphoma, bi-frontal (falcine) meningioma\n\n\n\u2022 Retinal \"blue cell tumor\"\n - Retinal lymphoma\n - Retinoblastoma\n - Chronic (benign) choroidal inflammation\n\n\u2022 Status-post vitrectomy\n - Intraocular silicone oil\n - Cataract\n - Angle closure glaucoma", "Case Diagnosis": "Retinal lymphoma, large B-cell type", "Diagnosis By": "Diagnostic vitrectomy and histopathology", "Treatment & Follow Up": "Diagnostic vitrectomy performed on the left eye in September, 2003. Specimen sent for Laser Scanning Cytometry: \n - \u201cmixed population of T and B lymphocytes with a T:B cell ratio of 1:1\u201d\n - equal populations of CD4+ and CD8+ cells\n - no expression of CD5 or CD10\n - \u201cpolyclonal expression of kappa and lambda\u2026\u201d\n - Cytologic preparation largely inadequate\n\nDecember, 2003: Decreased vision in the right eye\nLeft eye was blind and painful leading to Enucleation of the left eye" }, "Topic": { "Title": "Primary Intraocular Lymphoma", "Disease Discussion": "Primary intraocular lymphoma (PIOL) is a variant of primary central nervous system lymphoma(PCNSL). Initially the disease is confined only to the orbits. If detected early there is typically no evidence of disease in the brain or cerebrospinal fluid.\n\nThe true incidence of PIOL is yet to be defined, though it is thought to be more rare than PCNSL which has an incidence of 1/100,000. The patients at greatest risk of developing both PCNSL and PIOL are immunocompromised individuals. Recent studies suggests a possible underlying infectious etiology such as the presence of human herpesvirus 8 and Epstein-Barr virus. \n\nThe median age of onset is the fifth or sixth decade of life with an age range of 15-85.\nTypically the patients present with slowly worsening blurred vision and/or floaters present in their visual field. The disorder usually is present bilaterally (80%) but often has an asymmetric presentation. Initially most patients are diagnosed with chronic uveitis or posterior uveitis and the true diagnosis may delayed for several years.\n\nPIOL has been shown to be predominantly a B cell lymphoma which accumulate behind the retina producing a characteristic subretinal yellow infiltrate \"mound.\" The vitreous cavity contains a cellular infiltrate composed of neoplastic and reactive inflammatory cells.\n\nThe initial workup includes a chest radiograph, complete blood count, erythrocyte sedimentation rate and blood chemistries. Neuroimaging of the brain and orbits is required along with a lumbar puncture. MRI is not a good modality for revealing PIOL in the orbits. However it is very useful for seeing extensions of the primary tumor into the CNS as seen in this case. Typically the tumor cells can follow the optic nerve into the CNS proper and invade the surrounding structures. Typically, extension into the brain is accompanied by a neurologic deficit.\n\nIn the past the primary treatment of PIOL has been optic radiation. Despite a good clinical response rate of(60-100%) most patients do not opt for radiation due to the associated morbidities. Complications include radiation retinopathy, optic neuropathy, dry eyes, corneal epithelial defects, cataracts, glaucoma and a high incidence of recurrence. \n\nThe mainstay of chemotherapy is intra-vitreous injections of methotrexate. The methotrexate is augmented by a number of other chemotherapuetic agents as listed in the history. Optimal dosing regimens are still being determined in ongoing clinical trials. Many patients do achieve remission only to experience persistent recurrences and eventual CNS involvement.", "ACR Code": "1.3", "Category": "Ophthalmology", "Keywords": "MRICNS LymphomaOrbit", "Reference": "Buggage RR, Chan CC, Nussenblatt RB. Ocular manifestations of central nervous system lymphoma. Curr Opin Oncol 2001, 13(3):137-42\n\nAkpek EK, Ahmed I, Hochberg FH, et al. Intraocular-central nervous system lymphoma: clinical features, diagnosis, outcomes. Ophthalmology 1999, 106:1805-1810\n\nYanoff. Ophthalmology, 1st Ed. Chapt 24, Masquerade syndrome - intraocular lymphoma.\nChan, C.C., Blood, 1999, 93(8):2749-2751.\nBuhring, U. et al., Neurology, 57(3):393-396." } }, { "U_id": "MPX2482", "TAC": [], "MRI": [ "MPX2482_synpic46986", "MPX2482_synpic46987" ], "Case": { "Title": "Canavan Disease", "History": "2 y.o. girl whose parents noted irritability in early neonatal course. This improved by 5 months of age when patient was noted to be hypotonic.\n\nShe was also diagnosed in infancy with cortical blindness and has developmentally delay. Head size noted to be large.", "Exam": "Macrocephay", "Findings": "Diffuse, symmetric involvement of cerebral white matter\nSubcortical white matter preferentially affected early\nNo contrast enhancement\nMRS: Elevation of Naa", "Differential Diagnosis": "Alexander disease\nCanavan disease\nMetachromatic leukodystrophy", "Case Diagnosis": "Canavan Disease", "Diagnosis By": "Imaging and physical exam" }, "Topic": { "Title": "Canavan Disease", "Disease Discussion": "-AR (autosomal recessive)\n-Most common in Ashkenazi Jews\n-Deficiency in aspartoacylase\n-Macrocephaly, seizures\n-Death usually occurs in 2nd year of life\n\nImaging Findings:\n-Diffuse, symmetric involvement of cerebral white matter\n-SC WM preferentially affected early\n-No contrast enhancement\n-MRS: Elevation of NAA\nBoth the NAA to choline (Cho) and NAA to creatine (Cr) ratios are increased, with relatively normal Cho and Cr.\n\nhttp://pubs.rsna.org/doi/full/10.1148/radiol.2411040165\nhttp://www.medscape.com/viewarticle/495645_4", "ACR Code": "1.5", "Category": "Metabolic (see also Toxic)", "Keywords": "DysmyelinatingAlexander diseasemacrocephaly developmental delay blindness", "Reference": "Barkovich AJ. Pediatric Neuroimaging 4th ed. pp79-80." } }, { "U_id": "MPX2485", "TAC": [], "MRI": [ "MPX2485_synpic24204", "MPX2485_synpic24205" ], "Case": { "Title": "Achilles tendon tear", "History": "70 y/o male who felt a \u201cpop\u201d two days prior to presentation and has had pain in region of right Achilles tendon since that time.", "Exam": "Tenderness to palpation in posterior aspect of right ankle", "Findings": "MRI: Proton density without fat sat axial shows medium signal intensity in the region of the Achilles tendon and fat obliteration\nThis medium signal intensity becomes high signal intensity on T2 weighted with fat sat, with extensive edema medial, lateral, and posterior to the tendon\nT1 weighted sagittal reveals complete disruption approximately 5cm above the insertion site into the calcaneus. This disruption approximately 4cm proximally. \n\nSonography: longitudinal image on sonogram in region of Achilles tendon demonstrating heterogeneous echotexture with posttraumatic inflammation and hemorrhage.", "Differential Diagnosis": "Complete Achilles tendon tear", "Case Diagnosis": "Achilles tendon tear", "Treatment & Follow Up": "Treatment for patients with Achilles tendon tears remains controversial. Treatment strategies range from conservative treatment with serial casting to surgical repair. Treatment plan should be individualized to each patient", "Discussion": "): The Achilles tendon is the largest tendon in the body and is formed by the confluence of the gastrocnemius and soleus muscle complexes. The tendon is vulnerable to complete and partial tears. Trauma is involved In the majority of cases of Achilles tendon injury. However, there are many conditions that may weaken the tendon and predispose it to injury. These include degenerative changes, tissue ischemia, floroquinalone use, and systemic diseases such as rheumatoid arthritis, systemic lupus erythematosus, diabetes mellitus, and gout. The stereotypical patient is a middle-aged individual who is out of condition and starts playing a sport. The mechanism of injury is commonly forced dorsiflexion and the patient often reports an audible \u201cpop\u201d. Symptoms include pain, swelling, and weakness of plantar flexion, but often tears are asymptomatic.\n Diagnosis of an Achilles tendon rupture is often made by history and physical examination alone. However, up to 25% of cases can be missed without imaging. Physical exam findings include tenderness in the region of the tendon, positive Thompson test (absent plantar flexion on squeezing of the calf), or a palpable focal cleft at the insertion of the tendon. Imaging diagnosis is made either at MRI or sonography. With MRI, an intact tendon should have low signal intensity in all sequences. Increased intensity in any sequence is consistent with a tear in the tendon or tendonitis. Partial or complete disruption of the fibers is diagnostic for a tear in the tendon. With sonography the intact tendon has homogeneous low-level echoes oriented lengthwise along the tendon. Complete tears are characterized by discontinuity of the tendon, often with fluid in the gap and variable irregular echogenicity of Kager\u2019s fat pad due to hemorrhage and edema. Sonography has been shown to be highly reliable in diagnosing complete tendon rupture, as well as differentiating full from partial-thickness tears. Sonography can be used for diagnosis of both partial and complete tear of the tendon. \n Treatment is controversial and is largely based on the individual patient. Patients who are older, less active, or who are poor surgical candidates are generally treated with serial casting. This non-surgical approach is associated with re-rupture (particularly in the first four weeks after the cast has been removed) and venous thrombosis. Surgical repair is used for young, active patients; however, the prevalence of complications with surgical repair is reported to be 20%." }, "Topic": { "Title": "Achilles tendon tear", "Disease Discussion": "): The Achilles tendon is the largest tendon in the body and is formed by the confluence of the gastrocnemius and soleus muscle complexes. The tendon is vulnerable to complete and partial tears. Trauma is involved In the majority of cases of Achilles tendon injury. However, there are many conditions that may weaken the tendon and predispose it to injury. These include degenerative changes, tissue ischemia, floroquinalone use, and systemic diseases such as rheumatoid arthritis, systemic lupus erythematosus, diabetes mellitus, and gout. The stereotypical patient is a middle-aged individual who is out of condition and starts playing a sport. The mechanism of injury is commonly forced dorsiflexion and the patient often reports an audible \u201cpop\u201d. Symptoms include pain, swelling, and weakness of plantar flexion, but often tears are asymptomatic.\n Diagnosis of an Achilles tendon rupture is often made by history and physical examination alone. However, up to 25% of cases can be missed without imaging. Physical exam findings include tenderness in the region of the tendon, positive Thompson test (absent plantar flexion on squeezing of the calf), or a palpable focal cleft at the insertion of the tendon. Imaging diagnosis is made with either MRI or sonography. With MRI, an intact tendon should have low signal intensity in all sequences. Increased intensity in any sequence is consistent with a tear in the tendon or tendonitis. Partial or complete disruption of the fibers is diagnostic for a tear in the tendon. With sonography the intact tendon has homogeneous low-level echoes oriented lengthwise along the tendon. Complete tears are characterized by discontinuity of the tendon, often with fluid in the gap and variable irregular echogenicity of Kaeger\u2019s fat pad due to hemorrhage and edema. Ultrasound has been shown to be highly reliable in diagnosing complete tendon rupture, as well as differentiating full from partial-thickness tears. Ultrasound can be used for diagnosis of both partial and complete tear of the tendon. \n Treatment is controversial and is largely based on the individual patient. Patients who are older, less active, or who are poor surgical candidates are generally treated with serial casting. This non-surgical approach is associated with re-rupture (particularly in the first four weeks after the cast has been removed) and venous thrombosis. Surgical repair is suited for young, active patients; however, the incidence of complications with surgical repair is reported to be 20%.", "ACR Code": "4.4", "Category": "Trauma", "Keywords": "Achilles tendon tearAchillestendon tear", "Reference": "Stoller, David. Magnetic Resonance Imaging in Orthopedics and Sports Medicine. Lippincott Philadelphia, PA. 1997. pgs 448-461\n Lisa Dwornic, L M Lomansey, Terrence D Demos, L A Lavery. Orthopedics. Thorofare: Nov 2002. Vol 25: 1318-1320\n Hartgerinc et al. Full versus partial thickness Achilles tendon tears: sonographic accuracy and characterization in 26 cases with surgical correlation. Radiology 2001. vol 220: 406-412" } }, { "U_id": "MPX2497", "TAC": [], "MRI": [ "MPX2497_synpic11130", "MPX2497_synpic11131", "MPX2497_synpic11132", "MPX2497_synpic11133", "MPX2497_synpic11134" ], "Case": { "Title": "Medulloblastoma confirmed by pathology.", "History": "4 year old male with increasing ataxia over a one month period.", "Findings": "Sagittal and coronal T1, axial T2, and axial T1 post gadolinium images demonstrate a large enhancing mass in the posterior fossa with aossociated hydrocephalus.\n\nSagittal T1 weighted image post gadolinium of the spine demonstrated enhancing drop metastasis along the meninges of the distal spinal cord.", "Differential Diagnosis": "Ependymoma, malignant astrocytoma\nCSF dissemination (carcinomatous meningitis)", "Case Diagnosis": "Medulloblastoma confirmed by pathology." }, "Topic": { "Title": "Medulloblastoma", "Disease Discussion": "Between the ages of 2-5 and 12-15, intracranial neoplasms in children are most commonly located in the posterior fossa. Medulloblastoma (PNET - Primitive Neuroectodermal Tumors) and cerebellar astrocytomas account for two thirds of these neoplasms, and the remaining one-third are divided between ependymoma and brainstem glioma (usually astrocytoma).\n\nMedulloblastomas in children orignate most commonly from the vermis. They exhibit rapid growth, and frequently lead to hydocephalus. These tumors have a tendency to spread via the subarachnoid spaces. Up to 50% of patients will have CSF metastases at the time of diagnosis. These can be found within the ventricular system and in the thecal sac of the spinal canal. It is imperative that MR evaluation ot the spinal canal with gadolinium be performed prior to surgery. Metastases appear as brightly enhancing foci studding the meninges. After surgery, postoperative changes may become enhanced and might be indistinguishable from metastases. Systemic metastases also occur, with the skeleton being the most common site. Skeletal metastases may be desmoplastic and sclerotic. The 5 year survival rate is 50% - 86% with combination chemo-radiation therapy.\n\nOn CT, medulloblastomas are ususally midline, solid hyperdense masses. Small (< 10mm) cystic changes can be seen in up to 50 percent, and calcification occurs in up to 20 %. Hydrocephalus is present in 90 %. On MRI, they are usually hypointense to gray mattter on T1, and on T2 their appearance is variable. CSF seeding is seen in 30%. This tumor commonly and typically enhances intensely with both CT and MR contrast.", "ACR Code": "1.3", "Category": "Neoplasm, metastatic", "Keywords": "medulloblastomaPosterior fossa tumorCSF metastasis", "Reference": "Grossman, R and Yousem, D: Neuroradiology-The Requisites, St. Louis, 1994, Mosby. p 85\n\nBrant, W and Helms, C: Fundamentals of Diagnostic Radiology. 2nd Ed Lippincott: Philadelphia 1999. pp121-122" } }, { "U_id": "MPX2502", "TAC": [], "MRI": [ "MPX2502_synpic24909", "MPX2502_synpic24910" ], "Case": { "Title": "Stress fracture right femoral neck.", "History": "21 year old female with right hip pain after recent increase in physical activity.", "Exam": "Patient\u2019s chart unavailable for review", "Findings": "A-P radiograph of the hips shows no apparent fracture\nFollow-up A-P radiograph of the hips shows a sclerotic line in inferior aspect of the femoral neck consistent with a healing stress fracture.\nMRI- T1 weighted images showing linear hypointensity at the inferior aspect of the right femoral neck with consistent with a stress fracture. This area became high signal intensity on STIR MR images.", "Differential Diagnosis": "Stress fracture right femoral neck", "Case Diagnosis": "Stress fracture right femoral neck.", "Treatment & Follow Up": "Patient underwent closed reduction internal fixation of right femoral neck. Post-reduction films for this patient revealed three intertrochanteric screws and good alignment of the bony tissues.", "Discussion": "Stress fractures occur as a result of repetitive submaximal stress on normal bone, which results in a region of bone undergoing accelerated bone remodeling. This in turn can lead to microtrabecular breaks and ultimate cortical injury as the rate of osteoclast activity exceeds the rate of new bone formation. Two types of femoral neck stress fractures have been identified in adolescents/young adults-transverse fractures to the superior portion of the femoral neck, and compression fractures to the inferior portion of the femoral neck. Management of the more proximal fracture is with closed reduction and internal fixation. Initially, conservative therapy (non-weight bearing, reduction of physical activity) can be attempted for stress fractures involving the distal femoral neck, but failure of conservative therapy or delay in diagnosis will also lead to surgical intervention." }, "Topic": { "Title": "Stress fracture right femoral neck.", "Disease Discussion": "Stress fractures occur as a result of repetitive submaximal stress on normal bone, which results in a region of bone undergoing accelerated bone remodeling. This in turn can lead to microtrabecular breaks and ultimate cortical injury as the rate of osteoclast activity exceeds the rate of new bone formation. Two types of femoral neck stress fractures have been identified in adolescents/young adults-transverse fractures to the superior portion of the femoral neck, and compression fractures to the inferior portion of the femoral neck. Management of the more proximal fracture is with closed reduction and internal fixation. Initially, conservative therapy (non-weight bearing, reduction of physical activity) can be attempted for stress fractures involving the distal femoral neck, but failure of conservative therapy or delay in diagnosis will also lead to surgical intervention.", "ACR Code": "4.4", "Category": "Trauma", "Keywords": "Stress fracture right femoral neckfemoral neck", "Reference": "Browner: Skeletal Trauma: Basic Science, Management, and Reconstruction, 3rd ed.\nCanale: Campbell's Operative Orthopaedics, 10th ed. \nBencardino JT. Imaging of hip disorders in athletes. Radiol Clin North Am. 01-MAR-2002; 40(2): 267-87, vi-vii" } }, { "U_id": "MPX2514", "TAC": [], "MRI": [ "MPX2514_synpic19027", "MPX2514_synpic19028" ], "Case": { "Title": "L5-S1 disk herniation with sequestered disk material in the spinal canal, compressing the cauda equina and causing myelopathic symptoms", "History": "Patient heard his lower back \"pop\" during exercise. Within a few hours, he developed decreased sensation in his groin and urinary incontinence.", "Exam": "Decreased perineal sensation.", "Findings": "Image 1 is a sagittal T2 weighted MRI of the lumbar spine demonstrating a low signal structure compressing the cauda equina posterior to the superior sacrum\nImage 2 is an axial T-2 weighted image at the level upper sacrum demonstrating the low signal structure in the axial plane\nImage 3 is the same axial image with arrows pointing out the pertinent finding\nImage 4 is a magnified view of the sagittal image with arrows \nImage 5 demonstrates the utility of the cross-referencing function of a PACS.", "Differential Diagnosis": "L5-S1 Disk extrusion/sequestered disk with compression of cauda equina\n\nOther extradural spinal lesions, much less likely in light of patient's history:\nSpinal canal meningioma\nSpinal canal schwannoma\nSpinal canal neurofibroma\nChordoma\nDural or extradural metastatic disease (e.g. lymphoma)\nSpinal AVM\nOsteochondroma", "Case Diagnosis": "L5-S1 disk herniation with sequestered disk material in the spinal canal, compressing the cauda equina and causing myelopathic symptoms", "Diagnosis By": "The MRI morphology and signal characteristics of the lesion and the patient's history of hearing his back \"pop\" during exercise followed by the acute onset of perineal hypesthesia and urinary incontinence, essentially excludes all other diagnostic possibilities", "Treatment & Follow Up": "Neurosurgical extraction of the sequestered disk", "Discussion": "To define the disk material as sequestered (free fragment within the spinal canal) required the demonstration that the fragment was not contiguous with the parent disk. Scrolling through the images in the sagittal and axial planes revealed that the extruded disk material was, indeed, not attached to the parent disk." }, "Topic": { "Title": "Intervertebral Disk Herniation", "Disease Discussion": "Degenerative disk disease may be accompanied by disk herniation.\nDisk herniations may occur in the cervical, thoracic, or lumbar spine. Lower lumbar disk herniation is a particularly common clinical problem. Herniation is a localized displacement of disk material through a defect or tear in the annulus fibrosis. The protruding or extruded material is typically comprised of nucleus pulposus but may also include annular tissue, fragmented bone, or cartilage. Disk herniations can cause localized pain arising from nerve endings in the annular fibers at the location of the herniation. Disk herniations also commonly cause radicular symptoms due to compression of spinal nerve roots exiting the neuroforamen at the level of the herniation or by compression of nerve roots traversing the spinal canal to exit at lower levels. Myelopathic symptoms occur if the herniated disk material compresses the spinal cord sufficiently to interfere with normal cord function.\n\nThe disk space is defined cranio-caudally by the vertebral body endplates and peripherally by the outer edges of the vertebral body ring apophyses (excluding osteophytes). In the axial plane, a \"localized\" disk herniation is limited to 25% or less of the disk circumference. \"Broad based\" refers to disk herniations between 25% to 50% of the disk circcumference. \"Concentric broad based disk bulge\" refers to a concentric bulge of the disk occupying greater than 50% of the disk circumference. Herniations may be described as \"protusions\" or \"extrusions.\" Protusion implies that the widest dimension of the protruded material is less than the width of the separation in the annular fibers at the neck of the protusion. Extrusion implies that the widest dimension of extruded material exceeds the width of the annular fiber tear at the neck of the protusion. A \"sequestered disk\" is a free fragment of extruded disk material which is no longer in continuity with the disk material within the disk space. A free fragment can migrate to any location and lodge above or below the disk space and in rare instances can transgress the dura and lie intradurally. \n\nThe diagnosis of disk herniation can be made by MR or CT. On MR the presence of disk material may be seen extending beyond the confines of the disk space. The disk material may be seen circumferentially bulging or focally protruding or extruding and compressing the thecal sac or nerve roots. This can be demonstrated in the axial or sagittal planes, and, if detected, should be confirmed in the other plane. In general, the herniated disk material should have similar intensity or density to the parent disk. On MR, this is not always the case, depending on the state of hydration of the parent disk and the fragment and the particular pulse sequence used. [1]\n\nTreatment of disk herniation depends upon the level of the herniation, the severity of the herniation, and the nature of the symptoms it produces. Treatment ranges from very conservative therapies (e.g. bedrest, NSAIDs, analgesics, physical therapy) to minimally invasive therapies (e.g. steroid/analgesic epidural injections) to fully invasive surgical procedures (e.g. laminectomy, discectomy, vertebral body fusions.) Surgical interventions are typically reserved for patients who have failed conservative treatment, who have intractable pain, or who have significant neurological symptoms resulting directly from the herniation.", "ACR Code": "3.9", "Category": "Degenerative Disease", "Keywords": "disk herniationdisk protrusiondisk extrusion", "Reference": "Grossman R and Yousem D. (2003) Neuroradiology: The Requisites, 2nd Ed. Philadelphia: Mosby." } }, { "U_id": "MPX2521", "TAC": [], "MRI": [ "MPX2521_synpic52391", "MPX2521_synpic52392", "MPX2521_synpic52393", "MPX2521_synpic52394" ], "Case": { "Title": "Ulnar Collateral Ligament Tear, Stener Lesion", "History": "28yo male with no significant PMH presents with CC of \"sprained right thumb.\"", "Findings": "retracted ulnar collateral ligament with aponeurosis interposed between ligament and attachment site", "Differential Diagnosis": "Extensor tendon rupture\nFracture", "Case Diagnosis": "Ulnar Collateral Ligament Tear, Stener Lesion", "Diagnosis By": "MRI", "Treatment & Follow Up": "If stable, incomplete tear, then splinting or short arm cast. But this is unstable. If less than 3 weeks old, and/or Stener's lesion present, then surgical ligament fixation. If older than 3 weeks and non-healing, then consider surgical repair." }, "Topic": { "Title": "Ulnar Collateral Ligament Tear, Stener Lesion", "Disease Discussion": "Ulnar collateral ligament tears, also known as UCL rupture or gamekeeper's thumb, involves disruption of the UCL of the first metacarpophalangeal joint; it is often associated with proximal phalanx base fracture. The majority of the ruptures occur distally. Stener's lesion accounts for 50% of the complete tears and frequently found in skiers. \n\nThe mechanism involves forced abduction of the thumb causing hyperextension of the UCL. Displacement of the UCL proximal and superficial to the adductor pollicis aponeurosis is the Stener's lesion. An avulsed bone fragment or volar subluxation may also be seen. Localized joint pain is the common complaint. \n\nClassified as partial or complete tears (types I-III).\n\nMRI: T1-weighted or T2*-weighted coronal images show edema, thickening, disruption, displacement, or entrapment of the UCL, with the key sign being discontinuity of the UCL to the proximal phalanx. With the Stener's lesion, other findings may be: retracted mass of UCL, UCL trapped superficially or intersecting the adductor aponeurosis, gross displacement of the UCL medial to the aponeurosis, or \"yo-yo on a string\" appearance of a retracted and balled up UCL.\n\nUCL tears and Stener's lesions require coronal images through the first metacarpophalangeal joint acquired parallel to the plane of the collateral ligaments.\n\nRetracted UCL is seen with folded or horizontally directed fibers in Stener's lesion, which is defined by entrapment of the UCL by adductor pollicis aponeurosis.", "ACR Code": "4.4", "Category": "Sports Medicine", "Keywords": "ulnar collateral ligamentstener's lesiongamekeeper's thumb", "Reference": "http://www.wheelessonline.com/ortho/gamekeepers_thumb\nhttp://emedicine.medscape.com/article/97679-overview\nEssentials of Musculoskeletal Care, 3rd Edition\nMagnetic Resonance Imaging in Orthopaedics and Sports Medicine" } }, { "U_id": "MPX2527", "TAC": [], "MRI": [ "MPX2527_synpic20891", "MPX2527_synpic20892", "MPX2527_synpic20893", "MPX2527_synpic20894" ], "Case": { "Title": "macrodystrophia lipomatosa", "History": "enlarged finger for several years.", "Exam": "enlarged left index finger. otherwise normal exam", "Findings": "enlarged left index finger. There is diffuse fatty enlargement of the volar soft tissues with normal osseous structures and tendons.", "Differential Diagnosis": "macrodystrophia lipomatosa, neurofibromatosis, macrodactyly", "Case Diagnosis": "macrodystrophia lipomatosa", "Diagnosis By": "pathognomonic", "Treatment & Follow Up": "none", "Discussion": "neurofibromatosis will have usually have other body structures involved\nmacrodactyly will have enlargement of the bone, tendons, and fat\nmacrodystrophia lipomatosa typically is a non-heritable form of digit enlargement (usually solitary nerve or ray distributiuon) characterized by fatty overgrowth (especially distally)\nET call home!!!!" }, "Topic": { "Title": "Macrodystrophia lipomatosa", "Disease Discussion": "Macrodystrophia Lipomatosa produces enlargement of a ray (or sometimes multiple rays in a single nerve distribution). This overgrowth typically affects the more distal and volar aspects of the digit. Typically there is overgrowth of the bones and subcutaneous fatty hypertrophy. The enlarged ray is subject to premature osteoarthritis. The nerve may be enlarged and there may be an associated fibrolipomatous hamartoma. The hand is more commonly involved than the foot. This presents at birth but the growth may accelerate during the prepubescent years. Growth stops at puberty. It is non-inheritable. \n\nThe differential of an enlarged digit includes: neurofibromatosis type II (NF II), macrodactyly, juvenile rheumatoid arthritis, hemangioma, and osteoid osteoma. NF II typically has other findings of NF II and a lack of subcutaneous fatty hypertrophy while macrodactyly has an increase in all bony and soft tissue elements of the ray but lack of metacarpal/metatarsal involvement.", "ACR Code": "4.9", "Category": "Congenital, malformation", "Keywords": "macrodystrophialipomatosa", "Reference": "Mucsculoskeletal Imaging--A Teaching File\nChew, Felix et al\n1999\nLippincott" } }, { "U_id": "MPX2528", "TAC": [], "MRI": [ "MPX2528_synpic16720", "MPX2528_synpic16721", "MPX2528_synpic16722", "MPX2528_synpic16723", "MPX2528_synpic16724" ], "Case": { "Title": "MYXOID LIPOSARCOMA", "History": "34-year-old male with self-palpated slowly growing right thigh mass just above the knee. Mass painful with percussion.", "Exam": "The patient is a well-developed, muscular, well-nourished white man in no apparent distress. There is a palpable mass of the distal right anterior thigh. He weighs 214# and is 5'11\" tall. There is no palpable lymphadenopathy in the neck, supraclavicular, or axillary areas.", "Findings": "PLAIN RADIOGRAPH: A-P and lateral views of the right femur from 7/9/2002 demonstrate no bone abnormalities. No soft tissue abnormalities are evident. MRI: A right rectus femoris mass measuring 4.5x2.4x2.5cm shows intermediate- signal intensity periphery with low-signal-intensity center on T1-weighted MR images and predominantly high signal intensity mass on T2-weighted MR image with low-signal-intensity septae posteriorly. After contrast-enhancement, there is a thick rim of peripheral enhancement with non-enhancing areas centrally. These findings were consistent with a myxoid liposarcoma.", "Differential Diagnosis": "Myxoid liposarcoma, Myxoid malignant fibrous histiocytoma", "Case Diagnosis": "MYXOID LIPOSARCOMA", "Treatment & Follow Up": "Excisional biopsy of soft tissue mass was performed. Gross specimens consisted of one ovoid fragment of tan/pink, rubbery, glistening tissue measuring 5.1 x 3.3 x 1.5 cm. The specimen grossly appears to be enveloped by a tan/pink fibrous tissue capsule, which is focally disrupted in one area. The specimen is inked and serially sectioned to reveal homogeneous tan/pink, rubbery, glistening, cut surface. Histology showed positive margins. There were lobules of myxoid change, an \"alveolar\" or \"pulmonary edema\"-like pattern, delicate plexiform (Y-shaped) capillaries, and multiple small lipoblasts (many bi or uni-vacuolated, some multivacuolated. One month later, because of the positive margins, the patient underwent resection of the excision site (margins negative for residual sarcoma) followed by radiation therapy.Follow-up (5 months after second resection), follow-up contrast-enhanced CT of the chest, abdomen and pelvis showed no metastases. The MR image of the right femur showed interval resection of the previously noted intramuscular mass along with the mid-to-lower portions of the rectus femoris muscle, with a new tubular fluid collection in the surgical bed, probably representing a postoperative hygroma. Close interval MR follow-up of this area was recommended. The Physical Exam demonstrated a 20cm scar in the anterolateral right thigh from just above the knee to just below the groin. Therwas a soft tissue defect in the area of the resection." }, "Topic": { "Title": "MYXOID LIPOSARCOMA", "Disease Discussion": "Liposarcoma is second only to malignant fibrous histiocytoma as the most common malignant tumor of soft tissue. It occurs in both sexes with equal frequency and usually after the age of 40 years. It is found most often in the extremities. Pain is a late symptom related to the increasing mass size. Often the tumor grows slowly, but an occasional anaplastic tumor may grow rapidly. Physical examination reveals a mass with boundaries that may be ill defined. (Canale: Campbell's Operative Orthopaedics, 10th ed., Mosby, Inc 2003.). On radiographs, the presence of radiolucent fat in liposarcomas suggests a more differentiated form whereas soft tissue density is more consistent with more aggressive forms. (Reznick: Diagnosis of Bone and Joint Disorders, 4th ed. W.B. Saunders Co. 2002). On T1-weighted MR images, differentiatied liposarcomas show extensive areas of high signal intensity consistent with their fat content. Areas of low signal intensity and septae in lipomatous tumors suggest more aggressive lesions. On T2-weighted MR images with fat saturation, less differentiated liposarcomas show areas of high signal intensity whereas the differentiated fat is low signal intensity. Contrast-enhanced MRI shows enhancement of the more malignant regions of the liposarcoma. At MRI, the myxoid areas of myxoid liposarcoma characteristically show high signal intensity areas on T2-weighted images that do not enhance after contrast. (Shapeero: Dynamic contrast-enhanced MR imaging for soft tissue sarcomas. in Seminars in Musculoskeletal Radiology, Vol.3 No.2, 1999) At gross pathology, liposarcomas are large and lobulated and many are encapsulated. At histology, liposarcomas are divided into well-differentiated, myxoid, round cell, pleomorphic and dedifferentiated subtypes varying from the low-grade malignant type (well-differentiated) to myoid subtype of intermediate grade and the pleomorphic, round cell, and dedifferentiated of higher grades. Metastases occurs in approximately 50% of patients and 5-year survival rate of approximately 60%.", "ACR Code": "-1.-1", "Category": "Neoplasm, malignant (NOS)", "Keywords": "LIPOSARCOMA", "Reference": "See discussion" } }, { "U_id": "MPX2532", "TAC": [], "MRI": [ "MPX2532_synpic23154", "MPX2532_synpic23156", "MPX2532_synpic23157" ], "Case": { "Title": "Cavernous Malformation (preferred name)", "History": "Not reported by author.\n\nHowever, patient's with studies similar to the one presented for review here can present with headache or seizures", "Exam": "Not reported by author.", "Findings": "Multiple axial MR images demonstrate a lesion in the right cerebellar hemisphere which has a dark outer margin on all sequences. The remainder of the lesion has a coarsely heterogeneous signal intensity on the T1 sequence. The T2 bright signal within this lesion shows a characteristic \"popcorn\" like configuration. Axial GRE image demonstrates magnetic susceptibility \"blooming.\"", "Differential Diagnosis": "\u2022 Cavernous Malformation (a.k.a. Cavernous Angioma, Cavernous Hemangioma, Cavernoma)\n\u2022 Hemorrhagic Metastasis", "Case Diagnosis": "Cavernous Malformation (preferred name)", "Diagnosis By": "The MRI appearance of this entity is nearly pathomnemonic.", "Treatment & Follow Up": "In most cases treatement is comprised of medical management of symptoms.\nRadiosurgery is an option for lesions not associate with venous angiomas (which subserve normal brain). \nSurgerical resection is indicated for severe lesions.", "Discussion": "The internal portion of the lesion contains intravascular lacunes of stagnant or slow flowing blood and extravascular blood products in various stages of degradation. The dark outer ring that is most prominent on the gradient sequence is due to hemosiderin." }, "Topic": { "Title": "Cavernous Malformation (Cavernous Angioma)", "Disease Discussion": "Cavernous Angiomas make up approximately 10-15% of vascular malformations of the brain. They consist of large sinusoidal vascular spaces which lack normal endothelial tight juctions. As a result, bleeding is frequent. The majority of bleeds from these lesions, however, are subclinical with nearly 100% demonstrating hemosiderin staining of the adjacent parenchyma at diagnosis. There is a 0.5-1% incidence of symptomatic hemmorhage/year. The most common clinical presentation as a result of hemmorhage is the development of seizures or progressive neurologic deficits, with a seizure disorder being the presenting symptom in approximately 50% of patients with cavernous angiomas. The degree to which a lesion is symptomatic is,like most CNS abnormalities, dependent on location. Brainstem lesions tend to present earlier with neurologic deficits.\n\nCavernous angiomas may occur anywhere within the CNS with roughly 3/4 occurring supratentorially, 1/4 within the posterior fossa and brainstem, and occasional lesions within the spinal cord. While the occurrence may be sporadic, there is a strong familial association identified where close to 80% of members of affected families may demonstrate lesions. In about 50% of patients the lesions will be multiple. Whenever more than one cavernous malformation is identified in the CNS, there is probably an autosomal dominant inheritence. This should prompt an evaluation of all first-degree relatives.\n\nImaging findings are related to the degree of prior hemmorhage of the lesions. On CT, these lesions may be heavily calcified. MR often demonstrates blood products of various ages centrally and a rim of hemosiderin peripherally. Gradient-echo images may be helpful in identification of small lesions secondary to the gradient suseptibility or characteristic \"blooming\" artifact produced by hemosiderin. Following contrast administration, on either CT or MR, variable enhancement may occur.", "ACR Code": "1.3", "Category": "Vascular", "Keywords": "cavernous angiomacavernoma", "External Links": "rad.usuhs.mil/rad/home/vascmalf/malf0.html" } }, { "U_id": "MPX2557", "TAC": [], "MRI": [ "MPX2557_synpic17083", "MPX2557_synpic17084", "MPX2557_synpic17085", "MPX2557_synpic17086" ], "Case": { "Title": "Avascular necrosis (AVN) of femoral heads bilaterally", "History": "27 y.o. woman presents with L hip/groin that is exacerbated by activity and gradually worsening over several months but more so over last 2 weeks; denies red/hot/swollen L hip, trauma, recent increases in activity level, pain worse at night, recent illness, fevers/ chills/night sweats, new sexual contacts, or vesicular rash. She has a history of SLE and corticosteroid use.", "Exam": "Vital signs stable, well nourished, well developed, and no acute distress; exam remarkable for local tenderness to palpation at L hip; mildly reduced range of motion (ROM) in L hip; mild pain with passive ROM; moderate pain with active ROM; no erythema, edema, or swelling; no weakness or sensorimotor deficit; no rash. CBC and BMP were normal, +ANA, + APA, ESR 72.", "Findings": "1. AP and lateral radiographs show a C-shaped area of sclerosis \n2. T1W coronal MR image - shows focal area of low signal intensity in the R femoral head consistent with edema; also shows focal area of high signal intensity in the L femoral head surrounded by low signal intensity margin consistent with central fat and peripheral circumferential edema of the head and extension of the edema to the meta-diaphysis; additionally, there is evidence of a focal depression of the L femoral head and irregular L femoral epiphysis. \n3. FSE T2W with fat-sat coronal MR image \u2013 shows high signal intensity of edema in the R femoral head; also shows high signal intensity of edema surrounding the low signal intensity fat of the L femoral head with extension to the L femoral diaphysis 4. FSE proton density with fat-sat sagittal MR image - no collapse evident", "Differential Diagnosis": "Nearly pathognomonic for AVN", "Case Diagnosis": "Avascular necrosis (AVN) of femoral heads bilaterally", "Diagnosis By": "Characteristic imaging", "Treatment & Follow Up": "Rest, analgesiscs, limited weight-bearing, orthopedic referral for further evaluation (core decompression vs. osteotomy vs. arthroplasty)" }, "Topic": { "Title": "Avascular necrosis (AVN) of femoral heads bilaterally", "Disease Discussion": "Avascular necrosis (AKA osteonecrosis or aseptic/ischemic necrosis) is an incompletely understood pathology of bone arising from numerous etiologies whose commonality is compromised vasculature leading to loss of perfusion, tissue death (bone and marrow), and ultimately, to mechanical failure.\n\nEtiologies are numerous and include SLE (particularly if patient is APA+ and using corticosteroids; although primary lupus vasculitis can cause AVN), corticosteroid use (particularly over 20mg/day), alcoholism, trauma, hypercoagulability (such as from malignancy or FacV Leiden deficiency), HIV, and dysbaric injury seen in deep-water divers.\n\nPresentation commonly involves weight-bearing and movement-related pain (particularly with internal rotation and abduction), but up to 2/3 of pts also have rest pain, 1/3 have night pain, and a few are asymptomatic. Diagnosis is made through imaging, with MRI being the preferred modality secondary to much greater sensitivity than plain radiographs or CT; bone scans can be done when MRI is not available.\n\nPrior to MRI, AVN was staged according to Ficat staging on bone scans combined with conventional radiographs as follows: stage 0 shows only histopathological abnormalities (no radiographic findings); stage 1 shows an area of increased or decreased/absent radiopharmaceutical uptake on bone scan; stage 2 shows a sclerotic focus with osteopenic ring on radiographs or CT; stage 3 shows the typical \u2018crescent sign\u2019 of subchondral lucency; and stage 4 shows articular collapse with flattening of the femoral head and secondary osteoarthritic change. \n\nTreatment options include conservative medical management (rest, limited wt bearing, analgesics), joint replacement (arthroplasty), core decompression, and osteotomy. Current recommendations include core decompression for stage 0 to early stage 2, osteotomy for late stage 2 to stage 3, and total hip replacement for stage 4.", "ACR Code": "4.5", "Category": "Infarction and/or Necrosis", "Keywords": "AVNAvascular necrosis", "Reference": "1.\tDonahue JP. Osteonecrosis, Up To Date Online, Jul 2003. \n2.\tShapeero LG. Imaging of systemic lupus erythematosus. In Lahita, R. Systemic Lupus Erythematosus, 4th ed. Elsevier, 2004\n3.\tFunaki, B. Avascular Necrosis Staging, http://chorus.rad.mcw.edu/doc/01190.htm, 3-14-01\n4.\tResnick, D. Diagnosis Of Bone And Joint Disorders, WB Saunders, 1995, p3497." } }, { "U_id": "MPX2554", "TAC": [], "MRI": [ "MPX2554_synpic46958", "MPX2554_synpic46959", "MPX2554_synpic46960", "MPX2554_synpic46961", "MPX2554_synpic46962", "MPX2554_synpic46963" ], "Case": { "Title": "Autosomal Recessive Polycystic Kidney Disease", "History": "2 day old male with abdominal distention.", "Findings": "AP radiograph of the chest and abdomen demonstrates hypoinflated lungs, with a markedly distended abdomen.\nAP radiograph of the chest and abdomen demonstrates centrally placed loops of bowel, with prominent hepatic and renal shadows.\nCross table lateral radiograph demonstrates anteriorly displaced loops of bowel with a posterior abdominal mass. Hypoinflated lung volumes are also seen.\nLongitudal sonographic image through the right lobe of the liver reveals periportal heterogeneity, consistent with early hepatic fibrosis. No hepatic masses are seen. An enlarged hyperechoic right kidney is partially shown with loss of the corticomedullary differentiation.\nSonographic images through the kidneys reveals enlarged hyperechoic kidneys with loss of the corticomedullary differentiation. The right kidney measuring 16.6 cm and the left kidney measures 18.5 cm in greatest dimension.\nMR images through the kidneys demonstrates a morphologically abnormal and markedly enlarged right kidney. The patient is status-post left nephrectomy. Mild hepatosplenomegaly is also seen.", "Differential Diagnosis": "DDx of AP radiographs of the abdomen.\n\nNeonatal Ascites...Biliary Ascites (Perforation of Bile Duct), Urinary Ascites (Intraperitoneal bladder, ureteric, or upper tract perforation/ Posterior Urethral Valves), Chylous Ascites (congenital lymphatic abnormality)\n\nNeonatal Abdominal Mass....Renal (Multicystic Dysplastic Kidney, Hydronephrosis, Polycystic Disease, Posterior Urethral Valves, Renal Vein Thrombosis (dehydration/hemoconcentration, Mesoblastic Nephroma)), Adrenal Masses (Hemorrhage, Neuroblastoma), Liver (Cysts, Hepatoblastoma, Hemangioendothelioma, Mesenchymal hamartoma, Metastatic Disease), Choledochal cyst, Duplication of GI Tract, Pelvic and Genital Tract (Ovarian Cysts, Hydrometrocolpos, Distended Bladder, Teratoma, Anterior Meningomyelocele)", "Case Diagnosis": "Autosomal Recessive Polycystic Kidney Disease", "Diagnosis By": "Biopsy and surgical resection of the left kidney.", "Treatment & Follow Up": "The patient is currently status-post right renal transplantation and is undergoing work-up for liver transplant.\n\nIt is important to remember that in utero, severe renal disease is accompanied by oligohydramnios from decreased fetal urine production, with resultant pulmonary hypoplasia. In the neonatal period, patients are prone to pneumothorax, and may have associated VACTERL (Vertebral anomalies, Anal atresia, Cardiovascular anomalies, Tracheoesophageal fistula, Esophageal atresia, Renal and Limb anomalies) syndrome in conjunction with Potter facies (hypertelorism, epicanthus, low set ears, etc.)." }, "Topic": { "Title": "Autosomal Recessive Polycystic Kidney Disease", "Disease Discussion": "Lesions/Condition: Autosomal Recessive Polycystic Kidney Disease\n\nDiscussion: \n\nAutosomal recessive polycystic kidney disease (ARPKD) is a disease of tubular ectasia and fibrosis, affecting both the kidneys and liver, presenting in infancy and childhood. The frequency has been reported as between one in 6,000 and one in 55,000 births, and the gene responsible for ARPKD has been linked to the short arm of chromosome 6. \n\nIn the kidney, ARPKD manifests as nonobstructive collecting duct ectasia. Usually affecting both kidneys, the kidneys are enlarged, and the collecting ducts are dilated, elongated, and fibrosis develops in the renal interstitium. Clinically, this is manifested as hypertension, diminished urinary concentrating ability, and renal insufficiency and/or failure requiring dialysis or renal transplantation. Severe renal disease predominates in the very young infant, and may be seen in utero accompanied by oligohydramnios from decreased fetal urine production, with resultant pulmonary hypoplasia, and many infants die shortly after birth. For those patients with mild renal involvement most will develop some degree of renal insufficiency, and some will progress to renal failure.\n\nLiver disease is inevitably found in patients with ARPKD, with variable severity, involving the bile ducts and portal tracts. The bile ducts are abnormally formed, increased in number, and dilated, and the portal tracts are enlarged and fibrotic. This pattern is known as congenital hepatic fibrosis, and is always present in ARPKD, although is not by itself diagnostic of the disease. Generally, the liver is not enlarged, the hepatic parenchyma is normal, and there is normal hepatocellular function. The hepatic involvement is progressive, with patients commonly presenting between the ages of 5 and 13 years with resultant portal hypertension, splenomegaly, varices, and gastroesophageal hemorrhage. Interestingly, when the bile ducts are macroscopically dilated, ARPKD in the liver may be indistinguishable from Caroli disease. Further complications include ascending cholangitis, secondary to entry of nonsterile gastrointestinal contents into the dilated intrahepatic bile ducts.\n\nDisease manifestations and clinical presentations vary considerably, and ARPKD is viewed as a spectrum of kidney and liver disease, with renal and hepatic disease inversely proportional to each other in individual patients. Children with severe kidney disease have mild congenital hepatic fibrosis, and patients with minimal renal disease, may have no renal functional impairment, but rather progressive hepatic fibrosis leading to the development of portal hypertension. \n\nPathogenesis of Renal Involvement:\n\nRenal cysts develop from epithelial proliferation along the collecting duct of the nephron. Symmetric and circumferential epithelial proliferation results in tubular lengthening and fusiform dilatation of the collecting duct. The result is that the function of the epithelium changes from resorptive to secretory. \n\nPathologic Features:\n\nThere are numerous dilated and elongated tubular structures, radially oriented relative to the renal hilum. Obstruction is not the underlying cause of dilatation; the \u2018cysts\u2019 represent dilation and hyperplasia of the interstitial portions of the urteric bud branches that form the collecting ducts. The kidneys are symmetrically enlarged with a preserved reniform shape, with multiple, tiny cystic spaces throughout. The elongated, dilated collecting ducts extend from the medulla to the cortex, blurring the corticomedullary junction.\n\nSonography:\n\nAs the spectrum of renal involvement varies, so do the sonographic manifestations of ARPKD. Neonates and infants with moderate to severe renal disease may demonstrate kidneys that are smoothly enlarged and diffusely echogenic, which is the result of the many interfaces between the radially arrayed dilated ducts and the ultrasound beam. The degree of enlargement is directly proportional to the number of dilated ducts. Additionally, numerous, 1-2 mm cystic appearing structures may be identified throughout the cortex and medulla, causing loss of the corticomedullary differentiation. Occasionally, compressed cortex may be identified at the periphery of the kidney as a hypoechoic thin rim of parenchyma. Macrocysts may also be evident, becoming larger and more numerous over time. The bladder is usually small.\n\nThose children who present secondary to portal hypertension have milder renal involvement with normal, or near normal renal function. The kidneys may appear normal at US, or appear enlarged, echogenic, and have cysts of varying size. Older children who have progressed to renal fibrosis and demonstrate multiple macrocysts may have sonographic findings that mimic the appearance of autosomal dominant polycystic kidney disease, blurring the diagnosis of ARPKD.\n\nSonographic findings of the hepatobiliary manifestations of ARPKD are also variable. The liver displays patchy or diffusely increased echogenicity of the portal tracts, representing periportal fibrosis. The intrahepatic biliary tree may appear normal, or conversely numerous, dilated intrahepatic biliary ducts may be identified. As patients develop severe portal hypertension, enlarged splenic and portal veins may be demonstrated, and the liver and spleen may become enlarged. Sonographic evaluation of the portal and splenic veins for direction of flow may assess the progression of portal hypertension.\n\nTreatment: \n\nTreatment for ARPKD consists of symptomatic management of the sequelae of the disease, such as the control of systemic hypertension with appropriate medication. Renal failure is treated with dialysis or renal transplantation. Treatment of the hepatobiliary manifestations of ARPKD consist primarily of controlling variceal bleeding. Ascending cholangitis is also a possible complication, and prompt management is important.", "ACR Code": "8.6", "Category": "Congenital, genetic", "Keywords": "Autosomal Recessive Polycystic Kidney DiseaseCongenital Hepatic FibrosisARPKD", "Reference": "Lonergan et al. RadioGraphics 2000; 20:837-855.\nDonnelly. Fundamentals of Pediatric Radiology. Philadelphia. Elsevier \n Saunders. 2001." } }, { "U_id": "MPX2574", "TAC": [], "MRI": [ "MPX2574_synpic20243", "MPX2574_synpic20244", "MPX2574_synpic20245", "MPX2574_synpic20246" ], "Case": { "Title": "Hypoplastic A1 segment of ACA", "History": "30 year old male was admitted to the hospital after motor-vehicle accident. Initial CT of the head demonstrated area suspicion for an aneurism. MRI and MRA of the brain was performed to evaluate further.", "Findings": "MRA demonstrates hypoplastic right A1 segment of ACA. This is a conjenital variant and should be differentiated from dissection/occlusion of the vessel.\n\nRight A1 segment is not seen on a collapsed MIP image. Source images demonstrate string like signal compatible with A1 segment hypoplasia and not complete abscence.\n\nLeft ACA is of approximately the same size as left MCA. Right ICA is smaller than the left. This fingings confirm that the fingings related to the string like flow in right A1 are secondary to congenital hypoplastic A1. \nIn the case of dissection or partial occlusion, both ICAs would likely be of the same size. Additionally, contraleteral (left) A1 segment would be smaller than adjacent M1 segment.", "Differential Diagnosis": "Dissection\nPartial occlusion (in case of hypoplastic A1)\nTotal occlusion (in case of conjenitally absent A1).", "Case Diagnosis": "Hypoplastic A1 segment of ACA", "Treatment & Follow Up": "None necessary", "Discussion": "See factoid discussion" }, "Topic": { "Title": "Hypoplastic A1 segment of ACA", "Disease Discussion": "Absence or hypoplasia of A1 segment of anterior cerebral artery occurs approximately in 2% of general population. It is a conjenital vascular variant that usually does not cause any symptoms of vascular insufficiency. This finding is most often incidental.\n\nAbsence or hypoplasia of A1 segment should be differentiated from other more serious etiologies that can give similar appearance. These include dissection and occlusion. Complete occlusion (thrombotic or embolic) should be differentiated from a conjenital absence of A1. Dissection or partial occlusion should be differentiated from a hypoplastic A1. \nCertainly, clinical history and patients syptoms will most likely help in differentiation between variant and dissection/occlusion. However, the distinction can be made by looking for findings that are associated with conjenital variant of A1 segment. In most cases, an ipsilateral internal carotid artery (ICA) will be of smaller in diameter and contralateral ICA will be enlarged. Additionally, anterior cerebral artery (ACA) is usually smaller in diameter than an adjacent middle cerebral artery (MCA). In case of hypoplasia or absence of A1, a contralateral ACA is enlarged measuring closer to the adjacent MCA.\n\nPeople with either of these conjenital variants have increased chance of developing an ACOM artery aneurysm.", "ACR Code": "9.1", "Category": "Congenital, normal variant", "Keywords": "A1 segmenthypoplasia absencemra", "Reference": "AG Kane, WP Dillon, AJ Barkovich, D Norman, CF Dowd and TT Kane\nReduced caliber of the internal carotid artery: a normal finding with ipsilateral absence or hypoplasia of the A1 segment.\nAJNR, Vol 17, Issue 7 1295-1301, 1996." } }, { "U_id": "MPX2563", "TAC": [], "MRI": [ "MPX2563_synpic41792", "MPX2563_synpic41793", "MPX2563_synpic41794", "MPX2563_synpic41795", "MPX2563_synpic41796", "MPX2563_synpic41797", "MPX2563_synpic41798", "MPX2563_synpic41799", "MPX2563_synpic41800", "MPX2563_synpic41801", "MPX2563_synpic41802", "MPX2563_synpic41803", "MPX2563_synpic41804", "MPX2563_synpic41807", "MPX2563_synpic41808", "MPX2563_synpic41809", "MPX2563_synpic41810", "MPX2563_synpic41811", "MPX2563_synpic41814", "MPX2563_synpic41815", "MPX2563_synpic41816", "MPX2563_synpic41817" ], "Case": { "Title": "Right Vertebral Artery Dissection, Lateral Medullary Syndrome (Wallenberg Syndrome)", "History": "28 y.o. woman, four months postpartum, with onset of neck pain, severe vertigo associated with severe vomiting, anesthesia of the right hemi-facial region and loss of sensation in the region of the left upper and lower extremities immediately following cervical chiropractic manipulation. The patient was unsuccessfully treated for vertigo associated with Meniere\u2019s disease. The patient underwent a second cervical chiropractic treatment 15 days later, and presented with recurrent severe vertigo and associated hemi-anesthesia and difficulty phonating. Imaging was obtained one month following the initial chiropractic treatment", "Findings": "Occlusion of the right vertebral artery at the C1-2 level with subacute infarction of the right lateral medulla oblongata, and chronic infarction of the left flocculonodular lobe, as a result of traumatic chiropractic cervical manipulation.", "Differential Diagnosis": "Dissection\nRacemose Capillary Telangiectasia", "Case Diagnosis": "Right Vertebral Artery Dissection, Lateral Medullary Syndrome (Wallenberg Syndrome)", "Diagnosis By": "MRI and Angiogram", "Treatment & Follow Up": "Conservative", "Discussion": "Lateral Medullary Syndrome (Wallenberg Syndrome) is produced by infarction of a section of the lateral medulla supplied by a vertebral or posterior inferior cerebellar artery. The damaged structures may include the vestibular nuclei (nystagmus, oscillopsia, vertigo, nausea, vomiting); spinothalamic tract (contralateral impairment of pain and thermal sense over half the body); descending sympathetic fibers (ipsilateral Horner syndrome \u2013 miosis, ptosis, decreased sweating); fibers of the ninth and tenth cranial nerves (hoarseness, dysphagia, ipsilateral paralysis of the palate and vocal cord, diminished gag reflex); otolithic nucleus (vertical diplopia and illusion of tilting of vision); spinal trigeminal tract (pain, burning, and impaired sensation over ipsilateral half of face); nucleus and tractus solitarus (loss of taste); olivocerebellar or spinocerebellar fibers, restiform body and inferior cerebullum (ipsilateral ataxia of limbs, falling or toppling to the ipsilateral side). This syndrome is almost always secondary to infarction, with only a small portion being the result of hemorrhage or tumor. Most patients recover well, although reports of sudden and unexpected death may occur from respiratory or cardiac arrest in the absence of cerebellar swelling or basilar artery thrombosis.\n\nIt is interesting to note, there was no restricted diffusion indicating this was not an acute event. Burdette et al. report that infarctions greater than two weeks old, will demonstrate no signal abnormalities on diffusion-weighted imaging. Additionally, contrast enhancement in subacute strokes with iodinated contrast agents is well understood, and is secondary to extravasation of contrast material through a leaky blood-brain barrier. Likewise, similar findings were documented in this case with enhancement of the lateral medulla following the administration of gadolinium DTPA, consistent with a subacute infarct.\n\nReferences:\nAdams and Victor\u2019s Principles of Neurology. 7th Edition. New York. McGraw-Hill. 844-846. 2001.\nBurdette et al. AJR 1998;171:791-795.\nNorton et al. AJR 1978;131:881-885.\nElster et al. Radiology 1990; 177: 627-632." }, "Topic": { "Title": "Vertebral Basilar artery dissection with Pontine Infarct", "Disease Discussion": "Dissections may be spontaneous or traumatic; regardless of the etiology, the underlying pathology is the same: disruption of the intima with extravasation of blood into the vessel wall with subsequent extension of thrombus between the planes of the vessel wall (usually between the intima and media). The most common type is the subintimal dissection, although subadventitial dissections (clot extension in the plane between the media and adventitia) also occur. \n\nTwo theories exist with regard to the etiology of dissections, each of which invokes intimal injury as a final common pathway: \n1). An intimal tear occurs, allowing clot propagation within the vessel wall. \n2). A primary intramural hematoma develops and eventually ruptures through the intimal lining into the vessel lumen. \n\nTraumatic dissections result from three basic mechanisms of injury: \n\n1). Penetrating injuries, which include gunshot wounds, knife wounds, intra-oral trauma (pencils, sticks). With regard to characterizing the location of penetrating injuries, the neck is divided into three anatomic zones: \n*Zone 1: below the level of the cricoid cartilage. \n*Zone 2: between the level of the cricoid and the level of the mandibular angle. \n*Zone 3: superior to the level of the mandibular angle. \n\n2). Nonpenetrating injury due to spine fracture-subluxation injuries. \n\n3). Blunt injury to the carotid arteries. \n\nVertebral artery dissections account for approximately 20% of cases of cervical vascular injuries and most commonly occur between the skull base and the upper cervical spine. Less commonly, the injury occurs between the vessel\u2019s origin from the subclavian artery and the C6 foramen transversarium. Mid-cervical vertebral artery injuries occur in approximately 5% of patient with fractures involving the foramina transversaria. \n\nInternal carotid artery dissections are the most common of all craniocervical dissections, frequently (70% of cases) involve both the cervical and petrous segments of the ICA, and usually spare the carotid bulb. Dissections involving the intracranial internal carotid artery segments, while rare, do occur. \n\nThe radiographic appearance of the contrast-opacified vertebral artery on the lateral view is as follows: the vertebral artery takes a nearly vertical course as it traverses the C6 through C3 foramina transversaria. Immediately after passing through the vertebral canal of C2, the vessel forms an inverted L and turns laterally within C2. It then exits C2 and turns cephalad to pass through the vertebral canal of C1. On exiting the transverse foramen of the atlas, it then courses sharply posteriorly along the posterior ring of C1, completing the appearance of a half square. Finally, it turns anterosuperiorly (a hairpin turn) to pierce the dura as it passes through the foramen magnum.", "ACR Code": "1.9", "Category": "Vascular", "Keywords": "vertebral arterydissectionpontine infarct" } }, { "U_id": "MPX2586", "TAC": [], "MRI": [ "MPX2586_synpic16999", "MPX2586_synpic17000", "MPX2586_synpic17310" ], "Case": { "Title": "Cuneiform Stress Fracture", "History": "Foot pain. History of plantar fasciitis.", "Findings": "MRI: Bone marrow edema within the lateral cuneiform bone with transverse fracture line. Thickened plantar fascia with high T2 signal near calcaneal insertion also was seen consistent with plantar fasciitis.", "Differential Diagnosis": "-stress fracture\n-insufficiency fracture", "Case Diagnosis": "Cuneiform Stress Fracture", "Discussion": "This patient had a history of plantar fasciitis, confirmed by MR imaging and likely contributed to altered weight bearing with subsequent stress fracture of the cuneiform bones." }, "Topic": { "Title": "Cuneiform Stress Fracture", "Disease Discussion": "Stress fractures of the cuneiform bones are rare. More typical types of stress fractures include metatarsal (\"march\" fractures) and in the lower extremities in athletes, joggers, and dancers. Common sites include the calcaneus or other tarsal bones (ie navicular, less commonly), fibula, tibia, femur, metatarsal, pelvis, upper extremity and ribs. \nStress fractures can occur in normal or abnormal bones subjected to chronic loading. Resnick describes two types of stress fractures. 1. Fatigue fracture from abnormal stress to normal bone. and 2. Insuffieciency fracture, with normal stress on abnormal bone. \n\nCauses include RA, osteoporosis, Paget's, osteomalacia, renal osteodystrophy, and radiation.\n\nPlain film plays an essential role in stress fracture diagnosis; however, bone scan and MRI have better diagnostic sensitivity. MRI has comparable sensitivity and specificity superior to bone scan.\n\nStress fractures appear most typically as a linear zone of low signal on T1WI and a linear area of low SI surrounded by broader high SI on T2WI. Prompt diagnosis and treatment is key in preventing a tarsal stress fracture from becoming a chronic source of foot pain.", "ACR Code": "4.4", "Category": "Trauma", "Keywords": "stress fracturetarsal bonescuneiform", "Reference": "1. Bone and Joint Imaging. Resnick, 2nd ed. pgs 725-29. \n2. Meurman KO, Elfving S. Stress fracture of the cuneiform bones. British Jounal of Radiology. 53(626): 157-60, 1980 Feb\n3. Creighton RS, Gordon G. Stress fracture of the tarsal middle cuneiform bone. A case report. Journal of the American Podiatric Medical Association. 80(9): 489-95, 1990 Sep" } }, { "U_id": "MPX2594", "TAC": [], "MRI": [ "MPX2594_synpic20734", "MPX2594_synpic20735" ], "Case": { "Title": "Isolated Posterior Cruciate Ligament Tear", "History": "Patient is status post motor vehicle injury. He complains of difficulty walking and knee pain.", "Exam": "The physical examination noted a joint effusion.", "Findings": "MR images of the left knee demonstrate a large joint effusion. Heterogeneous high signal is seen within the posterior cruciate ligament, consistent with a complete tear. There is a significant degree of bone marrow edema within the anterior lateral tibial plateau, and an occult tibial plateau fracture cannot be completely excluded. Additionally, there is abnormal vertical high signal within the medical meniscus, consistent with a free edge traumatic tear. The lateral meniscus is normal. The medial and lateral collateral ligament complexes are normal. The anterior cruciate ligament is also normal.", "Differential Diagnosis": "A mid-substance interstitial lesion (most common).\nComplete disruption at the genu\nAvulsion at the tibial attachment (least common). \n\t- this requires reduction of osseus fragments to increase the chance of healing.", "Case Diagnosis": "Isolated Posterior Cruciate Ligament Tear", "Diagnosis By": "Surgically.", "Treatment & Follow Up": "Isolated partial tears require surgery. If the ACL is involved, surgery is also required with correction of the PCL first, and then the ACL at a later time in order to fix posterolateral instability. Complete PCL tears are treated conservatively with knee immobilization, crutches, ice, elevation and orthopedic referral. After 1-2 weeks, the patient should begin isometric quadriceps exercises.", "Discussion": "-Etiology and Pathogenesis: Classically a \u201cdashboard injury\u201d causes this where there is a direct blow to the tibia while the knee is in flexion with a posterior backwards flexion. However, rarely is there an isolated PCL tear as usually the ACL or MCL is involved. \n\n\n-Epidemiology: Rare, as only 30% of tears to the PCL are isolated.\n\n-Clinical Manifestations: Pain, pop, buckling sound. Pain is greater with a complete tear than with a partial tear. Pain increases with going down stairs or with pushing off in running.\n\nReferences\n\nRoberts DM. \u201cEmergency Department Evaluation and Treatment of Knee and Leg Injuries.\u201d Emergency Medicine Clinics of North America. 18(1): 67-84 v-vi.\n\nCarrino JA. \u201cImaging of Sports Related Knee Injuries.\u201d Radiology Clinics of North America. 01 Mar 2002; 40(2): 181-202.\n\nCosgarea AJ, Jay PR. \u201cPosterior Cruciate Ligament Injuries.\u201d Journal of the American Academy of Orthopedic Surgeons. 01-SEP-2001. 9(5): 297-307." }, "Topic": { "Title": "Posterior Cruciate Ligament Tear", "Disease Discussion": "Posterior Cruciate Ligament Tear\n\nPCL has it origin along the lateral aspect of medial femoral condyle and its attachement at the posterior intercondyloid fossa of the tibia. Both the PCL and ACL are intraarticular but extrasynovial\n\nThe PCL is a central stabilizer of the knee. It is composed of an anterolateral band and posteromedial band that tighten on flexion & extension respectively and restrict posterior tibial displacement on the femur. PCL is twice as strong as the ACL with a higher tensile strength and a larger cross sectional area. Therefore, the ACL is more commonly injured than the PCL. Injuries to PCL account for 5 \u2013 20 % of knee ligament injuries and are usually associated with ACL, meniscus or collateral ligament damage. The most common location for PCL tear is the midportion representing 76% of all PCL injuries. Avulsion from the femur (36 \u2013 55%) and from the tibia ( 22 \u2013 42%) are the other two locations of PCL tear. The mechanism of injury is excessive rotation, hyperextension, dislocation or direct trauma while the knee is flexed. The most common causes of PCL injury are dashboard strikes in MVAs and contact sports. Clinically, the posterior drawer sign will be positive in 60% of PCL injuries. \n\nTreatment for PCL tears include surgical repair and non-operative treatment. Isolated PCL tears are usually treated non-operatively. Surgical repair is usually reserved for symptomatic chronic PCL injury, acute bony avulsion, and combination injuries.", "ACR Code": "4.4", "Category": "Trauma", "Keywords": "PCLPosterior Cruciate LigamentKnee", "Reference": "Greenspan, A. Orthopedic Radiology, 2nd edition. Lippincott-Raven. Philadelphia. 1996. p. 234 \u2013 7, 268.\n\nStoller, D. Magnetic Resonance Imaging in Orthopaedics & Sports Medicine, 2nd ed. 1997. Lippincott-Raven, Philadelphia. Pp. 342 \u2013 349." } } ]