A 30-year-old male presented with cough, headache and progressive dyspnea one month before admission.
Two weeks later the patient developed mucopurulent expectoration and fever of 38oC.
The patient was advised to take amoxicillin and then moxifloxacin and tiotropium bromide.
She was admitted to the emergency room with dyspnea at rest, severe pain and fever.
He was not a smoker and had a history of bronchial asthma, which was treated with inhaled albuterol.
Physical examination revealed T.A: 110/70 mmHg, 37.5°C, conscious, tachypnea, sweating, and no jugular engorgement.
Pulmonary auscultation revealed diffuse bilateral crackles and cardiac auscultation revealed rhythmic tone, rapid without murmurs or extracts.
The abdomen was blando depressible and showed no organomegaly.
There were no edemas in the extremities and peripheral pulses were preserved.
Laboratory tests showed 18,500 leukocytes with left shift, hemoglobin 16.3 grams/dl, 474,000 platelets, prothrombin activity of 73%.
Dí¥ 920 mg/dl. Baseline arterial pressure: pH 7.53, pO2 47 mmHg, pCO2 23 mmHg, CO3H 19.2 mmol/l.
Normal biochemistry including troponin and CPK.
Chest radiography showed severe cardiomegaly and bilateral interstitial pattern.
A transthoracic echocardiogram showed a severe pericardial effusion with no signs of tamponade and a left ventricle with normal dimensions.
He was admitted to the intensive care unit and started treatment with furosemide, levofloxacin, acetylsalicylic acid and noninvasive mechanical ventilation.
In a new packing data were observed, so an evacuating pericentesis was performed, obtaining a polymorphous fluid U-cell sero53 with 98% LDH of the following 23 biochemical characteristics.
Seven days later, the patient was referred to the Internal Medicine Department where the study was initiated to determine the etiology of pericardial effusion and interstitial pattern. The following tests were performed: antinuclear antibodies, rheumatoid factor, Mantoux-negative.
Thyroid profile was normal.
The pericardial fluid culture was negative, as well as three blood cultures.
The pathological anatomy of the pericardial fluid was reported as acute intense inflammation and mesothelial cell groups with reactive admixtures, being negative for malignant cells.
High levels of collagen binding proteins (CEA) were found 21.53 ng/ml.
In addition, serology for human immunodeficiency virus, Mycoplasma pneumoniae, cytomegalovirus, Epstein and Chlamydia pneumonie was performed, which were negative except for IgM to cytomegalovirus that was positive.
A chest CT scan showed two mediastinal lymphadenopathies of pathological size of pretracheal localization of approximately 19 x 15 mm and 18 x 17 mm respectively, and a bilateral pleural effusion somewhat larger on the right side.
With the pulmonary window, bilateral and diffuse alterations of the pulmonary parenchyma were observed, with a nodular interstitial pattern septal reticulum and lobular center with areas of patched alveolar condensation of predominant distribution in the apical segment of the lower lobes.
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Bronchoscopy was performed, observing the upper airways, vocal cords and mucosa without alterations. There was widening in the subcarinal area.
The bronchial tree showed no alterations.
Bronchoalveolar lavage was performed in the apical segment of the culm, and the examination had to be suspended due to poor tolerance, without performing adenopathy puncture or transbronchial biopsy.
The pathological anatomy of the lavage revealed abundant macrophages and epithelial groups with reactive atypia, compatible with type II pneumocytes hyperplasia, secondary to acute lung injury.
It was thought that it could present a diffuse interstitial lung disease (DILD) due to the anatomopathological, clinical and radiological features.
The first possibility was eosinophilic pneumonia due to the presence of peripheral blood fever. Treatment with prednisone 1 mg/kg was initiated, with no favorable evolution and no dyspnea upon discharge 25 days after admission.
Seven days later, the patient presented with a cough with mucous expectoration, followed by hemoptoic cough.
The chest X-ray showed no changes, so a thoracic CT scan was performed, which revealed a ground glass pattern and moderate bilateral pleural effusion.
A lung biopsy was performed to obtain the diagnosis.
The report was about diffuse lymphocytic permeation (consciousing of a nodular interstitial pattern) due to acinar-papillary adenocarcinoma, well differentiated with abundant bodies of psamoma.
Pleural fluid showed cytological malignant cells consistent with adenocarcinoma.
Histochemical tests were performed confirming the pulmonary origin of adenocarcinoma.
She is currently receiving chemotherapy with the combination of cisplatin and gemcitabine.
Two cycles have been administered so far, so we do not yet have data on possible response.
