A 59-year-old male patient who travels in Cuzco, Peru, suddenly begins a picture of dyspnea at rest, adding epigastric abdominal pain, sensation of general abdominal distension and abdominal compromise.
The patient was misdiagnosed of acute height and received furosemide, acetazolamide, dexamethasone, ranitidine and ceftriaxone.
In Chile, 6 days later, the patient consulted due to identical symptoms and was referred to the Emergency Department of Hospital Clínico Universidad de Chile for suspected pulmonary thromboembolism.
The patient was admitted with fever, dyspnea, inspiratory cough and abdominal disfunction.
He had a history of sleep apnoea-hypopnea syndrome, bipolar disorder managed with valproic acid, allergic rhinitis, daily wine package, lower limbs, and a dexamethasone combination of 30, tabacco 10
Vital signs: fever 81, ventilation 18 per minute, blood pressure 102-67 mmHg, axillary temperature 36°C. On examination: supine, conscious, hydrated, well perfused, white skin, pale
The abdomen was painful in the left hypochondrium, with b increased in size, vacuum in the lower limbs.
The rest of the test was normal.
Laboratory tests: hematocrit 27.1%, hemoglobin 8.7 g/dl, normal MCV and MCHC, leukocytes 10.100/uL, ESR 28 mm/hr and prothrombin time.
ProBNP 4,683 ng/ml (normal < 500), LDH 1,247 (range: 313-618), GFR, CK, CK-MB and normal troponins.
Pulmonary CT angiography ruled out thromboembolism and demonstrated a perisplenic hematoma, subunit 17 cm. The patient was admitted to intermediate care with a probable diagnosis of splenic infarction with hemorrhagic transformation.
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Serial blood tests showed no changes, an echocardiography was performed which was normal and a control tomography revealed splenic hematoma growth at 19 cm in diameter.
Clinical stability was established in the operating room.
Clinical and laboratory findings did not suggest infectious etiologies of splenic hematoma, and there were no biochemical markers of myeloopiferative, lymphoproliferative or other neoplasms in tomography studies.
Blood counts prior to this event were normal.
Although the splenic syndrome is a rare cause, it was studied for a possible sickle cell trait with a positive test for sickle cell disease induction with metabis sodium 2%.
Given the favorable in-hospital evolution, accompanied by a general laboratory and progression free studies, it was decided not to intervene surgically and the patient was discharged.
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Hemoglobin electrophoresis in alkaline medium was requested in outpatient care unit because it revealed normal hemoglobin A 54.8% and 41.8% of fraction 3, compatible with hemoglobin S, and sickle cell trait was diagnosed.
