Edgard Wehbe

Spontaneous splenic rupture precipitated by cough: A case report and a review of the literature

Spontaneous rupture of a normal spleen without a history of trauma is a rare clinical entity. We report on a case of atraumatic splenic rupture in a 61-year-old man who presented to the emergency department for abdominal pain and hypotension. There was no evidence of hematologic or infectious disease involving the spleen. The chronic cough described by the patient was the main trigger for the rupture. Although, spontaneous splenic rupture is rare, it is vital that physicians consider this diagnosis when evaluating patients with abdominal pain and hypotension. Failure to consider splenic rupture could be catastrophic and early diagnosis is essential for a better outcome.

Lysis and thrombosis: Manifestation of the same disease

A 19-year-old female patient presented to the emergency department 6 hr after an episode of headache followed by brief loss of consciousness. The episode was associated with jerking of extremities and rapid recovery was reported without confusion or focal neurologic deficit. She reported having tension-like headaches for several months. She denied any fever, chills, nausea, vomiting, or head trauma. Physical examination revealed an obese, pale patient with flat affect. Her temperature was 99°F, pulse: 90 beats per minute, and blood pressure 110/75 mmHg without evidence of orthostasis. Neurological examination was pertinent for right Babinski sign. Her initial complete blood count revealed hemoglobin: 6.0 g/dL, hematocrit: 18%, MCV: 91.8 fl, platelet count: 116 x 10 3 per microliter, and leukocyte count: 6,700 per microliter.

Pleural effusion from a candy wrapper.

A 60-year-old man presents with worsening shortness of breath and productive cough. Flexible bronchoscopy reveals the surprising cause.

An unusual complication of sickle cell trait: intraureter thrombus.

A 37-year-old African American woman with sickle cell trait presented with 2 days history of right flank pain and macroscopic hematuria. She had a past history of non-Hodgkin lymphoma and splenectomy for splenic infarct. Physical examination showed right costovertebral angle tenderness. Laboratory evaluation was notable for a hemoglobin level of 12.7 g/dl, a creatinine level of 1.1 mg/dl, and red blood cells on urine microscopy. Contrast-enhanced computed tomography of the abdomen showed a filling defect involving the right collecting system, right ureter, and bladder. No stone or mass was identified. Urine culture and urine cytology were negative. Her symptoms resolved after 48 h of conservative treatment (intravenous fluid, bed rest and pain control). She underwent a cystoscopy with ureteroscopy which showed renal papillary necrosis and intraureter thrombus. Hemoglobin electrophoresis demonstrated 60% hemoglobin A and 40% hemoglobin S, consistent with sickle cell trait. A repeated computed tomography after 10 days showed complete resolution of the intraureter thrombus.

Reversible hepatic decerebration: a case report and review of the literature.

Hepatic encephalopathy is a syndrome of neuropsychiatric dysfunction caused by portosystemic venous shunting with or without the presence of intrinsic liver disease. Clinical presentations are variable ranging from an abnormal sleep pattern to somnolence and deep coma. Decerebrate and decorticate posturing, have been rarely reported with hepatic encephalopathy. We report a case of a 59-year-old-man with a history of Child-Pugh B liver disease secondary to chronic alcoholism who was admitted because of coma. He had a transjugular intrahepatic portosystemic shunt 3 months prior to his presentation. He was found to have decerebrating posture. He was treated for hepatic encephalopathy with complete recovery and resolution of the neurologic findings. The physician should be aware that decerebration and decortication posture can occur with hepatic encephalopathy and can be reversible.

GI stromal tumor presenting as a bleeding gastric ulcer

A 78-year-old woman with a long-standing history of hypertension was admitted for malaise, progressive dyspnea, and melena. There was no nausea, vomiting, abdominal pain, hematochezia, or hematemesis. Physical examination did not reveal any pertinent findings except for palor and a systolic heart murmur. A digital rectal examination confirmed the presence of melena. Laboratory examinations were pertinent for hemoglobin of 6.2 g/dL (normal 12-16 g/dL) and occult blood in the stool. EGD revealed a large gastric ulcer with raised smooth margins, measuring 5 cm in length and 3 cm in width along the anterior aspect of the greater curvature (A). Multiple deep biopsy specimens