A 58-year-old man with a prior history of coronary artery disease, hypertension, and radical prostatectomy for adenocarcinoma 6 years earlier presented with a 1-week history of headache and nausea, followed by a witnessed generalized tonic-clonic seizure. The history was positive for a 100 pack-year smoking history and an absence of intravenous drug use or sexual promiscuity. The physical examination, after resolution of the postictal state, was remarkable only for a tongue bite. Routine laboratory studies and toxicology screening were normal. An initial noncontrast computed tomography (CT) scan of the brain showed a questionable tiny arachnoid cyst adjacent to the right tentorium and ethmoid sinusitis (Fig 1). A magnetic resonance imaging (MRI) scan with contrast revealed a hypodense area with loss of gray-white differentiation on T1 imaging. Postgadolinium scan showed an enhanced 1.6 ϫ 1.3 cm mass in the left anteromedial temporal lobe (Figs 2A to 2C, arrows). There was also increased signal on T2 and flair images in the surrounding white matter suggestive of edema/mass effect (Figs 2D and 2E, arrows). There was a 0.65-cm area of increased signal on T2 and hypointense flair without enhancement on the postgadolinium measures in the right temporal region, likely representing a subarachnoid cyst. The differential included metastases, primary lymphoma, meningioma, and toxoplasmosis. A CSF
Cocaine has been associated with known adverse effects on cardiac, cerebrovascular and pulmonary systems. However, the effect of cocaine on other organs has not been extensively reported. A middle age man presented with abdominal pain and nausea after inhalation of crack cocaine. On admission, he was found to be hypertensive and tachycardic. Physical examination revealed mild abdominal tenderness without rebound. Laboratory investigations were significant for acute kidney failure with elevated serum creatinine (3.72 mg/dL), thrombocytopenia (platelet count 74,000/UL), elevated alanine and aspartate transaminases (ALT 331 U/L; AST 462 U/L) and elevated creatine phosphokinase (CPK 5885 U/L). Urine toxicology screening solely revealed cocaine. A clinical diagnosis of cocaine toxicity was made and patient was admitted to the intensive care unit because of multi organ failure. Despite downward trending of liver enzymes during the hospital course, he continued to have residual renal insufficiency and a low platelet count at the time of discharge. In a patient with history of recent cocaine use presenting with these manifestations, cocaine itself should be considered as a likely cause.
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