Case Presentation: A 54 year old woman with history of substance abuse(cocaine and recent synthetic marijuana use) presented to the emergency room with complaints of sudden onset, severe left upper and lower quadrant abdominal pain. Pain started at night waking her up from her sleep. Complete blood count showed microcytic anemia with hemoglobin of 8.4. Basic metabolic panel, lactic acid and lipase/amylase were within normal limits. Computed tomography(CT) of the abdomen/pelvis with contrast was obtained which showed large filling defects in the aorta, filling defect in the superior mesenteric artery, and wedge shaped attenuation in the left renal artery. CT angiography of the abdomen confirmed multiple thrombi in the thoracic and abdominal aorta with no calcification of the aortic wall, infarcts in the superior mesenteric and left renal artery. She was started on intravenous unfractionated heparin for thrombosis. Transesophageal echocardiograms were negative for intracardiac thrombus. Lupus antibodies were negative. Factor V leiden mutation testing was negative. Anti-thrombin 3 activity was low but the patient was on heparin when levels were obtained. Protein C activity,protein S activity and homocysteine levels were within normal limits. In this patient the aortic thrombosis with multi organ infarcts was secondary to cocaine abuse with possible synergistic effects from recent K2 use. She was discharged home on warfarin.
Discussion: Cocaine is a commonly abused drug, resulting in a multitude of detrimental health effects. Aside from the well known risk for myocardial infarction, another complication of cocaine abuse is predisposition to thrombus formation in vessels of smaller diameter. Rarely, it has been shown to be associated with thromboembolic events in large vessels with possible synergistic effects from concomitant synthetic marijuana abuse. Cocaine is one of the most commonly abused drugs and is associated with acute onset of cardiovascular complications such as myocardial infarction, arrhythmias, stroke, and kidney and spleen infarction. Rarely, cocaine use is associated with arterial and venous thrombosis. Arterial thrombosis mostly involves small diameter vessels such as coronary and cerebral vessels. The exact mechanism of thrombosis is unknown, but cocaine has been shown to induce the activation of platelets directly or indirectly. Our patient had a significant thrombus burden in a large diameter vessel leading to multiple thromboembolic events.
Conclusions: Considering this patient’s lack of risk factors except for cocaine abuse, recent concomitant use of K2, the large aortic thrombus and associated infarcts are postulated to be a result of cocaine and K2 synergism. Angiography is the diagnostic modality of choice. In certain cases arteriography shows acute thrombosis without underlying atherosclerosis. In patients with acute limb ischemia or large thrombus load, thrombectomy or intra-arterial thrombolysis is indicated. Alternatively, conservative management with systemic anticoagulation therapy is considered in patients without any ischemic symptoms.