A 55–year–old male with hypertension and polysubstance abuse presented after 3 days of bilateral flank and epigastric abdominal pain and chills. He was afebrile and exam revealed clear lungs, regular rhythm, no heart murmurs and mild costovertebral angle tenderness. Besides leukocytosis, the urinalysis, metabolic panel and pancreatic enzymes were unremarkable. Blood cultures grew Viridans streptococci and vancomycin was initiated. Abdominal CT scan revealed bilateral, wedge–shaped renal infarcts. Transesophageal echocardiography (TEE) showed no valvular vegetations, but demonstrated a 2.2 cm mobile (or floating) thrombus on the anterior wall of the ascending aorta, without evidence of aneurysm or dissection. On day 7, the patient complained of left arm weakness and numbness and exam revealed left pronator drift and decreased touch sensation in the left arm. A brain MRI showed infarcts involving the right parietal and posterior right frontal lobes. MRA of the aortic arch and TEE revealed no dissection and absence of the previously seen thrombus. At discharge, the patient had persistent left upper extremity numbness, but regained motor strength. Repeat blood cultures and a leukocyte scan were negative; hence, antibiotics were discontinued after 14 days. Subsequent hypercoagulable work–up revealed a positive dilute Russell viper venom test, suggesting a lupus anticoagulant, and a low Protein S level.
Mobile or floating ascending aortic arch thombi are rare causes of systemic embolization, although the true incidence is likely underestimated because there is no strict definition and some patients with unexplained systemic embolization may not undergo TEE. These have previously been described mostly in patients aged <60 years and are thought to be due to atherosclerotic plaques complicated by clot formation. Predisposing hypercoagulable states have been reported in several cases, including our patient, but the search for these conditions have not been uniformly performed. Therapeutic management remains ill–defined. In our patient, thrombolytic therapy could not be administered due to concerns of septic thrombus. Antiplatelet agents and systemic anticoagulation have not previously been shown to reduce recurrent embolization, and, indeed, our case illustrates the tremendous propensity for these events. Furthermore, anticoagulation was contraindicated in the setting of an acute stroke. Surgical intervention has been advocated in the literature, and would have been pursued in our patient had the aortic arch thrombus been visualized in subsequent evaluations.
In conclusion, in patients with unexplained embolic events, mobile aortic arch thrombi should be sought with TEE. Treatment involves surgical repair or anticoagulation in patients who are not surgical candidates.