A previously healthy, 8-year-old boy was admitted to the pediatric ICU following a motor vehicle accident. He had been an unrestrained passenger in a bus that overturned following a collision. After admission to a local rural hospital, he was conscious with stable vital signs. CT of the head was performed, and findings were unremarkable. Two days later, he was transferred to our institution. On admission, he was fully conscious, complaining only of pain in the right arm. Vital signs were normal. Physical examination revealed bruising of the left side of the face, bruising over the anterior abdominal wall, and a swollen, tender right elbow. Cardiovascular examination was normal. Total body tomography showed a fourth-degree splenic laceration, second-degree laceration of the left kidney, undisplaced fractures of the left inferior and superior ramis pubis, and a fracture of the right epicondyle. There was no collection of fluid in the pelvis or abdomen, vital signs were stable, and repeated blood counts were normal. The right arm was put in a cast, and the patient was admitted for observation and treated with analgesics and bed rest only. On the third day following hospital admission, the patient became somnolent and left hemiparesis with ipsilateral facialis developed. Emergent head CT showed signs of ischemic injury to the right internal capsule (Fig 1
). Ultrasound Doppler of the neck showed normal flow in the great vessels and vertebral arteries, with no signs of thrombi or dissection. Echocardiography showed normal left and right ventricular systolic function. However, within the left ventricle, a highly mobile mass (1 × 1.5 cm) was observed (Fig 2
; movie 1 and movie 2, online data), which originated from the left apex via a thin peduncle. Emergent splenectomy was performed, and anticoagulation with heparin was cautiously introduced in spite of the extensive injuries. No consequent bleeding complications were observed. Cardiac surgery for thrombectomy was planned; however, echocardiography the following day showed partial resolution of the cardiac mass to 1 × 1 cm. Three days after anticoagulation was begun, the mass disappeared and subsequent cardiac imaging was unremarkable (Fig 3
). Two weeks after the embolic event, a neurologic examination was remarkable only for slightly reduced strength in the left extremities. Results of further testing for coagulopathy were negative. Anticoagulation therapy was discontinued after 4 weeks, with no clinical or radiologic signs of recurrence 4 months after discharge.