Abstract

Blunt traumatic cerebrovascular injury (TCVI) is defined as a cerebrovascular structural defect that is directly attributable to high-energy, nonpenetrating trauma. TCVI is distinct from low-energy or spontaneous cerebrovascular injury, and this distinction has notable ramifications regarding diagnosis and management. The incidence of TCVI among all blunt trauma admission is approximately 1% to 2%. Given the initial asymptomatic presentation of the majority of patients with blunt traumatic injury, early risk of stroke in patients with TCVI, and technological improvements that have yielded high-quality noninvasive imaging, we recommend universal screening with neck CT angiography (CTA) of all patients after blunt trauma. The most common mechanism of ischemic stroke in TCVI is thromboembolism. TCVI can also result in complete artery occlusion, traumatic aneurysm formation, and arterial transection. It is practical to divide patients with asymptomatic TCVI into three categories with respect to risk of stroke: mild (arterial injury without occlusion); medium (single vertebral artery occlusion [up to 20% risk of stroke]); and high (bilateral vertebral artery occlusions [about 50% risk of stroke] and unilateral carotid artery occlusion [over 50% risk of stroke]). Treatment with antithrombotic medication forms the cornerstone of therapy for TCVI. Furthermore, all patients with convincing CTA evidence of TCVI should undergo observation and regular neurological examinations during the hospital admission, particularly during the 72-hour period after the injury, in which risk of thromboembolic stroke is greatest. We reserve endovascular therapy for selected patients with acute ischemic stroke, recurrent symptoms despite antithrombotic therapy, and traumatic aneurysms that demonstrate significant enlargement on follow-up imaging.

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