Delayed and prolonged hypotension and watershed cerebral infarction following coil embolization of an extracranial carotid artery aneurysm: A possible baroreceptor-mediated complication

Extracranial carotid artery aneurysms (ECAAs) are rare vascular lesions increasingly treated by endovascular approaches when open repair is unfavorable. Although hemodynamic depression related to carotid baroreceptor activation is recognized during carotid interventions, delayed and prolonged hypotension after primary coil embolization of an ECAA is rarely reported. A 64-year-old man underwent primary coil embolization for an enlarging high cervical ECAA because severe proximal internal carotid artery tortuosity precluded safe stent reconstruction. After an initially uneventful recovery, progressive hypotension developed approximately 1-2 hours after the procedure and ultimately required vasopressor support through postoperative day 16. Recurrent hypotension was followed by acute neurological deterioration. Computed tomography angiography showed no large-vessel occlusion, aneurysm rupture, or overt parent artery compromise, whereas diffusion-weighted magnetic resonance imaging demonstrated a left watershed infarction consistent with hypoperfusion. Blood pressure augmentation resulted in rapid neurological recovery. Because the aneurysm was adjacent to the carotid bulb, carotid baroreceptor activation related to post-embolization geometric change was considered a possible mechanism. This case highlights the need for careful hemodynamic monitoring after coil embolization of ECAAs near the carotid bulb, even without balloon angioplasty or stent deployment.