Neurologic deficit after carotid endarterectomy: pathogenesis and management

During a 7-year period, 818 patients underwent carotid endarterectomy (CE) and were evaluated for postoperative neurologic deficits. Three hundred and eighteen had CE performed with a shunt; transient deficits occurred in 2.9% (nine patients) and permanent deficits occurred in 1.6% (five patients). CE was performed without a shunt in 274 patients; transient deficits occurred in 2.9% (eight patients), while permanent deficits occurred in 2.2% (six patients). CE was monitored by surveillance in 226 patients; transient deficits were found in 2.2% (five patients), while permanent deficits occurred in 1.6% (four patients). There was no significant difference in the incidence of postoperative neurologic deficits between the groups (P greater than 0.25). The concept of inadequate collateral cerebral flow during endarterectomy could not, therefore, be indicted as the cause of the postoperative neurologic complications. Technical errors that caused carotid thrombosis or cerebral emboli, and not inadequate collateral cerebral flow, accounted for most of the neurologic deficits after CE. Deficits occurred most frequently in neurologically unstable patients, those who were first seen with stroke in evolution or with postreversible ischemic neurologic deficit and poststroke symptoms. Twenty-two patients awoke from CE with minor transient deficits, and neurologic function rapidly returned. Fifteen patients with profound postoperative deficits had reoperations immediately; intracranial emboli were identified in three patients, while a thrombosed CE site was demonstrated in seven. Three late (greater than 6 hours) postoperative deficits were due to thrombosis of the CE site. Patients with minimal postoperative deficits will improve without intervention, but reoperation is mandatory if a major deficit occurs in the immediate postoperative period. A protocol for the management of the post-CE neurologic deficit is presented.