Mechanisms of cerebral hemorrhage after carotid endarterectomy
Background: Intracerebral hemorrhage (IH) following carotid endarterectomy (CEA) has a high morbidity and mortality. Traditionally attention has focussed on the cerebral hyperperfusion (HP) syndrome as the leading cause of IH following CEA. Other mechanisms such as an intraoperative event, reperfusion into an old infarct and anticoagulation may also be important. Methods: We performed a case-control study to identify factors leading to IH following CEA. Over a ten year period (1990–9), all CEAs at the Mayo Clinic were assessed for the occurrence of IH within 30 days of the CEA. The relationship of IH to known cerebrovascular risk factors, perioperative EEG and xenon-133 cerebral blood flow (CBF) studies was compared with a control group of CEA patients. Clinical history and imaging of ischemic events and the IH were carefully reviewed in order to determine the possible underlying mechanism(s). HP was defined as the occurrence of doubling of CBF or the presence of hypertension with confusion, severe headache or seizures. Results: Twelve of 2747 (0.4%) CEAs had a subsequent IH. The most common underlying mechanism was HP. Doubling of xenon-133 CBF values were more likely to occur in patients with HP than controls but only one of three patients with a likely hyperperfusion IH had clinical features of the described syndrome. IH associated with HP occurred into the hemisphere surrounding the infarct except in one case of a recent infarct in which the hemorrhage occurred directly into the infarct. A peri-operative event and anticoagulation contributed to IH alone or in combination with other mechanisms in multiple patients. Seven of the 12 IH patients died or remained severely disabled. Conclusion: IH following CEA is an uncommon complication with a high mortality and morbidity. It usually occurs in the setting of HP, peri-operative event or anticoagulation with HP identifiable in the majority of cases. Identification of doubling of CBF at surgery may assist in identifying patients likely to develop HP following CEA and in these patients careful control of blood pressure and avoidance of anticoagulation is important.