OBJECT: Intracerebral hemorrhage (ICH) is an uncommon complication of carotid endarterectomy (CEA), and carries a high rate of mortality and morbidity. Traditionally, attention has been focused on the cerebral hyperperfusion syndrome (HPS) as the leading cause of ICH after CEA. Other mechanisms, such as a perioperative cerebral ischemic event, cerebral infarction, and use of postoperative anticoagulation therapy, may also be important. METHODS: The authors performed a retrospective case control study to identify factors leading to ICH after CEA. Records of CEAs performed over the past 10 years at the Mayo Clinic were searched for occurrences of ICH within 30 days of the procedure. The relationship of ICH to known cerebrovascular risk factors, perioperative electroencephalographic studies, and 133Xe cerebral blood flow (CBF) studies was compared with that in a control group. Hyperperfusion was defined as hypertension with symptoms of either severe headache, seizures, or confusion, or a doubling of intraoperative CBF values. The clinical history and imaging of ischemic events and the ICH were carefully reviewed to determine the possible underlying mechanism(s). Twelve (0.4%) of 2747 patients who underwent CEAs suffered a postoperative ICH. A doubling of CBF values was found in five of eight cases in which CBF studies were performed, and occurred more commonly in the patients with ICH than in controls. Clinical symptoms of the HPS were less common (three cases). A perioperative cerebral ischemic event (four cases) and anticoagulation therapy (six cases) were other contributors to a subsequent ICH. Seven of the 12 patients with ICHs died and five achieved a moderate outcome. CONCLUSIONS: An ICH following CEA is an unusual complication that occurs in the setting of hyperperfusion, perioperative cerebral ischemia, anticoagulation therapy, or multiple mechanisms. Identification of CBF doubling at surgery may assist in identifying patients at risk for ICH following CEA.
OBJECT: Intracerebral hemorrhage (ICH) is an uncommon complication of carotid endarterectomy (CEA), and carries a high rate of mortality and morbidity. Traditionally, attention has been focused on the cerebral hyperperfusion syndrome (HPS) as the leading cause of ICH after CEA. Other mechanisms, such as a perioperative cerebral ischemic event, cerebral infarction, and use of postoperative anticoagulation therapy, may also be important. METHODS: The authors performed a retrospective case control study to identify factors leading to ICH after CEA. Records of CEAs performed over the past 10 years at the Mayo Clinic were searched for occurrences of ICH within 30 days of the procedure. The relationship of ICH to known cerebrovascular risk factors, perioperative electroencephalographic studies, and 133Xe cerebral blood flow (CBF) studies was compared with that in a control group. Hyperperfusion was defined as hypertension with symptoms of either severe headache, seizures, or confusion, or a doubling of intraoperative CBF values. The clinical history and imaging of ischemic events and the ICH were carefully reviewed to determine the possible underlying mechanism(s). Twelve (0.4%) of 2747 patients who underwent CEAs suffered a postoperative ICH. A doubling of CBF values was found in five of eight cases in which CBF studies were performed, and occurred more commonly in the patients with ICH than in controls. Clinical symptoms of the HPS were less common (three cases). A perioperative cerebral ischemic event (four cases) and anticoagulation therapy (six cases) were other contributors to a subsequent ICH. Seven of the 12 patients with ICHs died and five achieved a moderate outcome. CONCLUSIONS: An ICH following CEA is an unusual complication that occurs in the setting of hyperperfusion, perioperative cerebral ischemia, anticoagulation therapy, or multiple mechanisms. Identification of CBF doubling at surgery may assist in identifying patients at risk for ICH following CEA.
Authors: M Leonardi; M Dall'olio; L Raffi; P Cenni; L Simonetti; R Marasco; F Giagnorio Journal: Interv Neuroradiol Date: 2008-06-30 Impact factor: 1.610