[show abstract][hide abstract] ABSTRACT: A series of 14 patients with intracerebral hemorrhage after carotid endarterectomy is reviewed. This complication occurred in 0.6% of 2362 consecutive carotid endarterectomies performed at the Mayo Clinic from 1972 through 1986. All hemorrhages occurred within the first 2 weeks after operation and were ipsilateral to the side of the operation. Eight patients died, and only two made a good recovery. Significant risk factors are hypertension and chronic hemispheric hypoperfusion with impaired autoregulation. The "normal pressure-hyperperfusion breakthrough" syndrome was considered to be operative in 12 of the 14 patients. Nine patients had documented hyperperfusion (at least 100% increase of baseline cerebral blood flow) at the time of surgery. In an additional three patients, normal perfusion-pressure breakthrough was inferred by the clinical course and radiological findings, as well as by the absence of alternative explanations. Patients at risk for postendarterectomy intracerebral hemorrhage include those who have a clinical history suggestive of hemodynamic cerebral ischemia, severe carotid stenosis with limited hemispheric collateral flow, and postendarterectomy hyperperfusion, as measured by intraoperative cerebral blood flow. To minimize the risk of hemorrhage in these patients, strict maintenance of blood pressure at normotensive or even relatively hypotensive levels during the intraoperative and early postoperative periods is advised.
Journal of Neurosurgery 05/1988; 68(4):532-6. · 3.15 Impact Factor
[show abstract][hide abstract] ABSTRACT: Correction of a very high grade carotid stenosis by endarterectomy in a normotensive man was followed by the development of severe unilateral head, eye, and face pain, seizures, and on the 6th day a fatal intracerebral hemorrhage. Autopsy revealed changes in the cerebral hemisphere ipsilateral to the endarterectomy that resembled the changes seen in malignant hypertension, whereas the opposite hemisphere was normal. These changes included hypercellularity and edema of arterial and arteriolar walls, with necrosis, extravasation of erythrocytes, and exudation of fibrin. We propose that the clinical and pathological features in this case were due to relative hyperperfusion of a cerebral hemisphere in which autoregulation had been impaired because of preoperative chronic hypoperfusion with chronic maximal dilatation of its blood vessels. This state of relative hyperperfusion is probably similar to the normal perfusion pressure breakthrough that occasionally occurs after the resection of cerebral arteriovenous malformations. It is similar to the breakthrough perfusion that occurs in severely hypertensive patients and results in hypertensive encephalopathy.
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