Cerebral vasospasm as a complication of aneurysmal subarachnoid hemorrhage: a brief review

Cerebral vasospasm is one of the most dreaded consequences of a ruptured intracranial aneurysm. Although exceptions may be found, the relationship between angiographic narrowing of cerebral arteries and deterioration of clinical status is supported by many authors. The cause of cerebral vasospasm still remains obscure. Several substances such as serotonin, prostaglandins, catecholamines appear to have a vasoconstrictive effect on the cerebral vessels. Recent evidence indicates that erythrocyte lysis within the subarachnoid spaces may play a major role in the genesis of delayed clinically relevant cerebral vasoconstriction following aneurysmal subarachnoid hemorrhage (SAH). The pathophysiology of brain ischemia following aneurysmal rupture, and the correlation between angiographic vasospasm, neurological condition, intracranial pressure (ICP) value, cerebral blood flow and CT findings are briefly discussed. It is concluded that, at present, blood volume expansion and/or induced hypertension, and pharmacological control of increased ICP provide the best basis for clinical management of the cerebral ischemic complications of SAH. Preoperative antifibrinolytic therapy and delayed surgical obliteration of the bleeding aneurysm, i.e. the policy at present most frequently adopted, are currently undergoing critical review in the light of the fact that antifibrinolytic therapy seems to be accompanied by a higher rate of ischemic SAH complications and vasospasm, whilst there are very recent suggestions that the results of early intracranial aneurysm surgery may be better than those of delayed surgery, if account is taken of the patients lost because of recurrent SAH or ischemia during the waiting period.