Current status of antifibrinolytic therapy for treatment of patients with aneurysmal subarachnoid hemorrhage.

ANEURYSMAL subarachnoid hemorrhage (SAH) accounts for approximately 8% of all acute cerebrovascular events, affecting approximately 26,000 Americans each year. Unlike other forms of cerebrovascular disease, the incidence of SAH is not declining. The ultimate mortality of this disease without treatment approaches 50%, most of the deaths occurring in the first two weeks after the hemorrhage, and disabling neurological sequelae are common among survivors. Death and disability result from the acute effects of SAH, including mass effects of a cerebral hematoma or cerebral edema. Acute hydrocephalus or convulsions may develop in the first few days after SAH. Fluid electrolyte imbalances secondary to inappropriate release of antidiuretic hormone may induce convulsions or coma. SAH causes profound rises in serum levels of catecholamines, which can lead to cardiac arrhythmias and myocardial infarction. Respiratory distress, hypoventilation, atelectasis, or pneumonia are known complications of SAH. The stress of the intracranial event may precipitate gastric mucosal ulceration and gastrointestinal hemorrhage. Cerebral vasospasm, a local or generalized narrowing of intracranial arteries, can complicate SAH and lead to cerebral infarction. Vasospasm reaches its peak severity during the first two weeks after SAH.