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  • Print publication year: 2009
  • Online publication date: April 2010

13 - Subarachnoid Hemorrhage

from SECTION III - MANAGEMENT OF SPECIFIC DISORDERS IN THE NEUROCRITICAL CARE UNIT

Summary

EPIDEMIOLOGY

Subarachnoid hemorrhage (SAH) includes the subset of intracranial hemorrhage that lies in the space between the thin arachnoid layer and pia mater. In the United States, the vast majority of SAH is caused by traumatic injury. Estimated prevalence of traumatic brain injury (TBI) worldwide is between 150 and 250 per 100,000 population per year. From 12% to 53% (a realistic figure is probably 40%) of traumatic brain injury patients have subarachnoid hemorrhage on initial computerized tomography (CT) scanning. Based on these data, approximately 240,000 persons in the United States suffer traumatic SAH per year.

The presence of traumatic SAH has a significant impact on patient outcome. In fact, the development of vasospasm – which has been demonstrated in various studies by angiography and transcranial Doppler – occurs in approximately 5–40% of head injuries with SAH. In one study, 10 (7.7%) of 130 head-injured patients who displayed SAH on initial CT scanning developed delayed ischemic neurologic deficits (DINDs), reportedly all attributable to vasospasm. In addition, severely head-injured patients (defined as Glasgow Coma Scale [GCS] score of 8 or less on admission, or deterioration to that level within 48 hours of admission) with SAH on CT scanning have a statistically significant increase in risk of death, with an odds ratio of 2.39.

In contrast to traumatic SAH, spontaneous SAH occurs less frequently, and its etiology is more diverse:

▪ Ruptured intracranial aneurysm (75–80%)

▪ “Angiogram negative SAH” (7–10%)

▪ Cerebral arteriovenous malformations (AVMs; 4–5%)

▪ Vasculitis

▪ Carotid or vertebral artery dissection

▪ Ruptured arterial infundibulum (rare)

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