Subarachnoid Hemorrhage

Excluding head trauma, most common cause of subarachnoid hemorrhage

(SAH) is rupture of an intracranial (saccular) aneurysm; other etiologies include

mycotic aneurysms in subacute bacterial endocarditis, vascular anomalies,

bleeding dyscrasias, and rarely infections or tumors. Approximately 2% of the

population harbor aneurysms; rupture risk for aneurysms _10 mm in size is

0.5–1% per year.

CLINICAL PRESENTATION Sudden, severe headache, often with

transient loss of consciousness at onset; vomiting is common. Bleeding

may injure adjacent brain tissue and produce focal neurologic deficits. A progressive third nerve palsy with severe headache suggests posterior communicating artery aneurysm. In addition to dramatic presentations, aneurysms can undergo small ruptures with leaks of blood into the subarachnoid space (sentinel bleeds).

LABORATORY EVALUATION Noncontrast CT is the initial study of

choice and usually demonstrates the hemorrhage. On occasion, LP is required

for diagnosis of suspected SAH if CT is nondiagnostic. Cerebral angiography

is necessary to define anatomy, location, and type of vascular malformation,

suchas aneurysm or arteriovenous malformation; also assesses vasospasm. Usually

performed as soon as possible after diagnosis of SAH is made. ECG may

reveal ST-segment changes, prolonged QRS complex, increased QT interval,

and prominent or inverted T waves; some changes reflect SAH, others indicate

associated myocardial ischemic injury.

TREATMENT

Standard management includes bed rest in a quiet darkened room, analgesics,

and stool softeners. Closely follow serum electrolytes and osmolality; hyponatremia frequently develops several days after SAH. Cerebral salt wasting

is common, and supplemental oral salt plus IV normal saline may be used to

overcome renal losses; some pts require hypertonic saline. Anticonvulsants

are begun at diagnosis and continued at least until the aneurysm is treated.

Risk of early rebleeding is high (20–30% over 2 weeks), thus early treatment

(within 1–3 days) is advocated to avoid rerupture and allow aggressive treatment

of vasospasm. Endovascular coiling of aneurysms in accessible locations

(via a catheter passed from the femoral artery) or neurosurgical clipping of

the aneurysm neck are the definitive treatments. Severe hydrocephalus may

require urgent placement of a ventricular catheter for external CSF drainage.

Blood pressure is carefully monitored and regulated to assure adequate cerebral

perfusion while avoiding excessive elevations. Symptomatic vasospasm

may occur by day 4 and continue through day 14, leading to focal

ischemia and possible stroke. Medical treatment, including nimodipine, may

reduce sequelae of vasospasm. Cerebral perfusion can be improved in

vasospasm by increasing mean arterial pressure withvasopressor agents

such as phenylephrine or dopamine. Intravascular volume can be expanded

withcrystalloid. Angioplasty of the cerebral vessels can be effective in severe

vasospasm when ischemic symptoms persist despite maximal medical

therapy.