35 SUBARACHNOID HEMORRHAGE
Harrison’s Manual of Medicine
Most common cause of nontraumatic subarachnoid hemorrhage (SAH) is rupture of an intracerebral aneurysm; other etiologies include mycotic aneurysms in subacute bacterial endocarditis, bleeding dyscrasias, and rarely infections or tumors. Approximately 3–4% of the population harbor aneurysms; rupture risk for aneurysms ³10mm in size is 0.5% 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 CT 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 Necessary to define the anatomy, location, and type of vascular malformation, such as aneurysm or arteriovenous malformation; also assesses vasospasm. Usually performed as soon as possible after diagnosis of SAH is made.
ECG ST-segment changes, prolonged QRS complex, increased QT interval, and prominent or inverted T waves often present; some changes reflect SAH, others indicate associated myocardial ischemic injury.
Blood Studies Closely follow serum electrolytes and osmolality; hyponatremia frequently develops several days after SAH. Cerebral salt wasting is common, and supplemental sodium is used to overcome renal losses.
Standard management includes bed rest in a quiet darkened room, analgesics, and stool softeners. 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. Neurosurgical clipping of the aneurysm neck is the most common treatment, although newer endovascular techniques are also possible. 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 minimize the neurologic sequelae of vasospasm. Cerebral perfusion can be improved in vasospasm by increasing mean arterial pressure with vasopressor agents such as neosynephrine or dopamine. Intravascular volume can be expanded with crystalloid. Angioplasty of the cerebral vessels can be effective in cases of severe vasospasm when ischemic symptoms appear despite maximal medical therapy.
For a more detailed discussion, see Smith WS, Hauser SL, Easton JD: Cerebrovascular Diseases, Chap. 361, p. 2369 in HPIM-15.