Harrisons Manual of Medicine, 18th Ed.

CHAPTER 19. Subarachnoid Hemorrhage

Excluding head trauma, the most common cause of subarachnoid hemorrhage (SAH) is rupture of an intracranial (saccular) aneurysm; other etiologies include bleeding from a vascular malformation (arteriovenous malformation or dural arterial-venous fistula), infective (mycotic) aneurysms, and extension into the subarachnoid space from a primary intracerebral hemorrhage. Approximately 2% of the population harbor aneurysms, and 25,000–30,000 cases of aneurysmal rupture producing SAH occur each year in the United States; rupture risk for aneurysms <10 mm in size is 0.1% per year; for unruptured aneurysms, the surgical morbidity risk far exceeds the percentage.


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, usually involving the pupil, along with 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). The initial clinical manifestations of SAH can be graded using established scales (Table 19-1); prognosis for good outcome falls as the grade increases.




• Noncontrast CT is the initial study of choice and usually demonstrates the hemorrhage if obtained within 72 h. LP is required for diagnosis of suspected SAH if the CT is nondiagnostic; xanthochromia of the spinal fluid is seen within 6–12 h after rupture and lasts for 1–4 weeks.

• Cerebral angiography is necessary to localize and define the anatomic details of the aneurysm and to determine if other unruptured aneurysms exist; angiography should be performed as soon as possible after the diagnosis of SAH is made.

• ECG may reveal ST-segment and T-wave changes similar to those associated with cardiac ischemia; caused by circulating catecholamines and excessive discharge of sympathetic neurons. A reversible cardiomyopathy producing shock or congestive heart failure may result.

• Studies of coagulation and platelet count should be obtained, and rapid correction should ensue if SAH is documented.

TREATMENT Subarachnoid Hemorrhage


• Early aneurysm repair prevents rerupture.

• The International Subarachnoid Aneurysm Trial (ISAT) demonstrated improved outcomes with endovascular therapy compared to surgery; however, some aneurysms have a morphology not amenable to endovascular treatment, and therefore surgery is still an important treatment option for some pts.


• Closely follow serum electrolytes and osmolality; hyponatremia (“cerebral salt wasting”) frequently develops several days after SAH, and supplemental oral salt plus IV normal saline or hypertonic saline may be used to overcome renal losses.

• Anticonvulsants may be begun until the aneurysm is treated, although most experts reserve this therapy only for pts in whom a seizure has occurred.

• Blood pressure should be carefully controlled, while preserving cerebral blood flow, in order to decrease the risk of rerupture until the aneurysm is repaired.

• All pts should have pneumatic compression stockings applied to prevent pulmonary embolism; unfractionated heparin administered subcutaneously for deep-vein thrombosis prophylaxis can be initiated immediately following endovascular treatment and within days following craniotomy and surgical clipping.


• Severe hydrocephalus may require urgent placement of a ventricular catheter for external CSF drainage; some pts will require permanent shunt placement.

• Deterioration of a SAH pt in the first hours to days should prompt repeat CT scanning to evaluate ventricular size.


• The leading cause of mortality and morbidity following initial rupture; may develop by day 4 and continue through day 14, leading to focal ischemia and possibly stroke.

• Medical treatment with the calcium channel antagonist nimodipine (60 mg PO q4h) improves outcome, probably by preventing ischemic injury rather than reducing the risk of vasospasm.

• Cerebral perfusion can be improved in symptomatic vasospasm by increasing mean arterial pressure with vasopressor agents such as phenylephrine or norepinephrine, and intravascular volume can be expanded with crystalloid, augmenting cardiac output and reducing blood viscosity by reducing the hematocrit; this so-called “triple-H” (hypertension, hemodilution, and hypervolemic) therapy is widely used.

• If symptomatic vasospasm persists despite optimal medical therapy, intra-arterial vasodilators and angioplasty of the cerebral vessels can be effective.


For a more detailed discussion, see Hemphill JC III, Smith WS, and Gress DR: Neurologic Critical Care, Including Hypoxic-Ischemic Encephalopathy and Subarachnoid Hemorrhage. Chap. 275, p. 2254, in HPIM-18.


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