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 arteriovenous fistula) 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 rate far exceeds the percentage.
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, 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 20-1 Grading Scales for Subarachnoid Hemorrhage); prognosis for good outcome falls as the grade increases.
Initial Evaluation
- Noncontrast CT is initial study of choice and usually demonstrates hemorrhage if obtained within 72 h. Lumbar puncture (LP) is required for diagnosis of suspected SAH if CT is nondiagnostic and the diagnosis is suspected; 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 diagnosis of SAH.
- ECG may reveal ST-segment and T-wave changes similar to 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, with rapid correction indicated if SAH is documented.
| TREATMENT |
Subarachnoid Hemorrhage
ANEURYSM REPAIR
- Early aneurysm repair prevents rerupture.
- The International Subarachnoid Aneurysm Trial (ISAT) demonstrated improved outcomes with endovascular therapy compared to surgery; however, some aneurysms have morphology not amenable to endovascular treatment, and therefore surgery is still an important treatment option for some pts.
MEDICAL MANAGEMENT
- 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 needed to overcome renal losses.
- Anticonvulsants are sometimes begun until the aneurysm is treated; 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 appear 4-14 days after the initial hemorrhage, leading to focal ischemia and stroke.
- Treatment with the calcium channel antagonist nimodipine (60 mg PO q4h) improves outcomes, perhaps by preventing ischemic injury rather than reducing 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, intraarterial vasodilators and angioplasty of the cerebral vessels can be effective.
|