Subarachnoid Hemorrhage
Wiley Hall
John P. Weaver
Majaz Moonis
I. GENERAL PRINCIPLES
A. Frequency and morbidity of subarachnoid hemorrhage (SAH).
1. Aneurysmal SAH accounts for 85% of nontraumatic SAH.
2. Perimesencephalic and other mechanisms of nontraumatic SAH account for the remaining 15% of cases and have lower incidences of morbidity and mortality from rebleeding and delayed ischemic deficits.
3. Intracranial hemorrhage secondary to the rupture of saccular aneurysms accounts for 2% to 5% of all new strokes and accounts for over 30,000 new cases in the United States annually.
B. Management of SAH caused by a ruptured aneurysm includes:
1. Early aneurysm repair to limit rebleeding.
2. Nimodipine to ameliorate cerebral injury secondary to vasospasm.
3. Hemodynamic and endovascular intervention to treat and overcome vasospasm.
II. PROGNOSIS. Prognostic indicators:
A. Unruptured aneurysms >10 mm in size and smaller aneurysms at the basilar tip are more likely to rupture as compared with smaller aneurysms in other locations.
B. Decerebration or coma at onset (Hunt and Hess grades 4 and 5) are associated with worse outcome.
C. Up to 51% of patients with SAH die, many before reaching medical care and most of the remainder in the first 2 weeks of care. Up to 33% of survivors need long-term care, and up to 46% of survivors suffer some form of long-term cognitive dysfunction.
III. PATHOGENESIS
A. Saccular (berry) aneurysms are distinguished from other types of intracerebral aneurysms caused by trauma, vascular dissection, or mycotic lesions and those related to tumors.
B. Of saccular aneurysms, 85% are located in the anterior circulation and 15% in the posterior circulation. Multiple aneurysms can occur in families or with systemic diseases such as polycystic kidney, Marfan syndrome, Ehlers-Danlos syndrome, pseudoxanthoma elasticum, fibromuscular dysplasia, and coarctation of the aorta.
C. Risk factors include tobacco use, heavy alcohol use, cocaine abuse, hypertension, and history of intracranial aneurysm in a first-degree relative.
IV. DIAGNOSIS
A. History.
1. Severe headache that is usually described as the worst ever and maximum intensity at onset. Reversible vasoconstriction syndrome and benign exertional headaches can mimic SAH.
2. Sudden loss of consciousness, nausea, vomiting.
3. Facial pain, pupillary dilation and ptosis (from oculomotor nerve compression), and visual field defects (from optic nerve or chiasm compression).
4. A warning leak, or sentinel hemorrhage affects 15% to 37% of patients. Physicians should have a high index of suspicion for aneurysmal expansion or warning leak when patients present with sudden, maximal headache because such events precede major hemorrhage.
B. Examination.
1. Neck stiffness.
2. Altered sensorium.
3. Focal signs (hemiparesis, oculomotor palsy, visual loss, paraparesis).
C. Laboratory studies.
1. A noncontrast head computed tomography (CT) is used to identify, localize, and quantify the hemorrhage. Modern CT is over 98% sensitive for SAH on the first day of hemorrhage.
2. Lumbar puncture (LP) is indicated if CT is nondiagnostic in a case with strong clinical suspicion.
3. When CT and LP are negative, in some cases escalation to computed tomography angiography (CTA) or conventional catheter angiography may be performed.
4. If surgery is emergent, CT angiography is the preferred study.
5. Four-vessel cerebral angiography is the most precise imaging study to localize the aneurysm(s), define the vascular anatomy, and assess vasospasm. Magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) or CTA can be performed to reveal aneurysms larger than 4 mm.
a. Imaging the upper cervical spine with angiography and MRI is important when cerebral angiography fails to reveal the source of hemorrhage.
b. If the initial angiogram fails to demonstrate the source of SAH, angiography may be repeated in 1 to 2 weeks. If clinically stable, patients may be discharged home after the second negative angiogram. In some cases, a third angiogram may be performed in several months’ time.
V. PREVENTION. Prevention of SAH is possible by screening for aneurysm in high-risk populations (e.g., polycystic kidney disease) and reducing risk factors (e.g., smoking). Early surgery may be considered in some patients with asymptomatic aneurysms at high risk of rupture, which depends on size and location.
VI. TREATMENT
A. Management.
