Subarachnoid Hemorrhage

Subarachnoid hemorrhage (SAH) refers to bleeding within the cerebrospinal fluid (CSF)-filled subarachnoid space. The majority of spontaneous cases are due to ruptured cerebral aneurysms, but 15%–20% are due to another mechanism. SAH, particularly aneurysmal SAH, carries a high rate of morbidity and mortality. Prevention of recurrent SAH is paramount, and determining the mechanism of initial SAH is necessary to select the proper therapy to prevent recurrence.

A.

Patients with SAH require intensive monitoring. Regardless of etiology, acute blood pressure management is critical. A goal of < 160/90 mmHg is reasonable, though the optimal target is unclear. Elevated intracranial pressure is a common complication of SAH, so the head of bed should be maintained > 30 degrees. If hydrocephalus is present, ventriculostomy should be placed to facilitate CSF drainage.
B.

Cortical/convexity SAH in elderly patients is likely to represent amyloid angiopathy. Magnetic resonance imaging (MRI) of the brain demonstrating chronic lobar hemorrhage or cortical microhemorrhages supports this diagnosis, but must be performed with gradient echo/susceptibility weighted images which are sequences sensitive to chronic hemorrhage. There is no specific treatment for SAH due to amyloid angiopathy, but all antithrombotic therapy should be stopped as there is a high risk of recurrent bleeding.
C.

Vascular imaging, starting with brain computed tomography angiography (CTA), is indicated in young patients with cortical/convexity SAH and in older patients without evidence of amyloid angiopathy on MRI. CTA is highly sensitive for identifying arteriovenous malformations and larger aneurysms, but less sensitive for dural arteriovenous fistulas, reversible segmental vasoconstriction syndrome, and smaller, particularly distal, aneurysms.
D.

Reversible cerebral vasoconstriction syndrome (RCVS) is a vasospastic condition associated with multifocal segmental narrowing of cerebral vessels. It is often visible only on catheter angiography; further, segmental narrowing seen on CTA is not infrequently artifactual. Consider catheter angiography to confirm the diagnosis. RCVS can be associated with conditions such as pregnancy and migraine, and may be triggered by use of vasoconstrictive drugs, including sympathomimetics, triptans, and decongestants. A thorough history of prescription, over-the-counter, and illicit drug use is essential. Potentially implicated drugs should be stopped. Calcium channel blockers such as verapamil are commonly used to mitigate vasoconstriction. Repeat vessel imaging in 1–3 months should confirm normalization of the vessels.
E.

If CTA is unrevealing, brain MRI with contrast should be performed; MR venography should also be considered if there is suspicion for cerebral venous thrombosis (i.e., prodromal progressive headache, known hypercoagulable state, or significant parenchymal edema, venous infarction, or adjacent parenchymal hemorrhage on imaging). Isolated cortical vein thrombosis and superficial cavernomas may also cause focal convexity SAH and are best visualized on brain MRI. If negative, catheter angiography should be pursued.
F.

When SAH is isolated to the perimesencephalic region, an underlying etiology is rarely identified; aneurysms are found in only about 5% of cases. Initial evaluation with CT and catheter angiography is appropriate, but if negative, repeat vascular imaging is not necessary.
G.

Hemorrhage in the basal cisterns typically represents aneurysm rupture. CTA is the preferred initial study, but MRA can also be considered. Both are very sensitive to aneurysms > 3 mm, but can miss smaller aneurysms. Catheter angiography is indicated regardless of the results of CTA (to ensure an aneurysm has not been missed if CTA is negative, and to better define aneurysm anatomy if previously identified), but CTA is useful to help target the catheter-based study to areas of concern. Also, occasionally a thrombosed aneurysm may be better seen on CTA.
H.

A ruptured aneurysm should be secured within 24 hours in order to reduce the risk of rebleeding. An unsecured aneurysm carries ~ 15% risk of early rebleeding; if this occurs, the mortality rate approaches 50%. An aneurysm can be secured via endovascular coiling or surgical clipping, a determination that is based on specific anatomic and clinical features of the patient.
I.

Medical management after aneurysmal SAH focuses on reducing the risk of secondary complications, specifically seizures, hydrocephalus, and vasospasm. Prophylactic levetiracetam is administered for 1 week; clinical seizures will require a longer course of antiepileptic drug therapy. Aside from rebleeding, vasospasm causing delayed cerebral ischemia is one of the most devastating consequences of SAH. Monitoring for vasospasm and ischemia is done with frequent neurological exams and daily transcranial Doppler ultrasonography. Elevations in blood flow velocities indicate evolving vasospasm. When present and severe, treatment options include induced hypertension and aggressive volume expansion, angioplasty of affected vessels, and direct intraarterial administration of vasodilators. Oral nimodipine (60 mg every 4 hours) for 21 days has been shown to improve outcome after SAH; the putative mechanism is reduction of vasospasm induced delayed cerebral ischemia.
J.

Small aneurysms may initially be obscured by hemorrhage, vasospasm, or thrombosis within the aneurysm, so if an underlying vascular abnormality is not identified catheter angiography should be repeated between 4 and 10 days.