Treatment of subarachnoid hemorrhage.

Nontraumatic subarachnoid hemorrhage from intracranial aneurysm rupture presents with sudden severe headache. Initial treatment focuses on airway management, blood pressure control, and extraventricular drain for hydrocephalus. After identifying the aneurysm, they may be clipped surgically or endovascularly coiled. Nimodipine is administered to maintain a euvolemic state and prevent delayed cerebral ischemia (DCI). Patients may receive anticonvulsants. Monitoring includes serial neurologic assessments, transcranial Doppler ultrasonography, computed tomography perfusion, and angiographic studies. Treatment includes augmentation of blood pressure and cardiac output, cerebral angioplasty, and intra-arterial infusions of vasodilators. Although early mortality is high, about one half of survivors recover with little disability.

Clinical review: Prevention and therapy of vasospasm in subarachnoid hemorrhage.

Vasospasm is one of the leading causes of morbidity and mortality following aneurysmal subarachnoid hemorrhage (SAH). Radiographic vasospasm usually develops between 5 and 15 days after the initial hemorrhage, and is associated with clinically apparent delayed ischemic neurological deficits (DID) in one-third of patients. The pathophysiology of this reversible vasculopathy is not fully understood but appears to involve structural changes and biochemical alterations at the levels of the vascular endothelium and smooth muscle cells. Blood in the subarachnoid space is believed to trigger these changes. In addition, cerebral perfusion may be concurrently impaired by hypovolemia and impaired cerebral autoregulatory function. The combined effects of these processes can lead to reduction in cerebral blood flow so severe as to cause ischemia leading to infarction. Diagnosis is made by some combination of clinical, cerebral angiographic, and transcranial doppler ultrasonographic factors. Nimodipine, a calcium channel antagonist, is so far the only available therapy with proven benefit for reducing the impact of DID. Aggressive therapy combining hemodynamic augmentation, transluminal balloon angioplasty, and intra-arterial infusion of vasodilator drugs is, to varying degrees, usually implemented. A panoply of drugs, with different mechanisms of action, has been studied in SAH related vasospasm. Currently, the most promising are magnesium sulfate, 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors, nitric oxide donors and endothelin-1 antagonists. This paper reviews established and emerging therapies for vasospasm.