Abstract
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.
Highlights
Vasospasm is a common complication that follows aneurysmal subarachnoid hemorrhage (SAH)
Skepticism regarding the association between angiographic vasospasm and clinical findings persisted [3], until CM Fisher and colleagues published a synopsis on the matter in 1977 [4]
SAHinduced vasospasm is a complex entity due in part to a delayed and reversible vasculopathy, impaired autoregulatory function, and hypovolemia causing a regional reduction of cerebral perfusion to the point of causing ischemia [5,6]
Summary
Vasospasm is a common complication that follows aneurysmal subarachnoid hemorrhage (SAH). Prophylactic hypervolemia In large prospective controlled studies, prophylactic volume expansion therapy failed to reduce the incidence of clinical or TCD-defined vasospasm, did not improve CBF, and had no effect on outcome [77,78,79]. In one of those studies, costs and complications were higher in the group treated with prophylactic hypervolemia [77]. A TCD study showed no improvement in elevated mean flow velocities in middle cerebral arteries of patients with clinical vasospasm after receiving a bolus infusion of Mg++ [135]. Other articles in the series can be found online at http://ccforum.com/articles/
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