In the context of SAH, the term "vasospasm" refers to a condition that is much more complex than simply constriction of blood vessels. Additional contributing factors include pathologic changes in arterial walls, with narrowing of the lumen and impairing vascular relaxation, altered vascular reactivity, and hypovolemia. The term "delayed ischemic deficit" (DID) more aptly describes the situation in which these multiple factors conspire to result in cerebral ischemia.

Vasospasm may be defined on the basis of angiographic, TCD, or clinical criteria. Angiographic segmental or diffuse narrowing of vessels occurs in up to 70% of patients. These changes are usually seen 5 to 14 days after the hemorrhage but may occur from as early as day 2 and as late as 3 weeks following the bleed. TCD criteria define vasospasm, using absolute linear blood flow velocity (LBFV), as mild (>120 cm/sec), moderate (>160 cm/sec), or severe (>200 cm/sec). The rate of rise in the LBFV may be a more sensitive indicator of vasospasm. When compared to angiography, TCD has a sensitivity of about 80%, reflecting that it samples only a small segment of the vasculature.

DIDs develop in approximately one-third of SAH patients, primarily in those with large amounts of subarachnoid blood. The syndrome presents as either a gradual decline in level of consciousness or the appearance of new focal neurologic deficits. These findings may fluctuate and can be exacerbated by hypovolemia or hypotension.

The disparity between the incidence of angiographic, TCD, and clinical vasospasm complicates management. All agree that when clinical symptoms develop, they should be treated aggressively; however, there is disagreement about how to respond to elevated TCD velocities or angiographic vasospasm in the absence of symptoms.

The management of vasospasm involves both the routine "prophylactic" measures used for all patients and the more aggressive intervention reserved for situations with signs of active vasospasm. Routine measures include the administration of the centrally acting calcium channel blocker nimodipine, avoidance of intravascular volume contraction, and mechanical means to remove subarachnoid blood at the time of surgery.

Nimodipine has been shown to reduce the incidence of ischemic infarctions and improve outcome in several prospective controlled studies; it is routinely administered to all patients

(77). Hypotension is infrequent with the usual doses (60 mg every 4 hr), especially if patients are well hydrated. In those treated with vasopressors for symptomatic vasospasm, dips in blood pressure following nimodipine administration could be more of a problem; therefore, changing the dose to 30 mg every 2 hr might be helpful.

It is routine practice to remove subarachnoid blood at surgery. Subarachnoid administration of recombinant tissue plasminogen activator completely prevented vasospasm in experimental models; however, in a randomized controlled trial of SAH patients, it did not alter neurologic outcome. Preliminary reports suggest a beneficial effect of a variation on this approach, using head shaking combined with cisternal irrigation with urokinase (78 ). Another recent study found improved outcome with reintroduction of the old practice of draining large volumes of CSF from the lumbar space to help clear subarachnoid blood (79).

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