Management of Vasospasm

Angiographic vasospasm occurs in up to 70% of patients after aneurysmal SAH, although only about 30-40% of patients become clinically symptomatic. Although nimodipine prophylaxis improves the neurological outcome of patients, it neither decreases the incidence nor alters the magnitude of vasospasm. Vasospasm typically occurs on day 3 after SAH, peaks on day 7, and generally subsides by the end of 14 days. Vasospasm is the main cause of delayed ischemic deficit, resulting in brain infarction or death. Early vasospasm results in elevated flow velocities, which can be detected by TCD, but the diagnosis must be confirmed with angiogra-phy in symptomatic patients. SPECT can detect regional differences in perfusion and facilitate management. Currently, the only medical treatment for symptomatic vasospasm is augmentation of cerebral perfusion by elevation of blood pressure, and cardiac output. Although its value has not been established with randomized clinical trials, triple-H therapy (hemodilution, hypervolemia, hypertension) is a standard management therapy for severe vasospasm in many neurointensive care units. This entails aggressive fluid therapy to maintain pulmonary wedge pressure at 14-16 mmHg, systolic blood pressure at 160-180 mmHg, and hematocrit at 30. Patients not responding to therapy may be

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