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What is cerebral vasospasm, and how is it treated?
Cerebral vasospasm is arterial narrowing and decreased blood flow following subarachnoid hemorrhage. The inci-dence of vasospasm following surgical treatment of rup-tured aneurysms is approximately 30%, with the overall incidence of severe cerebral infarct being approximately 10%. The occurrence of vasospasm following endovascular coiling may be higher, and is presumed to be due to the continued presence of subarachnoid blood, which is nor-mally evacuated during craniotomy. The mechanism lead-ing to vasospasm is poorly understood, but appears to result from the presence of blood degradation products in the subarachnoid space. Therapy usually consists of cal-cium channel blockers, such as nimodipine, and “triple H therapy”. This consists of deliberate hypertension, hyper-volemia, and hemodilution. However, hemodilution is rarely employed. Angioplasty and injection of endovascu-lar papaverine have more recently gained popularity. Papaverine is usually applied on day 8 after subarachnoid hemorrhage. Its effect persists for less than 24 hours and the magnitude of its effect is greater when vasospasm is severe. Angioplasty, by balloon dilation of the arterial narrowing, has a longer-lasting effect than papaverine but presents a greater risk of vessel rupture. In some patients, multiple interventions of papaverine or angioplasty are performed, as guided by repeat angiography. Of course, the patient’s clinical condition will also guide therapy
Treatment Options for Cerebral Vasospasm
Calcium channel blockers
“Triple H therapy”
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