Mechanical and pharmacologic treatment of vasospasm.

Introduction Subarachnoid hemorrhage-induced vasospasm is a well-recognized complication of aneurysm rupture and accounts for significant morbidity and mortality. The development and severity of vasospasm seems to be related to the amount of blood surrounding the vessel and the duration of exposure, indicating that some erythrocyte component, most likely hemoglobin, is ultimately responsible for its appearance. A variety of microscopic changes have been noted, including edema and thickening of the intima and media, necrosis and proliferation of the media, and adventitial inflammation resulting in luminal narrowing and rigidity of the vessel wall. The development of vasospasm can be recognized by transcranial Doppler ultrasonographic evaluation, cerebral blood flow studies, and/or changes in the patient’s neurologic examination results. Once detected, several therapeutic measures can be used to prevent or counteract vasospasm and its clinical sequelae, including medical treatment (eg, hypertensive, hypervolemic therapy) and pharmacologic regimens (eg, nimodipine). When these methods fail, timely application of endovascular procedures such as balloon angioplasty and intra-arterial infusion of papaverine may prove useful in reversing the effects of vasospasm. The following guidelines are intended for use in quality improvement programs to evaluate the endovascular treatment of vasospasm. Assessment guidelines include indications for treatment, success rates for achieving treatment goals, and complication rates.