Treatment of Cerebral Vasospasm With Continuous Intra-Arterial Nimodipine: A Case Report.

Aneurysmal subarachnoid hemorrhage (aSAH) is an important cause of death and disability, not just due to the initial event, but also because of the delayed complications. Cerebral vasospasm (CV) stands out as a serious complication, with high prevalence and association with permanent neurologic impairment. The treatment of CV includes non-invasive measures, like oral nimodipine and induced hypertension, but also invasive measures. Endovascular rescue treatment (ERT), with intra-arterial approaches, is linked with improvement of cerebral perfusion and thus associated with a better outcome. There are several, widely studied substances used in intra-arterial approaches, none showing clear superiority over the others. The main issues with these substances are the adverse systemic effects and the recurrence of CV, due to the short duration of action. Recent studies suggest that the use of continuous infusion of nimodipine, instead of bolus injection, may be related to better outcomes. The authors present a case of severe refractory vasospasm successfully treated with continuous intra-arterial nimodipine infusion. A 23-year-old female was admitted with aSAH, Fischer IV, and Hunt Hess 5. A brain CT scan showed an extensive and diffuse subarachnoid hemorrhage causing ill-defined hypodensity of the brainstem, bilateral hemispheric hypodensities, and alterations compatible with diffuse cerebral edema. The cerebral angiography revealed an aneurysm in the emergence of the left posterior communicating artery. Coil target detachment was performed with partial occlusion of the aneurysm. On the fifth day of hospitalization, transcranial Doppler (TCD) ultrasonography revealed hemodynamic signs suggestive of vasospasm. Cerebral angiography performed later showed vasospasm of the terminal segment of the left internal carotid artery (ICA) and the A1 and M1 segments. Intra-arterial verapamil was instilled, with angiographic control showing a slight increase in the caliber of these segments. On the 13th day of hospitalization, the patient maintained sonographic evidence of vasospasm in the left ICA and middle cerebral artery (MCA). Selective catheterization of the left ICA was performed with a microcatheter at the level of the petrous segment and continuous infusion of 1 mg/h intra-arterial nimodipine was started. A progressive improvement was documented after the beginning of the continuous infusion of intra-arterial nimodipine, which was maintained for five days, and angiographic control revealed improvement of vasospasm in the terminal portion of the ICA as well as in the A1 and M1 segments. Long-term continuous intra-arterial nimodipine infusion is a promising technique for the treatment of refractory CV and may be considered in selected cases.