gms | German Medical Science

Objective: For the treatment of delayed cerebral ischemia (DCI) after subarachnoid hemorrhage (SAH) the vasodilating agent nimodipine is widely employed. The mechanism and efficacy of the different application ways, oral vs. intravenous vs. intra-arterial (bolus and continuous), are not sufficiently understood.

Method: Neuromonitoring-Data (ICP, MAP, CPP, pbrO₂, vasoreactivity index PRx) of 105 SAH patients from the years 2009-2015 were retrospectively evaluated. The effect of intra-arterially applied nimodipine for the treatment of severe macrovasospasm either as bolus treatment (n=110) or as continuous infusion (n=20) was investigated. Focus was put on influence on the cerebrovascular autoregulation, assessed by PRx, and brain tissue oxygen (pbrO₂), as surrogate for cerebral perfusion, within the first 24 hours after nimodipine application. Additionally patients with intravenously applied nimodipine, both preemptive and therapeutic, were evaluated.

Results: Bolus nimodipine application results in a significant increase of pbrO₂ and PRx (as sign of an impaired cerebrovascular autoregulation). This effect is transient, however, and subsides within approximately 6 hours. A continuous intra-arterial nimodipine infusion shows a sustained elevation of pbrO₂ despite a continuously affected autoregulation. Nimodipine, both intravenous and intra-arterial, results in a significant impairment of cerebrovascular autoregulation, independent of the presence of vasospasm.

Conclusions: The assumed improvement of the cerebral perfusion after an intra-arterial bolus treatment with nimodipine seems limited to a few hours. The alteration of the cerebrovascular autoregulation associated with nimodipine correlates with the therapeutic effect. These data, however, do not allow a conclusion about the effectiveness of the different nimodipine application ways in the treatment of DCI after SAH.