Nimodipine-Induced Blood Pressure Changes Can Predict Delayed Cerebral Ischemia.

Corinne Fischer,Franca Wagner,Daniel Schöni,Andreas Raabe,Sonja Vulcu,Werner J Z'Graggen,Nicole Söll,Jürgen Beck,Christian Fung,Johannes Goldberg,Matthias Hänggi,Jörg Schefold

doi:10.3389/fneur.2019.01161

Abstract

Background: Early diagnosis of delayed cerebral ischemia (DCI) in patients after aneurysmal subarachnoid hemorrhage (aSAH) still poses a leading problem in neurointensive care. The aim of this study was to analyze the effect of oral Nimodipine administration on systemic blood pressure in patients with evolving DCI compared to patients without DCI.Methods: Systolic (SBP), mean (MAP), and diastolic (DBP) blood pressures were analyzed at the time of Nimodipine administration and additionally 30, 60, and 120 min thereafter on days 1, 3, and 5 after aSAH. Additionally, the 24 h period preceding DCI and in patients without DCI day 10 after aSAH were analyzed. Statistical analysis was performed for SBP, MAP and DBP at time of Nimodipine administration and for the maximal drop in blood pressure after Nimodipine administration.Results: Thirty patients with aSAH were retrospectively analyzed with 17 patients developing DCI (“DCI”) and 13 patients who did not (“Non-DCI”). DCI patients showed a more pronounced rise in MAP and DBP over the examined time period as well as a higher decrease in SBP following Nimodipine administration. A fall of 18 mmHg in SBP after Nimodipine administration showed a sensitivity of 82.4% and specificity of 92.3% for occurrence of DCI.Conclusion: An increase of MAP and DBP after aSAH and a heightened sensitivity to Nimodipine administrations may serve as additional biomarkers for early detection of evolving DCI.

Highlights

Cerebral vasospasm related ischemia remains the leading cause of disability for patients with aneurysmal subarachnoid hemorrhage who survive the initial bleed and in whom the ruptured aneurysm has been secured [1, 2]
The British aneurysm Nimodipine trial (1989) showed that poor outcome defined as death or severe disability was reduced by 40% in patients receiving 60 mg Nimodipine orally every 4 h for 21 days or until vasospasm occurred [8]
There were no statistical differences between the two groups when comparing age, sex, history of hypertension, method of aneurysm treatment or BNI and Fisher scores, there was a tendency for a higher percentage of female patients in the delayed cerebral ischemia (DCI) group

Summary

Introduction

Cerebral vasospasm related ischemia remains the leading cause of disability for patients with aneurysmal subarachnoid hemorrhage (aSAH) who survive the initial bleed and in whom the ruptured aneurysm has been secured [1, 2]. Several studies have reported that the L-type calcium channel blocker Nimodipine lowers the incidence of cerebral infarction and poor outcome in aSAH patients [6,7,8,9]. Diagnosis of delayed cerebral ischemia (DCI) in patients after aneurysmal subarachnoid hemorrhage (aSAH) still poses a leading problem in neurointensive care.

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