Intraarterial Nimodipine Versus Induced Hypertension for Delayed Cerebral Ischemia: A Modified Treatment Protocol

Miriam Weiss*, Walid Albanna, Catharina Conzen-Dilger, Nick Kastenholz, Katharina Seyfried, Hani Ridwan, Martin Wiesmann, Michael Veldeman, Tobias Philip Schmidt, Murad Megjhani, Henna Schulze-Steinen, Hans Clusmann, Marinus Johannes Hermanus Aries, Soojin Park, Gerrit Alexander Schubert

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

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Abstract

BACKGROUND: Rescue treatment for delayed cerebral ischemia (DCI) after subarachnoid hemorrhage can include induced hypertension (iHTN) and, in refractory cases, endovascular approaches, of which selective, continuous intraarterial nimodipine (IAN) is one variant. The combination of iHTN and IAN can dramatically increase vasopressor demand. In case of unsustainable doses, iHTN is often prioritized over IAN. However, evidence in this regard is largely lacking. We investigated the effects of a classical (iHTN+IAN) and modified (IANonly) treatment protocol for refractory DCI in an observational study.

METHODS: Rescue treatment for DCI was initiated with iHTN (target >180 mm Hg systolic) and escalated to IAN in refractory cases. Until July 2018, both iHTN and IAN were offered in cases refractory to iHTN alone. After protocol modification, iHTN target was preemptively lowered to >120 mm Hg when IAN was initiated (IANonly). Primary outcome was noradrenaline demand. Secondary outcomes included noradrenaline-associated complications, brain tissue oxygenation, DCI-related infarction and favorable 6-month outcome (Glasgow Outcome Scale 4-5).

RESULTS: N=29 and n=20 patients were treated according to the classical and modified protocol, respectively. Protocol modification resulted in a significant reduction of noradrenaline demand (iHTN+IAN 0.70±0.54 µg/kg per minute and IANonly 0.26±0.20 µg/kg per minute, P<0.0001) and minor complications (15.0% versus 48.3%, unadjusted odds ratio, 0.19 [95% CI, 0.05-0.79]; P<0.05) with comparable rates of major complications (20.0% versus 20.7%, odds ratio, 0.96 [0.23-3.95]; P=0.95). Incidence of DCI-related infarction (45.0% versus 41.1%, odds ratio, 1.16 [0.37-3.66]; P=0.80) and favorable clinical outcome (55.6% versus 40.0%, odds ratio, 1.88 [0.55-6.39]; P=0.32) were similar. Brain tissue oxygenation was significantly higher with IANonly (26.6±12.8, 39.6±15.4 mm Hg; P<0.01).

CONCLUSIONS: Assuming the potential of iHTN to be exhausted in case of refractory hypoperfusion, additional IAN may serve as a last-resort measure to bridge hypoperfusion in the DCI phase. With close monitoring, preemptive lowering of pressure target after induction of IAN may be a safe alternative to alleviate total noradrenaline load and potentially reduce complication rate.

Original languageEnglish
Pages (from-to)2607-2616
Number of pages10
JournalStroke
Volume53
Issue number8
Early online date8 Jun 2022
DOIs
Publication statusPublished - Aug 2022

Keywords

  • brain ischemia
  • Glasgow Outcome Scale
  • nimodipine
  • norepinephrine
  • subarachnoid hemorrhage
  • ANEURYSMAL SUBARACHNOID HEMORRHAGE
  • BLOOD-PRESSURE
  • VASOSPASM
  • THERAPY
  • GUIDELINES
  • MANAGEMENT
  • EVENT

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