Incremental Versus Immediate Induction of Hypertension in the Treatment of Delayed Cerebral Ischemia After Subarachnoid Hemorrhage

Michael Veldeman, Miriam Weiss, Walid Albanna, Omid Nikoubashman, Henna Schulze-Steinen, Hans Clusmann, Anke Hoellig, Gerrit Alexander Schubert, Michael Veldeman, Miriam Weiss, Walid Albanna, Omid Nikoubashman, Henna Schulze-Steinen, Hans Clusmann, Anke Hoellig, Gerrit Alexander Schubert

Abstract

Background: Delayed cerebral ischemia (DCI) is a common complication of aneurysmal subarachnoid hemorrhage and contributes to unfavorable outcome. In patients with deterioration despite prophylactic nimodipine treatment, induced hypertension (iHTN) can be considered, although the safety and efficacy of induction are still a matter of debate. In this study, two iHTN treatment algorithms were compared with different approaches toward setting pressure targets.

Methods: In a cohort of 325 consecutive patients with subarachnoid hemorrhage, 139 patients were treated by induced hypertension as a first tier treatment. On diagnosing DCI, blood pressure was raised via norepinephrine infusion in 20-mm Hg increments in 37 patients (iHTNincr), whereas 102 patients were treated by immediate elevation to systolic pressure above 180 mm Hg (iHTNimm). Treatment choice was based on personal preference of the treating physician but with a gradual shift away from incremental elevation. Both groups were evaluated for DCI-caused infarction, the need of additional endovascular rescue treatment, the occurrence of pressor-treatment-related complications, and clinical outcome assessed by the extended Glasgow outcome scale after 12 months.

Results: The rate of refractory DCI requiring additional rescue therapy was comparable in both groups (48.9% in iHTNincr, 40.0% in iHTNimm; p = 0.332). The type of induced hypertension was not independently associated with the occurrence of DCI-related infarction in a logistic regression model (odds ratio 1.004; 95% confidence interval 0.329-3.443; p = 0.942). Similar rates of pressor-treatment-related complications were observed in both treatment groups. Favorable outcome was reached in 44 (43.1%) patients in the immediate vs. 10 (27.0%) patients in the incremental treatment group (p = 0.076). However, only Hunt and Hess grading was identified as an independent predictor variable of clinical outcome (odds ratio 0.422; 95% confidence interval 0.216-0.824; p = 0.012).

Conclusions: Immediate induction of hypertension with higher pressure targets did not result in a lower rate of DCI-related infarctions but was not associated with a higher complication rate compared with an incremental approach. Future tailored blood pressure management based on patient- and time-point-specific needs will hopefully better balance the neurological advantages versus the systemic complications of induced hypertension.

Trial registration: ClinicalTrials.gov NCT02142166.

Keywords: Delayed cerebral infarction; Delayed cerebral ischemia; Induced hypertension; Subarachnoid hemorrhage.

Conflict of interest statement

There are no conflicts of interest to report.

© 2022. The Author(s).

Figures

Fig. 1
Fig. 1
Inclusion flowchart. DCI, delayed cerebral ischemia; ERT, endovascular rescue treatment; iHTNimm, immediate induced hypertension treatment group; iHTNincr, incremetal induced hypertension treatment group
Fig. 2
Fig. 2
Mean arterial and systolic pressure over time (hours) in both iHTN treatment groups. a Systolic blood pressure (mean ± SD) synchronized around the initial DCI event triggering hypertensive treatment (hours). b Mean arterial blood pressure (mean ± SD) synchronized around the initial DCI event triggering hypertensive treatment (hours). BP, blood pressure; DCI, delayed cerebral ischemia; MAP, mean arterial pressure; SD, standard deviation
Fig. 3
Fig. 3
Box plot (median, interquartile range, and range) comparison of blood pressure 24 h before DCI onset and 24 h after beginning of treatment with induced hypertension. a Systolic blood pressure before (24 h) and after (24 h) DCI treatment with incremental induced hypertension. b Mean arterial pressure before (24 h) and after (24 h) DCI treatment with incremental induced hypertension. c Systolic blood pressure before (24 h) and after (24 h) DCI treatment with immediate induced hypertension. d Mean arterial pressure before (24 h) and after (24 h) DCI treatment with immediate induced hypertension. BP blood pressure; DCI, delayed cerebral ischemia
Fig. 4
Fig. 4
The GOS-E in both induced hypertension treatment groups after 12 months. GOS-E, extended Glasgow outcome scale; iHTNimm, immediate induced hypertension treatment group; iHTNincr, incremetal induced hypertension treatment group

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