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高血压递增疗法与即刻诱导高血压疗法在蛛网膜下腔出血后迟发性脑缺血治疗中的比较。

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

机构信息

Department of Neurosurgery, RWTH Aachen University, Aachen, Germany.

Department of Diagnostic and Interventional Neuroradiology, RWTH Aachen University, Aachen, Germany.

出版信息

Neurocrit Care. 2022 Jun;36(3):702-714. doi: 10.1007/s12028-022-01466-7. Epub 2022 Mar 8.

DOI:10.1007/s12028-022-01466-7
PMID:35260962
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9110507/
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 (iHTN), whereas 102 patients were treated by immediate elevation to systolic pressure above 180 mm Hg (iHTN). 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 iHTN, 40.0% in iHTN; 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.

摘要

背景

迟发性脑缺血(DCI)是颅内动脉瘤性蛛网膜下腔出血的常见并发症,可导致预后不良。尽管预防性尼莫地平治疗后仍有恶化的患者,可考虑诱导高血压(iHTN),尽管诱导的安全性和疗效仍存在争议。在这项研究中,比较了两种 iHTN 治疗方案,它们采用了不同的方法来设定压力目标。

方法

在 325 例连续的蛛网膜下腔出血患者中,139 例患者接受诱导性高血压作为一线治疗。在诊断出 DCI 后,37 例患者(iHTN)通过去甲肾上腺素输注将血压升高 20mmHg,而 102 例患者立即将收缩压升高至 180mmHg 以上(iHTN)。治疗选择基于治疗医生的个人偏好,但逐渐倾向于逐步升高。评估两组患者的 DCI 引起的梗死、是否需要额外的血管内救援治疗、出现与升压治疗相关的并发症以及 12 个月后的格拉斯哥预后量表评估的临床结果。

结果

需要额外救援治疗的难治性 DCI 的发生率在两组中相似(iHTN 组为 48.9%,iHTN 组为 40.0%;p=0.332)。在逻辑回归模型中,诱导性高血压的类型与 DCI 相关梗死的发生无独立相关性(比值比 1.004;95%置信区间 0.329-3.443;p=0.942)。两组的升压治疗相关并发症发生率相似。即刻治疗组有 44 例(43.1%)患者预后良好,而逐步治疗组有 10 例(27.0%)患者预后良好(p=0.076)。然而,只有 Hunt 和 Hess 分级被确定为临床结果的独立预测变量(比值比 0.422;95%置信区间 0.216-0.824;p=0.012)。

结论

与逐步升高方法相比,即刻升高血压至较高的目标血压并不能降低 DCI 相关梗死的发生率,但与较高的并发症发生率无关。基于患者和时间点的具体需求进行的未来定制化血压管理有望更好地平衡诱导性高血压的神经学优势与系统性并发症。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79e5/9110507/76c39a8bcdb8/12028_2022_1466_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79e5/9110507/07b53ccab85d/12028_2022_1466_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79e5/9110507/fdf3f82e50f3/12028_2022_1466_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79e5/9110507/f33e75df2921/12028_2022_1466_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79e5/9110507/76c39a8bcdb8/12028_2022_1466_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79e5/9110507/07b53ccab85d/12028_2022_1466_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79e5/9110507/fdf3f82e50f3/12028_2022_1466_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79e5/9110507/f33e75df2921/12028_2022_1466_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79e5/9110507/76c39a8bcdb8/12028_2022_1466_Fig4_HTML.jpg

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