利用合成人血管紧张素II治疗儿茶酚胺抵抗性血管扩张性休克的危重儿童:单中心回顾性病例系列。

Critical Care Explorations Pub Date : 2023-09-12 eCollection Date: 2023-09-01 DOI:10.1097/CCE.0000000000000978
Oguzhan Tezel, Tamara K Hutson, Katja M Gist, Ranjit S Chima, Stuart L Goldstein, Natalja L Stanski
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引用次数: 0

摘要

目的:描述我们在儿茶酚胺抵抗性血管扩张性休克(CRVS)危重患儿中使用辅助合成血管紧张素II的机构经验。设计:单中心回顾性病例系列。环境:美国一家大型第四儿童医院的PICU和心脏ICU (CICU)。患者:2018年1月至2023年4月,23名CRVS儿科患者在床边临床医生的判断下使用合成血管紧张素II。干预措施:没有。测量和主要结果:23例患者(PICU 20例,CICU 3例)在研究期间接受了血管紧张素II治疗,中位年龄为10.4岁(四分位数范围[IQR] 1.5-18.5),其中70%死亡。在血管紧张素II启动时,17名患者(74%)正在接受一种或多种形式的体外治疗,在之前的24小时内,儿童Logistic器官功能障碍-2评分-2的中位数为9 (IQR 7-11)。开始使用第一种血管活性药物与血管紧张素II之间的中位时间为127小时(IQR 13-289),起始时的中位总去甲肾上腺素当量(NED)为0.65 μg/kg/min (IQR 0.36-0.78)。治疗的中位持续时间为27小时(IQR 4-68),在评估的每个时间点,患者在治疗后的NED和平均动脉压(MAP)中位改善。在血管活性过程中,幸存者开始使用血管紧张素II的时间提前了近3天(91.5小时vs 161小时,p = 0.23),并且在血管紧张素II停药时,患者的NED降低幅度更大(-75% [IQR -96 ~ -50] vs +2.1% [IQR -55 ~ 33], p = 0.008), MAP增加幅度更大(+15 mm Hg [IQR - 10 ~ 27] vs -1.5 mm Hg [IQR -27 ~ 18], p = 0.052)。结论:我们证明在CRVS的危重儿童开始使用血管紧张素II后,NED减少,MAP改善。需要进一步的前瞻性工作来检查血管紧张素II起始的最佳时机,适当的患者选择,以及在该人群中的安全性。
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Utilization of Synthetic Human Angiotensin II for Catecholamine-Resistant Vasodilatory Shock in Critically Ill Children: A Single-Center Retrospective Case Series.

Objectives: To describe our institutional experience utilizing adjunctive synthetic angiotensin II in critically ill children with catecholamine-resistant vasodilatory shock (CRVS).

Design: Single-center, retrospective case series.

Setting: PICU and cardiac ICU (CICU) at a large, quaternary children's hospital in the United States.

Patients: Twenty-three pediatric patients with CRVS who were prescribed synthetic angiotensin II at the discretion of bedside clinicians from January 2018 to April 2023.

Interventions: None.

Measurements and main results: Twenty-three patients (20 in PICU, 3 in CICU) with a median age of 10.4 years (interquartile range [IQR] 1.5-18.5) received angiotensin II over the study period, 70% of whom died. At the time of angiotensin II initiation, 17 patients (74%) were receiving one or more forms of extracorporeal therapy, and median Pediatric Logistic Organ Dysfunction-2 Score-2 in the prior 24 hours was 9 (IQR 7-11). The median time between initiation of the first vasoactive agent and angiotensin II was 127 hours (IQR 13-289), and the median total norepinephrine equivalent (NED) at initiation was 0.65 μg/kg/min (IQR 0.36-0.78). The median duration of therapy was 27 hours (IQR 4-68), and at each timepoint assessed, patients had median improvement in NED and mean arterial pressure (MAP) with treatment. Survivors initiated angiotensin II nearly 3 days earlier in vasoactive course (91.5 hr vs 161 hr, p = 0.23), and had both greater reduction in NED (-75% [IQR -96 to -50] vs +2.1% [IQR -55 to 33], p = 0.008) and greater increase in MAP (+15 mm Hg [IQR 10-27] vs -1.5 mm Hg [IQR -27 to 18], p = 0.052) at angiotensin II discontinuation.

Conclusions: We demonstrate reduction in NED and improved MAP following initiation of angiotensin II in critically ill children with CRVS. Further prospective work is needed to examine optimal timing of angiotensin II initiation, appropriate patient selection, and safety in this population.

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