氨氯地平暴露报告剂量与结果的关系:25年毒物中心回顾性回顾。

IF 3.3
Colleen P Cowdery, Courtney Temple
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引用次数: 0

摘要

简介:氨氯地平是一种二氢吡啶钙通道阻滞剂,在美国引起中毒死亡的原因越来越多。由于摄入氨氯地平后需要数小时才能达到血药浓度峰值,因此临床医生可能无法立即看出中毒的严重程度。本研究旨在根据临床结果的严重程度对报道的氨氯地平暴露剂量进行分层。方法:我们回顾了俄勒冈毒物中心25年的记录,以确定氨氯地平暴露,包括报告的摄入剂量,不涉及其他心脏活性共同摄入,并使用血管活性/肌力药物治疗。我们检查了报告的氨氯地平剂量、治疗期间同时使用的血管活性/肌力输注的最大次数、静脉-动脉体外膜氧合的使用和临床结果之间的关系。结果:41例符合纳入标准。据报道,≤250 mg (n = 20)的摄入很少需要两次以上的血管活性/肌力输注;只有1例患者需要静脉-动脉体外膜氧合,无死亡发生。据报道,在摄入401-1,000 mg (n = 14)的患者中,12例(86%)接受了4次或更多的血管活性/肌力输注,6例(43%)接受了静脉-动脉体外膜氧合,4例(29%)死亡。据报道,7名患者摄入701- 1000毫克;所有患者均接受了4次或更多的血管活性/肌力输注,其中4例(57%)接受了静脉-动脉体外膜氧合并存活。在没有接受体外膜氧合的3名患者中,2人死亡,1人存活,但需要进行血液透析。讨论:氨氯地平毒性可导致标准治疗无效的深度血管截瘫性休克。报告的摄入剂量与血管加压剂的需要量、静脉-动脉体外膜氧合的利用率和死亡率有关。结论:尽管受样本量的限制,这些研究结果表明,报告的氨氯地平摄入量≥400mg的患者发生难治性休克的风险较高,尽早转移到能够采取先进干预措施(如静脉-动脉体外膜氧合)的医疗中心可能有益。报告摄入剂量可作为临床医生早期危险分层的有用工具。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Relationship between reported dose and outcome in amlodipine exposures: a 25-year retrospective poison center review.

Introduction: Amlodipine, a dihydropyridine calcium channel blocker, is a growing cause of poisoning fatalities in the United States. As it takes several hours following ingestion for amlodipine peak plasma concentrations to be reached, the severity of poisoning may not be immediately apparent to clinicians. This study aimed to stratify reported amlodipine exposure doses with the severity of clinical outcomes.

Methods: We reviewed 25 years of Oregon Poison Center records to identify amlodipine exposures that included reported ingestion doses, did not involve other cardioactive co-ingestions and were treated with vasoactive/inotropic agents. We examined the relationship between the reported amlodipine dose, the maximum number of simultaneous vasoactive/inotropic infusions used during treatment, the use of veno-arterial extracorporeal membrane oxygenation, and clinical outcome.

Results: Forty-one cases met the inclusion criteria. Reported ingestions of ≤250 mg (n = 20) rarely required more than two vasoactive/inotropic infusions; only one patient required veno-arterial extracorporeal membrane oxygenation, and no deaths occurred. For patients who reportedly ingested 401-1,000 mg (n = 14), 12 (86%) received four or more vasoactive/inotropic infusions, six (43%) received veno-arterial extracorporeal membrane oxygenation, and four (29%) died. Seven patients reportedly ingested 701-1,000 mg; all received four or more vasoactive/inotropic infusions, and four (57%) received veno-arterial extracorporeal membrane oxygenation and survived. Of the three who did not receive extracorporeal membrane oxygenation, two died, and one survived but required ongoing hemodialysis.

Discussion: Amlodipine toxicity can result in profound vasoplegic shock refractory to standard therapy. Reported ingestion dose was associated with vasopressor requirements, utilization of veno-arterial extracorporeal membrane oxygenation, and mortality.

Conclusion: Although limited by sample size, these findings suggest that reported amlodipine ingestions of 400 mg or greater are at high risk for refractory shock and may benefit from early transfer to a medical center capable of advanced interventions such as veno-arterial extracorporeal membrane oxygenation. Reported ingestion dose may serve as a useful early risk stratification tool for clinicians.

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