{"title":"Relationship between reported dose and outcome in amlodipine exposures: a 25-year retrospective poison center review.","authors":"Colleen P Cowdery, Courtney Temple","doi":"10.1080/15563650.2025.2539300","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>Forty-one cases met the inclusion criteria. Reported ingestions of ≤250 mg (<i>n</i> = 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 (<i>n</i> = 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.</p><p><strong>Discussion: </strong>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.</p><p><strong>Conclusion: </strong>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.</p>","PeriodicalId":520593,"journal":{"name":"Clinical toxicology (Philadelphia, Pa.)","volume":"63 8","pages":"556-561"},"PeriodicalIF":3.3000,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinical toxicology (Philadelphia, Pa.)","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1080/15563650.2025.2539300","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/9/4 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
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.