Clinical toxicology (Philadelphia, Pa.)最新文献

{"title":"Correction.","authors":"","doi":"10.1080/15563650.2025.2510046","DOIUrl":"10.1080/15563650.2025.2510046","url":null,"abstract":"","PeriodicalId":520593,"journal":{"name":"Clinical toxicology (Philadelphia, Pa.)","volume":" ","pages":"524"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144176428","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acute oral toxic ingestion of lidocaine 4.","authors":"Kayla Leathem, Molly Chang, Katherine Weigartz","doi":"10.1080/15563650.2025.2519319","DOIUrl":"https://doi.org/10.1080/15563650.2025.2519319","url":null,"abstract":"","PeriodicalId":520593,"journal":{"name":"Clinical toxicology (Philadelphia, Pa.)","volume":" ","pages":"1-2"},"PeriodicalIF":0.0,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144328347","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Two cases of deliberate elemental arsenic ingestion with no apparent toxicologic consequences.","authors":"Kevin Baumgartner, David B Liss, Michael E Mullins, Annika J Strand, Sean P Boley, Jon B Cole","doi":"10.1080/15563650.2025.2496223","DOIUrl":"10.1080/15563650.2025.2496223","url":null,"abstract":"<p><strong>Introduction: </strong>Arsenic is a metalloid that is highly toxic in its inorganic and organic forms. Ingestion of elemental arsenic is rare.</p><p><strong>Case reports: </strong>A 33-year-old woman ingested elemental arsenic 10 g purchased online. She experienced brief gastrointestinal upset but was otherwise asymptomatic. She underwent chelation with succimer until it became apparent that she had no toxicologic consequences. She remained asymptomatic at 19-day follow-up. Her spot urine inorganic arsenic concentrations were >5,000 µg/L, 109 µg/L, and 87 µg/L at 12 days, 36 days, and 19 days post-ingestion, respectively. A 20-year-old woman similarly ingested elemental arsenic 10 g purchased online. She presented to care 30 min post-ingestion. Abdominal radiography confirmed the presence of multiple radiodensities. She underwent gastrointestinal decontamination without chelation. She developed no apparent signs or symptoms of arsenic poisoning. Her 24 h urine inorganic arsenic concentration (from hospital day 2) was 253 µg/L.</p><p><strong>Discussion: </strong>The poor water solubility and bioavailability of elemental arsenic may limit its toxicity in acute ingestion.</p><p><strong>Conclusions: </strong>Elemental arsenic ingestion resulted in no apparent toxicity, despite elevated arsenic concentrations in blood and urine. Elemental arsenic ingestion may not warrant emergent decontamination or chelation.</p>","PeriodicalId":520593,"journal":{"name":"Clinical toxicology (Philadelphia, Pa.)","volume":" ","pages":"442-444"},"PeriodicalIF":3.3,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144201350","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A 10-year retrospective review of mushroom exposures reported to the United Kingdom National Poisons Information Service between 2013 and 2022.","authors":"Ella P Edwards, Sachin Patel, Laurence A Gray, Aravindan Veiraiah, Sally M Bradberry, Ruben H K Thanacoody, James M Coulson","doi":"10.1080/15563650.2025.2507357","DOIUrl":"10.1080/15563650.2025.2507357","url":null,"abstract":"<p><strong>Introduction: </strong>Several poisonous mushroom species are present in the United Kingdom, but exposures that cause severe toxicity or death are rare. This study uses poison centre data to describe trends in mushroom poisoning in the United Kingdom over a 10-year period.</p><p><strong>Methods: </strong>A retrospective review of telephone enquiries from healthcare professionals to the National Poisons Information Service regarding mushroom ingestions between January 2013 and December 2022 was performed.</p><p><strong>Results: </strong>The service received 1,285 enquiries relating to 1,195 patients. Most enquiries were received from September to November, with a peak of 305 enquiries in October. Over half of the enquiries were from emergency departments (54%). Children made up 59.5% of the total exposures. Most exposures occurred at home (<i>n</i> = 802; 68.1%). The circumstance was unintentional in 84.2% of enquiries (<i>n</i> = 988). In 80% of cases, the species was recorded as \"mushroom not known.\" A mycologist was contacted for identification in 4.2% of cases. Most patients were asymptomatic (<i>n</i> = 697; 58.3%). Common features in symptomatic patients were gastrointestinal upset, kidney and liver injury, and somnolence. Patients with severe or moderate features presented later than patients with minor or no features. No fatalities were reported.</p><p><strong>Discussion: </strong>The highest number of enquiries corresponds to the peak of the mushroom growing season. Unintentional ingestions in children tend to be of unknown mushrooms. Garden mushrooms are unlikely to result in poisoning, which may explain the large number of asymptomatic patients. Mushroom poisoning in adults tends to produce more severe features, as they are likely to intentionally ingest mushrooms in larger quantities, or present to hospital later.</p><p><strong>Conclusion: </strong>Unintentional ingestions by children accounted for the majority of enquiries. Most exposures were asymptomatic. There is a need to increase safety messages, especially aimed at children, regarding the risks of ingesting unidentified mushrooms.</p>","PeriodicalId":520593,"journal":{"name":"Clinical toxicology (Philadelphia, Pa.)","volume":"63 6","pages":"426-433"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144510302","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nitazenes: review of comparative pharmacology and antagonist action.","authors":"Marcus Stangeland, Ola Dale, Arne Kristian Skulberg","doi":"10.1080/15563650.2025.2504133","DOIUrl":"10.1080/15563650.2025.2504133","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Introduction: &lt;/strong&gt;Nitazenes are a class of potent synthetic opioids that have emerged in illicit drug markets and have been identified in combination with other opioids in cases of poisoning and fatalities. Originally developed in the 1950s, these compounds were abandoned due to their high toxicity and unfavourable therapeutic index. Recent reports indicate that nitazenes exhibit a wide range of potencies, with some exceeding that of fentanyl. Understanding the pharmacological and toxicological profiles of nitazenes is critical for public health and clinical management. This review synthesizes literature on the pharmacology, toxicity, and antagonist action of nitazenes, particularly their response to naloxone.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;A comprehensive literature review was conducted using EMBASE, Ovid MEDLINE(R), APA PsycInfo, Scopus, and Web of Science up to 26 July 2024. The main search terms used were: \"nitazen*\", \"2-benzylbenzimidazole\", \"aminoisotonitazene\" OR \"butonitazeneor clonitazene\" OR \"desnitazene\" OR \"etodesnitazene\" OR \"etonitazene\" OR \"flunitazene\" OR \"isotonitazene\" OR \"metodesnitazene\" OR \"metonitazene\" OR \"protonitazene\". Inclusion criteria encompassed &lt;i&gt;in vitro&lt;/i&gt; and animal studies, post-mortem toxicology, clinical trials, and case reports on nitazene poisoning. Data regarding naloxone dosing in confirmed cases of nitazene poisoning were also analyzed.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;We identified 1,383 studies, and after removing duplicates, 557 abstracts were screened. Based on the eligibility criteria, 78 articles underwent full-text screening, and 35 were included in the final review. Nitazenes exhibit variability in potency and toxicity. &lt;i&gt;In vitro&lt;/i&gt; studies suggest that their receptor affinity and potency often surpass those of both morphine and fentanyl. Real-world data indicate that &lt;i&gt;in vivo&lt;/i&gt; potency is often lower than experimental findings. Case reports and clinical series indicate that naloxone remains an effective antidote for nitazene poisoning. A median dose of parenteral naloxone 1.20 mg effectively reversed poisoning, with a median dose of 0.8 mg in the pre-hospital setting. However, a subset of patients received prolonged naloxone infusions due to the persistence of opioid effects. Six out of 30 patients were treated with naloxone infusions. This ratio is higher than that reflected in current clinical guidelines, in which shorter observation time is deemed sufficient. Post-mortem toxicological analyses reveal highly variable nitazene concentrations, with overlap with those concentrations found in patients. This complicates the establishment of lethal thresholds. In several cases, nitazene metabolites were detected in isolation, suggesting independent pharmacological activity or alternative routes of administration. Additionally, nitazene poisoning often involves polysubstance use, further complicating diagnosis and management.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Discussion: &lt;/strong&gt;Data on nitazene","PeriodicalId":520593,"journal":{"name":"Clinical toxicology (Philadelphia, Pa.)","volume":" ","pages":"393-406"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144153176","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical characteristics of patients exposed to medetomidine in the illicit opioid drug supply in Philadelphia - a case series.","authors":"Lauren Murphy, Alex Krotulski, Brendan Hart, Matthew Wong, Rebeccah Overton, Rita McKeever","doi":"10.1080/15563650.2025.2500601","DOIUrl":"10.1080/15563650.2025.2500601","url":null,"abstract":"<p><strong>Introduction: </strong>Medetomidine is an emerging adulterant in the illicit opioid drug supply with minimal data regarding clinical effects or blood concentrations after uncontrolled exposures in humans.</p><p><strong>Methods: </strong>A retrospective case series was performed of patients presenting to the emergency department after illicit opioid overdose with confirmed exposure to medetomidine. Patient outcomes and clinical data were summarized with descriptive statistics.</p><p><strong>Results: </strong>Eleven patients were included in the series. Whole blood medetomidine concentrations ranged from 1.2 μg/L to 16 µg/L. Patients had sinus bradycardia for a median of 3.4 h, and hypotension was not common. Six cases were admitted to the hospital, one to the intensive care unit, and all survived. All cases tested positive for fentanyl and xylazine, and other adulterants were common.</p><p><strong>Discussion: </strong>Sinus bradycardia was the most salient finding of patients with confirmed medetomidine exposure from the illicit opioid supply. Bradycardia resolved within the expected five half-lives determined by early drug studies, and no patient required atropine, electrical pacing, or vasopressors for hypotension. The duration and degree of bradycardia did not correlate well with medetomidine concentrations.</p><p><strong>Conclusion: </strong>In this retrospective case series, patients who tested positive for medetomidine had sinus bradycardia and required prolonged monitoring.</p>","PeriodicalId":520593,"journal":{"name":"Clinical toxicology (Philadelphia, Pa.)","volume":" ","pages":"438-441"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144113293","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effectiveness of early activated charcoal administration in managing single-dose paracetamol overdose: a retrospective review in Hong Kong.","authors":"Cheung Lun William Wong, Chi Keung Chan, Fei Lung Lau","doi":"10.1080/15563650.2025.2499537","DOIUrl":"10.1080/15563650.2025.2499537","url":null,"abstract":"<p><strong>Introduction: </strong>This study aimed to assess the effectiveness of early activated charcoal administration for the management of single-dose paracetamol overdoses in Hong Kong.</p><p><strong>Methods: </strong>We retrospectively analyzed electronic records from 2010 to 2020 to identify patients with paracetamol overdose. The inclusion criteria comprised individuals over the age of 12 years with a known toxic dose (≥7.5 g) of a standard paracetamol preparation, available serum paracetamol concentration, and a known ingestion time within 4 h. Patients were categorized into either an activated charcoal group or a no activated charcoal group. The paracetamol ratio (serum paracetamol concentration divided by the corresponding concentration on the 150 mg/L at 4 h treatment line) and the need for acetylcysteine were compared. The effect of the timing of activated charcoal administration was also investigated.</p><p><strong>Results: </strong>Of the 1,274 screened cases, 601 met the inclusion criteria. Activated charcoal was administered to 366 patients at a median time of 89 min (IQR: 56-134 min) post-ingestion, including 140 who received pre-hospital activated charcoal at a median time of 55 min (IQR: 56-134 min). Acetylcysteine was required by 18.3% of the activated charcoal group and 35.3% of the no activated charcoal group. Odds ratios for acetylcysteine requirement decreased with earlier administration: 0.23 at 1 h (95% CI: 0.11-0.45; <i>P <</i>0.001), 0.24 at 1-2 h (95% CI: 0.13-0.42; <i>P</i> <0.001) and 0.49 at 2-3 h (95% CI: 0.25-0.94; <i>P</i> = 0.037).</p><p><strong>Discussion: </strong>Pre-hospital administration of activated charcoal is now feasible in Hong Kong. Although activated charcoal is not a life-saving intervention, it appears to reduce the need for antidote treatment. Early activated charcoal administration is associated with reducing acetylcysteine requirements in paracetamol overdoses up to 3 h post-ingestion. Elderly patients showed higher acetylcysteine needs (adjusted OR: 4.31; 95% CI: 1.53-11.96; <i>P</i> = 0.005).</p><p><strong>Conclusion: </strong>Early activated charcoal administration, including pre-hospital use, was significantly associated with a reduced acetylcysteine requirement for paracetamol overdose, with benefits observed up to 3 h post-ingestion.</p>","PeriodicalId":520593,"journal":{"name":"Clinical toxicology (Philadelphia, Pa.)","volume":" ","pages":"420-425"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144201349","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mortality risk factors for patients with cardiotoxic exposures treated with high-dose insulin: analysis of the National Poison Data System^®.","authors":"Jon B Cole, Alexandru Ulici, Samantha C Lee, Matthew E Prekker, Brian E Driver, Arthur R Jurao, Travis D Olives","doi":"10.1080/15563650.2025.2502613","DOIUrl":"10.1080/15563650.2025.2502613","url":null,"abstract":"<p><strong>Introduction: </strong>High-dose insulin/glucose is an inotrope, vasodilator, and standard therapy for beta-adrenoceptor and calcium channel blocker poisoning, yet no large database studies have examined its use. This study sought to describe high-dose insulin use in the United States using the National Poison Data System^®. Determining mortality risk factors was the primary aim.</p><p><strong>Methods: </strong>We identified all National Poison Data System® cases in which \"High dose insulin/glucose\" therapy was Recommended or Performed from 2019 to 2021, the first three years National Poison Data System^® allowed specific coding for high-dose insulin. We developed logistic regression models to determine clinical factors associated with death in patients receiving high-dose insulin. We also evaluated methylthioninium chloride (methylene blue) use as a refractory vasoplegia marker.</p><p><strong>Results: </strong>High-dose insulin was used in 1,856 patients, primarily for exposures to calcium channel blockers (<i>n</i> = 1,116 [60%]) and beta-adrenoceptor blockers (<i>n</i> = 985 [53%]), with the most common drugs being amlodipine (<i>n</i> = 677 [61%]) and metoprolol (<i>n</i> = 371 [38%]). Death occurred in 431 [23%] patients; amlodipine was the most common cardiotoxicant in fatal exposures (<i>n</i> = 202 [47%]). Calcium channel blocker exposure was significantly associated with death compared to beta-adrenoceptor blockers (odds ratio 2.2; 95% CI: 1.6-3.8). Exposure to verapamil, compared to amlodipine or diltiazem, was associated with death (odds ratio 1.7; 95% CI: 1.0-2.7). Increasing age, hyperglycemia, heart block, and concomitant treatment with mechanical ventilation or vasopressors were all associated with death. Methylthioninium chloride was more commonly used in patients with amlodipine exposures (110/677 [16%]) than with verapamil or diltiazem (7/325 [2%]; <i>P <</i>0.001).</p><p><strong>Discussion: </strong>Among patients treated with high-dose insulin, amlodipine-exposed patients were more commonly treated with methylthioninium chloride, suggesting they experienced more refractory vasoplegia. As high-dose insulin is a vasodilator, more data are needed to better define the role for high-dose insulin in amlodipine poisoning.</p><p><strong>Conclusion: </strong>In this study of patients treated with high-dose insulin, exposure to calcium channel blockers was more lethal than beta-adrenoceptor blocker poisoning. Amlodipine was the most common cardiotoxicant in patients who lived or died, while verapamil was the most lethal cardiotoxicant.</p>","PeriodicalId":520593,"journal":{"name":"Clinical toxicology (Philadelphia, Pa.)","volume":" ","pages":"407-419"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144218544","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Approaches to the treatment of nerve agent poisoning with oximes - from experimental studies to the intensive care unit.","authors":"Horst Thiermann, Franz Worek, Gabriele Horn","doi":"10.1080/15563650.2025.2501266","DOIUrl":"10.1080/15563650.2025.2501266","url":null,"abstract":"<p><strong>Introduction: </strong>Organophosphorus poisoning is still a continuing threat to military forces and the civilian health sector. The therapeutic value of clinically used oxime antidotes is frequently a matter of controversy. In this narrative review, we will focus on nerve agent poisoning in particular and show how experimental results can be integrated into the therapy of patients.</p><p><strong>Methods: </strong>This narrative review is based primarily on the extensive studies conducted by the authors over many years, supplemented by appropriate literature to provide the reader with currently available knowledge of the effects of different organophosphorus compounds on the inhibition kinetics, the post-inhibitory reactions and oxime-induced reactivation. The importance of species differences for the translation of animal experiments to humans is discussed by means of suitable published studies. The literature that describes tools that enable the monitoring of organophosphorus compound poisoning or the detection of skin exposure to organophosphorus compounds is reviewed.</p><p><strong>Organophosphorus compounds: structure and characteristics: </strong>Organophosphorus compounds, including nerve agents and pesticides, have a common general formula. In consequence, the variations in the structure and the physicochemical properties result in differences in the intrinsic toxicity of organophosphorus compounds as well as the onset, severity, and duration of clinical symptoms.</p><p><strong>Mechanisms of organophosphorus poisoning: </strong>The most toxicologically relevant mechanism of organophosphorus compounds is the inhibition of acetylcholinesterase, resulting in the overstimulation of cholinergic synapses in the neuromuscular junction as well as the central and the autonomic nervous system.</p><p><strong>Signs and symptoms of organophosphorus poisoning: </strong>After exposure by inhalation to nerve agent vapour, symptoms may develop very fast, and death can occur within minutes. The paralysis of respiratory muscles and the medullary respiratory centre, as well as bronchoconstriction and bronchorrhoea, may lead to death rapidly. In contrast, the onset of clinical signs may be delayed after percutaneous exposure.</p><p><strong>Treatment of organophosphorus poisoning: </strong>Current medical therapy includes atropine, oximes, and benzodiazepines. Oximes act by the reactivation of organophosphorus-inhibited acetylcholinesterase.</p><p><strong>Test systems for the investigation of interactions between organophosphorus compounds and acetylcholinesterase: </strong>Based on the spectrophotometric Ellman assay, static <i>in vitro</i> test systems for the determination of the inhibitory potency of an organophosphorus compound, post-inhibitory reactions, and oxime-induced reactivation have been developed, and their value is assessed. In addition, several dynamic models (real-time determination of acetylcholinesterase activity, kinetic compute","PeriodicalId":520593,"journal":{"name":"Clinical toxicology (Philadelphia, Pa.)","volume":" ","pages":"375-392"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144153174","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Indications for and complications of endotracheal intubation in gamma-hydroxybutyrate (GHB) overdoses admitted to a toxicology unit.","authors":"Ingrid Berling, Michael A Downes, Kylie McArdle, Caitlyn Lovett, Geoffrey K Isbister","doi":"10.1080/15563650.2025.2503442","DOIUrl":"10.1080/15563650.2025.2503442","url":null,"abstract":"<p><strong>Background: </strong>Gamma-hydroxybutyrate is a central nervous system depressant that can lead to a severely reduced level of consciousness, necessitating endotracheal intubation and intensive care admission. This study aims to analyse the clinical reasoning for endotracheal intubation in gamma-hydroxybutyrate overdoses, the incidence of complications, and length of stay.</p><p><strong>Method: </strong>We conducted a retrospective review of gamma-hydroxybutyrate overdoses between January 2000 and December 2024 in a single toxicology centre. Data collected included demographics, reason for endotracheal intubation, presence of aspiration pneumonitis, and length of stay.</p><p><strong>Results: </strong>There were 159 gamma-hydroxybutyrate presentations and 37 patients (23%) required endotracheal intubation. Aspiration pneumonitis was confirmed in 11 patients (30%), including six of eleven with vomiting, three of five with laryngeal obstruction and two of fourteen intubated for airway protection.</p><p><strong>Discussion: </strong>Vomiting and a perceived risk of inadequate airway protection were the main indications for endotracheal intubation in gamma-hydroxybutyrate overdose, which did not entirely prevent aspiration pneumonitis. Use of the Glasgow Coma Scale alone for airway risk assessment in toxicology presentations may result in unnecessary intervention and may increase complications.</p><p><strong>Conclusion: </strong>These data highlight the need to better identify patients requiring airway intervention and develop strategies to reduce aspiration risk in patients with gamma-hydroxybutyrate overdose.</p>","PeriodicalId":520593,"journal":{"name":"Clinical toxicology (Philadelphia, Pa.)","volume":" ","pages":"434-437"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144113295","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}