ArticleScandinavian journal of trauma, resuscitation and emergency medicine2016
Presentations to an urban emergency department in Switzerland due to acute γ-hydroxybutyrate toxicity.
Article in Scandinavian journal of trauma, resuscitation and emergency medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 19 citations in OpenAlex.
- Butanediol Conversion to Gamma-Hydroxybutyrate Markedly Reduced by the Alcohol Dehydrogenase Blocker Fomepizole.Clinical pharmacology and therapeutics · 2019Trial
- Effect of γ-hydroxybutyrate (GHB) on driving as measured by a driving simulator.Psychopharmacology · 2018Trial
- Article
- γ-Hydroxybutyric Acid: Pharmacokinetics, Pharmacodynamics, and Toxicology.The AAPS journal · 2021Review
- Designer drugs: mechanism of action and adverse effects.Archives of toxicology · 2020Review
- Effects of Recreational GHB Use and Multiple GHB-Induced Comas on Brain Structure and Impulsivity.Frontiers in psychiatry · 2020Article
- Recreational use of GHB is associated with alterations of resting state functional connectivity of the central executive and default mode networks.Human brain mapping · 2019Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundγ-Hydroxybutyrate (GHB) is a drug of abuse with dose-dependent sedative effects. Systematic data on the acute toxicity of GHB from emergency department (ED) presentations over a long period of time are currently missing from the literature. The present study described the clinical features of GHB toxicity.
methodsRetrospective case series of GHB intoxications seen in an urban ED.
resultsFrom January 2002 to September 2015, 78 GHB-related intoxication cases were recorded (71 % male patients). The mean ± SD age was 29 ± 8 years. The co-use of alcohol and/or other illicit drugs was reported in 65 % of the cases. Neurological symptoms other than central nervous system depression included agitation (40 %) and clonus (21 %). The most frequent reasons for admission were coma (64 %) and agitation (23 %). The median time to regain consciousness was 90 min (range, 3-400 min). Sudden recovery was reported in 25 cases (32 %). Coma was not significantly associated with polyintoxication. Coma occurred in 77 % of the alcohol co-users and in 62 % ofthe non-alcohol users (p=0.052). The mean recovery time in comatose patients was 142 min in patients with co-use of alcohol compared with 89 min in patients without alcohol co-use (p=0.07). Alcohol co-use was not significantly associated with nausea/vomiting (p=0.07). The co-use of stimulants was not significantly associated with non-responsive coma (Glasgow Coma Scale = 3) or mean recovery time. Analytical confirmation of GHB was available in 37 cases (47 %), with additional quantitative analysis in 20 cases. The median GHB concentration was 240 mg/L (range, 8.3-373 mg/L). Intoxication was severe in 72 % of the cases. No fatalities occurred, and 72 % of the patients were discharged directly home from the ED. DISCUSSION: There were trend associations between alcohol co-use and frequency and length of coma and nausea/vomiting which did not reach the significance level (all p=0.05-0.07) but may nevertheless be clinically relevant. As the exact time of use is not always known, and co-use of other substances can affect the severity of poisoning, no definitive conclusions can be drawn regarding the association between GHB concentration and severity.
conclusionImpaired consciousness and agitation were typical findings of GHB intoxication. The co-use of alcohol and/or other illicit substances is common but was not significantly associated with the severity of the intoxications in our study.
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