Citat:
AS FLUMAZENIL AN ANTAGONISTIC EFFECT IN GHB-INDUCED CNS DEPRESSION ?
Grob U, Schiltknecht M, Rentsch K, Kupferschmidt H. Department of Internal Medicine, Institute of Clinical Chemistry, Division of Clinical Pharmacology and Toxicology, Department of Medicine, University Hospital, Zurich, and Swiss Toxicological Information Centre, Zurich, Switzerland.
Background: The benzodiazepine antagonist flumazenil is not regarded as efficacious to reverse gammahydroxybutyrate (GHB)-induced CNS depression, although it interacts with the GABA receptor complex.
Case Report: A 36 year-old white caucasian male presented to our Emergency Department in frank coma (Glasgow Coma Scale 3) at time = 0. We only later learned that he had ingested GHB and some alcohol approximately one hour previously. His pupils were pinpoint, the physical examination was otherwise unremarkable, with no meningeal signs. At t = +5 min. blood was drawn for chemistry and an intravenous line was inserted. Because drug-induced coma was suspected, naloxone 0.4 mg was administered intravenously at t = +30 min. without effect. At t = +105 min. flumazenil 0.2 mg was given via the intravenous line, with a rapid and complete reversal of the coma (GCS rose from 3 to 14 within 5 minutes), with no relapse. Plasma GHB concentration was 137 mg/L; ethanol, benzodiazepines, zolpidem and zopiclone were non-detectable.
Conclusion: This well-documented report shows a striking effect of flumazenil on GHB-induced coma. The only alternative explanation is that arousal and flumazenil administration were coincidental. Against this view stands the close temporal relationship between the two events, the fact that plasma GHB concentration was very high 100 minutes earlier, and that the presence of flumazenil-sensitive drugs was excluded. The effect of flumazenil in this setting should be studied prospectively.
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