Gudrun Høiseth1, Grim Otto Berg-Hansen2, Jørg Mørland2. 1. Norwegian Institute of Public Health, Division of Forensic Medicine, Oslo, Norway; Center for psychopharmacology, Diakonhjemmet hospital, Oslo, Norway. Electronic address: gudrun.hoiseth@fhi.no. 2. Norwegian Institute of Public Health, Division of Forensic Medicine, Oslo, Norway.
Abstract
INTRODUCTION: The hip-flask defence (i.e. claiming ethanol intake after an incident) is difficult to refute by the use of ethanol analyses alone, as these may show decreasing concentrations shortly after intake of alcohol. The non-oxidative metabolites of ethanol, ethyl glucuronide (EtG) and ethyl sulphate (EtS) have a different pharmacokinetic profile, with peak concentrations in blood around 4h after intake. The aim of this study was to describe a method for using EtG-analysis for the purpose of estimating the time point of ethanol intake and to report cases in which this method is used. METHODS: Previously published studies are summarised. Also, in expert witness cases where the hip-flask defence is claimed, EtG and EtS were analysed in selected cases. Twelve such cases are reported. RESULTS: In previous studies, about 70 healthy volunteers have been included in different kinetic studies, demonstrating maximal individual concentrations of EtG always below 0.5 mg/L after 1 h, below 1 mg/L after 2 h and somewhat above 1 mg/L 4 h after a moderate alcohol intake (up to 80 grams of ethanol). Twelve cases are reported in the present study, where the suspect claimed no alcohol intake before driving, only intake after driving. In all 12 cases, ethanol concentration was lower in the second sample (taken approximately 30 min after the first). The median EtG concentration in the first sample was 4.13 mg/L (range 2.0-7.4) and 4.34 mg/L (range 2.1-7.2) in the second sample. One case showed an increase in EtG concentrations of 15% from first to second sample (the time difference between the samples was 32 min, with the first sample taken 41 min after driving). For the remainder of the cases, EtG concentrations were relatively stable. CONCLUSIONS: In all the presented cases, the levels of EtG were substantially higher than what would be expected only about 1-2h after a very recent alcohol intake. The relatively stable concentrations between the first and second sample also indicated that the high EtG concentrations were not caused by a rapid formation after a recent intake, as this would have demonstrated increasing concentrations over a time period of 30 min. In conclusion, EtG and EtS in blood could be a helpful tool in assessment of the hip-flask defence, in cases where the detected ethanol is claimed to be caused solely by a single intake after driving.
INTRODUCTION: The hip-flask defence (i.e. claiming ethanol intake after an incident) is difficult to refute by the use of ethanol analyses alone, as these may show decreasing concentrations shortly after intake of alcohol. The non-oxidative metabolites of ethanol, ethyl glucuronide (EtG) and ethyl sulphate (EtS) have a different pharmacokinetic profile, with peak concentrations in blood around 4h after intake. The aim of this study was to describe a method for using EtG-analysis for the purpose of estimating the time point of ethanol intake and to report cases in which this method is used. METHODS: Previously published studies are summarised. Also, in expert witness cases where the hip-flask defence is claimed, EtG and EtS were analysed in selected cases. Twelve such cases are reported. RESULTS: In previous studies, about 70 healthy volunteers have been included in different kinetic studies, demonstrating maximal individual concentrations of EtG always below 0.5 mg/L after 1 h, below 1 mg/L after 2 h and somewhat above 1 mg/L 4 h after a moderate alcohol intake (up to 80 grams of ethanol). Twelve cases are reported in the present study, where the suspect claimed no alcohol intake before driving, only intake after driving. In all 12 cases, ethanol concentration was lower in the second sample (taken approximately 30 min after the first). The median EtG concentration in the first sample was 4.13 mg/L (range 2.0-7.4) and 4.34 mg/L (range 2.1-7.2) in the second sample. One case showed an increase in EtG concentrations of 15% from first to second sample (the time difference between the samples was 32 min, with the first sample taken 41 min after driving). For the remainder of the cases, EtG concentrations were relatively stable. CONCLUSIONS: In all the presented cases, the levels of EtG were substantially higher than what would be expected only about 1-2h after a very recent alcohol intake. The relatively stable concentrations between the first and second sample also indicated that the high EtG concentrations were not caused by a rapid formation after a recent intake, as this would have demonstrated increasing concentrations over a time period of 30 min. In conclusion, EtG and EtS in blood could be a helpful tool in assessment of the hip-flask defence, in cases where the detected ethanol is claimed to be caused solely by a single intake after driving.