Cases reported "Alcoholic Intoxication"

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1/8. Fatal acute alcohol intoxication in an ALDH2 heterozygote: a case report.

    On an evening in November, a 25-year-old man was found dead in his bedroom. There were many empty snap-out sheets for flunitrazepam tablets in the trash at his bedside. He had been beaten by a gang of young people earlier in the morning of the same day. At the medico-legal autopsy, although there were many bruises and/or abrasions on the whole body, only slight subdural hemorrhage was observed, and none of them was thought to be the cause of death. flunitrazepam and its metabolites were not detected in his body fluid by gas chromatography-mass spectrometry (GC-MS). Marked lung edema and a severe congestion of organs were observed. His blood alcohol concentration from the femoral vein was 2.00 mg/ml. Fatal cases of acute alcohol intoxication usually have shown higher alcohol concentration (2.25-6.23 mg/ml). Although the genotype of aldehyde dehydrogenase 2 (ALDH2) has not previously been mentioned as a contributing factor in determining the cause of death, in this case the genotype of ALDH2 was ALDH2*1/2 and thus is important. Those who possess the ALDH2*2 gene show high concentrations of acetaldehyde (AcH) at even comparatively lower alcohol levels. Consequently, the cause of death was considered to be acute alcohol intoxication including AcH poisoning.
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2/8. Clinical experience with the benzodiazepine antagonist flumazenil in suspected benzodiazepine or ethanol poisoning.

    The clinical efficacy of different doses of the specific benzodiazepine antagonist flumazenil was studied in a total of 72 patients with benzodiazepine or ethanol overdose. In a randomized double-blind study, 18 patients (group 1) and eight patients (group 2) with suspected benzodiazepine overdose received 5 mg (group 1) or 1 mg (group 2) flumazenil or placebo, respectively. The stage of coma, heart rate, blood pressure and respiratory rate were monitored within the following 15 min. If no change in the stage of coma was observed, 5 mg (group 1) or 1 mg (group 2) flumazenil were given, and the stage of coma, heart rate and blood pressure were again monitored. In a similar way, the effect of 5 and 1 mg flumazenil was investigated in 13 patients (group 3) and four patients (group 4) with ethanol intoxication. In an open trial, the clinical efficacy of flumazenil for the diagnosis of benzodiazepine or ethanol overdose was studied in 29 patients (group 5). In all patients, a toxicological screening confirmed benzodiazepine or ethanol overdose. None of the patients receiving placebo showed effects on stage of coma, heart rate, blood pressure or respiratory rate. patients with benzodiazepine overdose who received 5 mg flumazenil regained consciousness about 1-2 min after the end of injection. The effect of 1 mg flumazenil (group 2) on benzodiazepine-induced coma was less pronounced. In patients with ethanol overdose (group 3), ethanol-induced coma was reversed after 5 mg flumazenil more slowly than in patients of group 1. No effect of flumazenil on ethanol-induced coma was observed in group 4. In group 5, flumazenil proved to be useful for diagnosing benzodiazepine or ethanol intoxication. In one patient with coma due to carbamazepine overdose, flumazenil was also found to be effective. Additionally, a possible analytical interference of flumazenil and its metabolites with the identification of other benzodiazepines by a toxicological screening procedure was studied. Even after an oral dose of 200 mg flumazenil, no interference with immunological benzodiazepine assays (EMIT, TDX, and RIA) was found. A metabolite and an artifact of flumazenil could be identified in urine by gas chromatography/mass spectrometry.
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3/8. A fatal interaction of methocarbamol and ethanol in an accidental poisoning.

    A case is presented of a fatal drug interaction caused by ingestion of methocarbamol (Robaxin) and ethanol. methocarbamol is a carbamate derivative used as a muscle relaxant with sedative effects. Therapeutic concentrations of methocarbamol are reported to be 24 to 41 micrograms/mL. Biological fluids were screened for ethanol using the Abbott TDx system and quantitated by gas-liquid chromatography (GLC). Determination of methocarbamol concentrations in biological tissue homogenates and fluids were obtained by colorimetric analysis of diazotized methocarbamol. Blood ethanol concentration was 135 mg/dL (0.135% w/v) and urine ethanol was 249 mg/dL (0.249% w/v). methocarbamol concentrations were: blood, 257 micrograms/mL; bile, 927 micrograms/L; urine, 255 micrograms/L; gastric, 3.7 g; liver, 459 micrograms/g; and kidney, 83 micrograms/g. The combination of ethanol and carbamates is contraindicated since acute alcohol intoxication combined with carbamate usage can lead to combined central nervous system depression as a result of the interactive sedative-hypnotic properties of the compounds.
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4/8. fluoxetine overdose: a case report.

    A fatality due to the ingestion of fluoxetine and ethanol is reported. Quantitation of the drug and its active normetabolite was accomplished by gas chromatography with a flame ionization detector. Identification of the compounds was performed by gas chromatography/mass spectrometry. tissue distribution of fluoxetine and norfluoxetine, as well as analytical details, is presented.
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5/8. Gas chromatographic and gas chromatographic-mass spectrometric determination of gasoline in a case of gasoline vapor and alcohol poisoning.

    A case of fatal poisoning due to the combined effect of alcohol and gasoline following an automobile accident is described. Toxicological analyses by means of gas chromatography and gas chromatography-mass spectrometry permitted the identification and quantitation of alcohol and several hydrocarbons in the heart blood and in the gas in the lung. Great variation was found in the estimates of blood gasoline concentration, depending on which of six constituents of gasoline was chosen for quantitation. The cause of this variation is discussed, together with the possible mechanisms leading to death.
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6/8. Death caused by triazolam and ethanol intoxication.

    gas chromatography-mass spectrometry was used for the quantification of the hypnotic drug triazolam in human samples. In our case, death was attributed to triazolam and ethanol intoxication. The whole blood concentration of triazolam was 7.0 ng/ml and that of ethanol was 230 mg/dl. Based on the literature, this is the lowest triazolam concentration that has been associated with death.
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7/8. Isopropanol interference with breath alcohol analysis: a case report.

    The presence of interfering substances, particularly acetone, has historically been a concern in the forensic measurement of ethanol in human breath. Although modern infrared instruments employ methods for distinguishing between ethanol and acetone, false-positive interferant results can arise from instrumental or procedural problems. The case described gives the analytical results of an individual arrested for driving while intoxicated and subsequently providing breath samples in two different BAC Verifier Datamaster infrared breath alcohol instruments. The instruments recorded ethanol results ranging from 0.09 to 0.17 g/210 L with corresponding interferant results of 0.02 to 0.06 g/210 L over approximately three hours. Breath and venous blood specimens collected later were analyzed by gas chromatography and revealed in the blood: isopropanol 0.023 g/100 mL, acetone 0.057 g/100 mL and ethanol 0.076g/100 mL. Qualitative analysis of the breath sample by GCMS also showed the presence of all three compounds. This individual had apparently consumed both ethanol and isopropanol with acetone resulting from the metabolism of isopropanol. An important observation is that the breath test instruments detected the interfering substances on each breath sample and yet they did not show tendencies to report false interferences when compared with statewide interferant data.
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8/8. Sudden death due presumably to internal use of methamphetamine.

    A 26-year-old male was found naked and excited in the backyard of his neighbor's house. He was carried to a nearby hospital, and returned home with his family, but took a sudden turn for the worse and died. In a judicial autopsy, the ethanol concentration of blood was found to be 0.58 milligrams, and methamphetamine (MA) was detected in his blood by thin-layer chromatography. The concentration of MA in his blood was 4.38 mumol/dl, higher than the fatal level. The amount of MA in his stomach was 5.8 mg (34.58 mumol/100 g), indicating that he ingested MA by internal use. Among the autopsy cases of acute MA poisoning reported in japan, hyperesthesia is known to last 1-3 h before death, whether the administration is by intravenous injection or orally. But the present case is quite unusual, as the death followed 6 h or more of hyperesthesia. This was attributed to the patient's combined intake of alcohol with MA, as it is known to decrease the mortality in mice.
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