Fatal intoxication because of trihexyphenidyl

Trihexyphenidyl (THP) is an anticholinergic agent with forensic toxicological interest. We present a case of a 59-year-old woman with a history of paranoid disorder, who was found dead in the house where she lived alone. The autopsy findings revealed no marked pathological changes. Toxicological analysis based on gas chromatography-mass spectrometry (GC-MS) analysis revealed THP and its major metabolite (hydroxy-THP) in blood and urine, with THP concentrations of 0.053 and 0.560 mg/L, respectively. The blood and urine ethanol concentrations were low 0.096 and 0.100 g/L, respectively. Based on these results, we determined the cause of death to be THP poisoning. It is suggested that rare case of death associated with THP overdosage should be taken in conjunction with central nervous system depressants (benzodiazepines, ethanol) and/or with other pathological disorders. Thus, our case could not be supportive for this allegation.     

Diagnostic implication of blood and urine morphine content in alcohol intoxication

A total of 198 cases of acute parenteral poisoning with opiates are characterized. The range of concentrations of opiates metabolites in the blood and urine, main causes of death due to opiate poisoning in alcohol intoxication are analysed. Opiates toxicity was assessed with the logit-regression method and dose-effect curves valid for analysis of relationships between probability of death and opiate metabolites concentration in blood and urine. Correlation between probability of death and detection of morphine and ethanol in biological media of the victims is considered. Concentrations of morphine in blood and urine definitely indicating opiates poisoning in alcohol intoxication as a cause of death are determined.     

The significance of ethanolemia for the diagnosis of death from acute ethanol poisoning

Foci of myolysis of cardiac muscle fibers are suggested to be used for evaluation of thanatogenetic significance of ethanol concentration in cadaveric blood. This sign of acute ethanol poisoning is absent in case of other cause of death in a state of ethanol intoxication, even in the presence of high ethanolemia. Therefore, foci of myolysis are a sign of ethanol tolerance.     

Forensic medical significance of enzymatic products of ethanol oxidation in cadaveric brain

The concentrations of ethanol, acetaldehyde, and the oxidizing enzymes alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (AIDH) were measured in neuronal cytoplasm, limbic cortical capillaries, and cardiovascular center of the medulla oblongata. The measurements were carried out by histochemical methods, gas-liquid chromatography, etc. The results were processed with consideration for the degree and stage of ethanol intoxication in case of death from ethanol poisoning and asphyxia in hanging. Increase of ethanol concentration in the blood was associated with a decrease and then increase in the brain concentrations of ADH and with an increase of AIDH concentration. Enzymatic changes predominated in capillary walls; the minimum shifts were observed in the neuronal cytoplasm of the cerebral limbic cortex, which confirms the neurohumoral nature of detoxication regulation. Lethal ethanol poisoning could occur during any stage of ethanol intoxication. The detected changes in ethanol, acetaldehyde, and metabolizing oxidoreductases in brain tissue can be used for forensic medical diagnosis of ethanol poisoning.     

Role of alcohol in heroin overdose

The relationship between ethanol and risk of heroin overdosage was studied. Statistical processing of the results of forensic chemical analysis (460 expert evaluations) carried out in Chelyabinsk Regional Bureau of Forensic Medical Expert Evaluations in 2000 was carried out. The results of morphine and ethanol measurements in the blood and urine from corpses where deaths ensued from narcotic or ethanol poisoning, were analyzed. The concentrations of morphine in the blood and urine were measured on a gaseous chromatographer with mass-selective detector (Hewlett Packard HP 6890/HP-5972). Methods for measuring urinary and blood morphine are described. The results of statistical analysis demonstrated relationships between the age and ethanol concentrations in the blood and urine; blood ethanol and total urinary and blood morphine concentrations; blood concentration of free morphine and presence of 6-monoacetylmorphine in the blood. The authors conclude that the presence of ethanol in the blood together with morphine drastically augments the risk of rapid death from respiration arrest. It can also lead to a relatively high risk of overdosage in experienced narcomaniacs using heroin and ethanol.     

Forensic medicine and toxicologic aspects of 2-propanol poisoning

Two cases of poisoning with 2-propanol (isopropylalcohol) are reported. In one case, nail polish remover was drunk by a 2-year-old child. The concentration of 2-propanol and its metabolite acetone in the blood could be observed over a period of approximately 50 h. The highest concentration of 2-propanol determined was 4.22 g/l. Acetone reached a maximum value of 2.27 g/l 12 h after ingestion. The child survived without any observable after-effects. In the second case, a 35-year-old man drank ethanol in addition to 2-propanol. The poisoning was lethal. The possible time of intake before death is discussed in relation to the estimated levels of ethanol, 2-propanol and acetone found in the blood and urine. The histomorphological findings are often important as well with regard to time of intake.     

Comparison of blood-ethanol concentration in deaths attributed to acute alcohol poisoning and chronic alcoholism

Ethanol concentrations were measured in femoral venous blood in deaths attributed to acute alcohol poisoning (N = 693) or chronic alcoholism (N = 825), according to the forensic pathology report. Among acute alcohol poisonings were 529 men (76%) with mean age 53 years and 164 women (24%) with mean age 53 years. In the chronic alcoholism deaths were 705 men (85%) with mean age 55 years and 120 women (15%) with mean age 57 years. The blood-ethanol concentrations were not related to the person's age (r = -0.17 in acute poisonings and r = -0.09 in chronic alcoholism). The distribution of blood-ethanol concentrations in acute poisoning cases agreed with a normal or Gaussian curve with mean, median, standard deviation, coefficient of variation, and spread of 0.36 g/100 mL, 0.36 g/100 mL, 0.086 g/100 mL, 24% and 0.074 to 0.68 g/100 mL, respectively. The corresponding concentrations of ethanol in chronic alcoholism deaths were not normally distributed and showed a mode between 0.01 and 0.05 g/100 mL and mean, median, and spread of 0.172 g/100 mL, 0.150 g/100 mL, and 0.01 to 0.56 g/100 mL, respectively. The 5th and 95th percentiles for blood-ethanol concentration in acute poisoning deaths were 0.22 and 0.50 g/100 mL, respectively. However, these values are probably conservative estimates of the highest blood-ethanol concentrations before death owing to metabolism of ethanol until the time of death. In 98 chronic alcoholism deaths (12%) there was an elevated concentration of acetone in the blood (>0.01 g/100 mL), and 50 of these (6%) also had elevated isopropanol (>0.01 g/100 mL). This compares with 28 cases (4%) with elevated blood-acetone in the acute poisoning deaths and 22 (3%) with elevated blood-isopropanol. We offer various explanations for the differences in blood-ethanol and blood-acetone in acute poisoning and alcoholism deaths such as chronic tolerance, alcohol-related organ and tissue damage (cirrhosis, pancreatitis), positional asphyxia or suffocation by inhalation of vomit, exposure to cold coupled with alcohol-induced hypothermia, as well as various metabolic disturbances such as hypoglycemia and ketoacidosis.     

Rare Death Via Histamine Poisoning Following Crab Consumption: A Case Report

Histamine poisoning (scombroid food poisoning) is a toxicity syndrome that results from eating spoiled fish. To date, however, few poisoning (or mortality) cases have been reported in relation to crab consumption. Here, we describe a very uncommon case in which a 37‐year‐old woman and her 14‐year‐old son ate cooked crabs (Scylla serrata), resulting in the death of the female. Samples of vomitus, food residue, liver tissue, gastric content, intestinal content, and cardiac blood were analyzed by high‐performance liquid chromatography. Toxicological analysis revealed that histamine concentrations were very high in the cooked crab (47.08 mg/100 g) and intestinal content (22.54 mg/100 g). Comparing our toxicological results, police investigations, and family member statements, it can be assumed that the decedent ingested spoiled crabs, and by excluding other causes of death, lethal intoxication with histamine poisoning was confirmed.     

Phase-contrast and polarization microscopic studies of the myocardium in forensic medical practice]

Describes the major acute pathologic changes in the myocardiocytes detectable by phase-contrast and polarization microscopy. Demonstrates the significance of these changes for a correct diagnosis of sudden coronary death, death from ethanol poisoning or closed injuries of the heart after blunt trauma of the chest.     

Urine/blood ratios of ethanol in deaths attributed to acute alcohol poisoning and chronic alcoholism

The concentrations of ethanol were determined in femoral venous blood (BAC) and urine (UAC) and the UAC/BAC ratios were evaluated for a large case series of forensic autopsies in which the primary cause of death was either acute alcohol poisoning (N=628) or chronic alcoholism (N=647). In alcohol poisoning deaths both UAC and BAC were higher by about 2g/l compared with chronic alcoholism deaths. In acute alcohol poisoning deaths the minimum BAC was 0.74 g/l and the distribution of UAC/BAC ratios agreed well with the shape of a Gaussian curve with mean+/-standard deviation (S.D.) and median (2.5th and 97.5th centiles) of 1.18+/-0.182 and 1.18 (0.87 and 1.53), respectively. In alcoholism deaths, when the BAC was above 0.74 g/l (N=457) the mean+/-S.D. and median (2.5th and 97.5th centiles) UAC/BAC ratios were 1.30+/-0.29 and 1.26 (0.87 and 2.1), respectively. When the BAC was below 0.74 g/l (N=190), the mean and median UAC/BAC ratios were considerably higher, being 2.24 and 1.58, respectively. BAC and UAC were highly correlated in acute alcohol poisoning deaths (r=0.84, residual S.D.=0.47 g/l) and in chronic alcoholism deaths (r=0.95, residual S.D.=0.41 g/l). For both causes of death (N=1275), the correlation between BAC and UAC was r=0.95 and the residual S.D. was 0.46 g/l. The lower UAC/BAC ratio observed in acute alcohol poisoning deaths (mean and median 1.18:1) suggests that these individuals died before absorption and distribution of ethanol in all body fluids were complete. The higher UAC/BAC ratio in chronic alcoholism (median 1.30:1) is closer to the value expected for complete absorption and distribution of ethanol in all body fluids.     

Deaths in Unlicensed Alcohol Rehabilitation Facilities,

Non‐English‐speaking people do not always seek medical care through established institutions. This paper reports a series of deaths in unlicensed alcohol rehabilitation facilities serving Spanish‐speaking men. These facilities are informal groups of alcohol abusing men who live together. New members receive various treatments, including administration of ethanol or isopropanol, restraint, and seclusion. We reviewed 42 deaths in unlicensed alcohol rehabilitation facilities in Los Angeles County during the years 2003–2014. Data gathered included age, length of time spent in the facility, blood alcohol and drugs at autopsy, and cause and manner of death. Causes of death included acute alcohol poisoning, alcohol withdrawal, and a variety of other causes. Three cases were considered homicides from restraint asphyxia. The Department of Medical Examiner‐Coroner has worked with the police, district attorney, and State Department of Health Services to try to prevent additional deaths in unlicensed alcohol rehabilitation facilities. Nevertheless, prevention has been difficult.     

Under-recording of ethanol intoxication and poisoning in cause-of-death data: causes and consequences

In the present study we examined how consistently and completely the role of acute alcohol (ethanol) intake as a cause of death is reported on death certificates, how complete and specific the statistical recording of cause-of-death data on acute alcohol-induced deaths is, and how the information ultimately appears in the national mortality statistics. Data on all alcohol-positive deaths with blood alcohol concentration of ≥ 0.5‰ (g/kg) in Finland in 2005 (N = 2348) were reviewed. Overall, a concentration-dependent association was found between forensic-toxicologically determined blood alcohol concentrations and acute alcohol-specific cause-of-death diagnoses. Based on a medico-legal re-evaluation of death certificates, acute alcohol-specific causes were found to be underreported nationally at a rate of 8%. For accidental alcohol poisonings alone, the figure was about 1%. This underreporting was not corrected during recording of the cause-of-death data, though individual corrections and changes were observed. Especially, recording of multiple causes suffers from this underreporting of acute alcohol-specific causes. ICD-10 seems to do well in fulfilling the demands for a specific classification of uncomplicated alcohol poisoning. In combined alcohol-drug poisonings, however, ICD-10 shows a bias towards drugs over alcohol, even when alcohol has been specified and reported as the most toxic component by the medico-legal pathologist. Since the national statistics is based on the underlying causes, this state of affairs is likely to result in the underestimation of the role of acute alcohol intake as a cause of death. This observation of underreporting of acute alcohol-specific causes on death certificates should result in a harmonisation of education and principles and practices used in death certification. To increase the coverage and specificity of mortality statistics, based on the underlying causes of death, the coding of all components of alcohol-drug combinations and their classification according to the most important intoxicant or combination of intoxicants is recommended.     

Fatal brodifacoum rodenticide poisoning: autopsy and toxicologic findings.

This report details the pathologic and toxicologic findings in the case of a 15-year-old girl who deliberately and fatally ingested brodifacoum, a commonly used rodenticide. The mechanism of death, massive pulmonary hemorrhage, has not been previously reported. Brodifacoum was quantitated in liver, spleen, lung, brain, bile, vitreous humor, heart blood, and femoral blood using HPLC with fluorescence detection. The highest brodifacoum concentrations were detected in bile (4276 ng/mL) and femoral blood (3919 ng/mL). No brodifacoum was detected in brain or vitreous humor. A brodifacoum concentration of 50 ng/g was observed in frozen liver while formalin fixed liver exhibited a concentration of 820 ng/g. A very high blood:liver brodifacoum concentration ratio suggested acute poisoning but the historical and pathologic findings suggested a longer period of anticoagulation. Though most cases of brodifacoum poisoning in humans are non-fatal, this compound can be deadly because of its very long half-life. Forensic pathologists and toxicologists should suspect superwarfarin rodenticides when confronted with cases of unexplained bleeding. Anticoagulant poisoning can mimic fatal leukemia or infectious diseases such as bacterial sepsis, rickettsioses, plague, and leptospirosis. A thorough death scene investigation may provide clues that a person has ingested these substances.     

Interpreting results of ethanol analysis in postmortem specimens: a review of the literature

We searched the scientific literature for articles dealing with postmortem aspects of ethanol and problems associated with making a correct interpretation of the results. A person's blood-alcohol concentration (BAC) and state of inebriation at the time of death is not always easy to establish owing to various postmortem artifacts. The possibility of alcohol being produced in the body after death, e.g. via microbial contamination and fermentation is a recurring issue in routine casework. If ethanol remains unabsorbed in the stomach at the time of death, this raises the possibility of continued local diffusion into surrounding tissues and central blood after death. Skull trauma often renders a person unconscious for several hours before death, during which time the BAC continues to decrease owing to metabolism in the liver. Under these circumstances blood from an intracerebral or subdural clot is a useful specimen for determination of ethanol. Bodies recovered from water are particular problematic to deal with owing to possible dilution of body fluids, decomposition, and enhanced risk of microbial synthesis of ethanol. The relationship between blood and urine-ethanol concentrations has been extensively investigated in autopsy specimens and the urine/blood concentration ratio might give a clue about the stage of alcohol absorption and distribution at the time of death. Owing to extensive abdominal trauma in aviation disasters (e.g. rupture of the viscera), interpretation of BAC in autopsy specimens from the pilot and crew is highly contentious and great care is needed to reach valid conclusions. Vitreous humor is strongly recommended as a body fluid for determination of ethanol in postmortem toxicology to help establish whether the deceased had consumed ethanol before death. Less common autopsy specimens submitted for analysis include bile, bone marrow, brain, testicle, muscle tissue, liver, synovial and cerebrospinal fluids. Some investigators recommend measuring the water content of autopsy blood and if necessary correcting the concentration of ethanol to a mean value of 80% w/w, which corresponds to fresh whole blood. Alcoholics often die at home with zero or low BAC and nothing more remarkable at autopsy than a fatty liver. Increasing evidence suggests that such deaths might be caused by a pronounced ketoacidosis. Recent research has focused on developing various biochemical tests or markers of postmortem synthesis of ethanol. These include the urinary metabolites of serotonin and non-oxidative metabolites of ethanol, such as ethyl glucuronide, phosphatidylethanol and fatty acid ethyl esters. This literature review will hopefully be a good starting point for those who are contemplating a fresh investigation into some aspect of postmortem alcohol analysis and toxicology.     

Fatal Intoxications in a Forensic Autopsy Material from Epirus,Greece, During the Period 1998‐2010

In this retrospective study, we report the epidemiological characteristics of all poisoning deaths in Epirus, Greece, from 1998 to 2010; we present the toxicological findings and the statistical evaluation of the results. This is the first detailed scientific report on all the officially certified poisoning deaths concerning part of the Greek population. A total of 126 poisoning fatalities were recorded, 67 of them being mono‐intoxications (53.2%). The cause of poisoning was as follows: drugs of abuse (60%); carbon monoxide (19.8%); pesticides (9.5%); corrosives (4.8%); pharmaceuticals (4.8%); and spider bite (0.8%). The most frequently detected poisonous substances were as follows: heroin (65 cases), ethanol (55), benzodiazepines (42), carbon monoxide (25), cocaine (17), cannabinoids (17) and pesticides (12). Increasing tendency in poisoning death rates was recorded, due to an increase in accidental poisoning deaths attributed mainly to drugs of abuse (total, accidental, and drugs‐of‐abuse poisoning death rates per 100,000 inhabitants per year were 1.87, 1.19, and 0.79, respectively, in the period 1998–2002 and 3.97, 3.41, and 2.55, respectively, in the period 2007–2010).     

54例氯化琥珀胆碱中毒案件的法医学分析

目的观察分析氯化琥珀胆碱中毒案件的法医学表现,以期提高氯化琥珀胆碱中毒的检验鉴定。方法收集54例氯化琥珀胆碱中毒案例,通过病理学、毒理学变化及案件特点进行回顾性分析,观察氯化琥珀胆碱中毒的检验鉴定规律。结果氯化琥珀胆碱中毒的病理学表现以急性肺淤血、肺水肿等一般猝死改变为主,部分死者心肌排列紊乱及断裂。死者心血中均检见琥珀胆碱成分,皮肤组织部分检见琥珀胆碱成分。结论氯化琥珀胆碱中毒具有死亡快、手段隐蔽、难以抢救、易漏检等特点。对于猝死案件、死因可疑案件应将氯化琥珀胆碱作为常规检验指标,防止此类案件的未检或漏检。     

Postmortem blood and vitreous humor ethanol concentrations in a victim of a fatal motor vehicle crash

A 20-year-old male was found on the passenger side of a small car after a collision with a semi-trailer truck. Postmortem blood, collected from the chest cavity, and vitreous humor samples were collected following harvesting of the heart and bones. Gas chromatographic analysis revealed a blood ethanol concentration of 0.32 g/dL and a vitreous humor ethanol concentration of 0.09 g/dL. The stomach was intact and full of fluid and food, but its contents were not collected. Possible explanations for the large difference between the two results include diffusion of ethanol from the stomach into the chest cavity, contamination of the blood sample prior to collection, and ingestion of a large quantity of ethanol shortly before death. This case demonstrates the importance of proper quality assurance procedures in collecting postmortem specimens and of collecting a vitreous humor sample for ethanol analysis in postmortem toxicology cases.     

Forensic-medical diagnostic implication of morphine levels in the blood and urine

Toxicological characteristics are presented for 198 cases of acute parenteral poisoning with morphine and heroin. The range of their metabolites concentration in the blood and urine encountered in practice are analysed. Principal causes of death due to opiate poisoning in inpatients are shown. Opiates toxicity was assessed by the method of logit-regression and dose-effect curves for analysis of probability of death depending on opiate metabolite concentration in blood and urine. Relations between probability of death and detection of morphine in biological media of the victims are considered. Morphine concentrations in the blood and urine undoubtedly indicating morphine poisoning are determined.     

Diagnostic role of organ-specific isoforms of lactate dehydrogenase in blood plasma

Changes in plasm isoenzymic spectrum of lactate dehydrogenase (LDG), a glycolytic enzyme, were studied in death of cardiovascular diseases, ethanol poisoning and a mechanical injury. The tests used electrophoresis in 1% solution of agarose. Isoenzymic composition differed between the groups with acute coronary failure, chronic coronary heart disease, alcohol cardiomyopathy and a mechanical injury. Ethanol poisoning caused two types of characteristic shifts in LDG isoenzymic spectrum. Nomograms were designed for practical application in forensic medical expertise of sudden death.