Histopathological Profile In Fatal Yellow Phosphorous Poisoning

Yellow phosphorous (YP) is the toxic form of elemental phosphorous and the chief constituent of firecrackers and rodenticides. In India, the rodenticide paste is frequently used for the suicidal purpose. This study is an autopsy‐based observational study which describes the histopathological features of heart, lungs, liver, and kidney of fatal cases of YP poisoning. The most common autopsy features in the viscera were congestion and petechial hemorrhage. The liver histopathology findings were microvesicular steatosis (68%), hepatic necrosis (62%), macrovesicular steatosis (50%), inflammatory cells (46%), sinusoidal congestion (40%), cholestasis (32%), and toxic hepatitis (18%). Hepatic necrosis ranged from being focal to centrizonal in distribution. Congestion was the most common feature observed in the lungs and the kidney. This is the largest autopsy‐based study on YP poisoning till date. The histopathological features of liver were consistent with YP poisoning whereas the findings of heart, lungs, and kidney were nonspecific in nature.     

Increased Lung Weights in Drug‐related Fatalities

This study is of autopsy data for potential validation as to whether increased weights of the lungs support toxic effects of drugs as the cause of death. This retrospective study compared data from 133 deaths resulting from the toxic effects of drugs with previously reported normal lung weights (Toxicol Mech Methods, 22, 2012, 159; Am J Forensic Med Pathol 33, 2012, 368). The lung weights and their standard errors were used in a two‐sample independent t‐test comparing the average drug‐related death weight to the average control weights. To account for multiple comparisons, a Bonferroni‐adjusted alpha level of 0.0125 was used. We are 98.75% confident that the mean right lung weight for female drug‐related deaths is between 227 and 377 g greater than the mean right lung weight for female non‐drug‐related deaths. We are 98.75% confident that the mean right lung weight for male drug‐related deaths is between 245 and 378 g greater than the mean right lung weight for male non‐drug‐related deaths.     

Sniffing-associated deaths in Denmark

An account is given of 20 deaths, which occurred in association with sniffing during the period 1959 – 1978. The annual number of deaths was almost constant during the period. Most of the deaths occurred in males. Ether and trichloroethylene were the predominant toxic substances. The material was divided into two groups. Group A, 14 cases, included real sniffing deaths, the cause of death being poisoning by the substance inhaled. In group B, 6 cases, sniffing was a contributory factor to death: 2 cases of suffocation by obstruction, one case of carbon monoxide poisoning during fire, one case of septicemia/severe anemia caused by bone marrow depression, and one case of bleeding to death from stab wounds inflicted by a sniffer against a non-sniffer. The circumstances before and at the time of death are reported, together with the autopsy and toxicological findings when these were performed.     

An analysis of toxic deaths, 1982 to 1985, Pima County, Arizona

Toxic deaths in Pima County, Arizona, were studied over a four-year period. The deaths were analyzed according to cause and manner of death, toxic substance, and demographic data. The age group 40 to 49 years had the highest rate of suicide from toxic substances. The accident death rate was highest for ages 20 to 29 years. Carbon monoxide was most often found to be the cause of deaths in this study. The most prevalent drugs were narcotics followed by antidepressants, cocaine, and barbiturates. Comparisons are made with similar studies.     

Pediatric toxicologic deaths: a 10-year retrospective study

A 10-year retrospective study of pediatric toxicologic deaths was performed at the Medical University of South Carolina (Charleston, SC) from January 1989 to December 1998. During this time, 709 pediatric forensic autopsies were performed on children younger than 18 years of age. Eleven deaths were determined to be secondary to toxic exposures (excluding carbon monoxide poisonings secondary to fires). The remaining deaths were reviewed for the presence of alcohol or illicit drugs. The 11 toxicologic deaths were analyzed for age, sex, race, type of toxic exposure, cause and manner of death, location of incident, witness, and, in the younger age group, the primary caregiver at the time of exposure. The deaths had a bimodal age distribution (6 deaths in victims ages 15 to 17 and 5 deaths in victims ages 4 or younger), involving a wide range of toxins. The teenage group was composed of five males and one female, all white. The preschool group had three females and three males, all black. The manner of death ranged from accidental to suicidal to homicidal. In addition, in eight neonatal and fetal deaths, the victims tested positive for maternal cocaine use, and five of these victims tested positive for cocaine or benzoylecgonine. However, the cause of death was not stated to be cocaine in any of these neonatal and fetal cases.     

Some observations concerning blood morphine concentrations in narcotic addicts

Blood samples from deceased narcotic addicts were analyzed for morphine, and the results form persons who died from narcotic addiction were compared with those from homicide victims. In most instances morphine was detectable in both types of death, and usually the values obtained were less than 30 microgram/dl. Narcotic addiction deaths involving only morphine, or morphine plus a combination of ethanol, quinine, or diazepam (Valium), were also evaluated. In some cases high quantities of ethanol were present, and death could be attributed to the combined CNS depressant effects of morphine and ethanol. The quinine levels would not normally be considered toxic, however, and it could not be ascertained that the quantity of this drug present contributed to death. Diazepam was present in elevated concentrations, and its depressant effect may have been a factor in some narcotic addiction deaths.     

Fatal cocaine interactions: a review of cocaine-related deaths in Bexar County, Texas

Although cocaine is a widely abused illicit substance that is known to cause death, deaths due to its use appear to occur in a minority of those who use it. This report was designed to review drug-related deaths due to cocaine, and the concomitant use of other drugs/medications. A retrospective review of drug deaths at the Bexar County Medical Examiner's Office in San Antonio, Texas, was undertaken for cases where cocaine was one of the drugs implicated in causing death. Analysis was performed comparing the concentrations of cocaine and benzoylecgonine present and the absence or presence of other drugs. The data obtained showed that cocaine was toxic over a large range with deaths occurring at concentrations ranging from 0.01 to 78 mg/L. Analyses also indicated an increased lethality when cocaine is used in combination with ethanol, heroin, opiates, and antidepressant/antipsychotic medications, which is consistent with previous reports and research. Antihistamine data showed that there may be relationship between increased toxicity and co-ingestion, although more research is necessary.     

Positional Asphyxia in Opioid-Related Deaths: Is It Being Overlooked?

The contribution of positional asphyxia in opioid-related deaths is currently unknown. Diagnostic criteria for positional asphyxia include finding the decedent in a position that does not allow for adequate respiration and an inability to extricate themselves from the position due to various conditions. Our primary objective was to assess whether positional asphyxia and the resulting airway compromise were a contributing factor to death due to the toxic effects of opioids. We evaluated 225 deaths where the death scene investigation contained adequate information to evaluate for positional asphyxia and performed a Pearson chi-square test to determine if the proportion of deaths found in an airway compromising position was higher when opioid(s) caused the death. The proportion of decedents found in a potential airway compromising position was greater when the death was related to opioid use (p < 0.0001). Further, narrowing the dataset to decedents who were definitely in an airway compromising position [Yes (24.49%) vs. No (11.02%)] showed a statistically significant association between positional asphyxia and deaths related to opioid use (p = 0.0021). Carefully documenting the position in which the decedent was initially found may be a significant factor in accurate reporting and in harm reduction efforts to decrease the opioid mortality rate.     

Trigemino‐Cardiac Reflex as Lethal Mechanism in a Suicidal Fire Death Case

In the vast majority of immediate fire deaths, the mechanism of death is inhalation of toxic gases (especially carbon monoxide), direct thermal injury, or neurogenic shock due to the redistribution of the body's blood volume produced by surface heat on the skin. We present a suicidal case that is unusual because the mechanism of immediate fire death could arguably be explained in terms of a primitive autonomic reflex/the trigemino‐cardiac reflex. Although this reflex is well known to surgeons and anesthetists, with possible lethal consequences in the course of invasive surgical procedures on the head and neck region, it is much less familiar to forensic pathologists.     

Acetyl Fentanyl: Trends and Concentrations in Metro Detroit

Acetyl fentanyl (N‐[1‐phenethylpiperidin‐4‐yl]‐N‐phenylacetamide) is a potent opioid analgesic with no medicinal uses. We report deaths between 2016 and 2017 at the Medical Examiner's Office in Detroit, MI where acetyl fentanyl was found in the decedent's blood and compare them to previously published deaths between 2015 and 2016. The recent cases (cohort B) had a mean acetyl fentanyl concentration of 0.9 ng/mL (range: 0.1–5.3 ng/mL) and an associated higher concentration of fentanyl along with multiple other drugs present. The older cases (cohort A) had higher concentrations of acetyl fentanyl (mean: 8.9 ng/mL; range: 0.28–37 ng/mL) with lower, yet still toxic, concentrations of fentanyl. We conclude that the cause of death in these recent cases was likely multiple drug toxicity with fentanyl and that the consistently observed lower peripheral blood concentrations of acetyl fentanyl are most likely an artifact in the manufacture of the consumed illicit fentanyl.     

Plastic bag asphyxia in southeast Scotland

Death resulting from plastic bag asphyxia has been recognized for >40 years, but relatively little is known about either its epidemiology or its pathophysiology. Over 15 years (1984-1998), 30 deaths were attributed to plastic bag asphyxia among the 14,560 autopsies performed in the Forensic Medicine Unit in Edinburgh. These 30 deaths involved 20 male and 10 female subjects, with an age range of 13 to 81 years. Eleven had some alcohol measurable in the blood, with four having levels >80 mg/dl. Only one individual appeared to have ingested a drug overdose, but inhaled substances within the plastic bag may have contributed to death in five cases. The absence of childhood accidental deaths may reflect successful preventive measures. The 3 accidental deaths involved adults (including 2 who died of autoerotic asphyxia), and the remaining deaths were 27 suicides. Of those who committed suicide, most (59%) had chronic psychiatric illness rather than chronic debilitating or terminal physical illness. In contrast with reports from the United States, publicity associated with "self-deliverance" did not result in an increased number of deaths from plastic bag asphyxia (4 deaths in this series). Analysis of the circumstances of all the deaths revealed them to be difficult to predict and hence prevent.     

Diagnosis of lethal poisoning with some substances used by toxicomaniacs

The authors analyze 62 expert conclusions on deaths from acute and chronic poisoning with various toxic substances used by toxicomaniacs. Forensic medical examination of corpses and forensic chemical analysis identified drugs, toluene, freon, organophosphorus compounds, and other toxins.     

Unusual facial markings and lethal mechanisms in a series of gasoline inhalation deaths

A review of deaths associated with hydrocarbon toxicity from gasoline sniffing in South Australia throughout a 10 year period from July 1987 to June 2002 revealed 4 cases. The victims were all Aboriginal people from remote inland communities. Each death had occurred while the victim was lying in bed sniffing gasoline from a can held to the face. Once unconsciousness had occurred, the mouth and nose had been pressed firmly against the can by the weight of the head. In each case, the effects of gasoline toxicity had been exacerbated by hypoxia and hypercapnia from rebreathing into the container once a tight seal had been established between the face and the can. The circular impressions left by the can edges on the faces of each of the victims provided an autopsy marker that assisted in clarifying the details of the fatal episodes. Discouraging solitary gasoline sniffing in bed may reduce the death rate in communities where this behavior is practiced.     

Immunohistochemical distribution of C-reactive protein in the hepatic tissue in forensic autopsy

Previously, we examined the expression of C-reactive protein (CRP) in hepatic tissues in fatal injuries (injury deaths) immunohistochemically, and classified the CRP distribution into three patterns: diffuse (D-) pattern, diffuse with strong positivity in the hepatic lobules; periportal (PP-) pattern, characterized by positive cells in the periportal region of some lobules; focal (F-) pattern, showing small islands of positive cells in some lobules. There was a relationship between the CRP distribution and the survival time. In this study, we further analyzed the deaths including those due to other than fatal injuries (non-injury deaths), and a study of a total of 314 deaths from various causes was performed. Generally, non-injury deaths showed findings similar to those in injury deaths. PP- and/or F-patterns were observed in 43.7% of cases having a short survival time (<6 h), but found in only 3% of those surviving longer (>6 h), showing that such findings are suggestive of a short survival time. D-pattern was found more frequently in non-acute deaths (60.4%), than in acute deaths (10.9%). In acute deaths, D-pattern was found in some cases showing extensive tissue injuries, such as burns and polytrauma, and inflammative predisposition. Immunohistochemical findings also showed some correlation with the serum CRP level. Our data suggest that hepatic CRP immunohistochemistry may be a useful tool for elucidating the dying process.     

Alcohol in a series of medico-legally autopsied deaths in northern Norway 1973-1992

It is well established that use of alcohol increases the risk of fatal injuries. The presence of blood alcohol in autopsied deaths is regularly encountered in medico-legal practices. The aim of this study was to investigate the prevalence and concentration of alcohol in 1539 medico-legal autopsies in two counties in northern Norway in the period 1973-1992, and the reporting of acute alcohol influence among these deaths to the official cause-of-death statistics. Blood alcohol concentration (BAC) >/=0.5 per thousand (50 mg/100 ml) was found in 47.6% (n=456) of violent deaths tested, and in 93% (n=426) of these the BAC was >/=1.0 per thousand. In 17.4% (n=55) of tested natural deaths the BAC was >/=0.5 per thousand. Acute alcohol-influenced violent deaths were under-reported to the cause-of-death statistics. Deaths by motor vehicle traffic accidents did not differ from other violent deaths in this respect. The under-reporting among violent deaths was 41% in cases with BAC >/=0. 5 per thousand and 37% where the BAC was >/=1.0 per thousand during the whole period. It is concluded that post-mortem BAC >/=0.5 per thousand, should be regarded as a possible contributory cause in all violent deaths, and reported accordingly.     

Postmortem detection of isopropanol in ketoacidosis

Isopropanol (IPA) detected in deaths because of diabetic ketoacidosis (DKA) or alcoholic ketoacidosis (AKA) may cause concern for IPA poisoning. This study addressed this concern in a 15-year retrospective review of 260 deaths in which concentrations of acetone and IPA, as well as their ratios, were compared in DKA (175 cases), AKA (79 cases), and IPA intoxication (six cases). The results demonstrated the frequency of detecting IPA in ketoacidosis when there was no evidence of IPA ingestion. IPA was detectable in 77% of DKA cases with quantifiable concentrations averaging 15.1 ± 13.0 mg/dL; 52% of AKA cases with quantifiable concentrations averaging 18.5 ± 22.1 mg/dL; and in cases of IPA intoxication, averaging 326 ± 260 mg/dL. There was weak correlation of IPA production with postmortem interval in DKA only (r = -0.48). Although IPA concentrations were much higher with ingestion, potentially toxic concentrations were achievable in DKA without known ingestion.     

U.S. Navy and Marine Corps recruit training deaths in San Diego, California, 1973-1985; a review of 31 cases.

The deaths of military recruits associated with training activities nearly always fall under close scrutiny from relatives of the deceased recruit and the media. The literature contains isolated case reports of recruit deaths but no comprehensive reviews of all deaths at a single training facility. The purpose of this study is to describe the circumstances and causes of all recruit deaths occurring at the Naval Training Command and the Marine Corps Recruit Depot in San Diego, California, from 1973 through 1985. Thirty-one male recruits died in training during this period; eight died from medical conditions not detected by preenlistment questioning or examination. In five of these cases, the conditions were probably known to the recruit but were not listed on a medical history form. Seven recruits died in incidents related to training, and there were six cases of "sudden cardiac death," as well as eight deaths caused by infectious diseases.     

曲马多中毒及其毒理作用

曲马多为中枢非麻醉镇痛药,通过作用于μ阿片受体、抑制去甲肾上腺素与5-羟色胺再摄取等双重作用机制的协同作用。镇痛效果较好。在世界范围内被广泛应用于中、重度急、慢性疼痛的治疗。但目前有关曲马多不良反应与曲马多滥用中毒的案例报道正日益增多。本文从曲马多的镇痛机制、不良反应以及依赖滥用等方面,综述了导致曲马多中毒的可能因素,以期唤起人们对曲马多安全性的注意。     

Evaluation of human brain damage in fire fatality by quantification of basic fibroblast growth factor (bFGF), glial fibrillary acidic protein (GFAP) and single-stranded DNA (ssDNA) immunoreactivities

Burns and inhalation of toxic gases, including carbon monoxide (CO) and cyanide, which are produced by combustion, are major factors involved in fire death. The present study immunohistochemically investigated basic fibroblast growth factor (bFGF), glial fibrillary acidic protein (GFAP) and single-stranded DNA (ssDNA) in the brains of fire fatalities (n=49) to examine the differences between fatal burns and CO intoxication, compared with those in cardiac deaths (n=24) and mechanical asphyxiation cases (n=23). In acute fire fatality, neuronal ssDNA immunopositivity in the cerebral cortex of the parietal lobe was high in both fatal burns and fatal CO intoxication, but that of the pallidum was higher for CO intoxication than for burns. The number of neurons was decreased in prolonged fire deaths, irrespective of the severity of burns or CO intoxication, but glias were increased in cases of fatal burns. Prolonged deaths due to burns had a higher glial bFGF immunopositivity in the cortex and white matter, higher and lower glial GFAP immunopositivity in the cortex and white matter, respectively, and a low neuronal ssDNA immunopositivity in the cerebral cortex and hippocampus. In prolonged deaths due to CO intoxication, however, glial bFGF and GFAP immunopositivities were low at each site, but neuronal ssDNA immunopositivity showed a higher value. These observations suggest increased cerebral neuronal ssDNA immunopositivity to be a finding of vitality in acute fire death, and a neuronal loss accompanied by active glial responses after severe burns, and a neuronal loss and progressive apoptosis without glial responses after CO intoxication to be characteristic in prolonged death.     

Fatal intoxication due to ackee (Blighia sapida) in Suriname and French Guyana. GC-MS detection and quantification of hypoglycin-A

Between 1998 and 2001 the deaths of 16 Surinamese children were recorded along the Maroni River, which forms the border between Suriname and French Guyana. After a metabolic origin was eliminated, ethnobotanical research in the field led to a hypothesis of intoxication through the ingestion of ackee. Ackee (Blighia sapida) is a large green leafy tree of West African origin. Its unripe fruit contains large quantities of two toxic molecules: hypoglycin-A and hypoglycin-B, the former being the more toxic. We have developed a GC-MS procedure allowing us to demonstrate the presence of hypoglycin-A in the gastric fluid of one of the deceased children, and to compare the content of hypoglycin-A in fruit collected on the road to Paramaribo in Suriname (5.1mg/g) with samples from Burkina Faso (8.1mg/g) and Jamaica (9.2mg/g). Field research showed the misuse of this little-known plant by Maroon witch doctors. The Bushinengue witch doctors were informed about the dangers of ackee, and no new cases have been reported to date.