Pesticide poisoning initially suspected as a natural death

A pesticide poisoning victim suspected initially as having died a natural death was autopsied. The victim was a 47-year-old male. Macroscopically, signs of acute death and, in particular, general erosion in the mucosa of the airways and esophagus were observed. In the gastric contents, which had a pungent smell and a greenish-brown color, 5.00 g/L of propanil, 1.27 g/L of carbaryl, 0.38 g/L of ethylbenzene, and 0.32 g/L of xylene were detected. In the blood (serum), 21.6 mg/L of propanil, 8.1 mg/L of carbaryl, 1.7 mg/L of ethylbenzene, and 4.0 mg/L of xylene were identified. Postmortem methemoglobinemia (45%) was recognized. The cause of death was considered to have been pesticide poisoning; propanil was probably most responsible for his death. The police considered the case to be "death with illness as the suspected cause." By performing an autopsy, however, we were able to clarify that the cause of death was pesticide poisoning.     

Atropine Eye Drops: An Unusual Homicidal Poisoning

In March 2009, the body of a 51‐year‐old man was found in the boot of his car. The body had been frozen before being dismembered at the abdomen. The autopsy failed to determine the cause of death. Systematic toxicological analyses of the victim's peripheral blood and urine showed the presence of atropine, a powerful anticholinergic. Atropine was therefore specifically detected and quantified throughout the victim's biologic samples by HPLC‐MS² in the biologic fluids and UHPLC‐MS² in the hair. The atropine concentrations were 887 ng/mL in the cardiac blood, 489 ng/mL in the peripheral blood, 6693 ng/mL in the gastric contents (1.1 μg), 6753 ng/mL in the urine, and 2290 pg/mg in the hair. The blood concentrations measured in the decedent were consistent with an overdose of atropine, which was determined as the cause of death. The manner of death was a homicide with criminal intent.     

Fatal Acute Poisoning from Massive Inhalation of Gasoline Vapors: Case Report and Comparison with Similar Cases

We describe a case of an acute lethal poisoning with hydrocarbons resulting from massive accidental inhalation of gasoline vapors. The victim, a 50‐year‐old man was found unconscious inside a control room for the transport of unleaded fuel. Complete autopsy was performed and showed evidence of congestion and edema of the lungs. Toxicological investigation was therefore fundamental to confirm exposure to fumes of gasoline. Both venous and arterial blood showed high values of volatiles in particular for benzene (39.0 and 30.4 μg/mL, respectively), toluene (23.7 and 20.4 μg/mL), and xylene isomers (29.8 and 19.3 μg/mL). The relatively low values found in the lungs are consistent with the fact that the subject, during the rescue, underwent orotracheal intubation followed by resuscitation techniques, while the low concentrations for all substances found in urine and kidneys could point to a death that occurred in a very short time after first contact with the fumes of gasoline.     

Post-mortem cases involving amphetamine-based drugs in the Netherlands: Comparison with driving under the influence cases

In this study we reviewed the post-mortem cases in the years 1999–2004 that were presented at the Netherlands Forensic Institute. The concentrations of amphetamine-based drugs in femoral blood from cases of suspected unnatural death were compared with concentrations in whole blood from non-fatal cases of driving under the influence (DUI cases) and with literature. Furthermore, the combinations with other drugs and/or alcohol were investigated. Amphetamine-based drugs were present in 70 post-mortem cases and 467 DUI cases. The most detected amphetamine-based drug was MDMA, followed by amphetamine. The presence of MDA could usually be explained by metabolism of MDMA. Methamphetamine and MDEA were rarely present. Frequently, the amphetamine-based drugs were taken in combination with alcohol and/or other non-amphetamine-based drugs such as cocaine or cannabinoids. The 70 post-mortem cases were divided into 38 amphetamine-based drug caused (i.e. the amphetamine-based drug directly caused or contributed to the death) and 32 amphetamine-based drug related deaths (i.e. death was not directly caused by the amphetamine-based drug). In the latter category, other (poly)drug intoxications and death by violence or drowning were the most frequent causes of death.In 30 cases, MDMA caused death directly. The range in blood concentrations of MDMA in these cases was substantial, i.e. 0.41–84 mg/L with a median concentration of 3.7 mg/L (n = 30). MDMA blood concentrations in the MDMA related deaths (n = 20) and in the DUI cases (n = 360) varied up to 3.7 and 4.0 mg/L, respectively. Seven victims died from the direct effects of amphetamine; the blood concentration of amphetamine ranged from 0.24 to 11.3 mg/L, with a median concentration of 1.7 mg/L (n = 7). The median concentrations of amphetamine in the amphetamine related deaths (n = 13) and the DUI cases (n = 208) were much lower, i.e. 0.28 and 0.22 mg/L, respectively. Amphetamine blood concentrations up to 6.0 and 2.3 mg/L were seen in the drug related deaths and DUI cases, respectively. The most frequently encountered amphetamine-based drugs in the investigated deaths were MDMA and amphetamine. The majority of MDMA- and amphetamine-caused deaths, i.e. 90% of these deaths, occurred with blood concentrations above 1.5 and 0.80 mg/L, respectively. MDMA and amphetamine blood concentrations in drug related deaths and DUI cases, however, overlap the range of fatal concentrations. Therefore, MDMA or amphetamine concentrations should never be used alone to establish the cause of death.     

Contributory and Incidental Blood Concentrations in Deaths Involving Citalopram

All cases presenting to the New South Wales Department of Forensic Medicine between January 1, 2001 and December 31, 2010 in which citalopram was detected were retrieved. A total of 348 cases were identified. Citalopram contributed to death in 21.0%, and was incidental in 79.0%. Cases in which citalopram was contributory to death had significantly higher blood citalopram concentrations than incidental cases (0.50 mg/L vs. 0.30 mg/L). Citalopram concentrations varied significantly by contributory status: sole citalopram toxicity (median = 1.30 mg/L), citalopram/other drug toxicity (0.50 mg/L), and incidental cases (0.30 mg/L). Citalopram concentrations also varied by suicide status, with the highest concentration found in suicides where citalopram contributed to death (0.70 mg/L) compared with 0.50 mg/L for nonsuicide cases where citalopram contributed to death. In almost all contributory cases (69/73), other psychoactive substances were also detected, most commonly benzodiazepines (47.9%), alcohol (45.2%), and opioids (40.1%).     

A Fatality Following Ingestion of the Designer Drug Meta‐Chlorophenylpiperazine (mCPP) in an Asthmatic—HPLC‐MS/MS Detection in Biofluids and Hair

A 20‐year‐old man, a cocaine addict and regular ecstasy user, with a medical history of allergic asthma died after ingesting half a tablet earlier the same day. The white tablet, stamped with a “smiling sun” logo looked very much like an ecstasy tablet and was sold as such. He experienced a severe asthma attack just after ingesting the half tablet and it evolved over the next few hours into fatal cardiorespiratory arrest. Biological samples, taken after embalming, were analyzed by high‐performance liquid chromatography tandem mass spectrometry (HPLC‐MS/MS). Analysis revealed meta‐chlorophenylpiperazine (mCPP) in concentrations of 45.8 mg in a similar tablet obtained later from the drug dealer, 5.1 ng/mL in the bile, 0.3 ng/g in the liver, 15.0 ng/mL in the urine, and its absence in a hair sample (<0.02 ng/mg), which indicated he was not a regular user (whereas strong concentrations of MDMA and cocaine were found in the hair). Interrogated by the police after his arrest, the dealer said that he had sold the victim and for the very first time two tablets with the same “smiling sun” logo. The tablet used for analysis was from the same brand as the one ingested by the victim. The autopsy excluded other causes of death, while the histological analyses showed a large number of polynuclear eosinophils in the bronchial walls, confirming the asthmatic pathology. None of the other organs examined (larynx, liver, heart, adrenal glands, and kidneys) showed any distinctive signs, and in particular no inflammatory infiltrate. The death was the result of an asthma attack in an asthmatic person, violently decompensated following ingestion of approximately 20 mg of mCPP.     

Reporting a sudden death due to accidental gasoline inhalation

The investigation of uncertain fatalities requires accurate determination of the cause of death, with assessment of all factors that may have contributed to it. Gasoline is a complex and highly variable mixture of aliphatic and aromatic hydrocarbons that can lead to cardiac arrhythmias due to sensitization of the myocardium to catecholamines or acts as a simple asphyxiant if the vapors displace sufficient oxygen from the breathing atmosphere. This work describes a sudden occupational fatality involving gasoline. The importance of this petroleum distillate detection and its quantitative toxicological significance is discussed using a validated analytical method. A 51 year-old Caucasian healthy man without significant medical history was supervising the repairs of the telephone lines in a manhole near to a gas station. He died suddenly after inhaling gasoline vapors from an accidental leak. Extensive blistering and peeling of skin were observed on the skin of the face, neck, anterior chest, upper and lower extremities, and back. The internal examination showed a strong odor of gasoline, specially detected in the respiratory tract. The toxicological screening and quantitation of gasoline was performed by means of gas chromatography with flame ionization detector and confirmation was performed using gas chromatography-mass spectrometry. Disposition of gasoline in different tissues was as follows: heart blood, 35.7 mg/L; urine, not detected; vitreous humor, 1.9 mg/L; liver, 194.7 mg/kg; lung, 147.6 mg/kg; and gastric content, 116,6 mg/L (2.7 mg total). Based upon the toxicological data along with the autopsy findings, the cause of death was determined to be gasoline poisoning and the manner of death was accidental. We would like to alert on the importance of testing for gasoline, and in general for volatile hydrocarbons, in work-related sudden deaths involving inhalation of hydrocarbon vapors and/or exhaust fumes.     

A fatal case of pure ethanol ingestion

An adult male was found dead in a car with two empty bottles (500 ml x 2) labeled dehydrated ethanol (>99.5%, v/v). At autopsy, extensive pancreatic necrosis with severe hemorrhage was observed. High concentrations of ethanol were detected in blood (8.14 mg/ml), urine (8.12 mg/ml) and tissue specimens. The cause of death was determined to be an acute alcohol intoxication caused by ingesting approximately 1l dehydrated ethanol.     

Acute Benztropine Intoxication and Fatality

A woman was found unresponsive with an empty bottle of Cogentin^® prescribed to another. Admitted to an area hospital, her condition steadily declined until death 29 h after admission. Following toxicological screening on hospital (admission) whole blood, the only significant compound detected was benztropine. Benztropine was confirmed at 0.28 mg/L – the highest antemortem blood concentration recorded in a case of toxicity or fatality uniquely associated with benztropine. A second serum antemortem specimen showed a benztropine concentration of 0.19 mg/L. Despite over 24 h in the hospital, benztropine was also found in the postmortem specimens collected at autopsy. Peripheral blood, central blood, liver, and gastric concentrations were 0.47 mg/L, 0.36 mg/L, 9.6 mg/kg, and 44 mg, respectively. These results indicate that benztropine exhibited a potential difference between whole‐blood and serum (plasma) concentrations. Additionally, in consideration of literature data, benztropine was found indicative of a compound prone to at least some postmortem redistribution.     

Characteristics and dose-effect relationship of clinical gamma-hydroxybutyrate intoxication: A case series

Gamma-Hydroxybutyrate (GHB) overdoses cause respiratory depression, coma, or even death. Symptoms and severity of poisoning depend on blood-concentrations and individual factors such as tolerance. A retrospective case study was conducted, evaluating GHB intoxication cases. GHB-concentrations in blood and urine were determined by gas chromatography-mass spectrometry (GC-MS) along with, in part, via enzymatic assay. GHB-concentrations, demographic data, and additional drug use, as well as specific clinical information, were evaluated. The correlation between GHB-levels in blood and associated symptoms were examined. In total, 75 cases originating from the Emergency Departments (EDs) of Hamburg and surrounding hospitals were included. Fifty-four of the patients (72%) were male. The mean GHB-concentration in blood was 248 mg/L (range 21.5–1418 mg/L). Out of the group with detailed clinical information (n = 18), the comatose group (n = 10/18) showed a mean of 244 mg/L (range 136–403 mg/L), which was higher than that of the somnolent and awake patients. Of the comatose collective, 70% (n = 7) showed co-use of one or more substances, with the additional use of cocaine being the most frequently detected (n = 5). In conclusion, a moderate dose-effect relationship was observed, although, there was some overlap in dosage concentration levels of GHB in awake and comatose patients. In GHB-intoxication cases, co-use was common as were clinical effects such as acidosis, hypotension, and impact on the heart rate. Timely analytical determination of the GHB-concentration in blood could support correct diagnosis of the cause of unconsciousness.     

Postmortem Fluid Concentrations of Heroin Biomarkers and Their Metabolites

Only limited data exist concerning the utility of complementary specimens in heroin-related deaths. As such, this report employed a validated LC-MS-MS method to quantify 6-monoacetylmorphine (6-MAM), 6-acetylcodeine (6-AC), and their metabolites morphine and codeine in blood with (BN) and without preservative (B) and the additional unpreserved specimens of vitreous humor, urine, stomach contents, and bile from 20 postmortem cases in which heroin was the primary cause of death. The median concentration of 6-MAM in BN was 0.011 mg/L, B was 0.008 mg/L, urine was 0.186 mg/L, vitreous humor was 0.022 mg/L, stomach contents was 0.147 mg/L, and bile was 0.012 mg/L. Only one case was found to be positive for 6-AC in B (case 6, 0.002 mg/L), and the median concentration of 6-AC was 0.002 mg/L in BN, 0.012 mg/L in urine, 0.003 mg/L in vitreous humor, 0.057 mg/L in stomach contents, and 0.004 mg/L in bile. These findings present new information on the distribution of these analytes in complementary matrices and support their inclusion for accurately determining the role of heroin in opioid-related deaths.     

Fatal cyclobenzaprine overdose with postmortem values

There are only two published cases of overdose with postmortem blood cyclobenzaprine concentrations, both with confounding factors. We report two additional cases of fatal cyclobenzaprine overdose with postmortem values. Case 1: a 56-year-old female was found in full cardiopulmonary arrest after a verbal suicide threat to a friend. Postmortem blood concentrations were cyclobenzaprine 0.96 mg/L and diazepam 0.3 mg/L. Case 2: a 37-year-old male was found in full arrest by a family member after an intentional ingestion of cyclobenzaprine. Postmortem blood concentrations were cyclobenzaprine 0.8 mg/L and ethanol 0.174 gm/dL. The concentrations of diazepam and ethanol reported in these two patients were not found in quantities usually associated with a fatal outcome, suggesting that the cyclobenzaprine was the primary cause of the fatality. Additionally, the blood was drawn from a femoral site, so that postmortem redistribution is not a likely factor. Blood concentration of > or = 0.8 mg/L cyclobenzaprine may be associated with a fatal outcome.     

Fatal bupivacaine intoxication following unusual erotic practices

A fatal drug overdose is described which involved unusual erotic practices. A 54-year-old male was discovered supine on the floor surrounded by sexual paraphernalia, syringes, and medications including three empty bottles of bupivacaine. Acute and chronic injection sites of the external genitalia with contusions, scarring, focal necrosis, and calcification were present at autopsy. Toxicology revealed femoral blood, heart blood, and vitreous bupivacaine concentrations of 3.8, 2.8 and 1.3 mg/L, respectively. The urine bupivacaine concentration was 11.4 mg/L. The cause of death was attributed to bupivacaine intoxication and the manner of death was accidental.     

Reporting a fatality during tumescent liposuction

Deaths of patients during elective surgery have drawn attention to the danger of anesthesia. Tumescent local anesthesia is subcutaneous infiltration of large volumes of dilute lidocaine with epinephrine to produce vasoconstriction while delivering anesthesia over large areas without lidocaine toxicity. This report documents the case of a 38-year-old woman who attended an outpatient clinic to undergo liposuction of the abdomen and bilateral hips and thighs. According to one witness, around 30 min after anesthesia administration, the victim suffered an episode of tonic–clonic convulsion. When the emergency medical services arrived the patient was in asystole. She died in spite of attempted cardiopulmonary resuscitation. The patient had no significant past medical history including no history of allergies or any known complications with anesthesia. A complete autopsy was performed and possible causes of death such as myocardial infarction, aspiration of food or foreign body, and pulmonary embolism were discarded. Anaphylactic shock was considered a possible but unlikely explanation for the fatality. Toxicological analyses revealed the presence of lidocaine and mepivacaine in heart blood, at concentrations of 4.9 and 16.2 mg/L, respectively. All drugs involved in the case were detected using gas chromatography with nitrogen–phosphorus detector and confirmed using gas chromatography–mass spectrometry full scan mode after solid-phase extraction using Chem-Elut columns. An additional high-performance liquid chromatography coupled to diode-array detection screening also obtained the same results. Based on the autopsy findings, case history, and toxicology results, the forensic pathologists ruled that the cause of death was an overdose of local anesthetic agents. The Court of Law ruled the death as an involuntary homicide due to gross negligence.     

Postmortem oxycodone and hydrocodone blood concentrations

There is limited data on postmortem oxycodone concentrations, consisting of three published reports with a total of 11 cases, many of which were polypharmacy cases. This report presents the results of a review of autopsy and coroner's reports from 10 counties for the years 2000 and 2001 to locate cases with oxycodone or hydrocodone exposure as a leading cause of death. Eighty-eight cases were located. Twenty-four deaths were attributed to oxycodone alone. Mean and median postmortem oxycodone blood concentrations were 1.23 mg/L and 0.43 mg/L, respectively. The range was 0.12 to 8.0 mg/L, with 13 cases (54%) < or = 0.5 mg/L. Seventeen deaths were attributed to hydrocodone alone. Mean and median postmortem hydrocodone blood concentrations were 0.53 mg/L and 0.40 mg/L, respectively. The range was 0.12 to 1.6 mg/L, with 11 cases (65%) < or = 0.5 mg/L. There were seven cases where the cause of death was attributed to the effects of a combination of hydrocodone and oxycodone. Mean oxycodone and hydrocodone blood concentrations were 0.34 mg/L and 0.14 mg/L, respectively. Forty cases involved polysubstance overdoses with significant involvement of other drugs and ethanol. Mean oxycodone and hydrocodone blood concentrations were 0.18 mg/L and 0.29 mg/L, respectively. The list of other substances involved was extensive but included ethanol, amitriptyline, methadone, codeine, propoxyphene, and acetaminophen. The findings of this study report oxycodone values associated with a fatality at blood concentrations lower than previously reported. This may represent enhanced information because of the larger sample group. Hydrocodone values associated with a fatality were similar to previously published values.     

The relationship of methanol and formate concentrations in fatalities where methanol is detected

An automated headspace gas chromatography method was developed for the determination of formate (formic acid) in postmortem specimens, based on the in situ sulfuric acid-methanol methylation of formic acid to methyl formate. Diisopropyl ether was used as an internal standard. The method was applied to over 150 postmortem cases where methanol was detected. Of the 153 cases presented, 107 deaths were attributed to acute methanol toxicity. In the vast majority of the remaining 46 deaths, the methanol was determined to be present as a postmortem or perimortem artifact, or was otherwise incidental to the cause of death. Of the 76 victims who were found dead and blood was collected by the medical examiner, all but one had a postmortem blood formate concentration greater than 0.50 g/L (mean 0.85 g/L; n = 74). The sole exception involved suicidal ingestion of methanol where the blood methanol concentration was 7.9 g/L (790 mg/100 mL) and blood formate 0.12 g/L. In 97% (72/74) of the cases where blood was available, the blood formate was between 0.60 and 1.40 g/L. In 31 of the 153 cases, the victim was hospitalized and blood obtained on admission or soon after was analyzed for methanol and formate during the subsequent death investigation; the vast majority (27/30) had antemortem blood formate concentrations greater than 0.50 g/L. Cases with samples taken prior to death with blood formate concentrations less than 0.5 g/L can readily be explained by active treatment such as dialysis. The blood formate method has also been useful in confirming probable perimortem or postmortem contamination of one of more fluids or tissues with methanol (e.g., windshield washer fluid or embalming fluid), where methanol ingestion was unlikely.     

Distribution of dimethoate in the body after a fatal organphosphateintoxication

Many organophosphate pesticides (OPs) such as dimethoate are used to eradicate household pests, and those occurring in agriculture and forestry sectors. Combinations of two or more different insecticides have been manufactured to increase their effectiveness. A case of death is presented as suspected organophosphates intoxication. Autopsy was unremarkable except for grayish fluid in the stomach, with garlicky odor. A systematic toxicological analysis on post-mortem specimens revealed high concentrations of dimethoate in blood 38 μg/mL, urine 0.47 μg/mL, brain 2.2 μg/g, myocardial muscle 7.6 μg/g, liver 4.6 μg/g, lung 7.6 μg/g, skeletal muscle 21 μg/g, kidney 55 μg/g and gall bladder 31 μg/g. Blood alcohol was 2.85 g/L, cyclohexanone and cyclohexanol were also detected in the blood but not quantified. The cause of death was determined as organophosphate intoxication.     

Gender effects in eyewitness accounts of a violent crime

Abstract

This research examined two aspects of gender effects in eyewitness accounts: whether there are gender differences in memory for a violent crime and how gender of perpetrator/victim affect witnesses' evaluations of perpetrator/victim behavior. Eighty male and 84 female university students saw a film showing a simulated manslaughter with either a male or female perpetrator stabbing a male or female victim. A female advantage was found in overall memory of the crime, and both a male perpetrator and a male victim were assigned more culpability than their female counterparts. It is suggested that females may have more elaborated categories for person information than males, which should facilitate female accuracy in person memory. Alternatively, the present findings may reflect a more general female advantage in episodic memory performance. Stereotype assimilation is suggested to account for the differential evaluations of a male and female perpetrator/victim.