Homicidal ethylene glycol intoxication: a report of a case

We report a case of a 75-year-old hypertensive, diabetic man who presented to the emergency room with symptoms and signs of nausea, acute intoxication, significant alteration in mental status with rapid neurologic deterioration, and blunt impact injuries sustained during a recent altercation with a 36-year-old female companion-caretaker. He denied a history of ethanol abuse or other recent toxic ingestion and had not been diagnosed with or treated for depression. Hospital laboratory tests revealed a metabolic acidosis and a negative urine toxicology screen. He was diagnosed with toxic encephalopathy with metabolic acidosis secondary to metformin. Despite treatments including hemodialysis, he expired after approximately 28 hours of hospitalization. A postmortem anatomic examination revealed recent blunt-impact injuries and cardiac and renal pathology. A subsequent histologic examination revealed the presence of calcium oxalate crystals in the kidneys and brain, in addition to cardiac and renal pathology. Comprehensive forensic toxicologic testing was performed on antemortem and postmortem samples and revealed lethal levels of ethylene glycol. The cause of death was as a result of acute intoxication by ethylene glycol with another condition of multiple blunt impacts to the head, trunk, and extremities. The manner of death was ruled as homicide. A trial by jury, involving the female companion-caretaker, resulted in her conviction, and she was sentenced to 23 years to life in prison. In this report, we present an unusual case of homicidal ethylene glycol intoxication in which legal proceedings have occurred.     

Heroin dependence as a rare cause of symmetrical globus pallidus necrosis

Long-term survival after carbon monoxide intoxication has been accepted for a long time as pathognomonic for elective cerebral tissue damage, especially in cases of isolated symmetrical necrosis of the globus pallidus. The results of old bilateral necrosis in the globus pallidus are described in a case of an acute heroin death after long-term drug abuse. The evaluation of such cerebral changes is discussed as they have to be interpreted as hypoxic or oligemic tissue damage. The different causes of symmetrical necrosis of the globus pallidus that are relevant for legal medicine are compiled and discussed.     

Acute intoxication with guaifenesin, diphenhydramine, and chlorpheniramine.

Mixed drug reactions are frequently encountered in emergency department overdose cases and also in fatal intoxications. Assessment of the relative contribution of each drug in producing adverse effects is often compounded by lack of case history and the paucity of cases reported in the literature. This report describes a fatal intoxication with three common over-the-counter medications: guaifenesin, diphenhydramine, and chlorpheniramine. A 48-year-old woman was found dead in the attic bedroom of her residence. Specimens obtained at autopsy for toxicologic analysis included heart blood, urine, bile, gastric contents, vitreous humor, and cerebrospinal fluid. The over-the-counter drugs were identified and quantitated by acid/neutral or basic liquid-liquid extraction followed by gas chromatographic analysis with nitrogen phosphorus detection. Concentrations of guaifenesin, diphenhydramine, and chlorpheniramine detected in the heart blood were 27.4, 8.8, and 0.2 mg/L, respectively. The cause of death was determined to be acute intoxication by the combined effects of guaifenesin, diphenhydramine, and chlorpheniramine, and the manner of death was determined to be suicide. To our knowledge, the blood guaifenesin concentration in this case is the highest reported concentration to date associated with an acute intoxication.     

Aspects of forensic medical diagnosis of acute opiate poisoning

The case study is dedicated to morphological changes occurring in the organs and tissues in lethal outcomes due to acute poisoning with narcotic substances; it is also dedicated to the structure of an acute respiratory insufficiency in unexpected "heroin" death and to delayed death after intoxication. The clinical-and-anatomical analysis of the material, involving the immunological, biochemical, chemical and spectral examination data, has been undertaken.     

Lethal Bentazone Intoxication – A Report of Two Cases

This study presents two cases of lethal bentazone poisonings, their clinical presentation, the course of the disease and the autopsy findings. The first is a 50‐year‐old male who had sprayed corn with a solution of bentazone and was admitted to the hospital with sweating, fever, nausea, vomiting of aqueous and hemorrhagic content, and bloody, watery stools. He was treated according to the symptoms including extracorporeal hemodialysis, but eventually suffered from multiorgan failure (acute respiratory failure, acute liver failure, coagulopathy, acute renal failure, metabolic acidosis, and gastrointestinal bleeding) and died 11.35 h after admittance. The cause of death was probable bentazone intoxication. The second case, also a male, aged 49 who committed suicide by ingesting a bentazone solution. He was transferred to the hospital prostrated and cyanotic and died 14.15 h after admittance despite all efforts by the hospital staff. The cause of death was acute bentazone intoxication.     

Brain changes in parathion poisoning: observations in 42 cases

A total of 42 cases were examined neuropathologically to determine possible toxic changes occurring in the brain after parathion intoxication. Sporadic anoxic alterations were observed in 7% of 41 cases in which the cause of death was acute intoxication. Nearly all cases (93%), however, showed marked hyperemia, often coupled with small reactionsless, periventricular hemorrhages which occurred in 40% of the cases. In one third of the cases (33%) there was moderate swelling of the oligodendroglia. Whereas histological evidence of edema was found in nearly one third of the cases (30%), comparison of the brain weights in these subjects with those of a large comparative collective showed definite pathologic brain weights in only five cases (12%) with 95% confidence limits. It is true that in 18 cases (42%) the brain weight was above the normal value if the confidence limit is ignored. Pronounced anoxic alterations were observed in only one case in which the individual survived the acute intoxication for 4 weeks after initial respiratory arrest. Predominantly toxic changes, however, could not be detected in any of the cases examined. This negative morphologic finding does not agree with the physiologic alterations reported by other investigators using animal models; they considered the cause of death in cases of parathion intoxication to be the result of toxic paralysis of the respiratory center. The literature was discussed.     

Death related to midazolam overdose during endoscopic retrograde cholangiopancreatography

We report a midazolam-related death that occurred during endoscopic retrograde cholangiopancreatography (ERCP). The acute intoxication due to midazolam overdose was confirmed by high-pressure liquid chromatography (HPLC) analysis of the blood samples taken from the patient in the intensive care unit (2.8 microg/ml) and postmortem (2.4 microg/ml). The case strongly emphasizes the necessity of the precautions that should be taken when midazolam is intravenously administered.     

Evaluation of certifier practices regarding alcohol-related deaths: Fulton County Medical Examiner's Center, Atlanta, Georgia, 2004

CONTEXT: Alcohol can contribute to various manners of death by acute intoxication that places a person at risk for fatal injury, acute fatal alcohol poisoning, or the various fatal complications of chronic abuse with or without superimposed acute intoxication. The reporting of alcohol use on the death certificate may vary with office policy or procedure, certifier judgment, and the timing of information received during investigation. OBJECTIVE: To determine the number of deaths including mention of alcohol use in the investigative case file, the number of death certificates on which alcohol use is reported, the number of discrepancies between the 2, and the possible reasons for observed discrepancies. DESIGN, SETTING, AND PARTICIPANTS: Retrospective case review of all deaths where alcohol use was mentioned in the investigative case file and/or on the death certificate for deaths investigated by the Fulton County Medical Examiner in Atlanta, Georgia, during a 1-year period between January 1, 2004, and December 31, 2004. MAIN OUTCOME MEASURES: Percentage of deaths with alcohol use reported on the death certificate, tabulation of where and how alcohol use is reported on the death certificate, and tabulation of the differences between the investigative case file and death certificate regarding alcohol's possible role in causing death. RESULTS: Among the 1324 deaths certified by the office, 105 (8%) had alcohol use reported on the death certificate. The majority (67%) of these cases were natural deaths. Sixty-nine (5%) deaths had mention of alcohol use in the investigative case notes but did not include it on the death certificate. Twenty-five (2%) deaths had mention of alcohol on the death certificate but did not have mention of it in the investigative case file based on our search criteria. However, subsequent review of additional case follow-up information disclosed a history of alcohol use or acute intoxication in each case. CONCLUSIONS: The data show that more natural deaths are considered to be directly caused by alcohol than other manners of death. For the unnatural manners of death (excluding acute alcohol poisoning), alcohol use is often viewed by medical examiners as an incidental, associated finding or risk factor surrounding the circumstances of death rather than being an actual cause of death. In such cases, alcohol use is often omitted from the death certificate. For deaths directly caused by alcohol, the proportion of cases involving possible underreporting or overreporting of alcohol involvement was relatively small and usually involved the omission of chronic alcohol use from the death certificate. Researchers need to be aware of potential limitations of death certificate data for studying alcohol-related deaths.     

Suspicious circumstances on discovery of the cadaver

The authors report on three autopsy cases in which the findings at the death scene gave rise to the suspect of non-natural, in two cases even violent causes of death. The medico-legal and criminalistic investigations led to surprising results: Death was due to acute intoxication with narcotics, supposed delirium tremens and a suicide attempt in the presence of bronchopneumonia. External force was ruled out in all three fatalities by cooperative work of police investigators and forensic medicine.     

Tissue distribution of olanzapine in a postmortem case

Olanzapine is a relatively new antipsychotic drug used in the United States for the treatment of schizophrenia. Since its release in the United States market in 1996, few cases of fatal acute intoxication have been reported in the literature. This article describes the case of a 25-year-old man found dead at home who had been prescribed olanzapine for schizophrenia. This case is unique because of the measurement of olanzapine in brain tissue obtained from seven regions in addition to the commonly collected biologic matrices. Olanzapine was detected and quantitated by basic liquid-liquid extraction followed by dual-column gas chromatographic analysis with nitrogen phosphorus detection. The assay had a limit of detection of 0.05 mg/L and an upper limit of linearity of 2 mg/L. The presence of olanzapine was confirmed by gas chromatography-mass spectrometry by use of electron impact ionization. The concentrations of olanzapine measured in this case were as follows (mg/L or mg/kg): 0.40 (heart blood), 0.27 (carotid blood), 0.35 (urine), 0.61 (liver), negative (cerebrospinal fluid), 0.33 mg in 50 ml (gastric contents). In the brain, the following distribution of olanzapine was determined (mg/kg): negative (cerebellum), 0.22 (hippocampus), 0.86 (midbrain), 0.16 (amygdala), 0.39 (caudate/putamen), 0.17 (left frontal cortex), and 0.37 (right frontal cortex). The cause of death was determined to be acute intoxication by olanzapine, and the manner of death was accidental.     

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.     

An unusual case of accidental poisoning: fatal methadone inhalation

In this report, the authors present a case of unusual, accidental methadone intoxication in a 40-year-old man, who had inhaled methadone powder. The drug dealer was a pharmacy technician; methadone had been stolen from a pharmacy and sold as cocaine. After having inhaled methadone powder, he suffered cardiopulmonary arrest. He was admitted to hospital where he died after 24 h of intensive care. The autopsy revealed congestion of internal organs and cerebral and pulmonary edema. Microscopically, the heart showed no changes. The toxicological analyses performed on blood and urine taken at the hospital revealed methadone, cannabinoids, and ethanol. The blood methadone concentration was 290 μg/L. The urine methadone concentration was 160 μg/L. Midazolam and lidocaine, which were administered to the patient at the hospital, were also detected in the blood. The cause of death was determined to be methadone intoxication. The literature has been reviewed and discussed. To date, and to our knowledge, only very few cases of accidental death resulting from methadone inhalation have been described up to the case presented herein.     

A Carbon Dioxide Fatality from Dry Ice

Abstract:  This report documents a rare case of carbon dioxide intoxication in a young healthy male. The deceased hid in a small plastic container, size 1.5 × 1 × 1 m, and within 5 min he was located suffering convulsions and was reported as dead within minutes. Scene investigation revealed dry ice in the container. Autopsy findings were unremarkable. The probable cause of the convulsions was carbon dioxide intoxication due to both the dry ice sublimation and the small confined space in which he was hiding. This report emphasizes the significance of scene investigation in establishing the cause of the death.     

Two fatal cases of selenium toxicity

Two patients, a 36-year-old female and a 36-year-old male, separately experienced new onset nausea, vomiting, diarrhea, abdominal pain, muscle weakness and pallor. Over a period of 14-16 h these symptoms continue and progress to include hypotension refractory to therapy, pulmonary edema and cardiovascular collapse. Autopsies show hemorrhagic pulmonary edema, splenomegaly and lack of anatomical cause for sudden death. Postmortem analysis, in one case post-embalming and exhumation, revealed elevated selenium concentrations and a determination of the cause of death. These two cases present several important features associated with selenium toxicity, two of which are previously unreported: (1) selenium as a potential homicidal agent, (2) the toxidrome and time frame of selenium toxicity, (3) selenium determination in exhumed, embalmed tissues, (4) postmortem urinary selenium concentration, and (5) decrease in tissue concentrations over time.     

Fatal mephenesin intoxication

This report describes a death related to the abuse of and intoxication by mephenesin. To the best of our knowledge, this is the first report case of lethal intoxication involving solely mephenesin and reporting mephenesin blood concentrations. The victim was a 48-year-old woman found unconscious at home. Resuscitation was unsuccessful. Toxicological analysis was performed on a blood sample collected during resuscitation. The results being negative, the body was exhumed for an autopsy, which revealed bronchial inhalation syndrome. Analysis in a second laboratory has revealed the presence of mephenesin in samples collected during autopsy. No other drug/toxin was found, and alcohol was negative. Reanalysis of the peripheral blood collected during resuscitation found a mephenesin concentration of 15.81 microg/mL (15-fold greater that the maximum concentration that would result from a single intake of a 500 mg formulation). The pathologist has concluded on a bronchial inhalation syndrome consecutive to a mephenesin overdose as the cause of death. The manner of this death is discussed in the light of the toxicological hair analysis and the medical past of the victim.     

Homicidal alcoholic intoxation versus manual neck compression

A case of homicide involving a 49-year-old man is reported. In the course of a booze-up he was forced to excessive consumption of alcohol and was pushed back into a sofa by repeated grasping his neck which finally left him dead. The postmortem examination revealed a small abrasion in the right mandibular region, a contusion of the subcutaneous tissue above the left clavicle, a haemorrhage in the deep muscles of the neck at the right side of the cervical spine, a fatty tissue haemorrhage between the left cornus of hyoid and thyroid cartilage as well as petechiae of the eyelids and conjunctivae. The blood alcohol concentration amounted to 4.00@1000, the urine alcohol concentration to 5.26@1000. Thus, a manual strangulation of the neck versus a lethal alcohol intoxication had to be taken into consideration as cause of death. The morphological findings of the postmortem examination and the pathophysiological concepts of the underlying mechanisms of death in manual strangulation versus lethal alcohol intoxication are discussed with regard to their significance for the juridical assessment.     

The diagnostic significance of the quantitative glycogen content in cadaveric tissues in different types of death

The author developed a method for glycogen content determination in histological sections of the liver, heart and the skeletal muscles, stained according to Best, in case of death from ischaemic heart disease, acute ethanol intoxication, overcooling. Different variation limits of glycogen level in these kinds of death as compared to data in case of death from lethal mechanical injuries ("normal value") were determined.     

Diagnostic significance of myofibrillar degeneration of cardiocytes in forensic pathology

The incidence of myofibrillar degeneration (MFD) was studied in the following different forensic-pathological diagnostic groups of 25 cases each: acute morphine intoxication, acute carbon monoxide intoxication, hanging, strangulation by hand/ligature, drowning, acute hemorrhagic shock, lethal acute brain injury, explainable death of babies or infants and sudden infant death syndrome, together with 18 cases of intoxication with various drugs. The MFD was demonstrated by the Luxol-fast-blue reaction, with two types of phenomena being differentiated, namely cross-band lesions and diffuse staining. All diagnostic groups included cases of MFD of differing degrees. Cross-band lesions were observed in practically all cases of hanging, strangulation and acute hemorrhagic shock. Diffuse stain was noted particularly in cases of drowning and acute brain injury. The diagnostic significance is discussed.     

Fetal death due to nonlethal maternal carbon monoxide poisoning

Fetal death due to acute carbon monoxide poisoning is rarely reported in the medical literature. Of the eight cases found in literature review, only one documented the fetal carboxyhemoglobin concentration. This paper reports a fetal death due to accidental nonlethal maternal carbon monoxide intoxication in which both maternal and fetal carboxyhemoglobin concentrations were obtained. The corrected carboxyhemoglobin concentration was 61% at the time of death in utero, while the maternal carboxyhemoglobin was measured at 7% after one hour of supplemental oxygen. The authors review the mechanisms of fetal death and emphasize the different carbon monoxide kinetics in the fetal circulation.