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.     

Single-stranded DNA as an immunohistochemical marker of neuronal damage in human brain: an analysis of autopsy material with regard to the cause of death

Single-stranded DNA (ssDNA) is a marker of apoptosis and programmed cell death, which appears prior to DNA fragmentation during delayed neuronal death. The present study investigated the immunohistochemical distribution of ssDNA in the brain to investigate apoptotic neuronal damage with regard to the cause of death in medicolegal autopsy cases (n=305). Neuronal immunopositivity for ssDNA was globally detected in the brain, independent of the age, gender of subjects and postmortem interval, and depended on the cause of death. Higher positivity was typically found in the pallidum for delayed brain injury death and fatal carbon monoxide intoxication, and in the cerebral cortex, pallidum and substantia nigra for drug intoxication. For mechanical asphyxiation, a high positivity was detected in the cerebral cortex and pallidum, while the positivity was low in the substantia nigra. The neuronal ssDNA increased during the survival period within about 24h at each site, depending on the type of brain injury, and in the substantia nigra for other blunt injuries. The neuronal positivity was usually lower for drowning and acute ischemic disease. Topographical analysis of ssDNA-positive neurons may contribute to investigating the cause of brain damage and survival period after a fatal insult.     

The spectrum of neuropathologic findings in deaths associated with seizure disorders

The pathologic and neuropathologic findings in 90 autopsied cases of death associated with a seizure disorder or complication thereof were reviewed. Most (69%) of the deceased individuals were between 21 and 40 years of age; two thirds were male. In 58% of patients, no cause of death other than seizure disorder was found. The ultimate cause of death in those patients was assumed to be a cardiac arrhythmia or respiratory arrest. Drowning accounted for 19% of deaths, and 17% of patients died of other contributory causes such as suicide, exposure, or atherosclerotic coronary vascular disease. Aspiration was found in the remaining 6%. Tongue lacerations or bite marks were observed in only one third of cases. The brain was normal in approximately two thirds of cases, with no focus for the origination of seizure found on neuropathologic examination. In the remainder of cases, a variety of lesions was found, with cavitary lesions, contusions, and dural lesions being the most common ones.     

The state of brain ventricles and their ependima in different scenarios of traumatic blood loss

The objective of the present study was to evaluate the state of ependima and the subependimal layer of the brain ventricles after death from the traumatic blood loss and in the cases of the blood loss under conditions of acute alcoholic and narcotic intoxication. The methods used for this purpose included light and scanning electron microscopy. It was shown that in subjects who died from the traumatic blood loss during acute alcoholic and narcotic intoxication ependima showed the signs of progressive polymorphism and had extensive areas of discontinued cell layers. Neuropil contained numerous vacuoles and blood effusion sites. The surface of ependima exhibited pathological erythrocytes, agglomerations of detritus, and crystalloid structures. The blood loss during combined alcoholic and narcotic intoxication resulted in more pronounced alterations in the ventricular walls.     

Increased lung weight in fatal intoxications is not unique to opioid drugs

Fatal intoxications with opioids are known to be associated with an increased lung weight, as well as with brain and pulmonary edema and urinary retention. However, there is evidence to suggest that fatal intoxications with non-opioid substances are also associated with increased lung weight; however, the latter aspect has not been comprehensively analyzed. To determine to what extent opioid and non-opioid substances are associated with increased lung and brain weight, we studied these organs in cases where the cause of death was attributed to intoxication with a single agent. Using data from cases autopsied at the National Board of Forensic Medicine (NBFM) in Sweden from 2009 through 2019 where the cause of death was attributed to a single substance, we created models of combined lung weight and brain weight. The models used age and sex as predictors as well as nested varying effects for the specific intoxicant and category of intoxicant. Suicidal hanging with negative toxicology cases served as controls. The population majority was male among both intoxications (68%) and controls (83%). The most common single substance group was opioids. All tested substances were associated with heavier lungs than controls, with the largest effect in the opioid group. Our findings show that several substances are associated with increased lung weight and that among intoxication deaths there is no difference in expected brain weight between substances. Hence, heavy lungs, without a reasonable explanation, should prompt a broad toxicological screening.     

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.     

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 cardiac arrhythmia after repeated exposure to 1,1-difluoroethane (DFE)

A 42-year-old man was found dead after repeated exposure to 1,1-difluoroethane (DFE, Freon 152a), a propellant found in CRC Duster, a product intended for the removal of dust and lint. Toxicologic analysis detected DFE in femoral blood 136.3 mg/L, brain 117.5 mg/kg, liver 87.6 mg/kg, lung 60.3 mg/kg, adipose 235.7 mg/kg, and vitreous fluid 25.1 mg/L. The cause of death was determined to be a fatal cardiac arrhythmia due to intoxication with 1,1-difluoroethane. After comparison to previously published cases involving DFE, we suggest that analysis of adipose tissue for DFE and similar compounds, along with blood and other tissues, may be useful in distinguishing between acute versus chronic exposure. Adipose may also be a valuable alternate specimen for detection in cases where loss or elimination from blood is likely to have occurred.     

The forensic medical diagnosis of intoxication of alcohol surrogates by morphological findings

The pathomorphology of intoxication of alcohol surrogates is described. A high frequency rate of DIC-syndrome is shown for the condition. A majority of thrombi accumulates at places with the highest concentrations of toxic substances as well as at those places, through which poisoning substances are brought out of the body, i.e. in the liver (since toxic substances are introduced perorally) and kidneys. Thrombi were detected in all internals, including the brain, in lethal intoxication. The immediate toxic effect from methanol and from higher spirits can matter in the genesis of changes, including acute swelling and chromatolysis with subsequent cell death. Exclusively cerebral or coagulopathic-cerebral types of thanatogenesis were registered in studied case of intoxication.     

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.     

Spontaneous umbilical cord hematoma: an unusual cause of fetal mortality: a report of 3 cases and review of the literature

Spontaneous hematoma of the umbilical cord represents a rare cause of fetal morbidity and mortality and the outcome is poor in half of the cases. There are many risk factors, such as infections, morphologic anomalies, alterations of the vessel walls, prolapses, twisting and traction of the cord, but in many cases the causes remain unknown. We present 3 cases of umbilical cord hematoma which took place at the end of the pregnancy and were followed by perinatal death of the fetus. In the 3 cases, which were autopsied including macroscopical and histopathologic examination of the placenta and the umbilical cord, a cordonal pathology was present; in all cases, there were alterations of the vascular wall, and in the third case inflammatory vasculopathy was found. In all 3 cases, the cause of death was attributed to acute anoxia due to the cordonal hematoma.     

Abnormally high alcohol concentration in the heart blood

A 46-year-old male alcoholic whose whereabouts had been unknown for about a month was found dead at the foot of a cliff 31 m deep. Fractures of the mandible, thorax and left patella were found at autopsy, but fatal injury to the brain or other organs was not observed. The alcohol distribution was 7.44 mg/g in the heart blood, 13.91 mg/g in the left thoracic cavity fluid and 1.88 mg/g in the urine. The high ethanol concentration in the heart blood was assumed to be mainly due to the diffusion of ethanol from the contents of the stomach and postmortem production of ethanol. It was decided that the cause of death was not acute alcohol intoxication but respiratory failure caused by fractures of the thorax.     

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.     

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.     

Causes of unexpected death in patients with multiple sclerosis: a forensic study of 50 cases

To determine the cause of death (as a result of neurologic or nonneurologic complications or accidents) in patients with multiple sclerosis (MS), we reviewed the autopsies of 50 subjects with MS from the Office of the Chief Medical Examiner of Maryland (OCME) between 1982 and 2004. The series included 32 females and 18 males (mean age, 45.8 years; range, 25-69 years) and the causes of death were classified into 3 categories: (A) neurologic complication directly related to MS; (B) nonneurologic complications or other medical causes; and (C) accidents, etc. Of the 50 cases, in 43 there was a history of MS, but in 7 subjects there was not, and the diagnosis was established by neuropathologic examination. In Group A, 21 (42%) cases, deaths were directly related to a neurologic complication; in Group B, 14 (28%) cases were related to the following nonneurologic and medical causes: ASCVD 9 (18%), metabolic disorder 1 (2%), pulmonary embolism 3 (6%), and bronchopneumonia 1 (2%); and in Group C, 15 (30%) cases, deaths were due to trauma, 9 (18%); intoxication, 5 (10%); and thermal injury, 1 (2%). Thus, among the 50 subjects, in 26, deaths occurred naturally; and in 24, from accidents, homicides, suicides, or undetermined causes. Pathologically, the majority of cases showed either chronic inactive (66.7%) or chronic active (15.6%) demyelinating lesions, mainly in the cerebral hemispheres. In some cases, it appears that demyelinating lesions, involving brain regions that regulate cardiorespiratory activity, could be considered as the immediate cause of death, but a large proportion appears to be due to other causes such as accidents and trauma. Thus, it seems likely that taking specific precautions could prevent some deaths in MS.     

Ascertainment of the cause and tempo of death in forensic medical practice

In order to develop a method of ascertaining a cause of death and of evaluating its tempo the authors undertook a histological study and a study of a dehydration degree in 76 cases of death due to the below reasons: mechanical trauma, mechanical asphyxia, burn shock, and carbon monoxide intoxication. Acute emphysema of lungs, lack of edemas in lungs and brain, desquamation of pulmonary macrophages, hyperemia of renal capillaries, primary urine in some glomerules, prevalence of ischemic changes with karyopyknosis in medulla and hypohydration of brain were typical of fast death. Prevalence of dystelectasis in lungs, emptying of pulmonary capillaries, evident edema of lungs and brain, desquamation of pulmonary macrophages, lack of primary urine in glomerular capsules, acute circulatory disorders of renal hemodynamics with sweating of fibrin and erythrocyte glomerules into cavities, necrotic nephrosis, pigment cylinders in renal tubules, thrombi in vessels, prevalence of chromatolysis, karyolysis and cytolysis in medulla, pronounced glial reaction as well as pronounced edema of brain and its hyperhydration were typical of slow death.     

Establishing the cause of death in finding a corpse on a flight of stairs

A total of 793 forensic medical conclusions concerning corpses found in vestibules are analyzed. The circumstances of death were unknown in the majority of cases. Causes other than injuries were responsible for the majority (72.4%) of deaths: coronary diseases, hanging, alcohol intoxication, or general hypothermia. Strikes with blunt objects and falling on the staircase or floor rank second among causes of death. Injuries caused by falling from staircase and cases with this cause suspected were responsible for 9.6% deaths. Murders with acute objects and guns were recorded in 6% cases. For facilitating differential diagnosis, a list of signs and injuries occurring as a result of falling from staircase and main causes of death in such injuries, made with consideration for the place where the corpses are found, is offered.     

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.     

Cerebral hypoxia and ischemia: the forensic point of view: a review

In cases with suspected brain anoxia/ischemia and hypoxia/hypoxemia a neuropathological investigation should give additional information to elucidate the cause of death and its pathophysiological mechanisms. Primary ischemic brain damage is associated with morphological and biochemical alterations. While acute ischemic neuronal injury reveals axon sparing and selective neuronal lesions due to the release of large quantities of glutamate, late neuronal death is associated with antiapoptotic growth factors, and decreased expression of microtubule-associated proteins and tubulin. On the morphological level ischemia can be detected by necrosis of neurons, proliferation of microglia, and astrocytes in vulnerable regions of the brain. In cases of permanent ischemia the so-called pale nervous cell injury is observed, in cases of partial perfusion the so-called dark nerve cell injury and apoptosis are detectable. In spite of the considerable advantages of recent research, presently there is no reliable qualitative marker to ascertain death due to acute hypoxic or ischemic events.     

Four deaths due to intravenous injection of cocaine

Cocaine is a potent psychotropic drug that alters mood and behavior by stimulating the central nervous system. Deaths from abuse of cocaine are relatively rare. Most such deaths appear to be related to the intravenous injection of the drug. Acute fatal cocaine intoxication is characterized by headache, cold sweats, rapid pulse, tremors and nausea, followed by convulsions, unconsciousness and death. The prime mode of death appears to be respiratory paralysis, secondary to the effects of cocaine on the medullary portion of the brain. This paper presents four deaths due to acute cocaine intoxication following intravenous injection. Blood concentrations of cocaine were 0.11, 0.37, 0.36 and 0.75 mg/dl.