An Autopsy Case Report of Homicide by Methanol Intoxication With Pinkish Bilateral Putamina.

ABSTRACT: Many deaths caused by methanol occur as a result of intentional suicide attempts or accidental ingestion, and several investigators have quantified methanol and formic acid in blood and organs. However, to the best of our knowledge, no reports have described regional differences in the concentration of methanol in the brain. A man in his 50s drank alcohol that had been deliberately contaminated with methanol by his wife, and he died of multiple-organ failure after 4 days of intensive medical treatment including hemodialysis. On medicolegal autopsy, cross sections of the brain showed scattered petechial hemorrhage in the brain stem and microscopic hemorrhage with congestion in the bilateral putamina, which showed pinkish discoloration. The concentrations of methanol, formic acid, and ethanol in autopsy samples were measured by headspace gas chromatography, revealing relatively high concentrations of residual methanol and formic acid in the brain (especially in the basal ganglia), although methanol had been eliminated from the blood. Even after 4 days of medical treatment, postmortem toxicological analysis of the brain tissue indicated methanol ingestion. The accumulation of formic acid and the consequent local metabolic acidosis may cause brain lesions.

Blunt traumatic aortic dissection death by falling: an autopsy case report.

A man in his early 60 s who worked at a waste disposal plant had fallen into the refuse pit and was immediately taken to the emergency department for treatment. After 8 days without recovering consciousness, the man died. Antemortem contrast-enhanced computed tomography at the emergency department indicated Stanford type B/DeBakey type IIIb aortic dissection. The autopsy showed a sharp and transverse intimal tear 0.6 cm in length in the aortic isthmus and fractures in the 5th-6th thoracic vertebrae. No structural abnormalities in arterial walls were noted on histopathological examination. The traumatic aortic dissection induced by falling is rare, compared with vehicle crash. Although the verification process was challenging, the cause of death was ultimately concluded as traumatic aortic dissection due to falling into the refuse pit. The following observations were cited as evidence: (1) the location and feature of the intimal tear, (2) the positional relationship between the impact site and the entry tear, and (3) the circumstance of clash impact onto the "cushion" of accumulated waste in the refuse pit. Inquiries into the cause of death, such as those made in this report, are required to provide detailed information on the circumstances of the accident, postmortem examinations, and careful consideration.

An autopsy case report of aortic dissection complicated with histiolymphocytic pericarditis and aortic inflammation after mRNA COVID-19 vaccination.

A male in his 90 s consulted a doctor because he experienced several days of general fatigue and dyspnea. He was diagnosed with heart failure, and diuretic medications taken for 3 days relieved his symptoms. However, he was found dead on the morning of the fourth day after consultation. He had received a third dose of coronavirus disease 2019 (COVID-19) vaccine approximately 2 weeks before death. An autopsy revealed dissection of the ascending aorta and pericardial hemotamponade. The heart showed a white villous surface, and the pericardium was fibrously thick. Microscopic examination revealed pericarditis with predominantly macrophage and lymphocyte infiltration. These histological findings were compatible with those of post-vaccination myocarditis. To the best of our knowledge, histopathologically proven pericarditis after COVID-19 vaccination has not been reported. In the present case, extended inflammation of the aortic adventitia was a possible cause of aortic wall fragility followed by dissection.

Immunohistochemical analysis of CD31 expression in myocardial tissues from autopsies of patients with ischemic heart disease.

CD31, a transmembrane protein expressed on endothelial and hematopoietic cells, plays important roles in leukocyte trafficking, mechanotransduction, angiogenesis, vascular permeability, and regulation of cellular responsiveness. CD31 immunoreactivity is employed as a sensitive and specific endothelial marker in diagnostic pathology. In this study, CD31 expression in myocardial tissues from deceased patients with ischemic heart disease and a mouse model of acute myocardial infarction were examined by immunohistochemical staining. We examined 24 neutral formalin-fixed, paraffin-embedded myocardial tissue samples obtained within 48 h postmortem from the autopsies of patients who were diagnosed with ischemic heart disease. CD31 expression was observed in vascular endothelial and endocardial cells. In necrotic myocardium, diffusion of CD31 antigen was observed. Elevated CD31 expression was observed around myocardial cells undergoing remodeling, suggesting that endothelial proliferation occurred at these sites. In contrast, fibrotic myocardial foci did not show upregulated CD31 expression. The same CD31 expression characteristics as those observed in the human samples were observed in the mouse model. CD31 immunostaining as an endothelial and microvasculature marker may be a useful complement to conventional staining techniques currently used in the diagnosis of ischemic heart disease, and may allow the timing and process of myocardial remodeling to be analyzed in detail.

Immunohistochemical analysis of vimentin expression in myocardial tissue from autopsy cases of ischemic heart disease.

Vimentin is a type III intermediate filament cytoskeletal protein that is expressed mainly in cells of mesenchymal origin and is involved in a plethora of cellular functions. In this study, myocardial tissues from patients with ischemic heart disease and a mouse model of acute myocardial infarction were subjected to immunohistochemistry for vimentin. We first examined 26 neutral formalin-fixed, paraffin-embedded myocardial tissue samples from autopsies of patients that were diagnosed with ischemic heart disease within 48 h postmortem. Myocardial cells were negative for vimentin, whereas non-myocardial cells, including vascular endothelium, vascular smooth muscle, fibroblasts, nerve fibers, adipocytes and mesothelial cells, showed positivity. Elevated vimentin expression was observed around myocardial cells undergoing remodeling, suggesting fibroblastic and endothelial proliferation in these locations. By contrast, myocardial foci that were completely fibrotic did not show upregulated vimentin expression. Inflammatory foci including macrophages and neutrophils were clearly visualized with vimentin immunostaining. The same vimentin expression phenomena as those found in human samples were observed in the mouse model. Our study indicates that immunostaining of vimentin as a marker for myocardial remodeling and the dynamics of all non-myocardial cell types may be useful for supplementing conventional staining techniques currently used in the diagnosis of ischemic heart disease.

Immunohistochemical analysis of von Willebrand factor expression in myocardial tissues from autopsies of patients with ischemic heart disease.

von Willebrand factor (VWF) plays a crucial role in hemostasis and thrombosis. VWF is involved in platelet attachment to the subendothelium, serving as a carrier protein for coagulation factor VIII. In this study, myocardial tissues from deceased patients with ischemic heart disease and a mouse model of acute myocardial infarction were subjected to immunohistochemistry to determine VWF expression. We examined 28 neutral formalin-fixed, paraffin-embedded myocardial tissue samples obtained from the autopsies of patients who were diagnosed with ischemic heart disease within 48 h postmortem. Most myocardial cells were negative for VWF, although some cells showed nonspecific positivity. Elevated VWF expression was observed around myocardial cells undergoing remodeling, suggesting that endothelial proliferation occurred at these sites. In contrast, completely fibrotic myocardial foci did not show upregulated VWF expression. Positivity in fibrin deposition and hemorrhagic sites was observed. The same VWF expression characteristics as those observed in the human samples were observed in the mouse model. VWF immunostaining as an endothelial marker may be a useful supplementation to conventional staining techniques that are currently used in the diagnosis of ischemic heart disease in terms of examining the timing of myocardial remodeling in detail and highlighting the remodeling process.

Immunohistochemical analysis of thrombomodulin expression in myocardial tissue from autopsy cases of ischemic heart disease.

Thrombomodulin is a transmembrane glycoprotein that is ubiquitously expressed on the surface of vascular endothelial cells. Thrombomodulin exerts its anticoagulant effects by combining with thrombin, activating protein C, and inactivating the coagulation factors FVa and FVIIIa. Clinically, thrombomodulin is also known as a marker of vascular injury because it circulates freely in response to endothelial injury. In this study, myocardial tissue from cases of ischemic heart disease was subjected to immunohistochemistry by thrombomodulin. We examined 40 neutral-formalin-fixed, paraffin-embedded myocardial tissue samples from autopsy cases that were diagnosed with ischemic heart disease (within 48 h postmortem). Thrombomodulin expression was observed in vascular endothelial cells between myocardial cells and in mesothelial cells of the epicardium. In necrotic myocardium, diffusion of thrombomodulin, which reflected endothelial injury, was observed. Upregulated thrombomodulin expression was observed around myocardial cells under ongoing remodeling, which suggested endothelial proliferation in these locations. Completed fibrotic foci of the myocardium did not show upregulated thrombomodulin expression. In a mouse model of acute myocardial infarction, the same phenomena as that found in human samples were observed by immunohistochemistry of thrombomodulin. Immunostaining of thrombomodulin, as a marker for endothelial injury or myocardial remodeling, may be useful for supplementing conventional staining techniques in the diagnosis of ischemic heart disease in forensic pathology.

Autopsy case of Rosai-Dorfman disease presenting as fibrinous pericarditis.

Rosai-Dorfman disease (RDD) is a rare non-Langerhans cell histiocytosis that is characterized histopathologically by accumulation of CD68-positive, S100-positive, and CD1a-negative histiocytes. Cardiac involvement of RDD is rare. We report here an autopsy case of cardiac involvement of RDD presenting as fibrinous pericarditis. A 14-year-old Japanese boy complained of loss of appetite and breathing difficulty when lying down. He was found dead on his back in his bedroom. One year before his death, he was diagnosed with RDD after skin biopsy. At autopsy, the deceased was 153 cm in height and weighed 38 kg with systemic edema. He had flat pigmented light-brown spots, as well as many pale reddish-brown papules on the abdomen and both thighs. Cervical and mediastinal lymphadenopathy was observed. A large amount of pleural and ascitic fluid was observed. The spleen weighed 381.9 g and showed splenomegaly. The heart weighed 620 g and showed acute fibrinous pericarditis with adhesion. Abundant fibrin was observed on the epicardial surface. The infiltrating cells were CD68-positive, S100-positive, and CD1a-negative histiocytes. The skin and spleen showed histiocytic involvement. Systemic edema, large amounts of pleural and ascitic fluid, a high brain natriuretic peptide level in blood, and hemosiderin-laden macrophages in the lungs suggested chronic heart failure. We speculate that the cause of death was extranodal cardiac involvement of RDD with chronic heart failure. This case highlights the need for forensic pathologists to perform a complete autopsy to determine the cause of sudden death when cardiac involvement of RDD is present.

Circumstances and factors of sleep-related sudden infancy deaths in Japan.

BACKGROUND: Sudden unexpected death in infancy (SUDI) comprises both natural and unnatural causes of death. However, few epidemiological surveys have investigated SUDI in Japan. OBJECTIVE: This retrospective study was conducted to investigate the latest trends of circumstances and risk factors of SUDI cases in which collapse occurred during sleep. METHODS: Forensic pathology sections from eight universities participated in the selection of subjects from 2013 to 2018. Data obtained from the checklist form were analyzed based on information at postmortem. RESULTS: There were 259 SUDI cases consisting of 145 male infants and 114 female infants with a mean birth weight of 2888 ± 553 and 2750 ± 370 g, respectively. Deaths most frequently occurred among infants at 1 month of age (18%). According to population data as the control, the odds ratio (95% confidence interval) of mother's age ≤19 years was 11.1 (6.9-17.7) compared with ages 30-39. The odds ratio for the fourth- and later born infants was 5.2 (3.4-7.9) compared with the frequency of first-born infants. The most frequent time of day for discovery was between 7 and 8 o'clock, and the time difference from the last seen alive was a mean of 4.1 h. Co-sleeping was recorded for 61%, and the prone position was found for 40% of cases at discovery. Mother's smoking habit exhibited an odds ratio of 4.5 (2.9-5.8). CONCLUSION: This study confirmed the trends that have been observed for sudden infant death syndrome; particularly, very high odds ratios were evident for teenage mothers and later birth order in comparison with those in other developed countries. Neglect was suspected in some cases of the prolonged time to discovery of unreactive infants. To our knowledge, this is the first report of an extensive survey of SUDI during sleep in Japan.

Anterior Tricuspid Leaflet Cleft in an Adult Male: An Autopsy Case Report.

The deceased was a 44-year-old male who was treated for a suspected Ebstein's anomaly observed using transthoracic echocardiogram. He was found dead in his bed at home. Autopsy revealed that the septal tricuspid leaflet was intact; however, a large anterior tricuspid leaflet cleft and right atrioventricular cavity dilation were observed. Pathological examination revealed a normal tricuspid valve, except for the presence of a cleft with local fibrosis of the left ventricle papillary muscle and hemosiderin-containing macrophages at both lungs. There were no other abnormalities that may have led to death. It was concluded that he died a cardiac death based on the right heart overload associated with the anterior tricuspid leaflet cleft. This case indicates the possibility that the anterior tricuspid leaflet cleft can cause death and also highlights the necessity of a detailed autopsy to accurately diagnose the cause of death.

An autopsy case of thyroid storm associated with chronic lymphocytic thyroiditis.

A Japanese woman in her 30s was found dead on a mattress. She had had fever, cough, and dyspnea for about 2 weeks. Gross examination at autopsy revealed slight enlargement of the thyroid gland and histopathological examination resulted in a diagnosis of chronic lymphocytic thyroiditis. The concentration of triiodothyronine in the cadaveric blood was extraordinarily high, whereas that of thyroid stimulating hormone was below the detection limit. Autoimmune antibodies against thyroid tissue were positive. The cause of death was assumed to be congestive heart failure caused by thyroid storm associated with chronic lymphocytic thyroiditis. Systemic histopathological examination of tissues and postmortem biochemistry can enable a diagnosis in medicolegal autopsies.

Unexpected neonatal death caused by interrupted aortic arch, an uncommon congenital great vessel malformation: An autopsy case report.

A 21-day-old Japanese male infant became inactive and then collapsed unexpectedly. On autopsy, there was no connection between the ascending and descending thoracic aorta. The site of interruption was the aortic isthmus. The heart showed hypertrophy and exhibited intracardiac malformations, including subaortic valve stenosis resulting from posterior deviation of the ventricular outlet septum and ventricular septal defect. The cause of death was diagnosed as prolonged physiological closure of the ductus arteriosus complicated by interrupted aortic arch and followed by assumed ductal shock.