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Objective In this study, the hemopericardium volume and pathological characteristics associated with cardiac ruptures caused by blunt violence, AMI, aortic dissection and CPR have been analyzed. The findings might provide reference and data support for deciphering the cause of heart rupture in forensic pathology. Method Pericardial water-injection tests were conducted in 22 noncardiac death subjects. Other study groups included 9 cases of myocardial infarction, 20 cases of aortic dissection rupture, 11 cases of cardiac rupture caused by trauma and 4 cases of cardiac rupture by CPR. The volume of hemopericardium and the pathological features were analyzed for each group. Result The hemopericardium volume in myocardial infarction and dissecting aneurysm rupture were significantly higher than the pericardial injection test in noncardiac subjects (p-value 0.05). The volume of hemopericardium in CPR-induced cardiac rupture had no difference with non-cardiac rupture and it was significantly lower than the pericardial injection test (p-value

The patient was an 88-year-old woman with a 10-year history of hypertension. She was suspected to have been hit by a car. At the time of the event, she was conscious and able to stand on her own and had no obvious injuries. She was sent home, but she lapsed into unconsciousness and was nonresponsive after 2 hours. She was sent to the hospital, and her heartbeat and breathing stopped. After half an hour of rescue attempts, her heartbeat did not recover, and she was declared dead. During the autopsy, a small subcutaneous hemorrhage was observed below the right knee joint. No obvious internal organ injuries or bone fractures were observed. The deceased also had mild atherosclerosis in the coronary arteries and an old cerebral infarction in the right cerebellum. The tissue histopathological tests showed distinct fat embolism in multiple organs, including the brain, lungs, kidneys, liver, and pancreas. A postmortem blood biochemistry test of the heart blood showed that the levels of low-density lipoprotein, cholesterol, triglycerides, and free fatty acids in the blood were increased, and the level of C-reactive protein was elevated. According to the autopsy results, the direct cause of death was multiorgan fat embolism. This case suggests that aging, hypertension, and hyperlipidemia may be risk factors for nontraumatic fat embolism under stressful conditions.

OBJECTIVE To discuss the collision relationship and the cause of the fracture caused by traffic accidents in which the front of a small car collides with the side of a pedestrian while braking. METHODS The surveillance videos of 42 traffic accidents involving the front of a small car colliding with the side of a pedestrian while braking were collected. By analyzing the surveillance videos and the paths, the speed of the collision, the relationship between the vehicle and the pedestrian upon collision, and the movement trajectory of the human body were clearly identified. The type and severity of the injuries were also determined through autopsy. The characteristics of the human injuries and vehicle paths were analyzed according to the collision speed (

Transverse fracture of the skull base is common both in the crushing of temporal regions of the skull and in the case of force acting on one temporal region. However, the mechanism of transverse skull base fracture caused by maxillofacial force has not been fully clarified. To provide an injury identification basis for forensic pathologists and clinicians, this paper combines accident reconstruction and finite element analysis methods to study the injury mechanism of an incomplete transverse fracture of skull base after the injured individual’s mandible was subjected to violence in a traffic accident. The results show that after the injured individual’s mandible was subjected to violence, forces in the direction of the left mandibular fossa and the right mandibular fossa were generated, creating the component forces. The combination of the two forces can produce a crushing effect toward the center of the skull base, as if the left and right temporal regions are being crushed, and the stress is concentrated at the joint of the mandible, the middle cranial fossa and the hypophyseal fossa. When the stress exceeds a certain limit, it will cause a transverse fracture of the skull base.

Methamphetamine (METH) is a major psychostimulant drug of abuse worldwide, and its neurotoxicity has been studied extensively. In addition to neurotoxicity, METH can also induce hepatotoxicity. The underlying mechanism of intestinal microorganisms in METH-induced hepatotoxicity remains unclear. In this study, mice have received antibiotics intragastrically or PBS once each day for 1 week, followed by METH or saline. The antibiotics attenuated METH-induced hepatotoxicity as evidenced by histopathological observation and biochemical analysis; furthermore, they alleviated METH-induced oxidative stress. The effect of antibiotics on METH-induced hepatotoxicity was investigated using RNA-sequencing (RNA-seq). The RNA-seq results demonstrated that antibiotics could regulate 580 differentially expressed genes (DEGs), of which 319 were upregulated after METH treatment and then downregulated with antibiotic pretreatment and 237 were first downregulated after METH administration and then upregulated after antibiotic pretreatment, in addition to 11 upregulated and 13 downregulated ones simultaneously in METH and antibiotic-pretreated groups. RNA-seq analyses revealed that TLR4 is one of the hub genes. Western blot analysis indicated that antibiotics inhibited the increase of TLR4, MyD88 and Traf6 induced by METH. This research suggests that antibiotics may play an important role in preventing METH-induced liver injury by regulating oxidative stress and TLR4/MyD88/Traf6 axis, though further investigation is required.

A full-term female baby born with an Apgar score of 10 exhibited a continual decrease in blood glucose and acid-base imbalance until she died at 40 h postpartum despite emergency rescue efforts. Autopsy showed a highly oedematous brain and a swollen liver. The cells of the myocardium, liver and kidney exhibited extensive microscopic vacuolar degeneration. The cardiac muscle and liver and kidney tissues were positive for Sudan III staining. Tandem mass spectrometry analysis revealed that the deceased was deficient in free carnitine, accompanied by an increase in multiple acylcarnitines. Genetic testing showed the parents of the deceased to be ETFDH mutation carriers, and the deceased carried a complex heterozygous mutation in ETFDH. Therefore, based on the results of autopsy, specific staining, genetic metabolic disease testing and genetic testing, we speculated that glutaric aciduria type IIc was the cause of death.

BACKGROUND Karoshi, which is sudden death associated with overwork, has become a serious problem in China. Many studies have examined the relationship between cardiovascular risks and karoshi, but there is little evidence that explains the exact mechanism by which overwork induces sudden death. In these cases, there are few obvious positive findings from forensic autopsies except for histories of overwork prior to death. Therefore, we assume that abnormalities, such as cardiac arrhythmia, rather than organic changes are the cause of karoshi. MATERIAL AND METHODS In the present study, the forced swim test (FST) was used to establish models of overwork. The myocardial tissues of SD rats taking FST (1 h per day, for 30 consecutive days) were collected. The arrhythmia-related molecule CX43 as well as its upstream regulation molecule Cav-1 and cSrc were tested by Western blot (WB) and immunohistochemistry (IHC). HE staining and Masson's staining were performed in the myocardium tissue section. RESULTS We observed downregulation of caveolin-1 (Cav1) followed by cSrc activation, resulting in the decrease of connexin43 (Cx43) levels in overwork models. Myocardial interstitial fibrosis, which is associated with electrophysiological aberrances that result in arrhythmia, was also found in the overwork models. CONCLUSIONS These data provide a mechanistic explanation for the speculated link between karoshi and cardiac arrhythmias.

This report describes a case of blunt cardiac injury and pericardial tamponade after video-assisted thoracoscopic surgery in a patient with lung cancer, hypertension, and cardiac hypertrophy. Anatomic findings included massive hemorrhage in the pericardium, cardiac hypertrophy, and a superficial contusion with a ruptured blood vessel on the epicardium at the lateral wall of the left ventricle. The patient died of pericardial tamponade secondary to blunt trauma from the tip of the thoracoscopic instrument. This case suggests that detailed assessment of the cardiovascular system, especially cardiac hypertrophy, careful preoperative preparation, and careful monitoring of postoperative conditions are important.

A full-term female baby born to parents who gave birth three years prior to a girl who survived only 31h postpartum died 36h after birth. An autopsy showed that the heart was markedly hypertrophic (32g). Microscopically, the myocardium, liver and kidney cells exhibited extensive vacuolar degeneration. Sudan III staining was positive in cardiac muscle, liver and kidney tissue. Tandem mass spectrometry analysis revealed that the deceased patient had a carnitine palmitoyl transferase II (CPT2) deficiency or a carnitine-acylcarnitine translocase deficiency. Genetic testing of the parents revealed heterozygous CPT2 mutations, indicating that their offspring would have a 25% chance of having a CPT2 deficiency. Therefore, we speculated that CPT2 deficiency might be the cause of death based on the results of staining, tandem mass spectrometry analysis and parental genetic testing.

A previously healthy 25-year-old man with no known risk factors was presented at the emergency room with a 3 h history of abdominal and loin pain. Physical examination and lab data showed no specific findings except tenderness, slight white cell count elevation and decreased haemoglobin level. The patient's condition deteriorated over the following hours and he died despite resuscitation attempts. Autopsy revealed a 2.5-cm longitudinal tear in the intima of the right common iliac artery, which formed a thrombosed false lumen extending to the abdominal aorta proximally and to the left common iliac artery. Histopathologic examination revealed the characteristic changes of fibromuscular dysplasia (FMD). FMD involving the common iliac arteries is extremely rare; only six cases have been reported previously, and only two of those included forensic findings. The presented case is the first case of FMD with intimal tearing in the right common iliac artery, with propagation to the left common iliac artery and abdominal aorta. When a previously healthy young adult without hypertension or other risk factors presents with acute abdominal and loin pain, systemic vascular disease should be on the list of differential diagnoses. Careful and complete evaluation of multiple arteries can be critical.

BACKGROUND Sudden death from ischemic heart disease while driving is an important cause of traffic accidents. This study discusses causes of traffic accidents in relation to risk factors for acute myocardial infarction such as hypertension and overwork and provides references for the early prevention and regulation of drivers' health conditions. MATERIAL AND METHODS Data on 21 cases of sudden death by ischemic heart disease while driving from January 2015 to December 2019 were collected. Age, symptoms, and cardiac pathological changes of patients were summarized by systematic anatomical and medical history data. RESULTS Patients were 21 men with an average age of 47±7.27 years (most aged 40 to 60 years), and the average weight of their hearts was 439.45±76.3 g. Twelve patients had a history of hypertension, 8 had previous myocardial infarction, and 4 had fatty liver. All had at least 1 severe narrowing of a major coronary artery. Twelve patients died within a short period; 9 died more than 12 h after myocardial infarction onset. Ten patients had worked more than 80 h of overtime per month, 4 patients, more than 45 h, and 7 patients, less than 45 h. CONCLUSIONS Regular physical examination and information about ischemic heart disease should be emphasized for men aged 40 to 60 years who drive frequently, especially for those with hypertension, overwork, or previous myocardial infarction. Incorporating objective evaluation criteria for the severity of ischemic heart disease and overwork into health condition-related driving regulations is needed.

Tyre imprints on the skin are usually considered to be the result of being run over by a motor vehicle. This article reports a traffic accident in which tyre marks on the victim’s skin were caused by a collision rather than by being run over. The mechanism of the injury in this case is analysed and discussed. A 23-year-old male drove a motorcycle while under the influence of alcohol and collided with a sign pillar on the side of the road. Both the victim and the motorcycle careened into the bottom of a tractor-trailer. No witnesses or surveillance videos could confirm the process of the accident. Because tyre imprints were found on the victim’s skin, traffic police believed that he had been run over during the accident. However, forensic autopsy and analysis of the accident process revealed that the true cause of the imprints was a collision between the victim’s body and a tyre.

Methamphetamine (MA) is a highly abused amphetamine‑like psychostimulant. At present, the mechanisms underlying MA‑induced cardiotoxicity are poorly understood. The cardiotoxic effects have yet not been clearly elucidated with respect to the apoptotic pathway. Insulin‑like growth factor binding protein‑5 (IGFBP5) is important for cell growth control and the induction of apoptosis. The aim of the present study was to analyze whether IGFBP5 is involved in MA‑induced apoptosis as a novel target. MA‑induced apoptosis was observed in neonatal rat ventricular myocytes (NRVMs) in a concentration‑dependent manner using a terminal deoxyribonucleotide transferase‑mediated dUTP nick end‑labeling assay. Using reverse transcription polymerase chain reaction and western blotting, MA was demonstrated to induce concentration‑dependent increases in the expression of IGFBP5. Silencing IGFBP5 with small interfering RNA significantly reduced apoptosis and suppressed the expression of caspase‑3 in NRVMs following treatment with MA. To the best of our knowledge, the present study provided the first evidence suggesting that IGFBP5 is a potential therapeutic target in MA‑induced apoptosis in vitro, providing a foundation for future in vivo studies.

Adrenocorticotropic hormone (ACTH) is involved in systemic reactions to stress. The aim of the present study was a comprehensive analysis of serum and cerebrospinal fluid (CSF) levels of ACTH, and the pituitary immunohistochemistry with special regard to fatal hypothermia in routine forensic autopsy cases (n=162: 5-97 years of age; 114 males and 48 females; 4 h to 3 days postmortem, median, 19.2 h). The ACTH concentrations were independent of the postmortem time, gender, or age of the subjects. The serum ACTH level was similar to the clinical reference value for sharp instrument injury, fire fatality, and hypothermia, but was lower in other groups including hyperthermia, in particular for asphyxia and poisoning. The CSF level was usually much higher than the serum level, but was significantly lower for hypothermia and hyperthermia than in other groups (p

The present report describes the unexpected death of a 6-month-old female infant who had been clinically diagnosed with Joubert syndrome. This is a relatively rare congenital neurological disorder characterized by hypoplasia/aplasia of cerebellar vermis, which transmits information from the body to the cerebellum, and is associated with respiratory dysfunction, abnormal eye movements, and developmental delay. The infant was found dead in bed and the immediate cause of death was determined as aspiration of vomit which may have been induced by a neurological disorder related to hypoplasia of the cerebellar vermis. These findings, together with a review of previous clinical case reports, suggest that Joubert syndrome should be considered as a predisposition to sudden unexpected death in infants mainly due to aspiration or complicated infection.

Glucose transporter 1 (GLUT1) and vascular endothelial growth factor (VEGF) have been established as being responsible for cellular adaptation to oxygen deficiency in tissue ischemia and hypoxia mediated by hypoxia-inducible factor 1. We hypothesized that mRNA quantification of these factors in autopsy tissue specimens could have diagnostic significance for investigating the pathology of death, especially after injury. Various cases (total, n = 119; less than 48 h postmortem) were examined, including fatal blunt injury (n = 71) and sharp instrument injury (n = 18), as well as asphyxia (strangulation/hanging, n = 12) and acute myocardial infarction/ischemia (n = 18) as controls. Quantification of mRNA by TaqMan real-time RT-PCR and immunostaining were performed for GLUT1 and VEGF in lung, kidney, and skeletal muscle specimens. The postmortem interval showed no significant influence on the relative quantification of mRNA during the early postmortem period. Characteristic results were found in blunt injury cases: both GLUT1 and VEGF mRNAs decreased in the lung but increased in the skeletal muscle depending on survival time. In the kidney, subacute deaths showed higher GLUT1 mRNA levels compared with acute deaths from blunt injury, but no significant change was found for VEGF mRNA. Immunohistochemistry showed visually predominant GLUT1 immunoreactivity in the renal cortex for cases with a longer survival time, coincident with the results at the mRNA level. Tissue-specific differences in mRNA quantification of GLUT1 and VEGF shed light on tissue ischemia/hypoxia and subsequent tissue-dependent pathophysiological changes leading to death after injury.

Catecholamines are major humoral factors and neurotransmitters that contribute to various stress responses. However, they have been considered unstable due to agony, terminal medical care and postmortem interference. The present study was a comprehensive investigation of postmortem serum levels of adrenaline (Adr), noradrenaline (Nad) and dopamine (DA) with regard to the cause of death in serial medicolegal autopsy cases (n = 542) including fatalities from various traumas and diseases. There was a slight tendency toward postmortem increases of Nad and DA in cardiac blood as well as Adr and Nad in peripheral blood, a slight age-dependent decrease in Adr and DA in right heart blood, and a marked increase in serum DA due to administration during critical medical care. When these factors were taken into consideration, significantly higher cardiac blood levels were observed for Adr and Nad in injury and asphyxiation cases and for Adr in fatal methamphetamine (MA) abuse and other poisoning cases, whereas those levels were lower in fatal hypothermia. Drowning, fire fatality, acute cardiac death and cerebrovascular disease showed intermediate Adr and Nad levels. The DA level was elevated in cases of injury, hyperthermia, MA fatality and other poisoning. Topographical analyses suggested that the major sources of increased serum catecholamines in cases of injury was abdominal viscera including adrenal glands, and that in cases of asphyxiation, drowning, fire fatality, hyperthermia, MA fatality, other poisoning, acute cardiac death and cerebrovascular disease was the extremities in addition to abdominal viscera. However, there was in part a large case-to-case difference in each marker related to individual causes of death. These findings differed markedly from clinical observations and suggest that the postmortem serum catecholamine levels may reflect the magnitude of physical stress responses during the process of death in individual cases.

We examined the immunohistochemical distributions of ubiquitin (Ub) and myoglobin (Mb) in human kidney tissues to assist the pathological assessment of death due to trauma. Medicolegal autopsy cases at our institute (n=138: 0-96 years of age, 105 males and 33 females) were examined. Causes of death were blunt injury (n=31), sharp injury (n=15), poisoning (n=11), drowning (n=10), fire fatalities (n=25), hypothermia (n=7), asphyxiation (n=14), hyperthermia (n=3), and natural diseases (n=22) for controls. Immunostaining of Ub and Mb was performed on the formalin-fixed paraffin-embedded kidney tissue sections. Quantitative analyses by estimating the proportion of Ub- and Mb-positive cells (%positivity) of renal tubule epithelial cells showed that the positivities for Ub and Mb were higher in subjects who died due to fire, blunt injury, sharp injury and fatal hypothermia than in other groups. The Ub-positivity correlated with the severity of airway thermal injury in fire deaths, survival time in blunt injury, and serum markers for renal failure in deaths due to sharp injury. Concomitant increases in the tubular Mb- and Ub-positivities were characteristic to deaths from injury and hypothermia. These findings suggest that Ub may serve as a sensitive indicator of the fatal influence of traumas.

There appears to be very poor investigation of postmortem serum calcium (Ca) and magnesium (Mg) for diagnostic evidence to determine the cause of death. The aim of the present study was a comprehensive analysis of the serum levels in relation to the causes of death in routine casework. Autopsy cases (total, n = 360; 5–48 h postmortem), including blunt injury (n = 76), sharp injury (n = 29), asphyxiation (n = 42), drownings (n = 28: freshwater, n = 11; saltwater, n = 17), fire fatalities (n = 79), methamphetamine (MA) poisoning (n = 8), delayed death from traumas (n = 37), and acute myocardial infarction/ischemia (AMI, n = 61), were examined. In total cases, there was no significant postmortem time-dependent rise in serum Ca and Mg. Both Ca and Mg levels in the heart and peripheral blood were significantly higher in saltwater drowning compared with those of the other groups. In addition, a significant elevation in the Ca level was observed in freshwater drowning and fire fatalities, and in the Mg level in fatal MA intoxication and asphyxiation. Topographic analyses suggested a rise in serum Ca and Mg due to aspirated saltwater in drowning, that in serum Ca in freshwater drowning and fire fatalities of peripheral skeletal muscle origin and that in serum Mg in MA fatality and asphyxiation of myocardial and/or peripheral origin. These markers may be useful especially for diagnosis and differentiation of salt- and freshwater drownings and may be also helpful to determine the causes of death involving skeletal muscle damage, including burns and MA intoxication. # 2004 Elsevier Ireland Ltd. All rights reserved.

Serum uric acid (UA) and creatinine (Cr) mainly derive from skeletal muscle tissues. Although, remarkable postmortem stability of the serum levels has been reported, there appears to be very poor knowledge of the diagnostic value in investigation of death, except for uremia. The aim of the present study was to evaluate postmortem serum UA and Cr levels using 395 forensic autopsy cases, in comparison with blood urea nitrogen (BUN), for investigation of the pathophysiology of death with special regard to the causes of death involving possible skeletal muscle damage, e.g. due to hypoxia, heat or agonal convulsions. Cr and BUN showed relatively good topographic stability in the cadaveric blood, whereas, UA was often much higher in the right heart blood than in the left heart and peripheral blood, independent of postmortem intervals. Moderate to marked elevation of Cr and BUN accompanied with hyperuricemia was observed in delayed death. In the acute death cases (survival time30 min), UA, especially in the right heart blood, showed a considerable elevation in mechanical asphyxiation and drowning. The Cr level in fire victims with a lower carboxyhemoglobin (COHb) level (60%) was significantly higher than in those with the possible fatal level (60%). A similar elevation of Cr was observed in fatalities from heat stroke and methamphetamine (MA) poisoning. The observations suggested that hyperuricemia in acute death may be indicative of advanced hypoxia and that elevated Cr level may reflect the skeletal muscle damage, especially due to thermal influence.

This study confirmed post-mortem ethanol concentrations in pericardial fluid and bone marrow aspirate in comparison with those in the blood in medicolegal autopsy cases (n = 140, within 48 h post-mortem). The specimens were examined by head-space gas chromatography/mass spectrometry. Ethanol concentrations in the pericardial fluid (y) were approximately equivalent to those in peripheral blood (x): y = 0.99x + 0.02, n = 44, r = 0.972. A high stomach ethanol concentration (> 10 mg/ml) appeared to mildly affect the pericardial levels. There was no significant interference in drowning cases. Ethanol concentrations in bone marrow aspirates (y) also showed a good correlation with those in the peripheral blood (x): y = 0.77x + 0.02, n = 20, r = 0.981. A dissociation was observed in cases of delayed death from hemorrhagic/traumatic shock and elderly victims. These findings suggest that pericardial fluid and bone marrow aspirate can be used as an alternative material when adequate blood specimens are not available.

We report a case of nontraumatic fat embolism syndrome with large amounts of macrophages with phagocytized fat droplets in the alveoli. A 46-year-old male presented with a glass-cut injury in his little finger. The wound was debrided and sutured at the hospital, but he was found dead 43 h after treatment. Autopsy results showed that the patient had steatohepatitis, accompanied by histological findings of fat droplets in the pulmonary capillaries. In the alveoli, we found a large number of macrophages with phagocytized fat droplets that showed stained. To the best of our knowledge, this is the first report of such a case, and the paper proposes that fat droplets phagocytized by a large number of macrophages may be a characteristic feature of fat embolism, which may be relevant to forensic pathology practice.

The glial fibrillary acidic protein (GFAP) is known as a peculiar marker of mature astrocytes of the central nervous system (CNS). However, we found distinct immunopositivity to a monoclonal anti-GFAP reagent in the hippocampus neurons in head injury fatalities. The present study investigated the neuronal and neuroglial GFAP-immunopositivity in the hippocampus in a series of head injury cases, which included acute and subacute/delayed deaths (n=17 and n=73, respectively), and acute cardiac death (n=13), delayed death due to multiple organ failure from nonhead injury (n=6), and pneumonia (n=9) cases were examined as controls. GFAP-immunopositivity in the neurons was frequently observed in CA4, CA3 and CA2 regions in cases of subacute/delayed head injury death that showed marked brain swelling accompanied by secondary brain stem hemorrhages, showing an inverse relationship to that in astrocytes. These findings suggest possible induction of GFAP or a related protein in hippocampus neurons depending on the severity of brain swelling following head injury.

Intracranial chordoma is a locally invasive, relatively rare tumour at the base of the skull. The tumour usually grows slowly but there have been several case reports of sudden death, all of which were due to tumour-associated haemorrhages. We report an autopsy case of a sudden unexpected death due to clinically undiagnosed intracranial chordoma in the brainstem without haemorrhage. A 44-year-old man was found dead at home. The autopsy revealed two small gelatinous and semi-translucent greyish tumours on the ventral surface of the brainstem between the midbrain and pons. The tumours were not attached to the dura or bone. The brain was markedly swollen, with enlarged lateral and third ventricles, but the aqueduct was compressed and narrowed. Microscopically, the tumour invaded the cerebral peduncles, and was classified as a chordoma. The cause of death was diagnosed as acute obstructive hydrocephalus due to a ventral brainstem tumour. Even a minor intracranial tumour that is not primarily life-threatening may cause sudden death due to subsequent obstructive hydrocephalus. The brainstem is one of the most vulnerable regions in the brain, and careful examination of this region is important for forensic pathologists.

This article reports an autopsy case of sudden death of an infant with an infrequent encephalopathy involving epileptic episodes. The infant was a 1-year and 10-month-old boy, who had a history of the first convulsive seizures in the third month after birth. The clinical diagnosis was described as 'an early infantile epileptic encephalopathy with suppression-bursts' (Ohtahara syndrome). On a winter day, he was collapsed following a high fever and was already dead on the arrival at a hospital. The body was small for the age and poorly nourished. The autopsy and postmortem magnetic resonance imaging scan (MRI) of formalin-fixed brain revealed advanced unsymmetric brain atrophy with cortical dysplasia, which were prominent in the left temporal and right occipital lobes, and sclerotic atrophy of the parahippocampal gyri, additionally showing a feature of the olivo-ponto-cerebellar atrophy. However, the cause of death was pathologically and microbiologically determined as bacterial bronchopneumonia following pulmonary infection of the influenza A virus. In sudden death cases of physically handicapped infants, the investigation of viral infection in consideration of an epidemiological survey is important even when the death can be pathomorphologically explained.