Search

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.

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.

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.

Karoshi is a term used to describe unexplained sudden death associated with overwork and has become a serious public health issue in China. Cases have occurred in physicians, university professors, engineers in high-tech companies, and blue-collar workers. The mechanisms associated with death by overwork are very complex. According to most researchers, karoshi is considered to be caused by an excessive workload that induces deterioration of underlying hypertension or atherosclerosis. These conditions inevitably lead to death from cardiovascular or cerebrovascular diseases. However, in our own experience, we have found that in some cases, the victims of karoshi were in a chronic state of overwork but without a history of cardiovascular or cerebrovascular diseases. In support of this, we have found that even autopsies have revealed few positive findings except for cardiac hypertrophy. In this article, we report 3 typical cases of karoshi but without the typical pathomorphological features of cardiovascular or cerebrovascular disease.

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.

An elevated serum tryptase concentration is considered a specific marker for systemic mast cell activation, a central feature of anaphylaxis. However, in some cases of acute cardiovascular death, high concentrations of serum tryptase are also observed. We compared the postmortem serum tryptase concentrations in 74 cases assigned to the following four groups: anaphylactic deaths (Group A, n = 20), acute cardiac deaths (Group ACD, n = 30), acute dissecting aneurysm ruptures (Group ADA, n = 10), and controls (Group C, n = 14). Additionally, the cutoff between Group A and the other groups was calculated using receiver-operating characteristic (ROC) curve analysis. Tryptase concentrations were markedly elevated in Group A (p < 0.001), Group ACD (p = 0.015), and Group ADA (p = 0.005). The optimal cutoff was 43 ng/mL, the sensitivity was 90%, and the specificity was 98%. While elevated concentrations of tryptase were noted in practical autopsy cases, due attention should be paid to the differential diagnosis between anaphylactic and acute cardiovascular deaths.