Polysarcia adiposa: morbid obesity

From October 1988 to March 2005, there were at least 92 autopsy cases where morbid obesity was present and/or where it was attributed to the cause of death in the coronial district of Auckland, New Zealand, a city with a population of over 1 million people. Obesity has been researched internationally, and much is known about associated comorbidities such as atherosclerotic disease, hypertension, and diabetes, to name a few. However, in the morbidly obese (body mass index>or=40 kg/m2), only 14 of 92 cases were found to have ischemic heart disease due to coronary atherosclerosis as the principal cause of death, and slightly over half (48/92) have some degree (mild, moderate, severe) of coronary atheroma. There is a strong positive correlation between heart weight and body weight. Only 8 livers were normal, all others showing some form of steatosis, venous congestion, and fibrosis/cirrhosis. The mean weights of the heart, lungs, and liver were above the normal reference range in almost all cases. In conclusion, the study did not follow the widely published finding of the positive correlation between morbid obesity and ischemic heart disease in terms of mortality, but the study was consistent with other studies on the organ manifestations of morbid obesity, particularly for the heart, lungs, and liver.     

急性博落回中毒的实验病理学研究

目的 探讨博落回中毒作用的靶器官、靶组织和病变特点,以及博落回中毒机理。方法 应用博落回水煎液对大鼠经口急性染毒,行组织病理学和重要脏器电镜检查及血清生化检测。结果 博落回对大鼠的半数致死量(LD50)为19.5g/kg,染毒大鼠血清谷丙转氨酶(GPT)、肌酐(Cr)、尿素氮(BUN)、肌酸激酶(CK)及其同功酶(CK-MB)增高;心电图(EKG)表现异常;肝、脾、肾脏器系数减小。光镜下中毒大鼠心、脑、肝、肾等器官呈淤血、出血性改变;电镜下中毒大鼠心、脑、肝、肾细胞内线粒体、内质网、核膜等膜性结构破坏。结论 博落回毒作用的主要靶器官或靶组织是心、脑、肝、肾,病变特点为受累脏器淤血、出血性变;毒作用的主要机理是对线粒体、内质网和核膜等膜性结构的破坏。     

Copper-binding protein in acute copper poisoning

This paper presents a suicide case of copper sulfate ingestion. Post-mortem autopsy revealed mucous membrane necrosis of the esophagus and the stomach. Histological examination revealed centrilobular necrosis in the liver and renal insufficiency. The quantitative determination of copper, zinc and cadmium in various tissues showed that the copper concentrations in blood, liver, kidney and lung were 3.5-24-fold higher than those of the normal level, whereas zinc and cadmium concentrations were within normal range. Chromatographical patterns on Sephadex G-75 showed that most of the accumulated copper in the liver and kidney was bound to metallothionein (MT), a low molecular weight protein with high metal binding capacity which plays a role in the detoxification of heavy metals, while no copper bound to MT was found in the lung. These results suggest that the formation of Cu-induced MT in the liver and kidney occurred at the early stage in fatal acute copper poisoning.     

多发性软组织挫伤后对肺及其他脏器的影响

目的观察多发性软组织挫伤后短时间内死亡案例的脏器病理学改变。方法应用常规组织学及免疫组织化学染色技术进行光学显微镜检查。结果光镜检查见肺组织毛细血管扩张充血，白细胞集聚，肺组织散在片状出血、灶状坏死及透明膜形成；心脏间质血管扩张充血，点灶状纤维溶解；脑组织充血水肿，肝脾充血。免疫组化发现肺泡腔及部分血管内纤维蛋白染色阳性，部分脾脏血管内及肾髓质集合管中肌红蛋白染色阳性。结论本研究结果提示多发性软组织挫伤后短时间内死亡的死因为成人呼吸窘迫综合征（ARDS）合并多脏器功能衰竭。     

急性斑蝥中毒的实验病理学研究

本文报告斑蝥急性中毒的实验病理学研究,结果显示,实验组大鼠血白细胞增高,淋巴细胞比值下降;血清GPT、GOT及BUN增高;肾G6P酶和ATP酶活性下降;脾、肾脏器系数增大;肾、肝细胞变性、坏死明显,淋巴器官的淋巴细胞变性坏死显著,胃、肠、膀胱等粘膜有出血、坏死。提示急性斑蝥中毒对淋巴组织具有免疫抑制作用,其中毒靶器官为淋巴器官、肾和肝。     

Disposition of fluoride in a fatal case of unsuspected sodium fluoride poisoning

A case of suicidal ingestion of sodium fluoride roach powder by a 33-year-old black woman is presented. Disposition of fluoride (mg/l or mg/kg) was: bile, 3.4; gastric content, 225; kidney, 16; liver, 8.6 and urine, 295. No history of roach powder ingestion was available at autopsy. This case illustrates the need for extensive toxicological screening to determine if fatal poisoning has occurred when histopathological findings are unremarkable.     

Fatal Acute Poisoning from Massive Inhalation of Gasoline Vapors: Case Report and Comparison with Similar Cases

We describe a case of an acute lethal poisoning with hydrocarbons resulting from massive accidental inhalation of gasoline vapors. The victim, a 50‐year‐old man was found unconscious inside a control room for the transport of unleaded fuel. Complete autopsy was performed and showed evidence of congestion and edema of the lungs. Toxicological investigation was therefore fundamental to confirm exposure to fumes of gasoline. Both venous and arterial blood showed high values of volatiles in particular for benzene (39.0 and 30.4 μg/mL, respectively), toluene (23.7 and 20.4 μg/mL), and xylene isomers (29.8 and 19.3 μg/mL). The relatively low values found in the lungs are consistent with the fact that the subject, during the rescue, underwent orotracheal intubation followed by resuscitation techniques, while the low concentrations for all substances found in urine and kidneys could point to a death that occurred in a very short time after first contact with the fumes of gasoline.     

Globus Pallidus Necrosis Unrelated to Carbon Monoxide Poisoning: Retrospective Analysis of 27 Cases of Basal Ganglia Necrosis

Bilateral globus pallidus necrosis is said to be characteristic of carbon monoxide (CO) poisoning. However, there has been no scientific test of this hypothesis. To examine the assertion that globus pallidus necrosis is typical of CO poisoning, this study examined autopsy cases from the King County Medical Examiner's Office (KCMEO) between 1994 and 2013. Twenty-seven cases with bilateral basal ganglia lesions were identified and examined for associated or causative disease or injury with the following results: 10 cases of drug overdose, seven heart disease, three asphyxia, two chronic ethanolism, two Huntington-like disorder, and one case each of remote trauma, rheumatic heart disease, and cerebral artery gas embolism. Additionally, review of all known cases at KCMEO of CO poisoning found no evidence of globus pallidus or basal ganglia necrosis. Thus, this study provides no support for the assertion that globus pallidus necrosis is characteristic of CO poisoning.     

脑死亡脑外器官病理变化的实验性研究

选用34只家猫研究脑死亡后脑外器官（心、肺、肝、肾）的病理学变化。经任内持续加压造成脑死亡模型,根据人工维持心跳和呼吸的时间分3组。结果脑死亡后出现：（1）缺血性心肌病变,心内膜下出血,心肌局灶性坏死及线粒体、微丝破坏;（2）肺淤血,水肿,间质炎症;（3）肝小叶中央带、中间带缺血性病变;（4）肾近曲小管缺血性病变。     

Sudden Unexplained Nocturnal Death Syndrome: Epidemiological and Morphological Characteristics in Thai Autopsy Cases

With limited knowledge on epidemiological and morphological characteristics of sudden unexplained nocturnal death syndrome (SUNDS), this study was aimed to identify such data in Thai SUNDS autopsy cases. All the cases were men and nondrug abusers aged 20–49 years old. Most cases were originated in the Northeastern region of Thailand. Half of them were found dead from midnight to 6 a.m., with a peak time at 2 a.m. The death rate was relatively higher in May and June. Most SUNDS cases were blue‐collar workers (93.2%) and nonsmokers (60%), with a normal BMI (72.1%). Approximately one‐fifth of the cases had detectable blood alcohol concentrations. Symptoms before death were respiratory difficulty, seizures, and urinary incontinence. Their mean heart weight was 329.8 ± 35.1 g. Their lungs (88.6%) had some degree of congestion. Acute pancreatitis was not found in these SUNDS cases, and approximately half (40.9%) of the cases had their gastric content <100 mL.     

丝穗金粟兰中毒病理学变化的初步研究

作者通过小白鼠动物试验，结合实际案例，初步证实了中草药丝穗金粟兰中毒的病理学变化，主要靶器官是肝脏、肾脏和全身血管，表现为弥漫性变性、坏死与充血出血．     

An investigation and pathological analysis of two fatal cases of cadmium poisoning

Pollution associated with population growth, and with industrial and urban development has led to a serious decline in the water quality of Chinese rivers. Cadmium (Cd) is recognized as one of the most toxic metals and is strongly accumulated by organisms. Humans are exposed to cadmium originating from the environment and from industrial pollution. In spite of thousands of published studies on Cd, there is little information on its pathological features seen in human autopsy. The gross and pathological findings of forensic autopsies of two case of cadmium poisoning are presented and related to an epidemiological investigation. In both cases, multiple organ damage was observed, involving brain, lung, liver, kidney, red blood cells, and platelets, which is consistent with reports in the literature. In particular, in both cases, transmission electron microscopy revealed a large number of dense lysosomal and phagocytic particles in the cytoplasm near the nucleus, indicating the need for a genotoxic study of cadmium. Our observations provide new clues for the future recognition and prevention of Cd poisoning.     

Homicide due to intravenous metallic mercury injection followed by sodium cyanide injection

We report a case of homicide due to intravenous mercury injection followed by meperidine and sodium cyanide injection. A 35-year-old woman was found dead in bed at home by her husband. Reportedly, she had been sick for more than 5 months. Initial death investigation revealed no evidence of foul play. Her death was believed to be natural. Therefore, her body was buried without an autopsy. Two months after death, her family requested an autopsy because they suspected her physician husband killed her. Her body was exhumed, and an autopsy was performed. Postmortem examination revealed numerous metallic mercury globules in the pulmonary arteries. Toxicological analysis revealed a high concentration of mercury in the tissue samples of the lungs, liver, heart, and kidney. In addition, cyanide and meperidine were also found in the heart and liver. The detailed case history and postmortem examination findings are described.     

Exogenous Lipoid Pneumonia as a Contributory Factor in a Drug‐related Death

Postmortem investigation often reveals various conditions, which may or may not have played a part in the death of the individual. The case of a 32‐year‐old woman is reported, with a long history of drug addiction. She was found dead in her bed. The autopsy revealed diffuse pulmonary edema with congestion of the lungs, brain, liver, and spleen. Microscopic examination of the lungs showed multiple intra‐alveolar and interstitial foamy macrophages and extracellular fat droplets surrounded by polynuclear giant cells. Death was attributed to acute polydrug intoxication. As microscopic examination had revealed severe pulmonary lesions, lipoid pneumonia was considered as a contributing factor to death. Lipoid pneumonia is an uncommon entity with the characteristic radiograph features and histologic findings of alveoli filled with vacuolated, lipid‐laden histiocytes. It can be either exogenous or endogenous in cause, based on the source of the lipid. Exogenous lipoid pneumonia usually results from aspiration or inhalation of fat‐like material, such as mineral oil or petroleum‐based lubricants and decongestants, resulting in pulmonary inflammatory reactions.     

How Reliable are Parenchymal Tissues for the Evaluation of Carbon Monoxide Poisoning? A Pilot Study

Dealing with burnt bodies, the forensic pathologist must first of all answer the question whether the victim was alive at the moment of the fire. This study aims at clarifying whether some human solid tissues may be reliably used for the forensic diagnosis of Co poisoning on burnt bodies providing no collectable blood during the autopsy. From 34 selected cases, both cardiac blood and parenchymal samples were collected to perform CO‐oxymeter, spectrophotometry, and gas chromatography tests: blood CO estimations (blood COHb% and blood[CO]) and parenchymal[CO] values have been compared with special focus on R values. The solid tissues having the best correlations with blood CO amount turned out to be the lung (R 0.84), the liver (R 0.83), the kidney (R 0.79), and the spleen (R 0.92).     

急性及己中毒的实验病理学研究

目的探讨及己对小鼠毒性作用的病理变化及其毒作用机制。方法应用及己水煎液对小鼠经口急性染毒,进行组织病理学观察血清生化、凝血机能检测。结果及己对小鼠的半数致死量(LD50)为41.12g/kg;染毒小鼠血清ALT和BUN升高;血液血小板计数减少、凝血时间延长;肝、脾、肾器官系数增大;肝、肾、心肌细胞变性、坏死明显,全身诸多器官淤血、出血性改变。结论及己毒作用的主要靶器官或靶组织是肝脏、肾脏、心脏和全身血管。毒作用机制是对线粒体、内质网等膜性结构及体内凝血机制的破坏。     

6例甲状腺功能亢进性心脏病猝死法医学分析

目的分析甲状腺功能亢进性心脏病(以下简称甲亢性心脏病)猝死案例,探讨其死亡的一般情况及法医病理学特点,为此类案件的法医病理学鉴定提供参考。方法收集中国医科大学法医学院2001—2016年6例甲亢性心脏病猝死案例,回顾性分析基本信息(性别与年龄)、临床表现、病史、解剖所见和组织病理学所见、生物化学检测指标、死亡原因。结果 6例案例多具有明确的甲状腺功能亢进病史,并表现出不同程度的心血管病症状;均具有明显的死亡诱因;甲状腺病理学检验符合弥漫性毒性甲状腺肿的表现;心脏质量均增加,心腔扩张,心肌肥大,灶状坏死;死后心包液的生物化学检测可作为甲亢性心脏病猝死的辅助手段。结论对甲亢性心脏病猝死案例进行诊断时应参考临床病史、尸体检验、组织病理学检验、死后毒(药)物检验等结果综合判定,必要时进行死后甲状腺和心功能的生物化学检测。     

A multiple drug fatality involving MK-801 (dizocilpine), a mimic of phencyclidine

MK-801 (dizocilpine) is a non-competitive antagonist at the N-methyl-D-aspartate (NMDA) family of glutamate receptors in the central nervous system. It is an anticonvulsant and also shares several pharmacological properties with phencyclidine and ketamine. It is not observed routinely as a substance of abuse. The deceased, a 45-year-old white male, obtained MK-801 surreptitiously in an attempt to treat a self-diagnosed depression. He was discovered the next morning, unresponsive on the bathroom floor. An empty bottle, labeled to contain 25mg of MK-801, was found near the body.The autopsy was performed at the Joseph A Jachimczyk Forensic Center, Houston, TX. Body weight at autopsy was 88kg. Lungs were edematous and congested (right: 775g; left 700g). The heart had proportionate chambers and was otherwise unremarkable. The kidneys (right: 220g; left 225g) were smooth surfaced. The brain (1550g) was congested and without trauma. Microscopic evaluation of the heart, kidneys and lungs showed normal histology and confirmed pulmonary congestion and edema. Samples of heart blood, liver, bile, vitreous humor, stomach contents and urine were collected at autopsy. There were 550ml of stomach contents.Drugs in blood were screened by EMIT II Plus immunoassay procedures and by gas chromatography/mass spectrometry (GC/MS) of an organic solvent extract of basified blood. Alcohol was determined by gas chromatography with headspace injection. MK-801, benzodiazepines and alcohol were detected in blood.Amounts of MK-801 present in blood, bile, liver, vitreous humor and urine were 0.15, 0.29, 0.92, less than 0.1 and 0.36 mg/l (kg), respectively.The cause of death was benzodiazepine, dizocilpine and ethanol toxicity and the manner accidental.     

大鼠急性八角莲中毒的组织病理学变化

目的观察大鼠急性八角莲中毒后主要器官的病理形态学改变,探讨急性八角莲中毒的作用机制及其对靶器官、靶组织的损伤影响。方法随机将40只SD大鼠,分为3个实验组(0.5、1.0和2.0倍LD50剂量的八角莲水煎剂灌胃)和1个对照组(1.0倍LD50剂量的生理盐水灌胃)。大鼠在八角莲急性染毒后14d处死,解剖取脑、心、肝、肺、肾,样品经组织病理学处理后,光镜和电镜下观察大鼠主要器官病理形态学改变。实验数据采用χ2检验进行统计学分析。结果光镜观察结果:神经元胞质疏松,大部分尼氏小体消失;心肌细胞肿胀,润盘及横纹结构消失;肝细胞水肿、气球样变;肾近曲小管上皮细胞肿胀,管腔内见蛋白质样红色淡染物质。电镜观察结果:神经元细胞膜及核膜结构破坏,胞质明显水肿,细胞器大多已破坏、消失。急性染毒后4组大鼠死亡率随着剂量的增加而增高(P0.05)。结论急性八角莲中毒可引起多器官病理形态学改变,其毒性作用与剂量呈正相关性,且主要靶组织、靶器官为脑(神经元)、心、肝和肾。