急性坏死性胰腺炎与死后胰腺自溶病理形态学变化

目的比较大鼠急性坏死性胰腺炎（acute necrotizing pancreatitis,ANP）与各种急性死亡大鼠死后48h胰腺的病理形态学变化,探讨两者的鉴别点。方法参照文献制作ANP和电击、机械性窒息（勒死）、急性毒鼠强中毒动物模型,采用半定量评分和图像分析定量分析,观察死后48h胰腺大体和光镜下组织病理变化。结果ANP组炎细胞浸润、脂肪坏死、钙沉积3项与其他组相比有显著意义（P〈0．05）。结论炎细胞浸润、脂肪坏死、钙沉积是ANP在普通光学显微镜下最重要的特异性形态学病理变化,对区别其他急性死亡和死后自溶胰腺有特别重要意义．     

Acute fatal poisoning with cyamemazine

A case of fatal poisoning with cyamemazine is presented. The cyamemazine was identified in post-mortem blood using a specific gas chromatographic/mass spectrometry method. The autopsy blood concentration of cyamemazine was 1800 ng/ml. Chronic use of cyamemazine was demonstrated by the presence of the drug in hair. Two other drugs were also detected (bromazepam and trimeprazine). We think that this current blood concentration (1800 ng/ml) is a fatal blood concentration because of the negativity of the other parameters, but careful interpretation of analytical findings are important, the possibility that this death was a consequence of the toxicity of combined drugs could not be excluded. Not many therapeutics and toxic levels were previously reported in overdosage cases in which cyamemazine was involved. We consider that this concentration is only of guidance value for a fatal cyamemazine poisoning.     

急性安妥中毒尸检1例

安妥 (Ａｎｔｕ)属硫脲类杀鼠剂 ,其分子式为Ｃ11Ｈ10 Ｎ2 Ｓ ,化学名α -萘硫脲或甲萘硫脲 (α -Ｎａｐｈｔｈｙｌ -ｔｈｉｏｕｒｅａ) ,1942年由ＣｕｒｔＰ .Ｒｉｃｈｔｅｒｔ合成本品 ,1945年用于防治褐家鼠。 1973年ＷＨＯ专家委员会主张禁用安妥 ,国内尚未见安妥中毒的尸检报道。同济医科大学法医病理学教研室曾检验一例如下 :某男 ,2 2岁 ,自服大量安妥后出现呕吐 ,呕吐大量黄色胃内容物。次日上午 10时被发现后送医院急救 ,患者烦躁不安、检查不合作、口唇及鼻腔周围有黄色血性物 ,颈软、瞳孔对光反射存在。肺呼吸音增强、心音快。病…     

急性安妥中毒尸检1例

安妥(Antu)属硫脲类杀鼠剂,其分子式为C11H10N2S,化学名α-萘硫脲或甲萘硫脲(α-Naphthyl-thiourea),1942年由Curt P.Richtert合成本品,1945年用于防治褐家鼠.1973年WHO专家委员会主张禁用安妥,国内尚未见安妥中毒的尸检报道.同济医科大学法医病理学教研室曾检验一例如下: 某男,22岁,自服大量安妥后出现呕吐,呕吐大量黄色胃内容物.次日上午10时被发现后送医院急救,患者烦躁不安、检查不合作、口唇及鼻腔周围有黄色血性物,颈软、瞳孔对光反射存在.肺呼吸音增强、心音快.病理反射阴性.裤上有大便.入院2小时后患者烦躁、神志不清,面色苍白、口唇紫绀、大小便失禁、吐黄色血性物,血压140/90mmHg,心律齐,呼吸急促,未闻及干湿性罗音.经洗胃、给氧、对症及抗感染等治疗,7.5小时后患者满肺湿性罗音,两眼瞳孔对光反射消失.12小时后血压降至90/70mmHg,约12.5小时血压已量不出,呈潮式呼吸,脉搏细弱,心跳弱而速,最终因呼吸心跳停止而死亡. 尸检见死者瞳孔直径0.5cm,口唇青紫,气管及支气管内多量白色泡沫状液体,两肺共重1450克,饱满,胸膜下少数点状出血,肺切面有多量泡沫状液体流出,轻度灶性肺气肿,镜下肺重度淤血水肿、部分肺泡腔内出血明显,有大量的肺透明膜形成(图1、图2),合并急性支气管肺炎.灶性肺气肿.胃内有约450克酱褐色液体,混有灰黑色粉末状物质及食物残渣,无特殊臭味,胃粘膜轻度充血,无明显腐蚀出血.十二指肠粘膜充血.脑淤血水肿.肝、肾水肿.心肌横纹尚清晰,心肌间质较增宽.肠壁粘膜下层水肿显著.膀胱内充满尿液,位于耻骨联合上12cm.胰无明显病变.病理诊断:肺重度淤血水肿、急性支气管肺炎;肝、肾、肠壁水肿;脑淤血水肿;膀胱内尿潴留.胃及胃内容物检出安妥成分.鉴定认为死者系口服安妥引起急性中毒,因重症肺水肿并发急性支气管肺炎而死亡. 讨论(1,2):安妥是中性化合物,市售商品为蓝灰色粉末,纯品为白色结晶,无臭,味苦,不溶于水,难溶于乙醇及醚,易溶于碱及有机溶剂(特别是丙酮),其溶液具有蓝色荧光.特别对家鼠有明显的选择性高效毒杀作用.对人毒性较低,故中毒案例极少,作为投毒他杀者罕见.安妥可经胃肠道、呼吸道吸收,吸收后主要分布在肺、肝、肾和神经系统,大部分由肾排出.安妥除对胃肠道粘膜有刺激作用外,主要由于损害毛细血管,促进毛细血管扩张和渗透性增加,引起肺水肿、胸膜炎、胸腔积液及肺出血,最终因呼吸困难、窒息而死亡;也可引起肝、肾脂肪变性及坏死.本例即因重度肺水肿而死亡.Round等1985年报道,用安妥腹腔内注射引起大鼠急性肺损伤,肺血管的反应性随急性安妥损伤增加而增强.反复安妥损伤可引起不可逆性肺动脉高压,从而导致右心室肥厚.也可引起肝肾变性坏死;此外它破坏胰腺β细胞,影响糖代谢,引起糖尿.安妥中毒致死的动物,常见重度肺水肿和多量胸水形成.狗或鼠还可有血糖显著升高,肝糖原含量降低,也可表现体温降低及血液浓缩等现象.因安妥对人中毒致死的报告不多,故其致死量各家意见不一,有报告成人口服致死量为4～10克,敏感者0.5克也可致死.小儿对安妥较第三较易引起中毒.大白鼠一次口服急性中毒LD50为6.25mg/kg,小白鼠为35mg/kg.     

Acute intoxication with orphenadrine and clozapine.

This report describes a fatal intoxication with two different drugs: clozapine and orphenadrine. A 38-year-old man was found dead in the bedroom of his residence. Near the body were found various empty pharmaceutical boxes, employed in schizophrenic therapy, two of them containing clozapine and orphenadrine. High concentrations of clozapine and orphenadrine detected in blood, urine and gastric content were related to death. These compounds were identified and quantitated by liquid-liquid extraction followed by gas chromatographic/mass spectrometry (GC/MS) analysis.     

Sudden unexpected death in a child with varicella caused by necrotizing fasciitis and streptococcal toxic shock syndrome

A 4-year-old child with chickenpox infection for 5 days prior to death complained of swelling and pain in his right leg that required medical assistance in the emergency department. Radiologic study was normal, and analgesic and bandage of the leg were prescribed. Some hours later, he presented cyanosis, dizziness, and vomiting and collapsed. A complete forensic autopsy was performed 12 hours after death. External examination of the body showed numerous crusty varicella skin lesions, especially over the trunk, and swelling and reddening of his right leg. The brain was swollen, with cerebellar herniation, and both adrenal glands were hemorrhagic.Microscopically, neutrophilic infiltration and muscle fiber necrosis were observed in soft tissues of his right leg, and fibrin microthrombus were numerous in capillaries of the plexus choroideus, larynx, lungs, and adrenals. Bacterial emboli were present in most of the tissues. Microbiologic cultures of blood and cerebrospinal fluid showed group A beta-hemolytic streptococcus (Streptococcus pyogenes). Death was attributed to fulminant streptococcal toxic shock syndrome, with necrotizing fasciitis as a complication of varicella.     

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。     

Acute intoxication with guaifenesin, diphenhydramine, and chlorpheniramine.

Mixed drug reactions are frequently encountered in emergency department overdose cases and also in fatal intoxications. Assessment of the relative contribution of each drug in producing adverse effects is often compounded by lack of case history and the paucity of cases reported in the literature. This report describes a fatal intoxication with three common over-the-counter medications: guaifenesin, diphenhydramine, and chlorpheniramine. A 48-year-old woman was found dead in the attic bedroom of her residence. Specimens obtained at autopsy for toxicologic analysis included heart blood, urine, bile, gastric contents, vitreous humor, and cerebrospinal fluid. The over-the-counter drugs were identified and quantitated by acid/neutral or basic liquid-liquid extraction followed by gas chromatographic analysis with nitrogen phosphorus detection. Concentrations of guaifenesin, diphenhydramine, and chlorpheniramine detected in the heart blood were 27.4, 8.8, and 0.2 mg/L, respectively. The cause of death was determined to be acute intoxication by the combined effects of guaifenesin, diphenhydramine, and chlorpheniramine, and the manner of death was determined to be suicide. To our knowledge, the blood guaifenesin concentration in this case is the highest reported concentration to date associated with an acute intoxication.     

Acute fatal intoxication with narcotic substances during their intracavitary transportation

The authors describe a case of sudden death of a passenger on the train from Uzbekistan bound for Russia via Kazakhstan. The death was attributed to the poisoning with an illegally transported narcotic substance that was detected in the subject's stomach and intestines.     

Ruptured cerebral artery aneurysm and bacterial meningitis in a man with osteogenesis imperfecta

This report describes a 38-year-old man with osteogenesis imperfecta who died of a ruptured cerebral artery aneurysm and bacterial meningitis. He had multiple long bone fractures in the past, and approximately 4 months before death, he had surgery to relieve symptoms of basilar impression. The surgery was complicated by a postoperative wound infection. For the next 4 months, he had intermittent headaches and vomiting. He was found dead in his bed at home. At autopsy, he had a ruptured anterior communicating artery aneurysm and bacterial meningitis. Cerebrospinal fluid and blood cultures had growth of Staphylococcus aureus. Osteogenesis imperfecta is a disorder of type I collagen. Type I collagen is present in many tissues, including blood vessels. The etiology of cerebral artery aneurysm formation is multifactorial. Some patients with cerebral artery aneurysms have been shown to have abnormalities in type III collagen. There has not been a reported relationship made between abnormalities in type I collagen and aneurysms. Meningitis can also result in cerebral artery aneurysms, but they are usually due to Aspergillus or Mycobacterium species. The case we report is unique; cerebral artery aneurysm formation may have been due to osteogenesis imperfecta and/or bacterial meningitis.     

Practical experiences with the determination of cadaver age by evaluation of bacterial metabolic products

In an experiment a corpse had been kept at room temperature (16 degrees-23 degrees C) for 1163 h. At regular intervals brain samples were taken and the content of free amino acids and related compounds was determined by column chromatography. It could be demonstrated that in a period of 4-20 days postmortem the age of the corpse could be calculated from the concentrations of alpha-aminobutyrate (ABU), gamma-aminobutyrate (GABA), and glutamic acid (GLU) in brain employing the previously [5] presented formula: (formula; see text) T is the postmortem time lapse (days). ABU, GABA, and GLU are the concentrations (mumol/g) wet tissue of the corresponding amino acids. During this postmortem interval there is nearly a linear correlation; from this interval a correct assignment between concentrations and time cannot be given. The determination method is in the range of about 15 degrees-25 degrees C (guarantees bacterial growth and metabolism) independent of ambient temperature. The brain samples (cortex or parts of the putrified brain mush) can be taken without any special precaution during normal autopsy. The results of the experiment (in Fig. 1) were supported by some practical cases where the time lapse since death was well (in Fig. 1) or reasonably (in Fig. 1) known. These results suggest that this method allows in many cases the determination of the age of a corpse found in a warm environment (approximately 15 degrees-25 degrees C) approximately 4-20 days after death.     

急性吗啡中毒大鼠主要脏器内吗啡分布变化的研究

研究急性吗啡中毒大鼠随给药和死后时间延长 ,主要脏器内吗啡的分布变化规律 ,为吗啡类毒品中毒死亡者尸检取材提供依据。采用免疫组织化学SP技术 ,观察 44只尾静脉注射吗啡的大鼠。从给药后 15min到 5h ,从死后即刻至 48h ,脑、肾、心、肝等脏器内吗啡分布的变化规律。结果表明 ,注射吗啡后短时间内各脏器均有吗啡存在 ,主要分布在某些实质细胞的胞浆内 ,且随时间延长吗啡含量上升 ,达高峰 ( 1h)后逐渐减少或消失。不同组织器官的吗啡含量及其变化速率差异巨大。脑内吗啡出现早 ( 15min) ,消失晚 ( 5h) ,峰值高 ,死后衰减慢 ( 4 8h仍呈强阳性 )。肾脏次之 ,但明显优于心、肝。免疫组化SP技术可作为一种鉴定吗啡类毒品中毒的特异性方法 ,脑、肾是其较理想的检材     

Acute cerebellar hemorrhage in a patient with Klinefelter syndrome: XXY karyotype obtained postmortem from cells from pericardial fluid

A case of Klinefelter syndrome and a spontaneous cerebellar hemorrhage in a 12-year-old boy is presented. Autopsy revealed that the hemorrhage was due to the rupture of a dilated artery in an arteriovenous malformation in the right cerebellar hemisphere. The small, undescended testes exhibited partial atrophy of the seminiferous tubules. Postmortem chromosome analysis of cells from the pericardial fluid demonstrated a 47, XXY karyotype. He had previous surgical treatment for bilateral thumb polydactyly and patent ductus arteriosus. In juvenile cases of sudden death with overlapping morphological dysgenesis, postmortem karyotyping may provide important diagnostic information.     

Detection of Acute Diazepam Exposure in Bone and Marrow: Influence of Tissue Type and the Dose‐Death Interval on Sensitivity of Detection by ELISA with Liquid Chromatography Tandem Mass Spectrometry Confirmation*

Abstract: Enzyme‐linked immunosorbent assay (ELISA) and liquid chromatography tandem mass spectrometry (LC/MS/MS) were used to detect diazepam exposure in skeletal tissues of rats (n = 15) given diazepam acutely (20 mg/kg, i.p.), and killed at various times postdose. Marrow, epiphyseal, and diaphyseal bone were isolated from extracted femora. Bone was cleaned, ground, and incubated in methanol. Marrow underwent ultrasonic homogenization. Extracts and homogenates were diluted in phosphate buffer, and then underwent solid‐phase extraction and ELISA. Relative sensitivity of detection was examined in terms of relative decrease in absorbance (ELISA) and binary classification sensitivity (ELISA and LC/MS/MS). Overall, the data showed differences in relative sensitivity of detection of diazepam exposure in different tissue types (marrow > epiphyseal bone > diaphyseal bone), which is suggestive of heterogenous distribution in these tissues, and a decreasing sensitivity with increasing dose‐death interval. Thus, the tissue type sampled and dose‐death interval may contribute to the probability of detection of diazepam exposure in skeletal tissues.