氯氮平急性中毒死亡1例

沈某,男,48岁,干部。1998年11月18日死在某宾馆卫生间地面上,经现场勘察发现其房间有氯氮平空药瓶3个。尸检所见:死者面部、双手及双下肢突出部位有多处散在小擦伤及皮下出血,皮肤擦伤生活反应不明显。大脑弥漫性肿胀,血管扩张充血,侧脑室内脑脊液呈红色;小脑扁桃体压迹明显,镜下见脑实质的组织间隙加宽,灰质和白质疏松,神经细胞和神经胶质细胞肿胀,血管周围间隙增宽,部分小血管周围可见漏出性出血。肺呈水气肿样改变,肺浆膜下点状出血;气管内有大量白色泡沫,镜下见肺泡壁毛细血管高度扩张、淤血,部分肺泡腔内充满粉染水肿液,局部肺组织出血…     

毒鼠强中毒实质性器官组织超微病理变化研究

目的观察不同浓度毒鼠强中毒大鼠实质性器官的超微病理变化。方法采用灌胃方法使大鼠毒鼠强染毒,制作大鼠中毒模型,并以健康大鼠灌服生理盐水为对照,提取大鼠的脑皮质、脑干桥脑部、心、肝、脾、肾等实质性器官,进行超微病理观察。结果不同浓度的毒鼠强可对心肌细胞、脑神经细胞、神经纤维和肝细胞造成一定损伤,而对肾、脾组织细胞损伤不明显。脑皮质神经元细胞结构模糊,内质网轻度扩张,线粒体扩张水肿,且无明显的剂量-反应关系;脑干桥脑部可见多处弥散性软化灶,神经细胞核溶解,神经纤维细胞有坏死,血管内皮细胞肿胀,血管周围有间隙出现,脑干损伤有明显的剂量-反应关系;心肌细胞表现为不同程度的心肌细胞坏死、线粒体弥漫性崩解或肿胀、肌丝断裂溶解、肌溶灶普遍存在等变化,并呈现出明显的剂量-效应关系;肝细胞表现弥漫性肿胀,细胞模糊,肝窦狭小,内皮细胞肿胀,结构模糊不清,细胞质内线粒体明显肿胀,糖原含量减少,与中毒剂量和时间均呈明显相关性。结论脑、心、肝可能为其毒性作用的主要靶器官或靶组织。     

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。     

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。     

不同时程吗啡依赖大鼠依赖相关脑区光镜和电镜观察

目的探讨吗啡依赖中枢神经系统毒理病理不同时程的变化。方法背部皮下递增注射吗啡建立吗啡依赖大鼠模型,光镜和透射电镜下观察不同时程大鼠吗啡依赖相关脑区,即蓝斑核、中脑导水管周围灰质、黑质、豆状核、杏仁核、海马的病理组织学变化,并对突触进行计数,比较与空白对照组的差异。结果吗啡依赖大鼠6个依赖相关脑区均出现神经细胞固缩或肿胀,神经纤维肿胀,线粒体肿胀、畸形,内质网扩张,多聚核糖体解聚,突触数量增多;胶质细胞、脑膜下淋巴细胞增多,随依赖时间的延长而更加显著,并可见胶质结节形成。吗啡依赖8周组、4周组, 大鼠突触数量较空白对照组增多,其差异具有非常显著性意义(P<0．01);吗啡依赖8周组大鼠突触数量的增多,与吗啡依赖1周组、2周组大鼠比较,其差异具有非常显著性意义(P<0．01)。结论吗啡依赖大鼠依赖相关脑区神经细胞呈缺血缺氧性及退行性改变,突触数量增多,并随吗啡依赖时限的延长而明显。     

小冠状动脉疾病合并冠状动脉畸形尸检1例

1案例某男，26岁，干部，某日上午被发现死于床上，现场勘验未发现异常情况。尸检：死者面、唇紫绀，体表无损伤。心脏重350g，心腔轻度扩张，左心室厚1.3cm，右心室厚0.3cm．心瓣膜未见异常；左、右冠状动脉开口处高出主动脉瓣缘0．3cm；右冠状动脉旁有一副冠状动脉；冠状动脉右优势型分布；窦房结动脉起始段外径0.05cm，结动脉来自右冠状动脉;冠状动脉主支未见粥样硬化斑。显微镜下见多处心肌壁内小冠状动脉壁纤维性增厚，管腔狭窄；心肌细胞浊肿、波状变性及嗜酸变性；部分心肌萎缩、肥大及间质纤维化；窦房结内肌细胞减少及脂肪浸润。肺…     

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 光敏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聚合管中肌红蛋白染色阳性。结果 本研究结果提示多     

有毒动物中毒4例尸检报告

<正> 斑蝥中毒例1,女,21岁。因未婚怀孕而以斑蝥约半两煎服企图堕胎。服后不久即呕吐、腹痛、乏力,23h后发生昏迷而送医院抢救。检查时血压测不到,心音低,心率140次/min,两肺底湿性罗音。于服药后24h死亡。尸检见两腋下、背、颈等处皮肤水泡形成;妊娠子宫(胎儿约3个月);胃粘膜点状出血。镜下见急性卡他性胃肠炎、小肠粘膜表层坏死;肾小管上皮显著浊肿及轻度坏     

外伤性复视损伤程度鉴定1例

<正>1案例资料1.1简要案情某女,44岁,被拳击致伤左眼。1.2病史摘要因左眼伤入院,左眼睑高度肿胀,睑裂消失,上睑伤口,结膜充血水肿,眼底无法检查。CT示:左侧眼眶内壁骨折,内直肌迂曲肿胀。后出现双眼复视。同视机检查结果示:Ⅰ:重复度0°;Ⅱ:融合范围-2°~+8°;Ⅲ级:200秒弧(图1)。HESS屏检查示左右视场图不对称,左眼外侧肌位点均向外扩张,其中上直肌点位扩张角度较大(图2)。     

烧死者皮肤电流斑样组织学改变一例

案例资料案精简介男性，25岁。某年1月因锅炉爆炸引起火灾，烧死。尸检尸体呈拳斗姿势，全身体表烧伤总面积达95？＜，其中淡化占体表面积的18％，其余77％为肝～I”度烧伤，有大易水池及红斑形料皮肤肌肉切面颜色呈鲜红色；口腔、喉头、气管与食管内有大量黑色炭主，粘膜明显充血；肺切面颜色鲜红。其余各脏器均呈淤血状。镜下见肺淤血水肿．气管胶粘膜面、食管粘膜面均见黑色炭尘粘附，粘膜及粘膜下血管明显扩张充血。皮肤表皮与真皮部分分离形成腔隙，表皮细胞呈现类似电流斑样改变。胞浆、胞核技长，呈极性排列。真皮内胶原纤维肿胀融…     

Liver damage in rats during acute carbon monoxide poisoning

Plasma leucine aminopeptidase (LAP) levels and respiration rates of isolated liver mitochondria were studied in carbon monoxide (CO)-poisoned rats sampled at respiratory arrest. An increase in LAP levels paralleled a decrease in the respiratory control ratio and the $\text{ADP}\text{O}$ ratio. The results suggest that the damage to mitochondria closely correlates with the liver damage in rats during acute CO poisoning.     

海洛因成瘾者神经、内分泌及免疫系统超微病理变化研究

目的 研究海洛因成瘾者中枢神经、内分泌、免疫及生殖系统的超微结构变化。方法 应用透射电镜技术对 4例海洛因成瘾者中枢神经系统、内分泌系统、免疫系统以及生殖系统进行了观察。结果 神经系统表现为线粒体肿胀、嵴断裂、空泡变、内质网扩张、神经纤维数量减少、细胞器减少;免疫系统表现为淋巴细胞数量减少,胞浆成分减少,死亡细胞增多;内分泌系统表现为线粒体扩张,局部嵴断裂,内质网扩张;生殖系统表现为男性生精细胞减少,细胞器减少。女性未见卵泡结构。结论 海洛因滥用者的亚细胞超微结构呈急、慢性缺氧性变性、坏死改变。     

Organic lesions after application of hashish in rats and rabbits (author's transl)]

Toxic lesions were found in liver, kidney and brain of rats and rabbits after oral application of hashish for 7 or 30 days. The brain tissue showed hyperemia and edema. The cerebral cortex, brain stem and cerebellum contained ganglion cells with eccentric nuclei and an icreased number of nucleoli. Different stages of cell lesions could be distinguished by nuclear vacuoles, pyknosis and karyolysis. The cytoplasma was loosened and showed numerous vacuoles. In the kidney we found, besides interstitial hemorrhage, cloudy swelling of the proximal tubules with vacuolous degeneration and nuclear pyknosis and karyolysis in all stages. The glomeruli were often enlarged with thickening of Bowman's capsule and surrounding cellular infiltration with cell fragments. The liver cells showed irregularities of nuclei and vacuolated nuclei, plasma vacuoles and cell necrosis. Infiltrations of round cells at the portal-biliary areas were usually combined with an activation of the Kupffer cells and intracellular bile stasis.     

Two cases of right ventricular ischemic injury due to massive pulmonary embolism

In general, massive pulmonary embolism induces severe right ventricular overload, but pathological changes in the right ventricle due to pulmonary embolism is rarely seen. In this report, we describe two autopsy cases of massive pulmonary embolism without pre-existing cardiopulmonary disease. Both cases were accompanied by myocarditis-like changes in the right ventricle and infiltration of a number of polymorphonuclear neutrophils and mononuclear cells into the dilated right ventricular wall. Transmural or subendocardial coagulation necrosis was not apparent. Almost all of the mononuclear cells were immunohistochemically revealed to be CD68-positive macrophages. We speculated that these findings resulted from ischemia due to massive pulmonary embolism.     

Fetal death due to nonlethal maternal carbon monoxide poisoning

Fetal death due to acute carbon monoxide poisoning is rarely reported in the medical literature. Of the eight cases found in literature review, only one documented the fetal carboxyhemoglobin concentration. This paper reports a fetal death due to accidental nonlethal maternal carbon monoxide intoxication in which both maternal and fetal carboxyhemoglobin concentrations were obtained. The corrected carboxyhemoglobin concentration was 61% at the time of death in utero, while the maternal carboxyhemoglobin was measured at 7% after one hour of supplemental oxygen. The authors review the mechanisms of fetal death and emphasize the different carbon monoxide kinetics in the fetal circulation.     

镇静催眠药自杀中毒——附六例尸检报告

本文分析6例镇静催眠药急性中毒死亡的临床症状,法医学尸检和毒物分析资料。镇静催眠药中毒临床表现为昏迷、呼吸抑制、低血压、反射消失、周围循环衰竭等。病理变化以肺、肝、肾、脑等脏器较明显,肺淤血、水肿、肝细胞脂肪变性、肾近曲小管上皮细胞变性、脑水肿等。病变程度与服药至死亡时间长短有关,中毒死亡与药物剂量、个体差异、所患疾病及中毒后抢救所致的临床并发症等因素有关。     

大鼠闭合性脑损伤酯化银和白蛋白组织化学研究

目的 研究闭合性脑损伤立即死亡和伤后 15min至 5天的大鼠脑组织病理变化。方法 应用 HE染色法观察闭合性脑损伤的组织形态学变化。结果 伤后立即死亡组大鼠脑干、大脑和小脑大量神经元表现为皱缩 (Ⅰ型变 )和肿胀 (Ⅱ型变 ),脑干大片神经纤维波浪样变形;伤后 2～ 8h,出现神经元水肿和轴索肿胀明显;伤后 8～ 24h,出现轴索收缩球。之后,Ⅰ型变、Ⅱ型变和收缩球随存活时间延长而增多加重。伤后 4～ 5天,组织水肿减轻或消失,收缩球仍存在。酯化银染色观察,各种损伤性改变均较 H.E.染色更清晰。 ABC法,血浆 Al随伤后时间延长,从血管周围逐渐向周围扩散,并进入损伤的神经元和胶质细胞。结论 脑震荡性损伤改变呈冲击性、对冲性和向心性分布。     

Heroin dependence as a rare cause of symmetrical globus pallidus necrosis

Long-term survival after carbon monoxide intoxication has been accepted for a long time as pathognomonic for elective cerebral tissue damage, especially in cases of isolated symmetrical necrosis of the globus pallidus. The results of old bilateral necrosis in the globus pallidus are described in a case of an acute heroin death after long-term drug abuse. The evaluation of such cerebral changes is discussed as they have to be interpreted as hypoxic or oligemic tissue damage. The different causes of symmetrical necrosis of the globus pallidus that are relevant for legal medicine are compiled and discussed.