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     

多发性软组织挫伤后成人呼吸窘迫综合征──组织学及免疫组织化学研究

本研究应用组织学Ｈ·Ｅ、Ｍａｌｌｏｒｙ、ＰＴＡＨ以及免疫组织化学染色方法对６例多发性软组织挫伤后成人呼吸窘迫综合征者肺组织改变进行了深入探讨。结果表明，所有外伤性呼吸窘迫综合征者肺组织均呈急性充血、出血及水肿改变，且免疫组织化学染色证明，水肿液中含有纤维蛋白（原）成份。在６例中２例可见肺组织局灶性出血坏死，３例有散在性血管内纤维蛋白柱形成及肺泡内透明膜形成。这些改变均属成人呼呼吸窘迫综合征的早期肺损伤。对多发软组织挫伤后呼吸窘迫综合征的形成机理进行阐述。     

广泛性软组织挫伤后肺脂肪栓塞1例

广泛性软组织挫伤后一般是由于继发休克、弥漫性血管内凝血（DIC）或者挤压综合征而导致死亡［1～3］,引起肺脂肪栓塞则少见。广泛性软组织挫伤后因血液中脂肪释放引起肺脂肪栓塞致死则更为罕见,笔者曾遇一例,现予以报道如下:     

急性吗啡中毒大鼠主要器官内吗啡的免疫组化定位研究

一次静脉注射１２．５ｍｇ／ｋｇ。ｂｗ的盐酸吗啡染毒雄性Ｓ－Ｄ大鼠，２小时后处死，取其脑、肾、肝、肺、心组织以２％戊二醛和４％多聚甲醛混合液固定后，常规石蜡切片。运用抗吗啡抗血清及ＳＡＢＣ技术染色。结果显示上述组织切片有不同程度的阳性染色，阳性着色主要见于肾髓质部分肾小管上皮细胞，肝脏中央静脉周围的肝细胞、肺泡上皮细胞及肺内小支气管粘膜上皮细胞、中脑部分神经细胞、室管膜细胞、心肌细胞．以及各器官小血管及毛细血管内皮细胞胞浆、血浆及肾小管腔内尿液。     

人脑挫伤后波形蛋白表达的免疫组化染色观察

目的观察人脑挫伤后波形蛋白（vimentin,Vim）的动态变化,探讨星形胶质细胞Vim表达变化与脑损伤时间的关系。方法42例闭合性脑损伤死亡者,根据伤后死亡时间分为6组（〈2h,〈24h,〈3d,〈7d,〈14d,≤30d）;取大脑挫伤灶进行HE和Vim免疫组织化学染色,对Vim染色阳性细胞面积进行图像分析。结果HE染色显示,脑挫伤后2h挫伤灶内脑组织挫碎、出血,5．5h挫伤灶周出现反应性星形胶质细胞,3d脑水肿明显,7d反应性星形胶质细胞明显增多,14d胶质结节形成,30d出现大量泡沫细胞,胶质瘢痕增多。Vim染色结果显示,脑挫伤后5．5hVim开始表达,少量Vim阳性细胞出现在挫伤灶周围,7d阳性反应性最强,14d逐渐下降,30d胶质瘢痕增多,Vim阳性表达又增强。Vim阳性细胞主要为反应性星形胶质细胞。结论Vim在反应性星形胶质细胞内表达呈现一定波动性,其表达部位在脑挫伤周围,Vim免疫组化染色结合图像分析技术可作为推断脑挫伤时间及部位的参考指标。     

广泛软组织挫伤后器官形态学的研究

目的探索法医病理学诊断广泛软组织挫伤、挤压综合征致死案例的形态学改变。方法采用大鼠广泛软组织挫伤模型和人体挤压综合征致死标本,对器官进行HE染色、肾肌红蛋白HSP免疫组化染色及电镜观察。 结果肾肌红蛋白的阳性率分别为60％、75％、95％;心肌、脑组织阳性染色率为90％;广泛软组织挫伤短期内死亡的大鼠肾电镜观察,可见多种组织细胞病理改变致使毛细血管腔狭窄、闭塞等。结论建立了较理想的大鼠广泛软组织挫伤形成的挤压综合征动物模型;为此类研究积累了具有一定实用价值的病理形态学资料。     

广泛软组织挫伤的病理分析

广泛软组织挫伤严重者可在较短时间内导致死亡。但由于文献中对这方面的研究报道较少,故对其所引起的全身病理改变和较详细的死亡机理尚知之不多,为此,作者将本教研室历年来遇到的五例尸体检查材料重新进行了观察分析。五例都作了全身尸体解剖,主要脏器经石蜡包埋切片,苏木素伊红染色,有的还作了磷钨酸苏木素染色。     

心房室结区挫伤致死尸检一例

案情李某，男，22岁。某日上午11时，被杨某用脚猛踢头、胸及要背部约10分钟，李某被打后呻吟不止．15分钟后死亡。尸检左锁骨中线下第五助处有5×2cm皮下出血，左第4、5肋间肌有9×4cm出血，左第5肋骨前端不完全性骨折。心脏重300g，心隔面房室交点上方有1.7×1.2cm出血灶（照片1）。切开见挫伤处心外膜、右心房肌层及心内膜下出血，尤以卵圆窝与冠状窦口间房室结区明显。冠状动脉未见异常。头顶部有6×2．5cm帽状健膜下出血。颅骨无骨折，其它脏器淤血。照片1．心膈面房室空点上方1．7×1．2cm挫伤灶病理检查挫伤灶内心房肌纤维挫碎、分离…     

87例大脑及脑干挫伤HSP70变化的研究

目的探讨人大脑及脑干挫伤后神经细胞HSP70变化与损伤时间的关系及大脑与脑干HSP70变化的差异。方法对87例闭合性颅脑损伤死亡脑挫伤组织进行病理学及HSP70免疫组织化学染色,结果进行图像分析。结果脑挫伤24h后.HSP70阳性神经细胞最多见,且免疫反应性最强,随后逐渐下降,14d组及30d组HSP70表达与对照组类似。脑挫伤部位可见较多HSP70阳性的淀粉样小体。图像分析显示大脑与脑干HSP70阳性细胞3个参数(A、IOD及AOD)之间呈高度显著正相关或显著正相关,由高至低排列为:A>IOD>AOD。结论神经细胞HSP70免疫组化染色结合图像分析技术作为推断脑挫伤经过时间的参考,大脑与脑干挫伤后神经细胞HSP70变化规律基本一致,但脑挫伤灶周围淀粉样小体形成的意义有待于进一步研究。     

迟发性外伤性脑内血肿脑组织病理形态学研究

运用组织病理学HE染色和Mallory染色,观察迟发性外伤性脑内血肿的病理学改变并探讨其发生机理。结果显示,迟发性外伤性脑内血肿伴有陈旧性脑挫伤、外伤性血管壁坏死及血管炎、挫伤灶或血管壁多发散在钙化,陈旧病灶有纤维包裹、胶质细胞增生和反应性肥大,但无创伤性脑脓肿形成。脑挫伤和外伤性脑内血管病变是脑出血的重要病理学基础,是迟发性外伤性脑内血肿的主要原因。     

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.     

Pulmonary edema in fatal heroin overdose: immunohistological investigations with IgE, collagen IV and laminin - no increase of defects of alveolar-capillary membranes

Pulmonary edema complicating heroin overdosage is a well recognized entity and regarded as the major mechanism contributing to death in heroin addicts. It's pathogenesis is unknown, several mechanisms are discussed: hypoxia-induced increase of pulmonary capillary permeability, depressed myocardial contractility, centrally induced respiratory depression, primary toxic effects on the alveolar capillaries and acute anaphylactic shock. The present study included opiate-related deaths (n=23) and a control group of sudden cardiovascular deaths (n=12) to verify the hypothesis, that defects of the alveolar capillary membranes and/or an acute anaphylactic reaction leads to pulmonary congestion, edema and hemorrhages. Lung specimens were obtained from these 35 autopsies of persons autopsied in the Institute of Forensic Medicine, University of Bonn, in 1997 and 1998. All specimens were examined with hematoxylin-eosin, prussian blue and investigated with immunohistological methods using primary antibodies against collagen IV, laminin and IgE. Defects of the basal laminae of the alveoli were found, demonstrated by laminin and collagen IV, and the number of IgE-positive cells was counted in both groups. There was an increased but not significant number of IgE-positive cells in the heroin-group and defects of the epithelial and endothelial basal laminae were found in both groups without significant differences.     

Suicidal hanging in Cardiff--a 15-year retrospective study.

A retrospective study of 84 cases of suicidal hanging was undertaken in which petechial haemorrhages or congestion were seen in 27%, soft tissue haemorrhage in 29% and fracture of the hyoid or laryngeal cartilages in 36%. Fractures were found to be related to increasing age and were not found when a soft ligature had been employed. Petechial haemorrhages and congestion were related to the completeness of suspension. Apart from the lack of fractures in the soft ligature group any of these findings, either singly or in combination, was found to occur without regard to age, suspension type or ligature type. No evidence was found of clustering or seasonality. The findings are compared to other series and discussed with regard to the mechanisms of causation.     

Pathology of peliosis

Peliosis is a pathological entity characterized by the gross appearance of multiple cyst-like, blood-filled cavities within parenchymatous organs. Peliosis has been related to several underlying debilitating illnesses such as tuberculosis, hematological malignancies, the acquired immunodeficiency syndrome (AIDS), and post-transplant immunodeficiency, as well as intravenous drug abuse, chronic alcoholism, and in conjunction with the intake of oral contraceptives or steroids. The classical pathoanatomical concept is based upon the opinion that peliosis exclusively develops in organs belonging to the mononuclear phagocytic system (liver, spleen, bone marrow, and lymph nodes). However, a paucity of studies indicates that other organs such as lungs, parathyroid glands, and kidneys may be affected too. Concerning the underlying pathogenetic mechanisms of onset and maintenance of peliosis, the morphological data obtained by different investigators suggest that there is more than one path of formal pathogenesis (e.g., congenital malformation of vessels manifesting under altered local intravascular pressure conditions, acquired vascular disorder triggered by toxic noxae, active proliferation of vessels corresponding to the benign end on the spectrum of neoplastic vascular lesions). In the liver, at gross inspection, the peliotic lesions give the cut sections a "swiss cheese" appearance. Microscopically, two different types of peliosis can be distinguished in the liver: (1) "parenchymal peliosis" consisting of irregular cavities that are neither lined by sinusoidal cells nor by fibrous tissue, and (2) "phlebectatic peliosis" characterized by regular, spherical cavities lined by endothelium and/or fibrosis. One of the differential diagnoses that most closely resembles peliosis hepatis is secondary hepatic congestion due to veno-occlusive disease or the Budd-Chiari syndrome. In the spleen, the peliotic lesions may be arranged sporadically, disseminated, or in clusters in an uneven distribution pattern. Histologically, the cavities show frequently well-demarcated margins that may appear focally lined by sinusoidal endothelium, or totally lack a clear cell lining. Differential diagnoses are hemangiomas and involvement of the spleen in hairy-cell leukaemia. Since the disease may culminate in spontaneous rupture of the affected organ and thus may mimic a violent death at autopsy, peliosis is far more than just another morphological curiosity. Awareness of peliosis at autopsy as well as an appreciation for the histopathological changes in less characteristic or advanced cases may become an important issue for both the forensic and clinical pathologist.     

Pneumomediastinum and Soft Tissue Emphysema in Pediatric Hanging

Postmortem computed tomography (CT) is increasingly being used as a tool in forensic pathology. The exact value of postmortem imaging in detecting specific conditions has not yet been established, but in specific cases, it can be used as a diagnostic tool demonstrating findings that remain undetected during autopsy, as in this case. Pneumomediastinum and soft tissue emphysema were detected with postmortem CT in a 3‐year‐old girl after hanging. It was not found during autopsy. This radiological finding matches 3 adult cases previously described. It is assumed that in this case, the first reported in a child, hanging was the most likely cause as well. In the adult cases, it was interpreted as a vital sign; the person must have been alive to create a pressure gradient causing rupture of the alveoli. This case demonstrates one of the added values of postmortem imaging, the possibility of demonstrating findings that remain undetected during autopsy.     

Longitudinal evaluation of immunohistochemical findings of milk aspiration: an experimental study using a murine model

To examine the longitudinal change of pathological findings of the lung and other organs in milk aspiration, an experimental study using a murine model was carried out. Either 0.5 or 1.0 ml cow's milk was instilled into the trachea of rats. From immediately after to 14 days after instillation, the animals were sacrificed, and the lungs, liver, kidneys, and spleen were removed. The results of immunostaining with anti-human α lactalbumin antibody indicated that not only the lung but also the kidney and spleen showed a positive reaction against the antibody over time. Experimentally aspirated milk was detectable in alveoli until 2 days after instillation. It was also detectable in renal tubules from 1 to 6h after instillation. Macrophages containing granules of aspirated milk were observed in splenic red pulp from 3h to 14 days after instillation. Detection of aspirated milk in other organs except the lung would be clear evidence of intravital milk aspiration and would suggest previous or recurrent milk aspiration.     

Immunohistochemical study of blood group activities in severely burned human tissue

The blood, livers and lungs obtained from donors or cadavers of known blood groups were experimentally burned, while the temperatures inside the tissue specimens were automatically measured. All the distinguishable portions with various thermo-changes in each burned tissue specimen were examined for their blood-group activities A, B, Lea, Leb and P1 by means of the immunofluorescence and immunoperoxidase techniques. In the layer immediately before charring of the blood masses (tissue temperature: ca. 200-250 degrees C), the activities A, B, Lea, Leb and P1 could be specifically demonstrated on the erythrocyte membranes. In case of the burned livers and lungs, the A- and B-activities could be detected in the small blood vessels in the layer immediately before charring (ca. 200-250 degrees C), though the layer was so severely thermo-changed, that their original tissue structures could be no more observed. In the severely thermo-coagulated, porous and hardened layer of both organ tissues, the A- and B-activities could be demonstrated on the endothelial cells of the hepatic sinus and small blood vessels (especially in the alveolar walls). The simply thermo-coagulated inner portions well retained their original tissue structures and the A- and B-activities remained on the epithelial cells of the alveoli and bronchioles of the lung as well as the cells described above. The Lewis blood-group activities could be demonstrated on the epithelial cells of the bronchioles in the simply thermo-coagulated inner portion of the lung. The P1-activity could not be demonstrated in the burned tissues of the livers and lungs.     

Vitality and age of conjunctival petechiae: The expression of P-selectin

Confocal laser scanning microscopy (CLSM) results in displaying multiple ruptures of capillaries and venules define conjunctival petechiae as a rhexis haemorrhage. In order to distinguish between petechiae which have arisen before death as opposed to post-mortem artefacts and the establishment of the age of the vessel's damage, we carried out an investigation on a collection of samples from medico-legal cases (positive petechiae: n = 65; post-mortem artefacts: n = 12; control: n = 19) to establish whether the expression of the endothelial adhesion molecule P-selectin as demonstrated by immunohistochemical methods is influenced by trauma before death and possibly by time. Except for cases with massive congestion in those cases where the victim had survived for around minutes, CLSM examination revealed a strong endothelial reaction at the site where the vessel had ruptured. It was impossible to detect a strong P-selectin expression signal in both those vessels which had not suffered any mechanical insult and those which had experienced post-mortem rupture. Therefore, the elevated expression of P-selectin can be used as a criterion to distinguish between those lesions which have occurred in life and those which are post-mortem artefacts.     

小儿感染与多系统器官功能衰竭──附12例临床及病理分析

本文对１２例小儿感染致多系统器官功能衰竭死亡病例进行临床及病理分析。临床表现有发热、外周血白细胞总数增高、心率增快、呼吸困难、呕吐、意识障碍、无尿等。其中发生二器官功能衰竭３例．三器官功能衰竭３例，四器官功能衰竭６例。病理学检查见多器官组织内炎细胞浸润；脏器充血、水肿、出血、ＤＩＣ形成；肠粘膜变性、坏死：淋巴免疫器官病变等。本文在形态学上进一步证实了多系统器官功能衰竭发生的炎症介质学说、微循环障碍、肠源性感染和免疫机能下降的综合作用机理。