外伤性脑梗死的形态学观察

目的 观察外伤性脑梗死的形态学特点,并探讨其与脑挫伤的鉴别。方法 从81例重型颅脑损伤中选出15例符合继发性出血坏死标准的脑标本,另选15例脑挫伤标本作对照,两者均经福尔马林固定后分别作冠状、矢状及水平切面,用肉眼与光镜观察。结果 外伤性脑梗死常见于5个部位,即基底节(3例)、扣带回(2例)、对称性枕部楔叶回(2例)、枕颞外侧回(6例,5例合并有中脑桥脑出血)和枕回(2例);梗死均不在直接受力点或其对冲点,范围明确局限,呈楔形或类楔形,且与脑疲密切相关。镜下见梗死区高度淤血、出血及坏死;水肿,并有白细胞浸润和胶质细胞反应。大脑各叶的梗死,严重者累及全皮层与蛛网膜下腔,未见软脑膜破裂;神经细胞缺氧或缺血性病变明显。脑挫伤的案例,见受力点或对冲部位的皮质及皮质下髓质处出血,挫伤处脑回顶部的软脑膜多破裂,挫伤的脑组织可有挫烂。结论 外伤性脑梗死在法医学上习惯称为继发性出血坏死;它是由于脑疝和水肿压迫颅内血管而形成。外伤性脑梗死和脑挫伤,根据其与脑疝的关系、病变部位、软脑膜是否完整,以及其它组织学改变,二者不难鉴别。     

11例脑皮质挫伤远区及脑干病变的光镜和扫描电镜观察报告

本文报告11例因脑外伤致死的案例。肉眼观察10例有轻重不等的大脑皮质挫伤；10例有蛛网膜下腔出血；3例有脑干出血；1例有视丘下部出血。光镜及扫描电镜下见大脑皮质挫伤10例；其余挫伤，在距大脑皮质挫伤3cm的脑白质6例，视丘下部8例，丘脑、中脑各6例，桥脑5例，延髓4例，侧脑室壁8例及视神经4例。镜下检查挫伤远较肉眼为多。10例神经细胞有不同程度变性、坏死及缺血性病变。9例大脑及脑干轴索、髓鞘有不同程度断裂、变性、排列紊乱、崩解及坏死，其中7例轴索断端查见收缩球。作者对脑外伤死因及法医学鉴定应注意的问题作了简要的讨论。     

大鼠脑损伤分级自由落体打击模型的建立

目的建立一个控制性与重复性好,并可分级的脑损伤动物模型。方法根据自由落体原理,使击锤从不同的高度下落,造成轻、中、重不同程度的大鼠脑损伤,肉眼、光镜观察损伤的程度。结果肉眼、光镜观察下出现可分级的病理学改变。轻度损伤组病理改变局限于大鼠大脑皮质浅层,中度损伤组病理改变可见于大脑皮质及深部白质内的基底核、海马、胼胝体、丘脑,重度损伤组病理改变除中度损伤累及部位外,还累及脑干。挫伤灶周围神经元变性、坏死范围和程度随损伤程度的加重而增大。各组内每只动物所受损伤程度一致。结论该模型制作出常见的闭合性颅脑加速伤损伤,致伤程度较一致,重复性好,可分级,是脑损伤实验研究较合适的动物模型。     

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     

132例滑动性脑挫伤类型与受力机制、受力部位的探讨

目的研究脑受力后在颅腔内滑动挫伤的类型与受力机制、受力部位的关系。方法按颅骨解剖部位划定受力部位，根据案情确定受力方式后，对132例滑动性脑挫伤的脑标本，经福尔马林固定后作冠状、矢状或连续切面，肉眼、镜下观察。结果滑动性脑挫伤按发生部位不同分3型：脑顶型，65例（49．24％）；脑底型，38例（28．78％）；混合型，29例（21．96％）。脑顶型多见于额顶部的加速性受力，脑底型多见于枕部的减速性受力，混合型多见于顶枕部的减速性受力。结论3种类型与头部的受力机制、受力部位有相应关系。     

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。     

法医颅脑损伤的研究进展(Ⅱ)

<正> 3 外伤性颅内出血3.1 外伤性蛛网膜下腔出血(traumatic subarachoid hamor-rhage,TSH) TSH能见于任何类型的头部外伤时,一般文献认为其占外伤性颅内出血的60％以上,是颅脑外伤常见死因之一。其法医学鉴定的关键和难点是与病理性蛛网膜下腔出血的鉴别,因为后者的发生率也很高。以往教科书和法医学专著中,都认为TSH与病理性蛛网膜下腔出血的发生部位有显著不同,描述TSH多见于大脑穹窿部,呈多灶性分布在脑挫伤周围,     

22例中毒死者胰腺出血坏死的法医病理学研究

研究了２２例中毒死者胰腺出血坏死的法医病理学特点，观察到口服中毒者出血坏死多发于胰腺头、体部，呈广泛、片状；吸入中毒者则多见于胰体、尾部，仅为间质或实质点、灶状出血坏死。并对其发生的机理作了探讨     

两例脑震荡所致立即死亡的案例报告

<正> 案例1.男性,50岁,农民。1987年5月29日与人争吵时,从禾田奔向大路,突然跌落在路旁水沟内,立即昏迷未醒至死亡。死亡当日法医剖验见头顶部有一长约4cm 创口。深达帽状筋腰,颅骨无骨折。送检固定的脑重1495g,大脑表面及切面正常,未见挫伤及出血,脑室大小正常,脑干及小脑肉眼未见损伤及病变。常规取各部位神经组织制片,经伊红苏木素和髓鞘染色镜检:脑实质毛细血管及小静脉     

变质性心肌炎致死1例

1案例案情：黄某，男，22岁，冈盗窃被收审，在审讯中突然呼吸困难、全身抽搐，送医院后已死亡。尸检主要所见：双下肢有挫伤，颅、胸、腹腔未见有出血，胸腺重309，心脏大小正常，左右心耳处有较多的脂肪，各瓣膜未见异常，其中右心室三尖瓣处粘附一较大血块，并向肺动脉延伸，大小为6cmX！．scm，质较硬，切面呈红白相间，心肌切面未见异常，冠状动脉未见粥样硬化及栓塞，其余器官未见有出血及其他病变。显微镜下：心肌间质见有散在分布的脂肪组织，在窦房结、房室结及传导束也有脂肪浸润，部分心肌纤维化，心肌纤维里节段性或全部变性和…     

Morphological damage to the central nervous system (CNS) following open heart surgery

We investigated 40 patients who had died following open heart surgery between January 1990 and May 1992. Between this time, 703 open heart procedures were carried out at the University Medical School of Debrecen, 2nd Department of Surgery's Cardiac Surgery Unit with a mortality rate of 8.3%. We studied each individual's clinical records, autopsy findings, and histology of defined portions of brain tissue. Clinical information used were: sex, age, clinical stage (according to New York Heart Association (NYHA) classification) at time of surgery, type of procedure performed, and duration of time of extracorporeal circulation. Autopsy records collected and studied focused on the macroscopic and microscopic alterations in the CNS. The most common morphological findings in the CNS for the 40 studies cases were, cerebral edema in all cases, reactive microgliosis and nuclear pyknosis in most cases, and in a minority of the cases focal microscopic hemorrhage or focal microscopic white emolition. Also found were, destructive brain hemorrhage and global cerebral necrosis. Of the 40 cases studied there was only one case in which brain death was diagnosed perioperatively, and which was clinically diagnosed to be caused by global cerebral hypoxia.     

人脑挫伤周围早期星形胶质细胞反应 定性定量分析初步研究

目的探讨脑挫伤灶周围早期反应性肿胀和增生胶质细胞的生物学特性和法医学意义。方法应用常规HE染色、GFAP免疫组化染色和图像分析技术,对尸检人脑组织挫伤周围星形胶质细胞反应进行定性定量分析。结果脑挫伤周围星形胶质细胞在伤后很短时间内（小于5分钟）即可反应性肿胀和增生;随伤后经过时间延长,肿胀程度逐渐减弱;星形胶质细胞反应与脑挫伤的部位有一定关系。结论这种反应性星形胶质细胞有可能作为诊断轻度脑挫伤和判断脑挫伤早期损伤经过时间的指标。     

Diverse morphological lesions and serious arrhythmias with hemodynamic insults occur in the early myocardial contusion due to blunt impact in dogs

To investigate the morphology and hemodynamics of the early myocardial contusion, an animal model of cardiac contusion was established by impact to the precordial region at sternum at velocity of 10.0m/s with a mechanical elastic-cord propelled impactor in 19 dogs. The electrocardiogram and both the left and right intra-ventricular pressures were recorded continuously throughout the experiment. Histological and immunohistochemical examinations of myoglobin, creatine kinase-MB and fibrinogen were conducted. At the moment of impact, abrupt over-pressures within the left and right ventricles occurred with concomitant serious arrhythmias followed by variety of cardiac conduction disorders and depressed left and right ventricular systolic pressures during the observation times. Histologically, lesions of myocardial contusions were identified at subepicardial, myocardial or subendocardial layer as interstitial hemorrhage, disruption or coagulative necrosis as well as contraction band necrosis of the muscle fibers, which might be categorized into the hemorrhagic, necrotized and mixed forms. The three forms of lesions were found to exist independently, or co-existed in a heart. However, severity of the lesions varied greatly with different parts even within a heart. Intravascular thromboses were occasionally discovered post-impact. Immunohistochemically, loss of myoglobin and creatine kinase-MB from cardiac cells, and accumulation of fibrinogen at the cell membranes were detected 5min post-impact. The intracellular accumulation of fibrinogen increased with extension of post-impact intervals. Our results indicate that diverse morphological lesions concomitant with hemodynamic compromise and serious, even fatal arrhythmias occur in the early myocardial contusion, and intravascular thromboses are occasionally produced, suggesting that traumatic myocardial ischemic lesion may be induced due to blunt impact to the precordial region.     

实验性心脏挫伤动物模型的建立

本研究应用自制机械式弹性拉力打击器以9．1～10．5m／s速度冲击动物胸骨心前区，不仅导致左右心室压力、心电图及心率发生改变，而且造成了心脏挫伤等宏观的病理形态学变化，成功地建立了心脏挫伤动物模型，为深入研究钝力性心脏外伤奠定了基础。     

心脏神经病

目的 研究心源性猝死的病理形态学。方法 用本组建立的CCS检查法对179例心源性猝死者作常规CCS组织学检查。结果 发现8例心脏神经或神经节内有出血、炎症或肿瘤浸润,伴神经组织水肿、变性、坏死,而其他病变不足以解释猝死。结论 一切原发或继发性心脏神经病均可致猝死。     

原发性脑干挫伤的HE染色观察

目的观察原发性脑干挫伤的形态学特点。方法从465例致死性颅脑损伤中,检出171例有脑干挫伤病变、均于伤后10min～7d死亡者。脑干标本经福尔马林固定后,以脑干各颅神经根水平面等处切取检材,每例共8块,HE染色,光镜观察。结果 171例中有24例颅底骨折致脑干挫伤者,脑干横切面见小灶出血,其余只有在镜下方可见有组织出血、挫碎或撕裂等脑挫伤改变,以及对损伤的应激反应现象。结论原发性脑干挫伤的形态学具有一定特点,故对鉴定脑干损伤有着重要的参考价值。     

Cardiac concussion: definition, differential diagnosis, and cases presentation and the legal ramification of a misdiagnosis

A cardiac concussion is caused by a sudden, nonpenetrating, localized impact to the chest that is theorized to result in almost simultaneous sudden death from a disruption to the conductive system. The detailed external/internal forensic examination of the body reveals no evidence of structural, pathologic, or histologic signs of trauma to the heart. A cardiac concussion is a rare and often overlooked cause of sudden death. This type of sudden death is typically seen among younger individuals participating in sports involving projectiles and, to a lesser degree, where collisions occur. Cardiac concussions are clinically, pathologically, and chemically different from a cardiac contusion. The objective of this paper will be to define cardiac concussion, differentiate between cardiac concussion and cardiac contusion, and describe the clinical and pathologic features of a 32-year-old white male who died of a cardiac concussion following a collision with a catcher during a softball game. The civil ramification of incorrectly diagnosing the manner of death in cases of death involving a cardiac concussion will also be addressed.     

大鼠挫伤肺组织中水通道蛋白1表达变化

目的探讨水通道蛋白1（aquaproin 1,AQP1）在大鼠挫伤肺组织中的表达变化及其与肺水肿的关系。方法将SD大鼠随机分为实验组和对照组,制备肺挫伤模型,用免疫组织化学方法检测肺组织中AQP1的分布和表达变化。结果肺挫伤后1和3h肺组织出现水肿、出血,炎性细胞浸润,5h炎性反应进一步加重。AQP1表达在挫伤后1、3和5h均明显高于对照组（P〈0．01）,随着伤后时间延长,水肿加重,AQP1持续上升。正常AQP1主要分布在支气管和肺泡壁的毛细血管内皮细胞及间质细胞,挫伤后肺AQP1的表达部位未发生改变,但积分光密度值（intergrated optical density,IOD）差异有统计学意义（P〈0．01）。结论挫伤肺组织可能存在AQPs的基因表达调控失衡,导致大量水的异常跨膜转运以及在肺组织中的异常聚集,这可能是挫伤肺组织水肿形成原因之一。     

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。