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。     

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     

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。     

头外伤短时死亡者脑干组织学改变的观察

ＨＥ染色,光镜下观察皮质挫伤及脑干损伤的形态学改变,在脑损伤组可见出血、水肿及神经元坏死等。可疑脑干损伤组也可见上述改变。     

人脑挫伤后GFAP,PCNA的法医病理学研究

采用在实际工作中所遇到的脑挫伤案例标本 ,利用免疫组织化学染色 ,观察人脑挫伤后GFAP ,PCNA的改变 ,用图象分析仪对免疫组织化学染色阳性细胞的面积和灰度等进行定量测量 ,EpiInfo统计软件分析 ,得出人脑挫伤后GFAP ,PCNA变化的时间性规律 ,为脑挫伤形成时间推断 ,提供新的形态学依据。GFAP阳性细胞面积、灰度伤后24h即有显著增加 (P<0 01) ,7天达高峰 (P<0 01) ,以后有逐渐下降的趋势 ;PCNA阳性细胞面积、灰度于伤后4天达到最大值 (P<0 01) ,以后逐渐下降。因此 ,伤后人脑组织GFAP、PCNA免疫组织化学染色阳性细胞面积、灰度改变有时间规律 ,GFAP、PCNA可作为2天到20天间不同时间脑损伤的推断指标。     

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。     

定量检测NSE和S-100推断脑挫伤时间的动物实验

观察实验性大鼠脑挫伤后NSE、S－100的时间性变化规律,为法医学推断脑挫伤形成时间提供新的手段。采用改进的Feeney氏落体打击致Wistar大鼠脑挫伤模型,进行免疫组织化学SP法染色,并利用图像分析仪对免疫组化染色阳性细胞灰度和面积进行测量,SAS统计软件分析,结果显示：NSE阳性神经元灰度与面积在伤后1h至2d呈下降趋势,至伤后12h阳性细胞灰度、面积降到最小值（P＜0．01）;S－100阳性细胞面积和灰度伤后呈上升趋势,至伤后4dS－100阳性细胞灰度、面积达到最大值,与对照组及其它实验组比较均有显著性差异（P＜0．01）,伤后5d仍保持较高水平;NSE、S－100免疫组织化学染色阳性细胞的数量、灰度、面积改变有时间规律。推断2d内脑挫伤可用NSE作为主要指标,推断2～5d的脑挫伤则以S－100改变为主。     

迟发性外伤性脑内血肿脑组织GFAP、S-100和NSE的免疫组织化学研究

应用免疫组织化学ABC法和S－P法，对6例伤后1．5天至2年发生的迟发性外伤性脑内血肿（DTICH）脑组织标本进行神经胶质细胞内胶质纤维酸性蛋白（GFAP）、S－100蛋白（S－100）和神经元细胞内特异性烯醇化酶（NSE）变化和应用价值的研究。尸检和组织学检查发现有脑挫伤等病变。6例DTICH脑组织挫伤及周围区均有明显的GFAP、S－100阳性的细胞变化，细胞数目增多，胞体肥大、增生，免疫组化反应产物增多、深染；神经元细胞NSE免疫组化染色均呈阴性改变。结果表明：6例DTICH脑组织中GFAP、S－100的NSE的免疫组织化学变化是有一定时间间隔的外伤性陈旧性改变，在DTICH的病理诊断上具有重要价值，可作为DTICH法医学鉴定的一个辅助手段。     

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:     

大鼠脑挫伤后脑与其他器官组织中TNF-α表达的比较

目的 比较大鼠脑挫伤组织及其他器官组织中肿瘤坏死因子α(tumor necrosis factor-α,TNF-α)表达的差异,期望为法医病理学脑挫伤的诊断以及损伤时间的判断提供理论依据.方法 对45例SD大鼠脑挫伤后脑组织及心、肝、脾、肺、肾等器官组织进行TNF-α免疫组织化学染色,观察脑挫伤对不同器官中TNF-α表...     

Immunohistochemistry of pulmonary surfactant apoprotein A in forensic autopsy: reassessment in relation to the causes of death

To reassess the immunohistochemical distribution of pulmonary surfactant apoprotein A (SP-A) in relation to the causes of death, 282 forensic autopsy cases were reviewed. The most intense and dense granular immunostaining of intra-alveolar SP-A was observed in the hyaline membrane syndrome from various traumas, protracted death from drowning, and perinatal aspiration of amniotic fluid. Similar granular staining pattern was found in fatal poisoning by a muscle relaxant and organophosphate pesticides. An evident increase of intra-alveolar granular staining was noted in most fatalities from mechanical asphyxia and drowning, and some cases of fire death. SP-A staining was usually very weak or sparse in alcohol intoxication, poisoning by hypnotics and also carbon monoxide poisoning. These findings suggest that the amount of intra-alveolar granular SP-A staining may be a possible indicator of severity and duration of respiratory distress (agony) from peripheral (non-central nervous system) origin and alveolar damage.     

Immunohistochemical investigation of pulmonary surfactant-associated protein A in fatal poisoning

To evaluate the immunohistochemical distribution of pulmonary surfactant-associated protein A (SP-A) in fatal poisoning in relation to the effects of drugs and poisons on respiratory function, 42 forensic autopsy cases were examined by scoring the staining intensity. The highest scores of SP-A staining, with dense granular deposits (aggregates) in the intra-alveolar space, were observed in fatalities from pancuronium bromide (muscle relaxant) injection and petroleum (butane) gas inhalation. Poisoning with organophosphate pesticides and arsenic (ingestion) showed a second grade SP-A score. However, The SP-A scores were relatively low in ethanol and sedative-hypnotic intoxication. Carbon monoxide intoxication showed a varied degree of SP-A score, and the aggregated SP-A score tended to be higher in cases of lower blood carboxyhemoglobin concentration. A varied SP-A score was also observed in methamphetamine fatalities, in which the score was relatively low in cases with a higher serum drug level. Increase of SP-A was not always associated with the intra-alveolar effusion or hemorrhages. The above-described observations suggested that the immunohistochemical score of SP-A may be a possible indication for intensity and duration of drug/poison-dependent respiratory distress.     

Two Fatal Cases of Hidden Pneumonia in Young People*

Abstract: Acute respiratory distress syndrome (ARDS) is a severe lung disease characterized by inflammation of the lung parenchyma leading to impaired gas exchange. This condition is often lethal, usually requiring mechanical ventilation and admission to an intensive care unit. We present two fatal cases of hidden pneumonia in young people and discuss the pathophysiological mechanism of ARDS with reference to the histological pattern. A complete forensic approach by means of autopsy and histological, immunohistochemical, and microbiological, examination was carried out. In both cases the cause of death was cardio‐respiratory failure following an acute bilateral pneumonia with diffuse alveolar damage and ARDS associated with sepsis and disseminated intravascular coagulation. Our cases suggest on one side the importance of an early diagnosis to avoid unexpected death while on the other that the diagnosis of ARDS has to be confirmed on the basis of a careful postmortem examination and a complete microscopy and microbiological study.     

Could Intra‐alveolar Hemosiderin Deposition in Adults be Used as a Marker for Previous Asphyxial Episodes in Cases of Autoerotic Death?

Intra-alveolar hemorrhage and hemosiderin have been cited as possible markers of recent and remote asphyxial events. Little study has been undertaken of the potential significance of intra-alveolar hemosiderin in adults as a potential marker of previous sublethal asphyxial episodes. Ten cases of lethal sexual asphyxia (an entity known to be associated with repetitive sublethal asphyxial episodes) and 20 randomly selected, age- and sex-matched controls had sections of lung stained for hemosiderin. Subsequently, intra-alveolar, iron-containing macrophages were counted. All cases were men (ages 15-50 years; mean 31.8). No significant increase in hemosiderin was found in victims of sexual asphyxia, indicating that asphyxial episodes in sublethal sexual asphyxial activities may not be sufficiently intense or prolonged to cause intra-alveolar hemorrhage or that intra-alveolar hemorrhage in adults is a relatively nonspecific finding. These results do not support intra-alveolar hemosiderin deposition as a marker for previous sublethal asphyxial events in autoerotic asphyxia.     

A comparison of pulmonary intra-alveolar hemorrhage in cases of sudden infant death due to SIDS in a safe sleep environment or to suffocation

The differentiation of SIDS from accidental or inflicted suffocation may be impossible without corroborating findings from the death scene or autopsy or in the absence of a confession from a perpetrator. Pulmonary intra-alveolar hemorrhage (PH) has been proposed as a potential clue to suffocation, but none of the previous studies on this topic have limited SIDS cases to those who were in a safe sleep environment, in which all were found supine and alone on a firm surface with their heads uncovered. Our aims are to: (1) compare PH in SIDS cases found in a safe sleep environment to a control group comprised of infants whose deaths were attributed to accidental or inflicted suffocation and (2) assess the effect of age, CPR, and postmortem interval (PMI), with regard to the severity of PH in this subset of safe-sleeping SIDS cases. We conducted a retrospective study of all postneonatal cases accessioned by the Office of the Medical Examiner in San Diego County, California who died of SIDS or suffocation between 1999 and 2004. A total of 74 cases of sudden infant death caused by SIDS (34 cases as defined above, comprising 8% of the total SIDS cases), accidental suffocation (37), and inflicted suffocation (3) from the San Diego SIDS/SUDC Research Project database were compared using a semiquantitative measure of pulmonary intra-alveolar hemorrhage. The most severe (grade 3 or 4) PH occurred in 35% of deaths attributed to suffocation, but in only 9% of the SIDS cases. Age, duration of CPR attempts and PMI had no effect on the severity of PH in SIDS. Our results indicate that the severity of PH cannot be used independently to differentiate SIDS from suffocation deaths. Each case must be evaluated on its own merits after thorough review of the medical history, circumstances of death, and postmortem findings.     

Childhood foreign body aspiration in Istanbul, Turkey

In this study, we present the data concerning 10 children (six boys, four girls) with a diagnosis of foreign body aspiration (FBA) amongst 19,951 cases that underwent autopsy between the years 1996-2002. Eight of the children were under 2 years old. All the incidents took place at home. One of the parents was in the company of the child at the time of incident. At least one of the risk factors was positive. Interestingly, all of the aspirated material was related to food except one. Only four cases had subpleural petechiae, whereas five of the seven subjects undergoing histopathological evaluation had edema, hyperemia or intra-alveolar fresh bleeding. The legal instructions, which regulate the standards of toy materials, came into force at the end of 2003. Even though the legal instructions regulating the size and consistency of toys are very important to prevent FBA, we believe that the education of the parents and carers in the prevention of food aspiration is of greater importance.     

Immunohistochemical studies on postmortem lividity

An immunohistochemical investigation of postmortem lividity was performed to illuminate localization of hemoglobin (Hb) and the mechanism of fixed lividity. The fixed lividity was defined as an unfading phenomenon by thumb finger pressure. Skin specimens were taken from 68 autopsy cases 7.5–336 h (2 weeks) postmortem. Localization of Hb of the specimens was examined by a labeled streptabidin biotin (LSAB) method using polyclonal (rabbit antihuman hemoglobin antibody) and monoclonal (mouse anti-human hemoglobin monoclonal antibody) antibodies. Positive staining for Hb was observed in various sites of the skin, i.e. in only intravascular erythrocytes, in vascular walls and perivascular tissue including sweat glands and sebaceous glands, in the dermal connective tissue, and in almost all of skin tissue except the horny layer. The diffusion of Hb into skin tissue was observed in 20 of 41 displaceable lividity cases (49%) and 11 of 27 fixed lividity cases (41%). Compared to displaceable lividity, superficial plexi in fixed lividity were filled with erythrocytes, which were markedly immunodetected. These findings support the hypothesis that the fixation of lividity is not due to diffusion of Hb into skin tissue but hemoconcentration in blood vessels.     

An autopsy case of intraoperative death due to pulmonary fat embolism--possibly caused by release of tourniquet after multiple muscle-release and tenotomy of the bilateral lower limbs

Acute interstitial pneumonitis (AIP), also known as Hamman-Rich syndrome, is a distinct type of idiopathic interstitial pneumonia affecting patients of both genders without pre-existing lung diseases. We describe the case of a fulminant form of AIP and discuss the pathophysiological mechanisms of AIP with reference to the histological pattern. A 15-year-previously-healthy male boy presented to the Hospital with a 6-day history of malaise, fever and cough. The clinical prodromes were followed by the acute onset of increasing shortness of breath rapidly progressing in acute respiratory failure. Chest X-ray demonstrated bilateral diffuse airspace opacification; the high resolution CT confirmed the presence of bilateral, symmetric diffuse ground-glass attenuation. The patient was admitted to the intensive care unit, but died after few hours. An autopsy was performed within 24h. The histological examination of lung specimens showed a pattern of diffuse alveolar damage. immunohistochemical, microbiological and toxicological tests were also carried out. The clinical presentation, the histological findings and the exclusion of infective, traumatic, toxic and metabolic causes of acute respiratory distress syndrome (ARDS) allowed us to conclude that the boy was affected by AIP. In conclusion, AIP is a diagnosis of exclusion. It has a mortality rate ranging about 50%, despite mechanical ventilation. In fatal cases of AIP diagnosis can be based on clinical presentation, radiological, histological and microbiological findings and can be further confirmed by immunohistochemical analysis.     

Pathological spectrum of the lung in cases of violent death: Part I. Lesion classification

The results are presented of the pathological study of the lungs in 66 cases of violent death observing the more frequent types of lesions and establishing 4 different groups of postlesioned pulmonary condition. 1. Inflammatory alveolar lesions without a diffused interstitial involvement (IAL) including contusions or direct aggressions, lobular pneumonias, or bronchopneumonias with a predominance of intra-alveolar inflammatory exudation. 2. Inflammatory alveolar lesions with a diffuse interstitial involvement (IALW) including generalized affectation of the parenchyma with lesions in the capillary structure of the wall. 3. Edemohemorrhagic lesions (EHL) presenting phenomena of capillary congestion with hematic extravasation and interstitial and intra-alveolar edema, without inflammatory involvement. This is the most numerous group and it can constitute the preliminary stage of any other. 4. Unspecific chronic lesions (UCL) not related to the cause of death, being chronically inflammatory and fibrotic alterations of limited interest in our study. We emphasize the importance of the inflammatory involvement of the alveolar wall in the pathogenia of diffuse alveolar damage (DAD) and the aggravation of pulmonary lesions by capillary structure alteration, direct lesion of alveolar epithelium, presence of macrophages, and liberation of certain intracellular enzymes.     

冠心病猝死心肌mcl-1蛋白检测及其意义

目的观察冠心病猝死(SCD)心肌mcl-1蛋白产物,探讨其免疫组化检测及其对SCD诊断的意义。方法运用免疫组织化学SABC法,对46例SCD和40例非猝死心肌(有冠心病和无冠心病)中mcl-1蛋白产物进行检测和观察,并比较其差异。结果(1)自症状出现至死亡,时间超过30min的SCD(36例),其心肌组织均出现mcl-1蛋白阳性染色;(2)自症状出现至死亡,时间短于30min的SCD(10例),其心肌组织mcl-1蛋白呈弱阳性染色;(3)冠心病非猝死样本(20例),4例心肌出现微弱的mcl-1蛋白阳性染色,无冠心病非猝死样本(20例)几乎没有出现阳性染色。结论心肌mcl-1蛋白的免疫组化检测可诊断自症状出现至死亡时间超过30min的SCD。