23例电击死尸检取材和法医鉴定方法研究

目的在前期动物实验基础上,结合电击死人体尸检病理组织学观察,确定电击死鉴定最佳的组织取材部位。方法选取23例明确"手-足路径"电击死者,明确死于交通事故颅脑损伤和冠心病猝死者各10例为对照组。所有案例提取双腕上前内侧、双踝上后部等部位软组织,观察并分析其骨骼肌(Sk MCs)和动脉血管平滑肌细胞(ASMCs)的核轴比变化。结果 23例电击死案例,年龄19~59岁,男性19例、女性4例;高压电击死3例,日用低压电击死20例;7例出现典型电流斑(31.18%);5例出现胸膜电击纹(22.7%)。电击死组的前腕、内踝的Sk MCs和ASMCs细胞核拉长、扭曲,呈波浪样、栅栏状排列,其核轴比与对照组相同部位比较,有显著性差异(P<0.001),而且ROC曲线分析,Sk MCs和ASMCs的核轴比的诊断临界值为分别4.84、3.81。结论在"手-足路径"电击死的最佳取材部位应为机体电流路径中最狭窄位置,即腕、踝部位,该部位Sk MCs和ASMCs细胞核的极向性拉长、靠近呈串珠状或直线状排列,为最具特征性和诊断价值的电损伤形态学变化。     

微束X射线荧光光谱法检测电流损伤皮肤金属化

目的建立微束X射线荧光光谱（μ-probe X-ray fluorescence,μ-XRF）检测电流损伤皮肤金属化的方法。方法新西兰大白兔32只,随机分为黄铜电击组、紫铜电击组、铁电击组、铝合金电击组,每组8只。电极一极固定于左后腿中部,另一极固定于左前腿,建立电击模型。提取左后腿触电部位皮肤,以及对侧右后腿相应部位皮肤作为对照,应用μ-XRF光谱仪对电流损伤皮肤内金属元素进行测定。结果正常对照组皮肤中检测出磷、氯、钾、钙元素成分;在电击组皮肤中,除正常皮肤检出的元素外,黄铜电击组检测出铜、锌元素,紫铜电击组检出铜元素,铁电击组检出铁元素,铝合金电击组检出铝元素。渗透到电流损伤皮肤内的金属元素呈不均匀分布。结论μ-XRF光谱法检测皮肤金属化可作为诊断电流损伤的特征性指标,并可为触电材料的推断提供依据。     

家兔皮肤低电压电损伤组织病理学研究

目的研究不同数值低电压对家兔皮肤电损伤的组织病理学变化,为皮肤电损伤的法医学鉴定提供一定依据。方法选取家兔35只,随机分为36V、110V、220V生前和死后电击组各3组及正常对照组,共7组,每组5只。应用自制电击装置对家兔进行生前不同数值电压电击和死后不同时间电击,然后对电击处皮肤取材,常规石蜡包埋及HE染色制片并进行组织病理学观察研究。结果 36V生前和死后电击皮肤组织学未见改变;110V、220V生前和死后不同时间予以电击均出现电流斑改变;220V和110V生前与死后电流斑形态无差异;220V较110V电击皮肤电流斑明显。结论电流斑与电压的数值大小存在相关性,电压越高电流斑越明显,36V交流电不能形成电流斑;相同数值电压下电击,生前和死后组电流斑无明显形态学差异,电流斑在36V、110V、220V电压时不能用于区分电击损伤是否为生前或死后所致。     

水、油污中无电流斑电击死大鼠皮肤和心肌的病变

目的探讨水中、油污中无电流斑电击死法医学鉴定的病理形态学依据。方法 SD大鼠28只,分为水中、油污中无电流斑电击死各1组,典型电流斑组、正常对照组、死后电击组、死后水中、油污中电击各1组共7组。采用肉眼、光镜及投射电镜观察水中、油污中无电流斑电击死大鼠皮肤和心肌组织病理学改变,并与其它各组进行比较。结果采用肉眼观察,生前水中、油污中无电流斑电击死大鼠皮肤未见明显电流斑。普通光镜观察,可见电击中心部位表皮变性坏死、脱落,表皮细胞变薄、致密,表皮细胞或/和毛囊、汗腺、皮脂腺发生极性化改变。电镜观察,透明层和角质层分离脱落,基底细胞肿胀、细胞器减少、核固缩,汗腺导管上皮肿胀,棘细胞中粗面内质网扩张融合成泡状,线粒体肿胀空泡化;但光镜与电镜的变化与生前电击死比较不明显、典型。而死后电击组皮肤则无明显病理学改变。实验各组大鼠心肌的改变与皮肤改变类同。结论采用光镜和投透射电镜观察在潮湿环境中电击死的组织病理学改变,可为无电流斑电击死提供依据。     

大鼠电击死心脑肺及皮肤超微结构的改变

目的 观察电击致死大鼠的心、脑、肺、皮肤超微结构形态学改变，寻找电击死的法医学鉴定依据。方法 大鼠12只，其中电击致死6只，另6只对照；取心、脑、肺、皮肤，用戊二醛固定、锇酸染色后透射电镜观察。结果 所取组织细胞均见明显细胞凋亡样改变，其中红细胞肿胀变形，充填整个毛细血管管腔。结论 心、脑、肺、皮肤组织细胞与血管内皮细胞的超微结构形态改变对鉴定电流死有参考价值。     

电感耦合等离子体质谱法检测电流损伤皮肤中金属元素

目的探讨应用电感耦合等离子体质谱(inductively coupled plasma mass spectrometry,ICP-MS)技术检测电流损伤皮肤中金属元素的可行性,建立检测电流损伤皮肤中金属元素的方法。方法用黄铜、紫铜、铝、铁电极材料以220V交流电电击家兔后肢,ICP-MS对电流损伤皮肤中金属元素进行检测。结果与对照组比较:黄铜电击组皮肤中的Cr、Ni、Cu、Zn、Pb含量升高(P0.05),紫铜电击组皮肤中的Cr、Cu、Pb含量升高(P0.05),铝电击组皮肤中的Al、Cr、Mn、Co、Ni、Cu、Pb含量升高(P0.05),铁电击组皮肤中的Cr、Mn、Fe、Ni含量升高(P0.05)。不同电极材料电击后皮肤中元素种类及含量也存在明显差异。结论ICP-MS可作为检测电流损伤皮肤中金属元素的有效方法,且可应用于触电材料的推断。     

电击伤组织的超微结构观察

目的 观察电流传导路径上器官、组织的超微结构变化。 方法 对 SD大鼠进行实验性低电压电击。结果 触电部位皮肤的上皮细胞胞浆内基质凝固、膜系统断碎;骨骼肌肌小节出现异常收缩带;心肌的变化也较明显,可见局灶性溶解坏死并出现异常收缩带;电流传导路径上外周血管、神经的改变以血管明显,血管内皮细胞胞浆中出现空泡,中膜平滑肌可见溶解坏死,神经纤维仅见部分髓鞘松解。 结论 电击伤组织的超微结构变化可作为诊断电击死组织学变化的补充,为解决无明显皮肤电损伤的电击死案件提供形态学指标。同时也探讨了电击伤超微结构变化的形成机制。     

电击死大鼠心肌细胞磷脂变化的研究

目的探讨无电流斑与有电流斑电击死心肌组织磷脂分布。方法 15只SD大鼠,无电流斑和有电流斑各6只,对照组3只。实验组通过自制电击装置通电致死,对照组采用脱颈处死。实验组和对照组大鼠死后0h、12h、24h三个时间段取心肌组织固定和冷冻,对其分别进行制片HE染色和磷脂染色。结果电击死均可见心肌纤维断裂、波浪状改变,血管内皮细胞极性化改变,部分心肌间质少量出血。磷脂染色:电击死0h、12h心肌细胞膜磷脂缺失,随时间延长,磷脂缺失程度加重。对照组仅可偶见单个磷脂位于细胞间质或少量心肌细胞膜磷脂缺损。死后24h,电击组、对照组均可见大面积心肌细胞膜磷脂缺失。结论心肌细胞膜磷脂染色可有助于电击死诊断,但死亡时间达到24h左右则诊断价值不大。     

甲醛溶液固定对ICP-MS检测电流损伤皮肤金属化的影响

目的探讨应用电感耦合等离子体质谱（inductively coupled plasma-mass spectrometry ICP-MS）技术检测甲醛溶液固定后电流损伤皮肤中金属元素。方法利用黄铜、铁电极材料以220V交流电电击兔子后肢,电损伤皮肤分别进行甲醛溶液固定1周、6个月后,应用ICP-MS对电流损伤皮肤中金属元素进行测定。结果与对照组皮肤比较,黄铜电击组皮肤中检测出Cr、Ni、Cu、Zn、Pb含量升高（P〈0.05）;固定1周、6个月后仍可检测出Cr、Ni、Cu、Zn、Pb成分,其中Cr、Cu、Zn、Pb含量电击组与固定组差异无统计学意义。与对照组比较,铁电击后皮肤中检测出Fe、Cr、Mn、Ni元素含量升高（P〈0.05）;固定组（1周和6个月）后Fe、Cr、Ni元素含量与电击组差异无统计学意义。结论 ICP-MS可作为检测电流损伤皮肤中金属元素的有效方法,甲醛溶液固定后触电皮肤仍可进行沉积的金属元素检测,且固定对皮肤金属元素的含量影响较小,该方法仍可为电流损伤诊断提供依据。     

电击死大鼠皮肤超微结构及心肌HIF-2α、H-FABP的表达变化

目的观察电击死大鼠皮肤超微结构,检测心肌细胞中缺氧诱导因子-2α(hypoxia-inducible factor-2α,HIF-2α)和心脏型脂肪酸结合蛋白(heart type-fatty acid-binding protein,H-FABP)的表达变化,为电击死的法医学鉴定提供依据。方法建立大鼠电击模型,将72只大鼠随机分为对照组、电击死组和死后电击组,每组又分为死后即刻、死后30 min和死后60 min 3个亚组。采用HE染色法观察大鼠皮肤改变,应用扫描电镜观察大鼠皮肤超微结构的改变,用免疫组织化学染色方法检测大鼠心肌HIF-2α、H-FABP的表达情况。结果电击死组和死后电击组皮肤的肉眼所见及HE染色结果均无明显差异,在扫描电镜下可见大量细胞碎屑,细胞界限不清,表面可见枯焦状龟裂,散在圆形和椭圆形小孔,边缘不规则,散在大量球形异物颗粒。与对照组相比,电击死各亚组HIF-2α表达均增多,且在死后即刻达到高峰,死后电击组仅在死后即刻表达增多,但低于电击死后即刻(P0.05)。与对照组相比,电击死和死后电击各亚组H-FABP表达均明显降低,在电击死组的表达均低于相应时间点死后电击组(P0.05)。结论电击可引起心肌HIF-2α表达升高、H-FABP表达降低,对电击死的判定以及生前电击和死后电击的鉴别具有法医学意义。     

血管电损伤的实验研究

观察电击后血管病理改变的规律及特点 ,探讨其损伤的发病机制和诊断电击伤 (死 )的价值。采用Wistar大鼠复制血管电击伤模型 ,通过HE、GS、Weigert弹力纤维染色和α actin免疫组化染色 ,观察电击后不同节段血管的病理变化。结果表明 :(1)电击后血管的损伤范围和程度均较其周围大 ;(2 )电击部位的血管常发生全层凝固性坏死 ,血管周围骨骼肌、脂肪细胞广泛坏死 ,大腔隙形成 ;距电击部位越远损伤越轻 ,血管损伤局限于管壁中内层 ,而血管周围组织相对完好 ;(3)光镜下 ,血管内皮细胞不同程度坏死、脱落 ;平滑肌肌浆凝聚 ,呈嗜碱性 (异染 ) ,胞核深染 ,扭曲伸长呈栅栏状排列 ,细胞内外大量汽化空泡形成 ,肌层中弹力纤维减少 ,网状纤维相互融合增粗、断裂 ,呈串珠状改变。TEM下见血管内皮细胞、平滑肌细胞内线粒体、内质网不同程度肿胀与扩张 ,甚至空泡化改变 ,平滑肌肌丝溶解 ,形成低电子密度区 ;汽化空泡边界清楚 ,无膜性结构 ,内无细胞器 ;SEM下见血管壁及腔面粗糙大小不等的腔隙形成 ;(4 ) 2 2 0V组血管的病理改变与 10 0 0V组相同 ,只是损伤程度较前者轻。电击后血管的病理改变是电热效应与电场作用的共同结果 ,血管的病理改变可以作为一种确证电击死的重要依据     

电击后心脏损伤的实验研究

将电击器电路连接家兔左前肢和右后肢，用200v5mA交流电定时电击，制造电击死和电击伤时心脏损伤的动物模型。结果显示：电击死前ECG出现室颤波，光镜下心肌纤维广泛断裂，间质出血，小血管周围水肿．心肌灶性坏死，心房心肌坏死累及心内膜时有微小附壁血栓形成；房室结细胞核空泡变，胞浆深嗜伊红性；电镜下心肌纤维闰盘撕裂；心肌Ⅰ带消失，肌节缩短，超收缩带（Hypercontractionbands）形成，或Ⅰ带扩大，肌节拉长，Z线移位；肌原纤维溶解等。电击伤动物出现心肌散在性坏死灶内炎性浸润，灶性心内膜炎，小冠状动脉狭窄或闭塞。传导系统炎性浸润。本实验对电击死的法医学鉴定和非致死性电击伤心脏并发症的诊断提供病理学基础。     

电击死心脏病理学研究

本文对三例因电击死亡尸体的心脏（包括传导系统）的病理改变进行了研究。研究中使用了三例非电击死尸体的心脏进行对照，并采用了多种染色方法以增加诊断的可靠性和消除假阳性。结果显示，两例２２０伏电压电击死的心脏除发现血管壁及其中的血细胞有改变外，心肌及传导系统未见文献所述的坏死性改变。而这种坏死改变在另一例因７５伏交流电电击死的心脏中却表现得相当明显。笔者分析了其中的原因，同时认为在进行类似的研究时，采用对照组和多种染色力“法是十分必要的。     

Satellite dish as source of electric current. Case report of a fatal and nearly fatal accident at the work site

The authors report on an initially unrecognized fatal accident caused by electric current at the place of work. The source of the current was a satellite dish which had been improperly connected to an old music box with subsequent connection to the household electrocution system (220 V, 50 Hz). Only when a second nearly fatal accident occurred, proper diagnosis and detection of the uncommon source of the electric current was made.     

电击兔肢体所致骨损伤后的实验性研究

目的220V交流电击兔肢体后,观察电击部位骨表面的病理改变,为法医病理诊断电击伤提供客观、量化的指标。方法用220V交流电作为损伤电压。动物分为:生前电击组、死后5m in电击组、腐败组及正常对照组。每组骨骼标本均进行肉眼检察、X线检测及SEM观察;同时运用能谱仪测量电击部位元素的种类及含量。结果①电击部位骨皮质SEM下骨皮质紊乱、小孔穴形成、周围高密度影环绕,且钙、磷元素升高,碳元素下降是诊断电击伤的指标,并能鉴别生前、死后电击伤及腐败骨。②小孔穴的形态及钙、磷、碳元素的变化可用于推断电击时间。结论电击造成骨组织的形态及电击部位元素的改变可作为鉴别生前、死后电击伤、腐败骨和推断电击时间的指标。     

Endothelial cell membrane perforation of aorta and pulmonary artery in the electrocution victims

Some electrocution deaths occur without detectable current marks on the skin, making forensic examination to determine the true cause of death more difficult. Because arterial thrombosis was a frequent finding in victims of electrocution, we investigated injury to the endothelium of the aorta and pulmonary artery with a scanning electron microscope in five cases of death known to be caused by electrocution. We found large pores on the surface of endothelial cells of the aorta and pulmonary artery in those who died of electrocution, but no endothelial membrane perforation was found in those who died of cardiac diseases. These findings were present within 12h after death. Therefore, scanning electron microscopic evidence of endothelial perforation in the aorta and pulmonary artery could be a useful marker to identify electrocution for those victims without detectable current marks on the skin.     

Suicide by electrocution with low-voltage current

Three cases of suicide by electrocution with low-voltage current were observed in five years (1994-1998) by medical clinical forensic examiners of an Emergency Forensic Unit of the Paris suburb among 2,000 external death examinations. The cases involved one woman, aged 72 and two men, aged 38 and 41. In the last two cases, electric burns were retrieved under bared electric wires, placed on the arms or fingers in order to realize a hand-to-hand electric circuit involving the heart muscle. In the other case, the electric circuit between mouth and foot also involved the heart muscle. Household low-voltage current delivered (220 V in France) had a sufficient strength to induce local muscular paralysis and heart fibrillation. In the three cases, blood samples taken have retrieved very high levels of muscular enzymes (CPK, LDH) correlated to the mechanism of electric death. The rareness of suicide by electrocution and its forensic characteristics are detailed in order to help the clinical forensic examiners, prosecutors, and police officers concerned by such death examinations.     

Experimental evaluation of rigor mortis. VII. Effect of ante- and post-mortem electrocution on the evolution of rigor mortis

The influence of electrocution on the evolution of rigor mortis was studied on rats. Our experiments showed that: (1) Electrocution hastens the onset of rigor mortis. After an electrocution of 90 s, a complete rigor develops already 1 h post-mortem (p.m.) compared to 5 h p.m. for the controls. (2) Electrocution hastens the passing of rigor mortis. After an electrocution of 90 s, the first significant decrease occurs at 3 h p.m. (8 h p.m. in the controls). (3) These modifications in rigor mortis evolution are less pronounced in the limbs not directly touched by the electric current. (4) In case of post-mortem electrocution, the changes are slightly less pronounced, the resistance is higher and the absorbed energy is lower as compared with the ante-mortem electrocution cases. The results are completed by two practical observations on human electrocution cases.     

Connexin 43, angiotensin II, endothelin 1, and type III collagen alterations in heart of rats having undergone fatal electrocution

Death due to accidental electrocution occurs frequently. The aim of this study was to investigate alterations in cardiac connexin 43 (Cx43), angiotensin II (Ang II), endothelin 1 (ET-1), and type III collagen associated with fatal electrocution.Twenty-four Sprague-Dawley rats were divided into control, fatal electrocution (220 V, 50 Hz, 60 seconds), and electrical injury (220 V, 50 Hz, 60 seconds) groups. Animals were deeply anesthetized with sodium pentobarbital before each treatment, with the anode connected to the left foreleg and the cathode to the right hindleg, followed by cervical dislocation. Control animals received cervical dislocation alone. Immunohistochemical analysis was performed to evaluate the cardiac protein expression of Cx43, Ang II, ET-1, and type III collagen. Sections were analyzed by digital image analysis.The expression of Cx43 was significantly reduced after fatal electrocution, with the integrated optical density also lower when compared with control (P < 0.05). Expression of both Ang II and ET-1 was significantly increased after fatal electrocution, supported by integrated optical density when compared with control (P < 0.05). But no significant difference was found in type III collagen expression between the fatal electrocution group and the control group.In summary, cardiac protein expression of Cx43, Ang II, and ET-1 was found to be significantly altered with fatal electrocution, suggesting that these 3 proteins may be important underlying mechanisms of death during fatal electrocution. The current findings indicate that such alterations would be reflected in abnormal cardiac function and a possible cause of sudden death.     

远离电击部位电流通路上骨骼肌的病理学研究

研究电损伤时骨骼肌中肌红蛋白(Mb)和纤维连接蛋白(Fn)的异常分布情况。采用大鼠模型和人体电击死标本,对电流通路上骨骼肌组织进行肌红蛋白、纤维连接蛋白免疫组化(LSAB)检测。结果显示:电流通路上肌细胞呈现深浅不同竹节样改变,免疫组化法见Mb脱失,Fn呈阳性,呈蟒蛇状纹理。电流通路上骨骼肌竹节样和蟒蛇纹理改变对无典型电流斑法医学鉴定有实用价值。