挤压伤——挤压综合征的实验病理学研究

观察挤压伤后挤压综合征的发生发展过程及肾脏病理改变特点。以家兔制造挤压伤—挤压综合征的动物模型 ,取血和尿进行生化检验并应用光镜、电镜及免疫组化等方法 ,观察肾脏的形态学改变。结果显示 :(1)挤压伤后血K+和血BUN明显升高 ,血CO2 CP明显下降 (P <0 0 5 ) ;(2 )在挤压综合征时 ,肾脏肾小球肿胀 ,肾小管上皮细胞不同程度的变性坏死 ,管腔内有以肌红蛋白为主要成分的管型 ,血BUN持续下降 ,血K+改变不明显。肾小管上皮细胞的变性坏死及肾小管内肌红蛋白管型形成可作为挤压综合征的法医病理学诊断依据之一 ,血K+升高是挤压伤后急性死亡的原因之一     

挤压综合征的法医学研究进展

目前挤压综合症(CrushSyndrome)的法医学鉴定一直没有全面、系统、量化的标准,其相关研究成为法医损伤学的热点。为此本文对挤压综合症的概念、病理生理学机制、重要器官的损伤以及相关症状的关系等问题进行了简要的综述。为挤压综合症的研究提供一些思路。     

广泛软组织挫伤致挤压综合征1例

挤压综合征是指遭受挤压伤的人在挤压解除后,出现以肌红蛋白尿和急性肾功能衰竭为主要特征的临床症候群[1]。挤压综合征虽可见于多种原因,但法医检案中遇到最多的是肢体广泛软组织挫伤和肢体被持续较长时间捆绑[1]。作者曾遇1例直接打击肢体所致挤压综合征的案例,现报道如下。1     

急性胸廊挤压综合征

据我们的临床资料,急性胸廓挤压综合征占胸部挤压伤的10%.占全部胸部严重损伤的0.5%.此综合征的描述是在19世纪初,当日于人们曾解剖研究了受惊吓人群中有窒息表现的死者(比如失火时).从那以后,急性胸廓挤压综合征被冠以各种各样的名称:其中有,淤斑面貌,创伤性窒息,奥利维尔或巴斯综合征.最后一个名称很少使用,除此以外每种传统的命名某种程度上都不很恰当,尤其是创伤性窒息的命名,因为此综合征有多种胸廓外影响因素,并不是总有原发损伤.     

广泛软组织损伤肾肌红蛋白免疫组化研究

目的探讨肌红蛋白对挤压综合征肾功能损害的病理形态学改变及法医病理学诊断价值。方法应用EnVision(两步法)免疫组化方法和LSAB免疫组化方法,对22例生前有较广泛肌肉软组织损伤的人尸体肾脏组织(损伤组)进行肌红蛋白检测,12例无上述病史的人尸体肾脏组织作对照(对照组)。结果损伤组有8例肾远曲小管及集合管管腔管型染色呈阳性或强阳性,均见于伤后36h至10d死亡者;有7例近曲小管、远曲小管和集合管上皮腔缘附近的胞浆及腔面肌红蛋白阳性或强阳性,最早见于伤后8h死亡者,伤后24h至48h死亡者最为显著;余9例未见上述改变。对照组12例上述部位均为阴性。结论肌红蛋白管型堵塞肾小管和肌红蛋白对肾小管上皮的直接损害是挤压综合征肾功能衰竭的重要病理形态学基础,两者对挤压综合征的法医病理诊断均具有重要价值。     

15例挤压综合征死亡的法医病理学研究

对 15例挤压伤后挤压综合征的致伤原因、损伤经过时间及尸检材料进行分析,并采用组织学和免疫组化 ABC法染色,观察肾脏的病理改变特点。结果发现：肾脏肿大,肾小管上皮细胞变性、坏死,远曲小管扩张,内有蛋白管型、细胞管型,并证实有肌红蛋白管型存在。     

挤压综合征致死一例探讨

挤压综合征,又称为挤压性肾衰综合征,是指在挤压伤(大多为四肢,肌肉丰富部位)的基础上并发休克、肌红蛋白尿,代谢性酸中毒、高血钾、氮质血症和急性肾衰的一组临床症候群.发生挤压综合征有两个关键因素:1.伤后肌肉缺血、坏死,大量毒性产物(如肌红蛋白、钾离子、组织分解产物等)释出致代谢紊乱,全身中毒.2.肾脏缺血导致急性肾功能衰竭.本症在法医检案中并非罕见,特报导一个曾经有过争议的实例并进行探讨.     

广泛软组织挫伤--挤压综合征

本文通过回顾国内外医学文献,对广泛性软组织挫伤--挤压综合征的研究现状和取得的成就进行了介绍,并对其今后的发展趋势进行了探讨.     

广泛软组织挫伤--挤压综合征

本文通过回顾国内外医学文献,对广泛性软组织挫伤－挤压综合征的研究现状和取得的成就进行了介绍,并对其今后的发展趋势进行了探讨。     

肌红蛋白染色在挤压综合征法医学鉴定中的应用

通过对软组织损伤后出现典型挤压综合征和其它原因死亡案件的分析,探讨检测肌红蛋白对挤压综合征的诊断价值。认为挤压综合征的诊断应从大面积软组织损伤史和急性肾功能衰竭的病理检验入手,肾小管内管型物质的肌红蛋白免疫组织化学染色作为证据之一,而非唯一依据。     

肢体挤压伤大鼠早期心电图及血清cTnI的变化

目的观察挤压伤大鼠早期心电图的改变,并检测血清心肌肌钙蛋白I(cTnI)的变化。方法复制挤压伤大鼠动物模型,标准Ⅱ导联记录心电图变化,化学发光法检测血清cTnI水平。结果挤压伤后心电图ST段明显抬高,并持续24h,伤后6h血清cTnI则显著升高,并持续24h以上。结论肢体挤压伤早期存在心肌细胞的损伤。     

挤压综合征大鼠血清酶浓度变化的初步研究

目的观察挤压伤大鼠血清肌酸激酶(CK)、肌酸激酶心肌同功酶(CK-MB)浓度的变化,阐明肢体挤压伤大鼠早期是否存在心脏损伤。方法复制挤压伤大鼠动物模型,全自动生化分析仪检测血清CK、CK-MB浓度的变化。结果挤压伤后12h,血清CK、CK-MB浓度显著升高,并持续48h以上。结论肢体挤压伤早期可能有心脏损伤的存在。     

挤压伤大鼠早期心脏损伤的细胞机制

目的观察挤压伤大鼠血清对培养的新生大鼠心肌细胞的某些作用,拟阐明挤压伤早期心肌细胞损伤的细胞机制。方法培养1～3d龄SD大鼠心肌细胞,观察挤压伤大鼠血清对心肌细胞搏动频率、表面积、蛋白质含量、3H-亮氨酸掺入、胞内钙浓度和Fos蛋白表达的影响。结果与正常大鼠血清组比较,挤压伤大鼠血清培养的心肌细胞搏动频率(次/min)由88.3±20.6降为26.4±16.7,心肌细胞表面积、蛋白质含量、3H-Leu掺入、胞内游离钙浓度(nmol/L)和Fos蛋白表达阳性指数增加。结论挤压伤大鼠血清通过抑制细胞搏动,增加胞内钙浓度诱导Fos蛋白的表达,引起心肌细胞肥大,介导挤压伤早期的心脏损伤。     

大鼠双后肢挤压伤后肺、肝细胞的凋亡

目的研究大鼠双后肢挤压伤后肺、肝细胞的凋亡过程,探讨挤压伤损伤机制。方法建立大鼠双后肢挤压伤模型,采用TUNEL法对大鼠肺、肝细胞凋亡进行检测,免疫组织化学法检测凋亡相关蛋白Bax、Bcl-2、caspase-3的表达。结果与对照组相比,损伤组大鼠双后肢局部肌肉组织明显损伤,肺、肝细胞凋亡明显增多(P0.05),凋亡相关蛋白Bax上调、Bcl-2下调、caspase-3被激活(P0.05)。结论大鼠双后肢挤压伤后引起肺、肝细胞凋亡明显增多,可能是损伤释放的相关因子介导了细胞凋亡的发生。     

Age‐Related Vulnerability to Lethal Craniocerebral Crush Injuries from Electrical Beds/Tables

Vulnerability to accidents characterizes the extremes of life for reasons that may be similar in each age group. Two cases are reported to demonstrate increased risks of entrapment and crushing injury involving the use of electrically controlled beds/tables. Case 1: A frail 98‐year‐old woman with a history of dementia suffered a lethal crush injury to her head when she fell out of bed and accidentally activated its lowering mechanism. Case 2: An 18‐month‐old girl suffered a lethal crush injury to her head when she became trapped under a lowered electric massage table. Common devices may be dangerous if individuals do not have the mental or physical capabilities to deal with them. The forensic assessment of such deaths involves an evaluation of the neurocognitive level and physical strength of the decedent as documented in previous clinical assessments, in addition to a careful examination of the structure and function of the bed/table.     

The Forensic Pathology of Fatal Attacks by the Large Mammals Inhabiting the Nordic Wilderness—A Literature Review

Fatalities due to animal attacks are rare in forensic medical work but have been known to pose problems due to their potential to mimic homicide. This review summarizes reported cases of fatal attacks by large mammals that inhabit the Nordic wilderness, namely brown bear, moose, wild boar, and wolf, and attempts to elucidate injury patterns that can guide the forensic pathologist to identifying the species and modus operandi of the attacker. A tendency toward a species‐specific injury pattern was observed. Injuries by bear and especially wolf are dominated by biting whereas moose and wild boar do not seem to bite their victims. The bear uses its paws, both for hitting, resulting in crush injury and fractures, and clawing with resulting excoriations and possible penetrating injuries. Crush injuries and fractures appear, on the other hand, to be minimal or absent in attacks by wolf and wild boar.     

Causes and Mechanisms of Death in Fatal Water Buffalo Attacks

Deaths due to buffalo attack have not been well described. A 72‐year‐old man was trampled by a water buffalo (Bubalus bubalis) while attempting to move the animal within an enclosed area at an abattoir. At autopsy, there were numerous injuries involving the chest, head, neck, and left upper arm. Blunt force injury had resulted in multiple rib fractures with a flail chest and fracture/dislocation of the mid‐cervical vertebrae caused either by physical crushing by the animal against the walls of the enclosure or by stomping. There was also evidence of crush asphyxia with bilateral conjunctival hemorrhages and petechial hemorrhages. In addition, there was a deep degloving injury of the upper left arm compatible with goring by one of the buffalo horns. While large animal attacks may result in death from multiple injuries, careful dissection and examination of specific injuries at autopsy may clarify the complex interaction of lethal mechanisms.     

Histological Changes in the Thyroid Gland in Cases of Infant and Early Childhood Asphyxia—A Preliminary Study

A retrospective blinded study of thyroid gland histology was undertaken in 50 infants and young children aged from 1 to 24 months. Deaths were due to (i) suffocation (N = 7), hanging (4), wedging (3), and chest and/or neck compression (4), and (ii) SIDS (20), noncervical trauma (7), organic disease, (4) and drug toxicity (1). In the asphyxia group (N = 18), thyroid gland congestion ranged from 0 to 3+ with 39% of cases (7/18) having moderate/marked congestion. In three cases, focal aggregates of red blood cells (blood islands) were observed within the intrafollicular colloid. These deaths involved chest compression, chest and/or neck compression, and crush asphyxia in a vehicle accident, and all had facial petechiae. Only 22% of the 32 control cases (7/32) had moderate/marked congestion with no blood islands being identified (p < 0.05). Blood islands within the thyroid gland may be caused by congestion associated with crushing or compression and may provide supportive evidence for this diagnosis.     

挤压伤大鼠血清对血管内皮细胞凋亡的作用及机制探讨

目的观察挤压伤大鼠血清对血管内皮细胞凋亡的影响及可能机制。方法培养小牛主动脉内皮细胞,观察挤压伤大鼠血清对培养的血管内皮细胞凋亡及胞内钙浓度的影响,并检测血浆内皮素-1(endothelin-1,ET-1)及心钠素(atrial natriuretic peptide,ANP)的含量。结果与正常大鼠血清相比,挤压伤大鼠血清致细胞的凋亡百分数由(8.26±1.75)%降为(2.75±0.90)%,胞内钙浓度由(96.98±3.95)nmol/L增加到(118.79±3.22)nmol/L,挤压伤大鼠血浆内皮素-1和心钠素含量显著增高。结论肢体挤压伤大鼠血清可抑制血管内皮细胞的凋亡,此效应可能与内皮素-1和心钠素诱发胞内钙浓度增加有关。     

高血压大鼠挤压伤后心功能指标与伤病关系分析

目的观察高血压病大鼠肢体挤压后的早期心肌损伤情况,并分析其在伤病关系分析中的意义。方法原发性高血压大鼠按打击程度随机分为4组,用自由落体装置打击大鼠右侧大腿,然后观察血压、心率变化,测量血清生化指标(肌酸激酶、肌酸激酶同功酶、乳酸脱氢酶、肌酐、尿素氮、α-羟丁酸脱氢酶、天门冬氨酸转移酶),并观察大鼠心、脑、肾的形态学改变。结果打击后大鼠血压、心率均有不同程度的上升,并且随着打击力度的增加而增加,但打击组间没有显著性差异。各组血清生化物表现为随打击力度的增加而上升,轻中重打击作为整体损伤组与对照组比较有显著性差异,天门冬氨酸转移酶、肌酸激酶、肌酸激酶同功酶在打击组间比较具有显著性差异。结论挤压性打击损伤造成了SHR早期心肌损伤,并且此指标可以运用于高血压病与损伤共存下的伤病关系分析。