利多卡因蛛网膜下腔麻醉致死的动物模型

目的 建立利多卡因麻醉致死的动物模型。方法 犬蛛网膜下腔注射利多卡因(37.01mg/kg体重),观察麻醉致死过程的生命体征变化及死后各器官的病理改变特点。结果 实验组犬心电、血压和呼吸消失的平均时间分别为23.8min(7-42min)、16.4min(7-35min)和18.6min(10～47min)。各器官病理改变均呈急死征象。结论 所建模型实验动物的表现和生命体征变化符合蛛网膜下腔麻醉致死的生前表现,可应用于利多卡因麻醉意外致死案件法医学鉴定的实验研究。     

利多卡因在蛛网膜下腔和静脉注射致死犬体内的死后分布

目的比较利多卡因在蛛网膜下腔和静脉注射致死犬体内的死后分布特点。方法犬12只,其中6只经蛛网膜下腔,另6只经股静脉匀速注入利多卡因(5×15mg/kg)致死,迅速解剖动物,取大脑、侧脑室脑脊液、腰段脊髓腔脑脊液、不同脊髓节段(颈髓、胸髓、腰髓、骶髓),心、肺、肝、脾、肾、胆汁、尿、心血、周围血、注射部位肌肉和注射部位20 cm以外肌肉等脏器组织和体液,用气质联用法定性,气相色谱法定量检测其中利多卡因含量。结果蛛网膜下腔注射致死犬体内利多卡因的含量由高到低顺序依次为腰段脊髓腔脑脊液、骶段脊髓、胸段脊髓、侧脑室脑脊液、腰段脊髓、颈段脊髓、肺、肾、注射部位肌肉、心、大脑、脾、心血、肝、周围血、胆汁、注射部位20 cm以外的肌肉、尿;静脉注射致死犬体内利多卡因的含量由高到低顺序依次为肾、心、肺、脾、大脑、肝、周围血、胆汁、心血、颈段脊髓、胸段脑脊液、注射部位肌肉、腰段脊髓、注射部位20 cm以外的肌肉、侧脑室脑脊液、尿、腰段脊髓腔脑脊液、骶段脊髓。结论蛛网膜下腔注射致死犬背侧脊髓液中利多卡因含量最高,静脉注射致死犬肾脏利多卡因含量最高,此分布特征可为利多卡因麻醉意外法医学鉴定中入体途径的判定提供参考。     

利多卡因及MEGX在蛛网膜下腔麻醉致死犬体内死后再分布

目的研究利多卡因及其代谢产物单乙基甘氨酰二甲苯胺(MEGX)在蛛网膜下腔麻醉致死犬体内的死后再分布规律。方法犬6只随机分为A、B两组,分别经蛛网膜下腔注射0.5倍(6.34mg/kg)和5倍(63.35mg/kg)硬膜外麻醉极量的盐酸利多卡因,于死后0h、12h、24h、36h、72h取心血、外周血、肝、脑等,采用高效液相色谱法(HPLC)检测其中利多卡因及MEGX的含量。结果 A组犬死后72h,心血、外周血和脑中利多卡因含量与死亡当时的比值(Ct/C0)分别为4.74,14.87,7.67,均呈上升趋势(P0.05),MEGX含量与死亡当时含量差异无统计学意义(P0.05);B组犬死后72h,心血中利多卡因含量Ct/C0值为0.36,呈下降趋势(P0.05),脑中为3.48(P0.05)呈升高的趋势,肝中MEGX含量与死亡当时相比差异无统计学意义(P0.05)。结论蛛网膜下腔不同剂量麻醉致死犬体内利多卡因均会发生死后再分布,MEGX未发生死后再分布。     

利多卡因在蛛网膜下腔麻醉致死犬体内的分布

目的 观察利多卡因蛛网膜下腔致死犬体内的分布及脊髓液、脊髓与血液中利多卡因含量的比值。方法薄层扫描法检测血、脊髓液、侧脑室液、各节段脊髓和各脏器组织中利多卡因含量。结果 蛛网膜下腔麻醉致死犬脊髓液、各节段脊髓、脑、血液和其它各脏器中利多卡因含量分别为485.6±51.5μg/ml、226.8±35.2-353.8±44.0μg/g、44.9±11.51μg/g、40.3±6.5μg/ml和13.5±13.7-38.0±9.8μg/g。脊髓液与血液中利多卡因含量之比为12.4±2.7,各节段脊髓与血液之比为5.7±0.9-9.0±2.6。结论 蛛网膜下腔麻醉致死犬脊髓液中利多卡因含量最高,脊髓中次之,血液和其它组织中含量较低。脊髓液/血液、脊髓/血液比值平均可达12.4和5.7-9.0。     

温度对硬膜外麻醉致死犬体内布比卡因死后再分布的影响

目的建立布比卡因在硬膜外麻醉犬体内死后再分布动物模型,观察温度对其死后再分布规律的影响。方法雄性杂种犬18只,盐酸布比卡因（5mg/kg）硬膜外麻醉致死,随机分3组,分别置于室温（20～23℃）、4℃和-20℃,于死后0、2、4、8、24、48、72、96、120h同一尸体提取心血、周围血、肝和大脑,GC-NPD、GC-MS法检测其中布比卡因含量,比较其各组含量变化。结果室温时心血、周围血和大脑的死后再分布现象较明显且复杂．4℃时死后再分布现象较室温下弱且缓慢。-20℃时4种检材中布比卡因的再分布现象进一步减弱。结论布比卡因在硬膜外麻醉致死犬体内可发生死后再分布．低温保存可延缓或阻止其发生。     

对一起非医疗事故纠纷案二审改判理由的几点思考

案情 1997年10月20日,原告庞某某因疝气入住被告某县人民医院诊治.同月22日,被告拟对原告进行手术,术前进行了普鲁卡因皮试,在实施硬膜外麻醉穿刺后,改为推入布比卡因和利多卡因.10分钟后,原告突然四肢抽搐、呼吸急促,继之呼吸、心跳骤停.经抢救,原告呼吸、心跳恢复.原告经被告治疗至同年12月21日方能下床活动,行走时偶尔双腿颤抖.     

延迟性全脊髓麻醉医疗纠纷尸体解剖1例

全脊髓麻醉 (简称全脊麻 )是硬膜外麻醉中最严重的并发症之一 ,系麻醉药物大部分或全部误入蛛网膜下腔 ,造成全部脊神经被阻滞。全脊麻在医疗纠纷中的麻醉事故报道中少见 ,本例系完整尸体解剖 ,包括整个脊髓打开暴露、脑脊液定量检查证实。现报道如下 :死者 ,女 ,4 2岁 ,农民。因反复右上腹疼痛 1年半 ,加重半月到某市第二人民医院住院治疗。入院检查 :体温 36 .7℃ ,脉搏 75次 /分 ,血压 92 / 6 0ｍｍＨｇ ,腹丰满 ,未见肠型及蠕动波 ,肝、脾未扪及 ,右上腹肌张力增高 ,有压痛、无反跳痛 ,莫非氏征阳性 ,肠鸣音正常。术前血常规、出凝血时…     

延迟性全脊髓麻醉医疗纠纷尸体解剖1例

全脊髓麻醉(简称全脊麻)是硬膜外麻醉中最严重的并发症之一,系麻醉药物大部分或全部误入蛛网膜下腔,造成全部脊神经被阻滞.全脊麻在医疗纠纷中的麻醉事故报道中少见,本例系完整尸体解剖,包括整个脊髓打开暴露、脑脊液定量检查证实.现报道如下:     

对一起非医疗事故纠纷案二审改判理由的几点思考

案　情1997年 10月 2 0日 ,原告庞某某因疝气入住被告某县人民医院诊治。同月 2 2日 ,被告拟对原告进行手术 ,术前进行了普鲁卡因皮试 ,在实施硬膜外麻醉穿刺后 ,改为推入布比卡因和利多卡因。 10分钟后 ,原告突然四肢抽搐、呼吸急促 ,继之呼吸、心跳骤停。经抢救 ,原告呼吸、心跳恢复。原告经被告治疗至同年 12月 2 1日方能下床活动 ,行走时偶尔双腿颤抖。原告住院期间共支付给被告医疗费 335 0元 ,后因无钱支付医疗费 ,被告停止对其治疗。经原告家属要求 ,被告又继续为原告治疗。 1998年 8月 5日 ,被告通知原告出院 ,原告家属以原告未愈为…     

无电流斑电击死兔骨骼肌il-6mRNA表达研究

目的探讨生前电击与死后电击的鉴别方法及电流通路的推断方法。方法15只新西兰兔，随机分为3组，每组5只，即电击死组、死后电击组、对照组。电击死组，用220V交流电的两极分别连接实验动物的左后肢与右前肢，通电致死。死后电击组，从耳缘静脉注射50ml空气致死，于死后即刻用220V交流电的两极分别连接实验动物的左后肢与右前肢通电3min。对照组直接从耳缘静脉注射50ml空气致死，不进行电击。用荧光RT—PCR技术检测骨骼肌白介素6信使核糖核酸（il-6mRNA）表达水平，所得结果进行统计学分析。结果电击死兔骨骼肌il-6mRNA水平远高于死后即刻电击者（P〈0．05）；电击死兔对称肢体中通电肢体骨骼肌il-6mRNA水平远高于非通电肢体（P〈0．05）。结论骨骼肌il-6mRNA表达变化可用于生前电击与死后电击的鉴别；机体对称部位骨骼肌il-6mRNA表达差异有助于推断电流通路。     

甲胺磷在犬体内的死后分布

目的建立甲胺磷的犬灌胃染毒致死模型,观察甲胺磷在犬体内的死后分布规律。方法犬经8倍LD50（7.4mg/kg）剂量甲胺磷灌胃后,观察其中毒症状,死亡后即刻解剖,分别取心、肝、脾、肺、肾、脑、右上肢肌、右下肢肌、胸肌、胃组织、心血、胆汁、玻璃体液和尿液,GC/MS和GC法检测其中甲胺磷含量。结果犬8倍LD50甲胺磷灌胃染毒后20min内出现中毒症状（,53.3±14.1）min死亡。各组织脏器及体液中甲胺磷含量由高到低分别为胃（99.84±0.87）μg/g、脾（46.87±28.67）μg/g、肝（43.82±22.74）μg/g、肾（43.79±29.04）μg/g、心血（35.36±13.98）μg/mL、肺（35.25±18.59）μg/g、尿34.81μg/mL、胸肌（19.23±17.18）μg/g、右上肢（16.92±8.98）μg/g、心（15.09±6.11）μg/g、右下肢（12.83±7.63）μg/g、脑（10.91±4.13）μg/g、胆汁（6.75±1.45）μg/mL、玻璃体液（6.22±4.97）μg/mL。结论甲胺磷在犬体内死后分布不均,胃、脾、肝、肾、心血、肺、尿检材中含量较高,可作为疑似甲胺磷中毒毒物分析的检材。     

Reporting a fatality during tumescent liposuction

Deaths of patients during elective surgery have drawn attention to the danger of anesthesia. Tumescent local anesthesia is subcutaneous infiltration of large volumes of dilute lidocaine with epinephrine to produce vasoconstriction while delivering anesthesia over large areas without lidocaine toxicity. This report documents the case of a 38-year-old woman who attended an outpatient clinic to undergo liposuction of the abdomen and bilateral hips and thighs. According to one witness, around 30 min after anesthesia administration, the victim suffered an episode of tonic–clonic convulsion. When the emergency medical services arrived the patient was in asystole. She died in spite of attempted cardiopulmonary resuscitation. The patient had no significant past medical history including no history of allergies or any known complications with anesthesia. A complete autopsy was performed and possible causes of death such as myocardial infarction, aspiration of food or foreign body, and pulmonary embolism were discarded. Anaphylactic shock was considered a possible but unlikely explanation for the fatality. Toxicological analyses revealed the presence of lidocaine and mepivacaine in heart blood, at concentrations of 4.9 and 16.2 mg/L, respectively. All drugs involved in the case were detected using gas chromatography with nitrogen–phosphorus detector and confirmed using gas chromatography–mass spectrometry full scan mode after solid-phase extraction using Chem-Elut columns. An additional high-performance liquid chromatography coupled to diode-array detection screening also obtained the same results. Based on the autopsy findings, case history, and toxicology results, the forensic pathologists ruled that the cause of death was an overdose of local anesthetic agents. The Court of Law ruled the death as an involuntary homicide due to gross negligence.     

Tissue distribution of lidocaine after fatal accidental injection

The accidental death of a 64-year-old heart patient as a result of the injection of an incorrect dose of lidocaine is presented. The attending nurse inadvertently administered an intravenous bolus of 10 mL of 20% lidocaine (2g). The patient should have received 5 mL of 2% lidocaine (0.1 g). Such iatrogenic overdoses of lidocaine arise from confusion between prepackaged dosage forms. Lidocaine concentrations (mg/L or mg/kg were: blood, 30; brain, 135; heart, 106; kidney, 204; lung, 89; spleen, 115; skeletal muscle, 20; and adipose, 1.3. The results indicate that even during cardiopulmonary resuscitation as much as 38% of the administered dose of lidocaine may be found in poorly perfused tissue such as skeletal muscle and adipose.     

人体皮肤创伤组织细胞因子表达的时间相关性

目的探讨TGF-β1、b—FGF和VEGF在人体皮肤创伤组织中的表达变化及其与损伤时间的关系。方法收集15例机械性致伤的人体皮肤组织(受伤5—120min内死亡),常规制作组织切片后进行免疫组化染色,并统计分析TGF-β1、b—FGF和VEGF因子的表达情况。结果 TGF-β1在16—50min组表达升高,60～120min组呈阳性至强阳性表达;b—FGF在16—50min组表达升高明显,强阳性表达亦出现在60～120min组;VEGF仅在60—120min组出现阳性表达。统计学分析表明,TGF—β1和b—FGF的表达升高分别在受伤60~120min(P<0.01)和在16—50min(P<0.01)有显著性意义,VEGF表达升高只在60~120min(P<0.05)有显著性意义。结论 TGF-β1、b—FGF和VEGF的表达时间和表达强度与损伤时间有关;TGF-β1、b—FGF和VEGF的表达可为人体短存活期损伤时间的推断提供参考。     

Death following spontaneous recovery from cardiopulmonary arrest in a hospital mortuary: 'Lazarus phenomenon' in a case of alleged medical negligence

We report a possibly first forensic autopsy case of death following a spontaneous recovery from cardiopulmonary arrest (CPA) after clinical declaration of death: 'Lazarus phenomenon'. A 65-year-old male with congenital deafness and dumbness was found unconscious in his room at a public home. During pre-hospital and clinical resuscitation including defibrillation and medications for about 35 min, CPA persisted under electrocardiographic (ECG) monitoring and therefore, his death was pronounced. However, about 20 min later, a police officer who had been called for the postmortem investigation found the patient moving in the mortuary. The patient subsequently showed typical ECG signs and laboratory findings of early inferior wall myocardial infarction and died 4 days later. The forensic autopsy, due to alleged medical negligence, revealed myocardial infarction with thrombotic occlusion of the right coronary artery and secondary hypoxic brain damage. The present case and the related clinical literature suggest that, especially in cases of acute myocardial infarction in elderly patients, a careful observation to confirm death after discontinuation of resuscitation is recommended to provide appropriate medical care, irrespective of the quality or duration of advanced life supporting efforts.     

Causes of death in hospitalized intravenous drug abusers

The authors reviewed at autopsy the causes of death of 274 patients with evidence of intravenous drug abuse who had been admitted to a large public hospital. There were 127 who died from diseases unrelated to intravenous drug abuse, and in 41% of these, chronic alcoholism was implicated. Deaths from overdose syndromes and drug-related organ pathology comprised only 11% of all cases. The mean age at death was 39 years. There was a male/female ratio of 3.6:1. Half of all patients died from infection--72 from acquired immunodeficiency syndrome (AIDS) alone. These findings indicate that persons hospitalized with a history of intravenous drug abuse usually die from causes other than overdose and that AIDS and chronic alcoholism are significant problems. Emphasis should be placed upon detecting "hidden" intravenous drug deaths to provide more accurate statistical information.     

A comparison of three computer models for prediction of dose in acute amitriptyline overdose

The pharmacokinetics of amitriptyline in overdose have been reported not to fit conventional compartmental models. In this study, the dose-concentration-time relationships of amitriptyline in overdose were modeled with discriminant analysis, with an evolutionary heuristic search program, and with a decision-tree model based on the entropy of uncertainty of classification. The computer models all used the same data from dogs administered treatment (80 mg/kg), toxic (250 mg/kg), or fatal (500 mg/kg) doses directly into the surgically isolated duodenum. All the models achieved a high degree of success (77 to 93%) in assigning records to the high-, low-, or middle-dose groups. Two of the models gave a probability of the assignment. Results of this analysis suggest that blood amitriptyline and nortriptyline concentrations are most useful in estimating dose in acute amitriptyline overdose.