人体敌敌畏中毒的血液致死浓度探讨

本文对4年间6家医院所有门急诊敌敌畏中毒病例(共50例)进行了调查分析。用气相色谱法对其血液敌敌畏浓度进行测定。运用Bliss法,计算其死亡率和昏迷率的机率单位的回归方程。并获得其经救治后血液半数致死浓度LC_(50)为45.80mg/l,半数致昏迷浓度CC_(50)为8.48mg/l。综合文献,认为其自然的血液半数致死浓度应在合并半数致死浓度LC_e50=19.69mg/l的附近。     

乙醇对小鼠口服地西泮半数致死量及早期代谢的影响

目的研究乙醇对地西泮半数致死量及早期代谢的影响。方法 1利用AOT425tat Pgm程序测定雌性小鼠经口灌服地西泮单独或与不同剂量乙醇联合染毒时的半数致死量;2低、中、高剂量(50、100、200mg/kg)地西泮单独或与不同剂量乙醇联合染毒,HPLC法测定染毒后15、30、60min时小鼠心血中地西泮及其主要代谢物去甲西泮、奥沙西泮血药浓度,观察染毒早期乙醇对地西泮代谢的影响。结果 1联合染毒使地西泮LD50值明显降低,且下降幅度随乙醇剂量增加而加剧;2各联合染毒组染毒15、30、60min时地西泮、奥沙西泮血药浓度较单独染毒时低;50、100mg/kg地西泮与乙醇联合染毒60min时去甲西泮浓度较单独染毒显著升高,但乙醇剂量影响不大;高剂量地西泮与低、中剂量乙醇联合染毒60min时去甲西泮浓度较单独染毒组时低。结论 1地西泮与乙醇确有毒性协同作用,联合中毒时地西泮半数致死量变化与乙醇剂量有关;2染毒早期,乙醇可使地西泮及奥沙西泮血药浓度降低,同时抑制去甲西泮的代谢,使其药浓度升高,在毒性协同效应发生中有意义。     

含甲醇假酒中毒致死的法医毒物分析9例

用工业酒精或直接用甲醇对水勾兑成假酒，冒充白酒流入市场而引起严重中毒甚至致死的事件时有发生。笔者曾检验了87例因饮用假酒而中毒和9例致死的案件，调查甲醇中毒者及死者生前中毒症状及尸体解剖所见，分析了中毒者血液、死者血液、尿液及玻璃体液的甲醇含量，并对其进行综合分析，以探讨鉴定这类案件时的要点。材料与方法1．检材来源本组案例均为男性，年龄25～50岁。假酒来源大多是私人酒坊用工业酒精或甲醇勾兑成的散装白酒，也有包装精美的瓶装白酒。2．对饮用假酒的中毒者和死者生前中毒症状、中毒环境和尸检所见进行回顾性调查。3…     

吸入二氯甲烷和氯仿中毒后溺水死亡案例的法医毒物学分析

国外曾有一些二氯甲烷在工业事故中引起死亡及氯仿用于自杀、谋杀和作为成痛剂吸食而致死的案例检验报道[1-6]，国内尚未见报道。本文采用顶空气相色谱分析方法测定了二氯甲烷和氯仿在3名死亡人员及1只死鱼鹰体内的分布情况，并习国外有关文献资料进行了比较讨论，确定了3人因吸入二氯甲烷和氯仿而引起中毒昏迷，但昏迷后落水溺死是其最终致死原因。案情摘要1991年1月22日上午，某乡数只捕鱼小船，途经某化工总厂正在排放废水、废气的排放口时，船上渔民及数只渔鹰接连落水，致使3人和6只渔鹰死亡。1人经抢救脱脸，据脱险者讲：他与其他3人…     

乙酰甲胺磷中毒血液灌流血药浓度的动态检测

目的探索乙酰甲胺磷中毒在血液灌流(HP)过程中血药浓度的变化规律及终末浓度。方法采用医院急诊病例病人股静脉血,通过气相色谱法分析血浆中的乙酰甲胺磷含量。结果经血液灌流后血浆中乙酰甲胺磷浓度迅速下降,并呈现出灌流前血药浓度越高下降速度越快的特性。结论血液灌流法能迅速降低血液中乙酰甲胺磷浓度,其下降的速度受制于乙酰甲胺磷的初始浓度和灌流开始时间等。     

海鸥洗净剂灌肠的法毒理学研究

本文以海鸥洗净剂为例,运用移动平均内插法,分别计算其灌肠和灌胃的LD_(50)。实验结果,其灌肠LD_(50)为0.67g/kg,参照大鼠一次经口毒性分级标准,属中等毒性,明显大于灌胃毒性(LD_(50)=7.33g/kg)。实验证实,碱性环境使洗净剂的毒性增强,酸性环境则无甚影响。综合文献,对洗净剂中的主要成分——表面活性剂的毒性及毒理机制进行了探讨。     

中毒致死者体内芬氟拉明的GC/NPD,GC/MS法测定

建立了生物检材中芬氟拉明的定性定量分析方法。体液及脏器组织经有机溶剂提取后 ,用GC/MS法进行药物筛选、定性 ,生物检材中的芬氟拉明浓度用4 -苯丁胺作内标、GC/NPD法测定。测得芬氟拉明中毒致死者的血液、尿液、肝等组织中浓度分别为7.8μg/ml、64.2μg/ml、31.3μg/g。并对尸体解剖所见及方法可行性进行讨论     

一起毒鼠强食物中毒的调查分析及其实验室筛查探索

目的 探讨原因不明性食物中毒的检查策略。方法 结合一起发生的原因不明性食物中毒案例，应用流行病学和简易急性动物试验等方法，对导致中毒的致病因素进行分析与判定。结果 中毒案例的暴露时间为早餐时，平均潜伏期为47．84分。中毒反应以神经症状和消化道症状为主。依病例的客观特征分层对其食谱分析，筛选出水煮豆腐是本次中毒的可凝食物。7种剩余食物进行的急性动物试验中发现，水煮豆腐的小白鼠灌注量与中毒反应呈剂量反应关系，半数致死剂量为LD50＝1．68mg/g。气相色谱－质谱仪分析确定水煮豆腐中的毒性性质为四次甲基二砚四胺。结论 本案通过采用症状分析、急性动物实验和毒物分析测定方法确定了一起原因不明性食物中毒的中毒原因。这种检查策略有助于原因不明性食物中毒及其它突发中毒事件的性质判定。     

度冷丁在家兔体内的代谢分布研究

建立生物检材中度冷丁及其代谢物去甲度冷丁的GC／NPD系统分析方法,研究染毒家兔体内度冷丁的原体及代谢物分布情况,测定1例肌肉注射度冷丁过量致死者体内度冷丁和去甲度冷丁浓度。组织检材经酸水解后,在碱性条件下用乙醚提取,残余物用25μl甲醇溶解后进行气相分析。度冷丁的提取回收率高于60％,相对标准偏差小于12％;染毒家兔体内度冷丁浓度下降很快,去甲度冷丁浓度较低;度冷丁和去甲度冷丁在染毒家兔各脏器中含量分布除血液外与度冷丁过量致死者体内分布一致,尿中度冷丁和去甲度冷丁浓度最高,肝脏中浓度明显低于其它脏器。此结果为中毒检案的最佳检材选择和对毒物分析结果评价提供了科学依据。     

一起毒鼠强食物中毒的调查分析及其实验室筛查探索

目的　探讨原因不明性食物中毒的检查策略。　方法　结合一起发生的原因不明性食物中毒案例 ,应用流行病学和简易急性动物试验等方法 ,对导致中毒的致病因素进行分析与判定。　结果　中毒案例的暴露时间为早餐时 ,平均潜伏期为 4 7.84分。中毒反应以神经症状和消化道症状为主。依病例的客观特征分层对其食谱分析 ,筛选出水煮豆腐是本次中毒的可疑食物。 7种剩余食物进行的急性动物试验中发现 ,水煮豆腐的小白鼠灌注量与中毒反应呈剂量反应关系 ,半数致死剂量为LD5 0 =1.68mg/ g。气相色谱 - -质谱仪分析确定水煮豆腐中的毒性性质为四次甲基二砜四胺。　结论　本案通过采用症状分析、急性动物实验和毒物分析测定方法确定了一起原因不明性食物中毒的中毒原因。这种检查策略有助于原因不明性食物中毒及其它突发中毒事件的性质判定。     

Dependence of acute opiate poisoning lethal outcome on the gender, age, and duration of addiction

The article presents toxicological characteristics of 198 cases of acute parenteral poisoning with morphine and heroin in the range of concentrations of their metabolites in the blood and urine which occur in practice. Risk of death is quantified in the range of possible morphine concentrations in the blood in acute opiates intoxication with reference to gender and age. Assessment of the criteria of quantitative opiates toxicity was made according to the method of logit regression and dose-effect curve suitable for analysis of correlations between probability of death and blood concentrations of opiates metabolites. Conditional lethal doses in respect to gender and age are calculated.     

Methadone-related deaths in Hennepin County,Minnesota: 1992-2002

Methadone maintenance therapy (MMT) is the only currently established medical therapy for heroin addiction. However, MMT still remains controversial. In Hennepin County, Minnesota, methadone is one of the top ten drugs reported in medical examiner investigated deaths and one of the most commonly diverted pharmaceuticals. This report reviews the role of methadone in medical examiner deaths over a 10-year period, 1992-2002. We compare cause and manner of death (accidental, natural, suicide) and methadone blood concentrations for decedents who were members of MMT programs with illicit users and those prescribed methadone for chronic pain. Findings reveal that 65% of decedents with measurable blood methadone concentrations were not participating in MMT programs. A total of 96 cases were identified, with the majority white (90.5%) and male (76.8%). MMTP program members were the minority (34.7%) of the methadone positive deaths and 39% were illicit users. Fifteen percent were chronic pain patients with almost half of this group dying from overdose. Methadone concentrations of drug caused/related deaths (0.18-3.99 mg/L) overlapped with those of deaths not attributable to methadone (0.18-3.03 mg/L) with no definable lethal level. Interpretation of methadone blood concentrations must be done in the context of the clinical history for determining cause of death, and may be confounded by postmortem redistribution.     

Renewal Acute Toxicity of Broad-Spectrum Herbicide,Paraquat Dichloride in Channa punctatus (Bloch)

Abstract

Paraquat dichloride (PD) is a major contaminant in aquatic environment and is a cause of concern to different organisms, especially to fishes, as it causes different changes in behavioral and morphological to aquatic creatures. Hence, the objectives of the study are to examine the acute toxicity, behavioral and morphological alterations in air-breathing teleost fish, Channa punctatus (CP) (Bloch). Renewal acute toxicity was performed to calculate the lethal concentration (LC₅₀) by Finney’s probit analysis to CP by exposure to wide range of PD concentrations (30, 60, 90, 120, 150?mg/L) for 24, 48, 72 and 96?h. The LC₅₀ values determined are 93.36, 82.22, 67.93 and 65.87?mg/L for 24, 48, 72 and 96?h, respectively. Maximum allowable toxicant concentrations (MATC) defined by LC₅₀ value is found to be 0.6587?mg/L. The upper and lower 95 percent confidence limit (Fiducial limit) are in narrow range for 24, 48, 72 and 96?h, respectively, and thus results of the experiments are considered good. Fiducial limit calculated helps us to state that the LC50 falls within the specified limit and helps in constructing of toxicity curve. LC50 value gradually decreases with increase in time. Mortality rate was dose-time dependent and increased with increase in concentration. The behavioral changes provide biologically relevant endpoints in evaluating toxicity testing. Deviation from baseline behavior was noticed. Morphological deformities were also seen. The present study provides a clear indication of the toxicity of PD, and is highly toxic even at low level. Hence, it is recommended that appropriate eco-toxicological risk assessment should be made and indiscriminate use of PD by farmers should be discouraged particularly in areas close to aquatic environment.     

The diagnostic value of postmortem blood glucose determinations in cases of diabetes mellitus

In 24 cases of death in diabetic coma the peripheral venous blood showed glucose levels exceeding 3.5 mg/ml (mean value 7.76 mg/ml). In a control material of deaths of other causes the blood glucose was usually low and often zero, and all values were well below the lower limit of the diabetic concentrations. The acetone contents of the diabetic blood varied widely and were of limited diagnostic value. We conclude that glucose concentrations above 3.5 mg/ml in the peripheral blood indicate that death occurred in diabetic coma.     

Diesel fumes do kill: a case of fatal carbon monoxide poisoning directly attributed to diesel fuel exhaust with a 10-year retrospective case and literature review*

While it is known that diesel fuel combustion engines produce much lower concentrations of carbon monoxide (CO) than gasoline engines, these emissions could certainly generate lethal ambient concentrations given a sufficient amount of time in an enclosed space and under suitable environmental conditions. The authors report a case of CO poisoning which was initially referred for autopsy as a presumed natural death of a truck driver found in the secure cab of a running diesel tractor trailer truck. Completion of the preliminary investigation ascribed death to complications of ischemic heart disease (IHD), pending toxicological analysis that included quantification of CO. When the toxicology results showed lethal blood COHbg, the cause of death was re-certified as CO intoxication secondary to inhalation of (diesel) vehicular exhaust fumes. Because of the unique source of fatal CO intoxication in this case, the contributory IHD and the possible contaminants in the putrefied blood, a 10-year retrospective review was conducted on all nonfire related CO deaths autopsied (n = 94) at the Office of the Chief Medical Examiner in Louisville, KY from 1994 to 2003. For validation of the COHbg detection method used by the Kentucky Office of Forensic Toxicology (KYOFT), blood samples from these cases along with controls were submitted to three laboratories using various analytical methods yielding no statistically significant differences. Lastly, an extensive literature review produced no scientifically reported cases of fatal CO poisoning attributed to diesel fuel exhaust.     

Clinical and forensic examinations of glycemic marker 1,5-anhydroglucitol by means of high performance liquid chromatography tandem mass spectrometry

Postmortem diagnosis of diabetes and a diabetic coma can be difficult because of the lack of characteristic morphological findings. 1,5-Anhydroglucitol (1,5-AG), the 1-deoxy form of glucose, competes with glucose for reabsorption in the kidneys. Therefore, diabetics with a permanent hyperglycemia show significantly lower serum concentrations of 1,5-AG than non-diabetics. A liquid chromatography-mass spectrometric method for the determination of 1,5-AG in serum and postmortem blood was developed and validated according to international guidelines. Linearity was given between 1μg/ml and 50μg/ml. Recovery rates ranged between 70.8% and 89.8%, the limit of quantification of the procedure was 0.20μg/ml, limit of quantification was 0.55μg/ml. Serum of 199 diabetics and 116 non-diabetics and femoral blood of 31 diabetic and 27 non-diabetic deceased was measured. Average concentrations were significantly (p<0.001) higher in non-diabetics compared to diabetics ante and postmortem. Seven of the diabetics may have died because of a hyperglycemic coma indicated by a sum formula of Traub>450mg/dl. 1,5-AG average concentrations in these deceased were not significantly different to diabetics which did not die because of a diabetic coma. Concentrations of 1,5-AG give a hint for not well controlled diabetes antemortem and postmortem and can be assumed as an additional and alternative information postmortem to the measurement of HbA1c or fructosamine.     

The role of hydrogen cyanide and carbon monoxide in fire casualties: a prospective study

Determinations of blood cyanide and carboxyhemoglobin concentrations were performed in 18 victims found dead in buildings after fires during a 2-year period. The results indicated that 50% of the victims had been exposed to toxic levels of hydrogen cyanide and 90% to toxic levels of carbon monoxide. Lethal concentrations of carbon monoxide were found in 83% of the victims. In one case a lethal blood cyanide but a non-toxic blood carboxyhemoglobin value was found. It is concluded that carbon monoxide appears to be more important than hydrogen cyanide as a toxic agent in the fire atmosphere, but cyanide poisoning without carbon monoxide poisoning may, under certain circumstances, be the cause of death in fire victims.     

Biochemical measurements of glucose metabolism in relation to cause of death and postmortem effects

This study was performed to examine the relationship between postmortem biochemical values and cause of death. The follow samples were taken from 399 corpses: cerebrospinal fluid (CSF; n = 376, suboccipital), blood (n = 158, femoral vein), and urine (n = 101, at autopsy). (See Table 1 for causes of death) All samples were stored at -80 degrees C. A further 100 samples of blood were later taken and stored at +4 degrees C before testing. Biochemical determinations made were: glucose in CSF, blood, and urine (hexokinase method); lactate (LDH/GPT) and free acetone (HS-gas chromatography) in CSF; hemoglobin A1 in blood (microcolumn technique). In 34 cases fatal diabetic coma was considered verified by morphological and chemical findings. One hundred cases of sudden cardiac death were chosen as the main control group. In 32 of the 34 cases defined above, the value of the formula of Traub (glucose + lactate in CSF) exceeded 415 mg/dl. It is not influenced significantly by hyperglycemia or hyperlactatemia due to factors other than diabetes (i.e., carbon monoxide, asphyxia). After death the value rose till the 30th hpm, then remained stable for at least 1 week. Fatal coma was defined as the ketoacidotic form if free acetone in CSF ranged above 21 mg/l. In these cases, CSF glucose and free acetone correlated positively. Hemoglobin A1 remained stable after death. Its amount was independent from postmortem blood glucose, postmortem interval and total hemoglobin. Furthermore, the manner of storage (-80 degrees or +4 degrees C) had no significant influence on its values. In 29 of 34 cases of fatal coma, Hb A1 exceeded 12.1%. Analysis of urine glucose showed elevated levels (over 500 mg/dl) in diabetic comas. On conclusion, fatal diabetic coma seems indicated as the cause of death if measured values of postmortem biochemistry exceed the following limits: CSF-Traub 415 mg/dl, free acetone (CSF) 21 mg/l; Hb A1 12.1%; urine glucose 500 mg/dl. Most important are the Traub formula and hemoglobin A1. Usually, in fatal coma both values are elevated. If both of them are normal, diabetic coma can nearly be excluded. Combined evaluation of all values is absolutely necessary. Morphology must also always be taken into account. Consequently, a diagnosis of fatal coma can be obtained by a process of elimination.     

阿维菌素在急性中毒死家兔体内的再分布研究

目的考察阿维菌素在急性中毒死家兔体内的再分布。方法按最小致死量一次性灌胃250mg/kg阿维菌素,HPLC法检测家兔死后0h、24h、48h和72h中阿维菌素的含量。结果给家兔一次性灌胃250mg/kg阿维菌素的临床死亡时间为120.6±9.2min(±s,n=10);测定了阿维菌素的致死血浓度和致死组织浓度;家兔死后0h~72h心血和各主要脏器组织中阿维菌素含量存在体内再分布现象;确定肝、肾、肺为最佳组织检材。结论阿维菌素在急性中毒死家兔体内的再分布数据,对法医办理此类案件具有重要参考价值。