Acute fatal poisoning with cyamemazine

A case of fatal poisoning with cyamemazine is presented. The cyamemazine was identified in post-mortem blood using a specific gas chromatographic/mass spectrometry method. The autopsy blood concentration of cyamemazine was 1800 ng/ml. Chronic use of cyamemazine was demonstrated by the presence of the drug in hair. Two other drugs were also detected (bromazepam and trimeprazine). We think that this current blood concentration (1800 ng/ml) is a fatal blood concentration because of the negativity of the other parameters, but careful interpretation of analytical findings are important, the possibility that this death was a consequence of the toxicity of combined drugs could not be excluded. Not many therapeutics and toxic levels were previously reported in overdosage cases in which cyamemazine was involved. We consider that this concentration is only of guidance value for a fatal cyamemazine poisoning.     

Acute fatal poisoning cases due to furathiocarb ingestion.

Seven cases involving acute fatalities due to ingestion of furathiocarb, a carbamate insecticide, are presented. Furathiocarb was detected in the gastric contents using thin layer chromatography (TLC) and gas chromatography/mass spectrophotometry (GC/MS), and quantified in the blood using a gas chromatograph equipped with a nitrogen-phosphorus detector (NPD). The fatal levels of furathiocarb in the blood ranged from 0.1 to 21.6 micrograms/ml.     

A fatal poisoning with LSD

Radioimmunoassay, high-performance liquid chromatography and capillary gas chromatography-mass spectrometry were used to detect and measure LSD in the first reported case of fatal poisoning by LSD. The levels found in ante-mortem serum and plasma and in post-mortem blood, liver blood and stomach contents are given.     

急性安妥中毒尸检1例

安妥 (Ａｎｔｕ)属硫脲类杀鼠剂 ,其分子式为Ｃ11Ｈ10 Ｎ2 Ｓ ,化学名α -萘硫脲或甲萘硫脲 (α -Ｎａｐｈｔｈｙｌ -ｔｈｉｏｕｒｅａ) ,1942年由ＣｕｒｔＰ .Ｒｉｃｈｔｅｒｔ合成本品 ,1945年用于防治褐家鼠。 1973年ＷＨＯ专家委员会主张禁用安妥 ,国内尚未见安妥中毒的尸检报道。同济医科大学法医病理学教研室曾检验一例如下 :某男 ,2 2岁 ,自服大量安妥后出现呕吐 ,呕吐大量黄色胃内容物。次日上午 10时被发现后送医院急救 ,患者烦躁不安、检查不合作、口唇及鼻腔周围有黄色血性物 ,颈软、瞳孔对光反射存在。肺呼吸音增强、心音快。病…     

急性安妥中毒尸检1例

安妥(Antu)属硫脲类杀鼠剂,其分子式为C11H10N2S,化学名α-萘硫脲或甲萘硫脲(α-Naphthyl-thiourea),1942年由Curt P.Richtert合成本品,1945年用于防治褐家鼠.1973年WHO专家委员会主张禁用安妥,国内尚未见安妥中毒的尸检报道.同济医科大学法医病理学教研室曾检验一例如下: 某男,22岁,自服大量安妥后出现呕吐,呕吐大量黄色胃内容物.次日上午10时被发现后送医院急救,患者烦躁不安、检查不合作、口唇及鼻腔周围有黄色血性物,颈软、瞳孔对光反射存在.肺呼吸音增强、心音快.病理反射阴性.裤上有大便.入院2小时后患者烦躁、神志不清,面色苍白、口唇紫绀、大小便失禁、吐黄色血性物,血压140/90mmHg,心律齐,呼吸急促,未闻及干湿性罗音.经洗胃、给氧、对症及抗感染等治疗,7.5小时后患者满肺湿性罗音,两眼瞳孔对光反射消失.12小时后血压降至90/70mmHg,约12.5小时血压已量不出,呈潮式呼吸,脉搏细弱,心跳弱而速,最终因呼吸心跳停止而死亡. 尸检见死者瞳孔直径0.5cm,口唇青紫,气管及支气管内多量白色泡沫状液体,两肺共重1450克,饱满,胸膜下少数点状出血,肺切面有多量泡沫状液体流出,轻度灶性肺气肿,镜下肺重度淤血水肿、部分肺泡腔内出血明显,有大量的肺透明膜形成(图1、图2),合并急性支气管肺炎.灶性肺气肿.胃内有约450克酱褐色液体,混有灰黑色粉末状物质及食物残渣,无特殊臭味,胃粘膜轻度充血,无明显腐蚀出血.十二指肠粘膜充血.脑淤血水肿.肝、肾水肿.心肌横纹尚清晰,心肌间质较增宽.肠壁粘膜下层水肿显著.膀胱内充满尿液,位于耻骨联合上12cm.胰无明显病变.病理诊断:肺重度淤血水肿、急性支气管肺炎;肝、肾、肠壁水肿;脑淤血水肿;膀胱内尿潴留.胃及胃内容物检出安妥成分.鉴定认为死者系口服安妥引起急性中毒,因重症肺水肿并发急性支气管肺炎而死亡. 讨论(1,2):安妥是中性化合物,市售商品为蓝灰色粉末,纯品为白色结晶,无臭,味苦,不溶于水,难溶于乙醇及醚,易溶于碱及有机溶剂(特别是丙酮),其溶液具有蓝色荧光.特别对家鼠有明显的选择性高效毒杀作用.对人毒性较低,故中毒案例极少,作为投毒他杀者罕见.安妥可经胃肠道、呼吸道吸收,吸收后主要分布在肺、肝、肾和神经系统,大部分由肾排出.安妥除对胃肠道粘膜有刺激作用外,主要由于损害毛细血管,促进毛细血管扩张和渗透性增加,引起肺水肿、胸膜炎、胸腔积液及肺出血,最终因呼吸困难、窒息而死亡;也可引起肝、肾脂肪变性及坏死.本例即因重度肺水肿而死亡.Round等1985年报道,用安妥腹腔内注射引起大鼠急性肺损伤,肺血管的反应性随急性安妥损伤增加而增强.反复安妥损伤可引起不可逆性肺动脉高压,从而导致右心室肥厚.也可引起肝肾变性坏死;此外它破坏胰腺β细胞,影响糖代谢,引起糖尿.安妥中毒致死的动物,常见重度肺水肿和多量胸水形成.狗或鼠还可有血糖显著升高,肝糖原含量降低,也可表现体温降低及血液浓缩等现象.因安妥对人中毒致死的报告不多,故其致死量各家意见不一,有报告成人口服致死量为4～10克,敏感者0.5克也可致死.小儿对安妥较第三较易引起中毒.大白鼠一次口服急性中毒LD50为6.25mg/kg,小白鼠为35mg/kg.     

A fatal methamphetamine poisoning associated with hyperpyrexia

After self-administration of 0.05g of methamphetamine hydrochloride intravenously on three occasions at intervals of 3h, a 25-year-old female methamphetamine abuser ingested approximately 1.5 g of methamphetamine hydrochloride, and was found dead 3–4 h later. Complete rigor mortis was observed 1–2 h after death and the rectal temperature was 38.4°C 3–4 h after death.Distribution of methamphetamine and amphetamine in the body was analyzed by chemical ionization mass fragmentography. Amphetamine/methamphetamine concentrations (μ mol/100 g) were $\text{0.26}\text{28.8}$ in blood, $\text{0.64}\text{68.2}$ in brain, $\text{0.96}\text{117.1}$ in liver, $\text{0.53}\text{50.6}$ in kidney, and $\text{1.49}\text{1045}$ in stomach contents. Total amount of methamphetamine hydrochloride in stomach contents was 11.6mg.Amphetamine in tissues was a metabolite of methamphetamine, and amphetamine in stomach contents resulted from excretion into saliva and gastric mucous excretion. With rectal temperature at death estimated at more than 41°C, it would seem that hyperpyrexia played an important role in causing death from methamphetamine poisoning.     

A fatal case of poisoning with cantharidin.

A case of fatal poisoning due to voluntary ingestion of cantharides powder for aphrodisiac purposes is reported. Clinical history, autopsy and analytical findings are described. Blood and urine samples collected during the 30 h of survival, as well as the cantharides product, were analyzed by gas chromatography-mass spectrometry. On the basis of the percentage of the active principle measured in the powder, an ingested dose of 26-45 mg of cantharidin could be estimated.     

A fatal interaction of methocarbamol and ethanol in an accidental poisoning

A case is presented of a fatal drug interaction caused by ingestion of methocarbamol (Robaxin) and ethanol. Methocarbamol is a carbamate derivative used as a muscle relaxant with sedative effects. Therapeutic concentrations of methocarbamol are reported to be 24 to 41 micrograms/mL. Biological fluids were screened for ethanol using the Abbott TDx system and quantitated by gas-liquid chromatography (GLC). Determination of methocarbamol concentrations in biological tissue homogenates and fluids were obtained by colorimetric analysis of diazotized methocarbamol. Blood ethanol concentration was 135 mg/dL (0.135% w/v) and urine ethanol was 249 mg/dL (0.249% w/v). Methocarbamol concentrations were: blood, 257 micrograms/mL; bile, 927 micrograms/L; urine, 255 micrograms/L; gastric, 3.7 g; liver, 459 micrograms/g; and kidney, 83 micrograms/g. The combination of ethanol and carbamates is contraindicated since acute alcohol intoxication combined with carbamate usage can lead to combined central nervous system depression as a result of the interactive sedative-hypnotic properties of the compounds.     

A fatal poisoning with 5-methoxy-N,N-diisopropyltryptamine, Foxy

A fatal overdose involving case by 5-methoxy-N,N-diisopropyltryptamine (5-MeO-DIPT) is reported. 5-MeO-DIPT and its two metabolites, 5-hydroxy-N,N-diisopropyltryptamine (5-OH-DIPT) and 5-methoxy-N-isopropyltryptamine (5-MeO-NIPT), were identified by LC-MS. The level of 5-MeO-DIPT, 5-OH-DIPT and 5-MeO-NIPT in blood and urine was 0.412, 0.327 and 0.020 microg/ml, and 1.67, 27.0 and 0.32 microg/ml, respectively. These blood and urine levels were higher than published data for such poisoning.     

A case of fatal salt water intoxication following an exorcism session

In response to a recent article published in this review, we present in this paper, an unusual case of fatal salt water intoxication. In this case, we point out three special features, the type of water ingested, the physiopathologic consequences of the ingestion and the very strange context of occurrence. This complex case allows us to point out complications due to salt poisoning and others caused by water intoxication.     

Fatal poisoning by protriptyline and haloperidol following an extreme overdose

In this paper the authors report on a case of lethal suicidal toxification with protriptyline and haloperidol after oral ingestion. Gas chromatographic and radioimmunologic investigations were used for quantitative determination of protriptyline and haloperidol in blood, urine, and tissues. The highest concentrations were found in lung and liver. These concentrations are discussed with reference to the cause of death.     

Acute fatal intoxication with narcotic substances during their intracavitary transportation

The authors describe a case of sudden death of a passenger on the train from Uzbekistan bound for Russia via Kazakhstan. The death was attributed to the poisoning with an illegally transported narcotic substance that was detected in the subject's stomach and intestines.     

A fatal doxepin poisoning associated with a defective CYP2D6 genotype

It has been suggested that the polymorphism of the CYP2D6 gene can contribute to occurrence of fatal adverse effects. We therefore investigated postmortem toxicology cases of fatal drug poisonings related to CYP2D6 substrates, with the manner of death denoted as accidental or undetermined. CYP2D6 genotypes were determined in 11 consecutive cases with samples available for DNA analysis. A case of fatal doxepin poisoning with an undetermined manner of death was found to coincide with a completely nonfunctional CYP2D6 genotype (*3/*4), indicating a total absence of CYP2D6 enzyme and suggesting a poor metabolizer phenotype. The doxepin concentration was 2.4 mg/L, the concentration of nordoxepin 2.9 mg/L, and the doxepin/nordoxepin ratio 0.83, the lowest found among the 35 nordoxepin-positive postmortem cases analyzed during the same year. No alcohols or other drugs were detected in the case. The CYP2C19 genotype was determined as that of an extensive metabolizer. The high N-desmethylmetabolite concentration is not consistent with acute intoxication. It is therefore probable that the defective genotype has contributed to the death, possibly involving repeated high dosage of doxepin. Our case strongly emphasizes that a pharmacogenetic analysis in postmortem forensic setting may reveal new insight to the cause or manner of death.     

A case of fatal poisoning with the aconite plant: quantitative analysis in biological fluid.

In recent years recorded cases of plant poisoning have become rare, this may in part be due to the possibility of plant ingestion not being indicated at the beginning of an investigation. Aconitum napellus (aconite, Wolfsbane, Monkshood) is one of the most poisonous plants in the UK. It contains various potent alkaloids such as aconitine, isoaconitine, lycaconitine and napelline. Ingestion of Aconitum plant extracts can result in severe, potentially fatal toxic effects. This paper describes the analytical findings in a recent death in the UK. resulting from deliberate ingestion of Aconitum napellus extract. The concentrations of aconitine measured by HPLC-DAD in the post mortem femoral blood and urine were 10.8 micrograms/L and 264 micrograms/L, respectively. The aconitine concentration in the ante mortem urine was 334 micrograms/L and was estimated to be 6 micrograms/L in the ante mortem serum. Hence, accidental, suicidal or homicidal poisoning due to the ingestion of plant material remains a possibility and should be borne in mind when investigating sudden or unexplained death.     

Child abuse with fatal sequelae in an Essen autopsy sample]

In the Institute of Forensic Medicine in Essen/Germany 24 cases of lethal child battering or neglect have been observed over 17 years from 1973 to 1989. The medicolegal and morphologic findings in these cases are presented and compared to the literature. The patterns of abuse/neglect in Essen compare to those frequently reported in the literature: skull/brain traumas caused by blunt impact, multiple hematomas, bone fractures, and symptoms of malnutrition, vitamin deficiency, and general neglect. In many cases the abuse could be shown to have been chronic. In the seven years 1983-1989 the cases of lethal child mistreatment and neglect amounted to 0.18 percent of all autopsies. Five cases of lethal sexual assault in children during the same period are compared to the mistreated cases.     

急性吗啡中毒大鼠主要脏器内吗啡分布变化的研究

研究急性吗啡中毒大鼠随给药和死后时间延长 ,主要脏器内吗啡的分布变化规律 ,为吗啡类毒品中毒死亡者尸检取材提供依据。采用免疫组织化学SP技术 ,观察 44只尾静脉注射吗啡的大鼠。从给药后 15min到 5h ,从死后即刻至 48h ,脑、肾、心、肝等脏器内吗啡分布的变化规律。结果表明 ,注射吗啡后短时间内各脏器均有吗啡存在 ,主要分布在某些实质细胞的胞浆内 ,且随时间延长吗啡含量上升 ,达高峰 ( 1h)后逐渐减少或消失。不同组织器官的吗啡含量及其变化速率差异巨大。脑内吗啡出现早 ( 15min) ,消失晚 ( 5h) ,峰值高 ,死后衰减慢 ( 4 8h仍呈强阳性 )。肾脏次之 ,但明显优于心、肝。免疫组化SP技术可作为一种鉴定吗啡类毒品中毒的特异性方法 ,脑、肾是其较理想的检材     

Suicidal carbon monoxide poisoning in an automobile with the engine switched off

Report is made on a suicidal carbon monoxide poisoning through entrance of exhaust fumes into the interior of the vehicle. The situation of discovery (switched-off engine) occasioned experimental examinations. The result showed that fatal carbon monoxide concentrations can obviously remain in the interior of a vehicle over a long period of time.     

Poisoning with sodium hypochlorite solution. Report of a fatal case, supplemented with an experimental and clinico-epidemiological study.

A case of fatal poisoning in a 1-year-old girl after ingestion of a household cleanser containing 4.5% sodium hypochlorite (Klorin) in an alkaline solution (pH 12.0) is reported. The forensic medical and toxicological investigations were supplemented by animal studies. These studies indicate that 5, 10, and 15 ml of Klorin/kg body wt given to rats is highly toxic, and that local tissue damage and secondary systemic involvement develops with a severity corresponding to the amount administered. The rats, all of which died, showed various degrees of degeneration and necrosis of the esophagoventricular mucosus membranes, changes analogous to those found at the autopsy of the child. A follow-up investigation of similar cases reported to the Swedish Poison Information Centre, during a limited time, was made to complete the picture.