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.     

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 diazinon poisoning

A case of fatal suicidal ingestion of diazinon insecticide is presented. Diazinon concentrations in post-mortem body fluids and tissues were determined using electron capture and flame ionization gas-liquid chromatography. The highest concentrations of diazinon were found in blood, stomach contents, bile and adipose tissue.     

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 chronic ketamine poisoning

A few papers in the literature reported incident deaths by acute ketamine poisoning. In this paper, we report an unusual homicide caused by chronic ketamine poisoning. The victim was a 34-year old married woman with no previous medical history (except as reported herein) who died in her own home. The court investigation revealed that she was chronically poisoned by her husband over a period of about one year in an act of homicide. Determination of ketamine concentrations in autopsy specimens was carried out with gas-chromatography/mass spectrometry (GC-MS). The results showed that ketamine concentration was 21 microg/mL in gastric contents, 3.8 microg/mL in blood and 1.2 microg/mL in urine. The most striking forensic findings were cardiac muscle fibrosis and hyaline degeneration of small arteries in victim's heart, the pathological features of ketamine poisoning previous reported only in animal studies.     

A fatal poisoning involving Bromo-Dragonfly

This paper reports a fatal overdose case involving the potent hallucinogenic drug Bromo-Dragonfly (1-(8-bromobenzo[1,2-b; 4,5-b′]difuran-4-yl)-2-aminopropane). In the present case, an 18-year-old woman was found dead after ingestion of a hallucinogenic liquid. A medico-legal autopsy was performed on the deceased, during which liver, blood, urine and vitreous humour were submitted for toxicological examination. Bromo-Dragonfly was identified in the liver blood using UPLC–TOFMS, and was subsequently quantified in femoral blood (0.0047 mg/kg), urine (0.033 mg/kg) and vitreous humour (0.0005 mg/kg) using LC–MS/MS. Calibration standards were prepared from Bromo-Dragonfly isolated from a bottle found next to the deceased. The structure and purity of the isolated compound were unambiguously determined from analysis of UPLC–TOFMS, GC–MS, HPLC–DAD, ¹H and ¹³C NMR data and by comparison to literature data.The autopsy findings were non-specific for acute poisoning. However, based on the toxicological findings, the cause of death was determined to be a fatal overdose of Bromo-Dragonfly, as no ethanol and no therapeutics or other drugs of abuse besides Bromo-Dragonfly were detected in the liver, blood or urine samples from the deceased. To our knowledge, this is the first report of quantification of Bromo-Dragonfly in a biological specimen from a deceased person. This case caused the drug to be classified as an illegal drug in Denmark on 5th December 2007.     

A fatal case of oleandrin poisoning

The study presents a case of fatal poisoning with oleander leaves in an adult diabetic male. After repeated vomiting, and gastrointestinal distress the patient was admitted at the hospital with cardiac symptoms 1h after the ingestion. Urine samples were assayed immunochemically and by GC-MS for drugs of abuse and for general toxicological screen. Blood was analyzed for alcohol and volatiles by static head space GC-MS. Blood and oleander leaves were analyzed by LC-MS/MS for oleandrin and related compounds, the main cardiac glycosides of Nerium oleander. Oleandrin was detected by LC-MS/MS in the blood sample at a concentration of approximately 10 ng/ml. Another cardiac glycoside with pseudo-molecular ion of m/z 577, a likely structural isomer of oleandrin, was also detected in the blood and oleander leaves. However, by using the response as a function of concentration for oleandrin, this cardiac glycoside was roughly estimated at a concentration of approximately 10 ng/ml in the deceased blood. This would give a total fatal blood concentration of cardiac glycosides of about approximately 20 ng/ml in the deceased blood.     

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 fatal case of pepper poisoning.

An 8 month old infant died as the result of administration of a traditional remedy, given orally as an infusion of a red powder. The symptoms on admission were coughing with diarrhoea and vomiting. Analysis of the powder using high-performance liquid chromatography (HPLC) confirmed the suspicion of capsaicin. Pepper preparations, which are used as traditional medicines, are highly toxic and their use on infants should be discouraged.     

A fatal case of mercuric cyanide poisoning

A 57-year-old pharmacist was found dead 11 days after his disappearance. At the autopsy, samples of blood, urine, gastric content were obtained. Presence of ethanol, cyanide and mercury were detected in some samples. Cyanide and mercury were identified and quantified using high-performance liquid chromatography with diode array detector (HPLC) in fluorescence mode and ICP with mass selective detector (ICP-MS) respectively. Whole blood concentrations of ethanol was 1.72 g/L. Cyanide and mercury concentrations in whole blood were respectively 0.16 and 3.8 mg/L. Concentrations of cyanide (27 mg/L) and mercury (150 mg/L) in gastric contents prove a massive oral ingestion of mercuric cyanide or mercuric oxycyanide occurred. In this case report, the death was attributed to the combined toxicity of cyanide and mercury.     

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 poisoning caused by methomyl and nicotine

A 35-year-old male was found lying in a prone position in his room. He was in cardiopulmonary arrest on arrival to hospital and was pronounced dead. There was no attempt at resuscitation. No miosis was observed on admission. At post-mortem his stomach contained 170 g greenish liquid with a small amount of shredded tobacco leaves. The serum cholinesterase activities were 47-90 IU (normal range for male: 200-440 IU). GC and GC-MS analyses showed nicotine (21.8 mg), methomyl (304 mg), and triazolam (1.69 mg) in his stomach. He had consumed tobacco leaves, Lannate containing water soluble methomyl (45%), and Halcion tablets containing 0.25 mg triazolam. Methomyl concentrations in blood were 3-8 ng/ml. Substantial amounts of methomyl (2260-2680 ng/ml) were detected in cerebrospinal fluid and vitreous humor. Nicotine concentrations in blood ranged from 222 to 733 ng/ml. A small amount of triazolam was detected only in bile (176 ng/ml) and liver (23 ng/g). The cause of death was respiratory paralysis produced by the additive effects of methomyl and nicotine shortly after consumption.     

An unusual case of fatal accidental paraquat poisoning

Paraquat, a useful contact herbicide is now used in over 130 countries of the world, including Sri Lanka. The number of cases of accidental poisoning reported with paraquat is small, relative to instances of suicide. When a clear history is not available, accidental paraquat poisoning is sometimes difficult to diagnose. A 9-year-old boy was admitted to a peripheral hospital with a history of diarrhoea and vomiting. He later developed abdominal pain, subcutaneous emphysema and difficulty in breathing. Following transfer to a district hospital and then to a teaching hospital, poisoning with paraquat was suspected only on day 11 of the illness. On persistent questioning, on day 13 of the illness the child remembered that the day prior to the onset of illness, on his way from a shop, he felt thirsty and having found an empty bottle of Gramoxone (paraquat) on the wayside he used it to drink water from a water tank. The child died on day 17 and the histology of the lung showed typical changes of paraquat poisoning. This tragic episode emphasises the need for proper disposal of empty containers of all poisonous substances.