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.     

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 case of parenteral paraquat poisoning.

The chief clinical and analytical aspects of the suicide of a 21-year-old male with psychiatric problems by parenteral administration of a 200 g/l aqueous solution of paraquat are described. Paraquat levels were determined in plasma, urine, kidney, liver and lung after autopsy. Tissue damage was studied by electron microscopy. The death ensued from pulmonary dysfunction 15 days after hospital admission.     

A case of fatal rotenone poisoning in a child

A case of a fatal rotenone poisoning in a three-and-a-half-year-old girl is described. The case report and autopsy findings are mentioned. For the extraction of rotenone out of biological samples, a solvent partitioning and silica gel open column chromatographic cleanup procedure has been used. The determination of rotenone was performed by high pressure liquid chromatography.     

A case of fatal aconitine poisoning by Monkshood ingestion

Accidental aconitine poisoning is extremely rare in North America. This report describes the confirmation of a case of accidental aconitine poisoning using a liquid chromatography-tandem mass spectrometry (LC-MS/MS) method. The case involved a 25-year-old man who died suddenly following a recreational outing with friends where he consumed a number of wild berries and plants including one that was later identified as Monkshood (Aconitum napellus). Postmortem blood and urine samples were available for analysis. All routine urine and blood toxicology screens were negative. The LC-MS/MS method allowed sensitive quantification of aconitine, the main toxin in A. napellus, and showed 3.6 and 149 microg/L in blood and urine, respectively. These concentrations were similar to that reported in other aconitine-related deaths. This case illustrates the dangers of consuming unidentified plants, and documents concentrations of aconitine in blood and urine in a fatal case of A. napallus-related poisoning.     

A fatal case of cocaine poisoning in a body packer

A 27-year-old man was carrying in his digestive tract 99 packages each containing about 10 g of a 86% cocaine powder. The courier died by acute cocaine intoxication due to inflation and rupture of four packages during a flight from Bogotá to Rome. At the autopsy, the external examination was unremarkable. The internal examination showed edema and generalized congestion of the organs. Toxicological analyses were performed by gas chromatography-mass spectrometry after solid phase extraction using Bond Elut Certify columns and derivatization with BSTFA/TMCS. High levels of cocaine and benzoylecgonine were found in blood (4.0 microg/mL and 17.0 microg/mL), urine (152.0 microg/mL and 512.0 microg/mL), bile (99.8 microg/mL and 54.0 microg/mL), vitreous humor (7.1 microg/mL and 5.8 microg/mL), brain (7.5 microg/mL and 3.5 microg/mL), and hair (55.5 ng/mg and 27.7 ng/mg). The presence of the cocaine and its metabolite in the hair suggested that the man was a cocaine user.     

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.     

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.     

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 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 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.     

Chlorobutanol poisoning. Report of a fatal case.

A fatal chlorobutanol intoxication is reported and a gas chromatographic method for the determination of this drug in human fluids and tissues is described. Analytical findings for blood, urine, stomach contents, bile, liver, kidney, spleen, and brain are reported.     

A rare fatal case of wood preservative,monochloro-naphthalene (MCN), poisoning

A rare case of poisoning by the wood preservative Xylamon^® TH-Clear (active ingredient: 60% 1-chloronaphthalene) is reported.A mentally disordered carpenter, 44 years old, ingested an unknown amount of Xylamon^® and died in about 2 hours. Analysis for 1-chloronaphthalene was performed by TLC, IR and GC methods. GC analysis for 1-chloronaphthalene showed the concentration in the peripheral blood to be 2.46 μg/ml and the bile concentration to be 75.5 μg/ml. The total amount in the stomach contents was 27.7 g.     

An unusual case of accidental poisoning: fatal methadone inhalation

In this report, the authors present a case of unusual, accidental methadone intoxication in a 40-year-old man, who had inhaled methadone powder. The drug dealer was a pharmacy technician; methadone had been stolen from a pharmacy and sold as cocaine. After having inhaled methadone powder, he suffered cardiopulmonary arrest. He was admitted to hospital where he died after 24 h of intensive care. The autopsy revealed congestion of internal organs and cerebral and pulmonary edema. Microscopically, the heart showed no changes. The toxicological analyses performed on blood and urine taken at the hospital revealed methadone, cannabinoids, and ethanol. The blood methadone concentration was 290 μg/L. The urine methadone concentration was 160 μg/L. Midazolam and lidocaine, which were administered to the patient at the hospital, were also detected in the blood. The cause of death was determined to be methadone intoxication. The literature has been reviewed and discussed. To date, and to our knowledge, only very few cases of accidental death resulting from methadone inhalation have been described up to the case presented herein.     

A fatal case of chlorate poisoning: confirmation by ion chromatography of body fluids

A 49-year-old male chemical industry worker was admitted to intensive care with a 24-hour history of respiratory failure, vomiting, headache, stupor, arterial hypotension, and cyanosed face and limbs. He had acute haemolysis (3.9 g/L plasma haemoglobin concentration) and 30% methaemoglobinaemia. Whereas the search for alcohol, barbiturates and opiates was negative, benzodiazepines and tricyclic antidepressants were present. The patient was in fact being treated with fluvoxamine, amitryptiline, and alprazolam. As the clinical and biological signs suggested chlorate poisoning, chlorate was looked for by using an aniline color reaction. It was found in gastric content and urine. Treatment consisted in mechanical ventilation, vasoactive amines, methylene blue, plasma exchange, exchange transfusion, and haemodialysis. Despite this, the patient had several cardiac arrests and refractory metabolic acidosis. He died 12 h after his admission. Specific ion chromatography was used afterhand to assay the chlorate in various body fluids. The technique was based on a separation on an ion exchange Dionex AS 12A column coupled with conductivity detection. A quantitative estimation was carried out by using external calibration with a four-point calibration curve which was linear between 1 and 15 mg/L. The measured plasma levels of chlorate were 78 and 29 mg/L respectively before and after exchange transfusion. Gastric-lavage liquid contained 1300 mg/L of chlorate and urine 4300 mg/L. Ion chromatography, which is routinely used in environmental studies helped to confirm a massive oral intake of chlorate by measuring the corresponding blood and urine chlorate concentrations, data which had only rarely been reported previously.     

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 rare fatal case of silicone resin precursor (SH792) poisoning.

A 39-year-old man committed suicide by ingesting a large quantity of SH792. SH792 is a silicone resin precursor used as a hardener for waterproof paints. It is polymerized in water; this process is then followed by the formation of silicone resin and the release of N,N-diethylhydroxylamine. In this decedent, analysis by infrared spectroscopy showed that polymerized silicone resin was present in the stomach contents. The amount of silica in his tissues was within levels seen in control subjects. N,N-diethylhydroxylamine was detected in the urine (0.7 microliters/ml) but not in the stomach contents. The data suggest that SH792 was polymerized in the stomach and the released N,N-diethylhydroxylamine (DEHA) was absorbed into the body. The mechanism of SH792 poisoning is also discussed.     

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.