A fatal case of aconite poisoning: accidental intake of a monkshood extract

Purpose

Monkshood is a wild growing plant which contains the very toxic alkaloid aconitine, and is often used in traditional Chinese medicine. In this case report, we describe a fatal accident after the unintentional consumption of an aconite extract.

Method

By applying high-performance liquid chromatography–tandem mass spectrometry, the distribution of the alkaloid aconitine in body fluids and organ tissues has been determined, as well as the concentration of the extract taken from the confiscated bottle.

Results

The concentration of aconitine in peripheral blood of the deceased was 19 ng/mL; the highest concentration in organ tissue was found in the liver specimen, which revealed a content of 205 ng/g, followed by the kidneys, lungs, muscle and the brain. Moreover, aconitine contents of the blossoms, roots and leaves of a wild growing monkshood were determined. The plant extract itself showed a high concentration (628 mg/L) of the alkaloid.

Conclusion

The present case report emphasizes the danger of aconite extracts and presents results of the distribution of the alkaloid in the human body.

     

A case of fatal arsenic poisoning

We describe a case of poisoning by arsenic trioxide of a young man found dead at home. There were no obvious external signs of arsenic poisoning; but we observed marked endocardial hemorrhages, hepatomegaly, diffuse gastric mucosal hemorrhages, and slight brain edema at autopsy. The Reinsch test for the stomach contents and liver homogenate was positive for arsenic. Wavelength-dispersive X-ray fluorescence spectrometry combined with the Reinsch test showed that fatal levels of arsenic were present in blood and tissues. The cause of death was diagnosed as circulatory collapse caused by arsenic trioxide.     

A fatal case of amlodipine poisoning

A fatal overdose of amlodipine, a calcium channel blocker, in a 50-year-old man is described. Biological samples obtained at autopsy were screened for common drugs and narcotics. The amlodipine determination was made by HPLC with diode-array detection and a post-mortem blood concentration of 2.3 mg/kg was determined. The only other drug detected was a blood alcohol concentration of 0.008%. The presence of amlodipine was confirmed in other tissues and in the stomach content. The overdose is assumed to be an accumulation of amlodipine due to the long half-life of this drug.     

A fatal case of poisoning by lormetazepam

Lormetazepam is a benzodiazepine widely used as a hypnotic for management of insomnia. It is considered to be a safe drug when not combined with alcohol or other psychoactive substances. Indeed, we could neither fi nd its toxic nor lethal concentrations in the literature. In the present article, we report a fatal case in which lormetazepam and its metabolite lorazepam were the only drugs found in body fl uids. The concentration measured in blood was more than 100 times higher than the therapeutic one. Therefore, we concluded that the death was due to the drug and that the measured levels could be regarded as lethal.     

A case of fatal trichlorfon and methidathion poisoning

A 50-year-old man, suspected of ingesting organophosphorus insecticides, was found dead in a graveyard. In the gas chromatography-mass spectrometric screening, trichlorfon and methidathion were detected in his gastric contents. The quantitative analysis for trichlorfon and methidathion was carried out by high-performance liquid chromatography. The concentrations (microg/ml or microg/g) of trichlorfon and methidathion were 409 and 1.9 in the heart blood, 281 and 0.4 in the femoral vein blood, 430 and 5.8 in the cerebrum, 385 and 5.1 in the brain stem, 256 and 2.8 in the right apex of lung, 449 and 15.1 in the left basal of lung, 856 and 131.0 in the liver, 460 and 1.6 in the right kidney, 390 and 1.9 in the left kidney, 524 and 3.4 in the spleen, 152 and 0.6 in the thigh muscle, 207 and 0.9 in the urine, 20,000 and 19,400 in the gastric contents, respectively. According to the autopsy finding and toxicological analysis, the cause of death was judged to be acute trichlorfon and methidathion poisoning.     

A fatal case of MAM-2201 poisoning

A 59-year-old man was found dead in his house, where three sachets containing herbal blends were found on a table. The sachet contents were analyzed by gas chromatography–mass spectrometry and found to contain [1-(5-fluoropentyl)-1H-indol-3-yl](4-methyl-1-naphthalenyl)methanone (MAM-2201). The deceased was subjected to forensic autopsy. There were neither external injuries nor endogenous diseases judged by macroscopic and microscopic observations. Liquid chromatography–electrospray ionization–tandem mass spectrometry was used to quantitate the concentrations of MAM-2201 in postmortem samples using deuterated MAM-2201 as internal standard. The MAM-2201 concentrations were: 12.4 ng/ml in whole blood; 18.1 ng/g in the liver; 11.2 ng/g in the kidney; 4.3 ng/g in the brain; and 1,535 ng/g in the adipose tissue. We concluded that the man’s death was caused by acute intoxication with MAM-2201. In addition, we propose that the adipose tissue is the specimen of choice to detect MAM-2201 in the unchanged form. To our knowledge, this is the first report of a fatal MAM-2201 poisoning case. In addition, this report is also the first to describe the distribution of the drug in postmortem human tissues and blood.     

A case of fatal benzalkonium chloride poisoning

Five elderly persons with senile dementia accidentally ingested Hoesmin, a 10% aqueous solution of benzalkonium chloride (BAC). The condition of one patient, an 84-year-old woman whose lips and oral cavity became erythematous, gradually deteriorated. Although gastric lavage was performed, the patient died 3 h after ingestion of Hoesmin. Autopsy revealed corrosive changes of the mucosal surfaces of the tongue, pharynx, larynx, esophagus and stomach which may have come in contact with BAC. In addition, BAC was detected in the serum. We conclude that the patient died of BAC poisoning. Fatal BAC poisoning is rare and autopsy findings in only a few cases of BAC poisoning have been reported. Our findings emphasize the risk of oral ingestion of BAC. Received: 11 August 1997 / Received in revised form: 10 December 1997     

A fatal poisoning case of acetone cyanohydrin and citalopram

Acetone cyanohydrin (ACH) is a readily available source of cyanide and is widely used in basic and applied sciences. In toxicology, ACH is classified as extremely hazardous as it readily decomposes on contact with water, with the potential rapid release of highly toxic hydrogen cyanide (HCN). We report the case of a young woman found dead from the intentional ingestion of ACH and citalopram, an antidepressant of the selective serotonin reuptake inhibitor class. The autopsy findings included bright reddish-purple hypostasis and mild pulmonary edema. As ACH can decompose to acetone and HCN, we quantified the concentration of each compound and thiocyanate separately in various body fluids and organs and determined their whole-body distributions by using gas chromatography–mass spectrometry (GC–MS). We observed high concentrations of both acetone and cyanide in the blood (0.63 mg/mL and 17.99 mM, respectively) and gastric contents (9.76 mg/mL and 472.44 mM). The whole-body distributions of acetone and cyanide were similar (i.e., the concentration of each compound was the highest in the lung, followed by the heart, and then the liver). Our results suggest that not only the route of administration but also the dose taken could greatly affect the body distributions of cyanide in humans. In addition, as toxicological screening detected citalopram, which was not prescribed to the deceased, we performed a chiral analysis by using liquid chromatography–tandem mass spectrometry (LC–MS/MS). We determined that only (S)-citalopram was ingested antemortem; its concentration was 0.36 μg/mL, which is in the toxic range.     

A fatal case of acetamiprid poisoning with turquoise urine

Acetamiprid is a member of neonicotinoid insecticides with a low risk of toxicity in humans. However, ingestion of large amounts may cause severe poisoning. This is the first case reported in the literature in which severe toxicity and death occurred after acetamiprid ingestion. A 57-year-old male patient consumed 50g/250mL of an insecticide formulation containing acetamiprid for suicidal purposes. The ambulance team performed cardiopulmonary resuscitation on the patient who had a cardiac arrest. His heart beat returned after a 15-min cardiopulmonary resuscitation, and afterward, he had tachycardia, hypotension, respiratory failure, high gap metabolic acidosis with a high lactate, hypokalemia, hypocalcemia, mydriasis, and coma. The patient underwent supportive treatment for a variety of symptoms. However, he died despite all supportive treatment. This case demonstrates that ingestion of large amounts of the acetamiprid and late presentation can be fatal despite all supportive care.     

A fatal case of n-butane poisoning after inhaling anti-perspiration aerosol deodorant

We report a case of sudden death due to n-butane poisoning after the inhalation of anti-perspiration aerosol deodorant. The deceased was a 15-year-old boy who was found unresponsive on the road, and was pronounced dead after 1.25h. A spray can of anti-perspiration deodorant and vinyl bags were found in a thicket near the scene. An autopsy revealed pulmonary edema, cerebral edema and congestion of the organs. Using qualitative gas chromatography/mass spectrometry, the existence of n-butane was ascertained. The concentration of n-butane (in microl/ml or microl/g) was estimated to be 15.3 in the blood, 13.3 in the brain, 26.6 in the liver, 7.5 in the lung, and 13.6 in the kidney. These n-butane levels in the blood and in the tissues were higher than those of previous reports of death associated with n-butane inhalation. We concluded that the cause of death was n-butane poisoning and presumed that n-butane in the can of anti-perspiration aerosol deodorant induced fatal cardiac arrhythmia.     

A curious autopsy case of accidental carbon monoxide poisoning in a motor vehicle

A 26-year-old man was found dead in his car. All doors and windows were locked inside. The ignition key was in the "on" position; but the engine was not running and the fuel tank was empty. His post-mortem lividity was cherry-pink, and marked congestion was observed in the lungs and brain macroscopically. Massive intracardiac blood containing a small amount of cruor was found in the heart. In histological examination of the heart, partial disarrangement or necrosis was found in the myocardium. The liver cells showed derangement and degenerative changes, with focal lymphocyte infiltration in the portal regions, although they were not severe. The chemical tests showed that the blood concentration of carboxyhemoglobin was 46.6%. Stimulants were also detected from his blood and urine; the concentrations of methamphetamine and amphetamine were 3.25 and 0.84 microg/ml, respectively, for his cardiac blood. Therefore, it seemed reasonable to judge that the cause of his death was carbon monoxide poisoning; the cardiomyopathy and the presence of stimulants in blood might facilitate his death. Upon careful investigation of his car, it was disclosed that exhaust gas, leaked from small holes of the exhaust pipe due to rust-through, invaded the interior through four holes on the floor of the car during parking with the engine being on for the purpose of air-conditioning of the interior. It is very common to commit suicide by introducing exhaust gas into an interior of a closed motor car, but the present accidental case of carbon monoxide poisoning in a car seems rare and worthwhile reporting.     

A fatal case of poisoning by fenitrothion without evidence of chemical exposure

We describe a mysterious fatal case of poisoning by fenitrothion of a male adult. No typical external signs of organophosphate poisoning were found; we observed patchy mucosal hemorrhages of the bronchi and slight parenchymal hemorrhages of the lower lobe of the left lung at autopsy. The stomach contained 10 g of a faintly purplish/reddish viscous fluid with no chemical smell. Gas chromatography and gas chromatography-mass spectrometry analyses of blood specimens revealed substantial amounts of fenitrothion. The concentrations in cerebrospinal fluid, vitreous humor, and urine are also presented. We concluded that the victim probably died of delayed respiratory insufficiency caused by acute fenitrothion poisoning.     

A fatal case of poisoning by lidocaine overdosage--analysis of lidocaine in formalin-fixed tissues: a case report

The death of a 76-year-old man with heart disease as a result of the injection of an excessive dose of lidocaine is presented. The patient was given 5 ml of 10% lidocaine hydrochloride (500 mg) intravenously instead of 2.5 ml of 2% lidocaine hydrochloride (50mg) in order to treat repeated paroxysmal ventricular arrhythmia. Immediately following the injection the patient had tonic clonic seizures and complete cardiopulmonary arrest followed. Although resuscitation attempts once successfully restarted his pulse and spontaneous respiration, the patient died on the eighth day after the injection. Toxicological examinations were carried out on the tissues obtained at the time of autopsy and which had been fixed in formalin solution for 40 days, and lidocaine was detected in each tissue examined. The concentrations were (ng/g or ml): parietal lobe, 308.0; occipital lobe, 208.7; temporal lobe, 318.0; frontal lobe, 223.2; cerebellum 200.9; pons 285.7; liver, 109.5; kidney 52.2; skeletal muscle 127.0; and formalin solution 8.4. In an experiment on rats we determined the concentration changes of lidocaine in formalin fixed tissues. The concentrations of lidocaine in these tissues significantly decreased to 1/3-1/4 from the original. This data shows that the cause of death was poisoning by lidocaine overdose.