Fatal hepatic failure following accidental tramadol overdose

A case of fatal overdose of tramadol is described, occurring in a 67-year-old man with painful rib fractures who accidentally ingested more than the recommended daily dose. The mode of death was acute liver failure due to fulminant hepatic necrosis. Post-mortem toxicology was negative apart from revealing a blood tramadol concentration well above the normal therapeutic range. This is the first report of fatal tramadol ingestion occurring in a therapeutic setting and also the first tramadol-related death where the mechanism was liver failure.     

Fatal poisoning by vanadium

We report here a fatal intoxication case involving ammonium vanadate. A 24-year-old woman was admitted to the Emergency Department for abdominal pain, nausea, vomiting, multiple daily diarrheas, hypoglycaemia (0.2g/L) and severe acute renal failure with glomerular filtration rate estimated at 21 ml/min. This patient had taken an undetermined amount of ammonium vanadate 12h after ingesting. She died next morning in the context of respiratory distress despite intensive care and oxygen therapy. The autopsy revealed widespread asphyxia syndrome and erosive gastritis. Determination of vanadium concentration in blood was carried out by means of mass spectrometer (ICP-MS) using rhodium ((103)Rh) as the internal standard. The vanadium concentration was 6.22 mg/L, corresponding to 6000 times higher than normal concentration in the general population. The latency and the brutality of clinical picture degradation seem to be in consideration of systemic poisoning by vanadium leading to inhibition of the cellular respiratory process.     

Fatal and nonfatal poisoning by hydrogen sulfide at an industrial waste site

An adult man (A) entered a pit to collect seepage at an industrial waste site in Japan. As he suddenly lost consciousness, three colleagues (B, C, D) entered the pit to rescue him. All of these men lost consciousness in the pit. Two workers (A and B) died soon after the accident, one worker (C) died 22 days after the accident, and one worker (D) survived. Since hydrogen sulfide gas was detected in the atmosphere of the pit, gas poisoning was suspected. Toxicological analyses of sulfide and thiosulfate, a metabolite of sulfide, in blood and urine of the victims were made using the extractive alkylation technique combined with gas chromatography/mass spectrometry (GC/MS). Sulfide was detected in the blood of A and B at levels of 0.13 and 0.11 mg/L, respectively, somewhat higher than in healthy persons. Thiosulfate was detected in whole blood of deceased victims A and B, in the plasma of deceased victim C, at concentrations of 10.53, 4.59, and 4.14 mg/L, respectively. These values were similar to those found in fatal cases of hydrogen sulfide poisoning. Thiosulfate was not detected in the plasma of survivor D. With respect to urine samples, thiosulfate was the highest in the non-acute death victim C (137.20 mg/L), followed by that in the survivor D (29.34 mg/L), and low (0.90 mg/L) and not detected in the acute death victims, A and B, respectively. Based on these results, all four patients were victims of hydrogen sulfide poisoning. The concentrations of thiosulfate in blood and urine were more useful than that for sulfide for determining hydrogen sulfide poisoning. Thiosulfate in urine was the only indicator of hydrogen sulfide poisoning in the non-fatal victim.     

Fatal overdose of zopiclone in an elderly woman with bronchogenic carcinoma

The death of a 72-year-old woman with respiratory debilitation due to bronchogenic carcinoma is described. She overdosed herself with probably 200 to 350 mg of zopiclone. Zopiclone, quantitated by HPLC in femoral postmortem blood, was found to be 1.9 mg/L (4.8 micromol/L). This level is higher than many other zopiclone fatalities reported. We report a case where only zopiclone was detected.     

Fatal poisoning by 1,1,1-trichloroethane after prolonged survival

A fatal case of 1,1,1-trichloroethane (methyl chloroform) poisoning, in which the patient survived, without recovering consciousness, for more than 3 years, is described. The brain showed symmetrical infarction of the lenticular nuclei and of the occipital cortex, changes which may have been the cause of neurological manifestations during life. The pattern of cerebral hypoxia was similar to, but not identical with that found in carbon monoxide poisoning, and might be specific for 1,1,1-trichloroethane poisoning.     

Fatal colchicine poisoning by accidental ingestion of meadow saffron-case report

A 62-year-old male died of colchicine poisoning after accidental ingestion of Colchicum autumnale (meadow saffron). He ate a salad of plant with green leaves regarded as wild garlic (Allium ursinum). A few hours later he developed symptoms of gastroenteritis and was admitted to hospital. In spite of gastric lavage, activated charcoal and supportive measures, multi-organ system failure developed over the next two days. Laboratory analysis showed highly elevated blood concentrations of hepatic enzymes, creatine kinase, lactate dehydrogenase and blood urea nitrogen, as well as leukocytopenia and thrombocytopenia. Mechanical ventilation, dopamine, noradrenaline, crystalloid solutions and fresh frozen plasma were applied but despite treatment the patient died five days after the ingestion. Post-mortem examination revealed hepatic centrilobular necrosis, nephrotoxic acute tubular necrosis, petechial bleeding in fatty tissue, blunt and shortened intestinal villi and cerebral toxic edema. Botanical identification of incriminated plant gave Colchicum autumnale which confirmed colchicine poisoning. Although the accidental ingestion of Colchicum autumnale is rare and to our knowledge only five such cases have been described in detail, this is the second fatal case in Croatia described in the last 3 years.     

Death following acute poisoning by moclobemide

A fatality due to ingestion of a reversible inhibitor of monoamine-oxidase A (MAO-A) is reported. Moclobemide is generally considered as a safe drug far less toxic than tricyclic anti-depressants. However, severe intoxications may result from interactions with other drugs and food such as selective serotonin reuptake inhibitors (SSRIs), anti-Parkinsonians of the MAOI-type (e.g. selegiline) or tyramine from ripe cheese or other sources. In the present case, high levels of moclobemide were measured in peripheral blood exceeding toxic values reported so far in the scientific literature. The body fluid concentrations of moclobemide were of 498 mg/l in peripheral whole blood, 96.3 mg/l in urine while an amount of approximately 33 g could be recovered from gastric contents. The other xenobiotics were considered of little toxicological relevance. The victim (male, 48-year-old) had a past history of depression and committed one suicide attempt 2 years before death. Autopsy revealed no evidence of significant natural disease or injury. It was concluded that the manner of death was suicide and that the unique cause of death was massive ingestion of moclobemide.     

Fatal outcome of poisoning with the benzodiazepines flunitrazepam and diazepam

On a wintry day a 29-year-old woman was found dead beside her car showing head injuries and signs of hypothermia. Several empty packets of sedative and hypnotic drugs were lying inside the car. Toxicological analysis revealed the presence of flunitrazepam (heart blood of the left and right chamber 0.033 mg/L each), norflunitrazepam (left heart blood 0.029 mg/L, right heart blood 0.027 mg/L), 7-amino-flunitrazepam (left heart blood 0.090 mg/L, right heart blood 0.104 mg/L), diazepam (left heart blood 0.395 mg/L, right heart blood 0.386 mg/L), nordazepam (left heart blood 0.112 mg/L, right heart blood 0.115 mg/L) and temazepam (left heart blood 0.034 mg/L, right heart blood 0.033 mg/L). Neither alcohol nor other drugs were found. It was concluded that benzodiazepine intake led to a disturbance of consciousness. Whether the woman died in this situation due to the icy temperature as a result of hypothermia or whether she died or would have died solely due to benzodiazepine overdosage could not be clarified.     

Fatal brodifacoum rodenticide poisoning: autopsy and toxicologic findings.

This report details the pathologic and toxicologic findings in the case of a 15-year-old girl who deliberately and fatally ingested brodifacoum, a commonly used rodenticide. The mechanism of death, massive pulmonary hemorrhage, has not been previously reported. Brodifacoum was quantitated in liver, spleen, lung, brain, bile, vitreous humor, heart blood, and femoral blood using HPLC with fluorescence detection. The highest brodifacoum concentrations were detected in bile (4276 ng/mL) and femoral blood (3919 ng/mL). No brodifacoum was detected in brain or vitreous humor. A brodifacoum concentration of 50 ng/g was observed in frozen liver while formalin fixed liver exhibited a concentration of 820 ng/g. A very high blood:liver brodifacoum concentration ratio suggested acute poisoning but the historical and pathologic findings suggested a longer period of anticoagulation. Though most cases of brodifacoum poisoning in humans are non-fatal, this compound can be deadly because of its very long half-life. Forensic pathologists and toxicologists should suspect superwarfarin rodenticides when confronted with cases of unexplained bleeding. Anticoagulant poisoning can mimic fatal leukemia or infectious diseases such as bacterial sepsis, rickettsioses, plague, and leptospirosis. A thorough death scene investigation may provide clues that a person has ingested these substances.     

Fatal tolperisone poisoning: autopsy and toxicology findings in three suicide cases

Tolperisone (Mydocalm) is a centrally acting muscle relaxant with few sedative side effects that is used for the treatment of chronic pain conditions. We describe three cases of suicidal tolperisone poisoning in three healthy young subjects in the years 2006, 2008 and 2009. In all cases, macroscopic and microscopic autopsy findings did not reveal the cause of death. Systematic toxicological analysis (STA) including immunological tests, screening for volatile substances and blood, urine and gastric content screening by GC-MS and HPLC-DAD demonstrated the presence of tolperisone in all cases. In addition to tolperisone, only the analgesics paracetamol (acetaminophen), ibuprofen and naproxen could be detected. The blood ethanol concentrations were all lower than 0.10 g/kg. Tolperisone was extracted by liquid-liquid extraction using n-chlorobutane as the extraction solvent. The quantification was performed by GC-NPD analysis of blood, urine and gastric content. Tolperisone concentrations of 7.0 mg/l, 14 mg/l and 19 mg/l were found in the blood of the deceased. In the absence of other autopsy findings, the deaths in these three cases were finally explained as a result of lethal tolperisone ingestion. To the best of our knowledge, these three cases are the first reported cases of suicidal tolperisone poisonings.     

Fatal poisoning from Nicotiana glauca leaves: identification of anabasine by gas-chromatography/mass spectrometry

Death of a worker occurred after ingestion of unknown amounts of Nicotiana glauca G leaves. The leaves were cooked after having been mistakenly considered to be spices of a type which grow in Thailand. After ingestion, two Thai workers collapsed, one with asystolia. Resuscitation efforts were successful only for one of the victims. A GC/MS method was used for the identification of anabasine as the main constituent in the leaves, food extract, blood, and the urine of the deceased. Lacking a standard, it was necessary to interpret the GC/MS spectrum to identify anabasine and establish its presence.     

Fatal cranial injuries caused by an electric angle grinder

A case of fatal cranial injuries caused by an angle grinder is reported. The scalp lesions were typical of those produced by a cutting disk in a side-slipping movement. On the cranial vault were two bony losses of substance, one of which was deep enough for intracranial penetration of the disk. Signs of deflection of the disk, identical to those found on the scalp, were observed on the external bony table. Because of the circumstances in which the victim was discovered, in particular the damage to the machine which had a broken handle, and the lack of any indication of homicide or suicide, an accident is the most likely hypothesis.     

Fatal carbon monoxide poisoning after the detonation of explosives in an underground mine: a case report.

An unusual death caused by carbon monoxide poisoning after the detonation of explosives in an underground mine was investigated by the Office of the Medical Investigator of the State of New Mexico. The 50-year-old miner had 18 years of mining experience but no documented safety training. He collapsed approximately 20 minutes after entering the mine and working at the bottom of the single vertical shaft. The tight confines of the mine shaft hindered rescue personnel from reaching him, and the body was not recovered until 2 days later. The autopsy showed severe coronary artery atherosclerosis with remote and resolving myocardial microinfarcts, as well as the characteristic pink lividity of carbon monoxide poisoning, which was confirmed by laboratory analysis. Detailed investigation of the scene revealed no sources of carbon monoxide other than the explosives. The case represents an uncommon cause of death in mining that may have been avoided through the use of proper safety procedures, and illustrates the importance of recognizing the many sources of carbon monoxide.     

Fatal thoracic compression after being partially run over by an automobile

The authors report on a fatal pedestrian accident in which the victim lay on the street and got under a car being run over by one of the front wheels. Both the car driver and the killed pedestrian were strongly alcohol-intoxicated at the time of the accident (2.45 a.m.). After the car had come to a standstill, the pedestrian remained trapped under the car until she was rescued by the fire brigade. On the basis of the autopsy findings and the technical expert opinion it could be reconstructed that the pedestrian's death was not caused by the consequences of being run over by the car, but by the subsequent compression of her thorax in the final accident position.     

Fatal Datura poisoning: identification of atropine and scopolamine by high performance liquid chromatography/photodiode array/mass spectrometry

A forensic method comprising solid phase extraction and HPLC analysis was developed for the detection and confirmation of atropine and scopolamine, the main toxic alkaloids of Datura stramonium and Datura ferox. This method allowed the direct coupling of an electrospray (ZMD) mass selective detector to the HPLC system. Under these conditions, atropine and scopolamine were well separated from other components and detected on the PDA (LOD = 1 microg/ml) and ZMD (LOD(atropine) = 10 pg/ml; LOD(scopolamine) = 100 pg/ml) detectors. Four geographically isolated populations of each of D. stramonium and D. ferox were analysed for seed alkaloids and it was found that the two species were diagnostically different in their atropine-scopolamine ratios. The optimised HPLC method was used to analyse three viscera samples of an adult Caucasian male whose death was ascribed to a fatal heart attack. Atropine and scopolamine were detected in the stomach and its contents, which contained Datura seeds. The chemical profile of the seeds found in the stomach contents was similar to those from four geographically different D. ferox plants.     

Diagnosis of carbon monoxide poisoning following embalming and exhumation

Clots of blood, which were found in the cardiac ventricles at an autopsy of an embalmed corpse, were to analyse for carbon monoxide. It was not possible to determine reliably the CO-Hb-content of the blood clots with the known methods. Therefore a new procedure was developed. Carbon monoxide was released by a solution of nitric acid and determined gas chromatographically by a headspace method. In the same vessel the iron-content of the sample was measured after decomposition with atomic absorption spectrometry. This procedure is especially suitable for samples like putrid or heat-clotted blood.     

Tissue distribution of tramadol and metabolites in an overdose fatality

Tramadol (Ultram) is a centrally acting, synthetic analgesic agent. Although it has some affinity for the opiate receptors, tramadol is believed to exert its analgesic effect by inhibiting the re-uptake of norepinephrine and serotonin. There are several published cases of tramadol's involvement in drug-related deaths and impairment. Reports of deaths involving tramadol alone with associated tissue concentrations are rare. This report documents a case in which tramadol overdose was identified as the cause of death. The following tramadol concentrations were found in various tissues: blood, 20 mg/L; urine, 110.2 mg/L; liver, 68.9 mg/kg; and kidney, 37.5 mg/kg. Tissue distributions of the two primary metabolites, N-desmethyl and O-desmethyl tramadol, are also reported. In each tissue or fluid except urine, the tramadol concentration was greater than either metabolite, consistent with other reports of drug-impaired drivers and postmortem cases. The O-desmethyl metabolite concentration was greater than the N-desmethyl metabolite concentration in all tissues; this is in contrast to other postmortem reports, in which the majority of cases report concentrations of O-desmethyl as less than those of N-desmethyl. This may be useful as an indicator of time lapse between ingestion and death.     

Fatal splenic rupture following Heimlich maneuver: case report and literature review

The most effective resuscitative procedure in choking by foreign bodies is the Heimlich maneuver, described for the first time by Henry Heimlich (1974) and recognized by the US Surgeon General (1985) as the "only method that should be used for the treatment of choking from foreign body airway obstruction." If performed correctly, this lifesaving maneuver is associated with rare complications, of which the most frequent are rib fractures and gastric or esophagus perforations. Other rare traumatic injuries such as pneumomediastinum, aortic valve cusp rupture, diaphragmatic herniation, jejunum perforation, hepatic rupture, or mesenteric laceration have been described.However, we are unaware of previous reports of splenic rupture after Heimlich maneuver. We present an interesting case of fatal hemoperitoneum due to a hilar laceration of the spleen following a correctly performed Heimlich maneuver.     

Fatal and non-fatal injuries caused by crossbows

Today in modern times, traumatic injuries caused by crossbows are a rarity. The largest collection of cases so far is presented in this study, consisting of four fatalities (two homicides and two suicides) and two non-fatal injuries (grievous bodily harm and an accident). All the victims were male having an age between 31 and 54. The weapons, which were used, were mainly high-performance precision crossbows with telescopic sights and hunting bolts. The parts of the body involved were the facial/head area in three of the cases and the thorax in three of them. There were either deep or total penetration injuries to the cranium and thorax with the bolt remaining in the wound in four out of six cases. The persons with non-fatal crossbow injuries exhibited comparatively few symptoms, despite the sometimes extensive involvement of the interior of the cranium (cerebrocranial penetration, in one instance). The two cases of suicide favoured the body areas often found with gun-users. The aetiological classification of crossbow injuries may be difficult after the removal of the bolt. The external morphology is strongly dependent on the type of tip used. Multiple-bladed hunting broadheads produce radiating incised wounds, whereas conical field tips produce circular to slitlike defects. Correspondingly, the external injuries can be reminiscent of the effects of a violent attack by sharp force or of a gunshot wound. The possibility, supported by clinical data, that the victim might have the ability to act or even to survive for a period of time, even with penetration of the brain, should be taken into account when the cause of death is being investigated.     

Fatal combined anileridine-pethidine poisoning. A gas chromatography, thin layer chromatography and mass spectrometry investigation.

Anileridine and pethidine were established by gas and thin layer chromatography and mass spectroscopy. In the mass spectrum the main peak of anileridine is found at m/e 246 and that of pethidine at m/e 71. The determination was made by gas chromatography from the blood, urine, liver, muscle and stomach contents.