Fatal overdose of tramadol and alprazolam

A 30-year-old woman, with history of depression, was found dead after the ingestion of an unknown quantity of Xanax (alprazolam), Tramal (tramadol) and alcohol. At the autopsy only a slight decomposition and a diffuse visceral congestion were noticed. Biological samples obtained at autopsy were analysed to detect the presence of alprazolam, tramadol and alcohol. Blood concentrations of alprazolam, alcohol and tramadol were 0.21 mg/l, 1.29 g/kg and 38.3 mg/l, respectively.     

Fatal overdose of the herbicide bentazone

A 59-year-old woman who intentionally ingested 100-200 ml Basagran was taken to the hospital with a cardiac arrest 2 days after she had consumed the herbicide. During this period she suffered vomiting, urination and diarrhoea and she was drowsy with a muddled speech. Biological samples obtained at the autopsy were analysed and presence of bentazone, alcohol and an active metabolite of citalopram were detected. Blood concentrations of bentazone, alcohol and desmethyl-citalopram were 625 mg/kg, 0.62 g/l and 0.03 mg/kg, respectively.     

Fatal cyclobenzaprine overdose with postmortem values

There are only two published cases of overdose with postmortem blood cyclobenzaprine concentrations, both with confounding factors. We report two additional cases of fatal cyclobenzaprine overdose with postmortem values. Case 1: a 56-year-old female was found in full cardiopulmonary arrest after a verbal suicide threat to a friend. Postmortem blood concentrations were cyclobenzaprine 0.96 mg/L and diazepam 0.3 mg/L. Case 2: a 37-year-old male was found in full arrest by a family member after an intentional ingestion of cyclobenzaprine. Postmortem blood concentrations were cyclobenzaprine 0.8 mg/L and ethanol 0.174 gm/dL. The concentrations of diazepam and ethanol reported in these two patients were not found in quantities usually associated with a fatal outcome, suggesting that the cyclobenzaprine was the primary cause of the fatality. Additionally, the blood was drawn from a femoral site, so that postmortem redistribution is not a likely factor. Blood concentration of > or = 0.8 mg/L cyclobenzaprine may be associated with a fatal outcome.     

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 intravenous drug abuse secondary to streptomycin overdose

A fatal case of chronic intravenous drug abuse involving the injection of a nonpsychoactive veterinary combination of penicillin G and streptomycin is reported. The circumstances surrounding the death indicate that the decedent died as a result of streptomycin induced paralytic neuromuscular blockade.     

Fatal venlafaxine overdose with acinar zone 3 liver cell necrosis

We present a case of fatal venlafaxine overdose in a 34-year-old male with a history of depression and previous suicide attempts. He presented unwell, and his condition deteriorated with the development of rhabdomyocytolysis and renal failure. Although treatment was provided, this was unsuccessful, and he died within a day of his admission. A postmortem examination was performed, and the findings included an acinar zone 3 pattern of liver cell necrosis and a very high level of serum venlafaxine in the deceased. No other elevated drug levels were detected. From this case, it is clear that venlafaxine overdose was the primary cause of a fatal acinar zone 3 pattern of liver cell necrosis. As far as we are aware, this is the first reported case of fatal acinar zone 3 liver necrosis caused by venlafaxine overdose alone.     

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.     

Fatal versus non-fatal heroin "overdose": blood morphine concentrations with fatal outcome in comparison to those of intoxicated drivers

The study was performed to distinguish fatal from non-fatal blood concentrations of morphine. For this purpose, blood levels of free morphine and total morphine (free morphine plus morphine conjugates) in 207 cases of heroin-related deaths were compared to those in 27 drivers surviving opiate intoxication. The majority of both survivors and non-survivors were found to show a concomitant use of depressants including alcohol or stimulants. Blood morphine levels in both groups varied widely, with a large area of overlap between survivors (free morphine: 0-128 ng/ml, total morphine: 10-2,110 ng/ml) and non-survivors (free morphine: 0-2,800 ng/ml, total morphine: 33-5,000 ng/ml). Five (18.5%) survivors and 87 (42.0%) non-survivors exhibit intoxication only by morphine. In these cases, too, both groups overlapped (survivors-free morphine: 28-93 ng/ml, total morphine: 230-1,451 ng/ml; non-survivors-free morphine: 0-2,800 ng/ml, total morphine: 119-4,660 ng/ml). Although the blood levels of free or total morphine do not allow a reliable prediction of survival versus non-survival, the ratio of free/total morphine may be a criterion to distinguish lethal versus survived intoxication. The mean of the ratio of free to total morphine for all lethal cases (N=207) was 0.293, for those that survived (N=27) 0.135, in cases of intoxication only by morphine 0.250 (N=87) and 0.080 (N=5), respectively. Applying a cut-off of 0.12 for free/total morphine and performing ROC analyses, fatal outcome can be predicted in 80% of the cases correctly, whereas 16% of the survivors were classified as dead. Nevertheless, in this study, all cases with a blood concentration of 200 ng/ml and more of free morphine displayed a fatal outcome.     

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 Diabetic Ketoacidosis—A Potential Complication of MDMA (Ecstasy) Use

A 19‐year‐old woman with insulin‐dependent diabetes mellitus was found dead in bed having allegedly recently taken ecstasy and consumed alcohol. At autopsy, there were microhemorrhages in the brain with subnuclear vacuolization and Armanni–Ebstein changes in renal tubules. Biochemical analyses confirmed diabetic ketoacidosis (vitreous glucose—46.5 mmol/L; β‐OH butyrate—13.86 mmol/L.). Toxicological analyses of blood showed a low level of 3,4‐methylenedioxy‐methamphetamine (MDMA) (0.01 mg/L), with acetone but no alcohol or other common drugs. Death was attributed to diabetic ketoacidosis most likely provoked by mixed MDMA/alcohol ingestion. Although the use of illicit drugs by young individuals with diabetes mellitus is being increasingly recognized, it has been noted that there is minimal information about the relationship between drug use and acute diabetic complications. Toxicological screening of cases of lethal diabetic ketoacidosis in the young may clarify lethal mechanisms in individual cases and also help to determine the extent of this problem.     

Fatal outcome of poisoning with ethylene glycol

After an act of violence, a delinquent swallowed about 250 ml ethylene glycol (EG) - probably to commit suicide before being arrested. During an interrogation by the police he appeared to be inebriated. A blood sample taken at this time did not contain ethanol but 5.1 g/l EG, as revealed by the analytical results. Only after a second examination was he taken to an intensive care unit in a hospital in spite of signs of pronounced intoxication after 12 h at the first examination. The patient died 30 h after taking EG without being effectively treated. The correct diagnosis, initiated by information from the poison control center, was made too late. At autopsy, findings were indicative of stage II of EG poisoning with a body burden of still 40-60 g EG. The mean rate of degradation in the blood was approximately 0.15 g/l per hour.     

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 outcome in a case of pontocerebellar hypoplasia type 2

Pontocerebellar hypoplasia (PCH) is a very rare congenital (autosomal recessive) condition with fetal onset. Only a few cases have been published on the basis of both clinical data (symptoms/neuroradiological imaging) and autopsy results. This paper reports on such a case involving a 1.5-year-old male infant. The child suffered from severe psychomotor delay, extrapyramidal dyskinesia and epileptic seizures, but did not exhibit signs of spinal muscular atrophy as related to PCH type 1. Magnetic resonance imaging (MRI) at the age of 6 months demonstrated olivo-pontine and bilateral cerebellar hypoplasia. The boy was unexpectedly found dead. Autopsy disclosed a severe aspiration of gastric contents as the final cause of death. The neuropathological examination confirmed PCH type 2 (according to Barth [Brain Dev., 15 (1993) 411-422]) with marked microcephaly and olivopontocerebellar hypoplasia. Histologically, decreased density of olivo-pontine neurons, reduction of granular and Purkinje's cell layers of the cerebellum, slight astroglial proliferation and fragmented appearance of the dentate nuclei were observed. The immunohistochemical expression pattern was determined using antibodies against glial fibrillary acidic protein, synaptophysin and neurofilament protein. Summarizing, typical features of PCH type 2 were present and proved by clinical course, MRI and autopsy. Despite severe symptoms due to a natural disease this rare neurogenetic entity can become of forensic interest, when sudden unexpected death occurs.     

Ecstasy and suicide

Deaths due to the ring-derivative amphetamines are not common and are usually accidental involving dehydration and hyperthermia. Suicides from 3,4-methylenedioxymethamphetamine (MDMA) and related ring-derivative amphetamines overdose are rare. A 15-year-old female who had a history of depression and previous suicide attempts was found dead with a suicide note. Toxicology demonstrated lethal serum concentrations of MDMA (9.3 mg/L), with 34 mg/kg of MDMA in the liver, 2.4 mg/L in the urine, and 530 mg/kg in the stomach. The cause of death was MDMA toxicity, the manner suicide. While MDMA may be detected in victims in other drug-related or traumatic deaths, it is only rarely used in isolation in suicide, with a predominance in the 21- to 25-year-old range. Despite the rarity of such events, the possibility of a nonaccidental manner of death should be considered when high levels of MDMA and associated amphetamines are found at autopsy.     

From chronic rhinitis to death: Fatal outcome of nasal polyposis treatment

Introduction

Nasal polyposis (NP) is considered to be the state of chronic inflammation of nasal mucosa and sinuses presenting with various nasal symptomatology. In most cases, it is treated conservatively. Recently, functional endoscopic sinus surgery (FESS) was developed as the valuable and advantageous surgical procedure to treat NP. Despite the inherited risks of this procedure, its complication rate is considered to be acceptable compared to potential benefits for the patient.

Case

Fifty-five-year-old man was admitted to the hospital for surgical removal of the nasal polypus. After the usual pre-surgery procedures, the patient underwent FESS. Under general anesthesia, left sphenoid sinus was opened and cleaned from the imflammatory discharge, polypus was excised, and following the trepanation the left maxillary sinus was left to drain out. Polypus and pieces of sinonasal mucosa were sent to pathohistological analysis, which yielded in diagnosis of inverted sinonasal papilloma.The early postoperative recovery was regular, but 2 h upon the surgery, the patient started to lose consciousness gradually falling into the state of coma. CT scan and angiography of the head revealed pneumocranium, defect of the left ethmoidal sinus, hematoma in the left frontal cerebral lobe, as well as the hemorrhage in all four cerebral ventricles. A series of neurosurgical procedures followed in the next 8 days. Despite the attempts to resolve above complications, the patient remained comatous and died 16 days after the polypectomy.Autopsy revealed the extensive oval-shaped defect on the skull base in the left posterior part of cribrous plate of the left ethmoid bone. The brain appeared swollen and heavily congested, showing the zone of subarachnoidal hemorrhage in basal face of left frontal lobe. Frontal serial sections revealed large intracerebral haematoma in basal periventricular structures of left frontal lobe extending to the whole ventricular system. Apart from the above, most prominent finding was bilateral bronchopneumonia. The cause of death was attributed to bronchopneumonia following the brain trauma, manner of death ruled as violent.

Conclusion

Although majority of the patients suffering from chronic rhinosinusitis or NP recover well after the endoscopic surgery, the possibility of undesirable outcome must not be ignored. This case calls for assessment of potential medical liability caused by malpractice. Having in mind rather high prevalence of chronic rhinosinusitis and NP, legal aspects of postoperative death should be carefully analyzed.