An unusual trichloroethanol fatality attributed to sniffing trichloroethylene.

We report the death of a 28-year-old man due to sniffing a contact cement containing trichloroethylene. Initial testing revealed the presence of 80 mg/L trichloroethanol in cardiac blood, and the death was ruled as being due to trichloroethanol toxicity resulting from chloral hydrate ingestion. However, further investigation of the case revealed that the trichloroethanol resulted from trichloroethylene abuse. Subsequent targeted analysis for trichloroethylene, four months after the death, confirmed its presence in cardiac blood (1.1 mg/L), bile (4.5 mg/L), and liver (2.5 mg/kg). Trichloroethanol was initially detected during routine drug screening that employed gas chromatography (GC) using an HP-5 column with electron capture detection and subsequently quantitated by GC using the same column as for the initial screen, but with flame-ionization detection (FID); ethchlorvynol was the internal standard. Trichloroethylene was quantitated by headspace GC with a Restek Rtx-BAC1 column and FID; 1,1,1-trichloroethane was the internal standard.

Loss of ethanol from vitreous humor in drowning death.

Two separate cases of drowning with extended periods underwater (2 and 4 weeks) are reported. The postmortem ethanol concentrations were 260 and 280 in central blood, 50 and 80 in vitreous, and 330 and 320 in urine (mg/100 mL) for cases 1 and 2, respectively. Determination of the urine 5-hydroxytryptophol/5-hydroxyindole-3-acetic acid ratios produced results of 713 and 41 pmol/nmol, respectively. The serotonin metabolite ratios support the explanation of diffusion of ethanol from the vitreous fluid into the surrounding water, rather than postmortem production of ethanol in blood, as the primary reason for the blood-vitreous ethanol differences.

The relationship of methanol and formate concentrations in fatalities where methanol is detected.

An automated headspace gas chromatography method was developed for the determination of formate (formic acid) in postmortem specimens, based on the in situ sulfuric acid-methanol methylation of formic acid to methyl formate. Diisopropyl ether was used as an internal standard. The method was applied to over 150 postmortem cases where methanol was detected. Of the 153 cases presented, 107 deaths were attributed to acute methanol toxicity. In the vast majority of the remaining 46 deaths, the methanol was determined to be present as a postmortem or perimortem artifact, or was otherwise incidental to the cause of death. Of the 76 victims who were found dead and blood was collected by the medical examiner, all but one had a postmortem blood formate concentration greater than 0.50 g/L (mean 0.85 g/L; n = 74). The sole exception involved suicidal ingestion of methanol where the blood methanol concentration was 7.9 g/L (790 mg/100 mL) and blood formate 0.12 g/L. In 97% (72/74) of the cases where blood was available, the blood formate was between 0.60 and 1.40 g/L. In 31 of the 153 cases, the victim was hospitalized and blood obtained on admission or soon after was analyzed for methanol and formate during the subsequent death investigation; the vast majority (27/30) had antemortem blood formate concentrations greater than 0.50 g/L. Cases with samples taken prior to death with blood formate concentrations less than 0.5 g/L can readily be explained by active treatment such as dialysis. The blood formate method has also been useful in confirming probable perimortem or postmortem contamination of one of more fluids or tissues with methanol (e.g., windshield washer fluid or embalming fluid), where methanol ingestion was unlikely.

Acute fatal acetaminophen overdose without liver necrosis.

Two unusual cases of suicidal overdose of acetaminophen (paracetamol) without the usual extensive centrilobular necrosis of the liver are reported. Both cases were subjected to comprehensive drug screening by immunoassay, and a combination of gas chromatography with mass spectrometry, nitrogen detection, and electron capture detection. Acetaminophen was detected in both cases. No other drugs were detected in case #1, and only a small amount of olanzapine (<0.1 mg/L) was detected in case #2. No anatomical cause of death was identified in either case. If untreated, the normal outcome of a large acetaminophen overdose would be massive hepatic necrosis with delayed death and low blood and tissue acetaminophen concentrations. In contrast, particularly high postmortem acetaminophen concentrations were measured in both our cases with little hepatic tissue damage. For case #1, femoral blood acetaminophen 1280 mg/L, vitreous 878 mg/L, and liver 729 mg/kg; in case #2, cardiac blood 1220 mg/L, vitreous 779 mg/L, liver 3260 mg/kg, and gastric 11,500 mg/500 g. Acetaminophen was measured using high performance liquid chromatography with UV detection (254 nm) using 3-hydroxyacetanilide as the internal standard. The very high concentrations of acetaminophen is these cases but relatively little hepatic damage suggests an alternative, possibly cardiac, mechanism of death.

An unusual autoerotic fatality associated with chloroform inhalation.

We report the death of a young male attributed to chloroform poisoning during autoerotic asphyxia. He was found lying on the floor of his apartment, prone on a piece of foam and a towel. His eyes were bound with a towel, his lower face and nose were almost entirely covered with duct tape surrounding a rubber hose in his mouth. The other end of the hose was loosely sitting inside an open bottle which was in a box beside him. He was bound-up by an intricate system of ropes, handles, and rods, ending with a noose around his neck. Toxicology testing indicated chloroform concentrations of 18.1 mg/L in femoral blood and 1.5 mg/L in urine. Chloroform was measured by headspace gas chromatography with flame-ionization detection using 1,1,1-trichloroethane as the internal standard. The cause of death was recorded as "chloroform toxicity" with "autoerotic asphyxia" as a contributing factor, and the manner of death was "accidental".

Application of LC-MS analysis to a colchicine fatality.

A 73-year-old man developed nausea, vomiting, and diarrhea 20-30 min after receiving a 1.0 mg intravenous dose of colchicine for the treatment of severe pain due to gouty arthritis in his physician's office. He was hospitalized 8 h later, and his condition deteriorated as he developed renal and respiratory failure. He subsequently died 10 h later, or a total of 18 h after he received the original 1 mg colchicine injection. The patient received a prescription for oral 0.6 mg colchicine tablets 8 days previously and consumed eight tablets during that period, an average of 0.6 mg/day (42 of 50 tablets remained at the time of death). Colchicine concentrations were measured by liquid chromatography-mass spectrometry in selected ion monitoring mode using positive ionization. Chromatography was performed using an Eclipse XDB C8 analytical column (30 mm x 2.1-mm i.d., 3-microm particle size) and a programmed mobile phase consisting of 50 mM pH 4 ammonium acetate buffer and acetonitrile. Colchicine concentrations were as follows: 50 microg/L in cardiac blood, 10 microg/L in vitreous humor, 575 microg/kg in liver, 12,000 microg/L in bile, and 4.4 microg in 60 g received gastric contents (estimated total gastric contents 100 g). The cause of death was ruled to be "acute colchicine toxicity" and the manner of death "accidental."