Search

Cigarette smoking is associated with a higher risk for suicide. The present study was conducted on the hypothesis that suicide smokers show higher nicotine and cotinine levels in blood and urine than non-suicide smokers. We determined nicotine and cotinine levels in blood and urine of 87 deceased individuals (18 suicides and 69 non-suicides) by gas chromatography. The smoking rate was 77.8% for individuals who committed suicide and 42.0% for those who did not commit suicide. Average nicotine and cotinine levels in blood were significantly higher in the suicide smokers than in the non-suicide smokers (nicotine: 93.2 ± 46.6 ng/ml versus 25.8 ± 14.4 ng/ml, p < 0.0001 and cotinine: 378 ± 235 ng/ml versus 201 ± 137 ng/ml, p < 0.005). Average levels of urinary nicotine and cotinine were also significantly higher in the suicide smokers than in the non-suicide smokers (nicotine: 1980 ± 2210 ng/ml versus 394 ± 376 ng/ml, p < 0.005 and cotinine: 1170 ± 1330 ng/ml versus 414 ± 290 ng/ml, p < 0.05). Twenty-six decedents were intoxicated with alcohol, and they included 7 suicides (7 smokers) and 19 non-suicides (15 smokers). Our data suggest that cigarette smokers who commit suicide smoke more heavily than other cigarette smokers.

We describe significantly elevated drug concentrations in the femoral venous blood due probably to postmortem diffusion from the bladder. A 16-year-old deceased male was found in a shallow ditch in winter. The estimated postmortem interval was 9 days and putrefaction was not advanced. The cardiac chambers contained fluid and coagulated blood and a small amount of buffy coat clots. Diffused hemorrhages were found in the gastric mucosa. The bladder contained approximately 600 ml of clear urine. Gas chromatographic-mass spectrometric analysis of the urine disclosed allylisopropylacetylurea (a fatty acid ureide sedative), diphenhydramine, chlorpheniramine and dihydrocodeine. The cause of death was considered to be drowning due to a drug overdose and cold exposure. The concentrations of diphenhydramine, free dihydrocodeine and total dihydrocodeine in the femoral venous blood (1.89, 3.27 and 3.30 microg/ml, respectively) were much higher than those in blood from the right cardiac chambers (0.294, 0.237 and 0.240 microg/ml, respectively). Urine concentrations of diphenhydramine, free dihydrocodeine and total dihydrocodeine were 22.6, 37.3 and 43.1 microg/ml, respectively. The stomach contained negligible amounts of diphenhydramine, free dihydrocodeine and total dihydrocodeine (0.029, 0.018 and 0.024 mg, respectively); concentrations of these drugs in the femoral muscle were 0.270, 0.246 and 0.314 microg/g, respectively. These results indicate that postmortem diffusion of diphenhydramine and dihydrocodeine from the bladder resulted in the elevated concentrations of these drugs in the femoral venous blood. Not only high urinary drug concentrations but also a large volume of urine in the bladder might accelerate the postmortem diffusion.

A rapid and accurate method, combining solid-phase extraction and second-order derivative spectrophotomety approaches, is developed for the simultaneous determination of diquat (DQ) and paraquat (PQ) in blood, tissue and urine samples. Supernatant resulting from the precipitation of protein (with trichloroacetic acid) in plasma and tissue or Amberlite IRA-401 resin treated urine are passed through a mini-column packed with Wakogel gel (Silica gel). Analytes are then eluted with a non-organic solvent, 0.2mol/l HCl solution containing 2mol/l NH(4)Cl. UV spectrum of the eluent in 220-350nm range provides effective screen to detect the presence of DQ and/or PQ. In the presence of DQ or PQ alone, the analyte present is quantitated by conventional zero- or second-order derivative spectrophotometry. The calibration curve in the 0.1-5.0mg/l range for either analyte obeys Beer's law. When both DQ and PQ are present, their concentrations are determined by the peak amplitudes of their respective second-derivative spectra after the addition of alkaline dithionite reagent. Interference is negligible when the DQ/PQ concentration ratio is within the 5.0-0.2 range. Using a 2-ml of sample size, the detection limits for DQ and PQ in plasma are 0.02 and 0.005mg/l. The corresponding detection limits for urine samples (10ml sample size) are 0.004 and 0.001mg/l. Recoveries of DQ and PQ in triplicate plasma and urine samples spiked with 0.5mg/l of analytes are 93 and 85%. The precision of the proposed method resulting from triplicate study of spiked urine samples varies from 3.2 to 4.6% at 0.5mg/l of DQ and PQ, respectively.

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.

We investigated tissue distribution of lidocaine in 33 patients after endotracheal intubation with Xylocaine jelly that contains 2% lidocaine hydrochloride. Blood levels of monoethylglycinexylidide (MEGX), an active metabolite of lidocaine, were also determined. Five patients (Group A) were alive on arrival and six patients (Group B) resumed heartbeats after cardiopulmonary resuscitation (CPR). The survival times for Groups A and B ranged from 3 to 72 h. The remaining 22 patients (Group C) did not survive cardiopulmonary arrest on arrival (CPAOA). Systemic distribution of lidocaine was measured in nine patients from Group C. The liver-to-kidney lidocaine ratios and cerebrum-to-cerebrospinal fluid lidocaine ratios were: Group A, 0.1-0.7 and 1.4-3.6, respectively; Group B, 0.2-0.8 and 1.2-2.3, respectively; Group C, 0.1-17 and 0.2-1.0, respectively. MEGX was detected in all blood samples from Group A and only two samples from Group B. No MEGX was detected in samples from Group C. Our results indicate that the absorption of tracheal lidocaine during natural circulation results in a cerebrum-to-cerebrospinal fluid lidocaine ratio of 1.2 or more, whereas absorption during artificial circulation by cardiac massage gives a ratio of 1.0 or less. The cerebrum-to-cerebrospinal fluid lidocaine ratio may be a more useful index to estimate circulatory dynamics of patients during CPR than the liver-to-kidney lidocaine ratio. MEGX was not a useful parameter for monitoring circulatory changes during cardiac massage.

We describe a case of massive hemorrhage in the cerebral ventricles, probably caused by methamphetamine abuse. A 44-year-old male was found dead in a prone position in a hotel room. Old and new injection marks were observed in his right cubital fossa. Petechiae were observed on the conjunctiva of his right eye, laryngeal mucosa, epicardium and under the capsule of the liver (to a slight or moderate degree). The brain, weighing 1.67 kg, was heavily edematous; the lateral and fourth ventricles were filled with hematomas. Subarachnoid, intracerebral hemorrhages were not observed. Cerebral vascular abnormalities were not evident. There were no remarkable changes in other organs, other than congestion. Gas chromatographic-mass spectrometric analysis of the urine disclosed the presence of methamphetamine and amphetamine. The concentration of methamphetamine within the femoral venous blood and intraventricular hematoma was 0.347 microg/ml and 0.189 microg/g, respectively. Amphetamine was not detected in either sample. Urine contained 3.15 microg/ml methamphetamine and 0.063 microg/ml amphetamine. These results indicate that intraventricular hemorrhage might have occurred shortly after intravenous self-administration of methamphetamine. Cerebral arterial spasm and hypertension resulting from the administration of methamphetamine might have resulted in intraventricular hemorrhage.

The effects of cocaine administration route on the formation of cocaethylene, an active metabolite of cocaine produced in the presence of ethanol, were investigated using rats. When 20 mg/kg cocaine was administered into the stomach together with 2 g/kg ethanol, maximum liver concentrations of cocaine and cocaethylene, 8410 +/- 3600 and 1680 +/- 520 ng/g, respectively, were observed at 15 min. In other tissues the maximum levels of both the substances were attained in 30 min, but were much lower than those in the liver. Intramuscular administration of 20 mg/kg cocaine with 2 g/kg oral ethanol gave levels of liver cocaine as low as 103 +/- 29 to 150 +/- 35 ng/g, resulting in no detection of liver cocaethylene over the entire 180-min study period, although gradual accumulation of cocaethylene was observed in other tissues. The accumulation patterns of cocaine and cocaethylene in blood of alcohol-intoxicated rats after the i.m. administration of cocaine were similar to those in blood of drinkers after nasal insufflation of cocaine. Despite i.v. administration of 1 mg/kg cocaine with 2 g/kg oral ethanol, no detectable amounts of cocaethylene appeared in any tissues over the entire 60-min study period. The present findings are considered to be of importance in the fields of forensic and clinical toxicology for clarifying (1) the rate of in vivo cocaethylene formation and (2) the distribution of cocaine and cocaethylene in blood and tissues.

An experiment was carried out on rats to determine whether or not a skeletal muscle sample was suitable for the determination of ethanol concentration in a carcass. Gas chromatography was used to estimate the ethanol and n-propanol concentrations in the femoral muscle and intracardial blood. The ethanol concentration of each sample was corrected according to the moisture ratio of circulating blood, viz., 78.5%. The ethanol concentration ratio of blood to muscle was 1.03 two hours after ethanol administration. When the carcasses of rats pre-treated with ethanol were stored at 15 degrees C and 25 degrees C, respectively, the ethanol concentrations in muscle and blood increased with time. At all times the concentration was higher in blood than in muscle, and also higher in samples collected from the carcass stored at 25 degrees C than at 15 degrees C. When the control carcass was stored in the same manner, the postmortem production of ethanol was noticed in both blood and muscle. As in the experimental rats, the control rats exhibited a higher blood ethanol than muscle ethanol level. Again, the ethanol concentration was higher in samples collected from the carcass stored at 25 degrees C than at 15 degrees C. The ratio of ethanol to n-propanol was less than 20:1 in blood and less than 10:1 in muscle. These results suggest that skeletal muscle may be a suitable tissue for the postmortem detection of ethanol.

Sudden and unexpected death and violent death of persons with a high risk of acquiring HIV-infections, especially homosexual males and intravenous drug abusers, have to be investigated by forensic autopsies. Therefore every forensic pathologist has to be aware of this infection and should try to make the proper diagnosis. Three typical cases are described: (1) suicide by hanging, (2) homicide by cutting the throat and (3) intravenous heroin overdose. Merely retro-spectively it could be cleared up that the deceased were homosexual but did not manifestly suffer from AIDS. The morphological findings in the lymph nodes and the postmortem serological findings are described in detail.