Digoxin, magnesium, and potassium levels in a forensic autopsy material of sudden death from ischemic heart disease

In 91 cases where the cause of death was heart disease, digoxin, Mg and K concentrations in serum and ventricular myocardium were measured post mortem. Forty per cent were positive for digoxin in both serum and myocardium. The mean serum level was 5.1 +/- 2.4 nmol/l and the mean myocardial level was 42.6 +/- 27.5 ng/g. Correlation could be established between serum and myocardial concentrations of digoxin. There were statistically significant differences in serum as well as in myocardial digoxin levels in persons on 0.13 mg and 0.25 mg per day, respectively. Myocardial levels of Mg and K were low as generally found in persons with ischemic heart disease. There was no correlation between these levels and myocardial digoxin concentrations. Caution must be exercised in the assessment of digoxin results from cadaver samples because of the postmortem rise of digoxin serum concentrations. Considering this fact, the results still indicate that the prevalence of toxic digoxin concentrations might be more common than previously thought.     

Classification of digoxin concentrations in blood and tissues in cases under suspicion of poisoning

The clarification of a suspicion of poisoning at all times poses a problem to the forensic toxicologist, when a narrow margin of therapeutic safety and a low dosage coincide as in cases of digoxin poisoning. Statistical methods may serve as an aid. The post mortem digoxin concentration in the tissues of heart, kidney, liver and in blood of 45 patients who had received therapeutic daily doses and of 13 cases of fatal poisoning are compared. After logarithmic transformation of the individual concentration values a two modal distribution is obtained. There is one concentration calculated with equal probability of being classified to "therapeutic or toxic", as well as the probability of observing the "critical" concentrations of 400 ng digoxin/g cardiac tissue, 500 ng/g kidney and 250 ng/g liver after therapeutic dosing. Using the discriminant analysis each of the cases clearly falls into one of the two collectives "therapeutic" and "toxic", when taken as a separate observation. Concentration data of fatal poisonings taken from the literature are as successfully classified as the analytical results of some exhumed bodies under suspicion but not poisoned. As expected the power of discrimination increases with the number of parameters. Because of the relatively slow body distribution of digoxin the blood taken from peripheral vessels is of most important evidence.     

Postmortem redistribution of digoxin in rats

Adult male Wistar rats were treated with either 0.1 or 3 mg/kg body weight X day of digoxin for five days, then killed and stored at 4 degrees C for 12 h in an attempt to mimic the normal preautopsy procedures in our hospital. In rats treated with 0.1 mg/kg body weight X day, the antemortem serum digoxin concentrations (SDC) were 1.1 +/- 0.4 ng/mL while the 12-h postmortem concentration was markedly increased (16.3 +/- 5.9 ng/mL) (P less than 0.01). In rats treated with 3 mg/kg body weight X day, SDC was not changed significantly (11.2 +/- 4.8 ng/mL antemortem and 13.3 +/- 6 ng/mL postmortem). Postmortem redistribution of digoxin was assessed by injection of 125I-labelled digoxin with or without pretreatment with the unlabelled drug. The results indicate that after death passive redistribution of digoxin may take place. When the SDC are within the therapeutic or low toxic range, digoxin may reenter the blood. High antemortem serum concentrations of digoxin may prevent such passive redistribution. Therefore, antemortem digoxin intoxication cannot be reliably inferred on the basis of high postmortem levels of the drug. Digoxin intoxication can be ruled out when postmortem SDC remain within the therapeutic range. The above changes cast doubt on some of the forensic and cardiologic literature, which has in the past been based on incorrect assumptions concerning postmortem behavior of digoxin.     

Cardiac glycosides and metabolites--problems of recovery in tissue extracts. Separation of visible substance spots in the nanogram range (author's transl)]

The recovery measurements in rat tissues performed via i.p. injected radioactive digoxin derivates (3H-digoxin, 125J-digoxin derivative) showed that approximately 50% of the total glycoside content will be extracted. Thus, an addition of digoxin standards to drug-free tissues may lead to false negative determinations. By comparison of the radioactivity before and after extraction the following results were obtained: Recovery from tissues 3H-digoxin 50% 125J-digoxin 40% from serum 3H-digoxin 60% added to drug free tissue homogenates 3H-digoxin 85% After i.p. application of 15 mg/kg of beta-methyldigoxin to BD9 (Berlin)-rats the resulting tissue concentrations were extracted by Amberlite XAD-2. beta-Methyldigoxin and its metabolites digoxin and digoxinbisdigitoxide could be separated and distinguished from artifacts by fluorescence detection on HPTLC-plates with a detection limit of 60 ng/spot. Concentration determined by radioimmunoassay are in satisfactory agreement with HPTLC results.     

Immunofluorescence demonstration of digoxin in human myocardial tissue and isolated rat cardiac myocytes with monoclonal antibodies

The aim of the present investigation was to identify the morphological correlates of digoxin binding sites in human heart muscle tissue and isolated viable rat heart myocytes. Cardiac glycoside linked to myocardial cells was demonstrated by monoclonal digoxin specific antibody and by FITC-conjugated anti-mouse immunoglobin serum. This versatile immunofluorescence method can be used in diagnostic and experimental studies of cardiac glycoside binding.     

The influence of sex hormones on the elimination kinetics of ethanol

The goal of the investigation was to research the influence of sex hormones on the elimination kinetics of ethanol. Forty-seven healthy men (average age 25+/-6.1 years) and 61 healthy women (average age 24+/-2.4 years) received 0.79-0.95g of ethanol/kg body weight in the form of an alcohol beverage of their choice. The target concentration for both sexes was a blood alcohol concentration (BAC) of 1.10g/kg. Blood samples for the determination of the ethanol concentration followed in the elimination phase in 10-20min intervals. The sex hormone levels (estradiol, progesterone and testosterone) were determined concomitantly from the serum. In men, the mean testosterone concentration was 5.3+/-1.6ng/ml, the mean estradiol concentration was 34.6+/-13.6pg/ml and the mean progesterone concentration was 0.9+/-0.3ng/ml. In women, the mean estradiol concentration was 47.6+/-52.6pg/ml and the mean testosterone concentration was 0.8+/-0.4ng/ml. Progesterone displayed a so-called dummy effect in women. In the high progesterone group (n=11), the mean concentration was 11.1+/-3.5ng/ml and in the low progesterone group (n=50) the mean was 0.6+/-0.3ng/ml. The mean hourly elimination rate (beta60) was 0.1677+/-0.0311g/kg/h in men. In women, the mean hourly elimination rate was 0.2044+/-0.0414g/kg/h in the high progesterone group and 0.1850+/-0.0276g/kg/h in the low progesterone group (p<0.05). The beta60 for women in the low progesterone group was significantly higher than that of the men, whose progesterone levels fell within a similar range (p>0.01). These results allow one to conclude that the gender differences in the pharmacokinetics of ethanol can partly, but not completely, be explained by progesterone levels.     

Forensic aspects of digoxin-poisoning: toxicological and morphological findings (author's transl)]

Case report. A 82 year old woman died 80 min after accidental ingestion of 5 mg beta-methyl-digoxin. The autopsy and the histological examination revealed non-specific alterations due to shock and preexisting coronary heart disease. Digoxin levels in various fluids and tissues were estimated by radioimmunoassay: bloodplasma 20--25 ng/ml, liquor 10--13 ng/ml, liver 100--110 ng/g, kidney 130--145 ng/g; the gastric fluid contained 0,6 mg. Forensic aspects of glycosid-intoxication, especially of the varying concentrations in different tissues, are discussed.     

UPLC-MS/MS法检测佐匹克隆及其在大鼠体内动态分布研究

目的建立安眠镇静药佐匹克隆的检测方法及其在大鼠体内动态分布模型。方法实验组大鼠用佐匹克隆橄榄油溶液(47.25mg/kg)灌胃给药,空白对照组大鼠采用橄榄油灌胃,分别于0.5、1、1.5、2.5、5、8、12h后采集心血后处死大鼠,分别取心、肝、肺、脾、肾、胃、大脑组织,采用超高效液相色谱-串联质谱法(UPLC-MS/MS)检测各组织中佐匹克隆的质量浓度。结果佐匹克隆与内标物SKF525A出峰时间分别为1.43、1.6min。各组织中佐匹克隆在5~5000ng/mL(g)线性关系良好。佐匹克隆在10、100、1000ng/mL三个浓度下日间、日内精密度良好,在各组织中平均萃取回收率高。灌胃给药后大鼠各组织中佐匹克隆含量在0.5~1h内呈上升趋势,在1h时达到峰值,在各时间点,佐匹克隆在胃壁组织中含量较其他组织高,心血和大脑组织中相对较少。结论本课题建立的UPLCMS/MS法动态检测大鼠各组织中佐匹克隆的含量具有高效性、可靠性的特点,这对今后法医学案件中涉及到佐匹克隆定性定量检验有一定的参考价值。     

Applicability of succinylmonocholine as a marker for succinylcholine administration--comparative analysis of samples from a fatal succinylcholine-intoxication versus postmortem control specimens

Doubts concerning the applicability of succinylmonocholine (SMC) as a succinylcholine (SUX) marker have been issued. A comparative analysis of previously discussed tissues, i.e. brain, liver and kidney, was conducted to further elucidate this question by searching for diagnostically useful differences in analyte content in samples of SUX- versus non-SUX-associated fatalities. Furthermore, possible advantages of vitreous humor as a novel and promising target matrix for SUX analytics were assessed. Sample material of SUX-negative controls as well as the fatal SUX-intoxication was derived from frozen archive material and current autopsies. Samples were analyzed according to a modified protocol of a previously published and validated method employing ion-pairing solid-phase extraction and subsequent HPLC-MS/MS analysis. Standard addition was employed for quantification as well as an estimation of the analytical limits of the method. In all tested matrices, the method was proven to be sufficiently sensitive for the intended application. No indication of native SMC was found in controls of fresh tissues, nor in fresh or frozen vitreous humor. However, most of the samples were found to be positive for a previously reported interference with SMC's main ion transition, thereby falsely suggesting an SMC content of up to 139 ng/g, 126 ng/g, 165 ng/g and 93 ng/ml in brain, liver, kidney and vitreous humor, respectively. Contrasting the results for fresh sample material, SMC was detectable in some of the initially non-putrefied liver samples after long-term storage, as well as in massively decomposed SUX-negative control bodies. In this context, a microbial origin of the analyte may be assumed. All tissues as well as the vitreous humor of the fatal SUX-intoxication were negative for SUX and SMC. Just like serum, tissue and vitreous humor samples therefore do not allow a reliable diagnosis of a SUX-intoxication: in tissues this is due to the pronounced instability of both target analytes in these esterase-containing matrices, for vitreous humor an additional reason could be their insufficient incorporation into this medium.     

Postmortem determination of the biological distribution of sufentanil and midazolam after an acute intoxication

A case is presented of a death caused by self-injection of sufentanil and midazolam. Biological fluids and tissues were analyzed for midazolam by high performance liquid chromatography (HPLC) and gas chromatography/mass spectrometry (GC/MS) and for sufentanil by GC/MS. Midazolam was extracted from basified fluids or tissues homogenated with n-butyl chloride and analyzed by HPLC by using a phosphate buffer: acetonitrile (60:40) mobile phase on a mu-Bondapak C18 column at 240 nm. Sufentanil was extracted from basified fluids and tissue homogenates with hexane:ethanol (19:1). GC/MS methodology for both compounds consisted of chromatographic separation on a 15-m by 0.25-mm inside diameter (ID) DB-5 (1.0-micron-thick film) bonded phase fused silica capillary column with helium carrier (29 cm/s) splitless injection at 260 degrees C; column 200 degrees C (0.8 min) 10 degrees C/min to 270 degrees C; and electron ionization and multiple ion detection for midazolam (m/z 310), methaqualone (IS, m/z 235), sufentanil (m/z 289), and fentanyl (IS, m/z 245). Sufentanil concentrations were: blood 1.1 ng/mL, urine 1.3 ng/mL, vitreous humor 1.2 ng/mL, liver 1.75 ng/g, and kidney 5.5 ng/g. Midazolam concentrations were: blood 50 ng/mL, urine 300 ng/mL, liver 930 ng/g, and kidney 290 ng/g. Cause of death was attributed to an acute sufentanil/midazolam intoxication and manner of death a suicide.     

A sandwich enzyme immunoassay for pulmonary surfactant protein D and measurement of its blood levels in drowning victims

A sensitive sandwich enzyme immunoassay for human pulmonary surfactant protein D (SP-D) was developed and used to examine the blood SP-D levels of drowning victims. Human SP-D was purified from amniotic fluid by chromatographic methods, and an antibody against human SP-D was prepared. A polystyrene ball coated with anti-SP-D IgG was incubated with purified human SP-D, and then with anti-SP-D Fab'-peroxidase conjugate. Peroxidase activity bound to the polystyrene ball was assayed by fluorometry using 3-(4-hydroxyphenyl)propionic acid as the hydrogen donor. The detection limit of human SP-D was 5.2 pg per assay tube. Examination of cross-reactions of this sandwich enzyme immunoassay with proteins from other human organs showed it to be highly specific for lung, and Northern blot analysis detected specific SP-D mRNA expression only in lung. The SP-D concentration of normal human serum was 6.4+/-2.7 (mean+/-S.D.) ng ml(-1) (n=20). The recovery rates of 0.52 ng and 5.2 ng SP-D added to 5 microl normal human serum were 93.6+/-2.7% and 93.6+/-6.1%, respectively. Blood SP-D levels of victims from the saltwater drowning group (n=14) revealed higher concentrations (105.8+/-53.7 ng ml(-1)), while freshwater drowning victims (n=12) were estimated to be 74.1+/-43.9 ng ml(-1). The SP-D levels of 15 subjects who died of hemorrhage (n=5), heart failure (n=8), traumatic shock (n=1), and electrocution (n=1) were lower (22.0+/-8.5 ng ml(-1)), and those of asphyxia victims (n=10) were slightly higher (36.2+/-17.1 ng ml(-1)) than those of other causes of death, except for drowning. These results suggest that in drowning victims, SP-D flowed into the systemic circulation by physiological and physical mechanisms, and the differences of blood SP-D levels between saltwater drowning and freshwater drowning victims are presumed to be influenced by the type of agony and/or the length of survival time in water.     

生物组织检材内异烟肼的薄层色谱扫描检测研究──附1例异烟肼中毒死亡者体内分布报告

改进血清中异烟肼的提取方法，建立了生物组织检材内异胭肼的提取和薄层色谱扫描检测方法，线性范围为2～32ug／ml或g，检出限为0．5ug／ml或g。l例异烟擀中毒死亡者体内异烟肼分布：肾31．6mg／100g、肝26．6mg／100g、脾22．1mg／100g、心21．3mg／100g、胃16．6mg／100g、脑15．5mg／100m、肺12．6mm／100g、小脑11．7mm／100g和10.5mm／100ml。     

Development and validation of a LC–MS/MS method for analysis of vortioxetine in postmortem specimens. First data from an authentic case

Vortioxetine is an antidepressant recently licensed in USA and EU for the treatment of major depressive disorder. Neither fatal case due to overdose nor data about postmortem concentrations on blood or other specimens have been reported. The aims of this study were the development and validation of a method for vortioxetine analysis by Liquid Chromatography Tandem Mass Spectrometry (LC–MS/MS) in postmortem samples and its application in an authentic case. The method was validated and applied on blood, vitreous humor, bile, brain, liver, kidney, and gastric content. After protein precipitation, the supernatant was directly injected into LC–MS/MS. Analysis was carried out by Multiple Reaction Monitoring (MRM) mode. The authentic case concerned a 38 years-old woman, affected by depression, who was found hanged at home. The method determined an acceptable sensitivity, selectivity, linearity, precision, and accuracy for all matrices. No interference was shown for all matrices. The matrices do not significantly reduce the peak intensity of vortioxetine. No carryover was shown. Toxicological analysis of the authentic case showed vortioxetine in blood (234 ng/ml), vitreous humor (10.5 ng/ml), brain (490 ng/g), lung (479 ng/g), liver (3751 ng/g), kidney (798 ng/g), bile (2267 ng/ml) and gastric content (253 ng/ml). Our case suggests that even at blood concentrations of vortioxetine equal to 234 ng/ml, the subject was able to stage and carry out the hanging. Vortioxetine concentrations found in the other cadaveric samples (biological fluids, organs, and gastric content) may be helpful to evaluate further similar comparable cases.     

Digoxin-like immunoreactive substance in postmortem blood of infants and children

A digoxin-like immunoreactive substance (DLIS) has been reported in the serum of infants not receiving digoxin. This study was undertaken to determine if DLIS is present in the postmortem blood and tissues of infants or children and whether the endogenous substance could interfere with forensic toxicological analysis in suspected overdose. Ninety blood specimens taken from the heart at autopsy of children or infants were screened for DLIS using commercial radioimmunoassay kits. The average age at death in these cases was 8.6 months, the median age was 2 months. DLIS equivalent to 0.25 to 2.0 ng/mL digoxin was found in one third of the cases. The incidence of positive findings was 5/6 stillborns, 10/45 Sudden Infant Death Syndrome (SIDS), 10/15 deaths as a result of infection, 4/7 homicides, 1/8 deaths caused by congenital defects, and 0/9 accidental deaths. The body distribution of DLIS was investigated and highest levels were found in the liver. Findings of DLIS in blood were correlated with renal failure, (elevated vitreous urea nitrogen), electrolyte imbalance, and liver trauma. Apparent concentrations were in the equivalent therapeutic range of digoxin and would not be confused with accidental or intentional overdose with digoxin.     

Ethyl glucuronide concentrations in two successive urinary voids from drinking drivers: relationship to creatinine content and blood and urine ethanol concentrations

The concentrations of alcohol in blood (BAC) and two successive urine voids (UAC) from 100 drunk drivers were compared with the concentration of ethyl glucuronide (EtG), a minor metabolite of ethanol in urine, and the urinary creatinine content as an indicator of dilution. The subjects consisted of 87 men with mean age 42.2+/-14.2 years (+/-standard deviation, S.D.) and 13 women with mean age 42.5+/-14.4 years. Ethanol was measured in blood and urine by headspace gas chromatography (GC) and EtG was determined in urine by liquid chromatography-mass spectrometry (LC-MS). The mean UAC was 2.53+/-1.15g/l for first void compared with 2.35+/-1.17g/l for second void, decreasing by 0.18+/-0.24g/l on average (P<0.001 in paired t-test). The ratios of UAC/BAC were 1.35+/-0.25 for first void and 1.20+/-0.16 for second void and the difference of 0.15+/-0.27 was statistically significant (P<0.001). The UAC/BAC ratio was not correlated with creatinine content of the urine specimens, whereas the concentration of urinary EtG was positively correlated with creatinine (r=0.64 for first void and r=0.62 for second void). The UAC was not correlated with urinary EtG directly (r=-0.03 for first void and r=0.08 for second void) but after adjusting for the relative dilution of the specimens (EtG/creatinine ratio) statistically significant positive correlations were obtained (r=0.58 for first void and r=0.57 for second void). The dilution of the urine, as reflected in creatinine content, is important to consider when EtG measurements are interpreted. The excretion of EtG in urine, like glucuronide conjugates of other drugs, is influenced by diuresis. EtG represents a sensitive and specific marker of acute alcohol ingestion with applications in clinical and forensic medicine.     

Determination of succinyldicholine in different tissue samples from guinea pigs after injection of a single intravenous dose

The distribution and postmortem stability of succinyldicholine in different tissues and urine from guinea-pigs has been studied. Succinyldicholine was extracted from tissue homogenates and urine samples from animals sacrificed by intravenous injections of succinyldicholine hydrochloride (40 mg/kg). The bis-quaternary ammonium compound was demethylated and the tertiary amine was analysed by gas chromatography/mass spectrometry. The concentrations found in muscle, kidney and urine were often low; in muscle below 5 pmol/g, in kidney from 5 to 1500 pmol/g and in urine from 5 to 650 pmol/ml. The eye proved to be the best tissue sample, with a rather high and constant concentration (280 +/- 36 pmol/g) of succinyldicholine. The postmortem stability was studied by storing the bodies at 4 degrees C. After 6 days storage the drug concentrations in the eyes started to decline. Four weeks after death it was not possible to detect any succinyldicholine in this tissue.     

Suicide due to oral ingestion of lidocaine: a case report and review of the literature

The Authors describe a rare case of suicide in a 31-year-old woman, due to oral ingestion of lidocaine; the histological and toxicological findings are discussed to provide useful information to the present experience with this particular modality of death. Histological examination revealed generalized stasis. In the myocardium we observed segmentation of the myocardial cells and/or widening of intercalated discs and associated group of hypercontracted myocardial cells with "square" nuclei in line with hyperdistended ones. Non-eosinophilic bands of hypercontracted sarcomeres alternating with stretched, often apparently separated sarcomeres, small foci of paradiscal contraction band necrosis, and perivascular fibrosis were observed too. Lidocaine was detected in the subject's urine through immunoenzymatic screening. Toxicological analysis by solid-liquid extraction and gas chromatography-mass spectrometry (GC-MS) analysis, was carried out to identify and quantify the individual substances present in the biological fluids and organs. Lidocaine concentrations were as follows: blood 31 microg/mL, gastric content 2.5 g, liver 10 microg/g, kidney 12 microg/g, brain 9 microg/g, spleen 24 microg/g, lung 84 microg/g, heart 9 microg/g, urine 9 microg/mL, and bile 6 microg/mL. No other drugs or alcohol were detected. When blood lidocaine reaches toxic levels, serious toxic symptoms associated with the central nervous system and cardiac system are noted. The overdose of lidocaine produces death from ventricular fibrillation or cardiac arrest. In this case, according to macroscopic and microscopic findings, the cause of death was most likely cardiac and possibly related to ventricular fibrillation.     

Nicotine and cotinine levels in body fluids of smokers who committed suicide

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.     

Distribution of ∆9‐Tetrahydrocannabinol and 11‐Nor‐9‐Carboxy‐∆9‐Tetrahydrocannabinol Acid in Postmortem Biological Fluids and Tissues From Pilots Fatally Injured in Aviation Accidents

Little is known of the postmortem distribution of ?⁹‐tetrahydrocannabinol (THC) and its major metabolite, 11‐nor‐9‐carboxy‐?⁹‐tetrahydrocannabinol (THCCOOH). Data from 55 pilots involved in fatal aviation accidents are presented in this study. Gas chromatography/mass spectrometry analysis obtained mean THC concentrations in blood from multiple sites, liver, lung, and kidney of 15.6 ng/mL, 92.4 ng/g, 766.0 ng/g, 44.1 ng/g and mean THCCOOH concentrations of 35.9 ng/mL, 322.4 ng/g, 42.6 ng/g, 138.5 ng/g, respectively. Heart THC concentrations (two cases) were 184.4 and 759.3 ng/g, and corresponding THCCOOH measured 11.0 and 95.9 ng/g, respectively. Muscle concentrations for THC (two cases) were 16.6 and 2.5 ng/g; corresponding THCCOOH, “confirmed positive” and 1.4 ng/g. The only brain tested in this study showed no THC detected and 2.9 ng/g THCCOOH, low concentrations that correlated with low values in other specimens from this case. This research emphasizes the need for postmortem cannabinoid testing and demonstrates the usefulness of a number of tissues, most notably lung, for these analyses.     

Methanol intoxication: distribution in postmortem tissues and fluids including vitreous humor

A 44-year-old man was found unconscious beneath an elevated rapid transit right-of-way. On admission to the emergency room, the patient was comatose in metabolic acidosis with high anion and osmolal gaps. The serum methanol was 583 mg/dL. The serum ethanol and ethylene glycol were negative. The patient was treated with ethanol, bicarbonate, and hemodialysis. He expired 40 h after admission. The postmortem methanol concentrations in body fluids were as follows: bile 175 mg/dL, vitreous humor 173 mg/dL, and blood 142 mg/dL. Urine was not available for analysis. Postmortem methanol concentrations in body tissues are given in decreasing order: brain 159 mg/100 g, kidney 130 mg/100 g, lung 127 mg/100 g, spleen 125 mg/100 g, skeletal muscle 112 mg/100 g, pancreas 109 mg/100 g, liver 107 mg/100 g, and heart 93 mg/100 g. The total amount of methanol in the gastric contents was 73 mg. Methanol determinations were performed on a Hewlett-Packard 5840A gas chromatograph with flame ionization detection using a glass column packed with 0.2% Carbowax 1500 on Carbopack C. The internal standard used was n-propyl alcohol.