Biomedical subjects
S Felby
Publications and source records attributed to S Felby.
A prospective toxicology analysis in alcoholics.
A prospective and comprehensive investigation was done on 73 medico-legal autopsies in alcoholics. The results of the toxicology analyses are described. Alcohol intoxication was the cause of death in 8%, combined alcohol/drug intoxication in 15% and drugs alone in 19%. Alcoholic ketoacidosis was found to be the cause of death in 7%. Altogether toxicology analyses were necessary for determining the cause of death in 51% of the cases. In four cases the cause of death would not have been found, had this investigation not been made. It is concluded that toxicology analyses should be the rule rather than the exception in deaths in alcoholics.
Alcoholic ketoacidosis as a cause of death in forensic cases.
Forensic pathologists are familiar with alcohol abusers, who are found dead and in whom the cause of death cannot be ascertained. In order to examine the possible role of ketoacidosis for the cause of death in this group of alcohol abusers, the concentrations of ketone bodies (acetone, acetoacetate, D-beta-hydroxybutyrate) were determined in post mortem blood specimens. Determination of the ketone body concentrations were made by a coupled enzymatic head-space gas chromatographic method. The material consisted of blood specimens from 131 deceased persons and was divided into three groups: Group 1: controls, 79 cases of non alcohol abusers; group 2: 35 cases of alcohol abusers with known causes of death and group 3: 17 cases of alcohol abusers without ascertainable cause of death. The geometric means for the sum of the ketone body concentrations in blood were: controls, 109 mumol/l; alcohol abusers with known causes of death, 152 mumol/l; and alcohol abusers without known cause of death, 590 mumol/l. The limit value between the controls and the group of alcoholics with unascertainable cause of death was by logistic regression found to be 531 mumol/l (343-1224 mumol/l). The term 'ketoalcoholic death' is, therefore, suggested, when the measured post mortem blood ketone body concentration in an alcoholic with otherwise unknown cause of death exceeds 531 mumol/l.
Congener production in blood samples during preparation and storage.
The possibility of congener production in blood during storage was studied. The material consisted of 216 blood specimens in which ethanol was not detected. We divided the specimens into two groups, A and B. Group A: 97 specimens were stored at 4 degrees C until alcohol analysis, and only exposed shortly to room temperature during the aseptic preparation for analysis. Group B: 119 specimens were stored at 17 degrees C until alcohol analysis were performed, and the handling during preparation was not aseptic. All specimens were subsequently stored at 4 degrees C. After three to twelve months of storage the blood specimens were analyzed for congeners. None of the forensic important congeners (n-propanol, isobutanol, or butanol-2) were detected in Group A, whereas in Group B n-propanol was detected in fourteen of the specimens, isobutanol in sixteen, and butanol-2 in two specimens.
Determination of ketone bodies in postmortem blood by head-space gas chromatography.
A method describing determination of the physiological ketone bodies: acetone, acetoacetate, and D-beta-hydroxybutyrate in postmortem blood by head-space gas chromatography. The method involves enzymic dehydrogenation of D-beta-hydroxybutyrate into acetoacetate and quantitative conversion of acetoacetate into acetone. The recoveries of acetone, acetoacetate and D-beta-hydroxybutyrate were 94-100%, 88-104% and 83-91%, respectively.
The postmortem blood alcohol concentration and the water content.
Determination of blood alcohol concentration and water content were performed on blood specimens from 71 bodies. Two blood specimens were sampled from each body. First-specimens (short-time-specimens) were sampled from 0 to 9.6 hours postmortem, in mean 2.1 hours. Second-specimens (long-time-specimens) were sampled from 8.0 to 229.9 hours postmortem. The relation between the blood alcohol concentration and the blood water content in the two blood specimens (first and second) is described by a multiple regression equation. The equation gave as result: if the body had no signs of putrefaction, the difference in water content between the short-time-specimens and the long-time-specimens has a significant influence on the blood alcohol concentration. This was not the case if the body had visible signs of putrefaction. Then other factors influence the blood alcohol concentration more than the water content. Our study also indicates that if a blood alcohol determination is performed on whole blood, and the blood specimen was sampled shortly after death from a case of bleeding shock, a correction of the blood alcohol concentration should be done if the blood water content is higher than 82%.
Alcoholism and ketoacidosis.
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Postmortem blood alcohol concentration.
The relation between the blood alcohol concentration and the vitreous humor alcohol concentration, blood propanol-1 concentration, and the signs of putrefaction of the body was described by a multiple regression equation. The calculations showed that the blood alcohol concentration increased 0.79/1000 when the vitreous humor alcohol concentration increased 1.00/1000, and that a blood propanol-1 content and signs of putrefaction had a significant influence on the postmortem ethanol concentration. The postmortem blood alcohol concentration increased 0.01/1000 in mean when the blood propanol-1 concentration increased 1 mg/kg, and increased 0.05/1000 when the body showed sign of putrefaction. The variance of the blood alcohol concentration between blood within the same body was independent of the ethanol concentration level. The pooled standard deviation was 0.05/1000.
Histologic changes and silicone concentrations in human breast tissue surrounding silicone breast prostheses.
Using a previously developed method for quantitative measurements of silicone concentrations in breast tissue, material from 86 biopsies from 67 breasts in 55 patients who had silicone implants was examined. In the 49 breast with unruptured prostheses, there was a positive relation between the concentrations and inflammatory reactions, the only exception being the amount of plasma cells, which showed a negative relation. It is concluded that silicone prostheses provoke an inflammatory response not only because they act as foreign bodies, but also because of silicone seepage through intact membranes.
Dibenzepine and its metabolites in blood, muscle, liver, vitreous body and urine from fatal poisoning.
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Morphine concentrations in blood and organs in cases of fatal poisoning.
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Concentrations of meprobamate in the blood and liver following fatal meprobamate poisoning.
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Identification of barbiturates in blood by gas chromatography.
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Comparative studies of postmortem barbiturate and meprobamate in vitreous humor, blood and liver.
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Comparative studies of postmortem ethyl alcohol in vitreous humor, blood, and muscle.
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Morphine: its quantitative determination in nanogram amounts in small samples of whole blood by electron-capture gas chromatography.
A method for the determination of nanogram quantities of morphine in hemolyzed whole blood taken post mortem, or other blood samples of poor quality, has been developed. Morphine was extracted into ethyl acetate from blood at pH 8.7-9.0, and purified by absorption onto a column of acid aluminium oxide and elution with methanol. Nalorphine was added as an internal standard, the compounds derivatized with pentafluoropropionic acid anhydride, and the derivatives formed quantified by electron-capture gas chromatography. The recovery of morphine added to whole blood was 83%, the coefficient of variation 6.7%. The method is capable of measuring morphine concentrations of 1 ng/g in 0.1-0.2 g of post-mortem blood.
Determination of organosilicon oxide polymers in tissue by atomic absorption spectroscopy using HGA graphite furnace.
A simple method of extraction and determination of organosilicon oxide polymers (silicones) in 0.1-0.5 g of formalin fixed tissue by atomic absorption spectroscopy is described. Before the tissue is extracted with n-heptane, it is dried in a desiccator containing concentrated sulphuric acid. The graphite tubes in the HGA graphite furnace are tubes with L'vov platform. The evaporation of n-heptane and a part of the charing of the tissue extract in the tube are done in the presence of oxygen (air). The significance of the employment of L'vov platform and the presence of oxygen are discussed. The methods detection limit (2 X S.D.) is about 0.009 microgram silicon/ml tissue extract which corresponds to about 0.5 microgram polydimethylsiloxane/g tissue.