PM formation of alcohol Flashcards
Can decomposing tissue produce EToh
Yes
First observed in early 1950s
Ethyl alcohol found as product of putrefaction in several cases
Could not have been from ante-mortem consumption Corry, J
However thought not to exceed 0.05g%
Is Pm etOh identical to bevarge
YES
Factors that affect rate of putrefaction
Ambient temperature
Humidity
Distribution and type of microorganisms
Microorganism
58 species of bacteria
17 species of yeasts
24 species of mold
That can produce ethyl alcohol under a variety of conditions
What is the greattedt microoragsims
Originally thought yeast Candida albicans was the primary organism, but the greatest increase observed was the result of Escherichia coli and not yeast
When can bacteria pentreate intestinal wall
Distributed through the bloodstream via the hepatic portal vein and intestinal lymph system as long as the
Body temperature exceeds 5 °C
How can microbial contamination be prevented
Refrigeration of body within 4 hours of death
Preserve specimens with 1% NaF after autopsy inhibits ethyl alcohol production by most organisms
Except C. albicans
what are some endogenous ethyl alcohol production results of microbial activity on
Glucose
Lactate
Glycerol
Amino acids
Will all microorganisms form ethyl alcohol
no
What is thje primary source of endogenous EtOH
Glucose
What tissue is high in glucose storage and the site of the greatest production
Liver
Skeletal muscles
Lungs
Heart
What is considered an ideal specimen for alcohol analysis
Vitreous humor
Why is vitreous humor ideal
Reflects antemortem ethyl alcohol concentration
Contains no glucose or microorganism
Protected from trauma and putrefaction
WHat is a poor medium for microbial ethyl alcohol
Urine except in diabetics
Case studies PM formation
12-57% of ethyl alcohol-positive cases was attributed to postmortem synthesis
Majority of cases attributed to postmortem synthesis did not have significant ethyl alcohol concentrations [<0.07 g%]
Cases with endogenous ethyl alcohol
ZUnmwalt
Evaluated for the degree of putrefaction
“SMELLBAD”
Skin slippage, mummification, changes in the eyes, marbling, state of rigor mortis [limpness], bloating, purging of fluids [appalling effusions], and discoloration
Cases with endogenous ethyl alcohol
Moorgate tube crash
London Northern City Line
Train failed to stop at the line’s end
13 hours to remove injured
42 passengers and motormen died
BAC 80 mg/dL [blood collected from kidney]
“Likely motorman was drinking”
However,
No evidence of drinking
Ante vs postmortem
History and scene, histology, blood/tissue distributn, Evaluation of chromatograpm, evaluation of ETOH metab, other volatile cmpds
Histroy and scene evidence
DUI and Evidence in car
Histology
Gross tissue and histologic evidence
Cirrhotic liver
Blood/tissue distribution
EtOH peak
Acetone peak
Evaluation of EtOH metabolites
Serotonin metabolites
Other biomarkers
Other volatile compounds
Other volatile compounds may be formed during the postmortem interval
Acetaldehyde
Acetone
Isopropanol
Butanol (1, 2, and iso-)
Volatile fatty acids
Gamma hydroxybutyric acid (GHB)
Serotonin Metabolite
Davis et al (1967) reported that the ratio of serotonin metabolites was altered by the ingestion of ethyl alcohol – remaining altered for up to 16 hours after cessation of drinking
5-hydroxyindoleacetic acid [5-HIAA]
5-hydroxytryptophol [5-HTOL]
Normally 5-HIAA is ~100 x greater than 5-HTOL
Helander et al )1992) found that when alcohol is consumed the formation of 5-HTOL is favored
Shifting the 5-HIAA:%-HTOL from 100:1 to 60:40
Evaluation of serotonin metabolites in urine will assist in the determination of whether the alcohol was from antemortem consumption or postmortem formation
Absence of alcohol ingestion
Normal HTOL/HITAA below 15 pmol/nmol [some 10 pmol/nmol]
