Asked Jan 31, 2010, 12:36 PM
The subject of this query was a 36 year old WF, H=63" W=200 lb. Death resulted from a high impact automobile collision. Death was instantaneous. The cause of death was blunt force trauma resulting in massive internal injuries including lacerations of pleural cavity, transection of descending aorta, transection of spinal cord at cervical as well as thoracic.
The autopsy was performed in a timely manner, within 15-17 hours of death. Three pathologists were involved. None reported an odor of alcohol during the prosection. There were no indications of chronic alcohol use or abuse. Personal history disclosed no alcohol abuse nor record of heavy drinking. In fact, all of the reprts indicated she drank very small amounts, infrequently and neither acquaintances or family had ever seen her intoxicated.
For the purpose of histologic examination and toxicology a blood sample was drawn from the R-chest cavity. A urine sample was obtained, also vitreous fluid, brain tissue and gastric contents. Tox testing (GCFID) disclosed a Blood Alcohol Content (BAC) of
.19 g/100ml; Urine Alcohol Content (UAC) of .25; Vitreous Alcohol Content (VAC) of .23Stomach Alcohol Content (gastric) was measured as 1.75 (each of these figures is expressed in g/100ml). The toxicologist further stated that the stomach contained 6 grams of unabsorbed alcohol (6g/350ml). I find these figures troubling. With VAC and UAC both higher than BAC would seem to indicate she was in the post-absorptive stage. Yet, this is contradicted by unabsorbed alcohol in the stomach. Second, the nature and extent of the injuries contraindicate central cavity blood sampling and particularly from pooled blood. Third, if the SAC reading is accurate, postmortem redistribution almost certainly contaminated the blood from which the sample was extracted.
Same case, another issue. THC and metabolites were found in blood and urine. Quantities as follows: THC, blood = 113 ng/ml; 11-OH-THC, blood = 5.6 ng/ml; THC-COOH, blood = 59 ng/ml; urine = 1638. I believe that the high level of THC in the blood had no effect on the high count in urine. Decedent was known to have used marijuana on a regular basis. I.e. In the evenings after she put the children to bed. Frequency of use is unknown. Given periodic use it would seem the urine count could be explained by the cumulative nature of THC and it's known system retention. Please correct if erroneous.
Given what is known of THC storage in adipose tissue, slow release (light bonding), I question if the high blood count 113 might be attributable to postmortem release from adipose tissue. I believe there are cased where panic situations catalyzed such activity. Could it be that her system was flooded with THC as a consequence of panic (the accident) and as a postmortem artifact (release from fatty tissue)? (Please recall R-chest cavity sample site). While liver sample was forwarded for tox it was not tested. The toxicologist without explanation chose not to do hair analysis.
Adding to this dilemma is the fact that there was no indication of alcohol or marijuana use found at the accident site. The decedent was seen by several people within two hours of the time of the accident and described as normal, steady and manifesting no discernble signs of intoxication.
The elements of the case do not blend with postmortem synthesis of ethanol. Too much alcohol, too short a period of time. I believe the pathologists, consequently the toxicologist, failed to consider redistribution, but ethanol can't be redistributed unless it's present. The time element(s) of this case strongly argue against the accuracy of the BAC, as does redistribution, but the VAC is generally protected from that factor and measured.