Ethanol
Although ethanol is a common and relatively well-understood intoxicant, interpretation of postmortem results can be complex. Ethanol can be formed by postmortem fermentation, degraded by bacterial action and redistributed within the body through trauma and other processes. The postmortem formation of ethanol in the blood, urine and tissues has been well described (Corry 1978). Under appropriate conditions ethanol can be formed in concentrations up to, and exceeding, those set as the statutory limit for driving a motor vehicle in many countries (e.g. 50–100 mg/100 mL blood). What is poorly understood is that concentrations as high as 200–400 mg/100 mL can be formed in exceptional circumstances (Harper and Corry 1988). Conversely, ethanol can also serve as a substrate for many microorganisms such that ethanol concentrations in blood and tissues may initially increase and later decrease. There is no known correlation between the degree of putrefaction of a specimen and the production of postmortem ethanol. Many severely decomposed specimens may contain no ethanol at all, whereas others that appearless severely decomposed may contain concentrations of 80 mg/100 mL or higher. Other factors can also cause ethanol to be present in postmortem blood as an artefact. It has been demonstrated that when the stomach contains a sufficiently large amount of ethanol, the ethanol may diffuse through the stomach wall and diaphragm and eventually enter into the heart and central blood vessels (Backer et al. 1980; Pounder and Smith 1995; Iwasaki et al. 1998). Severe trauma, sufficient to rupture the stomach and diaphragm, may allow gastric contents to pass into the chest cavity. In such cases it may be difficult to obtain blood from the usual peripheral vessels. The presence of a small amount of beer or wine, such as might be left after a single drink with lunch, could produce an enormously elevated, but artefactual chest blood ethanol concentration. Another mechanism by which blood alcohol may be elevated is the agonal, or postmortem, movement of gastric contents into the trachea and lungs (Pounder and Yonemitsu 1991). This can lead to elevated blood ethanol concentrations in the major central pulmonary and cardiac vessels and subsequently to erroneous interpretation.
For these reasons, analysis of a second alternative specimen in postmortem cases is recommended. Vitreous humour is the specimen of choice because it remains sterile for a period of days after death and therefore postmortem fermentation does not take place. Only in the case of very severe putrefaction, in which the eye dries out and little fluid is available, is a slight increase in ethanol concentration seen, but the extent of this effect is rarely, if ever, above 20 mg/100 mL (Zumwalt et al. 1982). Although an equilibrium between ethanol in the vitreous humour and blood is attained quickly, there may be a lag period during absorption when the vitreous ethanol concentration is slightly lower than that in the blood (Fernandez et al. 1989). After equilibrium has been attained, the concentration of ethanol in vitreous humour is about 1.15 times higher than that in blood. This is because ethanol is distributed in the body according to water content and, while vitreous humour contains more than 98% water, whole blood contains on average approximately 85–88% water. Cerebrospinal fluid may be similarly useful, but is more difficult to collect and therefore is less often available for analysis than vitreous humour.
Urine is also a useful fluid for the corroboration of ethanol concentrations in blood. Although concentrations of ethanol in urine average about 1.3 times those in blood, there is considerable variability. Urine is a waste fluid stored in the bladder and, once formed, is largely unaffected by the circulating blood ethanol concentration, unlike ethanol in vitreous humour, which is in equilibrium with the circulating blood. Ethanol can be present in urine and not in blood if sufficient time has elapsed between its consumption and death to allow for clearance from the blood into the bladder. Ethanol can also be detected in urine (sometimes at high concentrations) but not in blood if the donor is a poorly controlled diabetic and if high concentrations of glucose are present. The coexistence of a urinary tract infection (yeast or bacterial) can allow considerable in vitro post mortem fermentation to occur in the bladder (Alexander et al. 1988). It is virtually impossible to have significant concentrations of ethanol in blood but not in the urine, except as an artefact caused by postmortem fermentation or contamination. The only other exception is where the bladder has been irrigated with warm saline in an attempt to warm a hypothermia victim. Other postmortem specimens are less useful for ethanol measurement. Bile ethanol concentrations are roughly comparable to those in blood for uncontaminated specimens (Winek et al.1983). However, because of the proximity of the gallbladder to the stomach and liver, bile is of little value where postmortem fermentation or postmortem diffusion are of concern. Similarly, liver and other tissues can undergo postmortem fermentation when bacteria are present. In relatively fresh postmortem tissue, concentrations of ethanol are approximately 50–85% of the corresponding blood concentrations, because of the lower water content of solid tissues. The average liver: blood ratio for alcohol is approximately 0.6 (Jenkins et al. 1995). During metabolism, a small percentage of ethanol is converted to ethyl glucuronide and ethyl sulfate . These substances are not known to be formed post mortem (Kugelberg and Jones 2007; Høiseth et. al., 2007) and hence finding them in postmortem samples may give an indication of recent ethanol intake before death. Interpretation will depend upon the body fluids, tissues or other specimens in which these substances are found.
