The analysis of physiological chemical constituents of the body, as opposed to toxic substances, is often useful in investigating deaths from metabolic and biochemical disturbances.
Unfortunately, the concentration of many natural chem- ical substances in the dead body is rapidly distorted by post-mortem autolysis. Cell membranes become permeable to small molecules soon after the cells suffer ischaemic or anoxic damage, and agonal changes themselves may grossly alter the biochemical environment, even in the few minutes of the dying process. Thus both terminal and early post- mortem changes may render many of the analyses that are commonplace in clinical practice of little value – and indeed, quite misleading – when applied to body fluids obtained at autopsy. Some substances are more stable, how- ever, and when results are carefully interpreted, consider- able information can be obtained. Urea and creatinine are stable post-mortem, with little variation even up to 100 hours after death, so the diagnosis of ante-mortem nitrogen retention is quite reliable. The normal urea nitrogen range found in post-mortem serum is from 4.9 to 5.5mmol/l, creatine being from about 70.7 to 212.2 mol/l.
In the context of post-mortem chemistry the work of John Coe is best known in forensic pathology and his writ- ings should be consulted for detailed information. Another very useful source is Madea, especially for vitreous fluid.
The vitreous humour is much to be preferred to blood for post-mortem chemical analyses. Although still influenced by temperature changes, the vitreous is far less contam- inated by body autolysis and is remote from the large organs and blood vessels of the abdominothoracic cavity.
There is a large body of literature on vitreous potassium, much of it centred around the controversy over the in vivo concentration of potassium, which can naturally rarely be measured directly in healthy persons, and the slope of the regression graph for relating potassium levels with post- mortem interval.
After death, intracellular potassium leaches from the retina through the now permeable cell membranes, into the vitreous body, naturally with an uneven distribution depending on the distance from the wall of eyeball (which is why all or a substantial proportion of the fluid should be withdrawn for analysis, to obtain a mean level). If frag- ments of retina are aspirated by the syringe, due to excessive suction, then a falsely elevated potassium measurement will be obtained.
Differences in the recommended regression gradient are observed between various workers: Madea states that 0.19mmol/l/hour should be used, whereas Sturner claims 0.14 is preferable. The literature should be consulted for details (as in the 2002 book by Hennsge et al.); it is also pertinent to note that the methods of analysis can make a difference to the calculations. Generally speaking, the vitre- ous potassium method is of most use after the first 24–36 hours, when other methods have ceased to have applica- tion. Although the errors are great, some information can be derived for up to 100 hours post-mortem.
Caution must be used when interpreting results, as different analytical techniques provide different values. For instance, in relation to electrolytes, Coe and Apple (1985) state that flame photometric methods yield values about 5mmol/l less for sodium, 7mmol/l less for potassium and 10mmol/l less for chloride, compared with more modern specific electrode methods. Electrolyte concentration dif- ferences between left and right vitreous humor samples were studied by Pounder et al.(1998) in 200 medico-legal autopsies using an ion-specific electrode system. Between- eye concentration differences of sodium and chloride were tolerable using this methodology, whereas differences in potassium, even in biochemically nonputrefied cases (potassium15mmol/l), were 0–2.34 mmol/l (0–21.8 per cent of mean) averaging 0.37mmol/l (3.3 per cent), thus undermining the usefulness of vitreous potassium in esti- mation of time of death.
In relation to other vitreous electrolytes, the concentra- tion of sodium and chlorides decrease after death, while potassium rises. The latter can be used as a check on the reliability of the others, as if potassium is15mmol/l, then the sodium and chloride concentrations may be acceptable.
Chlorides decrease at less than 1 mmol/l/h and sodium by about 0.9mmol/l/h, so the loss of this and sodium is insignificant in the first few hours, differing from potassium, which rises appreciably.
Post-mortem chemistry
With the analysis of glucose in autopsy material, five different methods yielded five different results, presumably because interfering substances were included in varying amounts.
Returning to vitreous electrolytes, in mmol/l measured by flame photometry (in mmol/l), sodium155, chloride 135 and urea40 is a reliable indication of ante-mortem dehydration. When sodium and chloride are normal but the urea exceeds 150, a diagnosis of uraemia is acceptable.
These values can be distinguished from post-mortem decomposition, in which sodium is130, chloride105 and potassium20.
In relation to glucose, a common problem is the autopsy diagnosis of uncontrolled diabetes and of hypoglycaemia. The vitreous glucose usually falls after death and can reach zero within a few hours. In 6000 analyses, Coe (1973) found that a vitreous glucose of more than 11.1 mmol/l was an invariable indicator of diabetes mellitus. The agonal or post-mortem rise in blood sugar is not reflected in the vitreous concentrations.
In relation to hypoglycaemia, a vitreous glucose of less than 1.4 mmol/l was taken by Sturner et al.(1972) to be an indica- tion of a low ante-mortem blood sugar, but others feel that whatever the concentration, no reliable interpretation can be made. In hypothermia there is also an elevated vitreous glucose, but never greater than 11.1 mmol/l.
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