It is frequently important in deciding the cause of death to be able to determine chemical abnormalities which may have existed prior to demise. This is particularly true in cases where clinical history suggests the possibility of such chemical abnormalities, but opportunity for autopsy does not exist. Even when a postmortem examination is done, determination of chemical abnormalities may help establish the cause of death where the autospy findings are inconclusive or may validate the significance of recognizable organ changes. For this reason rather extensive studies have been made in the postmortem chemistry of blood. It has been found that abnormalities in concentrations of protein, calcium, urea nitrogen, creatinine, and bilirubin can be evaluated by study of the serum prior to the onset of intravascular hemolysis. Unfortunately there are many constituents in which postmortem changes occur rapidly and erratically so that extrapolation to probable antemortem values becomes impossible. Serum sodium and chloride concentrations begin to fall soon after death, but the rate of fall varies so markedly from individual to individual that it is impossible to detect electrolyte imbalance except in extreme cases and when the blood has been obtained very soon postmortem. Serum glucose will ordinarily decrease in the left heart and extremital vessels due to continued utilization by the red cells after death, but may be markedly elevated in cases where death results from asphyxia or is accompanied by a large output of epinephrine terminally. Glucose concentrations in blood obtained from the right heart or inferior vena cava frequently are found markedly elevated due to glycogenolysis in the liver but may be low in cases of starvation.
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