The post-mortem relationship between beta-hydroxybutyrate (BHB), acetone and ethanol in ketoacidosis

Abstract

A reduced blood pH (ketoacidosis) from the production of β-oxidative ketone bodies as a result of alcoholism (alcoholic ketoacidosis, AKA) or diabetes (diabetic ketoacidosis, DKA) can feature in many fatalities and analytical evidence can be used to support a pathological diagnosis, or provide a possible cause of death in the absence of other pathologically significant findings. Existing beliefs concerning the relationship of BHB concentrations, acetone and ethanol have been re-examined by analysis of BHB, acetone and ethanol in over 350 fatalities grouped into alcoholics, diabetics, alcoholic diabetics, coupled with speculative cases and those with an alternative cause of death. Uniquely, the concentrations of BHB were measured in post-mortem blood, urine and vitreous humour using selective GC–MS. The results showed that existing beliefs need to be re-evaluated. Ethanol is not always low (<10 mg/dL) or absent in cases of AKA. Also, the absence of acetone does not preclude a high BHB (>250 mg/L), therefore acetone can be used as an initial marker pathologically significant ketoacidosis. For blood and urine BHB concentrations the following interpretative ranges can be used (in mg/L); normal (<50 mg/L), raised (51–249 mg/L), high and pathologically significant (>250 mg/L). Initial data suggest vitreous humour BHB could be a useful alternative in the absence of blood (same interpretative ranges may also apply). Analytical recommendation for investigation of post-mortem ketoacidosis is also presented.