GHB Interpretation Issues and Post-mortem Production

Animal and human studies have demonstrated that endogenous GHB concentrations can rise post-mortem and under inappropriate specimen storage conditions. Doherty et al. (1978) observed an increase in the GHB concentrations in brain specimens after 6 h with a further increase if the specimens were left at room temperature. Snead et al. (1981) also observed an increase in GHB concentrations in CSF after 12 h of storage at room temperature. It was 

Another source of post-mortem GHB production is putrescine (1,4-butanediamine), a biogenic polyamine initially detected in decaying animal tissues, but now known to be present in all cells, both eukaryotic and prokaryotic, where it is important for cell 

Data from analyses of multiple specimens and a good case history can help tremendously, especially if litigation is involved. For example, in a case that involved the death of a young girl and GHB, a post-mortem blood GHB concentration of 15 pg mL was demonstrated. This concentration is in the range of post-mortem GHB production. However, a detailed case history plus a post-mortem urine GHB concentration of 150 pg mt, an ante-mortem blood concentration of 510 pg mL , an ante-mortem urine concentration of 2300 pg mL and the lack of any other significant autopsy findings made the cause of death an obvious GHB fatality. The decedent had a 14-h survival time in the hospital prior to death, which explains the low post-mortem blood GHB concentration (Marinetti et al., 2000). A second GHB fatality showed a heart blood concentration of 66 pg/mL, a femoral blood concentration of 77 pg/mL, an eye fluid concentration of 85 pg/mL and a urine concentration of 1260 pg/mL. This individual had an extensive history of chronic GHB use and no other cause of death (Marinetti et al., 2000). 

---