A cardiac blood GHB concentration above 50 mg/L does not, by itself, establish ingestion before death. Kintz and colleagues found 14 such results in a 71-autopsy series selected because the case investigations did not support GHB exposure. The study supports examining additional specimens, while leaving important limits on how confidently exposure can be excluded.
How the 71 cases were investigated
The 2004 study examined cardiac whole blood from 71 autopsies performed 12–72 hours after death. Pathologists assessed the circumstances and police records and considered GHB exposure excluded. This was a case-history classification, not a controlled experiment with independently verified lifetime nonexposure.
Specimens had no preservative, were refrigerated at 4°C and were analyzed within 48 hours after autopsy. Consequently, the findings reflect both the interval before collection and the subsequent handling conditions; the study did not experimentally separate formation in the body from formation in the specimen container.
GHB was measured using derivatization and GC–MS with deuterated GHB as the internal standard. The reported linear range was 1–200 mg/L and the quantification limit was 1 mg/L. The article reports some results below that quantification limit and others above the stated linear range, without detailing the handling of every out-of-range result. Its full reported cardiac range, 0.4–409 mg/L, should be read with those analytical limitations in view.
What happened above 50 mg/L?
Fourteen cardiac specimens exceeded 50 mg/L, with reported values of 50.8–409 mg/L. The authors interpreted these elevations as compatible with postmortem formation because the investigations supplied no evidence supporting intake. That interpretation is evidence against treating 50 mg/L as an automatic exposure rule; it does not prove the biochemical origin of every molecule in every case.
Other matrices were tested when available in these high-cardiac-result cases. They were not systematically tested across all 71 autopsies. Femoral blood was available in five, vitreous humor in six and bile in seven. These small, selected comparisons cannot establish population-wide diagnostic sensitivity or specificity.
Femoral blood, vitreous and bile gave different information
In one paired case, cardiac blood measured 96.6 mg/L while femoral blood measured 17.1 mg/L. In another, cardiac blood was 50.8 mg/L, femoral blood 39.7 mg/L and vitreous humor 10.8 mg/L. These are concentrations measured in separate specimens, not interchangeable estimates of one circulating concentration.
The six vitreous results ranged from 3.9 to 21.4 mg/L. By comparison, bile ranged from 6.1 to 238 mg/L in its seven paired cases. Because bile could also contain substantial GHB, the authors did not consider it a useful discriminator in this series. Femoral blood and particularly vitreous were more informative complements to cardiac blood under the studied conditions.
Obtaining another matrix provides biological corroboration. It is not the same step as confirming a presumptive immunoassay screen: these findings came from a quantitative GC–MS procedure. Even an analytically identified and quantified substance may have an uncertain source.
What a defensible interpretation should address
The collection site should appear beside the concentration. Reviewers should also examine the death-to-autopsy interval, refrigeration, preservative, analysis timing, availability of paired specimens and independent evidence of intake. An elevated cardiac result can justify further investigation without establishing ingestion, impairment or a contribution to death.
The study’s limited paired sample sizes and history-based exposure classification prevent a universal rule that a low femoral or vitreous result excludes intake. Conversely, its findings undermine the claim that a cardiac result above 50 mg/L necessarily proves it.
For the separate issue of change after collection, see GHB increases in stored postmortem blood.
Primary source
Kintz P, Villain M, Cirimele V, Ludes B. GHB in postmortem toxicology: Discrimination between endogenous production from exposure using multiple specimens. Forensic Science International. 2004;143:177–181. doi:10.1016/j.forsciint.2004.02.036.
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