Enzymatic Molecular Autopsy and Postmortem Thanatochemistry of Cyanide Poisoning: Multi-Organ Distribution, Cytochrome c Oxidase Inhibition and Manner of Death in Rabat, Morocco

Abstract

Background. Fatal cyanide poisoning causes histotoxic hypoxia through inhibition of cytochrome c oxidase, but postmortem interpretation is complicated by analyte volatility, redistribution and putrefactive artefact.

Objective. To describe multi-matrix cyanide distribution and cytochrome c oxidase inhibition in fatal cyanide poisoning and relate them to route and manner of death.

Methods. In this retrospective autopsy case series of 112 consecutive fatal cyanide poisonings in Rabat, Morocco, cyanide was quantified in six matrices by headspace gas chromatography–mass spectrometry, and cytochrome c oxidase activity was assayed in four tissues against matched controls. Peracute lethal outcome (death at the scene or within one hour) was analysed by logistic regression.

Results. Cyanide differed across matrices (F(5, 666) = 4380, p < 0.001): gastric contents 1250.0 ± 180.0, deep brain 200.5 ± 19.5 and femoral blood 100.2 ± 9.3 mg/L. Brain cyanide was highest after oral ingestion (228.1 ± 23.6 mg/L), lowest after transcutaneous absorption (105.0 ± 13.4 mg/L) and differed by manner of death (p < 0.001). Enzyme inhibition was tissue-dependent (brain 88.5 ± 5.2%, liver 45.6 ± 7.8%; p < 0.001). Brain cyanide correlated with femoral blood (r = +0.84) and enzyme inhibition (r = +0.79). Brain cyanide (adjusted OR 4.82 per 25 mg/L; 95% CI 2.56–9.08) and inhibition ≥ 75% (3.65; 1.88–7.10) independently predicted peracute lethal outcome; route did not.

Conclusion. Combining multi-organ thanatochemistry with enzymatic molecular autopsy may offer a more objective, corroborative basis for interpreting fatal cyanide poisoning, alongside scene and investigative evidence.