Some biochemical changes induced by cyanide intoxication during smoke inhalation

ABSTRACT

Cyanide poisoning is a major factor that contributes to death due to smoke inhalation. The aim of the current study is to explore the postmortem stability of cyanide concentration in blood and tissues of fire victims and to evaluate the relation between glucose, lactate, anion gap and acute cyanide poisoning in smoke inhalation. For this purpose 30 rats exposed to combustion products cotaining HCN for 1hour were used as the animal model. Biochemical data were obtained by measuring cyanide [CN-] concentration, carboxyhemoglobin [COHb] saturation, glucose, lactate, and anion gap levels in dead rats and living ones before and after treatment as well as by measuring CN -, COHb and lactate in fire victims specimens. Results showed a slight reduction in COHb saturation and a significant decrease in cyanide concentration in postmortem blood and tissues of rats during 24 hours to 3 days when left at 25-30C compared to zero time. There was a differential disposition of inhaled HCN, with the highest tissue levels found in the lung, brain, liver and spleen in decreasing order. Postmortem lactate [blood, lung, brain, and liver] of rats was elevated with respect to time and temperature with disappearance of glucose. From stability data, it was suggested that about 50% and 100% of the original blood cyanide disappeared during 24 hours and 3 days respectively, while about 14% remained in lung and brain at 3rd day. On the other hand, results revealed the close correlation between anion gap, lactic acidosis and whole blood cyanide levels in smoke inhalation-induced cyanide poisoning. The serial blood lactate measurements are useful in predicting survival in fire victims with severe smoke inhalation