Cyanide poisoning: pathophysiology and treatment recommendations

Abstract

This paper aims to assess and compare currently available antidotes for cyanide poisoning. Such evaluation, however, is difficult. Thus, extrapolation from the results of animal studies has potential pitfalls, as significant inter-species differences in response may exist, and these experiments often involve administration of toxin and antidote almost simultaneously, rather than incorporating a more realistic time delay before initiation of treatment. Direct inference from human case reports is also problematic; either because of uncertainties over the exposure levels involved (and hence the likely outcome without treatment), or because of difficulties in identifying the specific contribution of a particular antidote within the overall treatment regimen. Certainly an effort to compare the relative efficacy of cyanide antidotes produces equivocal findings, with no single regimen clearly standing out. Indeed, factors such as the risks of antidote toxicity to various individuals and other practical issues, may be more important considerations. There is therefore no single treatment regimen which is best for all situations. Besides individual risk factors for antidote toxicity, the nature of the exposure and hence its likely severity, the evolving clinical features and the number of persons involved and their proximity to hospital facilities, all need to be considered. Clinically mild poisoning may be treated by rest, oxygen and amyl nitrite. Intravenous antidotes are indicated for moderate poisoning. Where the diagnosis is uncertain, sodium thiosulphate may be the first choice. With severe poisoning, an additional agent is required. Given the various risks with methaemoglobin formers or with unselective use of kelocyanor, hydroxocobalamin may be preferred from a purely risk-benefit perspective. However the former alternatives will likely remain important.

Criteria for Safe Use of Plant Ingredients in Diets for Aquacultured Fish

“…The result is cessation of cellular respiration causing cytotoxic hypoxia and tissue anoxia and a reactive shift from aerobic to anaerobic metabolism. Respiratory arrest due to the depression of the central nervous system by a combination of cytotoxic hypoxia and lactic acidosis is the cause of death (Eisler, 1991;Beasley and Glass, 1998). Effects on the circulatory system are also postulated as significant contributors to fatalities, especially in severe poisoning, manifesting as reduced cardiac output and cardiac shock in extreme cases, pulmonary oedema and possibly release and detrimental activity of biogenic amines (Beasley and Glass, 1998).…”

A Review of Cyanogenic Glycosides in Edible Plants

“…Cyanide toxicity occurs when cytochrome oxidase a 3 inhibits the terminal enzyme in the respiratory chain and halts electron transport and oxidative phosphorylation (which is essential to the synthesis of adenosine triphosphate ("TP) and the continuation of cellular respiration) [48,49]. Cyanide poisoning occurs as a result of consumption of biter cassava, almond kernels, or apricot kernels and their products without proper processing.…”

Pathological effects of acetone cyanohydrin in swiss rats

“…These factors include: (i) the inability of hemoglobin to carry O 2 owing to the high affinity of cyanide to the ferric ion of heme, leading to tissue hypoxia (Hamel, 2011) and (ii) metabolic acidosis caused by high lactate concentrations that results in the inactivation of cytochrome oxidase a3 (Beasley;Glass, 1998). Inhibition of the respiratory chain (Sornyotha;Kyu;Ratanakhanokchai, 2010;Shama;Wasma, 2011) compromises ATP production and proper functioning of the calcium pump, leading to an imbalance in Ca ++ concentrations in the intra-and extracellular spaces.…”