Cyanide poisoning can present in multiple ways, given its widespread industrial use, presence in combustion
products, multiple physical forms, and chemical structures. The primary target of toxicity is mitochondrial cytochrome
oxidase. The onset and severity of poisoning depend on the route, dose, physicochemical structure and other variables.
Common poisoning features include dyspnea, altered respiratory patterns, abnormal vital signs, altered mental status, seizures,
and lactic acidosis. Our present knowledge supports cyanide poisoning treatment based on excellent supportive care
with adjunctive antidotal therapy. Multiple antidotes exist and vary in regional availability. All currently marketed antidotes
appear to be effective. Antidotal mechanisms include chelation, formation of stable, less toxic complexes, methemoglobin
induction, and sulfane sulfur supplementation for detoxification by endogenous rhodanese. Each antidote has
advantages and disadvantages. For example, hydroxocobalamin is safer than the methemoglobin inducers in patients with
smoke inhalation. Research for new, safer and more effective cyanide antidotes continues.
Keywords: Cyanides, antidotes, poisoning, amyl nitrite, cobinamide, edetic acid (dicobalt edetate), 4-dimethylaminophenol,
hydroxocobalamin, hydroxyacetone phosphate, sodium nitrite, sodium thiosulfate, thiosulfate sulfurtransferase, chemical structures, Multiple antidotes, physicochemical structure.
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