Acute cyanide (CN) poisoning leads to deterioration of body functions and often results in death. It can be accidental, suicidal, and at times homicidal. Since the historical period, CN has been the cause for several deaths, including fire accidents, industrial waste leakage, suicides of famous persons, and planned massacres. Several sources can lead to CN poisonings, such as smoke from the fire, mining and other industries, nitriles, and plants. The primary function of CN is to inhibit the cytochrome oxidase a3 enzyme due to the high binding affinity of CN to the ferric iron found in the haem moiety of the cytochrome oxidase a3 leads to uncoupling the mitochondrial oxidative phosphorylation and inhibiting the cellular respiration. Clinical signs and symptoms are primarily dose-related and range from gastrointestinal involvement to coma and death. In addition to decontaminating the poison and essential supportive treatment, effective antidotes are available. Last six years, fifteen Fatalities following CN poisoning were reported at Teaching Hospital, Jaffna. Social support and an adequate legal framework for controlling CN-containing substances could reduce the burden of cyanide toxicity.