Typically, cyanide toxicity treatment is initiated when there is high clinical suspicion of exposure. This process prevents aerobic metabolism, which results in diffuse clinical symptoms such as dizziness, headache, weakness, and tachypnea, with progression to seizures, paralysis, and coma. Once internalized, cyanide binds to cytochrome oxidase a 3, a terminal complex in the electron transport chain. Most commonly, cyanide is inhaled from the thermal breakdown of synthetic compounds during residential or industrial fires. Exposure to cyanide ions can occur through inhalation, skin absorption, and ingestion or even through metabolism. IntroductionĬyanide has well known adverse effects, some of which are rapidly fatal, documented as early as 1679.

Here, we present two cases resulting from the same source of cyanide poisoning and the use of both antidotes separately used with differing outcomes. These treatments act on different components of cyanide’s metabolism. Presently, there are two widely accepted antidotes: sodium thiosulfate and hydroxocobalamin. Remediation of symptoms and mortality is highly dependent on quick treatment with a cyanide antidote. The symptoms are diffuse and lethal and require high clinical suspicion. Cyanide is rapidly reacting and causes arrest of aerobic metabolism.

Cyanide poisoning antidote mechanism