Important sources of exposure in veterinary medicine include rumen contents of grazing animals that have consumed or been poisoned with plant cyanogenic glycosides (eg, during necropsy/sample collection procedures), handling or exposure to cyanide vertebrate pesticide agents (or animals poisoned by them), and combustion sources (particularly of nitrogen-containing materials such as plastics, wool, silk). Aqueous solutions of cyanide are commonly referred to as prussic acid, and hydrocyanic acid and formonitrile are commonly used synonyms. (Also see Cyanide Poisoning.)
Solutions of hydrogen cyanide are colorless or pale-blue liquid at room temperature. Cyanide is very volatile and highly toxic, and flammable/explosive concentrations can rapidly develop at normal temperatures and pressures, especially in enclosed spaces.
Hydrogen cyanide gas has a distinctive, bitter almond smell; however, the ability of people to detect the odor is genetically determined. Anosmic individuals (20%-40% of the human population) are not able to detect it. Accordingly, odor detection cannot be relied on in terms of detection and warning in relation to exposure. The wearing of cyanide detection devices and/or testing of breathing air with a Drӓger tube apparatus or similar test method is strongly recommended before entry into any environment where cyanide might be present.
The major potential route of workplace exposure in veterinary medicine is by inhalation. Substantial skin absorption can occur if the atmospheric concentration is high or if the skin comes into contact with cyanide solutions. High ambient temperatures and high humidity appear to increase skin absorption. Skin or clothing contamination with cyanide-containing materials can result in off-gassing of cyanide vapor and inhalation. Exposure by any route can cause systemic toxicity. Cyanide is also a skin and eye irritant. Children are more susceptible to poisoning because of their higher minute ventilation per kg.
Significant cyanide exposures result in death within a few minutes because of the arrest of mitochondrial oxidative phosphorylation, histotoxic hypoxia, and severe metabolic acidosis, which results in rapid onset CNS, cardiovascular, and respiratory effects. CNS signs and symptoms in people develop very quickly and are nonspecific: excitement, dizziness, nausea, vomiting, headache, and weakness, which progresses to drowsiness, tetanic spasm, lockjaw, convulsions, hallucinations, loss of consciousness, and terminal coma. Cardiovascular signs include arrhythmias and intractable hypotension. Respiratory signs typically include shortness of breath and chest tightness, rapid breathing and increased depth of respirations progressing to agonal respiration. Pulmonary edema and cyanosis of the skin may or may not be present. Severe, intractable anion-gap metabolic acidosis due to lactic acidosis typically develops rapidly. Cyanide poisoning survivors usually develop some form of hypoxic brain damage, and this can be associated with personality changes, memory deficits, disturbances in voluntary muscle movements, and appearance of involuntary movements (extrapyramidal syndromes).
Victims exposed only to hydrogen cyanide gas do not pose secondary contamination risks to rescuers, but resuscitation without a barrier should not be attempted. Victims whose clothing or skin is contaminated with hydrogen cyanide liquid or solution can secondarily contaminate response personnel by direct contact or through off-gassing vapor. Dermal contact with cyanide-contaminated victims or with gastric contents of victims who may have ingested cyanide-containing materials should be avoided.
Veterinarians poisoned by cyanide require speedy treatment, rapid administration of antidotes, and specialist care. Great care should be taken by rescuers who plan to enter a contamination “hot zone.” Many human casualties have occurred because of well-intentioned but misguided attempts at rescue from hydrogen cyanide–contaminated hot zones. Rescue and emergency treatment is best left to those with specialized training in these areas.
Last full review/revision December 2014 by Rhian B. Cope, BVSC, PhD, DABT, ERT, FACTRA