Treatment of cyanide toxicity should be initiated as soon as it is suspected; do not delay treatment while awaiting formal diagnosis by blood cyanide levels. Primarily, treatment is aimed at uncoupling cyanide from cytochrome oxidase, and allowing cells to return to aerobic metabolism via oxidative phosphorylation.
Patients who present with possible exposure (including iatrogenic exposure from the cyanogen sodium nitroprusside) who are found to have progressive or severe metabolic acidosis and elevated lactate should be treated presumptively. Monitoring must be initiated, as well as good IV access and fluid administration begun to aid in resuscitation. 100% O2 via facemask, or ETT if intubation is indicated, though theoretically useless has potentially been helpful in some cases.
Hydroxocobalamin: combines with cyanide, forming cyanocobalamin (vitamin B12), which is renally excreted; few side effects, well-tolerated by critically ill
Amyl nitrite: inhaled formulation, rapidly enters circulation generating methemoglobin which has higher affinity for CN than cytochrome oxidase
Sodium Nitrite: slower onset, longer lasting nitrite, as above frees up cytochrome oxidase to resume aerobic metabolism
Sodium Thiosulfate: regenerates sulfur-dependant rhodanese activity; this enzyme converts CN to thiocyanate, which is renally excreted; recommended co-administration with hydroxocobalamin or nitrites, especially in prolonged exposures
In addition to using antidotes, it is incumbent upon the provider to treat the associated abnormalities and symptoms of toxicity. Be prepared to treat with anticonvulsants, vasopressors and alkalinizing agents in addition to standard supportive measures.