Treatment

The mainstay of treatment is antidote therapy with hydroxocobalamin. Attention to supportive care is a critical part of the resuscitation. Airway management, intravenous access, and cardiac monitoring can support a cyanide-poisoned patient. Supplemental oxygen is beneficial and may enhance antidote efficacy and promote cyanide respiratory excretion along with other metabolic processes. Historically, cyanide was treated with the cyanide antidote kit consisting of amyl nitrite, sodium nitrite, and sodium thiosulfate. The nitrites induce methemoglobinemia, as a side effect which may be detrimental in a patient with concomitant trauma. The preferred antidote is now hydroxocobalamin (Cyanokit ®). However, if hydroxocobalamin is not available, the cyanide antidote kit can be used. An inhaled ampule of amyl nitrite can be a temporizing measure until IV/IO access is established.

Hydroxocobalamin (vitamin B12a) acts as a chelating agent and binds with cyanide to form cyanocobalamin (vitamin B12). The dose of hydroxocobalamin for cyanide toxicity is much higher than the dose used for other therapeutic indications, therefore the commercially prepared hydroxocobalamin is needed to get the optimal dose without volume overload: 5gm IV (70mg/kg in pediatric patients) over 15 minutes. The dose can be repeated for severe toxicity or inadequate response to the initial dose. It is as effective as epinephrine in the setting of cardiac arrest from cyanide. It may cause a red discoloration of the skin and urine that persists for several weeks. Other side effects are mild. The decision to administer hydroxocobalamin within the hot or warm zone has to be weighed against the tactical risk of stopping to gain IV or IO access and establishing the infusion.

Other treatment regimens as well as prophylactic measures have been explored in the literature and are summarized in the table below.