CP29 Thiocyanate Toxicity

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CP29 Thiocyanate Toxicity

Administer a cyanide antidote if the diagnosis of cyanide toxicity is strongly suspected, without waiting for laboratory confirmation. Available antidotes are hydroxocobalamin (Cyanokit) and sodium thiosulfate and sodium nitrite (Nithiodote). Both are given intravenously.

Patients who present with more than minimal symptoms that resolve without treatment should be admitted for observation and supportive care. In patients with acute poisoning from hydrogen cyanide (HCN) gas or soluble salts, the principal acute care concerns are hemodynamic instability and cerebral edema. The continuous cardiac monitoring, respiratory and cardiovascular support, and frequent neurologic evaluation these patients require is generally best provided in an intensive care unit.

Conversely, acute poisoning from cyanogens (nitriles) or poorly soluble salts may not manifest or become life-threatening for several hours after exposure. These patients require a 24-hour observation period.[24, 25]

Oxygenation should be optimized and continuous cardiac monitoring provided. Depending on the severity of symptoms, endotracheal intubation may be necessary to optimize oxygen delivery and protect the airway. Serum lactate concentrations, chemistries, and arterial or venous blood gases should be monitored.

Patients should be reevaluated 7-10 days after discharge from the hospital.[26]Delayed onset of Parkinson-like syndrome or neuropsychiatric sequelae may be noted on followup.

Special concerns in pregnancy

Fetal demise is possible in cyanide poisoning. Aggressive support and antidotal treatment of the mother is paramount. An obstetric evaluation following stabilization of the mother is essential. Therapeutic abortion may be indicated in the presence of fetal demise.

Cyanide Antidotes

Antidotes to cyanide include hydroxocobalamin and sodium nitrite and sodium thiosulfate. Sodium thiosulfate may be given in combination with sodium nitrite or hydroxocobalamin, or may be given alone. These agents are administered intravenously.


Hydroxocobalamin, which is considered the drug of choice in continental Europe and Australia, is approved by the US Food and Drug Administration (FDA) for treating known or suspected cyanide poisoning.[28, 29] Coadministration of sodium thiosulfate (through a separate line or sequentially) has been suggested to have a synergistic effect on detoxification.

Hydroxocobalamin combines with cyanide to form cyanocobalamin (vitamin B-12), which is renally cleared.[30] Alternatively, cyanocobalamin may dissociate from cyanide at a slow enough rate to allow for cyanide detoxification by the mitochondrial enzyme rhodanese.

A review by Hall et al notes that hydroxocobalamin has not been associated with clinically significant toxicity in antidotal doses compared with other cyanide antidotes. Hydroxocobalamin has a rapid onset of action, neutralizes cyanide without interfering with cellular oxygen use, is conducive to prehospital use due to its tolerability and safety profiles, and is safe for use in patients with smoke inhalation.[31]

Adverse effects of hydroxocobalamin administration include transient hypertension (a benefit in hypotensive patients), reddish brown skin, mucous membrane and urine discoloration, and rare anaphylaxis and anaphylactoid reactions. Because of its bright red color, it also interferes with co-oximetry (about a 5% increase in carboxyhemoglobin levels) and blood chemistry testing (bilirubin, creatinine kinase and possibly liver enzymes, creatinine, phosphorus, glucose, magnesium, and iron levels).[32] It can also interfere with hemodialysis.[33]

Certain medications should not be administered simultaneously or through the same line as hydroxocobalamin. These include diazepam, dopamine, dobutamine, and sodium thiosulfate.

Sodium nitrite and sodium thiosulfate

Sodium nitrite and sodium thiosulfate are often used in combination and are currently considered second-line therapy after hydroxocobalamin. Sodium nitrite is rapidly effective but can cause life-threatening toxicity, whereas sodium thiosulfate has a somewhat delayed effect but is far safer.

Sodium nitrite induces methemoglobin in red blood cells, which combines with cyanide, thus releasing cytochrome oxidase enzyme. Sodium thiosulfate donates a sulfur atom necessary for the transformation of cyanide to thiocyanate by rhodanese, thus increasing the activity of the endogenous detoxification system. The thiocyanate is then renally excreted.

Sodium nitrite should not be used in patients with smoke inhalation unless their carboxyhemoglobin concentration is very low (< 10%). The induction of methemoglobinemia by sodium nitrite compounds the effect of any existing carboxyhemoglobinemia, significantly reduces the oxygen-carrying capacity of blood. In addition, vasodilation from sodium nitrite may result in significant hypotension and cardiovascular collapse.[27]

Appropriate dosing of sodium nitrite has not been established in children. Consequently, these patients are at increased risk for excessive methemoglobinemia, hypotension, or both.

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