Elevated Methemoglobin Levels in a Patient Treated with Hydroxocobalamin After Suspected Cyanide Exposure.

Abstract

Cyanide (CN) toxicity commonly occurs during enclosed-space fires. Historically, the first step in treating CN toxicity utilized amyl nitrite and sodium nitrite to induce methemoglobinemia, which can be dangerous in this population. Hydroxocobalamin (OHCob), which binds to CN to form the nontoxic metabolite cyanocobalamin, is now the first-line antidote for CN toxicity, and has the advantage of not inducing methemoglobinemia. A 62-year-old man presented to the Emergency Department (ED) after a house fire. He was intubated for respiratory distress and hypoxia with an initial carboxyhemoglobin of 1.3%, methemoglobin 0.3%, and anion gap 19. Eleven hours after presentation, his serum lactic acid was 9mmol/L. Given his continued deterioration, 14h after arrival he received OHCob 5g i.v. for presumed CN toxicity. Methemoglobin concentration 4min prior to OHCob administration was 0.7%, and 2h after administration was 4.2%. This subsequently increased to 14.3% (16h after OHCob administration) and peaked at 16.3% (47h after OHCob administration), at which time he was administered a dose of methylene blue 50mg i.v., 60h after ED arrival. His methemoglobin concentrations fluctuated until a consistent downward trend starting at 92h from ED arrival. He continued to deteriorate and expired on hospital day 5 with a methemoglobin concentration of approximately 6.0%. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: CN toxicity requires immediate recognition and treatment. The antidote, OHCob, is believed to not induce methemoglobinemia. However, this potential side effect must be considered by emergency physicians when treating suspected CN toxicity, especially if the patient does not improve after antidotal therapy.