A 40-year-old man is unresponsive on arrival after having been found at a house fire. He is unconscious, hypotensive, and tachycardic with agonal respirations. You quickly secure the airway while the nurse establishes two large-bore intravenous lines. After placing the patient on 100% oxygen, you send an arterial blood gas: pH 7.01, Pco2 21, Po2 575, COHb level 20%, and blood lactate 12 mmol/L. You should now administer:
Intravenous sodium thiosulfate.
Inhaled amyl nitrate.
Intravenous methylene blue.
This patient needs to be emergently treated for cyanide toxicity. Cyanide poisoning can occur during a house fire secondary to combustion of materials such as silk, wool, and polyurethane. A lactate greater than 10 mmol/L in a patient who has been exposed to a fire is highly suggestive of concomitant cyanide poisoning. There are three steps in using the cyanide kit commonly found in United States emergency departments. The first recommended step is inhalation of amyl nitrate ampoules prior to establishing intravenous access (also known as “poppers” when abused). An unconscious patient will not be able to inhale amyl nitrate, and intravenous access has already been obtained. The second recommended step is administration of intravenous sodium nitrite, but this step is unnecessary and potentially harmful in a patient with a methemoglobin level greater than 10%, which would be expected in a patient suffering from smoke inhalation. Sodium nitrite works by increasing methemoglobin concentrations in red blood cells causing methemoglobin to combine with cyanide forming cyanomethemoglobin. The third and final step is critical in this patient: administration of sodium thiosulfate, which acts as a substrate for the conversion of cyanomethemoglobin into thiocyanate, which can be excreted in the urine. After initiation of treatment for cyanide toxicity, hyperbaric oxygen, and other appropriate therapies can be considered.