Maximal benefits of sodium nitrite are realized experimentally when sodium nitrite is given prophylactically, but benefits are still evident even when sodium nitrite is administered following cyanide poisoning. Sodium nitrite is clearly effective soon after administration, even when methemoglobin levels are low. Thus a target methemoglobin concentration should not be used to determine the correct dose of sodium nitrite, although care must be taken to avoid excessive methemoglobinemia.11 Administration of sodium nitrite should always be followed by sodium thiosulfate. Sodium thiosulfate donates a sulfur, which, with the help of rhodanese (cyanide sulfur transferase) and mercaptopyruvate sulfurtransferase, carries sulfane sulfur to bind to cyanide, producing thiocyanate. Thiocyanate is a much less toxic substance than cyanide and is renally eliminated.4
As early as 1952, the literature reported 16 cyanide-poisoned patients who survived following administration of nitrites and sodium thiosulfate.3 Even patients who were unconscious or apneic survived when given timely cardiopulmonary resuscitation and antidotal therapy.3 Case reports attest to the ability of amyl nitrite, sodium nitrite, and sodium thiosulfate to reverse the effects of cyanide if they are administered in a timely fashion.8,25 A 34 year-old man who ingested 1 g potassium cyanide became comatose within 45 minutes. One hour after ingestion, he arrived in the emergency department, became apneic, and was intubated. His blood pressure was 134/84 mm Hg and pulse 84 beats/min with fixed and dilated pupils. At 1 hour 15 minutes, he was given 300 mg sodium nitrite intravenously over 20 minutes, followed by 12.5 g sodium thiosulfate. Seizure activity that began just prior to sodium nitrite infusion resolved rapidly, and by the time the sodium thiosulfate was infused, his pupils were reactive and spontaneous respirations had returned.8
In another case, a 4 year-old boy ingested twelve 50 mg tablets of laetrile (amygdalin), became unresponsive, and developed seizures within 90 minutes.10 Upon arrival at a second hospital, the patient required intubation, had no blood pressure, and had dilated minimally responsive pupils. Arterial blood gas analysis revealed: pH, 6.85; PCO2, 15 mm Hg; PO2, 169 mm Hg on 100% oxygen with an anion gap of 26 mEq/L. His vital signs improved with intermittent inhalation of amyl nitrite pearls. Six hours after ingestion (and 1 hour 45 minutes after amyl nitrite administration), sodium nitrite and sodium thiosulfate obtained from another hospital were administered. Within 30 minutes of completion of 5 mL (0.33 mL/kg) 3% sodium nitrite solution by IV infusion, spontaneous respirations returned, and his blood pressure and pulse normalized. Over the next 3 hours, his mental status and acid–base status improved. Fifteen hours after ingestion, he was alert, oriented, and extubated. Elevated whole blood cyanide concentrations verified the ingestion.
A study in swine evaluated the effect of hydroxocobalamin plus sodium thiosulfate versus sodium nitrite and sodium thiosulfate in a model utilizing a continuous infusion of cyanide. There was no difference between the groups in metabolic acidosis with elevated lactate concentrations at times 20 and 40 minutes or in cardiac output and pulse rate at 40 minutes, or in mortality. The mean arterial pressure was higher in the hydroxocobalamin plus sodium thiosulfate group, beginning at 5 minutes and lasting for the entire 40 minute monitoring period.1