Severely poisoned patients have survived with supportive care, although survival in cases of massive exposure undoubtedly has been facilitated by antidotal therapy. The largest reported ingestion where survival occurred with supportive care alone was 600 mg. Patients have survived following much larger ingestions with use of specific antidotes. All patients with known or suspected cyanide poisoning should receive 100% oxygen by mask, be put on a cardiac monitor, and have an intravenous line in place. Patients with a history of ingestion should have careful gastric lavage, followed by endoscopic inspection of the esophagus to exclude caustic injury once the danger of death from the toxin is past. Ipecac is absolutely contraindicated because of the expected rapid onset of symptoms. Gastric decontamination should never take priority over resuscitation of the symptomatic patient. Superactivated charcoal has been shown to bind small amounts of cyanide and may be useful in decreasing the significance of an ingestion. Patients with inhalational exposures do not require gastric decontamination. Extensive decontamination of the skin with water should be accomplished in patients with cutaneous exposure, with adequate precautions to protect the staff from skin contamination. Patients with inhalational exposures often recover following their rescue from the toxic exposure. They do not require antidotal treatment if significant recovery has occurred prior to reaching medical attention.14
The decision to administer the sodium nitrite—thiosulfate antidote is straightforward when faced with a comatose, bradycardic patient with a clear history of cyanide exposure. Hypotension is not a contraindication to sodium nitrite therapy in this setting. Due to the potential toxicity of the nitrites, it is never appropriate to treat an asymptomatic patient. A patient with mild to moderate symptoms may be observed closely for more serious signs prior to the initiation of treatment. More difficult management decisions arise in (1) patients with smoke inhalation who have or may have carbon monoxide exposure as well as suspected cyanide exposure and (2) patients who are critically ill and acidotic without any history of cyanide exposure. In these patients, an antidote that is effective and has no toxicity obviously would be useful as empirical therapy for cyanide poisoning. The empirical administration of nitrites is problematic for two reasons. First, it may induce significant hypotension, and second, it may induce methemoglobinemia. Empirical administration of nitrites to patients who have or may have elevated carboxyhemoglobin levels has been considered to be contraindicated by some authors because of the decreased oxygen-carrying capacity caused by simultaneous induction of methemoglobinemia. 78 A limited study of seven patients with smoke inhalation and elevated cyanide and carboxyhemoglobin who were treated empirically with both sodium nitrite and sodium thiosulfate demonstrated that the measured decrease in oxygen-carrying capacity accounted for by combined carboxyhemoglobin and methemoglobin ranged from 10 to 21 percent and was not clinically significant. The maximum elevation of the methemoglobin level was 13 percent 1 h after treatment with sodium nitrite. None of these patients had initial carbon monoxide levels greater than 38 percent. 7 Due to limitations of this study, the safety of administering both agents in this setting remains unclear. The clinical detection of cyanide poisoning in victims of smoke inhalation also has been problematic because lactic acidosis may be the result of cyanide, carbon monoxide, hypoxia, severe burns, shock, or any state that induces anaerobic metabolism. A recent study of smoke inhalation victims showed a significant correlation between toxic cyanide levels and plasma lactate levels greater than 10 m MIL. This association was independent of the carbon monoxide concentration.8 For the critically ill victim of smoke inhalation with significant lactic acidosis, the safest immediate empirical therapy that avoids the hypotensive effects of nitrites and the concerns about decreased oxygen-carrying capacity due to methemoglobin formation is the administration of sodium thiosulfate in addition to 100% oxygen.8 The institution of hyperbaric oxygen therapy for patients with carbon monoxide poisoning obviates concern about induction of methemoglobinemia in the smoke inhalation victim with carbon monoxide poisoning.
The differential diagnosis of the comatose patient with metabolic acidosis is extensive. Empirical therapy in the unknown patient with suspected poisoning who is critically ill should include 100% oxygen, 50% dextrose, and naloxone, in addition to aggressive supportive care. When cyanide poisoning is considered, anecdotal reports support the utility of the empirical administration of sodium thiosulfate. 21 Significant hypotension is a contraindication to the empirical administration of sodium nitrite. Following the demonstration of adequate oxygenation and the absence of an elevated carboxyhemoglobin level, sodium nitrite may be administered after the sodium thiosulfate if the diagnosis is strongly entertained. A summary of nitrite and thiosulfate therapy is given in TabJeJi82:3.
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