Initial decontamination should include removal of clothes and cleansing of skin with soap and water. Because there is no proven antidote for SMFA or fluoroacetamide poisoning, orogastric lavage should be considered for exposed patients who present to the ED prior to significant emesis. Appropriate patients should receive 1 g/kg of activated charcoal (AC) orally. A rat study showed that colestipol is more effective than AC in binding SMFA.21 By extension, it seems reasonable to consider the use of colestipol, if available, for the treatment of life-threatening exposures in humans, although there are no human data to support this therapy. A suggested initial dose would be 5 g.
In a cat model, glycerol monoacetate (monacetin) at a dose of 0.5 mL/kg every 30 minutes prolonged survival. In this context, monacetin functions as an acetate donor for ultimate incorporation into citrate in place of fluoroacetate.29 Both ethanol and glycerol monoacetate are converted to acetyl-CoA and compete with monofluoroacetyl-CoA for binding of citrate synthase. This may prevent the “suicide-inhibition” of aconitase, subsequent increase in citrate, and the formation of the toxic metabolite fluorocitrate.29 Availability of monacetin for human use is limited, and appropriate human dosing is unknown.
Ethanol has been used in human cases, although the appropriate dose is unknown and there is not enough evidence to support its use as a single antidote.6,7,24 A reasonable therapeutic dose is the amount of ethanol required to obtain and sustain an ethanol serum concentration of 100 mg/dL (Antidotes in Depth: A31). One intriguing case report involves a patient who ingested 240 mg of SMFA (typically a lethal dose) mixed with a Taiwanese wine (30% ethanol) and survived.6 It is possible that the ethanol decreased or delayed the toxicity of SMFA.
In a mouse model, use of a combination of calcium salts, sodium succinate, and α-ketoglutarate improved survival.22 The rationale of using these antidotes is to provide tricarboxylic acid cycle intermediates distal to the inhibited aconitase in an attempt to improve energy production. These antidotes were not effective unless calcium was coadministered, emphasizing the importance of replenishing electrolytes, particularly the divalent cations that are chelated by citrate.14,28,23
If a patient develops hypotension and shock, rapid administration of intravenous 0.9% NaCl should be followed by a vasopressor, such as norepinephrine or vasopressin. Supportive care, correction of electrolyte abnormalities (especially calcium and potassium), ethanol infusion, and monitoring for dysrhythmias (prolonged QT interval) and seizures are the practical mainstays of treatment.