Fluoroacetate, also known as compound 1080, sodium monofluoroacetate (SMFA), and sodium fluoroacetate, is one of the most toxic substances known. In the past, it was used primarily as a rodenticide by licensed pest control companies, but it largely has been removed from the US market because of its hazardous nature. Compound 1080 use is currently restricted to livestock protection collars designed to protect sheep and cattle from coyotes. Occasionally, unlicensed product may be encountered. It is also still used in Australia and New Zealand for pest control. It is a tasteless, odorless water-soluble white crystalline powder. Fluoroacetamide (compound 1081) is a similar compound with similar toxicity.

1. Fluoroacetate is converted to fluorocitrate, a molecule that irreversibly inhibits the enzyme aconitase in the tricarboxylic acid (Krebs) cycle. Clinical manifestations of toxicity result from the accumulation of substrates proximal to and depletion of substrates distal to the inhibited aconitase. Accumulation of citrate, a calcium chelator, may cause hypocalcemia. ATP depletion with a subsequent shift to anaerobic metabolism causes a lactic acidosis.
2. Pharmacokinetics. Fluoroacetate is rapidly and well absorbed orally. There is little to no absorption through intact skin. The time to peak effect, volume of distribution, duration of action, and elimination half-life in humans are unknown. In sheep the serum half-life is 6.6-13.3 hours, and up to 33% may be excreted unchanged in urine over 48 hours.

Inhalation or ingestion of as little as 1 mg of fluoroacetate is sufficient to cause serious toxicity. Death is likely after ingestion of more than 2-10 mg/kg.

Following ingestion, an initial latent period of 30 minutes to several hours is described and consistent with the time necessary for cellular metabolism disruption. Nausea and vomiting are the most common initial symptoms. Other manifestations of diffuse cellular poisoning may become apparent and include acute kidney injury, agitation, coma, confusion, convulsions, diarrhea, hypotension, lactic acidosis, respiratory arrest, tetany, and ventricular dysrhythmias. Hypocalcemia and hypokalemia are described. ECG findings include QT prolongation, nonspecific ST and T wave changes, PVCs, atrial fibrillation, and ventricular tachycardia. Invasive hemodynamic monitoring in two hypotensive patients demonstrated decreased peripheral vascular resistance. Hypotension, acidemia, and elevated serum creatinine are the most sensitive predictors of mortality. Death is usually the result of respiratory failure or ventricular dysrhythmia.

Is based on a history of ingestion and clinical findings. Fluoroacetate poisoning may mimic other cellular toxins, such as hydrogen cyanide and hydrogen sulfide, although with these poisons the onset of symptoms is usually more rapid.

1. No readily available specific testing is available. Confirmatory tests for fluoroacetate, fluorocitrate, and elevated citrate have been described but will require analysis by a reference laboratory and will not return in time to affect clinical management.
2. Useful laboratory studies include electrolytes, glucose, BUN, creatinine, ionized or free calcium (ionized preferred), magnesium, blood gases, ECG, and chest radiography. Perform continuous ECG monitoring.

1. Emergency and supportive measures
   1. Maintain an open airway and assist ventilation if necessary. Administer supplemental oxygen.
   2. Replace fluid losses from gastroenteritis with IV saline or other crystalloids.
   3. Treat shock, seizures, and coma if they occur. Because of the reported potential delay in the onset of serious symptoms, it is prudent to monitor the patient for at least 36-48 hours.
2. Specific drugs and antidotes. Although several antidotes have been investigated, none has been proven efficacy in humans. Ethanol and monoacetin (glyceryl monoacetate) are thought to act as antidotes by increasing blood acetate levels, which may inhibit fluorocitrate conversion.
   1. In animal studies, ethanol is effective only if given within minutes of exposure. Ethanol has been used in humans. Although conclusive evidence of benefit is lacking, it is reasonable to attempt ethanol infusion with a target level of 100 mg/dL.
   2. Animal studies demonstrate benefit with hypocalcemia correction. Some human case reports (fluoroacetamide only) appear to corroborate this. Close monitoring and correction of hypocalcemia is recommended.
   3. Monoacetin (glycerol monoacetate) has been used experimentally in monkeys but is not available or recommended for human use.
3. Decontamination
   1. Prehospital. If it is available and the patient is alert, immediately administer activated charcoal.
   2. Hospital. Immediately administer activated charcoal (proven to adsorb fluoroacetate). Consider gastric lavage if it can be performed within 60 minutes of ingestion.
   3. Skin exposure. Fluoroacetate is poorly absorbed through intact skin, but a significant exposure could occur through broken skin. Remove contaminated clothing and wash exposed skin thoroughly.
4. Enhanced elimination. There is no known role for any enhanced removal procedure.