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INTRODUCTION

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 commonly in Australia and New Zealand for vertebrate pest control. It is a tasteless, odorless water-soluble white crystalline powder. Fluoroacetamide (compound 1081) is a similar compound with similar toxicity.

MECHANISM OF TOXICITY

  1. Fluoroacetate is metabolized to the toxic compound fluorocitrate, which blocks cellular metabolism by binding and inhibiting the aconitase enzyme within the Krebs cycle. This impairs ATP production leading to lactic acid production and metabolic acidosis. Krebs inhibition also causes citrate accumulation, which chelates calcium cations resulting in hypocalcemia.

  2. Pharmacokinetics. The onset of effect is reported to be 30 minutes to several hours after ingestion. 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, but there are reports of late-onset coma (36 hours in one report). 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.

TOXIC DOSE

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.

CLINICAL PRESENTATION

After a delay of minutes to several hours (most patients develop symptoms in 3–6 hours, although onset of coma was 36 hours in one report), manifestations of diffuse cellular poisoning become apparent; nausea, vomiting, diarrhea, metabolic acidosis (lactic acidosis), shock, renal failure, agitation, confusion, seizures, coma, respiratory arrest, pulmonary edema, and ventricular dysrhythmias may occur. One case series reported a high incidence of hypocalcemia and hypokalemia. Hypotension, acidemia, and elevated serum creatinine are the most sensitive predictors of mortality. Death is usually the result of respiratory failure or ventricular dysrhythmia.

DIAGNOSIS

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. Specific levels. There is no assay available.

  2. Other useful laboratory studies include electrolytes, glucose, BUN, creatinine, calcium, arterial blood gases, ECG, and chest radiography. Perform continuous ECG monitoring.

TREATMENT

  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 ...

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