VPT 421: Veterinary Toxicology (2+0)

SODIUM FLUROACETATE

• This is highly toxic to all species.
• Sodium fluroacetate is absorbed from the gastrointestinal tract, respiratory tract, abraded skin and mucous membrane.
• Sodium fluroacetae is metabolised to flurocitrate. This blocks the citric acid cycle.
• Flurocitrate inhibits aconitase and the oxidation of citric acid thus blocking tri carboxylic acid cycle.
• Energy depletion, accumulation of lactate and citrate and decrease in blood pH occur.
• Cellular respiration and metabolism of carbohydrates, proteins and fats are interfered with.
• It causes toxic effects by over stimulating the CNS, resulting in death by convulsions, and by causing alteration of cardiac function that results in myocardial depression, cardiac arrhythmias, ventricular fibrillation and circulatory collapse.
• CNS stimulation is the main effect in dogs, while the cardiac effects predominate in horses, sheep, goats and chickens.
• Pigs and cats appear about equally affected by both.
• Primates and birds are resistant while carnivores are more susceptible.
• A characteristic lag phase of ≥30 min after ingestion occurs before the onset of nervousness and restlessness.
• Affected animals rapidly become prostrate, and the pulse is weak and 2-3 times normal rate.
• Death is due to cardiac failure. Usually, dogs and pigs rapidly develop tetanic convulsions similar to those of strychnine poisoning.
• Many exhibit severe pain. Vomiting is prominent in pigs.
• Dogs usually have urinary and fecal incontinence and exhibit frenzied running.
• The course is rapid; affected animals die within hours after signs appear.
• Few animals that develop marked signs recover.
• Congestion of organs, cyanosis, subepicardial hemorrhages, and a heart stopped in diastole are common necropsy findings.
• No specific antidotal treatment is available.