Metaldehyde Poisoning in Animals

Metaldehyde can be purchased in liquid, powder, granular, or pelleted formulations. The concentration of the active ingredient may vary from 1.5%–5% by formulation. The bait is highly palatable, which often results in consumption of large quantities. Most avian and mammalian species are susceptible; the lethal oral dose ranges from ~100–600 mg/kg depending upon the species.

After ingestion, metaldehyde undergoes partial hydrolysis in the stomach to produce acetaldehyde. Both metaldehyde and acetaldehyde are readily absorbed from the GI tract. The type of stomach contents and the rate of gastric emptying influence the rate of absorption and the onset of clinical signs. After absorption, metaldehyde is rapidly metabolized. Enterohepatic circulation may prolong retention of metaldehyde, but ultimately, both metaldehyde and acetaldehyde are excreted in the urine. Clinical manifestations are attributed primarily to metaldehyde, although acetaldehyde does play a role. Metaldehyde ingestion affects a variety of neurotransmitter concentrations and enzyme activities. Metaldehyde decreases the concentration of gamma-aminobutyric acid, an inhibitory neurotransmitter that causes CNS excitation. Decreased concentrations of serotonin (5-hydroxytryptamine) and norepinephrine in the CNS decrease the threshold for seizures. Monoamine oxidase activity is increased following metaldehyde exposure. Muscle tremors and the production of acidic metaldehyde metabolites cause severe electrolyte disturbances and metabolic acidosis.

Clinical signs are dose-dependent and similar in most species. Neurologic manifestations, which predominate, develop within 1–3 hours after ingestion. Severe muscle tremors, anxiety, hyperesthesia, ataxia, tachycardia, and hyperthermia may be evident initially. As the acidosis becomes more severe, depression and hyperpnea may become more pronounced. With progression, opisthotonos and continuous tonic convulsions such that affected patients are unresponsive to external stimuli (in contrast to patients with strychnine poisoning) are typical manifestations. Vomiting, diarrhea, hypersalivation, abdominal pain, cyanosis, dyspnea, sweating (horses), mydriasis, and nystagmus (cats) are often reported.

No consistent pathognomonic gross or histologic lesions are seen with metaldehyde poisoning. Hepatic, renal, and pulmonary congestion and intestinal ecchymotic and petechial hemorrhages, which may be associated with prolonged hyperthermia, are common. Neuronal degeneration in the brain and hepatic degeneration with cellular swelling are often evident on histologic examination.

A history of exposure and the presence of typical clinical signs of disease is suggestive of metaldehyde poisoning. Stomach contents often have a distinctive apple cider–like odor. Rapid submission of a frozen sample of gastric contents for determination of metaldehyde and acetaldehyde concentration may be useful to confirm the diagnosis. Analysis of urine, blood or liver tissue specimens may be performed; however, the results are often unreliable.

Differential diagnoses include various neurologic, GI, and pulmonary diseases due to other toxins. These include poisonings from the ingestion of strychnine Strychnine Toxicosis in Animals Strychnine is a pesticide that typically causes toxicosis in companion and production animals by accidental ingestion or malicious poisoning. Onset of toxicosis is rapid and results in agitation... read more , roquefortine, sodium fluoroacetate, zinc phosphide Phosphide (Zinc, Magnesium, Aluminum) Poisoning in Animals Zinc phosphide was discovered as a chemical in 1740, and its use as a rodenticide was documented as early as 1911. Although zinc phosphide is most commonly and readily available in pelleted... read more , bromethalin, organophosphates, carbamate, organochlorine or pyrethroid insecticides, cyanide Cyanide Poisoning in Animals Cyanide poisoning results from exposure to a source of cyanide ions (CN^-). There are four main syndromes in animals: Classical acute cyanide poisoning is when CN^- binds... read more , blue-green algae, or compost (tremorgonic mycotoxins). Other diseases such as epilepsy, various encephalitic infections, lysosomal storage diseases, or metabolic derangements such as hypocalcemia Hypocalcemia in Dogs and Cats Hypocalcemia causes the major clinical manifestations of hypoparathyroidism by increasing the excitability of both the central and peripheral nervous systems. Peripheral neuromuscular signs... read more also may resemble metaldehyde poisoning.

There is no specific treatment for metaldehyde poisoning, although aggressive symptomatic treatment during the first 24 hours may allow for a full recovery in most patients within 2–3 days. Activated charcoal and cathartics may be administered to assist in decontamination and to reduce enterohepatic cycling of metaldehyde. Diazepam (2–5 mg/kg, IV, to effect) may be given to control neurologic signs such as seizures. Barbiturate treatment should be considered with caution, since these drugs compete with acetaldehyde metabolism and induce activity of cytochrome P450 enzymes involved in metaldehyde metabolism. Inhalation anesthesia may be a useful alternative. Administration of IV fluids containing sodium lactate or sodium bicarbonate is essential to correct the metabolic acidosis and associated electrolyte imbalances. Furthermore, provision of cold water to correct the hyperthermia, administration of methocarbamol (150 mg/kg, IV) for muscle relaxation, and IV dextrose or calcium borogluconate solutions may help to minimize liver damage. Xylazine is an effective treatment in horses with neurologic signs. Treatment options, dosages, and duration of treatment vary considerably between species.

Metaldehyde and acetaldehyde are rapidly eliminated. As such, tissue residues in food-producing animals are not a major concern. Withdrawal times, if established, are relatively short. The half-life of metaldehyde is approximately 27 hours.