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Overview of Metaldehyde Poisoning


Barry R. Blakley

, DVM, PhD, University of Saskatchewan

Last full review/revision Dec 2013 | Content last modified Dec 2013

Metaldehyde, a cyclic polymer of acetaldehyde, is the active component in molluscicides used to control slugs and snails. It is commonly used in wet coastal areas worldwide. This neurotoxicant has been associated with poisoning in a variety of domestic and wildlife species, although most poisonings have been reported in dogs and are related to careless placement of bait. Metaldehyde may be combined with other agents such as carbamate insecticides to enhance efficacy. It is not considered to be a persistent chemical. Under typical application circumstances, metaldehyde may remain effective for as long as 10 days.

Etiology and Pathogenesis:

Metaldehyde may be purchased in liquid, dust, granular, or pelleted formulations. The active ingredient may vary from 1.5%–5% in the formulation. The bait is highly palatable and potentially addictive, 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 in various 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 nature of the stomach contents and the rate of gastric emptying influence the rate of absorption and the onset of the clinical syndrome. After absorption, metaldehyde is rapidly metabolized. Enterohepatic circulation may prolong retention of metaldehyde in the animal, but ultimately, both metaldehyde and acetaldehyde are excreted in the urine. Clinical manifestations are attributed primarily to metaldehyde, although acetaldehyde does play a role in the clinical syndrome. Metaldehyde exposure alters a variety of neurotransmitter concentrations and enzyme activities. Metaldehyde reduces concentrations of γ-aminobutyric acid, an inhibitory neurotransmitter that causes CNS excitation. Reduced concentrations of brain serotonin (5-hydroxytryptamine) and norepinephrine decrease the threshold for convulsions. Monoamine oxidase activity is increased after metaldehyde exposure. Increased muscle activity and the production of acidic metaldehyde metabolites cause severe electrolyte disturbances and metabolic acidosis.

Clinical Signs and Lesions:

The clinical syndrome is similar in most species. Neurologic manifestations, which predominate, develop within 1–3 hr 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 evident. As the syndrome progresses, opisthotonos and continuous tonic convulsions that are unresponsive to external stimuli (in contrast to those in strychnine poisoning) are typical manifestations. Emesis, diarrhea, hypersalivation, colic, cyanosis, 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 present histologically.


A history of exposure plus the presence of typical clinical disease is suggestive of metaldehyde poisoning. Stomach contents often have a distinctive acetaldehyde or apple cider–like odor. Rapid analysis of stomach contents submitted frozen for metaldehyde and acetaldehyde may be useful to confirm the diagnosis. Analysis of urine, blood, or liver may be useful but is often unreliable.

Neurologic, GI, and pulmonary disease caused by other agents may be confused with metaldehyde poisoning. Potential differential diagnoses include poisonings by strychnine, roquefortine, sodium fluoroacetate, zinc phosphide, bromethalin, organophosphate, carbamate, organochlorine or pyrethroid insecticides, cyanide, blue-green algae, or compost (tremorgonic mycotoxins). Nontoxic conditions such as epilepsy, various encephalitic infections, lysosomal storage diseases, or metabolic diseases such as hypocalcemia also may resemble metaldehyde poisoning.


There is no specific treatment for metaldehyde poisoning, although aggressive symptomatic treatment during the first 24 hr will enable most affected animals to make a full recovery 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 used to control neurologic manifestations. Barbiturate treatment should be considered with caution, because barbiturates compete with acetaldehyde metabolism and induce cytochrome P450 enzymes involved in metaldehyde metabolism. Gas anesthesia may also be a useful alternative. Administration of IV fluids containing sodium lactate or sodium bicarbonate is essential to correct the metabolic acidosis and electrolyte imbalance. Cold water to correct the hyperthermia, methocarbamol (150 mg/kg, IV) to produce muscle relaxation, and dextrose (IV) or calcium borogluconate (IV) to minimize liver damage may be helpful. Xylazine is an effective treatment in horses to reduce neurologic manifestations. Treatment options, dosages, and duration of treatment vary considerably from species to species.

Metaldehyde and acetaldehyde are rapidly eliminated. Consequently, tissue residues in food-producing animals are not a major concern. Withdrawal times, if established, will be relatively short.

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