Metaldehyde is the active ingredient in molluscicides used especially during the wet season for slug and snail control in domestic gardens and crops. In certain circumstances, it is also used for control of rats, fish, frogs, and leeches. Metaldehyde is primarily a neurotoxicant, and poisoning has occurred in many domestic, wildlife, and avian species. Recently, the occurrence of metaldehyde poisonings has increased in North America.

Etiology and Pathogenesis

Metaldehyde comes as a liquid, dust, granules, or bait (3.5% active ingredient) combined with bran, either as flakes or pellets, and is highly palatable to pets and farm animals. Products other than bait may contain up to 10% metaldehyde. To reduce bait loss, some products also contain arsenic or a cholinesterase-inhibiting insecticide at concentrations that are less toxic than the metaldehyde. All species are susceptible to metaldehyde poisoning (lethal dose 100–300 mg/kg); dogs and cats are the species most frequently poisoned (3 oz of bait is toxic to a 30-lb dog).

When ingested, a portion of the metaldehyde is partially hydrolyzed in stomach acid to acetaldehyde and absorbed, while the remaining metaldehyde is well absorbed from the intestines. The great variability in onset of clinical signs of metaldehyde poisoning appears to be dependent on gastric contents and the rate of stomach emptying. Metaldehyde is excreted in urine and in bile, being trapped in an enterohepatic cycle. Toxicity was at first attributed to acetaldehyde but now appears to be due to both the parent chemical and metabolite. Clinical signs are due to a decrease in brain serotonin, noradrenaline, and γ-aminobutyric acid (GABA), and an increase in mono-amine oxidase. The altered enzyme effects are proportional to the increase in muscle activity and CNS excitatory signs. Metaldehyde also severely alters electrolyte and acid-base balance.

Clinical Signs and Lesions

Clinical signs of toxicosis are similar in all mammals. Nervous signs are prominent and may occur within 1–2 hr of ingestion. Initial signs include severe muscle tremors, anxiety, ataxia, and hyperesthesia. Severely affected animals show tachycardia, hyperthermia, and hyperpnea, followed by nystagmus, opisthotonos, and continuous tonic convulsions. Nystagmus is most severe in cats. Nervous signs are more continuous and less exaggerated by stimulation than in strychnine poisoning (see Strychnine Poisoning), which may appear clinically similar. Emesis, diarrhea, hypersalivation, and dyspnea, in all species, and profuse sweating in horses, are also seen.

Severe acidosis associated with CNS depression and hyperpnea develops due to acid metabolites and high muscle activity in all species. Cholinergic signs (especially pupillary constriction) and a drop in blood cholines-terase may occur if the product contains a carbamate or organophosphate. In high-level exposure, death (4–24 hr) is from respiratory failure, while survivors may develop kidney damage and liver failure (3–4 days).

Necropsy lesions are nonspecific and include congestion and edema of the liver, kidneys, and lungs, and intestinal hemorrhage.

Diagnosis

A mild formaldehyde-like odor may be present on opening the stomach or rumen. Stomach content, rapidly frozen, is the preferred sample for analysis of both metaldehyde and acetaldehyde. Acetaldehyde is rapidly lost from tissue. Residues of metaldehyde, not acetaldehyde, may be found in urine, blood, and liver. Detection of metaldehyde or acetaldehyde confirms the diagnosis.

Treatment

There is no specific antidote for metaldehyde poisoning. An emetic (eg, apomorphine) in acute exposure is usually not necessary because metaldehyde is a gastric irritant. However, gastric lavage with sodium bicarbonate or milk is recommended. Activated charcoal and catharsis are beneficial due to the enterohepatic cycling of metaldehyde. Diazepam (2–5 mg/kg, IV) to effect is preferred to reduce excitement and convulsions; acepromazine has been used successfully. Barbiturates (which compete with acetaldehyde degradation) are indicated only if the animal does not respond, and gas anesthesia is suggested to maintain severely affected animals. Horses benefit from xylazine plus acepromazine. In large animals, activated carbon (1–3 g/kg, repeated every 4–8 hr at half the original dose if necessary) reduces further absorption (metaldehyde is fat soluble). Aggressive fluid therapy with sodium lactate or sodium bicarbonate to reduce acidosis is essential. Dextrose or calcium borogluconate is used to prevent possible liver damage. Muscle relaxants, eg, methocarbamol, assist in reducing muscle activity and pain. Cold water rinses are recommended when fever is severe. Prognosis is good if hyperthermia and seizures are not severe and prolonged, but longterm aggressive therapy (up to 4 days) is required.

Last full review/revision March 2012 by Herman J. Boermans, DVM, MSc, PhD