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
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
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.
Last full review/revision December 2013 by Barry R. Blakley, DVM, PhD