Metaldehyde Poisoning in Animals

Metaldehyde baits are mostly available as granules (often dyed) and pellets but can also be purchased in liquid, powder, meal, or gels/pastes that can release metaldehyde for up to 14 days under moderately moist conditions. The concentration of the active ingredient in baits sold for residential use varies by formulation and ranges from 2% to 4%. In nonresidential (commercial) baits, metaldehyde concentration can be as high as 7%.

Oral median lethal dose (LD50) values for metaldehyde have been reported for dogs (210–600 mg/kg) and cats (207 mg/kg) (2, 3).

Most avian and mammalian species are susceptible to metaldehyde poisoning, with most cases reported in dogs.

Metaldehyde poisonings have been less commonly reported, as formulations have changed to make them less attractive and/or less accessible to dogs, and application rates have decreased because alternative molluscicides are available. Some countries, such as the UK, have banned outdoor use of metaldehyde slug pellets.

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 gastric contents and the rate of gastric emptying influence the rate of absorption and the onset of clinical signs.

Metaldehyde can cross the blood-brain barrier; it has been detected in brain of mice after PO administration of metaldehyde (4). After absorption, metaldehyde is rapidly metabolized, likely by cytochrome P450 enzymes; however, the exact metabolic fate of metaldehyde is not known. Enterohepatic circulation can prolong retention of metaldehyde, but metaldehyde is mostly metabolized. In dogs dosed with metaldehyde, urinary excretion was less than 1% (5). It is assumed that acetaldehyde is rapidly converted to carbon dioxide and eliminated via expiration.

Clinical manifestations are attributed primarily to metaldehyde; however, acetaldehyde does play a role.

Upon ingestion, metaldehyde irritates the mucous membranes of the GI tract.

Once absorbed, metaldehyde affects a variety of neurotransmitter concentrations and enzyme activities. Metaldehyde decreases the concentration of gamma-aminobutyric acid (GABA), an inhibitory neurotransmitter that causes CNS excitation (6). Metaldehyde increases monoamine oxidase activity in the CNS. Increased activity of monoamine oxidase causes decreased concentrations of serotonin and norepinephrine, which then decreases the threshold for seizures (7).

Muscle tremors and the production of acidic metaldehyde metabolites can cause severe electrolyte disturbances and metabolic acidosis.

Clinical signs of metaldehyde poisoning are dose-dependent and similar in most species. In dogs, neurological signs, which predominate, develop 30 minutes to 6 hours after ingestion. Severe muscle tremors, anxiety, hyperesthesia, ataxia, tachycardia, and hyperthermia (often exceeding 41–42°C [106–107°F]) can be evident initially.

As acidosis becomes more severe, depression and hyperpnea can become more pronounced.

With progression, opisthotonos and continuous tonic seizures 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.

Death from disseminated intravascular coagulation (DIC) or respiratory failure can occur soon after exposure (within 4–24 hours, although death from these causes can also occur later). Some animals that survive the acute phase of poisoning develop liver damage within 2 to 3 days after exposure; however, this is manageable through treatment. In rare cases, dogs become transiently blind but regain normal vision within several weeks after metaldehyde poisoning.

Dogs can require several days of hospitalization and several weeks to fully recover. In a study of 26 dogs with a diagnosis of metaldehyde poisoning, 21 survived (overall survival rate, 81%). Of the nine dogs in that study that developed reactive seizures and survived with long-term follow-up, none developed neurological sequelae (8).

Cats poisoned with metaldehyde can develop locomotor signs, dyspnea, hyperthermia, muscle spasms, mydriasis, and opisthotonos. In cats, nystagmus may be more pronounced than in dogs, and external stimuli can evoke seizures. Recovery takes approximately 2 weeks in cats with no sequelae. Secondary illness, such as liver disease or blindness, has not been reported in cats.

• History of exposure, combined with clinical signs

• Chemical analysis

A history of exposure with compatible neurological and GI signs of disease is suggestive of metaldehyde poisoning.

Metaldehyde baits are often formulated in pellets that resemble dog food, with some baits dyed blue or green; samples of bait can also be tested for metaldehyde. Gastric contents often have a distinctive formaldehyde-like odor.

Rapid submission of a frozen sample of gastric contents for determination of metaldehyde and acetaldehyde concentration can be useful to confirm the diagnosis. Analysis of feces, brain, and kidneys can be performed; however, the results are often unreliable.

Differential diagnoses include various neurological, GI, and pulmonary diseases due to other toxins. These include poisonings from the ingestion of many substances:

• strychnine

• penitrem A

• xylitol

• sodium fluoroacetate

• zinc phosphide

• bromethalin

• organophosphates

• carbamate

• organochlorine or pyrethroid insecticides

• hops

• chocolate

• cyanotoxins

• amphetamines

• 4-aminopyridine

• neurotoxic mushrooms

• cyanide

• illicit drugs

• certain prescription medications (eg, antidepressants, anxiolytics, sleep aids)

• methionine

Other diseases such as epilepsy, severe head trauma, various encephalitic infections, lysosomal storage diseases, neoplasms, or metabolic derangements (hypoglycemia, hypocalcemia) may also resemble metaldehyde poisoning.

• Supportive care

• Activated charcoal

• Intensive laboratory monitoring

No specific treatment exists for metaldehyde poisoning; however, rapid treatment during the first 24 hours can allow a full recovery in most patients within 2–3 days. Treatment should focus on decontamination; controlling hyperthermia, tremors, and seizures; maintaining adequate organ perfusion; and monitoring for and correction of metabolic acidosis.

Administration of activated charcoal (1–3 g/kg, PO, once, in combination with a cathartic) is recommended in recent ingestions, ideally within 60 minutes and before severe clinical signs have developed (9). Because of the lack of evidence for enterohepatic recirculation, multiple doses of activated charcoal are not recommended.

As an adjunctive to decontamination with activated charcoal, osmotic cathartics such as sorbitol 70% solution (1–2 mL/kg, PO, once [10]) or magnesium sulfate diluted to a 20% solution (250 mg/kg, PO, once [11]) can be used to help remove the metaldehyde from the intestinal tract (by inducing diarrhea); however, data on efficacy are lacking (12).

Controlling tremors and seizures with muscle relaxants and anticonvulsants is critical because persistent clinical signs can result in severe hyperthermia, rhabdomyolysis with secondary acute renal failure (rare), and DIC. For tremors, methocarbamol (55–220 mg/kg, slow IV to effect, repeated as needed) is the drug of choice, and large doses might be necessary (do not exceed 330 mg/kg in 24 hours) (13, 14).

Diazepam (0.5–1 mg/kg, IV, every 10 minutes to effect, up to 3 doses, or 0.5 mg/kg rectally) may be given to control seizures (15, 16). Diazepam has a short duration of action, ranging from 20 to 60 minutes, and can be repeated if necessary. If initial diazepam treatment has no effect or seizures continue once the drug wears off, a CRI of diazepam or midazolam may be used. Other anticonvulsants (eg, phenobarbital or levetiracetam) can be used to supplement diazepam.

In adult horses, midazolam (combined with ketamine and xylazine) can be considered for emergency seizure treatment.

Phenobarbital is given as a loading dose of four doses of 4 mg/kg, IV, slowly over 5 minutes, repeat every 20–30 minutes, with a maximum total phenobarbital dose of 20–24 mg/kg (17). Alternatively, a single dose of 12–20 mg/kg may be given IV slowly over at least 5 minutes, especially in cases of severe poisoning.

Carefully monitoring the patient for potential development of severe CNS depression and hypoventilation is critical. Because metaldehyde is likely degraded by cytochrome P450 enzymes, phenobarbital administration can increase the metabolic degradation of metaldehyde.

Levetiracetam (dogs: 30–60 mg/kg, IV [18]; cats: 20–25 mg/kg, IV [19]) may be used in place of or in combination with phenobarbital for seizure control.

If administration of the mentioned drugs is not able to control the patient’s seizures, general anesthetics (eg, propofol 2–8 mg/kg, IV to effect, followed by 0.1–0.25 mg/kg/min, IV CRI [20, 21]) or inhalant anesthetics may be used. All patients under general anesthesia require endotracheal intubation and ventilation.

Administration of IV fluids containing sodium lactate or sodium bicarbonate is essential to correct the metabolic acidosis and associated electrolyte imbalances and to control hyperthermia. Metaldehyde-poisoned patients typically develop severe hyperthermia from tremors and seizures, requiring direct and evaporative cooling measures such as ice baths, cold IV fluids, fans, and alcohol applied to the pinna and paw pads. To avoid hypothermia, cooling measures should be stopped once body temperature has been decreased to 39.7°C (103.5°F), and body temperature should be monitored every 1–2 hours thereafter.

Although rare, metaldehyde poisoning can lead to liver damage; thus it is important to evaluate hepatic parameters for 2–3 days after clinical resolution. Hepatoprotectants such as SAMe (20 mg/kg, PO, every 24 hours) can be considered (22). Treatment options, dosages, and duration of treatment vary considerably between species.

Intravenous lipid emulsion (ILE) is usually considered for lipophilic toxicants (ie, logP > 1.0 and logD [pH 7.4] > 1.0). LogP values for metaldehyde vary from 0.12 to 1.1 with a predicted logD (pH 7.4) of 0.90; thus, metaldehyde is not highly lipophilic, and ILE is unlikely to be helpful.

Hemodialysis and charcoal hemoperfusion are extracorporeal blood purification techniques and, when combined in vitro, effectively remove metaldehyde from canine plasma. Dogs with metaldehyde toxicosis can benefit from hemodialysis treatment because it can speed up clinical recovery, shorten anesthesia duration and hospitalization time, and decrease the incidence of aspiration pneumonia (23).

Laboratory monitoring should include venous blood gas analysis to assess and correct acid-base disturbances (especially metabolic acidosis), coagulation parameters to monitor for the development of DIC, renal and electrolyte parameters to monitor for the onset of acute renal failure secondary to rhabdomyolysis, and blood glucose concentrations for the presence of hyper- or hypoglycemia.

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 in humans; however, data in food-producing animals are lacking.

• Metaldehyde. WHO/FAO data sheet on pesticides. No. 93.

• Stebbins K, Hafner S. Metaldehyde: Draft Ecological Risk Assessment for Registration Review. EPA-HQ-OPP-2015-0649-0024. US Environmental Protection Agency. Office of Chemical Safety and Pollution Prevention. 2020.

• European Food Safety Authority. Conclusion on the peer review of the pesticide risk assessment of the active substance metaldehyde. EFSA J. 2010;8(10):1856.

• Also see pet owner content regarding metaldehyde poisoning.

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