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Metaldehyde Poisoning: Introduction |  |
| Metaldehyde is the active ingredient in molluscicides used especially during the wet season for slug and snail control in domestic gardens. In certain locations, it is also used for rat control. (See also
Rodenticide Poisoning: Introduction.) Metaldehyde comes as a liquid or bait (3.5%) combined with bran, either as flakes or pellets, and is palatable to pets and farm animals. Some products also contain arsenic or a cholinesterase-inhibiting insecticide, which is usually less toxic at the dosage used than the metaldehyde. All species are susceptible to metaldehyde poisoning (lethal dose 100-300 mg/kg); dogs 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 and acetaldehyde contribute to a decrease in brain serotonin, noradrenaline, and γ-aminobutyric acid (GABA), which is proportional to
the increase in muscle activity and CNS excitatory signs. |
| Clinical signs of toxicosis are similar in all mammals. Nervous signs are prominent. Initial signs may include severe muscle tremors, ataxia, hyperesthesia, 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 (
Strychnine Poisoning: Introduction), which may appear clinically similar. Emesis,
diarrhea, hypersalivation, and dyspnea, in all species, and profuse sweating in horses, are also seen. |
| Severe acidosis develops due to acid metabolites and high muscle activity in all species. Cholinergic signs (especially pupillary constriction) and a drop in blood cholinesterase 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 liver failure (3-4 days). Necropsy lesions are nonspecific and include congestion and edema of the liver, kidneys, and lungs, and intestinal
hemorrhage. A mild formaldehyde-like odor may be present on opening the stomach or rumen. Stomach content, rapidly frozen, is the preferred sample for analysis due to the low levels and rapid loss of acetaldehyde from tissue (liver and urine). |
| An emetic (eg, apomorphine) in acute exposure may not be necessary because metaldehyde is a gastric irritant. However, gastric lavage with sodium bicarbonate is recommended. 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 to reduce acidosis is essential, and 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 is required (≥4 days). |
