Metaldehyde poisoninig

Metaldehyde is a cyclic polymer of acetaldehyde. It has the form of a white or transparent powder or solid crystals. Metaldehyde is practically insoluble in water, but soluble in benzene and chloroform.

Metaldehyde is commonly used as a molluscicide to kill slugs and snails, especially in the wet seasons. Some products are also used to kill rats. The liquid formulations or solid bait (3.5%) combined with bran, in the form of both flakes and pellets, are attractive to companion animals and farm animals. Some metaldehyde-based products also contain arsenic and carbamate insecticides.

The brand names of some metaldehyde-based baits are: Escartox^® 4.9%, Gastrotox_^® 5%, Lumakill_^® 15%, and Metacid_^® 5%. The use of metaldehyde is authorised until December 31_^st, 2011. Metaldehyde is also the main compound in cigarette lighters and camping stove fuels.

MECHANISM OF ACTION

Metaldehyde works on molluscs by contact, causing an increase in mucus secretion with consequent dehydration to the point of death.

In mammals and birds, metaldehyde toxicity is manifested in the central nervous system, lungs (respiratory alkalosis) and as metabolic acidosis.

In the central nervous system, metaldehyde lowers the concentrations of gamma-amino-butyric acid (GABA), noradrenaline and serotonin, with contemporaneous stimulation of monoamine oxidases (MAO). The lack of inhibitory action of GABA and the lowering of the threshold of excitability of nerve cells cause the muscle contractions typical of poisoning by this compound.

METABOLISM

Following acid hydrolysis in the stomach, metaldehyde is partly transformed into acetaldehyde, rapidly absorbed and converted into carbon dioxide, and then eliminated through the lungs, and in part absorbed as such in the gastrointestinal system and then found in the central nervous system, liver and blood. The compound is excreted in the urine (dog: 1% of the oral dose administered) and in the faeces.

TOXICITY

The oral lethal dose, 50% (LD₅₀) is 100 mg/kg in the dog and 207 mg/kg in the cat.

CLINICAL SIGNS

The first toxic effects are manifested within 1-3 hours of ingestion and include:

• hyperaesthesia, muscle spasms, fasciculation, opisthotonus and convulsions that can last for more than 24 hours;
• mydriasis, nystagmus (particularly in the cat);
• dyspnoea, tachycardia, congestion or pallor of the visible mucosae;
• abundant salivation, vomiting [4]of gastric contents with a characteristic odour of formaldehyde, diarrhoea which may be green-coloured;
• severe hyperthermia (42-43°C) as a consequence of the muscle tremors.

DIFFERENTIAL DIAGNOSIS

The distinctive sign of poisoning by metaldehyde is hyperthermia. Other disorders that must be excluded are metabolic diseases (hypoglycaemia, uraemic syndrome, hypocalcaemia); bacterial or viral encephalitis; head injury; poisoning by strychnine, organophosphates or carbamates; and thiamine deficiency.

LABORATORY TESTS

The gastric contents must be frozen and subsequently analysed to determine whether metaldehyde/acetaldehyde is present. The levels of the poison in tissues is low, because the product is rapidly metabolised.

TREATMENT

There is no specific antidote. The treatment of metaldehyde poisoning is symptomatic and consists of:

• Removal of the metaldehyde still present in the gastrointestinal tract:
  • Hydrogen peroxide 3% per os, at a dose of 1-2 mg/kg, repeated after 10-20 minutes if vomiting has not been induced;
  • Syrup of ipecac 7%, at the dose of 1-2.5 ml/kg per os in the dog and 3.3 mg/kg in the cat. The emetic effect is obtained in 10-15 minutes; the dose can be repeated after 20-30 minutes if vomiting does not occur;
  • Gastric lavage.
• Administration of milk within 60 minutes of ingestion of the poison, in patients which have still not shown clinical signs (milk decreases absorption of the poison in the gastrointestinal tract).
• Administration of activated charcoal to decrease the intestinal absorption of the poison (1-4 g/kg per os, can be repeated every 6-8 hours).
• Decrease of metabolic acidosis: Ringer’s lactate. If blood-gas analyses can be performed, severe acidosis (pH< 7.05) should be treated with sodium bicarbonate, with a dose calculated using the following formula: HCO₃= 0.3 x body weight in kg x base excess. One quarter to one half of the calculated dose is given intravenously over 15-30 minutes and then blood gases and blood pH are re-evaluated.
• Control of convulsive crises: diazepam (dog: 0.4-5 mg/kg i.v., repeated three times at intervals of 10 minutes, if necessary; cat: 0.5-1 mg/kg i.v., repeated twice at an interval of 10 minutes, if necessary). If treatment with diazepam is not sufficient, general anaesthesia can be induced with pentobarbital (dog and cat: initial dose 3-15 mg/kg by slow i.v. infusion to induce the desired effect, then administered continuously at the dose of 1-6 mg/kg/hour i.v.). In the case in which the animal is anaesthetised, its ventilation must be controlled with monitoring of CO₂ and blood-gas measurements. Monitoring arterial and venous gases is useful in order to determine the acid-base balance of the patient.
• Muscle relaxants: methocarbamol (dog: 40-220 mg/kg i.v.; cat: 44.4 mg/kg).
• Treatment of hyperthermia: prompt action is required if the body temperature exceeds 41°C.
  • Airway patency must be ensured and the animal ventilated, if necessary;
  • Administration of i.v. fluids [5], in order to maintain blood pressure and to prevent or treat dehydration.
  • Cooling the animal from the exterior, for example by bathing the patient in cold water (advised).
  • Administration of agents that induce neuromuscular paralysis: e.g.. vecuronium, dog:10-20 μg/kg i.v.; cat: 20-40 μg/kg i.v. In this case it is essential to use assisted ventilation because the patient cannot breathe autonomously. Neuromuscular paralysis is one of the most effective methods of lowering hyperthermia, even though it is rarely used in veterinary medicine.
  • If the above mentioned measures do not lower the body temperature, antipyretic drugs can be tried, although their use is not generally advised in the case of ingestion of toxic substances.

PROGNOSIS

The prognosis is good for patients who survive beyond the first 24 hours after ingestion of metaldehyde. Death occurs in 4-24 hours from respiratory arrest. The most severe consequences occur in the liver (cirrhosis or liver failure) and, more rarely, kidneys (renal failure).

Suggested readings

1. Booze TF, Oheme FW. An investigation of metaldehyde and acetaldehyde toxicities in dogs. Fundam Appl Toxicol 1986;6:440-6.
2. Dolder LK. Metaldheyde toxicosis. Vet Med 2003;98:213-5.
3. Gfeller RW, Messonnier SP. Tossicologia ed Avvelenamenti nei Piccoli Animali. Poletto editore; 2004; pp. 15, 119-121.
4. Il Manuale Merk Veterinario. Ed. Giraldi, 2003, 8^th edn. pp. 2069, 2141.
5. Lorgue G, Lechenet J, Rivière A. Tossicologia Clinica Veterinaria. Ed. Cristiano Giraldi, 1999; pp.273-6.
6. Veterinary Toxicology: Basic and Clinical Principles. Ed. Gupta RC; pp.518-21.
7. Viganò F. Medicina d’Urgenza e Terapia Intensiva del Cane e del Gatto. Edizioni Masson SpA ed EV srl. 2004; pp.279.
8. Yas-Natan E, Segev G, Aroch I, et al. Clinical, neurological and clinicopathological signs, treatment and outcome of metaldehyde intoxication in 18 dogs. J Small Anim Pract 2007;48:438-43.

Useful links

Metaldehyde Toxicoses in Dogs, ASPCA