Metaldehyde is often found in slug and snail pellets. Metaldehyde ingestion and toxicity is a common presentation to the emergency centre. The mechanism for toxicity is unknown however an increase of excitatory neurotransmitters, decrease of inhibitory neurotransmitters and decrease in seizure threshold is suggested. Metaldehyde is toxic to both dogs and cats. It primarily affects the neurological system following ingestion and absorption of the toxin. The onset of activity is rapid with clinical signs occurring soon after ingestion however they can be delayed up to 3-4 hours post-ingestion.
Clinical signs most commonly consist of non-specific signs of excessive neurological stimulation and GIT signs which include panting, ptyalism, vomiting, ataxia, muscle tremors, altered mentation (often hypersensitive to stimuli), seizures and hyperthermia. Sometimes evidence of the toxin can be seen caught between the teeth or in stools and on rectal examination.
There is no antidote to metaldehyde toxicity and treatment consists of decontamination and supportive care. The treatment of each individual toxicity case is variable and dependent on how much toxin the patient has ingested and the clinical signs exhibited which is usually unable to be determined accurately from history hence aggressive ‘worst case scenario’ management of the patient is generally recommended.
Emesis should be performed if ingestion is recent and the patient is asymptomatic. If the patient is symptomatic then emesis is contraindicated as there is a high risk of aspiration. Symptomatic management of shock, dehydration, hyperthermia, muscle tremors, seizures and convulsions may be necessary. Methocarbamol appears to be an effective medication and muscle relaxant for controlling peripheral muscle tremors. Medications may also include a combination of benzodiazepines, barbiturates and general anaesthesia.
Prognosis is dependent on the amount of toxin ingested, duration and severity of clinical signs. However, prognosis in appropriately treated patients is generally good and animals tend to make a full recovery within 24-72hrs. A small proportion of animals presenting with severe or prolonged clinical signs refractory to treatment and a combination of anti-convulsant therapy and supportive care resulting in life threatening hyperthermia may go on to develop coagulation dysfunction, multi-organ dysfunction and death.