rather than plastic ones.
Management
Treatment is symptomatic since there is no known antidote and involves dermal (e.g. bathing) or gastrointestinal (e.g. emesis or gastric lavage, repeated administrations of activated charcoal due to enterohepatic recirculation) (Table 4.1) decontamination, skeletal muscle relaxants (Table 4.1), AEMs (see Table 4.1 and Chapters 12 and 24) and supportive care (including ventilator support in severely affected animals). Forced diuresis with 5% mannitol in 0.9% sodium chloride can enhance urinary excretion.
Prognosis
Signs of acute toxicosis usually abate in 1 to 2 days. Complete recovery may take weeks. The prognosis is guarded to good, depending on the dose of exposure, severity of neurological dysfunction and promptness of treatment.
Molluscicides
Metaldehyde
Overview
Metaldehyde is a cyclic tetramer of acetalde-hyde included in a variety of snail and slug baits, most commonly in the form of green granules, but also as liquid, powder or pellets (Yas-Natan et al., 2007).
Protein-rich material, such as bran or grain, is usually added to the bait to make it more attractive to slugs and snails, causing this type of bait to be palatable to dogs as well. Baits are sometimes mixed with other pesticides, most commonly with carbamate insecticides. In some countries, metaldehyde is also used as a fuel in small heating systems, such as camping stoves and lamps. Metaldehyde is degraded to various aldehydes in the stomach resulting in a formaldehyde odour of the gastric contents.
Mechanism of action
The exact mechanism of metaldehyde toxicity is currently unclear and may be associated with an increase in monoamine oxidase activity and a decrease in gamma-aminobutyric acid (GABA), norepinephrine and serotonin concentrations.
Clinical presentation
Clinical signs occur within 20 min to 3 h from ingestion and include tachycardia, tachypnea, hypersalivation, muscle tremors, vomiting, hyperesthesia, nystagmus (especially in cats), ataxia, opisthotonus, seizures, hyperthermia, diarrhoea and obtunded mental status to coma (Yas-Natan et al., 2007). The seizures are tonic, similar to those secondary to strychnine intoxication, but generally they do not worsen with stimuli in dogs. However, in cats seizures have been reported to be triggered or exacerbated by auditory, visual or tactile stimuli. Metabolic acidosis is common. Death may occur from respiratory failure 4 to 24 h after ingestion or from liver failure 3 to 4 days after ingestion in dogs. Post-metaldehyde intoxication liver disease has not been reported in cats.
Diagnosis
Diagnosis can be reached by laboratory analysis of gastric contents, serum, urine and liver. Samples must be kept frozen for analysis.
Management
Treatment includes induction of emesis (in mildly affected animals with no seizures and toxin ingestion <3 h), gastric lavage (toxin ingestion >3 h, ingestion of large volumes), activated charcoal (Table 4.1), methocarbamol for muscle tremors, AEMs (see Table 4.1 and Chapters 12 and 24), fluid therapy to correct metabolic acidosis, convective whole body cooling (e.g. wetting the fur, fan) and respiratory support. General anaesthesia may be necessary in animals that do not respond to AEMs (see Chapter 24). After the acute clinical signs have been controlled, treatment must focus on minimizing possible liver damage in dogs.
Prognosis
Prognosis is generally good in animals treated promptly and aggressively. A retrospective study including 18 dogs with metaldehyde intoxication reported a recovery rate of 83% (Yas-Natan et al., 2007). Prognosis is guarded in animals presenting with severe hyper-thermia (>41.6°C or 107°F). Prolonged status epilepticus following metaldehyde intoxication has not been associated with spontaneous recurrent seizures in dogs (Jull et al., 2011). Recovery may take approximately 2 weeks in cats (Puschner, 2006).
Rodenticides
Strychnine
Overview
Strychnine has been used as pest control of rodents and other animal species worldwide. Its sale has been restricted or banned without special permits in several countries. However, malicious and less commonly accidental or secondary (from ingestion of strychnine-poisoned rodents) poisonings of companion animals still occurs (Berny et al., 2010). The toxic dose in most animals ranges from 0.3 to 1.0 mg/kg with the lethal dose being 2.0 mg/kg in cats.
Mechanism of action
Strychnine antagonizes stereochemically and competitively the motor inhibitory neuro-transmitter glycine at the brainstem and spinal cord level and inhibits glycine release from Renshaw cells. Some supraspinal signs may also be associated with strychnine inhibition of GABA.
Clinical presentation
Clinical signs generally occur within 10 min to 2 h after toxin ingestion and typically begin with nervousness and restlessness, rapidly progressing to increased tone of both extensor and flexor muscles resulting in a stiff gait. All skeletal muscles including the appendicular, epaxial, facial, abdominal and respiratory muscles have tetanic spasms. Auditory (e.g. loud noise), visual (e.g. bright light) and tactile stimuli exacerbate the tetanic muscle spasms and can trigger tonic seizures. This feature, however, is not specific to strychnine and has been observed in other types of poisonings including metaldehyde, penitrem A, roquefortine and chlorinated hydrocarbons. Hyperthermia (secondary to the severe muscle contractions) is commonly observed. The animal remains conscious during seizures unless respiratory paralysis occurs. Apnea can lead to cerebral anoxia, loss of consciousness and death 30 min to 2 h following the onset of neurologic signs, if the animal is untreated (Murphy, 2002).
Diagnosis
Baits may have specific colours in some countries, which can help recognition during gastric decontamination. Definitive diagnosis is based on toxicologic analysis of stomach contents, urine, blood or hepatic and renal tissue. Ante-mortem analysis of stomach contents and
