Canine and Feline Epilepsy. Luisa De Risio
performed to correct possible dehydration, electrolyte imbalances and acidosis. Endotracheal intubation and ventilation may be necessary in cases of respiratory paralysis.
Pralidoxime chloride (2-PAM) is an AChE-reactivating oxime that acts specifically on the organophosphate-enzyme complex and counteracts the nicotinic cholinergic signs (Clemmons, 1990). Administration of 2-PAM should begin within 24 to 48 h of organophosphate intoxication as after this time the toxic compounds are irreversibly bound to AChE. The recommended dose is 10–20 mg/kg slowly IV with fluids over 30 min; or IM or SC. If nicotinic signs persist, the same dose can be repeated every 8–12 h, for 24 to 48 h. 2-PAM should be discontinued after three or four treatments if there is no response or nicotinic signs worsen. 2-PAM produces better results when atropine has already been administered; the atropine dose can be reduced when 2-PAM is used. Signs of muscle weakness and fasciculations usually disappear within 30 min. 2-PAM is not beneficial in treating carbamate toxicosis. If it is uncertain whether the toxicant is an organophosphate or a carbamate, 2-PAM should be used unless it is likely that the toxi-cant is carbaryl, in which case 2-PAM may be harmful. Administration of diphenhydramine (1 to 4 mg/kg PO every 8 h) has been recommended by one author to counteract the nicotinic signs 24 to 48 h after intoxication and to prevent signs of subacute intoxication (Clemmons et al., 1984; Clemmons, 1990). However, its use is controversial and other authors consider diphenhydramine contraindicated in animals with organophosphate and carbamate intoxication (Ellenhorn et al., 1997).
Prognosis
Prognosis depends on the dose and duration of exposure to the insecticide and promptness of adequate treatment (Blodgett, 2006). Generally, prognosis is considered good unless the animal shows signs of respiratory dysfunction or seizures (Wismer and Means, 2012).
Chlorinated hydrocarbons
Overview
Chlorinated hydrocarbons, also named organochlorines, have been used for prevention and control of insect infestations around farms, homes and on animals from the 1950s through the 1970s. Chlorinated hydrocarbons include endrin, aldrin, dieldrin, heptachlor, lindane, DDT and endosulfane. Most of these insecticides have been banned because of accumulating tissue residues and environmental persistence. Contaminated soils or leakage from old dump sites are possible sources of exposure for wildlife and domestic carnivores. The most likely source of exposure in dogs and cats is old stockpiles of insecticides and improper waste disposal. In addition, a few of these compounds may still be legal for ectoparasite control in dogs in certain countries. Exposure in dogs and cats may occur by ingestion, inhalation (less likely), or cutaneous absorption when the insecticide is applied topically and accidentally overdosed (Raisbeck, 2006).
Mechanism of action
The mechanism of action of most chlorinated hydrocarbons is poorly understood and they are considered to be nonspecific stimulants of the central nervous system (Hatch, 1988). Persistent opening of neuronal sodium channels and GABA inhibition are possible mechanisms.
Clinical presentation
Clinical diagnosis is based on history of exposure and clinical presentation. Clinical signs include hypersensitivity, nervousness, muscle tremors, spastic gait, ataxia, mydriasis, salivation, vomiting and severe generalized tonic-clonic seizures, which may be precipitated by external stimuli and may last for 2–3 days. Hyperthermia occurs as a result of the seizures. Death may occur within minutes or hours or after several days.
Diagnosis
Confirming the diagnosis is quite difficult as chlorinated hydrocarbon residues may be found in blood or tissue of normal animals due their persistence in tissues (particularly fat) (Raisbeck, 2006). Tissue samples should be submitted in glass or metal containers 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