Canine and Feline Epilepsy. Luisa De Risio
signs of toxicosis may occur within 3 to 72 h of exposure and include muscle fasciculations and tremors, hypersalivation, ataxia, vomiting, diarrhoea, obtundation, mydriasis, hyperexcitability, hyperactivity, paresthesia, hyperesthesia, seizures and dyspnoea. Type I pyrethroids tend to cause tremors and seizures, whereas type II pyrethroids cause depolarizing conduction blocks with weakness and paralysis (Wismer and Means, 2012). Death may occur but is uncommon.
Diagnosis
Clinical diagnosis is based on history of exposure and clinical presentation. The pet-owners should be specifically questioned on recent ectoparasite treatment either directly on the affected animal or other pets in the house.
Management
Treatment is symptomatic and supportive, including dermal decontamination by bathing with a mild hand-dishwashing detergent and water (in case of dermal exposure to spot-on preparations), methocarbamol (Table 4.1), AEMs (see Table 4.1 and Chapters 12 and 24), fluid therapy and oxygenation (if necessary). Activated charcoal (Table 4.1) can be used in case of oral exposure. The use of intravenous lipid emulsion (Table 4.1) as adjunctive treatment to reduce tissue concentrations of permethrin has produced encouraging results in cats with permethrin toxicosis (Haworth and Smart, 2012; Kuo and Odunayo 2013).
Paresthesia to spot-on preparations may be treated by rubbing vitamin E, corn or olive oil on the application area (Wismer and Means, 2012).
Prognosis
Clinical signs generally resolve within 72 h following appropriate treatment (Hansen, 2006). However, recovery may take a week or longer in some cases. Delayed treatment and generalized seizures are associated with a less favourable prognosis and increased probability of death. Mortality rates vary between 5% and 45% in cats.
Organophosphates and carbamates
Overview
Organophosphates (chlorpyrifos, diazinon, dichlorvos, fenthion) and carbamates (aldicarb, methomyl, carbofuran, carbaryl) are widely used for insect and nematode control in dogs and cats and for insect control in the household and garden. They are available as sprays, pour-ons, oral anthelminthics, baits, collars, dips, dusts and granules (Wismer and Means, 2012). Exposure commonly results from accidental cutaneous overdose or ingestion (Dorman and Fikes, 1993). Organophosphate toxicity may result in acute (<7 h), intermediate (7–96 h) and delayed (1–4 weeks) syndromes.
Mechanism of action
Organophosphates are irreversible inhibitors of acetylcholine esterase (AChE) and recovery depends upon synthesis of new AChE. Carbamates are reversible inhibitors of AChE with restoration of AChE activity when the carbamate insecticide and enzyme separate. Organophosphate and carbamate intoxication results in accumulation of the neuro-transmitter acetylcholine in the synaptic cleft and activation of muscarinic, nicotinic and CNS cholinergic synapses.
Clinical presentation
Clinical signs of acute organophosphate toxicity develop within minutes to hours depending on dose, route and toxicity of the compound and include:
• Muscarinic signs (associated with parasympathetic stimulation) such as hypersalivation, lacrimation, urination, increased gastrointestinal motility, defecation, bradycardia, dyspnoea and miosis;
• Nicotinic signs (associated with skeletal muscle stimulation) such as muscle fasciculations and tremors, which may result in a rigid stance and gait, and eventually weakness and paralysis;
• CNS signs including anxiety, restlessness, hyperactivity, obtundation to coma and generalized seizures.
All of the above clinical signs are not necessarily seen in every case and variability depends on toxicant type, dosage, formulation, route of exposure, poisoned species and stage of intoxication. Cats are generally more susceptible to AChE inhibitors than dogs. Death from either organophosphates or carbamates is associated with respiratory dysfunction resulting from respiratory tract secretions, bronchiolar constriction, intercostal and diaphragm muscle paralysis and CNS-mediated respiratory paralysis.
The intermediate and chronic (also named organophosphate-induced delayed neuropathy) syndromes are characterized by generalized neuromuscular weakness. The reader is referred to other textbooks for further information on these syndromes that are not characterized by seizures.
Diagnosis
Clinical diagnosis is based on history of ingestion, clinical presentation and improvement or resolution of muscarinic signs after atropine administration. If the diagnosis is uncertain, a test dose of atropine (0.02 mg/kg IV) can be administered after evaluating the baseline heart rate. If the heart rate increases, the pupils dilate and hypersalivation stops in 10–15 min, the animal is unlikely to have organophosphate or carbamate intoxication as it takes approximately 10 times this test dose to resolve clinical signs caused by these compounds.
Laboratory findings of heparinized whole blood cholinesterase (ChE) activity reduced by 50% of normal (based on the normal range for that laboratory) suggest exposure, whereas ChE activity less than 25% of normal indicates toxicosis in animals with characteristic clinical signs (Wismer, 2012). ChE activity of heparinized whole blood is a combination of true AChE activity of RBCs and pseudo-ChE activity of serum. Packed cell volume should be checked on blood samples for AChE testing as anaemia can result in decreased AChE activity. Blood should be kept refrigerated to prevent the loss of enzyme activity. ChE activity can remain decreased for 6 to 8 weeks following organophosphate exposure, whereas it may be normal in animals with carbamate intoxication. Carbamates bind reversibly with AChE in the body and they may also dissociate from AChE or pseudo-ChE in a blood tube or other specimen during transit. Stomach content, vomitus, hair, or suspected baits can be submitted to the laboratory for an organophosphate or carbamate residue screen.
Management
Treatment includes administration of atropine (0.2 to 0.4 mg/kg, one-fourth of the initial dose slowly IV and the rest IM or SQ) to counteract the muscarinic signs, decontamination and prevention of further toxin adsorption (Table 4.1), skeletal muscle relaxants (Table 4.1), AEMs (see Table 4.1 and Chapters 12 and 24) and supportive care. Dramatic cessation of para-sympathetic signs is usually observed within 3 to 5 min after administration of atropine IV. Repeated administration of atropine, IV, IM or SC, at one-half of the initial dose is often required, especially in cats with organophosphate toxicity. Glycopyrrolate (0.01–0.02 mg/ kg IV) may also be used to control the muscarinic signs. Cardiac activity should be monitored. In animals with dermal exposure, decontamination is performed by bathing with a mild hand-dishwashing detergent and water. The individuals bathing the animals should wear protective gloves and aprons. In animals with oral exposure, decontamination is performed by induction of emesis (in asymptomatic animals) or gastric lavage and administration of activated charcoal with a saline cathartic or sorbitol (Table 4.1). Fluid therapy should