Canine and Feline Epilepsy. Luisa De Risio
by high-performance liquid chromatography. This test is now commercially available in many countries and has replaced the erythrocyte transketolase activity assay because of its superior sensitivity and specificity for thiamine status (Marks et al., 2011). Diet samples can also be submitted for thiamine analysis. Pathologic changes include bilaterally symmetrical spongiosis, necrosis and haemorrhage of upper brainstem nuclei including caudal colliculus, lateral geniculate (Plate 2), medial vestibular and oculomotor nuclei.
Management
Treatment should be instituted immediately for any animal suspected of having thiamine deficiency. Thiamine should be administered at 50–100 mg per dog and 25–50 mg per cat IM, SC or PO every 12–24 h until a response is obtained or another diagnosis is established. Emergency management of seizures can be performed as described in Chapter 24. The underlying cause of thiamine deficiency should be identified and managed. The majority of affected dogs and cats respond rapidly to thiamine supplementation and diet change.
Exogenous Toxic Disorders Causing Seizures
Overview
Numerous exogenous toxins can induce seizures (see Box 3.1, Chapter 3) through different mechanisms including increased excitation, decreased inhibition, and interference with energy metabolism (O’Brien, 1998). Toxins may affect the nervous system directly or indirectly, by affecting other organs whose dysfunction secondarily affects the brain (e.g. HE due to toxin-induced hepatic failure, xylitol-induced hypoglycaemia). This chapter focuses predominantly on toxins with direct effect on the nervous system.
Clinical presentation
The suspicion of toxin exposure is often based on the history and the onset of acute neurological signs (including excitation and hyperactivity or obtundation, stupor, coma, muscle tremors and fasciculations, seizures and ataxia) often associated with vomiting, diarrhoea, salivation, bronchoconstriction, bradycardia or tachycardia and hyperthermia. The source of intoxication is not always obvious to the pet owner, and therefore veterinarians should be proactive in asking questions and mentioning possible sources of intoxication any time the clinical presentation raises the suspicion of toxin exposure. Seizure can occur in clusters or as status epilepticus (e.g. organophosphates, strychnine, mycotoxins) or less commonly may be isolated and recurrent (e.g. lead) (O’Brien, 1998).
Diagnosis
The presumptive diagnosis is often based on the history of toxin ingestion and clinical signs. Definitive diagnosis is made by identification of the toxin in feed or suspect bait material, gastric content from vomitus or lavage fluids, water, blood or urine (for urinary excreted toxins).
Management
Emergency treatment of neurotoxicity involves multiple simultaneous steps, including:
• Systemic stabilization (airway patency, ventilation, oxygenation, normalization of blood pressure, correction of any fluid, electrolyte or acid-base imbalances, management of cardiac arrhythmias);
• Seizure control (see Table 4.1 and Chapters 12 and 24);
• Excessive skeletal muscle tremor control (Table 4.1);
• Decontamination and prevention of further absorption of toxin (Table 4.1);
• Control of body temperature: convective whole body cooling (e.g. wetting the fur, placing a fan near the animal) in hyper-Thermic (≥40°C, 104°F) animals, or gradual warming in hypothermic animals. Body temperature should be closely monitored to avoid inducing hypo- or hyperthermia;
• Administration of an antidote when available;
• Nursing care.
Decontamination
The methods of decontamination and prevention of further toxin absorption depend on the route of entry of the toxin and its metabolic profile.
Cutaneous absorbed toxins
Bathing is the standard method of decontamination for cutaneous exposure to most toxic substances (Rosendale, 2002). The patient should be stabilized prior to bathing. The stimulation of bathing may trigger or exacerbate neurological and cardiovascular signs. People handling the animal should wear protective gloves and aprons. Liquid hand-dishwashing detergents are usually recommended over shampoo as they are more effective at removing lipid soluble substances. Sometimes bathing must be repeated to completely remove the toxin. Clipping may be the best way to remove adhesive substances.
Gastrointestinal absorbed toxins
When the toxin has been ingested, decontamination involves:
• Induction of emesis within 4–6 h of toxin ingestion (e.g. apomorphine in dogs and xylazine in cats, see Table 4.1), gastric lavage within 2–6 h of toxin ingestion or colonic lavage;
• Administration of activated charcoal with a cathartic (e.g. sodium sulphate or sorbitol; see Table 4.1);
• Providing demulscents (milk, kaolinpectin) for any gastrointestinal irritation.
Emetics that stimulate vomiting by direct irritation of the pharyngeal or gastric mucosa should not be used. Induction of emesis is contraindicated in case of ingestion of caustics or volatile substance, if vomiting has already occurred, and in animals with seizures, impaired mental status or abnormal gag reflex due to the risk of aspiration pneumonia (Rosendale, 2002).
Gastric lavage is performed in the anaesthetized animal by gastric intubation and irrigation of the stomach with warm water. A cuffed endotracheal tube must be in place during the procedure to minimize the risk of aspiration of stomach contents. Gastric lavage is indicated when induction of emesis is contraindicated (e.g. profound CNS depression or seizures) or when a large amount of toxin is likely to still be present in the stomach. Gastric lavage is contraindicated in the case of ingestion of: caustics, small volume of toxin (which can be decontaminated with activated charcoal) and moderate amount of toxin more than 2 h previously. The risks of general anaesthesia and of aspiration pneumonia need to be considered. The animal must be monitored continuously during recovery from general anaesthesia from gastric lavage.
Table 4.1. Medications used in animals with exogenous toxic disorders.
| Indication | Medication | Dosage |
| Seizure control | Diazepam | 0.5 to 1.0 mg/kg IV, up to a maximum total dose of 20 mg, or 0.5 to 2.0 mg/kg intrarectally in dogs and cats, repeated to effect or twice within 2 h; if seizures persist, diazepam can be administered as constant rate infusions of 2–5 mg/h in 5% dextrose in water (see Chapter 21) |
| Levetiracetam | 20–60 mg/kg IV, IM, PO once, followed after 8 h by 20 mg/kg IV, IM, PO q8h (see Chapter 16) | |
| Phenobarbital | 15-20 mg/kg IV, IM or PO divided in multiple |