Canine and Feline Epilepsy. Luisa De Risio
of activated charcoal) (Table 4.1), AEMs (see Table 4.1 and Chapters 12 and 24) in seizuring animals, methocarbamol or diazepam in animals with excessive tremors (Table 4.1), and supportive care. The repeated and prolonged administration of activated charcoal (1–5 g/kg every 6–8 h for up to 2–4 days in animals ingesting high dosage of bromethalin) is indicated due to the enterohepatic recirculation of bromethalin. Cerebral oedema can be treated with mannitol. Serum sodium levels should be closely monitored due to the potential for hypernatraemia of repeated administration of activated charcoal as well as mannitol.
Prognosis
Prognosis is fair with prompt and prolonged treatment in animals with mild clinical signs. Animals with obtundation and ataxia may recover over a period of 2 to 4 weeks. Prognosis is guarded in animals with severe neurological signs such as tremors, seizures, coma or paralysis.
Zinc phosphide
Overview
As with other rodenticides, zinc phosphide poisoning can be accidental or malicious in small animals. Secondary (or relay) poisoning has been reported in dogs feeding on the dead rodents and other animals poisoned by zinc phosphide. When zinc phosphide reaches the stomach, on exposure to moisture and an acidic environment, it hydrolyses to phosphine gas which is rapidly absorbed across the gastric mucosa and distributed systemically where it exerts its toxic effect (Proudfoot, 2009).
Mechanism of action
The corrosive action of zinc phosphide accounts for the early, acute and generally haemorrhagic emetic effect on the gastric mucosa. The systemic toxicity of zinc phosphide is caused by phosphine. Postulated mechanisms of action of phosphine include inhibition of cytochrome C oxidase with mitochondrial dysfunction and interruption of cellular respiration, inhibition of serum acetyl cholinesterase activity resulting in cholinergic overdrive and formation of reactive oxygen species (ROS) with resultant oxidative stress, damage to cell lipids, proteins and nucleic acids and cell death (Proudfoot, 2009).
Clinical presentation
Clinical signs occur within 15 min to 4 h after ingestion (but may be delayed by 12 to 18 h) and include vomiting (often with frank or dark blood clots), aimless pacing or running, vocalization, anxiety, discomfort, generalized muscle fasciculations, tremors, exaggerated response to external stimuli and tonic-clonic or tonic seizures. In addition, the production of phosphine gas within the stomach may lead to gastric or abdominal distension resulting in abdominal pain and potentially gastric dilatation-volvulus. Death can occur (Murphy, 2002; Proudfoot, 2009).
Diagnosis
The odour of phosphine is similar to rotten fish or acetylene gas and may be detected on the breath or in the stomach contents of intoxicated animals. However, some types of zinc phosphide may also be odourless. Owners should be warned about the risk of phosphine gas inhalational exposure during transit to the veterinary hospital and adequate precautions should be taken to minimize veterinary and support personnel exposure. The presence of zinc phosphide (phosphine gas) can be detected in stomach contents, vomitus, or suspect bait by laboratory analysis (gas chromatography-mass spectrometry or Dräger detector tube test) (Murphy, 2002; Proudfoot, 2009). The sample should be frozen in an airtight container soon after collection to prevent loss of phosphine gas.
Management
No specific antidote exists. Treatment involves decontamination (gastric lavage and activated charcoal), reducing phosphine production by decreasing the acidity of the gastric lumen through administration of a liquid antacid (e.g. magnesium or aluminium hydroxide and calcium carbonate) or 2–5% solution of sodium bicarbonate orally or through gastric lavage tube, symptomatic and supportive care (intravenous fluids, oxygen supplementation, gastro protectants, analgesia and hepatic supportive agents) and AEMs (see Table 4.1 and Chapters 12 and 24). Adequate room ventilation is imperative during gastrointenstinal decontamination (Gray et al., 2011).
Prognosis
Prognosis can be favourable in animals treated promptly and effectively (Murphy, 2002; Gray et al., 2011).
Sodium monofluoroacetate (Compound 1080)
Overview
Sodium monofluoroacetate was introduced as a rodenticide in the USA in 1946 and subsequently used as pest control particularly of non-native species such as the fox and possum in Australia and New Zealand, respectively. Sodium monofluoroacetate is one of the most toxic pesticides and its use is restricted to trained, licensed applicators. However, accidental or malicious poisoning of domestic animals can occur in baiting areas. Accidental or malicious poisoning of companion animals can occur directly from bait ingestion or secondarily following the ingestion of a poisoned carcass. Sodium monofluoroacetate can be absorbed from the gastrointestinal and respiratory tracts as well as across mucous membranes and abraded skin. Dogs are more susceptible than cats to this toxicant.
Mechanism of action
Fluoroacetate combines with acetyl-CoA to form fluoroacetyl-CoA, which then combines with oxaloacetate to produce fluorocitrate. Fluorocitrate is converted to 4-hydroxy-trans-aconitate, which binds and inactivates aconitase resulting in inhibition of citrate oxidation. This results in inhibition of the tricarboxylic acid (TCA) or Kreb’s cycle, cellular energy depletion, citric acid and lactic acid accumulation, a decrease in blood pH, and interference with cellular respiration and metabolism of carbohydrates, lipids and proteins. Organs with cells with a high metabolic rate, such as the heart, brain and kidneys, are most susceptible to dysfunction (Goh et al., 2005; Parton, 2006; Proudfoot et al., 2006). In addition to blockade of the TCA cycle, citrate accumulates within blood to toxic concentrations and binds to calcium resulting in serum ionized hypocalcaemia.
Clinical presentation
Clinical signs occur 30 min to 2 h after ingestion, depending on the dose, and include restlessness, hyperirritability, hyperesthesia, running, barking and howling episodes, vomiting, salivation, defecation, diarrhoea, urination, tremors, tonic-clonic seizures, hyperthermia (in dogs) and eventually coma and death 2 to 12 h after the onset of clinical signs. Hypothermia, vocalization, cardiac arrhythmias and episodes of bradycardia between seizures have been reported in cats.
Diagnosis
Diagnosis of sodium monofluoroacetate poisoning is usually based on characteristic clinical signs in conjunction with known access to the poison. Clinical pathological changes include metabolic acidosis, serum-ionized hypocalcaemia and elevations in serum citrate concentrations over two to three times greater than the reference range. Analysis of gastric content from vomitus or lavage fluids can confirm the diagnosis. The sample should be kept frozen until analysis to avoid bacterial breakdown of the toxin.
Management
Treatment involves decontamination (induction of emesis in asymptomatic animals