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 or gastric and colonic lavage in symptomatic animals, administration of activated charcoal with a cathartic) (Table 4.1), methocarbamol or diazepam in animals with excessive tremors (Table 4.1), AEMs (see Table 4.1 and Chapters 12 and 24) in seizuring animals, symptomatic and supportive care. Calcium gluconate (see hypocalcaemia) should be administered if serum-ionized calcium concentration is equal or lower than 0.8 mmol/l (3.2 mg/dl). In addition, administration of sodium bicarbonate or acetamide has shown promising results (O’Hagan, 2004; Parton, 2006). The recommended dosage of sodium bicarbonate is 300 mg/kg (3.6 ml/kg of 8.4% solution) IV over 15–30 min. Alternatively, half of the calculated dose may be given as a bolus and the remainder infused slowly. Administration of sodium bicarbonate may worsen hypocalcaemia and cause hypokalaemia and hyper-natraemia. Serum-ionized calcium, sodium and potassium levels should be monitored regularly in order to implement fluid therapy as well as calcium and potassium supplementations as required.
The recommended dosage of acetamide (15 g of acetamide granules dissolved in 1 l of warmed 5% dextrose) in dogs is 10 to 25 ml/kg IV (infused though a filter following sterilization) over a 60-min period followed by approximately 5 ml/kg/h IV for the next 12 to 18 h until resolution of clinical signs. In cats with fluoroacetate poisoning, the acetamide dose should be reduced by at least 75% (Parton, 2006). Electrolytes should be closely monitored as hyponatraemia may develop due to the large volume of administered free water.
Other treatment modalities are being investigated in Australia and New Zealand due to the higher prevalence of sodium monofluoroacetate poisoning than other countries.
Prognosis
The prognosis is poor to grave, depending on the amount of sodium monofluoroacetate ingested and the severity of clinical signs at initial evaluation (Goh et al., 2005). Early acetamide or sodium bicarbonate treatment and good supportive care can improve survival (O’Hagan, 2004; Parton, 2006).
Automotive Products
Ethylene glycol
Overview
Ethylene
