Ethylene Glycol Toxicity

Introduction

Ethylene Glycol is a sweet tasting fluid that is the main constituent of anti-freeze products.. Consequently in northern hemishpere ethylene glycol toxicity is frequently encountered in practice. It has a relatively low minimum lethal dose, and its sweet, palatable taste makes it attractive to dogs, cats and other small animals. , ,

Signalment

• Dogs: all ages, both sexes, following intoxication lower incidence of fatalities in dogs compared to cats
• Cats: all ages, both sexes
• Birds
• Other including pigs and cattle

Diagnosis

Clinical Signs

Severity of clinicals signs is inversely proportional to amount ingested. Time post-ingestion is also important..

• Dogs: Ataxia, mild to severe increasing depression and other neurological signs, tachycardia, tachypnoea, polydypsia, polyuria, dehydration, anorexia, emesis, miosis, hypothermia
  • if untreated coma and death, or if lesser amount ingested oliguric acute renal failure within 2 to 7 days after ingestion ., .
    • if untreated anuric acute renal failure
• Cats: Ataxia, pronounced depression and other neurological signs, tachycardia, tachypnoea, polyuria, dehydration, anorexia, emesis, miosis ,

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• • coma and death if untreated, or if lesser amount ingested oliguric acute renal failure within 1 day after ingestion
    • if untreated anuric acute renal failure

Laboratory Tests

• Metabolic Acidosis, increased serum osmolality, increased anion gap, decreased plasma bicarbonate concentration, decreased PCO2, decrease blood pH
• increased urea and creatinine, hyperkalaemia,
• Hyperphosphataemia due to acute renal failure .
  • Hypocalcaemia as a consequence of this.

Ultrasonography

• Renal accumulation of calcium oxalate crystals results in hyperechogenicity upon ultrasound examination .

Biopsy

• Needle or surgical wedge biopsy of kidney .

Pathology

Ethylene glycol toxicosis usually results from ingestion although there have been reports of skin contamination resulting in toxicosis in cats . It is absorbed relatively quickly from the gastrointestinal tract, hence the quick manifestation of clinical signs following intoxication. Following absorption transformation to its more toxic metabolites takes place in the liver and kidney. It is these substances, rather than ethylene glycol itself that are responsible for the more severe pathological changes in the body. The enzyme alcohol dehydrogenase, which is inhibited by 4-methylpyrazole, is responsible for the initial conversion of ethylene glycol to glycoaldehyde. Glycoaldehyde in turn is metabolised to glycolic acid. Following this glycolic acid is converted to glyoxylic acid. This reaction, along with the earlier conversion of ethylene glycol to glycoaldehyde, are the rate-limiting steps in the metabolism of ethylene glycol. Finally glycolic acid undergoes metabolic transformation to produce the end product, oxalic acid. Glycolic acid and oxalate are directly nephrotoxic. They are also reposponsible for the metabolic acidosis, which interferes with the normal ,metabolic pathways of the body. Glycolic acid is one such metabolite. It is a direct metabolite of glycoaldehyde which itself is produced following the actions of the enzyme alcohol dehydrogenase on ethylene glycol.

• Tetany results from the binding of Ethylene Glycol meatabolites to calcium ions present in serum .

Treatment

• Ethanol: useful in both dogs and cats .

• 4-methylpyrazole:Dogs only mode of action is to inhibit ADH in the liver. Recommended doses are 20mg per kg of a 50mg/ml solution (intravenous) followed by 15mg per kg (intravenous) 12 hours and 24 hours later and a final dose of 5mg per kg 36 hours later .

Ethylene Glycol is a weak acid. Therefore in order to increase the rate of renal clearance sodium bicarbonate can be administered to dogs. Intravenous administration of sodium bicarbonate at a concentration of 1-2 mmol/kg every 3 to 6 hours achieves sufficient alkalinisation of the urine.