Ethylene Glycol Toxicity in Pets
DIAGNOSIS AND TREATMENT
Ethylene glycol toxicity, commonly resulting from antifreeze ingestion, is a critical medical emergency in veterinary practice, notable for its high case fatality rates among small animals. For cats, the fatality rate ranges from 78% to 96%, and for dogs, it ranges from 44% to 70%. The minimum lethal dose of undiluted ethylene glycol is reported to be 1.5 mL/kg for cats and 4.4 to 6.6 mL/kg for dogs. Ethylene glycol is rapidly absorbed through the gastrointestinal tract, with primary metabolism occurring in the liver, leading to the production of toxic metabolites responsible for clinical signs of toxicosis.
Clinically, ethylene glycol toxicosis is characterized by acute renal tubular degeneration and necrosis with calcium oxalate monohydrate crystals formation. These crystals, unlike the dihydrate form found in some healthy animals, have a variable shape, including a flat, elongated appearance. Their presence in renal tissues often leads to severe degeneration and necrosis of renal tubules, highlighted by swollen epithelial cells with vacuolated cytoplasm and loss of cellular detail and nuclei. The metabolic acidosis associated with high anion gap is predominantly due to the production of ethylene glycol–derived organic acids. Moreover, hyperglycemia, hypocalcemia, and hyperkalemia are common biochemical abnormalities associated with ethylene glycol intoxication.
Ultrasonographic findings in affected animals can include hyperechoic renal cortex and the presence of a medullary rim sign, indicative of severe kidney damage. These changes, along with the presence of calcium oxalate monohydrate crystals in urine or renal tissues, support the diagnosis of ethylene glycol intoxication. It's important to note that while these ultrasonographic and histopathological findings are highly suggestive of ethylene glycol toxicosis, they are not pathognomonic.Treatment for ethylene glycol toxicity must be initiated promptly to improve prognosis.
The therapeutic approach often involves managing metabolic acidosis, preventing further metabolism of ethylene glycol into toxic metabolites, and supporting renal function. However, the prognosis remains guarded to poor, particularly if treatment is delayed or if the animal presents with severe azotemia or signs of intoxication at initial evaluation.The detection of specific ultrasonographic changes, such as the halo sign and increased renal cortical echogenicity, has been associated with a grave prognosis, especially in the context of clinical anuria. Early and aggressive treatment can be life-saving, highlighting the importance of prompt veterinary intervention in suspected cases of ethylene glycol intoxication.
References:
Pathology in Practice in: Journal of the American Veterinary Medical Association Volume 241 Issue 10
What Is Your Diagnosis? in: Journal of the American Veterinary Medical Association Volume 240 Issue 12
Ultrasonographic findings in dogs and cats with oxalate nephrosis attributed to ethylene glycol intoxication: 15 cases (1984-1988) in: Journal of the American Veterinary Medical Association Volume 199 Issue 4 (1991)
