Bovis ISSN 2398-2993

Ethylene glycol toxicosis

Synonym(s): Ethylene glycol, 1,2 ethanediol

Contributor(s): Nicola Bates , John Tulloch

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Introduction

Incidents of ethylene glycol toxicity are uncommon in livestock, but common in companion animals.
  • Cause:
    • Exposure to ethylene glycol, for example through leaks from farm vehicles, livestock access to open containers of ethylene glycol and other sources.
    • Ethylene glycol may be found in:
      • aeroplane de-icers
      • some windscreen/windshield de-icers.
      • some brake and transmission fluids
      • antifreeze used in vehicle coolant systems
  • Signs: depression, ataxia, convulsions, coma, death.
  • Diagnosis: history of exposure and clinical pathology.
  • Treatment: supportive care, hydration and removal from the source.
  • Prognosis: poor in non-ruminating calves and animals with severe signs.

Pathogenesis

Etiology

  • Possible sources of ethylene glycol exposure in cattle include:
    • Broken/leaking radiators in farm or other vehicles.
    • Antifreeze containing motor components discarded onto cattle pasture.
    • Antifreeze stored in open containers that are accessible to livestock.
    • Product spillage.
    • Accidental contamination of feed.

Pathophysiology

  • The development of metabolic acidosis Ruminal acidosis, plasma hyperosmolality, Hypocalcemia Hypocalcemia, oxalate nephrosis and uremia are characteristic of ethylene glycol toxicity.  
  • Ataxia is reflective of plasma hyperosmolality.   
  • Later observed clinical effects, such as anorexia, convulsions and coma, are due to uremia.
  • The increased plasma osmolality and accompanying thirst occur due to the effect of the parent compound, ethylene glycol. However, it is the metabolites of ethylene glycol that are the major toxins and not the parent compound.
  • Ethylene glycol and its metabolites are largely excreted through the kidneys in the urine.
  • The enzyme alcohol dehydrogenase acts on ethylene glycol to produce glycoaldehyde, which is metabolised to glycolic acid. Oxalic acid is a metabolite of glycolic acid. Glycine is also a metabolite of glycolic acid and is further metabolised to hippurate.
  • Glycolic acid causes acidosis. Tachycardia and dyspnoea may be seen as a result of acidosis. 
  • Both glycolic acid and oxalic acid can damage the kidneys.  
  • Oxalic acid causes kidney damage and hypocalcemia by binding with ionised calcium and forming calcium oxalate crystals.
  • Calcium oxalate crystals may be seen in the urine and can be found in large amounts in the kidneys .
  • The development of kidney damage worsens the acid/base and electrolyte imbalances.

Incubation and duration

  • The main clinical signs in cattle are progressive depression, Hypersalivation Hypersalivation, ataxia, a staggering gait, bruxism, recumbency, coma, convulsions and death.  
  • Clinical signs may be seen from 2.5-24 hours post ingestion, depending on the amount ingested. 
  • The higher the dose ingested, the quicker the onset and progression of clinical signs.
  • Azotemia may be seen as early as 24 hours post exposure, depending on the dose ingested.     
  • From 24 hours post ingestion, the levels of urea, creatinine and gamma glutamyl transferase (GGT) in the urine may also increase and the urine pH may decrease. The elevations in urine urea, creatinine and GGT are suggestive of renal damage.
  • Death may occur 1-6 days post ingestion, depending on the quantity ingested (with large doses resulting in earlier fatalities).     

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed Papers

  • Recent references from PubMed and VetMed Resource.
  • Barigye R, Mostrom M, Dyer N W, Newell T K & Lardy G P (2008) Case report – ethylene glycol toxicosis in adult beef cattle fed contaminated feeds. Can Vet J 49, pp 1018-1020 PubMed.
  • Hull W (2001) Ethylene glycol testing. Vet Tech 22 (4), pp 201-202, 216.
  • Singh D P, Kumar M & Sharma SP (1995) Clinico-haematological and biochemical alterations in EG induced acute nephrotoxicity in cow calves. Asian-Australasian Journal of Animal Sciences AJAS 8 (1), pp 7-11.
  • Singh D P, Kumar M & Sharma S P (1995) Changes in Urine in Experimental Ethylene Glycol Intoxication in Cow Calves. Journal of Applied Animal Research 7 (1), pp 75-80. 
  • Singh D P, Kumar M, Varshney K C (1994) Pathological changes in experimental Ethylene glycol intoxication in cow calves. Indian Journal of Animal Sciences 64 (12), pp 1361-1363.
  • Herd P (1992) Poison – ethylene glycol. In Practice 14 (6), pp 298-299.
  • Rhyan J C, Sartin E A, Powers R D, Wolfe W D, Dowling P M & et al (1992) Severe renal oxalosis in five young beefmaster calves. J Am Vet Med Assoc 201, pp 1907-1910.
  • Crowell W A, Whitlock R H, Stout R C & Tyler D E (1979) Ethylene glycol toxicosis in cattle.  Cornell Vet 69 (3), pp 272-279.
  • Gopal T, Leipold H W & Cook J E (1978) Renal oxalosis in neonatal calves. Vet Path 15, pp 519-524.

Other sources of information

  • Anon (2006) Diseases associated with inorganic and farm chemicals – ethylene glycol.  In: Veterinary medicine – A textbook of the diseases of cattle, horses, sheep, pigs and goats.10th Edn.  Eds: Radostits O M, Gay C C, Hinchcliff K W & Constable P D. Saunders, Elsevier. pp 1848.
  • Dalefield R (2004) Ethylene Glycol. In: Clinical Veterinary Toxicology. Ed: Plumlee K H. Mosby. pp 150-154.

Organisation(s)

  • Tiffany Blackett. Veterinary Poisons Information Service (VPIS), London. UK.


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