Changes

Severity of clinicals signs is inversely proportional to amount ingested. Time post-ingestion is also important.<ref name="multiples">http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/210900.htm, accessed on 31.10.2010 </ref>.

Severity of clinicals signs is inversely proportional to amount ingested. Time post-ingestion is also important.<ref name="multiples">http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/210900.htm, accessed on 31.10.2010 </ref>.

*'''Dogs:''' Ataxia, mild to severe increasing depression and other neurological signs, tachycardia, tachypnoea, polydypsia, polyuria, dehydration, anorexia, emesis, miosis, hypothermia

*'''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 .<ref name="multiples">http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/210900.htm, accessed on 31.10.2010 </ref>, <ref name="multiple"> '''BSAVA Manual of Canine and Feline Emergency Care'''(Second Edition 2007)</ref>.

**if untreated coma and death, or if lesser amount ingested oliguric acute renal failure within 2 to 7 days after ingestion .<ref name="multiples">http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/210900.htm, accessed on 31.10.2010 </ref>, <ref name="multiple"> '''BSAVA Manual of Canine and Feline Emergency Care'''(Second Edition 2007), p286-7 </ref>.

***if untreated anuric acute renal failure

***if untreated anuric acute renal failure

*'''Cats:''' Ataxia, pronounced depression and other neurological signs, tachycardia, tachypnoea, polyuria, dehydration, anorexia, emesis, miosis <ref name="multiple">'''The 5-Minute Veterinary Consult, Canine and Feline''' (Second Edition),''Lippencott, Williams and Wilkins </ref>,  

*'''Cats:''' Ataxia, pronounced depression and other neurological signs, tachycardia, tachypnoea, polyuria, dehydration, anorexia, emesis, miosis <ref name="multiple">'''The 5-Minute Veterinary Consult, Canine and Feline''' (Second Edition),''Lippencott, Williams and Wilkins </ref>,  

===Pathology===

===Pathology===

Ethylene glycol toxicosis usually results from ingestion although there have been reports of skin contamination resulting in toxicosis in cats <ref name="multiples">  http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/210900.htm, accessed on 17.11.2010 </ref>. It is absorbed relatively quickly from the gastrointestinal tract, hence the quick manifestation of clinical signs following intoxication. After 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, leading to necrosis of the renal tubules. Glycolic acid is the main metabolite reposponsible for the metabolic acidosis, although oxalate contributes, as does lactic acid, whose formation is increased as an indirect result of the metabolic pathway outlined above. The metabolic acidosis interferes with normal metabolic pathways. In addition to being directly nephrotoxic oxalate binds ionised calcium in the serum forming calcium oxalate crystals which are excreted by the kidney. Some of these crystals accumulate within the kidney tubules resulting in further nephrotoxicity and decreased urine production. The hypocalcaemia that is present is due not only to calcium oxalate crystal formation but also to the hyperphosphataemia that results from the acute renal failure. The decreased serum calcium level leads tetany <ref name="multiples"> '''Textbook of Veterinary Internal Medicine''', (Seventh Edition), ''Ettinger and Feldman''; p1747 </ref>.

Ethylene glycol toxicosis usually results from ingestion although there have been reports of skin contamination resulting in toxicosis in cats <ref name="multiples">  http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/210900.htm, accessed on 17.11.2010 </ref>. It is absorbed relatively quickly from the gastrointestinal tract <ref name="multiples">  http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/210900.htm, accessed on 17.11.2010 </ref>, hence the quick manifestation of clinical signs following intoxication. After absorption transformation to its more toxic metabolites takes place in the liver and kidney <ref name="multiples">  http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/210900.htm, accessed on 17.11.2010 </ref>. It is these substances, rather than ethylene glycol itself that are responsible for the more severe pathological changes in the body <ref name="multiples"> '''BSAVA Manual of Canine and Feline Emergency Care''',(Second Edition), p286-7 </ref> . 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, leading to necrosis of the renal tubules. Glycolic acid is the main metabolite reposponsible for the metabolic acidosis, although oxalate contributes, as does lactic acid, whose formation is increased as an indirect result of the metabolic pathway outlined above. The metabolic acidosis interferes with normal metabolic pathways. In addition to being directly nephrotoxic oxalate binds ionised calcium in the serum forming calcium oxalate crystals which are excreted by the kidney. Some of these crystals accumulate within the kidney tubules resulting in further nephrotoxicity and decreased urine production. The hypocalcaemia that is present is due not only to calcium oxalate crystal formation but also to the hyperphosphataemia that results from the acute renal failure. The decreased serum calcium level leads tetany <ref name="multiples"> '''Textbook of Veterinary Internal Medicine''', (Seventh Edition), ''Ettinger and Feldman''; p1747 </ref>.