|Clinical use:||To confirm if a patient has ingested the substance|
|Background:||Ethylene glycol, present in antifreeze products, may be ingested accidentally or for the purpose of inebriation or suicide. Ethylene glycol itself is relatively nontoxic, and its initial central nervous system (CNS) effects resemble those of ethanol. However, metabolism of ethylene glycol by alcohol dehydrogenase results in the formation of a number of acid metabolites, including oxalic acid and glycolic acid, These acid metabolites are responsible for much of the toxicity of ethylene glycol. Glycolic acid is cleared by the kidney and is largely responsible for the marked acidosis seen in severe cases. Patients will develop a high osmolar gap as they absorb the glycol over the first few hours. Thereafter, as the glycol is metabolised to acids, the osmolar gap will fall while the patient’s anion gap will climb and acidosis worsens. A severely poisoned patient can present early with a normal anion gap and a normal pH or hydrogen ion concentration; however, their osmolar gap will be high. Early treatment with an antidote will prevent the production of toxic metabolites and prevent the rise in anion gap.Typically, after a brief period of inebriation due to the intoxicating effect of ethylene glycol itself, metabolic acidosis develops, followed by tachypnoea, coma, seizures, hypertension, the appearance of pulmonary infiltrates and oliguric renal failure. If untreated, death from multi-organ failure usually occurs 24 to 36 hours after ingestion.
Stage 1 (30 minutes to 12 hours after ingestion) Apparent intoxication with alcohol (but no ethanol on breath), nausea, vomiting and haematemesis, coma and convulsions (often focal). ataxia, ophthalmoplegia, papilloedema, hypotonia, hyporeflexia, myoclonic jerks, tetanic contractions may occur. Metabolic acidosis develops.
Stage 2 (12-24 hours after ingestion) Increased respiratory rate, sinus tachycardia, hypertension, pulmonary oedema and congestive cardiac failure develop.
Stage 3 (24-72 hours after ingestion) Flank pain, renal angle tenderness, acute tubular necrosis, hypocalcaemia (as a consequence of calcium complexing with oxalate), calcium oxalate monohydrate crystalluria, hyperkalaemia and hypomagnesaemia develop.
|Reference ranges:||Indications for haemodialysis (or haemodiafiltration) are any one of the following:
|Patient preparation:||None required|
|Specimen requirements:||Plasma – Lithium Heparin or Serum (SST).
Discuss with the referring clinician and advise for them to speak with National Poisons Unit.
|Turnaround time:||1 week|
|Referred test:||Referred test|
|Location:||Royal Hallamshire Hospital|