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Example Content from MEDITEXT for 107-21-1:


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ACUTE EXPOSURE INFORMATION

  1. USES: Primarily used as an engine coolant (eg, antifreeze used in car radiators).
  1. PHARMACOLOGY: No medical use.
  1. TOXICOLOGY: Primary concern is the severe metabolic acidosis and nephrotoxicity from metabolites. Metabolized by alcohol dehydrogenase (ADH) to glycoaldehyde and then by aldehyde dehydrogenase to glycolic acid. Glycolic acid is metabolized by lactate dehydrogenase or glycolic acid oxidase to glyoxylic acid which can be metabolized to oxalic acid. Specifically, oxalic acid metabolite complexes with calcium to form calcium oxalate crystals in the renal tubules that can lead to acute renal failure. Other intermediate metabolites are believed to be nephrotoxic as well. May have CNS effects believed mediated through GABA receptors.
  1. EPIDEMIOLOGY: There are thousands of exposures and several deaths every year reported to poison centers. Inadvertent pediatric ingestions rarely develop severe toxicity.
  1. WITH POISONING/EXPOSURE
    1. MILD TO MODERATE TOXICITY: Initially, ethylene glycol ingestion may cause intoxication similar to ethanol with CNS depression, nystagmus, ataxia, and somnolence. Nausea and vomiting are also fairly common. If ethylene glycol metabolism is blocked early, there may be no other clinical manifestations.
    1. SEVERE TOXICITY: If ethylene glycol metabolism is not blocked early after a significant ingestion, patients develop increasing CNS depression (coma, hypotonia, hyporeflexia, eventually cerebral edema), anion gap metabolic acidosis (often severe, arterial pH less than 7 is common with severe ingestion), and renal failure. Seizures are common with severe toxicity, but usually not prolonged. Mild to moderate tachycardia is common, Kussmaul respirations develop with increasing acidosis, hypotension is rare. Hypocalcemia may result from precipitation of calcium oxalate crystals, which can (rarely) lead to cardiac dysrhythmias. In addition, there are reports of cranial nerve abnormalities developing 1 to 2 weeks post exposure in patients with severe intoxication, which may be secondary to calcium oxalate crystal formation in the brain.
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