Ethylene glycol is a colorless, odorless, sweet-tasting substance. It is highly water-soluble and rapidly absorbed when ingested orally, but not by the lungs or skin. Peak blood levels occur within 1 to 4 h of an ingestion. The volume of distribution is 0.83 L/kg and the plasma half-life is 3 to 5 h. Ethanol at a concentration of 100 to 200 mg/dL has an increased half-life of 17 h. Ethylene glycol is metabolized in the liver and kidneys to toxic metabolites—aldehydes, glycolate, oxalate, and lactate—which, in turn, cause toxicity to the lungs, heart, and kidneys. These metabolites also cause the metabolic acidosis associated with ethylene glycol poisoning.7

Ethylene glycol is metabolized to glycoaldehyde by the alcohol dehydrogenase ( Fig 160-3). This conversion involves the reduction of NAD+ to NADH, which causes inhibition of the citric acid cycle and formation of lactic acid. Glycoaldehyde is further metabolized to glycolic acid and to glyoxylic acid, which, in turn, are converted to several new compounds. Pyridoxal phosphate is a cofactor in the conversion of glyoxylic acid to glycine, which is nontoxic, while thiamine pyrophosphate is the cofactor in the conversion of glyoxylic acid to another nontoxic compound called a-hydroxy-b-ketoddipate. A deficiency of either pyridoxal phosphate or thiamine may shift the metabolism of ethylene glycol to the production of toxic metabolites.

FIG. 160-3. Metabolic pathway of ethylene glycol.

Glyoxylic acid is also metabolized to formic acid and oxalic acid. Glycolic acid contributes to the metabolic acidosis observed in ethylene glycol poisoning. Oxalate crystalluria is a striking feature caused by calcium oxalate salt deposition. Oxalate crystals are present in the urine in only about 50 percent of cases.

The potentially lethal dose in adults is 2 mL/kg, although survival has been reported after ingestions ranging from 240 to 970 mL.

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