ETHYLENE GLYCOL
Polyhydric
alcohols such as ethylene glycol (CH2OHCH2OH) are used as
heat exchangers, in antifreeze formulations, and as indus-trial solvents. Young
children and animals are sometimes attracted by the sweet taste of ethylene
glycol and, rarely, it is ingested intentionally as an ethanol substitute or in
attempted suicide. Although ethylene glycol itself is relatively harmless and
elimi-nated by the kidney, it is metabolized to toxic aldehydes and oxalate.
Three
stages of ethylene glycol overdose occur. Within the first few hours after
ingestion, there is transient excitation fol-lowed by CNS depression. After a
delay of 4–12 hours, severe metabolic acidosis develops from accumulation of
acid metabo-lites and lactate. Finally, delayed renal insufficiency follows
depo-sition of oxalate in renal tubules. The key to the diagnosis of ethylene
glycol poisoning is recognition of anion gap acidosis, osmolar gap, and oxalate
crystals in the urine in a patient without visual symptoms.
As
with methanol poisoning, early fomepizole is the standard treatment for
ethylene glycol poisoning. Intravenous treatment with fomepizole is initiated
immediately, as described above for methanol poisoning, and continued until the
patient’s serum ethylene glycol concentration drops below a toxic threshold
(20–30 mg/dL). Intravenous ethanol is an alternative to fomepi-zole in ethylene
glycol poisoning. Hemodialysis effectively removes ethylene glycol and its
toxic metabolites and is recommended for patients with a serum ethylene glycol
concentration above 50 mg/dL, significant metabolic acidosis, and significant
renal impairment. Fomepizole has reduced the need for hemodialysis, especially
in patients with less severe acidosis and intact renal function.
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