Pediatric emergency medicine trisk 3100 3100
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also be considered for high serum methanol levels (in excess of 70 mg/dL) after
alcohol dehydrogenase inhibition.
Ethylene Glycol
The ingestion of ethylene glycol, although uncommon, causes significant
morbidity and occasional mortality. The toxicity of ethylene glycol, like that of
methanol, is the result of drug metabolism; ethylene glycol has virtually no
toxicity in its parent state. However, metabolism by alcohol dehydrogenase
produces several toxic intermediates, including glycolaldehyde, glycolic acid, and
oxalate. These metabolites result in severe metabolic acidosis and deposition of
calcium oxalate crystals.
The clinical syndrome of ethylene glycol intoxication appears in three different
stages. The first stage consists predominantly of CNS manifestations and is
accompanied by a profound metabolic acidosis. In this early stage, mild
hypertension, tachycardia, and leukocytosis are often present. Nausea and
vomiting commonly occur, and with larger doses, coma and convulsions may
appear within a few hours. Another classic finding is the presence of
hypocalcemia. This is believed to result from the widespread formation of
calcium oxalate. Hypocalcemia may be severe enough to cause tetany and cardiac
conduction disturbances. Urinalysis usually reveals a low specific gravity,
proteinuria, microscopic hematuria, and crystalluria. The second distinct state is
coma and cardiopulmonary failure; it is usually the result of acidosis. The third
stage usually occurs after 24 to 72 hours. Here, renal failure emerges, generally
with a picture of acute tubular necrosis with either polyuria or anuria. Urine
sediment contains blood, protein, and casts. Patients often require dialysis for
extended periods and may be left with permanent renal insufficiency.
Consideration of ethylene glycol poisoning should be based either on the
history or, in the absence of diabetic ketoacidosis, the presence of any of the
following criteria: (i) alcohol-like intoxication without the odor of alcohol, (ii)
large anion-gap metabolic acidosis, and (iii) an elevated osmolar gap in the
absence of ethanol or methanol ingestion. A urinalysis that demonstrates oxalate
crystals, while neither highly sensitive nor specific for ethylene glycol poisoning,
can help corroborate the diagnosis. Serum chemistries or blood gas levels should
be obtained frequently because of the rapid evolution of metabolic acidosis. The
availability of ethylene glycol levels varies by institution.
Activated charcoal negligibly adsorbs ethylene glycol. As with methanol
intoxication, treatment of ethylene glycol poisoning falls into three areas:
supportive care, administration of pharmacologic agents, and enhancement of
