Citation

Saladino R, Shannon M. Pediatr. Emerg. Care 1991; 7(2): 93-96.

Affiliation

Division of Emergency Medicine, Children's Hospital, Boston, MA 02115.

Copyright

(Copyright © 1991, Lippincott Williams and Wilkins)

DOI

unavailable

PMID

2047315

Abstract

Ethylene glycol has long been recognized as a potentially lethal poison and remains available today as automotive antifreeze and windshield deicer fluids. Ethylene glycol is rapidly absorbed from the gastrointestinal tract, with peak levels measured one to four hours after ingestion. Metabolism of the parent compound and the production of several organic acids are responsible for the metabolic acidosis observed in ethylene glycol poisoning. Target organ cellular damage is seen in the kidney, brain, myocardium, pancreas, and blood vessel walls. Renal tubular deposition of calcium oxalate crystals is felt to be responsible for the development of the severe renal injury which may accompany ethylene glycol ingestion. The clinical course is quite varied and includes inebriation, hematuria, cardiorespiratory compromise, and neurologic effects. Prompt diagnosis and initiation of treatment, including ethanol therapy and hemodialysis, is necessary to ameliorate the effects of ethylene glycol ingestion. Two cases of ethylene glycol poisoning, one accidental and one intentional, are reviewed.

Language: en