Citation

Vale A. Medicine (Abingdon) 2012; 40(2): 89-93.

Copyright

(Copyright © 2012, Medicine Publishing)

DOI

10.1016/j.mpmed.2011.11.025

PMID

unavailable

Abstract

Ethanol is a central nervous system depressant and a peripheral vasodilator, thereby causing coma, hypothermia and hypotension in severe poisoning. Hypoglycaemia, particularly in children, is observed together with acid-base disturbances, which are common (respiratory acidosis is observed more frequently than metabolic acidosis, and metabolic alkalosis may be observed in those vomiting and hypovolaemic). Lactic acidosis (usually mild) is an uncommon but potentially serious complication. Haemodialysis may be considered if the blood ethanol concentration exceeds 7500 mg/L and severe metabolic acidosis is present.

The principal features of severe methanol poisoning are metabolic acidosis and blindness. The first priority of management is to inhibit methanol metabolism using either intravenous fomepizole or ethanol. In addition, sodium bicarbonate and folinic acid should be administered to correct acidosis and increase formate metabolism respectively. Haemodialysis will enhance methanol and formate elimination and correct acid−base disturbances.

Diethylene and ethylene glycols are both metabolized by alcohol and aldehyde dehydrogenases to produce toxic metabolites. Both glycols produce coma, seizures, metabolic acidosis and renal failure, though by different mechanisms. Management involves the administration of fomepizole or ethanol to prevent metabolism of the glycol, correction of acidosis, and the use of haemodialysis to remove the glycol and metabolites.