Objective: Toxic manifestations following ethylene glycol exposure are due
to accumulation of metabolites, particularly glycolate. We characterized gl
ycolate elimination kinetics and dialysis properties in a series of ethylen
e glycol poisonings. Methods: Patients who ingested ethylene glycol and rec
eived fomepizole (4-methylpyrazole; 4-MP) +/- hemodialysis were prospective
ly evaluated, Serial blood samples for ethylene glycol, glycolate, pH, and
bicarbonate were drawn to determine glycolate elimination rate, t(1/2), and
correlations between initial glycolate and initial markers of acidosis. Di
alyzer inlet and outlet samples were obtained to measure hemodialysis glyco
late clearance. Plasma ethylene glycol and glycolate were determined by gas
chromatography. Results: Ten patients, mean age 49 years (range 28-73 year
s), presented a mean of 10.5 hours (range 3.5-21.5 hours) after ethylene gl
ycol ingestion, Mean initial ethylene glycol was 18.5 mmol/L (range 0.8-62.
2 mmol/L) (115 mg/dL; range 5-386 mg/dL) and glycolate was 17.0 mmol/L (ran
ge 10.0-23.7 mmol/L). Nine of 10 underwent hemodialysis. Nonhemodialysis (n
= 4) elimination rate was 1.08 +/- 0.67 mmol/L/h (mean +/- SD) and t(1/2)
was 626 +/- 474 minutes. Elimination ty, during hemodialysis (n = 8) was 15
5 +/- 42 minutes. Hemodialysis clearance (n = 5) was 170 +/- 23 mL/min with
flow rates 250-400 mL/min. Pearson correlation coefficients were: anion ga
p vs glycolate r(2) = 0.65 (p = 0.005), bicarbonate vs glycolate r(2) = 0.1
0 (FJS), and pH vs glycolate r(2) = 0.06 (NS). Conclusion: Glycolate has a
slow elimination rate and long half-life. Hemodialysis effectively clears g
lycolate. An increased anion gap correlates with the presence of glycolate.
Hemodialysis is projected as useful for ethylene glycol-poisoned patients
with anion gap acidosis and low ethylene glycol blood levels.