Objective: To correlate serum glycolic acid levels with clinical severity a
nd outcome in ethylene glycol poisoning and to determine if glycolic acid l
evels are predictive of renal failure and the need for hemodialysis. Method
s: We measured serum ethylene glycol and glycolic acid levels by gas chroma
tography/mass spectrometry for 41 admissions (39 patients) for ethylene gly
col ingestion and performed retrospective chart reviews. Results: Eight pat
ients died, all of whom developed acute renal failure. Of the survivors, 15
also developed acute renal failure, whereas 18 did not, Of those with norm
al renal function, 8 had glycolic acid levels below detection limits (<0.13
mmol/L) despite ethylene glycol levels as high as 710 mg/dL; 7 of these pa
tients coingested ethanol. Pertinent initial laboratory data for each group
are as follows (mean; range): Deceased: pH 6.99 (6.82-7.22); bicarbonate,
4.8 mmol/L (2-9); anion gap, 28.6 mmol/L (24-40); glycolic acid, 23.5 mmol/
L (13.8-38.0); ethylene glycol, 136.5 mg/dL (6-272). Survived/acute renal f
ailure: pH 7.07 (6.75-7.32); bicarbonate, 5.6 mmol/L (1-12); anion gap, 28.
7 mmol/L (18-41); glycolic acid, 20.2 mmol/L (10.0-30.0); ethylene glycol,
238.8 mg/dL (12-810). No acute renal failure with glycolic acid >1.0 mmol/L
: pH 7.29 (7.12-7.46); bicarbonate, 14.7 mmol/L (4-23); anion gap, 16.5 mmo
l/L (10-26); glycolic acid, 6.8 mmol/L, (2.6-17.0); ethylene glycol, 269.1
mg/dL (6-675). No acute renal failure with glycolic acid <1.0 mmol/L: pH 7.
41 (7.38-7.47); bicarbonate, 23.4 mmol/L (17-25); anion gap, 11.8 mmol/L (8
-18); glycolic acid, 0.1 mmol/L (0-0.66); ethylene glycol, 211 mg/dL (8-710
). The mean time postingestion to admission generally correlated with sever
ity as follows: deceased, <greater than or equal to>10.4 h; survived/acute
renal failure, greater than or equal to9.9 h; no acute renal failure with g
lycolic acid >1.0 mmol/L greater than or equal to6.2 h; no acute renal,fail
ure with glycolic acid <1.0 mmol/L. <greater than or equal to>3.7 h. Hematu
ria was more prevalent than oxaluria (86% and 41%, respectively), but neith
er was individually predictive of acute renal failure. Good correlations we
re found between glycolic acid levels and anion gap (r(2) = 0.7724), pH (r(
2) = 0.7921), and bicarbonate (r(2) = 0.6579); poor correlations (r(2) <0.0
023) occurred between ethylene gl,col levels and glycolic acid, PH, anion g
ap, and bicarbonate. Measured ethylene glycol values were highly correlated
with ethylene glycol values calculated front the osmolal gap (r(2) = 0.933
9), but the latter overestimates the trite value by about 7%, on average. A
n initial glycolic acid level <greater than or equal to>10 mmol/L predicts
acute renal failure with a sensitivity, of 100%, a specificity of 94.4%, an
d an efficiency of 97.6%. Ethylene glycol levels are not Predictive of acut
e renal failure or central nervous system manifestations of toxicity. If on
ly ethylene glycol values are available (measured or calculated), an initia
l anion gap >20 mmol/L is 95.6% sensitive and 94.4% specific,for acute rena
l failure when ethylene glycol is present. Likewise, initial pH <7.30 is 10
0% sensitive and 88.5% specific for acute renal failure. Conclusion: We pro
pose glycolic acid >8 mmol/L as a criterion for the initiation of hemodialy
sis in ethylene glycol ingestion. Patients with glycolic acid <8 mmol/L pro
bably do not need dialysis, regardless of the ethylene glycol concentration
, it,hen metabolism of ethylene glycol is therapeutical inhibited. In the a
bsence of glycolic acid values, an anion gap >20 mmol/L or PH <7.30 predict
s acute renal failure.