Ethylene glycol toxicity


  • Component of antifreeze, automobile coolants, de-icing agents, industrial solvents and hydraulic brake fluid.
    • Fluoresces yellow/green under Wood's lamp (neither Sn nor Sp)
  • Sweet taste
  • Parent compound causes inebriation; metabolite (glycolic acid) causes toxicity


  • Peak serum concentration 1-4 hours, elimination half-life ~9 hours
  • Ethanol coingestion roughly doubles ethylene glycol half-life
  • Minimum lethal dose 1-1.5 mL/kg
    • Volume depends on percentage of ethylene glycol in solution, typically 0.6 g/mL
    • 60 kg patient lethal dose ~ 100 mL
  • Metabolites (eg. oxalate acid, glycolic acid) cause toxicity, but do NOT cause osmolal gap
Toxic alcohol ingestion - ethylene glycol.JPG

Clinical Features

Stage 1 - CNS

Stage 2 - Cardiopulmonary

Stage 3 - Renal

Differential Diagnosis

Sedative/hypnotic toxicity



May see:

  • Anion gap acidosis
    • Will not be present immediately after exposure (only metabolite causes acidosis)
  • Renal failure
  • Glucose - may be low in setting of decreased caloric intake

Serum osmolality

Osm gap:

  • Calculated serum osm - measured serum osm
  • Calculated serum osm = 2Na + BUN/2.8 + glucose/18 + ethanol/4.2)
  • Normal < 10
  • >50 highly suggestive of toxic alcohol poisoning

Note: Cannot rule out toxic ingestion with a "normal" osmol gap

  • Only parent alcohol is osmotically active
  • Delayed presentation may mean that much of it is already metabolized

Alcohol levels

May be useful however even if elevated, patients can still have ingested a toxic alcohol


  • Hematuria, proteinuria, pyuria
  • Calcium oxalate crystals (late finding; only seen in 50%)
  • Urinary fluorescence (may be seen 6 hours after ingestion), but lacks sensitivity and specificity

Total CK

Useful to assess for signs of rhabdomyolysis especially if the patient was found laying down

Venous blood gas

Needed to assess degree of acidosis. An ABG is not necessary since pH can be approximated with a clinical degree via a VBG


Acetaminophen or Aspirin levels

  • Useful to discern the cause of the anion gap as well as assess for other toxic ingestion


ADH enzyme blockade


  • Indications:
    • Ethylene glycol level >20mg/dL
    • Suspected significant ethylene glycol ingestion with ETOH level <100mg/dL
    • Coma or altered mental status in patient with unclear history and osm gap >10
    • Coma or altered mental status in patient with unclear history and unexplained met acidosis and ETOH level <100
  • Dosing
    • 15mg/kg IV over 30min; follow by 10mg/kg q12hr until level <20 or acidosis resolves


  • Ethanol drips are rarely used
  • BAL of 100-150 completely saturates alcohol dehydrogenase
  • Dosing:
    • IV: load 800mg/kg; then give 100mg/kg/hr
    • Oral: 3-4 1-oz "shots" of 80-proof liquor); then give 1-2 "shots" per hour

Correction of metabolic acidosis

  • Acidemia leads to protonation of oxalate which increases penetration to end organ tissues and causes more damage
  • Bicarbonate infusion is an option however the patient will need to compensate with an increased respiratory rate otherwise a concomitant respiratory acidosis will ensure.
  • Bicarbonate 1-2mEq/kg IV bolus to attain pH = 7.45-7.50
    • Follow by infusion of 150mEq/L in D5 @ 1.5-2 times maintenance fluid rate
  • Monitor for worsening hypocalcemia


  • Indications:
    • Refractory metabolic acidosis (pH <7.25) with AG >30 and base deficit < -15
    • Renal insufficiency (serum Cr >3.0 mg/dL or increase in Cr by 1.0 mg/dL)
    • Deteriorating vital signs despite aggressive supportive care
    • Electrolyte abnormalities refractory to conventional therapy
    • Ethylene glycol level >50mg/dL (controversial)
    • Glycolic acid level > 8 mmol/L (glycolic acid is metabolite that causes anion gap acidosis)

Decrease oxalate production


See Also


  1. Kraut JF, Kurtz I. Clin J Am Soc Nephrol 2008. PMID: 18045860