14. Acute Alcohol Toxicity

Toxic Alcohols

Includes methanol, ethylene glycol, isopropyl alcohol, diethylene glycol, and propylene glycol.

Diagnostic Evaluation

May be challenging given non-specific clinical presentation, difficulty detecting parent compound level, and lack of patient-provided history. Clinical presentation may evolve with formation of toxic metabolites.

Work Up:

  • Obtain BMP, ethanol level, POCT BG, POCT VBG, lactate, urinalysis.
  • Send toxic alcohol panel (if available, do not wait for results to pursue treatment).
  • Calculate osmolal gap: measured osmolality - 2xNa - BUN/2.8 - glucose/18. Normal range -14 to +10 mOsm/kg of water.
    • Accumulation of alcohol increases serum osmolality and the osmolal gap.
    • Accumulation of the parent alcohol initially elevates the osmolal gap, which decreases with metabolism.
  • Calculate the anion gap:
    • Accumulation of organic acid anions (toxic metabolites) increases serum anion gap.

Management

  • If high clinical suspicion for toxic alcohol ingestion (high risk exposure, elevated osmolal gap, elevated anion gap, AKI): treat with fomepizole.
    • Do NOT use fomepizole for isopropanol ingestion.
    • Administer fomepizole at 15 mg/kg loading dose, 10 mg/kg every 12 hours maintenance dose for 48 hours, followed by 15 mg/kg every 12 hours (if using dialysis, give immediately after).
  • Gastric decontamination is not helpful (GI absorption is too rapid).
  • Dialysis indicated for any one of the following:
    • pH <7.3.
    • AKI.
    • Amount and type of alcohol ingested (see chart).
  • Adjunct medications: based on type of alcohol ingested (see chart).

 

Alcohol Type

Mechanism

Clinical Features

Laboratory Features

(OG: osmolal gap, AG: anion gap)

Management

Ethylene glycol

(Automotive antifreeze, engine coolant, de-icing fluids)

Parent alcohol is innocuous; metabolized into oxalic and glycolic acid

Inebriation, cardiac dysfunction, pulmonary dysfunction, AKI 2/2 crystal deposition

Onset

Without ethanol: 12-24 hours

With ethanol: 48-72 hours

Increased OG, high AG metabolic acidosis, calcium oxylate crystalluria, hypocalcemia, lactate gap (discrepancy between point of care and lab test)

Fomepizole

Dialysis if concentration >50 mg/dl (or >300 mg/dl after antidote given)

Pyridoxine and thiamine products to promote metabolism of glycolic acid to less toxic metabolites

Methanol

(Windshield washer fluid, carburetor cleaner, octane booster, racing fuels, camp stove fuel, “moonshine”)

Parent alcohol is innocuous; metabolized into formic acid, which accumulates in retina and basal ganglia

Inebriation, abdominal pain, decreased vision with blindness, pulmonary dysfunction, Parkinson-like features (rare)

Onset

Without ethanol: 6-24 hours

With ethanol: 72-96 hours

Increased OG, high AG metabolic acidosis, increased formate, lactic acidosis with cellular hypoxia, spurious increase in creatinine

Fomepizole

Base solution to increase ionization of formate (increased urinary excretion, decreased penetration into optic nerve)

Dialysis if concentration > 50 mg/dl

Folic acid 1 mg/kg q4-6 hours to promote conversion of formic acid to CO2 and water

Propylene glycol

(Diluent in parenteral medication [lorazepam], automotive antifreeze, vaping nicotine liquid)

Parent compound and metabolites are toxic; metabolized into D-lactic and L-lactic acid

Look for in patients with underlying hepatic or renal disease receiving lorazepam (>10 mg/hr) for >48 hours.

Increased OG ONLY, unexplained lactic acidosis, acute AKI (rare)

Dialysis if severe, persistent lactic acidosis

Diethylene glycol

(Automotive brake fluids, hydraulic fluids, inappropriate substitution in liquid medication)

Metabolized to 2-hydroxyethoxy-acetic acid and glycolic acid  

 

Abdominal pain, nausea, vomiting, diarrhea, acute pancreatitis, AKI, AMS, hepatic dysfunction, central and peripheral neuropathy

Onset

Without ethanol: 24-48 hours (AKI can appear 8-24 hours after exposure)

With ethanol: 48-72 hours (CN palsy can occur after >5 days)

Increased OG, high AG acidosis, AKI

Fomepizole

Dialysis

Isopropanol

(Rubbing alcohol, hand sanitizer, industrial products)

Parent compound is toxic; metabolized directly to acetone and excreted in urine

Inebriation, depressed sensorium, abdominal pain, respiratory dysfunction, cardiovascular collapse, acute pancreatitis, hypotension

Onset

Without ethanol: 2-4 hours

Increased OG, acetonemia, ketonuria, lactic acidosis

Fomepizole is contraindicated

IV fluids

Dialysis if concentration >500 mg/dL, hypotension or lactic acidosis is present

 

Wang, C., Samaha, D., Hiremath, S. et al. Outcomes after toxic alcohol poisoning: a systematic review protocol. Syst Rev 7, 250 (2018). https://doi.org/10.1186/s13643-018-0926-z