Toxic Alcohols

Alcohols include:

  • Ethanol
  • Methanol
  • Ethylene Glycol

In toxicity:

  • All present with symptoms of alcohol intoxication
  • All contribute to the osmolar gap
  • Different toxicities occur due to the different metabolites


Ethanol is a weak alcohol with a complicated mechanism of action similar to volatile anaesthetic agents:

  • Enhanced GABA-mediated inhibition
    This is reversible with flumazenil.
  • Inhibition of Ca2+ entry
  • Inhibition of NMDA function
  • Inhibition of adenosine transport
Property Drug
Dosing One unit is ~8g/10ml of pure ethanol
Absorption Rapid PO absorption
Metabolism Saturatable kinetics at >4mmol.L-1 due to high doses requiring extensive NAD+ for oxidation, limiting metabolism to ~1 unit per hour. Low (0.2) extraction ratio, so high portal vein concentrations from rapid absorption (e.g. shots) causes a greater pharmacological effect. Ethanol is metabolised by alcohol dehydrogenase to acetylaldehyde, which is metabolised by aldehyde dehydrogenase to acetyl CoA.
Elimination 10% eliminated unchanged in air and urine
Resp Respiratory depression
CVS Vasodilatation increasing heat loss, reduced cardiovascular disease mortality due to increased HDL and inhibition of platelets. Alcoholic cardiomyopathy in abuse.
CNS Slurred speech, intellectual impediment, motor impediment, euphoria, dysphoria, increased confidence. Dementia, encephalopathy, peripheral neuropathy, and cerebellar atrophy with chronic use.
Endocrine Stimulates ACTH release and 'pseudo-Cushing's syndrome'. Inhibits testosterone release. May cause lactic acidosis and hypoglycaemia in toxicity.
Renal Inhibition of ADH release, causing diuresis. Ethanol is osmotically active and contributes to the osmolar gap.
GIT Gastritis. Fatty liver, progressing to hepatitis, necrosis, fibrosis and cirrhosis
GU Tocolytic effect
Haeme Inhibition of platelet aggregation
Metabolic High energy content comparble with fat (29kJ.g-1)
Other Synergistic with other CNS depressants. Metabolic interactions with warfarin, phenobarbitone, and steroids


  • Metabolised by alcohol dehydrogenase to formaldehyde and then formic acid
  • Formic acid is neurotoxic
    Damages retina and the optic nerve.

Ethylene Glycol

  • Metabolised by alcohol dehydrogenase to glycoaldehyde, and (via several intermediate steps) to oxalic acid
  • Oxalic acid binds calcium, which causes:
    • Hypocalcaemia
      • Long QT
    • Acute renal failure


  1. Rang HP, Dale MM, Ritter JM, Flower RJ. Rang and Dale's Pharmacology. 6th Ed. Churchill Livingstone.
  2. Holford NH. Clinical pharmacokinetics of ethanol. Clin Pharmacokinet. 1987 Nov;13(5):273-92.
  3. LITFL- Toxic Alcohol Ingestion
Last updated 2017-09-17

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