Ethyl Alcohol (Ethanol)

How to Cite This Chapter: Perri D, Klimaszyk D, Kołaciński Z, Szajewski J. Ethyl Alcohol (Ethanol). McMaster Textbook of Internal Medicine. Kraków: Medycyna Praktyczna. Accessed May 30, 2024.
Last Updated: February 17, 2022
Last Reviewed: February 17, 2022
Chapter Information

Unit conversion table: see Table 1 in Alcohols.

The contents of ethanol in alcoholic beverages are as follows: beer 4% to 9% by volume (ie, 4-9 mL of pure ethanol per 100 mL of beer), wine ≤16%, liqueurs and infusions 20% to 40%, and liquor (eg, vodka, gin, whiskey) ~40%. Ethanol is also used as an antiseptic (70%), in cosmetic products (eau de toilette, cologne; 70%), food flavorings (eg, vanilla, lemon extracts), mouthwash, pharmaceuticals (ie, elixirs), and as a household or industrial solvent. It is rapidly absorbed via the gastrointestinal (GI) tract, skin, and airways. Maximum blood levels are observed at 0.5 to 3 hours from ingestion, and ethanol is distributed in body water (volume of distribution, 0.5-0.7 L/kg). It is metabolized in the liver to acetaldehyde by alcohol dehydrogenase and is also cleared by microsomal ethanol-oxidizing systems. The average adult metabolizes 7 to 10 g of alcohol per hour. It is partially eliminated in unchanged form via the kidneys (2%-10%) and in exhaled air (>10%). It crosses the placenta and is excreted in breast milk.

Mechanism of toxicity: Ethanol is a central nervous system depressant. It has additive sedating effects when mixed with barbiturates, benzodiazepines, antidepressants, antipsychotics, or opioids. By inhibiting gluconeogenesis in the liver, it may cause hypoglycemia, especially in children or malnourished patients.

Toxic dose: Approximately 0.8 g/kg (1 mL/kg) of pure ethanol (roughly 3-4 drinks) will produce a blood ethanol concentration of 0.1 g/dL (equal to 100 mg/dL = 1 g/L = 0.1% = 21.7 mmol/L). In adults severe symptoms of ethanol intoxication may develop after ingestion of 1 to 1.5 mL/kg (50-100 mL) of pure ethanol. Death is usually associated with levels >80 to 90 mmol/L, but the lethal level may be much higher for chronic ethanol users.

Clinical FeaturesTop

1. Acute ethanol intoxication:

1) Mild to moderate intoxication leads to impaired judgment, disinhibition, agitation, and sometimes aggression. Patients may present with nausea, vomiting, abdominal pain, headache and vertigo, nystagmus, ataxia, diplopia, logorrhea (incoherent talkativeness), impaired concentration and posture, confusion, and slurred speech.

2) Severe intoxication may present with somnolence, coma, seizures, respiratory compromise, hypotension, bradycardia, hypothermia, and hypoglycemia. The pupils may be constricted, and patients are at risk of rhabdomyolysis from immobility.

3) In patients treated with disulfiram (or drugs causing a disulfiram-like reaction) (Table 1) the metabolism of ethanol is inhibited at the acetaldehyde stage and the accumulation of acetaldehyde results in earlier signs and symptoms of toxicity including nausea, vomiting, restlessness, anxiety, skin erythema, tremor, tachycardia, hypertension, and in severe cases hypotension and arrhythmias.

2. Chronic ethanol abuse may present with any number of complications including hepatic toxicity and cirrhosis, gastrointestinal bleeding, cardiomyopathy, alcoholic ketoacidosis, cerebral atrophy, cerebellar degeneration, peripheral neuropathy, acute or chronic pancreatitis, and Wernicke encephalopathy or Korsakoff psychosis.

3. Coingestions of methanol, ethylene glycol, and isopropyl alcohol may occur with ethanol either accidentally or intentionally. It is also important to consider that alcohol may have been taken with other medications.

4. Alcohol withdrawal syndrome.


The clinical diagnosis of ethanol intoxication is often based on history, smell of alcohol or acetaldehyde, and presence of ataxia, nystagmus, and altered mental status. Alcohol increases the risk of falls and head trauma, hypothermia, and coingestion of other drugs or toxins.

Diagnostic Tests

1. Specific measurement of blood ethanol levels can be done directly in serum or plasma. There is only a rough correlation between blood ethanol levels and clinical presentation:

1) Up to 4 mmol/L (~20 mg/dL): Asymptomatic.

2) 4-10 mmol/L (~20-50 mg/dL): Behavioral and cognitive changes.

3) Above 10 mmol/L (>50 mg/dL): Toxic levels; alcohol intoxication (in some countries the toxic level is assumed at 21.7 mmol/L [100 mg/dL; 0.1%] with driving limits set below this).

4) Equal to or above 65 mmol/L (≥300 mg/dL): Usually profound coma.

Coma with an ethanol level <65 mmol/L (300 mg/dL) should prompt investigation of other causes.

2. Other suggested investigations in patients with severe ethanol intoxication include levels of electrolytes, glucose (due to the risk of hypoglycemia), urea/blood urea nitrogen, creatinine, aminotransferase, as well as prothrombin time/international normalized ratio, arterial blood gas analysis, or pulse oximetry and chest radiographs to exclude aspiration pneumonitis or pneumonia if aspiration is a possibility. Twelve-lead electrocardiography (ECG) or cardiac monitoring may reveal arrhythmia (“holiday heart”). Exclude other ingestions in comatose or delirious patients with a toxicology screen and measurement of acetaminophen (INN paracetamol) level. We suggest measuring toxic alcohol and salicylate levels if an anion gap is present. If biochemistry testing does not reveal a cause of altered mental status and ethanol level is not remarkable (<65 mmol/L or ~300 mg/dL in a comatose patient), we suggest a computed tomography (CT) scan of the head to exclude other pathology. Serum osmolarity and calculation of the osmolar gap may help identify other toxins (formulas: see Alcohols). The contribution of ethanol to the osmolar gap is calculated as the level (in mmol/L) multiplied by 1.25. If a gap persists after calculating the ethanol level, and especially in the presence of an anion gap metabolic acidosis, diagnosis may include coingestion with toxic alcohols.


1. Decontamination: There are no known methods of decontamination. Activated charcoal does not adsorb ethanol but may be of use if coingestion of other drugs or toxins is suspected.

2. Antidotes and specific therapies: There is no commercially available antidote to ethanol. Rehydration, glucose, and thiamine are used both for acute intoxication and treatment of alcoholic ketoacidosis. Thiamine is also used for the prevention and treatment of Wernicke-Korsakoff syndrome. We suggest thiamine replacement (100-300 mg daily IV or orally for 3-5 days) in patients with presumed chronic ethanol ingestion or malnutrition. The utility of thiamine in acute intoxication is less clear but there is little harm to administering it. There is unclear benefit of multivitamin replacement for acute ethanol ingestion but there would be little harm associated with its use. We suggest using multivitamins for patients with chronic alcoholism and risk factors for malnutrition.

3. Accelerated elimination: Hemodialysis is effective at removing ethanol but is rarely needed because most patients recover within a few hours with supportive care only.

4. Supportive care:

1) Protect the intoxicated person from aspiration of vomitus by placing them in the safe position (see Figure 6 in Cardiac Arrest) or intubating and assisting ventilation if needed.

2) Support basic vital functions and correct metabolic disturbances.

3) Watch for and correct hypothermia with gradual rewarming.

5. Management of alcohol withdrawal syndrome.


Table 19.3-1. Selected drugs causing a disulfiram-like reaction

– Abacavir

– Cephalosporins (cefamandole, cefmenoxine, cefmetazole, cefoperazone, cefotetan, ceftriaxone)

– Chloramphenicol

– Griseofulvin

– Hydrazines (isoniazid, procarbazine)

– Ketoconazole

– Nitroimidazoles (benznidazole, metronidazole, ornidazole, tinidazole)

– Phenylbutazone

– Procarbazine

– Sulfonamides (including cotrimoxazole)

– Sulfonylureas (chlorpropamide, glyburide, tolbutamide)

– Tacrolimus

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