Commercial beer, wine, and liquors contain various amounts of ethanol. Ethanol is also found in a variety of colognes, perfumes, aftershaves, and mouthwashes; some rubbing alcohols; many food flavorings (eg, vanilla, almond, and lemon extracts); pharmaceutical preparations (eg, elixirs); hand sanitizers; and many other products. Ethanol is frequently ingested recreationally and is the most common coingestant with other drugs in suicide attempts. Ethanol may also serve as a competitive substrate in the emergency treatment of methanol and ethylene glycol poisonings ().

1. Central nervous system (CNS) depression is the principal effect of acute ethanol intoxication. Ethanol has additive effects with other CNS depressants, such as barbiturates, benzodiazepines, opioids, antidepressants, and antipsychotics.
2. Hypoglycemia may be caused by impaired gluconeogenesis in patients with depleted or low glycogen stores (particularly small children and poorly nourished persons).
3. Ethanol intoxication and chronic alcoholism also predispose patients to trauma, exposure-induced hypothermia, injurious effects of alcohol on the GI tract and nervous system, and a number of nutritional disorders and metabolic derangements.
4. In pregnancy, ethanol is absorbed by the mother and crosses the placenta. Fetal concentrations of ethanol rapidly approach those of the mother. Fetal excretion of ethanol into the amniotic fluid can lead to fetal reabsorption. Ethanol is a category C drug and ingestion during pregnancy can lead to fetal alcohol syndrome.
5. Pharmacokinetics. Ethanol is readily absorbed (peak, 30-120 minutes) and distributed into the body water (volume of distribution, 0.5-0.7 L/kg or ~50 L in the average adult). Elimination is mainly by oxidation in the liver and follows zero-order kinetics. The average adult can metabolize about 7-10 g of alcohol per hour, or about 12-25 mg/dL/h. This rate varies among individuals and is influenced by polymorphisms of the alcohol dehydrogenase enzyme and the activity of the microsomal ethanol-oxidizing systems.

Generally, 0.7 g/kg of pure ethanol (approximately 3-4 drinks) will produce a blood ethanol concentration of 100 mg/dL (0.1 g/dL). The legal limit for adult drivers of noncommercial vehicles in most of the United States is 80 mg/dL (0.08 g/dL or 0.08%).

1. A level of 100 mg/dL decreases reaction time and judgment and may be enough to inhibit gluconeogenesis and cause hypoglycemia in children and patients with liver disease, but by itself it is not enough to cause coma.
2. The level sufficient to cause deep coma or respiratory depression is highly variable, depending on the individual's degree of tolerance to ethanol. Although levels above 300 mg/dL usually cause coma in novice drinkers, persons with chronic alcoholism may be awake with levels of 500-600 mg/dL or higher.

1. Acute intoxication
   1. With mild-to-moderate intoxication, patients exhibit euphoria, mild incoordination, ataxia, nystagmus, and impaired judgment and reflexes. Social inhibitions are loosened, and boisterous or aggressive behavior is common. Hypoglycemia may occur, especially in children and persons with reduced hepatic glycogen stores.
   2. With deep intoxication, coma, respiratory depression, and pulmonary aspiration may occur. In these patients, the pupils are usually small, and the temperature, blood pressure, and pulse rate are often decreased. Rhabdomyolysis may result from prolonged immobility.
2. Chronic ethanol abuse is associated with numerous complications:
   1. Hepatic toxicity includes fatty infiltration of the liver, alcoholic hepatitis, and eventually cirrhosis. Liver injury can lead to portal hypertension, ascites, bleeding from esophageal varices and hemorrhoids; hyponatremia from fluid retention; and bacterial peritonitis. Production of clotting factors is impaired, leading to prolonged prothrombin time. Hepatic metabolism of drugs and endogenous toxins is impaired and may contribute to hepatic encephalopathy.
   2. Gastrointestinal bleeding may result from alcohol-induced gastritis, esophagitis, and duodenitis. Other causes of massive bleeding include Mallory-Weiss tears of the esophagus and esophageal varices. Acute pancreatitis is a common cause of abdominal pain and vomiting.
   3. Cardiac disorders include various dysrhythmias, such as atrial fibrillation, that may be associated with potassium and magnesium depletion and poor caloric intake (“holiday heart”). Cardiomyopathy has been associated with long-term alcohol use. (Cardiomyopathy was also historically associated with ingestion of cobalt used to stabilize beer.)
   4. Neurologic toxicity includes cerebral atrophy, cerebellar degeneration, and peripheral stocking-glove sensory neuropathy. Nutritional disorders such as thiamine (vitamin B₁) deficiency can cause Wernicke encephalopathy or Korsakoff psychosis.
   5. Hematologic toxicity may manifest as leukopenia, thrombocytopenia and macrocytosis with or without anemia. These hematologic effects result from ethanol's direct toxicity as well as its interference with folate metabolism.
   6. Alcoholic ketoacidosis is characterized by anion gap metabolic acidosis and elevated levels of beta-hydroxybutyrate and, to a lesser extent, acetoacetate. The osmolar gap may also be elevated, causing this condition to be mistaken for methanol or ethylene glycol poisoning.
3. Alcohol withdrawal. Sudden discontinuation after chronic high-level alcohol use often causes headache, tremulousness, anxiety, palpitations, and insomnia. Brief, generalized seizures may occur, usually within 6-12 hours of decreased ethanol consumption. Sympathetic nervous system overactivity may progress to delirium tremens (DTs), a life-threatening syndrome characterized by tachycardia, diaphoresis, hyperthermia, psychomotor agitation, hallucinations, and delirium, which usually manifests 48-72 hours after cessation of heavy alcohol use. Risk factors for the development of DTs include a history of previous severe alcohol withdrawal, previous DTs or withdrawal seizures, older age, heavy alcohol use, and abnormal liver function. Even with appropriate treatment, delirium tremens may cause mortality ranging from 5% to 15% due to cardiovascular and respiratory collapse.
4. Other problems. Ethanol users sometimes intentionally or accidentally ingest ethanol substitutes, such as isopropyl alcohol, methanol, and ethylene glycol. In addition, ethanol may be used for swallowing large numbers of pills in a suicide attempt. Disulfiram, a treatment for chronic alcoholism, can cause a serious acute reaction when ingested with ethanol.

Of ethanol intoxication is usually simple, based on the history of ingestion, the characteristic smell of fresh alcohol or the fetid odor of acetaldehyde and other metabolic products, and the presence of nystagmus, ataxia, and altered mental status. However, other disorders may accompany or mimic intoxication, such as hypoglycemia, head trauma, hypothermia, meningitis, Wernicke encephalopathy, and intoxication with other drugs or poisons.

1. Specific levels. Serum ethanol levels are typically available at most hospital laboratories and, depending on the method used, are accurate and specific. Note that serum levels are approximately 12-18% higher than corresponding whole-blood values.
   1. In general, there is only rough correlation between blood levels and clinical presentation; however, an ethanol level below 300 mg/dL in a comatose patient should initiate a search for alternative causes.
   2. If ethanol levels are not readily available, the ethanol concentration may be estimated by calculating the osmol gap.
   3. The metabolite ethyl glucuronide is present in urine for up to 5 days after heavy ethanol ingestion.
2. Alcohol breathalyzer. Hand-held breath alcohol analyzers reliably measure alcohol concentrations in exhaled breath, which is highly correlated with blood ethanol concentrations. Certain substances can produce false positives.
3. Suggested laboratory studies in the acutely intoxicated patient may include glucose, electrolytes, BUN, creatinine, liver aminotransferases, prothrombin time (PT/INR), magnesium, arterial blood gases or oximetry, and chest radiography (if pulmonary aspiration is suspected). Consider CT scan of the head if the patient has focal neurologic deficits or altered mental status inconsistent with the degree of blood alcohol elevation.

1. Emergency and supportive measures
   1. Acute intoxication. Treatment is mainly supportive.
      1. Protect the airway to prevent aspiration and intubate and assist ventilation if needed.
      2. Give glucose and thiamine, and treat coma and seizures if they occur.
      3. Correct hypothermia with gradual rewarming.
      4. Most patients will recover within 4-6 hours. Observe children until their blood alcohol level is below 50 mg/dL and there is no evidence of hypoglycemia.
   2. Alcoholic ketoacidosis. Treat with volume replacement, thiamine, and supplemental glucose. Most patients recover rapidly.
   3. Alcohol withdrawal. Treat with benzodiazepines (eg, diazepam, 5-10 mg IV initially and repeat as needed and/or phenobarbital (p 573).
   4. Alcohol use disorder. Treatment plans involve medical management to prevent acute withdrawal in addition to psychological counseling/support and oral medications (eg, acamprosate, disulfiram, naltrexone).
2. Specific drugs and antidotes. There is no available specific ethanol receptor antagonist.
3. Decontamination. Because ethanol is rapidly absorbed, gastric decontamination is usually not indicated unless other drug ingestion is suspected. Consider aspirating gastric contents with a small, flexible tube if the alcohol ingestion was massive and recent (within 30-45 minutes). Activated charcoal does not effectively adsorb ethanol but may be given if other drugs or toxins were ingested.
4. Enhanced elimination. Metabolism of ethanol normally occurs at a fixed rate of approximately 12-25 mg/dL/h. Elimination rates are faster in persons with chronic alcoholism and at serum levels above 300 mg/dL. Hemodialysis efficiently removes ethanol, but enhanced removal is rarely needed because supportive care is usually sufficient. Hemoperfusion and forced diuresis are not effective.