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Commercial beer, wine, and liquors contain various amounts of ethanol. Ethanol also is 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 co-ingestant with other drugs in suicide attempts. Ethanol may also serve as a competitive substrate in the emergency treatment of methanol and ethylene glycol poisonings (See Ethylene Glycol and Other Glycols).

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  1. Mechanism of toxicity

    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. 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.

  2. Toxic dose. 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 intoxication varies by state, with a range of 0.08–0.1 g/dL.

    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.

  3. Clinical presentation

    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 scarring leads to portal hypertension, ascites, and bleeding from esophageal varices and hemorrhoids; hyponatremia from fluid retention; and bacterial peritonitis. Production ...

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