Ethanol

CAS RN: 64-17-5

Treatment Overview

0.4.2 ORAL EXPOSURE
  • A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    • 1) Patients who appear mildly intoxicated may be simply managed with supportive care only. An ethanol concentration is generally not needed for management. Patients can be discharged when they are not clinically intoxicated (no ataxia, nystagmus, or slurred speech). Significant CNS depression indicates a more severe poisoning.
  • B) MANAGEMENT OF SEVERE TOXICITY
    • 1) Measure a serum ethanol level if ethanol is believed to be the cause of altered mental status, and consider and rule out other reversible causes of altered mental status, such as hypoglycemia, hypoxia, and opiate intoxication. Patients who are comatose may require airway protection. Other causes of altered mental status should be considered, because ethanol is often a coingestant with other drugs, and intoxicated patients are predisposed to traumatic injuries. Children may be susceptible to hypoglycemia following an ethanol ingestion. Alcoholic ketoacidosis is a condition that typically develops in chronic drinkers that results in impaired gluconeogenesis. It often develops after binge drinking combined with malnutrition. Vomiting, abdominal pain, and an anion-gap metabolic acidosis develop. Treatment is with fluid replacement and dextrose supplementation. Thiamine, folate, and other vitamins should also be provided intravenously. Ethanol withdrawal is a potentially life-threatening condition that may result in chronic drinkers following a period of abstinence. It usually begins with autonomic hyperactivity, tachycardia, tremor, hypertension, agitation leading to hallucinations, and seizures. Treatment is generally with benzodiazepines for sedation. In patients with resistant symptoms, consider the use of propofol or a barbiturate such as phenobarbital.
  • C) DECONTAMINATION
    • 1) PREHOSPITAL: There is no role for prehospital decontamination.
    • 2) HOSPITAL: Activated charcoal is not indicated, because it poorly adsorbs to ethanol, but it may be used in the appropriate conditions if there are coingestants. Consider the use of nasogastric suction for patients who present with massive ingestions within 30 minutes. This procedure is rarely indicated.
  • D) AIRWAY MANAGEMENT
    • 1) Patients who are comatose or with an altered mental status may need orotracheal intubation and mechanical ventilation.
  • E) ANTIDOTE
    • 1) There is no specific antidote.
  • F) ENHANCED ELIMINATION
    • 1) Hemodialysis can eliminate ethanol but is rarely indicated. Consider for patients with severe intoxication (eg, hypotension) not responding to supportive care.
  • G) PATIENT DISPOSITION
    • 1) HOME CRITERIA: Patients who are minimally intoxicated with no use of coingestants can be observed at home if there is another responsible, nonintoxicated adult. Symptomatic children or children with ingestions that are expected to cause more than minimal symptoms should be referred to a healthcare facility.
    • 2) OBSERVATION CRITERIA: Patients should be observed until they are not clinically intoxicated. If they are minimally intoxicated; there is a responsible, nonintoxicated adult who can provide care; and there is no evidence of trauma or other medical problems, they can potentially be discharged, depending on the circumstances. Refer patients with chronic alcoholism or high-risk drinking for detoxification and rehabilitation.
    • 3) ADMISSION CRITERIA: Admit patients with unstable vital signs, altered mental status that does not improve, concerning coingestants, associated serious trauma or medical conditions, or signs and symptoms of withdrawal.
    • 4) CONSULT CRITERIA: Consult a poison center or medical toxicologist for assistance in managing severe poisonings.
  • H) PITFALLS
    • 1) Ethanol is often a coingestant with other drugs. Intoxicated patients are predisposed to traumatic injuries, which may be more difficult to diagnose in an intoxicated patient. Ethanol can account for an elevated osmolar gap. Small amounts of concentrated ethanol solutions may result in significant toxicity in children.
  • I) PHARMACOKINETICS
    • 1) Ethanol is well absorbed (80% to 90%). Peak concentrations are achieved within 0.5 to 1.5 hours after a single ingestion. Volume of distribution is approximately 0.6 L/kg. Hepatically metabolized, primarily by alcohol dehydrogenase (which is saturable at low ethanol concentrations) and to a lesser extent by cytochrome P2E1 (which is inducible with chronic consumption) and by the peroxidase-catalase system.
  • J) TOXICOKINETICS
    • 1) Elimination changes from first-order to zero-order kinetics at low blood ethanol concentrations. Non-tolerant drinkers typically eliminate ethanol at a rate of approximately 15 to 20 mg/dL/hr, whereas chronic drinkers have an elimination rate of approximately 20 to 30 mg/dL/hr. Patients also develop tolerance to some effects.
  • K) DIFFERENTIAL DIAGNOSIS
    • 1) The differential diagnosis includes other xenobiotics that present with intoxication, including ingestions of isopropanol and methanol, benzodiazepines, barbiturates, and GHB. The differential diagnosis of altered mental status is extremely broad and includes toxicologic and nontoxicologic causes.
  • L) DRUG INTERACTIONS
    • 1) Coingestions with other CNS and respiratory depressants (eg, benzodiazepines, barbiturates, opioids) increases toxicity.
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