Select 5-Minute Pediatrics Topics

Alcohol (Ethanol) Intoxication

Basics

Description

  • Acute ingestion (accidental or intended) of alcohol, resulting in loss of inhibition, often associated with unruly/violent behavior, impaired judgment and/or coordination, diminished alertness/responsiveness, and sedation or coma
  • Accidental ingestion is more common in toddlers and younger children.
  • Frequency of intentional alcohol use increases with age.
  • Alcohol–drug interactions are common because acute intoxication reduces hepatic clearance for other drugs, thereby increasing their serum concentrations.

Epidemiology

Alcohol is 2nd only to caffeine in prevalence and incidence of use among substances of use/abuse.

Prevalence

  • >75% of high school students have had more than 1 drink in their lifetime; 37% had their 1st drink before 8th grade.
  • Rates of past 30-day alcohol use in 2009 were 3.5% (12–13 yo), 13.0% (14–15 yo), 26.3% (16–17 yo), 49.7% (18–20 yo), and 70.2% (21–25 yo).
  • Nearly 50% of high school students report current alcohol use, and 30% report heavy drinking in the past 30 days (>5 drinks).
  • Underage (12–20 yo) drinkers are 3 times more likely than adults to use illicit drugs with alcohol.
  • Almost 1/3 of high school students have ridden in a car with a driver who has been drinking alcohol.
  • Rates of driving under the influence are age-related: in 2009, 6.3% of 16–17 yo, 16.6% of 18–20 yo, and 24.8% of 21–25 yo reported driving under the influence in the past year.
  • Rates of binge alcohol use (5 or more drinks in 1 day in past 30 days) in 2009 were 1.6% (12–13 yo), 7.0% (14–15 yo), 17.0% (16–17 yo), 34.7% (18–20 yo), and 46.5% (21–25 yo).
  • Among full-time enrolled college students (18–22 yo), 63.9% were current drinkers, 43.5% were binge drinkers, and 16.0% were heavy drinkers (5 or more drinks in 1 day on 5 or more days in past 30 days); full-time college students have higher rates of alcohol use than part-time students or young adults not enrolled in college.

Risk Factors

Patients with psychiatric conditions are at an increased risk for abuse of alcohol and other drugs.

General Prevention

  • Promote family discussions about alcohol use and abuse.
  • Provide safety recommendations to prevent accidental ingestions.

Pathophysiology

  • Effects of alcohol ingestion are related to dose, the time in which alcohol was consumed and then absorbed, and the patient's history of alcohol exposure.
  • Alcohol absorption, decreased by the presence of food in the stomach and increased if liquid is carbonated, occurs rapidly and largely in the small intestine.
  • Minimal quantities of alcohol are excreted in urine, sweat, and breath.
  • >90% of alcohol oxidized in liver follows zero-order kinetics, primarily by alcohol dehydrogenase (ADH) and then acetaldehyde dehydrogenase (ALDH); rate of metabolism is fixed (not related to dose or time) and is proportional to body weight. Ethnic/racial and gender variabilities exist on quantity and efficacy of ADH.
  • Ethanol is metabolized by ADH to acetaldehyde, then to acetate, and finally to ketones, fatty acids, or acetone; ketosis and, infrequently, metabolic acidosis can occur.
  • Respiratory acidosis can occur secondary to carbon dioxide retention from respiratory depression due to ethanol intoxication.
  • Hypoglycemia occurs during acute ethanol intoxication owing to impaired gluconeogenesis resulting from changes in the NADH/NAD+ ratio associated with ethanol metabolism.
  • Alcohol affects the CNS primarily through the γ-aminobutyric acid (GABA) and glutamate neurotransmitter systems.

Etiology

Alcoholic beverages (water and ethanol) are produced from fermentation/distillation of sugar from grapes (wine), grains/corn (beer/whiskey), potatoes (vodka), or sugar cane (rum). After distillation, alcohol is mixed into solution to make specific beverages; products are marketed according to alcohol content or “proof,” which is twice the percent. Alcohol content ranges from 3–6% (6–12 proof) in beer to 40–75% (80–150 proof) in vodka/rum/whiskey. Alcohol is often consumed concurrently with other substances (licit and illicit), presenting a mixed clinical picture of intoxication.

Commonly Associated Conditions

  • Alcohol is involved in 30% of all drug overdoses.
  • A significant percentage of adolescent trauma patients, especially victims of gunshot wounds, have positive toxicology screens for alcohol and other drugs.

Diagnosis

History

  • Medical: Baseline health will affect patient's response to alcohol; diabetics, for example, may have worse hypoglycemia.
  • Type and dose of other drugs ingested:
    • Clinical effects of and treatment for other ingestions can vary depending on substance.
    • Polysubstance ingestion is very common.
  • Psychiatric history: Evaluate for possible suicidal ideation.
  • Gathering details regarding the alcohol consumed (type, amount, and over what time period) may help predict clinical course. For example, blood alcohol concentration (BAC) may continue rising if ingestion occurred recently.
  • Intoxication presents clinically with signs ranging from lack of coordination, slurred speech, and confusion (BAC of 20–200 mg/dL) to ataxia and nausea/vomiting (BAC 200–300 mg/dL) to amnesia, seizures, or coma (BAC >300 mg/dL).

Physical Exam

  • Bruises, lacerations, and fractures may suggest trauma and raise concern about CNS injury.
  • Neurologic exam, including mental status, will assess degree of intoxication and consciousness, including patient's ability to protect his or her airway, and risk for aspiration.
  • Tachycardia, hypotension may indicate dehydration.
  • Fever may suggest infection.
  • Average time for normalization of mental status in intoxicated adults is 3–3.5 hours; patients without clinical improvement in 3 hours should be evaluated for other causes of altered mental status.

Diagnostic Tests and Interpretation

Lab

  • Blood alcohol concentration:
    • Generally correlates with clinical picture.
    • In children, signs of intoxication may be present at levels of 50 mg/dL.
    • Serum levels of 600–800 mg/dL can be fatal.
  • Blood and/or urine toxicology screen:
    • Most urine toxicology screens do not test for alcohol.
    • Concurrent ingestions are common.
  • Acetaminophen level:
    • Usually not part of the general serum toxicology screen
    • Consider if polysubstance ingestion suspected and/or if patient has suicidal ideation
  • Serum electrolytes:
    • Alcohol is a diuretic. The associated nausea and vomiting seen with intoxication may result in severe dehydration.
    • Ketosis and, infrequently, metabolic acidosis can occur.
  • Serum glucose level: Ethanol inhibits gluconeogenesis and can be associated with hypoglycemia.
  • Blood gas can show both respiratory and metabolic acidosis.

Differential Diagnosis

  • Environmental:
    • Other ingestions (overdose of sedatives or illicit drugs, such as benzodiazepines, marijuana, narcotics, lysergic acid diethylamide [LSD], and phencyclidine [PCP])
    • Toxic exposures (ethylene glycol, methanol, carbon monoxide)
    • Head trauma
  • Infection
    • Meningitis
    • Encephalitis
    • Sepsis
  • Tumor: Brain tumor
  • Metabolic:
    • Hypoglycemia
    • Ketoacidosis
    • Hyperammonemia
    • Electrolyte imbalances (hyponatremia, hypernatremia)
  • Miscellaneous:
    • Increased intracranial pressure from hydrocephalus, mass, other
    • Stroke

Treatment

Medication

IV dextrose as needed for hypoglycemia

Additional Treatment

General Measures

  • Assess airway, breathing, and circulation (ABC).
  • Protect airway: The patient may require intubation and mechanical ventilation.
  • Mainstay is supportive therapy, as no specific ethanol antidote exists.
  • Appropriate trauma management as needed
  • Because alcohol is absorbed rapidly, gastric lavage is indicated only if the patient is seen immediately after ingestion (within minutes).

ISSUES FOR REFERRAL

  • Refer to substance abuse specialist (addiction medicine, psychiatrist, or certified addictions counselor) for detailed evaluation and treatment.
  • Refer for psychiatric evaluation if depression, anxiety, suicidal ideation, or any other mental health condition is suspected.
  • Assess for other risk-taking behaviors, including other substance use, sexual activity, use of motor vehicles while intoxicated, weapon carrying, and delinquency, and their sequelae, including pregnancy, sexually transmitted infections, and violence.

In-Patient Consideratons

Initial Stabilization

Keep patient awake; watch for vomiting as patients are at risk for choking owing to depressed gag reflex.

Admission Criteria

  • Unstable vital signs (hypotension)
  • Persistent CNS depression/impaired mental status
  • Potential severity of comorbid psychiatric conditions (depression/suicidality)
  • Inability to contact a parent/guardian

IV Fluids

IV fluids for dehydration and hypotension

Nursing

Observe and monitor vital signs and neurologic status.

Discharge Criteria

  • Stable vital signs
  • Patient awake, alert, responsive, and oriented
  • Decreasing BAC
  • Parent/guardian fully informed about patient's alcohol use

Ongoing Care

Diet

NPO secondary to depressed gag reflex

Prognosis

BAC serum levels of 600–800 mg/dL can be fatal.

Complications

  • Diuresis and dehydration
  • Vasodilation and hypotension
  • Vomiting, aspiration, potential respiratory arrest
  • Hypoglycemia
  • Metabolic acidosis
  • Impaired mental status
  • Engagement in risk-taking behaviors (e.g., other drug use, unprotected intercourse) while intoxicated
  • CNS depression
  • Gastritis
  • GI bleeding
  • Acute pancreatitis
  • Motor vehicle collisions associated with driving while intoxicated
  • Alcoholism
  • Alcohol withdrawal following a period of intoxication in chronic users (symptoms include tachycardia, elevated blood pressure, irritability, nausea, vomiting, and tremor)

Additional Reading

  1. Centers for Disease Control and Prevention. National drunk and drugged driving prevention month—December 2003. MMWR Morb Mortal Wkly Rep. 2003;52:1185–1186.
  2. Coupey SM. Specific drugs. In: Schydlower M, ed. Substance abuse: A guide for health professionals, 2nd ed. Elk Grove Village, IL: American Academy of Pediatrics; 2002:208–215.  [PMID:12653810]
  3. Foxcroft DR, Ireland D, Lister-Sharp DJ, et al. Longer-term primary prevention for alcohol misuse in young people: A systematic review. Addiction. 2003;98:397–411.
  4. Pitzele HZ, Tolia VM. Twenty per hour: Altered mental state due to ethanol abuse and withdrawal. Emerg Med Clin N Am. 2010;28:683–705.  [PMID:11063358]
  5. Porter RS. Alcohol and injury in adolescents. Pediatr Emerg Care. 2000;16(5):316–320.
  6. Substance Abuse and Mental Health Services Administration. Results from the 2009 National Survey on Drug Use and Health: Volume I. Summary of national findings (Office of Applied Studies, NSDUH Series H-38A, HHS Publication No. SMA 10-4856 Findings). Rockville, MD: Substance Abuse and Mental Health Services Administration; 2010.

Codes

ICD-9

980.0 Toxic effect of ethyl alcohol

ICD-10

  • F10.920 Alcohol use, unspecified with intoxication, uncomplicated
  • F10.929 Alcohol use, unspecified with intoxication, unspecified
  • T51.0X1A Toxic effect of ethanol, accidental (unintentional), initial encounter
  • T51.0X2A Toxic effect of ethanol, intentional self-harm, initial encounter
  • T51.0X4A Toxic effect of ethanol, undetermined, initial encounter

SNOMED

25702006 alcohol intoxication (disorder)

FAQ

  • Q: How quickly does a person metabolize alcohol?
  • A: The liver metabolizes ∼10 g of ethanol per hour, which corresponds to a decline in BAC of 18–20 mg/dL/hr.
  • Q: What is the legal level of BAC that defines driving under the influence of alcohol?
  • A: This varies by state, but generally is between 80 and 100 mg/dL.
  • Q: Why do some individuals, particularly of Asian descent, turn red or develop signs of pruritus after ingesting alcohol?
  • A: Flushing, pruritus, and nausea are due to high levels of acetaldehyde. Variations in the metabolic activity of dehydrogenase enzymes are associated with factors such as gender, history of alcohol use, and genetics. Decreased ALDH activity, which is more common in Native Americans and Asians, can result in increased levels of acetaldehyde (an estimated 50% of Asians).

Authors

Ann B. Bruner


© Wolters Kluwer Health Lippincott Williams & Wilkins

Alcohol (Ethanol) Intoxication is a sample topic found in
Medicine Central.

To find other Medicine Central topics
please login or purchase a subscription.

Content Manager
Related Content
Ethanol
Osmolality serum
Toxic Alcohols
Coma