eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Toxicology

Toxicity, Ethanol

Author: Christopher I Doty, MD, FAAEM, Assistant Professor of Emergency Medicine, Residency Program Director, Department of Emergency Medicine, Kings County Hospital Center, State University of New York Downstate Medical Center
Coauthor(s): Sage W Wiener, MD, Assistant Professor, Department of Emergency Medicine, State University of New York Downstate, Director of Medical Toxicology, Department of Emergency Medicine, Kings County Hospital Center; Binita R Shah, MD, FAAP, Professor of Clinical Pediatrics and Emergency Medicine, SUNY Health Science Center at Brooklyn, Director of Pediatric Emergency Medicine, Depts of Emergency Medicine and Pediatrics, Kings County Hospital Center
Contributor Information and Disclosures

Updated: Feb 8, 2008

Introduction

Background

Ethanol is a 2-carbon–chain alcohol; the chemical formula is CH2 CH3 OH. It is ubiquitous throughout the world and is a leading cause of morbidity across cultures. Ethanol is the most common psychoactive drug used by children and adolescents in the United States and is one of the most commonly abused drugs in the world. In a 1995 questionnaire study of high-school students, 88% admitted to using ethanol, and 37% admitted to consuming 5 or more drinks in one night during the previous 2 weeks.

Pathophysiology

Ethanol has a volume of distribution (0.6 L/kg) and is readily distributed throughout the body. The primary route of absorption is oral, although it can be absorbed by inhalation and even percutaneously.

Ethanol exerts its actions through several mechanisms. For instance, it binds directly to the gamma-aminobutyric acid (GABA) receptor in the CNS and causes sedative effects similar to those of benzodiazepines, which bind to the same GABA receptor. Furthermore, ethanol is also an N -methyl-D-aspartate (NMDA) glutamate antagonist in the CNS. Ethanol also has direct effects on cardiac muscle, thyroid tissue, and hepatic tissue.

Ethanol is rapidly absorbed, and peak serum concentrations typically occur 30-60 minutes after ingestion. Its absorption into the body starts in the oral mucosa and continues in the stomach and intestine. Both high and low concentrations of ethanol are slowly absorbed; the co-ingestion of food also slows absorption.

In young children, ethanol causes hypoglycemia and hypoglycemic seizures; these complications are not as common in older patients. Hypoglycemia occurs secondary to ethanol's inhibition of gluconeogenesis and secondary to the relatively smaller glycogen stores in the livers of young children. In toddlers who have not eaten for several hours, even small quantities of ethanol can cause hypoglycemia.

Ethanol is primarily metabolized in the liver. Approximately 90% of an ethanol load is broken down in the liver; the remainder is eliminated by the kidneys and lungs. In children, ethanol is cleared by the liver at the rate of approximately 30 mg/dL/h, which is more rapid than the clearance rate in adults.

In the liver, ethanol is broken down into acetaldehyde by alcohol dehydrogenase (ADH). Then, it is further broken down to acetic acid by acetaldehyde dehydrogenase. Acetic acid is fed into the Krebs cycle and is ultimately broken down into carbon dioxide and water. Also, a gastric isozyme of ADH breaks down a significant amount of ethanol before it can be absorbed; sex differences in ADH may, in part, account for differences in ethanol effects per given quantity consumed between men and women.

Frequency

United States

Ethanol use and intoxication in adolescents is widespread in the United States. In a 2004 sample of high-school students, 52% of those polled said they had "significant experiences" with ethanol prior to beginning high school.1 The actual incidence of ethanol poisoning in young children is unknown.

International

Ethanol use in countries other than the United States is common; however, literature about the incidence of ethanol intoxication in pediatric populations in other countries is scant.

Mortality/Morbidity

  • Trauma is the leading cause of mortality in children, and ethanol use is linked to a 3- to 7-fold increased risk of trauma. Ethanol use is also strongly linked to other risk-taking behaviors that can lead to minor trauma, assault, illicit drug use, and teenage pregnancy.
  • Approximately 40% of the 10,000 annual nonautomotive pediatric deaths (usually drownings and falls) are associated with ethanol. 
  • The concomitant use of ethanol and other drugs is common, and combinations of ethanol with other sedative-hypnotics or opioids may potentiate the sedative effects.
  • Ethanol greatly increases the risk of trauma, especially trauma due to motor vehicle collisions or violent crimes.
  • The intoxicated individual often engages in high-risk activities, even though his or her reflexes are substantially slowed.

Race

Data supporting a racial predilection in pediatric populations are limited. Studies of adult patients suggest a lower tolerance in patients of Asian descent. This is most likely due to differences in concentrations of ADH.

Sex

Data supporting a sex predilection in pediatric populations are limited. Studies in adults have reported that ADH breaks down a significant amount of ethanol before it can be absorbed, which may, in part, account for differences in tolerance between men and women.

Age

Ethanol intoxication can affect children and adults of all ages.

Clinical

History

  • Ethanol intoxication is often difficult to diagnose in young children and toddlers. Important questions to ask parents include the following:
    • Was a source of ethanol easily available to the child? For instance, was an open alcoholic drink left out after a party?
    • Is the alcohol in the house locked up? Are ethanol beverages in a place that the child can easily reach?
    • Is the child taking any over-the-counter medications that might contain alcohol, such as cough and cold medications?
    • Could older siblings in the house have given the child alcohol?
    • Did the parents give the child an alcohol bath?
    • Did the child drink an ethanol-containing substance (eg, perfume, cleaning fluids) not meant to be ingested?
  • If ingestion is known or suspected, determining exactly what and how much the patient ingested is important. The name, composition, and concentration of the alcohol are helpful.
    • If the amount is unknown, have the parents estimate how much was in the container and subtract that amount from the total volume of the container to estimate the amount ingested or possibly ingested.
    • The amount of ethanol in a product is often expressed as a percentage, which is the ratio of the volume of pure ethanol to the total volume of fluid.
      • The formula for determining the percentage of ethanol is as follows: X% = X g/100 mL
      • The concentration of ethanol in distilled spirits may be expressed as a proof, which is equal to twice the percentage of ethanol.
    • Ethanol concentrations in some common substances are as follows: liquid cold remedies, 2-25%; mouthwashes, 7-27%; rubbing alcohol, usually 70% (although most commonly, rubbing alcohol contains isopropanol); aftershave lotions, 15-80%; and perfumes and colognes, 25-95%. Other toxic alcohols are also often found in these products, such as methanol in perfume or cologne.
    • Ethanol concentrations in some common alcoholic beverages are as follows: whiskey, 40-60%; liqueurs, 22-50%; wine, 8-16%; and beer, 3-7%.
    • Be aware that patients often grossly underestimate the amount of Ethanol that they ingested.
  • Obtain a history from the emergency medical services (EMS) personnel, parents, relatives, or anyone else who accompanied the patient to the hospital.
  • Because ethanol predisposes patients to other causes of altered mental status (eg, trauma), consider the other causes as well.
  • Be aware of the other substances in the ingested fluid that may be toxins.
  • Because of potential legal implications in the United States, pediatric patients are often evasive in stating their history of possible ingestion. Outside the United States, ethanol consumption by children is often more culturally acceptable and less stigmatized.
  • Adolescents often present to the emergency department (ED) with acute illness or decreased mental status. Often, these patients do not admit to their use of alcohol. Assess for a history of possible ethanol use in all patients who present to the ED with an altered mental status.
  • A positive family history of alcohol abuse is significant because children of parents with alcoholism have a 2- to 4-fold increased risk of alcoholism.

Physical

Infants and toddlers have a clinical course significantly different from that of adolescents and adults. Ethanol ingestion and intoxication can lead to a marked hypoglycemic state in infants and young children. Ethanol has a CNS depressant action that can also lead to respiratory depression and hypoxia. Ethanol has a sedative effect, producing general CNS depression, respiratory depression, and often hypoglycemia. Young children often present to the ED after drinking discarded alcoholic beverages left within their reach during and after parties or after ingesting a fluid that contains ethanol. In the older children and adolescents, ethanol intoxication causes CNS depression, leading to respiratory depression. Hypoglycemia is less common in this group.

As with all patients, a careful physical examination is warranted. In patients in whom ethanol ingestion is suspected, carefully evaluate his or her mental status and perform a thorough neurologic examination. Evaluate for signs of trauma, neglect, and illicit drug use. Ethanol ingestion makes the patient more prone to trauma due to accidents or crime. The clinician's most crucial clues to ethanol ingestion are a change in the patient's mental status and the smell of alcohol on the patient's breath. The presence or absence of ethanol on breath cannot be used to diagnose or exclude ethanol intoxication.

Compared with nonintoxicated teenagers, intoxicated teenagers are much more likely to be affected by violence, even after drinking only one alcoholic beverage. Recent reports describe the use of sedatives with alcohol to create date-rape drug combinations. Therefore, possible sexual assault should be considered in teenaged patients.

Young children commonly ingest ethanol when they drink a liquid not meant for consumption, such as perfume or cleaning agents. Frequently, other chemicals in the ingested substance are more toxic than the ethanol. Therefore, a detailed physical examination is important to evaluate for any signs and symptoms caused by these other toxins. Also, give special attention to the examination of the oral cavity and airway because substances in cleaning agents can cause chemical burns to these areas.

In children, the classic triad of signs of ethanol intoxication includes coma, hypoglycemia, and hypothermia. These signs usually occur when the Ethanol level in the blood exceeds 50-100 mg/dL. However, hypoglycemia can be seen with serum Ethanol levels as low as 50 mg/dL. Relatively small amounts of ethanol can produce hypoglycemia, especially in patients with low glycogen stores, such as infants and small children who have not eaten for several hours.

  • Acute ethanol intoxication can cause the following:
    • CNS depression
    • Mild vasodilatation leading to a modest decrease in blood pressure
    • Flushed skin
    • Urticaria2
    • Inhibition of spermatogenesis
    • Hypothermia
    • Tachycardia
    • Myocardial depression
    • Variable pupillary response
    • Respiratory depression
    • Decreased pulmonary secretion clearance
    • Diuresis
    • Loss of behavior inhibitions
    • Hypoglycemia
    • Loss of fine motor control 
  • High doses of ethanol can cause the following:
    • Loss of gross muscle control (ataxia, slurred speech)
    • Acute pancreatitis
    • Severe myocardial depression
    • Hypotension
    • Atrial fibrillation
    • Lactic acidosis
    • Congestive heart failure
    • Pulmonary edema
    • Arrhythmias
    • Cardiovascular collapse
    • Sudden death 
  • Chronic ethanol use can lead to the following:
    • Fetal alcohol syndrome
    • Chronic pancreatitis
    • Hepatic dysfunction
    • Hematologic disorders
    • Numerous electrolyte abnormalities
    • Hypertension
    • Cardiomyopathy
    • Malnutrition
    • Obesity

Causes

Pediatric ethanol intoxication occurs in patterns that vary with the patient's age. Contributing factors may include poor parenting habits or inadequate supervision.

  • In infants and children, ethanol intoxication often has an unintentional cause.
    • Infants usually ingest alcohol as a result of their caregivers giving them over-the-counter cold medications that contain significant amounts of ethanol. 
    • Also, parents may be misinformed about how to treat an illness. In some cultures, caregivers commonly give infants fluids that contain alcohol to treat colic, or they may even put whiskey in an infant's mouth to soothe the discomfort of teething. 
    • In addition, infants and toddlers may be given ethanol orally or percutaneously. Usually, their caregivers do this to treat the child's cold symptoms. The parents may also give the child alcohol baths to treat a fever. This is also common with  isopropanol, but baths with isopropanol may have different effects 
  • Young children usually develop ethanol intoxication by drinking ethanol.
    • In children, the primary sources of ingested alcohol are beverages, often in the form of a discarded drink left within the child's reach during or after parties, especially during the Christmas holiday.
    • Other sources of alcohol include colognes or perfumes, mouthwashes, cold medicines or other medications, aftershave lotions, and cleaning fluids and other household fluids.
  • Adolescents may ingest alcohol as a response to peer pressure or a stressful home environment, as a way to assert their autonomy, as an escape from their daily life, or as an imitation of the habits of an adult caregivers.
  • Older children and adolescents frequently become intoxicated by knowingly drinking alcoholic beverages with a peer group or, less frequently, as part of a suicide attempt.

More on Toxicity, Ethanol

Overview: Toxicity, Ethanol
Differential Diagnoses & Workup: Toxicity, Ethanol
Treatment & Medication: Toxicity, Ethanol
Follow-up: Toxicity, Ethanol
References

References

  1. McKinnon SA, O'rourke KM, Thompson SE, Berumen JH. Alcohol use and abuse by adolescents: the impact of living in a border community. J Adolesc Health. Jan 2004;34(1):88-93. [Medline].

  2. Elphinstone PE, Kobza Black A, Greaves MW. Alcohol-induced urticaria. J R Soc Med. Apr 1985;78(4):340-1. [Medline].

  3. Mennella JA, Beauchamp GK. The transfer of alcohol to human milk. Effects on flavor and the infant's behavior. N Engl J Med. Oct 3 1991;325(14):981-5. [Medline].

  4. Baer JS, Barr HM, Bookstein FL, et al. Prenatal alcohol exposure and family history of alcoholism in the etiology of adolescent alcohol problems. J Stud Alcohol. Sep 1998;59(5):533-43. [Medline].

  5. Bates BA, Shannon MW, Woolf AD. Ethanol-related visits by adolescents to a pediatric emergency department. Pediatr Emerg Care. Apr 1995;11(2):89-92. [Medline].

  6. Beech DJ, Mercadel R. Correlation of alcohol intoxication with life-threatening assaults. J Natl Med Assoc. Dec 1998;90(12):761-4. [Medline].

  7. Caballeria J. Current concepts in alcohol metabolism. Ann Hepatol. Apr-Jun 2003;2(2):60-8. [Medline].

  8. Ceballos NA. Tobacco use, alcohol dependence, and cognitive performance. J Gen Psychol. Oct 2006;133(4):375-88. [Medline].

  9. Chabali R. Diagnostic use of anion and osmolal gaps in pediatric emergency medicine. Pediatr Emerg Care. Jun 1997;13(3):204-10. [Medline].

  10. Church AS, Witting MD. Laboratory testing in ethanol, methanol, ethylene glycol, and isopropanol toxicities. J Emerg Med. Sep-Oct 1997;15(5):687-92. [Medline].

  11. Eckardt MJ, File SE, Gessa GL, et al. Effects of moderate alcohol consumption on the central nervous system. Alcohol Clin Exp Res. Aug 1998;22(5):998-1040. [Medline].

  12. Ernst AA, Jones K, Nick TG, Sanchez J. Ethanol ingestion and related hypoglycemia in a pediatric and adolescent emergency department population. Acad Emerg Med. Jan 1996;3(1):46-9. [Medline].

  13. Gemma S, Vichi S, Testai E. Individual susceptibility and alcohol effects:biochemical and genetic aspects. Ann Ist Super Sanita. 2006;42(1):8-16. [Medline].

  14. Hernandez OH, Vogel-Sprott M, Ke-Aznar VI. Alcohol impairs the cognitive component of reaction time to an omitted stimulus: a replication and an extension. J Stud Alcohol Drugs. Mar 2007;68(2):276-81. [Medline].

  15. Hussain SZ, Rawal J, Henry JA. Gastric evacuation for acute ethanol intoxication in a three year old. J Accid Emerg Med. Jan 1998;15(1):54-62. [Medline].

  16. Kotwica M, Jarosz A, Kolacinski Z, Rogaczewska A. Sources of poisoning exposures in children during 1990-1995. An analysis of the National Poison Information Centre files. Int J Occup Med Environ Health. 1997;10(2):177-86. [Medline].

  17. Laitinen K, Lamberg-Allardt C, Tunninen R, et al. Transient hypoparathyroidism during acute alcohol intoxication. N Engl J Med. Mar 14 1991;324(11):721-7. [Medline].

  18. Lamminpaa A. Alcohol intoxication in childhood and adolescence. Alcohol Alcohol. Jan 1995;30(1):5-12. [Medline].

  19. Lamminpaa A, Vilska J, Korri UM, Riihimaki V. Alcohol intoxication in hospitalized young teenagers. Acta Paediatr. Sep 1993;82(9):783-8. [Medline].

  20. Lang RM, Borow KM, Neumann A, Feldman T. Adverse cardiac effects of acute alcohol ingestion in young adults. Ann Intern Med. Jun 1985;102(6):742-7. [Medline].

  21. Li J, Mills T, Erato R. Intravenous saline has no effect on blood ethanol clearance. J Emerg Med. Jan-Feb 1999;17(1):1-5. [Medline].

  22. Litovitz T. The alcohols: ethanol, methanol, isopropanol, ethylene glycol. Pediatr Clin North Am. Apr 1986;33(2):311-23. [Medline].

  23. Litt I. Alcohols. In: Behrman RE, Kliegman R, Jenson HB, eds. Nelson Textbook of Pediatrics. 16th ed. Philadelphia, Pa: WB Saunders; 2000:Chapter 113.1.

  24. Lopez GP, Yealy DM, Krenzelok EP. Survival of a child despite unusually high blood ethanol levels. Am J Emerg Med. May 1989;7(3):283-5. [Medline].

  25. O'Connor AD, Rusyniak DE, Bruno A. Cerebrovascular and cardiovascular complications of alcohol and sympathomimetic drug abuse. Med Clin North Am. Nov 2005;89(6):1343-58. [Medline].

  26. Osborn H. Ethanol. In: Goldfrank LR, Flomenbaum NE, Lewin NA, Weisman RS, Howland MA, Hoffman RS, eds. Goldfrank's Toxicologic Emergencies. 6th ed. McGraw-Hill Professional Publishing; 1998:1023-41.

  27. Ostrea EM Jr. Testing for exposure to illicit drugs and other agents in the neonate: a review of laboratory methods and the role of meconium analysis. Curr Probl Pediatr. Feb 1999;29(2):37-56. [Medline].

  28. Ragan FA Jr, Samuels MS, Hite SA. Ethanol ingestion in children. A five-year review. JAMA. Dec 21 1979;242(25):2787-8. [Medline].

  29. Rogers GC. Ethanol. In: Handbook of Common Poisonings in Children. 3rd ed. Elk Grove Village, IL: American Academy of Pediatrics, Committee on Injury and Poison Prevention; 1994.

  30. Rosett HL. A clinical perspective of the Fetal Alcohol Syndrome. Alcohol Clin Exp Res. Apr 1980;4(2):119-22. [Medline].

  31. Tovey C, Rana PS, Anderson DJ. Alcohol intoxication in a toddler. J Accid Emerg Med. Jan 1998;15(1):69-70. [Medline].

Further Reading

Keywords

ethanol, ethanol toxicity, alcohol intoxication, ethanol intoxication, drunkenness, inebriation, ethyl alcohol intoxication, alcohol overdose, ethanol poisoning, alcohol poisoning, drinking, psychoactive drug, hypoglycemia, alcohol abuse, hypoglycemia, hypoglycemic seizures, trauma risk, over-the-counter medication, alcoholism, respiratory depression, hypoxia, urticaria, hypothermia, myocardial depression, diuresis, acute pancreatitis, lactic acidosis, congestive heart failure, pulmonary edema, arrhythmia, cardiovascular collapse, sudden death, cardiomyopathy, obesity

Contributor Information and Disclosures

Author

Christopher I Doty, MD, FAAEM, Assistant Professor of Emergency Medicine, Residency Program Director, Department of Emergency Medicine, Kings County Hospital Center, State University of New York Downstate Medical Center
Christopher I Doty, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Sage W Wiener, MD, Assistant Professor, Department of Emergency Medicine, State University of New York Downstate, Director of Medical Toxicology, Department of Emergency Medicine, Kings County Hospital Center
Sage W Wiener, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Medical Toxicology, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Binita R Shah, MD, FAAP, Professor of Clinical Pediatrics and Emergency Medicine, SUNY Health Science Center at Brooklyn, Director of Pediatric Emergency Medicine, Depts of Emergency Medicine and Pediatrics, Kings County Hospital Center
Binita R Shah, MD, FAAP is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Medical Editor

Halim Hennes, MD, MS, Pediatric Emergency Medicine Research Director, Professor, Departments of Pediatrics and Emergency Medicine, Medical College of Wisconsin
Halim Hennes, MD, MS is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine.com, Inc
Disclosure: Pfizer Inc Stock Investment from broker recommendation; Avanir Pharma Stock Investment from broker recommendation

Managing Editor

Jeffrey R Tucker, MD, Assistant Professor, Department of Pediatrics, Division of Emergency Medicine, University of Connecticut and Connecticut Children's Medical Center
Jeffrey R Tucker, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Pediatrics, and Massachusetts Medical Society
Disclosure: Nothing to disclose.

CME Editor

Paul D Petry, DO, FACOP, FAAP, Consulting Staff, Freeman Pediatric Care, Freeman Health System
Paul D Petry, DO, FACOP, FAAP is a member of the following medical societies: American Academy of Osteopathy, American Academy of Pediatrics, American College of Osteopathic Pediatricians, and American Osteopathic Association
Disclosure: Nothing to disclose.

Chief Editor

Timothy E Corden, MD, Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin
Timothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, and Wisconsin Medical Society
Disclosure: Nothing to disclose.

RELATED INFORMATION FROM INDUSTRY
 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.