Pediatric Ethanol Toxicity

Updated: Feb 27, 2017
  • Author: Elizabeth Fernandez, MD; Chief Editor: Timothy E Corden, MD  more...
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Overview

Practice Essentials

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. [1]

Assessment of pediatric ethanol toxicity can be complicated by several factors. These include reluctance to admit ingestion, underestimation of the amount ingested, ingestion of other toxins (eg, methanol in perfume or cologne), and related trauma. (See Presentation.) The mainstay of treatment is supportive care. Hypoglycemia and respiratory depression are the two most immediate life-threatening complications that result from ethanol intoxication in children. (See Treatment.)

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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.

The pathway of ethanol metabolism. Disulfiram redu The pathway of ethanol metabolism. Disulfiram reduces the rate of oxidation of acetaldehyde by competing with the cofactor nicotinamide adenine dinucleotide (NAD) for binding sites on aldehyde dehydrogenase (ALDH).

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. However, the exact molecular targets of ethanol and the mechanism of action are still the subjects of ongoing research. [2, 3]

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.

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Epidemiology

Frequency

United States

Ethanol use and intoxication in adolescents is widespread in the United States. In the 2011 Youth Risk Behavior Survey, 21% of high school students admitted to drinking alcohol before age 13 years. The survey also found that 71% ever drank alcohol and 39% had at least one drink in the 30 days prior to the survey. More alarmingly, 24% rode in a vehicle with a driver who drank alcohol and 8% drove a vehicle after drinking alcohol. [4] 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-fold 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. In a study of 295 pediatrics patients aged 10-21 years presenting to the emergency department (ED) for treatment of any type of injury, Meropol et al found that 15 patients tested positive for alcohol; however, only 4 of these patients were tested upon initial ED evaluation. [5] Additionally, alcohol is frequently linked with injuries secondary to assault and motor vehicle crashes.

The intoxicated individual often engages in high-risk activities, despite the fact that his or her reflexes are substantially slowed. Adolescent binge drinking has been linked with high-risk behaviors such as riding in cars with intoxicated drivers, sexual activity, smoking cigarettes/cigars, suicide attempts, and illicit drug use and may be the victim of dating violence. [6] Early alcohol use has been linked to dating violence victimization, suicidal ideation, and suicide attempts. [5]

Race-, Sex-, and Age-related Demographics

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 expression or enzyme activity of ADH.

Data supporting a sex predilection in pediatric populations are limited. Studies in adults have reported that gastric 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. Interestingly, one study found that among children aged 12-20, more drinking without binges was reported among girls than among boys but that binge-drinking rates were still similar. [6]

In the 2015 report of the American Association of Poison Control Centers’ National Poison Data System, children younger than 6 years accounted for 1791 of the 2620 single exposures to non-beverage, non–rubbing-alcohol ethanol. Most single exposures to ethanol beverages involved adults; however, 1579 of the 6761 cases involved children under the age of 6 years; 882 involved teenagers. [7]

 

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