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.)
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.
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The pathway of ethanol metabolism. Disulfiram reduces the rate of oxidation of acetaldehyde by competing with the cofactor nicotinamide adenine dinucl....
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.
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]
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 alcoholic 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. Be aware that patients often grossly underestimate the amount of ethanol that they ingested.
In cases where parents bring in a young child who has ingested an unknown amount, 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%
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%
Beer, 3-7%
Other considerations include the following:
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-fold to 4-fold increased risk of alcoholism.
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 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
Urticaria
[8]
Inhibition of spermatogenesis
Hypothermia
Tachycardia
Myocardial depression
Variable pupillary response
Respiratory depression
Decreased pulmonary secretion clearance
Decreased sensitivity to airway foreign body
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)
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.
Serum glucose level: A bedside glucose finger stick is a quick and inexpensive method of assessing hypoglycemia. Hypoglycemia in a common in young children with ethanol intoxication.
Electrolyte levels: The anion gap measurement should be determined. Acute ethanol intoxication usually does not cause significant anion gap metabolic acidosis. The presence of a large anion gap or severe acidosis should suggest the ingestion of another substance, such as methanol or ethylene glycol. However, patients with multiple-trauma can also have marked metabolic acidosis, and ethanol intoxication predisposes patients to trauma.
Ethanol level
The serum ethanol concentration determined to obtain a starting level. Ethanol is metabolized at a fixed rate in an individual; however, alcohol metabolism rates widely vary, and predicting an individual's metabolism rate is impossible. If ethanol levels are obtained at two different times, one can reliably predict what a patient’s ethanol level would be at a given point in the future. However, one cannot predict whether the patient would be "intoxicated" without knowing the patient's tolerance to ethanol.
A blood alcohol concentration (BAC) that could make one person apneic may be a level at which another individual would suffer withdrawal. Also, a pharmacodynamic property, called the Mellanby effect, is observed when neurological impairment is greater at a given BAC when the BAC is increasing than the impairment observed at the same BAC when the BAC is decreasing.
Most hospitals use ethanol assays that function by enzymatic methods that utilize ADH. These assays detect ethanol only and do not have false-positive results when other toxic alcohols are present. Therefore, these assays cannot detect other toxic alcohols, and ingestion or co-ingestion of toxic alcohols or isopropanol may go unrecognized.
If ingestion of toxic alcohols is suspected, a specific assay for those alcohols or gas chromatography should be obtained.
Clinical findings and ethanol concentrations may be categorized as follows (these are rough estimates only and have not been validated in children):
Intoxication or inebriation - 100-150 mg/dL
Loss of muscle coordination - 150-200 mg/dL
Decreased level of consciousness - 200-300 mg/dL
Death - 300-500 mg/dL
The effects widely vary based on the patient’s BAC.
Human chorionic gonadotropin level: Urine pregnancy tests should be performed in all women of childbearing age.
Serum salicylate and acetaminophen levels: In intentional suicidal ingestions, the presence of other toxic substances must be determined, especially if the patient presents late or if he or she has ingested a substance that has a significant risk of morbidity (eg, acetaminophen, salicylate).
Urine drug levels: Older patients may have ingested recreational drugs such as cocaine, marijuana, benzodiazepines, amphetamines, and opiates.
ABG level
A determination of the pH is important when polysubstance ingestion or ketoacidosis is suspected. The partial pressure of carbon dioxide (pCO2) can be helpful in assessing respiratory depression.
The pH also can help in ruling out the co-ingestion of methanol and ethylene glycol, because significant academia is associated with those ingestions. However, reports in the literature have documented that the co-ingestion of ethanol and methanol does not cause significant acidosis.
Serum calcium and magnesium levels: High concentrations of ethanol and its chronic use can deplete these cations.
Serum osmolality: The osmolar gap can provide information about the ethanol concentration in the blood.
The osmolar gap is calculated using the following equation: gap = measured osmolality - (2 X [Na concentration]) + (glucose concentration/18) + (BUN concentration/2.8).
An osmolar gap of 22-25 mOsm/kg results for every 100 mg/dL of ethanol in the serum. A normal osmolar gap is 2 ± 6 mOsm/kg; 95% of the population have osmolar gaps between –14 and +10 mOsm/kg.
The predicted concentration of ethanol is calculated using the following equation: Ethanol concentration = (osmolar gap - 10) X 4.6. This equation may provide a gross estimate of the predicted level but varies based on the baseline osmolar gap.
Methanol levels: These results can be helpful if an ingestion of combined substances is suspected. A positive methanol level can alert the physician to a co-ingestion.
Head CT scanning is warranted in patients with a change of mental status, focal neurologic findings, or scalp bruises or lacerations and in patients in whom trauma cannot be excluded. C-spine precautions should also be used if trauma is a suspected comorbidity until the neck is thoroughly investigated.
If trauma is suspected, obtain appropriate radiography.
The mainstay of treatment of patients with ethanol toxicity is supportive care. Many modalities for treating ethanol intoxication and enhancing ethanol clearance have been attempted. In general, a conservative approach is recommended.
Hypoglycemia and respiratory depression are the 2 most immediate life-threatening complications that result from ethanol intoxication in children.
Initial care includes the following:
Assess the airway. If necessary, secure the airway with an endotracheal (ET) tube if the patient is not maintaining good ventilation or if a significant risk of aspiration is observed. Provide respiratory support and mechanical ventilation if needed.
Obtain intravenous (IV) access and replace any fluid deficit or use a maintenance fluid infusion. Use plasma expanders and vasopressors to treat hypotension, if present.
Ensure that the patient maintains a normal body temperature.
Quickly correct hypoglycemia. In children, 2-4 mL/kg of 25% dextrose solution is usually administered. A maintenance infusion of dextrose-containing IV fluids is often required. Note that this treatment does not clear ethanol from the blood
Correct any electrolyte abnormalities found with laboratory studies. Routine empiric electrolyte replacement is not helpful; only documented electrolytic abnormalities should be corrected.
If the ingestion occurred within 1 hour of presentation, placing a nasogastric tube and evacuating the stomach contents can be helpful.
In patients with chronic ethanol abuse, administer thiamine 100 mg IV/intramuscularly (IM) to prevent neurologic injury.
Additional care: If other substances have been co-ingested, initiate specific treatment for those substances, if available. For instance, naloxone can be used to reverse respiratory depression if opiate co-ingestion is suspected.
Treatments that are not recommended include the following:
The administration of medications to cause emesis is not recommended because of the rapid onset of central nervous system (CNS) depression and risk of aspiration.
The administration of activated charcoal is not recommended for isolated alcohol ingestions because it does not bind hydrocarbons or alcohols. If the clinician suspects a concomitant ingestion of other toxic products, activated charcoal may be effective in absorbing these toxins.
Forced diuresis is not helpful because 90% of ethanol metabolism occurs in the liver, and only 10% of the ethanol load is secreted in the urine.
Gamma aminobutyric acid (GABA) receptor antagonists such as naloxone and flumazenil have little effect on the CNS or respiratory depression caused by ethanol; their use is not recommended in isolated ethanol intoxication.
Fructose infusion can increase the ethanol clearance by 25%. However, the use of fructose is not recommended because significant adverse effects may occur, such as lactic acidosis, severe osmotic diuresis, and GI symptoms
The effects of insulin, glucose, caffeine, and several other medications have been studied, but none consistently increases ethanol metabolism or alleviate CNS depression.
Hemodialysis efficiently clears ethanol from the blood but is an invasive procedure; thus, its use is not routinely recommended. Hemodialysis can be used in patients whose clinical condition is deteriorating or in patients whose CNS depression, respiratory depression, or hypotension is refractory to standard therapy. Patients who have impaired hepatic function may require dialysis to clear an ethanol load.
Indications for hospital admission include the following:
Presence of hypoglycemia
Suspected neglect or inadequate social support at home
Unstable home environment or unreliable caregiver at home
Contact the regional or local poison control center for treatment guidance and reporting purposes.
Consider consulting social services personnel in all cases of ethanol intoxication in children.
Patients who chronically abuse alcohol may have serious nutritional deficiencies and may require a consultation with a nutritionist on an inpatient basis.
Vitamin and electrolyte replacement is recommended only for specific deficits detected by means of laboratory testing. Thiamine replacement is an exception because it is the only vitamin for which routine administration is recommended and it has been proved useful in patients with chronic alcohol abuse. Thiamine is given to prevent Wernicke syndrome.
Clinical Context:
An essential coenzyme of carbohydrate metabolism. Given to all patients with suspected chronic alcohol abuse. Only drug used in patients with ethanol intoxication without a documented deficit. Used in treatment and prevention of Wernicke syndrome.
Vitamins are organic substances required in small amounts for various metabolic processes. In the body, vitamins may be synthesized in small or insufficient amounts or not at all; thus, supplementation may be required. Vitamins are used in patients with suspected chronic ethanol abuse to prevent serious neurologic complications. If feasible, thiamine should be administered prior to glucose load to reduce risk of Wernicke encephalopathy.
Observe the patient with ethanol toxicity until his or her mental status has returned to normal.
Monitor the patient's blood glucose level until it is stable and is within the normal range.
Correct any electrolytic disturbances.
Watch for signs of ethanol withdrawal in patients who have abused alcohol for several years: Sympathetic discharge, tremor, and tongue fasciculations are typical; hallucinations may occur; seizures are possible.
Pediatric intensive care unit (PICU) monitoring is recommended in all patients who have continuing CNS or respiratory depression.
Thiamine administered daily on an inpatient basis is recommended in patients who have chronically abused ethanol. The length of therapy is well documented.
Risky behaviors (eg, increased likelihood of illicit drug use)
Increased risk of trauma
Legal consequences
Long-term complications of chronic ethanol abuse in children are not well described in the medical literature. Complications usually develop over several years. Because most pediatric patients do not start abusing ethanol until later in their adolescence, they do not present with long-term complications such as liver dysfunction (eg, cirrhosis) and cardiac problems until after they become adults.
Research has confirmed that intense neurologic development occurs both in utero and during adolescence. Heavy drinking in adolescents has been associated with deficits in visuospatial function. Heavy drinking in adolescents may also lead to chronic neurologic damage of a similar mechanism to that seen in fetal alcohol syndrome.
Current research is focusing on the effects of adolescent binge drinking on the hippocampus and frontal cortex. These areas appear to be particularly sensitive to the binge pattern of drinking, which predominates in adolescents.[10] Magnetic resonance imaging has demonstrated that adolescents who abuse alcohol have lower hippocampal volume than healthy controls.[11]
The prognosis for pediatric patients with ethanol toxicity is excellent, provided the patient can avoid both the long-term use of alcohol and the short-term complications of alcohol abuse.
Parents should be taught to prevent accidental ingestion at home by storing ethanol-containing liquids out of the reach of children and by disposing of unfinished alcoholic beverages.
Educating adolescents about alcohol abuse has proved challenging, as follows:
Few data indicate that educational programs to control drinking among adolescents are effective. However, the parents or pediatrician should still educate the patient about the dangers of alcohol consumption, including fetal alcohol syndrome in the pregnant patient.
Approaches that have traditionally been successful in adults, such as 12-step programs, are not as successful for adolescents. In fact, after treatment in aftercare or 12-step programs, only half of adolescents comply with the behavioral changes required by the program. However, about one third of adolescents are able to decrease their drinking using their own methods; exactly what these methods are has not been well studied. This is an area that may benefit from further study in order to design more effective treatment programs.[10]
One study used a laptop-based program to educate patients in the emergency department (ED) regarding the dangers of alcohol use. The authors found no decrease in the incidence of drinking behavior at 3- and 12-month follow-up. Of note, these patients had all presented to the ED, and were not patients with complaints specific to ethanol.[12]
Another study found that a motivational intervention for intoxicated patients in the ED or a combination of a motivational intervention and a family intervention did result in a reduction in drinking outcomes, but the effect attenuated over time.[13]
Elizabeth Fernandez, MD, Attending Physician, Department of Emergency Medicine, Long Island Jewish Medical Center
Disclosure: Nothing to disclose.
Coauthor(s)
Christopher I Doty, MD, FAAEM, FACEP, Professor of Emergency Medicine, Vice Chair, Department of Emergency Medicine, University of Kentucky-Chandler Medical Center
Disclosure: Nothing to disclose.
Specialty Editors
Mary L Windle, PharmD, Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Nothing to disclose.
Jeffrey R Tucker, MD, Assistant Professor, Department of Pediatrics, Division of Emergency Medicine, University of Connecticut School of Medicine, Connecticut Children's Medical Center
Disclosure: Received salary from Merck for employment.
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
Disclosure: Nothing to disclose.
Additional Contributors
Halim Hennes, MD, MS, Division Director, Pediatric Emergency Medicine, University of Texas Southwestern Medical Center at Dallas, Southwestern Medical School; Director of Emergency Services, Children's Medical Center
Disclosure: Nothing to disclose.
Acknowledgements
The author gratefully acknowledges the previous coauthors Dr. Sage Wiener and Dr. Binita Shah for their contributions to the development and writing of this article.
Drug Abuse Warning Network. Alcohol and Drug CombinationsAre More Likely to Have a SeriousOutcome Than Alcohol Alone inEmergency Department VisitsInvolving Underage Drinking. Substance Abuse and Mental Health Services Administration. Available at http://www.samhsa.gov/data/sites/default/files/spot143-underage-drinking-2014/spot143-underage-drinking-2014/spot143-underage-drinking-2014.pdf. Accessed: April 23, 2015.
[Guideline] U.S. Preventive Services Task Force. Alcohol Misuse: Screening and Behavioral Counseling Interventions in Primary Care. USPSTF. Available at http://www.uspreventiveservicestaskforce.org/Page/Topic/recommendation-summary/alcohol-misuse-screening-and-behavioral-counseling-interventions-in-primary-care. Accessed: April 24, 2015.
Rogers GC. Ethanol. Handbook of Common Poisonings in Children. 3rd ed. Elk Grove Village, IL: American Academy of Pediatrics, Committee on Injury and Poison Prevention; 1994.
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).
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).
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