US Pharm
. 2013;38(5):HS3-HS6.

ABSTRACT: The most common drug of abuse in adolescence, alcohol, is consumed primarily through binge drinking. The rapid rise in blood alcohol concentrations during binge drinking can cause alcohol intoxication. Treatment of alcohol intoxication and withdrawal in adolescents mimics that in adults. The main goals of treating acute alcohol intoxication are to ensure adequate respiration and to control associated agitation, nausea, and vomiting. The mainstay of therapy for acute alcohol withdrawal is benzodiazepines. Underage drinking, especially early initiation, can cause developmental problems that may continue into adulthood. Pharmacists can optimize the care of adolescents with alcohol poisoning by understanding the management of this prevalent condition.

In American teenagers, the most commonly abused drug is alcohol. An underage drinking epidemic is currently present, starting with elementary- and middle-school–aged children 9 to 13 years old and erupting during college. Underage drinking accounts for a significant amount of total alcohol consumption, with almost 20% of the alcohol consumed in the United States being by those under the age of 21 years.1

Increased risk-taking behaviors, low levels of harm avoidance, impulsivity, and anxiety may occur in adolescents (those aged 11-18 years). When accompanied with changes in gonadal steroid and stress-related hormone release, these may lead to initiation patterns of alcohol and drug consumption.2


When adolescents drink alcohol today, they consume a larger quantity with a clearer goal to “get drunk” versus earlier generations.2 The ingestion of large amounts of alcohol can lead to acute alcohol intoxication.3 Often toxicity is prevented because people pass out before they can ingest toxic amounts or vomiting eliminates the toxic contents.4

Since 1975, there has been an increase of almost one-third (27%-36%) in the proportion of children who have begun drinking by 8th grade. Further, there is no longer a gender gap for alcohol consumption.1,5 The results of community survey data revealed that by 8th grade, 51.7% of adolescents have tried alcohol, increasing to 80.3% by 12th grade.2

Binge drinking—consuming at least five alcoholic drinks in one episode—is the most common pattern for alcohol consumption in underage drinkers.1,5 Binge drinking can lead to acute alcohol poisoning, with rapid elevations in blood alcohol concentration (BAC).5 In 2011, binge drinking occurred in 22.6% of people over the age of 12 years, with a rate of 12.1% in adolescents specifically.6

Physiological Consequences

Throughout adolescence and into adulthood, the brain continues to develop, producing important structural and functional changes as well as cognitive, emotional, and social maturation.2,7 When the brain is exposed to ethanol during times of brain development, irreversible abnormalities in the function and structure of the brain may occur due to the vulnerability of the central nervous system (CNS) to alcohol’s effects. Memory deficit, abnormalities in brain structure, and poor academic performance also may occur in adolescents who drink alcohol.2

Alcohol use by an adolescent may lead to harmful consequences. The three top causes of teen deaths, accidents (traffic fatalities, drownings), suicide, and homicide, often involve alcohol use.1 Males aged 16 to 20 years who drove with a BAC of 0.08 g/dL were 52 times more likely to die in a single-vehicle crash than male drivers of the same age who were sober.5 Further, the primary source of adult alcoholism is teen drinking, with a four-fold increased rate of developing alcoholism if alcohol is initiated prior to the age of 15 compared to 21 years.1

Acute alcohol ingestion can have other consequences as well. Respiratory depression is the most life-threatening respiratory problem. Aspiration, nausea, vomiting, diarrhea, acute alcoholic hepatitis, and pancreatitis may also occur.3

Risk Factors

Childhood psychopathology can predict adolescent alcohol use disorders with conduct disorder, attention-deficit/hyperactivity disorder (ADHD), anxiety disorders, and major depressive disorders being the most clinically relevant childhood mental disorders.2

Several sociodemographic characteristics may influence adolescent alcohol involvement. Adolescents from single-parent families, lower socioeconomic status, or European American or Hispanic descent have higher levels of alcohol involvement.2,5 Timing of maturation also influences early alcohol consumption. Compared to girls who mature on time or late, girls who mature early are significantly more advanced with the trajectories of initiating alcohol use and binge drinking. Additionally, adolescents who mature early and are affiliated with older or more deviant peers and those who have increased parent-adolescent conflict have accelerated alcohol involvement.2


The mechanism of action of alcohol involves dose-dependent CNS depression.4 Alcohol primarily affects two neurotransmitters. It blocks the N-methyl- D-aspartate (NMDA) subtype of glutamate (an excitatory neuro-transmitter) and potentiates the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) at GABAA receptors. Tolerance develops from the augmented excitatory amino acid neurotransmission and upregulation of the NMDA receptor.8 A hyperexcitable state due to overactivity of the autonomic nervous system results when alcohol is abruptly withdrawn.8,9 The elimination of GABA inhibition when no alcohol is present during alcohol withdrawal syndrome results in excitation, which can lead to excitotoxic neuronal death.8

The gastrointestinal (GI) tract rapidly absorbs alcohol within 5 to 10 minutes of ingestion.4,8 Alcohol is primarily metabolized (95%-98%) in the liver by alcohol dehydrogenase (ADH).8 At low BACs, saturation of ADH occurs, causing the elimination of alcohol to be transformed from first-order to zero-order kinetics. With zero-order kinetics, a steady amount of alcohol is eliminated over time (15-22.2 mg/dL/h in nontolerant adults).4,8 A person’s BAC often correlates with the stage of intoxication. In nontolerant individuals, a BAC of 0.02 g/dL may lead to impaired driving-related skills. When the BAC is 0.05 g/dL, altered gross motor control and orientation and clinical ethanol intoxication are usually apparent. Legal intoxication is classified as a BAC of 0.08 g/dL. Individuals will experience varying degrees of impairment based on their BAC, so there is no specific BAC that classifies a person as experiencing acute alcohol poisoning.8


Symptoms of acute alcohol intoxication include abdominal pain, nausea, vomiting, and, less frequently, jaundice, shivering, and fevers.3

The Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR) criteria for alcohol withdrawal (TABLE 1) involve the cessation of alcohol use with at least two qualifying symptoms causing clinically significant impairment in the absence of another causative agent or medical disorder.8,10,11 Alcohol withdrawal syndrome features may begin to occur within 6 to 48 hours of the last alcoholic beverage and diminish over 24 to 48 hours.9,10 The initial symptoms of withdrawal include sweating, agitation, tremor, headache, disorientation, difficulty concentrating, irritability, anxiety, nausea, and vomiting. Transient hallucinations may occur in more serious cases. In addition, the first 24 hours of alcohol withdrawal may be accompanied by seizures in up to 25% of cases.9 It generally takes 2 to 3 days after the cessation of drinking for delirium to develop, which lasts 48 to 72 hours.10 Known as delirium tremens, this is the most serious and intense alcohol withdrawal syndrome. Severe agitation, persistent hallucinations, disorientation, tremor, and extreme tachycardia, tachypnea, and hypertension may occur as a result of delirium tremens.9

The Clinical Institute of Withdrawal Assessment for Alcohol, revised (CIWA-Ar) may be performed to assess for alcohol withdrawal and the need for benzodiazepine therapy.9,12 It has well-documented validity, reliability, and reproducibility. A high CIWA-Ar score is predictive of seizure or delirium development.12


It is difficult to find alcohol abuse programs specifically targeted for adolescents. Programs that do exist are based on models in adults with no evidence-based guidelines on effective alcohol poisoning treatment in adolescents. As a result, the focus of the pharmacotherapy discussion will be based on adult literature and guidelines.1

If a patient presents to the emergency room with known or suspected acute alcohol intoxication, a BAC and full toxicology screen for the possibility of co-ingestion should be drawn. A CT scan may be needed in patients with associated focal neurologic findings, seizures, and disproportionate mental status in relation to level of intoxication.4

In the management of acute alcohol intoxication, stabilizing the patient is generally the first priority. Respiratory function should be assessed. To prevent aspiration, the patient should be placed in a lateral position. In extreme cases of respiratory depression, mechanical ventilation may be needed. To correct dehydration and electrolyte abnormalities, an IV solution of dextrose 5%, magnesium sulfate 2 g, folate 1 mg, thiamine 100 mg, and multivitamins is commonly administered. To control symptoms of acute alcohol intoxication such as vomiting and agitation, antiemetics and sedative antipsychotics (e.g., haloperidol) may be administered.3

For moderate-to-severe alcohol withdrawal, pharmacologic therapy is warranted.9 The treatment of choice for alcohol withdrawal is benzodiazepines.12 The initial goal of therapy for alcohol withdrawal delirium (AWD) is to control agitation to decrease clinically important adverse events.10 The primary agents recommended for managing AWD are sedative-hypnotic agents (e.g., diazepam, chlordiazepoxide, pentobarbital) that have been shown to reduce mortality, reduce the duration of AWD symptoms, and have fewer associated complications versus neuroleptic agents (e.g., phenothiazines, haloperidol).10,12 Further, neuroleptic agents may reduce the seizure threshold.10

No specific sedative-hypnotic has shown superiority for the treatment of AWD. Because benzodiazepines have a favorable therapeutic and toxic effect index, they are most commonly recommended and used for AWD. Benzodiazepines are dosed by weight (mg/kg) in pediatric patients up to a maximum amount not to exceed the adult dosage. Pentobarbital or propofol may be considered if a patient requires extremely high doses of benzodiazepines and is still experiencing agitation.10

There are several factors to consider when choosing a benzodiazepine for alcohol withdrawal or AWD, including the patient’s age, liver function, and history of seizures.9 To control agitation quickly, a benzodiazepine with a rapid onset of action (e.g., diazepam or alprazolam) is ideal.4,10 Benzodiazepines with a longer duration of action (e.g., chlordiazepoxide) have less potential for breakthrough and rebound symptoms and may prevent withdrawal symptoms.10 However, in patients who have renal or hepatic dysfunction, a benzodiazepine with a short duration of action (e.g., oxazepam) may be preferred to prevent oversedation.9,10 The cost and potential for abuse should also be considered.10

Doses must be individualized with a goal to maintain light somnolence. A much higher dose of sedative-hypnotic is generally needed to suppress AWD compared to the dose for severe anxiety treatment or presurgical sedation. The preferred route of administration is IV because it provides the quickest onset of action. Erratic absorption occurs with intramuscular (IM) administration of benzodiazepines (except lorazepam), and it is not recommended. If a patient is stable from a cardiovascular stance, lorazepam may be given IM due to good IM absorption.10

There are two options for benzodiazepine therapy—fixed dosing and symptom-triggered therapy. Fixed dosing is characterized by a predetermined dosing schedule, regardless of the presence of withdrawal symptoms. Symptom-triggered therapy occurs when medications are given only when the patient experiences withdrawal symptoms.12 In two prospective, randomized, controlled trials, symptom-triggered therapy was proven to be as effective as fixed dosing with the added benefit of significantly less medication given and shorter duration of treatment.12-14 Fixed dosing may be reserved for patients with a history of withdrawal seizures due to strong risk of seizures with subsequent alcohol withdrawal.12

Alcohol withdrawal seizures (AWS) usually present as generalized tonic-clonic seizures, but partial seizures and rarely status epilepticus may occur.15,16 Supportive care is generally effective in treating AWS that are unrelated to delirium tremens. However, delirium tremens occurs in up to one-third of patients with AWS if left untreated.9 Further, patients who experience one withdrawal seizure are at an increased risk of subsequent seizures.16 The drug of choice for AWS in patients with no history of seizures is a benzodiazepine.9 Phenytoin has not been shown to be effective in the prevention or treatment of AWS.9,16,17

Depending on the patient’s presentation, adjunct therapy may need to be added to benzodiazepine management.10,12 In patients with uncontrolled agitation, perceptual disturbances, or disturbed thinking, adjunct neuroleptic agents may be beneficial. However, neuroleptic agents should not be used as AWD monotherapy due to higher associated mortality, longer delirium duration, and increased rate of complications than with sedative-hypnotics.10

Beta-adrenergic antagonists may reduce the autonomic manifestations of alcohol withdrawal. However, delirium may occur as a side effect of beta-blockers that have good CNS penetration (e.g., propranolol). Beta-adrenergic antagonists may also selectively mask development of other withdrawal symptoms due to selective reduction in certain withdrawal manifestations.12

Poor dietary habits and an impaired ability to absorb nutrients from the bloodstream due to alcohol-induced digestive tract changes may lead to vitamin deficiencies. A deficiency of folic acid can lead to anemia, and folic acid should be administered in the form of a multivitamin for a few weeks following alcohol withdrawal. Thiamine, which plays a major role in energy metabolism, is often deficient in people with alcohol dependence. Thiamine 100 mg daily for a minimum of 3 days should be given to all patients hospitalized with alcohol withdrawal.9 Thiamine deficiency may lead to Wernicke-Korsakoff syndrome, characterized by paralysis of certain eye muscles, an abnormal gait, and severe confusion, which may progress to irreversible dementia.9-10,12 Thiamine should be given before any form of glucose is administered in order to prevent the depletion of thiamine stores and precipitation of Wernicke-Korsakoff syndrome.9


Due to the commonality of alcohol abuse during adolescence, it is important to be familiar with the treatment options to relieve alcohol withdrawal. The use of benzodiazepines is beneficial to prevent alcohol withdrawal and AWD and to treat AWS. Benzodiazepine therapy should be individualized based on patient characteristics. Pharmacists should be well informed about the management of acute alcohol poisoning in adolescents to facilitate and optimize timely and appropriate patient care.


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