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Binge Drinking and Alcohol Poisoning inthe Adolescent PopulationTheresa Ringenberg, PharmD, Julie Kalabalik, PharmD, BCPS, ChristineRobinson, PharmDUS Pharmacist. 2013;38(5):HS3-HS6.

Abstract and IntroductionAbstract

The most common drug of abuse in adolescence, alcohol, is consumedprimarily through binge drinking. The rapid rise in blood alcoholconcentrations during binge drinking can cause alcohol intoxication.Treatment of alcohol intoxication and withdrawal in adolescents mimicsthat in adults. The main goals of treating acute alcohol intoxication are toensure adequate respiration and to control associated agitation, nausea,and vomiting. The mainstay of therapy for acute alcohol withdrawal isbenzodiazepines. Underage drinking, especially early initiation, can causedevelopmental problems that may continue into adulthood. Pharmacistscan optimize the care of adolescents with alcohol poisoning by

understanding the management of this prevalent condition.

Introduction

In American teenagers, the most commonly abused drug is alcohol. Anunderage drinking epidemic is currently present, starting with elementary-and middle-schoolaged children 9 to 13 years old and erupting duringcollege. Underage drinking accounts for a significant amount of totalalcohol consumption, with almost 20% of the alcohol consumed in theUnited 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 1118 years). Whenaccompanied with changes in gonadal steroid and stress-related hormonerelease, these may lead to initiation patterns of alcohol and drugconsumption.[2]
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EpidemiologyWhen adolescents drink alcohol today, they consume a larger quantity witha clearer goal to "get drunk" versus earlier generations.[2]The ingestion oflarge amounts of alcohol can lead to acute alcohol intoxication.[3]Oftentoxicity is prevented because people pass out before they can ingest toxicamounts or vomiting eliminates the toxic contents.[4]

Since 1975, there has been an increase of almost one-third (27%36%) inthe 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 ofcommunity survey data revealed that by 8th grade, 51.7% of adolescentshave tried alcohol, increasing to 80.3% by 12th grade.[2]

Binge drinkingconsuming at least five alcoholic drinks in one episodeisthe most common pattern for alcohol consumption in underage drinkers.[1,5]

Binge drinking can lead to acute alcohol poisoning, with rapid elevations inblood alcohol concentration (BAC).[5]In 2011, binge drinking occurred in22.6% of people over the age of 12 years, with a rate of 12.1% inadolescents specifically.[6]

Physiological ConsequencesThroughout adolescence and into adulthood, the brain continues todevelop, producing important structural and functional changes as well ascognitive, emotional, and social maturation.[2,7]When the brain is exposedto ethanol during times of brain development, irreversible abnormalities in

the function and structure of the brain may occur due to the vulnerability ofthe central nervous system (CNS) to alcohol's effects. Memory deficit,abnormalities in brain structure, and poor academic performance also mayoccur in adolescents who drink alcohol.[2]

Alcohol use by an adolescent may lead to harmful consequences. Thethree top causes of teen deaths, accidents (traffic fatalities, drownings),suicide, and homicide, often involve alcohol use.[1]Males aged 16 to 20years who drove with a BAC of 0.08 g/dL were 52 times more likely to diein 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 isinitiated prior to the age of 15 compared to 21 years.[1]

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


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also occur.[3]

Risk FactorsChildhood psychopathology can predict adolescent alcohol use disorderswith conduct disorder, attention-deficit/hyperactivity disorder (ADHD),anxiety disorders, and major depressive disorders being the most clinicallyrelevant childhood mental disorders.[2]

Several sociodemographic characteristics may influence adolescentalcohol involvement. Adolescents from single-parent families, lowersocioeconomic status, or European American or Hispanic descent havehigher levels of alcohol involvement.[2,5]Timing of maturation alsoinfluences early alcohol consumption. Compared to girls who mature ontime or late, girls who mature early are significantly more advanced withthe trajectories of initiating alcohol use and binge drinking. Additionally,

adolescents who mature early and are affiliated with older or more deviantpeers and those who have increased parent-adolescent conflict haveaccelerated alcohol involvement.[2]

PathophysiologyThe mechanism of action of alcohol involves dose-dependent CNSdepression.[4]Alcohol primarily affects two neurotransmitters. It blocks theN-methyl- D-aspartate (NMDA) subtype of glutamate (an excitatory neuro-transmitter) and potentiates the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) at GABAAreceptors. Tolerance develops from

the augmented excitatory amino acid neurotransmission and upregulationof the NMDA receptor.[8]A hyperexcitable state due to overactivity of theautonomic nervous system results when alcohol is abruptly withdrawn.[8,9]The elimination of GABA inhibition when no alcohol is present duringalcohol withdrawal syndrome results in excitation, which can lead toexcitotoxic neuronal death.[8]

The gastrointestinal (GI) tract rapidly absorbs alcohol within 5 to 10minutes of ingestion.[4,8]Alcohol is primarily metabolized (95%-98%) in theliver by alcohol dehydrogenase (ADH).[8]At low BACs, saturation of ADH

occurs, causing the elimination of alcohol to be transformed from first-orderto zero-order kinetics. With zero-order kinetics, a steady amount of alcoholis eliminated over time (1522.2 mg/dL/h in nontolerant adults).[4,8]Aperson's BAC often correlates with the stage of intoxication. In nontolerantindividuals, 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 orientationand clinical ethanol intoxication are usually apparent. Legal intoxication is


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classified as a BAC of 0.08 g/dL. Individuals will experience varyingdegrees of impairment based on their BAC, so there is no specific BACthat classifies a person as experiencing acute alcohol poisoning. [8]

SymptomsSymptoms 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 () involve thecessation of alcohol use with at least two qualifying symptoms causingclinically significant impairment in the absence of another causative agentor medical disorder.[8,10,11]Alcohol withdrawal syndrome features may beginto occur within 6 to 48 hours of the last alcoholic beverage and diminishover 24 to 48 hours.[9,10]The initial symptoms of withdrawal include

sweating, agitation, tremor, headache, disorientation, difficultyconcentrating, irritability, anxiety, nausea, and vomiting. Transienthallucinations may occur in more serious cases. In addition, the first 24hours 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 fordelirium to develop, which lasts 48 to 72 hours.[10]Known as deliriumtremens, this is the most serious and intense alcohol withdrawal syndrome.Severe agitation, persistent hallucinations, disorientation, tremor, andextreme tachycardia, tachypnea, and hypertension may occur as a resultof delirium tremens.[9]

Table 1. DSM-IV-TR Criteria for Alcohol Withdrawal

A. Cessation of (or reduction in) alcohol use that has been heavy and prolonged

B. Two (or more) of the following, developing within several hours to a few days after1. Autonomic hyperactivity (e.g., sweating or HR >100 bpm)

2. Increased hand tremor

3. Insomnia

4. Nausea or vomiting

5. Transient visual, tactile, or auditory hallucinations or illusions

6. Psychomotor agitation


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7. Anxiety

8. Grand mal seizures

C. The symptoms in Criterion B cause clinically significant distress or impairment in s

D. The symptoms are not due to a general medical condition and are not better acco

bpm: beats per minute; DSM-IV-TR: Diagnostic and Statistical Manual of Mental Diso11.

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

Treatment

It is difficult to find alcohol abuse programs specifically targeted foradolescents. Programs that do exist are based on models in adults with noevidence-based guidelines on effective alcohol poisoning treatment inadolescents. As a result, the focus of the pharmacotherapy discussion willbe based on adult literature and guidelines. [1]

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

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

For moderate-to-severe alcohol withdrawal, pharmacologic therapy iswarranted.[9]The treatment of choice for alcohol withdrawal isbenzodiazepines.[12]The initial goal of therapy for alcohol withdrawaldelirium (AWD) is to control agitation to decrease clinically importantadverse events.[10]The primary agents recommended for managing AWDare sedative-hypnotic agents (e.g., diazepam, chlordiazepoxide,


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pentobarbital) that have been shown to reduce mortality, reduce theduration of AWD symptoms, and have fewer associated complicationsversus 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 ofAWD. Because benzodiazepines have a favorable therapeutic and toxiceffect index, they are most commonly recommended and used for AWD.Benzodiazepines are dosed by weight (mg/kg) in pediatric patients up to amaximum amount not to exceed the adult dosage. Pentobarbital orpropofol may be considered if a patient requires extremely high doses ofbenzodiazepines and is still experiencing agitation.[10]

There are several factors to consider when choosing a benzodiazepine foralcohol withdrawal or AWD, including the patient's age, liver function, and

history of seizures.[9]

To control agitation quickly, a benzodiazepine with arapid 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 mayprevent withdrawal symptoms.[10]However, in patients who have renal orhepatic dysfunction, a benzodiazepine with a short duration of action (e.g.,oxazepam) may be preferred to prevent oversedation.[9,10]The cost andpotential 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 suppressAWD compared to the dose for severe anxiety treatment or presurgicalsedation. The preferred route of administration is IV because it providesthe quickest onset of action. Erratic absorption occurs with intramuscular(IM) administration of benzodiazepines (except lorazepam), and it is notrecommended. 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 therapyfixed dosing andsymptom-triggered therapy. Fixed dosing is characterized by apredetermined dosing schedule, regardless of the presence of withdrawalsymptoms. Symptom-triggered therapy occurs when medications are givenonly when the patient experiences withdrawal symptoms.[12]In twoprospective, randomized, controlled trials, symptom-triggered therapy wasproven to be as effective as fixed dosing with the added benefit ofsignificantly less medication given and shorter duration of treatment.[1214]Fixed dosing may be reserved for patients with a history of withdrawalseizures due to strong risk of seizures with subsequent alcohol


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withdrawal.[12]

Alcohol withdrawal seizures (AWS) usually present as generalized tonic-clonic seizures, but partial seizures and rarely status epilepticus mayoccur.[15,16]Supportive care is generally effective in treating AWS that are

unrelated to delirium tremens. However, delirium tremens occurs in up toone-third of patients with AWS if left untreated. [9]Further, patients whoexperience one withdrawal seizure are at an increased risk of subsequentseizures.[16]The drug of choice for AWS in patients with no history ofseizures is a benzodiazepine.[9]Phenytoin has not been shown to beeffective in the prevention or treatment of AWS.[9,16,17]

Depending on the patient's presentation, adjunct therapy may need to beadded to benzodiazepine management.[10,12]In patients with uncontrolledagitation, perceptual disturbances, or disturbed thinking, adjunct

neuroleptic agents may be beneficial. However, neuroleptic agents shouldnot be used as AWD monotherapy due to higher associated mortality,longer delirium duration, and increased rate of complications than withsedative-hypnotics.[10]

Beta-adrenergic antagonists may reduce the autonomic manifestations ofalcohol 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 otherwithdrawal symptoms due to selective reduction in certain withdrawal

manifestations.[12]

Poor dietary habits and an impaired ability to absorb nutrients from thebloodstream due to alcohol-induced digestive tract changes may lead tovitamin deficiencies. A deficiency of folic acid can lead to anemia, and folicacid should be administered in the form of a multivitamin for a few weeksfollowing alcohol withdrawal. Thiamine, which plays a major role in energymetabolism, is often deficient in people with alcohol dependence. Thiamine100 mg daily for a minimum of 3 days should be given to all patientshospitalized with alcohol withdrawal.[9]Thiamine deficiency may lead toWernicke-Korsakoff syndrome, characterized by paralysis of certain eyemuscles, an abnormal gait, and severe confusion, which may progress toirreversible dementia.[910,12]Thiamine should be given before any form ofglucose is administered in order to prevent the depletion of thiamine storesand precipitation of Wernicke-Korsakoff syndrome.[9]

ConclusionDue to the commonality of alcohol abuse during adolescence, it is


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important to be familiar with the treatment options to relieve alcoholwithdrawal. The use of benzodiazepines is beneficial to prevent alcoholwithdrawal and AWD and to treat AWS. Benzodiazepine therapy should beindividualized based on patient characteristics. Pharmacists should be wellinformed about the management of acute alcohol poisoning in adolescents

to facilitate and optimize timely and appropriate patient care.

References

1. Califano JA Jr. Teen tipplers: America's underage drinking epidemic. TheNational Center on Addiction and Substance Abuse at ColumbiaUniversity. Revised February 2003.www.casacolumbia.org/articlefiles/379-Teen%20Tipplers.pdf.

Accessed February 12, 2013.

2. Gurri C, Pascual M. Mechanisms involved in the neurotoxic, cognitive,and neurobehavioral effects of alcohol consumption duringadolescence.Alcohol. 2010;44:1526.

3. Vonghia L, Leggio L, Ferrulli A, et al. Acute alcohol intoxication. Euro JIntern Med. 2008;19:561567.

4. Doering PL, Kennedy WK, Boothby LA. Substance-related disorders:alcohol, nicotine, and caffeine. In: DiPiro JT, Talbert R, Yee GC, eds,et al. Pharmacotherapy: A Pathophysiologic Approach. 7th ed. NewYork, NY: McGraw-Hill; 2008:10841085.

5. Executive summary. Report to Congress on the prevention and reductionof underage drinking. Substance Abuse and Mental Health Services

Administration (SAMHSA). May 2011.http://store.samhsa.gov/shin/content/SMA114645/SMA114645.pdf. Accessed February 12, 2013.

6. SAMHSA. Results from the 2011 National Survey on Drug Use andHealth: Summary of National Findings. NSDUH Series H-44, HHSPub No. (SMA) 124713. Rockville, MD: SAMHSA; 2012.

7. Ehlers CL, Criado JR. Adolescent ethanol exposure: does it producelong-lasting electrophysiological effects?Alcohol. 2010;44:2737.

8. Nelson L, Lewin L, Howland MA, et al. Goldfrank's ToxicologicEmergencies. 9th ed. East Norwalk, CT: Appleton & Lange; 2011.


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9. Myrick H, Anton R. Treatment of alcohol withdrawal.Alcohol Health ResWorld. 1998;22:3843.

10. Mayo-Smith MF, Beecher LH, Fischer TL. Management of alcoholwithdrawal delirium. An evidence-based practice guideline.Arch

Intern Med. 2004;164:1405

1412.

11. American Psychiatric Association. Diagnostic and Statistical Manualof Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR).Washington, DC: American Psychiatric Association; 2000.

12. Mayo-Smith MF. Pharmacological management of alcoholwithdrawal. A meta-analysis and evidence-based practice guideline.JAMA. 1997;278:144151.

13. Saitz R, Mayo-Smith MF, Roberts MS, et al. Individualized treatmentfor alcohol withdrawal: a randomized double-blind controlled trial.JAMA. 1994;272:519523.

14. Manikant S, Tripathi BM, Chavan BS. Loading dose diazepamtherapy for alcohol withdrawal state. Ind J Med Res. 1993;98:170173.

15. Rogawski MA. Update on the neurology of alcohol withdrawalseizures. Epilepsy Curr. 2005;5:225230.

16. Chance JF. Emergency department treatment of alcohol withdrawalseizures with phenytoin.Ann Emerg Med. 1991;20:520522.

Alldredge BK, Lowenstein DH, Simon RP. Placebo-controlled trial ofintravenous diphenylhydantoin for short-term treatment of alcoholwithdrawal seizures.Am J Med. 1989;87:645648.

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