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EARN CATEGORY I CME CREDIT
by reading this article and the article beginning on page 40 and successfully
completing the posttest on page 45. Successful completion is defined as a cumulative score of at least 70%
correct. This material has been reviewed and is approved for 1 hour of clinical Category I (Preapproved) CME credit
by the AAPA. The term of approval is for 1 year from the publication date of September 2007.
CME LEARNING OBJECTIVES
● Describe the supposed mechanism of action of alcohol withdrawal● List the signs and symptoms associated with alcohol withdrawal● Discuss the steps in evaluating the hospitalized patient with suspected alcohol withdrawal● Outline treatment goals related to supportive care, pharmacologic choices, and posthospital therapy
Managing alcohol withdrawalin hospitalized patients
Therapy includes benzodiazepines to reduce withdrawal symptoms and prevent delirium.
Symptom-driven protocols may be more beneficial than scheduled-dosing plans.
Zachary Hartsell, MPAS, PA-C; Jennifer Drost, MMSc, PA-C;
James A. Wilkens, MD; Adriane I. Budavari, MD
Alcohol is currently the second most abused drug
in the United States and is abused by up to 9%of the population.1,2 Approximately 11 to 15million people report heavy alcohol intake, andthe costs of medical complications related to
alcohol abuse in the United States are estimated to be almost$100 billion per year.2 Although many definitions of alco-holism exist, the National Institute on Alcohol Abuse andAlcoholism (NIAAA) classifies women who consume morethan 7 drinks per week and men who consume more than 14drinks per week as being at high-risk of progressing to alco-holism. More than 4 drinks a day is considered heavy alcoholuse for women, more than 5 drinks a day for men.3
Heavy alcohol users are at risk for withdrawal symptoms,
with hospitalized patients who abuse alcohol at greatest risk.
Some reports suggest that at least 25% of general medical inpa-tients have alcohol use disorders.4 In trauma patients, the rateis much higher, with alcohol dependence or abuse present in25% to 47% of these patients.5 In a study of 242 trauma pa-tients admitted to a suburban US hospital, 43% were found to
have elevated blood alcohol levels and 33% were legally intoxi-cated.5 The incidence of patients with alcohol withdrawal syn-
drome is projected to be nearly 2 million per year, with morethan 500,000 per year having withdrawal symptoms severeenough to require pharmacologic treatment.6
Even though alcohol withdrawal is a common inpatient
disorder, studies suggest that many hospitalized patients arenot receiving appropriate diagnosis or treatment. Bostwickand colleagues found that in an urban Level I trauma center,approximately 75% of alcohol abusers were identified.7
Despite this, only 43% of these patients had withdrawal pro-
20 JAAPA •
SEPTEMBER 2007 •
phylaxis ordered, and only 38% were monitored for alcohol
by mild autonomic hyperactivity, manifesting as tremulous-
withdrawal signs and symptoms.7 This article reviews the
ness, mild anxiety, tachycardia, hypertension, GI upset, in-
pathophysiology of alcohol withdrawal, describes how to
somnia, and vivid dreams. Since the signs and symptoms
evaluate and monitor patients potentially suffering from this
of alcohol withdrawal are quite nonspecific at this stage, the
condition, and suggests treatment strategies.
diagnosis can often be missed. Symptoms of minor with-drawal typically resolve spontaneously in 24 to 48 hours,
Although the exact mechanism of action for alcohol with-
Major withdrawal syndromes tend to
drawal is unknown, the GABA inhibition theory is the most
occur approximately 48 to 72 hours after the last drink.
widely accepted. Alcohol enhances the inhibitory chloride
They include alcoholic hallucinosis, alcohol seizures, and
influx mediated by gamma-aminobutyric acid alpha (GABA-
A), resulting in clinical sedation. With chronic alcohol use,
First characterized in 1989, alcoholic hallucinosis occurs in
tolerance develops and GABA receptor function is down-
an estimated 10% to 25% of hospitalized alcoholics.9-11 Hallu-
regulated. Alcohol also inhibits the excitatory N
cinations can be tactile, visual, or auditory, but patients with
aspartate (NMDA) receptor, thus diminishing the excitatory
alcoholic hallucinosis—unlike those with DTs—maintain a
effects of glutamate and, over time, increasing neuroexcitato-
clear sensorium.6 Although definite risk factors for alcoholic
ry tone. Finally, alcohol causes alpha2-receptors to inhibit
hallucinosis have not been identified, a study of 643 patients
norepinephrine release. As a result, when alcohol is abruptly
in a Veterans Affairs drug and alcohol treatment center found
withdrawn, the unopposed hyperexcitable neurons cause the
that those who developed alcoholic hallucinosis were younger
at the onset of their alcoholism and tended to be heavier
Another key pathophysiologic concept in alcohol with-
drinkers than alcohol abusers who did not.11
drawal is the phenomenon of kindling
. Kindling begins as a
Alcoholic seizures occur in up to 10% of patients suffering
single electrical stimulus initially causing no overt clinical
alcohol withdrawal. They tend to occur 24 hours after the
manifestations but eventually results in the appearance of
last drink but can occur even while alcohol is still measurable
abnormal behavior (such as seizures) when the stimulus is
in the blood. Alcoholic seizures are single, short, generalized
administered repeatedly. Applied to alcoholism, kindling
tonic-clonic seizures that can recur successively but rarely
explains why each episode of alcohol withdrawal appears to
progress to status epilepticus.9 Status epilepticus, focal seizures
increase patients’ risk of withdrawal symptoms. Chronic
or seizures associated with fever or known head trauma, and
alcoholics typically experience progressively shorter intervals
seizures starting after the patient becomes delirious are not
between their last drink and onset of symptoms, as well as
typical of alcohol withdrawal and require further workup.
progressive worsening of symptoms during each subsequent
DTs is considered the end point of the alcohol withdrawal
spectrum and represents a medical emergency. DTs occurs inapproximately 5% of patients with alcohol withdrawal.6
Symptoms typically start 48 to 72 hours after the last drink
The signs and symptoms of alcohol withdrawal fall along a
and include confusion, disorientation, impaired attention,
spectrum, ranging from mild and self-limiting to life-threaten-
severe autonomic activity, and hallucinations. A history of
ing (see Figure 1, page 22). Importantly, these signs and
DTs, a long history of sustained drinking, age greater than
symptoms should be attributed to alcohol withdrawal only
65 years, concurrent medical comorbidities, and seizure
after other medical conditions are considered and ruled out.
activity during the present admission are risk factors. Earlier
The manifestations of mild alcohol with-
studies found mortality in patients with DTs to be as high
drawal typically start between 5 and 10 hours after the last
as 20% even with treatment, but more recently mortality is
drink. This early stage of alcohol withdrawal is characterized
cited at about 1%, with death generally occurring from
■ Early identification of patients who are experiencing an alcohol withdrawal syndrome
includes recognizing the spectrum of withdrawal indicators and monitoring carefully for signs and symptoms. With appropriate treatment, the risk of complications from alcohol
●●●●● Interpersonal & communication skills
withdrawal is significantly lessened.
■ Benzodiazepines are the drug of choice for the treatment of most patients who have alcohol
■ Studies suggest that use of a symptom-triggered dosing protocol may reduce treatment
times for patients with alcohol withdrawal syndrome.
■ In addition to recognizing alcohol withdrawal, clinicians should take the time to screen
●● Practice-based learning and improvement
patients for alcohol abuse. Proper identification can ensure appropriate outpatient follow-up.
SEPTEMBER 2007 •
www.jaapa.com • JAAPA 21
arrhythmias or concomitant illnesses. When DTs is unrecog-
the current status of the patient with respect to alcohol with-
nized and untreated, mortality can exceed 35%.12
drawal syndrome. The CAGE questions are designed to elic-it information about alcohol abuse in hopes of identifying
EVALUATING THE PATIENT
patients most at risk for withdrawal; therefore it is most
The first step in evaluating the hospitalized patient with sus-
appropriate to use during the admission interview, before the
pected alcohol withdrawal is ruling out other medical condi-
tions that could be causing the signs and symptoms. When
that may indicate alcohol abuse include
alcohol withdrawal remains likely, key historical information
elevations in mean corpuscular volume (MCV), gamma-
includes total duration of alcohol use, daily quantity of alco-
glutamyl transpeptidase (GGT), and liver transaminases.
hol ingestion, elapsed time since last drink, history of alcohol
Elevated liver transaminases with the pattern of AST being
withdrawal syndromes, abuse of other substances, and histo-
more than 2 times higher than ALT is the most common lab-
ry of major medical and/or psychiatric conditions. The physi-
oratory finding in patients who abuse alcohol. One study
cal examination should not only focus on identifying the
noted this finding in 83% of patients admitted with alcoholic
signs and symptoms of alcohol withdrawal but should also
hepatitis.15 Additionally, this pattern is generally not seen in
attempt to uncover any signs of complicating medical condi-
other forms of liver disease.15 GGT is commonly measured
tions—including (but not limited to) arrhythmias, heart fail-
to determine chronic alcohol use but has a sensitivity of only
ure, liver disease, pancreatitis, or infections.
30% to 40%.15 GGT can be elevated in patients with nonal-
Once alcohol withdrawal syndrome has been diagnosed,
coholic forms of liver disease or in those taking certain med-
the severity of the episode should be determined since severi-
ications. An elevated MCV is an index of RBC size. MCV
ty will guide further therapy. Although most patients under-
increases with excessive alcohol intake after 4 to 8 weeks.
going alcohol withdrawal need close observation, some war-
The mechanism of the elevation in chronic alcoholism is
rant admission to an ICU. These include patients with
unknown, but the elevation is found in 90% of alcoholics.
advanced age; hemodynamic instability; hyperthermia (per-
Patients who binge drink or who have started drinking heav-
sistent temperature higher than 39°C/103°F); a severe elec-
ily only recently (within 90 days) may have normal-size
trolyte disturbance or acid-base disorder; moderate to severe
RBCs.16 In more recent studies, elevations in carbohydrate-
cardiac, pulmonary, or renal disease; active infection; rhab-
deficient transferrin level was shown to be a more sensitive
domyolysis (as evidenced by an elevated creatine kinase
and specific biologic marker for detecting alcohol abuse, but
[CK] level combined with a normal CKMB/troponin level);
testing for this is impractical in the hospital setting.17
—that is, trying to identify which patients are at
DETERMINING SYMPTOM SEVERITY
high risk for alcohol withdrawal before
they become sympto-
In patients with suspected active alcohol withdrawal, the
matic—is considered the best practice. Although patients may
Clinical Institute Withdrawal Assessment for Alcohol scale,
be reluctant to discuss their drinking, the interview remains
revised (CIWA-Ar), is the best tool to determine severity and
the most reliable and accurate means of assessing alcohol
to guide therapeutic intervention (see Figure 2, page 24). The
intake and determining who is at risk for withdrawal.
CIWA-Ar is well-validated and has high reproducibility and
Although validated only in the outpatient setting, the
CAGE questionnaire can also be a useful interview tool for
The CIWA-Ar was created to assess and guide treatment
assessing inpatients suspected of alcohol abuse. It is com-
of acute alcohol withdrawal. It also has utility in triage. For
example, patients with a CIWA-Ar score of less than 10 can
• Have you ever felt the need to C
ut down on drinking?
be observed and in some cases may be treated as outpatients,
• Have you ever felt A
nnoyed by criticism of your drinking?
as long as they have a stable living situation with close follow-
• Have you ever felt G
uilty about your drinking?
up and no history of relapses or major comorbid mental or
• Have you ever taken a morning E
medical illness.19 Patients with a CIWA-Ar score greater than
The CAGE questionnaire has an overall sensitivity of 85%
10 should be admitted for inpatient treatment and close ob-
and a specificity of 89%; with three positive answers, its sen-
servation. Patients with a CIWA-Ar score greater than 15
sitivity is 100%.14 The main disadvantage of the CAGE is
will need initiation of treatment with benzodiazepines. After
that it does not distinguish between past and present alcohol
being used as a triaging tool, the CIWA-Ar can be used to
use, and it therefore does not provide any information about
guide therapy and monitor for worsening of the withdrawal.18
FIGURE 1. The spectrum of alcohol withdrawal syndrome
22 JAAPA •
SEPTEMBER 2007 •
Unfortunately, few clinicians report routinely using the
based on the score. In the 117 patients studied, symptom-
CAGE questionnaire or the CIWA-Ar with patients. Accord-
triggered dosing showed no difference in comfort levels.
ing to Friedmann and colleagues, although most clinicians
However, the mean duration of treatment was shorter in the
ask patients if they consume alcohol, only 13% report using
group treated in response to symptoms (20 hours vs 63
a validated screening tool such as the CAGE.20 In addition,
hours), and there was a marked decrease in the mean quanti-
the CIWA-Ar is rather labor-intensive, requiring high levels
ty of medication administered (37 mg vs 231 mg). There was
of nursing care to administer effectively. However, without
no difference in complications between the two groups.25
validated tools, diagnoses of alcoholism and alcohol with-
IV ethanol (IVE) historically was used for the treatment
drawal are delayed, as are necessary treatments.
and prevention of alcohol withdrawal. Discussion of its usewas confined to case reports, whose authors felt IVE to be
less sedating than benzodiazepines.26 A 2004 review of anec-
Treatment goals for alcohol withdrawal syndrome include
dotal reports of IVE in critically ill patients with alcohol with-
alleviating symptoms, preventing progression to DTs, control-
drawal similarly found no evidence to support its use.27 This
ling underlying comorbidities, and initiating rehabilitation.9
conclusion is a result of IVE’s inconsistent pharmacokinetic
Treating a patient in alcohol withdrawal
profile, relatively narrow therapeutic index, and enhance-
includes providing a quiet environment with supervision and
ment of drug interactions secondary to hepatic metabolism.27
precautions against falls. Electrolyte abnormalities should becorrected, but routine administration of magnesium has notproved effective.21 Similarly, IV fluids should be reserved for
patients with signs of excess fluid loss. Finally, a daily multi-
vitamin (orally if possible) and thiamine (100 mg by conven-tion) are generally recommended, though formal evidence to
support these interventions is lacking. A recent Cochranesystematic review found insufficient evidence from random-ized controlled trials to guide clinicians in the optimal dose,
Benzodiazepines are considered first-
route, frequency, or duration of thiamine for prophylaxis
line therapy for alcohol withdrawal syndrome, and adjunct
against or treatment of Wernicke-Korsakoff syndrome.22
medication should be used only in conjunction with benzodi-
Pharmacologic treatment of alcohol
azepines. Beta-blockers and alpha-blockers have been tradi-
withdrawal centers upon using medications that are cross-
tionally used in the management of alcohol withdrawal, par-
tolerant with alcohol. Benzodiazepines are considered first-line
ticularly to treat hypertension. The purpose of beta-blockade
therapy. Their mechanism of action is to enhance the depres-
in alcohol withdrawal is to reduce the result of increased car-
sant neurotransmitter GABA and replace the effects of alco-
diac autonomicity, including arrhythmias and increased car-
hol. A review of 57 trials with a total of 4,051 patients found
diac output. Adjunctive therapy with beta-blockers should be
that the risk of alcohol withdrawal seizure was reduced with
considered in patients with known coronary artery disease.
the use of benzodiazepines compared with placebo.23 Al-
Alpha-blockers, such as clonidine, work similarly to decrease
though no specific benzodiazepine has been shown to be
sympathetic tone and affect mainly the alpha-receptors.24
superior to another, certain agents are recommended, based
Historically, anticonvulsants have been widely used to con-
largely on their pharmacokinetics. For example, long-acting
trol alcohol withdrawal symptoms (particularly seizures).
agents such as diazepam and chlordiazepoxide effectively pre-
Carbamazepine is used widely throughout Europe for outpa-
vent rebound symptoms. In patients who are elderly, have
tient treatment of alcohol withdrawal. It appears to suppress
hepatic disease, or are critically ill, intermediate-acting agents
the kindling effect and to decrease the craving for alcohol
like lorazepam or oxazepam are preferred to prevent overse-
after withdrawal.9 A 2005 review of 48 studies found the use
dation. Lorazepam and diazepam are available for oral, IV,
of anticonvulsants controversial. Because of the heterogeneity
and IM administration, whereas chlordiazepoxide and oxaze-
of agents available and the limited studies performed, no rec-
pam have only oral formulations.24 Clonazepam, temazepam,
ommendation could be made on their use for alcohol with-
drawal. When compared to benzodiazepines, anticonvulsants
Fixed-dose versus symptom-triggered regimens
had equal efficacy in preventing seizures but a worse side
ential randomized controlled trial by Daeppen and colleagues
effect profile.28 Additionally, studies have shown no effect on
inspired a major change in how benzodiazepines are admin-
istered to hospitalized patients experiencing alcohol with-
Neuroleptics are often used to treat agitation and hallucina-
drawal syndrome. This study compared symptom-triggered
tions in alcohol withdrawal syndrome. In 2004, Mayo-Smith
benzodiazepine therapy (administering a dose in response to
and colleagues published a meta-analysis of nine prospective
symptoms) versus fixed-dose
(administering a fixed dose at
controlled trials which culminated in the formation of an
standard intervals regardless of symptoms) therapy. The
evidence-based practice guideline for the management of
CIWA-Ar was used to measure the severity of the withdraw-
alcohol withdrawal delirium.29 They suggested that sedative-
al, and an appropriate dose of benzodiazepine was given
hypnotics are more effective than neuroleptic agents in reduc-
SEPTEMBER 2007 •
www.jaapa.com • JAAPA 23
FIGURE 2. Clinical Institute Withdrawal Assessment for Alcohol Scale
Patient ________________________________________________________________ Date _____________________ Time __________________
Pulse or heart rate, taken for 1 min ________________________________________ Blood pressure______________________________________
Ask: “Do you feel sick to your stomach?
that is disturbing to you? Are you seeing
Do not rate for dizziness or lightheaded-
1 Barely perceptible sweating, palms moist
Rater’s initials _______________________
Adapted from Sullivan JT, Sykora K, Schneiderman J, et al. Assessment of alcohol withdrawal: the revised Clinical
Institute Withdrawal Assessment for Alcohol Scale (CIWA-Ar). Br J Addict. 1989;84:1353-1357.
24 JAAPA •
SEPTEMBER 2007 •
ing duration of delirium and mortality, with a relative risk of
death when using neuroleptics of 6.6, though the confidence
1. US Preventive Services Task Force. Screening and behavioral counseling interventions in pri-
mary care to reduce alcohol misuse: recommendation and statement. Ann Intern Med. 2004;
interval was very wide (95% CI, 1.2-34.7). Importantly, the
nine trials cited were decades old (1959-1978), occurring
2. Grant BF. Alcohol consumption, alcohol abuse and alcohol dependence. The United States as an
when diagnostic criteria were less clear and older neurolep-
3. NIAAA: Social work education for the prevention and treatment of alcohol use disorders.
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Module 1: epidemiology of alcohol use disorders in the United States. National Institute on
ommended haloperidol as first-line therapy for delirium
Alcohol Abuse and Alcoholism of the National Institutes of Health Web site. http://pubs.
niaaa.nih.gov/publications/Social/Module1Epidemiology/Module1.html. Accessed August 24,
In the absence of clear research evidence demonstrating
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6. Bayard M, McIntyre J, Hill KR, Woodside J Jr. Alcohol withdrawal syndrome. Am Fam Physician.
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for alcohol withdrawal. Baclofen is a GABA-B receptor ago-
11. Tsuang JW, Irwin MR, Smith TL, Schuckit MA. Characteristics of men with alcoholic hallucinosis.
nist. In several small studies, it reduced moderate and severe
symptoms in alcohol withdrawal syndrome, and it had a
12. Ferguson JA, Suelzer CJ, Eckert GJ, et al. Risk factors for delirium tremens development. J Gen
more favorable side effect profile than benzodiazepines. Fur-
13. Carlson RW, Keske B, Cortez A. Alcohol withdrawal syndrome: alleviating symptoms, preventing
thermore, baclofen exhibits less addictive properties and may
progression. J Crit Illness. 1998;13(5):311-317.
be more effective than benzodiazepines at helping to main-
14. Bush B, Shaw S, Cleary P, et al. Screening for alcohol abuse using the CAGE questionnaire. Am J
tain abstinence in alcoholics.31,32 Before widespread use of
15. Sorbi D, Boynton J, Lindor KD. The ratio of aspartate aminotransferase to alanine aminotrans-
baclofen can be recommended, however, larger studies com-
ferase: potential value in differentiating nonalcoholic steatohepatitis from alcoholic liver dis-
paring it directly to benzodiazepines are needed.
ease. Am J Gastroenterol. 1999;94(4):1018-1022.
16. Girard DE, Kumar KL, McAfee JH. Hematologic effects of acute and chronic alcohol abuse.
Treatment after hospitalization
Ensuring proper follow-up
Hematol/Oncol Clin N Am. 1987;1(2):321-334.
is one of the key steps in effectively managing patients with
17. Figlie NB, Benedito-Silva AA, Monteiro MG, Souza-Formigoni MLO, on behalf of the WHO/ISBRA
Study on State and Trait Markers of Alcohol Use and Dependence Investigators. Biological
alcohol-related disorders. Long-term abstinence should be the
markers of alcohol consumption in nondrinkers, drinkers, and alcohol-dependent Brazilian
goal, and the process can start with a brief intervention from
patients. Alcohol Clin Exp Res. 2002;26(7):1062-1069.
the provider. For example, a brief bedside intervention may
18. Sullivan JT, Sykora K, Schneiderman J, et al. Assessment of alcohol withdrawal: the revised
Clinical Institute Withdrawal Assessment for Alcohol Scale (CIWA-Ar). Br J Addict. 1989;84:1353-1357.
play a major role in helping patients achieve the long-term
19. Hayashida M, Aterman AI, McLellan AT, et al. Comparative effectiveness and costs of inpatient
goal of total abstinence. A large meta-analysis of 32 con-
and outpatient detoxification of patients with mild-to-moderate alcohol withdrawal syndrome.
trolled studies looking at the impact of brief interventions on
20. Friedmann PD, McCullough D, Chin MH, Saitz R. Screening and intervention for alcohol prob-
drinking behaviors found that brief intervention was superi-
lems: a national survey of primary care physicians and psychiatrists. J Gen Intern Med.
or to no intervention, and some studies found brief interven-
21. Wilson A, Vulcano B. A double-blind, placebo-controlled trial of magnesium sulfate in the
tion was as effective as extensive therapy.33
ethanol withdrawal syndrome. Alcohol Clin Exp Res. 1984;8(6):542-545.
Although inpatient psychiatry consultation is not mandato-
22. Day E, Bentham P, Callaghan R, et al. Thiamine for Wernicke-Korsakoff syndrome in people at
ry for every patient, it should be considered for those with
risk from alcohol abuse. Cochrane Database Syst Rev. 2006;4.
23. Ntais C, Pakos E, Kyzas P, Iodannidis JP. Benzodiazepines for alcohol withdrawal. Cochrane
withdrawal symptoms resistant to treatment, those with
comorbidities or multiple substance intoxications, and those
24. Physicians’ Desk Reference, electronic version. http://www.pdr.net. Accessed August 20, 2007.
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azepine for alcohol withdrawal: a randomized treatment trial. Arch Intern Med. 2002;162:1117-1121.
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29. Mayo-Smith MF, Beecher LH, Fischer TL, et al, for the Working Group on the Management of
practice in the Department of Hospital Internal Medicine, Mayo
Alcohol Withdrawal Delirium, Practice Guidelines Committee, American Society of Addiction
Clinic Hospital, Phoenix, Arizona. They have indicated no relationships to dis-
Medicine. Management of alcohol withdrawal delirium. An evidence-based practice guideline.
close relating to the content of this article.
Arch Intern Med. 2004;164(13):1405-1412.
30. Klijn IA, van der Mast RC. Pharmacotherapy of alcohol withdrawal delirium in patients admitted
to a general hospital [letter]. Arch Intern Med. 2005;165(3):346.
31. Addolorato G, Leggio L, Abenavoli L, et al. Baclofen in the treatment of alcohol withdrawal syn-
drome: a comparative study vs diazepam. Am J Med. 2006;119:276.e13-276.e18.
Haloperidol (Haldol, Haloperidol Intensol)
32. Addolorato G, Caputo F, Capristo E, et al. Baclofen efficacy in reducing alcohol craving and
intake: a preliminary double-blind randomized controlled study. Alcohol Alcohol. 2002;37(5):
33. Bien TH, Miller WR, Tonigan JS. Brief interventions for alcohol problems: a review. Addiction.
SEPTEMBER 2007 •
www.jaapa.com • JAAPA 25
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