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    Is your patient suffering from alcohol withdrawal?


    RN/DREXEL Home Study Program

    CE credit is no longer available for this article. Expired July 2005

    Originally posted February 2004


    ANN KELLY is an educator at Scripps Mercy Hospital and San Diego Veterans Affairs Healthcare System in San Diego. JACQUELINE SAUCIER is patient care manager for emergency services at Scripps Mercy Hospital.

    KEY WORDS: alcohol withdrawal, seizures, delirium tremens (DTs), hallucinosis, kindling,Wernicke-Korsakoff syndrome, benzodiazepines, symptom-triggered dosing

    Alcohol withdrawal can be life-threatening, but you may not know your patient is at risk until withdrawal is underway. Here's how to spot the signs and symptoms of this syndrome and initiate treatment.

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    In the United States, approximately 8.2 million people, including an estimated 15% – 20% of all primary care and hospitalized patients, are dependent on alcohol.1,2 This dependence often remains hidden until withdrawal signs appear.

    Alcohol withdrawal (AW) occurs when a person accustomed to regular alcohol intake either reduces his alcohol consumption or stops drinking alcohol altogether. The withdrawal produces a wide array of signs and symptoms that range in severity from mild to life-threatening. Because alcohol withdrawal is underdiagnosed in acute care patients,3 nurses need to understand the signs and complications of—and treatments for—this condition.

    Symptoms vary widely in type and severity

    Manifestations of AW develop when there's an interruption in the constant exposure of a patient's central nervous system to alcohol.4 Normally, nerve impulses travel from one neuron to another through small molecules called neurotransmitters, which either stimulate (excite) or inhibit these nerve cells. Under most circumstances, a balance is maintained between excitation and inhibition.

    Regular alcohol intake increases the activity of certain inhibitory neurotransmitters, suppressing neuronal activity. The body attempts to compensate for this depressant effect by increasing the excitability of neurons. When alcohol is removed, this compensation continues and results in excessive autonomic nervous system excitation, which causes the characteristic signs and symptoms of AW.4

    Early recognition of withdrawal is essential to preventing serious complications, such as seizures and delirium tremens (DTs). Signs and symptoms may begin hours after drinking has stopped and last for three to seven days.5 Initial symptoms may include headache, agitation, anxiety, irritability, nausea and vomiting, disorientation, difficulty concentrating, and heightened sensitivity to light and sound.6 These initial symptoms intensify and then diminish over 24 – 48 hours.6

    More serious manifestations include a low-grade fever, rapid breathing, tremor, and profuse sweating. The most severe manifestations of AW are seizures, hallucinosis, and DTs.4 About 25% of patients withdrawing from alcohol have seizures, which usually begin during the first 24 hours after drinking has stopped.6 Seizures can occur even in the absence of other withdrawal symptoms.4

    The likelihood and severity of seizures increases with the number of past withdrawals from alcohol. This phenomenon, known as kindling, is attributed to long-term changes in brain excitability.7 The risk of seizures also increases with the duration of alcohol abuse.

    The seizures that occur with alcohol withdrawal are usually generalized tonic-clonic; most patients experience only one.4 Although multiple seizures are rare, AW is one of the most common reasons for status epilepticus—continuous unrelenting seizures that can cause neurologic damage and death.4

    Alcoholic hallucinosis is a complication distinct from DTs and occurs in up to 10% of AW patients.7 The hallucinations can be visual, tactile, or auditory and occur while the patient is fully conscious and aware of his environment.4 They usually begin one to two days after alcohol intake has ceased.4

    DTs, the most severe symptom of AW, occurs in approximately 5% of AW patients and usually appears two to four days after the patient's last drink.6 It's characterized by severe agitation, disorientation, tremor, persistent hallucinations, and marked elevations in heart and respiratory rates and blood pressure.6 An estimated 5% of patients who experience DTs die from complications such as cardiac arrhythmias, respiratory arrest, dehydration, hyperthermia, circulatory collapse, and alcoholic ketoacidosis (AKA), an accumulation of ketones in the blood.6

    In addition to the above complications of AW, patients who are alcohol-dependent may develop Wernicke-Korsakoff syndrome, an irreversible degenerative brain disorder that's caused by thiamine deficiency.7 This syndrome is characterized by severe cognitive impairment, delirium, ataxia, and paralysis of certain eye muscles.7

    Currently, it's difficult to accurately predict which patients will develop which withdrawal symptoms.4 Risk factors for severe symptoms include higher levels of alcohol intake, longer duration of drinking, prior AW symptoms, abnormal liver function, older age, poor general health or concomitant acute illness, poor nutritional status, additional substance abuse, intense craving for alcohol, and past DTs or seizures.4

    Assess all patients for alcohol abuse and AW

    Screen all acute care patients at admission for alcohol use, abuse, and related problems.3 A simple screening tool, such as the CAGE questionnaire—shown in "The CAGE questionnaire" box—may be used to identify patients who might be alcohol-dependent. Those at high risk—trauma patients, for example—may warrant a blood alcohol concentration (BAC) test or a urine toxicology screen.

    Any acute care patient who has a high BAC or a CAGE score of 2 or higher should be assessed for AW using an evidenced-based, clinically-focused assessment tool.3 Two such withdrawal scales are the Alcohol Withdrawal Syndrome (AWS) Type Indicator and the revised Clinical Institute Withdrawal Assessment for Alcohol scale (CIWA-Ar).

    The AWS Type Indicator links types of symptoms to appropriate pharmacologic therapy.8 For example, CNS excitation (uneasiness, motor hyperactivity) would be treated with benzodiazepines, valproic acid (Depakene, Depakote), or carbamazepine (Tegretol, Carbatrol, others), while adrenergic hyperactivity (tachycardia, hypertension) would be treated with beta-blockers or clonidine HCl (Catapres).

    The most widely used AW assessment tool is the CIWA-Ar.9 It measures 10 manifestations of AW and takes three to five minutes to score. The higher the score, the greater the patient's risk for severe AW symptoms. Patients with a score higher than 15 have an increased risk of seizures and DTs.10 For a more detailed look at the CIWA-Ar, see the "Assessing alcohol withdrawal" box.

    First look for and treat underlying conditions

    When examining patients with AW, look for conditions that can exacerbate symptoms of AW, such as cardiac arrhythmias, heart failure, liver and pancreatic disease, infection, GI bleeding, and other conditions affecting the nervous system.6 Stabilize the patient's vital signs and correct any fluid and nutritional imbalances. Some patients may require IV fluids to correct severe dehydration from vomiting, diarrhea, sweating, or fever, while others may be at risk for volume overload because of fluid retention.6

    Alcohol-dependent patients are at risk of being thiamine-deficient, which increases their risk for Wernicke-Korsakoff syndrome. Administering thiamine (vitamin B1) can prevent this condition. All AW patients should receive 100 mg of thiamine as soon as treatment begins and then daily throughout the withdrawal period.6 Because it's necessary for glucose metabolism, thiamine should be administered before IV glucose.

    Patients' magnesium levels drastically drop during the course of withdrawal and spontaneously return to normal as symptoms subside.2 Unfortunately, though, there's no evidence that giving AW patients magnesium supplements reduces the severity of AW symptoms or the frequency of delirium or seizures.2

    Patients who have seizures should be evaluated using tests such as electroencephalography (EEG), computed tomography (CT), and magnetic resonance imaging (MRI). These tests will help detect or rule out other causes of seizures, such as head trauma or CNS infection.

    The treatment of patients with AW should be individualized.3 Most patients with mild symptoms (CIWA-Ar score <8) don't develop complications and can be treated without drug therapy.4 Some studies show that patients with mild symptoms benefit from supportive measures alone: a quiet environment, reduced lighting, limited interaction with others, nutrition and fluids, and reassurance and encouragement.6

    Patients with moderate to severe symptoms (CIWA-Ar score >8) need drug therapy to address their symptoms and reduce their risk of DTs.4 There are two primary approaches: traditional fixed- schedule dosing and symptom-triggered dosing.4

    In fixed-schedule dosing, the patient receives a specific dose of a specified medication—typically a benzodiazepine every six hours for two to six days, regardless of the presence or severity of symptoms. This fixed dose is decreased at regular intervals. In a symptom-triggered approach, the patient's CIWA-Ar score is determined hourly, and medication is administered only when the score is >8.2. Symptom-triggered therapy is generally preferred because it's just as effective as fixed-schedule dosing but it requires significantly less medication and leads to more rapid detoxification.10

    Currently, several types of medications, including benzodiazepines, beta-blockers, clonidine, anticonvulsants, and neuroleptic agents, are used to treat AW. In 1997, the American Society of Addiction Medicine (ASAM) developed practice guidelines for the pharmacological management of AW. In these guidelines, the ASAM recommends benzodiazepines for treating AW.2

    Benzodiazepines, such as chlordiazepoxide (Librium, Libritabs, others), diazepam (Valium, Valrelease), and lorazepam (Ativan), are recommended over other medications because they have better documented efficacy, are safer, and are less likely to lead to abuse.2 (The potential for abuse is higher with benzodiazepines with a rapid onset of action, such as diazepam, than it is for those with a slower onset, such as chlordiazepoxide.2) Benzodiazepines reduce the severity of AW, as well as the incidence of delirium and seizures.4 Dosage should be individualized, based on the severity of the withdrawal (as indicated by the withdrawal scale score), the presence or absence of co-morbid illness, and the presence or absence of seizures during previous episodes of withdrawal. For a patient with a CIWA-Ar >8, a typical dose would be: chlordiazepoxide 50 – 100 mg/hour; diazepam 10 – 20 mg/hour; or lorazepam 2 – 4 mg/hour.2

    Other medications may be used to treat AW but are not recommended as monotherapy; they should be used only in combination with benzodiazepines. Beta-blockers reduce the autonomic manifestations of AW but have no known anticonvulsant properties.2 Their effect on AW-related seizures has not been examined in large studies. In addition, delirium is a possible side effect of beta-blockers, particularly those with good central nervous system penetration, such as propranolol HCl (Inderal, Betachron ER, others). Furthermore, propranolol may mask symptoms of early withdrawal or impending seizures, making it difficult to use withdrawal scales to guide therapy.2,10

    Studies have shown that central acting alpha-adrenergic agonists, such as clonidine, alleviate symptoms in patients with mild to moderate AW; however, what effect these agents have on the rate of delirium and seizures is unknown.2

    In Europe, the anticonvulsants valproic acid and carbamazepine have been widely used in the management of AW.6 Both agents have well-documented anticonvulsant activity, and research shows that carbamazepine prevents AW seizures in animals2 and may prevent kindling.4 And, like the benzodiazepines that have slower onset of action such as chlordiazepoxide, anticonvulsants have a low likelihood of leading to abuse. For these reasons, you may see them used in conjunction with benzodiazepines to treat AW.2

    Using the popular anticonvulsant phenytoin (Dilantin) in the management of AW is controversial. Research has not shown it to be superior to placebo in the prevention of simple AW-induced seizures. However, you may need to give it to AW patients until other possible causes of seizures have been ruled out.4

    Neuroleptic agents, such as the phenothiazine chlorpromazine (Thorazine) and the butyrophenone haloperidol (Haldol), may reduce symptoms of AW but are significantly less effective than benzodiazepines in preventing delirium and seizures.10 Nonetheless, patients with severe agitation, thought disorders, or hallucinations may require haloperidol in addition to a benzodiazepine.

    All of that said, there is one other option for patients with AW that you need to be aware of. The oral or IV intake of ethyl alcohol can postpone the symptoms of AW, and some clinicians have used alcohol for this purpose. However, this practice is not recommended because there is well-documented evidence of ethyl alcohol's adverse effects, including hepatic, gastrointestinal, hematological, and neurological toxicity. In addition, there are no controlled trials evaluating alcohol's safety or efficacy in comparison to benzodiazepines.2,3

    While the above treatments are necessary to effectively address AW, treating alcohol dependence requires more than acute detoxification.3 All patients will need an individualized referral for additional treatment. A practitioner with expertise in substance abuse programs is the best person to discuss all available treatment options—including self-help programs such as Alcoholics Anonymous—with the patient prior to discharge.3 Let family members who are aware of the patient's situation know about community-based resources, such as Al-Anon and Alateen. These resources address the impact of alcoholism on families and friends of people with alcohol dependence.3

    By identifying and treating your patients' AW symptoms, you will do much more than relieve their discomfort and ward off complications. You'll be encouraging them to get treatment for their alcohol dependence. And that could quite possibly save their lives.


    1. Substance Abuse and Mental Health Services Administration. "Table 5.1A—Substance dependence for specific substances in the past year, by age group: Numbers in thousands, 2002." 2003. National survey on drug use and health. www.samhsa.gov/oasnhsda/2k2nsduh/2k2TabsCover.pdf (18 Nov. 2003)

    2. Mayo-Smith, M. F., Cushman, R., et al. (1997). Pharmacological management of alcohol withdrawal: A meta-analysis and evidenced-based practice guideline. JAMA, 278(2), 144.

    3. International Society of Psychiatric-Mental Health Nurses. "Assessment and identification management of alcohol withdrawal syndrome (AWS) in the acute care setting." 2000. www.ispn-psych.org/docs/10-00-aws.pdf (13 Nov. 2003).

    4. Saitz, R. (1998). Introduction to alcohol withdrawal. Alcohol Health Res World, 22(1), 5.

    5. McRae, A. L., Brady, K. T., & Sonne, S. C. (2001). Advances in the pathophysiology and treatment of psychiatric disorders: Implications for internal medicine. Med Clin North Am, 85(3), 779.

    6. Myrick, H., & Anton, R. F. (1998). Treatment of alcohol withdrawal. Alcohol Health Res World, 22(1), 38.

    7. Trevisan, L. A., Boutros, N., et al. (1998). Complications of alcohol withdrawal. Alcohol Health Res World, 22(1), 61.

    8. Depetrillo, P. B., & McDonough, M. K. 1999. Alcohol withdrawal treatment manual. Glen Echo, MD: Focused Treatment Systems.

    9. Williams, D., Lewis, J., & McBride, A. (2001). A comparison of rating scales for the alcohol-withdrawal syndrome. Alcohol Alcohol, 36(2), 104.

    10. Kosten, T. R., & O'Connor, P. G. (2003). Management of drug and alcohol withdrawal. N Engl J Med, 348(18), 1786.

    The CAGE questionnaire

    The complications of alcohol withdrawal (AW) are potentially fatal, so all acute care patients should be screened for alcohol dependence with a reliable and easy-to-use screening tool, such as the four-question CAGE questionnaire. (CAGE stands for Cutting down, Annoyance by criticism, Guilty feeling, and Eye-openers.) The questions are:

    • Have you ever felt you should cut down on your drinking?

    • Have people annoyed you by criticizing your drinking?

    • Have you ever felt bad or guilty about your drinking?

    • Have you ever had a drink first thing in the morning to steady your nerves or to get rid of a hangover?

    Answers are scored 0 for No and 1 for Yes. Patients with a score of 2 or higher require a more detailed assessment for AW.

    Sources: 1. Ewing, J. A., (1984). Detecting alcoholism. The CAGE questionnaire. JAMA, 252(14), 1905. 2. International Society of Psychiatric-Mental Health Nurses. "Assessment and identification management of alcohol withdrawal syndrome (AWS) in the acute care setting." 2000. www.ispn-psych.org/docs/10-00-aws.pdf (13 Nov. 2003).

    Assessing alcohol withdrawal

    The revised Clinical Institute Withdrawal Assessment for Alcohol scale (CIWA-Ar) is the most widely used tool for assessing alcohol withdrawal. It measures nine categories of symptoms on a scale of 0 – 7 and one symptom (clouding of sensorium) on a scale of 0 – 4. Mild symptoms translate into a total score of <8; moderate symptoms, 8 – 15; and severe symptoms, >15. Patients with a score >8 should receive drug therapy to treat their symptoms and reduce their risk of seizures and delirium tremens (DTs).


    Category Range of scores Scoring examples
    Agitation 0 – 7 0=normal activity;
    4=moderately fidgety and restless;
    7=constantly thrashes about
    Anxiety 0 – 7 0=no anxiety, at ease;
    4=moderately anxious or guarded;
    7=acute panic states
    Auditory disturbances 0 – 7 0=not present;
    4=moderately severe hallucinations;
    7=continuous hallucinations
    Clouding of sensorium 0 – 4 0=oriented and can do serial additions;
    2=disoriented for date by no more than two calendar days;
    4=disoriented for place and/or person
    Headache 0 – 7 0=not present;
    4=moderately severe;
    7=extremely severe
    Nausea or vomiting 0 – 7 0=no nausea and no vomiting;
    4=intermittent nausea with dry heaves;
    7=constant nausea; frequent dry heaves and vomiting
    Paroxysmal sweats 0 – 7 0=no sweat visible;
    4=beads of sweat obvious on forehead;
    7=drenching sweats
    Tactile disturbances 0 – 7 0=none;
    4=moderately severe hallucinations;
    7=continuous hallucinations
    Tremor 0 – 7 0=no tremor;
    4=moderate, with patient’s arms extended;
    7=severe, even without extended arms
    Visual disturbances 0 – 7 0=none;
    4=moderately severe hallucinations;
    7=continuous hallucinations


    Sources: 1. Kosten, T. R., & O'Connor, P. G. (2003). Management of alcohol and drug withdrawal. N Engl J Med, 348(18), 1786. 2. Saitz, R. (1998). Introduction to alcohol withdrawal. Alcohol Health Res World, 22(1), 5.


    Kathleen Moore, ed. Ann Kelly, Jacqueline Saucier. Is your patient suffering from alcohol withdrawal? RN Feb. 1, 2004;67:27.

    Published in RN Magazine.

    Jacqueline Saucier, RN, MSN, CEN, CCRN
    JACQUELINE SAUCIER is patient care manager for emergency services at Scripps Mercy Hospital.
    Ann E. Kelly, APRN, MSN
    ANN KELLY is an educator at Scripps Mercy Hospital and San Diego Veterans Affairs Healthcare System in San Diego.