Detox Article

January-February 2012 • Vol. 21/No. 1 9

Glenn Donnelly, PhD, MN, BSc(N), RN, ENC©, is Associate Professor, Faculty of Nursing,University of Regina, Regina, Saskatchewan, Canada.

Arlene Kent-Wilkinson, PhD, MN, BSN, RN, is Associate Professor, College of Nursing,University of Saskatchewan, Saskatoon, Saskatchewan, Canada.

Alecia Rush is a Nursing Student, Mount Royal University, Calgary, Alberta, Canada.

Note: The authors and all MEDSURG Nursing Editorial Board members reported no actual orpotential conflict of interest in relation to this continuing nursing education article.

The Alcohol-Dependent Patient inHospital: Challenges for Nursing

Alcohol dependence is thethird leading cause of disease burden in develop-ing countries worldwide

(World Health Organization, 2006).The ubiquitous presence of alcoholmeans nurses will encounter individ-uals in their acute care practices whouse or abuse alcohol. Some of theclinical problems presented by theseindividuals are examined and thecritical aspects of their care are high-lighted.

DefinitionsAlcohol abuse is a pattern of

drinking resulting in harm to a per-son’s health, interpersonal relation-ships, or ability to work (Anton,2008). Alcohol abuse can lead toalcohol dependence (Centers forDisease Control and Prevention,2008). Alcoholism is a behavior pat-tern characterized by uncontrolleddrinking of alcoholic beverages tothe extent of impairing health andsocial functioning. Alcoholism isthus one extreme in a range of drink-ing patterns that vary among indi-viduals in degree of dependency andtolerance, and in a host of otherways (e.g., timing or beveragechoice) (Pasch, 2010). Alcoholism isa pathological dependency onethanol (National Council onAlcoholism, 2011) that is character-ized by tolerance, physical depend-ency, and/or pathological organchanges (Schuckit, 2008).

Prevalence RatesIn Canada, an estimated 4% of

the population over age 15 isdependent on alcohol, with twice as

many males affected as females. Thehighest rate of alcoholism occurs inCanadians ages 20-24. In Canadiansurveys, about 20% of current andformer drinkers stated their alcoholicdrinking negatively affected them,usually impacting their jobs or theirfinances (Health Canada, 2008). Inthe United States, 7%-8% of theadult population is affected by alco-hol abuse and dependence (Sub -stance Abuse and Mental HealthServices Administration, 2007).Reportedly, 30%-50% of people whodrank in the past year experience atleast one adverse alcohol-relatedproblem, such as missing work orschool, driving after drinking, orhaving interpersonal problems, dur-ing their life times (Teesson, Baillie,Lynskey, Manor, & Degenhardt,2006).

In 2002, 2.4% of all deaths inCanada in people age 69 or youngerwere from chronic diseases attrib-uted to alcohol consumption. Thistranslated into nearly 43,000 years oflife lost prematurely, and nearly125,000 hospital admissions due to alcohol-related chronic diseases

(Rehm, Giesbrecht, Patra, & Roerecke,2006). Each year in the United States,85,000 deaths are attributed to alco-hol use, along with substantial dis-ability from medical and psychiatricconsequences, injuries, and second-hand effects (e.g., motor vehiclecrashes) (Saitz, 2005). In the UnitedKingdom, the number of alcohol-related deaths doubled from 4,144 in1991, to 8,758 in 2006 (Anderson &Baumberg, 2006).

Neurobiology of AlcoholDependence

The vulnerability of some personsto addiction seems to be multifac-toral, including genetic predisposi-tion, environmental factors, andneurophysiologic changes resultingfrom repeated use of the substance.Addictive or substance abuse disor-ders are more common in individu-als with mood and anxiety disorders,schizophrenia, and all conditionsassociated with the neurotransmitterdopamine (Cornwell & Lickteig,2006). Approximately 80% of per-sons with alcoholism complain of

Glenn Donnelly, Arlene Kent-Wilkinson, and Alecia Rush

Individuals who are alcohol dependent pose significant challengesfor nurses when they are admitted to hospital for treatment.Clinical problems presented by these individuals are examined andthe critical aspects of their care are highlighted.

CNE Objectives and Evaluation Form appear on page 15.

January-February 2012 • Vol. 21/No. 110

depressive symptoms, and 30% meetthe criteria for depressive episode(Bruinjnzeel, Repetto, & Gold, 2007).

Excessive use of alcohol alters theneurochemical transmitter systemsand makes a greater amount ofdopamine available in the nucleusaccumbens, the area of the brainthat mediates reward, pleasure, andassignment of salience to importantenvironmental stimuli (Guthrie,Brower, & Karam-Hage, 2008;Kalivus & Volkow, 2005). The result-ing increase in dopamine producesmood elevation and euphoria,which become strong motivators torepeat the experience (Pasch, 2010).

Alcohol influences other neuro-transmitters in modulating thedopaminergic pathway to increasethe amount of g-aminobutyric acid(GABA), glutamate, more dopamine,and endogenous opioids. The GABAand glutamate system is involvedprimarily in alcohol stimulation,sedation, and intoxication, as well asmany symptoms of alcohol with-drawal. The dopamine and opioidsystems are involved with reinforce-ment, reward, and some aspects ofcraving. This can result in sustaineduse of alcohol and potential relapseafter prolonged abstinence in thealcohol-dependent person (Kalivus& Volkow, 2005). Opioid-like proteinneurotransmitters, enkephalins, andB-endorphins increase their avail-ability and can be responsible for theeuphoria experienced with alcoholconsumption. Their release in alco-hol intoxication may contribute toaddiction by inhibiting the GABApathways and enhancing dopamin-ergic signaling, causing an evenheightened sense of euphoria(Anton, 2008).

Neural adaptation occurs when thechronic activation of the reward sys-tem results in depletion of the neuro-transmitter systems that were overactivated in an effort to maintainresponse to drug abuse. Sensitizationidentifies an increased response fol-lowing intermittent administrationof the substance, and may be akin tocraving. Tolerance, on the other hand,develops as continued use depletesthe neurotransmitters (Guthrie et al.,2008), and the dopa minergic recep-tors become less responsive (O’Brien,

2008). Greater amounts of alcoholthus are required to achieve positiverewarding effects (Guthrie et al.,2008).

During withdrawal, a decreaseoccurs in dopaminergic and seroton-ergic transmission through thenucleus accumbens. Also seen dur-ing withdrawal, an increase in opi-oid receptor activity occurs in con-junction with decreased GABA andincreased glutamate transmissionthrough the accumbens nuclei(Guthrie et al., 2008).

Once the brain has been exposedrepeatedly to high doses of alcohol,any sudden decrease in intake canproduce withdrawal symptoms. Theinhibition of the GABA pathway bycontinued exposure to high levels ofalcohol results in a neural adaptationmechanism. Abrupt cessation of pro-longed alcohol consumption resultsin brain hyperexcitablility becausethe pathway previously inhibited byalcohol is no longer inhibited(Bayard, McIntyre, Hill, & Woodside,2004). Alcohol withdrawal syndromeoccurs about 5-10 hours after the ces-sation of alcohol, and peaks in inten-sity in 2-3 days (Schuckit, 2008).

The most common withdrawalpattern is characterized by tremor ofthe hands, agitation and anxiety,nausea, and vomiting. In addition,autonomic nervous system overac-tivity results, including sweating,tachycardia, tachypnea, hyperten-sion, increasing body temperature,and insomnia sometimes accompa-nied by frightening dreams. Anxiety,insomnia, and mild central nervoussystem dysfunction may occur 4-6months following alcohol cessation(Schuckit, 2008).

Hallucinations occur in up to10% of patients, and are usually visu-al and tactile (Kahn, Barnhorst, &Bourgeois, 2009). Other individualsare likely to have auditory or visualhallucinations, or both (O’Brien,2008). Their onset usually occursafter several days of abstinence(Kahn et al., 2009).

Seizures occur as a result of alter-ation in neurobiology (Rogawski,2005). Approximately 2%-5% ofpersons with alcohol dependenceexperience withdrawal seizures, usu-ally within 48 hours of alcohol

intake cessation (Schuckit, 2008).Seizures present either as a singlegeneralized attack (Schuckit, 2008)or in groups (Rogawski, 2005).Withdrawal symptoms are notresponsive to the anticonvulsantmedication phenytoin (Dilantin®)(Rogawski, 2005). With drawalseizures are a repeated occurrence inapproximately 10% of heavydrinkers (Franklin & Francis, 2005).

Delerium tremens (DTs) is anepisode of intense alcohol withdraw-al characterized by disorientationand global confusion, agitation,severe tremor, fluctuating levels ofconsciousness, autonomic instabilityactivity (Kahn et al., 2009; Schuckit,2008), incontinence, and frighten-ing visual hallucinations (Carroll,2007). The condition usually begins3-5 days after the individual’s lastdrink. This serious condition is seenin less than 5% of individuals withalcohol dependence but has thepotential to be life-threatening, withdeath as a result of cardiovascular,metabolic, or infectious complica-tions (Schuckit, 2008). Early deathrates were estimated as high as 15%,with more recent estimates as low as0-1% with medical intervention(Kahn et al., 2009).

Health Effects of HeavyDrinking

Because alcohol is a central nerv-ous system depressant, people whoconsume large quantities of alcoholfrequently experience blackouts oracute retrograde amnesia during peri-ods of intoxication (Schuckit, 2008).Alcoholic-related amnestic episodesare associated with the quantity andfrequency of drinking. Althoughblackouts are not a sensitive indica-tor of the risk for developing alco-holism, they should be viewed as animportant warning sign of problemdrinking (Carroll, 2007; Schuckit,2008). Blackouts may be frighteningenough to some people to increaseawareness that they are drinking toomuch.

Alcohol intoxication affects everyorgan in the body, and chronicabuse of alcohol has deleteriouseffects on all body systems (Keys,2011). Hypertension, hyperlipi-


The Alcohol-Dependent Patient in Hospital: Challenges for Nursing

demia, cardiac arrhythmias, cardiacmyopathy (Schuckit, 2008), liver dis-ease, peptic ulcer disease, or pancre-atitis (Lucey, Mathurin, & Morgan,2009) may be the first physical indi-cation of alcohol abuse. Drinkingalso causes nutritional deficiencies.First, alcohol supplies calories butdoes not have essential nutrients,such as proteins, minerals, and vita-mins. In addition, alcohol interfereswith the absorption of vitaminsfrom the small intestine and theirstorage in the liver. Commonlyaffected are thiamine (B1), folic acid,pyridoxine (B6), niacin, and vitaminA (Schuckit, 2008). Pancreatitis, gas-tritis, and liver disease are commonco-morbid conditions. Alcohol keto-sis results from further starvation(Rampalla, 2008).

Alcohol and its metaboliteacetaldehyde are direct neurotoxins(Rampalla, 2008). As a result of alco-hol consumption, brain atrophyappears to be greater in drinkers thannon-drinkers (Mann et al., 2005).Alcohol-related nutritional deficien-cies and the toxic effects of alcoholcan lead to persistent neurologicalabnormalities. Wernicke’s encepha -lo pathy, an acute syndrome charac-terized by ataxia, abnormal eyemovements, and confusion, resultsfrom a severe thiamine deficiency. Ifuntreated, this condition can pro -gress to Korsakoff’s disease andinvolve lasting personality degenera-tion, confabulation, and memorydisturbances (Hannon, Pooler, &Porth, 2010). Hepatic encephalopa-thy, a deterioration of mental statusin patients with cirrhosis, occurswhen the liver fails to remove sever-al toxins (notably ammonia). In itsearly state, it is marked by inatten-tion, reversal of sleep wake cycle,and asterixis; symptoms mayprogress to delirium and coma(Lucey et al., 2009).

Alcohol has several cardiovascularconsequences. Two to three drinks aday increase blood pressure, low-density lipoprotein, and cholesterol(Schuckit, 2009). Acetaldehyde isdirectly toxic to the myocardium,with the toxicity playing a role inthe progression of cardiomyopathy(Schuckit, 2008). Cardiac arrhyth-mias and orthopnea generally are

considered antecedents of cardiomy-opathy in individuals who bingedrink, which can result in varyingdegrees of heart failure (Rampulla,2008).

Alcohol contributes to severalesophageal disorders, including eso -ph a gitis, esophageal varices, and eso -phageal adenocarcinoma (Rampalla,2008). Erosive gastritis can be a directresult of the toxic effects of alcoholand increased susceptibility toHelicobacter pylori bacteria. Excessivealcohol use is a major cause of pan-creatitis, which can lead to life-threatening necrosis (Rampulla,2008; Whitcomb, 2006). Heavy, pro-longed alcohol use also is associatedwith the progression of colon adeno-mas (Rampulla, 2008).

Alcoholic liver disease has threemain forms: fatty liver, alcoholichepatitis, and cirrhosis. Excessive useof alcohol can result in deposition offat in the hepatocytes of the liver.The mechanism by which thisoccurs is not understood completely(Porth, 2010), but it is postulatedthat impaired oxidation of fattyacids may contribute to the fat accu-mulation (Schuckit, 2008). Alcoholichepatitis usually manifests betweenthe occurrence of fatty changes andcirrhosis. It is characterized byinflammation and necrosis of livercells, and can lead to liver failure anddeath. Cirrhosis is the end result ofrepeated bouts of alcohol-relatedliver injury. It is characterized bydevelopment of fibrotic noduleswhich may compress hepatic veinsand thus cause portal hypertension.In addition to structural and func-tional changes in the liver, thealtered metabolism often results indepression of clotting factor andalbumin synthesis. This predisposesthe affected individual to hemor-rhage and development of edema(Lucey et al., 2009; Waken-Fleming& Mullen, 2005).

Assessment andIdentification of theAlcohol-Dependent Patient

Many patients admitted to hospi-tal for treatment of other health con-ditions have a drinking problem oralcohol dependence. The history of

alcohol use may be known by thehealth care team, but in many casesit is concealed from them. Detectionof alcohol problems is one way inwhich nurses can plan effectively forthe patient’s recovery (Keys, 2011).

The CAGE questionnaire is ascreening tool which may be helpfulwhen alcohol consumption hasbeen concealed. It consists of fourwell-validated questions that areeasy to use and are easily accessed(Hanson & Williams, 2001). A posi-tive response in two or more of thequestions is suggestive of alcoholmisuse (Mayfield, McLeod, & Hall,1974). This short questionnaire canbe used easily in hospital settings toscreen for heavy drinking and alco-hol disorders (Schuckit, 2009).

The nature of alcoholism, with itscharacteristic denial, intoxication,memory disturbances, anxiety, con-fusion, or disorientation, may makeit difficult for the nurse to obtain anaccurate history (Keys, 2011). Historyshould include the estimatedamount and duration of alcoholintake and the time of the last drink.Information about previous at temptsat detoxification (including compli-cations, such as seizures and halluci-nations), other health problems, andcurrent medications is part of theessential data (Kosten & O’Connor,2003; Schuckit, 2009). History takingalso should include seeking cultural-ly relevant data regarding thepatient’s condition (Canadian NursesAssociation, 2004). The initial assess-ment of the patient in withdrawalmust include a determinationwhether the patient is using otherdrugs as well as alcohol. Specific sub-stances must be identified becausesubstantial differences exist in associ-ated complications and treatmentcan vary greatly. Toxicology screen-ing also is useful to determine possi-ble abuse of other substances (Kosten& O’Connor, 2003).

First-encounter assessment in -cludes facial expression, self-careassessment, unusual odors, vitalsigns, height, weight, body move-ments and gait, balance, coordina-tion, level of consciousness, skin,hair and nails, and nutritional status(Monahan, 2009). Physical examina-tion usually reveals nothing unusual


unless the patient is intoxicated or inwithdrawal, or indulges in chronicheavy use of alcohol. The individ-ual’s mental status, vital signs, andblood glucose should be assessed.Postural hypotension and pulsechanges may indicate gastrointesti-nal bleeding. The patient’s headshould be assessed for signs of trau-ma (recent or past) and facial flush-ing. Facial puffiness usually follows adrinking binge. Unusual bruises,abrasions, and burns also shouldraise suspicion of a problem withalcohol use. Older drinkers, particu-larly those who take prescribed med-icines, are prone to falls. Ataxia,characterized by a wide steppinggait, may result from cerebellar dete-rioration. Early peripheral neuropa-thy is suggested by diminishedlower-extremity touch or tempera-ture sensation (Rampulla, 2008).

The revised Clinical InstituteWithdrawal Assessment for Alcohol(CIWA-Ar) scale is a valid, 10-itemassessment tool that can be used toquantify the severity of alcohol with-drawal. It also can be used to moni-tor and medicate patients as theyexperience withdrawal (Bayard et al.,2004). The nurse scores each of 10response categories using a Likertscale; the maximum possible score is67. Response categories include agi-tation, anxiety, auditory distur-bances, clouding of sensorium,headache, nausea or vomiting,paroxysmal sweats, tactile distur-bances, tremor, and visual distur-bances. Numerical criteria from 0 (nosymptoms) to 7 (severe or very frequent-ly) are used to determine mild, mod-erate, or severe withdrawal (Keys,2011). Each rise in score in a singlegroup is associated with a higher rel-ative risk of complications, such asconfusion, seizures, and hallucina-tions in untreated persons (Asplund,Aaronson, & Aaronson, 2004).

Srivastava (2007) suggested therange of medical treatment limitschoices and creates passivity. Nursescan encourage patients to take activeresponsibility in planning culturallyand socially acceptable treatmentoptions. By partnering with patients,nurses can advocate for an integra-tive health care approach that blendsknowledge of traditional healing

methods with current treatment pro-tocols which potentially can en -hance the single-model approachesto health and wellness (Srivastava,2007).

Treatment ProtocolsThe three goals of treatment for

alcohol withdrawal syndrome areinitiating abstinence; reducing with-drawal symptoms and severe com-plications; and retaining the patientin treatment (Kasser, Geller, Howell,& Wartenberg, 2004). About 50% ofpatients with alcohol dependencedevelop clinically relevant symp-toms of withdrawal, which occur asa rebound from usual effects of alco-hol intoxication (Schuckit, 2008).Meticulous, ongoing assessment iscritical for early identification ofsymptom severity and potentialcomplications so appropriate treat-ment can be provided, and thepatient evaluated in terms of overallprogress (Keys, 2011).

Delirium tremens can begin 48-72hours after the last drink. It is preced-ed by the typical signs of early with-drawal, although these may bemasked by medications such as ben-zodiazepines used for treatment ofsymptoms. Signs of sympathetichyperactivity, such as tachycardia,hypertension, fever, and diaphoresis,are often profound hallmarks ofalcohol withdrawal delirium (Bayardet al., 2004).

Nurses should recognize clinicalfeatures of alcohol withdrawal inany patient admitted to the hospital.Timely sedation will prevent theonset of convulsion or progressionto delirium tremens. The most effec-tive regimen is to control the agita-tion, sweating, and tremor withsymptom-triggered dosing (Harrison& Daly, 2006). With this method,the need for medication is signaledby signs and symptoms in thepatient withdrawing from alcohol(Bayard et al., 2004). In a double-blind, controlled trial, symptom-trig-gered therapy proved superior tofixed-dose sedative scheduling tomanage alcohol withdrawal. Personsreceiving symptom-triggered thera-py used less benzodiazepines andhad decreased duration of treatment

(Daeppen et al., 2002). Nurses’assessment skills are central to use ofsymptom-triggered dosing in anysetting. While standing orders arecommon for fixed-dose scheduling,the skilled nurse is able to provideoptimal care through symptom-trig-gered dosing (Keys, 2011; Kosten &O’Connor, 2003).

Benzodiazepines are considered afirst-line treatment, indicated rou-tinely for the patient with substan-tial symptoms of alcohol withdrawalas well as the person at increased riskfor complications of withdrawal(Saitz, 2005). They act as potentia-tors at inhibitory GABA receptors,which are relatively unoccupied inalcohol withdrawal (Kahn et al.,2009). Benzodiazepines should beadministered when the patientshows early signs of withdrawal toprevent progression of the symp-toms. The goal is to keep the patientmildly sedated or in a calm, tranquilstate while still allowing easy arousal(Sommers, Johnson, & Beery, 2007).Benzodiazepines may be adminis-tered via different regimens.Diazepam (Valium®) (0-20 mg every2 hours; maximum 100 mg in 24hours) is a common protocol(Harrison & Daly, 2006) in Canadaand the United Kingdom. TheAmerican Society for AddictionMedicine Practice Guidelines formanaging alcohol withdrawal rec-ommend starting doses of lorazepam(Ativan®) 1-4 mg every 15 minutes(Saitz, 2005).

Some patients appear to be resist-ant to large doses of benzodi-azepines and experience a pro-longed course of withdrawal symp-toms. When escalating doses ofbenzodiazepines ap pear to have lit-tle effect, alternative agents notdependent on GABA benzodi-azepine binding sites must besought. Combined or solitary dosesof the anticonvulsant drugs val-proic acid (Depakote®) and carba-mazepine (Tegretol®) for alcoholwithdrawal treat ment have notbeen supported by a meta-analysis(Polycarpou, Papanikolaou, Ioannidis,& Contopoulos-Ioanidis, 2005).Some evidence supports the use ofpropofol (Diprivan®) and barbituratesin alcohol withdrawal (Preuss, Zil, &


The Alcohol-Dependent Patient in Hospital: Challenges for Nursing

Koller, 2006). Antipsychotics andalpha agonists also may assist insymptom management (Kahn et al.,2009).

Nursing CarePatients with alcohol withdrawal

syndrome are usually apprehensiveor fearful. They may be acutely dis-turbed and hallucinating. Care thusshould be provided in a well-lit roomwith a calm, reassuring environment(Harrison & Daly, 2006).

Managing fluid volume deficit is atop priority in nursing care. If with-drawal occurs despite sedation,patients often will require intra-venous hydration, with fluid re -quirements of 4-10 liters in the first24 hours. A solution of 5% dextrosein saline or 0.45% saline can be usedfor rehydration if hypoglycemiaexists. Once the patient’s nausea andvomiting subside, fluids such as fruitjuices are encouraged, followed byprogression to a normal diet. Thepatient requires continual monitor-ing for signs of dehydration, such aspoor skin turgor, dry mucous mem-branes, weight loss, concentratedurine, flattened neck veins, andhypotension (Sommers et al., 2007).

Persons with alcohol dependencecan experience depletion of multi-ple electrolytes. Electrolytes shouldbe monitored and replaced as neces-sary (Sommers et al., 2007). Habitualdrinkers may be deficient in magne-sium, which will lower the seizurethreshold (Lohr, 2005). Thiaminedeficiency has been reported in30%-80% of people with alcoholdependence (Compton, 2002).Thiamine 25-50 mg given intra-venously is recommended to pre-vent Wernicke’s encephalopathy.The vitamin must be administeredbefore intravenous glucose becauseit is a co-factor necessary for glucosemetabolism (Harrison & Daly,2006). Caused by thiamine deficien-cy, Wernicke-Korsakoff syndrome ischaracterized by ataxia, encephalo -pathy, amnesia, nystagmus, andparalysis of external ocular muscles(Rampulla, 2008; Schuckit, 2008). Itcan occur quickly and have perma-nent effects if the patient receivesglucose without thiamine. The

symptoms are similar to those ofintoxication, making diagnosis moredifficult (Harrison & Daly, 2009).

Brief counseling interventions of10-15 minutes with feedback aboutdrinking, advice, and goal setting(Cooper, 2006) can be initiated withfollow-up contact after the patienthas progressed through withdrawal.Interventions should include coun-seling the patient about setting agoal for a reduction in alcohol con-sumption and identifying ways toachieve that goal. A systematicreview of 11 randomized, controlledtrials found persons who receivedsuch an intervention had signifi-cantly reduced their alcohol intakeat 6 months following treatment(McQueen, Howe, Allan, & Mains,2006). Planning for continued careshould begin while the patient isbeing detoxified. Referral and followup to other agencies, treatment pro-grams, self-help groups, and coun-selors is important for adequaterecovery from alcohol dependence.These services provide patients withthe tools to cope with situations thatmay precipitate heavy drinking.They should be initiated so as toavoid a lapse of time in differentcomponents of the treatment pro-gram (Keys, 2011; Saitz, 2005).

Nursing ImplicationsAlthough the understanding of

substance abuse has improved, thetendency remains for nurses to failto engage with persons who havealcohol dependence. Nurses may beuncertain whether this is withintheir scope of practice, or they mayperceive a lack of knowledge andskill in identifying and respondingto affected patients. For some profes-sionals, increased knowledge andunderstanding of alcohol depend-ence challenges their values, beliefs,and attitudes, and may result in neg-ative feelings that can affect theircare. In engaging with patients withalcohol dependence, nurses mustrecognize that excessive alcohol useis likely only one symptom of a larg-er problem (Cooper, 2006).

Nurses can play a critical role inidentifying patients with alcoholdependence, and also participate in a

comprehensive assessment thatincludes psychological state, effectsof alcohol use, motivation for treat-ment, social support, and physicalassessment. Nurses also should beprepared to provide brief interven-tion by sharing information and pro-viding motivational support. Theycan be pivotal in identifying andreferring patients to appropriatetreatment programs, counseling, orsocial support groups. Nurses’ effec-tive participation with an interdisci-plinary team of professionals is para-mount in providing effective sharedcare and treatment to patients withalcohol dependence (Keys, 2011).

ConclusionThe management of a patient

experiencing alcohol withdrawal isenhanced by nurses’ in-depth under-standing of the neurobiology of alco-hol dependence, the effects of alco-hol abuse on the body systems, andcurrent treatment of alcohol with-drawal syndromes. Nurses are placeduniquely to provide comprehensivecare to patients who are withdraw-ing from alcohol, and evidence-based practice will lead to improvedcare of affected patients.

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Pasch, S. (2010). Disorders of throughout,mood and memory. In R. Hannon, C.Pooler, & C. Porth (Eds.)., Porth patho-physiology: Concepts of altered healthstatus (1st Canadian edition) (pp. 1299-1325). Philadelphia, PA. Lippincott,Williams, & Wilkins.

Polycarpou, A., Papanikolaou, P., Ioannidis, J.,& Contopoulos-Ioanidis, D. (2005).Anticonvulsants for alcohol withdrawal.Cochrane Database of SystematicReviews, 3, CD005064.

Porth, C. (2010). Disorders of hepatocbiliaryand excocrine pancreas function. In R.Hannon, C. Pooler, & C. Porth (Eds.),Porth pathophysiology: Concepts ofaltered health status (1st Canadian ed.)(pp. 911-942). Philadelphia, PA: Lippincott,Williams, Wilkins.

Preuss, U., Zil, P., & Koller, G. (2006).Inotropic glutamate receptor geneGRK3SER320ALA functional polymor -

phism is related to delirium tremens inalcoholics. Pharmacogenomics Journal,6, 34-41.

Rampulla, J. (2008). Alcohol abuse. In T.Buttaro, J. Trybulski, P. Bailey, & J.Sandberg-Cook (Eds.), Primary care: Acollaborative practice (3rd ed.) (pp. 1372-1377). Philadelphia, PA: Mosby Elsevier.

Rehm, J., Giesbrecht, N., Patra, J., &Roerecke, M. (2006). Estimating chronicdisease deaths and hospitalizations dueto alcohol use in Canada in 2002:Implications for policy and preventionstrategies. Preventing Chronic Disease,3, A121.

Rogawski, M. (2005). Update on the neurobiol-ogy of alcohol withdrawal seizures.Epilepsy Current, 5(6), 225-230.

Saitz, R. (2005). Unhealthy alcohol use. NewEngland Journal of Medicine, 352, 596-607.

Schuckit, M. (2008). Alcohol and alcoholism. InA. Fauci, D. Kasper, D. Longo, E.Braunwald, S. Hauser, J. Jameson, & J.Loscatzo (Eds.). Harrison’s principles ofinternal medicine (17th ed.) (pp. 2724-2729). Philadelphia, PA: McGraw Hill.

Sommers, M., Johnson, S., & Beery, T. (2007).Diseases and disorders: A nursing thera-peutics manual (3rd ed.) (pp. 51-56).Philadelphia, PA: F.A. Davis.

Srivastava, R.H. (Ed.). (2007). Guide to clinicalcultural competence. Toronto, Ontario,Canada: Mosby/Elsevier.

Substance Abuse and Mental Health ServicesAdministration. (2007). Results from the2006 National Survey on Drug Use andHealth: National findings. NSDUH seriesH-32. Rockville, MD: Office of AppliedStudies.

Teesson, M., Baillie, A., Lynskey, A., Manor, B.,& Degenhardt, L. (2006). Substance use,dependence, and treatment seeking inthe United States and Australia: A crossnational comparison. Drug and AlcoholDependency, 81, 149-155.

Waken-Fleming, J., & Mullen, K. (2005). Longterm management of alcoholic liver dis-ease. Clinics in Liver Disease, 9, 135-149.

Whitcomb, D. (2006). Acute pancreatitis. NewEngland Journal of Medicine, 354, 2142-2150.

World Health Organization. (2006). Substanceabuse and mental health services admin-istration. Rockville, MD: Office of AppliedStudies.

ADDITIONAL READINGSAboriginal Nurses Association of Canada

[ANAC], Canadian Association ofSchools of Nursing, & Canadian NursesAssociation. (2009). Cultural compe-tence and cultural safety in First Nations,Inuit and Métis nursing education: Anintegrated review of the literature.Ottawa, Ontario, Canada: Author.

Connor, P. (2000). Screening for alcohol prob-lems in primary care: A systematicreview. Archives of Internal Medicine,160, 1977-1989.

continued on page 36


ANSWER FORM1. If you applied what you have learned from this activity into your practice, what would be different?

_______________________________________________________________________________________________________________

_______________________________________________________________________________________________________________

Answer/Evaluation Form: The Alcohol-Dependent Patient in Hospital: Challenges for Nursing

Deadline for Submission: February 28, 2014

MSN J1201

Strongly StronglyEvaluation disagree agree

2. By completing this activity, I was able to meet the following objectives:

a. Describe the prevalence and neurobiology of alcohol dependence. 1 2 3 4 5

b. Define the health effects of heavy drinking. 1 2 3 4 5

c. Discuss the assessment and treatment protocols for a patient with alcohol dependence. 1 2 3 4 5

d. Detail the nursing care and nursing implications of a patient with alcoholdependence. 1 2 3 4 5

3. The content was current and relevant. 1 2 3 4 5

4. The objectives could be achieved using the content provided. 1 2 3 4 5

5. This was an effective method to learn this content. 1 2 3 4 5

6. I am more confident in my abilities since completing this material. 1 2 3 4 5

7. The material was (check one) ___new ___review for me

8. Time required to complete the reading assignment: _____minutes

I verify that I have completed this activity: _______________________________________

Comments_______________________________________________________________________________________________________

_______________________________________________________________________________________________________________

OBJECTIVES

This continuing nursing educational (CNE) activity is designed fornurses and other health care professionals who care for and educat-ed patients and their families regarding alcohol dependence. Forthose wishing to obtain CNE credit, an evaluation follows. After study-ing the information presented in this article, the nurse will be able to:1. Describe the prevalence and neurobiology of alcohol dependence.2. Define the health effects of heavy drinking.3. Discuss the assessment and treatment protocols for a patient with

alcohol dependence.4. Detail the nursing care and nursing implications of a patient with

alcohol dependence.

CNE InstructionsPersons wishing to obtain CNE credit must read the article and completethe answer/evaluation form. Upon completion, a certificate for 1.4 contacthours will be awarded. Evaluations can be submitted two ways:

1. AMSN’s Online Library: Complete your evaluation online and print your CNE certificate immediately. Simply go towww.amsn.org/library, and select MEDSURG Nursing Journalfrom “My Library.”

Fee: AMSN Member: Free Regular: $15.00

2. Persons without access to the Internet may photocopy and sendthe answer/evaluation form along with a check or credit cardorder payable to AMSN to MEDSURG Nursing, CNE Series,East Holly Avenue Box 56, Pitman, NJ 08071-0056. Test returnsmust be post-marked by February 28, 2014. A CNE certificate willbe provided by mail.

Fee: AMSN Member: $10.00 Regular: $15.00

This independent study activity is co-provided by AMSN and Anthony J.Jannetti, Inc. (AJJ).

Accreditation status does not imply endorsement by the provider orANCC of any commercial product.

AJJ is accredited as a provider of continuing nursing education by theAmerican Nurses Credentialing Center’s Commission on Accreditation(ANCC-COA).

Anthony J. Jannetti, Inc. is a provider approved by the California Board ofRegistered Nursing, Provider Number, CEP 5387. Licensees in the stateof CA must retain this certificate for four years after the CNE activity iscompleted.

This article was reviewed and formatted for contact hour credit by DottieRoberts, MSN, MACI, RN, CMSRN, OCNS-C®, MEDSURG NursingEditor; and Rosemarie Marmion, MSN, RN-BC, NE-BC, AMSNEducation Director.

COMPLETE THE FOLLOWINGThis test may be copied for use by others.

Name: ______________________________________________

Address:_____________________________________________

City:_________________________State: _____ Zip: _________

Preferred telephone: (Home) ____________________________(Work)_____________________________

AMSN Member Expiration Date: _________________________

Check Enclosed Visa Mastercard

Credit Card # ________________________________________

Exp. Date ____________________________________________


Challenges for Nursingcontinued from page 14

Cross, T., Bazron, B., Dennis, K., & Isaacs, M.(1989). Toward a culturally competentsystem of care. Washington, DC:Georgetown University.

Davis-Murdoch, S. (2005). A cultural compe-tence guide for primary health care pro-fessionals in Nova Scotia. Halifax, NovaScotia, Canada: Primary Health Care,Nova Scotia Department of Health.

McNaughton-Dunn, A. (2002). Cultural com-petence and the primary care provider.Journal of Pediatric Health Care, 16(3),151-155.

Noutsias, M., Pauschinger, M., Poller, W.,Schultheiss, H., & Kuhl, U. (2003).Current insights into the pathogenesis,diagnosis, and therapy of inflammatorycardiomyopathy. Heart Failure Monitor,3(4), 127-135.

Smye, V., & Browne, A. (2002). ‘Cultural safety’and the analysis of health policy affectingaboriginal people. Nurse Researcher,9(3), 42-56.

Stewart, S. (2006). Cultural competence inhealth care (position paper). Sydney,Australia: Diversity Health Institute.

Copyright of MEDSURG Nursing is the property of Jannetti Publications, Inc. and its content may not be

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