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CLINICAL PRACTICE GUIDELINES FORTREATMENT OF ALCOHOL DEPENDENCEDr. N.G. Desal1, Dr. Rajesh Kumar2, Dr. S.N. Sengupta3, Dr. Parveen Sharma4

IntroductionTh e use of alcohol for purpos es of relaxation or socializing by mankind has been reported throughouthistory in m ost civilizations. The social approval to alcohol use has varied from strong disapproval tobeing actively encouraged. In the 20th Century Western World, the use of alcohol as well as therelated disorders, has been increasing rapidly. The recognition of alcoholism as a disease occurredduring the early 1950s by the World health Organization (WHO) Jellinek's description of "diseaseconcept of alcoholism" and the subtypes of alcoholism genera ted a lot of interest. It proved to bestimulus for systematic descriptions of alcohol related problems. Th e first description of "AlcoholDependence Syndrome" in 1976 by Edwards and Gross emphasized inability to controlconsumption, salience of drink seeking behaviour, and narrowing of drinking repertoire as thecharacteristics besides the phenom ena of tolerance and w ithdrawal. The concept of alcoholism canbe we ll understood by the entymological origin of the term . Like all other "isms", alcohol becomes away of life in persons with alcoholism. As in All other" isms", in this one too, alcohol becomes the"raison d ' et re" or the reaso n for existence. In India, although alcohol use in ancient times andcannabis and affim (raw opium) in more recent times have been know n and reported for some time ,substance use problems have been recognized to have a significant importance as a public healthproblems and in various other facets of life only very recently.A large number of pe rsons are involved in treating alcoho l dependent ind ividuals. They .include,General Physicians, Psychiatrists, Psychologist, Social Worker, lay volunteer, spiritual leader andeven recovered patient as a result, there is considerable difference of opinion on treatment issues.This is mainly due to their different conceptual models of treatment. Thus there is a need for acommon and uniform treatment guideline which can help in comprehensive management of thesepatients.II Current definitions and diagnostic guidelinesAlcohol consumption occurs along a continuum, with considerable variability in drinking patternsamong individuals. There is no sharp demarcation between "social or "moderate", drinking and"problem" or "harmful" drinking (Babor et al 1987a). It is clear, however, that as average alcoholconsumption and frequency of intoxication increase, so does the incidence of medical and psychosocialproblems (Kranzler et al. 1990). The most visible group of people affected by alcohol problems arethose who have developed a syndrome of alcohol dependence and w ho are comm only referred to asalcoholics. A less prominent group consists of those persons who experience problems with theirdrinking but who are not dependent on alcohol. These individuals are variously termed alcohol abusers,problem drinke rs, and harm ful drinkers. These two "worlds" of alcoho l problems may require differentapproaches to diagnosis and clinical management.1 -Professor, 2-Asstt. Professor, 3-Associate ProfessorInstitute of Human Behaviour & Allied Sciences (IHBAS) Dllshad Garden, Delhi-110095

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The definitions of alcoholism have been constantly in the process of change. The idea of consideringdepende nce to alcohol as significantly different from the depende nce on other drugs of abuse is notfavored any longer. The conditions of alcohol abuse and alcohol dependence are seen as being verysimilar in their clinical profile to these cond itions as in case of other substan ces. According to ICD-10"Dependence Syndrome" it is defined as a cluster of physiological, behavioural and cognitivephenom ena in which the use of a substance or a class of substances takes on a m uch higher priorityfor a given individual than other behaviours that once had great value. A central descriptivecharacteristic of the dependence syndrome is the desire to take psychoactive drugs, alcohol ortobacco. There may be evidence that return to substance use after a period of abstinence leads to amore rapid appearance of the synd rome than occurs with non dependent individuals. The diagnosticguidelines as per ICD-10 require that three or more of the six characteristics be established at somepoint during the previous year.D iagnos t ic gu ide l ines for Dependence Syndrome in ICD-10 (WHO, 1992)A definite diagnosis of dependence should usually be made only if three or more of the followinghave been exp erienced or exhibited at some time during the previous year:a) A strong desire or sense of compulsion to take the substance;b) Difficulties in con trolling substance -taking behaviour in terms of its onse t, term ination, or levels

of use;c) A physiological withdrawal state when substance use has ceased or has been reduced , asevidenced by the characteristic withdrawal syndrome for the substance; or use of the same (ora closely related) substance with the intention of relieving or avoiding withdrawal symptoms;d) Evidence of tolerance, such that increased doses of the psychoactive substance are required inorder to achieve effect originally produced by lower;e) Prog ressive neglect of alternative pleasures or interests because of psychoactive substanceuse, increased amou nt of time necessary to obtain or take the substance or to recover from itseffects;f) Persisting with substance use despite clear evidence of overtly harmful consequ ence, such asharm to the liver through excessive drinking, depressive m ood states consequent to periods ofheavy substance use or drug related impairment of cognitive functioning; efforts should bemade to de termine that user was actually, or could be expected to be, aware of the nature ofextent of the harm .The ICD-10 has opted for the newer concept of "Harmful Use" to define those individuals wh o do notsatisfy the definition of dependence syndrome and yet, do have problems due to substance use.Harm ful Use has been describe d as "a pattern of psychoactive substance use that is causing dam ageto health, the diagnosis requiring that actual damage should have been caused to the mental orphysical health of the user".I ll ETIOLOGY AND PATHOPHYSIOLOGYAlcoholism is a complex, multifaceted disorder which has long been recognized to run in families.There is substantial evidence from twin research and adoption studies that a major genetic componentis operative in the developm ent of alcoholism . None theless, the disorder is etiologically com plex, witha variety of other vulnerability factors (Gold man 1993, Gelernter 1995). It has been estimated that

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there is a sevenfold risk of alcoholism in first-degree relatives of alcohol-dependent individuals, withmale relatives of male alcohol-dependent individuals having the greatest risk for the disorder (Me rikangas 1990). However, the m ajority of alcohol dependent individuals do not have a first-degreerelative who is alcohol dependent. This underscores the fact that the risk for alcohol dependence isalso determined by environment factors, which may interact in complex ways with genetics.ETIOLOGICAL SUBTYPES OF ALCOHO LICSAnother approach to understanding the etiology of alcoholism is to identify distinct subtypes ofalcoho lics. A variety of typologic approaches have been proposed to simplify the diverse phenomenaassociated with alcoholism (Nixon 1993, Bohn and Meyer 1994, Bab oran d Laureman 1986). Theseinclude unidemensional approaches based on drinking history, drinking pattern, severity of alcoholdependence, family history of alcoholism, gender, personality style, comorbid psychopathology,cognitive impairment, and sociopathy, as well as multidimensional approaches that combine thesecharacteristics into meaningful clusters. The best known of these typologies is the Type1/Type2distinction developed by Cloninger and collegues (1981) from studies of adopted sons of Swedishalcoholics.Comparison of Two Typologies of Alcoholism

VariablesAge at onset (yr)SexSociopathy BingedrinkingInability to abstainComorbiddepressionHeritability

Late onsetType 1

After 25Male or femaleLow frequentUncommonHighLow

Type AMale>30Male: female=0.8Low frequentUncommonLowProbably low

Early onsetType2

Before 25Male-limitedHigh infrequentCommonLowHigh

TypeBMale

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Patterns of drinking and the types of problems associated with alcohol misuse differ markedlythroughout the world (Room et al. 200 2). Th irteen percent of the adult population in the U nited Stateshas history of alcohol dependence or alcohol abuse and the 12 month prevalence of alcoholdepend ence in between 4% and 5% (Grant et al 1997).Ana lyses of world trends in alcoho l consum ption indicates that levels of alcohol use have been stableor slightly decreasing in W estern Europe and the US since 1960.Despite increased availability of alcoholic beverages worldwide, cultural influences continue to exerta strong influence on national patterns of drinking. While the highest alcohol consum ption rates aregenerally found am ong the industrialized countries of Europe and North America continent, the lowestconsum ption rate are found in developing countries that are dom inated by Islam, which proscribe theuse of alcoh ol. The percentage of the d rinking adult population ranges from a high of 86% in N orthand Cen tral European co untries to less than 10 % of adults in Islamic countries such as Pakistan andIraq (Room eta l 2002).Several large-scale community studies conducted since 1980 have provided estimates of the lifetimeand past year prevalence of alcoho l use disorders in the general population. For example, the NationalCom orbidity Study (NC S), a representative household survey of 8,098 persons ag ed 15 to 54 yearsthat was conducted between 1990 and 1992, assessed lifetime and past-year alcohol disordersusing DSM-III-R criteria (American Psychiatry Association 1987). The NCS estimated that the lifetimeprevalence of alcohol abuse and alcohol dependence for adults 18 to 54 years old were 9.4 and14.1% respectively, indicating tha t more than one-in-five young to m iddle-aged adults in he US havehad a pattern of alcohol use that met criteria for lifetime alcohol abuse and d ependence during the 12months preceding the interview were 2.5 and 4.4%, respectively (Kessler et al. 1997).Summary of the Studies on Epidemiology of Alcohol Use in India (Singh, 1989)

Ever useUse in last one yearUse in last one m onth

Generalpopulation25.6-74.2%19.0-82.5%

-

Students21.6-58.4%

-9.3-12.7

MedicalProfessionals85-66.7%

-

i i STE PS FOR IDENTIFICATION OF ALCO HOL DEPENDENCEStep I - SUSPICIONThe suspicion about alcohol use disorders can arise by evidence for problems in the spheres ofwork, marriage, finances or with the law. Intoxications with alcohol or the occurrence of withdrawalfeatures of tremo rs, irritability, na usea & vomiting, insomnia or ha llucinations in any of their patientsshould ale rt clinicians. Report of excessive use of alcohol, even if it is in the form of a comp laint or acriticism, by the patient's spouse or any any other family member is well worth looking into. Somemedical or psycholog ical symptoms/conditions like Liver disease, acid peptic symptoms, neuropathy,anxiety, memory lapses and repeated accidents are well known to be more commonly associatedwith alcoho l dep enden ce. Tentative suspicion so aroused must be followed up by specific measuresfor identification.

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Step II - SCREENINGScreening Instrumen ts and Rating Scales1. Screening : MAST (Michigan Alcoholism Screening Test) (Selzer et

al, 1971) CAGE Questionnaire (Mayfield et al 1974)AUDIT (A lcohol Use Disorde rs Iden tification Test) (WHO1989)

2. Withdrawal rating scale : CIWA-A (Clinical Institute W ithdrawa l Asse ssm ent-Alcohol Scale) (Sellers 1980)

3. Scales for assessm ent of severity : ASI (Addiction Severity Index) (Mclellan 1980)

Biological ma rkers of alcoholism (Vasw ani et al 199 7)1. Asparate Aminotransferase (AST)

And A lanine Am inotransferase (ALT)2. Gammaglutamyl Transferase (GGT)

3. Mean Corpus cular Voume (MCV)4. Erythrocyte Aldehyde Dehydrogenase(ADH)5. Carbohyd rate Deficient Transferrin ( CDT)

If raised indicates liver damages from anycause. Useful when combined with other tests.Most commonly used test. High levels arestrongly suggestive of alcoholic liver damage,but can also be raised in liver damage due toother causes. Useful test in combination withother tests and also to monitor treatment resultsor in motivat ing pat ients to stop excessconsumption.Useful test in combination with other tests andcomm only used with GGT.Levels are decreased in long term abusers ofalcohol.Increased levels in long-term abusers of alcoho l.Can distinguish recent excessive consumptionfrom abstinence or very light drinking.

Laboratory tests, : Of the many tests used for screening, two routinely available tests viz. MeanCorpuscular Volume (MCV) an d Gamma - Glutamyl-Transpeptidase (GGT) are raised in a majorityof patients with alcohol dependence. Research on hospital and community based screening suggeststhat raised value of one or both of these measures, in the absence of other causes, is strongly linkedto the ultimate diagnosis of alcohol de pendence.Screening instrumen ts are used in epidemiological studies where large populations are to be screenedfor the presence of alcoho l related problem s. They are also useful in clinical settings like medical andsurgical outpatient departments where a detailed history of substance use in every patient is difficultto obtain due to time constraints. During the past 25 years a number of self-report screening tests

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have been developed to identify alcoholics as well as persons at risk of alcohol problems eg. TheMichigan Alcohol Screening Test (MAST), developed by Selzer (1971). Perhaps the most widelyused alcohol screening test is the CAG E (Ew ing 1984), which contains only four questions:CAGE Qu estionnaire for screening for alcohol abuse\dependence1. Have you ever felt you ought to cu t down on your dinking?2. Have people annoyed you by criticizing your drinking?3. Have you ever felt guilty about your drinking?4. Have you ever had a drink first thing in the morning (an eye opener) to steady your nerves or

get rid of a hangover?Note: Two or more positive answers indicates alcohol abuse/dependence.Another one is alcohol use disorders Identifications test (audit) (Saunders et al. 1993, Babor andHiggins-Biddle 2001a), a -10 item screening instrument, may be used as the f irst step in acomp rehensive an d sequen tial alcohol use history.Step III- CONFIRM ATIONThe final confirmation of alcohol depen dence in each individual patient will have to be made by oneor more c linical interview s, exploring the de tails of alcohol consump tion and its effects on the differentaspects of life. A gentle, persuasive approach on part of the interviewer is necessary, avoidingconfron tation or pro voca tion. The criteria and gu idelines require to be applied in order to arrive at anobjective and scientific diagnosis.iii types of treatme nt settings & levels of care types of treatment settings

/ primary care physicians/NGO /individual cham ber practiceII District hosp ital psyc hiatric units Ingo w ith inpatient facility/private hosp ital withpsychiatric unitIII general hospital psyc hiatric unit with spec ialist me ntal health personnel, non

psychiatric medical unit (gastroenterology)IV spec ialized d e add iction treatme nt settings (e.g aiims, nimh ans, pgi, ihbas)

Most of these treatment settings play a complementary role. Most patients move through each ofthese different setting over a period of time and many patients avail their services in more than onesetting during a particular treatment attempt. So these settings are not mutually exclusive.level of ca re/ optimum care - reasonable level of care (1,11)

II good paractice - comp rehensive level of care (multidisciplinary team app roach) (III,IV).

The level of care depends on the infrastructure of the treatment setting, expertise of the personnelinvolve and other facto rs.Each type of treatment setting would have specific components, variable duration and differenttechnique of treatment and different types of personnel involved :

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iv Phases of treatment for Alcohol DependencePretreatment:1. Identification2. Motivational Interviewing3. Role of family mem bers and physiciansDetoxification1. Diazepam (20-60 mgs. Per day) or Chlordiazepoxide (50-150 mgs. Per dayVLorazepam2. Thiam ine (or as part of Vitamin B-Complex) 50 mgs. Thrice a day orally or 100 mgs.lM daily3. Supportive Me asures viz fluids, electrolytes etcIntensiveTreatment:1. Brief Intervention/Simple advice2. Disulfiram (only with consent)/Anti craving drugs (NTX, A camprosate)3. Group Therapy4. Family Therapy5. Behaviour TherapyPosttreatment/ Aftercare:1. Treatment contact2. Relapse Prevention3. Social Reh abilitation4. Occup ational R ehabilitation5. Continued SupervisionViii GOALS OF ALCOHOLISM TREATMENT Promote complete abstinence Stablize acute medical (including alcohol withdrawal) and psychiatric conditions, as needed . Increase mo tivation for recovery Initiate treatment for chronic med ical and psychiatric conditions, as needed . Assist the patient in locating suitable housing (e.g. moving form a setting in which drinking is

widespread), as needed. Enlist social support for recovery. Enhance coping and relapse prevention skills. Improve occupational functioning. Promote ma intenance of recovery through ongoing participations in structured treatment or

self-help groupsThe goals of treatmen t vary according to the time frame and the scope envisaged. They will alsodiffer across individual patients and can be revised from time to time. Immediate goals can be

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detoxification, treatment of acuter medical sequel and crisis intervention; short term goals usuallytarget treatment of comorbid medical or psychiatric condit ions, maintaining abstinence, familyreintegration and vocational p lacem ent; and the long term goals focus on the larger issues of relapseprevention, occupational rehabilitation, social reintegration, abstinent life style and improvement ofquality of life.ix GUIDELINES FOR INPATIENT AND OUT PATIENT TREATMENTA. Indication for inpatient treatm ent1. Hea vily intoxicated patient2. Patient having complicated withdrawal (delirium tremens, withdrawal seizures)3. Significant physical complication, Wernicke's encephalopathy, hematemesis.4. patient with significant psychop athology5. Unsu ccessful outpatient treatment6. Poly substance dependence7. Crisis in social support8. Geo graphical consideration9. Academ ic and research reasonB. Indication for outpatient treatment1. Mild or mo derate level of depen dence2. Sho rt duration for depen dence3. Minimal health damage4. Good social supportC. Uns uitability for inpatient treatme nt1. Anti social personality disorder or traits2. Significant criminal record3. Disciplinary problems during inpatient treatment4. Seve ral aborted treatment attempts in inpatient settingsX ALCO HOL RELATED DISORDERSThe use of alcohol starts as a social phe nom enon , leading to abuse or depend ent use in some of theindividuals. The occurrenc e of alcohol related disorders is not necessarily associated with abuse ordependent use. In fact, the average persons with alcohol related problems is likely to be neatlydressed, to have no severe signs of alcohol withdrawals, to have a job and good family sup port, andmay have physical or psychiatric co mplications. In alcohol abuse, there is impairmen t of socia l, legal,interpersonal, and occupational functioning. Theamount of alcohol intake, frequency, pattern of alcoholintake, type of liquor and response of persons show great variability. One person may take alcoholoccasionally or dressed neatly an d yet show severe alcohol related complications, wherea s anotherperson may take alcoho l daily, throughou t the day and yet show no impairmen t.

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1. Alcohol IntoxicationAlcohol depresses the CN S and the extent of depression corresponds to blood alcohol concentration(BAC).CNS Effects at Different Blood Alcohol Concentrations (BAC) (Schuckit, 1995)

Blood alcohol concentration (BAC)20-30mg/dl30-80mg/dl80-200mg/dl200-300mg/dl>300mg/dl

CNS effectsSlowed motor performance and decreased thinkingabilityIncreases motor and cognitive problem.Increased in coordination and errors in judgment,mo od lability, deterioration in cognitionNystagmus, marked slurring of speech and alcoholblackoutsImpaired vital signs an d possible death

Clinical signs indicative of alcohol intoxication include slurred speech, lack of coordination unsteadygait, nystagmus, impairment of attention and memory, and in the most severe cases, stupor andcoma. Alcohol intoxication may also present with severe disturbances in consciousness and cognition(alcohol intoxication delirium), especially when large amounts of alcohol have been ingested or afteralcoholic intoxication has b een sustained for extended periods. Usually, this condition subsides shortlyafter alcohol intoxication e nds. Physical and m ental status exam ination a ccomp anied by analysis ofblood and urine allow the clinician to rule out general medical conditions or psychiatric disordersmimicking this condition. In this regard, urine toxicology is a valuable tool in ruling out intoxicationwith ben zodiazepines , barbitu-rates, or other sedatives that can present with a similar clinical picture.Collateral information from relatives or friends confirming the ingestion of alcohol is also useful, andshould be actively p ursued by the clinician.2. Alcohol Withdrawal

Alcohol withdrawal is a condition that follows a reduction in alcohol consu mp tion or an abruptcess ation of drinking in alcohol-dependent individuals. In add ition to significant distress, alcoholwithdrawal is also associated with impairment of social, occupational, and other areas offunctioning . Uncomplicated cases of alcohol withdrawal are characterized by signs and symptomsof autonomic hyperactivity, and may include increased heart rate, increased blood pressure,hype rtherm ia, diaphoresis, tremor, nausea, vomiting, insomnia, and anxiety. Onset of symptomsof uncomplicated alcohol withdrawal usually occurs between 4 and 12 hours following the lastdrink. Symp tom severity tends to peak around the second day, usually subsiding by the fourth orfifth day of abstine nce . After this period, less severe anxiety, insomnia, and autonom ic symptomsmay pe rsist for a few wee ks, with some individuals experienc ing a protracted alcohol withdrawalsyndrome up to 5 or 6 months after cessation of drinking. A small but singnificant number ofalcohol dependent individuals (10%) can experience complicated alcohol withdrawal episodes.Alcohol withdrawal delirium (also known as delirium tremens) can occur in 5% of the cases,usually between 36 an d 72 ho urs following alcoho l cessation. In addition to signs of autonomichyperactivity, this cond ition is characterized by illusions, auditory, visual, or tactile hallucinations,

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psychomotor agitation , fluctuating cloudiness of consciousness, disorientation. Grand malseizures a ssociated with alcohol w ithdrawal occur in 3 to 5% of the cases, typically within thefirst 48 hours following reduction or cessation of drinking. In both instances of complicatedalcohol w ithdrawal, lack or delay in instituting proper treatment is associated with an increasedmo rtality rate. Prior history of delirium treme ns and /or alcohol-withdrawal seizu res, older age,poor nu tritional status, com orbid medical conditions, and history of high tolerance to a lcohol arepredictors of increased severity of alcohol withdrawal.3. Alcoh ol induce d Persisting Am nestic Disorder

Continuous heavy alcohol consumption can lead to several neurological deficits caused bythiamin deficiency. Amon g them, alcohol-induced persisting amnestic diorder (AIPAD, also knownas a Korsakoff's psycho sis, due to the fantastic confabulatroy stories described by patientssuffering this con dition) is prom inent. Profound deficits in anterograde memory and so me deficitsin retrograde or learn characterize this condition. Cessation of drinking can lead to an improvementin memory w ith approximately 2 0% of the cases demon strating com plete recovery. However, inmost cases mem ory deficits remain unchanged, and in some instances long-term care is neededdespite sob riety.

4. Alcohol-induced Persisting DementiaContinuous heavy drinking is also associated with progressive and gradual development ofmultiple cognitive deficits characterized by mem ory impairment, apfax ia, agno sia, or disturbancein executive functioning. These deficits cause serious impairment in social and occupationalfunctioning and persist beyond the du ration of alcohol intoxication and alcohol withdrawa l. History,physical exam, and laboratory test should be utilized to determine whether these deficit areetiologically related to the toxic effects of alcohol use.

5. Alcohol-Induced Mood DisorderAlcohol-induced mood disorder (AIMD), characterized by depressed mood and anhedonia, aswell as e levated, expansive, or irritable m ood, frequently develops as a conseque nce of heavydrinking. Onset of symptoms can occur during episodes of alcohol intoxication or withdrawal,and may resemble a primary major depressive, manic, hypomanic or m ixed episode. Regardlessof the primary or secondary nature of mood symptoms, given the high prevalence of suicideamong alcoholics, clinicians should closely m onitor the patient for emerging suicidal though ts.

6. Alcohol-Induced Anxiety DisorderAlthough a lcohol has anxiolytic prope rties at low doses, heavy alcohol consumption can induceprominent anxiety sym ptoms. Alcohol-induced Anxiety (AIA) symptoms more comm only includegeneralized a nxiety sym ptoms, panic a ttacks, and phobias. In order to establish this diagnosis,clinicians mus t rule out other gene ral medical conditions or psychiatric disorders that can mimicthis problem .

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7. Alcoho l-Indu ced Psychotic DisorderThis d isorder is characterized by prominent hallucinations or delusions that are judged by theclinician to be due to the effects of alcohol. The psychotic symptoms usually occur within amo nth of a n alco hol intoxication or withdrawal episode , and the patient is characteristically fullyalert and o riente d, lacking insight that these symptoms are alcohol-induced . Although onset ofpsychotic symptoms can occur during or shortly after alcohol intoxication, delirium or alcoholwithdrawal delirium, alcohol-induced hallucinations, and/or delusions do not occur exclusivelyduring the delusions of these con ditions.

8. Alcoho l- Induced Sleep DisorderHeavy alcohol consumption can be associated with a prominent disturbance of sleep. Atintoxication B ALs, especially w hen b lood alcohol levels are declining, sedation and sleepinesscan be o bse rved. Alcohol intoxication induces an increase in non rapid eye movement (NREM)sleep, whereas rapid eye mom ent (REM ) sleep density decrease s. Subsequently, there is andincrease in w akefulness, restless sleep, and vivid dreams or nightmares related to a reductionin NREM sleep and rebound in REM sleep density. During alcohol withdrawal, sleep is fragmen tedand discontinuous with an increase in REM sleep. After withdrawal, patients frequently complainof sleep difficulties and may experience superficial and fragmented sleep for months or years.

9. Alcoho l-Induc ed Sexual DysfunctionAlthough sm all doses of a lcohol in healthy individuals appear to enhance sexual receptivity inwomen and facilitate arousal to erotic stimuli in men, continuous and/or heavy drinking maycause significant sexual impairment. Alcohol-induced sexual dysfunction is characterized byimpaired desire, impaired arousal, and impaired orgasm, or sexual pain. It is also associatedwith ma rked distress or interpersonal con flicts. Onset of these impairments usually occurs duringalcohol intoxication but duration of symptoms exceeds the uncomplicated course of alcoholintoxication. Symptoms usually subside after 3 to 4 w eeks of alcohol abstinence. Persistence ofsymptoms beyond this time may suggest a primary sexual dysfunction (PSD) or a sexualdysfunction due to the medical complications of alcoholism (e.g. neuropathy, alcoholic-liverdisease).

xi GOALS OF PHARMACOTHERAPY FOR ALCOHOLPROBLEMSThe goals of pharmacotherapy for alcohol abuse or dependence include1. The reversal of the pharmacologic effects of alcohol2. Treatment and prevention of withdrawal symptoms and com plications3. Ma intenance of abstinence and the prevention of relapse with agents that decreased craving

for alcoho l or the loss of control over drinking or make it unpleasant to ingest alco hol, and4. Treatment of coexisting psychiatric disorders that complicate recovery.

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xii ALGORITHM FOR THE IDENTIFICATION AND MANAGEMENT FOR PATIENT WITHALCOHOL ABUSE AND DEPENDENCEInitial assessment

AUDIT SCORE 16-40 AUDIT SCORE 8-15 AUDIT score

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XIII ASSESSMENT O F A PERSON WITH ALCOHO L RELATED PROBLEMS-BARRIERS ANDREMEDIESOnce an individual is confirmed to be suffering form alcohol abuse, dependence or other alcohol-related problems, it is necessary that a detailed assessment of the case is done before planningtreatmen t. Such an assessm ent should include :- Details of alcohol u se:- its onse t, duration, average daily consum ption, presence of w ithdrawalsymptom s if not used , over-intoxication with a lcohol, abuse of any other drugs, recent changesin pattern of drinking. Reasons for initiation and co ntinued drinking. Heal th damag e due to alcohol:- signs of medical consequences of alcohol use. Behavioral problems associated with alcohol use:- depression, memory problems,suspiciousness, interpersonal problems. Fam i l ia l , soc ia l and legal consequences of alcohol use:- Financial and occupational consequences:- includes cu rrent financial status an d current

occupational status. Previous treatment attem pts: reasons for seeking help this time, m otivation for getting changed.BARRIERS IN ASSESSMENTIt is not always simple to get the sensitive information required for the assessment of alcohol usecorrectly an d comp letely. Som e specific barriers on the part of the subject in the assessm ent include : Denial of the problem by the patient as well as ambivalence about the need for external help. Guilt abou t alcohol use and use related behav ioral pattern wh ich lead to withholding information. Feelings of sham e about having been 'weak' or 'failure' resulting in poor m otivation. Stigmatization of the patient and the family that hinders active help-seeking process. Dilemmas about physician's role and reactions may restrain a person form seeking help. Apprehension of possible legal and other punitive consequences may deter a person formapproaching treatment agencies.Even a clinician's personal characteristics may serve as a barrier in the assessment of potentialpatients. Some important issues are:- Scientific knowledge about the field of alcohol related problems, though expanding is still

limited. Judgmental attitude to persons with alcohol related problems affects effective delivery of

treatment. False opinion of therapeutic nihilism in cases of alcohol related problems leads to half hearted,non-proactive efforts on the part of treating teams. Fear of inability to manage alcohol related problems even at the most initial stages of

assessment.REMEDIES FOR BARRIERS IN ASSESSMENTThe barriers in assessment can be effectively overcome by remedial mea sures in the approach tothe assessm ent of pe rsons w ith alcohol related problems, for example:

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1. Ensuring privacy and confidentiality2. Remaining non-judgmental and non-moralistic.3. Showing no-possessive warmth and concern.4. Expressing em pathy and optimism .5. Read iness to listen and understand before reaching conclusions.6. Avoiding ambiguous messages.7. Being clear and firm regarding one's own role, functions, abilities and limitations.8. Deve loping introspective ability by the helper (physician, health worker or any other)XIV GOALS OF PHARMACOTHERAPY FOR ALCOHOL WITHDRAWALGoals for which substantial evidence of effectiveness exists Treatment of alcohol withdrawal symp toms Preven tion of initial and recurrent seizures Prevention and treatment of delirium tremensOther Goals Prevention of me dical and psychiatric complications of alcohol withdrawal Preven tion of kindling effect Prevention of Korsako ff's psychosis Improvement in the likelihood of abstinence Minimization of adverse drug effect Entry into ongo ing medical and addictions treatment Cost-effective treatment1 . Selecting Patients for Outpatient Treatment for Alcoho l W ithdrawal

Contraindications to outpatient withdrawal m anagement Severe alcohol withdrawal symptom s Delirium tremen s Coexisting acute or chronic illness nece ssitating inpatient treatment Pregnancy Follow-up not feasible

Relative contraindications to outpatient withdrawal management History of seizures History of delirium tremens Significant craving

2. RISK FACTORS FOR M ORE SEVERE ALCO HOL WITHDRAWAL SYMPTO MS, SEIZURES,AND DELIRIUM TREMENS Con com itant me dical or surgical

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Mod erate-to- severe withdrawal symptoms at baseline Older age Prior delirium tremens Prior detoxification (s) Prior seizures Time since last drink Severity of alcohol depend ence Elevated aspartate aminotransferase Greater degree of craving Greater quantity and frequency of alcohol intake Higher blood or breath alcohol Longer duration of alcoho lism More symptoms of alcohol depende nce Presence of alcohol associated gastrointestinal illness.

3. PHARMACOTHERAPIES FOR ALCOHO L WITHDRAWALIncidence of Symptomatic A lcohol WithdrawalBetween 13% and 71 % of persons presenting for alcohol detoxification develop significant symptomof alcoho l withdrawal. This wide-ranging incidence depends on the population studied and the severityof dependence in the subjects. In patients hospitalized for alcohol withdrawal receiving no specificpharmacologic treatments, 15% developed seizures, and 15% developed delirium tremens.A- Benzod iazepines:- are the drugs of choice for the management of alcohol withdrawal. The bestevidence for efficacy exists for the long-acting benzodiazepines. Benzodiazepines haven been show nnot only to ameliorate the sym ptoms of alcoho l withdrawal, but also to prevent seizures and deliriumtremens. The best evidence for efficacy in preventing the serious complications of seizures anddelirium tremens, however, lies with chlordiazepoxide (Librium) and diazepam.Benzodiazepines have been compared with other medications for the management of alcoholwithdrawal. A lthough phenothiazines, clonidine (Catapres), and carbamazepine (Tegretol) may reducesymptoms, no evidence supports their ability to prevent seizures or delirium tremens. In fact, seizuresare more common when phenothiazines are used, and delirium is more common when b-blockersare used as monotherapy for alcohol withdrawal. There are no control led data to guidepharmacotherapy of alcohol withdrawal in pregnancy. Although both chlordiazepoxide and diazepamare category D drugs , meaning that there is evidence of human fetal risk the benefit of using a proveneffective therapy for a brief course of therapy to prevent serious maternal and fetal complicationslikely outweighs the risks.B. Other Drugs and Adjunctive Pharmacologic TherapiesOther drugs that have been used in the management of alcohol withdrawal include barbiturates,sympa tholytics, carbamazepine, neuroleptics, magnesium, and thiamine.

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(i) Barbiturates:- Barbiturates are the second most common drug class used to treat alcoholwithdrawal in the United S tates. Although there is clinical experience suggesting efficacy, an danticonvulsant properties are well known, there is only on e controlled trial of barbiturate u se offor alcohol withdrawa l. A lthough evidence is lacking, favorable clinical experience an d consensussuggest that Phenobarbital is an acceptable alternative for the management of alcoh ol withdrawalin pregnant wom en.

(ii) Sympatholytics:- Because the symptoms of alcohol withdrawal are at least in part due toincreased sym pathetic outflow, sympatholytics would appear to be logical treatme nts. Clonidinehas been shown to be as effective as chlordiazepoxide and more effective than placebo intreating the signs and sym ptoms of alcohol withdrawal. But sympatholytics are not app ropriatemonotherapy for alcohol w ithdrawal. In fact, propranolol (Inderal) has been ass ociated with ahigher incidence of delirium.

(iii) Carbamazepine:- This anticonvulsant is as effective as oxazepam and more effective thanplacebo in treating the minor signs and symptoms of alcohol withdrawal. Currently, however,there is no evidence regarding treatment or prevention of delirium and insufficient evidence inhum ans to permit safety an d efficacy conclusions regarding the use of carbamazep ine to treatalcohol withdrawal.

'(iv) Neuroleptics:- Neuroleptics ca n reduce the symptoms of alcohol withdrawal, but they (particularlythe phenothiazines) are less efficacious in preventing delirium and may increase the risk ofseizu res during alcohol withdrawa l. Neuroleptics, however, particularly the butyrophenone s su chas haloperidol (Haldol), are useful as adjunctive therapy to treat agitation and hallucinations.

(v) Thiamine and Magnesium:- Neither thiamine nor magnesium has been shown to have anyimpact on the signs or symptom s of alcohol withdrawal or the incidence of seizures or deliriumduring alcohol withdrawal. Both thiamine and magenesium, however, have a role in thepharmacologic management of alcohol withdrawal. Although relatively uncommon as part of theacute presentation of alcohol withdrawal, Wernicke's encephalopathy (confusion, ataxia andophthalmoplegia) and Korsakoff's syndrome are disastrous complications if they develop. AcuteWernicke's encephlaopthy may go undiagnosed initially but can be prevented by parentraladm inistration of thiamine followed by daily oral doses and should be adm inistered to patientswithdrawing from alcohol. Hypom agnesaem ia is common in patients w ithdrawing from alcohol.Therefore, magnesium should be given to all persons with signs of deficiency and should beroutinely co nsidered for all patients w ithdrawing form alcohol. In severe m agnesium deficiency,the deficit is approximately 1 to 2 mEq/kg of body weight; greater than 50% of dose givenintravenously is excreted when renal function is normal. The goal is to replete half of the de ficiton the first day, then the remaining deficit on the following 4 days. For example, for 70-kg persons,administer 32 to 48 m Eq (4 to 6 ampoules) of magnesium sulfate in each of 2L intravenous fluidon the first day followed by half that amount da ily for 4 days.

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XV TREATMENT REGIMENS FOR ALCOHOL WITHDRAWALFixed-scheduled dosingFront-loadingSymptom-triggered therapyFor delirium tremens

Chlordiazepoxide orally every 6h for 3d (50-10Omg per dose day 1, then 25-50 m g per dose)Diazepam 20 mg ora l ly every 2h whi lesymptomatic until resolutionChlordiazepoxide 25-100 mg oral ly hourlywhenever symptomatic (CIWA-Ar>8)Diazepam 10 mg intravenously, then 5 mg every5 min until calm but awake.

I f unable to take oral medicat ion or in the presence of hepat ic synthet ic dysfunct ion(hypoalbuminemia, elevated prothrombin time), intramuscular, sublingual, oral, or intravenous(for delirium tremens only) lorazepam 1-4 mg may be substituted)Oral oxazepam 30-60 mg or lorazepam may be substituted in the elderly and those at risk ofexcessive sedation or its complications.All patients receive thiamine 50-100 mg daily, first dose parentally. Consider magnesiumadministrations (intravenously) 2-4 mEq/kg on day 1, 0.5-1 mEq/kg daily on days 2-4

CIWA-Ar= Clinical Institute Withdrawal Assessment- Alcohol revised scale.Choice of Appropriate Regimens:- The main consideration in choosing a treatment regimen iswhe ther medication must be delivered regardless of withdrawal symptom s (i.e, seizure history, acutemedical illness) or if medication administration can be safely guided by symptoms. Regardless ofregimen chosen, the key is frequent patient revaluation, particularly early on, with attention to thesymptoms and signs of alcohol withdrawal and to excessive sedation form med ication. A cookbookregimen does not obviate this requirement; therapy should be individualized. Significant symptomsand signs should be treated with more medication.The tendency to declare a particular benzodiazepineas a treatment failure w hen symptoms persist sho uld be resisted. This failure is usually due toinadequate dosing. Rather than switching specific drugs, larger additional doses usually treat allpersistent alcoh ol withdrawal symptoms.Treatment of Alcohol Withdrawal SeizuresAlcohol withdrawal seizures are generalized, occur early in the course of withdrawal (first 24 to 48hours), and usually are single or recur only once or twice. The seizure generally resolves spontaneously.Benzodiazepines, carbamazepine, and probably Phenobarbital prevent seizures, but phenytoin isineffective an d therefore not indicated for prophylaxis or treatment of seizures . (Alldredge at al 1989,Chance et al 1991)) If the seizure is not typical for alcohol withdrawal (e .g. focal seizures , focalneurologic exam ination, h ead fraum a, suspected intracranial bleeding) is reasonable. The mainstayof treatment as in the regimens previously described, preferably diazepam, chlordiazepoxide, orlorazepa m, all shown to prevent initial and recurrent seizures.Treatment of DeliriumTrem ens:- It is a Medical emergency. 20-50 % of patients die eventually if nottreated, there is 5-10% mortality even with treatment it requires immediate hosp italization in untreatedcases. Treatment of choice is intra venous diazepam (10 mg every 20 minutes till patient is sedated

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or signs and symptoms of w ithdrawal sub sides). Supported treatment should also continue. Safe andprotective environment should be se cured. With treatment it is usually co ntrolled within 3 to 4 days.XV MANAGEM ENT OF ALCOHO L DEPENDENCE

Pharmacological TreatmentNon P harmaco logical Treatment

a) Long term pha rmac ological treatment:-lt helps patients to maintain abstinence aftercomepletion of detoxification. As such 'cure' of dependence is improbable but successfultreatment with pharmacological agents is possible (Desai 1992). Disulfiram, naltrexone andAcamprosate are the drugs approved by US Food and Drug Administration (FDA)- for thepharmacotherapy of alcohol dependence.(i) Deterrent age nts (Alcoho l-Sensitizing Drugs ): - Medications such as disulfiram or calciumcarbam ide cause an unpleasant reaction when com bined with alcohol. The efficacy of suchdrugs in the prevention or limitation of relapse in alcoholics has not been dem onstrated. However,these drugs may be of utility in selected samples of alcoholics with whom special efforts are

made to ensure com pliance.Disulfiram:- It is the m ost comm only used alcohol-sensitizing m edication and the only one approvedfor use in the US . It was approved by US-FDA in 1948.Mechanism of Action:- It inhibits alcohol dehydrogenase enzyme which converts acetaldehyde toacetate in normal alcohol catabolism in the liver (larson et al 1992). Following disulfiram treatment,ingestion of alcohol increases acetaldehyde levels 5 to 10 times more than the levels without disulfiramtreatment. High concentrations of acetaldehyde are believed to mediate disulfiram-ethanol reaction,which is characterized by flushing, we akness, nau sea, tachycardia, hypotension and in severe casesdeath (chick et al 1999). Continuous treatment with disulfiram does not lead to the development oftolerance. Before disulfiram treatmen t is initiated, the patient should be abstinent from a lcoho l for atleast 12 hours. Disulfiram e ffects are observed 3 to 12 hours after its oral adm inistration. Disulfiram-alcohol reaction may occur as long as 1 to 2 weeks a fter the last dose of disulfiram. The standarddosage of disulfiram is 250 mg per day (range 125 to 500 mg daily). Goal is to achieve total abstinence .It is an aversive treatment that enhances motivation for continued abstinence by making the "high"unavailable, thus discou raging impulsive alcohol use. The cogn itive awareness of occurren ce ofDER and/or any previous experience of DER w ith use of alcohol while on disulfiram therapy, preventsa drinking response when exposed to alcohol use related cues (like persuation by friends, companyof other users social gatherings and parties). Prevention of drinking response helps to maintainabstinence. It should be rem embered that disulfiram does not reduce the craving but prevents responseto craving. It should not be given surreptiously. Patient to be taken in confidence and cliniciansshould never ever encourage the practice of giving this medicine without the informed consent ofpatient. Because of the hepatic toxicity and blood dyscrasias associated with disulfiram, themanufacturer recommends monitoring of liver function tests and complete blood count during treatment.Before starting treatment with disulfiram, patients should be warned to avoid alcohol containingproducts and food s.Side effects and adverse reactions: - The com monly experienced side effects are of drowsinessand gastric irritation. The a dverse effects, which occur most commonly with use of disulfiram, arehepatic, neuro logical, skin reactions and psychosis.The safety of disulfiram, estimated on the amount

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produced and the number of reactions reported, corresponds to an intermediate rate of adversereaction (1 per 200-2000 treatmen t year).Clinical reg imen:- Disulfiram shou ld always be given after obtaining informed consent and baselineinvestigations for mo nitoring the side effects. The usual dose is 250m g/day; however due to metabolicdifferences, some patients may require a higher dose 500-750mg/day to experience DER. It is generallydispersed in a single daily dose in the morning but a bedtime single dose has also been used.Supervised Disulfiram therapy: - Disulfiram works well when its use is supervised as it ensuresbetter com pliance. Supe rvision can be m ost effective when done by spouse, though it can be doneby an other fam ily member or a supervisor at work place. Supervision also ensures that the possibilityof DER is redu ced . Some training of supervisor in the detection of the techniques of evasion, whichthe patients use, is desirable.Treatment of DER: - In case of a DER induced by a challenge test, the resuscitation should be an dis usually available but the occurrence of a DER in uncontrolled situations is more likely to be fatal.Prompt treatment in such situation is necessary although it is mainly supportive and for controllingthe fall in blood p ressure. If DER is mild, assurance and oral fluids suffice. In patients w ith mode-rateor severe DER, intravenous fluids and in some patients dopamine infusion is necessary to controlthe severe hypotension. The use of antihistamines also has been recommended (Peterson et al1992). The use of 4-methylpyrazole, which blocks formation at acetaldehyde has been found to besuccessful but is still not common in clinical practice. (Lindros et al 1981).Compliance and efficacy:- Although disulfiram has been in use for more than 50 years but it hasbeen underused.(Brewer et al 1992) Azrin et al 1982 reported on a series of studies comparingsupervised and unsupervised disulfiram therapy, with a package of essen tially behavioral interventionstermed as community reinforcement therapy (CRT). The effectiveness of disulfiram therapy wasdem ons trated if it is properly supervised . The evidence for the effectiveness of supervised d isulfiramtherapy from American Studies has been confirmed in a multi -center British study by Chick et al1992, in which su pervised disulfiram therapy was compared with supervised vitam in C.The resultshave clearly favo red the disulfiram group with significant reductions in several measures of d rinkingbehavior including the level of GGT in the disulfiram group, compared to no reductions in theseme asures in the Vitamin C group. A review of controlled clinical trials with disulfiram concluded thatthere is unopposed evidence for its effectiveness.B) Anti craving age nts: A number of specific neurotransm itter systems have been implicated in thecontrol of alcohol co nsum ption, including endogenous o pioids, catecholamines, especially do pmine,and serotonin. Although these systems appear to function interactively in their effects on drinkingbehavior efforts to use medications to treat excessive drinking have increasingly focused on agentsthat have selective effects on specific neurotransmitter systems.1 . Naltrexone - An extensive literature supports the role of opioidinergic neurotransmitter in thepathphysiology of alcohol consumption and related phenomena. An analog of naloxone, is a relativelypure opioid antagonist with highest affinity of for the mu-opiate receptor type. Naltrexone is absorbe dbetter after oral adm inistration and has longer duration of action than naloxone. Naltrexone reducedalcoh ol crav ing, days of drinking per week, and the rate of relapse among those who drank (Volpicelliet al 1992). It shou ld be given to patients who categorically report craving and there are multipleinstances of lapse or relapses because of craving. There is evidence that naltrexone leads to a

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reduction in drinking quantity, maintain abstinence and helps prevent relapse to heavy drinking. Thesuperior efficacy of naltrexone for alcohol relapse prevention is well documented (Volpicelli et al1992). When administered at 50 mg /day for 3 months, this agent usually prevents relapse. It wasapproved by the Food a nd Drug Administration in 1994 for use in the treatment of alcohol dependence.Naltrexone is thought to attenuate the reinforcing effects but not the negative aspects of alcoholconsu mp tion, such as cogn itive impa irment and sed ation. Amo ng alcoholics in treatmen t, those whoconsumed alcoh ol rep orted fee ling less intoxicated and less craving for alcoho l. The e fficacy ofnaltrexone for use in alcohol dependence has been investigated in two placebo-controlled clinicaltrials. In a combined analysis of the data from the 186 alcohol dependent patients in these twostudies, patients random ized to receive 50 mg of naltrexone for 12 weeks w ere more likely to remainabstinent and to avoid relapse to heavy drinking 31 % of placebo patients remained abstinent comparedto 54% of patients on naltrexone 48 % of placebo patients avoided heavy drinking, whereas 75% ofnaltrexone patients succe ssfully avoide d drinking to excess. Craving for alcoh ol was also significantlylower for patients on naltrexone. The decision regarding the continuation of naltrexone beyond 12weeks is ba sed on clinical judgem ent. In making this decision, the physician considers w hether thepatient has made changes that could support continued abstinence, the patient's previous history ofresponse to treatment, and the patient's interest in continuing. Naltrexone may be particularly usefulfor subjects who present with high levels of craving and somatic symptoms (Volpicelli et al 1995).Another opioid a ntagonist, n almefene, has also been evaluated in alcohol dependent sub jects. In aninitial pilot study (Ma son e t al. 1994) and a subsequent larger trial (Mason et al 1999), the m edicationwas shown to be well tolerated an d to be superior to placebo in reducing relapse.In summa ry, naltrexone appears to produce a m odest effect on drinking behavior am ong alcoholics(Kranzler and Van Kirk 2001 ). However, given the com paratively sma ll overall effect of he medication,a variety of other factors, including medication compliance, the severity and chronicity of alcoholdepend ence, and the c hoice of concom itant psychotherapy, may de termine whether an effect of themedication is observe d. Com mon side effects are nausea, dizziness, headache.CONT RAINDICATIONS TO THE USE OF DISULFIRAM AND NALTREXONEConditions resulting in increased risk associated with the disulfiram ethanol reaction Cerebrovascular disorders Cardiovascular disease Severe pulmona ry disease Renal failure Cirrhosis with portal hypertension Occu lt atheroscelerosis (i.e >age 60, diabetes)Conditions that may be exacerbated by disulfiram Psychosis Significant depress ive illness Idiopathic seizure disorder Peripheral neuropathy

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Other contraindications to disulfiram Organic brain syndrom e: limited ability to understand risks of disulfiram ethanol reactions . Pregnancy: associated with birth defectsPrecautions for the use of disulfiram Concurrent use of adrenergic receptor antagonists Concurrent use of vasodilatorsAbsolute contraindications to naltrexone Acute hepa titis or liver failure Current depende nce on opiate or opiate withdrawal Need for opiate me dicationRelative contraindications to natlrexone Pregnancy Adolescence1 . Acamprosate -Aca mpros ate an amino acid derivative, affects both gamm a-aminobutyric acid(GABA) and excitatory amino acid (i.e. glutamate) neurotransmission (the latter effect mostlikely being the one that is important for its therapeutic effects in alcoholism). It inhibits theglutamine rgic excitatory activity, acting, probably, on a subclass of gultamate (NMDA) receptors,especially whe n there is hyperactivity of these receptors. It has been approved by FDA in 2004.Acamprosate has been considered a partial co-agonist of the NMDA receptor (Naassila et al1998). Acamprosate has a good oral absorption, which is, however, imp aired by the concom itantingestion of food. It is not metabolized, and completely eliminated by the kidneys. It has noprotein link. All these characteristics suggest that this medication has no preoccupying interactions

with drug s. It has been found efficacious for the treatment of alcoholism w ith long-term bene fits.In fourteen of the sixteen double blind placebo-controlled trials it has shown favorable results(Mason a nd Ownby, 2000). Meta analysis of the studies done between 1990 to 2002 has shownthat it increases ab stinent days and also increases cumulative abstinence days (C armen 2004).Acamprosate should be administered in alcohol dependent patients with more than 60 kg, inthree daily d oses, being two capsules with 333 m g in the three periods of the day, always beforeme als. For patients with less than 60 kg, most of the studies suggest the administration of lowerdoses i.e. a capsule with 333 mg in the three periods of the day. Maintenance time of theme dication is variable. The c linical trials performed used the dru g for 6 to 12 months (Wilde et al1997). This new medication has great promise in alcohol relapse prevention (Seas et al 1996).Common side effects include diarrhea and headache. However, some authors proscribe thedrug for patients with hepatic insufficiency CHILD-PUGH C, but not for CHILD-PUGH A or B.Pregnant women should not receive the medication, as there are no reliable data about itssafeness for the fetus (Saivin et al 1998).2. Selective Serotonergic Reuptake Inhibitors - Another major focus of research on medicationsto treat alcoholism has been the role of the indoleamine neurotransmitter serotonin (5-HT). 5-HT has been shown consistently to exert an influence over alcohol consumption in preclinicalmodels of drinking behavior (McBridge et al . 1990 , Le Ma rquand et al 1994a). In contrast to this

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preclinical literature, data on the effects of serotonergic m edication on human drinking behoaviorare more limited, and the results are less consistent (LeMarquand et al 1994b, Kranzler 2000).Naranjo and collegues (1990) found that fluoxetine 60mg/day reduced average daily alcoholconsu mp tion by approximately 17% from baseline levels, while treatment with fluoxetine 40m g/day or placebo had no effect. Decreased brain serotonin has been linked with impulsivenessand low s cores on the 'harm avoidance dime nsion of behaviour (Cloninger et al 1987). Thelargest study (Kranzler, Burleson, Korner et al 1995) involved 101 subjects, some of whom alsohad co mo rbid d epres sion. Studies have failed to show significant reduction in drinking or othermeasures of drinking (Kabel and Petty 1996:Johonson et al 1996). Three m onths trial of Fluoxetine(n=51) with comorbid major depression found a significant effect on both condition comparedwith placebo (Cornelius et al 1997). It is not as effective as naltrexone or acamprosate.Topiramate - It is an antiepiletic a nd adjuvant mood stabilizer. It inhibits release of dopamine inme so-co rtico-limbic pathway by augmenting GABA function and inhibiting specific glutaminergicpathway. It also inhibits carbonic anhydrase enzym e (Gibbs et al 2000, Shank et al 2000) Doseis 25-to 300-mg/per day. Most common side effects are weight loss, parasthesiae, cognitiveimp airment. A 12-week study using topiramate (25-300m g/day) has shown that it is significantlybetter than placebo in decreasing craving (Johnson et al 2003). Abstinence is not required tostart topiramate. It requires larger studies with control group and longer duration of the study.Ondansetron -Ondansetron, a selective 5-HT3 receptor antagonist, has shown promise inreducing overall alcoho l intake specifically among those with type I alcoholism (Cloninger et al1988). It reduces urge to drink. Dose is 4 micro gram/kg b id. It produces better result in earlyonset a lcohol de pend ence. (Johns on, 2000). It is not in comm on clinical use.Medications Used in Combination :- Drinking behavior is not dependent solely on a singleneurotransmit ter system. Rather, several systems have been implicated, including theopioidinergic, glutama tergic. GABAnergic, serotonergic, and dopam inergic systems as well asseveral neuroho rmones, such as thyrotropin releasing and adrenocorticotrophic hormones (Littenet al 1996: Roberts and Koob 1997). In light of this multi-determination, many options indevelopment of agents to reduce drinking merit exploration. One possibility is to use agents incom bination, pa rticularly to combine those that act on different receptors in the brain. This strategyhas been supp orted by several animal studies, demonstrating that combinations of m edicationsare m ore effective in reducing alcohol intake than the various drugs were used alone (Lankfordand Myers 1996; Yu et al 1997).e.g. DS+NTX,ACAMPROSATE+NTX.Depot Preparation:- Implanted disulfiram has been tried but not on large scale. Sustain releaseformulation of depot Disulfiram provoked only mild Disulfiram ethanol reaction (DER). DepotNaltrexone is better in patients with poor compliance. It holds promise in patients with poorcompliance.For optimu m benefits in the treatment of alcohol dependence pharmacological treatment has tobe given along with psychosocial treatments.Psychosocial treatmen ts in alcohol dependencePsychosocial intervention for substance use disorders is a broad "umbrella" term that bringsunder its folds a diverse array of non-pharmacological interventions for effective andcomprehens ive mana geme nt of drug abus e. A variety of treatment components are delivered

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within the context of rehabilitation services. Therapeutic approaches most often employed inboth residential and outpatient programs include behavior therapy., group therapy, familytreatment, and pharmacotherapy. Regarding specific treatment modalities, the weight of evidencesuggests that behavioral treatments are likely to be more effective than insight-oriented or familytherapy (Miller and Hester 1986). Nevertheless, recent research (Project MATCH Rese archGroup 1997a, 1997b 1998, Ouimette et al 1999) also indicates that Twelve Step Facilitation,wh ich is based on the principles of AA, is as effective as more theory-based therapies. Controlledstudies provide little support for the effectiveness of psychodynamic psychotherapy, althoughsuch treatment has been shown to be helpful in the treatment of drug abuse (Institute of Medicine1989, Miller and Hester 1980).GOALS OF PSYCHOSOCIAL TREATMENT Enhance efficacy of pharmacotherapy Achieving sustained drug free status Providing the relationsh ip Cha nge of life style Improv ed quality of lifeThough some of psychosocial interventional skills require specially trained professionals, most ofthese skills can be acquired by general physicians, nurses, social workers and counselors making itpossible to offer these interventions in a number of settings, including primary health care facilitiesand non governmental organizations working in the community.MODALITIES OF PSYCHOSOCIAL INTERVENTIONS1. Brief interventions - It is very popular because of its cot effectiveness. Brief interventions(studied mostly in relation to alcohol abuse so far) typically com prise of 1 -4 session. Contrary toprevious popular belief, relatively brief interventions have consistently been found to be effectivein reducing alco hol con sumption or achieving treatment referral or retention of problem drinkers,and a significant effect size was found in a meta analysis of 32 controlled studies across 14nations involving over 6000 problems d rinkers (Bien et al 1993). The com mon elements of briefintervention were summarized as the acronym FR AMES.F. Feedback, R- Personal responsibility, A- Advice, M- Menu.E- Em pathy,S- Self efficacy

Quite effective in brief contact contexts such as primary health care settings and employeeassistance programme. Although it requires much lesser time and cost, it was consistentlybetter than no coun seling and usually as good as other, more formal or long drawn therapies.2. Extended interventions - utilizes 5-12 sessions with patient, either in a group or alone. Patientsadvanced well into substance using patients, either in a group or alone. Patients advance wellinto substance using career, or those w ith multiple relapses, hospitalizations etc., are su itablefor this type of intervention.3. RELAPSE PREVENTION

Recovery - Process of initiating and maintaining abstinence from the substance Lapse - Isolated instances of substance use following a period of abstinence

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Relapse- Resum ption of a previous pattern of substance abuse or dependen ce following aperiod of abstinenceNEED AND SCOPE - Numerous reviews of treatment outcome literature have documentedhigh rates of relapse up to 65- 80 % in the first year of treatment amo ng substance dependenc edisorder patients (Hunt et al 1971, Catalano 1988).STRATEGIES OF RPIdentification and management of specific relapse precipitant situations/eventsMaintaining abstinenceCorrection of psychosocial and physical consequences of drug useSociooccupationalRehabilitation/reintegrationModifying or reverting underlying neuroadaptive process/changesDETERMINANTS OF RELAPSE (MARLATT AND GORD ON, 1995)INTERAPERSONAL FACTORS

Negative emotional states (most common)Negative phy sical statesPositive emotional statesTesting of personal co ntrol over urges an d temptations

INTRAPERSONAL FACTORS -Relationship conflictSocial pressure to use substancesPositive emotional states as a result of interpersonal intervention

OBJECTIVES OF RELAPSE PREVENTIONTo develop new coping skills for handling high risk situations and relapseWarning signsTo make life style changes to de crease the n eed for substancesTo increase healthy activitiesTo prepare for interrupting lapses , so that they do not end in a full blown relapseandTo prepare for mana ging relapses , so that adverse consequences c an be minimizedRELAPSE MANAGEMENTDetoxification and assessm ent of consequences of substance useAssessm ent of the reasons and precipitants for current relapse and the past history of relapsesAssessment of the reactions of the patient and the family members to the relapseAssessment of the recovery process, specifically the periods of abstinence and the factorscontributing to abstinence

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Intervention for the relapse precipitants and the reaction Prepa ration for future relapses3. COG NITIVE AND BEHAVIOUR THERAPY: - These therapies primarily focus on individualthoughts an d be haviors. These structured, focused, collaborative approaches are based on theassum ption that substance abuse is mediated by complex cognitive and b ehavioral processes,

which can be mo dified to decrease the drug using and other related behaviors.4. GROUP THERAPYGroup therapy for drug dependents can be defined as "an assembly of chemically dependent patientsusually 5-10 in number, who meet regularly under guidance of a professional leader (usually aprofessional therapist or an addiction counselor), for the purpose of promoting abstinence from allmo od altering ch emicals and recovery from ad diction (Washton 1997). Treatment goals in grouptherapy for substance dependent patients are enhancing motivation, establishing abstinence, psychoeducation, preventing relapse and addressing specific psycho social issues. Unfortunately in India,these the rapies have not bee n followed much . Our cultural characteristics of sharing life intimatelywith large number of people can be utilized by adopting the available models to our needs (Desai. 1992).5. FAMILY THE RAP YThe role of family transce nds genesis, maintenance, treatment seeking , recovery as well as relapseof substance used d isorders. There is a vicious cycle in which the patient's drug use adverselyaffects the family's well-being and coping resources. Dysfunctional and burdened families have strongly negative responses towards patients, resultingin increased substan ce use by patients. This is much true in the Indian context because of the intact family systems and support, with

family m embers having an imp ortant say in the matters of an individual and peculiar intra familialcharacteristics of the Indian families. "Fam ily as a u nit", "family as a context": - If the chem ical dependence seems to be mainlyowing to dysfunctional patterns in the family. Family as unit needs to be treated with intensivefamily or ma rital therapy. If chem ical dependence has led to dysfunction in the family, then a lessintensive but active and constant participation of family memb ers shall be sought to treat patientwhile focus on family as context.6. SELF help approach (Alcoholic Anonym ous)The 12 Steps of Alcoholics Anonymous1 . We ad mitted we w ere pow erless over alcohol-that our lives had become unmanageable.2. Came to believe that a Power greater than ourselves could restore us to sanity.3. Made a decision to turn our will and our lives over to the care of God as we understood Him.4. Made a sea rching and fearless moral inventory of ourselves.5. Adm itted to G od, to ourselves, and to another human being the exact nature of our wrongs.6. Were entirely ready to have God remove all these defects of character.7. Humbly asked Him to remove our shortcomings.

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8. Made a list of all persons we had harm ed, and became willing to make amends to them all.9. Made direct amends to such people wherever possible, except when to do so would injure themor others.10. Continued to take persona l inventory and wh en we were wrong , promptly admitted it.11. Sought through prayer and medication to improve our conscious contact with God as weunderstood Him, praying only for knowledge of His will for us and the power to carry that out.12. Having had a spiritual awakening as the result of these steps, we tried to carry this message toalcoholics, and to practice these principles in all our affairs.It is Group of individuals with similar problems. Mutual assistance is required among members tosatisfy a common need. It began in 1935 in Europe. The only requirement for membership is desireto stop drinking. Groups may or may not allow simultaneous treatment. AA meetings are of differenttype (closed meeting and open m eeting). It follows 12 tradition and 12 steps as mentioned above. AAviews alcoho lism as a disease or sp iritual illness. The central spiritual defect in alcoholic is describedas an excessive pre occupation with self. Treatment of preoccupation with self is the core of AAapproa ch. The theory of AA that ad diction is not the property of the d rug but a characteristics of theaddict being pow erless over drugs. Emotional sobriety rather than mere physical sobriety is the goal.Innumerable ind ividual accounts and collective impressions have been docum ented about the efficacyof these approaches. Efficacy depends on retention of members and extent of participation of AAmeeting. Clinical exp erience does su gges ts that participation in self help groups can be an importantadjunct to treatment for better ou tcome in many patients w ith substance use disorders. Patients, whohave experienced loss of control, believe in the need to abstain, have no significant psychopathology,are socially stable and show signs of religiosity, should be referred to self help groups, besides thetreatment they are receiving.Limitations of AA:-lt neither provides motivation nor detoxification there is no follow up and theydon't deal with the problems of multiple substance use.Self help groups in India:- It Started in 1957.Meetings are held mostly in churches. Mistakenimpression is that these are Christianity based, but principle of faith is followed it is necessary toencourage more active referrals to AA and other self help groupsxv Special FEATUR ES Influencing treatmentThere is considerable evidence that l inks the outcome of alcoholism treatment to comorbidpsychopathology. General measures of psychopathology (McLellan et al. 1983), as well as the specificdiagnoses of drug abuse, drug dependence, antisocial personality disorder and major depressivedisorder have been shown to predict poorer outcomes in alcoholics (Rounsaville et al 1987,Kranzleret al. 1996b). The extent to which treatment of concomitant psychopathology enhances alcoholismtreatment outcom e in unclear.Osher and K ofoed (198 9), in advocating an integrated approach to patients with comorbid psychiatricand addictive disorders, have described four phases of treatment with this patient population: (1)engagement of dually-diagnosed patients in the treatment programs, (2) persuading these patientsto accept long term abstinence as an appropriate goal of treatment, (3) active treatment, duringwhich efforts are focuse d on the deve lopment of attitudes and the acquisition of skills nece ssary forsobriety, and (4) relapse prevention, which involves the long term maintenance of sobriety an d extendbeyond the acute treatmen t period.

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D e mo g r a p h i c F e a tu r e sa ) A d o l e s c e n ts : - Despi te a pauci ty of control led, age-speci f ic t reatment outcome studies of

adolescents wi th alcohol use disorders, the need for prevent ion and special ized t reatment forthis group is clear. The l i terature indicates that in substance-abusing adolescents some treatmentis bet ter than no t reatment , re lapse rates are high, and there is no consistent support for thesuperior i ty of any single t reatment modal i ty (Brown et al 1989). However, several factors havebeen associated wi th bet ter t reatment outcome: later onset of problem drinking, pret reatmentat tend anc e at scho ol , voluntary entrance into t reatment , act ive paren tal input , and avai labi li ty ofanci l lary a dolescen t-speci f ic services, including those p ertaining to school , recreat ion, vocat ionalneeds, and contracept ion (Kaminer 1994, Catalano et a l . 1990-1991)Because many adolescents have not yet fu l ly developed formal operat ional th inking, t reatmentef forts sh ould be concrete an d goal-or iented . The use of age-ap propriate su ppo rt groups (e.gAlateen) may be part icular ly useful in th is regard.

b ) Geriatr ic Pat ients: - In addi t ion to the high prevalence of medical problems, pharmacokinet icand ph arm acod ynam ic v ariables can affect treatment outcom e in elderly alcohol ics. For exam ple,Liskow an d col legues (1989) found that elderly alcohol ics, despite having drunk less than you nge rp a t i e n t s d u r i n g t h e mo n t h p r i o r t o a d m i s s i o n , h a d mo re s e v e re a l c o h o l w i t h d ra w a lsymptomaotology and required a higher dosage of chlordiazepoxide. An important quest ion int reat ing elderly alcohol ics is the extent to which special ized t reatment services improve outco me .Kofoed and col leg ues (1987) found that pat ients t reated in special e lderly peer groups rem ainedin t reatm ent longer and we re l ikely to complete t reatmen t than thos e t reated in mixed age g roups .

c) Gen der ( Including Pregna ncy): - Epidem iological and cl in ical studies have shown that alcoh olabuse and dependence have become qu i te common among women, as h is tor ica l genderdi f ferences in dr inking pro blem s have dim inished during the past 25 yea rs. This trend haspromoted greater awareness of the impact of a lcohol use on women's heal th and importance ofgend er as a potent ia l determinant of treatmen t outco me . The recent requ i rement by the Na t ionalInst i tutes of Health and the FDA that women and minori t ies be act ively recruited to part icipate inheal th related research sho uld help to increase knowledg e about alcohol ism t reatme nt ou tcom ein these gro ups . To guide the t reatment of a lcohol ism in wo m en , Blume (1992 ) sugg ests thatevaluat ion sho uld include special at tent ion to the ident if ication of physical abu se, sexual ab use,me dical prob lem s, psychiatric com orbidity, the presence of alcohol ism and drug abuse in spouse s,and alcoh ol-related birth defects in chi ldren. Blume (1992) also l ists the fol lowing spec ial treatmen tneeds of women: informat ion about the ef fects of substance use on the fetus, parent ing ski l ls ,coup les an d fami ly therapy, sober fem ale role mo dels, asse rt iveness t raining, an d an awa renessof sex ism and i t s consequences.

d) Ethnic and Cul tural Issues and Treatmen t: - A l thou gh socioeconomic and cul tural issuesshou ld be addre sse d in alcohol ism t reatm ent (Frankl in 1989), guidel ines for such t reatment a rebas ed largely on com mo n sense , rather than systemat ic outco me evaluat ion. Obviously, wherelanguage barr iers exist , special ef forts must be made to ensure adequate communicat ion.Treatment providers shou ld also be aware of thei r pat ients t radi t ional pat terns of dr inking, howdrinking may be inf luenced by acculturat ion, di f ferences among ethnic groups in their perceptionof alcohol related p roblems, the impact of sociocultural dif ferences between patients an d providers,and how pre vai l ing social (e.g. fami ly) re lat ionships ca n affect t reatment o utco m e.

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xvi TREATM ENT OF PATIENTS WITH DUAL DIAGNOSESA number of patients of alcohol depe ndence may have another psychiatric disorder on ax is-l or axis-II. Managem ent of these patients puts a tough challenge at all phases viz. evaluation, early treatment,long-term treatment for maintenance of abstinence and rehabilitation.A. Problem in evaluation of patients with dua l diagnosisB. Problems in early treatment of patient with dual diagnosisC. Problems in long-term treatme nt of patients with dual diagnosisD. Treatm ent of spec ific com orbid cond itions

a) TREATMENT OF SPECIFIC COMO RBID CONDITIONS1. Alcoho lism patients with depressive symptom s:-ln the initial few days of detoxification manypatients of alcoholism experience subjective symptoms a nd or demonstrate objective signs ofdepressive nature. These abate at rapid pace in majority of the patients. It is crucial that any

decision of diagnosing these symptoms or initiating pharmacological treatment be de ferred fora minimum of two weeks, preferably for four weeks. In small group of patients, who continue tohave depressive symptoms, these have the potential of being relapse triggers. Appropriatepsychosocial treatment methods, if possible group therapy, must be considered for themana gemen t of these symptoms as well as for relapse prevention.2. Alcoholism patients with major depression:- Although it is necessary to observe thedepressive features in patients of alcoholism for a period of two to four weeks before arriving ata diagnosis, in some clinical situations, the imperative need for diagnosis and treatment isoverriding, viz. in cases of major depression (DSM-IV) or depressive disorder-moderate/severe

(ICD -10). Evidence from the past history as well as the family history ca n be helpful in reachingthe diagnosis in such patients. Antidepressants must be considered in all these patients. Thetraditionally used tricyclic antidepressants have been recognized to have limitation in such clinicalsituation due to their sedation, cardiac toxicity and low safety profile. The antidepressantsspecifically the ones like fluoxetine and tianeptine acting through the serotonergic system, aremore appropriate.3. Alcoholism with dysthymic disorder:- Dysthymic disorder (DSM-IV) or depressive disorder(mild) require ca refu l evaluation need for use of antidep ressants. Psychosocial therapies ,particularly supportive psycho-therapy or cognitive behavior therapy must be consideredacc ordin g to the suitability and feasibility. Th e course in these patients is marked with frequent

relapses and the prognosis of alcoholism is not too favorable.4. Treatment of anxiety in alcoholism: - Anxiety symptoms in alcoholism vary from anxietystates related to acute and protracted withdrawal to comorbid anxiety disorders. Prevalencerates for anxiety disorders in studies performed on patients in alcohol treatment programs rangefrom 16-60%. (Powell et al 1982; Bowen et al 1984). A proper assessment of symptomatologyand its temporal relationship w ith alcohol use is essential. It may be goo d to delay any definitediagnosis of an add itional anxiety disorder till the patient has abstained from alcohol for 2 weeks.Anxiolytic agents s hou ld be administered to patients who experience anxiety disorders separatelyfrom any problems related to alcoh ol. Longer acting benzod iazepines are preferred because of

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lower abuse liability, though day time drow siness and cumulative toxicity is problem . It has beenproposed that there is no clear evidence that alcohol interacts w ith buspirone and this drug canbe used in the treatment of anxiety syndromes in alcoholics. (Schckit et al 1987)

xvii Treatment issue in special groups1. Physician patients: - Physicians and other health care professionals, who are dependent onsubstance (s), require different treatment strategies and their rehabilitation in the same professionposes difficult p roblems. No specialized facilities exist in India for such patients. Th e general attitudinalbarriers in physicians and the other health professionals about their own health needs and the defensesspecific to the issue of substance use makes the treatment of such patient a m ore challenging task.All the same, the attitude of the treating team needs to be empathic and rooted strongly in thedisease m odel of use disorders.2. Ex patients on treatment team:- The phenomenon, so common in the West, of ex-patientcontinuing to work on treatment teams or health care professionals recovering form dependencealso continuing to function on treatment teams, is still very uncommon in India. Some voluntaryagencies have ex-patients on their teams . Some problems of such an arrangem ent can be raised butclearly there are many advantages for the team and the individuals in particular. The phenom enon isl ikely to catch on and some precaut ions need to be planned and implemented to avoidcounterproductive results.3. Children of patients:- With the proliferation of sub stance abuse problem in general and theincreased population of wom en patients in particular, there has been a recognition of distinct population,the children of substance abusers who are known to have unique characteristics, that require specialattention. It is being increasingly documented that these children are at risk for serious educational,medical and emotional problems and have the potential for abusing substances as we ll as an increasedrisk for HIV infection. Comprehensive drug treatment services must include services for parents aspatients and must address the special needs of the children of patients through services, like daycare facilities, parenting skill training and school facilities.XVIII CONCLUSIONDuring the past 25 years significant progress has been made in the scientific study of alcoholism andits treatment. A number of conclusions appear warranted at this time:1. Alcoholism is heterogeneous with respect to dem ographic features (e.g. gender, race/ethnicity),age of onset of heavy drinking, severity of alcohol dependence, comorbid psychopathology,genetic vulnerability, and other prognostic factors.2. The available evidence suggests that any treatment for alcoholism is better than not treatment.The majority of those treated demonstrate improvement, but many of these alcoholics mayimprove with minimal treatment.3. The intensity of treatment has not been shown to produce pronounced differences in outcome(Moos and Moos in press). Similarly, medical inpatient treatment, while more costly, is notdemonstrably more effective than nonmedical residential or outpatient treatment, for patientswith serious comorbid medical and psychiatric disorders, medical inpatient treatment may,none theless be necessary. Som e evidence indicates that continuing afterca re helps to maintainabstinence following short term intensive rehabilitation in patient settings.

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There is little evidence that any on e-treatme nt ap proach is superior. There is some sup port for certainkinds of behavior therapy, but the effectiveness of AA and disulfiram seem to depend on patientcharacteristics and compliance. Several kinds of carefully specified and theoretically derived therapeuticapproaches show prom ise as a basis for a new generation of amb ulatory treatments. The se includethe relapse prevention strategies that teach the alcoholic how to avoid high risk relapses situations,and new pharmacologic agents (e.g. naltrexone) that appear to reduce the alcoholic's risk of relapseby dampe ning the reinforcement potential of alcohol. Continued improvements in treatments outcomewill depe nd upon s uccessfully ma tching treatment se ttings a nd m odalities to the specific needs tothe individual patient.XXI SOME IMPORTANT M YTHS AND FACTS ABO UT TREATM ENT OF SUBSTANCE USE

DISORDERS

10 MythFact

1.2.3.

4.

5.

6.

7.

8.

9.

MythsFactsMythsFactsMythsFactsMythsFactMythFactMythFactsMyth :Facts :Myth :FactMythFact :

Detoxification is equivalent to treatmentDetoxification is only the initial phase in the long term process of treatmen tInpatient treatment is necessary and outpatient treatment does not workOutpatient treatment is feasible and is effective in selected patientMore intensive treatment is more likely to succee d.Sho rt-term, less intensive treatmen t or minimal treatment maybe effective in some patientsTotal abstinence is the only treatment goal for depend ence disorder.Other treatmen t goals like controlled use areFeasible and w orth pursuing in suitable patientsRelapse indicates that the treatment has failed: Relapse is a part of the recovery process and not failure of treatmentAnyone treatment method is superior to other treatment methods(s)Different treatment methods suit different patients and non onemethod is superior to the others for all patients.Com bining more than one treatment m ethod has no advantage.Mu ltimo dal treatme nt is superior to any single treatment m ethods.It is an individual's p roblem an d the treatment has to beFocused on the individualInvolvement of a key family member, preferably thespouse helps in the treatmentUniform structured programmes for all patients are more effectiveStructured programmes with flexibility for individualneeds and matching of patient with treatment methods are more effective.Patients who join treatmen t do so either entirely voluntarily or dueto coercion and those who join voluntarily fare better in treatment.There is some elem ent, in varying degrees, of voluntaries andCoe rcion in all patients an d there are no g roup differences in theOu tcome of voluntary and coerced patients.

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XXII optimal & go od practice dep ending on different level OF TREATMENT settingsLevel 1 - Primary care physician, non psychiatric physician in practice/individual cham berpracticeOptimal practice1. To be conversant w ith "disease mo del" of addiction2. To be able to recognize "problem drinking "3. To be able to relate phys ical problems to alcohol consumption4. To be able to commun icate the alcohol related harm to the client an d his/her family me mbe rs.Good practice1. To be able to draw a balance sheet of harm and benefits of alcohol drinking in problem drinkers2. To recognize specific alcohol related physical problems3. To offer me dical treatment for these problems4. To recognize alcohol withdrawal features & comm unicate the significance of the same to theclient5. To prescribe benzodiazepine detoxification for those having withdrawal features.6. To be able to refer those with heavy alcohol consumption patterns, those with past history ofpsychiatric problems, those with history or current evidence of fits, delirium, head injury, suspectedmetabolic disorders to GHPUs with inpatient facilities.Level 2 D istrict hosp ital psyc hiatrists, NGOs w ith inpatient FacilitiesOptimal practice1. To be able to recognize dependence syndrome, especially by the presence of alcohol withdrawalfeatures.2. To init iate and plan OP D detox if ication, by prescribing benz odiaz epn es (long acting)chlordizepoxide 60-100 mg d ivided doses for 4-5 days and then tapering the dose 25 mg oncein 2-3 days and withdrawing the dose by 10th to 12th day3. To mo tivate the clients to rema in abstinent by discussing the risk of develop ing dependence

syndrome and physical problems.Good Practice1. To recognize the needs of inpatient and outpatient detoxification2. To be able to accurately monitor the patient during detoxification3. To differentiate simple and com plicated with drawl states4. To initiate detoxification for complicated withdrawal states in emergency settings.5. To plan post detoxification mo tivation enhancement involving patient and family6. To offer option of DS therapy for 1 year to all patients who are well motivated and accepts the

treatment and are apparently free from relative contraindications of DS therapy7. To be able to mon itor patients on DS therapy

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8. To be able to refer those with mental disorders, comorbidity with heroirV/benzodiazepine/cannabis/injection users, for G HPU /specialized d eaddiction treatme nt settings.

Level 3 GHPUs- M edical College department Optimal1. To be able to differentiate depende nt and non dependent drinkers2. To detoxify (in patient/outpa tient) dependent drinker to use oxazepam /lorazep am for those with

liver disease and chlo rdiazep oxide for those without to differentiate severity of withdrawal statesan d predict DT by evaluating risk factor (heavy consum ption, past h/o DT head trauma, infection,metabolic disorder, dyselectrolyemia)

3. Post detoxification