Document 6478894

The Treatment of Alcohol Problems
A Review of the Evidence
Prepared for the Australian Government Department of Health and Ageing
by Elizabeth Proude, Olga Lopatko, Nicholas Lintzeris and Paul Haber
2009
1
Contents
List of Tables ............................................................................................................. 4
Chapter 1
Introduction......................................................................................... 5
Levels of evidence and strength of recommendations............................................ 5
Recommended drinking limits ............................................................................... 7
Healthy Adults........................................................................................................ 7
Minors.................................................................................................................... 7
Pregnancy and breastfeeding ................................................................................ 8
References ............................................................................................................ 8
Chapter 2
Prevalence of Alcohol Consumption and Related Harms in Australia.. 9
Key points.............................................................................................................. 9
Patterns of consumption ........................................................................................ 9
Gender differences in patterns of consumption .................................................... 10
Age differences in patterns of consumption.......................................................... 11
Alcohol consumption among Indigenous Australians ........................................... 11
Alcohol- related harm - Indigenous people........................................................... 12
Alcohol-related harm in general ........................................................................... 12
Regional variations in alcohol-related harms........................................................ 12
Mental health ....................................................................................................... 13
Physical health..................................................................................................... 13
Social costs.......................................................................................................... 14
References .......................................................................................................... 15
Chapter 3
Screening, assessment and treatment planning ............................... 17
Screening............................................................................................................. 17
Where to screen?................................................................................................. 17
How to screen?.................................................................................................... 19
Comprehensive Clinical Assessment ................................................................... 26
Purpose of assessment........................................................................................ 26
Diagnostic interviews ........................................................................................... 26
Treatment Planning.............................................................................................. 37
Identifying suitable interventions and developing treatment care plans ................ 37
References .......................................................................................................... 41
Chapter 4
Brief interventions............................................................................ 51
What are brief interventions? ............................................................................... 51
Who to target for brief interventions? ................................................................... 51
How to deliver brief intervention ........................................................................... 52
Who can deliver brief interventions? .................................................................... 54
Where should brief interventions be delivered?.................................................... 54
Limitations of Brief Interventions .......................................................................... 67
Summary ............................................................................................................. 68
References .......................................................................................................... 69
Chapter 5 Alcohol withdrawal management ............................................................ 74
Alcohol Withdrawal Syndrome: Clinical Presentation ........................................... 74
Assessment and Treatment Matching .................................................................. 76
Supportive Care................................................................................................... 82
Medications for Managing Alcohol Withdrawal ..................................................... 86
Treatment of Severe Withdrawal Complications................................................... 98
Wernicke’s Korsakoff’s Syndrome...................................................................... 104
References ........................................................................................................ 107
Chapter 6 Psychosocial Interventions for Alcohol Use Disorders ........................... 114
Overview of Psychosocial Interventions ............................................................. 114
When to Use Psychosocial Interventions ........................................................... 114
Choosing Psychosocial Interventions: A Stepped Care Approach...................... 115
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Motivational Interviewing.................................................................................... 115
Cognitive Behavioural Interventions................................................................... 119
Specific cognitive-behavioural interventions....................................................... 121
Other Counselling Strategies ............................................................................. 130
Relapse Prevention Strategies........................................................................... 131
Residential Rehabilitation Programs .................................................................. 132
References ........................................................................................................ 133
Chapter 7 Pharmacotherapies for alcohol dependence.......................................... 142
Overview of Pharmacotherapies ........................................................................ 142
Naltrexone ......................................................................................................... 144
Acamprosate...................................................................................................... 150
Combined Acamprosate and Naltrexone............................................................ 155
Disulfiram........................................................................................................... 156
Other medications.............................................................................................. 159
Integration with psychosocial treatments............................................................ 163
Increasing medication adherence ...................................................................... 163
Selecting medications for individual patients ...................................................... 164
References ........................................................................................................ 164
Chapter 8
Self-help programs ......................................................................... 170
Alcoholic Anonymous (AA)................................................................................. 170
SMART Recovery®............................................................................................ 174
Self-Help for Families......................................................................................... 175
References ........................................................................................................ 176
Chapter 9
Specific populations....................................................................... 179
Adolescents and Youth ...................................................................................... 179
Pregnant and breastfeeding women................................................................... 186
Aboriginal and Torres Strait Islander Australians................................................ 189
Older people ...................................................................................................... 193
Cognitively impaired patients ............................................................................. 199
References ........................................................................................................ 204
Chapter 10
Comorbidities.............................................................................. 217
Alcohol-related physical comorbidity .................................................................. 217
Co-occurring Mental Disorders........................................................................... 222
Polydrug use and dependence........................................................................... 239
References ........................................................................................................ 242
Chapter 11
Aftercare and long-term follow-up .............................................. 251
References ........................................................................................................ 255
3
List of Tables
Table 1.1: Categories of evidence and strength of recommendations ........................ 6
Table 2.1: Percentage of the population aged 14 years and over at risk of long-term
harm by gender, 2001 and 2007 .............................................................................. 10
Table 2.2: Percentage of the population aged 14 years and over at risk of short-term
harm by gender, 2001 and 2007 .............................................................................. 10
Table 2.3: Percentage of the population aged 14 years and over at risk of harm in the
long term by age group, 2001 and 2007 .................................................................. 11
Table 2.4: Prevalence of DSM-IV alcohol abuse and dependence by gender .......... 13
Table 4.1: FLAGS brief intervention structure .......................................................... 53
Table 5.1: Signs and symptoms of alcohol withdrawal ............................................. 74
Table 5.2 Post-ictal signs and symptoms: comparing epilepsy and alcohol withdrawal
seizures ................................................................................................................. 100
Table 8.1: The 12 steps of Alcoholics Anonymous................................................. 171
Table 10.1: Alcohol use and physical complications .............................................. 218
4
Chapter 1
Introduction
This review covers the major treatments currently available for treating alcohol use
disorders. We have included screening and assessment as a critical component of
the treatment process. The evidence on treatment setting, brief and early intervention
with problem drinkers is reviewed. The review also covers pharmacotherapies for
alcohol dependence, a range of psychosocial interventions, motivational interviewing,
cognitive behavioural, behavioural couples and family therapy and self-directed
treatment resources such as mutual support groups. Interventions for at-risk groups
(indigenous people, pregnant women, older people, adolescents and the cognitively
impaired) are discussed. Finally, the impact of psychological and physical
comorbidity and polysubstance use upon treatment outcomes is reviewed.
The focus of the review is on evidence that has emerged since the previous literature
review, The Treatment of Alcohol Problems: a Review of the Evidence (Shand et al.
2003). Developments since that time include a significant volume of research into
brief interventions, as well as more clinical trials in the use of acamprosate and
naltrexone in relapse prevention.
We have not revisited treatments that were considered previously to have little
potential. These included aversive therapy, relaxation training, systematic
desensitisation, interpretive therapy and hypnosis. Nor does the review give
extensive coverage to interventions for which there is no new evidence.
One of the challenges of preparing a review such as this is the selection of treatment
categories. Since it is not always possible to divide treatments into discrete
categories, readers may find that there is some overlap between treatment
categories.
The review of evidence is accompanied by a comprehensive set of guidelines for the
treatment of alcohol use disorders, the Guidelines for the Treatment of Alcohol
Problems (Haber et al. 2009).
The procedure used to identify research has involved searching relevant databases
for published clinical trials, hand searching references from journal articles, searching
the web for published guidelines, and contact with major research centres for
unpublished research and other relevant guidelines. Databases searched include
Medline, the Cochrane Database of Systematic Reviews, ISI Web of Knowledge,
PsychInfo and Evidence Based Medicine Reviews. Articles were ranked on their
order of strength of evidence according to the table below.
Levels of evidence and strength of recommendations
The preferred level of evidence was a meta-analysis of randomised controlled trials.
Overall, the quality of evidence available was high: meta-analyses have been
completed for most of the major treatment modalities. Each chapter of the review
presents first the evidence from meta-analytic reviews and findings from individual
randomised controlled trials, followed by block-randomised and non-randomised
controlled trials, and, if relevant, quasi-experimental studies, case-control studies and
descriptive studies.
Quality evidence is scant for the effectiveness of treatment of specific sub-groups:
indigenous people, adolescents, and those with comorbid mental disorders. For
5
these areas, we have reviewed clinical trials where available, or otherwise relied on
expert opinion.
A randomised controlled trial refers to a study that has at least one treatment group
and a control group, usually placebo or no treatment. The study uses outcome
measures before and after treatment, and randomly assigns participants to the
groups. Some trials, normally those testing medications, also use a double blind
where neither the participants nor the researcher know who is receiving which
treatment, or a single blind design where neither the participants nor the researcher
know who is receiving which treatment. Controlled trials allow the researcher to
conclude with a degree of certainty whether or not the treatment being tested is more
effective than no treatment. Sample size is important, with larger samples giving
greater statistical power to interpret differences in outcomes between groups. In field
research with patients, this ideal design is not always possible because of ethical
concerns. However it is still possible to draw conclusions from some of these quasiexperimental studies.
Meta-analysis is a statistical technique which combines a number of single trials to
increase the overall power and certainty of outcomes, provided the correct statistical
analysis is used to control for confounding variables. The conclusions drawn, though,
might be more tentative, especially if the samples are heterogeneous.
The strength of recommendation reflects the available evidence and the clinical
importance of research. In some circumstances, clinical recommendations are not
based upon systematic evidence, but erepresent a consencus (practical or ethical)
approach, indicated as S (standard of care) (See Table 1.1).
Recommendations are included in the Review of Evidence to enable cross-reference
with the Guidelines for the Treatment of Alcohol Problems (Haber et al. 2009).
Table 1.1: Categories of evidence and strength of recommendations
Categories of evidence for causal relationships and treatment
Ia: Evidence obtained from a systematic review or meta-analysis of randomised
controlled trials.
Ib: Evidence obtained from at least one properly designed randomised controlled trial.
IIa: Evidence obtained from at least one controlled study without randomisation
(alternate allocation or some other method)
IIb: Evidence from at least one other type of quasi-experimental study
III: Evidence from non-experimental descriptive studies, such as comparative studies,
correlation studies and case-control studies
IV Evidence from expert committee reports or opinions and/or clinical experience of
respected authorities
Categories of evidence for observational relationships
I:
II:
III:
III:
Evidence from large representative population samples
Evidence from small, well-designed but not necessarily representative samples
Evidence from non-representative surveys
Evidence from expert committee reports or opinions and/or clinical experience of
respected authorities
6
Strength of recommendation
A Directly based on category I evidence
B Directly based on category II evidence or extrapolated recommendation from
category I
C Directly based on category III evidence or extrapolated recommendation from
category I or II
D Directly based on category IV evidence or extrapolated recommendation from
category I, II, or III evidence
S Standard of care
Source: Shekelle et al. 1999; Lingford-Hughes et al. 2004.
Note: This table is also included in the Chapter 1 Introduction of the Guidelines for
the Treatment of Alcohol Problems (Haber et al. 2009).
Recommended drinking limits
The Australian Government NHMRC 2009 Guidelines to Reduce Health Risks from
Drinking Alcohol (NHMRC 2009) has taken a population health approach to the
subject. Their aim was to make the information simpler and easier to remember. In
general, the Guidelines state that the risk of harm from drinking alcohol increases
with the amount consumed. A ‘standard drink’ refers to the Australian measure,
which contains 10g of ethanol.
Guideline 1 advises on reducing the risk of alcohol-related harm over a lifetime;
Guideline 2 refers to risk of injury; Guideline 3 is for young people, and Guideline 4 is
for women who are pregnant or breastfeeding.
Healthy Adults
Guideline 1: Reducing risk of alcohol-related harm
For healthy men and women, drinking no more than two standard
drinks on any day reduces the lifetime risk of harm from alcoholrelated disease or injury
Guideline 2: Reducing the risk of injury on a single occasion of drinking
For healthy men and women, drinking no more than four standard
drinks on a single occasion reduces the risk of alcohol-related injury
arising from that occasion
Minors
Guideline 3: For children and young people under 18 years of age, not drinking is the
safest option
A. Parents and carers should be advised that children under 15
years of age are at the greatest risk of harm from drinking and that
for this age group, not drinking is the safest option
B. For young people aged 15-17 years, the safest option is to delay
the initiation of drinking for as long as possible
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Pregnancy and breastfeeding
Guideline 4: Maternal alcohol consumption can harm the developing foetus or
breastfeeding baby
A. For women who are pregnant or planning a pregnancy, not
drinking is the safest option
B. For women who are breastfeeding, not drinking is the safest
option
References
Haber, P, Lintzeris N, Proude E et al. 2009, Guidelines for the Treatment of Alcohol
Problems. Canberra: Australian Government Department of Health and Aged
Care.
Lingford-Hughes, AR, S Welch and DJ Nutt 2004, Evidence-Based Guidelines for the
Pharmacological Management of Substance Misuse, Addiction and
Comorbidity: Recommendations from the British Association for
Psychopharmacology. J Psychopharmacol 18(3): 293-335.
NHMRC 2009, Australian Guidelines to reduce Health Risks from Drinking Alcohol,
National Health & Medical Research Council and Commonwealth of Australia.
Shand, F, Gates J, Fawcett J et al. 2003, The Treatment of Alcohol Problems: a
review of the evidence. Canberra: Australian Government Department of
Health and Ageing.
Shekelle, PG, Woolf SH, Eccles M et al. 1999, Clinical guidelines: developing
guidelines. BMJ 318(7183): 593-596.
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Chapter 2
Prevalence of Alcohol Consumption and
Related Harms in Australia
Key points
•
Using the 2003 definitions, on which all the available data are based, the
prevalence of high risk drinking or dependence in Australia was estimated
at 5 percent of the population; 15% were considered ‘at risk’ (considering
both definitions of long- and short-term risk of harm) drinkers; 65% were
drinking at ‘low risk’ and 15% stated they were non-drinkers
•
Patterns of alcohol misuse differ by age group, place of residence,
including regional, rural and remote areas, and also by sex and cultural
group, including Indigenous or non-Indigenous status
•
Some of the adverse effects associated with excessive alcohol use, apart
from acts of violence, accidents and injury, include higher levels of
cancers, diabetes, overweight and obesity, cardiovascular disease, and
other nutritional deficiencies, as well as mental health effects including
cognitive impairment
•
Alcohol related harm can also result from the intoxicating effects of the
drug and also from its long term toxicity; this includes cancer of the liver
and the digestive system (including not only the bowel and colon, but also
the mouth and throat) and damaging effects on the brain, the heart, the
pancreas, and the peripheral nerves.
Introduction
As is well known, alcohol is commonly consumed in Australia; 83% of the population
in the 2007 Drug Strategy Household Survey aged over 14 years reported drinking
alcohol in the previous 12 months (AIHW 2008). Between 1996-7 and 2004-5,
apparent alcohol consumption (quantity consumed divided by the population aged
over 15 years) remained stable at 9.8 litres per person per annum, after declining
from 11.5 in 1990 (AIHW 2007). Australia ranks 14th among the OECD (Organisation
for Economic Co-operation and Development) countries for per capita pure alcohol
consumption, with the UK at 9th place (11.5 litres) and New Zealand at 17th with 9.4
litres (AIHW 2007). Wine consumption has grown over the last 40 years, while beer
has remained stable in comparison; however beer remains dominant in apparent
consumption, with 4.6 litres consumed per person, wine at 3.1 and spirits at 2.1 litres.
Patterns of consumption
The most comprehensive estimate of patterns and prevalence of drinking in Australia
has been obtained from the National Drug Strategy Household Survey which is
conducted every three years (AIHW 2002, 2005, 2008). It is recognised that one of
the drawbacks of population surveys include the omission of people who are not
living in households, such as the homeless and those in institutions, as well as those
who refuse to participate. This is taken into account by weighting and is somewhat
counterbalanced by the large sample sizes taken, 25,000 respondents in the case of
the 12th National Drug Strategy Household Survey and 10,600 in the National Survey
of Mental Health and Wellbeing 1997 (Hall et al. 1999).
9
Results from the 2007 National Drug Strategy Household Survey suggest that current
patterns of alcohol consumption are similar to those reported in 1998 and in 2001;
the main difference from 2001 to 2007 was that slightly fewer people are abstinent
and more are drinking at risky levels (AIHW 2008). The proportion of daily drinkers
fell significantly between 2004 and 2007 (from 8.9% to 8.1%).
In 2007, 72.6 percent of all persons aged 14 years and over consumed alcohol in
quantities considered to be low risk to health in the long-term and 17.1 were
abstainers (AIHW 2008). It was estimated that 6.9 percent of the population
consumed alcohol in a manner considered risky and a further 3.4 percent consumed
alcohol in a manner considered to be high risk to health in the long term (total 10%).
However the National Health Survey 2004-5 showed that 13% of people consumed
alcohol at levels which, if continued, would be risky to their health, compared with
11% in 2001 (ABS 2006).
Gender differences in patterns of consumption
Clear gender differences in patterns of alcohol consumption exist. On average men
usually begin drinking at a younger age than women (16 years compared to 18
years), and widespread problems in the areas of alcohol misuse and violence have
been identified as major health policy issues for men. Further, females are more
vulnerable to both the acute and chronic effects of alcohol misuse than males.
Females are more likely than males to be non-drinkers and males are more likely
than females to consume alcohol at levels considered high risk in the long term
(Table 2.1). Males are more likely than females to put themselves at risk of harm in
the short term (Table 2.2) and are almost twice as likely to drink daily (AIHW 2008).
Table 2.1: Percentage of the population aged 14 years and over at risk of longterm harm by gender, 2001 and 2007
Males
Females
Persons
Abstinent %
2001 (2007)
14.1 (14.0)
20.8 (20.1)
17.5 (17.1)
Low risk %
2001 (2007)
75.6 (75.8)
69.8 (69.4)
72.7 (72.6)
Risky %
2001 (2007)
6.7 (6.2)
7.2 (7.6)
7.0 (6.9)
High risk %
2001 (2007)
3.5 (3.9)
2.2 (2.8)
2.9 (3.4)
Overall, 35 percent of persons aged 14 years and over put themselves at risk of
alcohol-related harm in the short term at least once over a 12-month period, and
almost 8 percent place themselves at risk for short-term harm at least weekly. At all
ages, greater proportions of the population drink at risky or high-risk levels for shortterm harm, compared with risk for long-term harm (AIHW 2005).
Table 2.2: Percentage of the population aged 14 years and over at risk of shortterm harm by gender, 2001 and 2007
Males
Females
Persons
At least yearly %
2001 (2007)
15.5 (15.1)
12.7 (13.4)
14.1 (14.2)
At least monthly %
2001 (2007)
15.3 (14.3)
11.6 (10.9)
13.4 (12.6)
At least weekly %
2001 (2007)
8.5 (9.3)
5.3 (6.2)
6.9 (7.8)
10
Age differences in patterns of consumption
The proportions of Australians aged 14 years or over abstaining from alcohol
increased significantly between 2004 and 2007, with a greater change seen among
males than females (AIHW 2008). However, people in the 20-29 year age group
were most likely to consume alcohol at a level that put them at risk for long-term
(chronic) and short-term harm and were the least likely to abstain (Tables 2.3 and
2.4).
Rates of abstinence, therefore, are lowest in the 20-29 years age group; however
they tend to increase with increasing age (Table 2.3).
Table 2.3: Percentage of the population aged 14 years and over at risk of harm
in the long term by age group, 2001 and 2007
Age group
14-19
20-29
30-39
40-49
50-59
60+
Abstinent %
2001 (2007)
26.2 (29.0)
9.9 (12.9)
13.0 (12.2)
13.9 (12.4)
17.1 (14.0)
27.1 (24.7)
Low risk %
2001 (2007)
62.1 (62.2)
75.4 (71.1)
78.3 (77.5)
76.5 (76.8)
73.3 (75.6)
66.8 (68.9)
Risky %
2001 (2007)
8.0 (5.6)
10.2 (10.2)
6.3 (7.0)
7.1 (7.7)
6.6 (6.5)
4.4 (4.8)
High risk %
2001 (2007)
3.7 (3.2)
4.5 (5.8)
2.5 (3.3)
2.6 (3.1)
2.9 (3.9)
1.6 (1.6)
Table 2.4: Proportion of the population aged 14 years and over at risk of harm
in the short term by age group, 2001 and 2007
Age group
Risky and high risk*
At least yearly
At least monthly
At least weekly
2001 (2007)
2001 (2007)
2001 (2007)
14-19
13.4 (12.9)
20.5 (17.2)
10.7 (9.1)
20-29
21.1 (19.8)
27.3 (24.9)
12.0 (14.7)
30-39
20.5 (20.3)
16.5 (15.3)
6.3 (8.4)
40-49
16.0 (17.6)
11.1 (12.3)
6.2 (7.5)
50-59
10.2 (11.6)
6.4 (7.1)
5.8 (6.3)
60+
3.7 (5.1)
2.4 (3.2)
2.6 (2.7)
* For males, the consumption of 7 or more standard drinks on any one day; for
females 5 or more.
Alcohol consumption among Indigenous Australians
Although the overall proportion of Indigenous Australians who drink alcohol (71
percent) is smaller than in the general population (82 percent), those who do drink
tend to drink in larger and more harmful quantities (AIHW 2007). Twenty percent of
Indigenous Australians report drinking at risky or high-risk levels for long-term harm.
National statistics show that:
•
•
Heaviest drinking occurs amongst Aboriginal and Torres Strait Islander
people aged 25–34 years, while hazardous drinking in the general population
is most common among people aged 14–24 years
15% of Aboriginal and Torres Strait Islanders consume alcohol at risk of long
term alcohol related harm, compared to 9.8% of non-Indigenous Australians
11
•
31% of Aboriginal and Torres Strait Islanders had not consumed alcohol in
the last 12 months, compared to 13% of non-Indigenous Australians (AIHW
2007).
Alcohol- related harm - Indigenous people
•
•
•
•
Over the 5 year period from 2000 to 2004, an estimated 1,145 Indigenous
Australians died from alcohol-related injury and disease caused by drinking
Suicide (19%) and alcoholic liver cirrhosis (18%) account for almost 40% of
all alcohol-attributable deaths among Indigenous men
Alcohol liver cirrhosis (27%) haemorrhagic stroke (16%) and fatal injury
caused by assault 910%) are the most common causes of alcohol-attributable
death among Indigenous women
Average age at death from alcohol-related causes among Indigenous people
is about 35 years (Chikritzhs et al. 2007).
Alcohol-related harm in general
Alcohol is estimated to cause a net harm of 4.4% of the global burden of disease,
indicating that the beneficial effects of alcohol are small compared to the detrimental
effects. Alcohol causes a greater health burden for men than for women.
Neuropsychiatric disorders, mainly made up of alcohol use disorders, constitute the
category linked to most alcohol-attributable burden of disease, with unintentional
injury being the second most important category. Contrary to the assumption by
many that cirrhosis is the most important form of alcohol induced morbidity and
mortality, it only contributes to 10% of the burden of disease caused by alcohol. The
health burden is considerable both for acute and chronic health consequences
(World Health Organization 2007).
In Australia, alcohol consumption in total causes over 5000 deaths per year, and for
each death about 19 years of life are prematurely lost. The burden of deaths is
distributed unevenly across the population, with males being over-represented in
mortality and morbidity statistics compared to females, as are those living in nonmetropolitan regions compared to metropolitan regions. Problems associated with
drinking to intoxication are also unevenly distributed; with chronic diseases occurring
among people aged over 30 years, whereas deaths and hospitalisations, largely
caused by road accidents and violent assault, are much more common among
younger people. This may be attributed to different drinking patterns between
younger and older age groups (Chikritzhs et al. 2003).
Regional variations in alcohol-related harms
•
•
•
Rates of alcohol-caused death and hospitalisation were higher in nonmetropolitan than in metropolitan areas; the bulk of this was associated
with the effects of intoxication
The Northern Territory had the highest percentages of people aged 15
years or older who drank at risky or high-risk levels for acute harm (30% at
least monthly) and for chronic harm (18%) in 2001
The Northern Territory also had the highest alcohol-caused death and
hospitalisation rates of all jurisdictions; however Western Australia and
Queensland also had higher rates than other States (Chikritzhs et al.
2003).
12
Mental health
The 1997 National Survey of Mental Health and Well-Being, the first such national
survey conducted in Australia, examined the prevalence of alcohol and other
substance use disorders in the population aged 18 years and over. The prevalence
of alcohol dependence was estimated to be 3.5 percent, and 3 percent for harmful
use, using ICD-10 criteria (Hall et al. 1999), and using the DSM-IV-TR criteria for
substance dependence, the prevalence of dependence was 4.1%, with 75% of these
being male and 60% in the 18-34 year age group (Proudfoot and Teesson 2002).
This survey was conducted again between August and December 2007 but the
results were not available at the time of writing. Table 2.4, therefore, represents
figures from the 1997 survey. Men are more likely to meet criteria for an alcohol use
disorder than women, and prevalence also decreases with age; compared with those
aged 55 or older, people aged 18-34 were 6.4 times more likely to have an alcohol
use disorder.
Table 2.4: Prevalence of DSM-IV alcohol abuse and dependence by gender
Males
Females
Persons
Harmful use %
4.3
1.8
3.0
Dependence %
5.2
1.8
3.5
Source: (Hall et al. 1999)
Data from the 2007 Drug Strategy Household Survey report that high-risk drinkers
were twice as likely as low-risk drinkers (15.3% vs. 8.5%) to experience high or very
high levels of psychological distress, as measured by the Kessler-10; however risky
drinkers and abstainers were equally likely to experience high or very high levels of
distress (AIHW 2008).
Physical health
In general, higher overall levels of consumption in a population are associated with
higher levels of alcohol-related problems. Overall population levels of alcohol
consumption have been related to total mortality and to specific causes of death and
disease including liver cirrhosis, traffic accidents, suicide and criminal violence.
However, the greatest alcohol-related harm may come from problem drinkers who
are not likely to be alcohol dependent, compared with the minority who are, due to
the relatively larger numbers of the former. Particularly high rates of alcohol-related
harm have been found among low and moderate level drinkers on the occasions they
drink to intoxication. One US population-based survey reports that including binge
drinking into their calculations of average daily consumption and comparing it with
standard quantity- frequency questions raised the level of heavy drinking by 19% to
42%, (Stahre et al. 2006) and as a result half of female binge drinkers and half of
binge drinkers aged 55 and older met the criteria for heavy drinking. The former and
the recently updated NHMRC guidelines therefore consider pattern as well as
quantity of weekly consumption in considering level of risk associated with drinking.
It becomes even more important, when taking into account the reported surge in
binge drinking among young people, that reducing harm associated with lowdependent drinking patterns, such as episodes of intoxication, is at least as important
as reducing harm associated with average consumption level.
13
The relationship between consumption and harm varies substantially among age and
sex cohorts, since alcohol-related risk status is not necessarily stable over a person’s
lifetime (e.g. young people and males are at greater risk of harm) and also varies
between different defined sub-populations (e.g. Indigenous groups, those operating
machinery or driving vehicles, and pregnant women are at greater risk of harm) and
between different drinking situations (e.g. greater mortality and morbidity associated
with drink driving in rural areas). However, the general pattern of the relationship
between drinking and alcohol-related harm remains.
Low risk alcohol consumption is thought to have some health benefits, especially in
older men, where an association was found between moderate alcohol consumption
and decreased risk of myocardial infarction (Mukamal et al. 2003). Australian
studies, however, have found that benefits occur for women (Powers and Young
2008) but not for men, specifically when wine is the drink taken (Harriss et al. 2007).
Nevertheless, the evidence for other benefits is conflicting. Rather than a linear
relationship between consumption and harm, the relationship has been shown to be
U-shaped, where overall, moderate drinkers have better physical and outcomes than
either non-drinkers or heavy drinkers (O'Keefe et al. 2007). These authors warn that
the hypothesis is a two-edged sword; while there is evidence to show that light
drinking on a daily basis may significantly reduce the risks of coronary heart disease
and all-cause mortality, excessive alcohol intake and binge drinking are implicated in
types of cancer and are detrimental to the heart, liver and overall health. It is not
recommended, therefore, for non-drinkers to start drinking in order to gain indefinable
health benefits.
Social costs
The overall effects of alcohol-related harm extend beyond the individual to include
social and economic costs of harm to families, communities and society at large
(World Health Organization 2007). Alcohol abuse or intoxication is implicated in
violence, both domestic and public, unemployment, financial problems and poverty,
drink driving, traffic accidents, industrial and work accidents, fires, falls, and suicide
(Crombie et al. 2007).
There has been growing concern in the media both in Australia and in the UK and
Europe over youth drinking, especially binge drinking, and its association with
violence and accidents. One study that examined data from several Victorian
(Australia) surveys reports inconclusive evidence in this regard; both the Victorian
Emergency Minimum dataset and the Victorian Admitted Episodes dataset show an
increasing trend in hospitalisation for alcohol-related causes among people aged 1824 years between 1999-2006 (Livingston 2008). Contradictory results provided by the
Victorian Population Health Survey and the Victorian Youth Alcohol and Drug Survey
found no increases in rates of risky drinking among young people; the authors
conclude it is possible that, while the proportion of young people drinking at levels
that exceed NHMRC guidelines has not changed, more are drinking at extremely
high levels and thus are ending up in hospital (Livingston 2008).
Overall the proportion of respondents to the Drug Strategy Household Survey who
reported that they were likely to undertake potentially harmful activities while under
the influence of alcohol remained relatively stable between 2004 and 2007- in every
case males were more likely to undertake such activities. In 2007, 12.1 percent of
adults admitted to driving a motor vehicle while under the influence of alcohol (AIHW
2008). This figure fell slightly from 13.4% in 2004.
14
Since 1995, there has been a slow decrease in those who experienced verbal abuse
in the previous 12 months; down from 33 percent to 26.5 percent in 2001, to 24.9% in
2004 and 25.4% in 2007; the level of physical abuse (as victim) remained steady at
4.5%.
References
ABS 2006, National Health Survey 2004-5 Summary of Results. Cat no 4364.0.
Canberra: Australian Bureau of Statistics.
AIHW 2002, 2001 National Drug Strategy Household Survey. Canberra: Australian
Institute of Health & Welfare.
AIHW 2005, 2004 National Drug Strategy Household Survey. First results. AIHW cat
no. PHE 57. Canberra: Australian Institute of Health & Welfare.
AIHW 2007, Statistics on Drug Use in Australia 2006. Canberra: Australian Institute
of Health & Welfare.
AIHW 2008, 2007 National Drug Strategy Household Survey. First results. .
Canberra: Australian Institute of Health & Welfare.
Chikritzhs, T, Catalano P, Stockwell T et al. 2003, Australian Alcohol Indicators,
1990-2001: patterns of alcohol use and related harms for Australian States
and Territories. Perth and Melbourne, National Drug Research Institute,
Curtin University of Technology and Turning Point Alcohol & Drug Centre.
Chikritzhs, T, Pascal R, Gray D et al. 2007, Trends in alcohol-attributable deaths
among Indigenous Australians, 1998-2004. National Alcohol Indicators. Perth,
National Drug Research Institute, Curtin University of Technology.
Crombie, IK, Irvine L, Elliott L et al. 2007, How do public health policies tackle
alcohol-related harm: a review of 12 developed countries. Alcohol Alcohol
42(5): 492-499.
Hall, W, Teesson M, Lynskey M et al. 1999, The 12-month prevalence of substance
use and ICD-10 substance use disorders in Australian adults: finding from the
National Survey of Mental Health and Well-Being. Addiction 94(10): 15411550.
Harriss, LR, English DR, Hopper JL et al. 2007, Alcohol consumption and
cardiovascular mortality accounting for possible misclassification of intake:
11-year follow-up of the Melbourne Collaborative Cohort Study. Addiction
102(10): 1574-1585.
Livingston, M 2008, Recent trends in risky alcohol consumption and related harm
among young people in Victoria, Australia. Aust N Z J Pub Health 32(3): 266271.
Mukamal, KJ, Conigrave K, Mittleman MA et al. 2003, Roles of drinking pattern and
type of alcohol consumed in coronary disease in men. N Eng J Med 348(2):
109-118.
15
O'Keefe, JH, KA Bybee and CJ Lavie 2007, Alcohol and Cardiovascular Health: The
Razor-Sharp Double-Edged Sword. J Am College Cardiol 50(11): 1009-1014.
Powers, JR and AF Young 2008, Longitudinal analysis of alcohol consumption and
health of middle-aged women in Australia. Addiction 103(3): 424-432.
Proudfoot, H and M Teesson 2002, Who seeks treatment for alcohol dependence?
Findings from the Australian National Survey of Mental Health and Wellbeing.
Soc Psych Psych Epidemiol 37(10): 451-456.
Stahre, M, Naimi T, Brewer R et al. 2006, Measuring average alcohol consumption:
the impact of including binge drinks in quantity-frequency calculations.
Addiction 101: 1711-1718.
World Health Organization 2007, WHO Expert Committee on Problems Related to
Alcohol Consumption. World Health Organization. Available at:
http://www.who.int/substance_abuse/expert_committee_alcohol/en/index.html
16
Chapter 3
planning
Screening, assessment and treatment
Screening, assessment and diagnosis play a critical role in treatment planning and
clinical management. The level of detail collected during assessment will vary across
treatment settings and circumstances. In primary care settings such as general
medical practices and hospitals, screening is recommended to identify hazardous or
dependent drinkers.
Screening
Screening is intended to indicate the presence or absence of certain problems that
might need further investigation. It can lead to early intervention for problem drinkers
(see Chapter 4, Brief interventions), further investigation and problem management
as the setting or referral to specialist services if the client requires more intensive
assessment and treatment.
Risky drinking needs to be identified and targeted in its early stages, in order to
reduce its impact on the individual and the community. It is far more prevalent than
dependent drinking (AIHW 2008).
Where to screen?
Given the pervasiveness of risky alcohol consumption in Australia and the
seriousness of the health consequences of risky drinking, detection of risky alcohol
consumption has been evaluated in a wide range of health care settings.
General practice and relevant specialist settings
In routine general practice, without specific screening techniques, up to 70 percent of
risky/high risk drinkers are not detected (Reid et al. 1986). As indicated in the
Cochrane review by Kaner et al (2007), a number of studies, but not all, have shown
that screening and brief interventions are effective in primary care settings. There is
Australian evidence that screening and early intervention in primary care settings is
cost-effective (Wutzke et al. 2001).
One study examined current practices and barriers for screening and interventions
with primary care patients across randomly selected clinics in a large health care
system in the USA. Focus groups and mailed structured surveys were sent to
practising GPs. Results indicated that 85% of patients treated in primary care
received some screening for alcohol use disorders (Barry et al. 2004). However
CAGE was the predominant screening tool; the drawback of this approach is that the
primary clinical focus falls on patients who meet abuse/dependence criteria. This
shows the importance of using an appropriate screening instrument. Lack of time
was the most important perceived barrier to implementing screening and brief
interventions for problem drinkers.
Another study examining barriers to screening conducted focus groups with primary
care practitioners (GPs) in Pennsylvania. Their key barriers included lack of time,
lack of access to treatment, and financial resources, both from the patient
perspective and their own, of reimbursement from insurers. Additional barriers
17
included the negative attitude toward AOD use, their lack of self-efficacy in managing
AOD use disorders, and lack of knowledge in this area (Holland et al. 2009).
However, screening is the most important first step towards identification of problems
and has been proven valuable in other common conditions such as raised
cholesterol. GPs are well placed to undertake this important first step, as 85% of the
Australian population have contact with a GP annually. Moreover, one
comprehensive study (of 78,974 adult patients from 2470 GPs in Australia) found that
heavy drinkers (n = 5,753) were more likely to see their GP for management of
chronic problems, psychological problems and physical injuries than were light- or
non-drinkers (Proude et al. 2006), thus providing perfect opportunities for early
intervention.
A number of initiatives to encourage screening were undertaken as part of the
Smoking, Nutrition, Alcohol and Physical Activity (SNAP) Framework for General
Practice (Harris et al. 2005). The Drink-Less package, developed by the University of
Sydney in 1990s (Gomel et al. 1994) and revised and re-released in 2004 (Proude et
al. 2005; Proude et al. 2006), has been implemented mainly within NSW, although it
has been used in other countries, notably the UK (Institute of Health & Society,
Newcastle University, Gateshead).
Screening and brief interventions are feasible in specialist settings where prevalence
of alcohol use is high such as opioid treatment services (Watson et al. 2007) and
sexual health services (Lane et al. 2008). See also Chapter 4.
Hospital settings, including emergency, mental health and general wards
Several studies have shown that alcohol use disorders are commonly not identified in
hospitalised patients (Proude et al. 2008; Shourie et al. 2007; Williams et al. 2008).
Screening and brief interventions in emergency departments have proved to be
effective in reducing risky levels of alcohol intake and binge drinking episodes (see
Chapter 4).
It is considered a good clinical practice to provide routine screening procedures for
excessive alcohol consumption among inpatients and outpatients and have
procedures for appropriate intervention in all hospital settings.
Notwithstanding this consensus recommendation, studies in medical and surgical
wards have not shown improved health outcomes as a consequence of screening
and intervention for alcohol disorders in hospital inpatients (Shourie et al. 2007),
(Saitz et al. 2007). However, the major benefit may lie in earlier recognition
prevention and treatment of alcohol withdrawal and alcohol-related medical toxicity.
Welfare and general counselling services
In these settings, there is a need to develop a structure where screening can occur in
a routine way, thereby increasing the likelihood that it will become and will remain a
part of the normal for detecting unsafe drinking patterns (Piccinelli et al. 1997a).
However, there are significant barriers to the widespread adoption of screening and
intervention procedures. For instance, there are few incentives and some
disincentives to primary health caseworkers and others becoming involved in
screening activities (Babor et al. 2005).
18
The Workplace
There is evidence of high rates of problem drinking in some of these settings,
suggesting that the workplace is a suitable venue for detection of risky drinking and
intervention (Richmond et al. 2000; Roche et al. 2008). Detection of unsafe alcohol
consumption should form part of any routine health evaluation in the workplace.
Although appealing in concept, brief intervention is not always effective in this setting
(Anderson and Larimer 2002; Matano et al. 2007), and strategies for more intensive
interventions have not been well studied (see also Chapter 4). Accordingly,
widespread implementation of brief intervention in this setting cannot be
recommended at this time.
Workplace occupational health and safety procedures should identify appropriate
strategies and referral options for those workers identified as having alcohol-related
problems.
Recommendation
3.1 Screening for risk levels of alcohol
consumption and appropriate intervention
systems should be widely implemented in
general practice and emergency departments.
3.2 Screening for risk levels of alcohol
consumption and appropriate intervention
systems should be widely implemented in
hospitals.
3.3 Screening for risk levels of alcohol
consumption and appropriate intervention
systems should be widely implemented in
community health and welfare settings.
3.4 Screening for risk levels of alcohol
consumption and appropriate intervention
systems should be widely implemented in highrisk workplaces.
Strength of
recommendation
A
Level of
evidence
Ia
D
IV
D
IV
D
IV
How to screen?
The methods for detecting risky drinkers include quantity-frequency estimates of
alcohol consumption, screening questionnaires, physical examination for intoxication
or signs of harmful use of alcohol and biological markers of excessive alcohol
consumption.
Evaluation of all methods for assessing alcohol intake suffers from the absence of a
“gold standard” against which they can be tested.
Quantity-frequency estimates
A quantitative alcohol history can be a reliable method of detecting risk patterns of
alcohol consumption. It comprises the daily average consumption (grams per day or
standard drinks per day) of alcohol, the number of drinking days per week (or month)
and the pattern of drinking. Where use exceeds recommended NHMRC guidelines, a
more detailed assessment is indicated to exclude harmful use and/or dependence.
19
Recommendation
3.5 Quantity–frequency estimates is the
recommended way to detect levels of
consumption in excess of the NHMRC 2009
guidelines in the general population.
Strength of
recommendation
D
Level of
evidence
IV
Screening questionnaires
In specialist alcohol and drug treatment settings, diagnostic interviews and
questionnaires help to assess the severity of alcohol dependence, including
consumption levels, so that appropriate treatment goals and strategies can be
selected. A range of questionnaires is available for both uses.
The list of assessment instruments reviewed below is by no means exhaustive. For a
more comprehensive review of alcohol and other drug instruments, see Teesson et
al. (2000). For a review of screening and diagnostic tools for other substances and
mental disorders, see the review by Dawe et al. (2002).
Validated alcohol screening questionnaires include the Alcohol Use Disorders
Identification Test (AUDIT) and its short version, AUDIT-C, the Michigan Alcoholism
Screening Test (MAST) and its shortened versions, b-MAST, S-MAST, CAGE, TACE and TWEAK. To be effective, a questionnaire needs to be sensitive (capable of
correctly identifying patients with the condition) and specific (capable of
discriminating those who do not have the condition). Thus, a sensitivity of 0.90
indicates that 90 percent of those with the condition will be correctly identified; and a
specificity of 0.90 indicates that the test correctly identifies 90 percent of those who
do not have the condition.
Alcohol Use Disorders Identification Test
The AUDIT is a 10-item instrument designed to screen for a range of drinking
problems, particularly hazardous and harmful consumption. A cut-off score of 8 is
used to identify risky drinkers. Developed by a World Health Organisation (WHO)
collaborative study in six countries, it is the only questionnaire designed for
international use and has been translated into several languages. The questions
cover four conceptual domains: alcohol consumption, drinking behaviour, adverse
reactions and alcohol-related problems (Saunders et al. 1993). For more detailed
administration and scoring information, refer to the World Health Organization
Guidelines (Babor et al. 1992). It effectively distinguishes between risky and nonrisky drinkers, identifies dependent drinkers, and has cross-cultural validity. It is
short (10 items) may be self-administered, and is suitable for primary health care
settings.
Its short version, AUDIT-C (the first 3 questions of AUDIT) also performs well at
identifying alcohol misuse (Bradley et al. 2007), especially in primary care. A score of
3 or above for women, or 4 and above for men, has maximum sensitivity and
specificity (Bradley et al. 2007; Dawson et al. 2005).
AUDIT-C has been used successfully with male Veterans’ Affairs patients to screen
for heavy drinking, performing similarly to the full AUDIT. Patients were considered to
be heavy drinkers if they drank more than 14 drinks a week or five or more drinks on
one occasion in the past or a typical month (Bush et al. 1998).
20
The third question of the AUDIT taken alone (AUDIT-3), has been shown to have
almost as good sensitivity and specificity as the longer forms (level 1 evidence)
(Bradley et al. 2007).
At a cut-off score of eight to identify hazardous and harmful drinking, the full AUDIT
has demonstrated a sensitivity of 0.92 and specificity of 0.94 (Saunders et al. 1993).
When validated against a diagnostic interview, physical examination and laboratory
tests, the AUDIT was better than the MAST at distinguishing between hazardous and
non-hazardous drinkers (Fiellin et al. 2000). Both instruments effectively identified
dependent drinkers. The AUDIT performed as well as the MAST and the CAGE when
validated against Composite International Diagnostic Interview (CIDI) scores for
dependent drinking and had higher sensitivity and specificity for detecting risky, nondependent drinking (Piccinelli et al. 1997b).
MAST and CAGE questionnaire
The prototype alcohol dependence questionnaire is the MAST (Selzer 1971).
Instruments such as the MAST and the CAGE questionnaire were derived on the
basis of their ability to distinguish chronic alcohol dependent individuals from nonalcohol dependent individuals (Mayfield et al. 1974).
The MAST is a 24-item instrument designed to identify alcohol abuse and
dependence. It has adequate sensitivity and specificity at a cut-off score of 13 in
identifying both of these disorders, but is very long, taking at least 10 minutes. The SMAST, a shorter 13-item version of the MAST, has also demonstrated good reliability
as a self-administered questionnaire. However there is little recent published
research on these instruments. The Brief Michigan Alcohol Screening Test (b-MAST)
has been recently validated against AUDIT, found significantly correlated, and proved
effective in measuring severity of problem drinking in a treatment-seeking population
(Connor et al. 2007). The MAST and its shorter versions have been criticised for their
lack of sensitivity in detecting alcohol problems among women (Dawe et al 2002).
The CAGE is a four-item screening instrument intended to identify alcohol abuse and
dependence. Because of its brevity, it is less sensitive than the AUDIT or the MAST.
It is not a diagnostic instrument, however a ‘yes’ to two or more questions indicates
the need for further assessment for alcohol abuse (Mayfield et al. 1974).
In a study with drink drivers, the MAST correlated more highly than the AUDIT with
the Diagnostic and Statistical Manual (DSM-IV) criteria for alcohol use disorders,
although both had acceptable internal validity (Conley 2001). Almost no new
literature has been found in this area; one study examined the test-retest reliability of
a new instrument to assess intoxicated driving, the FORM 90-DWI (Hettema et al.
2008) and found it demonstrated high levels of reliability for this purpose. However,
this is not a brief screening test as it takes 45 minutes to administer.
Japanese translations of AUDIT and CAGE have also been tested against a semistructured interview diagnosis; results showed that AUDIT had superior sensitivity
and specificity for detecting dependent and problem drinkers (Volk et al. 1997).
CAGE was found to have poor validity with a sample of USA university students
(Heck and Lichtenberg 1990).
When used with a group of drug-dependent patients, the AUDIT and the MAST were
equally able to detect alcohol dependence, but the AUDIT was better at identifying
21
hazardous drinking (Skipsey et al. 1997). The AUDIT has also been evaluated in
psychiatric patients and in one study demonstrated very high sensitivity and
specificity at detecting alcohol abuse using a cut- off of 10 (Cassidy et al. 2008). The
AUDIT-C also performed well against the S-MAST and CAGE in detecting risk
drinking among people with any past-year mood disorder (Dawson et al. 2005). In
another study of patients affected by a mood disorder, AUDIT and CAGE were
compared with the first 2 questions of the NIAA guide (“do you sometimes drink
alcohol?” and “how many times in the past year have you had 5 drinks [men] 4
[women] in a day?”). Both instruments achieved high sensitivity, using a cut-off of 5
for AUDIT and 1 for CAGE (Agabio et al. 2007).
Overall it appears that the AUDIT is superior to other instruments in detecting various
aspects of a range of alcohol problems. CAGE is proven to be insufficient to detect
lower levels of alcohol abuse among primary care patients, and conventional
laboratory tests were proved in at least one study to be of no use in this setting
(Aertgeerts et al. 2001).
The AUDIT can be also used effectively to identify hazardous, problem and
dependent alcohol consumption amongst psychiatric patients; AUDIT-C can be used
to detect alcohol use disorders, using a cut-off of 5 (Dawson et al. 2005).
Other questionnaires
The Alcohol, Smoking and Substance Involvement Screening Test (ASSIST) is a
useful screening questionnaire, recommended by the World Health Organization,
which includes alcohol with other substances (World Health Organization 2002).
A number of other screening instruments have been developed to overcome the
limitations of existing inventories. These are most useful for research rather than
clinical settings and are not considered further in these guidelines.
Recommendation
3.6 AUDIT is the most sensitive of the currently
available screening tools and is recommended
for use in the general population.
Strength of
recommendation
A
Level of
evidence
I
Screening for alcohol use in special populations: Pregnant Women
The NHMRC guidelines recommend that it is safest to consume no alcohol during
pregnancy (NHMRC 2009). The low levels of consumption highlighted as a concern
in recent guidelines cannot be identified using current questionnaires. A clinical
history to estimate the quantity and frequency of alcohol use is the preferred method.
In light of the potential for adverse effects on the foetus, screening for alcohol use
should be included in the usual antenatal history. All pregnant women should be
asked about their level of alcohol consumption.
TWEAK and T-ACE questionnaires
22
Two screening instruments – TWEAK and T-ACE – have been developed for use
with pregnant women. Both were designed in the 1980’s.
TWEAK is a modified five-item version of MAST and has five items; a score of two or
more suggests the patient is drinking at risky levels. Further assessment should be
recommended.
T-ACE consists of three CAGE questions and a tolerance question (see Appendix 1).
It is quick and easy to administer; a score of two or more indicates the patient may be
drinking at risky levels, and should be further investigated.
Both T-ACE and TWEAK are more specific and sensitive than either MAST or CAGE
in identifying risky drinking levels (Russell et al 1994). TWEAK and T-ACE have been
tested against CAGE with pregnant women in Brazil and both were found to be
clearly more reliable than CAGE (Moraes et al. 2005). TWEAK and AUDIT also both
perform better than the CAGE when validated against standard cut-off points on the
Composite International Diagnostic Interview (CIDI)(Piccinelli et al. 1997b).
Both Both T-ACE and TWEAK identify levels of drinking associated with a significant
risk of fetal alcohol-related harms and, until new tools are developed to better reflect
the NHMRC 2009 guidelines, can be recommended for use in this population.
The ASSIST questionnaire that screens for alcohol and other substances can also be
used in this population (World Health Organization 2002).
Recommendation
3.7 In pregnant women, quantity–frequency
estimation is recommended to detect any
consumption of alcohol. T-ACE and TWEAK
questionnaires may be used in this population to
detect consumption at levels likely to place the
foetus at significant risk of alcohol-related harm.
Strength of
recommendation
D
Level of
evidence
IV
Physical examination for intoxication or signs of harmful use of alcohol
Clinical presentations related to alcohol use cover a diverse spectrum, varying across
health and welfare settings: a characteristic is multiplicity of problems across these
domains.
Certain physical disorders or signs are indicative of hazardous alcohol use. Common
physical indicators include hypertension, a pattern of accidents, dilated facial
capillaries, blood shot eyes, hand or tongue tremor, history of gastrointestinal
disorders, duodenal ulcers and cognitive deficits (Saunders and Hanratty 1990;
Skinner et al. 1986). Conditions such as liver cirrhosis and pancreatitis are commonly
alcohol-induced. More subtle signs include job, financial, marriage and relationship
problems, insomnia, depression and anxiety, and domestic violence (Scouller et al.
2000).
Whilst the above problems are indicative of alcohol misuse, it should be noted that
they are not conclusive, nor does their absence rule out the existence of hazardous
alcohol consumption.
23
However, patients presenting with such problems should be screened for alcohol
use, and if appropriate, proceed to a more comprehensive assessment. General
practitioners and other health and welfare workers encountering these presentations
should have screening systems in place.
Biological markers of excessive alcohol consumption
Biological markers of excessive alcohol use include direct measures of alcohol (e.g.
alcohol in breath or blood) and a range of indirect indices such as liver enzymes
activity, the levels of carbohydrate-deficient transferrin, characteristics of blood
erythrocytes (e.g. mean corpuscular volume) and others.
Measures of alcohol levels
Alcohol concentrations may be measured in breath, blood and urine. Use of breath
alcohol testing has been incorporated into Emergency Department practice by a
number of groups (Cherpitel 1995; Robinson et al. 1992; Walsh and Macleod 1983)
as part of screening and brief intervention programs. There is evidence that such
programs prevent readmission with alcohol-related trauma (Longabaugh et al. 2001).
False positive detection may result from technical failure but may also be rarely
encountered in low levels due to endogenous production of ethanol (Spinucci et al.
2006). Endogenous production of ethanol by yeasts is accentuated by
gastrointestinal stasis and dietary sucrose and is reduced by antibiotics (Baraona et
al. 1986).
Recommendation
3.8 Direct measures of alcohol in breath and/or
blood can be useful markers of recent use and
in the assessment of intoxication.
Strength of
recommendation
D
Level of
evidence
II
Indirect Markers
A number of biological markers can be used to detect alcohol consumption:
gamma glutamiltransferase (GGT), aspartate aminotransferase (AST), alanine
aminotransferase (ALT), mean cell volume (MCV), carbohydrate-deficient transferrin
(CDT) and uric acid (Conigrave et al. 2003; Hannuksela et al. 2007).
Serum GGT, a liver enzyme, is elevated in 60-80 percent of alcohol dependent
people (Conigrave et al. 2002). CDT has similar sensitivity to GGT but higher
specificity (Scouller et al. 2000). CDT results vary depending on the laboratory
method used (the more commonly used modified test is less sensitive than the
original test) and consequently may be no more sensitive than GGT (Scouller et al.
2000).
A multi-site international study comparing CDT, GGT and AST found that CDT was
little better than GGT in detecting high- or intermediate-risk alcohol consumption,
although both were better than AST. CDT and GGT levels were influenced by body
mass index, sex, age, and smoking status (Conigrave et al 2002). False positives
occur with most CDT test kits in the presence of advanced liver disease of any cause
(Anton et al. 2001).
24
CDT and GGT are used in some clinical settings, however with a clinical detection
rate of around 30-40 percent in some studies, they are not recommended as a standalone screening technique. Some CDT assay methods (i.e. liquid chromatography
and isoelectric focusing) appear promising, but more research is required before firm
conclusions are drawn (Scouller et al. 2000).
The other generally available laboratory tests are less sensitive: for example, an
elevated mean cell volume (MCV) is found in only five to twenty percent of alcoholic
patients. The value of these tests in detecting non-alcohol dependent people with
risky/harmful alcohol consumption is correspondingly lower.The combination of a
number of biological markers can provide a rate of detection above the rate
achievable by any biochemical marker alone, with a sensitivity of 78 percent (Vanclay
et al. 1991). However, combinations of tests are not recommended for clinical use
because of reduced specificity (Musshoff and Daldrup1998).
Recommendation
3.9 Indirect biological markers (liver function tests or
carbohydrate-deficient transferrin) should only be
used as an adjunct to other screening measures as
they have lower sensitivity and specificity in detecting
at-risk people than structured questionnaire
approaches (such as AUDIT).
Strength of
recommendation
A
Level of
evidence
Ia
Other Screening methods for binge drinking: The Quantity-Frequency Index
(QFI) and the Retrospective Diary
A comparison of a 30-day quantity-frequency index with a seven day retrospective
diary and item three on AUDIT showed that the quantity-frequency question was
comparable to the AUDIT item in detecting binge drinking (95 percent positive
predictive value). All three methods were administered using a computer. The
retrospective diary requires patients to identify the type and quantity of alcoholic
beverage consumed beginning with the previous day and work back through each
day of the week. It was less sensitive than the QFI (ranging from 23.1 percent to 36.7
percent) (Shakeshaft et al. 1999).
The quantity-frequency question asked respondents to indicate the number of
occasions during the previous 30 days on which they had consumed four different
levels of standard drinks (defined by the NHMRC as the equivalent of 10g of ethanol)
(NHMRC 2001).
Item 3 (AUDIT-3) asks “how often do you have six or more drinks on one occasion?”
Possible responses are “never”, “less than monthly”, “monthly”, “weekly”, and “daily
or almost daily”.
Although the retrospective diary took longer to administer than the QFI (mean
completion times of three min, 38 sec and one min, 41 sec respectively) it provides
two important pieces of information: weekly and binge consumption. Further,
although the retrospective diary was inferior in detecting binge drinking, the QFI
underestimated overall drinking relative to the retrospective diary (Shakeshaft et al.
1999). The researchers suggested that there is greater potential for improving the
reliability and validity of the RD relative to the QFI.
25
Comprehensive Clinical Assessment
A comprehensive clinical assessment should be conducted before developing a
comprehensive treatment plan for those drinkers who have not responded to advice
to reduce their consumption of alcohol, have severe alcohol-related problems and in
patients who asked for or need help to deal with their drinking.
Assessment should combine a variety of techniques for gathering information about
the patient, including diagnostic interviews, physical examination, biological markers
and clinical investigations as well as collateral information from significant others.
The areas for assessment include: motivation to change, alcohol consumption
pattern and severity of dependence, alcohol-related harms (such as physical and
psychological health problems, relationship problems, occupational problems and
legal problems), family factors and cognitive functioning.
The need for comprehensive assessment must be balanced with the desire to
engage and retain the patient in treatment. If the patient perceives that little or no
progress is being made in the first sessions, their motivation to stay in treatment may
reduce.
Purpose of assessment
Assessment has three important functions:
a) to assist the patient and clinician to identify shared treatment goals and
develop a treatment plan;
b) to engage the patient in the assessment and treatment process;
c) to motivate the patient to change drinking patterns and related behaviour.
The patient’s perception of a gap between their goals and their present state may
improve motivation for change (Miller and Rollnick 2002; Miller 1995).
Recommendation
3.10 Assessment should include patient
interview, structured questionnaires, physical
examination, clinical investigations and
collateral history. The length of the assessment
should be balanced against the need to keep
the patient in treatment and address immediate
concerns.
Strength of
recommendation
D
Level of
evidence
IV
Diagnostic interviews
The initial assessment procedure ideally takes the form of an open-ended, semistructured interview where the patient and the clinician compile a narrative history,
using questionnaires as appropriate and necessary. This has the advantage of
clinician involvement which is personal and responsive to the drinker, rather than
mechanical and impersonal. Yet, it should maintain a purposeful structure so as to
avoid a vague, directionless discussion of the drinker’s history.
Standardised questionnaires are not often used, but a number of validated
26
instruments may be useful in selected cases. Structured diagnostic interviews are
available but infrequently used in clinical practice. Examples include: Composite
International Diagnostic Interview (CIDI), the Schedules for Clinical Assessment in
Neuropsychiatry (SCAN) and the Alcohol Use Disorder and Associated Disabilities
Interview Schedule-Alcohol/Drug-Revised (AUDADIS-ADR).
The Composite International Diagnostic Interview (CIDI) is a standardised and
comprehensive interview designed to assess psychological disorders against the
International Classification of Diseases (ICD) and DSM-IV diagnoses (World Health
Organisation 1990). It must be administered or supervised by a fully trained mental
health professional who has undertaken recognised CIDI training. As well as
substance use disorders, it covers eating disorders, organic mental disorders,
schizophrenic disorders, paranoid disorders, affective disorders, anxiety disorders,
somatisation disorders, dissociative disorders, and psychosexual disorders. WHO
also recently produced the World Mental Health (WMH) Survey Initiative version
(Kessler and Ustun 2004). However, one study found that CIDI performed poorly,
especially in diagnosing social phobia and post-traumatic stress disorder, compared
to clinical assessment (Komiti et al. 2001).
The CIDI, the Schedules for Clinical Assessment in Neuropsychiatry (SCAN) and the
Alcohol Use Disorder and Associated Disabilities Interview Schedule-Alcohol/DrugRevised (AUDADIS-ADR) all have reasonable test-retest reliability and diagnostic
concordance for alcohol dependence, but not for risky alcohol use or abuse.
Assessing level and history of alcohol consumption
The assessment process should gather information about the drinking history,
including how the drinking pattern evolved, fluctuated and/or progressed over time.
The history should include the daily average consumption (grams per day or
standard drinks per day) of alcohol, the number of drinking days per week (or month)
and the pattern of drinking.
There is limited community recognition of a standard drink (Kaskutas and Kerr 2008)
(Gill et al. 2007). Based on cumulative population self-report, overall alcohol use is
under-reported, but interviewing style influences the accuracy of self-report
(Stockwell et al. 2004; Stockwell et al. 2008). For example, the Lifetime Drinking
History that examines alcohol use throughout the life span has been shown to be a
valid assessment (Koenig et al. 2009).
There are several structured methods available to perform assessment of alcohol
consumption, although these are not routinely used in clinical practice. The Timeline
Follow-back Method (TLFB) helps to obtain an accurate, retrospective account of
alcohol consumption over a particular period, typically three months. This method
requires the patient and clinician to fill in a blank calendar with a detailed description
of alcohol consumption. The patient is first asked to note all events that may assist
with recall, for example public holidays or significant personal events. Any personal
diaries may help with recall. The patient then fills in the drinking days, noting the
amount consumed, and perhaps also the number of hours of consumption. This can
be extended to obtain a life-time drinking history which is useful for research and
occasionally for other purposes, but is time consuming and of moderate accuracy
(Sobell and Sobell 1992).
27
Recommendation
3.11 A quantitative alcohol history should be
recorded.
Strength of
recommendation
A
Level of
evidence
I
Assessing motivation
According to the model developed by Prochaska and DiClemente (Prochaska et al.
1992), readiness for change may be conceptualised as involving five (or six if precontemplation is included) stages:
AC TION
PREPARATION
M AINTENANC E
C O N T EM PLAT I O N
RELAPSE
Design: Author
•
•
•
•
•
•
A pre-contemplative stage, during which the person is not considering
changing
A contemplative stage, during which the person becomes more aware of the
benefits of changing, but is ambivalent about changing and does not act
A preparation stage, during which the person formulates plans for change,
may take steps to monitor their problem behaviour and initiate behaviour
change
An action stage, during which the person will engage in active attempts to
moderate or to cease the behaviour
A maintenance stage, which occurs after the behaviour has been moderated
or stopped but during which the person could relapse and return to an earlier
stage
A relapse stage, when the individual resumes or even increases the intensity
or frequency of the previous behaviour
The model, also known as the transtheoretical model (TTM), includes change
processes and levels of change. However, the assessment tool’s primary purpose is
to measure stages of change and our discussion is limited to this aspect. The TTM
28
theory has been tested widely, most often with smoking cessation, and correlational
data supports its predictive validity (DiClemente et al. 1991); however this has
recently been challenged by others (Dijkstra et al. 2006; West 2005).
There is only slim evidence of its ability to predict treatment outcome with alcohol
dependent patients. Project MATCH assessed readiness to change using a subset of
the University of Rhode Island Change Assessment (URICA) scale, and
hypothesised that patients low in motivation would do better in the motivational
enhancement therapy than in cognitive behaviour therapy. On an analysis of data,
overall a median of only 3% of the drinking outcome at follow-up could be attributed
to treatment; however the effect appeared to be present before most of the treatment
had been delivered, with the zero treatment group showing the most improvement.
The long-term results found that patient-treatment matching was unsuccessful and
that the three treatments produced essentially the same results (Cutler and Fishbain
2005).
Callaghan’s additional analysis found that, contrary to expectations, the individuals
who made a progressive stage transition to action-oriented stages did not manifest
greater improvements in drinking than those remaining in preparatory stages
(Callaghan et al. 2007). A similar effect, that greater readiness to change was not
predictive of reduced alcohol consumption, was found in a prospective cohort study
(Williams et al. 2007), where patient confidence in their ability to change was more
predictive of a favourable outcome. Others have challenged the concept that welldefined ‘stages’ actually exist; West’s criticism partly rests on the premise that people
sometimes change their behaviour on strong situational determinants without any
prior evidence of motivation (West 2005).
In an Australian study of brief interventions, heavy drinkers who were less ready to
change did better with a brief motivational interviewing intervention than with a skills
based intervention; however, those classified as ready to change did not do better in
the skills-based intervention (Heather et al. 1996). In a more recent study of hospital
patients, Saitz et al found that brief motivational counselling did not reduce alcohol
consumption significantly among the intervention group of heavy drinkers (1.8 drinks
per day) compared to ‘usual care’ patients (2.6 drinks per day) at 12 months; neither
did it reduce the need for alcohol assistance in the intervention group at 3 months.
However, both groups reduced their drinking and this may be attributable to the
screening and feedback process in itself (Saitz et al. 2007).
Results of these studies suggest that factors other than ‘stage of change’ (e.g.
confidence, peer group behaviour) play an important part in behaviour change and
must be considered in all assessments. However, treatment planning should take
motivational state into account so as to maintain and enhance motivation to control
excessive drinking.
Recommendation
3.12 Motivation to change should be assessed
through direct questioning, although expressed
motivation has only a moderate impact on
treatment outcome.
Strength of
recommendation
B
Level of
evidence
II
29
Assessing dependence and alcohol-related harms
When assessing the patient’s dependence on alcohol and the related harms he/she
may be consequently suffering, clinicians should examine patient’s severity of
dependence, the consequences of drinking and any previous experiences of
abstinence and treatment.
Severity of dependence
DSM-IV criteria or ICD-10 diagnoses are more often currently used to define alcohol
dependence than the older questionnaires (American Psychiatric Association 2000;
World Health Organization 1992).
A number of instruments are available to assess the severity of alcohol dependence.
However there is little current research on some of the questionnaires described
below.
The Severity of Alcohol Dependence Questionnaire (SADQ-C) is most useful as an
assessment tool with problem drinkers rather than as a screening tool (Stockwell et
al. 1994). It takes about five minutes to complete and has five subscales: physical
withdrawal symptoms, affective withdrawal symptoms, craving and withdrawal relief
drinking, consumption and reinstatement. An addition, the Impaired Control Scale
(ICQ) part of SADQ assesses the extent to which subjects perceive themselves to be
out of control with respect to their alcohol use (Marsh et al. 2002).
The original SADQ had good concordance with clinician ratings of alcohol
dependence (Stockwell et al. 1979), high test-retest reliability, and significant
correlations with observed withdrawal severity and narrowing of drinking repertoire
(Stockwell et al. 1983) A cut-off score of 30 was found to indicate severe
dependence. However, a lower cut-off score may be appropriate for females due to
the contribution of consumption questions to the total score. The shortened version of
the SADQ (SADQ-C) demonstrated good reliability and validity in a general
(Australian) population sample (Stockwell et al. 1994). A key difference between the
SADQ and the SADQ-C is that the latter focuses on the last three months, rather
than a ‘recent period’ of heavy drinking.
The Short Alcohol Dependence Data Questionnaire (SADD), a 15-item
questionnaire, is similar to the SADQ, although less focused on the experience of
withdrawal symptoms. The SADD and the SADQ are thought to measure the same
theoretical construct, i.e. the alcohol dependence syndrome (Raistrick et al. 1983;
Heather 1995).
The Severity of Dependence Scale (SDS) was the subject of a recent Australian
study aiming to determine a cut-off point that discriminated between the presence
and absence of a DSM-IV diagnosis of alcohol dependence. It was found that a score
of 3 or above on the SDS was the optimal cut-off to detect alcohol dependence
(Lawrinson et al. 2007).
The Alcohol Dependence Scale (ADS), a 25-item questionnaire, is designed to
identify and assess alcohol abuse and dependence. It assesses four aspects of the
alcohol dependence syndrome: loss of behavioural control, psychoperceptual
withdrawal symptoms, psychophysical withdrawal symptoms and obsessive-
30
compulsive drinking style. The validation study for the ADS reported high correlations
with daily consumption of alcohol, lifetime use of alcohol, social consequences from
drinking, prior treatment for alcohol abuse, use of alcohol to change mood, feelings of
guilt over drinking, and MAST scores (Skinner and Holm 1984). For alcohol use
disorders, a cut-off score of six or seven had a sensitivity of 0.97 and 0.75 specificity.
An early study found high correlations between the ADS and the MAST, with an ADS
score of eight or nine accurately classifying 88 percent of patients with an alcohol use
disorder (Ross et al. 1990). The ADS was also found to correlate well with a
structured diagnostic interview amongst a sample of homeless women
(Chantarujikapong et al. 1997).
A more recent study identified nine of the 25 ADS items as reliably discriminating
between those with no or minimal alcohol problems and those with symptoms of
excessive or abusive drinking, in a sample of high-risk drinkers mandated to a
domestic violence program (Kahler et al. 2003). However, another study evaluated
the concurrent validity of the ADS as a general measure of severity and the
screening accuracy of the total score and subscales to detect DSM-IV physiological
dependence, with patients entering the COMBINE study. These authors conclude
that the ADS reflected variation in symptom severity, but did not adequately identify
physiological dependence or withdrawal in treatment-seeking individuals with DSMIV alcohol dependence (Saxon et al. 2007).
Consequences of drinking
The clinician should assess the range of problems the patient has encountered as a
result of their drinking. In addition to physical and mental health, the patient’s drinking
may have led to family problems, detrimentally affected work performance, social
relations or financial stability. Alcohol-related offences such as drink–driving are also
relevant. A specific crisis in one of these areas may have been the impetus for
seeking help, and this should be explored. Discussion of the ‘less good things’ about
drinking can enhance the patient’s readiness for change. Alcohol harms are usually
assessed using unstructured clinical interviewing.
The Alcohol Problems Questionnaire (APQ) is a reliable instrument that covers eight
domains: friends, money, police, physical, affective, marital, children and work
(Drummond 1990).
Previous experiences of abstinence and treatment
Previous episodes of abstinence or reduced drinking and treatment exposure are
important to record and understand as it helps to plan future treatment, both in terms
of what worked and what did not, as well as to clarify patient experiences, tolerances.
Recommendation
3.13 Assessment of the patient’s alcohol-related
problems, diagnosis and severity of dependence
should be recorded.
Strength of
recommendation
S
Level of
evidence
Assessing physical well-being
31
According to the professional background and skills of the health professional, all
patients should be assessed regarding their physical health. If there are any active
medical issues, it is appropriate to encourage the patient to see his/her GP or other
medical practitioner. If there are no significant symptoms but the alcohol history
places the patient at risk of medical illness, medical referral for physical examination
and blood tests should also be recommended. Medical practitioners should conduct a
thorough assessment, including history, examination and clinical investigations.
Physical examination should at least assess signs intoxication or withdrawal, signs of
liver disease, vital signs (temp, blood pressure, pulse) and screen for organic brain
damage (Miller et al. 1988).
There is demonstrated value in the simple act of feeding back to the patient the
results of the medical examination and any clinical investigations. For example,
discussion about the implications of abnormal liver function tests has been shown to
reduce subsequent alcohol consumption.The Drinker’s Check-up is an example of a
computer software program that relies heavily on this motivating function of feeding
back objective information (Hester et al. 2005; Miller et al. 1988).
The advantages of feedback are less clear when the medical tests show normal
results. However, the whole assessment process should allow patients to assess
accurately the degree of their alcohol- related problems and normal medical results
should not detract from this process. The issue of normal results can be looked at
within the context of a clinical interaction and is further discussed in the motivational
interviewing material in Chapter 6: Psychosocial interventions.
Recommendation
3.14 Assessment for alcohol-related physical
health problems should be routinely conducted.
A medical practitioner should assess patients at
risk of physical health problems.
Strength of
recommendation
S
Level of
evidence
Assessing psychological and psychiatric disorders
Alcohol use disorders are associated with a range of mental health problems. It is
therefore critical to assess for comorbid disorders and symptoms, particularly
depression and anxiety symptoms. A range of short questionnaires is available for
assessing mental health disorders.
Around one in five (20 percent) Australians with alcohol dependence also have an
anxiety disorder, whilst 24 percent have an affective (mood) disorder. Heavy alcohol
use is also associated with other substance misuse, greater levels of psychological
distress and high levels of psychosis (Teesson et al. 2000; Cleary et al. 2008).
Patients with post-traumatic stress disorder (PTSD) also have increased rates of
alcohol-related disorders, and both of these may also be associated with a range of
personality disorders (American Psychiatric Asscoation 2000). However, care must
be taken not to make a personality disorder diagnosis based solely on behaviours
that are a result of alcohol intoxication or withdrawal.
Thus, it is critical to assess for comorbid disorders and symptoms, and suicidal
ideation. Referral for further specialist assessment may be required if significant
mental problems are suspected.
32
A limited range of measures of mental health is outlined below. Their use will depend
to some extent on the setting (i.e. the type of patients being seen; the amount of time
available for assessment; the skill level/qualifications of the clinician). However, at
least a brief assessment for depression and anxiety should be routinely carried out
for patients with a suspected alcohol use disorder such as the Kessler 10 Symptom
Scale or the General Health Questionnaire (Kessler et al. 2002; Goldberg 1972).
The following list is a sample of the available assessment tools. For a more extensive
review of instruments, see Dawe et al (2002).
•
The Kessler 10 Symptom Scale is a scale of psychological distress, suitable
for use as an outcome measure in people with anxiety and depressive
disorders (Kessler et al. 2002).
• The General Health Questionnaire (GHQ) is designed as a screening
instrument to identify likely non-psychotic psychiatric ‘cases’ in general health
settings (Goldberg 1972).
• The Short Form 12 (SF-12) assesses possible limitations in both physical
and mental health (Ware et al. 1996).
• The Beck Depression Inventory measures depression and its symptoms
(Beck and Steer 1987a).
• The Beck Hopelessness Scale measures hopelessness and negative views
about the future, as well as being an indicator of suicide attempts (Beck and
Steer 1987b).
• The Spielberger State-Trait Anxiety Scale measures current anxiety (state
anxiety) and a more enduring personality characteristic (trait anxiety)
(Speilberger et al. 1983).
• The Social Anxiety Interaction Scale and the Social Phobia Scale are useful
for assessing social phobia (Mattick and Clarke 1998).
• The Modified PTSD Symptom Scale is a brief (17-item) measure of post
traumatic stress disorder symptoms (Falsetti et al. 1993).
Note: The Kessler 10, the GHQ, the SF-12, the Mattick scales and the Modified
PTSD Symptom Scale are all in the public domain. The other scales need to be
purchased.
Recommendation
3.15 Assessment for mental health problems,
such as anxiety, depressive symptoms and
suicidal risk, should be routine, including mental
stage examination. Referral for further specialist
assessment may be needed if significant mental
problems are suspected.
Strength of
recommendation
S
Level of
evidence
Assessment of cognitive functioning
There is a high prevalence of cognitive dysfunction among people with alcohol
problems (Cook 2000). It is estimated that more than 50 percent of patients over the
age of 45 who have lengthy histories of drinking at risky levels will show some
degree of cognitive dysfunction, although this may not be permanent (Lishman
1987). Between 75 and 100 percent of patients admitted to alcohol treatment
facilities perform below normal for their age groups on tests of cognitive function
(Goldman 1995).
33
Many patients can report that there has been a decline in memory function as shown
by a number of changes in memory ability. However, some commentators caution
against relying upon the self-report of patients, especially in the case of damage to
the frontal lobes, as they may not be aware that the changes have occurred
(Lennane 1986).
Wernicke–Korsakoff’s syndrome is one of the forms of alcohol-related cognitive
deficit, and has high prevalence in alcohol dependent people. It is a potentially fatal
neurological disorder caused by thiamine (Vitamin B1) deficiency (see Chapters 5
and 9). Other medical causes of cognitive impairment include cerebrovascular
disease, dementia, Alzheimer’s disease, chronic subdural haematoma, cerebral
neoplasm, syphilis and HIV/AIDS.
While not the most common form of alcohol-related cognitive deficit, Wernicke
Korsakoff’s syndrome (WKS) can have severe consequences for its sufferers
(Donnino et al. 2007). WKS is characterised most notably by cognitive impairments in
memory (i.e. anterograde amnesia) as well as deficits in abstraction and problem
solving. However, overall intelligence usually remains intact. The acute phase
(Wernicke’s encephalopathy) is characterised by confusion, ocular and gait
disturbances, apathy and amnesia. Once this acute phase resolves, some patients
are left with an irreversible and dense amnesia, usually accompanied by apathy (the
chronic phase, known as Korsakoff syndrome) (Thomson and Marshall 2006a;
Thomson and Marshall 2006b; Donnino et al. 2007).
Autopsy studies in the 1980s showed that Australia had amongst the highest
recorded prevalence of WKS in the world, 80% of which cases had not been
diagnosed during life (Harper et al. 1989), although this rate of under-diagnosis is still
common today (Donnino et al. 2007). The introduction of thiamine into bread flour in
1991 dramatically reduced the incidence of WKS in Sydney hospitals, most notably in
the two years following its introduction (Ma and Truswell 1995), although some
doubts were voiced at the time about ‘mass medication’.
The condition is much more frequent in alcohol dependent individuals than in others
(although by no means confined to alcohol drinkers) with a prevalence of around 12
to 13 percent. There is also some evidence that some single symptoms of WKS are
present in around one-third of alcohol-dependent people, and that lower estimates
are due to the difficulty in diagnosing WKS (Cook 2000).
Some cognitive deficits such as impairment in verbal abilities, visual-spatial abilities,
problem-solving skills and memory often improve with a period of abstinence from
alcohol (Goldman 1995).
Screening instruments for cognitive Impairment
A brief assessment of cognitive functioning should be an integral part of the
assessment procedure and results should be used to guide treatment planning. If
significant impairment is suspected, a more thorough assessment by an
appropriately qualified professional is indicated.
For the non-psychologist seeking a quick assessment of cognitive dysfunction, the
Mini-Mental State Examination (MMSE) is helpful (Kurlowicz and Wallace 1999).
However, among elderly Australians aged 65 and over, taken from the National
Mental Health and Wellbeing Survey, total scores on the MMSE were influenced by
34
education, ethnic background, language spoken at home, socio-economic status,
occupation, prevalence of a mood disorder, sex and age (Anderson et al. 2007), and
the authors suggest appropriate cut-off points to take some of these variables into
account.
One study among alcohol-dependent, psychiatric patients, and those with dual
diagnosis found higher rates of cognitive impairment among dual diagnosis patients
compared to the schizophrenia or alcohol patients, and age was a considerable
confounding factor. Despite its common usage, global MMSE scores were insensitive
to the cognitive impairments typically found in these clinical groups (Manning et al.
2007).
Therefore the MMSE should be used with caution, and referral to a specialist for
further assessment is recommended.
For a more extensive assessment, a variety of tests have been shown to be sensitive
to alcohol-related brain damage. These tests include the Rey Complex Figure Test,
designed to test perceptual organisation and visual memory, the Rey Auditory-Verbal
Learning Test which measures verbal memory recall and recognition and the Trail
Making Test which tests visual concepts and visuomotor tracking. However, some of
these tests have very limited normative data available and they are not specific to
alcohol-related brain damage, so that their confident interpretation is made difficult.
Some of the tests relevant to the detection of cognitive dysfunction (e.g. Wechsler
Adult Intelligence Scale-III (WAIS-III)) should only be administered by psychologists
who have been trained in their interpretation. Two subtests are especially useful in
this context, although the entire WAIS-III should be administered to determine if there
is significant scatter among the various subtests, rather than relying upon a single
subtest result. The most relevant subtests of the WAIS-III are the Digit Symbol
subtest and the Block Design subtest (Ryan et al. 2000). The Wechsler logical testing
materials are available, depending upon professional qualifications, from the
Australian Council for Educational Research and the Psychological Corporation.
The Clock Drawing Test is another widely used screening test for cognitive
dysfunction that can be recommended but to achieve optimal performance (Pinto and
Peters 2009).
Caution needs to be applied to ensure testing is not conducted while the patient is
intoxicated or undergoing detoxification, or while affected by benzodiazepines or
other sedatives. As well, the clinician must be aware of other factors, such as
concomitant anxiety or depression, when interpreting tests of cognitive dysfunction.
Recommendation
3.16 Screening for cognitive dysfunction should
be conducted if the clinician suspects the patient
has cognitive impairment. Referral to a clinical
psychologist or neuropsychologist for further
testing may be appropriate. The need for formal
cognitive assessment is generally deferred until
the patient has achieved several weeks of
abstinence.
Strength of
recommendation
S
Level of
evidence
35
Gathering collateral information
Excessive alcohol use and its consequences are stigmatised problems that many
patients are reluctant to acknowledge. Collateral interviews play a central role where
the patient does not self-report their use of alcohol or its consequences. Collateral
information is particularly needed where a discrepancy appears likely.
There are significant barriers that limit access to collateral reports, including legal
(privacy legislation limits the distribution of personal information without consent),
ethical and financial (the enquiry can be time consuming). Patients may object to
such enquiries and the therapeutic relationship may be disrupted.
Recommendation
3.17 Collateral reports should be incorporated in
the assessment where inconsistencies appear
likely, with the patient’s permission where
possible, and subject to legal and ethical
boundaries.
Strength of
recommendation
S
Level of
evidence
Family factors
Patients should be encouraged to explore relevant family issues during assessment
including the relationships with their spouse or partner, their parents, their children,
and other significant people in their lives including any attributions about the effects
of the patient’s drinking.
Domestic violence and sexual abuse, either as perpetrator and/or victim, are
common and serious problems associated with alcohol and other substance use.
Because of the sensitivity of these issues, it may not be appropriate to raise them in
the first contact session unless there is reason to believe there may be a current
safety risk. It is important to determine whether the patient wishes to discuss these
issues. Specialist assessment and intervention is typically required.
When it is possible the clinician should interview the spouse or the family members.
The family interview is an opportunity for family members to ask questions and to
voice their concerns. It may also help the family see the drinking problem in
perspective.
While this kind of complex information is best obtained by clinical interview, Alcohol
Problems Questionnaire has a subscale assessing family problems and one
assessing marital/relationship problems (see Appendix) (Drummond 1990).
Recommendation
3.18 The social support for the patient should be
assessed and this information should be
incorporated into the management plan.
3.19 Clinicians should determine if the patient
cares for any children under the age of 16, and
act according to jurisdictional guidelines if there
are any concerns about child welfare.
Strength of
recommendation
S
Level of
evidence
S
36
Assessing risk
Full risk assessment involves assessment of a number of aspects of safety of the
patient or others, including suicide risk, violence risk, physical safety (for example,
self-care, risk of accidental injury), childcare, driving and workplace safety. Detailed
considerations of full risk assessment are beyond the scope of these guidelines. In
many cases, intervention to help the patient abstain from alcohol will substantially
reduce many risks. However, where concern about safety of the patient or others
remains, specialist consultation should be advised.
Recommendation
3.20 In the event of suspected or continuing
concerns over safety of the patient or others,
specialist consultation is advised.
Strength of
recommendation
S
Level of
evidence
Treatment Planning
As part of treatment planning it is important to identify suitable interventions, set
goals, and plan long-term follow-up aftercare to prevent relapse.
Identifying suitable interventions and developing treatment care plans
The factors that promote change in individuals are broader than treatment alone, but
treatment can help patients change by learning to think and act differently in relation
to drinking (Orford et al. 2006).
The cumulative evidence from the results of the large scale treatment trials, such as
Project MATCH (Project MATCH Research Group 1997) and the United Kingdom
Alcohol Treatment Trial (UKATT Research Team 2005) ssuggests that there are a
range of effective interventions and treatment approaches for alcohol disorders. No
single intervention is effective for all people with alcohol problems. There may be
treatment processes that reduce the likelihood of finding large differential effects
between empirically supported interventions.
Assessment and feedback
A comprehensive assessment is fundamental in treatment planning. Feedback of
assessment information to patients, that is sharing this information in plain, nonjudgemental language, should be standard practice in a collaborative and
motivationally oriented approach to treatment (Miller and Rollnick 2002), and can
increase the patient’s understanding, motivation to change and engagement in the
treatment process.
Recommendation
3.21 Assessment should lead to a clear,
mutually acceptable comprehensive treatment
plan that structures specific interventions to
meet the patient’s needs.
Strength of
recommendation
D
Level of
evidence
IV
37
Engaging the patient in treatment
Patient engagement may be viewed in terms of intensity and duration of treatment
participation. Higher levels of engagement are predictive of positive treatment
outcomes and are, in turn, contingent upon patient, clinician and clinic
characteristics.
• Patient characteristics include pre-treatment motivation, severity of disorder
and prior treatment experiences, strength of therapeutic relationship,
perceived helpfulness of the treatment services.
• Clinician factors include degree of empathy, therapeutic relationship and
counselling skills.
• Clinic factors include removal of practical access barriers such as
transportation, fees, hours, physical surroundings, and perceptions about
other patients of the service.
In addition to identifying clinical disorders and effective interventions, negotiation of
treatment goals requires clarification of the patient’s insight, values and expectation.
There is also evidence that providing the patient with a choice of treatment options
improves treatment retention (Rokke et al. 1999).
Treatment adherence and completion are prominent issues in alcohol and other drug
treatment and the factors that improve it are not yet well understood (Mattson and
Friedman 1994; Mattson et al. 1998). A focus in early interactions with patients
should be on maximising engagement with the professional and the service and
fostering a sense of collaboration (Zweben 2002; Zweben and Zuckoff 2002).
Central to the provision of any intervention is a strong bond and therapeutic alliance
alliance between patient and clinician (Shand et al. 2003). Basic counselling “micro
skills” including warmth, empathy and optimism, and strong interpersonal skills are
associated with better retention in treatment and indirectly with better treatment
outcomes (Shand et al. 2003; Miller and Rollnick 2002).
Goal setting: abstinence, moderation and reduced drinking
Identifying and agreeing upon treatment goals regarding alcohol consumption is an
important process for many patients.
For patients with no or low levels of dependence, and who are not experiencing
significant alcohol related harms, a goal of moderation may be achievable (Sitharthan
et al. 1997; Heather 1995).
For patients with severe alcohol dependence, and/or those presenting with
associated problems such as organ damage, cognitive impairment and co-existing
mental health problems, the most realistic drinking goal is likely to be abstinence
(Edwards et al. 2003).
Often patients may wish to drink at levels that can continue to cause harm, or may
not be realistically sustained. Several options can be considered when the patient’s
38
expressed preference for moderation is at odds with clinician advice (Miller and Page
1991; Jarvis et al. 2005). Options include
• to decline assistance explaining that it would be unethical for you to support your
patient’s goal. However, this approach is unlikely to engage and retain the patient
in treatment;
• to accept the patient’s goal on a provisional basis for a stipulated period of time,
and:
1. negotiate a period of abstinence (e.g. one to three months) with the
rationale that this would allow the patient to get through withdrawal (if
relevant), provide some much needed recovery from the effects of
alcohol, and provide time to acquire new skills that can be applied to
learning moderation (controlled drinking strategies);
2. agree on a gradual tapering down of drinking towards abstinence, setting
realistic, intermediate goals, and monitoring the number of drinks
consumed daily;
3. negotiate a period of trial moderation, with daily drink monitoring and
controlled drinking strategies (coping skills training).
Central to this process is ongoing review and monitoring of drinking against identified
goals. If these goals are too difficult to achieve, then abstinence may seem a more
reasonable goal, and this should be clearly identified and agreed upon with the
patient from the outset. Interventions with some patients require protracted but
important negotiation for goal setting (Miller and Page 1991; Jarvis et al. 2005).
Recommendation
3.22 Patients should be involved in goal setting
and treatment planning.
Strength of
recommendation
A
Level of
evidence
I
Development of treatment care plan
Information obtained during assessment is used to develop a case formulation with
patients, that entails a shared understanding of alcohol and other drug problems, coexisting health and social problems and other concerns, and to formulate hypotheses
about their development, maintenance and inter-relationships (Baker et al. 2007).
Any treatment plan must address the patient’s presenting problem. Often, the
presenting problem is alcohol-related (e.g. liver disease, depression, domestic
violence), and it will be necessary to also address the patient’s alcohol use in order
for comprehensive and longer term changes to take effect. However, the sequence of
interventions is often determined by immediate needs (e.g. hospitalisation for hepatic
failure or suicidal attempt, emergency shelter to avoid further violence).
Treatment options should be discussed with patients (and their families or carers as
relevant), identifying
•
what is involved with each treatment approach,
•
the likely outcomes (including potential adverse outcomes), and
•
provide the patient the opportunity to raise questions or concerns.
As in any health care intervention, informed consent is essential.
A stepped care model is proposed that serves as a guide to clinical decision making
and treatment planning (Sobell and Sobell 2000). Stepped care identifies that
39
patients should be offered the least “restrictive” intervention appropriate to their
presentation. Should the first intervention prove to be insufficient to achieve the
agreed treatment goals for the patient, the next level of intensity of treatment should
be offered until the desired treatment goals are achieved. This approach requires
regular review and monitoring of the patient, their response to treatment and any
changes in their presentation (ie continuous assessment).
Relapse prevention, aftercare and long-term follow-up
Relapse is a common problem in alcohol treatment, with approximately 60% of
treated patients relapsing to problematic drinking within the first 12 months (Connors
et al. 1996).
It has long been observed that specific situations or mood states are associated with
relapse. Factors include: negative emotional states (e.g. frustration, anger, anxiety,
depression or anger); interpersonal conflict (e.g. relationships with partner, work
colleagues, friends); and direct or indirect social pressure to drink (Marlatt and
George 1984).
Relapse prevention addresses itself to the maintenance of change, and to the
development of self-efficacy and coping skills (Edwards et al. 2003). Relapse
prevention can be assisted through the use of medication, including alcohol
pharmacotherapies for reducing alcohol use (e.g. naltrexone, acamprosate,
disulfiram), or medication directed towards addressing psychological problems such
as anxiety or depression (See Chapter 6).
Aftercare or extended care refers to the period immediately following intensive
treatment (See Chapter 11). Aftercare acknowledges the fact that severe alcohol
problems are prone to recurrence and that maintenance of change may require some
ongoing monitoring and assistance beyond the active phase of initial treatment. It is
particularly suited to people with severe dependence whose likelihood of relapse is
greater. It consists of planned telephone or face-to-face contact following a period of
treatment to discuss progress and any problems that may have arisen since the end
of active treatment.
Structured aftercare is more effective than patient-initiated, unstructured aftercare
(See Chapter 11).
Many clinicians may use referral to self-help programs (such as Alcoholic
Anonymous and SMART Recovery) as forms of continuing care, although aftercare
generally refers to contact with the treating clinician or service with the goal of
maintaining treatment gains. Often primary care workers (e.g. general practitioners)
can provide this function through ongoing follow-up of other health issues (See
Chapter 8).
Recommendation
3.23 Treatment plans should be modified
according to reassessment and response to
interventions (stepped care approach).
3.24 Evidence-based treatment should be
offered in a clinical setting with the appropriate
resources based on the patient’s needs.
Strength of
recommendation
S
Level of
evidence
S
40
References
Aertgeerts, B, Buntinx F, Ansoms S et al. 2001, Screening properties of
questionnaires and laboratory tests for the detection of alcohol abuse or
dependence in a general practice population. Br J Gen Pract 51(464): 206217.
Agabio, R, Marras P, Gessa GL et al. 2007, Alcohol use disorders, and at-risk
drinking in patients affected by a mood disorder, in Cagliari, Italy: sensitivity
and specificity of different questionnaires. Alcohol Alcoho 42(6): 575-581.
AIHW 2008, 2007 National Drug Strategy Household Survey. First results. Canberra
Australian Institute of Health and Welfare.
American Psychiatric Association 2000, Diagnostic and Statistical Manual of Mental
Disorders, 4th edition, text revision (DSM-IV-TR) American Psychiatric
Association, Washington, DC.
Anderson, BK and ME Larimer 2002, Problem drinking and the workplace: an
individualized approach to prevention. Psychol Addict Behav 16(3): 243-251.
Anderson, TM, Sachdev PS, Brodaty H et al. 2007, Effects of sociodemographic and
health variables on Mini-Mental State Exam scores in older Australians. Am J
Geriatr Psychiatry 15(6): 467-476.
Anton, RF, Dominick C, Bigelow M et al. 2001, Comparison of Bio-Rad %CDT TIA
and CDTect as laboratory markers of heavy alcohol use and their
relationships with gamma-glutamyltransferase. Clin Chem 47(10): 1769-75.
Babor, T, de la Fuente J, Sounders J et al. 1992, The Alcohol Use Disorders
Identification Test: Guidelines for use in Primary Health Care. World Health
Organisation.
Babor, T, Higgins-Biddle J, Dauser D et al. 2005, Alcohol screening and brief
intervention in primary care settings: implementation models and predictors. J
Stud Alcohol 66: 361-368.
Baker, A, Bucci S, Kay-Lambkin F et al. 2007, Cognitive behaviour therapy for people
with co-existing mental health and drug and alcohol problems. In: Baker, A
and R, Velleman (eds) Clinical handbook of co-existing mental health and
drug and alcohol problems. London: Rountledge.
Baraona, E, Julkunen R, Tannenbaum L et al. 1986, Role of intestinal bacterial
overgrowth in ethanol production and metabolism in rats. Gastroenterol.
90(1):103-10.
Barry, K, Blow FC, Willenbring M et al. 2004, Use of alcohol screening and brief
interventions in primary care settings: implementation and barriers. Subst
Abuse 25(1): 27-36.
Beck, A and R Steer 1987a, Beck depression inventory: Manual. USA, Harcourt,
Brace, Jovanovich.
41
Beck, A and R Steer 1987b, Beck Hopelessness Scale Manual. San Antonio, The
Psychological Corporation. Harcourt Brace Jovanovich Inc.
Bradley, KA, DeBenedetti AF, Volk RJ et al. 2007, AUDIT-C as a brief screen for
alcohol misuse in primary care. Alcohol Clin Exp Res 31(7): 1208-1217.
Bush, K, Kivlahan DR, McDonell MB et al. 1998,The AUDIT alcohol consumption
questions (AUDIT-C): an effective brief screening test for problem drinking.
Ambulatory Care Quality Improvement Project (ACQUIP). Alcohol Use
Disorders Identification Test. Arch Intern Med 158(16): 1789-1795.
Callaghan, RC, L Taylor and JA Cunningham 2007, Does progressive stage
transition mean getting better? A test of the Transtheoretical Model in
alcoholism recovery. Addiction 102(10): 1588-1596.
Cassidy, CM, N Schmitz and A Malla 2008, Validation of the alcohol use disorders
identification test and the drug abuse screening test in first episode
psychosis. Can J Psychiatry 53(1): 26-33.
Chantarujikapong, SI, EM Smith and LW Fox 1997, Comparison of the Alcohol
Dependence Scale and diagnostic interview schedule in homeless women.
Alcohol Clin Exp Res 21(4): 586-595.
Cherpitel, CJ 1995, Screening for alcohol problems in the emergency department.
Ann Emerg Med 26(2): 158-166.
Cleary, M, Hunt G, Matheson S et al. 2008, Psychosocial interventions for people
with both severe mental illness and substance misuse. Cochrane Database
Syst Rev (1).
Conigrave, KM, Degenhardt LJ, Whitfield JB et al. 2002, CDT, GGT, and AST as
markers of alcohol use: the WHO/ISBRA collaborative project. Alcohol Clin
Exp Res 26: 332–339.
Conigrave, KM, Davies P, Haber P et al. 2003, Traditional markers of excessive
alcohol use. Addiction 98 (Suppl 2): 31-43.
Conley, T 2001, Construct validity of the MAST and AUDIT with multiple offender
drunk drivers. J Subst Abuse Treat 20(4): 287-295.
Connor, JP, M Grier, GF Feeney et al. 2007, The validity of the Brief Michigan
Alcohol Screening Test (bMAST) as a problem drinking severity measure. J
Stud Alcohol 68(5): 771-779.
Connors, G, S Maisto and W Zywiak 1996, Understanding relapse in the broader
context of post-treatment functioning. Addicition, 91(Suppl), S173-S190.
Cook, CC 2000, Prevention and treatment of Wernicke-Korsakoff syndrome. Alcohol
Alcohol Suppl 35(1): 19-20.
Cutler, RB and DA Fishbain 2005, Are alcoholism treatments effective? The project
MATCH data. BMC Public Health 14 (5): 75.
42
Dawe, S, Loxton N, Hides L et al. 2002, Review of diagnostic screening instruments
for alcohol and other drug use and other psychiatric disorders. Canberra:
Commonwealth Department of Health & Ageing.
Dawson, DA, BF Grant and FS Stinson 2005, The AUDIT-C: screening for alcohol
use disorders and risk drinking in the presence of other psychiatric disorders.
Compr Psychiatry 46(6): 405-416.
DiClemente, CC, Prochaska JO, Fairhurst SK et al. 1991, The Process of Smoking
Cessation: An Analysis of Precontemplation, Contemplation, and Preparation
Stages of Change. J Consult Clin Psychol 59(2): 295-304.
Dijkstra, A, B Conijn and H De Vries 2006, A match-mismatch test of a stage model
of behaviour change in tobacco smoking. Addiction 101: 1035-1043.
Donnino, MW, Vega J, Miller J et al. 2007, Myths and misconceptions of Wernicke's
encephalopathy: What every emergency physician should know. Ann Emerg
Med 50(6): 715-721.
Drummond, C 1990, The relationship between alcohol dependence and alcohol
related problems in a clinical population. Addiction 85(3): 357-366.
Edwards, G, EJ Marshall and CCH Cook 2003, The treatment of drinking problems:
A guide for the helping professions. Cambridge: Cambridge University Press.
Falsetti, S, Resnick H, Resnick P et al. 1993, The Modified PTSD Symptom Scale: A
brief self-report measure of posttraumatic stress disorder. Behav Ther 16:
161-162.
Fiellin, D, Reid MC and P O'Connor 2000, Screening for alcohol problems in primary
care: a systematic review. Arch Int Med 160(3): 1977-1989.
Gill, JS, Donaghy M, Guis J et al. 2007, Descriptors and accounts of alcohol
consumption: methodological issues piloted with female undergraduate
drinkers in Scotland. Health Educ Res 22(1): 27-36.
Goldberg, D 1972, The detection of psychiatric illness by questionnaire. London, UK:
Oxford University Press.
Goldman, M 1995, Recovery of cognitive functioning in alcoholics - the relationship to
treatment. Alcohol Health Res World 190: 148-154.
Gomel, MK, Saunders JB, Burns L et al. 1994, Dissemination of early intervention for
harmful alcohol consumption in general practice. Health Promot J Austr 4(2):
65-69.
Hannuksela, ML, Liisanantti MK, Nissinen AE et al. 2007, Biochemical markers of
alcoholism. Clin Chem Lab Med 45(8): 953-61.
Harper, C, Gold J, Rodriguez M et al. 1989, The prevalence of the WernickeKorsakoff syndrome in Sydney, Australia - a prospective necropsy study J
Neurol Neurosurg Psych 52(2): 282-285.
43
Harris, MF, Hobbs C, Powell Davies G et al. 2005, Implementation of a SNAP
intervention in two divisions of general practice: a feasibility study. Med J Aust
183(10 Suppl): S54-58.
Heather, N. 1995, Brief intervention strategies. In: Hester, R and WR Miller (eds),
Handbook of Alcoholism Treatment Approaches (pp. 105-122). Boston: Allyn
and Bacon.
Heather, N, Rollnick S, Bell A et al. 1996, Effects of brief counselling among male
heavy drinkers identified on general hospital wards. Drug Alcohol Rev 15(1):
29-38.
Heck, EJ and JW Lichtenberg 1990, Validity of the CAGE in screening for problem
drinking in college students. J College Student Devel 31: 359-364.
Hester RK, D Squires and H Delaney 2005, The Drinker's Check-up: 12-month
outcomes of a controlled clinical trial of a stand-alone software program for
problem drinkers. J Subst Abuse Treat 28(2): 159-169.
Hettema, JE, Miller WR, Tonigan JS et al. 2008, The test-retest reliability of the Form
90-DWI: an instrument for assessing intoxicated driving. Psych Addict Behav
22(1): 117-121.
Holland, CL, JL Pringle and V Barbetti 2009, Identification of Physician Barriers to the
Application of Screening and Brief Intervention for Problem Alcohol and Drug
Use. Alcohol Treat Q 27(2): 174 - 183.
Kahler, CW, Strong DR, Stuart GL et al. 2003, Item functioning of the alcohol
dependence scale in a high-risk sample. Drug Alcohol Depend 72(2): 183192.
Kaner, EFS, Beyer F, Dickinson HO et al. 2007, Effectiveness of brief alcohol
interventions in primary care populations. Cochrane Database of Syst Rev.
Kaskutas, LA and WC Kerr 2008, Accuracy of photographs to capture respondentdefined drink size. J Stud Alcohol Drugs 69(4): 605-610.
Kessler, RC, Andrews G, Colpe LJ et al. 2002, Short screening scales to monitor
population prevalences and trends in non-specific psychological distress.
Psychol Med 32(6): 959-976.
Kessler, RC and TB Ustun 2004, The World Mental Health (WMH) Survey Initiative
Version of the World Health Organization (WHO) Composite International
Diagnostic Interview (CIDI). Int J Methods Psychiatr Res 13(2): 93-121.
Koenig, LB, T Jacob and JR Haber 2009, Validity of the lifetime drinking history: a
comparison of retrospective and prospective quantity-frequency measures. J
Stud Alcohol Drugs 70(2):296-303.
Komiti, AA, Jackson HJ, Judd FK et al. 2001, A comparison of the Composite
International Diagnostic Interview (CIDI-Auto) with clinical assessment in
diagnosing mood and anxiety disorders. Aust N Z J Psychiatry 35(2): 224230.
44
Kurlowicz, L and M Wallace 1999, The Mini Mental State Examination (MMSE).
Director 7(2): 62.
Lane, J, Proude EM, Conigrave KM et al. 2008, Nurse-provided screening and brief
intervention for risky alcohol consumption by sexual health clinic patients. Sex
Transm Infect 84(7):524-527.
Lawrinson, P, Copeland J, Gerber S et al. 2007, Determining a cut-off on the Severity
of Dependence Scale (SDS) for alcohol dependence. Addict Behav 32(7):
1474-1479.
Lennane, KJ 1986, Management of moderate to severe alcohol-related brain damage
(Korsakoff's syndrome). Med J Aust 145(3-4): 136, 141-143.
Lishman, W 1987, Organic psychiatry: psychological consequences of cerebral
disorder (2nd edition). Oxford: Blackwell Scientific Publications.
Longabaugh, R, Woolard RE, Nirenberg TD et al. 2001, Evaluating the effects of a
brief motivational intervention for injured drinkers in the emergency
department. J Stud Alcohol 62(6): 806-816.
Ma, JJ and AS Truswell 1995, Wernicke-Korsakoff syndrome in Sydney hospitals:
before and after thiamine enrichment of flour. Med J Aust 163(10): 531-534.
Manning, V, Wanigaratne S, Best D et al. 2007, Screening for cognitive functioning in
psychiatric outpatients with schizophrenia, alcohol dependence, and dual
diagnosis. Schizophr Res 91(1-3): 151-158.
Marlatt GA and WH George 1984, Relapse prevention: introduction and overview of
the model. Br J Addict 79(3):261-73.
Marsh, A, Smith L, Saunders B et al. 2002, The Impaired Control Scale: confirmation
of factor structure and psychometric properties for social drinkers and
drinkers in alcohol treatment. Addiction 97(10): 1339-1346.
Matano, RA, Koopman C, Wanat SF et al. 2007, A pilot study of an interactive web
site in the workplace for reducing alcohol consumption. J Subst Abuse Treat
32(1): 71-80.
Mattick, R and J Clarke 1998, Development and validation of measures of social
phobia scrutiny fear and social interaction anxiety. Behav Res Ther 36(4):
455-470.
Mattson, ME and LM Friedman 1984, Issues in medication adherence assessment in
clinical trials of the National Heart, Lung, and Blood Institute. Control Clin
Trials 5(4 Suppl):488-496.
Mattson, ME, Del Boca F, Carroll KM et al. 1998, Compliance with Treatment and
Follow-up Protocols in Project MATCH: Predictors and Relationship to
Outcome. Alcohol Clin Exp Res, 22 (6), 1328-1339.
Mayfield, D, G McLeod and P Hall 1974, The CAGE questionnaire: validation of a
new alcoholism screening instrument. Am J Psychiatry 131(10): 1121-1123.
45
Miller, W 1995, Increasing motivation for change. In: Hester, RK and W Miller (eds)
Handbook of Alcoholism Treament Approaches. Boston: Allyn & Bacon.
Miller, WR and AC Page 1991, Warm turkey: other routes to abstinence. J Subst
Abuse Treat 8(4):227-32.
Miller, WR, RG Sovereign and B Krege 1988, Motivational interviewing with problem
drinkers: 2. The Drinkers Checkup as a preventive intervention. Behav
Psychother 16(4): 251-268.
Miller, W and S Rollnick 2002, Motivational interviewing: preparing people for
change. New York: Guilford Press.
Moraes, CL, EF Viellas and ME Reichenheim 2005, Assessing alcohol misuse during
pregnancy: evaluating psychometric properties of the CAGE, T-ACE and
TWEAK in a Brazilian setting. J Stud Alcohol 66(2): 165-173.
Musshoff, F and T Daldrup 1998, Determination of biological markers for alcohol
abuse. J Chromatogr B Biomed Sci Appl 713(1):245-264.
NHMRC 2001, Australian Alcohol Guidelines: Health Risks and Benefits. Canberra:
National Health & Medical Research Council.
NHMRC 2009, Australian Guidelines To Reduce Health Risks from Drunking Alcohol.
Canberra: National Health & Medical Research Council.
Orford, J, Hodgson R, Copello A et al. 2006, The clients’ perspective on change
during treatment for an alcohol problem: qualitative analysis of follow-up
interviews in the UK Alcohol Treatment Trial. Addiction 101, 60-68.
Piccinelli, M, Tessari E, Bortolomasi M et al. 1997a, Efficacy of the alcohol use
disorders identification test as a screening tool for hazardous alcohol intake
and related disorders in primary care: a validity study. BMJ 314(7078): 420424.
Piccinelli, M, Tessari E, Bortolomasi M et al. 1997b, Efficacy of the alcohol use
disorders identification test as a screening tool for hazardous alcohol intake
and related disorders in primary care: a validity study. BMJ 314(7078): 420424.
Pinto, E and R Peters 2009, Literature review of the Clock Drawing Test as a tool for
cognitive screening. Dement Geriatr Cogn Disord. 27(3):201-13.
Prochaska, JO, CC DiClemente and JC Norcross 1992, In search of how people
change. Applications to addictive behaviors. Am Psychol 47(9): 1102-1114.
Project MATCH Research Group 1997, Matching alcoholism treatments to client
heterogeneity: Project MATCH posttreatment drinking outcomes. J Stud
Alcohol 58(1): 7-29.
Project MATCH Research Group 1998, Matching alcoholism treatments to client
heterogeneity: Project MATCH three-year drinking outcomes. Alcohol Clin
Exp Res 22(6): 1300.
46
Proude, E, Britt H, Valenti L et al. 2006, The relationship between self-reported
alcohol intake and the morbidities managed by GPs in Australia. BMC Fam
Pract 7:17.
Proude, E, KM Conigrave and P Haber 2006, Effectiveness of skills-based training
using the Drink-less package to increase family practitioner confidence in
intervening for alcohol use disorders. BMC Med Educ 6: 8.
Proude, E, Saunders J, Conigrave K et al. 2005, The Drink-less Program. Retrieved
25 April 2009, from http://www.cs.nsw.gov.au/drugahol/drinkless/.
Proude, EM, Conigrave KM, Britton A et al. 2008, Improving Alcohol and Tobacco
History Taking by Junior Medical Officers. Alcohol Alcohol: 43(3): 320-325.
Raistrick, D, G Dubar and R Davidson 1983, Development of a questionnaire to
measure alcohol dependence. Br J Addict 78:89-95.
Reid, ALA, Webb GR, Hennrikus D et al. 1986, General practitioners' detection of
patients with high alcohol intake. BMJ 293: 735-737.
Richmond, R, Kehoe L, Heather N et al. 2000, Evaluation of a workplace brief
intervention for excessive alcohol consumption: the workscreen project. Prev
Med 30(1): 51-63.
Robinson, GM, H Leslie and BJ Robinson 1992, Detection of problem-drinkers in an
emergency department using a breathalyser and questionnaire. Drug Alcohol
Rev 11(3): 259-264.
Roche, AM, Pidd K, Berry JG et al. 2008, Workers' drinking patterns: the impact on
absenteeism in the Australian work-place. Addiction 103(5): 738-748.
Rokke, PD, JA Tomhave and Z Jocic 1999, The role of client choice and target
selection in self-management therapy for depression in older adults. Psychol
Aging 14(1): 155-169.
Ross, HE, DR Gavin and HA Skinner 1990, Diagnostic validity of the MAST and the
alcohol dependence scale in the assessment of DSM-III alcohol disorders. J
Stud Alcohol 51(6): 506-513.
Russell M, Martier SS, Sokol RJ et al. 1994, Screening for pregnancy risk-drinking.
Alcohol Clin Exp Res 18(5):1156-61.
Ryan, JJ, Arb JD, Paul CA et al. 2000, Reliability of the WAIS-III subtests, indexes,
and IQs in individuals with substance abuse disorders. Assessment 7(2): 151156.
Saitz, R, Palfai TP, Cheng DM et al. 2007, Brief intervention for medical inpatients
with unhealthy alcohol use: a randomized, controlled trial. Ann Int Med1
46(3): 167-176.
Saunders, JB, Aasland OG, Babor TF et al. 1993, Development of the Alcohol Use
Disorders Identification Test (AUDIT): WHO Collaborative Project on Early
47
Detection of Persons with Harmful Alcohol Consumption - II. Addiction 88:
791-804.
Saunders, JB and SJ Hanratty 1990, Early intervention for harmful alcohol
consumption. National Workshop on Early and brief interventions, National
Drug and Alcohol Research Centre, Sydney.
Saxon, AJ, Kivlahan DR, Doyle S et al. 2007, Further validation of the alcohol
dependence scale as an index of severity. J Stud Alcohol Drugs 68(1): 149156.
Scouller, K, Conigrave KM, Macaskill P et al. 2000, Should we use carbohydrate
deficient transferrin instead of gamma-glutamyltransferase for detecting
problem drinkers? A systematic review and metaanalysis. Clin Chem 46(12):
1894 1902.
Selzer, ML 1971, The Michigan Alcoholism Screening Test: the quest for a new
diagnostic instrument. Am J Psychiatry 12: 1653-1658.
Shakeshaft, AP, JA Bowman and RW Sanson-Fisher 1999, A comparison of two
retrospective measures of weekly alcohol consumption: diary and
quantity/frequency index. Alcohol Alcohol 34(4): 636-645.
Shourie, S, Conigrave KM, Proude EM et al. 2007, Detection of and intervention for
excessive alcohol and tobacco use among adult hospital in-patients. Drug
and Alcohol Review 26(2): 127-133.
Skinner, HA and S Holt 1984, Alcohol Dependence Scale (ADS) Users Guide.
Toronto: Addiction Research Foundation.
Skinner, HA, Holt S, Sheu WJ et al. 1986, Clinical versus laboratory detection of
alcohol abuse: the alcohol clinical index. BMJ 292: 1703-1708.
Skipsey, K, JA Burleson and HR Kranzler 1997, Utility of the AUDIT for identification
of hazardous or harmful drinking in drug-dependent patients. Drug Alcohol
Depend 45(3): 157-163.
Sobell, L and M Sobell 1992, Timeline follow-back: A technique for assessing selfreported alcohol consumption. In: Litten, R and J Allen (eds) Measuring
Alcohol Consumption. Humana Press.
Speilberger, C, Gorsuch R, Lushene R et al. 1983, Manual for the State-Trait Anxiety
Inventory (Form Y). Palo Alto: Consulting Psychologist Press, Inc.
Spinucci. G, Guidetti M, Lanzoni E et al. 2006, Endogenous ethanol production in a
patient with chronic intestinal pseudo-obstruction and small intestinal bacterial
overgrowth. Eur J Gastroenterol Hepatol 18(7): 799-802.
Stockwell, T, Donath S, Cooper-Stanbury M et al. 2004, Under-reporting of alcohol
consumption in household surveys: a comparison of quantity-frequency,
graduated-frequency and recent recall. Addiction 99(8): 1024-1033.
48
Stockwell, T, Hodgson R, Edwards G et al. 1979, The development of a
questionnaire to measure severity of alcohol dependence. Br J Addict Alcohol
Other Drugs 74(1): 79-87.
Stockwell, T, D Murphy and R Hodgson 1983, The severity of alcohol dependence
questionnaire: its use, reliability and validity. Br J Addict 78(2): 145-155.
Stockwell, T, Sitharthan T, McGrath D et al. 1994, The measurement of alcohol
dependence and impaired control in community samples. Addiction 89(2):
167-174.
Stockwell, T, Zhao J, Chikritzhs T et al. 2008, What did you drink yesterday? Public
health relevance of a recent recall method used in the 2004 Australian
National Drug Strategy Household Survey. Addiction 103(6): 919-928.
Teesson, M, Clement N, Copeland J et al. 2000, The Measurement of Outcome in
Alcohol and Other Drug Treatment: A Review of Available Instruments.
Sydney: National Drug and Alcohol Research Centre.
Teesson, M, Hall W, Lynskey M et al. 2000, Alcohol- and drug-use disorders in
Australia: implications of the National Survey of Mental Health and WellBeing. Aust N Z J Psychiatry 34: 206-213.
Thomson, A and EJ Marshall 2006a, The natural history and pathophysiology of
Wernicke’s Encephalopathy and Korsakoff’s psychosis. Alcohol Alcohol 41:
151-158.
Thomson, AD and EJ Marshall 2006b, The treatment of patients at risk of developing
Wernicke's Encephalopathy in the community. Alcohol Alcohol 41(2): 159167.
UKATT Reaearch Team 2005, Effectiveness of treatment for alcohol problems:
findings of the randomised UK alcohol treatment trial (UKATT) BMJ 331: 331541.
Vanclay, F, Raphael B, Dunne M et al. 1991, A community screening test for high
alcohol consumption using biochemical and haematological measures.
Alcohol Alcohol 26(3): 337-346.
Volk, RJ, Steinbauer JR, Cantor SB et al. 1997, The Alcohol Use Disorders
Identification Test (AUDIT) as a screen for at-risk drinking in primary care
patients of different racial/ethnic backgrounds. Addiction 92(2): 197-206.
Walsh, ME and D Macleod 1983, Breath alcohol analysis in the accident and
emergency Department. Injury 15: 62-66.
Ware, J, M Kosinski and S Keller 1996, A 12-item Short Form Health Surveyconstruction of scales and preliminary tests of reliability and validity. Med
Care 34: 220-233.
Watson, B, Conigrave KM, Wallace C et al. 2007, Hazardous alcohol consumption
and other barriers to antiviral treatment among hepatitis C positive people
receiving opioid maintenance treatment. Drug Alcohol Rev 26(3): 231-239.
49
West, R 2005, Time for a change: putting the Transtheoretical (Stages of Change)
Model to rest. Addiction 100: 1036-1037.
World Health Organization 1990, Composite International Diagnostic Interview.
Geneva, Switzerland: World Health Organization.
World Health Organization 1992, The ICD-10 Classification of Mental and
Behavioural Disorders: Clinical descriptions and diagnostic guidelines, F10–
F19 Mental and behavioural disorders due to psychoactive substance use,
Geneva: World Health Organization. Available at
<http://www.who.int/substance_abuse/terminology/ICD10ClinicalDiagnosis.pd
f>.
World Health Organization 2002, Alcohol, Smoking and Substance Involvement
Screening Test (WHO ASSIST) Working Group, The Alcohol, Smoking and
Substance Involvement Screening Test (ASSIST); development, reliability
and feasibility. Addiction 97: 1183–94.
Williams, EC, Horton NJ, Samet JH et al. 2007, Do brief measures of readiness to
change predict alcohol consumption and consequences in primary care
patients with unhealthy alcohol use? Alcohol Clin Expe Res 31(3): 428-435.
Williams, G, Daly M, Proude EM et al. 2008, The influence of alcohol and tobacco
use in orthopaedic inpatients on complications of surgery. Drug Alcohol Rev
27(1): 55-64.
Wutzke, SE, Shiell A, Gomel MK et al. 2001, Cost effectiveness of brief interventions
for reducing alcohol consumption. Social Science & Medicine 52(6): 863-870.
Zweben, JE 2002, Addiction: selecting appropriate treatment and using the self-help
system. Occup Med 17(1):41-49.
Zweben, A and A Zuckoff 2002, Motivational interviewing and treatment adherence.
In: Miller, WR and S Rollnick (eds) Motivational interviewing: preparing people
for change.New York: The Guilford Press.
50
Chapter 4
Brief interventions
Brief interventions represent an important and effective way to reduce alcohol related
harm, especially in primary care (Kaner et al. 2007, 2009). This treatment strategy
has been shown to be as effective for heavy drinkers as more intensive interventions,
more cost-effective due to their length and can be used in a wide variety of primary
care settings to reach a large number of patients. Significant reductions of up to 30%
in alcohol consumption have been achieved in a variety of health care settings,
including hospital and general practice (Bertholet et al. 2005; Kaner et al. 2007)
(Kaner et al. 2009). Brief interventions in primary care are also cost-effective (Wutzke
et al. 2001).
What are brief interventions?
Brief interventions comprise clinical interventions that include screening and
assessment, and provide information and advice designed to achieve a reduction in
risky alcohol consumption, and/or alcohol-related problems (Bien et al. 1993). They
typically target individuals drinking at risky levels before they develop into abuse or
dependence disorders (Babor et al. 2000).
Opportunistic brief interventions are usually delivered to people who have not sought
help for a problem with alcohol but are identified as drinking at risk levels via
screening. They are viewed as a component of a public health approach to alcoholrelated harm; at least one study showed long-term effects of up to 9 years (Nilssen
2004), and while the effect shown in another study had faded at 10 years (Wutzke et
al. 2002), this is still a worthwhile strategy. However, despite years of research and
positive evidence for their effect, routine screening, identification of alcohol use
disorders, and the implementation of brief intervention remains remarkably low
(Cheeta et al. 2008).
Who to target for brief interventions?
Brief interventions are a recognised treatment approach to responding to individuals
with risky patterns of drinking who may or may not already have experienced alcohol
related harms, but without a diagnosis of alcohol dependence (Kaner et al. 2007).
There is strong scientific evidence for their effectiveness in reducing levels of alcohol
intake in people who drink above recommended levels and are at risk of developing
alcohol related problems, but do not seek treatment (Moyer et al. 2002).
This effectiveness has been demonstrated across a variety of settings.
Meta-analyses
In the first meta-analysis of brief interventions in various settings, Bien, Miller and
Tonigan pooled the findings of 18 studies that compared opportunistic brief
interventions to a control condition and 13 studies comparing less-intensive
treatments with more extended therapy (Bien et al. 1993). The mean pooled effect
size (values above zero indicate higher effect) for brief interventions versus a control
condition favoured brief interventions (0.38), indicating that brief interventions were
more effective than usual care (no intervention) in reducing alcohol consumption. The
mean pooled effect size for less-intensive treatment versus extended treatment was
negligible (0.06), indicating that the interventions were effective regardless of
51
intensity. However, in this review, mean effect sizes were not weighted by study
size/variance and no homogeneity tests or significance tests for overall effect sizes
were conducted, thus making it unclear as to whether the types of studies examined
were comparing similar treatment interventions. Nevertheless, this was the first metaanalysis that has clearly demonstrated that brief intervention is effective in reducing
alcohol consumption when compared to no intervention.
Wilk et al reviewed 12 randomised controlled trials of brief interventions (i.e. less than
1 hour) focusing on studies with adult participants and sample sizes greater than
thirty, conducted in a variety of settings (Wilk et al. 1997). Only eight of these
reported outcome data that allowed calculation of individual odds ratios. These odds
ratios were calculated based on the estimate that the heavy drinkers had moderated
their drinking six or 12 months after intervention compared to the untreated control
group. The odds ratio was 1.95. Heavy drinkers were defined as those who were
drinking more than 2 or 3 drinks daily, but were non-dependent. This level of drinking
is shown to increase the risk of accidents, injuries and subsequent alcohol-related
problems (Saunders et al. 1993). Conclusions were that heavy drinkers who received
an intervention were twice as likely to moderate their drinking 6 to12 months postintervention as controls. The results of Wilk’s meta-analysis also confirm that brief
interventions are effective in reducing alcohol consumption when compared to no
intervention.
The more recent meta-analyses and randomised controlled studies are discussed
below and are classified according to the settings in which the studies were
conducted. The results are consistent in suggesting that opportunistic brief
interventions are effective in reducing alcohol consumption compared to screening
alone or to no intervention. There is no consistent evidence that less-intensive
treatments are less effective than more intensive treatment interventions for more
severe cases of alcohol abuse and dependence.
Brief interventions are not usually effective in individuals who have developed
dependence, or who are experiencing severe alcohol related harms. For these
individuals, more intensive treatment interventions are recommended (Heather et al.
2004). However, there is some evidence that brief interventions can be effective in
dependent individuals (Guth et al. 2008). This study is discussed later in the text.
Recommendation
4.1 Brief interventions are effective in reducing
alcohol use in people with risky pattern of
alcohol use and in non-dependent drinkers
experiencing alcohol-related harms and should
be routinely offered to these populations.
4.2 Brief interventions are not recommended for
people with more severe alcohol-related
problems or alcohol dependence.
Strength of
recommendation
A
Level of
evidence
Ia
A
Ib
How to deliver brief intervention
As a general rule, brief interventions should include at least the five components
identified in the acronym FLAGS, the two most crucial of which are Feedback and
Advice (see Table 4.1) (Proude et al. 2005).
52
Table 4.1: FLAGS brief intervention structure
Feedback • Provide individualised feedback about the risks associated with
continued drinking, based on current drinking patterns, problem
indicators, and health status.
• Discuss the potential health problems that can arise from risky alcohol
use.
Listen
•
•
Advice
•
Goals
•
Strategies
•
•
Listen to the patient’s response.
This should spark a discussion of the patient’s consumption level and
how it relates to general population consumption and any false beliefs
held by the patient.
Give clear advice about the importance of changing current drinking
patterns and a recommended level of consumption.
• A typical five to 10 minute brief intervention should involve advice on
reducing consumption in a persuasive but non-judgemental way.
• Advice can be supported by self-help materials, which provide
information about the potential harms of risky alcohol consumption and
can provide additional motivation to change.
Discuss the safe drinking limits and assist the patient to set specific
goals for changing patterns of consumption.
• Instil optimism in the patient that his or her chosen goals can be
achieved.
• It is in this step, in particular, that motivation-enhancing techniques are
used to encourage patients to develop, implement and commit to plans
to stop drinking.
Ask the patient to suggest some strategies for achieving these goals.
This approach emphasises the individual’s choice to reduce drinking
patterns and allows them to choose the approach best suited to their
own situation.
• The individual might consider setting a specific limit on alcohol
consumption, learning to recognise the antecedents of drinking, and
developing skills to avoid drinking in high-risk situations, pacing one’s
drinking and learning to cope with everyday problems that lead to
drinking.
There are alternative acronyms such as FRAMES (Bien et al. 1993) and 5A’s (Ask,
Advise, Assess, Assist, Arrange, usually used in interventions for tobacco) (Zwar et
al. 2005) with comparable structures for guiding an intervention, which can be used.
However, for people who drink above recommended levels but are not experiencing
alcohol-related harm, brief advice may be sufficient.
Recommendation
4.3 Brief interventions may consist of the five
components of the FLAGS acronym: feedback,
listening, advice, goals, and strategies (or
equivalent).
4.4 Brief advice may be sufficient for those
drinking above NHMRC recommendations but
not experiencing harm.
Strength of
recommendation
A
Level of
evidence
Ia
S
53
Who can deliver brief interventions?
Any health professional or treatment provider with adequate training can deliver brief
interventions.
Generalist health professionals can be successfully trained in the delivery of brief
interventions within a 1-2 hour training program (Field et al. 2005).
Where should brief interventions be delivered?
Brief interventions can be effectively delivered in a variety of settings including
general practice settings, general hospital wards, emergency departments, trauma
centres and community counselling centres.
General practice setting
Universal screening in general practice can identify excessive drinkers suitable for
brief interventions, as about 85 percent of the population visit their general
practitioner each year (Beich et al. 2003b; AIHW 2004). general practitioners have
the resources and skills to offer an intervention and thus, the general practitioners
has the ability and potential to have a substantial effect on risky levels of drinking.
The level of evidence for its effect is strong, especially for male patients (Kaner et al.
2007). However, about 25 percent of patients presenting to general practitioner
settings in Australia who are drinking at risk levels are likely to remain undetected
(Britt et al. 2003).
General practice setting: Meta-analyses
There have been a number of meta-analyses examining the effectiveness of brief
interventions in various settings, the most recent of which was carried out by Kaner
and colleagues (Kaner et al. 2007). The majority of these studies are in agreement
that brief interventions are effective in this setting.
To demonstrate the depth of research in this area and the consistency of results this
chapter briefly reviews each meta-analysis and has a more detailed explanation of
the most recent and comprehensive one.
The first two meta-analyses of brief interventions conducted in various settings,
including primary care (Bien et al. 1993; Wilk et al. 1997), are described above. Their
results demonstrate that brief interventions are effective in reducing alcohol
consumption when compared to no intervention.
The next review concentrated on randomised controlled trials of brief interventions
delivered in primary health care (Poikolainen 1999). Results from the 7 publications
selected, with the inclusion criterion of follow-up at 6-12 months, indicated that very
brief interventions (5-20 minutes) did not result in a significant change in alcohol
consumption; however, extended brief interventions (several visits) produced a
significant pooled effect estimate of change in alcohol intake among women and
among the whole sample. Among men, the statistical heterogeneity among studies
meant that no significant conclusions could be reached. One of the author’s
conclusions was that ‘excessive drinking’ should be based in standard criteria so that
trials could be compared more efficiently (Poikolainen 1999). Therefore, the results of
this meta-analysis suggest that a single brief intervention may be less effective than
an extended brief intervention delivered and reinforced over several sessions.
54
The next meta-analysis of brief interventions was a comprehensive examination of
the brief intervention literature, resulting in 56 trials (Moyer et al. 2002). Studies were
classified according to both the type of comparison (brief treatment compared to a
control or a more extended treatment) and the type of patient population (treatmentseeking compared to non-treatment-seeking). Comparing brief intervention and
control conditions, effect sizes were significant at less than 3 months (p<0.01), more
than 3-6 months (p<0.001), and more than 6-12 months (p<0.001) follow-up points
for the composite variable of drinking related outcomes, and at a significance level of
p<0.001 at all follow-up points for reductions in alcohol consumption. Their results
indicated that brief interventions were effective when compared to no intervention in
reducing alcohol consumption. The effect was significant until twelve months after the
intervention. The results also suggest that brief interventions are more effective in
studies of treatment-seeking populations who do not have severe alcohol problems
than in non-treatment-seeking people.
Beich et al conducted a meta-analysis of screening and brief intervention trials in
general practice, with the aim of discovering the number needed to treat, proportion
of patients positive to screening, proportion given brief intervention and effect of
screening (as opposed to intervention) (Beich et al. 2003b). Their conclusions were
that only two to three patients per thousand would benefit from screening, and
therefore universal screening was not a viable proposition, a statement that was
widely challenged in the online responses to the article (Vinson 2003; Conigrave et
al. 2003).
Following this, Ballesteros et al published the results of a meta-analysis of thirteen
studies of brief intervention with non-dependent patients in primary care (Ballesteros
et al. 2004). One of their aims was to examine whether there was a dose-effect trend
which aligned with the number or intensity of interventions. Studies were selected on
the basis that intention-to-treat analyses were available and there was a six to 12
month follow-up. Studies were published between 1987 and 2003. The only
measurable and reported effect was the change in proportion of hazardous drinkers
6-12 months after randomisation (i.e. decrease in numbers drinking at hazardous
levels); other outcomes such as changes in consumption, biochemical markers and
psychosocial outcomes were not used in the meta-analysis. No dose-effect of the
intervention was found. Findings from this meta-analysis showed clear support for
the efficacy of brief intervention at consultations in primary care (odds ratio =1.41;
NNT= 12).
Bertholet et al. also conducted a systematic review and meta-analysis, focussing on
non-treatment-seeking patients in primary care, the setting and population group that
is most recommended for brief interventions (Bertholet et al. 2005). Nineteen trials
were selected that fulfilled the criteria. Follow-up rates ranged from 32.5% to 92.4%.
No studies reported negative effects. Meta-analysis was restricted to those 10 trials
for which the reduction of alcohol consumption could be calculated, and was the only
outcome that was pooled for the analysis. The other variables were too disparate to
allow pooling. The adjusted intention-to-treat analysis showed a mean pooled
difference of -38 g of ethanol (approximately 4 drinks) per week (95% confidence
interval, -51 to -24 g/wk) in favor of the brief alcohol intervention group. Results
indicated that brief intervention is effective for both men and women in reducing
alcohol consumption at 6 and 12 months; reductions were similar for both 6 and 12
months. Most studies they reviewed, however, also reported a 10-30% reduction of
drinking in the control group, a common effect which can be caused by several
reasons including natural changes over the course of time, regression to the mean,
the Hawthorne effect, or just the effect of screening (McCambridge et al. 2008). Nine
55
studies also reported data related to mental or physical health perception, well-being
and alcohol-related problems. There were significant differences among 9 of the 21
measures reported, showing a more improved quality of life in the intervention group
than in the control group (Bertholet et al. 2005). Therefore, according to this review,
brief intervention delivered in primary care setting is effective in reducing alcohol
consumption by 4 standard drinks a week in a population of non-treatment-seeking
patients (both in men and women) at 6 and 12 months post-intervention.
A high-quality review carried out for the U.S. Preventive Services Taskforce by
Whitlock et al was published in the Annals of Internal Medicine (Whitlock et al. 2004).
All studies in this review were published prior to 2002 and almost all of them were
included in the above meta-analyses. In order to avoid repetition of results, the main
findings only are summarised here. Twelve trials of intervention in primary care met
the study criteria of randomised controlled trial with 6-12 month follow-up data.
Results showed that intervention group participants reduced the average number of
drinks per week by 13-34% more than the control group, and the proportion of
patients drinking at moderate or safe levels was 10-19% greater than controls at
follow-up.
The latest and most comprehensive meta-analysis of the effectiveness of brief
alcohol interventions in primary care was a Cochrane review by Kaner et al (2007).
The previous meta-analyses by Ballesteros, Bertholet, Moyer, and Poikolainen were,
as they mention, similar and directly relevant to their review. While their exercise
might be viewed as needless repetition, there are still evidence gaps, namely in
subgroups, e.g. young people; in different countries and cultures; in identifying the
‘active ingredient’ of brief intervention; and lastly the efficacy/effectiveness issue. As
mentioned above, while evidence for the efficacy of brief intervention is plentiful, the
effectiveness (will it work in actual clinical practice?) is the sticking point. This review
therefore undertook a secondary subgroup analysis to assess the impact of brief
intervention in efficacy (ideal world) and effectiveness (real world) trials to account for
variability in treatment exposure relating to frequency, duration and theoretical basis
of the brief intervention. The main results: primary meta-analyses of 22 trials with
7.619 participants showed that, compared to controls, brief intervention reduced the
quantity of alcohol consumed per week by 38g (95% CI: 23 to 54); which equates to
between 4 to 5 (UK) units of alcohol. This analysis was repeated excluding trials of
uncertain quality (e.g. insufficient reporting of procedures for randomisation) and
excluding participants lost to follow-up, with the results still showing a statistically
significant benefit of brief intervention. The secondary subgroup analysis of the issue
of efficacy/effectiveness showed no evidence of any difference in effect of brief
intervention between the two types of trials (Kaner et al. 2007). Final conclusions
from the data were that: brief intervention in primary care results in significant
reductions in weekly consumption for men, with an average drop of about 6 standard
drinks per week; however there was no significant reduction in alcohol consumption
for women. Although this may have been due to low statistical power (only 499
female participants), it seems from this analysis as though brief interventions in
primary care for women are not yet justified. Further research should focus on
women and on finding the most effective components of interventions.
General Practice Setting: Selected randomised controlled trials
As so many trials of rigorous quality have been published about brief intervention, we
have selected only the most recent, significant, or unusual trials of methods or
settings or with unexpected results for this section of the review.
56
General Practice: Negative outcome
Beich et al trialled screening and brief intervention in Danish general practices (Beich
et al. 2007). Their aims were to conduct a pragmatic controlled trial aimed at
evaluating the effectiveness of the WHO recommendations for screening and brief
intervention in general practice. The trial involved 39 Danish general practitioners.
Systematic screening of 6897 adults led to inclusion of 906 risky drinkers; 537 of
whom were followed up at 12-14 months. Outcome measures focused on patients'
acceptance of screening and intervention and their self-reported alcohol
consumption. Their results showed that although all the intervention group subjects
(n = 442) were exposed to an instant brief counselling session, only 18% (79/442)
attended a follow-up consultation that was offered by their general practitioner. At
one-year follow-up, average weekly consumption had increased by 0.7 drinks in both
groups. Secondary findings were an indiscriminate absolute risk reduction (ARR =
0.08 (95% confidence interval, CI: 0.02-0.18)) in male binge drinking, but adverse
intervention effects for women on the secondary outcomes (binge drinking ARR =
0.30 (95% CI: 0.47-0.09)). The authors’ conclusions were that the results of
systematic screening and brief interventions in everyday general practice fell short of
their theoretical expectations and therefore could not be considered effective.
General Practice: Stepped-care approach
Another trial was conducted to look for gender differences in response to brief
intervention with a stepped care approach (Reinhardt et al. 2008). In "Stepped
Interventions for Problem Drinkers," 10,803 patients from 85 general practitioners
were screened using alcohol related questionnaires; 408 patients (32% female) were
randomised to a control (booklet only) or two different intervention groups: stepped
care (feedback, manual, and up to three counselling sessions depending on the
success of the previous intervention) and fixed care (four sessions). Response rate
for the 12 month follow-up was 91.7%. Regression analysis revealed a significant
effect size (R2) only in women (R2 = 0.029; p = 0.039) when both interventions
together were compared with the control group. After excluding alcohol dependents
and binge drinkers an effect size (R2) of 0.031 (p = 0.05) in women and an effect size
(R2) of 0.069 (p = 0.057) in men was obtained. Among the patients in stepped care
who, by the first assessment point, had reduced drinking to within safe drinking limits,
there was a tendency for females to have achieved this more often than males (40%
vs. 24%; p = 0.09). Authors did not report mean values. Number needed to treat
(NNT) to achieve reduction in alcohol consumption as a relust of an intervention
(either fixed or stepped care) was 10 for women and 17 for men. Conclusions were
that in a heterogeneous sample the intervention was only effective for women, and
also that women tended to benefit more from the less intensive intervention than did
men.
General Practice: Young adults
An article by Grossberg et al. (2004) reports the results of a subanalysis of young
adults (aged 18 to 30 years) who participated in Project TrEAT (Trial of Early Alcohol
Treatment) conducted in the offices of 64 primary care physicians located in 10
counties in southern Wisconsin. Project TrEAT was a randomised clinical trial
designed to test the efficacy of a brief intervention protocol to reduce alcohol use,
improve health status, and decrease health care utilisation. A total of 226 young
adults were randomly assigned to either a usual care or brief intervention group.
Results showed that during the 4-year follow-up period, there were significant
57
reductions in the intervention group in number of persons drinking more than 3 drinks
per day, average 7-day alcohol use, number of persons drinking 6 or more drinks per
occasion, and number of binge drinking episodes in the previous 30 days (p<0.01 to
p<0.001). There were also significant differences (p<0.05) in emergency department
visits (103 vs. 177), motor vehicle crashes (9 vs. 20), total motor vehicle offences
(114 vs. 149), and arrests for controlled substances or possession of liquor (0 vs. 8),
between intervention and control groups. Conclusions were that long-term effects on
drinking could be achieved by intervention with young adults and should be more
widely implemented.
A University health care service in New Zealand was the setting for a randomised
controlled trial of a web-based screening and intervention (Kypri et al. 2008).
Participants were 975 students (aged 17-29 years) screened using AUDIT. Of 599
students who scored in the hazardous or harmful range, 576 (50% male) consented
to the trial and were randomised to receive an information pamphlet (control group),
a web-based motivational intervention (single-dose e-SBI group), or a web-based
motivational intervention with further interventions 1 and 6 months later (multidose eSBI group). Results showed that relative to the control group, the single-dose group
reported a lower frequency of drinking at 6 months (rate ratio [RR], 0.79; 95%
confidence interval [CI] 0.68-0.94), less total consumption (RR, 0.77; 95% CI, 0.630.95), and fewer academic problems (RR, 0.76; 95% CI, 0.64-0.91). At 12 months,
statistically significant differences in total consumption and in academic problems
remained, and the AUDIT scores were 2.17 points lower (95% CI, -1.10 to -3.24).
Relative to the control group, the multidose group reported a lower frequency of
drinking at 6 months (RR, 0.85), reduced total consumption (RR, 0.79, [equivalent to
3 standard drinks per week]), reduced episodic heavy drinking (RR, 0.65), and fewer
academic problems (RR, 0.78). At 12 months, statistically significant differences in
academic problems remained (RR, 0.75), while the AUDIT scores were 2.02 points
lower. The conclusions were that the single-dose intervention reduced hazardous
drinking significantly with an effect lasting for 12 months. The additional sessions
seemed not to add any benefit.
A more unusual (and partially inconclusive) study compared 10 hours of intervention
with a mailed intervention comprising the student’s AUDIT score, advice to cut down
and suggested sources of help (e.g. telephone numbers of treatment organisations)
(Johnsson et al. 2006). In total 693 freshmen at Lund University, Sweden, took part.
A cognitive behavioural alcohol program or mailed intervention was randomly
assigned to high-risk drinkers (n = 177). The AUDIT was used at baseline and at a 12
month follow-up to measure any changes in drinking. Results showed no significant
differences between the cognitive behavioural and the mailed intervention groups.
Both groups reduced their AUDIT scores, which could be explained by effects of
regression to the mean. No significant differences occurred between the groups. This
result suggests that mailed intervention was as effective as the much more intensive
cognitive behavioural intervention.
General Practice: Effect of mental comorbidities
In a randomised controlled brief intervention study with two intervention groups and
one control group, data were collected from 408 general practice patients with
alcohol use disorders, at-risk drinking or binge drinking (Grothues et al. 2008).
Eighty-eight participants were diagnosed with comorbid anxiety and/or depressive
disorders. The effectiveness of the intervention was assessed at a 12-month followup in relation to the presence and absence of comorbidity. Reduction of drinking in
six ordered categories (g/alcohol) between baseline and follow-up served as the
58
outcome variable. Results showed that the brief intervention significantly reduced
drinking in the non-comorbid (p = 0.03) but not in the comorbid subsample (p = 0.76).
Compared to non-comorbid participants, a significantly higher reduction of drinking
was found for comorbid individuals (p = 0.01). Ordinal regression analysis revealed
comorbidity to be a positive predictor for reduction of drinking (p<0.01). When
entering the variables (i) amount of drinking at baseline, (ii) intervention and (iii)
classification of problematic drinking, these became significant predictors, whereas
comorbidity showed only a tendency. As brief interventions are known to be less
effective for dependent drinkers, a larger proportion of dependents among the
comorbid might have limited its effectiveness.
General Practice: Dependent drinkers
At least one study tested brief interventions with dependent drinkers and compared
the results with non-dependent drinkers (Guth et al. 2008). Retrospective analyses
were performed on participants (n = 326) enrolled in a randomised trial designed to
examine the impact of interactive voice response following brief intervention. All
participants had received a brief intervention from their primary care provider before
enrolling in the study. Daily consumption data were collected using the Timeline
Followback method for the period prior to intervention (mean = 71 days) and for 6
months following. Dependent participants had significantly higher pre-brief
intervention consumption than non-dependent patients. At the initial assessment 15
days after the brief intervention, both dependent and non-dependent participants
reported significant reductions in total drinks per week and drinking days per week.
Dependent participants significantly reduced their drinks per drinking day and no
longer differed significantly from non-dependent participants on these measures.
Similar decreases were observed in both groups over the following 6 months,
although dependent participants drank on fewer days, but in significantly higher
amounts than did non-dependent drinkers. Regression analyses showed that
baseline consumption was the only significant predictor of post-intervention
consumption. Conclusions were that there was no evidence that dependent
participants gained less benefit on measures of alcohol consumption following brief
intervention than non-dependent participants.
Recommendation
4.5 Brief interventions should be implemented in
general practice and other primary care settings.
Strength of
recommendation
A
Level of
evidence
Ia
Emergency departments and trauma centres
There is a high rate of alcohol-related injuries and conditions among people attending
accident and emergency departments, 1.5 to 3 times the rate seen in primary care.
Data suggest that recent trauma or a life-threatening experience increases the
receptivity of patients to interventions, thus increasing the likelihood of brief
intervention being effective in reducing alcohol consumption among these patients
(D'Onofrio et al. 2002; Neumann et al. 2006).
Interventions in emergency departments have proved to be effective in reducing risky
levels of alcohol intake and binge drinking episodes (D'Onofrio et al. 2004/05;
Bazargan-Hejazi et al. 2005; Soderstrom et al. 2007; Walton et al. 2008; Nilsen et al.
2008) and reducing subsequent alcohol-related injuries in the 6-12 months
subsequent to intervention (Havard et al. 2008; Dinh-Zarr t al. 2005) although Dinh-
59
Zarr’s Cochrane review was not able to correlate this benefit with the effect of the
intervention on abstinence, consumption, or drinking-related hazardous behaviour
(Dinh-Zarr et al. 2005).
Reduction of heavy alcohol consumption in the subsequent 12 months is less likely
(Havard et al. 2008), but has been shown in some studies (Bazargan-Hejazi et al.
2005; Walton et al. 2008).
A number of studies reported reductions in alcohol consumption from risky to low risk
levels in emergency department/trauma patients who did not receive structured brief
intervention, but were asked about their levels of alcohol consumption and
participated in the study as a control or standard care group (Daeppen et al. 2007;
Dent et al. 2008; D'Onofrio et al. 2004/05). Highlighting the alcohol/injury connection
as part of brief intervention in this setting may increase the effect of the intervention
(Walton et al. 2008). Uptake of opportunistic screening by emergency department
staff in one Australian study (Dent et al. 2008) was poor, as was patient compliance
with off-site counselling.
Computer-assisted brief interventions in emergency department settings have
demonstrated reductions in alcohol use over the subsequent 6 to 12 months, and
appears a promising dissemination strategy (Neumann et al 2006).
Emergency Departments and Trauma Centres: Meta-analyses
A review and meta-analysis of strategies targeting alcohol problems in emergency
departments (ED) was recently published (Havard et al. 2008). Thirteen studies with
reasonable methodological quality were identified, with the exception that some had
poor reporting of effect size or inconsistent selection of outcome measures. Sample
sizes ranged from 85 to 1334. Selected outcome measures were quantity/frequency
of alcohol consumption at 12 month follow-up; frequency of high-volume drinking at 3
months and 12 months; consequences from drinking at 6 and 12 months, and
alcohol-related injuries at 6 and 12 months. Ten randomised controlled trials fulfilled
these criteria. Findings were that ED-based interventions were found to have no
effect on quantity/frequency or on high volume drinking at 12 months. Effects on
frequency of heavy drinking at 3 months and consequences of drinking at 6 or 12
months were inconclusive; the only statistically significant effect found from the
analysis was that intervention patients had half the probability (OR: 0.59) of controls
in sustaining an alcohol-related injury in the 6 or 12 months following their ED visit.
However, there were limitations in the data that prevented more thorough analyses
being conducted.
A Cochrane review that examined interventions to prevent injuries in problem
drinkers (Dinh-Zarr et al. 2005) was published prior to the Havard paper above.
Settings were various, participants included dependent and non-dependent drinkers,
partners of drinkers, men convicted of drink driving (DUI) and settings included
Emergency departments, outpatient and inpatient settings, and others not described.
Interventions ranged from brief intervention to a one hour consultation with a
psychologist and included blood test results, medications, probation, rehabilitation
programs, and AA attendance. The most common intervention studied was brief
counselling in the clinical setting for problem drinking. The majority of trials of brief
counselling showed beneficial effects on diverse non-fatal injury outcomes: motorvehicle crashes and related injuries, falls, suicide attempts, domestic violence,
assaults and child abuse, alcohol-related injuries and injury emergency visits, and
hospitalisations; seven trials demonstrated reductions in injury-related deaths
60
(relative risk (RR) 0.65; 95% confidence interval (CI) 0.21-2.00). Reductions ranged
from 27% to 65%. Because few trials were sufficiently large to assess effects on
injuries, individual effect estimates were generally imprecise. The results were not
combined quantitatively because the interventions, patient populations, and
outcomes were so diverse. The major conclusions were that interventions for
problem drinking appear to reduce injuries and their antecedents (e.g. falls, motor
vehicle crashes, suicide attempts). The time frames for follow-up varied from 3 to 48
months.
Several studies have reported on the results of brief intervention delivered during a
visit to an ED or trauma centre. D’Onofrio and Degutis compared 4 studies
conducted between 1999 and 2004: Monti et al. (1999); Gentilello et al. (1999);
Longabaugh et al. (2001) and Spirito et al. (2004). Findings suggested that, from the
evidence presented, brief intervention to patients whose injuries are alcohol-related
may decrease their alcohol consumption. However, the standard care groups also
reduced their drinking in every case, and three of the studies had very high refusal
rates, perhaps skewing the results in favour of more compliant patients (D'Onofrio et
al. 2004/05). The follow-up intervals were 3 and 6 months (Monti); 3, 6 and 12
months (Spirito); 6 and 12 months (Gentilello); and 12 months only (Longabaugh).
Nilsen et al carried out a systematic review of emergency care brief interventions for
injured patients, selecting 14 studies for analysis (Nilsen et al. 2008). Of the 12
studies that compared pre- and post-brief intervention results, 11 observed a
significant effect of brief intervention on the following outcomes: alcohol intake, risky
drinking practices, alcohol-related negative consequences, and injury frequency. Two
studies assessed only post- brief intervention results. More intensive interventions
tended to yield more favourable results. brief intervention patients achieved greater
reductions than control group patients, although there was a tendency for the control
group(s) to also show improvements. Five studies failed to show significant
differences between the compared treatment conditions. Variations in the study
protocol, alcohol-related recruitment criteria, screening and assessment methods,
and injury severity limited the specific conclusions that could be drawn.
Emergency departments and trauma centres: RCTs
One study in ED with patients that were not randomised, but allocated alternately to
control and intervention groups, showed that brief motivational intervention delivered
by peer educators significantly reduced moderately risky drinking and associated
problems in the intervention group patients who scored 7-18 on AUDIT at baseline
(Bazargan-Hejazi et al. 2005). No such effect was found, however, for intervention
group patients in the high-risk group (defined by AUDIT scores above 19).
Two recent randomised controlled trials in Switzerland and in Australia were not able
to demonstrate any effect on alcohol use in either intervention or control groups
(Daeppen et al. 2007; Dent et al. 2008). The aims of the Swiss study were to
evaluate the effectiveness of brief intervention (BI) in reducing alcohol use among
hazardous drinkers treated in the ED after an injury; it also tested whether
assessment of alcohol use without intervention was sufficient to reduce hazardous
drinking. A total of 5136 consecutive patients completed a seven-item general and a
three-item alcohol screen; 1472 (28.7%) were positive for hazardous drinking
according to the National Institute on Alcohol Abuse and Addiction definition; 987
(67.1%) were randomised into a BI group (n = 310), a control group with screening
and assessment (n = 342), or a control group with screening only (n = 335). A total of
770 patients (78%) completed the 12-month follow-up. The intervention was a single
61
standardised 10-15-minute session conducted by a trained research assistant. At
follow-up similar proportions of participants reduced their level of drinking to low-risk
in the intervention and both control groups with and without assessment (35.6%,
34.0%, 37.0%, respectively, p = 0.71). Data also indicated similar reductions in
drinking frequency, quantity, binge drinking frequency and AUDIT scores across
groups. A model including age groups, gender, AUDIT and injury severity scores
indicated that BI had no influence on the main alcohol use outcome. This study
provided evidence that a 10-15-minute intervention did not decrease alcohol use and
health resource utilisation in hazardous drinkers attending ED. The authors also state
that commonly-found decreases in hazardous alcohol use in control groups cannot
be solely attributed to the baseline alcohol assessment. There are three possible
explanations for this; either a very minimal intervention (the assessment) is sufficient
to change behaviour; having an injury is of itself enough reason to reduce drinking; or
the brief Intervention of 10-15 minutes had no effect over and above the minimal
intervention, due to regression to the mean.
The Australian study (Dent et al. 2008) aimed to evaluate the feasibility and efficacy
of opportunistic screening and brief intervention by ED staff to reduce high-risk
alcohol consumption. It was an open, randomised controlled trial with allocation
blinding, performed over 12 months. Adult patients were screened using the
Paddington Alcohol Test. Consenting patients screened positive were randomised to
standard care (control group), same-day brief intervention (BI) by an emergency
nurse or doctor, or motivational intervention (MI) within 1 week by off-site drug and
alcohol counsellors. Telephone follow up was performed at 1 and 3 months. The
primary outcome was maximum self-reported daily standard drinks consumed. Of
32,965 eligible patients, 10,274 (31%) were screened, 1043 (10%) were positive, 468
(45%) consented to the study, and 161, 159 and 148 were allocated to SC, BI and MI
respectively. Results showed a loss to follow-up of about 50%. In the MI group, 133
declined intervention or failed to attend the counselling session. At 3 months, 96
(60%), 81 (51%) and 74 (50%) participants in the control, BI and MI groups,
respectively, were contactable and consented to telephone interview. Overall,
maximum daily alcohol consumption decreased from a median of 13.5 standard
drinks at enrolment to 9.25 drinks at 3 months. At 3 months, control participants
reported fewer drinks than those randomised to MI. The authors’ conclusions were
that neither BI nor MI was better in this case than standard care in reducing high-risk
alcohol consumption. However, the uptake of opportunistic screening by ED staff was
poor, as was patient compliance with off-site counselling, which would have had an
impact on the lack of significant results.
The aim of the latest study published by D’Onofrio et al was to determine the efficacy
of emergency practitioner-performed brief intervention for hazardous/harmful drinkers
in reducing alcohol consumption and negative consequences (D'Onofrio et al. 2008).
A randomised clinical trial was conducted in an urban ED. Patients who screened
above National Institute for Alcohol Abuse and Alcoholism guidelines for low-risk
drinking or presented with an alcohol-related injury were eligible. The mean number
of drinks per week and binge-drinking episodes during the past 30 days were
collected at 6 and 12 months; negative consequences and use of treatment services
at 12 months. A brief negotiation Interview performed by emergency practitioners
was compared to a scripted discharge instruction sheet. A total of 494 drinkers took
part and each group was similar with respect to baseline characteristics. In the Brief
Negotiation Interview group, the mean number of drinks per week at 12 months was
3.8 fewer than the 13.6 reported at baseline. The discharge instructions group
decreased their mean number of drinks to 2.6 from 12.4 at baseline. Likewise, bingedrinking episodes per month decreased from 6.0 to 4.0 in the brief interview group
and from 5.4 to 3.9 in the discharge instructions group. For each outcome, the time
62
effect was significant and the treatment effect was not. The authors conclude that
brief interventions among ED patients with hazardous/harmful drinking were effective
in reducing alcohol consumption at 3 months and there was no difference in efficacy
between the two types of interventions.
Yet another randomised controlled study (Soderstrom et al. 2007) tested the
effectiveness of two different brief interventions to reduce both drinking and the
consequences of drinking. Trauma patients defined as at-risk alcohol users (n=497)
were randomised into two treatment options: a brief personalised motivational
intervention (MI), or brief information and advice (BI). After a brief assessment, MI
subjects received a motivational session, feedback letter, and two post-discharge
telephone contacts, whereas the BI group received a brochure and one postdischarge telephone contact. Both groups were followed up and reassessed at 6 and
12 months post-injury. Results show that both groups had statistically significant
reductions in drinking, binge episodes, and consequences related to drinking that
persisted from the 6- to the 12-month follow-up. Although not statistically significant,
for those classified as lower-level drinkers (<1 drink per day), there was a consistent
pattern of maintaining reductions for the MI group at 12 months compared with the BI
group. Their results suggest that brief interventions that link alcohol consumption with
trauma injury and consequences of drinking can be effective in reducing drinking and
consequences related to drinking in non-dependent drinkers.
Walton et al carried out a study with an aim of determining what influence the stage
of change and other attitudes might have on advice given to injured patients visiting
ED for non-life- threatening injuries (Walton et al. 2008). Patients (n = 4,476)
completed a computerised survey; 575 at-risk drinkers were randomly assigned to
one of four brief intervention conditions, and 85% were interviewed again at 3-month
and 12-month follow-ups. The results produced by regression models examined
interaction effects between intervention/control condition (advice/no advice) and
hypothesised moderator variables (stage of change, self-efficacy, acute alcohol use,
attribution of injury to alcohol) on alcohol outcomes over time. Overall, participants
who reported higher levels of self-efficacy had lower weekly consumption, whereas
those with higher readiness to change had greater weekly consumption. In addition,
individuals who attributed their injury to alcohol and received advice had significantly
lower levels of average weekly alcohol consumption and less frequent heavy drinking
from baseline to 12-month follow-up, compared with those who did not receive
advice. This study provides more data regarding attribution for alcohol-related injury
as an important moderator of change and suggests that highlighting the alcohol/injury
connection in ED-based alcohol interventions can augment their effectiveness.
Use of Computers in Emergency Department screening and intervention
Neumann et al hypothesised that the use of computer technology to screen and
provide an intervention could reduce at-risk drinking in injured ED patients (Neumann
et al. 2006). Sub-critically injured patients were screened for an alcohol use disorder,
using a laptop computer that administered the AUDIT and assessed motivation to
reduce drinking. Patients with a positive AUDIT (n = 1,139) were randomised to an
intervention (n = 563) or control (n = 576) condition. The computer generated a
customised printout based on the patient's own alcohol use pattern, level of
motivation, and personal factors, which was provided in the form of feedback and
advice. Most patients (85%) used the computer with minimal assistance. At study
entry, a similar proportion in each group met criteria for at-risk drinking (49.6% versus
46.8%, p = 0.355). At 6 months, 21.7% of intervention and 30.4% of control patients
met criteria for at-risk drinking (p = 0.008). Intervention patients also had a 35.7%
63
decrease in alcohol intake, compared with a 20.5% decrease in controls (p = 0.006).
At 12 months, alcohol intake decreased by 22.8% in the intervention group versus
10.9% in controls (p = 0.023), but the proportion of at-risk drinkers did not
significantly differ (37.3% versus 42.6%, p = 0.168). The results suggest that this is a
practical and effective option to assist the implementation of screening and
intervention in ED.
Recommendation
4.6 Brief interventions should be implemented in
emergency departments and trauma centres.
Strength of
recommendation
A
Level of
evidence
Ia
Hospital settings
Clear associations have been found between admissions for traumatic incidents or
medical problems and alcohol consumption (Saitz 2005). There is a high prevalence
of problem drinkers among hospital inpatients (Shourie et al. 2007), making general
hospital wards a good environment in which to offer brief interventions to a large
number of risky drinkers who already demonstrate or may be at risk of developing
alcohol problems. It is likely that the experience of being admitted to hospital
provides an ideal opportunity for brief alcohol intervention, which is rarely done
(Hosking et al. 2007; Williams et al. 2008). Hospital wards can be a particularly
effective setting for advice, as patients are often more motivated and willing to
change their drinking behaviours after being hospitalised. However, to date the
evidence for the effectiveness of brief intervention in this setting is limited (Emmen et
al. 2004; Freyer-Adam et al. 2008; Saitz et al. 2007). See also Chapter 3.
The existing studies (described in more detail below) could suggest that minimal
intervention (or even simply a participation in a research trial) in these settings is as
successful as a more intensive intervention, or conversely, that all interventions are
ineffective and the impact of hospital admittance is sufficient to effect changes in
alcohol-related behaviour, including rate of consumption.
However, there seems to be more influences at work than is yet fully explored. “What
explains the range of findings?” is a question asked in an editorial (Bernstein et al.
2008); possibilities for negative influences include low sample size, low AUDIT score
cut-off for eligibility; length of the intervention, lack of booster session, possible
contamination, patient characteristics, social desirability bias, etc. These issues have
been addressed fully in primary care and it seems too early to dismiss the usefulness
of brief intervention in hospital settings; the fact that there are conflicting results,
some positive and some negative, seems to indicate that the most effective
combination of intervention elements have not yet been found (Bernstein et al. 2008).
Routine screening for excessive alcohol consumption should be implemented in
general hospital settings; however the evidence for brief intervention is limited
Hospital Settings: Meta-analyses
Eight studies of opportunistic brief intervention conducted in hospitals were reviewed
by Emmen et al (2004) for their effectiveness in reducing alcohol consumption. Some
were individually randomised, some were cluster randomised and one was nonrandomised (group allocation, 6 hospitals, 3 control and 3 intervention). The sole
64
outcome measure was change in alcohol consumption. Weaknesses in study
reporting meant that the authors had difficulty in drawing any conclusions; these
weaknesses included irretrievable data, gaps in data collection or reporting, small
sample sizes and losses to follow-up (from 9% to 50%). Only one study, with a short
follow-up period, showed any significant effect, a larger reduction in weekly drinking
by the intervention group (mean difference -309g; range -470g to -148g). These were
outpatients in a hypertension clinic, 91% of whom were followed up. Changes in the
control group patients are not described. Results from this particular review,
therefore, are inconclusive.
Hospital settings: Randomised controlled trials
Two recent studies have trialled brief alcohol intervention in a hospital setting, by
Saitz et al. (2007) and Freyer-Adam et al. (2008).
The Saitz et al (2007) study included dependent drinkers (77% of whom fulfilled the
CIDI criteria for dependence) and included the outcome measure of treatment by a
specialist for this group, as well as change in mean number of drinks which was
applied to all participants (Saitz et al. 2007). The intervention was a 30-minute
session of motivational counselling by a trained counsellor. Results showed that the
intervention was not significantly associated with receipt of alcohol assistance by 3
months among alcohol-dependent patients (adjusted proportions receiving
assistance, 49% for the intervention group and 44% for the control group;
intervention-control difference, 5% [95% confidence interval, CI, -8%-19%]) or with
drinks per day at 12 months among all patients (adjusted mean decreases, 1.5 for
patients who received the intervention and 3.1 for patients who received usual care;
adjusted mean group difference was -1.5 (CI, -3.7-0.6). There was no significant
interaction between the intervention and alcohol dependence in statistical models
predicting drinks per day (p = 0.24). The conclusions these authors drew are that
brief intervention is insufficient to link medical inpatients with treatment for alcohol
dependence, and is ineffective in reducing levels of alcohol consumption.
Freyer-Adam et al (2008) screened all inpatients of 29 wards from 4 hospitals in
Germany, and 595 were randomised into 3 groups; a control condition or to two
intervention groups which included motivational interviewing by either the specialist
consultation liaison service or by hospital physicians. At baseline, the three groups
differed regarding motivation, with higher motivation among the controls. At 12-month
follow-up, the groups did not differ in alcohol consumption, alcohol-related problems
or measure of well-being. All groups significantly decreased their alcohol
consumption. Regarding motivation, longitudinal analyses revealed significant
interaction effects of time and intervention (p<0.05), indicating a stronger increase of
readiness to change drinking and a small increase in readiness to seek help among
those who received intervention compared to the controls. The conclusions were that
the intervention was not effective in reducing alcohol consumption when compared to
controls (who, however, had higher motivation to reduce drinking, thereby affecting
the results) or in increasing well-being 12 months after hospitalisation. However, it
had a positive effect on readiness to change drinking and on readiness to seek
formal help for alcohol problems.
Recommendation
4.7 Brief interventions should be implemented in
general hospital settings.
Strength of
recommendation
D
Level of
evidence
IV
65
Community counselling and welfare services
Patients may present to community counselling services with a variety of complaints
that may be related to their alcohol or other drug use, including financial, relationship,
employment or parenting problems. Brief interventions may be appropriate for those
drinking at risky levels (O'Connor et al. 2007) (Sullivan et al. 2005); however as yet
there is little evidence as to their effectiveness in these settings (see Chapter 3) .
Recommendation
4.8 Brief interventions in community health and
welfare settings may be used, but should not be
a sole intervention strategy.
Strength of
recommendation
D
Level of
evidence
IV
Workplace settings
Rates of alcohol consumption are particularly high in some workplace settings. In
particular, hospitality, agriculture and construction industries have been identified as
having a large proportion of people drinking at levels leading to both short-term and
long-term risk of harm (Berry et al. 2007), which can lead to increased rates of
accidents and absenteeism (Roche et al. 2008).
Web-based feedback, with or without motivational counselling, proved an effective
method for reducing risky drinking among young employed people (Doumas et al.
2008); 124 participants were randomly assigned to one of three conditions: webbased feedback, web-based feedback plus a 15-minute motivational interviewing
session, or a control group. Both intervention groups reported significantly lower
levels of drinking than those in the control group at a 30-day follow-up. No
differences were found between the two intervention conditions, indicating that the
addition of the motivational interview did not increase the efficacy of the web-based
feedback program. However the small sample size limits any generalisations that can
be made from this study.
Another study found challenges in getting people to access and participate in the
workplace-initiated website program (Matano et al. 2007). Matano‘s pilot study gave
145 employees working in Silicon Valley access to a web site that provided feedback
on their levels of stress and use of coping strategies. Participants randomised to
receive full individualised feedback also received individualised feedback about their
risk for alcohol-related problem. The major drawback is that only 3% took up the offer
of participation, severely limiting the results and any conclusions that could be made.
A substance misuse prevention training program designed to change work culture,
combined with random workplace testing, in a large US transportation company, was
successful in reducing injuries (Miller et al. 2007). This program focussed on
changing workplace attitudes toward on-the-job substance use, in addition to training
workers to recognise and intervene with co-workers who have a problem. The main
benefit to the company was that the combination of the peer-based program and
testing was associated with an approximate one-third reduction in injury rate,
avoiding a $48m in employer costs. The cost-benefit ratio was 1:26, thereby making
the program extremely worthwhile both for participants and employers. However, the
project had the benefit of being backed up by a federally mandated testing program.
66
There is at present not enough evidence to recommend implementation of brief
interventions in this setting
Recommendation
4.9 Brief interventions in high-risk workplaces
may be used, but should not be a sole
intervention strategy.
Strength of
recommendation
D
Level of
evidence
IV
The wider community- and the internet
Research on the efficacy of correspondence or web-based interventions is emerging.
For example, Kypri et al identified nine acceptability or feasibility studies of these
approaches and seven efficacy trials covering a wide range of settings in 2003-4
(Kypri et al. 2005). These modes of intervention are acceptable to patients and the
public, and with careful planning can be implemented in a variety of settings.
Treatment trials demonstrate the efficacy of these interventions in reducing
hazardous drinking by university students, in delaying initiation of heavy drinking in
children and adolescents, and, intriguingly, in addressing insomnia among recovering
alcoholics.
There is strong support among potential users for alcohol interventions that employ
telephone assistance, written correspondence, and the Internet.
These new technologies offer the prospect of increasing the reach of interventions for
problem drinking and being cost-effective alternatives or supplements to face-to-face
interventions.
One study is presently examining two alternative modes of electronic intervention
(Murray et al. 2007). In a two-arm randomised controlled trial, an on-line
psychologically enhanced interactive computer-based intervention is compared with
a flat, text-based information web-site. Recruitment, consent, randomisation and data
collection are all on-line. The primary outcome is to be total past-week alcohol
consumption; secondary outcomes include hazardous or harmful drinking,
dependence, harm caused by alcohol, and mental health.
Web-based interventions show promise, especially in university students (Bewick et
al. 2008b; Bewick et al. 2008a) and young people. Web-based feedback, with or
without motivational counselling, proved an effective method for reducing risky
drinking among young employed people (Doumas et al. 2008), although another
study found challenges in getting people to access and participate in the website
program through their workplace (Matano et al. 2007).
Limitations of Brief Interventions
The outcomes can be perceived as modest and discourage clinicians from using brief
interventions routinely.
One of the limitations of brief interventions is that the clinician often does not see
beneficial results of the intervention (e.g. the number needed to treat can be
substantial in order to create a measurable effect). In order to get one drinker to
return within recommended limits, brief intervention needs to be delivered to 10
67
patients (this is the number needed to treat, or NNT) (Beich et al. 2003a; Beich et al.
2003b; Vinson 2003). To identify those individuals one must screen 100 (the number
needed to screen). However this is a quarter of the number (400) needed to screen
for high cholesterol before 1 person can benefit, which is a routine, expensive and
invasive test (Vinson 2003; Shepherd et al. 1995).
Another factor that must be mentioned is that screening alone can raise the patients’
awareness and have a similar effect to a brief intervention (Kaner et al. 2007; Kaner
et al. 2009).
There is no evidence that brief interventions are effective among people with more
severe alcohol problems and dependence disorders. Typically, interventions offered
to treatment-seeking populations or those with severe alcohol problems require more
comprehensive treatment approaches, that will usually include intensive interventions
(e.g. detoxification), or extended follow-up sessions.
A number of barriers to the uptake and implementation of brief interventions in health
care settings have been identified (Aalto et al. 2003). These include:
•
Lack of confidence, knowledge, or skills
•
Difficulty in identifying risky drinkers
•
Uncertainty of the justification for initiating discussion about alcohol
•
Lack of simple guidelines
•
Lack of financial incentives
Summary
Most alcohol-related harm in the community is caused by excessive drinkers whose
consumption exceeds recommended drinking levels, not the drinkers with severe
alcohol dependency problems. One way to reduce consumption levels in a
community is to provide a brief intervention in primary care over one to four sessions,
provided by healthcare workers such as general physicians, nurses or psychologists.
In general practice, patients should be routinely asked about alcohol consumption
during registration, general health checks and as part of health screening (using a
questionnaire). The intervention would ideally include feedback on alcohol use and
harms, identification of high risk situations for drinking, coping strategies, increased
motivation and the development of a personal plan to reduce drinking.
Brief interventions for non-dependent drinkers have been proved efficacious in
primary care; at present there is conflicting evidence for their effectiveness in
emergency departments and other hospital settings.
68
References
Aalto, M, P Pekuri and K Seppa 2003, Obstacles to carrying out brief intervention for
heavy drinkers in primary health care: a focus group study. Drug Alcohol Rev
22: 169-173.
AIHW 2004, General practice activity in Australia 2003-4. Available at
http://www.aihw.gov.au/publications/index.cfm/title/10079
Babor, T and J Higgins-Biddle 2000, Alcohol acreening and brief intervention:
dissemination strategies for medical practice and public health. Addiction
95(5): 677-686.
Ballesteros, J, Duffy JC, Querejeta I et al. 2004, Efficacy of brief interventions for
hazardous drinkers in primary care: systematic review and meta-analyses.
Alc Clin Exper Res 28(4): 608-618.
Bazargan-Hejazi, S, Bing E, Bazargan M et al. 2005, Evaluation of a Brief
Intervention in an Inner-City Emergency Department. Ann Emerg Med 46(1):
67-76.
Beich, A, Gannik D, Saelan H et al. 2007, Screening and brief intervention targeting
risky drinkers in Danish general practice. A pragmatic controlled trial. Alcohol
Alcohol 42(6): 593-603.
Beich, A, T Thorsen T and S Rollnick 2003a, Screening in brief intervention trials
targeting excessive drinkers in general practice: systematic review and metaanalysis. BMJ 327: 536.
Beich, A, T Thorsen and S Rollnick 2003b, Screening in brief intervention trials
targeting excessive drinkers in general practice: systematic review and metaanalysis. BMJ 327(7414): 536-542.
Bernstein, E and J Bernstein 2008, Effectiveness of Alcohol Screening and Brief
Motivational Intervention in the Emergency Department Setting. Ann Emerg
Med 51(6): 751-754.
Berry, J, Pidd K, Roche A et al. 2007, Prevalence and patterns of alcohol use in the
Australian workplace: findings from the 2001 National Drug Strategy
Household Survey. Addiction 102(9): 1399-1410.
Bertholet, N, Daeppen J-B, Wietlisbach V et al. B 2005, Reduction of alcohol
consumption by brief alcohol intervention in primary care: systematic review
and meta-analysis. Arch Int Med 165(9): 986-995.
Bewick, BM, Trusler K, Barkham M et al. 2008a, The effectiveness of web-based
interventions designed to decrease alcohol consumption - A systematic
review. Prev Med 47(1): 17-26.
Bewick, BM, Trusler K, Mulhern B et al. 2008b, The feasibility and effectiveness of a
web-based personalised feedback and social norms alcohol intervention in
UK university students: A randomised control trial. Addict Behav 33(9): 11921198.
Bien, T, W Miller and J Tonigan 1993, Brief interventions for alcohol problems: a
review. Addiction 88: 315-336.
69
Britt, H, Millerm GC, Knox S et al. 2003, General practice activity in Australia 200203. Cat. No. GEP 16, Canberra: Austrlian Institute of Health and Welfare &
University of Sydney.
Cheeta, S, Drummond C, Oyefeso A et al. 2008, Low identification of alcohol use
disorders in general practice in England. Addiction 103(5): 766-773.
Conigrave, K, E Proude and J Saunders 2003, Doctors should ask every patient
about alcohol (in rapid responses to Beich et al). BMJ 327(7414): 536-542.
D'Onofrio, G and L Degutis 2002, Preventive care in the emergency department:
screening and brief intervention for alcohol problems in the Emergency
department: a systematic review. Acad Emerg Med 9:627-638.
D'Onofrio, G and P Degutis 2004/05, Screening and brief intervention in the
Emergency Department. Alcohol Res Health 28(2): 63-72.
D'Onofrio, G, Pantalon MV, Degutis LC et al. 2008, Brief Intervention for Hazardous
and Harmful Drinkers in the Emergency Department. Ann Emerg Med 51(6):
742-750.
Daeppen, JB, Gaume J, Bady P et al. 2007, Brief alcohol intervention and alcohol
assessment do not influence alcohol use in injured patients treated in the
emergency department: a randomized controlled clinical trial. Addiction
102(8): 1224-1233.
Dent, AW, Weiland TJ, Phillips GA et al. 2008, Opportunistic screening and cliniciandelivered brief intervention for high-risk alcohol use among emergency
department attendees: a randomized controlled trial. Emerg Med Australas
20(2): 121-128.
Dinh-Zarr, T, Goss C, Heitman E et al. 2005, Interventions for preventing injuries in
problem drinkers [Systematic Review]. Cochrane Database Syst Rev 3:3.
Doumas, D and E Hannah 2008, Preventing high-risk drinking in youth ein the
workplace: a web-based normative feedback program. J Subst Abuse Treat
34:263-271.
Emmen, MJ, Schippers GM, Bleijenberg G et al. 2004, Effectiveness of opportunistic
brief interventions for problem drinking in a general hospital setting:
systematic review. BMJ 328(7435): 318-310.
Field, C, DW Hungerford and C Dunn 2005, Brief motivational interventions: an
introduction. J Trauma 59(3 Suppl): S21-26.
Freyer-Adam, J, Coder B, Baumeister SE et al. 2008, Brief alcohol intervention for
general hospital inpatients: A randomized controlled trial. Drug and Alcohol
Dependence 93(3): 233-243.
Gentilello, L, Rivara F, Donovan D et al. 1999, Alcohol interventions in a trauma
center as a means of reducing the risk of injury recurrence. Annals of Surgery
230(4): 473-483.
70
Grossberg, PM, DD Brown and MF Fleming 2004, "Brief physician advice for highrisk drinking among young adults. Ann Fam Med 2(5): 474-480
Grothues, J, Bischof G, Reinhardt S et al. 2008, Effectiveness of brief alcohol
interventions for general practice patients with problematic drinking behavior
and comorbid anxiety or depressive disorders. Drug Alcohol Depend 94(1-3):
214-220.
Guth, S, Lindberg SA, Badger GL et al. 2008, Brief intervention in alcohol-dependent
versus nondependent individuals. J Stud Alcohol Drugs 69(2): 243-250.
Havard, A, A Shakeshaft and R Sanson-Fisher 2008, Systematic review and metaanalyses of strategies targeting alcohol problems in emergency departments:
interventions reduce alcohol-related injuries. Addiction 103(3): 368-376.
Heather, N and T Stockwell 2004, The essential handbook of treatment and
prevention of alcohol problems Chichester, England; Hoboken, NJ, Wiley.
Hosking, J, S Ameratunga, C Bullen et al. 2007, Screening and intervention for
alcohol problems among patients admitted following unintentional injury: a
missed opportunity? N Z Med J 120(1249): U2417.
Johnsson, KO and M Berglund 2006, Comparison between a cognitive behavioural
alcohol programme and post- mailed minimal intervention in high-risk drinking
university freshmen: results from a randomized controlled trial. Alcohol
Alcohol 41(2): 174-180.
Kaner, E, Beyer F, Dickinson H et al. 2007, Effectiveness of brief alcohol
interventions in primary care populations. Cochrane Database Syst Rev.
Kaner, E, Dickinson H, Beyer F et al. 2009, The effectiveness of brief alcohol
interventions in primary care settings: A systematic review. Drug Alcohol Rev
28(3): 301-323.
Kypri, K, Langley JD, Saunders JB et al. 2008, Randomized Controlled Trial of WebBased Alcohol Screening and Brief Intervention in Primary Care. Arch Intern
Med 168(5): 530-536.
Kypri, K, Sitharthan T, Cunningham JA et al. 2005, Innovative approaches to
intervention for problem drinking. Curr Opin Psychiatry 18(3): 229-234.
Longabaugh, R, Woolard RE, Nirenberg TD et al. 2001, Evaluating the effects of a
brief motivational intervention for injured drinkers in the emergency
department. J Stud Alcohol 62(6): 806-816.
Matano, RA, Koopman C, Wanat SF et al. 2007, A pilot study of an interactive web
site in the workplace for reducing alcohol consumption. J Subst Abuse Treat
32(1): 71-80.
McCambridge, J and M Day 2008, Randomized controlled trial of the effects of
completing the Alcohol Use Disorders Identification Test questionnaire on
self-reported hazardous drinking. Addiction 103(2): 241-248.
71
Miller, T, E Zaloshnja and R Spicer 2007, Effectiveness and benefit-cost of peerbased workplace substance abuse prevention coupled with random testing.
Accid Anal & Prev 39: 565-573.
Monti, P, Colby S, Barnett N et al.1999, Brief intervention for harm reduction with
alcohol-positive older adolescents in a hospital emergency department. J
Consul Clin Psychol 67(6): 989-994.
Moyer, A, Finney JW, Swearingen CE et al. 2002, Brief interventions for alcohol
problems: a meta-analytic review of controlled investigations in treatmentseeking and non-treatment-seeking populations. Addiction 97(3): 279-292.
Murray, E, McCambridge J, Khadjesari Z et al. 2007, The DYD-RCT protocol: an online randomised controlled trial of an interactive computer-based intervention
compared with a standard information website to reduce alcohol consumption
among hazardous drinkers. BMC Public Health 7: 306.
Neumann, T, Neuner B, Weiss-Gerlach E et al. 2006, The effect of computerized
tailored brief advice on at-risk drinking in subcritically injured trauma patients.
J Trauma 4: 805-814.
Nilsen, P, Baird J, Mello MJ et al. 2008, A systematic review of emergency care brief
alcohol interventions for injury patients. J Subst Abuse Treat 35(2): 184-201.
Nilssen, ODD 2004, Long-term effect of brief intervention in at-risk alcohol drinkers: a
9-year follow-up study. Alcohol and Alcohol 39(6): 548-551.
O'Connor, MJ and SE Whaley 2007, Brief intervention for alcohol use by pregnant
women. Am J Pub Health 97(2): 252-258.
Poikolainen, K 1999, Effectiveness of brief interventions to reduce alcohol intake in
primary health care populations: a meta-analysis. Prevent Med 28(5): 503509.
Proude, E, Saunders JB, Conigrave K et al. 2005, The Drink-less Program.
Retrieved 25 April 2009 from http://www.cs.nsw.gov.au/drugahol/drinkless/.
Reinhardt, S, Bischof G, Grothues J et al. 2008, Gender differences in the efficacy of
brief interventions with a stepped care approach in general practice patients
with alcohol-related disorders. Alcohol Alcohol 43(3): 334-340.
Roche, A, Pidd K, Berry J et al. 2008, Workers' drinking patterns: the impact on
absenteeism in the Australian workplace. Addiction 103: 738-748.
Saitz, R 2005, Unhealthy alcohol use. N Eng J Med 352(6): 596-607.
Saitz, R, Palfai TP, Cheng DM et al. 2007, Brief Intervention for Medical Inpatients
with Unhealthy Alcohol Use: A Randomized, Controlled Trial. Ann Int Med
146(3):167-176.
Saunders, J, Aasland OG, Amundsen A et al.1993, Alcohol consumption and related
problems among primary health care patients: WHO Collaborative Project on
Early Detection of Persons with Harmful Alcohol Consumption-I. Addiction 88:
349-362.
72
Shepherd, J, Cobbe SM, Ford I et al.1995, Prevention of coronary heart disease with
pravastatin in men with hypercholesterolemia. West of Scotland Coronary
Prevention Study Group. N Engl J Med 333(20):1301-1307.
Shourie, S, Conigrave KM, Proude EM et al. 2007, Detection of and intervention for
excessive alcohol and tobacco use among adult hospital in-patients. Drug
Alcohol Rev 26(2): 127-133.
Soderstrom, CA, DiClemente CC, Dischinger PC et al. 2007, A controlled trial of brief
intervention versus brief advice for at-risk drinking trauma center patients. J
Trauma 62(5): 1102-1111.
Spirito, A, Monti P, Barnett N et al. 2004, A randomized clinical trial of a brief
motivational intervention for alcohol-positive adolescents treated in an
emergency department J Paediatr 145: 396-402.
Sullivan, LE, DA Fiellin and PG O'Connor 2005, The prevalence and impact of
alcohol problems in major depression: a systematic review. Am J Med 118(4):
330-341.
Vinson, D 2003, Number needed to treat and the prevention paradox. (In rapid
responses to Beich et al). BMJ 327 (7414): 536-542.
Walton, M, Goldstein A, Chermack S et al. 2008, Brief alcohol intervention in the
emergency department: moderators of effectiveness. J Stud Alcohol Drugs
69(4):550-560.
Whitlock, E, Polen MR, Green CA et al. 2004, Behavioral counseling interventions in
primary care to reduce risky/harmful alcohol use by adults: a summary of the
evidence for the U.S. Preventive Services Task Force. Ann Int Med 140: 557568.
Wilk, A, N Jensen and T Havighurst 1997, Meta-analysis of randomized control trials
addressing brief interventions in heavy alcohol drinkers. J Gen Int Med 12(5):
274-283.
Williams, G, Daly M, Proude EM et al. 2008, The influence of alcohol and tobacco
use in orthopaedic inpatients on complications of surgery. Drug Alcohol Rev
27(1): 55-64.
Wutzke, S, Conigrave K, Saunders J et al. 2002, The long-term effectiveness of brief
interventions for unsafe alcohol consumption: a 10-year follow-up. Addiction
97(6): 665-675.
Wutzke, S, Shiell A, Gomel M et al. 2001, Cost effectiveness of brief interventions for
reducing alcohol consumption. Soc Sci Med 52(6): 863-870.
Zwar, N, Richmond R, Borland R et al. 2005, Smoking cessation guidelines for
Australian general practice. Aust Fam Physician 34(6): 461-466.
73
Chapter 5 Alcohol withdrawal management
Alcohol Withdrawal Syndrome: Clinical Presentation
This section discusses the clinical signs and symptoms, onset and duration, and
common complications of alcohol withdrawal.
Signs and symptoms of alcohol withdrawal
Alcohol withdrawal syndrome is characterised by central nervous system
hyperactivity that occurs when an alcohol dependent individual abruptly stops or
significantly reduces alcohol consumption. About 50% of alcohol-dependent patients
develop clinically relevant symptoms of withdrawal, ranging from 13% to 71% (Victor
and Adams 1953; Saitz et al. 1994; Degenhardt et al. 2000).
The signs and symptoms of alcohol withdrawal may be grouped into three major
classes (autonomic, gastro-intestinal and cognitive and perceptual changes), and
may be uncomplicated or complicated withdrawal (American Psychiatric Association
2000).
Table 5.1: Signs and symptoms of alcohol withdrawal
Uncomplicated
withdrawal
features
Severe
withdrawal
complications
Autonomic
hyperactivity
Sweating
Tachycardia
Hypertension
Tremor
Fever (generally
<38°C)
Gastrointestinal
features
Anorexia
Nausea
Vomiting
Dyspepsia
Diarrhoea
Dehydration and
electrolyte
disturbances
Cognitive and
perceptual changes
Poor concentration
Anxiety
Psychomotor
agitation
Disturbed sleep, vivid
dreams
Seizures
Hallucinations or
perceptual
disturbances (visual,
tactile, auditory)
Delirium
Onset and duration of withdrawal symptoms
Onset of alcohol withdrawal is usually between six and 24 hours after the last drink or
following significant reduction in alcohol consumption. In some individuals (usually
relatively fit and healthy), the withdrawal syndrome is short-lived and inconsequential,
with the acute phase resolving well within five days with minimal or no medical
intervention. However, in others it increases in severity over the first 48 to 72 hours of
abstinence (Saitz 1998; Shuckitt 2006; Prescrire 2007).
In some severely dependent drinkers, withdrawal can occur when the blood alcohol
level (BAL) is decreasing, even if the patient is still intoxicated or has consumed
74
alcohol recently, with a significant proportion of dependent drinkers experiencing the
onset of withdrawal symptoms before the BAL reaches zero (Victor and Brausch
1967).
Psychological symptoms of alcohol withdrawal, including dysphoria, sleep
disturbance and anxiety often persist for 1-2 weeks after drinking cessation and can
continue for months (Satel et al. 1993; Shuckitt 2006).
Severe withdrawal complications
Severe withdrawal complications include seizures, delirium and hallucinations.
Alcohol Withdrawal Seizures
Alcohol withdrawal seizures are usually generalised (tonic-clonic) seizures. Seizures
may occur 6 to 48 hours after the last drink is consumed in alcohol dependent
individuals , and can occur even if the blood alcohol level is high (e.g. greater than
0.10 g%) in severely dependent drinkers (Victor and Brausch 1967; Tartara et al
1983).
The prevalence of alcohol-withdrawal seizures is estimated at between 2 and 9% of
alcohol dependent individuals (Chan 1985). Individuals who have experienced an
alcohol withdrawal seizure are more likely to experience further seizures in
subsequent alcohol withdrawal episodes (Trevisan et al. 1998). The risk of seizure
recurrence within 6-12 hours is estimated at between 13% and 24% in untreated
patients (Hillbom et al 2003).
Alcohol withdrawal delirium
The features of alcohol withdrawal delirium (also known as delirium tremens, DTs)
are disturbance of consciousness and changes in cognition or perceptual disturbance
(American Psychiatric Association 2002). The terms “alcohol withdrawal delirium”
and “delirium tremens” can be used interchangeably.
The incidence of alcohol withdrawal delirium in un-medicated alcohol dependent
patients averages at 5%, although the incidence is much lower with effective
treatment of alcohol withdrawal. Early studies of delirium tremens reported mortality
rates as high as 15%, however, mortality rates have fallen with advances in
management to less than 1% (Mayo-Smith et al. 2004).
Alcohol withdrawal delirium usually occurs 48 to 96 hours after the last drink is
consumed but may take up to seven days to appear. The delirium usually lasts for 2
to 3 days, although can persist for several days (Mayo-Smith et al. 2004).
Hallucinations
During any stage of the alcohol withdrawal, transient hallucinations either visual or
tactile may occur in 3-10% of patients with severe withdrawal, however they have no
prognostic significance (Trevisan et al. 1998). Some patients may also experience
paranoia, psychomotor disturbances, abnormal affect and other delusions.
Hallucinations may appear within the first 24 hours and in some cases last up to
three days; however they can resolve within 24 to 48 hours.
75
Assessment and Treatment Matching
Assessment of patients undergoing alcohol withdrawal requires a comprehensive
history, examination, investigations and collateral history and is described in detail in
Chapter 3. This section discusses common predictors of alcohol withdrawal severity,
withdrawal treatment services and their objectives, treatment matching and
monitoring during withdrawal and the use of alcohol withdrawal scales are also
discussed.
Predictors of withdrawal severity
Development of severe withdrawal in an individual patient is difficult to predict.
However, a number of patient characteristics have been identified that are likely to be
associated with more severe withdrawal symptoms or complications (Saitz 1998).
These include: current drinking pattern, past withdrawal experience, concomitant
substance use and coexisting medical and psychiatric conditions.
The severity of withdrawal is only moderately predicted by amounts of alcohol
consumed. Large numbers of patients can be safely managed without medication
(Benzer 1990; Whitfield et al. 1978). Severe withdrawal is more likely with the higher
the levels of chronic alcohol consumption (e.g. 150 grams of alcohol per day), but
individuals with lower levels can experience severe withdrawal and withdrawal
complications. The minimal quantity and frequency of alcohol consumption that may
lead to withdrawal is not known. In a recent review of alcohol withdrawal syndromes
no studies identified the minimal level of alcohol consumption required to produce
physical dependence (Prescrire 2007).
Duration of heavy alcohol use for 6 years or longer increases the odds of developing
withdrawal symptoms 15 times (Ballenger and Post 1978).
Early morning drinking to alleviate withdrawal symptoms is a predictor of higher
alcohol withdrawal severity (Benzer 1990; Essardas Darayanani et al. 1994;
Prescrire 2007). Individuals with heavy but irregular (e.g. 2-3 days per week) alcohol
consumption (sometimes referred to as ‘binge’ drinking) generally do not experience
severe withdrawal, but are still at risk of such. Patients with a history of severe
alcohol withdrawal syndrome (e.g. severe anxiety, seizures, delirium, hallucinations)
are more likely to experience such complications in future withdrawal episodes
(Essardas Darayanani et al.1994; Trevisan et al. 1998; Saitz 1998).
Patients with heavy or regular use of other substances (e.g. benzodiazepines,
stimulants, opiates) may experience more severe withdrawal features. In particular,
withdrawal from both alcohol and benzodiazepines may increase the risk of
withdrawal complications (Saitz 1998; Soyka et al. 1989).
Patients with concomitant medical (e.g. sepsis, epilepsy, severe hepatic disease,
head injury, pain and nutritional depletion) or psychiatric conditions (e.g. anxiety,
psychosis or depression) are more likely to experience severe withdrawal
complications (Wetterling et al. 1994; Myrick and Anton 1998; Saitz 1998).
The presence of moderate to severe withdrawal symptoms (e.g. CIWA-Ar ≥ 15, see
discussion of alcohol withdrawal scales below) left untreated is one of the stronger
predictors of seizures and confusion (Foy et al. 1988).
76
It is important to monitor all patients carefully during the alcohol withdrawal period,
particularly those with heavy alcohol use and with a history of alcohol withdrawal.
Recommendation
5.1 The risk of severe alcohol withdrawal should
be assessed based on current drinking patterns,
past withdrawal experience, concomitant
substance use, and concomitant medical or
psychiatric conditions.
Strength of
recommendation
Level of
evidence
B
II
Objectives of alcohol withdrawal services
Research suggests that withdrawal treatment alone has little, if any, impact on longterm alcohol use (Vaillant 1988). All existing literature assessing efficacy of relapse
prevention medication indicates high levels of relapse in the first 3 month after
detoxification in placebo group. For example in the study by Kiefer et al. (2004)
comparing acamprosate and naltrexone, 75% of placebo group relapsed at 12 weeks
and 80% at 24 weeks post-withdrawal. Withdrawal management should not be seen
as a stand-alone treatment that is likely to result in prolonged periods of abstinence,
but instead as a transitional step on the long road to abstinence.
Many commentators have described objectives for alcohol and drug withdrawal
services (e.g. Saitz and O’Malley 1997; Myrick and Anton 1998). A consensus
approach developed for opiate withdrawal services in Australia (Lintzeris et al 2006)
can also be applied to alcohol withdrawal services.
The realistic set of objectives adapted for alcohol withdrawal services is as follows:
1. To interrupt a pattern of heavy and regular alcohol use. Some individuals require
the structure and support of withdrawal services in order to stop drinking. Whilst
many have a longer term goal of achieving abstinence, some individuals may be
seeking a temporary break from their alcohol use.
2. To alleviate withdrawal symptoms. Palliation of the discomfort of alcohol
withdrawal symptoms is an important reason for patients presenting for treatment,
and one of the primary aims of withdrawal services.
3. To prevent severe withdrawal complications. Management of alcohol withdrawal
aims to prevent or manage potentially life threatening complications such as
seizures, delirium and Wernicke’s encephalopathy. Furthermore, alcohol
withdrawal can complicate concomitant medical or psychiatric conditions.
4. Facilitate linkages to ongoing treatment for alcohol dependence. Withdrawal
services are acute services with short-term outcomes. However alcohol
dependence is a chronic relapsing condition and positive long-term outcomes are
more often associated with participation in ongoing treatment such as counselling,
self-help, residential rehabilitation and pharmacological approaches (see Chapter
7). Managed withdrawal provides an opportunity to plan and engage in postwithdrawal treatment services.
5. To get help with any other problems. While some people will be unwilling or
unable to continue in ongoing drug treatment programs, they may benefit from
77
linkages with primary or specialist health services or welfare services (e.g.
accommodation, employment services).
Recommendation
Strength of
recommendation
Level of
evidence
5.2 Successful completion of alcohol withdrawal
does not prevent recurrent alcohol consumption
and additional interventions are needed to
achieve long-term reduction in alcohol
consumption.
A
Ia
5.3 Realistic goals of clinicians, patients and
their carers for withdrawal services include:
interrupting a pattern of heavy and regular
alcohol use, alleviating withdrawal symptoms,
preventing severe withdrawal complications,
facilitating links to ongoing treatment for alcohol
dependence, providing help with any other
problems (such as accommodation,
employment services).
D
IV
Settings for alcohol withdrawal
Alcohol withdrawal management can occur in a variety of settings, ranging from
hospital inpatient, community residential (e.g. specialised detoxification unit) to
ambulatory services (outpatient or home-based detoxification services).
Outpatient withdrawal management is an effective, safe, and low-cost treatment for
patients with mid-to-moderate symptoms of alcohol withdrawal. One randomised
controlled study comparing inpatient and outpatient treatment of withdrawal found
that the cost and duration of treatment were significantly lower in the outpatient
group. The completion rates were higher in the inpatient group than in the outpatient
(95% vs 72%) and abstinence rates were higher in the inpatient group at one month
follow up. The abstinence rates were not different at 6 months. There were no
serious medical complications in either group (Hayashida et al. 1989).
Soyka and Horak (2004) examined the effectiveness and safety of alcohol outpatient
detoxification in an open prospective study. Patients were screened for relevant
neuropsychiatric disorders and other exclusion criteria and then seen on a daily
outpatient basis for 5-7 days. Psychotropic or symptomatic medications to alleviate
withdrawal symptoms were prescribed if necessary (CIWA-A score >16).
Psychotherapeutic interventions were conducted to motivate the patient for further
alcohol therapy. Of 557 patients screened 331 entered the study. Ninety four percent
(n = 312) of the study participants successfully completed treatment. Sixty percent of
them required psychotropic medication. Ninety one percent of the initial sample
patients entered a consecutive 3-month motivational treatment program. Forty six
percent of patients successfully completed the 1-year consecutive outpatient
treatment. The patients who were not included into the study required inpatient
management of withdrawal for medical reasons. It should be noted that this study
does not compare outpatient vs inpatient management. However, it provides
evidence for safe and effective management of alcohol withdrawal in an outpatient
setting.
78
Selecting withdrawal settings
The withdrawal setting should be carefully selected for each individual patient.
Withdrawal can be managed in an ambulatory setting (i.e. outpatient, home-based
detoxification), a community residential unit or in a hospital.
The choice of withdrawal setting requires a comprehensive clinical assessment and
discussion with the patient (and where possible family or carers) regarding the
advantages and disadvantages of each approach (Saitz and O’Malley 1997; Saitz
1998; Myrick and Anton 1998).
Factors to be considered in determining the most appropriate withdrawal setting for
an individual include:
likely severity of alcohol withdrawal and occurrence of severe withdrawal
complications (seizures, delirium, hallucinations);
use of other substances: individuals who report heavy use of other drugs (e.g.
benzodiazepines, psychostimulants, opiates), may be at increased risk of
withdrawal complications and generally require close monitoring and supervision
(e.g. community residential unit);
concomitant medical or psychiatric conditions: patients with significant comorbidity may require hospital admission until medically cleared. Patients may be
able to be ‘step-down’ to less intensive withdrawal settings to complete
withdrawal once medically stable.
social circumstances, the availability of a safe environment and ‘home’ supports;
outcome of prior withdrawal attempts: repeated failure at ambulatory withdrawal
may be an indication for referral to a residential detox unit;
patient preference and availability of resources;
Some patients wish to attempt ambulatory withdrawal despite multiple failed prior
attempts. Further attempts at outpatient withdrawal may be appropriate, however
clinicians should identify how this attempt will be different to previous attempts (e.g.
increased home supports and monitoring), and negotiate with the patient mutually
agreed criteria to be met in order to continue with the withdrawal attempt (e.g. no
alcohol use in first 2 days).
Patients on waiting-lists for residential withdrawal units may require support in
maintaining motivation and avoiding high risk activities until admission.
Prescribing benzodiazepines in an attempt to alleviate withdrawal prior to admission
is not recommended, and may increase the risk of adverse events from the
combination of alcohol and benzodiazepines.
Based on the assessment of these factors, patients with no history of severe
withdrawal complications and without severe concomitant medical, psychiatric or
other substance use disorders are likely to experience withdrawal of mild to moderate
severity. They are suitable for ambulatory withdrawal setting, if they have a safe
‘home’ environment and good social support enabling daily monitoring by reliable
support person and good access to health care services.
79
Patients with predicted moderate to severe withdrawal, who have a history of severe
withdrawal complications (such as seizure, hallucinations) or withdrawing from
multiple substances should be recommended withdrawal management in a
community residential setting, if they have no severe medical or psychiatric
comorbidity. Patients without safe home environment or social supports and those
with repeated failed ambulatory withdrawal attempts would also benefit from
residential withdrawal.
Inpatient hospital treatment should be recommended for those with severe
withdrawal complications (such as delirium or seizures of unknown cause), and/or
severe medical or psychiatric comorbidity. Hospital addiction medicine consultation
liaison services should be accessible in hospitals to aid assessment, management
and discharge planning.
Recommendation
Strength of
recommendation
Level of
evidence
5.4 Ambulatory withdrawal is appropriate for
those with mild to moderate predicted
withdrawal severity, a safe ‘home’ environment
and social supports, no history of severe
withdrawal complications, and no severe
concomitant medical, psychiatric or other
substance use disorders.
5.5 Community residential withdrawal is
appropriate for those with predicted moderate to
severe withdrawal, a history of severe
withdrawal complications, withdrawing from
multiple substances, no safe environment or
social supports, repeated failed ambulatory
withdrawal attempts, and with no severe
medical or psychiatric comorbidity.
D
IV
D
IV
5.6 Inpatient hospital treatment is appropriate
for those with severe withdrawal complications
(such as delirium or seizures of unknown
cause), and/or severe medical or psychiatric
comorbidity.
S
5.7 Hospital addiction medicine consultation
liaison services should be accessible in
hospitals to aid assessment, management and
discharge planning.
S
Monitoring during alcohol withdrawal
Patients with moderate to severe withdrawal symptoms left untreated are more likely
to develop withdrawal complications (Foy et al. 1988). Other factors, such as
patient’s compliance with treatment, level of motivation and perception of treatment
effectiveness may influence treatment outcome. It is important to carefully monitor
patients during the alcohol withdrawal period paying particular attention to the
following:
• physical parameters, including level of hydration, pulse rate, blood pressure,
temperature, level of consciousness (especially if medicated);
80
•
•
severity of alcohol withdrawal. It is beneficial to use an alcohol withdrawal
rating scale to assess the severity of withdrawal, to guide treatment, and to
assist clinicians in communicating more objectively about the severity and
management of alcohol withdrawal. Alcohol withdrawal scales are described
below.
general progress during withdrawal episode. This includes ongoing level of
motivation, alcohol and other drug use during ambulatory withdrawal
(breathalyser readings and/or urine drug screens may be clinically indicated);
response to any medication(s); and patient concerns or difficulties.
Clinical Institute Withdrawal Assessment for Alcohol Scale
The Clinical Institute Withdrawal Assessment for Alcohol revised CIWA-Ar is a 10item, validated scale. CIWA-Ar scores below 10 are considered mild withdrawal;
between 10 and 20 are moderate withdrawal, and above 20 are considered severe
withdrawal. Patients with CIWA-Ar scores of >10 are at greater risk of developing
withdrawal complications if not medicated (Sullivan et al. 1989).
Frequency of CIWA-Ar monitoring depends upon treatment setting and clinical
condition of the patient. Patients with CIWA-Ar scores of >10 require more frequent
monitoring (e.g. at least 4 hourly), and patients with severe withdrawal (CIWA-Ar>20)
should be monitored every 2 hours (Saitz and O’Malley 1997; NSW Department of
Health 2007).
Alcohol Withdrawal Symptoms – Rating Scale
An alternative scale is the Alcohol Withdrawal Symptoms - Rating Scale (AWS). The
AWS has not been validated, however it has been widely used in Australian
conditions and is considered acceptable for use (NSW Department of Health 1999).
Short Alcohol Withdrawal Scale
The Short Alcohol Withdrawal Scale (SAWS) is a self-completion scale used once a
day, and is suited to ambulatory withdrawal settings (Gossop et al. 2002). Other
validated scales may be used according to local preference.
Limitations of withdrawal scales
Alcohol withdrawal rating scales are not to be used as diagnostic tools, as many
other medical conditions (e.g. sepsis, hepatic encephalopathy, severe pain),
psychiatric conditions (e.g. anxiety disorder) or other drug withdrawal syndromes
(e.g. benzodiazepine, stimulant or opiate withdrawal), will produce signs and
symptoms that rate on these scales, and can lead to an inappropriate diagnosis of
alcohol withdrawal (Foy et al. 1988).
These scales have not been validated for management of seriously ill patients. For
example, there is evidence of inappropriate use of CIWA-Ar to guide treatment of
alcohol withdrawal in hospitalised medical and surgical patients (Bostwick and Lapid
2004; Hecksel et al. 2008), particularly in patients with limited communication
abilities.
81
Therefore, alcohol withdrawal scales should not be used to guide medication (e.g.
symptom-triggered regimes) in patients with significant medical or psychiatric comorbidity, or those withdrawing from other substances. Health professionals should
consult a specialist drug and alcohol clinician about monitoring and management
needs. Scoring is typically highly variable in clinical practice and often not
reproducible. Clinicians should review scores before making management decisions.
Recommendation
5.8 Patients withdrawing from alcohol should be
regularly monitored for physical signs, severity
of alcohol withdrawal and general progress
during withdrawal.
5.9 Alcohol withdrawal scales (CIWA-Ar, AWS)
can be used to assess withdrawal severity, to
guide treatment (such as symptom-triggered
medication regimes) and to aid objective
communication between clinicians; but should
not be used as diagnostic tools.
5.10 Alcohol withdrawal scales should not be
used to guide treatment in patients concurrently
withdrawing from other substances, or with
significant medical or psychiatric comorbidity.
Health professionals should consult a specialist
drug and alcohol clinician about monitoring and
management needs.
5.11 Scores on alcohol withdrawal scales are
not always reproducible and should be checked
before using them to make management
decisions.
Strength of
recommendation
Level of
evidence
S
A
Ia
B
Ib
S
Supportive Care
This section discusses strategies used to improve withdrawal outcomes, including
patient information, environment and support, counselling, diet and rehydration,
thiamine supplementation, sleep and relaxation and strategies to facilitate links with
other services for further treatment and support.
Patient Information
Patients (and carers) generally benefit from information regarding the likely nature,
severity and duration of symptoms during withdrawal, strategies for coping with
symptoms and cravings, strategies to reduce high-risk situations and the role of
medication (NSW Department of Health 2007).
Recommendation
5.12 Patients (and carers) should be provided
with information about the likely nature and
course of alcohol withdrawal, and strategies to
cope with common symptoms and cravings.
Strength of
recommendation
Level of
evidence
C
III
82
Environment and support
Patients attempting alcohol withdrawal are vulnerable to psychological stress.
Treatment is more effective in an environment that is quiet, non-stimulating, and nonthreatening. Easy availability of alcohol and other drugs reduces the likelihood of
treatment completion (Ozdemir et al. 1994; Myrick and Anton 1998).
Recommendation
5.13 Treatment environment should be quiet,
non-stimulating, and non-threatening, and
where alcohol and other drugs are not available.
Strength of
recommendation
Level of
evidence
S
Supportive counselling
Counselling during the withdrawal episode should be aimed specifically at providing
patient with strategies for coping with withdrawal symptoms, including cravings,
maintaining motivation, and facilitating post-withdrawal links. While no studies
directly assessed the effectiveness of these strategies in management of alcohol
withdrawal, a recent meta-analysis of treatments for opioid dependence has shown
that psychosocial interventions implemented during withdrawal management were
effective in terms of completion of treatment, use of opioids, results at follow-up and
compliance (Amato et al. 2008).
Recommendation
5.14 Supportive counselling should be provided
to maintain motivation, provide strategies for
coping with symptoms, and reduce high-risk
situations.
Strength of
recommendation
Level of
evidence
D
III
Diet, nutrition and rehydration
Many patients experience nausea and/or diarrhoea during withdrawal. It appears that
frequent, light meals are generally better tolerated in the first few days of withdrawal.
Patients with such withdrawal symptoms as diarrhoea, nausea/vomiting or profuse
sweating may develop dehydration. Dehydration can cause severe disturbances of
fluid and electrolyte balance and provoke withdrawal complications and should be
corrected with oral fluids or via intravenous infusion, if necessary. In patients with
fluid retention water balance should be maintained by oral administration of fluids as
intravenous infusion may cause fluid overload leading to heart failure (Myrick and
Anton 1998).
Recommendation
5.15 Clinicians should ensure oral rehydration is
adequate. Intravenous fluids may be necessary
in severe dehydration and/or in those not
tolerating oral fluids.
Strength of
recommendation
Level of
evidence
S
83
Thiamine and other supplements
Thiamine deficiency is common in patients with alcohol dependence, particularly in
those with poor nutritional status (Sgouros et al. 2004). Thiamine supplements are
recommended for all individuals undergoing alcohol withdrawal (Cook 2000).
According to the recent Cochrane review there is insufficient evidence from
randomised controlled trials to guide the clinician as to the optimum dose, frequency,
route, or duration of thiamine treatment for prophylaxis or treatment of Wernicke's
encephalopathy due to alcohol misuse (Day et al. 2004). There is one randomised,
double-blind, multidose study of thiamine treatment in 107 subjects who were
detoxifying from alcohol (Ambrose et al. 2001). The results did not reveal a simple
dose-response relationship. However, the study has demonstrated that the dose of
200mg IM thiamine for two consecutive days was more effective that the 5mg dose in
improving participants’ performance in the test of working memory (a delayed
alteration task).
The existing recommendations currently used in the UK and Australia (Thomson et al.
2002; Lingford-Hughes et al. 2004; NSW Department of Health 2007; Feeney and
Connor 2008) are mostly based on studies by Cook et al. (e.g. 1998, 2000) and
Thomson et al. (e.g. 2000; 2006). See also Sechi (2007) for review. In patients
showing no clinical features of Wernicke’s Encephalopathy or memory impairment,
thiamine is recommended as a prophylactic measure (Cook et al. 1998).
The dose, route and duration of thiamine administration depend on patient’s nutritional
status.
Healthy patients with good dietary intake may be administered oral thiamine. The
recommended dose is 300mg per day (e.g. 100mg tds) for 3 to 5 days, and
maintained on 100mg oral thiamine for a further 4 to 9 days (total of 1 -2 weeks of oral
thiamine).
Intestinal absorption of oral thiamine supplements is slow and may be incomplete in
patients with poor nutritional status (Thomson et al. 2000). Chronic drinkers with poor
dietary intake and general poor nutritional state require parenteral thiamine doses.
The recommended dose of thiamine 300mg IM or IV per day for 3-5 days, with
subsequent oral thiamine doses of 300mg per day for several weeks (Cook 2000).
The intramuscular route should not be used for patients with coagulopathy as
absorption of thiamine will be reduced.
Parenteral carbohydrates can cause rapid utilisation of thiamine in peripheral tissues
and precipitate Wernicke’s Encephalopathy. Therefore, thiamine (oral or
intramuscular) should be given BEFORE any carbohydrate load (e.g. IV glucose)
(Thomson et al. 2002).
Deficiencies of other B complex vitamins, vitamin C, folic acid, zinc and magnesium
are not uncommon and an oral multi-vitamin preparation can be given for several days
in nutritionally depleted individuals (Myrick and Anton 1998).
Thiamine supplementation should be continued indefinitely in an alcohol-dependent
patient who continues to drink alcohol.
84
Recommendation
Strength of
recommendation
Level of
evidence
5.16 Thiamine should be provided to all patients
undergoing alcohol withdrawal to prevent
Wernicke’s encephalopathy.
5.17 Thiamine should be given before any
carbohydrate load (such as intravenous
glucose) as carbohydrates can cause rapid use
or depletion of thiamine and precipitate
Wernicke’s encephalopathy.
D
IV
D
III
5.18 Healthy patients with good dietary intake
should be administered oral thiamine 300 mg
per day for 3 to 5 days, and maintained on 100
mg oral thiamine for a further 4 to 9 days (total
of 1 to 2 weeks of thiamine).
5.19 Chronic drinkers with poor dietary intake
and general poor nutritional state should be
administered parenteral (intramuscular or
intravenous) thiamine doses of 300 mg per day
for 3 to 5 days, with subsequent oral thiamine
doses of 300 mg per day for several weeks. The
intramuscular route should not be used for
patients with coagulopathy.
D
IV
D
Ib
5.20 Thiamine supplementation should be
continued indefinitely in an alcohol-dependent
patient who continues to drink alcohol.
S
Sleep and relaxation
Heavy drinkers commonly report sleep disturbances (Benca et al. 1992). Insomnia is
a frequent symptom of alcohol withdrawal (Caetano et al. 1998) and a predictor of
relapse during early recovery (Foster and Peters 1999; Brower et al. 2001; Malcolm
et al. 2007).
However, there is no role for continuing treatment with long-term benzodiazepines or
other sedatives to improve sleep following alcohol withdrawal (i.e. more than one
week). Sleep hygiene practices should be encouraged. Patient literature should be
provided regarding sleep and relaxation techniques.
Similarly, there is limited role for benzodiazepines or other sedatives for management
of anxiety after alcohol withdrawal, and behavioural approaches to relaxation and
anxiety management should be encouraged.
Recommendation
5.21 Sedatives (such as benzodiazepines)
should not be continued beyond the first week of
withdrawal. Behavioural approaches to
management of anxiety and sleep problems
should be encouraged.
Strength of
recommendation
Level of
evidence
D
IV
85
Facilitating links with other services for further treatment and support
It has long been recognised that effective management of patients’ alcohol
withdrawal symptoms presents a window of opportunity to initiate further treatment of
their alcohol dependence (Saitz 1998). Post-withdrawal treatment options include
counselling (e.g. relapse prevention), residential rehabilitation, self-help, and
medications for relapse prevention. Medications such as naltrexone and
acamprosate can be initiated during alcohol withdrawal treatment as a way of
enhancing uptake, and indeed acamprosate may also reduce calcium mediated
neuronal damage during the withdrawal process (Mann et al. 2008). These are
generally commenced after at least three days of abstinence (see Chapter 7).
Based on the meta-analysis of studies investigating the effect psychosocial
interventions during withdrawal from opioids (Amato et al. 2008), counselling
strategies during alcohol withdrawal should focus on examining post-withdrawal
treatment options, and facilitating engagement with these services (See section on
Supportive counselling, above).
Recommendation
5.22 Clinicians should facilitate links to postwithdrawal treatment services during withdrawal
treatment.
Strength of
recommendation
Level of
evidence
D
III
Medications for Managing Alcohol Withdrawal
The following describes the use of medications for managing alcohol withdrawal.
Benzodiazepines
Benzodiazepines are safe and effective for the treatment of alcohol withdrawal. In
general, long acting benzodiazepines with a rapid onset of action are most commonly
recommended. The recommendations are based on the evidence from earlier metaanalyses (Mayo-Smith 1997; Holbrook et al. 1999) and reviews (Lingford-Hughes et
al. 2004; Mayo-Smith et al. 2004).
There is significant evidence that benzodiazepines are effective in reducing
symptoms of alcohol withdrawal and in reducing the risk of seizures and alcohol
withdrawal delirium when compared to placebo (Mayo-Smith 1997; Holbrook et al.
1999).
The most recent meta-analysis (Ntais et al. 2005) has also found that
benzodiazepines are effective in reducing withdrawal symptoms and, in particular, in
treatment and prevention of withdrawal seizures (see below).
Diazepam is the benzodiazepine of choice in many countries, including Australia.
Chlordiazepoxide, a long acting and rapid onset benzodiazepine, is widely used
internationally but is not registered in Australia.
The choice among different agents is guided by duration of action, rapidity of onset,
and cost. Meta-analyses show no differences in relative efficacies of different
benzodiazepines (Mayo-Smith 1997; Ntais et al. 2005). Earlier randomised controlled
86
trials have shown that lorazepam was more effective than placebo (Naranjo 1998)
and as effective as diazepam in reducing symptoms of moderate alcohol withdrawal
(Miller and McCurdy 1983). Long-acting benzodiazepines may be more effective in
preventing seizures than short acting benzodiazepines (Mayo-Smith 1997).
Benzodiazepines with shorter duration of action, such as midazolam, lorazepam,
oxazepam lorazepam are recommended when there is concern about prolonged
sedation (e.g., in elderly, in patients with significant comorbidities or liver disease)
(Saitz 1998; Mayo-Smith et al. 2004).
Benzodiazepines should not be continued beyond the first week for managing
alcohol withdrawal due to the risk of rebound phenomenon and dependence (Saitz
and O’Malley 1997).
Benzodiazepines: Recent Meta-analysis
A Cochrane review of the use of benzodiazepines for alcohol withdrawal was carried
out in 2005 by Ntais et al (2005). Fifty-seven trials included a total of 4,051 people.
There was a very large variety of outcomes and of different rating scales, and this
limited the data analyses. It was found that benzodiazepines offered a large benefit
against alcohol withdrawal seizures compared to placebo (relative risk [RR] 0.16;
95% confidence interval [CI] 0.04 to 0.69; p = 0.01). Benzodiazepines had similar
success rates to other drugs (RR 1.02; 95% CI 0.92 to 1.12), particularly,
anticonvulsants (RR 1.00; 95% CI 0.87 to 1.16) in reducing symptoms of alcohol
withdrawal. Seizures were better prevented with benzodiazepines than with nonanticonvulsants (RR 0.23; 95% CI 0.07 to 0.75; p = 0.02). However, no differences in
this outcome were found between benzodiazepines and anticonvulsants (RR 1.99;
95% CI 0.46 to 8.65). Thirteen trials with the total of 571 patients showed no
difference in efficacy, adverse effects or drop-out rate among patients treated with
the following benzodiazepines for 5-28 days: alprazolam, chlordiazepoxide,
clobazam, diazepam, halazepam, lopirazepam, lorazepam, and prazepam.
Small sample sizes, inadequate reporting of patient status (inpatient or outpatient), or
of randomisation techniques, limited the possibilities for further pooling of data. It was
not possible to draw definite conclusions about the relative effectiveness and safety
of benzodiazepines against other drugs (including carbamazepine, clonidine,
propranolol, bromocriptine) in alcohol withdrawal, because of the large heterogeneity
of the trials both in interventions and assessment of outcomes.
The main conclusion reached by the authors was that benzodiazepines were
effective against alcohol withdrawal symptoms, in particular seizures, when
compared to placebo. This conclusion is in concordance with previous meta-analyses
and in general justifies the current status of benzodiazepines as first-line treatment
for alcohol withdrawal, although clear superiority over other agents has not been
demonstrated.
Recommendation
5.23 Benzodiazepines are the recommended
medication in managing alcohol withdrawal. In
Australia, diazepam is recommended as ‘gold
standard’ and as first-line treatment because of
its rapid onset of action, long half-life and
evidence for effectiveness.
Strength of
recommendation
Level of
evidence
A
Ia
87
5.24 Shorter-acting benzodiazepines
(lorazepam, oxazepam, midazolam) may be
indicated where the clinician is concerned about
accumulation and over sedation from diazepam,
such as in the elderly, severe liver disease,
recent head injury, respiratory failure, in obese
patients, or where the diagnosis is unclear.
5.25 Benzodiazepines should not be continued
beyond the first week for managing alcohol
withdrawal due to the risk of rebound
phenomenon and dependence.
D
III
D
III
Symptom-triggered therapy
Symptom-triggered medication regimen relies upon linking medication (e.g.
diazepam doses) to scores on a frequently administered withdrawal scale (e.g.
CIWA-Ar or AWS) (e.g. four times a day). Medication is administered only when the
patient develops moderate alcohol withdrawal symptoms. Symptom-triggered
regimens have the advantage of better tailoring medication to the needs of
individuals, and have been shown to result in less benzodiazepine use than fixeddose regimens in specialist residential detoxification settings (Saitz et al. 1994;
Reoux and Miller 2000; Daeppen et al. 2002; Spies et al. 2003).
The meta-analysis described above (Ntais et al. 2005) included three of the above
studies (Saitz et al. 1994; Daeppen et al. 2002; Spies et al. 2003) with the total of
262 patients. While there was a trend towards a higher effectiveness of symptomtriggered dosing schedules when compared to fixed-dose regimens, in terms of
CIWA-Ar score at the end of treatment, therapeutic success and number of
completed withdrawals per arm, the statistical significance was not reached.
This regimen is not suitable for ambulatory settings or for patients with a history of
seizures (Saitz and O’Malley 1997).
It should be noted that the appropriateness of symptom-triggered regimen in
seriously ill, medically or surgically unstable patients with an established drinking
history is unproven. This is particularly the case for patients with limited
communication abilities (Hecksel et al. 2008).
In the latter study (Hecksel et al. 2008) 25% of all hospital patients who received
symptom-triggered therapy according to CIWA-Ar protocol were randomly selected
(n=124) and assessed for appropriateness of treatment administered. It was found
that although scoring with CIWA-Ar requires communication between the patient and
nursing staff, 23% of cases involved patients unable to interact meaningfully.
Furthermore, 44% of patients assessed with CIWA-Ar had no history of recent
drinking. As a result, 64% of non-drinkers were treated as if they were experiencing
alcohol withdrawal syndrome. All these patients could communicate appropriately
with the nursing staff, but were not specifically asked about their current drinking
status. The situation was especially problematic for patients who had a history of
heavy drinking but who had since achieved sobriety. In this study, post-operative
status was most likely to result in inappropriate initiation of the CIWA-Ar protocol,
probably because the delirium common in the hours and days after surgery is more
88
likely to be mistaken for alcohol withdrawal syndrome. Patients with liver disease
were more likely to receive appropriate treatment.
Similarly, the symptom-triggered schedule may not be appropriate for management
of patients with psychiatric comorbidity or polysubstance dependence.
Recommendation
5.26 Diazepam should be administered in a
symptom-triggered regimen in residential
withdrawal settings for people with no
concomitant medical, psychiatric or substance
use disorders.
Strength of
recommendation
Level of
evidence
B
Ia
Loading dose therapy
Loading dose regimens (also referred to as “front-loading”) administer high doses of
benzodiazepines in the early stages of alcohol withdrawal. These regimens are used
in managing patients with a prior history of severe withdrawal complications and in
patients presenting in severe alcohol withdrawal and/or severe withdrawal
complications (Saitz and O’Malley 1997). Diazepam is safe to administer in loading
regime (Heinala et al. 1990). A common loading diazepam regime under these
circumstances is 20mg orally every 2 hours until reaching 60 to 80mg or the patient
is sedated (Saitz and O’Malley 1997).
Hillbom et al (2003) performed a meta-analysis of 22 randomised controlled studies
investigating medications for treatment and prevention of alcohol withdrawal seizures
(see below, in Anticonvulsants: Meta-analyses and reviews). They also recommend
an administration of the loading dose of diazepam of 10-20mg orally or parenterally
to all patients presenting in withdrawal seizures. They emphasised the importance of
prevention and treatment of first seizures as every subsequent seizure increases the
risk of status epilepticus and other life-threatening complications. Status epilepticus
increases the risk of seizures in future withdrawal episodes (Hesdorffer 1998, cited in
Hillbom et al. 2003).
Two small RCTs examined the effectiveness of diazepam loading dose (Sellers et
al.1983, Manikant et al. 1993). Sellers et al (1983) showed that the loading dose
regimen using 20mg diazepam was more effective than placebo. Manikant et al.
(1993) compared conventional and loading doses. The total dose of diazepam in the
conventional treatment and in the loading dose groups were 200 mg and 67 +/- 9.3
mg, respectively. Clinical response was comparable in both groups. None of the
subjects developed diazepam related side effects.
Patients with a history of severe withdrawal complications (seizures, delirium) and
those presenting in severe alcohol withdrawal with or without complications should
be treated according to the loading dose regimen.
Recommendation
5.27 Diazepam should be administered in a
loading regimen (20 mg 2 hourly until 60 to 80
mg or light sedation) in patients with a history of
Strength of
recommendation
Level of
evidence
B
Ib
89
severe withdrawal complications (seizures,
delirium); in patients presenting in severe
alcohol withdrawal and/or severe withdrawal
complications (delirium, hallucinations, following
withdrawal seizure).
Fixed-schedule therapy
Benzodiazepines given at fixed dosing intervals are a common therapy for alcohol
withdrawal management, and are well suited to ambulatory withdrawal, community
residential and inpatient withdrawal settings (Saitz and O’Malley 1997; Saitz 1998).
Fixed schedule regimens may be supplemented with additional diazepam as needed
for people with low tolerance of withdrawal discomfort (for example, 5 mg 6 hourly as
needed, based on clinical observation or alcohol withdrawal scale scores) (Saitz and
O’Malley 1997).
In general hospitals, patients with a history of alcohol dependence are the most likely
to experience complications of alcohol withdrawal, such as delirium and seizures,
when receiving symptom-triggered therapy according to the CIWA-Ar protocol. Such
patients should be monitored more closely and may require more frequent doses of
benzodiazepines than the CIWA-Ar protocol permits (Hecksel et al. 2008).
In patients with concomitant medical, psychiatric or substance use disorders a fixedschedule therapy is more appropriate.
Recommendation
Strength of
recommendation
Level of
evidence
C
Ib
5.28 Diazepam should be administered in a
fixed dose regimen in ambulatory settings, or for
those with concomitant medical, psychiatric or
substance use disorders.
Alternative, symptomatic and other medications
Alternative medications may need to be considered in patients who abuse
benzodiazepines, particularly if they continue drinking. In minority of patients
benzodiazepines cause paradoxical reactions (such as violence, agitation) or
confusion and delirium and are not recommended for use in these patients.
However, the alternative medications should be effective in preventing serious
complications of alcohol withdrawal, such as seizures and delirium.
Anticonvulsant medications should be continued in patients who take them regularly
(such as for epilepsy not related to withdrawal).
Anticonvulsants: Meta-analyses and reviews
A Cochrane review of clinical trials assessing safety and effectiveness of
anticonvulsants in the treatment of alcohol withdrawal (Polycarpou et al. 2005),
analysed forty-eight studies with the total number of 3610 patients. However,
90
because these studies assessed a large variety of outcomes and used different
withdrawal rating scales, quantification of the data was limited. While certain trends
were noted, no statistical significance was shown for the benefit of anticonvulsants in
reducing severity of withdrawal symptoms (relative risk [RR] 1.32; 95% confidence
interval [CI] 0.92 to 1.91) or preventing alcohol withdrawal seizures (RR 0.57; 95% CI
0.27 to 1.19) when compared to placebo. When anticonvulsants were compared to
other drugs (such as oxazepam) no significant differences were found in CIWA-Ar
scores at the end of treatment (weighted mean difference [WMD] -0.73; 95% CI -1.76
to 0.31). In a subgroup analysis of three studies, carbamazepine was found to be
significantly more effective than a benzodiazepine (oxazepam and lorazepam), in
reducing severity of some alcohol withdrawal symptoms (WMD -1.04; 95% CI -1.89
to -0.20; p = 0.02); however this result was based on only 260 participants. The
incidence of alcohol withdrawal seizures post-treatment tended to be lower with
anticonvulsants than with placebo or other drugs, but the difference did not reach
significance. Phenytoin assessed alone was found to be ineffective in preventing
seizures when compared to placebo (RR 0.78; 95% CI 0.35 to 1.77; p = 0.56). The
side-effects tended to be less common in the anticonvulsant-group (RR 0.56; 95% CI
0.31 to 1.02). The authors state that it was not possible to draw definite conclusions
about the effectiveness and safety of anticonvulsants in alcohol withdrawal in this
review, due to the heterogeneity of the trials both in interventions and the
assessment of outcomes.
An earlier review by Hillbom et al (2003) provides a meta-analysis of twenty two
randomised controlled trials examining the efficacy of different drugs for the primary
prevention of seizures. This study found that benzodiazepines significantly reduced
the risk of seizures while antipsychotics significantly increased the risk seizures.
Short-acting benzodiazepines (oxazepam and lorazepam) appeared less effective as
tapering off the drugs caused additional seizures in some cases. Anticonvulsants
were as effective as benzodiazepines in preventing primary alcohol withdrawal
seizures but adding them to benzodiazepines did not further reduce the risk of
seizures. A meta-analysis of three randomised controlled trials examining the efficacy
of drugs for prevention of the secondary (recurrent) seizures, found phenytoin to be
ineffective. The authors conclude that benzodiazepines should be the first line of
treatment as they effectively prevent both first seizures and recurrent seizures during
alcohol withdrawal episode. Non-sedative anticonvulsants are the second choice.
Ait-Daoud et al. (2006) provide an overview on a number of medications for
treatment of alcohol dependence, including treatment of withdrawal. They examined
the results of eight trials of valproate for treatment of withdrawal, including openlabel, case-report and randomised controlled studies. They also reported in detail the
results of a double-blind trial comparing carbamazepine with lorazepam (Malcolm et
al. 2002). The authors concluded that ‘valproate and carbamazepine have been
shown to be safe and effective alternatives to benzodiazepines for treating alcohol
withdrawal’. However, the effectiveness of these drugs for prevention of secondary
seizures was not discussed.
Carbamazepine
Carbamazepine for treatment of alcohol withdrawal has been studied for many years
and is widely used in Europe for this indication (Mayo-Smith 1997; Mayo-Smith
2004). It is a safe alternative to benzodiazepines, but it is usually is not
recommended for use as the first line of treatment because it has significant side
effects and may not prevent secondary seizures (Hillbom et al. 1989).
91
Prince and Turpin (2008) reviewed six randomised double-blind trials investigating
carbamazepine, gabapentin and nitrous oxide as alternatives to symptom-triggered
benzodiazepine administration for the treatment of alcohol withdrawal syndrome
(Prince and Turpin 2008). The results of the review suggested that carbamazepine
200mg four times daily was as effective as 30 mg of lorazepam four times daily in
reducing symptoms of alcohol withdrawal. It is therefore, may be useful for treatment
of alcohol withdrawal, particularly in outpatient settings, although adverse effects and
drug interactions may limit its usefulness. The role of gabapentin was unclear
because of the lack of randomised, double-blind, controlled trials and the conflicting
results of existing case series and open-label trials. Two trials of nitrous oxide were
poorly designed and had conflicting results. The authors conclude that because of
the limitations in evidence, the routine use of carbamazepine and gabapentin for the
treatment of alcohol withdrawal cannot be recommended, and the use nitrous oxide
should be avoided.
Valproate
One study looked at the role of valproic acid, conducting a literature review of
controlled clinical trials (Lum et al. 2006). The results were inconclusive.
Comparisons were made among various regimens of valproic acid and traditional
therapy with benzodiazepine or non-benzodiazepine agents. Only 2 of 6 trials
reported a statistically significant difference in favour of valproic acid on endpoints of
alcohol withdrawal. However, these differences were of marginal clinical significance.
The number of patients included in these studies did not allow for adequate
evaluation of safety. The authors conclude that the existing limited efficacy and
safety data suggest that valproic acid should not replace conventional therapy or be
used as adjunct therapy for management of mild-to-moderate alcohol withdrawal
syndrome.
Anticonvulsants: Randomised controlled trials
Oxcarbazepine
A pilot study of oxcarbazepine vs. carbamazepine was conducted in Germany (Schik,
et al. 2005) with 29 patients. Results showed that the oxcarbazepine group had a
significant decrease of withdrawal symptoms and reported significantly less 'craving
for alcohol' compared to the carbamazepine group. Subjectively experienced side
effects, normalisation of autonomic parameters and improvement in the cognitive
processing speed did not differ between groups. Therefore, the authors suggest that
oxcarbazepine might be an interesting alternative to carbamazepine, and having
almost no addictive potential, no clinically relevant interaction with alcohol and no
prominent sedatory effect, it might also offer an alternative to other drugs such as
benzodiazepines or clomethiazole.
A study by Koethe et al examined the role of oxcarbazepine’s efficacy and tolerability
during alcohol withdrawal (Koethe et al. 2007), with limited results. The trial was
conducted in 50 inpatients during a 6-day treatment of alcohol withdrawal in a 4-site,
double-blind, randomised, placebo-controlled pilot study. The amount of rescue
medication of clomethiazole capsules needed was chosen as the primary variable.
Results showed no differences in the need for rescue medication clomethiazole,
decrease of withdrawal symptoms, or craving for alcohol between the oxcarbazepine
and the placebo group. Subjectively experienced side effects, normalisation of
vegetative parameters, craving, or improvement of psychopathological parameters
92
were not different between the groups. The authors state that despite the negative
finding, which may be attributable to the design of the study, oxcarbazepine still
poses an interesting alternative to carbamazepine and other drugs because other
studies have found it not only as efficient but also as having no addictive potential,
while additionally possessing an anti-craving effect. They also suggests that it may
have been better to trial it against benzodiazepine instead of placebo.
Gabapentin
A small trial was carried out comparing gabapentin and phenobarbital for the
treatment of alcohol withdrawal (Mariani et al. 2006). A randomised, open-label,
controlled trial had 27 inpatient participants. Results showed no significant
differences in the proportion of treatment completers between treatment groups or
the proportion of patients in each group requiring rescue medication for breakthrough
signs and symptoms of alcohol withdrawal. There were no significant treatment
differences in withdrawal symptoms or psychological distress, nor were there serious
adverse events. The authors suggest that gabapentin may be as effective as
phenobarbital in the treatment of alcohol withdrawal. However phenobarbital is no
longer used in the management of alcohol withdrawal. The small sample size and the
choice of a comparison drug, make it difficult to draw any firm conclusions from this
study.
A recent double-blind study of 100 patients compared 2 doses of gabapentin (900 mg
tapering to 600 mg or 1200 tapering to 800 mg) with lorazepam (6 mg tapering to 4
mg) for 4 days. They found that gabapentin was well tolerated and was clinically
similar to lorazepam in reducing alcohol withdrawal symptoms, especially at the high
dose. The gabapentin groups reported less craving, anxiety, and sedation compared
to lorazepam (Myrick et al. 2009).
Topiramate
In a small study, Choi et al. (2005, cited in Ait-Daoud et al. 2006) found that
topiramate 50 mg/day (N =25) was as efficacious as lorazepam up to 4 mg/day
(N=27) at treating alcohol withdrawal symptoms in an inpatient setting.
Anticonvulsants: Summary
While some anticonvulsants, such as carbamazepine are effective in minimising
alcohol withdrawal symptoms and in preventing primary withdrawal seizures, there is
no clear evidence that anticonvulsants are effective in preventing secondary seizures
or delirium. There is appears to be no advantage in adding anticonvulsants to
benzodiazepines for preventing withdrawal seizures. Phenytoin and valproate are not
effective in preventing the onset of alcohol withdrawal seizures. The role of newer
anticonvulsants (e.g. gabapentin and topiramate) is yet to be demonstrated in
controlled studies against gold standard treatment, such as diazepam.Anticonvulsant
medications should be continued in patients who take them regularly (such as for
epilepsy not related to withdrawal).
Recommendation
5.29 Carbamazepine is safe and effective as an
alternative to benzodiazepines, although it is not
effective in preventing further seizures in
Strength of
recommendation
Level of
evidence
A
Ia
93
withdrawal episodes.
5.30 Phenytoin and valproate are not effective in
preventing alcohol withdrawal seizures and are
not recommended.
5.31 Newer anticonvulsant agents (such as
gabapentin) are not recommended at this stage
due to lack of clinical evidence.
5.32 There is no benefit in adding
anticonvulsants to benzodiazepines to manage
alcohol withdrawal.
5.33 Anticonvulsant medications should be
continued in patients who take them regularly
(such as for epilepsy not related to withdrawal).
A
Ia
D
IV
A
Ia
S
Antipsychotic medications: Meta-analyses
Anti-psychotic medication when used alone may increase seizure risk (for example
phenothiazines) and do not prevent the onset of delirium, as has been shown in the
meta-analyses by Hillbom et al. (2003) (see above in Anticolvulsants) and MayoSmith et al. (2004) (see below, in Alcohol Withdrawal Delirium).
Antipsychotics should only be used in conjunction with benzodiazepines in the
management of hallucinations or agitation associated with delirium that have not
responded to adequate doses of benzodiazepines.
Antipsychotic medications: Randomised controlled studies
There are no placebo-controlled studies of neuroleptics or newer atypical
antipsychotics (such as olanzapine and risperidon) for treatment of alcohol
withdrawal. Nevertheless, neuroleptics, especially haloperidol, are commonly used
(with sedative-hypnotic drugs) in patients with alcohol withdrawal delirium.
Studies reported below provide evidence for safety and effectiveness of some
antipsychotic medications either alone or in combination with anticonvulsants in
treatment of alcohol withdrawal. These studies, however, are relatively small and the
results should be interpreted with caution.
Cyamemazine
Cyamemazine is a phenothiazine derivative with a pharmacological profile close to
that of atypical antipsychotics and with some anxiolytic effect. It is not available in
Australia. It has been shown to reduce convulsions in animal studies and there is one
clinical trial of its efficacy and safety in alcohol-dependent patients (Favre et al.
2005). This was a small multicentre, randomised double-blind study investigating
cyamemazine for its efficacy and tolerability in alcohol-dependent patients electing an
alcohol withdrawal procedure, in comparison with diazepam. Eighty-nine alcohol
dependent patients were randomised to receive cyamemazine or diazepam to
compare it for efficacy and tolerability. On day 1, cyamemazine or diazepam (50 mg
and 10 mg capsule, respectively) were administered at hourly intervals, with effects
measured by reduction in CIWA-Ar (withdrawal scale) scores, up to a maximum of
eight administrations. Starting from day 2, the compounds were given twice a day in
progressively decreasing doses during a maximum period of 13 days. Similarity of
94
therapeutic effects and safety were confirmed in both medications. The authors’
conclusions were that cyamemazine showed similar efficacy and tolerability to
diazepam for the treatment of alcohol withdrawal symptoms at therapeutic doses in
the range 100-300 mg. The incidence of delirium tremors or alcohol withdrawal
seizures after initiation of treatment was 2.3% (one patient out of 44 for each). It is
not clear from the protocol how many patients had a previous history of alcohol
withdrawal seizures.
Tiapride/carbamazepine combination
Benzodiazepines can cause respiratory depression, especially in combination with
alcohol. Administration of diazepam to patients with blood alcohol concentrations
above 0.1% is usually discouraged. Because intoxicated patients quite often seek
treatment for alcohol withdrawal, the search for alternative medications continues.
Tiapride is an atypical neuroleptic with a dopamine receptor-antagonist activity, often
used in treatment of hyperkinesias, including tremor. Tiapride does not prevent
delirium or withdrawal seizures and has been studied in a combination with
carbamazepine for treatment of alcohol withdrawal.
One small open-label study has compared four treatment conditions for alcohol
withdrawal in intoxicated and non-intoxicated patients (Lucht al. 2003). Patients were
assigned in blocks of 10 to one of the following: tiapride and carbamazepine (group
A) vs clomethiazole (group B) vs diazepam (group C) in non-intoxicated patients and
vs tiapride/carbamazepine in intoxicated patients (group D). Findings were that
efficacy and safety were not different between groups (total group: delirium, 3.9%;
seizure, 0.8%). While treatment could be initiated safely in intoxicated patients, in
18% of cases the tiapride/carbamazepine combination was ineffective in controlling
withdrawal symptoms after the blood alcohol concentration fell below 0.1% and a
change of medication was required. The authors’ conclusions were that treatment
with tiapride/carbamazepine can be used in alcohol-intoxicated and in nonintoxicated patients without delirium.
Soyka et al. (2006) used a retrospective study, pooling data from 540 patients to
examine the efficacy, practicability and medical safety of a combination of tiapride
and fast-acting formula of carbamazepine. Details of alcohol history and comorbid
disorders were extracted from patient files. Patients had a long-term history of
alcohol dependence and a significant alcohol intake before detoxification. Most
patients were still intoxicated at the moment of hospitalisation (median respiratory
alcohol 1.6g/l). Most patients had moderate-to-severe withdrawal (baseline CIWA-Ascore 12.3). A pooled analysis of the results showed that, in general, medication safe
and effective. Withdrawal symptomatology as indicated by CIWA-A scores decreased
from baseline to 3.9 on day 5 and 2.6 on day 9). A total of 5 (0.9%) patients
developed seizures, 5 on the initial, 2 on the second and 1 on the fourth day. Of the
151 patients who had a previous history of alcohol withdrawal seizures, only 4
developed seizures during treatment. Although a significant number of patients had a
history of alcohol withdrawal delirium (103), only 5 of these patients developed
delirium. Three patients had first episode of alcohol withdrawal delirium. Only 24
(4.4%) patients dropped out because of lack of efficacy or change of medication, and
15 (2.8%) because of side effects. No case of malignant neuroleptic syndrome was
recorded. Severe withdrawal complications were more frequent in men compared to
women and in patients with repeated inpatient treatment.
95
The authors conclude that, in line with previous research, the results from this study
give further evidence that a combination of the anticonvulsant carbamazepine and
tiapride is an effective and safe combination for the treatment of alcohol withdrawal.
Antipsychotic medications: Summary
Antipsychotic medications should not be a stand alone treatment of alcohol
withdrawal but can be used in conjunction with benzodiazepines to treat
hallucinations or agitation in patients who do not respond well to benzodiazepines
alone.There is insufficient evidence at this stage to recommend cyamemazine or
tiapride/carbamazepine combination for treatment of alcohol withdrawal.
Recommendation
5.34 Antipsychotic medications should only be
used as an adjunct to adequate benzodiazepine
therapy for hallucinations or agitated delirium.
They should not be used as stand-alone
medication for withdrawal.
Strength of
recommendation
Level of
evidence
A
Ia
Anti-hypertensive agents
Elevated blood pressure during alcohol withdrawal is usually well managed by
adequate doses of benzodiazepines. In cases where blood pressure remains
markedly elevated despite adequate benzodiazepine loading, a beta-blocker (e.g.
atenolol or propranolol) is recommended. However, the use of propranolol in these
patients is limited due to its association with hallucinations (Zilm et al. 1980; Saitz
1998).
Recommendation
5.35 Anti-hypertensive agents (beta-blockers)
should be used for managing extreme
hypertension that has not responded to
adequate doses of diazepam for alcohol
withdrawal.
Strength of
recommendation
Level of
evidence
D
IV
Symptomatic medication
Despite the absence of an empirical evidence base in alcohol withdrawal,
symptomatic medications are commonly used in the management of alcohol
withdrawal.
Recommendation
5.36 A range of symptomatic medications may
be used for addressing specific symptoms (such
as paracetamol for headache, anti-emetics, antidiarrhoeal agents).
Strength of
recommendation
Level of
evidence
D
IV
96
Electrolyte disturbances
Hypokalaemia and hypomagnesaemia should be corrected using oral supplements
(Saitz and O’Malley 1997; Myrick and Anton 1998). Hyponatraemia is usually selflimiting and should not be aggressively corrected because of the risk of central
pontine myelinolysis (Laureno and Karp 1997; Leens et al. 2001).
Recommendation
5.37 Electrolyte replacement may be a
necessary adjunctive treatment for patients with
electrolyte abnormalities (such as
hypomagnesaemia, hypokalaemia).
Hyponatraemia should not be aggressively
corrected due to the risk of central pontine
myelinolysis.
Strength of
recommendation
Level of
evidence
S
Other medications
Chlormethiazole (also spelled as clomethiazole) is a short-acting sedative and
anticonvulsant medication that was historically widely used for treating alcohol
withdrawal before the advent of benzodiazepines. It is no longer recommended for
managing alcohol withdrawal due to its risk of respiratory depression and death in
overdose or in combination with alcohol or other sedatives.
The use of barbiturates, clonidine and beta-blockers is not recommended for routine
management of alcohol withdrawal, based on the meta-analysis by Mayo-Smith
(1997). Alcohol (ethanol) (Mayo-Smith 1997; Saitz and O’Malley 1998; Weinberg et
al. 2008) and GHB currently have no role in the treatment of alcohol withdrawal.
Studies on effectiveness of GHB in reducing alcohol withdrawal symptoms have
been published, but there is no evidence to suggest that they are effective in
preventing alcohol withdrawal seizures or delirium. Magnesium is used to correct
hypomagnesaemia in patients with alcohol withdrawal, but is not a stand alone
treatment (Mayo-Smith 1997).
Recommendation
5.38 Chlormethiazole, barbiturates, alcohol,
beta-blockers, clonidine and gammahydroxybutyric acid (GHB) are not
recommended in the routine management of
alcohol withdrawal.
Strength of
recommendation
Level of
evidence
A
Ia
97
Treatment of Severe Withdrawal Complications
Severe complications of alcohol withdrawal include seizures, hallucinations and
alcohol withdrawal delirium.
Alcohol Withdrawal Seizures
Alcohol acts on the brain through various mechanisms that influence seizure
threshold, including calcium and chloride ion flow through glutamate (N-methyl-daspartate, NMDA) and gamma aminobutyric acid (GABA) receptors. Chronic alcohol
use results in adaptive changes to the effects of alcohol, and the seizure threshold is
lowered as a rebound phenomenon when alcohol intake is stopped.
Clinical presentation and prevalence
Alcohol withdrawal seizures (AWS) typically occur 6 to 48 hours after the last drink is
consumed (50% between 13 and 24 hours, 90% within 48 hrs), and are usually
generalised (tonic-clinic) seizures (Rueff 1995, cited in Prescrire 2007). New-onset
alcohol withdrawal seizures are linked to heavy alcohol consumption (Hillbom et al.
2003).
Withdrawal seizures occur as blood alcohol levels fall, and in some severely
dependent drinkers, seizures can occur even if the patient is still intoxicated or has
consumed alcohol recently and the blood alcohol level is high (for example, greater
than 0.10) (Victor and Brausch 1967).
Hillbom et al. (2003) reviewed the placebo arms of four studies of secondary
prevention of seizures and estimated that the risk of seizure recurrence within 6-12
hours after a seizure was between 13% and 24%. Whilst the incidence of status
epilepticus is low, alcohol withdrawal is major cause of status epilepticus.
The prevalence of alcohol-withdrawal seizures is estimated at between 2 and 9% of
alcohol dependent individuals (8% in placebo arms in controlled studies of heavy
drinkers in inpatient studies. Individuals who have experienced an alcohol withdrawal
seizure are more likely to experience further seizures in subsequent alcohol
withdrawal episodes (Hillbom et al. 2003).
The prevalence of seizures in alcohol dependent individuals when all causes are
included is up to 15% (Chan 1985). This is at least three times higher than the
general population. It is estimated that alcohol-related seizures account for one third
of all seizure-related hospital admissions (Chan 1985; Bråthen et al. 2000).
Other causes of seizures in heavy drinkers
Heavy alcohol use can also contribute to seizures through other conditions including
concurrent metabolic, infectious, traumatic, neoplastic or cerebrovascular conditions,
or through concomitant use of other substances (particularly benzodiazepines).
Furthermore, it has been suggested that long-term neurotoxic effects of alcohol may
lead to epilepsy (Hauser et al. 1988). Seizures under these circumstances may be
atypical of alcohol-withdrawal seizures in onset or type (e.g. partial-onset seizures).
98
However, other causes of seizures can present clinically as alcohol withdrawal
seizures. In a series of 259 individuals with recent alcohol abuse and first onset
seizures with no obvious cause other than alcohol withdrawal, 6% showed
intracranial lesions on CT scan (Earnest et al. 1988).
Pharmacological approaches to prevention of seizures
Systematic reviews indicate that benzodiazepines effectively prevent alcohol
withdrawal seizures, and are effective in preventing recurrent (further) seizures in a
withdrawal episode (Mayo-Smith 1997; Hillbom et al. 2003).
In patients with prior seizure history, or in severe alcohol withdrawal diazepam
loading is recommended. Carbamazepine effectively prevents alcohol withdrawal
seizures, but is not effective in preventing recurrent (further) seizures in a withdrawal
episode (Hillbom et al. 2003).
There appears to be no advantage in adding anticonvulsants to benzodiazepines for
preventing alcohol withdrawal seizures (Hillbom et al. 2003).
Phenytoin and valproate do not effectively prevent the onset of alcohol withdrawal
seizures and are not recommended (Hillbom et al. 2003). The role of other
anticonvulsants (such as gabapentin, topiramate) is yet to be demonstrated, and
while their GABA-ergic actions suggest they may be useful, they are not
recommended at this stage.
See ‘Medications for managing alcohol withdrawal’ above for more detail.
Assessing and managing seizures in heavy drinkers
Many heavy drinkers present to services (e.g. hospital, paramedic) following a
seizure, and can pose a diagnostic dilemma for clinicians. The diagnosis of alcohol
withdrawal seizures is one of exclusion of other causes of seizures, such as epilepsy,
seizures due to head injury, subdural hematoma or metabolic, neoplastic, infectious,
cardiovascular and other causes (Saitz 1998; Rathlev 2002, cited in Hughs 2008;
Hillbom et al. 2003; Bråthen et al. 2005).
Studies investigating the diagnosis and management of alcohol withdrawal seizures
have been reviewed by Hillbom et al. (2003) and the European Federation of
Neurological Societies task force (Bråthen et al. 2005).
An alcohol withdrawal seizure can be diagnosed if none of the following criteria are
present:
•
clinical features or suspicion of other causes of seizures (such as head injury,
metabolic, infectious, neoplastic, cerebrovascular disorders)
•
no previous seizure history
•
the patient experiences two or more seizures in succession
•
partial-onset (focal) seizures
•
seizure occurring more than 48 hours after last drink
99
•
no recent heavy alcohol use or other features of alcohol withdrawal.
•
If any of the above criteria are present, alcohol withdrawal seizures should not
be assumed. (Hillbom et al. 2003; Bråthen et al. 2005)
•
The patient should be admitted into hospital, assessed for other causes of
seizures, and monitored for at least 24 hours. Careful collateral history should
be taken where possible (Bråthen et al. 2005).
•
Clinical examination should focus on differentiation between epileptic and
alcohol withdrawal seizures.
•
Table 5.2 identifies common differences between alcohol withdrawal seizures
and epileptic seizures.
Table 5.2 Post-ictal signs and symptoms: comparing epilepsy and alcohol
withdrawal seizures
Epilepsy
Alcohol withdrawal
seizures
Consciousness level
Post-ictal sleep/drowsy
Sleeplessness
Mood
Tremor
Sweating
Calm
No
No
Anxiety, agitated
Yes
Yes
BP, PR
Temperature
Arterial bloods
Normal
Normal/slight fever
Normal
Elevated
Fever (lower than 38.5°C)
Respiratory alkalosis
EEG
Pathology
Normal, low-amplitude
Notes: EEG – electroencephalogram; BP, PR – blood pressure, pulse rate
Source: EFNS guideline on the diagnosis and management of alcohol-related
seizures: Report of the European Federation of Neurological Societies task force
(2005) .available at
<http://www.guideline.gov/summary/summary.aspx?doc_id=9648>
Where the likely diagnosis is alcohol withdrawal seizures, patients should be
administered benzodiazepines to prevent further (secondary) seizures (see Loadingdose therapy above).
Where the diagnosis of alcohol withdrawal seizures can be established against
criteria (above), the patients should be admitted into a supervised withdrawal setting
for at least 48 to 72 hours and monitored for vital signs, alcohol withdrawal symptoms
and neurological symptoms. Thiamine administration (100 mg three times daily
intramuscular or intravenous) before carbohydrate is recommended as prophylaxis of
Wernicke’s encephalopathy. Supportive management, including nursing in a quiet
environment away from excessive sensory stimuli and rehydration should be
provided. Diazepam loading to prevent further alcohol withdrawal seizures is
recommended as described above, in Loading-dose therapy.
Recommendation
5.39 Alcohol withdrawal seizure should only be
Strength of
recommendation
Level of
evidence
B
II
100
assumed if the clinical presentation is typical of
an alcohol withdrawal seizure, no other causes
of seizure are suspected, and the patient has a
history of previous alcohol withdrawal seizures.
All other cases need full investigation.
5.40 Heavy drinkers with a seizure of unknown
cause should be admitted to hospital and
monitored for at least 24 hours. Investigations
include biochemical tests and neuro-imaging,
and possibly EEG.
5.41 Loading with benzodiazepines (diazepam,
lorazepam) and close monitoring for at least 24
hours is recommended after an alcohol
withdrawal seizure.
5.42 Anticonvulsants are not effective in
preventing further seizures in the withdrawal
episode.
C
III
A
Ia
A
Ia
Role of long-term anticonvulsants for patients with alcohol withdrawal seizures
Patients should not be initiated on long-term anticonvulsants unless there are other
causes of seizure activity. Alcohol withdrawal seizures will not recur if the patient
remains abstinent, and most patients have very poor adherence with anticonvulsants
if they recommence alcohol use, and indeed may even increase the risk of seizures
due to erratic anticonvulsant use (Hillbom et al. 2003).
Recommendation
5.43 Long-term anticonvulsant treatment is not
recommended to prevent further alcohol
withdrawal seizures.
Strength of
recommendation
Level of
evidence
D
IV
Hallucinations
Patients may experience hallucinations or other perceptual disturbances (e.g.
misperceptions) at any stage of the alcohol withdrawal phase and are not a predictor
of alcohol withdrawal delirium (Holloway 1984, cited in Turner et al. 1989).
Hallucinations may be visual, tactile or auditory. Visual hallucinations commonly
reported by patients include bugs crawling on the walls or patient’s bed. Auditory
hallucinations are often voices that are accusatory in nature and patients appear
frightened and paranoid. Visual and auditory hallucinations may occur
simultaneously. Hallucinations occur on the background of clear sensorium in
contrast with the clouded consciousness characteristic of alcohol withdrawal delirium
(Turner et al. 1989). The autonomic symptoms of withdrawal may be absent.
Assessment and monitoring
Thorough psychiatric evaluation is required in order to exclude concomitant medical
or psychiatric conditions.
101
Medication
There are no controlled trials demonstrating the superiority of different antipsychotic
medications, and practitioners should use medications with which they are most
familiar.
Antipsychotic medication should not be used in isolation (i.e. without adequate
benzodiazepine loading) as they do not adequately prevent the onset of alcohol
withdrawal delirium and may lower seizure threshold.
Alcoholic hallucinosis
Chronic alcohol use can result in an organic psychotic disorder, most commonly with
hallucinatory features (alcoholic hallucinosis), that can be difficult to differentiate from
other causes of psychosis, such as paranoid schizophrenia (Soyka 1990; Glass
1989a). Hallucinations (usually auditory) occur whilst patients are drinking, although
may persist during withdrawal, and can be mistaken for alcohol withdrawal
hallucinations.
Alcoholic hallucinosis is a rear syndrome, compared to alcohol withdrawal delirium,
with estimated prevalence of 0.6% (Soyka 2008).
Treatment with antipsychotic medications is recommended until long-term abstinence
is achieved and symptoms ameliorate. The prognosis is usually good if long-term
abstinence is maintained, although a minority (10-20%) will develop a chronic
schizophrenia-like syndrome (Glass 1989b).
Treatment of alcoholic hallucinosis with sodium valproate has been investigated in a
double-blind placebo-controlled study (Aliyev and Aliyev 2008). The results of the
study suggest that valproate reduces auditory hallucinations in patients with alcoholic
hallucinosis.
Alcohol Withdrawal Delirium
Alcohol withdrawal delirium is also referred to as delirium tremens or DTs and the
terms can be used interchangeably.
Clinical presentation and prevalence
The features of alcohol withdrawal delirium are disturbance of consciousness and
changes in cognition or perceptual disturbance developing in a short period of time
during or shortly after alcohol withdrawal syndrome (American Psychiatric
Association 2000). It is accompanied by other symptoms of withdrawal, such as high
fever, tachycardia, hypertension and diaphoresis (Mayo-Smith et al. 2004).
The incidence of alcohol withdrawal delirium in placebo-treated alcohol dependent
patients entered into inpatient clinical trials averages at 5% (Mayo-Smith 1997). Early
studies reported mortality rates as high as 15%, however, mortality rates have fallen
with advances in management to less than 1% (Mayo-Smith et al. 2004),
102
Concomitant medical conditions are common and may include dehydration,
electrolyte abnormalities, renal failure, unrecognised head trauma, infections
(including meningitis), gastrointestinal haemorrhage, pancreatitis, liver failure,
Management
The initial treatment goal in patients with AWD is control of agitation. Rapid control of
agitation reduces the incidence of subsequent adverse events. Hospitalisation is
recommended.
Mayo-Smith et al. (2004) have reviewed 49 studies investigating treatment of alcohol
withdrawal delirium and conducted a meta-analysis of nine randomised clinical trials.
Sedative hypnotics were found more effective than neuroleptics in reducing mortality
from alcohol withdrawal delirium (relative risk of mortality with neuroleptic treatment
compared with sedative-hypnotic treatment was 6.6 (95% confidence interval, 1.234.7). Sedative-hypnotic agents were superior to neuroleptic agents in reducing the
duration of alcohol withdrawal delirium. The authors recommend that control of
agitation should be achieved using parenteral rapid-acting sedative-hypnotic agents.
Adequate doses should be used to maintain light somnolence for the duration of
delirium. Coupled with comprehensive supportive medical care, this approach is
highly effective in preventing morbidity and mortality.
Monitoring and assessment
There are no controlled studies assessing these issues, the literature includes
recommendations from clinical experts and case reports reviewed by Mayo-Smith et
al. (2004). Thorough medical evaluation is required in order to identify complications
of alcohol withdrawal delirium (such as electrolyte disturbances) and concomitant
medical conditions.
Close monitoring and supervision (preferably one-to-one) may be needed to ensure
safety of the patient from harm to self or others. Vital signs (including pulse, blood
pressure, temperature) should be monitored frequently. Patient should be managed
in a quiet room with minimal sensory stimulation.
Recommendation
5.44 Alcohol withdrawal delirium requires
hospitalisation, medical assessment, and close
monitoring.
5.45 Patient should be managed in a quiet
environment with minimal sensory stimulation.
Strength of
recommendation
Level of
evidence
A
I
C
III
IV fluids and nutritional supplements
Electrolyte abnormalities should be corrected. In particular, hypomagnesaemia is
often reported in patients with AWD, and magnesium administration may help reduce
neuromuscular activity and agitation (Saitz and O’Malley 1997).
Recommendation
5.46 Dehydration and electrolyte imbalance
should be corrected.
Strength of
recommendation
Level of
evidence
S
103
Medication
Benzodiazepines are recommended as the primary medication in managing AWD,
reducing mortality, duration of delirium and with fewer complications than with
neuroleptics in controlled trials (Mayo-Smith et al. 2004).
Controlled studies are lacking with regards to the most effective benzodiazepine, or
route of administration.
Antipsychotic medications should be used as second-line medication in controlling
agitation of AWD, as an adjunct to (not instead of) adequate benzodiazepine doses
(Mayo-Smith et al. 2004). There are no controlled trials demonstrating the superiority
of different antipsychotic medications, and practitioners should use medications with
which they are most familiar.
The newer antipsychotic agents (e.g. risperidone, olanzapine, quetiapine) have a
better safety profile.
Recommendation
Strength of
recommendation
Level of
evidence
A
1a
A
1a
5.47 Benzodiazepines should be used to
achieve light sedation. Oral diazepam or
lorazepam loading until desired effect is the
treatment of choice. Intravenous diazepam or
midazolam is appropriate if rapid sedation is
needed.
5.48 Antipsychotic medications should be used
to control agitation of alcohol withdrawal as an
adjunct to (not instead of) adequate
benzodiazepine doses.
Wernicke’s Korsakoff’s Syndrome
Wernicke’s encephalopathy is a form of acute brain injury resulting from a lack of
thiamine (vitamin B1) that most commonly occurs in chronically alcohol dependent
individuals (Victor et al. 1989). In alcohol dependent patients thiamine deficiency
occurs due to poor dietary intake and due to intestinal malabsorption. It is estimated
that healthy subjects absorb 4.5% of an oral dose of thiamine, compared to 1.5% in
alcohol-dependent patients (Thomson et al. 2002). The condition is initially
reversible, but if untreated or inadequately treated can lead to Korsakoff’s syndrome,
a chronic and disabling condition characterised by severe anterograde amnesia and
often presents with confabulation. Korsakoff’s is not associated with dementia or
delirium.
Approximately one quarter of patients with Wernicke’s encephalopathy recover
completely, a quarter show significant improvement, a quarter only partially recover,
and one quarter no improvement with time. Approximately one quarter require longterm institutional care (Cook et al. 1998).
There is no effective treatment of Korsakoff’s Syndrome.
104
Clinical presentation and diagnosis
The initial diagnosis of Wernicke’s encephalopathy remains clinical. The classic triad
of signs of Wernicke’s encephalopathy syndrome are:
Confusion or mental impairment (estimated to occur in 80% of cases)
Ataxia (approximately 20-25% of cases)
Eye signs - nystagmus, opthalmoplegia (approximately 30% of cases) (Harper
1986).
Only a minority of patients with Wernicke’s encephalopathy (estimated at 10%)
exhibit all three signs. In rare cases, untreated Wernicke’s encephalopathy may
result in hypothermia, hypotension, coma and death (Harper et al. 1986).
Wernicke’s encephalopathy is grossly under-diagnosed (Thomson et al. 2002). Postmortem studies reveal changes diagnostic for Wernicke’s encephalopathy in 12.5%
of heavy drinkers (compared to 1.5% of general population). Fewer than 80% of
these cases are diagnosed before post-mortem (Harper et al. 1986; Cook et al.
1998).
Clinical features of Wernicke’s encephalopathy may be misinterpreted as alcohol
intoxication, alcohol withdrawal, head injury, or other causes of confusion in heavy
drinkers. Whilst there are no specific routine diagnostic tests for Wernicke’s
encephalopathy, magnetic resonance imaging (MRI) remains a valuable technique
(Sechi and Serra 2007). It can usually detect symmetric alterations in the mamillary
bodies, medial thalami, tectal plate, and periaqueductal area (Chung et al. 2003;
Estruch et al. 1998; Sechi and Serra 2007). In patients with a history of alcohol
abuse, contrast media and other methods of enhanced MRI can often identify
mamillary body lesions typical for Wernicke’s encephalopathy, even in the presence
of normal unenhanced MR images. MRI has low sensitivity (53%) but high specificity
(93%) for Wernicke’s encephalopathy (Antunez et al. 1998). Valuable adjuncts for an
early diagnosis of Wernicke’sencephalopathy are MR fluid-attenuated inversion
recovery (FLAIR) sequence and diffusion-weighted MRI (Sullivan and Pfefferbaum
2009).
Diagnosis of Wernicke’s encephalopathy requires a high index of suspicion in heavy
or chronic drinkers, especially if there are any clinical features consistent with
Wernicke’s encephalopathy or Korsakoff syndrome (e.g. memory impairment).
Recommendation
Strength of
recommendation
Level of
evidence
D
III
5.49 Clinicians should consider MR contrast
neuro-imaging where the diagnosis of
Wernicke’s encephalopathy is not clinically
established.
Preventing and treating Wernicke’s encephalopathy
The most recent meta-analysis of studies examining efficacy of thiamine in
preventing and treating Wernicke’s encephalopathy in patients with alcohol
dependence (Day et al. 2009) found insufficient evidence to guide clinicians in the
105
choice of thiamine dose, frequency and route of administration or duration of
treatment. Only two randomised controlled studies were identified and only one
contained data sufficient for quantitative analysis. The current approach described in
this section, is based on uncontrolled trials and expert opinion (e.g. Thomson et al.
2002; Lingford-Hughes et al. 2004; Thomson and Marshall 2006; Feeney and
Connor. 2008).
Is recommended that:
• all heavy or chronic drinkers should be considered at risk of Wernicke’s
encephalopathy
• all patients undergoing alcohol withdrawal should be treated with thiamine to
prevent Wernicke’s encephalopathy and
• all patients with any features of WE should be treated as though Wernicke’s
encephalopathy is established.
Prophylaxis
In patients showing no clinical features of WE or memory impairment, thiamine is
recommended as a prophylactic measure. See Section on Thiamine and other
supplements in this chapter.
Treatment
All heavy drinkers with any features of WE (e.g. confusion, ataxia, eye signs), coma,
memory impairment, hypothermia with hypotension, or delirium tremens should be
treated as though WE is established (even if intoxicated). Thiamine should be given
BEFORE any carbohydrate load (e.g. IV glucose). Parenteral doses of at least
500mg per day thiamine (IM or IV diluted in saline over 30 minutes) should be
administered daily for at least 3 to 5 days, with subsequent doses of at least 300mg
(oral or parenteral) per day for 1 to 2 weeks. Any electrolyte disturbances, including
hypomagnesaemia, should be corrected.
Recommendation
Strength of
recommendation
Level of
evidence
5.50 All patients exhibiting any features of
Wernicke’s encephalopathy should be treated
as though Wernicke’s encephalopathy is
established.
D
III
5.51 All patients suspected of Wernicke’s
encephalopathy should be treated with highdose parenteral thiamine (at least 500 mg daily)
for at least 3 to 5 days. The intramuscular route
should not be used for patients with
coagulopathy. Subsequent oral thiamine doses
of 300 mg per day for several weeks.
5.52 Patients suspected of Wernicke’s
encephalopathy should have hypomagnesaemia
corrected in order for thiamine supplements to
be effective.
D
III
D
III
Long-term thiamine use in persistent drinkers
Oral thiamine (e.g. 100mg daily) should be maintained until long term abstinence has
been achieved. Persistent drinkers should be maintained on oral thiamine
supplements.
106
References
Ait-Daoud, N, Malcolm RJ, Jr. and BA Johnson 2006, An overview of medications for the
treatment of alcohol withdrawal and alcohol dependence with an emphasis on the
use of older and newer anticonvulsants. Addict Behav 31(9): 1628-1649.
Aliyev, ZN and NA Aliev 2008, Valproate treatment of acute alcohol hallucinosis: a doubleblind, placebo-controlled study. Alcohol Alcohol 43(4): 456-459.
Amato, L, Minozzi S, Davoli M et al. 2008, Psychosocial and pharmacological treatments
versus pharmacological treatments for opioid detoxification. Cochrane Database Syst
Rev. (4):CD005031.
Ambrose, ML, Bowden SC and G Whelan 2001, Working memory impairments in alcoholdependent participants without clinical amnesia. Alcohol Clin Exp Res. 25(2): 185191.
American Psychiatric Association 2000, Diagnostic and Statistical manual of Mental
Disorders, Fourth Edition, Text Revision. Washington DC: American Psychiatric
Association.
Antunez, E, Estruch R, Cardenal C et al. 1998, Usefulness of CT and MR imaging in the
diagnosis of acute Wernicke's encephalopathy. AJR AM J Roentgenol 171(4): 11311137.
Ballenger, JC and RM Post 1978, Kindling as a model for alcohol withdrawal syndromes. Br
J Psychiatry 133: 1-14.
Benca, RM, Obermeyer WH, Thisted RA et al. 1992, Sleep and psychiatric disorders. A
meta-analysis. Arch Gen Psychiatry 49(8): 651-668;
Benzer, DG 1990, Quantification of the alcohol withdrawal syndrome in 487 alcoholic
patients. J Subst Abuse Treat 7(2): 117-123.
Bostwick, JM and MI Lapid 2004, False positives on the Clinical Institute Withdrawal
Assessment for Alcohol - Revised: is this scale appropriate for use in the medically
ill? Psychosomatics 45(3): 256-261.
Bråthen, G, Ben-Menachem E, Brodtkorb E et al. 2005, EFNS guideline on the diagnosis
and management of alcohol-related seizures: report of an EFNS task force. Eur J
Neurol 12(8): 575-581.
Brower, KJ, Aldrich MS, Robinson EA et al. 2001, Insomnia, self-medication, and relapse to
alcoholism. Am J Psychiatry 158(3): 399-404.
Caetano, R, Clark CL and TK Greenfield 1998, Prevalence, trends, and incidence of alcohol
withdrawal symptoms: analysis of general population and clinical samples. Alcohol
Health Res World 22: 73–79.
Chan, AW 1985, Alcoholism and epilepsy. Epilepsia 26(4): 323-333.
Chung, SP, Kim SW, Yoo IS et al. 2003, Magnetic resonance imaging as a diagnostic
adjunct to Wernicke’s encephalopathy in the ED. Am J Emerg Med 21(6): 497–502.
107
Cook, CCH, Hallwood PM and AD Thomson 1998, B-vitamin deficiency and neuropsychiatric syndromes in alcohol misuse, Alcohol Alcohol Suppl 33 (4): 317–336.
Cook, CC 2000, Prevention and treatment of Wernicke-Korsakoff Syndrome, Alcohol Alcohol
Suppl 35(1): 19–20.
Daeppen, JB, Gache P, Laundry U et al. 2002, Symptom-triggered vs fixed-schedule doses
of benzodiazepine for alcohol withdrawal: a randomized treatment trial. Arch Intern
Med. 162(10): 1117-1121.
Day, E, Benthan P, Callaghan R et al. 2004, Thiamine for Wernicke-Korsakoff syndrome in
people at risk from alcohol abuse. Cochrane Database Syst Rev 1, CD004003.
Degenhardt, L, Hall W, Teesson M et al. 2000, Alcohol use disorders in Australia: findings
from the National Survey of Mental Health and Well-Being. Technical Report no. 97.
Sydney: National Drug and Alcohol Research Centre.
Earnest, MP, Feldman H, Marx JA et al. 1998, Intracranial lesions shown by CT scans in 259
cases of first alcohol-related seizures. Neurology 38(10): 1561-1565.
Essardas Daryanani, H, Santolaria FJ, Reimers EG et al. 1994, Alcoholic withdrawal
syndrome and seizures. Alcohol Alcohol 29(3): 323-328.
Estruch, R, Bono G, Laine P et al. 1998, Brain imaging in alcoholism. Eur J Neurol 5(2):
119-135.
Favre, J-D, Allain H, Aubin H-J et al. 2005, Double-blind study of cyamemazine and
diazepam in the alcohol withdrawal syndrome. Hum Psychopharmacol 20(7): 511519.
Feeney, GF and JP Connor 2008, Wernicke-Korsakoff syndrome (WKS) in Australia: no
room for complacency. Drug Alcohol Rev 27(4): 388-392.
Foster JH and TJ Peters 1999, Impaired sleep in alcohol misusers and dependent alcoholics
and the impact upon outcome. Alcohol Clin Exp Res 23 (6): 1044–1051.
Foy, A, March S and V Drinkwater 1988, Use of an objective clinical scale in the assessment
and management of alcohol withdrawal in a large general hospital. Alcohol Clin Exp
Res 12(3): 360-364.
Glass, IB 1989a, Alcoholic hallucinosis: a psychiatric enigma, 1, the development of an idea.
Br J Addiction 84: 29-41.
Glass, IB 1989b, Alcoholic hallucinosis: a psychiatric enigma, 2, Follow-up studies. Br J
Addiction 84: 151-164.
Gossop, M, Keaney F, Stewart D et al. 2002, Short Alcohol Withdrawal Scale (SAWS)
development and psychometric properties. Addict Biol 7(1): 37–43.
Harper, CG, M Gilesn and R Finlay-Jones 1986, Clinical signs in the Wernicke-Korsakoff
complex: a retrospective analysis of 131 cases diagnosed at necropsy. J Neurol
Neurosurg Psychiatry 49(4): 341-345.
108
Hauser, WA, SK Ng and JC Brust 1988, Alcohol, seizures, and epilepsy. Epilepsia 29 Suppl
2: S66-78.
Hayashida, M, Alterman AI, McLellan AT et al. 1989, Comparative effectiveness and costs of
inpatient and outpatient detoxification of patients with mild-to-moderate alcohol
withdrawal syndrome. N Engl J Med 320(6): 358-365.
Hecksel, KA, Bostwick JM, Jaeger TM et al. 2008, Inappropriate Use of Symptom-Triggered
Therapy for Alcohol Withdrawal in the General Hospital. Mayo Clin Proc 83(3):274279.
Heinälä P, Piepponen T and H Heikkinen 1990, Diazepam loading in alcohol withdrawal:
clinical pharmacokinetics. Int J Clin Pharmacol Ther Toxicol 28(5): 211-7.
Hillbom, M, Tokola R, Kuusela V et al. 1989, Prevention of alcohol withdrawal seizures with
carbamazepine and valproic acid. Alcohol, 6: 223-226.
Hillbom, M, I Pieninkeroinen and M Leone 2003, Seizures in alcohol-dependent patients:
epidemiology, pathophysiology and management. CNS Drugs 17(14): 1013-1030.
Holbrook AM, Crowther R, Lotter A, et al. 1999, Diagnosis and management of acute alcohol
withdrawal. CMAJ 160(5): 675-80.
Hughes, JR (2008) Alcohol withdrawal seizures. Epilepsy and Behavior 15: 92-97
Kiefer, F, Andersohn C, Otte K, et al. 2004, Long-term effects of pharmacotherapy on
relapse prevention in alcohol dependence. Acta Neuropsychiatr. 16: 233–238.
Koethe, D, Juelicher A, Nolden BM et al. 2007, Oxcarbazepine--efficacy and tolerability
during treatment of alcohol withdrawal: a double-blind, randomized, placebocontrolled multicenter pilot study. Alcohol Clin Exp Res 31(7): 1188-1194.
Leens C, Mukendi R, Forêt F et al. 2001, Central and extrapontine myelinolysis in a patient
in spite of a careful correction of hyponatremia. Clin Nephrol 55(3): 248-253.
Lingford-Hughes, AR, S Welch and DJ Nutt 2004, Evidence-based guidelines for the
pharmacological management of substance misuse, addiction and comorbidity:
recommendations from the British Association for Psychopharmacology British
Association for Psychopharmacology. J Psychopharmacol 18(3): 293-335.
Lintzeris N, Clark N, Winstok A et al. 2006, National clinical guidelines and procedures for
the use of buprenorphine in the treatment of opioid dependence. Canberra:
Australian Government Department of Health and Ageing.
Laureno, R and BI Karp 1997, Myelinosis after correction of hyponatremia. Ann Intern Med
126(1): 57-62.
Lucht, M, Kuehn KU, Armbruster J et al. 2003, Alcohol withdrawal treatment in intoxicated
vs. non-intoxicated patients: a controlled open-label study with
tiapride/carbamazepine, clomethiazole and diazepam. Alcohol Alcohol 38(2): 168175.
Lum, E, SK Gorman and RS Slavik 2006, Valproic Acid Management of Acute Alcohol
Withdrawal. Ann Pharmacother 40(3): 441-448.
109
Malcolm, R, Myrick H, Roberts J et al. 2002, The differential effects of medication on mood,
sleep disturbance, and work ability in outpatient alcohol detoxification. Am J Addict
11(2): 141-150.
Malcolm, R, Myrick LH, Veatch LM et al. 2007, Self-reported sleep, sleepiness, and repeated
alcohol withdrawals: a randomized, double blind, controlled comparison of lorazepam
vs gabapentin. J Clin Sleep Med 3(1): 24-32.
Manikant, S, BM Tripathi and BS Chavan 1993, Loading dose diazepam therapy for alcohol
withdrawal state. Indian J Med Res 98: 170-173.
Mann, K, F Kiefer, R Spanagel, et al. 2008, Acamprosate: recent findings and future
research directions Alcohol Clin Exp Res 32(7): 1105-1110.
Mariani, JJ, Rosenthal RN, Tross S et al. 2006, A randomized, open-label, controlled trial of
gabapentin and phenobarbital in the treatment of alcohol withdrawal. Am J Addict
15(1): 76-84.
Mayo-Smith, MF 1997, Pharmacological management of alcohol withdrawal. JAMA 278 (2):
144-151
Mayo-Smith, MF, Beecher LH, Fischer TL, et al. 2004, Management of alcohol withdrawal
delirium. An evidence-based practice guideline. Arch Intern Med 164: 1405-1412.
Miller, WC Jr and L McCurdy 1984, A double-blind comparison of the efficacy and safety of
lorazepam and diazepam in the treatment of the acute alcohol withdrawal
syndrome.Clin Ther 6(3): 364-371.
Myrick, H and RF Anton 1998, Treatment of Alcohol Withdrawal. Alcohol Health Res World
22(1):38-43
Myrick, H, Malcolm R, Randall PK, et al. 2009, A double-blind trial of gabapentin versus
lorazepam in the treatment of alcohol withdrawal. Alcohol Clin Exp Res 33(9): 15821588.
Naranjo, CA, Sellers EM, Chater K et al. 1983, Nonpharmacologic intervention in acute
alcohol withdrawal. Clin Pharmacol Ther 34: 214-219
NSW Department of Health 2007, NSW drug and alcohol withdrawal clinical practice
guidelines. Mental Health and Drug and Alcohol Office, NSW Department of Health.
NSW Health Department 1999, New South Wales Detoxification Clinical Practice Guidelines,
NSW Health Department
Ntais, C, Pakos E, Kyzas P et al. 2005, Benzodiazepines for alcohol withdrawal. Cochrane
Database Syst Rev. (3):CD005063.
Ozdemir, V, KE Bremner and CA Naranjo 1994, Treatment of alcohol withdrawal syndrome.
Ann.Med 26(2): 101-105.
EFNS 2005, EFNS guideline on the diagnosis and management of alcohol-related seizures:
Report of the European Federation of Neurological Societies task force. available at
<http://www.guideline.gov/summary/summary.aspx?doc_id=9648>
110
Polycarpou, A, Papanikolaou P, Ioannidis JPA et al. 2005, Anticonvulsants for alcohol
withdrawal. Cochrane Database Syst Rev (3): CD005064.
Prescrire 2007, Alcohol withdrawal syndrome: how to predict, prevent, diagnose and treat it.
Prescrire International 16(87): 24-31.
Prince, V and KR Turpin 2008, Treatment of alcohol withdrawal syndrome with
carbamazepine, gabapentin, and nitrous oxide. Am J Health Syst Pharm 65(11):
1039-1047.
Reoux, JP and K Miller 2000, Routine hospital alcohol detoxification practice compared to
symptom triggered management with an Objective Withdrawal Scale (CIWA-Ar). Am
J Addict 9(2): 135-144.
Saitz, R, Mayo-Smith MF, Roberts MS et al. 1994, Individualized treatment for alcohol
withdrawal: a randomized double-blind controlled trial. JAMA 272(7): 519-23.
Saitz, R and SS O’Malley 1997, Pharmacotherapies for Alcohol Abuse: Withdrawal and
Treatment. In: Samet. JH, Stein. MD and O’Connor. PG (eds) The Medical Clinics of
North America: Alcohol and Other Substance Abuse. 81(4), pp 881-907, WB
Saunders Company Pennsylvania.
Saitz, R 1998, Introduction to alcohol withdrawal. Alcohol Health Res World 22(1): 5-12.
Satel, SL, Kosten TR, Schuckit MA et al. 1993, Should protracted withdrawal from drugs be
included in the DSM-IV? Am J Psych 150: 695-704.
Schik, G, Wedegaertner FR, Liersch J et al. 2005, Oxcarbazepine versus carbamazepine in
the treatment of alcohol withdrawal. Addict Biol 10(3): 283-288.
Schuckitt, MA 2006, Drug and alcohol abuse: a clinical guide to diagnosis and treatment (6th
edn.) New York: Springer.
Sechi, G and A Serra 2007, Wernicke’s encephalopathy: new clinical settings and recent
advances in diagnosis and management. Lancet Neurol 6: 442–455.
Sellers, EM, Naranjo CA, Harrison M et al. 1983, Diazepam loading: simplified treatment of
alcohol withdrawal. Clin Pharmacol Ther 34(6): 822-826.
Sgouros, X, Baines M, Bloor RN et al. 2004, Evaluation of a clinical screening instrument to
identify states of thiamine deficiency in inpatients with severe alcohol dependence
syndrome. Alcohol Alcohol 39(3): 227–232.
Soyka, M, Lutz W, Kauert G et al. 1989, Epileptic seizures and alcohol withdrawal:
Significance of additional use (and misuse) of drugs and electroencephalographic
findings. J Epilepsy 2(2): 109-113.
Soyka, M 1990, Psychopathological characteristics in alcohol hallucinosis and paranoid
schizophrenia. Acta Psychiatrica 81:255-259.
Soyka, M and M Horak 2004, Outpatient alcohol detoxification: implementation efficacy and
outcome effectiveness of a model project. Eur Addict Res. 10(4): 180-187.
111
Soyka, M, Schmidt P, Franz M et al. 2006, Treatment of alcohol withdrawal syndrome with a
combination of tiapride/carbamazepine: results of a pooled analysis in 540 patients.
Eur Arch Psychiatry Clin Neurosci 256(7): 395-401.
Soyka, M 2008, Prevalence of alcohol-induced psychotic disorders. Eur Arch Psychiatry Clin
Neurosci 258(5): 317-318.
Spies, CD, Otter HE, Hüske B et al. 2003, Alcohol withdrawal severity is decreased by
symptom-orientated adjusted bolus therapy in the ICU. Intensive Care Med. 29(12):
2230-2238.
Sullivan, J, Sykora K, Schneiderman J et al. 1989, Assessment of alcohol withdrawal: the
revised clinical institute withdrawal assessment for alcohol scale (CIWA-Ar), Br J
Addiction 84 (11): 1353-1357.
Sullivan, EV and A Pfefferbaum 2009, Neuroimaging of the Wernicke–Korsakoff Syndrome
Alcohol Alcohol 44(2): 155-165.
Tartara, A, Manni, R and Mazella, G. 1983, Epileptic seizures and alcoholism: clinical and
pathogenetic aspects. Acta Neurol. Belg. 83(2): 88-94.
Thomson, AD 2000, Mechanisms of vitamin deficiency in chronic alcohol misusers and the
development of the Wernicke–Korsakoff syndrome. Alcohol Alcohol Suppl 35(1): 2–7.
Thomson, AD, Cook CCH, Touquet R et al. 2002, The Royal College of Physicians report on
alcohol: guidelines for managing Wernicke's encephalopathy in the accident and
emergency department, Alcohol Alcohol Suppl 37(6): 513–521.
Thomson, AD and EJ Marshall 2006, The treatment of patients at risk of developing
Wernicke's Encephalopathy in the community, Alcohol Alcohol Suppl 41(2): 159–167.
Trevisan, LA, Boutros N, Petrakis IL et al. 1998, Complications of Alcohol Withdrawal:
Pathophysiological insights. Alcohol Health Res World 22(1): 61-66.
Turner, RC, Lichsyein P, Peden JG et al. 1989, Alcohol withdrawal syndromes: A review of
pathophysiology, clinical presentation and treatment. J Gen Int Med 4(5): 432-444.
Valliant, GE 1988, What can long-term follow up teach us about relapse and prevention of
relapse in addiction? Br J Addict 83(10): 1147-1157.
Victor, M and RD Adams 1953, The effect of alcohol on the nervous system. Research
Publications of the Association for Research on Nervous and Mental Disorders 32:
526-573.
Victor, M and C Brausch 1967, The role of abstinence in genesis of alcoholic epilepsy.
Epilepsia 8(1): 1-20.
Victor, M, RD Adams and GH Collins 1989, The Wernicke-Korsakoff Syndrome and related
Neurological disorders due to alcoholism and malnutrition. Philadelphia: F A Davis
Company.
Wetterling, T, Kanitz RD, Veltrup C et al. 1994, Clinical predictors of alcohol withdrawal
delirium. Alcohol Clin Exp Res 18(5): 1100-1102.
Whitfield, CL, Thompson G, Lamb A et al. 1978, Detoxification in 1024 alcoholic patients
without psychoactive drugs. JAMA 239(14): 1409-1410.
112
Weinberg, JA, Magnotti LJ, Fischer PE, et al. 2008, Comparison of intravenous ethanol
versus diazepam for alcohol withdrawal prophylaxis in the trauma ICU: results of a
randomized trial. J Trauma. 64(1): 99-104.
Zilm, DH, Jacob MS, MacLeod SM et al. 1980, Propranolol and chlordiazepoxide effects on
cardiac arrhythmias during alcohol withdrawal. Alcohol Clin Exp Res 4(4): 400-405.
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Chapter 6 Psychosocial Interventions for Alcohol Use
Disorders
Overview of Psychosocial Interventions
Psychosocial interventions for treatment of alcohol and drug problems cover a
diverse array of treatment interventions (Raistrick and Tober 2004; Carroll and
Onken 2005; Raistrick et al. 2006; Bottlender et al. 2006).These interventions
generally focus on the individual (their beliefs, feelings and behaviour), their social
context, including family, community and cultural factors and the interaction between
these two domains.
Psychosocial interventions encompass treatment content (that is, the skills,
strategies and the theoretical orientation of treatment) and treatment process (that is,
the interaction between the clinician and patient which includes the strength of
engagement, interpersonal processes and ability to work on shared treatment goals
(Marsh and Dale 2006).
The effectiveness of treatment depends not only on the treatment itself but also who
delivers it and how it is delivered (Raistrick et al. 2006). The process of natural
change also has a part to play, as most people (estimated 70-80%) experience major
changes in their substance use without any formal help or treatment. However, the
evidence shows that people who receive substance abuse treatment do better than
those who do not (Raistrick and Tober 2004) .
The most widely used empirically supported psychosocial approaches are brief
interventions (discussed in Chapter 4), motivational interviewing and cognitivebehaviour therapy (CBT), including coping skills training, relapse prevention and
behavioural couples therapy (Miller et al. 1995; Miller and Wilbourne 2002; Raistrick
and Tober 2004; Carroll and Onken 2005).
When to Use Psychosocial Interventions
Psychosocial interventions can be used in a variety of treatment settings. They can
be implemented individually or in groups and delivered by a range of health workers.
Psychological treatments can be brief or intensive and specialised (e.g., cognitive
behaviour therapy, couples therapy). Brief interventions are most suited for nondepended drinkers (see Chapter 4). Motivational strategies are often used early in
treatment and engage patient into the process of change. Cognitive behavioural or
other specialised therapy is added as appropriate to provide patients with necessary
skills to maintain change.
In general, low intensity psychosocial interventions are indicated for people with low
dependence, increasing the level of intensity for those with more severe dependence
and co-existing mental health concerns.
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Choosing Psychosocial Interventions: A Stepped Care Approach
Stepped care model is a practical approach to implementing psychosocial and other
interventions in which patients are offered the least “restrictive” intervention
appropriate to their presentation (Sobell and Sobell 2000; Raistrick and Tober 2004;
Raistrick et al. 2006). The next level of intensity is offered if the first treatment fails to
provide sufficient benefit to the patient.
An adaptation of this model detailing a stepped care process for the application of
psychosocial interventions has been developed. This adaptation presupposes that
issues relating to risk management, withdrawal, and rehabilitation options have been
ruled out and a psychosocial intervention is indicated (NSW Health Department,
2008).
There is no published literature evaluating effectiveness of the stepped care
approach. However, this model has been accepted as a useful guide in selecting
treatment strategies and using resources efficiently (Raistrick et al. 2006). At present,
there is limited evidence to support ‘patient–treatment’ matching based upon patient
characteristics. The stepped care approach provides an adjunct to decision-making
and does not replace clinical judgment and expert advice (NSW Department of
Health 2008).
Recommendation
6.1 A stepped care approach is recommended
as a framework for selecting psychosocial
interventions, incorporating assessment,
monitoring, implementation of a treatment plan,
regular review of progress, and increasing
intervention intensity in the absence of a
positive response to treatment.
Strength of
Level of
recommendation evidence
D
IV
Motivational Interviewing
Motivational interviewing, introduced by Miller and Rollnick in 1991, is an interviewing
style which employs empathic counselling skills in an attempt to alter patient views of
the implications of continued alcohol use. As defined by Miller and Rollnick (2002),
motivational interviewing is a “client-centred, directive method for enhancing intrinsic
motivation to change by exploring and resolving ambivalence”.
One of the key elements in motivation for change is self-efficacy. Self-efficacy refers
to a person’s belief in their ability to carry out and succeed with a specific task. and is
a reasonable predictor of change (Miller and Rollnick 2002). A clinician’s own
expectations about a person’s likelihood of change can also have a powerful effect
on outcome (Miller and Mount 2001).
Motivational Interviewing: Meta-analyses
A meta-analysis by Hettema et al. (2005) published in 2005 studied 72 clinical trials
spanning a range of target problems, 31 of which focused on alcohol. The results of
this meta-analysis indicate that there is a high variability in effectiveness of
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motivational interviewing across providers, settings and target groups. Overall it
shows small to medium effectiveness in improving health outcomes. Motivational
interviewing is effective when used on its own when compared to no treatment or
education, with the average short-term between-group combined effect size (dc,) of
0.77 (95% CI 0.35, 1.19) at 1 month post-treatment, decreasing to 0.39 (95%
confidence interval, CI, 0.27, 0.50) at >1 to 3 months and 0.3 (95% CI 0.16, 0.43) at
one year (where dc = 1.0 represents a between-group difference of one standard
deviation). Motivational interviewing also appears to improve outcomes when added
to other treatment approaches. Manual guided motivational interviewing does not
appear to be an efficient way of delivering this intervention, particularly where a
therapist strictly follows a manual’s instructions ignoring the patient’s current
motivational status. The authors suggest that when motivational interviewing is
offered as an independent intervention, its effect could be prolonged by offering
booster sessions or stepped care. They also note that when motivational interviewing
is used as a prelude to treatment, its effect remains significant over a longer period of
time, ‘suggesting a synergistic effect of motivational interviewing with other treatment
procedures’. Motivational interviewing is often more effective in patients who are
more resistant to change at the start of treatment and is not effective in those who
are already motivated to changing behaviour and are committed to begin treatment.
A meta-analysis by Vasilaki et al (2006) of 22 studies reviewed the evidence for the
efficacy of motivational interviewing as a brief intervention for excessive drinking. Of
these studies, 7 were conducted among college students; six were tested in
outpatient settings; five in emergency rooms or clinics; and two in specialist treatment
agencies. They analysed a final sample of 15 studies (2767 participants), once
others had been rejected for methodological problems. Brief motivational interviewing
(of 87 minutes) was found to be statistically significantly more effective than no
treatment in nine studies, with the aggregate Cohen’s effect size of 0.18 (95%CI
0.07, 0.29) (positive effect sizes indicate better outcomes for motivational
interviewing). The effect size was largest at 3-month follow-up (0.6 (95% CI 0.36,
0.83)). It was also found that brief motivational interviewing of 53 minutes was more
effective than other types of treatment in another nine studies, with aggregate effect
size of 0.43 (CI 0.17, 0.7). Other treatments included brief advice/standard care in
five studies, and one study of each, directive confrontational counselling, educational
intervention, skill based counselling and cognitive behavioural treatment. The
conclusions of this meta-analysis were that brief motivational interviewing was an
effective treatment modality for reducing hazardous alcohol consumption, particularly
in the short-term (within the first 3 months of treatment). It was more effective with
young people, in those with occasional heavy drinking pattern and low dependence,
than with older drinkers or those with a more severe dependence. Specifically, helpseeking low-dependent drinkers benefited the most. The authors suggest that future
studies should focus on factors such as age, gender, employment status, mental
health, marital status and readiness to change.
Motivational Interviewing: Randomised controlled trials
The largest randomised controlled study of psychosocial interventions for alcohol use
disorders was the Project MATCH study (Project MATCH Research Group 1997;
1998a; 1998b). The effectiveness data from this study was included in both metaanalyses discussed above. Its aim was to assess benefits of matching of patients
with the DSM-IIIR diagnosis of alcohol dependence or abuse (with at least 3 months
of active drinking prior to entrance into the study) to three types of psychosocial
treatments. It compared four sessions over 12 week period of motivational
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enhancement therapy (a manual guided motivational interviewing) to 12 weekly
sessions of either cognitive behavioural therapy (CBT) or twelve-step facilitation.
There were two groups of patients, one from outpatient clinics (n = 952) and the other
involving clients receiving aftercare following inpatient treatment (n = 774).
Participants in all treatment groups showed significant improvements on all drinking
measures with no consistent differences between groups. Overall, in the first year
there was an increase in days abstinent from 20-30% to 80-90% at 12-month follow
up and the amount of alcohol consumed on a drinking day fell from 12-20 to 1-4
standard drinks (Project MATCH Research Group 1997). During the treatment
phase, small but statistically significant differences among treatments were found
only in the outpatient arm on measures of alcohol consumption and alcohol-related
negative consequences. Abstinence or moderate alcohol consumption (without
alcohol-related consequences) was reported by 41% of patients receiving CBT and
twelve-step facilitation, compared with 28% of those receiving motivational
enhancement therapy (Project MATCH Research Group 1998a).
At 3-year follow up the reductions in alcohol consumption, observed in the first year
after treatment, were sustained. Almost 30% of the patients were totally abstinent.
Those who continued drinking reported abstinence on an average of two-thirds of the
time in the last 3 months. There were no significant differences between the
treatment groups (Project MATCH Research Group 1998b).
No matching effect was found. It was concluded that the three treatments were
equally effective. In the outpatient setting there appears to be a temporary advantage
to assigning individuals to CBT or twelve-step facilitation rather than motivational
enhancement therapy.
The secondary analysis of data from the above study (Cutler and Fishbain 2005)
showed that the drop out patients (that the authors used as a zero treatment/control
group) also improved, showing 72% days abstinent at 1 year follow-up. Further, most
of the effect occurred after the first session. The conclusions of the latter paper were
that the current psychosocial treatments for people with alcohol problems are not
particularly effective and untreated patients in clinical trials also show significant
improvement. The improvements appear to be due to “selection effect’ whereby
patients who are motivated to enter treatment are likely to reduce drinking regardless
of treatment provided. The authors indicate that while treatments were not
particularly effective when compared to the drop out patients, it is likely that many
patients would benefit from them. The authors further suggest that these treatments
should not be discontinued or reduced on the basis of these findings, but their
effectiveness should not be over-emphasised and perhaps better attention should be
paid to patient characteristics and beliefs.
Two forms of motivational intervention (individual vs group treatment) were tested in
alcohol-dependent patients by John et al. (2003). In this trial, 322 in-patients
undergoing detoxification were randomised to group or individual counselling. The
aim was to examine whether 3 sessions of individual counselling (40 minutes
duration each) was more effective than the more costly 2-week group treatment
program (9 sessions, 90 minutes each and four outpatient sessions after discharge)
in enhancing motivation to seek help with alcohol problems and to live abstinently. At
6-month follow-up, group treatment participants showed a higher rate of participation
in self-help groups; however this effect had disappeared at 12 months. Abstinence
rates did not differ between groups (27.3 % and 29.2% were abstinent at 6 month
follow up in the individual counselling and group treatment respectively). This study
suggests that in patients with alcohol dependence, an intensive motivational
117
treatment may not provide any benefit over a less intensive counselling approach in
the long term.
Another large study of psychosocial treatment for alcohol problems, was the UK
Alcohol Treatment Trial (UKATT ) (UKATT Research Team 2005a). It was a
pragmatic randomised trial that compared socially based treatment (social behaviour
and network therapy) with motivational enhancement therapy, with the hypothesis
that they would prove equally effective. It was carried out in 7 UK sites with 742
participants. Social behaviour and network therapy comprised eight 50 minute
sessions over 8 to 12 weeks that focused on cognitive and behavioural strategies to
help clients build social networks supportive of change. The motivational
enhancement therapy comprised three 50 minute sessions over 8 to 12 weeks. It
combined counselling in the motivational style with objective feedback. Findings
showed that both groups reported substantial reductions in alcohol consumption,
dependence and problems and better mental-health-related quality of life at 12
months. The two therapies did not differ in effectiveness. Participants in both groups
reported that the number of abstinence days increased from 29% to 43% at 3 months
and to 46% at 12 months. Alcohol consumption reported by patients continuing to
drink fell from 27 drinks per drinking day to 18 drinks at 3 months and to 19 drinks at
12 months (mean adjusted values). Therefore, total alcohol consumption decreased
by 48% at 3 months and by 45% at 12 months. The Leeds dependence
questionnaire score reduced from 17 to 12 at 3 months and to 11 at 12 months. The
alcohol problem questionnaire score fell from 12 to 7 at 3 months and to 6 at 12
months. The mental component of the SF-36 score rose from 30 to 37 at 3 months
and to 39 at 12 months indicating improvement in mental health (UKATT Research
Team 2005a). The results of the trial have demonstrated effectiveness of the two
treatment modalities in reducing alcohol consumption and associated problems and
improving mental health of alcohol dependent patients.
The cost-analysis study showed that both types of treatment were cost effective.
Each saved ‘about five times as much in expenditure on health, social, and criminal
justice services as they cost’ (UKATT Research Team 2005b).
Monti et al. (2007) examined the effect of a motivational interview versus personal
feedback in a hospital setting (emergency department) in young patients (18 to 24
years of age) who either tested positive on alcohol at admission and/or were
identified on screening as having alcohol problems. Patients (n = 198) were randomly
assigned to receive either a 35 - 40 minute motivational interviewing session (that
included personal feedback), or personal feedback only. All patients received
additional booster telephone calls at 1 and 3 months. At six-month follow-up, both
patient groups showed reductions in alcohol consumption that were sustained at 12months follow up. Average number of drinks per week reduced from 13 standard
drinks at baseline to 6 drinks at 12 months in the motivational interview group and
from 11 to 9 respectively in the feedback only group. Patients who received the
motivational interview drank on significantly fewer days, had fewer heavy drinking
days, and drank fewer drinks per week, compared with patients who received
feedback only. It was estimated that twice as many patients who received a
motivational interview reliably reduced their alcohol consumption at 12 months as
those who received a personalised feedback only. The results of this study provide
support for effectiveness of motivational intervention in reducing alcohol consumption
in young people in emergency department setting.
In a study of rural community health care centres, 26 patients achieving an AUDIT
score indicating hazardous alcohol use were randomised to receive a motivational
interview session with a nurse practitioner or to a control condition (no treatment)
118
(Beckham and Beckham 2007). At 6 weeks, there was a significant reduction in
number of drinks per day and also in GGT levels in the treatment group compared to
the controls. The number of drinks reduced from 4.4 to 3.8 in the control group and
from 4.7 to 2 drinks in the intervention group. The results of this small study indicate
that one session of motivational interviewing can be effective in reducing hazardous
alcohol consumption in patients attending rural community health care clinics.
Motivational Interviewing: Summary
The evidence base for motivational interviewing is still strong. It is effective as a
stand alone treatment, as a prelude to treatment and as an adjunct to other treatment
modalities in addressing patient’s ambivalence to change their drinking or other
behaviours. It is effective in reducing alcohol consumption and associated problems
and improving mental health of alcohol dependent patients. The effect is more
evident in the short term (e.g. within the first 3 months of treatment).
The effect varies between providers, settings and target groups. It is particularly
effective in ethnic minority populations, young people and those with occasional
heavy drinking pattern and in treatment-seeking populations with low level of
dependence. There is some evidence to suggest that motivational interviewing is
effective in emergency department and rural settings.
The cost-effectiveness studies suggest that both motivational interviewing and CBT
approaches can save ‘about five times as much in expenditure on health, social, and
criminal justice services as they cost’ in the UKATT study. Motivational interviewing
may be more cost-effective than other treatment modalities, such as CBT and 12step facilitation. For example, in the Project MATCH four sessions of motivation
enhancement therapy were found to be equal in efficacy to twelve sessions of
cognitive behaviour therapy and twelve sessions of twelve step facilitation. In the
UKATT study, three sessions of motivation enhancement therapy were equivalent to
8 sessions of social behaviour and network therapy. Motivation enhancement
therapy, in these studies, was less intensive, about one third the number of sessions
but equally efficacious, hence it was more cost effective than other treatments.
More intensive motivational interviewing approaches (e.g. 13 group sessions) may
not provide additional benefit over a less intensive approach (e.g. 3 sessions of
individual counselling).
Recommendation
6.2 Motivational interviewing approaches can be
used as a first-line or stand-alone treatment, or
as an adjunct to other treatment modalities in
addressing patient’s ambivalence to change
their drinking or other behaviours.
Strength of
Level of
recommendation evidence
A
Ia
Cognitive Behavioural Interventions
Cognitive behavioural interventions, also called cognitive behavioural therapy (CBT)
comprise a range of approaches that are broadly based on learning principles and
the idea that behaviour is influenced by cognitive processes (Dobson 2000).
119
The cognitive-behavioural approach implies that excessive alcohol use is a
maladaptive way of coping with problems (Bandura 1986). Inability to cope with life
stresses in general and alcohol cues in particular are thought to maintain excessive
drinking and lead to a resumption of drinking following unsuccessful cessation
attempts. This learned behaviour can be changed through the application of
combined cognitive and behavioural interventions (Kadden 1994). Interventions are
designed to enhance patient motivation to stop or reduce drinking, to increase patient
understanding of alcohol effect and consequences of excessive drinking and to
challenge maladaptive beliefs and thought patterns that lead to problematic alcohol
use.
CBT approach: Reviews
The Mesa Grande project (Miller and Wilbourne 2002) is a review of clinical trials of
treatment for alcohol use disorders. The trials cover treatment modalities such as
brief intervention, motivational enhancement, pharmacotherapies, skills training,
psychotherapy, marital and family therapies, mutual help approaches, aversion
therapies, specific behavioural procedures, and milieu therapy (i.e. inpatient vs.
outpatient). This particular paper describes the progress up to and including 2000 (59
new trials, 361 in total). The main finding at that date was that the strongest evidence
of efficacy was found for brief intervention, community reinforcement, case
management and cognitive behavioural approaches such as social skills training,
behaviour contracting and behavioural marital therapy. Among pharmacological
approaches naltrexone and acamprosate appeared most supported by evidence.
Least supported were methods designed to educate, confront, or to foster insight
regarding the nature and causes of alcoholism. The review suggests that CBT
interventions such as social skills training, behaviour contracting and behavioural
marital therapy are effective treatments of alcohol use disorders.
CBT approach: Randomised Clinical Trials
The Project MATCH (see above under Motivational Interviewing for more detail) was
an earlier study aimed to assess benefits of matching alcohol dependent patients to
three types of psychosocial treatments: motivational enhancement therapy and
twelve-step facilitation (Project MATCH Research Group 1997; 1998a; 1998b). As
stated above, CBT was as effective as motivational enhancement therapy and 12step facilitation in reducing alcohol consumption in patients with alcohol use
disorders. With regard to patient-treatment matching it was found that: a) patients
with high degree of anger were more likely to benefit from motivational enhancement
than from CBT; b) patients with higher degree of alcohol dependence had better
outcomes with 12 step programs than with CBT; c) patients with lower psychiatric
severity at baseline did better with 12-step facilitation than with CBT; d) there was a
trend (not statistically significant) for patients with high psychiatric severity at baseline
to have better outcomes with CBT than 12-step facilitation.
The UKATT study described above (UKATT Research Team 2005a) that compared
socially based treatment (based on a CBT approach) with motivational enhancement
therapy. According to this study, CBT is as effective as motivational enhancement
therapy in reducing alcohol consumption and associated problems and improving
mental health of alcohol dependent patients.
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The COMBINE study (Anton et al. 2006) was designed to evaluate the efficacy or
pharmacotherapy, behavioural therapy and their combinations for treatment of
alcohol dependence and to evaluate placebo effect on overall outcome. This large
RCT involved 1383 patients with the diagnosis of alcohol dependence, recently
abstinent from alcohol. The treatments included naltrexone and acamprosate (alone
or together), placebo (single or double), each with or without a combined behavioural
intervention (CBI). The CBI integrated cognitive behavioural therapy, motivational
interviewing and 12-step facilitation and was delivered by trained behavioural health
specialists in up to 20 sessions of 50 min duration. All the above groups received
medical management. One group received a CBI only (no pills or medical
management). The treatment was of 16 weeks duration. It was found that by the end
of the treatment period, participants in all nine different treatments and combined
interventions showed reductions in drinking, including the placebo group. No
combination was more effective than naltrexone or CBI alone in the presence of
medical management. Patients who received CBI with placebo or naltrexone (both in
conjunction with medical management) had higher percent days abstinent when
compared to those receiving placebo with medical management without CBI.
However, CBI alone was less effective (e.g. resulted in lower percent days abstinent)
than medical management and placebo or when CBI was combined with medical
management and placebo. At one year follow up the differences were similar but no
longer significant. Overall the percent days abstinent declined across groups at 1
year follow up.
The results of this study suggest that although CBI, consisting of cognitive
behavioural therapy, motivational interviewing and 12-step facilitation, may reduce
alcohol consumption, placebo pills and a meeting with a health care professional can
have a stronger positive effect than CBI alone.
The COMBINE study aimed to determine whether improvements in outcome could
be achieved by combining pharmacotherapy and behavioural interventions, but no
such combining effect had been detected. It has been suggested that the variability
between treatment providers may be more important than the variability between
treatments (Bergmark 2008; Buhringer and Pfeiffer-Gerschel 2008).
Specific cognitive-behavioural interventions
Despite core similarities of cognitive behavioural interventions, they differ in duration,
modality, content and treatment setting (Kadden 1994). This section discusses the
effectiveness of specific cognitive-behavioural interventions, including behavioural
self-management (controlled drinking programs), coping skills training, cue exposure
and behavioural couples therapy. We have also included a study investigating the
effect of CBT for insomnia on relapse to heavy drinking.
Behavioural self-management or self-control: Controlled Drinking Programs
This approach teaches individuals to reduce their alcohol consumptions. It is most
suitable for individuals at the less severe end of the dependence spectrum
(Ambrogne 2002; Edwards et al. 2003). The components of behavioural selfmanagement include: goal setting; self-monitoring of daily drinking; controlling the
rate of drinking; and identifying problematic drinking situations and triggers to
drinking (Heather, 1995).
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The controlled drinking approach is widespread in Australia, Norway, Britain and
Switzerland but it has not receive much support from the treatment services in some
countries, such as the USA and Canada until relatively recently (Ambrogne 2002;
Gastfriend 2007).
Behavioural self control: Reviews and meta-analyses
Behavioural self control is ranked seventh in the Mesa Grander review of
effectiveness of psychosocial interventions (Miller and Wilbourne 2002).
A meta-analysis by Walters (2000) included 17 randomised controlled trials
investigating the efficacy of behavioural self-control training for problem drinking and
showed that this treatment modality was superior to no intervention in reducing both
alcohol consumption and problematic drinking. It was also superior to alternative nonabstinence-oriented interventions. There was a trend (not statistically significant)
towards higher effectiveness of behavioural self-control training over traditional
abstinence-oriented treatment. Self-control training was equally effective for use with
alcohol-dependent and problem-drinking subjects. The effect lasted at follow-ups
spanning several months to several years.
Behavioural self control: Other studies
A consistent finding in a number of earlier studies, not included in the meta-analysis,
is that patients with alcohol problems of various severity are able to maintain problem
free drinking at least over the 1-2 years of follow up and that treatment outcomes are
similar for patients who choose drinking moderation goal and for those with the goal
of abstinence (Booth et al. 1984; Booth et al. 1992; Miller et al. 1992). Also, patients,
who choose the goal of moderation and begin to learn behavioural self-management
strategies, are likely to move towards abstinence by the 4th month of treatment
(Hodgins et al. 1997).
Behavioural self control: Summary
Behavioural self control therapy is an effective treatment modality in reducing
problematic alcohol consumption is patients with and without dependence. There is,
however, a reason to believe that studies failing to find a benefit for BSCT were
conducted mainly on alcohol patients with more severe problems. This treatment
modality is currently recommended for patients with no or low level of dependence
and those considered suitable for moderation goal (Berglund et al. 2003; Raistrick et
al. 2006).
Recommendation
6.3 Behavioural self-management (controlled
drinking program) can be recommended as a
treatment strategy for people with no or low
level dependence and for when both patient and
clinician agree that moderation is an appropriate
goal.
Strength of
Level of
recommendation evidence
A
Ib
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Coping Skills Training
Based on Bandura’s (1969, 1997) Social Learning Theory, skills training assumes
that developing effective coping skills can help individuals deal with stressful social
situations (Dobson 2002).
Coping skills training is based on the premise that drinking has become a way of
coping with interpersonal stress (Monti et al. 1994). Skills training provides alternative
strategies to cope with social skills deficits and teach clients to deal with
interpersonal stress without drinking to excess.
Examples of social skills training include communication skills, listening techniques,
assertiveness, problem solving, drink refusal skills, coping with urges to drink,
relaxation, anger management and stress management skills training. Skills training
is usually delivered in conjunction with other interventions such as broad spectrum
cognitive behavioural approaches, cue exposure and more recently, with
pharmacotherapies such as naltrexone and acamprosate.
Coping Skills Training: Reviews
Coping skills training has been regarded as one of the best-established and
empirically supported interventions. A number of earlier reviews have stated that
there is consistent evidence that coping skills training is effective in reducing alcohol
consumption among alcohol dependent people (Mattick and Jarvis 1993; Monti et al.
1994; Miller et al. 1995; Shand et al. 2003; Raistick et al. 2006). It has been
suggested that skills training is more effective than other approaches when included
as a component of a more comprehensive treatment, but not when delivered as a
stand-alone treatment or as aftercare (Longabaugh and Morgenstern 1999). Social
skills training was identified as the ninth best supported treatment for alcohol use
disorders in the Mesa Grande review discussed above (Miller and Wilbourne 2002).
There are no recent reviews or meta-analyses of coping skills training.
Coping Skills Training: Randomised controlled trials
Randomised clinical trials provide some more evidence in support of coping skills
training as an effective treatment modality.
The form of CBT, evaluated in the Project MATCH (Project MATCH Research Group
1997), included coping skills training as a prominent part of the treatment
intervention. As discussed above, this approach was as effective as motivational
interviewing and 12-step facilitation in reducing alcohol consumption in patients with
alcohol use disorders.
Ferrell and Galassi (1981) specifically selected alcohol dependent patients with poor
social skills for their study. Patients who received assertion training had better
interpersonal skills and a longer period of sobriety as compared to those who
received human relations training. Therefore, there may be additional advantages in
offering skills training to patients who are identified at assessment as specifically
lacking in social skills.
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A prospective cohort study assessed the effectiveness of coping skills training in
2376 participants treated in community residential facilities (Forys et al. 2007).
Patients completed self-efficacy measures at baseline and at one year follow-up.
Findings were that alcohol-specific and ‘general approach coping’ was significantly
associated with less alcohol consumption and drug use at follow-up and ‘avoidance
coping’ was associated with more alcohol use and drug problems. Patients who had
greater participation in life skills and vocational training were more likely to rely on
alcohol-specific and general approach coping than on avoidance type coping at one
year follow up. Authors conclude that life skills and vocational training is an effective
way to promote healthy coping in patients with substance use disorders.
Ball et al (2007) have compared brief coping skills training, brief motivational
enhancement (each comprising 3 weekly sessions) and a waiting list control group
(who received delayed brief intervention of their choice in the 3-week post-treatment
phase of the study) in a clinical trial with non-dependent heavy drinkers (n = 98). The
authors chose to compare the coping skills and motivational enhancement
treatments because they considered them the two brief psychotherapies with the
most empirical support (Carroll et al. 2004). They found that all study participants
reduced their drinking. The control patients had more drinks per drinking day at all
study phases, i.e. before, during and after the treatment period. All three groups
reduced their drinking in the first phase (3-week pre-treatment monitoring). The lack
of difference between the two treatments could be attributed to an intensive preintervention monitoring that used a hand-held computer and included an extensive
baseline and daily assessment of alcohol consumption. It appears that this intensive
pre-intervention monitoring in the first 3 weeks of the study had a positive effect of its
own and may have rendered the three-session brief interventions of limited additional
benefit (Ball et al. 2007). This is in agreement with the findings of the project MATCH
study (Project MATCH Research Group 1997) suggesting that a cognitivebehavioural intervention, motivational enhancement and 12-step facilitation were
equally effective in reducing alcohol consumption. The results of the secondary
analysis of the data (Cutler and Fishbain 2005) showed that most of the effect also
occurred prior to the treatment intervention in all groups, including the drop-outs
(secondary analysis control group).
In addition, there is some evidence that teaching coping skills to spouses of alcohol
dependent patients may help improve the mental health and wellbeing of spouses
but may not have much effect on patients’ alcohol consumption. Hansson et al.
(2004) individual coping skills training (4 monthly 90-minutes sessions) and group
support (12 fortnightly 90-minute sessions of CBT focusing on communication skills,
coping with partner’s drinking and stress management) were found to be significantly
more effective than an ‘information only’ session of 60 minutes duration for spouses
(n=38) of alcohol-dependent individuals, with most improvement in spouses’ mental
health and wellbeing shown in the first year. There were no significant changes in the
second year and no differences between the treatment groups in the effect on
partners’ drinking levels. Of the 38 participants, 16 (2 of these had divorced) reported
that their partners had improved (drinking less or less often) by 24 months, and 22 (7
divorced) reported no reduction in drinking. In general, divorce was commoner in the
treatment groups than in the information only group. One of the drawbacks of this
study is the small sample size; however the follow-up rate was very high (38 out of
39 spouses participated in the 24 months follow up).
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Recommendation
6.4 Coping skills training is recommended for
people who appear to lack the relevant skills to
achieve and remain abstinent.
Strength of
Level of
recommendation evidence
A
Ib
Cue exposure
Cue exposure is a variant of cognitive behavioural intervention. It is based on the
associative learning principle (Gossop et al. 2002), which assumes that people,
places and events that regularly precede drinking (or drug-taking, for example)
become associated with the pleasant effects of taking the drink or drug, and
consumption becomes a conditioned response to these cues; the Pavlovian effect
(Pavlov 1927). Repeated exposure to these stimuli (such as the sight and smell of
alcohol) with instructions to resist craving and without subsequent reinforcement in a
laboratory/clinic setting, eventually leads to extinction of some of the conditioned
responses in real life situation, thereby reducing craving, expending time to first
relapse and reducing alcohol consumption. However, some conditioned responses
are difficult to extinguish and the effect is of a variable duration. There are earlier
reports of spontaneous and rapid re-instatement of previously extinguished
conditioned responses after a priming dose of alcohol (Drummond et al. 1990). Later
studies incorporated priming doses before patients attempted to resist drinking
(Sitharthan et al. 1997; Dawe et al. 2002). Negative effective states have been
shown to trigger relapse. Adding negative emotional cues to cue exposure therapy is
a useful approach, but it does not seem to add to effectiveness of this therapy
compared to standard CBT (Kavanagh et al. 2006). Using virtual reality environments
in cue exposure treatment may achieve more effective extinction of responses to
cues in rehabilitation settings. However, at present there are only a few small studies
investigating this approach in alcohol dependent patients (Kuntze et al. 2001; Lee et
al. 2007).
Cue exposure therapy usually consists of 6-12 sessions, each of 50-90min duration.
Sessions can be run on a daily basis or less frequently (Conklin and Tiffany 2002).
Cue Exposure: Meta-analyses
Cue exposure can be applied with a treatment goal of either abstinence or
moderation with moderately good results. In their meta-analysis of 9 studies
investigating effectiveness of cue exposure therapy, Conklin and Tiffany (2002) have
reported effect sizes ranging from 0.17 to 0.74, indicating variable effectiveness.
Authors suggested that evidence from animal studies should be better utilised to
increase effectiveness of cue exposure therapy in humans.
A number of studies have been published since the time of this meta-analysis,
showing that cue exposure therapy is effective in reducing alcohol consumption, but
not more effective than other cognitive-behavioural treatments. At present cue
exposure therapy is often used in conjunction with coping skills training to increase
the patient’s ability to deal with cravings if they arise, but the effectiveness of this
approach remains equivocal (Dawe et al. 2002, Kavanagh et al. 2006).
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Kadden’s (2001) status report and review of research priorities for NIAAA stated that:
“A number of gaps in knowledge and consequent research opportunities were
identified. Additional work on cue exposure is needed to identify the most potent cues
for drinking, and strategies for reducing the impact of drinking cues. … research
should identify its most effective elements and ways to sustain gains following
treatment. The mediating role assigned to coping skills in the cognitive-behavioral
model needs to be substantiated, and the effectiveness of various coping skills
components must be determined”. The gaps identified in this statement appear not to
be fully closed.
Cue Exposure: Randomised controlled trials
In a study examining the efficacy of cue exposure, Sitharthan et al. (1997) compared
cue exposure (with a priming dose) to standard cognitive behavioural therapy
consisting of goal setting, self-monitoring and behavioural and cognitive strategies to
moderate drinking. This was a randomised controlled trial that recruited patients
without severe alcohol dependence (n = 53). Both interventions were delivered in six
90-minute sessions. Cue exposure produced significantly greater reductions than
standard cognitive behavioural therapy in participant reports of drinking frequency
and consumption at six month follow-up, suggesting that cue exposure was an
important component of cognitive-behavioural approach.
Heather et al. (2000) conducted a randomised controlled trial comparing ModerationOriented Cue Exposure (MOCE) to Behavioural Self-control Training (BSCT).
Patients (N = 91) were randomised to receive either MOCE or BSCT and had weekly
sessions with trained therapists for 16 weeks. At six-month follow-up, both MOCE
and BSCT were effective in reducing alcohol consumption. From the results, it is
unclear whether MOCE and BSCT are both effective cognitive-behavioural
interventions, or whether treatment itself, regardless of type, is effective in reducing
consumption.
Using the same interventions, Dawe et al. (2002) compared the effectiveness of
moderation-oriented cue exposure (following a priming alcohol dose) with cognitivebehavioural intervention in a community sample of problem drinkers including those
with severe dependence. Participants (n = 100) were randomly assigned to one of
the two treatments and received a mean of 5.84 sessions. At eight-month follow-up,
there were significant decreases in alcohol consumption, severity of dependence,
impaired control, and alcohol-related problems in both groups compared to pretreatment levels. Both treatments were as effective in patients with a mild-tomoderate level of dependence as they were in those with severe dependence.
Negative effective states have been shown to increase the risk of relapse. One
recent study explored the effect of negative emotional states as an additional cue of
the cue exposure therapy. The study looked at the addition of two variants of cue
exposure to cognitive-behaviour therapy for alcohol misuse (Kavanagh et al. 2006).
This was conducted with 163 outpatients of treatment centres in Brisbane and
Sydney. The selection criteria included reports of an increased desire to drink when
dysphoric. Eight weekly 75-minute sessions were given to all participants. One group
received CBT and a moderation-oriented cue exposure and another received CBT
and an emotional cue exposure (with negative cue induction). The groups were
compared to CBT alone. The CBT sessions focused on developing skills in selfcontrol of alcohol use. Average improvements were highly significant across all
conditions (including reduction of alcohol consumption, related problems, alcohol
expectancies and depression and increase in self-efficacy), with an acceptable level
126
of maintenance of all effects at 12 months. However, treatment retention and effects
on alcohol consumption were progressively weaker in groups that received additional
cue exposure or emotional cue exposure compared to CBT alone. The authors
conclude that the results do not indicate that the addition of either versions of cue
exposure to CBT improves outcomes.
Cue exposure: Other study designs
As discussed in Shand et al. (2003), Rohsenow et al. (2001) compared the efficacy
of cue exposure, coping skills and communication skills. In a 2 x 2 design, the effect
of cue exposure (CE), in conjunction with coping skills (CS), (CE/CS) was compared
to a meditation-relaxation control, and communication skills training was compared to
an education control. These treatments were added to an intensive treatment
program for persons dependent on alcohol. Both CE/CS and communication skills
training appeared to be effective in decreasing number of heavy drinking days at six
and twelve month follow-ups. In the second six months after treatment, those who
received both CE/CS and communication skills training consumed a lower number of
drinks on drinking days than did those in the other treatment combinations. CE/CS
also resulted in reports of more use of coping skills during follow-up, and many of the
strategies taught in the CE/CS condition were associated with reduced drinking.
These results suggest that cue exposure, coping skills and communication skills are
promising elements of comprehensive alcohol treatment programs.
Loeber et al. (2006) tested cue exposure alone against standard CBT in a quasiexperimental study. Patients with a diagnosis of alcohol dependence (n = 63) were
recruited from an in-patient alcohol-detoxification facility and were sequentially
assigned to either treatment. Outcome measures were self-reports of craving and
self-efficacy before and after treatment; drinking behaviour was assessed at 3 and 6month follow-up. It was found that both treatments were associated with a reduction
of self-reported craving and an increase in self-reported measures of self-efficacy. A
significant time x treatment interaction indicated a greater increase in self-reported
measures of self-efficacy after cue exposure treatment. Measures of drinking
behaviour showed clearly that both treatments were efficacious. For example, in the
first 3-months period the number of days abstinent increased by 371 and 331 percent
in the cue exposure and CBT group respectively, decreasing to 309 and 285 percent
respectively at 6 months. The authors conclude that cue exposure and standard
cognitive-behavioural treatment are equally effective on drinking behaviour for
patients with a moderate severity of alcohol dependence.
Virtual reality programs have been increasingly used in behavioural science
research, including the field of substance abuse. The virtual reality cue reactivity
programs appear feasible in nicotine, cocaine and alcohol dependent individuals
(Kuntze et al. 2001; Bordnick et al. 2005; Bordnick et al. 2008; Cho et al. 2008). In a
small study Lee et al. (2007) used virtual reality to create two lifelike situations and
applied cue exposure therapy (CET) to 8 members of an Alcohol Anonymous group
for 8 x 30-minute sessions. The scenes were a Japanese-style pub and a Western
bar. This was a pre-test post-test design study with no comparison or control group.
Outcomes were measured by the Alcohol Urge Questionnaire; mean score on the
first session was 15.75 (SD = 10.91) which decreased to 11.50 (SD = 5.76) at the
final session. These initial reports support the use of virtual reality settings in cuebased treatment for alcohol problems.
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Cue exposure: summary
There is evidence to suggest that cue exposure is at least as effective as standard
CBT.
Elements of self-control skills training and other supporting interventions are often
included as part of cue exposure therapy. However, it should be noted that when
standard CBT and cue exposure treatments are combined, the additive effect may be
masked. This may occur due to excessive complexity of the resulting intervention
(i.e. more may not necessarily be better) (Kavanagh et al. 2006) and some degree of
overlap in the content of these therapies (Dawe et al. 2002).
It has been suggested that cue exposure may be particularly effective in patients with
stronger cue reactivity (Heinz et al. 2009). Imaging studies indicate that such
heightened sensitivity of neuronal circuits to alcohol related cues in some patients
may be partly genetically influenced (Heinz et al. 2005). Identifying such patients may
provide opportunities for targeted use of cue exposure treatment and enhance
treatment effectiveness in this subgroup of patients in future. Ways to increase the
effectiveness of cue exposure therapy are continued to be explored (Taylor et al.
2009).
Based on studies of cue exposure in treatment of post-traumatic stress disorder
(PTSD) and phobias, disruption of re-consolidation of memories related to drug cues
using pharmacological agents, such as propranolol or glucocorticosteriods, appears
a feasible treatment strategy but it has not yet been tested in patients with alcohol
problems (Taylor et al. 2009).
Recommendation
6.5 Cue exposure in conjunction with other
psychosocial interventions can be an effective
intervention for treating alcohol dependence.
Strength of
Level of
recommendation evidence
A
Ib
Behavioural couples therapy (BCT)
Behavioural couples therapy is based on an assumption that problematic alcohol use
and relationship functioning are reciprocal. Excessive alcohol use causes
deterioration of relationships in a family unit which often results in further increase in
drinking. However, functional relationships can help patients to achieve abstinence or
controlled drinking, and reduce a risk of relapse (O’Farrell and Fals-Stewart 2000;
O’Farrell et al. 1993). BCT has a long standing evidence of effectiveness in reducing
alcohol consumption and improving marital and partner relationship functioning when
compared to treatments that do not include spouses (Epstein and McCrady 1998;
O’Farrell and Fals-Stewart 2000).
BCT: Meta-analyses
Evidence from a meta-analysis presented by Powers et al. (2008) further supports
the conclusions of the narrative reviews quoted above and indicates that BCT is an
effective treatment. Their meta-analysis of 12 randomised controlled trials (total of
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754 participants; including 8 trials of alcohol use disorders, published in 1985-2008)
concludes that there is a clear overall advantage of including BCT compared to
individual-based treatments (Cohen’s effect size, d = 0.54). Immediately posttreatment BCT showed an advantage only in the relationship satisfaction measure,
however, at 3 months the advantage was evident across all 3 outcome domains:
(frequency of use, d = 0.45; consequences of use, d = 0.50; and relationship
satisfaction, d = 0.51). The difference was maintained for at least a year. BCT was
more effective than CBT with the focus on relationships (d = 0.44). There was no
dose-response effect (i.e. the number of consecutive BCT sessions did not influence
the outcome). The authors therefore conclude that behavioural couples therapy is
more effective than individual treatment. It appears that relationship improvement
evident immediately post-treatment later lead s to reduction of patient’s drinking and
its consequences. Compared to individual-based treatment BCT produces better
child adjustment, reduced interpersonal violence and higher cost-effectiveness
(Powers et al. 2008). However, BCT is a more costly intervention, given that
treatment sessions lasted almost twice as long as individual CBT sessions (Vedel et
al. 2008). It suggests that BCT is an option that should be explored if available.
Recommendation
6.6 Behavioural couples’ therapy, which focuses
on drinking behaviour as the problem, can
improve drinking outcomes following treatment
and should be delivered by an appropriately
trained clinician.
Strength of
Level of
recommendation evidence
A
Ia
CBT for adolescents
Thush et al. (2007) have investigated the effectiveness of a targeted intervention
program designed to change cognitive determinants of drinking and thus reduce
hazardous alcohol consumption in at-risk adolescents (n = 107). The program
consisted of 7 weekly sessions that combined intervention methods which have been
proven effective in reducing drinking in young adults, such as an alcohol social and
sexual expectancy challenge, cognitive behavioral skill training (including drink
refusal skills) and brief motivational feedback. The outcomes in the treatment group
were compared to those of the control (information only) group. Results showed that
the intervention was effective in changing several of the targeted cognitive
determinants, such as a significantly increased perception of risk factors for
developing alcohol problems and a significant decrease of positive expectancies for
high dose of alcohol in the experimental group compared to control. However,
despite these positive changes, the experimental group did not show a significant
decrease or difference in decrease in drinking at post-test or at 6 and 12 months
follow up, compared with controls.
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CBT for treatment of insomnia
Insomnia has a high prevalence in alcohol dependent patients (36-67%) compared to
general population (17-30%) (Brower et al. 2001). Insomnia during early recovery
has been linked to relapse (Foster and Peters 1999; Brower et al. 2001).
One study has investigated the effect of CBT for insomnia on relapse to heavy
drinking in a group of outpatients with a diagnosis of alcohol dependence who had at
least one month of continuous abstinence and were suffering from insomnia (N=60)
(Currie et al. 2004). This trial tested 5 sessions of CBT against a self-help manual
with telephone support for the treatment of insomnia or a waiting list control
condition. The quality of sleep improved in patients in both treatment conditions.
Patients in the CBT group had better sleep outcomes than those in the self-group or
placebo. Similar proportion of patients relapsed to drinking in all three groups. It
should be noted that about 30% of participants had more than 12 months of
abstinence prior to the study. The results indicate that the shorter period of
abstinence pre-treatment predicted relapse at post-treatment and 3 and 6 months
follow up. The conclusions of this preliminary study were that CBT assisted to reduce
the insomnia but did not have an effect in reducing relapses to drinking alcohol. More
intensive sleep interventions are needed for patients in early recovery.
It should be noted that while it would be expected that CBT works through increasing
cognitive and behavioural coping skills, a review of ten studies that examined the
mechanism of action of CBT found it difficult to establish why CBT is an effective
treatment for alcohol dependence (Morgenstern and Longabaugh 2000).
Other Counselling Strategies
Contingency management is based on operant conditioning theory that assumes that
behaviour is controlled and shaped by its consequences. It is a strategy that uses
positive reinforcement to improve treatment outcomes by providing incentives to
encourage behavioural changes. Withholding incentives when desirable behaviour is
not maintained (that is, negative reinforcement) may also be used.
There is a strong evidence that contingency management is an effective strategy in
treatment substance use disorders, particularly, opioids , tobacco, and polysubstance
use (Griffith et al. 2000; Lussier et al. 2006; Prendergast et al. 2006). Its use in
treatment of alcohol use disorders has been studied during the 1960s, 1970s, and
1980s. It has been shown to be effective in reinforcing abstinence and improving
medication compliance (with disulfiram) and treatment attendance (Higgins and Petry
1999; Petry et al. 2000a). Most of the recent studies focus on the treatment of illicit
drug problems. However, the research has not been routinely translated into clinical
practice either in the USA or UK (Petry et al. 2000b) or in Australia (Cameron and
Ritter 2007).
This is largely due to perceived high costs of provision of such interventions,
including the costs of reinforcers and additional staff involvement (Helmus et al.
2003). However, implementing contingency management for alcohol use disorders
has additional difficulties.
Unlike with most other drugs, it is difficult to reliably detect recent alcohol use as
neither blood nor breath tests can detect alcohol use that occurred more than 12
hours previously (Kadden 2001). Providing reinforcement on the basis of other
130
factors, such as counselling session attendance, in addition to the negative
breathalyzer test may be an effective strategy (Helmus et al. 2003).
A number of other approaches are being increasingly used in counselling settings,
including for patients with alcohol problems. Examples include: solution-focused
approaches (such as solution-focus brief therapy) mindfulness-based stress
reduction, psychodynamic, narrative therapy.
Solution focused therapy focuses on patient’s strengths and successes rather than
weaknesses and is aimed at helping the patient to look for exceptions to the problem
patterns and to find new solutions.
Mindfulness-based stress-reduction is an approach that utilises a specific meditative
technique that focuses on increasing patient’s awareness of their feelings, emotions
and thoughts by bringing conscious attention to what they experience at the present
moment.
Psychodynamic therapy focuses not only on the present problem but also on the
patient’s life history and encourages them to look for unconscious drivers for their
motivation and behaviour patterns. Interpersonal therapy is a variation of this
approach.
Narrative therapy encourages patients to talk about their problems in terms of
personal life stories that define the meaning of their lives and relationships, assess
the impact of these on the current behaviour and assists patients in the process of
“re-authoring” or re-writing these stories in a way that would help overcome
presenting problems.
These counselling approaches are not supported by a strong evidence base,
particularly in the field of treatment of alcohol use disorders, and so are not yet widely
recommended.
Relapse Prevention Strategies
Relapse is a common problem in alcohol treatment, with approximately 60% of
treated clients relapsing to problematic drinking within the first 12 months (Connors et
al. 1996). It has long been observed that specific situations or mood states are
associated with relapse, including negative emotional states (e.g. frustration, anger,
anxiety, depression or anger); interpersonal conflict (e.g. relationships with partner,
work colleagues, friends); and direct or indirect social pressure to drink (Marlatt and
Gordon 1985).
Relapse prevention is not so much a specific intervention but rather a set of
strategies that aim to help the client maintain treatment gains (Jarvis et al. 2005).
These include psychosocial interventions described above such as skills training and
cognitive restructuring that deal with immediate triggers of relapse and more global
strategies that address long-term factors of relapse such as lifestyle balancing and
after care (Larimer et al. 1999) (see also Chapter 11).
Relapse prevention may also incorporate medications for reducing alcohol use (e.g.
naltrexone, disulfiram, acamprosate), or for addressing concomitant conditions linked
to relapse (e.g. anxiety, depression) (see Chapters 7 and 10 respectively).
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All moderately and severely alcohol dependent patients should be offered the
opportunity to learn relapse-prevention strategies. These are best discussed after
acute withdrawal symptoms have subsided. Relapse prevention addresses itself to
the maintenance of change, and to the development of self-efficacy and coping skills
(Edwards et al. 2003).
Recommendation
6.7 Psychosocial relapse prevention strategies
are recommended for use with all moderately to
severely alcohol-dependent patients.
6.8 Psychosocial relapse prevention strategies
are best delivered as soon as acute withdrawal
symptoms have subsided.
Strength of
Level of
recommendation evidence
A
Ib
C
III
Residential Rehabilitation Programs
Residential rehabilitation programs (sometimes called therapeutic communities) are
usually long-term programs where people live and work in a community of other
substance users, ex-users and professional staff. Programs can last anywhere
between 1 and 24 months (or more). The aim of residential rehabilitation programs is
to help people develop the skills and attitudes to make long-term changes towards an
alcohol- and drug-free lifestyle. Programs usually include activities such as
employment, education and skills training, life skills training (such as budgeting and
cooking), counselling, group work, relapse prevention, and a ‘re-entry’ phase where
people are helped return to their community.
The effectiveness data are sparse. The results of meta-analysis by Smith et al.
(2006) of seven studies investigating the effectiveness of therapeutic communities for
substance related disorders, including alcohol indicate that there is little evidence that
residential rehabilitation programs are more effective than other residential
treatments (such as community residence) in terms of treatment completion or drug
use related outcomes or that one type of therapeutic community is better than
another. Prison based therapeutic communities are effective in preventing reincarceration, criminal activity and alcohol and drug offences in the 12 month period
after release from prison. No comparison could be made with other treatment
modalities. The authors concluded that the use therapeutic communities for
treatment of alcohol and drug use disorders is not based on sound evidence.
Programs with directed treatment orientation are more effective that those with
undifferentiated approach (e.g. safety and security oriented, mostly shelter and food
provision with limited counselling and active treatment) (Moos et al. 1999). Program
completion and a longer period of care are associated with better outcomes at one
year (Moos et al. 1999). Some programs are based on 12-step Alcoholics
Anonymous (AA) approaches (Forys et al. 2007; Polcin and Henderson 2008).
An extended period of abstinence can be beneficial in reversing cognitive and
physical harm arising from chronic heavy alcohol use.
132
Residential rehabilitation programs can be effective for people needing structured
long-term support, and are more attractive to those with moderate to severe
dependence, and limited social supports.
Recommendation
6.9 Residential rehabilitation programs can be
effective for patients with moderate to severe
dependence who need structured residential
treatment settings.
Strength of
Level of
recommendation evidence
D
IV
Summary
In summary, there is strong support for the efficacy of motivational interviewing as a
treatment intervention. There is also sufficient support for the efficacy of cognitivebehavioural treatment approaches, such as behavioural self-management, coping
skills training, cue exposure and behavioural couples therapy, although there are
variations in effectiveness across studies, settings and providers. However, there is
less evidence for contingency management and residential rehabilitation programs
and no sufficient evidence for solution-focused approaches, mindfulness-based
stress reduction, psychodynamic, narrative therapy or other counselling techniques
for use in treatment of alcohol problems at his stage. There is little evidence that
patient-treatment matching is effective as a technique to reduce alcohol
consumption.
References
Ambrogne, JA 2002, Reduced-risk drinking as a treatment goal: what clinicians need
to know. Subst Abuse Treat 22(1): 45-53.
Anton, RF, O'Malley SS, Ciraulo DA et al. 2006, Combined pharmacotherapies and
behavioral interventions for alcohol dependence: the COMBINE study: a
randomized controlled trial. JAMA 295(17): 2003-2017.
Baker, A, Bucci S, Kay-Lambkin F et al. 2007. Cognitive behaviour therapy for people
with co-existing mental health and drug and alcohol problems. In: A. Baker
and R. Velleman (eds) Clinical handbook of co-existing mental health and
drug and alcohol problems. London: Routledge.
Ball, SA, Todd M, Tennen H et al. 2007, Brief motivational enhancement and coping
skills interventions for heavy drinking. Addict Behav 32(6): 1105-1118.
Bandura, A 1969, Principles of behaviour modification. New York: Holt, Reinhart &
Winston.
Bandura, A 1986, Social Foundations of Thought and Action: a Social Cognitive
Theory. Englewood Cliffs, New Jersey: Prentice Hall.
Bandura, A 1997, Self-efficacy: The exercise of control. New York: Freeman.
133
Beckham, N and N Beckham 2007, Motivational interviewing with hazardous
drinkers. J Amer Acad Nurse Pract 19(2): 103-110.
Berglund, M, Thelander S, Salaspuro M et al. 2003, Treatment of alcohol abuse: an
evidence-based review. Alcohol Clin Exp Res 27(10): 1645-56.
Bergmark, A 2008, On treatment mechanisms; what can we learn from the
COMBINE study? Addiction 103(5): 703-705.
Bien, T, W Miller and J Boroughs 1993, Motivational interviewing with alcohol
outpatients. Behav Cogn Psychother: 347-356.
Bien, T.H., WR Miller and JS Tonigan 1993, Brief interventions for alcohol
problems:a review. Addiction, 88, 315-336.
Booth, PG, B Dale and J Ansari 1984, Problem drinkers' goal choice and treatment
outcome: a preliminary study. Addict Behav 9(4): 357-64.
Booth, PG, Dale B, Slade PD et al. 1992, A follow-up study of problem drinkers
offered a goal choice option. J Stud Alcohol 53(6): 594-600.
Bordnick, PS, Graap KM, Copp HL et al. 2005, Virtual reality cue reactivity
assessment in cigarette smokers. Cyberpsychol Behav 8(5): 487-92.
Bordnick, PS, Traylor A, Copp HL et al. 2008, Assessing reactivity to virtual reality
alcohol based cues. Addict Behav. 33(6): 743-56.
Borsari, B and KB Carey 2000, Effects of a brief motivational intervention with college
student drinkers. J Consult Clin Psychol 68(4): 728-733.
Bottlender, M, J Kohler and M Soyka 2006, The Effectiveness of Psychosocial
Treatment Approaches for Alcohol Dependence - A Review. Fortschr Neurol
Psychiatr 74(1): 19-31.
Brower, KJ, Aldrich MS, Robinson EA et al. 2001, Insomnia, Self-Medication, and
Relapse to Alcoholism. Am J Psychiatry 158: 399–404.
Brown, J and W Miller 1993, Impact of motivational interviewing on participation &
outcome in residential and alcoholism treatment. Psychol Addict Behav 7(4):
211-218.
Buhringer, G and TIM Pfeiffer-Gerschel 2008, [Commentary] COMBINE and MATCH:
the final blow for large-scale black box randomized controlled trials. Addiction
103(5): 708-710.
Burns, L and M Teesson 2002, Alcohol use disorders comorbid with anxiety,
depression and drug use disorders: Findings from the Australian National
Survey of Mental Health and Well Being. Drug Alcohol Depend 68 (3): 299307.
Cameron, J and A Ritter 2007, Contingency management: perspectives of Australian
service providers. Drug Alcohol Rev 26(2): 183-9.
134
Carroll, K, S Ball and S Martino 2004, Cognitive, behavioral and motivational
therapies. In: M Galanter and H Kleber (eds) Textbook of Substance Abuse
Treatment. Washington DC, American Psychiatric Association Press.
Carroll, KM and LS Onken 2005, Behavioural therapies for drug abuse. Am J
Psychiatry 162:1452-1460.
Cho, S, Ku J, Park J et al. 2008, Development and verification of an alcohol cravinginduction tool using virtual reality: craving characteristics in social pressure
situation. Cyberpsychol Behav 11(3): 302-9.
Conklin, C and S Tiffany 2002, Applying extinction research and theory to cue
exposure addiction treatments. Addiction 97: 155-167.
Connors, G, S Maisto and W Zywiak 1996, Understanding relapse in the broader
context of post-treatment functioning. Addiction 91(Suppl): S173-S190.
Currie, SR, Clark S, Hodgins DC et al. 2004, Randomized controlled trial of brief
cognitive-behavioural interventions for insomnia in recovering alcoholics.
Addiction 99(9): 1121-1132.
Cutler, RB and DA Fishbain 2005, Are alcoholism treatments effective? The project
MATCH data. BMC Public Health 14 (5): 75.
Dawe, S, Rees VW, Mattick R et al. 2002, Efficacy of Moderation-Oriented Cue
Exposure for Problem Drinkers: A Randomized Controlled Trial. J Consult
Clin Psychol 70(4): 1045-1050.
Dobson, KS 2000, (Ed) Handbook of cognitive-behavioral therapies. Second Edition.
New York: Guilford Press.
Drummond, DC, T Cooper and SP Glautier 1990, Conditioned learning in alcohol
dependence: implications for cue exposure treatment. Br J Addict 85(6): 72543.
Edwards, G, EJ Marshall and CCH Cook 2003, The treatment of drinking problems:
A guide for the helping professions. Cambridge: Cambridge University Press.
Epstein, EE and BS McCrady 1998, Behavioral couples treatment of alcohol and
drug use disorders: current status and innovations. Clin Psychol Rev 18(6):
689-711.
Ferrell, WL and JP Galassi 1981, Assertion training and human relations training in
the treatment of chronic alcoholics. Int J Addict 16(5): 959-68.
Forys, K, J McKellar and R Moos 2007, Participation in specific treatment
components predicts alcohol-specific and general coping skills. Addict Behav
32(8): 1669-1680.
Foster, JH and TJ Peters 1999, Impaired sleep in alcohol misusers and dependent
alcoholics and the impact upon outcome. Alcohol Clin Exp Res. 23(6): 104451.
135
Gastfriend, DR, Garbutt JC, Pettinati HM et al. 2007, Reduction in heavy drinking as
a treatment outcome in alcohol dependence. J Subst Abuse Treat 33(1): 7180.
Gentilello, L, Rivara F, Donovan D et al. 1999, Alcohol interventions in a trauma
center as a means of reducing the risk of injury recurrence. Ann Surg 230(4):
473-483.
Gossop, M, Keaney F, Stewart D, et al. 2002, A Short Alcohol Withdrawal Scale
(SAWS): development and psychometric properties. Addict Biol 7(1): 37-43.
Griffith, JD, Rowan-Szal GA, Roark RR et al. 2000, Contingency management in
outpatient methadone treatment: a meta-analysis. Drug Alcohol Depend 58(12): 55-66.
Handmaker, NS, WR Miller and M Manicke 1999, Findings of a pilot study of
motivational interviewing with pregnant drinkers. J Stud Alcohol 60(2): 285287.
Hansson, H, Zetterlind U, Aberg-Orbeck K et al. 2004, Two-year outcome of coping
skills training, group support and information for spouses of alcoholics: a
randomized controlled trial. Alcohol Alcohol 39(2): 135-140.
Heather, N 1995, Brief intervention strategies. In: Hester, R and WR Miller (eds),
Handbook of Alcoholism Treatment Approaches. Boston: Allyn and Bacon.
Heather, N, Brodie J, Wale S et al. 2000, A randomized controlled trial of ModerationOriented Cue Exposure. J Stud Alcohol 61(4): 561-570.
Heather, N, Rollnick S, Bell A et al. 1996, Effects of brief counselling among male
heavy drinkers identified on general hospital wards. Drug Alcohol Rev 15(1):
29-38.
Heinz, A, Beck A, Grüsser SM et al. 2009, Identifying the neural circuitry of alcohol
craving and relapse vulnerability. Addict Biol 14(1): 108-18.
Heinz, A, Braus DF, Smolka MN et al. 2005, Amygdala-prefrontal coupling depends
on a genetic variation of the serotonin transporter. Nat Neurosci 8:20–21.
Helmus, TC, Saules KK, Schoener EP et al. 2003, Reinforcement of counseling
attendance and alcohol abstinence in a community-based dual-diagnosis
treatment program: a feasibility study. Psychol Addict Behav 17(3): 249-51.
Hettema, J, Steele J and R Miller 2005, Motivational interviewing. Ann Rev Clin
Psychol 1: 91-111.
Higgins, ST and NM Petry 1999, Contingency management. Incentives for sobriety.
Alcohol Res Health 23(2): 122-7.
Hodgins, DC, Leigh G, Milne R et al. 1997, Drinking goal selection in behavioral selfmanagement treatment of chronic alcoholics. Addict Behav 22(2): 247-55.
136
Jarvis, T, Tebbutt J, Mattick RP et al. 2005, Treatment approaches for alcohol and
drug dependence: An introductory guide. Second edition. Chichester: John
Wiley & Sons.
John, U, Veltrup C, Driessen M et al. 2003, Motivational intervention: an individual
counselling vs a group treatment approach for alcohol-dependent in-patients.
Alcohol Alcohol 38(3): 263-269.
Kadden, R 1994, Cognitive-behavioral approaches to alcoholism treatment. Alcohol
Health Res World 18(4): 279-286.
Kadden, RM 1996, Project MATCH: Treatment Main Effects and Matching Results.
Alcoholism: Clin Exper Res 20(s8): 196a-197a.
Kadden, RM 2001, Behavioral and cognitive-behavioral treatments for alcoholism:
research opportunities. Addict Behav 26(4): 489-507.
Kavanagh, DJ, Sitharthan G, Young RM et al. 2006, Addition of cue exposure to
cognitive-behaviour therapy for alcohol misuse: a randomized trial with
dysphoric drinkers. Addiction 101(8): 1106-1116.
Kelly, AB, WK Halford and RM Young 2000, Maritally distressed women with alcohol
problems: the impact of a short-term alcohol-focused intervention on drinking
behaviour and marital satisfaction. Addiction 95(10): 1537-1549.
Kuntze, MF, Stoermer R, Mager R et al. 2001, Immersive virtual environments in cue
exposure. Cyberpsychol Behav. 4(4): 497-501.
Larimer, ME, RS Palmer and GA Marlatt 1999, Relapse prevention. An overview of
Marlatt's cognitive-behavioral model. Alcohol Res Health 23(2): 151-60.
Lee, JH, Kwon H, Choi J et al. 2007, Cue-exposure therapy to decrease alcohol
craving in virtual environment. Cyberpsychol Behav 10(5): 617-623.
Loeber, S, B Croissant, A Heinz et al. 2006, Cue exposure in the treatment of alcohol
dependence: Effects on drinking outcome, craving and self-efficacy. Br J Clin
Psychol 45: 515-529.
Longabaugh, R, Woolard RE, Nirenberg TD et al. 2001, Evaluating the effects of a
brief motivational intervention for injured drinkers in the emergency
department. J Stud Alcohol 62(6): 806-816.
Longabaugh, R and J Morgenstern 1999, Cognitive-behavioural coping skills therapy
for alcohol dependence. Current status and future directions. Alcohol Res
Health 23(2): 78-85.
Lussier, JP, Heil SH, Mongeon JA et al. 2006, A meta-analysis of voucher-based
reinforcement therapy for substance use disorders. Addiction. 101(2):192203.
Maisto, S, Conigliaro J, McNeil M et al. 2001, Effects of two types of brief intervention
and readiness to change on alcohol use in hazardous drinkers. J Stud Alcohol
62(5): 605-614.
137
Marlatt, G, Baer J, Kivlahan D et al. 1998, Screening and brief intervention for highrisk college student drinkers: results from a 2-year follow-up assessment. J
Consult Clin Psychol 66(4): 604-615.
Marlatt, G. and J Gordon 1985, Relapse Prevention: Maintenance Strategies in the
Treatment of Addictive Behaviors. New York: The Guildford Press.
Marsh, A. and A Dale 2006, Addiction counseling: Content and process. Victoria: IP
Communications.
Mattick, R and T Jarvis 1993, An outline for the management of alcohol problems:
Quality Assurance in the Treatment of Drug Dependence Project. Monograph
no. 20. National Drug Strategy, Canberra: Commonwealth Department of
Human Services and Health,.
Mattson, M.E, Del Boca F, Carroll KM et al. 1998, Compliance with Treatment and
Follow-up Protocols in Project MATCH: Predictors and Relationship to
Outcome. Alcohol Clin Exper Res 22 (6), 1328-1339.
Miller, W, R Sovereign and B Krege 1988, Motivational interviewing with problem
drinkers: 2. The drinkers' checkup as a preventive intervention. Behav
Psychother 16(4): 251-268.
Miller, WR and AC Page 1991, Warm Turkey: Other routes to abstinence. J Subst
Abuse Treat 8(4): 227-232.
Miller, WR, Leckman AL, Delaney HD et al. 1992, Long-term follow-up of behavioral
self-control training. J Stud Alcohol. 53(3): 249-61.
Miller, W, R Benefield and J Tonigan 1993a, Enhancing motivation for change in
problem drinking: A controlled comparison of two therapist styles. J Consult
Clin Psychol 61: 455-461.
Miller, WR, R Benefield and J Tonigan 1993b, Enhancing motivation for change in
problem drinking: A controlled comparison of two therapist styles. J Consult
Clin Psychol logy 61(3): 455-461.
Miller, W, Brown J, Simpson T et al. 1995, What works? A methodological analysis of
the alcohol treatment outcome literature. In: Hester, R and WR Miller (eds)
Handbook of Alcoholism Treatment Approaches: Effective Alternatives.
Boston: Allyn & Bacon.
Miller, W. and K Mount 2001, A small study of training in motivational interviewing:
Does one workshop change clinician and client behaviour? Behav Cogn
Psychother 29: 457-471.
Miller, W and S Rollnick 2002, Motivational interviewing: preparing people for
change. New York: Guilford Press.
Miller, WR and PL Wilbourne 2002, Mesa Grande: a methodological analysis of
clinical trials of treatments for alcohol use disorders. Addiction 97(3): 265-277.
138
Miller, WR, Locastro JS, Longabaugh R et al. 2005, When worlds collide: blending
the divergent traditions of pharmacotherapy and-psychotherapy outcome
research. J Stud Alcohol Suppl(15): 17-23; discussion 16-17.
Monti, P, S Gulliver and M Myers 1994, Social skills training for alcoholics:
assessment and treatment. Alcohol Alcohol 29(6): 949-964.
Monti, PM, Barnett NP, Colby SM et al. 2007, Motivational interviewing versus
feedback only in emergency care for young adult problem drinking. Addiction
102(8): 1234-1243.
Moos, RH, Moos BS, Andrassy JM 1999, Outcomes of four treatment approaches in
community residential programs for patients with substance use disorders.
Psychiatr Serv 50(12): 1577-83.
Morgenstern, J and R Longabaugh 2000, Cognitive-behavioral treatment for alcohol
dependence: a review of evidence for its hypothesized mechanisms of action.
Addiction 95(10): 1475-90.
Murphy, JG, Duchnick JJ, Vuchinich RE et al. 2001, Relative efficacy of a brief
motivational intervention for college student drinkers. Psychol Addict Behav
15(4): 373-379.
NSW Department of Health 2008, NSW Health Drug and Alcohol Psychosocial
Interventions Professional Practice Guidelines. Sydney: NSW Department of
Health.
O’Farrell, TJ, Choquette KA, Cutter HSG et al. 1993, Behavioral marital therapy with
and without additional couples relapse prevention sessions for alcoholics and
their wives. J Stud Alcohol 54: 652-666.
O’Farrell, T and W Fals-Stewart 2000,Behavioral couples therapy for alcoholism and
drug abuse. J Subst Abuse Treat 18: 51-54.
Orford, J, Hodgson R, Copello A et al. 2006, The clients’ perspective on change
during treatment for an alcohol problem: qualitative analysis of follow-up
interviews in the UK Alcohol Treatment Trial. Addiction 101: 60-68.
Pavlov, IP 1927, Conditioned reflexes; an investigation of the physiological activity of
the cerebral cortex. Translated and edited by GV Anrep. London: Oxford
University Press, Humphrey Milford.
Petry, NM, Martin B, Cooney JL et al. 2000, Give them prizes, and they will come:
contingency management for treatment of alcohol dependence. J Consult Clin
Psychol 68(2): 250-7
Petry, NM. 2000b, A comprehensive guide to the application of contingency
management procedures in clinical settings. Drug Alcohol Depend 58(1-2): 925.
Polcin, DL and DM Henderson 2008, A clean and sober place to live: philosophy,
structure, and purported therapeutic factors in sober living houses. J
Psychoactive Drugs 40(2): 153-9.
139
Powers, MB, E Vedel and PMG Emmelkamp 2008, Behavioral couples therapy
(BCT) for alcohol and drug use disorders: A meta-analysis. Clin Psychol Rev
28(6): 952-962.
Prendergast, M, Podus D, Finney J et al. 2006, Contingency management for
treatment of substance use disorders: a meta-analysis. Addiction. 101(11):
1546-60.
Project MATCH Research Group 1997, Matching alcoholism treatments to client
heterogeneity: Project MATCH posttreatment drinking outcomes. J Stud
Alcohol 58(1): 7-29.
Project MATCH Research Group 1998a, Matching alcoholism treatments to client
heterogeneity: treatment main effects and matching effects on drinking during
treatment. J Stud Alcohol 59(6):631-9.
Project MATCH Research Group 1998b, Matching alcoholism treatments to client
heterogeneity: Project MATCH three-year drinking outcomes. Alcohol Clin
Exp Res. 22(6): 1300-11.
Raistrick, D, N Heather and C Godfrey 2006, Review of the effectiveness of
treatment for alcohol problems. London, UK, National Treatment Agency for
Drug Abuse.
Raistrick, D and G Tober 2004, Psychosocial interventions. Psychiatry 3(1): 36-39.
Rohsenow, DJ, Monti PM, Rubonis AV et al. 2001, Cue exposure with coping skills
training and communication skills training for alcohol dependence: 6- and 12month outcomes. Addiction 96(8): 1161-1174.
Rotunda, R, D Scherer and P Imm 1995, Family systems and alchol misuse:
research on the effects of alcoholism on family functioning and effective
family interventions. Prof Psychol Res Pract 26(1): 95-104.
Sanchez-Craig, M, K Spivak and R Davila 1991, Superior outcome of females over
males after brief treatment for the reduction of heavy drinking: replication and
report of therapist effects. Br J Addict 86(7): 867-876.
Sellman, D, Sullivan P, Dore G et al. 2001, A Randomized Controlled Trial of
Motivational Enhancement Therapy (MET) for Mild to Moderate Alcohol
Dependence. J Stud Alcohol 62: 389-396.
Shakeshaft, AP, Bowman JA, Burrows S et al. 2002, Community-based alcohol
counselling: a randomized clinical trial. Addiction 97(11): 1449-1463.
Shand, F, J Gates and J Fawcett 2003, The treatment of alcohol problems: A review
of the evidence. Canberra: Australian Commonwealth Department of Health
and Ageing.
Sim, K, KP Gwee and A Bateman 2005, Case Formulation in Psychotherapy:
Revitalizing Its Usefulness as a Clinical Tool. Acad Psychiatry 29: 289-292.
140
Sitharthan, T and DJ Kavanagah 1990, Role of self-efficacy in predicting outcomes
from a programme for controlled drinking. Drug Alcohol Depend 27: 87–94.
Sitharthan, T, Sitharthan G, Hough MJ et al. 1997, Cue exposure in moderation
drinking: A comparison with cognitive-behavioural therapy. J Consult Clin
Psychol 65: 878-882.
Smith, AJ, Hodgson RJ, Bridgeman K et al. 2003, A randomized controlled trial of a
brief intervention after alcohol-related facial injury. Addiction 98(1): 43-52.
Smith, LA, S Gates and D Foxcroft 2006, Therapeutic communities for substance
related disorder. Cochrane Database Syst Rev. 25(1):CD005338.
Sobell, MB and LC Sobell 2000, Stepped care as a heuristic approach to the
treatment of alcohol problems’. J Consul Clin Psychol 68(4): 573–579.
Taylor JR, Olausson P, Quinn JJ et al. 2009, Targeting extinction and reconsolidation
mechanisms to combat the impact of drug cues on addiction.
Neuropharmacol 56 (Suppl 1): 186-95.
Thush, C, Wiers RW, Theunissen N et al. 2007, A randomized clinical trial of a
targeted intervention to moderate alcohol use and alcohol-related problems in
at-risk adolescents. Pharmacol Biochem Behav 86(2): 368-376.
UKATT Research Team 2005a, Effectiveness of treatment for alcohol problems:
findings of the randomised UK alcohol treatment trial (UKATT) BMJ 331: 331541.
UKATT Research Team 2005b, Cost effectiveness of treatment for alcohol problems:
findings of the randomised UK alcohol treatment trial (UKATT). BMJ
331(7516): 544-548.
Vasilaki, EI, SG Hosier and WM Cox 2006, The efficacy of motivational interviewing
as a brief intervention for excessive drinking: a meta-analytic review. Alcohol
Alcohol 41(3): 328-335.
Vedel, E, Emmelkamp PM and GM Schippers 2008, Individual cognitive-behavioral
therapy and behavioral couples therapy in alcohol use disorder: a
comparative evaluation in community-based addiction treatment centers.
Psychother Psychosom 77(5): 280-8.
Walters, GD 2000, Behavioral Self-Control Training for Problem Drinkers:A MetaAnalysis of Randomized Control Studies. Behav Ther 31: 135—149.
Zweben, A and A Zuckoff 2002, Motivational interviewing and treatment adherence.
In: WR Miller and S Rollnick (eds) Motivational interviewing: preparing people
for change.New York: The Guilford Press.
141
Chapter 7 Pharmacotherapies for alcohol dependence
Overview of Pharmacotherapies
Three medications: acamprosate, naltrexone and disulfiram have been approved for
use as part of a comprehensive treatment plan for alcohol dependence.
Acamprosate and naltrexone have been shown to improve treatment outcomes when
combined with a psychosocial intervention (e.g. Mann et al. 2004; Bauza et al. 2004).
For patients who are motivated to take the medication, both are potential tools for
reducing the core symptoms of alcohol dependence.
The evidence for disulfiram is weaker, but the drug remains an option for relapse
prevention in certain circumstances, and can be effective as part of a comprehensive
treatment approach (e.g. Laaksonen et al. 2008).
Pharmacotherapy should be considered for all alcohol-dependent patients following
management of withdrawal. They are best used in association with psychosocial
supports as part of an after-care treatment plan.
Overview of Pharmacotherapies: Reviews and meta-analyses
An extensive overview of the clinical data on pharmacotherapy for alcohol
dependence was published by Mann et al. (2004). This review concentrates on
naltrexone, acamprosate and disulfiram but also mentions SSRIs, tricyclic
antidepressants, benzodiazepines and all other drugs for which data were available
at the time, with results of all the published clinical trials. Acamprosate produced the
most beneficial effects in maintaining abstinence, having been evaluated in 16
controlled clinical trials with 4500 patients. Naltrexone appeared to have different
effects and proved to be useful in reducing craving (i.e. in reducing relapses rather
than maintaining abstinence). The conclusions reached were that pharmacotherapy
should be considered for all alcohol-dependent patients, and be used in association
with psychosocial support.
A systematic review and analysis of 33 studies was carried out by Bouza et al (2004).
The number of patients involved was 4000 with DSM-III or DSM-IV criteria for
dependence (all had undergone detoxification). Thirteen trials compared
acamprosate with placebo; 19 compared naltrexone with placebo, and 1 compared
acamprosate with naltrexone. The main findings were that acamprosate was
associated with a significant improvement in abstinence rate and days of cumulative
abstinence, and that short-term administration of naltrexone reduced the relapse rate
significantly but was not associated with significant improvement in the abstinence
rate. The side-effects of naltrexone were more numerous, but it was tolerated
acceptably without compromising adherence to treatment. The overall conclusions
were that acamprosate appeared to be better in achieving abstinence, whereas
naltrexone seemed to be better directed at treatments where controlled drinking is
the goal.
142
This thesis is discussed and elaborated on in a recent meta-analysis of unreported
data (Rosner et al. 2008). The authors say that their primary objective was to
complete the efficacy profiles for acamprosate and naltrexone and compare them
with each other. Another (unstated) goal perhaps was to diminish publication bias,
when negative trial results are less likely to be reported. Unreported results of
registered clinical trials were requested from study investigators; they were restricted
to randomised placebo-controlled trials of either acamprosate or naltrexone or both.
Intention-to-treat analysis was carried out for all dichotomous variables. There were
21 trials of acamprosate, and 20 with naltrexone. Confounding and defining factors
were that some patients were abstinent and a subgroup were not; some were
outpatients and others not, recruitment procedures differed, and different types of
psychosocial interventions were utilised. Conclusions reached were that there are
specific therapeutic advantages in each drug, as they have different mechanisms of
action: acamprosate is more effective in aiding abstinence and naltrexone in reducing
of craving.
Overview of Pharmacotherapies: Randomised controlled trials
Efficacy of naltrexone and acamprosate were compared in a multi-centre,
randomised double-blind, placebo controlled trial conducted in Australia (Morley et al.
2006). Results from 94 subjects who completed the study (of 169) showed that there
were no differences between groups on outcome measure of drinking, craving or
biochemical markers. Intention-to-treat analysis also showed similar results. A
secondary survival analysis, on subjects with low baseline levels of dependence, did,
however, demonstrate the efficacy of naltrexone in increasing the number of days to
relapse relative to acamprosate. A further analysis comparing naltrexone to
acamprosate in reducing craving showed that naltrexone had a greater effect on
drinking when level of craving was high (Richardson et al. 2008).
The COMBINE study conducted in the USA (Anton et al. 2006) was designed to
evaluate the efficacy or pharmacotherapy, behavioural therapy and their
combinations for treatment of alcohol dependence and to evaluate placebo effect on
overall outcome. This large RCT involved 1383 patients with the diagnosis of alcohol
dependence, recently abstinent from alcohol. The treatments included naltrexone
and acamprosate (alone or together), placebo (single or double), each with or without
a combined behavioural intervention (CBI). The CBI integrated cognitive behavioural
therapy, motivational interviewing and 12-step facilitation and was delivered by
trained behavioural health specialists in up to 20 sessions of 50 min duration. All the
above groups received medical management. The treatment was of 16 weeks
duration. It was found that at the end of the treatment period, participants in all nine
different treatments and combined interventions showed reductions in drinking,
including the placebo group. Patients who received naltrexone alone, naltrexone with
CBI or CBI and placebo had higher percent of days abstinent (80.6, 79.2 and 77.1
respectively) when compared to placebo group (i.e. medical management only).
Naltrexone significantly increased the time to the first heavy drinking day (Hazard
Risk, 0.72; 97.5% confidence interval, CI, 0.53-0.98; p = 0.02). Patients receiving
acamprosate either alone or in combination with CBI and/or naltrexone had not
significantly reduce their drinking when compared to placebo group. At one year
follow up the between group differences maintained a similar trend but were no
longer significant. The results of this clinical trial are in contradiction with many
previously conducted studies investigating the efficacy of acamprosate in treatment
of alcohol dependence.
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The study found no beneficial effect of combining pharmacotherapy and behavioural
interventions on improvements in outcome. It has been suggested that the variability
between treatment providers may be more important than the variability between
treatments (Bergmark 2008; Buhringer and Pfeiffer-Gerschel 2008).
A randomised open-label trial conducted in Finland compared the effectiveness of
disulfiram, acamprosate and naltrexone in 243 treatment-seeking alcohol dependent
patients over two and a half years (Laaksonen et al. 2008). In the first 12 weeks of
the trial patients received supervised naltrexone, acamprosate or disulfiram (50,
1998, or 200 mg, respectively, per day) plus a brief manual-based cognitivebehavioural intervention. By the end of this period, 25% had dropped out. The
second phase took place over weeks 13-52, during which patients were instructed to
take the medication in connection with craving or when a relapse was imminent (a
targeted medication phase). Intake during the targeted medication phase was
relatively low, with 87% taking medication once a week. At the end of the second
phase period, 52% of the original sample had dropped out, with no significant
differences between medication groups, thereby diluting the power of the study.
During the fist 12 weeks disulfiram was better than naltrexone and acamprosate in
reducing time to first incidence of heavy drinking in reducing the number of heavy
drinking days (p<0.001), increasing time to the first drink (p<0.0002) and increasing
the number of abstinent days (p<0.0001). During the second phase there were no
significant differences in most of the above measures between groups, but
abstinence days were significantly more frequent in the disulfiram group than in the
naltrexone group (p = 0.0005) and in the acamprosate group (p = 0.0097). The
average alcohol consumption in all groups remained significantly lower than at the
baseline. Over the entire 52-week period disulfiram was significantly better than
naltrexone or acamprosate in increasing the time to first drink (p = 0.001). Supervised
disulfiram appeared superior to naltrexone and acamprosate, especially during the
continuous medication period.
Summary
There is evidence of effectiveness for all three types of pharmacotherapies in
reducing alcohol consumption in patients with alcohol dependence. Evidence is
stronger for naltrexone and acamprosate, but disulfiram remains an option for some
patients. The majority of effectiveness trials of the pharmacotherapies involved some
type of psychosocial interventions, or structured medical management. There is
evidence of an additive effect of psychosocial interventions such as cognitive
behavioural therapy (CBT), and naltrexone (see below).
Recommendation
7.1 Pharmacotherapy should be considered for
all alcohol-dependent patients, in association
with psychosocial supports.
Strength of
Level of
recommendation evidence
A
Ia
Naltrexone (NTX)
Naltrexone is an opioid receptor antagonist. By blocking mu- opioid receptors,
naltrexone reduces levels of dopamine (the major reward neurotransmitter in the
brain) and reduces alcohol intake (Gonzales and Weiss 1998).
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Effectiveness of naltrexone: Meta-analyses and reviews
The most recent (and only) meta-analysis comes in the Cochrane review of 2004
(Srisurapanont and Jarusuraisin 2005). Articles selected for review were from the
period 1966-2001. There were 2 trials of nalmefene and all the others (n = 27) were
of naltrexone; the total number of participants was 3048. The authors’ findings were
(i) that several lines of high-quality evidence supported the short-term treatment with
naltrexone for preventing relapse- the relative risk ratio (RR) for decreasing shortterm relapse was 36%, with the number needed to treat (NNT) at 7, compared to
placebo; (ii) that alcohol-dependent patients using naltrexone were more likely to
accept the treatment program; and (iii) apart from its small benefits on time to first
drink and craving, no available evidence supported a meaningful benefit after 12
weeks of treatment (Srisurapanont and Jarusuraisin 2005). There was no evidence to
support the use of nalmefene in clinical practice for alcohol dependence.
Roozen et al. (2006) conducted a systematic review of the effectiveness of
naltrexone in the maintenance both of opioid and alcohol dependence, summarising
the evidence existing up until March 2004. We only discuss the alcohol studies here.
The aims were to study the effects of naltrexone compared to placebo in the
maintenance treatment of dependence; and to study whether combining naltrexone
with psychological treatment was more effective than naltrexone alone. Seventeen
alcohol studies were identified as fitting the Cochrane quality criteria. Conclusions
from the analyses were that there is: (i) strong evidence that naltrexone is superior to
placebo regarding medium term relapse rates; (ii) strong evidence that there is no
difference in terms of continuous abstinence; (iii) strong evidence in favour of
naltrexone reducing percentage of drinking days; (iv) conflicting evidence regarding
time to first relapse; and (v) strong evidence that there is no difference in time to first
drink; (v) CBT increases effectiveness of naltrexone. In a number of individual
studies treatment compliance was significantly correlated with positive outcomes. Six
studies were included that reported follow-up or long-term results. Conclusions drawn
from the pooled effects of these studies were that there is moderate evidence in
favour of the use naltrexone concerning relapse rate, and there was no difference in
the long-term effects of naltrexone on percentage of drinking days and time to
relapse in when compared to placebo.
Almost all studies provided some form of psychosocial treatment. Although it was not
detailed in many cases, cognitive behaviour therapy including relapse prevention and
coping skills were used in most. It is recommended in the review above that
naltrexone should be delivered in combination with psychological interventions
(Srisurapanont and Jarusuraisin 2005). Conclusions drawn from the analysis by
Roozen et al. (2006) were that there was evidence that the combination with CBT
increases the effectiveness of naltrexone treatment, as discussed above.
Effectiveness of naltrexone: Randomised controlled trials
Anton et al. (2005) conducted a USA-based randomised controlled trial with 4 arms
(naltrexone or placebo combined with either CBT or with Motivational Enhancement
Therapy, MET) among 160 outpatient alcohol dependent patients. The authors
conclude that the CBT- naltrexone group did better than the others on a variety of
outcome measures. Naltrexone increased the time to first relapse. They also state
that although MET is easier to deliver, the combination of MET and naltrexone was
less effective than CBT in this case. They also note that the positive CBT- naltrexone
145
outcomes emerged over time; it is possible that the skills acquired and augmented by
CBT in conjunction with the pharmacological assistance provided by naltrexone have
a complementary effect in mutually reinforcing the active ingredients of each.
Another randomised controlled trial of naltrexone was conducted with 153 early
problem drinkers, of whom 130 (86%) completed the 8-week program (Kranzler et al.
2004). This study compared naltrexone with placebo on a daily or targeted basis.
‘Targeted’ treatment was defined as encouraging patients to take at least 2 and a
maximum of 5 tablets per week in anticipation of high-risk situations. All patients
received additional brief skills training. Both the targeted and daily basis groups
reduced their drinking days (14% fewer days) when compared to placebo. Patients
receiving targeted naltrexone showed an initial decline in heavy drinking, followed by
an increase when the number of tablets they had been given became fewer, while
the daily naltrexone group continued their decline in heavy drinking all through the
trial. Daily diaries were kept by all patients to record drinks and medications taken.
Conclusions reached by the authors were that targeted naltrexone – providing
adequate numbers of tablets are available – and combined with at least some skills
training, is effective in reducing heavy drinking, at least in highly-educated and
compliant patients. A substudy of this one examined the effects of daily interpersonal
events on heavy drinkers (Armeli et al. 2006), and found that participants had at least
one drink more on days that were characterised by higher levels of either positive or
negative interpersonal events, especially events that were celebratory in nature.
Tidey et al. (2008) randomised 180 non-treatment-seeking heavy drinkers 63% of
whom were alcohol-dependent, to daily naltrexone or placebo for 3 weeks.
Naltrexone was effective in reducing the percentage of drinking days in all
participants and also decreased the percentage of heavy drinking days in those with
the D4 dopamine receptor (DRD4) gene polymorphism (DRD4-L genotype). The muopiate receptor (OPRM1) gene polymorphism did not operate in any of the
naltrexone effects. No counselling interventions were reported; however, participants
received regular prompted messages on handheld computers reminding them to
complete their daily diaries of alcohol consumption, mood and urge to drink, activity,
location and setting for drinking and this may have helped to reinforce their
treatment.
Effectiveness of naltrexone: Summary
Effectiveness of naltrexone in reducing the rate of relapse to heavy drinking and
increasing the number of abstinence days in alcohol dependent patients has been
supported by a number of meta-analyses and reviews. Meta-analyses suggest that
compared to placebo, naltrexone reduces the relative risk ratio (RR) for relapse to
heavy alcohol use by 36%, with the number needed to treat (NNT) at 7, suggesting a
moderate effect size for maintaining abstinence (Streeton and Whelan 2001;
Krantzler and Van Kirk 2001; Srisurapanont and Jarusuraisin 2005; Roozen et al.
2006).
Naltrexone reduces the rate of relapse to heavy drinking and increases the number
of abstinence days in alcohol dependent patients. Naltrexone decreases excessive
drinking by reducing the reward associated with drinking alcohol. It reduces craving
induced by environmental stimuli and decreases the amount and frequency of
drinking when relapse occurs. It is, therefore, more effective in reducing rate and
severity of relapses rather than in maintaining abstinence (Mann et al. 2004;
Srisurapanont and Jarusuraisin 2005; Rosner et al. 2008).
146
Naltrexone is usually not prescribed without a support of some type of psychological
counselling (Srisurapanont and Jarusuraisin 2005; Donovan et al. 2008). It appears
to work best when supported by psychosocial interventions, particularly those aimed
at relapse prevention (Roozen et al. 2006). While most controlled studies of
naltrexone treatment have been in conjunction with intensive psychosocial services
(such as counselling), it has nevertheless also been effective in physician-led
treatment with regular monitoring, as has been shown in COMBINE study (Anton et
al. 2006).
Suitability for naltrexone
There is still little evidence to directly inform decisions about what patient populations
are more suitable for naltrexone. The following points should be taken into account
(O’Malley 1998, Anton 2008):
1) Patients who are moderately to severely alcohol dependent and are medically
stable are suitable for naltrexone. For example, a person who drinks on more
than 50% of days, consumes more than five drinks a day, and has some
alcohol-related problems (Anton 2008);
2) Naltrexone may be more effective for preventing relapse to heavy or problem
drinking than for maintaining abstinence from alcohol (Rosner et al. 2008);
3) Patients currently using opioids or who require opiate-based pain relief are
not suitable (Anton 2008). Due to its antagonist properties at the mu-opioid
receptor, naltrexone will precipitate acute opioid withdrawal in patients
currently using opioids. For the same reason, being on naltrexone will render
opioid analgesia ineffective.
4) While hepatotoxicity has not emerged as a wide-spread problem (Croop et al
1997), naltrexone is contraindicated for people with acute hepatitis or severe
liver failure. It is also contraindicated in patients with a history of sensitivity to
naltrexone.
5) There are no well controlled studies of the safety of naltrexone during
pregnancy or lactation.
6) There are some reports that patients with significant depression or more
severe alcohol dependence respond less well to naltrexone treatment.
Regular monitoring for depression is recommended (Latt et al 2002; Morley et
al. 2006).
Recommendation
7.2 Naltrexone is recommended as relapse
prevention for alcohol-dependent patients.
7.3 Naltrexone is not suitable for people who are
opioid dependent or who have pain disorders
needing opioid analgesia.
Strength of
Level of
recommendation evidence
A
Ia
S
Interaction with other drugs
Naltrexone is a mu-opioid receptor antagonist and induces precipitated opiate
withdrawal in patients who are currently opiate dependent. It is contraindicated in
patients with current or recent use of opioid medication (e.g. codeine, morphine,
oxycodone, methadone).
Naltrexone is a long-acting drug and will block the effects of opioids when they are
used after commencement of naltrexone treatment. Naltrexone should be
147
discontinued 48-72 hours prior to any situation where opioid analgesia may be
required (e.g. in patients undergoing elective surgery).
Naltrexone does not appear to alter the absorption or metabolism of alcohol; however
some patients have reported nausea after drinking alcohol while taking naltrexone.
The interaction of naltrexone and most other medications has not been tested.
However, caution should be exercised when combining naltrexone with other drugs
known to have hepatotoxicity (e.g. disulfiram).
Concurrent administration with antidepressants appears to be safe (Croop et al
1997).
Starting treatment
It is not known whether patients with a diagnosis of alcohol dependence achieve
better outcomes if abstinent before taking naltrexone. However, some period of
abstinence (at least 3 days) was the requirement of most clinical trials investigating
the effectiveness of naltrexone. The patient’s ability to achieve abstinence in this
period is a good indication of their motivation to adhere to a course of naltrexone. It
has been suggested that such abstinence is the most judicious approach (Anton
2008).
Naltrexone dosing is recommended to begin 3-7 days after the patient’s last drink
and after resolution of acute withdrawal symptoms. In most randomised controlled
studies (e.g. reviewed by Srisurapanont and Jarusuraisin 2005) investigating
effectiveness of naltrexone, treatment was initiated within one week of completing
managed withdrawal.
Recommendation
7.4 Naltrexone should be started as soon as
possible after completion of withdrawal (usually
3 to 7 days after last drink).
Strength of
Level of
recommendation evidence
A
Ib
Dosage
Naltrexone is formulated in tablets of 50mg, with the recommended dose being 50mg
(1 tablet/day orally) with meals. It may be preferable to commence with ½ tablet
(25mg/day) for several days, and increase to 50mg after any adverse effects have
subsided.
There has been only one study comparing several doses of naltrexone (O’Malley et
al 2008). This was a placebo-controlled dose-range study, investigating the effect of
oral naltrexone (25mg, 50mg and 100mg) on alcohol consumption in hazardous
drinkers (not seeking treatment), combined with open-label transdermal nicotine
patch for enhancing smoking cessation. The lowest dose (25mg) was more effective
in reducing levels of drinking. The authors conclude that given its efficacy, favourable
side-effect profile and a lower cost when compared to higher doses, the 25-mg dose
should be considered for future studies of combination therapy.
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Adverse effects and their management
Naltrexone is usually well tolerated. Common adverse effects include nausea,
headache, dizziness, fatigue, nervousness, insomnia, vomiting, and anxiety in about
10 percent of patients. These generally subside with time (usually days) (e.g.
Srisurapanont and Jarusuraisin 2005).
Based on clinical practice, the following strategies may help reduce the impact of
potential side effects on treatment outcome:
1) Patient education about expected side effects and duration
2) Timing of doses: establish a routine; ideally taken in the morning with food or
splitting the dosage between the morning and evening
3) Gradual introduction of medication (25mg for 1-2 days)
4) Dose reduction (half tablets at 25mg/day), slow titration, and stopping the
medication for three to four days before reintroducing it at a lower dose
5) Distinguishing between prolonged alcohol withdrawal symptoms and side
effects of naltrexone by beginning treatment once the major features of
alcohol withdrawal have subsided (generally 3-5 days after drinking
cessation) may be important.
Treatment duration
The most appropriate duration of treatment continuation in an alcohol-dependent
patient is not yet known. The usual treatment period used in majority of randomised
controlled studies (e.g. Srisurapanont and Jarusuraisin 2005) as well as in clinical
practice is 3-6 months and in some cases up to 12 months.
However, the decision on the treatment duration should be made on a case-by-case
basis between the patient and doctor, based on side effects, history of relapse, social
and family circumstances, and other individual factors.
Recommendation
7.5 Naltrexone is usually taken for at least 3 to 6
months.
Strength of
Level of
recommendation evidence
D
IV
Clinical considerations during treatment
Treatment should continue even if the patient lapses; psychosocial relapse
prevention techniques should be used to deal with the lapse or relapse (see Chapter
6a: Psychosocial interventions)
Monitoring and attending to physical and mental health is important. Depression and
dysphoria have been reported as side effects of naltrexone (Farren and O’Malley
1999; Mendelson et al 1978)
Ending naltrexone therapy
There is no evidence of a withdrawal syndrome or development of dependence
following the use of naltrexone. Psychosocial relapse prevention should continue
beyond the end of pharmacotherapy.
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Acamprosate
Acamprosate is thought to reduce drinking by modulating the brain GABA (gammaaminobutyric acid) and glutamate function which is implicated in withdrawal
symptoms. The drug only reaches desired levels in the brain after one to two weeks
(Wright and Myrick 2006; Mann et al. 2008).
Effectiveness of Acamprosate: Reviews and Meta-analyses
A meta-analysis by Mann et al. (2004) examined results of 17 randomised clinical
trials investigating efficacy of acamprosate in the maintenance of abstinence in
alcohol dependent patients. A total of 4087 patients were included, of whom 53%
received the intervention medication. Findings showed that continuous abstinence
rates at 6 months were significantly higher in the acamprosate-treated patients than
in placebo group (36.1 and 23.4% respectively, with the relative risk ratio of 1.47
(95% CI, 1.29–1.69; p<0.001). At 12 months, the pooled difference in success rates
between acamprosate and placebo was 13.3%, with number needed to treat (NNT)
at 7.5. The conclusions of this study were that acamprosate had a significant
beneficial effect in enhancing abstinence in detoxified alcohol-dependent individuals.
Another study evaluated the results of 3 double-blind, placebo-controlled trials
carried out in Belgium and France, France alone, and Germany (Kranzler and Gage
2008). Acamprosate was delivered in doses of either 1332mg or 1998mg per day. In
one study of 48 weeks (in Germany), the doses were assigned according to body
weight (as recommended) and in the other two (13- and 52-week studies) they were
randomly assigned. All patients received counselling. Drinking outcomes were
measured by blood tests (GGT and MCV), breath, blood or urine alcohol
concentrations, and by reports from patients and family members. Results showed
that 54% of patients receiving acamprosate completed the trials versus 39% of
control group patients. Intention-to-treat analysis was used; patients with missing
data or unknown status were assumed to relapse to non-abstinence. The
intervention group reported significantly higher percentage of days abstinent than
placebo patients in all 3 studies (p<0.01). Differences ranged from 18% in the 52week study (p = 0.001) to 38% in the 13-week study (p<0.001). Overall, the rate of
complete abstinence was significantly higher with acamprosate than placebo
(p<0.05). Acamprosate significantly increased percent days abstinent and time to first
drink compared to placebo patients (p<0.01). Conclusions were that acamprosate is
an effective medication and was also the first to demonstrate efficacy in maintaining
complete abstinence, when combined with psychosocial support.
Effectiveness of Acamprosate: Randomised controlled trials
One pragmatic trial of acamprosate was undertaken over 149 general practices in
France with 422 alcohol dependent patients (Kiritze-Topor et al. 2004). Patients were
randomised to receive acamprosate with standard care (which in France includes a
rehabilitation program, often with some type of psychosocial therapy) or standard
care alone. The purpose of the trial was to test its efficacy in routine practice. The
principal outcome measure was change from baseline on the Alcohol-Related
Problems Questionnaire (ARPQ), a questionnaire that measures the influence of
alcohol consumption on patients’ lives with respect to health, work, financial, family
and relationship and legal/judicial problems. Secondary outcome measures were
abstinence (measured by proportion of days abstinent during the trial), and the
success of the treatment from the physician’s point of view. Results from the 12
150
month follow-up showed a level of significance in favour of acamprosate, with a
relative risk ratio (RR) of 1.26. The number needed to treat was 7.14; i.e. 7 patients
need to be treated to save one additional patient from alcohol-related problems. Half
of all patients reported no alcohol-related problems during the study period. Study
completion rate was high at 82.5%; intention-to-treat analysis was used. Conclusions
of the study were that acamprosate is successful in reducing alcohol-related
problems, and also that the treatment can be practically carried out in routine general
practice with alcohol-dependent patients.
Psychosocial treatment was the subject of two trials where it was tested with alcoholdependent patients and compared with acamprosate. A study conducted in
Netherland compared acamprosate alone with acamprosate plus minimal
motivational enhancement, and acamprosate plus brief cognitive behavioural therapy
(de Wildt et al. 2002). Another similar study in Sweden compared two types of
intervention: minimal psychosocial intervention and extended psychosocial
intervention; both arms contained treatment with acamprosate (Hammarberg et al.
2004).
The de Wildt et al. (2002) study was conducted with 248 alcohol-dependent
outpatients from 14 addiction treatment centres in the Netherlands; the study period
was 28 weeks. Minimal intervention (group 2) was 3 sessions of 20 minutes each in
weeks 2, 3, and 4. Extended intervention (group 3) was 5 standard and 2 elective
weekly 60-minute sessions of CBT in weeks 2-8. In contrast, ‘no intervention’ (group
1) patients were seen by the physician 6 times in 28 weeks. All patients were
prescribed acamprosate for 28 weeks. At the end of the treatment period 114
patients (47%) remained in the study. Outcome measures were number of abstinent
days, time to first relapse and number of drinks per drinking day. The results showed
that adding a psychosocial intervention did not enhance drinking outcomes or
medication compliance. Total number of abstinent days was 108.5 for group 1, 119.1
for group 2, and 108.1 for group 3; rates of continuous abstinence were 13%, 21%
and 10% respectively; time to first relapse was 53.4, 65.5 and 55.4 days respectively.
Intention-to-treat analysis was used. No statistical differences were found between
the treatment groups; the authors suggest that this may partly have been explained
by the ‘no intervention’ group spending the same amount of time in consultations as
the ‘minimal intervention’ group. Although the protocol was strictly adhered to,
sources of potential bias were addressed in the randomisation of patients to
treatment arms, and the sample size was powerful enough to detect differences in
outcomes, it remains unknown why the interventions did not produce a larger effect
than expected. It concludes that this trial could not demonstrate an effect for brief
psychosocial treatments and either a much more intensive treatment is needed or
that acamprosate with medical management is adequate to produce decreases in
drinking.
The study by Hammarberg et al. (2004) compared two intensities of psychosocial
interventions (extensive and minimal) with 70 alcohol dependent patients, all being
treated with acamprosate. Results showed that the extended intervention was not
more effective in prolonging time to first drink, with reducing either the number of
drinking days or of heavy drinking days than the minimal intervention. There were no
differences between groups in compliance to medication during the trial, or in AST,
GGT or CDT levels in blood tests conducted after 24 weeks. There was a slight
reduction in ALT levels in the minimal intervention group. The authors suggest that
the extended intervention may not have been intensive enough to produce a doseresponse effect, or conversely (similar to the above study) medication with minimal
intervention is sufficient to reduce drinking levels.
151
Patient motivation was found to have a significant effect on the outcome in a study
conducted in the USA which tested the dose-dependent effectiveness of
acamprosate in alcohol-dependent patients in a double-blind placebo- controlled trial
(Mason et al. 2006). There were 3 arms to the trial; 3 placebo tablets (nil dose); 2
tablets of acamprosate and one placebo (2g); or 3 tablets of acamprosate (3g); all
given twice daily. All patients received brief counselling and self-help materials at 8
study visits, for 24 weeks. The primary outcome measure was alcohol-free days,
measured by the timeline follow-back method. Results show no statistically
significant difference in alcohol-free days across all arms, although a slight trend was
noticed (54% for nil dose, 56% for 2g, and 61% for 3g. However, by examining
results from a subgroup whose goal at baseline was to be completely abstinent, it
was found acamprosate had a significant linear dose effect, with 3g superior to 2g
(p=0.01) and 2g superior to nil dose (p=0.04), using both intention-to-treat analysis
and actual completers’ results.
Reid et al. (2005) conducted a small randomised trial (n = 40) to evaluate the
effectiveness of compliance therapy in increasing adherence to treatment with
acamprosate in patients with alcohol dependence. Patients received acamprosate,
with or without compliance therapy for 4 months (n = 20 in each group). All subjects
received routine medical care (seven medical reviews each of 15 minutes duration
over 4 months. Compliance therapy consisted of four to six individual sessions (60
minute duration) and included motivational interviewing and cognitive behaviour
therapy techniques with the focus on exploration of beliefs about medication side
effects, the benefits of treatment ambivalence and relapse prevention. Intention-totreat analyses of data showed no differences between the two groups in the number
of days taking acamprosate, days to first drink, days to first relapse. However, it was
found that participation in three or more sessions of compliance therapy was
associated with better adherence to acamprosate and better overall treatment
outcomes.
The COMBINE study (Anton et al. 2006), described above, found that acamprosate
was not more effective in reducing drinking than placebo (with medical management)
either alone or in combination with psychological intervention or with naltrexone or
both. It should be noted, however, that in this study percent days abstinent at the end
of the 16-week treatment period was similar in placebo, acamprosate and naltrexone
groups (mean, placebo acamprosate 77.6 vs acamprosate 78.4; placebo naltrexone
77.2 vs naltrexone 78.8). The assessment of interactions between treatment
combinations showed that naltrexone, but not acamprosate, was significantly more
effective than placebo in reducing the number of percent days abstinent, although the
actual difference was small (mean, placebo naltrexone without CBI 75.1 vs
naltrexone without CBI 80.6).
There was a significant "placebo effect" in the COMBINE study resultingt from pill
taking and meetings with a medical professional. The latter may have contributed by
repeated advice to attend Alcoholics Anonymous and instilling sense of optimism
about a medication effect (Weiss et al. 2008).
Effectiveness of acamprosate: Summary
Acamprosate is effective in maintaining abstinence from alcohol following withdrawal
in dependent drinkers; the relative risk ratio is 1.3 to 1.5 in the first 6 months, and the
number needed to treat is 7.5 over placebo (Mann et al. 2004). Acamprosate
increases the number of days of continuous abstinence as well as the percent of
days abstinent and time to first drink (Kranzler and Gage 2008).
152
Acamprosate is more likely to be effective in patients motivated to stay abstinent at
the start of treatment (Mason et al. 2006).
While there is no sufficient evidence to suggest that acamprosate is more effective
when used together with psychosocial interventions, the current approach is to use
acamprosate as part of a more comprehensive treatment plan that may include
psychosocial interventions.
Suitability for acamprosate
There is still little evidence to inform decisions about what patient groups are most
suitable for acamprosate.
Verheul et al. (2005) pooled the results of 7 European trials with the aim of identifying
if there was a particular subgroup of patients who responded better to acamprosate.
They analysed the results of 1485 patients with alcohol dependence using the
outcome measures of cumulative abstinence duration, continuous abstinence, and
time to first relapse. The overall results concluded that acamprosate can be
considered potentially effective for all patients with alcohol dependence, as despite
the large sample size and sufficient statistical power to detect any variations, no
differences were detected for any of the variables (craving, anxiety, study, and
treatment) entered into the analysis. It is posited by the authors, however, that
evidence from 2 other studies suggests that naltrexone or disulfiram combined with
acamprosate would improve its effectiveness.
Based on available evidence, acamprosate is a suitable treatment option for patients
with alcohol dependence (usually, moderate to severe), who are medically stable and
are willing to comply with the dosing regimen may benefit for acamprosate (Reid et
al. 2005).
Acamprosate may be more effective for patients with an abstinence goal rather than
preventing excessive drinking in non-abstinent patients (Mason et al. 2006; Rosner et
al. 2008).
Acamprosate is contraindicated in patients with a known hypersensitivity to the drug,
renal insufficiency or severe hepatic failure (Childs Pugh classification C) (MIMS
2008).
The safety of acamprosate in pregnancy or lactation has not been established so it
should not be administered to women who are pregnant or breastfeeding (MIMS
2008).
Recommendation
7.6 Acamprosate is recommended as relapse
prevention for alcohol-dependent patients.
Strength of
Level of
recommendation evidence
A
Ia
Interaction with other drugs
Acamprosate does not interact with alcohol. Tetracyclines may be rendered inactive
by the calcium component in acamprosate.
153
Starting treatment
Acamprosate dosing is recommended to begin 3-7 days after the patient’s last drink,
and after resolution of any acute withdrawal symptoms. Acamprosate can be safely
initiated during alcohol withdrawal (Gual and Lehert 2001) and its potential
neuroprotective effect may be useful early in withdrawal (Koob et al. 2002).
Starting acamprosate at the beginning of detoxification versus after completion of
detoxification has not been shown to improve treatment outcomes (Kampman et al.
2009).
However, pre-treatment with acamprosate 8 days prior to withdrawal management
has been shown to improve sleep during withdrawal and in a post-withdrawal period
(Staner et al. 2006).
Medical history should be taken, as per Chapter 3: Screening and assessment.
Physical examination may include assessment for signs of chronic liver disease and
hepatic failure. Investigations may include tests of kidney function (urea and
electrolytes), since 90 percent of acamprosate is excreted through the kidney, and
liver function tests.
Recommendation
7.7 Acamprosate should be started as soon as
possible after completion of withdrawal (usually
3 to 7 days after last drink).
Strength of
Level of
recommendation evidence
A
Ib
Dosage
Acamprosate is formulated in tablets of 333 mg, with the recommended dose for
adults being 1998mg with meals (six tablets/day, orally in three doses: 2; 2; 2). Adults
under 60kg should take 1332 mg/day (four tablets/day in three doses: 2; 1; 1).
Adverse effects and their management
Acamprosate is usually well tolerated. Its predominantly gastrointestinal adverse
effects, commonly diarrhoea, usually resolve spontaneously within days. Mild
abdominal pain, rash or isolated pruritus, parasthesiae, altered libido and confusion
have been reported at low frequencies (Wilde and Wagstaff 1997).
The following strategies are recommended:
1) Patient education about expected side effects and duration.
2) Distinguishing between prolonged alcohol withdrawal symptoms and side effects
of acamprosate by beginning treatment once more pronounced features of
withdrawal have subsided (after first 3-5 days).
Treatment duration
The usual treatment period is 3-6 months (Mann et al. 2004). However, the decision
on the duration of treatment should be made on a case-by-case basis between the
154
patient and doctor, based on side effects, history of relapse, social and family
circumstances and other individual factors.
Recommendation
7.8 Acamprosate is usually taken for at least 3
to 6 months.
Level of
Strength of
recommendation evidence
D
IV
Clinical considerations during treatment
Treatment should continue even if the patient lapses; psychosocial relapse
prevention techniques should be used to deal with the lapse or relapse (see Chapter
6a: Psychosocial interventions) (Mann et al. 2004).
Some clinicians do not prescribe acamprosate during continued drinking. This is not
because of drug interactions but due to the belief that medication is of most use for
patients that possess a higher motivation to change
Regular monitoring and attending to physical, mental health and social issues is
necessary.
Some patients will have difficulty adhering to a medication regime that involves taking
tablets three times a day for prolonged periods (Reid et al. 2005) (see also material
later in this chapter on increasing medication adherence).
Ending acamprosate therapy
There is no evidence of a withdrawal syndrome following the use of acamprosate or
developing dependence. Psychosocial relapse prevention interventions should
continue beyond the end of pharmacotherapy.
Combined Acamprosate and Naltrexone
Some clinicians administer acamprosate and naltrexone concurrently given the
different theoretical approaches of the two medications in reducing alcohol
consumption. Studies have found this to be a safe and promising approach.
Nonetheless, most evidence suggests that while combined naltrexone and
acamprosate may be more effective than acamprosate alone, the combination is no
more effective than naltrexone alone (Kiefer et al. 2003; Anton et al. 2006).
Combined acamprosate and naltrexone: Meta-analyses and reviews
An evidence-based risk-benefits assessment was carried out by Mason (2003) who
assessed all published double-blind placebo-controlled trials of acamprosate and
naltrexone. Sixteen studies of acamprosate were found, of which 15 used
standardised methodology and were included; 14 studies were found of naltrexone
and 3 of the two medications combined. The naltrexone trials differed more in their
methodology than the others. The advantages of this were that the drug was
evaluated under many conditions, from short- to long-term, and with and without
accompanying psychosocial treatment. Based on this review, the conclusions were
that both medications are useful in the treatment of alcohol dependence. However,
155
as the two drugs act in different ways and have different effects on the brain, there is
a case for combining the two, and it was suggested that this may offer an advantage
for some patients.
Combined acamprosate and naltrexone: Randomised controlled trials
Kiefer et al. (2003) compared naltrexone, acamprosate, and a combination of the two
in a double-blind placebo-controlled study. After detoxification, 160 alcohol
dependent patients were randomised to receive naltrexone, acamprosate, both, or
placebo for 12 weeks. All patients attended group therapy weekly, utilising CBT and
coping skills training. Full blood tests were also carried out, and breath and urine
were randomly tested for alcohol. Results were that both medications were superior
in achieving abstinence compared to placebo, with a tendency for a better outcome
in the naltrexone group compared to acamprosate in maintenance of abstinence.
There was no significant difference in time to first drink between naltrexone and
acamprosate. Additional benefits were observed in combining naltrexone and
acamprosate (p = 0.002). The combined medication group had a relapse rate of 25%.
At follow-up (week 24) patients who received combined medication had rates
significantly lower relapse rate than placebo, but not lower than acamprosate. Both
naltrexone and acamprosate were superior to placebo. Relapse rates were 80%
(placebo), 54% (acamprosate), 53% (naltrexone) and 34% (combined medication).
The results of COMBINE study (Anton 2006), discussed above, showed no
advantage of adding acamprosate to naltrexone.
Disulfiram
Disulfiram primarily works by inhibiting the action of an enzyme (aldehyde
dehydrogenase) involved in the second step in the metabolism of alcohol, namely the
conversion of acetaldehyde to acetate. This leads to the accumulation of
acetaldehyde following consumption of alcohol while on disulfiram. The resulting
symptoms are unpleasant including flushing, dizziness, nausea and vomiting,
irregular heart beat, breathlessness and headaches. Disulfiram acts as a deterrent to
drinking because the patient expects to experience these negative consequences
(Heather 1989). Evidence indicates that the maximal effect of disulfiram is achieved
when the medication is provided to the patient under supervision (Chick et al. 1992;
Hughes and Cook 1997; Laaksonen et al. 2008).
There is one recently reported trial of disulfiram and acamprosate (De Sousa and De
Sousa 2005), which was randomised but not blinded. Better outcomes were noticed
with disulfiram as the trial progressed, and it was found significantly better both at
preventing relapse during the study (p = 0.0003), maintaining abstinence (p =
0.0002) and increasing days to first relapse (p = 0.0001).
Another trial in Finland compared disulfiram, acamprosate and naltrexone in a
randomised open-label study with 243 treatment-seeking alcohol dependent patients
over two and a half years (Laaksonen et al. 2008). Results show that during the fist
12 weeks disulfiram was better than naltrexone and acamprosate in reducing time to
first incidence of heavy drinking (p<0.001). During the second phase (dosing
targeted to risk situations) there were no significant differences in these measures
between groups, but abstinence days were significantly more frequent in the
disulfiram group (p = 0.0005 in the naltrexone group; p = 0.0097 in the acamprosate
156
group). Supervised disulfiram appeared superior to naltrexone and acamprosate,
especially during the continuous medication period. This trial is described in more
detail in Section 1.2 above.
Suitability for disulfiram
Based on the results of the recent studies discussed above and previous clinical
experience, disulfiram is an appropriate medication for patients who are motivated to
abstain from alcohol. It is beneficial for patients that accept a need for an external
control on their drinking and are prepared to be supervised in the daily dosing of the
medication (Chick et al. 1992; Hughes and Cook 1997). Since it is most effectives
with supervised administration, willingness of patient’s spouse, family member or a
friend is an important factor.
Disulfiram can cause significant toxicity if relapse occurs. It should only be prescribed
to patients that display no medical or psychosocial contraindications as described
below.
Recommendation
7.9 Disulfiram is recommended in closely
supervised alcohol-dependent patients
motivated for abstinence and with no
contraindications.
Strength of
Level of
recommendation evidence
A
Ia
Precautions
The intensity of the disulfiram-alcohol reaction varies amongst patients and in rare
cases may result in cardiovascular collapse, myocardial infarction, respiratory
depression, convulsion and death. Accordingly, treatment is contraindicated for
patients with significant cardiovascular, hepatic or pulmonary disease. Several of the
patients most suited to disulfiram in other terms may suffer from these problems. A
risk-benefit analysis of the treatment should therefore be undertaken by the treating
clinician. Careful monitoring of cardiac and liver condition is recommended if
disulfiram treatment is started.
The enzyme that metabolizes dopamine into norepinephrine and epinephrine is
inhibited by disulfiram, which may result in an exacerbation of psychosis.
Nonetheless, a trial in a psychotic population did not reveal significant problems
(Petrakis et al. 2006).
Interaction with Other Drugs
Disulfiram interacts with the metabolism of alcohol. It increases the blood
concentration of benzodiazepines, caffeine, phenytoin, the active ingredient in
marijuana, isoniazid, barbiturates, anticoagulants, tricyclic agents and paraldehyde
(MIMS 2008). Disulfiram should not be given concomitantly with paraldehyde
because paraldehyde is metabolized to acetaldehyde in the liver. Disulfiram should
not be combined with naltrexone as both medications are potentially hepatotoxic.
157
Starting Treatment
Treatment should begin after detoxification, approximately 24-48 hours after drinking
cessation. Medical history should be taken. It is important to discuss the effects of the
drug when alcohol is taken, including potential severe, life threatening reaction. The
patient’s anticipation of its effects will greatly enhance the drug’s effectiveness as a
deterrent against drinking. Disulfiram should be seen as an aid that does not detract
from the patient’s own responsibility in maintaining abstinence.
Dosage
Disulfiram is formulated in tablets of 200mg, with the recommended dose being 200400mg (1-2 tablets/day orally). Some patients can continue to drink on 200-400 mg
without significant aversive effects, and the dose should be increased. The
maintenance dosage should generally not exceed 600 mg a day. In many patients,
two or three doses per week may be sufficient, and this approach may be more
practical and easier to schedule with supervision.
Clinical considerations during treatment
Treatment should be suspended if the patient lapses; psychosocial relapse
prevention techniques should be used to deal with the lapse or relapse (see Chapter
6a: Psychosocial interventions). Disulfiram may be recommenced after 48 hours
abstinence.
Supervision
Based on the outcomes of the recent studies discussed above, disulfiram treatment
is best suited to individuals with social supports (e.g. family) who will help supervise
medication adherence (Chick et al. 1992; Hughes and Cook 1997; Laaksonen et al.
2008). Supervision has a marked effect on adherence and may greatly improve the
effectiveness of this intervention.
A spouse/partner is an obvious choice for married/de facto patients. It is important to
stress that the spouse cannot be expected to control the other person’s drinking. A
written ‘disulfiram contract’ should be considered between a carer and patient. This
contract should include an outline of the likely effects of drinking and products that
may need to be avoided (e.g. facial products), the recognition that the patient will
allow the medication to be supervised, that the carer will be the supervisor and that
the supervisory role includes contacting the health professional if medication
compliance becomes a problem.
Treatment duration
Disulfiram is likely to be a useful treatment for the first 3-6 months of treatment. After
that the benefits of continuing use are less clear and the patient should be
encouraged to maintain abstinence without disulfiram.
Recommendation
7.10 Disulfiram is usually taken for at least 3 to
6 months.
Strength of
Level of
recommendation evidence
D
IV
158
Other medications
Serotonergic agents
There is minimal evidence for the efficacy of serotonergic agents (e.g. SSRIs,
buspirone and ondansetron) for treating the main symptoms of alcohol dependence.
However, these agents may have a role in certain patients that have concomitant
symptoms of anxiety or depression and there is evidence they are effective for these
symptoms in the presence of alcohol use (see Chapter 8: special population groups
and Chapter 9: comorbidity).
Other formulations and medications
There are several new agents emerging in the literature. These include
anticonvulsants such as gabapentin (Furieri and Nakamura-Palacios 2007) and
topiramate (Johnson et al. 2007), a gamma aminobutyric acid type B (GABA-B)
receptor agonist baclofen (Addolorato et al. 2007), a N-methyl-d-aspartate (NMDA)
receptor antagonist memantine (Evans et al 2007) and antipsychotic medications
such as olanzapine (Guardia et al. 2004) and aripiprazole (Anton et al. 2008). Whilst
some of these medications appear promising as agents in reducing alcohol relapse,
the need for further controlled trials and the cost of these agents means that they
cannot be recommended for use as first line treatments for alcohol dependence at
this time.
A long-acting (monthly) depot intramuscular injected preparation of naltrexone has
been developed and is licensed in the USA (e.g. Garbutt et al. 2005). This agent
looks promising and avoids problems of poor adherence, however it is not yet
available for use in Australia.
Whilst benzodiazepines are commonly sought after by some patients, there are no
studies to support the use of benzodiazepines beyond the immediate withdrawal
period in reducing alcohol use, and indeed there may be adverse effects of
benzodiazepines dependence and interactions with alcohol.
Gabapentin
The efficacy of gabapentin (an anticonvulsant) in reducing alcohol consumption and
craving has been examined by Furieri and Nakamura-Palacios (2007) in a
randomized, double-blind, placebo-controlled trial performed in a Brazilian public
outpatient drug treatment clinic. Subjects (n = 60) with alcohol dependence who
received routine management of withdrawal with diazepam were randomised on
treatment with gabapentin (300 mg twice daily) or placebo for 4 weeks. At the end of
the treatment period patients receiving gabapentin had a significant reduction in both
number of drinks per day and mean percentage of heavy drinking days (p = 0.02 for
both), and an increase in the percentage of days of abstinence (p = 0.008),
compared to the placebo group. Gabapentin was well tolerated.
159
Topiramate
Oral topiramate (an anticonvulsant) has also been trialled as an antagonist for
alcohol’s rewarding effects. It was tested against placebo with 150 alcohol-dependent
treatment-seeking individuals in a double-blind randomised controlled study (Johnson
et al. 2003) in the USA, and later in an identical study with 371 individuals at 17 US
sites (Johnson et al. 2007). Outcome measures of the first study were, using the
timeline followback method: number of drinks per day; average number of drinks per
drinking day; percentage of heavy drinking days, and percentage of days abstinent.
Results showed that topiramate was significantly more effective than placebo on all
outcome measures. Secondary outcome measures included plasma GGT levels and
self-reported craving and these also fell significantly. The dosage of topiramate was
increased slowly for the first 8 weeks and so a time effect cannot be separated from
a dosage effect. The authors conclude that topiramate is a safe and effective
medication for alcohol dependence.
Other favourable results of this study have been reported elsewhere; namely one of
improvement of quality of life and physical health associated with the use of
topiramate (Johnson et al. 2008).
The later and larger trial of more sites and subjects, but using more rapid titration of
dose (Johnson et al. 2007), replicated the findings of the first trial but with more
rigorous statistical testing and therefore was able to conclude that the therapeutic
effect of topiramate was replicable. The dropout rate, however, was found to be
higher in the intervention group due to side-effects and they recommend slower
titration of dose, as in the first trial. One of the drawbacks of the trial, as they report,
is that no follow-up was conducted and so it is not known if the effects on reduction of
drinking persisted.
Another study tested the effects of topiramate on urge to drink (Miranda et al. 2008)
and found no conclusive effects on this feature, but did confirm others’ findings that it
reduced the frequency of drinking; it also reduced the stimulating effects of alcohol
but was only significant in the 200mg group. As the authors report, the sample size
was small (n = 61) and was a preliminary study only.
The scientific concepts and clinical evidence for the development of topiramate in the
treatment of alcohol dependence have been reviewed by Johnson (2005).
Baclofen
The effectiveness and safety of baclofen (a muscle relaxant acting through activation
of the GABA-B receptor) was assessed in a double-blind randomised controlled trial
of 84 alcohol-dependent patients in Italy with liver cirrhosis (Addolorato et al. 2007).
Results from this study showed that 71% of baclofen patients achieved and
maintained abstinence compared with 12% of placebo. The drug was well tolerated.
Memantine
Memantine is an N-methyl-d-aspartate (NMDA) receptor antagonist that may have
potential for the treatment of alcohol disorders. Memantine has been shown to
decrease alcohol craving in moderate drinkers. A double-blinded pilot study in the
USA of memantine with 34 patients randomised to medication or placebo produced
inconclusive results (Evans et al. 2007). Eighty percent of patients completed the 16week trial; both groups significantly reduced their alcohol use, with no difference
160
between the groups. The authors conclude that there is no evidence from this pilot to
support its use to reduce either alcohol consumption or relapse from abstinence.
Olanzapine
Similar results were found in a double-blind randomised parallel group trial of
olanzapine (an antipsychotic) in Spain, where both placebo and treatment groups
also received psychotherapy (Guardia et al. 2004). Olanzapine was well tolerated;
side-effects were mostly weight gain (32%), increased appetite (25%), drowsiness
(18%), constipation (11%) and dry mouth (11%). Both groups reduced drinking and
no differences were found between groups on any of the measured psychological
variables, in the relapse rate or in any other drinking variables.
Another trial was carried out in the USA by Hutchison et al. (2006) with 128 patients
who were randomised to receive placebo or olanzapine with the aim of reducing
craving. The patients were further analysed by sub-groups (those who had and did
not have a particular allele (described as the seven-repeat allele of the DRD4
variable number of tandem repeats). Results of this study show that olanzapine
reduced cue-elicited craving for alcohol in the DRD4-L (positive) individuals after 2
weeks of treatment. It also decreased the quantity of drinking over 12 weeks. It did
not have this effect on the DRD4-S (negative) individuals. Side-effects from
olanzapine included weight gain, with average weight gain being 6.5 lbs (approx 3
kilos) in the treatment group.
Aripiprazole
Finally, trials of aripiprazole have been recently reported. Aripiprazole is a
dopaminergic/serotonergic agent with partial agonist properties at the D2 dopamine
receptor and 5-hydrdoxytryptamine 1A (5-HT(1A)) receptor and antagonist properties
at the 5-HT(2A) receptor.
Anton et al. (2008) conducted a randomised multi-centred double-blind, placebocontrolled study of efficacy and safety of aripiprazole in treatment of alcohol
dependence. The primary efficacy measure was percentage of days abstinent over
12 weeks. Patients (n = 295) with DSM-IV alcohol dependence were randomised to
placebo or oral aripiprazole in an increasing dose from 5mg to 30mg per day.
Subjects also received weekly psychotherapy sessions. Time line follow-back
method was used to measure alcohol consumption. More patients in the treatment
group dropped out (41% vs 17% of controls); more dropouts in the treatment group
were due to adverse effects than in the control group, and dropout also occurred
sooner. Results indicated that aripiprazole patients consumed fewer drinks when
they did drink and rated themselves as having fewer problems at study end.
Statistically significant items favouring aripiprazole were ‘made me not want to drink’
(p = 0.034); ‘felt better the next day if I did drink’ (p = 0.010); and ‘felt less high or
intoxicated when I did drink’ (p<0.0001). The authors conclude that this antipsychotic,
or others, may be useful in treating alcoholism or other addictions.
Martinotti et al (2008) compared aripiprazole with naltrexone in a double-blind
comparison trial of 75 patients who were committed to abstinence. Outcome
measures were maintenance of abstinence and relapse to drinking, defined as 5 or
more drinks on 5 days in a week; secondary was time to first drink, number of
abstinent days and reduction in craving. Intention-to-treat analysis was used.
Results: number of subjects alcohol free and relapsed during the study period were
not significantly different in the two groups. The authors conclude that aripiprazole
161
was effective at flexible doses in improving alcohol–related outcomes, with a relapse
rate and number of patients retained in treatment not significantly different from
naltrexone.
Injectable naltrexone
Two randomised controlled trials were identified that tested intramuscular injection of
naltrexone. Kranzler et al. (2004) conducted a multicentre trial of 315 patients who
received a monthly injection of naltrexone or placebo for 12 weeks. Patients also
received 5 sessions of motivational enhancement therapy. Outcomes of interest were
self-reported alcohol use and GGT levels; 74% completed all injections, which were
well tolerated. Results favoured the naltrexone group in reducing alcohol
consumption and lowering GGT levels but did not reach statistical significance;
however, the naltrexone group did have significantly fewer drinking days than the
placebo group and a significantly greater abstinence rate (18% vs. 10%).
A study by Garbutt et al. (2005) was also a multicentre trial, which took place over 6
months at 24 hospitals and clinics in the USA with 624 participants. This study used
two doses of long-acting naltrexone 380mg and 190mg, vs. placebo, delivered in
monthly intramuscular injections. Patients also received 12 sessions of low-intensity
psychosocial intervention. The principal outcome measure was the rate of heavy
drinking days. Intent-to-treat analysis was used. Results showed that 380mg of
naltrexone resulted in a 25% decrease in heavy drinking, while 190mg doses
resulted in 17% decrease compared to placebo, with the medication being well
tolerated. Patients who entered with the goal of abstinence had a greater degree of
reduction in drinking than those who aimed to reduce their drinking. These patients in
both groups benefited more from the trial (placebo vs. both doses of naltrexone);
however, patients who had already abstained when entering the trial benefited the
most (see the study by O’Malley et al. 2007 below). Authors conclude that longacting naltrexone is beneficial in the treatment of alcohol dependence.
Furthermore, patients who received 380 mg extended release naltrexone as part of
the Garbutt et al. (2005) trial had significantly greater improvements from baseline in
mental health (p = 0.0496), social functioning (p = 0.010), general health (p = 0.048),
and physical functioning (p = 0.028), compared with placebo. Reductions in drinking
from the baseline (percentage of drinking days and percentage of heavy drinking
days in the last 30 days) were significantly (p < 0.05) correlated with improvements in
quality of life (Pettinati et al. 2009).
O’Malley et al. (2007) analysed the data from a subgroup of patients who participated
in the Garbut et al. (2005) study. The subgroup included patients with 4 days or more
of voluntary abstinence before the injection of the extended release naltrexone (n =
82). Patients on 380 mg naltrexone (n = 28) has significantly better treatment
outcomes when compared to placebo (n = 28), including a longer time to first drink
(median of 41 days versus 12 days in placebo group) and to first heavy drinking
event (>180 days vs 20 days respectively, p = 0.04). They also had only 0.7 drinking
days per months, which is a 90% decrease when compared to 7.2 days in placebo
groups (p = 0.005). The rate of continuous abstinence at six months was 32% versus
11% respectively (p = 0.02). The 190 mg dose of (n = 26) showed intermediate
outcomes, indicating a dose-response effect. Therefore, a period of abstinence of as
little as 4 days before commencement of treatment with the extended release
naltrexone is sufficient to significantly prolong abstinence and reduce drinking in
alcohol dependent patients.
162
Benzodiazepines
Benzodiazepines are not recommended for use beyond the withdrawal management
period (See Chapter 5).
Antidepressants
Despite an expensive research into the role of SSRIs in treatment of alcohol
dependence, there is limited evidence of their effectiveness (Johnson 2008). Their
use in treatment of comorbid depression and alcohol dependence is discussed in
Chapter 10.
Recommendation
7.11 A range of medications appear promising
agents in reducing alcohol relapse (such as
topiramate, gabapentin, baclofen, aripiprazole);
however, need further research and are not
recommended as first-line options at this stage.
7.12 Benzodiazepines and antidepressants are
not recommended as relapse prevention agents
in alcohol dependence.
Strength of
Level of
recommendation evidence
B
II
B
II
Integration with psychosocial treatments
Pharmacological treatment is considered to be significantly more successful when
the patient is receiving concurrent psychosocial treatment or structured medical
supervision. Referral to a specialist alcohol and drug counselling service may be
appropriate (see Chapter 6a: Psychological Interventions for more information).
Pharmacotherapy for relapse prevention should always be accompanied by close
follow-up by the prescribing doctor.
Increasing medication adherence
Alcohol pharmacotherapy has been shown to be more effective than placebo among
highly compliant participants (Volpicelli et al. 1997). However, adherence rates of
alcohol dependent patients are generally low.
Poor medication adherence may be due to: adverse side effects; stigma attached to
taking medication for an alcohol use disorder; no immediate reward for complying
with these pharmacotherapies; fears about the safety and side effects of the
medication (O'Malley 1998; Kranzler et al. 2000).
Adherence to pharmacotherapies may be assisted by:
1) Eliciting the patient’s thoughts and concerns about taking medication and
using cognitive restructuring techniques to help them change unhelpful or
maladaptive thoughts about taking medication
2) Providing the patient with a realistic view of the way in which the medication
can help, its side effects, and any risks associated with its use
163
3) Using motivational interviewing techniques to help the patient to identify their
personal costs and benefits of taking the medication
4) Providing the patient with some take-home reading material about the
medication
5) Tailoring the psychosocial intervention according to the patient’s drinking
goal: some studies show that coping skills training combined with naltrexone
is better for helping patients cope with lapses and relapses, whereas
supportive therapy is more effective in helping patients to maintain
abstinence.
6) Following up patients who miss appointments.
Compliance therapy, based on these cognitive-behavioural and motivational
interviewing techniques, has demonstrated effectiveness in increasing medication
compliance in alcohol dependent patients (Reid et al. 2005) (for the manual see
Teesson et al. 2003).
Adherence may also be a problem in patients that suffer cognitive impairment from
chronic drinking. Aids to enhance adherence in such instances include: family
supervision, medication calendars, special containers, dispensing systems,
reminders and follow-up monitoring from health professionals.
Recommendation
7.13 Medication compliance can be improved
with use of adherence enhancing strategies.
Strength of
Level of
recommendation evidence
B
Ia
Selecting medications for individual patients
Available evidence does not enable clear recommendations as to which medication
is best suited to different patients. Decision of choice of medication includes:
•
•
Available evidence: the general conclusions from various meta-analyses suggest
that acamprosate and disulfiram appear better suited to those seeking to achieve
complete abstinence from alcohol, whereas naltrexone seems better directed at
treatments where reduced or controlled drinking is the goal.
Individual patient factors: such as side effects, prior experience, treatment goals,
capacity to adhere to treatment regime, concomitant medical conditions.
Resource factors: the cost of some medications will be prohibitive for some patients
(e.g. topiramate, gabapentin, aripiprazole). Disulfiram treatment is best suited to
individuals with social supports (e.g. family) who will help supervise medication
adherence.
References
Addolorato, G, Leggio L, Ferrulli A et al. 2007, Effectiveness and safety of baclofen
for maintenance of alcohol abstinence in alcohol-dependent patients with liver
cirrhosis: randomised, double-blind controlled study. Lancet 370(9603): 19151922.
164
Anton, RF, Moak DH, Latham P et al. 2005, Naltrexone combined with either
cognitive behavioral or motivational enhancement therapy for alcohol
dependence. J Clin Psychopharmacol 25(4): 349-357.
Anton, RF, O'Malley SS, Ciraulo DA et al. 2006, Combined pharmacotherapies and
behavioral interventions for alcohol dependence: the COMBINE study: a
randomized controlled trial. JAMA 295(17): 2003-2017.
Anton, RF 2008, Naltrexone for the management of alcohol dependence. N Engl J
Med. 359: 715-721.
Anton, RF, Kranzler H, Breder C et al. 2008, A randomized, multicenter, double-blind,
placebo-controlled study of the efficacy and safety of aripiprazole for the
treatment of alcohol dependence. J Clin Psychopharmacol 28(1): 5-12.
Armeli, S, Feinn R, Tennen H et al. 2006, The effects of naltrexone on alcohol
consumption and affect reactivity to daily interpersonal events among heavy
drinkers. Exp Clin Psychopharmacology 14(2): 199-208.
Bergmark, A 2008 On treatment mechanisms--what can we learn from the COMBINE
study? Addiction 103(5): 703-705.
Bouza, C, Angeles M, Magro A et al. 2004, Efficacy and safety of naltrexone and
acamprosate in the treatment of alcohol dependence: a systematic review.
Addiction 99(7): 811-828.
Bühringer, G and T Pfeiffer-Gerschel 2008, Combine and match: the final blow for
large-scale black box randomized controlled trials. Addiction 103(5): 708-710.
Chick, J, Gough K, Falkowski W et al.1992, Disulfiram treatment of alcoholism. Br J
Psychiatry 161: 84–89.
Croop, RS, EB Faulkner and DF Labrida 1997, The safety profile of naltrexone in the
treatment of alcoholism. Results from a multicentre usage study. The
naltrexone usage study group. Arh. Gen. Psychiatry 54(12): 1130-1135.
De Sousa, A and A De Sousa 2005, An open randomised study comparing disulfiram
and acamprosate in the treatment of alcohol dependence. Alcohol Alcohol
40(6): 545-548.
de Wildt, W, Schippers GM, van den Brink W et al. 2002, Does psychological
treatment enhance the efficacy of acamprosate in patients with alcohol
problems? Alcohol Alcohol 37(4): 375-382.
Donovan, DM, Anton RF, Miller WR et al. 2008, Combined pharmacotherapies and
behavioral interventions for alcohol dependence (The COMBINE Study):
examination of posttreatment drinking outcomes. J Stud Alcohol Drugs 69(1):
5-13.
Evans, SM, Levin FR, Brooks DJ et al. 2007, A pilot double-blind treatment trial of
memantine for alcohol dependence. Alcohol Clin Exp Res 31(5): 775-782.
165
Farren, CK and SS O’Malley 1999, Occurrence and management of depression in
the context of naltrexone treatment of alcoholism Am J Psychiatry 156(8):
1258-1262.
Furieri, FA and E M Nakamura-Palacios 2007, "Gabapentin reduces alcohol
consumption and craving: a randomized, double-blind, placebo-controlled
trial." J Clin Psychiatry 68(11): 1691-1700.
Garbutt, JC, Kranzler HR, O'Malley SS et al. 2005, Efficacy and Tolerability of LongActing Injectable Naltrexone for Alcohol Dependence: A Randomized
Controlled Trial. JAMA 293(13):1617-1625.
Gonzales, RA and F Weiss 1998, Suppression of ethanol-reinforced behavior by
naltrexone is associated with attenuation of the ethanol-induced increase in
dialysate dopamine levels in the nucleus accumbens. J Neurosci 18: 16631671.
Gual, A and P Lehert 2001, Acamprosate during and after acute alcohol withdrawal:
a double-blind placebo-controlled study in Spain. Alcohol Alcohol 36: 413–
418.
Guardia, J, Segura L, Gonzalvo B et al. 2004, A double-blind, placebo-controlled
study of olanzapine in the treatment of alcohol-dependence disorder. Alcohol
Clin Exp Res 28(5):736-745.
Hammarberg, A, Wennberg P, Beck O et al. 2004, A comparison of two intensities of
psychosocial intervention for alcohol dependent patients treated with
acamprosate. Alcohol Alcohol 39(3): 251-255.
Heather, N 1989, Disulfiram treatment for alcoholism. BMJ 299(6697): 471-472.
Hughes, J and C Cook 1997, The efficacy of disulfiram: a review of outcome studies.
Addiction 92: 381–395.
Hutchison, KE, Ray L, Sandman E et al. 2006, The effect of olanzapine on craving
and alcohol consumption. Neuropsychopharmacol 31(6): 1310-1317.
Johnson, BA, Ait-Daoud N, Bowden CL et al. 2003 Oral topiramate for treatment of
alcohol dependence: a randomised controlled trial. Lancet 361(9370): 16771685.
Johnson, BA 2005, Recent advances in the development of treatments for alcohol
and cocaine dependence: focus on topiramate and other modulators of GABA
or glutamate function. CNS Drugs 19(10): 873-896.
Johnson, BA, Rosenthal N, Capece JA et al. 2007, Topiramate for treating alcohol
dependence: a randomized controlled trial. JAMA 298(14): 1641-1651.
Johnson, BA 2008, Update on neuropharmacological treatments for alcoholism:
Scientific basis and clinical findings. Biochem Pharmacol 75(1): 34-56.
166
Johnson, BA, Rosenthal N, Capece JA et al. 2008, Improvement of physical health
and quality of life of alcohol-dependent individuals with topiramate treatment:
US multisite randomized controlled trial. Arch Intern Med 168(11): 1188-1199.
Kampman KM, Pettinati HM, Lynch KG et al. 2009, Initiating acamprosate withindetoxification versus post-detoxification in the treatment of alcohol
dependence. Addict Behav 34(6-7): 581-586.
Kiefer, F, Jahn H, Tarnaske T et al. 2003, Comparing and combining naltrexone and
acamprosate in relapse prevention of alcoholism: a double-blind, placebocontrolled study. Arch Gen Psychiatry 60(1): 92-99.
Kiritze-Topor, P, Huas D, Rosenzweig C et al. 2004, A pragmatic trial of acamprosate
in the treatment of alcohol dependence in primary care. Alcohol Alcohol 39(6):
520-527.
Koob, G, Mason B, De Witte, P et al. 2002, Potential neuroprotective effects of
acamprosate. Alcohol Clin Exp Res 26: 586–592.
Kranzler, HR, V Modesto-Lowe and J Van Kirk 2000, Naltrexone vs. nefazodone for
treatment of alcohol dependence. A placebo-controlled trial.
Neuropsychopharmacol 22(5): 493-503.
Kranzler, HR and J Van Kirk 2001, Efficacy of naltrexone and acamprosate for
alcoholism treatment: a meta-analysis. Alcohol Clin Exp Res 25(9): 13351341.
Kranzler, HR, Armeli S, Feinn R et al. 2004, Targeted naltrexone treatment
moderates the relations between mood and drinking behavior among problem
drinkers. J Consult Clin Psychol 72(2): 317-327.
Kranzler, HR and A Gage 2008, Acamprosate Efficacy in Alcohol-Dependent
Patients: Summary of Results from Three Pivotal Trials. Am J Addictions
17(1): 70-76.
Laaksonen, E, Koski-Jannes A, Salaspuro M et al. 2008, A randomized, multicentre,
open-label, comparative trial of disulfiram, naltrexone and acamprosate in the
treatment of alcohol dependence. Alcohol Alcohol 43(1): 53-61.
Latt, NC, Jurd S, Houseman J et al. 2002, Naltrexone in alcohol dependence: a
randomised controlled trial of effectiveness in a standard clinical setting. Med
J Aust 176(11): 530-4.
Mann, K, P Lehert and MY Morgan 2004, The efficacy of acamprosate in the
maintenance of abstinence in alcohol-dependent individuals: Results of a
meta-analysis. Alcohol Clin Exp Res 28: 51–63.
Mann, K, Kiefer F, Spanagel R et al. 2008, Acamprosate: recent findings and future
research directions. Alcohol Clin Exp Res 32(7): 1105-1110.
Martinotti, G, Di Nicola M, Di Giannantonio M et al. 2008, Aripiprazole in the
treatment of patients with alcohol dependence: a double-blind, comparison
trial vs naltrexone. J Psychopharmacol 23(2): 123-9.
167
Mason, BJ 2003, Acamprosate and naltrexone treatment for alcohol dependence: an
evidence-based risk-benefits assessment. Eur Neuropsychopharmacol 13(6):
469-475.
Mason, BJ, Goodman AM, Chabac S et al. 2006, Effect of oral acamprosate on
abstinence in patients with alcohol dependence in a double-blind, placebocontrolled trial: the role of patient motivation. J Psych Res 40(5): 383-393.
Mendelson, JH, Ellingboe J, Keuhnle JC et al. 1978, Effects of naltrexone on mood
and neuroendocrine function in normal adult males. Psychoneuroendocrinol
3(3-4): 231-236.
MIMS 2008, MIMS Annual. CMPMedica. 32nd edition.
Miranda, R Jr, MacKillop J, Monti PM et al. 2008, Effects of Topiramate on Urge to
Drink and the Subjective Effects of Alcohol: A Preliminary Laboratory Study.
Alcohol Clin Exp Res 32(3): 489-497.
Morley, KC, Teesson M, Reid SC et al. 2006, Naltrexone versus acamprosate in the
treatment of alcohol dependence: a multi-centre, randomized, double-blind,
placebo-controlled trial. Addiction 101(10): 1451-1462.
O'Malley, S 1998, Naltrexone And Alcoholism Treatment: Treatment Improvement
Protocol (TIP). Rockville, MD.
O'Malley, SS, Garbutt JC, Gastfriend DR et al. 2007, Efficacy of extended-release
naltrexone in alcohol-dependent patients who are abstinent before treatment.
J Clin Psychopharmacol 27(5): 507-12.
O'Malley, SS, Krishnan-Sarin S, McKee SA et al. 2008, Dose-dependent reduction of
hazardous alcohol use in a placebo-controlled trial of naltrexone for smoking
cessation. Int J Neuropsychopharmacol 17: 1-9.
Petrakis, IL, C Nich C and E Ralevski 2006, Psychotic spectrum disorders and
alcohol abuse: a review of pharmacotherapeutic strategies and a report on
the effectiveness of naltrexone and disulfiram. Schizophr Bull 32(4): 644-54.
Pettinati, HM, Gastfriend DR, Dong Q et al. 2009, Effect of extended-release
naltrexone (XR-NTX) on quality of life in alcohol-dependent patients. Alcohol
Clin Exp Res 33(2): 350-356.
Raistrick, D, N Heather and C Godfrey 2006, Review of the effectiveness of
treatment for alcohol problems. London, UK, National Treatment Agency for
Drug Abuse.
Reid, SC, Teesson M, Sannibale C et al. 2005, The efficacy of compliance therapy in
pharmacotherapy for alcohol dependence: a randomized controlled trial. J
Stud Alcohol 66(6): 833-41.
Richardson K, Baillie A, Reid S et al. 2008, Do acamprosate or naltrexone have an
effect on daily drinking by reducing craving for alcohol? Addiction 103: 953959.
168
Roozen, H, de Waart R, van der Windt DA et al. 2006, A systematic review of the
effetiveness of nalterxone on the maintenance treatment of opioid and alcohol
dependence. Eur Neuropsychopharmacol 16: 311-323.
Rosner, S, Leucht S, Lehert P et al. 2008, Acamprosate supports abstinence,
Naltrexone prevents excessive drinking: evidence from a meta-analysis with
unreported outcomes. J Psychopharmacol 22(1): 11-23.
Sinclair, JD 2001 Evidence about the use of naltrexone and for different ways of
using it in the treatment of alcoholism. Alcohol Alcohol 36(1): 2-10.
Srisurapanont, M and N Jarusuraisin 2005, Opioid antagonists for alcohol
dependence. Cochrane Database of Systematic Reviews (2).
Staner, L, Boeijinga P, Danel T et al. 2006, Effects of acamprosate on sleep during
alcohol withdrawal: A double-blind placebo-controlled polysomnographic
study in alcohol-dependent subjects. Alcohol Clin Exp Res 30(9): 1492-1499.
Streeton, C and G Whelan 2001 Naltrexone, a relapse prevention maintenance
treatment of alcohol dependence: a meta-analysis of randomized controlled
trials. Alcohol Alcohol 36(6): 544-552.
Teesson, M, Sannibale C et al. 2003, Manual for Compliance Therapy in Alcohol
Pharmacotherapy. Sydney: National Drug and Alcohol Research Centre,
technical report number 157.
Tidey, JW, Monti PM, Rohsenow DJ et al. 2008, Moderators of Naltrexone's Effects
on Drinking, Urge, and Alcohol Effects in Non-Treatment-Seeking Heavy
Drinkers in the Natural Environment. Alcolol Clin Exp Res 32(1): 58-66.
Verheul, R, Lehert P, Geerlings PJ et al. 2005, Predictors of acamprosate efficacy:
results from a pooled analysis of seven European trials including 1485
alcohol-dependent patients. Psychopharmacology (Berl) 178(2-3): 167-173.
Volpicelli, JR, Rhines KC, Rhines JS et al. 1997, Naltrexone and alcohol
dependence. Role of subject compliance. Arch Gen Psychiatry 54(8): 737-42.
Weiss, RD, O'Malley SS, Hosking JD et al. 2008, Do patients with alcohol
dependence respond to placebo? Results from the COMBINE Study. J Stud
Alcohol Drugs 69(6): 878-84.
Wilde, MI and AJ Wagstaff 1997, Acamprosate. A review of its pharmacology and
clinical potential in the management of alcohol dependence after
detoxification. Drugs 53(6): 1038-1053.
Wright, TH and H Myrick 2006, Acamprosate: a new tool in the battle against alcohol
dependence. Neuropsychiatr Dis Treat 2(4): 445-453.
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Chapter 8
Self-help programs
This chapter discusses self-help approaches for patients, including Alcoholics
Anonymous and Smart Recovery®, and their families.
Recommendation
8.1 Long-term participation in Alcoholics
Anonymous can be an effective strategy to
maintain abstinence from alcohol for some
patients.
8.2 Assertive referral practices to Alcoholics
Anonymous increase participation and improve
outcome.
8.3 SMART Recovery® may be an effective
self-help alternative to Alcoholics Anonymous
for reducing alcohol consumption.
8.4 Self-help groups for families may provide
support for those affected by people with
alcohol dependence.
Strength of
Level of
recommendation evidence
B
II
A
I
D
IV
D
IV
Alcoholic Anonymous (AA)
What is AA?
Established in the US in 1935, over 100,000 groups exist worldwide with a total
membership of approximately two million (Alcoholics Anonymous 2001). AA is
founded on the assumption that shared experience and mutual support are
necessary for recovery from addiction (Alcoholics Anonymous 2001). In particular,
AA proposes that sobriety is only possible by first acknowledging one’s inability to
control the drinking habit, committing to a comprehensive overhaul of one’s identity
and lifestyle, and assisting new members in their recovery process (Alcoholics
Anonymous 2001). AA is the prototype for many self-help groups, with its core
program based around 12 steps (see Table 8.1) that promote increased selfawareness and heighten a sense of meaning in life. It is important to note that the
concept of God or a ‘higher power’ includes anything of a transpersonal nature that
can be drawn on for strength, including the AA group (Browne 1991; 1994).
How it works
AA is founded on the assumption that shared experience and mutual support are
necessary for recovery from addiction. In particular, AA proposes that sobriety is only
possible by first acknowledging one’s inability to control the drinking habit, committing
to a comprehensive overhaul of one’s identity and lifestyle, and assisting new
members in their recovery process. Several studies have also suggested that AAfacilitated abstinence is partly due to an increase in self-efficacy that arises from its
recovery.
170
Table 8.1: The 12 steps of Alcoholics Anonymous
1. We admitted we were powerless 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 searching and fearless moral inventory of ourselves.
5. Admitted to God, 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.
8. Made a list of all persons we had harmed, 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 them or others.
10. Continued to take personal inventory and when we were wrong promptly
admitted it.
11. Sought through prayer and meditation to improve our conscious contact with
God as we understood 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 to alcoholics and to practice these principles in all our
affairs.
Affiliation with Alcoholics Anonymous in addition to a structured aftercare program
may benefit patients, as the AA program strengthens the individual’s sense of selfefficacy (see Tonigan and Connors 2008) and provides a social network supportive
of abstinence (Bond et al. 2003; Litt et al. 2007; Vaillant, 2005).
Research also suggests that patients who attend AA as part of a structured aftercare
program in addition to individual outpatient sessions, and begin attendance early in
the treatment process, demonstrate better outcomes than individuals attending either
AA or treatment alone (Ito and Donovan 1990; Moos and Moos 2005; Moos Moos,
2006a; Moos and Moos 2006b; Ouimette et al.1998).
In Australia, about 1,700 groups are currently in operation in all states and territories
on a daily basis; for those unable to access physical groups, a number of groups are
available online (http://www.alcoholicsanonymous.org.au/). Based on the 12
traditions adopted by AA’s organisational body (Alcoholics Anonymous 1978), the
only requirement for membership is a desire to stop drinking, with meeting
attendance incurring no cost.
Evidence for AA effectiveness
Whilst literally hundreds of studies that examine the effectiveness of AA have been
conducted, it should be noted that the literature base is subject to several serious
limitations. Very few randomised controlled trials exist, most participants have had
exposure to other treatment programs in addition to AA, and naturalistic studies only
include participants who have elected to attend treatment (suggesting a higher
degree of motivation to change).
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Further, the majority of studies have limited the examination of AA participation to the
frequency and duration of meeting attendance, which fails to capture the breadth of
involvement in the program. Several recent studies have suggested that the level of
engagement with various aspects of AA are more important determinants of its
effectiveness than meeting attendance alone (Timko et al. 2006; Timko and
DeBenedetti 2007; Weiss et al. 2005). These studies have prompted a move away
from attendance-only measurement of AA involvement, with a growing literature base
adopting more refined measures of affiliation.
Despite these limitations, a substantial body of methodologically sound naturalistic
research suggests that AA is beneficial in promoting abstinence and facilitates the
maintenance of long-term sobriety (see Moos and Timko, 2008, for a review). In a 16
year longitudinal study, Moos and Moos (2006a; see also Moos and Moos, 2005 and
2006b) examined how the duration of various treatment approaches in the first year
of help-seeking behaviour influenced drinking outcomes. Whilst both professional
treatment and AA affiliation for a period of 27 weeks or more in the first year of
recovery were associated with better 16 year abstinence rates, the improvements
gained by professional treatment were mediated by AA attendance; only participants
who concurrently participated in AA showed better long-term outcomes. Further,
continued involvement in AA (yrs 2-8) was associated with a higher likelihood of
remission at each follow up point.
Due to the difficult nature of running randomised controlled trials into AA’s efficacy,
most RCTs have compared Twelve Step Facilitation Therapy (TSF) – a program
designed to foster increased commitment to AA as part of an extended care strategy
– to traditional treatment approaches (Nowinski et al.1995). To date, several studies
have demonstrated that TSF is as effective as CBT and Motivational Interviewing in
facilitating sobriety and is actually more effective than these modalities when
abstinence is the goal (Ouimette et al. 1997; Project MATCH Research Group 1997;
see Ries et al. 2008 for a review).
One Cochrane review undertook to compare AA and other 12-step programs to other
psychosocial interventions, looking for any evidence in reducing alcohol intake,
achieving abstinence, maintaining abstinence, improving the quality of life of affected
people and their families, and reducing alcohol associated accidents and health
problems (Ferri et al 2006). Their main findings were that no experimental studies
unequivocally demonstrated the effectiveness of AA or TSF approaches to reduce
alcohol dependence or problems. However this does not detract from the social
benefits of either of these approaches.
Additionally, Timko et al. (2006; see also Timko and DeBenedetti, 2007) have
demonstrated that therapists’ referral practices influence the depth of the client’s
participation in AA. Intensive referral (IR) practices include providing meeting
schedule and public transport timetables, finding a temporary sponsor and organising
for AA volunteers to accompany the client to meetings, and asking the client to use a
‘meeting journal’ (signed off by the AA meeting convener) to record attendance and
reactions to the meeting. Compared to the standard referral condition where only
minimal information about local AA meeting schedules was provided, participants
randomly allocated to the IR group were more fully involved in the AA program (e.g.,
service, sponsorship, ‘spiritual awakening’) and demonstrated significantly better
substance use outcomes over the ensuing 12 months.
Several studies have also suggested that AA-facilitated abstinence is partly due to an
increase in self-efficacy which arises from its recovery program (Project MATCH
172
Research Group, 1997; Tonigan and Connors 2008). AA provides a new social
network supportive of abstinence; for the patient who lacks such support in their
home environment, this aspect of AA involvement plays an important role in relapse
prevention (Bond et al. 2003; Litt et al. 2007; Vaillant, 2005).
Clinicians using Twelve-Step Facilitation therapy to encourage AA involvement
deepen their patients’ commitment to the use of AA as part of an extended care plan,
resulting in improved abstinence rates and greater treatment retention (Ouimette et
al. 1997; Nowinski et al. 1995; Project MATCH Research Group, 1997; Timko et al.
2006; Timko and DeBenedetti 2007).
A recent study by Walitzer et al. (2009) illustrates one method that was effective in
increasing AA involvement and abstinence from alcohol. A total of 169 alcoholic outpatients (57 women) were assigned randomly to one of three conditions: a directive
approach to facilitating AA, a motivational enhancement approach to facilitating AA or
treatment as usual, with no special emphasis on AA. The results showed that
participants in the directive condition for facilitating AA involvement reported more AA
meeting attendance, more evidence of active involvement in AA and a higher
percentage of days abstinent than people in the treatment-as-usual group. The
effect of the directive strategy on abstinent days was also somewhat influenced
through the involvement in AA. The motivational enhancement approach to
facilitating AA had no effect on the percentage of abstinent days or the percentage of
heavy drinking days.
For whom is AA appropriate?
A common misconception concerning 12 step groups is that members need to be
religious to benefit from the program. In a study of 3,018 male substance abusers,
individuals involved with AA demonstrated improved outcomes whether or not they
identified with a particular religious or spiritual belief system (Winzelberg and
Humphreys 1999). AA may also be appropriate for dually diagnosed clients, although
the efficacy of AA depends on the nature of the additional diagnosis (see Moos and
Timko 2008). In particular, depressed clients require more intensive outpatient
support, particularly in the early stages of aftercare treatment, to facilitate the social
elements of AA involvement (including finding an appropriate sponsor) and to reduce
the likelihood of dropping out of the program (Curran et al. 2002; Kelly et al. 2003;
Moos and Timko, 2008).
Clients who demonstrate a higher level of symptom severity are more likely to affiliate
with AA (Tonigan et al. 2006) and appear to benefit more as the amount of
involvement increases (Morgenstern et al, 2003).
Further, AA provides a new social network supportive of abstinence that assists in
promoting recovery. Litt et al. (2007) randomly assigned 210 participants to either a
network support (NS), NS and contingency management, or case management
experimental condition. In the NS conditions TSF was employed to promote AA
attendance, thereby increasing the number of social contacts supportive of
abstinence. As hypothesised, participants in the NS groups demonstrated heightened
attitudinal and behavioural support for abstinence at post-treatment and a 15 month
follow-up, with AA involvement correlated to improved drinking outcomes.
Participation in AA would thus also be appropriate for clients with limited social
support or a social network comprised of other substance users.
173
Referring to AA
A growing body of research is demonstrating that the use of TSF and ‘intensive AA
referral’ as part of outpatient treatment improves AA meeting attendance and
involvement, and is associated with better long-term outcomes (Nowinski et al. 1995;
Project MATCH Research Group 1997; Connors et al. 2001; Timko et al. 2006;
Timko and DeBenedetti 2007; see Rieset al. 2008 for a review).
TSF is designed to increase the client’s commitment to and involvement with AA; the
clinician works through the core features of the AA ideology (e.g., acceptance of the
inability to control the addiction) with the client over 12 sessions in 3 months. If
adopted as part of an extended care plan following inpatient treatment, TSF and AA
attendance can assist in helping the client through the initial 3 month ‘danger period’.
Intensive referral practices can also be used as a means of removing barriers to
aftercare participation, reducing the likelihood of treatment dropout, and increasing
the level of AA involvement. These include providing meeting schedule and public
transport timetables, organising for AA volunteers to accompany the client to
meetings, using a ‘meeting journal’ (signed off by the AA meeting convener) to record
attendance and reactions to the meeting, and organise for a temporary sponsor
(Timko et al. 2006; Timko and DeBenedetti 2007). As each AA group is different in
terms of its overall atmosphere, it is also recommended that clinicians attend several
meetings across different groups to assist in matching the client to a suitable
situation (Passetti and Godley 2008; Ries et al. 2008).
A longer duration of AA attendance in the first year of treatment and sustained
involvement across years 2-8 of a longitudinal follow-up study has been linked to
better long-term outcomes (Moos and Moos 2006a),
SMART Recovery®
An alternative to the AA self-help approach is Self Management and Recovery
Training (SMART), a not-for-profit mutual-aid group aimed at facilitating recovery
from any addictive behaviour. SMART Recovery® (originally the non-profit Rational
Recovery Self-Help Network) officially began in the US in 1994 and is a spin-off from
the original. At present approximately 16 online and 300 face-to-face meetings are
sponsored worldwide by SMART (http://www.smartrecovery.org/). Although relatively
new to Australia, over 50 groups are currently operating across most states on a
weekly basis (http://www.smartrecoveryaustralia.com.au/).
Founded on scientifically validated addiction treatment principles (at present, the
organisation adopts a Cognitive Behavioural Therapy (CBT) framework), SMART
Recovery® differs from AA in that it eliminates the focus on spirituality inherent to the
12-step approach (Li et al. 2000). Instead, it aims to tackle addiction through using a
four-point recovery program designed to enhance members’ motivation and teach
techniques that help to manage lifestyle and behavioural difficulties (Horvath and
Velten 2000) (see also http://www.smartrecovery.org/intro/index.htm). Skills training
involves exposure to (among other things) cost–benefit analyses, identifying and
rectifying irrational thoughts, and role-playing.
Although based on an empirically supported theoretical framework, SMART
Recovery® is a relatively young organisation, and very little research has assessed
174
its efficacy in comparison to other self-help groups. The only two studies that have
investigated SMART Recovery® and AA have done so with dual-diagnosis patients,
rather than alcohol-specific patients in aftercare (Penn and Brooks 2000; Brooks and
Penn 2003). The SMART (CBT) program was compared to 12-step program, with
112 patients alternately assigned to the two treatment conditions; 50 completed the
6-month treatment program. Assessments occurred at baseline, 3 months, and 6
months during treatment, and at 3- and 12-month follow-ups. Analyses were
conducted at the 3 month follow-up. The 12-step intervention was found to be more
effective in decreasing alcohol use and increasing social interactions; however, it was
associated with a worsening of medical problems, health status, employment status,
and psychiatric hospitalisation. Positive changes in health and employment were
associated with the SMART intervention, and alcohol use also decreased, although
not as much as in the 12-step group.
Whilst the 12-step intervention in these studies appeared to impact more positively
on alcohol-related outcomes than SMART, the findings indicate that SMART patients
exhibited greater improvements to overall health and employment. It is necessary,
however, to exercise caution in interpreting such findings, given that both AA and
SMART Recovery® groups operate as self-help rather than as specialised inpatient
treatment programs.
Self-Help for Families
Family therapy is a viable treatment for the patient and major changes often have to
be made in the family to support the patient’s recovery (Higgins 1998). According to
Higgins, the interpersonal dynamics of the family may support and maintain the
addictive behaviour; this is why addressing the family unit as a whole is more
productive than changing the addict’s behaviour in isolation. This change has the
potential to be perceived as a threat, destabilising the family unit.
Again, there is little empirical evidence in the form of randomised controlled trials to
demonstrate the benefit of family involvement on treatment for alcohol use disorders.
However, Barnett (2003) conducted an extensive review of current research,
literature, and internet-based resources. The conclusion of her article was that
alcohol dependency flourishes within the social context of the family system and is
one of the leading causes of family dysfunction. She stresses that, therefore,
understanding the impact of alcoholism on the family and being familiar with
resources and referrals is critical to the management of treatment for the patient and
family. It is imperative that the family be recognised as the unit of treatment and be
included in the treatment plan. Barnett also states that involving the patient and the
family in the treatment for alcohol problems is validated and supported by the
principles of family systems theory (Lipps 1999).
175
References
Alcoholics Anonymous 1978, Twelve steps and twelve traditions. New York:
Alcoholics Anonymous World Services.
Alcoholics Anonymous 2001, Alcoholics Anonymous. New York: Alcoholics
Anonymous World Services.
Barnett, MA 2003, All in the family: resources and referrals for alcoholism. J Am Acad
Nurse Pract 1510: 467-472.
Bond, J, Kaskutas LA and C Weisner 2003, The persistent influence of social
networks and Alcoholics Anonymous on abstinence. J Stud Alcohol 644: 579588.
Brooks, AJ and PE Penn 2003, Comparing treatments for dual diagnosis: Twelvestep and Self-Management And Recovery Training. Am J Drug Alc Abuse
292: 359-383.
Browne, BR 1991, The selective adaptation of the Alcoholics Anonymous program by
Gamblers Anonymous. J Gambl Stud 73: 187-206.
Browne, BR 1994, Really not God: Secularization and pragmatism in Gamblers
Anonymous. J Gambl Stud 103: 247-260.
Connors, GJ, JS Tonigan and WR Miller 2001, A longitudinal model of intake
symptomatology, AA participation and outcome: retrospective study of the
project MATCH outpatient and aftercare samples. J Stud Alcohol 626: 817825.
Curran, GM, Kirchner JE, Worley M et al. 2002, Depressive symptomatology and
early attrition from intensive outpatient substance use treatment. J Behav
Health Serv Res 292: 138-43.
Ferri, M, L Amato and M Davoli 2006, Alcoholics Anonymous and other 12-step
programmes for alcohol dependence. Cochrane Database Syst Rev 3:
CD005032.
Higgins, MP 1998, Alcoholic families, the crisis of early recovery. Fam Ther 253: 203219.
Horvath, AT and E Velten 2000 SMART Recovery®: Addiction recovery support from
a Cognitive-Behavioral perspective. J Rational-Emotive and CognitiveBehavioral Ther 183: 181-191.
Ito, JR and DM Donovan 1990, Predicting drinking outcome: Demography, chronicity,
coping, and aftercare. Addict Behav 156: 553-559.
Kelly, JF, JD McKellar and R Moos 2003, Major depression in patients with
substance use disorders: Relationship to 12-Step self-help involvement and
substance use outcomes. Addiction 984: 499-508.
176
Li, EC, C Feifer and M Strohm 2000, A pilot study: Locus of control and spiritual
beliefs in Alcoholics Anonymous and SMART Recovery members. Addict
Behav 254: 633-640.
Litt, MD, Kadden RM, Kabela-Cormier E et al. 2007, Changing network support for
drinking: Initial findings from the Network Support Project. J Consult Clin
Psychol 754: 542-555.
Lipps, AJ 1999. Family therapy in the treatment of alcohol-related problems: A review
of behavioral family therapy, family systems therapy and ttreatment matching
research. Alcohol Treat Q, 173: 13-23.
Moos, RH and BS Moos 2005, Paths of entry into Alcoholics Anonymous:
Consequences for participation and remission. Alcohol Clin Exper Res 2910:
1858-1868.
Moos, RH and BS Moos 2006a. Participation in Treatment and Alcoholics
Anonymous: A 16-Year Follow-Up of Initially Untreated Individuals. J Clin
Psychol, 626: 735-750.
Moos, RH and BS Moos 2006b, Treated and untreated individuals with alcohol use
disorders: Rates and predictors of remission and relapse. Int J Clin Health
Psychol 63: 513-526.
Moos, RH and C Timko 2008, Outcome research on 12-step and other self-help
programs. In: Galanter, M and HD Kleber (eds) The American Psychiatric
Publishing Ttextbook of Substance Abuse Ttreatment 4th ed., American
Psychiatric Publishing.
Morgenstern, J, Bux DA, Labouvie E et al. 2003, Examining mechanisms of action in
12-Step community outpatient treatment. Drug Alcohol Depend 723: 237-247.
Nowinski, J, S Baker and K Carroll 1995, Twelve Step Facilitation Therapy Manual.
Rockville, MD: National Institute on Alcohol Abuse and Alcoholism.
Ouimette, PC, JW Finney and RH Moos 1997, Twelve-step and cognitive-behavioral
treatment for substance abuse: A comparison of treatment effectiveness. J
Consult Clin Psychol 652: 230-240.
Ouimette, PC, RH Moos and JW Finney 1998, Influence of outpatient treatment and
12-step group involvement on one-year substance abuse treatment
outcomes. J Stud Alcohol 595: 513-522.
Passetti, LL and SH Godley 2008, Adolescent substance abuse treatment: clinicians
self-help meeting referral practices and adolescent attendance rates. J
Psychoactive Drugs 401: 29-40.
Penn, PE and AJ Brooks 2000, Five years, twelve steps, and REBT in the treatment
of dual diagnosis. J Rational-Emotive and Cognitive-Behavioral Ther 184: 97208.
177
Project MATCH Research Group 1997, Matching alcoholism treatments to client
heterogeneity: Project MATCH Post-treatment drinking outcomes. J Stud
Alcohol 581, 7-29.
Ries, RK, M Galanter and JS Tonigan 2008, Twelve-step facilitation: An adaptation
for psychiatric practitioners and patients. In: Galanter M and HD Kleber
(eds).The American Psychiatric Publishing Textbook of Substance Abuse
treatment 4th ed., American Psychiatric Publishing.
Timko, C and A Debenedetti 2007, A randomized controlled trial of intensive referral
to 12-step self-help groups: One-year outcomes. Drug Alcohol Depend 902-3:
270-279.
Timko, C, A DeBenedetti and R Billow 2006, Intensive referral to 12-Step self-help
groups and 6-month substance use disorder outcomes. Addiction 1015: 678688.
Tonigan, JS, MP Bogenschutz and WR Miller 2006, Is alcoholism typology a
predictor of both Alcoholics Anonymous affiliation and disaffiliation after
treatment? J Subst Abuse Treat 304: 323-330.
Tonigan, JS and GJ Connors 2008, Psychological mechanisms in Alcoholics
Anonymous. In: Galanter, M and HD Kleber (eds).The American Psychiatric
Publishing Textbook of Substance Abuse Treatment 4th ed. American
Psychiatric Publishing.
Vaillant, GE 2005, Alcoholics Anonymous: Cult or cure? Aust N Z J Psychiatry 396:
431-436.
Walitzer, KS, KH Dermen and C Barrick 2009, Facilitating involvement in Alcoholics
Anonymous during out-patient treatment: a randomized clinical trial. Addiction
1043: 391-401.
Weiss, RD, Griffin ML, Gallop RJ et al. 2005, The effect of 12-step self-help group
attendance and participation on drug use outcomes among cocainedependent patients. Drug Alcohol Depend 772: 177-184.
Winzelberg, A and K Humphreys 1999, Should patients' religiosity influence
clinicians' referral to 12-step self-help groups? Evidence from a study of 3,018
male substance abuse patients. J Consult Clin Psychol 675: 790-794.
178
Chapter 9
Specific populations
This chapter reviews management of alcohol problems in adolescents and young
people, pregnant and breastfeeding women, Aboriginal and Torres Strait Islander
Australians as well as people from other cultures, older people and cognitively
impaired patients.
Adolescents and Youth
Recommendation
9.1 NHMRC guidelines recommend that not
drinking alcohol is the safest option for children
and young people under 18 years of age.
9.2 Screening and brief intervention for
tobacco, alcohol and other drug use should
occur routinely. Binge drinking and polydrug
use are common among adolescent problem
drinkers.
9.3 A broad medical and psychosocial history
is needed to work effectively with young
people.
9.4 Engagement and therapeutic relationships
require an understanding of adolescent
development and a cognitively and
developmentally appropriate approach.
9.5 Brief interventions may suit some young
people drinking excessively and/or
experiencing alcohol-related harms.
9.6 Motivational interviewing, cognitive
behavioural and family therapies have been
shown to be of benefit in reducing alcohol and
other drug use and related harms.
9.7 Limited evidence exists on the role of
pharmacotherapies in reducing alcohol use in
adolescents.
9.8 Adolescent drinkers may experience a
range of psychosocial crises. In these cases,
outreach and crisis interventions should be
engaged.
9.9 Mental health disorders, including
depression, suicidal ideation, anxiety, sexual
abuse and antisocial behavior, are common in
young people with alcohol and other drug
problems, and should be addressed in the
treatment plan.
Strength of
Level of
recommendation evidence
D
IV
D
IV
S
S
A
Ia
A
Ia
B
II
D
IV
D
IV
179
Introduction
There has been considerable concern shown in the media, both in Australia and in
the UK and Europe over youth drinking, especially binge drinking. However, as latest
figures show, it is the young adult age group in Australia that has increased drinking
at levels of risk for long-term harm, not the teenage group (Australian Institute of
Health and Welfare 2008). More evidence for underage drinking is shown in data
from the European School Survey Project, suggesting that young people in the UK
are among the heaviest drinkers in the world (Hibell et al. 2004).
The adolescent years are a period for experimentation and socialisation with peers,
which may include engaging in high-risk substance abuse behaviours.
The 2002 national survey on the use of alcohol by Australian secondary school
students (White and Hayman 2004) found that experience with alcohol was high
among secondary school students. Alcohol consumption became more common as
age increased:
•
•
•
by the age of 14, around 90 per cent of students had tried alcohol;
by the age of 17, around 70 per cent of students had consumed alcohol in the
month prior to the survey; and
the proportion of students drinking in the week prior to the survey increased with
age, from 19 per cent of 12-year-olds to reach a peak of 50 per cent among 17year-olds.
Experimentation is much more common than progression to regular use. Binge
drinking and deliberate drinking to become intoxicated is common, with 8.8% percent
of those aged 14-19 years and 16% percent of those aged 20-29 years drinking at
risky or high risk levels for long-term harm (Australian Institute of Health and Welfare
2008). This rate has fallen in Australia in the 14-19 year age group, compared to
2001 figures, but has risen in the 20-29 year age group (see Chapter 2).
Rates of drinking above NHMRC 2001 guideline levels among 14–19 year-olds are
similar to the rates for the general population — about 9 per cent for alcoholrelated
disease risk (longterm harm) and 39 per cent for accident and injury risk (shortterm
harm) (Australian Institute of Health and Welfare 2008). People in the 20–29 year
age group show the riskiest drinking profile. About 60 per cent of this group drink
above NHMRC 2001 guideline levels for accidents and injuries and about 16 per cent
drink above NHMRC 2001 guideline levels for alcoholrelated diseases (Australian
Institute of Health and Welfare 2008).
Among school students aged 16–17 years who report drinking in the past week,
there has been a slight increase in numbers drinking above NHMRC 2001 guideline
levels for accidents and injuries (White and Hayman 2004). This may be because of
changes in the type of alcohol young people are drinking. The 2002 survey found that
among male adolescent drinkers, the proportion consuming beer decreased while
consumption of spirits, in either their un-premixed or their premixed form, increased.
Among adolescent female drinkers, the proportion drinking premixed spirits as
opposed to un-premixed spirits increased significantly (White and Hayman 2004).
180
Polysubstance use is common among young people and it is therefore important to
screen for use of tobacco and other drugs in addition to alcohol. Around 16% of 1419 year olds smoke cigarettes (Australian Institute of Health and Welfare 2005).
Uptake of cannabis use usually peaks around the age of 16-17 years. Around 25% of
14-19 year olds and 54% of 20-29 year olds report using cannabis in their lifetime.
Weekly use occurs in 20% of 14 to 29 year olds and daily use in 10-15% (Australian
Institute of Health and Welfare 2005).
Excessive alcohol use in adolescence is also associated with a wide range of other
co-existing problems, including difficulty with relationships (especially with parents),
homelessness, poor school performance, low employment prospects. Early alcohol
use also increases the likelihood of alcohol abuse and alcohol dependence
continuing into adulthood; the risk highest appears associated with heavy alcohol
consumption before 16 years. Early intervention with adolescents at risk of alcohol
problems is therefore very important. The NHMRC Guidlelines 2009 recommend that
children and young people under the age of 18 not drink alcohol at all (see Guideline
3 in Chapter 2)
Assessment
Working effectively with young people experiencing difficulties with alcohol requires
the establishment of good rapport. Barriers to effective consultation with adolescents
have been extensively described in the past two decades and can be classified into
four broad categories: availability, accessibility, acceptability and equity of health
services (Tylee et al. 2007). Concerns about confidentiality has been identified to be
a particularly significant barrier to seeking professional assistance among young
people (Sanci et al. 2005). A non-judgemental approach is needed that encourages
the young person to be honest about reporting ongoing difficulties with alcohol.
A broad medical and psychosocial history is needed to work effectively with young
people. A familial history of heavy alcohol and drug use also impacts on adolescents.
Social and environmental factors, such as being exposed to a family culture that
accepts heavy drinking, may contribute to development of dependence in the
children of heavy drinkers. DSM-IV criteria for alcohol use disorders have limitations
when used with adolescents (Martin and Winters 1998).
‘Problem drinking’ in young people is variably defined and may refer to quantity of
alcohol consumed, frequency of drinking and/or to adverse outcomes attributable to
drinking. Adolescent alcohol problems commonly constitute recurrent binge drinking,
and related short term adverse consequences, including trauma, assaults and
memory loss. Adverse outcomes related to alcohol consumption in young people are
highly correlated to male gender and conduct disorder (Toumbourou et al. 2007).
A psychosocial history includes information about the social, cultural, educational and
vocational background of the adolescent. There are different acronyms such as
HEADSS that provide a framework for taking a broad psychosocial history from
adolescents (see Chapter 9 of the Guidelines for the Treatment of Alcohol Problems).
What is the difference between adult and adolescent drinking?
Adolescents tend to take more than one drug at a time (polydrug use), are more
inclined to binge drink, and are at a time of rapid social and physical change in their
lives. Excessive alcohol or drug use in adolescence is implicated in a wider range of
co-existing life problems such as homelessness, poor performance at school, difficult
181
parental relationships and low employment prospects. In addition, regular heavy
alcohol or other drug use frequently inhibits adolescent development, especially in
impairing cognitive maturation and reducing educational achievement (Bonomo et al.
2004). Early alcohol use also increases the likelihood of adult heavy drinking and
dependence, with the risk highest if drinking begins before 16 years (Pitkanen et al.
2005; Bonomo et al. 2004). This provides motives for the importance of screening
and early intervention with adolescents at risk before problems occur.
Treatment
Engaging adolescents and families in treatment
Engaging adolescents in treatment is a critical issue.The principles are similar to
treatment of other chronic disorders in young people. Establishment of good rapport
is required (see Section on Assessment above).
Engagement and therapeutic relationships require an understanding of adolescent
development and a cognitively and developmentally appropriate approach. Young
people are influenced by the ‘here and now’ rather than future benefits of changing
current drinking patterns. It is also important for health professionals to remember
that young people are more interested in achieving the goals of adolescence rather
than focusing on improving their health. Given this, treatment goals need to be
framed as ‘relevant’ to young people. Approaches include examination of how
alcohol affects their appearance, peer-reputation, ability to socialize, recreational,
educational, employment or sporting achievements, or impact upon finances. These
discussions need to be delivered by the health professional at a level that is
developmentally and cognitively appropriate. Working with the young person to
develop concrete short term goals (weeks to months) is recommended.
Encouraging the young person to participate in negotiation of treatment plans
facilitates engagement in treatment and empowers change (Sawyer et al. 2007). In
some cases, disengagement with family may have occurred as a result of heavy
drinking and other drug use. Families are an integral part of the adolescent’s world
and it is therefore important to try to assist the young person to re-build the
connection. Depending on the individual circumstance this may be through mediation
buy the health professional or more formally with family counselors.
In cases where adolescents are not engaging well with alcohol or drug services,
specific outreaching and proactive services that cater appropriately for their
developmental stage and incorporate a consideration of their cultural background,
lifestyle and in many cases their family are required.
Psychosocial treatments
Early intervention for alcohol problems in young people is important. Alcohol and
other substance use intereferes with normal adolescent brain development, and
neurodevelopment, especially in regions linked to regulation of behaviour and
emotion is not complete until early adulthood (ref). Once young people have
developed an alcohol use disorder, abstinence appears an unlikely outcome of
treatment (Cornelius et al. 2003; Winters et al. 2000).
Brief interventions may suit some young people drinking excessively and/or
experiencing alcohol-related harms. Brief interventions, motivational interviewing,
cognitive behavioural therapies and family therapies in general have been shown to
182
be of benefit, especially in conferring improved knowledge about alcohol related
harms and at least a short term reduction in alcohol and other drug use (Toumbourou
et al. 2007; Grella et al. 2001; Winters et al. 2000; Spooner et al. 2001).
Certain factors pre-treatment predict outcomes. A poorer prognosis is associated
with more severe alcohol problems at the outset (Anderson et al. 2007) and with
other drug use problems (Chung et al. 2003). Poor psychosocial functioning pretreatment and lack of longer term engagement in health services are also associated
with negative outcomes (Chung et al. 2003). Abstinent peers in a young person’s
social network, on the other hand, increase the odds of remaining abstinent four-fold
(Anderson et al. 2007).
Few differences in outcome have been found when comparing treatment settings and
types of adolescents (Winters et al. 2000; Spooner et al. 2001; Rice et al 1993),
although as with adult services, longer treatment retention is associated with better
outcomes (Winters et al. 2000). Studies of longer term outcomes from inpatient and
outpatient treatment settings are less readily available.
Many of the research studies on adolescents have examined treatment impact on
substance abuse generally, not specifically alcohol, and the previous literature review
included papers about other substances for this reason. We include only the studies
on alcohol here.
Psychosocial treatments: Earlier studies
A Cochrane Review was published in 2002 (Foxcroft et al. 2008) which showed very
mixed evidence for interventions for alcohol misuse with young people. Two of the
US studies included in that review were Monti et al. (1999) and Marlatt et al. (1998);
in these, brief and motivational interventions appeared to be effective for adolescent
heavy drinkers. Monti and colleagues (1999) found that a brief intervention, used with
older adolescents in an emergency department setting after an alcohol-related event,
resulted in fewer alcohol-related injuries and reduced the likelihood to drink-drive
compared with adolescents who received standard hospital care (Monti et al. 1999).
Similar results were obtained by Marlatt et al (1998 in a high school setting.
In addition, a study not mentioned in the Cochrane review, (Borsari and Carey 2000),
found that college students who were binge drinkers and received a single-session of
motivational interviewing exhibited significant reductions on the number of drinks
consumed per week and the number of times drinking alcohol was recorded in the
month. Also in the month to follow up, the frequency of binge drinking fell significantly
on number of drinks consumed per week, the number of times drinking alcohol and
the frequency of binge drinking when compared to a no-treatment group. All these
trials had small sample sizes (from 60 to 94 participants).
Psychosocial treatments: Recent studies
During the past decade, much progress has been made in treating adolescent
alcohol use disorders with evidenced-based modalities developed specifically for
adolescents (Deas 2008). This review by Deas discusses psychosocial treatments
such as family-based interventions, motivational interviewing, behavioural therapy
and cognitive-behavioural therapy as well as the limited pharmacotherapy studies
available. All of the studies used assessment tools validated for use in adolescent
populations. The authors’ conclusions are that, overall, great strides have been made
183
in the area of adolescent alcohol treatment, and the treatment modalities used have
more than adequate potential for replication.
There is little recent rigorous evidence on youth-oriented interventions from the UK or
Europe (McArdle 2008). However, we found some recent work from the Netherlands,
Australia and the USA.
A pilot randomised controlled trial in Australia (Bailey et al. 2004) aimed to identify
whether a brief motivational interviewing and cognitive behavioural-based alcohol
intervention group program was feasible with young people at risk of developing a
problem with alcohol, and to assess the short-term effectiveness of the intervention.
Sample size was 34 and the follow-up intervals were at 1 and 2 months posttreatment. The intervention took place over 4 weeks of group sessions. The
Intervention group showed an increase in readiness to reduce their alcohol
consumption and reduced their frequency of drinking both at post-treatment (4 weeks
after randomisation) and the 1-month follow-up assessment, while the control group
reported increased drinking at the 2-month follow-up assessment. The control group
also increased hazardous drinking and frequency of binge drinking compared to the
Intervention group. These results provide preliminary evidence for the effectiveness
of the program in training young people to set limits on alcohol consumption and
reduce consumption, and also to increase their awareness of safe drinking levels and
the effects of alcohol abuse.
Four US studies were conducted in different settings; one in the course of a family
practice visit (Boekeloo et al. 2004) and three in emergency departments (Spirito et
al. 2004) (Maio et al. 2005) (Monti et al. 2007). The Boekeloo trial aimed to
determine whether office-based interventions changed adolescents' alcohol beliefs
and alcohol use, with largely contradictory findings. Participants were 409 12- to 17year-olds seeing primary care providers for general check-ups, randomised to 3
groups. Most (79%) were African American, 44% male; 16% currently drank. All
received a randomised audio program; usual care group (I) listened to self-selected
music, group II had an audio program about alcohol with alcohol self-assessment just
prior to check-up and group III had the same program with an additional brochure. At
exit interview, Groups II and III reported they knew that less alcohol was needed for
impaired thinking and also reported a greater intent to drink alcohol in the next 3
months than Group I. At 6 months, Group III reported more resistance to peer
pressure to drink, and Groups II and III reported more bingeing than Group I. At 1year follow-up Groups II and III reported more bingeing in the last 3 months than
Group I; Group II reported more drinking in the last 30 days and in the last 3 months
than Group I. The authors’ conclusions are that brief office-based interventions were
ineffective in reducing alcohol use but may increase adolescent reporting of alcohol
use.
Conflicting evidence is provided by three emergency department studies with
adolescents; however the motivation may have been different between the
participants. One trial (Spirito et al. 2004) tested whether a brief motivational
interview (MI) would reduce alcohol-related consequences and use among
adolescents treated after an alcohol-related event. Patients aged 13 to 17 years
(N = 152) with a positive blood alcohol concentration were recruited in the ED and
randomly assigned to either MI or standard care. Both conditions resulted in reduced
quantity of drinking during the 12-month follow-up; alcohol-related negative
consequences were relatively low at baseline and remained low at follow-up.
Adolescents who screened positive for problematic alcohol use at baseline reported
significantly more improvement, decreasing both the average number of drinking
184
days per month and the frequency of high-volume drinking if they had received MI.
The authors conclude that that brief interventions are recommended for adolescents
who present to an ED with an alcohol-related event and report problematic alcohol
use. (Level Ib evidence)
The other, also a randomised controlled trial (Maio et al. 2005) used a laptop
computer to deliver both the screening and the intervention. It also had a much larger
number of subjects (n=580) aged 14-18 years who attended ED with a minor injury.
Main outcome measures were Alcohol Misuse Index (AMIDX) and binge-drinking
episodes. Follow-up occurred by telephone at 3 and 12 months. Overall, there were
no significant effects on alcohol misuse or binge drinking (effect size 0.04). Subgroup
analysis suggested that the intervention may have had an effect among subjects who
had experienced drinking and driving (5% of the sample). The conclusions of the
study were that the intervention was ineffective in decreasing alcohol misuse.
Another trial in ED was conducted by Monti et al (2007) with 198 18-24-year-old
patients who were either alcohol positive upon hospital admission or met screening
criteria for alcohol problems. Participants were assigned randomly to receive a onesession motivational intervention (MI) that included personalised feedback, or the
personalised feedback report only (FO). All received telephone contact at 1 month
and 3 months. Six months post-intervention MI participants drank on fewer days, had
fewer heavy drinking days and drank fewer drinks per week in the past month than
did FO patients. These effects were maintained at 12 months. Twice as many MI
participants as FO participants reliably reduced their volume of alcohol consumption
from baseline to 12 months. Reductions in alcohol-related injuries and driving
offences and increases in alcohol treatment-seeking were observed across both
groups at both follow-ups with no differences between conditions. This study
provides new data supporting the potential of motivational intervention to reduce
alcohol consumption among high-risk youth.
Thush et al (2007) investigated the effectiveness of a targeted intervention program
aimed at 107 at-risk adolescents in a randomised clinical trial in schools. This
program combined intervention methods which have been proven effective in
reducing drinking in young adults, such as an expectancy challenge, cognitive
behavioural skill training and brief motivational feedback. The intervention contained
the new element of discussing biological, cognitive and social risk factors for
developing alcohol problems; outcome measures were cognitive determinants of
drinking behaviour, moderating alcohol use and the development of alcohol-related
problems. The intervention was effective in changing several of the targeted cognitive
determinants; however, despite this, the intervention group did not show a significant
difference in decrease of drinking at posttest compared with the control group. These
results did not yield support for any differential long term effects of the intervention.
The authors therefore conclude that although the intervention successfully changed
important cognitive determinants of drinking, a more intensive intervention is needed
to change subsequent drinking behaviour.
These studies suggest that an alcohol-related injury that results in presentation to the
acute hospital context provides more impetus for reducing drinking than does
attendance at a family practice or participation in school-based program; however
further research is required to confirm this.
Pharmacotherapies
185
The evidence base for pharmacotherapy for alcohol use disorders in young people
remains limited (Deas 2008). Naltrexone has been confined to case reports (Lifrak et
al. 1997; Wold et al. 1997) and two small open label studies (Deas et al.2005;
Leeman et al. 2008). Acamprosate was examined in one small RCT (Niederhofer et
al. 2003). These studies demonstrate short term benefits; however, longer term
outcomes were not described.
Addressing comorbidity
Treatment of young people with alcohol problems needs to include screening for a
history of sexual abuse and screening and management of common mental health
disorders especially depression, suicidal ideation, anxiety, and antisocial behavior.
Reduced substance use has been noted when co-morbid mental conditions are
appropriately treated (Toumbourou et al. 2007; Roberts 2007).
Pregnant and breastfeeding women
Recommendation
9.10 Women who are or may become
pregnant should be advised of new NHMRC
guidelines that recommend abstinence.
Clinicians who provide advice to pregnant
women should familiarise themselves with the
risk analysis described in those guidelines.
Women who drink alcohol sparingly (less than
one standard drink per drinking day without
intoxication) may be reassured that there is no
consistent evidence this is harmful.
9.11 Breastfeeding women should be advised
of current NHMRC guidelines that recommend
abstinence from drinking. If a woman wishes to
drink, it is recommended that she breastfeeds
before drinking. Otherwise, wait until the blood
alcohol returns to zero (one hour per standard
drink consumed) before resuming
breastfeeding. It is not necessary to express or
discard milk before this time.
9.12 Brief interventions are recommended for
use during pregnancy, including the partner
where relevant. Follow-up evaluation of
response to the intervention is important.
9.13 If a woman presents intoxicated during
pregnancy, hospital admission is
recommended to assess fetal safety, maternal
safety, and for comprehensive assessment
and care planning.
9.14 Alcohol withdrawal during pregnancy
should be managed in a general hospital,
ideally in a high-risk maternity unit in
Strength of
Level of
recommendation evidence
S
S
B
II
D
IV
S
186
consultation with a specialist drugs-inpregnancy team. Diazepam may be given as
needed to control withdrawal. Nutritional
intervention should be initiated, including
parenteral thiamine, folate replacement and
assessment for other supplementation in
hospital.
9.15 Women who present during pregnancy
with serious alcohol (and/or other drug)
problems should be admitted to an appropriate
hospital unit for stabilisation, comprehensive
assessment and care planning.
9.16 Assertive follow-up is recommended for
antenatal care, substance misuse treatment,
and welfare support and child protection.
9.17 Pharmacotherapy to maintain abstinence
from alcohol cannot be recommended during
pregnancy due to insufficient safety data.
9.18 Assertive antenatal care, including
monitoring of fetal growth and health, is
recommended.
9.19 Management of infants with neonatal
alcohol withdrawal should be undertaken in
consultation with a specialist unit.
9.20 Infants born to women who have
consumed alcohol regularly during pregnancy
should be carefully assessed for fetal alcohol
spectrum disorders by a pediatrician aware of
the maternal history, with further management
directed by the appropriate experts.
9.21 Assessment of the family unit is an
essential aspect of managing substance use in
women. Intervention should be directed to the
whole family unit to reduce consumption of
alcohol.
9.22 Indigenous women should be offered
referral to culturally appropriate clinical
services.
9.23 Comprehensive mental health
assessment is an essential component of an
integrated care plan for pregnant women with
alcohol problems.
S
S
S
S
S
S
S
D
IV
S
Introduction
The negative effects of alcohol on the developing foetus were described about 40
years ago, with the first articles published in the 1970’s (Jones and Smith 1973;
Ouellette et al. 1977; Cooper 1978). Jones was the first to coin the term foetal
alcohol syndrome (FAS). More recently, the designation foetal alcohol spectrum
disorder (FASD) has emerged, which characterises a spectrum of problems (Sokol et
al. 2003). Characteristics include unusual facial features and poor physical, cognitive
and behavioural outcomes; in addition, alcohol exposure is a strong predictor of
premature or preterm birth and low birth weight for gestational age. Heavy drinking
187
(defined in one study as 1 or more drinks per day) was associated with a 5-fold
increase in the likelihood of low birth weight (Jaddoe et al. 2007).
Therefore it is imperative to advise all pregnant women, or those planning a
pregnancy, to avoid drinking alcohol altogether. While low levels of drinking are not
always necessarily associated with FAS, it seems sensible to advise every woman to
abstain. Women who are or may become pregnant and should be advised of new
NHMRC guidelines that recommend abstinence. Women who drink alcohol sparingly
(less than one standard drink per drinking day without intoxication) may be reassured
that there is no consistent evidence this is harmful. Similarly, breastfeeding women
should be adviced that abstinence is recommended.
Brief interventions are recommended for use during pregnancy, including the partner
where relevant. Follow-up evaluation of response to the intervention is important.
Brief interventions in pregnancy: Randomised controlled trials
A subanalysis of data from ProjectTrEAT (Fleming et al. 2002) was carried out to
evaluate the results of the intervention on the 205 women at 48-month follow-up
(Manwell et al. 2000). A significant treatment effect was found in reducing both 7 day
alcohol use (p = 0.0039) and binge drinking episodes (p = 0.0021) over the 48 month
follow-up period. Women in the experimental group who became pregnant during the
follow-up period had the most dramatic decreases in alcohol use.
Another trial of a brief intervention with 304 pregnant women also studied the effect
of including the woman’s partner in the single intervention session, given by a nurse
practitioner or the doctor (Chang et al. 2005). All women had screened positive on
the T-ACE questionnaire. Fewer than 20% of participants (median 11.5 weeks of
gestation) were abstinent at study enrolment, averaging more than 1.5 drinks per
episode. Nearly 30% had 2 or more drinks at a time while pregnant. Prenatal alcohol
use declined in both the treatment and control groups, based on a 95% follow-up
rate. Factors associated with increased prenatal alcohol use after randomisation
included more years of education, extent of previous alcohol consumption, and
temptation to drink in social situations. Brief interventions for prenatal alcohol
reduced subsequent consumption most significantly for the women with the highest
consumption initially (p<0.01). The effects of the brief intervention were significantly
enhanced when the partner participated (p< 0.05).
A study with 255 participants examined the efficacy of brief intervention given by a
nutritionist and also assessed outcomes for the newborns (O'Connor and Whaley
2007). Women in the intervention group were 5 times more likely to report abstinence
compared with women in the assessment-only (with no intervention) condition.
Newborns whose mothers received brief intervention had higher birth-weights and
birth lengths, and foetal mortality rates were 3 times lower (0.9%) compared with
newborns in the assessment-only (2.9%) group.
A larger trial used a brief motivational intervention delivered to 830 nonpregnant
women at risk (defined as drinking more than 5 drinks per day, and not currently
using contraception). They were randomised to receive four counselling sessions and
one contraception consultation, or information only (Floyd et al. 2007), with the aim of
preventing alcohol-affected pregnancies (AEP). Follow-up was at 3, 6, and 9 months.
Results showed that across the follow-up period, the odds ratios (ORs) of being at
reduced risk for AEP were twofold greater in the intervention group: 3 months, 2.31
(95% confidence interval [CI] =1.69-3.20); 6 months, 2.15 (CI=1.52-3.06); 9 months,
188
2.11 (CI=1.47-3.03). Between-groups differences by time phase were 18.0%, 17.0%,
and 14.8%, respectively.
These studies provide clear evidence for the effectiveness of intervention for alcohol
with non-dependent women who are pregnant or contemplating pregnancy.
Aboriginal and Torres Strait Islander Australians
Recommendation
9.23a Given late presentation of alcohol
problems, active detection is recommended.
9.24 Indigenous Australians, like all other
Australians should have access to the full
range of treatment services, including early
intervention and where appropriate, relapse
prevention medications.
9.25 Indigenous Australians should be offered
access to trained Indigenous health care
workers and services where possible.
9.26 Non-Indigenous clinicians should work in
partnership with Indigenous health
professionals and/or agencies to improve
treatment access and appropriateness for
communities.
9.27 A respectful, holistic and integrated
approach to assessment and management is
necessary, considering the patient in the
context of both the family and the community.
9.28 Indigenous cultures and customs vary.
Use of language and approach to
communication should be appropriate for both
the individual and the community.
9.29 Given the high prevalence of physical and
mental comorbidities in the Indigenous
population, clinicians should consider the
possibility of physical and/or mental
comorbidity in all presentations.
9.30 The ongoing impact of colonisation
should be considered and efforts to provide a
range of treatment options for alcohol
problems to Indigenous population should be
combined with wider community measures
addressing both alcohol misuse-related
problems and underlying social determinants
of alcohol misuse.
Strength of
Level of
recommendation evidence
D
IV
D
IV
D
IV
D
IV
D
IV
D
IV
A
I
D
IV
189
Introduction
The number of people identified as being of Aboriginal and/or Torres Strait Islander
origin in the 2006 Census was 455,000, representing 2.3% of the total Australian
population, of whom 90% identified as Aboriginal. Around three-quarters (76%) of the
Indigenous population were living in major cities and regional areas in 2006, with the
remaining 24% in remote areas (Australian Institute of Health and Welfare and
Australian Bureau of Statistics 2008). In contrast, only 2% of non-Indigenous people
live in remote areas.
Indigenous Australians are less likely to drink alcohol than are non-Indigenous
Australians; however, among those who do drink, a greater proportion consumes
alcohol at risky or high-risk levels, often resulting in serious harm to themselves and
others. Indigenous Australian youth are nearly 2½ times more likely to die from
alcohol-related causes than are non-Indigenous. Overall, 60% of Indigenous
Australian drinkers are estimated to directly or indirectly experience some alcoholrelated harm compared with 35% of non-Indigenous Australian drinkers (Australian
Institute of Health and Welfare 2008). Early intervention is required before serious
harms and problems emerge.
Evidence for the effectiveness of treatment specific to Indigenous clients is scant.
However, guidelines have recently been developed for the management of alcohol
problems in Indigenous primary care settings (Commonwealth Government Dept of
Health and Ageing 2007). This practical guide provides recommendations for
managing intoxication, withdrawal, medical and psychiatric comorbidity, and for
providing screening, brief interventions and continuing care.
A number of evaluations of individual clinics or programs have been undertaken
(Gray et al. 2000) with mixed results, and limited data are available in some cases.
We could not locate any completed trials for treatment of Indigenous clients with
alcohol use disorders. Challenges in implementing randomised controlled trials in
Indigenous settings have been described e.g. (Sibthorpe et al. 2002; Brady, M. et al.
2002).
Appropriate ways to conduct research in Indigenous communities were highlighted in
an article by Foster et al, emphasising that the communities need to take control over
the research (Foster et al. 2006). The paper provides a model for conducting
research for Indigenous community-controlled organisations and can inform nonIndigenous researchers about ways of working with those communities to address
substance misuse and other health problems.
There has been very limited research into the best approach for detecting alcohol
problems earlier among Indigenous Australians. Qualitative research by Brady et al
(2002) during their trial of brief intervention showed that they had limited success
using AUDIT in an urban Aboriginal health centre. The Indigenous health workers
said they felt ‘intrusive’ at first asking the questions; question 8 (How often during the
last year have you had a feeling of guilt or remorse after drinking?) sometimes
needed clarification, and health workers believed that clients sometimes ‘fudged’
their responses. This may have been influenced by the closeness of this particular
community. Anecdotally, in other settings the AUDIT and its shorter form, AUDIT-C,
have been used successfully.
A number of constraints to delivering brief interventions in this particular health
service included lack of time, crowded waiting rooms, patients who became irritated
190
when alcohol was raised as an issue, and the “…severity of illness and the
complexity of the physical, social and psychological problems with which patients
present” (Brady et al. 2002). However, again, anecdotally in other settings
Indigenous Health Workers have delivered opportunistic brief intervention and found
it acceptable to the patient. Indigenous persons with past alcohol dependence at
times report having stopped because of the advice of a doctor (Brady 2001).
Caution needs to be applied in using questionnaires and instruments designed for
and by the dominant Australian culture, as they may give misleading results
(Chikritzhs and Brady 2006). One brief questionnaire has been developed and
validated specifically for use in the Indigenous setting. This questionnaire, known as
the Indigenous Risk Impact Screen (IRIS), jointly screens for alcohol and other drug
disorders, as well as mental health disorders (Schlesinger et al. 2007). It has been
applied in a number of settings, particularly in Queensland, and an associated brief
intervention has been developed.
One survey of an Indigenous community-controlled health service revealed that
nearly half (42.6 percent) of all consultations (N = 583) were with Indigenous health
workers, not GPs, a finding with relevance for the implementation of alcohol
screening and treatment services (Thomas et al. 1998). Further, almost all patients
(96.1 percent) saw an Indigenous health worker before seeing a GP. Female patients
made up on average 57 percent of all the consultations in the survey.
In remote areas, the range and quality of general and specialist health care facilities
are below the level of those in regional centres In addition, both distance and limited
availability of qualified health workers present obstacles to treatment, including early
intervention.
Treatment in specialist settings
There may be many barriers to Indigenous clients in accessing mainstream alcohol
treatment services (Teasdale et al. 2008). While there are few data on how to
improve access specifically to alcohol treatment services, methods used in services
for injecting drug users including more flexibility, increasing Indigenous staffing and
cultural appropriateness have increased service uptake.
While indigenous-specific services may be more culturally acceptable, Brady (1995)
found that the range of available services at that time was limited. She points out that
Indigenous drinkers show varied patterns of alcohol use and it should not be
assumed that one treatment approach will be appropriate for all Indigenous patients
(Brady 1995). Available Indigenous treatment services have a strong orientation
towards the disease model of alcoholism and the 12-step facilitation model. Brady
(1995) stresses the need for a range of treatment options, including brief
interventions and motivational interviewing. Brady also points out that approaches
using ‘culture as treatment’ (the notion that reclaiming culture will in itself heal the
alcohol problem) are more likely to work if “…they succeed in helping clients to form
peer groups (both adolescent and adult) which disvalue drug and alcohol use and
which assist individuals to deal with the persuasive pressures of their kin and
associates”.
Where studies exist, Gray (2000) found that effectiveness of specialised treatment
programs was equivocal. There is some suggestion that sobering up centres have
been a catalyst to further local actions to address alcohol misuse and associated
harm and certainly the regular visitors present a pressing case for referral to
191
treatment. The sobering-up centres do not pretend to solve the problems of alcohol
abuse in the community, but play a vital role in keeping people out of police custody,
reducing alcohol-related harm and offering practical care in a safe environment for a
short time (Brady et al. 2006). They also provide opportunities for brief interventions
by drug and alcohol workers and other personnel. An evaluation of two residential
programs and one non-residential program concluded that attendance at a family
oriented program had modest effects on drinking behaviour and that communitybased field workers are an essential complement to residential programs (Gray et al.
2000; Gray et al. 2006).
Community-wide measures to reduce alcohol problems
Chikritzhs et al discuss the results of some strategies implemented in the Northern
Territory (NT) to reduce alcohol-related harm (Chikritzhs et al. 2005). The Living With
Alcohol (LWA) program incorporated education, increased control on alcohol
availability, and expansion of treatment and rehabilitation services. An important
component of this program was the support and engagement of communities to
address alcohol (Chikritzhs et al. 2005). Trends in age-standardised rates of acute
and chronic alcohol-attributable deaths in the NT were examined before, during and
after the combined implementation of the LWA program and an alcohol beverage
levy. The program was associated with significant declines in acute alcoholattributable deaths in the NT overall, as well as Indigenous deaths between 1992 and
1997. A significant but delayed decline in chronic deaths was evident towards the
end of the study period (1998 – 2002). The authors conclude that the combined
impact of the LWA program, the levy, and the programs and services funded by the
levy reduced the burden of alcohol-attributable injury to the NT in the short term and
may have contributed to a reduction in chronic illness in the longer term. The results
of this study present a strong argument for the effectiveness of combining alcohol
taxes with comprehensive programs and services designed to reduce the harm from
alcohol, and underline the need to distinguish between the acute and chronic effects
of alcohol in population level studies. Unfortunately, ongoing funding for this program
was not provided.
One of the most successful methods to reduce alcohol consumption and associated
harm is to implement restrictions on the sale of alcohol, either by hours (of opening),
persons (by residency) or quantity allowances, including complete bans on supply
(‘dry’ areas) and reducing the density of outlets (Hogan et al. 2006). The best results
are achieved by plans that have been initiated by the Indigenous communities
themselves in consultation with residents, elders, and organisations such as Land
Councils in partnership with other agencies such as police, hospital and health
workers and tavern or club licensees; and often accompanied by State Government
support (Martin and Brady 2004; Brady 2007; Conigrave et al. 2007) . Such ‘dry’
areas have only been feasible to set up and maintain in more isolated communities.
Currently, measures are being trialled in urban areas such as families declaring their
houses as dry and obtaining the support of agencies, such as Housing Commission
to enforce this (anecdotal evidence). Research conducted in the general Australian
population measuring the impact of the enforcement of responsible service of alcohol
can reduce harms (Loxley et al. 2004), so this would be expected to also be effective
in other specific population groups.
192
Older people
Recommendation
9.31 Older Australians should be screened for
alcohol use and related harms (such as
trauma, exacerbation illness, drug interactions,
violence or physical neglect) across a range of
health and welfare settings.
9.32 Brief interventions should be employed
for older people drinking at risky levels or
experiencing alcohol-related harms (such as
falls, driving 0impairment, drug interactions).
9.33 Concurrent physical or mental illness,
medications, social conditions and functional
limitations need to be considered when
assessing older drinkers.
9.34 Abstinence can be associated with
marked physical, mental and cognitive
improvements; alternatively, alcohol use may
have been masking underlying illness.
Consequently, the severity and management
of concomitant physical and mental conditions
should be reviewed several weeks to months
after cessation of drinking.
9.35 Withdrawal management of older
dependent drinkers requires close monitoring,
nutritional supplements, careful use of
sedative medication, and management of
comorbid conditions.
9.36 Caution should be exercised when
prescribing medications to older drinkers.
Short-acting benzodiazepines (such as
oxazepam, lorazepam) are preferred for
alcohol withdrawal management over longacting benzodiazepines (such as diazepam).
9.37 Psychological and pharmacological
treatment approaches should be tailored to
physical, cognitive and mental health of older
patients.
Strength of
Level of
recommendation evidence
D
IV
A
Ia
D
IV
D
IV
S
D
IV
D
IV
Introduction
Australia, like other developed countries, has a rapidly ageing population. The 2006
national census indicated that the number of Australians aged 65 years and older
was 2,644,374 representing 13.3% of the total population (Australian Bureau of
Statistics 2007). Over the next 50 years the number of older people in Australia is
expected to increase to 6.5 million, representing approximately 25% of the total
population (Australian Bureau of Statistics 2000).
193
The term older-person has been defined by the United Nations (2003) as any person
over 60 years of age. However, in Australia, the term older-person has been used to
refer to anyone aged 65 years and older. As this definition can encompass people
whose ages vary by many decades, the term older-person has been further divided
into three age groups: people aged 85 years and older; people aged 75 to 84 years
and those aged 65 to 74 years (Australian Association of Gerontology 2005; Broe
2004; Maddox 1985; Selvanathan and Selvanathan 2004).
Based upon the 2007 National Drug Strategy Household Survey (Australian Instutute
of Health and Welfare 2008), of Australians aged 60 years and older, it is estimated
that:
•
•
•
15.6% drank alcohol on a daily basis and 34.6% drank alcohol on a weekly basis;
14.9% of older men and 7.5% of older women drank at levels that potentially put
their health at risk in the short term;
7.4% of men and 5.5% of older women drank at levels that put them at risk of
long term harm.
As with younger populations, older people drink alcohol for a variety of reasons.
However, increased alcohol use amongst older people can be associated with later
life events such as bereavement and loss, and related conditions such as social
isolation and psychiatric co-morbidity. Retirement can also have an impact on
drinking. Some authors (Alexander and Duff 1988; Ekerdt et al. 1989; Perreira and
Sloan 2001) have argued that retirement can increase alcohol consumption as it is
associated with a loss of status, a sense of rolelessness and feelings of social
marginalisation.
Although some people may increase their alcohol consumption after retirement,
epidemiological evidence indicates that alcohol consumption does tend to decrease
with increasing age and that declining health is an important predictor of declining
alcohol use (Khan et al. 2006; Paganini-Hill et al. 2007; Moos et al. 2005). In
Australia, depending on the methodology used to assess harm, the prevalence of
women potentially at risk from alcohol varies from 1% to 26% (Fleming 1996).
Amongst men, these figures vary from 7.9% to 23.8% (Australian Institute of Health
and Welfare 2005; O'Halloran et al. 2003). The lower estimates of at-risk alcohol
consumption have typically arisen from studies based upon NHMRC alcohol
guidelines, whereas the higher estimates have occurred in those studies which have
used screening tools such as the AUDIT (Saunders et al. 1993b). The issue of
screening for the presence of alcohol-related problems amongst older people is
however problematic, as some of the diagnostic criteria used in screening
instruments may be inappropriate (e.g. employment) for use with older people (Dawe
et al. 2002). In addition, harmful and hazardous drinking in elderly people is not
adequately described by the use of quantity/frequency screening measures alone as
older people have lowered tolerance to alcohol, may have chronic illnesses, be
taking medications (Evans 2000) or have functional impairments that need to be
taken into account as part of any comprehensive assessment.
Benefits of light to moderate alcohol use in older adults
There are a number of studies that suggest that light to moderate alcohol use (one
to two drinks per day) may convey some health benefits to older adults, including:
reduced bone loss in males and females (Bakhireva et al 2004; Mukamal et al.
2007);
194
reduced risk of cardiovascular conditions such as heart failure (Bryson et al.
2006), stroke (Mukamal et al. 2005) and atherosclerosis (e.g. Mattace-Raso et al.
2005).
reduced risk of cognitive impairment and dementia in older adults (e.g. Mukamal
et al. 2003; Cassidy et al. 2004; Ganguli et al. 2005; Deng et al. 2006; McGuire et
al 2007).
Although there have now been more than 100 epidemiological studies suggesting
that moderate alcohol consumption is cardio protective (Gulbransen and McCormick
2007), recent critical literature has found that people who never drink were at no
greater risk than light drinkers (Filmore et al. 2003) Because of the systematic error
of misclassification that has occurred in much research (Fillmore et al. 2006), the
contention surrounding alcohol’s cardio protective effects is likely to continue (e.g.
(Ellison et al. 2007; Rimm et al. 2007). In addition, confounding factors such as diet
need to be considered; in one study people who drank a little wine with meals tended
to consume a more healthy diet (higher intake of fish, vegetables, and more use of
olive oil) (Tjonneland et al. 1999). While research continues, the comment by
Goldberg (2003) is relevant: ”If alcohol were a newly discovered drug (instead of one
dating back to the dawn of human history) we can be sure that no pharmaceutical
company would develop it to prevent cardiovascular disease”(p.164).
In contrast, the mortality data from the Australian Longitudinal Study on Women’s
Health (ALSWH) on the cohort of women aged 70 -75 years in 1996 demonstrated
that women who did not consume alcohol or drank rarely had a higher rate of
mortality than women in the low-level consumption category. Non-drinkers also
scored lower on General Health, Physical Functioning, Mental Health and Social
Functioning subscales of the SF-36 (Byles et al. 2006). US studies among men
(Mukamal et al. 2003) and women (Stampfer et al. 2005) found protective effects
from moderate drinking, and a reduced risk of Type 2 diabetes in both sexes
(Djousse et al. 2007).
Health risks of alcohol use in older adults
Older people warrant special consideration in relation to alcohol use for a number of
reasons. Four of these reasons include: the physiological changes that occur with
ageing; medication use; the link between alcohol and cancer; alcohols impact on
cognitive function and the conflict surrounding alcohol’s impact on coronary vascular
disease.
Important age-related physiological changes include a reduction in total body water
and changes in hepatic metabolism of alcohol, producing a higher blood alcohol
concentration for a given dose.
A higher blood alcohol concentration (BAC) can be produced with a standard quantity
of alcohol if it is absorbed more quickly, eliminated more slowly or the total body
water (TBW) for distribution is less (Vogel-Sprott and Barrett 1984). While neither
alcohol absorption nor elimination are affected with ageing, TBW does decrease with
age (Schoeller 1989; Watson et al. 1980). TBW also varies across gender with
females having a lower TBW (on average) than males. As women of all ages have
less lean muscle mass than men, they are more susceptible to the effects of alcohol.
With age there is a decrease in lean body mass versus total volume of fat, and the
decrease in total body mass increases the total distribution of alcohol in the body
(Blow and Barry 2002).
195
There is an increased possibility of drug interactions: many older people take
medications that may have interactions (and may be contraindicated) with alcohol.
While older people comprise between 12% and 15% of the population of most
developed nations, it has been estimated that they use approximately 33% of all
prescription medicines (Evans 2000). They also have a high use of over-the-counter
medications, the most common of which are analgesics, vitamins, antacids and
laxatives (Evans 2000). Problems can result from the concomitant use of many
prescription drugs commonly used by older people and alcohol (Tanaka 2003). For
example, alcohol increases the sedative effects of antidepressants, antihistamines,
muscle relaxants, benzodiazepines and opioids (National Institute on Alcohol Abuse
and Alcoholism 1995). This interaction can have serious consequences such as
increasing the risk of falls, motor vehicle accidents and overdose (Tanaka 2003;
Weathermon and Crabb 1999). Alcohol use in combination with non-steroidal antiinflammatory drugs (NSAIDS) can result in stomach bleeding, gastric inflammation
and liver damage (Bush et al. 1991; Dart 2001; Kaufman 1999; Korrapati 1995;
Tanaka 2003).
There is an increased risk of falls and impaired driving ability in older people who
drink alcohol (Chikritzhs and Pascal 2005). Cognitive function, and in particular
memory, may be more vulnerable to the effects of alcohol in older drinkers.
Between 1994 and 2003 over 10,000 Australians aged 65 years and older died from
alcohol attributable injury and disease caused by risky and high-risk drinking
(Chikritzhs and Pascal 2005). There is also evidence that over the past decade
alcohol-attributable hospitalisations amongst older people have increased in Victoria,
Tasmania and Western Australia. The most common causes of alcohol attributable
hospitalisations were: falls, supraventricular cardiac dysrhythmias, and alcohol
dependence (Chikritzhs and Pascal 2005).
Long term alcohol use is also an important consideration in relation to cancer. In
Australia in 2001, it was estimated that 2,791 (3.2%) of all new cases of cancer and
1,291 cancer deaths were attributed to alcohol consumption (Australian Institute of
Health and Welfare and Australasian Association of Cancer Registries 2004). In their
most recent publication, the World Cancer Research Fund and American Institute of
Cancer Research (2007) expert panel concluded that since the mid-1990’s the
evidence that alcohol is a cause of cancer has become stronger and that there is
ample evidence from case-control and cohort studies of a dose-response relationship
between alcohol and breast cancer. The panel also stated that ”the evidence that
alcoholic drinks are a cause of pre-menopausal and post-menopausal breast cancer
is convincing”(p.168) (World Cancer Research Fund/ American Institute for Cancer
Research 2007).
The issue of alcohol and cognitive function is also complex. Several longitudinal
studies have shown an association of light drinking (up to 20/10grams of alcohol per
day for men and women respectively) with a reduced risk of cognitive impairment and
dementia (Bryan and Ward 2002; Cassidy et al. 2004; DeCarli et al. 2001; Deng et al.
2006; Ganguli et al. 2005; Lyndsay et al. 2002; McGuire et al. 2007; Rodgerset al.
2005; Ruttenberg et al. 2002; Zimmerman et al. 2004). Conversely, other research
shows no association (Truelsen et al. 2002; Tyas et al. 2001) or an acceleration in
cognitive deterioration (Anttila et al. 2004) and the development of early onset
dementia (McMurtray et al. 2006). Complementing the psychometric testing on
cognitive function has been research examining the association between alcohol use
and brain atrophy. Anstey et al. (2006) conducted MRI brain scans on a sample of
196
478 persons aged 60 to 64 years and found evidence of a positive association
between brain atrophy and alcohol consumption.
Who to target for screening and interventions?
Diagnosis of alcohol use disorders may be difficult, as alcohol use and related
disorders may be mistaken for the effects of aging or other conditions.
Every person over the age of 60 should be screened for their concomitant alcohol
and other drug use, with a particular focus on patients on multiple medications,
medications such as sedatives. Alcohol abuse or dependence may mimic the effects
of aging and many conditions prevalent in this age-group. A high index of suspicion
and thorough history taking can aid early detection and appropriate management.
As with younger age groups, screening is recommended in general practice settings,
general hospital wards, emergency departments and community counselling settings.
As older people are unlikely to present at traditional alcohol or other drug treatment
settings, it is important that opportunistic screening in mainstream and gerontology
settings occur.
What is effective?
Older people have typically been excluded from large scale outcome studies, but
there is some evidence that brief intervention and other treatment options are also
valid with older people (Gordon et al. 2003). Brief interventions in this age
populations are effective in significant reductions in overall alcohol use and frequency
of excessive drinking.
Bruef interventions for older people: Randomised controlled trials
One randomised controlled trial evaluated the economic cost and benefits of brief
intervention for at-risk drinking older adults (Mundt et al. 2005). This trial with 24month follow-up tested the effectiveness of brief physician advice in reducing alcohol
use, health care utilisation and other consequences among adult problem drinkers
aged 65 or more. Patients were screened for problem drinking in 24 communitybased primary care practices; 158 were randomised into control (n = 71) or
intervention (n = 87) group. Intervention group patients received two 10- to 15-minute
physician-delivered counselling sessions including professional advice, education
and contracting using scripted workbooks. The intervention group demonstrated
significant reductions in alcohol use (p= 0.001) and frequency of excessive drinking
(p= 0.03) compared with the control group over 24 months, but no significant
differences emerged in economic outcomes, including hospital days, emergency
department visits, office visits, medications, lab and x-ray procedures, injuries, legal
events or mortality. The authors conclude that the economic results of brief
intervention in this age group are less certain than the effects on alcohol
consumption; older adult problem drinkers may require more intensive and costly
interventions to achieve economic benefits similar to those seen in younger adults.
Another trial reproduced similar effects of brief intervention on alcohol consumption
with the conclusion that brief intervention is as effective for elderly patients as for
younger (Gordon et al. 2003). This study compared patients in 2 treatment arms
(brief advice [BA] and motivational enhancement [ME] with one control arm [SC].
Patients were assessed at 1, 3, 6, 9 and 12 months. Post-hoc analysis compared the
elderly (>65 years, n=45) with non elderly (n=256) patients over all outcome
197
measures. During the 12 months following intervention, the elderly in ME, BA, and
SC intervention arms increased the number of days abstained, decreased the
number of drinks per day, and reduced the number of total days per month drinking.
There were trends toward decreases in the alcohol consumption measures in the ME
and BA treatment arms compared to SC. The elderly patients’ response to all
interventions was similar to that of the younger cohort. (Level 1a evidence) However,
the refusal rate was high (75% of eligible patients) and the sample size was
correspondingly small (Zimmerman et al. 2004).
Assessment and screening
Routine screening for alcohol consumption amongst older people is recommended
as older people tend not to discuss their drinking and health professionals can often
mistake the effects of alcohol for a physical or mental health problem.
•
•
Attention should be given to assessing alcohol related harms in this agegroup (including falls, exacerbation of medical conditions, drug interactions,
violence or abuse).
Comprehensive assessment should include physical and mental health,
chronic pain, social conditions, overall general functioning, and a review of
medications.
Older drinkers taking other medications, in particular those taking multiple
medications or psychoactive medications (e.g. sedatives, anti-depressants), should
have medications reviewed by their medical practitioner to assess for any drug
interactions. See Appendix xx for alcohol-drug interactions.
Withdrawal management for dependent drinkers
Older dependent drinkers attempting alcohol withdrawal should be closely monitored,
generally in a supervised withdrawal setting (detoxification unit or hospital).
•
•
•
Poor diet and housing, physical inactivity, and concomitant illness may make
patients more vulnerable to complications during withdrawal such as
dehydration, nutritional deficiency (e.g. Wernicke’s), hypertension or
infections.
Patients should receive adequate thiamine, rehydration and nutritional
support, and close monitoring of other conditions (e.g. blood pressure, blood
glucose, mental state).
Diazepam has the potential for over-sedation due to accumulation in older
people (delayed hepatic clearance of long-acting active metabolites). Shorter
acting benzodiazepines such as oxazepam or lorazepam should be
considered as first line medication for moderate to severe alcohol withdrawal
(see Chapter 5). Doses should be titrated according to clinical effect.
The severity and management of concomitant physical and mental conditions should
be reviewed several (2 to 4) weeks after cessation of drinking and completion of
withdrawal. Abstinence can be associated with marked improvements in other
conditions (e.g. hypertension, cognitive function, mental state); alternatively, alcohol
use may have been masking underlying illness.
198
Treatment of dependence
Treatment is becoming of increasing importance as the population ages; however, to
date there are very few experimental studies conducted with the older age groups,
especially those aged over 70. Most studies are longitudinal studies or retrospective
analyses of data.
One retrospective study compared long-term outcomes for men and women (Satre et
al. 2007). These authors examined participants at seven-year follow-up to assess the
outcomes for women (n = 25) and men (n = 59) aged 55 and over in an outpatient
addiction program. It measured demographic characteristics, alcohol and drug use,
psychiatric symptoms, Addiction Severity Index, treatment length, and outcomes. At
seven years, 76.0% of women reported abstinence in the prior 30 days versus 54.2%
of men (p = 0.05). Logistic regression analysis found that longer treatment stay
predicted abstinence. The authors conclude that their findings indicate that older
women have better long-term addiction outcomes than older men, but treatment
length is more significant than gender in predicting outcome.
Cognitively impaired patients
Recommendation
9.38 A brief assessment of cognitive
functioning should be a routine part of
assessment upon treatment entry.
9.39 More detailed diagnostic and functional
assessment should be carried out where brief
assessment suggests that a patient suffers
from significant cognitive deficits.
9.40 The possibility of improvement in
cognitive functioning should be taken into
account by allowing a sufficient period of
abstinence from alcohol to elapse before
finalising treatment planning.
9.41 Where cognitive impairment is confirmed,
information presented to patients should be
concrete and patients should be given
opportunities to practice behaviours taught in
treatment.
9.42 Clinicians should engage cognitively
impaired patients in treatment by providing
information about treatment, discussing
different treatment options and maintaining
contact with the patient.
9.43 Cognitively impaired patients should be
taught relapse prevention strategies.
Strength of
Level of
recommendation evidence
S
S
D
IV
B
II
S
D
IV
Introduction
Chronic excessive alcohol use has been consistently associated
199
with cognitive impairment, including impairements in decision making, problem
solving cognitive flexibility and propensity for risky behaviour (e.g. Moselhy et al,
2001; Davies et al. 2005; Glass et al. 2009). Higher frequency and a longer duration
of alcohol consumption are associated with greater decline of frontal lobe function of
alcohol-dependent patients (e.g. Fein et al., 1990). It has been suggested that
cognitive impairment in alcohol dependent patients is associated with frontal lobe
dysfunction (Noel et al. 2001; Uekermann and Daum 2008; Chanraud et al. 2007).
Many studies suggest that impaired cognitive functioning is related to poorer
treatment outcome, particularly for treatments that require the acquisition of new
skills. Thus, a brief assessment of cognitive functioning should be an integral part of
the assessment procedure and results should be used to guide treatment planning
(Allsop et al. 2000) (see below). If significant impairment is suspected, a more
thorough assessment by an appropriately qualified professional is indicated. Where
severe cognitive impairment is present, treatment in an inpatient facility may be more
effective than outpatient treatment (Rychtarik et al. 2000).
People who suffer from alcohol abuse or dependence may have difficulty processing
all the relevant information about their problem and may be inflexible about changing
behaviour (Goldman 1995). Cognitive impairment can impair motivation, attention
span, the capacity to evaluate situations critically and the ability to acquire new skills,
but they can and often do improve with a period of abstinence from alcohol (Goldman
1995). Where cognitive impairment is apparent, treatment elements that require
heavy cognitive processing should not be used as they are likely to be ineffective
(Allsop et al. 2000).
There is significant variability in the severity of cognitive deficits present in patients
(Harper 1998). Many studies suggest that a substantial minority or perhaps a majority
of patients seeking treatment for alcohol dependence will exhibit signs of cognitive
impairment after the withdrawal phase has passed (e.g. Parsons et al. 1994).
Cognitive impairment is especially pronounced in early abstinence (Loeber et al.
2009).
Wernicke-Korsakoff’s syndrome (WKS) is the most common form of cognitive
impairment associated with alcohol abuse and dependence (See Chapter 5). WKS is
a potentially fatal neurological disorder caused by thiamine (vitamin B1) deficiency
(Harper et al. 1998). Much confusion persists regarding the existence of a separate
alcohol related dementia, because of the under-recognition of the variability of
cognitive impairment manifested in WKS (Sechi and Serra 2007; Torvik 1991).
Although the hypothesis has aroused enormous interest, the tangible basis for
ethanol neurotoxicity remains to be demonstrated.
Further, thiamine deficiency is now recognised as a primary underlying cause of
cerebellar degeneration and peripheral neuropathy associated with alcohol abuse
(Sechi and Serra, 2007) although these conditions were for many years thought to be
attributable to ethanol neurotoxicity. Of course, WKS may be seen in patients with
thiamine deficiency from any cause. For example in patients with gastrointestinal
tract disease, recurrent vomiting, malignancy, or other medical conditions, or even in
people lost in the bush or at sea without food for some time (Donnino et al. 2007).
One of the most common causes of WKS may be iatrogenic, arising from inadequate
clinical management of patients at risk of severe malnutrition or requiring refeeding,
200
where dietary supplementation does not include sufficient thiamine (Sechi and Serra,
2007).
To understand the wide variability in clinical manifestations of WKS, and therefore
the importance of thiamine treatment in many patients with alcohol abuse or
dependence, it is instructive to briefly review evidence regarding the variable
spectrum of clinical symptoms in WKS. Although sometimes still described as
though different conditions (Sechi and Serra, 2007), the neuropathology of
Wernicke’s encephalopathy (WE) and Korsakoff’s syndrome (KS) is identical,
recency of onset varying widely in individual patients (Harper et al. 1986; Torvik
1991).
Most patients observed to have an acute episode of WE will display the severe
cognitive impairment of KS at follow-up (Victor et al., 1989). Beyond the period of
acute hospitalization and the well established benefits of high dose thiamine on the
acute symptoms of WE (Thomson, et al., 2002; Victor et al., 1989) some patients
with WKS recover from the severe illness, including from the severe cognitive
impairment, although recovery may occur over months or years. It is surprising how
little appreciated is the potential for cognitive recovery despite Korsakoff highlighting
the potential for recovery in his original case descriptions (Korsakoff, translated by
Victor and Yakovlev, 1954). At the present time we have poor understanding of the
factors underlying recovery of cognitive impairment after severe episodes of WKS,
the obvious explanation being refeeding and re-establishing adequate thiamine
intake (Ambrose, Bowden and Whelan, 2001). Post recovery, obtaining a good selfreport history of past episodes of WKS is obviously difficult because many patients
have little of no clear recollection of their periods of exacerbation. The stereotype of
a severe, permanent Korsakoff’s amnesia requiring long-term, high-level care,
although reiterated in recent editions of the Diagnostic and Statistical Manual
(American Psychiatric Association, 2000) was recognised many years ago as an
artefact of a clinical research strategy focussing on those patients with WKS who
were most impaired. In contrast to patients suffering acute episodes requiring
medical attention, many patients with WKS may have an insidious course with less
obvious episodes of exacerbation and then recovery (Bowden, 1990; Lishman 1998).
Perhaps the most important variant of cognitive impairment associated with WKS is
dementia-like deterioration (Bowden 1990). Indeed, it has been suggested, on the
basis of large retrospective post-mortem series, that the most common explanation
for a clinical diagnosis of dementia associated with alcohol abuse and dependence is
unrecognised WKS neuropathology (Lishman 1998). The classic diagnostic triad of
WKS, namely eye signs, cerebellar signs and mental impairment is known to have
low diagnostic sensitivity, perhaps somewhere between 1-20% (Torvik 1991). Some
years ago, Harper and colleagues (Caine et al, 1997) published revised clinical
diagnostic criteria for WKS in patients with a history of alcohol dependence. These
criteria comprised any two of the following signs in patients with a history of alcohol
dependence: dietary deficiencies, cerebellar signs, eye signs or cognitive
impairment. This revised diagnostic approach was shown to have better that 90%
diagnostic sensitivity and 90% specificity against the gold standard of post mortem
identification. To date there is only one RCT cited in the Cochrane review of thiamine
treatment for WKS and alcohol related dementia (Day et al. 2004). Clearly there is a
need for further detailed study of these issues.
Although thiamine fortification of bread making flour was recommended by the
NHMRC in 1987, the poor diets of many alcohol abusing and dependent people may
diminish the benefits of this initiative (Feeney and Connor 2008). In addition, in the
201
absence of systematic evaluation there is no tangible evidence that this initiative has
led to changes in the incidence of WKS. Fortification elsewhere has not prevented a
high prevalence of reported cases of WKS (Feeney and Connor 2008; Sechi and
Serra 2007). It is likely that the perceived prevalence of WKS in diverse clinical
settings still depends greatly on the vigilance of clinicians (Victor et al. 1989). The
most important implications for treatment of WKS and cognitive impairment
associated with alcohol abuse and dependence is to assume that WKS is the cause
of any symptoms of cognitive impairment, instituting prompt with high dose
intramuscular or parenteral thiamine (Thomson et al. 2002).
Effect of cognitive impairment on treatment efficacy
Although many studies have examined cognitive impairment in alcohol dependent
patients, few studies have systematically examined the effect of cognitive impairment
on treatment outcomes. However there is reason to believe that cognitive deficits
may impact on some of the skills and behaviours taught in treatment because
impaired cognitive functioning impacts on a variety of processes, such as impulsivity,
planning and decision-making skills (Smith and McCrady 1991). There is some
evidence suggesting that cognitive functioning relates to various aspects of
treatment, including treatment outcome, but findings are mixed. In the late 1970s and
early 1980s many studies claimed that cognitive impairment was one of the best
predictors of poor treatment outcome (Allsop et al. 2000). Others have found no
relationship between cognitive deficits and treatment success (Goldman 1995).
Does cognitive functioning affect treatment outcome?
Smith and McCrady examined the impact of cognitive impairment on drink refusal
skills, acquisition and treatment outcome in thirty-three alcohol dependent males
receiving inpatient treatment (Smith and McCrady 1991). Two month follow-up data
indicated that patients with less cognitive impairment had better treatment outcomes.
Overall, patients with less impairment tended to respond more rapidly than more
impaired patients on a behavioural test of drink skills, patients higher in verbal
abstraction were signif-icantly better in their ability to describe an effective drink
refusal, higher abstraction patients and patients with generally greater learning ability
demonstrated marginally different improvement on a quiz about effective drink refusal
strategies from pre to post training and individuals higher in verbal abstraction
evidenced greater outpatient aftercare involvement. These data suggest that
cognitive deficits adversely affect treatment outcome. Further, the authors suggest
that the relationship between cognitive impairment and aftercare involvement indicate
that impaired individuals may be vulnerable to relapse. While suggestive, these data
should be viewed cautiously due to the small sample size.
One study examined the relationship between executive function impairment, change
process factors and substance use outcomes in a sample of substance users (N =
118) participating in intensive 12-step treatment (Morgenstern and Bates 1999).
Change processes were self-efficacy, commitment to abstinence, negative substance
abuse expectancies and affiliation with Alcoholics Anonymous. More than half of the
sample showed some form of executive impairment, but executive impairment did not
predict worse substance use outcomes six months following treatment. However,
change processes were strongly related to outcome for unimpaired individuals but
weakly related for impaired individuals, suggesting that impaired and unimpaired
individuals traverse different pathways in achieving equivalent outcomes.
202
Although Smith and McCrady reported that cognitive impairment adversely affected
treatment outcome for drink refusal skills training, executive impairment was not
found to adversely affect outcome for twelve-step treatment in Morgenstern and
Bates’ study. Although these results could be taken to suggest that compared to 12step programs, cognitive behavioural interventions may be too difficult for cognitively
impaired individuals, there is not enough evidence to make such a judgement.
Outcomes could differ due to the treatments given, type of cognitive functioning
assessed and the measures used, outcome measures, length of follow-up or type of
patients participating, as Smith and McCrady examined alcohol dependent patients,
whereas Morgenstern and Bates examined patients with substance abuse.
Is cognitive impairment associated with an increased risk of relapse?
In a study examining gender differences in reasons for relapse after treatment,
Saunders et al. (Saunders et al. 1993a) found that the best predictors of a return to
drinking were comparatively low cognitive abilities plus few prior periods of
abstinence. The authors postulated that low neuropsychological scores may suggest
the inability to acquire new skills during treatment, and/or could be indicative of past
heavy drinking and acquired brain damage, with the concomitants of impulsivity and
poor planning. Interestingly, in this study high scores on executive functioning were
predictive of poorer outcomes for women but not for men. This finding is confusing,
but suggests that cognitive functioning may affect treatment outcome differently for
men and women.
Allsop, Saunders and Phillips (Allsop et al. 2000) also investigated factors
hypothesised to influence the relapse process, with a focus on the roles of selfefficacy, alcohol dependence and cognitive functioning. Participants (N = 60, male)
were recruited from patients attending an alcohol treatment unit. Poorer cognitive
functioning was significantly associated with being categorised as a problem drinker
at six-month follow-up, which is consistent with results reported in other studies
(Parsons et al. 1990). Poorer cognitive functioning was also associated with higher
risk of lapse over the 12-month follow-up. The authors speculated that those with
comparatively poor cognitive functioning might have had difficulty learning new skills.
Further, poor cognitive functioning may impair the ability to make the decision to
change and increase the likelihood of poor decision-making skills, which would
increase the risk of relapse.
Do outcomes for cognitively impaired patients differ according to treatment
setting?
In a study focused on the impact of treatment setting on treatment outcome,
Rychtarik and colleagues (Rychtarik et al. 2000) found that patients low in cognitive
functioning appeared to benefit more from inpatient than outpatient care. However,
Alcoholics Anonymous attendance appeared to moderate and perhaps mediate this
effect. Among this population of inpatients there was a tendency for low cognitive
functioning to be associated with higher Alcoholics Anonymous attendance, whereas
no significant relationship was suggested for patients who received outpatient
treatment. The authors speculate that successfully increasing Alcoholics Anonymous
attendance among outpatients low in cognitive functioning may negate any additional
benefits derived from inpatient care.
203
Cognitively impaired patients: Randomised controlled trials
In a study designed to test the patient-treatment matching hypothesis (Cooney et al.
1991), patients (N = 96) were randomly assigned to aftercare group treatment with
either coping skills training or interactional therapy. Two-year outcome data indicated
that patients with cognitive impairment had better outcomes in interactional
treatment, and patients without cognitive impairment had better outcomes with
coping skills treatment. An explanation of this finding is that cognitively impaired
participants found the coping skills treatment too complex, whereas the interactional
therapy may have been less cognitively demanding. This would suggest that keeping
treatments simple would improve outcomes for persons suffering from cognitive
impairment.
In Project MATCH’s first post-treatment report (Project MATCH Research Group
1997), cognitive impairment was found not to interact significantly with treatment type
on treatment outcome. That is, treatment outcomes for cognitively impaired patients
were similar, regardless of whether patients received motivational enhancement
therapy, cognitive behavioural therapy or 12-step facilitation. However, the 3-year
follow-up (Project MATCH Research Group 1998) showed that patients whose social
networks were more supportive derived greater benefit from 12-step facilitation
compared to motivational enhancement therapy. Readiness to change and selfefficacy were the strongest predictors of long-term drinking outcome. It is further
posited in another article by Buckman et al that cognitive impairment may increase
the positive influence of the social network on drinking outcomes (Buckman et al.
2007). These findings suggest that patients with cognitive deficits respond in different
ways, but almost equally well, to motivational enhancement therapy, cognitive
behavioural therapy and twelve-step facilitation. In an attempt to replicate Project
MATCH findings, a pragmatic, multi-centre RCT with blind follow-up at 12 months
examined six matching criteria on drinking outcomes (Heather et al. 2008). Although
specific aspect of cognitive impairment were not examined in this study, one
treatment matching criterion was general psychiatric morbidity, but none of the
matching variables were shown to enhance treatment outcome (Heather et al. 2008).
Although evidence about the impact of cognitive deficits on addiction treatment
outcome is limited, available research consistently indicates that cognitive
impairment mostly in is common in alcohol dependent patients seeking treatment.
There is no clear evidence from a systematic study at the present time for the
benefits of treatment matching (i.e. treatment type based on some patient attributes)
being more effective than non-matched treatment.
References
Alexander, F and RW Duff 1988, Social interaction and alcohol use in retirement
communities. Gerontologist 5: 632-636.
Allsop, S, B Saunders and M Phillips 2000, The process of relapse in severely
dependent male problem drinkers. Addiction 95(1): 95-106.
204
Ambrose, ML, SC Bowden and G Whelan 2001, Working memory impairments in
alcohol-dependent participants without clinical amnesia. Alcohol Clin Exp
Res. 25(2): 185-191.
American Psychiatric Association 2000, Diagnostic and Statistical manual of Mental
Disorders, Fourth Edition, Text Revision. Washington DC: American
Psychiatric Association.
Anderson KG, Ramo DE, Schulte MT et al. 2007, Substance use treatment outcomes
for youth: integrating personal and environmental predictors. Drug Alcohol
Depend 88(1): 42-48.
Anstey, K, Jorm AF, Meslin C et al. 2006, Alcohol consumption, brain atrophy and
white matter hyperintensities in a community based sample of 60-64 year
olds. Psychosom Med 68: 778-785.
Anttila, T, Helkala E, Viitanen M et al. 2004, Alcohol drinking in middle age and
subsequent risk of mild cognitive impairment in old age: a prospective
population based study. BMJ 329: 539-545.
Australian Association of Gerontology 2005, Ageing well, Ageing Productively. from
http://www7.health.gov.au/nhmrc/publications/_files/sub27.pdf.
Australian Bureau of Statistics 2000, Population projections Australia 1999-2101.
Canberra: Australian Bureau of Statistics.
Australian Bureau of Statistics. 2007, Census: QuickStats: Australia. Retrieved
29/10/2007.
Australian Government Department of Health and Aging 2007, Alcohol Treatment
Guidelines for Indigenous Australians. Canberra: Australian Government
Department of Health and Aging.
Australian Institute of Health and Welfare 2008, 2007 National Drug Strategy
Household Survey. First results. Drug Statistics Series number 20. Cat. no.
PHE98. Canberra: Australian Institute of Health and Welfare.
Australian Institute of Health and Welfare 2005, 2004 National Drug Strategy
Household Survey: First Results. Canberra: Australian Institute of Health and
Welfare.
Australian Institute of Health and Welfare and Australasian Association of Cancer
Registries 2004, Cancer in Australia 2001. Cancer Series no. 28. Canberra:
Australian Institute of Health and Welfare.
Australian Institute of Health and Welfare and Australian Bureau of Statistics 2008,
The health and welfare of Australia's Aboriginal and Torres Strait Islander
peoples (IHW 21). Canberra: Australian Institute of Health and Welfare and
Australian Bureau of Statistics.
Bakhireva, LN, Barrett-Connor E, Kritz-Silverstein D et al. 2004, Modifiable predictors
of bone loss in older men: a prospective study. Am J Prev Med 26(5): 436442.
205
Bailey, KA, Baker AL, Webster RA et al. 2004, Pilot randomized controlled trial of a
brief alcohol intervention group for adolescents. Drug Alcohol Rev 23(2): 157166.
Blow, FC and K Barry 2002, Use and misuse of alcohol among older women. Alc Res
Health 26(4): 308-315.
Boekeloo, BO, Jerry J, Lee-Ougo WI et al. 2004, Randomized trial of brief officebased interventions to reduce adolescent alcohol use. Arch Pediatr Adolesc
Med 158(7): 635-642.
Bonomo, YA, Bowes G, Coffey C et al. 2004, Teenage drinking and the onset of
alcohol dependence: a cohort study over seven years. Addiction 99(12):
1520-1528.
Borsari B and KB Carey 2000, Effects of a brief motivational intervention with college
student drinkers. J Consult Clin Psychol 68(4): 728-733.
Bowden, SC 1990, Separating cognitive impairment in neurologically asymptomatic
alcoholism from Wernicke-Korsakoff syndrome: is the neuropsychological
distinction justified? Psychol Bull 107(3): 355-366.
Brady, M 1995, Culture in treatment, culture as treatment. A critical appraisal of
developments in addictions programs for indigenous North Americans and
Australians. Soc Sci Med 41(11): 1487-1498.
Brady, M 2001, Giving away the grog: a positive strategy for addressing substance
abuse, Australia. Indigenous peoples and international development: case
study profiles. Inuit Circumpolar Conference 2001. KK Gray C, Weitzner V,
editors, Canada.
Brady, M 2007, Equality and difference: persisting historical themes in health and
alcohol policies affecting Indigenous Australians. J Epidemiol Community
Health 61(9): 759-763.
Brady, M, Nicholls R, Henderson G et al. 2006, The role of a rural sobering-up centre
in managing alcohol-related harm to Aboriginal people in South Australia.
Drug Alcohol Rev 25(3): 201-206.
Brady, M, Sibthorpe B, Bailie R et al. 2002, The feasibility and acceptability of
introducing brief intervention for alcohol misuse in an urban aboriginal
medical service. Drug Alcohol Rev 21(4): 375-380.
Broe, GA 2004, From the president. Australian Association of Gerontology
Newsletter July: 1.
Bryan, J and L Ward 2002, Smoking, alcohol use and engagement in exercise and
cognitive performance among older adults. Australas J Ageing 21(2): 67-73.
Bryson, CL, Mukamal KJ, Mittleman MA et al. 2006, The association of alcohol
consumption and incident heart failure: the Cardiovascular Health Study. J
Am Coll Cardiol 48(2): 305-311.
206
Buckman, JF, Bates ME and RA Cisler 2007, Social networks and their influence on
drinking behaviors: differences related to cognitive impairment in clients
receiving alcoholism treatment. J Stud Alcohol Drugs 68(5): 738-747.
Bush, TM, T Shlotzhauer and K Imai 1991, Nonsteroidal anti-inflammatory drugs:
proposed guidelines for monitoring toxicity. West J Medicine 155(1): 39-42.
Byles, J, Young A, Furuya H et al. 2006, A Drink to Healthy Aging: The Association
Between Older Women's Use of Alcohol and Their Health-Related Quality of
Life. J Am Geriatr Soc 54(9): 1341-1347.
Caine, D, Halliday GM, Kril JJ et al. 1997, Operational criteria for the classification of
chronic alcoholics: identification of Wernicke's encephalopathy. J Neurol
Neurosurg Psychiatry 62(1): 51-60.
Cassidy, K, Kotynia-English R, Acres J et al. 2004, Association between lifestyle
factors and mental health measures among community-dwelling older
women. Austr N ZJ Psychiatry 38: 940-947.
Chang, G, McNamara TK, Orav EJ et al. 2005, Brief intervention for prenatal alcohol
use: a randomized trial. Obstet Gynecol 105(5 Pt 1): 991-998.
Chanraud, S, Martelli C, Delain F et al. 2007, Brain morphometry and cognitive
performance in detoxified alcohol-dependents with preserved psychosocial
functioning. Neuropsychopharmacol 32: 429-438.
Chikritzhs, T and M Brady 2006, Fact or fiction? A critique of the National Aboriginal
and Torres Strait Islander Social Survey 2002. Drug Alcohol Rev 25(3): 277287.
Chikritzhs, T and R Pascal 2005a, Trends in alcohol consumption and related harms
for Australians aged 65 to 74 years (the 'young-old'), 1990-2003, National
Alcohol Indicators. Perth: National Drug Research Institute, Curtin University
of Technology.
Chikritzhs, T, T Stockwell and R Pascal 2005, The impact of the Northern Territory's
Living With Alcohol program, 1992-2002: revisiting the evaluation. Addiction
100(11): 1625-1636.
Chung, T, Martin CS, Grella CE et al. 2003, Course of alcohol problems in treated
adolescents. Alcohol Clin Exp Res 27(2): 253-61.
Conigrave, K, E Proude and P d'Abbs 2007, Evaluation of the Groote Eylandt and
Bickerton Island Alcohol Management System: a report produced for the
Department of Justice, Northern Territory Governmen. University of Sydney;
Menzies School of Health Research, Darwin; James Cook University, Cairns.
Cooney, NL, Kadden RM, Litt MD et al. 1991, Matching alcoholics to coping skills or
interactional therapies: two-year follow-up results. J Consult Clin Psychol
59(4): 598-601.
Cooper, SJ 1978, Poisoned people: psychotropic drugs in pregnancy: morphological
and psychological adverse effects on offspring. J Biosoc Sci 10(3): 321-334.
207
Cornelius, JR, Maisto SA, Pollock NK et al. 2003, Rapid relapse generally follows
treatment for substance use disorders among adolescents. Addict Behav
28(2): 381-386.
Dart, RC 2001, The use and effect of analgesics in patients who regularly drink
alcohol. Am J Manag Care 7: 597-601.
Dawe, S, Loxton NJ, Hides L et al. 2002, Review of diagnostic screening instruments
for alcohol and other drug use and other psychiatric disorders. Canberra:
Australian Government Department of Health and Aging.
Davies, SJ, Pandit SA, Feeney A et al 2005, Is there cognitive impairment in clinically
‘healthy’ abstinent alcohol dependence? Alcohol Alcohol 40: 498-503.
Day, E, Benthan P, Callaghan R et al. 2004, Thiamine for Wernicke-Korsakoff
syndrome in people at risk from alcohol abuse. Cochrane Database Syst Rev
1, CD004003.
Deas, D 2008, Evidence-based treatments for alcohol use disorders in adolescents.
Pediatrics 121 Suppl 4: S348-354.
Deas, D, May K, Randall C et al. 2005, Naltrexone treatment of adolescent
alcoholics: An open-label pilot study. J Child Adolesc Psychopharmacol 15(5):
723-728.
DeCarli, C, Miller BL, Swan GE et al. 2001, Cerebrovacualr and brain morpholic
correlates of mild cognitive eimpairment in the National Heart, Lung and
Blood Institute Twin Study. Arch Neurol 58: 643-647.
Deng, J, Zhou DHD, Li J et al. 2006, A 2-year follow-up study of alcohol consumption
and risk of dementia. Clin Neurol Neurosurg 108: 378-383.
Djousse, L, Biggs ML, Mukamal KJ et al. 2007, Alcohol consumption and type 2
diabetes among older adults: the Cardiovascular Health Study. Obesity
(Silver Spring) 15(7): 1758-1765.
Donnino, MW, Vega J, Miller J et al. 2007, Myths and misconceptions of Wernicke's
encephalopathy: What every emergency physician should know. Ann Emerg
Med 50(6): 715-721.
Ekerdt, DJ, DeLabry LO, Glynn R et al. 1989, Change in drinking behaviors with
retirement: findings from the normative aging study. J Stud Alcohol 50: 347353.
Ellison, RC, Wannamethee SG, Rimm EB et al. 2007, Panel Discussion 1: Does
alcohol consumption prevent cardiovascular disease? Ann Epidemiol 17:
S37-S39.
Evans, JG 2000, Oxford Textbook of Geriatric Medicine. Oxford, Oxford University
Press.
Feeney, GF and JP Connor 2008, Wernicke-Korsakoff syndrome (WKS) in Australia:
no room for complacency. Drug Alcohol Rev 27(4): 388-392.
208
Fillmore, KM, Kerr WC, Stockwell T et al. 2006, Moderate alcohol use and mortality
risk: Systematic error in prospective studies. Addict Res Theory 14(2).
Filmore, K, Kerr WC, Stockwell T et al. 2003, Changes in drinking status, serious
illness, and mortality. J Stud Alcohol 64(2): 278-285.
Fleming, J 1996, The epidemiology of alcohol use in Australian women: findings from
a national survey of women's drinking. Addiction 91(6): 1325-1334.
Fleming, MF, Mundt MP, French MT et al. 2002, Brief physician advice for problem
drinkers: long-term efficacy and benefit-cost analysis. Alcohol Clin Exp Res
26(1): 36-43.
Floyd, RL, Sobell M, Velasquez MM et al. 2007, Preventing Alcohol-Exposed
Pregnancies: A Randomized Controlled Trial. Am J Prevent Med 32(1): 1-10.
Foster, D, Williams R, Campbell D et al. 2006, Researching ourselves back to life:
new ways of conducting Aboriginal alcohol research. Drug Alcohol Rev 25(3):
213-217.
Foxcroft, DR, Ireland D, Lowe G et al. 2008, Primary prevention for alcohol misuse in
young people. Cochrane Database of Systc Rev (2).
Ganguli, M, Bilt JV, Saxton JA et al. 2005, Alcohol consumption and cognitive
function in late life - A longitudinal community study. Neurology 65(8): 12101217.
Glass, JM, Buu A, Adams KM et al 2009 Effects of alcoholism severity and smoking
on executive neurocognitive function. Addiction 104: 38–48.
Goldberg, I 2003, To drink or not to drink? (editorial). N Eng J Med 348(2): 163-164.
Goldman, M 1995, Recovery of cognitive functioning in alcoholics- the relationship to
treatment. Alc Health Res World 190: 148-154.
Gordon, AJ, Conigliaro J, Maisto SA et al. 2003, Comparison of consumption effects
of brief interventions for hazardous drinking elderly. Subst Use Misuse 38(8):
1017 - 1035.
Gray, D, Pulver LJ, Saggers S et al. 2006, Addressing indigenous substance misuse
and related harms. Drug Alcohol Rev 25(3): 183-188.
Gray, D, Saggers S, Sputore B et al. 2000, What works? A review of evaluated
alcohol misuse interventions among aboriginal Australians. Addiction 95(1):
11-22.
Grella CE, Hser YI, Joshi V et al. 2001, Drug treatment outcomes for adolescents
with comorbid mental and substance use disorders. J Nerv Ment Dis
189(6):384-392.
Gulbransen, G and R McCormick 2007, Drink to your health- is alcohol really
cardioprotective? NZ Fam Physician 34(2): 122-126.
209
Harper, C 1998, The neuropathology of alcohol-specific brain damage, or does
alcohol damage the brain? J Neuropathol Exp Neurol 57(2): 101-110.
Harper, CG, M Giles and R Finlay-Jones 1986, Clinical signs in the WernickeKorsakoff complex: a retrospective analysis of 131 cases diagnosed at
necropsy. J Neurol Neurosurg Psychiatry 149(4): 341-345.
Harper, CG, Sheedy DL, Lara AI et al. 1998, Prevalence of Wernicke-Korsakoff
syndrome in Australia: has thiamine fortification made a difference? Med J
Aust 168(11): 542-545.
Heather, N, Copello A, Godfrey C et al. 2008, UK Alcohol Treatment Trial: clienttreatment matching effects. Addiction 103: 228-238.
Hibell, B, Andersson B, Bjarnasson T et al. 2004, The ESPAS Report 2003. Alcohol
and other drug use among students in 35 European countries. Stockholm,
Sweden.
Hogan, E, Boffa J, Rosewarne C et al. 2006, What price do we pay to prevent
alcohol-related harms in Aboriginal communities? The Alice Springs trial of
liquor licensing restrictions. Drug Alcohol Rev 25(3): 207-212.
Jaddoe, VW, Bakker R, Hofman A et al. 2007, Moderate alcohol consumption during
pregnancy and the risk of low birth weight and preterm birth. The generation
R study. Ann Epidemiol 17(10): 834-840.
Jones, KL and DW Smith 1973, Recognition of the fetal alcohol syndrome in early
infancy. Lancet 2(7836): 999-1001.
Kaufman, DW, Kelly JP, Wiholm BE et al. 1999, The risk of acute major
gastrointestinal bleeding among users of aspirin and ibuprofen at various
levels of alcohol consumption. Am J Gastronenterol 94(11): 3189-3196.
Khan, N, TJ Wilkinson and S Keeling 2006, Reasons for changing alcohol use
among older people in New Zealand. Australas J Ageing 25: 97-100.
Korrapati, MR and RE Vestal 1995, Alcohol and medications in the elderly: Complex
interactions. New York, Oxford University Press.
Leeman, RF, Palmer RS, Corbin WR et al. 2008, A pilot study of naltrexone and
BASICS for heavy drinking young adults. Addict Behav 33(8): 1048-1054.
Lifrak, PD, Alterman AI, O'Brien CP et al. 1997, Naltrexone for alcoholic adolescents.
Am J Psychiatry 154(3): 439-441.
Lishman, WA 1998, Cerebral beriberi (Wernicke's encephalopathy). J Psychosom
Res 44(6): 631-632.
Loeber, S, Duka T, Welzel H et al. 2009, Impairment of cognitive abilities and
decision making after chronic use of alcohol: the impact of multiple
detoxifications. Alcohol Alcohol 44(4): 372-81.
210
Loxley, W, Toumbourou J, Stockwell T et al. 2004, The Prevention of Substance
Use, Risk and Harm in Australia: A review of the evidence. Canberra:
Australian Government Department of Health and Ageing.
Lyndsay, J, Laurin D, Verreault R et al. 2002, Risk factors for Alzheimer's disease: a
prospective analysis from the Canadian Study of Health and Aging. Am J
Epidemiol 156: 445-453.
Maddox, GL 1985, Intervention strategies to enhance well-being in later life: the
status and prospect of guided change. Health Serv Res 19: 1007-1018.
Maio, RF, Shope JT, Blow FC et al. 2005, A Randomized Controlled Trial of an
Emergency Department-Based Interactive Computer Program to Prevent
Alcohol Misuse Among Injured Adolescents. Ann Emerg Med 45(4): 420-429.
Manwell, LB, Fleming MF, Mundt MP et al. 2000, Treatment of problem alcohol use
in women of childbearing age: results of a brief intervention trial. Alcohol: Clin
Exp Res 24(10): 1517-1524.
Marlatt, GA, Baer JS, Kivlahan DR et al. 1998, Screening and brief intervention for
high-risk college student drinkers: results from a 2-year follow-up
assessment. J Consult Clin Psychol 66(4): 604-615.
Martin, C and K Winters 1998, Diagnosis and assessment of alcohol use disorders
among adolescents. Alcohol Health and Research World 22(2): 95.
Martin, D and M Brady 2004, Human rights, drinking rights? Alcohol policy and
Indigenous Australians. Lancet 364(9441): 1282-1283.
Mattace-Raso, FU, van der Cammen TJ, van den Elzen AP et al. 2005, Moderate
alcohol consumption is associated with reduced arterial stiffness in older
adults: the Rotterdam study. J Gerontol A Biol Sci Med Sci 60(11): 14791483.
McArdle, P 2008, Alcohol abuse in adolescents. Arch Dis Child 93(6): 524-527.
McGuire, LC, Ajani UA, and ES Ford 2007, Cognitive impairment in late life: the
impact of moderate alcohol consumption. Ann Epidemiol 17: 93-99.
McMurtray, A, Clark DG, Christine D et al. 2006, Early-onset dementia: Frequency
and causes compared to late-onset dementia. Dement Geriatr Cogn Disord
21: 59-64.
Monti, PM, Barnett NP, Colby SM et al. 2007, Motivational interviewing versus
feedback only in emergency care for young adult problem drinking. Addiction
102(8): 1234-1243.
Monti, PM, Colby SM, Barnett NP et al. 1999, Brief intervention for harm reduction
with alcohol-positive older adolescents in a hospital emergency department. J
Consult Clin Psychol 67(6): 989-994.
Moos, RH, Brennan PL, Schutte KK et al. 2005, Older adults' health and changes in
late-life drinking patterns. Aging Ment Health 9(1): 49 - 59.
211
Morgenstern, J and ME Bates 1999, Effects of executive function impairment on
change processes and substance use outcomes in 12-step treatment. J Stud
Alcohol 60(6): 846-855.
Moselhy, HF, G Georgiou and A Kahn 2001, Frontal lobe changes in alcoholism: a
review of the literature. Alcohol Alcohol 36: 357-368.
Mukamal KJ, Chung H, Jenny NS et al. 2005, Alcohol use and risk of ischemic stroke
among older adults: the cardiovascular health study. Stroke 36(9): 18301834.
Mukamal KJ, Jenny NS, Tracy RP et al. 2007, Alcohol consumption, interleukin-6
and apolipoprotein E genotypes, and concentrations of interleukin-6 and
serum amyloid P in older adults. Am J Clin Nutr 86(2): 444-450
Mukamal, K, Kuller L, Fitzpatrick A et al. 2003, Prospective study of alcohol
consumption and risk of dementia in older adults. JAMA 289(11): 1405-1417.
Mundt, M, French MT, Roebuck MC et al. 2005, Brief physician advice for problem
drinking among older adults: an economic analysis of costs and benefits. J
Stud Alcohol 66: 389-394.
National Institute on Alcohol Abuse and Alcoholism 1995, Alcohol alert. Bethesda,
MD, National Institute on Alcohol Abuse and Alcoholism.
Niederhofer, H and W Staffen 2003, Acamprosate and its efficacy in treating alcohol
dependent adolescents. Eur Child Adolesc Psychiatry 12(3): 144-148.
Noel X, Paternot J, Van Der Linden M et al. 2001, Correlation between inhibition,
working memory and delimited frontal area blood flow measure by 99mTcBicisate SPECT in alcohol-dependent patients. Alcohol Alcohol 36: 556–63.
O'Connor, MJ and SE Whaley 2007, Brief intervention for alcohol use by pregnant
women. Am J Public Health 97(2): 252-258.
O'Halloran, J, Britt H, Valenti L et al. 2003, Older patients attending general practice
in Australia 2000-02. Canberra: Australian Institute of Health and Welfare.
Ouellette, EM, Rosett HL, Rosman NP et al. 1977, Adverse effects on offspring of
maternal alcohol abuse during pregnancy. N Engl J Med 297(10): 528-530.
Paganini-Hill, A Kawas C and M Corrada 2007, Type of alcohol consumed, changes
in intake over time and mortality: the Leisure World Cohort Study. Age Ageing
36: 203-209.
Parsons, OA, Schaeffer KW and SW Glenn 1990, Does neuropsychological testperformance predict resumption of drinking in posttreatment alcoholics?
Addict Behav 15(3): 297-307.
Perreira, KM and FA Sloan 2001, Life events and alcohol consumption among
mature adults: A longitudinal analysis. J Stud Alcohol 62: 501-508.
212
Pitkanen, T, Lyyra A-L and Pulkkinen, L 2005, Age of onset of drinking and the use of
alcohol in adulthood: a follow-up study from age 8-42 for females and males.
Addiction 100(5): 652-661.
Project MATCH Research Group 1997, Matching alcoholism treatments to client
heterogeneity: Project MATCH posttreatment drinking outcomes. J Stud
Alcohol 58(1): 7-29.
Project MATCH Research Group 1998, Matching alcoholism treatments to client
heterogeneity: Project MATCH three-year drinking outcomes. Alcoholism:
Clinical and Experimental Research 22(6): 1300.
Rice, C, Longabaugh R, Beattie M et al. 1993, Age group differences in response to
treatment for problematic alcohol use. Addiction 88: 1369-1375.
Rimm, E, Booyse FM, Fillmore K et al. 2007, Panel discussion IV: Implications for
future research. Ann Epidemiol 17: S95-S97.
Roberts, RE, CR Roberts and Y Xing 2007, Comorbidity of substance use disorders
and other psychiatric disorders among adolescents: evidence from an
epidemiologic survey. Drug Alcohol Depend 88 (Suppl 1): S4-13.
Rodgers, B, Windsor TD, Anstey K et al. 2005, Non-linear relationships between
cognitive function and alcohol consumption in young, middle-aged and older
adults: the PATH Through Life Project. Addiction 100: 1280-1290.
Ruttenberg, A, Van Swieten JC, Witteman JC et al. 2002, Alcohol consumption and
risk of dementia: the Rotterdam study. Lancet 359: 281-286.
Rychtarik, RG, Connors GJ, Whitney RB et al. 2000, Treatment settings for persons
with alcoholism: evidence for matching clients to inpatient versus outpatient
care. J Consult Clin Psychol 68(2): 277-289.
Sanci LA, Sawyer SM, Kang MS et al. 2005 Confidential health care for adolescents:
reconciling clinical evidence with family values. Med J Aust 183(8): 410-414.
Satre, DD, Blow FC, Chi FW et al. 2007, Gender differences in seven-year alcohol
and drug treatment outcomes among older adults. Am J Addict 16(3): 216221.
Saunders, B, Baily S, Phillips M et al. 1993a, Women with alcohol problems- do they
relapse for reasons different to their male counterparts? Addiction 88(10):
1413-1422.
Saunders, JB, Aasland OG, Babor TF et al. 1993b, Development of the Alcohol Use
Disorders Identification Test (AUDIT): WHO Collaborative Project on Early
Detection of Persons with Harmful Alcohol Consumption - II. Addiction 88:
791-804.
Sawyer, SM, Drew S, Yeo MS et al. 2007 Adolescents with a chronic condition:
challenges living, challenges treating. Lancet 369(9571): 1481-1489.
213
Schlesinger, C, Ober C, McCarthy M et al. 2007, The development and validation of
the Indigenous Risk Impact Screen (IRIS): a 13-item screening instrument for
alcohol and drug and mental health risk. Drug Alcohol Rev (26): 109-117.
Schoeller, DA 1989, Changes in total body water with age. Am J Clin Nutr 50: 11761181.
Sechi, G and A Serra 2007, Wernicke's encephalopathy: new clinical settings and
recent advances in diagnosis and management. Lancet Neurol 6(5): 442-455.
Selvanathan, EA and S Selvanathan 2004, Economic and demographic factors in
Australian alcohol demand. Appl Economics 36(21): 2405-2418.
Sibthorpe, B, Bailie RS, Brady MA et al. 2002, The demise of a planned randomised
controlled trial in an urban Aboriginal medical service. Med J Aust 176: 273276.
Smith, DE and BS McCrady 1991, Cognitive impairment among alcoholics: impact on
drink refusal skill acquisition and treatment outcome. Addict Behav 16(5):
265-274.
Sokol, R, V Delaney-Black and B Nordstrom 2003, Fetal Alcohol Spectrum Disorder
(brief report). JAMA 290: 2996-2999.
Spirito, A, Monti PM, Barnett NP et al. 2004, A randomized clinical trial of a brief
motivational intervention for alcohol-positive adolescents treated in an
emergency department. J Pediatr 145(3): 396-402.
Spooner, C, R Mattick and W Noffs 2001, Outcomes of a comprehensive treatment
program for adolescents with a substance disorder. J Subst Abuse Treat
20(3): 205-213.
Stampfer, MJ, Kang JH, Chen J et al. 2005, Effects of Moderate Alcohol
Consumption on Cognitive Function in Women. N Engl J Med 352(3): 245253.
Tanaka, E 2003, Toxicological interactions involving psychiatric drugs and alcohol:
An update. J Clin Pharm Therap 28: 81-95.
Teasdale, KE, Conigrave KM, Kiel KA et al. 2008, Improving services for prevention
and treatment of substance misuse for Aboriginal communities in a Sydney
Area Health Service. Drug Alcohol Rev 27(2):152-159.
Thomas, DP, Heller RF and JM Hunt 1998, Clinical consultations in an aboriginal
community-controlled health service: a comparison with general practice.
Aust N Z J Public Health 22(1): 86-91.
Thomson, AD, Cook CCH, Touquet R et al. 2002, The Royal College of Physicians
report on alcohol: guidelines for managing Wernicke's encephalopathy in the
accident and emergency department, Alcohol Alcohol Suppl 37(6): 513–521.
214
Thush, C, Wiers RW, Theunissen N et al. 2007, A randomized clinical trial of a
targeted intervention to moderate alcohol use and alcohol-related problems in
at-risk adolescents. Pharmacol Biochem Behav 86(2): 368-376.
Tjonneland, AM, Gronbaek MN, Stripp C et al. 1999, [The connection between food
and alcohol intake habits among 48.763 Danish men and women. A crosssectional study in the project "Food, cancer and health"]. Ugeskr Laeger
161(50): 6923-6927.
Torvik, A 1991, Wernicke's encephalopathy--prevalence and clinical spectrum.
Alcohol Alcohol Suppl 1:381-384.
Toumbourou, JW, Hemphill SA, Tresidder J et al. 2007, Mental health promotion and
socio-economic disadvantage: lessons from substance abuse, violence and
crime prevention and child health. Health Promot J Austr 18(3):184-90.
Truelsen, T, Thudium D and M Gronbaek 2002, Amount and type of alcohol and risk
of dementia: the Copenhagen City Heart Study. Neurology 59: 1313-1319.
Tyas, SL, Manfreda J., Strain LA et al. 2001, Risk factos for Alzheimer's disease: a
population-based, longitudinal study in Manitoba, Canada. Int J Epidemiol
30: 590-597.
Tylee A, Haller DM, Graham T et al. 2007 Youth-friendly primary-care services: how
are we doing and what more needs to be done? Lancet 369(9572): 1565-73.
Uekermann J and I Daum 2008, Social cognition in alcoholism: a link to prefrontal
cortex dysfunction? Addiction 103(5): 726-35.
United Nations Department of Economic and Social Affairs 2003, Report on the
World Social Situation 2003. Social Vulnerability: Sources and Challenges.
New York, United Nations.
Victor, M, RD Adams and GH Collins 1989, The Wernicke-Korsakoff Syndrome and
related Neurological disorders due to alcoholism and malnutrition.
Philadelphia: F A Davis Company.
Vogel-Sprott, M and P Barrett 1984, Age, drinking habits and the effects of alcohol. J
Stud Alcohol 45: 517-521.
Watson, PE, IA Watson and RD Batt 1980, Total body water volumes for adult males
and females from simple anthropometric measurements. Am J Clin Nutr 33:
27-39.
Weathermon, R and DW Crabb 1999, Alcohol and medication interactions. Alcohol
Res Health 23: 40-54.
White, V and J Hayman 2004 Australian secondary students' use of alcohol in 2002.
National Drug Strategy Monograph Series No. 55. Canberra: Australian
Government Department of Health and Aging.
215
Winters, K, Stinchfield R, Opland E et al. 2000, The effectiveness of the Minnesota
Model approach in the treatment of adolescent drug abusers Addiction 95(4):
601-612.
Wold, M and Y Kaminer 1997, Naltrexone for alcohol abuse. J Am Acad Child
Adolesc Psychiatry 36(1): 6-7.
World Cancer Research Fund/ American Institute for Cancer Research 2007, Food,
nutrition, physical activity and cancer: a global perspective. Washington, DC.,
American Institute of Cancer Research.
Zimmerman, T, McDougall GJ and H Becker 2004, Older women's cognitive and
affective response to moderate drinking. Int J Geriatr Psychiatry 19: 10951102.
216
Chapter 10
Comorbidities
This chapter discusses treatment approaches to patients with alcohol-related
physical comorbidity, co-occurring mental and alcohol use disorders, and people
using multiple drugs (the latter section primarily focusing on people who are polydrug
dependent).
Alcohol-related physical comorbidity
Recommendation
10.1 Comprehensive assessment is indicated
for patients with physical comorbidity related to
alcohol, as multiple pathology is the rule.
10.2 Abstinence is recommended for those
with physical comorbidity related to alcohol
unless mild and reversible pathology is
present. In particular, pancreatitis may recur
after a single drink.
10.3 Comprehensive management requires a
single practitioner with a broad range of clinical
skills or close coordination between an
appropriate team.
Strength of
Level of
recommendation evidence
A
1
D
IV
S
People with alcohol use disorders often have associated physical comorbidities.
These include peripheral neuropathy, brain damage, liver disease, gastritis and
pancreatitis; heart and vascular diseases, nutritional disorders (e.g. malnutrition or
thiamine deficiency), metabolic disorders (e.g. hypoglaecemia), endocrine
deficiencies (e.g. reduced fertility) and cutaneous problems (e.g. porphyria, psoriasis,
excema); malignancies, and infections (see table).
Accidents, injuries and poisonings are also associated with excessive alcohol use
and intoxication (Adrian and Barry 2003). Adrian et al compared the nature and
extent of treated health problems in patients with problems related to the use of
alcohol and drugs (including both licit and illicit drugs) with the morbidity levels of all
patients treated in Ontario, Canada, hospitals for 1985-86, using age-sex
standardised morbidity ratios. The morbidities of all inpatients with alcohol or drug
diagnoses (n = 52,200) were examined retrospectively through the medical records.
Excess morbidity for alcohol patients affected more diagnostic categories and body
systems, and was at a higher level than for drug patients. Both had particularly high
morbidity for mental disorders, infectious and parasitic diseases, and injury and
poisoning (Adrian and Barry 2003). Alcohol dependence and misuse is also
implicated in the risk of suicide, especially in the elderly (Waern 2003).
217
Table 10.1: Alcohol use and physical complications
Gastrointestinal
Cardiovascular
Neurological
•
Liver disease, including alcohol-related fatty liver,
alcoholic hepatitis, alcohol-related cirrhosis and multiple
complications of cirrhosis and portal hypertension
•
Liver cell cancer – hepatocellular carcinoma
•
Acute and chronic pancreatitis
•
Parotid enlargement
•
Gastro-oesophageal reflux
•
Peptic ulcer, gastritis, duodenitis
•
Oesophageal rupture from violent vomiting bouts
•
Small bowel damage leading to malabsorption
•
Altered bowel habit with diarrhoea predominating
•
Hypertension
•
High output cardiac failure
•
Cardiomyopathy
•
Acute rhythm disturbances in alcohol intoxication
•
Coronary artery disease
•
Cortical atrophy
Cerebellar damage (midline structures maximally
affected)
•
•
Peripheral neuropathy
•
Autonomic neuropathy
•
Wernicke’s encephalopathy
•
Wernicke–Korsakoff syndrome
•
Central pontine myelinolysis
•
Marchiafava–Bignami syndrome
•
Myopathy
•
Cerebrovascular accidents
•
Withdrawal delirium and neuronal damage
218
Musculoskeletal
Haematological
•
Rhabdomyolysis
•
Compartment syndromes
•
Gout
•
Osteopaenia
•
Osteonecrosis
•
Thrombocytopaenia from bone marrow suppression
•
Pancytopaenia from hypersplenism
Haemolytic anaemia with advanced liver disease - spur
cell anaemia
•
Immunological
•
Macrocytic anaemia
•
Folate and B12 deficiency anaemias
•
Coagulopathies from liver disease
•
Impaired B and T cell function mediated by alcohol toxicity
•
Autoimmune phenomena triggered by acetaldehyde
adducts acting as immunogenic targets
Respiratory
Endocrine
•
IgA nephropathy
•
Increased predisposition to respiratory infection
•
TB as a common infection
•
Aspiration pneumonia
•
Sleep apnoea
•
Syndrome of inappropriate antidiuretic hormone secretion
(SIADH)
•
Altered thyroid function
•
Altered oestrogen metabolism associated with liver
damage
Renal
•
Masculinisation in women
•
Pseudo Cushing’s disease
•
Altered calcium and bone metabolism
•
Hypoglycaemia
•
Aggravation of diabetes mellitus
•
Ketoacidosis
•
Hypertriglyceridaemia
•
Testicular atrophy
•
Hypoparathyroidism
•
IgA nephropathy
219
Infectious
diseases
Nutritional
disorders
•
Hepatitis C virus
•
Pneumonia
•
Tuberculosis
•
Sexually transmitted diseases
Vitamin and mineral deficiencies; B1, B6, riboflavin,
niacin, calcium, phosphate, zinc, magnesium.
•
•
Alcohol and
malignancy
Protein calorie malnutrition
The risk of developing certain malignancies increases from base
risk levels with any alcohol consumption. These include breast,
oropharyngeal and oesophageal cancers. Other malignancies
such as colon, pancreatic, hepatic and ovarian are more
prevalent in those drinking more than 40 gm per day.
Whereas low or moderate alcohol consumption can be cardioprotective, heavy
drinking is associated with increased risks of hypertension, coronary heart disease,
and ischemic stroke, possibly due to alcohol-induced sympathetic activation. Chronic
excessive alcohol consumption is a strong risk factor for various types of cancer,
particularly of the respiratory tract, but also of the digestive system, liver, breast, and
ovaries, while heavy drinking is associated with various forms of alcoholic liver
disease such as cirrhosis. Alcohol dependence is also a major cause of mortality and
is associated with psychiatric conditions, neurologic impairment, cardiovascular
disease, liver disease, and malignant neoplasms. Dependence also increases the
risk of injury, possibly due to alcohol-related factors such as diminished coordination
and balance, increased reaction time, and impaired attention, perception, and
judgement (Cargiulo 2007).
A meta-analysis carried out by Corrao et al on the risk of 14 major alcohol-related
neoplasms and non-neoplastic diseases plus injuries showed, from 156 studies with
116,702 patients, strong trends in the risk for cancers of the oral cavity, oesophagus
and larynx, hypertension, liver cirrhosis, chronic pancreatitis, and injuries and
violence. Weaker direct trends were observed for cancers of the colon, rectum, liver,
and breast (Corrao et al. 2004). For all these conditions, significant increased risks
were found at ethanol intake of 25g per day. Threshold values were observed for
ischemic and hemorrhagic strokes. For coronary heart disease, a J-shaped relation
was observed with a minimum relative risk of 0.80 at 20 g/day, a significant protective
effect up to 72 g/day, and a significant increased risk at 89 g/day. No clear relation
was observed for duodenal ulcer. The authors conclude that there was no clear
evidence of a threshold effect for both neoplasms and several non-neoplastic
diseases.
A European study investigated physical health problems among patients with alcohol
use disorders at alcohol treatment agencies in six European cities (Gossop et al.
2007). The sample comprised 315 patients with a primary alcohol use disorder. Data
were collected at admission to treatment using a structured research protocol, and
ratings were made by a doctor after a physical examination of the patient. Physical
health problems were extremely common: 79% of the sample had at least one, and
59% had two or more problems. These were often serious, and 60% had at least one
problem that required treatment. The most common were gastrointestinal and liver
disorders, but about a quarter of the sample had cardiovascular or neurological
problems. Frequency of drinking, duration of alcohol use disorder, and severity of
220
alcohol dependence were associated with increased physical morbidity. Current
smoking status and age were also associated with poorer physical health. Older
drinkers had more physical health problems, although they were less severely
alcohol dependent than the younger patients. The authors conclude that the high
prevalence of physical health problems among problem drinkers provides
opportunities of screening for alcohol use disorders, not only in specialist alcohol
treatment services but also in other health-care settings. They recommend that
alcohol treatment agencies should provide a full routine health screen of patients at
admission to treatment with provision or referral to appropriate treatment.
The most commonly alcohol-associated physical condition is alcohol-related liver
disease, either fatty liver or cirrhosis. Alcohol-dependent individuals die from cirrhosis
at a much higher rate than does the general population (Cargiulo 2007). However,
patients with alcoholic liver disease have been considered less desirable liver
transplant candidates than patients with other types of liver disease (DiMartini et al.
2004). These authors examined the pre-transplant prevalence of comorbid physical
and psychological problems in 112 alcoholic liver disease patients who received a
liver transplant. Fifty-six percent of the patients had comorbid hepatitis C or hepatitis
B, 40% had used other substances in addition to alcohol, 25% met the criteria for a
lifetime DSM-IV non-alcohol substance use disorder, 36% for a lifetime depressive
disorder, and 12% for a lifetime anxiety disorder. They recommend that pretransplant psychiatric evaluation should be undertaken with alcoholic liver disease
patients to identify other substance use disorders and other psychiatric disorders that
may require treatment prior to admission.
Vascular diseases are another complication associated with alcohol consumption.
Epidemiologic studies have shown a J-shaped association between alcohol
consumption and vascular diseases, as also demonstrated in the meta-analysis
above (Corrao et al. 2004). However, only a few studies have reported on the
association between alcohol intake and subclinical atherosclerosis.
The aim of a German study (Schminke et al. 2005) was to investigate the relation
between alcohol intake and carotid intima-media thickness (IMT) in participants in a
very large study, the population-based Study of Health in Pomerania. In 1230 men
and 1190 women, the mean IMT of the right and left common carotid arteries was
measured by ultrasonography. Alcohol consumption was assessed at interview,
calculating the quantities of alcohol consumed from the ethanol content of the
specific drinks reported by patients. Linear regression controlled for age, diabetes,
systolic blood pressure, physical activity, eating patterns and frequency, smoking
status, and education revealed a significant inverse association between IMT and
alcohol intake < 80 g/d in men (p<0.02), which became insignificant after further
controlling for HDL cholesterol and fibrinogen. In women, no significant differences in
IMT were found between the two groups. The authors can conclude that alcohol
consumption was inversely correlated with carotid IMT in men but not in women;
however, the reported total daily level of alcohol intake was above the threshold
where severe alcohol related comorbidity and organ damage have been reported,
and correspondingly any potential protective effect of alcohol was accordingly lost.
Another study describes the relation between eating disorders and alcohol and drug
abuse (Conason et al. 2006). Eating-disordered patients are already at an increased
risk for morbidity and mortality, so that alcohol and drug use pose additional dangers
for these patients. Anorexics, binge eaters, and bulimics appear to be distinct
subgroups within this population, with binge eaters and bulimics more prone to
alcohol and drug use. Impulsivity has also been linked to both bulimia nervosa and
221
substance abuse. The authors say that interviewing is generally the most useful tool
in diagnosing alcohol and substance abuse disorders in these individuals (rather than
questionnaires etc), and they also recommend obtaining information from third
parties as patients may be unwilling to disclose their substance use.
The above studies suggest that all patients with alcohol use disorders should be
carefully assessed for physical (and psychological) comorbidities that would
otherwise be overlooked in treating the primary presenting condition. Abstinence
from alcohol is to be recommended for patients with comorbid physical problems,
especially pancreatitis (Strum 1995; Pelli et al. 2008; Tsujimoto et al. 2008) to
improve their quality of life and relief from pain.
Co-occurring Mental Disorders
Introduction
In Australia, of the 10,641 people surveyed for the National Survey of Mental Health
and Well Being in 1997, 1.9 percent met the criteria for alcohol abuse, and 4.1
percent met the criteria for alcohol dependence. Of this latter group around one in
five (20 percent) met criteria for an anxiety disorder and almost one in four (24
percent) met criteria for an affective or mood disorder. Other disorders associated
with alcohol dependence include other substance use disorders and psychosis
(Degenhardt et al. 2000).
One rural New South Wales health service’s data showed that 43% of inpatient and
20% of ambulatory mental health admission records indicated problem drinking or
drug-taking. Information gathered from focus groups conducted with consumer
groups and service providers indicated a reasonable level of awareness of comorbidity, and changes were underway to better meet patient needs; however, the
results indicated a lack of formalised care coordination, unclear treatment pathways,
and a lack of specialist care and resources to treat such patients (Hoolahan et al.
2006).
Indig et al. (2007) looked at presentations to Emergency Departments (ED) in New
South Wales and found that high-risk alcohol consumption, high psychological
distress and current smoking were all significantly and independently associated with
a greater likelihood of presenting to an emergency department in the last year. ED
presentation was found to be three times more likely for women aged 30-59 years
with all three risk factors, and ten times more likely for women aged 60 years or more
who reported high risk alcohol consumption and high psychological distress, than
similar-aged women without these risk factors. For individuals aged 16-29 years,
being a high-risk drinker and a current smoker doubled the risk of presentation to ED.
The authors conclude that the combination of being a high-risk consumer of alcohol,
having high psychological distress, and being a current smoker are associated with
increased presentations, independent of age and sex.
Scher et al studied 505 depressed subjects with and without co-occurring alcohol use
disorders (AUDs) between 2000 and 2005 (Sher et al. 2008). A total of 318 had
DSM-IV major depressive disorder without a history of any alcohol or substance
abuse/dependence and 187 had depression and a history of alcohol
abuse/dependence. Demographic, clinical, and psychiatric history measures of
patients in the two groups were examined and compared. Dual diagnosis patients
222
were significantly younger at their first psychiatric hospitalisation, their first major
depressive episode, and their first suicide attempt. They reported more previous
major depressive episodes, suicide attempts, and recent life events and had higher
lifetime aggression, impulsivity, and hostility. These patients were also more likely to
report tobacco smoking, a lifetime history of abuse, and a history of alcohol problems
among first-degree relatives, compared to depressive patients. They also had
significantly higher childhood, adolescent and adult aggression scores and reported
more behavioural problems during childhood. Scher’s findings suggest that in
addition to obtaining a history of depression and suicidal behaviour, clinicians should
also assess for an alcohol use disorder; conversely patients with alcohol use
disorders should be assessed for depression. Comorbididity may result from worse
antecedents and lead to early onset, more comorbidity, and a more severe course of
illness.
Co-occurrence of anxiety and depressive symptoms with alcohol consumption/abuse
was analysed by Almeida-Filho et al in a sample of 2,302 adults in Bahia, Brazil
(Almeida-Filho et al. 2007). A cross-sectional household survey collected selfreported information on social and personal health, as well as individual
psychological status. Prevalence was 15% for anxiety, 12% for depressive disorders
and 7% for alcohol abuse/ dependence. Symptom co-occurrence was more frequent
for depression (94% of cases), followed by anxiety disorders (82%), and alcoholism
(20%). There was a 74% prevalence of anxiety symptoms among depressives, and a
61% of anxiety sufferers also suffered depression. The combination of depression
plus anxiety was the most prevalent, ranging from 17% for women to 5% for men.
Levander et al (2007) conducted a structured clinical interview for DSM-IV with
bipolar men and women. They were then divided into (i) subjects meeting current or
lifetime criteria for an alcohol use disorder (n = 213), and (ii) those subjects who did
not (n=137). Lifetime rates of comorbid anxiety disorder were evaluated between
groups. Their results showed that of 350 subjects, 163 (46.5%) met criteria for an
anxiety disorder. Panic disorder and obsessive compulsive disorder (OCD) were the
most common anxiety disorders in both groups. OCD and specific phobia were
significantly less prevalent in patients with alcohol use disorders than those without,
and bipolar women with an alcohol use disorder had a significantly higher rate of
post-traumatic stress disorder than those without.
Thus there is clear evidence for increased prevalence of mental disorders in people
with alcohol use disorders. The co-occurrence of mental and alcohol use disorders
presents special challenges in the treatment of individuals with alcohol problems.
There is some evidence that the co-occurrence is associated with greater disability
and poorer response to treatment (Schneider et al. 2001; Farrell et al. 1998; Project
MATCH Research Group 1997; Terra et al. 2006; Tomasson and Vaglum 1996;
Tomasson and Vaglum 1998a). In addition, a higher readiness to change problem
drinking has been found in outpatients with dual diagnoses (Velasquez et al. 1999),
although it could also be that the more psychiatric distress the person is
experiencing, the more tempted they are to drink.
There are diagnostic dilemmas. Some of the co-occurrence appears to be a direct or
withdrawal effect of alcohol which remits with abstinence of at least three weeks
duration (Schuckit and Hesselbrock 1994; Schuckit and Monteiro 1988). In other
cases mental disorders are in parallel with alcohol use disorders. Still further cases
show signs of mental disorders and alcohol interacting to cause greater problem
severity, disability and poorer response to treatment.
223
Recommendation
10.4 Patients with comorbid disorders of
alcohol use and persisting mental health
comorbidity should be offered treatment for
both disorders.
10.5 More intensive interventions are needed
for comorbid patients, as this population tends
to be more disabled and carries a worse
prognosis than those with single pathology.
Strength of
Level of
recommendation evidence
A
1b
B
I
Assessment and diagnosis
Firstly, given the high prevalence of other disorders amongst patients with an alcohol
use disorder, it is essential that checking for particularly common problems such as
anxiety and depression symptoms is a routine part of the assessment. Secondly, the
AUDIT appears to be a suitable screening tool for identifying risky, problem and
dependent alcohol consumption amongst psychiatric patients (Cassidy et al. 2008;
Dawson et al. 2005). Physical comorbidities and sociodemographic factors have an
effect on neurocognitive functioning and also need to be assessed (Durazzo et al.
2008).
Recommendation
10.6 AUDIT is recommended for screening
psychiatric populations.
Strength of
Level of
recommendation evidence
A
Ib
The key issue in the assessment of co-occurring mental disorders is whether they
are an effect of alcohol or a separate comorbid disorder. Some epidemiological data
suggest that social phobia but not panic disorder begins before alcohol consumption
and may have a distinct genetic vulnerability (Merikangas et al. 1998) suggesting that
the age of onset may be one way to determine whether co-occurring symptoms of
mental disorders are an artefact of alcohol consumption or withdrawal. A period of
abstinence is the most widely used method to make a differential diagnosis (Brown et
al. 1991; Schuckit et al. 1994; Schuckit et al. 1988).
It may be possible to differentiate between primary and secondary depressive
disorders, which may have implications for treatment strategies, since secondary
depression often abates once the alcohol use disorder is addressed (Schuckit et al.
1997). In this study, individuals who met DSM-III criteria for alcohol dependence
were selected from a particular ongoing US cohort study. Almost 42 percent of
dependent drinkers met criteria for a diagnosis of a concomitant major depressive
episode. Of those, more than 60 percent reported a substance-induced period of
depression. Those with primary depression also had a higher prevalence of
independent depressive disorders in first-degree relatives. These individuals typically
had experience with fewer drugs and less treatment for alcohol problems and were
more likely to have attempted suicide. However, the clinical presentation of
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symptoms did not differ substantially between substance-induced and primary
depressive disorders.
Recommendation
10.7 Assessment for comorbid disorders
should take place once the patient’s
withdrawal syndrome has diminished, since
some anxiety and depressive symptoms may
abate once alcohol consumption is reduced or
ceased.
Strength of
Level of
recommendation evidence
B
II
Co-occurring alcohol dependence and mental disorders: Reviews and metaanalyses
A study in the USA by Sullivan et al (2005) reviewed the literature looking for
answers to the following questions. How common are alcohol problems in patients
with depression? Does alcohol affect the course of depression, response to
antidepressant therapy, risk of suicide/death, social functioning and health care
utilisation? In which alcohol categories and treatment settings have patients with
depression and alcohol problems been evaluated? Studies were selected using
predefined criteria of reporting on either the prevalence or the effects of alcohol
problems in depression. Thirty-five studies were included and revealed a median
prevalence of current or lifetime alcohol problems in depression of 16% (range 567%) and 30% (range 10-60%), respectively, compared to 7% for current and 1624% for lifetime alcohol problems in the general population. The majority of the
studies evaluated alcohol abuse and dependence, and 25 of 35 (71%) were
conducted in psychiatric inpatients. They found evidence that antidepressants
improved depression outcomes in persons with alcohol dependence. Alcohol
problems were associated with worse outcomes with respect to course of
depression, suicide/death risk, social functioning, and use of health care services.
The authors conclude that alcohol problems are more common in depression than in
the general population, are associated with adverse clinical and health care
outcomes, and that antidepressants can be effective in treatment of depression
associated with alcohol dependence. In addition, one of the drawbacks of their
search was that the literature they found seemed to focus almost exclusively on
patients with alcohol use disorders, including dependence, in psychiatric inpatient
locations, and excluded individuals with less severe alcohol problems and in
outpatient settings.
Davis et al (2008) reviewed a recent systematic research on distinguishing baseline
characteristics, including demographics and the influence of family history, clinical
features such as depressive symptoms and suicidal ideation, and the outcome of
treatment for depression, in patients with comorbid major depressive disorder and
substance use disorders. They also addressed the possible explanations cited in the
literature as to why these two disorders tend to co-occur and the implications of the
comorbidity of these illnesses on treatment. Their findings showed that nearly onethird of patients with a major depressive disorder also had a substance use disorder,
and the comorbidity resulted in a higher risk of suicide and greater social and
personal impairment, as well as other psychiatric conditions. Although the treatment
of comorbid major depressive disorder and substance use disorders with medication
can often be effective, this has not yet been the subject of many rigorous studies to
225
date. The authors’ conclusions are that the emerging results of recent studies
comparing the outcome of major depressive disorder patients with comorbid major
depressive disorder and substance use disorders suggest that there are fewer
differential effects based on comorbidity than previously anticipated by older
assumptions from smaller, less methodologically rigorous studies.
Degenhardt and Hall described patterns of co-morbidity between alcohol use and
other substance use problems in the Australian population using data from the 1997
National Survey of Mental Health and Well-Being (Degenhardt, Louisa and Hall
2003). Multiple regression analyses examined whether the observed associations
between alcohol and other drug use disorders were explained by other variables,
including demographic characteristics and neuroticism. They also assessed whether
the presence of co-morbid substance use disorders affected treatment seeking for a
mental health problem. Alcohol use was related strongly to the use of other
substances; those who did not drink alcohol within the past 12 months were less
likely to report using tobacco, cannabis, sedatives, stimulants or opiates. Half (51%)
of those who were alcohol-dependent were regular tobacco smokers and one-third
had used cannabis (32%); 15% reported other drug use; 15% met criteria for a
cannabis use disorder and 7% met criteria for another drug use disorder. Co-morbid
substance use disorders (sedatives, stimulants or opioids) predicted a high likelihood
of seeking treatment for a mental health problem among alcohol-dependent people.
Anxiety: impact on treatment of alcohol dependence
There are several studies that have addressed the impact of comorbid anxiety
disorders on outcomes of treatment for alcohol dependence. Evidence from these is
conflicting. Results from some of the earlier studies (Tomasson and Valgum 1996,
1998a, 1998b; Driessen et al. 2001) suggest that comorbidity is associated with
worse alcohol treatment outcome, relapse and readmissions.
Tomasson’s 1996 study (Tomasson and Valgum 1996) looked at the association
between psychopathology and alcohol consumption in a sample of inpatient
dependent alcoholics (n = 245) who were examined at intake and at 15 month
follow-up. At baseline, men and women with antisocial personality disorder or
cognitive impairment consumed more alcohol in the month prior to admission than
those without these disorders. In contrast, men with panic disorder drank less than
those not so affected. The prognosis for men consuming more than the median
amount of alcohol was worse than that of women. However, after controlling for
psychiatric distress and alcohol consumption at baseline, the prognosis of women
was worse. Women who had stopped drinking had a higher degree of psychiatric
distress at follow-up compared with those still drinking at a low level. Among men,
panic disorder predicted continued drinking. Psychiatric distress and alcohol
consumption at baseline both interacted to predict alcohol consumption at follow-up.
Another study by the same authors (Tomasson and Valgum 1998a) was a
prospective study over a 28-month period in Iceland using a representative sample (n
= 351), examining the association among patients seeking detoxification between
comorbid psychopathology and (1) number of lifetime admissions, (2) readmissions
for detoxification, and (3) a repeating (revolving-door) pattern of admission (>4
admissions within 30 months). Patients with no comorbid diagnoses had the fewest
lifetime admissions. Agoraphobia or panic disorder predicted readmission (odds ratio
5.8) for those with fewer than two prior admissions. For those with 3 or more prior
admissions, readmissions were primarily related to polysubstance abuse. The
development of the revolving-door pattern was rare (6%) among those with less than
226
4 prior admissions. Among others (27%), it was primarily predicted by polysubstance
abuse.
Another Tomasson study (Tomasson and Valgum 1998b) produced similar results in
that polysubstance use had clear implications for worse outcomes. Controlling for
alcohol consumption, polysubstance abuse predicted accidents (odds ratio, OR =
2.9) and fights (OR = 3.9) among men, while phobia (OR = 4.3) and antisocial
personality disorder (OR = 3.0) predicted fights in both men and women.
A cluster analysis by Driessen et al (2001) examined the association between
drinking behaviour and the course of anxiety and depression in 100 alcohol
dependent patients with and without these comorbid disorders during the early and
late post-detoxification periods. At 6 months, abstinence rates differed significantly
between groups: 60.5% non-comorbid vs. 30.5% comorbid anxiety and depression
vs. 23.5% anxiety alone). Although not definitive, it appears that comorbid anxiety
disorders may be associated with a poorer treatment outcome for alcohol
dependence.
However, in contrast, Marquerie et al (2006) examined whether the outcome of
treatment-seeking alcohol dependent patients with a comorbid phobic disorder was
worse than that of similar patients without comorbidity. The probabilities of resuming
drinking and relapsing into regular heavy drinking in 81 alcohol-dependent patients
with comorbid social phobia or agoraphobia were compared with 88 alcoholdependent patients without anxiety disorders. Their results showed that the risk ratio
for the association of phobic disorders with resumption of drinking was 1.05, (p =
0.66) and the adjusted hazard ratio for the association of phobic disorders with a
relapse into regular heavy drinking was 1.02 (p = 0.89). The findings of this study did
not confirm the idea that alcohol-dependent patients who have undergone treatment
are at greater risk of a relapse if they have a comorbid anxiety disorder. No
differences were found in abstinence duration or time to relapse into regular heavy
drinking between patients with and without comorbid phobic disorders.
In addition, Terra et al (2006) in Brazil investigated the impact of social phobia on
adherence to and outcomes 6 months following standard alcohol treatment and
Alcoholics Anonymous group meetings among alcohol-dependent patients with and
without social phobia. Alcohol-dependent patients (n = 300) were interviewed during
admission for detoxification and at 3 and 6 months afterwards. At both follow-ups,
treatment adherence was low and relapse rates were high among both groups of
patients, and no significant differences were seen between the two groups in amount
of relapse, adherence to AA, or adherence to psychotherapy. Although the social
phobics showed a tendency to be less committed to treatment, or felt less integrated
with their AA group, social phobia was not a significant risk factor for alcohol use
relapse or loss of adherence to psychotherapy.
Treatment
Co-occurring mental and substance use disorders use disorders should be managed
in parallel with evidence-based treatments provided for both problems (Horsefall et
al. 2009).
Comorbid mental disorders that do not abate within 3 to 6 weeks of abstinence (or
significantly reduced drinking) or that emerge from such a period should be treated
227
according to the clinical practice guidelines for those specific disorders (Tiet and
Mausbach 2007).
Limited evidence supports integrating the content of treatment (Tiet and Mausbach
2007; Hesse 2009). Patient engagement in treatment planning and goal setting is
particularly important in this population of patients. Adequate duration of treatment is
essential to successful outcome. Clinicians should emphasise the patient’s education
and rising awareness of the interaction between alcohol use and symptoms of mental
disorder. Patients with comorbid mood and alcohol use disorder should be regularly
assessed and monitored for risk of suicide.
Brief interventions
Grothues et al (2008b) examined the effectiveness of brief interventions in general
practice patients with comorbid anxiety or depressive disorders, because of the
recent strong evidence that brief interventions are effective in this setting (Kaner et
al. 2007). In an RCT with two intervention groups and one control group, data were
collected from 408 patients with alcohol use disorders, at-risk drinking or binge
drinking; 88 patients were diagnosed with comorbid anxiety and/or depression. The
effectiveness of brief intervention (BI) was assessed at a 12-month follow-up in
relation to the presence and absence of comorbidity. Reduction of drinking in six
ordered categories (g/alcohol) between baseline and follow-up served as the
outcome variable. The brief intervention was significantly effective in reducing
drinking in the non-comorbid (p = 0.03) but not in the comorbid patients (p = 0.76). As
brief interventions are known to be less effective for dependent drinkers, a larger
proportion of dependent drinkers in this group might have limited their effectiveness.
Grothues et al also tested the theory that the comorbid patients would seek help
more often than the others after brief intervention (Grothues et al. 2008a), using data
from patients participating in the above study. At 12-months follow-up, differences in
help-seeking for drinking problems were assessed between comorbid and noncomorbid individuals. In a logistic regression analysis, comorbidity (p = 0.01) and
previous help seeking (p< 0.001) were found to be positive predictors for utilising
formal help. The authors conclude that individuals with problematic drinking and
comorbid anxiety or depressive disorders might benefit from more specialised
support.
Psychosocial interventions
Comorbid mental disorders that last beyond a 3 to 6 week period of abstinence (or
significantly reduced drinking) or that emerge from such a period should be treated
according to the clinical practice guidelines for those specific disorders. The service
that provides care should be integrated, but little evidence supports use of specific
packages that integrate the content of psychological interventions. The psychosocial
treatments discussed in Chapter 6 can be tailored to individual needs. Regardless of
whether services follow integrated or parallel models, they should be well
coordinated and provide for long-term follow-up (Tiet and Mousebach 2007; Harsefall
et al. 2009; Hesse 2009).
Depression
In one study, cognitive behavioural therapy (CBT) was shown to have greater
benefits for depressed alcohol dependent patients than standard alcohol treatment
combined with relaxation training (Brown et al. 1997). Thirty five participants with a
diagnosis of DSM-III-R alcohol dependence and a Beck Depression Inventory score
228
of 10 or greater were recruited from an alcohol and drug treatment service day
hospital program at a psychiatric hospital. Women made up 29 percent of the
participants in the study. Participants received either CBT or relaxation training with
the standard day hospital treatment. Post-treatment, patients in the CBT group had
greater reductions in depressive symptoms and a higher percentage of days
abstinent than the standard treatment group. At three and six-month follow-up, the
CBT group also had significantly better outcomes for total abstinence (47 percent vs.
13 percent), proportion of days abstinent (91 percent vs. 68 percent), and drinks per
day (0.46 vs. 5.71).
Kavanagh et al (2006) reported that cue exposure and cue exposure with a negative
mood induction did not significantly add to CBT, based on the work of Sitharthan in
reducing drinking or depression (Sitharthan et al. 1996). The patients in this RCT
drank when they were dysphoric, but those with current major depressive episodes
were excluded.
Anxiety
The effect of anxiety management procedures such as relaxation training in more
severely dependent drinkers has shown reductions in anxiety but not in drinking.
Ormrod and Budd (1991) compared a multi-component cognitive behavioural anxiety
management program and a progressive muscle relaxation program with a health
education control group for outpatients with anxiety and alcohol problems. Both
anxiety management and relaxation training reduced anxiety levels compared with
the control group but there was no difference in drinking outcomes. Those who
reported that they drank to reduce anxiety were no more likely to show reductions in
drinking from an anxiety-reducing intervention than those who reported no such link.
The study analysis was, however, limited by its small sample size (n=36).
Lehman, Brown and Barlow (1998) report on three cases of people suffering panic
disorder and agoraphobia and co-existing alcohol abuse who were treated with CBT
for panic disorder and agoraphobia which ignored their alcohol use. At a six month
follow-up only one had a diagnosis of alcohol abuse. These patients did not meet
criteria for alcohol dependence, and, from their histories, it appears that the two
whose alcohol use had declined from diagnostic levels had milder initial drinking
patterns. These patients sought help from a specialist anxiety disorders clinic and
were motivated to deal with their panic disorder and agoraphobia.
Bowen et al. (2000) found that for alcohol dependent patients with comorbid panic
disorder, CBT was no better than a standard alcohol treatment program in reducing
problem drinking. Participants were randomised to receive either CBT (n = 146) or
the standard alcohol treatment (n = 85). Follow-ups were conducted at three, six and
twelve months. The CBT treatment consisted of six-two hour group-based panic
management training sessions. The article does not describe the standard treatment
program, but the authors suggest that it may have contained enough active anxietytreatment ingredients to reduce any differences between it and CBT.
One sub-analysis of data reported that CBT delayed relapse for female, alcohol
dependent patients with comorbid social phobia. Using data from Project MATCH,
patients receiving CBT were compared with those who received 12-step facilitation.
Socially phobic women, but not men, who received CBT had a longer time to relapse
than matched counterparts in the 12-step group, and for socially phobic males, there
was a trend towards better outcomes in the 12-step group (Thevos et al. 2000).
229
In contrast, Bowen, D’Arcy Keegan and Senthilselvan found that for alcohol
dependent patients with comorbid panic disorder, CBT was no better than a standard
alcohol treatment program in reducing problem drinking (Bowen et al. 2000).
Participants were randomised to receive either CBT (n = 146) or the standard alcohol
treatment (n = 85). Follow-ups were conducted at three, six and twelve months. The
CBT treatment consisted of six-two hour group-based panic management training
sessions. Unfortunately the article does not describe the standard treatment
program, but the authors suggest that it may have contained enough active anxietytreatment components to reduce any differences between it and CBT. While the
sample size was initially large, nearly a third (46) dropped out of the CBT group;
however there was still sufficient power to compare groups. There were no
statistically significant differences between the groups on anxiety or drinking
outcomes. One of the possible explanations given by the authors is the resistance
from other staff to introducing the program, and the relatively brief nature of the CBT
intervention. They also raise the possibility that the anxiety disorder experienced by
people with co-existing substance use disorders may be different from those who
have no co-existing problems.
One study found that treatment for both alcohol dependence and social phobia
produced worse alcohol use outcomes than treatment for alcohol dependence alone
(Randall et al. 2001). A total of 93 participants were randomised to either 12 weeks of
CBT for alcoholism only or concurrent treatment for both alcohol and social anxiety
problems. Participants were followed up after the 12 weeks and again three months
after the end of treatment. Whilst both groups improved on alcohol-related and social
anxiety outcomes, the dual treatment group had worse outcomes than the alcohol
dependence treatment group on three of the four alcohol use measures. They also
reported no significant correlation between reductions in drinking and social anxiety
measures indicating the processes of change for these two outcomes were
unrelated. A lack of integration between the CBT for social phobia and alcohol and
resulting patient confusion may account for the lack of additional effects for additional
anxiety treatment.
The unexpected finding of worse alcohol outcome in the dual treatment group in the
above study (Randall et al. 2001) was attributed to several limitations, including
individual rather than group treatment when group anxiety treatment is regarded by
some as the preferred mode; parallel presentation of two unintegrated manualised
treatments, in which alcohol was addressed during the first 45 minutes of each
session and social phobia in the next 45 minutes; and a loss of alcohol treatment
time in the dual treatment condition. The authors comment that the sample was
drawn from “severe population of treatment-seeking alcoholics”. Thus those with
higher initial alcohol dependence may not do as well if they are distracted from a
focus on their alcohol problems. In addition, the intervention for social phobia was
based on an unknown treatment manual (Holmstrom and Thevos, 1993,
unpublished) the efficacy of which cannot be determined. An intervention supported
by empirical evidence may have yielded different results.
Another study of alcohol dependence and social phobia (Schadé et al. 2005) was a
randomised controlled trial of 96 abstinent alcohol dependent patients with comorbid
anxiety disorder (social phobia or agoraphobia). The patients were randomly
assigned to an intensive, comprehensive 32 week psychosocial program, involving 34 months of inpatient groups followed by up to 16 weeks of aftercare, relapseprevention and disulfiram on its own or in combination with an anxiety treatment
program comprising CBT and optional pharmacotherapy. The anxiety treatment
consisted of 12 weekly 60-minute sessions of cognitive therapy delivered individually
230
at an anxiety clinic; the first six sessions of treatment dealt with alcohol only. The
authors found that additional therapy for anxiety significantly reduced anxiety
symptoms and avoidance behaviour but did not affect the alcohol relapse rates.
While 13 of the 49 (26%) who were allocated to Alcohol only treatment were
abstinent for 30 days before each of the three assessments, 18 of the 47 (38%) who
were allocated to alcohol and anxiety treatment were similarly abstinent, giving an
effect size of 0.13. While this difference was not statistically significant there was
only a 23% chance that this size of effect would be detected with this sample size. In
addition there was a trend of greater reduction of heavy drinking days in the dual
treatment group: the reduction in mean number of days drinking 5 or more drinks
from baseline to follow-up, was greater (but not significantly) in the combined (mean
reduction 9.4) than in the alcohol-only treatment (mean 7.1). The inclusion of both
panic/agoraphobia and social phobia comorbidities with alcohol use disorder leaves
the results less clear.
Schade et al (2007) report on predictors of outcome in the 34 completers in their
combined phobia and alcohol treatment groups. While severity of alcohol
dependence did not predict anxiety outcomes, later age of onset for alcohol problems
was related to better anxiety outcomes.
One quasi-randomised experiment was carried out by Nielsen et al (2007). They
theorised that personality-guided treatment for alcohol dependence, an approach that
integrates cognitive therapy for addictive behaviours with a strategic intervention for
certain personality traits, may be helpful for patients with co-morbid alcohol
dependence and personality disorders. They compared patients admitted for alcohol
dependence in Denmark (n = 108) and allocated them to either standard inpatient
treatment with cognitive therapy for alcohol dependence, or to the personality- guided
treatment. Follow-up was conducted by mail at six months after treatment.
Personality-guided treatment was associated with better retention, longer time to first
relapse, and less time spent drinking post-treatment, although few differences
reached statistical significance. Differences in results were mainly found in the
subgroup with higher levels of personality disorder. These results suggest that
personality-guided treatment is a promising approach, directed at the particular
personality disorders and the typical function fulfilled by drinking. This complex
instrument is described in the article, but it is available only in Danish.
Psychosis and chronic mental disorders
A recent update by Cleary et al (2008) was conducted of Ley et al’s (2000) Cochrane
Review of Psychosocial Interventions for people with both severe mental illness and
substance misuse. They suggest that the evidence is poor at best, with very few
studies. They examined 25 RCTs and found no compelling evidence to support one
psychosocial treatment over another to reduce substance use or improve mental
state for people with a serious mental health problem.
We just mention a few positive studies here. Integrating motivational interviewing,
CBT and family intervention with routine psychiatric care produced greater benefits
for patients with comorbid schizophrenia and substance use disorders than routine
psychiatric care alone (Barrowclough et al. 2001).Thirty-six participants and their
caregivers were randomised to receive either (i) motivational interviewing, CBT and
family intervention plus routine care or (ii) routine care alone. At 12-month follow-up,
the integrated treatment group had better general functioning, a reduction in positive
symptoms, and an increase in the percentage of days abstinent from alcohol or
drugs.
231
Herman et al (2000) randomly assigned patients with a serious mental illness and a
substance use disorder to either an integrated mental health and substance use
treatment program or to a standard hospital treatment program. A total of 429
participants were randomised at a ratio of 2:1 into either the integrated treatment or
the standard short-term treatment ward. Two months after treatment, those receiving
integrated treatment had fewer days of alcohol use than those in the standard
treatment program. This study also found that patients who had no family
involvement, low intentions to stay sober and who had low attendance at self-help
groups post-treatment had the worst outcomes.
In a more recent study Salloum et (2005) reported on a 24-week double-blind
placebo-controlled RCT of divalproex sodium (valproate) for alcohol dependence and
bipolar I disorder. In 59 patients, valproate led to significant reductions in alcohol but
had no differential effect on bipolar outcomes compared to placebo.
Graeber et al (2003) conducted a pilot study with 30 patients who had comorbid
schizophrenia and alcohol use disorders. They were randomly assigned to receive
either a Motivational Interviewing (MI) or Educational Treatment (ET) intervention
with treatment goals of abstinence and/or decreased alcohol use. Subjects were
followed up at 4, 8 and 24-weeks after completing the interventions. Outcome
measures included number of drinking days, abstinence rates, average blood alcohol
concentration and standard ethanol content per drinking day. MI subjects had a
significant reduction in drinking days and an increase in abstinence rates when
compared to subjects receiving ET. These authors conclude that motivational
Interviewing may be a useful adjunct to intervention for individuals with comorbid
schizophrenia and alcoholism.
Recommendation
10.8 Comorbid mood and anxiety disorders
that do not abate within 3 to 6 weeks after
alcohol withdrawal is complete should be
treated with integrated/concurrent cognitive
behavioural therapy for the comorbid disorder.
10.9 Cognitive behavioural therapy, behaviour
therapy, cognitive therapy, and interpersonal
therapy should be considered for treatment of
patients with comorbid mental and alcohol use
disorders because of their demonstrated
effectiveness in non-comorbid cases.
10.10 Integrating psychosocial treatment for
mood disorders and psychoses with
psychosocial treatment for alcohol-use
disorder may be beneficial in treating patients
with such comorbidity.
Strength of
Level of
recommendation evidence
B
II
B
Ib
D
IV
Pharmacotherapy
Pharmacological treatments have proved effective in treating anxiety, depression and
psychosis in patients exhibiting co-occurring mental and alcohol use disorders.
However they should not be used as primary treatments of alcohol dependence as
232
there is little evidence that treatment of co-morbid mental disorder alone leads to a
reduction of alcohol intake.
Depression
A meta-analysiss of randomised controlled trials by Nunes and Levin (2004) indicates
that antidepressant medication has a modest beneficial effect for patients with
combined depressive and substance-use disorders. It is not recommended as a
stand-alone treatment. Concurrent treatment directly targeting substance
dependence is also indicated. The findings also suggest a clinical approach that
begins with an evidence-based psychosocial intervention, followed by antidepressant
medication if depression does not improve.
Evidence for the capacity of SSRIs to reduce alcohol intake is mixed, and several
trials have examined the effectiveness of SSRIs with comorbid patients. Three very
early studies (Naranjo et al. 1995; Kabel and Petty 1996) found little advantage for
SSRIs over placebo in reducing alcohol consumption in the long term (after 12
weeks); however fluoxetine was found to be effective in reducing depression
symptoms (Kranzler et al. 1995).
Cornelius et al. (1997) administered fluoxetine or placebo over a 12-week period to a
randomised group of 51 alcohol dependent patients diagnosed with major depressive
disorder in an inpatient setting. Depression and alcohol consumption ratings were
collected weekly during the 12-week period. Both depressive symptoms and total
alcohol consumption over the trial were significantly lower in the fluoxetine group
than in the placebo group. One 12 week double-blind RCT of patients with posttraumatic stress disorder (PTSD) (Labbate, Sonne et al. 2004) investigated the role
of sertraline in the treatment of patients with comorbid PTSD and an alcohol use
disorder. Patients (n = 93) were stratified into four groups depending on presence or
absence of additional anxiety or depressive disorders and evaluated for the effects of
comorbidity on PTSD symptoms, depressive symptoms, and drinking behaviours,
hypothesising that additional comorbidity would be associated with poorer outcomes.
Patients in all four subgroups showed marked and clinically significant improvement
in alcohol drinking behaviours over the course of the study (p<0.001). There were,
however, no significant differences among groups. All patients showed moderate
improvement in Hamilton Depression Rating Scale scores and a clinicianadministered PTSD scale scores. Hence, having additional anxiety or mood disorder
comorbidity did not decrease their response to treatment.
Gual et al. (2003) performed a double-blind, placebo-controlled randomised trial of
sertraline in recently detoxified alcohol-dependent patients with current depressive
symptoms. The objectives of the study were to evaluate the efficacy of sertraline at
achieving stable abstinence, at ameliorating depressive symptoms and at improving
quality of life in these patients. 83 patients received either sertraline (50-150 mg/day)
or placebo for 24 weeks. The primary outcome criteria were the rate of relapse into
alcohol consumption and the rate of response on the Montgomery and Asberg
Depression Rating Scale (MADRS). At the end of treatment, relapse rates were
23.1% in the placebo group and 31.8% in the sertraline group. Responder rates for
depression were 38.5% for the placebo group and 44.2% for the sertraline group.
There was no significant difference between treatment groups with either variable.
However, when patients were stratified into severe (MADRS score >or=26) and
moderate (MADRS score <26) depression at inclusion, a significant treatment benefit
with sertraline was observed in the former group. Quality of life, determined by the
SF-36, improved in both groups, with more benefit observed for the sertraline group
233
on mental health items. Sertraline was well tolerated, and the incidence of adverse
events was similar in the two treatment groups. The authors conclude that the
explanation for the overall good outcome in both treatment groups and for the
inability to demonstrate a clear treatment effect may rest in the clinical features of the
patients.
In Kranzler’s 2006 study, following a 1-week, single-blind, placebo lead-in period, 328
patients with co-occurring major depressive disorder and alcohol dependence were
randomly assigned to receive 10 weeks of treatment with sertraline (at a maximum
dose of 200 mg/d) or matching placebo (Kranzler et al. 2006). Randomisation was
stratified, based on whether initially elevated scores on the 17-item Hamilton
Depression Rating Scale (HDRS) declined with cessation of heavy drinking, resulting
in a sample of 189 patients with HDRS scores >17 (group A) and 139 patients with
HDRS scores < 16 (group B). Results showed that both the depressive symptoms
and alcohol consumption decreased substantially over time in both groups. There
were no reliable group differences on depressive symptoms or drinking behavior in
either group A or B patients. Therefore this study did not provide consistent support
for the use of sertraline to treat co-occurring major depressive disorder and alcohol
dependence.
Yet another study, of 42 subjects with social anxiety and a co-occurring alcohol use
disorder, participated in a 16-week, double-blind, placebo-controlled clinical trial to
determine the efficacy of paroxetine for social anxiety in patients with co-occurring
alcohol problems (Book et al. 2008). Paroxetine proved to be superior to placebo in
reducing social anxiety, as measured by the Liebowitz Social Anxiety Scale total and
subscale scores and additional measures of social anxiety.
However, SSRIS still do not appear to have any significant effects on the reduction of
alcohol consumption, either during or subsequent to the trial periods of the studies.
Most importantly, Nunes and Levin’s 2004 systematic review and meta-analysis
which included 14 double-blinded RCTs and 848 patients to quantify the efficacy of
antidepressant medications for treatment of combined depression and substance use
disorders (Nunes and Levin 2004) reached the conclusion that antidepressant
medication exerts a modest beneficial effect for patients with combined depressiveand substance-use disorders. Their principal measure of effect size was the
standardised difference between means on the Hamilton Depression Scale (HDS);
the pooled effect size from the random-effects model was 0.38 (95% confidence
interval, 0.18-0.58). Heterogeneity of effect on the depression scale across studies
was significant (p<0.02), and studies with low placebo response showed larger
effects. It is clear from their results that when the medication is effective in treating
depression, it helps diminish quantity of substance use; however, sustained
abstinence or remission is harder to achieve. They conclude that antidepressant
medication is not a stand-alone treatment, and concurrent therapy directly targeting
the addiction is also indicated.
Torrens et al reviewed the literature for randomised controlled trials on the efficacy of
antidepressant drugs in subjects with drug abuse disorders, including alcohol,
cocaine, nicotine and opioids, with and without comorbid depression (Torrens et al.
2005). They conducted a meta-analysis of studies that used common evaluation
procedures in alcohol, cocaine and opioid dependence. Based on this review, the
authors propose some recommendations: (i) the prescription of antidepressants for
drug abuse seems only clear for nicotine dependence with or without previous
comorbid depression (bupropion and nortryptiline); (ii) in alcohol dependence without
234
comorbid depression the use of any antidepressant seems not justified and the use
of antidepressants in alcohol, cocaine or opioid dependence with comorbid
depression needs more studies in well-defined samples, adequate doses and
duration of treatment to be really conclusive. They also conclude that SSRIs do not
seem to offer significant advantages compared with tricyclic drugs in substance
abuse disorders.
Some noradrenergic antidepressants show promise for reducing relapse or drinking
in comorbid patients. For example, nortriptyline (a noradrenergic antidepressant)
reduces drinking in patients diagnosed with antisocial personality disorder, but not in
those patients with affective/anxiety disorders or those without a comorbid disorder
(Powel et al 1995).
A controlled trial with desipramine (a tricyclic antidepressant) showed reduced
relapse in alcohol dependent patients diagnosed with major depression, but not in
those without major depression (Mason et al. 1996). Tricyclic antidepressants should
be used with caution in this population due to high risk of poor treatment adherence,
abuse and overdose.
There are two fairly recent trials of nefazodone. Hernandez-Avila and colleagues
(2004) reported a reduction in alcohol use, but no reduction on depression symptoms
(Hernandez-Avila et al. 2004). In contrast, Roy-Byrne et al. (2000) reported no effect
on depression symptoms, substance use, or craving for alcohol.
Ondansetron reduced depression in 161 early onset alcohol dependent patients but
not in those 160 with late onset (Anton et al. 2006). The effect on drinking was not
reported but there was no relationship between antidepressant effects in early onset
drinkers and reductions in drinking. Those whose anxiety reduced during treatment
also drank less (Sloan et al. 2003).
In addition, Petrakis et al (2006) studied the effects of naltrexone and disulfiram on
alcohol dependent veterans with current DSM-IV major depressive disorders, to find
that their response was similar to those without current depression; subjects with
PTSD had better alcohol outcomes with active medication (naltrexone, disulfiram or
the combination) than they did on placebo, while overall psychiatric symptoms of
PTSD improved. The results suggest that disulfiram and naltrexone are effective and
safe for individuals with PTSD and comorbid alcohol dependence.
In conclusion, antidepressants should not be the first line of treatment in patients with
comorbid alcohol use disorders, unless there is high level of suicidal ideation, severe
depressive symptoms or a history of pre-existing depressive illness.
Recommendation
10.11 Selective serotonin reuptake inhibitor
antidepressants are not recommended as
primary therapy to reduce alcohol consumption
in patients with comorbid mood or anxiety
disorders.
Strength of
Level of
recommendation evidence
B
II
235
Anxiety
Typical pharmacological treatments for anxiety and mood disorders also reduce
anxiety and depression when they co-occur with alcohol use disorders. However,
treating only a comorbid mental disorder usually does not lead to a reduction of
alcohol consumption.
Selective serotonin reuptake inhibitors (SSRIs) reduce symptoms of anxiety in
patients with comorbid anxiety and alcohol dependence. They are indicated for
treatment of obsessive-compulsive disorder and panic attacks in these patients.
However, little sound evidence supports their capacity to reduce alcohol intake in the
longer-term in patients with comorbid anxiety disorders.
Buspirone, an anxiolytic, has been tested with anxious alcohol dependent outpatients
with some success. Approximately half of the participants met current diagnostic
criteria for an anxiety disorder; others had high levels of anxiety. Participants
received either buspirone or placebo over a 12-week period, and weekly,
manualised, individual CBT which focused on relapse prevention and skills training.
Outcomes were measured at the end of treatment and at a six-month follow-up
evaluation. Buspirone patients were more likely to remain in treatment for the 12
weeks, had reduced anxiety, a slower return to heavy alcohol consumption, and
fewer drinking days during the follow-up period (Kranzler et al. 1994).
Benzodiazepines are not recommended for treatment of comorbid anxiety in patients
with alcohol-use disorders due to high risk of dependence and a potential synergistic
interaction with alcohol.
Recommendation
10.12 Benzodiazepines are not recommended
for treatment of comorbid anxiety in patients
with alcohol-use disorders due to high risk of
dependence and a potential synergistic
interaction with alcohol.
Strength of
Level of
recommendation evidence
S
Psychosis
A qualified mental health practitioner usually provides pharmacological treatment of
psychotic illness. Atypical antipsychotics appear to be the first line of treatment of
comorbid psychotic illness and substance use disorders (Wobrock and Soyka 2009).
Limited evidence shows that among schizophrenic patients, two atypical antipsychotics
(risperidone and clozapine) may reduce alcohol misuse, smoking, and possibly some
other substance misuse (Kavanah et al. 2002).
Addition of psychosocial support to pharmacological treatment has been shown to be
effective in treatment of patients with comorbid psychosis and alcohol use disorders
(Drake 2007).
236
.
.
Pharmacotherapy combined with psychosocial interventions
In an early study, Kranzler et al (1995) tested the hypothesis that fluoxetine, when
used in combination with relapse prevention psychotherapy, would reduce relapse
frequency and severity for alcohol dependent patients. This was a randomised,
placebo-controlled trial of fluoxetine (up to a maximum of 60 mg/day) for 12 weeks in
combination with weekly psychotherapy for 101 alcohol-dependent subjects.
Outcomes were measured at the end of treatment and 6 months later. Placebotreated subjects were more compliant with the medication regimen and remained in
the study longer than fluoxetine-treated subjects. There was significantly less alcohol
consumption in both groups during treatment than before treatment, and these
effects persisted at follow-up. Although fluoxetine had no significant effects on
alcohol consumption, it reduced Hamilton Depression Rating Scale scores more than
placebo among subjects with current major depression. The authors concluded that
Fluoxetine at a dose of 60 mg/day was not useful for relapse prevention in lowerlevel alcoholics without comorbid depression. In alcoholics with major depression, the
drug may reduce depressive symptoms.
There have been three placebo-controlled trials of sertraline in combination with
psychological therapies (Deas et al. 2000; Moak et al. 2003; Oslin 2005). Deas et al
undertook a 12-week double-blind, placebo-controlled trial of sertraline plus cognitive
behaviour group therapy (CBT) to preliminarily evaluate the efficacy, safety and
tolerability of the serotonin reuptake inhibitor, sertraline, in the treatment of
adolescents with a primary depressive disorder and a comorbid alcohol use disorder.
Subjects were 10 outpatient treatment-seeking adolescents. Baseline assessment
included several psychiatric diagnostic instruments (K-SADS, HAM-D, SCID), and
the Time-Line Follow-Back method of assessing alcohol consumption. The HAM-D
and the Time-Line Follow-Back were performed weekly thereafter. Both groups
showed a significant reduction in depression scores with an average reduction
between baseline and endpoint HAM-D score of -9.8 (p< 0.001), although there were
no significant group differences. There was an overall reduction in percentage of
days drinking (p < 0.02) and in drinks per drinking day (p < 0.002); however, again
there were no group differences. Depression patients who responded tended to have
higher baseline percentage of drinking days than non-responders (p = 0.08) and the
change in HAM-D scores tended to correlate with change in the percentage of
drinking days (p = 0.09). These data support the evidence that sertraline is safe and
well tolerated in the treatment of adolescents with depression and alcohol
dependence. Small sample size and the CBT group therapy, which was given to all
subjects, may have limited the group differences.
Moak et al (2003) looked at the role of sertraline and CBT for depressed alcohol
dependent patients, because while SSRIs have proved effective in the treatment of
depression and decreased drinking in some studies, the reported effect of these
237
medications on alcohol intake had not been consistent. Also, at this time most
previous studies had not investigated the use of an SSRI in the context of cognitive
behavioural therapy, a known efficacious treatment for both alcoholism and
depression. They conducted a randomised placebo-controlled 12-week trial of
sertraline combined with individual CBT focussing on both alcoholism relapse
prevention and depressive symptoms. There were 82 subjects with either primary
major depression (70 subjects) or substance-induced mood disorder and at least 1
first-degree relative with an affective disorder (12 subjects). Depression and alcohol
consumption outcomes were measured weekly over 12 weeks. Sertraline was well
tolerated and all subjects had decreases in both depression and alcohol use during
the study compared with baseline. Subjects who received sertraline had fewer drinks
per drinking day than subjects who received placebo, but other drinking outcomes
were not different between the 2 treatment groups. Treatment with sertraline was
associated with less depression at the end of treatment in female subjects compared
with females who received placebo. Lower alcohol consumption during the study was
also associated with improvements in depression. The findings in this study suggest
that sertraline, compared with placebo, may provide some modest benefit in terms of
drinking and also may lead to improved depression in female alcohol-dependent
subjects. Additionally, alcohol relapse prevention CBT, delivered with modifications
that provide specific attention to depression, appeared to be of benefit to subjects,
although this is limited by the study design.
Oslin (2005) tested the efficacy of naltrexone combined with sertraline for the
treatment of older adults with major depression and alcohol dependence. The sample
was 74 subjects, age 55 and older, who met criteria for a depressive disorder along
with alcohol dependence. All subjects were randomly assigned to 12 weeks of
naltrexone 50 mg/day or placebo. All subjects also received sertraline 100 mg/day
and individual weekly psychosocial support. Treatment response for alcohol
consumption and depression was measured during the 12 weeks of treatment. At
baseline, subjects were drinking an average of 10.7 drinks per drinking day. The
overall results are encouraging; 42% of the subjects had a remission of their
depression and had no drinking relapses during the trial. There was no evidence for
an added benefit of naltrexone in combination with sertraline, but there was
significant correlation between any alcohol relapse during the trial and poor response
to depression treatment.
The same group (Oslin et al. 2008) also undertook a 24-week double-blind placebocontrolled study of naltrexone to examine the impact of 3 types of psychosocial
treatment combined with either naltrexone or placebo treatment on alcohol
dependency over 24 weeks of treatment: (i) Cognitive-Behavioural Therapy (CBT) +
medication clinic; (ii) BRENDA (an intervention promoting pharmacotherapy) +
medication clinic; and (iii) a medication clinic model with limited therapeutic content.
Two hundred and forty alcohol-dependent subjects were also randomly assigned to 1
of 3 psychosocial interventions. All patients were assessed for alcohol use,
medication adherence, and adverse events at regularly scheduled research visits.
There was a modest treatment effect for the psychosocial condition favouring those
subjects randomised to CBT. Intent-to-treat analyses suggested that there was no
overall efficacy of naltrexone and no medication by psychosocial intervention
interaction. There was a relatively low level of medication adherence (50% adhered)
across conditions, and this was associated with poor outcome. Results from this 24week treatment study demonstrate the importance of the psychosocial component in
the treatment of alcohol dependence. Moreover, results demonstrate a substantial
association between medication adherence and treatment outcomes.
238
Summary
The evidence supports the assumption that antidepressants help to relieve
depressive symptoms but have little effect on reducing alcohol consumption, unless
accompanied and supported by psychosocial treatment. Naltrexone and disulfiram
may be safely used to help reduce alcohol consumption in patients with comorbid
psychiatric disorders. Psychosocial interventions are recommended for comorbid
patients, with or without the addition of pharmacotherapy.
Polydrug use and dependence
Recommendation
Strength of
Level of
recommendation evidence
10.13 All patients with alcohol-use disorders
should be screened for other substance use
using quantity–frequency estimates, or through
structured screening instruments such as the
ASSIST questionnaire.
D
IV
10.14 Polydrug dependence is typically
associated with higher levels of physical,
psychiatric and psychosocial comorbidity that
should be addressed in comprehensive
treatment plans.
D
IV
10.15 Use of other drugs can be affected by
cessation or reduction in alcohol use, and
treatment plans should address use of alcohol
and other drugs together.
D
IV
10.16 Patients undergoing polydrug withdrawal
need close monitoring, increased psychosocial
care, and increased medication. Consider
specialist advice.
D
IV
10.17 Fixed diazepam dosing regimens are
preferred for managing alcohol withdrawal in
the context of other drug withdrawal, with
regular review of dosing regimens. Withdrawal
scales (such as CIWA-Ar) need careful
interpretation in patients withdrawing from
multiple drugs, and should not be used to
direct medication.
D
IV
10.18 Patients dependent on alcohol and
benzodiazepines or opioids should be
stabilised on substitution medications while
undergoing alcohol withdrawal.
D
IV
239
Introduction
There is published evidence from several countries that other substances; legal, illicit
or prescribed, are commonly used in combination with alcohol (Martin et al. 1996;
Barrett et al. 2006; Brecht et al. 2008; McCabe et al. 2006), but little has been
published about the influence of polydrug use on alcohol withdrawal (Degenhardt and
Dunn 2008). The last 40 years has seen a rapid expansion in the availability, range
and popularity of psychoactive drugs, with lifetime experience of their use almost
normalised as behaviour. A recent study of 3000 second year University students in
the UK reported that over 50 % reported lifetime use of cannabis, with a third having
used other drugs such as LSD or ecstasy (Webb et al. 1996). Although historically
demonised by society, the true image of the average consumer of illicit substances is
more benign. Drug policies driven by political will and social expectancies have
compounded significantly the harm associated with their use.
Polydrug users and alcohol
While simultaneous polysubstance use is a common phenomenon among nonalcoholic populations, alcohol is most commonly one of the substances used in
combination with other drugs, discounting tobacco (Barrett et al. 2006). The authors
of this article recruited 149 drug-using university students to complete structured
interviews about their use of various substances. For each substance ever used,
participants provided details about the type, order and amount of all substances coadministered during its most recent administration. Alcohol, tobacco and cannabis
were frequently taken with each other and with all other substances. Chi-squared
tests revealed that when alcohol was consumed in combination with any of cannabis,
psilocybin, MDMA, cocaine, amphetamines, or the prescription stimulant drug
methylphenidate (p<0.01) or LSD (p<0.05), alcohol use preceded the administration
of the other substance. Paired samples t-tests revealed that when alcohol was used
with cocaine (p <0.01) or the stimulant, methylphenidate, (p <0.05) it was ingested in
greater quantities than when used in their absence. Patterns of cannabis use were
not systematically related to other substances. Tobacco use was demonstrated to
increase relative to 'straight/sober' smoking rates when used with alcohol, cannabis,
psilocybin, MDMA, cocaine, amphetamine (p<0.001), LSD (p<0.01) or
methylphenidate (p<0.05).
An earlier study of 3075 UK university students (Webb et al. 1996) showed that while
11% were non-drinkers, 61% of men and 48% of the women exceeded
recommended limits of 14 units per week for women and 21 for men. Hazardous
drinking (> 36 units per week for women, > 51 for men) was reported by 15% of the
drinkers. Binge drinking was declared by 28% of drinkers. 60% of the men and 55%
of the women reported having used cannabis once or twice and 20% of the sample
reported regular cannabis use (weekly or more often). Experience with other illicit
drugs was reported by 33% of the sample, most commonly LSD (lysergic acid
diethylamide), amphetamines, ecstasy, and amyl nitrate which had each been used
by 13-18% of students, and 34% of these had used several drugs.
Problem drinkers and polydrug use
Studying polydrug use among problem drinkers, Martin et al (1996) found that a
majority (61%) of their 212 subjects reported simultaneous polydrug use (SPU)
during the assessment interval of 120 days prior to admission for treatment, using
Timeline Follow-back. Subjects who reported SPU were disproportionately younger,
male, and unmarried, compared with those who did not report such use.
240
The most common alcohol/drug combinations were alcohol with cocaine (60% of
subjects who reported SPU), alcohol with marijuana (51% of SPU subjects), and
alcohol with sedatives (31% of SPU subjects). The most common three-drug
combination was alcohol, cocaine, and marijuana (23% of SPU subjects). Alcohol
use and drug use were associated at the event level, significantly more than
associations predicted by the base rates of the individual behaviours. Their results
suggest that polydrug use is an important focus for assessment and intervention in
alcohol treatment programs.
Population studies
One US study examined rates of remission from substance-use disorders based on
type of disorder (abuse vs. dependence), type of substance (alcohol vs. other drug),
and polysubstance involvement (alcohol or drug vs. alcohol and drug) (Karno et al.
2008). Participants in the National Epidemiologic Survey on Alcohol and Related
Conditions were included if they met criteria for a prior-to-past-year alcohol- and/ or
drug-use disorder (n = 12,297). Odds ratios were computed to examine differences in
the rate of remission as of the past year. Individuals with a diagnosis of alcohol
misuse (as opposed to dependence) were more likely to have recovered than
dependent drinkers. Individuals with both alcohol- and drug-use disorders were less
likely to have recovered, compared with those with only one substance disorder. No
differences were observed in remission rates between those with an alcohol-use
disorder and those with a drug-use disorder. These findings support prior research in
suggesting a worse prognosis for individuals with a diagnosis of dependence and
problematic use of both alcohol and drugs.
The 1997 National Survey of Mental Health and Well-Being in Australia (Degenhardt
et al. 2003) showed that alcohol use was related strongly to the use of other
substances. Those who did not report alcohol use within the past 12 months were
less likely to report using tobacco, cannabis, sedatives, stimulants or opiates. Higher
rates again were observed among those with alcohol use disorders: half (51%) of
those who were alcohol-dependent were regular tobacco smokers, one-third had
used cannabis (32%); 15% reported other drug use; 15% met criteria for a cannabis
use disorder and 7% met criteria for another drug use disorder.
Also in Australia, Degenhardt’s paper about GHB and ketamine use, derived from a
subsection of respondents (aged 14-39 years only) to the 2004 Australian Household
Drug Survey (Australian Institute of Health and Welfare 2005), supplies some
information about other drug use. While the prevalence of GHB and ketamine use
was quite low, they found high rates of polydrug use among illicit drug users
(Degenhardt and Dunn 2008). The most commonly used drug was alcohol, used by
95% of the total surveyed population (n =11,595), with 28% of the total consuming
more than 11 drinks in one day in the previous year, and 49% of 115 GHB-users and
57% of ketamine-users consuming 11 drinks or more in one day in the previous year.
This may suggest either that use of GHB or ketamine lowers personal resistance to
drinking alcohol, or conversely it opposes its effects (thereby reducing intoxication, as
do amphetamines, for example). However, no evidence is available on this aspect.
Comorbidities and cognitive impairment
The comorbidities most commonly associated with polysubstance use, as
demonstrated in at least one study (Skinstad and Swain 2001) include anxiety and
mood disorders, followed by personality disorders. However, cognitive deficits are
the characteristics most often associated with alcohol dependence.
241
Cognitive deficits were assessed in one study of dependent alcoholics (Durazzo et al.
2008). The goal of Durazzo’s study was to investigate the influence of several
common co-morbid medical conditions (primarily hypertension and hepatitis C),
psychiatric (primarily unipolar mood and anxiety disorders), and substance use
(primarily psychostimulant and cannabis) disorders, and chronic cigarette smoking on
the neurocognitive functioning in short-term abstinent, treatment-seeking individuals
with an alcohol use disorder. Seventy-five alcohol-dependent participants (average
51 years; 72 male) completed comprehensive neurocognitive testing after
approximately 1 month of abstinence. Smoking status (smoker/nonsmoker) and age
were significant independent predictors of cognitive efficiency, general intelligence,
postural stability, processing speed, and visuospatial memory after adjustment for
age norms and also controlling for estimated verbal intelligence, education, alcohol
consumption, and medical, psychiatric, and substance-misuse co-morbidities.
Results indicated that chronic smoking accounted for a significant portion of the
variance in the neurocognitive performance of this cohort.
Several tests of visuospatial cognition are also known to be sensitive to chronic
alcohol abuse. Beatty et al (1997) examined spatial cognition in a sample of 94
alcohol-dependent people, compared to controls, and looked for any influences on
effects resulting from the use of other drugs. Groups that had misused only alcohol,
alcohol and marijuana, or alcohol and multiple other drugs (A/P) were compared to
the controls recruited from the community. Testing occurred after at least 3 weeks of
treatment for the drug abusers. On all measures of visuospatial perception and
construction, and on all measures of visuospatial learning and memory, all groups of
alcoholics were impaired relative to controls, but there were no significant differences
among the groups that misused alcohol. By contrast, on all measures of geographical
knowledge that required more detailed place localisation, subjects in the A/P group
were impaired, while subjects who misused only alcohol or alcohol and marijuana
performed as well as controls. Their results seem to indicate that alcohol is the most
disabling substance, and those who also use cannabis and other drugs have no
more impairments than those associated with their alcohol use.
Another study of polydrug users tested for associated cognitive deficits (Nixon et al.
1998). Healthy control subjects (n=63) were compared with 40 individuals who
misused alcohol only, 24 individuals who misused alcohol and stimulants, 16
individuals who misused alcohol and marijuana, and 41 individuals who misused
alcohol and depressants/narcotics, or alcohol and two or more other drugs. All
subjects were administered tests of short-term memory, spatial orientation, visualspatial perception, and problem-solving. Results from the study indicated that control
subjects and individuals who misused both alcohol and marijuana performed
significantly better than the other groups on most tests. Gender was not significant.
These results were not attributable to differences on measures of affect, or the years
of chronic alcohol consumption.
Summary
The above studies all indicate that any assessment of alcohol use or misuse should
include questioning on the use of other drugs. This should be taken into account as
they can adversely influence the outcome of treatment.
References
242
Adrian, M and SJ Barry 2003, Physical and mental health problems associated with
the use of alcohol and drugs. Subst Use Misuse 38(11-13): 1575-1614.
Almeida-Filho, N, Lessa I, Magalhaes L, et al. 2007, Co-occurrence patterns of
anxiety, depression and alcohol use disorders. Eur Arch Psychiatry Clin
Neurosci 257(7): 423-431.
Anton, RF, O'Malley SS, Ciraulo DA, et al. 2006, Combined Pharmacotherapies and
Behavioral Interventions for Alcohol Dependence: The COMBINE Study: A
Randomized Controlled Trial. JAMA 295(17): 2003-2017.
Australian Institute of Health and Welfare 2005, 2004 National Drug Strategy
Household Survey. First results. AIHW cat no. PHE 57. Canberra: Australian
Institute of Health and Welfare.
Barrett, SP, C Darredeau and RO Pihl 2006, Patterns of simultaneous polysubstance
use in drug using university students. Hum Psychopharmacol 21(4): 255-263.
Barrowclough, C, Haddock G, Tarrier N, et al. 2001, Randomized controlled trial of
motivational interviewing, cognitive behavior therapy, and family intervention
for patients with comorbid schizophrenia and substance use disorders. Am J
Psychiatry 158(10): 1706-1713.
Beatty, WW, Blanco CR, Hames KA, et al. 1997, Spatial cognition in alcoholics:
influence of concurrent abuse of other drugs. Drug Alcohol Depend 44(2-3):
167-174.
Book, SW, Thomas SE, Randall PK, et al. 2008, Paroxetine reduces social anxiety in
individuals with a co-occurring alcohol use disorder. J Anxiety Disord 22(2):
310-318.
Bowen, RC, D'Arcy C, Keegan D, et al. 2000, A controlled trial of cognitive behavioral
treatment of panic in alcoholic inpatients with comorbid panic disorder. Addict
Behav 25(4): 593-597.
Brecht, M-L, Huang D, Evans E, et al. 2008, Polydrug use and implications for
longitudinal research: ten-year trajectories for heroin, cocaine, and
methamphetamine users. Drug Alcohol Depend 96(3): 193-201.
Brown, R, Evans D, Miller I et al. 1997, Cognitive-behavioral treatment for depression
in alcoholism. J Consult Clin Psychol 65(5): 715-726.
Brown, S, M Irwin and M Schuckit 1991, Changes in anxiety among abstinent
alcoholics. J Stud Alcohol 52: 55-61.
Cargiulo, T 2007, Understanding the health impact of alcohol dependence. American
J Health-Syst Pharmacy 64: S5-S11.
Cassidy, CM, N Schmitz and A Malla 2008, Validation of the alcohol use disorders
identification test and the drug abuse screening test in first episode
psychosis. Can J Psychiatry 53(1): 26-33.
243
Cleary, M, Hunt G, Matheson S et al. 2008, Psychosocial interventions for people
with both severe mental illness and substance misuse. Cochrane Database of
Syst Rev (1).
Conason, AH, A Brunstein Klomek and L Sher 2006, Recognizing alcohol and drug
abuse in patients with eating disorders. QJM 99(5): 335-339.
Cornelius, JR, Salloum IM, Ehler JG et al. 1997, Fluoxetine in depressed alcoholics.
A double-blind, placebo-controlled trial. Arch Gen Psychiatry 54(8): 700-705.
Corrao, G, Bagnardi V, Zambon A et al. 2004, A meta-analysis of alcohol
consumption and the risk of 15 diseases. Prevent Med 38(5): 613-619.
Davis, L, Uezato A, Newell JM et al. 2008, Major depression and comorbid
substance use disorders. Curr Opin Psychiatry 21(1): 14-18.
Dawson, DA, BF Grant and FS Stinson 2005, The AUDIT-C: screening for alcohol
use disorders and risk drinking in the presence of other psychiatric disorders.
Comprehensive Psychiatry 46(6): 405-416.
Deas, D, Randall CL, Roberts JS et al. 2000, A double-blind, placebo controlled trial
of sertraline in depressed adolescent alcoholics: a pilot study. Hum
Psychopharmacol 15: 461-469.
Degenhardt, L and M Dunn 2008, The epidemiology of GHB and ketamine use in an
Australian household survey. Int J Drug Policy 19(4): 311-316.
Degenhardt, L and W Hall 2003, Patterns of co-morbidity between alcohol use and
other substance use in the Australian population. Drug Alcohol Rev 22(1): 713.
Degenhardt, L, Hall W, Teesson M et al. 2000. Alcohol use disorders in Australia:
Findings from the National Survey of Mental Health and Well-being. Sydney,
National Drug and Alcohol Research Centre.
DiMartini, A, Dew MA, Javed L et al. 2004, Pretransplant psychiatric and medical
comorbidity of alcoholic liver disease patients who received liver transplant.
Psychosomatics 45(6): 517-523.
Drake, RE. 2007, Management of substance use disorder in schizophrenia patients:
current guidelines. CNS Spectr 12(10 Suppl 17): 27-32.
Driessen, M, Meier S, Hill A et al. 2001, The course of anxiety, depression and
drinking behaviours after completed detoxification in alcoholics with and
without comorbid anxiety and depressive disorders. Alcohol Alcohol 36(3):
249-255.
Durazzo, TC, Rothlind JC, Gazdzinski S et al. 2008, The relationships of
sociodemographic factors, medical, psychiatric, and substance-misuse comorbidities to neurocognition in short-term abstinent alcohol-dependent
individuals. Alcohol 42(6): 439-449.
244
Farrell, M, Howes S, Taylor C et al. 1998, Substance misuse and psychiatric
comorbidity: An overview of the OPCS national psychiatric morbidity survey.
Addict Behav 23(6): 909-918.
Frye, MA and IM Salloum 2006, Bipolar disorder and comorbid alcoholism:
prevalence rate and treatment considerations. Bipolar Disord 8(6): 677-685.
Gossop, M, Domingos N, Radovanovic M et al. 2007, Physical health problems
among patients seeking treatment for alcohol use disorders: a study in six
European cities. Addict Biol 12(2): 190-196.
Graeber, DA, Moyers TB, Griffith G, et al. 2003, A pilot study comparing motivational
interviewing and an educational intervention in patients with schizophrenia
and alcohol use disorders. Community Mental Health Journal 39(3): 189-202.
Grothues, J, Bischof G, Reinhardt S et al. 2008a, Differences in help seeking rates
after brief intervention for alcohol use disorders in general practice patients
with and without comorbid anxiety or depressive disorders. Int J Methods
Psychiatr Res 17(1 Suppl): S74-77.
Grothues, J, Bischof G, Reinhardt S et al. 2008b, Effectiveness of brief alcohol
interventions for general practice patients with problematic drinking behavior
and comorbid anxiety or depressive disorders. Drug Alcohol Depend 94(1-3):
214-220.
Gual, A, Balcells M, Torres M et al. 2003, Sertraline for the prevention of relapse in
detoxicated alcohol dependent patients with a comorbid depressive disorder:
A randomized controlled trial. Alcohol Alcohol 38: 619-625.
Hesse, M. 2009 Integrated psychological treatment for substance use and co-morbid
anxiety or depression vs. treatment for substance use alone. A systematic review of
the published literature. BMC Psychiatry. 20;9: 6.
Herman, S, Frank K, Mowbray C et al. 2000, Longitudinal effects of integrated
treatment on alcohol use for persons with serious mental illness and
substance use disorders. J Behav Health Serv Res 27: 286-302.
Hernandez-Avila, CA, Modesto-Lowe V, Feinn R et al. 2004, Nefazodone treatment
of comorbid alcohol dependence and major depression. Alcohol Clin Exp Res
28(3): 433-440.
Hoolahan, B, Kelly B, Stain HJ et al. 2006, Co-morbid drug and alcohol and mental
health issues in a rural New South Wales Area Health Service. Aust J Rural
Health 14(4): 148-153.
Horsfall, J, Cleary M, Hunt GE et al. 2009, Psychosocial treatments for people with
co-occurring severe mental illnesses and substance use disorders (dual
diagnosis): a review of empirical evidence. Harv Rev Psychiatry 17(1): 24-34.
Indig, D, Eyeson-Annan M, Copeland J et al. 2007, The effects of alcohol
consumption, psychological distress and smoking status on emergency
department presentations in New South Wales, Australia. BMC Public Health
7(147): 46.
245
Kabel, DI and F Petty 1996, A placebo-controlled, double-blind study of fluoxetine in
severe alcohol dependence: adjunctive pharmacotherapy during and after
inpatient treatment. Alcohol Clin Exp Res 20(4): 780-784.
Kaner, EFS, F Beyer, HO Dickinson et al. 2007, Effectiveness of brief alcohol
interventions in primary care populations. Cochrane Database of Syst Rev.
Karno, MP, Grella CE, Niv N et al. 2008, Do substance type and diagnosis make a
difference? A study of remission from alcohol- versus drug-use disorders
using the National Epidemiologic Survey on Alcohol and Related Conditions.
J Stud Alcohol Drugs 69(4): 491-495.
Kavanagh, DJ, McGrath J, Saunders J et al. 2002, Substance misuse in patients with
schizophrenia: epidemiology and management. Drugs 62(5): 743-755.
Kavanagh, DJ, Sitharthan G, Young RM et al. 2006, Addition of cue exposure to
cognitive-behaviour therapy for alcohol misuse: a randomized trial with
dysphoric drinkers. Addiction 101(8): 1106-1116.
Kranzler, H, Burleson J, Korner P et al. 1995, Placebo-controlled trial of fluoxetine as
an adjunct to relapse prevention in alcoholics. Am J Psychiatry 152(3): 391397.
Kranzler, HR, Burleson JA, Del Boca FK et al. 1994, Buspirone treatment of anxious
alcoholics: A placebo-controlled trial. Arch Gen Psych 51(9): 720-731.
Kranzler, HR, Mueller T, Cornelius J et al. 2006, Sertraline treatment of co-occurring
alcohol dependence and major depression. J Clin Psychopharmacol 26(1):
13-20.
Labbate, LA, Sonne SC, Randal CL, et al. 2004, Does comorbid anxiety or
depression affect clinical outcomes in patients with post-traumatic stress
disorder and alcohol use disorders? Compr Psychiatry 45(4): 304-310.
Lehman, CL, TA Brown and DH Barlow 1998, Effects of cognitive-behavioral
treatment for panic disorder with agoraphobia on concurrent alcohol abuse.
Behav Ther 29(3): 423-433.
Levander, E, Frye MA, McElroy S et al. 2007, Alcoholism and anxiety in bipolar
illness: differential lifetime anxiety comorbidity in bipolar I women with and
without alcoholism. J Affect Disord 101(1-3): 211-217.
Marquenie, LA, Schade A, Van Balkom AJ et al. 2006, Comorbid phobic disorders do
not influence outcome of alcohol Dependence treatment. Results of a
naturalistic follow-up study. Alcohol Alcohol 41(2): 168-173.
Martin, CS, Clifford PR, Maisto SA, et al. 1996, Polydrug use in an inpatient
treatment sample of problem drinkers. Alcohol Clin Exp Res 20(3): 413-417.
Mason, B, Kocsis J, Ritvo E et al. 1996, A double-blind, placebo-controlled trial of
desipramine for primary alcohol dependence stratified on the prersence or
absence of major depression. JAMA 275(10):761-767.
246
McCabe, SE, Cranford JA, Morales M, et al. 2006, Simultaneous and concurrent
polydrug use of alcohol and prescription drugs: prevalence, correlates, and
consequences. J Stud Alcohol 67(4): 529-537.
Merikangas, KR, Mehta RL, Molnar BE, et al. 1998, Comorbidity of substance use
disorders with mood and anxiety disorders: Results of the international
consortium in psychiatric epidemiology. Addict Behav 23(6): 893-907.
Moak, DH, Anton RF, Latham PK et al. 2003, Sertraline and cognitive behavioral
therapy for depressed alcoholics: results of a placebo-controlled trial. J Clin
Psychopharmacol 23(6): 553-562.
Naranjo, CA, KE Bremner and KL Lanctot 1995, Effects of citalopram and a brief
psycho-social intervention on alcohol intake, dependence and problems.
Addiction 90(1): 87-99.
Nielsen, P, S Rojskaer and M Hesse 2007, Personality-guided treatment for alcohol
dependence: a quasi-randomized experiment. Am J Addict 16(5): 357 - 364.
Nixon, SJ, R Paul and M Phillips 1998, Cognitive efficiency in alcoholics and
polysubstance abusers. Alcohol Clin Exp Res 22(7): 1414-1420.
Nunes, EV and FR Levin 2004, Treatment of Depression in Patients With Alcohol or
Other Drug Dependence: A Meta-analysis. JAMA 291(15): 1887-1896.
Ormrod, J and R Budd 1991, A comparison of two treatment interventions aimed at
lowering anxiety levels and alcohol consumption amongst alcohol abusers.
Drug Alcohol Depend 27(3): 233-243.
Oslin, DW 2005, Treatment of late-life depression complicated by alcohol
dependence. Am J Geriatr Psychiatry 13(6): 491-500.
Oslin, DW, Lynch KG, Pettinati HM et al. 2008, A placebo-controlled randomized
clinical trial of naltrexone in the context of different levels of psychosocial
intervention. Alcohol Clin Exp Res 32(7): 1299-1308.
Pelli, H, Lappalainen-Lehto R, Piironen A et al. 2008, Risk factors for recurrent acute
alcohol-associated pancreatitis: a prospective analysis. Scand J
Gastroenterol 43(5): 614-621.
Petrakis, IL, Poling J, Levinson C, et al. 2006, Naltrexone and disulfiram in patients
with alcohol dependence and comorbid post-traumatic stress disorder. Biol
Psychiatry 60(7): 777-783.
Powell, B, Campbell J, Lamndon J et al. 1995, A double-blind, placebo-controlled
study of nortriptillyne and bromocriptine in male alcoholics subtyped by
comorbid paychiatric disorders. Alcohol Clin Exp Res 19(2): 452-468.
Project MATCH Research Group 1997, Matching alcoholism treatments to client
heterogeneity: Project MATCH posttreatment drinking outcomes.J Stud
Alcohol 58: 7-29.
247
Randall, CL, S Thomas and AK Thevos 2001, Concurrent alcoholism and social
anxiety disorder: A first step toward developing effective treatments. Alcohol
Clin Exp Res 25(2): 210-220.
Roy-Byrne, PP, Pages KP, Russo JE et al. 2000, Nefazodone treatment of major
depression in alcohol-dependent patients: A double-blind, placebo-controlled
trial. J Clin Psychopharmacol 20: 129-136.
Salloum, IM, Cornelius JR, Daley DC et al. 2005, Efficacy of Valproate Maintenance
in Patients With Bipolar Disorder and Alcoholism: A Double-blind PlaceboControlled Study. Arch Gen Psychiatry 62(1): 37-45.
Schadé, A, Marquenie LA, van Balkom AJ et al. 2005, The Effectiveness of Anxiety
Treatment on Alcohol-Dependent Patients with a Comorbid Phobic Disorder:
A Randomized Controlled Trial. Alcohol Clin Exp Res 29(5): 794-800.
Schadé, A, Marquenie LA, van Balkom AJ et al. 2007 Anxiety disorders: treatable
regardless of the severity of comorbid alcohol dependence. Eur Addict Res,
109-115
Schminke, U, Luedemann J, Berger K et al. 2005, Association between alcohol
consumption and subclinical carotid atherosclerosis: the Study of Health in
Pomerania. Stroke 36(8): 1746-1752.
Schneider, U, Altmann A, Baumann M et al. 2001, Comorbid anxiety and affective
disorder in alcohol-dependent patients seeking treatment: the first Multicentre
Study in Germany. Alcohol Alcohol 36(3): 219-223.
Schuckit, MA and V Hesselbrock 1994, Alcohol dependence and anxiety disorders:
what is the relationship? Am J Psychiatry 151(12): 1723-1734.
Schuckit, MA and MG Monteiro 1988, Alcoholism, anxiety and depression. Br J
Addict 83(12): 1373-1380.
Schuckit, MA, JE Tipp, M Bergman et al. 1997, Comparison of induced and
independent major depressive disorders in 2,945 alcoholics. Am J Psychiatry
154(7): 948-957.
Sher, L, Stanley BH, Harkavy-Friedman JM et al. 2008, Depressed patients with cooccurring alcohol use disorders: a unique patient population. J Clin Psychiatry
69(6): 907-915.
Sitharthan, T, DJ Kavanagh and G Sayer 1996, Moderating drinking by
correspondence: an evaluation of a new method of intervention. Addiction
91(3): 345-355.
Skinstad, AH and A Swain 2001, Comorbidity in a clinical sample of substance
abusers. Am J Drug Alcohol Abuse 27(1): 45-64.
Sloan, TB, JD Roache and BA Johnson 2003, The role of anxiety in predicting
drinking behaviour. Alcohol Alcohol 38(4): 360-363.
248
Strum, WB 1995, Abstinence in alcoholic chronic pancreatitis. Effect on pain and
outcome. J Clin Gastroenterol 20(1): 37-41.
Sullivan, LE, DA Fiellin and PG O'Connor 2005, The prevalence and impact of
alcohol problems in major depression: a systematic review. American Journal
of Medicine 118(4): 330-341.
Tiet QQ and Mausbach B 2007, Treatments for patients with dual diagnosis: a
review. Alcohol Clin Exp Res 31: 513–36.
Terra, MB, Barros HMT, Stein AT et al. 2006, Does co-occurring social phobia
interfere with alcoholism treatment adherence and relapse? J Subst Abuse
Treat 31(4): 403-409.
Thevos, AK, Roberts JS, Thomas SE et al. 2000, Cognitive behavioral therapy
delays relapse in female socially phobic alcoholics. Addict Behav 25(3): 333345.
Tomasson, K and P Vaglum 1996, Psychopathology and alcohol consumption
among treatment-seeking alcoholics: a prospective study. Addiction 91(7):
1019-1030.
Tomasson, K and P Vaglum 1998a, The role of psychiatric comorbidity in the
prediction of readmission for detoxification. Compr Psychiatry 39(3): 129-136.
Tomasson, K and P Vaglum 1998b, Social consequences of substance abuse: the
impact of comorbid psychiatric disorders. A prospective study of a nation-wide
sample of treatment-seeking patients. Scand J Soc Med 26(1): 63-70.
Torrens, M, Fonseca F, Mateu G et al. 2005, Efficacy of antidepressants in
substance use disorders with and without comorbid depression: A systematic
review and meta-analysis. Drug Alcohol Depend 78(1): 1-22.
Tsujimoto, T, Kawaratani H, Yoshiji H et al. 2008, Recent developments in the
treatment of alcoholic chronic pancreatitis. Curr Drug Abuse Rev 1(2): 197202.
Velasquez, MM, JP Carbonari and CC Diclemente 1999, Psychiatric severity and
behavior change in alcoholism: The relation of the transtheoretical model
variables to psychiatric distress in dually diagnosed patients. Addict Behav
24(4): 481-496.
Waern, M 2003, Alcohol dependence and misuse in elderly suicides. Alcohol Alcohol
38(3): 249-254.
Webb, E, Ashton CH, Kelly P et al. 1996, Alcohol and drug use in UK university
students. Lancet 348(9032): 922-925.
Wobrock T and Soyka M 2009, Pharmacotherapy of patients with schizophrenia and
substance abuse. Expert Opin Pharmacother 10(3): 353-367.
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250
Chapter 11
Aftercare and long-term follow-up
Recommendation
11.1 Long-term follow-up of patients following
an intensive treatment program is
recommended as part of a comprehensive
treatment plan, reflecting the chronic relapse
possibility of alcohol dependence.
Strength of
Level of
recommendation evidence
D
IV
A number of studies have examined various methods of continuing care for patients
with alcohol use disorders. For example, a telephone intervention was tested for
acceptability and feasibility by Burleson and Kaminer for short-term follow-up of
adolescents (Burleson and Kaminer 2007). Four therapists and 43 adolescents who
completed a series of manualised guided follow-up telephone interventions
responded favourably and consistently to a questionnaire concerning its
acceptability, feasibility, and confidentiality.
Three other studies tested the effect of continuing care by telephone on abstinence
rates (Rus-Makovec and Cebasek-Travnik 2008; McKay et al. 2004; McKay et al.
2005; Horng and Chueh 2004). The first study showed a positive influence on quality
of life in the telephone follow-up group but had no effect on abstinence rates at the
long term (Rus-Makovec and Cebasek-Travnik 2008). Positive indicators of therapy
success (abstinence or decrease in drinking, stable social relations, and more
positive self-evaluation of well-being) were found in 53% of patients at 3 months,
44% at 6 months, and 31% at 12 months in the telephone group. However, groups
did not significantly differ in abstinence level (telephone group=28%, control
group=24%) at the 24-month mark. There were significant differences in measure of
well-being, with the telephone group scoring higher on self-assessment of
psychological health, self-evaluation of financial status, and general quality of life.
The McKay studies showed more positive effects. The 2004 publication (McKay et al.
2004) looked at continuing care for 359 substance dependent (alcohol and/or
cocaine) patients, using a randomised procedure, comparing a telephone-based
monitoring and brief counselling intervention (TEL) with 2 face-to-face interventions,
relapse prevention (RP) and standard 12-step group counselling. Self-report,
collateral, and biological measures of alcohol and cocaine use were obtained over a
12-month follow-up. The treatment groups did not differ on abstinence-related
outcomes; however, in participants solely with alcohol dependence (n = 91), the
telephone group (TEL) improved more than did the 12-step group; heavy drinking
days decreased from 40-50% prior to follow-up care, to 5% of days at 3 months and
8-18% at 12 months.
At 24-month follow-up the results were similar but were no longer significant between
the groups (McKay et al. 2005). However the TEL group did not deteriorate faster, as
might have been expected, over time; they still had higher rates of abstinence than
the 12-step group, and had lower GGT levels than the RP group, at the 24- month
mark. It seems apparent from this study that telephone-based counselling following
an intensive stabilisation period is as effective as more intensive face-to-face
treatments and is more cost-effective.
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A smaller study of patients (34 in each group) recruited from a psychiatric centre
(Horng et al. 2004) used a quasi-experimental pre-post control group design to
compare abstinence rates, re-admission rates, alcohol consumption, addiction
severity and social adjustment between the two groups. The experimental group
received regular telephone counselling at 1, 3, 5, 9, and 13 weeks after discharge.
These sessions were 30 minutes to one hour in length. All outcome measures
showed significant differences between the groups at 3 month follow-up.
Readmissions in the control group were 38% while in the experimental group was
9%; both groups decreased alcohol consumption; the experimental group’s average
alcohol consumption was 28g compared to the control group’s average 119g;
however the control group had a higher level of consumption at baseline. The
authors conclude that telephone counselling is highly recommended to help reduce
readmission, to improve social functioning, and to reduce alcohol consumption postdischarge for alcoholism. They do recognise that the experimental group was more
highly motivated to change, as participants were not randomly selected, and that it
may have been difficult to continue beyond 3 months due to mobility of their patients.
This limits the generaliseability of their results.
Another study of follow-up focussed on improving compliance with aftercare
treatment by 74 patients on disulfiram, following their admission to an inpatient
program (Neto et al. 2007). This study focussed on attendance at aftercare groups,
psychiatric appointments, and attendance at AA. The results, using intention-to-treat
analysis, show that 39% of patients were abstinent at 6 months; the largest
percentage of relapses occurred at 3 months. However 80% were abstinent at 30
days and the relapse rate slowed, with the median time to first relapse at 120 days. A
closer inspection showed that 47% of patients had not attended their monthly
outpatient psychiatric appointment, 20% had not attended the fortnightly aftercare
groups, and 34% had not attended the AA sessions. This matter of compliance would
seem to be major factor in the success (or failure) of such a program.
A randomised controlled trial of adolescents with alcohol use disorders (Kaminer et
al. 2008) also looked at the effect of outpatient aftercare on abstinence rates,
frequency of drinking, and cannabis use (n = 177). Participants were assigned to 5
face-to-face sessions (active aftercare), brief telephone follow-up, or no contact. All
had completed 9 weekly cognitive behavioural therapy group sessions to address
their alcohol problems. Results at three months showed the likelihood of relapse
increased significantly in the no contact condition, although all groups relapsed to a
degree. The differential treatments were more effective for females; there was a
significant change in abstinence rate for girls from baseline to follow-up in the active
aftercare 5-session group. The results are not clearly presented in the paper;
however the active aftercare produced better outcomes than did the control
condition. Youths enrolled in active aftercare showed significantly fewer drinking
days (p =.044) and fewer heavy drinking days (p =.035) per month relative to
controls. The authors conclude that, in general, active aftercare was effective in
slowing the expected relapse to higher frequency and amount of alcohol use;
however, maintenance of treatment gains was only achieved for females.
Other studies reinforce the evidence for longer treatment and longer follow-up having
more beneficial results for patients. Moos and Moos looked at the influence of
duration and intensity of treatment on 473 previously untreated patients with alcohol
use disorders (Moos and Moos 2003). They found that, compared with patients who
did not enter treatment immediately, individuals who started treatment relatively
quickly and who obtained a longer duration of treatment had better short- and longterm alcohol-related outcomes and better short-term social functioning. Patients were
252
followed up at 1-year, 3-year and 8-year intervals. It was found that patients who
underwent a longer duration of additional treatment had better alcohol-related
outcomes than others who had no additional treatment but, in those who delayed
treatment entry, the duration of treatment was not associated with improved
outcomes. In general, the intensity of treatment was not related to better outcomes;
rather the length of treatment was the deciding factor, with 68% being abstinent at an
8-year interval after 53 or more weeks of continuing additional treatment. The
message from this particular study seems to be – start treatment immediately and
keep in continued contact (at least once weekly) for at least one year.
Two other longitudinal studies followed patients over 16 and 20 years. The first one
(Ilgen et al. 2008) surveyed 420 US patients who had not received treatment for
alcohol use disorders at baseline and 1 year and reassessed them at 8 and 16 years.
It is not stated whether any treatment was delivered to these people; it appears to be
a naturalistic study. In the 6 months prior to the 1-year assessment, 36% reported
abstinence from alcohol, 48% reported drinking problems, and 16% reported nonproblem drinking. At each follow up, between 16% and 21% of the entire sample
were problem-free. Those who were problem-free at 1 year had reported, at baseline,
fewer days of intoxication, fewer drinks per drinking day, fewer alcohol dependence
symptoms and alcohol-related problems, less depression, and more adaptive coping
mechanisms than did the abstinent and problem-drinking participants. In addition,
48% of participants who were problem-free at 1 year continued to report positive
outcomes (either no problem drinking or abstinence) throughout the long-term followup, whereas 77% of those who were abstinent at 1 year reported the same positive
outcomes throughout the same period.
Gual et al’s 20-year follow-up (Gual et al. 2009) covered 850 patients in 8 addiction
centres in Catalonia, evaluating long-term outcomes after outpatient treatment. This
treatment focussed on abstinence, building on awareness of alcohol dependence as
an illness, the acquisition of new lifestyle habits, and improvement of quality of life,
delivered over a 2-year period. Participants were followed up at 1, 5 and 10 years,
and then 20 years, using quantity-frequency measures of alcohol consumption over
the previous 12 months. All information was collected at interview with either a
psychiatrist or clinical psychologist from the initial study centres. Data were also
collected about chronic illnesses, medications, hospital visits, alcohol-related
accidents, employment, financial or legal problems, or disability; psychosocial stress
was assessed using DSM-III-R Axis IV. Results show that 50% were abstinent at
year 5, 42% at year 10 and 33% of the original sample at year 20 (32% were
deceased by that time, and 10% lost to followup). Women had better outcomes, with
84% abstinent at 20 years, compared to 66% of men; mortality rates were
significantly different (22% of women compared to 34.5% men; p = 0.03). A factor
that is recognised by the authors is that heavy drinkers had double the mortality rates
than controlled drinkers or abstainers, with 5-year drinking status predicting mortality
rates at 10 and 20 years, thus abstinence rates remain high in the surviving cohort
(70% of those who answered questions at 20 years).
Recommendation
11.2 A range of clinical strategies should be
used to reduce alcohol-related harm in people
who continue to drink heavily and resist
treatment. These include attending to medical,
psychiatric, social and medico-legal issues,
maintaining social supports, and facilitating
Strength of
Level of
recommendation evidence
D
IV
253
reduction in alcohol intake.
The authors of one of the studies above also examined the personal and social
resources that predicted positive alcohol-related outcomes in that particular study,
following up 461 patients (Moos and Moos 2007). They found that in general, social
learning (self-efficacy and approach coping), health and financial resources,
association with Alcoholics Anonymous, and bonding with family members, friends,
and co-workers predicted better alcohol-related and psychosocial outcomes. In
particular, more self-confidence and financial resources at one year independently
predicted less 3-year alcohol consumption and fewer drinking problems. Better health
and participation in AA also predicted fewer drinking problems, while more selfconfidence and more health and financial resources predicted less depression. The
social learning and health and financial resources also tended to predict better 8-year
outcomes. The authors conclude that the application of social learning theory,
economic behaviour, and social control theories may help to identify predictors of
remission. If these are tackled at the same time as treatment for alcohol problems in
isolation, better results may be achieved.
Other factors affecting positive outcomes include the length of initial stay in treatment
and attendance at 12-step programs. One such study looked at gender differences in
seven year outcomes among older adults (Satre et al. 2007). The sample was 25
women and 59 men aged 55 and over who took part in one of two treatment options
in the same abstinence-based program. Average length of stay in treatment,
including after care of up to one year, was 142.6 days among women and 80.1 days
among men. At seven years, 76% of women reported abstinence in the prior 30
days while 56% of men did so. Also at 7 years, more frequent attendance at 12-step
programs (mean 3.9 meetings in previous 30 days) was significantly associated with
abstinence in the same period. Abstinent people also reported attending significantly
more meetings in the prior 12 months (mean 42.8) vs a mean of 2.3 meetings for
non-abstinent participants (p = 0.005). The authors consider that, given the projected
rate of growth in the older population, the influential factors for successful treatment
of older people for alcohol problems need to be carefully assessed and implemented.
There are several other studies that report on various dimensions that influence
continuity of care. One article (Schaefer et al. 2008) looked at staff practices and
engagement in care, and whether they mediated or moderated the interaction
between the patient and treatment factors. They compared the 18 different intensive
outpatient substance use disorder programs that varied in their continuity of care
practices, in which 429 patients were enrolled. Methadone maintenance programs
were excluded; however most patients (82%) had an alcohol and drug problem. They
found that abstinence was more likely to occur when the patient’s discharge plan
specified at least one follow-up care appointment per week, appointments were
arranged before discharge, drug-free or sober living arrangements were available,
and when patients were engaged for a longer time (up to 6 months, in this case) in
continuing care. They also state that psychiatric or clinic use in the year prior to entry
for treatment, completion of treatment, access to transport for appointments, and
more patient motivation for continuing care also predicted abstinence. The follow-up
rate was 78% and almost all patients were male (98%); therefore this study may not
be generalisable to females. Average age was 47 (standard deviation, SD = 7.9)
years; 58% were divorced or separated, and at discharge 25% were employed.
A pilot study by Passetti et al (Passetti et al. 2008) examined community treatment
methods to engage alcohol-dependent patients in treatment. They compared two
clinics which differed in the degree of assertiveness with which they tried to engage
people with a history of repeat presentation for alcohol problems. The usual care
254
clinic sent patients an opt-in letter and they had to telephone for an appointment. The
flexible access clinic operated a walk-in service; caseloads were smaller, and the
staff telephoned patients reminding them to attend a session. Failure to attend was
followed up. Staff role composition was similar at each clinic. Results of this study
show that retention in treatment of recidivist patients was more likely in the flexible
care clinic, with 35% completing withdrawal compared to 26% of usual care patients
(p<0.05), and 23% entering aftercare compared to 14% (p<0.02). However, as
patients were not randomly assigned, selection bias may have occurred.
A small quasi-experimental study (n = 40) evaluated whether social reinforcement
would further improve aftercare attendance and treatment outcome (Lash et al.
2004). Socila reinforcement in this case was personal verbal recognition by the
therapist, a certificate of attendance at the 6th visit, their name on an honour roll and
a medallion on completion of 8 sessions. At 6-month follow-up, patients who received
social reinforcement had less alcohol use, and were also more likely to be abstinent
form alcohol than the standard care patients (76% versus 40%; p = 0.036). They
were also more likely to attend aftercare for a longer time (up to 12 months). This
seems a very simple strategy, but it was effective in encouraging attendance and
reduction in alcohol use. Randomisation was not possible due to patients’ personal
schedules but the two groups were very similar on demographic variables, diagnostic
criteria or Addiction Severity Index scores at baseline. However it must be noted that
drug use was not affected by the social reinforcement technique; it was only effective
for alcohol.
Another method of keeping patients engaged in treatment is presented in a paper by
Collins et al. (2007). These authors describe three case studies of patients for whom
email was utilised between patient and physician as an adjunct to the ongoing
treatment for alcohol or substance dependency. They applied this method to selected
patients who were at higher risk due to previous relapse or to complacency, and they
were invited to communicate with their addiction specialists. They have continued for
between 6 months and 5 years. It comes through from these selected studies that the
support gained by patients was highly effective in aiding their continuance and
perseverance in recovery programs. Patients using this method (or selected to use
this method) are commonly high-functioning professionals who might otherwise feel
isolated and who benefit from the constant responses of their provider. They are
accustomed to self-analysis, able to express themselves clearly and are willing to
email daily. For one patient it also served as a map of progress.
It is important therefore to utilise all and any method of retaining patients in after care
using whatever method is available, cost-effective, and feasible to both the patient
and the provider of care
References
Burleson, JA and Y Kaminer 2007, Aftercare for adolescent alcohol use disorder:
feasibility and acceptability of a phone intervention. Am J Addict 16(3): 202205.
Collins, GB, MS McAllister and DB Ford 2007, Patient-provider e-mail communication
as an adjunctive tool in addiction medicine. J Addict Dis 26(2): 45-52.
255
Gual, A, Bravo F, Lligona A et al. 2009, Treatment for alcohol dependence in
Catalonia: health outcomes and stability of drinking patterns over 20 years in
850 patients. Alcohol Alcohol 44(4): 409-415.
Horng, F-F and K-H Chueh 2004, Effectiveness of telephone follow-up and
counseling in aftercare for alcoholism. J Nurs Res 12(1): 11-20.
Ilgen, MA, Wilbourne PL, Moos BS et al. 2008, Problem-free drinking over 16 years
among individuals with alcohol use disorders. Drug and Alcohol Dependence
92(1-3): 116-122.
Kaminer, Y, JA Burleson and RH Burke 2008, Efficacy of outpatient aftercare for
adolescents with alcohol use disorders: a randomized controlled study. J Am
Acad Child Adolesc Psychiatry 47(12): 1405-1412.
Lash, SJ, Burden JL, Monteleone BR et al. 2004, Social reinforcement of substance
abuse treatment aftercare participation: Impact on outcome. Addict Behav
29(2): 337-342.
McKay, JR, Lynch KG, Shepard DS et al. 2005, The effectiveness of telephonebased continuing care for alcohol and cocaine dependence: 24-month
outcomes. Arch Gen Psychiatry 62(2): 199-207.
McKay, JR, Lynch KG, Shepard DS, et al. 2004, The effectiveness of telephonebased continuing care in the clinical management of alcohol and cocaine use
disorders: 12-month outcomes. J Consult Clin Psychol 72(6): 967-979.
Moos, RH and BS Moos 2003, Long-term influence of duration and intensity of
treatment on previously untreated individuals with alcohol use disorders.
Addiction 98(3): 325-337.
Moos, RH and BS Moos 2007, Protective resources and long-term recovery from
alcohol use disorders. Drug and Alcohol Dependence 86(1): 46-54.
Neto, D, R Lambaz and JE Tavares 2007, Compliance with aftercare treatment,
including disulfiram, and effect on outcome in alcohol-dependent patients.
Alcohol Alcohol 42(6): 604-609.
Passetti, F, Jones G, Chawla K et al. 2008, Pilot study of assertive community
treatment methods to engage alcohol-dependent individuals. Alcohol Alcohol
43(4): 451-455.
Rus-Makovec, M and Z Cebasek-Travnik 2008, Long-term abstinence and well-being
of alcohol-dependent patients after intensive treatment and aftercare
telephone contacts. Croat Med J 49(6): 763-771.
Satre, DD, Blow FC, Chi FW et al. 2007, Gender differences in seven-year alcohol
and drug treatment outcomes among older adults. American Journal on
Addictions 16(3): 216-221.
Schaefer, JA, Harris AHS, Cronkite RC et al. 2008. Treatment staff's continuity of
care practices, patients' engagement in continuing care, and abstinence
following outpatient substance-use disorder treatment. J Stud Alcohol Drugs
69(5): 747-756.
256