CNE Objectives and Evaluation Form appear on page 15.
The Alcohol-Dependent Patient in
Hospital: Challenges for Nursing
Glenn Donnelly, Arlene Kent-Wilkinson, and Alecia Rush
lcohol dependence is the
third leading cause of
disease burden in developing countries worldwide
(World Health Organization, 2006).
The ubiquitous presence of alcohol
means nurses will encounter individuals in their acute care practices who
use or abuse alcohol. Some of the
clinical problems presented by these
individuals are examined and the
critical aspects of their care are highlighted.
A
Definitions
Alcohol abuse is a pattern of
drinking resulting in harm to a person’s health, interpersonal relationships, or ability to work (Anton,
2008). Alcohol abuse can lead to
alcohol dependence (Centers for
Disease Control and Prevention,
2008). Alcoholism is a behavior pattern characterized by uncontrolled
drinking of alcoholic beverages to
the extent of impairing health and
social functioning. Alcoholism is
thus one extreme in a range of drinking patterns that vary among individuals in degree of dependency and
tolerance, and in a host of other
ways (e.g., timing or beverage
choice) (Pasch, 2010). Alcoholism is
a pathological dependency on
ethanol (National Council on
Alcoholism, 2011) that is characterized by tolerance, physical dependency, and/or pathological organ
changes (Schuckit, 2008).
Individuals who are alcohol dependent pose significant challenges
for nurses when they are admitted to hospital for treatment.
Clinical problems presented by these individuals are examined and
the critical aspects of their care are highlighted.
many males affected as females. The
highest rate of alcoholism occurs in
Canadians ages 20-24. In Canadian
surveys, about 20% of current and
former drinkers stated their alcoholic
drinking negatively affected them,
usually impacting their jobs or their
finances (Health Canada, 2008). In
the United States, 7%-8% of the
adult population is affected by alcohol abuse and dependence (Substance Abuse and Mental Health
Services Administration, 2007).
Reportedly, 30%-50% of people who
drank in the past year experience at
least one adverse alcohol-related
problem, such as missing work or
school, driving after drinking, or
having interpersonal problems, during their life times (Teesson, Baillie,
Lynskey, Manor, & Degenhardt,
2006).
In 2002, 2.4% of all deaths in
Canada in people age 69 or younger
were from chronic diseases attributed to alcohol consumption. This
translated into nearly 43,000 years of
life lost prematurely, and nearly
125,000 hospital admissions due
to alcohol-related chronic diseases
(Rehm, Giesbrecht, Patra, & Roerecke,
2006). Each year in the United States,
85,000 deaths are attributed to alcohol use, along with substantial disability from medical and psychiatric
consequences, injuries, and secondhand effects (e.g., motor vehicle
crashes) (Saitz, 2005). In the United
Kingdom, the number of alcoholrelated deaths doubled from 4,144 in
1991, to 8,758 in 2006 (Anderson &
Baumberg, 2006).
Neurobiology of Alcohol
Dependence
The vulnerability of some persons
to addiction seems to be multifactoral, including genetic predisposition, environmental factors, and
neurophysiologic changes resulting
from repeated use of the substance.
Addictive or substance abuse disorders are more common in individuals with mood and anxiety disorders,
schizophrenia, and all conditions
associated with the neurotransmitter
dopamine (Cornwell & Lickteig,
2006). Approximately 80% of persons with alcoholism complain of
Glenn Donnelly, PhD, MN, BSc(N), RN, ENC©, is Associate Professor, Faculty of Nursing,
University of Regina, Regina, Saskatchewan, Canada.
Arlene Kent-Wilkinson, PhD, MN, BSN, RN, is Associate Professor, College of Nursing,
University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
Prevalence Rates
In Canada, an estimated 4% of
the population over age 15 is
dependent on alcohol, with twice as
Alecia Rush is a Nursing Student, Mount Royal University, Calgary, Alberta, Canada.
Note: The authors and all MEDSURG Nursing Editorial Board members reported no actual or
potential conflict of interest in relation to this continuing nursing education article.
January-February 2012 • Vol. 21/No. 1
9
depressive symptoms, and 30% meet
the criteria for depressive episode
(Bruinjnzeel, Repetto, & Gold, 2007).
Excessive use of alcohol alters the
neurochemical transmitter systems
and makes a greater amount of
dopamine available in the nucleus
accumbens, the area of the brain
that mediates reward, pleasure, and
assignment of salience to important
environmental stimuli (Guthrie,
Brower, & Karam-Hage, 2008;
Kalivus & Volkow, 2005). The resulting increase in dopamine produces
mood elevation and euphoria,
which become strong motivators to
repeat the experience (Pasch, 2010).
Alcohol influences other neurotransmitters in modulating the
dopaminergic pathway to increase
the amount of g-aminobutyric acid
(GABA), glutamate, more dopamine,
and endogenous opioids. The GABA
and glutamate system is involved
primarily in alcohol stimulation,
sedation, and intoxication, as well as
many symptoms of alcohol withdrawal. The dopamine and opioid
systems are involved with reinforcement, reward, and some aspects of
craving. This can result in sustained
use of alcohol and potential relapse
after prolonged abstinence in the
alcohol-dependent person (Kalivus
& Volkow, 2005). Opioid-like protein
neurotransmitters, enkephalins, and
B-endorphins increase their availability and can be responsible for the
euphoria experienced with alcohol
consumption. Their release in alcohol intoxication may contribute to
addiction by inhibiting the GABA
pathways and enhancing dopaminergic signaling, causing an even
heightened sense of euphoria
(Anton, 2008).
Neural adaptation occurs when the
chronic activation of the reward system results in depletion of the neurotransmitter systems that were over
activated in an effort to maintain
response to drug abuse. Sensitization
identifies an increased response following intermittent administration
of the substance, and may be akin to
craving. Tolerance, on the other hand,
develops as continued use depletes
the neurotransmitters (Guthrie et al.,
2008), and the dopaminergic receptors become less responsive (O’Brien,
10
2008). Greater amounts of alcohol
thus are required to achieve positive
rewarding effects (Guthrie et al.,
2008).
During withdrawal, a decrease
occurs in dopaminergic and serotonergic transmission through the
nucleus accumbens. Also seen during withdrawal, an increase in opioid receptor activity occurs in conjunction with decreased GABA and
increased glutamate transmission
through the accumbens nuclei
(Guthrie et al., 2008).
Once the brain has been exposed
repeatedly to high doses of alcohol,
any sudden decrease in intake can
produce withdrawal symptoms. The
inhibition of the GABA pathway by
continued exposure to high levels of
alcohol results in a neural adaptation
mechanism. Abrupt cessation of prolonged alcohol consumption results
in brain hyperexcitablility because
the pathway previously inhibited by
alcohol is no longer inhibited
(Bayard, McIntyre, Hill, & Woodside,
2004). Alcohol withdrawal syndrome
occurs about 5-10 hours after the cessation of alcohol, and peaks in intensity in 2-3 days (Schuckit, 2008).
The most common withdrawal
pattern is characterized by tremor of
the hands, agitation and anxiety,
nausea, and vomiting. In addition,
autonomic nervous system overactivity results, including sweating,
tachycardia, tachypnea, hypertension, increasing body temperature,
and insomnia sometimes accompanied by frightening dreams. Anxiety,
insomnia, and mild central nervous
system dysfunction may occur 4-6
months following alcohol cessation
(Schuckit, 2008).
Hallucinations occur in up to
10% of patients, and are usually visual and tactile (Kahn, Barnhorst, &
Bourgeois, 2009). Other individuals
are likely to have auditory or visual
hallucinations, or both (O’Brien,
2008). Their onset usually occurs
after several days of abstinence
(Kahn et al., 2009).
Seizures occur as a result of alteration in neurobiology (Rogawski,
2005). Approximately 2%-5% of
persons with alcohol dependence
experience withdrawal seizures, usually within 48 hours of alcohol
intake cessation (Schuckit, 2008).
Seizures present either as a single
generalized attack (Schuckit, 2008)
or in groups (Rogawski, 2005).
Withdrawal symptoms are not
responsive to the anticonvulsant
medication phenytoin (Dilantin®)
(Rogawski, 2005). Withdrawal
seizures are a repeated occurrence in
approximately 10% of heavy
drinkers (Franklin & Francis, 2005).
Delerium tremens (DTs) is an
episode of intense alcohol withdrawal characterized by disorientation
and global confusion, agitation,
severe tremor, fluctuating levels of
consciousness, autonomic instability
activity (Kahn et al., 2009; Schuckit,
2008), incontinence, and frightening visual hallucinations (Carroll,
2007). The condition usually begins
3-5 days after the individual’s last
drink. This serious condition is seen
in less than 5% of individuals with
alcohol dependence but has the
potential to be life-threatening, with
death as a result of cardiovascular,
metabolic, or infectious complications (Schuckit, 2008). Early death
rates were estimated as high as 15%,
with more recent estimates as low as
0-1% with medical intervention
(Kahn et al., 2009).
Health Effects of Heavy
Drinking
Because alcohol is a central nervous system depressant, people who
consume large quantities of alcohol
frequently experience blackouts or
acute retrograde amnesia during periods of intoxication (Schuckit, 2008).
Alcoholic-related amnestic episodes
are associated with the quantity and
frequency of drinking. Although
blackouts are not a sensitive indicator of the risk for developing alcoholism, they should be viewed as an
important warning sign of problem
drinking (Carroll, 2007; Schuckit,
2008). Blackouts may be frightening
enough to some people to increase
awareness that they are drinking too
much.
Alcohol intoxication affects every
organ in the body, and chronic
abuse of alcohol has deleterious
effects on all body systems (Keys,
2011). Hypertension, hyperlipi-
January-February 2012 • Vol. 21/No. 1
The Alcohol-Dependent Patient in Hospital: Challenges for Nursing
demia, cardiac arrhythmias, cardiac
myopathy (Schuckit, 2008), liver disease, peptic ulcer disease, or pancreatitis (Lucey, Mathurin, & Morgan,
2009) may be the first physical indication of alcohol abuse. Drinking
also causes nutritional deficiencies.
First, alcohol supplies calories but
does not have essential nutrients,
such as proteins, minerals, and vitamins. In addition, alcohol interferes
with the absorption of vitamins
from the small intestine and their
storage in the liver. Commonly
affected are thiamine (B1), folic acid,
pyridoxine (B6), niacin, and vitamin
A (Schuckit, 2008). Pancreatitis, gastritis, and liver disease are common
co-morbid conditions. Alcohol ketosis results from further starvation
(Rampalla, 2008).
Alcohol and its metabolite
acetaldehyde are direct neurotoxins
(Rampalla, 2008). As a result of alcohol consumption, brain atrophy
appears to be greater in drinkers than
non-drinkers (Mann et al., 2005).
Alcohol-related nutritional deficiencies and the toxic effects of alcohol
can lead to persistent neurological
abnormalities. Wernicke’s encephalopathy, an acute syndrome characterized by ataxia, abnormal eye
movements, and confusion, results
from a severe thiamine deficiency. If
untreated, this condition can progress to Korsakoff’s disease and
involve lasting personality degeneration, confabulation, and memory
disturbances (Hannon, Pooler, &
Porth, 2010). Hepatic encephalopathy, a deterioration of mental status
in patients with cirrhosis, occurs
when the liver fails to remove several toxins (notably ammonia). In its
early state, it is marked by inattention, reversal of sleep wake cycle,
and asterixis; symptoms may
progress to delirium and coma
(Lucey et al., 2009).
Alcohol has several cardiovascular
consequences. Two to three drinks a
day increase blood pressure, lowdensity lipoprotein, and cholesterol
(Schuckit, 2009). Acetaldehyde is
directly toxic to the myocardium,
with the toxicity playing a role in
the progression of cardiomyopathy
(Schuckit, 2008). Cardiac arrhythmias and orthopnea generally are
considered antecedents of cardiomyopathy in individuals who binge
drink, which can result in varying
degrees of heart failure (Rampulla,
2008).
Alcohol contributes to several
esophageal disorders, including esophagitis, esophageal varices, and esophageal adenocarcinoma (Rampalla,
2008). Erosive gastritis can be a direct
result of the toxic effects of alcohol
and increased susceptibility to
Helicobacter pylori bacteria. Excessive
alcohol use is a major cause of pancreatitis, which can lead to lifethreatening necrosis (Rampulla,
2008; Whitcomb, 2006). Heavy, prolonged alcohol use also is associated
with the progression of colon adenomas (Rampulla, 2008).
Alcoholic liver disease has three
main forms: fatty liver, alcoholic
hepatitis, and cirrhosis. Excessive use
of alcohol can result in deposition of
fat in the hepatocytes of the liver.
The mechanism by which this
occurs is not understood completely
(Porth, 2010), but it is postulated
that impaired oxidation of fatty
acids may contribute to the fat accumulation (Schuckit, 2008). Alcoholic
hepatitis usually manifests between
the occurrence of fatty changes and
cirrhosis. It is characterized by
inflammation and necrosis of liver
cells, and can lead to liver failure and
death. Cirrhosis is the end result of
repeated bouts of alcohol-related
liver injury. It is characterized by
development of fibrotic nodules
which may compress hepatic veins
and thus cause portal hypertension.
In addition to structural and functional changes in the liver, the
altered metabolism often results in
depression of clotting factor and
albumin synthesis. This predisposes
the affected individual to hemorrhage and development of edema
(Lucey et al., 2009; Waken-Fleming
& Mullen, 2005).
Assessment and
Identification of the
Alcohol-Dependent Patient
Many patients admitted to hospital for treatment of other health conditions have a drinking problem or
alcohol dependence. The history of
January-February 2012 • Vol. 21/No. 1
alcohol use may be known by the
health care team, but in many cases
it is concealed from them. Detection
of alcohol problems is one way in
which nurses can plan effectively for
the patient’s recovery (Keys, 2011).
The CAGE questionnaire is a
screening tool which may be helpful
when alcohol consumption has
been concealed. It consists of four
well-validated questions that are
easy to use and are easily accessed
(Hanson & Williams, 2001). A positive response in two or more of the
questions is suggestive of alcohol
misuse (Mayfield, McLeod, & Hall,
1974). This short questionnaire can
be used easily in hospital settings to
screen for heavy drinking and alcohol disorders (Schuckit, 2009).
The nature of alcoholism, with its
characteristic denial, intoxication,
memory disturbances, anxiety, confusion, or disorientation, may make
it difficult for the nurse to obtain an
accurate history (Keys, 2011). History
should include the estimated
amount and duration of alcohol
intake and the time of the last drink.
Information about previous attempts
at detoxification (including complications, such as seizures and hallucinations), other health problems, and
current medications is part of the
essential data (Kosten & O’Connor,
2003; Schuckit, 2009). History taking
also should include seeking culturally relevant data regarding the
patient’s condition (Canadian Nurses
Association, 2004). The initial assessment of the patient in withdrawal
must include a determination
whether the patient is using other
drugs as well as alcohol. Specific substances must be identified because
substantial differences exist in associated complications and treatment
can vary greatly. Toxicology screening also is useful to determine possible abuse of other substances (Kosten
& O’Connor, 2003).
First-encounter assessment includes facial expression, self-care
assessment, unusual odors, vital
signs, height, weight, body movements and gait, balance, coordination, level of consciousness, skin,
hair and nails, and nutritional status
(Monahan, 2009). Physical examination usually reveals nothing unusual
11
unless the patient is intoxicated or in
withdrawal, or indulges in chronic
heavy use of alcohol. The individual’s mental status, vital signs, and
blood glucose should be assessed.
Postural hypotension and pulse
changes may indicate gastrointestinal bleeding. The patient’s head
should be assessed for signs of trauma (recent or past) and facial flushing. Facial puffiness usually follows a
drinking binge. Unusual bruises,
abrasions, and burns also should
raise suspicion of a problem with
alcohol use. Older drinkers, particularly those who take prescribed medicines, are prone to falls. Ataxia,
characterized by a wide stepping
gait, may result from cerebellar deterioration. Early peripheral neuropathy is suggested by diminished
lower-extremity touch or temperature sensation (Rampulla, 2008).
The revised Clinical Institute
Withdrawal Assessment for Alcohol
(CIWA-Ar) scale is a valid, 10-item
assessment tool that can be used to
quantify the severity of alcohol withdrawal. It also can be used to monitor and medicate patients as they
experience withdrawal (Bayard et al.,
2004). The nurse scores each of 10
response categories using a Likert
scale; the maximum possible score is
67. Response categories include agitation, anxiety, auditory disturbances, clouding of sensorium,
headache, nausea or vomiting,
paroxysmal sweats, tactile disturbances, tremor, and visual disturbances. Numerical criteria from 0 (no
symptoms) to 7 (severe or very frequently) are used to determine mild, moderate, or severe withdrawal (Keys,
2011). Each rise in score in a single
group is associated with a higher relative risk of complications, such as
confusion, seizures, and hallucinations in untreated persons (Asplund,
Aaronson, & Aaronson, 2004).
Srivastava (2007) suggested the
range of medical treatment limits
choices and creates passivity. Nurses
can encourage patients to take active
responsibility in planning culturally
and socially acceptable treatment
options. By partnering with patients,
nurses can advocate for an integrative health care approach that blends
knowledge of traditional healing
12
methods with current treatment protocols which potentially can enhance the single-model approaches
to health and wellness (Srivastava,
2007).
Treatment Protocols
The three goals of treatment for
alcohol withdrawal syndrome are
initiating abstinence; reducing withdrawal symptoms and severe complications; and retaining the patient
in treatment (Kasser, Geller, Howell,
& Wartenberg, 2004). About 50% of
patients with alcohol dependence
develop clinically relevant symptoms of withdrawal, which occur as
a rebound from usual effects of alcohol intoxication (Schuckit, 2008).
Meticulous, ongoing assessment is
critical for early identification of
symptom severity and potential
complications so appropriate treatment can be provided, and the
patient evaluated in terms of overall
progress (Keys, 2011).
Delirium tremens can begin 48-72
hours after the last drink. It is preceded by the typical signs of early withdrawal, although these may be
masked by medications such as benzodiazepines used for treatment of
symptoms. Signs of sympathetic
hyperactivity, such as tachycardia,
hypertension, fever, and diaphoresis,
are often profound hallmarks of
alcohol withdrawal delirium (Bayard
et al., 2004).
Nurses should recognize clinical
features of alcohol withdrawal in
any patient admitted to the hospital.
Timely sedation will prevent the
onset of convulsion or progression
to delirium tremens. The most effective regimen is to control the agitation, sweating, and tremor with
symptom-triggered dosing (Harrison
& Daly, 2006). With this method,
the need for medication is signaled
by signs and symptoms in the
patient withdrawing from alcohol
(Bayard et al., 2004). In a doubleblind, controlled trial, symptom-triggered therapy proved superior to
fixed-dose sedative scheduling to
manage alcohol withdrawal. Persons
receiving symptom-triggered therapy used less benzodiazepines and
had decreased duration of treatment
(Daeppen et al., 2002). Nurses’
assessment skills are central to use of
symptom-triggered dosing in any
setting. While standing orders are
common for fixed-dose scheduling,
the skilled nurse is able to provide
optimal care through symptom-triggered dosing (Keys, 2011; Kosten &
O’Connor, 2003).
Benzodiazepines are considered a
first-line treatment, indicated routinely for the patient with substantial symptoms of alcohol withdrawal
as well as the person at increased risk
for complications of withdrawal
(Saitz, 2005). They act as potentiators at inhibitory GABA receptors,
which are relatively unoccupied in
alcohol withdrawal (Kahn et al.,
2009). Benzodiazepines should be
administered when the patient
shows early signs of withdrawal to
prevent progression of the symptoms. The goal is to keep the patient
mildly sedated or in a calm, tranquil
state while still allowing easy arousal
(Sommers, Johnson, & Beery, 2007).
Benzodiazepines may be administered via different regimens.
Diazepam (Valium®) (0-20 mg every
2 hours; maximum 100 mg in 24
hours) is a common protocol
(Harrison & Daly, 2006) in Canada
and the United Kingdom. The
American Society for Addiction
Medicine Practice Guidelines for
managing alcohol withdrawal recommend starting doses of lorazepam
(Ativan®) 1-4 mg every 15 minutes
(Saitz, 2005).
Some patients appear to be resistant to large doses of benzodiazepines and experience a prolonged course of withdrawal symptoms. When escalating doses of
benzodiazepines appear to have little effect, alternative agents not
dependent on GABA benzodiazepine binding sites must be
sought. Combined or solitary doses
of the anticonvulsant drugs valproic acid (Depakote®) and carbamazepine (Tegretol®) for alcohol
withdrawal treatment have not
been supported by a meta-analysis
(Polycarpou, Papanikolaou, Ioannidis,
& Contopoulos-Ioanidis, 2005).
Some evidence supports the use of
propofol (Diprivan®) and barbiturates
in alcohol withdrawal (Preuss, Zil, &
January-February 2012 • Vol. 21/No. 1
The Alcohol-Dependent Patient in Hospital: Challenges for Nursing
Koller, 2006). Antipsychotics and
alpha agonists also may assist in
symptom management (Kahn et al.,
2009).
Nursing Care
Patients with alcohol withdrawal
syndrome are usually apprehensive
or fearful. They may be acutely disturbed and hallucinating. Care thus
should be provided in a well-lit room
with a calm, reassuring environment
(Harrison & Daly, 2006).
Managing fluid volume deficit is a
top priority in nursing care. If withdrawal occurs despite sedation,
patients often will require intravenous hydration, with fluid requirements of 4-10 liters in the first
24 hours. A solution of 5% dextrose
in saline or 0.45% saline can be used
for rehydration if hypoglycemia
exists. Once the patient’s nausea and
vomiting subside, fluids such as fruit
juices are encouraged, followed by
progression to a normal diet. The
patient requires continual monitoring for signs of dehydration, such as
poor skin turgor, dry mucous membranes, weight loss, concentrated
urine, flattened neck veins, and
hypotension (Sommers et al., 2007).
Persons with alcohol dependence
can experience depletion of multiple electrolytes. Electrolytes should
be monitored and replaced as necessary (Sommers et al., 2007). Habitual
drinkers may be deficient in magnesium, which will lower the seizure
threshold (Lohr, 2005). Thiamine
deficiency has been reported in
30%-80% of people with alcohol
dependence (Compton, 2002).
Thiamine 25-50 mg given intravenously is recommended to prevent Wernicke’s encephalopathy.
The vitamin must be administered
before intravenous glucose because
it is a co-factor necessary for glucose
metabolism (Harrison & Daly,
2006). Caused by thiamine deficiency, Wernicke-Korsakoff syndrome is
characterized by ataxia, encephalopathy, amnesia, nystagmus, and
paralysis of external ocular muscles
(Rampulla, 2008; Schuckit, 2008). It
can occur quickly and have permanent effects if the patient receives
glucose without thiamine. The
symptoms are similar to those of
intoxication, making diagnosis more
difficult (Harrison & Daly, 2009).
Brief counseling interventions of
10-15 minutes with feedback about
drinking, advice, and goal setting
(Cooper, 2006) can be initiated with
follow-up contact after the patient
has progressed through withdrawal.
Interventions should include counseling the patient about setting a
goal for a reduction in alcohol consumption and identifying ways to
achieve that goal. A systematic
review of 11 randomized, controlled
trials found persons who received
such an intervention had significantly reduced their alcohol intake
at 6 months following treatment
(McQueen, Howe, Allan, & Mains,
2006). Planning for continued care
should begin while the patient is
being detoxified. Referral and follow
up to other agencies, treatment programs, self-help groups, and counselors is important for adequate
recovery from alcohol dependence.
These services provide patients with
the tools to cope with situations that
may precipitate heavy drinking.
They should be initiated so as to
avoid a lapse of time in different
components of the treatment program (Keys, 2011; Saitz, 2005).
Nursing Implications
Although the understanding of
substance abuse has improved, the
tendency remains for nurses to fail
to engage with persons who have
alcohol dependence. Nurses may be
uncertain whether this is within
their scope of practice, or they may
perceive a lack of knowledge and
skill in identifying and responding
to affected patients. For some professionals, increased knowledge and
understanding of alcohol dependence challenges their values, beliefs,
and attitudes, and may result in negative feelings that can affect their
care. In engaging with patients with
alcohol dependence, nurses must
recognize that excessive alcohol use
is likely only one symptom of a larger problem (Cooper, 2006).
Nurses can play a critical role in
identifying patients with alcohol
dependence, and also participate in a
January-February 2012 • Vol. 21/No. 1
comprehensive assessment that
includes psychological state, effects
of alcohol use, motivation for treatment, social support, and physical
assessment. Nurses also should be
prepared to provide brief intervention by sharing information and providing motivational support. They
can be pivotal in identifying and
referring patients to appropriate
treatment programs, counseling, or
social support groups. Nurses’ effective participation with an interdisciplinary team of professionals is paramount in providing effective shared
care and treatment to patients with
alcohol dependence (Keys, 2011).
Conclusion
The management of a patient
experiencing alcohol withdrawal is
enhanced by nurses’ in-depth understanding of the neurobiology of alcohol dependence, the effects of alcohol abuse on the body systems, and
current treatment of alcohol withdrawal syndromes. Nurses are placed
uniquely to provide comprehensive
care to patients who are withdrawing from alcohol, and evidencebased practice will lead to improved
care of affected patients.
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ADDITIONAL READINGS
Aboriginal Nurses Association of Canada
[ANAC], Canadian Association of
Schools of Nursing, & Canadian Nurses
Association. (2009). Cultural competence and cultural safety in First Nations,
Inuit and Métis nursing education: An
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January-February 2012 • Vol. 21/No. 1
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MSN J1201
Answer/Evaluation Form:
The Alcohol-Dependent Patient in Hospital: Challenges for Nursing
Deadline for Submission: February 28, 2014
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those wishing to obtain CNE credit, an evaluation follows. After studying the information presented in this article, the nurse will be able to:
1. Describe the prevalence and neurobiology of alcohol dependence.
2. Define the health effects of heavy drinking.
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_______________________________________________________________________________________________________________
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Evaluation
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2. By completing this activity, I was able to meet the following objectives:
3.
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7.
8.
a. Describe the prevalence and neurobiology of alcohol dependence.
b. Define the health effects of heavy drinking.
c. Discuss the assessment and treatment protocols for a patient with
alcohol dependence.
d. Detail the nursing care and nursing implications of a patient with alcohol
dependence.
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I verify that I have completed this activity: _______________________________________
Comments _______________________________________________________________________________________________________
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January-February 2012 • Vol. 21/No. 1
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Challenges for Nursing
continued from page 14
Cross, T., Bazron, B., Dennis, K., & Isaacs, M.
(1989). Toward a culturally competent
system of care. Washington, DC:
Georgetown University.
Davis-Murdoch, S. (2005). A cultural competence guide for primary health care professionals in Nova Scotia. Halifax, Nova
Scotia, Canada: Primary Health Care,
Nova Scotia Department of Health.
McNaughton-Dunn, A. (2002). Cultural competence and the primary care provider.
Journal of Pediatric Health Care, 16(3),
151-155.
Noutsias, M., Pauschinger, M., Poller, W.,
Schultheiss, H., & Kuhl, U. (2003).
Current insights into the pathogenesis,
diagnosis, and therapy of inflammatory
cardiomyopathy. Heart Failure Monitor,
3(4), 127-135.
Smye, V., & Browne, A. (2002). ‘Cultural safety’
and the analysis of health policy affecting
aboriginal people. Nurse Researcher,
9(3), 42-56.
Stewart, S. (2006). Cultural competence in
health care (position paper). Sydney,
Australia: Diversity Health Institute.
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