The alcohol-dependent patient in hospital: challenges for nursing.
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).
In Canada, an estimated 4% of the population over age 15 is dependent on alcohol, with twice as 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 second-hand effects (e.g., motor vehicle crashes) (Saitz, 2005). In the United Kingdom, the number of alcohol-related 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 multifactotal, 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 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, 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[R]) (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, hyperlipidemia, 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 ([B.sub.1]), folic acid, pyridoxine ([B.sub.6]), 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, low-density 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 life-threatening 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 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 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 methods with current treatment protocols which potentially can enhance the single-model approaches to health and wellness (Srivastava, 2007).
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 double-blind, 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[R]) (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[R]) 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[R]) and carbamazepine (Tegretol[R]) 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[R]) and barbiturates in alcohol withdrawal (Preuss, Zil, & Koller, 2006). Antipsychotics and alpha agonists also may assist in symptom management (Kahn et al., 2009).
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).
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 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).
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 evidence-based practice will lead to improved care of affected patients.
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Glenn Donnelly, PhD, MN, BSc(N), RN, ENC[c], is Associate Professor, Faculty of Nursing, University of Regina, Regina, Saskatchewan, Canada.
Arlene Kent-Wilkinson, PhD, MN, BSN, RN, is Associate Professor, College of Nursing, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
Alecia Rush is a Nursing Student, Mount Royal University, Calgary, Alberta, Canada.
Note: The authors and all MEDSURG Nursing Editorial Board members reported no actual or potential conflict of interest in relation to this continuing nursing education article.
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|Title Annotation:||CNE SERIES|
|Author:||Donnelly, Glenn; Kent-Wilkinson, Arlene; Rush, Alecia|
|Date:||Jan 1, 2012|
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