Critical Care Nurse. 2005;25: 40-48
Copyright © 2005 by the American Association of Critical-Care Nurses.
Clinical Article
CE Article
Alcohol Withdrawal Syndrome Overlooked and Mismanaged?
Mary G. McKinley, RN, MSN, CCRN
Mary G. McKinley is a graduate of Ohio Valley General Hospital Diploma School of Nursing, Wheeling College (now Wheeling Jesuit University), Wheeling, WV. She received her master’s degree from West Virginia University, Morgantown, WV. She has maintained her CCRN certification since 1985. She is past president of the American Association of Critical-Care Nurses. She has published in the area of critical care and has spoken nationally on topics related to critical care and nursing.
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* This article has been designated for CE credit. A closed-book, multiple-choice examination follows this article, which tests your knowledge of the following objectives:- Describe pathophysiology involved between alcohol and alterations of neurotransmission in the brain
- Define the relationship between alcohol and thiamine deficiency
- Examine the management of patients undergoing alcohol withdrawal syndrome
Patients are admitted to critical care with a myriad of problems. A problem easily overlooked is alcohol dependency and the potential development of alcohol withdrawal syndrome (AWS). Fourteen million persons in the United States abuse alcohol or are alcohol dependent. Nearly 27% of persons in the United States between the ages of 18 and 64 years meet the diagnostic criteria for alcohol dependency, making it the most prevalent addictive disease in this country. According to estimates, 1 of every 5 patients admitted to a hospital is an alcohol abuser.1
When patients are admitted for problems such as trauma, alcohol is often associated as a factor, and trauma patients are more likely than other patients to be assessed for AWS. Admissions to a critical care unit because of nontrauma conditions, however, are not always so clearly linked to alcohol abuse, and AWS can easily be overlooked. Overlooking AWS can have devastating consequences and complications. Persons who abuse alcohol have mortality and morbidity rates 2 to 4 times greater than those of the general population.2 The toxic effects of alcohol abuse on organs and tissues put these patients at increased risk for multiple system dysfunction. Early detection of and intervention for AWS can prevent, or at least minimize, the complications and consequences of the syndrome.
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Terminology
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Because confusion can exist about the different terms associated with AWS, clarification is necessary (see Sidebar). Alcohol abuse cannot be diagnosed on the basis of a set amount or frequency of alcohol consumption. Signs and symptoms of withdrawal rarely occur in persons who drink only occasionally. AWS usually occurs in persons who have been heavy drinkers for weeks or months who suddenly stop drinking. An example is a patient admitted to a critical care unit for treatment of an acute hypertensive episode who is a heavy drinker but because of the admission cannot continue the alcohol intake. An understanding of the signs and symptoms and behavioral indicators is key in recognizing patients who are at risk for AWS.
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Pathophysiology
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The complex mechanisms of alcohol intoxication, tolerance, dependence, and withdrawal are not completely understood, but a clear relationship exists between alcohol and alterations in neurotransmission in the brain. Neurotransmitters are chemical messengers that transmit information from one neuron to another across synapses. Neurotransmitters in the brain either promote (excitatory) or slow down (inhibitory) impulses along the neurons.
One of the main neurotransmitters in the brain affected by alcohol is the inhibitory neurotransmitter 
-aminobutyrate A (GABAA). GABAA allows more chloride to enter the neuron, making the neuronal cell membranes less likely to depolarize, thereby inhibiting the cell. A second neurotransmitter of importance in alcohol abuse is the excitatory neurotransmitter N-methyl-D-aspartate (NMDA). NMDA regulates neuron excitability, increasing depolarization of the neuronal membrane by regulating the flow of calcium into the neuron. Initially, in short-term use (1 or 2 drinks occasionally), alcohol enhances the GABAA receptors and inhibits the NMDA receptors.3 The result of short-term alcohol use therefore is depression of the behavioral inhibitory centers in the cerebral cortex and the reticular activating system, causing initial euphoria, exaggerated feelings of well-being, and reduced self-control and then sedation and anesthesia (Figure 1
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Figure 1 Schematic representation of the effects of alcohol exposure and withdrawal. The zero line represents the excitability of the brain. Short-term alcohol intake produces a depression of the inhibitory centers of the cerebral cortex, which results in the initial symptoms of intoxication (euphoria, exaggerated feelings of well-being, and loss of self-control followed by sedation). Long-term alcohol intake causes the initial decrease with tolerance that occurs during continued exposure to alcohol. Removal of alcohol causes a rebound stimulatory effect, increasing excitability in the nervous system.
Adapted from Finn and Crabbe.3
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The pathophysiological effects of long-term use of alcohol involve the same neurotransmitters but are complicated by tolerance and physical dependence as contributing factors to the problem of withdrawal of alcohol. Long-term alcohol intake (see Sidebar for indicators of alcohol dependence) results in a decrease in GABAA inhibitory function and an increase in NMDA excitatory function.3 Continued intake of alcohol causes adaptation of the central nervous system, reducing the initial, short-term effects. Abrupt cessation of intake of alcohol or withdrawal produces a rebound stimulatory effect, resulting in adrenergic hypersensitivity of the limbic system and brain stem, which can lead to irritability (manifested as aggrssive behavior), tremors, and seizures.1
An additional problem that occurs with long-term use of alcohol is tolerance or a need to increase the amount of alcohol to obtain desired effects. Three types of tolerance develop.
The first type is metabolic tolerance or an increase in the rate of ethanol metabolism in the liver. As the ethanol is more rapidly metabolized, larger and still larger amounts of alcohol are needed to achieve the desired effects. The second type is cellular tolerance, which develops through the continued exposure of the cells in the brain to the neurochemical changes, the activities of GABAA, NMDA, and other neurotransmitters. Prolonged use of alcohol results in adaptation of the neurons to the use of alcohol, and larger doses of alcohol are needed to produce the same result. The third type is behavioral tolerance, learning to adapt behavior so the person can function under the influence of alcohol.1
These 3 forms of tolerance can complicate the management of patients who have alcohol problems. For example, cellular tolerance may result in the need for increased dosages of medication to produce the desired results for a patient who has AWS.
Long-term exposure to alcohol also leads to dependence. In alcohol dependence, the neuronal adaptation to alcohol has become pronounced and the continued presence of alcohol is required for proper neuronal functioning. The metabolic and cellular changes caused by long-term use of alcohol do not resolve with cessation of drinking. The management of patients with AWS requires knowledge of the physical dependency caused by long-term use of alcohol.
Long-term alcohol dependency also leads to thiamine deficiency, a contributing factor to the pathophysiology of AWS.4 Thiamine deficiency occurs for 2 reasons: inadequate intake due to a poor nutritional state and interruption of the metabolism of thiamine by alcohol. Thiamine plays a key role in glucose metabolism. Thiamine pyrophosphate (the active form of thiamine) acts as a coenzyme for 2 enzymes in the Krebs or tricarboxylic acid cycle: ketoglutarate dehydrogenase and pyruvate dehydrogenase. Most likely, a deficiency in thiamine pyrophosphate alters neuronal energy metabolism in the central nervous system and diminishes nerve transmission. The major organs affected by thiamine deficiency are those that depend on energy from the metabolism of carbohydrates: the peripheral nerves, heart, and brain.
Peripheral neuropathy with myelin degeneration is the result of thiamine deficiency in the peripheral nerves. Cardiomyopathy and hypertension can occur because of effects of thiamine deficiency on the heart.1 Wernicke encephalopathy and Korsakoff syndrome are the result of chronic thiamine deficiency in the brain. Wernicke encephalopathy is characterized by ophthalmoplegia (paralysis of the eye muscles), nystagmus (horizontal and vertical involuntary, rapid, rhythmic movements of the eyeballs), and ataxia (slow, uncertain, short-stepped gait). Signs and symptoms of Korsakoff syndrome include retrograde amnesia (inability to recall information), anterograde amnesia (inability to assimilate new information), decreased spontaneity, decreased initiative, and confabulation (filling in memory gaps with distorted facts).1 Understanding the role of thiamine deficiency in long-term alcohol abuse is helpful in recognizing important clinical manifestations and in managing patients with AWS.
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Clinical Features
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Signs and symptoms of autonomic hyperreactivity and neuropsychiatric alterations characterize AWS. Autonomic hyperreactivity includes tremors, sweating, nausea, and vomiting. Neuropsychiatric alterations include agitation, anxiety, auditory disturbances, clouding of sensorium, and disturbances in visual or tactile senses. These signs and symptoms are somewhat nonspecific and therefore are easily confused with other problems common in critical care patients, such as electrolyte imbalances, pain, and infection.
The signs and symptoms of AWS usually occur within 24 hours after the last drink. They peak in 24 to 36 hours and end after 48 hours.5
Alcohol withdrawal delirium or delirium tremens can occur within 48 to 72 hours after the last drink. Delirium tremens is a serious and life-threatening complication of alcohol withdrawal and should be treated as a medical emergency. The peak time for occurrence of delirium is usually day 4 after cessation of alcohol use, and the delirium can persist for 2 to 3 days, or in severe cases, up to 2 weeks.1 The pronounced autonomic hyperreactivity signs and symptoms of delirium include hypertension, tachycardia, tachypnea, and tremors. If untreated, these can lead to respiratory and cardiovascular collapse. Neuropsychiatric indications of delirium include hallucinations, confusion, disorientation, and impaired attention. (See Table 1 for a summary comparison of the manifestations of AWS and delirium tremens.)
Laboratory values that may assist in recognition of AWS include mean corpuscular volume and serum levels of -glutamyl transferase, uric acid, and carbohydrate-deficient transferrin6 (Table 2). The values are abnormally increased with regular consumption of 180 to 240 mL (6-8 oz) of alcohol per day.5
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Assessment Tools
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As a part of assessment at the time of admission to the critical care unit, all patients should be screened for alcohol abuse. The usual assessment includes an alcohol use history that includes the frequency and quantity of regular alcohol consumption, how many years the use has been occurring, and the most recent intake.
One tool that has been suggested as an assessment questionnaire for alcohol use is the CAGE tool7 (Table 3). Guidelines suggest that patients with a CAGE score greater than 2 or a score greater than 1 and at least 1 positive laboratory result (Table 2
) should be considered alcohol dependent and at risk for AWS.2 The CAGE tool has been used in multiple studies and has documented reliability and validity in clinical settings. The advantage to using CAGE is that it is quick, easy to use, and easy to score.7
The Clinical Institute Withdrawal Assessment of Alcohol Scale, revised (CIWA-Ar; Figure 2) is a tool that can be used to objectively assess patients for the development of AWS. This scale has well-documented reliability and validity.8 It is a refined tool with a list of 10 signs and symptoms that is quick, easy to use, and useful in a variety of hospital settings, including psychiatric and general medical surgical units. The categories assessed in the CIWA-Ar include agitation, anxiety, auditory disturbances, orientation and clouding of sensorium, headache, nausea and vomiting, paroxysmal sweats, tactile disturbances, tremor, and visual disturbances.
The CIWA-Ar is used not only for diagnosis and monitoring but also as a basis for pharmacological management of patients with AWS. Scores of less than 8 to 10 on the CIWA-Ar indicate minimal to mild withdrawal.8 Scores of 8 to 15 indicate moderate withdrawal, and scores of 15 or more indicate severe withdrawal and impending delirium.8 By using the CIWA-Ar to assess patients, nurses can quantify the potential for the development of AWS and therefore initiate treatment for patients who require therapy. The CIWA-Ar is not copyrighted and can be downloaded from the following Web site: www .erowid.org/chemicals/alcohol/alcohol_ARF_withdrawal_scale.shtml.
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Management of Patients With AWS
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The treatment plan for patients with AWS includes pharmacological management and supportive care.
Pharmacological Management
Most signs and symptoms of alcohol withdrawal are caused by the rapid removal of the depressant effects of alcohol in the central nervous system. Although many pharmacological agents have depressant effects on the central nervous system, the cornerstone of pharmacological management for AWS patients is benzodiazepines. These drugs are the only agents that have been proved in placebo-controlled trials to reduce the severity of the effects of alcohol withdrawal and prevent progression to the serious complications of AWS.9 Benzodiazepines work by potentiating the responses of the GABAA receptors, thereby enhancing neuronal inhibition, or putting on the brakes. At this time, no specific benzodiazepine is recommended for use. The choice of agent to be used should be guided by the agent’s duration of action, potential for abuse, and cost.9
Benzodiazepines with a short-half life (eg, oxazepam, with a half-life of 4-14 hours, or lorazepam, with a half-life of 10–20 hours) result in rapid changes of drug levels in the blood and may have to be given at an interval of every 4 hours to avoid abrupt fluctuations of the drug levels, which may precipitate seizures. These short-duration agents may be particularly useful in patients with serious liver impairment or encephalopathy or when rapid control of signs and symptoms is needed. Agents with a longer duration of action (eg, diazepam, with a half-life of 20–90 hours, or chlordiazepoxide, with a half life of 24–48 hours) may be used because they maintain the therapeutic levels more evenly and consistently and so provide more effective control of signs and symptoms.
Another consideration in selecting an agent for treatment is the potential for abuse of the drug. The results of some clinical trials indicate that certain agents are preferred by patients with addictive disorders.8 Agents with a rapid onset of action, such as diazepam or lorazepam, have a higher abuse potential than do agents with a slower onset, such as chlordiazepoxide or oxazepam.
In the current healthcare environment, cost of pharmacological management is also a consideration. Table 4 includes the approximate average wholesale costs of some of the benzodiazepines.9
Because the goal of therapy is to alleviate the signs and symptoms of withdrawal, providing a fixed standardized dose of the selected benzodiazepine is not effective in treating alcohol withdrawal.8 Individualizing therapy according to the signs and symptoms (symptom-triggered therapy) of each patient results in administration of less medication and shorter treatment.8
The CIWA-Ar can be used to provide guidance and to monitor effective treatment with benzodiazepines. Monitoring should be completed by using the CIWA-Ar every 4 hours, and if the score is greater than 8 to 10, the selected benzodiazepine should be administered (Table 4). One hour after administration of the drug, the CIWA-Ar should be used again to determine if further medication is needed. Monitoring should continue until the CIWA-Ar score is less than 8 to 10 for 24 hours.8
Comorbid conditions and history of previous withdrawal seizures should also be considered when dosages of benzodiazepines are determined. The goal is to administer enough of the drug to alleviate the signs and symptoms and then to decrease the dose as the signs and symptoms abate.
Thiamine is another pharmacological agent recommended in the treatment of patients with AWS. The purpose of thiamine replacement is to avoid the severe and irreversible complications (as discussed earlier) that can occur as a result of thiamine deficiency. A dose of 50 to 100 mg of thiamine is given parenterally or orally daily for 3 days or more.5
Supportive Care
The effects of alcohol on the body should be taken into consideration in supportive care (Table 5). Reducing environmental stimuli and providing uninterrupted periods of rest can help minimize the severity of signs and symptoms. Use of restraints should be avoided because they may worsen the neuropsychiatric alterations. Orientation should be provided as necessary with clocks and calendars. Use of television may contribute to a patient’s confusion and hallucinations, particularly if the program is unfamiliar to the patient. Because malnutrition is a concern with patients with AWS, providing adequate nutritional support is important. Monitoring fluid balance is important because fluid retention occurs as a result of the inhibition of vasopressin secretion, which occurs with increases in blood alcohol levels.1 In order to help reduce the stress of critical illness, which can exacerbate AWS, the concomitant medical disorder that brought the patient to the critical care unit should be aggressively treated.
Discharge planning should include encouragement to seek treatment for addictive disease. A nonjudgmental explanation of the effects of alcohol abuse and the possible complications can help patients make appropriate behavioral changes. Patients who abuse alcohol may be noncompliant with self-care management and are at risk for chronic AWS complications and increased likelihood of experiencing injury or trauma. Psychiatric support services and referrals are appropriate for follow-up.
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Summary
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Because alcohol abuse and alcohol dependency are widespread, many critical care patients may have AWS. AWS has marked consequences that affect the care of these patients, and critical care nurses must actively assess and intervene to prevent or at least minimize the complications of AWS. By increasing awareness, using reliable assessment tools, and knowing guidelines for the management of these patients, nurses can reduce the consequences of overlooking AWS and mismanaging patients who have the syndrome.
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Acknowledgments
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The author wishes to thank Kathy Kaminski, RN, for her encouragement and assistance in identifying the focus for this article.
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References
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- Schuckit M. Alcohol and alcoholism. In: Brunwald E, Fauci AS, Kasper DL, Hauser SL, Longo DL, Jameson JL. Harrison’s Principles of Internal Medicine. Vol. 2. 15th ed. New York, NY: McGraw-Hill Professional Publishing; 2001:2561–2566.
- Alcohol: What You Don’t Know Can Harm You. Bethesda, Md: US Dept of Health and Human Services, National Institute on Alcohol Abuse and Alcoholism; 2001. NIH publication 96 4153.
- Finn DA, Crabbe JC. Exploring alcohol withdrawal syndrome. Alcohol Health Res World. 1997;21:149–156.[Medline]
- Bridges KJ, Trujillo EB, Jacobs DO. Alcohol-related thiamine deficiency and malnutrition. Crit Care Nurse. December 1999;19:80–85.[Medline]
- Tierney LM, McPhee SJ, Papadakis MA, eds. Current Medical Diagnosis and Treatment 2003. 42nd ed. New York, NY: Apple-ton & Lange: 2003.
- Chernecky CC, Berger BJ, eds. Laboratory Tests and Diagnostic Procedures. 3rd ed. Philadelphia, Pa: WB Saunders Co; 2001.
- Bisson J, Nadeau L, Demers A. The validity of the CAGE scale to screen for heavy drinking and drinking problems in a general population survey. Addiction. 1999;94:715–722.[Medline]
- Jaeger T, Lohr R, Pankratz S. Symptom-triggered therapy for alcohol withdrawal syndrome in medical inpatients. Mayo Clin Proc. 2001;76:695–701.[Abstract]
- Mayo-Smith MF. Pharmacological management of alcohol withdrawal: a meta-analysis and evidence-based practice guideline. American Society of Addiction Medicine Working Group on Pharmacological Management of Alcohol Withdrawal. JAMA. 1997;278:144–151.[Abstract/Free Full Text]
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Terminology
Pathophysiology
