Alcohol, a central nervous system depressant, is used socially in our society for many reasons: to enhance the flavor of food, to encourage relaxation and conviviality, for celebrations, and as a sacred ritual in some religious ceremonies. Therapeutically, it is the major ingredient in many OTC/prescription medications. It can be harmless, enjoyable, and sometimes beneficial when used responsibly and in moderation.
It is rapidly absorbed from the stomach and small intestine into the bloodstream. On the other hand, alcohol withdrawal refers to symptoms that may occur when a person who has been drinking too much alcohol every day suddenly stops drinking alcohol.
Alcohol withdrawal symptoms usually occur within 8 hours after the last drink but can occur days later. Symptoms usually peak by 24 – 72 hours, but may persist for weeks. Common symptoms include anxiety or nervousness, depression, fatigue, irritability, jumpiness or shakiness, mood swings, nightmares and not thinking clearly.
Nursing care planning for patients who are undergoing alcohol withdrawal includes: maintaining physiological stability during the acute withdrawal phase, promoting safety, providing appropriate referral and followup, and involvement of SO in the process.
May be related to
- Cessation of alcohol intake/physiological withdrawal
- Situational crisis (hospitalization)
- Threat to self-concept, perceived threat of death
Possibly evidenced by
- Feelings of inadequacy, shame, self-disgust, and remorse
- Increased helplessness/hopelessness with loss of control of own life
- Increased tension, apprehension
- Fear of unspecified consequences; identifies object of fear
- Verbalize reduction of fear and anxiety to an acceptable and manageable level.
- Express sense of regaining some control of situation/life.
- Demonstrate problem-solving skills and use resources effectively.
|Determine cause of anxiety, involving patient in the process. Explain that alcohol withdrawal increases anxiety and uneasiness. Reassess level of anxiety on an ongoing basis.||Person in acute phase of withdrawal may be unable to identify and accept what is happening. Anxiety may be physiologically or environmentally caused. Continued alcohol toxicity will be manifested by increased anxiety and agitation as effects of medication wear off.|
|Develop a trusting relationship through frequent contact being honest and nonjudgmental. Project an accepting attitude about alcoholism.||Provides patient with a sense of humanness, helping to decrease paranoia and distrust. Patient will be able to detect biased or condescending attitude of caregivers.|
|Maintain a calm environment, minimizing noise.||Reduces stress.|
|Inform patient about what you plan to do and why. Include patient in planning process and provide choices when possible.||Enhances sense of trust, and explanation may increase cooperation and reduce anxiety. Provides sense of control over self in circumstance where loss of control is a significant factor. Note: Feelings of self-worth are intensified when one is treated as a worthwhile person.|
|Reorient frequently.||Patient may experience periods of confusion, resulting in increased anxiety.|
|Orient the patient to reality.||He may also experience hallucinations and may try to harm himself and others.|
|Monitor patient for signs of depression.||To prevent suicidal attempts.|
|Administer medications as indicated:|
||Antianxiety agents are given during acute withdrawal to help patient relax, be less hyperactive, and feel more in control.|
||These drugs suppress alcohol withdrawal but need to be used with caution because they are respiratory depressants and REM sleep cycle inhibitors.|
|Arrange “Intervention” (confrontation) in controlled setting||Process wherein SO and family members, supported by staff, provide information about how patient’s drinking and behavior have affected each one of them, helps patient acknowledge that drinking is a problem and has resulted in current situational crisis.|
|Provide consultation for referral to detoxification and
crisis center for ongoing treatment program as soon as medically stable (oriented to reality).
|Patient is more likely to contract for treatment while still hurting and experiencing fear and anxiety from last drinking episode. Motivation decreases as well-being increases and person again feels able to control the problem. Direct contact with available treatment resources provides realistic picture of help. Decreases time for patient to “think about it,” change mind or restructure and strengthen denial systems.|
- Sensory/Perceptual Alterations
May be related to
- Chemical alteration: Exogenous (e.g., alcohol consumption/sudden cessation) and endogenous (e.g., electrolyte imbalance, elevated ammonia and BUN)
- Sleep deprivation
- Psychological stress (anxiety/fear)
Possibly evidenced by
- Disorientation to time, place, person, or situation
- Changes in usual response to stimuli; exaggerated emotional responses, change in behavior
- Bizarre thinking
- Listlessness, irritability, apprehension, activity associated with visual/auditory hallucinations
- Regain/maintain usual level of consciousness.
- Report absence of/reduced hallucinations.
- Identify external factors that affect sensory-perceptual abilities.
|Assess level of consciousness; ability to speak, response to stimuli and commands.||Speech may be garbled, confused, or slurred. Response to commands may reveal inability to concentrate, impaired judgment, or muscle coordination deficits.|
|Observe behavioral responses such as hyperactivity, disorientation, confusion, sleeplessness, irritability.||Hyperactivity related to CNS disturbances may escalate rapidly. Sleeplessness is common due to loss of sedative effect gained from alcohol usually consumed before bedtime. Sleep deprivation may aggravate disorientation and confusion. Progression of symptoms may indicate impending hallucinations (stage II) or DTs (stage III).|
|Provide calm environment, minimizing noise and shadows.||To reduce the incidence of delusions and hallucinations.|
|Avoid restraining the patient unless necessary.||To protect patient and others.|
|Note onset of hallucinations. Document as auditory, visual, and tactile.||Auditory hallucinations are reported to be more frightening and threatening to patient. Visual hallucinations occur more at night and often include insects, animals, or faces of friends and enemies. Patients are frequently observed “picking the air.” Yelling may occur if patient is calling for help from perceived threat (usually seen in stage III AWS).|
|Provide quiet environment. Speak in calm, quiet voice. Regulate lighting as indicated. Turn off radio and TV during sleep.||Reduces external stimuli during hyperactive stage. Patient may become more delirious when surroundings cannot be seen, but some respond better to quiet, darkened room.|
|Provide care by same personnel whenever possible.||Promotes recognition of caregivers and a sense of consistency, which may reduce fear.|
|Monitor patient for signs of depression.||To avoid harming himself and attempts of suicide.|
|Encourage SO to stay with patient whenever possible.||May have a calming effect, and may provide a reorienting influence.|
|Reorient frequently to person, place, time, and surrounding environment as indicated.||May reduce confusion, prevent and limit misinterpretation of external stimuli.|
|Avoid bedside discussion about patient or topics unrelated to the patient that do not include the patient.||Patient may hear and misinterpret conversation, which can aggravate hallucinations.|
|Provide environmental safety (place bed in low position, leave doors in full open or closed position, observe frequently, place call light or bell within reach, remove articles that can harm patient).||Patient may have distorted sense of reality or be fearful or suicidal, requiring protection from self.|
|Provide seclusion, restraints as necessary.||Patients with excessive psychomotor activity, severe hallucinations, violent behavior, and suicidal gestures may respond better to seclusion. Restraints are usually ineffective and add to patient’s agitation, but occasionally may be required to prevent self-harm.|
|Orient the patient to reality.||He may experience hallucinations and may try to harm himself and others.|
|Monitor laboratory studies: electrolytes, magnesium levels, liver function studies, ammonia, BUN, glucose, ABGs.||Changes in organ function may precipitate or potentiate sensory-perceptual deficits. Electrolyte imbalance is common. Liver function is often impaired in the chronic alcoholic, and ammonia intoxication can occur if the liver is unable to convert ammonia to urea. Ketoacidosis is sometimes present without glycosuria; however, hyperglycemia or hypoglycemia may occur, suggesting pancreatitis or impaired gluconeogenesis in the liver. Hypoxemia and hypercarbia are common manifestations in chronic alcoholics who are also heavy smokers.|
|Administer medications as indicated: Antianxiety agents as indicated||Reduces hyperactivity, promoting relaxation and sleep. Drugs that have little effect on dreaming may be desired to allow dream recovery (REM rebound) to occur, which has previously been suppressed by alcohol use.|
Risk for Injury
Risk factors may include
- Cessation of alcohol intake with varied autonomic nervous system responses to the system’s suddenly altered state
- Involuntary clonic/tonic muscle activity (seizures)
- Equilibrium/balancing difficulties, reduced muscle and hand/eye coordination
- Demonstrate absence of untoward effects of withdrawal.
- Experience no physical injury.
|Identify stage of AWS (alcohol withdrawal syndrome); i.e., stage I is associated with signs and symptoms of hyperactivity (tremors, sleeplessness, nausea and vomiting, diaphoresis, tachycardia, hypertension). Stage II is manifested by increased hyperactivity plus hallucinations and seizure activity. Stage III symptoms include DTs and extreme autonomic hyperactivity with profound confusion, anxiety, insomnia, fever.||Prompt recognition and intervention may halt progression of symptoms and enhance recovery or improve prognosis. In addition, recurrence or progression of symptoms indicates need for changes in drug therapy and more intense treatment to prevent death.|
|Monitor and document seizure activity. Maintain patent airway. Provide environmental safety (padded side rails, bed in low position).||Grand mal seizures are most common and may be related to decreased magnesium levels, hypoglycemia, elevated blood alcohol, or history of head trauma and preexisting seizure disorder. Note: In absence of history and other pathology causing seizures, they usually stop spontaneously, requiring only symptomatic treatment. Note: Antiepileptic drugs are not indicated for alcohol withdrawal seizures.|
|Check deep-tendon reflexes. Assess gait, if possible.||Reflexes may be depressed, absent, or hyperactive. Peripheral neuropathies are common, especially in malnourished patient. Ataxia (gait disturbance) is associated with Wernicke’s syndrome (thiamine deficiency) and cerebellar degeneration.|
|Assist with ambulation and self-care activities as needed.||Prevents falls with resultant injury.|
|Provide for environmental safety when indicated.||May be required when equilibrium, hand and eye coordination problems exist.|
|Administer medications as indicated:|
||BZDs are commonly used to control neuronal hyperactivity because of their minimal respiratory and cardiac depression and anticonvulsant properties. Studies have also shown that these drugs can prevent progression to more severe states of withdrawal. IV and PO administration is preferred route because IM absorption is unpredictable. Muscle-relaxant qualities are particularly helpful to patient in controlling “the shakes,” trembling, and ataxic quality of movements. Patient may initially require large doses to achieve desired effect, and then drugs may be tapered and discontinued, usually within 96 hr. Note: These agents are used cautiously in patients with known hepatic disease because they are metabolized by the liver, although Serax has a shorter half-life.|
||May be used in conjunction with BZDs for patients experiencing hallucinations.|
||Thiamine deficiency (common in alcohol abuse) may lead to neuritis, Wernecke’s syndrome, and Korsakoff’s psychosis.|
||Reduces tremors and seizure activity by decreasing neuromuscular excitability.|
Risk for Decreased Cardiac Output
- Risk for Decreased Cardiac Output
Risk factors may include
- Direct effect of alcohol on the heart muscle
- Altered systemic vascular resistance
- Electrical alterations in rate, rhythm, conduction
- Display vital signs within patient’s normal range; absence of/reduced frequency of dysrhythmias.
- Demonstrate an increase in activity tolerance.
|Monitor vital signs frequently during acute withdrawal.||Hypertension frequently occurs in acute withdrawal phase. Extreme hyperexcitability, accompanied by catecholamine release and increased peripheral vascular resistance, raises BP and heart rate; however, BP may become labile and progress to hypotension. Note:Patient may have underlying cardiovascular disease, which is compounded by alcohol withdrawal.|
|Monitor cardiac rate and rhythm. Document irregularities and dysrhythmias.||Long-term alcohol abuse may result in cardiomyopathy or HF. Tachycardia is common because of sympathetic response to increased circulating catecholamines. Irregularities and dysrhythmias may develop with electrolyte shifts and imbalance. All of these may have an adverse effect on cardiac function and output.|
|Monitor body temperature.||Elevation may occur because of sympathetic stimulation, dehydration, and infections, causing vasodilation and compromising venous return and cardiac output.|
|Monitor I&O. Note 24-hr fluid balance.||Preexisting dehydration, vomiting, fever, and diaphoresis may result in decreased circulating volume that can compromise cardiovascular function. Note: Hydration is difficult to assess in the alcoholic patient because the usual indicators are not reliable, and overhydration is a risk in the presence of compromised cardiac function.|
|Be prepared and assist in cardiopulmonary resuscitation.||Causes of death during acute withdrawal stages include cardiac dysrhythmias, respiratory depression and arrest, oversedation, excessive psychomotor activity, severe dehydration or overhydration, and massive infections. Mortality for unrecognized and untreated delirium tremens (DTs) may be as high as 25%.|
|Monitor laboratory studies: serum electrolyte levels.||Electrolyte imbalance: potassium, magnesium, potentiate risk of cardiac dysrhythmias and CNS excitability.|
|Administer fluids and electrolytes, as indicated||Severe alcohol withdrawal causes the patient to be susceptible to fluid losses (associated with fever, diaphoresis, and vomiting) and electrolyte imbalances, especially potassium, magnesium, and glucose.|
|Administer medications as indicated: Clonidine (Catapres), atenolol (Tenormin);Potassium.||Although the use of benzodiazepines is often sufficient to control hypertension during initial withdrawal from alcohol, some patients may require more specific therapy. Note: Atenolol and other b-adrenergic blockers may speed up the withdrawal process and eliminate tremors, as well as lower the heart rate, blood pressure, and body temperature.
Corrects deficits that can result in life-threatening dysrhythmias.
Risk for Ineffective Breathing Pattern
- Risk for Ineffective Breathing Pattern
Risk factors may include
- Direct effect of alcohol toxicity on respiratory center and/or sedative drugs given to decrease alcohol withdrawal symptoms
- Tracheobronchial obstruction
- Presence of chronic respiratory problems, inflammatory process
- Decreased energy/fatigue
- Maintain effective breathing pattern with respiratory rate within normal range, lungs clear; be free of cyanosis and other signs/symptoms of hypoxia.
|Monitor respiratory rate and depth and pattern as indicated. Note periods of apnea, Cheyne-Stokes respirations.||Frequent assessment is important because toxicity levels may change rapidly. Hyperventilation is common during acute withdrawal phase. Kussmaul’s respirations are sometimes present because of acidotic state associated with vomiting and malnutrition. However, marked respiratory depression can occur because of CNS depressant effects of alcohol if acute intoxication is present. This may be compounded by drugs used to control alcohol withdrawal symptoms (AWS).|
|Auscultate breath sounds. Note presence of adventitious sounds: rhonchi, wheezes.||Patient is at risk for atelectasis related to hypoventilation and pneumonia. Right lower lobe pneumonia is common in alcohol-debilitated patients and is often due to chronic aspiration. Chronic lung diseases are also common: emphysema, bronchitis.|
|Elevate head of bed.||Decreases potential for aspiration; lowers diaphragm, enhancing lung inflation.|
|Encourage cough and deep-breathing exercises and frequent position changes.||Facilitates lung expansion and mobilization of secretions to reduce risk of atelectasis and pneumonia.|
|Have suction equipment, airway adjuncts available.||Sedative effects of alcohol and drugs potentiates risk of aspiration, relaxation of oropharyngeal muscles, and respiratory depression, requiring intervention to prevent respiratory arrest.|
|Administer supplemental oxygen if necessary.||Hypoxia may occur with CNS and respiratory depression.|
|Review serial chest x-rays, ABGs and pulse oximetry as available and indicated||Monitors presence of secondary complications such as atelectasis and pneumonia; evaluates effectiveness of respiratory effort, identifies therapy needs.|
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