Excessive alcohol consumption (EAC) increases the risks of injury and chronic physical and mental health problems, negatively affects relationships and social status, and strains the economy.1-3 People who engage in EAC may be diagnosed with alcohol use disorder (AUD).1-3 AUD affects an estimated 100 million people globally, including 15 million people aged 12 and older in the US.1-3 AUD is a medical diagnosis occurring when a person cannot control their alcohol consumption, resulting in physical and mental health deterioration and problems at home, work, and in the community.4 A person with AUD who abruptly decreases the quantity of alcohol consumption may experience alcohol withdrawal syndrome (AWS), which may be mild to life-threatening.5 This article presents the pathophysiology, clinical manifestations, and management of patients with AWS.
Epidemiology
Approximately 50% of people with AUD experience AWS after abruptly decreasing or abstaining from alcohol consumption.6 AWS is caused by altered neurotransmitters in the brain, causing an increase in neuron activity.6 People with mild AWS may be managed on an outpatient basis, while moderate to severe AWS requires hospitalization.6
Approximately 500,000 episodes of severe AWS occur annually in the US.7 People at the highest risk for developing AWS include those with a history of withdrawal; using sedatives, anxiolytics, and opioids; are older adults; have chronic physical and mental illnesses; have insufficient intake of nutrients; are impoverished; or are homeless.5,6,8
The incidence of AWS is greater than 80% in people with AUD who are homeless or hospitalized.8 AWS is an incidental finding in 2% to 7% of people hospitalized for a medical problem whose history of alcohol consumption is not known to the healthcare team.7
Neurotransmitters
Several mechanisms mediate AWS. Inhibitory and excitatory neurotransmitters in the brain balance neurochemicals.6,7,9 Neurotransmitters initiate and transmit nerve conduction through the nervous system; alcohol consumption affects each one.6,7,9
Thiamine (vitamin B-1) is a cofactor for synthesizing neurotransmitters, enhancing neuronal function, and converting carbohydrates into energy.10,11 Thiamine is not manufactured in the body and must be acquired from the diet.10,11 Thiamine deficiency may occur in AUD from poor intake or absorption, leading to severe headaches, paresthesia, neuropathy, gait imbalance, visual disturbances, anxiety, cognitive impairment, confusion, and dementia, known as Wernicke-Korsakoff (WK) Syndrome.10,11 Thiamine deficiency often coexists with AWS and thiamine is administered to help glucose form adenosine triphosphate (ATP) to enhance neurotransmission and energy.10,11 Acetylcholine, an excitatory neurotransmitter, and ATP are synthesized simultaneously to facilitate the conduction of other neurotransmitters (see Function of select neurotransmitters).10,11
Gamma-aminobutyric acid (GABA), glutamate, and dopamine are major neurotransmitters impacted by EAC.6,7,12 GABA is an inhibitory neurotransmitter that decreases cell excitability and produces a calming effect in a person who has not consumed alcohol.6,7,12 The calming effect is described as feeling normal.6,7,12 Alcohol increases GABA in the brain, causing relaxation, euphoria, and various levels of sedation depending on the amount of alcohol consumed.6,7,12 However, tolerance develops with chronic EAC, in which alcohol suppresses the production of GABA, and a person requires more alcohol to achieve the desired effect.6,7,12 A person with a tolerance needs to consume just enough alcohol to feel normal and more elevated amounts to experience euphoria.6,7,12
Glutamate binding to N-methyl-D-aspartate (NMDA) receptor sites, an excitatory neurotransmitter, promotes cognition and motor movement and increases energy.6,7,12 Alcohol consumption inhibits glutamine production, causing a calming effect.6,7,12 The steady consumption of alcohol causes suppression of glutamate.6,7,12
Dopamine is a neurotransmitter with inhibitory and excitatory properties that mediates motor control, memory, motivation, lactation, sleep, arousal, eating, and pleasure.6,7,12 Elevated dopamine levels occur in the mesolimbic pathway (reward pathway), with EAS causing euphoria.6,7,12 Dopamine levels increase even when a person anticipates drinking alcohol, which leads to craving more alcohol.6,7,12
Epinephrine and norepinephrine are excitatory neurotransmitters that regulate the heart, blood vessels, lungs, and muscles.12 These neurotransmitters are suppressed by alcohol.12 Serotonin is an inhibitory neurotransmitter that mediates mood, pain perception, sexual response, sleep, rest, and appetite.12 Alcohol consumption can temporarily increase serotonin levels.12 Endogenous opioids (endorphins) are depleted with EAC.12 When a person with AUD abruptly decreases alcohol consumption or stops drinking altogether, neurotransmitters respond with a rebound effect wherein the brain is in a hyperexcitability state affecting all body tissues and organs.5-7
Clinical manifestations
The hyperexcitability state occurs 6 to 24 hours after a person's last drink following a period of EAC and may last 3 to 7 days.7,13,14 EAC is defined as when a man consumes 4 or more drinks in a day or 14 or more in 7 days, and a woman consumes 3 or more drinks in a day or 7 or more in 7 days.15 A person who consumes more than 8 drinks daily for several days is more likely to experience AWS (see US standard drink sizes).16,17 The AWS combines physical and psychological signs and symptoms involving autonomic hyperactivity, motor disturbances, and cognitive and perceptual disturbances (see AWS common disturbances).8,16
Lab analysis reflects EAC. Gamma-glutamyltransferase is elevated anytime a person consumes alcohol; however, the level is much higher in a person who engages in EAC.18,19 An increase in carbohydrate-deficient transferrin is a specific marker of EAC and is especially useful when correlated with liver enzyme elevation.18,19 An aspartate aminotransferase (AST) to alanine aminotransferase (ALT) ratio, in which AST is greater than ALT, is suggestive of liver injury secondary to EAC.18,19 An increased mean corpuscular volume may reveal the toxic effects of alcohol on the bone marrow and poor nutritional intake.18,19 Alcohol blood levels and urine toxicology may reveal the presence of alcohol and other substances.18,19 Hypomagnesemia, hypophospatemia, hypernatremia, elevated blood urea nitrogen, elevated creatinine, and hypoglycemia may be noted.18,19 Dehydration and hypoglycemia are common signs of EAC.18,19 Electroencephalography may reveal abnormal conduction in the brain from EAC.20
Diagnosis
Differential diagnoses should be explored.5 For example, AWS may mimic withdrawal from sedatives and opioids, amphetamine or cocaine toxicity, sensory and perceptual symptoms in mental illness, hypoglycemia, diabetic ketoacidosis, thyrotoxicosis, and central nervous system infection or tumors.5
The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition's (DSM-5) criteria for AWS include the cessation or reduction in alcohol consumption after prolonged and heavy use and the signs and symptoms cause the development of significant personal, social, and occupational impairment.5 Two or more of the following signs or symptoms that are not caused by other medical conditions are required to diagnose AWS:5-8 (1) An increase in autonomic nervous system activity, such as diaphoresis, tachycardia, hypertension, tachypnea, and pupillary dilatation, (2) Tremors or uncontrollable shaking, (3) Seizures, (4) Illusions or hallucinations, (5) Nausea and vomiting, (6) Psychomotor agitation, (7) Anxiety, and (8) Insomnia.5-8
The Clinical Institute Withdrawal Assessment for Alcohol-Revised (CIWA-Ar) is a reliable tool to evaluate the severity of withdrawal and initiate management strategies quickly.21-23 The CIWA-Ar consists of 10 questions that assess symptoms such as headache, tremors, anxiety, agitation, nausea, vomiting, diaphoresis, and sensory disturbances.21-23 Each question is evaluated on a 0 (no symptoms) to 7 (severe) scale. The final question evaluates orientation on a 0 to 4 scale.21-23 The total number of possible points is 67.21-23 The severity of AWS is determined by the total points on the CIWA-Ar: (1) 0 to 9, very mild, (2) 10 to 15, mild, (3) 16 to 20 modest, and (4) 21 to 67, severe. Quantification reduces morbidity and mortality through early intervention to prevent the progression of AWS.21-23
Management
Goals
The goals for a patient with AWS are to provide a safe and humane withdrawal from alcohol, protect the person's dignity, and prepare them for treatment and recovery.24
The terms AWS and alcohol detoxification (detox) are frequently used synonymously but differ.24 AWS is the syndrome; detox is a process wherein the alcohol is eliminated from the body through abstinence so the body and mind can heal.24 Detox may be managed at home in mild AWS but requires hospitalization in severe AWS.24
Nursing considerations
The nurse's initial step in caring for a patient with AWS is to perform a health history interview and head-to-toe assessment and correlate the findings with lab data and the severity of withdrawal indicated by the total points on the CIWA-Ar.13,21,23,25,26 The assessment should include an evaluation of physical and mental comorbidities, history of prescribed and nonprescribed medications, and history of illicit drug use (see Selected assessment findings suggestive of AUD).6,8,13,14
The nurse should be alert for the development of delirium tremens (DTs), the most severe form of AWS, when a patient presents with acute confusion; hypertensive crisis; high fever; extreme fear; apprehension and agitation; extreme sensitivity to touch, sound, and light; and seizures.8,13,14,16,29 DTs are life-threatening and require hospitalization.8,13,14,16,29 Common causes of death in patients with DTs are respiratory failure and cardiac dysrhythmias.8,13,14,16,29 Priority assessments include oxygen saturation, respiratory rate, depth and rhythm, cardiac rate and rhythm, BP, temperature, and mental status.8,13,14,16,29 Instability in assessment findings requires interventions including but not limited to supplemental oxygen, oral and nasopharyngeal airways, endotracheal intubation, and intravenous fluids (IVF).8,13,14,16,29 Environmental stimuli, including but not limited to televisions, pictures, room decor, and bright colors might create perceptual problems.8,13,14,16,29
Perceptual alterations can include having nightmares, hearing voices, and seeing animals crawling in the room or on the person.29 Nonpharmacologic interventions include frequent reality orientation and reassurance.8,13,14,16,29 Approximately 3% to 10% of people with AWS develop DTs.8,13,14,16,29
Nutrition and fluids
Hypoglycemia is a common assessment finding in AWS.8,27,28,31 Administration of I.V. fluids with glucose should improve mental status alterations.8,27,28,31 Altered mental status may also be related to beer potomania, severe dilutional hyponatremia from EAC of beer, poor nutrition, and reduced fluid intake.32,33
Beer has little sodium content, reducing the solute load in the kidneys and impairing the kidneys' ability to excrete excess free water from the body.32,33 Overcorrecting dilutional hyponatremia with rapid administration of IVF with sodium can lead to osmotic demyelination syndrome, also referred to as central pontine myelinolysis, confirmed by MRI, and is manifested by altered mental status, dysarthria, dysphagia, muscle weakness, and paralysis in severe cases.32,33 Fluid restriction for 24 hours will likely increase serum sodium levels.32,33 I.V. fluids of 0.45% sodium chloride solution, infused slowly, is added to the treatment strategy if sodium levels do not increase in 24 hours.32,33
Thiamine should be administered orally or parenterally to promote optimal functioning of the central and peripheral nervous systems, including the prevention of WK Syndrome, alcohol-induced cerebellar syndrome manifested by gait disturbances, decreased muscle tone, diplopia, and nystagmus, and alcohol-induced neuropathy.10,11,34 Nurses should encourage foods rich in thiamine, including pork, vegetables, legumes, and enriched foods, when the patient is stable enough to consume a meal.35 Cobalamin, pyridoxine, and niacin are additional B vitamins that need replacement.8,36 Magnesium deficiency is common during EAC. Magnesium is required for thiamine synthesis.36,37 Foods rich in magnesium include yogurt, legumes, whole grains, and dark green, leafy vegetables.36,37
Pharmacotherapy
Benzodiazepines (BZDs) are the first-line medications used in treating AWS because they are generally safe, effective, and reduce anxiety by stimulating GABA receptors.7,8,37,38 The evidence indicates BZDs lessen the severity of AWS and progression to DTs.7,8,37,38
The selection of a specific BZD should be determined by the patient's clinical status, rapidity of onset, and duration of action.7,8,37,38 The efficacy of BZDs is contingent on maintaining a calm and quiet environment.7,8,37,38
The misuse and overdose possibility with BZDs indicate they are best administered within a controlled inpatient setting.8,37 However, medically supervised outpatient management of mild AWS with BZDs is safe and effective in patients who adhere to the treatment plan.8,37 Patients in severe AWS, including having seizures, need I.V. BZDs in an inpatient setting, preferably the ICU (see Benzodiazepines in AWS).13,14 Naltrexone, acamprosate, and disulfiram are additional options when a person with AUD wants to stop consuming alcohol, whether they have experienced AWS or not.39-43
The American Psychiatric Association recommends naltrexone, acamprosate, and disulfiram for anyone who is trying to decrease alcohol consumption and cannot.39
Adjuvant medications for AWS
Barbiturates, such as phenobarbital, have been used as an adjuvant alternative to BZDs because they stimulate GABA receptors and inhibit the production of NMDA receptor sites.8,13,14,44 However, phenobarbital produces more respiratory depression than BZDs, especially in older adults and patients with pulmonary disease.13,14,44 Dexmedetomidine (I.V.) is an alpha-2 agonist that reduces anxiety and autonomic hyperactivity and has shown promising results as an adjuvant to BZDs for patients with AWS in the ICU.13 Propofol (I.V.), a sedative-hypnotic agent, stimulates GABA receptors, inhibits glutamate binding to NMDA receptor sites, and is used as an adjuvant to BZDs in the ICU.13 Preliminary research evidence indicates propofol helps to decrease BZD dosage needs.13 While antiepileptic medications such as carbamazepine, gabapentin, and valproic acid may have a role in the outpatient management of mild alcohol withdrawal, convincing evidence that these medications effectively treat patients with DT or other severe symptoms is lacking.
Antiepileptic drugs (AEDs), such as carbamazepine and gabapentin, have been used as an adjuvant treatment to decrease the incidence of seizures in mild AWS, reduce alcohol cravings, and improve mood and affect.45 Another benefit of AEDs is the low potential for abuse, while BZDs and phenobarbital have a high potential for abuse.44,45 Preliminary research evidence indicates phenobarbital and gabapentin, when combined with BZDs, might be more efficacious in managing inpatient AWS than using BZDs alone.37,44,45 Alpha-2 agonists, such as clonidine, and a beta-blocker, such as propranolol, reduce autonomic hyperactivity, and improve symptoms of AWS.13 They lower BP and heart rate and are a valuable adjuvant to BZDs, but they do not prevent seizures or DTs.8,13 Baclofen, a selective agonist of the GABA-B receptor, treats muscle spasticity. Baclofen has been used as an adjuvant treatment to reduce agitation and alcohol cravings in AWS.46 More evidence-based research is required to confirm its efficacy.46
Recovery
Recovery from AUD is achieved when a person abstains from alcohol consumption over time and shows improvement in the adverse reactions of alcohol on physical and mental health, fulfillment of basic needs, functional ability, and relationships.47-49 Sustainable recovery usually brings transformative interpersonal growth, renewed health and purpose, and a sense of joyful serenity.47-49 Remission requires a person not meet the DSM-5 criteria for AUD, excluding craving, over time and is categorized in the following manner: (1) Initial: Up to 3 months, (2) Early: 3 months to 1 year, (3) Sustained: 1 to 5 years, and (4) Stable: Longer than 5 years.47 Recovery involves a personal understanding and acknowledging the damaging effects of their alcohol addiction and having the motivation to recover.47
Nurses and interdisciplinary teams can include the following strategies to help improve a patient's quality of life after detoxification and withdrawal.13,25,26,39-43,48-60
12-step programs
These programs are available for many addictive behaviors but the key 12-step program associated with alcohol is Alcoholics Anonymous (AA). AA provides peer support and sponsors through a sense of community to help a person struggling with alcohol addiction identify healthy coping skills. AA is based on 12 guiding steps and 12 traditions and has many affiliated texts or books. It is nonprofessional, self-supporting, and free. Programs are available face-to-face in most communities and virtually.
Other support resources
Examples include but are not limited to Women for Sobriety, SMART Recovery, and LifeRing. These groups are free and have their own framework of guiding principles or values, materials, meetings, and retreats.
Cognitive behavioral therapy (CBT)
CBT strategies include self-help tools for people with AUD to enhance an understanding of alcohol and addiction, promote communication skills, build relationships, manage stress, and recognize and remove themselves from an environment that may trigger craving alcohol. Triggers may include people, places, and events. CBT therapies show how a person's thoughts, feelings, and actions impact recovery.
A framework for successful outcomes of these strategies is mindfulness-an intentional process where people meditate about their thoughts, feelings, and environment.
Focus on health
A person in recovery may have numerous health problems from the damaging effects of AUD on the body. Physical activity, such as yoga, walking, jogging, hiking, bicycling, and swimming, sufficient rest and sleep, a balanced diet, and sufficient fluid intake can improve symptoms. Physical activity and healthy hobbies and interests take energy and time and stimulate dopamine production that might have been spent craving and consuming alcohol. Replacing nutrients and fluids is a priority in recovery. A dietitian can develop an individualized nutrition plan. Alternatively, consider a functional medicine or naturopathic practitioner, or a health coach for additional health and wellness expertise.
Inpatient or outpatient treatment programs should be considered when a person cannot at stop drinking independently.
Conclusion
AUD is a chronic, often relapsing illness. More than half of people with AUD experience AWS. AWS causes substantial morbidity and mortality and exacerbates coexisting physical and mental conditions. Depending on the severity of AWS, people can be managed as an outpatient or inpatient in the hospital, mental health facility, or detoxification center. Medication management, nutrition, lifestyle adjustment, engaging in 12-step programs or similar support groups, and abstaining from alcohol consumption are crucial to a person's recovery from AUD and AWS.
There is a need to conduct more research to influence policy development and elevate standards of care in AUD and AWS, seek funding to establish more detoxification centers, and increase awareness of the impact of alcohol misuse and abuse globally. Finally, community education programs need to have an elevated focus on alcohol as a toxic, psychoactive, and addictive substance.
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