Approximately 16 million American adults meet criteria for alcohol use disorder (AUD), which is the third-leading cause of preventable death in the US.1,2 In 2016, AUD accounted for around 3 million or 5.3% of all deaths globally.3 Data indicate that 40% of US-admitted hospital patients suffer from this disease with approximately 500,000 episodes of alcohol withdrawal syndrome (AWS) per year.4,5 One study found that 50% of people with AUD will develop AWS when they reduce or discontinue their alcohol consumption.6 Alcohol use plays a significant role in other substance and opioid use disorders, contributing to the opioid mortality epidemic.7
Nurses should be aware of the possibility of polysubstance abuse in their patients. So, it is important to determine the likelihood of withdrawal from other substances as well. Consequently, hospital nurses caring for these complex patients are on the front line for preventing, recognizing, and helping treat patients with AWS. Yet, patients at risk are not always obvious and signs of alcohol abuse can be obscure.8 Patients who drink heavily may not recognize that they have a problem, or be embarrassed and minimize their drinking pattern, not realizing that alcohol withdrawal can be life-threatening. Patients with unhealthy alcohol use are prevalent in hospitals, particularly young men who consume more than 2 to 4 drinks daily or more than 14 drinks per week.4 As a result of this population's high acuity, incomplete assessments, misinterpretation of signs and symptoms, and/or the inability to identify these patients, management of patients with AWS is extremely challenging.
The urgency of critical care admissions leads to abrupt alcohol cessation with potential for serious AWS. A large percentage of patients in the ED are at risk for AWS because of increased lengths of stay and unrecognized signs and symptoms. The ED staff plays an important role as the initial or only medical care for some patients with AUD. ICUs, EDs, CCUs, and trauma unit healthcare providers routinely treat patients with AUD, and up to 33% of patients progress to severe AWS and delirium tremens (DTs).9 AUD accounts for 21% of medical ICU admissions and approximately 44% of these patients die within 7 years.10,11 Alcohol abuse is not uncommon in patients with traumatic injuries, with 1 in 10 experiencing DTs requiring prompt and aggressive treatment.12
A focused nursing assessment is essential in identifying the potential for AWS in all hospital units. This article discusses how to assess patients at risk and how to use these assessment findings as a basis for nursing interventions for improved safe patient outcomes.
Coming to terms
AUD, also called alcoholism, is defined by the National Institute on Alcohol Abuse and Alcoholism (NIAAA) as a chronic relapsing brain disease characterized by compulsive alcohol use, loss of control over alcohol intake, and a negative emotional state when not using. There are four cardinal symptoms:2
- craving—a strong need or urge to drink alcohol
- loss of control—inability to stop drinking when drinking has begun
- physical dependence—appearance of withdrawal signs and symptoms after stopping drinking
- tolerance—the need to drink higher amounts of alcohol to get “high.”
The clinical signs and symptoms associated with cessation of alcohol consumption are known collectively as AWS.9 Signs and symptoms indicating or consistent with alcohol withdrawal include hand tremors, poor appetite, chills, cravings for alcohol, muscle cramps, irritability, labile mood, palpitations, odor of alcohol, disorientation, tachycardia, hypertension, fever, mood changes, slurred speech, impaired gait, poor dexterity, fatigue, insomnia, and abdominal pain.5,13-15
The potential for AWS can easily be overlooked when patients are debilitated in critical care areas. For example, alcohol abuse among older adults is a national epidemic, and those who underreport their use may fail to get appropriate treatment.16 Baby boomers comprise 30% of the US population, and, unlike previous older adults, there is strong evidence that alcohol abuse has been underidentified and reported for decades in this population. There is a 22% rate of AUD in older adults in healthcare settings.17 Aging causes an increased vulnerability for higher blood alcohol levels (BALs) related to decreased liver function, body water, body mass, and neuronal receptor sensitivity in the brain. The baby boom generation will create a new urgency for assessment and interventions in the prevention and treatment of AWS.
Be aware that complex critically ill patients may falsely present with signs and symptoms of alcohol withdrawal because of other medical conditions, such as pneumonia, postoperative delirium, septicemia, uremia, pancreatitis, and adverse drug reactions. If AUD is suspected, it is important to quantify the regular amount of alcohol consumption by corroborating with family members or friends and to review drug test results and results of serum biochemical markers such as electrolytes, mean corpuscular volume, carbohydrate-deficient transferrin, blood alcohol, and liver function tests.18 In addition, it is important to remember many patients with AUD have comorbid psychiatric disorders, such as mood, anxiety, posttraumatic, and personality disorders potentially requiring interventions.
Because patient admission assessment is unlikely to identify all patients with an AUD, it is recommended that clinicians routinely screen all patients for unhealthy drinking behaviors (such as three or four standard drinks per day) as part of both the initial and ongoing patient assessment.19 In the US, a standard drink contains about 14 g of pure alcohol (about 1.2 tablespoons).20 Validated screening tools have been developed to identify alcohol problems but are not validated in critically ill patients.
The CAGE (cut-annoyed-guilty-eye) questionnaire is a simple, internationally recognized assessment instrument for identifying problems with alcohol. It is a helpful tool to use in the ED, particularly with intoxicated patients. Nurses can easily include this quick, effective tool in routine assessments if the patient is alert and oriented. Two out of four positive answers to the following questions indicate AUD.21
- Have you ever felt you should cut down on your drinking?
- Have people annoyed you by criticizing your drinking?
- Have you ever felt bad or guilty about your drinking?
- Have you ever had a drink first thing in the morning to steady your nerves or get rid of a hangover (eye-opener)?
Nurses should ask reliable people when the patient had his or her last drink, how much was consumed, and what type of alcohol. Find out how long (months or years) they have been drinking heavily and any substance abuse or treatment history. Patients who develop AWS more than 2 days after their last drink are more likely to experience severe signs and symptoms than patients who develop AWS in a shorter time.13 In addition, patients with a long history of intoxication and withdrawals will experience more severe withdrawal. A history of seizures, delirium, elevated heart rate, and BALs greater than 100 mg/dL further increase the risk of more severe withdrawal symptoms.22
The Joint Commission initiated and recommends screening for unhealthy use of alcohol in hospitalized patients using screening, brief intervention, and referral to treatment. Patient outcome evidence in this approach is not robust but has increased provider comfort in alcohol use assessments.4,23 Two additional tools that are being increasingly used to identify AUD are the AUDIT (Alcohol Use Disorders Identification Test) published by the World Health Organization, and Alcohol Screening and Brief Intervention for Youth: A Practitioner's Guide published by the National Institutes of Health (NIH)/NIAAA.4,24
Although a skillful clinical assessment may successfully identify patients with obvious alcohol-related problems, those with covert problems or who are critically ill may remain undetected until signs and symptoms develop.8
Signs of trouble
In patients who are physically dependent on alcohol, the central nervous system (CNS) adapts to the presence of alcohol and loses the ability to function normally in its absence, resulting in CNS hyperexcitability. Chronic alcohol use results in the loss of homeostasis in neurotransmitter pathways and receptors in the CNS. There is a decrease in the number of inhibitory gamma-aminobutyric acid (GABA) receptors (downregulation), and activation of the (upregulation) glutamate N-methyl-d-aspartate (NMDA) receptors resulting in an excitatory effect. Dopamine, another neurotransmitter, is increased during AWS and contributes to hyperexcitability and hallucinations.9,11 The brain adapts to alcohol after repeated exposure by altering opiate receptor sites requiring higher alcohol amounts to have the same feeling resulting in cravings and an increase in the number of NMDA receptors. Signs and symptoms of AWS reflect declining BALs. These usually appear within a few hours to a few days after cessation of alcohol consumption, although in some patients signs and symptoms may develop up to 10 days after the last drink.6,25
Under diagnostic criteria specified by the Diagnostic Statistical Manual of Mental Disorders (DSM-5), alcohol withdrawal has these components:26
- Cessation of (or reduction in) alcohol use that has been heavy and prolonged
- Two (or more) of the following, developing within several hours to a few days after the above criterion
- autonomic hyperactivity
- increased hand tremor
- nausea or vomiting
- transient visual, tactile, or auditory hallucinations or illusions
- psychomotor agitation
- generalized tonic-clonic seizures
- The diagnostic criteria also specify that signs and symptoms cause “clinically significant” distress or impairment that are not due to another medical condition and are not better accounted for by another mental disorder, including intoxication or withdrawal from another substance.
DTs: A medical emergency
The most severe form of alcohol withdrawal is DTs, defined and characterized by disturbance in attention, awareness, language, visuospatial ability, memory, orientation, and perception that fluctuates during the day.6,26 The altered mental status and severe autonomic hyperactivity may lead to cardiovascular collapse.4,6,25 Usually, DTs begin 3 days after AWS or may appear within 8 hours from the last drink and may last for 1 to 8 days.6 Approximately, 5% of patients with alcohol withdrawal progress to DTs, but about 5% of these patients die.27
Because of its high mortality, DTs is a medical emergency often requiring ICU admission. Patients with untreated seizures have a 33% risk of DTs. Signs and symptoms, which may worsen abruptly, include body tremors, diaphoresis, tachycardia, hypertension, fever, delirium, severe anxiety or agitation, disorientation, hallucinations, and seizures.25,27 Patients with a history of DTs and Clinical Institute Withdrawal Assessment, revised (CIWA-Ar) scores ≥15 are at higher risk for DTs.14 DTs is most common in patients with a history of prolonged AUD, admission hypokalemia, and in those who have experienced previous withdrawal episodes. It is important to remember that trauma patients with AWS have a higher incidence of DTs that is associated with mortality. Neuronal changes related to repeated alcohol withdrawal increase the risk of progressively frequent and severe withdrawal episodes, a phenomenon known as kindling, considered to increase the risk of DTs.15,27
Alcoholic hallucinosis, termed in 1916, is a rare complication of chronic alcohol abuse with predominantly auditory hallucinations, prevalence of 0.6% to 0.7%, with no consensus of the etiology of the illness but is not synonymous with DTs.28,29 (See A matter of timing: When withdrawal symptoms may appear.)
Treatment for AWS is individualized according to symptom severity. Some patients with minor withdrawal signs and symptoms require supportive care only; others with moderate or severe withdrawal require medication and other interventions. Supportive care includes fluid and electrolyte replacement; nutritional support; and supplemental thiamine, glucose, and multivitamins (the banana bag). If medication is indicated, benzodiazepines are the standard pharmacologic prophylaxis and treatment for all the phases of AWS.6,10 Their safety and efficacy in easing the discomfort of withdrawal, especially for preventing or treating seizures and delirium, is well documented.5 However, there is a lack of evidence-based guidelines for the treatment of AWS in critical care areas resulting in a varied selection of sedatives.29
Traditionally, the treatment approach has been fixed-schedule dosing in which the healthcare provider prescribes a routine benzodiazepine regimen. Fixed dosing prevents individualized treatment based on close monitoring of signs and symptoms. In contrast, symptom-triggered administration of benzodiazepines is based on administration of medication as needed depending on signs and symptom severity.29
As direct caregivers, nurses are ideally positioned to improve patient outcomes by using the symptom-triggered approach. Based on an objective withdrawal severity scale, a symptom-triggered approach provokes faster and more-effective relief of withdrawal symptoms than treatment based on clinicians' subjective judgment alone.29 There is evidence that length of stay may be reduced as well. Increased severity of AWS is associated with prolonged hospitalization and longer ICU length of stay. (See Assessment of Alcohol Withdrawal: CIWA-Ar.)
The CIWA-Ar is the gold standard withdrawal assessment rating scale in both hospital and outpatient settings but has limited research for critically ill patients. This evidence-based, validated objective observer-rated assessment tool is designed to maintain consistency in patient assessment and treatment.30 Studies indicate that the CIWA-Ar is an effective tool for alert patients having AWS but is not validated in critical care areas. The patient who is cognitively impaired, unconscious, endotracheally intubated, sedated, or severely ill is not able to communicate an alcohol history requiring early identification of the problem. As a result, the safe management of AWS can be problematic because of poor alcohol assessment such as determining a patient's alcohol consumption or underrecognition of active withdrawal. Unfortunately, a patient's inability to communicate because of mechanical ventilation, delirium, sedation, trauma, or disease is a major barrier. In a retrospective review of 2,000 trauma patients, only 7.3% had adequate alcohol history assessment making it difficult to make recommendations to nurses caring for these patients.30
Clinicians use the CIWA-Ar tool to rate 10 signs/symptoms on numeric scales to determine the severity of signs and symptoms. The total score can range from 0 (no symptoms) to a maximum of 67. Any score over 18 indicates severe withdrawal.22 The tool takes approximately 5 minutes to administer.
The CIWA-Ar provides a measure of withdrawal severity and helps to guide treatment, enabling clinicians to intervene early in withdrawal to prevent poor patient outcomes. Signs and symptoms of severe AWS include withdrawal seizures (generalized clonic-tonic seizures), alcoholic hallucinosis, and DTs. Although withdrawal seizures are usually singular or present only in short bursts, they may progress to DTs in one-third of patients if untreated.13
Individualized drug therapy based on symptom assessment is guided by a sliding benzodiazepine scale per institution and unit protocol. Generally, when the CIWA-Ar score is greater than 9, a benzodiazepine is indicated.31
In a typical protocol, the CIWA-Ar scale is repeated hourly until the score is less than 10. Benzodiazepine use is continued until the score is less than 9 for four consecutive assessments.31 Then, the CIWA-Ar can be done every 8 hours until the score is less than 6 for four consecutive assessments.
Symptom-triggered treatment is safe and effective and generally manages signs and symptoms with lower medication doses compared with a fixed-schedule dosing approach.32
Assessing withdrawal trend
The Withdrawal Trend Profile (WTP) was developed by nursing staff at the NIAAA, a part of the US NIH. Like the CIWA-Ar, this tool is not copyrighted and may be freely used and modified as needed. (See Withdrawal Trend Profile.)
The WTP provides an ongoing record of the patient's condition, and can be used as an adjunct to the CIWA-Ar to assess withdrawal trends and the patient's response to treatment. If the patient is alert and able, the nurse takes the breath alcohol concentration (BrAC), which measures the alcohol content of air in the patient's lungs and reflects the BAL. Otherwise, a BAL level should be drawn. The nurse must review the BAL or BrAC value. The higher the value, the greater the potential for withdrawal symptoms.
The nurse also documents the patient's vital signs, looking for an upward trend indicating increased withdrawal symptoms. On a scale of 0 (none) to 3 (severe), the nurse then rates key signs and symptoms such as nausea/vomiting; tremors; diaphoresis; anxiety; agitation; tactile, auditory, and visual disturbances; headache; and orientation. For example, a patient whose arms or body are visibly shaking while in bed rates a score of 3 for tremors. A patient who has tremors only when extending the arms would rate a score of 2. A patient who has fingertip tremors that are not visible but can be felt by the nurse rates a score of 1.
Combined with the CIWA-AR score, the WTP identifies trends in the patient's condition and helps the nurse determine whether withdrawal symptoms require the p.r.n. use of medication. For example, a noncompromised patient with a CIWA-Ar of 7 and normal vital signs would require standard nursing support and reassurance with no medication intervention. However, 1 hour later the same patient might have an increased heart rate (greater than 100 beats/minute) and systolic BP (greater than 150 mm Hg), indicating an upward trend in withdrawal symptoms and the need for medication.15
Using medications to manage AWS
The individualized, symptom-triggered approach to benzodiazepine use satisfies the need to use medication only when needed and may also reduce inpatient hospital stays. Benzodiazepines stimulate GABA receptors causing a decrease in neuronal activity resulting in sedation.32 Many patients can be safely managed with supportive care only, avoiding the risks and costs of unnecessary medication.33,34 When indicated, the most commonly used benzodiazepines are diazepam, lorazepam, chlordiazepoxide, and oxazepam.15 These drugs mimic the effects of alcohol in the CNS because brain receptors previously inhibited by alcohol are now hyperexcitable.35 Although all benzodiazepines have similar properties, certain agents may be recommended over others based on their pharmacokinetics. For example, long-acting drugs such as diazepam and chlordiazepoxide help prevent recurrent withdrawal signs and symptoms. Intermediate-acting drugs such as lorazepam or oxazepam may be indicated for older adults, critically ill patients, or those with hepatic dysfunction to minimize the risk of oversedation.17
Older adults have more difficulty metabolizing and excreting alcohol than younger patients and eliminate benzodiazepines at a slower rate.17 Carefully assess and monitor withdrawal signs and symptoms in these patients and administer lower doses of intermediate-acting benzodiazepines as prescribed to prevent medication accumulation and oversedation, which could lead to respiratory depression.
Patients experiencing seizures or DTs require I.V. benzodiazepine administration, so maintain I.V. access for any patient at risk for severe AWS. Avoid giving I.M. injections because they are painful and drug absorption is unpredictable.
Data indicate that some ICUs use midazolam as an adjunct agent due to available ready-to-use bags.35 Some clinicians advocate for barbiturate use in the ED and ICU because they are fast and long-acting.34 Their use may be helpful in certain clinical conditions such as a one-time dose in the ED, or for severe withdrawal. However, the risk of respiratory and cardiac depression, and drug interactions requires more studies for efficacy.34 Beta-blockers cannot treat DTs or seizures.10 A Cochrane systematic review could not conclude safety and effectiveness in using antiepileptic drugs, such as phenytoin, for preventing and treating seizures during AWS.5,14,27
For patients in the ICU who are intubated, or unresponsive to benzodiazepines, propofol and dexmedetomidine have been used as adjunct medications.6,14 Propofol is a rapid-onset, short-acting agent. It causes global CNS depression, which might explain its effectiveness in treating status epilepticus, DTs, and resistant alcohol withdrawal (nonresponsive to benzodiazepines). However, it may cause respiratory depression/infection, hypotension, and bradycardia; increase intubation rates, mortality, and morbidity; and is not FDA-approved for AWS.36,37 Recently, dexmedetomidine has been FDA-approved for sedation without intubation but not approved for the treatment of AWS. It has anxiolytic properties without respiratory depression and safety evidence in the prevention of seizures.35,37 Animal data demonstrate its efficacy in AWS, but there is limited evidence in humans. Antipsychotic agents are used with frequency despite paucity of research evidence; haloperidol is used by clinicians for severe, uncontrolled agitation or hallucinosis but use with caution because it lowers the seizure threshold, prolongs the QT interval, and can result in neuroleptic malignant syndrome.4,6,11 These patients are generally treated in ICUs for closer observation. There is no evidence that baclofen is effective and safe in controlling AWS.32 Carbamazepine has been used effectively in Europe to treat AWS for a few decades. Its efficacy in improving patient response overall, preventing relapse, decreasing cravings, and anticonvulsant properties is well documented. Also, its use in outpatient detoxification helps patients return to normal activities more quickly.37 However, its use in the US lacks evidence.14 Ketamine is readily available in the ED and used to depress the CNS for AWS but further research is needed.14 Phenobarbital is the most commonly studied barbiturate because it is long-acting, inexpensive, and available in multiple formulations (I.V., I.M., P.O.). However, there is insufficient evidence for first-line AWS treatment and the body of literature for its use has small sample sizes and retrospective study designs.10,35,38
It is important to remember that these medications have not been studied like the benzodiazepines during AWS and potential hazards must be assessed. In some institutions, AWS is treated with I.V. ethanol replacement therapy. Current research supports the use of benzodiazepines as the gold standard; ethanol replacement therapy is outmoded and not recommended. Therapy with benzodiazepines is safer, more effective, and well supported by the evidence.5,13,29,37
Nursing care for patients in withdrawal
Frequently assess the patient as indicated throughout the withdrawal process using the CIWA-Ar. Initiate fall and seizure precautions as indicated. Elevate the head of the bed to reduce the risk of aspiration. Provide nonjudgmental, supportive, nonreactive, empathetic, and comprehensive emotional care.
Current recommendations for evidence-based nursing interventions during alcohol withdrawal include the following:5,14
- Ensure a patent airway; suction as needed. Frequently monitor vital signs, observing for respiratory distress.
- Use individualized symptom-triggered therapy.
- Assess skin for abnormalities such as jaundice, pressure injuries, rashes, signs of dehydration, and ecchymoses; inspect for needle tracks from I.V. drug use.
- Use the CIWA-Ar tool to guide medication administration with benzodiazepines.
- Encourage the patient to rest by controlling minimal interpersonal contact with the patient. Decrease environmental stimuli with controlled lighting, and provide a calm, quiet private room.
- Provide adequate nutrition and fluid intake. Obtain a dietary consult as indicated to treat malnutrition. Administer thiamine (I.V., I.M. for absorption) to prevent Wernicke-Korsakoff syndrome and Wernicke encephalopathy, and additional vitamins (folate) as prescribed.
- Document fluid intake and output. Maintain I.V. access and administer I.V. fluids as prescribed.
- Review all lab results and closely monitor for illicit drugs, opioids, electrolyte imbalances, including hypomagnesemia, hypokalemia, and hypophosphatemia. Also watch for liver biochemical test abnormalities, including serum aspartate aminotransferase, alanine aminotransferase, and gamma glutamyl transferase. A serum carbohydrate-deficient transferrin level can identify chronic heavy alcohol consumption.29 Ethyl glucuronide is a biomarker for recent alcohol consumption.
- Assess mental status, suicide risk (up to 15% of AUD patients are at risk for death), sleep pattern, and provide emotional support to reduce anxiety. Reassure the patient that depressive symptoms and sleep disturbances during withdrawal are common but temporary.
- Control agitation.
- Control seizures.
The rate of alcohol metabolism varies depending on various factors, such as the patient's health status, age, gender, liver function, and ethnicity. On average, however, patients eliminate the equivalent of one standard drink or 0.6 oz (14 g) of pure alcohol per hour. When caring for older adults, keep in mind that the speed of alcohol metabolism diminishes with age, resulting in higher blood levels.17,39
In addition, assess dental hygiene and document recent weight loss. Assess for bladder distension or incontinence of urine and feces. Use therapeutic management techniques and medications to prevent the use of physical restraints. Be prepared to initiate cardiac monitoring and emergency life support depending on the severity of AWS.
When interacting with the patient, be matter-of-fact, respectful, and maintain a positive, supportive, calm, quiet, and caring milieu.5 Communicate with short, simple statements in a calm manner, using a low tone of voice. Use concrete language and statements beginning with “I” rather than “You.”
If the patient is hallucinating, do not agree or disagree with the patient's statements. For example, using an “I” statement, you might respond, “I see the curtain moving next to you,” instead of, “You are hallucinating.”
Present reality without challenging or escalating the patient's anxiety and thought disturbances. Build a therapeutic rapport with the patient by providing relief from his or her symptoms and meeting physiologic and safety needs. Meet the patient's needs promptly to reduce the risk of violence or aggression. Do not approach the patient with loose items that the patient could grab if he or she becomes agitated, such as a clipboard or dangling ID badge or phone.
It is imperative to examine your own feelings and beliefs about working with patients who have alcohol problems to provide nonbiased care. You want to remain objective so you can provide nonjudgmental support to the patient and family. If needed, discuss with a healthcare professional your own feelings, thoughts, and bias, especially if you have a personal or family history of alcohol abuse, or close friends who have AUD.
AUD is a chronic and relapsing disease requiring complex treatment strategies to improve patient outcomes. Abstinence is the only effective treatment. Many patients with AUD have other psychiatric disorders, such as anxiety, depression, bipolar, posttraumatic stress, or personality disorders, so involve the appropriate clinicians immediately in discharge planning. Referrals for short-term and/or long-term rehabilitation centers, counselors who specialize in addiction, cognitive behavioral therapy, motivational enhancement therapy (helps individuals resolve their ambivalence about engaging in treatment and stop drinking), medical and medication management, sober housing, and Twelve Step (Alcoholics Anonymous) modalities are important for patient recovery.40
Intervene early to improve outcomes
AWS is a frequently encountered medical consequence of AUD. Closely monitor your patient during your shift to identify subtle changes and intervene rapidly and appropriately. The consistent use of the CIWA-Ar as the gold standard can help clinicians accurately identify patients at high risk for alcohol withdrawal and meet the same standard of care throughout the hospital.
Benzodiazepines and the CIWA-Ar remain the gold standards and most widely used medications and tool for effective and safe management of AWS. It is important to prevent serious medical consequences, decrease the enormous impact on healthcare resources, and costs (approximately $26 billion) from AWS.9 Clinicians' early recognition and treatment of AWS is critical for positive patient outcomes. Unfortunately, few physicians have been adequately trained to identify and treat AWS.6 However, nurses are well versed in quickly establishing rapport and trust with patients and their families.41 Therefore, nurses may be able to obtain more accurate information regarding patients' alcohol history and contribute to a comprehensive approach to treatment.
Because of the paucity of AWS research for critically ill and resistant alcohol withdrawal patients, identification and interventions are challenging and complex. The lack of research studies precludes the development of evidence-based practice nursing guidelines.9,30 The lack of evidence for the treatment of resistant alcohol withdrawal endorses the use of varied sedatives, and provider preference without evidence.
There are no validated AWS tools or scales to initiate prompt assessment and treatment in critically ill patients. The Richmond Agitation Sedation Score (RASS) has been used in practice for patients in severe withdrawal in the ED and ICU. Alternatives to benzodiazepines have shown limited outcomes and serious complications. Research and publications are needed to provide best practices and clear standards of care versus the current multimodal interventions for critically ill patients.14
1. National Institutes of Health/National Institute on Alcohol Abuse and Alcoholism. Alcohol Use Disorder
2. National Institutes of Health/National Institute on Alcohol Abuse and Alcoholism. Alcohol Facts and Statistics: Alcohol use disorder
. 2018. www.niaaa.nih.gov/alcohol-health/overview-alcohol-consumption/alcohol-facts-and-statistics
3. World Health Organization. Management of substance abuse. Global status report on alcohol and health 2018. www.who.int/substance_abuse/publications/global_alcohol_report/en
4. Makdissi R, Stewart SH. Care for hospitalized patients with unhealthy alcohol use: a narrative review. Addict Sci Clin Pract
5. Ackley B, Ladwig G, Swan BA, Tucker S. eds. Evidence-Based Nursing Care Guidelines: Medical-Surgical Interventions
. St. Louis, MO: Mosby, Inc.; 2008.
6. Schuckit MA. Recognition and management of withdrawal delirium (delirium tremens
). N Engl J Med
7. Singh AK. Alcohol interaction with cocaine, methamphetamine, opioids, nicotine, cannabis, and _-hydroxybutyric acid. Biomedicines
8. Jane L. How is alcohol withdrawal syndrome
best managed in the emergency department. Int Emerg Nurs
9. Ferreira JA, Wieruszewski PM, Cunningham DW, Davidson KE, Weisberg SF. Approach to the complicated alcohol withdrawal patient. J Intensive Care Med
10. Martin K, Katz A. The role of barbiturates for alcohol withdrawal syndrome
11. Dixit D, Endicott J, Burry L, et al. Management of acute alcohol withdrawal syndrome
in critically ill patients. Pharmacotherapy
12. Salottolo K, McGuire E, Mains CW, van Doorn EC, Bar-Or D. Occurrence, predictors, and prognosis of alcohol withdrawal syndrome
and delirium tremens
following traumatic injury. Crit Care Med
13. Pace C. Alcohol withdrawal: epidemiology, clinical manifestations, course, assessment, and diagnosis. UpToDate. 2018. www.uptodate.com
14. Long D, Long B, Koyfman A. The emergency medicine management of severe alcohol withdrawal. Am J Emerg Med
15. Mainerova B, Prasko J, Latalova K, et al. Alcohol withdrawal delirium—diagnosis, course and treatment. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub
16. Mathews S, Oslin DW. Alcohol misuse among the elderly: an opportunity for prevention. Am J Psychiatry
17. Kuerbis A, Sacco P, Blazer DG, Moore AA. Substance abuse among older adults. Clin Geriatr Med
18. U.S. Department of Health and Human Services: Substance Abuse and Mental Health Services Administration. Treatment Improvement Protocol (TIP) Series, No. 45. Detoxification and Substance Abuse Treatment. 2006.
19. Schuckit MA. Alcohol-use disorders. Lancet
20. National Institutes of Health/National Institute on Alcohol Abuse and Alcoholism. Rethinking drinking: alcohol and your health. http://rethinkingdrinking.niaaa.nih.gov
21. O'Brien CP. The CAGE questionnaire
for detection of alcoholism: a remarkably useful but simple tool. JAMA
22. Miller SC, Fiellin DA, Rosenthal RN, eds. The ASAM Principles of Addiction Medicine
. 6th ed. Philadelphia, PA: Lippincott Williams and Wilkins; 2018.
23. Yale School of Medicine. Screening, brief intervention, and referral to treatment tool. http://medicine.yale.edu/SBIRT
24. National Institutes of Health/National Institute on Alcohol Abuse and Alcoholism. Alcohol Screening and Brief Intervention for Youth: A Practitioner's Guide. www.niaaa.nih.gov/publications/clinical-guides-and-manuals/alcohol-screening-and-brief-intervention-youth
25. U.S. National Library of Medicine/National Institutes of Health. MedlinePlus: Delirium tremens
26. Diagnostic and Statistical Manual of Mental Disorders: DSM-5
. 5th ed. American Psychiatric Association; 2013.
27. Burns MJ. Delirium tremens
(DTs). Medscape Reference. 2018. http://emedicine.medscape.com/article/166032-overview
28. Bhat PS, Ryali V, Srivastava K, Kumar SR, Prakash J, Singal A. Alcoholic hallucinosis. Ind Psychiatry J
29. Hoffman RS, Weinhouse GL. Management of moderate and severe alcohol withdrawal syndromes. UpToDate. 2018. www.uptodate.com
30. Sutton LJ, Jutel A. Alcohol withdrawal syndrome
in critically ill patients: identification, assessment, and management. Crit Care Nurse
31. McKeon A, Frye MA, Delanty N. The alcohol withdrawal syndrome
. J Neurol Neurosurg Psychiatry
32. Amato L, Minozzi S, Davoli M. Efficacy and safety of pharmacological interventions for the treatment of the Alcohol Withdrawal Syndrome
. Cochrane Database Syst Rev
33. Cassidy EM, O'Sullivan I, Bradshaw P, Islam T, Onovo C. Symptom-triggered benzodiazepine therapy for alcohol withdrawal syndrome
in the emergency department: a comparison with the standard fixed dose benzodiazepine regimen. Emerg Med J
34. Stehman CR, Mycyk MB. A rational approach to the treatment of alcohol withdrawal in the ED. Am J Emerg Med
35. Wong A, Benedict NJ, Kane-Gill SL. Multicenter evaluation of pharmacologic management and outcomes associated with severe resistant alcohol withdrawal. J Crit Care
36. Chico JI, Rivero C, Casado R, et al. Severe alcohol withdrawal syndrome
in ICU: is propofol a safe option. Crit Care
. 2010;14(suppl 1):P491.
37. Maldonado JR. Novel algorithms for the prophylaxis and management of alcohol withdrawal syndromes-beyond benzodiazepines. Crit Care Clin
38. Tidwell WP, Thomas TL, Pouliot JD, Canonico AE, Webber AJ, et al. Treatment of alcohol withdrawal syndrome
: phenobarbital vs CIWA-Ar
protocol. Am J Crit Care
39. Intoximeters, Inc. Alcohol and the Human Body: Alcohol's Properties
; 2009–2012. www.intox.com/t-physiology.aspx
40. American Psychological Association. Understanding alcohol use disorders and their treatments. 2012. www.apa.org/helpcenter/alcohol-disorders.aspx