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Emergency Department Management of Patients with Alcohol Intoxication, Alcohol Withdrawal, and Alcohol Use Disorder: A White Paper Prepared for the American Academy of Emergency Medicine

      1. Introduction

      Alcohol is the most-used intoxicant in the world, and the repercussions of unhealthy alcohol use are of corresponding magnitude. A six-fold increase in all-cause mortality and six percent of overall deaths are related to the use of alcohol, (1,2) which is the most important risk factor for ill health among working-age people worldwide. (3) Alcohol intoxication (AI) is strongly tied to serious trauma (especially motor vehicle collisions (4)), suicide, (5) domestic abuse and sexual assault, crime, (6) and thousands of Americans die from alcohol poisoning every year. (7) In addition to the myriad medical consequences of chronic alcohol use, addiction to alcohol–suffered by over 14 million Americans (8)–leads to the destruction of relationships, families and social function, including unemployment and homelessness. Mortality among patients with AUD increased by over 20% in 2020 and 2021, during the COVID-19 pandemic. (9,10)
      As with other conditions that cause medical, psychological, and social deterioration, patients with AUD present frequently to the emergency department (ED) for care. Alcohol-related ED visits are rapidly escalating, (5,11) and these patients are at high risk for poor outcomes, especially frequent presenters for care, nearly 1 in 10 of whom will die within one year. (12) The routine nature of these visits and the gradual pace of their decline conceals this risk; alcohol-related presentations in many centers are so common, and alcohol use so broadly accepted, that its impact is easily overlooked, when in fact every harm caused by alcohol is preventable.
      Because so many patients with or at risk for AUD access care in the ED and often only in the ED, emergency physicians are uniquely positioned to meaningfully intervene on the ruinous trajectory of alcoholism by identifying at-risk drinking and initiating effective treatment. This may include withdrawal management, addressing comorbid medical, social, substance, or psychiatric conditions, referral to a mutual help organization, prescription of anti-craving medications, or mobilizing community-based wraparound care. This guideline aims to reduce alcohol-related harms by providing consensus-based, evidence supported recommendations for clinicians in acute care settings who manage patients with AUD or at risk for AUD, including the management of AI and alcohol withdrawal.
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        Q1. When should Alcohol Withdrawal Syndrome (AWS) be suspected and how is AWS diagnosed?
      AWS is a constellation of uncomfortable symptoms and dangerous physiologic derangements that occurs when a person with alcohol dependence reduces or ceases consumption of alcohol. There is great variability in how patients manifest AWS and its course is notoriously unpredictable. In most patients AWS will self-resolve after several days of autonomic excess colloquially referred to as the shakes, however the features of AWS classically proceed as described in Table 1. Delirium tremens is often incorrectly used to describe severe AWS; DTs refer to a specific set of dangerous findings that generally occur in a subset of patients with AWS, 2-3 days after their last drink.
      Table 1Clinical Features of AWS
      6-10 hours:
      Typical time ranges after the last drink. Time ranges are significantly variable and overlapping
      “The Shakes”
      Restlessness, irritability, anxiety, agitation, insomnia
      Tremor, diaphoresis
      Nausea, vomiting, anorexia, headache
      Mild tachycardia, hypertension
      12-36 hours: “Rum Fits” and “The Horrors”
      Convulsions
      Hallucinosis: auditory, visual, or tactile hallucinations, paranoid/persecutory delusions
      24-72 hours: Delirium Tremens
      Tachycardia, hypertension, hyperthermia
      Delirium: disturbance in attention and awareness, as well as disturbance in orientation, language, or perception, often with fluctuating level of consciousness
      low asterisk Typical time ranges after the last drink. Time ranges are significantly variable and overlapping
      Patients known to drink recently, regularly, and heavily, or with a history of complicated withdrawal, should be evaluated for the presence or prospect of developing AWS. (13) Patients with signs and symptoms consistent with AWS, especially patients in a hyperadrenergic state or with seizure, should be specifically evaluated for AWS. Appropriate history can be elicited with questions such as How much alcohol do you drink every day? When was your last drink? Have you ever had trouble when you stop drinking? Why did you stop drinking?
      Screening tools for unhealthy alcohol use such as AUDIT-C or CAGE and collateral inquiry of the patient's relations are valuable assessments of AWS risk, see Table 2. Biologic tests of the breath, blood, or urine detect recent use and may indicate chronic use but have a limited role in diagnosing or predicting AWS in the ED. Patients with an elevated ethanol concentration but with no or minimal signs of AI are at higher risk for AWS, and patients who develop AWS with a positive alcohol level are at risk for more severe withdrawal. (13)
      Table 2AUD Assessment Tools
      ToolFull NameUse
      AUDIT-CAlcohol Use Disorder Identification Test ConsumptionIdentifies at-risk problem drinking
      AWTTAlcohol Withdrawal Triage ToolPredicts patients who will develop severe AWS
      BAWSBrief Alcohol Withdrawal ScaleAWS severity score
      CAGECut down, Annoyed, Guilty, Eye-openerScreens for problem drinking and AUD
      CIWA-ArClinical Institute Withdrawal Assessment of Alcohol Scale, RevisedAWS severity score
      LARSLuebeck Alcohol Withdrawal Risk ScalePredicts patients who will develop severe AWS
      PAWSSPrediction of Alcohol Withdrawal Severity ScalePredicts patients who will develop severe AWS
      RASSRichmond Agitation-Sedation ScaleLevel of arousal (sedation to agitation) score
      SAWSShort Alcohol Withdrawal ScaleAWS severity score
      SEWSSeverity of Ethanol Withdrawal ScaleAWS severity score
      Though prior episodes of AWS are most predictive, no single risk factor, symptom, or finding can accurately rule in or exclude the possibility of developing AWS. AWS severity scales (CIWA-Ar, SEWS, RASS) and AWS severity prediction scores (PAWSS, LARS) are confounded by comorbidities and AWS mimics; they should be used only after the diagnosis is established. The differential diagnosis includes the range of causes of hyperadrenergic tone, altered mental status, and seizure; examples of misdiagnoses include stimulant or anticholinergic intoxication, opioid withdrawal, thyrotoxicosis, serotonin syndrome, diabetic ketoacidosis, alcoholic ketoacidosis, and sepsis.
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        Q2. Which patients with AWS or at risk for AWS are appropriately managed as an outpatient and which require inpatient management?
      Patients with severe AWS requiring inpatient management are readily identified as demonstrating progressive hyperadrenergic signs (tachycardia, hypertension, diaphoresis, tremor) despite treatment, altered mental status (agitation or confusion), or convulsions. If a severity score is used, American Society of Addiction Medicine (ASAM) recommends that patients with CIWA-Ar score ≥19 receive inpatient treatment. Pregnant patients should be offered inpatient management of AWS given the risk to the fetus of both withdrawal and ongoing alcohol use.
      Determining which patients can be safely managed in an outpatient setting can be challenging. The most important predictor of severe AWS is prior severe AWS as characterized by convulsions, delirium tremens, or prior ICU admission. (14) Other recognized risk factors for complicated withdrawal include multiple prior episodes of AWS, age >65, medical comorbidities, longer and heavier alcohol use, use of benzodiazepines or barbiturates, elevated blood alcohol concentration (BAC) on presentation, and at least moderate AWS on presentation (CIWA-Ar≥10, RASS ≥2). Thrombocytopenia and elevated ALT suggest chronic heavy alcohol use and are associated with more severe withdrawal. (13)
      Severity scoring systems such as CIWA-Ar, Richmond Agitation-Sedation Scale (RASS), Severity of Ethanol Withdrawal Scale (SEWS), and Brief Alcohol Withdrawal Scale (BAWS) can be used to quantify withdrawal intensity but are not predictive of clinical course. Several scores have been developed to predict severity, including the Luebeck Alcohol Withdrawal Risk Scale (LARS) and the Alcohol Withdrawal Triage Tool (AWTT), however the only validated score is the Prediction of Alcohol Withdrawal Severity Scale (PAWSS), a 10-question tool designed to predict AWS complications in inpatients. PAWSS includes several interview questions that may be challenging to administer in a busy ED, but the elements of these scores may inform the clinician's risk assessment.
      Patients who do not demonstrate significant withdrawal with a zero BAC are less likely to develop dangerous AWS, and patients who show significant withdrawal with a high BAC are at greater risk and should not be discharged without a very specific plan for withdrawal management. However, because progression to severe AWS cannot be reliably predicted, the primary criteria guiding disposition in patients with mild-moderate AWS being considered for discharge is the likelihood to return if AWS worsens, ability to follow up, or capacity to access alcohol. As progression of AWS itself impairs the patient's cognition and therefore their ability to seek care, outpatient safety corresponds to the capacity for monitoring, either by friends and family, or at an outpatient facility. Outpatient AWS treatment programs vary widely in their capabilities, and providers should verify that a prospective discharge destination is properly matched to the patient's needs.
      If minimal or no monitoring is available to a patient being considered for discharge, a period of observation, either in the ED or under an ED-based observation protocol, will often clarify the patient's withdrawal trajectory and inform disposition. Table 3 lists features that suggest safety in outpatient management of AWS.
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        Q3. In which patients should AWS be treated before the appearance of signs or symptoms?
      Table 3Safety Factors in Outpatient Management of AWS
      In good physical and mental health
      Supportive social network and stable living environment; able to be monitored at home by family or
      friends and return to care if worsening symptoms
      No previous withdrawal episodes; if previous AWS, no severe AWS
      Mild AWS in ED and control of withdrawal symptoms over a period of ED or hospital-based observation
      Not also dependent on benzodiazepines or opioids
      Able to acquire and take oral medications
      The role of AWS prophylaxis in the ED is controversial, and there are no ED-based studies to guide decision-making. Most patients at risk for AWS who present with AI are discharged prior to the development of significant withdrawal. However, many patients with AUD are held in the ED to address medical, psychiatric, social, or substance use concerns. Preventing AWS in these patients has a variety of benefits: AWS is dangerous, and early signs of withdrawal may not be detected in a busy ED, putting the patient at risk. Furthermore, each episode of AWS makes future episodes more severe and less responsive to treatment, a phenomenon known as kindling. (15,16) Lastly, though inpatient management may facilitate treatment of AUD, in the absence of such treatment, the development of AWS in a patient who would otherwise be discharged may lead to low-value hospital admissions.
      On the other hand, administering a sedating medication to patients who would not have needed it carries important harms such as oversedation or delirium, falls, depression of respiration or airway reflexes, and prolongation of stay.
      SAMHSA recommends that high-risk AUD patients receive prophylaxis, (15) and AWS prophylaxis for inpatients is well-described and effective; (17-21) emergency physicians should consider administering withdrawal prophylaxis to patients at high risk for AWS who cannot be discharged in the “window of safety” between sobriety and withdrawal. Oral agents used for prophylaxis include chlordiazepoxide (50-100 mg), lorazepam (1-2 mg), and gabapentin (600-1200 mg, avoid in patients with renal impairment). (22)
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        Q4. Which medications should be used to treat patients with mild to moderate AWS?
      Emergency physicians commonly manage mild to moderate AWS, however treatment is guided by few established standards and therefore practice is highly variable. Symptom-triggered dosing is preferred over scheduled dosing for AWS management as it reduces the risk of under or overtreating symptoms and is more appropriate for ED workflows. (13) Patients with AWS who are stable enough to be discharged from the ED and are interested in decreasing alcohol use should be provided a prescription for the indicated medication(s), with the goal to bridge them to a follow up appointment.
      Mild AWS includes mild anxiety, insomnia, diaphoresis, and presence of minor tremor and corresponds to a CIWA-Ar score of <10 or RASS 0 or 1. (13,23) In these patients who have a low risk of developing severe or complicated withdrawal, pharmacotherapy and/or supportive care are reasonable. Carbamazepine or gabapentin are appropriate choices in this group.
      Moderate AWS includes headache, anxiety, retching, conspicuous tremor, and tachycardia and is defined by a CIWA-Ar score of 10-18 or RASS 2. (13) Traditionally, benzodiazepines have been the first line treatment of patients with moderate to severe AWS, however carbamazepine, valproic acid, and gabapentin are increasingly used as alternative or adjunctive treatment options (Table 4).
      Table 4Medications that can be used to manage mild to moderate AWS
      DiazepamMild AWS: 10 mg PO q6h x 4 doses then prn
      all prn dosing is “as needed for withdrawal symptoms.” Dosing recommendations may need to be adjusted for patient specific and situational reasons.
      for 3-5 days (disp#20 10 mg tabs)
      Moderate AWS: 20 mg PO q2h x 3 doses, then prn for 3-5 days (disp#30 10 mg tabs)
      Chlordiazepoxide50-100 mg PO q6h prn for 1 week (disp#50 25 mg tabs)
      LorazepamMild AWS: 0.5-1 mg PO q6h as needed for 3-5 days (disp#20 0.5 mg tabs)
      Moderate AWS: 1-2 mg PO q2h as needed for 3-5 days (disp#30 1 mg tabs)
      Carbamazepine400 mg PO BID for 1 week (disp#14 400 mg tabs)
      Valproic Acid500 mg PO TID for 1 week (disp#21 500 mg tabs)
      low asterisk all prn dosing is “as needed for withdrawal symptoms.” Dosing recommendations mayneed to be adjusted for patient specific and situational reasons.

      1.2 Benzodiazepines

      Benzodiazepines enhance the activity of GABA on its receptor. The literature endorses no benzodiazepine as superior, but diazepam and chlordiazepoxide (CDZ) have the best evidence to support their use (24,25) and feature a long duration of action to provide ongoing reduction in breakthrough symptoms and prevention of progression to seizures. (13,26) However, long-acting benzodiazepines can cause prolonged sedation, particularly in geriatric patients or patients with COPD or liver disease. If a scheduled, rather than a symptom-triggered approach is used in these patients, a shorter acting agent such as lorazepam or oxazepam may be more appropriate. When considering an oral long-acting benzodiazepine, diazepam has a faster onset of action compared to chlordiazepoxide; (27) unfortunately, this therapeutically attractive property also increases the risk of misuse and diversion. (26) Though no standard exists, the risk of benzodiazepine misuse and dependence suggest that with the exception of the less misuse-prone chlordiazepoxide, benzodiazepines prescriptions should be limited to 3-5 days. (13)

      1.3 Non-benzodiazepine/barbiturate treatment of mild-moderate AWS

      Non-benzodiazepine, non-barbiturate agents such as carbamazepine, gabapentin, and valproic acid have a growing body of evidence supporting their use in managing AWS, although these agents remain infrequently utilized. Because GABAergic drugs are sedating, dependence-forming, and misuse-prone, alternatives are attractive as monotherapy or adjunctive treatment in the management of patients with mild to moderate AWS. (13, 22, 28-30)

      1.4 Carbamazepine

      Carbamazepine, a sodium channel blocker that may potentiate GABAergic neurotransmission, is safe and effective in treating AWS in patients at low risk for seizures or delirium. (28,31) Evidence supports carbamazepine for use in AWS management as it decreases the severity of illness and psychiatric distress as well as reducing the likelihood of return to alcohol use and the amount of alcohol consumed after detoxification. (22,28,32-39) The drug is safe for use in patients with liver and renal disease and does not cause oversedation when combined with alcohol. (22,34,36)

      1.5 Gabapentin

      Gabapentin is a calcium channel modulator used as an anticonvulsant, anxiolytic, and sedative that is emerging as a safe and effective alternative to benzodiazepines in the management of mild to moderate AWS. (22, 40) Dosed at 400-600 mg three times per day, gabapentin is as effective as lorazepam and chlordiazepoxide for mild-moderate AWS treatment, with the benefit of reduced cravings, alcohol use, anxiety and daytime sedation, and improvements in sleep and ability to work, as well as promoting abstinence and reducing heavy drinking. (41-44). Unlike benzodiazepines, gabapentin can be continued as an anti-craving medication for maintenance treatment. (29,45-47)
      Gabapentin misuse has become an important concern; it is currently a Schedule V medication in some states, with high rates of misuse among patients prescribed the medication regardless of indication. Though safer in overdose than other drugs with misuse potential, substance use disorder (SUD), and opioid use disorder (OUD) in particular, is a risk factor for gabapentin misuse and gabapentinoids are increasingly found in postmortem toxicology analyses. (48,49) Gabapentin is advantageous for its extrahepatic metabolism, however it should be renally dosed or avoided in patients with renal impairment and used with caution in the elderly or patients with COPD. (50)

      1.6 Valproic Acid

      Valproic acid (VPA) modulates GABA transmission and is well tolerated in patients with AWS, decreases irritability, is effective in mood stabilization, and reduces the risk of relapse to heavy drinking when compared to placebo. (51,52) It is not for use as monotherapy in the management of AWS; instead it may have a role as an adjunct for patients with persistent AWS despite adequate doses of benzodiazepines. (13,28,30,33,53,54) VPA added to benzodiazepines decreases the progression and duration of AWS, in addition to improvements in outcomes for patients admitted for AWS (37,55,56). VPA should not be used in pregnant patients or those with hepatic or hematologic abnormalities. (13,29,30,53)

      1.7 Phenobarbital

      Phenobarbital has been in use since the 1920s and was the first medication to successfully and predictably manage AWS. (13) It enhances the binding of GABA to the GABA-A receptor, thus depressing central nervous system activity while also blocking the effects of glutamate signaling. (13,57) Although very effective for the management of AWS, it has an array of dangerous adverse effects including respiratory depression, especially when combined with benzodiazepines (or alcohol). (27,57,58) Phenobarbital's long half-life is an important advantage when used in a monitored setting, (see question #5) but is a dangerous liability when prescribed at discharge. Phenobarbital, whether used as an adjunct or as monotherapy, is best reserved for patients with moderate to severe AWS being admitted to the hospital. (13)
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        Q5. How should severe AWS be identified and managed in the ED?
      Severe AWS is characterized by psychomotor agitation, delirium, hallucinations, seizures, or autonomic hyperactivity (e.g. marked tachycardia, hypertension or tachypnea) among patients with known or suspected AUD. Clinical assessment tools such as CIWA-Ar can be used to score severity, but these are often impractical for use in the ED. (59) Though other etiologies (such as infections, metabolic derangements, or intoxications) may present similarly and require evaluation, treatment for severe AWS should be initiated as soon as it is suspected. (60)
      Severe AWS requires treatment with parenteral benzodiazepines or barbiturates. (13) Existing clinical data does not strongly support the use of one intravenous benzodiazepine over another. (61) IV diazepam or lorazepam are often used as a first-line medication, with some preferring diazepam for its favorable pharmacokinetics (see Table 5). Among patients who are at risk of developing severe AWS, usual initial doses are 10 mg of IV diazepam or 2 mg of IV lorazepam, however variability in patient presentations make it difficult to standardize dosing. For patients manifesting signs of severe AWS, escalating benzodiazepine doses may be required every 5-20 minutes. Inadequate dosing of benzodiazepines occurs more frequently than overdosing; in the treatment of progressive or unabating symptoms, benzodiazepine dose may be increased by 50% or doubled with subsequent administrations.
      Table 5Parenteral benzodiazepines for severe AWS
      MedicationInitial IV doseComment
      Diazepam10-20mg IVRapid onset and active metabolites, which prolong duration of action, are ideal characteristics for treatment of severe AWS
      Lorazepam2-4mg IVSlower onset and lack of active metabolites, however long history of effective use
      Midazolam5-10mg IMFavored for intramuscular dosing. Rapid onset may be useful though short half-life and lack of active metabolites will often mandate switching to a longer-acting benzodiazepines for continuing doses
      Though benzodiazepine tolerance in patients with severe AWS may be extremely high, the large doses often required confer the risk of respiratory depression and loss of protective airway reflexes. Endotracheal intubation may be required and may be particularly dangerous as patients with severe AWS have high oxygen consumption and can desaturate quickly. Patients who demonstrate high benzodiazepine resistance, as evidenced by marginal benefit after 200-400 mg IV diazepam or equivalent, require alternative treatments. Although supported by fewer data, these non-benzodiazepine medications have an evolving role in the treatment of severe AWS.
      Phenobarbital has been used both as monotherapy for treatment of severe AWS and in combination with benzodiazepines to reduce the required doses of each. (62) Phenobarbital has demonstrated benefit in some studies of benzodiazepine-refractory AWS, may cause less delirium than benzodiazepines, and, when used as monotherapy, its notably long half-life provides a self-tapering effect that may lessen the intensity of downstream inpatient care, reducing ICU admissions and mechanical ventilation. (63-67) Phenobarbital has a comparatively delayed onset of action, which hinders rapid titration, and intramuscular administration further prolongs the onset. Symptom-triggered dosing is 130-260 mg IV, and is generally given as adjunctive therapy. For monotherapy, some data suggest best outcomes with a substantially larger loading dose of 10 mg/kg given over 15-30 minutes. The broad range of dose recommendations (between 130 and 780 mg) highlights both the wide therapeutic index of phenobarbital and lack of consensus around optimal dosing. Though evidence is supportive and many severe AWS protocols now include phenobarbital, it remains an emerging treatment, especially as monotherapy for severe AWS.
      Data on other anti-epileptic drugs for treatment of severe AWS and seizures in the setting of AWS are conflicting. Placebo-controlled studies demonstrate no improvement in frequency of seizures between patients who received non-benzodiazepine/barbiturate anti-epileptic drugs and those who received placebo. (68,69) Some guidelines support the use of carbamazepine, valproic acid, or gabapentin as adjunctive therapy in severe AWS; (13) however, when treating seizures associated with severe AWS, these drugs may be used in addition to, but not in lieu of benzodiazepines or phenobarbital.
      There are reports of successful treatment of refractory AWS with ketamine; for example starting with a ketamine infusion dose of 0.5mg/kg/hour and titrating to a maximum of 4.5mg/kg/hour. (70) Dexmedetomidine may also be considered as adjunctive therapy for patients whose AWS is not well controlled with benzodiazepines. (71,72) Similarly, propofol may be useful for intubated patients with refractory signs of AWS, though data do not uniformly demonstrate benefit compared to conventional treatments. (73) For patients with benzodiazepine-refractory psychosis and agitation, treatment with a parenteral antipsychotic may be useful.
      In addition to treatment of the hyperadrenergic manifestations of AWS described above, patients with severe AWS often require volume resuscitation and nutrient replacement. Severe AWS patients frequently have other substance dependencies (especially nicotine) that should be specifically sought and treated. Patients with severe AWS are critically ill and should be dispositioned accordingly: the risk of recurrent symptoms, seizures, agitation, and iatrogenic respiratory depression, as well as high medication and nursing demands, requires an inpatient setting capable of close observation and prompt treatment. Patients with severe AWS who have been stabilized in the ED and observed over a period of hours may be appropriate for management in non-ICU settings.
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        Q6. Which medications to manage cravings should be offered to AUD patients being discharged from the ED?
      Though benzodiazepines are central to the treatment of AWS, there is no evidence that short-term prescriptions of benzodiazepines reduce the return to heavy drinking in patients with AUD. (74-76) Medications that reduce cravings and therefore reduce compulsive alcohol use are underutilized in most care settings, and certainly from EDs. (77,78) However, there is growing interest in, and developing evidence to support, initiation of anti-craving medications from the ED. (78,79) Naltrexone, acamprosate, and disulfiram are FDA-approved anti-craving treatments for AUD; gabapentin and topiramate are often used (off-label) as well. (80) See Table 6.
      Table 6Anti-craving medications to assist with sustained alcohol use reduction or abstinence
      MedicationSummaryContraindicationsUsual DoseTips
      NaltrexoneFirst line agent from the ED (PO)Opioid dependence50 mg PO dailyMust inquire about current opioid dependence, including medications for opioid use disorder; if in doubt perform naloxone challenge
      Abstinence not required before initiation (only clinical sobriety for patient consent)Severe hepatic impairmentXR-NTX: 380 mg IM every 3-4 weeks.Does not treat withdrawal –consider combining with gabapentin
      Severe renal impairment
      AcamprosateRenally cleared and can be used in severe liver diseaseRenal impairment (can decrease dose in mild/moderate renal impairment)666 mg (two 333 mg tabs) PO TIDGI side effects are common; may have to be gradually increase to therapeutic dose
      More effective if initiated when patient abstinent (after detoxification)May require prior authorization or be cost prohibitive
      Efficacy requires 3X daily dosing
      GabapentinCan be used to treat AWS and to decrease cravingsRequires renal dose adjustment300-600 mg PO TIDPatients with AUD generally require high doses
      Sobriety not required to initiateCaution in elderly or fall risk as medication is sedatingMay be used as a single agent or adjunctively with NTX or AC
      TopiramateDose needs to be titrated up to an effective dose (usually over a period of weeks)Caution in patients with balance difficulty (fall risk)Starting dose is 50 mg PO nightlyIndicated for some forms of epilepsy, migraine, behavioral health conditions
      Only recommend to be initiated from the ED if prompt and reliable clinic follow upTitrated to 50-300 mg PO daily, usually divided BIDAdverse effects (tremor, disequilibrium, confusion) are common may prevent reaching a therapeutic dose
      DisulfiramNot recommended for initiation from the EDMedically compromised patients250 mg PO daily, may increase to 500 mg dailyAdherence is poor outside of an institutional or other daily supervised setting
      Aversion therapy–does not reduce alcohol cravings.Patients lacking observation or supervisionCan cause dangerous adverse effects
      Naltrexone (NTX) exerts its therapeutic action by disrupting the reward cascade initiated by alcohol intake, which is modulated by endogenous opioids at the mu-opioid receptor. (80) NTX can be administered as either an oral medication or as a depot extended-release intramuscular injection (XR-NTX).
      Treatment of patients with AUD with oral NTX results in significantly fewer drinking days and lower rates of relapse to heavy drinking, with a number needed to treat of ∼12, (81,82) as well as decreased rates of hospital readmission and ED utilization at 30 days. (78) The standard oral dose of NTX is 50 mg/day. NTX is usually well-tolerated; side effects such as insomnia, headache, nausea, abdominal pain, dizziness, and decreased appetite are generally mild and treatable. (83) A limitation of oral naltrexone is the need for daily dosing, which is difficult for many patients to achieve without a strong support system.
      XR-NTX is administered intramuscularly every 4 weeks at a dose of 380 mg. The most-commonly reported adverse effect is persistent pain at the injection site, which is avoidable with optimal administration technique; personnel who administer XR-NTX must therefore receive product-specific training. The cost and need for pre-authorization are potential limitations to the use of this formulation in the ED.
      NTX is contraindicated in patients with ongoing illicit or prescribed opioid use because it can precipitate severe opioid withdrawal; patients must therefore be screened for opioid dependence. Most patients can be effectively screened with a directed, non-judgmental history, and if opioid dependence remains a possibility, a naloxone challenge test can be performed (e.g. 0.4 mg IN, IM, or SC or 0.2 mg IV). Caution should be exercised using naltrexone in patients with acute hepatitis, severe hepatic impairment, or severe renal impairment; SAMHSA guidelines endorse initiation of naltrexone when hepatic transaminases are less than 5 times the upper limit of normal. (84,85)
      Acamprosate (AC) is thought to promote abstinence by correcting the balance between the GABA and glutamate systems that is disrupted in patients with AUD. (86,87) AC is dosed at 666 mg orally TID and unlike NTX, is renally cleared and can be taken by patients with hepatic failure. (86) AC achieves better abstinence outcomes when begun after the period of alcohol withdrawal is complete, (88,89) and is comparatively expensive. (90) Although demonstrated to improve abstinence, (87,88,89) issues around timing of initiation, minor but troublesome adverse effects, cost and frequent need for a prior authorization limit the opportunities to initiate acamprosate in the ED.
      Gabapentin (GAB) is FDA approved to treat epilepsy and neuropathic pain and is prescribed for multiple off-label conditions. (91) GAB is renally cleared and requires dose adjustment in patients with kidney disease, but can be taken by patients with hepatic failure. (91) GAB has been studied in the treatment of AUD in doses of 300mg/day (92) to 3600mg/day, (93) and at doses >1800mg/day reduces heavy drinking days, (43,91) increases abstinent days, and improves the symptoms of insomnia, dysphoria, and craving that lead to relapse. (44,45,91,93) GAB is well tolerated in combination with alcohol and can be safely initiated in patients who are actively drinking. (93-95) GAB is particularly efficacious in AUD patients with a history of AWS (96) and when used in combination with NTX may improve drinking outcomes over NTX alone. (97)
      GAB is relatively safe and adverse effects are most commonly neuropsychiatric, including dizziness, somnolence, and unsteady gait. (80,98) GAB should be prescribed cautiously to elderly patients or others at risk for falls. (99) Misuse of GAB, either alone or in combination with other substances (including alcohol), is frequent (see Question #4); (100-103) however, considering the low rate of severe adverse events involving the misuse of GAB, especially when compared to benzodiazepines, (102,104,105) and balancing the risk of harms from continued alcohol misuse, emergency clinicians can consider prescribing GAB for AUD.
      Topiramate (TOP), FDA approved as an antiepileptic, migraine preventative, and appetite suppressant, (80) reduces craving for alcohol by targeting glutamate brain pathways and inhibiting dopamine release. (106,107) TOP decreases binge drinking and increases days of abstinence, with efficacy comparable to naltrexone. (108) TOP also has mood stabilizing properties and is used to treat several comorbid psychiatric disorders. (106) Unfortunately, adverse medication reactions are common including paresthesias, disturbance of taste and appetite, and disruption of concentration or dizziness. (107) These reactions require slow and careful titration, and may prevent reaching a therapeutic dose. (107) TOP is a valuable treatment in a carefully selected and monitored subset of AUD patients, and can be initiated in the ED in consultation with a following outpatient provider or established followup pathway.
      Disulfiram (DIS) irreversibly inhibits the enzyme aldehyde dehydrogenase, leading to the accumulation of acetaldehyde when ethanol is consumed. (109) This causes the disulfiram ethanol reaction (DER), which includes facial flushing, nausea, palpitations, malaise and a pulsating headache (80,110). Instead of acting as a true anti-craving medication, the anticipation of the DER is how disulfiram reduces alcohol consumption (aversion therapy), however adherence is poor outside the setting of supervised treatment. (109,111,112) Monitoring transaminases is recommended for patients treated with DIS, (113,114) and the DER can cause dangerous systemic toxicity. (110) DIS is therefore not recommended for prescription from the ED.
      Medications to treat AUD can significantly reduce alcohol use, particularly heavy alcohol use, and thus reduce the myriad harms of AI and chronic alcohol consumption. Initiating anti-craving medications from the ED should be considered for all willing AUD patients. First-line treatment is naltrexone, unless the patient has significant hepatic impairment, in which case acamprosate is an appropriate choice. Gabapentin may be a valuable adjunct, especially in patients with a history of AWS, with caution and dose adjustment in the elderly and patients with renal impairment, and consideration of the potential for misuse, especially in patients who use opioids or other psychoactive substances.
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        Q7. What are the general management principles for patients presenting with presumed isolated AI?
      The goals in the management of patients with presumed isolated AI are to identify dangerous medical conditions, provide a safe environment for the patient to recover, and address underlying alcohol use disorder, if present. There is a high incidence of subclinical medical and traumatic pathology in patients who present with presumed isolated AI; (115,116) therefore, all such patients should be rapidly and carefully assessed for the degree of mental status impairment, evidence of dangerous medical conditions, and signs of trauma. Initial vital signs, including pulse oximetry and finger stick glucose, should be assessed, and abnormalities addressed. Mild tachycardia, hypotension and hypothermia are common in AI, but marked or sustained abnormalities require investigation. AI causes respiratory depression, and patients with decreased level of consciousness must be monitored according to their risk for hypoventilation. Risk for hypoventilation does not strictly correlate with blood alcohol concentration, and can be influenced by the patient's degree of tolerance to alcohol, comorbid cardiopulmonary disease, co-exposure to sedating substances prior to arrival, and medications given in the ED for agitation.
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        Q8. What ancillary studies, including measurement of Blood Alcohol Concentration, should be considered in patients presumed to be alcohol intoxicated?
      Patients with isolated AI in whom there is limited concern for traumatic, metabolic, or other coexisting conditions require little ancillary testing. Because nearly all patients will have an altered mental status, and because alcohol predisposes patients to the development of hypoglycemia, a blood glucose level should be obtained routinely.
      Basic laboratory studies (e.g., CBC, serum electrolytes, liver and renal function testing) should not be routinely performed. Patients who demonstrate features of concomitant medical comorbidities such as blood loss, persistent vomiting, or abnormal vital signs should be appropriately investigated. Urine drug testing is not indicated for patients who present with AI unless another indication is present.
      Given the high incidence of subclinical intracranial pathology in AI patients, the threshold for obtaining a head CT should be relatively low. Conversely, the liberal use of CT imaging carries a variety of potential harms and competes for a limited resource. (117) Patients without a history or evidence of trauma and who do not demonstrate other concerning clinical features can be managed with frequent reassessments to verify improvement of mental status; this “watchful waiting” approach limits CT utilization but is resource intensive. (118,119)
      Alcohol concentration can be measured in patients using blood (BAC) or breath (BrAC) analyses, though BrAC is only reliable when the patient is cooperative. (120) Routine measurement of alcohol concentration (BAC or BrAC) is not recommended. (121) For patients with uncomplicated presentations who are easily arousable and endorse using alcohol, the BAC/BrAC value is unlikely to be useful, incurs a variety of resource costs (especially serum testing, which also subjects patients and staff to the risk of needlestick), and may delay disposition. In these cases, limited ancillary testing and frequent reassessments to verify appropriate recovery of mentation is appropriate. Conversely, if the etiology of the patient's altered mental status is in question, a negative or low BAC/BrAC may be useful to exclude the presumed diagnosis of AI. A high concentration supports–but never confirms–the diagnosis of uncomplicated AI, and will inform the pursuit of additional diagnostics based on the physician's judgment. Factors that suggest alternative etiologies of altered mental status include a patient who is deeply unconscious and unassessable, has significant trauma, or is without evidence of recent alcohol use.
      The ability of the BAC (or BrAC) to determine a time of safe discharge is limited. Although serial measurements can identify when a patient has reached a predetermined BAC, such as 80 mg/dL (the legal limit to operate a motor vehicle in most states), it often requires that patients with tolerance to ethanol, and therefore a very high BAC, remain in the ED long enough to develop AWS. Examination for signs of AI, such as unstable gait or impaired decision-making, allows discharge at a clinically safe time independent of the measured BAC. The use of a single BAC to predict a BAC at a later point in time based on presumed metabolic rate is limited by the variability in alcohol kinetics (absorption and elimination) among patients and may carry legal liability. (122,123) See Question#12. Early BAC/BrAC measurements are useful in AI patients who subsequently develop AWS because the concentration, early in withdrawal, correlates with the ultimate AWS severity. (124)
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        Q9. What is the role of vitamins and fluids in the management of the alcohol intoxicated patient?
      Data do not support the routine administration of intravenous fluid to hydrate patients; this practice extends ED the length of stay, (125,126) and does not enhance the clearance rate of ethanol. (127) Additionally, administration of a large volume of fluid may lead to spontaneous urination or injury if the patient attempts to stand or ambulate to urinate. Oral fluid is generally sufficient to provide adequate hydration, though clinically dehydrated patients may benefit from crystalloid fluid replacement. The addition of potassium and magnesium, while often provided routinely, is ideally done on an individualized basis.
      Thiamine deficiency and Wernicke's encephalopathy occur frequently in those with long-term heavy alcohol use, and is often subclinical based on postmortem findings. The empiric administration of thiamine therefore represents an important public health approach to preventing deficiency-related syndromes in this population and is cost effective. Intermittent treatment with intramuscular thiamine is likely to be of benefit to patients who use alcohol daily, and though without evidentiary base, routine treatment with an oral multivitamin is low-cost, without harm, and of possible benefit. Because other vitamin deficiencies, such as vitamin B12 and folate, are rare in most patients who present with AI, the use of an infused multivitamin (e.g., banana bag) is not cost effective. (128,129)
      There is a prevalent misconception that thiamine must be administered before glucose administration, based on the potential for the precipitation of acute thiamine deficiency due to its cofactor role in glycolysis; in a hypoglycemic patient, a delay in glucose administration is likely to be more deleterious. (130)
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        Q10. How is agitation related to alcohol intoxication best managed in the ED?
      Agitation is a common component of encounters for AI. (131) Agitation, particularly when associated with psychomotor activity or violence, puts the patient and staff at significant risk for morbidity, and thus warrants prompt treatment.
      The first-line treatment for agitation in most patients with AI should be verbal de-escalation, unless the patient is actively exhibiting violent behavior or poses an imminent threat. (132) Verbal de-escalation may adequately address the patient's agitation by creating a collaborative and noncoercive environment in which the patient is encouraged to control their own behavior. De-escalation entails listening to the patient and attempting to identify the issues underlying their agitation; however it is still important to set clear limits and boundaries in a respectful manner. Specific de-escalation techniques are described in Table 7, and specialized training programs are also available. (132,133)
      Table 7Verbal De-escalation Techniques
      De-Escalation TechniqueExamples
      Respect patient's autonomyUtilize periods of intent listening
      Respect personal space
      Introduce yourself and orient the patientEmphasize to the patient that you are their medical provider to help care for them, and that they are in a hospital setting
      Identify wants or needsOffer comfort objects (warm blankets)
      Facilitate using the restroom
      Offer food or drink (if patient can tolerate)
      Provide support/validation of the situation“I would be upset too”
      “Let's figure this out together”
      Providing step-by-step expectations“Here is what you can expect during your visit today”
      Offering patient choices or optionsOffering oral anxiolytics
      Discuss physical restraint removal (if applicable)
      If verbal de-escalation is not successful and the AI patient remains agitated, medications to treat agitation should be utilized. Though treatment preferences are often dictated by individual and departmental experience and driven by regional or institutional custom, the treating clinician should consider each unique patient scenario when choosing an appropriate medication. Table 8 summarizes medications commonly used. Although there are no comprehensive head-to-head comparisons of all relevant medications, doses, and routes, several conclusions can be drawn from the literature.
      Table 8Medications for Treating Agitation in the Alcohol-Intoxicated Patient
      MedicationStarting Dose, Formulation, RouteAdministration Notes
      AntipsychoticsPreferred treatments if agitation is thought to be driven by underlying psychiatric disease
       Haloperidol5-10 mg, IMDiphenhydramine should not be co-administered empirically, treat EPS if they occur
      2-5 mg, IVIV use is off label
       Droperidol2.5-10 mg, IM or IV
       Olanzapine5-10 mg, oralMust be reconstituted with sterile water
      10 mg, IM
       Ziprasidone10-20 mg, IMMust be reconstituted with sterile water
       Risperidone1-2 mg, oral
      BenzodiazepinesPreferred treatments for patients with concomitant stimulant intoxication or withdrawal from alcohol or other sedatives
       Midazolam2-10 mg, IMHigh doses (≥5mg IM or any dose IV) may increase risk of respiratory depression, must be monitored
      2-5 mg, IV
       Lorazepam2-4 mg, IM or IVIM has slow onset
      1-4 mg, oral
       Diazepam2-10 mg, oral or IVShould not be given IM
      Others
       Ketamine4-5 mg/kg IMPatients receiving ketamine for agitation must have continuous cardiorespiratory monitoring after administration, until recovery from dissociation
      1-2 mg/kg IV
      Among the benzodiazepines, midazolam is superior to lorazepam and diazepam when given intramuscularly, due to its rapid and reliable absorption by this route. Intramuscular midazolam also produces a faster time to sedation compared to the antipsychotics haloperidol, olanzapine, and ziprasidone, and is similar to droperidol. (134-139) These efficacy benefits must be weighed against the potential for benzodiazepines to cause respiratory depression in AI patients, especially at higher doses. (137,139) However, clinically important respiratory depression is very uncommon at usual doses of benzodiazepines (e.g., midazolam ≤5 mg) and is safe practice with appropriate monitoring, as outlined below. (135,136)
      Intramuscular olanzapine, droperidol, and ziprasidone have more rapid onset and result in adequate sedation more often compared to haloperidol, though ziprasidone has a slower onset than olanzapine and droperidol. (134-136,140-143) The butyrophenone antipsychotics haloperidol and droperidol cause more extrapyramidal side effects than newer alternatives, though even with the butyrophenones they are uncommon and manageable.
      Intramuscular combination of a benzodiazepine and an antipsychotic (134,138,139,144, 145) allows for lower doses of each medication, which may mitigate side effects associated with larger doses of either. However, combination treatment increases the spectrum of possible side effects. Commonly used combinations are 5 mg of intramuscular midazolam or 2 mg of lorazepam with 5 mg of droperidol, olanzapine, or haloperidol. Respiratory depression has been associated with the combination of olanzapine with benzodiazepines, leading to a drug warning about its use; however, this combination, as with any combination of sedating medications, is a safe practice when given at usual doses with appropriate monitoring. (146,147)
      For agitated patients who are uncontrollably violent with concern for immediate harm to self or others, or if there is a concern for an immediately life-threatening medical condition whose diagnosis and management is hindered by agitation, dissociative-dose ketamine (4-5 mg/kg IM or 1-2 mg/kg IV) should be considered. (148-150) These patients require procedural sedation level care with an airway-capable clinician available and vigilant attention paid to ventilation until dissociation resolves or the patient is intubated.
      Clinicians should consider continuous monitoring of oxygenation or ventilation in patients with AI who are deeply unconscious or receive any sedating medication, based on an assessment of risk to develop respiratory depression. Monitoring should be supplemented with frequent bedside evaluations and re-assessments of mental status.
      Despite the risk of QTc prolongation associated with certain antipsychotics, an ECG is not required prior to medication administration because the risk of dysrhythmias is very low in this population when the discussed agents are used in the recommended doses. For patients with cardiac disease or at risk for QT prolongation, it is reasonable to obtain an ECG after the patient calms. (151-154)
      Physical restraints for extreme agitation and violent behavior may be necessary to provide an immediate mechanism to prevent harm to the patient, to ED staff, and to nearby patients and property. Physical restraints should not be used routinely in the management of agitation. If physical restraints are used, the patient must be re-assessed frequently, with the goal of removing physical restraints as soon as safely possible. Documentation of restraints using a “face to face” note is imperative, and must include the date and time of the in-person assessment, the rationale for restraints, alternatives attempted, and criteria for discontinuation. (155,156) A detailed description of the patient's impairment, including the suspected etiology of agitation, BAC/BrAC values (if obtained), and results of urine toxicology screens (if obtained) will likely prove valuable if issues concerning civil liberties or battery arise.
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        Q11. What are the medical conditions or complications that commonly occur in patients with AI and/or AUD?
      The most common medical consequences of AUD are metabolic and nutritional. This is primarily a function of inadequate dietary consumption with typical caloric intake being replaced by alcohol, which lacks nutritional value. (157) Common vitamin deficiencies and their potential clinical effects are shown in Table 9. Though routine vitamin supplementation in AUD is without strong evidentiary support, it is well established that these nutritional deficiencies occur, and their treatment using a daily oral multivitamin is low cost and low risk. (157,158) However, routine administration of intravenous fluids and multivitamin is not recommended. (See Question#9)
      Table 9Common nutritional deficiencies in AUD and their clinical effects.
      B-Complex VitaminsClinical effects of deficiency
      Thiamine (B1)Wernicke encephalopathy, Korsakoff syndrome
      Riboflavin (B2)Mucosal inflammation, dermatitis, depression, peripheral neuropathy
      Pyridoxine (B6)Stomatitis, depression, peripheral neuropathy
      Folic Acid (B9)Anemia, intestinal malabsorption
      Minerals
      ZincEndocrine abnormalities, retinal dysfunction
      SeleniumMuscle Pain
      Hyponatremia may occur in AUD patients by beer potomania, (a dilutional hyponatremia caused by excessive intake of a hypotonic fluid such as beer), SIADH, or cirrhosis. Hypomagnesemia may cause neuromuscular and cardiovascular manifestations, and impair the treatment of hypokalemia, which is also commonly seen in patients with AUD. Emergency physicians should consider screening for electrolyte deficiencies or empiric replacement of vitamins in AUD patients with suspected malnutrition or metabolic disorder. (157,158)
      Alcoholic ketoacidosis (AKA) is a starvation ketosis related to free fatty acid breakdown in the absence of appropriate carbohydrate and protein intake. The metabolism of ethanol indirectly leads to an acidosis from excess beta-hydroxybutyrate and acetoacetate. AKA frequently presents with gastrointestinal symptoms, hypovolemia, and electrolyte disturbances. Ketonuria may or may not be present, and an elevated beta-hydroxybutyrate level may be helpful to confirm the diagnosis. Treatment consists of volume repletion, dextrose, and vitamin and electrolyte supplementation. (158,159,160) A mildly elevated lactate is often present in AI patients, however a wide anion gap metabolic acidosis should prompt consideration of alternative diagnoses such as AKA, toxic alcohol ingestion, renal failure, or sepsis.
      Severe thiamine deficiency causes Wernicke encephalopathy (WE) and, if untreated, the irreversible Korsakoff syndrome. WE is a clinical diagnosis, and should be considered in a patient with any combination of suspected nutritional deficiency, altered mental status, oculomotor impairment, and cerebellar dysfunction. (161) The treatment for WE is parenteral thiamine at an initial dose of 500 mg IV. (162) Contrary to often-repeated recommendations, administration of glucose should not be delayed for thiamine administration in patients who are at risk for thiamine deficiency and found to be hypoglycemic. (157,158,161,163,164,165) (See Question#9)
      Long term alcohol use can be associated with cardiac, renal, immunological, and liver disease, and patients with nutritional deficiencies associated with AUD may be more susceptible to infections and have prolonged recovery time from disease. (166,167,168)
      Occult traumatic injuries, including acute and chronic subdural hemorrhage, are common in patients with either AI or AUD and should be carefully assessed for, especially in patients who present with decreased level of consciousness or with agitation. Seizures in people with AUD may represent alcohol withdrawal, but may also be related to head injury, metabolic disturbance, or exacerbation of a preexisting seizure disorder by AI. (118)
      Separate from the consequences of chronic alcohol use, severe AI can mask critical illness and cause dangerous hypoventilation as well as loss of airway reflexes and resultant aspiration; 1-4% of patients presenting with AI will require intubation or critical care. (115,116,169) This small minority can be identified by appropriately screening for trauma, hypoglycemia, and other common co-occurring conditions.
      Pregnant patients with AUD deserve special attention because of the risks to both mother and fetus. Emergency physicians should be prepared to counsel patients on the risks of Fetal Alcohol Spectrum Disorders associated with AUD and either admit for high intensity addiction care and high risk obstetric care, or arrange followup with outpatient resources targeted at both the mother and the newborn, including developmental screening. (170) Pregnant patients with AWS are particularly vulnerable and should be strongly considered for inpatient management regardless of AWS severity. Though benzodiazepines and barbiturates have potentially teratogenic effects, this risk with short-term use is small and generally outweighed by the risks of untreated AWS, which include placental abruption, preterm delivery, and fetal distress. (13)
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        Q12. What are the key considerations when discharging a patient who presented with alcohol intoxication?
      Discharging a patient who presented to the ED with AI is associated with medical, social, and legal risk that requires clinicians to apply a deliberate approach and individualized assessment. The key considerations include the exclusion of concomitant dangerous medical, psychiatric, and social conditions as well as determination of neurocognitive status and safety as it relates to the patient's discharge environment and the capacity of the patient to harm themself or others if discharged prematurely.
      The determination of discharge safety in a patient who presented to the ED with AI is based on the physician's evaluation of neurocognitive function as assessed by the patient's understanding of their circumstance, ability to care for self, and psychomotor fitness, e.g. steady gait. (171,172) These features of safe discharge should be documented in the chart prior to the patient's exit. Although case law differs from state to state, emergency physicians are responsible for protecting impaired patients under their care, which may include holding an at-risk patient in the ED against their will. The risk of allowing a patient whose mental or physical functioning is impaired by AI to leave must be weighed against the harms of forcibly holding that patient until assessment demonstrates evident discharge safety; these harms include the dangers associated with physical and chemical restraint, (173,174) as well as the abridgement of the patient's autonomy.
      Discharge safety is tightly linked to the discharge environment. A mildly or moderately intoxicated patient is appropriately discharged to the care of guardians or companions who are able to remain with the patient until sobriety. (171) However, the less safety offered by the discharge environment, the more capacity the patient must demonstrate prior to discharge. Homelessness, inclement weather, and nighttime discharges require special consideration as darkness impairs safety, public transportation may cease, shelters may not allow late arrivals, and detoxification/sobering centers may be at capacity. (121) In these cases, it is prudent to allow patients to remain overnight in the ED, in some cases for discharge planning or social worker consultation in the morning. Patients presenting with AI and suicidal ideation require reassessment of suicidality once intoxication has resolved.
      A targeted evaluation of the clinical parameters described above, rather than blood or breath alcohol concentration (BAC/BrAC), should be used to determine safety. (175) However, BAC/BrAC poorly correlates with degree of clinical intoxication and discharge safety, despite being frequently measured in the ED. (121,176,177) Though scoring systems aimed to assist clinicians in their assessment of sobriety have been described, these tools are infrequently used and do not have demonstrated benefit over gestalt. (178,179) Though BAC or elements of sobriety scores may usefully inform clinical assessment, strict adherence to numerical tools or using metabolism formulas to “clear by numbers” are likely to result in holding some patients long enough to develop AWS. (See Question #8)
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        Q13. What ED-based behavioral, psychosocial, detoxification and harm reduction strategies are most likely to improve the health of patients with AUD?
      Alcohol Screening, Brief Intervention, and Referral to Treatment (SBIRT) is an evidence-based pathway for identifying patients with AUD and engaging them in treatment. (180) SBIRT consists of screening for AUD using an evidence-based tool (See Question#15), engagement of the patient in a brief conversation to focus on risky alcohol use, and referral to an appropriate AUD treatment resource. Techniques to facilitate patient engagement include motivational Interviewing (MI) and brief cognitive behavioral therapy (CBT). MI is a form of counseling that elicits behavioral change by addressing and resolving ambivalence, and CBT helps patients identify risky situations and learn coping strategies for relapse and cravings. (181,182) Though SBIRT is an evidence-based, effective tool in the primary care setting, when performed in the ED it demonstrates only a modest salutary effect on ED utilization, recidivism, and alcohol consumption. (180,183-187) SBIRT can be performed by any healthcare professional but requires 15-30 minutes and in many settings will be most effectively carried out by trained advanced practice providers, nurses, social workers, psychologists, community health workers, medical students, or peer recovery coaches. (180,188,189)
      Detoxification, or withdrawal management, refers to the medical and psychological care of patients who are experiencing AWS as a result of ceasing or reducing their substance use. Detoxification can occur across a range of settings that vary in treatment intensity including the patient's home, residential treatment facilities, and inpatient units. The setting and type of detoxification best suited for an individual patient is based on the severity of withdrawal, medical and psychiatric comorbidities, social supports, and treatment resources available. (13) Patients should be treated in the lowest intensity setting that can safely and effectively treat their AWS and the underlying use disorder, however inpatient treatment may contribute to decreased relapse rates and increased abstinence. (190)
      Mutual Help Organizations are peer support organizations that assist patients with AUD in achieving abstinence, improving social relationships, and quality of life. (191) Alcoholics Anonymous (AA), centered on a 12-step framework, is the most prominent, with over 2 million members and presence in 180 countries. Meetings are community based, convened frequently (in some communities, multiple times per day), last 1-2 hours and focus on sharing personal addiction and recovery stories with a goal of improvement of personal interactions and coping. Free, widespread availability promotes continued participation and access. Many locales offer alternatives to AA that provide the benefits of mutual help within, for example, a secular, gender-specific, or non abstinence-based framework. In addition, 12-Step Facilitation Treatment programs catalyze recovery by offering individual and group therapy to patients wishing to transition to community AA programs. Mutual Help Organizations improve continuous abstinence and remission, reduce alcohol related harms, amount of drinking, and severity of addiction. (192) Family and friends of people with AUD may benefit from referral to a Mutual Help Organization for relations such as Al-Anon. (193)
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        Q14. What are the unique considerations relevant to people with AUD who frequently present to the ED with AI?
      The definition of frequent presenter varies greatly in the literature, but is generally defined by a minimum of 2-4 presentations to the ED within a 12 month period. (12, 194) Alcohol is a contributing factor in a significant number of these patients, who are often trapped in a vortex of substance use disorders, medical conditions, psychiatric disease, and social disadvantages from which they are profoundly incapacitated. Patients who present frequently to the ED with AI should be evaluated for AUD and its common comorbidities. (195,196)
      Emergency departments are not designed to address the majority of these issues, and these patients can be difficult to engage and direct to community-based services that can provide the longitudinal wrap-around care often required. (194) Patients may be cynical about the efforts of emergency physicians to provide holistic care due to previous poor experiences with healthcare facilities, the persistence of unmet needs, and discrimination and judgmental attitudes of healthcare staff. (197) Poor participation with both hospital and community-based referrals can be difficult to overcome and is compounded by the lack of coordination and communication among these services.
      Patients who have two or more alcohol-related ED visits in one year are a high-risk group, with one cohort demonstrating a 12 month all-cause mortality rate of 5.4%. (12) This rate increases to 8.8% in those that have 5 or more presentations over the same time period. The majority of these deaths are caused by suicide, unintentional alcohol poisoning, trauma, and diseases of the gastrointestinal system.
      There are several strategies that can be used to deliver health and social care that is accessible to this vulnerable cohort of patients. (198) Strategies that have evidence of effectiveness in decreasing ED presentations, reducing healthcare costs, and improving social determinants of health include enhanced treatment plans (also called “care plans” or “management plans”), referrals for ongoing case management, diversion to community or outpatient-based services, and social work involvement. (199) These patients are heavily stigmatized and reframing the mindsets of treating clinicians may prevent their own bias from affecting the patient's care.
      Enhanced treatment plans are documents that are created to identify the spectrum of medical and psychosocial needs of an individual patient and attempt to coordinate the services involved in their ongoing care. They aim for a holistic approach that fast tracks provision of resources, limits unnecessary investigations, and attempts to redirect patients away from the ED to community-based services that are better equipped to provide ongoing care. Enhanced treatment plans reduce ED visits (199,200) though their rates of success vary, (194) they require a stigmatizing alert being placed in the patient's health record, and they may improperly narrow the emergency physician's focus.
      Every interaction with a person with frequent alcohol-related ED visits is an opportunity to intervene on the extraordinary morbidity and mortality associated with their condition. (12,201) Rather than viewing frequent presentations as the dominant problem, emergency physicians can do better by recognizing repeat visits as the symptom of what is usually a long history of misfortune, wrong turns, and needs unmet by their social network and community. (201)
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        Q15. What is the role of the emergency department in screening for alcoholism?
      There were an estimated 3.8 million ED visits in the US specifically for alcohol-related concerns in 2011, (202) however the prevalence of patients with diseases and injuries attributable to alcohol use far exceeds this number. (203) Patients with AUD are also more likely to utilize the ED for any reason. (204,205) Patients often do not disclose their alcohol use to physicians, (206) and emergency physicians may fail to recognize patients with problem alcohol use. (207)
      Universal screening of hospitalized patients indicates that 11% of patients have moderate- or high-risk alcohol use, (208) and the US Preventive Services Task Force recommends screening of primary care patients. (209) As many patients with AUD access the ED as their sole point of contact with medical care, screening is also recommended from the ED. (210-212) However, many EDs do not take the first step of screening their patients. (213)
      There are at least five reasons to screen patients for AUD in the ED: 1) informing medical care, such as determining if a patient will be at risk for AWS or have underlying liver disease, which, for example, may be a contraindication to certain medications; 2) identifying the need for intervention, as the first step of the SBIRT model; 3) informing population health, which can lead to care innovations, 4) engaging patients and reducing stigma, particularly if the screening is universal and not biased, and 5) an alcohol-related ED visit (even if not initially disclosed as such) may also be a teachable moment in which the patient is open to change. (214,215)
      There are myriad screening tools available for alcohol misuse. (214) We recommend use of one of three tools given their brevity, sensitivity/specificity profiles, and use in prior ED-based studies:
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        SISQ-Alc (Single-Item Screening Question-Alcohol): This tool is recommended by the National Institute on Alcohol Abuse and Alcoholism. A pre-screening question is asked: “Do you sometimes drink beer, wine, or other alcoholic beverages?” If the answer is “yes”, then the quick screen question is asked: “How many times in the past year have you had X or more drinks in a day?” (X = 5 for men, X = 4 for women). Any response greater than zero indicates a positive screen. (216,217)
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        CAGE: The CAGE questionnaire is an acronym of four questions. Two or more positive answers are a common threshold for detecting alcohol use disorder (218,219), although it is suggested that a positive response to the “eye opener” question is highly concerning for AUD even if the other questions are answered negatively.
      Have you ever felt you should Cut down on your drinking?
      Have people Annoyed you about 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 to get rid of a hangover (Eye opener)?
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        AUDIT-C (Alcohol Use Disorder Identification Test Consumption): (220) This tool was developed by the World Health Organization and consists of three questions with point assignments. Although various thresholds have been suggested, scores ≥3 in women and ≥4 in men are positive:
      How often do you have a drink containing alcohol? Never (0 points), Monthly or less (1 points), Two to four times a month (2 points), Two to three times a week (3 points), Four or more times a week (4 points)
      How many drinks containing alcohol do you have on a typical day when you are drinking? 1 or 2 (0 points), 3 or 4 (1 points), 5 or 6 (2 points), 7 to 9 (3 points), 10 or more (4 points)
      How often do you have six or more drinks on one occasion? Never (0 points), Less than monthly (1 points), Monthly (2 points), Weekly (3 points), Daily or almost daily (4 points)
      Regardless of the screening method used, a positive screen should be followed by a brief intervention and referral to treatment resources (206), as covered in Question #13.
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        Q16. What is the role of the ED in reporting impairment in driving and performing forensic sampling?
      Alcohol-related motor vehicle crashes continue to be a public health problem, with 10,142 deaths from alcohol-impaired driving in 2019, representing 28% of all driving fatalities. (221) As providers of care for individuals who experience motor vehicle collisions and injuries after impaired driving, emergency physicians face a dilemma with competing priorities: the duty to treat the patient confidentially versus protecting the public by reporting dangerous and illegal activity. (222) Most impaired drivers injured in a motor vehicle collision and seen in the ED are neither charged nor convicted of a crime, but as many as 40% had a previous driving under the influence conviction on their record. A small but notable number (2-10%) had a subsequent driving under the influence conviction (223) although enforcement is variable and may depend on jurisdiction. (224)
      States have taken three broad stances on reporting, and do not focus specifically on alcohol. Rather they address broader recognition of impairment that would prevent the driver from operating a vehicle safely, including conditions like epilepsy and Alzheimer's disease. (225-228) A small minority of states (e.g. Oregon) require physicians to report impaired drivers. (229) Other states (e.g. Montana) permit voluntary reporting and provide protections from liability to the physician who reports. (230) In states with no statute related to reporting, the physician must use their own judgment, because reporting may not be a sanctioned reason for breaching confidentiality. Therefore, it is imperative that physicians learn the regulations in whichever states they practice. In states where reporting is voluntarily permitted or there is no statute related to reporting, it is recommended to talk to the patient about the risk of future harm to the patient and others, and report if that risk is deemed to be high. (226) In all situations, EPs should follow their institutionally sanctioned policy or discuss with their risk managers in real time to avoid personal repercussions.
      The American College of Emergency Physicians’ policy statement on reporting of potentially impaired drivers states: “Reporting of potentially impaired drivers should be individualized to the patient's clinical condition and the clear risk posed to the patient and public by continued driving; physicians exercising good faith clinical judgments should have protection from liability for their reporting actions.” (231) The American Medical Association's Code of Medical Ethics emphasizes a patient-centered approach, including “formulate a plan to reduce risks, including options for treatment or therapy if available, changes in driving behavior, or other adjustments.” (232). An exception may be the case of a minor passenger involved in a collision in which the driver was impaired. Reporting this event to child protective services may be required by the state.
      Another special circumstance arises when law enforcement requests BAC sampling for patients in the ED for forensic purposes. (233) If the patient is awake and able to consent, this is generally permitted, and such consent should be clearly documented. If the patient is unconscious or not consenting, despite a court order or warrant, physicians should rely on the policies of their hospital informed by state law. In the absence of specific guidance developed by the hospital legal/risk management team, it is prudent to err on the side of patient autonomy and decline to acquire samples from the unconscious or non-consenting patient.

      2. Conclusion

      Emergency physicians manage patients brought to the department by consequences of acute or chronic alcohol use every shift; in some centers, alcohol-related ED visits comprise a significant proportion of all patients, especially at night. (5,234-236) ED patients with AI and AUD are so prevalent that their treatment is foundational to the practice of emergency medicine, but treatment is rarely complete: The consequences of alcohol use–the broken hand in a drunken fistfight, the alcohol withdrawal seizure, the request for emergency contraception–are readily and routinely managed, but what of their underlying cause?
      In response to the opioid addiction and overdose epidemic, over the past decade many emergency physicians have deepened their expertise in the management of opioid intoxication, opioid withdrawal, and opioid use disorder (OUD). The specialty has expanded its scope of practice in the recognition that an ED visit is a critical and perhaps the only opportunity to move the OUD patient to treatment or harm reduction, to great benefit. (237-239)
      A similar opportunity exists with AUD. Patients who present with dangerous consequences of alcohol use may be screened for problem drinking, patients with clear evidence of problem drinking may be treated with anti-craving medications and linked to community resources such as mutual support organizations, and the sickest AUD patients may be managed with an intensity that correlates to their substantial medical risk. Intense management of the most distressed and debilitated AUD patients includes supplementing nutritional deficiencies, identifying and treating comorbid medical conditions, prevention and optimal treatment of AWS, and the application of enhanced treatment plans that engage wraparound services to address their unmet medical, psychiatric, substance, and social needs.
      There are many barriers to improving ED care of AUD patients. In contrast to opioids, alcohol is legally obtained and its use is not only accepted but widely encouraged. Unlike the opioid overdose that suddenly kills an otherwise healthy person and often leaves a shocked and devastated family in its wake, the harms of alcohol accumulate over decades and insidiously destroy the patient's relationships, leaving the most severely affected patients destitute, alone, and incapable of self-effectuated recovery. Science has not yet provided a medication that protects the AUD patient from cravings, overdose and withdrawal in the way that buprenorphine treats OUD, which is why detoxification and abstinence-based treatment is an acceptable goal for AUD, despite how difficult it is to initiate and maintain.
      The most important obstacle to advancing AUD care, however, may be long-established patterns of practice that exclude it from the emergency physician's purview and encourage an attitude of futility or even irritation. (240) The lessons learned in the successful adoption of ED-initiated treatment of OUD in many departments may provide a path forward. Meaningful and sustained progress relies on local champions implementing best-practice AUD programming through educational efforts, linkages to hospital and community resources, EHR order screens and collective or individual dashboards that track provider and patient outcomes. (241-245) The most powerful force for change is the witnessed effects of successful AUD treatment. Initial efforts can focus on motivated, well-supported patients; as these cases accumulate, enthusiasm for addiction treatment spreads and bigger challenges can be undertaken. We hope that the recommendations presented here will inform these efforts to once again expand our scope of practice to meet our patients’ needs and improve their lives.

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