Alcohol use disorder

Alcohol use disorder (AUD) is a chronic condition in which a pattern of alcohol use leads to significant physical and psychosocial impairment or distress. Not all individuals with heavy alcohol use develop AUD, and not all individuals with AUD have a history of heavy alcohol use. If screening for unhealthy alcohol use suggests AUD, diagnosis is confirmed using the DSM-5 criteria for AUD. An evaluation for alcohol-related complications is recommended at the point of diagnosis for early identification and treatment. The management of AUD depends on whether the patient wishes to reduce their alcohol consumption. For patients who want to reduce their intake or abstain from alcohol, psychotherapy and/or pharmacotherapy for AUD may be utilized. For patients who do not wish or are unable to change their alcohol use, the mainstays of management are harm reduction strategies and regular monitoring for complications of alcohol use.

• Prevalence ^[1]
  • Lifetime prevalence is ∼ 29%.
  • More common in White and Native American individuals
• Peak incidence: 18–25 years ^[2]
• Sex: ♂ > ♀ (2.5:1) ^[3]
• Associated comorbidities ^[1]
  • Personality disorders (most commonly borderline personality disorder)
  • Anxiety, mood disorders (e.g., depression, bipolar disorder), posttraumatic stress disorder, and psychosis
  • Other substance-related disorders (e.g., stimulants, sedatives, cannabis)
  • Attention deficit hyperactivity disorder

Epidemiological data refers to the US, unless otherwise specified.

• Genetic factors
• Neurobiological factors
• Psychosocial factors
  • Family history of AUD ^[4]
  • Environmental influences: e.g., social pressure to consume alcohol, economic disadvantage (e.g., unemployment), stressful life events

References:^[5][6]

General principles

• AUD is normally detected during screening for unhealthy alcohol use.
• The diagnosis is confirmed if DSM-5 criteria for AUD are met.
• For patients who meet the DSM-5 criteria for AUD, perform diagnostic studies for:
  • Laboratory confirmation of alcohol use
  • Evaluation for alcohol-related complications

Liver chemistries and an abdominal ultrasound are recommended for all patients with AUD to assess for alcohol-associated liver disease. ^[7]

DSM-5 diagnostic criteria ^[8][9]

All patients ^[10]

• Urgently treat acute complications of AUD; see: ^[10][11]
  • “Management of alcohol withdrawal”
  • “Management of Wernicke encephalopathy”
  • “Management of alcohol intoxication”
• Provide counseling on AUD.
  • Educate patients on the health complications of alcohol use.
  • Discuss the risk of harm to others; follow state law for mandatory reporting requirements.
• Screen for and treat comorbid psychiatric conditions (e.g., depression). ^[10]
• Assess the patient's insight and motivation to make changes. ^[12]
• Discuss lifestyle modifications to reduce the risk of complications of alcohol use.
  • Encourage healthy eating. ^[13]
    • Refer to food banks and other nutritional support programs if needed.
    • Consider multivitamins containing vitamin B₁ (thiamine), vitamin B₆ (pyridoxine), and folic acid. ^[13][14]
  • Discuss smoking cessation. ^[15][16]
• Encourage the patient to involve individuals (e.g., family, friends) who can provide support. ^[10][11][17]

Friends and family of patients with AUD can experience significant distress; offer support, including referral to community support groups for family and friends such as Al-Anon. ^[18]

Patients who want treatment for AUD

• Create and document a plan based on the patient's goals, using shared decision-making. ^[10]
  • Refer for psychotherapy, e.g., cognitive behavioral therapy and family therapy. ^[17][19]
  • Provide resources for community support groups, e.g., Alcoholics Anonymous. ^[12][20]
  • Patients with moderate to severe AUD: Offer medication-assisted treatment (see “Pharmacotherapy for AUD”).
• Identify potential triggers that can cause relapse. ^[12][17]
• Schedule follow-up visits to monitor for clinical improvement and treatment adherence; adjust management as necessary. ^[10][11]

For patients with a court-mandated treatment plan, ascertain the testing and reporting requirements. ^[10]

Patients who do not want treatment for AUD

• Use patient-centered care.
• Discuss harm mitigation strategies.
• Advise patients they can return at any point to start treatment.
• Regularly review patients for complications of alcohol use.

Psychosocial therapy can improve treatment adherence and outcomes and should be offered to all patients. ^[11]

Indications ^[10][17][20]

• Individuals ; with moderate to severe AUD who want to decrease the amount of alcohol consumed or abstain from use ^[10][17][21]
• Consider on a case-by-case basis for patients with mild AUD who have either: ^[10]
  • A preference for pharmacotherapy
  • An insufficient response to nonpharmacological treatments

Choice of medication

Approach

• Obtain baseline laboratory studies to ascertain suitable medications.
  • CBC
  • Liver chemistries ^[10]
  • Renal function ^[10][17]
  • Urine toxicology ^[10]
  • Pregnancy test ^[22]
• Determine whether the patient is abstaining, or plans to abstain, from alcohol use. ^[20]
• Screen for comorbidities, e.g., opioid use disorder (OUD). ^[10]
• Inquire about risk factors for poor adherence.
• Check if patients receiving court-mandated treatment require a particular pharmacotherapy. ^[23]

Give patients a wallet card with details of their medication-assisted treatment to show medical personnel in the event of an emergency or if a procedure is needed (e.g., dental surgery). ^[10][11]

First-line options ^[10][20]

• Naltrexone and acamprosate are preferred. ^[10][20]
• Both medications reduce cravings and can be used for patients who: ^[10][17]
  • Continue to drink alcohol
  • Use other substances recreationally
• Interactions with other medications are minimal. ^[17]

Naltrexone

• Naltrexone can be given orally or IM. ^[10][11][17]
• Mechanism of action: central μ-opioid receptor antagonist
• Considerations
  • Check liver chemistries before and after starting naltrexone because of the risk of hepatic dysfunction in patients with liver disease. ^[10]
  • Advise patients to abstain from opioid use 7–14 days before starting naltrexone. ^[10]

Acamprosate ^[10][17]

• Acamprosate requires frequent oral dosing to be effective. ^[10][17]
• Mechanism of action: may modulate central glutamate receptors ^[10][17]
• Considerations: Check serum creatinine before initiating treatment. ^[10][17]

Avoid concurrent use of opioids and naltrexone because of the risk of opioid withdrawal. ^[10]

Alternative options

Alternative medications may be considered, especially for patients who do not improve with first-line options. ^[10]

Disulfiram

• Disulfiram is given orally once daily. ^[17]
• Deters patients from drinking alcohol by precipitating a disulfiram-alcohol reaction; symptoms include ; : ^[24][25][26]
  • Cutaneous vasodilation
  • Headache
  • Nausea and vomiting
  • Tachycardia and other cardiac arrhythmias
  • Hypotension
  • Seizures
  • Breathing difficulties (including bronchospasm and dyspnea)
• To prevent disulfiram-alcohol reactions: ^[17]
  • Ensure patients have been abstinent for at least 12 hours before starting disulfiram. ^[20]
    • Advise patients to maintain abstinence during treatment and for 14 days after. ^[17]
• Considerations
  • Check liver transaminases before and up to 2 weeks after starting treatment; although rare, a rise in enzyme levels can occur. ^[11]
  • Consider obtaining a baseline ECG for at-risk individuals (e.g., those with a history of cardiac disease). ^[11]
  • Do not prescribe if patients have recently received metronidazole, because of the risk of psychosis. ^[10]
  • Not recommended for initiation in the emergency department because monitoring is required. ^[14]

During treatment with disulfiram, advise alcohol abstinence, avoidance of alcohol-containing products (e.g., some mouthwashes), and certain medications such as metronidazole. ^[10][14][17]

Topiramate

• Topiramate (off-label) is given orally and requires slow titration. ^[10][20]
• Reduces cravings (and can assist in weight loss)

Gabapentin

• Gabapentin (off-label) is given orally and requires slow titration. ^[10]
• Reduces cravings and may help with comorbid anxiety ^[10][27]
• Has the potential for misuse; monitor patients carefully. ^[10][28]

Monitoring

• Follow up regularly to assess for treatment adherence, changes in alcohol use, and cravings. ^[11][12]
• Monitor for signs of improvement, e.g.: ^[11]
  • Mood: e.g., less irritability, better sleep hygiene
  • Social interactions: e.g., participation in recreational activities
  • Better performance at school or work
  • No new legal violations
• Consider using serial measurements of GGT and carbohydrate deficient transferrin to monitor progress. ^[29]
• Regularly perform evaluations for alcohol-related complications. ^[7]

Patients started on treatment for AUD in the emergency department should be followed up within 48 hours of discharge. ^[25]

Adjusting management

• If patients struggles with treatment adherence or relapse, consider the following: ^[11]
  • Increase the frequency of follow-up visits to provide counseling and support.
  • Adjust treatment as necessary.
  • Consider referral to a special treatment program. ^[12]
• If patients on pharmacotherapy for AUD develop adverse effects or contraindications, consider : ^[17]
  • Changing the medication dosage
  • Switching to a different medication ^[17]

Discontinuing pharmacotherapy

• The ideal treatment duration is unclear and should be agreed upon using shared decision-making. ^[11][17]
• Consider the following when discussing whether treatment can be stopped: ^[11]
  • Improvement in cravings and maintenance of abstinence
  • The patient feels ready to stop treatment and is engaged in a community support group.
  • Development of any contraindications to pharmacotherapy
• Tapering medications is not necessary.
• Advise patients that adverse effects and drug interactions may occur a few weeks after discontinuing disulfiram and IM naltrexone. ^[17]

See also “Complications of alcohol use.”

Alcoholic ketoacidosis ^[25]

• Definition: elevated anion gap metabolic acidosis due to increased production of ketone bodies with normal or low glucose levels resulting from the combined effects of alcohol and starvation on glucose metabolism
• Etiology
  • Most commonly occurs in malnourished individuals with AUD
  • Associated with recent episodes of binge drinking complicated by poor food intake, dehydration, and vomiting
• Onset: typically occurs 1–3 days after binge drinking
• Pathophysiology: accumulation of ketone bodies (see ketogenesis) as a result of:
  • Depleted glycogen stores in the liver (malnutrition/decreased carbohydrate intake)
  • Increased lipolysis and free fatty acid release
    • Decreased energy intake (e.g., starvation) → decreased insulin secretion and excess secretion of glucagon, catecholamines, and cortisol
    • Increased NADH:NAD⁺ ratio: regular heavy alcohol use ; → impaired hepatic gluconeogenesis → hypoglycemia → decreased insulin secretion
  • Volume depletion (e.g., vomiting, poor oral fluid intake) → impaired renal perfusion → decreased ability to excrete ketone bodies
• Clinical features of alcoholic ketosis
  • Nausea, vomiting, and abdominal pain
  • Tachypnea
  • Features of dehydration and electrolyte imbalance (e.g., hyponatremia, hypokalemia, hypophosphatemia), including hypotension and altered mental status
  • Features of alcohol withdrawal: e.g., tremors, seizures, tachycardia
• Diagnostics
  • Arterial blood gas analysis: elevated anion gap metabolic acidosis
  • Ketonemia (acetoacetate, β-hydroxybutyrate, acetone in blood) and ketonuria
  • Blood glucose: low, normal, or only moderately increased
  • Blood ethanol: not detectable or low ^[30]
• Treatment
  • Initially: parenteral administration of thiamine to prevent Wernicke encephalopathy
  • Followed by: IV fluid therapy with 5% dextrose in 0.9% saline
  • Correction of electrolyte imbalances
  • Treatment of alcohol withdrawal and complications of alcohol use
• Prognosis: The condition is reversible with appropriate treatment.

In contrast to diabetic ketoacidosis, blood glucose levels are normal or low in alcoholic ketoacidosis.

We list the most important complications. The selection is not exhaustive.

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