Alcohol Use Disorder

Alcohol is one of the most commonly used addictive substances in the world. Alcohol use disorder (AUD) is defined as pathologic consumption of alcohol leading to impaired daily functioning. Acute alcohol intoxication presents with impairment in speech and motor functions and can be managed in most cases with supportive care. Withdrawal from chronic alcohol use can have fatal consequences, including delirium and seizures, and is managed with benzodiazepines. Chronic AUD affects almost every part of the human body and has serious impacts on a person’s mental and physical health. Alcohol user disorder can be managed with psychotherapy as well as medications; however, the prognosis is usually poor, with high rates of relapse and complications.

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Overview

Definition

Alcohol use disorder (AUD) is a chronic (> 12 months), problematic pattern of alcohol use causing significant distress.

Classification

There are varying definitions by different organizations for the classification of alcohol consumption.

  • Intoxication: 
    • Recent history of use
    • Symptoms such as stupor, unsteady gait, and slurred speech
  • Withdrawal: 
    • Development of a substance-specific syndrome due to the cessation (or reduction) of substance after heavy and prolonged use
    • Individuals experience physical (nausea, diarrhea, chills, and body aches) and/or psychological symptoms (compulsive or perceived need to use the substance). 
  • Tolerance: 
    • Need to increase the dose of the substance to achieve the same desired effect (diminished effect while using the same amount of the substance)
  • Moderate and at-risk drinking:
    • 1 standard drink contains roughly 14 g of pure alcohol. 
      • 350 mL (12 oz) of regular beer
      • 150 mL (5 oz) of wine
      • 45 mL (1.5 oz) of distilled spirits
    • Moderate consumption:
      • Women: ≤ 3 drinks on any single day and no more than 7 drinks per week
      • Men: ≤ 4 drinks on any single day and no more than 14 drinks per week
    • At-risk consumption:
      • Exceeds moderate drinking limits but without physical/psychological ill effects from AUD
      • Includes heavy-episodic drinking (binge drinking) or consumption of > 60 g of alcohol on a single occasion at least once a month

Epidemiology

  • Prevalence: 7% of adults in the United States have AUD.
  • Lifetime prevalence: 10% in men, 3%–5% in women
  • Caucasians have the highest rate of alcohol use. 
  • Only 8% of those who meet criteria for AUD seek treatment. 
  • 3rd leading preventable cause of death in the United States
  • Risk factors: Studies suggest a strong genetic predisposition to AUD.
  • Early onset of AUD associated with higher risk for developing future complications
  • Older population with AUD at higher risk of severe consequences of alcohol intoxication

Pharmacology

Biochemistry of ethanol metabolism

  • Roughly 90% of alcohol is metabolized by an oxidative process in the liver; the rest is excreted unchanged through the lungs and kidneys.
  • Ethanol is metabolized into acetaldehyde (enzyme: alcohol dehydrogenase).
  • Acetaldehyde is metabolized into acetate (enzyme: acetaldehyde dehydrogenase).
  • In chronic alcohol consumers, enzymes are up-regulated.
  • Individuals of Asian ethnicity have less aldehyde dehydrogenase (gene variation) → accumulation of acetaldehyde → flushing and nausea → less likely to develop AUD
  • Drugs that inhibit ethanol metabolism:
    • Fomepizole (antidote for methanol or ethylene glycol overdose) → inhibits alcohol dehydrogenase
    • Disulfiram → inhibits acetaldehyde dehydrogenase

Other types of alcohol

  • Methanol poisoning: 
    • Some individuals might drink methanol as an alternative to ethanol.
    • Intoxication:
      • Visual blurring
      • Central scotoma
      • Afferent pupillary defect
      • Headaches
      • Mental status changes
      • Nausea
      • Vomiting
      • Anion gap metabolic acidosis
    • Most dangerous complications: vision loss and coma
  • Ethylene glycol poisoning:
    • Some individuals might drink ethylene glycol as an alternative to ethanol.
    • Intoxication: 
      • Flank pain
      • Hematuria
      • Oliguria
      • Anion gap metabolic acidosis
      • Calcium oxalate crystals in urine
      • Kidney damage

Effects on the body

  • Alcohol is a potent CNS depressant: 
    • Activation of inhibitory receptors (GABA, dopamine, serotonin)
    • Inhibition of excitatory receptors (glutamate, voltage-gated calcium channels)
  • Alcohol withdrawal
    • With chronic alcohol use, body increases activity of excitatory receptors (e.g., glutamate) while decreasing activation of inhibitory receptors (e.g., GABA). 
    • Cessation of alcohol use leads to unchecked glutamate activation, presenting as withdrawal.

Clinical Presentation and Diagnosis

Alcohol intoxication

Signs and symptoms of acute alcohol intoxication differ depending on the blood alcohol level. 

Mild intoxication:

  • Talkativeness 
  • Feeling of tranquility and relaxation 
  • Mild feelings of sedation 
  • Impairment in tasks requiring skill and/or fine motor coordination

Moderate intoxication:

  • Uncontrolled eye movements
  • Clumsiness and unsteady gait (positive field sobriety test)
  • Slowed reaction time
  • Slurred speech
  • Impaired judgment
  • Altered perception of the environment
  • Changes in mood, behavior, and personality

Severe intoxication:

  • Nausea and vomiting
  • Dizziness
  • Problems speaking and articulating
  • Double vision
  • Amnesia
  • Delirium
  • Hypothermia, or feeling very cold
  • Lethargy
  • Respiratory depression
  • Seizures
  • Coma
  • Death

Diagnosis: 

  • If possible, obtain a history of alcohol use.
  • Breath alcohol test with breathalyzer
  • Increased blood alcohol level  
  • Liver function tests:
    • AST is 2 × more elevated than ALT. Mnemonic: “take A ShoT for me”
    • Elevation of AST and ALT is < 500 U/L.
    • Gamma glutamyl transpeptidase (GGT) might be elevated and is specific for recent use.
  • Monitor arterial blood gases (ABGs) and anion gap. 
  • Obtain amylase/lipase levels to rule out alcoholic pancreatitis: considered positive if serum lipase is > 3 × normal limits

Alcohol withdrawal

Clinical Institute Withdrawal Assessment for Alcohol Scale (CIWA-A): 

  • Helps in determining the severity of withdrawal
  • Maximum score: 67 
  • Individuals who score < 10 usually do not need additional medication for withdrawal.
  • Assesses the following symptoms, most of which have a maximum score of 7 points:
    • Nausea and vomiting
    • Tactile disturbances
    • Tremor
    • Auditory disturbances
    • Paroxysmal sweating
    • Visual disturbances
    • Anxiety
    • Headache, fullness in head
    • Agitation
    • Orientation and clouding of sensorium (maximum: 4 points)

Diagnosis:

  • Must obtain detailed history of alcohol use, including most recent use
  • Alcohol withdrawal is a lethal condition if not treated. 
  • Complete mental status examination to assess severity 
  • Manifestations vary depending on the time of most recent alcohol consumption.
  • Urine drug screen
  • Blood alcohol level cannot independently predict severity of alcohol withdrawal symptoms. 
Table: Signs and symptoms of alcohol withdrawal
Signs and symptomsMost recent drink
Mild
  • Anxiety, insomnia, and irritability
  • Tremors
  • GI upset (nausea and vomiting)
  • Mild autonomic hyperactivity (diaphoresis, tachycardia, hypertension)
6–24 hours
SeizuresGeneralized tonic clonic seizures (single or multiple)12–48 hours
HallucinationsPredominantly visual (other types can also occur)12–48 hours
Delirium tremens
  • Life-threatening condition
  • CNS changes: confusion, agitation, hallucinations, gross tremors
  • Severe hemodynamic instability: fever, tachycardia, and diaphoresis
> 48 hours

Alcohol use disorder

Screening for misuse of alcohol must be incorporated into routine visits.

  • Initial screening: How many times in the past year have you had > 5 drinks in 1 sitting? 
  • CAGE questionnaire: 
    • Have you felt you should Cut down on your drinking?
    • Have people Annoyed you by criticizing your drinking?
    • Have you felt Guilty about your drinking?
    • Have you felt you needed a drink early in the morning to steady yourself (Eye opener)
  • Alcohol Use Disorders Identification Test (AUDIT):
    • Issued by WHO 
    • Aim: Identify persons whose alcohol consumption has become harmful to their health. 
    • 10-item screening questionnaire
      • 3 questions on amount and frequency of drinking
      • 3 questions on alcohol dependence
      • 4 questions on harmful impact of alcohol consumption
    • Maximum: 4 points per question
      • 1–7 points: suggests low-risk consumption 
      • 8–14 points: suggests hazardous or harmful alcohol consumption
      • ≥ 15 points: suggests alcohol dependence (moderate-to-severe AUD)

Laboratory findings

  • Carbohydrate-deficient transferrin (CDT): 
    • Chronic heavy alcohol consumption elevates CDT
    • Used to distinguish chronic heavy drinkers from light or “social drinkers”
  • RBCs:
    • Total number
    • ↑ MCV and MCH 
    • Changes can be observed after 4–8 weeks of excessive alcohol consumption
    • May be present even with normal folate levels 
  • WBCs
  • Electrolytes:
    • Hypomagnesemia 
    • Hypokalemia 
  • Note: Individuals with increased tolerance may not show alcohol intoxication symptoms even with increased blood alcohol level.

Management and Complications

Alcohol intoxication

  • Primarily supportive
  • Airway, breathing, circulation assessment (ABC): Check regularly.
  • Thiamine (vitamin B₁): 
    • Should be administered to all individuals with alcohol intoxication–induced coma
    • To prevent or treat Wernicke encephalopathy
    • Administer before glucose → giving glucose alone worsens Wernicke encephalopathy
  • Regularly monitor: 
    • Glucose
    • Electrolytes
    • Acid–base status
  • Agitation: Administer benzodiazepines or 1st-generation antipsychotics. 
  • GI evaluation:
    • Not generally indicated in the treatment of alcohol intoxication
    • Might be considered if a significant amount of alcohol was ingested within the preceding 30–60 minutes
    • Options include gastric lavage, induction of emesis, and/or administration of charcoal.

Alcohol withdrawal

  • Setting:
    • Treatment method depends on the severity of withdrawal symptoms. 
    • Otherwise healthy individuals with mild symptoms can be treated in an outpatient setting.
    • Individuals with CIWA-A > 15 or with medical comorbidities should be treated in an inpatient setting.
    • If hemodynamically unstable or nonresponsive to benzodiazepines → intensive care level treatment 
  • Medications:
    • Benzodiazepines (chlordiazepoxide, diazepam, lorazepam) 
      • 1st-line treatment
      • Given orally or IV (in severe cases) 
      • Lorazepam preferred in individuals with liver abnormalities
      • Usually given on as-needed basis in conjunction with CIWA-A
      • Start at a high dosage and then taper or titrate as condition improves
    • Antipsychotics (caution: lower seizure threshold) 
    • Barbiturates: can be used as adjunct to benzodiazepines 
    • Sedatives (dexmedetomidine, propofol): used in severe benzodiazepine-resistant alcohol withdrawal
  • Thiamine (vitamin B₁) and folic acid (vitamin B₉) 
  • Correct electrolyte and fluid abnormalities

Alcohol use disorder

  • 1st step is identification.
  • Followed by intervention, detoxification, and rehabilitation 
  • Relapse prevention: social support, individual and group counseling, self-help groups (Alcoholics Anonymous) 
  • Factors predicting poor prognosis:
    • Preexisting major psychiatric diagnosis (bipolar disorder, schizophrenia)
    • Preexisting personality disorder (antisocial personality disorder) 
    • Other substance use disorder
    • Lack of social stability
Table: 3 most important drugs for the management of alcohol use disorder
MedicationMechanism of actionFeatures
NaltrexoneOpioid receptor antagonists
  • 1st-line option
  • Used in individuals who are still drinking
  • Decreases craving
  • Precipitates withdrawal in individuals with opioid dependence
  • Contraindicated in individuals with liver failure
AcamprosateModulates glutamate transmission
  • 1st-line option
  • Used to prevent relapse in individuals who stopped drinking (after detoxification phase)
  • Decreases craving
  • Suitable for individuals with liver disease
  • Contraindicated in individuals with renal disease
DisulfiramInhibits aldehyde dehydrogenase
  • Results in accumulation of aldehyde, causing severe toxic symptoms → aversive reaction to alcohol
  • Symptoms include flushing, headache, nausea/vomiting, palpitations, shortness of breath.
  • Contraindicated in cardiac disease, pregnancy, and psychosis
  • Indicated for highly motivated individuals

Complications

  • Wernicke encephalopathy (WE): neurologic symptoms caused by thiamine (vitamin B₁) deficiency, which is common in individuals with AUD. Wernicke encephalopathy is marked by 3 features: ataxia (broad-based), oculomotor dysfunction, and encephalopathy (confusion, altered mental status). Treatment is supplementation with thiamine. 
  • Korsakoff syndrome: neurologic disorder that occurs as a result of damage to the medial dorsal nucleus of the thalamus and mammillary bodies. Korsakoff syndrome can occur in combination with WE or separately. Korsakoff syndrome is characterized by confabulation (unconsciously producing fabricated memories about oneself or the world), personality changes, and permanent memory loss (impaired recent memory, anterograde amnesia). Treatment is replacement of thiamine as well as proper hydration and nutrition. 
  • Pancreatitis: One of the top causes of pancreatitis, both acute and chronic, is recurrent alcohol consumption. Alcohol stimulates pancreatic cells to secrete lytic enzymes, producing an inflammatory process and inducing autolysis. Both forms of pancreatitis present with severe abdominal pain, nausea, and vomiting. Treatment involves supportive care as well as cessation of alcohol use. 
  • Alcoholic liver disease: spectrum of liver disorders that occur as a result of excessive alcohol consumption. Alcoholic liver disease can range from fatty liver to liver cirrhosis, and it affects up to 20% of heavy drinkers. Liver function tests and liver biopsy are helpful in establishing the diagnosis. Individuals with alcoholic liver diseases are susceptible to further damage to their liver by infection and drugs. Alcohol abstinence is key at all stages of this disease. 
Long-term effects of ethanol consumption

Important long-term effects resulting from low to high alcohol consumption

Image by BioDigital, edited by Lecturio

Alcohol consumption during pregnancy:

  • Cardiac congenital defects: ventricular and atrial septal defects, tetralogy of Fallot, patent ductus arteriosus 
  • Fetal alcohol syndrome:
    • Marked by 3 specific facial dysmorphisms:
      • Small palpebral fissures
      • Smooth philtrum
      • Thin vermilion border
    • Associated with low height and/or weight, microcephaly, and cognitive and behavioral impairments

Differential Diagnosis

  • Hepatic encephalopathy: altered mental status secondary to severe liver disease. Hepatic encephalopathy often presents with cognitive impairment, ataxia, and findings of chronic liver disease, which are commonly found in those with a history of chronic alcohol use. Even in individuals with severe AUD, a full workup to determine other potential causes of hepatic encephalopathy must be completed. Treatment is supportive.   
  • Sedatives and hypnotics intoxication: Sedative and hypnotic agents include benzodiazepines (BDZs), barbiturates and non-BDZs. Medically, sedative and hypnotic agents are used as anxiolytics, hypnotics, anticonvulsant medications, and muscle relaxants. Symptoms include ataxia and short-term memory loss. History and urine drug screen can distinguish sedative and hypnotic use from AUD; however, alcohol is often taken with sedatives and hypnotics, resulting in synergistic effects. Treatment is supportive, with special attention to airways (aspiration, respiratory failure) and cardiac arrhythmias.

References

  1. Sadock, B. J., Sadock, V. A., Ruiz, P. (2014). Substance use and addictive disorders. Chapter 20 of Kaplan and Sadock’s Synopsis of Psychiatry: Behavioral Sciences/Clinical Psychiatry, 11th ed. Philadelphia: Lippincott Williams & Wilkins, pp. 659–666.
  2. Thompson, A. (2021). Alcohol and drug withdrawal syndromes and their clinical management. DeckerMed Medicine. Retrieved February 16, 2021. doi:10.2310/im.13042
  3. Tetrault, J. (2020). Risky drinking and alcohol use disorder: epidemiology, pathogenesis, clinical manifestations, course, assessment, and diagnosis. UpToDate. Retrieved March 4, 2021 from  https://www.uptodate.com/contents/risky-drinking-and-alcohol-use-disorder-epidemiology-pathogenesis-clinical-manifestations-course-assessment-and-diagnosis 
  4. Sullivan, J. T., Sykora, K., Schneiderman, J., Naranjo, C. A., Sellers, E. M. (1989). Assessment of alcohol withdrawal: the revised Clinical Institute Withdrawal Assessment for Alcohol Scale (CIWA-Ar). British Journal of Addiction 84:1353–1357. https://doi.org/10.1111/j.1360-0443.1989.tb00737.x
  5. Alcohol and its Biomarkers. (2015). Alcohol Biomarkers: An Overview. Chapter 4 of Clinical Aspects and Laboratory Determination. Elsevier, pp. 91–120. https://www.sciencedirect.com/science/article/pii/B9780128003398000043 
  6. National Institute on Alcohol Abuse and Alcoholism. Alcohol Use Disorders Identification Test (AUDIT). Retrieved July 31, 2021, from https://pubs.niaaa.nih.gov/publications/audit.htm 
  7. Babor, T.F., de la Fuente, J.R., Saunders, J., Grant, M. AUDIT: the Alcohol Use Disorders Identification Test: guidelines for use in primary health care. Geneva, Switzerland: World Health Organization, 1992.

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