Diagnosis Sheet
Substance-Related and Addictive Disorders DSM-5-TR 303.90/305.00 | ICD-10-CM F10.10, F10.20
Alcohol Use Disorder
Compulsive alcohol use with impaired control, tolerance, and withdrawal that persists despite mounting medical and social harm.
Lifetime prevalence~29% (US adults)
Typical onsetLate teens to mid-20s
Sex ratio~1.7:1 male:female
CourseChronic, relapsing-remitting
Clinical picture
- Escalating quantity and frequency with failed cutdown attempts, morning drinking, and blackouts that patients reframe as ordinary social use.
- Tolerance shows as high-dose functioning; withdrawal emerges 6-24 hours after the last drink as tremor, sweating, tachycardia, nausea, and anxiety.
- Craving is cue-driven and situational, intensifying with stress, negative affect, and exposure to drinking environments or social pressure.
- Physical signs include hypertension, elevated GGT and MCV, spider angiomata, palmar erythema, gastritis, peripheral neuropathy, and unexplained trauma.
- Interpersonal fallout precedes medical presentation: absenteeism, DUIs, marital conflict, and role failure often bring the patient in before symptoms do.
- Comorbid insomnia, depressed mood, and anxiety typically improve substantially within 2 to 4 weeks of sustained abstinence.
Criteria snapshot
- Requires at least 2 of 11 problematic use indicators within 12 months, spanning impaired control, social impairment, risky use, and pharmacologic criteria.
- Severity is graded by symptom count: mild 2-3, moderate 4-5, and severe 6 or more, replacing the older abuse and dependence split.
- Craving, a strong desire or urge to drink, was added to the criterion set, while recurrent legal problems were removed from it.
- Tolerance and withdrawal are not counted when alcohol is taken solely under appropriate medical supervision, a rare situation for alcohol.
- Specifiers cover early remission (3 to under 12 months), sustained remission (12 months or more), and being in a controlled environment.
Neurobiology
- Alcohol potentiates GABA-A inhibition and blocks NMDA glutamate receptors; chronic use reverses this balance, driving withdrawal hyperexcitability.
- Mesolimbic dopamine release in the nucleus accumbens, amplified by endogenous opioid signaling at mu receptors, underlies reinforcement and craving.
- Repeated withdrawals kindle progressively severe episodes, raising seizure and delirium tremens risk with each successive detoxification.
- Allostatic shift recruits extended amygdala CRF and dynorphin systems, converting drinking from reward-seeking to negative-reinforcement relief.
- Heritability is roughly 50%, and ADH1B and ALDH2 variants that produce flushing are strongly protective in East Asian populations.
- Chronic use causes thiamine depletion with Wernicke encephalopathy risk, cerebellar atrophy, hepatic steatosis to cirrhosis, and cortical volume loss.
Psychology
- Negative reinforcement dominates late-stage use: drinking relieves withdrawal dysphoria, anxiety, and insomnia rather than producing euphoria.
- Alcohol expectancies for tension reduction and social ease, learned early from family and media, predict initiation and heavier adolescent consumption.
- Alcohol myopia narrows attention to immediate cues, impairing consideration of long-term consequences and inflating disinhibited behavior.
- Shame-based self-concept and stigma drive concealment, delayed help-seeking, and abstinence violation effects after a single lapse.
- Classical conditioning links people, places, and moods to craving, and cue reactivity persists for many months into abstinence.
Differential & comorbidity
- Substance-induced depressive and anxiety disorders resolve within weeks of abstinence, while independent disorders persist and need their own treatment.
- Screen with AUDIT-C or AUDIT, and differentiate from unhealthy drinking without disorder, bipolar disorder, and PTSD-driven self-medication.
- Comorbidity includes mood and anxiety disorders, PTSD, ADHD, tobacco use disorder, and other sedatives; polysubstance use raises overdose risk.
- Suicide risk is elevated roughly two to threefold, and acute intoxication increases impulsive attempts and the lethality of chosen means.
- Assess withdrawal severity with CIWA-Ar; scores above 8 to 10 warrant medication, and prior seizures or delirium tremens indicate inpatient detox.
Pharmacologic treatment
- Naltrexone 50 mg/day oral or 380 mg IM monthly is first-line, reducing heavy drinking days; check LFTs and avoid with any opioid agonist.
- Acamprosate 666 mg TID supports abstinence maintenance and is preferred in hepatic impairment; reduce the dose for CrCl of 30 to 50 mL/min.
- Disulfiram 250 mg/day works only with supervised dosing and high motivation, and the aversive reaction can itself be medically dangerous.
- Off-label topiramate 200-300 mg/day and gabapentin 900-1800 mg/day have supporting trial data, especially with comorbid anxiety or insomnia.
- Withdrawal management uses symptom-triggered lorazepam or chlordiazepoxide plus thiamine 100 mg given before any glucose load.
Psychotherapy
- Motivational interviewing and brief interventions of 1 to 4 sessions reliably reduce consumption in risky drinkers who are not yet dependent.
- CBT with relapse prevention over 12 to 16 sessions targets high-risk situations, coping skills, and abstinence violation cognitions.
- Contingency management yields the largest short-term effect sizes, and the community reinforcement approach restructures competing reinforcers.
- Behavioral couples therapy improves both drinking outcomes and relationship functioning more than individual therapy delivered alone.
- Twelve-step facilitation produces abstinence rates equal to or better than CBT and durably increases mutual-help group engagement.
Adjunct options
- AA and secular alternatives such as SMART Recovery provide free, sustained recovery capital, and active linkage clearly beats passive referral.
- Use ASAM criteria to match level of care, from outpatient counseling through medically managed inpatient withdrawal.
- Monitor with AUDIT, timeline followback, and biomarkers such as phosphatidylethanol, carbohydrate-deficient transferrin, and GGT.
- Treat comorbid insomnia behaviorally with CBT-I rather than sedatives, and correct thiamine, folate, and magnesium deficits.
- Screen for hepatitis C, vaccinate against hepatitis A and B, and coordinate hepatology follow-up for patients with advanced liver disease.
Clinical pearls
- Two or more of 11 criteria in 12 months makes the diagnosis; the count sets severity.
- Give thiamine before any glucose load to avoid precipitating Wernicke encephalopathy.
- Naltrexone works even while the patient is still drinking; abstinence is not required.
References
- American Psychiatric Association. (2018). Practice guideline for the pharmacological treatment of patients with alcohol use disorder. https://www.psychiatry.org/psychiatrists/practice/clinical-practice-guidelines
- American Psychiatric Association. (2022). Diagnostic and statistical manual of mental disorders (5th ed., text rev.). https://doi.org/10.1176/appi.books.9780890425787
- Jonas, D. E., Amick, H. R., Feltner, C., Bobashev, G., Thomas, K., Wines, R., Kim, M. M., Shanahan, E., Gass, C. E., Rowe, C. J., & Garbutt, J. C. (2014). Pharmacotherapy for adults with alcohol use disorders in outpatient settings: A systematic review and meta-analysis. JAMA, 311(18), 1889-1900. https://doi.org/10.1001/jama.2014.3628
- National Institute on Alcohol Abuse and Alcoholism. (n.d.). Understanding alcohol use disorder. National Institutes of Health. https://www.niaaa.nih.gov/publications/brochures-and-fact-sheets/understanding-alcohol-use-disorder
- Sadock, B. J., Sadock, V. A., & Ruiz, P. (2021). Kaplan & Sadock's synopsis of psychiatry (12th ed.). Wolters Kluwer.
- Stahl, S. M. (2021). Stahl's essential psychopharmacology (5th ed.). Cambridge University Press.
- U.S. Department of Veterans Affairs & U.S. Department of Defense. (2021). VA/DoD clinical practice guideline for the management of substance use disorders. https://www.healthquality.va.gov/guidelines/MH/sud/