Alcohol use disorder

Alcohol use disorder (AUD) is the most examinable substance-use presentation in psychiatry fellowship. Examiners punish three failures: thin nosology (DSM versus ICD), incomplete withdrawal/Wernicke emergencies, and vague pharmacology without agent, dose, route, monitoring, and contraindications.[4][6][12]

Overview and definition

AUD is a maladaptive pattern of alcohol use leading to clinically significant impairment or distress. DSM-5-TR collapsed older abuse/dependence categories into a single spectrum disorder with eleven criteria spanning impaired control, social impairment, risky use, and pharmacological features (tolerance, withdrawal).[6][8][12]

ICD-11 keeps a more traditional public-health ladder: hazardous alcohol use, harmful pattern of use, and alcohol dependence (impaired control, alcohol taking precedence, physiological features). In viva answers, name the system you are using — examiners mark candidates who mix severity counts with ICD dependence language carelessly.[6][12]

Classification — DSM-5-TR and ICD-11

DSM-5-TR (reproduce for exam)

At least two of eleven criteria within a twelve-month period, with severity:[8][12]

[8] [12]

Domains (paraphrased accurately for teaching): 1. Impaired control — larger/longer use; desire/unsuccessful cut-down; time spent; craving; 2. Social impairment — role failure; continued use despite interpersonal problems; activities given up; 3. Risky use — hazardous situations; continued use despite physical/psychological harm; 4. Pharmacological — tolerance; withdrawal (or alcohol to relieve/avoid withdrawal).[8][12]

Specifiers include early/sustained remission and controlled environment when relevant.[12]

ICD-11 contrast (high-yield divergence)

• Hazardous use — risk-elevating pattern without established disorder.
• Harmful pattern of use — alcohol causing physical or mental harm without full dependence.
• Alcohol dependence — strong internal drive, impaired control, prioritisation, persistence despite harm, often with tolerance/withdrawal.

[6] [12]

Related coded states examiners still ask: alcohol intoxication, alcohol withdrawal (with/without perceptual disturbance), alcohol-induced mental disorders, and amnestic syndromes (Korsakoff).[12]

Epidemiology and risk factors

[8] [6]

In NESARC-III, twelve-month DSM-5 AUD prevalence was approximately 13.9% and lifetime approximately 29.1% among US adults, with higher rates in men, younger adults, and substantial comorbidity with other mental and substance disorders.[8] Global patterns vary by culture, policy, and availability, but the clinical message is consistent: AUD is common, undertreated, and a major driver of injury, liver disease, cancer risk, cardiovascular harm, suicide, and health-system use.[6][12]

Risk amplifiers: family history and substantial heritability; early onset of heavy drinking; trauma and adverse childhood experiences; other substance use; mood/anxiety/psychotic disorders; social isolation; high availability and low price environments.[6][12] Genetic variants affecting alcohol metabolism (for example ALDH2*2-associated flushing in East Asian populations) modulate risk and can shape culturally informed counselling.[12]

Pathophysiology

Intoxication/reinforcement. Alcohol facilitates GABA-A signalling and inhibits NMDA glutamatergic transmission; mesolimbic dopamine contributes to rewarding and habit-forming effects.[12]

Neuroadaptation. With sustained heavy use, GABAergic tone is relatively downregulated and glutamatergic/NMDA systems upregulated. Abrupt cessation produces CNS hyperexcitability — tremor, anxiety, seizures, autonomic surge, and risk of delirium tremens.[9][12]

Thiamine and Wernicke. Poor intake, gastrointestinal losses, reduced hepatic storage, and increased metabolic demand deplete thiamine (vitamin B1). Critical regions (mammillary bodies, medial thalamus, periaqueductal grey) fail oxidative metabolism → Wernicke encephalopathy; incomplete recovery yields Korsakoff amnestic syndrome.[3][11][17]

Clinical presentation

Use history that examiners want

• Quantity, frequency, binge pattern, beverage type, time of last drink
• Previous withdrawal severity, seizures, DT, detox failures
• Morning drinking, relief drinking, blackouts, drink-driving, occupational impact
• Other substances (especially benzodiazepines — dual withdrawal)
• Psychiatric comorbidity and suicide attempts

[6] [12]

Intoxication

Disinhibition, impaired judgement, ataxia, dysarthria, nystagmus, progressive CNS and respiratory depression at high levels. Trauma and aspiration risk are part of the assessment, not afterthoughts.[12]

Withdrawal spectrum and timing

Hallucinosis without full delirium can occur earlier. DT mortality is material if untreated — this is a medical emergency.[9][12]

Atypical presentations

Older adults with falls, confusion, or "failure to thrive"; perioperative patients whose dependence is unrecognised until day two; women and some cultural groups under-detected by quantity-focused history; dual diagnosis masking primary mood/psychosis timelines.[6][12]

Differential diagnosis

[3] [9] [12] [17]

Also separate: benzodiazepine or GHB withdrawal; primary anxiety/panic; primary psychotic disorders versus alcohol-induced psychotic disorder; post-ictal states; head injury; thyrotoxicosis/sepsis mimics of autonomic surge.[9][12]

Clinical and bedside assessment

1. ABCDE, vitals, glucose, SpO2; trauma survey if intoxicated.[12]
2. Structured alcohol and substance history + psychiatric + medical + forensic/social.[6][12]
3. AUDIT (10 items) for screening/severity signal in clinic and ED interfaces.[16]
4. CIWA-Ar for symptomatic withdrawal severity when the patient can be assessed reliably.[1]
5. MSE: intoxication versus withdrawal versus delirium; hallucinations; insight; capacity.[12]
6. Risk: suicide, violence, vulnerability, driving, childcare, occupational safety.[6][12]
7. Motivation and goals (abstinence versus reduction) — honest negotiation, not moralising.[6]
8. Collateral and pharmacy/GP records when history is incomplete.[12]
9. Legal status if incapacity or acute risk requires jurisdiction-specific mental health or guardianship pathways — do not invent section numbers across countries.[6][12]

AUDIT (what it is)

The WHO Alcohol Use Disorders Identification Test is a ten-item screen developed for early detection of hazardous and harmful drinking. Interpret thresholds using local protocol cut-points; higher scores increase the probability of dependence-range problems and need for full assessment.[16]

CIWA-Ar (reproduce accurately)

The revised Clinical Institute Withdrawal Assessment for Alcohol (CIWA-Ar) rates ten items (nausea/vomiting, tremor, paroxysmal sweats, anxiety, agitation, tactile/auditory/visual disturbances, headache, orientation and clouding of sensorium). Maximum total 67.[1] Local protocols map score bands to PRN benzodiazepine dosing and reassessment frequency (commonly every 1–2 hours in active withdrawal).[1][18]

Limitations: not validated as a stand-alone tool in severe medical illness, inability to communicate, or concurrent delirium of other cause — treat the physiology and do not withhold benzos solely because a score cannot be completed.[1][9]

Investigations

There is no single lab that diagnoses AUD. Labs risk-stratify and find reversible drivers of delirium.[12]

Do not delay parenteral thiamine for a thiamine level when Wernicke is clinically plausible.[11][13][17]

Management — resuscitation and withdrawal

Immediate priorities

1. Airway/breathing/circulation, recovery position if vomiting/intoxicated, aspiration precautions.[9][12]
2. Thiamine early — parenteral when malnourished, confused, ataxic, oculomotor signs, or otherwise high Wernicke risk. Classic teaching: do not give glucose without thiamine cover in this population; if hypoglycaemia requires glucose, give thiamine concurrently/promptly.[11][13][17]
3. Benzodiazepines — first-line for alcohol withdrawal (meta-analytic and guideline support).[9][19]
4. Correct magnesium, potassium, phosphate and dehydration carefully.[9][12]
5. Seizure management: protect airway, benzodiazepines; investigate alternative causes if first seizure or focal features.[9]

Benzodiazepine strategy

Symptom-triggered regimens guided by CIWA-Ar reduce total benzodiazepine exposure and treatment duration compared with fixed schedules in appropriate monitored settings, without loss of efficacy for preventing severe withdrawal when protocols are followed.[18][9] Fixed schedules remain useful when CIWA-Ar is impractical or risk is very high.

Agent choice (exam standard): Diazepam — long-acting; common front-line oral/IV agent where liver function allows; symptom-triggered PRN dosing per local CIWA-Ar band (example teaching band: treat when CIWA-Ar is elevated, often from around 8–10 upward depending on protocol). Lorazepam — preferred when advanced liver disease, elderly, or risk of diazepam accumulation; typical intermittent IV/oral PRN doses in protocols (commonly 1–2 mg increments, titrated). Chlordiazepoxide — still used in some UK protocols as fixed or triggered regimens.[9][18][19]

Always cite local protocol for exact milligram bands; fellowship answers must still name agents and the symptom-triggered principle.[9][18]

Setting of detox

Inpatient/supervised if: history of withdrawal seizures or DT; significant medical or psychiatric comorbidity; pregnancy; unstable housing or lack of support; polydrug dependence; failed ambulatory attempts; high suicide risk.[4][6][12]

Ambulatory detox only with reliable supports, daily review capacity, lower predicted severity, and clear escalation plan.[6][12]

Management — definitive and stepwise (post-detox)

Pharmacotherapy for relapse prevention

APA pharmacological guidance supports offering evidence-based medications; naltrexone and acamprosate have the strongest overall evidence base for reducing return to heavy drinking or supporting abstinence depending on goal and population.[4][5][7]

Naltrexone

• Mechanism: mu-opioid receptor antagonist; reduces alcohol reward/heavy drinking days.[10][5]
• Oral dose (standard teaching): 50 mg once daily (some start 25 mg for a few days if tolerability concern).[4][7][10]
• Long-acting injectable naltrexone (XR-NTX): monthly IM formulation improves adherence for selected patients (classic trial evidence for efficacy/tolerability).[15]
• Prerequisites: opioid-free (risk of precipitated withdrawal); counsel that opioids will not work as usual in emergency analgesia — medical alert; baseline and follow-up LFTs; avoid in acute hepatitis/liver failure per product guidance.[4][7]
• COMBINE: naltrexone with medical management improved outcomes; interpret alongside behavioural platforms.[2]

Acamprosate

• Mechanism: modulates glutamatergic (NMDA-related) hyperactivity; supports abstinence maintenance after detox.[14][5]
• Dose (standard adult with normal renal function): 666 mg three times daily (two 333 mg tablets TDS).[4][7][14]
• Renal impairment: dose-reduce or avoid in severe renal failure per product information — always check eGFR before prescribing.[4][14]
• Start: typically after detoxification when abstinence is established; does not treat acute withdrawal.[4][14]
• COMBINE nuance: acamprosate did not show expected benefit in COMBINE’s specific design — quote the trial carefully rather than over-generalising that acamprosate "does not work". Meta-analyses still support efficacy in appropriate abstinence-oriented samples.[2][5][14]

Disulfiram

• Mechanism: aldehyde dehydrogenase inhibition → aversive acetaldehyde reaction with alcohol (flushing, nausea, tachycardia, hypotension risk).[20]
• Dose: commonly 200–250 mg daily after specialist assessment (regional product strengths differ; UK often discusses 200 mg, US product teaching often 250 mg).[4][20]
• Mandatory: informed consent; supervised dosing when possible; absolute alcohol education (including some mouthwashes/foods); not for impulsive patients or those likely to drink through the reaction; caution/contraindication in significant cardiac disease, psychosis, and when adherence/supervision impossible.[4][20]
• Evidence is strongest in supervised contexts; unsupervised use underperforms.[20][7]

Other agents (know, do not over-claim)

Baclofen and nalmefene (marketed in some European settings for reduction) appear in stems as controversies or regional options — not universal first-line replacements for naltrexone/acamprosate in ANZ teaching. State evidence uncertainty and local approval status.[4][6][7]

Psychosocial interventions

Medication is adjunctive, not a complete treatment. Evidence-aligned packages include:[2][6][12]

• Motivational enhancement therapy (MET) / motivational interviewing
• Cognitive behavioural therapy for alcohol (urge surfing, high-risk planning, cognitive restructuring)
• Contingency management where available
• Twelve-step facilitation and mutual aid (AA, SMART Recovery) — offer, do not coerce ideology
• Residential rehabilitation for high severity, unstable environment, or failed community treatment
• Family interventions and social work (housing, employment, legal)
• Brief intervention for hazardous use that does not meet full dependence thresholds

[6] [12]

Specific subtypes and scenarios

Alcohol withdrawal seizures

Usually generalised tonic-clonic within the 12–48 hour window; prior seizures predict recurrence. Benzodiazepines are the cornerstone; chronic antiepileptic drugs are not routine substitutes for adequate withdrawal management unless another epilepsy diagnosis exists.[9][19]

Delirium tremens

Fluctuating consciousness, severe autonomic hyperactivity, vivid hallucinations, global disturbance — typically day 2–3 after cessation. High-dose benzodiazepines, medical/ICU support, thiamine, electrolytes, infection and metabolic work-up.[9][12]

Wernicke encephalopathy and Korsakoff

Caine operational criteria (any two of four) improve identification over waiting for the incomplete classic triad of ophthalmoplegia, ataxia, and confusion:[3]

1. Dietary deficiency / malnutrition
2. Oculomotor abnormalities
3. Cerebellar dysfunction
4. Altered mental state or mild memory impairment

[3]

Treatment intensity: EFNS and RCP-linked emergency guidance support high-dose parenteral thiamine for suspected Wernicke (commonly taught regimens use 500 mg IV three times daily for several days, then step-down — follow local product-compatible protocol and EFNS/RCP sources).[13][17] Oral thiamine alone is inadequate for established Wernicke. Prevention doses for lower-risk admitted drinkers are lower but still systematic — local protocols apply.[11][13][17]

Korsakoff syndrome: dense anterograde amnesia, confabulation variable, poor insight — rehabilitation and long-term support after the acute thiamine emergency.[3][11]

Alcohol-induced psychotic disorder / hallucinosis

Hallucinations (often auditory) with clearer sensorium than DT; still exclude medical delirium. Manage withdrawal physiology and safety; antipsychotic short-term if needed after medical stabilisation; reassess for primary psychosis after sustained abstinence.[12]

Dual diagnosis pointer

Depression, anxiety, PTSD, bipolar disorder, schizophrenia, and personality disorders commonly co-occur. Integrated care outperforms sequential "treat one then the other" in principle — see the dual-diagnosis topic for full models. Acute safety and withdrawal come first; restart or adjust psychotropics with hepatic status and interaction awareness.[6][12]

Liver disease and transplant interface

Prefer lorazepam over long-acting diazepam when cirrhosis risks accumulation. Avoid disulfiram in significant liver disease. Naltrexone needs careful LFT review. Addiction psychiatry input improves transplant candidacy processes in specialised centres.[4][12]

Complications and pitfalls

• Missing Wernicke because the classic triad is incomplete.[3][17]
• Underdosing benzodiazepines → seizure/DT; oversedation → aspiration and respiratory failure.[9][19]
• Glucose without thiamine cover in malnutrition.[13][17]
• Naltrexone started on ongoing opioids.[4]
• Unsupervised disulfiram and covert drinking.[20]
• Calling DT "behavioural" and under-treating medically.[9]
• Ignoring suicide risk in early recovery and intoxication.[6][12]
• Fixed belief that one medication works for all goals (reduction vs abstinence phenotypes differ).[5][7]

Prognosis and disposition

AUD is typically relapsing–remitting. Many people improve substantially with engagement; severity, comorbidity, social capital, and treatment adherence predict course.[6][12] After detox, default disposition packages medication plus psychosocial follow-up within days to weeks, not "discharge and good luck". Step up to residential or intensive outpatient when community care fails or risk remains high.[4][6]

Special populations

Pregnancy. Alcohol is teratogenic (FASD spectrum). Detox is specialist (obstetric + addiction); avoid disulfiram; individualise other pharmacotherapy with extreme caution; prioritise psychosocial support and safeguarding.[4][12]

Older adults. Lower consumption may still be hazardous; falls, cognitive impairment, polypharmacy, and atypical withdrawal presentations.[6][12]

Adolescents. Family-based interventions; developmental framing; careful off-label pharmacology thresholds.[6][12]

Indigenous and culturally diverse communities. Stigma, access, and historical trauma shape engagement — culturally safe care and local services matter as much as the script.[12]

Intellectual disability. Collateral history, simplified interventions, capacity assessment for treatment decisions.[6][12]

Evidence, guidelines, and regional differences

Landmark anchors to name in viva: Volpicelli naltrexone; COMBINE; Jonas outpatient pharmacotherapy meta-analysis; Maisel naltrexone/acamprosate meta-analysis; Rösner acamprosate Cochrane; Sullivan CIWA-Ar; Caine Wernicke criteria; Galvin EFNS Wernicke guideline; Daeppen/Saitz symptom-triggered detox trials.[1][2][3][5][7][10][14][17][18]

Exam pearls

• Last drink time drives the seizure/DT prediction window.[9]
• DSM severity = count of criteria; ICD-11 dependence = pattern features — do not conflate.[8][12]
• CIWA-Ar max 67; ten items; symptom-triggered benzos.[1]
• Caine: any two of four → treat as Wernicke.[3]
• Naltrexone 50 mg daily; acamprosate 666 mg TDS; disulfiram supervised 200–250 mg range.[4][7][20]
• DT is medical, not "just psych".[9]
• Dual diagnosis: stabilise withdrawal/safety, then integrated care — do not dump one disorder for the other.[6][12]

Self-test: 54-year-old day-2 post-admission

A man with decades of heavy drinking, last drink 48 hours ago, becomes agitated, sweaty, HR 128, BP 178/100, disoriented, pulling at lines, describing insects on the walls. CIWA-Ar is high. What is the working diagnosis and first-line treatment ladder?[9]

Answer. Working diagnosis: delirium tremens (timing, autonomic hyperactivity, fluctuating sensorium, hallucinations). Immediate: medical emergency pathway — IV access, monitoring, high-dose benzodiazepines titrated to control agitation/autonomics, parenteral thiamine, electrolytes (Mg/K/phosphate), exclude infection/metabolic/head injury, ICU/HDU if refractory. Not antipsychotics-first. Not "behavioural specialling" alone.[9][13][19]

References

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2. [2]Anton RF, O'Malley SS, Ciraulo DA, et al. Combined pharmacotherapies and behavioral interventions for alcohol dependence: the COMBINE study: a randomized controlled trial. JAMA, 2006.PMID 16670409
3. [3]Caine D, Halliday GM, Kril JJ, et al. Operational criteria for the classification of chronic alcoholics: identification of Wernicke's encephalopathy. J Neurol Neurosurg Psychiatry, 1997.PMID 9010400
4. [4]Reus VI, Fochtmann LJ, Bukstein O, et al. The American Psychiatric Association Practice Guideline for the Pharmacological Treatment of Patients With Alcohol Use Disorder. Am J Psychiatry, 2018.PMID 29301420
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6. [6]Knox J, Hasin DS, Larson FRR, et al. Prevention, screening, and treatment for heavy drinking and alcohol use disorder. Lancet Psychiatry, 2019.PMID 31630982
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8. [8]Grant BF, Goldstein RB, Saha TD, et al. Epidemiology of DSM-5 Alcohol Use Disorder: Results From the National Epidemiologic Survey on Alcohol and Related Conditions III. JAMA Psychiatry, 2015.PMID 26039070
9. [9]Mayo-Smith MF Pharmacological management of alcohol withdrawal. A meta-analysis and evidence-based practice guideline. American Society of Addiction Medicine Working Group on Pharmacological Management of Alcohol Withdrawal. JAMA, 1997.PMID 9214531
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11. [11]Day E, Bentham PW, Callaghan R, et al. Thiamine for prevention and treatment of Wernicke-Korsakoff Syndrome in people who abuse alcohol. Cochrane Database Syst Rev, 2013.PMID 23818100
12. [12]Connor JP, Haber PS, Hall WD Alcohol use disorders. Lancet, 2016.PMID 26343838
13. [13]Thomson AD, Cook CC, Touquet R, et al. The Royal College of Physicians report on alcohol: guidelines for managing Wernicke's encephalopathy in the accident and Emergency Department. Alcohol Alcohol, 2002.PMID 12414541
14. [14]Rösner S, Hackl-Herrwerth A, Leucht S, et al. Acamprosate for alcohol dependence. Cochrane Database Syst Rev, 2010.PMID 20824837
15. [15]Garbutt JC, Kranzler HR, O'Malley SS, et al. Efficacy and tolerability of long-acting injectable naltrexone for alcohol dependence: a randomized controlled trial. JAMA, 2005.PMID 15811981
16. [16]Saunders JB, Aasland OG, Babor TF, et al. Development of the Alcohol Use Disorders Identification Test (AUDIT): WHO Collaborative Project on Early Detection of Persons with Harmful Alcohol Consumption--II. Addiction, 1993.PMID 8329970
17. [17]Galvin R, Bråthen G, Ivashynka A, et al. EFNS guidelines for diagnosis, therapy and prevention of Wernicke encephalopathy. Eur J Neurol, 2010.PMID 20642790
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20. [20]Fuller RK, Gordis E Does disulfiram have a role in alcoholism treatment today? Addiction, 2004.PMID 14678055