Can you integrate both of them and teach me alcohol use disorders treatment very nicely step by step… you can also take other informations and also mention any latest guidelines or advances in aid treatment.. dont miss anything.. also give viva tips

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"alcohol use disorder" AND treatment

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alcohol use disorder treatment guidelines 2024 2025 NICE ASAM pharmacotherapy

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Note: The synopsis_clinical_practice.pdf is a scanned image-based PDF with no extractable text layer - it could not be read by any text extraction method. If you can share what specific content it covers, I can incorporate it. All other sources have been fully integrated.

Here is your complete, integrated guide on Alcohol Use Disorder Treatment:

🍺 ALCOHOL USE DISORDER (AUD) - COMPLETE TREATMENT GUIDE

Integrated from: IPS Clinical Practice Guidelines (SUD), Maudsley Prescribing Guidelines 15th Ed, Textbook of Family Medicine 9e + Latest Evidence 2023-2026


PART 1: FOUNDATIONS

What is AUD?

AUD (per IPS) encompasses the spectrum: intermittent binge drinking → hazardous drinking → chronic abuse → dependence. DSM-5 uses a unified diagnosis (mild/moderate/severe).
DSM-5 Criteria (2+ in 12 months = AUD):
  1. Drinking more/longer than intended
  2. Unsuccessful efforts to cut down
  3. Much time spent obtaining/using/recovering
  4. Craving
  5. Failure to fulfill role obligations
  6. Continued use despite interpersonal problems
  7. Important activities given up
  8. Use in hazardous situations
  9. Continued use despite knowing it causes harm
  10. Tolerance
  11. Withdrawal
Severity: Mild = 2-3 | Moderate = 4-5 | Severe = 6+

PART 2: STEP-BY-STEP CLINICAL ASSESSMENT

Step 1 - History

  • Alcohol use pattern (units/day, binge vs. daily)
  • Prior withdrawal history: seizures, DTs, prior hospital admissions
  • Prior treatment attempts
  • Psychiatric comorbidity (60% of adolescent SUD patients have one)
  • Family history of AUD
  • Psychosocial functioning: academic/occupational, family, legal

Step 2 - Screening Tools

ToolPurposeKey Cutoff
AUDITPrimary screening≥8 hazardous; ≥16 harmful; ≥20 dependence
SADQDependence severity>30 = severe (inpatient detox needed)
CIWA-ArMonitor withdrawal symptoms>10 = pharmacotherapy needed
SAWSSelf-report withdrawal>12 = assisted withdrawal
CRAFFTAdolescents (6 items)Brief primary care screen
Standard Drink = 14g / 18mL absolute alcohol = 360mL beer (5%) = 150mL wine = 45mL spirit (40%)
Binge (to BAC ≥80mg%): Males ≥16y: 5 drinks; 14-15y: 4 drinks; Females 9-17y: 3 drinks

Step 3 - Investigations

  • BAC/Breath analysis - detect recent intake
  • CDT (Carbohydrate-Deficient Transferrin) - best biomarker for chronic use + monitoring treatment
  • GGT, AST, ALT - elevated with recent heavy use; AST:ALT >2:1 suggests alcoholic hepatitis
  • MCV - raised (macrocytosis)
  • Ethyl glucuronide (urine) - sensitive marker; false positives possible
  • Thiamine, B12, folate, pyridoxine, Vitamin D - check if poor nutritional status suspected
  • LFTs, KFTs - baseline before pharmacotherapy
  • Urine toxicology - rule out polysubstance use
  • USG abdomen - hepatorenal status
  • FibroScan - early cirrhosis detection
  • ECG - before initiating pharmacotherapy, if malnourished

PART 3: TREATMENT PHASES

PHASE 1: ACUTE DETOXIFICATION (Alcohol Withdrawal Management)
                    ↓
PHASE 2: MAINTENANCE / RELAPSE PREVENTION (Anti-craving drugs)
                    ↓
PHASE 3: PSYCHOSOCIAL REHABILITATION (Long-term recovery)

PHASE 1: ALCOHOL WITHDRAWAL SYNDROME (AWS)

Timeline of Withdrawal Features

Hours After Last DrinkFeatures
6-24hTremor, sweating, anxiety, tachycardia, hypertension, insomnia
12-48hWithdrawal seizures (grand mal), alcoholic hallucinosis
48-96hDelirium Tremens (DTs) - confusion + autonomic storm
Weeks-monthsProtracted withdrawal - insomnia, dysphoria, anxiety
DTs mortality: 5-15% untreated; <1% with proper treatment

AWS Severity (IPS Classification)

GradeFeatures
MildAtaxia, nystagmus, reduced consciousness, conjunctival injection
ModerateCoarse tremor, restlessness, nausea/vomiting, autonomic hyperactivity (tachycardia, hypertension, hyperthermia), anxiety/depression, headache, insomnia
SevereRespiratory depression, seizures, stupor, coma, death
ComplicatedHallucinations, delirium, (pancreatitis, cirrhosis - rare in adolescents)
PathologicalBelligerent, combative, psychotic state even with small amounts

Community vs. Inpatient Detox Decision

Community detox possible when: Mild-moderate dependence, 24h carer available, SADQ <30, no prior DTs/seizures, agreed plan with contingency.
Inpatient detox REQUIRED (Maudsley 15th Ed.) when:
  • Regular consumption >30 units/day OR SADQ >30
  • History of withdrawal seizures or DTs
  • Concurrent benzodiazepine use + alcohol
  • Polysubstance misuse
  • Comorbid mental/physical illness, cognitive impairment
  • Pregnant, homeless, or no social support
  • Minor or elderly
  • Failed community detox previously

PHARMACOTHERAPY - ACUTE DETOX

A. BENZODIAZEPINES - Cornerstone

Cross-react at GABA-A receptors → suppress CNS hyperexcitability → prevent seizures and DTs.
Drug choice by liver function:
  • Normal liver: Long-acting BZDs - Chlordiazepoxide (1st choice), Diazepam, Clonazepam
  • Impaired liver (cirrhosis/elderly): "LOT" drugs - Lorazepam, Oxazepam, Temazepam (no active metabolites via glucuronidation; not oxidized)
Why long-acting preferred? Self-tapering effect; smoother withdrawal curve; less interdose withdrawal.

Chlordiazepoxide Fixed-Dose Regimens (Maudsley):

Rule of thumb: Starting dose (mg QID) ≈ daily units consumed. E.g., 20 units/day → 20mg QID.
DayModerate (SADQ 15-30)Severe (SADQ >30)
120mg QID (80mg total)40mg QID + 40mg PRN (up to 200mg)
215mg QID (60mg)40mg QID (160mg)
310mg QID (40mg)30mg QID (120mg)
45mg QID (20mg)25mg QID (100mg)
55mg BD (10mg)20mg QID (80mg)
6-10-Continue tapering
Symptom-triggered dosing (preferred in monitored settings): BZD given only when CIWA-Ar >10 - reduces total BZD consumed, shortens treatment.
Paediatric/Adolescent (IPS):
  • Diazepam 0.2-0.5mg/kg/dose IV (max 10mg) or 0.5mg/kg PR
  • Pathological intoxication: Lorazepam 1-5mg PO PRN or Haloperidol 1-5mg q4-8h IM (with BZD cover)

B. MANDATORY ADJUNCTS

Thiamine - Non-negotiable:
  • 50-100mg IM (first dose IM/IV - BEFORE giving glucose)
  • Reason: Glucose → pyruvate → demands thiamine (TPP). Thiamine deficiency → Wernicke's encephalopathy
  • Then oral supplementation
Wernicke's Triad: W-O-A = Walking difficulty (ataxia) + Ophthalmoplegia + Altered consciousness/confusion. Only 10-15% show all three - treat any suspected case promptly.
  • Wernicke's (acute, reversible) → Korsakoff's (chronic, largely irreversible: amnesia + confabulation)
Magnesium: 2-4 mEq/kg IV Day 1; 0.5-1 mEq/kg/day Days 2-4 (reduces seizure threshold)
Multivitamins: Pyridoxine, folate, B12, Vitamin D
Why nutritional deficiencies occur in AUD (IPS):
  • Poor dietary intake
  • Alcoholic gastritis + GI bleeding
  • Reduced pancreatic enzyme secretion
  • Damaged GI wall → malabsorption
  • Reduced fat absorption → fat-soluble vitamin deficiency
  • Folate deficiency → further GI wall changes → vicious cycle

C. DELIRIUM TREMENS - Emergency Management

  • ICU admission, airway protection, ventilatory support
  • IV diazepam loading (or phenobarbital for refractory DTs)
  • IV thiamine + electrolyte correction
  • Haloperidol for agitation - only with adequate BZD cover (antipsychotics alone lower seizure threshold)
  • Lateral decubitus position (aspiration prevention)
  • Continuous monitoring: BP, pulse, SpO2, temperature, glucose

PHASE 2: MAINTENANCE / RELAPSE PREVENTION

Principles

  • Treat like a chronic disease - long-term (even indefinite) medication is reasonable
  • Indicated for: moderate-to-severe dependence post-detox; mild dependence failed psychosocial alone
  • Always combine with psychosocial interventions
  • Pre-treatment baseline: physical exam, LFTs, KFTs, toxicology

DRUG 1: NALTREXONE

Mechanism: Mu-opioid receptor antagonist → blocks alcohol-induced dopamine release in mesolimbic reward pathway (nucleus accumbens) → reduces euphoric "high" and craving
FeatureDetail
DoseStart 12.5-25mg/day × 1-2 wks; target 50mg OD
When to start3-7 days after last drink (must be opioid-free)
DurationMinimum 3 months; ideally 6-12 months
Injectable form380mg IM monthly (Vivitrol) - superior adherence + efficacy
SC implant170-340mg; lasts ≥6 months (not yet in India)
Who benefits most:
  • Strong cravings | Family history of AUD | History of opioid use seeking AUD treatment
  • Intense alcohol urges during treatment | More somatic complaints
  • OPRM1 Asp40 (G allele) carriers - pharmacogenomics marker for naltrexone response
Adverse effects: Nausea (give with food), vomiting, headache, dizziness, fatigue; hepatotoxicity (rare)
LFT monitoring: Baseline, 1 month, 3 months, 6 months, yearly. Discontinue if AST/ALT >5x ULN.
Absolute contraindication: Current opioid use (precipitates severe withdrawal).
Key point: No abuse potential, no withdrawal on stopping. Continue even after a slip - limits relapse severity.

DRUG 2: ACAMPROSATE

Mechanism: Modulates NMDA glutamate receptors + GABA → normalizes glutamate hyperactivity after chronic alcohol use → reduces protracted withdrawal symptoms (insomnia, anxiety, dysphoria) that drive relapse
FeatureDetail
Dose666mg TID (2 × 333mg tablets, 3 times daily)
When to startDay 1 of abstinence (no need to wait, unlike naltrexone)
EliminationRenally excreted unchanged (no hepatic metabolism)
Advantages (IPS):
  • Safe in severe hepatic failure - drug of choice for AUD with liver disease
  • Safe with opioid maintenance therapy
  • No drug-drug interactions
  • Extremely safe in overdose (up to 56g studied)
  • No abuse potential
Adverse effects: Diarrhea (most common, treat with loperamide), GI cramps, nausea; rarely suicidal ideation (monitor depression)
Contraindication: Severe renal impairment (eGFR <30); dose-adjust in moderate renal disease

DRUG 3: DISULFIRAM

Mechanism: Irreversibly inhibits ALDH (aldehyde dehydrogenase) in liver + dopamine-β-hydroxylase in brain → acetaldehyde accumulation → Disulfiram-Ethanol Reaction (DER) within 15-30 minutes
FeatureDetail
Loading dose250-500mg/day starting 12-24h after last drink × 1-2 weeks
Maintenance125-250mg/day
DurationUntil stable long-term abstinence
SupervisionDirect supervised ingestion (by family/clinician) - ESSENTIAL
Disulfiram-Ethanol Reaction (DER):
Mild-ModerateSevere
Flushing, sweating, tachycardiaAcute heart failure, MI
Hypotension, chest painArrhythmias, severe hypotension
Acetaldehyde breath, respiratory distressRespiratory depression, seizures
Nausea/vomiting, severe headache, vertigoOccasional death
DER Management:
  • Mild (BAC 5-10mg%): Reassurance + oral fluids
  • Moderate-Severe (BAC 50-150mg%): IV Vitamin C 1g, ephedrine sulphate, antihistamines IV, oxygen/carbogen
  • Refractory: Fomepizole (4-methyl pyrazole) 15mg/kg IV single dose
Contraindications:
AbsoluteRelative
Cardiac failure, CAD, arrhythmiaLiver disease
Hypertension, cerebrovascular diseasePeripheral/optic neuropathy
Pregnancy, breastfeedingSevere mental illness
Alcohol within 24hMetronidazole, ritonavir, sertraline concurrent use
Monitoring: LFTs at 2 weeks post-initiation, monthly × 6 months, then every 3 months.
NICE CG115: Use disulfiram when naltrexone/acamprosate are not suitable or preferred; combine with psychological intervention; supervised administration by carer.
Unique facts: No tolerance on long-term use; no withdrawal on stopping; duration of supervised therapy directly correlates with abstinence duration.

DRUG 4: NALMEFENE (Newer)

Mechanism: Mu + delta opioid receptor antagonist + kappa partial agonist → prevents alcohol-induced dopamine release
FeatureDetail
Dose18mg, taken 1-2 hours BEFORE anticipated drinking (PRN)
Unique advantageAs-needed dosing - targets harm reduction, not just abstinence
ApprovalEU 2013; not yet in India
LFT monitoringNot required (no dose-dependent hepatotoxicity)
Use whenNaltrexone not tolerated; patient wants to reduce rather than abstain

DRUG COMPARISON TABLE

FeatureNaltrexoneAcamprosateDisulfiramNalmefene
MechanismOpioid antagonistGlutamate/GABA modulatorALDH inhibitor (aversive)Opioid antagonist (mixed)
Start after last drink3-7 daysDay 112-24hFlexible/PRN
GoalReduce reward/cravingReduce protracted withdrawalDeter drinkingReduce intake
Liver safetyCaution (hepatotoxic)SAFE (renally excreted)ContraindicatedSafer than naltrexone
Evidence levelFirst-line (JAMA 2023)First-line (JAMA 2023)Second/third-lineSecond-line
Opioid usersCONTRAINDICATEDSafeSafeCaution

DRUGS UNDER INVESTIGATION (IPS + Maudsley)

DrugClassStatus
BaclofenGABA-B agonist2023 Cochrane: benefit for abstinence post-detox; second-line in UK
TopiramateGABA/glutamate modulatorMay = naltrexone for heavy drinking reduction
GabapentinAnticonvulsantSome evidence; safety concerns limit use
Ondansetron5-HT3 antagonistEarly-onset AUD; under trial
VareniclinenAChR partial agonistUnder RCT evaluation
GLP-1 agonists (semaglutide)Incretin mimeticHot 2024-2025 topic; mesolimbic reward modulation
Sodium oxybateGHB analogueApproved Italy/Austria; safety concerns elsewhere
OxytocinNeuropeptidePre-clinical; blocks drug reinforcement

PHASE 3: PSYCHOSOCIAL INTERVENTIONS

A. Brief Interventions (BI) - FRAMES Model

For hazardous/harmful drinkers (not yet dependent). Delivered opportunistically in primary care/ED.
  • Feedback about personal risk | Responsibility (patient's) | Advice to change
  • Menu of options | Empathy | Self-efficacy enhanced

B. Motivational Enhancement Therapy (MET)

  • 1-4 sessions, 45-90 minutes each
  • Empathetic, non-confrontational
  • Explore ambivalence; develop discrepancy; "roll with resistance"; reinforce change talk
  • Moves patient: Pre-contemplation → Contemplation → Preparation → Action
  • Used as gateway before CBT

C. Cognitive Behavioral Therapy (CBT)

  • Identifies triggers, teaches coping/refusal skills
  • Cognitive restructuring for negative beliefs
  • Role-playing drink-refusal; relapse management skills
  • CBT + MET combination shows best outcomes

D. Family Systems Approaches

  • Functional Family Therapy (FFT), Brief Strategic Family Therapy (BSFT)
  • Multisystemic Therapy (MST), Multidimensional Family Therapy (MDFT) - esp. effective in adolescents
  • Goals: psychoeducation, establish supervision/boundaries, improve communication, engage family in treatment

E. 12-Step Programs (AA)

  • Spiritual fellowship (not religious), only requirement is desire to stop drinking
  • Open meetings (anyone), closed meetings (alcoholics/those wanting to stop only)
  • Anonymity is foundational
  • Caution in adolescents - deviancy training effect from deviant peer groups

F. Contingency Management (CM)

  • Vouchers/rewards for confirmed abstinence (urinalysis/breathalyzer)
  • Escalating reinforcement; effective adjunct to MET/CBT

G. Mindfulness-Based Relapse Prevention (MBRP)

  • Urge-surfing techniques; present-moment awareness; adjunct to CBT

SPECIAL POPULATIONS

Pregnancy

  • No safe level of alcohol → Fetal Alcohol Syndrome (FAS): growth retardation, CNS dysfunction, characteristic facies (smooth philtrum, thin vermillion border, short palpebral fissures), intellectual disability
  • Management: psychosocial + nutritional (needs 10-30% higher than baseline)
  • All medications avoided unless benefit clearly outweighs risk (specialist only)

Psychiatric Comorbidity (Dual Diagnosis)

  • 60% of adolescents with SUD have comorbid psychiatric disorder
  • Treat both simultaneously; better outcomes than treating either alone
  • Common comorbidities: ADHD, Conduct Disorder, Depression, Anxiety, PTSD

Liver Disease

  • Use Acamprosate (safest - renally excreted)
  • For detox: Lorazepam / Oxazepam (LOT rule)
  • Avoid or extreme caution: Naltrexone, Disulfiram (both hepatotoxic)

LATEST GUIDELINES & ADVANCES (2023-2026)

1. JAMA Meta-Analysis 2023 (PMID: 37934220 - 118 RCTs, 20,976 patients)

  • First-line: Oral naltrexone 50mg + Acamprosate - both with strong evidence
  • Naltrexone NNT = 11 (heavy drinking prevention) and 18 (any drinking prevention)
  • Acamprosate NNT = 11 (prevention of return to any drinking)
  • Injectable naltrexone: -4.99 fewer drinking days/30 days vs. placebo
  • Must always combine with psychosocial interventions

2. NICE CG115 (UK) - Key Points

  • Community detox with 24h carer + agreed plan = standard
  • Inpatient if SADQ >30, prior DTs/seizures, severe comorbidity
  • Disulfiram: third-line with psychological intervention + supervised administration
  • Monitor: 2-weekly × 2 months → monthly × 4 months → 6-monthly thereafter

3. GRACE-4 ED Guidelines 2024 (PMID: 38747203)

  • Detox alone is insufficient - initiate underlying SUD treatment concurrently in ED
  • Systematic monitoring, team communication, regular reassessment emphasized

4. ASAM 2025-2026

  • New assessment guide for level of addiction care (Jan 2025)
  • New standards for adolescent SUD care (March 2026)
  • Hospital/ED implementation guide for SUD (March 2026)

5. GLP-1 Agonists - Emerging Frontier

  • Semaglutide and liraglutide showing signals for reducing alcohol consumption in preclinical models and early trials
  • Mechanism: GLP-1 receptors in limbic/mesolimbic system modulate reward
  • Multiple trials underway; not yet approved for AUD

6. Pharmacogenomics

  • OPRM1 A118G (Asp40 variant): G allele carriers respond significantly better to naltrexone - moving toward personalized AUD treatment

7. Maudsley 15th Ed. Updates (2024)

  • Baclofen: officially recognized as second-line option (2023 Cochrane data)
  • Topiramate: may equal naltrexone; still off-label
  • FibroScan now recommended for early cirrhosis detection in AUD patients

🎓 VIVA TIPS - 20 MUST-KNOW Q&As

Q1: First-line pharmacotherapy for AUD?
Naltrexone 50mg OD and Acamprosate 666mg TID - both first-line per JAMA 2023 and NICE CG115. Choice depends on: acamprosate preferred in liver disease; naltrexone for those with strong craving/reward component.
Q2: Why give thiamine BEFORE glucose?
Glucose → pyruvate → needs thiamine (TPP cofactor). In deficient AUD patients, glucose without thiamine precipitates Wernicke's encephalopathy. Always IM/IV thiamine first.
Q3: Contraindications to disulfiram?
Cardiac failure/CAD/arrhythmia, hypertension, cerebrovascular disease, pregnancy, breastfeeding, active liver disease, peripheral/optic neuropathy, severe mental illness, alcohol within 24h.
Q4: BZD of choice when liver is damaged?
Lorazepam or Oxazepam - "LOT" rule (Lorazepam, Oxazepam, Temazepam). They undergo glucuronidation (not oxidation) → no active metabolites → safe in hepatic failure.
Q5: What is CIWA-Ar?
Clinical Institute Withdrawal Assessment for Alcohol - Revised. 10-item, 5-minute scale (objective). Score >10 = pharmacotherapy needed. Used for symptom-triggered BZD dosing in monitored settings.
Q6: How does naltrexone work in AUD?
Blocks mu-opioid receptors → prevents alcohol-induced dopamine release in nucleus accumbens (mesolimbic reward pathway) → reduces euphoric reinforcement and craving → alcohol becomes less rewarding.
Q7: Mechanism of acamprosate?
Modulates NMDA glutamate receptors (and GABA) → normalizes the glutamate hyperactivity (excitotoxicity) that develops after chronic alcohol use → reduces protracted withdrawal symptoms (insomnia, anxiety, dysphoria) that trigger relapse.
Q8: DER management?
Mild: reassurance + oral fluids. Moderate-severe: IV Vitamin C 1g, ephedrine sulphate, antihistamines IV, oxygen. Refractory: Fomepizole 15mg/kg IV (ALDH inhibitor reversal agent).
Q9: Alcoholic hallucinosis vs. Delirium Tremens?
Hallucinosis: vivid hallucinations (usually auditory) with clear sensorium and intact orientation; 12-48h. DTs: hallucinations + disorientation + autonomic storm + fluctuating consciousness; 48-96h; mortality 5-15% untreated.
Q10: Wernicke-Korsakoff syndrome?
Wernicke (acute): WOA triad - W ataxia, O phthalmoplegia, A ltered consciousness; due to thiamine deficiency; reversible if treated promptly with IV thiamine. Korsakoff (chronic): anterograde + retrograde amnesia + confabulation; largely irreversible.
Q11: When to use nalmefene over naltrexone?
Patient does NOT want complete abstinence (goal = harm reduction/reduced drinking), or naltrexone not tolerated. Nalmefene taken PRN (1-2h before anticipated drinking session) - gives patient autonomy.
Q12: Best biomarker for monitoring AUD treatment?
CDT (Carbohydrate-Deficient Transferrin) - most sensitive/specific for chronic heavy drinking (>50g/day × 2 weeks); normalizes with abstinence. GGT also used but less specific.
Q13: Why injectable naltrexone is superior to oral?
Superior adherence (monthly injection), avoids first-pass metabolism (higher plasma levels), eliminates the "drinking window" exploited with oral dosing, and removes daily pill burden.
Q14: FRAMES model (Brief Interventions)?
Feedback-personal risk, Responsibility lies with patient, Advice clearly given, Menu of options, Empathy shown, Self-efficacy enhanced. (Miller & Sanchez model)
Q15: Fetal Alcohol Syndrome features?
Pre/postnatal growth retardation; CNS dysfunction (intellectual disability, microcephaly, ADHD); characteristic facies (smooth philtrum, thin vermillion upper lip border, short palpebral fissures). No safe level of alcohol in pregnancy.
Q16: Chlordiazepoxide dosing rule of thumb?
Starting dose QID (mg) ≈ daily units consumed. 20 units/day → 20mg QID. Taper over 5-7 days (moderate) or 7-10 days (severe).
Q17: Three FDA-approved drugs for AUD?
(1) Disulfiram (Antabuse) - aversive; (2) Acamprosate (Campral) - anti-craving; (3) Naltrexone - anti-craving (oral ReVia + injectable Vivitrol).
Q18: Pharmacogenomics of naltrexone?
OPRM1 A118G (Asp40 variant) - G allele carriers show significantly better response to naltrexone. Also: ALDH2*2 allele (East Asians) causes endogenous disulfiram-like reaction (natural DER).
Q19: Five drugs under investigation for AUD?
Baclofen, Topiramate, Gabapentin, Ondansetron, GLP-1 agonists (semaglutide - 2024 frontier), Varenicline, Sodium oxybate.
Q20: How long to continue naltrexone/acamprosate?
Naltrexone: minimum 3 months, ideally 6-12 months; no withdrawal on stopping. Acamprosate: until stable abstinence + diminished craving + sound recovery plan. Both may be used indefinitely in chronic severe AUD - analogous to long-term medication for hypertension or diabetes.

Quick Mnemonics

MnemonicWhat It Represents
LOTLiver-safe BZDs: Lorazepam, Oxazepam, Temazepam
WOAWernicke's triad: W alking (ataxia), O phthalmoplegia, A ltered consciousness
FRAMESBrief Intervention model components
DTs = Day 2-4DTs typically onset 48-96h (day 2-4) after last drink
"Thiamine before glucose"Critical rule for AWS management
ACdN = AUD drugsAcamprosate, C (disulfiram = classic), Naltrexone - 3 FDA-approved
CDT = Chronic Detection ToolBest biomarker for chronic AUD monitoring

Sources: IPS Clinical Practice Guidelines on SUD in Children & Adolescents | Maudsley Prescribing Guidelines 15th Ed | Textbook of Family Medicine 9th Ed | McPheeters et al. JAMA 2023 (PMID: 37934220) | NICE CG115 | ACG Guideline 2024 (PMID: 38174913) | GRACE-4 Guidelines 2024 (PMID: 38747203) | ASAM 2025-2026 Standards
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