Alcohol-Related Disorders

Clinically reviewed Aug 13, 2026 Updated Aug 30, 2026

Clinical Snapshot

Alcohol-related disorders require a biopsychosocial treatment approach and span a continuum: at-risk drinking (exceeding Canada's low-risk drinking guidance but not meeting diagnostic criteria for a disorder), alcohol use disorder (AUD) (a chronic, relapsing-remitting condition of impaired control over alcohol use with continued use despite consequences), and alcohol withdrawal (physical symptoms occurring hours to days after heavy or prolonged drinking is stopped or reduced).[1] Relapse is a normal, expected part of this disorder, not a treatment failure — communicate this to patients directly. Two withdrawal-related presentations are genuine medical emergencies covered throughout this chapter: delirium tremens (severe confusion, disorientation, and/or hallucinations with severe autonomic hyperactivity) and Wernicke encephalopathy (a preventable, treatable, but potentially fatal or permanently disabling consequence of thiamine deficiency).[1]

Recognize the Condition

Alcohol use disorder — severity by criteria count

Mild

2-3 diagnostic indicators present within a 12-month period.

Moderate

4-5 diagnostic indicators present within a 12-month period.

Severe

6 or more diagnostic indicators present within a 12-month period.

Diagnosis (per DSM-5-TR criteria, as used in the current Canadian guideline[1]) requires 2 or more of the following indicators within a 12-month period; if fewer than 2 are present, assess instead for at-risk drinking:

  • Craving — a strong desire, urge, or preoccupation with drinking.
  • Time and effort — spending considerable time obtaining, using, or recovering from alcohol.
  • Loss of control over use — drinking more or longer than planned; repeated unsuccessful attempts to cut down or stop.
  • Disruption of responsibilities — prioritizing drinking over work, school, or home obligations.
  • Reduced activities — giving up or cutting back important social, occupational, or recreational activities in favour of drinking.
  • Interpersonal conflict — continuing to drink despite ongoing relationship problems caused or worsened by alcohol.
  • Risky behaviour — using alcohol in physically hazardous situations (driving, operating machinery).
  • Health consequences — continuing to drink despite awareness that it is causing or worsening a physical or psychological problem.
  • Tolerance — needing more alcohol for the same effect, or a reduced effect from the same amount.
  • Withdrawal symptoms — experiencing physical or psychological withdrawal symptoms after stopping or reducing intake (see below).

Alcohol withdrawal — presentation by symptom domain

DomainSymptoms
AutonomicTachycardia, sweating, hypertension.
NeuromuscularHand tremor, psychomotor agitation; generalized tonic-clonic seizures mark severe withdrawal. Withdrawal seizures are typically brief and generalized, occurring 6-48 hours after the last drink or significant dose reduction.[2]
GastrointestinalNausea, vomiting.
PsychologicalAnxiety, insomnia, brief visual/tactile/auditory hallucinations or illusions; delirium tremens marks the most severe form.

2 or more of these symptoms, occurring within hours to a few days of reducing or stopping heavy alcohol use and not explained by another medical or psychiatric condition, support a diagnosis of alcohol withdrawal, especially when they cause distress or impair functioning.[1] Delirium tremens is a serious, potentially life-threatening manifestation of withdrawal characterized by severe confusion, disorientation, and/or hallucinations together with severe autonomic hyperactivity — it is a medical emergency, not simply "severe" ordinary withdrawal.[1]

Risk Factors

  • Heavy or prolonged alcohol consumption pattern, and any consumption above Canada's Guidance on Alcohol and Health low-risk thresholds.
  • Family history of alcohol use disorder.
  • Comorbid psychiatric conditions, particularly depression, anxiety, and trauma-related disorders.
  • Concurrent use of other substances, including opioids, sedative-hypnotics, cannabis, and tobacco.
  • For severe withdrawal complications specifically: a personal history of past withdrawal seizures or past delirium tremens is one of the strongest predictors of a repeat severe episode — always ask about this directly.[1]
  • Older age, and comorbid conditions such as heart disease, cirrhosis, or other significant medical illness, which increase both withdrawal severity and complication risk.
  • Unstable housing or lack of a reliable support person, which affects the safety of outpatient withdrawal management specifically rather than withdrawal risk itself.
  • Concurrent use of opioids or other benzodiazepines, which increases both withdrawal complexity and combined-CNS-depressant risk.

Red Flags & Refer

The following require immediate escalation to emergency or inpatient care rather than routine outpatient management:

  • Delirium tremens — severe confusion, disorientation, and/or hallucinations with severe autonomic hyperactivity (marked tachycardia, hypertension, fever, diaphoresis). This is a medical emergency requiring inpatient, often critical-care, management.[1]
  • Any active or recent withdrawal seizure.
  • Suspected Wernicke encephalopathy — the classic triad of confusion, ataxia, and eye-movement abnormalities (nystagmus, ophthalmoplegia); treat empirically on suspicion alone since not all three features need be present and delay risks permanent injury.[3]
  • A personal history of past withdrawal seizures or past delirium tremens — mandates a high-risk withdrawal pathway regardless of the current presentation's apparent severity.[1]
  • PAWSS score ≥4, indicating high risk of severe/complicated withdrawal — refer for inpatient withdrawal management where available.[2]
  • Pregnancy with alcohol withdrawal — always requires inpatient management with fetal monitoring capability.[1]
  • Severe or uncontrolled comorbid medical conditions (decompensated cirrhosis, uncontrolled diabetes, unstable cardiac or respiratory disease).
  • Acute confusion or cognitive impairment of any cause during withdrawal assessment.
  • Active suicidal ideation, psychosis, or another unstable psychiatric emergency.
  • Lack of a safe, substance-free setting or a reliable support person, for a patient who would otherwise be a candidate for outpatient withdrawal management.

Assessment & Diagnosis

History and screening

Take a detailed history of alcohol and other substance use (amount, frequency, duration), impact on occupational/social/family functioning, prior withdrawal episodes (including seizures or delirium tremens), and comorbid medical/psychiatric conditions. All patients should be screened for high-risk drinking at regular intervals, even when a problem is not suspected.[1]

Begin with the ultra-brief single-question screen: "How many times in the past year have you had X or more drinks in a day?" (X = 5 for men, 4 for women). An answer of 1 or more is a positive screen and should be followed by a more detailed tool.[4]

AUDIT-C questionScoring (0-4 per item)
How often do you have a drink containing alcohol?Never (0) to 4+ times/week (4)
How many standard drinks do you have on a typical drinking day?1-2 (0) to 10+ (4)
How often do you have 6 or more drinks on one occasion?Never (0) to daily/almost daily (4)

Total AUDIT-C score 0-4 = low-risk alcohol use (offer encouragement, re-screen annually); 5-7 = moderate-risk (explore reasons for drinking, offer brief advice, re-screen annually); 8 or higher = high-risk alcohol use or possible AUD — proceed to a diagnostic interview using DSM-5-TR criteria.[5][1]

Withdrawal risk stratification — PAWSS

The Prediction of Alcohol Withdrawal Severity Scale (PAWSS) is a clinician-administered, 10-item cumulative screening tool used alongside clinical judgment (especially a history of past seizures or delirium tremens) to decide the withdrawal management pathway.[2][1] It is not validated for self-administration, in outpatient settings, in youth, or in pregnancy, and requires alcohol use or a positive blood alcohol level within the relevant window before scoring.

PAWSS item (1 point each if present)Domain
Recently intoxicated within the last 30 daysPatient interview
Prior alcohol use disorder treatment (inpatient, outpatient, or AA)Patient interview
Any previous episode of alcohol withdrawal, any severityPatient interview
Any previous blackout (transient retrograde amnesia without loss of consciousness)Patient interview
Any previous alcohol withdrawal seizurePatient interview
Any previous delirium tremensPatient interview
Combined alcohol with benzodiazepines/barbiturates in the last 90 daysPatient interview
Combined alcohol with any other substance in the last 90 daysPatient interview
Blood alcohol level >200 mg/dL, equivalent breath alcohol, or any alcohol consumed in the past 24 hoursClinical evidence
Evidence of increased autonomic activity (heart rate >120 bpm, tremor, agitation, sweating, nausea)Clinical evidence

Maximum score 10. A score of 4 or higher indicates high risk for moderate-to-severe (complicated) withdrawal — inpatient management and prophylaxis are indicated; a score under 4 generally allows an outpatient pathway provided no other exclusion criteria are present (see Choose Initial Treatment).[2]

Withdrawal severity monitoring — CIWA-Ar

Once withdrawal management is underway, the Clinical Institute Withdrawal Assessment for Alcohol, Revised (CIWA-Ar) is the most widely used symptom-severity scale, used both to grade severity and to drive symptom-triggered medication dosing.[6] It has 10 clinician-scored items; 9 are scored 0 (absent) to 7 (most severe), and orientation/clouding of sensorium is scored 0-4, for a maximum of 67.

ItemScore rangeWhat is assessed (top-anchor example)
Nausea/vomiting0-77 = constant nausea, frequent dry heaves and vomiting
Tremor0-77 = severe, even with arms not extended
Paroxysmal sweats0-77 = drenching sweats
Anxiety0-77 = equivalent to acute panic states
Agitation0-77 = paces constantly or thrashes about
Tactile disturbances0-77 = continuous tactile hallucinations
Auditory disturbances0-77 = continuous auditory hallucinations
Visual disturbances0-77 = continuous visual hallucinations
Headache/fullness in head0-77 = extremely severe
Orientation/clouding of sensorium0-44 = disoriented for place and/or person

A total score under 10 usually does not need additional withdrawal medication; scores of roughly 10-18 indicate moderate withdrawal, and 19 or higher indicates severe withdrawal with the highest seizure/delirium tremens risk — see Drug Tables for how this score drives symptom-triggered dosing.[6]

Investigations

  • Pregnancy test where relevant, CBC, renal and liver function, electrolytes including magnesium and phosphate.
  • AST, ALT, GGT, and mean corpuscular volume may be elevated with chronic use but are nonspecific and not required to make the diagnosis.
  • Toxicology, including urine ethanol and ethyl glucuronide; a blood alcohol level reflects only recent intoxication (hours), not chronic use. A phosphatidylethanol blood test, where available, indicates heavy use over the preceding 2-4 weeks.
  • Directed imaging or further labs (chest x-ray, CT head, abdominal ultrasound) as clinically indicated for suspected complications, not routinely.

Treatment Targets

  • Assess and address immediate safety issues — ability to care for dependents, driving, or operating machinery.
  • Change the pattern of alcohol use according to the patient's own goal: complete abstinence or reduction.
  • Assess for and treat withdrawal, including preventing progression to seizures, delirium tremens, or Wernicke encephalopathy.
  • Assess for and treat medical complications and psychiatric comorbidities concurrently, not sequentially.
  • Integrate pharmacologic and nonpharmacologic (psychosocial) treatment.
  • Prevent relapse, while treating any relapse that occurs as an expected part of a chronic, relapsing-remitting condition rather than a treatment failure.

Choose Initial Treatment

Direct treatment rule

Withdrawal risk stratification and care setting

PAWSS < 4, no exclusion criteria outpatient withdrawal management is appropriate: prefer a non-benzodiazepine agent (gabapentin first-line; carbamazepine or clonidine as alternatives), with daily follow-up for the first 3-5 days.[1]

PAWSS ≥ 4, or any history of past withdrawal seizures/delirium tremens, or another inpatient-level exclusion criterion use a short-term benzodiazepine, ideally in an inpatient/withdrawal-management-facility setting; if inpatient care is genuinely unavailable, benzodiazepines can be used outpatient only with close monitoring.[1]

Dosing schedule: use symptom-triggered dosing (CIWA-Ar or an equivalent scale drives each dose) in a setting where frequent reassessment is feasible — it lowers total benzodiazepine exposure and treatment duration versus a fixed schedule in mild-to-moderate withdrawal. Use a fixed/tapering schedule instead for severe withdrawal, or whenever frequent symptom reassessment is not feasible (e.g., outpatient without close monitoring).[1]

Wernicke encephalopathy prevention — applies to every patient

Give thiamine before, or together with, any glucose-containing fluid or food in a patient with heavy alcohol use, at-risk drinking, or suspected thiamine deficiency — glucose metabolism consumes thiamine and can precipitate or worsen Wernicke encephalopathy in a deficient patient.[3]

Give oral thiamine 100-200 mg daily to every patient undergoing withdrawal management; give parenteral thiamine 200-300 mg IV/IM daily for a minimum of 5 days (until Wernicke encephalopathy is excluded) to any patient with suspected Wernicke encephalopathy, or who presents to hospital with malnourishment or decompensated liver disease.[1]

Ongoing AUD pharmacotherapy selection

1st line — goal is abstinence or reduced drinking naltrexone.

1st line — goal is abstinence specifically, or significant hepatic impairment acamprosate.

2nd line — inadequate response to, contraindication to, or preference against both first-line agents topiramate or gabapentin.

Special situation — motivated patient who can be supervised, especially with a history of prior disulfiram success disulfiram, only after full informed consent and counselling on the disulfiram-alcohol reaction.[1]

Non-Pharmacologic Treatment

  • Approach alcohol use disorder as a treatable medical condition, not a moral failing — a nonjudgmental stance is itself part of effective treatment.[1]
  • Match counselling to the patient's stage of change: precontemplation (open, non-confrontational discussion of use and consequences), contemplation (build a decisional balance of pros/cons, reinforce any "change talk"), preparation (plan practical details of a quit/reduction attempt, discuss withdrawal management and anti-craving medication options), action (monitor progress, reinforce successes, troubleshoot difficulties), maintenance (reinforce successes, build relapse-prevention skills and a support network), and relapse (normalize relapse as part of the disease process rather than a failure, and use motivational techniques to move the patient back toward preparation/action).
  • Brief interventions (including motivational interviewing) are effective alone for at-risk drinking that does not yet meet AUD criteria.
  • Offer referral to specialist-led psychosocial treatment for every patient with mild-to-severe AUD: psychoeducation, relapse-prevention training, trauma therapy, cognitive behavioural therapy (CBT), motivational enhancement therapy, interpersonal therapy, and group/family therapy. Combined motivational interviewing plus CBT is associated with higher abstinence rates, including in patients with comorbid depression or anxiety.
  • Offer information about and referral to peer-support and recovery-oriented community programs (e.g., Alcoholics Anonymous, SMART Recovery) for every patient with mild-to-severe AUD — no single modality has demonstrated clear superiority, so base the choice on patient preference, cost, and accessibility.[1]
  • During outpatient withdrawal management: provide a 24-hour contact number, arrange a reliable support person where possible, encourage increased fluid and electrolyte intake with a restricted, mild diet, advise minimal exercise, and advise against driving until symptoms subside. Discuss the risk/benefit of activities that increase sweating (hot baths, saunas) and of caffeine intake.[1]
  • Managed alcohol programs are a harm-reduction option in some communities for patients with chronic, severe AUD who are unstably housed, providing individually tailored, regularly dispensed alcohol doses to reduce non-beverage alcohol use and stabilize withdrawal risk.

Pharmacologic Treatment Options

Drug / interventionRoleDose / useImportant adverse effectsTeaching points
Thiamine
Preferred
Wernicke encephalopathy prevention — every patient with heavy/at-risk drinking or AUDOral: 100-200 mg daily. Parenteral (suspected Wernicke's, or hospital presentation with malnourishment/decompensated liver disease): 200-300 mg IV/IM daily x 5 days minimumGenerally well tolerated; rare anaphylactoid reaction with rapid IV administrationAlways give before or with glucose-containing fluids/food in an at-risk patient.
Diazepam
Preferred
1st-line benzodiazepine, high-risk withdrawal (PAWSS ≥4)Symptom-triggered per CIWA-Ar, or fixed-schedule tapering over 4-7 days — see Drug TablesSedation, ataxia, respiratory depression with concurrent CNS depressantsLong-acting; avoid in significant hepatic impairment or older adults — use lorazepam/oxazepam instead.
Lorazepam
Preferred
Benzodiazepine of choice in hepatic impairment, cirrhosis, or older adultsSymptom-triggered per CIWA-Ar, or fixed-schedule tapering over 4 days — see Drug TablesSedation, ataxia, respiratory depression with concurrent CNS depressantsNo active metabolites; cleared by glucuronidation only, giving predictable clearance in hepatic disease.
Gabapentin
Preferred
1st-line outpatient withdrawal (PAWSS under 4, no seizure history); 2nd-line ongoing AUD pharmacotherapyWithdrawal: 300 mg PO up to QID (max 1200 mg/day) x 5 days. AUD maintenance: 100-300 mg PO TID, titrate PRN to max 1800 mg/daySedation, ataxia, dizziness; risk of misuse/diversionContraindicated with any seizure history for withdrawal use — does not reliably prevent seizures.
Naltrexone
Preferred
1st-line AUD pharmacotherapy — goal of abstinence or reduced drinking25 mg PO daily x 3-4 days, then 50 mg daily; may increase to max 150 mg daily if cravings persist with normal LFTsNausea, headache, dizziness; hepatotoxicity riskContraindicated with any current opioid use — patient must be opioid-free ≥7-10 days before starting.
Acamprosate
Preferred
1st-line AUD pharmacotherapy — goal of abstinence, or hepatic impairment2 x 333 mg tablets PO TID (666 mg TID); reduce for weight under 60 kg or moderate renal impairmentDiarrhea, nausea, abdominal painRenally cleared — treatment of choice in hepatic impairment. Contraindicated if CrCl ≤30 mL/min. Start after ≥4 days abstinence.
Disulfiram
Special situation
2nd-line AUD pharmacotherapy, motivated patient who can be supervised250 mg PO daily (125-500 mg range); patient must be alcohol-free ≥24-48 hours before first doseMetallic taste, dermatitis; rare but serious hepatotoxicityNot commercially available in Canada — must be compounded. Full informed consent on the disulfiram-alcohol reaction required before starting.
Phenobarbital
Special situation
Resistant/severe withdrawal not controlled by large benzodiazepine doses, incl. delirium tremensWeight-based IV dosing per institutional critical-care protocolNarrow therapeutic index; respiratory depression, oversedationCritical-care setting only, with continuous monitoring — not an outpatient or ward-level medication.

Special Populations

Pregnancy

Alcohol use in pregnancy increases the risk of fetal alcohol spectrum disorder, alcohol-related birth defects, and spontaneous abortion. Alcohol withdrawal in pregnancy must always be managed as an inpatient, with fetal heart rate and movement monitoring — CIWA-Ar-guided benzodiazepine loading follows the same approach used outside pregnancy, preferring a shorter-acting agent (lorazepam or oxazepam).[1] There are no controlled studies of AUD pharmacotherapy in pregnancy; the safety of naltrexone, acamprosate, disulfiram, and baclofen has not been established, so the risks of medication must be weighed directly against the risks of continued alcohol use with the patient. Gabapentin may be considered for mild withdrawal in pregnancy. Topiramate is associated with an increased risk of fetal malformations and should not be used in pregnancy. Give thiamine at standard replacement doses — it is a required nutrient in pregnancy, not a drug to be avoided.

Breastfeeding

Disulfiram is contraindicated during breastfeeding. Naltrexone transfers minimally into breast milk and does not require discontinuation. Acamprosate has limited safety data but systemic infant effects are considered unlikely — monitor the infant for diarrhea. Gabapentin at maternal doses under 2100 mg/day produces low infant serum levels; use caution combined with other sedating medications. Topiramate at maternal doses up to 200 mg/day produces relatively low infant serum levels, though infant sedation and diarrhea have been reported. Thiamine is compatible with breastfeeding.

Older adults

Older patients are more sensitive to alcohol's effects (reduced metabolizing-enzyme activity, lower total body water) and tend to have earlier-onset, more severe withdrawal and a higher risk of Wernicke encephalopathy. Avoid diazepam — its long half-life and active metabolites risk accumulation, particularly with reduced renal clearance. Lorazepam (or oxazepam) is preferred for withdrawal management in this population. A commonly used older-adult-specific thiamine protocol is 200 mg parenteral thiamine IM or IV daily for 3-5 days. Weigh relapse-prevention pharmacotherapy carefully against this population's increased sensitivity to adverse effects and drug interactions.[1]

Hepatic impairment

Lorazepam and oxazepam are preferred over diazepam given hepatic glucuronidation-only clearance without active metabolites. Acamprosate (renally cleared, no hepatotoxicity) is the treatment of choice for AUD pharmacotherapy in hepatic insufficiency. Naltrexone and disulfiram both carry hepatotoxicity risk and require caution or avoidance with significant hepatic impairment/dysfunction, with baseline and periodic liver function monitoring for naltrexone specifically. Carbamazepine and valproic acid are both contraindicated in hepatic disease.

Renal impairment

Acamprosate is contraindicated at CrCl ≤30 mL/min and requires dose reduction at CrCl 30-50 mL/min. Gabapentin requires dose adjustment in renal impairment, with GFR-guided monitoring. Topiramate requires dose adjustment in renal impairment and carries a nephrolithiasis risk — maintain adequate fluid intake.

Youth (age 12-19)

Withdrawal on cessation is relatively uncommon in youth with AUD, and only a subset of those who experience it require pharmacological management; no empirical dosing data exist specifically for adolescents. Where pharmacological withdrawal management is genuinely needed, the general adult approach is used, but a consultation with an addiction medicine specialist is strongly recommended before initiating any outpatient withdrawal management in a youth patient, even with a PAWSS score under 4, since PAWSS is not validated in this age group.[1]

Monitoring & Follow-Up

During withdrawal management: assess vital signs, withdrawal symptoms (CIWA-Ar or equivalent), hydration, cognition, and general condition at every visit; see patients daily during the acute phase (roughly the first 3-5 days), then space out follow-up as symptoms allow. Confirm a reliable support person or virtual-care connection is in place for outpatient management.[1]

After withdrawal management: withdrawal management alone is not adequate treatment for AUD — connect every patient to ongoing pharmacotherapy, psychosocial treatment, or both immediately on completion, since a return to drinking without ongoing care is common in the days to weeks that follow.[1]

On AUD pharmacotherapy: for naltrexone, check liver function tests at baseline and at 1, 3, and 6 months (more often if elevated), and advise the patient to stop treatment and seek care for signs of acute hepatitis (fatigue, anorexia, nausea, vomiting). For disulfiram, obtain baseline and periodic liver function tests and CBC/blood chemistries. For carbamazepine, obtain a baseline CBC (including platelets) before starting and monitor hepatic function periodically, particularly in older adults or those with liver disease. For topiramate, monitor for signs of metabolic acidosis or hyperammonemia (unexplained vomiting, lethargy, confusion, hyperventilation) with long-term use.

Reassess treatment goals and psychiatric comorbidities at every visit, and treat depression or anxiety concurrently with AUD rather than sequentially.[1]

Treatment Failure / Next Step

  1. Outpatient withdrawal symptoms not controlled with a non-benzodiazepine regimen after 24-48 hours: escalate to inpatient care and a benzodiazepine regimen.
  2. Withdrawal symptoms persist despite adequate benzodiazepine doses (e.g., 50 mg or more of diazepam-equivalent in the first hour, or 200 mg or more in the first 3 hours): this defines resistant withdrawal — transfer to a critical-care setting and add phenobarbital as adjunctive therapy under continuous monitoring.[1]
  3. Inadequate response to a full trial of naltrexone or acamprosate: switch to the other first-line agent if not already tried, or move to a second-line option (topiramate or gabapentin) if both first-line agents have been tried or are contraindicated.
  4. Persistent postacute withdrawal symptoms (anxiety, irritability, sleep disturbance, lasting up to 6 months and a known predictor of relapse): consider behavioural therapy or a GABA-modulating agent such as gabapentin.
  5. Continued return to drinking despite optimized pharmacotherapy and psychosocial treatment: refer to an addiction medicine specialist, intensify psychosocial supports and peer-support connections, and reassess specifically for an undertreated psychiatric comorbidity.

Common Errors to Avoid

  • Giving glucose-containing fluids before or without thiamine in a patient with heavy alcohol use — this can precipitate or worsen Wernicke encephalopathy.[3]
  • Estimating withdrawal risk from drinking history alone rather than using a validated tool (PAWSS) and, once withdrawal starts, a validated severity scale (CIWA-Ar).
  • Using clonidine as monotherapy for anything beyond mild withdrawal in a low-risk patient — it does not protect against seizures and can mask the true severity of autonomic withdrawal, risking undertreatment.
  • Prescribing benzodiazepines as ongoing, long-term "maintenance" treatment for AUD — this is not indicated and creates a separate dependence risk.
  • Treating alcohol use disorder without addressing a comorbid psychiatric condition (depression, anxiety) at the same time, rather than sequencing one after the other.
  • Prescribing an antipsychotic or an SSRI specifically to treat AUD itself — neither is recommended for this indication, including in patients with a concurrent anxiety or depressive disorder.
  • Starting naltrexone without confirming the patient has been opioid-free for at least 7-10 days — this can precipitate acute opioid withdrawal.
  • Discharging a patient after completing withdrawal management without a concrete connection to ongoing AUD pharmacotherapy and/or psychosocial care.
  • Judging disulfiram a failure based on unsupervised, placebo-controlled trial evidence alone — supervised, witnessed daily administration is what the evidence supports as effective, and adherence (not drug efficacy) is usually the real issue in an unsupervised failure.
  • Confusing a PAWSS "blackout" (transient amnesia without loss of consciousness) with simply "passing out," which can lead to a falsely elevated risk score if not clarified with the patient.

Clinical Decision Algorithm

Screening, diagnosis, and withdrawal risk stratification
Any patient — routine screening, or a positive single-question screen (5+ drinks/day for men, 4+ for women, in the past year)
AUDIT-C (3 questions, scored 0-12)
Score 0-4: low risk
Offer encouragement; re-screen annually
Score 5-7: moderate risk
Explore reasons for drinking; brief advice/intervention; re-screen annually
Score ≥8: high risk / possible AUD
DSM-5-TR diagnostic interview (≥2 of 10 indicators = AUD)
If AUD confirmed and withdrawal management needed or abstinence is the goal: assess withdrawal risk with PAWSS
PAWSS under 4, no other exclusion criteria
Outpatient withdrawal management — proceed to next algorithm
PAWSS ≥4, or history of withdrawal seizures/DTs, or other exclusion
Inpatient withdrawal management — proceed to next algorithm
Withdrawal management
Withdrawal management pathway assigned
Start oral thiamine 100-200 mg daily before/with any glucose; parenteral 200-300 mg IV/IM daily x5 days if Wernicke encephalopathy suspected or malnourished/decompensated liver disease
Outpatient, low risk
Gabapentin 300 mg PO up to QID (no seizure history); alternatives: carbamazepine or clonidine
Reassess daily x3-5 days using CIWA-Ar or SAWS
Inadequate response after 24-48h, or any severe symptoms emerge: escalate to inpatient benzodiazepine pathway
Inpatient, high risk
Benzodiazepine (diazepam, or lorazepam/oxazepam if hepatic impairment/older adult) — symptom-triggered dosing per CIWA-Ar if frequent reassessment feasible, otherwise fixed tapering schedule
Adequately controlled
Taper over 4-7 days; discontinue once CIWA-Ar consistently under 8-10
Resistant: symptoms persist despite ≥50mg diazepam-equivalent in 1st hour or ≥200mg in first 3h
Resistant withdrawal — transfer to critical care; add phenobarbital under continuous monitoring
Delirium tremens or withdrawal seizure at any point: manage as a medical emergency in an inpatient/critical-care setting regardless of the original pathway
On completion of withdrawal management: connect every patient to ongoing AUD pharmacotherapy and/or psychosocial care before discharge
Ongoing AUD pharmacotherapy selection
AUD confirmed; patient ready to discuss ongoing pharmacotherapy (with or without preceding withdrawal management)
Establish the patient's treatment goal: abstinence, or reduced drinking
Goal: abstinence or reduced drinking
Naltrexone 25 mg daily x3-4 days, then 50 mg daily (opioid-free ≥7-10 days first)
Goal: abstinence specifically, or hepatic impairment present
Acamprosate 666 mg PO TID, started after ≥4 days abstinence
Inadequate response, contraindication, or preference against both first-line agents
Topiramate (titrated over 4-8 weeks) or gabapentin (100-300mg TID, titrate PRN)
Motivated, can be supervised, prior disulfiram success
Disulfiram 250 mg daily after full informed consent and counselling on the disulfiram-alcohol reaction — supervised/witnessed administration preferred
Adequate response to first-line/second-line agent
Continue with regular monitoring and integrated psychosocial care; reassess goals at every visit

Drug Tables

How to use this table: Doses are adult doses and require patient-specific confirmation (renal/hepatic function, weight, allergy history). Pediatric dosing is weight-based per the current product monograph unless stated. Drug pricing is intentionally omitted. Select any drug name to open its complete Pharmasist Drug Database page.

Benzodiazepines (withdrawal management)

First-line for high-risk withdrawal (PAWSS ≥4). No single benzodiazepine has proven superior; agent choice depends on hepatic status, age, and dosing schedule. Symptom-triggered dosing (dose given only when CIWA-Ar/SAWS crosses a threshold) reduces total dose and treatment duration versus fixed dosing in mild-moderate withdrawal, but a fixed, individually-tailored schedule may be safer for severe withdrawal or when frequent reassessment is not feasible.

DrugDosageAdverse effectsComments
Diazepam
Symptom-triggered (CIWA-Ar ≥10): 20 mg PO Q1-2H until symptoms resolve and CIWA-Ar under 8 on 2 consecutive readings ≥1h apart; max 80 mg/day
Fixed schedule (outpatient example): Day 1: 10 mg PO Q4H (max 60 mg). Day 2: 10 mg Q8H. Day 3: 10 mg Q12H. Day 4: 10 mg daily. Day 5: 5 mg daily, then follow-up
Fixed schedule (inpatient example): Day 1: 5-10 mg QID. Day 2: 5-10 mg TID. Day 3: 5-10 mg BID. Day 4: 5-10 mg HS
Sedation, ataxia, respiratory depression with other CNS depressants, paradoxical agitation (rare)Long-acting with active metabolites — avoid in significant hepatic impairment and in older adults. Give with, or after, thiamine.
Lorazepam
Symptom-triggered (CIWA-Ar ≥10): 4 mg PO/SL Q1H until symptoms resolve and CIWA-Ar under 8 on 2 consecutive readings ≥1h apart; max 16 mg/day
Fixed schedule (outpatient example): Day 1: 2 mg PO/SL Q4H (max 12 mg). Day 2: 2 mg Q8H. Day 3: 2 mg Q12H. Day 4: 2 mg daily. Day 5: 1 mg daily, then follow-up
Fixed schedule (inpatient example): Day 1-2: 1-2 mg Q4H. Day 3-4: 0.5-1 mg Q4H
Sedation, ataxia, respiratory depression with other CNS depressantsNo active metabolites, cleared by glucuronidation only — preferred in hepatic impairment/cirrhosis and in older adults.
Oxazepam
Anxiety/withdrawal: 10-30 mg PO 3-4 times daily; elderly/debilitated start at 10 mg 2-3 times daily
Sedation, ataxia, respiratory depression with other CNS depressantsNo active metabolites; preferred alternative to lorazepam in hepatic impairment/older adults when lorazepam is unavailable.

Non-benzodiazepine agents (outpatient/low-risk withdrawal)

Preferred for outpatient management of mild-moderate withdrawal (PAWSS under 4) given a superior safety profile versus benzodiazepines, though evidence that they prevent seizures or delirium tremens is insufficient — do not use them for high-risk patients.

DrugDosageAdverse effectsComments
Gabapentin
Regular dose (CIWA-Ar 10-14 or SAWS ≥12): 300 mg PO TID, titrate up to 600 mg TID if not responding
PRN: 300 mg PO PRN (leave 2h between regular and PRN doses); 300-600 mg PRN at bedtime
Maximum: 3600 mg/day; taper over 3-5 days once CIWA-Ar/SAWS consistently below threshold
Sedation, ataxia, tremor, dizziness; misuse/diversion riskContraindicated with any seizure history for this indication. Also usable, at a different dosing pattern, for ongoing AUD pharmacotherapy (see below).
Carbamazepine
Day 1: 200 mg PO QID
Day 2: 200 mg PO TID
Day 3: 200 mg PO BID
Days 4-5: 200 mg PO daily, then discontinue
Dizziness, pruritus, ataxia, headache, drowsiness, nausea; rare blood dyscrasias/Stevens-Johnson syndromeAvoid in patients of Asian ethnicity unless HLA-B*15:02 testing excludes the high-risk variant. Contraindicated in hepatic disease.
Clonidine
Start: 0.1-0.2 mg PO BID, last dose at bedtime
Titrate: May add 0.2 mg PRN
Maximum: 0.1-0.6 mg BID
Hypotension, dry mouth, dizziness, sedationAdjunct-only for autonomic symptoms (sweating, tachycardia, tremor) or standalone only for mild withdrawal, low risk (PAWSS under 4). Does not protect against seizures — never a sole agent for higher-risk withdrawal.
Valproic acid
CIWA-Ar under 10 at treatment start: 250 mg PO TID x5 days; titrate to 500 mg TID x1-3 days if symptoms persist, then taper
CIWA-Ar ≥10 at treatment start: 500 mg PO TID days 1-3, then 250 mg TID days 4-5, then discontinue
Sedation, GI upset, confusion, tremorLimited evidence of efficacy — use only when all other withdrawal agents are contraindicated. Contraindicated in hepatic disease; avoid in pregnancy/childbearing potential (teratogenic).

Barbiturate (resistant/severe withdrawal)

Reserved for the small proportion of patients with withdrawal resistant to large benzodiazepine doses, including delirium tremens — critical-care setting with continuous monitoring only.

DrugDosageAdverse effectsComments
Phenobarbital
Resistant/severe withdrawal: Weight-based incremental IV dosing per institutional critical-care protocol
Narrow therapeutic index; respiratory depression, oversedation, hypotensionAdjunctive to (or in place of) escalating benzodiazepine doses once resistant withdrawal is defined (e.g., ≥50 mg diazepam-equivalent in the 1st hour, or ≥200 mg in the first 3 hours) without adequate response.

Vitamins (Wernicke encephalopathy prevention)

Give before or together with any glucose-containing fluid or food in an at-risk patient — glucose metabolism consumes thiamine and can precipitate or worsen Wernicke encephalopathy.

DrugDosageAdverse effectsComments
Thiamine (vitamin B1)
Prophylaxis (outpatient/withdrawal): 100-200 mg PO daily for the duration of withdrawal and until malnutrition risk resolves (commonly ~2 weeks, longer if risk factors persist)
Suspected Wernicke encephalopathy: 200-300 mg IV or IM daily x5 days minimum, or until the diagnosis is excluded, then switch to oral
Older-adult-specific protocol: 200 mg parenteral (IM or IV) daily x3-5 days
Well tolerated orally; rare anaphylactoid reaction with rapid IV administrationBest practice is to give thiamine to every patient with alcohol use disorder, not only those with overt signs of deficiency.
Folic acid
Supplementation: 1 mg PO daily
Well toleratedLow folate is common with chronic alcohol use and can cause severe megaloblastic anemia; supplement alongside thiamine during withdrawal/detoxification.

First-line AUD pharmacotherapy

Naltrexone and acamprosate are equally recommended first-line; selection follows the patient's treatment goal rather than one agent being generally superior.

DrugDosageAdverse effectsComments
Naltrexone
Start: 25 mg PO daily x3-4 days
Usual maintenance: 50 mg PO daily
Maximum: 150 mg PO daily, only if LFTs are normal and cravings persist at 50 mg
Nausea, headache, dizziness, abdominal pain; hepatotoxicity risk at high doses or with hepatic impairmentContraindicated with any current opioid use — confirm the patient is opioid-free for at least 7-10 days before the first dose to avoid precipitating opioid withdrawal. Monitor LFTs at baseline and 1, 3, 6 months.
Acamprosate
Usual dose: 2 x 333 mg tablets (666 mg) PO TID
Lower-weight adjustment (under 60 kg): 666 mg at breakfast, then 333 mg at midday and evening
Diarrhea, nausea, vomiting, abdominal pain, pruritus; rare reports of suicidalityRenally excreted — preferred in hepatic impairment. Contraindicated at CrCl ≤30 mL/min; reduce dose at CrCl 30-50 mL/min. Start after ≥4 days of abstinence. TID dosing can challenge adherence.

Second-line / alternative AUD pharmacotherapy

Consider after an inadequate trial of, a contraindication to, or a documented preference against both first-line agents.

DrugDosageAdverse effectsComments
Topiramate
Week 1: 25 mg PO HS
Weeks 2-3: 25 mg PO BID
Weeks 3-4: 50 mg PO BID
Further titration: Increase by 50 mg/week as needed, max 400 mg/day
Paresthesia, dysgeusia, anorexia, cognitive/concentration difficulty, dizziness, pruritus, nephrolithiasisTitrate slowly to reduce side effects. Contraindicated in pregnancy (teratogenic) and narrow-angle glaucoma; caution with conditions predisposing to acidosis.
Gabapentin (AUD maintenance)
Start: 100-300 mg PO TID
Titrate: PRN for anxiety/cravings, up to 1800 mg/day max
Sedation, ataxia, dizziness, peripheral edema; misuse/diversion riskDistinct dosing pattern from withdrawal-management use above. Renally eliminated — adjust dose in renal impairment; safe in hepatic disease.
Disulfiram
Usual dose: 250 mg PO once daily
Lower dose (daytime sedation): 125 mg PO once daily
Maximum: 500 mg PO once daily
Metallic/garlic aftertaste, dermatitis, drowsiness, erectile dysfunction; rare but serious hepatotoxicityNot commercially available in Canada — must be compounded. Blocks aldehyde dehydrogenase; if the patient drinks alcohol, acetaldehyde accumulates and produces the disulfiram-alcohol reaction (flushing, throbbing headache, nausea, vomiting, sweating, chest pain, palpitations, hypotension — rarely fatal). Reaction risk persists up to 2 weeks after the last dose given irreversible enzyme inhibition. Contraindicated within 2 weeks of metronidazole use. Most effective with supervised/witnessed daily administration. Obtain baseline and periodic LFTs.

Investigational / not routinely recommended

Baclofen, ondansetron, ketamine, and GLP-1 receptor agonists (e.g., semaglutide) have each been studied for alcohol use disorder or withdrawal, but current evidence is insufficient to recommend routine use of any of them, and none has an established Canadian dosing protocol for this indication — they are not included as a drug-table row for that reason. Clonidine, similarly, is never a sole agent for anything beyond mild, low-risk withdrawal, since it provides no seizure protection and can mask the true severity of autonomic withdrawal symptoms.

References

  1. Canadian guideline for the clinical management of high-risk drinking and alcohol use disorder — CMAJ, Canadian Research Initiative in Substance Misuse / BC Centre on Substance Use (Wood E, Bright J, Hsu K, et al.; Canadian Alcohol Use Disorder Guideline Committee). CMAJ 2023;195(40):E1364-E1379
  2. The "Prediction of Alcohol Withdrawal Severity Scale" (PAWSS): systematic literature review and pilot study of a new scale for the prediction of complicated alcohol withdrawal syndrome — Alcohol (Maldonado JR, Sher Y, Ashouri JF, et al.). Alcohol 2014;48(4):375-390
  3. EFNS guidelines for diagnosis, therapy and prevention of Wernicke encephalopathy — European Journal of Neurology, European Federation of Neurological Societies (Galvin R, Bråthen G, Ivashynka A, Hillbom M, Tanasescu R, Leone MA). Eur J Neurol 2010;17(12):1408-1418
  4. Screening for high-risk drinking and alcohol use disorder: update of the 2023 national clinical practice guideline — CMAJ (Wood E, Wong SC, Corace K, et al.). CMAJ 2026;198(17):E655-E665
  5. The AUDIT alcohol consumption questions (AUDIT-C): an effective brief screening test for problem drinking — Archives of Internal Medicine (Bush K, Kivlahan DR, McDonell MB, Fihn SD, Bradley KA). Arch Intern Med 1998;158(16):1789-1795
  6. Assessment of alcohol withdrawal: the revised clinical institute withdrawal assessment for alcohol scale (CIWA-Ar) — British Journal of Addiction (Sullivan JT, Sykora K, Schneiderman J, Naranjo CA, Sellers EM). Br J Addict 1989;84(11):1353-1357

Professional reference only. Apply clinical judgment and verify patient-specific decisions against current authoritative guidance and product information.

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