Alcohol-Related Disorders

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]

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

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]

• 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.

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]

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.

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.

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.

• 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.

• 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.

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]

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]

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.

• 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.

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.

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.

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.

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.

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.

Second-line / alternative AUD pharmacotherapy

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

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.