Lucan · Conditions
Alcohol use disorder
Australian guidance: RACGP Alcohol/Drug Consensus + eTG Psychotropic
1. Definition and epidemiology
Alcohol use disorder (AUD) is a chronic relapsing condition characterised by compulsive alcohol use, loss of control over intake, and continued use despite harmful consequences including physical, psychiatric, and social sequelae. In Australia, alcohol consumption accounts for approximately 3.3% of the total burden of disease and injury, and alcohol is responsible for the majority of drug-related deaths and hospitalisations among people aged 15 to 34. Data from general practice encounters shows that approximately 23% of adult patients attending Australian general practices drink at "at-risk" levels, indicating a high prevalence in primary care settings.
2. Pathophysiology
Alcohol exerts its primary central nervous system effects through positive allosteric modulation of gamma-aminobutyric acid type A (GABA-A) receptors and inhibition of N-methyl-D-aspartate (NMDA) glutamate receptors. Acute intoxication potentiates inhibitory GABAergic tone and suppresses excitatory glutamatergic activity, producing sedation and anxiolysis. With chronic heavy use, the brain undergoes adaptive neuroplastic changes: GABA-A receptors are downregulated and desensitised, while NMDA receptors are upregulated and sensitised. When alcohol is abruptly ceased, this neuroadaptation is unmasked as a state of CNS hyperexcitability. The resulting withdrawal syndrome is driven by unopposed excitatory neurotransmission and can culminate in autonomic instability, seizures, and delirium tremens. Dopaminergic mesolimbic pathways mediating reward and reinforcement are also implicated in craving and relapse. Chronic alcohol use additionally causes hepatotoxicity through acetaldehyde accumulation, oxidative stress, and activation of the innate immune system via Kupffer cell stimulation, contributing to alcoholic liver disease along a spectrum from steatosis to cirrhosis.
3. Clinical presentation and diagnostic criteria
AUD presents across a severity spectrum from hazardous drinking through to dependence. In the history, key features include craving, tolerance (needing more alcohol to achieve the same effect), unsuccessful attempts to cut down, continued use despite physical or psychological harm, withdrawal symptoms on cessation, and neglect of other activities. DSM-5 diagnosis requires two or more of eleven criteria within a twelve-month period, with severity graded as mild (2 to 3 criteria), moderate (4 to 5 criteria), or severe (6 or more criteria). On examination, signs of chronic use may include hepatomegaly, spider naevi, palmar erythema, parotid enlargement, Dupuytren's contracture, peripheral neuropathy, and cerebellar signs. Alcohol withdrawal presents 6 to 24 hours after the last drink with tremor, diaphoresis, tachycardia, hypertension, nausea, and anxiety; severe withdrawal may progress to seizures (approximately 5% of dependent drinkers) and delirium tremens in the most severe cases.
4. Investigations and AU-specific cutoffs
Screening is recommended every 2 to 4 years in all patients aged 15 and older. The Alcohol Use Disorders Identification Test (AUDIT) is the standard screening instrument. The abbreviated AUDIT-C (3 items, scored 0 to 12) is practical in general practice: a score of 4 or more in men, or 3 or more in women, is considered positive for hazardous drinking or active AUD. Where the AUDIT-C total is derived entirely from Question 1 alone, the clinician should review consumption history before concluding a disorder is present. The full AUDIT score of 20 or more, or AUDIT-C score of 5 or more, should prompt assessment for assisted withdrawal.
Additional investigations: - Liver function tests including gamma-glutamyl transferase (GGT) and alanine aminotransferase (ALT): GGT is elevated in chronic heavy use but is not specific; carbohydrate-deficient transferrin (CDT) has higher specificity - Full blood count: macrocytosis with elevated mean corpuscular volume (MCV) is a sensitive marker of chronic use - Electrolytes, urea, and creatinine: hypokalaemia, hypomagnesaemia, and hypophosphataemia are common - Blood glucose: hypoglycaemia may complicate withdrawal - Coagulation studies: prothrombin time is prolonged in advanced hepatic disease - Severity of Alcohol Dependence Questionnaire (SADQ): a 20-item self-administered tool used to classify mild, moderate, or severe dependence and guide withdrawal setting; a score above 30 indicates inpatient or residential withdrawal is required - Clinical Institute Withdrawal Assessment of Alcohol State, revised (CIWA-Ar) or Alcohol Withdrawal Scale (AWS): monitor symptom severity during managed withdrawal
5. Management
Management follows the 5As model in Australian primary care (Ask, Assess, Advise, Assist, Arrange). Brief interventions delivered by the general practitioner for patients drinking at hazardous or high-risk levels have Level I Grade A evidence, with studies in Australia and the United Kingdom showing a 25 to 30% reduction in alcohol consumption and a 45% reduction in the number of excessive drinkers.
Low-risk drinking targets are no more than two standard drinks on any single day and no more than four drinks on any one occasion. An Australian standard drink contains 10 g of alcohol, equivalent to 12.5 mL of pure alcohol. Pregnant women and those planning pregnancy should be advised that non-drinking is the safest option.
Patients with at-risk patterns should be offered brief advice, motivational interviewing, and goal setting around reducing intake. Patients not ready to change should be provided information about risks and have follow-up arranged within 1 to 3 months to review goals and assess for relapse.
For patients with moderate to severe dependence, managed withdrawal is required. Community-based withdrawal is appropriate when the patient has no history of seizures or delirium tremens, no suicide risk, adequate social support, no significant polydrug use, and no concurrent benzodiazepine dependence. Inpatient or residential withdrawal is required when any of these safety criteria are not met, when the patient drinks more than 30 standard drinks per day, has a SADQ score above 30, or has significant psychiatric or physical comorbidities.
Three assisted withdrawal approaches are used in practice: benzodiazepine loading (large initial dose, typically up to 80 mg of diazepam on day one in an inpatient setting), tapering fixed-dose regimens over 2 to 6 days, and symptom-triggered sedation titrated to CIWA-Ar score.
After successful withdrawal for moderate to severe dependence, pharmacotherapy combined with psychological intervention should be considered. Cognitive behavioural therapy (CBT), social network and environment-based therapies, and behavioural therapies that focus specifically on alcohol misuse have established efficacy and should be offered alongside pharmacotherapy.
Patients who fail brief interventions or who have complex needs should be referred to a local drug and alcohol counsellor or specialist service. The Alcohol and Drug Information Service (ADIS) provides a 24-hour hotline in each state and territory, including Western Australia (08) 9442 5000.
6. Pharmacology and AU PBS notes
Withdrawal phase:
Diazepam and oxazepam are the benzodiazepines of choice for acute alcohol withdrawal, with Grade A evidence supporting their use for up to a maximum of 7 days. Diazepam is preferred for its long half-life and active metabolites, which provide a smoother withdrawal curve. Oxazepam is preferred in patients with significant hepatic impairment as it undergoes direct glucuronidation without hepatic oxidation. Benzodiazepines should not be prescribed to alcohol-dependent patients before enrolling them in or referring them to a managed withdrawal program, as they can increase alcohol cravings and relapse rates. Benzodiazepines are available under PBS for alcohol withdrawal (Schedule 4 in most jurisdictions; dispensing within the context of a managed withdrawal program).
Relapse prevention (post-withdrawal):
Acamprosate (Campral): modulates glutamatergic and GABAergic neurotransmission to reduce craving. Dose is 666 mg three times daily (approximately 60 kg) to 999 mg three times daily (above 60 kg). It is PBS-listed on the Repatriation Pharmaceutical Benefits Scheme (RPBS) and is available on the Pharmaceutical Benefits Scheme (PBS) under authority prescription for patients with established alcohol dependence. Contraindicated in severe renal impairment and pregnancy.
Naltrexone (Revia, Vivitrol): an opioid receptor antagonist that reduces the reinforcing effects of alcohol. Oral dose is 50 mg daily. PBS-listed under authority for alcohol dependence. Contraindicated in patients using opioid analgesics and in those with acute hepatitis or liver failure. Monthly injectable formulation (Vivitrol) is available but not PBS-listed. Both acamprosate and naltrexone are contraindicated in pregnancy. Informed consent should be obtained before prescribing.
Disulfiram (Antabuse): produces an unpleasant acetaldehyde reaction when alcohol is consumed. Use requires close supervision; not a first-line agent. Not PBS-listed.
Thiamine (vitamin B1): all patients with AUD should receive prophylactic thiamine to prevent Wernicke's encephalopathy. High-dose parenteral thiamine (Pabrinex) is given in hospital settings for at-risk patients or those with signs of deficiency. Oral thiamine 100 mg three times daily is standard in ambulatory prevention.
7. Complications and monitoring
Key complications include:
- Neurological: Wernicke's encephalopathy (classic triad of confusion, ataxia, and ophthalmoplegia) progressing to Korsakoff's psychosis with irreversible anterograde amnesia; alcoholic peripheral neuropathy; cerebellar degeneration
- Hepatic: alcoholic fatty liver, alcoholic hepatitis, and cirrhosis; hepatocellular carcinoma complicating cirrhosis
- Gastrointestinal: oesophageal varices, Mallory-Weiss tears, pancreatitis (both acute and chronic), gastritis
- Cardiovascular: dilated cardiomyopathy, arrhythmias (particularly atrial fibrillation), hypertension
- Haematological: macrocytic anaemia, thrombocytopenia, coagulopathy
- Psychiatric: major depressive disorder, anxiety disorders, alcohol-induced psychosis, suicidal ideation
- Foetal alcohol spectrum disorder in offspring of drinking mothers
- Immune suppression increasing susceptibility to infections including pneumonia and tuberculosis
Surveillance schedule:
- Follow-up at 1 to 3 months after initial intervention to review drinking goals, assess for relapse, and monitor comorbidities
- Liver function tests, full blood count, and GGT at baseline and every 6 to 12 months in ongoing heavy use
- Annual screening for anxiety and depression given high comorbidity
- Vitamin B12 and folate annually in patients with macrocytosis or dietary insufficiency
- Patients on acamprosate: renal function at baseline and annually
- Patients on naltrexone: liver function tests at baseline, 3 months, and annually thereafter
- Patients with cirrhosis: 6-monthly hepatic ultrasound and alpha-fetoprotein for hepatocellular carcinoma surveillance per gastroenterology guidelines
Written for Australian practice and grounded in the guidance named above. Study material only — not medical advice. Always check against current guidelines.