📋 Key Information Summary
- Alcohol-related liver disease (ALD) encompasses a spectrum from hepatic steatosis through steatohepatitis (ASH), fibrosis, cirrhosis, and hepatocellular carcinoma (HCC); it remains one of the leading causes of liver-related morbidity and mortality in Australia.
- An estimated 1.4 million Australians exceed NHMRC guideline limits for alcohol intake (>10 standard drinks/week or >4 on any single occasion); risky drinking is the strongest modifiable risk factor for ALD.
- Screening with the AUDIT-C (≥3 women, ≥4 men) or full AUDIT questionnaire should be performed annually in primary care; the AUDIT-C can be embedded in routine electronic health record templates.
- Brief motivational interventions (BI) — typically 1–3 sessions of 10–30 minutes — reduce alcohol consumption and are cost-effective in Australian general practice settings.
- Evaluate for liver damage with LFTs (AST, ALT, GGT), platelet count, INR, FIB-4 score, and liver ultrasound; an AST:ALT ratio >2 is highly suggestive of ALD.
- Transient elastography (FibroScan®) is available at most major Australian hospitals (MBS item 13020 or 55063) and is the preferred non-invasive test for staging fibrosis.
- Complete alcohol abstinence is the single most effective intervention — it can reverse steatosis, halt fibrosis progression, and improve survival even in decompensated cirrhosis.
- Alcohol withdrawal syndrome (AWS) should be assessed with the Clinical Institute Withdrawal Assessment for Alcohol–Revised (CIWA-Ar); benzodiazepines (diazepam or chlordiazepoxide) are first-line for moderate–severe withdrawal, preferably in a supervised medical setting.
- Patients with decompensated cirrhosis (ascites, variceal bleeding, hepatic encephalopathy) or severe alcoholic hepatitis (Maddrey DF ≥32) require urgent hepatology referral and consideration of corticosteroids (prednisolone 40 mg/day for 28 days).
- Pharmacotherapy for alcohol use disorder includes naltrexone (oral or extended-release IM injection), acamprosate, and disulfiram — all PBS-listed; choice depends on comorbidities, hepatic function, and patient preference.
- HCC surveillance with 6-monthly ultrasound ± AFP is mandatory for all patients with ALD-related cirrhosis, and liver transplant assessment should be considered early in eligible patients.
- Aboriginal and Torres Strait Islander Australians experience ALD at 3–5× the rate of non-Indigenous Australians; culturally safe, trauma-informed, and community-led approaches are essential to closing the gap.
Introduction & Australian Epidemiology
Alcohol-related liver disease (ALD) is a chronic hepatocellular injury caused by sustained excessive alcohol consumption. It encompasses a histological continuum — hepatic steatosis (fatty liver), alcoholic steatohepatitis (ASH), progressive fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). ALD is a leading cause of liver transplantation in Australia and accounts for approximately 25–30% of all liver-related hospital admissions nationally.
In the 2022–2023 National Drug Strategy Household Survey, 16.8% of Australians aged 14 and over exceeded the NHMRC single-occasion risk guideline (≥5 standard drinks on one occasion) at least monthly, and 23% exceeded the lifetime risk guideline (>10 standard drinks per week). The annual economic burden of alcohol-related harm in Australia has been estimated at over billion (including healthcare, lost productivity, and social costs).
ALD disproportionately affects Aboriginal and Torres Strait Islander peoples, people experiencing socioeconomic disadvantage, rural and remote populations, and middle-aged men (40–65 years). However, ALD in women is increasing, and women are more susceptible to alcohol-related liver injury at lower consumption thresholds due to differences in body composition, gastric alcohol dehydrogenase activity, and hormonal factors.
The natural history of ALD is highly variable. Approximately 90% of heavy drinkers develop steatosis, but only 10–35% develop ASH, and 10–20% progress to cirrhosis over two or more decades. Genetic polymorphisms (PNPLA3 rs738409, TM6SF2, MBOAT7), obesity, metabolic syndrome, and concurrent viral hepatitis (especially hepatitis C) accelerate disease progression. Critically, alcohol cessation at any stage — even after decompensation — confers a survival benefit.
Key national data: Alcohol-attributable liver disease was responsible for an estimated 2,600 deaths in Australia in 2022, with a sharp rise in alcohol-related liver admissions during and after COVID-19 pandemic lockdowns (AIHW, 2023).
| Epidemiological Metric | Statistic | Source |
|---|---|---|
| Australians exceeding weekly risk guideline | ~1.4 million (23% of drinkers) | NDSHS 2022–23 |
| Alcohol-related liver deaths (annual) | ~2,600 | AIHW 2023 |
| ALD as proportion of liver transplants | ~30–35% | ANZOLT Registry |
| ATSI rate ratio for alcohol-related liver hospitalisation | 3.1× non-Indigenous rate | AIHW 2023 |
| Peak incidence age group | 40–65 years | ABS Causes of Death |
Pathophysiology
Alcohol (ethanol) is metabolised in the liver primarily by alcohol dehydrogenase (ADH) and, to a lesser extent, by the microsomal ethanol-oxidising system (MEOS / CYP2E1) and catalase. The resultant acetaldehyde and reactive oxygen species (ROS) drive the pathological cascade:
1
Hepatic Steatosis
Acetaldehyde inhibits fatty-acid β-oxidation and promotes lipogenesis via SREBP-1c activation. Fat droplets accumulate in hepatocytes. This stage is fully reversible with abstinence (weeks to months).
2
Alcoholic Steatohepatitis (ASH)
Gut-derived endotoxin (lipopolysaccharide / LPS) translocates across an alcohol-damaged intestinal barrier and activates hepatic Kupffer cells via TLR4 signalling. Pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) recruit neutrophils. Mallory–Denk bodies form. Hepatocyte ballooning and necrosis occur.
3
Fibrosis & Cirrhosis
Persistent inflammation activates hepatic stellate cells (HSCs) to produce extracellular matrix (collagen I and III). Fibrosis progresses from pericentral/perisinusoidal (zone 3) → bridging fibrosis → regenerative nodules → cirrhosis. PNPLA3 I148M polymorphism accelerates this step.
4
Decompensation & HCC
Portal hypertension develops from increased intrahepatic resistance (sinusoidal remodelling) and splanchnic vasodilation. Decompensation manifests as ascites, variceal haemorrhage, hepatic encephalopathy, and jaundice. Cirrhotic liver also carries a 1–6% annual risk of HCC development.
Spectrum reversibility: Steatosis and even early ASH are fully reversible with abstinence. Established cirrhosis is not reversible, but abstinence still reduces portal pressure, improves synthetic function, and halts further progression.
Screening & Brief Intervention
Screening for risky alcohol consumption is a core component of preventive health care in Australian general practice (RACGP Red Book). All adults should be screened at least annually, and more frequently in those with known liver disease, mental health comorbidities, or a history of substance use disorders.
Screening Tools
| Tool | Items | Positive Threshold | Setting |
|---|---|---|---|
| AUDIT-C | 3 items | ≥3 (women), ≥4 (men) | Primary care — rapid screen |
| Full AUDIT | 10 items | ≥8 hazardous; ≥20 dependence | Confirmed risky drinking, assessment |
| CAGE | 4 items | ≥2 positive responses | Quick bedside screen (less sensitive) |
| FAST | 4 items | ≥3 total | Emergency department |
Recommended approach: Use the AUDIT-C as the initial screening tool embedded in practice software. If positive (≥3 women / ≥4 men), proceed to the full AUDIT to quantify risk level and guide intervention intensity. The AUDIT is freely available under WHO copyright with permission for clinical use.
Brief Motivational Interventions (BI)
Brief interventions in primary care are a Level I evidence-based strategy for reducing harmful alcohol consumption. The FRAMES approach is the foundation of effective BI in Australian general practice:
- Feedback — provide personalised results (AUDIT score, LFTs, elastography)
- Responsibility — emphasise the patient's autonomy in choosing to change
- Advise — give clear, non-judgemental advice to reduce or cease drinking
- Menu — offer a range of strategies (goal-setting, self-monitoring, referral)
- Empathy — use reflective listening, open-ended questions
- Self-efficacy — express confidence in the patient's ability to change
For patients with mild risky drinking (AUDIT 8–15), a single brief session (5–15 minutes) with follow-up is appropriate. For moderate risky drinking (AUDIT 16–19), 3–4 sessions of 15–30 minutes (extended BI) or referral to a psychologist with addiction expertise is recommended. For probable alcohol dependence (AUDIT ≥20), referral to specialised addiction medicine services, consideration of pharmacotherapy, and planned withdrawal management are required.
Medicare-funded counselling: Under MBS items 2700 and 2701, GPs can provide focused psychological strategies for alcohol-related problems. Additionally, the Australian Government funds free telephone counselling via the National Alcohol and Other Drug Hotline (1800 250 015) and online support via Counselling Online (counsellingonline.org.au).
NHMRC Guideline Thresholds
| Risk Level | Single Occasion | Weekly Total | Action |
|---|---|---|---|
| Low risk | ≤4 standard drinks | ≤10 standard drinks | Reinforce low-risk drinking |
| Risky | >4 on any occasion | >10/week | Brief intervention + BI follow-up |
| High risk | >6 on any occasion (frequent) | >20/week (men), >15/week (women) | Extended BI, pharmacotherapy, LFT screen |
| Dependence likely | AUDIT ≥20 or clinical features | Daily drinking to avoid withdrawal | Addiction medicine referral, withdrawal plan |
Evaluation for Liver Damage
All patients identified as drinking above NHMRC guideline thresholds should undergo liver evaluation. Patients with any abnormal liver biochemistry in the context of regular alcohol use require structured assessment for the degree of liver injury, fibrosis stage, and complications of portal hypertension.
First-Line Investigations
Essential
Liver function tests (AST, ALT, GGT, ALP, bilirubin, albumin)
AST:ALT ratio >2 strongly suggests ALD. GGT is the most sensitive marker of recent heavy drinking. Albumin and bilirubin reflect synthetic function and are components of Child–Pugh and MELD scores. Available at all Australian pathology providers.
Essential
Full blood count with platelets
Thrombocytopenia (platelets <150 × 10⁹/L) is an early marker of portal hypertension and hypersplenism. Macrocytosis (MCV >100 fL) is common with heavy alcohol use. Used in FIB-4 calculation.
Essential
INR / Prothrombin time
Elevated INR indicates impaired hepatic synthetic function. Part of MELD score calculation. INR >1.7 in the setting of alcoholic hepatitis confers higher mortality risk (Maddrey discriminant function).
Available
FIB-4 score (calculated)
FIB-4 = (Age × AST) / (Platelets × √ALT). Score <1.3 suggests low fibrosis risk (NPV ~90%); >3.25 suggests advanced fibrosis. Can be calculated in practice software. No MBS item — free calculation.
Available
Liver ultrasound
First-line imaging. Detects steatosis (increased echogenicity), splenomegaly, ascites, portal vein dilation, and hepatic nodules. Available at all Australian radiology practices. MBS item 55039 (abdomen).
Referral
Transient elastography (FibroScan®)
Non-invasive measure of liver stiffness (kPa). Scores <7.5 kPa exclude advanced fibrosis; >12.5 kPa suggest cirrhosis; >20 kPa are highly suggestive of clinical significant portal hypertension. Available at most tertiary hospitals and some community hepatology clinics. MBS item 55063 or 13020.
FIB-4 Score Interpretation
| FIB-4 Value | Interpretation | Action |
|---|---|---|
| <1.3 | Low risk of advanced fibrosis | Repeat in 2–3 years if drinking continues; otherwise reassurance |
| 1.3–3.25 | Indeterminate — may have significant fibrosis | Refer for transient elastography or hepatology assessment |
| >3.25 | High probability of advanced fibrosis / cirrhosis | Urgent hepatology referral; initiate HCC screening if cirrhosis confirmed |
Assessing for Cirrhosis and Portal Hypertension
Clinical features suggesting established cirrhosis include spider naevi, palmar erythema, gynaecomastia, caput medusae, splenomegaly, ascites, and asterixis. However, compensated cirrhosis is frequently clinically silent. The following findings on examination, bloods, and imaging should prompt concern:
- Platelets <150 × 10⁹/L (hypersplenism from portal hypertension)
- Albumin <35 g/L or INR >1.3 (impaired synthetic function)
- AST:ALT ratio >1 (reversal of normal ratio) with AST rarely >300 IU/L in ALD
- Ultrasound: splenomegaly (>13 cm), ascites, portal vein >13 mm, recanalised umbilical vein
- FibroScan® >12.5 kPa (suggests cirrhosis); >20 kPa suggests clinically significant portal hypertension
Critical safety point: An AST >300 IU/L in the setting of alcohol use is NOT typical of ALD alone and should prompt evaluation for alternative aetiologies: acetaminophen (paracetamol) overdose, viral hepatitis (hepatitis A, B, C), ischaemic hepatitis, or autoimmune hepatitis. Acute alcoholic hepatitis typically produces AST 100–300 IU/L with the classic AST:ALT ratio >2.
Second-Line / Specialist Investigations
Specialist
Upper GI endoscopy (OGD)
To screen for oesophageal and gastric varices in confirmed cirrhosis. Recommended at diagnosis and then every 1–3 years depending on variceal size and liver stiffness score. Available at all major hospitals.
Specialist
CT or MRI liver with contrast
For characterisation of liver lesions detected on ultrasound; HCC screening protocol (LI-RADS). Multiphase CT or gadoxetate-enhanced MRI preferred. MBS items 56806/56814.
Specialist
Liver biopsy
Gold standard for histological grading. Reserved for diagnostic uncertainty, atypical features, or when concurrent aetiology suspected. Transjugular route preferred in coagulopathic patients.
Referral
Hepatitis B & C serology
Essential to exclude concurrent viral hepatitis, which accelerates ALD progression. HBsAg, anti-HBs, anti-HBc (core), anti-HCV. HCV RNA if anti-HCV positive.
Clinical Presentation & Diagnostic Criteria
ALD may be identified at any point on the disease spectrum — from an incidental finding of elevated GGT at a routine health check to presentation with decompensated cirrhosis or acute variceal haemorrhage. The diagnosis is clinical, supported by laboratory and imaging findings, and requires a history of significant alcohol intake.
Presentation by Disease Stage
Stage 1
Steatosis
Usually asymptomatic. May have mild hepatomegaly, mildly elevated GGT, or incidental fatty liver on ultrasound. AST and ALT often normal or mildly raised.
Setting: Primary care
Stage 2
Alcoholic Steatohepatitis (ASH)
Hepatomegaly, RUQ tenderness, nausea, anorexia. LFTs elevated (AST 100–300 IU/L, AST:ALT >2). Leukocytosis, fever possible. Severe ASH: Maddrey DF ≥32, MELD ≥21.
Setting: Hospital / Hepatology
Stage 3
Cirrhosis — Compensated
Often asymptomatic. May have thrombocytopenia, mild coagulopathy, spider naevi, or splenomegaly. Diagnosed by elastography or biopsy. Patients feel well.
Setting: Hepatology outpatient
Stage 4
Cirrhosis — Decompensated
Ascites, spontaneous bacterial peritonitis, variceal bleeding, hepatic encephalopathy, jaundice, hepatorenal syndrome. MELD >15 associated with 1-year mortality >20%.
Setting: Tertiary hospital / Transplant centre
Alcoholic Hepatitis — Specific Presentation
Severe alcoholic hepatitis (SAH) is a distinct clinical syndrome with rapid onset of jaundice, fever, tender hepatomegaly, and systemic inflammatory response. It carries a short-term mortality of 30–50% if untreated. Key diagnostic features include:
- Recent heavy drinking (often >80 g/day for >6 months), though presentation may lag 4–8 weeks after a drinking binge
- Jaundice (bilirubin >80 µmol/L) developing over days to weeks
- AST 100–300 IU/L (rarely >500 IU/L), AST:ALT ratio >2
- Neutrophil leukocytosis, elevated CRP
- Maddrey discriminant function (DF) = 4.6 × (patient PT − control PT) + bilirubin (mg/dL); DF ≥32 = severe disease
Rule out other causes before diagnosing SAH: Acetaminophen toxicity (check paracetamol level), viral hepatitis (HAV IgM, HBsAg, anti-HCV), biliary obstruction (ultrasound + MRCP), ischaemic hepatitis, autoimmune hepatitis (ANA, ASMA, IgG), and Wilson disease (if <40 years, ceruloplasmin, urinary copper).
Risk Stratification & Severity Scoring
Accurate risk stratification guides treatment intensity, determines the need for corticosteroid therapy in alcoholic hepatitis, and informs transplant eligibility. Multiple validated scoring systems are used in Australian hepatology practice:
Scoring Systems for Alcoholic Hepatitis
| Score | Components | Threshold for Severe Disease | Utility |
|---|---|---|---|
| Maddrey DF | PT difference + bilirubin (mg/dL) | ≥32 | Standard for corticosteroid initiation |
| MELD score | Bilirubin, INR, creatinine | ≥21 | Predicts 90-day mortality; transplant listing |
| ABIC score | Age, bilirubin, INR, creatinine | >6.71 = high risk | Alternative to Maddrey; predicts 90-day mortality |
| Lille model | Change in bilirubin at day 7 of corticosteroid treatment | ≥0.45 = non-responder | Futility assessment — stop steroids if Lille ≥0.45 |
| Child–Pugh | Bilirubin, albumin, INR, ascites, encephalopathy | Class B (7–9) / C (10–15) | Cirrhosis severity; surgical risk; HCC management |
Lille Score at Day 7 — Futility Check
1
Start corticosteroids
Prednisolone 40 mg PO daily if Maddrey DF ≥32 or MELD ≥21, after excluding active infection.
2
Reassess at Day 7
Calculate Lille score using bilirubin at day 0 and day 7, plus other clinical variables.
3
Lille ≥0.45 → Stop steroids
Non-responders have <20% 6-month survival. Consider palliative care, transplant assessment, or clinical trials.
4
Lille <0.45 → Continue
Complete 28-day course of prednisolone, then taper and discontinue. Monitor for infection.
Cirrhosis Risk Stratification
For patients with established ALD-related cirrhosis, ongoing risk stratification includes:
- HCC risk: 1–6% per year in cirrhosis; 6-monthly ultrasound ± AFP surveillance (MBS item 55039)
- Variceal bleeding risk: Endoscopy at diagnosis; non-selective β-blocker (carvedilol or propranolol) for medium/large varices or small varices with red wale signs
- Decompensation risk: Baveno VII criteria — liver stiffness <20 kPa AND platelets >150 × 10⁹/L can safely exclude clinically significant portal hypertension and high-risk varices
- Transplant eligibility: MELD-Na score, 6-month abstinence requirement (varies by state), psychosocial assessment
Management & Referral
The Centrality of Abstinence
Abstinence is the most effective treatment for ALD at every stage. Sustained alcohol cessation improves survival, reverses steatosis, halts or slows fibrosis progression, reduces portal pressure, and improves hepatic synthetic function — even in decompensated cirrhosis. There is no safe level of ongoing alcohol intake for patients with established liver disease.
Counselling for Abstinence
Counselling should be delivered in a non-judgemental, empathic manner using motivational interviewing techniques. Key messages include:
- Personalised feedback linking the patient's current liver results to their alcohol intake
- Explanation of the disease trajectory with and without continued drinking
- Setting of specific, measurable, achievable, relevant, time-bound (SMART) goals
- Development of a relapse prevention plan with identification of triggers
- Involve family/support persons with patient consent
- Refer to peer support programs (e.g., SMART Recovery Australia, Alcoholics Anonymous)
Alcohol Withdrawal Management
Patients with alcohol dependence who reduce or cease drinking are at risk of alcohol withdrawal syndrome (AWS), which can range from mild tremor and anxiety to life-threatening delirium tremens (DT). AWS typically onset 6–24 hours after the last drink, peaks at 24–72 hours, and resolves by 5–7 days.
Mild
CIWA-Ar <10
Tremor, anxiety, insomnia, nausea, mild tachycardia. Onset 6–12 hours.
Setting: Outpatient / GP with close follow-up
Moderate
CIWA-Ar 10–20
Pronounced tremor, diaphoresis, tachycardia, nausea/vomiting, transient hallucinations. Onset 12–48 hours.
Setting: Hospital / supervised detox unit
Severe
CIWA-Ar >20 or DT
Seizures (onset 12–48h), delirium tremens (onset 48–96h), autonomic instability, disorientation, visual/tactile hallucinations. Mortality 5–15% if untreated.
Setting: ICU / HDU admission
Pharmacotherapy for Withdrawal
Diazepam
Valium® · Generic · Benzodiazepine
Adult dose (symptom-triggered)
10–20 mg PO/IV PRN based on CIWA-Ar score (score ≥10: give dose; reassess in 1 hour)
Adult dose (fixed schedule)
20 mg PO QID day 1; taper by 5 mg/day over 5–7 days
Paediatric dose
Not routinely used; specialist management only
Renal adjustment
Use with caution; active metabolites accumulate in renal impairment
Hepatic adjustment
Reduce dose by 50% in severe hepatic impairment; lorazepam preferred if decompensated cirrhosis
PBS status
✔ PBS General Benefit
Chlordiazepoxide
Librium® · Generic · Benzodiazepine
Adult dose
25–50 mg PO TDS–QID day 1; taper by 10–20% per day over 7–10 days
Renal / hepatic adjustment
Avoid in severe hepatic impairment; use lorazepam as alternative
PBS status
✔ PBS General Benefit
Lorazepam
Ativan® · Generic · Benzodiazepine (preferred in liver disease)
Adult dose
1–2 mg PO/IV/IM QID PRN based on CIWA-Ar; hepatically safe (no active metabolites)
Key advantage
Preferred in decompensated cirrhosis — undergoes glucuronidation only, does not accumulate
PBS status
✔ PBS General Benefit
Thiamine (vitamin B1)
Generic · Essential adjunct in all alcohol withdrawal
Adult dose
IV: 300–500 mg IV TDS for 3–5 days, then 100–300 mg PO daily. Must be given BEFORE or WITH glucose.
Indication
Prevention/treatment of Wernicke encephalopathy (confusion, ataxia, ophthalmoplegia)
PBS status
✔ PBS General Benefit
Thiamine before glucose: In malnourished or dependent drinkers, IV thiamine MUST be administered before or concurrently with any glucose-containing fluids. Giving glucose without thiamine can precipitate Wernicke encephalopathy, which may progress to irreversible Korsakoff syndrome. Thiamine is water-soluble and has no toxicity; err on the side of higher doses.
Pharmacotherapy for Alcohol Use Disorder (AUD) Maintenance
Naltrexone
ReVia® · Depot injection: Vivitrol® · Opioid antagonist
Adult dose (oral)
50 mg PO daily; may use 100 mg Mon/Wed/Fri (targeted dosing before anticipated drinking situations)
Adult dose (IM depot)
380 mg IM every 4 weeks (gluteal injection by healthcare professional)
Key contraindication
Active opioid use (precipitates severe withdrawal); acute hepatitis or liver failure (avoid if ALT/AST >5× ULN); concurrent opioid analgesics
Hepatic adjustment
Avoid in decompensated cirrhosis; use with caution and regular LFT monitoring in compensated cirrhosis
PBS status
🔶 PBS Authority Required
Acamprosate
Campral® · NMDA receptor modulator
Adult dose
666 mg (2 × 333 mg tablets) PO TDS; start when patient is abstinent
Key advantage
No hepatic metabolism — safe in liver disease; renally cleared
Renal adjustment
Contraindicated if eGFR <30 mL/min; reduce to 333 mg TDS if eGFR 30–50
PBS status
🔶 PBS Authority Required
Disulfiram
Antabuse® · Aldehyde dehydrogenase inhibitor
Adult dose
200 mg PO daily (range 125–500 mg); must be fully informed and motivated
Mechanism
Blocks acetaldehyde metabolism → acetaldehyde accumulation → severe flushing, nausea, vomiting, tachycardia if alcohol consumed (aversive therapy)
Contraindications
Severe hepatic impairment, cardiovascular disease, psychosis, concurrent metronidazole or cephalosporins
PBS status
✔ PBS General Benefit
Management of Severe Alcoholic Hepatitis
Patients with severe alcoholic hepatitis (Maddrey DF ≥32 or MELD ≥21) require inpatient management under hepatology supervision. The treatment algorithm is:
1
Exclude active infection
Blood cultures, urine culture, chest X-ray, diagnostic ascitic tap (PMN >250 cells/mm³ = SBP). Do NOT start corticosteroids if infection is present — treat infection first.
2
Nutritional support
Target 35 kcal/kg/day, 1.2–1.5 g protein/kg/day. Supplement thiamine, folate, zinc, vitamin D. NG tube feeding if oral intake inadequate. Avoid protein restriction.
3
Prednisolone 40 mg/day × 28 days
If no active infection and Maddrey DF ≥32. Use prednisolone (PO), not prednisone (requires hepatic conversion). Calc Lille at day 7.
4
Lille at day 7
<0.45 → continue prednisolone to day 28. ≥0.45 → stop steroids (futile), discuss palliative/comfort care, transplant evaluation.
Pentoxifylline is no longer recommended: The STOPAH trial (Lancet, 2015) demonstrated no mortality benefit from pentoxifylline in severe alcoholic hepatitis. It is no longer included in eTG or AASLD guidelines as a treatment option.
Hepatology Referral Criteria
- FIB-4 >3.25 or FibroScan >12.5 kPa (suggesting advanced fibrosis/cirrhosis)
- Any evidence of decompensation: ascites, variceal bleeding, jaundice, encephalopathy
- Maddrey DF ≥32 or MELD ≥21 (severe alcoholic hepatitis)
- Suspected HCC on imaging
- Diagnostic uncertainty — atypical LFT pattern, suspected concurrent liver disease
- Consideration of liver transplant assessment (MELD >15, sustained abstinence or likely compliance)
- Failure to improve with abstinence over 3–6 months
General Practice Management of ALD Without Decompensation
Patients with early ALD (steatosis, mild fibrosis) can be managed in primary care with:
- Motivational interviewing and structured brief intervention for alcohol cessation
- Consideration of AUD pharmacotherapy (acamprosate or naltrexone, with LFT monitoring)
- Repeat LFTs, FIB-4, and platelets at 3–6 months post-abstinence to assess response
- Cardiovascular risk factor management (BP, lipids, diabetes — MetS is common in ALD)
- Hepatitis B vaccination if non-immune, hepatitis C treatment if HCV RNA positive
- Annual review with LFTs and FIB-4; onward referral if no improvement or deterioration
Monitoring
Monitoring Schedule
Baseline
LFTs (AST, ALT, GGT, ALP, bilirubin, albumin), FBC with platelets, INR, FIB-4, liver ultrasound, hepatitis B/C serology, AUDIT-C. Document alcohol consumption patterns (quantity, frequency, duration).
3 months
Repeat LFTs, platelets, INR. Assess adherence to abstinence (PEth blood test or CDT if available). Review AUD pharmacotherapy efficacy and side effects. FIB-4 recalculation.
6 months
LFTs, FIB-4. If cirrhosis confirmed: begin HCC surveillance (6-monthly ultrasound ± AFP). Repeat FibroScan if available. Liver transplant referral if MELD >15 and appropriate candidate.
12 months
Comprehensive review. LFTs, platelets, INR, albumin. Assess for clinical improvement with sustained abstinence. If LFTs normalised: continue annual monitoring with 6-monthly HCC surveillance (if cirrhosis). If not improved: reassess diagnosis, referral, or consider concurrent aetiology.
Ongoing (annually)
Annual LFTs, FBC, INR, AUDIT-C, and AUD management review. 6-monthly ultrasound for HCC surveillance (cirrhosis). Variceal surveillance per hepatology schedule. Bone density (DEXA) every 2 years if chronic corticosteroid exposure or other risk factors.
Biomarkers of Alcohol Consumption
| Biomarker | Window | Sensitivity/Specificity | Notes |
|---|---|---|---|
| GGT | 2–6 weeks | Moderate / moderate | Elevated in obesity, cholestasis, drugs; not specific |
| CDT (carbohydrate-deficient transferrin) | 2–4 weeks | Moderate–high / high | Most specific biomarker for heavy drinking; MBS item 66832 |
| PEth (phosphatidylethanol) | 2–4 weeks | High / high | Direct alcohol metabolite; not yet widely available in Australia; definitive proof of alcohol intake |
| MCV (mean cell volume) | Variable | Low / low | Non-specific; slow to normalise after cessation |
| Urine ethyl glucuronide (EtG) | 24–80 hours | High / moderate | Detects recent intake; useful for monitoring compliance |
Self-report is still valuable: Despite the availability of biomarkers, validated self-report instruments (AUDIT, Timeline Followback) are the cornerstone of monitoring in primary care. Combining self-report with objective biomarkers (CDT, GGT) provides the most reliable assessment of drinking status.
Special Populations
Pregnancy
Alcohol in pregnancy
There is NO safe level of alcohol consumption during pregnancy. ALD in pregnancy is rare but carries high maternal and fetal morbidity. Alcohol is a known teratogen causing fetal alcohol spectrum disorder (FASD). NHMRC guidelines advise abstinence from alcohol when planning pregnancy and throughout pregnancy and breastfeeding.
Pharmacotherapy in pregnancy
Naltrexone and acamprosate are contraindicated in pregnancy (Category B3 / insufficient safety data). Disulfiram is contraindicated (teratogenicity concerns). Benzodiazepines carry teratogenic risk (Category D); lorazepam is preferred if withdrawal management is required, under specialist supervision only. Thiamine and folate supplementation are safe and essential.
Monitoring
Pregnant women with ALD or heavy alcohol use require multidisciplinary care including obstetrics, addiction medicine, and hepatology. GGT is unreliable in pregnancy (physiologically elevated). CDT and PEth are preferred biomarkers.
Paediatrics & Adolescents
Epidemiology
ALD is uncommon in adolescents but may be seen in the context of severe binge drinking or early-onset AUD. FASD affects an estimated 2–5% of Australian school-age children. All adolescents should be screened with CRAFFT or AUDIT-C at annual health checks.
Benzodiazepines
Not routinely recommended for paediatric withdrawal. Specialist (addiction medicine/paediatric hepatology) management is mandatory. Dosing is weight-based and not well standardised for paediatric withdrawal.
Pharmacotherapy for AUD
Naltrexone, acamprosate, and disulfiram are NOT approved for use in patients <18 years in Australia. Psychosocial interventions (CBT, family therapy, motivational enhancement therapy) are first-line.
Elderly (>65 years)
Increased vulnerability
Reduced hepatic blood flow, lower volume of distribution, decreased albumin, and polypharmacy increase susceptibility to alcohol-related harm and drug interactions. Falls risk is markedly elevated. FIB-4 is less reliable in the elderly (age is in the numerator); consider FibroScan as an alternative.
Benzodiazepines
Use with extreme caution. Risk of oversedation, falls, cognitive impairment. Lower doses (50% reduction); prefer short-acting agents (lorazepam, oxazepam). Avoid long-acting diazepam if possible.
Naltrexone
Can be used with dose adjustment and LFT monitoring. Caution with concurrent opioids for pain management. Acamprosate is preferred if renal function adequate (eGFR >30).
Renal Impairment
Acamprosate
Contraindicated if eGFR <30 mL/min. Reduce dose to 333 mg TDS if eGFR 30–50 mL/min. Renally cleared; significant accumulation in CKD.
Benzodiazepines
Lorazepam is preferred (no active metabolites). Avoid chlordiazepoxide and diazepam in renal impairment — active metabolites accumulate.
Hepatorenal syndrome
Type 1 HRS (doubling of creatinine to >226 µmol/L in <2 weeks) is a complication of advanced cirrhosis with ascites. Treat with terlipressin (2 mg IV Q4–6h) + albumin (1 g/kg initially, then 20–40 g/day). Refer to transplant centre urgently. Terlipressin is available via compassionate access / TGA Special Access Scheme in Australia.
Hepatic Impairment (Advanced ALD)
Naltrexone
Avoid in decompensated cirrhosis (Child–Pugh B/C). Hepatotoxic risk if ALT/AST >5× ULN. Can be used cautiously in compensated cirrhosis with monthly LFTs.
Disulfiram
Absolutely contraindicated in any degree of hepatic impairment — hepatotoxic.
Preferred agents
Acamprosate is the safest AUD pharmacotherapy in liver disease (no hepatic metabolism). Lorazepam is the preferred benzodiazepine for withdrawal (glucuronidation only). Avoid diazepam and chlordiazepoxide.
Immunocompromised
HIV and ALD
Alcohol accelerates liver fibrosis in HIV/HCV co-infection. Antiretroviral drug hepatotoxicity is synergistic with ALD. Monitor LFTs closely. Some ARVs (e.g., nevirapine, ritonavir-boosted regimens) require dose adjustment. Coordinate care between hepatology and infectious disease.
Post-transplant
Alcohol relapse post-liver transplant occurs in 10–30% of patients. Tacrolimus and cyclosporine are metabolised by the liver; ALD recurrence increases immunosuppressant toxicity risk. Lifelong monitoring is required.
Aboriginal and Torres Strait Islander Health
Aboriginal and Torres Strait Islander Health Considerations
Aboriginal and Torres Strait Islander Australians experience significantly higher rates of alcohol-related liver disease compared to non-Indigenous Australians. According to AIHW data (2023), the rate of alcohol-attributable liver disease hospitalisation among Indigenous Australians is approximately 3.1 times the non-Indigenous rate. ALD is a leading contributor to the gap in life expectancy between Indigenous and non-Indigenous Australians. Culturally safe, trauma-informed, community-led approaches are essential.
Key Epidemiological Disparities
- Indigenous Australians are 3–5× more likely to be hospitalised for alcohol-related liver disease than non-Indigenous Australians.
- Despite lower overall per-capita alcohol consumption (a higher proportion of Indigenous Australians abstain), those who do drink consume alcohol at higher-risk levels and experience greater harm.
- ALD mortality rates are highest in remote and very remote areas of the Northern Territory, Western Australia, and Queensland, where specialist hepatology and addiction services are scarce.
- Hepatitis B prevalence is 5–10× higher in Indigenous communities, compounding ALD progression when co-infection is present.
- Younger age of onset of ALD and higher rates of decompensated cirrhosis at first presentation are observed in Indigenous patients.
Barriers and Enablers
Closing the Gap: ALD is a preventable contributor to the Indigenous health gap. Screening for risky alcohol use, early liver disease assessment, and culturally safe intervention should be incorporated into every Indigenous health check (MBS item 715). The MBS 715 health check includes alcohol screening and provides an opportunity for brief intervention within a holistic health assessment framework.
📚 References
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