Liver Cirrhosis and Failure

Red flags

Suspected/known cirrhosis with acute decompensation (encephalopathy, GI bleeding, new-onset ascites — especially with pain, fever, or other systemic symptoms); acute liver failure (encephalopathy + severe derangement, especially INR >1.5 or bilirubin >60); sepsis in a patient with cirrhosis; suspected ascending cholangitis; severe hepatic encephalopathy; suspected spontaneous bacterial peritonitis.

Background

Cirrhosis results from repeated liver inflammation/injury causing progressive fibrosis that replaces normal tissue, impeding blood flow and synthetic function. Diagnosis combines clinical findings, imaging, endoscopy, non-invasive tests (transient elastography), and/or histology — it’s often asymptomatic and can occur without signs of chronic liver disease. A risk factor for liver failure and hepatocellular carcinoma (HCC) — regular monitoring and cancer screening are needed once diagnosed.

• Compensated: usually asymptomatic, normal synthetic function, may have asymptomatic portal hypertension.
• Decompensated: ascites, hepatic encephalopathy, variceal bleeding, or jaundice.

Most common causes: excess alcohol, fatty liver disease, hepatitis B/C. First Nations people are at greater risk of liver disease, especially hepatitis B.

Assessment

Causes to consider

Common: alcoholic liver disease (chronic/heavy/binge use); chronic hepatitis C (see viral-hepatitis.md for risk factors); chronic hepatitis B; metabolic dysfunction-associated steatohepatitis (MASH — see fatty-liver-nash.md).

Less common: autoimmune hepatitis; genetic disorders (haemochromatosis, alpha-1-antitrypsin deficiency, Wilson’s disease); biliary disease (primary biliary cholangitis; secondary biliary cirrhosis from prior biliary injury/ligation; primary sclerosing cholangitis); severe drug reactions; prolonged environmental toxin exposure; schistosomiasis; heart failure with hepatic congestion.

Symptoms (may be absent until complications develop)

Exhaustion/fatigue, loss of appetite, nausea, weakness, decreased mental functioning, weight loss, abdominal pain, itching, easy bruising.

Signs of chronic liver disease / complications

Spider naevi, leg oedema/ascites, bruising/bleeding, jaundice, leukonychia, palmar erythema, gynaecomastia, muscle wasting (most visible proximally in the upper limbs), sepsis, encephalopathy/confusion, and signs of portal hypertension (usually indicated by thrombocytopenia): splenomegaly, ascites, gastro-oesophageal varices, variceal GI bleeding. Also screen for HCC, and be aware of multi-organ effects: immune dysfunction/infection risk (including spontaneous bacterial peritonitis), subfertility/sexual dysfunction, renal dysfunction, osteoporosis.

Investigations

• EUC, LFTs (may be only mildly abnormal even in severe disease), INR, FBC (thrombocytopenia suggests cirrhosis/portal hypertension), iron studies, HIV, hepatitis A IgG + hepatitis B (HBsAg/HBcAb/HBsAb), HCV Ab (or RNA if known HCV-positive with reinfection risk).
• Cause-directed tests: autoimmune hepatitis (ANA, SMA, LKM, IgG); primary biliary cholangitis (AMA); Wilson’s disease (ceruloplasmin); haemochromatosis (HFE gene test if abnormal LFTs, hepatomegaly, or ferritin >1000µg/L).
• Abdominal ultrasound — liver structure/HCC, ascites, splenomegaly, varices. A normal ultrasound does not exclude cirrhosis.
• Liver fibrosis assessment: FIB-4 score (simple primary-care estimate) or liver stiffness measurement (Fibroscan, via public/private providers).
• Alpha-fetoprotein (AFP) in confirmed cirrhosis, to screen for HCC — if raised, arrange contrast CT abdomen and annotate “elevated AFP” on the request.
• Child-Pugh score to determine severity/prognosis.

Management

Practice point — paracetamol is generally fine

Most patients with cirrhosis can use paracetamol up to 2g/day maximum (lower still if they drink alcohol).

General principles

Treat the underlying cause to slow progression; treat complications; arrange ongoing monitoring and HCC screening.

Referral

Emergency assessment for any red flag above.

Urgent gastroenterology assessment if suspected/known cirrhosis (on imaging, non-invasive testing, or pathology) with any of: a current or previous decompensation event (jaundice, ascites, confusion, GI bleeding); high-risk labs (Child-Pugh >B7, MELD >9, platelets <150); or elevated AFP/a space-occupying lesion on imaging.

Non-urgent gastroenterology assessment if: an underlying liver disease needs specialist-level treatment (viral hepatitis at the referrer’s discretion, haemochromatosis, autoimmune liver disease, PSC, Wilson’s disease); a new cirrhosis diagnosis with no prior specialist plan; or routine care (varices/HCC screening, nutrition) is due within 6 months.

Medication review

Check for hepatotoxic medications (consider a Home Medicines Review) — no need to routinely stop statins.

Lifestyle and nutrition

• Compensated cirrhosis + metabolic syndrome: weight loss may help — a 10% weight loss can reverse fibrosis in MASH.
• Decompensated cirrhosis: malnutrition/sarcopenia are common — needs a diet preserving muscle mass and reducing encephalopathy risk (see GESA’s high- protein, high-energy diet resource); dietitian referral.
• Stop alcohol entirely (any amount worsens liver damage regardless of cause), smoking (nicotine or cannabis), and other substance/injecting use — consider drug and alcohol service referral.

Vaccination

Hepatitis A and B, yearly influenza, COVID-19, pneumococcus — vaccinate as early as possible, since antigenic response weakens as cirrhosis progresses.

Treating the underlying cause

• Viral hepatitis: see viral-hepatitis.md. All HBsAg-positive cirrhotic patients should receive entecavir or tenofovir irrespective of viral load — HCC surveillance continues even with a good antiviral response (risk reduced, not eliminated).
• Alcohol-related: address alcohol use disorder.
• Autoimmune hepatitis: non-urgent gastroenterology referral for immunosuppressant therapy.
• Haemochromatosis: see haemochromatosis.md.
• Wilson’s disease: non-urgent referral for copper chelators or zinc.

Managing complications (often shared care with gastroenterology)

Oesophageal varices — asymptomatic unless ruptured (haematemesis/melaena; acute bleeding mortality 10–20%). Screening endoscopy at diagnosis, repeat interval per gastroenterology. Consider non-selective beta-blockers targeting a 25% resting heart-rate reduction (not below 60bpm): carvedilol 6.25mg daily, up-titrated to 12.5mg daily (preferred but not currently PBS-listed for this indication), or propranolol 10–20mg twice daily up-titrated to 80mg twice daily. Variceal band ligation may be done at gastroscopy.

Ascites — the goal is symptom control, not complete fluid removal. Advise a low-salt diet and adequate protein/energy intake. Diuretics: spironolactone 50mg mane ± furosemide 40mg (max 400mg/160mg respectively); monitor renal function/electrolytes weekly with dose changes; weight loss target ≤1kg/day (with oedema) or ≤0.5kg/day (without). Refractory ascites (no response to maximum tolerated diuretics, or diuretics not tolerated e.g. renal disease) → seek gastroenterology advice or emergency assessment.

Hepatic encephalopathy — covert (subtle: sleep disturbance, reduced concentration, personality/mood change, impaired judgement) or overt (disorientation, drowsiness, asterixis); 64% one-year mortality. Usually transient, triggered by sedatives, constipation, dehydration, infection, or GI bleeding. Assess fitness to drive (consider formal driving assessment) — see Fitness to Drive (Austroads) for the reporting-duty framework. A high-protein diet may help. Lactulose is first-line (titrate to 2–3 loose stools/day); add rifaximin (non-absorbed antibiotic) if encephalopathy recurs on lactulose alone — reduces recurrence risk from 46% to 21% (PBS Authority criteria apply).

Hepatocellular carcinoma — 90% arises in cirrhosis (though chronic HBV or MASH can cause HCC without cirrhosis). Routine 6-monthly surveillance: abdominal ultrasound + AFP; if AFP raised, contrast CT abdomen (annotate “elevated AFP” on the request).

Spontaneous bacterial peritonitis (SBP) — poor prognosis in ascites; suspect if a patient with ascites becomes unwell (abdominal pain may be absent). Refer all suspected SBP for emergency assessment. Primary prophylaxis for high-risk patients (Child-Pugh C + low-protein ascites); after a first episode, secondary prophylaxis reduces recurrence: trimethoprim+sulfamethoxazole 160/800mg daily (preferred) or norfloxacin 400mg daily.

Infection

Cirrhosis increases infection risk — in descending frequency: SBP, UTI, pneumonia, spontaneous bacteraemia, skin/soft tissue infection. Infection is a common decompensation trigger; risk rises with disease severity; treat promptly.

Type 2 diabetes in cirrhosis

More prevalent in cirrhosis, and diabetes itself increases cirrhosis-complication risk. HbA1c may be unreliable in decompensated disease — aim HbA1c <7% as a general rule; insulin can be used in decompensated disease but needs close hypoglycaemia monitoring.

Analgesia principles

• Paracetamol up to 2g/day (lower if the patient drinks alcohol).
• Avoid NSAIDs entirely — risk of GI bleeding, renal dysfunction, hepatorenal syndrome, and ascites.
• Avoid naloxone-containing combinations — increased naloxone bioavailability can blunt opioid analgesic effect.
• Half-life/bioavailability of most analgesics is increased in decompensated disease — use lower doses, longer intervals, avoid slow-release formulations when starting, titrate slowly.
• All opioids can cause or worsen hepatic encephalopathy; avoid codeine specifically (unpredictable metabolism in severe liver disease); monitor for sedation/constipation.
• Neuropathic pain: gabapentinoids or TCAs (nortriptyline less sedating than other TCAs); avoid SNRIs; duloxetine specifically may cause liver injury.
• Consider a Home Medicines Review for patients needing long-term analgesia.

Transplantation

Considered by the specialist team when the prognosis from liver disease is worse than the expected outcome from transplant (decompensation or HCC with cirrhosis) — current 5-year post-transplant survival is >80%.

Long-term monitoring

• Every 6 months: EUC, LFTs, FBC, INR, AFP, abdominal ultrasound.
• Bone mineral density scan every 2 years (chronic liver disease is an osteoporosis risk factor; Medicare-rebatable at this interval).
• Serum testosterone every 2 years in male patients.