Clinical Features
Examination
- Bedside clues: Look for medications such as lactulose, inhalers (alpha 1 AT deficiency)
- General CLD: leukonychia, dupuytren contracture, palmar erythema, bruising, encephelopathy, jaundice, spider naevi, gynaecomastia, ascitis, and muscle wasting.
- Alcohol-related clues: fine tremors on outstretched hands
- Metabolic/MASLD (formerly called NAFLD) clues: central obesity, libre device, acanthosis nigricans and dyslipidaemia-associated xanthelasma.
- Viral hepatitis clues: tattoos, injection marks or haemodialysis exposure may suggest acquisition risk.
- Autoimmune liver disease clues: vitiligo, thyroid disease (check for scars), inflammatory arthritis, sicca/systemic-autoimmune features; cholestatic autoimmune disease may give scratch marks and xanthelasma.
- Haemochromatosis: bronze/slate pigmentation (see image), MCP arthropathy, diabetes clues, hypogonadism (not to be assessed in PACES) and cardiomyopathy (cardiac device).
- Wilson disease: Kayser–Fleischer rings (see skills library) or parkinsonism in a younger patient.
- Alpha-1 antitrypsin deficiency: bedside inhaler, examine the chest for hyperinflation, reduced air entry, prolonged expiration or wheeze from emphysema.
- PSC/PBC: look for signs of intestinal or extra-intestinal IBD
Presentation tip
- Present as chronic liver disease, ?decompensated (bruising, encephalopathy - flapping tremors, jaundice, spider naevi, gynaecomastia, ascites) or compensated, ?obvious etiology, signs of treatment such as scar marks ascitic tap/liver transplant
Red flags of deterioration
- New confusion, drowsiness or asterixis suggests hepatic encephalopathy and decompensation.
- Haematemesis or melaena in cirrhosis should be treated as possible variceal bleeding until proven otherwise.
- New ascites, rapidly increasing abdominal distension or peripheral oedema indicates decompensation.
- Fever, abdominal pain or unexplained renal deterioration in a patient with ascites should raise concern for spontaneous bacterial peritonitis.
- New jaundice with coagulopathy, encephalopathy or rapid systemic deterioration may represent acute-on-chronic liver failure.
Differential Diagnosis
Most common causes of DCLD, from more common to less common:
Chronic viral hepatitis: Hepatitis B, Hepatitis C
Alcohol-related liver disease
MASLD/MASH (formerly NAFLD/NASH)
Autoimmune liver disease:
Autoimmune hepatitis
Primary biliary cholangitis (PBC)
Primary sclerosing cholangitis (PSC)
Genetic/metabolic:
Haemochromatosis
Wilson disease
Alpha-1 antitrypsin deficiency
Drug-induced chronic liver injury:
Methotrexate
Amiodarone
Vascular:
Budd–Chiari syndrome
Chronic right-sided heart failure / cardiac cirrhosis
Long-standing portal vein thrombosis
Differentials for ascites:
SAAG ≥1.1 g/dL: suggests portal hypertension
Cirrhosis
Cardiac failure
Budd–Chiari syndrome
Portal vein thrombosis
SAAG <1.1 g/dL: suggests non-portal hypertensive ascites
Malignancy
Tuberculosis
Pancreatitis
Nephrotic syndrome
Serositis
Investigations
A to E assessment for unwell patients
- Focused history
- Baseline blood tests: FBC, U&E, LFT, bilirubin, albumin, INR and glucose/HbA1c to assess severity, synthetic function and complications.
- Aetiology screen: HBV/HCV testing; autoimmune serology/immunoglobulins; ferritin/transferrin saturation; caeruloplasmin/urinary copper where appropriate; alpha-1 antitrypsin level/phenotype; metabolic risk assessment.
- Ultrasound liver ± portal Doppler: Assess liver morphology, portal hypertension, ascites, focal lesions and portal/hepatic venous flow.
- Fibrosis assessment: Use transient elastography and/or validated non-invasive fibrosis tools according to aetiology and stage.
- Endoscopy: Assess oesophageal/gastric varices when indicated by cirrhosis/portal-hypertension pathways.
- HCC surveillance: Use 6-monthly liver ultrasound surveillance in people with cirrhosis, with AFP according to local pathway.
- Cause-specific testing: Respiratory assessment for alpha-1 antitrypsin disease, cardiac assessment for haemochromatosis and slit-lamp/neurological assessment when Wilson disease is suspected.
Management
Think treating cause, complications, and the need for monitoring.
Lifestyle and General Measures
No alcohol, stop smoking.
Maintain adequate calories/protein, optimise weight and exercise.
Avoid hepatotoxic drugs/NSAIDs in advanced disease.
Ensure vaccination (HAV, HBV, pneumococcal, influenza).
Specialist / MDT
Hepatology, liver nurse, dietetics.
Add alcohol/addiction, metabolic/diabetes, respiratory/genetics, or other MDT input depending on cause.
Treat the Aetiology
Remove ongoing injury and treat the underlying disease.
Condition‑Specific
Alcohol‑related disease: Complete abstinence, structured support, relapse‑prevention therapy, thiamine, nutrition.
MASLD/MASH: Sustained weight loss; aggressive control of diabetes, BP, lipids; specialist metabolic therapy if needed.
Viral hepatitis: HBV antivirals (tenofovir/entecavir when indicated); curative DAAs for HCV.
Autoimmune hepatitis: Steroids for induction; azathioprine for maintenance.
Haemochromatosis: Venesection; manage systemic complications.
Wilson disease: Lifelong copper‑lowering therapy (chelators or zinc); urgent transplant review if acute failure.
A1AT deficiency: Absolute smoking avoidance; optimise COPD care; family testing; assess for transplant if advanced.
Complications and Transplant
Manage portal hypertension, ascites, encephalopathy, infection, malnutrition, osteoporosis.
Continue HCC surveillance.
Transplant referral.