Spectrum of Liver Disease
| Stage | Description | Reversibility | Key Intervention |
|---|---|---|---|
| Simple steatosis (fatty liver / NAFLD) | Fat deposits; normal inflammation | Fully reversible | Weight loss; alcohol reduction |
| NASH (non-alcoholic steatohepatitis) | Fat + inflammation | Largely reversible | Same; plus address metabolic syndrome |
| Fibrosis (stages F1–F3) | Scarring: degree varies | Partially reversible | Weight loss; treat cause; avoid hepatotoxins |
| Cirrhosis (F4) | Advanced scarring; altered architecture | Largely irreversible | Prevent complications; transplant if end-stage |
| Decompensated cirrhosis | Jaundice, ascites, encephalopathy, variceal bleeding | Emergency | Specialist/hospital management |
Signs of Advanced Liver Disease
- Jaundice (yellow skin and eyes): reduced bilirubin conjugation
- Ascites: fluid in abdomen from low albumin + portal hypertension
- Spider naevi, >5 on upper chest and arms, sinister
- Palmar erythema: red palms
- Caput medusae: dilated abdominal veins
- Hepatic encephalopathy: confusion, asterixis ('liver flap') from ammonia
- Splenomegaly: portal hypertension causes back-pressure
References
The clinical information on this page is drawn from peer-reviewed sources indexed by the US National Library of Medicine. Links go to the source so you can read it yourself.
- Hepatic Cirrhosis. In: StatPearls. Treasure Island (FL): StatPearls Publishing. NCBI Bookshelf NBK482419
- Acute Liver Failure. In: StatPearls. Treasure Island (FL): StatPearls Publishing. NCBI Bookshelf NBK482374
References
Sources cited on this page. PubMed links open the original abstract.
- Chalasani N, Younossi Z, Lavine JE, et al. The diagnosis and management of nonalcoholic fatty liver disease: practice guidance from AASLD. Hepatology. 2018;67(1):328–357. PMID 29427967 · doi:10.1002/hep.29367
Fibrosis staging – from mild to cirrhosis
Chronic liver disease progresses through stages of fibrosis (scar tissue formation), from minimal to cirrhosis (complete architectural distortion of the liver). Staging was traditionally done by liver biopsy, but non-invasive methods now allow fibrosis to be estimated without a procedure:
- FIB-4 score: A simple calculation using age, ALT, AST, and platelet count. FIB-4 below 1.3 indicates low risk of advanced fibrosis (F0–F1); above 2.67 indicates high risk (F3–F4). NICE recommends FIB-4 as the primary non-invasive fibrosis assessment in NAFLD.
- Transient elastography (FibroScan): Uses ultrasound to measure liver stiffness – stiffer = more fibrosis. Liver stiffness below 7 kPa = minimal fibrosis; above 12 kPa = cirrhosis likely. Particularly useful in hepatitis C monitoring after antiviral therapy (fibrosis can regress).
- Enhanced liver fibrosis (ELF) panel: A blood-based test measuring three components of the extracellular matrix (TIMP-1, PIIINP, HA) – direct markers of the fibrosis process. Score above 9.8 indicates advanced fibrosis. Used in specialist practice when FIB-4 and FibroScan are inconclusive.
Signs of decompensated cirrhosis and their blood test correlates
Decompensated cirrhosis – when the liver can no longer maintain essential functions – presents through four main complications. Each has characteristic blood test findings:
- Ascites (fluid in abdomen): Caused by portal hypertension plus low albumin (the liver can no longer synthesise sufficient albumin to maintain oncotic pressure). Serum albumin below 30 g/L indicates impaired synthetic function. Serum-ascites albumin gradient (SAAG) above 11 g/L on ascitic fluid analysis confirms portal hypertension as the cause.
- Hepatic encephalopathy: Ammonia accumulates as the liver fails to detoxify gut-derived nitrogen compounds. Serum ammonia is elevated but imperfectly correlates with clinical grade – bedside assessment (orientation, asterixis, number connection test) is more reliable for monitoring.
- Variceal bleeding: Portal hypertension causes oesophageal varices – dilated veins at risk of rupture. This is the most immediately life-threatening complication. FBC shows thrombocytopenia (splenomegaly traps platelets); INR is prolonged (impaired clotting factor synthesis).
- Spontaneous bacterial peritonitis (SBP): Infection of ascitic fluid, usually by gut bacteria. Diagnosed by ascitic fluid neutrophil count above 250 cells/µL – no positive culture is required. CRP is elevated; blood cultures often positive (same organism).
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