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Gastroenterology

Liver Cirrhosis

End-stage chronic liver injury with fibrosis and nodular regeneration. Portal hypertension causes ascites, varices and hepatic encephalopathy; hepatocellular dysfunction causes coagulopathy and jaundice.

Last reviewed 9 Jun 2026 - MedicoMedics editorial team

Progression of chronic liver disease from steatosis to cirrhosis

Aetiology & pathophysiology

Chronic hepatocyte injury (alcohol, HCV, HBV, MASLD/NAFLD, autoimmune, haemochromatosis, Wilson, primary biliary cholangitis, PSC) activates hepatic stellate cells, which lay down type I/III collagen. Regenerative nodules and fibrous septa disrupt architecture, raise intrahepatic resistance and cause portal hypertension.

Sources: AASLD Practice Guidance on Cirrhosis (Hepatology 2021;74:1014); Baveno VII Consensus on Portal Hypertension (J Hepatol 2022;76:959)

Clinical presentation

Fatigue, weight loss, jaundice, spider naevi, palmar erythema, Dupuytren, gynaecomastia, testicular atrophy, easy bruising, ascites, splenomegaly, caput medusae. Decompensation: variceal bleeding, ascites, spontaneous bacterial peritonitis, hepatic encephalopathy, hepatorenal and hepatopulmonary syndromes, HCC.

Sources: AASLD Practice Guidance on Cirrhosis (Hepatology 2021;74:1014); Baveno VII Consensus on Portal Hypertension (J Hepatol 2022;76:959)

Diagnosis & staging

Labs: elevated INR, hypoalbuminaemia, thrombocytopenia, hyponatraemia, hyperbilirubinaemia. AST usually > ALT in cirrhosis. Non-invasive fibrosis assessment: FIB-4, transient elastography (FibroScan). Ultrasound with duplex; MRI/CT for HCC surveillance. Biopsy remains gold standard when needed. Prognosis by Child-Pugh (A-C) and MELD-Na (used for transplant priority).

Sources: AASLD Practice Guidance on Cirrhosis (Hepatology 2021;74:1014); Baveno VII Consensus on Portal Hypertension (J Hepatol 2022;76:959)

Management of complications

Ascites: sodium restriction (<2 g/day) + spironolactone/furosemide, large-volume paracentesis with albumin >5 L. Refractory: TIPS. SBP (>250 PMNs/mm³): ceftriaxone + albumin, secondary prophylaxis with norfloxacin. Variceal bleed: octreotide, ceftriaxone, endoscopic band ligation, TIPS if uncontrolled. Encephalopathy: lactulose + rifaximin, identify precipitants (infection, GI bleed, dehydration, sedatives).

Sources: AASLD Practice Guidance on Cirrhosis (Hepatology 2021;74:1014); Baveno VII Consensus on Portal Hypertension (J Hepatol 2022;76:959)

Surveillance & transplant

Screen for HCC with US ± AFP every 6 months in all cirrhotics. Vaccinate against HAV, HBV, influenza, pneumococcus and COVID-19. Alcohol cessation, weight management for MASLD, hepatitis therapy. Liver transplantation for decompensated cirrhosis, MELD ≥15 or HCC within Milan criteria.

Sources: AASLD Practice Guidance on Cirrhosis (Hepatology 2021;74:1014); Baveno VII Consensus on Portal Hypertension (J Hepatol 2022;76:959)

Sample USMLE-style MCQs

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Question 1

A cirrhotic with ascitic fluid PMN 320 cells/mm³ and no surgical source has?

Question 2

Which regimen is first-line for hepatic encephalopathy?

Question 3

A cirrhotic bleeds from oesophageal varices. Which prophylaxis is given at admission?

Question 4

The MELD score is calculated from which set of variables?

Question 5

Which is the recommended HCC surveillance strategy in cirrhosis?

References

Primary guidelines and peer-reviewed sources used for this entry. Reviewed 9 Jun 2026 by MedicoMedics editorial team.

  1. AASLD Practice Guidance on Cirrhosis (Hepatology 2021;74:1014)
  2. Baveno VII Consensus on Portal Hypertension (J Hepatol 2022;76:959)

Frequently asked

When should HCC surveillance begin?

At diagnosis of cirrhosis and in chronic HBV even without cirrhosis (in high-risk groups) - 6-monthly ultrasound ± AFP.

Which fluid is used with large-volume paracentesis?

25% albumin at 6-8 g per litre of ascites removed above 5 L to prevent post-paracentesis circulatory dysfunction.

What defines SBP?

Ascitic fluid PMN count ≥250 cells/mm³ in cirrhotic ascites without a surgical source; treat with third-generation cephalosporin plus albumin.

Why do cirrhotics develop hyponatraemia?

Portal hypertension causes splanchnic vasodilation, activating RAAS and ADH; free-water retention dilutes serum sodium.

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