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This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.
The Bottom Line
- Cirrhosis = irreversible hepatic fibrosis with regenerative nodules. Commonest UK causes: alcohol, NAFLD, hepatitis C
- Compensated: may be asymptomatic. Decompensated: ascites, variceal bleeding, hepatic encephalopathy, jaundice (any one = decompensation)
- Assess severity: Child-Pugh score (A/B/C) for prognosis; MELD/UKELD score for transplant listing
- Key management: treat underlying cause, manage complications (spironolactone for ascites, propranolol/band ligation for varices, lactulose/rifaximin for encephalopathy)
- HCC surveillance: 6-monthly USS ± AFP in ALL cirrhotic patients. Consider liver transplant if UKELD ≥49
Overview
Cirrhosis is the end-stage of chronic liver disease characterised by diffuse fibrosis, loss of normal hepatic architecture, and formation of regenerative nodules. Portal hypertension develops as fibrosis increases intrahepatic resistance to blood flow. Compensated cirrhosis may be clinically silent for years. Decompensation occurs when the liver can no longer maintain its synthetic, metabolic, and excretory functions, manifesting as ascites, variceal haemorrhage, hepatic encephalopathy, and/or jaundice. Transition to decompensation marks a major prognostic shift, with median survival dropping from >12 years (compensated) to ~2 years (decompensated) without transplantation.
Epidemiology
Liver disease is the third most common cause of premature death in the UK. There are approximately 60,000 people living with cirrhosis in England. The leading causes are alcohol (~60%), NAFLD (~20%), and hepatitis C (~10%). Other causes include autoimmune hepatitis, primary biliary cholangitis (PBC), primary sclerosing cholangitis (PSC), haemochromatosis, Wilson disease, and alpha-1-antitrypsin deficiency. Approximately 700 liver transplants are performed annually in the UK.
Clinical Features
Symptoms
Compensated: often asymptomatic or non-specific fatigue
Abdominal distension (ascites)
Haematemesis or melaena (variceal bleeding)
Confusion, drowsiness, personality change (hepatic encephalopathy)
Jaundice and pruritus
Easy bruising and bleeding (coagulopathy)
Peripheral oedema
Signs
Jaundice
Spider naevi (≥5 = significant — territory of SVC)
Palmar erythema
Dupuytren contracture (alcohol-related)
Gynaecomastia and testicular atrophy
Hepatomegaly (early) or shrunken liver (late)
Splenomegaly (portal hypertension)
Ascites (shifting dullness, fluid thrill)
Caput medusae (periumbilical venous distension)
Asterixis/flapping tremor (hepatic encephalopathy)
Fetor hepaticus (sweet musty breath)
Leukonychia (hypoalbuminaemia)
Investigations
First-line
LFTsMay show raised bilirubin, low albumin (<35 g/L), raised ALP/GGT. Transaminases may be normal in "burnt-out" cirrhosis
FBCThrombocytopenia (hypersplenism — early marker of portal hypertension), macrocytic anaemia, leucopenia
Coagulation (INR/PT)Prolonged — impaired hepatic synthetic function. Used in Child-Pugh and MELD scores
U&EsHyponatraemia (dilutional, poor prognostic marker), renal function (hepatorenal syndrome)
Second-line
Liver screen (for aetiology)Hepatitis B/C serology, autoantibodies (ANA, SMA, AMA, LKM), immunoglobulins (IgG raised in autoimmune, IgM in PBC), ferritin/transferrin saturation (haemochromatosis), caeruloplasmin (Wilson), alpha-1-antitrypsin
Abdominal USS with DopplerLiver morphology (nodular, shrunken), splenomegaly, ascites, portal vein patency and flow direction
FibroScan/transient elastographyNon-invasive fibrosis assessment — >12.5 kPa highly suggestive of cirrhosis
Child-Pugh scoreA (5–6): well-compensated. B (7–9): significant functional compromise. C (10–15): decompensated. Uses bilirubin, albumin, INR, ascites, encephalopathy
Specialist
OGD (variceal screening)All patients with newly diagnosed cirrhosis — screen for oesophageal/gastric varices. Repeat 2-yearly if no varices, annually if small varices
6-monthly HCC surveillanceUSS ± AFP every 6 months — for all cirrhotic patients regardless of aetiology
MELD/UKELD scoreFor liver transplant listing. UKELD ≥49 = eligible for transplant assessment. Uses bilirubin, INR, creatinine, sodium
Ascitic tap (diagnostic paracentesis)If new-onset ascites: albumin, cell count and differential (PMN >250/mm³ = spontaneous bacterial peritonitis), MC&S, protein, cytology
Management
NICE NG50 (Cirrhosis in over 16s), 20161
Treat underlying cause
- Alcohol: abstinence (most important single intervention)
- HCV: DAA therapy (cure halts progression)
- HBV: antiviral therapy (tenofovir/entecavir)
- Autoimmune hepatitis: prednisolone + azathioprine
- NAFLD: weight loss, metabolic risk factor management
2
Ascites
- First-line: spironolactone 100 mg OD (titrate up to 400 mg), add furosemide 40 mg OD if insufficient response
- Dietary sodium restriction (<2 g/day = 88 mmol/day)
- Therapeutic paracentesis (large-volume) for tense/refractory ascites + IV albumin replacement (8 g per litre drained if >5 L removed)
- TIPSS for refractory ascites
- SBP prophylaxis: ciprofloxacin 500 mg OD or norfloxacin if previous episode of SBP or ascitic protein <15 g/L
3
Variceal management
- Primary prophylaxis: carvedilol 6.25–12.5 mg OD (preferred) or propranolol 40 mg BD (titrate to resting HR 55–60), OR endoscopic band ligation if beta-blocker intolerant
- Acute variceal bleed: terlipressin + antibiotics + urgent OGD with band ligation (see Upper GI Bleed)
- Secondary prophylaxis: combination of non-selective beta-blocker + endoscopic band ligation programme
4
Hepatic encephalopathy
- Identify and treat precipitants: infection (SBP), GI bleeding, constipation, dehydration, electrolyte disturbance, sedative drugs
- First-line: lactulose (titrate to 2–3 soft stools/day)
- Second-line: rifaximin 550 mg BD (non-absorbable antibiotic — reduces ammonia-producing gut bacteria)
- Protein restriction is NOT recommended (patients need adequate nutrition)
5
Transplant
- Assess for liver transplantation if: UKELD ≥49, repeated decompensation, HCC within Milan criteria, or acute-on-chronic liver failure
- Abstinence from alcohol ≥6 months (some centres allow earlier listing in select cases)
- Contraindications: active sepsis, active substance misuse, advanced cardiopulmonary disease, extrahepatic malignancy
Complications
- Ascites and spontaneous bacterial peritonitis (SBP): Ascitic PMN >250/mm³ → treat with IV cefotaxime 2 g TDS (without waiting for culture). Mortality ~20%
- Variceal haemorrhage: See Upper GI Bleed entry
- Hepatic encephalopathy: Ranges from subclinical to coma. Graded West Haven I–IV
- Hepatorenal syndrome (HRS): Functional renal failure — type 1 (rapid deterioration, poor prognosis), type 2 (gradual). Treat with terlipressin + albumin
- Hepatocellular carcinoma: 1–5% annual risk — hence 6-monthly surveillance
- Coagulopathy: Paradoxically, cirrhosis carries risk of BOTH bleeding AND thrombosis (rebalanced haemostasis)
UKMLA Exam Tips
- 1Decompensation = any ONE of: ascites, variceal bleeding, encephalopathy, jaundice
- 2SBP: diagnostic paracentesis is essential in ALL new ascites and ANY cirrhotic admission. PMN >250 = treat immediately with cefotaxime
- 3Spironolactone is first-line diuretic for ascites (aldosterone antagonist). Furosemide is added second
- 4Hepatorenal syndrome: rising creatinine + refractory ascites + no response to fluid challenge. Treat with terlipressin + albumin
- 5Child-Pugh uses: Bilirubin, Albumin, INR (PT), Ascites, Encephalopathy (mnemonic: BAAIE)
- 6Thrombocytopenia is often the earliest laboratory clue to cirrhosis/portal hypertension
- 7Protein restriction is NOT recommended in hepatic encephalopathy — adequate nutrition is essential
practicetest your knowledge on cirrhosisApply what you've learnt with UKMLA-style questions from the iatroX Q-Bank — gastroenterology and beyond.
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