Cirrhosis
Exam Tips
- In OSCEs, actively distinguish compensated from decompensated cirrhosis: ask about ascites, encephalopathy, jaundice, and variceal bleeding.
- A normal ALT/AST does not exclude cirrhosis; thrombocytopenia and low albumin are often more useful for chronic severity.
- Always state: any new ascites in cirrhosis needs diagnostic tap to exclude SBP (PMN >=250 cells/mm3).
- For prescribing stations, mention safety checks with diuretics (U&E/creatinine, weight trajectory, blood pressure, encephalopathy status).
- For viva answers, use Child-Pugh/MELD-Na to communicate prognosis and transplant priority succinctly.
- See Figure from page X (standard hepatology textbook) for classic stigmata of chronic liver disease and variceal pathway overview.
Definition
Cirrhosis is the end stage of chronic liver injury in which normal hepatic architecture is replaced by diffuse fibrosis and regenerative nodules, causing irreversible structural distortion. This leads to progressive loss of synthetic, metabolic, and detoxification function, with clinical progression from compensated disease (often minimally symptomatic) to decompensated disease marked by portal hypertension and liver failure complications.
Pathophysiology
Repeated hepatocyte injury (for example from alcohol, viral hepatitis, or metabolic dysfunction-associated steatotic liver disease) activates stellate cells and drives collagen deposition in the space of Disse. Fibrous septa and nodular regeneration distort sinusoidal blood flow, increasing intrahepatic resistance and portal venous pressure. Portal hypertension causes splanchnic vasodilation, effective arterial underfilling, RAAS activation, sodium/water retention, and ascites; portosystemic shunting and reduced hepatocyte clearance permit neurotoxins (including ammonia) to accumulate, contributing to hepatic encephalopathy. Falling hepatocyte reserve causes hypoalbuminaemia, coagulopathy, jaundice, immune dysfunction, and susceptibility to sepsis, while chronic inflammation and regeneration increase hepatocellular carcinoma risk.
Risk Factors
- Harmful alcohol intake (classically sustained high intake, e. g. >50 units/week in men or >35 units/week in women)
- Chronic hepatitis B infection
- Chronic hepatitis C infection
- Obesity and type 2 diabetes (especially with MASLD/NAFLD)
- Autoimmune liver disease (autoimmune hepatitis, primary biliary cholangitis, primary sclerosing cholangitis)
- Genetic/metabolic disease (haemochromatosis, Wilson disease, alpha-1 antitrypsin deficiency, cystic fibrosis)
- Drug-induced liver injury (e. g. long-term methotrexate, amiodarone, methyldopa)
- Vascular causes (Budd-Chiari syndrome, veno-occlusive disease)
Clinical Features
Symptoms
- Fatigue, malaise, anorexia, nausea
- Unintentional weight loss and muscle wasting
- Pruritus
- Easy bruising or bleeding tendency
- Abdominal distension/discomfort from ascites
- Confusion, sleep-wake reversal, personality change (hepatic encephalopathy)
- Haematemesis or melaena from variceal bleeding
Signs
- Spider naevi, palmar erythema, clubbing
- Hepatomegaly and/or splenomegaly
- Proximal nail-bed pallor (Terry-type nail change)
- Jaundice (best seen in sclera in natural light)
- Ascites (shifting dullness, fluid thrill) and peripheral oedema
- Asterixis, dysarthria, ataxia in encephalopathy
- Gynaecomastia and testicular atrophy in men
- Cachexia/sarcopenia
Investigations
Management
Lifestyle Modifications
- Treat and remove the driver of liver injury: strict alcohol abstinence, antiviral treatment where indicated, and weight loss/metabolic risk control in MASLD
- High-protein, energy-adequate nutrition with late-evening carbohydrate snack; assess for malnutrition/sarcopenia and involve dietetics early
- Vaccinate against influenza, pneumococcus, hepatitis A and B (if non-immune)
- Avoid hepatotoxic drugs where possible and avoid NSAIDs in decompensated cirrhosis/ascites due to AKI risk
- Regular surveillance for varices and HCC, and early transplant assessment when decompensation develops
Pharmacological Treatment
Ascites control (first-line diuretics)
- Spironolactone 100 mg once daily, titrate every 3-5 days up to 400 mg/day
- Furosemide 40 mg once daily, titrate up to 160 mg/day (commonly with spironolactone in 100:40 ratio)
Monitor U&E, creatinine, blood pressure, and weight. Stop/reduce if AKI, severe hyponatraemia, encephalopathy worsening, or hypotension. Spironolactone can cause hyperkalaemia and gynaecomastia.
Hepatic encephalopathy
- Lactulose 25-30 mL orally 2-4 times daily, titrated to 2-3 soft stools/day
- Rifaximin 550 mg orally twice daily as add-on for recurrent episodes
Identify precipitants (infection, GI bleed, constipation, dehydration, sedatives). Avoid or minimise benzodiazepines and opioids where possible.
Primary/secondary variceal bleed prophylaxis
- Carvedilol 6.25 mg once daily, increase to 12.5 mg once daily if tolerated
- Propranolol 40 mg twice daily, titrated to resting heart rate about 55-60 bpm (specialist-guided)
Contraindications/cautions: asthma with bronchospasm, marked bradycardia, hypotension, advanced AKI/shock. Combine with endoscopic band ligation where indicated.
Spontaneous bacterial peritonitis (SBP) and prophylaxis
- Ceftriaxone 2 g IV once daily (typical inpatient empirical option; local antimicrobial policy may vary)
- Ciprofloxacin 500 mg orally once daily for secondary prophylaxis in selected high-risk patients
Urgent treatment is life-saving; send ascitic fluid before antibiotics where possible. Review QT-risk, tendon toxicity, and C. difficile risk with fluoroquinolones.
Acute variceal haemorrhage adjuncts (specialist emergency care)
- Terlipressin 2 mg IV every 4 hours initially, then step-down per response/protocol
Use with urgent endoscopy and prophylactic antibiotics. Terlipressin can cause ischaemia and hyponatraemia; avoid/caution in coronary, peripheral vascular, or cerebrovascular disease.
Surgical / Interventional
- Large-volume paracentesis with human albumin solution replacement for tense/refractory ascites
- Endoscopic variceal band ligation for primary prophylaxis in selected patients and for treatment of variceal bleeding
- Transjugular intrahepatic portosystemic shunt (TIPS) for refractory ascites or recurrent variceal bleeding in appropriate candidates
- Liver transplantation for end-stage disease or recurrent decompensation after specialist assessment
Complications
- Portal hypertension with oesophageal/gastric varices and life-threatening upper GI bleeding
- Ascites, including refractory ascites and umbilical hernia
- Spontaneous bacterial peritonitis
- Hepatic encephalopathy (episodic or persistent)
- Hepatorenal syndrome/acute kidney injury
- Hyponatraemia
- Coagulopathy and thrombocytopenia-related bleeding risk
- Sepsis from immune dysfunction
- Malnutrition, sarcopenia, frailty, and osteoporosis
- Hepatocellular carcinoma
Prognosis
Compensated cirrhosis may remain stable for years, but progression to decompensation occurs in roughly 5-7% per year and sharply worsens survival. Typical median survival is over 12 years in compensated disease but around 2 years once decompensated, although recompensation is possible if the underlying cause is effectively treated (for example sustained alcohol abstinence or successful viral suppression). Outcomes are poorer with ongoing liver injury, recurrent admissions, infection, renal dysfunction, and alcohol-related aetiology.
Sources & References
🏥BMJ Best Practice(2)
💊BNF Drug References(1)
- Metaraminol[cautions]
✅NICE Guidelines(1)
- Cirrhosis[overview]
📖Textbook References(7)
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 761, 762)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 750, 751)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 762, 763)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 759, 760)[context]
- Oxford Handbook of Clinical Diagnosis (Huw Llewelyn, Hock Aun Ang, Keir Lewis etc.) (Z-Library).pdf(pp. 384, 385)[context]
- Oxford Handbook of Clinical Diagnosis (Huw Llewelyn, Hock Aun Ang, Keir Lewis etc.) (Z-Library).pdf(pp. 385, 386)[context]
- Oxford Handbook of Clinical Diagnosis (Huw Llewelyn, Hock Aun Ang, Keir Lewis etc.) (Z-Library).pdf(pp. 385, 386, 387)[context]