Cirrhosis
Summary
Cirrhosis is the end-stage of chronic liver disease, characterised by diffuse fibrosis, nodular regeneration, and distortion of hepatic architecture. It results from any cause of chronic liver injury, most commonly alcohol-related liver disease, non-alcoholic fatty liver disease (NAFLD/MASLD), and viral hepatitis (B and C). Cirrhosis is classified as compensated (no major complications) or decompensated (ascites, variceal bleeding, encephalopathy, jaundice). Child-Pugh and MELD scores assess severity and prognosis. Management focuses on treating the underlying cause, preventing and managing complications, HCC surveillance, and liver transplant evaluation in suitable candidates.
Key Facts
- Definition: Diffuse hepatic fibrosis with nodular regeneration
- Prevalence: ~1-2% of population; rising due to NAFLD
- Common Causes: Alcohol (40%), NAFLD/MASLD (30%), Hepatitis B/C (20%), other (10%)
- Staging: Compensated vs Decompensated
- Scoring: Child-Pugh (prognosis), MELD (transplant prioritisation)
- Screening: HCC surveillance (USS ± AFP every 6 months)
Clinical Pearls
"Compensated vs Decompensated": The transition from compensated to decompensated cirrhosis is the key prognostic event. Median survival in compensated cirrhosis is >12 years; in decompensated, it drops to 2-4 years without transplant.
"Decompensation = AVEJ": Ascites, Variceal bleeding, Encephalopathy, Jaundice — presence of any defines decompensated cirrhosis.
"Always Think About Underlying Cause": Treating the cause (alcohol abstinence, antiviral therapy) can halt progression and even lead to regression of fibrosis.
Why This Matters Clinically
Cirrhosis is a major cause of morbidity and mortality. Early identification can prevent progression to decompensation. Management of complications significantly improves survival and quality of life. Liver transplant is curative in suitable candidates.
Incidence & Prevalence
- Global Prevalence: ~2 million deaths/year from liver disease; 50% from cirrhosis
- UK Prevalence: ~600,000 people with cirrhosis
- Trend: Increasing due to NAFLD and alcohol
Demographics
| Factor | Details |
|---|---|
| Age | Increases with age; peak 50-70 |
| Sex | Male > Female (alcohol); Female > Male in autoimmune |
| Socioeconomic | Higher in lower SES (alcohol, viral hepatitis) |
Causes
| Cause | Proportion | Notes |
|---|---|---|
| Alcohol | ~40% | Leading cause in developed countries |
| NAFLD/MASLD | ~30% | Rising; associated with metabolic syndrome |
| Hepatitis C | ~15% | Declining with DAA therapy |
| Hepatitis B | ~5% | Higher in endemic areas |
| Autoimmune | ~5% | AIH, PBC, PSC |
| Other | ~5% | Haemochromatosis, Wilson's, A1AT, Budd-Chiari |
Mechanism
Step 1: Chronic Injury
- Hepatocyte necrosis and inflammation
- Kupffer cell activation (resident macrophages)
Step 2: Stellate Cell Activation
- Hepatic stellate cells transform to myofibroblasts
- Collagen deposition (fibrosis)
Step 3: Architectural Distortion
- Fibrous septa form
- Nodular regeneration
- Loss of normal lobular architecture
Step 4: Functional Consequences
- Portal hypertension (increased intrahepatic resistance)
- Synthetic failure (coagulopathy, hypoalbuminaemia)
- Detoxification failure (encephalopathy)
- Hormonal changes (gynaecomastia, spider naevi)
Portal Hypertension
Portal pressure >10 mmHg leads to:
- Varices (oesophageal, gastric)
- Ascites
- Splenomegaly
- Portosystemic shunting
Symptoms
Compensated (Often Asymptomatic):
Decompensated:
Signs
Chronic Liver Disease Signs:
Decompensation Signs:
Red Flags
[!CAUTION] Red Flags — Urgent Assessment:
- Variceal bleeding (haematemesis, melaena, shock)
- Hepatic encephalopathy (confusion, altered consciousness)
- SBP (abdominal pain, fever in cirrhotic with ascites)
- Hepatorenal syndrome (rising creatinine + low urine output)
- Acute-on-chronic liver failure
Structured Approach
General:
- Jaundice (sclera, skin)
- Nutritional status (cachexia, muscle wasting)
- Signs of chronic liver disease (spider naevi, palmar erythema)
Hands:
- Clubbing, Dupuytren's contracture
- Palmar erythema, leukonychia
Arms:
- Spider naevi
- Bruising
- Needle marks
Face/Chest:
- Jaundice, spider naevi
- Gynaecomastia
Abdomen:
- Hepatomegaly (may be small/shrunken in advanced cirrhosis)
- Splenomegaly
- Ascites (shifting dullness, fluid thrill)
- Caput medusae
Neurological:
- Asterixis (flapping tremor)
- Confusion, drowsiness (encephalopathy)
First-Line
| Test | Purpose | Expected Findings |
|---|---|---|
| LFTs | Assess liver function | Raised bilirubin, low albumin, prolonged PT/INR |
| FBC | Thrombocytopenia (splenomegaly) | Low platelets; may have anaemia |
| U&E | Renal function | May have low sodium (dilutional); raised creatinine (HRS) |
| Coagulation | Synthetic function | Prolonged PT/INR |
| USS Abdomen | Liver appearance, ascites, splenomegaly | Nodular liver, portal hypertension signs |
Aetiology Screen
| Test | Condition |
|---|---|
| Hepatitis B/C serology | Viral hepatitis |
| Autoimmune screen (ANA, SMA, AMA, IgG) | AIH, PBC |
| Iron studies, Ferritin | Haemochromatosis |
| Caeruloplasmin, urinary copper | Wilson's disease |
| Alpha-1 antitrypsin | A1AT deficiency |
| Immunoglobulins | IgG (AIH), IgM (PBC) |
Further Investigations
| Test | When |
|---|---|
| Fibroscan (TE) | Non-invasive fibrosis assessment |
| Liver Biopsy | Uncertain aetiology; assess fibrosis stage |
| OGD | Varices screening |
| AFP ± USS | HCC surveillance (6-monthly) |
| Ascitic Tap | New ascites; suspected SBP |
| EEG | Subtle encephalopathy |
General Measures
- Treat underlying cause (most important)
- Alcohol abstinence
- Nutrition (high protein unless encephalopathy)
- Vaccinations (Hepatitis A/B, Influenza, Pneumococcal)
- Avoid hepatotoxins (NSAIDs, excessive paracetamol)
- HCC surveillance (USS ± AFP every 6 months)
Complications Management
Ascites:
- Salt restriction (<2g sodium/day)
- Spironolactone 100mg OD ± Furosemide 40mg OD (100:40 ratio)
- Large volume paracentesis (LVP) with albumin (8g/L drained)
- TIPS if refractory
SBP:
- Diagnostic paracentesis: Ascitic PMN ≥250/μL
- IV Ceftriaxone + IV Albumin
- Prophylaxis: Norfloxacin or Co-trimoxazole
Hepatic Encephalopathy:
- Identify and treat precipitant (infection, GI bleed, constipation, drugs)
- Lactulose (titrate to 2-3 soft stools/day)
- Rifaximin for recurrent episodes
Variceal Bleeding:
- Resuscitation, IV access, blood transfusion (target Hb 70-80)
- IV Terlipressin or Octreotide
- IV Ceftriaxone (prophylaxis)
- Urgent OGD + band ligation
- TIPS if refractory
Hepatorenal Syndrome:
- Stop diuretics, NSAIDs
- IV Albumin + Terlipressin
- Urgent transplant evaluation
Liver Transplant
Indications:
- MELD ≥15
- Decompensated cirrhosis
- HCC within Milan criteria
- Acute liver failure
Outcomes:
- 1-year survival >90%
- 5-year survival ~75%
Acute Complications
| Complication | Mechanism | Management |
|---|---|---|
| Variceal Bleeding | Portal hypertension | Terlipressin, OGD, TIPS |
| SBP | Bacterial translocation | Antibiotics, albumin |
| Hepatic Encephalopathy | Ammonia accumulation | Lactulose, rifaximin |
| Hepatorenal Syndrome | Renal vasoconstriction | Terlipressin + albumin |
| ACLF | Acute insult on chronic | ICU, transplant |
Chronic Complications
| Complication | Notes |
|---|---|
| HCC | Risk 1-8%/year; surveillance essential |
| Hepatopulmonary Syndrome | Intrapulmonary shunts; hypoxia |
| Portopulmonary Hypertension | Pulmonary arterial hypertension |
| Malnutrition | Common; high protein intake advised |
Natural History
Compensated cirrhosis can remain stable for years if cause addressed. Decompensation marks a critical transition with significantly reduced survival.
Outcomes
| Stage | 5-Year Survival |
|---|---|
| Compensated | 80-90% |
| Decompensated | 30-50% |
| With transplant | ~75% |
Prognostic Scores
Child-Pugh:
- Class A: 100% 1-year survival
- Class B: 80% 1-year survival
- Class C: 45% 1-year survival
MELD:
- Higher score = worse prognosis
- Used for transplant allocation
Key Guidelines
-
EASL Clinical Practice Guidelines on Cirrhosis (2018) — Comprehensive guidance.
-
BSG Guidelines on Ascites (2020) — Ascites management.
Landmark Studies
HALT-C Trial — Long-term maintenance interferon
- Key finding: No benefit of maintenance interferon in non-responders
- Clinical Impact: Informed treatment duration decisions
STOPAH Trial (2015) — Alcoholic hepatitis
- Key finding: Prednisolone improved 28-day mortality
- Clinical Impact: Steroids for severe alcoholic hepatitis (Maddrey ≥32)
Evidence Strength
| Intervention | Level | Key Evidence |
|---|---|---|
| Beta-blocker for varices | 1a | Meta-analyses |
| Lactulose for encephalopathy | 1a | Cochrane reviews |
| DAA for Hepatitis C | 1a | Multiple RCTs |
| Liver transplant | 1a | Registry data |
What is Cirrhosis?
Cirrhosis is scarring of the liver. When the liver is injured over many years (from alcohol, fatty liver, or viruses), it tries to repair itself, but this leads to scar tissue replacing normal liver tissue. Eventually, the liver can't work properly.
What causes it?
The most common causes are:
- Alcohol: Long-term heavy drinking
- Fatty liver disease: Linked to obesity and diabetes
- Viral hepatitis: Hepatitis B or C infection
What are the symptoms?
Early on, there may be no symptoms. As it gets worse:
- Tiredness, weakness
- Yellowing of skin and eyes (jaundice)
- Swelling in the belly (fluid build-up) and legs
- Confusion
- Vomiting blood (from bleeding in the gullet)
How is it treated?
- Treat the cause: Stop drinking, treat hepatitis, lose weight
- Manage complications: Tablets to remove fluid, prevent bleeding, prevent confusion
- Liver transplant: For severe cases where the liver is failing
What to expect
- If caught early and the cause is treated, the liver can recover somewhat
- You'll need regular check-ups and screening for liver cancer
- If cirrhosis is advanced, a transplant may be the best option
When to seek urgent help
Call 999 or go to A&E if:
- You vomit blood or have black, tarry stools
- You become confused or drowsy
- You have a fever with a swollen belly
- You feel very unwell
Primary Guidelines
- European Association for the Study of the Liver. EASL Clinical Practice Guidelines for the management of patients with decompensated cirrhosis. J Hepatol. 2018;69(2):406-460. PMID: 29653741
Key Trials
- Thursz MR, Richardson P, Allison M, et al. Prednisolone or pentoxifylline for alcoholic hepatitis (STOPAH). N Engl J Med. 2015;372(17):1619-1628. PMID: 25901427
Further Resources
- British Liver Trust: britishlivertrust.org.uk
- BASL (British Association for Study of the Liver): basl.org.uk
Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate guidelines and specialists for patient care.