Gastroenterology
General Practice
High Evidence

Chronic Liver Disease and Cirrhosis

Updated 2026-01-04
5 min read

Chronic Liver Disease (CLD) and Cirrhosis

1. Clinical Overview

Summary

Chronic Liver Disease (CLD) represents a spectrum of progressive liver injury and fibrosis, culminating in Cirrhosis. Cirrhosis is defined histologically as diffuse hepatic fibrosis with the formation of regenerative nodules, leading to distortion of the vascular architecture.

This structural distortion causes the two major pathophysiological consequences of cirrhosis:

  1. Portal Hypertension: Increased resistance to portal blood flow.
  2. Hepatocellular Insufficiency: Loss of metabolic and synthetic function.

Clinically, patients are categorised into two phases:

  • Compensated Cirrhosis: Asymptomatic or mild fatigue. Median survival > 12 years.
  • Decompensated Cirrhosis: Defined by the onset of Ascites, Variceal Bleeding, Encephalopathy, or Jaundice. Median survival less than 2 years without transplant.

Management focuses on treating the underlying cause (e.g., Alcohol cessation, Viral cure) to halt progression, and managing the complications of decompensation. Liver Transplantation remains the only curative option for end-stage disease.

Key Facts

  • Prevalence: The 3rd most common cause of premature death in the UK.
  • Alcohol: Remains the leading cause in the West, but NAFLD (Fatty Liver) is rapidly overtaking it.
  • Assessment: The Child-Pugh Score and MELD Score are the gold standards for prognostication.
  • Bleeding: Variceal haemorrhage has a 20% mortality per episode. Prophylactic Beta-Blockers (Carvedilol) are life-saving.
  • Infection: Patients are functionally immunosuppressed. Spontaneous Bacterial Peritonitis (SBP) is common and lethal if missed.
  • Cancer Risk: All cirrhotics require 6-monthly Ultrasound surveillance for Hepatocellular Carcinoma (HCC).

Clinical Pearls

The "Platelet" Pearl: Thrombocytopenia (less than 150) is often the first sign of portal hypertension (due to hypersplenism). In a patient with "fatty liver", a dropping platelet count suggests transition to Cirrhosis.

The "Alcohol" Pearl: "If you stop drinking, you stop dying." Even in advanced cirrhosis, abstinence significantly improves survival and can reverse decompensation. Be direct but non-judgemental.

The "Albumin" Pearl: Albumin is not just a protein; it is a volume expander and antioxidant. In SBP and Hepatorenal Syndrome, IV Albumin is a specific drug therapy, not just nutritional support.

The "Spider" Pearl: > 5 Spider Naevi in the SVC distribution is highly specific for chronic liver disease (> 95% specificity).

2. Epidemiology

Burden of Disease

  • Rising Mortality: Liver disease is the singular major cause of death still increasing year-on-year in the UK (unlike Heart Disease/Stroke/Cancer which are falling).
  • Age: Peak incidence 40-60 years ("Working age"). High economic burden.

Aetiology (Causes)

Think "vitamin" logic or "ABCDE".

1. Alcohol (ALD)

  • Most common. Dose-dependent risk.
  • Pattern: AST:ALT ratio > 2:1. Macrocytosis.

2. Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD)

  • Formerly NAFLD/NASH.
  • Linked to Obesity, T2DM, Metabolic Syndrome.
  • Rapidly becoming the #1 indication for transplant.

3. Viral Hepatitis

  • Hepatitis B: Global/Asian prevalence.
  • Hepatitis C: IVDU/Blood products. Now curable with DAAs.

4. Autoimmune

  • Autoimmune Hepatitis (AIH): Young females. Anti-Smooth Muscle Antibody (ASMA). High IgG.
  • Primary Biliary Cholangitis (PBC): Middle-aged females. Anti-Mitochondrial Antibody (AMA). Pruritus.
  • Primary Sclerosing Cholangitis (PSC): Young males. Associated with Ulcerative Colitis (IBD). p-ANCA.

5. Metabolic / Genetic

  • Haemochromatosis: "Bronze Diabetes". High Ferritin. HFE gene.
  • Wilson's Disease: Copper accumulation. Low Ceruloplasmin. Kayser-Fleischer rings.
  • Alpha-1 Antitrypsin Deficiency.

6. Drugs

  • Methotrexate, Amiodarone.

3. Pathophysiology

From Inflammation to Fibrosis

  1. Injury: Chronic insult (Alcohol/Virus/Fat) kills hepatocytes.
  2. Activation: This activates Hepatic Stellate Cells (Ito cells), which transform into myofibroblasts.
  3. Collagen Deposition: Stellate cells lay down Collagen Type I and III in the Space of Disse.
  4. Capillarisation: The fenestrated sinusoids lose their pores ("Defenestration"), impairing exchange between blood and hepatocytes.
  5. Nodularity: Surviving hepatocytes regenerate in chaotic nodules surrounded by fibrous septa.

Consequences of Portal Hypertension (HVPG > 10mmHg)

The stiff liver resists blood flow from the Portal Vein.

  • Varices: Blood seeks collateral routes to the SVC (Oesophagus/Stomach/Rectum).
  • Ascites: High hydrostatic pressure + Low Albumin + Splanchnic Vasodilation -> Fluid leak into peritoneum.
  • Splenomegaly: Back pressure causes congestive splenomegaly -> Sequesters platelets (Thrombocytopenia).

Consequences of Liver Failure

  • Coagulopathy: Loss of Clotting Factors (II, VII, IX, X). Elevated INR.
  • Hypoalbuminaemia: Loss of synthesis. Oedema.
  • Jaundice: Failure to conjugate/excrete bilirubin.
  • Encephalopathy: Failure to clear Ammonia (NH3), which crosses the blood-brain barrier.
  • Immune Paresis: Reduced Kupffer cell function -> Bacteraemia risk.

4. Clinical Presentation

Symptoms

Compensated:

  • Often Asymptomatic.
  • Fatigue / Malaise.
  • Anorexia / Muscle wasting.
  • Loss of Libido / Amenorrhoea.

Decompensated:

  • Yellow skin/eyes (Jaundice).
  • Swollen tummy (Ascites).
  • Swollen legs (Oedema).
  • Vomiting blood (Variceal bleed).
  • Confusion / Sleep disturbance (Encephalopathy).
  • Bruising (Coagulopathy).

History Taking (The "Screening" Questions)

  • Alcohol: Units per week? Morning drink? CAGE questionnaire.
  • Risk Factors: Tattoos? Blood transfusions pre-1991? IVDU? Travel?
  • Family History: Liver disease? (Hemochromatosis/Wilson's).
  • Metabolic: Diabetes? Obesity?

Differential of Jaundice (Expanded)

The "Three Boxes" Approach.

1. Pre-Hepatic (Excess Production)

  • Mechanism: Haemolysis.
  • Blood Picture: Unconjugated Hyperbilirubinaemia. Normal LFTs. Reticulocytosis.
  • Causes: Malaria, Sickle Cell, Autoimmune Haemolysis.

2. Hepatic (Uptake/Conjugation Failure)

  • Mechanism: Hepatocyte death.
  • Blood Picture: Mixed Hyperbilirubinaemia. High ALT/AST.
  • Causes: Viral Hepatitis (A/B/C/E), Alcohol, Paracetamol Overdose, Ischaemic Hepatitis ("Shock Liver").

3. Post-Hepatic (Obstruction)

  • Mechanism: Blockage of bile flow.
  • Blood Picture: Conjugated Hyperbilirubinaemia. High ALP/GGT. Pale Stools / Dark Urine.
  • Causes: Gallstones, Pancreatic Cancer, Cholangiocarcinoma, Primary Biliary Cholangitis.

5. Clinical Examination (Stigmata of CLD)

(CRITICAL EXAM SECTION - The "Spot Diagnosis")

Hands and Arms

  1. Clubbing: Loss of Schamroth's window. (Causes: Shunting, Hypoxia).
  2. Leukonychia: White nail beds (Hypoalbuminaemia).
  3. Palmar Erythema: Red thenar/hypothenar eminences (High Oestrogen).
  4. Dupuytren's Contracture: Thickening of palmar fascia (Alcohol specific).
  5. Asterixis (Flapping Tremor): Ask patient to "Stop traffic". Coarse flap of wrist. (Encephalopathy / CO2 retention / Uraemia).
  6. Bruising / Track Marks: Coagulopathy or IVDU.

Face and Neck

  1. Scleral Icterus: Jaundice visible when Bilirubin > 50. Lift eyelid.
  2. Parotid Encounterment: "Chipmunk cheeks" (Alcohol specific).
  3. Fetors Hepaticus: "Pear drop" or sweet faecal smell on breath.
  4. Kayser-Fleischer Rings: Copper ring in cornea (Wilson's).

Chest

  1. Spider Naevi: Central arteriole with radiating legs using glass slide. Fills from centre. Distribution: SVC territory (above nipples). > 5 is significant. (High Oestrogen).
  2. Gynaecomastia: In men. Palpable breast tissue. (Spironolactone or High Oestrogen).
  3. Loss of Axillary Hair: In men.

Abdomen

  1. Distension: Ascites? Everted umbilicus?
  2. Caput Medusae: Dilated veins radiating from umbilicus (Portal Hypertension). Do not confuse with IVC obstruction.
  3. Hepatomegaly:
    • Early: Large fatty liver.
    • Late: Small shrunken liver (often not palpable).
  4. Splenomegaly: Massive spleen suggests Portal Hypertension.
  5. Shifting Dullness: Percuss from centre to flank. Keep finger there. Roll patient. Wait 10s. Percuss again. Does it become resonant? (Ascites).

6. Risk Stratification (Child-Pugh & MELD)

Child-Pugh Score (Prognosis)

Mnemonic: "Pour Another Beer At Eleven" (PT, Ascites, Bilirubin, Albumin, Encephalopathy).

Parameter1 Point2 Points3 Points
Bilirubin (umol/L)less than 3434 - 50> 50
Albumin (g/L)> 3528 - 35less than 28
INRless than 1.71.7 - 2.3> 2.3
AscitesNoneMild / Diuretic ResponsiveModerate / Refractory
EncephalopathyNoneGrade 1-2Grade 3-4

Scoring:

  • Class A (5-6): 100% 1-year survival.
  • Class B (7-9): 80% 1-year survival.
  • Class C (10-15): 45% 1-year survival.

MELD Score (Model for End-Stage Liver Disease)

  • Uses Creatinine, Bilirubin, INR. (And recently Sodium).
  • Objective (no subjective assessment of ascites).
  • Used to prioritise Transplant Waiting List. High score = Top of list.

7. Investigations

Laboratory (The "Liver Screen")

  • LFTs:
    • Bili/Albumin/INR: Markers of FUNCTION (Synthetic).
    • ALT/AST: Markers of INJURY (Hepatocellular).
    • ALP/GGT: Markers of CHOLESTASIS (Biliary).
  • FBC: Thrombocytopenia (Hypersplenism). Macrocytosis (Alcohol).
  • U&Es: Hyponatraemia (Dilutional - bad sign). Creatinine (HRS?).
  • Screen:
    • Viral Serology (Hep B sAg, Hep C Ab).
    • Autoimmune (ANA, AMA, ASMA, LKM, IgG/IgM).
    • Ferritin (Haemochromatosis).
    • Caerunoplasmin (Wilson's).
    • Alpha-1 Antitrypsin.
  • AFP (Alpha Feto-Protein): HCC tumour marker.

Imaging

  • Ultrasound:
    • First line.
    • Looks for: HCC, Ascites, Portal Vein Thrombosis, Splenomegaly.
    • Cirrhosis: "Coarse echotexture"
  • "Nodular surface".
  • FibroScan (Transient Elastography):
    • Measures liver stiffness (kPa). Replaces biopsy.

    • 15 kPa = Cirrhosis.

  • CT/MRI: For HCC characterisation.

Invasive

  • Liver Biopsy: Gold standard but rarely done now due to FibroScan risk. Used for uncertain diagnosis (e.g., AIH vs Drug injury).
  • Ascitic Tap: Mandatory in all new ascites.
    • Send for: MC&S (Neutrophil count), Albumin (SAAG), Cytology.

8. Management: Decompensated Cirrhosis

1. Ascites Management

A. Salt Restriction: less than 5g salt/day. (No added salt). B. Diuretics:

  • Spironolactone (Aldosterone antagonist) is key. Start 100mg OD. Titrate to 400mg.
  • Furosemide: Added for potency and preventing Hyperkalaemia. Start 40mg.
  • Goal: Weight loss 0.5kg/day. C. Paracentesis (Drainage):
  • For Large Volume Ascites (LVP).
  • Albumen Replacement Rule: If drain > 5 Litres, give 100ml of 20% Human Albumin Solution (HAS) for every 3 Litres removed. Prevention of Post-Paracentesis Circulatory Dysfunction (PPCD). D. TIPS (Transjugular Intrahepatic Portosystemic Shunt):
  • Metal stent connecting Hepatic Vein to Portal Vein. Relieves pressure.
  • Risk: Worsens Encephalopathy (bypasses liver cleaning).

2. Spontaneous Bacterial Peritonitis (SBP)

Infection of ascites without a surgical source.

  • Diagnosis: Ascitic Neutrophil Count > 250 cells/mm3.
  • Treatment: IV Ceftriaxone / Piperacillin-Tazobactam. PLUS IV Albumin (Day 1 and Day 3) to protect kidneys.
  • Prophylaxis: Ciprofloxacin 500mg Daily for life if previous SBP or low Ascitic Protein (less than 15g/L).

3. Variceal Bleeding

Medical Emergency.

  • Resuscitate: Blood (Target Hb 70-80). Don't overfill (increases portal pressure).
  • Drugs: Terlipressin (splanchnic vasoconstrictor) + IV Antibiotics.
  • Endoscopy: Band Ligation.
  • Sengstaken Tube: Balloon tamponade as bridge to TIPS.
  • Prevention: Non-selective Beta-Blocker (Carvedilol / Propranolol) OR Banding program.

4. Hepatic Encephalopathy (HE)

Ammonia intoxication.

  • Trigger Hunt: Look for Infection (SBP), GI Bleed (Protein load), Constipation, Dehydration, Sedatives.
  • Lactulose: Osmotic laxative. Traps ammonia as ammonium (NH4+) in gut. Aim for 2-3 soft stools/day.
  • Rifaximin: Non-absorbable antibiotic. Kills ammonia-producing gut bacteria. Add if recurrrent.

5. Hepatorenal Syndrome (HRS)

Functional renal failure due to extreme vasodilation.

  • Diagnosis: AKI in cirrhosis not responding to fluid challenge.
  • Treatment: Terlipressin + Albumin. (Vasoconstrict splanchnic bed + Fill intravascular volume).

9. Holistic Management (Expanded)

(CRITICAL SECTION for Exam/Practice)

1. Alcohol Withdrawal Management

Crucial in ALD admissions.

  • Risk: Seizures, Delirium Tremens (DTs).
  • Protocol (CIWA or Fixed Dose):
    • Chlordiazepoxide (Librium): Long-acting benzo. CAUTION in cirrhosis (accumulates). Use reduced doses (e.g. 10mg rather than 30mg) or switch to Lorazepam (short acting) in severe liver failure.
    • Pabrinex (IV B Vitamins): Essential to prevent Wernicke's Encephalopathy. Give 2 pairs TDS for 3 days.

2. Liver Cancer (HCC) Screening & Staging

  • Screening: US Liver + AFP every 6 months.
  • Staging (BCLC - Barcelona Clinic Liver Cancer):
    • Stage 0/A (Single lesion less than 2cm): Ablation / Resection.
    • Stage B (Multinodular): TACE (Trans-Arterial Chemo-Embolization).
    • Stage C (Portal invasion): Sorafenib (Systemic Chemo).
    • Stage D (Terminal): Palliation.

3. Palliation in Liver Disease

Symptom control in end-stage disease (Class C).

  • Pruritus (Itch): Caused by bile salts.
    • Step 1: Cholestyramine (Sachet).
    • Step 2: Rifampicin / Naltrexone.
  • Muscle Cramps: Very common.
    • Treatment: Quinine Sulphate / Magnesium.
  • End of Life: Avoid Morphine (toxic metabolite accumulation). Use Fentanyl or Alframanil (low dose) for pain.

4. Viral Hepatitis Therapy (New Era)

The landscape has changed with Direct Acting Antivirals (DAAs).

  • Hepatitis C:
    • Curative treatment now exists (> 95% SVR - Sustained Virologic Response).
    • Regimen: Sofosbuvir + Velpatasvir (Epclusa) for 12 weeks. Pan-genotypic.
  • Hepatitis B:
    • Suppressive (not curative) treatment. Indefinite.
    • Regimen: Tenofovir or Entecavir.
  • Hepatitis E:
    • Usually self-limiting but chronic in immunosuppressed. Treat with Ribavirin.

10. Procurment & Transplant

  • Compensated: Median survival > 12 years.
  • Decompensated: Median survival less than 2 years. Indication for Transplant Assessment.
  • UKELD Score: Used in UK to list for transplant. Score > 49 means 1-year mortality without transplant (> 9%) > 1-year mortality WITH transplant.
  • Transplant Contraindications:
    • Active Alcoholism (less than 6 months abstinence).
    • Extra-hepatic malignancy.
    • Severe cardiopulmonary disease.

11. Evidence & Guidelines

Guidelines

  1. EASL (European Association for the Study of the Liver): Clinical Practice Guidelines on Decompensated Cirrhosis (2018).
  2. BSG (British Society of Gastroenterology): Guidelines on Management of Ascites and SBP (2020).

Key Trials

  • Basso et al (Prednisolone in Alcoholic Hepatitis): STOPAH Trial. Showing benefit of steroids in severe Alcoholic Hepatitis (MDF > 32) for short term survival.
  • Sort et al (IV Albumin in SBP): Demonstrated that giving Albumin with Antibiotics reduces renal failure and mortality compared to antibiotics alone. (Seminal paper).
  • Villaneuva et al (Beta Blockers): Demonstrated survival benefit of Beta Blockers in preventing variceal bleed.

12. Patient Explanation

What is Cirrhosis?

The liver is like a factory that cleans blood and makes proteins. Cirrhosis means the factory is scarred and stiff.

  1. It's Stiff: Blood can't flow through easily, so pressure builds up (Portal Hypertension), causing veins to swell (Varices) and fluid to leak (Ascites).
  2. It's Failing: It stops making muscle protein (wasting) and stops clearing toxins (confusion).

Is it reversible?

The scarring is mostly permanent, but the function can improve massively if you remove the cause. If you have alcoholic cirrhosis and stop drinking today, your liver can "re-compensate" and keep you going for many years. If you continue drinking, liver failure is inevitable.

Why do I need to eat late at night?

Your liver usually stores sugar energy for the night. In cirrhosis, the cupboard is bare. If you don't eat a snack before bed, your body will "eat its own muscles" for energy while you sleep. A slice of toast or cereal at 10pm protects your muscles.

Driving?

If you have had confusion (encephalopathy), you must stop driving and inform the DVLA. It is unsafe.

13. References

  1. European Association for the Study of the Liver. EASL Clinical Practice Guidelines for the management of patients with decompensated cirrhosis. J Hepatol. 2018 Aug;69(2):406-460. PMID: 29653741

  2. Moore KP et al (BSG). Guidelines on the management of ascites in cirrhosis. Gut. 2006 Oct;55 Suppl 6:vi1-12. PMID: 16966752

  3. Runyon BA (AASLD). Introduction to the revised American Association for the Study of Liver Diseases Practice Guidelines management of adult patients with ascites due to cirrhosis 2012. Hepatology. 2013 Apr;57(4):1651-3. PMID: 23463408

  4. Sort P et al. Effect of intravenous albumin on renal impairment and mortality in patients with cirrhosis and spontaneous bacterial peritonitis. N Engl J Med. 1999 Aug 5;341(6):403-9. PMID: 10432325

  5. Thursz MR et al (STOPAH). Prednisolone or pentoxifylline for alcoholic hepatitis. N Engl J Med. 2015 Apr 23;372(17):1619-28. PMID: 25901427

14. Examination Focus

Common Exam Questions

  1. "Causes of clubbing?"
    • Answer: Respiratory (Cancer, Fibrosis, Suppuration), Cardiac (Cyanotic, Endocarditis), GI (Cirrhosis, IBD, Coeliac).
  2. "Identify 3 causes of massive splenomegaly."
    • Answer: CML, Myelofibrosis, Malaria, Leishmaniasis, Portal Hypertension (Cirrhosis).
  3. "Management of INR 1.8 in cirrhosis pre-biopsy?"
    • Answer: Do NOT give Vitamin K (it won't work, synthesis failure). Give FFP or use Trans-jugular route.
  4. "Antibiotic for SBP?"
    • Answer: IV Ceftriaxone or Tazocin.

Viva Points

  • Child-Pugh vs MELD: Know that MELD is objective (Creatinine/INR/Bili) and used for transplant listing. Child-Pugh uses subjective measures (Ascites/Encephalopathy).
  • Terlipressin: Mechanism of action (Splanchnic vasoconstriction -> Reduces portal inflow).
  • SBP Diagnosis: Neutrophils > 250.

Last Reviewed: 2026-01-04 | MedVellum Editorial Team