by | 4 Dec, 2020

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Cirrhosis refers to scarring of liver tissue due to long-term damage. It occurs as a result of necrosis of liver cells, which is followed by diffuse fibrosis and nodule formation. This interferes with liver function and blood flow, producing portal hypertension and impaired liver cell function.


The commonest cause worldwide is viral hepatitis. However, the most common cause in the developed world is alcohol.

Cirrhosis is the most of common cause of portal hypertension.


Causes include any condition that leads to: persistent or recurrent hepatocyte death, prolonged biliary damage or obstruction, or persistent blockage of venous return from the liver.

  • Alcohol (accounts for 50% of all cases)
  • Viral hepatitis especially, hepatitis B and C
  • Non-alcoholic fatty liver disease
  • Autoimmune: autoimmune hepatitis, primary sclerosing cholangitis
  • Biliary: primary biliary cirrhosis, cystic fibrosis
  • Drug-induced e.g. methotrexate
  • Genetic: haemochromatosis, Wilson’s disease, alpha1-antritrypsin deficiency
  • Idiopathic
  • Chronic venous outflow obstruction
  • Lysosomal acid lipase deficiency


Chronic injury to the liver leads to cytokine release from Kuppfer cells and hepatocytes. This activates stellate cells in the space of Disse. Stellate cells transform into a myofibroblast-like cell, which produces collagen, pro-inflammatory cytokines and other mediators that promote damage and fibrosis.

Pathological changes in cirrhosis usually affect the whole liver, although they maybe patchy in biliary cirrhosis. There are 2 types of cirrhosis:

  • Micronodular: Small nodules <1-3 mm in diameter. Typically seen in alcoholic cirrhosis and biliary tract disease
  • Macronodular: Larger nodules of various sizes. Normal acini may be seen within the larger nodules. Typically seen following chronic viral hepatitis.

Clinical features

Clinical presentation is highly variable. Some patients are asymptomatic and are incidentally diagnosed on ultrasound scans. If symptoms are present, they are usually non-specific e.g. weight loss, fatigue. Clinical features may relate to hepatic insufficiency or portal hypertension

  • Change in liver size: may be hepatomegaly (especially if hepatitis is present) or, more commonly in the long-term, liver shrinkage
  • Jaundice
  • Reduced albumin production: ascites (which may become complicated with infections, producing spontaneous bacterial peritonitis) and peripheral oedema
  • Upper limb changes: palmar erythema, clubbing, Dupuytren’s contracture, leuconychia
  • Portal hypertension: splenomegaly, variceal bleeding
  • Endocrine changes: loss of libido. Males may have gynaecomastia, testicular atrophy and impotence and spider naevi (due to increased oestrogen). Females can develop breast atrophy, irregular menses and amenorrhoea.
  • Bleeding tendency (e.g. bruises, epistaxis) due to reduced production of clotting factors
  • Hepatic encephalopathy

Advanced disease may lead to hepatorenal syndrome or hepatocellular carcinoma.

Decompensated liver disease

Signs of decompensation include:

  1. Jaundice
  2. Ascites
  3. Variceal bleeding
  4. Hepatic encephalopathy



  • Viral serology: hepatitis A-E, EBV, CMV
  • Clotting studies: prolonged INR and APTT in advanced cirrhosis
  • Ferritin: raised in haemochromatosis
  • FBC: check for anaemia (gastrointestinal bleeding) and macrocytosis
  • U&E: check for hepatorenal syndrome
  • LFT and GGT: check for raised bilirubin, ALT and ALP
  • Autoantibodies: ANCA, ANA, AMA
  • Immunoglobulin levels: IgM, IgG
  • Caeruloplasmin: reduced in Wilsons’s disease
  • Alpha1-antitrypsin levels


  • Ultrasound scan: check liver size, shape and elasticity
  • CT abdomen: checks for hepatosplenomegaly and collateral vessels
  • Endoscopy: visualise and treat varices

Special tests:

  • Ascitic tap
  • Liver biopsy: assesses severity of cirrhosis and support diagnosis


A multidisciplinary approach is required for cirrhotic patients. The main principles of management include:

  1. Treating the underlying disease
  2. Maintenance of nutrition e.g. thiamine
  3. Treating complications. For examples, ascites can be managed with spironolactone, salt restriction and therapeutic ascitic taps. Varices can be managed prophylactically with beta-blockers (e.g. carvedilol) or treated with terlipressin and band ligation

Once a diagnosis is made, endoscopy should be performed to check for varices and be repeated every 2 years.

Liver transplantation may also be considered in advanced disease.


Poor prognosis but highly variable. Many patients present with advanced disease and/or serious complications. 5 year survival is 25%.

Prognosis is more favourable if the cause is correctable e.g. alcohol, Wilson’s disease.


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