Liver Cirrhosis

Liver cirrhosis is the result of chronic inflammation and damage to liver cells. When the liver cells are damaged they are replaced with scar tissue (fibrosis) and nodules of scar tissue form within the liver.

This fibrosis affects the structure and blood flow through the liver, which causes increased resistance in the vessels leading in to the liver. This is called portal hypertension.


Most Common Causes

It is worth remembering the four most common causes of liver cirrhosis.

  • Alcoholic liver disease
  • Non Alcoholic Fatty Liver Disease
  • Hepatitis B
  • Hepatitis C


Rarer Causes

Cirrhosis also has a large number of rarer causes of liver damage that should also be considered as some of them are potentially reversible:

  • Autoimmune hepatitis
  • Primary biliary cirrhosis
  • Haemochromatosis
  • Wilsons Disease
  • Alpha-1 antitrypsin deficiency
  • Cystic fibrosis
  • Drugs (e.g. amiodarone, methotrexate, sodium valproate)


Signs of Cirrhosis

  • Jaundice – caused by raised bilirubin
  • Hepatomegaly – however the liver can shrink as it becomes more cirrhotic
  • Splenomegaly – due to portal hypertension
  • Spider Naevi – these are telangiectasia with a central arteriole and small vessels radiating away
  • Palmar Erythema – caused by hyperdynamic cirulation
  • Gynaecomastia and testicular atrophy in males due to endocrine dysfunction
  • Bruising – due to abnormal clotting
  • Ascites
  • Caput Medusae – distended paraumbilical veins due to portal hypertension
  • Asterixis – “flapping tremor” in decompensated liver disease




  • Liver biochemistry is often normal, however in decompensated cirrhosis all of the markers (ALT, AST, ALP and bilirubin) become deranged.
  • Albumin and prothrombin time are useful markers of the “synthetic function” of the liver. The albumin level drops and the prothrombin time increases as the synthetic function becomes worse.
  • Hyponatraemia indicates fluid retention in severe liver disease.
  • Urea and creatinine become deranged in hepatorenal syndrome.
  • Further bloods can help establish the cause of the cirrhosis if unknown (such as viral markers and autoantibodies).
  • Alpha-fetoprotein is a tumour marker for hepatocellular carcinoma and can be checked every 6 months as a screening test in patients with cirrhosis along with ultrasound.

Enhanced Liver Fibrosis (ELF) blood test. This is the first line recommended investigation for assessing fibrosis in non-alcoholic fatty liver disease but it is not currently available in many areas and cannot be used for diagnosing cirrhosis of other causes. It measures three markers (HA, PIIINP and TIMP-1) and uses an algorithm to provide a result that indicates the fibrosis of the liver:

  • < 7.7 indicates none to mild fibrosis
  • ≥ 7.7 to 9.8 indicates moderate fibrosis
  • ≥ 9.8 indicates severe fibrosis



In cirrhosis ultrasound may show:

  • Nodularity of the surface of the liver
  • A “corkscrew” appearance to the arteries with increased flow as they compensate for reduced portal flow
  • Enlarged portal vein with reduced flow
  • Ascites
  • Splenomegaly

Ultrasound is also used as a screening tool for hepatocellular carcinoma. NICE recommend screening patients with cirrhosis for HCC every 6 months.



FibroScan” can be used to check the elasticity of the liver by sending high frequency sound waves into the liver. It helps assess the degree of cirrhosis. This is called “transient elastography” and should be used to test for cirrhosis. NICE recommend retesting every 2 years in patients at risk of cirrhosis:

  • Hepatitis C
  • Heavy alcohol drinkers (men drinking > 50 units or women drinking > 35 units per week)
  • Diagnosed alcoholic liver disease
  • Non alcoholic fatty liver disease and evidence of fibrosis on the ELF blood test
  • Chronic hepatitis B (although they suggest yearly for hep B)



Endoscopy can be used to assess for and treat oesophageal varices when portal hypertension is suspected.


CT and MRI scans

CT and MRI can be used to look for hepatocellular carcinoma, hepatosplenomegaly, abnormal blood vessel changes and ascites.


Liver Biopsy

Liver biopsy can be used to confirm the diagnosis of cirrhosis.


Child-Pugh Score for Cirrhosis

Each factors is taken into account and given as score of 1, 2 or 3. Therefore the minimum score is 5 and the maximum score is 15. The score then indicates the severity of the cirrhosis and the prognosis.


Score 1

Score 2

Score 3
















Moderate or severe




Moderate or severe


MELD Score

The MELD score is recommended by NICE to be used every 6 months in patients with compensated cirrhosis. It is a formula that takes into account the bilirubin, creatinine, INR and sodium and whether they are requiring dialysis. It gives a percentage estimated 3 month mortality and helps guide referral for liver transplant.


General Management

  • Ultrasound and alpha-fetoprotein every 6 months for hepatocellular carcinoma
  • Endoscopy every 3 years in patients without known varices
  • High protein, low sodium diet
  • MELD score every 6 months
  • Consideration of a liver transplant
  • Managing complications as below


Complications of Cirrhosis

The course of the disease is variable. 5 year survival is overall about 50% once cirrhosis has developed. The Child-Pugh score and the MELD score can be used as prognostic tools. There are several important complications of cirrhosis that we will go through below:

  • Malnutrition
  • Portal Hypertension, Varices and Variceal Bleeding
  • Ascites and Spontaneous Bacterial Peritonitis (SBP)
  • Hepato-renal Syndrome
  • Hepatic Encephalopathy
  • Hepatocellular Carcinoma



Cirrhosis leads to malnutrition and muscle wasting. A simplified explanation of this is that it leads to increased use of muscle tissue as fuel and reduces the protein available in the body for muscle growth. Cirrhosis affects the metabolism of proteins in the liver and reduces the amount of protein produced. It also disrupts the livers ability to store glucose as glycogen and release it when required. This results in the body using muscle tissue as fuel leading to muscle wasting and weight loss.



  • Regular meals (every 2-3 hours)
  • Low sodium (to minimise fluid retention)
  • High protein and high calorie (particularly if underweight)
  • Avoid alcohol


Portal Hypertension and Varices

The portal vein comes from the superior mesenteric vein and the splenic vein and delivers blood to the liver. Liver cirrhosis increases the resistance of blood flow in the liver. As a result, there is increased back-pressure into the portal system. This is called “portal hypertension”. This back-pressure causes the vessels at the sites where the portal system anastomoses with the systemic venous system to become swollen and tortuous. These swollen, tortuous vessels are called varices. They occur at the:

  • Gastro oesophageal junction
  • Ileocaecal junction
  • Rectum
  • Anterior abdominal wall via the umbilical vein (caput medusae)

Varices do not cause symptoms or problems until they start bleeding. Due to the high blood flow through varices, once they start bleeding patients can exsanguinate (bleed out) very quickly.


Treatment of stable varices

  • Propranolol reduces portal hypertension by acting as a non-selective beta blocker
  • Elastic band ligation of varices
  • Injection of sclerosant (less effective than band ligation)

Transjugular Intra-hepatic Portosystemic Shunt (TIPS) is a technique where an interventional radiologist inserts a wire under xray guidance into the jugular vein, down the vena cava and into the liver via the hepatic vein. They then make a connection through the liver tissue between the hepatic vein and the portal vein and put a stent in place. This allows blood to flow directly from the portal vein to the hepatic vein and relieves the pressure in the portal system and varices. This is used if medical and endoscopic treatment of varices fail or if there are bleeding varices that cannot be controlled in other ways.


Bleeding Oesophageal Varices


  • Vasopressin analogues (i.e. terlipressin) cause vasoconstriction and slow bleeding in varices
  • Correct any coagulopathy with vitamin K and fresh frozen plasma (which is full of clotting factors)
  • Giving prophylactic broad spectrum antibiotics has been shown to reduce mortality
  • Consider intubation and intensive care as they can bleed very quickly and become life threateningly unwell

Urgent endoscopy

  • Injection of sclerosant into the varices can be used to cause “inflammatory obliteration” of the vessel
  • Elastic band ligation of varices

Sengstaken-Blakemore Tube is an inflatable tube inserted into the oesophagus to tamponade the bleeding varices. This is used when endoscopy fails.



Ascites is basically fluid in the peritoneal cavity. The increased pressure in the portal system causes fluid to leak out of the capillaries in the liver and bowel and in to the peritoneal cavity. The drop in circulating volume caused by fluid loss into the peritoneal space causes a reduction in blood pressure entering the kidneys. The kidneys sense this lower pressure and release renin, which leads to increased aldosterone secretion (via the renin-angiotensin-aldosterone system) and reabsorption of fluid and sodium in the kidneys. Cirrhosis causes a transudative, meaning low protein content, ascites.

Management of Ascites

  • Low sodium diet
  • Anti-aldosterone diuretics (spironolactone)
  • Paracentesis (ascitic tap or ascitic drain)
  • Prophylactic antibiotics against spontaneous bacterial peritonitis (ciprofloxacin or norfloxacin) in patients with less than 15g/litre of protein in the ascitic fluid
  • Consider TIPS procedure in refractory ascites
  • Consider transplantation in refractory ascites


Spontaneous Bacterial Peritonitis (SBP)

This occurs in around 10% of patients with ascites secondary to cirrhosis and can have a mortality of 10-20%. It involves an infection developing in the ascitic fluid and peritoneal lining without any clear cause (e.g. not secondary to an ascitic drain or bowel perforation).


  • Can be asymptomatic so have a low threshold for ascitic fluid culture
  • Fever
  • Abdominal pain
  • Deranged bloods (raised WBC, CRP, creatinine or metabolic acidosis)
  • Ileus
  • Hypotension

Most common organisms

  • Escherichia coli
  • Klebsiella pnuemoniae
  • Gram positive cocci (such as staphylococcus and enterococcus)

Management of SBP

  • Take an ascitic culture prior to giving antibiotics
  • Usually treated with an IV cephalosporin such as cefotaxime


Hepatorenal Syndrome

Hepatorenal syndrome occurs in liver cirrhosis. Hypertension in the portal system leads to dilation of the portal blood vessels, stretched by large amounts of blood pooling there. This leads to a loss of blood volume in other areas of the circulation, including the kidneys. This leads hypotension in the kidney and activation of the renin-angiotensin system. This causes renal vasoconstriction, which combined with low circulation volume leads to starvation of blood to the kidney. This leads to rapid deteriorating kidney function. Hepatorenal syndrome is fatal within a week or so unless liver transplant is performed.


Hepatic Encephalopathy

This is also known as portosystemic encephalopathy. It is thought to be caused by the build up of toxins that affect the brain. One toxin that is particularly worth remembering is ammonia, which is produced by intestinal bacteria when they break down proteins and is absorbed in the gut. There are two reasons that ammonia builds up in the blood in patients with cirrhosis: Firstly, the functional impairment of the liver cells prevents them metabolising the ammonia into harmless waste products. Secondly, collateral vessels between the portal and systemic circulation mean that the ammonia bypasses liver altogether and enters the systemic system directly.

By giving laxatives we help clear the ammonia from the gut before it is absorbed and by giving antibiotics we reduce the number of bacteria in the gut producing ammonia.

Acutely, it presents with reduced consciousness and confusion. It can present in a more chronically with changes to personality, memory and mood.

Precipitating Factors

  • Constipation
  • Electrolyte disturbance
  • Infection
  • GI bleed
  • High protein diet
  • Medications (particularly sedative medications)


  • Laxatives (i.e. lactulose) promote the excretion of ammonia. The aim is 2-3 soft motions daily. They may require enemas initially.
  • Antibiotics (i.e. rifaximin) reduces the number of intestinal bacteria producing ammonia. Rifaximin is useful as it is poorly absorbed and so stays in the GI tract.
  • Nutritional support. They may need nasogastric feeding.


Last updated January 2019
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