Cirrhosis

Cirrhosis is a description of the extent of scarring of the liver. With cirrhosis, the scarring or fibrosis has advanced to the point where the structure of the liver has been altered. As a result, the liver’s smooth texture starts to become nodular and lumpy.

Nodules are areas of liver cells which have become cut off from the rest of the liver by circular bands of scarring. Inside these bands, liver cells have unsuccessfully tried to regenerate. The free flow of blood throughout the liver then starts to be compromised. You can read about how hepatitis C damages the liver here.

Studies suggest that chronic infection with hepatitis C will almost invariably result in cirrhosis. The time that this takes varies. From those who develop a chronic or long term infection (between 70-80% of those infected with hepatitis C) around 20-30% will develop cirrhosis within 20 years. For some it may be quicker while for others it may take up to sixty years meaning they will probably die of unrelated causes first.

Cirrhosis is categorised by two stages, depending on the extent to which the liver has become damaged:

  • Compensated cirrhosis: This is when the liver is still able to cope with the damage and continues to carry out most (or even all) of its functions.
  • Decompensated cirrhosis: This is when the liver is unable to cope and is no longer functioning.

Compensated cirrhosis

Like fibrosis, cirrhosis ranges from mild (at the beginning) to moderate or severe. Severe cirrhosis can then progress to decompensated cirrhosis, which means the liver cannot carry out all of its normal functions. Its symptoms include jaundice, ascites and internal bleeding. If you experience this development, you should contact a medical professional as soon as possible as survival rates are low for people who develop decompensated cirrhosis.

The rate of progression of cirrhosis is different in everyone but does not appear to be related to genotype. Progression is affected by similar factors to fibrosis, but at this stage the effect of alcohol on liver damage is even greater.

Once they have developed compensated cirrhosis, many people do not experience symptoms that differ from those they may have had during the chronic phase of the disease. Many people experience no symptoms at all.

There is also no evidence of portal hypertension. Over time and without treatment for hepatitis C, compensated cirrhosis does seem to progress inevitably to decompensated cirrhosis. This can take many years and some people may die from other unrelated causes before this occurs. Studies have suggested that the annual rate of decompensation among people with hepatitis C with cirrhosis is 4%.

On average 18% of people with compensated cirrhosis will progress to decompensated cirrhosis after five years. After ten years the rate rises to 30%.

As with the chronic stage of hepatitis C, people’s experiences and symptoms during compensated cirrhosis can vary significantly.

Below is a list of symptoms that are more specifically associated with compensated cirrhosis. These can be included with any of the other symptoms experienced with hepatitis C. It does not necessarily mean that will experience them if you do cirrhosis. Equally, experiencing this symptoms does not necessarily mean you have cirrhosis.

  • Symptoms
  • Tiredness and weakness
  • Loss of appetite
  • Nausea and vomiting
  • A build-up of fluid in the legs and abdomen.
  • Weight loss
  • The tendency to bruise easily.
  • Jaundice (yellowing of the skin and the white of the eyes).
  • Itchiness
  • Sensitivity to drugs due to the reduced ability of the liver to deactivate them.
  • Spider naevi – these are small capillaries visible on the surface of your skin. Branches grow out from one capillary making it look like a small red spider. They can only be found above the waist, usually on the chest, upper arms, shoulders, face, neck and upper back.

Decompensated cirrhosis

Decompensated cirrhosis is when the scarring of the liver is so extensive that the parts of the liver that are still functioning efficiently can no longer compensate for the parts that are damaged. At this stage the liver will have nodules of scar tissue, which are visible on ultrasound. It will be shrunken in size and will no longer be able to carry out its essential functions. Once decompensated cirrhosis has occurred, serious complications are almost inevitable. There is usually a high frequency of readmissions to hospital.

The most serious symptoms of decompensated cirrhosis are:

  • Portal Hypertension: When blood cannot properly flow through the liver and pressure rises in the portal vein leading into the liver.
  • Variceal Bleeding: When the portal hypertension forces blood to re-route through veins that are too small and consequently burst, often in the oesophagus (between the throat and the stomach), causing potentially life-threatening internal bleeding.
  • Oedema: When the liver stops producing enough albumin. This regulates the amount of fluid in cells. This fluid then builds up, typically in the stomach, and is known as ‘ascites’.
  • Hepatic Encephalopathy: When the liver stops properly filtering poisons and toxins. These then build up in the brain leading to serious mental confusion and sometimes coma.