Cirrhosis is a condition that develops with long-term, ongoing liver damage. With cirrhosis, the normal structure of the liver has been replaced by islands of liver tissue separated by nonfunctional bands of scar tissue. Chronic liver disease/cirrhosis is among the top 10 causes of death in the United States for people aged 25 to 64, reports the Centers for Disease Control and Prevention. The most common causes of cirrhosis in the US are chronic hepatitis C infection and alcoholic liver disease. Several different systems are used to stage the severity of cirrhosis. The 4-stage system is based on the presence or absence of specific complications of cirrhosis. These complications develop because of failing liver function and/or blockage of blood flow through the liver caused by extensive scarring within the organ.
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Stage 1 Cirrhosis
Stage 1 is the earliest stage of cirrhosis and is characterized by the absence of two significant complications known as varices and ascites. Varices are dilated, ballooned veins. They are most often located in the lining of the esophagus and/or stomach. Acsites refers to an accumulation of fluid in the abdominal cavity. Both varices and ascites develop primarily because of obstructed blood flow through the liver, a condition known as portal hypertension. While people with stage 1 cirrhosis have extensive liver scarring, it is not severe enough to cause substantial portal hypertension and its complications.
Stage 1 cirrhosis is considered compensated cirrhosis. This means that despite extensive damage, the liver is not yet so severely scarred that clinically apparent signs of liver failure have developed. People with stage 1 cirrhosis generally do not experience many symptoms other than perhaps lack of energy and fatigue. Stage 1 cirrhosis is potentially reversible if the underlying cause of the cirrhosis is eliminated or cured.
Stage 2 Cirrhosis
Stage 2 cirrhosis is marked by the development of esophageal varices, due to worsening portal hypertension, but without the presence of ascites. While the development of esophageal varices indicates worsening cirrhosis and an increased risk of dying in the next 12 months, stage 2 cirrhosis is still considered compensated cirrhosis. There remains the potential for at least partial reversal of liver damage if the underlying cause of cirrhosis is eliminated or cured.
Stage 3 Cirrhosis
Stage 3 cirrhosis is marked by the development of ascites, with or without the presence of varices. The volume of ascites varies from being detectable only with imaging tests, such as abdominal ultrasound, to obvious bloating of the abdomen. The development of ascites signals worsening portal hypertension due to advancing liver scarring and deterioration of liver function. Stage 3 cirrhosis signals decompensated cirrhosis, meaning the liver is failing. Once decompensated cirrhosis develops, liver scarring is irreversible and evaluation for liver transplantation is generally recommended. A variety of signs and symptoms may be present with stage 3 cirrhosis, including:
- pale and/or yellowish skin
- weight loss and loss of appetite
- shortness of breath
- extreme fatigue
- persistent, widespread itchiness
- swelling of the feet, ankles and lower legs
- wasting of the muscles of the arms and legs
Stage 4 Cirrhosis
The defining feature of stage 4 is gastrointestinal bleeding, usually from ruptured varices in the esophagus or stomach. This type of bleeding can be immediately life threatening if not controlled. Even if bleeding stops or is medically controlled, however, individuals with stage 4 cirrhosis still face a high risk of dying within 12 months. Persons with stage 4 cirrhosis have end-stage liver disease and urgent evaluation for possible liver transplantation is necessary. Signs and symptoms that might develop include those that may occur with stage 3 cirrhosis as well as others, such as:
- confusion, personality changes and/or extreme sleepiness
- hand tremors
- reduced urination, which may indicate kidney failure
- high fever, signalling infection of the abdominal cavity
Reviewed and revised by: Tina M. St. John, M.D.