What is cirrhosis?

Cirrhosis is a complication of many liver diseases characterized by abnormal structure and function of
the liver. The diseases that lead to cirrhosis do so because they injure and kill liver cells, after which the
inflammation and repair that is associated with the dying liver cells causes scar tissue to form. The liver
cells that do not die multiply in an attempt to replace the cells that have died. This results in clusters of
newly formed liver cells (regenerative nodules) within the scar tissue. There are many causes of cirrhosis
including chemicals (such as alcohol, fat, and certain medications), viruses, toxic metals (such as iron and
copper that accumulate in the liver as a result of genetic diseases), and autoimmune liver disease in
which the body's immune system attacks the liver.

What are the signs and symptoms of cirrhosis?

People with cirrhosis may have few or no symptoms and signs of liver disease. Some of the symptoms
may be nonspecific and don't suggest the liver is their cause. Common symptoms and signs of cirrhosis
include:

 Yellowing of the skin (jaundice) due to the accumulation of bilirubin in the blood
 Fatigue
 Weakness
 Loss of appetite
 Itching
 Easy bruising from decreased production of blood clotting factors by the diseased liver.

What are the stages of cirrhosis of the liver?

 Stage 1 cirrhosis involves some scarring of the liver, but few symptoms. This stage is
considered compensated cirrhosis, where there are no complications.
 Stage 2 cirrhosis includes worsening portal hypertension and the development of
varices.
 Stage 3 cirrhosis involves the development of swelling in the abdomen and advanced
liver scarring. This stage marks decompensated cirrhosis, with serious complications
and possible liver failure.
 Stage 4 cirrhosis can be life threatening and people have developed end-stage liver
disease (ESLD), which is fatal without a transplant.
Complications of cirrhosis
Edema and ascites
As cirrhosis of the liver becomes severe, signals are sent to the kidneys to retain salt and water
in the body. The excess salt and water first accumulates in the tissue beneath the skin of the
ankles and legs because of the effect of gravity when standing or sitting. This accumulation of
fluid is called peripheral edema or pitting edema.
As cirrhosis worsens and more salt and water are retained, fluid also may accumulate in the
abdominal cavity between the abdominal wall and the abdominal organs (called ascites)
causing swelling of the abdomen, abdominal discomfort, and increased weight.
Spontaneous bacterial peritonitis (SBP)
Fluid in the abdominal cavity (ascites) is the perfect place for bacteria to grow. Normally, the
abdominal cavity contains a very small amount of fluid that can resist infection well, and
bacteria that enter the abdomen (usually from the intestine) are killed or find their way into the
portal vein and to the liver where they are killed. In cirrhosis, the fluid that collects in the
abdomen is unable to resist infection normally. In addition, more bacteria find their way from
the intestine into the ascites. Infection within the abdomen and the ascites, called spontaneous
bacterial peritonitis or SBP, is likely to occur. SBP is a life- threatening complication. Some
patients with SBP have no symptoms, while others have fever, chills, abdominal pain and
tenderness, diarrhea, and worsening ascites.
Bleeding from esophageal varices
In the cirrhotic liver, the scar tissue blocks the flow of blood returning to the heart from the
intestines and raises the pressure in the portal vein (portal hypertension). When pressure in the
portal vein becomes high enough, it causes blood to flow around the liver through veins with
lower pressure to reach the heart. The most common veins through which blood bypasses the
liver are the veins lining the lower part of the esophagus and the upper part of the stomach.

As a result of the increased flow of blood and the resulting increase in pressure, the veins in the
lower esophagus and upper stomach expand and then are referred to as esophageal and gastric
varices; the higher the portal pressure, the larger the varices and the more likely a patient is to
bleed from the varices into the esophagus or stomach.
What are common causes of cirrhosis?

 Alcohol
 Nonalcoholic fatty liver disease
 Cryptogenic causes
 Chronic viral hepatitis (A, B, and C)
 Autoimmune hepatitis
 Inherited (genetic) disorders
 Primary biliary cirrhosis (PCB)
 Infants born without bile ducts
 How is cirrhosis diagnosed and evaluated?

The single best test for diagnosing cirrhosis is biopsy of the liver. Liver biopsies carry a small risk for
serious complications, and biopsy often is reserved for those patients in whom the diagnosis of the
type of liver disease or the presence of cirrhosis is not clear. The history, physical examination, or
routine testing may suggest the possibility of cirrhosis. Examples of how doctors diagnose and
evaluate cirrhosis are:

 The patient's history. The doctor may uncover a history of excessive and prolonged intake of
alcohol, a history of intravenous drug abuse, or a history of hepatitis. This can suggest the
possibility of liver disease and cirrhosis.
 Patients who are known to have chronic viral hepatitis B or C have a higher probability of
having cirrhosis.
 Some patients with cirrhosis have enlarged livers and/or spleens. A doctor can often feel
(palpate) the lower edge of an enlarged liver below the right rib cage and feel the tip of the
enlarged spleen below the left rib cage. A cirrhotic liver also feels firmer and more irregular
than a normal liver.
 Some patients with cirrhosis, particularly alcoholic cirrhosis, have small red spider-like
markings (telangiectasias) on the skin, particularly on the chest that are made up of
enlarged, radiating blood vessels. However, these spider telangiectasias also can be seen in
individuals without liver disease.
 Jaundice (yellowing of the skin and of the whites of the eyes due to elevated bilirubin in the
blood) is common among patients with cirrhosis, but jaundice can occur in patients with
liver diseases without cirrhosis and other conditions such as hemolysis (excessive break
down of red blood cells).
 Swelling of the abdomen (ascites) and/or the lower extremities (edema) due to retention of
fluid is common among patients with cirrhosis, although other diseases can cause them
commonly, for example, congestive heart failure.

How is cirrhosis treated?

 Preventing further damage to the liver
 Treating the complications of cirrhosis
 Preventing liver cancer or detecting it early
 Liver transplant
 Consuming a balanced diet and a multivitamin daily. Patients with PBC with impaired absorption
of fat-soluble vitamins may need additional vitamins D and K.
 Avoiding drugs (including alcohol) that cause liver damage.
 All people with cirrhosis should avoid alcohol. Most of those with alcohol induced cirrhosis
experience an improvement in liver function with abstinence from alcohol. Even people with
chronic hepatitis B and C can substantially reduce liver damage and slow the progression
towards cirrhosis with abstinence from alcohol.
 Avoiding nonsteroidal anti-inflammatory drugs (NSAIDs, such as ibuprofen or naproxen).
Patients with cirrhosis can experience worsening of liver and kidney function with NSAIDs.
 Eradicating hepatitis B and hepatitis C virus by using anti-viral medications. Not all patients with
cirrhosis due to chronic viral hepatitis are candidates for drug treatment. Some patients may
experience serious deterioration in liver function and/or intolerable side effects during
treatment. Decisions to treat viral hepatitis have to be individualized, after consulting with
doctors experienced in treating liver diseases (hepatologists).
 Removing blood from patients with hemochromatosis to reduce the levels of iron and prevent
further damage to the liver. In Wilson disease, medications can be used to increase the
excretion of copper in the urine to reduce the levels of copper in the body and prevent further
damage to the liver.
 Suppressing the immune system with drugs such as prednisone and azathioprine (Imuran) to
decrease inflammation of the liver in autoimmune hepatitis.
 Treating patients with PBC with a bile acid preparation, ursodeoxycholic acid (UDCA), also called
ursodiol (Actigall). Results of an analysis that combined the results from several clinical trials
showed that UDCA increased survival among PBC patients during 4 years of therapy. The
development of portal hypertension also was reduced by the UDCA. Despite producing clear
benefits, UDCA treatment primarily slows progression and does not cure PBC. Other
medications such as colchicine (Colcrys) and methotrexate (Rheumatrex, Trexall) also may have
benefit in subsets of patients with PBC.
 Immunizsing people with cirrhosis against infection with hepatitis A and B to prevent a serious
deterioration in liver function. There are currently no vaccines available for immunizing against
hepatitis C.

https://www.medicinenet.com/cirrhosis/article.htm#what_research_is_ongoing_to_prevent_an
d_treat_cirrohsis_of_the_liver