SCHOOL OF NURSNG – KANDY.

MEDICAL NURSING CARE STUDY OF A

PATIENT WITH CIRRHOSIS

SUBMITED TO :- SPECIAL GRADE NURSING TUTOR AJITH DASSANAYAKA

SUBMITTED BY :- W.M.D.D.WIJEKOON.

INDEX NO :- 9501

BATCH :- 2016 - A
AKNOWLEDGEMENT.

I am glad to

Dedicate this care study

To

Madam K.C. THENNAKOON ,

Who is guided me

For this

“Cirrhosis”

Care study.

THANK YOU…
 TABLE OF CONTENT.

1. Introduction
2. Objectives
3. Cirrhosis
4. Why does cirrhosis case probles?
5. Anatomy and Physiology of the liver
6. Anatomy of the liver
7. Physiology of the liver
8. About the liver
9. Stages of cirrhosis of the liver
10. Symptoms
11. Causes
12. Complication
13. Risk Factors
14. Prevention
15. Diagnosis
16. Treatment
17. Pathophysiology
18. Etiology
19. Clinical Manifestation
20. Classification
21. Risk Factors
22. Complication
23. Diagnosis
24. Nursing Document.
25. Conclusion
26. References
 INTROUCTION.

Cirrhosis, also known as liver cirrhosis or hepatic cirrhosis, is a condition in

which the liver does not function properly due to long-term damage. This damage is
characterized by the replacement of normal liver tissue by scar tissue Typically, the
disease develops slowly over months or years

Cirrhosis is most commonly caused by alcohol, hepatitis B, hepatitis C, and non-

alcoholic fatty liver disease. Typically, more than two or three alcoholic drinks per
day over a number of years is required for alcoholic cirrhosis to occur. Non-alcoholic
fatty liver disease has a number of causes, including
being overweight, diabetes, high blood fats, and high blood pressure. A number of
less common causes of cirrhosis include autoimmune hepatitis, primary biliary
cholangitis, hemochromatosis, certain medications, and gallstones. Diagnosis is
based on blood testing, medical imaging, and liver biopsy

Cirrhosis affected about 2.8 million people and resulted in 1.3 million deaths in 2015.
Of these deaths, alcohol caused 348,000, hepatitis C caused 326,000, and hepatitis
B caused 371,000. In the United States, more men die of cirrhosis than women. The
first known description of the condition is by Hippocrates in the 5th century BCE. The
term cirrhosis was invented in 1819, from a Greek word for the yellowish color of a
diseased liver.

This care study includes the information regarding cirrhosis, treatment for cirrhosis
and prevention.
 OBJECTIVES.

 To identify patient’s condition and his problem.

 To establish good interpersonal relationship with patient and his family.

 To obtain whole knowledge about this disease condition.

 Getting know about solution through the understanding of nursing diagnosis.

 To develop skills in health education.

 To recognize the ways to prevent this disease.

 To carry this knowledge for the community.

 Human Anatomy & Physiology of the Liver

Anatomy of the Liver

Weighing in at around 3 pounds, the liver is the body’s second largest organ; only
the skin is larger and heavier. The liver performs many essential functions related to
digestion, metabolism, immunity, and the storage of nutrients within the body. These
functions make the liver a vital organ without which the tissues of the body would
quickly die from lack of energy and nutrients. Fortunately, the liver has an incredible
capacity for regeneration of dead or damaged tissues; it is capable of growing as
quickly as a cancerous tumor to restore its normal size and function.
Gross Anatomy

The liver is a roughly triangular organ that extends across the entire abdominal
cavity just inferior to the diaphragm. Most of the liver’s mass is located on the right
side of the body where it descends inferiorly toward the right kidney. The liver is
made of very soft, pinkish-brown tissues encapsulated by a connective tissue
capsule. This capsule is further covered and reinforced by the peritoneum of the
abdominal cavity, which protects the liver and holds it in place within the abdomen.

The peritoneum connects the liver in 4 locations: the coronary ligament, the left and
right triangular ligaments, and the falciform ligament. These connections are not true
ligaments in the anatomical sense; rather, they are condensed regions of peritoneal
membrane that support the liver.

 The wide coronary ligament connects the central superior portion of the liver
to the diaphragm.
 Located on the lateral borders of the left and right lobes, respectively, the left
and right triangular ligaments connect the superior ends of the liver to the
diaphragm.
 The falciform ligament runs inferiorly from the diaphragm across the anterior
edge of the liver to its inferior border. At the inferior end of the liver, the
falciform ligament forms the round ligament (ligamentum teres) of the liver
and connects the liver to the umbilicus. The round ligament is a remnant of
the umbilical vein that carries blood into the body during fetal development.

The liver consists of 4 distinct lobes – the left, right, caudate, and quadrate lobes.
  The left and right lobes are the largest lobes and are separated by the
falciform ligament. The right lobe is about 5 to 6 times larger than the tapered
left lobe.
 The small caudate lobe extends from the posterior side of the right lobe and
wraps around the inferior vena cava.
 The small quadrate lobe is inferior to the caudate lobe and extends from the
posterior side of the right lobe and wraps around the gallbladder.

Bile Ducts

The tubes that carry bile through the liver and gallbladder are known as bile ducts
and form a branched structure known as the biliary tree. Bile produced by liver cells
drains into microscopic canals known as bile canaliculi. The countless bile canaliculi
join together into many larger bile ducts found throughout the liver.

These bile ducts next join to form the larger left and right hepatic ducts, which carry
bile from the left and right lobes of the liver. Those two hepatic ducts join to form the
common hepatic duct that drains all bile away from the liver. The common hepatic
duct finally joins with the cystic duct from the gallbladder to form the common bile
duct, carrying bile to the duodenum of the small intestine. Most of the bile produced
by the liver is pushed back up the cystic duct by peristalsis to arrive in the
gallbladder for storage, until it is needed for digestion.

Blood Vessels

The blood supply of the liver is unique among all organs of the body due to the
hepatic portal vein system. Blood traveling to the spleen, stomach, pancreas,
gallbladder, and intestines passes through capillaries in these organs and is
collected into the hepatic portal vein. The hepatic portal vein then delivers this
blood to the tissues of the liver where the contents of the blood are divided up into
smaller vessels and processed before being passed on to the rest of the body. Blood
leaving the tissues of the liver collects into the hepatic veins that lead to the vena
cava and return to the heart. The liver also has its own system of arteries and
arterioles that provide oxygenated blood to its tissues just like any other organ.
Lobules

The internal structure of the liver is made of around 100,000 small hexagonal
functional units known as lobules. Each lobule consists of a central vein surrounded
by 6 hepatic portal veins and 6 hepatic arteries. These blood vessels are connected
by many capillary-like tubes called sinusoids, which extend from the portal veins
and arteries to meet the central vein like spokes on a wheel.
Each sinusoid passes through liver tissue containing 2 main cell types: Kupffer cells
and hepatocytes.
 Kupffer cells are a type of macrophage that capture and break down old, worn
out red blood cells passing through the sinusoids.
 Hepatocytes are cuboidal epithelial cells that line the sinusoids and make up
the majority of cells in the liver. Hepatocytes perform most of the liver’s
functions – metabolism, storage, digestion, and bile production. Tiny bile
collection vessels known as bile canaliculi run parallel to the sinusoids on the
other side of the hepatocytes and drain into the bile ducts of the liver.
 Physiology of the Liver

Essential Functions of the Liver are

 Production of Energy instantly

 Making proteins for body building and tissue repair
 Storing vitamins, minerals, and sugars for various functions
 Regulating fat transport across the body
 Regulating Blood clotting activities
 Regulating levels of chemicals and drugs in the blood
 Regulating hormone balance
 Helping in digestion by production of bile
 Helping to eliminate excess cholesterol levels
 Neutralizing poisonous substances
 Metabolism of alcohol
 A vital organ in blood formation before birth
 Helping to resist infection
 Regenerating its own damaged tissue
 Resisting infections by helping to remove bacteria from blood
 Cleansing Blood by discharging waste products

Digestion

The liver plays an active role in the process of digestion through the production of
bile. Bile is a mixture of water, bile salts, cholesterol, and the pigment bilirubin.
Hepatocytes in the liver produce bile, which then passes through the bile ducts to be
stored in the gallbladder. When food containing fats reaches the duodenum, the
cells of the duodenum release the hormone cholecystokinin to stimulate the
gallbladder to release bile. Bile travels through the bile ducts and is released into the
duodenum where it emulsifies large masses of fat. The emulsification of fats by bile
turns the large clumps of fat into smaller pieces that have more surface area and are
therefore easier for the body to digest.

Bilirubin present in bile is a product of the liver’s digestion of worn out red blood
cells. Kupffer cells in the liver catch and destroy old, worn out red blood cells and
pass their components on to hepatocytes. Hepatocytes metabolize hemoglobin, the
red oxygen-carrying pigment of red blood cells, into the components heme and
globin. Globin protein is further broken down and used as an energy source for the
body. The iron-containing heme group cannot be recycled by the body and is
converted into the pigment bilirubin and added to bile to be excreted from the body.
Bilirubin gives bile its distinctive greenish color. Intestinal bacteria further convert
bilirubin into the brown pigment stercobilin, which gives feces their brown color.
Metabolism

The hepatocytes of the liver are tasked with many of the important metabolic jobs
that support the cells of the body. Because all of the blood leaving the digestive
system passes through the hepatic portal vein, the liver is responsible for
metabolizing carbohydrate, lipids, and proteins into biologically useful materials.

Our digestive system breaks down carbohydrates into the monosaccharide

glucose, which cells use as a primary energy source. Blood entering the liver through
the hepatic portal vein is extremely rich in glucose from digested food. Hepatocytes
absorb much of this glucose and store it as the macromolecule glycogen, a branched
polysaccharide that allows the hepatocytes to pack away large amounts of glucose
and quickly release glucose between meals. The absorption and release of glucose
by the hepatocytes helps to maintain homeostasis and protects the rest of the body
from dangerous spikes and drops in the blood glucose level. (See more about
glucose in the body.)

Fatty acids in the blood passing through the liver are absorbed by hepatocytes and
metabolized to produce energy in the form of ATP. Glycerol, another lipid
component, is converted into glucose by hepatocytes through the process of
gluconeogenesis. Hepatocytes can also produce lipids like cholesterol,
phospholipids, and lipoproteins that are used by other cells throughout the body.
Much of the cholesterol produced by hepatocytes gets excreted
from the body as a component of bile.
Dietary proteins are broken down into their component amino acids by the digestive
system before being passed on to the hepatic portal vein. Amino acids entering the
liver require metabolic processing before they can be used as an energy source.
Hepatocytes first remove the amine groups of the amino acids and convert them into
ammonia and eventually urea. Urea is less toxic than ammonia and can be excreted
in urine as a waste product of digestion. The remaining parts of the amino acids can
be broken down into ATP or converted into new glucose molecules through the
process of gluconeogenesis.

Detoxification

As blood from the digestive organs passes through the hepatic portal circulation, the
hepatocytes of the liver monitor the contents of the blood and remove many
potentially toxic substances before they can reach the rest of the body. Enzymes in
hepatocytes metabolize many of these toxins such as alcohol and drugs into their
inactive metabolites. And in order to keep hormone levels within homeostatic limits,
the liver also metabolizes and removes from circulation hormones produced by the
body’s own glands.
Storage

The liver provides storage of many essential nutrients, vitamins, and minerals
obtained from blood passing through the hepatic portal system. Glucose is
transported into hepatocytes under the influence of the hormone insulin and stored
as the polysaccharide glycogen. Hepatocytes also absorb and store fatty acids from
digested triglycerides. The storage of these nutrients allows the liver to maintain the
homeostasis of blood glucose. Our liver also stores vitamins and minerals - such
as vitamins A, D, E, K, and B12, and the minerals iron and copper - in order to
provide a constant supply of these essential substances to the tissues of the body.

Production

The liver is responsible for the production of several vital protein components of
blood plasma: prothrombin, fibrinogen, and albumins. Prothrombin and fibrinogen
proteins are coagulation factors involved in the formation of blood clots. Albumins
are proteins that maintain the isotonic environment of the blood so that cells of the
body do not gain or lose water in the presence of body fluids.

Immunity

The liver functions as an organ of the immune system through the function of the
Kupffer cells that line the sinusoids. Kupffer cells are a type of fixed macrophage that
form part of the mononuclear phagocyte system along with macrophages in the
spleen and lymph nodes. Kupffer cells play an important role by capturing and
digesting bacteria, fungi, parasites, worn-out blood cells, and cellular debris. The
large volume of blood passing through the hepatic portal system and the liver allows
Kupffer cells to clean large volumes of blood very quickly.
 Pathophysiology.

Normal liver vs. liver cirrhosis

Cirrhosis is a late stage of scarring (fibrosis) of the liver caused by many forms of
liver diseases and conditions, such as hepatitis and chronic alcoholism.
Each time your liver is injured — whether by disease, excessive alcohol consumption
or another cause — it tries to repair itself. In the process, scar tissue forms. As
cirrhosis progresses, more and more scar tissue forms, making it difficult for the liver
to function (decompensated cirrhosis). Advanced cirrhosis is life-threatening.
The liver damage done by cirrhosis generally can't be undone. But if liver cirrhosis is
diagnosed early and the cause is treated, further damage can be limited and, rarely,
reversed.

Etiology
A wide range of diseases and conditions can damage the liver and lead to cirrhosis.
Some of the causes include:

 Chronic alcohol abuse

 Chronic viral hepatitis (hepatitis B, C and D)
 Fat accumulating in the liver (nonalcoholic fatty liver disease)
 Iron buildup in the body (hemochromatosis)
 Cystic fibrosis
 Copper accumulated in the liver (Wilson's disease)
 Poorly formed bile ducts (biliary atresia)
 Alpha-1 antitrypsin deficiency
 Inherited disorders of sugar metabolism (galactosemia or glycogen storage
disease)
 Genetic digestive disorder (Alagille syndrome)
 Liver disease caused by your body's immune system (autoimmune hepatitis)
 Destruction of the bile ducts (primary biliary cirrhosis)
 Hardening and scarring of the bile ducts (primary sclerosing cholangitis
 Infection, such as syphilis or brucellosis
 Medications, including methotrexate or isoniazid

Clinical Manifestation.
Cirrhosis often has no signs or symptoms until liver damage is extensive. When
signs and symptoms do occur, they may include:

 Fatigue
 Easily bleeding or bruising
 Loss of appetite
 Nausea
 Swelling in your legs, feet or ankles (edema)
 Weight loss
 Itchy skin
 Yellow discoloration in the skin and eyes (jaundice)
 Fluid accumulation in your abdomen (ascites)
 Spiderlike blood vessels on your skin
 Redness in the palms of the hands
 For women, absent or loss of periods not related to menopause
 For men, loss of sex drive, breast enlargement (gynecomastia) or testicular
atrophy
 Confusion, drowsiness and slurred speech (hepatic encephalopathy)

Classification.
Alcohol and nonalcoholic fatty liver disease

Alcohol

Alcohol is a very common cause of cirrhosis, particularly in the Western world.

Chronic, high levels of alcohol consumption injure liver cells. Thirty percent of
individuals who drink daily at least eight to sixteen ounces of hard liquor or the
equivalent for fifteen or more years will develop cirrhosis. Alcohol causes a range of
liver diseases, which include simple and uncomplicated fatty liver (steatosis), more
serious fatty liver with inflammation (steatohepatitis or alcoholic hepatitis), and
cirrhosis.

Nonalcoholic fatty liver disease (NAFLD)

Nonalcoholic fatty liver disease (NAFLD) refers to a wide spectrum of liver diseases
that, like alcoholic liver disease, range from simple steatosis, to nonalcoholic
steatohepatitis (NASH), to cirrhosis. All stages of NAFLD have in common the
accumulation of fat in liver cells. The term nonalcoholic is used because NAFLD
occurs in individuals who do not consume excessive amounts of alcohol, yet in many
respects the microscopic picture of NAFLD is similar to what can be seen in liver
disease that is due to excessive alcohol. NAFLD is associated with a condition
called insulin resistance, which, in turn, is associated with metabolic
syndrome and diabetes mellitus type 2. Obesity is the main cause
of insulin resistance, metabolic syndrome, and type 2 diabetes. NAFLD is the most
common liver disease in the United States and is responsible for up to 25% of all
liver disease. The number of livers transplanted for NAFLD-related cirrhosis is on the
rise. Public health officials are worried that the current epidemic of obesity will
dramatically increase the development of NAFLD and cirrhosis in the population.

Hepatitis, primary biliary cirrhosis, and primary

sclerosing cholangitis
Chronic viral hepatitis (hep B and C)
Chronic viral hepatitis is a condition in which hepatitis B or hepatitis C virus infects
the liver for years. Most patients with viral hepatitis will not develop chronic hepatitis
and cirrhosis. The majority of patients infected with hepatitis A recover completely
within weeks, without developing chronic infection. In contrast, some patients
infected with hepatitis B virus and most patients infected with hepatitis C virus
develop chronic hepatitis, which, in turn, causes progressive liver damage and leads
to cirrhosis, and, sometimes, liver cancers.

Autoimmune hepatitis
Autoimmune hepatitis is a liver disease found more commonly in women that is
caused by an abnormality of the immune system. The abnormal immune activity in
autoimmune hepatitis causes progressive inflammation and destruction of liver cells
(hepatocytes), leading ultimately to cirrhosis.

Primary biliary cirrhosis (PBC)

Primary biliary cirrhosis (PBC) is a liver disease caused by an abnormality of the
immune system that is found predominantly in women. The abnormal immunity in
PBC causes chronic inflammation and destruction of the small bile ducts within the
liver. The bile ducts are passages within the liver through which bile travels to the
intestine. Bile is a fluid produced by the liver that contains substances required for
digestion and absorption of fat in the intestine, as well as other compounds that are
waste products, such as the pigment bilirubin. (Bilirubin is produced by the
breakdown of hemoglobin from old red blood cells.). Along with the gallbladder, the
bile ducts make up the biliary tract. In PBC, the destruction of the small bile ducts
blocks the normal flow of bile into the intestine. As the inflammation continues to
destroy more of the bile ducts, it also spreads to destroy nearby liver cells. As the
destruction of the hepatocytes proceeds, scar tissue (fibrosis) forms and spreads
throughout the areas of destruction. The combined effects of progressive
inflammation, scarring, and the toxic effects of accumulating waste products
culminates in cirrhosis.

Primary sclerosing cholangitis (PSC)

Primary sclerosing cholangitis (PSC) is an uncommon disease frequently found in
patients with Crohn's disease and ulcerative colitis. In PSC, the large bile ducts
outside of the liver become inflamed, narrowed, and obstructed. Obstruction to the
flow of bile leads to infections of the bile ducts and jaundice, eventually causing
cirrhosis. In some patients, injury to the bile ducts (usually because of surgery) also
can cause obstruction and cirrhosis of the liver.

Inherited disorders, cryptogenic cirrhosis, and

biliary atresia in infants

Inherited (genetic) disorders

Inherited (genetic) disorders that result in the accumulation of toxic substances in the
liver, which leads to tissue damage and cirrhosis. Examples include the abnormal
accumulation of iron (hemochromatosis) or copper (Wilson disease). In
hemochromatosis, patients inherit a tendency to absorb an excessive amount of iron
from food. Over time, iron accumulation in different organs throughout the body
causes cirrhosis, arthritis, heart muscle damage leading to heart failure, and
testicular dysfunction causing loss of sexual drive. Treatment is aimed at preventing
damage to organs by removing iron from the body through phlebotomy (removing
blood). In Wilson disease, there is an inherited abnormality in one of the proteins that
controls copper in the body. Over time, copper accumulates in the liver, eyes, and
brain. Cirrhosis, tremor, psychiatric disturbances and other neurological difficulties
occur if the condition is not treated early. Treatment is with oral medication, which
increases the amount of copper that is eliminated from the body in the urine.

Cryptogenic cirrhosis

Cryptogenic cirrhosis (cirrhosis due to unidentified causes) is a common reason for

liver transplantation. It is termed called cryptogenic cirrhosis because for many years
doctors have been were unable to explain why a proportion of patients developed
cirrhosis. Doctors now believe that cryptogenic cirrhosis is due to NASH
(nonalcoholic steatohepatitis) caused by long standing obesity, type 2 diabetes, and
insulin resistance. The fat in the liver of patients with NASH is believed to disappear
with the onset of cirrhosis, and this has made it difficult for doctors to make the
connection between NASH and cryptogenic cirrhosis for a long time. One important
clue that NASH leads to cryptogenic cirrhosis is the finding of a high occurrence of
NASH in the new livers of patients undergoing liver transplant for cryptogenic
cirrhosis. Finally, a study from France suggests that patients with NASH have a
similar risk of developing cirrhosis as patients with long standing infection
with hepatitis C virus. (See discussion that follows.) However, the progression to
cirrhosis from NASH is thought to be slow and the diagnosis of cirrhosis typically is
made in people in their sixties.

Biliary atresia

Infants can be born without bile ducts (biliary atresia) and ultimately develop
cirrhosis. Other infants are born lacking vital enzymes for controlling sugars that
leads to the accumulation of sugars and cirrhosis. On rare occasions, the absence of
a specific enzyme can cause cirrhosis and scarring of the lung (alpha-1 antitrypsin
deficiency).
Less common causes of cirrhosis include unusual reactions to some drugs and
prolonged exposure to toxins, as well as chronic heart failure (cardiac cirrhosis). In
certain parts of the world (particularly Northern Africa), infection of the liver with a
parasite (schistosomiasis) is the most common cause of liver disease and cirrhosis.

Risk factors
 Drinking too much alcohol.
Excessive alcohol consumption is a risk factor for cirrhosis.
  Being overweight.
Being obese increases your risk of conditions that may lead to cirrhosis, such
as nonalcoholic fatty liver disease and nonalcoholic steatohepatitis.

 Having viral hepatitis.

Not everyone with chronic hepatitis will develop cirrhosis, but it's one of the
world's leading causes of liver disease.

Complications
Complications of cirrhosis can include:
 High blood pressure in the veins that supply the liver (portal
hypertension). Cirrhosis slows the normal flow of blood through the liver, thus
increasing pressure in the vein that brings blood to the liver from the intestines
and spleen
.
 Swelling in the legs and abdomen. The increased pressure in the portal vein
can cause fluid to accumulate in the legs (edema) and in the abdomen
(ascites). Edema and ascites also may result from the inability of the liver to
make enough of certain blood proteins, such as albumin.

 Enlargement of the spleen (splenomegaly). Portal hypertension can also

cause changes to and swelling of the spleen, and trapping of white blood cells
and platelets. Decreased white blood cells and platelets in your blood can be
the first sign of cirrhosis.

 Bleeding. Portal hypertension can cause blood to be redirected to smaller

veins. Strained by the extra pressure, these smaller veins can burst, causing
serious bleeding. Portal hypertension may cause enlarged veins (varices) in the
esophagus (esophageal varices) or the stomach (gastric varices) and lead to
life-threatening bleeding. If the liver can't make enough clotting factors, this also
can contribute to continued bleeding.

 Infections. If you have cirrhosis, your body may have difficulty fighting
infections. Ascites can lead to bacterial peritonitis, a serious infection.

 Malnutrition. Cirrhosis may make it more difficult for your body to process
nutrients, leading to weakness and weight loss.

 Buildup of toxins in the brain (hepatic encephalopathy). A liver damaged by

cirrhosis isn't able to clear toxins from the blood as well as a healthy liver can.
These toxins can then build up in the brain and cause mental confusion and
difficulty concentrating. With time, hepatic encephalopathy can progress to
unresponsiveness or coma.

 Jaundice. Jaundice occurs when the diseased liver doesn't remove enough
bilirubin, a blood waste product, from your blood. Jaundice causes yellowing of
the skin and whites of the eyes and darkening of urine.

 Bone disease. Some people with cirrhosis lose bone strength and are at
greater risk of fractures.

 Increased risk of liver cancer. A large proportion of people who develop liver
cancer have pre-existing cirrhosis.

 Acute-on-chronic cirrhosis. Some people end up experiencing multiorgan

failure. Researchers now believe this is a distinct complication in some people
who have cirrhosis, but they don't fully understand its causes.
 Stages of cirrhosis of the liver

Cirrhosis in itself is already a late stage of liver damage. In the early stages of liver
disease there will be inflammation of the liver. If this inflammation is not treated it can
lead to scarring (fibrosis). At this stage it is still possible for the liver to heal with
treatment.

If fibrosis of the liver is not treated, it can result in cirrhosis. At this stage, the scar
tissue cannot heal, but the progression of the scarring may be prevented or slowed.
People with cirrhosis who have signs of complications may develop end-stage liver
disease (ESLD) and the only treatment at this stage is liver transplantation.

 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 develop end-stage
liver disease (ESLD), which is fatal without a transplant.
 Prevention
Reduce your risk of cirrhosis by taking these steps to care for your liver:
  Do not drink alcohol if you have cirrhosis. If you have liver disease, you
should avoid alcohol.

 Eat a healthy diet. Choose a plant-based diet that's full of fruits and
vegetables. Select whole grains and lean sources of protein. Reduce the
amount of fatty and fried foods you eat.

 Maintain a healthy weight. An excess amount of body fat can damage your
liver. Talk to your doctor about a weight-loss plan if you are obese or
overweight.

 Reduce your risk of hepatitis. Sharing needles and having unprotected sex
can increase your risk of hepatitis B and C. Ask your doctor about hepatitis
vaccinations.
If you're concerned about your risk of liver cirrhosis, talk to your doctor about ways
you can reduce your risk.

Diagnosis

Liver biopsy
People with early-stage cirrhosis of the liver usually don't have symptoms. Often,
cirrhosis is first detected through a routine blood test or checkup. To help confirm a
diagnosis, a combination of laboratory and imaging tests is usually done.

Tests

Your doctor may order one or more tests that may suggest a problem with your liver,
including:

 Laboratory tests. Your doctor may order blood tests to check for signs of liver
malfunction, such as excess bilirubin, as well as for certain enzymes that may
indicate liver damage. To assess kidney function, your blood is checked for
creatinine. You'll be screened for the hepatitis viruses. Your international
normalized ratio (INR) is also checked for your blood's ability to clot.
Based on the blood test results, your doctor may be able to diagnose the
underlying cause of cirrhosis. He or she can also use blood tests to help identify
how serious your cirrhosis is.

 Imaging tests. Magnetic resonance elastography (MRE) may be

recommended. This noninvasive advanced imaging test detects hardening or
stiffening of the liver. Other imaging tests, such as MRI, CT and ultrasound,
may also be done.

 Biopsy. A tissue sample (biopsy) is not necessarily needed for diagnosis.

However, your doctor may use it to identify the severity, extent and cause of
liver damage.

Treatment
Treatment for cirrhosis depends on the cause and extent of your liver damage. The
goals of treatment are to slow the progression of scar tissue in the liver and to
prevent or treat symptoms and complications of cirrhosis
Treatment for the underlying cause of cirrhosis

In early cirrhosis, it may be possible to minimize damage to the liver by treating the
underlying cause. The options include:

 Treatment for alcohol dependency. People with cirrhosis caused by

excessive alcohol use should try to stop drinking. If stopping alcohol use is
difficult, your doctor may recommend a treatment program for alcohol addiction.
If you have cirrhosis, it is critical to stop drinking since any amount of alcohol is
toxic to the liver.
 Weight loss. People with cirrhosis caused by nonalcoholic fatty liver disease
may become healthier if they lose weight and control their blood sugar levels.
 Medications to control hepatitis. Medications may limit further damage to
liver cells caused by hepatitis B or C through specific treatment of these
viruses.
 Medications to control other causes and symptoms of
cirrhosis. Medications may slow the progression of certain types of liver
cirrhosis. For example, for people with primary biliary cirrhosis that is diagnosed
early, medication may significantly delay progression to cirrhosis.

Other medications can relieve certain symptoms, such as itching, fatigue and pain.
Nutritional supplements may be prescribed to counter malnutrition associated with
cirrhosis and to prevent weak bones (osteoporosis).

Treatment for complications of cirrhosis

Your doctor will work to treat any complications of cirrhosis, including:

 Excess fluid in your body. A low-sodium diet and medication to prevent fluid
buildup in the body may help control ascites and swelling. More-severe fluid
buildup may require procedures to drain the fluid or surgery to relieve pressure.
 Infections. You may receive antibiotics or other treatments for infections. Your
doctor also is likely to recommend vaccinations for influenza, pneumonia and
hepatitis.
 Increased liver cancer risk. Your doctor will likely recommend periodic blood
tests and ultrasound exams to look for signs of liver cancer.
 Hepatic encephalopathy. You may be prescribed medications to help reduce
the buildup of toxins in your blood due to poor liver function.
 Portal hypertension. Certain blood pressure medications may control
increased pressure in the veins that supply the liver (portal hypertension) and
prevent severe bleeding. Your doctor will perform an upper endoscopy at
 regular intervals to look for enlarged veins in the esophagus or stomach
(varices) that may bleed.
If you develop varices, you likely will need medication to reduce the risk of
bleeding. If you have signs that the varices are bleeding or are likely to bleed,
you may need a procedure (band ligation) to stop the bleeding or reduce the
risk of further bleeding. In severe cases, you may need a small tube — a
transjugular intrahepatic portosystemic shunt — placed in your vein to reduce
blood pressure in your liver.

Liver transplant surgery

In advanced cases of cirrhosis, when the liver ceases to function, a liver transplant
may be the only treatment option. A liver transplant is a procedure to replace your
liver with a healthy liver from a deceased donor or with part of a liver from a living
donor. Cirrhosis is one of the most common reasons for a liver transplant.
Candidates for liver transplant have extensive testing to determine whether they are
healthy enough to have a good outcome following surgery.

Historically, those with alcoholic cirrhosis have not been liver transplant candidates
because of the risk that they will return to harmful drinking after transplant. Recent
studies, however, suggest that carefully selected people with severe alcoholic
cirrhosis have post-transplant survival rates similar to those of liver transplant
recipients with other types of liver disease.
For transplant to be an option if you have alcoholic cirrhosis, you would need:

 To find a program that works with people who have alcoholic cirrhosis
 To meet the requirements of the program, which would include lifelong
commitment to alcohol abstinence as well as other requirements of the specific
transplant center

Potential future treatments

Scientists are working to expand current treatments for cirrhosis, but success has
been limited. Because cirrhosis has numerous causes and complications, there are
many potential avenues of approach. A combination of increased screening, lifestyle
changes and new medications may improve outcomes for people with liver damage,
if started early.
Researchers are working on therapies that will specifically target liver cells, helping
to slow or even reverse the fibrosis that leads to cirrhosis. While no targeted therapy
is quite ready, the framework for developing such treatments is in place, and
progress is accelerating.