LIVER CIRRHOSIS

I. Definition

Cirrhosis of the liver is a chronic disease that causes cell destruction and fibrosis (scarring) of
hepatic tissue. Fibrosis alters normal liver structure and vasculature, impairing blood and lymph
flow and resulting in hepatic insufficiency and hypertension in the portal vein. Complications
include hyponatremia, water retention, bleeding esophageal varices. Coagulopathy, spontaneous
bacterial peritonitis, and hepatic encephalopathy.

Cirrhosis is a potentially life-threatening condition that occurs when scarring damages the liver.
This scarring replaces healthy tissue and prevents the liver from working normally. Cirrhosis
usually develops after years of liver inflammation. When chronic diseases cause the liver to
become permanently injured and scarred, the condition is called Cirrhosis. Cirrhosis harms the
structure of the liver and blocks the flow of blood. The loss of normal liver tissue slows the
processing of nutrients, hormones, drugs, and toxins by the liver. Also, the production of proteins
and other substances made by the liver is suppressed. People with cirrhosis often have few
symptoms at first. The person may experience fatigue, weakness, and exhaustion. Loss of
appetite is usual, often with nausea and weight loss. As liver function declines, water may
accumulate in the legs and the abdomen (ascites). A decrease in proteins needed for blood
clotting makes it easy for the person to bruise, bleeding or infection. In the later stages of
cirrhosis, jaundice (yellow skin) may occur, caused by the buildup of bile pigment that is passed
by the liver into the intestines. The liver of a person with cirrhosis also has trouble removing
toxins, which may build up in the blood. Drugs taken usually are filtered out by the liver, and
this cleansing process also is slowed down by cirrhosis. People with cirrhosis often are very
sensitive to medications and their side effects. The doctor often can diagnose cirrhosis from the
patient’s symptoms and from laboratory tests. During a physical exam, the doctor could notice a
change in how your liver feels or how large it is. If the doctor suspects Cirrhosis, you will be
given blood tests. The purpose of these tests is to find out if liver disease is present. In some
cases, other tests that take pictures of the liver are performed such as the computerized axial
tomography (CAT) scan, and ultrasound. The doctor may decide to confirm the diagnosis by
putting a needle through the skin (biopsy) to take a sample of tissue from the liver. In some
cases, cirrhosis is diagnosed during surgery when the doctor is able to see the entire liver.

Three major forms

1. Laennec’s (alcohol induced) Cirrhosis

 Fibrosis occurs mainly around central veins and portal areas.

 This is the most common form of cirrhosis and results from chronic alcoholism and
malnutrition.
2. Postnecrotic (micronodular) Cirrhosis

 Consist of broad bands of scar tissue and results from previous acute viral hepatitis or
drug-induced massive hepatic necrosis.
3. Biliary Cirrhosis

 Consist of Scarring of bile ducts and lobes of the liver and results from chronic biliary
obstruction and infection (cholangitis), and is much rarer than the preceding forms
 II.ANATOMY AND PHYSIOLOGY:
The liver is located in the upper right-hand portion of the abdominal cavity, beneath the
diaphragm and on top of the stomach, right kidney and intestines. The liver, a dark reddish-
brown organ that weighs about 3 pounds, has multiple functions.

There are two distinct sources that supply blood to the liver:

 oxygenated blood flows in from the hepatic artery

 nutrient-rich blood flows in from the portal vein

The liver holds about one pint (13 percent) of the body’s blood supply at any given moment.

The liver consists of two main lobes, both of which are made up of thousands of lobules. These
lobules are connected to small ducts that connect with larger ducts to ultimately form the hepatic
duct. The hepatic duct transports the bile produced by the liver cells to the gallbladder and
duodenum (the first part of the small intestine).

The liver regulates most chemical levels in the blood and excretes a product called “bile,” which
helps carry away waste products from the liver. All the blood leaving the stomach and intestines
passes through the liver. The liver processes this blood and breaks down the nutrients and drugs
into forms that are easier to use for the rest of the body. More than 500 vital functions have been
identified with the liver. Some of the more well-known functions include the following:

 Production of bile, which helps carry away waste and break down fats in the small
intestine during digestion.
 Production of certain proteins for blood plasma.
 Production of cholesterol and special proteins to help carry fats through the body.
 Conversion of excess glucose into glycogen for storage. (This glycogen can later be
converted back to glucose for energy.)
  Regulation of blood levels of amino acids, which form the building blocks of proteins.
 Processing of hemoglobin for use of its iron content. (The liver stores iron.)
 Conversion of poisonous ammonia to urea. (Urea is one of the end products of protein
metabolism that is excreted in the urine.)
 Clearing the blood of drugs and other poisonous substances.
 Regulating blood clotting.
 Resisting infections by producing immune factors and removing bacteria from the blood
stream.

When the liver has broken down harmful substances, its by-products are excreted into the bile or
blood. Bile by-products enter the intestine and ultimately leave the body in the feces. Blood by-
products are filtered out by the kidneys, and leave the body in the form of urine.

III.ETIOLOGY / CAUSES

Alcoholic liver disease

For many people, cirrhosis of the liver is synonymous with chronic alcoholism, but in fact,
alcoholism is only one of the causes. Alcoholic cirrhosis usually develops after more than a
decade of heave drinking. The amount of alcohol that can injure the liver varies greatly from
person to person. In women, as few as two to three drinks per day have been linked with
cirrhosis and in men, as few as three to four drinks per day. Alcohol seems to injure the liver by
blocking the normal metabolism of protein, fats, and carbohydrates.

Chronic hepatitis C

The hepatitis C virus ranks with alcohol as a major cause of chronic liver disease and cirrhosis in
the US. Infection with this virus causes inflammation of and low grade damage to the liver that
over several decades can lead to cirrhosis.

Chronic hepatitis B and D

The hepatitis B virus is probably the most common cause of cirrhosis worldwide, but less
common in the US and other western countries. Hepatitis B, like hepatitis C, causes liver
inflammation and injury that over several decades can lead to cirrhosis. Hepatitis D is another
virus that infects the liver, but only in people who already have hepatitis B.

Autoimmune hepatitis

This disease appears to be caused by the immune system attacking the liver and causing
inflammation, damage, and eventually scarring and cirrhosis.

Inherited Disease

Alpha-1 antitrypsin deficiency, hemochromatosis, Wilson disease, galactosemia, and glycogen

storage diseases are among the inherited diseases that interfere with the way the liver produces,
processes, and stores enzymes, proteins, metals, and other substances the body needs to function
properly.

Nonalcoholic steatohepatitis (NASH)

In NASH, fat builds up in the liver and eventually causes scar tissue. This type of hepatitis
appears to be associated with diabetes, protein malnutrition, obesity, coronary artery disease, and
treatment with corticosteroid medications.

Blocked bile ducts

When the ducts that carry bile out of the liver are blocked, bile backs up and damages liver
tissue. In babies, blocked bile ducts are most commonly caused by biliary atresia, a diseases in
which the bile ducts are absent or injured. In adults, the most common cause is primary biliary
cirrhosis, a disease in which the ducts become inflamed, blocked, and scarred. Secondary biliary
cirrhosis can happen after gall bladder surgery if the ducts are inadvertently tied off or injured.

IV. Signs and Symptoms

Early Signs

 Weakness, fatigue
 Anorexia
 Stomatitis
 Urine – tea color
 Stool – clay color
 Amenorrhea
 Decrease sexual urge
 Loss of puic hair, axilla hair
 Hepatomegaly
 Jaundice
 Pruritus or urticaria

Late Signs

 Hematological changes – all blood cells decrease

o Leukopenia – decrease
o Thrombocytopenia – decrease
o Anemia – decrease

 Endocrine changes
o Spider angiomas, Gynecomastia
o Caput medusa, Palmar errythema
 GIT changes
o Ascitis, bleeding esophageal varices – due to portal Hypertension
  Neurological Changes

V. Complications

1. Portal Hypertension

In cirrhosis, liver cell damage slows down blood flow. This causes a backup of blood through the
portal vein, a condition called portal hypertension. The effects of portal hypertension can be
widespread and serious, including fluid buildup and bleeding.

2. Ascites and Fluid Buildup

Ascites is fluid buildup in the abdomen. It is uncomfortable and can reduce breathing function
and urination. Ascites is usually caused by portal hypertension, but it can result from other
conditions. Swelling can also occur in the arms and legs and in the spleen. Although ascites itself
is not fatal, it is a marker for severe progression. Once ascites occurs, only half of patients
survive after 2 years. In fact, some experts refer to the phases of cirrhosis as preascitic and
ascitic . Some doctors even believe that ascites signals the need for liver transplantation,
particularly in alcoholic cirrhosis.

3. Variceal Bleeding

One of the most serious repercussions of portal hypertension is the development of varices ,
which are blood vessels that enlarge to provide an alternative pathway for blood diverted from
the liver. In about two-thirds of patients they form in esophagus. Varices pose a high risk for
rupture and bleeding because of the following characteristics:

 They are thin-walled.

 They are often twisted.
 They are subject to high pressure.
 Internal bleeding from these varices (variceal bleeding) occurs in 20 – 30% of patients
with cirrhosis. The risk of death from a single episode can reach 70%.

Bleeding commonly recurs within 2 weeks of the first episode, but after 6 weeks, the risk for
recurrence is the same as for patients who have not had a bleeding event.

Factors that predict variceal bleeding include:

 Ascites.
 Encephalopathy.
 Large veins.

Factors that can increase the danger for a bleeding episode in high-risk individuals include the
following:

 Moderate to intense exercise.

  Bacterial infection.
 Certain times of the day. Eating increases portal pressure, and there is a greater risk for
bleeding in the evening. A lesser but still significant risk occurs in the early morning.

It is important for patients to be screened for esophageal varices and treated with preventive beta
blockers if they show signs of risk. Between 30 – 40% of patients with cirrhosis experience
bleeding. this complication has a mortality rate of 20 – 35%. Some experts recommend that all
newly diagnosed patients be screened using endoscopy. Screening should also be considered for
all previously diagnosed patients who have not been screened but would benefit from preventive
treatments.

4. Kidney Failure

Portal hypertension can cause several secondary complications, including kidney failure. Non-
steroidal anti-inflammatory drugs (NSAIDs), such as naproxen, may increase the risk for kidney
failure.

5. Gastrointestinal Bleeding

Gastrointestinal (GI) bleeding can occur from abnormal blood clotting, which can be result of a
combination of complications associated with cirrhosis. They include vitamin K deficiencies and
thrombocytopenia — a drop in platelets (the blood cells that normally initiate the clotting
process). Some research now suggests that thrombocytopenia itself may be associated with more
advanced liver failure.

6. Infections

Bacterial infections are very common in advanced cirrhosis, and may even increase the risk for
bleeding. Most bacterial infections, including those in the urinary, respiratory, or gastrointestinal
tracts, develop when patients are in the hospital. Abdominal infections are a particular problem
in cirrhosis and occur in up to 25% of patients with cirrhosis within a year of diagnosis.

7. Mental Impairment and Encephalopathy

Mental impairment is a common event in advanced cirrhosis. In severe cases, the disease causes
encephalopathy (damage to the brain), with mental symptoms that range from confusion to coma
and death. A combination of conditions associated with cirrhosis causes this serious
complication:

 Buildup in the blood of harmful intestinal toxins, particularly ammonia.

 An imbalance of amino acids that affect the central nervous system.

Encephalopathy is often triggered by certain conditions, including:

  Gastrointestinal bleeding
 Constipation
 Excessive dietary protein
 Infection
 Surgery
 Dehydration

Alcoholics with cirrhosis are believed to be at higher risk for this complication than are
nonalcoholic cirrhosis, but one study suggested that alcoholics simply tend to have more severe
cirrhosis. Even minimal hepatic encephalopathy (MHE) can have detrimental effects on
functional ability. One study suggested that MHE impairs the ability to safely drive a car, and
that all patients with cirrhosis be tested for MHE.

8. Symptoms of Encephalopathy.

Early symptoms of hepatic encephalopathy include forgetfulness, unresponsiveness, and trouble

concentrating. Sudden changes in the patient’s mental state, including agitation or confusion,
may indicate an emergency condition. Other symptoms include bad fruity-smelling breath and
tremor. Late stage symptoms of encephalopathy are stupor and eventually coma.

9. Hepatorenal Syndrome

Hepatorenal syndrome occurs if the kidneys drastically reduce their own blood flow in response
to the altered blood flow in the liver. It is a life-threatening complication of late-stage liver
disease that occurs in patients with ascites. Symptoms include dark colored urine and a reduction
in volume, yellowish skin, abdominal swelling, mental changes (delirium, confusion), jerking or
coarse muscle movement, nausea, and vomiting.

10. Liver Cancer

Cirrhosis greatly increases the risk for liver cancer, regardless of the cause of cirrhosis. Although
few studies have been conducted on the risk for liver cancer in patients with primary biliary
cirrhosis, one study reported an incidence of 2.3%. About 4% of patients with cirrhosis caused
by hepatitis C develop liver cancer. In Asia about 15% of people who have chronic hepatitis B
develop liver cancer, but this high rate is not seen in other parts of the world. (One Italian study
that followed a group of hepatitis B patients for 11 years found no liver cancer over that period
of time.)

11. Osteoporosis

About 30% of patients with chronic liver disease develop osteoporosis (loss of bone density),
which is twice the usual incidence. Patients with primary biliary cirrhosis have a particularly
high risk for osteoporosis. Treating osteoporosis in patients with cirrhosis can be complicated.
One study found that calcitriol (a form of vitamin D) is especially helpful in preventing bone loss
in patients with cirrhosis.

12. Insulin Resistance

Nearly all patients with cirrhosis are insulin resistant. Insulin resistance is a primary feature in
type 2 diabetes and occurs when the body is unable to use insulin. This hormone is important for
delivering blood sugar and amino acids into cells and helps determine whether these nutrients
will be burned for energy or stored for future use.

VI. Pathophysiology

VII. Diagnostic Tests

 Liver biopsy – detects destruction and fibrosis of hepatic tissue.

 Liver scan – shows abdominal thickening and a liver mass.
 CT scan – determines the size of the liver and its irregular nodular surface.
 Esophagoscopy – to determine esophageal varices.
 Paracentesis – to examine ascetic fluid for cell, protein, and bacterial counts.
 PTC – differentiates extrahepatic from intrahepatic obstructive jaundice.
 Laparoscopy and liver biopsy – permit direct visualization of the liver.
  Serum liver function test – results are elevated

VIII. Medical Management

 Provide asymptomatic relief measures such as pain medications and antiemetics.

 Diuretic therapy, frequently with spironolactone, a potassium-sparing diuretic that
inhibits the action of aldosteroe on the kidneys.
 I.V albumin to maintain osmotic pressure and reduce ascites.
 Administration of lactulose or neomycin through a nasogastric tube or retention enema to
reduce ammonia levels during periods of hepatic encephalopathy.

IX. Surgical Interventions

 Transjugular intrahepatic portosystemic shunt may be performed in patients whose

ascites prove resistant. This percutaneous procedure creates a shunt from the portal to
systemic circulation to reduce portal pressure and relieve ascites.
 Orthotropic liver transplantation may be necessary.

X. Nursing Interventions

Promoting Activity Tolerance:

 Encourage alternating periods of rest and ambulation.

 Maintain some periods of bed rest with legs elevated to mobilize edema and ascites.
 Encourage and assist with gradually increasing periods of exercise.

Improving Nutritional Status:

 Encourage patient to eat high calorie, moderate protein meal and to have supplementary
feedings.
 Suggest small, frequent feedings and attractive meals in an aesthetically pleasing setting
at meal time.
 Encourage and assist withgradually increasing periods of exercise.

Protecting Skin Integrity:

 Note and record degree of jaundice of skin and sclerae and scratches on the body.
 Encourage frequent skin care, bathing without soap, and massage with emollient lotions.
 Advise patient to keep fingernails short.

Patient Education and Health Maintenance:

 Stress the necessity of giving up alcohol completely.

 Urge acceptance of assistance from a substance abuse program.
 Provide written dietary instructions.
  Encourage daily weighing for self-monitoring of fluid retention depletion.
 Discuss adverse effects of diuretic therapy.
 Emphasize the importance of rest, a sensible lifestyle, and an adequate, well-balanced
diet.
 Involve the person closest to the patient because recovery usually is not easy and relapses
are common.
 Stress the importance of continued follow –up for laboratory test and evaluation by a
health care provider.

XI. Nursing Care Plan

Assessment Diagnosis Inference Planning Intervention Rationale Evaluation

SUBJECTIVE: Fluid volume Cirrhosis of the *After 8 hours INDEPENDENT: After 8 hours of
“Napansin ko na excess liver is a chronic of nursing nursing
lumalaki ang tiyan ko” related to disease that causes interventions, interventions, the
(I feel that my tummy compromise cell destruction the patient will *Measure intake *Reflects patient was able
is getting bigger) d regulatory and fibrosis demonstrate and output, weigh circulating volume to demonstrate
As verbalized by the mechanism. (scarring) of stabilized fluid daily, and note status. Positive stabilized fluid
patient. hepatic tissue. volume and weight gain more balance/ weight volume and
Fibrosis alters decreased than 0.5 kg/day. gain often reflects decreased edema.
OBJECTIVE: normal liver edema. continuing fluid
 Anasarca structure and retention.
 Weight gain vasculature,
 Altered
electrolyte
impairing blood
and lymph flow *Assess respiratory *Indicative of
status, noting pulmonary
levels and resulting in
increased respiratory congestion.
 Oliguria hepatic
insufficiency and rate, dyspnea.
V/S taken as follows: hypertension in the
T: 37.3 portal vein.
*Monitor blood *Blood pressure
P: 89 Complications elevation usually
include pressure.
R: 20 associated with
BP: 120/80 hyponatremia, fluid volume excess
water retention, but may not occur
bleeding because of fluid
esophageal shifts out of the
varices. vascular space.
Coagulopathy,
spontaneous
bacterial
*Auscultate lungs, *Increasing
peritonitis, and pulmonary
hepatic noting diminished/ congestion may
encephalopathy absent breath sounds result in
. and developing consolidation,
adventitious sounds. impaired gas
exchange, and
complications.
*Assess degree of
peripheral/ *Fluid shift into
dependent edema. tissues as a result of
sodium and water
retention, decreased
albumin, and
increased anti
 diuretic hormone
(ADH).

*Measure *Reflects
abdominal girth.
accumulation of
fluid (ascites)
resulting from loss
of plasma proteins
or fluid into
peritoneal space.

*Encourage bed rest *May promote

when ascites is recumbency-
present. induced diuresis.

COLABORATIVE:

*Administer *To control edema

and ascites.
medications as
indicated. Such as
diuretics.

*Monitor *To correct further

electrolytes.
imbalances.
 WESLEYAN UNIVERSITY PHILIPPINES
CABANATUAN CITY
COLLEGE OF NURSING

CASE STUDY OF
LIVER CIRRHOSIS

SUBMITTED BY:
JOEY R. GREGORIO
SUBMITTED TO:
GENELYN GRACE G. CORONEL, RN