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 – decreaseo Thrombocytopenia – decreaseo Anemia – decrease

Endocrine changes o Spider angiomas, Gynecomastiao 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 EvaluationSUBJECTIVE:“Napansin ko na lumalaki ang tiyan ko” (I feel that my tummy is getting bigger)As verbalized by the patient.

OBJECTIVE: Anasarca Weight

gain Altered

electrolyte levels

Oliguria

V/S taken as follows:T: 37.3P: 89R: 20BP: 120/80

Fluid volume excess related to compromised regulatory mechanism.

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.

*After 8 hours of nursing interventions, the patient will demonstrate stabilized fluid volume and decreased edema.

INDEPENDENT:

*Measure intake and output, weigh daily, and note weight gain more than 0.5 kg/day.

*Assess respiratory status, noting increased respiratory rate, dyspnea.

*Monitor blood pressure.

*Auscultate lungs, noting diminished/ absent breath sounds and developing adventitious sounds.

*Reflects circulating volume status. Positive balance/ weight gain often reflects continuing fluid retention.

*Indicative of pulmonary congestion.

*Blood pressure elevation usually associated with fluid volume excess but may not occur because of fluid shifts out of the vascular space.

*Increasing pulmonary congestion may result in consolidation, impaired gas exchange, and complications.

After 8 hours of nursing interventions, the patient was able to demonstrate stabilized fluid volume and decreased edema.

*Assess degree of peripheral/ dependent edema.

*Measure abdominal girth.

*Encourage bed rest when ascites is present.

COLABORATIVE:

*Administer medications as indicated. Such as diuretics.

*Monitor electrolytes.

*Fluid shift into tissues as a result of sodium and water retention, decreased albumin, and increased anti diuretic hormone (ADH).

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

*May promote recumbency-induced diuresis.

*To control edema and ascites.

*To correct further 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