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. 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: y oxygenated blood flows in from the hepatic artery y nutrient-rich blood flows in from the portal vein y 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. PREDISPOSING FACTORS: 1. Chronic Alcoholism 2. Malnutrition decrease Vitamin B, thiamin main cause 3. Virus 4. Toxicity e.g. carbon tetrachloride 5. Use of hepatotoxic agents

SIGNS AND SYMPTOMS: I. Early Signs y Weakness, fatigue y Anorexia y Stomatitis y Urine tea color y Stool clay color y Hepatomegaly y Jaundice y Pruritus or urticaria II. Late Signs A. Hematological changes all blood cells decrease y Leukopenia decrease y Thrombocytopenia decrease y Anemia decrease B. Endocrine changes y Spider angiomas, Gynecomastia y Caput medusa, Palmar errythema C. GIT changes y Ascitis, bleeding esophageal varices due to portal Hypertension D. Neurological Changes PATHOPHYSIOLOGY:

Cirrhosis is characterized by diffuse fibrotic bands of connective tissue that distort the liver s normal architecture. Inflammation caused by either toxins or disease results in extensive degeneration and destruction of hepatocytes ( liver cells ). As cirrhosis develops, the tissue becomes nodular. These nodules can block lile ducts and normal blood flow throughout the liver. Flow alterations in the vascular system and lymphatic bile duct channels result from compression caused by the proliferation of fibrous tissue. In early disease, the liver is usually enlarged, firm and hard. As the pathologic process continues, the liver shrinks in size. COMPLICATIONS: Cirrhosis is the eleventh leading cause of death by disease in the United States, killing more than 25,000 people each year. A damaged liver affects almost every bodily process, including the functions of the digestive, hormonal, and circulatory systems. The most serious complications are those associated with so-called decompensation, which occur when cirrhosis progresses. They include the following:  Bleeding and fluid buildup (ascites).  Infections.  Damage to the brain (encephalopathy). Impaired brain function occurs when the liver cannot detoxify harmful substances. Liver cancer is also a long-term risk with cirrhosis. Cirrhosis is irreversible, but the rate of progression can be very slow, depending on its cause and other factors. Five-year survival rates are about 85% and can be lower or higher depending on severity.    For example, alcoholics with cirrhosis who abstain can have a 5-year or more survival rate of as high as 85%. For those who continue drinking, the chance for living beyond 5 years is no higher than 60%. In patients with hepatitis B or C, the 5-year survival rate after a diagnosis of cirrhosis ranges between 71 85%. About two-thirds of patients with primary biliary cirrhosis never develop symptoms and can have a normal life span. Once symptoms of liver damage, such as jaundice, occur, however, the average survival time declines. In one study of women diagnosed with primary biliary cirrhosis, about 36% developed symptoms over an 11-year period, and 11% either died or required liver transplantation.

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 aspreascitic 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 withcirrhosis. 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 incirrhosis 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 severecirrhosis. 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. DIAGNOSTIC EVALUATION:     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

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

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