I.

INTRODUCTION Present History Leonida Malto, a 67 year-old mother of four, was admitted at BRTTH last July 1, 2011 at the Gastro Unit of Medical Ward. She currently resides at Guinobatan, Albay together with the family of his third son, and occupies herself as a street vendor to help the family financially. The written medical diagnosis is T/C Liver Cirrhosis, decompensated, not in PSE. On my interview, his son claims that the mother is a non-drinker and a non-smoker; but declares that she used to have her regular diet with high sodium content. This might have been the predisposing factor to her current diagnosis. Their low financial stability concludes the fact that they cannot afford to have a balanced-diet, or nutritious meal, everyday. She, being a vendor at day and a care-taker of her grandchildren at night, may also be the reason why she failed to have achieved a healthier lifestyle. In patients with previously stable cirrhosis, decompensation may occur due to various causes, such as constipation, infection, increased alcohol intake, medication, bleeding from esophageal varices or dehydration. It may take the form of any of the complications of cirrhosis listed above. Patients with decompensated cirrhosis generally require admission to hospital, with close monitoring of the fluid balance, mental status, and emphasis on adequate nutrition and medical treatment - often with diuretics, antibiotics, laxatives and/or enemas, thiamine , and steroids. Administration of saline is generally avoided as it would add to the already high total body sodium content that typically occurs in cirrhosis. 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 patients 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. Development History

Medical History Upon interview, his son stated that her mother had already been admitted at their district hospital with the same diagnosis several weeks ago with complaints of onset symptoms like loss of appetite, weakness, and jaundice. Her mother had stayed for less than a month in the district hospital before they were advised to transfer to BRTTH. Social History On Mrs. Maltos stay at the Medical Ward, her third son, who was also my interviewee, is the one who used to stay with her in the hospital even before she was admitted at BRTTH. At times, her sons wife took care of her alternately.

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 bodys 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 byproducts are filtered out by the kidneys, and leave the body in the form of urine.

III. PATHOPHYSIOLOGY Cirrhosis is characterized by diffuse fibrotic bands of connective tissue that distort the livers 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. The liver plays a vital role in synthesis of proteins (e.g., albumin, clotting factors and complement), detoxification and storage (e.g., vitamin A). In addition, it participates in the metabolism of lipids and carbohydrates. Cirrhosis is often preceded by hepatitis and fatty liver (steatosis), independent of the cause. If the cause is removed at this stage, the changes are still fully reversible. The pathological hallmark of cirrhosis is the development of scar tissue that replaces normal parenchyma, blocking the portal flow of blood through the organ and disturbing normal function. Recent research shows the pivotal role of the stellate cell, a cell type that normally storesvitamin A, in the development of cirrhosis. Damage to the hepatic parenchyma leads to activation of the stellate cell, which becomes contractile (called myofibroblast) and obstructs blood flow in the circulation. In addition, it secretes TGF-1, which leads to a fibrotic response and proliferation of connective tissue. Furthermore, it secretes TIMP 1 and 2, naturally occurring inhibitors of matrix metalloproteinases, which prevents them from breaking down fibrotic material in the extracellular matrix.

The fibrous tissue bands (septa) separate hepatocyte nodules, which eventually replace the entire liver architecture, leading to decreased blood flow throughout. The spleen becomes congested, which leads to hypersplenism and increased sequestration of platelets. Portal hypertension is responsible for most severe complications of cirrhosis.

IV. DIAGNOSTIC EVALUATIONS/LABORATORY EXAMS

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.

The following findings are typical in cirrhosis:

Aminotransferases - AST and ALT are moderately elevated, with AST > ALT. However, normal aminotransferases do not preclude cirrhosis. Alkaline phosphatase - usually slightly elevated. Gamma-glutamyl transferase correlates with AP levels. Typically much higher in chronic liver disease from alcohol. Bilirubin - may elevate as cirrhosis progresses. Albumin - levels fall as the synthetic function of the liver declines with worsening cirrhosis since albumin is exclusively synthesized in the liver Prothrombin time - increases since the liver synthesizes clotting factors. Globulins - increased due to shunting of bacterial antigens away from the liver to lymphoid tissue. Serum sodium - hyponatremia due to inability to excrete free water resulting from high levels of ADH and aldosterone. Thrombocytopenia - due to both congestive splenomegaly as well as decreased thrombopoietin from the liver. However, this rarely results in platelet count < 50,000/mL. Leukopenia and neutropenia - due to splenomegaly with splenic margination. Coagulation defects - the liver produces most of the coagulation factors and thus coagulopathy correlates with worsening liver disease.

There is now a validated and patented combination of 6 of these markers as non-invasive biomarker of fibrosis (and so of cirrhosis):FibroTest. Other laboratory studies performed in newly diagnosed cirrhosis may include:

Serology for hepatitis viruses, autoantibodies (ANA, anti-smooth muscle, anti-mitochondria, anti-LKM) Ferritin and transferrin saturation (markers overload), copper and ceruloplasmin (markers of copper overload) of iron

Immunoglobulin levels (IgG, IgM, IgA) - these are non-specific but may assist in distinguishing various causes Cholesterol and glucose Alpha 1-antitrypsin

V. MEDICAL AND EVALUATION TREATMENT

VI. DRUG STUDY Antiviral Medications: Ribavirin for treatment of chronic hepatitis C in adult patients Lamivudine for treatment of patients with chronic hepatitis B and evidence of hepatitis B virus replication Entecavir (Baraclude) for treatment of chronic hepatitis B virus infection in adults with evidence of active liver inflammation Telbivudine (Sebivo) for treatment of chronic hepatitis B with evidence of viral replication and active viral disease Chronic viral hepatitis B and C may respond to treatment with antiviral medications. These may include interferon (for hepatitis B and C) or a combination of interferon and ribavirin (hepatitis C). For hepatitis C, combination therapy consistently yields higher rates of sustained response than treatment with just one drug. At present, use of interferon alone is generally reserved for people who should not use ribavirin. Interferon is given subcutaneously (injected beneath the skin) once every week. Treatment of hepatitis C usually lasts for 24-48 weeks depending on the HCV genotype. Ribavirin is an oral antiviral agent that is given twice a day. Lamivudine, adnovir, entecavir, telbivudine is used to treat hepatitis B infection. It is usually provided in an oral form that is taken once a day for a year or more. Sometimes these drugs are combined with interferon. Possible side effects associated with antiviral use include:

Abdominal or stomach pain (severe) Feeling of fullness Nausea Tingling, burning, numbness, or pain in the hands, arms, feet, or legs Flu-like symptoms (fever, body aches, chills) Anti-inflammatory Medications (Corticosteroids) Azathioprine (Imuran) to reduce the corticosteroid requirements of renal transplant recipients, treatment of auto-immune chronic active hepatitis

Metal Chelating Agent Deferoxamine (Desferal) treatment for aldosterone overload for patients with ESRF (under maintenance with dialysis encephalopathy) Vitamin K Phytonadione (AquaMEPHYTON, Mephyton) Bleeding abnormalities are common in cirrhosis. Vitamin K plays an important role in blood clotting. Because your liver metabolizes this vitamin, liver diseases can affect vitamin K levels and its ability to function, and thereby alter clotting ability. Possible side effects associated with vitamin K use include:

Flushing of the face Redness, pain, or swelling at the site of injection Unusual taste Diuretics *Loop diuretics: Bumetanide (Bumex) Furosemide (Lasix) *Thiazide diuretics: Hydrochlorothiazide (HydroDIURIL, Esidrix) Chlorothiazide (Diuril) *Potassium-sparing diuretics: Amiloride (Midamor) Triamterene (Dyrenium) Diuretics are used to treat the buildup of excess fluid in the body that occurs with cirrhosis (as well as other diseases). These drugs act on the kidneys to increase urine output, which reduces the amount of fluid in the bloodstream. This can help reduce portal vein hypertension and help alleviate some of the symptoms of cirrhosis, such as fluid accumulation in the abdomen and legs. Possible side effects associated with diuretic use include:

Loss of appetite Nausea and vomiting Dizziness Headache Lethargy Low or high blood potassium level Low sodium level Bleeding from Varices Octreotide (Sandostatin, Sandostatin LAR) This drug is often used with endoscopic treatment to treat bleeding from esophageal varices. It reduces the pressure in the varices. Once started, it is continued five days after bleeding. Possible side effects associated with the use of this drug include:

Abdominal cramps Nausea Vomiting

Diarrhea Constipation Slow heart rate Hypothyroidism Greasy stools Upset stomach Antihypertensives (Beta-Blockers) Atenolol (Tenormin) Metoprolol (Lopressor) Nadolol (Corgard) Propranolol (Inderal) Timolol (Blocadren) In cirrhosis, these are used to reduce venous blood pressure in the abdomen (called portal hypertension) and thereby reduce the risk of esophageal variceal bleeding and other complications. These drugs come in capsule, tablet, liquid, and injectable forms. Possible side effects associated with beta-blocker use include:

Drowsiness and dizziness Cold sensitivity Sleep disorders Laxatives Beta-galactosidofructose (Lactulose) Although laxatives are usually prescribed to treat constipation, they can help treat cirrhosis by absorbing or binding toxins, such as ammonia, in the intestine and remove them from the body. Not all laxatives are equally effective, and your doctor may be more likely to prescribe betagalactosidofructose (Lactulose). Possible side effects associated with laxative use include:

Diarrhea Abdominal cramping, flatulence, and bloating Dehydration and weakness Multivitamin/Mineral Supplements Centrum This may be recommended to help correct any nutrient deficiencies may have developed if dietary intake was reduced because of liver disease. It will also promote healing of damaged liver tissue.

VII. NURSING CARE MANAGEMENT Ongoing Assessment 1. Measure I&O, noting positive balanceintake in excess of output. Weigh daily and note gain more than 0.5 kg/day. 2. Monitor BP and CVP, if available. Note JVD and abdominal vein distention.

3. Assess respiratory status, noting increased respiratory rate and dyspnea. 4. Auscultate lungs, noting diminished or absent breath sounds and developing adventitious soundscrackles. 5. Monitor for cardiac dysrhythmias. 6. Assess degree of peripheral and dependent edema. 7. Measure abdominal girth. 8. Encourage bedrest when ascites is present. 9. Monitor serum albumin and electrolytes, particularly potassium and sodium. Diet 1. Provide frequent mouth care and occasional ice chips, particularly if NPO; schedule fluid intake around the clock. 2. Advice to have Soft diet as ordered, taking egg whites in particular. Possible Complications 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 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. Nonsteroidal 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 in concentrating. Sudden changes in the patients 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 byhepatitis 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. Osteoporosis is a condition characterized by progressive loss of bone density, thinning of bone tissue, and increased vulnerability to fractures. Osteoporosis may result from disease, dietary or hormonal deficiency, or advanced age. Regular exercise and vitamin and mineral supplements may reduce and even reverse loss of bone density. 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.

VIII. NCP DISCHARGE PLAN Medications Client was advised to take medications regularly at home. Also, not altering the dosage and schedule of medications was highly emphasized. Having a regular check-up was also encouraged. Exercise In order to promote activity tolerance, Mrs. Malto was encouraged to do alternating periods of rest and ambulation. Maintaining some periods of bed rest with legs elevated to mobilize edema and ascites, and, was encouraged to be assisted with gradually increasing periods of exercise. Health education To better protect the skin integrity of the client, I advised his son to note and record the degree of jaundice of skin and sclera and the scratches on her body as well. Also, having frequent skin care, bathing without soap, and to keep fingernails short were also emphasized. In connection with her health maintenance, his son was asked to provide written dietary instructions; to encourage her daily weighing for self-monitoring of fluid retention depletion; discussed the adverse effects of diuretic therapy; emphasized the importance of rest, a sensible lifestyle, and an adequate, well-balanced diet; to be involved to the person closest to the patient because recovery usually is not easy and relapses are common; and lastly, gave importance of having continued follow up for laboratory test and evaluation by a health care provider.

Diet To improving nutritional status of the client, patient was encouraged to eat high calorie, moderate protein meal and to have supplementary feedings. Taking small, frequent feedings and attractive meals in an aesthetically pleasing setting at meal time was also suggested.

IX. REFERENCES Brunner and Suddarth. Textbook of Medical-Surgical Nursing 12th Edition. Cales P, Masliah C, Bernard B, Garnier PP et al. Early Administration of Vapreotide for variceal Bleeding in Patients with Cirrhosis. New E J Med. 2001;344:23-28 . Heidelbaugh JJ, Bruderly M: Cirrhosis and Chronic Liver Failure. Part I. Diabnosis and Evaluation. Am Fam Phy. 2006;74:756-62. Minio AM, Heron MP, Murphy SL, Kochanek KD. Deaths: Final data for 2004. Centers for Disease Control and Prevention Web site National Digestive Diseases Information Clearinghouse http://www.digestive.niddk.nih.gov http://www.google.com http://www.nurseslab.com http://www.cdc.gov/nchs/data/nvsr/nvsr55/nvsr55_19.pdf http://www.liverfoundation.org/ . Accessed March 8, 2006.

BICOL UNIVERSITY COLLEGE OF NURSING LEGAZPI CITY

CASE STUDY: LIVER CIRRHOSIS

Prepared By: PAULINE G. BALUIS BSN 3 B

Submitted To: RICHARD L. BARTOLATA, RN, MAEd, MN