Cirrhosis essay

I. Abstract

            Hepatic dysfunction results from damage to the liver’s parenchymal cells, either directly from primary liver diseases or indirectly from obstruction of bile flow or derangements of hepatic circulation. Liver dysfunction may be acute or chronic; chronic dysfunction is far more common that acute.

            Chronic liver disease, including cirrhosis, is the seventh most common cause of death in the United States among young and middle-aged adults. More than 40% of those deaths are associated with alcohol. The rate of chronic liver disease for men is twice that from women, and chronic liver disease is more common among African Americans than Caucasians.

            Disease processes that lead to hepatocellular dysfunction may be caused by infectious agents such as bacteria and viruses and by anoxia, metabolic disorders, toxins and medications, nutritional deficiencies, and hypersensitivity states. The most common cause of parenchymal damage is malnutrition, especially that related to alcoholism.

            The parenchymal cells respond to most noxious agents by replacing glycogen with lipids, producing fatty infiltration with or without cell death or necrosis. This is commonly associated with inflammatory cell infiltration and growth of fibrous tissue. Cell regeneration can occur if the disease process is the shrunken, fibrotic liver seen in cirrhosis.

            The consequences of liver disease are numerous and varied. Their ultimate effects are often incapacitating or life-threatening, and their presence is ominous. Treatment often is difficult. Among the most common and significant symptoms of liver disease are the following:

·         Jaundice, resulting from increased bilirubin concentration in the blood.

·         Portal hypertension, ascites, and varices, resulting from circulatory changes within the diseased liver and producing severe GI hemorrhages and marked sodium and fluid retention.

·         Butritional deficiencies, which result from the inability of the damaged liver cells to metabolize certain vitamins; responsible for impaired functioning of the central and peripheral nervous systems and for abnormal bleeding tendencies.

·         Hepatic encephalopathy or coma, reflecting accumulation of ammonia in the serum due to impaired protein metabolism by the diseased liver.

            This paper intents to study the

II. Introduction

            Cirrhosis is a disease of the liver in which that organ is extensively damaged and scarred. The vital functions of the liver are partially lost, and circulation of blood through the liver is often obstructed by extensive scarring (Angulo, 2002). The obstructed vessels can become overfilled with blood and rupture, often causing fatal hemorrhages.

            Cirrhosis can be due to chronic alcoholism, infectious hepatitis, diseases of the circulatory system, malnutrition, or other conditions. Patients can be aided considerably by treatment with specific diets, vitamins, and drugs. Sometimes surgery can be aided considerably by treatment with specific diets, vitamins, and drugs. Sometimes surgery is performed to relieve the high pressure in the performed to relieve the high pressure in the obstructed branches of the circulatory system. In extreme cases, liver transplants may be performed.

III. Hepatic Cirrhosis

A. Overview

            Cirrhosis is a chronic disease characterized by replacement of normal liver tissue with diffuse fibrosis that disrupts the structure and function of the liver (Blow, F.C., Walton, M.A., Barry, K.L., et al., 2000). There are three types of cirrhosis or scarring of the liver:

·         Alcoholic cirrhosis, in which the scar issue characteristically surrounds the portal areas. This is most frequently due to chronic alcoholism and is the most common type of cirrhosis.

·         Postnecrotic cirrhosis, in which there are broad bands of scar tissue as a late result of a precious bout of acute viral hepatitis.

·         Biliary cirrhosis, in which scarring occurs in the liver around the bile ducts. This type usually is the result of chronic biliary obstruction and infection (cholangitis);   it is much less common than the other two types.

            The portion of the liver chiefly involved in cirrhosis consists of the portal and the periportal spaces, where the bile canaliculi of each lobule communicate to form the liver bile ducts. These areas become the sites of inflammation, and the bile ducts become occluded with inspissated (thickened) bile and pus. The liver attempts to form new bile channels; hence, there is an over-growth of tissue made up largely of disconnected, newly formed bile ducts and surrounded by scar tissue.

            Clinical manifestations include intermittent jaundice and fever. Initially the liver is enlarged, hard, and irregular, but eventually it atrophies.

B. Pathophysiology

            Although several factors have been implicated in the etiology of cirrhosis, alcohol consumption is considered the major causative factor. Cirrhosis occurs with greatest frequency among alcoholics. Although nutritional deficiency with reduced protein intake contributes to liver destruction in cirrhosis, excessive alcohol intake is the major causative factor in fatty liver and its consequences. Cirrhosis, however, has also occurred in people who do not consume alcohol and in those who consume a normal diet and have a high alcohol intake (Orozco, H., & Mercado, M.A., 2000).

            Some people appear to be more susceptible than others to this disease, whether or not they are alcoholics or malnourished. Other factors may play a role, including exposure to certain chemicals (carbon tetrachloride, chlorinated naphthalene, arsenic, or phosphorus) or infectious schistosomisasis. Twice as many men as women are affected, although women are at greater risk of developing alcohol-induced liver disease for a yet undiscovered reason. Most patients are between 40 and 60 years of age. Each year more than 25,000 people die of chronic liver diseases and cirrhosis in the United States (Bravo, A.A., Sheth, S.G., & Chopra, S., 2001).

            Alcoholic cirrhosis is characterized by episodes of necrosis involving the liver cells, sometimes occurring repeatedly throughout the course of the disease. The destroyed liver cells are replaced gradually by scar tissue; eventually the amount of scar tissue exceeds that of the functioning liver tissue. Islands of residual normal tissue and regenerating liver tissue may project from the constricted areas, giving the cirrhotic liver its characteristic hobnail appearance. The disease usually has an insidious onset and a protracted course, occasionally proceeding over a period of 30 or more years.

            The prognosis of different forms of cirrhosis caused by various liver diseases has been investigated in several studies. Of the many prognostic indicators, the Child’s classification seems most useful in predicting the outcome of patients with liver disease. It is also used in choosing management approaches.

C. Clinical Manifestations

            Signs and symptoms of cirrhosis increase in severity as the disease progresses. The severity of the manifestations helps to categorize the disorder into two main presentations.

            Compensated cirrhosis, with its less severe, often vague symptoms, may be discovered secondarily at a routine physical examination. The hallmarks of decompensated cirrhosis result from failure of the liver to synthesize proteins, clotting factors, and other substances and manifestations of portal hypertension (Chikritzhs, T.N., Jonas, H.A. Stockwell, T.R. et al., 2001).

v  Liver Enlargement

            Early in the course of cirrhosis, the liver tends to be large and its cells loaded with fat. The liver is firm and has a sharp edge noticeable on palpation. Abdominal pain may be present because of recent, rapid enlargement of the liver, producing tension on the fibrous covering of the liver (Glisson’s capsule). Later in the disease, the liver decreases in size as scar tissue contracts the liver tissue. The liver edge, if palpable, is nodular (Chikritzhs, T.N., Jonas, H.A. Stockwell, T.R. et al., 2001).

v  Portal Obstruction and Ascites

            These late manifestations are due partly to chronic failure of liver function and partly to obstruction of the portal circulation. Practically, all the blood from the digestive organ is collected in the portal veins and carried to the liver. Because a cirrhotic liver does not allow the blood free passage, it backs up into the spleen and the GI tract and these organs become the seat of chronic passive congestion; that is, they are stagnant with blood and thus cannot function properly. Indigestion and altered bowel function result. Fluid rich in may accumulate in the peritoneal cavity, producing ascites. This can be demonstrated through percussion for shifting dullness or a fluid wave (Garcia, N., Jr.  & Sanyal, A. J., 2001).

v  Infection and Peritonitis

            Bacterial peritonitis may develop in cirrhotic patients with ascites in the abscess. This condition is referred to as spontaneous bacterial peritonitis. Bacteremia is believed to be the most likely route of infection. Clinical signs may be absent; paracentesis may be necessary for diagnosis. Antibiotic therapy is effective in the treatment and prevention of recurrent episodes of spontaneous bacterial peritonitis (Garcia, N., Jr.  & Sanyal, A. J., 2001).

v  Gastrointestinal Varices

             The obstruction to blood flow through the liver resulting from the fibrotic changes also results in the formation of collateral blood vessels in the GI system and shunting of blood from the portal vessels into blood vessels with lower pressures. As a result, the patient with cirrhosis often has prominent, distended abdominal blood vessels, which are visible on abdominal inspection (caput medusae), and distended blood vessels throughout the GI tract. The esophagus, stomach, and lower rectum are common sites of collateral blood vessels. These intended blood vessels form varices or hemorrhoids, depending on their location (Jonsen, P.L., 2002).

            Because these vessels were not intended to carry the high pressure and volume of blood imposed by cirrhosis, they may rupture and volume of blood imposed by cirrhosis, they may rupture and bleed. Therefore, assessment must include observation for occult and frank bleeding from the GI tract. Approximately 25% of patients develop minor hematemesis; others have profuse hemorrhage fro gastric and esophageal varices (Hussain, H., Lapin, S., & Cappell, M.S., 2000).

v  Edema

            Another late symptom of cirrhosis is edema, which is attributed to chronic liver failure. A reduced plasma albumin concentration predisposes the patient to the formation of edema. Edema is generalized but often affects lower extremities, upper extremities, and the presacral area. Facial edema is not typical. Overproduction of aldosterone occurs, causing sodium and water retention and potassium excretion.

v  Vitamin Deficiency and Anemia

            Because of inadequate formation, use, and storage of certain vitamins (notably vitamins A, C, and K), signs deficiency are common, particularly hemorrhagic phenomena associated with vitamin K deficiency. Chronic gastritis and impaired GI function, together with inadequate dietary intake and impaired liver function, account for the anemia often associated with cirrhosis. The anemia and the patient’s poor nutritional status and poor state of health result severe fatigue, which interferes with the ability to carry out routine daily activities (Kaptanoglu, L., & Blei, A.T., 2000).

v  Mental Deterioration

            Additional clinical manifestations include deterioration of mental function with impending hepatic encephalopathy and hepatic coma. Neurologic assessment is indicated and includes the patient’s general behavior, cognitive abilities, orientation to time and place, and speech patterns.

IV. Assessment and Diagnostic Findings

A. Overview

            The extent of liver disease and the type of treatment are determined after reviewing the laboratory findings. Because the functions of the liver are complex, there are many diagnostic tests that may provide information about the liver function. The patient needs to know why these tests are being performed and ways to cooperate.

            In severe parenchymal liver dysfunction, the serum albumin level tends to decrease and the serum globulin level rises. Enzyme tests indicate liver cell damage: serum alkaline phosphate, AST, ALT, and GGT levels increase and the serum cholinesterase level may decrease. Bilirubin tests are performed to measure bile excretion or bile retention; elevated levels can occur with cirrhosis and other liver disorders. Prothrombin time is prolonged (Kaptanoglu, L., & Blei, A.T., 2000).

            Ultrasound scanning is used to measure the difference in density of parenchymal cells and scar tissue. CT, MRI, and radioisotope liver scans give information about liver size and hepatic blood flow and obstruction. Diagnosis is confirmed by liver biopsy. Arterial blood gas analysis may reveal a ventilation-perfusion imbalance and hypoxia.

B. Medical Management

            The management of the patient with cirrhosis is usually based on the presenting symptoms. For example, antacids are prescribed to decrease gastric distress and minimize the possibility of GI bleeding. Vitamins and nutritional supplements promote healing of damaged liver cells and improve the general nutritional status. Potassium-sparing diuretics (spironolactone [Aldactone], triamterene [Dyrenium] may be indicated to decrease ascites, if present; these diuretics are preferable to other diuretic agents because they may minimize the fluid and electrolyte changes common with other agents. An adequate diet and avoidance of alcohol are versed; its progression may be halted or slowed by such measures.

            Preliminary studies indicate that colchicines, an anti-inflammatory agent used to treat the symptoms of gout, may increase the length of survival in patients with mild to moderate cirrhosis. Improved survival has been observed in patients with alcoholic cirrhosis. Colchicine is believed to reverse the fibrotic processes in cirrhosis, and this has improved survival (Lake, J.R., 2000).

V. Nursing Process: The patient with Hepatic Cirrhosis

            Nursing assessment focuses on the onset of symptoms and the history of precipitating factors, particularly long-term alcohol abuse, as well as dietary intake and changes in the patient’s physical and mental status. The patient’s past and current patterns of alcohol use (duration and amount) are assessed and documented. It is also important to document any exposure to toxic agents encountered in the workplace or during recreational activites. The nurse documents and reports exposure to potentially hepatotoxic substances (medications, illicit IV/injection drugs, inhalants) or general anesthetic agents.

            The nurse assesses the patient’s mental status through the interview and other interactions with the patient; orientation to person, place, and time is noted. The patient’s ability to carry out a job or household activities provides some information about physical and mental status. The patient’s relationship with family, friends, and coworkers may give some indication about incapacitation secondary to alcohol abuse and cirrhosis. Abdominal distention and bloating, GI bleeding, bruising, and weight changes are noted (Pratt, D. S., & Kaplan, M.M., 2000).

            The nurse assesses nutritional status, which is of major importance in cirrhosis, by daily weights, and monitoring of plasma proteins, transferring, and creatinine levels.

v  Diagnosis

            Nursing Diagnosis

            Based on all the assessment data, the patient’s major nursing diagnosis may include the following:

·                    Activity intolerance related to fatigue, general debility, muscle chronic, and discomfort.

·                    Imbalanced nutrition, less than body requirements, related to chronic gastritis, decreased GI mobility, and anorexia.

·                    Impaired skin integrity related to compromised immunologic status, edema, and poor nutrition.

·                    Risk for injury and bleeding related to altered clotting mechanisms.

VI. Planning and Goals

A. Overview

            The goals for the patient may include increased participation in activities, improvement of nutritional status, improvement skin integrity, and decreased potential for injury, improvement of mental status, and absence of complications (Reynolds, T.B., 2000).

B. Nursing Interventions

v  Promoting Rest

            The patient with active liver disease requires rest and other supportive measures to permit the liver to reestablish its functional ability. If the patient is hospitalized, weight and fluid intake and output are measured and recorded daily. The nurse adjusts the patient’s position in bed for maximal respiratory efficiency, which is especially important if ascites is marked because it interferes with adequate thoracic excursion. Oxygen therapy may be required in liver failure to oxygenate the damage cells and prevent further cell destruction (Menon, K.V., & Kamath, P.S., 2000).

            Rest reduces the demands on the liver and increases the liver’s blood supply. Because the patient is susceptible to the hazards of immobility, efforts to prevent respiratory, circulatory, and vascular disturbances are initiated. These measures may help prevent such problems as pneumonia, thrombophlebitis, and pressure ulcers. When nutritional status improves and strength increases, the nurse encourages the patient to increase activity gradually. Activity and mild exercise, as well as rest, are planned (Yu, A.S., & Hu, K.Q., 2001).

v  Improving Nutritional Status

            The patient with cirrhosis who has no ascites or edema and exhibits no signs of impending hepatic coma should receive a nutritious, high-protein diet if tolerated (including vitamins A, C, K and folic acid). Because proper nutrition is so important, the nurse makes every effort to encourage the patient to eat. This is as important as any medication. Often small, frequent meals are tolerated well than three large meals because of the abdominal pressure exerted by ascites. Protein supplements may also be indicated.

            Patient preferences are considered. Patients with prolonged or severe anorexia, or those who are vomiting or eating poorly for any reason, may receive nutrients enterally or parenteral nutrition (Zimmerman, H. J., 2000).

            Patient preferences are considered. Patients with prolonged or severe anorexia, or those who are vomiting or eating poorly for any reason, may receive nutrients enterally or parenteral nutrition.

            Patients with fatty stools (steatorrhea) should receive water-soluble forms of fat-soluble vitamins—A, D, and E (Aquasol A, D and E0. Folic acid and iron are prescribed to prevent anemia. If the patient shows signs of impending or advancing coma, the amount of protein in the diet is decreased temporarily. In the absence of hepatic encephalopathy, a moderate-protein, high-calorie intake is provided, with protein foods of high biologic value. A diet containing 1 to 1.5 g of protein per kilogram of body weight per day is required unless the patient is malnourished. Protein is restricted if encephalopathy develops (Chasalani, N., & Imperiale, T.F., 2001). Incorporating vegetable protein to meet protein needs may decrease the risk of encephalopathy. Sodium restriction is also indicated to prevent ascites.

VII. Conclusion

            It is possible for a person to have a cirrhotic liver but not suffer from any symptoms. This is known as latent cirrhosis. The symptoms caused by active cirrhosis include abdominal pain, liver tenderness, diarrhoea, lack of appetite, ascites (accumulation of fluid in the peritoneal cavity), jaundice, weakness, muscle wasting, and weight loss. Ascites is caused because of the increased pressure in the portal vein and the lack of albumin in the plasma (albumin is normally made by the liver). An individual with cirrhosis often has a characteristic appearance: they have thin arms and legs but a large stomach due to the combination of weight loss and ascites. Jaundice is caused by abnormally high levels of bilirubin in the blood because the liver is not removing it as it normally does. There may be mental changes caused by toxins in the blood passing to the brain without being metabolized by the liver. These symptoms range from confusion, irritability, and childishness, to coma. There is often a fluctuation in these symptoms. The portal hypertension can lead to gastrooesophageal bleeding (bleeding in the gut), which is one of the most severe symptoms and carries a high risk of mortality

            Complete recovery is impossible. However, since the healthy cells may regenerate, it is sometimes possible for some degree of normal liver function to return. Alcohol should be avoided, unless there is firm evidence that the cirrhosis was not caused by alcohol. Because there is no treatment for the irreversible liver damage, only the symptoms can be treated; this normally requires treatment in hospital.

VIII. References:

Angulo, P. (2002). Nonalcoholic fatty liver disease. New England Journal of Medicine, 346 (16), 121-1231.
Blow, F.C., Walton, M.A., Barry, K.L., et al. (2000). The relationship between alcohol problems and health functioning of older adults in primary care settings. Journal of American Geriatrics Society, 48 (7), 856-908.
Bravo, A.A., Sheth, S.G., & Chopra, S. (2001). Liver biopsy. New England Journal of Medicine, 344 (7), 495-500.
Chikritzhs, T.N., Jonas, H.A. Stockwell, T.R. et al.  (2001). Mortality and life years lost due to alcohol: A comparison of acute and chronic causes. Medical Journal of Australia, 174 (6), 281-284.
Garcia, N., Jr.  & Sanyal, A. J. (2001). Portal Hypertension. Clinics in Liver Disease, 5 (2), 509-540.
Hussain, H., Lapin, S., & Cappell, M.S. (2000). Clinical scoring systems for determining the prognosis of gastrointestinal bleeding. Gastroenterology Clinics, 29(2), 711-729.
Kaptanoglu, L., & Blei, A.T. (2000). Current status of liver support systems. Clinics in Liver Disease, 29 (2), 46-59.
Jonsen, P.L. (2002). Liver disease in the elderly. Best Practice and research in Clinical Gastroenterology, 16 (1), 149-158.
Lake, J.R. (2000). The role of transjugular portosystematic shunting in patients with ascites. New England Journal of Medicine, 342 (23), 1745-1747.
Maddrey, W.C. (2000). Alcohol-induced liver disease. Clinics in Liver Disease, 4 (1), 115-131.
Pastorelli, R., Bardozzi, G., Saieva, C., et al. (2001). Genetic determinants of alcohol addiction and metabolism: A survey in Italy. Alcoholism: Clinical and Experimental Research, 25 (2), 221-(227).
Pratt, D. S., & Kaplan, M.M. (2000). Primary care: Evaluation of abnormal liver-enzyme results in asymptomatic patients. New England Journal of medicine, 342 (17), 1266-1271.
Reynolds, T.B. (2000). Ascites. Clinics in Liver Disease, 4(1), 151-168. 132 (60, 460-466.
Yu, A.S., & Hu, K.Q. (2001). Management of ascites. Clinics in Liver Disease, 5 (2), 541-568.
Zimmerman, H. J. (2000). Drug-induced liver disease. Clinics in Liver Disease, 4(1), 73-96.
Chasalani, N., & Imperiale, T.F. (2001). Screening for varices in patients with cirrhosis: Where do we stand? American Journal of gastroenterology, 96(3), 623-624.
Menon, K.V., & Kamath, P.S. (2000). Managing the complications of cirrhosis. Mayo Clinic Proceedings, 75 (5), 501-509.
Orozco, H., & Mercado, M.A. (2000). The evolution of portal hypertension: Lessons from 1,000 operations and 50 years’ experience. Archives of Surgery, 135 (12), 1389-1393.


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