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Control cirrhosis complications

Fenimore, George S. RN, MSN; Manno, Martin S. RN, APRN, BC, MSN

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doi: 10.1097/01.CCN.0000304289.63546.7c
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Cirrhosis, a term used to represent an end-stage consequence for a wide variety of chronic liver diseases, is characterized by the development of scar tissue that replaces normal parenchyma. The most common causes of cirrhosis include hepatitis C, alcoholic liver disease, cryptogenic causes, hepatitis B, and a variety of other miscellaneous causes (such as primary biliary cirrhosis or hemochromatosis).

According to the U.S. Centers for Disease Control and Prevention, chronic liver diseases and cirrhosis are the 12th leading causes of death in the United States, representing 1.2% of total deaths. Each year, more than 474,000 people in the United States are discharged from inpatient care with chronic liver disease or cirrhosis, and 27,000 people die yearly.1,2 It affects twice as many men as women, with most patients being between 40 and 60 years of age.

The disease's prognosis varies from patient to patient and depends on the type of cirrhosis, the presence and severity of complications, and compliance with recommended care and treatments, such as maintaining proper nutrition and ceasing alcohol consumption. Therefore, it's important for nurses to be mindful of the breadth of cirrhosis, its etiologies, specific assessments, and treatment options.

Pathophysiology

In cirrhosis, which culminates in hepatic failure, normal liver tissue is damaged and replaced by diffuse fibrosis (tough fibrous scar tissue), which disrupts the structure and normal functions of the liver. The progression of liver injury to cirrhosis may occur over weeks to years. There are four types of cirrhosis, each resulting from a different etiology, namely, Laënnec's (alcoholic cirrhosis), postnecrotic cirrhosis, biliary cirrhosis, and cardiac cirrhosis. (See Types of cirrhosis.)

The pathophysiologic course of cirrhosis involves the portal and periportal spaces that communicate to eventually form the liver bile ducts. These spaces become inflamed and narrowed, resulting in the formation of thickened bile and pus. The liver attempts to compensate by forming new bile channels that cause an overgrowth of tissue, which, along with inflammation, adds to early enlargement of the liver.

In alcoholic and postnecrotic cirrhosis, destroyed hepatocytes (liver cells) are replaced by scar tissue. Eventually, the amount of scar tissue exceeds functional liver tissue, resulting in the clinical manifestations and complications associated with cirrhosis. Liver damage is classified histopathologically, based on grade (extent of inflammatory activity) and stage (extent of fibrosis). The grade or stage and underlying cause of cirrhosis are important considerations in directing appropriate treatment. (See Cirrhosis.)

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Figure

Clinical presentation

Clinical manifestations of cirrhosis are many and will vary depending on the underlying etiology and the extent of disease progression.3 The signs and symptoms of cirrhosis result from disruption of the liver's metabolic functions, which include glucose metabolism and regulation; conversion of ammonia into urea, which is then excreted by the kidneys; protein and fat metabolism; vitamin and iron storage; bile production; and drug metabolism.

In early or compensated cirrhosis, many patients will report vague symptoms, including:

  • generalized weakness
  • fatigue
  • intermittent low-grade fevers
  • ankle edema
  • right upper quadrant abdominal pain
  • various gastrointestinal (GI) symptoms, including anorexia, nausea and vomiting, dyspepsia, and changes in bowel patterns.

Further, cutaneous manifestations include spider angioma.

In late or decompensated cirrhosis, signs that indicate deteriorating hepatic function include:

  • progression of earlier signs and symptoms
  • jaundice
  • mental status changes
  • muscle wasting
  • weight loss
  • ascites
  • epistaxis
  • clubbing of fingers
  • nail changes (Muehrcke's nails or Terry's nails)
  • loss of body hair
  • GI bleeding
  • spontaneous bruising
  • gonadal atrophy
  • palmar erythema
  • Dupuytren's contracture
  • peripheral neuropathy
  • hypotension.

Assessment

The history and physical examination should include questioning and inquiry regarding specific influences on the diagnosis of cirrhosis. In addition to the chief complaint, patient history areas to explore include details regarding the onset of symptoms, history of lifestyle, and other precipitating factors, such as long-term alcohol abuse, infections, exposure to hepatotoxins, and other psychosocial influences. (See “Lifestyle and precipitating factors.”) Patients with long-term alcohol abuse should be monitored for alcohol withdrawal syndrome.

Family history, as well as current and past medical conditions, requires further discussion, especially if liver or biliary diseases are noted. Current nutritional and mental status may also contribute information regarding the patient's overall health status.

Focused assessment of mental status is particularly important, as changes may indicate worsening cirrhosis.

In addition to the general head-to-toe physical examination, focus needs to be directed to body systems and structures more likely to be affected by cirrhosis. These areas include but aren't limited to GI, integumentary, musculoskeletal, neurologic, and cardiopulmonary body systems. (See Key assessments.)

Psychosocial assessment of the patient is also important in order to gather information to incorporate in the nursing plan of care. Specific items should include sexual ability, role function, body image, and self-esteem. Lastly, the nurse should assess the patient's safety risk, because the severity of the disease process may increase the likelihood of incurring an avoidable injury.

Diagnostic tests

There are many diagnostic tests that can provide information about the overall integrity and functioning of the liver. Blood samples are analyzed to determine specific blood enzyme levels, which are referred to as markers or disease indicators. Other blood tests provide information directly related to the function of the liver. The liver can be visualized with various imaging techniques, such as computed tomography (CT) and GI radiographic imaging. Biopsy is the definitive determinant of cirrhosis.

Laboratory: In addition to standard laboratory tests (such as complete blood cell count, electrolyte panel, and coagulation studies) a hepatic panel is important. Many liver enzymes, such as alanine aminotransferase (ALT), aspartate transaminase (AST), lactate dehydrogenase (LDH), and gamma-glutamyl transferase (GGT), become elevated in liver disease. Measuring these enzymes enables the healthcare provider to detect liver damage, but doesn't give a good indication of a specific disease, because the results usually aren't helpful in distinguishing between the different causes of liver damage. Other tests can be performed to evaluate the ability of the liver to manufacture proteins (such as albumin and other globulins), as the tests show characteristic abnormalities with abnormal liver function.

Serum levels of ALT, AST, LDH, and GGT are elevated as these enzymes are released into the blood with hepatic cell damage. Alanine aminotransferase is the enzyme produced within the liver and is generally increased with damage to liver cell membranes, indicating inflammation.4 Liver inflammation can be caused by fatty infiltration, some drugs and medications, alcohol, and liver and bile duct disease. Aspartate transaminase is less specific for liver disease, and may be elevated in other disease states. As AST is elevated with damage to hepatic cells, it's most often considered in conjunction with ALT, because the ratio between the two may be helpful in assessing the etiology of liver enzyme abnormalities. For example, in alcoholic liver disease the AST:ALT ratio is typically greater than 2.0.

Alkaline phosphatase is an enzyme also associated with, but not specific to, the biliary tract. If the alkaline phosphatase is elevated, biliary tract damage and inflammation should be considered. It's common to assess the etiology of the elevated alkaline phosphatase by determining whether GGT is elevated or whether other tests are abnormal (such as bilirubin level). Considering these tests in combination may give a more accurate assessment of the etiology of the enzyme elevations.

Gamma-glutamyl transferase (transpeptidase) is produced by the bile ducts, but it isn't very specific to the liver or bile ducts. It's often used to confirm that the alkaline phosphatase is of hepatic etiology. Gamma-glutamyl transferase is often elevated in those who excessively use alcohol or are exposed to other toxic substances. Total serum protein and albumin levels are decreased in severe or chronic liver disease as the liver's ability to synthesize them becomes diminished. Serum globulin levels (alpha, beta, and gamma) are elevated because of their increased synthesis, indicating an immune response to liver disease. Total serum bilirubin levels rise in cirrhosis. Indirect bilirubin levels rise because of the diseased liver's inability to conjugate bilirubin. Prothrombin time is prolonged as the liver decreases the synthesis of prothrombin. In the presence of advanced liver disease, ammonia levels are elevated because the conversion of ammonia to urea is decreased.

Radiographic: Abdominal X-ray studies may be useful as they may reveal hepatomegaly, cysts, or gas in the biliary tract or liver, calcification of the liver, or massive ascites. Abdominal ultrasound is also an important diagnostic tool to evaluate morphologic abnormalities and to assess for complications, such as ascites, varices, portal vein thrombosis, and portal hypertension.

Upper GI radiographic studies may reveal esophageal varices or ulcerations of the stomach or duodenum. A CT scan may reveal ascites not large enough to be visualized on X-ray, identify the presence of masses, visualize hepatic blood flow and obstruction, and provide additional information about fluid collections. Esophagogastroduodenoscopy (EGD) may reveal variceal bleeding, irritation, or ulceration of the upper GI tract. Sclerotherapy may be performed during the EGD to palliate variceal bleeding.

Biopsy: Liver biopsy is considered the definitive test to establish the diagnosis of cirrhosis and also may help in determining its cause. Samples are usually obtained by percutaneous biopsy and may be guided by ultrasound or CT scan.

Collaborative management

Management of patients with cirrhosis requires a dedicated multidisciplinary team approach that will provide and oversee a holistic and comprehensive plan of care. In addition to medicine and nursing, typical team members might include nutritional professionals, physical and occupational therapy, case management or social services, psychology professionals, and pastoral care.

When standard medical and procedural therapy hasn't controlled cirrhosis complications, liver transplantation is usually considered. Early referral to a transplant center is important for potential liver transplant patients to allow time for the patient, family, referring physician, and transplant center staff to meet and identify potential issues. The United Network for Organ Sharing has developed a system for prioritizing candidates waiting for liver transplants based on a formula for predicting those in need of liver transplant most urgently.5

The Model for End-Stage Liver Disease (MELD) is used for transplant candidates 12 years of age and older. The MELD is calculated by a formula using bilirubin, international normalized ratio, and creatinine. Similarly, Pediatric End-Stage Liver Disease Model (PELD) is used for candidates 11 years of age and younger. Though PELD is similar to MELD, it uses several different factors to calculate the score to recognize the specific growth and development needs of children. The nursing plan of care should focus on not only addressing the patient's immediate needs, but also preventing future complications and promoting lifestyle changes and health maintenance activities that alone can improve survivability.

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Figure

Nursing considerations

The following eight considerations are important for nurses providing care to cirrhosis patients:

  1. Activity intolerance—Promote rest to help the liver reestablish its functional ability. This reduces the metabolic demands on the liver and increases blood supply, promoting regeneration of hepatocytes. However, take care to prevent complications related to immobility, such as pneumonia, deep vein thrombosis, phlebitis, and pressure ulcers. Activity and mild exercise, balanced with rest, will reduce the risk of complications and support the patients need to conserve energy.
  2. Impaired skin integrity—Skin care and monitoring of skin integrity is important due to the effects of edema, poor nutrition, jaundice, dryness, and excoriations. Patients should avoid irritants such as harsh soaps and adhesive tape. Lotion may be soothing and provide lubrication to dry areas. Jaundice is likely to lead to pruritus, therefore, patients should be advised to refrain from scratching.
  3. Imbalanced nutrition—Proper nutrition in the patient with cirrhosis is extremely important. Nurses should make every effort to encourage the patient to eat. Interventions such as arranging for preferred foods, providing oral hygiene prior to meals, and offering small frequent meals may help improve nutritional intake and tolerance. Patients with ascites or edema should have sodium restricted in their diet. In the early stages of cirrhosis without signs of hepatic encephalopathy or elevated serum ammonia levels, a nutritionally sound diet should be high in protein and supplemented with vitamins such as B complex, A, C, K, and folic acid. Protein supplements may be helpful; however, if the patient has experienced severe anorexia or vomiting, enteral or parenteral nutrition may be required. Patients who are demonstrating signs of impending or advancing hepatic coma (as evidenced by decreased level of conscious or increased serum ammonia) should have dietary protein restricted. Although dietary protein is necessary in the early stages of cirrhosis to promote hepatocyte regeneration, as liver function deteriorates, ammonia levels increase because the liver can no longer eliminate ammonia by converting it to urea for renal elimination.
  4. High risk for injury—Patients with cirrhosis are at high risk for injury related to issues resulting from changes in mental status and abnormal coagulation. The nurse must be vigilant to ensure a safe, protective environment at all times. Changes in mental status as a result of increased metabolic toxins (such as ammonia) may manifest as a decreased level of consciousness, agitation, restlessness, or disorientation. The nurse should monitor the patient's level of consciousness and compare it to his or her baseline. (See Mental status assessment.) Barbiturates and sedatives should be avoided, because they mask the symptoms of hepatic coma and aren't metabolized by the already compromised liver. Injuries such as falls may be avoided when the nurse orients the patient to place and time, explains all procedures, provides a calm, quiet environment, and assures close supervision and surveillance. Physical restraints should be avoided and the bed should be in a low position. Instructions on using the call bell and providing assistance for getting out of bed may also help prevent injuries.
  5. Because of abnormal clotting, the nurse should evaluate the patient for signs of internal and external bleeding. Frequently seen indications of hemorrhage include blood observed or detected in the stool, emesis, or urine. Patients may also demonstrate decreased hemoglobin and hematocrit levels, hypotension, ecchymosis, epistaxis, and petechiae. Using an electric razor and soft-bristle toothbrush may minimize minor bleeding episodes. In addition, pressure should be applied to all venipuncture sites to minimize bleeding.
  6. Fluid volume excess—Patients with advanced liver disease are predisposed to excessive fluid retention, and as a result, may develop cardiac and pulmonary complications. Circulating plasma volume is increased, and in the presence of severe cirrhosis, it may cause cardiovascular and respiratory compromise. There's an increase in cardiac output and a decrease in peripheral vascular resistance, causing a hyperdynamic circulatory state. The nurse should assess for signs of acute fluid overload by monitoring lung sounds for crackles, observing for peripheral and generalized edema, and evaluating the patient for jugular venous distension. Poor nutrition and protein intake contribute to fluid balance issues. Decreased total serum protein, especially serum albumin, results in decreased osmotic pressure which results in edema. Assessment of daily weights, accurate intake and output measurement, abdominal girth, and edema (especially in the extremities) will provide data regarding fluid balance.
  7. Other key interventions aimed at controlling fluid balance include fluid restrictions, a low sodium diet, and diuretics. Potassium-sparing diuretics such as spironolactone (Aldactone) and triamterene (Dyrenium) are useful to reduce excessive fluid while preventing potassium excretion. Patients who are experiencing issues with fluid balance should have their electrolytes monitored and treated accordingly.
  8. Comfort and pain management—The pain associated with cirrhosis is usually related to an enlarged liver and ascites. However, fatigue, weakness, nausea, vomiting, abdominal cramping, pruritus, peripheral edema, hyperthermia, and dyspnea may contribute to the patient's overall well-being, comfort, and motivation to comply with recommended care measures. Because the compromised state of the liver may not be able to adequately metabolize medications, caution needs to be observed when administering agents aimed at relieving pain and discomforts, such as analgesics.
  9. Accurate and ongoing pain assessment is necessary to evaluate the patient's baseline pain level and to decide on interventions and further care. Care measures should be individualized to the patient's needs, holistically involving the patient's support systems. For example, rest and paced activity may alleviate fatigue and weakness. Antiemetics may be used to treat nausea and vomiting, and antispasmodics for abdominal spasms. Positioning may assist with the discomfort associated with edema, ascites, and dyspnea, and cool moist compresses may sooth pruritus and reduce fevers. A paracentesis relieves the discomfort associated with ascites by removing fluid from the abdominal cavity. The reduced intra-abdominal volume reduces pressure, thus decreasing abdominal discomfort as well as dyspnea.
  10. Disturbed body image—A disturbed body image may be related to changes in appearance, sexual ability, and role function. Psychosocial support for the patient with cirrhosis should include the caretakers and significant others because the insidious progression of the disease will require lifestyle changes, new coping strategies, and adjustment to many emotional responses such as anxiety, sadness, or anger.
  11. It's important for the nurse to know what the changes in body image and function mean to the patient. Assess previous coping strategies and help the patient to verbalize feelings and frustrations. Empowering the patient to discuss options and make decisions allows him or her to regain a sense of control. Referrals to other support resources, such as counselors, spiritual advisors or religious leaders, may assist the patient's coping ability. In addition, if the patient has had issues with alcohol or some other substance abuse, a referral to a support group may prove to be useful. The overall goals for interventions regarding psychosocial support are aimed at providing positive reinforcement to increase self-esteem and a sense of well-being.
  12. Ongoing care and patient teaching—Hospitalization is only part of the patient's healthcare plan. From the time of admission, planning for transition to home offers challenges. Two of the greatest needs for promoting seamless transition from acute care to the home or less acute care settings are the exclusion of alcohol consumption and diet modifications. Referral to Alcoholics Anonymous or an alcohol rehabilitation center should be considered for the patient with a history of alcohol abuse. Counsel him or her on the long-term effects and risks associated with chronic alcohol use. The patient must be instructed regarding sodium and fluid restrictions, especially the specific protein requirements depending on the stage of the disease process.
  13. Another goal for transition from the acute care setting is to promote self-care activities to support health maintenance and independence. Written instructions and performing teaching with patients and caretakers promotes compliance with the plan of care and supports positive outcomes. Education should also include the importance of recognizing and reporting signs and symptoms of hepatic coma, bleeding, and infections. The nurse should reinforce with patients and caretakers the concept that recovery is slow and lifestyle changes are challenging; however, with vigilant education and homecare resources, positive outcomes are a realistic reality.

Complications

Cirrhosis is associated with numerous complications that must be managed in order for the patient to have a successful outcome.

Portal hypertension: Portal hypertension refers to an elevated blood pressure in branches of the portal vein. It's caused by increased volume of blood flowing through the vessels and increased resistance to the blood flow through the liver.5 Portal hypertension may lead to the development of GI varices. Antihypertensive medications are given to reduce portal hypertension.

Gastrointestinal varices: The resistance of blood flow through the liver results in the development of collateral blood vessel formation in the GI tract and shunting of blood from vessels of higher resistance to those of lower resistance. As a result, the patient with cirrhosis may develop distended blood vessels, called varices, throughout the GI tract as a result of those with lower resistance to flow becoming engorged. Because these vessels don't have the capacity to carry the high pressure and volume of blood, they may rupture, causing significant hemorrhage. The esophagus, stomach, and rectum are common sites for development of varices. Varices may be treated by several nonsurgical interventions, including gastric intubation; balloon tamponade with an esophagogastric tube (such as a Sengstaken-Blakemore tube); medication, such as propranolol (Inderal), to control heart rate and blood pressure; vasoconstrictors, such as vasopressin (Pitressin), to control hemorrhage by lowering pressure within the portal blood flow system; replacement of blood products; injection sclerotherapy; or a transjugular intrahepatic portal-systemic shunt (TIPS). Surgical treatment may be necessary as a last-resort intervention for patients with portal hypertension and esophageal varices. Surgical bypass shunting procedures, most commonly portacaval or splenorenal shunts, are performed to decrease portal hypertension and reduce variceal bleeding. Finally, liver transplantation has increasingly become an option for cirrhosis.

Ascites: This accumulation of excessive fluid in the peritoneal cavity may interfere with lung expansion leading to orthopnea and dyspnea. Individuals with ascites may present with shifting dullness or a fluid wave upon percussion. Dietary restrictions and medications, such as diuretics, are typically indicated in the treatment of patients with ascites. Failure of these treatment measures may warrant paracentesis.

Coagulation defects: Decreased vitamin K absorption results in decreased hepatic production of factors II, VII, IX, and X, making patients susceptible to bleeding and bruising. Patients with cirrhosis also may experience fibrinolysis and disseminated intravascular coagulation. Treatment may include factor replacement and transfusion of blood products.

Portal-systemic encephalopathy: Portal-systemic encephalopathy, or hepatic encephalopathy, results when brain function deteriorates as a result of the buildup of toxic substances (such as ammonia) in the blood that are normally removed by the liver. In the earliest stages, subtle changes appear in logical thinking, personality, and behavior. In later stages, the person may lose consciousness and develop hepatic coma. Medications such as lactulose and neomycin sulfate are commonly given to eliminate or reduce ammonia levels in the blood.

Quality of life

Overall, a collaborative approach by nurses and other members of the multidisciplinary team works best to achieve optimal outcomes for patients with cirrhosis. From the time of a diagnosis, to complex acute care issues, to supporting the patient's needs in the home, nurses provide the clinical leadership, coordination skills, and insight to guide the continuum of care. Cirrhosis may be a devastating, multifaceted chronic disease striking individuals in the prime of their lives, but with genuine caring, appropriate education, and strong partnership with patients, significant others, and nurses, the patient may be able to experience a satisfactory quality of life with minimal discomfort, managed symptoms, and prevention of complications.

Cirrhosis

Cirrhosis is characterized by widespread destruction of hepatic cells. The destroyed cells are replaced by fibrotic cells in a process called fibrotic regeneration. As necrotic tissue yields to fibrosis, regenerative nodules form and the liver parenchyma undergo extensive and irreversable fibrotic changes. The disease alters normal liver structure and vasculature, impairs blood and lymphatic flow and, ultimately, causes hepatic insufficiency.

Types of cirrhosis

Laënnec's, or alcoholic cirrhosis

Laënnec's cirrhosis, the most common type of cirrhosis, is caused by chronic alcohol use. In its early stages, the liver becomes enlarged and hardens as scar tissue forms and surrounds the portal areas. As the disease progresses, the liver shrinks in size. Poor nutrition with reduced protein intake also contributes to progression of the disease.

Postnecrotic cirrhosis

Postnecrotic cirrhosis most often results from acute viral hepatitis or exposure to drugs or other liver-damaging chemicals, such as carbon tetrachloride, arsenic, or phosphorus. It's often suspected in individuals without a history of chronic alcohol use.

Biliary cirrhosis

Biliary cirrhosis develops as a result of prolonged obstruction of biliary ducts or from infection of gallbladder origin. Scarring occurs in the liver around the bile ducts.

Cardiac cirrhosis

An uncommon complication of severe heart failure, cardiac cirrhosis occurs when the heart isn't able to pump back into the systemic circulation venous blood that has accumulated in the liver.

Key assessments

Gastrointestinal

Abdominal girth for distension and bloating, enlarged, irregular or tender liver, upper or lower GI bleeding, appetite changes, GI disturbances, weight loss, dilated abdominal wall veins

Integumentary

Skin color such as pallor or jaundice, areas of excoriation, spider veins, unexplained bruising, pruritus

Musculoskeletal

Muscle tone, muscle wasting or atrophy, fatigue, weakness

Neurologic

Tremors including asterixis, peripheral neuropathies, slurred speech, chronic pain

Cardiopulmonary

Edema, shortness of breath, hypotension, or hypertension

Other

Skin infections, hyperthermia, chronic pain

Mental status assessment

  • Orientation to person, place, and time
  • General behavior
  • Ability to carry out activities of daily living
  • Status of relationships with others
  • Sleep patterns
  • Cognitive recall and memory
  • Abstract thinking
  • Speech patterns
  • Mood and affect

Lifestyle and precipitating factors

Alcohol abuse

Past and present patterns of alcohol use, including type, amount, and duration

Infections

Hepatitis, HIV, chronic cholecystitis, or other viral infections

Hepatotoxins

Medication that includes over-the-counter, herbals and dietary supplements, illicit intravenous drug use, inhalants, and other occupational or industrial exposures

Psychosocial

Sexual practices and history of foreign travel

REFERENCES

1. CDC. National Hospital Discharge Survey: 2003 Annual Summary With Detailed Diagnosis and Procedure Data. Available at: http://www.cdc.gov/nchs/data/series/sr_13/sr13_160.pdf. Accessed December 2, 2007.
2. CDC. Table 2. Percentage of total deaths, death rates, age-adjusted death rates for 2003, percentage change in age-adjusted death rates from 2002 to 2003 and ratio of age-adjusted death rates by race and sex for the 15 leading causes of death for the total population in 2003: United States. Available at: http://www.cdc.gov/nchs/data/hestat/finaldeaths03_tables.pdf#2. Accessed December 2, 2007.
3. Smeltzer S, Bare B. Brunner & Suddarth's Textbook of Medical Surgical Nursing. 10th ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 2004:1101–1112.
4. American Liver Foundation. Liver health articles. Liver function tests factsheet. Available at: http://www.liverfoundation.org/db/articles/1077. Accessed December 2, 2007.
5. United Network for Organ Sharing. Resources. MELD/PELD Calculator. Available at: http://www.unos.org/resources/meldPeldCalculator.asp. Accessed December 2, 2007.
6. Portal hypertension. Available at: http://www.merck.com/mmhe/sec10/ch135/ch135e.html. Accessed December 2, 2007.
    © 2008 Lippincott Williams & Wilkins, Inc.