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Care and management of the patient with Ascites.

Cirrhosis is a relatively common disorder that may be difficult to manage. Cirrhosis combined with chronic liver failure accounts for 26,549 deaths per 100,000 persons in the United States (Minino, Heron, & Smith, 2006). Causes of the majority of preventable cases of cirrhosis include excessive alcohol consumption, viral hepatitis C, and nonalcoholic steatohepatitis (NASH) related to obesity (Feldman, 2006; Heidelbaugh & Bruderly, 2006). Information on ascites, its pathogenesis, evaluation, diagnosis, and management, particularly in patients with cirrhosis, is presented.

Definition and Development of Ascites

Ascites is the accumulation of fluid in the peritoneal cavity and is the most common complication of liver failure in cirrhosis, followed by hepatic encephalopathy and variceal hemorrhage (Feldman, 2006; Heidelbaugh & Bruderly, 2006; Saadeh & Davis, 2004). The most common presenting symptom of ascites is the increase of abdominal girth with weight gain and lower-extremity edema. The fluid accumulation may occur over several weeks or rapidly over a few days (Sargent, 2006). If the fluid accumulation is extensive, it may produce abdominal discomfort, respiratory compromise, umbilical hernia, impaired sense of well-being, and early satiety (Noble, 2001).

About 15% of patients with ascites have a non-hepatic cause of fluid retention (Heidelbaugh & Sherbondy, 2006; Saadeh & Davis, 2004). Ascites can be associated with heart failure, constrictive pericarditis, abdominal malignancies, nephrotic syndrome, and malnutrition (see Table 1) (Huether, 2006a).

Development of ascites is predictive of mortality, especially in liver disease. Two years after the development of ascites associated with alcoholic cirrhosis, an affected individual has a 50% chance of survival. Development of ascites associated with chronic hepatitis C suggests a 5-year survival time (Saadeh & Davis, 2004).

The most recent theory of cirrhotic ascites formation is the peripheral arterial vasodilation hypothesis, which proposes that portal hypertension develops prior to the development of ascites (see Figure 1). Portal hypertension occurs because of increased pressure in the portal venous system (Whiteman & McCormick, 2005), which consists of the portal veins, sinusoids (small capillaries), and hepatic veins. Its normal pressure is 3 mmHg; an increase of pressure to at ]east 10 mmHg constitutes portal hypertension (Huether, 2006a). The portal system carries blood from the intestines, pancreas, and spleen to the liver. Blood in the liver flows through the sinusoids to the hepatic veins into the inferior vena cava, then to the right atrium (Huether, 2006a; Whiteman & McCormick, 2005). The increased pressure occurs due to fibrosis and scarring of the liver from chronic liver disease, causing obstruction to venous flow (Whiteman & McCormick, 2005).

[FIGURE 1 OMITTED]

As the portal pressure increases, circulating levels of nitric oxide also increase and vasodilation results (Rockey, 2003). Systems to counteract this effect are stimulated (renin-angiotensin-aldosterone, antidiuretic hormone). These result in renal function compromise, sodium and fluid retention, and eventual ascites (Feldman, 2006). Specifically, the vasodilation signals the kidneys to release renin; this converts angiotensinogen (produced by the liver) to angiotensin, which is converted to angiotensin II and causes vasoconstriction (see Figure 2). The angiotensin II signals the adrenal glands to release aldosterone, which causes the kidneys to retain more sodium and water. This sodium retention, coupled with inadequate levels of albumin, facilitates the shift of fluid from the intravascular space into the interstitial space of the abdomen and creates ascites ("Patho Puzzler," 2005).

Assessment of the Patient with Ascites

History. A careful history of the patient with ascites should include information that places a patient at risk for liver disease, including quantity and duration of alcohol use, transfusion of blood products, and personal or family history of autoimmune or hepatic diseases. In addition, risk factors for hepatitis B and/or C transmission, such as intravenous or intranasal drug use, travel to or birth in an endemic area, body piercing or tattooing, sexual history exposure risk, and accidental exposure to contaminated blood and body fluids, also should be assessed (Heidelbaugh & Bruderly, 2006).

[FIGURE 2 OMITTED]

Cirrhotic liver disease can be asymptomatic until decompensation occurs. Ascites may not develop until the patient's first decompensatory episode of liver disease. The discovery of liver disease can occur during routine tests showing abnormal results of liver function tests or a coagulation screen. Therefore, the nurse should be aware of several key areas regarding the patient's clinical history to screen for liver disease (Saadeh & Davis, 2004; Starr & Hand, 2002).

Symptoms, such as anorexia, weight loss, weakness, and fatigue, also may be present in early and compensated cirrhosis. Osteoporosis secondary to vitamin D malabsorption, which contributes to a calcium deficiency, may be evident (Heidelbaugh & Bruderly, 2006). Clinical symptoms of ascites include jaundice of the eyes or skin, increasing abdominal girth, shortness of breath, and weight gain. In addition mental status changes, coagulopathy, gastrointestinal bleeding, and pruritus may indicate signs of impaired liver function (Day & Taylor, 2006; Heidelbaugh & Bruderly, 2006; "Patho Puzzler," 2005).

The timing of the development of ascites, even in those with liver disease, is significant. Patients with a long history of stable cirrhosis and the sudden development of ascites should be evaluated for hepatocellular carcinoma, which may have caused the decompensation. Associated symptoms also may be informative. The presence of abdominal pain may be a defining feature. Malignancy-related ascites frequently is painful, while cirrhotic ascites generally is not painful unless associated with bacterial peritonitis or alcoholic hepatitis (Feldman, 2006).

Physical examination. When a patient presents with a history of multiple symptoms, a thorough examination by the health provider is warranted. In the patient with cirrhosis, the exam may lead to focused hepatic and gastrointestinal diagnostics (Heidelbaugh & Bruderly, 2006). During the abdominal exam, the health care provider should determine the presence of ascites based on the presence of a full, bulging abdomen. The next step is to percuss the flanks for dullness. An accumulation of approximately 1,500 ml of intraperitoneal fluid must be present before dullness is detected (Feldman, 2006). A normal abdomen percussed with the patient in the supine position should produce predominately tympany because air rises. If ascites is suspected in a patient with distended and bulging flanks, a physical exam maneuver called shifting dullness can be used to detect ascites. Shifting dullness is identified by first marking the border where dullness occurs with the patient in the supine position; then the patient turns to one side and the provider percusses from the top of the abdomen down to the level of dullness. If fluid is present, the level of dullness shifts higher upward to the umbilicus (Jarvis, 2004).

Overall, the abdominal physical exam has limited value in identifying ascites. Cattau, Benjamin, Knuff, and Castell (1982) studied 21 patients who were evaluated with a diagnosis of questionable ascites. Three investigators who performed five different physical examination maneuvers examined them independently. Ultrasonography determined that six patients had ascites. However, the sensitivity and specificity of the five physical examination maneuvers were 50%-94% and 29%-82% respectively, with overall accuracy of only 58%. The absence of flank dullness had a 90% accuracy for the absence of ascites. In questionable cases, ultrasonography is recommended. In addition, if flank dullness is absent, there is no need to check for shifting fluid as described because the patient has less than 10% chance of having ascites (Feldman, 2006). Other findings of note on physical exam include palmar erythema, large pulsatile spider angiomata, large abdominal wall collateral veins, or fetor hepaticus (breath odor described as sweet, fecal smell), which suggest parenchymal liver disease and portal hypertension (Feldman, 2006; Whiteman & McCormick, 2005). Vascular spiders (spider angiomata, spider telangiectasias) are vascular lesions found on the trunk, face, and upper extremities. Although the lesions are not specific for cirrhosis, the number and size of them correlate with the severity of chronic liver disease, also placing a patient at risk for ascites and variceal hemorrhage (Heidelbaugh & Bruderly, 2006).

Diagnostics

Because ascites is most often associated with liver disease, diagnostics for hepatic abnormalities are a priority. These should include a liver panel, complete blood count with platelets, and prothrombin time. Further testing also should include a viral hepatitis panel. To determine other causes of liver disease, more serologic testing would be performed (Heidelbaugh & Bruderly, 2006).

In the initial assessment of new onset ascites, renal function should be evaluated using serum creatinine, electrolytes, and 24-hour urinary sodium and potassium (Sandhu & Sanyal, 2005). An abdominal ultrasound is recommended unless there is high suspicion for a malignancy or pancreatic disease (Saadeh & Davis, 2004). Ultrasound can detect as little as 50-100 ml of fluid in the peritoneal cavity and also can confirm patency of the hepatic and portal veins for other causes of ascites (Heidelbaugh & Bruderly, 2006; Saadeh & Davis, 2004).

Diagnostics to Detect Cause of Ascites

Ultrasound should be followed by an abdominal paracentesis to diagnose the cause of ascites (Saadeh & Davis, 2004). The American Association for the Study of Liver Diseases recommends a diagnostic abdominal paracentesis performed on patients with clinical evidence of new onset ascites (Runyon, 2004). Ascitic fluid should be collected in blood culture bottles before antibiotics are started to rule out a true infection.

Initial evaluation of an ascitic fluid specimen should include a differential leukocyte count, total protein level, and a serum-ascites albumin gradient (SAAG) (Heidelbaugh & Sherbondy, 2006). A gram stain and culture should be obtained for suspicion of peritoneal infection (Saadeh & Davis, 2004).

The SAAG is a strong indicator of the likelihood of portal hypertension or pressure caused by cirrhosis or liver disease. It is calculated by subtracting the ascitic albumin concentration from the serum albumin concentration in specimens obtained at the same time. A SAAG of 1.1 g per dL (11 g per L) or greater is highly suggestive of portal hypertension. If the value is less than 1.1 g per dL, other causes for ascites should be investigated (Heidelbaugh & Sherbondy, 2006; Saadeh & Davis, 2004). Even though the SAAG can suggest portal hypertension, it is not exclusive to cirrhosis as the cause (Saadeh & Davis, 2004).

Treatment Recommendations for Ascites

Abstinence from alcohol is a critical component in the treatment of ascites from alcoholic liver disease. In the pre-cirrhotic alcoholic hepatitis stage of disease, alcohol reduction or abstinence may decrease the predisposition to fluid retention and therefore the level of ascites. In addition, alcohol abstinence at this early stage may reverse the portal hypertension and resulting sodium retention (Feldman, 2006; Runyon, 2004).

Evidence is accumulating that nonalcoholic cirrhosis also can be reversible with effective therapy. Whether a decompensated nonalcoholic cirrhotic liver can revert to normal, however, remains to be seen. Many patients with cirrhosis and ascites will require liver transplantation (Feldman, 2006). The nurse plays an important role in caring for the patient with cirrhosis due to alcoholism, offering support and providing information about counseling and treatment regarding alcohol abuse for the family and patient (Heitkemper, Croghan, & Cox-North, 2007).

Diet. Sodium restriction of two grams per day is the first-line treatment recommended in the literature. Protein is not restricted unless the patient has refractory hepatic encephalopathy. There is no recommendation for fluid restriction unless serum sodium is less than 120-125 mEq per liter (Feldman, 2006; Heidelbaugh & Sherbondy, 2006). All patients with ascites should receive a referral for dietary counseling regarding a low-sodium diet and proper overall nutrition. Nurses caring for patients with ascites should be familiar with foods that should be allowed, restricted, or omitted in the diet (Sargent, 2006). Nurses need to monitor food intake for nutritional content and calories and encourage frequent small meals, oral hygiene, and between-meal nourishment because anorexia and nausea are typical in patients with cirrhosis (Heitkemper et al., 2007).

Diuretics. Diuretics are the mainstay of treatment for cirrhotic ascites, with spironolactone (Aldactone[R]) as the most commonly used therapy. Spironolactone is an aldosterone antagonist which blocks the effect of aldosterone that contributes to sodium retention in the development of ascites. The starting dose of 100 mg daily may be titrated at weekly intervals to a maximum of 400 mg per day (Sandhu & Sanyal, 2005).

The diuretic furosemide (Lasix[R]) is used in combination with spironolactone. It is started at a dose of 40 mg per day and titrated up to 160 mg per day. Furosemide acts by delivering increased amounts of sodium, chloride, and water to the distal tubule to cause diuresis. Sodium is reabsorbed during this process. The spironolactone aids by blocking sodium reabsorption at the distal tubule, which allows natriuresis or sodium loss. The combination of the two drugs, which are started together to begin treatment, is the most effective regimen of diuretics, initiated in a ratio of 100:40, to maintain normokalemia (Runyon, 2004; Sandhu & Sanyal, 2005; Schouten & Michielsen, 2007).

Weight loss of 1-2 pounds per day is a reasonable goal for diuresis as electrolytes are monitored carefully for volume depletion and renal functioning (Mathews, McGuire, & Estrada, 2006). Nurses contribute to fluid monitoring by carefully weighing the patient daily before breakfast in the same amount of clothing (Sargent, 2006). They also should teach the patient to weigh himself or herself at home and report a weight gain of more than 2 pounds in a day to the health care provider. Nurses monitor fluid intake and output to assess renal function, and they also assist the patient to maintain fluid restriction if needed. Other nursing measures include administering diuretics, obtaining labs concerning fluid or electrolytes, and monitoring changes in peripheral edema and abdominal girth (Heitkemper et al., 2007).

Due to the resulting changes in fluid balance, the patient may have problems with skin breakdown, pruritus, and tautness due to peripheral edema and ascites. Nurses can protect the skin by frequently turning immobilized patients every 2 hours, evaluating the need for an alternating air pressure mattress, and avoiding use of alkaline soap. They support edematous areas, applying medicated creams or lotions to decrease itching and teaching patients to keep fingernails short to prevent excoriation (Heitkemper et al., 2007).

Refractory ascites. Approximately 5%-10% of patients with cirrhosis experience refractory ascites and more than 50% die within 2 years after the onset (Mathews et al., 2006). Therapies that are used to assist in managing refractory ascites include large-volume paracentesis, and transjugular intrahepatic portosystemic stent-shunts (TIPS) (Gines, Cardenas, Arroyo, & Rodes, 2004; Saadeh & Davis, 2004; Sandhu & Sanyal, 2005; Sargent, 2006).

Large-volume abdominal paracentesis with removal of more than five liters of fluid is standard therapy (Sargent, 2006). Removal of 4-6 liters of fluid is considered safe, but greater than 10 L should be performed no more often than every 2 weeks (Yeung & Wong, 2002). The procedure can be performed in an outpatient setting and is usually required about every 2-4 weeks with administration of albumin as a plasma volume expander (Gines et al., 2004; Mathews et al., 2006). The nurse must have the patient void prior to the procedure and later monitor for hypovolemia and electrolyte abnormalities, as well as check the dressing for bleeding or leakage (Heitkemper et al., 2007).

A pilot study (Lenaerts, Codden, Henry, Legros, & Ligny, 2005) compared repeated large-volume paracentesis with the combination of clonidine (Catapres[R]) and spironolactone as treatment for refractory ascites, and found that paracentesis was more effective in relieving ascites. Clonidine-spironolactone may be beneficial in long-term treatment as it led to reduced time to first readmission, lower readmission rates, and requirements for diuretics, although larger controlled studies are needed to validate these findings. A review of randomized clinical trials comparing transjugular intrahepatic portosystemic stent-shunts with paracentesis concluded that TIPS was more effective at removing ascites without an increase in mortality (Saab, Nieto, Ly, & Runyon, 2006). Although an increased risk of hepatic encephalopathy occurred in patients with TIPS, no difference in mortality, gastrointestinal bleeding, infection, or acute renal failure was found between the two groups. Another comparison of TIPS to paracentesis plus albumin in 66 patients with severe ascites associated with cirrhosis found improvement in survival but rates of hospitalization and complications were similar between the groups (Salerno et al., 2004). The number of patients with hepatic encephalopathy was greater (although not significantly) in those receiving TIPS.

Paracentesis is effective in removing fluid and providing patients with immediate symptomatic relief (Sargent, 2006). The primary disadvantage is the frequent recurrence of ascites (Mathews et al., 2006; Sargent, 2006). TIPS as alternative therapy may increase hepatic encephalopathy and mortality in patients with advanced liver disease (Mathews et al., 2006). Because the prognosis for refractory ascites is poor, patients should be referred for evaluation for liver transplantation as soon as possible (Dib, Oberti, & Cales, 2006; Mathews et al., 2006).

Conclusion

Excessive alcohol consumption, hepatitis C, and NASH account for the majority of preventable cirrhosis cases, with NASH possibly increasing in the future as obesity continues to rise. Ascites is a common complication of cirrhosis, which worsens as decompensation of the liver occurs regardless of its cause. Management of ascites includes a combination of spironolactone and furosemide, and a 2-gram sodium diet. Treatment options for refractory ascites include large-volume paracentesis and TIPS. Prompt recognition and management of ascites are crucial because prognosis for refractory ascites is poor and patients will need referral for liver transplantation. Nurses play a vital part in all aspects of care for patients with cirrhosis, including education on prevention of alcohol abuse and obesity, and lifestyle behaviors and risks associated with hepatitis C transmission. They also assist patients in preparation for diagnostic evaluations and treatments, and institute interventions to manage symptoms associated with ascites.

Reference

Becket, G., Galandi, D., & Blum, H.E. (2006). Malignant ascites: Systematic review and guideline for treatment. European Journal of Cancer, 42, 589-597.

Cattau, E.L., Jr., Benjamin, S.B., Knuff, T.E., & Castell, D.O. (1982). The accuracy of the physical examination in the diagnosis of suspected ascites. The Journal of the American Medical Association, 247, 1164-1166.

Day, H.L., & Taylor, R.M. (2006). The liver part 4: Chronic liver disease. Nursing Times, 102, 22-23.

Dib, N., Oberti, E, & Cales, P. (2006). Current management of the complications of portal hypertension: Variceal bleeding and ascites. Canadian Medical Association Journal 174, 1433-1443.

Feldman, M. (2006). Sleisenger and Fordtran's gastrointestinal and liver disease (8th ed.) Philadelphia: Saunders.

Gines, P., Cardenas, A., Arroyo, V., & Rodes, J. (2004). Management of cirrhosis and ascites. New England Journal of Medicine, 350, 1646-1654.

Heidelbaugh, J.J., & Bruderly, M. (2006). Cirrhosis and chronic liver failure: Part I. Diagnosis and evaluation. American Family Physician, 74, 756-762.

Heidelbaugh, J.J., & Sherbondy, M. (2006). Cirrhosis and chronic liver failure: Part II. Complications and treatment. American Family Physician, 74, 767-776.

Heitkemper, M.M., Croghan, A. & Cox-North, R (2007). Liver, pancreas and biliary problems. In S.L. Lewis, M.M. Heitkemper, S.R. Dirksen, P.G. O'Brien, & L. Bucher (Eds.), Medical-surgical nursing: Assessment and management of clinical problems (7th ed., pp. 1110-1114). St. Louis: Mosby.

Huether, S.E. (2006a). Alterations of digestive function. In K.L. McCance & S.E. Huether (Eds.), Pathophysiology: The biological basis for disease in adults and children (5th ed., pp. 1414-1416). St. Louis: Mosby, Inc.

Huether, S.E. (2006b). Alterations of renal and urinary tract function In K.L. McCance & S.E. Huether (Eds.), Pathophysiology: The biological basis for disease in adults and children (5th ed., pp. 1320-1321). St. Louis: Mosby, Inc.

Jarvis, C. (2004). Physical examination and health assessment (5th ed.). Philadelphia: W.B. Saunders.

Lenaerts, A., Codden, T., Henry, J.R, Legros, F., & Ligny, G. (2005). Comparative pilot study of repeated large volume paracentesis vs the combination on clonidine-spironolactone in the treatment of cirrhosis-associated refractory ascites. Gastroenterologie Clinique et Biologique, 29, 1137-1142.

Mathews, R.E., McGuire, B.M., & Estrada, C.A. (2006). Outpatient management of cirrhosis: A narrative review. Southern Medical Journal, 99, 600-606.

Minino, A.M., Heron, M.P., & Smith, B.L. (2006). National vital statistics reports. Centers for Disease Control and Prevention [Online]. Retrieved November 16, 2006, from http://www.cdc.gov/nchs/data/nvsr/ nvsr54/nvsr54_19.pdf

Noble, J. (2001). Textbook of primary care medicine (3rd ed.). St. Louis: Mosby, Inc.

Patho puzzler. A puzzling complication of liver disease. (2005). Nursing Made Incredibly Easy, 3, 54-56.

Rockey, D.C. (2003). Vascular mediators in the injured liver. Hepatology, 37, 4-12.

Runyon, B.A. (2004). Management of adult patients with ascites due to cirrhosis. Hepatology, 39, 841-856.

Saab, S., Nieto, J.M., Ly, D., & Runyon, B.A. (2006, October 18). TIPS versus paracentesis for cirrhotic patients with refractory ascites. Cochrane Library, (4): CD004889.

Saadeh, S. & Davis, G. L. (2004). Management of ascites in patients with end-stage liver disease. Review of Gastroenterologic Disorders, 4, 175-185.

Salerno, F., Merli, M, Riggio, O., Cazzaniga, M., Valeriano, V., Pozzi, M., et al. (2004). Randomized controlled study of TIPS versus paracentesis plus albumin in cirrhosis with severe ascites. Hepatology, 40, 629-635.

Sandhu, B.S., & Sanyal, A.J. (2005). Management of ascites in cirrhosis. Clinics in Liver Disease, 9, 715-32, viii.

Sargent, S. (2006). Hepatology. The management and nursing care of cirrhotic ascites. British Journal of Nursing, 15, 212-219.

Schouten, J., & Michielsen, P. (2007). Treatment of cirrhotic ascites. Acta Gastroenterologica Belgica, 70, 217-222.

Starr, S., & Hand, H. (2002). Nursing care of chronic and acute liver failure. Nursing Standard, 16, 47-56.

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Lisa Lee, MS, RN, ANP, Instructor, Adult Health Department, School of Nursing, Virginia Commonwealth University, Richmond, VA.

Mary Jo Grap, PhD, RN, ACNP, FAAN, is a Professor, Adult Health Department, School of Nursing, Virginia Commonwealth University, Richmond, VA.

Note: The authors and all MEDSURG Nursing Editorial Board members reported no actual or potential conflict of interest in relation to this continuing nursing education article.

Note: A related article on this topic, "Ascites: What You Should Know," can be found in the November/December 2008 issue of Medsurg Matters, the official newsletter of the Academy of Medical-Surgical Nurses (www.amsn.org).
Table 1.
Non-Hepatic Causes of Fluid Retention

Heart failure and     The heart loses its ability to pump blood;
constrictive          this causes a back up of blood and increased
pericarditis          pressure into the portal venous system,
                      leading to portal hypertension (PH) and
                      ascites (Huether, 2006a).

Abdominal             Ascites development is dependent on the
malignancies          location of the tumor. In peritoneal
                      carcinomatosis, tumor cells line the
                      peritoneal cavity and produce a protein-like
                      fluid. Extracellular fluid is drawn into the
                      cavity due to the increased oncotic pressure
                      of the peritoneal fluid. Fluid also develops
                      in liver metastases and hepatocellular cancer
                      due to PH. These malignancies induce PH when
                      stenosis or occlusion of the portal vein
                      occurs by thrombosis, tumor emboli, or tumor
                      nodules (Feldman, 2006). Tumor cells also may
                      obstruct lymphatic drainage, decreasing fluid
                      removal and blood volume. This reduction
                      activates the renin-angiotensin-aldosterone
                      system and leads to sodium retention, which
                      then further exacerbates the ascites (Becker,
                      Galandi, & Blum, 2006).

Nephrotic             Contributes to ascites due to protein loss
syndrome              from damaged kidneys. This loss of protein and
                      concomitant reduction of plasma albumin
                      results in a decrease in oncotic pressure that
                      also stimulates the
                      renin-angiotensin-aldosterone system and
                      antidiuretic hormone production, resulting in
                      sodium and water retention, edema, and ascites
                      (Huether 2006a, 2006b).

Malnutrition and      May also cause ascites due to reduced protein
the lack of           synthesis and insufficient albumin resulting
dietary amino         in generalized edema, increased total body
acids                 water and extracellular fluid (Huether,
                      2006a).
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Date:Dec 1, 2008
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