CHAPTER 18. ASCITES
Debra E. Heidrich
DEFINITION AND INCIDENCE
Ascites is the abnormal accumulation of fluid in the peritoneal cavity. The majority of patients with ascites have advanced liver disease—usually cirrhosis (Runyon, Montano, Akriviadis et al., 1992). Other nonmalignant diseases associated with ascites include right-sided heart failure, tuberculous peritonitis, nephrotic syndrome, complications of pancreatitis, and chylous ascites from trauma or surgery (Hostetter, Marincola, & Schwartzentruber, 2005; Runyon, 2004). Approximately 10% of patients with ascites have a malignancy as the primary cause (Runyon et al., 1992). Cancer diagnoses most often associated with ascites are ovarian, endometrium, breast, large bowel, stomach, and pancreas (Kichian & Bain, 2004). About 6% of patients entering hospices have ascites (Waller & Caroline, 2000).
Common symptoms associated with ascites include abdominal bloating, abdominal pain, nausea, decreased appetite, and constipation. Large-volume ascites leads to dyspnea and orthopnea. Patients with cirrhosis and ascites have higher variceal pressure than those without ascites and thus are at greater risk for variceal bleeding, which is associated with a high mortality rate (Kravetz, Bildozola, Argonz et al., 2000). The presence of malignancy-associated ascites is a poor prognostic sign, with a 1-year survival rate of 40% (Kichian & Bain, 2004). The median length of survival in a patient with symptomatic malignant ascites is reported to be 1 to 4 months. However, there is some variability in survival based on cancer type; women with breast or ovarian cancer may have a longer survival (Adam & Adam, 2004; Hostetter et al., 2005). Prolongation of survival has been documented in response to aggressive and more-targeted treatment approaches, but few randomized clinical trials exist in these patient populations (Hostetter et al., 2005).
ETIOLOGY AND PATHOPHYSIOLOGY
Ascites with Liver Disease
Common aspects of all postulated mechanisms for the development of ascites in liver disease involve a combination of sodium retention and portal hypertension (Lingappa, 2003). Portal hypertension can arise from hepatic venous outflow blockage caused by nodules and fibrosis in the liver (Wongcharatrawee & Garcia-Tsao, 2001). Three possible effects of portal hypertension are (1) diversion of the vascular volume to the lymphatics, resulting in overloading of the lymphatic drainage and weeping of fluid into the peritoneum; (2) portal-to-systemic shunting causing irritants that are normally cleared by the liver to be released into circulation where they initiate activities that decrease renal perfusion and increase renal tubular sodium resorption; or (3) endothelin-1 secretion, causing renal vasoconstriction, decreased glomerular filtration rate, and sodium retention. Regardless of the causal mechanism involved, depletion of the intravascular volume activates the renin-angiotensin-aldosterone system and vasopressin, causing sodium and water retention, which further contributes to fluid accumulation (Lingappa, 2003).
Ascites with Malignancy
Several mechanisms have been proposed for the development of malignancy-associated ascites. Patients with liver cancer may develop portal hypertension, resulting in ascites formation in much the same way as those with cirrhosis (Kichian & Bain, 2004). In addition, tumors that have seeded the peritoneum may release high levels of vascular endothelial growth factor (VEGF) that increase capillary permeability. Zebrowski, Liu, Ramirez et al. (1999) showed that VEGF protein levels were markedly increased in malignant ascites compared to levels in ascites associated with cirrhosis and that inhibiting VEGF activity decreased endothelial cell permeability in vitro. Further, animal studies show that ascites recurrence can be blocked by inhibiting VEGF expression (Stoelcker, Echtenacher, Weich et al., 2000). When the vascular permeability increases, proteins enter the peritoneal cavity. In mice, proteins in the peritoneal cavity make ascites worse by functionally impairing lymphatic drainage (Nagy, Herzberg, Masse et al., 1989). These proteins also increase the oncotic pressure pulling in more fluids via osmosis. In addition, obstruction or invasion of lymphatic channels by tumors may lead to chylous ascites (Kichian & Bain, 2004).
Effects of Ascites
The accumulation of abnormal amounts of fluid in the peritoneal cavity causes many uncomfortable symptoms. Pain occurs due to stretching or compression of tissues. Also, inflammation from a peritoneal infection may cause severe pain. Increased pressure on the stomach causes early satiety and nausea. Constipation, due to pressure on the bowel, is also a common complication of ascites. Dyspnea may result from pressure on the diaphragm and leakage of ascitic fluid into the pleural space (Kichian & Bain, 2004).
ASSESSMENT AND MEASUREMENT
An observable enlargement of a patient’s abdomen is a somewhat late sign of ascites. It has been estimated that 1.5 liters of ascitic fluid must be present before flank dullness is detected and 2 liters must be present before bulging is appreciated on physical examination (Cattau, Benjamin, Knuff et al., 1982; Tabbarah & Casciato, 1990). Patients of short stature may show these physical signs with less fluid accumulation. The earliest signs of ascites are often patient complaints of bloating, abdominal discomfort or pain, and increasing weight or waist size (e.g., clothes do not fit). Patients may also complain of fatigue, inability to sit upright, heartburn, nausea, early satiety, and constipation. As ascites becomes more pronounced, dyspnea and orthopnea may occur. Edema of the legs is also possible with progressive ascites (Kichian & Bain, 2004). Abdominal girth measurement provides a baseline that can be used to monitor worsening ascites, effectiveness of interventions, or recurrence of ascites after treatment.
HISTORY AND PHYSICAL EXAMINATION
Review the Patient’s History
Determine the underlying pathophysiology of the ascites (e.g., liver disease, heart disease, renal disease, or cancer).
Assess for Symptoms Associated with Ascites
Ask about onset and severity:
▪ Weight gain
▪ Increasing abdominal girth or a change in the way clothes fit
▪ Indigestion, nausea, and early satiety
▪ Sensation of fullness or bloating
▪ Ankle swelling
▪ Dyspnea
▪ Constipation
▪ Urinary frequency
Perform a Physical Examination
▪ Compare weight to baseline, taking weight loss due to anorexia and cachexia into account.
▪ Measure abdominal girth.
▪ Assess abdomen:
Note distension with bulging flanks when the patient is supine. This may be difficult to discern if the patient is obese or if less than 2 liters of fluid is present.
Percuss abdomen. (Note: percussion may not be sensitive or specific in diagnosing ascites [Cattau et al., 1982].)
Note any shifting dullness on percussion with position changes. In the supine patient with ascites, tympany is heard near the umbilicus but dullness is noted when the clinician percusses away from the umbilicus and reaches the level of fluid. When the patient turns to one side, the dullness shifts to the dependent areas.
Feel for evidence of a fluid wave (i.e., when flank is tapped on one side, an impulse is felt on the opposite side). Be sure to block transmission of a wave through subcutaneous fat by having an assistant place the medial edges of both hands firmly down the midline of the abdomen.
Observe skin across abdomen for signs of tightness or stretch marks.
Look for abdominal venous engorgement.
Identify changes in umbilicus; may be flattened or everted.
Assess for scrotal and/or lower-extremity edema.
Assess for associated complications:
Note any respiratory changes due to pressure on diaphragm or pleural effusion:
Assess rate and depth of respiration.
Listen for diminished or absent breath sounds.
Assess for dehydration or malnutrition due to nausea and early satiety:
Assess hydration of mucous membranes.
Assess general nutritional status.
DIAGNOSTICS
Abdominal radiographic studies, ultrasound, and computed tomography scans do verify the presence of free fluid in the abdomen, but these tests are generally not required after a thorough history and physical examination. On radiography, ascites appears with hazy or ground-glass features, distended and separated loops of bowel, and poor definition of abdominal organs (Hostetter et al., 2005; Kichian & Bain, 2004).
Cytology and examination of the protein concentration of the peritoneal fluid are tests that assist in determining the cause of ascites. However, in end-of-life care, the cause is often evident, so a diagnostic paracentesis is rarely required. More commonly, the peritoneal fluid is examined for cell count, Gram stain, and culture to select the appropriate antibiotic intervention when infection is suspected.
INTERVENTION AND TREATMENT
Sodium Restriction and Diuretics
Sodium restriction and diuretics may be effective for ascites caused by increased portal hypertension (e.g., cirrhosis or cancer in the liver) but are rarely effective for other types of malignant ascites (Adam & Adam, 2004). When portal hypertension is contributing to ascites, restrict sodium to 2000 mg/day or less; fluid restriction is not necessary for any cause of ascites unless serum sodium is less than 120 to 125 mmol/L (Runyon, 2004). In end-of-life care, it is important to balance the potential therapeutic effects of sodium and fluid restriction with the quality of living benefits of allowing patients to eat whatever foods taste good to them. As the appetite decreases, the appropriateness of a sodium-restricted diet also decreases.
When diuretic therapy is appropriate, that is, when portal hypertension is contributing to the ascites, spironolactone is more effective than loop diuretics (Kichian & Bain, 2004). However, a combination of spironolactone and loop diuretics (e.g., furosemide) may be even more effective. It may be reasonable to begin with an oral regiment of 100 mg of spironolactone and 40 mg of furosemide. Doses of both diuretics can be increased every 3 to 5 days, maintaining the 100:40 mg ratio, if weight loss and sodium excretion are inadequate (Runyon, 2004). The recommended maximum oral dose of spironolactone is 400 mg/day and of furosemide is 160 mg/day (Sandhu & Sanyal, 2005). Potential complications of diuretics, especially overuse of diuretics, include fluid and electrolyte imbalances, postural hypotension, hepatic encephalopathy, and pre–renal failure (Kichian & Bain, 2004; Sandhu & Sanyal, 2005).
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