Ascites is the condition in which there is free fluid in the peritoneal cavity. The most common cause is portal hypertension. Symptoms usually result from abdominal distention. Diagnosis is based on physical examination, ultrasound, or CT. Treatments include bed rest, dietary Na restriction, diuretics, and therapeutic paracentesis. Ascitic fluid can become infected (spontaneous bacterial peritonitis), often with pain and fever. Diagnosis of infection involves analysis and culture of ascitic fluid. Infection is treated with antibiotics.

Etiology

Ascites can result from chronic, but not acute, liver diseases. More than 90% of hepatic cases result from portal hypertension, usually due to cirrhosis. Other hepatic causes, which are uncommon, include chronic hepatitis, severe alcoholic hepatitis without cirrhosis, and hepatic vein obstruction (Budd-Chiari syndrome). Portal vein thrombosis does not usually cause ascites unless hepatocellular damage is also present.

Nonhepatic causes include generalized fluid retention associated with systemic diseases (eg, heart failure, nephrotic syndrome, severe hypoalbuminemia, constrictive pericarditis) and peritoneal disorders (eg, carcinomatous or infectious peritonitis, biliary leak due to surgery or another medical procedure). Less common causes include renal dialysis, pancreatitis, SLE, and endocrine disorders (eg, myxedema).

Pathophysiology

Mechanisms are complex and incompletely understood. Factors include altered Starling's forces in the portal vessels (low oncotic pressure due to hypoalbuminemia plus increased portal venous pressure), avid renal Na retention (urinary Na concentration is typically < 5 mEq/L), and possibly increased hepatic lymph formation.

Mechanisms that appear to contribute to renal Na retention include activation of the renin-angiotensin-aldosterone system; increased sympathetic tone; intrarenal shunting of blood away from the cortex; increased formation of nitric oxide; and altered formation or metabolism of ADH, kinins, prostaglandins, and atrial natriuretic factor. Vasodilation in the splanchnic arterial circulation may be a trigger, but the specific roles and interrelationships of these abnormalities remain uncertain.

Spontaneous bacterial peritonitis (SBP) is infection of ascitic fluid without an apparent source. SBP is particularly common in cirrhotic ascites, especially in alcoholics. It can produce serious sequelae or death. The most common bacteria causing SBP are the gram-negative Escherichia coli and Klebsiella pneumoniae and the gram-positive Streptococcus pneumoniae ; usually only a single organism is involved.

Symptoms and Signs

Small amounts of ascitic fluid cause no symptoms. Moderate amounts cause increased abdominal girth and weight gain. Massive amounts may cause nonspecific diffuse abdominal pressure, but actual pain is uncommon. If ascites results in elevation of the diaphragm, dyspnea may occur. Symptoms of SBP may include new abdominal discomfort and fever.

Signs include shifting dullness on abdominal percussion and a fluid wave. Volumes <1500 mL may not produce physical findings. Massive ascites produces tautness of the abdominal wall and flattening of the umbilicus. In liver diseases or peritoneal disorders, ascites is usually isolated or disproportionate to peripheral edema; in systemic diseases (eg, heart failure), the reverse is usually true.

Signs of SBP may include fever, malaise, encephalopathy, worsening hepatic failure, and unexplained clinical deterioration. Peritoneal signs (eg, abdominal tenderness and rebound) are present but may be somewhat diminished by the presence of ascitic fluid.

Diagnosis

Diagnosis may be based on physical examination if there is a large amount of fluid, but imaging tests are more sensitive. Ultrasound and CT reveal much smaller volumes of fluid (100 to 200 mL) than does physical examination. SBP is suspected in a patient with ascites who also has abdominal pain, fever, or unexplained deterioration.

Diagnostic paracentesis (see Diagnostic and Therapeutic GI Procedures: Abdominal Paracentesis) should be performed if ascites is newly diagnosed, if its cause is unknown, or if SBP is suspected. About 50 to 100 mL of fluid is removed and analyzed for gross appearance, protein content, cell count and differential, cytology, culture, and, as clinically indicated, acid-fast stain and/or amylase. In contrast to ascites due to inflammation or infection, ascites due to portal hypertension produces fluid that is clear and straw-colored, has a low protein concentration (usually < 3 g/dL, but occasionally > 4 g/dL), a low PMN count (< 250 cells/μL), and, most reliably, a high serum-to-ascites albumin concentration, which is the serum albumin concentration minus the ascitic albumin concentration. Gradients > 1.1 g/dL suggest ascites due to portal hypertension. In ascitic fluid, turbidity and a PMN count > 500 cells/μL suggest infection, whereas bloody fluid usually signals a tumor or TB. The rare milky (chylous) ascites is most common with lymphoma.

Clinical diagnosis of SBP can be difficult; its diagnosis requires a high index of suspicion and liberal use of diagnostic paracentesis, including culture. Blood cultures are also indicated. Transferring ascitic fluid to blood culture media before incubation increases the sensitivity of culture to almost 70%. Because SBP usually results from a single organism, obtaining mixed flora on culture suggests a perforated abdominal viscus or contaminated specimen.

Treatment

(See also the American Association for the Study of Liver Disease's practice guideline Management of Adult Patients with Ascites Due to Cirrhosis.) Bed rest and dietary Na restriction (20 to 40 mEq/day) are the first, and least risky, treatments for ascites due to portal hypertension. Diuretics should be used if rigid Na restriction fails to initiate diuresis within a few days. Spironolactone is usually effective (in oral doses ranging from 50 to 200 mg bid). A loop diuretic (eg, furosemide 20 to 160 mg po usually once/day, or 20 to 80 mg po bid) should be added if spironolactone is insufficient. Because spironolactone can cause K retention and furosemide K depletion, the combination of these drugs often provides optimal diuresis with a lower risk of K abnormalities. Fluid restriction is helpful only if serum Na is < 130 mEq/L. Changes in body weight and urinary Na determinations reflect response to treatment. Weight loss of about 0.5 kg/day is optimal, because the ascitic compartment cannot be mobilized much more rapidly. More aggressive diuresis depletes fluid from the intravascular compartment, especially when peripheral edema is absent; this may cause renal failure or electrolyte imbalance (eg, hypokalemia) that may precipitate portal-systemic encephalopathy. Inadequate dietary Na restriction is the usual cause of persistent ascites.

Therapeutic paracentesis is an alternative. Removal of 4 L/day is safe, provided that salt-poor albumin (about 40 g/paracentesis) is concomitantly infused IV as needed to prevent intravascular volume depletion. Even single total paracentesis may be safe. Therapeutic paracentesis shortens the hospital stay with relatively little risk of electrolyte imbalance or renal failure; nevertheless, patients require ongoing diuretics and tend to reaccumulate fluid more rapidly than those treated without paracentesis.

Techniques for the autologous infusion of ascitic fluid (eg, the LeVeen peritoneovenous shunt) often produce complications and are generally no longer used. Transjugular intrahepatic portal-systemic shunting (TIPS) can lower portal pressure and successfully treat ascites resistant to other treatments, but TIPS is invasive and may produce complications, including portal-systemic encephalopathy and worsening hepatocellular function. (See also the American Association for the Study of Liver Disease's practice guideline The Role of Transjugular Intrahepatic Portosystemic Shunt in the Management of Portal Hypertension.)

If SBP is suspected and > 500 PMNs/μL of ascitic fluid are found, an antibiotic such as cefotaxime 2 g IV q 4 to 8 h (pending Gram stain and culture results) is given for at least 5 days, until ascitic fluid shows < 250 PMNs/μL. Antibiotics increase the chance of survival. Because SBP recurs within a year in up to 70% of patients, prophylactic antibiotics are indicated; quinolones (eg, norfloxacin 400 mg po once/day) are most widely used. Prophylaxis in ascitic patients with variceal hemorrhage decreases the risk of SBP.

Last full review/revision November 2005