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Ascites: causes, symptoms, diagnosis, treatment
Last reviewed: 12.07.2025
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Ascites is a condition in which free fluid accumulates in the abdominal cavity. Most often, the cause is portal hypertension. The main symptom of ascites is an increase in the size of the abdomen.
Diagnosis is based on physical examination, ultrasonography, or CT. Treatment of ascites includes bed rest, a sodium-restricted diet, diuretics, and therapeutic paracentesis. Ascitic fluid may become infected (spontaneous bacterial peritonitis), which is often accompanied by pain and fever. Diagnosis of ascites involves examination and culture of ascitic fluid. Treatment of ascites is based on antibacterial therapy.
What causes ascites?
Ascites is usually a manifestation of (portal) hypertension (>90%) resulting from chronic liver disease leading to cirrhosis. Other causes of ascites are less common and include chronic hepatitis, severe alcoholic hepatitis without cirrhosis, and hepatic vein obstruction (Budd-Chiari syndrome). Portal vein thrombosis does not usually cause ascites unless the hepatocellular structure of the liver is affected.
Extrahepatic causes of ascites include generalized fluid retention associated with systemic diseases (eg, heart failure, nephrotic syndrome, severe hypoalbuminemia, constrictive pericarditis) and intra-abdominal diseases (eg, carcinomatosis or bacterial peritonitis, bile leakage after surgery or other medical procedures). Less common causes include renal dialysis, pancreatitis, systemic lupus erythematosus, and endocrine disorders (eg, myxedema).
Pathophysiology of ascites
The mechanism of ascites development is complex and not fully understood. Known factors include altered portal venous Sterling pressure (low oncotic pressure due to hypoalbuminemia and elevated portal venous pressure), active renal sodium retention (normal urinary sodium concentration < 5 mEq/L), and possibly increased hepatic lymph formation.
Mechanisms influencing renal sodium retention include activation of the renin-angiotensin-aldosterone system; increased sympathetic tone; intrarenal shunting of blood past the cortex; increased nitric oxide production; and altered production and metabolism of antidiuretic hormone, kinins, prostaglandins, and atrial natriuretic peptide. Vasodilation of splanchnic arterial blood flow may be a trigger, but the significance of these disturbances and the relationships between them remain poorly understood.
Spontaneous bacterial peritonitis (SBP) is associated with infection of ascitic fluid without an obvious source. Spontaneous bacterial peritonitis usually occurs in cirrhotic ascites, is particularly common in alcoholics, and is often fatal. It can cause severe complications and death. Spontaneous bacterial peritonitis is most often caused by the gram-negative bacteria Escherichia coli and Klebsiella pneumoniae, and the gram-positive Streptococcus pneumoniae; typically, only one organism is cultured from the ascitic fluid.
Symptoms of ascites
A small amount of ascitic fluid does not cause symptoms. A moderate amount leads to an increase in abdominal volume and body weight. A large amount leads to non-specific diffuse abdominal tension without pain. If ascites compresses the diaphragm, shortness of breath may occur. Symptoms of spontaneous bacterial peritonitis may be accompanied by a feeling of abdominal discomfort and fever.
Objective signs of ascites include shifting dullness to abdominal percussion and fluctuation. Fluid volumes less than 1500 mL may not be detected by physical examination. Large ascites cause abdominal wall tension and protrusion of the umbilicus. In liver disease or peritoneal involvement, ascites is usually unrelated to or disproportionate to peripheral edema; in systemic diseases (eg, heart failure), peripheral edema is more pronounced.
Symptoms of spontaneous bacterial peritonitis may include fever, malaise, encephalopathy, worsening liver failure, and unexplained clinical deterioration. Peritoneal signs of ascites (eg, abdominal tenderness and the Shchetkin-Blumberg sign) may appear but may be obscured by the presence of ascitic fluid.
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Diagnosis of ascites
The diagnosis can be made based on physical examination if there is a significant amount of fluid, but instrumental studies are more informative. Ultrasonography and CT can detect a significantly smaller volume of fluid (100-200 ml) compared to physical examination. Suspicion of spontaneous bacterial peritonitis arises when a patient with ascites has abdominal pain, fever, or unexplained deterioration in condition.
Diagnostic dye laparocentesis is indicated when ascites is new, the cause is unknown, or spontaneous bacterial peritonitis is suspected. Approximately 50–100 mL of fluid is withdrawn for gross evaluation, protein content, cell count and differentiation, cytology, culture, and, if clinically indicated, Ziehl-Neelsen staining and/or amylase testing. In contrast to ascites from inflammation or infection, ascitic fluid from portal hypertension appears 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 a higher serum-to-ascitic albumin concentration gradient, which is defined as the difference between the serum albumin concentration and the ascitic albumin concentration (more informative). A gradient greater than 1.1 g/dL indicates that portal hypertension is the most likely cause of ascites. Turbid ascitic fluid and a PMN count greater than 500 cells/μL indicate infection, whereas hemorrhagic fluid is usually a sign of tumor or tuberculosis. Milky (chylous) ascites is rare and is usually associated with lymphoma.
Clinical diagnosis of spontaneous bacterial peritonitis can be difficult; its verification requires a thorough examination and mandatory diagnostic laparocentesis, including bacteriological culture of the fluid. Bacteriological blood culture is also indicated. Inoculation of ascitic fluid for blood culture before incubation increases sensitivity by almost 70%. Since spontaneous bacterial peritonitis is usually caused by a single microorganism, detection of mixed flora in bacteriological culture may suggest perforation of a hollow organ or contamination of the examined material.
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Treatment of ascites
Bed rest and a sodium-restricted diet (20-40 mEq/day) are the primary and least safe treatments for ascites in portal hypertension. Diuretics should be used if strict sodium restriction does not result in adequate diuresis within a few days. Spironolactone (50-200 mg orally, on average, twice daily) is usually effective. If spironolactone is ineffective, a loop diuretic (eg, furosemide 20-160 mg orally, usually once daily or on average 20-80 mg twice daily) may be added. Because spironolactone can cause potassium retention and furosemide can cause excess potassium excretion, the combination of these drugs often provides optimal diuresis with little risk of hyper- or hypokalemia. Fluid restriction is beneficial, but only if the serum Na level is less than 130 mEq/L. Changes in body weight and urinary sodium reflect the effectiveness of treatment. A loss of approximately 0.5 kg/day is optimal, since ascites accumulation cannot be more intense. Greater diuresis reduces intravascular fluid volume, especially in the absence of peripheral edema; this may cause renal dysfunction or electrolyte imbalance (eg, hypokalemia), which may accelerate the development of portosystemic encephalopathy. Inadequate dietary sodium restriction is usually the cause of persistent ascites.
An alternative is therapeutic laparocentesis. Removal of 4 L of ascitic fluid per day is safe, provided that low-salt albumin (about 40 g per procedure) is given intravenously to prevent fluid from leaving the vascular bed. Therapeutic laparocentesis shortens the hospital stay with a relatively small risk of electrolyte imbalance or renal dysfunction; however, patients require continued diuretics, and ascites may recur much more quickly than without laparocentesis.
The technique of autologous ascitic fluid infusion (eg, LeVeen peritoneovenous shunt) is often associated with complications and is generally no longer used. Transjugular intrahepatic portal-systemic shunting (TIPS) can reduce portal pressure and effectively resolve ascites refractory to other treatments, but carries significant risks and can lead to complications including portosystemic encephalopathy and deterioration of hepatocellular function.
If spontaneous bacterial peritonitis is suspected and ascitic fluid levels are greater than 500 PMN/μL, an antibiotic such as cefotaxime 2 g IV every 4 to 8 hours (Gram stain and culture) should be given for at least 5 days until ascitic fluid levels are less than 250 PMN/μL. Antibiotics increase the likelihood of survival. Because spontaneous bacterial peritonitis recurs within 1 year in 70% of patients, antibacterial prophylaxis is indicated; quinolones (eg, norfloxacin 400 mg/day orally) are the most widely used. Prophylactic antibiotics in patients with ascites and variceal bleeding reduce the risk of spontaneous bacterial peritonitis.