Ascites

Background

• Ascites is a pathologic accumulation of fluid in the peritoneal cavity most often caused by cirrhosis, but other causes include malignancy, nephrotic syndrome, heart failure, malnutrition, and infections such as peritoneal tuberculosis.
• Ascites results from an osmotic pressure imbalance which may occur with increased resistance to portal blood flow, hypoalbuminemia, and/or sodium intake exceeding excretion.

Evaluation

• Clinical diagnosis based on symptoms and signs is not well established to diagnose or rule out ascites.
  • Large-volume ascites may be clinically evident on physical exam (increased abdominal girth, fluid wave, and shifting dullness).
• Consider ultrasound for equivocal diagnosis and for assessing the liver for cirrhosis, signs of portal hypertension (such as splenomegaly), tumors, and portal or hepatic vein thrombosis (Weak recommendation).
• Perform diagnostic paracentesis on patients with new-onset moderate (grade 2) or large (grade 3) ascites (Strong recommendation) or in patients hospitalized for decompensated liver disease.
  • Assess ascitic fluid for cell count with differential, total protein, and albumin (Strong recommendation).
  • The serum-ascites albumin gradient correlates directly with portal pressures.
    • A SAAG gradient ≥ 1.1 g/dL suggests portal hypertension, most likely due to cirrhosis. Other causes include venous congestion such as from right sided heart failure.
    • A SAAG gradient < 1.1 g/dL suggests other causes of ascites such as peritoneal carcinomatosis, chronic peritoneal infection, nephrotic syndrome, pancreatic ascites, and protein-losing enteropathy.
    • Myxedema associated ascites in hypothyroidism may have high or low SAAG.
    • Consider lactate dehydrogenase (LDH) and cytology if concerned about malignancy, and other studies as indicated by the probability of disease (Weak recommendation).
    • Order Gram stain, culture, and glucose if concerned about infection prior to initiating antibiotics (Strong recommendation).
  • Laboratory evaluation may include serum electrolytes, renal function, hepatic function, albumin, coagulation tests, complete blood count, and 24-hour urinary protein and sodium.

Management

• Recommend sodium restriction in diet (reducing added salt and improved awareness of high sodium content in many pre-packaged and canned foodstuffs) (Strong recommendation) along with cessation of alcohol use if hepatic etiology (Strong recommendation).
• Treat ascites with a SAAG gradient of ≥ 1.1 g/dL with diuretics along with moderate sodium restriction in patients with cirrhosis (Strong recommendation).
  • Consider starting with spironolactone 100 mg once daily, and adding furosemide 40 mg orally once daily in patients with edema (Weak recommendation).
  • Consider increasing doses every 3-5 days if weight loss and natriuresis is inadequate, up to spironolactone 400 mg/day and furosemide 160 mg/day (Weak recommendation).
  • Consider withholding furosemide if there is hyponatremia and decreasing dose of spironolactone if there is hyperkalemia (Weak recommendation). Consider withholding diuretics if renal insufficiency develops.
• Treat ascites with a SAAG gradient of <1.1 g/dL by addressing the underlying etiology as diuretics are often ineffective and may lead to volume depletion.
• To treat or prevent bacterial peritonitis:
  • Use empiric antibiotic therapy (such as cefotaxime 2 g IV every 8 hours) for patients with polymorphonuclear leukocyte counts in ascites of ≥ 250 cells/mm³ or signs of infection (Strong recommendation).
  • Use short-term (7 day) antibiotic prophylaxis for patients with cirrhosis and active upper gastrointestinal bleeding (Strong recommendation).
  • Consider long-term antibiotic prophylaxis for patients with cirrhosis and ascites if the ascitic fluid protein level < 1.5 g/dL (15 g/L) and there is impaired renal function (Cr>1.2 mg/dL, BUN>25 mg/dL, or Na<130 mmol/L) or liver failure (Child score ≥9 and bilirubin ≥3 mg/dl) (Weak recommendation).
  • Consider long-term antibiotic secondary prophylaxis for patients with cirrhosis and a previous episode of spontaneous bacterial peritonitis.
• Perform therapeutic large volume paracentesis for large ascites with marked abdominal distension (Strong recommendation).
• Consider albumin (6-8 g/L ascitic fluid removed) (Strong recommendation if > 5 L removed, Weak recommendation if < 5 L removed). Limit albumin dose to ≤ 1.5 g/kg/day.
• Consider transjugular intrahepatic portosystemic shunt (TIPS) for ascites or associated hydrothorax that is not responsive to sodium restriction and diuretic therapy, or patients who require paracentesis more than once every two weeks.
  • TIPS increases the risk of hepatic encephalopathy.
  • TIPS may not be appropriate in patients with a cardiac ejection fraction < 60% or diastolic dysfunction, portopulmonary hypertension, renal parenchymal disease, hemodialysis, hepatocellular carcinoma, repeated episodes of hepatic encephalopathy, or complete portal vein thrombosis.
• Consider liver transplant evaluation for patients with cirrhosis and ascites, with expedited evaluation if there is worsening renal dysfunction or rapid liver decompensation (Weak recommendation).
• For refractory ascites, consider discontinuation of beta blockers (Weak recommendation) and refer for liver transplant evaluation (Strong recommendation).
• Patients with hemorrhagic ascites may require immediate hemodynamic stabilization followed by identification and control of peritoneal bleeding.