> Table of Contents > Ascites
Daniel J. Stein, MD, MPH
Stephen K. Lane, MD, FAAFP
image BASICS
  • Accumulation of fluid in the peritoneal cavity; may occur in conditions that cause generalized edema.
  • Men generally have no fluid in peritoneal cavity; women may have up to 20 mL depending on menstrual phase.
  • Ascites comes from Greek word askos (bag).
  • Children: nephrotic syndrome and malignancy most common
  • Adults: cirrhosis (81%), cancer (10%), heart failure (3%), other (6%)
˜ 50-60% of patients with cirrhosis will develop ascites within 10 years (1).
10% of patients with liver cirrhosis have ascites.
Portal hypertensive versus nonportal hypertensive etiologies
  • Cannot reliably establish/confirm etiology without paracentesis
  • Serum-ascites albumin gradient (SAAG), which is the (serum albumin level) - (ascites albumin level) differentiates causes
High portal pressure (SAAG ≥1.1)
  • Cirrhosis
  • Hepatitis (alcoholic, viral, autoimmune, medications)
  • Acute liver failure
  • Liver malignancy (primary or metastatic)
  • Elevated right-sided filling pressures from heart failure or constrictive pericarditis
  • Hepatic venous thrombosis (Budd-Chiari syndrome)
  • Portal vein thrombosis
Normal portal pressure (SAAG <1.1)
  • Peritoneal carcinomatosis
  • Tuberculosis
  • Severe hypoalbuminemia (nephrotic syndrome; severe enteropathy with protein loss)
  • Meigs syndrome (ovarian cancer)
  • Lymphatic leak (chylous ascites)
  • Pancreatitis
  • Inflammatory (vasculitis, lupus serositis, sarcoidosis)
  • Other infections (parasitic, fungal)
  • Hemoperitoneum from trauma or ectopic pregnancy
Pathophysiology of ascites is partially understood. It is best described for portal hypertensive (typically cirrhotic) ascites
  • Most ascites is due to portal hypertension, with preferentially dilated splanchnic vasculature causing systemic hypotension.
  • Reduced renal and carotid perfusion activates systemic vasoconstrictors and antinatriuretic mechanisms. This stimulates the sympathetic nervous system and renin-angiotensin-aldosterone system, culminating in sodium and water retention ascites and edema.
  • Abdominal distention, flank dullness, shifting dullness, and puddle splash are most sensitive (83%) and specific (56%) exam findings (1).
  • Edema (penile/scrotal, pedal), pleural effusion, rales
  • Stigmata of cirrhosis (palmar erythema, spider angiomata, dilated abdominal wall collateral veins)
  • Other signs of advanced liver disease: jaundice, muscle wasting, gynecomastia, leukonychia
  • Signs of underlying malignancy: cachexia; umbilical (Virchow) node suggests upper abdominal malignancy.
Initial Tests (lab, imaging)
  • Diagnostic paracentesis for fluid analysis should be obtained in all patients with ascites requiring hospital admission and in any new-onset or new-to-treatment patients with ascites (1)[C] to determine etiology and rule out infection.
    • Paracentesis has a complication rate of 1% (despite high prevalence of coexisting coagulation abnormalities). Routine attempts to correct platelet or coagulation defects are not needed (1)[B].
    • Ascitic fluid analysis should include (1)[C]:
      • Cell count and differential:
        • Polymorphonuclear leukocytes ≥250 cells/mm3 suggests infection.
      • Albumin level to calculate SAAG:
        • <1.1 g indicates a low portal pressure exudative process (i.e., inflammatory, biliary/pancreatic, carcinomatosis, TB)
        • ≥1.1 g indicates portal hypertensive/transudative process (cirrhosis, CHF, constrictive pericarditis, thrombosis)
      • Total protein (low in cirrhosis, nephrotic disease, and high in cardiac ascites. Cutoff approximately 25 g/L)
    • Other tests based on clinical scenario (1)[C]:
      • Bacterial gram stain/culture, if infection suspected (cirrhotic patients with ascites can fail to mount adequate fever or significant leukocytosis)
        • Fluid cultures are positive in 50-90% of cases of SBP.
        • Yield improved if inoculated to blood culture bottles at bedside and obtained before first dose of antibiotics.
      • Amylase (suspicion for bowel perforation, choledocholithiasis, or pancreatitis)
      • Triglyceride if fluid appears milky
      • Cytology if concern for malignancy (less sensitive in the absence of carcinomatosis)
      • Lactate dehydrogenase (LDH): An ascitic fluid-to-serum LDH ratio >1.0 can indicate infection, perforation, or tumor.
      • Carcinoembryonic antigen and alkaline phosphatase (elevated in viscous perforation)
  • Myobacterial culture/TB complex PCR for suspicion of tuberculosis.
  • Blood tests: BUN/creatinine, electrolytes (renal function)
    • Brain natriuretic peptide (heart failure)
    • Liver function tests and hepatitis serologies (hepatitis)
    • Albumin (needed for SAAG)
  • Abdominal ultrasound can confirm ascites; highly sensitive, cost-effective, involves no radiation
  • Portal Doppler can be obtained with ultrasound as first line to evaluate for thrombosis or cirrhosis.
  • CT scan to rule out intra-abdominal pathology (e.g., malignancy)
  • MRI preferred for evaluation of liver disease or confirmation of portal vein thrombosis
Diagnostic Procedures/Other
Laparoscopy: preferred if imaging and paracentesis are nondiagnostic
  • Allows for direct visualization and biopsy of peritoneum, liver, and intra-abdominal lymph nodes
  • Preferred for evaluating suspected peritoneal tuberculosis or malignancies
Test Interpretation
Cytology may reveal malignant cells: adenocarcinoma (ovary, breast, GI tract) or primary peritoneal carcinoma (most commonly associated with ascites)
For all patients:
  • Daily weight
  • Restrict dietary sodium to ≤2 g/day if the cause is due to portal hypertension (high SAAG) (1)[A].
  • Water restriction (1 to 1.5 L/day) only necessary if serum sodium <120 to 125 mEq/L (1)[C]
  • Creatinine >2.0 mg/dL: decrease diuretic doses, peritoneal paracentesis
  • Avoid alcohol and ensure adequate nutrition if liver disease (1)[A].
  • Baclofen may be used to reduce alcohol craving/consumption (1)[C].
First Line
  • Sodium restriction and diuretics are the mainstay of treatment for patients with elevated portal pressures (1)[A]; other causes (e.g. carcinomatosis) are less likely to respond to medical therapy.
    • Spironolactone 100 to 400 mg daily PO; typical initial dose is 100 to 200 mg given in AM
      • Diuretic of choice due to its antialdosterone effects; can be used as single agent in patients with minimal ascites
    • P.85

    • Furosemide 40 to 160 mg daily PO (avoid IV if possible); typical initial dose is 40 mg given in AM
      • Antinatriuretic effect helps to achieve negative sodium balance.
      • Not first-line as monotherapy but is an effective adjunct to potentiate the effect of spironolactone
    • Most common (and preferred) regimen is spironolactone and furosemide together (maintaining a 100:40 ratio) for maximum efficacy and to maintain potassium homeostasis.
      • Titrate dose to desired result and monitor renal function regularly.
      • Follow daily weight.
  • Diuretic-intractable ascites (10% of patients): persistent or worsening ascites despite maximum doses of spironolactone (400 mg/day) and furosemide (160 mg/day) and sodium restriction or progressive rise in creatinine to 2.0
    • Ensure compliance with dietary sodium restriction using 24-hour urine sodium excretion: in general, if <78 mEq/day, patient is compliant with 2-g dietary sodium restriction.
    • Therapeutic paracentesis or serial large-volume paracentesis (LVP) (see “Surgery/Other Procedures”)
Second Line
  • Midodrine 7.5 mg TID can be added to diuretic resistant or hypotensive patients and may improve survival (1)[B].
  • Alternatives to spironolactone: amiloride up to 40 mg/day; triamterene up to 200 mg/day in divided doses (1)[C]
  • Alternatives to furosemide: torsemide up to 100 mg/day; bumetanide up to 4 mg per day (1)[C]
  • Vaptans may have a beneficial effect on hyponatremia and ascites, but routine use in ascites is not yet supported (2)[A].
Consider referral for liver transplant in patients with decompensated liver disease, whether or not ascites is present/controlled. Liver transplant is the definitive treatment for portal hypertension (1)[B].
  • Therapeutic paracentesis
    • Initial therapy if tense ascites is present (1)[C].
    • Serial (generally every 2 weeks) paracentesis can be used as second-line after diuretics in patients with elevated portal pressures (3)[B].
    • Complications: infection, hemodynamic collapse, acute renal failure
    • Similar complication rate as diuretics (3)[B]
    • Replace albumin when removing >5 L of ascites: 5.5 to 8 g albumin for each liter removed has been shown to decrease renal dysfunction, hyponatremia post paracentesis, and overall morbidity (4)[A] for patients with portal hypertension; likely not needed for malignant ascites
    • Continue diuretics at 1/2 previous dose if transitioning to serial paracentesis in patients who fail diuretics alone.
  • Transjugular intrahepatic portosystemic shunt (TIPS)
    • Used only in patients with elevated portal pressures
    • Fluoroscopically placed conduit from portal to hepatic vein for intractable ascites (5)[A]
      • At time of placement, portal pressure should drop ≥20 mm Hg or to <12 mm Hg, and ascites should be readily controlled with diuretics.
      • Yearly US to confirm shunt is functional.
      • 4 weeks after TIPS, urinary sodium and serum creatinine improve significantly and can normalize after 6 to 12 months in combination with diuretics (5). Dilation/replacement may be needed after 2 years.
      • Encephalopathy is a primary complication.
      • TIPS is superior to paracentesis for controlling ascites. No difference in mortality (5)[A].
  • Peritoneovenous shunt (LeVeen or Denver shunt): drains ascites directly into the inferior vena cava
    • Clinical trials show poor long-term shunt patency, no survival advantage compared with medical therapy.
    • Complications include:
      • Bacteremia, bowel obstruction, and variceal bleed as a result of rapid volume overload from ascitic fluid into systemic circulation
      • Usually reserved for patients with refractory ascites who are not candidates for TIPS or liver transplant, and who have numerous abdominal adhesions, making repeated paracentesis unsafe (1)[A].
  • Indwelling catheters with external drainage
    • Most useful in malignant ascites as a palliative measure
    • Overall low rate of infection
    • Can be drained at home
  • Percutaneous endoscopic gastrostomy should be avoided in patients with ascites due to an associated high mortality rate following this procedure (1)[B].
Caution advices with many herbal and other dietary supplements (risk drug interactions, hepatotoxicity, coagulopathy)
  • Prognosis varies depending on underlying cause.
  • Ascites in itself is rarely life threatening but can signify life-threatening disease (e.g., cancer, end-stage liver disease)
1. Runyon BA. Management of adult patients with ascites due to cirrhosis: update 2012. http://www.aasld.org/sites/default/files/guideline_documents/adultascitesenhanced.pdf. Accessed May 5, 2015.
2. Watson H, Jepsen P, Wong F, et al. Satavaptan treatment for ascites in patients with cirrhosis: a metaanalysis of effect on hepatic encephalopathy development. Metab Brain Dis. 2013;28(2):301-305.
3. Ginés P, Arroyo V, Quintero E, et al. Comparison of paracentesis and diuretics in the treatment of cirrhotics with tense ascites. Results of a randomized study. Gastroenterology. 1987;93(2):234-241.
4. Bernardi M, Caraceni P, Navickis RJ, et al. Albumin infusion in patients undergoing large-volume paracentesis: a meta-analysis of randomized trials. Hepatology. 2012;55(4):1172-1181.
5. Rössle M, Gerbes AL. TIPS for the treatment of refractory ascites, hepatorenal syndrome and hepatic hydrothorax: a critical update. Gut. 2010;59(7):988-1000.
6. Fernández J, Navasa M, Planas R, et al. Primary prophylaxis of spontaneous bacterial peritonitis delays hepatorenal syndrome and improves survival in cirrhosis. Gastroenterology. 2007;133(3):818-824.
Additional Reading
  • Becker G, Galandi D, Blum HE. Malignant ascites: systematic review and guideline for treatment. Eur J Cancer. 2006;42(5):589-597.
  • Perumalswami PV, Schiano TD. The management of hospitalized patients with cirrhosis: the Mount Sinai experience and a guide for hospitalists. Dig Dis Sci. 2011;56(5):1266-1281.
See Also
  • Cirrhosis of the Liver; Hepatorenal Syndrome
  • Algorithms: Congestive Heart Failure: Differential Diagnosis; Nephrotic Syndrome
  • R18.8 Other ascites
  • R18.0 Malignant ascites
  • K70.31 Alcoholic cirrhosis of liver with ascites
Clinical Pearls
  • Cirrhosis remains the most common cause of ascites.
  • Patients with new-onset ascites or hospitalized patients with ascites should have a diagnostic paracentesis.
  • ACE inhibitors, ARBs, and β-blockers should be avoided in patients with ascites.
  • Most common cause of “diuretic-intractable ascites” is noncompliance with dietary sodium restriction.
  • First-line management of ascites is diuretics. Serial paracentesis or TIPS are second-line therapies.
  • Ensure early referral of cirrhosis patients who are potential candidates for liver transplant.