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Information ⬇

Author(s): Ben Warner and Mark Wilkinson

Ascites is the accumulation of fluid within the peritoneal cavity. Assessment and management of the patient with ascites is summarized in Figure 24.1. The clinical features, together with findings on diagnostic paracentesis (of which the serum-to-ascites albumin gradient is of particular importance), will narrow the differential diagnosis and direct further investigation.

Priorities ⬆ ⬇

  • Perform a diagnostic aspirate (30–50 mL) immediately on admission for new-onset ascites or if there is evidence of sepsis. The technique of diagnostic paracentesis is described in Box 24.1 Diagnostic tests on ascitic fluid are summarized in Table 24.1.
  • If there is clinical or radiological evidence of cirrhosis, the cause of decompensation must be identified and treated: see Chapter 77.
  • The management of spontaneous bacterial peritonitis is summarized in Appendix 24.1.
  • Budd-Chiari syndrome is suspected in patients who present with sudden onset ascites in the absence of a known chronic liver disease. Presentation can range from asymptomatic to fulminant liver failure. Similarly, portal vein thrombosis can be asymptomatic, but typically presents with abdominal pain or features of portal hypertension such as varices or ascites. It is more common in patients with known chronic liver disease or who are in a hypercoagulable state. Duplex ultrasonography can be done if these are suspected, although CT and MRI are more diagnostic.
  • Ascites may complicate cardiac disease (severe tricuspid regurgitation, other causes of right-sided heart failure, and constrictive pericarditis). If the jugular venous pressure is raised, or there are other features of heart disease, check plasma BNP/NT-proBNP and arrange echocardiography.
  • Nephrotic syndrome as the cause of ascites can be confirmed or excluded by measurement of urinary protein excretion on a 24-hour urine collection (>3.5g/day is nephrotic-range proteinuria) or by calculating the albumin-to-creatinine ratio (ACR) in a spot urine sample (ACR is usually >220 mg/mmol in nephrotic syndrome).

Further Management of Ascites Due to Cirrhosis

In all patients with ascites, avoid nephrotoxic drugs, including NSAIDs, ACE inhibitors and α-adrenergic blockers.

Grade 1 or 2 (mild or moderate) ascites

Unless the ascites is new or complicated, both of these grades of ascites can be managed as an outpatient.

Restrict dietary sodium intake to 80–120 mmol/day.

Start diuretic therapy with spironolactone 100 mg daily and increase by 100 mg weekly with monitoring of electrolytes and creatinine to a maximum of 400 mg daily. If spironolactone resistant, add in furosemide 40 mg daily and increase weekly by 40 mg to a maximum of 160 mg with biochemical monitoring.

Monitor daily weight. Target weight loss is 0.5kg daily in patients without peripheral oedema and 1kg daily in those with peripheral oedema.

Aim for the minimum dose of diuretics once ascites has resolved.

Complications from diuretics include gynaecomastia (amiloride 10–40 mg daily can be substituted for spironolactone), renal failure, hyperkalaemia (either reduce the spironolactone or add in furosemide), and encephalopathy. Stop diuretics if plasma sodium levels fall below 120 mmol/L as this may be consistent with diuretic-induced hypovolaemic hyponatraemia (Chapter 85).

Grade 3 (large volume) ascites, or diuretic-resistant ascites

Severe ascites can cause breathlessness and this can be alleviated by paracentesis. If there is tense ascites, consider a single paracentesis, followed by dietary sodium restriction and diuretic therapy. Human albumin solution (100 mL of 20% HAS per 2L of ascites removed) should be given IV during paracentesis. Seek advice from a hepatologist.

In the case of diuretic-resistant ascites and where the urinary sodium concentration remains below 30 mmol/L, the patient should be referred for a transjugular intrahepatic portosystemic shunt (TIPS) or consideration of liver transplantation.

Further Reading ⬆

Hernaez R, Hamilton JP. (2016) Unexplained ascites. Clinical Liver Disease 7, 53–56. http://onlinelibrary.wiley.com/doi/10.1002/cld.537/full.

Pericleous M, Sarnowski A, Moore A, Fijten R, Zaman M. (2016). The clinical management of abdominal ascites, spontaneous bacterial peritonitis and hepatorenal syndrome: a review of current guidelines and recommendations. Eur J Gastroenterol Hepatol , 28, e10–18.

Solà E, Solé C, Ginès P. (2016) Management of uninfected and infected ascites in cirrhosis. Liver Int 36 (suppl 1), 109–115.