Ascites is the accumulation of fluid in the peritoneal cavity. The most common causes of ascites are cirrhosis, peritoneal malignancy, and heart failure.

In patients with cirrhosis, ascites is one of the complications that marks the transition from a compensated to a decompensated stage. Initially, ascites is “uncomplicated,” that is, it responds well to diuretics and is not infected. As cirrhosis progresses and the mechanisms that lead to ascites formation worsen, ascites ceases to respond to diuretics (refractory ascites). Bacteria may infect ascites, an entity known as spontaneous bacterial peritonitis (SBP) that occurs mainly in hospitalized patients with severe liver disease. With further progression of cirrhosis, the patient with ascites may develop hyponatremia and functional renal failure (hepatorenal syndrome). The hemodynamic alterations that lead to ascites and refractory ascites are the same as those that lead to hyponatremia and hepatorenal syndrome, differing only in the degree of abnormality, with the latter complications denoting a more deranged circulatory status. The approach to a patient with ascites depends on the setting surrounding its presentation (Figures 59.1–59.19 and Tables 59.1–59.4).

Suspected ascites

In a patient with suspected ascites (by history and physical examination), the least invasive and most cost‐effective method to confirm the presence of ascites is abdominal ultrasonography. This test can be accompanied by doppler examination of the hepatic venous system, an important initial test to rule out the presence of hepatic vein obstruction, which is a frequently overlooked cause of ascites.

New‐onset ascites

In a patient with new‐onset ascites, the priority is to determine the etiology of ascites as this will determine its management. A diagnostic paracentesis should be the first test performed in such a patient. The serum‐ascites albumin gradient (SAAG) and the ascites total protein are two inexpensive tests that, taken together, are most useful. The three main causes of ascites (cirrhosis, peritoneal pathology [malignancy or tuberculosis], and heart failure) can be easily distinguished by combining the results of SAAG (a measure of sinusoidal pressure) and ascites total protein. In cirrhosis, the SAAG is high (>1.1 g/dL) and ascites protein is low (<2.5 g/dL); in peritoneal disease, the SAAG is low and ascites protein is high; in heart failure, both the SAAG and the ascites protein are high. The decisive test to determine the source of ascites (sinusoidal or not) is by measuring the hepatic venous pressure gradient. When the source is likely to be peritoneal (carcinomatosis or tuberculosis), the decisive test is a laparoscopy with peritoneal biopsy, culture, and histological examination.

Cirrhotic ascites

In a patient with cirrhotic ascites, management depends on the phase of ascites at which the patient with cirrhosis is situated, from the patient with uncomplicated ascites to the patient with hepatorenal syndrome.

Therapy of cirrhotic ascites is not an emergency as the risk of death is not implicit unless the fluid is infected. The mainstay of therapy is aimed at achieving a negative sodium balance (i.e., sodium restriction and diuretics). Sodium intake should be restricted to ~90 mEq (2 g) of sodium/day. Diuretic treatment should only be initiated in the patient with cirrhosis in whom complications, such as gastrointestinal (GI) hemorrhage, bacterial infection, and renal dysfunction, are absent or have resolved. In a patient with tense ascites who experiences not only abdominal discomfort but also respiratory distress, a single large‐volume paracentesis (LVP) should be performed prior, or concomitant to, starting diuretics.

Diuretic therapy should be spironolactone based, either with spironolactone alone (initial dose of 100 mg in a single daily dose, increased to a maximum of 400 mg/day) or in combination with furosemide (range 20–160 mg/day). Both schedules are equally effective but dose adjustments are needed more frequently in patients in whom treatment is initiated with combination therapy.

Before considering that ascites is refractory to diuretics, it is necessary to ascertain whether the patient has adhered to the prescribed sodium‐restricted diet and has restrained from using nonsteroidal antiinflammatory drugs.

Refractory ascites

First‐line therapy for patients with refractory ascites is serial LVP, adding albumin (6–8 g/L of ascites removed) if more than 5 L are removed at once. To increase the time between paracenteses, patients should continue on the maximally tolerated diuretic dose provided that the urinary sodium is >30 mEq/L. In patients requiring LVP every 3 weeks or so or in those in whom ascites is loculated and cannot be entirely removed with a single LVP, evaluation for transjugular intrahepatic portosystemic shunt (TIPS) placement should be undertaken. In general, TIPS should not be performed in patients with age >70 years, Child–Turcotte–Pugh (CTP) score >12, serum bilirubin >6 mg/dL, evidence of heart failure or pulmonary hypertension and those with recurrent overt encephalopathy, as these factors are associated with poorer survival and poorer shunt function. Patients with refractory ascites who seem to benefit most from TIPS are those with a Model for End‐Stage Liver Disease (MELD) score of around 12. Covered TIPS stents should be used as they have been associated with an increased survival in these patients. In patients who are requiring frequent LVP and who are not TIPS candidates, a peritoneovenous shunt (PVS) may be considered.