Definition and Etiology

Ascites is defined as the accumulation of fluid in the peritoneal cavity. It is a common clinical finding, with various extraperitoneal and peritoneal causes (Box 1), but it most often results from liver cirrhosis. The development of ascites in a cirrhotic patient generally heralds deterioration in clinical status and portends a poor prognosis.

Prevalence

Ascites is the most common major complication of cirrhosis and is an important landmark in the natural history of chronic liver disease. If observed for 10 years, approximately 60% of patients with cirrhosis develop ascites requiring therapy.

Pathophysiology

Cirrhotic ascites forms as the result of a particular sequence of events. Development of portal hypertension is the first abnormality to occur. As portal hypertension develops, vasodilators are locally released. These vasodilators affect the splanchnic arteries and thereby decrease the effective arterial blood flow and arterial pressures. The precise agent(s) responsible for vasodilation is a subject of wide debate; however, most the recent literature has focused on the likely role of nitric oxide.

Progressive vasodilation leads to the activation of vasoconstrictor and antinatriuretic mechanisms, both in an attempt to restore normal perfusion pressures. Mechanisms involved include the renin-angiotensin system, sympathetic nervous system, and antidiuretic hormone (vasopressin). The ultimate effect is sodium and water retention. In the late stages of cirrhosis, free water accumulation is more pronounced than the sodium retention and leads to a dilutional hyponatremia. This explains why cirrhotic patients with ascites demonstrate urinary sodium retention, increased total body sodium, and dilutional hyponatremia, a challenging concept for many physicians.

Signs and Symptoms

The symptoms of ascites vary from patient to patient and largely depend on the quantity of fluid. If trace ascites is present, the patient may be asymptomatic and fluid can be detected only on physical or radiologic examination. If a large amount of fluid is present, the patient might complain of abdominal fullness, early satiety, abdominal pain, or shortness of breath.

Physical examination findings are equally variable. The accuracy of detecting ascites depends on the amount of fluid present and the body habitus of the patient: ascites may be more technically difficult to diagnose in obese patients. If ascites is present, typical findings include generalized abdominal distention, flank fullness, and shifting dullness. If the physical examination is not definitive, abdominal ultrasonography can be used to confirm the presence or absence of ascites.

Two grading systems for ascites have been used in the literature (Table 1). An older system has graded ascites from 1+ to 4+, depending on the detectability of fluid on physical examination. More recently, a different grading system has been proposed, from grade 1 to grade 3. The validity of this grading system has yet to be established.

Table 1 Grading Systems for Ascites

Diagnosis

If a noncirrhotic patient develops ascites, diagnostic paracentesis with ascites fluid analysis is an essential part of the medical evaluation. In a patient with well-established cirrhosis, the exact role of a diagnostic paracentesis is less clear. Our opinion is that for a highly functional outpatient with documented cirrhosis, the new development of ascites does not routinely require paracentesis. Cirrhotic patients should, however, undergo paracentesis in the case of unexplained fever, abdominal pain, or encephalopathy or if they are admitted to the hospital for any cause. It is common for hospitalized cirrhotic patients to have infected ascites fluid (spontaneous bacterial peritonitis, SBP) even if no symptoms are present. This is particularly true in the case of a significant gastrointestinal hemorrhage.

Complications from abdominal paracentesis are rare, occurring in less than 1% of cases. A low platelet count or elevated prothrombin time is not considered a contraindication, and prophylactic transfusion of platelets or plasma is almost never indicated. Insertion of the paracentesis needle is most commonly performed in the left or right lower quadrant, but it can also be performed safely in the midline. An abdominal ultrasound can guide the procedure if the fluid is difficult to localize or if initial attempts to obtain fluid are unsuccessful.

Valuable clinical information can often be obtained by gross examination of the ascites fluid (Table 2). Uncomplicated cirrhotic ascites is usually translucent and yellow. If the patient is deeply jaundiced, the fluid might appear brown. Turbidity or cloudiness of the ascites fluid suggests that infection is present and further diagnostic testing should be performed. Pink or bloody fluid is most often caused by mild trauma, with subcutaneous blood contaminating the sample. Bloody ascites is also associated with hepatocellular carcinoma or any malignancy-associated ascites. Milky-appearing fluid usually has an elevated triglyceride concentration. Such fluid, commonly referred to as chylous ascites, can be related to thoracic duct injury or obstruction or lymphoma, but it is often related primarily to cirrhosis.

Table 2 Gross Appearance of Ascites Fluid

Many ascites fluid tests are currently available, yet the optimal testing strategy has not been well established. Generally, if uncomplicated cirrhotic ascites is suspected, only a total protein and albumin concentration and a cell count with differential are determined (Box 2). Less than 10 mL of fluid is required to perform these basic tests. The albumin concentration is used to confirm the presence of portal hypertension by calculating the serum-to-ascites albumin gradient, or SAAG. The SAAG is determined by subtracting the ascites albumin value from a serum albumin value obtained on the same day:

The SAAG has been proved in prospective studies to categorize ascites better than any previous criteria. The presence of a gradient higher than 1.1 g/dL indicates that the patient has portal hypertension–related ascites with 97% accuracy. Portal hypertension is usually caused by liver cirrhosis or, less commonly, outflow obstruction from right-sided heart failure or Budd-Chiari syndrome. A SAAG value lower than 1.1 g/dL indicates that the patient does not have portal hypertension–related ascites, and another cause of the ascites should be sought. Determination of the SAAG does not need to be repeated after the initial measurement.

The cell count and differential are used to determine if the patient is likely to have SBP. Patients with an ascites polymorphonuclear (PMN) count greater than 250 cells/mm³ should receive empiric antibiotics, and additional fluid should be inoculated into blood culture bottles to be sent for culture. The PMN count is calculated by multiplying the white cells/mm³ by the percentage of neutrophils in the differential. In a bloody sample, which contains a high concentration of red blood cells, the PMN count must be corrected: 1 PMN is subtracted from the absolute PMN count for every 250 red cells/mm³ in the sample.

Based on clinical judgment, additional testing can be performed on ascites fluid including total protein, lactate dehydrogenase (LDH), glucose, amylase, triglyceride, bilirubin, cytology, or tuberculosis smear and culture. These tests are generally only useful when there is suspicion of a condition other than sterile cirrhotic ascites. Tests that are not routinely helpful include determination of pH, lactate levels, and Gram staining. Results of Gram staining are of particular low yield unless a large concentration of bacteria, such as in the case of a free gut perforation, is suspected.

Treatment

Successful treatment of cirrhotic ascites is defined as the minimization of intraperitoneal fluid without intravascular volume depletion. Despite a lack of data supporting decreased mortality, minimizing the amount of ascites fluid can decrease infection-related morbidity in the cirrhotic patient. Treatment of ascites can dramatically improve quality of life by decreasing abdominal discomfort or dyspnea, or both. General ascites management in all patients should include minimizing consumption of alcohol, nonsteroidal anti-inflammatory drugs (NSAIDs), and dietary sodium. The use of more-aggressive interventions largely depends on the severity of ascites and includes oral diuretics, therapeutic (or large-volume) paracentesis, transjugular intrahepatic portosystemic shunt (TIPS), and orthotopic liver transplantation (Fig. 1).

Figure 1 Treatment options for cirrhotic ascites.

Refractory Ascites

Refractory ascites occurs in 5% to 10% of cirrhotic ascites patients and portends a poor prognosis. The definition of refractory ascites is (1) lack of response to high-dose diuretics (400 mg of spironolactone and 160 mg of furosemide/day) while remaining compliant with a low-sodium diet or (2) frequent ascites recurrence shortly after therapeutic paracentesis. Patients with recurrent side effects from diuretic therapy, including symptomatic hyponatremia, hyperkalemia or hypokalemia, renal insufficiency, or hepatic encephalopathy, are also considered to have refractory ascites. Treatment options include large-volume paracentesis with albumin infusion, placement of a TIPS, or liver transplantation. Surgical shunts (e.g., LeVeen or Denver shunt) have essentially been abandoned because controlled trials have shown poor long-term patency, excessive complications, and no survival advantage over medical therapy.

Frequent therapeutic paracentesis with or without albumin infusion is the most widely accepted treatment for patients with refractory ascites (see “Large-Volume Ascites” for controversy and dosing of albumin use). For those who have loculated fluid or are unwilling or unable to receive frequent paracentesis, TIPS placement can also be considered. In the appropriately selected patient, TIPS is highly effective for preventing ascites recurrence by decreasing the activity of sodium-retaining mechanisms and improving renal function. Ongoing studies will determine whether TIPS might also provide a survival benefit.

In the United States, TIPS is most commonly performed under conscious sedation by an interventional radiologist. The portal system is accessed through the jugular vein, and the operator inserts a self-expanding shunt between the portal (high-pressure) and hepatic (low-pressure) veins. The ultimate goal of the procedure is to lower portal pressures to less than 12 mm Hg, the level at which ascites begins to accumulate. Complications are relatively common and include hemorrhage (intrahepatic or intra-abdominal) and stent stenosis or thrombosis. Other important complications include hepatic encephalopathy and decompensation of liver or cardiac function. Therefore, TIPS is generally not recommended for patients with pre-existing encephalopathy, an ejection fraction lower than 55%, or a Child-Pugh Score higher than 12 (Table 3). Additional disadvantages of the procedure are high cost and lack of availability at some medical centers.

Table 3 Child-Pugh Classification*

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