Ascites can result from hepatic disorders, usually chronic but sometimes acute; conditions unrelated to the liver can also cause ascites.
Hepatic causes include the following:
Portal vein thrombosis does not usually cause ascites unless hepatocellular damage is also present.
Nonhepatic causes include the following:
Generalized fluid retention associated with systemic diseases (eg, heart failure, nephrotic syndrome, severe hypoalbuminemia, constrictive pericarditis)
Peritoneal disorders (eg, carcinomatous or infectious peritonitis, biliary leak due to surgery or another medical procedure)
Mechanisms are complex and incompletely understood. Factors include nitric oxide-induced splanchnic vasodilation, altered Starling forces in the portal vessels (low oncotic pressure due to hypoalbuminemia plus increased portal venous pressure), avid renal sodium retention (urinary sodium concentration is typically < 5 mEq/L [5 mmol/L]), and possibly increased hepatic lymph formation.
Mechanisms that seem to contribute to renal sodium retention include activation of the renin-angiotensin-aldosterone system; increased sympathetic tone; intrarenal shunting of blood away from the cortex; increased formation of nitric oxide; and altered formation or metabolism of antidiuretic hormone, kinins, prostaglandins, and atrial natriuretic factor. Vasodilation in the splanchnic arterial circulation may be a trigger, but the specific roles and interrelationships of these abnormalities remain uncertain.
Small amounts of ascitic fluid cause no symptoms. Moderate amounts cause increased abdominal girth and weight gain. Massive amounts may cause nonspecific diffuse abdominal pressure, but actual pain is uncommon and suggests another cause of acute abdominal pain. If ascites results in elevation of the diaphragm, dyspnea may occur. Symptoms of spontaneous bacterial peritonitis (SBP) may include new abdominal discomfort and fever.
Signs include shifting dullness (detected by abdominal percussion) and a fluid wave. Volumes < 1500 mL may not cause physical findings. Massive ascites causes tautness of the abdominal wall and flattening of the umbilicus. In liver diseases or peritoneal disorders, ascites is usually isolated or disproportionate to peripheral edema; in systemic diseases (eg, heart failure), the reverse is usually true.
Diagnosis may be based on physical examination if there is a large amount of fluid, but imaging tests are more sensitive. Ultrasonography and CT reveal much smaller volumes of fluid (100 to 200 mL) than does physical examination. Spontaneous bacterial peritonitis (SBP) is suspected if a patient with ascites also has abdominal pain, fever, or unexplained deterioration. However, SBP can also be asymptomatic with the only signs being worsening hepatic synthetic function or acute kidney injury. And because treatment delays lead to a high mortality, the treatment threshold should be low.
Diagnostic abdominal paracentesis should be done if any of the following occur:
About 50 to 100 mL of fluid is removed and analyzed for gross appearance, protein content, cell count and differential, culture, and, as clinically indicated, cytology, acid-fast stain, and/or amylase. In contrast to ascites due to inflammation or infection, ascites due to portal hypertension produces fluid that is clear and straw-colored, has a low protein concentration, a low polymorphonuclear (PMN) leukocyte count (< 250 cells/mcL), and, most reliably, a high serum-to-ascites albumin concentration gradient (SAAG), which is the serum albumin concentration minus the ascitic albumin concentration. SAAG ≥ 1.1 g/dL (11 g/L) is relatively specific for ascites due to portal hypertension. In ascitic fluid, a PMN count of > 250 cells/mcL indicates SBP, whereas bloody fluid can suggest a tumor or tuberculosis. The rare milky (chylous) ascites is most common with lymphoma or lymphatic duct occlusion.
(See also the American Association for the Study of Liver Diseases [AASLD] practice guideline Management of Adult Patients with Ascites Due to Cirrhosis.)
Dietary sodium restriction (2000 mg/day) is the first and least risky treatment for ascites due to portal hypertension. Diuretics should be used if rigid sodium restriction fails to initiate diuresis within a few days. Spironolactone is usually effective (in oral doses ranging from 50 mg once a day to 200 mg twice a day). A loop diuretic (eg, furosemide 20 to 160 mg orally usually once a day or 20 to 80 mg orally twice a day) should be added if spironolactone is insufficient. Because spironolactone can cause potassium retention and furosemide can cause potassium depletion, the combination of these drugs often provides optimal diuresis with a lower risk of potassium abnormalities. Fluid restriction is indicated only for treatment of hyponatremia (serum sodium < 125 mEq/L [125 mmol/L]).
Changes in body weight and urinary sodium determinations reflect response to treatment. Weight loss of about 0.5 kg/day is optimal because the ascitic compartment cannot be mobilized much more rapidly. More aggressive diuresis depletes fluid from the intravascular compartment, especially when peripheral edema is absent; this depletion may cause renal failure or electrolyte imbalance (eg, hypokalemia) that may precipitate portosystemic encephalopathy. If peripheral edema is present, more aggressive diuresis up to 1 kg/day is usually well tolerated (1). Inadequate dietary sodium restriction is the usual cause of persistent ascites.
Therapeutic paracentesis can be combined with diuretics. If more than 5 liters of ascites are removed, 6 to 8 g of 25% albumin should be given for each liter removed. Albumin helps reduce the risk of post-paracentesis hypotension (post-paracentesis circulatory dysfunction), which can precipitate hepatorenal syndrome. Therapeutic paracentesis can reduce ascites more quickly than diuretics; however, patients require ongoing diuretics to prevent reaccumulation of ascites.
Techniques for the autologous infusion of ascitic fluid (eg, the LeVeen peritoneovenous shunt) often cause complications and are generally no longer used. Transjugular intrahepatic portosystemic shunting (TIPS) can lower portal pressure and successfully treat ascites resistant to other treatments, but TIPS is invasive and may cause complications, including portosystemic encephalopathy and worsening hepatocellular function.
Refractory ascites is defined as ascites that persists and requires paracentesis despite maximal dose diuretics (furosemide 160 mg and spironolactone 400 mg daily) or inability to tolerate diuretics due to acute kidney injury or hypotension. Refractory ascites is an indication for referral for liver transplantation.
(See also the AASLD practice guideline The Role of Transjugular Intrahepatic Portosystemic Shunt [TIPS] in the Management of Portal Hypertension: Update 2009.)
1. European Association for the Study of the Liver: EASL clinical practice guidelines for the management of patients with decompensated cirrhosis. J Hepatol 69:406-460, 2018. doi.org/10.1016/j.jhep.2018.03.024
Ascites is free fluid in the abdominal cavity, usually caused by portal hypertension and sometimes by other hepatic or nonhepatic conditions.
Moderate amounts of fluid can increase abdominal girth and cause weight gain, and massive amounts can cause abdominal distention, pressure, and dyspnea; signs may be absent if fluid accumulation is < 1500 mL.
Unless the diagnosis is obvious, confirm the presence of ascites using ultrasonography or CT.
If ascites is newly diagnosed, its cause is unknown, or spontaneous bacterial peritonitis is suspected, do paracentesis and test ascitic fluid.
Recommend dietary sodium restriction; if insufficiently effective, consider use of diuretics and therapeutic paracentesis.
Promptly refer patients with refractory ascites for liver transplantation.
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