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  • All patients with cirrhosis and ascites on admission should undergo diagnostic paracentesis.
  • Diagnosis of spontaneous bacterial peritonitis (SBP) is usually established by an elevated ascitic fluid polymorphonuclear leukocyte (PMN) count >250 cells/mL. Whereas some patients with ascites have peritoneal fluid PMN counts >250 cells/mL, all patients with SBP do.
  • The most useful parameter for classifying ascites is the serum–albumin peritoneal fluid albumin gradient (SAAG).
  • With 98% accuracy a SAAG value >1.1 g/dL is consistent with ascites secondary to portal hypertension.
  • SAAG values <1.1 g/dL can occur in ascites due to infection, inflammation, or neoplasm.

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General Considerations

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The major causes of ascites are listed in Table 45–1. In North America and Europe, 90% of the cases of ascites are due to cirrhosis, malignancy, and congestive heart failure. In Europe and other countries tuberculous peritonitis is not uncommon. Ascites is a cardinal manifestation of decompensated cirrhosis of the liver. Approximately 50% of patients with cirrhosis will develop ascites within 10 years. The development of ascites in patients with cirrhosis provides important prognostic information as up to 50% of such patients will die within 5 years.

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Table Graphic Jump Location
Table 45–1. Causes of Ascites.
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Pathogenesis

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Development of Cirrhotogenic Ascites

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Five major factors are involved in the pathogenesis of cirrhotogenic ascites: portal hypertension, hypoalbuminemia, sodium retention, water retention, and increased lymph formation.

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Portal hypertension is universally present in patients with ascites secondary to cirrhosis of the liver. Two major mechanisms contribute to the development of portal hypertension: (1) distortion of the hepatic vascular architecture caused by reduction in the intrahepatic arterial bed as a result of fibrosis and nodule formation, and (2) increased production of vasodilatory substances, most importantly nitric oxide synthase.

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Hypoalbuminemia results from decreased albumin synthesis that, in turn, is secondary to impaired hepatocellular synthetic function. It should be emphasized that there is no critical level of serum albumin at which ascites formation takes place. In one large series of cirrhotic patients with ascites, serum albumin levels ranged from 2.3 g% to 3.8 g%.

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Increased sodium retention appears to be related primarily to abnormalities of proximal tubular function, and increased proximal tubular reabsorption of sodium. The latter occurs due to increased aldosterone secretion in response to changes in effective circulating blood volume. Activation of the renin-angiotensin-aldosterone system contributes to abnormal sodium retention.

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It has long been appreciated that cirrhotic ...

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