B9781416049197X50014 B9781416049197501791 Main
B9781416049197X50014 B9781416049197501791 Main
B9781416049197X50014 B9781416049197501791 Main
Chapter 177
Ascites
DEFINITION
DIFFERENTIAL DIAGNOSIS
Ascites is the accumulation of excess uid in the peritoneal cavity, most commonly caused by liver cirrhosis.
CLINICAL PRESENTATION
CAUSE
Pathophysiology of ascites: increased hepatic resistance to portal ow leads to portal hypertension. The splanchnic vessels
respond by increased secretion of nitric oxide causing splanchnic artery vasodilation. Early in the disease increased plasma
volume and increased cardiac output compensate for this vasodilation. However, as disease progresses the effective arterial
blood volume decreases causing sodium and uid retention
through activation of the renin-angiotensin system. The change
in capillary pressure causes increased permeability and retention of uid in the abdomen.
LABORATORY TESTS
Fig 1771
Fig 1772
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Fig 1773
Ascites. On a plain lm of the abdomen (A), only gross amount of ascites (a) can be identied. This is usually seen, because the ascites have
caused a rather gray appearance of the abdomen and pushed the gas-containing loops of small bowel (SB) toward the most nondependent and
central portion of the abdomen. A transverse computed tomography scan (B) shows a cross-sectional view of the same appearance with the airand contrast-lled small bowel (SB) oating in the ascitic uid (A).
(From Mettler FA, Guibertau MJ, Voss CM, Urbina CE: Primary Care Radiology. Philadelphia, Elsevier, 2000.)
Liver biopsy in select patients (i.e., those with portal hypertension of uncertain etiology).
TREATMENT
Fig 1774
Transjugular intrahepatic portosystemic stent-shunt (TIPS). An intrahepatic tract has been created between the right hepatic vein and the
right portal vein. The tract is dilated and stented, creating a shunt as
demonstrated on shuntogram. (Courtesy of Dr. W. K. Tso.)
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