Medicina

Ascites
Fredric D. Gordon,
KEYWORDS  Ascites  Cirrhosis  Spontaneous bacterial peritonitis  Hepatorenal syndrome
MD
a,b,

*

Ascites is the pathologic accumulation of fluid in the peritoneum. It is the most common complication of cirrhosis, with a prevalence of approximately 10%. Over a 10-year period, 50% of patients with previously compensated cirrhosis are expected to developascites.1 As a marker of hepatic decompensation, ascites is associated with a poor prognosis with only a 56% survival 3 years after onset.2 In addition, morbidity is increased because of the risk of additional complications, such as spontaneous bacterial peritonitis (SBP) and hepatorenal syndrome. Understanding the pathophysiology of ascites is essential for the proper management of this highlysymptomatic and potentially lethal complication of cirrhosis.

PATHOPHYSIOLOGY

Ascites develops in cirrhosis from the complex interaction among the endogenous vasoactive systems, portal hypertension, and renal function. The specific timeline of events and interplay among these abnormally functioning systems is not clearly understood. Nonetheless, three theories have been advanced to explain thedevelopment of ascites.
Backward Theory of Ascites Formation

The first theory to explain the development of ascites was the backward theory of ascites formation. This theory states that portal hypertension and ascites formation occur first with subsequent circulatory dysfunction and renal impairment.3,4 Portal hypertension and hypoalbuminemia lead to increased splanchnic lymph formation. Excessivelymph production overwhelms the ability of the thoracic duct to return lymph to the heart, resulting in extravasation of fluid into the abdominal cavity. These changes impact circulatory and renal function and result in diminished plasma volume and cardiac output and increased peripheral vascular resistance.

The author has nothing to disclose. a Tufts Medical School, Boston, MA, USA; b LaheyClinic Medical Center, 41 Mall Road, 4 West, Burlington, MA 01805, USA * Lahey Clinic Medical Center, 41 Mall Road, 4 West, Burlington, MA 01805. E-mail address: Fredric_D_Gordon@lahey.org Clin Liver Dis 16 (2012) 285–299 doi:10.1016/j.cld.2012.03.004 1089-3261/12/$ – see front matter Ó 2012 Elsevier Inc. All rights reserved. liver.theclinics.com

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Overflow Theory of AscitesFormation

When it became clear that the plasma volume and cardiac output were, in fact, increased and vascular resistance decreased in patients with cirrhosis, the backward theory of ascites formation had to be dismissed. According to the newer overflow theory of ascites formation, the primary event was sodium retention before impairment in the circulatory function.5 For this hypothesis to beexplanatory, sodium retention had to be caused by portal hypertension.6 These effects would result in increased plasma volume and cardiac output and decreased systemic peripheral vascular resistance, as expected. The arterial hypovolemia and further increase in portal hypertension would induce overflow ascites.7 Later, this theory was undermined by the fact that arterial vasodilation is not systemicbut rather restricted to the splanchnic circulation. Also, according to this theory, one would expect that administration of angiotensin II antagonists would improve arterial pressure and peripheral vascular resistance; however, this does not occur, suggesting that primary sodium retention is not the inciting event.8,9
Peripheral Arterial Vasodilation Theory

This hypothesis is the currentunderstanding of the cause of ascites in cirrhosis. The primary abnormality is the impairment in circulatory function characterized by a reduction in systemic vascular resistance (SVR) from arterial vasodilation of the splanchnic circulation caused by portal hypertension.10 This abnormality has been further evaluated and is attributed to the increased production and activity of vasodilator factors,...