Ascites

Updated: Aug 24, 2016
  • Author: Rahil Shah, MD; Chief Editor: Praveen K Roy, MD, AGAF  more...
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Overview

Background

The word ascites is of Greek origin (askos) and means bag or sac. Ascites describes the condition of pathologic fluid collection within the abdominal cavity. Healthy men have little or no intraperitoneal fluid, but women may normally have as much as 20 mL, depending on the phase of their menstrual cycle. This article focuses only on ascites associated with cirrhosis.

See the image below.

This computed tomography scan demonstrates free in This computed tomography scan demonstrates free intraperitoneal fluid due to urinary ascites.

For  patient education resources, see Digestive Disorders Center and Heart Health Center, as well as Cirrhosis, Hepatitis B (HBV, HepB), Hepatitis C, and Congestive Heart Failure.

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Pathophysiology

The accumulation of ascitic fluid represents a state of total-body sodium and water excess, but the event that initiates the unbalance is unclear. Although many pathogenic processes have been implicated in the development of abdominal ascites, about 75% likely occur as a result of portal hypertension in the setting of liver cirrhosis, with the remainder due to infective, inflammatory, and infiltrative conditions. [1]

Three theories of ascites formation have been proposed: underfilling, overflow, and peripheral arterial vasodilation.

The underfilling theory suggests that the primary abnormality is inappropriate sequestration of fluid within the splanchnic vascular bed due to portal hypertension and a consequent decrease in effective circulating blood volume. This activates the plasma renin, aldosterone, and sympathetic nervous system, resulting in renal sodium and water retention.

The overflow theory suggests that the primary abnormality is inappropriate renal retention of sodium and water in the absence of volume depletion. This theory was developed in accordance with the observation that patients with cirrhosis have intravascular hypervolemia rather than hypovolemia.

The most recent theory, the peripheral arterial vasodilation hypothesis, includes components of both of the other theories. It suggests that portal hypertension leads to vasodilation, which causes decreased effective arterial blood volume. As the natural history of the disease progresses, neurohumoral excitation increases, more renal sodium is retained, and plasma volume expands. This leads to overflow of fluid into the peritoneal cavity. The vasodilation theory proposes that underfilling is operative early and overflow is operative late in the natural history of cirrhosis.

Although the sequence of events that occurs between the development of portal hypertension and renal sodium retention is not entirely clear, portal hypertension apparently leads to an increase in nitric oxide levels. Nitric oxide mediates splanchnic and peripheral vasodilation. Hepatic artery nitric oxide synthase activity is greater in patients with ascites than in those without ascites.

Regardless of the initiating event, a number of factors contribute to the accumulation of fluid in the abdominal cavity. Elevated levels of epinephrine and norepinephrine are well-documented factors. Hypoalbuminemia and reduced plasma oncotic pressure favor the extravasation of fluid from the plasma to the peritoneal fluid, and, thus, ascites is infrequent in patients with cirrhosis unless both portal hypertension and hypoalbuminemia are present.

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Epidemiology

Mortality/Morbidity

Ambulatory patients with an episode of cirrhotic ascites have a 3-year mortality rate of 50%. The development of refractory ascites carries a poor prognosis, with a 1-year survival rate of less than 50%. [2]

Sex

Healthy men have little or no intraperitoneal fluid, but women may normally have as much as 20 mL, depending on the phase of their menstrual cycle.

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Prognosis

The prognosis for patients with ascites due to liver disease depends on the underlying disorder, the degree of reversibility of a given disease process, and the response to treatment.

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Patient Education

The most important aspect of patient education is determining when therapy is failing and recognizing the need to see a physician. Unfortunately, in most cases, liver failure has a dismal prognosis. All patients must be taught which complications are potentially fatal and the signs and symptoms that precede them.

Abdominal distention and/or pain despite maximal diuretic therapy are common problems, and patients must realize the importance of seeing a physician immediately.

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