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new england journal

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medicine

review article

current concepts

Management of Cirrhosis and Ascites
Pere Ginès, M.D., Andrés Cárdenas, M.D., Vicente Arroyo, M.D., and Juan Rodés, M.D.
From the Liver Unit, Hospital Clinic and University of Barcelona, Institut d’Investigacions Biomèdiques August Pi-Sunyer, Barcelona, Spain (P.G., A.C., V.A., J.R.); and the Division ofGastroenterology and Hepatology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston (A.C.). Address reprint requests to Dr. Ginès at the Liver Unit, Hospital Clinic, Villarroel 170, 08036 Barcelona, Spain, or at gines@medicina.ub.es. N Engl J Med 2004;350:1646-54.
Copyright © 2004 Massachusetts Medical Society.

c

irrhosis, most frequently caused by hepatitis c or alcoholism,was the 12th leading cause of death in the United States in 2000, accounting for more than 25,000 deaths.1 Ascites is the most common complication of cirrhosis and is associated with a poor quality of life, increased risks of infections and renal failure, and a poor long-term outcome.2,3 In recent years, important advances have been made in the management of cirrhosis and ascites.pathophysiology of ascites
The chief factor contributing to ascites is splanchnic vasodilatation.4 Increased hepatic resistance to portal flow due to cirrhosis causes the gradual development of portal hypertension, collateral-vein formation, and shunting of blood to the systemic circulation. As portal hypertension develops, local production of vasodilators, mainly nitric oxide, increases, leading tosplanchnic arterial vasodilatation.5 In the early stages of cirrhosis, splanchnic arterial vasodilatation is moderate and has only a small effect on the effective arterial blood volume, which is maintained within normal limits through increases in plasma volume and cardiac output.4 In the advanced stages of cirrhosis, splanchnic arterial vasodilatation is so pronounced that the effective arterial bloodvolume decreases markedly, and arterial pressure falls. As a consequence, arterial pressure is maintained by homeostatic activation of vasoconstrictor and antinatriuretic factors, resulting in sodium and fluid retention. The combination of portal hypertension and splanchnic arterial vasodilatation alters intestinal capillary pressure and permeability, facilitating the accumulation of retained fluidwithin the abdominal cavity. As the disease progresses, there is marked impairment in renal excretion of free water and renal vasoconstriction — changes that lead to dilutional hyponatremia and the hepatorenal syndrome, respectively4,6 (Fig. 1).

evaluation of patients with ascites
general assessment

The evaluation of patients with cirrhosis and ascites should include not only an assessmentof liver function but also an assessment of renal and circulatory function (Table 1). Ideally, patients should be evaluated when they are not receiving diuretic agents, since some variables related to renal function may be altered by the administration of these medications. Ascitic fluid should be examined to rule out spontaneous bacterial peritonitis in patients with new-onset ascites, whether ornot they are hospitalized, and especially in those who have signs of infection, abdominal pain, encephalopathy, or gastrointestinal bleeding.

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n engl j med 350;16

www.nejm.org

april 15, 2004

Downloaded from www.nejm.org at MAYO CLINIC LIBRARY on September 26, 2005 . Copyright © 2004 Massachusetts Medical Society. All rights reserved.

current concepts

CirrhosisIncreased resistance to portal flow

Portal hypertension

Splanchnic vasodilatation

Increase in splanchnic capillary pressure

Arterial underfilling

Arterial and cardiopulmonary receptors

Lymph formation that exceeds lymph return

Activation of vasoconstrictor and antinatriuretic factors

Ascites

Sodium and water retention

Impaired free-water excretion

Renal vasoconstriction...