الفهرس 
Physical examination
AscitesOnly 14 pages are availabe for public view
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Abstract
Summary Ascites is the most common complication of cirrhosis. Once ascites develops, the prognosis worsens and the patient becomes susceptible to complications such as bacterial peritonitis, hepatic hydrothorax, hyponatremia, and complications of diuretic therapy. Following the development of ascites, the patient’s quality of life declines significantly and survival is about 50% after 5 years of follow-up. Once the ascites becomes refractory to medical therapy, the prognosis is worse, with only 40–60% of patients alive after 2 years without liver transplantation. The pathophysiology of ascites is complex, and various mechanisms have been proposed. Splanchnic and systemic vasodilatation related to excess nitric oxide has been associated with systemic hypotension and increased portal flow. This is associated with hemodynamic compensatory mechanisms via activation of the renin-angiotensin aldosterone and sympathetic nervous systems and the non-osmotic release of antidiuretic hormones. Refractory ascites develops in approximately 5-10% of all cases of ascites and 50% of such patients die within 6 months of its development. Portal hypertension and splanchnic vasodilatation causes more marked arterial under filling and the sodium retaining mechanisms become permanently activated. The therapeutic options available for patients with refractory ascites are serial therapeutic paracentesis, liver transplantation, transjagular intrahepatic portosystemic shunts (TIPS), and peritoneovenous shunt.