Ascites



Ascites is the accumulation of excess fluid in the peritoneal cavity. Although cirrhosis is the commonest cause of ascites, it may result from numerous other causes . Ascites due to cirrhosis is commonly a transudate (protein concentration <3 grams per dl), whereas inflam­matory and neoplastic causes usually lead to for­mation of an exudate (protein >3 grams per dl). Ascites becomes clinically detectable when more than 500 ml has accumulated. Shifting dullness to percussion is the most sensitive clinical sign of ascites, the presence of which can be confirmed by ultrasound examination.

Ascites in cirrhosis is the result of several path­ogenetic factors, including portal hypertension, increased hepatic and splanchnic lymph produc­tion and transudation, and impaired renal sodium and water excretion secondary to hyperaldoster-onism, increased levels of antidiuretic hormone, and other less well-understood factors.

Treatment of ascites consists initially of bed rest with restriction of sodium intake. Restricted fluid intake may be necessary if hyponatremia is present. These measures are commonly inade­quate, and administration of spironolactone, an aldosterone antagonist, supplemented with a loop diuretic (e.g., furosemide) is often effective. Di­uresis should be promoted cautiously, as aggres­sive diuretic therapy may result in hypokalemia and a depleted plasma volume, leading to hepatic encephalopathy and impaired renal function. Some patients may be extremely refractory to medical measures and may benefit from a surgi­cally implanted plastic shunt between the peri­toneal cavity and the superior vena cava (LeVeen shunt).
Two important complications occur in patients with cirrhotic ascites: spontaneous bacterial per­itonitis and the hepatorenal syndrome.

Spontaneous Bacterial Peritonitis. Infection of ascites may occur in patients with cirrhosis, usually with coliform bacteria. Fever, abdominal pain, and tenderness may be present or the infec­tion may be clinically silent. Hepatic encepha­lopathy may be precipitated. The diagnosis is strongly suspected if the ascitic fluid white cell count is greater than 500/cu mm with greater than 50 per cent polymorphonuclear leukocytes, and is confirmed by Gram’s stain and culture. Vigor­ous antibiotic treatment is indicated, but mortal­ity from this complication is high.





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