Ascites:
Ascites is present when there is accumulation of free fluid in the peritoneal cavity. Small amounts of ascites are asymptomatic, but with larger accumulations of fluid (> 1 L) there is abdominal distension, fullness in the flanks, shifting dullness on percussion and, when the ascites is marked, a fluid thrill.
Ascites is caused by a variety of diseases and conditions, for example, cirrhosis of the liver, cancer within the abdomen, congestive heart failure, and tuberculosis.
In obese patients, much larger volumes of ascites may accumulate before they are detectable clinically.
• If cirrhosis has caused ascites, an individual may benefit from reducing salt and taking water tablets (diuretics).
• Water tablets cause urine to pass more frequently and can prevent further fluid retention.
• While this is an effective approach in many situations, some types of ascites are resistant to diuretics.
Other features include
distortion or eversion of the umbilicus, herniae, abdominal striae, divarication of the recti and scrotal oedema.
Dilated superficial abdominal veins may be seen if the
ascites is due to portal hypertension.
Pathophysiology:-
Ascites may result from several different causes, the
most common of which are malignant disease, cirrhosis or heart failure. Many primary disorders of the
peritoneum and visceral organs can also cause ascites,
and these need to be considered even in a patient with
chronic liver disease . Splanchnic vasodilation is thought to be the main factor leading to ascites in
cirrhosis.
This is mediated by vasodilators (mainly nitric oxide) that are released when portal hypertension causes shunting of blood into the systemic circulation.
Systemic arterial pressure falls due to pronounced splanchnic vasodilatation as cirrhosis advances. This leads to activation of the renin–angiotensin system with secondary aldosteronism, increased sympathetic nervous activity, increased atrial natriuretic hormone secretion and altered activity of the kallikrein–kinin system .
These
systems tend to normalise arterial pressure but produce
salt and water retention. In this setting, the combination
of splanchnic arterial vasodilatation and portal hypertension alters intestinal capillary permeability, promoting accumulation of fluid within the peritoneum.
