liver health

Ascites

Ascites and Peritoneum

Ascites, from the Greek askos = sack, is a pathological collection of liquids in the abdominal cavity. In healthy individuals the volume of these fluids is rather small (10-30 ml), and helps the sliding of peritoneal surfaces.

The peritoneum is a membrane made up of two sheets, of which the most external or parietal forms the lining of the abdominal cavity and the innermost, or visceral, covers most of the viscera contained within it. Between the two sheets there is a virtual space, called peritoneal cavity, containing a small quantity of serous liquid, which is continually renewed and allows the two sheets to slide over each other, facilitating the active and passive movements of the abdominal organs . The excessive accumulation of liquids in this intraperitoneal cavity is called ascites.

Causes of Ascites

In 75-80% of cases ascites is related to cirrhosis, a degenerative liver disease in which the normal liver tissue is replaced by a fibrous (cicatricial) connective tissue. In turn, cirrhosis is very often the long-term complication of viral, autoimmune, alcoholic or other substances (drugs, prolonged exposure to toxic agents of various kinds). Ascites occurs in 50% of patients with cirrhosis within 10 years of diagnosis; 40% of cirrhotic patients with ascites die within 2 years, while life expectancy at 5 years after diagnosis is 30%. If possible, therefore, the appearance of ascites should lead to the consideration of a liver transplant.

Among the possible causes of ascites we also find heart failure (3% of cases), cancers affecting the abdominal organs (colon, liver, stomach, pancreas, ovary) (10%), infectious diseases such as tuberculosis (2% ), pancreatitis (1%) and more rarely severe forms of intestinal malabsorption or severe malnutrition (Kwashiorkor).

Whatever the origin, ascites is caused by the loss of water and salt balance, with excessive body water and sodium retention. Presumably the origin of the problem is portal hypertension; we remember that the portal vein collects the blood coming from the spleen, and from the subdiaphragmatic portion of the digestive tract, to convey it to the liver; in the presence of a liver disease, such as cirrhosis, the structural alterations of the organ hinder the blood flow inside the liver, increasing the blood pressure in the portal vein. Due to this pressure increase, the quantity of blood seized by the spleen increases (which significantly increases in volume → splenomegaly), with a consequent reduction in the amount of circulating blood (hypovolemia).

The activation of the sympathetic system and the renin-angiotensin-aldosterone system in response to hypovolemia, increases the amount of sodium and fluids considered to be renal, while on the other hand the baroreceptors push the heart to increase its frequency and contractility, in addition to stimulating arteriolar vasoconstriction. The entire mechanism feeds the portal hypertension, which increases the hydrostatic pressure inside the hepatic sinusoids favoring the transudation of liquids in the peritoneal cavity (ascites).

Finally, hepatic impairment leads to a reduction in protein synthesis, including that related to albumin; it is the most important plasma protein, which alone is responsible for 80% of the oncotic (colloid-osmotic) blood pressure. As such albumin favors the passage of water from the interstitial liquid to the capillaries; consequently, hypoalbuminemia leads to the formation of edema and ascites due to fluid accumulation in the intercellular spaces (although its role in the development of ascites is now considered a minority).