In patients with chronic diseases of the liver, fibrosis (scarring) of the liver often occurs.
November 23, 2005 (Press Release) --
Why do patients with liver disease develop ascites and edema?
In patients with chronic diseases of the liver, fibrosis (scarring) of the liver often occurs. When the scarring becomes advanced, the condition is called cirrhosis of the liver. Ascites is fluid that accumulates in the abdominal (peritoneal) cavity. It is a complication of cirrhosis and appears as an abdominal bulge. The peritoneum is the inner lining of the abdominal cavity, which also folds over to cover the organs inside the abdomen such as the liver, gallbladder, spleen, pancreas, and intestines. Ascites develops because of a combination of two factors: (1) increased pressure in the vein system that carries blood from the stomach, intestines, and spleen to the liver (portal hypertension); and (2) a low level of the protein albumin in the blood (hypoalbuminemia). Albumin, which is the predominant protein in the blood and which helps maintain blood volume, is reduced in cirrhosis primarily because the damaged liver is not able to produce enough albumin.
Other consequences of portal hypertension include dilated veins in the esophagus (varices), prominent veins on the abdomen, and an enlarged spleen. Each of these conditions is due primarily to the increased pressure and accumulation of blood in the abdominal blood vessels. Other signs of chronic liver disease are spider nevi (distinctive vascular malformations) on the skin, certain characteristic changes in the nails, gynecomastia (enlarged breasts), and shrinkage of the testicles (testicular atrophy). The fluid of ascites can be removed from the abdominal cavity by using a syringe and a long needle. This procedure is called paracentesis. Analysis of the fluid can help differentiate ascites that is caused by cirrhosis from other causes of ascites, such as cancer, tuberculosis, congestive heart failure, and nephrosis. Sometimes, when ascites does not respond to treatment with diuretics, paracentesis can be used to remove large amounts of the ascitic fluid.
Peripheral edema, which is usually seen as pitting edema of the legs and feet, also occurs in cirrhosis. The edema is a consequence of the hypoalbuminemia and activation of the renin-angiotensin- aldosterone hormonal system, which prompt the kidneys to retain salt and water. The presence or absence of edema in patients with cirrhosis and ascites is an important consideration in the treatment of the ascites. In patients with ascites without edema, diuretics must be given with extra caution. The reason for this is that a diuresis (induced increased volume of urine) that is too depleting or rapid in these patients can lead to a low blood volume (hypovolemia), which can possibly be followed by kidney and liver failure. In contrast, when patients who have both edema and ascites undergo diuresis, the edema fluid in the interstitial space serves as somewhat of a buffer against the development of low blood volume. The excess interstitial fluid moves into the blood vessel spaces to rapidly replenish the depleted blood volume.
In patients with chronic diseases of the liver, fibrosis (scarring) of the liver often occurs. When the scarring becomes advanced, the condition is called cirrhosis of the liver. Ascites is fluid that accumulates in the abdominal (peritoneal) cavity. It is a complication of cirrhosis and appears as an abdominal bulge. The peritoneum is the inner lining of the abdominal cavity, which also folds over to cover the organs inside the abdomen such as the liver, gallbladder, spleen, pancreas, and intestines. Ascites develops because of a combination of two factors: (1) increased pressure in the vein system that carries blood from the stomach, intestines, and spleen to the liver (portal hypertension); and (2) a low level of the protein albumin in the blood (hypoalbuminemia). Albumin, which is the predominant protein in the blood and which helps maintain blood volume, is reduced in cirrhosis primarily because the damaged liver is not able to produce enough albumin.
Other consequences of portal hypertension include dilated veins in the esophagus (varices), prominent veins on the abdomen, and an enlarged spleen. Each of these conditions is due primarily to the increased pressure and accumulation of blood in the abdominal blood vessels. Other signs of chronic liver disease are spider nevi (distinctive vascular malformations) on the skin, certain characteristic changes in the nails, gynecomastia (enlarged breasts), and shrinkage of the testicles (testicular atrophy). The fluid of ascites can be removed from the abdominal cavity by using a syringe and a long needle. This procedure is called paracentesis. Analysis of the fluid can help differentiate ascites that is caused by cirrhosis from other causes of ascites, such as cancer, tuberculosis, congestive heart failure, and nephrosis. Sometimes, when ascites does not respond to treatment with diuretics, paracentesis can be used to remove large amounts of the ascitic fluid.
Peripheral edema, which is usually seen as pitting edema of the legs and feet, also occurs in cirrhosis. The edema is a consequence of the hypoalbuminemia and activation of the renin-angiotensin- aldosterone hormonal system, which prompt the kidneys to retain salt and water. The presence or absence of edema in patients with cirrhosis and ascites is an important consideration in the treatment of the ascites. In patients with ascites without edema, diuretics must be given with extra caution. The reason for this is that a diuresis (induced increased volume of urine) that is too depleting or rapid in these patients can lead to a low blood volume (hypovolemia), which can possibly be followed by kidney and liver failure. In contrast, when patients who have both edema and ascites undergo diuresis, the edema fluid in the interstitial space serves as somewhat of a buffer against the development of low blood volume. The excess interstitial fluid moves into the blood vessel spaces to rapidly replenish the depleted blood volume.
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