What Are the Causes of Ascites in Liver Cirrhosis?
Jun 06, 2022
Source: Cainiu Health
Dr. Jin Zhongkui
Introduction
The primary causes of ascites in liver cirrhosis include the following:
1. Decreased plasma albumin levels.
2. Elevated portal pressure. Studies indicate that during cirrhosis, intrahepatic fibrous tissue proliferation obstructs hepatic blood vessels, thereby increasing portal pressure and reducing plasma colloid osmotic pressure—facilitating fluid transudation from the portal system into the peritoneal cavity.
3. Increased lymphatic leakage.
Hepatic cirrhotic ascites—commonly referred to as “hepatic ascites”—refers to the accumulation of fluid in the peritoneal cavity resulting from chronic liver disease and recurrent hepatic inflammation. What, then, are the underlying causes of hepatic cirrhotic ascites?
Causes of Hepatic Cirrhotic Ascites
The primary causes of hepatic cirrhotic ascites include the following:
1. Decreased Plasma Albumin Levels
Plasma albumin is synthesized by hepatocytes. In cirrhosis, impaired hepatocyte function leads to markedly reduced albumin synthesis, thereby lowering plasma colloid osmotic pressure. Under the influence of elevated portal venous pressure, part of the plasma transudates from the portal venous vessels into the peritoneal cavity, forming ascites.
2. Increased Portal Venous Pressure
Research indicates that during cirrhosis, intrahepatic fibrous tissue proliferation obstructs hepatic vasculature, elevating portal venous pressure and reducing plasma colloid osmotic pressure. Consequently, fluid within the portal venous system more readily transudates into the peritoneal cavity.
3. Increased Lymphatic Leakage
In cirrhosis, regenerative nodules may cause post-sinusoidal hepatic venous obstruction, leading to impaired hepatic lymphatic drainage, increased lymphatic pressure, and enhanced lymphatic leakage. Some lymphatic fluid inevitably enters the peritoneal cavity, contributing to ascites formation. During surgery, lymphatic leakage may be observed from the hilar lymphatic plexus and subcapsular hepatic lymphatic vessels; additionally, the thoracic duct is often markedly dilated—sometimes reaching a caliber comparable to that of the subclavian vein.
Dietary management must ensure adequate nutritional intake. A varied diet is recommended, while coarse, high-fiber foods should be avoided to prevent injury to esophageal varices and subsequent life-threatening hemorrhage. In cases of elevated blood ammonia levels or severely compromised liver function, protein intake should be carefully moderated to avoid precipitating hepatic encephalopathy. Monitor closely for signs such as bleeding, purpura, fever, or changes in mental status or neurological function, and promptly inform your physician. We hope this information proves helpful!
