What are the mechanisms of ascites formation in decompensated cirrhosis?
Nov 03, 2025
Source: Cainiu Health
Dr. Huang Yuhong
Introduction
In cirrhosis, increased fibrous tissue and formation of regenerative nodules in the liver compress intrahepatic blood vessels, leading to elevated portal venous pressure. Excessive portal pressure increases hydrostatic pressure in the visceral vascular beds of the abdominal cavity, causing fluid leakage from blood vessels into the peritoneal cavity and resulting in ascites, which is a key initiating factor in ascites formation. Cirrhosis also impairs hepatocyte synthesis of albumin, leading to decreased plasma albumin levels.
The mechanisms of ascites formation in decompensated cirrhosis generally include increased portal venous pressure, hypoalbuminemia, secondary hyperaldosteronism, insufficient effective circulating blood volume, and excessive production of hepatic lymph. Detailed analysis is as follows:
1. Increased portal venous pressure: In cirrhosis, fibrous tissue proliferation and regenerative nodule formation compress intrahepatic blood vessels, leading to elevated portal pressure. High portal pressure increases hydrostatic pressure in the splanchnic vascular bed, causing fluid to leak from blood vessels into the abdominal cavity, forming ascites. This is a key initiating factor in ascites development.
2. Hypoalbuminemia: Cirrhosis impairs hepatocyte synthesis of albumin, resulting in reduced plasma albumin levels. Albumin is the main contributor to plasma colloid osmotic pressure. A decrease in albumin reduces this osmotic pressure, making it difficult for fluid to remain within blood vessels, thus promoting its leakage into the peritoneal cavity and worsening ascites.
3. Secondary hyperaldosteronism: In cirrhosis, the liver's ability to inactivate aldosterone is diminished, leading to elevated systemic aldosterone levels. Aldosterone enhances sodium reabsorption in the renal distal tubules, resulting in sodium and water retention, increased blood volume, and subsequent leakage of excess fluid into the abdominal cavity, further aggravating ascites.
4. Insufficient effective circulating blood volume: Portal hypertension causes significant pooling of blood in the splanchnic circulation, leading to relative deficiency in effective circulating volume. The body responds by activating the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS), prompting the kidneys to reduce urine output. This exacerbates sodium and water retention, creating favorable conditions for ascites formation.
5. Excessive hepatic lymph production: In cirrhosis, compression of intrahepatic vessels and impaired blood flow increase pressure in the liver sinusoids, stimulating overproduction of hepatic lymph. When the rate of lymph formation exceeds the drainage capacity of the thoracic duct, excess lymph leaks from the surface of the liver capsule into the peritoneal cavity, becoming one of the major sources of ascites.
Once ascites develops, prompt medical evaluation is essential. Patients must strictly follow medical advice regarding restriction of sodium and fluid intake; regularly monitor body weight and abdominal girth to assess changes in ascites; and avoid strenuous activities to prevent sudden increases in intra-abdominal pressure that may cause discomfort.
