5.22
Ascites is the buildup of fluid in the peritoneal cavity. The most accepted explanation is the splanchnic vasodilation model.
In cirrhosis, excess nitric oxide and other vasodilators cause dilation of the splanchnic arteries. This lowers the effective circulating blood volume, despite an increase in total body fluid.
The body responds by activating the renin–angiotensin–aldosterone system and antidiuretic hormone. These responses promote sodium and water retention.
Plasma volume expansion then raises sinusoidal pressure in the liver. This pressure forces lymph to leak into the peritoneal cavity, resulting in the formation of ascites, also known as ascitic fluid.
As fluid continues to accumulate, the adequate circulating volume continues to fall further. This leads to the underfill stage, which triggers even stronger fluid retention.
Besides this mechanism, systemic inflammation, intestinal and mesenteric changes, malignancies, and cardiac or renal dysfunction can also worsen ascites.
Ascites is the buildup of fluid inside the peritoneal cavity. It occurs when fluid moves out of the vascular system faster than the peritoneal lymphatics can remove it. This fluid shift is most commonly seen in liver cirrhosis but can also appear in several other systemic disorders.
Cirrhosis remains the leading cause of ascites. Other conditions that can contribute include:
These disorders disrupt the normal balance of vascular and lymphatic systems, making fluid accumulation more likely.
The splanchnic vasodilation model is the main explanation for how ascites forms and progresses. In cirrhosis, excess nitric oxide and other vasodilators widen the splanchnic arteries. This dilation causes blood to pool in the splanchnic region, lowering the adequate circulating blood volume, even though total body fluid volume increases.
The body senses this low effective volume and activates the renin–angiotensin–aldosterone system and antidiuretic hormone. These responses promote sodium and water retention as an attempt to restore arterial filling. As fluid is retained, plasma volume expands, but the continued vasodilation prevents proper redistribution, creating an underfill state. Underfill enhances sodium and water retention, driving ongoing fluid accumulation.
At the same time, pressure inside the liver rises, leading to increased lymph formation. When the liver can no longer clear this lymph load, fluid leaks into the peritoneal space and becomes ascitic fluid. Systemic inflammation, intestinal changes, malignancy, and cardiac or renal dysfunction can further worsen this process.
Ascites is the buildup of fluid in the peritoneal cavity. The most accepted explanation is the splanchnic vasodilation model.
In cirrhosis, excess nitric oxide and other vasodilators cause dilation of the splanchnic arteries. This lowers the effective circulating blood volume, despite an increase in total body fluid.
The body responds by activating the renin–angiotensin–aldosterone system and antidiuretic hormone. These responses promote sodium and water retention.
Plasma volume expansion then raises sinusoidal pressure in the liver. This pressure forces lymph to leak into the peritoneal cavity, resulting in the formation of ascites, also known as ascitic fluid.
As fluid continues to accumulate, the adequate circulating volume continues to fall further. This leads to the underfill stage, which triggers even stronger fluid retention.
Besides this mechanism, systemic inflammation, intestinal and mesenteric changes, malignancies, and cardiac or renal dysfunction can also worsen ascites.
From Chapter 5:
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