pathophysiology of ascites
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- Опубликовано: 26 сен 2024
- Ascites is a pathological accumulation of fluid in the peritoneal cavity.
It can result from either increased portal venous pressure, low plasma proteins, chronic peritoneal irritation, leakage of lymphatic fluid into the peritoneal cavity or fluid overload.
Pathophysiology of ascites
Like we have mentioned above, one of the major causes of ascites is increased portal venous pressure related to cirrhosis. In discussing the pathophysiology of ascites we shall do it as per the causes because all have different mechanisms.
Increased portal venous pressure.
The presence of portal hypertension contributes to the development of ascites in patients who have cirrhosis. Apart from cirrhosis, any cause of increases resistance to hepatic or portal venous flow can lead to ascites
There is an increase in intrahepatic resistance, causing increased portal pressure. This increased pressure within the hepatic veins or post sinusoidal level increases hydrostatic pressure within the hepatic sinusoids and portal veins.
In late stages of liver cirrhosis there is collateral vein formation, shunting of blood to the systemic circulation and also vasodilation of the splanchnic arterial system, which, in turn, results in an increase in portal venous inflow.
All these abnormalities result in increased production of splanchnic lymph. Lymphatic flow is increased proximal to the point of vascular obstruction and when the normal capacity of the lymphatic system is overwhelmed the transudate fluid moves across the surfaces of the liver, mesentery and intestines into the peritoneal cavity.
Vasodilating factors such as nitric oxide are responsible for the vasodilator effect.
These hemodynamic changes result in sodium retention by causing activation of the renin-angiotensin-aldosterone system with the development of hyperaldosteronism. The renal effects of increased aldosterone leading to sodium retention also contribute to the development of ascites.
Sodium retention is the consequence of a homeostatic response caused by underfilling of the arterial circulation secondary to arterial vasodilation in the splanchnic vascular bed. Because the retained fluid is constantly leaking out of the intravascular compartment into the peritoneal cavity, the sensation of vascular filling is not achieved, and the process continues
The increased portal venous pressure in combination with splanchnic vasodilation alters normal permeability and capillary pressure. This alteration enables movement of vascular fluid through the poles between capillary vascular endothelial cells of the portal system into extravascular space of the liver and intestines.
Any condition that causes obstruction to hepatic venous flow may lead to ascites as a result of increasing portal venous pressure like in the case of Budd-Chiari Syndrome. The site of this obstruction can be anywhere from hepatic venules, large hepatic veins, inferior vena cava or right atrium of the heart. This is why right heart failure causes ascites.
Hypoalbuminemia and ascites
Low concentration of plasma proteins mainly albumin and reduced plasma oncotic pressure also contribute to the loss of fluid from the vascular compartment into the peritoneal cavity. Hypoalbuminemia is due to decreased synthetic function in a cirrhotic liver.
In a normal healthy being, there is relatively high osmotic pressure of intravascular plasma which tends to draw extravascular fluid back to intravascular compartment.
This osmotic gradient is reduced in hypoproteinemia or low protein levels in blood so that less fluid is removed from the extravascular space. In decreased synthetic function of the liver, the capacity of intestinal and hepatic lymphatics to remove fluid from extravascular interstitial space is exceeded and ascites eventually develops.
Malignant infiltration (Carcinomatosis Peritonei)
Abdominal cancers cause ascites as a result of inflammation, exudation, shedding of cells and in some instances bleeding.
This case usually occurs in late stages of cancer. The most common cancers associated are gastric cancers and ovarian cancers because of their ease of trans peritoneal spread.
Ascites due to peritoneal inflammation
Like any form of inflammation, peritoneal inflammation results in increased in flow within peritoneal blood and lymphatic vessels.
Peritoneal wall micro vascular permeability increases with consequent exudation of plasma proteins and fluid into extravascular spaces.
When the ability of the lymphatics to absorb the fluid is exceeded it accumulates within the peritoneal cavity. Due to high protein in this fluid, reabsorption of the fluid is also impaired.
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Nice
Thank you for the video. I have a question: does portal hypertension cause hypoalbuminemia? Because I dont understand this. I know that cyrrosis causes hypoalbuminemia but does portal hypertenion in general cause hypoalbuminemia or we have it just in case there s an hepatic damage?
Hello.
Portal hypertension doesnt cause Hypoalbuminemia. Hypoalbuminemia is due to decreased synthetic function in a cirrhotic liver.Also the most common cause of portal hypertension is cirrhosis whereby there is increased vascular resistance and increased blood flow.
Hypoalbuminemia generally comes about in case of hepatic damage and not due to portal hypertension.
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thank you
I don't understand why ascitic protein levels vary in various causes of ascites. Why is ascitic protein low in cirrhosis and high in cardiac ascites?
Ascitic fluid protein is low in case of cirrhosis because in cirrhosis the sinusoids gets defenestrated and so large protein like albumin don't leak out and only smaller proteins leak. That's the reason. Forgive me if I am wrong🤗 🤗