Portal hypertension - Pathogenesis

The main pathogenetic factors of portal hypertension are the following:

1. Mechanical obstruction of blood flow.

In subhepatic and posthepatic portal hypertension, the obstruction of blood flow is caused by thrombosis, obliteration, or (pressure from outside) large vessels (portal vein, hepatic veins).

Postsinusoidal intrahepatic block is caused by obliteration of the terminal branches of the hepatic vein or (pressure on them by regeneration nodes, centrilobular formation of fibrous tissue (for example, hyaline central sclerosis in chronic alcoholic hepatitis, etc.). Disruption of blood flow in the hepatic sinusoids is caused by the growth of connective tissue inside the liver lobule, proliferation of endothelial cells.

Presinusoidal intrahepatic block is associated with infiltration and fibrosis in the portal and periportal areas.

2. Increased blood flow in the portal veins.

This may be due to difficulty in the outflow of blood from the liver through the hepatic veins, the presence of arteriovenous fistulas, myeloproliferative diseases, liver cirrhosis, etc.

3. Increased resistance of portal vessels.

There are no valves in the portal venous system and any structural changes in it cause an increase in pressure. In patients with liver cirrhosis, resistance to blood flow can increase in different parts of the intrahepatic vascular bed.

The increase in vascular resistance is caused by the presence of regeneration nodes that compress the hepatic and portal veins, as well as the formation of collagen around the sinusoids, terminal hepatic venules, and disruption of the liver architecture.

4. Formation of collaterals between the portal vein pool and the systemic blood flow.

The development of these anastomoses is a consequence of portal hypertension.

In prehepatic portal hypertension, porto-portal anastomoses develop. They restore blood flow from the sections of the portal system located below the block to the intrahepatic branches of the portal vein.

With intrahepatic and suprahepatic portal hypertension, portocaval anastomoses develop, which ensure the outflow of blood from the portal vein system into the basins of the superior and inferior vena cava, bypassing the liver.

Anastomoses in the cardiac region of the stomach and esophagus are especially important, since bleeding from these veins is a severe complication of portal hypertension.

5. The development of ascites, the most important symptom of portal hypertension, is caused by the following factors:

• increased lymph production in the liver due to blockage of venous blood outflow from the liver. Lymph leaks through the lymphatic vessels of the liver capsule directly into the abdominal cavity or enters through the lymphatic ducts in the area of the hepatic portal into the thoracic duct. The capacity of the thoracic lymphatic duct becomes insufficient and lymphatic congestion occurs, promoting fluid exudation into the abdominal cavity;
• a drop in the colloid osmotic pressure of plasma, which is associated with a disruption in protein synthesis in the liver; a decrease in colloid osmotic pressure promotes the release of water into the extravascular space, i.e. into the abdominal cavity;
• increased activity of the renin-angiotensin-aldosterone system;
• impaired renal function (decreased renal blood flow, glomerular filtration, increased sodium reabsorption) due to impaired venous outflow from the kidneys or decreased blood flow to the kidneys;
• an increase in the content of estrogens in the blood due to a decrease in their destruction in the liver; estrogens have an antidiuretic effect.

6. Splenomegaly is a consequence of portal hypertension. Splenomegaly is caused by congestion, as well as the growth of connective tissue in the spleen and hyperplasia of cells of the reticulohistiocytic system.
7. Portal hypertension with the development of portocaval anastomoses gradually leads to hepatic (porto-systemic) encephalopathy.

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