Consequences of portal blood flow disturbance

When the amount of portal blood flowing to the liver decreases in connection with the development of collateral circulation, the role of the hepatic artery increases. The liver decreases in volume, its ability to regenerate decreases. This is probably due to inadequate intake of hepatotropic factors, including insulin and glucagon, produced by the pancreas.

In the presence of collaterals usually refers to portal hypertension, although sometimes with significant development of collaterals, pressure in the portal vein can be reduced. At the same time, short-term portal hypertension can occur without the development of collateral circulation.

With significant portosystemic shunting, hepatic encephalopathy, sepsis caused by intestinal bacteria, and other circulatory and metabolic disorders can develop.

Morphological changes in portal hypertension

On autopsy signs of significant collateral circulation are almost not detected, as varicose-dilated veins are in a collapsed state.

The spleen is enlarged, its capsule is thickened. From the surface of the cut, dark blood oozes (fibrous-stagnant splenomegaly), Malpighian corpuscles are invisible.With histological examination, the sinusoids are broadened and lined with thickened endothelium.Histocytes proliferation, sometimes accompanied by erythrocyte phagocytosis, can be transformed into nodes of siderosis and fibrosis.

Vessels of the portal system and spleen. The splenic artery and portal vein are enlarged, crimped, and there may be aneurysms in them. In the portal and splenic veins, subendothelial hemorrhages, parietal thrombi, plaques in the intima, calcinosis are revealed. On such veins, surgical procedures can not be performed.

In 50% of cases with cirrhosis, small aneurysms of the spleen artery are found.

Changes in the liver depend on the cause of portal hypertension.

The relationship between the degree of increase in pressure in the portal vein and the severity of cirrhosis and especially of fibrosis is weak. More distinct communication is noted between portal hypertension and the number of nodes in the liver.

Phlebeurysm

Esophagus

If there is no varicose veins of the esophagus and stomach and bleeding from them, then portal hypertension has no clinical significance. In the varicose veins of the esophagus, blood flows mainly from the left gastric vein. Its posterior branch usually falls into the unpaired vein system, and the anterior one communicates with the varicose veins immediately below the junction of the esophagus with the stomach, forming in this place a bundle of thin parallel veins that pass into the large convoluted veins in the lower part of the esophagus. The esophageal veins are arranged in 4 layers. Intraepithelial veins with portal hypertension can endoscopically have the appearance of red spots, their presence indicates the possibility of rupture of varicose-dilated veins. The superficial venous plexus is drained into the larger deep veins of the submucosal plexus. Perforating veins connect the submucosal plexus to the fourth layer of veins - the adventitious plexus. Usually the largest of the varicose-dilated veins refer to the deep submucosal plexus, which connects to the varicose-dilated veins of the stomach.

The anatomical structure of the veins of the region of the esophageal-gastric junction, through which the connection between portal and systemic circulation is realized, is very difficult. The increase in blood flow and its redistribution into the system of the inferior vena cava with portal hypertension have been studied little. Between the zone of perforating veins and the stomach zone is the transition zone. In this zone, the blood flow is directed to both sides, it ensures the deposition of blood between the portal and unpaired veins systems. The turbulent nature of the blood flow in the perforating veins that connect the varicose-dilated veins with adventitia allows one to explain the high incidence of ruptures in the lower third of the esophagus. Recurrences of varicose veins after endoscopic sclerotherapy are apparently due to the presence of messages between different venous trunks or the expansion of veins of the superficial venous plexus. The lack of effect from sclerotherapy can also be explained by the fact that it is not possible to achieve thrombosis of perforating veins.

Stomach

The blood in the varicose-dilated veins of the stomach comes mainly from the short veins of the stomach and flows into the submucous venous plexus of the esophagus. Especially pronounced varicose veins of the stomach with extrahepatic form of portal hypertension.

Roentgenologically varicose-dilated veins of the duodenum look like filling defects. The presence of expanded collaterals around the bile duct makes the operation dangerous.

Colon and rectum

Varicose veins of the colon and rectum develop as a result of the formation of collaterals between the inferior mesenteric and internal iliac vein. The first clinical manifestation of them may be bleeding. They can be identified with a colonoscopy. The source of bleeding can be localized by scintigraphy with erythrocytes labeled with ^99m Tc. After successful sclerotherapy of the esophagus, rapid development of varicose veins of the colon takes place.

The presence of collaterals between the upper (portal vein system) and the middle and lower (lower vena cava system) hemorrhoidal veins promotes varicose enlargement of the anorectal veins.

The defeat of the intestinal vessels with portal hypertension

In chronic portal hypertension, not only varicose veins develop, but also various changes in the intestinal mucosa due to microcirculation disorders.

Pathology of the stomach with portal hypertension. The blood supply of the stomach is disturbed: the number of arteriovenous shunts between the own muscular plate of the mucous membrane and the expanded precapillary and veins of the submucosal layer increases, vascular ectasia. Increased blood flow in the mucous membrane of the stomach. The likelihood of its damage and development of bleeding, for example, under the influence of non-steroidal anti-inflammatory drugs (NSAIDs), significantly increases. After sclerotherapy of the esophagus, changes in the gastric mucosa may increase. They can only be reduced if portal pressure is reduced.

Stagnant nejino-and a colonopathy. In the duodenum and jejunum, similar changes develop. Histologically, in the villi of the jejunum, an increase in the number and diameter of the vessels is revealed. There is swelling and hyperemia of the mucous membrane, it becomes light-headed.

Stagnant colonopathy is indicated by the expansion of capillaries of the mucous membrane with a thickening of the basal membrane in the absence of signs of mucosal inflammation.

Vascular changes in other structures

Portosystemic collaterals can also form in spasms of the abdominal cavity organs with the abdominal wall, which are formed after operations or inflammatory diseases of the pelvic organs. In addition, varicose veins are noted in the areas of mucous membranes and skin, for example after ileostomy or colostomy.

[1], [2], [3], [4], [5], [6], [7], [8], [9], [10], [11], [12]