Consequences of impaired portal blood flow

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

In the presence of collaterals, portal hypertension is usually implied, although sometimes with significant development of collaterals, the pressure in the portal vein can decrease. 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 may develop.

Morphological changes in portal hypertension

At autopsy, signs of significant collateral circulation are almost not detected, since varicose veins are in a collapsed state.

The spleen is enlarged, its capsule is thickened. Dark blood oozes from the cut surface (fibrocongestive splenomegaly). Malpighian bodies are not visible. Histological examination reveals dilated sinusoids lined with thickened endothelium. Histiocyte proliferation is noted, sometimes accompanied by erythrocyte phagocytosis. Periarterial hemorrhage foci may develop into siderosis and fibrosis nodes.

Vessels of the portal system and spleen. The splenic artery and portal vein are enlarged, tortuous, and may contain aneurysms. Subendothelial hemorrhages, parietal thrombi, intimal plaques, and calcification are detected in the portal and splenic veins. Such veins cannot be used for surgical interventions.

In 50% of cases of cirrhosis, small aneurysms of the splenic artery are detected.

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

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

Varicose veins

Esophagus

If there are no varicose veins of the esophagus and stomach and bleeding from them, then portal hypertension has no clinical significance. Blood flows into the varicose veins of the esophagus mainly from the left gastric vein. Its posterior branch usually flows into the azygos vein system, and the anterior one communicates with the varicose veins immediately below the junction of the esophagus with the stomach, forming a bundle of thin parallel veins in this place, which pass into large tortuous veins in the lower part of the esophagus. The veins of the esophagus are located in 4 layers. Intraepithelial veins in portal hypertension can endoscopically look like red spots, their presence indicates the possibility of rupture of varicose veins. The superficial venous plexus drains into larger deep veins of the submucous plexus. Perforating veins connect the submucous plexus with the fourth layer of veins, the adventitial plexus. Typically, the largest varicose veins belong to the deep submucous plexus, which connects with the varicose veins of the stomach.

The anatomical structure of the veins of the esophagogastric junction, which provide a connection between the portal and systemic circulation, is very complex. Increased blood flow and its redistribution into the superior vena cava system in portal hypertension have been little studied. Between the perforating vein zone and the gastric zone there is a transition zone. In this zone, the blood flow is directed in both directions; it ensures blood deposition between the portal and azygos vein systems. The turbulent nature of the blood flow in the perforating veins connecting varicose veins with adventitial veins helps explain the high frequency of ruptures in the lower third of the esophagus. Recurrence of varicose veins after endoscopic sclerotherapy is apparently due to the presence of communications between different venous trunks or dilation of the veins of the superficial venous plexus. The lack of effect from sclerotherapy can also be explained by the failure to achieve thrombosis of the perforating veins.

Stomach

Blood in the varicose veins of the stomach comes mainly from the short veins of the stomach and flows into the submucosal venous plexus of the esophagus. Varicose veins of the stomach are especially pronounced in the extrahepatic form of portal hypertension.

Radiographically, varicose veins of the duodenum appear as filling defects. The presence of dilated 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 veins. Their first clinical manifestation may be bleeding. They can be identified during colonoscopy. The source of bleeding can be localized by scintigraphy with erythrocytes labeled with ^99m Tc. After successful sclerotherapy of the esophageal veins, varicose veins of the colon rapidly develop.

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

Intestinal vascular lesions in portal hypertension

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

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

Congestive jejuno- and colonopathy. Similar changes develop in the duodenum and jejunum. Histologically, an increase in the number and diameter of vessels is detected in the villi of the jejunum. Edema and hyperemia of the mucous membrane are noted, it becomes easily injured.

Congestive colonopathy is indicated by dilation of the capillaries of the mucous membrane with thickening of the basement membrane in the absence of signs of inflammation of the mucous membrane.

Vascular changes in other structures

Portosystemic collaterals may also form in adhesions of abdominal organs to the abdominal wall that occur after surgery or pelvic inflammatory disease. Varicose veins also occur in areas where mucous membranes and skin meet, such as after ileostomy or colostomy.

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