Formation of portal collateral circulation

Introduction There is a wide communication branch between the portal vein and the body vein. In the case of cirrhotic portal hypertension, in order to stagnant blood in the portal system, these traffic branches are largely open, and the dilated or varicose veins are matched with the veins of the systemic circulation. The collateral circulation, so the portal vein blood can go straight back to the right heart without the liver. In the case of hepatic insufficiency, the activity of monoamine oxidase in the liver is reduced or the collateral circulation of the portal is formed. Hepatic insufficiency: refers to the serious damage to liver cells caused by certain causes, which can cause damage to the liver's morphological structure and cause serious disorders such as secretion, synthesis, metabolism, detoxification, immune function, etc., jaundice, bleeding tendency, serious infection, liver Pathological processes or clinical syndromes of clinical manifestations such as renal syndrome and hepatic encephalopathy.

Cause

Various pathogenic factors cause severe damage to liver parenchyma cells and Kupffer cells.

Its main collateral circulation has the following ways:

(1) At the bottom of the stomach, the gastric coronary veins of the portal vein are anastomosed with the intercostal veins, septal veins, esophageal veins, and semi-singular veins of the vena cava, forming the lower esophagus and gastric varices. These varicose veins are supported by weak submucosal tissue, which is often eroded by food friction and reflux of the whole esophagus acidic gastric juice, which is prone to rupture and bleeding. In severe cases, it can be fatal. Traditionally, the two hypotheses of gastric acid reflux erosion of esophageal mucosa and portal pressure increase explain the rupture of esophageal and gastric varices. Increased portal pressure, large varicose vein volume, and thin wall can cause the varicose vein wall pressure to rise above the elastic limit and cause rupture. Determination of varicose vein wall pressure has important clinical significance for predicting variceal hemorrhage.

(2) The subcutaneous vein around the umbilicus communicates with the umbilical vein during the fetal period, and the umbilical vein is occluded after birth. Subcutaneous varices are visible around the umbilicus and in the upper abdomen as the umbilical vein reopens and expands during portal hypertension.

(3) The superior iliac vein of the portal vein is anastomosed to the middle and lower iliac veins of the intestinal venous system to form the nucleus.

(4) The establishment of collateral circulation in all the abdominal organs and the retroperitoneal tissue or in the site of adhesion to the abdominal wall, including the umbilical vein of the liver to the septum, the spleen and renal ligament and the vein in the omentum, the lumbar vein or the posterior The abdominal wall vein, and the vein formed in the scar tissue of the laparotomy staff.

an examination

Related inspection

Liver ultrasound examination of liver function tests

1, insidious onset, fatigue, loss of appetite, abdominal distension, diarrhea, weight loss and so on.

2, hepatomegaly, hard edges, often nodular, spider mites, liver palm, splenomegaly, abdominal varicose veins, ascites and so on.

3, often with mild anemia, decreased platelets and white blood cells. Combined with increased bilirubin, ALT, AST, GGT, prolonged prothrombin time, decreased plasma albumin, inverted A/G ratio, and increased alpha-fetoprotein.

4, B ultrasound can prompt diagnosis. Esophageal barium meal seeing X-ray positive signs of varicose veins also has a decisive diagnostic significance.

Differential diagnosis

(1) Hepatomegaly should be differentiated from chronic hepatitis, primary liver cancer, liver echinococcosis, clonorchiasis, chronic leukemia, and hepatolenticular degeneration.

(2) Ascites should be differentiated from cardiac insufficiency, kidney disease, tuberculous peritonitis, constrictive pericarditis.

(3) Splenomegaly should be differentiated from malaria, chronic leukemia, and schistosomiasis.

(4) Acute upper gastrointestinal bleeding should be differentiated from peptic ulcer, erosive hemorrhagic gastritis, and gastric cancer.

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