Portal hypertension

Introduction to portal hypertension Portalhypertension is a group of syndromes caused by persistent increase in portal pressure. The vast majority of patients are caused by cirrhosis, and a small number of patients are secondary to portal vein or hepatic vein obstruction and some unexplained factors. basic knowledge Sickness ratio: 0.1% Susceptible people: no special people Mode of infection: non-infectious Complications: upper gastrointestinal bleeding esophageal varices and rupture of bleeding gastric ulcer liver and kidney syndrome

A. Sinusoidal space shrinkage: The main reasons are the collagenization of Disse space, the increase in the volume of hepatocytes and macrophages, the accumulation of fat in adipocytes, the proliferation of fibrous tissue, the infiltration of tumor cells outside the sinus, and the formation of sinus thrombosis. Due to the large lumen of the sinusoidal vessels and no pressure-resistant structure, when the internal and external pressure changes, the lumen can be passively expanded or contracted. Hypertrophy, on the one hand, compresses the sinus wall, reducing and narrowing the sinusoidal space. Since the vascular resistance is inversely proportional to the fourth power of its radius, a mild stenosis of the sinusoidal space can significantly increase the blood flow resistance and aggravate the intrahepatic Microcirculation disorders. On the other hand, due to the narrowing of the sinusoidal space, the micropores on the endothelial cells are reduced and the number is reduced, which narrows the Disse space, thereby affecting the nutrient uptake and excretion of the liver cells themselves, further aggravating the damage of the liver cells, and forming a vicious circle. . In alcoholic liver disease, not only liver cells are severely fatty, but also amyloid deposition in the Disse space, collagenization and fibrin deposition, hepatic artery damage, and increased blood flow resistance. The increase of hepatocyte volume and the collagenization of Disse space are the main reasons for the narrowing of intrahepatic vascular space. In patients with chronic vitamin A poisoning, the accumulation of intrahepatic fat-storage cells can also narrow the sinusoidal space and increase blood flow resistance. The infiltration and proliferation of various tumor cells and extramedullary hematopoiesis caused by various reasons can also increase sinus circulation disorders. Sinusoidal thrombosis caused by DIC can block intrahepatic microcirculation and is also one of the factors that seriously affects portal hypertension.

B. Capillary vascularization of hepatic sinusoids: This is due to the unique and complex structure of the above-mentioned intrahepatic microcirculation. The inner diameter of the sinusoid is only 7-15 μm, and there is no basement membrane outside the sinus. The sinus wall is composed of endothelial cells, hepatic macrophages, fat-storage cells, lacuna cells, and a very small amount of reticular fibers and nerve fibers. Its endothelial cells have many micropores with a diameter of about 0.1 μm. Only solutes and particulate matter in the blood can enter the Disse space through these micropores, while blood cells cannot. Sinusoidal blood is in direct contact with hepatocytes. Hepatocyte injury, inflammation, immune response, etc. caused by various reasons cause increased collagen synthesis, fibrous tissue proliferation, formation of basement membrane under endothelial cells, and de-microporation of endothelial cells, leading to capillary vascularization of hepatic sinusoids, hindering blood and liver The contact of cells not only affects the exchange of substances inside and outside the cells, but also hinders the passage of blood cells, increases blood flow resistance, and participates in the formation of portal hypertension.

C. Intrahepatic blood flow redistribution: due to chronic liver inflammation and other chronic injuries, under the long-term action of cytokines and other factors, necrosis and proliferation of liver cells occur simultaneously or sequentially, and the original mesh scaffold collapses, collagen Metabolism, diffuse proliferation of fibrous tissue, resulting in structural changes in the original hepatic lobules and the formation of pseudolobules. The shape of the intrahepatic blood vessels is widely deformed, and the direct communicating branches between the hepatic artery and the portal vein are opened to form various anastomosis such as portal vein-hepatic vein, portal vein-portal vein, hepatic vein-hepatic vein, and hepatic artery-portal vein, among which the main one is the hepatic artery- Hepatic veins and portal-hepatic shunts. In addition, due to the obstruction of portal venous return during portal hypertension and the natural portosystemic shunt outside the liver, the total blood flow of the liver decreases. The proportion of hepatic artery and portal venous blood changes with the development of the disease, the proportion of portal venous blood is less and less, and the proportion of hepatic artery blood is more and more. The effects of this redistribution of intrahepatic blood flow on portal hypertension include: through the arteriovenous anastomotic branch, the hepatic artery pressure can be directly transmitted to the portal vein, increasing the portal vein pressure; reducing the blood flow in the sinusoidal space, thereby allowing the blood perfusion of hepatocytes Insufficient amount will aggravate liver cell damage, increase sinusoidal blood flow resistance, and aggravate portal hypertension.

D. Post-sinusoidal factors in the liver: In addition to the factors of increased extrahepatic venous resistance caused by post-sinusoidal causes such as hepatic vein thrombosis or embolism, Budd-Chiari syndrome, etc., in some patients with liver cirrhosis, intrahepatic post-sinusoidal factors also Participate in the occurrence of this disease, which is due to increased resistance or even obstruction of hepatic venule outflow tract due to perivascular sclerosis between hepatic sinusoids and hepatic venules, nodule formation in liver regeneration, fibrosis, liver cell inflammation, and edema. , in the formation of portal hypertension may also be partially involved in its pathogenesis.

Liver cirrhosis is the most common cause of portal hypertension, so various liver diseases should be actively treated to avoid cirrhosis caused by liver damage. There are no symptoms in the early stage of the disease, and once symptoms appear, it will be more dangerous. Therefore, it is necessary to regularly follow up patients with post-hepatitis cirrhosis and schistosomiasis cirrhosis in combination with physical examinations; early detection and early treatment.

Complications of portal hypertension Complications Upper gastrointestinal bleeding Esophagogastric varices and ruptured bleeding gastric ulcer Hepatorenal syndrome
1. Stomach fundus and esophageal variceal bleeding are the most common and dangerous complications of portal hypertension.

2. In patients with hepatic encephalopathy and cirrhosis, upper gastrointestinal bleeding is the most common and most serious complication, whether it is variceal bleeding, gastric mucosa or ulcer bleeding.

3. Gastrointestinal bleeding This bleeding mainly comes from the esophagus, gastric varices, acute gastric mucosal erosion and duodenal or gastric ulcer, mainly caused by portal hypertension, belonging to portal gastropathy and portal enteropathy Fan, is the most common serious complication of chronic liver disease.

4. Hepatorenal syndrome After upper gastrointestinal hemorrhage in patients with portal cirrhosis, liver function and systemic failure can easily lead to the formation of hepatorenal syndrome.

portal hypertension symptoms
Portal hypertension is mainly caused by various liver cirrhosis, most of which are caused by hepatitis liver cirrhosis in my country, followed by schistosomiasis liver cirrhosis and alcoholic liver cirrhosis. Check the characteristics of liver cirrhosis. This disease is more common in middle-aged men, and the disease develops slowly. The main clinical manifestations are: spleen enlargement, ascites, formation of portal collateral circulation and portal hypertensive gastroenteropathy. The formation of systemic collateral circulation is the most characteristic, and these clinical manifestations are often accompanied by corresponding complications, such as hypersplenism, primary peritonitis, gastrointestinal bleeding, hepatic encephalopathy and hypoalbuminemia.

1. Enlarged spleen

Hypersplenism and congestive splenomegaly is one of the main clinical manifestations of this disease, and it is also the earliest clinical sign. Sherlock believes that if the patient cannot touch the spleen clinically, and B-ultrasound or X-ray examination cannot show splenomegaly, the diagnosis of this disease is made. Insufficient evidence and doubtful, its incidence is about 80%.

(1) Causes of splenomegaly:

①Splenic artery dilatation: due to splenic artery dilation, blood flow increases, splenic venous output blood resistance increases and portal vein pressure is reversed to the spleen, causing passive congestion of the spleen, hyperplasia of spleen tissue and fibrous tissue in the spleen, leading to splenomegaly .

②Splenic mononuclear macrophage hyperplasia: Recent studies have shown that about 1/3 of patients with hypersplenism cannot be relieved after various portal shunts, and even individual patients' hypersplenism occurs after portal decompression. The reason is: because the intestinal antigen material enters the systemic circulation through the portal system collateral circulation, and is recognized and taken up by the spleen; or directly flows backward into the spleen through the splenic vein, the antigen stimulates the proliferation of splenic mononuclear macrophages, resulting in hypersplenism and splenomegaly.

(2) Clinical features and manifestations: When splenomegaly is accompanied by hypersplenism, the patient presents with leukopenia, proliferative anemia and thrombocytopenia, and is prone to anemia, fever, infection and bleeding tendency, and the spleen may be tender when there is perisplenitis.

Under normal circumstances, portal hypertension is often accompanied by splenomegaly and hypersplenism, but there is a lack of correlation among the three, disproportion, and the size, activity, and texture of the spleen are related to the course of the disease. Small nodular cirrhosis patients have obvious splenomegaly, and schistosomiasis cirrhosis is more prominent than alcoholic cirrhosis patients.

2. Ascites

In normal people, there is only a small amount of fluid in the abdominal cavity, which is serous fluid, no more than 200ml. It plays a lubricating role. It mainly contains water and a small amount of other substances. It enters and exits through the visceral layer of the peritoneum. When portal hypertension occurs in the late stage of liver cirrhosis, the rate of ascites formation exceeds The speed of reabsorption is often accompanied by ascites. The volume of ascites often exceeds 500ml, mostly around 1 to 4L, sometimes more than 5 to 6L, and up to 30L. The ascites mainly comes from the infiltration of extracellular fluid in the body.

portal hypertension

1. Blood routine, urine, feces, liver function, immunological examination and serum markers of liver fibrosis, etc.

2. Paracentesis

The ascites was aspirated by paracentesis, and routine, biochemical, culture and tumor cell examinations were performed on the ascites.

(1) Routine ascites: ascites is generally clear, light yellow, grass green or bile color, if the appearance is cloudy, 3/4 cases are primary purulent peritonitis or cancerous ascites; the remaining 1/4 cases have no infection or other complications The ascites contains lipidoid or pancreatic ascites, and smoke-like ascites may also appear. There are also cases where the cause is unclear. Whether the ascites is cloudy or not, it is uncertain whether there is inflammation or other complications. White or chylous ascites is more common in tumors. Found in trauma, intestinal obstruction, etc., bloody ascites is more common in malignant tumors.

(2) Determination of the protein content of ascites: the content of ascites is generally 10-20g/L, which is proportional to the albumin in the blood. If the protein content in ascites exceeds 25g/L, it may be infection, liver cancer or hepatic vein obstruction.

(3) Ascites cytology: In the ascites of liver cirrhosis, there are often cells (0.02-0.1)×109/L, mainly epithelial cells. Sometimes these cells resemble malignant cells and cannot be easily diagnosed as a tumor. Diploidy suggests malignant ascites.

(4) Bacteriology of ascites: acute infection of ascites, often caused by gram-negative bacteria, can also be pneumococcal infection, or tuberculous peritonitis, infection is also prone to occur after the application of corticosteroids, symptoms are full abdominal pain and Tenderness, fever, and leukocytosis persisted.

(5) Determination of carcinoembryonic antigen (CEA) and alpha-fetoprotein (AFP): Benign ascites CEA<15μg/L, more than this value in malignant ascites, AFP in ascites caused by primary liver cancer metastasis increases.

(6) Others:

①Determination of lactic acid in ascites: It is a method for the early and rapid diagnosis of bacterial infection, and the fermentation is enhanced due to infection, but lactic acidosis must be excluded.

②Ascites fibronectin (FN) determination: the concentration of FN is higher in cancerous ascites, lower in liver cirrhosis ascites, FN in cancerous ascites is more than 75mg/L, and lower than this value in primary bacterial peritonitis .

③Cholesterol determination: it is the most valuable for distinguishing benign and malignant ascites. Ascites cholesterol >1.24mmol/L is likely to be a tumor, but some primary bacterial peritonitis and tuberculous peritonitis ascites cholesterol levels can also increase.

3. Ultrasound imaging

Real-time imaging, two-dimensional ultrasonography and color Doppler flow imaging can be combined to detect portal hypertension.

Differential diagnosis

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