Portal hypertension

Introduction to portal hypertension Portal hypertension is a group of syndromes caused by a persistent increase in portal pressure. Most are caused by cirrhosis, a few secondary to the portal vein or hepatic vein obstruction and other factors of unknown cause. When the portal vein blood does not flow smoothly through the liver into the inferior vena cava, it will cause an increase in portal pressure. The performance is that the portal-to-venous communication is open. A large amount of portal vein blood enters the systemic circulation directly through the traffic branch before entering the liver, resulting in abdominal wall and esophageal vein dilation, splenomegaly and hypersplenism, liver function decompensation and ascites. . The most serious is the dilatation of the veins at the junction of the esophagus and the stomach. Once ruptured, severe acute upper gastrointestinal bleeding is life-threatening. basic knowledge The proportion of illness: 0.06% Susceptible people: no special people Mode of infection: non-infectious Complications: esophageal varices and rupture of hemorrhage Upper gastrointestinal bleeding Hypersplenism

Causes of portal hypertension

Cirrhosis of the liver (60%):

According to the pathological morphology, it can be divided into two types: anterior sinus obstruction The common cause of anterior sinus obstruction is schistosomiasis cirrhosis. Schistosomiasis matures in the portal system, spawns, forms egg emboli, and the blood flow from the portal vein reaches the small branch of the portal vein in the portal area of the hepatic lobules, causing thrombotic endometritis and fibrosis around them. The blood flow to the portal vein is blocked and the portal vein pressure is increased. A common cause of post-sinus occlusion is cirrhosis after hepatitis. The main pathological changes are fibrous tissue hyperplasia and hepatocyte proliferation in the hepatic lobule. Due to the compression of the proliferating fiber cord and the regenerating hepatocyte nodules, the hepatic sinus is narrowed and blocked in the hepatic lobules, so that the portal vein blood does not easily flow to the central vein of the hepatic lobules, and the blood flow stagnates, causing the portal vein pressure to rise. Post-sinus obstruction, due to the narrowing or occlusion of the hepatic sinus in many hepatic lobes, so that some of the high-pressure hepatic arterial blood flows through the arterial traffic in the hepatic lobular region, directly injecting a small portal vein with low pressure, making the portal pressure higher. .

Extrahepatic portal vein occlusion (30%):

Mainly due to the main thrombosis of the extrahepatic portal vein, the portal vein is mainly caused by obstruction of the branch. The most common is splenic vein thrombosis. Obstruction of the extrahepatic portal vein, stagnant blood flow at the distal end of the obstruction, elevated venous pressure, esophageal varices and upper gastrointestinal bleeding can occur. Such patients are more common in children, and liver function is mostly normal.

Portal hypertension prevention

The early stage of the disease can be without any symptoms, and once the symptoms appear, it is often more dangerous. Therefore, it is necessary to regularly follow up the health checkups in patients with post-hepatitis cirrhosis and schistosomiasis cirrhosis; early detection and early treatment.

1, the law of life, do not do strenuous exercise. Rest in multiple beds and do a deep, rhythmic breath to help the blood flow back.

2, adjust the diet, should eat nutritious and digestible soft food, must not eat rough and hard food. Most patients have ascites and should limit salt intake. When there is no hepatic coma, you can eat good quality protein.

3, to prevent any activity that can increase abdominal pressure, such as vomiting, constipation, cough, laughter, force and so on.

4, regular visits to specialist hospitals, if necessary, do esophagus and gastroscopy to understand the varicose veins. Appropriately take some drugs to reduce the pressure of the portal vein, or vaginal vein ligation, or surgery. In short, the portal hypertension must not be taken lightly, otherwise the consequences are unimaginable.

Portal hypertension complications Complications Esophageal and gastric varices and their rupture and bleeding upper gastrointestinal bleeding hypersplenism

Gastroesophageal varices bleeding is a major complication of portal hypertension.

Symptoms of portal hypertension Common symptoms Portal hypertension splenomegaly ascites left upper abdominal mass accompanied by... Huangqi liver hydropsyma urinary upper gastrointestinal bleeding thrombocytopenia

Portal hypertension is more common in middle-aged men, and the disease develops slowly. Symptoms and signs vary according to the etiology. The clinical manifestations are splenomegaly, hypersplenism, and esophageal varices, hematemesis and melena and ascites. Symptoms and signs, but mainly splenomegaly, hypersplenism, hematemesis and ascites.

(A) splenomegaly: most of the spleen combined with symptoms of hypersplenism, such as anemia, blood cells and thrombocytopenia, in general, the larger the spleen, the more prominent spleen function.

(2) Upper gastrointestinal bleeding: When the portal pressure is increased, the fundus vein and the lower esophageal varices are caused. Therefore, the lower esophageal varices are an important manifestation of portal hypertension, often due to ulcers, trauma and bleeding, due to liver Functional damage leads to coagulation dysfunction, bleeding is not easy to stop, the clinical manifestations of hematemesis and tar-like stools and other upper gastrointestinal bleeding symptoms.

(3) Ascites: In the late stage of intrahepatic portal hypertension, the appearance of ascites is a manifestation of impaired liver function. In patients with ascites, the superficial veins of the abdominal wall tend to be more pronounced, sometimes accompanied by jaundice.

Examination of portal hypertension

Auxiliary inspection

1, most patients have a history of hepatitis, alcohol history or history of schistosomiasis, a small number of patients with unknown history of jaundice, usually may be easy to nosebleed or bleeding gums, chronic diarrhea, abdominal distension, lower extremity edema and other abnormal performance.

2, if you go to the hospital for a physical examination, you may find jaundice, palm redness (liver palm), spider sputum and abdominal wall varicose veins, splenomegaly and ascites.

3. In order to make a preliminary judgment, the doctor first prescribes routine non-invasive tests, such as testing hematuria, coagulation, liver function (mainly bilirubin, albumin, transaminase), alpha-fetoprotein (screening for liver cancer). ), check for hepatitis B or hepatitis C infection, suspected schistosomiasis for the fecal hatching test or serum ring egg test.

4, color ultrasound is also very common, you can roughly understand the size of the liver, spleen and with or without cirrhosis, ascites and its severity, and scan the portal vein for thrombosis, portal patency, blood flow and blood flow direction.

5, abdominal enhanced CT scan is a diagnostic value for the diagnosis of portal hypertension, can clearly observe the diameter of the portal vein, the presence or absence of thrombosis, the presence of a large number of varicose vessels, the extent of liver disease and the presence or absence of liver cancer, spleen, ascites The amount. CT is a key check and has a guiding role in the next step of treatment.

6. If you want to know whether the patient's esophagus and fundus have varicose veins and their extent, the simple method is X-ray barium meal examination. The high accuracy is to make a fiber endoscope, which can simultaneously determine whether there is a risk of bleeding and treatment.

7. Measurement of portal pressure is a direct evidence for the diagnosis of portal hypertension. Invasive measurements are rarely used at present. Generally, the ratio of nuclear to blood flow (H/L) is used to indirectly estimate portal pressure.

Diagnosis and diagnosis of portal hypertension

Diagnosis can be based on medical history, clinical symptoms, and laboratory tests.

When esophageal varices rupture, it should be differentiated from gastroduodenal ulcer, erosive gastritis, gastric cancer and vomiting esophageal mucosal rupture, detailed medical history, comprehensive physical examination and laboratory tests, including blood and liver function tests. Blood ammonia determination, etc., gastroduodenal ulcer bleeding, general history of ulcer, spleen is not swollen, liver function is normal, after the major bleeding, there is generally no jaundice, ascites, these are helpful to identify, sometimes difficult to identify, feasible X-ray barium meal examination, fiber gastroscopy or selective celiac angiography to make a diagnosis.

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