Portal vein thrombosis

　　The etiology of portal vein thrombosis (PT) is complex, mainly including inflammatory, tumor, coagulation dysfunction, postoperative abdominal surgery, traumatic, and idiopathic causes. 25% to 30% of adult cases of portal vein thrombosis are secondary to liver cirrhosis. Portal vein thrombosis in infants and young children is often secondary to congenital portal vein atresia, umbilical vein sepsis, appendicitis, and other conditions. PT can be classified into primary and secondary types. Local factors account for 40% of the risk factors for PT formation, and the presence of local factors promotes the formation of portal vein thrombosis. These local factors are mainly divided into four categories: local infection foci, portal vein system injury, abdominal tumors, and liver cirrhosis, with liver cirrhosis complicated by PT being the most common in clinical practice. PT can also occur during pregnancy (especially in preeclampsia patients), in patients taking oral contraceptives, and in those with portal vein congestion (such as hepatic vein obstruction, chronic heart failure, restrictive pericarditis). The specific details are as follows:

　　1. Portal hypertension is mostly caused by liver cirrhosis and congestive splenomegaly due to various etiologies. It is mainly due to the increase in portal vein pressure, resulting in a decrease in the amount and slow blood flow of the hepatic portal blood flow, causing eddies and platelet accumulation to form thrombi.

　　2. Abdominal infection is caused by bacteria from intestinal infectious foci entering the portal venous system, such as neonatal umbilical inflammation, umbilical venous sepsis, and in adults, common conditions include acute appendicitis, pancreatitis, cholecystitis, perforation of hollow organs, inflammatory lesions of the small intestine, abdominal pelvic abscesses, and postoperative infections in the abdomen.

　　3. Abdominal surgery and trauma: Various abdominal surgeries can lead to thrombosis in the portal venous system, especially after splenectomy, which is the most common. It may be related to an increase in platelets and an increase in blood viscosity after surgery. After splenectomy, the reduction in portal vein blood flow and the accelerated decrease in portal vein pressure accelerate the formation of thrombosis. In addition, the slow blood flow in the expanded splenic vein after surgery, in a hypercoagulable state, also promotes the formation of splenic vein thrombosis.

　　4. Hypercoagulable state of blood: Abdominal tumors, especially those in the colon and pancreas, often have a hypercoagulable state in the portal venous system, which can lead to thrombosis. In recent years, it has also been found that hereditary coagulation dysfunction also participates in the formation of portal vein thrombosis, including protein C, protein S, and antithrombin deficiency, etc.

　　5. Compression of the portal vein by tumors: Compression by tumors (such as pancreatic tumors, hepatocellular carcinoma) and intestinal volvulus can lead to obstruction of blood flow in the portal venous system, resulting in portal vein thrombosis.

　　6. Other causes: include primary venous sclerosis, extension of splenic vein or mesenteric vein thrombosis, a history of long-term use of oral contraceptives in some patients, and rare factors such as various congestive heart failure, polycythemia, etc.

　　7. Primary portal vein thrombosis: A small part of extrahepatic portal vein thrombosis has no clear etiology. There may be a history of deep vein thrombosis in the limbs or migratory thrombophlebitis.

　　Esophageal varices and gastroesophageal varices with rupture and bleeding are common complications of portal vein thrombosis, which seriously threaten the patient's life. After the first bleeding stops, there is a possibility of recurrent bleeding, but it is not a symptom that every patient must have.

　　The clinical manifestations of portal vein thrombosis are divided into acute and chronic types:
　　1. Acute type
　　Sudden onset of the disease, with severe abdominal pain, distension, and vomiting, mainly caused by intestinal congestion. If the thrombus spreads to the superior mesenteric vein, symptoms such as diarrhea, hematochezia, abdominal pain, distension, abdominal tenderness, muscular tension, and percussion pain may occur, indicating peritonitis or paralytic ileus. In infants and young children, it may manifest as sudden upper gastrointestinal bleeding, with an enlarged spleen being mild in most cases. If the thrombus spreads to the main portal vein and intrahepatic branches, a large amount of ascites may occur.
　　2. Chronic type
　　If the patient passes through the acute phase, due to the extensive collateral circulation established between the portal and systemic veins - that is, the formation of natural shunts, ascites may be relieved or reduced. Splenomegaly is often a prominent symptom, and the degree of splenic enlargement generally depends on the duration of the disease. After long-term congestion of the spleen, splenic pulp cells proliferate and fibrous tissue accumulates, and a large number of inhibitory blood cells cause an increase in blood cell destruction, leading to hypersplenism. Clinical manifestations include varying degrees of anemia, decreased platelet count, and in some patients, nosebleeds, but rarely purpura.

　　Active treatment of the primary disease is the key to preventing portal vein thrombosis. The diet of patients should be light and easy to digest, with an emphasis on eating more vegetables and fruits, properly balanced meals, and ensuring adequate nutrition. In addition, patients should also pay attention to avoiding spicy, greasy, and cold foods.

　　The following are the items and content of the laboratory tests for the diagnosis of portal vein thrombosis:
　　1. Abdominal X-ray: In cases of combined intestinal necrosis or paralytic ileus, there is visible intestinal dilatation and thickening with air-fluid levels.
　　2. Abdominal Ultrasound: It shows the location, size, and extent of portal vein thrombosis formation. The main findings are the widening of the main portal vein, splenic vein residual end, and superior mesenteric vein trunk. There are abnormal echoes in the veins, which are实质性 irregular strong light points or isoechogenic light points. In patients with cavernous transformation of the portal vein, the main portal vein and branches disappear, and the portal vein is replaced by a small and irregular tubular structure.
　　3. Color Doppler: The diameter of the portal vein, splenic vein, or superior mesenteric vein is widened, and substantial echoes are detected. The blood flow becomes finer, and the blood flow signal disappears when completely blocked. The distal veins to the embolism are dilated.
　　4. Abdominal CT: Including conventional unenhanced and enhanced scans (arterial phase and venous phase), the CT typical sign of portal vein thrombosis is the appearance of non-enhanced low-density strips or masses within the portal vein lumen, and visible collateral veins and abnormal intestinal segments, as well as the detection of splenomegaly or splenic thickening.
　　5. Angiography: Direct or indirect portal vein angiography can show the location and extent of thrombosis. At the site of portal vein or splenic vein thrombosis, there is a filling defect or complete absence of contrast agent. The distal to the obstruction and splenic vein are dilated, tortuous, elongated, and displaced. The proximal to the obstruction and intrahepatic portal vein branches do not show contrast agent filling. There is a large amount of contrast agent retention in the spleen.
　　6. Magnetic Resonance Angiography (MRA): This examination provides a highly accurate evaluation of the portal venous system and can provide more information about collateral circulation than ultrasound or CT. It can understand the patency of the portal venous system, thrombosis, varicose veins, spontaneous shunts, and others. It has very high sensitivity and specificity.

The diet of patients with portal vein thrombosis should be light and easy to digest, with an emphasis on eating more vegetables and fruits, properly balanced meals, and ensuring adequate nutrition. In addition, patients should also pay attention to avoiding spicy, greasy, and cold foods.

　　For the acute type of portal vein thrombosis, medical treatment should be performed, such as anticoagulation, antithrombosis, thrombolysis, and antispasmodics. For cases with bleeding, hemostasis and antishock should be the main focus.
　　For chronic cases, the overall goal is to stop the rupture of esophageal and gastric fundus varices, save lives; reduce portal vein pressure, prevent recurrence of bleeding; relieve hypersplenism.
　　1. Hemostatic Measures
　　For bleeding, it is difficult for clinical physicians to estimate how much blood the patient will bleed and what methods can prevent the recurrence of bleeding permanently. Therefore, even for patients with small amounts of hematemesis or melena, attention should be paid. Firstly, medical treatment is adopted, such as patients resting in bed, fasting, supplementing nutrition, applying hemostatic agents, applying three-chamber two-sac tube compression (children can use an appropriate model of Foley catheter), and also injecting sclerosing agents into the varices under esophageal endoscopy.
　　2. Surgical Treatment for Hemorrhage Prevention
　　Due to the relatively mild liver function damage at the time of portal vein thrombosis, the tolerance for shunt surgery is better, and the effect is also reliable; while the long-term effect of the occlusion surgery is often not satisfactory, therefore, shunt surgery should be the first choice for such patients. The following is a brief introduction to several types of shunt surgery:
　　1. Portal bypass surgery: Also known as shunt bypass, which is to bridge or short-circuit anastomosis between the proximal and distal ends of the obstructed portal vein, so that the venous blood flow of the viscera flows into the portal vein of the liver, thereby restoring the normal circulation of portal vein blood flow, which is in line with physiology. However, it must be available in the superficial location of the liver with the corresponding口径 of the portal vein branches that can be anastomosed, and there have been no reports in China at present.
　　2. Modified spleen and greater omentum pleural fixation: Many clinical practices have achieved good effects and are suitable for various types of portal hypertension.
　　3. C-shaped bridge surgery for superior mesenteric vein-inferior vena cava artificial blood vessel with combined ligation of coronary vein and splenic artery: This operation is also known as 'triple surgery', during which, after entering the abdomen, the splenic artery, coronary vein, and posterior gastric vascular branches in the gastric plicae of the pancreas are ligated through the omentum. If the spleen is large, a partial resection can be performed. An artificial blood vessel (Gore-Tex) with a diameter of 1.0 cm and a ring is used for the C-shaped bridge between the intestine and the cavity.
　　3. Intestinal Resection
　　For patients with mesenteric thrombosis who have intestinal necrosis, the only treatment method is the resection of the necrotic intestinal segment and mesentery. Postoperative continuous anticoagulation is used to prevent the recurrence of thrombosis.