Mesenteric venous thrombosis

　　The etiology of mesenteric venous thrombosis (MVT) is relatively complex and can be divided into two major categories: secondary and primary.
　　First, secondary factors
　　1. Liver cirrhosis complicated with portal hypertension: Due to portal hypertension, the blood flow of the mesenteric vein is slow, so thrombosis is sometimes easy to occur.
　　2. Infection of abdominal organs: such as acute appendicitis, acute pancreatitis, small intestinal inflammatory lesions, organ perforation, sepsis after abdominal surgery, abdominal abscess, or pelvic abscess. These inflammatory lesions can directly affect the blood flow of the mesenteric vein or cause MVT due to the action of bacterial toxins and the released coagulation factors.
　　3. Changes in mesenteric venous blood flow or vascular injury: including abdominal surgery, abdominal trauma, and radiation injury. Some scholars have found that after splenectomy and portocaval shunt surgery, MVT can be induced. It has been confirmed that some patients have a thrombocytosis phenomenon after splenectomy, which increases the coagulation factors in the blood and also increases the blood viscosity.
　　4. Abdominal closed injuries may occasionally damage the mesenteric vein and induce MVT.
　　5. High blood coagulation state: It is believed that abdominal malignant tumors such as a few pancreatic cancers and colon cancers may be accompanied by a high blood coagulation state, which is prone to MVT. In addition, long-term use of oral contraceptives can also trigger MVT, and the cause is also related to changes in blood flow.
　　6. Other rare causes include congestive heart failure, polycythemia vera, myocardial infarction, and diabetes, etc.
　　Second, primary factors

      In the past, mesenteric venous thrombosis without the above secondary factors was called primary or idiopathic mesenteric thrombosis. However, recent research has found that nearly half of the patients with primary or idiopathic MVT have a history of thrombophlebitis in peripheral veins or a family history of thromboembolism, so it is believed that the disease may be a special type of thrombophlebitis. In addition, hereditary hypercoagulable states such as the lack of C protein, S protein, or antithrombin III can explain many primary or idiopathic cases. Therefore, coagulation and anticoagulation factor tests should be performed on patients with unknown causes to determine whether their occurrence is due to hereditary or congenital dysfunction of the coagulation system.
　　Most mesenteric venous thrombosis occurs in the branches emitted by the superior mesenteric vein, generally not in the main trunk, and only 5% to 6% occur in the inferior mesenteric vein. After MVT, it is mostly segmental small bowel infarction, and a few involve the entire small bowel. The large intestine rarely develops infarction after MVT due to the existence of collateral circulation between the renal vein, splenic vein, paraaortic vein, and systemic circulation. The involved intestinal segments, due to the obstruction of blood circulation, show congestion, edema, hemorrhage, and focal necrosis of the mucosa. The wall of the small intestine thickens, and the lumen is filled with dark red blood. The mesentery of the involved intestinal segment also becomes significantly thickened, showing a rubbery change. The mesenteric small arteries often show spasm and slow blood flow but are not occluded.

　　Intestinal fistula is a major complication after the operation of mesenteric venous thrombosis (MVT). Nutritional support is of great significance for ensuring the nutritional supplement of patients, preventing negative nitrogen balance, enhancing immune function, and reducing the occurrence of other complications, which is worthy of application.

　　Due to the varying extent and speed of the lesion of mesenteric venous thrombosis, the severity of clinical manifestations varies from person to person. For example, patients with fewer involved intestinal segments and slow thrombosis may only show decreased appetite and abdominal discomfort, with symptoms lasting for several days to several weeks; if the lesion is extensive and the thrombosis is rapid, there are often acute onset and severe abdominal pain. Therefore, the clinical manifestations of patients are often lacking in specificity.
　　1. Most cases have abdominal discomfort as the prodromal symptom, followed by abdominal pain, which gradually intensifies, mostly paroxysmal colic pain, and only a few cases start with severe abdominal pain. The range of abdominal pain varies with the severity of the lesion, with mild cases showing localized pain and severe cases showing diffuse abdominal pain. Most patients have a relatively long history of abdominal pain before admission, ranging from a few days to several weeks. In a few patients with severe abdominal pain, the abdominal signs are often not proportional to the degree of pain, which is a characteristic of the disease.
　　2. About half of the patients may have nausea and vomiting.
　　3. A few patients may have diarrhea or accompanied by thin bloody stool.
　　4. A few patients may have fever, but it is generally not more than 38℃, and high fever often suggests concurrent infection.
　　5. Signs: There is often tenderness and rebound tenderness in the abdomen, but the degree is mild and muscle tension is not obvious. In a few patients, when palpated, the dilated and thickened intestinal loops can be felt, and the bowel sounds are normal in the early stage, but often weaken or disappear in the later stage. When the abdominal puncture draws out pale red blood-containing fluid, it is helpful for the diagnosis of the disease.

　　The prevention of mesenteric venous thrombosis (MVT) focuses on effective prevention and treatment of secondary factors of MVT etiology (such as: liver cirrhosis complicated with portal hypertension, infection of abdominal organs, hypercoagulable state of blood, etc.) to avoid further development of the disease and the occurrence of MVT.

　　The laboratory examination of mesenteric venous thrombosis (MVT) mostly shows an abnormal increase in blood leukocytes that does not correspond to the signs, most of which are as high as 20×10⁹above and there is a phenomenon of blood concentration, occult blood in stool can be positive.

　　Recent experiments have shown that fatty acid-binding protein and dimer (dimer > 20μg/ml) have certain specificity in the diagnosis of mesenteric vascular lesions, but they are still less used in clinical practice. The auxiliary examination of this disease has the following characteristics:
　　First, X-ray examination There is intestinal distension, thickening of the intestinal wall, and fluid accumulation in the intestinal lumen. The incomplete obstruction sign is of certain significance for the diagnosis of the disease.
　　Second, abdominal CT This disease diagnosis is helpful, and it can support the diagnosis of the disease from the following aspects:
　　1. After thrombosis, the superior mesenteric vein often becomes dilated, and the diameter of the vessel before and after the thrombosis area is not proportional.
　　2. The thrombus in the intestinal blood vessels appears as a higher density shadow on plain scan, and the density is lower than that of the surrounding veins after enhancement.
　　3. The mesentery becomes obviously thickened and denser due to edema.
　　4. Intestinal wall edema and thickening, CT shows 'finger print sign'.
　　Selective mesenteric superior arterial angiography can detect the interruption of mesenteric vessels, and the diagnostic rate of color Doppler ultrasound, CT, and other examinations can reach about 70%, and selective vascular angiography can reach about 90%, but the final determination still depends on surgical exploration.

　　Patients with mesenteric venous thrombosis (MVT) should eat more fruits and vegetables, such as watermelons, which have the functions of clearing heat and detoxifying, relieving irritability and thirst, and diuretic and antihypertensive effects. They are rich in a large amount of sugar, vitamins, and proteases. In addition, they should also eat more foods rich in potassium, such as kelp, rice bran, wheat bran, apricot kernel, dried grapes, and bananas.

　　After the diagnosis of mesenteric venous thrombosis (MVT), early application of anticoagulant drugs and vasodilators can be used, including heparin anticoagulation, urokinase thrombolysis, and dextran treatment. Heparin anticoagulation is generally 5-7 days, urokinase 7-10 days, and warfarin is given 2 days before stopping heparin. After stopping heparin, warfarin is changed to maintenance dose, and anticoagulation therapy should be at least 3-6 months. During conservative treatment, close observation is required, and timely surgery is needed once signs of intestinal necrosis appear. Venous thrombosis often involves branches, so necrosis may only affect a segment of the intestine, but there is a possibility of thrombus extension. There are also reports that the use of local thrombolysis through the superior mesenteric artery during surgery has a more ideal effect. The range of resection for this disease should be wider, including the entire mesentery containing the venous thrombus. When the length of the involved small intestine is less than 1/2, the involved intestine and mesentery should be completely resected, and the range of resection should be appropriately widened. When the length of the involved small intestine is more than 1/2 or more, the range of resection should be strictly controlled. There is a high risk of recurrent thrombosis after surgery, and commonly used drugs include 40% dextran (low molecular weight dextran), heparin, urokinase, salvia miltiorrhiza, and so on. These drugs are changed to oral anticoagulant drugs for maintenance after 7-14 days, and anticoagulation therapy should be maintained for 3-6 months.
　　After surgical treatment and anticoagulation therapy for mesenteric venous thrombosis (MVT), the prognosis is better than that of arterial栓塞, with a mortality rate of about 20%.