Acute superior mesenteric venous thrombosis

　　First, etiology

　　Superior mesenteric vein thrombosis is divided into primary and secondary types. The former has an unknown cause, with an incidence rate of 10% to 20%, and some of these patients have a history of peripheral venitis such as migratory venitis. The latter often occurs secondary to:

　　1. Hepatic cirrhosis or extracorporeal compression causing portal vein congestion and blood stasis.

　　2. Abdominal infections such as suppurative appendicitis, pelvic inflammatory disease, etc.

　　3. Certain blood diseases such as polycythemia vera, as well as hypercoagulable states caused by oral contraceptives.

　　4. Trauma or surgery caused by abdominal trauma, which is often severe and often accompanied by shock.

　　5. Direct compression and obstruction of mesenteric venous blood flow by abdominal malignant tumors.

　　6. Congenital abnormalities in coagulation function, such as hereditary antithrombin III deficiency, hereditary protein C deficiency, and hereditary protein S deficiency, which are more common in young patients with a history of deep vein thrombosis.

　　Second, pathogenesis

　　After venous thrombosis, thrombosis can spread to the proximal and distal ends. When the venous return in the involved intestinal area is completely blocked, the intestinal vessels become congested and edematous, and there are punctate hemorrhages under the serosa, which gradually spread into patchy hemorrhages, until the hemorrhagic necrosis of the intestines. A large amount of bloody fluid leaks from the intestinal wall and mesentery into the intestinal lumen and abdominal cavity, leading to a decrease in blood volume, blood concentration, and failure of the cardiovascular and pulmonary functions. Moreover, acute venous occlusion can also reflexively cause vasoconstriction of visceral arteries and accelerate thrombosis, thereby accelerating the process of intestinal necrosis. Venous thrombosis often only involves a segment of jejunum or ileum venous thrombosis, and rarely causes complete intestinal necrosis. However, thrombosis is prone to recurrence, and sometimes multiple surgical operations may be required.

　　1. Intestinal necrosis is a severe complication of the disease. Thrombosis can spread to the proximal and distal ends. When the venous return in the involved intestinal area is completely blocked, the intestinal vessels become congested and edematous, and there are punctate hemorrhages under the serosa, which gradually spread into patchy hemorrhages, until the hemorrhagic necrosis of the intestines. A large amount of bloody fluid leaks from the intestinal wall and mesentery into the intestinal lumen and abdominal cavity, leading to a decrease in blood volume, blood concentration, and failure of the cardiovascular and pulmonary functions. Moreover, acute venous occlusion can also reflexively cause vasoconstriction of visceral arteries and accelerate thrombosis, thereby accelerating the process of intestinal necrosis. Venous thrombosis often only involves a segment of jejunum or ileum venous thrombosis, and rarely causes complete intestinal necrosis. However, thrombosis is prone to recurrence, and sometimes multiple surgical operations may be required.

　　2. Intestinal necrosis is commonly seen in intestinal obstruction. Intestinal obstruction, caused by intestinal contents such as ascaris clumps, gallstones, feces, or other foreign bodies blocking the intestinal lumen, is a simple mechanical intestinal obstruction. It is more common for ascaris to aggregate into clumps and cause local intestinal spasm, leading to intestinal lumen obstruction. It is most common in children, with a higher incidence in rural areas. Clinical manifestations include episodic abdominal pain around the umbilicus and vomiting, and there may be a history of passing ascaris or vomiting ascaris.

　　1. General abdominal pain

　　Early symptoms are only mild abdominal pain or discomfort, constipation or diarrhea, about 27% of patients may have abdominal pain for more than 30 days, and physical examination shows severe abdominal pain, but the signs are mild.

　　2. Peritonitis

　　With the progression of the disease, venous blood return is obstructed, intestinal function is severely impaired, and sudden severe abdominal pain occurs, accompanied by vomiting, diarrhea, and blood in the stool, which is more common than in arterial occlusion. Physical examination: There may be obvious peritoneal irritation signs, decreased or absent bowel sounds, elevated body temperature, and blood-containing fluid can be aspirated through abdominal puncture.

　　2. Do not eat too much salty and spicy food, do not eat overheated, cold, expired, or deteriorated food; for the elderly and weak, or those with certain genetic predisposition to diseases, eat some cancer-preventive foods and alkaline foods with high alkalinity as appropriate, and maintain a good mental state.

　　1. Develop good living habits, quit smoking and limit alcohol. The World Health Organization predicts that if people stop smoking, cancer in the world will decrease by one-third after 5 years; secondly, do not drink excessively. Smoking and drinking are highly acidic substances, and people who smoke and drink for a long time are prone to acid体质.

　　First, blood routine

　　1. White blood cell count significantly increases.

　　2. Hemoglobin and hematocrit increase, indicating blood concentration.

　　3. Serum phosphates, amylase, and creatine phosphokinase increase, but lack specificity.

　　4. The positive rate of serum lactate determination can reach 85.1% to 91.4%, but it often appears after ischemia and intestinal necrosis, and is not very helpful for early diagnosis of the disease.

　　Second, blood gas analysis

　　pH decreases, SB decreases, BE is negative, the carbon dioxide binding power decreases, indicating the occurrence of metabolic acidosis.

　　Third, X-ray examination

　　1. Abdominal plain film: It shows intestinal gas or liquid level.

　　2. CT scan: It can display thrombosis in the portal venous system, with an accuracy of over 90%.

　　3. Selective superior mesenteric artery angiography: Arteriography can only provide indirect signs of the disease, and selective superior mesenteric artery angiography has great significance for the venous diagnosis. A few patients can show thrombosis in the portal or superior mesenteric veins, while most show delayed or no venous phase.

　　Fourth, color Doppler

　　It can be detected early in the mesenteric blood vessels, especially when there is thrombosis in the portal vein, the positive rate can reach 100%, but color Doppler ultrasound is easily interfered by intestinal gases, and higher technical and experiential requirements are placed on the examiner.

　　Fifth, paracentesis

　　There may be blood-containing fluid extracted.

　　Dietary requirements vary according to different symptoms, and specific dietary standards should be formulated according to specific diseases after consulting a doctor. The patient's diet should be light and easy to digest, with an emphasis on eating more vegetables and fruits, and a reasonable dietary combination should be maintained, with attention to adequate nutrition. In addition, patients should also pay attention to avoiding spicy, greasy, and cold foods.

　　First, Non-Surgical Treatment

　　1. Thrombolysis and Anticoagulation:Once the diagnosis of acute superior mesenteric venous thrombosis is established, anticoagulation therapy should be administered immediately. Thrombolytic therapy should be given at the same time if the onset time is less than 1 week, while anticoagulation therapy is the main approach if it exceeds 1 week. Conservative treatment should be performed in the early stage of thrombosis formation, with heparin (2.5～4.0)×104U/d administered intravenously or subcutaneously; urokinase (60～120)×104U/d or defibrase 10U/d administered intravenously, which can achieve good results. For patients receiving conservative treatment, the duration of anticoagulation therapy should be controlled within 2 weeks, and thrombolytic therapy should last for 5 to 7 days. During medication, the platelet count and activated partial thromboplastin time of the patient should be monitored to keep them within 2 to 2.5 times of the pre-medication level. All patients should continue to take warfarin orally for 3 months after stopping heparin, and those with hypercoagulable states may require lifelong anticoagulation.

　　2. Blood Volume Support:Blood transfusion and fluid resuscitation to correct severe circulatory blood volume insufficiency.

　　3. Gastrointestinal Decompression.

　　4. Antimicrobial Therapy:Administer high-dose broad-spectrum antibiotics and continue until after surgery.

　　During conservative treatment, symptoms and signs should be closely observed. If the patient shows no significant improvement or has signs of intestinal necrosis, emergency surgery should be performed immediately.

　　Second, Surgical Treatment

　　1. Resection of Necrotic Intestinal Tract:Unlike arterial occlusion, venous thrombosis often occurs more frequently in peripheral branches rather than the main trunk, so the affected segment of the small intestine is usually shorter, and therefore, the devitalized intestinal tract and end-to-end anastomosis can generally be resected. To reduce the absorption of toxins, the necrotic intestinal tract can be first resected during surgery.

　　2. Venous Thrombectomy:The extension of thrombosis often exceeds the visible infarction area, and the main trunk of the superior mesenteric vein and the portal vein often have thrombi, and the latter is an important cause of postoperative recurrence of intestinal necrosis. Therefore, in addition to completely removing the thrombi in the blood vessels of the mesenteric residual ends after intestinal resection, incisions also need to be made in the superior mesenteric vein or portal vein to remove the thrombi inside.

　　3. Intraoperative Anticoagulation:For emergency surgery patients, heparin anticoagulation should start immediately during surgery and continue for 6 to 8 weeks postoperatively. After reviewing a large number of literature, Abdu and others noticed that the survival rate of patients with intestinal resection and anticoagulation therapy is 80%, while the survival rate of those with only intestinal resection is 50%.