Sulger Elisabeth, Dhaliwal Harpal S., Oropallo Alisha, Gonzalez Lorena
NYU Langone Hospital Long Island
Christian Medical College and Hospital, Ludhiana, Punjab, India
Mesenteric venous thrombosis is a clot within the superior or inferior mesenteric vein or its branches. Thrombosis may be secondary to an inherited or acquired thrombophilia or as a consequence of or in conjunction with a proinflammatory state. Factors contributing to mesenteric venous thrombus formation include injury, stasis, malignancy, infection, trauma, and systemic inflammation. While greater than 25% of cases of mesenteric venous thrombosis may initially appear idiopathic, with thorough evaluation, many are shown to have an identifiable etiology. The thrombosis can originate in the vena rectae or a major vein and may involve the portal vein. The superior mesenteric vein is involved in more than 90% of cases of mesenteric vein thrombosis, whereas the inferior mesenteric vein is only implicated in up to 11% of cases. Mesenteric venous thrombosis may be an acute, subacute, or chronic process. Venous thrombi account for 5% to 15% of cases of acute mesenteric ischemia and are responsible for 1 in 5000 to 15,000 inpatient admissions and 1 in 1000 emergency department visits. Chronic mesenteric venous thrombosis accounts for 20% to 40% of all cases and is often an incidental finding. Although mesenteric venous thrombosis is a relatively rare condition, mortality remains high due to nonspecific symptoms and delayed diagnosis. The location, acuity, and extent of the thrombus affect the prognosis. Patients with chronic thrombosis may have complications stemming from venous hypertension, including malnutrition and esophageal or gastric varices. Chronic thrombi promote the formation of collaterals that protect the bowel from ischemic changes, but when a thrombus arises acutely, mesenteric ischemia may develop quickly; acute ischemia disrupts the intestinal mucosal barrier, promoting bacterial translocation and resulting in sepsis, multisystem organ failure, and death. Treatment of mesenteric venous thrombosis ranges from temporary anticoagulation with management of the underlying proinflammatory disorder to prolonged intensive care unit admission and urgent surgical intervention. The goal of treatment is to protect tissue, prevent the extension of the thrombosis, and minimize the chances of recurrence. Anticoagulation is often a mainstay of therapy. Anticoagulation is recommended even for those patients with varices, but patients with symptomatic varices may require decompression of their venous hypertension before they are anticoagulated.
肠系膜静脉血栓形成是指在肠系膜上静脉或下静脉及其分支内形成的血栓。血栓形成可能继发于遗传性或获得性易栓症，或者是促炎状态的结果或与之相关。促成肠系膜静脉血栓形成的因素包括损伤、血流淤滞、恶性肿瘤、感染、创伤和全身炎症。虽然超过25%的肠系膜静脉血栓形成病例最初可能表现为特发性，但经过全面评估，许多病例显示出可识别的病因。血栓可起源于直静脉或主要静脉，可能累及门静脉。超过90%的肠系膜静脉血栓形成病例累及肠系膜上静脉，而肠系膜下静脉仅在高达11%的病例中受累。肠系膜静脉血栓形成可能是急性、亚急性或慢性过程。静脉血栓占急性肠系膜缺血病例的5%至15%，导致每5000至15000例住院病例中有1例发病，每1000例急诊就诊病例中有1例发病。慢性肠系膜静脉血栓形成占所有病例的20%至40%，通常是偶然发现。尽管肠系膜静脉血栓形成是一种相对罕见的疾病，但由于症状不特异和诊断延迟，死亡率仍然很高。血栓的位置、严重程度和范围影响预后。慢性血栓形成的患者可能会出现静脉高压引起的并发症，包括营养不良和食管或胃静脉曲张。慢性血栓会促进侧支循环的形成，保护肠道免受缺血性改变，但当血栓急性形成时，可能会迅速发展为肠系膜缺血；急性缺血会破坏肠黏膜屏障，促进细菌移位，导致败血症、多系统器官衰竭和死亡。肠系膜静脉血栓形成的治疗范围从针对潜在促炎疾病进行临时抗凝治疗到延长重症监护病房住院时间和紧急手术干预。治疗的目标是保护组织、防止血栓扩展并尽量减少复发机会。抗凝治疗通常是主要治疗方法。即使是患有静脉曲张的患者也建议进行抗凝治疗，但有症状的静脉曲张患者在抗凝治疗前可能需要降低静脉高压。
