Mesenteric Venous Thrombosis

Elisabeth Sulger; Harpal  Dhaliwal; Alisha Oropallo; Lorena Gonzalez

Mesenteric Venous Thrombosis

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Continuing Education Activity

Mesenteric venous thrombosis, characterized by acute, subacute, or chronic thrombosis in the superior or inferior mesenteric vein and branches, poses a significant risk of life-threatening intestinal infarction, accounting for 5% to 15% of mesenteric ischemic events. Patients with mesenteric venous thrombosis present with a range of signs and symptoms, from mild abdominal pain to hemodynamic instability secondary to septic shock. Mesenteric venous thrombosis may occur due to a primary coagulopathy or an underlying infectious, traumatic, or inflammatory condition. The acuity and extent of the thrombus will dictate the course of the disease and the recommended intervention. However, delays in diagnosis and treatment cause significant increases in morbidity and mortality.

This activity for healthcare professionals reviews the epidemiology, etiology, pathophysiology, clinical manifestations, evaluation, management, and complications of acute, subacute, and chronic mesenteric venous thrombosis. The activity also highlights the critical role of the interprofessional team in improving outcomes for patients with mesenteric venous thrombosis.

Objectives:

Identify patients at risk for or who may have a mesenteric venous thrombosis based on their clinical history and presentation.
Select the most appropriate diagnostic imaging modality for a patient with a suspected mesenteric venous thrombosis.
Create a tailored treatment plan for a patient with a mesenteric venous thrombosis.
Develop and implement effective interprofessional team strategies to improve outcomes for patients with mesenteric venous thrombosis.

Introduction

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.[1][2]

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.

Etiology

Hypercoagulable states are present in 60% to 75% of patients with mesenteric venous thrombosis. Often, an inherited or acquired thrombophilia coexists with trauma, infection, inflammation, or surgery to give rise to a thrombotic process. Thrombosis may also arise from stasis, such as heart failure or cirrhosis. Hypercoagulable conditions include malignancies, heparin-induced thrombocytopenia, essential thrombocythemia, polycythemia vera, antiphospholipid antibodies, oral contraceptive use, and pregnancy. Heritable hypercoagulable conditions include sickle cell disease, Factor V Leiden, excess prothrombotic factors, and deficiencies in antithrombin III or proteins C or S.[3][4][5]

Patients with a thrombus in a major mesenteric vein often have concurrent portal vein thrombosis; such persons are more likely to have an underlying localized condition such as inflammatory bowel disease, pancreatitis, diverticulitis, myeloproliferative neoplasms, and malignancies. Portal vein involvement is also higher in persons with cirrhosis and has been reported in 15% of people awaiting liver transplantation. Patients with smaller vessel thrombosis in the vena rectae are more likely to have systemic thrombophilia.[6]

While up to 25% of cases of mesenteric vein thrombosis may initially be construed as idiopathic, thorough evaluation often reveals the causative etiology. For example, the gain-of-function JAK2V617F mutation results in a blood cell line proliferation; an assay for this mutation helps diagnose those with subclinical myeloproliferative disorders and can distinguish an inherited prothrombotic state from a reactive condition. The mutation is detected in most cases of polycythemia vera and 50% of cases of essential thrombocythemia and myelofibrosis. In addition, the JAK2V617F mutation is reported in up to 46% of cases without overt myeloproliferative neoplasms.[6][7][8]

Epidemiology

Acute mesenteric venous thrombosis causes 5% to 15% of all cases of mesenteric ischemia and accounts for 1 in 5,000 to 15,000 inpatient admissions and 1 in 1000 emergency department visits. The incidence of mesenteric venous thrombosis is estimated to be 2.7 per 100,000 persons. Computed tomography (CT) has increased the number of cases diagnosed during evaluation for other reasons, and this imaging modality identifies approximately 90% of mesenteric venous thromboses. Although mortality remains between 19% and 23%, there has been a trend toward earlier diagnosis and improved outcomes. Mesenteric venous thrombosis is slightly more common in men and most frequently presents in persons between the ages of 40 and 60.[9][3]

Pathophysiology

The superior mesenteric vein returns blood from the bowel from the second portion of the duodenum to the proximal two-thirds of the transverse colon, joining the splenic vein posterior to the neck of the pancreas, forming the portal vein. The left gastric vein drains the lower part of the esophagus and a portion of the lesser curvature of the stomach and enters the portal system at the formation of the portal vein. The inferior mesenteric vein drains the left colon and enters the splenic vein.

The pathophysiology of mesenteric venous thrombosis depends on the acuity, location, and causative etiology of the thrombus. Systemic thrombophilia causes thrombi within the vena rec. In contrast, local factors, such as intraabdominal malignancy, pancreatitis, and diverticulitis, produce thrombi in the superior mesenteric vein, often with extension into the portal vein.

Thrombi within the small, more distal venous branches pose a risk for bowel infarction. Blood return from the bowel is impeded, resulting in venous engorgement and subsequent ischemia. Arterial spasms can also contribute to irreversible ischemia. The bowel mucosa becomes permeable at sites of infarction, permitting the translocation of bacteria and leading to sepsis.[3][4]

In chronic mesenteric venous thrombosis, collateral circulation develops in the form of extensive cavernoma around the chronically thrombosed area. Often, portal hypertension, varices, and thrombocytopenia coexist with chronic venous thrombosis, and those with portal venous thrombosis have splenomegaly secondary to tissue fibrosis. If the thrombosis is distal to the junction of the left gastric and portal vein, both esophageal and gastric varices are seen. However, if the thrombosis is proximal to this point, gastric varices predominate.[10][11]

Patients with chronic mesenteric venous thrombosis are at risk for many impairments of the gastrointestinal system. Significant bowel edema arises in the setting of extensive chronic thrombosis within the portal, superior mesenteric, and splenic veins. Over time, a patient with considerable chronic thrombosis may develop clinically significant small bowel and biliary strictures that can cause malnutrition and cholangitis.[12]

History and Physical

The history and physical of a patient with mesenteric venous thrombosis will vary depending on the acuity and etiology of the thrombosis. The presentation can range from an asymptomatic patient whose thrombosis is an incidental finding to an acutely ill patient with peritonitis and sepsis. Often, a patient with mesenteric venous thrombosis will describe several days of diffuse abdominal pain with anorexia, nausea, and vomiting. The history may involve an antecedent infectious or inflammatory condition. Patients may have a personal or family history of thrombosis; this should raise the suspicion of a hereditary coagulopathy. A patient with a chronic mesenteric venous thrombosis may have any underlying condition of greater concern, such as portal hypertension.[3][13]

In a patient with chronic mesenteric venous thrombosis, the physical examination may be unremarkable, or there may be stigmata of portal hypertension and cirrhosis such as spider nevi, palmar erythema, caput medusae, or evidence of esophageal variceal bleeding. Abdominal distension, discomfort, and ascites may be present.[14]

Patients with acute mesenteric venous thrombi often experience pain out of proportion to physical findings, along with nausea, vomiting, and diarrhea. Fever may indicate a concurrent infection, such as phlebitis, or an intraabdominal process, such as appendicitis or diverticulitis. A patient may exhibit dehydration and hemodynamic instability.

Patients with subacute mesenteric venous thrombosis experience symptoms over days to weeks; the average duration of symptoms varies from 6 to 14 days. In patients with a subacute thrombotic process, abdominal distension may be present, and pain is often mild-to-moderate and diffuse. Ascites may be evident.[12]

Evaluation

Imaging Studies

Abdominal imaging is the most useful diagnostic tool to evaluate mesenteric venous thrombosis. An abdominopelvic CT with intravenous contrast can diagnose mesenteric venous thrombosis in 90% of cases. Plain abdominal radiographs reveal abnormalities in 50% to 75% of cases but demonstrate nonspecific findings such as dilated bowel, thumbprinting, and, in cases of perforation, free air. Magnetic resonance imaging (MRI), angiography, and abdominal Doppler ultrasonography are less commonly employed imaging modalities when evaluating patients with suspected mesenteric venous thrombosis. Abdominal Doppler ultrasonography can detect thrombosis in larger veins but has only 73% to 80% sensitivity and cannot visualize smaller vena recta.[15][16]

A venous thrombus will be seen as a focal lucency on CT images. Radiographic signs of ischemia include bowel wall thickening greater than 3mm with thickened mesentery and surrounding fluid. In the setting of a transmural bowel infarction, the bowel wall may be greater than 10 mm thick. The presence of portal venous gas and pneumatosis suggest necrotic bowel. Intraabdominal free air indicates bowel perforation.[17]

When a mesenteric venous thrombosis is identified on CT, magnetic resonance cholangiopancreatography (MRCP) or endoscopic retrograde cholangiopancreatography (ERCP) permits further assessment of the biliary system and degree of portal hypertension; ERCP carries a risk of bleeding from catheter injury. Esophagogastroduodenoscopy (EGD) is recommended to evaluate for esophageal and gastric varices.[18]

Laboratory Testing

Routine laboratory testing is not specific for mesenteric venous thrombosis but provides general clinical information. Recommended laboratory studies include a complete blood count with a differential, comprehensive metabolic panel, coagulation tests, and a thrombophilia screen. An elevated lactate level is a late marker of ischemia, and amylase levels can also be elevated with bowel ischemia; amylase levels greater than 1000 U/L suggest pancreatitis. Blood cultures should be obtained from patients with fevers and hemodynamic instability. Patients with portal vein involvement or sepsis will have elevated liver enzymes.[3][19][20]

Treatment / Management

Treatment for acute and subacute mesenteric venous thromboses can range from bowel rest, resuscitation, and anticoagulation to extensive surgery with bowel resection. Treatment goals are to prevent bowel infarction, mitigate blot extension, and minimize recurrence risk. Initial treatment depends on clinical presentation, the acuity of the thrombosis, and the underlying etiology. Stable patients may be treated nonoperatively with bowel rest, electrolyte replacement, and anticoagulation. Nasogastric decompression is often necessary, and total parenteral nutrition may be indicated. Febrile patients may benefit from broad-spectrum antibiotics to treat thrombophlebitis or enteric bacterial translocation.[21]

Significant clot burden and clinical deterioration warrant invasive intervention. Historically, the only option for urgent intervention was open surgery. Interventional radiology (IR) can offer precise therapy such as catheter-directed thrombolysis, thrombectomy, and focal administration of pharmacologic agents, including papaverine for vasodilation, or tissue-type plasminogen activator (tPA) or streptokinase for clot lysis. These IR measures often result in symptomatic improvement and lower bowel resection rates, even with persistent radiographic thrombus.[3]

During an IR procedure, access is obtained percutaneously via a transjugular or transhepatic approach.[22][23] A 4F or 5F angiographic catheter over a 0.035-inch hydrophilic guidewire is used to cross the thrombus. The angiographic catheter is exchanged with a multi-sidehole perfusion catheter, and the tip is placed in the mesenteric vein. If using tPA, an initial dose of 5 mg is given, followed by continuous tPA infusion at 0.5 mg/h. Heparin sodium 40 mg every 12 hours and 80,0000 U/day of urokinase can also be used. A post-procedural venogram is performed. Contraindications for catheter-directed fibrinolysis include intracranial hemorrhage, a history of stroke, primary or metastatic central nervous system disease, recent surgery, trauma, and mesenteric infarction.[21][22][23]

Open surgery is indicated if a patient becomes septic from ischemic bowel or a perforated viscus. The area of thrombosis is identified, and the affected bowel segment is resected. The goal of surgery is bowel conservation while resecting necrotic segments, and the average length of resection is 50 to 60 cm. Intraoperative Doppler ultrasonography may be used to assess the mesenteric blood supply. The surgeon may return in 24 hours for a second look before completing the anastomosis if there are concerns for ongoing ischemia.[2][20][24][25]

Anticoagulation is the cornerstone of mesenteric venous thrombosis treatment. While there remains a possibility of invasive intervention, or for patients with renal insufficiency, the initial anticoagulant of choice is unfractionated heparin. Once the patient is stable, the anticoagulant is changed to an oral medication such as warfarin or a direct oral anticoagulant (DOAC). Patients with reversible causes of thrombosis should complete a 6-month course of anticoagulation therapy, while those with heritable or acquired thrombotic states continue lifelong anticoagulation.

Despite the risks, anticoagulation remains the mainstay of management, even in those patients with portal venous thrombosis who have cirrhosis and portal hypertension. Anticoagulation helps recanalize the vein. Patients with mesenteric venous thrombosis awaiting liver transplantation who receive anticoagulation experience recanalization in 50% of cases, while those not taking anticoagulation do not experience recanalization of the portal vein. Factors associated with failure of recanalization include splenic vein involvement, ascites, and significant clot burden.[3]

Patients with portal hypertension may require intervention such as a transjugular intrahepatic portosystemic shunt (TIPS) to minimize bleeding risks before anticoagulation. The goal of a TIPS is mechanical recanalization of the portal vein to maintain flow across the occluded segment. In patients with cirrhosis, a shunt can be created between the left portal vein and the superior mesenteric vein, and splenectomy is effective in those patients with isolated gastric varices from splenic vein thrombosis. Stenting may be required for biliary strictures formed as a consequence of chronic portal vein thrombosis. Rarely a hepaticojejunostomy is required to overcome the stenotic bile ducts.[26][27]

Differential Diagnosis

The symptoms of mesenteric venous thrombosis can be vague and nonspecific and range from mild to severe. Physical examination and laboratory values alone generate a broad differential diagnosis, including a spectrum of intraabdominal pathology, myocardial infarction, and aortic dissection. It is also essential to distinguish mesenteric venous thrombosis from mesenteric arterial thrombosis, as the etiology and approach to treatment are different. Mesenteric venous thrombosis may exist concurrently with an inciting infectious or inflammatory process.

Prognosis

While overall mortality has decreased due to earlier diagnosis and treatment, mesenteric venous thrombosis remains a life-threatening condition, and a delay in diagnosis directly correlates with worse outcomes. The most common causes of death in patients with mesenteric venous thrombosis are sepsis, pulmonary emboli, and the sequelae from recurrent thrombi. Patient age, comorbidities, time to diagnosis, and successful revascularization impact outcomes.[21]

Acute mesenteric venous thrombosis has a 30-day mortality of up to 32%. Timely diagnosis reduces mortality to less than 10%; the mortality rate approaches 60% when diagnosis is delayed.[28][21] If treatment is delayed longer than 24 hours from symptom onset, mortality ranges between 80% and 100%.[29] For patients with chronic mesenteric venous thrombosis, 5-year survival rates are up to 82%. In the paradigm of chronic thrombosis, the prognosis is determined by the severity of the underlying condition.[30]

Complications

Complications of mesenteric venous thrombosis arise from the thrombosis, the treatments, and the underlying condition. Thrombosis recurrence usually occurs within the first 30 days and may be as low as 0% to 3% in those who receive anticoagulation. Recurrence or extension of thrombosis may give rise to bowel infarction, sepsis, and death. Short bowel syndrome may be a consequence of bowel resection, and some patients require lifelong total parenteral nutrition.[31]

Complications from catheter-directed thrombolysis include major and minor bleeding, fever, hematoma formation, pain, and infection. Transhepatic access for thrombolytic therapy carries an increased risk of bleeding, and the transileocolic approach may require surgical access. The bleeding risk from anticoagulation is less than 10%, and bleeding is usually within the gastrointestinal system. Patients with varices have a higher bleeding risk and should be pretreated with beta blockers or undergo definitive management of varices.[21][32]

Chronic thrombosis can give rise to biliary strictures, gallstones, and recurrent cholangitis; major reconstructive surgery is required occasionally. The myeloproliferative neoplasms that predispose some patients to thrombosis can convert to leukemia and myelodysplasia. Patients with chronic thrombosis also suffer from chronic fatigue, bone pain, pruritis, weight loss, and bleeding from platelet dysfunction.[12]

Postoperative and Rehabilitation Care

The intensity of postoperative and rehabilitative care depends on the etiology and clinical impact of the mesenteric venous thrombosis. Those who progress to multisystem organ failure requiring critical care support will face a long recovery period with many potential pitfalls, including recurrent thrombus, pulmonary emboli, gastrointestinal bleeding, need for prolonged invasive ventilation, and parenteral nutrition. Those patients who underwent surgery may require repeat surgical interventions, possible intestinal reconstruction, and delayed abdominal closure. A subset of patients will require chronic nutritional monitoring and supplementation. Lifelong anticoagulation is indicated in those patients for whom the etiology of the venous thrombosis was idiopathic or secondary to a chronic condition.

Consultations

It is important to include interventional radiology and general surgery in the decision-making early in the clinical course of patients diagnosed with mesenteric venous thrombosis. Pharmacists also play an important role in helping to administer anticoagulation and fibrinolytic therapy. Additional frequently needed consultants include nutritionists and intensivists.

Deterrence and Patient Education

It is important to identify those patients who may be at an increased risk for developing mesenteric venous thrombosis, such as those with a personal or family history of blood clots, chronic inflammatory conditions, or known portal hypertension and cirrhosis. These individuals should understand the importance of seeking prompt medical evaluation for severe or unrelenting abdominal pain. A subset of patients with increased risk may benefit from prophylactic anticoagulation.[33]

Pearls and Other Issues

Severe pain in the absence of definitive physical findings should raise the suspicion for a mesenteric venous thrombosis. While the finding of ascites confers a broad differential diagnosis, mesenteric venous thrombosis should always be considered in this setting. Any radiographic diagnosis of venous thrombosis should prompt a thorough evaluation for either a local source, such as inflammation, infection, intraabdominal malignancy, or a heritable or acquired thrombophilic condition.

Individuals with a personal or family history of deep vein thrombosis or other thrombophilia presenting with acute abdominal pain should be promptly evaluated for mesenteric venous thrombosis.

Enhancing Healthcare Team Outcomes

Mesenteric venous thrombosis can be challenging to diagnose and treat and requires collaboration amongst the interprofessional team, including internal medicine providers, surgeons, interventional radiologists, critical care specialists, and pharmacists. Patients diagnosed with mesenteric venous thrombosis require close monitoring, and patient outcomes depend on timely communication between the interprofessional team, and the ability to rapidly adjust to clinical circumstances.

Details

References

[1]

Brunaud L, Antunes L, Collinet-Adler S, Marchal F, Ayav A, Bresler L, Boissel P. Acute mesenteric venous thrombosis: case for nonoperative management. Journal of vascular surgery. 2001 Oct:34(4):673-9 [PubMed PMID: 11668323]

Level 3 (low-level) evidence

[2]

Acosta S, Alhadad A, Svensson P, Ekberg O. Epidemiology, risk and prognostic factors in mesenteric venous thrombosis. The British journal of surgery. 2008 Oct:95(10):1245-51. doi: 10.1002/bjs.6319. Epub [PubMed PMID: 18720461]

[3]

Singal AK, Kamath PS, Tefferi A. Mesenteric venous thrombosis. Mayo Clinic proceedings. 2013 Mar:88(3):285-94. doi: 10.1016/j.mayocp.2013.01.012. Epub 2013 Feb 27 [PubMed PMID: 23489453]

[4]

Duran R, Denys AL, Letovanec I, Meuli RA, Schmidt S. Multidetector CT features of mesenteric vein thrombosis. Radiographics : a review publication of the Radiological Society of North America, Inc. 2012 Sep-Oct:32(5):1503-22. doi: 10.1148/rg.325115100. Epub [PubMed PMID: 22977032]

[5]

Gaspary MJ, Auten J, Durkovich D, Gable P. Superior mesenteric vein thrombosis mimicking acute appendicitis. The western journal of emergency medicine. 2011 May:12(2):262-5 [PubMed PMID: 21691540]

[6]

Holl K, Chatain N, Krapp S, Baumeister J, Maié T, Schmitz S, Scheufen A, Brock N, Koschmieder S, Moreno-Andrés D. Calreticulin and JAK2V617F driver mutations induce distinct mitotic defects in myeloproliferative neoplasms. Scientific reports. 2024 Feb 2:14(1):2810. doi: 10.1038/s41598-024-53240-8. Epub 2024 Feb 2 [PubMed PMID: 38308077]

[7]

Marconato R, Nezi G, Capovilla G, Moletta L, Baldan N, Canton SA, Spirch S, Salvador R, Merigliano S. Primary mesenteric vein thrombosis: a case series. Journal of surgical case reports. 2020 Mar:2020(3):rjaa016. doi: 10.1093/jscr/rjaa016. Epub 2020 Mar 24 [PubMed PMID: 32226599]

Level 2 (mid-level) evidence

[8]

Nielsen C, Birgens HS, Nordestgaard BG, Kjaer L, Bojesen SE. The JAK2 V617F somatic mutation, mortality and cancer risk in the general population. Haematologica. 2011 Mar:96(3):450-3. doi: 10.3324/haematol.2010.033191. Epub 2010 Dec 15 [PubMed PMID: 21160067]

[9]

Salim S, Zarrouk M, Elf J, Gottsäter A, Sveinsdottir S, Svensson P, Acosta S. Clinical implications of different risk factor profiles in patients with mesenteric venous thrombosis and systemic venous thromboembolism: a population-based study. Journal of thrombosis and thrombolysis. 2019 May:47(4):572-577. doi: 10.1007/s11239-019-01816-x. Epub [PubMed PMID: 30756343]

[10]

Yoshida H, Shimizu T, Yoshioka M, Matsushita A, Kawano Y, Ueda J, Kawashima M, Taniai N, Mamada Y. The Role of the Spleen in Portal Hypertension. Journal of Nippon Medical School = Nippon Ika Daigaku zasshi. 2023:90(1):20-25. doi: 10.1272/jnms.JNMS.2023_90-104. Epub [PubMed PMID: 36908126]

[11]

Mayer P, Venkatasamy A, Baumert TF, Habersetzer F, Pessaux P, Saviano A, Felli E. Left-sided portal hypertension: Update and proposition of management algorithm. Journal of visceral surgery. 2024 Feb:161(1):21-32. doi: 10.1016/j.jviscsurg.2023.11.005. Epub 2023 Dec 22 [PubMed PMID: 38142180]

[12]

Stancu B, Chira A, Coman HF, Mihaileanu FV, Ciocan R, Gherman CD, Andercou OA. Intestinal Obstruction as Initial Presentation of Idiopathic Portal and Mesenteric Venous Thrombosis: Diagnosis, Management, and Literature Review. Diagnostics (Basel, Switzerland). 2024 Jan 30:14(3):. doi: 10.3390/diagnostics14030304. Epub 2024 Jan 30 [PubMed PMID: 38337820]

[13]

Monita MM, Gonzalez L. Acute Mesenteric Ischemia. StatPearls. 2024 Jan:(): [PubMed PMID: 28613722]

[14]

Dajti E, Alemanni LV, Marasco G, Montagnani M, Azzaroli F. Approaches to the Diagnosis of Portal Hypertension: Non-Invasive or Invasive Tests? Hepatic medicine : evidence and research. 2021:13():25-36. doi: 10.2147/HMER.S278077. Epub 2021 Mar 18 [PubMed PMID: 33776492]

[15]

Kunychka M, Váňa J, Žáček M, Chromčiková M. Acute mesenteric ischemia - a persistent problem. Rozhledy v chirurgii : mesicnik Ceskoslovenske chirurgicke spolecnosti. 2024:102(6):228-235. doi: 10.33699/PIS.2023.102.6.228-235. Epub [PubMed PMID: 38286651]

[16]

Reintam Blaser A, Mändul M, Björck M, Acosta S, Bala M, Bodnar Z, Casian D, Demetrashvili Z, D'Oria M, Durán Muñoz-Cruzado V, Forbes A, Fuglseth H, Hellerman Itzhaki M, Hess B, Kase K, Kirov M, Lein K, Lindner M, Loudet CI, Mole DJ, Murruste M, Nuzzo A, Saar S, Scheiterle M, Starkopf J, Talving P, Voomets AL, Voon KKT, Yunus MA, Tamme K, AMESI Investigators (Collaborators). Incidence, diagnosis, management and outcome of acute mesenteric ischaemia: a prospective, multicentre observational study (AMESI Study). Critical care (London, England). 2024 Jan 23:28(1):32. doi: 10.1186/s13054-024-04807-4. Epub 2024 Jan 23 [PubMed PMID: 38263058]

Level 2 (mid-level) evidence

[17]

Li B, Wu Z, Wang J. The target sign: a significant CT sign for predicting small-bowel ischemia and necrosis. La Radiologia medica. 2024 Feb 14:():. doi: 10.1007/s11547-024-01793-z. Epub 2024 Feb 14 [PubMed PMID: 38355906]

[18]

Bayraktar Y, Harmanci O. Etiology and consequences of thrombosis in abdominal vessels. World journal of gastroenterology. 2006 Feb 28:12(8):1165-74 [PubMed PMID: 16534866]

[19]

Nielsen C, Lindholt JS, Erlandsen EJ, Mortensen FV. d-lactate as a marker of venous-induced intestinal ischemia: an experimental study in pigs. International journal of surgery (London, England). 2011:9(5):428-32. doi: 10.1016/j.ijsu.2011.04.004. Epub 2011 Apr 19 [PubMed PMID: 21530695]

[20]

Morasch MD, Ebaugh JL, Chiou AC, Matsumura JS, Pearce WH, Yao JS. Mesenteric venous thrombosis: a changing clinical entity. Journal of vascular surgery. 2001 Oct:34(4):680-4 [PubMed PMID: 11668324]

[21]

Russell CE, Wadhera RK, Piazza G. Mesenteric venous thrombosis. Circulation. 2015 May 5:131(18):1599-603. doi: 10.1161/CIRCULATIONAHA.114.012871. Epub [PubMed PMID: 25940967]

[22]

Barah A, Al-Hashimi I, Kassamali R, Aldebyani Q, Almokdad O, Elmagdoub A, Khader M, Rehman SU, Omar A. Catheter-Directed Thrombolysis in the treatment of acute Portomesenteric Vein Thrombosis after Laparoscopic Sleeve Gastrectomy. Thrombosis journal. 2022 Sep 29:20(1):57. doi: 10.1186/s12959-022-00415-w. Epub 2022 Sep 29 [PubMed PMID: 36175959]

[23]

Gao Z, Yin L, Pan Y, Chen B. Treatment of Superior Mesenteric Vein Thrombus by Catheter-Directed Thrombolysis. Annals of vascular surgery. 2020 May:65():286.e9-286.e13. doi: 10.1016/j.avsg.2019.11.021. Epub 2019 Nov 16 [PubMed PMID: 31743781]

[24]

Kaplan JL, Weintraub SL, Hunt JP, Gonzalez A, Lopera J, Brazzini A. Treatment of superior mesenteric and portal vein thrombosis with direct thrombolytic infusion via an operatively placed mesenteric catheter. The American surgeon. 2004 Jul:70(7):600-4 [PubMed PMID: 15279182]

[25]

Kozuch PL, Brandt LJ. Review article: diagnosis and management of mesenteric ischaemia with an emphasis on pharmacotherapy. Alimentary pharmacology & therapeutics. 2005 Feb 1:21(3):201-15 [PubMed PMID: 15691294]

[26]

Liu X, Wang Y, Zheng L, Zhu J. Risk factors analysis of endoscopy and TIPS in the treatment of secondary esophagogastric varicose bleeding with cirrhosis. African health sciences. 2023 Sep:23(3):655-663. doi: 10.4314/ahs.v23i3.76. Epub [PubMed PMID: 38357146]

[27]

Shalvoy MR, Ahmed M, Weinstein JL, Ramalingam V, Malik MS, Ali A, Shenoy-Bhangle AS, Curry MP, Sarwar A. Transjugular Intrahepatic Portosystemic Shunt and Thrombectomy (TIPS-Thrombectomy) for Symptomatic Acute Noncirrhotic Portal Vein Thrombosis. Journal of vascular and interventional radiology : JVIR. 2023 Aug:34(8):1373-1381.e3. doi: 10.1016/j.jvir.2023.05.009. Epub 2023 May 12 [PubMed PMID: 37182668]

[28]

Schoots IG,Koffeman GI,Legemate DA,Levi M,van Gulik TM, Systematic review of survival after acute mesenteric ischaemia according to disease aetiology. The British journal of surgery. 2004 Jan [PubMed PMID: 14716789]

Level 1 (high-level) evidence

[29]

Klar E, Rahmanian PB, Bücker A, Hauenstein K, Jauch KW, Luther B. Acute mesenteric ischemia: a vascular emergency. Deutsches Arzteblatt international. 2012 Apr:109(14):249-56. doi: 10.3238/arztebl.2012.0249. Epub 2012 Apr 6 [PubMed PMID: 22536301]

[30]

Orr DW, Harrison PM, Devlin J, Karani JB, Kane PA, Heaton ND, O'Grady JG, Heneghan MA. Chronic mesenteric venous thrombosis: evaluation and determinants of survival during long-term follow-up. Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association. 2007 Jan:5(1):80-6 [PubMed PMID: 17142105]

[31]

Bagley K, Schuller JG. Mesenteric ischemia in the acute care setting. Nursing. 2024 Feb 1:54(2):48-55. doi: 10.1097/01.NURSE.0000998028.77929.e0. Epub [PubMed PMID: 38271132]

[32]

Kim HS, Patra A, Khan J, Arepally A, Streiff MB. Transhepatic catheter-directed thrombectomy and thrombolysis of acute superior mesenteric venous thrombosis. Journal of vascular and interventional radiology : JVIR. 2005 Dec:16(12):1685-91 [PubMed PMID: 16371536]

[33]

Rybicki F Jr, Ojiaku M. Patient-Friendly Summary of the ACR Appropriateness Criteria: Imaging of Mesenteric Ischemia. Journal of the American College of Radiology : JACR. 2019 May:16(5):e21. doi: 10.1016/j.jacr.2019.01.015. Epub [PubMed PMID: 31054704]