Endovascular Options Offer Relief for Venous Occlusion in Select Patients With NETs

Interventional radiology procedures, including transhepatic stenting of the superior mesenteric vein (SMV) and portal vein and catheter-directed recanalization of thrombosed veins, can relieve symptoms and restore venous flow in carefully selected patients with neuroendocrine tumors (NETs) and portomesenteric venous occlusion. However, the supporting evidence comes largely from small retrospective series and case reports, according to Erica S. Alexander, MD, assistant attending radiologist at Memorial Sloan Kettering Cancer Center, who reviewed the topic at the 2026 North American Neuroendocrine Tumor Society (NANETS) Symposium.¹

For fibrotic encasement of the SMV in small intestinal NETs (SI-NETs), some of the most direct evidence comes from a series of 7 patients who underwent transhepatic SMV stenting for large mesenteric masses.² Symptoms resolved in 4 patients, 2 were unchanged, and 1 was slightly worse, with clinical benefit associated with normalization of venous flow. A separate analysis of 824 patients with SI-NETs identified 20 with critically symptomatic central mesenteric fibrosis, most of whom benefited from interventions that included SMV stenting or resection. A case report also described retrograde transmesenteric SMV stenting that stopped life-threatening collateral bleeding.

“So, broadly, these are multiple different small series, and most of them show that patients that are critically symptomatic [have] a decent improvement,” Alexander said.

Because NET-specific data are sparse, Alexander also discussed outcomes extrapolated from portal vein and SMV stenting studies involving other malignancies. In those series, technical success ranged from 86% to 97%, primary patency was approximately 80% at a median follow-up of 20 months, and symptom improvement was reported in 80% to 85% of patients. Stent choice appeared to matter: in a study of malignant portal vein occlusion, 6-month patency was 90.0% with stent grafts compared with 52.2% with bare-metal stents.

For thrombotic occlusion, direct catheter-directed thrombolysis, with or without thrombectomy, performed through transhepatic, transjugular, or transsplenic access, achieved recanalization in 75% to 100% of patients in reported series. Thrombectomy assisted by a transjugular intrahepatic portosystemic shunt (TIPS), which provides both portal decompression and access for thrombolysis or aspiration, produced 30-day patency rates of 70% to 90%. Indirect thrombolysis through the superior mesenteric artery (SMA) was less effective, requiring longer infusions and higher doses. Large-bore aspiration or rotational thrombectomy devices, angioplasty, and stenting of residual stenosis can serve as adjunctive approaches.

Risks, Technical Pitfalls, and Evidence Limits

Several technical factors predict poorer outcomes with portomesenteric stenting. An occlusion longer than 4 cm predicted technical failure, and preexisting thrombus predicted early stent thrombosis. In an analysis of 182 patients, anticoagulation after stenting did not improve patency.

For thrombotic occlusion, the evidence supporting interventional treatment of acute mesenteric venous thrombosis is graded no higher than class IIb, level C. Practice guidance from the American Association for the Study of Liver Diseases (AASLD) notes that endovascular procedures carry procedural morbidity and that recanalization rates may be similar to those achieved with anticoagulation alone, reserving local thrombolysis for very select patients.³ Evidence for stenting in fibrotic encasement is also limited to small case series and case reports.

As a result, patient selection is central. Successful portal venous recanalization requires adequate inflow, from the SMV or splenic vein, and adequate outflow through intrahepatic portal vein branches. The extent and location of thrombosis, including whether the thrombus is confined to the main portal vein or extends into the mesenteric veins, are important considerations in determining technical feasibility.

“Patient selection is critical for endovascular recanalization,” Alexander said.

Two Distinct Mechanisms of Venous Occlusion

Alexander emphasized that venous occlusion in NETs arises from 2 distinct processes, and treatment diverges accordingly. Venous occlusion spans a clinical spectrum from chronic venous stasis and malabsorption to mesenteric ischemia and acute bowel infarction. About 35% of patients with advanced midgut NETs present with obstruction, ischemia, or both, according to the presentation.

The first mechanism is fibrotic encasement, seen predominantly in SI-NETs. Nodal metastases and tumor deposits release serotonin and growth factors such as transforming growth factor-beta, connective tissue growth factor, and platelet-derived growth factor, driving dense mesenteric fibrosis that progressively entraps the superior mesenteric vessels. Mesenteric fibrosis is reported in 5% to 50% of patients with SI-NETs, although the prevalence varies depending on the population and definition used. As the fibrosis shrinks and fixes the mesenteric root to the retroperitoneum, patients can develop vessel obstruction, segmental ischemia, and venous stasis; bowel edema, obstruction, malabsorption, postprandial pain, diarrhea, and ascites; and retroperitoneal complications such as obstructive uropathy, hydronephrosis, and renal failure.

“So the key message here is to recognize [fibrosis] early,” Alexander said, noting that the process tends to worsen over time.

The second mechanism is thrombosis associated with a tumor-related hypercoagulable state, reported particularly in pancreatic, functioning, and high-grade NETs. A systematic review found a pooled venous thromboembolism prevalence of approximately 11% in patients with neuroendocrine neoplasms, ranging from 7.5% to 33% across series, with portal vein thrombosis among the most common sites.⁴ Thrombosis in atypical or visceral veins is characteristic. Risk factors include a pancreatic primary, poorly differentiated or advanced-stage disease, and functioning tumors such as glucagonomas and adrenocorticotropic hormone-secreting neoplasms. However, thrombosis can occur in both functioning and nonfunctioning tumors.

A Framework for Management

For fibrotic disease, Alexander described the Koea classification of mesenteric disease as a guide to treatment.⁵ Type A disease is resectable, type B is borderline resectable, with fibrosis adjacent to but not encasing the main SMA or SMV, and type C is locally advanced or unresectable, with encasement of the SMA and SMV. Type C accounts for only about 5% of cases in reported series, but nearly all patients with this disease are symptomatic from ischemia or obstruction.

Patients with type A or B disease are generally evaluated for surgery or cytoreduction. National Comprehensive Cancer Network guidelines support resection of the primary ileal or jejunal tumor and mesenteric nodes in symptomatic patients and consideration of resection in selected asymptomatic patients to prevent obstruction, ischemia, bleeding, or perforation. For cytoreductive surgery in metastatic disease, a threshold of more than 90% of the disease burden is generally considered. Alexander noted that about 80% of patients deemed unresectable elsewhere could undergo debulking at experienced, high-volume centers, where en bloc resection with portal vein or SMV reconstruction is feasible in selected patients.

Systemic therapies, including somatostatin analogues, lutetium Lu 177 dotatate, everolimus, and chemotherapy, can control tumor growth but do not reliably reverse established mesenteric fibrosis. For unresectable, asymptomatic disease, observation plus a somatostatin analogue is reasonable, whereas symptomatic patients may need palliative bypass, vascular stents, or nephrostomy for obstructive uropathy.

Transhepatic SMV stenting is considered for patients with unresectable mesenteric root disease and SMA and SMV encasement who have symptoms of venous stasis, such as postprandial pain, diarrhea, malnutrition, bowel-wall edema, chylous ascites, or collateral gastrointestinal bleeding. The procedure involves transhepatic portal access, venoplasty of the SMV stenosis or occlusion, and placement of a self-expanding stent, with stent grafts preferred.

For thrombotic occlusion, anticoagulation, typically initiated with heparin, is first-line therapy. Treatment is often continued long term, depending on the underlying cause, ongoing thrombotic risk, and bleeding risk. Interventional radiology is generally reserved for patients who deteriorate despite anticoagulation, have impending bowel infarction, or develop complications of chronic portal hypertension.

“Transhepatic SMV stenting is primarily a palliative option for [carefully] selected patients,” Alexander said.

References

1. Alexander ES. Presented at: 2026 North American Neuroendocrine Tumor Society (NANETS) Symposium; November 5-7, 2026; Las Vegas, NV.

2. Hellman P, Hessman O, Åkerström G, et al. Stenting of the superior mesenteric vein in midgut carcinoid disease with large mesenteric masses. World J Surg. 2010;34:1373-1379. doi:10.1007/s00268-009-0361-3

3. Northup PG, Garcia-Pagan JC, Garcia-Tsao G, et al. Vascular liver disorders, portal vein thrombosis, and procedural bleeding in patients with liver disease: 2020 practice guidance by the American Association for the Study of Liver Diseases. Hepatology. 2021;73(1):366-413. doi:10.1002/hep.31646

4, Massironi S, Gervaso L, Fanizzi F, et al. Venous thromboembolism in patients with neuroendocrine neoplasms: a systematic review of incidence, types, and clinical outcomes. Cancers (Basel). 2025;17(2):212. doi:10.3390/cancers17020212

5. Koea J. Management of locally advanced and unresectable small bowel neuroendocrine tumours. World J Surg. 2021;45(1):219-224. doi:10.1007/s00268-020-05740-7