The therapeutic effect of portal vein (PV) stenting for PV stenosis following nontransplant hepato-pancreato-biliary (HPB) surgery has not been fully investigated.

Changes in portal venous pressure (PVP) gradient before and after stenting, complications, symptomatic improvement, and stent patency were evaluated.

We identified 14 consecutive patients undergoing PV stenting for malignant (n = 8) and benign (n = 6) PV stenosis. Signs of PV stenosis were composed of refractory ascites in 6 patients, varices with hemorrhagic tendencies in 5, and abnormal liver function in 5. The median PVP gradient after PV stenting was 3.0 cm H2O (range, 1.5-3.0), which was significantly smaller than that before PV stenting (median, 15 cm H2O [range, 2.5-25]; P < 0.01). Thirteen out of 14 (93%) achieved clinical success with symptomatic improvement, except one patient with sustained refractory ascites because of peritoneal seeding. During the median follow-up time of 7.3 months (range, 1.0-87), stent occlusion occurred in two patients (14%) because of intrastent tumor growth. The 1-year cumulative stent patency rate was 76% in the entire cohort.

Based on durable effect on patency, we deemed PV stenting for PV stenosis after HPB surgery to be safe and beneficial for improving symptoms.

To evaluate the long-term outcomes of percutaneous transhepatic stent placement for portal vein (PV) stenosis after liver transplantation (LT) and hepato-pancreato-biliary (HPB) surgery.

Retrospective study of 455 patients who underwent LT and 522 patients who underwent resection of the pancreatic head between June 2011 and February 2016. Technical success, clinical success, patency, and complications were evaluated for both groups.

A total of 23 patients were confirmed to have postoperative PV stenosis and were treated with percutaneous transhepatic PV stent placement. The technical success rate was 100%, the clinical success rate was 80%, and the long-term stent patency was 91.3% for the entire study population. Two procedure-related hemorrhages and two early stent thromboses occurred in the HPB group while no complications occurred in the LT group. A literature review of selected studies reporting PV stent placement for the treatment of PV stenosis after HPB surgery and LT showed a technical success rate of 78-100%, a clinical success rate of 72-100%, and a long-term patency of 57-100%, whereas the procedure-related complication rate varied from 0-33.3%.

Percutaneous transhepatic PV stent is a safe and effective treatment for postoperative PV stenosis/occlusion in patients undergoing LT regardless of symptoms. Due to increased risk of complications, the indication for percutaneous PV stent placement after HPB surgery should be limited to patients with clinical symptoms after an individual assessment.

Two patients presented with bleeding duodenal varices secondary to mesenteric and portal vein chronic occlusion. After a failed transhepatic recanalization, a combined transmesenteric and transhepatic approach was used to recanalize the chronic portal and mesenteric venous obstruction. The occluded segment was treated with transmesenteric stent placement in one patient and stent placement and coil embolization of varices in the second patient. Follow-up imaging and endoscopy showed decompression of the duodenal varices in both patients and absence of further bleeding episodes.

Treatment options for patients with portal vein (PV) stenosis or occlusion after surgery are limited. The purpose of this study was to investigate the efficacy and safety of PV stent placement in patients with portal vein occlusion or stenosis after radical operation for hepatobiliary pancreatic malignant tumour.

We retrospectively reviewed the records of 59 patients who underwent portal venous stent placement at the Asan Medical Center, Seoul, Korea, for PV stenosis or occlusion between February 2008 and February 2012.

Stents were placed in the portal venous system across stenotic (n = 47) and occlusive (n = 12) lesions after percutaneous transhepatic portography. Reasons for stent placement were tumour recurrence (n = 30), portal vein resection and anastomosis (n = 18) and post-operative inflammatory changes (n = 11). Pressure gradients (superior mesenteric vein, main PV) decreased immediately after stent placement, from 10.5 mm Hg ± 4.4 (standard deviation) to 2.5 mm Hg ± 2.6 (P < 0.0001). Liver function was improved post-stenting (P < 0.05). The median time between the original surgery and stent placement was 16 (1-137) days in the vascular-orientated group and 306 (13-3703) days in the tumour recurrence group (P < 0.0001). Transient fever developed in 11 patients, but resolved in 2-5 days. Stents were occluded in 15 of the 59 patients (25.4%).

PV stent placement is a safe choice, has an acceptable success rate and provides marked relief from portal hypertension due to portal vein occlusion or stenosis after hepatobiliary pancreatic surgery. Liver function data are also improved after portal venous stent placement.

To review the technical success and results of attempted transcatheter management of portal vein (PV) stenosis and occlusion in the nontransplant population.

All patients referred for percutaneous management of PV stenosis or occlusion between January 1997 and July 2007 were included in this review. Patients were included on an intent-to-treat basis, but liver transplant recipients were excluded. Intervention was attempted in 18 patients. Access to the portal system was achieved by the transhepatic route in 17 of 18 patients and by way of a preexisting transjugular intrahepatic portosystemic shunt in the other one. Indications for intervention included gastrointestinal bleeding (n = 8), ascites (n = 3), hemorrhage and ascites (n = 4), preoperative decompression of varices (n = 2), and intestinal angina (n = 1). Etiology of the PV stenosis or occlusion was postsurgical (n = 9), tumor encasement (n = 5), pancreatitis (n = 3), and unknown (n = 1).

Lesions were successfully crossed with a stent in 14 of 18 patients. Successful decompression of the portal system was achieved in 13 of 14. In one of 14 patients, the varices were not decompressed as a result of competitive flow. In four of 18 patients, the lesion could not be crossed. In the 13 technically successful cases in which the portal varices were decompressed, there was resolution of clinical symptoms with no immediate periprocedural complications.

PV stent placement is safe, with an acceptable success rate, and provides symptomatic relief from the sequelae of presinusoidal portal hypertension.

This article evaluates the results of portal vein (PV) stent placement in patients with malignant extrinsic lesions stenosing or obstructing the PV and causing symptomatic PV hypertension (PVHT). Fourteen patients with bile duct cancer (n = 7), pancreatic adenocarcinoma (n = 4), or another cancer (n = 3) underwent percutaneous transhepatic portal venous stent placement because of gastroesophageal or jejunal varices (n = 9), ascites (n = 7), and/or thrombocytopenia (n = 2). Concurrent tumoral obstruction of the main bile duct was treated via the transhepatic route in the same session in four patients. Changes in portal venous pressure, complications, stent patency, and survival were evaluated. Mean +/- standard deviation (SD) gradient of portal venous pressure decreased significantly immediately after stent placement from 11.2 mmHg +/- 4.6 to 1.1 mmHg +/- 1.0 (P < 0.00001). Three patients had minor complications, and one developed a liver abscess. During a mean +/- SD follow-up of 134.4 +/- 123.3 days, portal stents remained patent in 11 patients (78.6%); stent occlusion occurred in 3 patients, 2 of whom had undergone previous major hepatectomy. After stent placement, PVHT symptoms were relieved in four (57.1%) of seven patients who died (mean survival, 97 +/- 71.2 days), and relieved in six (85.7%) of seven patients still alive at the end of follow-up (mean follow-up, 171.7 +/- 153.5 days). Stent placement in the PV is feasible and relatively safe. It helped to relieve PVHT symptoms in a single session.

The purpose of this study was to retrospectively evaluate interventional radiological management of patients with symptomatic portal hypertension secondary to obstruction of splanchnic veins.

Twenty-four patients, 15 males and 9 females, 0.75 to 79 years old (mean, 36.4 years), with symptomatic portal hypertension, secondary to splanchnic venous obstruction, were treated by percutaneous methods. Causes and extent of splanchnic venous obstruction and methods are summarized following a retrospective evaluation.

Obstructions were localized to the main portal vein (n = 22), intrahepatic portal veins (n = 8), splenic vein (n = 4), and/or mesenteric veins (n = 4). Interventional treatment of 22 (92%) patients included recanalization (n = 19), pharmacological thrombolysis (n = 1), and mechanical thrombectomy (n = 5). Partial embolization of the spleen was done in five patients, in two of them as the only possible treatment. TIPS placement was necessary in 10 patients, while an existing occluded TIPS was revised in two patients. Transhepatic embolization of varices was performed in one patient, and transfemoral embolization of splenorenal shunt was performed in another. Thirty-day mortality was 13.6% (n=3). During the follow-up, ranging between 2 days and 58 months, revision was necessary in five patients. An immediate improvement of presenting symptoms was achieved in 20 patients (83%).

We conclude that interventional procedures can be successfully performed in the majority of patients with obstruction of splanchnic veins, with subsequent improvement of symptoms. Treatment should be customized according to the site and nature of obstruction.

Rapid development of diagnostic radiological methods during recent decades has been followed by development of new interventional procedures involving portal circulation. The majority of these interventions were developed for treatment of patients with symptoms secondary to portal hypertension (PH). Interventions involving portal vein circulation have an established position in the treatment of PH and other diseases, and further development of these methods can be expected.

Portal vein thrombosis (PVT) is an uncommon cause for presinusoidal portal hypertension. PVT can be caused by one of three broad mechanisms: (1) spontaneous thrombosis when thrombosis develops in the absence of mechanical obstruction, usually in the presence of inherited or acquired hypercoagulable states; (2) intrinsic mechanical obstruction because of vascular injury and scarring or invasion by an intrahepatic or adjacent tumor; or (3) extrinsic constriction by adjacent tumor, lymphadenopathy or inflammatory process. Usually, several combined factors are necessary to result in PVT. The consequences of portal vein thrombosis are mostly related to the extension of the clot within the vein. Gastrointestinal bleeding from gastroesophageal varices is the most frequent presentation. Noninvasive imaging techniques are currently used for the screening of patients and the initial diagnosis of PVT. The invasive techniques are reserved for cases when noninvasive techniques are inconclusive, before percutaneous interventional treatment, or in preoperative assessment of patients who are candidates for surgery. Recanalization of the portal vein with anticoagulation alone may not be consistent or appropriate in highly symptomatic patients. Catheterization of the superior mesenteric artery (SMA) is helpful for diagnosis as well as for therapy by allowing the intra-arterial infusion of thrombolytic drugs in the same setting. Direct transhepatic portography allows precise determination of the degree of stenosis and extension within the portal vein, as well as pressure measurements. Thrombotic occlusions of the portal, mesenteric, and splenic veins can be managed by mechanical thrombectomy (MT) or pharmacologic thrombolysis. Underlying occlusions because of organized or refractory thrombus or fixed venous stenosis are best corrected by balloon angioplasty and stent placement. Access into the portal venous system can also be established through creating a transjugular intrahepatic portosystemic shunt (TIPS). Creating a TIPS is also important in the setting of PVT associated with cirrhosis to decompress portal hypertension and improve portal venous flow. PVT involving the portal, splenic, and/or mesenteric veins can also complicate a preexisting TIPS in which case the shunt can be readily used as therapy access. Several techniques may be used to recanalize the shunt and portal venous system, including thrombolytic therapy, balloon angioplasty/embolectomy, suction embolectomy, basket extraction of clots, and mechanical thrombectomy with a variety of devices. Advantages of MT include the potential to rapidly remove thrombus without the need for prolonged thrombolytic infusions, and reducing the potential life-threatening complications of thrombolytic therapy. Possible drawbacks include the risk of intimal or vascular trauma to the portal vein, which may promote recurrent thrombosis.

A case of portal vein thrombosis (PVT) secondary to pancreatitis is presented. Patient was treated with catheter-directed thrombolysis using urokinase solution. Because the percutaneous transhepatic approach is associated with higher risk of hemorrhage we used the catheter-directed thrombolysis via the transjugular intrahepatic access to restore the patency of the thrombosed portal vein. This case shows that catheter-directed thrombolysis with transjugular approach can be effectively used in the treatment of PVT.