Portal Vein Occlusion Research Articles

Long-term liver deportalisation in stable and time prolonged prehepatic portal hypertension model affects expression of hypoxia, angiogenesis, apoptosis, and autophagy markers in the young rats’ liver

prehepatic portal hypertension in children cause severe and life-threatening complications, that highlights the need in in-depth investigations of pathogenetic mechanisms, which contribute to prehepatic portal hypertension-associated liver pathology. In developed stable experimental prehepatic portal hypertension model in adolescent rat males we aimed to assess the expression levels of the key molecular markers of hypoxia, angiogenesis, autophagy, and apoptosis in the liver tissue after 6-month deportalization. Partial portal vein ligation was performed in 4-week old male rats. After 6-months tissue samples from PHP-model, sham operated and control animals were studied by western blot to identify protein levels of markers related to prehepatic portal hypertension -induced liver injury. Partial portal vein occlusion upregulated hypoxia inducible factor -1α (by 4.67 folds vs. control, p<0.001) and vascular endothelial growth factor protein expression levels (by 2.33 folds vs. control, p<0.001) suggesting chronic hypoxia development. Abnormally high levels of angiostatin isoforms were found (by 9.88 folds vs. control, p<0.001) to signify angiogenesis dysregulation. Significant caspase-3 (23.4-fold increase vs. control, p<0.001) overexpression is executive phase of apoptotic cell death evidence. Dramatic LC3 level expression indicates existence of crosstalk between autophagy and apoptosis that contribute to fibrotic changes. Hypoxia-induced events, impaired angiogenesis regulation, enhanced autophagy and apoptosis are contributing factors of prehepatic portal hypertension -induced liver injury. A better understanding of subtle molecular mechanisms of this pathology may pave the way for innovative treatment options.

Portal Hypertensive Mayhem: A Case Report of Colonic Variceal Bleeding Treated by Antegrade Embolization

AbstractIn patients with cirrhosis of the liver, acute variceal bleeding can be fatal. Bleeding colonic varices is a very rare cause of lower gastrointestinal bleeding that can result in massive hemorrhage in patients with cirrhosis. Here we present the case of a 50-year-old gentleman, having cirrhosis of the liver with chronic portal vein occlusion, who presented with massive bleeding per rectum. Contrast computed tomography (CT) revealed a large shunt arising from the superior mesenteric vein forming submucosal colonic varices and joining the right renal vein. He underwent successful obliteration of the varix by antegrade endovascular embolization via the trans-splenic access. Endovascular embolization could be an effective and life-saving treatment option for colonic variceal bleeding.

Imaging and Pathological Feature Analysis of Idiopathic Portal Hypertension

Background: Idiopathic portal hypertension (IPH) is a rare clinical condition often misdiagnosed as cirrhosis. The management of IPH focuses on preventing and treating complications related to portal hypertension, such as bleeding from esophagogastric fundal varices. In contrast, the management of cirrhosis focuses on symptomatic treatment based on etiology, protecting hepatocyte function, and inhibiting hepatic inflammation and fibrosis. Therefore, it is crucial to correctly recognize both diseases and take appropriate therapeutic measures. Objectives: The aim of this study was to summarize and analyze the imaging, pathological, and serological features of idiopathic portal hypertension and cirrhosis to reduce misdiagnosis in clinical practice. Patients and Methods: Pathological, radiological parameters [computed tomography (CT)/magnetic resonance imaging (MRI)], and serological examinations were retrospectively evaluated for 14 patients with IPH and 30 patients with cirrhosis. We analyzed and compared their imaging manifestations in terms of spleen thickness and length, liver morphology, hepatic lobe atrophy, hyperplasia, portal vein thrombosis, arteriovenous phase liver perfusion, regenerative nodules, focal nodular hyperplasia-like lesions of the liver, portal vein morphology, splenorenal shunt, and hepatorenal shunt. The aim was to investigate the correlation between the imaging manifestations and the pathological manifestations. Results: There were significant differences between the IPH and cirrhosis groups in individual indicators of liver function, routine blood tests, and coagulation function (P < 0.05). Significant differences in spleen thickness and length were also observed between the IPH and cirrhosis groups (P < 0.05). Atrophy and hyperplasia of the hepatic lobe differed between the two groups. Changes in liver morphology and parenchyma were observed in both the IPH and cirrhosis groups, with diffuse regenerative nodules and focal nodular hyperplasia-like lesions being significant for distinguishing between IPH and cirrhosis. Focal nodular hyperplasia-like lesions were more common in patients with idiopathic portal hypertension, whereas diffuse regenerative nodules were more common in patients with cirrhosis. All 14 IPH patients had abnormalities in the portal vein system, including main portal vein dilation, stiffness, straightening, and distal branch vein stenosis or occlusion, while 9 cirrhosis patients had portal vein abnormalities, primarily thinning of the portal vein. Pathology revealed that patients in the cirrhosis group had varying degrees of cell necrosis and edema, and pseudolobule formation was observed in all patients. Patients with IPH showed varying degrees of fibrosis in the portal and confluent areas, but lobular inflammation was not evident. Some IPH patients experienced portal vein occlusion and stenosis. Conclusion: Idiopathic portal hypertension is relatively rare in clinical practice and is characterized by mostly normal liver function and hypersplenism, which may lead to a decrease in platelets, red blood cells, and white blood cells. If a giant spleen is found on imaging and the liver surface is smooth, IPH should be considered. Additionally, fibrosis, stenosis, and occlusion of the portal venous system, as well as focal nodular hyperplasia-like lesions, are suggestive of idiopathic portal hypertension. In contrast, diffuse regenerative nodules and pseudolobule formation are often indicative of cirrhosis. Furthermore, atrophy and hyperplasia of the liver are significant in differentiating the two diseases.

Beyond the Rex: an innovative meso-intrahepatic portal vein bypass for late-onset extrahepatic portal vein occlusion after living donor liver transplantation.

The Meso-Rex bypass (MRB) is recognized as an effective treatment for portal hypertension secondary to extrahepatic portal vein occlusion (EHPVO) both in the pediatric and adult population, within or outside the context of liver transplantation. It is the preferred surgical treatment in most centers because not only does it addresses the portal hypertension, but also restores physiologic portal hepatopetal flow. However, the Rex recess, the landmark for this technique, may not be safely accessible in some patients. We present a 22-year-old male who underwent living donor liver transplant (LDLT) for neonatal hepatitis. He presented with variceal bleeding due to EHPVO at 13 years after transplant. Various endoscopic, radiologic, and surgical interventions were employed to address the recurrent gastrointestinal bleeding, but results have been unsatisfactory. We performed a meso-intrahepatic portal vein bypass (MIPVB), an innovative alternative to the MRB, for this patient with extensive post-operative adhesions, perihilar collaterals, and cavernous transformation. MIPVB creation in patients where the Rex recess is inaccessible is technically challenging. But with a multidisciplinary team approach, meticulous preoperative planning, and close follow-up, the authors have demonstrated that it is a safe and feasible option for patients with late-onset EHPVO after liver transplantation.

Embolization with or without portal vein stenting for bleeding ectopic jejunal varices in hepatopetal portal collaterals due to extrahepatic portal vein occlusion or stenosis after hepatobiliary and pancreatic surgery

PurposeTo evaluate the efficacy and safety of embolization with or without portal vein stenting for bleeding ectopic jejunal varices in the hepatopetal portal collateral due to extrahepatic portal vein occlusion or stenosis after hepatobiliary and pancreatic surgery.Materials and methodsThis study included consecutive patients who underwent embolization for bleeding ectopic jejunal varices in the hepatopetal collateral due to extrahepatic portal vein occlusion or stenosis after hepatobiliary and pancreatic surgery between September 2012 and December 2020. The safety, technical and clinical success rates (no re-bleeding within 1 month) and re-bleeding-free survival after the first therapy and overall survival were assessed.ResultsFourteen sessions in 11 patients were included. Four patients (7 sessions) underwent variceal embolization only, and the remaining seven patients (7 sessions) underwent portal vein stenting and variceal embolization. Technical success was achieved in all 14 sessions (100%). Clinical success was achieved in 13 of 14 sessions (92.9%). No treatment-related serious complications including liver failure were observed. One-year and 2-year re-bleeding-free survival rate after the first endovascular therapy in all 11 patients was 90.9 and 60.6%, respectively. Two patients who experienced re-bleeding had repeat embolization treatment. There was no significant difference in re-bleeding-free survival after endovascular therapy between the combination with stenting and embolization group and the embolization-only group (p = 0.13).ConclusionEmbolization with or without portal vein stenting of bleeding ectopic jejunal varices in the hepatopetal portal collateral due to extrahepatic portal vein occlusion or stenosis after hepatobiliary and pancreatic surgery can be considered a safe, effective, and repeatable therapy for long-term hemostasis of uncontrollable bleeding.

Protocolo diagnóstico y terapéutico de la trombosis portal

Portal vein thrombosis (PVT) is occlusion of the vein by thrombotic material with or without extension to other segments of the splanchnic venous system (splenic and mesenteric vein). Portal vein occlusion due to a thrombus occurs most frequently in patients with cirrhosis. It is most often diagnosed as an incidental finding on routine imaging tests. However, non-cirrhotic DVT, despite being a rare disease with a prevalence between 0.7–3.7 per 100,000 individuals, is the second most frequent cause of portal hypertension. The clinical manifestations depend on the duration (acute or chronic) of the event. PVT is diagnosed via Doppler ultrasound and the extent and presence of associated factors is confirmed via contrast-enhanced CT/MRI. It is essential for the therapeutic approach to differentiate whether there is an underlying cirrhosis or if it has occurred in a non-cirrhotic patient. In both cases, anticoagulation is the indicated treatment. However, the duration of anticoagulation depends on other factors, including the extent, temporality, and the existence or not of associated untreatable prothrombotic disease. In addition, alternative treatments are available in the case of anticoagulation failure, including transjugular intrahepatic postosystemic shunting.

The effect of an endovascular Heaney maneuver to achieve total hepatic isolation on survival, hemodynamic stability, retrohepatic bleeding, and collateral flow in a porcine model

PurposeCombining resuscitative endovascular balloon occlusion of the aorta (REBOA) and the inferior vena cava (REBOVC) with open surgery is a new hybrid approach for treating retrohepatic vena caval injuries. We compared endovascular total hepatic isolation with supraceliac REBOA ± suprahepatic REBOVC and no occlusion in experimental retrohepatic vena cava bleeding regarding survival, bleeding volume, hemodynamic stability, and arterial collateral blood flow.MethodsTwenty-five anesthetized pigs (n = 6–7/group) were randomized to REBOA; REBOA + REBOVC; REBOA + infra and suprahepatic REBOVC + portal vein occlusion (endovascular Heaney maneuver, four-balloon-occlusion, 4BO) or no occlusion. After balloon inflation, free bleeding was initiated from an open sheath in the retrohepatic vena cava. Bleeding volume, right internal thoracic artery (RITA) blood flow, hemodynamics, and arterial blood variables were measured until death or up to 90 min.ResultsThe REBOA group had a longer median survival time (63 min) compared with the 4BO (24 min, P = 0.02) and no occlusion (30 min, P = 0.02) groups, not versus the REBOA + REBOVC group (49 min, P > 0.05). The first 15 min accumulated bleeding was comparable in all groups (P > 0.05); Thereafter, bleeding volume was higher in the REBOA group versus the 4BO group (P < 0.05), not versus the other groups. RITA blood flow and MAP were higher in the REBOA group versus the other groups after 10 min of bleeding (P < 0.05).ConclusionsEndovascular Heaney maneuver was not beneficial for survival or hemodynamic stability in this porcine model, whereas supraceliac REBOA was. Anatomical differences in thoracoabdominal collaterals between pigs and humans must be considered when interpreting these results.

Transjugular intrahepatic portosystemic shunt for portal hypertension with chronic portal vein occlusion

PurposeThis study aims to evaluate the long-term patency of transjugular intrahepatic portosystemic shunt (TIPS) and determine the predictors of shunt dysfunction in patients with chronic portal vein occlusion (CPVO). MethodThis retrospective study was conducted from December 2010 to December 2020 in patients with portal hypertension and CPVO. Patients were followed up from initial TIPS insertion to December 2022 or death. Details of TIPS procedure, adverse events and clinical outcomes were recorded. The cumulative rate of shunt patency was calculated by the Kaplan-Meier method and compared by using the log-rank test. Independent predictors of shunt dysfunction were calculated with the Cox regression model. A nomogram comprising independent variables was developed to enhance the predictive accuracy of shunt patency. ResultsOne hundred six patients (mean age, 45.3 years ± 13.6; 71 males and 35 females) were enrolled in the study. TIPS procedure was technically successful in 100 of 106 patients (94.3 %). The primary shunt patency rates for all 100 patients were 78.9 %, 74.7 %, 67.2 %, and 62.4 % at 6, 12, 24, and 36 months, respectively, and the overall shunt patency rates were 88.9 %, 86.8 %, 83.6 %, and 81.2 % at 6, 12, 24, and 36 months, respectively. Independent predictor of shunt dysfunction were inadequate inflow from superior mesenteric vein or splenic vein (the maximum diameter < 8 mm) and platelet count ≥ 300 × 109/L. The developed nomogram is a simple tool for accurately predicting shunt patency. ConclusionsIn patients with CPVO, inadequate inflow and high platelet count are important factors for TIPS dysfunction.

Evaluation of portal vein occlusion with or without parenchymal splitting in the management of irresectable liver tumors

Evaluation of portal vein occlusion with or without parenchymal splitting in the management of irresectable liver tumors

The mechanism of intestinal stem cells differentiation after ischemia-reperfusion injury in a rat model.

Notch and Wnt/β-catenin signaling are responsible for regulation of intestinal stem cells (ISCs) proliferation and differentiation. The purpose of the study was to evaluate Wnt/β-catenin and Notch signaling roles in regulation of ISC differentiation following ischemia-reperfusion (IR) injury in a rat. Rats were assigned into two groups: Sham rats underwent laparotomy without vascular intervention and IR rats underwent occlusion of SMA and portal vein for 20min followed by 48h of reperfusion. Wnt/β-catenin and Notch-related gene expression were determined using Real-Time PCR. Enterocyte proliferation, differentiation and Wnt-related proteins were determined by immunohistochemistry. IR rats demonstrated a significant decrease in β-catenin gene expression, a decrease in cyclin D1 and β-catenin positive cells in jejunum and ileum compared to Sham rats. IR rats demonstrated a significant increase in Notch-related gene expression in jejunum and ileum compared to Sham rats. The number of secretory cells was higher mainly in the jejunum and number of absorptive cells was significantly lower in jejunum and lower in ileum in IR rats compared to Sham rats. Intestinal stem-cell differentiation is toward secretory cells 48h after IR injury; however, Wnt/β-catenin pathway inhibition and Notch-related gene expression stimulation suggest crosstalk between pathways.

Refining MRI-based criteria for portal vein invasion in hepatocellular carcinoma: improving sensitivity beyond portal vein tumor thrombosis.

To investigate the imaging features indicating portal vein invasion (PVI) of hepatocellular carcinoma (HCC) on gadoxetic acid-enhanced MRI and to create more accurate diagnostic criteria than the presence of portal vein tumor thrombosis (PVTT) on MRI. This retrospective study included patients with surgically resected HCC larger than 5 cm, and the presence of PVI was investigated. On MRI, we evaluated the image findings of portal vein occlusion, the parenchymal signal change caused by hemodynamic alterations of the portal vein, and their combination showing the highest odds ratio (OR) to define the diagnostic criteria for radiological PVI detection (rPVI criteria). The diagnostic performance and recurrence-free survival were compared between the rPVI criteria and the presence of PVTT using McNemar's test and Kaplan-Meier method, respectively. Interobserver agreement was evaluated using Cohen's weighted ĸ statistics. Of 189 enrolled patients, 25 (13.2%) had PVI on histology. To diagnose PVI on MRI, either peripheral wedge-shaped arterial peritumoral hyperemia with an abrupt cut-off of a portal vein or the presence of PVTT had the highest OR (41.67, p<0.001). The sensitivity of PVI was significantly increased under this diagnostic criterion (64.0% to 88.0%; p=0.031) with comparable accuracy (95.2% vs. 94.7%; p>0.999). In terms of recurrence-free survival, the patient group with rPVI was significantly worse (p=0.017) compared with the patients without rPVI. Interobserver agreement of radiologic findings was substantial (ĸ=0.64). Diagnostic criteria for radiologically PVI detection increase the sensitivity more than the only presence of PVTT.

Fibrolamellar hepatocellular carcinoma: a case report and gene analysis

BackgroundFibrolamellar hepatocellular carcinoma (HCC) (FL-HCC) is rare in Japan. FL-HCC develops in young patients with no history of cirrhosis and tends to manifest lymphatic metastasis with clinical features similar to those of HCC. We present a case of FL-HCC in a young male patient.Case presentationA 14-year-old male patient underwent abdominal computed tomography (CT) to diagnose appendicitis, wherein a hepatic tumor was detected. Dynamic enhanced CT revealed a 35-mm solid tumor, which contrasted at the early phase of dynamic enhanced study of the right hepatic segments, with occlusion of the right portal vein. We performed right hepatectomy for these lesions. The patient experienced a single lymphatic recurrence on the hepatoduodenal ligament 12 months after the initial surgery. We performed lymphadenectomy for the recurrent tumor. We performed RNA sequencing (RNA-seq) and targeted DNA sequencing of the resected specimens (primary tumor, lymphatic metastasis, and normal liver). RNA-seq detected DNAJB1-PRKACA in both primary and metastatic lesions as previously reported. Furthermore, The Cancer Genome Atlas (TCGA) database was used to compare other gene expressions in this case with those of previously reported cases of FL-HCC and HCC in young patients. Principal component analysis of differentially expressed genes in the top 10% revealed that the gene expression in our case was similar to that of previous FL-HCC cases but was a different cluster from that in HCC cases in young patients. Mutational analysis did not detect any somatic mutations associated with carcinogenesis, including previously reported mutations (Kastenhuber et al. in Proc Natl Acad Sci USA 114: 13076–84, 2017).ConclusionWe encountered a case of FL-HCC, a rare hepatic tumor in an adolescent patient, and evaluated the genetic background. Our findings could contribute to the elucidation of the mechanisms underlying carcinogenesis and progression in patients with FL-HCC and thereby contribute to the development of new therapeutic strategies in the future that may improve patient prognosis.

Ectopic Variceal Bleeding from the Hepaticojejunostomy due to Extrahepatic Portal Vein Occlusion: How to Treat?

Atypical variceal bleeding, which primarily stems from extrahepatic portal vein obstruction (EHPVO), is a severe complication of pancreatic hepatobiliary surgery. This review provides insights into this condition's incidence, diagnosis, and management strategies. The treatment modalities for atypical variceal bleeding resulting from EHPVO range from endoscopic intervention to surgical procedures, including direct variceal ligation and shunt surgery. Here, we discuss the efficacy and potential limitations of each treatment approach. Additionally, we explored the utility and therapeutic advantages of the meso-Rex shunt, a particularly promising surgical technique for mitigating the hemodynamic and metabolic impacts of EHPVO.

Intravascular Ultrasound-Guided Percutaneous Creation of a Gastric Vein to Cava Shunt in a Patient with Variceal Hemorrhage and Portal Vein Occlusion

Intravascular Ultrasound-Guided Percutaneous Creation of a Gastric Vein to Cava Shunt in a Patient with Variceal Hemorrhage and Portal Vein Occlusion

Portal Vein Recanalization–Transjugular Intrahepatic Portosystemic Shunt (PVR-TIPS) with superior mesenteric vein access and balloon-assisted shunt placement

BackgroundTo report the technique and outcome of ultrasound-guided percutaneous access to the superior mesenteric vein (SMV) for balloon-assisted portal vein recanalization–transjugular intrahepatic portosystemic shunt (PVR-TIPS) in a patient with chronic portal venous and splenic vein occlusion.Case presentationA 51-year-old, non-cirrhotic patient with severe portal hypertension was admitted for PVR-TIPS. Neither splenic nor hepatic access was feasible due to chronic portal and splenic vein occlusion. Percutaneous ultrasound-guided direct puncture of the SMV was performed to obtain access for balloon-assisted PVR-TIPS. The transmesenteric approach in combination with a balloon puncture technique for PVR-TIPS was successful, and no immediate complications were observed post-procedure. The subsequent follow-up exams showed patent TIPS and SMV without signs of intraabdominal hemorrhage.ConclusionPercutaneous ultrasound-guided superior mesenteric vein access for balloon-assisted PVR-TIPS is a feasible option in cases where hepatic or splenic access is not.

Extrahepatic portal vein aneurysm in which the acute thrombogenic process triggered by trauma confirmed by abdominal ultrasonography: a case report.

Extrahepatic portal vein aneurysm (PVA) is a rare condition in which the extrahepatic portal vein is partially dilated into a sac-like or spindle-like shape. Usually, patients are followed, but surgery is considered in cases of rupture, thrombus, or enlargement. We report a case of thrombus formation in an extrahepatic portal vein aneurysm following trauma that resulted in regression of the aneurysm and extrahepatic portal vein occlusion. Immediately after the trauma, ultrasonography showed moderately hyperechoic structures and comet signs along the vessel wall of the aneurysm and turbulent blood flow in the aneurysm, like in a whirlpool. There were floating point-like echogenic features, which were presumed to be microthrombi. In other words, the trauma might have triggered Virchow's triad: changes in the vessel wall, changes in blood properties, and blood stagnation. This is a valuable case in which ultrasonography imaging revealed interesting changes during the thrombus formation process inside an extrahepatic portal vein aneurysm. The aneurysm's size was reduced by thrombus-induced organization, but the main trunk of the portal vein became deficient in blood flow, resulting in extrahepatic portal vein occlusion. This case is suggestive of the mechanism of extrahepatic portal vein occlusion.

Anesthetic Challenges in Pregnancy with Wilson’s Disease Associated with Massive Splenomegaly Complicated with Intramyometrial Carboprost: A Case Report

Wilson’s disease is a rare autosomal recessive condition, that affects the liver and brain mainly. Pregnancy in these patients is of high risk due to involvement of liver and high incidence of abortion, preeclampsia, HELLP syndrome. We report a case of a 24year old G2A1 (35+2 weeks) diagnosed with wilson’s disease 6 years ago, currently on tab zinc. She presented with thrombocytopenia, anemia, extrahepatic portal vein occlusion with splenomegaly and mild ascites. She was taken up for elective section at 35+2 weeks, under general anesthesia. With intramyometrial injection of carboprost, there was sudden desaturation and bronchospasm. However, we managed the case successfully with safe outcome of both the mother and child. There are only very few case reports of Wilson’s disease in pregnancy undergoing C-section under general anesthesia in the presence of hepatic dysfunction.

A133 PORTAL VENOUS STENTING FOR THE TREATMENT OF NON-CIRRHOTIC PORTAL HYPERTENSION-RELATED GASTRIC ANTRAL VASCULAR ECTASIA: A CASE REPORT

Abstract Background Pancreatic and hepatobiliary cancers account for 15-24% of extrahepatic portal hypertension. Treating portal hypertensive bleeding associated with these tumors has been challenging with the delayed effect of chemoradiation and patients with active bleeding being unfit for such therapies. Portal vein stenting has been described in the literature for the treatment of variceal bleeding in such patients. We present the first report of its use for the successful treatment of refractory gastric vascular ectasia (GAVE)-related bleeding. Purpose To review portal vein stenting as a treatment for non-cirrhotic portal hypertension-related GAVE bleeding. Method Chart review was performed with the patient's informed consent. Result(s) A 53-year-old female patient with locally invasive pancreatic cancer presented with one week of melena and presyncope. She had a history of gastroesophageal reflux disease. Her tumor encased the celiac trunk, hepatic and splenic arteries, and abutted the superior mesenteric artery. She had been treated with chemotherapy and radiation. On examination, she was afebrile, blood pressure was 132/87, pulse 110 beats/min, and oxygen saturation 99% on room air. Her abdomen was soft and non-tender. Her hemoglobin was 63 g/L, which represented a 64-point drop over 4 months, leukocytes 4.5 x109/L, platelets 238 x109/L, INR 1.1 and normal electrolytes and creatitine. Alkaline phosphatase was 399 U/L, aminotransferases normal, albumin 38 g/L and total bilirubin 6 umol/L. She was started on pantoprazole and octreotide. On admission, gastroscopy revealed copious blood in the stomach with no clear source despite gastric lavage; hemospray was applied. Given persistent bleeding, repeat gastroscopy the following day revealed 4 columns of Baveno grade III esophageal varices with no high-risk stigmata, as well as severe portal hypertensive gastropathy and GAVE. Argon plasma coagulation and esophageal banding were performed. Over the next month, she continued to have maroon-colored stools. CT angiogram revealed portal vein occlusion and contrast extravasation within the gastric lumen, in keeping with her known gastric antral bleed, with no evidence of lower gastrointestinal bleeding. She had 5 further gastroscopies where APC and GAVE banding were performed. Despite that, she developed hematemesis. Interventional radiology was consulted and performed transhepatic portal venous recanalization, angioplasty and stenting using a 10mm x 60mm self expandable nitinol stent from the superior mesenteric vein to the main portal vein. After stenting, previously seen collateral veins and cavernous transformation were significantly reduced on angiography. She was started on clopidogrel to maintain stent patency. Two days following stent insertion, she stopped clinically bleeding and her hemoglobin stabilized. She was discharged home one month later. Conclusion(s) In patients with GAVE-related bleeding refractory to standard therapeutics, portal venous stenting is possibly an effective treatment modality. Please acknowledge all funding agencies by checking the applicable boxes below None Disclosure of Interest None Declared

Reply: Discussing the place of TIPS in non-cirrhotic patients with chronic extra hepatic portal vein occlusion refractory to standard of care therapy.

Department of Radiology, Section of Vascular and Interventional Radiology, Northwestern University, Chicago, Illinois, USA CorrespondenceRiad Salem ([email protected])

Safety of Laparoscopic Right Hepatectomy after Portal Vein Occlusion: Results from a Multicenter Study

Safety of Laparoscopic Right Hepatectomy after Portal Vein Occlusion: Results from a Multicenter Study