Extrahepatic Portal Hypertension Research Articles

Portal Cavernoma

Portal cavernoma corresponds to the abnormal development of a venous network whose caliber is initially microscopic, with hepatopetal portal blood flow. It is a consequence of chronic portal thrombosis in a healthy or slightly fibrous liver. The causes are essentially those of portal thrombosis. However, portal thrombosis remains an undetermined cause in 50% of the cases. The clinical manifestations of cavernoma reflect extrahepatic portal hypertension and are exceptionally biliary. The diagnosis of portal cavernoma is radiological. Ultrasound Doppler and CT confirmed the diagnosis. MRI offers a better analysis of biliary impact. The treatment is essentially medically based on anticoagulants. Recording to surgery was reserved for complications.

S4892 Isolated Jejunal Varices: A Hidden Source of Gastrointestinal Bleeding in Patient With Extrahepatic Portal Hypertension and Altered Anatomy

S4892 Isolated Jejunal Varices: A Hidden Source of Gastrointestinal Bleeding in Patient With Extrahepatic Portal Hypertension and Altered Anatomy

A clinical case of liver iron overload in a child with liver cavernoma and extrahepatic portal hypertension

A clinical case of liver iron overload in a child with liver cavernoma and extrahepatic portal hypertension

HYPERAMMONEMIA IN NEONATOLOGY: DIAGNOSTIC DIFFICULTIES, MANAGEMENT FEATURES

There are primary and secondary hyperammonemia. Primary hyperammonemia is a hereditary disorder of the urea formation cycle. Secondary hyperammonemia can occur both in hereditary diseases (mitochondrial diseases, organic aciduria/aminoacidopathies) and in asphyxia suffered in childbirth, liver damage of various etiologies (toxic, infectious, etc.), extrahepatic portal hypertension, renal failure, infections caused by urease-producing microorganisms, diseases accompanied by increased catabolism, etc. transient nature. Regardless of the etiology, hyperammonemia can cause irreversible damage to brain cells, which determines the exceptional importance of early diagnosis and timely therapy.

Curcumol Attenuates Portal Hypertension and Collateral Shunting Via Inhibition of Extrahepatic Angiogenesis in Cirrhotic Rats.

Liver cirrhosis can cause disturbances in blood circulation in the liver, resulting in impaired portal blood flow and ultimately increasing portal venous pressure. Portal hypertension induces portal-systemic collateral formation and fatal complications. Extrahepatic angiogenesis plays a crucial role in the development of portal hypertension. Curcumol is a sesquiterpenoid derived from the rhizome of Curcumae Rhizoma and has been confirmed to alleviate liver fibrosis by inhibiting angiogenesis. Therefore, our study was designed to explore the effects of curcumol on extrahepatic angiogenesis and portal hypertension. To induce cirrhosis, Sprague Dawley rats underwent bile duct ligation (BDL) surgery. Rats received oral administration with curcumol (30mg/kg/d) or vehicle (distilled water) starting on day 15 following surgery, when BDL-induced liver fibrosis had developed. The effect of curcumol was assessed on day 28, which is the typical time of BDL-induced cirrhosis. The results showed that curcumol markedly reduced portal pressure in cirrhotic rats. Curcumol inhibited abnormal splanchnic inflow, mitigated liver injury, improved liver fibrosis, and attenuated portal-systemic collateral shunting in cirrhotic rats. These protective effects were partially attributed to the inhibition on mesenteric angiogenesis by curcumol. Mechanically, curcumol partially reversed the BDL-induced activation of the JAK2/STAT3 signaling pathway in cirrhotic rats. Collectively, curcumol attenuates portal hypertension in liver cirrhosis by suppressing extrahepatic angiogenesis through inhibiting the JAK2/STAT3 signaling pathway.

Ectopic biliary varices as a cause of portal biliopathy and mechanical jaundice syndrome

The authors consider ectopic biliary varices as a possible cause of portal biliopathy in extrahepatic portal hypertension. The main diagnostic methods including ultrasound CT, MRI, endoscopic ultrasonography, cholangioscopy, difficulties of differential diagnosis and clinical manifestations of portal biliopathy are presented. Various treatment options including portosystemic shunting and endoscopic biliary decompression are discussed. The authors emphasize the role of differentiated treatment depending on bile duct lesions. The study not only reviews this problem, but also highlights the issues requiring further analysis for selection of optimal diagnostic and treatment methods.

Extrahepatic portal hypertension in myeloproliferative diseases, features of diagnosis and therapeutic tactics

Extrahepatic portal hypertension in myeloproliferative diseases, features of diagnosis and therapeutic tactics

Surgical Treatment of Portal Hypertension in Children.

Introduction: Portal hypertension is a syndrome characterized by increased pressure in the portal vein system and can be caused by impaired blood flow in the portal vein, hepatic veins, or inferior vena cava. The main complications of this condition are bleeding from varicose veins of the esophagus (in our study in 100% of patients), splenomegaly with hypersplenism (in our study in 98% of patients), ascites (in our study in 1 patient). The main goal of treating portal hypertension is to prevent bleeding from esophageal varices. However, today the goal of surgical treatment of portal hypertension in children is not only to prevent the development of bleeding but also the possible restoration of intrahepatic blood flow. Materials and Methods: A retrospective analysis of the results of treatment of portal hypertension in 75 children (41 boys, 34 girls) operated in our Center for the period from 2019 to 2022 was carried out. The mean age of the patients was 7 ± 1 years. Sixty-nine patients had an extrahepatic form of portal hypertension, and 6 patients had an intrahepatic form (liver fibrosis). In 14 patients (18.6%), the operation was repeated (a vascular shunt was previously applied in another hospital; 4 children were operated on repeatedly). Results: A good result was obtained in all children, and the risk of bleeding from varicose veins of the esophagus was eliminated. Vascular bypass surgery was performed in all cases: mesoportal bypass in 17 (22.7%) patients, splenorenal bypass in 37 (49.3%) patients, mesocaval bypass in 21 (28%) patients. In 10 (13%) cases, repeated bypass surgery was required due to dysfunction or thrombosis of the previously performed bypass. In 14 (18.6%) patients with mesoportal shunts, blood flow in the liver was completely restored. Conclusions: The main method of surgical treatment of portal hypertension today is portosystemic bypass surgery, which effectively prevents bleeding from varicose veins of the esophagus. Mesoportal shunting is a definitive treatment for extrahepatic portal hypertension that restores portal perfusion of the liver.

Portosinusoidal Vascular Disorder: A Heretofore Unrecognized Manifestation of Sickle Cell Disease?

Portosinusoidal vascular disorder (PSVD) is a recently proposed histopathologic entity that encompasses a spectrum of often subtle hepatic microvascular lesions and related microarchitectural abnormalities. Clinical manifestations may arise years after histologic diagnosis and include extrahepatic portal vein thrombosis and portal hypertension. While the histopathologic features of PSVD have been associated with numerous clinical conditions, most notably prothrombotic/vasculopathic disorders, PSVD has not yet been described in sickle cell disease. This gap is striking given the central role of microvascular dysfunction in sickle cell disease and well-described patterns of hepatic injury and dysfunction in this population. This case series is the first to explore the prevalence and pathogenesis of PSVD in sickle cell disease. Forty-one diagnostically adequate liver biopsies from patients with sickle cell disease were identified across the archives of 5 tertiary medical centers. All biopsies exhibited at least 1 histopathologic feature associated with PSVD (mean 3.8 features/case). Overall, 90.2% of patients met the criteria for a diagnosis of PSVD based on the presence of specific histopathologic and/or clinical findings. Immunohistochemical stains for von Willebrand factor, CD34, and glutamine synthetase were performed on 36 cases (87.8%). Aberrant (centrilobular sinusoidal) CD34 and von Willebrand factor staining was present in 97.2% and 86.1% of cases, respectively. Glutamine synthetase reactivity was at least mildly decreased in zone 3 hepatocytes in 52.8% of cases. We posit that chronic erythrocyte sickling results in dysfunction and remodeling of the portal microvasculature, culminating in regression of zone 3 hepatocytes. The presence of PSVD may explain, at least in part, the hepatic dysfunction observed in this patient population. These patients may also benefit from extended clinical surveillance for portal hypertension and other complications. While subtle and prone to overdiagnosis, the features of PSVD should be carefully considered when interpreting liver biopsies from patients with sickle cell disease.

Two Cases of Gastric Varices with Left-sided Portal Hypertension due to Essential Thrombocythemia Treated with Gastric Devascularization or Partial Splenic Embolization.

Left-sided portal hypertension (LSPH) is a condition of extrahepatic portal hypertension that often results in bleeding from isolated gastric varices (GVs). LSPH is sometimes caused by myeloproliferative diseases, such as essential thrombocythemia (ET). We herein report two cases of GVs with LSPH due to ET that were successfully controlled by gastric devascularization (GDS) or partial splenic embolization (PSE). Since each patient with LSPH due to ET has a different pathology, optimal treatment should be performed depending on the patient's condition, such as platelet counts, hemodynamics, or the prognosis. We believe that these cases will serve as a reference for future cases.

Liver reportalization in extrahepatic portal hypertension

The study involved literature review of history and current state of surgical treatment in extrahepatic portal hypertension in children and adults. The author analyzed Russian and foreign publications on surgical repair of hepatopetal blood flow in extrahepatic portal hypertension. The issue is a high priority in Russia, which is confirmed by the fact that the author found out the pioneer studies of Russian authors, which were published earlier than the works of foreign researchers. It was found that the role of hepatopetal blood flow restoration in extrahepatic portal hypertension in adults had been much less studied than in children. More clinical material is to be gathered to determine the feasibility of such interventions in adults.

Portal Hypertension in Children at the Department of Pediatric Gastroenterology & Nutrition, BSMMU, Dhaka, Bangladesh

Background: Portal hypertension is the hemodynamic abnormality frequently associated with serious liver disease, although it is recognized in a variety of extrahepatic diseases also. Portal hypertension is an important cause of morbidity and mortality in Bangladeshi children. Development of esophageal varices and bleeding is one of the major complications of CLD. The mortality from each episode of variceal bleeding is 30-50% depending on the clinical status of the patient. All conditions that interfere with blood flow at any level within the portal system can lead to portal hypertension. For better management of this disorder, it is important to determine the underlying cause. Objective: To assess the portal hypertension in children at the Department of Pediatric Gastroenterology & Nutrition, BSMMU, Dhaka, Bangladesh. Methods: This cross-sectional descriptive study was conducted at the Department of Pediatric Gastroenterology & Nutrition, BSMMU during the period Jan 2018 to July 2019. 50 patients who were diagnosed as portal hypertension were determined by Upper GI Endoscopy. Doppler USG was also done for supporting the diagnosis of Portal HTN as well as to differentiate between extrahepatic Portal HTN and CLD with portal HTN. Demographic data and other related information regarding etiology and complications were recorded in a standard datasheet. Results: Results: A total of 50 cases were included in this study. Their age range was 1.5-16 years. It was observed that 21 (42.0%) patients belonged to age group 6-10 years. The mean age was 9.22±9.85 years with ranged from 2.5 to 16 years. It was observed that almost two third 31 (62.0%) patients were male and 19 (38.0%) were female. Among 50 patients 29 were diagnosed as extrahepatic portal hypertension and 21 were diagnosed as CLD with portal HTN. Shows the etiology of portal hypertension of studied patients. Extrahepatic portal hypertension was the most common etiology (58.0%). Among CLD patients Wilson disease was the most common (13; 26.0%). Two (4.0%) patients were cryptogenic CLD and two (4.0%) were Budd Chiari Syndrome. One patient was Biliary cirrhosis and one patient had Auto immune hepatitis. Conclusion: We concluded that Extrahepatic Portal HTN is the most common cause of portal hypertension in children in this center. Among the intrahepatic causes of portal HTN Wilson disease was the

Roux-en-Y biliary reconstruction as a definitive treatment for serious complications of portal biliopathy. Case series.

Portal biliopathy (PB) is an abnormality of the biliary tree wall due to extrahepatic portal hypertension. Among the complications of portal biliopathy are digestive bleeding, jaundice, and cholangitis. Surgical treatment is an exception when medical management is not possible. This is a case series study of four patients with severe PB complications requiring surgical management in our center from 2005 to 2016. Two of them had previous surgical procedures related to portal hypertension. All presented with severe biliary stenosis and recurrent cholangitis, and two also had massive upper gastrointestinal bleeding. Because of endoscopic management failure, a Roux-en-Y hepaticojejunostomy was performed in all cases. Two patients presented morbidity Clavien-Dindo>IIIA, requiring reoperation. During follow-up, no one developed other complications related to PB. Surgical treatment for PB complications is a challenge and mainly implies a portosystemic shunt as a first step. When it fails, an alternative is perform a biliodigestive anastomoses, with high risk of bleeding given the prominent collaterals present in the hepatoduodenal pedicle secondary to portal cavernomatosis. Our patients after YRGB didn't present new complications due to PB. The surgery could be a definite solution for PB complications. It has only been made for selective cases because it implies high complexity and risk.

A History of Umbilical Vein Catheterization Does Not Preclude Children from a Successful Meso-Rex Bypass.

Umbilical vein catheterization (UVC) can cause portal venous thrombosis, leading to the development of extrahepatic portal venous obstruction (EHPVO) and portal hypertension (PHT). The feasibility of the Meso-Rex bypass (MRB) for the treatment of EHPVO in patients with a history of UVC has been questioned. We compared the feasibility of performing an MRB in patients with or without a history of previous UVC. A retrospective review of patients with EHPVO and known UVC status explored for a possible MRB at our institution was performed (1997-2022). Patients were categorized in two groups: with (UVC(+)) or without (UVC(-)) a history of UVC for comparison. A p-value less than 0.05 was considered significant. One hundred and eighty-seven patients were included (n = 57 in UVC(+); n = 130 in UVC(-)). Patients in the UVC group were significantly younger at surgery and the incidence of prematurity was higher. Other risk factors for the development of EHPVO were similar between the groups, but only history of UVC could predict the ability to receive MRB (odds ratio [OR]: 7.4 [3.5-15.4]; p < 0.001). The success rate of MRB was significantly higher in patients with no history of UVC (28/57 [49.1%] in UVC(+) vs. 114/130 [87.7%] in UVC(-); p < 0.001). However, MRB patency at discharge (25/28 [89.3%] in UVC(+) vs. 106/114 [94.7%] in UVC(-); p = 0.3) was equally high in both groups. Our results indicate that a history of UVC is not a contraindication to MRB. Half of the patients were able to successfully receive an MRB. Patients with symptomatic PHT from EHPVO should not be excluded from consideration for MRB based on UVC history.

An Audit of Extrahepatic Portal Vein Obstruction: Experience from Tertiary Referral Center.

Extrahepatic portal vein obstruction (EHPVO) is a common cause of portal hypertension in India. (1) To evaluate the clinical presentation and the natural history of EHPVO; (2) to describe the risk factors, rebleeding rates and development of portal biliopathy on follow-up; and requirement of surgery in EHPVO at a tertiary care center. Data from 318 consecutive patients with EHPVO from June 2012 to October 2020 were analyzed. All patients underwent liver biochemistry, ultrasonography (USG) abdomen, upper gastrointestinal (GI) endoscopy, and viral serology. Color Doppler, computed tomography (CT) abdomen and magnetic resonance cholangiopancreatography (MRCP) were done as indicated. Mean age of presentation was 15.08 years [standard deviation (SD) 12.74; 6 months-60 years; 210 males)]. The presenting features were upper GI bleed (n = 227) (age at first bleed 11 years; 4 months-56 years), left hypochondrium pain or lump (n = 67), and only lower GI bleed (n = 1). Incidentally detected EHPVO on USG was seen in 10.69% (n = 34) patients. Postbleed ascites were seen in 10.69% (n = 34) patients. Six patients had symptomatic portal biliopathy and 14 had hypersplenism. Around 14.77% (n = 47) of patients had a history of being delivered at home, while 3.45% (n = 11) had a history of umbilical sepsis. During follow-up, 35.3% (n = 82) of patients had rebled. On imaging, associated splenic vein (SV) collaterals and superior mesenteric vein (SMV) collaterals were seen in 35.84% (n = 114) and 11.01% (n = 35) patients, respectively. Gallbladder varices were seen in 44.3% (n = 106), while gallstones in 5.66% (n = 18). On endoscopy, 87.42% (n = 278) patients had esophageal varices, 18.86% (n = 60) had isolated fundic varices, and three had ectopic varices. Only two patients had rectal varices and colopathy. Emergency devascularization was required in 3.45% (n = 14) patients for the failure of variceal bleed control, 1.88% (n = 7) underwent splenectomy, and four patients had proximal splenorenal shunt (PSRS) surgery. Extrahepatic portal hypertension (EHPVO) is an important cause of portal hypertension (PHT) in our country. The majority of them present with GI bleed; postbleed ascites were seen only in ~10%. Rebleed occurs in one-third of cases. Gallbladder varices were common; portal biliopathy occurred in 10% and were usually asymptomatic.

Vascular bypass surgery in the treatment of extrahepatic portal hypertension in children (review)

In children with extrahepatic portal hypertension (EPHT), the most frequent and life-threatening complication is bleeding from varicose veins of the esophagus and stomach. Therefore, the main task of HSV treatment is to prevent bleeding from the veins of the upper gastrointestinal tract. The most effective treatment is portosystemic bypass surgery, with effectiveness of 94%97%. However, the use of these operations is limited precisely by a decrease in portal liver perfusion and development of portosystemic encephalopathy. This study aimed to analyze domestic and foreign publications devoted to the surgical treatment of portal hypertension and the development of portosystemic encephalopathy during the postoperative period. A systematic search was carried out in PubMed, Web of Science, Scopus, MEDLINE, eLibrary, RSCI, and Cyberleninka; 345 references were analyzed, 110 articles were reviewed, and 97 publications on the surgical treatment of portal hypertension were selected for the review. The development of portosystemic encephalopathy during the postoperative period often occurs after the imposition of total portosystemic bypass surgery. To reduce the risk of developing portosystemic encephalopathy, selective shunts have been developed, which to some extent preserve the PPP. With distal splenorenal anastomosis, the frequency of portosystemic encephalopathy is 10%15%. An intermediate position is occupied by a side-to-side splenorenal anastomosis, which has signs of selective surgery. The results of the analysis of literature sources showed that discussions are still underway regarding the choice of the optimal treatment strategy for patients with EPHT, place and role of endoscopic methods for the prevention of gastrointestinal bleeding, and mesoportal shunt in the treatment of patients with EPHT. Nevertheless, the majority of world experts consider mesoportal shunt to be the most optimal operation for the primary and secondary prevention of varicose bleeding and other HSV complications. If it is impossible to perform, selective bypass surgery of the distal splenorenal anastomosis can be an alternative to a mesoportal shunt.

“Etiology of Portal Hypertension in Children at the Department of Pediatric Gastroenterology &amp; Nutrition, Bangladesh Shishu Hospital &amp; Institute, Dhaka, Bangladesh”

Background: Portal hypertension is an important cause of morbidity and mortality in Bangladeshi children. Development of esophageal varices and bleeding is one of the major complications of CLD. The mortality from each episode of variceal bleeding is 30-50% depending on the clinical status of the patient. All conditions that interfere with blood flow at any level within the portal system can lead to portal hypertension. For better management of this disorder, it is important to determine the underlying cause. Objective: To assess the Etiology of Portal Hypertension in Children. Methods: This cross-sectional descriptive study was conducted at the Emergency, Observation and Referral Unit, Bangladesh Shishu Hospital and Institute, Dhaka, Bangladesh during the period Jan 2018 to July 2019. 47 patients who were diagnosed as portal hypertension were determined by liver biopsy, abdominal sonography, abdominal computed tomography scan, and liver doppler so¬nography. Demographic data and other related information regarding etiology and complications were recorded in a standard datasheet. Results: Total 47 cases were included in this study. Their age range was 1.5-16 years. It was observed that 20 (42.6%) patients belonged to age group 6-10 years. The mean age was 9.22±9.85 years with ranged from 2.5 to 16 years. It was observed that almost two third (67.7%) patients were male and 18 (38.3%) were female. Among 47 patients 27 were diagnosed as extrahepatic portal hypertension and 20 were diagnosed as CLD with portal HTN. Shows the etiology of portal hypertension of studied patients. Extrahepatic portal hypertension was the most common etiology (57.4%). Among CLD patients Wilson disease was the most common (12; 25.5%). Two (4.3%) patients were cryptogenic CLD and two (4.3%) were Budd Chiari Syndrome. One patient was Biliary cirrhosis and one patient had Auto immune hepatitis. Conclusion: We concluded that intrahepatic diseases are the most common causes of portal .............

Etiology, Presenting Features, and Endoscopic Findings of Portal Vein Hypertension in Children

Background: Portal hypertension (PH) refers to a clinical syndrome characterized by an elevation in the pressure gradient between the portal and hepatic veins. It is necessary to identify the underlying causes to manage this disorder effectively. Objectives: This study aimed to investigate the etiology, clinical manifestations, and endoscopic findings in children with PH. Methods: This analytic cross - sectional study was performed on patients (&lt; 18 years) with PH who were referred to the Pediatric Gastroenterology Clinic of Mofid Children’s Hospital in Tehran, Iran, within 2014 - 2020. The demographic details of the patients were collected from their medical records. Clinical manifestations, age at diagnosis, family history, and endoscopic findings were also recorded. Results: A total of 102 patients participated in this study. The subjects’ mean age was 6.81 ± 4.46 years. The results revealed that 50 (49.0%) and 46 (45%) cases had PH due to extrahepatic and intrahepatic diseases, respectively. Autoimmune hepatitis and portal vein thrombosis were the most common etiology of intrahepatic and extrahepatic PH, respectively. Based on the endoscopic analysis, esophageal varices were the most common findings (95.8%) observed in patients with PH. Conclusions: Extrahepatic diseases were the most prevalent PH etiology in children referred to the Pediatric Gastroenterology Clinic of Mofid Children’s Hospital.

Minimal invasive prophylaxis of bleeding from esophageal varices in children with extrahepatic portal hypertension

The objective of the work was to study the efficacy of minimally invasive endoscopic treatment of esophageal varices (EV) in children with extrahepatic portal hypertension (EHPH).Methods and Materials. Eighty children aged 3 to 17 years of age with EHPH included in this study. The patients were divided into three analysis groups. The group I (n=14) included children with EHPH who had not previously undergone any surgical interventions and endoscopic ligation of EV was performed against the background of acute bleeding or after medical hemostatic treatment. The group II (n=37) included patients who had undergone the endoscopic treatment of EV after an unsatisfactory outcome of previously performed surgical interventions. The group III included 29 children who underwent only azygos-portal disconnection procedures. We performed the comparative analysis of the severity of EV before and after sessions of the endoscopic treatment of EV, as well as the analysis of the frequency of recurrent bleedings in comparison groups.Results. According to the research results, recurrent gastroesophageal hemorrhages were noted in 44.4 % of cases in the group I. In the group II, 37 patients underwent a total of 68 sessions of the stage endoscopic treatment of EV. According to the control endoscopic examinations, there was a significant reduction in the risk of bleeding from EV between ligation sessions (p=0.001) of the endoscopic treatment of EV. During the follow-up period, in the group II, recurrent bleedings from EV were noted in 6 (16.2 %) patients. Whereas in 10 (34.5 %) children of the group III, recurrent gastroesophageal hemorrhages were noted in the postoperative period. The analysis showed a significant correlation of the presence of «red flags» with recurrent episodes of bleedings in children of the group II after the endoscopic treatment of EV (r=0.32 p=0.05). Analysis of the causes of recurrent gastroesophageal bleedings in children of the group III did not reveal significant differences in such parameters as the degree of EV and «red flags».Conclusion. Thus, the endoscopic treatment of EV is a safe and effective method of secondary prevention of bleedings from EV. The question concerning the primary prevention of gastroesophageal hemorrhages require further study.

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