Etiology Of Portal Hypertension Research Articles

Safety and efficacy of EUS-guided coil and glue injection for the primary prophylaxis of gastric variceal hemorrhage

Gastric variceal bleeding (GVB) is associated with high morbidity and mortality. EUS-guided coil and cyanoacrylate (CYA) injection (EUS-CCI) has been shown to be an effective therapy in acute bleeding and secondary prophylaxis; however, there is a paucity of data on primary prophylaxis. In this single-center observational study, adult patients with high-risk gastric varices (GV; size >10mm or cherry red spot) without prior bleeding underwent EUS-CCI for the primary prophylaxis of GVB between June 2009 and December 2019. The primary outcome was post-treatment GVB. Eighty patients with a mean variceal size of 22.5 ± 9.4mm and a mean length of follow-up of 3.0 ± 2.4 years were included. The etiology of portal hypertension was cirrhosis in 71 patients (88.7%) and noncirrhotic in 9 (11.3). The mean model for end-stage liver disease score was 12.3 ± 3.7 in patients with cirrhosis. The mean coil number was 1.5 (range, 1-3) and mean glue volume injected 2 mL (range, .5-5). Technical success was achieved in 100%, 96.7% had EUS confirmation of GV obliteration, and 67.7% were obliterated with 1 treatment session. Post-treatment GVB occurred in 2 patients (2.5%) and adverse events in 4 (4.9%). No deaths related to GVB occurred, and emergent transjugular intrahepatic shunts were not needed during the follow-up period. In patients with high-risk GV, EUS-CCI for primary prophylaxis is highly effective at preventing GVB with a low rate of adverse events. Primary prophylaxis of high-risk GV with coil and CYA glue injection should be considered in centers with the appropriate expertise.

Natural Course of Pediatric Portal Hypertension

The etiology of portal hypertension (pHTN) in children differs from that of adults and may require different management strategies. We set out to review the etiology, management, and natural history of pHTN at a pediatric liver center. From 2008 to 2018, 151 children and adolescents with pHTN were identified at a free‐standing children’s hospital. Patients were stratified by etiology of pHTN (intrahepatic disease [IH], defined as cholestatic disease and fibrotic or hepatocellular disease; extrahepatic disease [EH], defined as hepatic vein obstruction and prehepatic pHTN). Patients with EH were more likely to undergo an esophagoduodenscopy for a suspected gastrointestinal bleed (77% vs. 41%; P < 0.01). Surgical interventions differed based on etiology (P < 0.01), with IH more likely resulting in a transplant only (65%) and EH more likely to result in a shunt only (43%); 30% of patients with IH and 47% of patients with EH did not undergo an intervention for pHTN. Kaplan‐Meier analysis revealed a significant increase in mortality in the group that received no intervention compared to shunt, transplant, or both and lower mortality in patients with prehepatic pHTN compared to other etiologies (P < 0.01 each). Multivariate analysis revealed increased odds of mortality in patients with refractory ascites (odds ratio [OR], 4.34; 95% confidence interval [CI], 1.00, 18.88; P = 0.05) and growth failure (OR, 13.49; 95% CI, 3.07, 58.99; P < 0.01). Conclusion: In this single institution study, patients with prehepatic pHTN had better survival and those who received no intervention had higher mortality than those who received an intervention. Early referral to specialized centers with experience managing these complex disease processes may allow for improved risk stratification and early intervention to improve outcomes.

Etiology of portal hypertension in rural India

Etiology of portal hypertension in rural India

Analysis Of The Natural Course Of Pediatric Portal Hypertension

Presenter: Al-Faraaz Kassam MD | Cincinnati Children's Hospital Medical Center Background: The etiology of portal hypertension (pHTN) in children varies from that of adults and requires understanding of the differences in management strategies. We set out to assess the epidemiology and natural history of pediatric pHTN. Methods: 154 patients with pHTN from 2008-2018 were identified at a free-standing children’s hospital. Etiology, disease course, and interventions were assessed. Patients were then stratified by etiology of pHTN. The primary outcome was overall survival, with a secondary outcome of understanding the interventions and management required. Survival was calculated using Kaplan-Meier survival analysis. Statistical significance was set at p<0.05. Results: The distribution of etiology included 105 (68%) patients with cholestatic disease (CD), 16 (10%) with fibrotic or hepatocellular disease (HFD), four (3%) with hepatic vein obstruction (HVO), and 29 (19%) with pre-hepatic pHTN (PRE) caused by portal vein obstruction or portal vein sclerosis. Median follow-up for the cohort was 4.63 (IQR 2.02-7.25) years. Median age at diagnosis (years) varied between etiologies (0.34, IQR 0.06-0.9 CD vs 0.51, 0.06-3.33 HFD vs 5.85, 1.26-9.52 HVO vs 2.51, 0.85-5.09 PRE; p<0.01). There were no differences in sex, comorbidities, or years of follow up. Patients with PRE were more likely to require an EGD (79.3% vs 40% CD, 50% HFD, 50% HVO, p<0.01) and patients with PRE (2.0±0.4) and HVO (1.8±1.0) required more endoscopic interventions than CD (1.1±0.2) or HFD (1.4±0.5) (p<0.01). However, there were no differences regarding gastrointestinal bleeding or need for banding or sclerotherapy (p=0.31 and p=0.94 respectively). Interventions differed based on etiology (p<0.01) with CD more likely undergoing a transplant only (71.4%) and PRE more likely to undergo a shunt only (44.8%). 24.8% of CD, 62.5% of HFD, 100% of HVO, and 41.4% of PRE patients did not undergo an intervention. Kaplan-Meier analysis revealed no difference in survival based on etiology, however, analysis by type of intervention revealed a significant increase in mortality in the group who received no intervention compared to shunt, transplant, or both (p<0.01) (Figure 1). Of the 18 patients who died without intervention, 7 patients died while listed for transplant, five patients were not candidates due to progression of disease, and six patients had clinical deterioration before workup was completed. Of the 36 patients who are alive and have not undergone intervention, 27 have stable pHTN, six are waitlisted for organs, and three are not candidates for intervention due to severity of disease. Conclusion: The sequelae of pHTN in children is distinct from the adult process and a better understanding of this disease is necessary. In this single institution study, we found that most patients presented with CD as the cause of pHTN followed by PVO. While no difference in overall survival was noted between groups, patients who received no intervention had higher mortality than those who received an intervention. Early referral to specialized centers with experience managing these complex disease processes may allow for improved risk stratification and early intervention which may improve outcomes. Further work is needed to understand the predictors of mortality in patients with pHTN.

Update on the management of gastrointestinal varices.

Cirrhosis of liver is a major problem in the western world. Portal hypertension is a complication of cirrhosis and can lead to a myriad of pathology of which include the development of porto-systemic collaterals. Gastrointestinal varices are dilated submucosal veins, which often develop at sites near the formation of gastroesophageal collateral circulation. The incidence of varices is on the rise due to alcohol and obesity. The most significant complication of portal hypertension is life-threatening bleeding from gastrointestinal varices, which is associated with substantial morbidity and mortality. In addition, this can cause a significant burden on the health care facility. Gastrointestinal varices can happen in esophagus, stomach or ectopic varices. There has been considerable progress made in the understanding of the natural history, pathophysiology and etiology of portal hypertension. Despite the development of endoscopic and medical treatments, early mortality due to variceal bleeding remains high due to significant illness of the patient. Recurrent variceal bleed is common and in some cases, there is refractory variceal bleed. This article aims to provide a comprehensive review of the management of gastrointestinal varices with an emphasis on endoscopic interventions, strategies to handle refractory variceal bleed and newer endoscopic treatment modalities. Early treatment and improved endoscopic techniques can help in improving morbidity and mortality.

Diagnosing the Etiology of Portal Hypertension by Colonoscopy

Diagnosing the Etiology of Portal Hypertension by Colonoscopy

Colonic Indole And Hydrogen Sulfide, Gut Bacterial Metabolites, Affect Portal Blood Pressure in Healthy And Cirrhotic Rats

Liver cirrhosis is a leading cause of portal hypertension, and is often accompanied by systemic hypotension. Accumulating evidence suggests that gut bacteria may affect hemodynamics, however, the mechanisms are not clear. We investigated the effect of colon‐administered gut bacteria metabolites on portal blood pressure (PBP), portal blood flow (PBF) and systemic arterial blood pressure (ABP) in healthy (controls) and cirrhotic rats (CRH).10‐week‐old, male, Sprague Dawley rats were maintained either on tap water (controls) or water solution of thioacetamide for 18 weeks to induce liver cirrhosis (CRH). PBP, PBF and ABP were measured in anaesthetized rats at baseline and after the intracolonic administration of either a vehicle, indole, or Na2S, a hydrogen sulfide (H2S) donor into the colon.CRH showed significantly higher PBP but lower ABP than controls. The intracolonic administration of indole increased portal blood level of indole, and peripheral blood level of indoxyl sulfate, a liver metabolite of indole. Rats treated with Na2S showed increased portal blood levels of thiosulfate and sulfane sulfur, products of H2S oxidation. The intracolonic administration of vehicle did not affect hemodynamic parameters. In controls intracolonic H2S increased PBP but decreased PBF and ABP. In contrast, intracolonic indole increased both BPB and PBF, whereas did not affect significantly ABP. In comparison to controls, CRH showed significantly greater hemodynamic responses to H2S but not to indole. Cirrhotic livers had a significantly higher concentration of H2S but lower expression of rhodanese, an enzyme converting H2S to sulfate.Colon‐administered indole and H2S increase portal blood pressure via distinct hemodynamic mechanisms. Indole increases, whereas H2S decreases portal blood flow. Indole and H2S signaling in the gut‐liver axis may be involved in the control of portal blood pressure and in the etiology of portal hypertension. Further studies on the effects of gut bacterial metabolites on portal circulation are needed.Support or Funding InformationThis work was supported by the National Science Centre, Poland grant no. UMO‐2016/22/E/NZ5/00647This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Clinicopathological Correlation of Portal Hypertension in Children and Management Strategies

We studied 51 children with clinical setting of portal hypertension over a period of one and half years. Out of these, 27 (52.94%) were males and 24 (47.05%) were females. All the cases were subjected to biochemical, diagnostic, radiological investigations and liver biopsy. Portal hypertension was diagnosed by demonstrating on USG abdomen/ Doppler, the presence of collaterals of portal vein and esophageal varices on endoscopy. Treatment was initiated depending upon clinical presentation. The most common presenting complaints were hematemesis and malena (35.3%) followed by their combination with abdominal distension (19.6%). 86.3% patients had anemia mostly due to upper GI bleed. 35.3% patients had leucopenia while 47.1% had thrombocytopenia. Only 18 (i.e. 35.3%) had Hypersplenism. Maximum patients who bled more than twice had a mild (41.2%) or severe (29.4%) derangement of prothrombin time. The etiology of portal hypertension turned out to be extra- hepatic portal vein obstruction in 86.3% cases. There were 2 cases each (3.9% each) of Wilson’s disease and Budd-Chiari syndrome. One (2%) was secondary to chronic liver disease due to hepatitis C infection, one was extra- hepatic biliary atresia and one was autoimmune hepatitis. 9.8% cases required drugs in the form of somatostatin drip and all these required a packed cell transfusion as well. 23 patients (45.1%) required only blood transfusion without a somatostatin infusion. Those with severe acute bleeding usually were given somatostatin infusion. The variceal size at presentation was a very important predictor of the morbidity and outcome.

Etiology of Portal Hypertension among Pediatric Patient: Hospital based Study

Etiology of Portal Hypertension among Pediatric Patient: Hospital based Study

Splenoadrenal Shunt for Noncirrhotic Portal Hypertension

Portosystemic shunt surgery is an established treatment option for preventing variceal rebleeding in patients with noncirrhotic portal hypertension (NCPH). The proximal splenorenal shunt is a widely performed procedure in these patients. In this study, the use of adrenal vein as an alternative conduit has been investigated. A retrospective analysis of patients with NCPH who underwent proximal splenoadrenal and splenorenal shunt between 2011 and 2015 was performed. Demographic findings, etiology of portal hypertension, clinical presentation, hematological parameters, liver function test, intraoperative findings, postoperative morbidity, and shunt patency were studied and compared between the two groups. All patients were followed up for a minimum of 12 months with Doppler study of the shunt to assess shunt patency and upper gastrointestinal endoscopy to assess regression of varices. During the study period, 97 patients with NCPH underwent shunt surgery (proximal splenoadrenal shunt, 8; proximal splenorenal shunt, 74; and interposition mesocaval shunt, 15). Anomalous anatomy of the left renal vein was the main indication (5/8 patients) for a splenoadrenal shunt. Median fall in portal pressure in patients who underwent splenoadrenal shunt was 11.5 mmHg (range, 2–14 mmHg). The median (range) operative time was 4.5 (3–6) hours and median (range) intraoperative blood loss was 160 (100–200) mL. During a median (range) follow-up of 32 (12–48) months, shunt thrombosis developed in one patient. Comparison of intraoperative parameters and postoperative outcomes showed no significant difference in median fall in portal pressure (p = 0.39), median operative time (p = 0.51), median blood loss (p = 0.80), Grade III/IV postoperative complications (p = 0.56), shunt thrombosis (p = 0.93), and varices regression rate (p = 0.72) between patients undergoing proximal splenorenal and splenoadrenal shunt. In conclusion, left adrenal vein is a suitable vascular conduit for porto-systemic shunt surgery. This is especially so if the performance of splenorenal shunt is precluded because of anatomic abnormality of the renal vein.

Transjugular intrahepatic portosystemic shunt: Indications, complications, survival and its use as a bridging therapy to liver transplant in Western Australia.

Insertion of transjugular intrahepatic portosystemic shunt (TIPS) is an established therapeutic option to treat the complications of portal hypertension. The purpose of this study is to review the experience of a single Australian institute with TIPS and evaluation of result to emphasize the indication, aetiology of portal hypertension, prognostic factors, complications and survival. Use of TIPS as a bridge to liver transplantation was also analysed. A retrospective cohort study of patients treated with TIPS at The Western Australian Liver Transplant Unit, Sir Charles Gairdner Hospital, over a period of 12years. Kaplan-Meier method was used for survival analysis and cox-regression analysis was used to analyse the predictors of survival. Fifty-three patients underwent TIPS between January 2000 and March 2012. The cumulative survival at 1month, 1year and 5years was 90%, 70.9% and 43.9%, respectively. The predictors of survival were indication (variceal bleeding versus ascites, hazard ratio 3.19, CI 95%: 1.164-8.794, P=0.024) and Model of End Stage Liver Disease score (Hazard ratio 2.513, CI 95%: 1.087-5.810, P=0.031). Patients who underwent TIPS as a bridge to liver transplant had a 5-year survival of 71% that is comparable to the overall survival of Western Australian liver transplant unit. Transjugular intrahepatic portosystemic shunt is a safe and effective method of treatment of complications of portal hypertension. TIPS can be safely used as a bridging therapy to liver transplant. Despite small number of TIPS being performed at our institute, our technical results are comparable to the institutes with bigger number of patients.

Spectrum of small-bowel mucosal abnormalities identified by capsule endoscopy in patients with portal hypertension of varied etiology

Bleeding from small intestinal ectopic varices and persistent anemia caused by portal hypertensive enteropathy (PHE) can be very challenging. Capsule endoscopy (CE) is one of the best noninvasive modalities in identifying such lesions. The aims of this study are to study the prevalence of small-bowel changes related to portal hypertension (PHT) and to correlate them with the observations related to the effects of portal hypertension in the esophagus, stomach, and colon. Thirty-two patients with various etiologies of PHT with either anemia or gastrointestinal bleed were included along with age- and sex-matched controls without PHT. All patients underwent blood tests, gastroscopy, colonoscopy, and CE. The small-bowel findings by CE were categorized as inflammatory-like and vascular lesions. The small-bowel changes were analyzed to find out any association with various demographic, clinical, and endoscopic variables. Thirty-one out of 32 patients with PHT (96.8%) had PHE identified by CE. Of them, 31 (96.8%) had inflammatory-like appearance, 11 (34.4%) had vascular lesions, and 2 (6.2%) had small-bowel varices. Inflammatory-like appearance was noted in eight (25%) and angiodysplastic lesions in two (6.2%) controls. Findings compatible with PHE were detected in 96.8% of the patients and 25% of the controls (X 2 =34.72, p=0.000).The presence of PHE was not associated with any of the above-mentioned variables. Small-bowel mucosal changes were seen in significantly higher number of patients with PHT with anemia.

LDRf classification for ectopic varices in gastrointestinal tract

Objective To study the feasibility of LDRf classification for gastrointestinal tract ec- topic varices （EcV） outside the esophagus. Methods Data of 914 patients with gastrointestinal EcV were classified by LDRf and analyzed for EeV location （ L）, vascular diameter （D） , and risk factor （Rf）. The etiology of the portal hypertension （PH） was determined, and the patients were treated and followed up. Results The EeVs were located in duodenum of 198 cases, in jejunum and ileum of 93, in bile duct of 105, in colon of 65, and in rectum of 453. Diameters of blood vessels of EcV varied from 0. 3 to 3.5 cm. PH causes were cirrhosis with portal hypertention in 630 patients （68. 9% ）, in which 3 were autoimmune cirrhosis and 3 were portal spongiform fiver disease （0. 6% ）. Combined esophageal and gastric varices were found in 252 cases （27.6 % ） , including 4 cases （0. 5% ） of splenectomy. Various treatments were applied in 315 patients, including endoscopic tissue adhesive injection in 43, endoscopic sclerotherapy in 76, endo- scopic ligation in 74, interventional treatment in 52, and surgical laparotomy in 70. A total of 19 patients died of variceal bleeding. The patients were followed up for 13 to 36 months, no varices relapsed, and 1-year survival rate was 100%. Conclusion LDRf classification, simple, applicable, standardized, is suitable for the whole gastrointestinal varicose veins. Key words: Varicose veins, heterotopic ; Endoscopy; Hypertension, portal; LDRf typing

Ectopic varices.

Ectopic varices.

Selective surgical shunts for treating complications of portal hypertension: 10-year experience in a single institution in eastern Taiwan

ObjectiveSurgical portosystemic shunts are safe and effective for treating rebleeding gastric varices (GV) in portal hypertensive patients with well-preserved liver function. The aim of this study is to investigate the clinical outcomes of using selected surgical shunts for managing rebleeding GV at a single institution in eastern Taiwan. Materials and MethodsWe retrospectively recruited 12 patients who received distal splenorenal shunts (DSRS) following the indication of rebleeding GV or hypersplenism from January 2001 through December 2010. Their demographic data, etiology of portal hypertension, associated treatments, perioperative complications and clinical outcomes were reviewed. ResultsAll patients received DSRS, including 10 adults and two children, and were examined for a median follow-up period of 53 months. No postoperative encephalopathy, major complications, or surgical mortality occurred. Two of the patients were waiting for liver transplants. Late rebleeding in esophageal varices developed in two patients who were successfully managed using endoscopic treatment. The etiology of portal hypertension had no significant impact on the postoperative complications. ConclusionAlthough there were a limited number of cases in this series, our results indicate that the DSRS is an effective treatment for rebleeding GV, especially for patients with well-preserved liver function and taking into account the realities of organ shortages.

Nodules in antrum after variceal eradication a new finding in patients with portal hypertension

Portal hypertension is known to cause esophageal varices, gastric varices and portal hypertensive gastropathy (PHG). The prevalence of gastric varices and PHG is known to increase after eradication of esophageal varices. PHG includes the presence of a mucosal mosaic pattern, cherry red spots, and/or black-brown spots and gastric vascular ectasia (GAVE). Patients with portal hypertension in whom esophageal varices were eradicated were on follow up endoscopy for detection of recurrence of esophageal varices. Their status of PHG was assessed and patients antral nodules were enrolled. Twenty patients with antral nodules were identified over one year. Fifteen out of 20 patients had cirrhosis as etiology of portal hypertension, three had non-cirrhotic portal hypertension and two had extra-hepatic portal vein thrombosis. GAVE was seen more commonly (n=8, 40%) in patients with PHG with nodules. PHG with antral nodules is a novel endoscopic finding present both in cirrhotic and non-cirrhotic portal hypertension with unknown pathogenesis, and is seen more commonly in patients with eradicated varices who are on long-term follow up.

Measuring of gastric emptying in Egyptian pediatric patients with portal hypertension by using real-time ultrasound

Background/Aim:Among the various methods for evaluating gastric emptying, the real-time ultrasound is safe, does not require intubation, or rely on either radiologic or radionuclide technique. The aim of our work was to measure the gastric emptying in pediatric patients with portal hypertension by using the real-time ultrasound.Patients and Methods:Forty patients with portal hypertension with mean age 7 ± 2.8 years and 20 healthy children as a control group underwent gastric emptying study by using real-time ultrasound. The cross-sectional area of the gastric antrum was measured in the fasting state and then each subject was allowed to drink tap water then calculated by using formula area (π longitudinal × anteroposterior diameter/4). The intragastric volume was assumed to be directly proportional to the cross-sectional area of the antrum.Results:The mean gastric emptying half-time volume was significantly delayed in portal hypertension patients (40 ± 6.8 min) compared with the control subjects (27.1 ± 3.6) min (P<0.05). Patients with extrahepatic portal vein obstruction had significant delayed gastric emptying in comparison to patients with portal hypertension due to other etiologies (36.14 ± 4.9 vs 44.41 ± 6.04 min; P<0.01).Conclusion:Ultrasound is a noninvasive and a reliable method for measuring gastric emptying in pediatric patients. Gastric emptying was significantly delayed in patients with portal hypertension. Etiology of portal hypertension may influence gastric emptying time in patients with chronic liver disease.

Confocal Endomicroscopy Improves Detection of Gastric Intestinal Metaplasia

in 20 consecutive patients ( M 9/20,45%; F 11/20, 55%; mean age 66.2+/7.6 SD). With portal hypertension diagnosed by clinical, ultra sonographic (US) and endoscopic criteria. The etiology of portal hypertension was hepatic cirrhosis in 15 patients (75%), portal cavernomatosi in 4 patients (20%) and portal vein thrombosis in 1 (5%). All patients underwent US and gastroscopy before performing CE examination. Results: Upper endoscopy showed F1 varices in 5 patients (25%), F2 varices in 7 patients (35%) and F3 varices in 6 patients (30%). Two patients (10%) did not present oesophageal varices. Ascites was present in 11/20 patients (55%). CE examination showed small bowel lesions due to portal hypertension in 16/20 patients (80%). Duodenal involvement occurred in 9 (40%) and jejunal lesions in 13 patients (65%) (<Lesions were found 7 times in proximal-, 9 times in mid, 8 times with distal jejunal involvement).Conclusion: Clinically relevant small bowel abnormalities are frequent in patients with portal hypertension, more so if oesophageal varices and/or ascites are present. Capsule endoscopy is an effective tool for their diagnosis Terminal ileum showed abnormal findings in 11 patients (55%). The entire jejunum was involved in 6 patients (30%). Lesions were classified as: bleeding or not-bleeding erosions and mucosal congestion with vascular ectasia. Most patients with positive CE had both erosions and mucosal congestion (12/16, 75%), 4 patients (25%) had erosions alone. All patients with positive CE had oesophageal varices. there was a significant association between abdominal ascites and CE findings (OR 1.7).

Colorectal Cancer Screening in Patients With Ulcerative and Crohn's Colitis Using Chromoendoscopy and Confocal Endomicroscopy

in 20 consecutive patients ( M 9/20,45%; F 11/20, 55%; mean age 66.2+/7.6 SD). With portal hypertension diagnosed by clinical, ultra sonographic (US) and endoscopic criteria. The etiology of portal hypertension was hepatic cirrhosis in 15 patients (75%), portal cavernomatosi in 4 patients (20%) and portal vein thrombosis in 1 (5%). All patients underwent US and gastroscopy before performing CE examination. Results: Upper endoscopy showed F1 varices in 5 patients (25%), F2 varices in 7 patients (35%) and F3 varices in 6 patients (30%). Two patients (10%) did not present oesophageal varices. Ascites was present in 11/20 patients (55%). CE examination showed small bowel lesions due to portal hypertension in 16/20 patients (80%). Duodenal involvement occurred in 9 (40%) and jejunal lesions in 13 patients (65%) (<Lesions were found 7 times in proximal-, 9 times in mid, 8 times with distal jejunal involvement).Conclusion: Clinically relevant small bowel abnormalities are frequent in patients with portal hypertension, more so if oesophageal varices and/or ascites are present. Capsule endoscopy is an effective tool for their diagnosis Terminal ileum showed abnormal findings in 11 patients (55%). The entire jejunum was involved in 6 patients (30%). Lesions were classified as: bleeding or not-bleeding erosions and mucosal congestion with vascular ectasia. Most patients with positive CE had both erosions and mucosal congestion (12/16, 75%), 4 patients (25%) had erosions alone. All patients with positive CE had oesophageal varices. there was a significant association between abdominal ascites and CE findings (OR 1.7).

Abstract No. 73: What variables predict the need for revisions in patients undergoing TIPS with PTFE-covered stents?

To determine what clinical, laboratory, or procedural variables predict the need for TIPS revisions in individuals with PTFE-covered TIPS. Between 2003–2009, a total of 141 patients underwent TIPS venographic evaluation following TIPS placement with PTFE-covered stents. Of these, a total of 43 patients required TIPS revisions. Twenty-three (23) different variables were modeled using univariate analysis, and then evaluated using a Cox proportional hazards model. Of the variables tested, only the presence of a previous intervention predicted the need for further interventions (p=0.03). This variable also had an interaction with time (e.g. the hazard ratio increased over time), so that there was a greater likelihood of a need for a second revision as the time from the previous intervention increased. Other variables, including the size of the stent, etiology of portal hypertension, post-TIPS portosystemic gradient, and intrahepatic stent location failed to predict the need for future interventions. Individuals requiring one TIPS reinterventions should be aggressively screened for TIPS failures because of the increased likelihood that they will require another intervention. No correlation with other clinical, laboratory, or procedural variables was noted with the need for TIPS revisions.