Portal Venous Pressure Gradient Research Articles

Development of a new Cox model for predicting long-term survival in hepatitis cirrhosis patients underwent transjugular intrahepatic portosystemic shunts.

Transjugular intrahepatic portosystemic shunt (TIPS) placement is a procedure that can effectively treat complications of portal hypertension, such as variceal bleeding and refractory ascites. However, there have been no specific studies on predicting long-term survival after TIPS placement. To establish a model to predict long-term survival in patients with hepatitis cirrhosis after TIPS. A retrospective analysis was conducted on a cohort of 224 patients who underwent TIPS implantation. Through univariate and multivariate Cox regression analyses, various factors were examined for their ability to predict survival at 6 years after TIPS. Consequently, a composite score was formulated, encompassing the indication, shunt reasonability, portal venous pressure gradient (PPG) after TIPS, percentage decrease in portal venous pressure (PVP), indocyanine green retention rate at 15 min (ICGR15) and total bilirubin (Tbil) level. Furthermore, the performance of the newly developed Cox (NDC) model was evaluated in an internal validation cohort and compared with that of a series of existing models. The indication (variceal bleeding or ascites), shunt reasonability (reasonable or unreasonable), ICGR15, postoperative PPG, percentage of PVP decrease and Tbil were found to be independent factors affecting long-term survival after TIPS placement. The NDC model incorporated these parameters and successfully identified patients at high risk, exhibiting a notably elevated mortality rate following the TIPS procedure, as observed in both the training and validation cohorts. Additionally, in terms of predicting the long-term survival rate, the performance of the NDC model was significantly better than that of the other four models [Child-Pugh, model for end-stage liver disease (MELD), MELD-sodium and the Freiburg index of post-TIPS survival]. The NDC model can accurately predict long-term survival after the TIPS procedure in patients with hepatitis cirrhosis, help identify high-risk patients and guide follow-up management after TIPS implantation.

Hepatic venous pressure gradient: Inaccurately estimates portal venous pressure gradient in alcoholic cirrhosis and portal hypertension.

Portal hypertension (PHT) in patients with alcoholic cirrhosis causes a range of clinical symptoms, including gastroesophageal varices and ascites. The hepatic venous pressure gradient (HVPG), which is easier to measure, has replaced the portal venous pressure gradient (PPG) as the gold standard for diagnosing PHT in clinical practice. Therefore, attention should be paid to the correlation between HVPG and PPG. To explore the correlation between HVPG and PPG in patients with alcoholic cirrhosis and PHT. Between January 2017 and June 2020, 134 patients with alcoholic cirrhosis and PHT who met the inclusion criteria underwent various pressure measurements during transjugular intrahepatic portosystemic shunt procedures. Correlations were assessed using Pearson's correlation coefficient to estimate the correlation coefficient (r) and determination coefficient (R2). Bland-Altman plots were constructed to further analyze the agreement between the measurements. Disagreements were analyzed using paired t tests, and P values < 0.05 were considered statistically significant. In this study, the correlation coefficient (r) and determination coefficient (R2) between HVPG and PPG were 0.201 and 0.040, respectively (P = 0.020). In the 108 patients with no collateral branch, the average wedged hepatic venous pressure was lower than the average portal venous pressure (30.65 ± 8.17 vs. 33.25 ± 6.60 mmHg, P = 0.002). Hepatic collaterals were identified in 26 cases with balloon occlusion hepatic venography (19.4%), while the average PPG was significantly higher than the average HVPG (25.94 ± 7.42 mmHg vs 9.86 ± 7.44 mmHg; P < 0.001). The differences between HVPG and PPG < 5 mmHg in the collateral vs no collateral branch groups were three cases (11.54%) and 44 cases (40.74%), respectively. In most patients, HVPG cannot accurately represent PPG. The formation of hepatic collaterals is a vital reason for the strong underestimation of HVPG.

Interventional treatment for portal vein complications utilizing a hybrid operating room after liver transplantation

BackgroundVascular complications after liver transplantation (LT) can be lethal and require immediate treatment to prevent graft failure. Nowadays, with interventional radiology (IR), approaches such as the percutaneous transhepatic (PTH) and transileocolic venous (TIC), have become major treatment options. We reviewed the safety and efficacy of a hybrid operating room (OR) for portal vein complications after LT. MethodsPatients who underwent IR for post-LT vascular complications in the hybrid OR from May 2014 to May 2022 were enrolled. Patients who underwent post-LT IR in conventional angiography rooms were excluded. ResultsNine patients developed portal vein complications; eight after living donor LT and one after deceased donor LT. Six patients had portal vein stenosis, two had portal vein thrombosis, and one had both. In the hybrid OR, PTH and TIC were used in five and three cases, respectively. The Rendezvous technique was used in one case. Angioplasty was performed in all patients. A stent was placed in four patients. The portal venous pressure gradient across the stenotic site significantly decreased after IR (P &= 0.031). The IR success rate in the hybrid OR was 100%. ConclusionThe hybrid OR enables us to accomplish IR for post-LT vascular complications safely and effectively.

S3168 Sinusoidal Obstruction Syndrome: A Known and Often Missed Complication of Oxaliplatin Therapy

Introduction: Sinusoidal obstruction syndrome (SOS) is caused by sinusoidal endothelial injury due to hematopoietic cell transplantation, liver irradiation or exposure to chemotherapy such as oxaliplatin and may occur days to weeks following exposure. SOS can be a life-threatening complication and its presentation may include jaundice, volume overload or hepatic failure. We present the case of a 32-year-old male with gastroesophageal adenocarcinoma who underwent oxaliplatin-based chemotherapy and developed SOS. Case Description/Methods: A 32-year-old male with no significant medical history presented with dysphagia and weight loss. Esophagogastroduodenoscopy showed a mass at the gastroesophageal junction. He underwent diagnostic laparoscopy which showed peritoneal metastasis. Tissue biopsy was consistent with stage 4 gastroesophageal junction adenocarcinoma. He was started on 5-fluorouracil (5-FU), oxaliplatin and nivolumab. The patient developed thrombocytopenia and moderate aminotransferase elevation after 6 cycles of chemotherapy. An abdominal ultrasound obtained after 10 of 12 cycles of chemotherapy showed portal hypertension. Subsequent abdominal imaging showed worsening ascites (serum ascites to albumin gradient > 1.1), anasarca and splenomegaly. Transjugular liver biopsy showed elevated portal hepatic venous pressure gradient, focal sinusoidal dilatation and centrizonal ischemic changes suggesting drug induced hepatopathy, and a diagnosis of oxaliplatin induced SOS was made. The patient was not a candidate for defibrotide and was treated conservatively. He continued to have worsening ascites with severe direct hyperbilirubinemia and moderately elevated aminotransferases without biliary obstruction (Figure). Discussion: Oxaliplatin-based chemotherapies are known to cause the potentially life-threatening complication of SOS which is oftentimes missed. Our patient developed signs and symptoms suggestive of SOS by cycle 10 of oxaliplatin therapy. These changes included thrombocytopenia, elevated liver associated enzymes, volume overload and portal hypertension. He went on to complete 12 cycles of oxaliplatin with eventual worsening of his portal hypertension related symptoms and worsening of his hepatic function. This case highlights the importance of having a high index of suspicion for the development of SOS with plans to pursue patient-centered discussions regarding alternative chemotherapeutic regimens, instituting prophylactic therapies and timely SOS screening protocols.Figure 1.: Timeline of events leading up to SOS diagnosis.

Correlation between hepatic venous pressure gradient and portal venous pressure gradient in hepatitis B cirrhosis with different hepatic veins anatomy

PurposeThe hepatic venous pressure gradient (HVPG) has been employed as the gold standard for indicating the portal venous pressure gradient (PPG) in the diagnosis of portal hypertension (PHT). However, little has been reported on whether the HVPG can accurately estimate the PPG in patients with hepatic vein collateral shunts. We aimed to explore the correlation between the HVPG and the PPG in hepatitis B cirrhosis patients with different hepatic vein anatomies. MethodsA total of 461 hepatitis B cirrhosis patients with portal hypertension (PHT) who were treated with a transjugular intrahepatic portosystemic shunt (TIPS) between January 2016 and June 2020 were included. All patients underwent various venous pressure measurements and balloon-occluded compression hepatic venography during the TIPS operation. Agreements were evaluated by Pearson’s correlation and the Bland–Altman method. Disagreements were assessed by paired t tests. ResultsThe correlation coefficient (r) values (P < 0.001) between the HVPG and the PPG of the early (151 patients, 32.8 %), middle (73 patients, 15.8 %), late (46 patients, 10.0 %), portal vein (151 patients, 32.8 %), and no lateral branch development groups (40 patients, 8.7 %) were 0.373, 0.487, 0.569, 0.690, and 0.575, respectively; the determination coefficient (R2) values were 0.139, 0.238, 0.323, 0.475, and 0.330, respectively. According to the Bland–Altman method, agreement was the greatest in the portal vein development group, with the 95 % limits of agreement (95 % LoA, mean differences ± 1.96 SD) being the smallest. The differences were statistically significant (P < 0.05). ConclusionThe correlation between the HVPG and the PPG is the worst in early lateral branch development, followed by middle development, and the influence of lateral branches becomes significantly reduced in late development. Hepatic venous collateral formation is a vital factor for underestimation of the HVPG, which is the most accurate predictor of PPG in patients with portal vein development. Patients with no collateral channel development in the hepatic vein have a higher HVPG than PPG, which is an important reason for overestimation of the HVPG.

Effects of plasma lipopolysaccharide changes on platelet release of vascular endothelial growth factor and thromobospondin-1 in patients with cirrhotic portal hypertension after TIPS procedure

Objective: To investigate the effects of plasma lipopolysaccharide (LPS) concentration changes on platelet release of vascular endothelial growth factor (VEGF) and thrombospondin (TSP)-1 in patients with decompensated cirrhotic portal hypertension after transjugular intrahepatic portosystemic shunt (TIPS) procedure. Methods: 169 cases with cirrhotic portal hypertension were enrolled, of which 81 cases received TIPS treatment. LPS, VEGF, and TSP-1 concentrations with different Child-Pugh class in peripheral blood plasma of patients were measured. After pre-incubation of normal human platelets with different concentrations of LPS and stimulated by collagen in vitro, platelet PAC-1 expression rate, VEGF, and TSP-1 concentrations were detected. PAC-1 expression rate and the concentrations of LPS, VEGF and TSP-1 in peripheral blood plasma of patients before and after TIPS procedure were detected. The relationship between plasma LPS, VEGF and TSP-1 concentrations and Child-Pugh score changes in patients after TIPS procedure was analyzed. Statistical analysis was performed by t-test, one-way ANOVA or Pearson's rho according to different data. Results: Plasma LPS and TSP-1 concentrations were significantly higher in Child-Pugh class C patients than class A and B, but the concentration of plasma VEGF was significantly lower than class A and B (P < 0.01). In vitro experiments showed that concentration of LPS, TSP-1, and platelet PAC-1 expression rate was higher in the supernatant, but the difference in the concentration of VEGF in the supernatant was not statistically significant. Portal vein pressure and platelet activation were significantly decreased (P < 0.01) in patients after TIPS procedure. Portal venous pressure, platelet activation, plasma LPS, and TSP-1 levels were significantly decreased continuously, while VEGF levels were significantly increased continuously after TIPS procedure. Plasma LPS concentration was positively correlated with TSP-1 concentration (r = 0.506, P < 0.001), and negatively correlated with VEGF concentration (r = -0.167, P = 0.010). Child-Pugh score change range was negatively correlated with change range of plasma VEGF concentration (r = -0.297, P = 0.016), and positively correlated with change range of plasma TSP-1 concentration (r = 0.145, P = 0.031) after TIPS. Conclusion: Portal venous pressure gradient, plasma LPS concentration and corresponding platelet activation was decreased in cirrhotic portal hypertension after TIPS procedure, and with TSP-1 reduction and VEGF elevation it is possible to reduce the liver function injury caused by portal venous shunt.

The Etiology of Portal Hypertension in Egyptian Children and Adolescents

Abstract Background Portal hypertension is a clinical syndrome in which the portal venous pressure gradient between portal vein and inferior vena cava exceeding 5mmHg. Clinically significant portal hypertension is diagnosed when clinical manifestations of the disease appear or the portal pressure gradient exceeding 10 mmHg. For better management, it is important to determine the underlying cause. Objective To evaluate the aetiology of portal hypertension in pediatric who attending the hepatology clinic at El-Demerdash hospital, Ain Shams University. Materials and Methods This cross sectional study was done in the department of pediatric hepatology clinic at El-Demerdash hospital, Ain Shams University on 91 consecutive cases of portal hypertension enrolled from 2016 to 2019. All pediatric patients were subjected to full history, clinical examination, investigations and questionnaire about effect of portal hypertension and its complications on QOL. Results Age of children and adolescent was 5 months to 16 years with mean age of 5.55±4.30y and male to female ration was 1.5:1. Out of 91 children (51, 56.1%) developed portal hypertension due to extrahepatic causes and (39, 42.9%) due to hepatic causes. In extrahepatic causes (portal vein thrombosis was found 36, (39.6%) and Budd Chiari syndrome 15(16.5%)). On the other hand, hepatic causes (cong. hepatic fibrosis (CHF) was found in 21(23.1%), cases, hepatic cirrhosis 12(13.2%), extrahepatic biliary atresia 3(3.3%) and autoimmune hepatitis with secondary hepatic fibrosis 3(3.3%)). In extrahepatic cases first variant bleed much earlier than hepatic cases. Conclusion Extrahepatic disease were the most common aetiology of portal hypertension in studied cases. Portal vein thrombosis in extrahepatic cases and congenital hepatic fibrosis in intrahepatic cases were the most common causes.

Somatostatin Therapy Improves Stellate Cell Activation and Early Fibrogenesis in a Preclinical Model of Extended Major Hepatectomy

Background: Liver resection is effective treatment for primary and secondary liver tumors, though clinical applicability is limited by remnant liver mass and quality. Aims: Perform major hepatic resections in pigs to define changes associated with sufficient and insufficient remnants and improve liver-specific outcomes through continuous somatostatin infusion. Methods: Three experimental groups were performed: 75% hepatectomy (75H), 90% hepatectomy (90H), and 90% hepatectomy with somatostatin (90H+SST). In each group, animals were followed for 24 hours (N=6) and 5 days (N=6). Results: After hepatectomy, portal venous pressure gradient was higher in 90H versus 75H and 90H+SST (8[3-13] mmHg vs. 4[2-6] mmHg and 4[2-6] mmHg, respectively, P <0.001). After 24 hours, changes were observed in 90H associated with stellate cell activation and collapse of sinusoidal lumen (area 23.5±3.6% 90H vs. 31.1±3.5% 75H, P <0.001, and 30.9±4.3% 90H+SST, P=0.008). Collagen chain type 1 alpha 1 mRNA expression was higher, extracellular matrix width less, and percentage of collagen-staining areas greater at 24 hours in 90H versus 75H and 90H+SST.After 5 days, remnant liver mass was higher in 75H and 90H+SST versus 90H (469±33 g and 463±79 g vs. 313±107, respectively, P=0.003), and Ki-67 immunostaining was higher in 90H+SST versus 75H and 90H (10±7 high-power field-1 vs. 2±2 high-power field-1 and 5±6 high-power field-1, respectively, P<0.001). More TUNEL-staining cells were observed in 90H versus 75H and 90H+SST at 5 days. Conclusions: Perioperative somatostatin modified portal pressure, injury, apoptosis, and hepatic stellate cell activation, stemming early changes related to hepatic fibrogenesis seen in liver remnants not receiving treatment. Funding: Research was supported by FIS Grant 15/01092 from the Instituto de Salud Carlos III, Ministerio de Ciencia e Innovacion, Spain. Amelia J. Hessheimer was supported by the “Ajut Josep Font” from the Hospital Clinic Barcelona. Lilia Martinez de la Maza was supported by the Fundacio Catalana de Trasplantament. Declaration of Interest: Amelia J. Hessheimer and Constantino Fondevila have received research funding and consultancy fees from Guanguong Shunde Innovative Design Institute, Guangdong, China. The remainder of the authors have nothing to declare. Ethical Approval: The University of Barcelona Animal Experimentation Unit is authorized by the Catalan Department of Agriculture, Husbandry, and Fisheries (authorization number B9900020), registered in the General Registry of Livestock Facilities (ES080190036536), and accredited by the International Standards Organization (ISO 9001:2015). Animals were cared for according to the guidelines of the Catalan Department of the Environment Commission on Animal Experimentation and University of Barcelona Committee on Ethics in Animal Experimentation, which approved the study protocol.

Increase of Portal Vein Pressure Gradient After Hepatectomy Predicts Post-operative Liver Dysfunction.

Background. Post-hepatectomy liver failure (PHLF) is an important cause of mortality and morbidity. Whether Child-Pugh A patients with varying degrees of cirrhosis are good candidates for hepatectomy is disputed. The purpose of this study was to analyze the impact of portal venous pressure gradient (PVPG) variation during surgery on PHLF. Methods. PVPG, the pressure gradient between the portal vein and central vein, was measured in consecutive patients before and after liver resection. The optimal cutoff of PVPG to predict PHLF was determined by receiver operating characteristic curve analysis. Risk factors for PHLF were subjected to univariate and multivariable analysis. Results. Sixty Child-Pugh A patients were recruited. The mean PVPG was increased from 5.17 ± 4.78mm of mercury (mmHg) to 6.37 ± 4.44mmHg after liver resection. The optimal cutoff value of PVPG increments to predict PHLF was 1.5mmHg. Multivariable analysis showed prothrombin time (PT), post-hepatectomy PVPG increments of 1.5mmHg or greater, and resected liver segments of 3 or more to be independent predictors of PHLF. Conclusions. Acute PVPG increase after hepatectomy is associated with a higher risk of PHLF in Child-Pugh A patients.

Portal hypertension among Egyptian children and adolescents (single center study).

Portal hypertension is a clinical syndrome in which the portal venous pressure gradient between the portal vein and inferior vena cava exceeding 5 mmHg. Clinically significant portal hypertension is diagnosed when clinical manifestations of the disease appear or the portal pressure gradient exceeding 10 mmHg. For better management, it is important to determine the underlying cause. This study aimed to evaluate the aetiology, presentation and quality of life in pediatric portal hypertension patients. This cross-sectional study was done on ninety-one consecutive cases of portal hypertension enrolled from 2016 to 2019. Demographic data, etiology, clinical presentation, endoscopic interventions, and quality of life were all assessed. The mean age of participants was 5.55 ± 4.30 years with a male to female ratio of 1.5:1. Out of 91 children, 56.1% developed portal hypertension due to extrahepatic causes and 42.9% due to hepatic causes. In extrahepatic causes portal vein obstruction was the most common aetiology representing 39.6% Splenomegaly was the commonest presentation of PHT and esophageal varices were the commonest complication. QoL scores, total and individual domains, were lower in all our PHT children. Conclusion: Extra hepatic portal vein obstruction was the most common etiology of portal hypertension in studied cases. Poor QOL was reported in all patients irrespective of the etiology of portal hypertension.

Therapeutic effect of portal vein stenting for portal vein stenosis after upper-abdominal surgery

BackgroundThe therapeutic effect of portal vein (PV) stenting for PV stenosis following nontransplant hepato-pancreato-biliary (HPB) surgery has not been fully investigated. MethodsChanges in portal venous pressure (PVP) gradient before and after stenting, complications, symptomatic improvement, and stent patency were evaluated. ResultsWe 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. ConclusionsBased on durable effect on patency, we deemed PV stenting for PV stenosis after HPB surgery to be safe and beneficial for improving symptoms.

Pathophysiological role of prostanoids in coagulation of the portal venous system in liver cirrhosis.

BackgroundProstanoids are important regulators of platelet aggregation and thrombotic arterial diseases. Their involvement in the development of portal vein thrombosis, frequent in decompensated liver cirrhosis, is still not investigated.MethodsTherefore, we used pro-thrombotic venous milieu generation by bare metal stent transjugular intrahepatic portosystemic shunt insertion, to study the role of prostanoids in decompensated liver cirrhosis. Here, 89 patients receiving transjugular intrahepatic portosystemic shunt insertion were included in the study, and baseline levels of thromboxane B2, prostaglandin D2 and prostaglandin E2 were measured in the portal and the hepatic vein.ResultsWhile the hepatic vein contained higher levels of thromboxane B2 than the portal vein, levels of prostaglandin E2 and D2 were higher in the portal vein (all P<0.0001). Baseline concentrations of thromboxane B2 in the portal vein were independently associated with an increase of portal hepatic venous pressure gradient during short term follow-up, as an indirect sign of thrombogenic potential (multivariable P = 0.004). Moreover, severity of liver disease was inversely correlated with portal as well as hepatic vein levels of prostaglandin D2 and E2 (all P<0.0001).ConclusionsElevated portal venous thromboxane B2 concentrations are possibly associated with the extent of thrombogenic potential in patients with decompensated liver cirrhosis.Trial registrationClinicalTrials.gov identifier: NCT03584204.

Efficacy of transjugular intrahepatic portosystemic shunt in treatment of sinusoidal obstruction syndrome caused by gynura segetum

Objective To evaluate the safety and efficacy of transjugular intrahepatic portosystemic shunt (TIPS) in the treatment of sinusoidal obstruction syndrome (SOS) caused by gynura segetum. Methods The clinical data of 9 patients with SOS caused by gynura segetum (5 males and 4 females) who underwent TIPS were retrospectively analyzed from February 2017 to June 2018. The Child-Pugh scores were (9.5±1.3) and the MELD scores were (12.5±5.0). The success rates, complications and follow-up results were evaluated. Results TIPS was performed successfully in all the 9 patients. The portal venous pressure gradient dropped from (22.4±2.7) mmHg to (10.4±3.2) mmHg (P<0.05). There was no complication such as abdominal hemorrhage and biliary peritonitis. Nine patients were followed-up for 1~17months, mean 7.8±6.0 months. One month after treatment, the Child-Pugh scores were (7.1±1.8), compared with that of the preoperative scores, the difference was statistically significant (P<0.05). The MELD scores were (5.3±4.6), compared with that of the preoperative scores, the difference was also statistically significant (P<0.05). At the end point of the follow-up, color Doppler ultrasound and portal CTA showed that the TIPS shunt was patent and hepatic congestion was relieved in all the 9 patients. All patients were alive. Conclusion TIPS was a safe and efficacious treatment for SOS caused by gynura segetum. Key words: Portasystemic shunt, transjugular intrahepatic; Gynura segetum; Sinusoidal obstruction syndrome

Hepatic venous pressure gradient after portal vein embolization: An accurate predictor of future liver remnant hypertrophy

BackgroundThe impact of portal hemodynamic variations after portal vein embolization on liver regeneration remains unknown. We studied the correlation between the parameters of hepatic venous pressure measured before and after portal vein embolization and future hypertrophy of the liver remnant after portal vein embolization. MethodsBetween 2014 and 2017, we reviewed patients who were eligible for major hepatectomy and who had portal vein embolization. Patients had undergone simultaneous measurement of portal venous pressure and hepatic venous pressure gradient before and after portal vein embolization by direct puncture of portal vein and inferior vena cava. We assessed these parameters to predict future liver remnant hypertrophy. ResultsTwenty-six patients were included. After portal vein embolization, median portal venous pressure (range) increased from 15 (9–24) to 19 (10–27) mm Hg and hepatic venous pressure gradient increased from 5 (0–12) to 8 (0–14) mm Hg. Median future liver remnant volume (range) was 513 (299–933) mL before portal vein embolization versus 724 (499–1279) mL 3 weeks after portal vein embolization, representing a 35% (7.4–83.6) median hypertrophy. Post–portal vein embolization hepatic venous pressure gradient was the most accurate parameter to predict failure of future liver remnant to reach a 30% hypertrophy (c-statistic: 0.882 [95% CI: 0.727–1.000], P < 0.001). A cut-off value of post–portal vein embolization hepatic venous pressure gradient of 8 mm Hg showed a sensitivity of 91% (95% CI: 57%–99%), specificity of 80% (95% CI: 52%–96%), positive predictive value of 77% (95% CI: 46%–95%) and negative predictive value of 92.3% (95% CI: 64.0%–99.8%). On multivariate analysis, post–portal vein embolization hepatic venous pressure gradient and previous chemotherapy were identified as predictors of impaired future liver remnant hypertrophy. ConclusionPost–portal vein embolization hepatic venous pressure gradient is a simple and reproducible tool which accurately predicts future liver remnant hypertrophy after portal vein embolization and allows early detection of patients who may benefit from more aggressive procedures inducing future liver remnant hypertrophy. (Surgery 2018;143:1-2.)

A High Portal Venous Pressure Gradient Increases Gut-Related Bacteremia and Consequent Early Mortality After Living Donor Liver Transplantation.

Portal hypertension (PHT) is defined as a portal venous pressure gradient (PVPG) exceeding 5 mm Hg, which results in severe clinical manifestations. However, the validity of intraoperative PVPG monitoring and the association between PHT and bacterial translocation after liver transplantation remain unclear. In this retrospective study, 223 patients who underwent primary adult-to-adult living donor liver transplantation from 2008 to 2015 were divided into 2 groups based on the PVPG at the end of the operation: high PVPG (>5 mm Hg, n = 69) and low PVPG (≤5 mm Hg, n = 154). The clinical factors were compared between the groups, and the association between a high PVPG and posttransplant bacteremia/bacterial infections was investigated. The high PVPG group had a significantly higher incidence of bacteremia (46% vs 24%, P < 0.001), higher 90-day mortality rate (20% vs 7%, P = 0.002), and poorer 1-year survival (71% vs 86%, P = 0.006). The high PVPG group had a particularly higher incidence of bacteremia caused by "gut bacteria" including Enterobacteriaceae, Bacteroides spp., and Enterococcus spp. (29% vs 12%, P = 0.003). Multivariate analysis showed that a PVPG greater than 5 mm Hg (odds ratio, 2.55; 95% confidence interval, 1.18-5.55; P = 0.017) was an independent predictor of bacteremia due to gut bacteria. Monitoring of the PVPG is clinically meaningful for predicting patients' prognosis. In particular, a high PVPG with a threshold of 5 mm Hg at the end of adult-to-adult living donor liver transplantation may increase gut-related bacteremia through the mechanism of bacterial translocation, resulting in early mortality.

APTR is a prognostic marker in cirrhotic patients with portal hypertension during TIPS procedure

Portal hypertension is a major cause of mortality and morbidity in cirrhotic patients. In this study, we aimed to analyze the clinical characteristics of Alu-mediated p21 transcriptional regulator (APTR) during transjugular intrahepatic portosystemic shunt (TIPS) procedure. Portal and hepatic venous blood was drawn from 84 patients with liver cirrhosis and portal hypertension before and after TIPS treatment. Then, we detected biochemical, hemodynamic parameters and APTR expression before and after TIPS treatment. Indeed, TIPS treatment could markedly ameliorate the serum blood urea nitrogen (BUN) level and portal vein hemodynamics in cirrhotic patients. We found that portal venous levels of APTR was significantly decreased after TIPS treatment and its aberrant expression levels were positively correlated with Model for End Stage Liver Disease (MELD), portal hepatic venous pressure gradient (PHPG) in patients. Higher APTR expression in portal vein was associated with poor prognosis. APTR level in portal vein was an independent predictors of mortality. Our data indicated that APTR may serve as a novel biomarker for cirrhotic patients with portal hypertension before and after receiving TIPS.

Is Portal Venous Pressure or Porto-systemic Gradient Really A Harbinger of Poor Outcomes After Living Donor Liver Transplantation?

Portal hyperperfusion as a cause of small for size syndrome (SFSS) after living donor liver transplantation (LDLT) remains controversial. Portal venous pressure (PVP) is often measured indirectly and may be confounded by central venous pressure (CVP). In 42 adult cirrhotics undergoing elective LDLT, PVP was measured by direct canulation of portal vein and porto systemic gradient (PSG) was obtained after subtracting CVP from PVP. None underwent portal inflow modulation. SFSS was looked in 27 patients after excluding 15 with technical complications. Clinical features of SFSS found in 6 patients, 5 with graft recipient weight ratio (GRWR)>0.8% and PVP<20mm of Hg. One with GRWR<0.8% could truly be labeled as SFSS. Incidence of SFSS was not higher in patients with elevated PVP>20mm of Hg (14.3% vs 0%, P=0.259) or PSG>13mm of Hg (33.3% vs 0%, P=0.111). Intensive care unit (ICU) stay was longer in patients with elevated PVP (14.55 vs 9.13 days, P=0.007) and PSG (16.8 vs 9.72 days, P=0.009). There was no difference in graft functions, post-operative complications and mortality in first month post-LDLT. Elevated PVP or PSG increased morbidity but neither predicted SFSS nor affected survival.

Non Cirrhotic Portal Fibrosis - Current concepts

Non cirrhotic portal fibrosis (NCPF) is characterized by perivenular fibrosis of the small and medium branches of the portal vein resulting in portal hypertension (PHT) while the liver structure and function remain normal. This results in an increased portal venous pressure gradient in the absence of a known cause of liver disease. It has been commonly described from India and Japan, and is being increasingly recognised in the West. The etiology of NCPF in unclear but postulated to be chronic infections, exposure to medication or toxins, thrombophilia, immunological disorders or genetic disorders. Multifactorial etiology can also be encountered. The majority of patients present with signs or complications of (PHT), mainly well controlled episodes of variceal bleeding and splenomegaly. They usually have preserved liver function. Patients can be misdiagnosed as having liver cirrhosis, but awareness of this condition (presence of portal hypertension with disproportionately large splenomegaly but preserved liver functions) along with a diligent search to rule out other causes of non cirrhotic PHT, can identify this subset of patients who have a better prognosis than cirrhotic patients with similar symptoms. The recommendations for prophylaxis and treatment of variceal bleeding are similar to cirrhotic patients. While endotherapy can successfully manage most of the varieal bleeding episodes, surgical portocaval shunts are indicated in patients with failure of endotherapy, bleeding from sites not amenable to endotherapy and symptomatic splenomegaly. Since NCPF is a benign disorder with overall good prognosis except for need for frequent endoscopic surveillance and therapy, there is deep interest in role of prophylactic surgery to prevent the first bleeding episode all together and to offer a onetime permanent solution to patients who have recovered from a bleeding episode. But shunt surgery is not entirely innocuous and technically demanding, so the debate continues.

Usefulness of Intraoperative Measurement of Portal Venous Pressure for Confirming the Most Appropriate Hepatectomy in Patients with Borderline Hepatic Functional Reserve

Background We investigated whether portal venous pressure (PVP) measured immediately before surgery and then immediately after clamping of the Glissonian pedicle can be used to predict postoperative complications (ascites or jaundice) and thus select the extent of resection in patients with liver disease requiring hepatectomy. Methods Thirty-seven patients with hepatic functional reserve near the advisable limit and in whom direct measurement of PVP was done just before surgery and after clamping of the Glissonian pedicle were divided into two groups, an Event group (n = 9) and a Non-event group (n = 28), according to whether postoperative complications developed. The relation between PVP and the complication rate was analyzed, and a PVP safety margin was dent 昀ed. Results PVP obtained after the Glissonian pedicle was clamped was s gn 昀cantl higher in the Event group than in the Non-event group (18.8 vs. 15.7 cmH2O; p = 0.03). The PVP gradient de 昀ned as PVP after Glisso‐ nian clamping – PVP before surgery) tended to be greater in the Event group (5.1 versus 3.6 cmH2O; p = 0.13). PVP after Glissonian clamping plotted against the PVP gradient revealed safety margins of PVP gradient < 5 cmH2O and PVP < 20 cmH2O, respectively. Conclusion PVP after Glissonian clamping and the PVP gradient may be useful for predicting post-hepatec‐ tomy complications.

Hagen-Poiseuille's law: The link between cirrhosis, liver stiffness, portal hypertension and hepatic decompensation.

The onset of hepatic decompensation in cirrhosis heralds an accelerated downhill course with poor outcome. The sole predictor of this decompensation in cirrhosis is increased hepatic vein to portal vein gradient hepatic venous pressure gradient (HVPG). Surrogate markers of liver function or hepatic reserve appear to be less relevant. The hepatic sinusoids become less elastic and more rigid as liver fibrosis and cirrhosis progress. We propose that the Hagen-Poiseuille's law, which applies to rigid, but not elastic vessels, determines the pressure-flow characteristics in the sinusoids. In the rigid cirrhotic liver, HVPG rises dramatically with any change in net surface area or radius, r(4) of the vasculature that follows surgical resection. This review relates liver stiffness to the risk of decompensation in patients with cirrhosis. The liver has a unique dual blood supply comprising a low pressure portal vein and high pressure hepatic artery. We compare the complexity of autoregulation in the normal elastic liver with that in the rigid cirrhotic liver. Therapeutic modalities to reduce portal pressure may reduce the risk of hepatic decompensation and improve outcomes in cirrhosis.