To assess the role of portal hemodynamics in the development of postshunt encephalopathy, we studied 19 patients after small-diameter portacaval H grafting (SD-PCHG). We used contrast studies as well as technetium-labeled macroaggregated albumin injected into the portal vein to assess direction of portal flow. We then quantitated the mesenteric fraction of flow perfusing the liver by injecting macroaggregated albumin into a peripheral mesenteric vein tributary. We found that none of seven patients with prograde flow by both scintigraphy and angiography developed postoperative encephalopathy, but the incidence was 58% in the remaining patients (p = 0.02). The fraction of mesenteric flow perfusing the liver after SD-PCHG was 12% +/- 4%, but this did not significantly correlate with encephalopathy rates. We conclude that after SD-PCHG, prograde portal flow minimizes encephalopathy rates. Although encephalopathy occurs in patients with predominantly reversed flow, a subgroup of patients with reversed flow remain without symptoms. The absolute fraction of mesenteric flow perfusing the liver has less influence on encephalopathy rates than has direction of portal flow. This study identifies a complex relationship between portal hemodynamics and encephalopathy.
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Clin Transplant
February 2025
Department of Transplant Surgery, University of California, California, San Francisco, USA.
Background: Multiple intraoperative hemodynamic parameters are associated with an increased risk of early allograft dysfunction (EAD) following living donor liver transplantation (LDLT); however, there is significant center-to-center variability in terms of which parameters are used. We sought to determine which intraoperative hemodynamic parameters are most predictive of EAD following LDLT.
Methods: This is a systematic review following PRISMA guidelines (PROSPERO ID: CRD42023409711).
J Biomech
January 2025
School of Mechanical Engineering, Hefei University of Technology, Hefei, Anhui 230009, PR China. Electronic address:
Hemodynamic processes from the portal vein(PV) to the inferior vena cava(IVC) were mimicked for three patients with portal hypertension(PH) and the effects of stent parameters on the outcomes of transjugular intrahepatic portosystemic shunt(TIPS) were investigated through computational fluid dynamics(CFD). The liver region was simulated with porous media model and the spatial distributions of superior mesenteric vein(SMV) and splenic vein(SV) blood were solved through the Eulerian multiphase model. The present method is able to simulate the PH flow and predict the PV pressure, the stent shunt rate and the SMV blood proportion after TIPS treatment.
View Article and Find Full Text PDFActa Radiol
January 2025
Department of Radiology, Chonnam National University Medical School, Gwangju, Republic of Korea.
Background: Non-invasive approach other than conventional endoscopy could be effectively used for screening and monitoring esophageal variceal bleeding (EVB).
Purpose: To retrospectively investigate the role of four-dimensional (4D) flow magnetic resonance imaging (MRI) as an add-on tool to endoscopy for predicting EVB in cirrhotic patients with esophageal varices (EVs).
Material And Methods: A cohort of 109 cirrhotic patients with EVs was divided into four groups: A = negative red color [RC] sign, no EVB, n = 60; B = negative RC sign, EVB, n = 13; C = positive RC sign, no EVB, n = 10; and D = positive RC sign, EVB, n = 26.
Life (Basel)
January 2025
Department of Radiology, University Medical Center Regensburg, 93053 Regensburg, Germany.
Background: Portal vein thrombosis (PVT) leads to portal hypertension (PH) with its sequelae. Computed tomography spleno-mesenterico-portography (CT-SMPG) combines sequential CT spleno-portography and CT mesenterico-portography. CT-SMPG comprehensively illustrates the venous hemodynamic changes due to PH.
View Article and Find Full Text PDFMedicina (Kaunas)
December 2024
Clinic for Gastroenterology and Hepatology, University Clinical Centre of Serbia, 11 000 Belgrade, Serbia.
Cirrhotic cardiomyopathy (CCM) is a diagnostic entity defined as cardiac dysfunction (diastolic and/or systolic) in patients with liver cirrhosis, in the absence of overt cardiac disorder. Pathogenically, CCM stems from a combination of systemic and local hepatic factors that, through hemodynamic and neurohormonal changes, affect the balance of cardiac function and lead to its remodeling. Vascular changes in cirrhosis, mostly driven by portal hypertension, splanchnic vasodilatation, and increased cardiac output alongside maladaptively upregulated feedback systems, lead to fluid accumulation, venostasis, and cardiac dysfunction.
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