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Electrical Analog Models to Simulate the Impact of Partial Hepatectomy on Hepatic Hemodynamics

[+] Author Affiliations
Charlotte Debbaut, David De Wilde, Manuel Dierick, Luc Van Hoorebeke, Patrick Segers

Ghent University, Gent, Belgium

Christophe Casteleyn

University of Antwerp, Wilrijk, Belgium

Pieter Cornillie

Ghent University, Merelbeke, Belgium

Diethard Monbaliu

University Hospitals Leuven, Leuven, Belgium

Ye-Dong Fan

Military Hospital Queen Astrid, Brussel, Belgium

Paper No. SBC2013-14266, pp. V01AT19A004; 2 pages
doi:10.1115/SBC2013-14266
From:
  • ASME 2013 Summer Bioengineering Conference
  • Volume 1A: Abdominal Aortic Aneurysms; Active and Reactive Soft Matter; Atherosclerosis; BioFluid Mechanics; Education; Biotransport Phenomena; Bone, Joint and Spine Mechanics; Brain Injury; Cardiac Mechanics; Cardiovascular Devices, Fluids and Imaging; Cartilage and Disc Mechanics; Cell and Tissue Engineering; Cerebral Aneurysms; Computational Biofluid Dynamics; Device Design, Human Dynamics, and Rehabilitation; Drug Delivery and Disease Treatment; Engineered Cellular Environments
  • Sunriver, Oregon, USA, June 26–29, 2013
  • Conference Sponsors: Bioengineering Division
  • ISBN: 978-0-7918-5560-7
  • Copyright © 2013 by ASME

abstract

Due to the growing shortage of donor livers, more patients are waiting for liver transplantation. Efforts to expand the donor pool include the use of living donor liver transplantation (LDLT) and split liver transplantation. LDLT involves a healthy person undergoing a partial hepatectomy to donate a part of his liver to a patient with severe liver failure. Afterwards, the regenerative capacity of the organ allows the livers of both donor and recipient to regrow to normal liver masses. The procedure is not without risk as serious complications may occur (such as cholestasis, ascites, gastrointestinal bleeding and renal impairment). An inadequate liver mass compared to the body mass may result in the small-for-size syndrome (SFSS). In both donor and recipient, LDLT may lead to portal hypertension associated with the elevated intrahepatic resistance of a smaller liver, and an increased portal venous (PV) inflow per gram of liver tissue compared to the total liver before resection. Excessive hyperperfusion and shear stress may damage the sinusoidal endothelial cells and lead to graft dysfunction.

Copyright © 2013 by ASME
Topics: Hemodynamics , Liver

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