TY - JOUR
T1 - Graft inflow modulation in recipients with portal hypertension
AU - Cassese, Gianluca
AU - Montalti, Roberto
AU - Giglio, Mariano Cesare
AU - Rompianesi, Gianluca
AU - Troisi, Roberto Ivan
N1 - Publisher Copyright:
© Italian Society of Surgery (SIC) 2024.
PY - 2024
Y1 - 2024
N2 - The extended application of living donor liver transplantation (LDLT) has revealed the problem of graft size mismatching, potentially leading to the “small-for-size syndrome” (SFSS). SFSS is a rare dysfunction that may affect a partial liver graft, characterized by coagulopathy, cholestasis, ascites, and encephalopathy. A key role in the physiopathology of SFSS is played by portal hypertension (PHT) to which a small allograft is submitted after reperfusion, resulting in sinusoidal congestion and hemorrhage. Portal overflow injures the liver directly through nutrient excess, endothelial activation, and sinusoidal shear stress, and indirectly through arterial vasoconstriction. Thus, SFSS prevention relies not only on increasing graft volume (implementing the use of larger grafts or auxiliary/dual liver transplantation), but also on the control of the increased portal vein pressure (PVP) and portal vein flow (PVF). To this aim, surgical graft inflow modulation techniques (GIM) such as splenic artery ligation (SAL), splenectomy and hemiportocaval shunts, can be considered when an imbalance between the PVP and the hepatic arterial flow (HAF) is acknowledged. However, such strategies have their pros and cons, and a deep knowledge of the indications and complications is needed. Furthermore, pharmacological modulation has also been proposed. This review is aimed to update available literature on the current knowledge and strategies for modulating portal vein flow in LDLT.
AB - The extended application of living donor liver transplantation (LDLT) has revealed the problem of graft size mismatching, potentially leading to the “small-for-size syndrome” (SFSS). SFSS is a rare dysfunction that may affect a partial liver graft, characterized by coagulopathy, cholestasis, ascites, and encephalopathy. A key role in the physiopathology of SFSS is played by portal hypertension (PHT) to which a small allograft is submitted after reperfusion, resulting in sinusoidal congestion and hemorrhage. Portal overflow injures the liver directly through nutrient excess, endothelial activation, and sinusoidal shear stress, and indirectly through arterial vasoconstriction. Thus, SFSS prevention relies not only on increasing graft volume (implementing the use of larger grafts or auxiliary/dual liver transplantation), but also on the control of the increased portal vein pressure (PVP) and portal vein flow (PVF). To this aim, surgical graft inflow modulation techniques (GIM) such as splenic artery ligation (SAL), splenectomy and hemiportocaval shunts, can be considered when an imbalance between the PVP and the hepatic arterial flow (HAF) is acknowledged. However, such strategies have their pros and cons, and a deep knowledge of the indications and complications is needed. Furthermore, pharmacological modulation has also been proposed. This review is aimed to update available literature on the current knowledge and strategies for modulating portal vein flow in LDLT.
KW - Graft inflow modulation
KW - Living donor liver transplantation
KW - Portal hypertension
KW - Small-for-size syndrome
UR - http://www.scopus.com/inward/record.url?scp=85212201269&partnerID=8YFLogxK
U2 - 10.1007/s13304-024-02048-2
DO - 10.1007/s13304-024-02048-2
M3 - Review article
SN - 2038-131X
JO - Updates in Surgery
JF - Updates in Surgery
ER -