Low-Pressure Tactic: A Novel Intrahepatic Shunt Improves Outcomes in Experimental Small-for-Size Syndrome

Excerpt

Due to the rapidly growing demand for organ donations, the global severe donor shortage remains a major impediment to liver transplantation. To address this imbalance, living donor liver transplantation has been instituted as an alternative to deceased donor transplantation. Although living donors increase the number of available organs, small-for-size syndrome (SFSS) is a key adverse event that occurs after liver transplantation with small-size grafts, especially for partial liver grafts from living donors. SFSS, defined as dysfunction of a smaller liver graft within 1–2 weeks post-transplantation in the absence of other identifiable causes, is characterized by evidence of hepatic decompensation such as ascites, coagulopathy, cholestasis, and hepatic encephalopathy [1]. SFSS is considered when graft volume/standard liver volume is < 40–50% or the graft/recipient weight ratio (GRWR) is < 0.8–1.0% [2, 3]. Although many factors contribute to the SFSS including donor and recipient status, the primary mechanism is considered to be excessive portal vein flow to the small graft. Portal venous hyperperfusion triggers sinusoidal shear stress, endothelial activation, and nutrient excess that are all thought to directly damage hepatocytes, [4, 5] and to induce arterial vasoconstriction, sinusoidal congestion, and hemorrhage [6]. …