Abstract: Small-for-size grafts and small-for-size syndrome remain the greatest limiting factor for the expansion of living donor liver transplantation. Graft to recipient weight ratio less than 0.8% or the ratio of graft volume to standard liver volume of the recipient less than 40% is termed as small-for-size graft. A partial liver graft unable to meet the functional demands of the recipient results in liver failure characterized by development of coagulopathy, ascites, prolonged cholestasis and encephalopathy, often associated with pulmonary and renal failure, and frequently leads to death of the recipient in the absence of re-transplantation. This ill-defined clinical picture is termed “small-for-size syndrome”. The pathogenesis of small-for-size syndrome is related to graft size, underlying liver disease, regenerative response, vascular inflow and outflow, and recipient’s health status. Portal hypertension, venous pathology, and the arterial buffer response importantly contribute to early and late clinical and histopathologic manifestations of the small-for-size syndrome. The strategies to prevent and treat small-for-size syndrome include using larger graft and modulation of portal pressure and portal inflow. Modulation of portal inflow seems to be the key for successful adult living donor liver transplantation with smaller grafts.

Key words: liver transplantation, living donors, small-for-size graft, small-for-size syndrome