Small-for-size syndrome in adult liver transplantation: A review

Abstract

Small-for-size syndrome remains the greatest limiting factor for the expansion of liver transplantation (apart from cadaveric organ donation) and has been the major cause of worse short-term prognoses after LDLT. The size of the graft, ( GRWR < 0.8 or graft to SLV ratio <30–40%, portal hyperperfusion, obstructed hepatic venous drainage, MELD score, and graft steatosis may be responsible for the pathogenesis of SFSS. Sinusoidal shear stress may be the principal common pathway in the pathogenesis. Living donor grafts with portal pressure more than 20 mmHg or portal flow exceeding 250 mL/min per 100 g have a higher risk of graft failure. The role of decrease arterial flow in response to portal hyperflow remains to be elucidated. Acute portal hypertension and increased shear stress caused by a partial hepatectomy triggers the regeneration of the remaining liver, though liver dysfunction is seen to be due to sudden portal hypertension, microcirculatory ischemia, reduced oxygen delivery, and hepatocellular dysfunction. The differences in sinusoidal pressure, or differences in the hepatotropic substances delivered to the graft or the liver remnant may be the difference between grafts that survive and grafts that don't. We need to find the threshold level of hyperperfusion that does more harm than good.