Has "Small-for-Size" Reached Its "Sell-By" Date.

Abstract

We read with interest the article by Pomposelli et al,1 presenting the Adult to Adult Living Donor Liver Transplant Cohort (A2ALL) data on early allograft dysfunction (EAD) after adult living donor liver transplantation (LDLT). The article reinforces the knowledge that EAD after LDLT is multifactorial. We support their suggestion that it is necessary to take another look at the current practice of attributing all EAD after adult LDLT to “small for size” syndrome (SFSS), apart from that caused by technical, infectious, or immunological complications. SFSS is a syndrome characterized by hepatocyte injury related to portal hyperperfusion.2 The current definitions of SFSS are based on the presence of cholestasis, coagulopathy, encephalopathy, and ascites.3 These are nonspecific consequences of allograft dysfunction and therefore include patients with causes for allograft dysfunction unrelated to portal hyperperfusion, such as high Model for End Stage Liver Disease score, increased donor age, graft steatosis, and prolonged warm ischemia times1—all well known to be associated with EAD after deceased donor liver transplantation. Nor should portal hyperperfusion caused by inadequate anterior sector outflow in a right lobe graft be included as part of SFSS, particularly when it occurs due to thrombosis of a v5/v8 vascular graft, the latter being a technical complication. The best possible hepatic venous outflow to the graft must be ensured before making a diagnosis of portal hyperperfusion. The phenomenon of portal steal is increasingly recognized as another potential cause for EAD after LDLT, indistinguishable by the current definitions.4 The fact that EAD indistinguishable from SFSS is recognized across all sizes of liver grafts is yet another reason to take another look at the term “small for size.”4 We propose therefore that the term SFSS be replaced by the term “portal hyperperfusion syndrome” or “small for flow syndrome,” the latter as suggested by Asencio et al in 2013.2 This syndrome should be defined by EAD associated with elevated portal flow and portal pressure and the consequent need for portal inflow modulation. A consensus is yet to be reached regarding the limits of portal flow and pressure consistent with this syndrome, but going by current knowledge, they could be as follows: Portal flow greater than 4 times the portal flow in the right portal vein of the donor, that is, greater than 360 mL/min per 100 g graft weight.4 A combination of portal pressure above 15 mm Hg5 along with portal vein flow greater than twice the portal flow in the right portal vein of the donor, that is, greater than 180 mL/min per 100 g graft weight (or >1 L/min).4 The second criterion is favored by the recent literature. Portal flow must be taken into consideration along with portal pressure to avoid portal steal syndrome, especially as Sainz-Barriga et al4 reported that 27% of their patients had portal flow below 90 mL/min per 100 g graft weight despite a portal pressure above 15 mm Hg.