Splenic artery occlusion for small‐for‐size syndrome: Better late than never but early is the best

Small-for-size syndrome (SFSS) has emerged as a distinct clinical problem that adversely affects graft survival when partial liver grafts from living donors or split from deceased donors are used in adult recipients. A partial liver graft is frequently small in comparison with the size of an adult recipient and hence small for size. When the graft volume is too small to meet the metabolic demand of the recipient, a clinical picture of graft dysfunction, characterized by cholestasis, ascites, and coagulopathy, develops, and this is termed SFSS. A small-for-size graft not only may be functionally inadequate but also will sustain injury characterized by histologic features of ischemia and cholestasis after implantation. Both clinical experience and animal experiments have shown the presence of portal hypertension and established excessive portal flow or portal hyperperfusion injury as the underlying cause of the damage to a small-for-size graft. The excessive portal flow results in ischemia secondary to irreversible endothelial damage and arterial buffer response, and portal hyperperfusion and graft injury perpetuate each other in a vicious cycle, culminating in graft failure. Various methods of portal decompression using surgical or pharmacologic means have been described to prevent SFSS. Once established, however, SFSS generally carries a poor prognosis with progressive graft failure that predisposes to fatal complications such as gastrointestinal bleeding and sepsis, and there have been only a few reports of successful treatment. In this issue of Liver Transplantation, Humar et al. present a series of 7 patients who had a diagnosis of SFSS based on clinical features after receiving partial liver grafts with a graft weight to recipient body weight ratio of 0.51% to 1.58%. Reduction of portal flow by splenic artery ligation or embolization was performed to treat established SFSS at 8 to 16 days after transplantation. Afterward, graft function improved in 6 patients, and only 1 patient required retransplantation for graft failure. The case series highlights the importance of considering SFSS as a cause of early dysfunction of a partial graft, but it also illustrates the difficulties encountered with the diagnosis of SFSS as there is currently no consensus on its precise definition. A diagnosis of SFSS is generally made when dysfunction of a small-for-size partial liver graft occurs in the absence of any identifiable causes. There are several confusing issues. First, the clinical and biochemical criteria for graft dysfunction vary. Proposals have been made to distinguish small-for-size dysfunction from small-for-size nonfunction and to set an arbitrary cutoff for biochemical values in order to make it more objective. Second, the threshold for defining a graft as small for size has not been determined. Although a living donor graft of 40% of the standard liver volume or 0.8% of the body weight of the recipient is associated with inferior graft survival, the exact limit may vary with recipient factors such as pretransplant status and severity of portal hypertension, and even a graft larger than this lower limit may develop SFSS. On the other hand, SFSS should be diagnosed only if the primary cause of the graft dysfunction is insufficient graft size, generally when the graft is less than 50% of the standard liver volume or 1% of the body weight of the recipient. Third, confusion has arisen because various graft