The Increasingly Limited Basis for Portal Venous Pressure Modulation in Living Donor Liver Transplantation.

Abstract

SEE ARTICLE ON PAGE 1578 Potential conflict of interest: Nothing to report. Since its inception, living donor liver transplantation (LDLT) has had the arduous task of minimizing risk to donors while concurrently providing adequate liver parenchyma for the recipient. Surgeons began stratifying graft size either via the graft‐to‐recipient weight ratio (GRWR) or graft volume–to–standard liver volume ratio. Early on, it became apparent that a GRWR ratio <1% to 0.8% predicted an increased rate of complications and diminished survival.1 Termed small‐for‐size syndrome (SFSS), it implies dysfunction of a small graft within the first 1‐2 posttransplant weeks in the absence of any other identifiable cause, and it is characterized by coagulopathy, cholestasis, ascites, and encephalopathy.2 A key mechanism is believed to be excessive portal venous pressure (PVP) and flow transmitted to the allograft in the postreperfusion setting, resulting in sinusoidal congestion and hemorrhage. Portal hyperperfusion also results in diminished hepatic arterial flow from the hepatic artery buffer response.3 Various techniques have been described to help obviate this physiology. The goal is to either decrease portomesenteric inflow via splenic artery ligation and splenectomy or partially divert flow away from the liver via a portosystemic shunt. As previously detailed by the Kyoto group, success depends on lowering the PVP to less than a specific threshold, which in their experience was determined to be 15 mm Hg. This results in diminishing rates of SFSS and improved graft survival. In this issue of Liver Transplantation, Yao et al.4 have updated their experience with inflow modification by splenectomy, but they depict significant risk reduction only among >44‐year‐old donors or ABO‐incompatible recipients. They also reveal that GRWR <0.8% was independently associated with elevated risk of failed PVP modulation. They did not, however, stratify their treatment arm to correspond with a specific GRWR cutoff.4 This methodology is not without controversy. Some of the techniques employed, eg, splenectomy, have been shown to increase operative times, transfusion requirements, and perioperative infectious risks.5 In addition, other groups have noted equivalent results without undertaking any such interventions. The Asan group, as described in their comprehensive review of LDLT, no longer routinely measures portal pressures. Rather, providing excellent venous outflow is deemed a key mechanism for avoiding SFSS in grafts as small as GRWR 0.7%. They maintain that PVP >20 mm Hg was not associated with increased SFSS or graft loss as long as perfect venous outflow was maintained and portal flow steal was interrupted via portosystemic shunt ligation.6 The group from Juntendo University showed similar results in left segment allografts. In their series of 42 patients receiving left lobe LDLT without any portal flow augmentation and a median GRWR of 0.81, none met SFSS criteria despite PVP values >20 mm Hg in 19 of 31 recipients. Interestingly, this cohort did not have an increase in PVP postimplantation despite a significant increase in portal flow rate, a fact that was attributed to the enhanced compliance of the healthy allografts.7 The team from University of Tokyo reported on their series of LDLT comprising 395 patients. Selected patients were subjected to splenectomy at the time of transplant if medically indicated but never for PVP augmentation. There was no decrease in SFSS incidence in the splenectomized patients. Notably, the recipients in both Juntendo and Tokyo were ABO compatible and had the advantage of a younger donor pool than used in Kyoto. The Tokyo group limited their allografts to those over 40% graft‐to‐recipient standard liver volume.5 Variances in published series are not surprising given the multitude of confounding variables. Adequate allograft function is the result of a complex interplay between graft size, functional mass, anatomic variability, and recipient factors that include comorbidities, severity of underlying liver disease, and severity of portal hypertension. Surgical technique, including method and degree of outflow reconstruction, is also critically important.8 Even when considering PVP in isolation, it has been shown that increased flow is complementary to graft hypertrophy. Furthermore, there is often little correlation between measured PVP and portal flow volume. An allograft may exhibit suboptimal portal flow while concurrently having elevated portal pressures. Thus, a careful balance must be maintained.9 Taken together, these reports help corroborate the notion that routine PVP measurement and augmentation is not indicated. Optimized allograft and recipient pairing in combination with pristine surgical technique can alone substantially mitigate the incidence of SFSS even with GRWR ratios in the 0.7%‐0.8% range. Rather, as concluded by the Kyoto group, such modulation should be segregated to the exceptional cases using the least invasive techniques available.