The portal hyperperfusion, or small-for-size syndrome (SFSS), is a widely recognized clinical complication that may occur after segmental liver transplantation. Several surgical strategies have been proposed to reduce portal blood inflow and portal pressure after partial liver transplantation. In particular, splenic artery ligation and splenectomy have been used without a firm hemodynamic basis for these procedures. Our group recently demonstrated that, in patients with cirrhosis and portal hypertension, the occlusion of the splenic artery causes a significant reduction in the portal pressure gradient, which is directly related to the spleen volume and indirectly related to the liver volume. This concept is at the center of our strategy for performing early splenic artery embolization (SAE) for the treatment of SFSS after living-related liver transplantation (LRLT). Six patients developed smallfor-size syndrome, defined as: onset within the first week after LRLT of progressive hyperbilirubinemia without mechanical cause; marked cholestasis; centrilobular sinusoidal dilatation and hepatocyte atrophy at liver biopsy; and refractory ascites in the absence of vascular complications. All six patients who underwent SAE rapidly improved their clinical condition, with an evident decrease in the value of bilirubin in the serum, in the production of ascites, and improvement in condition of pancytopenia. Coagulopathy expressed by the international normalized ratio value (INR) was not a reliable early marker of SFSS in this series; in fact a slight improvement in the result of this test was already present immediately after LRLT and before SAE. Because splenic flow clearly contributes to portal hyperperfusion, an early SAE can relieve the partial graft from the deleterious effect of this portal overflow.
COMMENTS
To prevent small-for-size syndrome (SFSS) in liver transplantation, the obvious-but not practical-solution is to always use an adequately sized graft. 1 Because factors in addition to graft size contribute to this syndrome and because of the inevitable emergencies and the limited organ supply, most surgeons will face SFSS. 2 What is the best strategy: prevention of SFSS for patients at risk or treatment for those who develop SFSS?
Rat and pig transplant models are well suited for studying SFSS in liver transplantation. These models have enabled numerous publications, and numerous clinical solutions have been proposed.
In this review, Gruttadauria et al. report that even though splenic artery ligation and splenectomy have been used in the past to prevent SFSS, there has been no firm hemodynamic basis for these procedures. In an earlier report published in Liver Transplantation, 3 these authors wrote that occlusion of the splenic artery in patients with cirrhosis and portal hypertension significantly reduces the elevated portal pressure gradient, which is the underlying etiology of SFSS in liver transplantation. In 67 adult recipients of living related liver transplants at the authors' institution from January 2002 until April 2007, all patients except one had a graft/body weight ratio ΟΎ 0.8%, and 6 developed confirmed SFSS. Following antibiotic prophylaxis, selective catheterization using the right femoral approach to embolize the splenic artery was performed. All 6 patients had splenic artery embolization within 1 week of transplantation and showed rapid improvement, with a decrease in bilirubin levels, decreased ascites, and improvement in their pancytopenia. One patient developed massive splenic colliquation 3 weeks after embolization, eventually requiring surgical exploration and abdominal washout. Another patient underwent a liver biopsy at 27 days after transplantation to rule out acute cellular rejection and developed a large intrahepatic hematoma. The patient developed septic shock and irreversible liver failure and was successfully retransplanted. In the follow-up to this report, all patients were found to be well with normal liver function, with the exception of one patient who developed a spontaneous large bowel perforation unrelated to the splenic artery embolization and died. The authors point out that their study lacked a control group, precluding comment on the possibility of spontaneous regression of the SFSS in their patients.
Lo et al. 4 described a case in which they successfully used splenic artery ligation to salvage a small-for-size liver allograft. Tanaka and Ogura 5 related their experience with surgical ligation of the splenic artery for the prevention or treatment of small-for-size grafts. Troisi et al. 6 reviewed their series of 13 adult living donor recipients who underwent surgical splenic artery ligations at the time of transplantation to prevent SFSS