The safety and efficacy of proximal splenic artery embolization after liver transplantation are still not clearly defined

In this issue of Liver Transplantation, Presser et al. present an elegant description of their results from embolizing the proximal splenic artery in recipients after whole organ liver transplantation. They recount how empirical observations relating hepatic artery thrombosis to early arterial insufficiency were expanded to the treatment of portal hyperperfusion (PHP) and recurrent ascites. PHP and the importance of the hepatic artery buffer response are essential areas of research in the transplantation of whole and partial liver grafts. Clearly, the authors and their colleagues in interventional radiology have developed significant expertise in optimizing the intrahepatic hemodynamics after orthotopic liver transplantation and are facile with spleen-preserving proximal splenic artery embolization (SAE). The authors also reinforce the evidence supporting 2 risk factors for PHP: the spleen volume and the spleen/liver volume ratio. Although the current study is an important starting point for discussion, it suffers from some design flaws that make the data difficult to extrapolate for use by a wider audience. A lack of randomization and the absence of standardized indications for SAE limit the generalizability of the data. The primary outcome of the study is the improvement of intrahepatic arterial flow and the reduction of portal venous flow. There is no doubt that this is a theoretically important result, but it would be helpful to demonstrate that proximal SAE produced a clinical effect such as a reduction in the rate of development of intractable ascites or that the volume of ascites was reduced after SAE. Along that line of thinking, the authors treated all recipients who had an elevated resistive index (RI) with SAE, but 12 patients still went on to develop intractable ascites. If all patients with elevated RIs were captured and an elevated RI led to intractable ascites, then how did these 12 patients progress to intractable ascites? These patients were shown to have a lower RI than those with elevated RIs, but where is the evidence that this was due to poor compliance of the liver graft? Moreover, the RI is affected by numerous factors, including blood volume, pressure, and heart rate, and to confuse matters further, it is also closely related to vascular compliance. Another issue with the design of the study is that the authors combine 2 different groups of patients into the study arm: those with high RIs and those with intractable postoperative ascites. These groups are undoubtedly different, and subsequently, attempting to draw conclusions from the data is difficult. The pathology of PHP in the first few days after transplantation is likely distinct from the pathophysiology in the weeks after transplantation, so treatment with proximal SAE is likely to have different consequences and effectiveness on day 3 versus day 88 after transplantation. The authors link a persistently elevated RI to the development of postoperative ascites, which mechanistically makes sense, but they have not provided a control group that confirms this assumption. The