“Splenic artery steal syndrome” is a misnomer: The cause is portal hyperperfusion, not arterial siphon

Quintini, Cristiano; Hirose, Kenzo; Hashimoto, Koji; Diago, Teresa; Aucejo, Federico; Eghtesad, Bijan; Vogt, David; Pierce, Gregory; Baker, Mark E.; Kelly, D. G.; Miller, Charles M.

doi:10.1002/lt.21386

Cited by 107 publications

(106 citation statements)

References 14 publications

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“…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). 2,3 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.…”

supporting

confidence: 62%

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

Roll

Muiesan

2015

Liver Transpl

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In this issue of Liver Transplantation, Presser et al. 1 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). 2,3 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...

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supporting

confidence: 62%

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

Roll

Muiesan

2015

Liver Transpl

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“…15 Hepatic artery buffer response indicates that an increase in portal flow causes intraparenchymal Abbreviations: PVV, maximal velocity resistance, which in turn causes a decrease in arterial inflow. 16 Decreases in PVV and improvements in PSV of the hepatic artery after coil embolization support the idea that portal hyperperfusion may play a role in SASS. Selective arterial embolization is effective in treating SASS and has been shown to be safe, especially when coil deployment is placed in the proximal or midportion of the splenic artery.…”

Section: Discussionmentioning

confidence: 75%

Doppler Ultrasonography Findings of Splenic Arterial Steal Syndrome After Liver Transplant

Uslu

Aslan²,

Töre³

et al. 2012

Exp Clin Transplant

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“…4,[18][19][20] Our results agree with the HA buffer response theory in which the HA shows compensatory vasoconstriction reducing the arterial blood flow in response to portal hyperperfusion, thus leading to a high RI. 21,22 This phenomenon had been demonstrated intraoperatively by temporary clamping of the PV, which resulted in improved HA flow. 19 Other theories have related the early and transient elevation of the HA RI after DDLT to the older donor grafts, prolonged period of cold ischemia and preservation injury, graft steatosis, and chronic cholestatic disease as an indication for trans plant.…”

Section: Omar Abdelaziz Et Al/experimental and Clinical Transplantatimentioning

confidence: 93%

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Abdelaziz

Emad‐Eldin²,

Hussein³

et al. 2017

Exp Clin Transplant

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Objectives: Our aim was to investigate the early changes that occur after graft perfusion in livingdonor liver transplant by Doppler ultrasonography. Materials and Methods: We prospectively evaluated liver grafts of 30 patients who underwent living-donor liver transplant during an 18-month period and who were followed for 1 year postoperatively. The hepatic artery peak systolic velocity, resistivity index, portal vein velocity, portal vein anastomotic velocity ratio, and hepatic vein pattern were compared after excluding patients who developed vascular complications and acute rejection episodes. Results: We observed intraoperative increases in the mean hepatic artery peak systolic velocity (96.3 ± 65 cm/s), the resistivity index (0.78 ± 0.091), and the portal vein velocity (99.6 ± 48 cm/s), which started to normalize after 2 weeks. In comparing the mean portal vein velocity, portal vein anastomotic velocity ratio, hepatic artery peak systolic velocity, and resistivity index after excluding 5 patients who developed vascular complications, we observed overall significance levels of P < .001, P = .039, P < .001, and P = .040. After we excluded 9 patients who developed acute rejection, our comparison of the portal vein velocity, hepatic artery peak systolic velocity, and resistivity index showed overall significance (P < .001, P < .001, and P = .043). Conclusions: Early and transient increases in portal vein velocity, anastomotic velocity ratio, hepatic artery peak systolic velocity, and resistivity index are common after living-donor liver transplant, with significant declines in the first 2 weeks posttransplant.

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“Splenic artery steal syndrome” is a misnomer: The cause is portal hyperperfusion, not arterial siphon

Cited by 107 publications

References 14 publications

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

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

Doppler Ultrasonography Findings of Splenic Arterial Steal Syndrome After Liver Transplant

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