Abstract
There are numerous causes of reduced arterial inline flow to the liver transplant
despite a patent hepatic artery. These include causes of increased peripheral resistance
in the hepatic arterial bed, siphoning of the hepatic arterial flow by a dominant
splenic artery (splenic steal syndrome), functional reduction of hepatic arterial
flow in response to hyperdynamic portal inline flow, and small hepatic graft relative
to normal portal inline flow (relative increase of portal flow). These causes are
incompletely understood, and perhaps the most controversial of all is the splenic
steal syndrome, which is possibly an underrecognized cause of graft ischemia in the
United States. Splenic steal syndrome presents nonspecifically as graft dysfunction;
if overlooked, it may lead to graft failure. Its incidence is reported to be 0.6 to
10.1% in liver transplant recipients, with some institutions performing prophylactic
and/or posttransplant treatment procedures in up to a quarter of their transplant
recipients. This wide disparity in the incidence of the diagnosis is probably because
there are no objective diagnostic imaging criteria. This article presents a review
of the literature that addresses the differential diagnostic considerations of hepatic
artery hypoperfusion (splenic steal syndrome included) in the absence of an anatomical
defect (hepatic artery stenosis, thrombosis, and/or kinks).
Keywords transplant - liver - vascular complications - splenic steal - hypoperfusion - buffer
response
