"Splenic artery steal syndrome" is a misnomer: the cause is portal hyperperfusion, not arterial siphon.
Splenic artery embolization (SAE) improves hepatic artery (HA) flow in liver transplant (OLT) recipients with so-called splenic artery steal syndrome. We propose that SAE actually improves HA flow by reducing the HA buffer response (HABR). Patient 1: On postoperative day (POD) 1, Doppler ultrasonography (US) showed patent vasculature with HA resistive index (RI) of 0.8. On POD 4, aminotransferases rose dramatically; his RI was 1.0 with no diastolic flow. Octreotide was begun, but on POD 5 US showed reverse diastolic HA flow with no signal in distal HA branches. After SAE, US showed markedly improved flow, RI was 0.6, diastolic flow in the main artery, and complete visualization of all distal branches. By POD 6, liver function had normalized. RI in the main HA is 0.76 at 2 months postsurgery. Patient 2: On POD 1, RI was 1.0. US showed worsening intrahepatic signal, with no signal in the intrahepatic branches and reversed diastolic flow despite good graft function. On POD 7, SAE improved the intrahepatic waveform and RI (from 1.0 to 0.72). Patient 3: Intraoperative reverse diastolic arterial flow persisted on PODs 1, 2, and 3, with progressive loss of US signal in peripheral HA branches. SAE on POD 4 improved the RI (0.86) and peripheral arterial branch signals. Patient 4: US on POD 1 showed good HA flow with a normal RI (0.7). A sudden waveform change on POD 2 with increasing RI (0.83) prompted SAE, after which the wave form normalized, with reconstitution of a normal diastolic flow (RI 0.68). In conclusion, these reports confirm the usefulness of SAE for poor HA flow but suggest that inflow steal was not the problem. Rather than producing an increase in arterial inflow, SAE worked by reducing portal flow and HABR, thereby reducing end-organ outflow resistance. Evidence of this effect is the marked reduction of the RI after the SAE to 0.6, 0.72, 0.86, and 0.68, in patients 1-4, respectively. SAE reduces excessive portal vein flow and thereby ameliorates an overactive HABR that can cause graft dysfunction and ultimately HA thrombosis.
Quintini
Cristiano
C
Department of General Surgery, Liver Transplant Center, Cleveland, OH 44195, USA.
Hirose
Kenzo
K
Hashimoto
Koji
K
Diago
Teresa
T
Aucejo
Federico
F
Eghtesad
Bijan
B
Vogt
David
D
Pierce
Gregory
G
Baker
Mark
M
Kelly
Dympna
D
Miller
Charles M
CM
D000368:Aged; D005260:Female; D006499:Hepatic Artery / Q000000981:diagnostic imaging / Q000503:physiopathology*; D006801:Humans; D008099:Liver / Q000098:blood supply* / Q000000981:diagnostic imaging; D008102:Liver Circulation / Q000502:physiology; D016031:Liver Transplantation / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D012039:Regional Blood Flow / Q000502:physiology; D013154:Spleen / Q000098:blood supply* / Q000000981:diagnostic imaging; D013157:Splenic Artery / Q000000981:diagnostic imaging / Q000503:physiopathology*; D013577:Syndrome; D009626:Terminology as Topic; D014463:Ultrasonography; D014655:Vascular Resistance / Q000502:physiology; D014661:Vasoconstriction / Q000502:physiology