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

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

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish (US)
Pages (from-to)374-379
Number of pages6
JournalLiver Transplantation
Volume14
Issue number3
DOIs
StatePublished - Mar 2008
Externally publishedYes

Fingerprint

Splenic Artery
Hepatic Artery
Ultrasonography
Buffers
Transplants
Doppler Ultrasonography
Octreotide
Liver
Portal Vein
Transaminases
Thrombosis
Arteries

ASJC Scopus subject areas

  • Surgery
  • Transplantation

Cite this

Quintini, C., Hirose, K., Hashimoto, K., Diago, T., Aucejo, F., Eghtesad, B., ... Miller, C. M. (2008). "Splenic artery steal syndrome": Is a misnomer: The cause is portal hyperperfusion, not arterial siphon. Liver Transplantation, 14(3), 374-379. https://doi.org/10.1002/lt.21386

"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; Kelly, Dympna; Miller, Charles M.

In: Liver Transplantation, Vol. 14, No. 3, 03.2008, p. 374-379.

Research output: Contribution to journalArticle

Quintini, C, Hirose, K, Hashimoto, K, Diago, T, Aucejo, F, Eghtesad, B, Vogt, D, Pierce, G, Baker, M, Kelly, D & Miller, CM 2008, '"Splenic artery steal syndrome": Is a misnomer: The cause is portal hyperperfusion, not arterial siphon', Liver Transplantation, vol. 14, no. 3, pp. 374-379. https://doi.org/10.1002/lt.21386
Quintini, Cristiano ; Hirose, Kenzo ; Hashimoto, Koji ; Diago, Teresa ; Aucejo, Federico ; Eghtesad, Bijan ; Vogt, David ; Pierce, Gregory ; Baker, Mark ; Kelly, Dympna ; Miller, Charles M. / "Splenic artery steal syndrome" : Is a misnomer: The cause is portal hyperperfusion, not arterial siphon. In: Liver Transplantation. 2008 ; Vol. 14, No. 3. pp. 374-379.
@article{cb6c23f5604d4651a129374bdff03908,
title = "{"}Splenic artery steal syndrome{"}: Is a misnomer: The cause is portal hyperperfusion, not arterial siphon",
abstract = "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.",
author = "Cristiano Quintini and Kenzo Hirose and Koji Hashimoto and Teresa Diago and Federico Aucejo and Bijan Eghtesad and David Vogt and Gregory Pierce and Mark Baker and Dympna Kelly and Miller, {Charles M.}",
year = "2008",
month = "3",
doi = "10.1002/lt.21386",
language = "English (US)",
volume = "14",
pages = "374--379",
journal = "Liver Transplantation",
issn = "1527-6465",
publisher = "John Wiley and Sons Ltd",
number = "3",

}

TY - JOUR

T1 - "Splenic artery steal syndrome"

T2 - Is a misnomer: The cause is portal hyperperfusion, not arterial siphon

AU - Quintini, Cristiano

AU - Hirose, Kenzo

AU - Hashimoto, Koji

AU - Diago, Teresa

AU - Aucejo, Federico

AU - Eghtesad, Bijan

AU - Vogt, David

AU - Pierce, Gregory

AU - Baker, Mark

AU - Kelly, Dympna

AU - Miller, Charles M.

PY - 2008/3

Y1 - 2008/3

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=41149102901&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=41149102901&partnerID=8YFLogxK

U2 - 10.1002/lt.21386

DO - 10.1002/lt.21386

M3 - Article

C2 - 18306381

AN - SCOPUS:41149102901

VL - 14

SP - 374

EP - 379

JO - Liver Transplantation

JF - Liver Transplantation

SN - 1527-6465

IS - 3

ER -