| "Splenic artery steal syndrome" is a misnomer: the cause is portal hyperperfusion, not arterial siphon. | |
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MedLine Citation:
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PMID: 18306381 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Cristiano Quintini; Kenzo Hirose; Koji Hashimoto; Teresa Diago; Federico Aucejo; Bijan Eghtesad; David Vogt; Gregory Pierce; Mark Baker; Dympna Kelly; Charles M Miller |
Publication Detail:
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Type: Case Reports; Journal Article |
Journal Detail:
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Title: Liver transplantation : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society Volume: 14 ISSN: 1527-6473 ISO Abbreviation: Liver Transpl. Publication Date: 2008 Mar |
Date Detail:
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Created Date: 2008-03-04 Completed Date: 2008-06-05 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 100909185 Medline TA: Liver Transpl Country: United States |
Other Details:
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Languages: eng Pagination: 374-9 Citation Subset: IM |
Affiliation:
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Department of General Surgery, Liver Transplant Center, Cleveland, OH 44195, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Aged Female Hepatic Artery / physiopathology*, ultrasonography Humans Liver / blood supply*, ultrasonography Liver Circulation / physiology Liver Transplantation / physiology* Male Middle Aged Regional Blood Flow / physiology Spleen / blood supply*, ultrasonography Splenic Artery / physiopathology*, ultrasonography Syndrome Terminology as Topic Vascular Resistance / physiology Vasoconstriction / physiology |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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