Small for size syndrome following living donor and split liver transplantation
The field of liver transplantation is limited by the availability of donor organs. The use of living donor and split cadaveric grafts is one potential method of expanding the donor pool. However, primary graft dysfunction can result from the use of partial livers despite the absence of other causes...
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Published in: | World journal of gastrointestinal surgery Vol. 2; no. 12; pp. 389 - 394 |
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Main Authors: | , , , |
Format: | Journal Article |
Language: | English |
Published: |
United States
Baishideng Publishing Group Co., Limited
27-12-2010
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Subjects: | |
Online Access: | Get full text |
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Summary: | The field of liver transplantation is limited by the availability of donor organs. The use of living donor and split cadaveric grafts is one potential method of expanding the donor pool. However, primary graft dysfunction can result from the use of partial livers despite the absence of other causes such as vascular obstruction or sepsis. This increasingly recognised phenomenon is termed "Small-for-size syndrome" (SFSS). Studies in animal models and humans have suggested portal hyperperfusion of the graft combined with poor venous outflow and reduced arterial flow might cause sinusoidal congestion and endothelial dysfunction. Graft related factors such as graft to recipient body weight ratio < 0.8, impaired venous outflow, steatosis > 30% and pro- longed warm/cold ischemia time are positively predictive of SFSS. Donor related factors include deranged liver function tests and prolonged intensive care unit stay greater than five days. Child-Pugh grade C recipients are at relatively greater risk of developing SFSS. Surgi- cal approaches to prevent SFSS fall into two categories: those targeting portal hyperperfusion by reducing inflow to the graft, including splenic artery modulation and portacaval shunts; and those aiming to relieve paren-chymal congestion. This review aims to examine thecontroversial diagnosis of SFSS, including current strate-gies to predict and prevent its occurrence. We will also consider whether such interventions could jeopardize the graft by compromising regeneration. |
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Bibliography: | Hector Daniel Gonzalez, Zi Wei Liu, Sophia Cashman, Giuseppe K Fusai, Centre for HPB Surgery and Liver Transplantation, Royal Free Hospital, Pond Street, NW3 2QG, London, United Kingdom ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Author contributions: Gonzalez HD, Liu ZW, Cashman S and Fusai GK contributed equally to this paper. Telephone: +44-20-77940500 Fax: +44-20-74726226 Correspondence to: Giuseppe K Fusai, Consultant Surgeon, Centre for HPB Surgery and Liver Transplantation, Royal Free hospital, Pond Street, NW3 2QG, London, United Kingdom. gfusai@medsch.ucl.ac.uk |
ISSN: | 1948-9366 1948-9366 |
DOI: | 10.4240/wjgs.v2.i12.389 |