Copyright
©The Author(s) 2016.
World J Hepatol. Jan 8, 2016; 8(1): 36-57
Published online Jan 8, 2016. doi: 10.4254/wjh.v8.i1.36
Published online Jan 8, 2016. doi: 10.4254/wjh.v8.i1.36
Summary of the clinical characteristics about PVT |
The incidence of PVT is uncommon and ranges from < 3% following OLT |
PVT incidence is higher in pediatric transplantation, LDLT and split liver transplantation |
Early PVT is more frequent than late PVT with a median time to diagnosis of 5 d following OLT (range: 1 to 15 d) |
The clinical presentation of early PVT ranges from portal hypertension manifestations (abdominal pain, ascites, gastrointestinal bleeding, splenomegaly) to severe allograft dysfunction and multiorgan failure |
The most common causes leading to PVT are technical errors and anatomic complications such as venous redundancy, kinking and/or stenosis of the anastomosis |
Risk factors are the presence of portal thrombosis prior OLT, small diameter of the portal vein, previous splenectomy, large portosystemic collaterals and the use of cryopreserved venous conduits for PV reconstruction |
DUS, CEUS, contrast-enhanced CT, MRI and portography are imaging tools used for a positive diagnosis |
PVT treatment includes systemic anticoagulation therapy, catheter-based thrombolytic therapy by percutaneous radiological intervention (transhepatic or transjugular access depending of the coagulation state) with or without stent placement to portosystemic shunting (TIPS) to retransplantation in highly unresolvable cases |
PVT is associated with poor survival without treatment, but with prompt management, outcomes in terms of morbidity and mortality are satisfying |
- Citation: Piardi T, Lhuaire M, Bruno O, Memeo R, Pessaux P, Kianmanesh R, Sommacale D. Vascular complications following liver transplantation: A literature review of advances in 2015. World J Hepatol 2016; 8(1): 36-57
- URL: https://www.wjgnet.com/1948-5182/full/v8/i1/36.htm
- DOI: https://dx.doi.org/10.4254/wjh.v8.i1.36