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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
Table 6 Portal vein thombosis highlights
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