In the early period of liver transplantation (LT), portal vein thrombosis (PVT) was considered a contraindication for operation because of the technical difficulties it entailed, especially the inability to gain an adequate portal supply [1-3]. In 1985, Shaw et al. [4] reported the first successful deceased donor liver transplantation (DDLT) for a PVT patient and since then, many innovative surgical techniques have been introduced such as thrombectomy, portal vein (PV) reconstruction using vein grafts, and cavoportal hemitransposition [5-9]. Current PVT patients are no longer regarded to be contraindicated for LT and the results for patients with PVT is now comparable to that of patients without PVT [1,2,9,10]. Nevertheless, PVT is considered to add high risk to LT because of the complexity of LT procedures, resulting in significant surgical morbidity and mortality [10,11].

In living donor liver transplantation (LDLT), the issue of subjecting a healthy donor to potentially significant morbidity and mortality has led to a critical reassessment of the recipient selection criteria that are considered acceptable in DDLT [12]. In addition, there are some technical difficulties due to these innovations for preexisting PVT patients; necessity of distal dissection of vascular pedicle of the hilum and restricted availability of deceased donor vein graft [10,11].

Therefore, based on greater technical difficulties and the results from DDLT in this group of patients, the presence of PVT has often been considered to be a relative or absolute contraindication in LDLT [13,14].

From this point of view, the purpose of this report is to analyze single-center experiences in management of PVT, and to assess the impact of PVT on the outcomes in adult LDLT patients.

We retrospectively studied the records of 97 LDLT patients using data collected prospectively among 109 cases of consecutive adult LDLT performed at our center from July 2008 to June 2010. In our center, PVT has not been a contraindication for LDLT except where the preoperative radiologic studies demonstrate a gross tumor thrombus in the main portal vein. All PVT patients were diagnosed using abdominal computed tomography (CT) performed within 3 months before transplantation, and intraoperative detection. For standardization purposes, 12 patients were excluded for the following reasons: 1) no availability of preoperative and postoperative CT scans, 2) insufficient records of the intraoperative findings, or 3) tumor thrombus confirmed by postoperative pathology.

PV flow was monitored routinely after transplantation by Doppler ultrasound at post-transplant days 1,4, and 7, and dynamic CT scan at days 14 and 21.

PVT was diagnosed preoperatively and/or intraoperatively in 18 cases (18.5%). These patients with preoperatively and/or intraoperatively confirmed PVT formed the study group. Patients without PVT and transplanted during the same period were used as the control group.

All patients with confirmed PVT were retrospectively classified into four grades according to the extent of thromboses, as described by Yerdel et al. [15]: Grade I: minimally or partially thrombosed PV, in which the thrombus is mild or, at the most, confined to <50% of the vessel lumen with or without minimal extension into the superior mesenteric vein (SMV). Grade II showed >50% occlusion of the PV, including total occlusion with or without minimal extension into the SMV. Grade III were complete thromboses of both PV and proximal SMV with an open distal SMV. Grade IV was complete thrombosis of the portal vein as well as the proximal and distal SMV.

The preoperative, intraoperative, and postoperative parameters in these two groups were compared. The patients with PVT and those with non-PVT were followed up for a median time of 15.3 months (range, 1.2 to 36.5 months) and 14.9 months (range, 2.4 to 36.3 months).

The PVT is a well-established complication among patients with end-stage liver disease, and its incidence ranges from 2 to 26% in various centers [8,14], reaching as high as 39% in certain patient populations [16]. The incidence of PVT in LDLT patients at our center was 18.5%.

The etiology is not completely understood, but is believed to be related to anatomic change in the liver owing to the cirrhotic process, increased portal pressure, endothelial injury or coagulation changes [1,15,17,18]. In past studies, high-risk factors for developing PVT included autoimmune hepatitis, cryptogenic cirrhosis, chronic active hepatitis, Budd-Chiari syndrome, male gender, increased age, trauma, hypercoagulative states, Child-Pugh C, and treatment of portal hypertension (splenectomy, shunt operation, TIPS) [4,14,15,19]. But, this study found that previous treatment of portal hypertension was an independent risk factor for PVT prior to LDLT.

PVT was considered for 2 decades to be an absolute contraindication for LT [17]. However, in 1985, two successful liver transplantations were reported despite PVT [4]. Since then, progress in LT has allowed surgeons to utilize multiple techniques including thrombectomy of native veins, extensive thromboendovenectomy up to splenomesenteric confluence, venous interposition graft, renoportal anastomosis, cavoportal hemitransposition for overcoming this major problem and restoring PV flow [6,15,20,21]. But, there are some problems with technical difficulties and restricted availability of vein graft in LDLT as of yet [10,11,18]. The ideal surgical technique to resolve PVT during LT is not defined. The treatment depends on the characteristics of thrombosis (whether acute or chronic), degree (partial or complete), and especially, degree of extension to the splanchnic venous system [1,17].

In our study, 93.3% (n = 14) of patients with grade I and II PVT were successfully managed by classic PV-PV anastomosis with or without simple or eversion thrombectomy. In only one patient with grade II PVT, we performed thrombosed PV resection and portal vein reconstruction using interposition vein graft between the donor's PV and the recipient's proximal PV close to spleno-portal junction because of severe porta hepatis fibrotic change and incomplete eversion thrombectomy.

In one grade III PVT patient eversion thrombectomy failed, interposition vein graft was used and intraoperative PV stenting was performed due to residual thrombus at portomesenteric confluence level. And in the other case of grade III PVT with large splenorenal shunt, we experienced portal vein reconstruction using an interposition iliac vein graft connected to the left renal vein in a side-to-end fashion.

Regarding to blood transfusion, operation time, and in-hospital stay including ICU stay, no statistical difference was observed between the PVT and non-PVT groups in our study, indicating that proper management of PVT is a controllable procedure of LDLT.

The greater technical difficulty in patients with pre-existing PVT has demonstrated an increased risk of complications like hepatic artery thrombosis, relaparotomy, postoperative pancreatitis, sepsis, and renal failure in the different studies [9,15,22]. In our center, comparisons of the PVT patients and controls showed no statistical differences except postoperative bleeding. This increased risk is related to pre-existing PV pathology, high blood loss, the development of coagulopathy and severe acidosis [23]. Therefore, meticulous operative procedures and close monitoring for postoperative bleeding are required.

Initially, patients with PVT undergoing LT showed a high mortality rate in some papers [24]. But, recent studies such as that of Lladó et al. [25] have described similar survival in patients with PVT compared to patients without PVT. In our study, the results (in-hospital mortality, 1-and 3-year survival rates) obtained in patients undergoing LDLT with preoperative PVT are not significantly different to patients without PVT, despite short-term follow-up. Moreover, PVT of grade II to III can be managed with different techniques, with good postoperative results. The results suggest that accurate preoperative evaluation and detailed surgical planning are essential for restoring PV patency in LDLT patients.

In conclusion, the results are similar to non-PVT group in terms of in-hospital mortality, survival rates, and postoperative complications, and PV patency. Therefore, our experience suggests that PVT cannot be considered to be a contraindication for LDLT in spite of operative complexity.

In PVT of grade II and III, LDLT could be undertaken successfully with accurate preoperative diagnosis and proper surgical techniques and good postoperative outcomes can be obtained. Furthermore, innovations of therapeutic approaches and accumulation of experience could be required to improve the outcomes in LDLT with the more extensive PVT patients.