DISCUSSION
PVT occurs in 5%–26% of end-stage liver disease patients.^(2,3) Cirrhotic patients with end-stage liver disease have increased intrahepatic resistance to portal flow. The increased resistance, along with the disseminated intravascular coagulopathy of cirrhosis, and endothelial injury due to portal hypertension, increases the incidence of PVT. It is more common for patients with cryptogenic cirrhosis, post-necrotic cirrhosis, autoimmune chronic active hepatitis, trauma, previous dissection of porta hepatis, tumours and previous splenectomy, to have PVT.^(4-7) PVT is also more common in male patients.⁽⁵⁾ Viability of an allograft is dependent on portal flow, and hence patency of the portal vein needs to be maintained.⁽⁸⁾ Lerut et al reported 100% mortality when the liver is deprived of portal venous inflow.⁽¹⁾

Patients with PVT have a shrunken liver, large spleen, ascites and oesophageal varices. Doppler ultrasound and helical CT scans are highly accurate for diagnosing splanchnic vein thrombosis.^(9,10) All the patients on the waiting list at National University Hospital undergo trimonthly Doppler screening. There have been reports of 35%–57% incidence of unexpected PVT, found at transplantation, in patients who had negative results on previous duplex examinations.^(5-7,11-13) The higher false negative rate is attributed to post-duplex PVT, while patients are on the waiting list, and the identification of large portal collateral veins as the portal vein.⁽¹¹⁾ PVT can be graded preoperatively (Table II).⁽¹⁴⁾

Shaw et al first reported successful OLTs in patients with PVT using portal vein grafts.⁽¹⁵⁾ Presently, almost all patients with splanchnic vein thrombosis can have OLT. If the patients have PVT, the high-risk nature of surgery should be explained to the patient and informed consent should be obtained. In unsuspected PVT cases, the surgeon should be able to modify the surgery based on intraoperative evaluation and grading of the thrombus. In either case, the careful planning of the surgery and vigilant intraoperative assessment by experienced personnel is essential. However, with improved imaging modalities, this should be a rarity. Dissection of collateral rich hepatoduodenal ligament and thrombosed splanchnic veins, along with restoration of portal perfusion, demands high levels of surgical expertise. Portal perfusion can be restored from simple procedures like thromboendovenectomy, to the use of complex procedures using venous bypass and reconstruction. Isolated segmental PVT can be dealt with thromboendovenectomy.

When the thrombus involves the whole portal vein up to the splenomesenteric confluence, thromboendovenectomy can still be done, as in both of our cases. In some cases where there is sclerosis of the portal vein along with thrombosis, the portal vein can be excised and an interposition iliac vein graft can be used to anastomose the donor portal vein to the recipient splenomesenteric confluence. Common iliac veins are hence routinely harvested at the time of cadaveric multiorgan retrieval. Extensive splanchnic venous thrombosis involving the splenic and/or superior mesenteric veins can be dealt with by the use of an extra anatomic jump graft from the superior mesenteric vein to the donor portal vein. When an appropriate superior mesenteric vein segment is not available for jump graft, a jump graft from the left renal vein to the portal vein of the donor graft can be used for reconstruction. This is usually brought anterior to the pancreas and duodenum. In a living-related transplantation, a cryopreserved vascular graft of similar nature can be used.

Techniques using the internal jugular vein, saphenous vein or inferior mesenteric vein of the recipient have also been described. However, these not only carry higher risks, but also the experience of evidence for them is limited. Arterialisation of portal vein⁽¹⁶⁾ and cavoportal hemitransposition (CPHT)⁽¹⁷⁾ has been reported by others to restore the portal perfusion. Table III shows various case series on PVT and liver transplantation. The results of surgery involving PVT have improved with experience, and are comparable to results of OLT in patients without PVT.^(11,14,18) In a study by Francoz, the proportion of partial or complete recanalisation was higher in those who received anticoagulation than in those who did not.⁽¹⁷⁾ We do not anticoagulate our patients routinely, except for Budd-Chiari syndrome or rethrombosis.

A recent meta-analysis of 15 studies including 56 OLTs with CPHT and renoportal anastomosis (RPA), revealed early encouraging results at short-term followup. Ascites, renal dysfunction, lower extremity and torso oedema, and variceal bleeding were common postoperative complications after CPHT and RPA.⁽¹⁹⁾ When PVT extends diffusely to the peripheral parts of the mesenteric veins, a combined small intestine and liver transplantation may be the only option. Experience with cluster transplantation is very limited and is usually reserved if there is associated intestinal failure. Many series report that the results of surgery for PVT in OLT improve with experience, and the results are comparable to OLT in patients without PVT. Although it is not an absolute contraindication to liver transplantation, PVT is still a factor that adds to the technical challenge, complexity, morbidity and mortality of the procedure. Our early experience shows that with careful case selection and meticulous surgical technique, OLT can be safely done in patients with PVT without significant complications.

Correspondence to:
Dr Ravishankar K Diddapur
Specialist Surgery
Singapore Pte Ltd,
#02-35, Gleneagles Hospital (Annexe Block),
6A Napier Road,
Singapore 258500
Tel: (65) 9181 7293
Fax: (65) 6479 7608
Email: ravi_diddapur@hotmail.com