Portal vein complications after adult-to-adult living donor liver transplantation

Abstract

Summary Successful management of portal vein (PV) complications after liver transplantation is crucial to long‐term success. Little information is available, however, regarding the incidence and treatment of PV complications after adult‐to‐adult living donor liver transplantation (LDLT). Between January 1996 and October 2006, 310 adult LDLTs were performed at our institution. PV thrombus was present in 54 patients at the time of LDLT. The incidence of PV complications, choice of therapeutic intervention, and outcomes were retrospectively analyzed. Among the 310 recipients, PV complications were identified in 28 (9%). Risk factors included smaller graft size, presence of PV thrombus at the time of LDLT, and use of jump or interposition cryo‐preserved vein grafts for PV reconstruction. When divided into early (within 3 months, n = 11) and late (after 3 months, n = 17) complications, the use of vein grafts for PV reconstruction predisposed to the occurrence of late, but not early, PV complications. Portal vein thrombosis occurred more frequently in the early period (eight out of 11, 73%), whereas stenosis occurred more frequently in the later period (14 out of 17, 82%). Surgical interventions were favored in the earlier period, whereas interventional radiologic approaches were selected for later events. Overall 3‐ and 5‐year survival rates were 81% and 77%, respectively, in patients with PV complications and 88% and 84%, respectively, in those without PV complications (P = 0.21, log‐rank test). PV complications are a significant problem following LDLT with both early and late manifestations. Acceptable long‐term results, however, are achievable with periodic ultrasonographic surveillance and timely conventional therapeutic interventions. The use of cryo‐preserved vein grafts for reconstructing portal flow should be discouraged.

Vascular complications following liver transplantation: A literature review of advances in 2015

“…In contrast, liver failure is rare [30,90,96] . Langnas et al [30] (1991) reported a mean diagnosis time of 5 d following OLT (range: 1 to 15 d), which was confirmed by Kyoden et al [101] (2008), who reported that PVT occurred more frequently in the early period, i.e., 8/11 cases (72%).…”

“…From the UCLA experience, Duffy et al [5] (2009) reported a PVT incidence of 2% in more than 4200 patients. However, the incidence of PVT is close to 4% in adult LDLT due to technical difficulties in PV reconstructions, mainly related to a shorter vessel pedicle and limited vessel graft [101] . In LDLT, PVT occurs more frequently in the early period, defined as within 3 mo by Kyoden et al [101] (2008) (73% of cases from Table 5 Hepatic artery rupture highlights…”

“…Other reported risk factors include prior surgery on the portal or splanchnic venous system or a pretransplant portal thrombosis requiring thrombectomy during the operation, a small diameter of the portal vein (< 5 mm), previous splene ctomy, hypoplastic portal vein, large portosystemic collaterals and the use of venous conduits for portal vein reconstruction [90,96] . Specific risk factors found in adult LDLT are: Small PV size, liver graft position and the type of venous conduits used to connect the PV of the donor to the recipient such as a cryopreserved vein, the use of which is discouraged by Kyoden et al [101] (2008) [30,90,96,102105] . DUS should be the first imaging tool used and is easily employed to evaluate vascular patency.…”

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“…1,2 Additionally, the incidence of biliary anastomotic stricture developing within 5 to 8 months after a liver transplant ranges from 16% to 32%. 3 The incidence of anastomotic biliary stricture because of the placement of stents by endoscopic retrograde cholangiopancreatography ranges from 0% to 24%.…”

Living Donor Liver Transplantation

“…Early PVT is treated with surgical thrombectomy and revision of the anastomosis. Late PVT may require surgical shunting to decompress the portal system as treatment of the complications of portal hypertension (Kyoden Y, et al, 2008).…”