- Email: [email protected]
Outcome of modified portal vein anastomosis for recipients with portal vein thrombosis or stenosis before living donor liver transplantation
Journal of Pediatric Surgery (2011) 46, 2291–2295
www.elsevier.com/locate/jpedsurg
Outcome of modified portal vein anastomosis for recipients with portal vein thrombosis or stenosis before living donor liver transplantation Toshiharu Matsuura ⁎, Yusuke Yanagi, Isamu Saeki, Makoto Hayashida, Tomoaki Taguchi Department of Pediatric Surgery, Reproductive and Developmental Medicine, Graduate School of Medical Sciences, Kyushu University, 3-1-1, Maidashi, Higashi-ku, Fukuoka, Japan Received 23 August 2011; accepted 3 September 2011
Key words: Portal vein thrombosis; Modified portal vein anastomosis; Vessel graft; Living donor liver transplantation
Abstract Background: Portal vein thrombosis (PVT) or stenosis (PVS) often requires challenging techniques for reconstruction in living donor liver transplantation (LDLT). Materials and Methods: A total of 57 LDLTs were performed between October 1996 and December 2010. There were 16 cases (28%) with PVT/PVS that underwent modified portal vein anastomosis (mPVa). The m-PVa techniques were classified into 3 groups: patch graft (Type-1), interposition graft (Type-2), and using huge shunt vessels (Type-3). The reconstruction patterns were evaluated with regard to age, graft vessels, PV flow, and complication rate. Results: The m-PVas were Type-1 in 10 cases, Type-2 in 3 cases, and Type-3 in 3 cases. The vessel graft in Type-1 was the inferior mesenteric vein (IMV) in 8 and the jugular vein in 2 cases, whereas the vessel graft in Type-2 was IMV in 2 and the saphenous vein in 1 case; in Type-3, the vessel grafts were renoportal, gonadal-portal, and coronary-portal anastomoses, respectively. The postoperative PV flow was sufficient in all types and slightly higher in Type-3. The postoperative complications occurred in 20% of the patients who underwent Type-1, in 33% who underwent Type2, and in 0% who underwent Type-3. Conclusion: The m-PVa was effective to overcome the surgical difficulty during transplantation. Pretransplant planning for the selection of the type of reconstruction is important for recipients with PVT/PVS. © 2011 Elsevier Inc. All rights reserved.
Portal vein thrombosis (PVT) is caused by a decreased portal flow resulting from progressing liver cirrhosis, the development of periportal lymphangitis, and fibrosis. Presented at the Pacific Association of Pediatric Surgeons 44th Annual Meeting, Cancun, Mexico, April 10-14, 2011. ⁎ Corresponding author. Tel.: +81 92 642 5573; fax: +81 92 642 5580. E-mail address: [email protected] (T. Matsuura). 0022-3468/$ – see front matter © 2011 Elsevier Inc. All rights reserved. doi:10.1016/j.jpedsurg.2011.09.015
Enhanced coagulability related with decreased levels of natural anticoagulants such as protein C, and protein S, as well as coagulation factors, was also observed in patients with PVT [1]. The incidence of PVT in cirrhotic end-stage liver disease patients is reported 5% to 15% [2]. The presence of PVT or stenosis (PVS) remains a technical difficulty during living donor liver transplantation (LDLT), even if it may no longer be considered an
2292
T. Matsuura et al.
absolute contraindication for LDLT. Innovative surgical techniques, such as thrombectomy and portal vein reconstruction using vein grafts, are successfully performed in most PVT cases. Moreover, advanced PVT recipients can now be successfully treated with more complex procedures, such as cavoportal hemitransposition and renoportal anastomosis [3]. The present study describes the surgical pattern for portal vein reconstruction in a series of 57 recipients who underwent LDLT. Moreover, the study also retrospectively reviewed the outcome of the portal vein reconstruction using vessel graft or shunt vessel in LDLT for recipients with PVT/PVS.
1. Patients and methods A total of 57 patients underwent LDLT at our department between October 1996 and December 2010. There were 15 male and 42 female recipients. Their mean age was 8.9 years ranged from 6 months to 28 years, and their body weight ranged from 5.2 to 71.3 kg. Their primary diagnostic indications for LDLT are biliary atresia (n = 42), fulminant hepatitis (n = 6), hepatoblastoma (n = 3), Alagille syndrome (n = 2), congenital absence of the portal vein (n = 2), and congenital metabolic liver disease (n = 2) (Table 1). Sixteen cases (28%) PVT/PVS required modified portal vein anastomosis (m-PVa), which was defined as the reconstruction of the portal vein with a vein graft or anastomosis to the shunt vessels. In the other 41 recipients, the portal vein reconstruction was simple end-to-end anastomosis without any vein grafts, including branch patch anastomosis at the bifurcation of the right and left branches of the recipient portal vein. Portal vein thrombosis was found in 6 of the 16 m-PVa recipients (10.5% of total cases), and PVS was found in 10 cases. Both were diagnosed by either preoperative computed tomographic (CT) or intraoperative findings. The portal vein anastomosis was Table 1
mostly performed with 7-0 PDS (Johnson & Johnson K.K., Tokyo, Japan) continuous sutures with growth factor, in some cases, continuous sutures only in the back wall with interrupted sutures in the front wall of the portal vein to prevent anastomotic stenosis. The m-PVa technique was classified into 3 types: patch graft (Type-1), interposition graft (Type-2), and the use of the huge collateral shunt vessels (Type-3) (Fig. 1). Modalities for portal vein reconstruction were chosen according to the diameter, wall status, and length of the recipient's portal vein and the diameter and length of the graft portal vein. The planning algorithm for portal vein reconstruction for PVT/ PVS is shown in Fig. 2. At dissection of the recipient portal vein during hepatectomy, we assessed the recipient portal vein and the amount of portal flow by unclamping the portal vein. When there was no stenosis or slightly diameter mismatch leading to reduced portal flow, we used the native trunk including branch patch technique for anastomosis. When there was diameter mismatch because of significant stenosis (smaller than 4 mm), the venoplasty using patch graft was performed from the level of the confluence. When the distance between the graft portal vein and the recipient portal vein was too far, the interposition graft was applied. When the PVT was advanced and the huge collateral shunt vessel existed, the anastomosis between the graft portal vein and the shunt vessel was performed. The intraoperative portal vein blood flow volume was measured after anastomosis using electromagnetic flow probes. The hepatic flow was monitored by Doppler ultrasonography twice a day for the first week after LDLT and once a day during hospitalization. No anticoagulant therapy was applied in any recipients after LDLT. Vessel complications were assessed by thin slice CT to select the optimal treatment, reoperation, anticoagulant therapy, or interventional therapy. The pretransplant clinical data in the m-PVa recipients was retrospectively reviewed, especially episodes of treatment of portal hypertension. Moreover, the reconstruction patterns were also evaluated based on the age of recipients, type of graft vessels, PV flow, and complication rate.
The comparison between m-PVa and s-PVa recipients' profiles
Age at LDLT (y)
Approximately 1 1-5 6-10 11-18 Approximately N18 Biliary atresia, 16
Primary disease
CAPV indicates congenital absence of the portal vein.
m-PVa (n = 16)
s-PVa (n = 41)
6 (55%) 4 (21%) 1 (20%) 4 (31%) 1 (11%)
5 15 4 9 8 Biliary atresia, 26 Acute liver failure, 6 Hepatoblastoma, 3 Alagille syndrome, 2 CAPV, 2 Metabolic disease, 2
Modified portal vein anastomosis
2293
Fig. 1 Reconstruction methods for m-PVa. Type-1, patch graft technique; Type-2, interposition graft technique; Type-3, anastomosis with huge shunt vessel.
All operations were performed with informed consent of the recipients or their parents and the donors and approved by the Ethics Committee of Kyushu University. This study was performed according to ethical guidelines for clinical studies of the Ministry of Health, Labour and Welfare of Japan.
2. Results The overall survival rate of the 57 cases after LDLT was 89.5% (51/57), and there was no significant difference in comparison with the 87.5% survival (14/16) in recipients with m-PVa. The causes of death in the two m-PVa
recipients were graft failure because of insufficient portal flow and complications because of a brain tumor found after LDLT. The age distribution and primary diagnostic indications for LDLT were summarized in Table 1. Although the infant patients had higher tendency to m-PVa application for reconstruction (55%), this method was applied in all age groups. The primary disease for LDLT was biliary atresia in all m-PVa recipients. Nine recipients with m-PVa (56%) had episodes of treatment of portal hypertension before LDLT (data not shown). Endoscopic injection sclerotherapy or endoscopic varices ligation and was applied for esophageal varices in 4 cases. The other 4 cases were treated with β-blocker to decrease the portal blood pressure. Splenectomy was
Fig. 2 The planning algorithm to choose techniques for portal vein reconstruction with PVT/PVS. Diameter matching was considered whether the recipient portal vein diameter was smaller than 4 mm. s-PVa indicates simple portal vein anastomosis.
2294
T. Matsuura et al.
performed before LDLT in one case because of severe hypersplenism with near normal liver function. The comparison among the types of portal vein reconstruction in m-PVa recipients was summarized in Table 2. Type-1 m-PVa was performed in 10 cases, Type-2 in 3 cases, and Type-3 in 3 cases. The mean age of the patients in these groups at LDLT was 4.6 ± 2.3, 3.0 ± 1.4, and 10.6 ± 6.2 years, respectively. The recipients in the Type-3 group were significantly older than those in other two groups. The liver graft was mostly used left lateral segment in Type-1 and -2 and the extended left lobe graft was used in all Type-3 recipients. The vessel graft in the Type-1 group was the donor inferior mesenteric vein (IMV) in 8 cases and the recipient jugular vein in 2. The vessel graft in the Type-2 group was the donor IMV in 2 and the donor saphenous vein in 1, and the 3 cases in the Type-3 group received renoportal, gonadal-portal, and coronary-portal anastomoses. The intraoperative portal vein flow (PVF) volume measured just after graft liver reperfusion was sufficient in all types of m-PVa, and slightly higher flow volume was obtained in Type-3 (mean PVF: Type-1, 177.2 ± 21.3; Type-2, 132.4 ± 16.4; Type-3, 291.8 ± 29.2 mL/min per 100 g liver). The clinical data of the liver function test after LDLT showed no significant differences among all 3 types except for the data during biopsy-proven acute cellular rejection. Postoperative portal vein complications occurred in 20% of the Type-1 patients (PVT in 2 cases), 33% of the Type-2 patients (PVS in 1 case), and 0% of the Type-3 patients. One complicated Type-1 case died because of insufficient portal flow despite re-reconstruction, and the other case was successfully re-reconstructed using a jumping graft. The Type-2 PVS case was successfully treated by interventional therapy and experienced no recurrence of PVS. Table 2 The comparison among the types of portal vein reconstruction in m-PVa recipients
Age at LDLT (y) Graft liver
Graft vessels
PVF/GV (mL/min per 100 g) Post portal vein complications
Type-1 (n = 10)
Type-2 (n = 3)
Type-3 (n = 3)
4.6 ± 2.3 LLS, 7 ex LL, 2 RL, 1 IMV, 8 Jugular vein, 2
3.0 ± 1.4
10.6 ± 6.2
LLS, 3
Ex LL, 3
IMV, 2 Saphenous vein, 1
177 ± 21.3
132 ± 16.4
Renoportal, 1 Gonadal vein, 1 Coronary vein, 1 291 ± 29.2
PVT 2 (20%)
PVS 1 (33%)
None (0%)
LLS indicates left lateral segment; ex LL, extended left lobe; RL, right lobe; GV, graft volume.
3. Discussion Portal vein thrombosis is no longer considered to be a contraindication for LDLT because of technical achievements such as the introduction of vessel grafting by Shaw in 1985 [4]. This technique also enabled surgeons to overcome the technical difficulties in cases with PVS or size-mismatched portal vein. Although vessel grafts can be easily obtained from a cadaveric donor, the availability of vessel grafts in LDLT is limited. Therefore, portal vein reconstruction with vessel grafts is still a challenging operation in LDLT. The incidence of pre-LDLT PVT was 10.5% (6/57 cases) in the current series, in contrast to 5% to 15% reported elsewhere [2]. Portal vein sclerosis is frequently seen in patients with biliary atresia because of repeated cholangitis. Saad et al reported that the pathologic examination of the portal vein showed the fibrous change at LDLT in 80% of post-Kasai cases [5]. The present study found that of 56% recipients with m-PVa had episodes of treatment of portal hypertension before LDLT. There are several risk factors for PVT, such as advanced age, Child-Pugh C, previous treatment of portal hypertension (sclerotherapy, Transjugular intrahepatic portosystemic shunt, shunt surgery, splenectomy), and previous surgical interventions [6]. The treatments of portal hypertension may change the hemodynamic state to low perfusion or reversed flow in the PV [7]. Pretransplant examinations, such as Doppler ultrasonography and CT, enable surgeons to plan the portal reconstruction. It is therefore necessary to harvest a vein graft from the donor when those data show a native portal vein diameter of ≤4 mm. Portal vein reconstruction requires a huge shunt vein when the PVT is extended to the bifurcation and accompanied by cavernous transformation. The potential surgical options for advanced PVT cases include different types of venous jump graft reconstruction or arterializations of the portal vein [8]. Cavoportal hemitransposition or renoportal anastomosis [3] had been recently advocated as creative surgical strategies. Regarding the type of vessel grafts, we think the donor IMV is the most ideal graft in Type-1 or -2 m-PVa because it is not only suitable for diameter and length but also safely obtained from the same surgical field. In recent years, the use of cryopreserved veins are reported to be useful from limited centers, but long-term outcome remains unstudied [8,9]. In our series, the portal vein reconstruction using shunt vessel (Type-3) was useful for the extended PVT recipients with huge shunt vessel, resulting to no experience of postoperative complications. However, because the vascular wall of the shunt vessel is usually thin, the anastomosis should be performed carefully not to split the vessel wall. The recipients in the Type-3 group were significantly older than those in other two groups. Because the long-term portal hypertensive state may result in the severe PVT and the formation of huge collateral shunt vessel, the age of Type-3 is higher than other two groups.
Modified portal vein anastomosis The optimal PVF volume to match the graft liver size is a controversial problem. Hypoperfusion often leads to graft failure; however, hyperperfusion can injure the hepatocytes, as observed in small-for-size syndrome. Troisi and de Hemptinne reported that the recovery of liver function is slower and not better with PVF/graft volume greater than 250 (mL/min per 100 g liver) after LDLT [10]. The optimal PVF was obtained (100-250 mL/min per 100 g liver) in Type-1 and -2 m-PVa. The mean PVF in Type-3 was slightly higher (291.8 mL/min per 100 g liver), but the postoperative course was excellent, and there were no PV complications after LDLT. Although the PVF was measured intraoperatively just after reperfusion in the current study, the PVF may decrease some time after reperfusion because of the graft edema or regulation of arterial and portal flows that occur over the sinusoids. Ou et al reported that slow portal flow (b10 cm/s) is a strongly predictable sign of post-LDLT PVT in patients with biliary atresia [11]. Therefore, obtaining optimal PVF is the most important factor in portal vein reconstruction. In conclusion, it is suggested that m-PVa was able to effectively overcome the operative the surgical difficulty and postoperative complications. The most important matter in portal anastomosis is to obtain a sufficient diameter and length to allow for sufficient portal blood flow volume. Pretransplant planning for selecting the optimal type of reconstruction is important for the success in LDLT for recipients with PVT/PVS.
Acknowledgments The authors would like to thank Dr Brian Quinn for reading the article. This work was supported in part by a
2295 grant-in-aid for scientific research from the Japanese Society for the Promotion of Science. This study was performed according to ethical guidelines for clinical studies of the Ministry of Health, Labour and Welfare of Japan.
References [1] Webster GJ, Burroughs AK, Riordan SM. Review article: portal vein thrombosis—new insights into aetiology and management. Aliment Pharmacol Ther 2005;21:1-9. [2] Nonami T, Yokoyama I, Iwatsuki S, et al. The incidence of portal vein thrombosis at liver transplantation. Hepatology 1992;16:1195-8. [3] Paskonis M, Jurgaitis J, Mehrabi A, et al. Surgical strategies for liver transplantation in the case of portal vein thrombosis—current role of cavoportal hemitransposition and renoportal anastomosis. Clin Transplant 2006;20:551-62. [4] Shaw BW, Iwatsuki S, Bron K, et al. Portal vein grafts in hepatic transplantation. Surg Gynecol Obstet 1985;161:66-8. [5] Saad S, Tanaka K, Inomata Y, et al. Portal vein reconstruction in pediatric liver transplantation from living donors. Ann Surg 1998;227: 275-81. [6] Ramos AP, Reigada CPH, Ataide EC, et al. Portal vein thrombosis and liver transplantation: Long term. Transplant Proc 2010;42:498-501. [7] Tao YF, Teng F, Wang ZX, et al. Liver transplant recipients with portal vein thrombosis: a single center retrospective study. Hepatobiliary Pancreat Dis Int 2009;8:34-9. [8] Kim SJ, Kim DJ, Park JH, et al. Clinical analysis of living donor liver transplantation in patients with portal vein thrombosis. Clin Transplant 2011;25:111-8. [9] Sugawara Y, Makuuchi M, Tamura S, et al. Portal vein reconstruction in adult living donor liver transplantation using cryopreserved vein grafts. Liver Transpl 2006;12:1233-6. [10] Troisi R, de Hemptinne B. Clinical relevance of adapting portal vein flow in living donor liver transplantation in adult patients. Liver Transpl 2003;9:S36-41. [11] Ou HY, Concejero AM, Huang TL, et al. Portal vein thrombosis in biliary atresia patients after living donor liver transplantation. Surgery 2011;149:40-7.
www.elsevier.com/locate/jpedsurg
Outcome of modified portal vein anastomosis for recipients with portal vein thrombosis or stenosis before living donor liver transplantation Toshiharu Matsuura ⁎, Yusuke Yanagi, Isamu Saeki, Makoto Hayashida, Tomoaki Taguchi Department of Pediatric Surgery, Reproductive and Developmental Medicine, Graduate School of Medical Sciences, Kyushu University, 3-1-1, Maidashi, Higashi-ku, Fukuoka, Japan Received 23 August 2011; accepted 3 September 2011
Key words: Portal vein thrombosis; Modified portal vein anastomosis; Vessel graft; Living donor liver transplantation
Abstract Background: Portal vein thrombosis (PVT) or stenosis (PVS) often requires challenging techniques for reconstruction in living donor liver transplantation (LDLT). Materials and Methods: A total of 57 LDLTs were performed between October 1996 and December 2010. There were 16 cases (28%) with PVT/PVS that underwent modified portal vein anastomosis (mPVa). The m-PVa techniques were classified into 3 groups: patch graft (Type-1), interposition graft (Type-2), and using huge shunt vessels (Type-3). The reconstruction patterns were evaluated with regard to age, graft vessels, PV flow, and complication rate. Results: The m-PVas were Type-1 in 10 cases, Type-2 in 3 cases, and Type-3 in 3 cases. The vessel graft in Type-1 was the inferior mesenteric vein (IMV) in 8 and the jugular vein in 2 cases, whereas the vessel graft in Type-2 was IMV in 2 and the saphenous vein in 1 case; in Type-3, the vessel grafts were renoportal, gonadal-portal, and coronary-portal anastomoses, respectively. The postoperative PV flow was sufficient in all types and slightly higher in Type-3. The postoperative complications occurred in 20% of the patients who underwent Type-1, in 33% who underwent Type2, and in 0% who underwent Type-3. Conclusion: The m-PVa was effective to overcome the surgical difficulty during transplantation. Pretransplant planning for the selection of the type of reconstruction is important for recipients with PVT/PVS. © 2011 Elsevier Inc. All rights reserved.
Portal vein thrombosis (PVT) is caused by a decreased portal flow resulting from progressing liver cirrhosis, the development of periportal lymphangitis, and fibrosis. Presented at the Pacific Association of Pediatric Surgeons 44th Annual Meeting, Cancun, Mexico, April 10-14, 2011. ⁎ Corresponding author. Tel.: +81 92 642 5573; fax: +81 92 642 5580. E-mail address: [email protected] (T. Matsuura). 0022-3468/$ – see front matter © 2011 Elsevier Inc. All rights reserved. doi:10.1016/j.jpedsurg.2011.09.015
Enhanced coagulability related with decreased levels of natural anticoagulants such as protein C, and protein S, as well as coagulation factors, was also observed in patients with PVT [1]. The incidence of PVT in cirrhotic end-stage liver disease patients is reported 5% to 15% [2]. The presence of PVT or stenosis (PVS) remains a technical difficulty during living donor liver transplantation (LDLT), even if it may no longer be considered an
2292
T. Matsuura et al.
absolute contraindication for LDLT. Innovative surgical techniques, such as thrombectomy and portal vein reconstruction using vein grafts, are successfully performed in most PVT cases. Moreover, advanced PVT recipients can now be successfully treated with more complex procedures, such as cavoportal hemitransposition and renoportal anastomosis [3]. The present study describes the surgical pattern for portal vein reconstruction in a series of 57 recipients who underwent LDLT. Moreover, the study also retrospectively reviewed the outcome of the portal vein reconstruction using vessel graft or shunt vessel in LDLT for recipients with PVT/PVS.
1. Patients and methods A total of 57 patients underwent LDLT at our department between October 1996 and December 2010. There were 15 male and 42 female recipients. Their mean age was 8.9 years ranged from 6 months to 28 years, and their body weight ranged from 5.2 to 71.3 kg. Their primary diagnostic indications for LDLT are biliary atresia (n = 42), fulminant hepatitis (n = 6), hepatoblastoma (n = 3), Alagille syndrome (n = 2), congenital absence of the portal vein (n = 2), and congenital metabolic liver disease (n = 2) (Table 1). Sixteen cases (28%) PVT/PVS required modified portal vein anastomosis (m-PVa), which was defined as the reconstruction of the portal vein with a vein graft or anastomosis to the shunt vessels. In the other 41 recipients, the portal vein reconstruction was simple end-to-end anastomosis without any vein grafts, including branch patch anastomosis at the bifurcation of the right and left branches of the recipient portal vein. Portal vein thrombosis was found in 6 of the 16 m-PVa recipients (10.5% of total cases), and PVS was found in 10 cases. Both were diagnosed by either preoperative computed tomographic (CT) or intraoperative findings. The portal vein anastomosis was Table 1
mostly performed with 7-0 PDS (Johnson & Johnson K.K., Tokyo, Japan) continuous sutures with growth factor, in some cases, continuous sutures only in the back wall with interrupted sutures in the front wall of the portal vein to prevent anastomotic stenosis. The m-PVa technique was classified into 3 types: patch graft (Type-1), interposition graft (Type-2), and the use of the huge collateral shunt vessels (Type-3) (Fig. 1). Modalities for portal vein reconstruction were chosen according to the diameter, wall status, and length of the recipient's portal vein and the diameter and length of the graft portal vein. The planning algorithm for portal vein reconstruction for PVT/ PVS is shown in Fig. 2. At dissection of the recipient portal vein during hepatectomy, we assessed the recipient portal vein and the amount of portal flow by unclamping the portal vein. When there was no stenosis or slightly diameter mismatch leading to reduced portal flow, we used the native trunk including branch patch technique for anastomosis. When there was diameter mismatch because of significant stenosis (smaller than 4 mm), the venoplasty using patch graft was performed from the level of the confluence. When the distance between the graft portal vein and the recipient portal vein was too far, the interposition graft was applied. When the PVT was advanced and the huge collateral shunt vessel existed, the anastomosis between the graft portal vein and the shunt vessel was performed. The intraoperative portal vein blood flow volume was measured after anastomosis using electromagnetic flow probes. The hepatic flow was monitored by Doppler ultrasonography twice a day for the first week after LDLT and once a day during hospitalization. No anticoagulant therapy was applied in any recipients after LDLT. Vessel complications were assessed by thin slice CT to select the optimal treatment, reoperation, anticoagulant therapy, or interventional therapy. The pretransplant clinical data in the m-PVa recipients was retrospectively reviewed, especially episodes of treatment of portal hypertension. Moreover, the reconstruction patterns were also evaluated based on the age of recipients, type of graft vessels, PV flow, and complication rate.
The comparison between m-PVa and s-PVa recipients' profiles
Age at LDLT (y)
Approximately 1 1-5 6-10 11-18 Approximately N18 Biliary atresia, 16
Primary disease
CAPV indicates congenital absence of the portal vein.
m-PVa (n = 16)
s-PVa (n = 41)
6 (55%) 4 (21%) 1 (20%) 4 (31%) 1 (11%)
5 15 4 9 8 Biliary atresia, 26 Acute liver failure, 6 Hepatoblastoma, 3 Alagille syndrome, 2 CAPV, 2 Metabolic disease, 2
Modified portal vein anastomosis
2293
Fig. 1 Reconstruction methods for m-PVa. Type-1, patch graft technique; Type-2, interposition graft technique; Type-3, anastomosis with huge shunt vessel.
All operations were performed with informed consent of the recipients or their parents and the donors and approved by the Ethics Committee of Kyushu University. This study was performed according to ethical guidelines for clinical studies of the Ministry of Health, Labour and Welfare of Japan.
2. Results The overall survival rate of the 57 cases after LDLT was 89.5% (51/57), and there was no significant difference in comparison with the 87.5% survival (14/16) in recipients with m-PVa. The causes of death in the two m-PVa
recipients were graft failure because of insufficient portal flow and complications because of a brain tumor found after LDLT. The age distribution and primary diagnostic indications for LDLT were summarized in Table 1. Although the infant patients had higher tendency to m-PVa application for reconstruction (55%), this method was applied in all age groups. The primary disease for LDLT was biliary atresia in all m-PVa recipients. Nine recipients with m-PVa (56%) had episodes of treatment of portal hypertension before LDLT (data not shown). Endoscopic injection sclerotherapy or endoscopic varices ligation and was applied for esophageal varices in 4 cases. The other 4 cases were treated with β-blocker to decrease the portal blood pressure. Splenectomy was
Fig. 2 The planning algorithm to choose techniques for portal vein reconstruction with PVT/PVS. Diameter matching was considered whether the recipient portal vein diameter was smaller than 4 mm. s-PVa indicates simple portal vein anastomosis.
2294
T. Matsuura et al.
performed before LDLT in one case because of severe hypersplenism with near normal liver function. The comparison among the types of portal vein reconstruction in m-PVa recipients was summarized in Table 2. Type-1 m-PVa was performed in 10 cases, Type-2 in 3 cases, and Type-3 in 3 cases. The mean age of the patients in these groups at LDLT was 4.6 ± 2.3, 3.0 ± 1.4, and 10.6 ± 6.2 years, respectively. The recipients in the Type-3 group were significantly older than those in other two groups. The liver graft was mostly used left lateral segment in Type-1 and -2 and the extended left lobe graft was used in all Type-3 recipients. The vessel graft in the Type-1 group was the donor inferior mesenteric vein (IMV) in 8 cases and the recipient jugular vein in 2. The vessel graft in the Type-2 group was the donor IMV in 2 and the donor saphenous vein in 1, and the 3 cases in the Type-3 group received renoportal, gonadal-portal, and coronary-portal anastomoses. The intraoperative portal vein flow (PVF) volume measured just after graft liver reperfusion was sufficient in all types of m-PVa, and slightly higher flow volume was obtained in Type-3 (mean PVF: Type-1, 177.2 ± 21.3; Type-2, 132.4 ± 16.4; Type-3, 291.8 ± 29.2 mL/min per 100 g liver). The clinical data of the liver function test after LDLT showed no significant differences among all 3 types except for the data during biopsy-proven acute cellular rejection. Postoperative portal vein complications occurred in 20% of the Type-1 patients (PVT in 2 cases), 33% of the Type-2 patients (PVS in 1 case), and 0% of the Type-3 patients. One complicated Type-1 case died because of insufficient portal flow despite re-reconstruction, and the other case was successfully re-reconstructed using a jumping graft. The Type-2 PVS case was successfully treated by interventional therapy and experienced no recurrence of PVS. Table 2 The comparison among the types of portal vein reconstruction in m-PVa recipients
Age at LDLT (y) Graft liver
Graft vessels
PVF/GV (mL/min per 100 g) Post portal vein complications
Type-1 (n = 10)
Type-2 (n = 3)
Type-3 (n = 3)
4.6 ± 2.3 LLS, 7 ex LL, 2 RL, 1 IMV, 8 Jugular vein, 2
3.0 ± 1.4
10.6 ± 6.2
LLS, 3
Ex LL, 3
IMV, 2 Saphenous vein, 1
177 ± 21.3
132 ± 16.4
Renoportal, 1 Gonadal vein, 1 Coronary vein, 1 291 ± 29.2
PVT 2 (20%)
PVS 1 (33%)
None (0%)
LLS indicates left lateral segment; ex LL, extended left lobe; RL, right lobe; GV, graft volume.
3. Discussion Portal vein thrombosis is no longer considered to be a contraindication for LDLT because of technical achievements such as the introduction of vessel grafting by Shaw in 1985 [4]. This technique also enabled surgeons to overcome the technical difficulties in cases with PVS or size-mismatched portal vein. Although vessel grafts can be easily obtained from a cadaveric donor, the availability of vessel grafts in LDLT is limited. Therefore, portal vein reconstruction with vessel grafts is still a challenging operation in LDLT. The incidence of pre-LDLT PVT was 10.5% (6/57 cases) in the current series, in contrast to 5% to 15% reported elsewhere [2]. Portal vein sclerosis is frequently seen in patients with biliary atresia because of repeated cholangitis. Saad et al reported that the pathologic examination of the portal vein showed the fibrous change at LDLT in 80% of post-Kasai cases [5]. The present study found that of 56% recipients with m-PVa had episodes of treatment of portal hypertension before LDLT. There are several risk factors for PVT, such as advanced age, Child-Pugh C, previous treatment of portal hypertension (sclerotherapy, Transjugular intrahepatic portosystemic shunt, shunt surgery, splenectomy), and previous surgical interventions [6]. The treatments of portal hypertension may change the hemodynamic state to low perfusion or reversed flow in the PV [7]. Pretransplant examinations, such as Doppler ultrasonography and CT, enable surgeons to plan the portal reconstruction. It is therefore necessary to harvest a vein graft from the donor when those data show a native portal vein diameter of ≤4 mm. Portal vein reconstruction requires a huge shunt vein when the PVT is extended to the bifurcation and accompanied by cavernous transformation. The potential surgical options for advanced PVT cases include different types of venous jump graft reconstruction or arterializations of the portal vein [8]. Cavoportal hemitransposition or renoportal anastomosis [3] had been recently advocated as creative surgical strategies. Regarding the type of vessel grafts, we think the donor IMV is the most ideal graft in Type-1 or -2 m-PVa because it is not only suitable for diameter and length but also safely obtained from the same surgical field. In recent years, the use of cryopreserved veins are reported to be useful from limited centers, but long-term outcome remains unstudied [8,9]. In our series, the portal vein reconstruction using shunt vessel (Type-3) was useful for the extended PVT recipients with huge shunt vessel, resulting to no experience of postoperative complications. However, because the vascular wall of the shunt vessel is usually thin, the anastomosis should be performed carefully not to split the vessel wall. The recipients in the Type-3 group were significantly older than those in other two groups. Because the long-term portal hypertensive state may result in the severe PVT and the formation of huge collateral shunt vessel, the age of Type-3 is higher than other two groups.
Modified portal vein anastomosis The optimal PVF volume to match the graft liver size is a controversial problem. Hypoperfusion often leads to graft failure; however, hyperperfusion can injure the hepatocytes, as observed in small-for-size syndrome. Troisi and de Hemptinne reported that the recovery of liver function is slower and not better with PVF/graft volume greater than 250 (mL/min per 100 g liver) after LDLT [10]. The optimal PVF was obtained (100-250 mL/min per 100 g liver) in Type-1 and -2 m-PVa. The mean PVF in Type-3 was slightly higher (291.8 mL/min per 100 g liver), but the postoperative course was excellent, and there were no PV complications after LDLT. Although the PVF was measured intraoperatively just after reperfusion in the current study, the PVF may decrease some time after reperfusion because of the graft edema or regulation of arterial and portal flows that occur over the sinusoids. Ou et al reported that slow portal flow (b10 cm/s) is a strongly predictable sign of post-LDLT PVT in patients with biliary atresia [11]. Therefore, obtaining optimal PVF is the most important factor in portal vein reconstruction. In conclusion, it is suggested that m-PVa was able to effectively overcome the operative the surgical difficulty and postoperative complications. The most important matter in portal anastomosis is to obtain a sufficient diameter and length to allow for sufficient portal blood flow volume. Pretransplant planning for selecting the optimal type of reconstruction is important for the success in LDLT for recipients with PVT/PVS.
Acknowledgments The authors would like to thank Dr Brian Quinn for reading the article. This work was supported in part by a
2295 grant-in-aid for scientific research from the Japanese Society for the Promotion of Science. This study was performed according to ethical guidelines for clinical studies of the Ministry of Health, Labour and Welfare of Japan.
References [1] Webster GJ, Burroughs AK, Riordan SM. Review article: portal vein thrombosis—new insights into aetiology and management. Aliment Pharmacol Ther 2005;21:1-9. [2] Nonami T, Yokoyama I, Iwatsuki S, et al. The incidence of portal vein thrombosis at liver transplantation. Hepatology 1992;16:1195-8. [3] Paskonis M, Jurgaitis J, Mehrabi A, et al. Surgical strategies for liver transplantation in the case of portal vein thrombosis—current role of cavoportal hemitransposition and renoportal anastomosis. Clin Transplant 2006;20:551-62. [4] Shaw BW, Iwatsuki S, Bron K, et al. Portal vein grafts in hepatic transplantation. Surg Gynecol Obstet 1985;161:66-8. [5] Saad S, Tanaka K, Inomata Y, et al. Portal vein reconstruction in pediatric liver transplantation from living donors. Ann Surg 1998;227: 275-81. [6] Ramos AP, Reigada CPH, Ataide EC, et al. Portal vein thrombosis and liver transplantation: Long term. Transplant Proc 2010;42:498-501. [7] Tao YF, Teng F, Wang ZX, et al. Liver transplant recipients with portal vein thrombosis: a single center retrospective study. Hepatobiliary Pancreat Dis Int 2009;8:34-9. [8] Kim SJ, Kim DJ, Park JH, et al. Clinical analysis of living donor liver transplantation in patients with portal vein thrombosis. Clin Transplant 2011;25:111-8. [9] Sugawara Y, Makuuchi M, Tamura S, et al. Portal vein reconstruction in adult living donor liver transplantation using cryopreserved vein grafts. Liver Transpl 2006;12:1233-6. [10] Troisi R, de Hemptinne B. Clinical relevance of adapting portal vein flow in living donor liver transplantation in adult patients. Liver Transpl 2003;9:S36-41. [11] Ou HY, Concejero AM, Huang TL, et al. Portal vein thrombosis in biliary atresia patients after living donor liver transplantation. Surgery 2011;149:40-7.