LIVER TRANSPLANTATION 20:245–246, 2014
LETTER FROM THE FRONTLINE
Functional Distal Splenorenal Shunt and Splenic Artery Ligation as Portal Flow Modulation in Left Lobe Living Donor Transplantation Received June 16, 2013; accepted October 22, 2013.
TO THE EDITORS: Here we present a living donor liver transplant with simultaneously performed distal splenorenal shunting and splenic artery ligation. The recipient was an 18year-old, 83.5-kg male with autoimmune hepatitis and end-stage liver disease who had a Model for End-Stage Liver Disease score of 23 (total bilirubin level 5 5.8 mg/ dL, creatinine level 5 0.6 mg/dL, international normalized ratio 5 2.51). The patient’s brother, a healthy 24year-old male weighing 88.6 kg, was the donor. A donor computed tomography angiogram demonstrated a nonreplaced arterial vasculature, a normal biliary anatomy, and patent hepatic veins. The portal vein had an anomaly in which the right posterior portal vein branch bifurcated from the main portal vein, and the right anterior portal vein branch bifurcated separately from the left portal vein. The total donor liver volume was 1780.5 mL, with 1274.4 mL coming from the right lobe and 506.1 mL coming from the left lobe (Fig. 1). Because the remnant liver volume (28.4%) was less than our standard for right lobe procurement and the donor had a portal vein variant that generally indicates donation of the left lobe, we proposed an inflow modification (as detailed by Hill et al.1) and the use of the smaller left lobe graft. Opting initially for splenic artery ligation, we would combine this maneuver with a portal vein shunt to further guard against small-forsize syndrome; the actual graft weight was noted to be 457 g on the back table (graft-weight/recipient ratio 5 0.55). As such, we dissected out the splenic vein and the left renal vein below the transverse mesentery to perform a distal splenorenal shunt. Notably, the left adrenal vein was found to be sizeable when we isolated the renal vein, and it was used as a conduit. Thus, after dividing the gonadal vein to ensure greater renal vein mobility, we anastomosed the adrenal vein in an end-to-side fashion to the splenic vein as described by Aydin et al.2 After the recipient liver was removed, the donor graft was implanted with the standard piggyback tech-
nique. We then ligated the splenic artery to optimize this undersized graft. Balancing the possibly reduced portal inflow against relative splanchnic hypertension, we opted to formally ligate the proximal splenic vein and convert the end-to-side spleno-adrenal shunt into a functional distal splenorenal shunt and establish a gradient of 2 mm Hg (Fig. 1). Recovery was prolonged by a bile leak from the liver’s cut surface and early graft dysfunction consistent with small-for-size syndrome, which was completely resolved within 2 months. At the time of this writing, the patient was symptom-free with normal hepatic function on standard immunosuppression. The use of the left lobe and the acceptance of donors with a predicted graft weight/recipient ratio < 0.8 increases access to living donor liver transplantation, although theoretically there is an augmented risk of graft failure.3 The use of portal flow modulation has been postulated to increase the utilization of small grafts in living donor liver transplantation.4,5 Guided by the principle that a selective shunt could lower the portal vein pressure without diverting the flow, we preferred to create a functional distal splenorenal shunt. Admittedly, in the comparison of shunts, there has been limited inquiry into the hemodynamics involved in living donor liver transplantation. Contrastingly, possibly because of the technical ease, splenic artery modulation in living donor liver transplantation has been more frequently explored and chronicled. Recently, Umeda et al.6 demonstrated that recipients with a graft weight/recipient ratio < 0.8 who underwent splenic artery embolization or ligation had decreased portal flow volume in comparison with nonmodulated cohorts. Moreover, splenic artery embolization has been shown to dramatically counter the effects of small-for-size syndrome in the postoperative period.7,8 Therefore, given our very real concerns about small-for-size syndrome in the recipient, we opted to ligate the splenic artery in combination with the creation of a functional distal splenorenal shunt.
Address reprint requests to Tomoaki Kato, M.D., Abdominal Organ Transplant and Hepatobiliary Surgery, Department of Surgery, Center for Liver Disease and Transplantation, 622 West 168th Street, PH 14 Center, Room 202, New York, NY 10032. Telephone: 212-305-4199; E-mail: [email protected] DOI 10.1002/lt.23790 View this article online at wileyonlinelibrary.com. LIVER TRANSPLANTATION. DOI 10.1002/lt. Published on behalf of the American Association for the Study of Liver Diseases
C 2013 American Association for the Study of Liver Diseases. V
246 LETTER FROM THE FRONTLINE
LIVER TRANSPLANTATION, February 2014
way at our center as part of the Adult-to-Adult Living Donor Liver Transplantation Cohort Study to address these issues. This experience may provide yet another impetus for exploring the use of smaller grafts and the technical methods that make this more permissible. Jay A. Graham, M.D. Benjamin Samstein, M.D. Jean C. Emond, M.D. Tomoaki Kato, M.D. Department of Surgery Columbia University College of Physicians and Surgeons New York, NY
REFERENCES
Figure. 1. The splenoadrenal shunt is seen with the adrenal vein (a) anastomosed to the splenic vein (s). Notably, the proximal splenic vein has been ligated (arrow) to created a functional distal splenorenal shunt. The implanted donor liver (L) is noted. Inset: the splenorenal shunt is demonstrated before ligation of the proximal splenic vein.
We present here a novel dichotomous strategy of inflow modulation and portal vein flow diversion that has yet to be described. Appropriately, we submit that the utility of such an intervention may be questioned because of our inability to abrogate small-for-size syndrome in this patient. Contrastingly, the counterargument presupposes that without the aforementioned portal venous flow alteration, the resultant graft dysfunction may have been worse. Perhaps, in hindsight, intraoperative flow studies may have been of use, but it is unclear what clinical role a static assessment of the portal vein should play in the setting of intravenous pressors, large volume shifts, and a hyperdynamic cardiac state. Moreover, changes in the graft resistance interposed between the systemic and splanchnic venous circulations may occur long after the patient leaves the operating room.9,10 A large, multicenter, prospective study of flow modulation in living donor liver transplantation is under-
1. Hill MJ, Hughes M, Jie T, Cohen M, Lake J, Payne WD, Humar A. Graft weight/recipient weight ratio: how well does it predict outcome after partial liver transplants? Liver Transpl 2009;15:1056-1062. 2. Aydin U, Yazici P, Kilic M. Porto-systemic shunt using adrenal vein as a conduit; an alternative procedure for spleno-renal shunt. BMC Surg 2007;7:7. 3. Campos BD, Botha JF. Strategies to optimize donor safety with smaller grafts for adult-to-adult living donor liver transplantation. Curr Opin Organ Transplant 2012; 17:230-234. 4. Troisi R, Cammu G, Militerno G, De Baerdemaeker L, Decruyenaere J, Hoste E, et al. Modulation of portal graft inflow: a necessity in adult living-donor liver transplantation? Ann Surg 2003;237:429-436. 5. Botha JF, Langnas AN, Campos BD, Grant WJ, Freise CE, Ascher NL, et al. Left lobe adult-to-adult living donor liver transplantation: small grafts and hemiportocaval shunts in the prevention of small-for-size syndrome. Liver Transpl 2010;16:649-657. 6. Umeda Y, Yagi T, Sadamori H, Matsukawa H, Matsuda H, Shinoura S, et al. Effects of prophylactic splenic artery modulation on portal overperfusion and liver regeneration in small-for-size graft. Transplantation 2008;86:673680. 7. Gruttadauria S, Mandala’ L, Miraglia R, Caruso S, Minervini MI, Biondo D, et al. Successful treatment of small-for-size syndrome in adult-to-adult living-related liver transplantation: single center series. Clin Transplant 2007;21:761-766. 8. Humar A, Beissel J, Crotteau S, Cohen M, Lake J, Payne WD. Delayed splenic artery occlusion for treatment of established small-for-size syndrome after partial liver transplantation. Liver Transpl 2009;15:163-168. 9. Kita Y, Harihara Y, Sano K, Hirata M, Kubota K, Takayama T, et al. Reversible hepatofugal portal flow after liver transplantation using a small-for-size graft from a living donor. Transpl Int 2001;14:217-222. 10. Cho SY, Kim SH, Lee KW, Park SJ, Han SS, Kim YK. Ligation of left renal vein as a salvage procedure for splenorenal shunt after living donor liver transplantation: a case report. Transplant Proc 2009;41:4243-4245.
LETTER FROM THE FRONTLINE
Functional Distal Splenorenal Shunt and Splenic Artery Ligation as Portal Flow Modulation in Left Lobe Living Donor Transplantation Received June 16, 2013; accepted October 22, 2013.
TO THE EDITORS: Here we present a living donor liver transplant with simultaneously performed distal splenorenal shunting and splenic artery ligation. The recipient was an 18year-old, 83.5-kg male with autoimmune hepatitis and end-stage liver disease who had a Model for End-Stage Liver Disease score of 23 (total bilirubin level 5 5.8 mg/ dL, creatinine level 5 0.6 mg/dL, international normalized ratio 5 2.51). The patient’s brother, a healthy 24year-old male weighing 88.6 kg, was the donor. A donor computed tomography angiogram demonstrated a nonreplaced arterial vasculature, a normal biliary anatomy, and patent hepatic veins. The portal vein had an anomaly in which the right posterior portal vein branch bifurcated from the main portal vein, and the right anterior portal vein branch bifurcated separately from the left portal vein. The total donor liver volume was 1780.5 mL, with 1274.4 mL coming from the right lobe and 506.1 mL coming from the left lobe (Fig. 1). Because the remnant liver volume (28.4%) was less than our standard for right lobe procurement and the donor had a portal vein variant that generally indicates donation of the left lobe, we proposed an inflow modification (as detailed by Hill et al.1) and the use of the smaller left lobe graft. Opting initially for splenic artery ligation, we would combine this maneuver with a portal vein shunt to further guard against small-forsize syndrome; the actual graft weight was noted to be 457 g on the back table (graft-weight/recipient ratio 5 0.55). As such, we dissected out the splenic vein and the left renal vein below the transverse mesentery to perform a distal splenorenal shunt. Notably, the left adrenal vein was found to be sizeable when we isolated the renal vein, and it was used as a conduit. Thus, after dividing the gonadal vein to ensure greater renal vein mobility, we anastomosed the adrenal vein in an end-to-side fashion to the splenic vein as described by Aydin et al.2 After the recipient liver was removed, the donor graft was implanted with the standard piggyback tech-
nique. We then ligated the splenic artery to optimize this undersized graft. Balancing the possibly reduced portal inflow against relative splanchnic hypertension, we opted to formally ligate the proximal splenic vein and convert the end-to-side spleno-adrenal shunt into a functional distal splenorenal shunt and establish a gradient of 2 mm Hg (Fig. 1). Recovery was prolonged by a bile leak from the liver’s cut surface and early graft dysfunction consistent with small-for-size syndrome, which was completely resolved within 2 months. At the time of this writing, the patient was symptom-free with normal hepatic function on standard immunosuppression. The use of the left lobe and the acceptance of donors with a predicted graft weight/recipient ratio < 0.8 increases access to living donor liver transplantation, although theoretically there is an augmented risk of graft failure.3 The use of portal flow modulation has been postulated to increase the utilization of small grafts in living donor liver transplantation.4,5 Guided by the principle that a selective shunt could lower the portal vein pressure without diverting the flow, we preferred to create a functional distal splenorenal shunt. Admittedly, in the comparison of shunts, there has been limited inquiry into the hemodynamics involved in living donor liver transplantation. Contrastingly, possibly because of the technical ease, splenic artery modulation in living donor liver transplantation has been more frequently explored and chronicled. Recently, Umeda et al.6 demonstrated that recipients with a graft weight/recipient ratio < 0.8 who underwent splenic artery embolization or ligation had decreased portal flow volume in comparison with nonmodulated cohorts. Moreover, splenic artery embolization has been shown to dramatically counter the effects of small-for-size syndrome in the postoperative period.7,8 Therefore, given our very real concerns about small-for-size syndrome in the recipient, we opted to ligate the splenic artery in combination with the creation of a functional distal splenorenal shunt.
Address reprint requests to Tomoaki Kato, M.D., Abdominal Organ Transplant and Hepatobiliary Surgery, Department of Surgery, Center for Liver Disease and Transplantation, 622 West 168th Street, PH 14 Center, Room 202, New York, NY 10032. Telephone: 212-305-4199; E-mail: [email protected] DOI 10.1002/lt.23790 View this article online at wileyonlinelibrary.com. LIVER TRANSPLANTATION. DOI 10.1002/lt. Published on behalf of the American Association for the Study of Liver Diseases
C 2013 American Association for the Study of Liver Diseases. V
246 LETTER FROM THE FRONTLINE
LIVER TRANSPLANTATION, February 2014
way at our center as part of the Adult-to-Adult Living Donor Liver Transplantation Cohort Study to address these issues. This experience may provide yet another impetus for exploring the use of smaller grafts and the technical methods that make this more permissible. Jay A. Graham, M.D. Benjamin Samstein, M.D. Jean C. Emond, M.D. Tomoaki Kato, M.D. Department of Surgery Columbia University College of Physicians and Surgeons New York, NY
REFERENCES
Figure. 1. The splenoadrenal shunt is seen with the adrenal vein (a) anastomosed to the splenic vein (s). Notably, the proximal splenic vein has been ligated (arrow) to created a functional distal splenorenal shunt. The implanted donor liver (L) is noted. Inset: the splenorenal shunt is demonstrated before ligation of the proximal splenic vein.
We present here a novel dichotomous strategy of inflow modulation and portal vein flow diversion that has yet to be described. Appropriately, we submit that the utility of such an intervention may be questioned because of our inability to abrogate small-for-size syndrome in this patient. Contrastingly, the counterargument presupposes that without the aforementioned portal venous flow alteration, the resultant graft dysfunction may have been worse. Perhaps, in hindsight, intraoperative flow studies may have been of use, but it is unclear what clinical role a static assessment of the portal vein should play in the setting of intravenous pressors, large volume shifts, and a hyperdynamic cardiac state. Moreover, changes in the graft resistance interposed between the systemic and splanchnic venous circulations may occur long after the patient leaves the operating room.9,10 A large, multicenter, prospective study of flow modulation in living donor liver transplantation is under-
1. Hill MJ, Hughes M, Jie T, Cohen M, Lake J, Payne WD, Humar A. Graft weight/recipient weight ratio: how well does it predict outcome after partial liver transplants? Liver Transpl 2009;15:1056-1062. 2. Aydin U, Yazici P, Kilic M. Porto-systemic shunt using adrenal vein as a conduit; an alternative procedure for spleno-renal shunt. BMC Surg 2007;7:7. 3. Campos BD, Botha JF. Strategies to optimize donor safety with smaller grafts for adult-to-adult living donor liver transplantation. Curr Opin Organ Transplant 2012; 17:230-234. 4. Troisi R, Cammu G, Militerno G, De Baerdemaeker L, Decruyenaere J, Hoste E, et al. Modulation of portal graft inflow: a necessity in adult living-donor liver transplantation? Ann Surg 2003;237:429-436. 5. Botha JF, Langnas AN, Campos BD, Grant WJ, Freise CE, Ascher NL, et al. Left lobe adult-to-adult living donor liver transplantation: small grafts and hemiportocaval shunts in the prevention of small-for-size syndrome. Liver Transpl 2010;16:649-657. 6. Umeda Y, Yagi T, Sadamori H, Matsukawa H, Matsuda H, Shinoura S, et al. Effects of prophylactic splenic artery modulation on portal overperfusion and liver regeneration in small-for-size graft. Transplantation 2008;86:673680. 7. Gruttadauria S, Mandala’ L, Miraglia R, Caruso S, Minervini MI, Biondo D, et al. Successful treatment of small-for-size syndrome in adult-to-adult living-related liver transplantation: single center series. Clin Transplant 2007;21:761-766. 8. Humar A, Beissel J, Crotteau S, Cohen M, Lake J, Payne WD. Delayed splenic artery occlusion for treatment of established small-for-size syndrome after partial liver transplantation. Liver Transpl 2009;15:163-168. 9. Kita Y, Harihara Y, Sano K, Hirata M, Kubota K, Takayama T, et al. Reversible hepatofugal portal flow after liver transplantation using a small-for-size graft from a living donor. Transpl Int 2001;14:217-222. 10. Cho SY, Kim SH, Lee KW, Park SJ, Han SS, Kim YK. Ligation of left renal vein as a salvage procedure for splenorenal shunt after living donor liver transplantation: a case report. Transplant Proc 2009;41:4243-4245.
