LIVER TRANSPLANTATION 21:135–139, 2015
LETTER FROM THE FRONTLINE
Successful Living Donor Liver Transplantation With Cavoportal Hemitransposition in Diffuse Portomesenteric Thrombosis Received July 22, 2014; accepted September 16, 2014.
TO THE EDITORS: Portal vein thrombosis (PVT) is not uncommon in patients with end-stage liver disease who are undergoing orthotopic liver transplantation (OLT). The prevalence of PVT at the time of OLT is variable and has been reported in the literature to be between 2.1% and 26%.1 PVT was once considered to be an absolute contraindication to OLT because of the inherent technical difficulties that it posed and the accompanying high rate of mortality. These technical difficulties included an increased risk of intraoperative bleeding and an inability to establish adequate portal blood flow with resulting allograft nonfunction. However, with greater experience and improved surgical techniques, PVT is no longer an absolute contraindication. The surgical techniques that are used depend on the extent of PVT.1 In the presence of diffuse thrombosis of the splenomesenteric venous system, the ideal treatment is a multivisceral transplant. However, in India, where there are few deceased donors, cavoportal hemitransposition (CPHT) is one of the options used to obtain portal inflow to the liver. This procedure is surgically complex and has traditionally had high postoperative morbidity and mortality rates.2-4 Most of the literature on CPHT has come from centers performing deceased donor liver transplantation (DDLT).2-4 The literature on CPHT in living donor liver transplantation (LDLT) has been limited to a few case reports.5 CPHT is still considered to be a relative or even absolute contraindication for LDLT by numerous groups.6 Here we describe a successful case of LDLT with CPHT performed in a patient who had end-stage liver disease from cryptogenic cirrhosis with diffuse portomesenteric thrombosis (Yerdel grade 4).
CASE REPORT
Preoperative Evaluation and Operative Technique A 36-year-old man presented with abdominal distension, jaundice, 2 bouts of hematemesis, and 1 episode of hepatic encephalopathy. Investigations were suggestive of cryptogenic cirrhosis leading to end-stage liver disease with diffuse portomesenteric thrombosis (Yerdel grade 4). The patient had undergone upper gastrointestinal endoscopy and successful esophageal variceal ligation twice for hematemesis. He had ascites, for which he was taking diuretics, and had undergone paracentesis once. Also, anticoagulation therapy for PVT had failed. His Child-Turcotte-Pugh score was 10/15, and his Model for End-Stage Liver Disease score was 22. Before coming to our center, the patient had been refused liver transplantation at 3 centers in our country because of his diffuse portomesenteric thrombosis. A preoperative computed tomography (CT) angiogram revealed features of chronic liver disease; diffuse thrombosis of the splenic vein, superior mesenteric vein (SMV), main portal vein (PV), and right and left PVs; extensive collaterals; massive splenomegaly; ascites; and a naturally occurring mesocaval shunt (Fig. 1). The blood investigations also revealed pancytopenia resulting from hypersplenism. The decision to perform LDLT with CPHT was made in light of the CT findings (Fig. 2) because DDLT is not a readily available option in our country and the decision to perform renoportal or cavoportal transposition is driven by the location of the shunts. If we find predominant splenorenal shunts joining the left renal vein, then a renoportal transposition is preferred, but a cavoportal anastomosis is chosen if the shunts are predominantly in the cava. The
Potential conflict of interest: Nothing to report. The institutional review board of Sir Ganga Ram Hospital has approved this case for publication, provided that the patient’s identity is not revealed. Address reprint requests to Manish Srivastava, M.B.B.S., M.S., D.N.B., Department of Surgical Gastroenterology and Liver Transplantation, Sir Ganga Ram Hospital, Old Rajinder Nagar, New Delhi, India 110060. Telephone: 191-9910276749; Fax: -91-11-42252224; E-mail: [email protected] DOI 10.1002/lt.24008 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 2014 American Association for the Study of Liver Diseases. V
136
LIVER TRANSPLANTATION, January 2015
Figure. 1. Preoperative CT angiogram showing diffuse thrombosis of the portomesenteric system and portosystemic collaterals draining into the IVC.
preoperative CT findings were confirmed during surgery. Recipient hepatectomy was performed in a piggyback fashion. The splenic artery was ligated to reduce portal hypertension and hypersplenism. The graft was a living donor right lobe with the middle hepatic vein (MHV). Its weight was 690 g, and the graft-to-recipient weight ratio was 1.06. In back-table reconstruction, hepatic venoplasty of the MHV and a segment 8 vein was performed. MHV reconstruction was carried out with a cryopreserved vein graft as a conduit. The hepatic venous reconstruction used an anastomosis of the graft right hepatic vein to the recipient right hepatic vein with the inferior vena cava (IVC) with a 4-0 Prolene continuous suture and the MHV conduit to the IVC with a 5-0 Prolene continuous suture. The suprarenal IVC was stapled with a vascular stapler and then divided just below the staple line. The lower end of the IVC was partially closed with 5-0 Prolene suture to reduce the caliber of the IVC to match the graft PV caliber. The end-to-end cavoportal anastomosis was fashioned between the lower end of the recip-
Figure. 2.
Diagram of LDLT with CPHT (with a right lobe graft).
ient IVC and the graft PV with a 5-0 Prolene continuous suture and the use of a growth factor to adjust for the size discrepancy between the veins (Fig. 3). The hepatic artery (HA) anastomosis (7-0 Prolene interrupted sutures) and the bile duct anastomosis (Roux-en-Y hepaticojejunostomy, 6-0 polydioxanone interrupted sutures) were then performed. The cold ischemia time was 119 minutes, and the warm ischemia time was 64 minutes. The total operative time was 960 minutes, and there was an intraoperative transfusion of 8 U of blood. The small bowel remained well perfused throughout the procedure. The patency of the vascular anastomosis was assessed with serial intra- and postoperative Doppler ultrasonography. Intraoperative Doppler ultrasonography demonstrated good flow through all the anastomoses, including the cavoportal anastomosis (Fig. 3).
Postoperative Outcome The patient was extubated on postoperative day (POD) 1. An oral diet was started on POD 4. He was shifted from the transplant intensive care unit to a room in the ward on POD 6 and was discharged from the hospital to his home on POD 10. He developed transient renal dysfunction in the postoperative period, with his serum creatinine level rising to 3 mg/dL on POD 5; it returned to normal levels by POD 19. He also developed bilateral lower limb edema and mild ascites that improved gradually over 3 months. However, he did not develop any venous thrombosis or small bowel ischemia. The patient was immunosuppressed with a dual-agent regimen of tacrolimus and prednisone. On POD 18, he was again admitted with pancytopenia. He was administered 2 U of blood and discharged. CT angiography and Doppler ultrasonography showed a patent cavoportal anastomosis with a good flow of 1.1 L/minute (Fig. 4). His renal and liver function tests were normal. He was again admitted with an episode of hematemesis resulting from unrelieved portal hypertension and persistent pancytopenia. He was discharged after medical management of this problem. At the time of this writing, after a follow-up period of 26 months, he was alive and well. Doppler ultrasonography during his last visit showed a patent
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Figure. 3. Intraoperative photographs of the PV completely occluded by thrombosis, the IVC transection just below the stapled line, and the completed cavoportal anastomosis. Intraoperative Doppler ultrasonography demonstrates good flow through the cavoportal anastomosis.
cavoportal anastomosis with a good flow of 1 L/minute. His blood investigations showed normal liver and renal function along with persistent pancytopenia.
Figure. 4. Postoperative CT angiogram showing the patent cavoportal anastomosis.
DISCUSSION We have summarized the 26-month outcome of successful LDLT with CPHT for end-stage liver disease with diffuse portomesenteric thrombosis. LDLT with end-to-end CPHT is thus a feasible option. There may be some complications related to portal hypertension in the initial postoperative period, but in the long term, the graft liver function remains normal, and there is also improvement in the portal hypertension. PVT is being increasingly recognized in patients with end-stage liver disease who are undergoing OLT. In the past, PVT has been considered to be an absolute contraindication to OLT. However, with improvements in surgical techniques and with the experience gained with DDLT at various centers, liver transplantation is now considered feasible even in the presence of PVT.2-4 The reported incidence of PVT in published DDLT series has been 2.1% to 26%,1 but in the LDLT scenario, the experience has been different, with the reported incidence of PVT in LDLT recipients being only 1%.6 Sixty-two percent of centers still consider PVT to be a relative or absolute contraindication to LDLT.6
138
CPHT, a technique in which the IVC is used for portal inflow to the allograft, is proposed as a salvage procedure in the presence of diffuse PVT when no other option is technically feasible. Starzl and coworkers studied complete cavoportal transposition in dogs to determine the effects of systemic venous inflow on liver function and histology, and they found that liver function and histology remained normal when systemic venous blood was used as the portal inflow into the liver.7 The use of this technique in clinical liver transplantation was first reported in 1998 by Tzakis et al.2 in a 4-center experience of 9 patients and a later series of 11 successfully treated patients. In a series of 23 patients undergoing liver transplantation with CPHT described by Selvaggi et al.,3 the overall survival was 60% at 1 year and 38% at 3 years. The most common cause of death was sepsis with multiorgan failure, and this was followed by pulmonary embolism. Seven patients had postoperative gastrointestinal bleeding episodes, 6 developed thrombosis of the vena cava, and almost all patients had some degree of postoperative ascites. Renal dysfunction was commonly seen even beyond the first month after transplantation. In a review of 23 publications, Borchert8 found 71 reported cases of CPHT worldwide before 2008. Among these patients, 62 had whole cadaveric grafts, and 7 pediatric patients had left lateral segment grafts. Thirty-two of 71 patients did not survive: 12 of these patients died within 4 weeks of transplantation. The most common cause of death was sepsis with multiorgan failure, and this was followed by pulmonary embolism, primary nonfunction of the allograft, rejection, and cardiac failure. However, all these series were from centers running mainly a DDLT program. In contrast to DDLT, reports on LDLT with CPHT are scarce. Egawa et al.9 described a series of 39 patients with PVT among 404 LDLT recipients. They found that candidates with complete PVT and a Model for End-Stage Liver Disease score > 25 were poor candidates for LDLT. The single patient who underwent end-to-end CPHT in their series died within 2 weeks of transplantation from multiorgan failure. This led them to conclude that end-to-end CPHT might be a contraindication to adult LDLT with a hemiliver. In another article, Kim et al.10 reported their experience of 18 patients with PVT in a series of 97 LDLT recipients. No patient underwent CPHT in their series. There are only a few case reports of LDLT with CPHT in the literature.5 Therefore, our report of a successful case of LDLT with CPHT with allograft and patient survival 26 months after transplantation seems worthy of attention. CPHT necessitates performing an anastomosis between the allograft PV and the suprarenal recipient IVC in an end-to-side or end-to-end manner. When the PV does not reach the IVC easily, an interposition vein graft is necessary. Blood flow through the IVC is diverted toward the new liver either by ligation of the IVC with a clip or by formal division; this creates a functional end-to-end anastomosis. Drawbacks of this
LIVER TRANSPLANTATION, January 2015
procedure include the persistence of portal hypertension and the continuing risk of bleeding from gastroesophageal varices and hypertensive gastropathy, which is reported to have occurred in 37% of cases in 1 series.11 Spontaneous shunts or surgical shunts constructed during previous operations or during transplantation may have a protective effect against these complications. These complications have been treated by splenectomy, gastric devascularization, splenic artery embolization, and endoscopic intervention. The use of intraoperative splenectomy and gastric devascularization as prophylaxis was proposed in earlier series,2,12 but later reports3 have found it unnecessary. Diverting the total IVC flow through the liver may result in small-for-size syndrome with associated hyperperfusion, especially in LDLT. A small living donor graft would be susceptible to injury from a high inflow. Therefore, we would require a graft-torecipient weight ratio of at least 1% in these cases, although we would go as low as 0.7% in otherwise technically straightforward living donor transplants. However, in India, we do not have the luxury of listing a patient for a deceased donor graft because the mortality rate on the waiting list for the few deceased donor grafts available is more than 90%. In this scenario, if only 1 prospective donor is available, a somewhat higher than optimal risk may be acceptable to the recipient and to the transplant team. The excessive systemic flow from the IVC through the hepatic microvascular bed after reperfusion may produce flow injury to the sinusoidal endothelial cells and activation of Kupffer cells and cause a severe reperfusion injury. There may be a risk of primary nonfunction of the allograft. Another hemodynamic implication of all IVC blood passing through a sievelike barrier (the liver) instead of the retrohepatic vena cava, which provides minimum resistance to the flow, is the development of complications such as ascites, renal dysfunction, and lower-body edema along with an increased risk of deep venous thrombosis (DVT).2,12 Persistent ascites, lower extremity edema, and renal dysfunction improve with time and are treated through the avoidance of fluid overload and the judicious use of diuretic therapy until resolution occurs.12 Prophylaxis against DVT is required. In a recent review4 of 17 series on CPHT covering 56 patients, ascites and lower body edema developed in 55% of patients, gastrointestinal bleeding developed in 30%, and renal dysfunction developed in 48%. Our patient twice received endoscopic treatment for bleeding varices in the preoperative period. Intraoperatively, we ligated the splenic artery in an attempt to ameliorate the portal hypertension and hypersplenism. In the postoperative period, he had 1 episode of hematemesis from persistent portal hypertension that was successfully managed medically. Although he continued to have pancytopenia resulting from the hypersplenism and required blood and platelet transfusions, his gastroesophageal varices and hypertensive gastropathy improved with time. He developed postoperative ascites, lower limb edema,
LIVER TRANSPLANTATION, Vol. 21, No. 1, 2015
and transient renal dysfunction that improved with conservative management, but he had no episodes of DVT or pulmonary embolism. Twenty-six months after transplantation, the patient was alive and had a patent cavoportal anastomosis with normal liver and renal function. In conclusion, LDLT with CPHT is feasible, safe, and effective in select recipients who have diffuse thrombosis of the portomesenteric system. Final recipient selection depends on the experience of the liver transplant surgeon and team. Manish Srivastava, M.B.B.S., M.S., D.N.B. Vinay Kumaran, M.B.B.S., M.S., M.Ch. Samiran Nundy, M.A., M.Chir., F.R.C.S., F.R.C.P. Naimish Mehta, M.B.B.S., M.S., F.A.C.R.S.I., F.E.B.S. Department of Surgical Gastroenterology and Liver Transplantation Sir Ganga Ram Hospital Old Rajinder Nagar, New Delhi, India
REFERENCES 1. Yerdel MA, Gunson B, Mirza D, Karayalc¸in K, Olliff S, Buckels J, et al. Portal vein thrombosis in adults undergoing liver transplantation: risk factors, screening, management, and outcome. Transplantation 2000;69: 1873-1881. 2. Tzakis AG, Kirkegaard P, Pinna AD, Jovine E, Misiakos EP, Maziotti A, et al. Liver transplantation with cavoportal hemitransposition in the presence of diffuse portal vein thrombosis. Transplantation 1998;65:619-624. 3. Selvaggi G, Weppler D, Nishida S, Moon J, Levi D, Kato T, Tzakis AG. Ten-year experience in porto-caval hemitransposition for liver transplantation in the presence
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of portal vein thrombosis. Am J Transplant 2007;7: 454-460. 4. Bhangui P, Lim C, Salloum C, Andreani P, Sebbagh M, Hoti E, et al. Caval inflow to the graft for liver transplantation in patients with diffuse portal vein thrombosis: a 12-year experience. Ann Surg 2011;254:1008-1016. 5. Shi Z, Yan L, Wen T, Chen Z. Cavoportal hemitransposition in an adult-to-adult, living-donor liver transplantation. Dig Liver Dis 2011;43:e2. 6. Kadry Z, Selzner N, Handschin A, M€ ullhaupt B, Renner EL, Clavien PA. Living donor liver transplantation in patients with portal vein thrombosis: a survey and review of technical issues. Transplantation 2002;74:696-701. 7. Meyer WH Jr., Starzl TE. The reverse portacaval shunt. Surgery. 1959;7:531-534. 8. Borchert DH. Cavoportal hemitransposition for the simultaneous thrombosis of the caval and portal systems—a review of the literature. Ann Hepatol 2008;7: 200-211. 9. Egawa H, Tanaka K, Kasahara M, Takada Y, Oike F, Ogawa K, et al. Single center experience of 39 patients with preoperative portal vein thrombosis among 404 adult living donor liver transplantations. Liver Transpl 2006;12:1512-1518. 10. Kim JD, Choi DL, Han YS. An early single-center experience of portal vein thrombosis in living donor liver transplantation: clinical feature, management and outcome. J Korean Surg Soc 2011;81:35-42. 11. Gerunda GE, Merenda R, Neri D, Angeli P, Barbazza F, Valmasoni M, et al. Cavoportal hemitransposition: a successful way to overcome the problem of total portosplenomesenteric thrombosis in liver transplantation. Liver Transpl 2002;8:72-75. 12. Pinna AD, Nery J, Kato T, Levi D, Nishida S, Tzakis AG. Liver transplant with portocaval hemitransposition: experience at the University of Miami. Transplant Proc 2001; 33:1329-1330.
LETTER FROM THE FRONTLINE
Successful Living Donor Liver Transplantation With Cavoportal Hemitransposition in Diffuse Portomesenteric Thrombosis Received July 22, 2014; accepted September 16, 2014.
TO THE EDITORS: Portal vein thrombosis (PVT) is not uncommon in patients with end-stage liver disease who are undergoing orthotopic liver transplantation (OLT). The prevalence of PVT at the time of OLT is variable and has been reported in the literature to be between 2.1% and 26%.1 PVT was once considered to be an absolute contraindication to OLT because of the inherent technical difficulties that it posed and the accompanying high rate of mortality. These technical difficulties included an increased risk of intraoperative bleeding and an inability to establish adequate portal blood flow with resulting allograft nonfunction. However, with greater experience and improved surgical techniques, PVT is no longer an absolute contraindication. The surgical techniques that are used depend on the extent of PVT.1 In the presence of diffuse thrombosis of the splenomesenteric venous system, the ideal treatment is a multivisceral transplant. However, in India, where there are few deceased donors, cavoportal hemitransposition (CPHT) is one of the options used to obtain portal inflow to the liver. This procedure is surgically complex and has traditionally had high postoperative morbidity and mortality rates.2-4 Most of the literature on CPHT has come from centers performing deceased donor liver transplantation (DDLT).2-4 The literature on CPHT in living donor liver transplantation (LDLT) has been limited to a few case reports.5 CPHT is still considered to be a relative or even absolute contraindication for LDLT by numerous groups.6 Here we describe a successful case of LDLT with CPHT performed in a patient who had end-stage liver disease from cryptogenic cirrhosis with diffuse portomesenteric thrombosis (Yerdel grade 4).
CASE REPORT
Preoperative Evaluation and Operative Technique A 36-year-old man presented with abdominal distension, jaundice, 2 bouts of hematemesis, and 1 episode of hepatic encephalopathy. Investigations were suggestive of cryptogenic cirrhosis leading to end-stage liver disease with diffuse portomesenteric thrombosis (Yerdel grade 4). The patient had undergone upper gastrointestinal endoscopy and successful esophageal variceal ligation twice for hematemesis. He had ascites, for which he was taking diuretics, and had undergone paracentesis once. Also, anticoagulation therapy for PVT had failed. His Child-Turcotte-Pugh score was 10/15, and his Model for End-Stage Liver Disease score was 22. Before coming to our center, the patient had been refused liver transplantation at 3 centers in our country because of his diffuse portomesenteric thrombosis. A preoperative computed tomography (CT) angiogram revealed features of chronic liver disease; diffuse thrombosis of the splenic vein, superior mesenteric vein (SMV), main portal vein (PV), and right and left PVs; extensive collaterals; massive splenomegaly; ascites; and a naturally occurring mesocaval shunt (Fig. 1). The blood investigations also revealed pancytopenia resulting from hypersplenism. The decision to perform LDLT with CPHT was made in light of the CT findings (Fig. 2) because DDLT is not a readily available option in our country and the decision to perform renoportal or cavoportal transposition is driven by the location of the shunts. If we find predominant splenorenal shunts joining the left renal vein, then a renoportal transposition is preferred, but a cavoportal anastomosis is chosen if the shunts are predominantly in the cava. The
Potential conflict of interest: Nothing to report. The institutional review board of Sir Ganga Ram Hospital has approved this case for publication, provided that the patient’s identity is not revealed. Address reprint requests to Manish Srivastava, M.B.B.S., M.S., D.N.B., Department of Surgical Gastroenterology and Liver Transplantation, Sir Ganga Ram Hospital, Old Rajinder Nagar, New Delhi, India 110060. Telephone: 191-9910276749; Fax: -91-11-42252224; E-mail: [email protected] DOI 10.1002/lt.24008 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 2014 American Association for the Study of Liver Diseases. V
136
LIVER TRANSPLANTATION, January 2015
Figure. 1. Preoperative CT angiogram showing diffuse thrombosis of the portomesenteric system and portosystemic collaterals draining into the IVC.
preoperative CT findings were confirmed during surgery. Recipient hepatectomy was performed in a piggyback fashion. The splenic artery was ligated to reduce portal hypertension and hypersplenism. The graft was a living donor right lobe with the middle hepatic vein (MHV). Its weight was 690 g, and the graft-to-recipient weight ratio was 1.06. In back-table reconstruction, hepatic venoplasty of the MHV and a segment 8 vein was performed. MHV reconstruction was carried out with a cryopreserved vein graft as a conduit. The hepatic venous reconstruction used an anastomosis of the graft right hepatic vein to the recipient right hepatic vein with the inferior vena cava (IVC) with a 4-0 Prolene continuous suture and the MHV conduit to the IVC with a 5-0 Prolene continuous suture. The suprarenal IVC was stapled with a vascular stapler and then divided just below the staple line. The lower end of the IVC was partially closed with 5-0 Prolene suture to reduce the caliber of the IVC to match the graft PV caliber. The end-to-end cavoportal anastomosis was fashioned between the lower end of the recip-
Figure. 2.
Diagram of LDLT with CPHT (with a right lobe graft).
ient IVC and the graft PV with a 5-0 Prolene continuous suture and the use of a growth factor to adjust for the size discrepancy between the veins (Fig. 3). The hepatic artery (HA) anastomosis (7-0 Prolene interrupted sutures) and the bile duct anastomosis (Roux-en-Y hepaticojejunostomy, 6-0 polydioxanone interrupted sutures) were then performed. The cold ischemia time was 119 minutes, and the warm ischemia time was 64 minutes. The total operative time was 960 minutes, and there was an intraoperative transfusion of 8 U of blood. The small bowel remained well perfused throughout the procedure. The patency of the vascular anastomosis was assessed with serial intra- and postoperative Doppler ultrasonography. Intraoperative Doppler ultrasonography demonstrated good flow through all the anastomoses, including the cavoportal anastomosis (Fig. 3).
Postoperative Outcome The patient was extubated on postoperative day (POD) 1. An oral diet was started on POD 4. He was shifted from the transplant intensive care unit to a room in the ward on POD 6 and was discharged from the hospital to his home on POD 10. He developed transient renal dysfunction in the postoperative period, with his serum creatinine level rising to 3 mg/dL on POD 5; it returned to normal levels by POD 19. He also developed bilateral lower limb edema and mild ascites that improved gradually over 3 months. However, he did not develop any venous thrombosis or small bowel ischemia. The patient was immunosuppressed with a dual-agent regimen of tacrolimus and prednisone. On POD 18, he was again admitted with pancytopenia. He was administered 2 U of blood and discharged. CT angiography and Doppler ultrasonography showed a patent cavoportal anastomosis with a good flow of 1.1 L/minute (Fig. 4). His renal and liver function tests were normal. He was again admitted with an episode of hematemesis resulting from unrelieved portal hypertension and persistent pancytopenia. He was discharged after medical management of this problem. At the time of this writing, after a follow-up period of 26 months, he was alive and well. Doppler ultrasonography during his last visit showed a patent
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Figure. 3. Intraoperative photographs of the PV completely occluded by thrombosis, the IVC transection just below the stapled line, and the completed cavoportal anastomosis. Intraoperative Doppler ultrasonography demonstrates good flow through the cavoportal anastomosis.
cavoportal anastomosis with a good flow of 1 L/minute. His blood investigations showed normal liver and renal function along with persistent pancytopenia.
Figure. 4. Postoperative CT angiogram showing the patent cavoportal anastomosis.
DISCUSSION We have summarized the 26-month outcome of successful LDLT with CPHT for end-stage liver disease with diffuse portomesenteric thrombosis. LDLT with end-to-end CPHT is thus a feasible option. There may be some complications related to portal hypertension in the initial postoperative period, but in the long term, the graft liver function remains normal, and there is also improvement in the portal hypertension. PVT is being increasingly recognized in patients with end-stage liver disease who are undergoing OLT. In the past, PVT has been considered to be an absolute contraindication to OLT. However, with improvements in surgical techniques and with the experience gained with DDLT at various centers, liver transplantation is now considered feasible even in the presence of PVT.2-4 The reported incidence of PVT in published DDLT series has been 2.1% to 26%,1 but in the LDLT scenario, the experience has been different, with the reported incidence of PVT in LDLT recipients being only 1%.6 Sixty-two percent of centers still consider PVT to be a relative or absolute contraindication to LDLT.6
138
CPHT, a technique in which the IVC is used for portal inflow to the allograft, is proposed as a salvage procedure in the presence of diffuse PVT when no other option is technically feasible. Starzl and coworkers studied complete cavoportal transposition in dogs to determine the effects of systemic venous inflow on liver function and histology, and they found that liver function and histology remained normal when systemic venous blood was used as the portal inflow into the liver.7 The use of this technique in clinical liver transplantation was first reported in 1998 by Tzakis et al.2 in a 4-center experience of 9 patients and a later series of 11 successfully treated patients. In a series of 23 patients undergoing liver transplantation with CPHT described by Selvaggi et al.,3 the overall survival was 60% at 1 year and 38% at 3 years. The most common cause of death was sepsis with multiorgan failure, and this was followed by pulmonary embolism. Seven patients had postoperative gastrointestinal bleeding episodes, 6 developed thrombosis of the vena cava, and almost all patients had some degree of postoperative ascites. Renal dysfunction was commonly seen even beyond the first month after transplantation. In a review of 23 publications, Borchert8 found 71 reported cases of CPHT worldwide before 2008. Among these patients, 62 had whole cadaveric grafts, and 7 pediatric patients had left lateral segment grafts. Thirty-two of 71 patients did not survive: 12 of these patients died within 4 weeks of transplantation. The most common cause of death was sepsis with multiorgan failure, and this was followed by pulmonary embolism, primary nonfunction of the allograft, rejection, and cardiac failure. However, all these series were from centers running mainly a DDLT program. In contrast to DDLT, reports on LDLT with CPHT are scarce. Egawa et al.9 described a series of 39 patients with PVT among 404 LDLT recipients. They found that candidates with complete PVT and a Model for End-Stage Liver Disease score > 25 were poor candidates for LDLT. The single patient who underwent end-to-end CPHT in their series died within 2 weeks of transplantation from multiorgan failure. This led them to conclude that end-to-end CPHT might be a contraindication to adult LDLT with a hemiliver. In another article, Kim et al.10 reported their experience of 18 patients with PVT in a series of 97 LDLT recipients. No patient underwent CPHT in their series. There are only a few case reports of LDLT with CPHT in the literature.5 Therefore, our report of a successful case of LDLT with CPHT with allograft and patient survival 26 months after transplantation seems worthy of attention. CPHT necessitates performing an anastomosis between the allograft PV and the suprarenal recipient IVC in an end-to-side or end-to-end manner. When the PV does not reach the IVC easily, an interposition vein graft is necessary. Blood flow through the IVC is diverted toward the new liver either by ligation of the IVC with a clip or by formal division; this creates a functional end-to-end anastomosis. Drawbacks of this
LIVER TRANSPLANTATION, January 2015
procedure include the persistence of portal hypertension and the continuing risk of bleeding from gastroesophageal varices and hypertensive gastropathy, which is reported to have occurred in 37% of cases in 1 series.11 Spontaneous shunts or surgical shunts constructed during previous operations or during transplantation may have a protective effect against these complications. These complications have been treated by splenectomy, gastric devascularization, splenic artery embolization, and endoscopic intervention. The use of intraoperative splenectomy and gastric devascularization as prophylaxis was proposed in earlier series,2,12 but later reports3 have found it unnecessary. Diverting the total IVC flow through the liver may result in small-for-size syndrome with associated hyperperfusion, especially in LDLT. A small living donor graft would be susceptible to injury from a high inflow. Therefore, we would require a graft-torecipient weight ratio of at least 1% in these cases, although we would go as low as 0.7% in otherwise technically straightforward living donor transplants. However, in India, we do not have the luxury of listing a patient for a deceased donor graft because the mortality rate on the waiting list for the few deceased donor grafts available is more than 90%. In this scenario, if only 1 prospective donor is available, a somewhat higher than optimal risk may be acceptable to the recipient and to the transplant team. The excessive systemic flow from the IVC through the hepatic microvascular bed after reperfusion may produce flow injury to the sinusoidal endothelial cells and activation of Kupffer cells and cause a severe reperfusion injury. There may be a risk of primary nonfunction of the allograft. Another hemodynamic implication of all IVC blood passing through a sievelike barrier (the liver) instead of the retrohepatic vena cava, which provides minimum resistance to the flow, is the development of complications such as ascites, renal dysfunction, and lower-body edema along with an increased risk of deep venous thrombosis (DVT).2,12 Persistent ascites, lower extremity edema, and renal dysfunction improve with time and are treated through the avoidance of fluid overload and the judicious use of diuretic therapy until resolution occurs.12 Prophylaxis against DVT is required. In a recent review4 of 17 series on CPHT covering 56 patients, ascites and lower body edema developed in 55% of patients, gastrointestinal bleeding developed in 30%, and renal dysfunction developed in 48%. Our patient twice received endoscopic treatment for bleeding varices in the preoperative period. Intraoperatively, we ligated the splenic artery in an attempt to ameliorate the portal hypertension and hypersplenism. In the postoperative period, he had 1 episode of hematemesis from persistent portal hypertension that was successfully managed medically. Although he continued to have pancytopenia resulting from the hypersplenism and required blood and platelet transfusions, his gastroesophageal varices and hypertensive gastropathy improved with time. He developed postoperative ascites, lower limb edema,
LIVER TRANSPLANTATION, Vol. 21, No. 1, 2015
and transient renal dysfunction that improved with conservative management, but he had no episodes of DVT or pulmonary embolism. Twenty-six months after transplantation, the patient was alive and had a patent cavoportal anastomosis with normal liver and renal function. In conclusion, LDLT with CPHT is feasible, safe, and effective in select recipients who have diffuse thrombosis of the portomesenteric system. Final recipient selection depends on the experience of the liver transplant surgeon and team. Manish Srivastava, M.B.B.S., M.S., D.N.B. Vinay Kumaran, M.B.B.S., M.S., M.Ch. Samiran Nundy, M.A., M.Chir., F.R.C.S., F.R.C.P. Naimish Mehta, M.B.B.S., M.S., F.A.C.R.S.I., F.E.B.S. Department of Surgical Gastroenterology and Liver Transplantation Sir Ganga Ram Hospital Old Rajinder Nagar, New Delhi, India
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