Ligation of left renal vein for large spontaneous splenorenal shunt to prevent portal flow steal in adult living donor liver transplantation

Lee, Sung‐Gyu; Ahn, Curie; Kim, Ki‐Hun; Hwang, Shin; Park, Kwang-Min; Ha, Tae‐Yong; Ko, Gi‐Young; Sung, Kyu‐Bo; Song, Gi‐Won; Jung, Dong‐In; Moon, Ki-Myung; Kim, Bum Soo; Cho, Yong‐Pil

doi:10.1111/j.1432-2277.2006.00392.x

Cited by 108 publications

(108 citation statements)

References 21 publications

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“…1,2,5,8,10,[14][15][16][17][18][19][20][21][22][23][24][25][26][27] Possible treatment options include preoperative further selective shunting of flow such as transjugular intrahepatic portosystemic shunts, intraoperative assessment of portal flow with a decision to intervene if there is evidence of inadequate flow to the allograft, automatic intraoperative ligation of the shunt, close monitoring of the shunt and the functional status of the transplant liver without intervention, creation of portorenal anastomosis in the case of portal vein thrombosis, or postoperative percutaneous interventions to embolize a symptomatic shunt. …”

Section: Interventionmentioning

confidence: 99%

Perioperative Management of Spontaneous Splenorenal Shunts in Orthotopic Liver Transplant Patients

Awad

Horrow²,

Parsikia³

et al. 2012

Exp Clin Transplant

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Objectives: Spontaneous splenorenal shunts cause significant vascular steal from the liver. There is no accepted algorithm for treating spontaneous splenorenal shunts before, during, or after liver transplant, and evidence for efficacy of treatments remains limited. Materials and Methods: We reviewed the literature, and our institution's experience regarding spontaneous splenorenal shunts, including a case series of 6 patients with spontaneous splenorenal shunts undergoing transjugular intrahepatic portosystemic shunts, a case of intraoperative ligation of a large spontaneous splenorenal shunts during transplant, and 1 patient requiring multiple endovascular interventions to embolize recurrent spontaneous splenorenal shunts after orthotopic liver transplant.

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Section: Interventionmentioning

confidence: 99%

Perioperative Management of Spontaneous Splenorenal Shunts in Orthotopic Liver Transplant Patients

Awad

Horrow²,

Parsikia³

et al. 2012

Exp Clin Transplant

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“…[1][2][3][4] In advanced stages of chronic liver disease, the portal vein (PV) flow may become hepatofugal, and this may lead to a portal steal phenomenon with a dramatic decrease in hepatic perfusion. 3,[5][6][7][8][9] Not infrequently, this is associated with PV thrombosis. [10][11][12] However, large portosystemic shunts such as SSRSs may jeopardize the portal flow and lead to graft dysfunction due to portal hypoperfusion.…”

mentioning

confidence: 99%

Hemodynamic consequences of spontaneous splenorenal shunts in deceased donor liver transplantation

2011

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The presence of large spontaneous splenorenal shunts (SSRSs) is a risk factor for poor portal vein flow and liver dysfunction. The disconnection of splenorenal shunts by left renal vein (LRV) ligation has been suggested as a potential solution for improving portal flow. We reviewed the hemodynamic consequences of splenorenal shunts in deceased donor liver transplantation and investigated the role of LRV ligation. In 10 patients who underwent liver transplantation at our institution between January 2006 and April 2010, an SSRS was diagnosed preoperatively. Intraoperative portal and hepatic artery flows were measured with a transit time flowmeter. The shunt was disconnected in 6 patients for whom the portal flow after reperfusion was less than or equal to 1200 mL/minute. LRV ligation resulted in significant increases in the portal flow. There were no differences in renal function for the patients who underwent renal vein ligation and the patients who did not undergo ligation. In conclusion, LRV ligation disconnects splenorenal shunts and modulates the portal inflow without any detrimental effects on renal function. Liver Portal hypertension leads to the development of an extensive network of portosystemic collateral vessels. In 5% to 12% of patients, these collaterals include spontaneous splenorenal shunts (SSRSs).

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“…2,3 In living donor liver transplantation, management of a large SRS becomes more complicated because closure of an SRS to increase portal flow may increase portal pressure and shear stress and result in small-for-size syndrome (SFSS). 4 Therefore, the management of a large SRS during living donor liver transplantation has become a dilemma.…”

Section: To the Editorsmentioning

confidence: 99%

“…Alternatively, the left renal vein can be ligated to prevent portal vein flow diversion; however, it may cause sustained renal dysfunction in 9.1% of patients. 2 Furthermore, both procedures can cause SFSS. We have no doubt that ligation of the proximal SV was less complicated than closure of a large SRS or ligation of the left renal vein.…”

mentioning

confidence: 99%

Ligation of the proximal splenic vein to overcome the effects of a large splenorenal shunt during living donor liver transplantation

Lee

Cheng

et al. 2014

Liver Transpl

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TO THE EDITORS:Patients with severe cirrhosis with portal hypertension may develop a splenorenal shunt (SRS) spontaneously to divert portal flow. After transplantation, the SRS may be occluded spontaneously. However, a large SRS may persist. This persistent SRS can steal portal flow and cause portal vein thrombus, hepatic encephalopathy, and graft dysfunction.1 The methods to manage a large SRS in deceased donor liver transplantation include splenectomy, ligation of the SRS, ligation of the left renal vein, and percutaneous transfemoral embolization. 2,3 In living donor liver transplantation, management of a large SRS becomes more complicated because closure of an SRS to increase portal flow may increase portal pressure and shear stress and result in small-for-size syndrome (SFSS). 4 Therefore, the management of a large SRS during living donor liver transplantation has become a dilemma. Here we introduce ligation of the proximal splenic vein (SV) to resolve this dilemma. This study was approved by local ethic committee of ChangGung Memorial Hospital (IBR No. 101-2410B).A 51-year-old male patient had hepatitis C-related cirrhosis and hepatocellular carcinoma. Liver transplantation was performed because of tumor recurrence after radiofrequency ablation and transarterial chemoembolization. His body height was 168 cm, and his body weight was 81 kg. The liver cirrhosis status was Child-Pugh B, and the Model for End-Stage Liver Disease score was 13. Pretransplant computed tomography (CT) showed the diameter of the portal vein to be very small, and the portal flow was shunted into the renal vein via a large spontaneous SRS (Fig. 1). The living donor was the patient's 45-year-old sister, whose body height was 162 cm and whose body weight was 56.4 kg. The liver volume calculated by CT volumetry was 1272.9 cm 3 . The right lobe of the liver was 51.8% as calculated by Lee's formula with the diameters of right and left portal veins, 5 and the estimated graft weight was 659 g. During the donor operation, the right lobe of the liver without the middle hepatic vein was procured and weighed 650 g. The graft-to-recipient weight ratio was 0.80%. During the recipient's operation, we found that the caliber of the portal vein was small, and the portal flow was 200 mL/minute as measured by a flowmeter (Transonic Systems, Ithaca, NY). Therefore, the infrapancreas superior mesenteric vein (SMV) was identified and exposed. The tunnel between the pancreatic neck and the SMV was made. The junction between the SMV and SV was hooked upward and snared with a 1-0 silk thread (Fig. 2). Subsequently, the native liver was removed, and the liver graft was implanted. The portal vein was reconstructed via the grafting of the recipient's native portal vein to the graft portal vein. The portal flow was 500 mL/minute as measured by the flowmeter immediately the graft was reperfused. When the proximal SV was ligated, the portal flow was increased to 800 mL/minute. The hepatic artery was reconstructed by a microscopic technique, and the flow was 220 mL/...

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Ligation of left renal vein for large spontaneous splenorenal shunt to prevent portal flow steal in adult living donor liver transplantation

Cited by 108 publications

References 21 publications

Perioperative Management of Spontaneous Splenorenal Shunts in Orthotopic Liver Transplant Patients

Perioperative Management of Spontaneous Splenorenal Shunts in Orthotopic Liver Transplant Patients

Hemodynamic consequences of spontaneous splenorenal shunts in deceased donor liver transplantation

Ligation of the proximal splenic vein to overcome the effects of a large splenorenal shunt during living donor liver transplantation

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