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Keywords:

  • EMS, hepatic vein stenosis, liver regeneration, LRLT

Abstract

  1. Top of page
  2. Abstract
  3. Introduction
  4. Case Report
  5. Discussion
  6. References

Although the incidence of stenosis and obstruction of the hepatic venous anastomosis after right hepatic living-related liver transplantation (LRLT) has been found to be higher than after orthotopic liver transplantation (OLT), to the best of our knowledge, intrahepatic stenosis of the venous trunk in the early period after right hepatic LRLT has never been reported in the literature. A 53-year-old man who underwent right hepatic LRLT, postoperatively, developed liver dysfunction and an increasing amount of ascites, and a Doppler sonogram showed a flat waveform and low-flow velocity in the hepatic vein. Based on these findings an outflow block was suspected, and a hepatic venogram and manometry revealed intrahepatic stenosis of a tortuous hepatic venous trunk and a pressure gradient of 14 mmHg at the site of the stenosis. We inserted an expandable metallic stent (EMS) at the site of intrahepatic venous stenosis, and its insertion was followed by a decrease in pressure gradient. Liver function recovered, and the volume of ascitic fluid decreased after placement of the EMS. The results of an analysis of the venogram and CT volumetric data suggested that the pathogenesis of the stenosis was twisting of the venous trunk during hypertrophy of the liver parenchyma.


Introduction

  1. Top of page
  2. Abstract
  3. Introduction
  4. Case Report
  5. Discussion
  6. References

Right hepatic living-related liver transplantation (LRLT) is now commonly used to treat adults, and although stenosis of the right hepatic vein anastomosis has been found to occur as a postoperative complication, to our knowledge early intrahepatic hepatic venous stenosis not at the site of the anastomosis has never been reported. We report such a case and describe the radiological findings obtained by hepatic venography and the hepatic vein manometric data in a patient treated with an expandable metallic stent (EMS). We discuss the possible pathogenetic mechanism of the intrahepatic stenosis of the hepatic vein that developed during the period of liver regeneration after right hepatic LRLT.

Case Report

  1. Top of page
  2. Abstract
  3. Introduction
  4. Case Report
  5. Discussion
  6. References

A 53-year-old man was referred to our department for LRLT. At 39 years of age he had been diagnosed with liver dysfunction secondary to hepatitis B virus (HBV) infection. Liver cirrhosis and hepatocellular carcinoma (HCC) subsequently developed, and he was treated by trans-arterial embolization at 48 years of age. The HCC recurred at 52 years of age, and he developed an umbilical hernia caused by a huge volume of ascitic fluid. Living-related liver transplantation of an ABO-compatible right hepatic lobe donated by his wife was performed. Preoperative three-dimensional dynamic enhanced computed tomography of the donor revealed that drainage veins from the middle hepatic vein had not developed in Couinaud segments V and VIII, that the main drainage route of venous return from right lobe of the liver was the right hepatic vein, and that there was no stenosis (Figure 1). The graft-to-recipient weight ratio was 0.89%. The main hepatic vein of the donor was anastomosed to the right hepatic vein of the recipient without reconstruction of the middle hepatic vein. The length of the orifice and the cuff of the right hepatic vein of the graft were 27 mm and 14 mm, respectively, and the length of the remnant right hepatic vein of the recipient was 8  mm. The detailed surgical procedure for hepatic vein reconstruction was as follows. The vascular clamp holding the stump of the right hepatic vein was positioned vertically on the inferior vena cava (IVC). The IVC was incised at the inferior end of the right hepatic vein orifice to adjust it to the length of the orifice of the hepatic vein of the graft. A portion of the anterior wall of the IVC was removed to make the orifice oval-shaped. End stitches of 5–0 polypropylene monofilament suture were placed on the superior and inferior ends. The superior stitch of 5–0 polypropylene monofilament suture was knotted, and one arm of the knotted stitch was passed through the posterior wall of the graft vein from the outside in, close to the first knot, and continued intraluminally to the inferior end. The anterior wall closure was completed in simple running suture fashion with the same stitch. There were no areas of congestion in the graft. Cold ischemic time was 47 min, and warm ischemic time was 59 min. Intraoperative Doppler ultrasound examinations showed no evidence of either stenosis or obstruction of the hepatic venous, portal venous, or hepatic arterial blood flow after reperfusion. Portal venous pressure was monitored with a catheter inserted into the superior mesenteric vein via a branch of the ileocolic vein. Before hepatectomy, it was 33 mmHg, but it decreased to 20 mmHg after transplantation, and ultimately to 9 mmHg on postoperative day (POD) 7. HBIg and lamivudine were given postoperatively, and immunosuppressive treatment with tacrolimus was started immediately after transplantation. On POD 10 the serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and total bilirubin (T-bil) values had decreased to 56 international units (IU)/mL, 41 IU/mL, and 2.8 mg/dL, respectively (Figure 2), and by POD 12 they had increased to 103  IU/mL, 81 IU/mL, and 3.6 mg/dL, respectively. The daily volume of ascitic fluid increased from less than 5000  mL to more than 10 000 mL on POD 11 (Figure  2). Ascitic fluid cultures were negative for mycobacteria and fungi, and no cytomegalovirus–antigen was detected on granulocytes in the ascitic fluid. A Doppler ultrasound examination on POD 12 revealed flat waveforms and low-flow velocity of 9.6 cm/s in the right hepatic vein (Figure 2), and a low-flow velocity of 11.7 cm/s in the right main portal vein. A hepatic venogram was performed on POD 13 because of clinical suspicion that hepatic venous obstruction had developed. The venogram showed stenosis of an intrahepatic vein, not of the anastomosis (Figure  3A), and examination of both the anterior-posterior view and lateral view (Figure  3B) hepatic venograms revealed that the stenotic intrahepatic vein was tortuous. Manometric venous pressure data obtained by withdrawing the catheter from the intrahepatic vein into the inferior vena cava showed a gradient of 14 mmHg across the intrahepatic stenosis (Figure  3C). The wedge pressure of the distal hepatic vein branch was 33  mmHg. We immediately inserted an EMS (diameter: 1.4  cm, length: 5 cm; Wallsten™, Boston Scientific, Nagoya, Japan K. K) into the right hepatic vein via the right internal jugular vein (Figure  4A), and the venous pressure gradient was found to have decreased to 4 mmHg (Figure  4B). A Doppler ultrasound examination after EMS placement showed a pulsatile waveform in the right hepatic vein and an increase in flow velocity at the same sites in the intrahepatic vein and the right main portal vein of 30.9 cm/s and 23.9 cm/s, respectively. The AST and ALT values had decreased to 31 IU/L and 30 IU/L, respectively, on POD 14. The daily volume of ascitic fluid decreased to less than 5000 mL from POD 18 onward, and continued decreasing to less than 500 mL from POD 25 onward. The patient developed to severe sepsis caused by coagulase-negative Staphylococcus aureus associated with increasing AST- and T-bil-values and decreasing flow velocity from POD 16 to POD 24, but treatment with Vancomycin was followed by recovery of their values. The patient was discharged on POD 55, and he has been working and enjoying a good quality of life for the past 7 months.

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Figure 1. Three-dimensional dynamic-enhanced computed tomography of the donor's liver showing that the main drainage route of venous return of the right lobe was the right hepatic vein (white arrow), and absence of stenosis.

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Figure 2. Sequential changes in the serum total bilirubin level (•), volume of ascitic fluid (□), and flow velocity (▵) measured by Doppler sonography of the right hepatic vein after the operation. Flow velocity increased greatly after placement of an expandable metallic stent, and the volume of ascitic fluid decreased. The serum total bilirubin level increased to 15 mg/dL because of sepsis, but decreased in response to Vancomycin therapy.

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Figure 3. (A) Hepatic venogram (anterior-posterior view) and (B) hepatic venogram (lateral view). A tortuous stenotic intrahepatic vein ([RIGHTWARDS ARROW]) is seen, and the hepatic venous anastomosis is intact (dotted arrow). (C) Manometric hepatic venous pressure data. The hepatic venous pressure gradient was measured at the point indicated by the arrow.

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Figure 4. (A) Hepatic venogram after placement of the expandable metallic stent. (B) Manometric hepatic venous pressure data. No steep decline in pressure is seen.

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Discussion

  1. Top of page
  2. Abstract
  3. Introduction
  4. Case Report
  5. Discussion
  6. References

The use of right hepatic lobe grafts is a major development in LRLT and has significantly increased the graft supply. Right hepatic LRLT is a relatively new and technically challenging method. The hepatic venous anastomosis in a right-lobe graft is unique in terms of the variety of patterns of venous drainage, i.e. in some cases, such as our own, the right hepatic vein alone drains the entire graft, whereas in other cases the major anterior segment (Couinaud segments V and/or VIII) veins drain into a middle hepatic vein, or inferior hepatic veins may provide the main venous drainage of the posterior segment. While hepatic venous complications of orthotopic liver transplantations are rare, the anatomical variations may lead to hepatic venous congestion in the absence of reconstruction of drainage branches in LRLT, or to outflow obstruction owing to an insufficient anastomotic orifice. Egawa et al. reported two cases of early onset (1 week postoperatively) and six cases of late onset (2 months or more postoperatively) hepatic vein occlusion among 152 LRLTs (45 left lobe grafts, 106 lateral segment grafts, and one right lobe graft) (1). Inomata et al. reported outflow block in one case with multiple, separate hepatic vein anastomoses among 26 right hepatic LRLTs, and they suspected that a shift in the position of the graft may have led to the obstruction of the multiple hepatic venous anastomoses (2). Other surgeons and radiologists have reported incidences of outflow block after right hepatic LRLT of 0%[0/20 (3), 0/30 (4), 0/46 (5)] and 4% (1/256). Ko et al. treated 27 cases of hepatic venous outflow obstruction after LRLT by balloon angioplasty and insertion of an EMS, and analyzed the etiologies of the obstruction (7). They concluded that the causes were fibrosis or intimal hyperplasia in the perianastomotic area, kinking or buckling of a redundant hepatic vein, external compression by a hypertrophied liver graft, a tight suture line, and iatrogenic obstruction after stent placement in the IVC (7). In our patient, the site of stenosis was in an intrahepatic vein far from the site of the anastomosis, which provided a sufficient orifice according to the venogram. The CT volumetric data of the right hepatic lobe graft showed that graft volume had increased approximately twofold on POD 7, and approximately 2.5-fold on POD 14 (Table 1). The increase in liver volume until POD 14 may have been secondary to venous congestion of the graft. The daily volume of ascitic fluid after the operation was ranged from approximately 1000–3000 mL until POD11, however, those volumes did not indicate liver congestion because of hepatic vein stenosis caused by a technical error in the anastomosis, because daily ascitic fluid volumes of greater than 1000 mL until POD 14 have sometimes been observed in cirrhotic patients after LRLTs. As the hepatic venous obstruction appeared to have occurred around POD 13 based on the Doppler ultrasound findings, we concluded that the doubling of the preoperative graft volume on POD 7 was attributable to regeneration of liver parenchyma rather than congestion of hepatic venous return. We suspect that relatively rapid hypertrophy of the right lobe graft that was asymmetric may have led to intrahepatic twisting of the hepatic vein like a hollow tube, and resulted in outflow block. The CT volumetric data on POD 70 showed that the volume had decreased to approximately the same level as on POD 7, when there was no venous congestion. Inomata et al. reported that a relatively small lateral-segment or left-lobe graft in LRLTs may twist around the hepatic venous anastomosis (extrahepatic) during hepatic regeneration and cause outflow block (8). They inserted a tissue expander into the space adjacent to the graft in order to stabilize its position. Our case, in which the pathogenesis of the venous outflow blockage may have been intrahepatic twisting of the venous trunk during hypertrophy of the liver parenchyma, may be the first such case ever reported. Another possible etiology of the intrahepatic vein stenosis in our case is ischemic stricture of an intrahepatic vein, because 59 min of warm ischemic time was considered relatively long. The mean warm ischemic time in the adult 31 cases in our LRLT series was 40.3 min (range: 21–73 min), but no intrahepatic hepatic vein stricture was found in a further seven cases in which the warm ischemic time was greater than 50 min. Interventional radiologic procedures like balloon angioplasty and EMS placement are useful treatment modalities for hepatic venous outflow obstruction after LRLT and split-liver transplantation (7,9). We inserted an EMS at a site of intrahepatic stenosis of the hepatic vein, so that the proximal portion of the EMS did not extend beyond the anastomosis. The EMS has been retained at the site and has been effective in combination with anticoagulant therapy with warfarin over the past 7 months of follow up to date.

Table 1.  CT volumetric data of the recipient
 PreoperativePostoperative day
7142870
Graft volume (cm3)8601700215720511636

In conclusion, we have reported a case of intrahepatic venous stenosis resembling outflow block after right hepatic LRLT in which we treated the stenosis by insertion of an EMS. We suspect that the pathogenesis of the stenosis was twisting of the venous trunk during hypertrophy of the liver parenchyma.

References

  1. Top of page
  2. Abstract
  3. Introduction
  4. Case Report
  5. Discussion
  6. References
  • 1
    Egawa H, Inomata Y, Uemoto S et al.. Hepatic vein reconstruction in 152 living-related donor liver transplantation patients. Sugery 1997; 121: 250257.
  • 2
    Inomata Y, Uemoto S, Asonuma K et al.. Right lobe graft in living donor liver transplantation. Transplantation 2000; 69: 258264.
  • 3
    Ghobrial RM, Saab S, Lassman C et al.. Donor and recipient outcomes in right lobe adult living donor liver transplantation. Liver Transpl 2002; 8: 901909.
  • 4
    Sugawara Y, Makuuchi M, Sano K et al.. Vein reconstruction in modified right liver graft for living donor liver transplantation. Ann Surg 2003; 237: 180185.
  • 5
    Zeytunlu M, Icoz G, Kilic M, Yuzer Y, Tokat Y. Optimal venous drainage for right lobe living donor liver grafts. Transplant Proc 2002; 34: 33273330.
  • 6
    De Villa VH, Chen CL, Chen YS et al.. Right lobe living donor liver transplantation-addressing the middle hepatic vein controversy. Ann Surg 2003; 238: 275282.
  • 7
    Ko GY, Sung KB, Yoon HK et al.. Endovascular treatment of hepatic venous outflow obstruction after living-donor liver transplantation. J Vasc Interv Radiol 2002; 13: 591599.
  • 8
    Inomata Y, Tanaka K, Egawa H et al.. Application of a tissue expander for stabilizing graft position in living-related liver transplantation. Clin Transplant 1997; 11: 5659.
  • 9
    Mazariegos GV, Garrido V, Jaskowski-Phillips S, Towbin R, Pigula F, Reyes J. Management of hepatic venous obstruction after split-liver transplantation. Pediatr Transplant 2000; 4: 322327.