Gastrointestinal Intervention 2017; 6(3): 176-179
Percutaneous transhepatic hepatic venous stenting after extracorporeal hepatic resection and autotransplantation: A case report
Jung Hwan Park1, Ung Bae Jeon1,*, Ki Seok Choo1, Tae Un Kim1, Chong Woo Chu2, and Je Ho Ryu2
1Department of Radiology, Pusan National University Yangsan Hospital, Yangsan, Korea, 2Department of Surgery, Pusan National University Yangsan Hospital, Yangsan, Korea
Department of Radiology, Medical Research Institute, Pusan National University School of Medicine and Research Institute for Convergence of Biomedical Science and Technology, Pusan National University Yangsan Hospital, 20 Geumo-ro, Mulgeum-eup, Yangsan 50612, Korea. E-mail (U.B. Jeon).
Received: April 14, 2016; Revised: June 8, 2016; Accepted: June 10, 2016; Published online: October 31, 2017.
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We report a case of percutaneous transhepatic stent placement for the treatment of hepatic venous outflow obstruction after extracorporeal hepatic resection and autotransplantation. A 63-year-old woman with a large mass in the liver was asymptomatic with no hepatic virus infection. Because the tumor was unresectable by conventional means, we used extracorporeal hepatic resection and autotransplantation for operation. Two days after surgery, hepatic venous outflow obstruction of the right and right inferior hepatic veins was suspected on computed tomography. After failure of the transjugular approach, hepatic venous stenting was performed successfully via the percutaneoustranshepatic approach.

Keywords: Autografts, Budd-Chiari syndrome, Hepatic veins, Liver, Stents

With the development of surgical techniques and clinical experience, the incidence of vascular complications after hepatic surgery such as liver transplantation has become low. Hepatic venous outflow obstruction (HVOO) is relatively rare, with an incidence of 1.5% to 2.5% in orthotopic liver transplantation and 2% to 9% in living-donor liver transplantation.1 The clinical manifestation of HVOO can be varied, such as ascites, edema, hepatomegaly, pleural effusion, and renal or hepatic dysfunction.2 Percutaneous angioplasty and stent insertion in the hepatic vein have gained worldwide acceptance as effective treatment modalities for patients with HVOO.1 However, to the best of our knowledge, the incidence or treatment of HVOO after extracorporeal hepatic resection and autotransplantation (ECHRA) has not been reported yet. We report a case of percutaneous transhepatic venous stenting for HVOO after ECHRA after failure of the transjugular approach.

Case Report

History and preoperative evaluation

A 63-year-old woman without any symptoms was admitted to the hospital because of a hepatic mass detected during routine examination. She had no history of liver disease and alcohol abuse. Physical examination revealed no specific finding. Laboratory analysis revealed the following values: aspartate aminotransferase, 31 IU/L (reference range, 10–40 IU/L); alanine aminotransferase, 25 IU/L (reference range, 6–40 IU/L); alkaline phosphatase, 357 IU/L (reference range, 95–280 IU/L); γ-glutamyl transpeptidase, 144 IU/L (reference range, 5–63 IU/L); total bilirubin, 0.5 mg/dL (reference range, 0.3–1.3 mg/dL); hemoglobin, 12.1 g/dL (reference range, 12.5–15.0 g/dL); and carbohydrate antigen 19-9 (CA 19-9), 73.6 U/mL (reference range, 0–39 U/mL). Other laboratory values, including albumin level, prothrombin time, white blood cell count, platelet count, and α-fetoprotein level, were normal. Results were positive for antibody to the anti-hepatitis B virus antigen but negative for hepatitis B surface antigen.

Imaging findings

Abdominal computed tomography (CT) and magnetic resonance imaging (MRI) revealed a large lobulated mass with a maximum diameter of 10 cm in the liver, occupying S2, S3, S4, and S8. The mass showed peripheral enhancement with central low attenuation on CT and enhanced T1-weighted MRI. Adjacent portal and hepatic veins and biliary tracts were pressed and displaced (Fig. 1).

Operative and postoperative data

Because of the possibility of a hepatic malignant tumor, the mass was resected. However, the tumor was conventionally unresectable because the inferior vena cava (IVC), right hepatic vein (RHV), and right inferior hepatic vein (RIHV) were compressed. Thus, we decided to use the ECHRA technique. An artificial graft (Gore-Tex; WL Gore & Associates Inc., Newark, DE, USA) was used for hepatic venous anastomosis with IVC (Fig. 1C). Piggyback anastomosis was used during the IVC anastomosis. The affected segments of the liver were resected after total hepatectomy, and the autograft was reimplanted. Final histopathologic examination of the surgical specimen revealed a cholangiocarcinoma. Routine postoperative abdominal CT performed 2 days after surgery showed an anastomotic stenosis and a suspicious small outpouching lesion at the RHV, and an anastomotic stenosis and suspicious flap-like lesion at the RIHV (Fig. 2). These outpouching and flap-like lesions are supposed to be surgical materials such asa polytetrafluoroethylene graft. Color Doppler ultrasonography performed 6 days after surgery showed suspected findings of stenosis on RHV and RIHV.

Intervention and follow-up

For hepatic venography, the transjugular approach was performed via the right internal jugular vein, accessed by using the standard Seldinger technique, under local anesthesia. A 9-Fr sheath (Flexor Check-Flo; Cook, Bloomington, IN, USA) containing a 9-Fr dilator was advanced into the IVC by using a 5-Fr cobra catheter and 0.035-inch hydrophilic guidewire (Terumo, Tokyo, Japan). RHV or RIHV selection was attempted several times but failed due to the severe stenoses of the lesions. For the alternative approach, the transhepatic approach was attempted. The RIHV was punctured with a 22-G needle (PTC needle; M.I.Tech, Seoul, Korea) under ultrasonographic guidance. Then, after confirmation of the hepatic venous puncture with a test dose injection of contrast media, a 0.018-inch nitinol guidewire (Cope Mandril Guide Wire; Cook) was advanced to the right atrium (RA) through the stenotic anastomotic site. After changing the nitinol guidewire to a 0.035-inch hydrophilic guidewire (Terumo), a 7-Fr sheath (Cook) was inserted. Right inferior hepatic venography using the sheath revealed an occlusion at the anastomotic site of the RIHV (Fig. 3). For treatment of the occlusion, a 10 × 40 mm nitinol stent (SMART; Cordis, Miami, FL, USA) was inserted. The final right inferior hepatic venography revealed improved blood flow (Fig. 3B). The pressure gradient between the RA and the RIHV was 2 mmHg. To improve the patient’s condition, RHV stenting was attempted by using the same method. Angiography revealed an occlusion at the anastomotic site of the RHV (Fig. 3C). A 10 × 60 mm nitinol stent (SMART) was applied in the lesion. However, the pressure gradient between RHV and RA was 6 mmHg, and additional balloon dilatation was performed by using a 10 × 40 mm balloon (Mustang; Boston Scientific, Galway, Ireland). The final right hepatic venography revealed good blood flow to the RA (Fig. 3D). The pressure gradient between the RA and the RHV was 2 mmHg. Transhepatic access route was embolized with gelfoam slurry (Cutanplast; Mascia Brunelli Spa, Milano, Italy) all the time. Abdominal CT performed 1 month later demonstrated a patent blood flow in both stents (Fig. 4).


Hepatic resection is the gold standard treatment of liver neoplasm. However, for some cases, owing to the size or extension of the lesion or its location close to critical structures, resection using conventional techniques is extremely difficult and risky. For tumors considered unresectable by conventional means, ECHRA has been proposed as analternative.3 Long-term experience with ECHRA showed that the early postoperative mortality rate is high and early tumor recurrence remained to be the important problem.4 Improved experiences with liver transplantation and resection have promoted the development of ex situ liver surgery in recent years. Sugimachi et al5 reported a case of far advanced hepatocellular carcinoma that was successfully treated with ECHRA with favorable long-term survival.

HVOO is a relatively uncommon but important complication of liver transplantation. Thus, management of HVOO is highly important. Because HVOO immediately after liver transplantation is a surgical emergent condition, reoperation might be needed for correction.6

Although the internal jugular approach provides a good route to the hepatic veins and the associated morbidity is low, in the presence of hepatic vein stenosis or obstruction, hepatic vein catheterization via the transjugular approach is difficult. Thus, the transhepatic approach could be a useful alternative approach.7 Access to the stenoticsite is easier with the transhepatic approach owing to its straightforward direction. It results in shorter procedure time and less radiation exposure. However, the hepatic parenchyma is vulnerable to injury because of its active regeneration during the early postoperative period after living donor liver transplantation.8 However, we thought that the transhepatic approach was not worrisome because our patient underwent ECHRA and did not take any immunosuppressive agent.

The indications for primary stent placement in HVOO are as follows. First, the risk of disruption after balloon angioplasty at a relatively fresh anastomosis. Second, kinking of a redundant hepatic vein itself or an interposed vein graft. These could not be resolved effectively by balloon angioplasty alone. Third, the risk of elastic restenosis.9 In our case, HVOO occurred in the early postoperative period (< 28 days) but was successfully treated with percutaneous transhepatic hepatic venous stenting.

In conclusion, percutaneous transhepatic hepatic venous stent insertion were safe and effective for the HVOO of ECHRA in our patient.

Fig. 1. Axial (A) and coronal (B) views of a portal venous phase abdominal computed tomography image showing a large lobulated mass at the central area of the liver, which is abutting to the hepatic inferior vena cava (IVC) and right hepatic vein (RHV) (arrowheads). (C) During the surgery, the IVC and RHV were reconstructed by using a 32-mm polytetrafluoroethylene graft. The anastomosis was made with continuous running sutures (6-0 monofilaments).
Fig. 2. The portal venous phase on abdominal computed tomography (CT) 2 days after surgery. (A) Axial CT scan at the level of the right hepatic vein (RHV) showing an anastomotic stenosis (arrow) and a suspicious small outpouching lesion looks like condensation of extravasated contrast agent around anastomotic site (arrowheads) on the RHV. (B) Axial CT scan at the level of the right inferior hepatic vein (RIHV) showing stenosis of the RIHV and a flap-like lesion at the inferior vena cava (IVC) (arrow). (C) Coronal CT scan showing a well-demarcated flap-like lesion in the IVC near the two anastomoses (arrow).
Fig. 3. Percutaneous transhepatic hepatic venous stenting. (A) A right inferior hepatic venography obtained via the percutaneous transhepatic approach, showing total occlusion at the anastomosis between the right inferior hepatic vein (RIHV) and the inferior vena cava (IVC) (arrow). (B) A right inferior hepatic venography after stent placement showing restorationof RIHV flow. The pressure gradient between the RIHV and the right atrium (RA) was 2 mmHg. (C) A right hepatic venogram obtained via the percutaneous transhepatic approach showing occlusion at the anastomosis between the right hepatic vein (RHV) and the IVC (arrow). The RHV was drained to the RIHV via the capsular vein of the liver (arrowheads). (D) RHV stent placement was performed, and pressure gradient between the RHV and the RA was 6 mmHg. Thus, additional balloon dilatation was performed for stent expansion. The final right hepatic venography after stent placement and balloon dilatation, showing good flow to the IVC. The final pressure gradient between the RHV and the RA was 2 mmHg.
Fig. 4. Follow-up abdominal computed tomography images obtained 1 month later, demonstrating a patent blood flow in the right hepatic vein (A) and right inferior hepatic vein (B) stents (arrows).
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