A 67-year-old woman with hepatitis C was found to have a liver tumor located in segment 8 during follow-up computed tomography (CT) for pyogenic spondylitis. She also had a past medical history of cirrhosis due to hepatitis C infection and diabetes mellitus. Laboratory examination showed normal levels of carcinoembryonic antigen, carbohydrate antigen 19–9, and α-fetoprotein but elevated protein induced by vitamin K antagonist-II at a level of 106 mAU/mL. Other laboratory studies showed the following: total bilirubin 0.6 mg/dL, albumin 3.2 g/dL, prothrombin time 13.7 s, aspartate aminotransferase 28 IU/L, alanine aminotransferase 22 IU/L, blood urea nitrogen 16 mg/dL, and creatinine 0.54 mg/dL. The Child-Pugh score was grade A (6 points), and the indocyanine green retention rate at 15 min was 16.6%. A diagnosis of hepatocellular carcinoma (HCC) located in segment 8 was indicated by CT (Fig. ), magnetic resonance imaging (Fig. ), and ultrasonography. The tumor was attached to the MHV. CT scans also showed multiple varices (Fig. ). MHV resection was necessary to obtain sufficient surgical margins. Central bisectionectomy (S4, S5, and S8 resection) was suggested but could not be tolerated because of her poor liver function and low future liver remnant volume, which preoperatively was only 56% by CT volumetry. Therefore, we decided to perform partial hepatectomy with MHV resection. Preoperative CT scans revealed the existence of duplicated IVC (Fig. ), so we chose to use the left IVC as the graft for reconstructing the MHV.\nThe surgery started with an inverted L-shaped incision. Intraoperative ultrasonography confirmed a 3.5-cm tumor that was touching the MHV. After mobilization of the right lobe, the liver parenchyma was transected, preserving the right hepatic vein and right anterior glissonian pedicle. A 3-cm portion of the MHV was resected around the tumor to obtain sufficient surgical margins. Immediately before resecting the MHV, we harvested the left IVC for use as the graft. After incising the retroperitoneum beside the Treitz ligament, the LRV, which had ramified from the IVC, was detected. The left IVC, which had ramified 3 cm peripherally from the origin of the LRV, was then isolated and harvested for 5 cm from the confluence of the LRV. The cut ends of the left IVC were closed with 4–0 polypropylene running sutures. The venous graft was anastomosed first to the proximal end of the MHV and then to the distal end using 6–0 polypropylene (Fig. ). A good Doppler flow through the graft was confirmed after the reconstruction. The operation required 394 min, and the estimated blood loss was 1,894 mL.\nMacroscopic evaluation showed a 35-mm bile-stained tumor (Fig. ). Histologic examination revealed moderately differentiated HCC without direct invasion of the MHV and a tumor-free surgical margin (Fig. ). The tumor was classified as stage II (T2N0M0) according to the TNM staging system for HCC. The patient recovered uneventfully and was discharged on postoperative day 12.\nThe patency of the reconstructed MHV was confirmed postoperatively by ultrasonography and dynamic CT (Fig. ). Laboratory examination 2 years after surgery showed normal levels of total bilirubin (0.6 mg/dL), albumin (4.0 g/dL), aspartate aminotransferase (24 IU/L), alanine aminotransferase (24 IU/L), prothrombin time of 13.5 s, blood urea nitrogen (15 mg/dL), and creatinine (0.46 mg/dL).\nNew lesions were found in the left lobe of the liver 4 months after surgery and in the right lobe 26 months after surgery. Both lesions were treated using transabdominal catheter embolization.
A 48-year-old male patient underwent surgical correction of interrupted CoA at the age of 22 years using EABG from the LSCA to the descending aorta. He presented with shortness of breath. The patient was found to be hypertensive with a BP of 170/90 mmHg on both arms. The BP in the lower limbs was 125/85 mmHg with obvious brachiofemoral delay. The patient was taking amlodipine 10 mg and valsartan 160 mg, both once a day. The ECG revealed LV hypertrophy. His TTE revealed normal LV systolic function, with LV hypertrophy and impaired relaxation. A CT angiography revealed stenosis at the proximal anastomosis site of the EABG (Figure ).\nThe plan was to proceed with cardiac catheterization and stenting the proximal stenosis after measuring the gradient but the patient refused any kind of intervention. The patient was sent home after adding a third antihypertensive medication, which wass bisoprolol 5 mg once a day. After six months, the patient's symptoms improved and his BP was 145/80 mmHg. His repeated TTE revealed no major changes.