Vascular reconstruction techniques in hepato-pancreato-biliary (HPB) surgery


Over the three last decades, advances in liver surgery have included extensive experience in living and deceased donor-liver transplantation (see Chapters 105 and 125 ), induction of liver hypertrophy by interventional radiology (portal vein embolization and radioembolization) (see Chapters 94B and 102C ) or surgical techniques (associating liver partition and portal vein ligation for staged hepatectomy) (see Chapter 102D ), and increased use of neoadjuvant chemotherapeutic drugs to downstage liver disease (see Chapters 97 and 98 ).

The combination of these medical and surgical advances has led surgeons to push the limits of tumor resectability. The presence of vascular invasion, which can be a common finding in advanced liver tumors, is now not considered as a contraindication for surgery if a radical resection can be reasonably performed with acceptable postoperative morbidity and mortality rates. The risk and benefits of such extended liver resections combined with vascular resection should be balanced against the survival offered by medical treatment. In some cases, the increased perioperative risk of these resections is justified in selected patients undergoing an R0 resection. Vascular invasion, however, either of the vessel wall or as a tumoral thrombus, reflects an aggressive tumoral behavior and is a poor prognostic factor. Tumoral thrombosis of the portal vein (PV) and hepatic vein (HV) occurs more often with hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (ICC) and represents one of the prognostic factors predictive of poor survival. , Indeed, tumoral invasion of the vascular wall occurs more frequently with adenocarcinoma, notably for ICC and metastatic tumors.

Liver resection in the presence of vascular invasion requires meticulous preoperative preparation for surgery. First, the need for extensive vascular clamping requires appropriate study of the function (indocianine green retention test, functional scintigraphy) and the volume (three-dimensional volumetry) of the future liver remnant (see Chapters 4 and 102 ). Second, the presence of vascular venous invasion and thrombosis, mainly of the inferior vena cava (IVC) and HVs, promotes the progressive development of intrahepatic venous shunts, which are sources of profuse bleeding during liver transection. These collaterals should be extensively mapped preoperatively and surgical strategy should be adapted to decrease intraoperative bleeding. Third, segmental resection of the involved vessels (vena cava, PV, HV, and hepatic artery) might require vascular interposition grafts. The length and the type of these grafts should be planned preoperatively and grafts should be rapidly available in the operating room. Accurate study of preoperative imaging is of paramount importance in this regard in order to plan the length of the resected vessels and the vascular graft. Fourth, given the bulkiness of some tumors and the need for caval replacement, the use of total vascular exclusion with an extracorporeal venovenous bypass (VVB) can be very common. Specific experience with this technique and the use of VVB is then mandatory before attending these complex procedures. Finally, vascular resection should be performed by well-trained surgeons who should have extensive expertise in both liver surgery and vascular resection to afford the complexity of these resections and give patients the lowest risk of postoperative mortality. In the absence of this experience, patients requiring these complex surgeries should be addressed to tertiary centers experienced in vascular resection during liver surgery (see Chapters 101A and 101B ).

Resection and reconstruction of the inferior vena cava

Generalities

Different types of vascular infiltration of the IVC can be encountered in routine practice. For general rules one can differentiate (1) macrovascular venous invasion as direct extension of a tumoral thrombus into the caval vein, which is frequent in case of renal cell carcinomas, adrenocortical carcinomas, and HCCs; and (2) invasion of the caval venous wall (most frequently seen in ICC and colorectal liver metastasis). , , , , Based on radiologic examination, tumoral invasion of the IVC can be classified into three groups according to venous segment involved: segment I, infrarenal; segment II, interrenal and suprarenal up to but not including the three hepatic veins; and segment III, suprahepatic with possible intracardiac extension. According to this radiologic classification, clinical symptoms may range from leg edema to life-threatening Budd-Chiari syndrome (see Chapter 86 ).

Preoperative prediction of histologic IVC invasion remains difficult to assess even with improvements in preoperative imaging and intraoperative exploration by an experienced surgeon. With IVC resection, true histologic vascular wall involvement has been reported to range from 22% to 72% according to different series. , , , In many cases, however, attempts to separate the tumor from the IVC wall, even without histologic involvement, can result in tumoral rupture or sudden entry into the IVC. This occurs frequently in ICC, which can have a desmoplastic reaction between the tumor and IVC wall. Some preoperative computed tomography (CT) findings have been identified as highly suspicious of IVC invasion, such as compression of more than 50% of caval circumference, presence of a peaked deformity of the IVC wall, and extent of the IVC circumference attached to the tumor greater than 25% compared with the whole IVC circumference (see Chapters 14 and 15 ). The development of large collateral veins between the origins of the hepatic veins mainly in the inferior liver segments is a reliable indirect sign of venous obstruction at the level of the hepatic vein confluence and should be systematically identified before surgery.

Hepatectomy with caval resection should be planned preoperatively and the incidental discovery of caval invasion should remain a rare event. Some basic rules should be used as a guide to such extended resections. Full vascular control below and above the liver of the inferior vena cava as well as the control of the hepatic pedicle and of an eventual accessory left hepatic artery should be the rule. Very often, the presence of a bulky tumor and/or venous thrombus makes liver mobilization difficult and/or risky. In such conditions control of the IVC above the liver should be performed as high as possible without liver mobilization. Different intrapericardial transabdominal approaches of the IVC have been described (see later in this chapter). For parenchymal transection an anterior approach is mostly used and recommended. The presence of venous compression and/or obstruction enhances the development of intrahepatic venous collateral shunts, which can be the source of massive bleeding during parenchymal transection. One should not be reluctant to perform total vascular exclusion (TVE) to reduce bleeding and speed up the procedure. The use of VVB can also reduce the hemodynamic consequences of TVE and provides stability for a longer period.

Control of the inferior vena cava

Resection and reconstruction of the IVC at the time of liver resection requires control of the IVC below and above the liver. Control of the IVC below the liver is easily achieved just below segment I and above the renal veins by a large right angle directed from right to left. On the contrary, control of the IVC above the liver varies according to the extent and location of IVC involvement. The extension of the abdominal incision to the sternum or the thoracic cavity will be determined by the need for controlling the IVC into the thoracic cavity or the need for placing a cardiopulmonary bypass. As a general rule, when the segment of the IVC involved by the tumor is below the hepatic veins, an abdominal incision is sufficient to achieve safe control of the IVC above and below the liver.

A classic method of controlling the IVC entails control of the IVC above the liver after full liver mobilization and ligation of the inferior diaphragmatic veins bilaterally, as described for liver transplantation. This approach could be hazardous in the presence of tumors encasing the hepatocaval confluence, tumoral thrombosis of the retrohepatic IVC, and bulky tumors. In these circumstances, several approaches have been described to achieve safer control of the suprahepatic IVC, either directly into the pericardium by a sternotomy or by a purely abdominal approach. A transabdominal transdiaphragmatic approach to the suprahepatic IVC can often be achieved without the need for sternotomy. The isolation of the suprahepatic IVC can be obtained into the intrapericardial or extrapericardial space (see Chapter 118A ).

For the transabdominal transdiaphragmatic intrapericardial approach to the suprahepatic IVC, three different approaches have been described. A first approach entails a transverse incision of the bilateral diaphragm just below the pericardial cavity and then sectioning the bottom of the pericardium. A second approach consists of dissecting off the central tendon of the diaphragm circumferentially. The falciform ligament is divided with cautery, and the incision is continued around each portion of the divided falciform ligament to the right superior coronary ligament. The left triangular ligament and the central diaphragm tendon are dissected until the supradiaphragmatic intrapericardial IVC is identified. The dissection has to be circumferential so that the intrapericardial IVC can be encircled below or above the confluence into the right atrium. A third approach entails the isolation of the IVC through a transdiaphragmatic pericardial window. After mobilizing the left liver, the diaphragm and bottom of the pericardium are vertically incised, and the intrapericardial IVC is isolated. These approaches are mainly used when, for technical or oncologic reasons, clamping of the IVC must be performed close to the right atrium. Although all these approaches avoid sternotomy, the opening of the pericardium increases right ventricular end-diastolic and end-systolic volumes, resulting in diminished right ventricular ejection fraction. In addition, postoperative pericardial effusion, constrictive pericarditis, and cardiac tamponade can develop. Pericardial drainage should be the rule every time that the pericardium is opened (see Chapter 118A ).

Two additional transabdominal transdiaphragmatic extrapericardial approaches to the IVC can be used as alternatives to the previous techniques. The first includes dissecting the diaphragm from the pericardium just below the xiphoid process, cutting the diaphragm vertically toward the IVC, and then taping the IVC after dissecting the fusion space between the pericardium and the diaphragm. In the second approach, after opening the posterior part of the falciform ligament and lowering the liver, the IVC is isolated in the same space while making a 5- to 7-cm transverse incision of the diaphragm 2 to 3 cm above the vena cava foramen. The dissection between the diaphragm and the inferior side of the pericardium allows identification of the IVC that can be taped. In both approaches, the diaphragm must be closed at the end of the procedure.

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