Chapter 33 Trisectionectomy
INTRODUCTION
As experience with hepatic resection has evolved since the late 1980s, significant improvements in perioperative morbidity and mortality have been realized. Nonetheless, because it involves the resection of up to 70% to 80% of functional hepatic mass, trisectionectomy places patients at considerable risk for postoperative morbidity. In a study of over 1800 liver resections performed at Memorial Sloan-Kettering from 1991 to 2001, investigators found that the incidence of postoperative morbidity and mortality increased significantly as the number of segments involved in the resection increased. For patients undergoing trisectionectomy at that institution, the complication rate of 75% and operative mortality rate of 7.8% were significantly higher than for patients undergoing less extensive resections.1 When the same authors analyzed a subgroup of 226 patients undergoing only extended hepatic resections, they were able to identify a total of five factors that were most predictive of in-hospital mortality: cholangitis, creatinine greater than 1.3 mg/dl, total bilirubin greater than 6 mg/dl, intraoperative blood loss greater than 3 L, and vena caval resection.2 The presence of any two of these factors was associated with 100% mortality, whereas the absence of any of these factors was associated with only 3% mortality. In the largest series of left hepatic trisectionectomies published to date, from Nishio and colleagues,3 revealed an overall morbidity rate of 46% and a 30-day mortality rate of 7%. Preoperative jaundice and intraoperative blood transfusion were identified by multivariate analysis to be the major risk factors for postoperative morbidity in this group of 70 patients.
Knowledge of the variables most predictive of postoperative morbidity has stimulated a number of modifications in the preoperative and intraoperative management of patients undergoing extended hepatic resection. Preoperative management options such as portal venous embolization and biliary drainage, as well as intraoperative techniques aimed at limiting blood loss, have enabled trisectionectomy to be performed with minimal perioperative mortality and major postoperative morbidity. One analysis of 58 major hepatic resections, including 49 trisectionectomies, reported 0% perioperative mortality and a 43% morbidity rate, with no cases of postoperative liver failure.4 Other groups are reporting similar outcomes, indicating that trisectionectomy for oncologic diagnoses can be performed with minimal short-term mortality.5,6
OPERATIVE STEPS COMMON TO BOTH RIGHT AND LEFT TRISECTIONECTOMY7
Step 3 Abdominal exploration and intraoperative ultrasonography of hepatic lesions and major vascular structures
Step 5 Confirmation of arterial anatomy via palpation of gastrohepatic ligament and gastroduodenal ligament to rule out accessory/replaced hepatic arteries
OPERATIVE STEPS SPECIFIC TO RIGHT TRISECTIONECTOMY
Step 7R Control of inflow vessels via extrahepatic dissection and ligation
• Open sheath of porta hepatis, dissection of plane between common bile duct and portal vein, ligation and division of right portal vein, ligation and division of right hepatic artery
Step 8R Control of right hepatic vein
• Ligation/division of small hepatic venous tributaries from caudate process and posterior aspect of right lobe to inferior vena cava (IVC)
OPERATIVE STEPS SPECIFIC TO LEFT TRISECTIONECTOMY
OPERATIVE PROCEDURE
Skin Incision
Inadequate Exposure
• Consequence
Difficulty in hepatic venous identification and control owing to inadequate liver mobilization increases the potential for hepatic venous injury and subsequent massive hemorrhage.
• Repair
Maximizing the position of a self-retaining retractor may permit better visualization of the suprahepatic and retrohepatic IVC.8 In cases in which manipulation of the retractor still does not provide adequate exposure, extension of the subcostal incision further to the right or left may help to improve exposure. Rarely, creating a modified thoracoabdominal incision permits exposure to the chest and supradiaphragmatic vena cava and may be especially useful in patients with bulky tumors of the superoposterior portions of the right hepatic lobe, especially in large patients.9
• Prevention
An alternative to the bilateral subcostal incision is an upper midline incision from the xyphoid process to 2 cm superior to the umbilicus connecting to a right transverse abdominal incision extending to the midaxillary line halfway between the lowest rib and the right iliac crest.7 This incision usually provides sufficient exposure for all types of hepatic resection, including resections involving the right lobe of the liver. A right anterolateral thoracoabdominal incision will permit access to both the chest and the abdominal cavity and should be considered preoperatively either in patients with a large tumor of the right lobe or in those who require repeat resection after a previous right hepatic lobectomy. In the Memorial Sloan-Kettering series of over 1800 hepatic resections, a thoracoabdominal incision was required in only 3% of patients.1
Mobilization of the Liver
Postoperative Pleural Effusion
Pleural effusion is one of the most common complications after major hepatectomy and likely has a multifactorial etiology. A retrospective review of 254 patients undergoing liver resection for hepatocellular carcinoma at one institution found the incidence of patients developing postoperative intractable pleural effusion to be 5.9%.10 The pressure differential between the abdominal and the thoracic spaces, combined with compromise of the diaphragmatic barrier owing liver mobilization, can cause ascitic fluid to traverse the diaphragm and accumulate in the right pleural space. Patients with some degree of underlying cirrhosis are also commonly hypoalbuminemic and may also have high portal venous pressures that are transmitted to the azygous vein, thus promoting transudation into the pleural space.11
• Consequence
Although often asymptomatic, postoperative pleural effusions may compromise the respiratory function of posthepatectomy patients. The effusion can cause pulmonary atelectasis and poses a risk factor for nosocomial pneumonia. In patients on the ventilator, significant pleural effusion can increase the number of days that mechanical ventilation is necessary, whereas in patients who have already been extubated, pleural effusion may increase the incidence of reintubation.
• Repair
Intraoperatively, pleural drainage using an indwelling central venous catheter in the pleural cavity has been shown to be efficacious in preventing the accumulation of pleural fluid after hepatectomy.12 Postoperative drainage for pleural effusion is indicated either in patients who are experiencing difficulty weaning from mechanical ventilation or in those who have marginal respiratory function postextubation. Management options include diuretic administration, pleural drainage via either thoracentesis or a pleural drainage catheter, and pleurodesis. In a study of 10 patients with postoperative pleural effusion, 4 responded to conservative management with diuretics, 4 required pleural drainage, and 2 required pleurodesis.11
• Prevention
Multivariate analysis of patients with intractable posthepatectomy pleural effusion revealed increased serum levels of type IV collagen, preoperative transcatheter arterial embolization, and resections including segments 7 and/or 8 to be independent risk factors for the development of this complication.10 A separate investigation confirmed that resections involving segments 7 and 8, via either right hepatectomy or posterior segmentectomy, led to increased risk of postoperative pleural effusion.13
The difference between the positive pressure of the abdominal cavity and the negative pressure of the intrathoracic space may contribute to the unidirectional diffusion of ascitic fluid into the pleural space, especially as the dissociation of the liver from its diaphragmatic attachments can lead to an increase in the development of small holes in the diaphragm. Simply extending the duration of postoperative mechanical ventilation by 1 day postoperatively has been shown to reduce the development of pleural effusion after hepatectomy, presumably by providing persistent positive intrathoracic pressure to allow fibrin deposits to seal the small diaphragmatic communications between the abdomen and the thoracic cavity and thus preventing the migration of ascitic fluid.14
Alternatively, argon beam coagulation of the dissected diaphragmatic surfaces may help to seal these tiny routes for fluid migration intraoperatively. Yan and colleagues12 compared two groups of hepatectomy patients, one who underwent separation of the liver from the diaphragm using argon beam coagulation and the other undergoing suture ligation of bleeding points from the diaphragmatic attachments. Patients in the argon beam coagulation group had a 3.8% incidence of postoperative pleural effusion, whereas patients in the suture ligation group had a 10.5% incidence (P < .01). In a separate prospective, randomized trial of 60 patients undergoing hepatectomy, 28 underwent argon beam coagulation of the cut surface of the hepatic ligaments and bare area of the retroperitoneum whereas 32 did not. The two groups of patients were similar with respect to demographic characteristics as well as preoperative and postoperative liver function. One of the 28 patients receiving argon beam coagulation developed postoperative pleural effusion at 3 days postoperatively compared with 9 of the 32 patients who did not receive argon beam coagulation.11
An alternative to the use of argon beam coagulation is to apply fibrin sealant to the cut surface of the diaphragmatic attachments after liver mobilization. This technique resulted in a significant reduction in the development of postoperative pleural effusion among 25 patients undergoing hepatectomy compared with a control group of 39 patients in whom fibrin sealant was not used.15 Avoidance of routine use of the thoracoabdominal approach to liver resection has also been suggested as a means to reduce the incidence of postoperative pleural effusion and the necessity for subsequent thoracentesis because up to 73% of patients in whom this incision is used will develop pleural effusion postoperatively.16
Control of Inflow Vessels
Hepatic Necrosis due to Hepatic Arterial or Portal Venous Injury or Thrombosis
• Consequence
The hepatic artery is responsible for up to 50% of the oxygen supply to the liver. Because the oxygen consumption is expected to be elevated after hepatectomy as the remnant liver undergoes regeneration, compromise of oxygen delivery to the remnant liver owing to hepatic arterial injury can result in acute necrosis of the remaining hepatic tissue. In addition, compromise of the portal venous flow postoperatively can also result in hepatic necrosis because the portal vein normally provides 75% of blood flow to the liver. Acute hepatic necrosis is typically characterized by acute abdominal pain and abrupt, marked increases in transaminase levels. Other sequelae of fulminant hepatic failure may soon follow. The diagnosis can be confirmed by duplex ultrasonography, which will document reduced or absent hepatic arterial or portal venous flow and hypoechogeneic areas within the remnant liver. Computed tomography can verify the absence of portal flow and arteriography can verify the absence of hepatic arterial flow, if ultrasound is equivocal.17
• Repair
Injuries to the hepatic artery or portal vein that are recognized intraoperatively can usually be repaired. Hepatic arterial injuries that do not involve excessive segment lengths can be repaired using a direct end-to-end anastomosis or a saphenous vein interposition graft. Portal venous injuries, meanwhile, can usually be repaired by venoplasty using the greater saphenous vein. Vascular reconstruction of either the hepatic artery or the portal vein in patients undergoing hepatic resection for cholangiocarcinoma has been shown to result in survival rates comparable with those in patients who do not require such reconstruction.6
Unrecognized hepatic arterial injuries that lead to hepatic arterial thrombosis postoperatively are usually not necessary to repair because the resulting hepatic necrosis is irreversible. However, in order to maximize the function of the remaining liver tissue, some groups have reported performing portal arterialization in these situations. This procedure involves the construction of a shunt between the portal vein and a mesenteric artery, thereby increasing the delivery of oxygen to regenerating hepatic tissue that is spared of necrosis.17,18
• Prevention
The best way to prevent hepatic arterial injury is to have a thorough knowledge of variants to normal hepatic arterial anatomy and to carefully assess the anatomy of individual patients through preoperative multisection computed tomographic arteriography. “Normal” hepatic arterial anatomy, which is present in only 55% of patients, consists of a common hepatic artery coming off of the celiac axis, giving off a gastroduodenal branch to then become the proper hepatic artery.19 The proper hepatic artery travels toward the liver within the hepatoduodenal ligament, lying anterior to the portal vein and to the left of the common bile duct. In up to 20% to 30% of patients, a left hepatic artery arises from the left gastric artery. This can be either an accessory left hepatic artery (which occurs in addition to a left branch of the proper hepatic artery) or a replaced left hepatic artery (which represents the sole arterial supply to the left segments of the liver). In approximately 17% of patients, a right hepatic artery arises from the superior mesenteric artery. This artery, which can also serve as either an accessory or a replaced right hepatic artery, travels within the hepatoduodenal ligament posterior to the common bile duct, then to the right of the common hepatic duct as it approaches the hilum of the liver.20
Portal venous anatomy tends to be more consistent from patient to patient, although variants do exist. The portal vein lies posterior to both the common bile duct and the hepatic artery within the hepatoduodenal ligament. The most common anomaly requiring attention during left trisectionectomy is trifurcation of the portal vein, in which the portal vein branches to the right paramedian and lateral sectors originate from the main portal vein in addition to the left portal vein.21 In patients with a normal portal vein bifurcation undergoing left trisectionectomy, care must be taken in dissecting the right portal vein because this branch is much shorter than the left portal vein (Fig. 33-1).
In addition to thorough knowledge of these types of variants, avoiding injury or excessive manipulation of the hepatic artery and portal vein that is to supply the remnant liver is also essential for preventing postoperative hepatic necrosis owing to hepatic arterial injury. For example, when performing a Pringle maneuver, a tourniquet made from a Penrose drain to obtain vascular inflow occlusion should be used in order to avoid intimal disruption within the proper hepatic artery that can be caused by direct application of vascular clamps.17 In addition, verification of pulsatile blood flow to the planned hepatic remnant during occlusion of arterial inflow into liver to be resected will assist in prevention of this complication.
Injury to the Arterial Supply of the Biliary System
• Consequence
Injury to the right hepatic artery, or its branches that supply the major bile ducts, can result in ischemic injury to the duct and subsequently long-term bile duct stenosis. Such stenosis can subsequently lead to recurrent episodes of cholangiitis or even the development of cirrhosis of the remnant liver.
• Repair
Accidental division of the major bile duct that is to drain the remnant liver after trisectionectomy requires intraoperative reestablishment of biliary continuity. This can be accomplished either through a direct end-to-end anastomosis of the proximal duct and distal common bile duct or by Roux-en-Y hepaticojejunostomy. Although primary anastomosis can be considered for dilated ducts, a bilioenteric anastomosis is usually preferred for ducts that are of normal caliber because the risk of postoperative biliary stenosis is minimized.
In cases of unrecognized biliary injury due to ischemic damage to the major bile duct draining remnant liver, repair involves reoperation and Roux-en-Y hepaticojejunostomy. If the patient presents with postoperative cholangiitis due to biliary obstruction, the percutaneous transhepatic drainage of the remnant biliary system should be performed prior to definitive repair.
• Prevention
Knowledge of the arterial blood supply to the extrahepatic biliary system is important in order to avoid ischemic insult to the biliary drainage of the remnant liver after trisectionectomy. The epicholedochal plexus at the biliary bifurcation derives its blood supply primarily from the right hepatic artery, which sends a branch to the plexus when it passes posterior to the common bile duct. Therefore, dissection and division of the right hepatic artery during right trisectionectomy should be performed to the right of the common bile duct in order to avoid damaging this branch.21 Furthermore, division of biliary structures during major hepatectomy should be delayed until after parenchymal resection in order to avoid biliary injury. Minimization of hilar dissection is also preferable in order to avoid injury to the vascular supply of the remnant biliary duct. Recently described techniques in which the glissonian sheaths of the segments to be resected are isolated and divided individually can help limit the degree of hilar dissection necessary to achieve resection.22
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