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Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1114_Библиотеки_им_академика_М_И_Перельмана

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M anagement: M alignant P rimary Liver N eoplasms ............................................................................. 189
Types of hepatic resection
FIGURE 6.20. Hepatic resections. The type of liver resection per­formed depends on the type and extent of the pathology. (Adapted with permission from Schwartz SI, ed. Principles of Surgery. 6th ed. New York: McGraw-Hill, Inc., Health Professions Division, 1994.)
requiring dissection along the main interlobar fissure in the right and left segmental fissure.
Hepatic lobectomy. In hepatic lobectomy, all liver tissue to one side of the main interlobar fissure is removed, either all tissue to the left in a left hepatic lobectomy or all tissue to the right in a right hepatic lobectomy. In either case, full mobilization of the liver is required (see below).
Trisegmentectomy. Also known as extended right hepa­tectomy, trisegmentectomy involves removing the right
lobe as well as the medial segment of the left lobe. This procedure can be considered only when the hepatic parenchyma in the left lateral segment is normal.
ECHNIQUE OF LIVER RESECTION Several steps are
T
involved in performing liver resection:
1. Incision. Either a long midline incision or a large right subcostal incision can be used. If necessary, either can be extended into medial sternotomy (Figure 6.21).
2. Mobilization. Key to major liver resection is ade­quate mobilization of the liver by dividing ligamentous attachments. The type of resection to be performed deter­mines the degree of mobilization required (Figure 6.22).
3. Portal dissection. Dissection of the hepatoduodenal ligament allows accurate application of a noncrushing clamp, should the Pringle maneuver be required at any time in the course of the operation (Figure 6.23).
4. Intraoperative ultrasound. Intraoperative ultrasound provides precise identification of the size of the tumor and its relationship to major ducts and vessels, particularly the hepatic veins. Hence, resection margins and avoidance of the unintended hepatic venous injury can be planned before embarking on the parenchymal dissection.
mentectomy, lobectomy, and trisegmentectomy (Figure
6.20). The selection of one approach over another depends on the type and extent of the pathology. The usual operations performed for HCC are hepatic lobectomy or trisegmentectomy:
Wedge resection. Benign tumors superficially located in the liver are amenable to wedge resection that involves removal of less than one segment of liver. The procedure usually requires little mobilization of the liver and no anatomic plane dissection. Resection is usually accom­plished with electrocautery and bleeding controlled by heavy mattress sutures using #1 absorbable suture.
Segmentectomy. This operation requires anatomic plane dissection along the lines of Couinaud. The simplest segmental resection is left lateral segmentectomy, also known as left hepatic lobectomy. An alternate procedure, left medial segmentectomy, is a more complicated approach
FIGURE 6.21. Surgical incision for liver resection. A modified chevron incision is often used. If necessary, the incision can be extended up into the chest, either as a median sternotomy or right lateral thoracotomy.
190 ................................................................................................................................................. Liver
A
B
C
D
FIGURE 6.22. Mobilization of the liver. The extent to which the liver must be mobilized depends on the type of resection to be performed. (A–C) Trisegmentectomy requires complete liver mobilization, which involves division of the triangular and coronary ligaments, the ligamentum teres and the falci­form ligament. (D) The liver is then rotated to the left and posterior attachments are dissected to expose the inferior vena cava and hepatic veins as they enter it. (Adapted from Blumgart LH, ed. Surgery of the Liver and Biliary Tract. 3rd ed. London: W.B. Saunders Company Ltd.; 2000.)
M anagement: M alignant P rimary Liver N eoplasms ............................................................................. 191
A
B
FIGURE 6.23. Portal dissection. (A) The hepatic artery, portal vein and bile duct are dissected in the hepatoduodenal ligament. (B) Dissection is carried to the liver parenchyma so that the right and left divisions of these structures can be identified and, if possible, encircled individually with tape before subsequent division between ligatures.
192 ................................................................................................................................................. Liver
A
B
C
FIGURE 6.24. Parenchymal and hepatic vein dissection. (A) The relevant vascular structures in the porta hepatis are clamped and the liver capsule incised along the surgical plane with scalpel or elec­trocautery. The surgical plane is developed by blunt dissection using the scalpel handle or by finger fracture technique. Vessels and bile ductal structures are clamped as they are encountered and individ­ually ligated (B). At the conclusion of the hepatic parenchymal division, the right, middle, and left hepatic veins can be isolated and the appropriate vein divided between vascular clamps and (C) the proximal end closed with continuous suture. (Adapted from Warren KW, Jenkins RL, Steele GD, Jr. Atlas of Surgery of the Liver, Pancreas and Biliary Tract. Norwalk, CT.: Appleton & Lange; 1991.)
5. Parenchymal dissection (Figure 6.24). Several other techniques may be used to aid in parenchymal dissection, including electrocautery, water-jet dissection, and ultra­sonic dissector. The procedure described above uses the technique of selective inflow control. Total inflow control by the Pringle maneuver may also be used but requires inflow restoration for several minutes every half hour to avoid warm ischemic injury to the liver.
6. Hepatic vein division. The intrahepatic dissection is continued posteriorly until the major hepatic veins are identified. Those draining the portion of the liver to be removed are doubly ligated in continuity and divided; care must be taken not to damage the venous drainage of the portion of the liver that is to be left behind. Now, the portion of liver to be excised is completely freed and removed. At this point, any clamps previously applied on
M anagement: M alignant P rimary Liver N eoplasms ............................................................................. 193
the vessels in the porta hepatis are unclamped and the cut surface of the liver examined for any bleeding. Bleeders are individually controlled and ligated. When all bleeding has stopped, the raw surface of liver is covered with omentum.
Another technique used for major hepatic resection is total vascular isolation of the liver, in which total inflow is controlled and the inferior vena cava is clamped below and above the liver. Total vascular isolation is safe for up to 60 minutes and is appropriate only for technically demanding cases in which hepatic vein dissec­tion is complicated by pathology in that region of the liver.
7. Drainage. Two large closed sump drains are inserted, one posteriorly in the right subphrenic space and the other more anteriorly, close to the porta hepatis.
194 ................................................................................................................................................. Liver
POSTOPERATIVE COMPLICATIONS
1. Functional complications. Patients who undergo 50%
or more resection may develop metabolic complications:
a. Hypoglycemia may occur when the remaining liver cannot provide adequate glycogenolysis. It can be pre­vented by administering 10% glucose solution intra­venously and frequently monitoring blood glucose levels.
b. Hypoalbuminemia may require administration of albumin but is rarely serious.
c. Coagulopathy may occur because of inadequate synthesis of prothrombin, fibrinogen, and factor ix. Proth­rombin time should be monitored and vitamin K adminis­tered intravenously if prothrombin time is prolonged.
d. Hyperbilirubinemia and AST and LDH elevation may occur but are temporary and resolve in 3 to 5 days.
2. Postoperative hemorrhage. The incidence of hemor­rhage is significantly reduced by ensuring meticulous hemostatis during the operation. Occasionally, significant postoperative bleeding requires control angiographically or with reoperation.
3. Sepsis. Subphrenic or perihepatic abscess may develop, causing fever and leukocytosis. These abscesses are usually successfully treated by percutaneous drainage.
4. Stress ulcer. Upper gastrointestinal bleeding from stress ulcer is now very rare because of the prophylactic use of histamine H
2
-receptor antagonists and antacids.
Total Hepatectomy and Liver Transplantation
Liver transplantation is emerging as a viable option in patients with lesions of less than 5 cm in size, three or fewer lesions, and with associated cirrhosis, which renders partial hepatectomy risky. Recently reported studies indi­cate 5-year survival of 19% to 70%.
16
Favorable prognos­tic factors are tumor size of 5 cm or less, unicentric tumors, absence of vascular invasions, presence of pseudocapsulae, and low histologic grade. In one report by Mazzaferro et al.,
17
the 4-year survival for single nodules less than 5 cm or fewer than three nodules each less than 3cm in size was 92%.
Palliative Therapy
When curative resection or transplantation are not possible a number of palliative therapeutic modalities are available.
1. Transarterial chemoembolization with doxorubicin may be helpful because the blood supply of HCC is derived from the hepatic artery. A 1-year survival rate of 40% to 50% has been achieved.
18
2. Hepatic artery ligation can be performed to produce tumor necrosis and may be combined with chemoembolization.
3. Percutaneous ethanol injection may lead to partial regression.
4. Cryosurgery with liquid nitrogen may help shrink the tumor.
5. Systemic chemotherapy is particularly useful in chil­dren with hepatoblastoma, in which subsequent resec­tion might achieve very high cure rates of 80% to 90%.
19
CHOLANGIOCARCINOMA
The incidence of cholangiocarcinoma in patients is about 5% of the incidence of HCC. Its incidence is much higher in areas of the world where chronic infestation of liver flukes (Clonorchis sinensis and Opisthorchis viverrini) occurs in the biliary tree (i.e., Thailand, Hong Kong, and Canton Province of China). Other conditions associated with cholangiocarcinoma are sclerosing cholangitis and
a
1
-antitrypsin deficiency. While the symptoms and signs are similar to those of HCC, jaundice is more common and more severe. The picture is one of progressive obstruc­tive jaundice.
Investigations
Liver function studies show a mixture of obstructive and hepatocellular abnormality. AFP is infrequently elevated. CT and ultrasound show the tumor. Hepatic angiography reveals a tumor that is not hypervascular,and the branches of the hepatic artery are diminished in number and size because of the associated fibrosis that occurs. Endoscopic retrograde cholangiopancreatography (ERCP) or tran­shepatic cholangiography are useful localizing techniques.
Treatment
Resection is rarely possible because the lesion is diagnosed late. Similarly, the tumor is unresponsive to radiotherapy or chemotherapy. Resection of hilar tumors is discussed separately in Chapter 7.
METASTATIC NEOPLASMS OF THE LIVER
The liver is a common site for metastatic cancer. Metasta­tic cancer accounts for 95% of all neoplasms in the liver. The liver represents the first hematogenous filter of tumor cells spread from abdominal organs via the portal vein. Thus, it is a frequent site of metastasis from the pancreas, stomach, and small and large intestine. Secondary spread to the liver can also occur via the systemic circulation, and common primary tumors that metastasize there are breast, lung, kidney, ovary, and uterus.
The clinical picture is usually dominated by that of the primary neoplasm. Since liver metastasis represents advanced malignancy, patients frequently exhibit weight loss, anorexia, and fatigue. The liver lesions, however, may be painful and become palpable on abdominal examina­tion. Jaundice is a rare symptom.
Investigations
Abnormal liver function is seen in more than 50% of patients. Elevated alkaline phosphatase is more common than elevated bilirubin levels. CT, ultrasound, or MRI will show the lesion. MRI is the superior imaging modality because it provides information about venous invasion. Needle biopsy can be obtained under CT or ultrasound guidance, at laparoscopy, or laparotomy.
Treatment
In ninety percent of patients with liver metastases, the disease will have spread to other organs. Only nonsurgical palliative therapy can be offered to these patients. In some, presence of multiple lesions precludes surgical treat­ment, and in others, the known aggressive biological behavior of the primary makes consideration of surgical treatment of liver secondaries futile. Hence, second­aries from the esophagus, stomach, pancreas, lung, and usually breast and liver are not considered for surgical extirpation.
Patients with colorectal primary neoplasms have been shown to benefit most from resection of hepatic metasta­sis. Even here, fewer than 5% of patients are candidates for liver resection. Patients who should be considered for removal of hepatic secondaries include those with:
1. No extrahepatic disease.
2. A single metastatic tumor or not more than three or four lesions.
3. A time lapse of 1 year from colectomy or proctectomy.
4. Duke B stage of primary tumor.
Other patients who may be candidates for resection of
hepatic metastases are those with carcinoid syndrome and other neuroendocrine tumors. Hepatic resection may be limited to wedge resection or may involve hepatic lobec­tomy (see Figure 6.20).
Outcome
Some 25% of patients with colorectal cancer who meet the criteria for resection of hepatic metastasis will live 5 years after resection.
20
Patients who undergo palliative liver resection for the carcinoid syndrome or for other malig­nant neuroendocrine tumors (e.g., VIPoma, insulinoma) experience significant improvement of their symptoms and are more successfully managed postoperatively phar­macologically with octreotide.
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2. Iwatsuki S, Stieber AC, Marsh JW, et al. Liver transplantation for fulminant hepatic failure. Transplant Proc 1989;21(1 Pt 2): 2431–2434.
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8. Fillmore DJ, Miller FJ, Fox LF, et al. Transjugular intrahepatic portosystemic shunt: midterm clinical and angiographic follow­up. J Vasc Interv Radiol 1996;7:255–261.
9. Orloff MJ, Orloff MS, Orloff SL, et al. Three decades of experi­ence with emergency portacaval shunt for acutely bleeding esophageal varices in 400 unselected patients with cirrhosis of the liver. JAmCollSurg1995;180:257–272.
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13. Rikkers LF, Sorrell WT, Jin G. Which portosystemic shunt is best? Gastroenterol Clin North Am 1992;21:179–196.
14. Stanley MM, Ochi S, Lee KK, et al. Peritoneovenous shunting as compared with medical treatment in patients with alcoholic cir­rhosis and massive ascites.Veterans Administration Cooperative Study on Treatment of Alcoholic Cirrhosis with Ascites. NEngl JMed1989;321:1632–1638.
15. Lai EC, Fan ST, Lo CM, et al. Hepatic resection for hepatocellu­lar carcinoma. An audit of 343 patients. Ann Surg 1995;221: 291–298.
16. Simonetti RG, Liberati A, Angiolini C, et al. Treatment of hepa­tocellular carcinoma: a systematic review of randomized con­trolled trials. Ann Oncol 1997;8:117–136.
17. Mazzaferro V, Regalia E, Doci R, et al. Liver transplantation for the treatment of small hepatocellular carcinomas in patients with cirrhosis. NEnglJMed1996;334:693–699.
18. Liu CL, Fan ST. Nonresectional therapies for hepatocellular car­cinoma. Am J Surg 1997;173:358–365.
19. Reynolds M, Douglass EC, Finegold M, et al. Chemotherapy can convert unresectable hepatoblastoma. J Pediatr Surg 1992;27: 1080–1084.
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20. Ohlsson B, Stenram U, Tranberg KG. Resection of colorectal liver metastases: 25-year experience. WorldJSurg1998;22: 268–277.
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Dixon JL, Ginsberg HN. Hepatic synthesis of lipoproteins and
apolipoproteins. Semin Liver Dis 1992;12:364–372.
Mammen EF. Coagulation defects in liver disease. Med Clin North
Am 1994;78:545–554.
Meier PJ. Molecular mechanisms of hepatic bile salt transport from
sinusoidal blood into bile. Am J Physiol 1995;269(6 Pt 1): G801–G812.
Nathanson MH, Boyer JL. Mechanisms and regulation of bile secre-
tion. Hepatology 1991;14:551–566.
Pilkis SJ, Granner DK. Molecular physiology of the regulation of
hepatic gluconeogenesis and glycolysis. Annu Rev Physiol 1992;54:885–909.
Rothschild MA, Oratz M, Schreiber SS. Serum albumin. Hepatology
1988;8:385–401.
Steer CJ. Liver regeneration. FASEB J 1995;9:1396–1400.
Portal Hypertension
Collins JC, Rypins EB, Sarfeh IJ. Narrow-diameter portacaval shunts
for management of variceal bleeding. WorldJSurg1994;18: 211–215.
Klein AS, Sitzmann JV, Coleman J, et al. Current management of the
Budd–Chiari syndrome. Ann Surg 1990;212:144–149.
Langer B, Taylor BR, Mackenzie DR, et al. Further report of a
prospective randomized trial comparing distal splenorenal shunt with end-to-side portacaval shunt. An analysis of enceph­alopathy, survival, and quality of life. Gastroenterology 1985;88: 424–429.
Millikan WJ Jr, Warren WD, Henderson JM, et al. The Emory
prospective randomized trial: selective versus nonselective shunt to control variceal bleeding. Ten year follow-up. Ann Surg 1985;201:712–722.
Patch D, Sabin CA, Goulis J, et al. A randomized, controlled trial of
medical therapy versus endoscopic ligation for the prevention of variceal rebleeding in patients with cirrhosis. Gastroenterol- ogy 2002;123:1013–1019.
Resnick RH, Chalmers TC, Ishihara AM, et al. A controlled study of
the prophylactic portacaval shunt. A final report. Ann Intern Med 1969;70:675–688.
Rikkers LF, Jin G. Emergency shunt.Role in the present management
of variceal bleeding. Arch Surg 1995;130:472–477.
Stanley MM, Ochi S, Lee KK, et al. Peritoneovenous shunting as
compared with medical treatment in patients with alcoholic cir­rhosis and massive ascites.Veterans Administration Cooperative Study on Treatment of Alcoholic Cirrhosis with Ascites. NEngl JMed1989;321:1632–1638.
Terblanche J, Kahn D, Bornman PC. Long-term injection scle-
rotherapy treatment for esophageal varices. A 10-year prospec­tive evaluation. Ann Surg 1989;210:725–731.
Liver Abscess
Donovan AJ, Yellin AE, Ralls PW. Hepatic abscess. WorldJSurg
1991;15:162–169.
Huang CJ, Pitt HA, Lipsett PA, et al. Pyogenic hepatic abscess.
Changing trends over 42 years. Ann Surg 1996;223:600–609.
Echinococcus (Hydatid) Cyst
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pared with surgery for hepatic hydatid cysts. NEnglJMed 1997;337:881–887.
Lewall DB. Hydatid disease: biology, pathology, imaging and classi-
fication. Clin Radiol 1998;53:863–874.
Xynos E, Pechlivanides G, Tzortzinis A, et al. Hydatid disease of
the liver. Diagnosis and surgical treatment. HPB Surg 1991;4: 59–67.
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Belli L, De Carlis L, Beati C, et al. Surgical treatment of symptomatic
giant hemangiomas of the liver. Surg Gynecol Obstet 1992;174: 474–478.
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Hepatocellular Carcinoma and Cholangiocarcinoma
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resection or transplantation. J Hepatobiliary Pancreat Surg 1998; 5:18–23.
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Liver Transpl 2000;6(6 Suppl 2):S30–S34.
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carcinoma metastases: a multi-institutional study of indications for resection. Surgery 1988;103:278–288.
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Bismuth H, Dennison AR. Segmental liver resection. Adv Surg
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S uggested R eadings............................................................................................................................. 197
198 ...........................................................................................................................................................
The biliary tree and liver develop from a diverticulum of the embryonic foregut at approximately 18 days of gesta­tion. Between the fourth and fifth weeks, the diverticulum consists of a solid cranial portion and a hollow caudal portion. The solid cranial portion differentiates into the liver with the development of hepatocytes and intrahe­patic bile ducts, while the hollow caudal portion gives rise to the gallbladder, the extrahepatic bile ducts, and the ventral pancreas (Figure 7.1).
GALLBLADDER
In the adult, variability in the anatomy of the biliary tree is more the norm than the exception.The gallbladder (GB) is a pear-shaped organ (50ml volume) consisting of the fundus, corpus, infundibulum, and neck, which tapers into the cystic duct. Its wall is made up of smooth muscle encased in fibrous tissue. The mucosa is made up of columnar epithelial cells with tight junctions and micro­villi suited for absorption. The cystic duct connects the GB to the common bile duct (CBD) and contains the spiral valve of Heuser, which provides a measure of resistance to outward flow.
COMMON BILE DUCT
The left and right hepatic ducts form the common hepatic duct. The cystic duct entrance into the common hepatic
7
Biliary Tract
EMBRYOLOGY AND ANATOMY
duct represents the beginning of the CBD, which then runs inferiorly toward the duodenum in the free edge of the lesser omentum to the right of the hepatic artery and ante­rior to the portal vein. The CBD passes behind the first part of the duodenum and then courses within the pan­creas to enter the second part of the duodenum. The CBD is about 7 cm long and less than 1 cm wide when assessed intraoperatively with the naked eye or with a choledo­chogram. When seen by ultrasonography, however, normal CBD width should be less than 0.7 cm. The mucosa is cuboidal epithelium, and the wall of the CBD is fibrous tissue with small amounts of smooth muscle.
CHOLEDOCHAL SPHINCTER COMPLEX OR SPHINCTER OF ODDI
The entrance of the CBD into the second portion of the duodenum is oblique and surrounded by the choledochal sphincter complex, which controls bile flow into the duo­denum in a manner that is coordinated with GB contrac­tion. The choledochal sphincter complex or sphincter of Oddi (Figure 7.2) is composed of several portions:
1. The choledochal sphincter, comprised of a compact area of circular muscle around the intramural part of the duct.
2. The pancreatic duct sphincter, present in about one­third of individuals.
Management of biliary tract disease constitutes an important segment of gastrointestinal surgery. Patients recovering from biliary tract surgery once accounted for a significant number of inpatients on the surgical wards. The advent of minimally invasive surgery and advances in both interventional endoscopy and interventional radiology has changed all this. Following laparoscopic cholecystectomy and endoscopic sphincterotomy and removal of common duct stones, most patients now are admitted for only 24 to 48 h or need not be admitted at all. Nonetheless, the incidence of biliary tract surgery has not decreased.