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Surgery_Schwartz. rate was 50%, but the recurrence-free survival rate was only 10%.200 In a report of 67 patients undergoing a second resection for HCC, over-all 1-, 3-, and 5-year survival rates were 93%, 70%, and 56%, respectively.201 Multivariate analysis showed that absence of portal invasion at the second resection, single HCC at primary hepatectomy, and disease-free interval of ≥1 year after primary hepatectomy were independent prognostic factors after the sec-ond resection.LAPAROSCOPIC LIVER RESECTIONCherqui and colleagues first reported in 2000 that laparoscopic hepatic surgery was feasible.202 Since this initial report, laparo-scopic liver surgery has expanded from the simple unroofing of hepatic cysts to resection of peripheral benign lesions to formal anatomic lobectomies for malignancy and laparoscopic hepa-tectomy for living donor liver transplantation. While minimally invasive approaches have been widely adopted in other areas of abdominal surgery, there was initial apprehension regarding


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Surgery_Schwartz. hepa-tectomy for living donor liver transplantation. While minimally invasive approaches have been widely adopted in other areas of abdominal surgery, there was initial apprehension regarding laparoscopic liver resection (LLR), hampering its widespread adoption.203 Great strides have been made in the past decade with techniques of laparoscopic liver resection,204,205 and two International Laparoscopic Liver Resection Consensus Confer-ences have been convened in Louisville (2008) and Morioko (2014).206,207 Indications for liver resection should not be altered by the availability of minimally invasive liver resection tech-niques. Currently, over 9500 cases of laparoscopic liver resec-tion have been reported worldwide, with over 50% of the cases being done for malignancy.208Pure laparoscopic and hand-assisted laparoscopic liver resection are the two most commonly used techniques for mini-mally invasive liver resection surgery,209,210 while robotic liver resection is being used by several


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Surgery_Schwartz. and hand-assisted laparoscopic liver resection are the two most commonly used techniques for mini-mally invasive liver resection surgery,209,210 while robotic liver resection is being used by several groups.211 Advantages of the hand-port include tactile feedback, facilitation of liver mobiliza-tion, and ease of ability to control bleeding. Also, when doing a large parenchymal resection, the hand-port can be comparable in size to the extraction port utilized in the purely laparoscopic Brunicardi_Ch31_p1345-p1392.indd 138620/02/19 2:37 PM 1387LIVERCHAPTER 31approach. The hand-assisted approach can be ideal for surgeons beginning the transition to laparoscopic liver resection and for more experienced laparoscopic HPB surgeons doing laparo-scopic major hepatectomies or as an alternative to conversion to open surgery.Benefits of laparoscopic liver resection include less blood loss, decreased morbidity, decreased postoperative pain and narcotic requirements, faster return of bowel


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Surgery_Schwartz. to conversion to open surgery.Benefits of laparoscopic liver resection include less blood loss, decreased morbidity, decreased postoperative pain and narcotic requirements, faster return of bowel function, and shorter length of hospital stay compared to open hepatic resection.212 Long-term oncologic outcomes for HCC and CLM have been shown to be comparable for laparoscopic vs. open liver resection using propensity score matching and meta-analysis studies.213-215 The learning curve for laparoscopic liver resection has been reported to be around 60 cases,216 although this may be greater for laparoscopic major hepatectomy.217-219 Cost analy-sis has shown that laparoscopic liver resection is cost effective compared to open liver resection, where the added cost of the operating room disposables are more than offset by the savings associated with ∼50% reduction in the hospital length of stay.221,222Initial experience with laparoscopic living-donor hepatec-tomy for transplantation was with


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Surgery_Schwartz. are more than offset by the savings associated with ∼50% reduction in the hospital length of stay.221,222Initial experience with laparoscopic living-donor hepatec-tomy for transplantation was with left lateral segmentectomy during liver allograft procurement for pediatric transplants.222 With continued advances in laparoscopic liver surgery, LLR has been applied to adult-to-adult donor right hepatectomy,223,224 although this approach remains controversial.In summary, laparoscopic liver resection can now be per-formed safely by experienced surgeons in selected patients. Compared to open hepatic resection, the laparoscopic approach has benefits of less blood loss, reduced postoperative pain, and a shorter length of hospital stay, with similar oncologic out-comes for resection of HCC and limited colorectal liver metastases.REFERENCESEntries highlighted in bright blue are key references. 1. Wikipedia. Prometheus. Available at: http://en.wikipedia.org/wiki/Prometheus. Accessed July 26,


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Surgery_Schwartz. limited colorectal liver metastases.REFERENCESEntries highlighted in bright blue are key references. 1. Wikipedia. Prometheus. Available at: http://en.wikipedia.org/wiki/Prometheus. Accessed July 26, 2018. 2. Keen WW IV. Report of a case of resection of the liver for the removal of a neoplasm, with a table of seventy-six cases of resection of the liver for hepatic tumors. Ann Surg. 1899;30(3):267-283. 3. Fortner JG, Blumgart LH. A historic perspective of liver sur-gery for tumors at the end of the millennium. J Am Coll Surg. 2001;193(2):210-222. 4. Pringle JH V. Notes on the arrest of hepatic hemorrhage due to trauma. Ann Surg. 1908;48(4):541-549. 5. Cantlie J. On a new arrangement of the right and left lobes of the liver. Proc Anat Soc Great Britain Ireland. 1897;32:4-9. 6. Couinaud C. Lobes de segments hepatiques: notes sur l’architecture anatomique et chirurgical de foie. Presse Med. 1954;62(33):709-712. 7. Abdalla EK, Vauthey JN, Couinaud C. The caudate lobe of the liver:


Surgery_Schwartz

Surgery_Schwartz. C. Lobes de segments hepatiques: notes sur l’architecture anatomique et chirurgical de foie. Presse Med. 1954;62(33):709-712. 7. Abdalla EK, Vauthey JN, Couinaud C. The caudate lobe of the liver: implications of embryology and anatomy for surgery. Surg Oncol Clin N Am. 2002;11(4):835-848. 8. Bismuth H. Surgical anatomy and anatomical surgery of the liver. World J Surg. 1982;6(1):3-9. 9. Nordlie RC, Foster JD, Lange AJ. Regulation of glucose pro-duction by the liver. Annu Rev Nutr. 1999;19:379-406. 10. Merriman R. Approach to the patient with jaundice. In: Yamada T, ed. Textbook of Gastroenterology. 4th ed. Philadelphia: Lippincott Williams & Williams; 2003:911. 11. Ramadori G, Christ B. Cytokines and the hepatic acute-phase response. Semin Liver Dis 1999;19(2):141-155. 12. Tsung A, Geller DA. CD14 and Toll Receptor. In: Dufour JF, Clavien PA, eds. Signaling Pathways in Liver Diseases. Berlin: Springer; 2005:165-171. 13. Su GL. Lipopolysaccharides in liver injury: molecular


Surgery_Schwartz

Surgery_Schwartz. A, Geller DA. CD14 and Toll Receptor. In: Dufour JF, Clavien PA, eds. Signaling Pathways in Liver Diseases. Berlin: Springer; 2005:165-171. 13. Su GL. Lipopolysaccharides in liver injury: molecular mecha-nisms of Kupffer cell activation. Am J Physiol Gastrointest Liver Physiol. 2002;283:G256-G265. 14. Geller DA, Billiar TR. Molecular biology of nitric oxide syn-thases. Cancer Metastasis Rev. 1998;17:7-23. 15. Prince JM, Billiar TR. Nitric Oxide. In: Dufour JF, Clavien PA, eds. Signaling Pathways in Liver Diseases. Berlin: Springer; 2005:299-310. 16. Tsuchihashi S, Busuttil RW, Kupiec-Weglinski JW. Heme Oxygenase System. In: Dufour JF, Clavien PA, eds. Sig-naling Pathways in Liver Diseases. Berlin: Springer; 2005: 291-298. 17. Zuckerbraun BS, Billiar TR. Heme oxygenase-1: a cellular Hercules. Hepatology. 2003;37:742-744. 18. Akira S, Takeda K. Toll-like receptor signalling. Nat Rev Immunol. 2004;4:499-511. 19. Mollen KP, Anand RJ, Tsung A, Prince JM, Levy RM, Billiar TR. Emerging


Surgery_Schwartz

Surgery_Schwartz. Hepatology. 2003;37:742-744. 18. Akira S, Takeda K. Toll-like receptor signalling. Nat Rev Immunol. 2004;4:499-511. 19. Mollen KP, Anand RJ, Tsung A, Prince JM, Levy RM, Billiar TR. Emerging paradigm: toll-like receptor 4-sentinel for the detection of tissue damage. Shock 2006;26:430-437. 20. Farombi EO, Surh YJ. Heme oxygenase-1 as a potential therapeutic target for hepatoprotection. J Biochem Mol Biol 2006;39:479-491. 21. Kruskal JB, Kane RA. Intraoperative US of the liver: techniques and clinical applications. Radiographics. 2006;26(4):1067-1084. 22. Martinez SM, Crespo G, Navasa M, Forns X. Noninvasive assessment of liver fibrosis. Hepatology. 2011;53(1):325-335. 23. Federle MP, Blachar A. CT evaluation of the liver: principles and techniques. Semin Liver Dis. 2001;21(2):135-145. 24. Hyodo T, Kumano S, Kushihata F, et al. CT and MR cholan-giography: advantages and pitfalls in perioperative evaluation of biliary tree. Br J Radiol. 2012;85(1015):887-896. 25. Ros PR, Davis GL. The


Surgery_Schwartz

Surgery_Schwartz. T, Kumano S, Kushihata F, et al. CT and MR cholan-giography: advantages and pitfalls in perioperative evaluation of biliary tree. Br J Radiol. 2012;85(1015):887-896. 25. Ros PR, Davis GL. The incidental focal liver lesion: photon, proton, or needle? Hepatology. 1998;27(5):1183-1190. 26. Wald C, Scholz FJ, Pinkus E, Wise RE, Flacke S. An update on biliary imaging. Surg Clin North Am. 2008;88(6):1195-1220. 27. Wiering B, Krabbe PF, Jager GJ, Oyen WJ, Ruers TJ. The impact of fluor-18-deoxyglucose-positron emission tomogra-phy in the management of colorectal liver metastases. Cancer. 2005;104(12):2658-2670. 28. Sacks A, Peller PJ, Surasi DS, Chatburn L, Mercier G, Sub-ramaniam RM. Value of PET/CT in the management of liver metastases, part 1. AJR Am J Roentgenol. 2011;197(2): W256-W259. 29. Bernal W, Auzinger G, Dhawan A, Wendon J. Acute liver failure. Lancet. 2010;376(9736):190-201. An outstanding review of pathophysiology, treatment, and evidence based outcomes for patients with acute


Surgery_Schwartz

Surgery_Schwartz. W, Auzinger G, Dhawan A, Wendon J. Acute liver failure. Lancet. 2010;376(9736):190-201. An outstanding review of pathophysiology, treatment, and evidence based outcomes for patients with acute liver failure. 30. Polson J, Lee WM. Etiologies of acute liver failure: location, location, location! Liver Transpl. 2007;13(10):1362. 31. Agopian V, Petrowsky H, Kaldas FM, et al. The evolution of liver transplantation during three decades: analysis of 5347 consecutive liver transplants at a single center. Ann Surg. 2013;258(3):409-421. 32. Escorsell A, Mas A, de la Mata M, Spanish Group for the Study of Acute Liver F. Acute liver failure in Spain: analysis of 267 cases. Liver Transpl. 2007;13(10):1389-1395. 33. Larson AM, Polson J, Fontana RJ, et al. Acetaminophen-induced acute liver failure: results of a United States multi-center, prospective study. Hepatology. 2005;42(6):1364-1372. 34. Ostapowicz G, Fontana RJ, Schiodt FV, et al. Results of a pro-spective study of acute liver failure at 17


Surgery_Schwartz

Surgery_Schwartz. of a United States multi-center, prospective study. Hepatology. 2005;42(6):1364-1372. 34. Ostapowicz G, Fontana RJ, Schiodt FV, et al. Results of a pro-spective study of acute liver failure at 17 tertiary care centers in the United States. Ann Intern Med. 2002;137(12):947-954. 35. Hodgman MJ, Garrard AR. A review of acetaminophen poi-soning. Crit Care Clin. 2012;28(4):499-516.10Brunicardi_Ch31_p1345-p1392.indd 138720/02/19 2:37 PM 1388SPECIFIC CONSIDERATIONSPART II 36. Kortsalioudaki C, Taylor RM, Cheeseman P, Bansal S, Mieli-Vergani G, Dhawan A. Safety and efficacy of N-acetylcysteine in children with non-acetaminophen-induced acute liver fail-ure. Liver Transpl. 2008;14(1):25-30. 37. O’Grady JG, Alexander GJ, Hayllar KM, Williams R. Early indicators of prognosis in fulminant hepatic failure. Gastroen-terology. 1989;97(2):439-445. 38. Bismuth H, Samuel D, Castaing D, et al. Orthotopic liver transplantation in fulminant and subfulminant hepatitis. The Paul Brousse experience. Ann


Surgery_Schwartz

Surgery_Schwartz. failure. Gastroen-terology. 1989;97(2):439-445. 38. Bismuth H, Samuel D, Castaing D, et al. Orthotopic liver transplantation in fulminant and subfulminant hepatitis. The Paul Brousse experience. Ann Surg. 1995;222(2):109-119. 39. Antoniades CG, Berry PA, Bruce M, et al. Actin-free Gc globulin: a rapidly assessed biomarker of organ dysfunc-tion in acute liver failure and cirrhosis. Liver Transpl. 2007;13(9):1254-1261. 40. Renner EL. How to decide when to list a patient with acute liver failure for liver transplantation? Clichy or King’s College criteria, or something else? J Hepatol. 2007;46(4):554-557. 41. Faybik P, Krenn CG. Extracorporeal liver support. Curr Opin Crit Care. 2013;19(2):149-153. 42. Ekser B, Gridelli B, Tector AJ, Cooper DK. Pig liver xenotrans-plantation as a bridge to allotransplantation: which patients might benefit? Transplantation. 2009;88(9):1041-1049. 43. Yu Y, Fisher JE, Lillegard JB, Rodysill B, Amiot B, Nyberg SL. Cell therapies for liver diseases. Liver


Surgery_Schwartz

Surgery_Schwartz. allotransplantation: which patients might benefit? Transplantation. 2009;88(9):1041-1049. 43. Yu Y, Fisher JE, Lillegard JB, Rodysill B, Amiot B, Nyberg SL. Cell therapies for liver diseases. Liver Transpl. 2012;18(1):9-21. 44. Faraj W, Dar F, Bartlett A, et al. Auxiliary liver trans-plantation for acute liver failure in children. Ann Surg. 2010;251(2):351-356. 45. Wanless IR, Nakashima E, Sherman M. Regression of human cirrhosis. Morphologic features and the gen-esis of incomplete septal cirrhosis. Arch Pathol Lab Med. 2000;124(11):1599-1607. 46. Fattovich G, Giustina G, Degos F, et al. Morbidity and mortal-ity in compensated cirrhosis type C: a retrospective follow-up study of 384 patients. Gastroenterology. 1997;112(2):463-472. 47. Rinella ME, Sanyal AJ. Management of NAFLD: a stage-based approach. Nat Rev Gastroenterol Hepatol. 2016:13:196-205. 48. Loomba R, Sanyal AJ. The global NAFLD epidemic. Nat Rev Gastroenterol Hepatol. 2013;10:686-690. 49. Michelotti GA, Machado MV, Diehl


Surgery_Schwartz

Surgery_Schwartz. approach. Nat Rev Gastroenterol Hepatol. 2016:13:196-205. 48. Loomba R, Sanyal AJ. The global NAFLD epidemic. Nat Rev Gastroenterol Hepatol. 2013;10:686-690. 49. Michelotti GA, Machado MV, Diehl AM. NAFLD, NASH and liver cancer. Nat Rev Gastroenterol Hepatol. 2013;10:656-665. 50. Schuppan D, Afdhal NH. Liver cirrhosis. Lancet. 2008;371:838-851. 51. Bhala N, Angulo P, van der Poorten D, et al. The natural his-tory of nonalcoholic fatty liver disease with advanced fibrosis or cirrhosis: an international collaborative study. Hepatology. 2011;54:1208-1216. 52. Sanyal AJ, Banas C, Sargeant C, et al. Similarities and differ-ences in outcomes of cirrhosis due to nonalcoholic steatohepa-titis and hepatitis C. Hepatology. 2006;43:682-689. 53. Lehmann K, Rickenbacher A, Weber A, et al. Chemotherapy before liver resection of colorectal metastases: friend or foe? Ann Surg. 2012;255:237-247. 54. Vetelainen R, van Vliet A, Gouma DJ, van Gulik TM. Steatosis as a risk factor in liver surgery. Ann


Surgery_Schwartz

Surgery_Schwartz. before liver resection of colorectal metastases: friend or foe? Ann Surg. 2012;255:237-247. 54. Vetelainen R, van Vliet A, Gouma DJ, van Gulik TM. Steatosis as a risk factor in liver surgery. Ann Surg. 2007;245:20-30. 55. Reddy SK, Marsh JW, Varley PR, et al. Underlying steato-hepatitis, but not simple hepatic steatosis, increased morbid-ity after liver resection: a case-control study. Hepatology. 2012;56(6):221-230. 56. Doberneck RC, Sterling WA, Jr, Allison DC. Morbidity and mortality after operation in nonbleeding cirrhotic patients. Am J Surg. 1983;146(3):306-309. 57. Northup PG, Wanamaker RC, Lee VD, Adams RB, Berg CL. Model for End-Stage Liver Disease (MELD) predicts non-transplant surgical mortality in patients with cirrhosis. Ann Surg. 2005;242(2):244-251. 58. Farnsworth N, Fagan SP, Berger DH, Awad SS. ChildTurcotte-Pugh versus MELD score as a predictor of outcome after elective and emergent surgery in cirrhotic patients. Am J Surg. 2004;188(5):580-583. 59. Hanje AJ, Patel T.


Surgery_Schwartz

Surgery_Schwartz. Berger DH, Awad SS. ChildTurcotte-Pugh versus MELD score as a predictor of outcome after elective and emergent surgery in cirrhotic patients. Am J Surg. 2004;188(5):580-583. 59. Hanje AJ, Patel T. Preoperative evaluation of patients with liver disease. Nat Clin Pract Gastroenterol Hepatol. 2007;4(5):266-276. 60. Shah V. Cellular and molecular basis of portal hypertension. Clin Liver Dis. 2001;5(3):629-644. 61. Poynard T, Cales P, Pasta L, et al. Beta-adrenergic-antagonist drugs in the prevention of gastrointestinal bleeding in patients with cirrhosis and esophageal varices. An analysis of data and prognostic factors in 589 patients from four randomized clini-cal trials. Franco-Italian Multicenter Study Group. N Engl J Med. 1991;324(22):1532-1538. 62. Garcia-Pagan JC, Bosch J. Endoscopic band ligation in the treatment of portal hypertension. Nat Clin Pract Gastroenterol Hepatol. 2005;2(11):526-535. 63. Valla DC. The diagnosis and management of the Budd-Chiari syndrome: consensus and


Surgery_Schwartz

Surgery_Schwartz. band ligation in the treatment of portal hypertension. Nat Clin Pract Gastroenterol Hepatol. 2005;2(11):526-535. 63. Valla DC. The diagnosis and management of the Budd-Chiari syndrome: consensus and controversies. Hepatology. 2003;38(4):793-803. 64. Henderson JM, Warren WD, Millikan WJ, Jr, et al. Surgical options, hematologic evaluation, and pathologic changes in Budd-Chiari syndrome. Am J Surg. 1990;159(1):41-50. 65. Barnes PF, De Cock KM, Reynolds TN, Ralls PW. A com-parison of amebic and pyogenic abscess of the liver. Medicine (Baltimore). 1987;66(6):472-483. 66. Pedrosa I, Saiz A, Arrazola J, Ferreiros J, Pedrosa CS. Hydatid disease: radiologic and pathologic features and complications. Radiographics. 2000;20(3):795-817. 67. Khuroo MS, Zargar SA, Mahajan R. Hepatobiliary and pan-creatic ascariasis in India. Lancet. 1990;335(8704):1503-1506. 68. Scaglione SJ, Lok AS. Effectiveness of hepatitis B treatment in clinical practice. Gastroenterology. 2012;142(6):1360-1368. 69. Corey KE,


Surgery_Schwartz

Surgery_Schwartz. ascariasis in India. Lancet. 1990;335(8704):1503-1506. 68. Scaglione SJ, Lok AS. Effectiveness of hepatitis B treatment in clinical practice. Gastroenterology. 2012;142(6):1360-1368. 69. Corey KE, Mendez-Navarro J, Gorospe EC, Zheng H, Chung RT. Early treatment improves outcomes in acute hepatitis C virus infection: a meta-analysis. J Viral Hepat. 2010;17(3):201-207. 70. Tsung A, Geller DA. Workup of the incidental liver lesion. Adv Surg. 2005;39:331-341. 71. Caremani M, Vincenti A, Benci A, Sassoli S, Tacconi D. Eco-graphic epidemiology of non-parasitic hepatic cysts. J Clin Ultrasound. 1993;21(2):115-118. 72. Tahvanainen P, Tahvanainen E, Reijonen H, Halme L, Kaari-ainen H, Hockerstedt K. Polycystic liver disease is genetically heterogeneous: clinical and linkage studies in eight Finnish families. J Hepatol. 2003;38(1):39-43. 73. Drenth JP, Chrispijn M, Nagorney DM, Kamath PS, Torres VE. Medical and surgical treatment options for polycystic liver disease. Hepatology.


Surgery_Schwartz

Surgery_Schwartz. in eight Finnish families. J Hepatol. 2003;38(1):39-43. 73. Drenth JP, Chrispijn M, Nagorney DM, Kamath PS, Torres VE. Medical and surgical treatment options for polycystic liver disease. Hepatology. 2010;52(6):2223-2230. 74. Robinson TN, Stiegmann GV, Everson GT. Laparo-scopic palliation of polycystic liver disease. Surg Endosc. 2005;19(1):130-132. 75. Caroli J. Disease of the intrahepatic biliary tree. Clin Gastro-enterol. 1972;2:147-161. 76. Yoon SS, Charny CK, Fong Y, et al. Diagnosis, management, and outcomes of 115 patients with hepatic hemangioma. J Am Coll Surg. 2003;197(3):392-402. 77. Geller DA, Tsung A, Marsh JW, Dvorchik I, Gamblin TC, Carr BI. Outcome of 1000 liver cancer patients evaluated at the UPMC Liver Cancer Center. J Gastrointest Surg. 2006;10(1):63-68. 78. International Agency for Research on Cancer. GLOBOCAN 2008. Available at: http://globocan.iarc.fr/. Accessed July 26, 2018. 79. Liaw YF, Tai DI, Chu CM, et al. Early detection of hepatocel-lular carcinoma in


Surgery_Schwartz

Surgery_Schwartz. Agency for Research on Cancer. GLOBOCAN 2008. Available at: http://globocan.iarc.fr/. Accessed July 26, 2018. 79. Liaw YF, Tai DI, Chu CM, et al. Early detection of hepatocel-lular carcinoma in patients with chronic type B hepatitis. A prospective study. Gastroenterology. 1986;90(2):263-267. 80. Schwartz M, Roayaie S, Uva P. Treatment of HCC in patients awaiting liver transplantation. Am J Transplant. 2007;7(8):1875-1881.Brunicardi_Ch31_p1345-p1392.indd 138820/02/19 2:37 PM 1389LIVERCHAPTER 31 81. Zarrinpar A, Kaldas F, Busuttil RW. Liver transplantation for hepatocellular carcinoma: an update. Hepatobiliary Pancreat Dis Int. 2011;10(3):234-242. 82. Bruix J, Sherman M, American Association for the Study of Liver Disease. Management of hepatocellular carcinoma: an update. Hepatology. 2011;53(3):1020-1022. BCLC algo-rithm for management of hepatocellular carcinoma (HCC). 83. DeOliveira ML, Kambakamba P, Clavien PA. Advances in liver surgery for cholangiocarcinoma. Curr Opin


Surgery_Schwartz

Surgery_Schwartz. 2011;53(3):1020-1022. BCLC algo-rithm for management of hepatocellular carcinoma (HCC). 83. DeOliveira ML, Kambakamba P, Clavien PA. Advances in liver surgery for cholangiocarcinoma. Curr Opin Gastroen-terol. 2013;29(3):293-298. 84. Jarnagin WR, Fong Y, DeMatteo RP, et al. Staging, resect-ability, and outcome in 225 patients with hilar cholangiocarci-noma. Ann Surg. 2001;234(4):507-519. 85. Hidalgo E, Asthana S, Nishio H, et al. Surgery for hilar chol-angiocarcinoma: the Leeds experience. Eur J Surg Oncol. 2008;34(7):787-794. 86. Nagino M, Kamiya J, Nishio H, Ebata T, Arai T, Nimura Y. Two hundred forty consecutive portal vein embolizations before extended hepatectomy for biliary cancer: surgical outcome and long-term follow-up. Ann Surg. 2006;243(3): 364-372. 87. Gores GJ, Nagorney DM, Rosen CB. Cholangiocarci-noma: is transplantation an option? For whom? J Hepatol. 2007;47(4):455-459. 88. Marsh JW, Geller DA, Finkelstein SD, Donaldson JB, Dvor-chik I. Role of liver transplantation


Surgery_Schwartz

Surgery_Schwartz. Rosen CB. Cholangiocarci-noma: is transplantation an option? For whom? J Hepatol. 2007;47(4):455-459. 88. Marsh JW, Geller DA, Finkelstein SD, Donaldson JB, Dvor-chik I. Role of liver transplantation for hepatobiliary malignant disorders. Lancet Oncol. 2004;5(8):480-488. 89. Rea DJ, Heimbach JK, Rosen CB, et al. Liver transplanta-tion with neoadjuvant chemoradiation is more effective than resection for hilar cholangiocarcinoma. Ann Surg. 2005;242(3):451-461. 90. Hassoun Z, Gores GJ, Rosen CB. Preliminary experience with liver transplantation in selected patients with unre-sectable hilar cholangiocarcinoma. Surg Oncol Clin N Am. 2002;11(4):909-921. 91. Darwish Murad S, Kim WR, Harnois DM, et al. Efficacy of neoadjuvant chemoradiation, followed by liver transplanta-tion, for perihilar cholangiocarcinoma at 12 US centers. Gas-troenterology. 2012;143(1):88-98. 92. Weber SM, Jarnagin WR, Klimstra D, DeMatteo RP, Fong Y, Blumgart LH. Intrahepatic cholangiocarcinoma: resect-ability,


Surgery_Schwartz

Surgery_Schwartz. cholangiocarcinoma at 12 US centers. Gas-troenterology. 2012;143(1):88-98. 92. Weber SM, Jarnagin WR, Klimstra D, DeMatteo RP, Fong Y, Blumgart LH. Intrahepatic cholangiocarcinoma: resect-ability, recurrence pattern, and outcomes. J Am Coll Surg. 2001;193(4):384-391. 93. Jan YY, Yeh CN, Yeh TS, Chen TC. Prognostic analysis of surgical treatment of peripheral cholangiocarcinoma: two decades of experience at Chang Gung Memorial Hospital. World J Gastroenterol. 2005;11(12):1779-1784. 94. Hong JC, Jones CM, Duffy JP, et al. Comparative analysis of resection and liver transplantation for intrahepatic and hilar cholangiocarcinoma: a 24-year experience in a single center. Arch Surg. 2011;146(6):683-689. 95. Smith GC, Parks RW, Madhavan KK, Garden OJ. A 10-year experience in the management of gallbladder cancer. HPB (Oxford). 2003;5(3):159-166. 96. Bartlett DL, Fong Y, Fortner JG, Brennan MF, Blumgart LH. Long-term results after resection for gallbladder can-cer. Implications for staging and


Surgery_Schwartz

Surgery_Schwartz. cancer. HPB (Oxford). 2003;5(3):159-166. 96. Bartlett DL, Fong Y, Fortner JG, Brennan MF, Blumgart LH. Long-term results after resection for gallbladder can-cer. Implications for staging and management. Ann Surg. 1996;224(5):639-646. 97. Shoup M, Fong Y. Surgical indications and extent of resection in gallbladder cancer. Surg Oncol Clin N Am. 2002;11(4):985-994. 98. Pawlik TM, Gleisner AL, Vigano L, et al. Incidence of finding residual disease for incidental gallbladder carci-noma: implications for re-resection. J Gastrointest Surg. 2007;11(11):1478-1486. 99. Chan SY, Poon RT, Lo CM, Ng KK, Fan ST. Management of carcinoma of the gallbladder: a single-institution experience in 16 years. J Surg Oncol. 2008;97(2):156-164. 100. Goetze TO, Paolucci V. Benefits of reoperation of T2 and more advanced incidental gallbladder carcinoma: analysis of the German registry. Ann Surg. 2008;247(1):104-108. 101. Fong Y, Fortner J, Sun RL, Brennan MF, Blumgart LH. Clini-cal score for predicting


Surgery_Schwartz

Surgery_Schwartz. more advanced incidental gallbladder carcinoma: analysis of the German registry. Ann Surg. 2008;247(1):104-108. 101. Fong Y, Fortner J, Sun RL, Brennan MF, Blumgart LH. Clini-cal score for predicting recurrence after hepatic resection for metastatic colorectal cancer: analysis of 1001 consecutive cases. Ann Surg. 1999;230(3):309-318. 102. Poston G, Adam R, Vauthey JN. Downstaging or downsizing: time for a new staging system in advanced colorectal cancer? J Clin Oncol. 2006;24(18):2702-2706. 103. Minagawa M, Makuuchi M, Torzilli G, et al. Extension of the frontiers of surgical indications in the treatment of liver metastases from colorectal cancer: long-term results. Ann Surg. 2000;231(4):487-499. 104. Kornprat P, Jarnagin WR, Gonen M, et al. Outcome after hepatectomy for multiple (four or more) colorectal metas-tases in the era of effective chemotherapy. Ann Surg Oncol. 2007;14(3):1151-1160. 105. Charnsangavej C, Clary B, Fong Y, Grothey A, Pawlik TM, Choti MA. Selection of patients


Surgery_Schwartz

Surgery_Schwartz. more) colorectal metas-tases in the era of effective chemotherapy. Ann Surg Oncol. 2007;14(3):1151-1160. 105. Charnsangavej C, Clary B, Fong Y, Grothey A, Pawlik TM, Choti MA. Selection of patients for resection of hepatic colorectal metastases: expert consensus statement. Ann Surg Oncol. 2006;13(10):1261-1268. 106. Abdalla EK, Adam R, Bilchik AJ, Jaeck D, Vauthey JN, Mahvi D. Improving resectability of hepatic colorectal metastases: expert consensus statement. Ann Surg Oncol. 2006;13(10):1271-1280. 107. Pawlik TM, Schulick RD, Choti MA. Expanding criteria for resectability of colorectal liver metastases. Oncologist. 2008;13(1):51-64. Summary of the paradigm shift for resection of colorectal cancer liver metastases based on adequate liver remnant rather than actual number of liver tumors. 108. Clavien PA, Petrowsky H, DeOliveira ML, Graf R. Strategies for safer liver surgery and partial liver transplantation. N Engl J Med. 2007;356(15):1545-1559. 109. Adam R, Wicherts DA, de Haas RJ,


Surgery_Schwartz

Surgery_Schwartz. PA, Petrowsky H, DeOliveira ML, Graf R. Strategies for safer liver surgery and partial liver transplantation. N Engl J Med. 2007;356(15):1545-1559. 109. Adam R, Wicherts DA, de Haas RJ, et al. Patients with initially unresectable colorectal liver metastases: is there a possibility of cure? J Clin Oncol. 2009;27(11):1829-1835. 110. Que FG, Nagorney DM, Batts KP, Linz LJ, Kvols LK. Hepatic resection for metastatic neuroendocrine carcinomas. Am J Surg. 1995;169(1):36-42. 111. Touzios JG, Kiely JM, Pitt SC, et al. Neuroendocrine hepatic metastases: does aggressive management improve survival? Ann Surg. 2005;241(5):776-783. 112. Sarmiento JM, Heywood G, Rubin J, Ilstrup DM, Nagorney DM, Que FG. Surgical treatment of neuroendocrine metasta-ses to the liver: a plea for resection to increase survival. J Am Coll Surg. 2003;197(1):29-37. 113. Kianmanesh R, Sauvanet A, Hentic O, et al. Two-step surgery for synchronous bilobar liver metastases from digestive endo-crine tumors: a safe approach for


Surgery_Schwartz

Surgery_Schwartz. J Am Coll Surg. 2003;197(1):29-37. 113. Kianmanesh R, Sauvanet A, Hentic O, et al. Two-step surgery for synchronous bilobar liver metastases from digestive endo-crine tumors: a safe approach for radical resection. Ann Surg. 2008;247(4):659-665. 114. Mazzaferro V, Pulvirenti A, Coppa J. Neuroendocrine tumors metastatic to the liver: how to select patients for liver trans-plantation? J Hepatol. 2007;47(4):460-466. 115. Adam R, Aloia T, Krissat J, et al. Is liver resection justified for patients with hepatic metastases from breast cancer? Ann Surg. 2006;244(6):897-907. 116. Abbott DE, Brouquet A, Mittendorf EA, et al. Resection of liver metastases from breast cancer: estrogen receptor status and response to chemotherapy before metastasectomy define outcome. Surgery. 2012;151(5):710-716. 117. Jarnagin W, Chapman WC, Curley S, et al. Surgical treatment of hepatocellular carcinoma: expert consensus statement. HPB (Oxford). 2010;12(5):302-310. 118. Belghiti J, Hiramatsu K, Benoist S,


Surgery_Schwartz

Surgery_Schwartz. W, Chapman WC, Curley S, et al. Surgical treatment of hepatocellular carcinoma: expert consensus statement. HPB (Oxford). 2010;12(5):302-310. 118. Belghiti J, Hiramatsu K, Benoist S, Massault P, Sauvanet A, Farges O. Seven hundred forty-seven hepatectomies in the 1990s: an update to evaluate the actual risk of liver resection. J Am Coll Surg. 2000;191(1):38-46.Brunicardi_Ch31_p1345-p1392.indd 138920/02/19 2:37 PM 1390SPECIFIC CONSIDERATIONSPART II 119. Jarnagin WR, Gonen M, Fong Y, et al. Improvement in perioperative outcome after hepatic resection: analysis of 1,803 consecutive cases over the past decade. Ann Surg. 2002;236(4):397-406. 120. Imamura H, Seyama Y, Kokudo N, et al. One thousand fifty-six hepatectomies without mortality in 8 years. Arch Surg. 2003;138(11):1198-1206. 121. Mullen JT, Ribero D, Reddy SK, et al. Hepatic insufficiency and mortality in 1,059 noncirrhotic patients undergoing major hepatectomy. J Am Coll Surg. 2007;204(5):854-862. 122. Hamady ZZ, Cameron IC,


Surgery_Schwartz

Surgery_Schwartz. JT, Ribero D, Reddy SK, et al. Hepatic insufficiency and mortality in 1,059 noncirrhotic patients undergoing major hepatectomy. J Am Coll Surg. 2007;204(5):854-862. 122. Hamady ZZ, Cameron IC, Wyatt J, Prasad RK, Toogood GJ, Lodge JP. Resection margin in patients undergoing hepatec-tomy for colorectal liver metastasis: a critical appraisal of the 1 cm rule. Eur J Surg Oncol. 2006;32(5):557-563. 123. Pawlik TM, Vauthey JN. Surgical margins during hepatic sur-gery for colorectal liver metastases: complete resection not mil-limeters defines outcome. Ann Surg Oncol. 2008;15(3):677-679. 124. Andreou A, Aloia TA, Brouquet A, et al. Margin status remains an important determinant of survival after surgical resection of colorectal liver metastases in the era of modern chemotherapy. Ann Surg. 2013;257(6):1079-1088. 125. Hemming AW, Mekeel KL, Zendejas I, Kim RD, Sicklick JK, Reed AI. Resection of the liver and inferior vena cava for hepatic malignancy. J Am Coll Surg.


Surgery_Schwartz

Surgery_Schwartz. Ann Surg. 2013;257(6):1079-1088. 125. Hemming AW, Mekeel KL, Zendejas I, Kim RD, Sicklick JK, Reed AI. Resection of the liver and inferior vena cava for hepatic malignancy. J Am Coll Surg. 2013;217:115-124. 126. Schwartz M, Roayaie S, Konstadoulakis M. Strategies for the management of hepatocellular carcinoma. Nat Clin Pract Oncol. 2007;4(7):424-432. Excellent summary of the current strategies for multi-disciplinary management of hepa-tocellular carcinoma (HCC). 127. Duffy JP, Vardanian A, Benjamin E, et al. Liver transplanta-tion criteria for hepatocellular carcinoma should be expanded: a 22-year experience with 467 patients at UCLA. Ann Surg. 2007;246(3):502-509. 128. Organ Procurement and Transplantation Network. Available at: http://www.optn.org. Accessed May 6, 2017. 129. Mazzaferro V, Regalia E, Doci R, et al. Liver transplanta-tion for the treatment of small hepatocellular carcinomas in patients with cirrhosis. N Engl J Med. 1996;334(11): 693-699. Landmark article showing


Surgery_Schwartz

Surgery_Schwartz. V, Regalia E, Doci R, et al. Liver transplanta-tion for the treatment of small hepatocellular carcinomas in patients with cirrhosis. N Engl J Med. 1996;334(11): 693-699. Landmark article showing excellent outcomes of liver transplantation for small HCC that established the size and tumor number criteria that was adopted by the MELD system and is now widely accepted. 130. Wiesner RH, Freeman RB, Mulligan DC. Liver transplantation for hepatocellular cancer: the impact of the MELD allocation policy. Gastroenterology. 2004;127(5 suppl 1):S261-S267. 131. de Villa V, Lo CM. Liver transplantation for hepatocellular carcinoma in Asia. Oncologist. 2007;12(11):1321-1331. 132. McGahan JP, Browning PD, Brock JM, Tesluk H. Hepatic ablation using radiofrequency electrocautery. Invest Radiol. 1990;25(3):267-270. 133. Rossi S, Fornari F, Pathies C, Buscarini L. Thermal lesions induced by 480 KHz localized current field in guinea pig and pig liver. Tumori. 1990;76(1):54-57. 134. Curley SA, Izzo F,


Surgery_Schwartz

Surgery_Schwartz. S, Fornari F, Pathies C, Buscarini L. Thermal lesions induced by 480 KHz localized current field in guinea pig and pig liver. Tumori. 1990;76(1):54-57. 134. Curley SA, Izzo F, Delrio P, et al. Radiofrequency ablation of unresectable primary and metastatic hepatic malignancies: results in 123 patients. Ann Surg. 1999;230(1):1-8. 135. Bilchik AJ, Wood TF, Allegra D, et al. Cryosurgical abla-tion and radiofrequency ablation for unresectable hepatic malignant neoplasms: a proposed algorithm. Arch Surg. 2000;135(6):657-662. 136. Poon RT, Ng KK, Lam CM, et al. Learning curve for radio-frequency ablation of liver tumors: prospective analysis of initial 100 patients in a tertiary institution. Ann Surg. 2004;239(4):441-449. 137. Abdalla EK, Vauthey JN, Ellis LM, et al. Recurrence and out-comes following hepatic resection, radiofrequency ablation, and combined resection/ablation for colorectal liver metasta-ses. Ann Surg. 2004;239(6):818-825. 138. Sutherland LM, Williams JA, Padbury RT, Gotley


Surgery_Schwartz

Surgery_Schwartz. hepatic resection, radiofrequency ablation, and combined resection/ablation for colorectal liver metasta-ses. Ann Surg. 2004;239(6):818-825. 138. Sutherland LM, Williams JA, Padbury RT, Gotley DC, Stokes B, Maddern GJ. Radiofrequency ablation of liver tumors: a systematic review. Arch Surg. 2006;141(2):181-190. 139. Berber E, Siperstein AE. Perioperative outcome after laparo-scopic radiofrequency ablation of liver tumors: an analysis of 521 cases. Surg Endosc. 2007;21(4):613-618. 140. Martin AP, Goldstein RM, Dempster J, et al. Radiofrequency thermal ablation of hepatocellular carcinoma before liver transplantation—a clinical and histological examination. Clin Transplant. 2006;20(6):695-705. 141. Cheng BQ, Jia CQ, Liu CT, et al. Chemoembolization com-bined with radiofrequency ablation for patients with hepato-cellular carcinoma larger than 3 cm: a randomized controlled trial. JAMA. 2008;299(14):1669-1677. 142. Sucandy I, Cheek S, Golas BJ, Tsung A, Geller DA, Marsh JW. Longterm


Surgery_Schwartz

Surgery_Schwartz. for patients with hepato-cellular carcinoma larger than 3 cm: a randomized controlled trial. JAMA. 2008;299(14):1669-1677. 142. Sucandy I, Cheek S, Golas BJ, Tsung A, Geller DA, Marsh JW. Longterm survival outcomes of patients undergoing treatment with radiofrequency ablation for hepatocellular carcinoma and metastatic colorectal cancer liver tumors. HPB (Oxford). 2016;18:756-763. 143. Iannitti DA, Martin RC, Simon CJ, et al. Hepatic tumor abla-tion with clustered microwave antennae: the US Phase II trial. HPB (Oxford). 2007;9(2):120-124. 144. Lo CM, Ngan H, Tso WK, et al. Randomized controlled trial of transarterial lipiodol chemoembolization for unresectable hepatocellular carcinoma. Hepatology. 2002;35(5):1164-1171. 145. Llovet JM, Real MI, Montana X, et al. Arterial embolisation or chemoembolisation versus symptomatic treatment in patients with unresectable hepatocellular carcinoma: a randomised controlled trial. Lancet. 2002;359(9319):1734-1739. 146. Takayasu K, Arii S, Ikai I,


Surgery_Schwartz

Surgery_Schwartz. versus symptomatic treatment in patients with unresectable hepatocellular carcinoma: a randomised controlled trial. Lancet. 2002;359(9319):1734-1739. 146. Takayasu K, Arii S, Ikai I, et al. Prospective cohort study of transarterial chemoembolization for unresectable hepa-tocellular carcinoma in 8510 patients. Gastroenterology. 2006;131(2):461-469. 147. Sotiropoulos GC, Druhe N, Sgourakis G, et al. Liver transplan-tation, liver resection, and transarterial chemoembolization for hepatocellular carcinoma in cirrhosis: which is the best onco-logical approach? Dig Dis Sci. 2009;54(10):2264-2273. 148. Lewandowski RJ, Geschwind JF, Liapi E, Salem R. Transcath-eter intraarterial therapies: rationale and overview. Radiology. 2011;259(3):641-657. 149. Kemeny N, Huang Y, Cohen AM, et al. Hepatic arterial infusion of chemotherapy after resection of hepatic metastases from colorectal cancer. N Engl J Med. 1999;341(27):2039-2048. 150. Ibrahim SM, Lewandowski RJ, Sato KT, et al. Radioem-bolization


Surgery_Schwartz

Surgery_Schwartz. infusion of chemotherapy after resection of hepatic metastases from colorectal cancer. N Engl J Med. 1999;341(27):2039-2048. 150. Ibrahim SM, Lewandowski RJ, Sato KT, et al. Radioem-bolization for the treatment of unresectable hepatocellu-lar carcinoma: a clinical review. World J Gastroenterol. 2008;14(11):1664-1669. 151. Gulec SA, Fong Y. Yttrium 90 microsphere selective inter-nal radiation treatment of hepatic colorectal metastases. Arch Surg. 2007;142(7):675-682. 152. Sato KT, Lewandowski RJ, Mulcahy MF, et al. Unresectable chemorefractory liver metastases: radioembolization with 90Y microspheres—safety, efficacy, and survival. Radiology. 2008;247(2):507-515. 153. Tse RV, Hawkins M, Lockwood G, et al. Phase I study of indi-vidualized stereotactic body radiotherapy for hepatocellular carcinoma and intrahepatic cholangiocarcinoma. J Clin Oncol. 2008;26(4):657-664. 154. Mendez Romero A, Wunderink W, Hussain SM, et al. Ste-reotactic body radiation therapy for primary and metastatic


Surgery_Schwartz

Surgery_Schwartz. carcinoma and intrahepatic cholangiocarcinoma. J Clin Oncol. 2008;26(4):657-664. 154. Mendez Romero A, Wunderink W, Hussain SM, et al. Ste-reotactic body radiation therapy for primary and metastatic liver tumors: a single institution phase I-II study. Acta Oncol. 2006;45(7):831-837. 155. Chapman WC, Majella Doyle MB, Stuart JE, et al. Outcomes of neoadjuvant transarterial chemoembolization to downstage hepatocellular carcinoma before liver transplantation. Ann Surg. 2008;248(4):617-625. 156. Yao FY, Kerlan RK, Jr, Hirose R, et al. Excellent outcome following down-staging of hepatocellular carcinoma prior to Brunicardi_Ch31_p1345-p1392.indd 139020/02/19 2:37 PM 1391LIVERCHAPTER 31liver transplantation: an intention-to-treat analysis. Hepatology. 2008;48(3):819-827. 157. Llovet JM, Ricci S, Mazzaferro V, et al. Sorafenib in advanced hepatocellular carcinoma. N Engl J Med. 2008;359(4):378-390. Randomized clinical trial that showed benefits of Sorafenib compared to placebo in advanced


Surgery_Schwartz

Surgery_Schwartz. S, Mazzaferro V, et al. Sorafenib in advanced hepatocellular carcinoma. N Engl J Med. 2008;359(4):378-390. Randomized clinical trial that showed benefits of Sorafenib compared to placebo in advanced HCC and led to FDA drug approval. 158. American Hepato-Pancreato-Biliary Association. IHPBA Brisbane liver terminology. Available at: http://www.ahpba.org/resources/liver.asp. Accessed June 4, 2013. 159. Pang YY. The Brisbane 2000 terminology of liver anatomy and resections. HPB (Oxford). 2002;4(2):99-100; author reply 99. 160. Strasberg SM. Nomenclature of hepatic anatomy and resec-tions: a review of the Brisbane 2000 system. J Hepatobiliary Pancreat Surg. 2005;12(5):351-355. 161. Weber JC, Navarra G, Jiao LR, Nicholls JP, Jensen SL, Habib NA. New technique for liver resection using heat coagulative necrosis. Ann Surg. 2002;236(5):560-563. 162. Geller DA, Tsung A, Maheshwari V, Rutstein LA, Fung JJ, Marsh JW. Hepatic resection in 170 patients using saline-cooled radiofrequency


Surgery_Schwartz

Surgery_Schwartz. heat coagulative necrosis. Ann Surg. 2002;236(5):560-563. 162. Geller DA, Tsung A, Maheshwari V, Rutstein LA, Fung JJ, Marsh JW. Hepatic resection in 170 patients using saline-cooled radiofrequency coagulation. HPB (Oxford). 2005;7(3): 208-213. 163. Saiura A, Yamamoto J, Koga R, et al. Usefulness of LigaSure for liver resection: analysis by randomized clinical trial. Am J Surg. 2006;192(1):41-45. 164. McEntee GP, Nagorney DM. Use of vascular staplers in major hepatic resections. Br J Surg. 1991;78(1):40-41. 165. Jurim O, Colonna JO II, Colquhoun SD, Shaked A, Busuttil RW. A stapling technique for hepatic resection. J Am Coll Surg. 1994;178(5):510-511. 166. Kaneko H, Otsuka Y, Takagi S, Tsuchiya M, Tamura A, Shiba T. Hepatic resection using stapling devices. Am J Surg. 2004;187(2):280-284. 167. Schemmer P, Friess H, Hinz U, et al. Stapler hepatectomy is a safe dissection technique: analysis of 300 patients. World J Surg. 2006;30(3):419-430. 168. Balaa FK, Gamblin TC, Tsung A, Marsh


Surgery_Schwartz

Surgery_Schwartz. P, Friess H, Hinz U, et al. Stapler hepatectomy is a safe dissection technique: analysis of 300 patients. World J Surg. 2006;30(3):419-430. 168. Balaa FK, Gamblin TC, Tsung A, Marsh JW, Geller DA. Right hepatic lobectomy using the staple technique in 101 patients. J Gastrointest Surg. 2008;12(2):338-343. 169. Blumgart L. Liver resection for benign disease and for liver and biliary disease. In: Blumgart L, ed. Surgery of the Liver and Biliary Tract. 3rd ed. London: WB Saunders; 2000:1639. 170. Launois B, Jamieson GG. The importance of Glisson’s capsule and its sheaths in the intrahepatic approach to resection of the liver. Surg Gynecol Obstet. 1992;174(1):7-10. 171. Azoulay D, Marin-Hargreaves G, Castaing D, Adam R, Savier E, Bismuth H. The anterior approach: the right way for right massive hepatectomy. J Am Coll Surg. 2001;192(3):412-417. 172. Liu CL, Fan ST, Cheung ST, Lo CM, Ng IO, Wong J. Anterior approach versus conventional approach right hepatic resection for large


Surgery_Schwartz

Surgery_Schwartz. right massive hepatectomy. J Am Coll Surg. 2001;192(3):412-417. 172. Liu CL, Fan ST, Cheung ST, Lo CM, Ng IO, Wong J. Anterior approach versus conventional approach right hepatic resection for large hepatocellular carcinoma: a prospective randomized controlled study. Ann Surg. 2006;244(2):194-203. 173. Makuuchi M, Mori T, Gunven P, Yamazaki S, Hasegawa H. Safety of hemihepatic vascular occlusion during resection of the liver. Surg Gynecol Obstet. 1987;164(2):155-158. 174. Man K, Fan ST, Ng IO, Lo CM, Liu CL, Wong J. Prospective evaluation of Pringle maneuver in hepatectomy for liver tumors by a randomized study. Ann Surg. 1997;226(6):704-711. 175. Belghiti J, Noun R, Malafosse R, et al. Continuous versus intermittent portal triad clamping for liver resection: a con-trolled study. Ann Surg. 1999;229(3):369-375. 176. Figueras J, Llado L, Ruiz D, et al. Complete versus selective portal triad clamping for minor liver resections: a prospective randomized trial. Ann Surg.


Surgery_Schwartz

Surgery_Schwartz. study. Ann Surg. 1999;229(3):369-375. 176. Figueras J, Llado L, Ruiz D, et al. Complete versus selective portal triad clamping for minor liver resections: a prospective randomized trial. Ann Surg. 2005;241(4):582-590. 177. Clavien PA, Yadav S, Sindram D, Bentley RC. Protec-tive effects of ischemic preconditioning for liver resection performed under inflow occlusion in humans. Ann Surg. 2000;232(2):155-162. 178. Clavien PA, Selzner M, Rudiger HA, et al. A prospective ran-domized study in 100 consecutive patients undergoing major liver resection with versus without ischemic preconditioning. Ann Surg. 2003;238(6):843-850. 179. Kinoshita H, Sakai K, Hirohashi K, Igawa S, Yamasaki O, Kubo S. Preoperative portal vein embolization for hepatocel-lular carcinoma. World J Surg. 1986;10(5):803-808. 180. Makuuchi M, Thai BL, Takayasu K, et al. Preoperative por-tal embolization to increase safety of major hepatectomy for hilar bile duct carcinoma: a preliminary report. Surgery.


Surgery_Schwartz

Surgery_Schwartz. M, Thai BL, Takayasu K, et al. Preoperative por-tal embolization to increase safety of major hepatectomy for hilar bile duct carcinoma: a preliminary report. Surgery. 1990;107(5):521-527. 181. Abdalla EK, Hicks ME, Vauthey JN. Portal vein emboliza-tion: rationale, technique and future prospects. Br J Surg. 2001;88(2):165-175. 182. Chun YS, Ribero D, Abdalla EK, et al. Comparison of two methods of future liver remnant volume measurement. J Gas-trointest Surg. 2008;12(1):123-128. 183. Abdalla EK, Barnett CC, Doherty D, Curley SA, Vauthey JN. Extended hepatectomy in patients with hepatobiliary malig-nancies with and without preoperative portal vein emboliza-tion. Arch Surg. 2002;137(6):675-680. 184. Vauthey JN, Chaoui A, Do KA, et al. Standardized mea-surement of the future liver remnant prior to extended liver resection: methodology and clinical associations. Surgery. 2000;127(5):512-519. 185. Farges O, Belghiti J, Kianmanesh R, et al. Portal vein emboli-zation before right hepatectomy:


Surgery_Schwartz

Surgery_Schwartz. to extended liver resection: methodology and clinical associations. Surgery. 2000;127(5):512-519. 185. Farges O, Belghiti J, Kianmanesh R, et al. Portal vein emboli-zation before right hepatectomy: prospective clinical trial. Ann Surg. 2003;237(2):208-217. 186. Hemming AW, Reed AI, Howard RJ, et al. Preoperative por-tal vein embolization for extended hepatectomy. Ann Surg. 2003;237(5):686-691. 187. Azoulay D, Castaing D, Smail A, et al. Resection of nonre-sectable liver metastases from colorectal cancer after percu-taneous portal vein embolization. Ann Surg. 2000;231(4): 480-486. 188. Kubota K, Makuuchi M, Kusaka K, et al. Measurement of liver volume and hepatic functional reserve as a guide to decision-making in resectional surgery for hepatic tumors. Hepatology. 1997;26(5):1176-1181. 189. Ribero D, Abdalla EK, Madoff DC, Donadon M, Loyer EM, Vauthey JN. Portal vein embolization before major hepatec-tomy and its effects on regeneration, resectability and out-come. Br J Surg.


Surgery_Schwartz

Surgery_Schwartz. D, Abdalla EK, Madoff DC, Donadon M, Loyer EM, Vauthey JN. Portal vein embolization before major hepatec-tomy and its effects on regeneration, resectability and out-come. Br J Surg. 2007;94(11):1386-1394. 190. Covey AM, Brown KT, Jarnagin WR, et al. Combined portal vein embolization and neoadjuvant chemotherapy as a treat-ment strategy for resectable hepatic colorectal metastases. Ann Surg. 2008;247(3):451-455. 191. Hwang S, Lee SG, Ko GY, et al. Sequential preoperative ipsi-lateral hepatic vein embolization after portal vein embolization to induce further liver regeneration in patients with hepatobili-ary malignancy. Ann Surg. 2009;249(4):608-616. 192. Jaeck D, Oussoultzoglou E, Rosso E, Greget M, Weber JC, Bachellier P. A two-stage hepatectomy procedure combined with portal vein embolization to achieve curative resection for initially unresectable multiple and bilobar colorectal liver metastases. Ann Surg. 2004;240(6):1037-1049. 193. Adam R, Miller R, Pitombo M, et al. Two-stage


Surgery_Schwartz

Surgery_Schwartz. to achieve curative resection for initially unresectable multiple and bilobar colorectal liver metastases. Ann Surg. 2004;240(6):1037-1049. 193. Adam R, Miller R, Pitombo M, et al. Two-stage hepatec-tomy approach for initially unresectable colorectal hepatic metastases. Surg Oncol Clin North Am. 2007;16(3):525-536. Very useful summary of the two-stage hepatectomy approach for resection of hepatic colorectal cancer metastases. 194. Schnitzbauer AA, Lang SA, Goessmann H, et al. Right portal vein ligation combined with in situ splitting induces rapid left lateral liver lobe hypertrophy enabling 2-staged extended right hepatic resection in small-for-size settings. Ann Surg. 2012;255(3):405-414. Initial paper describing the ALPPS technique to induce massive future liver remnant hypertrophy and outcomes.Brunicardi_Ch31_p1345-p1392.indd 139120/02/19 2:37 PM 1392SPECIFIC CONSIDERATIONSPART II 195. Adam R, Bismuth H, Castaing D, et al. Repeat hepatectomy for colorectal liver metastases.


Surgery_Schwartz

Surgery_Schwartz. outcomes.Brunicardi_Ch31_p1345-p1392.indd 139120/02/19 2:37 PM 1392SPECIFIC CONSIDERATIONSPART II 195. Adam R, Bismuth H, Castaing D, et al. Repeat hepatectomy for colorectal liver metastases. Ann Surg. 1997;225(1):51-60. 196. Petrowsky H, Gonen M, Jarnagin W, et al. Second liver resec-tions are safe and effective treatment for recurrent hepatic metastases from colorectal cancer: a bi-institutional analysis. Ann Surg. 2002;235(6):863-871. 197. Sa Cunha A, Laurent C, Rault A, Couderc P, Rullier E, Saric J. A second liver resection due to recurrent colorectal liver metastases. Arch Surg. 2007;142(12):1144-1149. 198. Antoniou A, Lovegrove RE, Tilney HS, et al. Meta-analysis of clinical outcome after first and second liver resection for colorectal metastases. Surgery. 2007;141(1):9-18. 199. Nakajima Y, Ko S, Kanamura T, et al. Repeat liver resec-tion for hepatocellular carcinoma. J Am Coll Surg. 2001;192(3):339-344. 200. Itamoto T, Nakahara H, Amano H, et al. Repeat hepatec-tomy for


Surgery_Schwartz

Surgery_Schwartz. Y, Ko S, Kanamura T, et al. Repeat liver resec-tion for hepatocellular carcinoma. J Am Coll Surg. 2001;192(3):339-344. 200. Itamoto T, Nakahara H, Amano H, et al. Repeat hepatec-tomy for recurrent hepatocellular carcinoma. Surgery. 2007;141(5):589-597. 201. Minagawa M, Makuuchi M, Takayama T, Kokudo N. Selec-tion criteria for repeat hepatectomy in patients with recurrent hepatocellular carcinoma. Ann Surg. 2003;238(5):703-710. 202. Cherqui D, Husson E, Hammoud R, et al. Laparoscopic liver resections: a feasibility study in 30 patients. Ann Surg. 2000;232(6):753-762. 203. Reddy SK, Tsung A, Geller DA. Laparoscopic liver resection. World J Surg. 2011;35(7):1478-1486. 204. Nguyen KT, Gamblin TC, Geller DA. World review of laparoscopic liver resection – 2,804 patients. Ann Surg, 2009;250:831-841. Comprehensive review of the indications, techniques, benefits, and outcomes of laparoscopic liver resection. 205. Koffron AJ, Auffenberg G, Kung R, Abecassis M. Evaluation of 300 minimally


Surgery_Schwartz

Surgery_Schwartz. Comprehensive review of the indications, techniques, benefits, and outcomes of laparoscopic liver resection. 205. Koffron AJ, Auffenberg G, Kung R, Abecassis M. Evaluation of 300 minimally invasive liver resections at a single institu-tion: less is more. Ann Surg. 2007;246(3):385-392. 206. Buell JF, Cherqui D, Geller DA, et al. The international posi-tion on laparoscopic liver surgery: the Louisville statement, 2008. Ann Surg. 2009;250:825-830. 207. Wakabayashi G, Cherqui D, Geller DA, et al. Recommen-dations for laparoscopic liver resection: a report from the second international consensus conference held in Morioka. Ann Surg. 2015;261:619-629. Up-to-date recommendations from the second international consensus conference consist-ing of a 9-member jury and an expert panel that addressed 17 questions for laparoscopic liver resection. 208. Ciria R, Cherqui D, Geller DA, Briceno J, Wakabayashi G. Comparative short term benefits of laparoscopic liver resec-tion: 9,000 cases and climbing.


Surgery_Schwartz

Surgery_Schwartz. questions for laparoscopic liver resection. 208. Ciria R, Cherqui D, Geller DA, Briceno J, Wakabayashi G. Comparative short term benefits of laparoscopic liver resec-tion: 9,000 cases and climbing. Ann Surg. 2016;263:761-777. 209. Cardinal JS, Reddy SK, Tsung A, Marsh JW, Geller DA. Lap-aroscopic major hepatectomy: pure laparoscopic approach versus hand-assisted technique. J Hepatobiliary Pancreat Sci. 2013;20:114-119. 210. Cheek SM, Sucandy I, Geller DA. Hand-assisted laparoscopic left hepatectomy: how I do it. J Hepatobiliary Pancreat Sci. 2016;23(12):E30-E32. 211. Tsung A, Geller DA, Sukato DC, et al. Robotic versus lapa-roscopic hepatectomy: a matched comparison. Ann Surg. 2014;259:549-555. 212. Nguyen KT, Marsh JW, Tsung A, Steel JL, Gamblin TC, Geller DA. Comparative benefits of laparoscopic versus open hepatic resection: a critical appraisal. Arch Surg. 2011;146:348-356. 213. Takahara T, Wakabayashi G, Beppu T, et al. Long-term and perioperative outcomes of laparoscopic versus


Surgery_Schwartz

Surgery_Schwartz. versus open hepatic resection: a critical appraisal. Arch Surg. 2011;146:348-356. 213. Takahara T, Wakabayashi G, Beppu T, et al. Long-term and perioperative outcomes of laparoscopic versus open liver resection for hepatocellular carcinoma with propensity score matching: a multi-institutional Japanese study. J Hepatobiliary Pancreat Sci. 2015;22:721-727. 214. Zhou YM, Shao WY, Zhao YF, Xu DH, Li B. Meta-analysis of laparoscopic versus open resection for hepatocellular carci-noma. Dig Dis Sci. 2011;56(7):1937-1943. 215. Schiffman SC, Kim KH, Tsung A, Marsh JW, Geller DA. Laparoscopic versus open liver resection for metastatic colorectal cancer: a meta-analysis of 610 patients. Surgery. 2015;157:211-222. 216. Vigano L, Laurent A, Tayar C, et al. The learning curve in laparoscopic liver resection: improved feasibility and repro-ducibility. Ann Surg 2009;250:772-782. 217. Brown KM, Geller DA. What is the learning curve for laparoscopic major hepatectomy? J Gastrointest Surg.


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Surgery_Schwartz. liver resection: improved feasibility and repro-ducibility. Ann Surg 2009;250:772-782. 217. Brown KM, Geller DA. What is the learning curve for laparoscopic major hepatectomy? J Gastrointest Surg. 2016;20:1065-1071. 218. Dagher I, O’Rourke N, Geller DA, et al. Laparoscopic major hepatectomy: an evolution in standard of care. Ann Surg. 2009;250:856-860. 219. Lin NC, Nitta H, Wakabayashi G. Laparoscopic major hepa-tectomy: a systematic literature review and comparison of 3 techniques. Ann Surg. 2013;257:205-213. 220. Vanounou T, Steel JL, Nguyen KT, Tsung A, Marsh JW, Geller DA, Gamblin TC. Comparing the clinical and economic impact of laparoscopic versus open liver resection. Ann Surg Oncol. 2010;17:998-1009. 221. Cleary SP, Han HS, Yamamoto M, Wakabayashi G, Asbun HJ. The comparative costs of laparoscopic and open liver resec-tion: a report for the 2nd International Consensus Con-ference on Laparoscopic Liver Resection. Surg Endosc. 2016;30(11):4691-4696. 222. Cherqui D, Soubrane O,


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Surgery_Schwartz. of laparoscopic and open liver resec-tion: a report for the 2nd International Consensus Con-ference on Laparoscopic Liver Resection. Surg Endosc. 2016;30(11):4691-4696. 222. Cherqui D, Soubrane O, Husson E, et al. Laparoscopic living donor hepatectomy for liver transplantation in children. Lancet 2002;359:392-396. 223. Koffron AJ, Kung R, Baker T, Fryer J, Clark L, Abecassis M. Laparoscopic-assisted right lobe donor hepatectomy. Am J Transplant. 2006;6:2522-2525. 224. Soubrane O, Perdigao Cotta F, Scatton O. Pure laparo-scopic right hepatectomy in a living donor. Am J Transplant. 2013;13:2467-2471.Brunicardi_Ch31_p1345-p1392.indd 139220/02/19 2:37 PM


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Surgery_Schwartz. Gallbladder and the Extrahepatic Biliary SystemKelly R. Haisley and John G. Hunter 32chapterANATOMYGallbladderThe gallbladder is a pear-shaped sac that measures around 7 to 10 cm long, with an average capacity of 30 to 50 mL. When obstructed, the gallbladder can distend markedly and contain up to 300 mL of fluid. The gallbladder is located in an anatomic fossa on the inferior surface of the liver. Cantle’s line, a vertical plane running from the gallbladder fossa anteriorly to the infe-rior vena cava (IVC) posteriorly divides the liver into right and left lobes. The gallbladder itself is divided into four anatomic areas: the fundus, the body, the infundibulum, and the neck. The fundus is the rounded, blind end that normally extends 1 to 2 cm beyond the liver’s margin and contains most of the smooth muscle of the organ. The body functions as the main storage area and contains most of the elastic tissue allowing for disten-tion. As the body tapers towards the neck of the gallbladder, a


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Surgery_Schwartz. the smooth muscle of the organ. The body functions as the main storage area and contains most of the elastic tissue allowing for disten-tion. As the body tapers towards the neck of the gallbladder, a mucosal outpouching is present at the junction of the neck and the cystic duct, known as the infundibulum or Hartmann’s pouch. Beyond this, the neck of the gallbladder lies in the deep-est part of the gallbladder fossa and can extend slightly into the free portion of the hepatoduodenal ligament, where it connects with the cystic duct (Fig. 32-1).1The same peritoneal lining that covers the liver extends to cover the fundus and the inferior surface of the gallblad-der. Occasionally, part or all of the gallbladder is embedded deep inside the liver parenchyma (an intrahepatic gallbladder). Rarely, the gallbladder has a complete peritoneal covering on all sides and is suspended in a mesentery off the inferior surface of the liver.The mucosal lining of the gallbladder is formed by a single,


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Surgery_Schwartz. the gallbladder has a complete peritoneal covering on all sides and is suspended in a mesentery off the inferior surface of the liver.The mucosal lining of the gallbladder is formed by a single, highly redundant, simple columnar epithelium that contains cholesterol and fat globules. The mucus secreted into the gall-bladder originates in tubuloalveolar glands that are found in the mucosal lining of the infundibulum and neck of the gallbladder, but are absent from the body and fundus. The epithelial lining of the gallbladder is supported by a lamina propria. The gallblad-der differs histologically from the rest of the gastrointestinal (GI) tract in that it lacks a muscularis mucosa and submucosa. The muscular layer has circular, longitudinal, and oblique fibers, but without well-defined layers. The adventitia contains connective tissue, nerves, vessels, lymphatics, and adipocytes. The gallbladder is covered by serosa except where the gallblad-der is embedded in the liver.The cystic


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Surgery_Schwartz. layers. The adventitia contains connective tissue, nerves, vessels, lymphatics, and adipocytes. The gallbladder is covered by serosa except where the gallblad-der is embedded in the liver.The cystic artery that supplies the gallbladder is usually a branch of the right hepatic artery (>90% of the time). The course of the cystic artery may vary, but it nearly always is found within the hepatocystic triangle (triangle of Calot), the area bound by the cystic duct, common hepatic duct, and the inferior edge of the liver. When the cystic artery reaches the neck of the gall-bladder, it divides into anterior and posterior divisions. Venous return is carried either through small veins that enter directly into the liver or, rarely, to a large cystic vein that carries blood back to the portal vein. Gallbladder lymphatics drain into nodes Anatomy 1393Gallbladder / 1393Bile Ducts / 1394Anatomic Variants / 1396Physiology 1396Bile Formation and Composition / 1396Gallbladder Function / 1397Sphincter


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Surgery_Schwartz. Gallbladder lymphatics drain into nodes Anatomy 1393Gallbladder / 1393Bile Ducts / 1394Anatomic Variants / 1396Physiology 1396Bile Formation and Composition / 1396Gallbladder Function / 1397Sphincter of Oddi / 1397Diagnostic Studies 1398Blood Tests / 1398Transabdominal Ultrasonography / 1398Computed Tomography / 1398Hepatobiliary Scintigraphy / 1399Magnetic Resonance Imaging / 1399Endoscopic Retrograde Cholangiopancreatography / 1400Endoscopic Choledochoscopy / 1400Endoscopic Ultrasound / 1401Percutaneous Transhepatic Cholangiography / 1401Gallstone Disease 1401Prevalence and Incidence / 1401Natural History / 1401Gallstone Formation / 1402Symptomatic Gallstones / 1404Cholangiohepatitis / 1410Procedural Interventions for Gallstone Disease 1410Percutaneous Transhepatic Cholecystostomy Tubes / 1410Endoscopic Interventions / 1410Cholecystectomy / 1410Common Bile Duct Exploration / 1413Common Bile Duct Drainage Procedures / 1414Other Benign Diseases and Lesions 1414Biliary Dyskinesia


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Surgery_Schwartz. / 1410Endoscopic Interventions / 1410Cholecystectomy / 1410Common Bile Duct Exploration / 1413Common Bile Duct Drainage Procedures / 1414Other Benign Diseases and Lesions 1414Biliary Dyskinesia and Sphincter of Oddi Dysfunction / 1414Acalculous Cholecystitis / 1415Choledochal (Biliary) Cysts / 1417Primary Sclerosing Cholangitis / 1417Bile Duct Strictures / 1418Injury to the Biliary Tract 1419Gallbladder / 1419Extrahepatic Bile Ducts / 1419Tumors 1421Carcinoma of the Gallbladder / 1421Cholangiocarcinoma / 1423Brunicardi_Ch32_p1393-p1428.indd 139311/02/19 2:42 PM 1394at the neck of the gallbladder. Frequently, a visible lymph node (Lund’s or Mascagni’s node, often referred to as Calot’s node) overlies the insertion of the cystic artery into the gallbladder wall. The gallbladder receives parasympathetic, sympathetic and sensory innervation through nerve fibers running largely through the gastro hepatic ligament. Parasympathetic (cholinergic) fibers arise from the hepatic branches


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Surgery_Schwartz. parasympathetic, sympathetic and sensory innervation through nerve fibers running largely through the gastro hepatic ligament. Parasympathetic (cholinergic) fibers arise from the hepatic branches of the vagus nerve to stimulate activity in the gallbladder, bile ducts, and liver. These vagal branches also have peptide-containing nerves contain-ing agents such as substance P, somatostatin, enkephalins, and vasoactive intestinal polypeptide (VIP).2 The sympathetic and sensory braches of the gallbladder, liver, and bile ducts pass through the celiac plexus and control gallbladder relaxation and mediate the pain of biliary colic.Bile DuctsThe extrahepatic biliary tree consists of the right and left hepatic ducts, the common hepatic duct, the cystic duct, and the com-mon bile duct. Exiting the liver, the left hepatic duct is longer than the right and has a greater propensity for dilatation as a consequence of distal obstruction. The two ducts join close to their emergence from the liver to


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Surgery_Schwartz. liver, the left hepatic duct is longer than the right and has a greater propensity for dilatation as a consequence of distal obstruction. The two ducts join close to their emergence from the liver to form the common hepatic duct. The common hepatic duct typically extends 1 to 4 cm, has a diameter of approximately 4 mm, and lies anterior to the portal vein and to the right of the hepatic artery.The cystic duct exits the gallbladder and joins the common hepatic duct at an acute angle to form the common bile duct. The segment of the cystic duct immediately adjacent to the gall-bladder neck bears a variable number of mucosal folds called the spiral valves of Heister. While they do not have any valvular function, they can make cannulation of the cystic duct difficult. The length and course of the cystic duct can be quite variable. It may be short or absent and have a high union with the hepatic duct, or it may be long and running parallel to, behind, or spiral-ing around to the common


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Surgery_Schwartz. of the cystic duct can be quite variable. It may be short or absent and have a high union with the hepatic duct, or it may be long and running parallel to, behind, or spiral-ing around to the common hepatic duct before joining it, some-times as far distally as at the duodenum. Variations of the cystic duct and its point of union with the common hepatic duct are surgically important and misidentification can lead to bile duct injuries (Fig. 32-2).The union of the cystic duct and the common hepatic duct marks the start of the common bile duct. This segment is typi-cally about 7 to 11 cm in length and 5 to 10 mm in diameter, ijoklmabdefgchqrptnsFigure 32-1. Anterior aspect of the biliary anatomy. a = right hepatic duct; b = left hepatic duct; c = common hepatic duct; d = portal vein; e = proper hepatic artery; f = gastroduodenal artery; g = right gastro-epiploic artery; h = common bile duct; i = fundus of the gallbladder; j = body of gallbladder; k = infundibulum of the gallbladder; l =


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Surgery_Schwartz. hepatic artery; f = gastroduodenal artery; g = right gastro-epiploic artery; h = common bile duct; i = fundus of the gallbladder; j = body of gallbladder; k = infundibulum of the gallbladder; l = cystic duct; m = cystic artery; n = superior pancreaticoduodenal artery; o = neck of the gallbladder; p = pancreatic duct; q = common hepatic artery; r = right gastric artery; s = ampulla of Vater; t = supraduodenal artery. Note the situation of the hepatic bile duct confluence anterior to the right branch of the portal vein, and the posterior course of the right hepatic artery behind the common hepatic duct.Key Points1 The physiology of the gallbladder, biliary tree, and sphincter of Oddi are regulated by a complex interplay of hormones and neuronal inputs designed to coordinate bile release with food consumption. Dysfunctions related to this activity are linked to the development of gallbladder pathologies as de-scribed in this chapter.2 In Western countries, the most common type of


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Surgery_Schwartz. with food consumption. Dysfunctions related to this activity are linked to the development of gallbladder pathologies as de-scribed in this chapter.2 In Western countries, the most common type of gallstones are cholesterol stones. The pathogenesis of these stones relates to supersaturation of bile with cholesterol and sub-sequent precipitation.3 Laparoscopic cholecystectomy has been demonstrated to be safe and effective, and it has become the treatment of choice for symptomatic gallstones. Knowledge of the various ana-tomic anomalies of the cystic duct and artery is critical in guiding the dissection of these structures and avoiding injury to the common bile duct during cholecystectomy.4 Common bile duct injuries, although uncommon, can be devastating to patients. Proper exposure of the hepatocystic (Calot’s) triangle to obtain the critical view of safety and careful identification of the anatomic structures are keys to avoiding these injuries. Once a bile duct injury is diag-nosed,


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Surgery_Schwartz. hepatocystic (Calot’s) triangle to obtain the critical view of safety and careful identification of the anatomic structures are keys to avoiding these injuries. Once a bile duct injury is diag-nosed, the best outcomes are seen at large referral centers with experienced biliary surgeons, and patient transfer may be required.5 The main risk factor for gallbladder disease in Western coun-tries is cholelithiasis. The main complications include cho-lecystitis, choledocholithiasis, cholangitis, and biliary pancreatitis. Cholelithiasis is also the major risk factor for the development of gallbladder cancer.6 Carcinomas of the gallbladder or bile ducts generally have a poor prognosis because patients usually present late in the disease process and have poor response to chemotherapy and radiation. Surgery offers the best chance for survival and has good long-term outcomes in patients with early-stage disease.Brunicardi_Ch32_p1393-p1428.indd 139411/02/19 2:42 PM 1395GALLBLADDER AND THE


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Surgery_Schwartz. Surgery offers the best chance for survival and has good long-term outcomes in patients with early-stage disease.Brunicardi_Ch32_p1393-p1428.indd 139411/02/19 2:42 PM 1395GALLBLADDER AND THE EXTRAHEPATIC BILIARY SYSTEMCHAPTER 32though its diameter can increase slightly with age and follow-ing cholecystectomy. The upper third (supraduodenal portion) passes downward in the free edge of the hepatoduodenal liga-ment, to the right of the hepatic artery and anterior to the portal vein. The middle third (retroduodenal portion) of the common bile duct curves behind the first portion of the duodenum and diverges laterally from the portal vein and the hepatic arteries. The lower third (pancreatic portion) can curve behind the head of the pancreas in a groove, or traverse through it to enter the wall of the second portion of the duodenum. The duct then runs obliquely downward within the wall of the duodenum for 1 to 2 cm before opening on a papilla of mucous membrane (ampulla of Vater),


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Surgery_Schwartz. the wall of the second portion of the duodenum. The duct then runs obliquely downward within the wall of the duodenum for 1 to 2 cm before opening on a papilla of mucous membrane (ampulla of Vater), about 10 cm distal to the pylorus.The union of the common bile duct and the main pan-creatic duct follows one of three configurations. In about 70% of people, these ducts unite outside the duodenal wall and tra-verse the duodenal wall as a single duct. In about 20%, they join within the duodenal wall and have a short or no common duct, but open through the same opening into the duodenum. In about 10%, they exit via separate openings into the duodenum, termed pancreas divisum. The sphincter of Oddi, a thick coat of circular smooth muscle, surrounds the common bile duct at the ampulla of Vater (Fig. 32-3). It controls the flow of bile, and in some cases pancreatic juice, into the duodenum.The extrahepatic bile ducts are lined by a columnar mucosa with numerous mucous glands that are


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Surgery_Schwartz. Vater (Fig. 32-3). It controls the flow of bile, and in some cases pancreatic juice, into the duodenum.The extrahepatic bile ducts are lined by a columnar mucosa with numerous mucous glands that are concentrated in the com-mon bile duct. A fibro areolar tissue containing scant smooth muscle cells surrounds the mucosa. A distinct muscle layer is not present in the human common bile duct. The arterial supply to the bile ducts is derived from the gastroduodenal and the right hepatic arteries, with major trunks running along the medial and lateral walls of the common duct (sometimes referred to as 3 o’clock and 9 o’clock). The nerve supply to the common bile duct is the same as for the gallbladder, with the density of nerve fibers and ganglia increasing near the sphincter of Oddi.1,2ABCDEFGHFigure 32-2. Variations of the cystic duct anatomy. A. Low junction between the cystic duct and common hepatic duct. B. Cystic duct adher-ent to the common hepatic duct. C. High junction between the


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Surgery_Schwartz. 32-2. Variations of the cystic duct anatomy. A. Low junction between the cystic duct and common hepatic duct. B. Cystic duct adher-ent to the common hepatic duct. C. High junction between the cystic and the common hepatic duct. D. Cystic duct drains into right hepatic duct. E. Long cystic duct that joins common hepatic duct behind the duodenum. F. Absence of cystic duct. G. Cystic duct crosses posterior to common hepatic duct and joins it anteriorly. H. Cystic duct courses anterior to common hepatic duct and joins it posteriorly.Pancreatic ductCommonbile duct Sphincterof OddiDuodenumAmpulla ofVaterDuodenal wallFigure 32-3. The sphincter of Oddi.Brunicardi_Ch32_p1393-p1428.indd 139511/02/19 2:43 PM 1396SPECIFIC CONSIDERATIONSPART IIABCDEFFigure 32-5. Variations in the arterial supply to the gallbladder. A. Cystic artery from right hepatic artery, about 80% to 90%. B. Cystic artery off the right hepatic artery arising from the superior mesenteric artery (accessory or replaced),


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Surgery_Schwartz. to the gallbladder. A. Cystic artery from right hepatic artery, about 80% to 90%. B. Cystic artery off the right hepatic artery arising from the superior mesenteric artery (accessory or replaced), about 10%. C. Two cystic arteries, one from the right hepatic, the other from the common hepatic artery, rare. D. Two cystic arteries, one from the right hepatic, the other from the left hepatic artery, rare. E. The cystic artery branching from the right hepatic artery and running anterior to the common hepatic duct, rare. F. Two cystic arteries arising from the right hepatic artery, rare.Anatomic VariantsThe classic description of the extrahepatic biliary tree and its arteries applies only in about one-third of patients.3 The gall-bladder may have abnormal positions, be intrahepatic, be rudi-mentary (a small, nonfunctional hypoplastic remnant), or have anomalous forms or duplications. A partially or completely intrahepatic gallbladder is associated with an increased inci-dence of


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Surgery_Schwartz. be rudi-mentary (a small, nonfunctional hypoplastic remnant), or have anomalous forms or duplications. A partially or completely intrahepatic gallbladder is associated with an increased inci-dence of cholelithiasis, and may be encountered at the time of cholecystectomy. Isolated congenital absence of the gallblad-der is very rare, with a reported incidence of 0.03%. Before the diagnosis is made, the presence of an intrahepatic gallbladder or anomalous position must first be ruled out. Duplication of the gallbladder with two separate cavities and two separate cystic ducts has an incidence of about one in every 4000 persons. This occurs in two major varieties: the more common form in which each gallbladder has its own cystic duct that empties indepen-dently into the same or different parts of the extrahepatic biliary tree, and the less common variant in which the two cystic ducts merge before they enter the common bile duct. Duplication is only clinically important when some pathologic


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Surgery_Schwartz. of the extrahepatic biliary tree, and the less common variant in which the two cystic ducts merge before they enter the common bile duct. Duplication is only clinically important when some pathologic process affects one or both organs. Even rarer variants include a left-sided gallbladder (often with a cystic duct that empties into the left hepatic or common bile duct), retrodisplacement of the gall-bladder at the posterior-inferior surface of the liver, transverse positioning of the gallbladder, or a floating gallbladder in which the gallbladder is hanging by a mesentery (Fig. 32-4).Additional small bile ducts (of Luschka) may drain directly from the liver fossa into the body of the gallbladder. If present, but not recognized at the time of a cholecystectomy, a bile leak and subsequent accumulation of bile (biloma) may occur in the abdomen. An accessory right hepatic duct occurs in about 5% of cases. Variations in how the common bile duct enters the duode-num are described earlier, in


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Surgery_Schwartz. of bile (biloma) may occur in the abdomen. An accessory right hepatic duct occurs in about 5% of cases. Variations in how the common bile duct enters the duode-num are described earlier, in the “Bile Ducts” section.Anomalies of the hepatic artery and the cystic artery are quite common, occurring in as many as 50% of cases. While the right hepatic artery usually originates from the proper hepatic branch of the celiac trunk, up to 20% of patients will have a replaced right hepatic artery coming off the superior mesenteric artery. In about 5% of cases, there are two right hepatic arteries, one from the proper hepatic artery and the other from the superior mesenteric artery (accessory right hepatic artery). While the right hepatic artery typically runs posterior to the bile ducts, variations may allow it to course anterior to the common duct, making it vulnerable during surgical procedures, particularly if it runs par-allel to the cystic duct or in the mesentery of the gallbladder. The


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Surgery_Schwartz. may allow it to course anterior to the common duct, making it vulnerable during surgical procedures, particularly if it runs par-allel to the cystic duct or in the mesentery of the gallbladder. The cystic artery arises from the right hepatic artery in about 90% of cases, but it may arise from the left hepatic, common hepatic, gastroduodenal, or superior mesenteric arteries (Fig. 32-5).3Figure 32-4. Floating gallbladder suspended on mesenteryPHYSIOLOGYBile Formation and CompositionThe liver produces bile continuously and excretes it into the bile canaliculi. Bile leaves the liver through the right and left hepatic ducts, into the common hepatic duct and then the com-mon bile duct. With an intact sphincter of Oddi, tonic contrac-tion diverts bile flow into the gallbladder for storage, while mealtime stimulation allows for its passage into the duode-num. The normal adult consuming an average diet produces 500 to 1000 mL of bile a day. The secretion of bile is respon-sive to neurogenic,


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Surgery_Schwartz. mealtime stimulation allows for its passage into the duode-num. The normal adult consuming an average diet produces 500 to 1000 mL of bile a day. The secretion of bile is respon-sive to neurogenic, hormonal, and chemical stimuli. Parasym-pathetic stimulation from the hepatic branches of the vagus nerve increases secretion of bile, whereas sympathetic nerve stimulation via the celiac plexus results in decreased bile flow. Hydrochloric acid, partly digested proteins, and fatty acids entering the duodenum from the stomach after a meal stimulate the release of secretin from the S-cells of the duodenum, and increases bile production and flow.Bile is mainly composed of water, mixed with bile salts and acids, cholesterol, phospholipids (lecithin), proteins, and bilirubin. It also contains several minor components such as Brunicardi_Ch32_p1393-p1428.indd 139611/02/19 2:43 PM 1397GALLBLADDER AND THE EXTRAHEPATIC BILIARY SYSTEMCHAPTER 32electrolytes and vitamins. Sodium, potassium, calcium,


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Surgery_Schwartz. minor components such as Brunicardi_Ch32_p1393-p1428.indd 139611/02/19 2:43 PM 1397GALLBLADDER AND THE EXTRAHEPATIC BILIARY SYSTEMCHAPTER 32electrolytes and vitamins. Sodium, potassium, calcium, and chlorine have the same concentration in bile as in plasma or extracellular fluid. The pH of hepatic bile is usually neutral or slightly alkaline, though a high protein diet will shift the bile to a more acidic ph. The primary bile salts, cholate and che-nodeoxycholate, are synthesized in the liver from cholesterol metabolism. They are conjugated there with taurine and glycine and act within the bile as anions (bile acids) that are balanced by sodium. These bile acids are then excreted into the bile by hepatocytes and aid in the digestion and absorption of fats in the intestines.4 About 80% of the secreted conjugated bile acids are reabsorbed in the terminal ileum. The remainder is dehydroxyl-ated (deconjugated) by gut bacteria, forming the secondary bile acids deoxycholate and


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Surgery_Schwartz. 80% of the secreted conjugated bile acids are reabsorbed in the terminal ileum. The remainder is dehydroxyl-ated (deconjugated) by gut bacteria, forming the secondary bile acids deoxycholate and lithocholate. These are absorbed in the colon and can then be transported back to the liver. Eventu-ally, about 95% of the bile acid pool is reabsorbed, the so-called enterohepatic circulation. Only a small amount (5%) is excreted in the stool, allowing the relatively small quantity of bile acids produced to have maximal effect.The color of the bile is due to the presence of the pigment bilirubin (orange or yellow) and its oxidized form, biliverdin (green), which are the metabolic products of the breakdown of hemoglobin, and are present in bile in concentrations 100 times greater than in plasma. Bilirubin conjugated in the liver can be excreted through the urine as urobilinogen (yellow). Remaining excess bile pigment passes into the intestines where bacteria con-vert it into stercobilinogen


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Surgery_Schwartz. Bilirubin conjugated in the liver can be excreted through the urine as urobilinogen (yellow). Remaining excess bile pigment passes into the intestines where bacteria con-vert it into stercobilinogen (brown), which is excreted through the stool.Gallbladder FunctionThe gallbladder, bile ducts, and the sphincter of Oddi act together to store and regulate the flow of bile. The main function of the gallbladder is to concentrate and store hepatic bile in order to deliver it in a coordinated fashion to the duode-num in response to a meal. Absorption and Secretion. In the fasting state, approxi-mately 80% of the bile secreted by the liver is stored in the gallbladder. This storage is made possible by the fact that the gallbladder mucosa has the greatest absorptive power per unit area of any structure in the body. It rapidly absorbs sodium, chloride, and water against significant gradients, concentrating the bile as much as 10-fold and leading to a marked change in bile composition. This rapid


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Surgery_Schwartz. in the body. It rapidly absorbs sodium, chloride, and water against significant gradients, concentrating the bile as much as 10-fold and leading to a marked change in bile composition. This rapid absorptive capacity is one of the protective mechanisms that prevent a potentially dangerous rise in pressure within the biliary system as bile is produced and stored. In addition, gradual relaxation of the gallbladder as well as routine emptying of the gallbladder’s excess bile stores during the fasting period also play a role in maintaining a low resting intraluminal pressure in the biliary tree.The mucosal cells of the gallbladder itself secrete at least two important products into the gallbladder lumen: glycopro-teins and hydrogen ions. The mucosal glands in the infundibu-lum and the neck of the gallbladder secrete mucus glycoproteins that are believed to protect the mucosa from the corrosive action of bile and to facilitate the passage of bile through the cystic duct. This same mucus


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Surgery_Schwartz. of the gallbladder secrete mucus glycoproteins that are believed to protect the mucosa from the corrosive action of bile and to facilitate the passage of bile through the cystic duct. This same mucus creates the colorless “white bile” seen in hydrops of the gallbladder as a result of cystic duct obstruction blocking the entry of bile pigments into the gallbladder. The transport of hydrogen ions by the gallbladder epithelium also plays an important role in decreasing the pH of stored bile. This acidification helps prevent the precipitation of calcium salts, which can act as a nidus for stone formation.4Motor Activity. Normal gallbladder filling is facilitated by tonic contraction of the sphincter of Oddi, which creates a small but effective pressure gradient between the bile ducts and the gallbladder. In association with phase II of the interdigestive migrating myenteric motor complex (MMC) in the gut, the gallbladder repeatedly empties small volumes of bile into the duodenum. This


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Surgery_Schwartz. gallbladder. In association with phase II of the interdigestive migrating myenteric motor complex (MMC) in the gut, the gallbladder repeatedly empties small volumes of bile into the duodenum. This process is mediated at least in part by the hormone motilin. In response to a meal, the gallbladder delivers larger volumes to the intestine by a combination of gallbladder contraction and synchronized sphincter of Oddi relaxation. One of the main stimuli to this coordinated effort of gallbladder emp-tying is the hormone cholecystokinin (CCK). CCK is released endogenously from the enteroendocrine cells in the duodenum in response to a meal.5 When stimulated by eating, the gallbladder empties 50% to 70% of its contents within 30 to 40 minutes. Over the following 60 to 90 minutes, the gallbladder gradually refills as CCK levels drop. Other minor hormonal and neural pathways also are involved in the coordinated action of the gall-bladder and the sphincter of Oddi. Defects in the motor activity


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Surgery_Schwartz. gradually refills as CCK levels drop. Other minor hormonal and neural pathways also are involved in the coordinated action of the gall-bladder and the sphincter of Oddi. Defects in the motor activity of the gallbladder that inhibit correct emptying are thought to play a role in cholesterol nucleation and gallstone formation.Neurohormonal Regulation. Neurally mediated reflexes are very important in maintaining the functions of the gallbladder, sphincter of Oddi, stomach, and duodenum to coordinate the flow of bile into the intestines at the correct times. The vagus nerve stimulates contraction of the gallbladder by parasympa-thetic innervation while splanchnic sympathetic nerves from the celiac plexus are inhibitory to its motor activity. For this reason, parasympathomimetic or cholinergic drugs, including nicotine and caffeine, contract the gallbladder. Conversely, anticholiner-gic drugs such as atropine lead to gallbladder relaxation. Antral distention of the stomach causes both


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Surgery_Schwartz. drugs, including nicotine and caffeine, contract the gallbladder. Conversely, anticholiner-gic drugs such as atropine lead to gallbladder relaxation. Antral distention of the stomach causes both gallbladder contraction and relaxation of the sphincter of Oddi.In addition to neural inputs, hormonal receptors are located on the smooth muscles, vessels, nerves, and epithelium of the gallbladder and biliary tree. CCK is a peptide that comes from the enteroendocrine cells of the duodenum and proximal jejunum. CCK is released into the bloodstream in response to the presence of hydrochloric acid, fat, and amino acids in the duodenum.6 CCK has a plasma half-life of 2 to 3 minutes and is metabolized by both the liver and the kidneys. CCK acts directly on smooth muscle receptors of the gallbladder and stimulates gallbladder contraction. It also relaxes the terminal bile duct, the sphincter of Oddi, and the duodenum to allow forward bile flow. CCK stimulation of the gallbladder and biliary tree


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Surgery_Schwartz. and stimulates gallbladder contraction. It also relaxes the terminal bile duct, the sphincter of Oddi, and the duodenum to allow forward bile flow. CCK stimulation of the gallbladder and biliary tree is also mediated by cholinergic vagal neurons. For this reason, patients who have had a vagotomy may have a diminished response to CCK stimulation, resulting in an increase in the size and volume of the gallbladder.Hormones such as vasoactive intestinal polypeptide (VIP) and somatostatin are potent inhibitors of gallbladder contrac-tion. Patients treated with somatostatin analogues and those with somatostatinomas have a high incidence of gallstones, presum-ably due to the inhibition of gallbladder contraction and empty-ing. Other hormones such as substance P and enkephalin affect gallbladder motility, but their exact physiologic role is less clear.5Sphincter of OddiThe sphincter of Oddi regulates the flow of bile and pancre-atic juice into the duodenum, prevents the regurgitation of


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Surgery_Schwartz. motility, but their exact physiologic role is less clear.5Sphincter of OddiThe sphincter of Oddi regulates the flow of bile and pancre-atic juice into the duodenum, prevents the regurgitation of duodenal contents into the biliary tree, and diverts bile into 1Brunicardi_Ch32_p1393-p1428.indd 139711/02/19 2:43 PM 1398SPECIFIC CONSIDERATIONSPART IIthe gallbladder. It is a complex structure that is functionally independent from the duodenal musculature and creates a high-pressure zone between the bile duct and the duodenum. The sphincter of Oddi spans approximately 4 to 6 mm in length and has a basal resting pressure of about 13 mmHg above the duodenal pressure. On manometry, the sphincter shows pha-sic contractions with a frequency of about four per minute and amplitude of 12 to 140 mmHg. The spontaneous motility of the sphincter of Oddi is regulated by the interstitial cells of Cajal through intrinsic and extrinsic inputs from hormones and neu-rons acting on the smooth muscle


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Surgery_Schwartz. mmHg. The spontaneous motility of the sphincter of Oddi is regulated by the interstitial cells of Cajal through intrinsic and extrinsic inputs from hormones and neu-rons acting on the smooth muscle cells.7 Relaxation occurs in response to raising levels of the gastrointestinal hormones CCK, glucagon, and secretin. This leads to diminished amplitude of phasic contractions and reduced basal pressure of the sphinc-ter, allowing increased flow of bile into the duodenum. During fasting, the sphincter of Oddi activity is coordinated with the periodic partial gallbladder emptying that occurs during phase II of the migrating myoelectric motor complexes.8 Pharmacologic administration of certain gastrointestinal hormones, such as glucagon, can temporarily decrease sphincter of Oddi baseline pressure and facilitate diagnostic studies.7DIAGNOSTIC STUDIESA variety of diagnostic modalities are available for the patient with suspected disease of the gallbladder or bile ducts. In 1924, the diagnosis


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Surgery_Schwartz. and facilitate diagnostic studies.7DIAGNOSTIC STUDIESA variety of diagnostic modalities are available for the patient with suspected disease of the gallbladder or bile ducts. In 1924, the diagnosis of gallstones was revolutionized by the intro-duction of oral cholecystography by Graham and Cole. For decades, it was the mainstay of investigation for gallstones. It involved oral administration of a radiopaque compound that is absorbed, excreted by the liver, and passed into the gallblad-der. Stones are noted on a film as filling defects in a visualized, pacified gallbladder. In the later half of the 20th century, bili-ary imaging improved dramatically with the development of hepatobiliary scintigraphy (radionucleotide scanning), as well as transhepatic and endoscopic retrograde cholangiography (ERCP), which allowed for more detailed imaging of the bili-ary tree. Later, ultrasonography, computed tomography (CT), and magnetic resonance imaging (MRI) would further improve the ability to


Surgery_Schwartz

Surgery_Schwartz. (ERCP), which allowed for more detailed imaging of the bili-ary tree. Later, ultrasonography, computed tomography (CT), and magnetic resonance imaging (MRI) would further improve the ability to image the biliary tract.Blood TestsWhen patients with suspected diseases of the gallbladder or the extrahepatic biliary tree are evaluated, a complete blood count and liver function tests are routinely requested. An elevated white blood cell (WBC) count may indicate or raise suspicion of acute cholecystitis (infection within the gallbladder). If asso-ciated with an elevation of bilirubin, alkaline phosphatase, and transaminases, cholangitis (infection within the biliary tree) should be suspected. Cholestasis (an obstruction to bile flow) is generally characterized by an elevation of conjugated bilirubin and a rise in alkaline phosphatase, but it may have no transa-minitis. Such a pattern may suggest choledocholithiasis (stones in the common bile duct) or an obstructing lesion such as a


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Surgery_Schwartz. bilirubin and a rise in alkaline phosphatase, but it may have no transa-minitis. Such a pattern may suggest choledocholithiasis (stones in the common bile duct) or an obstructing lesion such as a stricture or cholangiocarcinoma. In patients with simple symp-tomatic cholelithiasis, biliary colic, or chronic cholecystitis (a chronic inflammatory state of the gallbladder without infec-tion), blood tests will often be normal.Transabdominal UltrasonographyTransabdominal ultrasound is the initial investigation of any patient suspected to have disease of the biliary tree.9 It is non-invasive, painless, does not submit the patient to radiation, and can be performed on critically ill patients. Adjacent organs can also frequently be examined at the same time. However, its reliability and interpretation are dependent upon the skills and experience of the operator. In addition, obese patients, patients with ascites, and patients with distended bowel may be difficult to examine with ultrasound as


Surgery_Schwartz

Surgery_Schwartz. are dependent upon the skills and experience of the operator. In addition, obese patients, patients with ascites, and patients with distended bowel may be difficult to examine with ultrasound as the quality of the images obtained in these situations can be poor.Ultrasound will show stones in the gallbladder with sen-sitivity and specificity of >90%, and can also reliably detect other pathologies of the biliary tree. Stones are acoustically dense and reflect the ultrasound waves back to the ultrasonic transducer. Because stones block the passage of sound waves to the region behind them, they also produce an acoustic shadow (Fig. 32-6). Stones move with changes in position. Polyps, on the other hand, may be calcified and reflect shadows, but they do not move with change in posture. Some stones form a layer in the gallbladder; others a form sediment or sludge. A thickened gallbladder wall, pericholecystic fluid, and local tenderness with direct pressure by the ultrasound probe over the


Surgery_Schwartz

Surgery_Schwartz. form a layer in the gallbladder; others a form sediment or sludge. A thickened gallbladder wall, pericholecystic fluid, and local tenderness with direct pressure by the ultrasound probe over the fundus of the gallbladder (sonographic Murphy’s sign) may indicate acute cholecystitis. When a stone obstructs the neck of the gallbladder, the gallbladder may become very large, but thin walled. A contracted, thick-walled gallbladder can be indicative of chronic cholecystitis.The extrahepatic bile ducts are also well visualized by transabdominal ultrasound, with the exception of the retro-duodenal portion. Dilation of the biliary tree in a patient with jaundice suggests an extrahepatic obstruction as the cause for the jaundice. Frequently, the site and, sometimes, the cause of the obstruction can be determined by ultrasound. Small stones in the common bile duct frequently get lodged at the distal end of it, behind the duodenum, and are, therefore, difficult to detect. A dilated common bile


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Surgery_Schwartz. be determined by ultrasound. Small stones in the common bile duct frequently get lodged at the distal end of it, behind the duodenum, and are, therefore, difficult to detect. A dilated common bile duct on ultrasound, small stones in the gallbladder, and a classic clinical presentation allows one to assume that a stone or stones are causing the obstruction. Peri-ampullary tumors can be difficult to diagnose on ultrasound, but above the retroduodenal portion, the level of obstruction and the cause may be visualized quite well. Ultrasound can also be helpful in evaluating tumor invasion and flow in the portal vein, an important guideline for resectability of periampullary tumors.10Computed TomographyAbdominal CT scans are frequently used in the workup of undif-ferentiated abdominal pain and thus often diagnose gallbladder Figure 32-6. An ultrasonography of the gallbladder. White arrows indicate stones within the gallbladder; black arrowheads show acoustic shadows from


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Surgery_Schwartz. abdominal pain and thus often diagnose gallbladder Figure 32-6. An ultrasonography of the gallbladder. White arrows indicate stones within the gallbladder; black arrowheads show acoustic shadows from stones.Brunicardi_Ch32_p1393-p1428.indd 139811/02/19 2:43 PM 1399GALLBLADDER AND THE EXTRAHEPATIC BILIARY SYSTEMCHAPTER 32disease. CT scanning is inferior to ultrasonography in diagnos-ing gallstones but is similar in sensitivity for acute cholecystitis. The major application of CT scan, however, is to define the course and status of the extrahepatic biliary tree and adjacent structures, and to evaluate for alternate causes of a patients clini-cal presentation.11 CT is also the initial test of choice in evaluat-ing patients with suspected malignancy of the gallbladder, the extrahepatic biliary system, or nearby organs such as the head of the pancreas. Use of CT scan is an integral part of the dif-ferential diagnosis of obstructive jaundice of unknown origin (Fig. 32-7).Hepatobiliary


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Surgery_Schwartz. system, or nearby organs such as the head of the pancreas. Use of CT scan is an integral part of the dif-ferential diagnosis of obstructive jaundice of unknown origin (Fig. 32-7).Hepatobiliary ScintigraphyHepatobiliary scintigraphy, or hepatobiliary iminodiace-tic acid (HIDA) scanning, is another option for noninvasive evaluation of the liver, gallbladder, bile ducts, and duode-num that provides both anatomic and functional information. 99mTechnetium-labeled derivatives of iminodiacetic acid are injected intravenously, taken up by the Kupffer cells in the liver, and excreted in the bile. Uptake by the liver is usually detected within 10 minutes, and the gallbladder, bile ducts, and duodenum are typically visualized within 60 minutes in fasting subjects. The primary use of biliary scintigraphy is in the diag-nosis of acute cholecystitis, which appears as a nonvisualized gallbladder, with prompt filling of the common bile duct and duodenum. The lack of gallbladder filling is due to


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Surgery_Schwartz. is in the diag-nosis of acute cholecystitis, which appears as a nonvisualized gallbladder, with prompt filling of the common bile duct and duodenum. The lack of gallbladder filling is due to inflamma-tory closure of the cystic duct preventing bile backflow into the gallbladder (Fig. 32-8). Evidence of cystic duct obstruction on biliary scintigraphy is highly diagnostic for acute cholecys-titis. The sensitivity and specificity for the diagnosis are about 95% each. False-positive results can occur in patients in the nonfasting state, those receiving parenteral nutrition, or in the setting of gallbladder stasis, recent narcotic use, or alcoholism. Filling of the gallbladder and common bile duct with delayed or absent filling of the duodenum indicates an obstruction at the ampulla. Biliary leaks as a complication of surgery of the gallbladder or the biliary tree can be confirmed and frequently localized by biliary scintigraphy.12 HIDA scanning with evalu-ation of the gallbladder ejection