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Surgery_Schwartz_9202
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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. 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
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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. 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
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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. 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,
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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. 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
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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. 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
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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. 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
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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. 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,
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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. 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
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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. 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,
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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. 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,
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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. 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.
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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. 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
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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. 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,
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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. 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
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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. 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.
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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. 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
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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. 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
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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. 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.
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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. 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
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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.
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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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,
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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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
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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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
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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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,
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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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
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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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
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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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
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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/ 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
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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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
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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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
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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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 =
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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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
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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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,
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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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
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 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),
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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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
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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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
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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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),
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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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
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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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
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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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
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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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
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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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,
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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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,
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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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
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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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
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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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
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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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
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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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
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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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
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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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
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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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
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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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
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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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
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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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
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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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. 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
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(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
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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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. 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
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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. 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
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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
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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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
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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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
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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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
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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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
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
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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 fraction with or without CCK provocation may also be helpful in diagnosing chronic bili-ary dyskinesia in patients with atypical symptoms. While an ejection fraction of <35% is considered abnormal, the exact interpretations and clinical implications of this finding remain a matter of some debate.13Magnetic Resonance ImagingAvailable since the mid-1990s, MRI provides anatomic details of the liver, gallbladder, and pancreas similar to those obtained from CT. Many MRI techniques (i.e., heavily T2-weighted sequences, pulse sequences with or without contrast materials) can generate high-resolution anatomic images of the biliary tree and the pancreatic duct. MRI with magnetic resonance chol-angiopancreatography (MRCP) offers a focused, noninvasive test for the diagnosis of biliary tract and
Surgery_Schwartz. 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 fraction with or without CCK provocation may also be helpful in diagnosing chronic bili-ary dyskinesia in patients with atypical symptoms. While an ejection fraction of <35% is considered abnormal, the exact interpretations and clinical implications of this finding remain a matter of some debate.13Magnetic Resonance ImagingAvailable since the mid-1990s, MRI provides anatomic details of the liver, gallbladder, and pancreas similar to those obtained from CT. Many MRI techniques (i.e., heavily T2-weighted sequences, pulse sequences with or without contrast materials) can generate high-resolution anatomic images of the biliary tree and the pancreatic duct. MRI with magnetic resonance chol-angiopancreatography (MRCP) offers a focused, noninvasive test for the diagnosis of biliary tract and
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anatomic images of the biliary tree and the pancreatic duct. MRI with magnetic resonance chol-angiopancreatography (MRCP) offers a focused, noninvasive test for the diagnosis of biliary tract and pancreatic disease (Fig. 32-9).14 It has a sensitivity and specificity of 95% and 89%, respectively, for detecting choledocholithiasis.15 In many centers, MRCP is the preferred imaging modality for precise evaluation of biliary and pancreatic duct pathology, reserving endoscopic retrograde cholangiopancreatography (ERCP) for therapeutic purposes only.Figure 32-7. Computed tomography scan of the upper abdomen from a patient with cancer of the distal common bile duct. The cancer obstructs the common bile duct as well as the pancreatic duct. 1 = the portal vein; 2 = a dilated intrahepatic bile duct; 3 = dilated cystic duct and the neck of the gallbladder; 4 = dilated common hepatic duct; 5 = the bifurcation of the common hepatic artery into the gastroduodenal artery and the proper hepatic
Surgery_Schwartz. anatomic images of the biliary tree and the pancreatic duct. MRI with magnetic resonance chol-angiopancreatography (MRCP) offers a focused, noninvasive test for the diagnosis of biliary tract and pancreatic disease (Fig. 32-9).14 It has a sensitivity and specificity of 95% and 89%, respectively, for detecting choledocholithiasis.15 In many centers, MRCP is the preferred imaging modality for precise evaluation of biliary and pancreatic duct pathology, reserving endoscopic retrograde cholangiopancreatography (ERCP) for therapeutic purposes only.Figure 32-7. Computed tomography scan of the upper abdomen from a patient with cancer of the distal common bile duct. The cancer obstructs the common bile duct as well as the pancreatic duct. 1 = the portal vein; 2 = a dilated intrahepatic bile duct; 3 = dilated cystic duct and the neck of the gallbladder; 4 = dilated common hepatic duct; 5 = the bifurcation of the common hepatic artery into the gastroduodenal artery and the proper hepatic
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duct; 3 = dilated cystic duct and the neck of the gallbladder; 4 = dilated common hepatic duct; 5 = the bifurcation of the common hepatic artery into the gastroduodenal artery and the proper hepatic artery; 6 = dilated pancreatic duct; 7 = the splenic vein.ABFigure 32-8. HIDA scanning. A. Normal HIDA scan showing filling of the extrahepatic biliary tree and gallbladder (white arrow). B. HIDA san in a patient with acute cholecystitis showing no filling of the gallbladder.Brunicardi_Ch32_p1393-p1428.indd 139911/02/19 2:43 PM 1400SPECIFIC CONSIDERATIONSPART IIEndoscopic Retrograde CholangiopancreatographyWhile the use of endoscopic retrograde cholangiopancrea-tography (ERCP) in biliary disease is particularly valuable for its therapeutic capabilities, its diagnostic role should not be overlooked. Using a side-viewing endoscope, the common bile duct can be cannulated through the ampulla of Vater and a cholangiogram performed using fluoroscopy (Fig. 32-10). The procedure requires at
Surgery_Schwartz. duct; 3 = dilated cystic duct and the neck of the gallbladder; 4 = dilated common hepatic duct; 5 = the bifurcation of the common hepatic artery into the gastroduodenal artery and the proper hepatic artery; 6 = dilated pancreatic duct; 7 = the splenic vein.ABFigure 32-8. HIDA scanning. A. Normal HIDA scan showing filling of the extrahepatic biliary tree and gallbladder (white arrow). B. HIDA san in a patient with acute cholecystitis showing no filling of the gallbladder.Brunicardi_Ch32_p1393-p1428.indd 139911/02/19 2:43 PM 1400SPECIFIC CONSIDERATIONSPART IIEndoscopic Retrograde CholangiopancreatographyWhile the use of endoscopic retrograde cholangiopancrea-tography (ERCP) in biliary disease is particularly valuable for its therapeutic capabilities, its diagnostic role should not be overlooked. Using a side-viewing endoscope, the common bile duct can be cannulated through the ampulla of Vater and a cholangiogram performed using fluoroscopy (Fig. 32-10). The procedure requires at
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overlooked. Using a side-viewing endoscope, the common bile duct can be cannulated through the ampulla of Vater and a cholangiogram performed using fluoroscopy (Fig. 32-10). The procedure requires at least intravenous (IV) sedation and in some cases general anesthesia. The advantages of ERCP include direct visualization of the ampullary region and direct access to the distal common bile duct for cholangiography or choledochoscopy. The test is rarely needed for uncomplicated gallstone disease. However, for cases of choledocholithiasis, obstructive jaundice, biliary strictures, or cholangitis, ERCP has the advantage of being both diagnostic and therapeutic. If ductal stones are identified on the endoscopic cholangiogram, biliary sphincterotomy and stone extraction can be performed, clearing the common bile duct of stones. If another etiology such as a biliary stricture is found, diagnostic brushings can be obtained at the time of the procedure. In the hands of experts, the success rate
Surgery_Schwartz. overlooked. Using a side-viewing endoscope, the common bile duct can be cannulated through the ampulla of Vater and a cholangiogram performed using fluoroscopy (Fig. 32-10). The procedure requires at least intravenous (IV) sedation and in some cases general anesthesia. The advantages of ERCP include direct visualization of the ampullary region and direct access to the distal common bile duct for cholangiography or choledochoscopy. The test is rarely needed for uncomplicated gallstone disease. However, for cases of choledocholithiasis, obstructive jaundice, biliary strictures, or cholangitis, ERCP has the advantage of being both diagnostic and therapeutic. If ductal stones are identified on the endoscopic cholangiogram, biliary sphincterotomy and stone extraction can be performed, clearing the common bile duct of stones. If another etiology such as a biliary stricture is found, diagnostic brushings can be obtained at the time of the procedure. In the hands of experts, the success rate
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the common bile duct of stones. If another etiology such as a biliary stricture is found, diagnostic brushings can be obtained at the time of the procedure. In the hands of experts, the success rate of common bile duct cannulation and cholan-giography is >90%. Notable complications of diagnostic ERCP include pancreatitis, which occurs in approximately 3.5% of patients, as well as rare occurrences of bleeding, perforation, or infection (cholangitis).16,17Endoscopic CholedochoscopyThe development of small fiber-optic cameras that can be threaded through endoscopes used for endoscopic retrograde cholangiopancreatography (ERCP) has facilitated the develop-ment of intraductal endoscopy. By providing direct visualiza-tion of the biliary and pancreatic ducts, this technology has been shown to increase the effectiveness of ERCP in the diag-nosis of certain biliary diseases.18 Intraductal endoscopy has been shown to have therapeutic applications that include bili-ary stone lithotripsy and
Surgery_Schwartz. the common bile duct of stones. If another etiology such as a biliary stricture is found, diagnostic brushings can be obtained at the time of the procedure. In the hands of experts, the success rate of common bile duct cannulation and cholan-giography is >90%. Notable complications of diagnostic ERCP include pancreatitis, which occurs in approximately 3.5% of patients, as well as rare occurrences of bleeding, perforation, or infection (cholangitis).16,17Endoscopic CholedochoscopyThe development of small fiber-optic cameras that can be threaded through endoscopes used for endoscopic retrograde cholangiopancreatography (ERCP) has facilitated the develop-ment of intraductal endoscopy. By providing direct visualiza-tion of the biliary and pancreatic ducts, this technology has been shown to increase the effectiveness of ERCP in the diag-nosis of certain biliary diseases.18 Intraductal endoscopy has been shown to have therapeutic applications that include bili-ary stone lithotripsy and
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increase the effectiveness of ERCP in the diag-nosis of certain biliary diseases.18 Intraductal endoscopy has been shown to have therapeutic applications that include bili-ary stone lithotripsy and directed stone extraction in high-risk surgical patients.19 It can also allow for direct visualization and sampling of concerning lesions in order to evaluate for malig-nancy (Fig. 32-11). Studies have thus far shown intraductal endoscopy to be safe and effective, though complications such as bile duct perforation, minor bleeding, and cholangitis have Figure 32-9. Magnetic resonance cholangiopancreatography. This view shows the course of the extrahepatic bile ducts (arrow) and the pancreatic duct (arrowheads).BAFigure 32-10. Endoscopic retrograde cholangiography. A. A schematic picture showing the side-viewing endoscope in the duodenum and a catheter in the common bile duct. B. An endoscopic cholangiogram showing stones in the common bile duct. The catheter has been placed through the
Surgery_Schwartz. increase the effectiveness of ERCP in the diag-nosis of certain biliary diseases.18 Intraductal endoscopy has been shown to have therapeutic applications that include bili-ary stone lithotripsy and directed stone extraction in high-risk surgical patients.19 It can also allow for direct visualization and sampling of concerning lesions in order to evaluate for malig-nancy (Fig. 32-11). Studies have thus far shown intraductal endoscopy to be safe and effective, though complications such as bile duct perforation, minor bleeding, and cholangitis have Figure 32-9. Magnetic resonance cholangiopancreatography. This view shows the course of the extrahepatic bile ducts (arrow) and the pancreatic duct (arrowheads).BAFigure 32-10. Endoscopic retrograde cholangiography. A. A schematic picture showing the side-viewing endoscope in the duodenum and a catheter in the common bile duct. B. An endoscopic cholangiogram showing stones in the common bile duct. The catheter has been placed through the
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the side-viewing endoscope in the duodenum and a catheter in the common bile duct. B. An endoscopic cholangiogram showing stones in the common bile duct. The catheter has been placed through the ampulla of Vater into the distal common bile duct (arrow). Note the duodenal shadow indicated with arrowheads.Brunicardi_Ch32_p1393-p1428.indd 140011/02/19 2:43 PM 1401GALLBLADDER AND THE EXTRAHEPATIC BILIARY SYSTEMCHAPTER 32been described.20 Further refinement of this technology will likely enhance ERCP as a diagnostic and therapeutic tool.Endoscopic UltrasoundEndoscopic ultrasound (EUS) has improved significantly in recent years and offers additional diagnostic utility to the workup of biliary disease. It requires a specialized 30° endo-scope with either a radial or linear ultrasound transducer at its tip. The results are operator dependent and require a skilled endoscopist but offer noninvasive imaging of the bile ducts and adjacent structures. Endoscopic ultrasound can also be used to
Surgery_Schwartz. the side-viewing endoscope in the duodenum and a catheter in the common bile duct. B. An endoscopic cholangiogram showing stones in the common bile duct. The catheter has been placed through the ampulla of Vater into the distal common bile duct (arrow). Note the duodenal shadow indicated with arrowheads.Brunicardi_Ch32_p1393-p1428.indd 140011/02/19 2:43 PM 1401GALLBLADDER AND THE EXTRAHEPATIC BILIARY SYSTEMCHAPTER 32been described.20 Further refinement of this technology will likely enhance ERCP as a diagnostic and therapeutic tool.Endoscopic UltrasoundEndoscopic ultrasound (EUS) has improved significantly in recent years and offers additional diagnostic utility to the workup of biliary disease. It requires a specialized 30° endo-scope with either a radial or linear ultrasound transducer at its tip. The results are operator dependent and require a skilled endoscopist but offer noninvasive imaging of the bile ducts and adjacent structures. Endoscopic ultrasound can also be used to
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at its tip. The results are operator dependent and require a skilled endoscopist but offer noninvasive imaging of the bile ducts and adjacent structures. Endoscopic ultrasound can also be used to identify choledocholithiasis. It is useful for evaluation of the retroduodenal potion of the bile duct, which is difficult to visu-alize with transabdominal ultrasonography. Although EUS is less sensitive than ERCP for biliary stones, the technique is less invasive as it does not require cannulation of the sphincter of Oddi. EUS is also of particular value in the evaluation of tumors near or behind the duodenum and their resectability. Using a linear EUS scope that has a biopsy channel, fine-needle aspira-tion (FNA) of tumors or lymph nodes, therapeutic injections, or drainage procedures under direct ultrasonic guidance can be performed.21Percutaneous Transhepatic CholangiographyIn settings in which the biliary tree cannot be accessed endo-scopically, antegrade cholangiography can be
Surgery_Schwartz. at its tip. The results are operator dependent and require a skilled endoscopist but offer noninvasive imaging of the bile ducts and adjacent structures. Endoscopic ultrasound can also be used to identify choledocholithiasis. It is useful for evaluation of the retroduodenal potion of the bile duct, which is difficult to visu-alize with transabdominal ultrasonography. Although EUS is less sensitive than ERCP for biliary stones, the technique is less invasive as it does not require cannulation of the sphincter of Oddi. EUS is also of particular value in the evaluation of tumors near or behind the duodenum and their resectability. Using a linear EUS scope that has a biopsy channel, fine-needle aspira-tion (FNA) of tumors or lymph nodes, therapeutic injections, or drainage procedures under direct ultrasonic guidance can be performed.21Percutaneous Transhepatic CholangiographyIn settings in which the biliary tree cannot be accessed endo-scopically, antegrade cholangiography can be
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under direct ultrasonic guidance can be performed.21Percutaneous Transhepatic CholangiographyIn settings in which the biliary tree cannot be accessed endo-scopically, antegrade cholangiography can be performed by accessing the intrahepatic bile ducts percutaneously with a small needle under fluoroscopic guidance. Once the position in a bile duct has been confirmed, a guidewire is inserted and a catheter is passed over the wire (Fig. 32-12). Through the catheter, an antegrade cholangiogram can be obtained and therapeutic inter-ventions such as tissue sampling, biliary drain insertions, or stent placements performed. Percutaneous transhepatic cholangiog-raphy (PTC) can also be performed through previously placed percutaneous biliary drainage tubes, if present. PTC has little role in the management of patients with uncomplicated gallstone disease but can be useful in patients with bile duct strictures or tumors, as it can define the anatomy of the biliary tree proximal to the affected
Surgery_Schwartz. under direct ultrasonic guidance can be performed.21Percutaneous Transhepatic CholangiographyIn settings in which the biliary tree cannot be accessed endo-scopically, antegrade cholangiography can be performed by accessing the intrahepatic bile ducts percutaneously with a small needle under fluoroscopic guidance. Once the position in a bile duct has been confirmed, a guidewire is inserted and a catheter is passed over the wire (Fig. 32-12). Through the catheter, an antegrade cholangiogram can be obtained and therapeutic inter-ventions such as tissue sampling, biliary drain insertions, or stent placements performed. Percutaneous transhepatic cholangiog-raphy (PTC) can also be performed through previously placed percutaneous biliary drainage tubes, if present. PTC has little role in the management of patients with uncomplicated gallstone disease but can be useful in patients with bile duct strictures or tumors, as it can define the anatomy of the biliary tree proximal to the affected
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of patients with uncomplicated gallstone disease but can be useful in patients with bile duct strictures or tumors, as it can define the anatomy of the biliary tree proximal to the affected segment. As with any invasive procedure, there are potential risks. For PTC, these are mainly bleeding, cholan-gitis, bile leak, and other catheter-related problems.12GALLSTONE DISEASEPrevalence and IncidenceGallstone disease (cholelithiasis) is one of the most common afflictions of the digestive tract. Autopsy reports show that gallstones are present in between 10% and 15% of adults.22 The prevalence of gallstones is related to many factors, including diet, age, gender, BMI, and ethnic background with increased prevalence in patients of Native American and Latin American descent. Certain conditions also predispose to the development of gallstones including pregnancy, non-HDL hyperlipidemia, Crohn’s disease, and certain blood disorders such as heredi-tary spherocytosis, sickle cell disease, and
Surgery_Schwartz. of patients with uncomplicated gallstone disease but can be useful in patients with bile duct strictures or tumors, as it can define the anatomy of the biliary tree proximal to the affected segment. As with any invasive procedure, there are potential risks. For PTC, these are mainly bleeding, cholan-gitis, bile leak, and other catheter-related problems.12GALLSTONE DISEASEPrevalence and IncidenceGallstone disease (cholelithiasis) is one of the most common afflictions of the digestive tract. Autopsy reports show that gallstones are present in between 10% and 15% of adults.22 The prevalence of gallstones is related to many factors, including diet, age, gender, BMI, and ethnic background with increased prevalence in patients of Native American and Latin American descent. Certain conditions also predispose to the development of gallstones including pregnancy, non-HDL hyperlipidemia, Crohn’s disease, and certain blood disorders such as heredi-tary spherocytosis, sickle cell disease, and
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also predispose to the development of gallstones including pregnancy, non-HDL hyperlipidemia, Crohn’s disease, and certain blood disorders such as heredi-tary spherocytosis, sickle cell disease, and thalassemia. Sur-geries that alter the normal neural or hormonal regulation of the biliary tree including terminal ileal resection and gastric or duodenal surgery increase the risk of cholelithiasis. Rapid weight loss following bariatric surgery or lifestyle changes can also precipitate gallstone formation by creating an imbal-ance in bile composition. Medications such as somatostatin analogues and estrogen-containing oral contraceptives are also associated with an increased risk of developing gallstones.22 Women are three times more likely to develop gallstones than men, and first-degree relatives of patients with gallstones have a twofold greater prevalence, possibly indicating a genetic predisposition.23Natural HistoryDespite the high prevalence of cholelithiasis, most patients will
Surgery_Schwartz. also predispose to the development of gallstones including pregnancy, non-HDL hyperlipidemia, Crohn’s disease, and certain blood disorders such as heredi-tary spherocytosis, sickle cell disease, and thalassemia. Sur-geries that alter the normal neural or hormonal regulation of the biliary tree including terminal ileal resection and gastric or duodenal surgery increase the risk of cholelithiasis. Rapid weight loss following bariatric surgery or lifestyle changes can also precipitate gallstone formation by creating an imbal-ance in bile composition. Medications such as somatostatin analogues and estrogen-containing oral contraceptives are also associated with an increased risk of developing gallstones.22 Women are three times more likely to develop gallstones than men, and first-degree relatives of patients with gallstones have a twofold greater prevalence, possibly indicating a genetic predisposition.23Natural HistoryDespite the high prevalence of cholelithiasis, most patients will
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of patients with gallstones have a twofold greater prevalence, possibly indicating a genetic predisposition.23Natural HistoryDespite the high prevalence of cholelithiasis, most patients will remain asymptomatic from their gallstones throughout life. For unknown reasons, some patients progress to a symptom-atic stage, with typical symptoms of postprandial right upper quadrant pain (biliary colic) caused by a stone obstructing the cystic duct. In addition to pain, gallstones may progress to cause complications such as acute cholecystitis, choledocholithiasis, cholangitis, gallstone pancreatitis, gallstone ileus, and gallblad-der cancer. Rarely, one of these complications of gallstones may be the initial presenting picture.Gallstones in patients without biliary symptoms are com-monly diagnosed incidentally during unrelated abdominal imag-ing or at the time of surgery for an unrelated diagnosis. Several studies have examined the likelihood of developing biliary colic or developing
Surgery_Schwartz. of patients with gallstones have a twofold greater prevalence, possibly indicating a genetic predisposition.23Natural HistoryDespite the high prevalence of cholelithiasis, most patients will remain asymptomatic from their gallstones throughout life. For unknown reasons, some patients progress to a symptom-atic stage, with typical symptoms of postprandial right upper quadrant pain (biliary colic) caused by a stone obstructing the cystic duct. In addition to pain, gallstones may progress to cause complications such as acute cholecystitis, choledocholithiasis, cholangitis, gallstone pancreatitis, gallstone ileus, and gallblad-der cancer. Rarely, one of these complications of gallstones may be the initial presenting picture.Gallstones in patients without biliary symptoms are com-monly diagnosed incidentally during unrelated abdominal imag-ing or at the time of surgery for an unrelated diagnosis. Several studies have examined the likelihood of developing biliary colic or developing
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diagnosed incidentally during unrelated abdominal imag-ing or at the time of surgery for an unrelated diagnosis. Several studies have examined the likelihood of developing biliary colic or developing significant complications of gallstone disease after incidental diagnosis in the asymptomatic patient. About 80% of these patients will remain symptom free.24 However, 2% to 3% will become symptomatic per year (i.e., develop biliary colic). Once symptomatic, patients tend to have recurring bouts of biliary colic. Complicated gallstone disease (cholecystitis, choledocholithiasis, gallstone pancreatitis, etc.) develops in 3% to 5% of symptomatic patients per year.25Because few patients develop complications without previ-ous biliary symptoms, prophylactic cholecystectomy in asymp-tomatic persons with gallstones is rarely indicated.24 Exceptions exist for individuals who will be isolated from medical care for extended periods of time, or in populations with increased risk of gallbladder
Surgery_Schwartz. diagnosed incidentally during unrelated abdominal imag-ing or at the time of surgery for an unrelated diagnosis. Several studies have examined the likelihood of developing biliary colic or developing significant complications of gallstone disease after incidental diagnosis in the asymptomatic patient. About 80% of these patients will remain symptom free.24 However, 2% to 3% will become symptomatic per year (i.e., develop biliary colic). Once symptomatic, patients tend to have recurring bouts of biliary colic. Complicated gallstone disease (cholecystitis, choledocholithiasis, gallstone pancreatitis, etc.) develops in 3% to 5% of symptomatic patients per year.25Because few patients develop complications without previ-ous biliary symptoms, prophylactic cholecystectomy in asymp-tomatic persons with gallstones is rarely indicated.24 Exceptions exist for individuals who will be isolated from medical care for extended periods of time, or in populations with increased risk of gallbladder
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with gallstones is rarely indicated.24 Exceptions exist for individuals who will be isolated from medical care for extended periods of time, or in populations with increased risk of gallbladder cancer, in which case a prophylactic cholecys-tectomy may be advisable. The presence of porcelain gallblad-der, marked by significant calcifications thought to be related to Figure 32-11. A view from the choledochoscope showing cholangiocarcinoma.Brunicardi_Ch32_p1393-p1428.indd 140111/02/19 2:43 PM 1402SPECIFIC CONSIDERATIONSPART IIgallstones, is a rare premalignant condition and is an absolute indication for cholecystectomy, even when asymptomatic.Gallstone FormationGallstones form as a result of solids settling out of solution. The major organic solutes in bile are bilirubin, bile salts, phospho-lipids, and cholesterol. Gallstones are classified by their choles-terol content as either cholesterol stones or pigment stones. Pigment stones can be further classified as either black or brown.
Surgery_Schwartz. with gallstones is rarely indicated.24 Exceptions exist for individuals who will be isolated from medical care for extended periods of time, or in populations with increased risk of gallbladder cancer, in which case a prophylactic cholecys-tectomy may be advisable. The presence of porcelain gallblad-der, marked by significant calcifications thought to be related to Figure 32-11. A view from the choledochoscope showing cholangiocarcinoma.Brunicardi_Ch32_p1393-p1428.indd 140111/02/19 2:43 PM 1402SPECIFIC CONSIDERATIONSPART IIgallstones, is a rare premalignant condition and is an absolute indication for cholecystectomy, even when asymptomatic.Gallstone FormationGallstones form as a result of solids settling out of solution. The major organic solutes in bile are bilirubin, bile salts, phospho-lipids, and cholesterol. Gallstones are classified by their choles-terol content as either cholesterol stones or pigment stones. Pigment stones can be further classified as either black or brown.
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and cholesterol. Gallstones are classified by their choles-terol content as either cholesterol stones or pigment stones. Pigment stones can be further classified as either black or brown. In Western countries, about 80% of gallstones are cholesterol stones and about 15% to 20% are black pigment stones.22 Brown pigment stones account for only a small percentage. Both types of pigment stones are more common in Asia.Cholesterol Stones. Pure cholesterol stones are uncommon and account for <10% of all stones. They usually occur as a sin-gle large stone with a smooth surface. The majority of choles-terol stones are mixed but are at least 70% cholesterol by weight in addition to variable amounts of bile pigments and calcium. These stones are usually multiple, of variable size, and may be 2SafetywireinsertedExternaldrainagecatheter21-guageneedleBileducttumorGuidewire insertedthrough introducerDrainagecatheterABCDEFFigure 32-12. Schematic diagram of percutaneous transhepatic cholangiogram and
Surgery_Schwartz. and cholesterol. Gallstones are classified by their choles-terol content as either cholesterol stones or pigment stones. Pigment stones can be further classified as either black or brown. In Western countries, about 80% of gallstones are cholesterol stones and about 15% to 20% are black pigment stones.22 Brown pigment stones account for only a small percentage. Both types of pigment stones are more common in Asia.Cholesterol Stones. Pure cholesterol stones are uncommon and account for <10% of all stones. They usually occur as a sin-gle large stone with a smooth surface. The majority of choles-terol stones are mixed but are at least 70% cholesterol by weight in addition to variable amounts of bile pigments and calcium. These stones are usually multiple, of variable size, and may be 2SafetywireinsertedExternaldrainagecatheter21-guageneedleBileducttumorGuidewire insertedthrough introducerDrainagecatheterABCDEFFigure 32-12. Schematic diagram of percutaneous transhepatic cholangiogram and
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insertedthrough introducerDrainagecatheterABCDEFFigure 32-12. Schematic diagram of percutaneous transhepatic cholangiogram and drainage for obstructing proximal cholangiocarcinoma. A. Dilated intrahepatic bile duct is entered percutaneously with a fine needle. B. Small guidewire is passed through the needle into the duct. C. A plastic catheter has been passed over the wire, and the wire is subsequently removed. A cholangiogram can be performed through the catheter. D. An external drainage catheter in place. E. Long wire placed via the catheter and advanced past the tumor and into the duodenum. F. Internal stent has been placed through the tumor.Brunicardi_Ch32_p1393-p1428.indd 140211/02/19 2:43 PM 1403GALLBLADDER AND THE EXTRAHEPATIC BILIARY SYSTEMCHAPTER 32Figure 32-13. Gallbladder with cholesterol stones. A. Stones of multiple shapes and sizes. B. Solitary large stone. C. Multiple stones of varying composition. (Reproduced with permission from Slesinger MH, Fordtran JS:
Surgery_Schwartz. insertedthrough introducerDrainagecatheterABCDEFFigure 32-12. Schematic diagram of percutaneous transhepatic cholangiogram and drainage for obstructing proximal cholangiocarcinoma. A. Dilated intrahepatic bile duct is entered percutaneously with a fine needle. B. Small guidewire is passed through the needle into the duct. C. A plastic catheter has been passed over the wire, and the wire is subsequently removed. A cholangiogram can be performed through the catheter. D. An external drainage catheter in place. E. Long wire placed via the catheter and advanced past the tumor and into the duodenum. F. Internal stent has been placed through the tumor.Brunicardi_Ch32_p1393-p1428.indd 140211/02/19 2:43 PM 1403GALLBLADDER AND THE EXTRAHEPATIC BILIARY SYSTEMCHAPTER 32Figure 32-13. Gallbladder with cholesterol stones. A. Stones of multiple shapes and sizes. B. Solitary large stone. C. Multiple stones of varying composition. (Reproduced with permission from Slesinger MH, Fordtran JS:
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with cholesterol stones. A. Stones of multiple shapes and sizes. B. Solitary large stone. C. Multiple stones of varying composition. (Reproduced with permission from Slesinger MH, Fordtran JS: Gastrointestinal Diseases. Philadelphia, PA: Elsevier/Saunders; 1989.)100100Moles % Bile salts100808080606060Moles % CholesterolMoles % LecithinMicellarliquidMetastablesupersaturatedzone4040402020200002 or morephasesFigure 32-14. The three major components of bile plotted on triangular coordinates, cholesterol, bile salts and phospholipids (lecithin). A given point represents the relative molar ratios of each. The area labeled “micellar liquid” shows the range of concentrations in which cholesterol is fully solubilized. The shaded area directly above this region corresponds to a metastable zone, supersaturated with cholesterol. Above the shaded area, bile has exceeded the solubilization capacity of cholesterol and precipitation of cholesterol crystals and stones occurs.hard and faceted or
Surgery_Schwartz. with cholesterol stones. A. Stones of multiple shapes and sizes. B. Solitary large stone. C. Multiple stones of varying composition. (Reproduced with permission from Slesinger MH, Fordtran JS: Gastrointestinal Diseases. Philadelphia, PA: Elsevier/Saunders; 1989.)100100Moles % Bile salts100808080606060Moles % CholesterolMoles % LecithinMicellarliquidMetastablesupersaturatedzone4040402020200002 or morephasesFigure 32-14. The three major components of bile plotted on triangular coordinates, cholesterol, bile salts and phospholipids (lecithin). A given point represents the relative molar ratios of each. The area labeled “micellar liquid” shows the range of concentrations in which cholesterol is fully solubilized. The shaded area directly above this region corresponds to a metastable zone, supersaturated with cholesterol. Above the shaded area, bile has exceeded the solubilization capacity of cholesterol and precipitation of cholesterol crystals and stones occurs.hard and faceted or
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supersaturated with cholesterol. Above the shaded area, bile has exceeded the solubilization capacity of cholesterol and precipitation of cholesterol crystals and stones occurs.hard and faceted or irregular, multilobed, and soft (Fig. 32-13). Colors range from whitish yellow to green or black. Most cho-lesterol stones (>90%) are radiolucent, though some have a high calcium carbonate component and become radioopaque.The primary event in the formation of cholesterol stones is supersaturation of bile with cholesterol. Cholesterol is highly nonpolar and its solubility in water and bile depends on the relative concentration of cholesterol, bile salts, and lecithin (the main phospholipid in bile). Cholesterol is secreted into bile and is surrounded by bile salts and phospholipids to form a soluble vesicle complex. When cholesterol hypersecretion is present, either through increased intake or dysfunctional processing, supersaturation occurs. When cholesterol concentrations exceed the ability
Surgery_Schwartz. supersaturated with cholesterol. Above the shaded area, bile has exceeded the solubilization capacity of cholesterol and precipitation of cholesterol crystals and stones occurs.hard and faceted or irregular, multilobed, and soft (Fig. 32-13). Colors range from whitish yellow to green or black. Most cho-lesterol stones (>90%) are radiolucent, though some have a high calcium carbonate component and become radioopaque.The primary event in the formation of cholesterol stones is supersaturation of bile with cholesterol. Cholesterol is highly nonpolar and its solubility in water and bile depends on the relative concentration of cholesterol, bile salts, and lecithin (the main phospholipid in bile). Cholesterol is secreted into bile and is surrounded by bile salts and phospholipids to form a soluble vesicle complex. When cholesterol hypersecretion is present, either through increased intake or dysfunctional processing, supersaturation occurs. When cholesterol concentrations exceed the ability
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vesicle complex. When cholesterol hypersecretion is present, either through increased intake or dysfunctional processing, supersaturation occurs. When cholesterol concentrations exceed the ability of the bile salts and phospholipid to maintain solu-bility, the cholesterol precipitates out of solution into a solid, forming a cholesterol stone (Fig. 32-14).26 Cholesterol hyperse-cretion is almost always the cause of supersaturation rather than reduced secretion of phospholipid or bile salts.2Pigmented Stones. Pigmented stones contain <20% choles-terol and are dark because of the presence of calcium bilirubi-nate. Black and brown pigment stones have little in common and should be considered as separate entities.Black pigment stones are usually small, brittle, dark, and sometimes spiculated. They are formed by supersaturation of unconjugated bilirubin within the bile. Deconjugation of bili-rubin occurs normally in bile at a slow rate. Thus, excessive levels of conjugated bilirubin
Surgery_Schwartz. vesicle complex. When cholesterol hypersecretion is present, either through increased intake or dysfunctional processing, supersaturation occurs. When cholesterol concentrations exceed the ability of the bile salts and phospholipid to maintain solu-bility, the cholesterol precipitates out of solution into a solid, forming a cholesterol stone (Fig. 32-14).26 Cholesterol hyperse-cretion is almost always the cause of supersaturation rather than reduced secretion of phospholipid or bile salts.2Pigmented Stones. Pigmented stones contain <20% choles-terol and are dark because of the presence of calcium bilirubi-nate. Black and brown pigment stones have little in common and should be considered as separate entities.Black pigment stones are usually small, brittle, dark, and sometimes spiculated. They are formed by supersaturation of unconjugated bilirubin within the bile. Deconjugation of bili-rubin occurs normally in bile at a slow rate. Thus, excessive levels of conjugated bilirubin
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They are formed by supersaturation of unconjugated bilirubin within the bile. Deconjugation of bili-rubin occurs normally in bile at a slow rate. Thus, excessive levels of conjugated bilirubin excretion, as occurs in hemolytic disorders like hereditary spherocytosis and sickle cell disease will lead to an increased rate of production of unconjugated bilirubin. Cirrhosis and hepatic dysfunction may also lead to increased secretion of unconjugated bilirubin directly from the liver. The insoluble unconjugated bilirubin will then precipitate with calcium as insoluble calcium bilirubinate, forming a pig-ment stone. Due to their high calcium content, pigment stones are often radiopaque. Like cholesterol stones, they almost always form in the gallbladder. In Asian countries such as Japan, black stones account for a much higher percentage of gallstones than in the Western hemisphere.Brown stones are usually <1 cm in diameter, brownish-yel-low, soft, and often mushy. They may form either in
Surgery_Schwartz. They are formed by supersaturation of unconjugated bilirubin within the bile. Deconjugation of bili-rubin occurs normally in bile at a slow rate. Thus, excessive levels of conjugated bilirubin excretion, as occurs in hemolytic disorders like hereditary spherocytosis and sickle cell disease will lead to an increased rate of production of unconjugated bilirubin. Cirrhosis and hepatic dysfunction may also lead to increased secretion of unconjugated bilirubin directly from the liver. The insoluble unconjugated bilirubin will then precipitate with calcium as insoluble calcium bilirubinate, forming a pig-ment stone. Due to their high calcium content, pigment stones are often radiopaque. Like cholesterol stones, they almost always form in the gallbladder. In Asian countries such as Japan, black stones account for a much higher percentage of gallstones than in the Western hemisphere.Brown stones are usually <1 cm in diameter, brownish-yel-low, soft, and often mushy. They may form either in
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stones account for a much higher percentage of gallstones than in the Western hemisphere.Brown stones are usually <1 cm in diameter, brownish-yel-low, soft, and often mushy. They may form either in the gallblad-der or in the bile ducts secondary to bacterial infection and bile stasis. Bacteria such as Escherichia coli secrete β-glucuronidase that enzymatically cleaves conjugated bilirubin to produce the insoluble unconjugated bilirubin. This unconjugated bilirubin then precipitates with calcium, and along with dead bacterial cell bodies, forms soft brown stones in the biliary tree. Brown stones are typically found in Asian populations and are associated with stasis secondary to parasite infection with Ascaris lumbricoides BCABrunicardi_Ch32_p1393-p1428.indd 140311/02/19 2:43 PM 1404SPECIFIC CONSIDERATIONSPART II(roundworm) or Clonorchis sinensis (liver fluke). In Western populations, brown stones most often occur as primary bile duct stones in patients with biliary strictures or
Surgery_Schwartz. stones account for a much higher percentage of gallstones than in the Western hemisphere.Brown stones are usually <1 cm in diameter, brownish-yel-low, soft, and often mushy. They may form either in the gallblad-der or in the bile ducts secondary to bacterial infection and bile stasis. Bacteria such as Escherichia coli secrete β-glucuronidase that enzymatically cleaves conjugated bilirubin to produce the insoluble unconjugated bilirubin. This unconjugated bilirubin then precipitates with calcium, and along with dead bacterial cell bodies, forms soft brown stones in the biliary tree. Brown stones are typically found in Asian populations and are associated with stasis secondary to parasite infection with Ascaris lumbricoides BCABrunicardi_Ch32_p1393-p1428.indd 140311/02/19 2:43 PM 1404SPECIFIC CONSIDERATIONSPART II(roundworm) or Clonorchis sinensis (liver fluke). In Western populations, brown stones most often occur as primary bile duct stones in patients with biliary strictures or
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CONSIDERATIONSPART II(roundworm) or Clonorchis sinensis (liver fluke). In Western populations, brown stones most often occur as primary bile duct stones in patients with biliary strictures or other common bile duct stones that cause stasis and bacterial contamination.2,27Symptomatic GallstonesSymptomatic Cholelithiasis. Patients with symptomatic gall-stone disease typically present with recurrent attacks of pain. The pain develops when a stone obstructs the cystic duct, resulting in a progressive increase of tension in the gallbladder wall as it contracts in response to a meal. This postprandial right upper quadrant or epigastric pain is often referred to as biliary colic. If untreated, about two-thirds of these patients will develop chronic noninfectious inflammation of the gallbladder wall, termed chronic cholecystitis. The pathologic changes, which often do not correlate well with symptoms, vary from an apparently nor-mal gallbladder with minor chronic inflammation in the mucosa,
Surgery_Schwartz. CONSIDERATIONSPART II(roundworm) or Clonorchis sinensis (liver fluke). In Western populations, brown stones most often occur as primary bile duct stones in patients with biliary strictures or other common bile duct stones that cause stasis and bacterial contamination.2,27Symptomatic GallstonesSymptomatic Cholelithiasis. Patients with symptomatic gall-stone disease typically present with recurrent attacks of pain. The pain develops when a stone obstructs the cystic duct, resulting in a progressive increase of tension in the gallbladder wall as it contracts in response to a meal. This postprandial right upper quadrant or epigastric pain is often referred to as biliary colic. If untreated, about two-thirds of these patients will develop chronic noninfectious inflammation of the gallbladder wall, termed chronic cholecystitis. The pathologic changes, which often do not correlate well with symptoms, vary from an apparently nor-mal gallbladder with minor chronic inflammation in the mucosa,
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wall, termed chronic cholecystitis. The pathologic changes, which often do not correlate well with symptoms, vary from an apparently nor-mal gallbladder with minor chronic inflammation in the mucosa, to a shrunken, nonfunctioning gallbladder with transmural fibro-sis and adhesions to nearby structures. The mucosa is initially normal or hypertrophied but later becomes atrophied, with the epithelium protruding into the muscle coat, leading to the forma-tion of the so-called Aschoff-Rokitansky sinuses.Clinical Manifestations The chief symptom associated with symptomatic cholelithiasis is pain (biliary colic). The pain is con-stant and increases in severity over the first half hour or so after a meal and can last 1 to 5 hours. It is located in the epigastrium or right upper quadrant and frequently radiates to the right upper back or between the scapulae (Fig. 32-15). The pain is severe and comes on abruptly, typically during the night or after a fatty meal. It often is associated with
Surgery_Schwartz. wall, termed chronic cholecystitis. The pathologic changes, which often do not correlate well with symptoms, vary from an apparently nor-mal gallbladder with minor chronic inflammation in the mucosa, to a shrunken, nonfunctioning gallbladder with transmural fibro-sis and adhesions to nearby structures. The mucosa is initially normal or hypertrophied but later becomes atrophied, with the epithelium protruding into the muscle coat, leading to the forma-tion of the so-called Aschoff-Rokitansky sinuses.Clinical Manifestations The chief symptom associated with symptomatic cholelithiasis is pain (biliary colic). The pain is con-stant and increases in severity over the first half hour or so after a meal and can last 1 to 5 hours. It is located in the epigastrium or right upper quadrant and frequently radiates to the right upper back or between the scapulae (Fig. 32-15). The pain is severe and comes on abruptly, typically during the night or after a fatty meal. It often is associated with