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Surgery_Schwartz_9902
Surgery_Schwartz
of the interval once sta-bility is established. Patients with noninvasive MCNs require no surveillance after resection, but patients with IPMNs need surveillance after resection. In the absence of residual lesions, repeat MRI at 2 and 5 years may be reasonable. If there is low or moderate-grade dysplasia at the margin, MRI every 6 months is recommended.Resection is indicated in all surgically fit patients with MD-IPMN, and additional resection is indicated if there is high-grade dysplasia at the margin. Resection is also indicated in all surgically fit patients with MCN. BD-IPMN <3 cm without wor-risome features or high-risk stigmata can undergo surveillance.When patients are deemed unacceptable for resection due to comorbidities, ablation of the cyst can be considered. How-ever, at this time, cyst ablation is considered experimental and should be done as part of a clinical trial. Gastroenterologists have limited experience with injection of a cytotoxic agent into the cyst in an
Surgery_Schwartz. of the interval once sta-bility is established. Patients with noninvasive MCNs require no surveillance after resection, but patients with IPMNs need surveillance after resection. In the absence of residual lesions, repeat MRI at 2 and 5 years may be reasonable. If there is low or moderate-grade dysplasia at the margin, MRI every 6 months is recommended.Resection is indicated in all surgically fit patients with MD-IPMN, and additional resection is indicated if there is high-grade dysplasia at the margin. Resection is also indicated in all surgically fit patients with MCN. BD-IPMN <3 cm without wor-risome features or high-risk stigmata can undergo surveillance.When patients are deemed unacceptable for resection due to comorbidities, ablation of the cyst can be considered. How-ever, at this time, cyst ablation is considered experimental and should be done as part of a clinical trial. Gastroenterologists have limited experience with injection of a cytotoxic agent into the cyst in an
Surgery_Schwartz_9903
Surgery_Schwartz
this time, cyst ablation is considered experimental and should be done as part of a clinical trial. Gastroenterologists have limited experience with injection of a cytotoxic agent into the cyst in an attempt to ablate the cyst epithelium. Ethanol has been used and more recently this has been combined with paclitaxel. The combination of ethanol and paclitaxel injection resulted in elimination of the cysts, as determined by CT scan-ning, in 29 out of 47 (62%) of patients in a median follow-up period of 21.7 months.377Recently, the American Gastroenterological Association (AGA) published guidelines for asymptomatic mucinous cysts (http://www.gastro.org/guidelines/pancreatic-cysts) that are different from all previously published guidelines in the following areas: 2-year interval for cyst of any size undergoing surveillance, stopping surveillance after 5 years if no change, surgery only if more than one concerning feature on MRI confirmed on EUS and only in centers with high volumes of
Surgery_Schwartz. this time, cyst ablation is considered experimental and should be done as part of a clinical trial. Gastroenterologists have limited experience with injection of a cytotoxic agent into the cyst in an attempt to ablate the cyst epithelium. Ethanol has been used and more recently this has been combined with paclitaxel. The combination of ethanol and paclitaxel injection resulted in elimination of the cysts, as determined by CT scan-ning, in 29 out of 47 (62%) of patients in a median follow-up period of 21.7 months.377Recently, the American Gastroenterological Association (AGA) published guidelines for asymptomatic mucinous cysts (http://www.gastro.org/guidelines/pancreatic-cysts) that are different from all previously published guidelines in the following areas: 2-year interval for cyst of any size undergoing surveillance, stopping surveillance after 5 years if no change, surgery only if more than one concerning feature on MRI confirmed on EUS and only in centers with high volumes of
Surgery_Schwartz_9904
Surgery_Schwartz
any size undergoing surveillance, stopping surveillance after 5 years if no change, surgery only if more than one concerning feature on MRI confirmed on EUS and only in centers with high volumes of pancreatic surgery, and no surveillance after surgery if no invasive cancer or dysplasia. Although based on extensive literature review and synthesis, these recommendations have resulted in significant controversy because, in an effort to reduce the costs of health care delivery and perhaps decrease inadvertent harm to patients, they advocate less frequent follow-up and a higher threshold before offering EUS and/or surgery.Solid-Pseudopapillary Tumor. Solid-pseudopapillary tumors are rare and typically occur in young women. Previous names for this entity include, solid and cystic, solid and papillary, cystic and papillary, and papillary-cystic tumor. They are typically well circumscribed on CT (Fig. 33-83). The cysts are not true epithelial-lined cysts but rather represent a
Surgery_Schwartz. any size undergoing surveillance, stopping surveillance after 5 years if no change, surgery only if more than one concerning feature on MRI confirmed on EUS and only in centers with high volumes of pancreatic surgery, and no surveillance after surgery if no invasive cancer or dysplasia. Although based on extensive literature review and synthesis, these recommendations have resulted in significant controversy because, in an effort to reduce the costs of health care delivery and perhaps decrease inadvertent harm to patients, they advocate less frequent follow-up and a higher threshold before offering EUS and/or surgery.Solid-Pseudopapillary Tumor. Solid-pseudopapillary tumors are rare and typically occur in young women. Previous names for this entity include, solid and cystic, solid and papillary, cystic and papillary, and papillary-cystic tumor. They are typically well circumscribed on CT (Fig. 33-83). The cysts are not true epithelial-lined cysts but rather represent a
Surgery_Schwartz_9905
Surgery_Schwartz
solid and papillary, cystic and papillary, and papillary-cystic tumor. They are typically well circumscribed on CT (Fig. 33-83). The cysts are not true epithelial-lined cysts but rather represent a necrotic/degenerative process. Histology may be similar to neuroendocrine tumors, but they do not stain positive for neuroendocrine markers such as chromogranin. Most are cured by resection, but liver and peritoneal metastases have been reported.Other Cystic Neoplasms. Rarely, typical ductal adenocarci-noma of the pancreas may undergo cystic degeneration due to central necrosis. Occasionally, this will create difficulty in the proper preoperative diagnosis and should be kept in mind when deciding to conservatively follow a cystic pancreatic neoplasm. It is more common, 5% to 10%, for neuroendocrine tumors of the pancreas to contain cysts. These cysts are filled with sero-sanguineous fluid rather than necrotic debris. Lymphoepithelial Figure 33-82. Operative specimen of pancreas with
Surgery_Schwartz. solid and papillary, cystic and papillary, and papillary-cystic tumor. They are typically well circumscribed on CT (Fig. 33-83). The cysts are not true epithelial-lined cysts but rather represent a necrotic/degenerative process. Histology may be similar to neuroendocrine tumors, but they do not stain positive for neuroendocrine markers such as chromogranin. Most are cured by resection, but liver and peritoneal metastases have been reported.Other Cystic Neoplasms. Rarely, typical ductal adenocarci-noma of the pancreas may undergo cystic degeneration due to central necrosis. Occasionally, this will create difficulty in the proper preoperative diagnosis and should be kept in mind when deciding to conservatively follow a cystic pancreatic neoplasm. It is more common, 5% to 10%, for neuroendocrine tumors of the pancreas to contain cysts. These cysts are filled with sero-sanguineous fluid rather than necrotic debris. Lymphoepithelial Figure 33-82. Operative specimen of pancreas with
Surgery_Schwartz_9906
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tumors of the pancreas to contain cysts. These cysts are filled with sero-sanguineous fluid rather than necrotic debris. Lymphoepithelial Figure 33-82. Operative specimen of pancreas with multifocal intraductal papillary mucinous neoplasms (black arrow) and a focus of invasive adenocarcinoma (white arrow). (Reproduced with permission from Asiyanbola B, Andersen DK. IPMN. Editorial Update. accesssurgery.com McGraw-Hill Education; 2008.)Brunicardi_Ch33_p1429-p1516.indd 150401/03/19 6:47 PM 1505PANCREASCHAPTER 33Figure 33-83. Abdominal computed tomographic scan of a 25-year-old woman demonstrating a well-circumscribed cystic lesion with septation in body/tail of pancreas. At surgery, the tumor was adherent to the splenic artery. Pathologic diagnosis was solid-pseudopapillary carcinoma.cysts of the pancreas usually occur in men in their fifth to sixth decade. These benign lesions may be unilocular or multilocular and vary widely in size. The contents of the cyst are also vari-able and
Surgery_Schwartz. tumors of the pancreas to contain cysts. These cysts are filled with sero-sanguineous fluid rather than necrotic debris. Lymphoepithelial Figure 33-82. Operative specimen of pancreas with multifocal intraductal papillary mucinous neoplasms (black arrow) and a focus of invasive adenocarcinoma (white arrow). (Reproduced with permission from Asiyanbola B, Andersen DK. IPMN. Editorial Update. accesssurgery.com McGraw-Hill Education; 2008.)Brunicardi_Ch33_p1429-p1516.indd 150401/03/19 6:47 PM 1505PANCREASCHAPTER 33Figure 33-83. Abdominal computed tomographic scan of a 25-year-old woman demonstrating a well-circumscribed cystic lesion with septation in body/tail of pancreas. At surgery, the tumor was adherent to the splenic artery. Pathologic diagnosis was solid-pseudopapillary carcinoma.cysts of the pancreas usually occur in men in their fifth to sixth decade. These benign lesions may be unilocular or multilocular and vary widely in size. The contents of the cyst are also vari-able and
Surgery_Schwartz_9907
Surgery_Schwartz
of the pancreas usually occur in men in their fifth to sixth decade. These benign lesions may be unilocular or multilocular and vary widely in size. The contents of the cyst are also vari-able and may be thin serous fluid or cheesy/caseous material if there is increased keratin formation. A substantial number of patients with von Hippel-Lindau syndrome develop pancreatic cysts that resemble serous cystadenomas. There may be mul-tiple lesions scattered throughout the pancreas. Patients with polycystic kidney and hepatic disease may also develop benign pancreatic cysts (cystadenomas). With all of these rare cystic neoplasms, careful clinical history, high-quality pancreatic imaging, and sampling of the cyst fluid for analysis will guide proper treatment.Pancreatic Lymphoma. Lymphoma can affect the pancreas. Primary involvement of the pancreas with no disease outside the pancreas also occurs. The clinical presentation often is similar to pancreatic adenocarcinoma, with vague abdominal
Surgery_Schwartz. of the pancreas usually occur in men in their fifth to sixth decade. These benign lesions may be unilocular or multilocular and vary widely in size. The contents of the cyst are also vari-able and may be thin serous fluid or cheesy/caseous material if there is increased keratin formation. A substantial number of patients with von Hippel-Lindau syndrome develop pancreatic cysts that resemble serous cystadenomas. There may be mul-tiple lesions scattered throughout the pancreas. Patients with polycystic kidney and hepatic disease may also develop benign pancreatic cysts (cystadenomas). With all of these rare cystic neoplasms, careful clinical history, high-quality pancreatic imaging, and sampling of the cyst fluid for analysis will guide proper treatment.Pancreatic Lymphoma. Lymphoma can affect the pancreas. Primary involvement of the pancreas with no disease outside the pancreas also occurs. The clinical presentation often is similar to pancreatic adenocarcinoma, with vague abdominal
Surgery_Schwartz_9908
Surgery_Schwartz
the pancreas. Primary involvement of the pancreas with no disease outside the pancreas also occurs. The clinical presentation often is similar to pancreatic adenocarcinoma, with vague abdominal pain and weight loss. Identification of a large mass often involving the head and body of the pancreas should raise suspicion. Percuta-neous or EUS-guided biopsy will confirm the diagnosis in most cases. If the diagnosis cannot be confirmed preoperatively, lapa-roscopic exploration and biopsy are indicated.378 There is no role for resection in the management of pancreatic lymphoma. Endoscopic stenting to relieve jaundice followed by chemo-therapy is the standard treatment, and long-term remission is often achieved.REFERENCESEntries highlighted in bright blue are key references. 1. Silen W. Surgical anatomy of the pancreas. Surg Clin North Am. 1964;44:1253. 2. Havel PJ, Taborsky GJ, Jr. The contribution of the autonomic nervous system to changes of glucagon and insulin secretion during
Surgery_Schwartz. the pancreas. Primary involvement of the pancreas with no disease outside the pancreas also occurs. The clinical presentation often is similar to pancreatic adenocarcinoma, with vague abdominal pain and weight loss. Identification of a large mass often involving the head and body of the pancreas should raise suspicion. Percuta-neous or EUS-guided biopsy will confirm the diagnosis in most cases. If the diagnosis cannot be confirmed preoperatively, lapa-roscopic exploration and biopsy are indicated.378 There is no role for resection in the management of pancreatic lymphoma. Endoscopic stenting to relieve jaundice followed by chemo-therapy is the standard treatment, and long-term remission is often achieved.REFERENCESEntries highlighted in bright blue are key references. 1. Silen W. Surgical anatomy of the pancreas. Surg Clin North Am. 1964;44:1253. 2. Havel PJ, Taborsky GJ, Jr. The contribution of the autonomic nervous system to changes of glucagon and insulin secretion during
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Surgical anatomy of the pancreas. Surg Clin North Am. 1964;44:1253. 2. Havel PJ, Taborsky GJ, Jr. The contribution of the autonomic nervous system to changes of glucagon and insulin secretion during hypoglycemic stress. Endocr Rev. 1989;10:332-350. 3. Davenport HW. Pancreatic secretion. In: Davenport HN, ed. Physiology of the Digestive Tract. 5th ed. Chicago: Year Book Medical Publishers; 1982:143. 4. Valenzuela JE, Weiner K, Saad C. Cholinergic stimulation of human pancreatic secretion. Dig Dis Sci. 1986;31:615-619. 5. Konturek SJ, Becker HD, Thompson JC. Effect of vagotomy on hormones stimulating pancreatic secretion. Arch Surg. 1974;108:704-708. 6. Ebert R, Creutzfeldt W. Gastrointestinal peptides and insulin secretion. Diabetes Metab Rev. 1987;3:1-26. 7. Leahy JL, Bonner-Weir S, Weir GC. Abnormal glucose regulation of insulin secretion in models of reduced B-cell mass. Diabetes. 1984; 33:667-673. 8. Brunicardi FC, Sun YS, Druck P, et al. Splanchnic neural regulation of insulin and
Surgery_Schwartz. Surgical anatomy of the pancreas. Surg Clin North Am. 1964;44:1253. 2. Havel PJ, Taborsky GJ, Jr. The contribution of the autonomic nervous system to changes of glucagon and insulin secretion during hypoglycemic stress. Endocr Rev. 1989;10:332-350. 3. Davenport HW. Pancreatic secretion. In: Davenport HN, ed. Physiology of the Digestive Tract. 5th ed. Chicago: Year Book Medical Publishers; 1982:143. 4. Valenzuela JE, Weiner K, Saad C. Cholinergic stimulation of human pancreatic secretion. Dig Dis Sci. 1986;31:615-619. 5. Konturek SJ, Becker HD, Thompson JC. Effect of vagotomy on hormones stimulating pancreatic secretion. Arch Surg. 1974;108:704-708. 6. Ebert R, Creutzfeldt W. Gastrointestinal peptides and insulin secretion. Diabetes Metab Rev. 1987;3:1-26. 7. Leahy JL, Bonner-Weir S, Weir GC. Abnormal glucose regulation of insulin secretion in models of reduced B-cell mass. Diabetes. 1984; 33:667-673. 8. Brunicardi FC, Sun YS, Druck P, et al. Splanchnic neural regulation of insulin and
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Abnormal glucose regulation of insulin secretion in models of reduced B-cell mass. Diabetes. 1984; 33:667-673. 8. Brunicardi FC, Sun YS, Druck P, et al. Splanchnic neural regulation of insulin and glucagon secretion in the isolated perfused human pancreas. Am J Surg. 1987;153:34-40. 9. Yamada Y, Post SR, Wang K, et al. Cloning and functional characterization of a family of human and mouse somatostatin receptors expressed in brain, gastrointestinal tract, and kidney. Proc Natl Acad Sci U S A. 1992;89:251-255. 10. Voss M, Pappas T. Pancreatic fistula. Curr Treat Options Gastroenterol. 2002;5:345-353. 11. Floyd JC, Jr, Fajans SS, Pek S. Regulation in healthy subjects of the secretion of human pancreatic polypeptide, a newly recognized pancreatic islet polypeptide. Trans Assoc Am Physicians. 1976;89:146-158. 12. Adrian TE, Bloom SR, Besterman HS, et al. Mechanism of pancreatic polypeptide release in man. Lancet. 1977;1:161-163.Brunicardi_Ch33_p1429-p1516.indd 150501/03/19 6:47 PM
Surgery_Schwartz. Abnormal glucose regulation of insulin secretion in models of reduced B-cell mass. Diabetes. 1984; 33:667-673. 8. Brunicardi FC, Sun YS, Druck P, et al. Splanchnic neural regulation of insulin and glucagon secretion in the isolated perfused human pancreas. Am J Surg. 1987;153:34-40. 9. Yamada Y, Post SR, Wang K, et al. Cloning and functional characterization of a family of human and mouse somatostatin receptors expressed in brain, gastrointestinal tract, and kidney. Proc Natl Acad Sci U S A. 1992;89:251-255. 10. Voss M, Pappas T. Pancreatic fistula. Curr Treat Options Gastroenterol. 2002;5:345-353. 11. Floyd JC, Jr, Fajans SS, Pek S. Regulation in healthy subjects of the secretion of human pancreatic polypeptide, a newly recognized pancreatic islet polypeptide. Trans Assoc Am Physicians. 1976;89:146-158. 12. Adrian TE, Bloom SR, Besterman HS, et al. Mechanism of pancreatic polypeptide release in man. Lancet. 1977;1:161-163.Brunicardi_Ch33_p1429-p1516.indd 150501/03/19 6:47 PM
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1976;89:146-158. 12. Adrian TE, Bloom SR, Besterman HS, et al. Mechanism of pancreatic polypeptide release in man. Lancet. 1977;1:161-163.Brunicardi_Ch33_p1429-p1516.indd 150501/03/19 6:47 PM 1506SPECIFIC CONSIDERATIONSPART II 13. Kono T, Wang XP, Fisher WE, Andersen DK, Brunicardi FC. Pancreatic Polypeptide (PP). In: L Martini, ed. Encyclopedia of Endocrine Diseases. Volume 3. Philadelphia: Elsevier; 2004:488-496. 14. Andersen DK. Mechanisms and emerging treatments of the metabolic complications of chronic pancreatitis. Pancreas. 2007;35:1-5. 15. Wierup N, Svensson H, Mulder H, Sundler F. The ghrelin cell: anovel developmentally regulated islet cell in the human pancreas. Regul Pept. 2002;107:63-69. 16. Prado CL, Pugh-Bernard AE, Elghazi L, Sosa-Pineda B, Sussel L. Ghrelin cells replace insulin-producing beta cells in two mouse models of pancreas development. Proc Natl Acad Sci U S A. 2004;101:2924-2429. 17. Sun Y, Asnicar M, Saha PK, Chan L, Smith RG. Ablation of
Surgery_Schwartz. 1976;89:146-158. 12. Adrian TE, Bloom SR, Besterman HS, et al. Mechanism of pancreatic polypeptide release in man. Lancet. 1977;1:161-163.Brunicardi_Ch33_p1429-p1516.indd 150501/03/19 6:47 PM 1506SPECIFIC CONSIDERATIONSPART II 13. Kono T, Wang XP, Fisher WE, Andersen DK, Brunicardi FC. Pancreatic Polypeptide (PP). In: L Martini, ed. Encyclopedia of Endocrine Diseases. Volume 3. Philadelphia: Elsevier; 2004:488-496. 14. Andersen DK. Mechanisms and emerging treatments of the metabolic complications of chronic pancreatitis. Pancreas. 2007;35:1-5. 15. Wierup N, Svensson H, Mulder H, Sundler F. The ghrelin cell: anovel developmentally regulated islet cell in the human pancreas. Regul Pept. 2002;107:63-69. 16. Prado CL, Pugh-Bernard AE, Elghazi L, Sosa-Pineda B, Sussel L. Ghrelin cells replace insulin-producing beta cells in two mouse models of pancreas development. Proc Natl Acad Sci U S A. 2004;101:2924-2429. 17. Sun Y, Asnicar M, Saha PK, Chan L, Smith RG. Ablation of
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cells replace insulin-producing beta cells in two mouse models of pancreas development. Proc Natl Acad Sci U S A. 2004;101:2924-2429. 17. Sun Y, Asnicar M, Saha PK, Chan L, Smith RG. Ablation of ghrelin improves the diabetic but not obese phenotype of ob/ob mice. Cell Metab. 2006;3:379-386. 18. Westermark P, Wilander E, Westermark GT, et al. Islet amyloid polypeptide-like-immunoreactivity in the islet B-cells of type 2 (non-insulin-dependent) diabetic and non-diabetic individuals. Diabetologia. 1987;30:887-892. 19. Tatemoto K, Efendic S, Mutt V, Makk G, Feistner GJ, Barchas JD. Pancreastatin, a novel pancreatic peptide that inhibits insulin secretion. Nature. 1986;324:476-478. 20. Efendic S, Tatemoto K, Mutt V, Quan C, Chang D, Ostenson CG. Pancreastatin and islet hormone release. Proc Natl Acad Sci U S A. 1987:84:7257-7260. 21. Funakoshi A, Miyasaka K, Nakamura R, Kitani K, Tatemoto K. Inhibitory effect of pancreastatin on pancreatic exocrine secretion in the conscious rat. Reg
Surgery_Schwartz. cells replace insulin-producing beta cells in two mouse models of pancreas development. Proc Natl Acad Sci U S A. 2004;101:2924-2429. 17. Sun Y, Asnicar M, Saha PK, Chan L, Smith RG. Ablation of ghrelin improves the diabetic but not obese phenotype of ob/ob mice. Cell Metab. 2006;3:379-386. 18. Westermark P, Wilander E, Westermark GT, et al. Islet amyloid polypeptide-like-immunoreactivity in the islet B-cells of type 2 (non-insulin-dependent) diabetic and non-diabetic individuals. Diabetologia. 1987;30:887-892. 19. Tatemoto K, Efendic S, Mutt V, Makk G, Feistner GJ, Barchas JD. Pancreastatin, a novel pancreatic peptide that inhibits insulin secretion. Nature. 1986;324:476-478. 20. Efendic S, Tatemoto K, Mutt V, Quan C, Chang D, Ostenson CG. Pancreastatin and islet hormone release. Proc Natl Acad Sci U S A. 1987:84:7257-7260. 21. Funakoshi A, Miyasaka K, Nakamura R, Kitani K, Tatemoto K. Inhibitory effect of pancreastatin on pancreatic exocrine secretion in the conscious rat. Reg
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Natl Acad Sci U S A. 1987:84:7257-7260. 21. Funakoshi A, Miyasaka K, Nakamura R, Kitani K, Tatemoto K. Inhibitory effect of pancreastatin on pancreatic exocrine secretion in the conscious rat. Reg Peptides. 1989;25: 157-166. 22. Bottcher G, Sjoberg J, Ekman R, et al. PYY in the mammalian pancreas: Immunocytochemical localization and immunochemical characterization. Regul Pept. 1993; 43:115-130. 23. Gorelick FS, Jamieson JD. Structure-function relationship of the pancreas. In: Johnson LR, ed. Physiology of the Gastrointestinal Tract. New York: Raven Press; 1981:773. 24. Kennedy FP. Pathophysiology of pancreatic polypeptide secretion in human diabetes mellitus. Diabetes Nutr Metab. 1990;2:155. 25. Petrov MS, Shanbhag S, Chakraborty M, Phillips AR, Windsor JA. Organ failure and infection of pancreatic necrosis as determinants of mortality in patients with acute pancreatitis. Gastroenterology. 2010;139:813-820. 26. Peery AF, Dellon ES, Lund J, et al. Burden of gastrointestinal disease in
Surgery_Schwartz. Natl Acad Sci U S A. 1987:84:7257-7260. 21. Funakoshi A, Miyasaka K, Nakamura R, Kitani K, Tatemoto K. Inhibitory effect of pancreastatin on pancreatic exocrine secretion in the conscious rat. Reg Peptides. 1989;25: 157-166. 22. Bottcher G, Sjoberg J, Ekman R, et al. PYY in the mammalian pancreas: Immunocytochemical localization and immunochemical characterization. Regul Pept. 1993; 43:115-130. 23. Gorelick FS, Jamieson JD. Structure-function relationship of the pancreas. In: Johnson LR, ed. Physiology of the Gastrointestinal Tract. New York: Raven Press; 1981:773. 24. Kennedy FP. Pathophysiology of pancreatic polypeptide secretion in human diabetes mellitus. Diabetes Nutr Metab. 1990;2:155. 25. Petrov MS, Shanbhag S, Chakraborty M, Phillips AR, Windsor JA. Organ failure and infection of pancreatic necrosis as determinants of mortality in patients with acute pancreatitis. Gastroenterology. 2010;139:813-820. 26. Peery AF, Dellon ES, Lund J, et al. Burden of gastrointestinal disease in
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pancreatic necrosis as determinants of mortality in patients with acute pancreatitis. Gastroenterology. 2010;139:813-820. 26. Peery AF, Dellon ES, Lund J, et al. Burden of gastrointestinal disease in the United States: 2012 update. Gastroenterology. 2012;143(5):1179-1187. 27. Banks PA. Epidemiology, natural history, and predictors of disease outcome in acute and chronic pancreatitis. Gastrointesi Endosc. 2002;56(6 suppl):S226-S230. 28. Akhtar AJ, Shaheen M. Extrapancreatic manifestations of acute pancreatitis in African-American and Hispanic patients. Pancreas. 2004;29(4):291-297. 29. Lowenfels AB, Maisonneuve P. Acute pancreatitis: is smoking a risk factor for acute pancreatitis. Nat Rev Gastroenterol Hepatol. 2011;8(11):603-604. 30. Acosta JM, Ledesma CL. Gallstone migration as a cause of acute pancreatitis. N Engl J Med. 1974;290(9):484-487. 31. Lee SP, Nicholls JF, Park HZ. Biliary sludge as a cause of acute pancreatitis. N Engl J Med. 1992;326(9):589-593. 32. Lankisch PG, Apte M,
Surgery_Schwartz. pancreatic necrosis as determinants of mortality in patients with acute pancreatitis. Gastroenterology. 2010;139:813-820. 26. Peery AF, Dellon ES, Lund J, et al. Burden of gastrointestinal disease in the United States: 2012 update. Gastroenterology. 2012;143(5):1179-1187. 27. Banks PA. Epidemiology, natural history, and predictors of disease outcome in acute and chronic pancreatitis. Gastrointesi Endosc. 2002;56(6 suppl):S226-S230. 28. Akhtar AJ, Shaheen M. Extrapancreatic manifestations of acute pancreatitis in African-American and Hispanic patients. Pancreas. 2004;29(4):291-297. 29. Lowenfels AB, Maisonneuve P. Acute pancreatitis: is smoking a risk factor for acute pancreatitis. Nat Rev Gastroenterol Hepatol. 2011;8(11):603-604. 30. Acosta JM, Ledesma CL. Gallstone migration as a cause of acute pancreatitis. N Engl J Med. 1974;290(9):484-487. 31. Lee SP, Nicholls JF, Park HZ. Biliary sludge as a cause of acute pancreatitis. N Engl J Med. 1992;326(9):589-593. 32. Lankisch PG, Apte M,
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acute pancreatitis. N Engl J Med. 1974;290(9):484-487. 31. Lee SP, Nicholls JF, Park HZ. Biliary sludge as a cause of acute pancreatitis. N Engl J Med. 1992;326(9):589-593. 32. Lankisch PG, Apte M, Banks PA. Acute pancreatitis. Lancet. 2015;386(9988):85-96. 33. Elmunzer BJ, Scheiman JM, Lehman GA, et al. A randomized trial of rectal indomethacin to prevent post-ERCP pancreatitis. N Engl J Med. 2012; 66:1414-1422. 34. Akbar A, Abu Dayyeh BK, Baron TH, Wang Z, Altayar O, Murad MH. Rectal non-steroidal anti-inflammatory drugs are superior to pancreatic duct stentsin preventing pancreatitis after endoscopic retrograde cholangiopancreatography: a network meta-analysis. Clin Gastroenterol Hepatol. 2013;13: 778-783. 35. Whitcomb DC. Genetics of alcoholic and nonalcoholic pancreatitis. Curr Opin Gastroenterol. 2012;28(5):501-506. 36. Saluja A, Steer M. Pathophysiology of pancreatitis. Role of cytokines and other mediators of inflammation. Digestion. 1999;60:27-33. 37. Hofbauer B, Saluja AK,
Surgery_Schwartz. acute pancreatitis. N Engl J Med. 1974;290(9):484-487. 31. Lee SP, Nicholls JF, Park HZ. Biliary sludge as a cause of acute pancreatitis. N Engl J Med. 1992;326(9):589-593. 32. Lankisch PG, Apte M, Banks PA. Acute pancreatitis. Lancet. 2015;386(9988):85-96. 33. Elmunzer BJ, Scheiman JM, Lehman GA, et al. A randomized trial of rectal indomethacin to prevent post-ERCP pancreatitis. N Engl J Med. 2012; 66:1414-1422. 34. Akbar A, Abu Dayyeh BK, Baron TH, Wang Z, Altayar O, Murad MH. Rectal non-steroidal anti-inflammatory drugs are superior to pancreatic duct stentsin preventing pancreatitis after endoscopic retrograde cholangiopancreatography: a network meta-analysis. Clin Gastroenterol Hepatol. 2013;13: 778-783. 35. Whitcomb DC. Genetics of alcoholic and nonalcoholic pancreatitis. Curr Opin Gastroenterol. 2012;28(5):501-506. 36. Saluja A, Steer M. Pathophysiology of pancreatitis. Role of cytokines and other mediators of inflammation. Digestion. 1999;60:27-33. 37. Hofbauer B, Saluja AK,
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Gastroenterol. 2012;28(5):501-506. 36. Saluja A, Steer M. Pathophysiology of pancreatitis. Role of cytokines and other mediators of inflammation. Digestion. 1999;60:27-33. 37. Hofbauer B, Saluja AK, Lerch MM, et al. Intra-acinar cell activation of trypsinogen during caerulein-induced pancreatitis in rats. Am J Physiol. 1998;275(2 pt 1):G352-G362. 38. Saluja AK, Lerch MM, Phillips PA, Dudeja V. Why does pancreatic overstimulation cause pancreatitis? Annu Rev Physiol. 2007;69:249-269. 39. Dawra R, Sah RP, Dudeja V, et al. Intra-acinar trypsinogen activation mediates early stages of pancreatic injury but not inflammation in mice with acute pancreatitis. Gastroenterol. 2011;141(6):2210-2217 e2212. 40. Gaiser S, Daniluk J, Liu Y, et al. Intracellular activation of trypsinogen in transgenic mice induces acute but not chronic pancreatitis. Gut. 2011;60(10):1379-1388. 41. Whitcomb DC, Gorry MC, Preston RA, et al. Hereditary pancreatitis is caused by a mutation in the cationic trypsinogen
Surgery_Schwartz. Gastroenterol. 2012;28(5):501-506. 36. Saluja A, Steer M. Pathophysiology of pancreatitis. Role of cytokines and other mediators of inflammation. Digestion. 1999;60:27-33. 37. Hofbauer B, Saluja AK, Lerch MM, et al. Intra-acinar cell activation of trypsinogen during caerulein-induced pancreatitis in rats. Am J Physiol. 1998;275(2 pt 1):G352-G362. 38. Saluja AK, Lerch MM, Phillips PA, Dudeja V. Why does pancreatic overstimulation cause pancreatitis? Annu Rev Physiol. 2007;69:249-269. 39. Dawra R, Sah RP, Dudeja V, et al. Intra-acinar trypsinogen activation mediates early stages of pancreatic injury but not inflammation in mice with acute pancreatitis. Gastroenterol. 2011;141(6):2210-2217 e2212. 40. Gaiser S, Daniluk J, Liu Y, et al. Intracellular activation of trypsinogen in transgenic mice induces acute but not chronic pancreatitis. Gut. 2011;60(10):1379-1388. 41. Whitcomb DC, Gorry MC, Preston RA, et al. Hereditary pancreatitis is caused by a mutation in the cationic trypsinogen
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Surgery_Schwartz. or with-out pylorus preservation. Hepatogastroenterol. 2001;48: 1479-1485. 336. Ohtsuka T, Yamaguchi K, Ohuchida J, et al. Comparison of quality of life after pylorus-preserving pancreatoduodenectomy and Whipple resection. Hepatogastroenterol. 2003; 50:846-850.Brunicardi_Ch33_p1429-p1516.indd 151301/03/19 6:47 PM 1514SPECIFIC CONSIDERATIONSPART II 337. Van Buren G, Bloomston M, Hughes SJ, et al. A ran-domized prospective multicenter trial of pancreatico-duodenectomy with and without routine intraperitoneal drainage. Ann Surg. 2014;259(4):605-612. doi: 10.1097/SLA.0000000000000460 338. Van Buren G, Bloomston M, Schmidt CR, et al. A prospective randomized multicenter trial of distal pancreatectomy with and without routine intraperitoneal drainage. Ann Surg. 2017;266(3):421-431. doi: 10.1097/SLA.0000000000002375 339. Bassi C1, Molinari E, Malleo G, et al. Early versus late drain removal after standard pancreatic resections: results of a prospective randomized trial. Ann Surg.
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10.1097/SLA.0000000000002375 339. Bassi C1, Molinari E, Malleo G, et al. Early versus late drain removal after standard pancreatic resections: results of a prospective randomized trial. Ann Surg. 2010;252(2):207-214. doi: 10.1097/SLA.0b013e3181e61e88 340. Keane FK, Wo JY, Ferrone CR, et al. Intraoperative radiotherapy in the era of intensive neoadjuvant chemotherapy and chemoradiotherapy for pancreatic adenocarcinoma. Am J Clin Oncol. Post Author Corrections: October 12, 2016. 341. Birkmeyer JD, Finlayson SR, Tosteson AN, et al. Effect of hospital volume on in-hospital mortality with pancreaticoduodenectomy. Surgery. 1999;125(3):250-256. 342. Gordon TA, Bowman HM, Tielsch JM, et al. Statewide regionalization of pancreaticoduodenectomy and its effect on in-hospital mortality. Ann Surg. 1998;228:71-78. 343. Buchler M, Friess H, Klempa I, et al. Role of octreotide in the prevention of postoperative complications following pancreatic resection. Am J Surg. 1992;163:125-130; discussion
Surgery_Schwartz. 10.1097/SLA.0000000000002375 339. Bassi C1, Molinari E, Malleo G, et al. Early versus late drain removal after standard pancreatic resections: results of a prospective randomized trial. Ann Surg. 2010;252(2):207-214. doi: 10.1097/SLA.0b013e3181e61e88 340. Keane FK, Wo JY, Ferrone CR, et al. Intraoperative radiotherapy in the era of intensive neoadjuvant chemotherapy and chemoradiotherapy for pancreatic adenocarcinoma. Am J Clin Oncol. Post Author Corrections: October 12, 2016. 341. Birkmeyer JD, Finlayson SR, Tosteson AN, et al. Effect of hospital volume on in-hospital mortality with pancreaticoduodenectomy. Surgery. 1999;125(3):250-256. 342. Gordon TA, Bowman HM, Tielsch JM, et al. Statewide regionalization of pancreaticoduodenectomy and its effect on in-hospital mortality. Ann Surg. 1998;228:71-78. 343. Buchler M, Friess H, Klempa I, et al. Role of octreotide in the prevention of postoperative complications following pancreatic resection. Am J Surg. 1992;163:125-130; discussion
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1998;228:71-78. 343. Buchler M, Friess H, Klempa I, et al. Role of octreotide in the prevention of postoperative complications following pancreatic resection. Am J Surg. 1992;163:125-130; discussion 130-131. 344. Montorsi M, Zago M, Mosca F, et al. Efficacy of octreotide in the prevention of pancreatic fistula after elective pancreatic resections: a prospective, controlled, randomized clinical trial. Surgery. 1995;117:26-31. 345. Pederzoli P, Bassi C, Falconi M, et al. Efficacy of octreotide in the prevention of complications of elective pancreatic surgery. Italian Study Group. Br J Surg. 1994;81:265-269. 346. Barnett SP, Hodul PJ, Creech S, et al. Octreotide does not prevent postoperative pancreatic fistula or mortality following pancreaticoduodenectomy. Am Surg. 2004;70:222-226; discussion 227. 347. Hesse UJ, DeDecker C, Houtmeyers P, et al. Prospectively randomized trial using perioperative low-dose octreotide to prevent organ-related and general complications after pancreatic
Surgery_Schwartz. 1998;228:71-78. 343. Buchler M, Friess H, Klempa I, et al. Role of octreotide in the prevention of postoperative complications following pancreatic resection. Am J Surg. 1992;163:125-130; discussion 130-131. 344. Montorsi M, Zago M, Mosca F, et al. Efficacy of octreotide in the prevention of pancreatic fistula after elective pancreatic resections: a prospective, controlled, randomized clinical trial. Surgery. 1995;117:26-31. 345. Pederzoli P, Bassi C, Falconi M, et al. Efficacy of octreotide in the prevention of complications of elective pancreatic surgery. Italian Study Group. Br J Surg. 1994;81:265-269. 346. Barnett SP, Hodul PJ, Creech S, et al. Octreotide does not prevent postoperative pancreatic fistula or mortality following pancreaticoduodenectomy. Am Surg. 2004;70:222-226; discussion 227. 347. Hesse UJ, DeDecker C, Houtmeyers P, et al. Prospectively randomized trial using perioperative low-dose octreotide to prevent organ-related and general complications after pancreatic
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227. 347. Hesse UJ, DeDecker C, Houtmeyers P, et al. Prospectively randomized trial using perioperative low-dose octreotide to prevent organ-related and general complications after pancreatic surgery and pancreatico-jejunostomy. World J Surg. 2005;29:1325-1328. 348. Lowy AM, Lee JE, Pisters PW, et al. Prospective, randomized trial of octreotide to prevent pancreatic fistula after pancreaticoduodenectomy for malignant disease. Ann Surg. 1997;226:632-641. 349. Suc B, Msika S, Piccinini M, et al. Octreotide in the prevention of intra-abdominal complications following elective pancreatic resection: a prospective, multicenter randomized controlled trial. Arch Surg. 2004;139:288-294; discussion 295. 350. Allen PJ, Mithat G, Brennan MF, et al. Pasireotide for postoperative pancreatic fistula. N Engl J Med. 2014;370: 2014-2022. doi:10.1056/NEJMoa1313688 351. Yeo CJ, Cameron JL, Maher MM, et al. A prospective ran-domized trial of pancreaticogastrostomy versus pancreati-cojejunostomy after
Surgery_Schwartz. 227. 347. Hesse UJ, DeDecker C, Houtmeyers P, et al. Prospectively randomized trial using perioperative low-dose octreotide to prevent organ-related and general complications after pancreatic surgery and pancreatico-jejunostomy. World J Surg. 2005;29:1325-1328. 348. Lowy AM, Lee JE, Pisters PW, et al. Prospective, randomized trial of octreotide to prevent pancreatic fistula after pancreaticoduodenectomy for malignant disease. Ann Surg. 1997;226:632-641. 349. Suc B, Msika S, Piccinini M, et al. Octreotide in the prevention of intra-abdominal complications following elective pancreatic resection: a prospective, multicenter randomized controlled trial. Arch Surg. 2004;139:288-294; discussion 295. 350. Allen PJ, Mithat G, Brennan MF, et al. Pasireotide for postoperative pancreatic fistula. N Engl J Med. 2014;370: 2014-2022. doi:10.1056/NEJMoa1313688 351. Yeo CJ, Cameron JL, Maher MM, et al. A prospective ran-domized trial of pancreaticogastrostomy versus pancreati-cojejunostomy after
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N Engl J Med. 2014;370: 2014-2022. doi:10.1056/NEJMoa1313688 351. Yeo CJ, Cameron JL, Maher MM, et al. A prospective ran-domized trial of pancreaticogastrostomy versus pancreati-cojejunostomy after pancreaticoduodenectomy. Ann Surg. 1995;222(4):580-588; discussion 588-592. 352. Wente MN, Shrikhande SV, Muller MW, et al. Pancreaticojejunostomy vs. pancreaticogastrostomy: systematic review and meta-analysis. Am J Surg. 2007;193:171-183. 353. Suzuki Y, Fujino Y, Tanioka Y, et al. Selection of pancreaticojejunostomy techniques according to pancreatic texture and duct size. Arch Surg. 2002;137:1044-1047; discussion 1048. 354. Reid-Lombardo KM, Farnell MB, Crippa S, et al. Pancreatic anastomotic leakage after pancreaticoduodenectomy in 1,507 patients: a report from the Pancreatic Anastomotic Leak Study Group. J Gastrointest Surg. 2007;11:1451-1458. 355. Dong Z, Xu J, Wang Z, Petrov MS. Stents for the prevention of pancreatic fistula following pancreaticoduodenectomy. Cochrane Database Syst
Surgery_Schwartz. N Engl J Med. 2014;370: 2014-2022. doi:10.1056/NEJMoa1313688 351. Yeo CJ, Cameron JL, Maher MM, et al. A prospective ran-domized trial of pancreaticogastrostomy versus pancreati-cojejunostomy after pancreaticoduodenectomy. Ann Surg. 1995;222(4):580-588; discussion 588-592. 352. Wente MN, Shrikhande SV, Muller MW, et al. Pancreaticojejunostomy vs. pancreaticogastrostomy: systematic review and meta-analysis. Am J Surg. 2007;193:171-183. 353. Suzuki Y, Fujino Y, Tanioka Y, et al. Selection of pancreaticojejunostomy techniques according to pancreatic texture and duct size. Arch Surg. 2002;137:1044-1047; discussion 1048. 354. Reid-Lombardo KM, Farnell MB, Crippa S, et al. Pancreatic anastomotic leakage after pancreaticoduodenectomy in 1,507 patients: a report from the Pancreatic Anastomotic Leak Study Group. J Gastrointest Surg. 2007;11:1451-1458. 355. Dong Z, Xu J, Wang Z, Petrov MS. Stents for the prevention of pancreatic fistula following pancreaticoduodenectomy. Cochrane Database Syst
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Study Group. J Gastrointest Surg. 2007;11:1451-1458. 355. Dong Z, Xu J, Wang Z, Petrov MS. Stents for the prevention of pancreatic fistula following pancreaticoduodenectomy. Cochrane Database Syst Rev. 2016;(5):CD008914. doi: 10.1002/14651858.CD008914.pub3 356. Jang JY, Chang YR, Kim SW, et al. Randomized multicentre trial comparing external and internal pancreatic stenting during pancreaticoduodenectomy. Br J Surg. 2016;103(6):668-675. doi: 10.1002/bjs.10160. 357. Sutton CD, Garcea G, White SA, et al. Isolated Roux-loop pancreaticojejunostomy: a series of 61 patients with zero postoperative pancreaticoenteric leaks. J Gastrointest Surg. 2004;8:701-705. 358. Yang YM, Tian XD, Zhuang Y, et al. Risk factors of pancreatic leakage after pancreaticoduodenectomy. World J Gastroenterol. 2005;11:2456-2461. 359. Di Carlo V, Chiesa R, Pontiroli AE, et al. Pancreatoduodenectomy with occlusion of the residual stump by Neoprene injection. World J Surg. 1989;13:105-110; discussion
Surgery_Schwartz. Study Group. J Gastrointest Surg. 2007;11:1451-1458. 355. Dong Z, Xu J, Wang Z, Petrov MS. Stents for the prevention of pancreatic fistula following pancreaticoduodenectomy. Cochrane Database Syst Rev. 2016;(5):CD008914. doi: 10.1002/14651858.CD008914.pub3 356. Jang JY, Chang YR, Kim SW, et al. Randomized multicentre trial comparing external and internal pancreatic stenting during pancreaticoduodenectomy. Br J Surg. 2016;103(6):668-675. doi: 10.1002/bjs.10160. 357. Sutton CD, Garcea G, White SA, et al. Isolated Roux-loop pancreaticojejunostomy: a series of 61 patients with zero postoperative pancreaticoenteric leaks. J Gastrointest Surg. 2004;8:701-705. 358. Yang YM, Tian XD, Zhuang Y, et al. Risk factors of pancreatic leakage after pancreaticoduodenectomy. World J Gastroenterol. 2005;11:2456-2461. 359. Di Carlo V, Chiesa R, Pontiroli AE, et al. Pancreatoduodenectomy with occlusion of the residual stump by Neoprene injection. World J Surg. 1989;13:105-110; discussion
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2005;11:2456-2461. 359. Di Carlo V, Chiesa R, Pontiroli AE, et al. Pancreatoduodenectomy with occlusion of the residual stump by Neoprene injection. World J Surg. 1989;13:105-110; discussion 110-111. 360. Tran K, Van Eijck C, Di Carlo V, et al. Occlusion of the pancreatic duct versus pancreaticojejunostomy: a prospective randomized trial. Ann Surg. 2002;236:422-428, discussion 428. 361. Fisher WE, Chai C, Hodges SE, Wu MF, Hilsenbeck SG, Brunicardi FC. Effect of BioGlue on the incidence of pancreatic fistula following pancreas resection. J Gastrointest Surg. 2008;12:882-890. 362. Lillemoe KD, Cameron JL, Kim MP, et al. Does fibrin glue sealant decrease the rate of pancreatic fistula after pancreaticoduodenectomy? Results of a prospective randomized trial. J Gastrointest Surg. 2004;8:766-772, discussion 772-774. 363. Kazanjian KK, Hines OJ, Eibl G, Reber HA. Management of pancreatic fistulas after pancreaticoduodenectomy: results in 437 consecutive patients. Arch Surg.
Surgery_Schwartz. 2005;11:2456-2461. 359. Di Carlo V, Chiesa R, Pontiroli AE, et al. Pancreatoduodenectomy with occlusion of the residual stump by Neoprene injection. World J Surg. 1989;13:105-110; discussion 110-111. 360. Tran K, Van Eijck C, Di Carlo V, et al. Occlusion of the pancreatic duct versus pancreaticojejunostomy: a prospective randomized trial. Ann Surg. 2002;236:422-428, discussion 428. 361. Fisher WE, Chai C, Hodges SE, Wu MF, Hilsenbeck SG, Brunicardi FC. Effect of BioGlue on the incidence of pancreatic fistula following pancreas resection. J Gastrointest Surg. 2008;12:882-890. 362. Lillemoe KD, Cameron JL, Kim MP, et al. Does fibrin glue sealant decrease the rate of pancreatic fistula after pancreaticoduodenectomy? Results of a prospective randomized trial. J Gastrointest Surg. 2004;8:766-772, discussion 772-774. 363. Kazanjian KK, Hines OJ, Eibl G, Reber HA. Management of pancreatic fistulas after pancreaticoduodenectomy: results in 437 consecutive patients. Arch Surg.
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2004;8:766-772, discussion 772-774. 363. Kazanjian KK, Hines OJ, Eibl G, Reber HA. Management of pancreatic fistulas after pancreaticoduodenectomy: results in 437 consecutive patients. Arch Surg. 2005;140:849-854, discussion 854-856. 364. Bilimoria KY, Bentrem DJ, Ko CY, et al. National failure to operate on early stage pancreatic cancer. Ann Surg. 2007;246(2):173-180. doi: 10.1097/SLA.0b013e3180691579 365. Group GTS. Further evidence of effective adjuvant combined radiation and chemotherapy following curative resection of pancreatic cancer. Cancer. 1997;59:2006-2010. 366. Neoptolemos JP, Dunn JA, Stocken DD, et al. Adjuvant chemoradiotherapy and chemotherapy in resectable pancreatic cancer: a randomised controlled trial. Lancet. 2001;358:1576-1585. 367. Rocha FG1, Hashimoto Y, Traverso LW, et al. Interferon-based adjuvant chemoradiation for resected pancreatic head cancer: long-term follow-up of the Virginia Mason Protocol. Ann Surg. 2016;263(2):376-384. doi:
Surgery_Schwartz. 2004;8:766-772, discussion 772-774. 363. Kazanjian KK, Hines OJ, Eibl G, Reber HA. Management of pancreatic fistulas after pancreaticoduodenectomy: results in 437 consecutive patients. Arch Surg. 2005;140:849-854, discussion 854-856. 364. Bilimoria KY, Bentrem DJ, Ko CY, et al. National failure to operate on early stage pancreatic cancer. Ann Surg. 2007;246(2):173-180. doi: 10.1097/SLA.0b013e3180691579 365. Group GTS. Further evidence of effective adjuvant combined radiation and chemotherapy following curative resection of pancreatic cancer. Cancer. 1997;59:2006-2010. 366. Neoptolemos JP, Dunn JA, Stocken DD, et al. Adjuvant chemoradiotherapy and chemotherapy in resectable pancreatic cancer: a randomised controlled trial. Lancet. 2001;358:1576-1585. 367. Rocha FG1, Hashimoto Y, Traverso LW, et al. Interferon-based adjuvant chemoradiation for resected pancreatic head cancer: long-term follow-up of the Virginia Mason Protocol. Ann Surg. 2016;263(2):376-384. doi:
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Hashimoto Y, Traverso LW, et al. Interferon-based adjuvant chemoradiation for resected pancreatic head cancer: long-term follow-up of the Virginia Mason Protocol. Ann Surg. 2016;263(2):376-384. doi: 10.1097/SLA.0000000000001190 368. Russo S, Saif MW. Neoadjuvant therapy for pancreatic cancer: an ongoing debate. Therap Adv Gastroenterol. 2016;9(4):429-436. 369. Tachezy M, Gebauer F, Petersen C, et al. Sequential neoadjuvant chemoradiotherapy (CRT) followed by curative surgery vs. primary surgery alone for resectable, non-metastasized pancreatic adenocarcinoma: NEOPA—a randomized multicenter phase III study (NCT01900327, DRKS00003893, ISRCTN82191749). BMC Cancer. 2014;14:411. 370. Gingras MC, Covington KR, Chang DK, et al. Ampullary cancers harbor ELF3 tumor suppressor gene mutations and exhibit frequent WNT dysregulation. Cell Rep. 2016;14(4):907-919. 371. Laffan TA, Horton KM, Klein AP, et al. Prevalence of unsuspected pancreatic cysts on MDCT. AJR Am J Roentgenol.
Surgery_Schwartz. Hashimoto Y, Traverso LW, et al. Interferon-based adjuvant chemoradiation for resected pancreatic head cancer: long-term follow-up of the Virginia Mason Protocol. Ann Surg. 2016;263(2):376-384. doi: 10.1097/SLA.0000000000001190 368. Russo S, Saif MW. Neoadjuvant therapy for pancreatic cancer: an ongoing debate. Therap Adv Gastroenterol. 2016;9(4):429-436. 369. Tachezy M, Gebauer F, Petersen C, et al. Sequential neoadjuvant chemoradiotherapy (CRT) followed by curative surgery vs. primary surgery alone for resectable, non-metastasized pancreatic adenocarcinoma: NEOPA—a randomized multicenter phase III study (NCT01900327, DRKS00003893, ISRCTN82191749). BMC Cancer. 2014;14:411. 370. Gingras MC, Covington KR, Chang DK, et al. Ampullary cancers harbor ELF3 tumor suppressor gene mutations and exhibit frequent WNT dysregulation. Cell Rep. 2016;14(4):907-919. 371. Laffan TA, Horton KM, Klein AP, et al. Prevalence of unsuspected pancreatic cysts on MDCT. AJR Am J Roentgenol.
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mutations and exhibit frequent WNT dysregulation. Cell Rep. 2016;14(4):907-919. 371. Laffan TA, Horton KM, Klein AP, et al. Prevalence of unsuspected pancreatic cysts on MDCT. AJR Am J Roentgenol. 2008;191(3):802-807. doi: 10.2214/AJR.07.3340 372. Tanaka M, Adsay V, Chari S, et al. International consensus guidelines 2012 for the management of IPMN and MCN of the pancreas. Pacreatology. 2012(12):183-197.Brunicardi_Ch33_p1429-p1516.indd 151401/03/19 6:47 PM 1515PANCREASCHAPTER 33 373. Brugge WR, Lewandrowski K, Lee-Lewandrowski E, et al. Diagnosis of pancreatic cystic neoplasms: a report of the cooperative pancreatic cyst study. Gastroenterology. 2004;126:1330-1336. 374. Khalid A, Zahid M, Finkelstein SD, et al. Pancreatic cyst fluid DNA analysis in evaluating pancreatic cysts: a report of the PANDA study. Gastrointest Endosc. 2009;69:1095-1102. 375. Yoon WJ, Brugge WR. Pancreatic cystic neoplasms: diagnosis and management. Gastroenterol Clin North Am.
Surgery_Schwartz. mutations and exhibit frequent WNT dysregulation. Cell Rep. 2016;14(4):907-919. 371. Laffan TA, Horton KM, Klein AP, et al. Prevalence of unsuspected pancreatic cysts on MDCT. AJR Am J Roentgenol. 2008;191(3):802-807. doi: 10.2214/AJR.07.3340 372. Tanaka M, Adsay V, Chari S, et al. International consensus guidelines 2012 for the management of IPMN and MCN of the pancreas. Pacreatology. 2012(12):183-197.Brunicardi_Ch33_p1429-p1516.indd 151401/03/19 6:47 PM 1515PANCREASCHAPTER 33 373. Brugge WR, Lewandrowski K, Lee-Lewandrowski E, et al. Diagnosis of pancreatic cystic neoplasms: a report of the cooperative pancreatic cyst study. Gastroenterology. 2004;126:1330-1336. 374. Khalid A, Zahid M, Finkelstein SD, et al. Pancreatic cyst fluid DNA analysis in evaluating pancreatic cysts: a report of the PANDA study. Gastrointest Endosc. 2009;69:1095-1102. 375. Yoon WJ, Brugge WR. Pancreatic cystic neoplasms: diagnosis and management. Gastroenterol Clin North Am.
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pancreatic cysts: a report of the PANDA study. Gastrointest Endosc. 2009;69:1095-1102. 375. Yoon WJ, Brugge WR. Pancreatic cystic neoplasms: diagnosis and management. Gastroenterol Clin North Am. 2012;41(1):103-118. 376. Furukawa T, Hatori T, Fujita I, et al. Prognostic relevance of morphological types of intraductal papillary mucinous neoplasms of the pancreas. Gut. 2011;60(4):509-516. 377. Brugge WR. Management and outcomes of pancreatic cystic lesions. Dig Liver Dis. 2008;40(11):854-859. 378. Boni L, Benevento A, Dionigi G, Cabrini L, Dionigi R. Primary pancreatic lymphoma. Surg Endosc. 2002;16:1107-1108.Brunicardi_Ch33_p1429-p1516.indd 151501/03/19 6:47 PM
Surgery_Schwartz. pancreatic cysts: a report of the PANDA study. Gastrointest Endosc. 2009;69:1095-1102. 375. Yoon WJ, Brugge WR. Pancreatic cystic neoplasms: diagnosis and management. Gastroenterol Clin North Am. 2012;41(1):103-118. 376. Furukawa T, Hatori T, Fujita I, et al. Prognostic relevance of morphological types of intraductal papillary mucinous neoplasms of the pancreas. Gut. 2011;60(4):509-516. 377. Brugge WR. Management and outcomes of pancreatic cystic lesions. Dig Liver Dis. 2008;40(11):854-859. 378. Boni L, Benevento A, Dionigi G, Cabrini L, Dionigi R. Primary pancreatic lymphoma. Surg Endosc. 2002;16:1107-1108.Brunicardi_Ch33_p1429-p1516.indd 151501/03/19 6:47 PM
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The SpleenAdrian E. Park, Eduardo M. Targarona, Adam S. Weltz, and Carlos Rodriguez-Otero Luppi 34chapterHISTORICAL BACKGROUNDThe spleen has been the subject of man’s musings since almost the establishment of the written word. It has been largely mis-understood, often maligned, and certainly underappreciated as a major organ for more than two millennia. The ancients, pre-sumably through patient observation and occasional anatomic exploration, often consigned the spleen to a vestigial role.Our current understanding of the central role played by the spleen in regulating the immune system and influencing meta-bolic and endocrine functions has been built upon knowledge gleaned only over the past few decades. Our early notions of the spleen as a dispensable filter of blood or seat of emotion have been dispelled as our understanding of its structure and function has evolved, informing our surgical approach to this worthy and fascinating organ. Many of the “founding fathers of medicine”
Surgery_Schwartz. The SpleenAdrian E. Park, Eduardo M. Targarona, Adam S. Weltz, and Carlos Rodriguez-Otero Luppi 34chapterHISTORICAL BACKGROUNDThe spleen has been the subject of man’s musings since almost the establishment of the written word. It has been largely mis-understood, often maligned, and certainly underappreciated as a major organ for more than two millennia. The ancients, pre-sumably through patient observation and occasional anatomic exploration, often consigned the spleen to a vestigial role.Our current understanding of the central role played by the spleen in regulating the immune system and influencing meta-bolic and endocrine functions has been built upon knowledge gleaned only over the past few decades. Our early notions of the spleen as a dispensable filter of blood or seat of emotion have been dispelled as our understanding of its structure and function has evolved, informing our surgical approach to this worthy and fascinating organ. Many of the “founding fathers of medicine”
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have been dispelled as our understanding of its structure and function has evolved, informing our surgical approach to this worthy and fascinating organ. Many of the “founding fathers of medicine” have weighed in on the anatomy and function of the spleen over the centuries. Hippocrates in the fourth century BC was one of the first to write on the spleen.1-3 He taught broadly on the need for balance and equilibrium between the patient and his environment. Illness arose from disharmony in nature, particularly among the patient’s four humors: blood, phlegm, black bile (melancholia), and yellow bile. Hippocrates wrote of a direct connection between the brain and spleen and its particu-lar association with the black bile. These ideas would influence thinking about the role of the spleen for more than 1000 years.2Aristotle, later in the same era, famously stated that, “Nature makes nothing in vain,” yet held the spleen to be an organ of minor importance whose main role was to
Surgery_Schwartz. have been dispelled as our understanding of its structure and function has evolved, informing our surgical approach to this worthy and fascinating organ. Many of the “founding fathers of medicine” have weighed in on the anatomy and function of the spleen over the centuries. Hippocrates in the fourth century BC was one of the first to write on the spleen.1-3 He taught broadly on the need for balance and equilibrium between the patient and his environment. Illness arose from disharmony in nature, particularly among the patient’s four humors: blood, phlegm, black bile (melancholia), and yellow bile. Hippocrates wrote of a direct connection between the brain and spleen and its particu-lar association with the black bile. These ideas would influence thinking about the role of the spleen for more than 1000 years.2Aristotle, later in the same era, famously stated that, “Nature makes nothing in vain,” yet held the spleen to be an organ of minor importance whose main role was to
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spleen for more than 1000 years.2Aristotle, later in the same era, famously stated that, “Nature makes nothing in vain,” yet held the spleen to be an organ of minor importance whose main role was to counterbal-ance the liver.4 He also described how the “hot character” of the spleen aided in digestion.Galen, in the second century AD, engaged in more seri-ous anatomic investigation espousing the early belief that func-tion followed structure. His investigations, though pioneering, lacked sufficient rigor, evidenced by his contention that black bile or melancholia flowed from the liver to the spleen and then through the short gastric vessels into the stomach to be excreted. The influence of Galen’s teaching endured for more than 1200 years. All the more remarkable considering the cur-rent hallowed measure of influence of surgical publication, the impact factor, which is most commonly calculated using a 2-year frame of reference.5,6In the early 17th century, several physician scientists,
Surgery_Schwartz. spleen for more than 1000 years.2Aristotle, later in the same era, famously stated that, “Nature makes nothing in vain,” yet held the spleen to be an organ of minor importance whose main role was to counterbal-ance the liver.4 He also described how the “hot character” of the spleen aided in digestion.Galen, in the second century AD, engaged in more seri-ous anatomic investigation espousing the early belief that func-tion followed structure. His investigations, though pioneering, lacked sufficient rigor, evidenced by his contention that black bile or melancholia flowed from the liver to the spleen and then through the short gastric vessels into the stomach to be excreted. The influence of Galen’s teaching endured for more than 1200 years. All the more remarkable considering the cur-rent hallowed measure of influence of surgical publication, the impact factor, which is most commonly calculated using a 2-year frame of reference.5,6In the early 17th century, several physician scientists,
Surgery_Schwartz_9997
Surgery_Schwartz
measure of influence of surgical publication, the impact factor, which is most commonly calculated using a 2-year frame of reference.5,6In the early 17th century, several physician scientists, Mal-pighi being the most prominent, began testing hypotheses on splenic function by splenectomizing dogs. He reportedly fol-lowed several dogs 5 years postoperatively, noting their healthy survival though apparent ravenous hunger and enhanced sexual appetites. The spleen, still in the era of “balanced humors,” was thus felt to play a role in balancing various appetites as well. In addition to melancholy, the spleen became associated with anger and, paradoxically, was also seen as the “seat of laughter.”7The claim for the first human splenectomy may have pre-dated that of canine splenectomy. Andriano Zaccavello was credited in 1549 with having performed a splenectomy on a middle-aged woman. This claim remains shrouded in contro-versy, and the indication for the surgery and whether in fact
Surgery_Schwartz. measure of influence of surgical publication, the impact factor, which is most commonly calculated using a 2-year frame of reference.5,6In the early 17th century, several physician scientists, Mal-pighi being the most prominent, began testing hypotheses on splenic function by splenectomizing dogs. He reportedly fol-lowed several dogs 5 years postoperatively, noting their healthy survival though apparent ravenous hunger and enhanced sexual appetites. The spleen, still in the era of “balanced humors,” was thus felt to play a role in balancing various appetites as well. In addition to melancholy, the spleen became associated with anger and, paradoxically, was also seen as the “seat of laughter.”7The claim for the first human splenectomy may have pre-dated that of canine splenectomy. Andriano Zaccavello was credited in 1549 with having performed a splenectomy on a middle-aged woman. This claim remains shrouded in contro-versy, and the indication for the surgery and whether in fact
Surgery_Schwartz_9998
Surgery_Schwartz
Zaccavello was credited in 1549 with having performed a splenectomy on a middle-aged woman. This claim remains shrouded in contro-versy, and the indication for the surgery and whether in fact splenectomy was performed have been called into question. The patient apparently survived, but may in fact have under-gone resection of an ovarian cyst rather than her spleen!8 Most patients who underwent splenectomy in the three centuries that followed fared badly. The vast majority of splenectomies per-formed were partial. Most of these patients required surgery for Historical Background 1517Embryology and Anatomy 1518Physiology and Pathophysiology 1520Indications for Splenectomy 1522Benign Disorders / 1524Malignant Conditions / 1527Miscellaneous Disorders and Lesions / 1529Imaging for Evaluation of Size and Pathology 1532Preoperative Considerations 1532Vaccination and Patient Education / 1532Deep Vein Thrombosis Prophylaxis / 1533Splenectomy Techniques 1533Patient Preparation / 1533Open
Surgery_Schwartz. Zaccavello was credited in 1549 with having performed a splenectomy on a middle-aged woman. This claim remains shrouded in contro-versy, and the indication for the surgery and whether in fact splenectomy was performed have been called into question. The patient apparently survived, but may in fact have under-gone resection of an ovarian cyst rather than her spleen!8 Most patients who underwent splenectomy in the three centuries that followed fared badly. The vast majority of splenectomies per-formed were partial. Most of these patients required surgery for Historical Background 1517Embryology and Anatomy 1518Physiology and Pathophysiology 1520Indications for Splenectomy 1522Benign Disorders / 1524Malignant Conditions / 1527Miscellaneous Disorders and Lesions / 1529Imaging for Evaluation of Size and Pathology 1532Preoperative Considerations 1532Vaccination and Patient Education / 1532Deep Vein Thrombosis Prophylaxis / 1533Splenectomy Techniques 1533Patient Preparation / 1533Open
Surgery_Schwartz_9999
Surgery_Schwartz
of Size and Pathology 1532Preoperative Considerations 1532Vaccination and Patient Education / 1532Deep Vein Thrombosis Prophylaxis / 1533Splenectomy Techniques 1533Patient Preparation / 1533Open Splenectomy / 1533Laparoscopic Splenectomy / 1534Hand-Assisted Splenectomy / 1534Single-Incision Laparoscopic Surgery Splenectomy / 1535Robotic Splenectomy / 1536Partial Splenectomy / 1536Inadvertent Intraoperative Splenic Injury / 1538Preoperative Grading Score to Predict Technical Difficulty in Laparoscopic Splenectomy / 1536Splenectomy Outcomes 1538Overwhelming Postsplenectomy Infection / 1538Complications / 1539Hematologic Outcomes / 1539Cancer / 1539Ultrasound / 1540Computed Tomography / 1540Plain Radiography / 1540Magnetic Resonance Imaging / 1540Angiography / 1541Nuclear Imaging / 1541Brunicardi_Ch34_p1517-p1548.indd 151723/02/19 2:36 PM 1518left upper quadrant stab wounds sustained in battles or duels resulting in partial or complete splenic prolapse.9It was in the early 18th
Surgery_Schwartz. of Size and Pathology 1532Preoperative Considerations 1532Vaccination and Patient Education / 1532Deep Vein Thrombosis Prophylaxis / 1533Splenectomy Techniques 1533Patient Preparation / 1533Open Splenectomy / 1533Laparoscopic Splenectomy / 1534Hand-Assisted Splenectomy / 1534Single-Incision Laparoscopic Surgery Splenectomy / 1535Robotic Splenectomy / 1536Partial Splenectomy / 1536Inadvertent Intraoperative Splenic Injury / 1538Preoperative Grading Score to Predict Technical Difficulty in Laparoscopic Splenectomy / 1536Splenectomy Outcomes 1538Overwhelming Postsplenectomy Infection / 1538Complications / 1539Hematologic Outcomes / 1539Cancer / 1539Ultrasound / 1540Computed Tomography / 1540Plain Radiography / 1540Magnetic Resonance Imaging / 1540Angiography / 1541Nuclear Imaging / 1541Brunicardi_Ch34_p1517-p1548.indd 151723/02/19 2:36 PM 1518left upper quadrant stab wounds sustained in battles or duels resulting in partial or complete splenic prolapse.9It was in the early 18th
Surgery_Schwartz_10000
Surgery_Schwartz
151723/02/19 2:36 PM 1518left upper quadrant stab wounds sustained in battles or duels resulting in partial or complete splenic prolapse.9It was in the early 18th century that the growing body of anatomic microstructural knowledge began to turn the tide on the long-held theory of health and disease deriving from a balance of the four humors. William Henson believed the spleen to be a ductless vascular gland similar to the thyroid and adrenals. In 1777, he wrote of the lymphatic nature of the spleen and its filtering function and even suggested its role in hematopoiesis.10Rudolf Virchow, one of the first to discover leukemia, implicated the spleen as figuring prominently in all leukemia patients. He suspected that the spleen was responsible for gen-erating the leukocytes in large quantities in these patients. There soon followed an enthusiastic effort by surgeons to cure leu-kemia by splenectomy. Dr. Thomas Bryant performed the first splenectomy in 1866 in a patient with leukemia.
Surgery_Schwartz. 151723/02/19 2:36 PM 1518left upper quadrant stab wounds sustained in battles or duels resulting in partial or complete splenic prolapse.9It was in the early 18th century that the growing body of anatomic microstructural knowledge began to turn the tide on the long-held theory of health and disease deriving from a balance of the four humors. William Henson believed the spleen to be a ductless vascular gland similar to the thyroid and adrenals. In 1777, he wrote of the lymphatic nature of the spleen and its filtering function and even suggested its role in hematopoiesis.10Rudolf Virchow, one of the first to discover leukemia, implicated the spleen as figuring prominently in all leukemia patients. He suspected that the spleen was responsible for gen-erating the leukocytes in large quantities in these patients. There soon followed an enthusiastic effort by surgeons to cure leu-kemia by splenectomy. Dr. Thomas Bryant performed the first splenectomy in 1866 in a patient with leukemia.
Surgery_Schwartz_10001
Surgery_Schwartz
in these patients. There soon followed an enthusiastic effort by surgeons to cure leu-kemia by splenectomy. Dr. Thomas Bryant performed the first splenectomy in 1866 in a patient with leukemia. The patient died, as did all 14 patients who underwent splenectomy for leukemia over the next 15 years. After his second consecutive mortality in this setting, Bryant declared that “the operation is physiologically unsound & surgically unsafe for leukemia and should not be performed.”11 In 1908, Johnson reported a series of 99 splenectomies for leukemia with an 85% mortality rate. Unfortunately, it took several decades for his words to be heeded.In 1916, a medical student from Prague named Paul Kaznelson wrote on the key role played by the spleen in the destruction of platelets leading to the first reported (and success-ful) splenectomy for a patient with idiopathic thrombocytopenia purpura.2As surgeons’ experience with the procedure grew, the associated morbidity and mortality decreased. By
Surgery_Schwartz. in these patients. There soon followed an enthusiastic effort by surgeons to cure leu-kemia by splenectomy. Dr. Thomas Bryant performed the first splenectomy in 1866 in a patient with leukemia. The patient died, as did all 14 patients who underwent splenectomy for leukemia over the next 15 years. After his second consecutive mortality in this setting, Bryant declared that “the operation is physiologically unsound & surgically unsafe for leukemia and should not be performed.”11 In 1908, Johnson reported a series of 99 splenectomies for leukemia with an 85% mortality rate. Unfortunately, it took several decades for his words to be heeded.In 1916, a medical student from Prague named Paul Kaznelson wrote on the key role played by the spleen in the destruction of platelets leading to the first reported (and success-ful) splenectomy for a patient with idiopathic thrombocytopenia purpura.2As surgeons’ experience with the procedure grew, the associated morbidity and mortality decreased. By