Surgery_Schwartz

Surgery_Schwartz. emptying scans are helpful in evaluating these possibilities.Bile reflux may be quantified with gastric analysis or esophageal impedance testing or with scintigraphy (bile reflux scan). Typically, enterogastric reflux is greatest after Billroth II gastrectomy or gastrojejunostomy, and least after vagotomy and pyloroplasty, with Billroth I gastrectomy giving intermediate values. Patients who are well into the abnormal range of bile reflux may be considered for remedial surgery if symptoms are severe. Remedial surgery will eliminate the bile from the vomi-tus and may improve the patient’s pain, but it is quite unusual to render these patients completely asymptomatic, especially if they are narcotic dependent.Bile reflux gastritis after distal gastric resection may be treated by one of the following options: Roux-en-Y gastroje-junostomy; interposition of a 40-cm isoperistaltic jejunal loop between the gastric remnant and the duodenum (Henley loop); Billroth II gastro jejunostomy with


Surgery_Schwartz

Surgery_Schwartz. following options: Roux-en-Y gastroje-junostomy; interposition of a 40-cm isoperistaltic jejunal loop between the gastric remnant and the duodenum (Henley loop); Billroth II gastro jejunostomy with Braun enteroenterostomy; total gastrectomy with Roux esophagojejunostomy. To mini-mize reflux of bile into the stomach or the esophagus, the Roux limb should be at least 45 cm long (preferably 60 cm). The Braun enteroenterostomy should be placed at a similar distance from the stomach. Excessively long limbs may be associated with obstruction or malabsorption. All of these operations can result in marginal ulceration on the jejunal side of the gastrojeju-nostomy and thus are combined with a generous distal gastrec-tomy. If this has already been done at a previous operation, the Roux or Braun operations may be attractively simple. Whether truncal vagotomy should be considered to decrease the risk of marginal ulceration is controversial because acid-suppressing medications may be equally


Surgery_Schwartz

Surgery_Schwartz. operations may be attractively simple. Whether truncal vagotomy should be considered to decrease the risk of marginal ulceration is controversial because acid-suppressing medications may be equally effective. In addition, the benefits of decreased acid secretion following vagotomy may be out-weighed by problems with vagotomy-associated dysmotility in the gastric remnant. The Roux operation may be associated with an increased risk of emptying problems compared to the other two options, but controlled data are lacking. Patients with debilitating bile reflux after gastrojejunostomy can be consid-ered for simple takedown of this anastomosis provided that the pyloric channel is open.Primary bile reflux gastritis (i.e., no previous operation) is rare, and may be treated with the duodenal switch operation, essentially an end-to-end Roux-en-Y to the proximal duodenum (see Fig. 26-68). The Achilles’ heel of this operation is, not sur-prisingly, marginal ulceration. Thus, it should be combined


Surgery_Schwartz

Surgery_Schwartz. operation, essentially an end-to-end Roux-en-Y to the proximal duodenum (see Fig. 26-68). The Achilles’ heel of this operation is, not sur-prisingly, marginal ulceration. Thus, it should be combined with highly selective vagotomy, and/or long-term acid suppressive medication.Bile gastritis or esophagitis is a recognized complication after esophagogastrectomy with or without pyloroplasty. This can be effectively treated by division of the duodenum immedi-ately distal to the pylorus with drainage of the prepyloric antrum into a Roux limb. Preservation of the right gastroepiploic pedi-cal is important. Proximal subtotal gastrectomy with esophago-antral anastomosis should be avoided, but when performed, the pylorus should be left intact.Roux SyndromeA subset of patients who have had distal gastrectomy and Roux-en-Y gastrojejunostomy will have great difficulty with gastric emptying in the absence of mechanical obstruc-tion. These patients present with vomiting, epigastric pain, and weight


Surgery_Schwartz

Surgery_Schwartz. and Roux-en-Y gastrojejunostomy will have great difficulty with gastric emptying in the absence of mechanical obstruc-tion. These patients present with vomiting, epigastric pain, and weight loss. This clinical scenario has been labeled the Brunicardi_Ch26_p1099-p1166.indd 115801/03/19 7:13 PM 1159STOMACHCHAPTER 26Roux syndrome. Endoscopy may show retained food or bezoars, dilation of the gastric remnant, and/or dilation of the Roux limb. Anastomotic inflammation and stricture from mar-ginal ulceration is a confounding finding. An upper GI series confirms these findings and may show delayed gastric empty-ing. This is better quantified by a gastric emptying scan, which always shows delayed solid emptying and may show delayed liquid emptying as well.GI motility testing shows abnormal motility in the Roux limb, with much of the propulsive activity toward, rather than away from, the stomach.212 Gastric motility also may be abnor-mal. Presumably, the disordered motility in the Roux


Surgery_Schwartz

Surgery_Schwartz. motility in the Roux limb, with much of the propulsive activity toward, rather than away from, the stomach.212 Gastric motility also may be abnor-mal. Presumably, the disordered motility in the Roux limb occurs in all patients with this operation. Why only a subset develops the Roux syndrome is unclear. Perhaps patients with disordered gastric motility are at most risk. The disorder seems to be more common in patients with a generous gastric remnant. Truncal vagotomy also has been implicated.Medical treatment consists of promotility agents. Surgi-cal treatment consists of paring down the gastric remnant. Care should be taken to preserve adequate blood supply to the new gastric pouch. If the left gastric artery is intact, a vertically ori-ented lesser curvature based pouch (similar to gastric bypass) with excision of the fundus can be considered. If gastric motility is severely disordered, 95% gastrectomy or total gastrectomy should be considered. The Roux limb should be resected if it


Surgery_Schwartz

Surgery_Schwartz. bypass) with excision of the fundus can be considered. If gastric motility is severely disordered, 95% gastrectomy or total gastrectomy should be considered. The Roux limb should be resected if it is dilated and flaccid, unless doing so puts the patient at risk for short bowel.GallstonesGallstone formation following gastric surgery generally is thought to be secondary to vagal denervation of the gallblad-der with attendant gallbladder dysmotility and stasis. Although prophylactic cholecystectomy is not justified with most gas-tric surgery, it should be considered if the gallbladder appears abnormal, especially if subsequent cholecystectomy is likely to be difficult. If preoperative evaluation reveals sludge or gall-stones, or if intraoperative evaluation reveals stones, incidental cholecystectomy should be considered.Weight LossWeight loss is common in patients who have had a vagotomy and/or gastric resection. The degree of weight loss tends to par-allel the magnitude of the


Surgery_Schwartz

Surgery_Schwartz. cholecystectomy should be considered.Weight LossWeight loss is common in patients who have had a vagotomy and/or gastric resection. The degree of weight loss tends to par-allel the magnitude of the operation. It may be insignificant in the obese but devastating in the asthenic patient. The surgeon should always consider the possible nutritional consequences before performing a gastric resection for benign disease in a thin patient. The causes of weight loss after gastric surgery generally fall into one of two categories: altered dietary intake or malabsorption. If a stool stain for fecal fat is negative, it is likely that decreased caloric intake is the cause. This is the most common cause of weight loss after gastric surgery, and it may be due to small stomach syndrome, postoperative gastroparesis, anorexia due to loss of ghrelin, or self-imposed dietary modifi-cation because of dumping and/or diarrhea. Consultation with an experienced dietitian may prove invaluable.AnemiaIron


Surgery_Schwartz

Surgery_Schwartz. gastroparesis, anorexia due to loss of ghrelin, or self-imposed dietary modifi-cation because of dumping and/or diarrhea. Consultation with an experienced dietitian may prove invaluable.AnemiaIron absorption takes place primarily in the proximal GI tract, and it is facilitated by an acidic environment. Intrinsic factor, essential for the enteric absorption of vitamin B12, is made by the parietal cells of the stomach. Vitamin B12 bioavailability also is facilitated by an acidic environment. Folate-rich vegetables may be poorly tolerated if gastric emptying is delayed or if 10gastric capacity is limited. Since iron, B12, and folate play vital roles in hematopoiesis, it is easy to understand why patients who have had a gastric operation are at risk for anemia. Ane-mia is the most common metabolic side effect in patients who have had a gastric bypass for morbid obesity. It also occurs in up to one-third of patients who have had a vagotomy and/or gastric resection. Iron deficiency is the


Surgery_Schwartz

Surgery_Schwartz. side effect in patients who have had a gastric bypass for morbid obesity. It also occurs in up to one-third of patients who have had a vagotomy and/or gastric resection. Iron deficiency is the most common cause, but vitamin B12 or folate deficiency also occurs, even in patients who have not had total gastrectomy. Of course, patients who have had a total gastrectomy will all develop B12 deficiency with-out some type of regular nonenteral vitamin B12 administration. Gastric bypass patients should be given oral iron supplements and monitored for iron, B12, and folate deficiency. Patients who have had a vagotomy and/or gastrectomy should be similarly monitored with periodic determination of hematocrit, red blood cell indices, iron and transferrin levels, B12, and folate levels. Marginal nutrient status should be corrected with oral and/or parenteral supplementation.Bone DiseaseGastric surgery sometimes disturbs calcium and vitamin D metabolism. Calcium absorption occurs primarily in the


Surgery_Schwartz

Surgery_Schwartz. status should be corrected with oral and/or parenteral supplementation.Bone DiseaseGastric surgery sometimes disturbs calcium and vitamin D metabolism. Calcium absorption occurs primarily in the duo-denum, which is bypassed with gastrojejunostomy. Fat mal-absorption may occur because of blind loop syndrome and bacterial overgrowth or because of inefficient mixing of food and digestive enzymes. This can significantly affect the absorp-tion of vitamin D, a fat-soluble vitamin. Both abnormalities of calcium and vitamin D metabolism can contribute to metabolic bone disease in patients following gastric surgery. The prob-lems usually manifest as pain and/or fractures many years after the index operation. Musculoskeletal symptoms should prompt a study of bone density. Dietary supplementation of calcium and vitamin D may be useful in preventing these complications. Routine skeletal monitoring of patients at high-risk (e.g., elderly males and females and postmenopausal females) may prove


Surgery_Schwartz

Surgery_Schwartz. of calcium and vitamin D may be useful in preventing these complications. Routine skeletal monitoring of patients at high-risk (e.g., elderly males and females and postmenopausal females) may prove useful in identifying skeletal deterioration that may be slowed or stopped with appropriate treatment after gastric surgery.LAPAROSCOPIC GASTRIC OPERATIONSThe most common laparoscopic gastric operations performed today are for GERD and obesity. However, all conventional gastric operations can be performed with minimal access techniques.213 Some are more technically challenging (e.g., partial or total gastric resection) are of debatable advantage over conventional open approaches. Certainly, highly selective vagotomy, vagotomy and gastrojejunostomy, and gastrostomy lend themselves to a minimal access approach. Laparoscopic local excision is often feasible for GI stromal tumors, leiomyo-mas, or gastric diverticula. Difficult to access lesions near the GE junction or pylorus may be removed


Surgery_Schwartz

Surgery_Schwartz. access approach. Laparoscopic local excision is often feasible for GI stromal tumors, leiomyo-mas, or gastric diverticula. Difficult to access lesions near the GE junction or pylorus may be removed through an anterior gastrotomy; more recent approaches utilizing transgastric ports or combined laparoscopic and endoscopic approaches show promise in allowing removal of practically any small gastric lesion with limited incisions.In Japan and Korea, laparoscopic and robotic assisted approaches have been applied increasingly in the manage-ment of gastric cancer.214,215 Indeed, laparoscopic subtotal gas-trectomy has supplanted the traditional open operation as the preferred operation for patients with earlier stage tumors, and laparocopic total gastrectomy for proximal tumors is performed with regularity and excellent outcomes. The Asian experience Brunicardi_Ch26_p1099-p1166.indd 115901/03/19 7:13 PM 1160SPECIFIC CONSIDERATIONS PART IIhas firmly established the feasibility of safe


Surgery_Schwartz

Surgery_Schwartz. regularity and excellent outcomes. The Asian experience Brunicardi_Ch26_p1099-p1166.indd 115901/03/19 7:13 PM 1160SPECIFIC CONSIDERATIONS PART IIhas firmly established the feasibility of safe laparoscopic D2 gastrectomy. Translation of this experience to the United States, however, is not easily accomplished. Studies from Asia suggest that expertise in the laparoscopic approach require upwards of 40 cases, a challenging baseline given the much lower incidence of gastric cancer in the United States.216-219 A more advanced spectrum of disease and higher mean BMI in Western coun-tries are additional barriers to widespread implementation of laparoscopic resection for gastric cancer. Notwithstanding, several high volume centers in the United States have reported excellent outcomes after laparoscopic gastrectomy. As robotic technology that facilitates dissection and anastomosis with articulated instrumentation and enhanced visualization becomes increasingly ubiquitous, the pendulum


Surgery_Schwartz

Surgery_Schwartz. laparoscopic gastrectomy. As robotic technology that facilitates dissection and anastomosis with articulated instrumentation and enhanced visualization becomes increasingly ubiquitous, the pendulum will likely swing toward increasing utilization of minimal access approaches for all gas-tric operations.220REFERENCESEntries highlighted in bright blue are key references. 1. Beaumont W. Experiments and Observations on the Gastric Juice and the Physiology of Digestion. Plattsburgh: PP Allen; 1833. 2. Wangensteen OH, Wangensteen SD. Gastric surgery. In: The Rise of Surgery. Minneapolis: University of Minnesota Press; 1978. 3. Herrington JL. Historical aspects of gastric surgery. In: Scott HW, Jr, Sawyers JL, eds. Surgery of the Stomach, Duodenum, and Small Intestine. 2nd ed. Boston: Blackwell; 1992. 4. Dragstedt LR. Vagotomy for the gastroduodenal ulcer. Ann Surg. 1945;122:973-989. 5. Zollinger RM, Ellison EH. Primary peptic ulcerations of the jejunum associated with islet cell tumors of


Surgery_Schwartz

Surgery_Schwartz. 1992. 4. Dragstedt LR. Vagotomy for the gastroduodenal ulcer. Ann Surg. 1945;122:973-989. 5. Zollinger RM, Ellison EH. Primary peptic ulcerations of the jejunum associated with islet cell tumors of the pancreas. Ann Surg. 1955;142:709-728. 6. Flora ED, Wilson TG, Martin IJ, et al. A review of natural orifice translumenal endoscopic surgery (NOTES) for intraab-dominal surgery: experimental models, techniques, and appli-cability to the clinical setting. Ann Surg. 2008;247:583-602. 7. Mercer DW, Liu TH, Castaneda A. Anatomy and physiology of the stomach. In: Zuidema GD, Yeo CJ, eds. Shackelford’s Surgery of the Alimentary Tract. 5th ed. Vol 2. Philadelphia: WB Saunders; 2002:3. 8. Warren WD, Zeppa R, Fomon JJ. Selective trans-splenic decompression of gastroesophageal varices by distal spleno-renal shunt. Ann Surg. 1967;166:437-455. 9. Orringer MB, Marshall B, Chang AC, et al. Two thousand transhiatal esophagectomies: changing trends, lessons learned. Ann Surg. 2007;246:363-372. 10. Leung


Surgery_Schwartz

Surgery_Schwartz. shunt. Ann Surg. 1967;166:437-455. 9. Orringer MB, Marshall B, Chang AC, et al. Two thousand transhiatal esophagectomies: changing trends, lessons learned. Ann Surg. 2007;246:363-372. 10. Leung WK, et al. Tumors of the stomach. In: Yamada T, et al, eds. Textbook of Gastroenterology. 4th ed. Philadelphia: Lip-pincott, Williams & Wilkins; 2003:1416. 11. Japanese Gastric Cancer Association. Japanese classifications of gastric carcinoma: 3rd English edition. Gastric Cancer. 2011;14:101-112. 12. Jansen EPM, Boot H, Verheij M, van de Velde CJ. Opti-mal locoregional treatment in gastric cancer. J Clin Oncol. 2005:23:4509-4517. 13. Johnson LR, ed. Physiology of the Gastrointestinal Tract. 5th ed. New York: Elsevier; 2012. 14. Browning KN, Verheijden S, Boeckxstaens GE. The vagus nerve in appetite regulation, mood, and intestinal inflamma-tion. Gastroenterology. 2017;152(4):730-744. 15. Matteoli G, Boeckxstaens GE. The vagal innervation of the gut and immune homeostasis. Gut.


Surgery_Schwartz

Surgery_Schwartz. nerve in appetite regulation, mood, and intestinal inflamma-tion. Gastroenterology. 2017;152(4):730-744. 15. Matteoli G, Boeckxstaens GE. The vagal innervation of the gut and immune homeostasis. Gut. 2013;62(8):1214-1222. 16. Fawcett DW, Jensh R. In: Bloom and Fawcett: Concise Histol-ogy. 2nd ed. Oxford University Press: London. 17. Ashley SW, Evoy D, Daly JM. Stomach. In: Schwartz SI, ed. Principles of Surgery. 7nd ed. New York:McGraw-Hill; 1999:1181. 18. Antonioli DA, Madara JL. Functional anatomy of the gas-trointestinal tract. In: Ming S-C, Goldman H, eds. Pathology of the Gastrointestinal Tract. 2nd ed. Baltimore: Williams & Wilkins; 1998:13. 19. Aloia L, McKie MA, Huch M. Cellular plasticity in the adult liver and stomach. J Physiol. 2016;594(17):4815-4825. 20. Feldman M. Gastric secretion. In: Feldman M, ed. Sleisenger and Fordtran’s Gastrointestinal and Liver Disease. 7nd ed. Philadelphia: Saunders; 2002;715. 21. Minalyan A, Gabrielyan L, Scott D, Jacobs J, Pisegna JR. The


Surgery_Schwartz

Surgery_Schwartz. secretion. In: Feldman M, ed. Sleisenger and Fordtran’s Gastrointestinal and Liver Disease. 7nd ed. Philadelphia: Saunders; 2002;715. 21. Minalyan A, Gabrielyan L, Scott D, Jacobs J, Pisegna JR. The gastric and intestinal microbiome: role of proton pump inhibi-tors. Curr Gastroenterol Rep. 2017;19(8):42. 22. Loo VG, Bourgault AM, Poirier L, et al. Host and pathogen factors for Clostridium Difficile infection and colonization. N Engl J Med. 2011;365:1693-1703. 23. Canani RB, Terrin G. Gastric acidity inhibitors and the risk of intestinal infections. Curr Opin Gastroenterol. 2010;26:31-35. 24. Kopic S, Murek M, Geibel JP. Revisiting the parietal cell. Am J Physiol Cell Physiol. 2010;298:C1-C10. 25. Wolfe MM, Soll AH. The physiology of gastric acid secretion. N Engl J Med. 1988;319:1707-1715. 26. Schubert ML. Physiologic, pathophysiologic, and pharmaco-logic regulation of gastric acid secretion. Curr Opin Gastro-enterol. 2017;33(6): pp. 430-438. 27. Schubert ML, Peura DA. Control of


Surgery_Schwartz

Surgery_Schwartz. ML. Physiologic, pathophysiologic, and pharmaco-logic regulation of gastric acid secretion. Curr Opin Gastro-enterol. 2017;33(6): pp. 430-438. 27. Schubert ML, Peura DA. Control of gastric acid secretion in health and disease. Gastroenterology. 2008;134(7):1842-1860. 28. Lloyd KCK, Debas HT. Hormonal and neural regulation of gastric acid secretion. In: Johnson LR, ed. Physiology of the Gastrointestinal Tract. 3rd ed. New York: Raven; 1993. 29. Del Valle J, Todisco A. Gastric secretion. In: Yamada T, et al, eds. Textbook of Gastroenterology. 4nd ed. Philadelphia: Lippincott, Williams & Wilkins; 2003:266. 30. Norlén P, Ericsson P, Kitano M, Ekelund M, Håkanson R. The vagus regulates histamine mobilization from rat stomach ECL cells by controlling their sensitivity to gastrin. J Physiol. 2005;564(pt 3):895-905. 31. Holst JJ, Knuhtsen S, Orskov C, et al. GRP nerves in pig antrum: role of GRP in vagal control of gastrin secretion. Am J Physiol. 1987;253(5 pt 1):G643-G649. 32. Helgadottir


Surgery_Schwartz

Surgery_Schwartz. 3):895-905. 31. Holst JJ, Knuhtsen S, Orskov C, et al. GRP nerves in pig antrum: role of GRP in vagal control of gastrin secretion. Am J Physiol. 1987;253(5 pt 1):G643-G649. 32. Helgadottir H, Metz DC, Yang YX, Rhim AD, Björnsson ES. The effects of long-term therapy with proton pump inhibitors on meal stimulated gastrin. Dig Liver Dis. 2014;46(2):125-130. 33. Lodrup AB, Reimer C, Bytzer P. Systematic review: symptoms of rebound acid hypersecretion following proton pump inhibi-tor treatment. Scand J Gastroenterol. 2013;48(5):515-522. 34. Boyce M, et al. Randomised trial of the effect of a gastrin/CCK2 receptor antagonist on esomeprazole-induced hyper-gastrinaemia: evidence against rebound hyperacidity. Eur J Clin Pharmacol. 2017;73(2):129-139. 35. Agreus L, et al. Rationale in diagnosis and screening of atro-phic gastritis with stomach-specific plasma biomarkers. Scand J Gastroenterol. 2012;47(2):136-147. 36. Wallace JL. Prostaglandins, NSAIDs, and gastric mucosal pro-tection: why


Surgery_Schwartz

Surgery_Schwartz. and screening of atro-phic gastritis with stomach-specific plasma biomarkers. Scand J Gastroenterol. 2012;47(2):136-147. 36. Wallace JL. Prostaglandins, NSAIDs, and gastric mucosal pro-tection: why doesn’t the stomach digest itself? Physiol Rev. 2008;88:1547-1565. 37. Choi SR, Lee SA, Kim YJ, et al. Role of heat shock proteins in gastric inflammation and ulcer healing. J Physiol Pharmacol. 2009;60:5-17. 38. Yandrapu H, Sarosiek J. Protective factors of the gastric and duodenal mucosa: an overview. Curr Gastroenterol Rep. 2015;17(6):24. 39. Cummings DE, Overduin J. Gastrointestinal regulation of food intake. J Clin Invest. 2007;117(1):13-23. 40. Dimaline R, Varro A. Novel roles of gastrin. J Physiol. 2014;592(14):2951-2958.Brunicardi_Ch26_p1099-p1166.indd 116001/03/19 7:13 PM 1161STOMACHCHAPTER 26 41. Bartfeld S, et al. In vitro expansion of human gastric epithelial stem cells and their responses to bacterial infection. Gastroen-terology. 2015;148(1):126-136 e6. 42. Winsett OE, et


Surgery_Schwartz

Surgery_Schwartz. 26 41. Bartfeld S, et al. In vitro expansion of human gastric epithelial stem cells and their responses to bacterial infection. Gastroen-terology. 2015;148(1):126-136 e6. 42. Winsett OE, et al. Gastrin stimulates growth of colon cancer. Surgery. 1986;99(3):302-307. 43. Johnson LR. The trophic action of gastrointestinal hormones. Gastroenterology. 1976;70(2):278-288. 44. Murray CD, Kamm MA, Bloom SR, et al. Ghrelin for the gastroenterologist: history and potential. Gastroenterology. 2003;125:1492-1502. 45. Muller TD, et al. Ghrelin. Mol Metab. 2015;4(6):437-460. 46. Ariyasu H, Takaya K, Tagami T, et al. Stomach is a major source of circulating ghrelin, and feeding state determines plasma ghrelin-like immuno reactivity levels in humans. J Clin Endocrinol Metab. 2001;86:4753-4758. 47. Anderson B, et al. The impact of laparoscopic sleeve gastrec-tomy on plasma ghrelin levels: a systematic review. Obes Surg. 2013;23(9):1476-1480. 48. Steinert RE, et al. Ghrelin, CCK, GLP-1, and PYY(3-36):


Surgery_Schwartz

Surgery_Schwartz. B, et al. The impact of laparoscopic sleeve gastrec-tomy on plasma ghrelin levels: a systematic review. Obes Surg. 2013;23(9):1476-1480. 48. Steinert RE, et al. Ghrelin, CCK, GLP-1, and PYY(3-36): secretory controls and physiological roles in eating and glycemia in health, obesity, and after RYGB. Physiol Rev. 2017;97(1):411-463. 49. Cummings DE, Weigle DS, Frayo RS, et al. Plasma ghrelin levels after diet-induced weight loss or gastric bypass surgery. N Engl J Med. 2002;346:1623-1630. 50. Karamanakos SN, Vagenas K, Kalfarentzos F, et al. Weight loss, appetite suppression, and changes in fasting and post-prandial ghrelin and peptide-YY levels after Roux-en-Y gas-tric bypass and sleeve gastrectomy: a prospective, double blind study. Ann Surg. 2008;247:401. 51. Delhanty PJ, Neggers SJ, and van der Lely AJ. Mechanisms in endocrinology: ghrelin: the differences between acyland des-acyl ghrelin. Eur J Endocrinol. 2012;167(5):601-608. 52. Badman MK, Flier JS. The gut and energy balance:


Surgery_Schwartz

Surgery_Schwartz. van der Lely AJ. Mechanisms in endocrinology: ghrelin: the differences between acyland des-acyl ghrelin. Eur J Endocrinol. 2012;167(5):601-608. 52. Badman MK, Flier JS. The gut and energy balance: visceral allies in the obesity wars. Science. 2005;307(5717):1909-1914. 53. Bado A, et al. The stomach is a source of leptin. Nature. 1998;394(6695):790-793. 54. Sanjeevi A. Gastric motility. Curr Opin Gastroenterol. 2007;23:625. 55. Parkman HP, Jones MP. Tests of gastric neuromuscular func-tion. Gastroenterology. 2009;136:1526-1543. 56. Hasler WL. Physiology of gastric motility and gastric empty-ing. In: Yamada T, et al, eds. Textbook of Gastroenterology. 4nd ed. Philadelphia: Lippincott, Williams & Wilkins; 2003:195. 57. Chial HJ, Camilleri M. Motility disorders of the stomach and small intestine. In: Friedman SL, McQuaid KR, Grendell JH, eds. Current Diagnosis and Treatment in Gastroenterology. 2nd ed. New York:McGraw-Hill; 2003:355. 58. Sanders KM, Koh SD, Ro S, Ward SM. Regulation of


Surgery_Schwartz

Surgery_Schwartz. In: Friedman SL, McQuaid KR, Grendell JH, eds. Current Diagnosis and Treatment in Gastroenterology. 2nd ed. New York:McGraw-Hill; 2003:355. 58. Sanders KM, Koh SD, Ro S, Ward SM. Regulation of gastro-intestinal motility—insights from smooth muscle biology. Nat Rev Gastroenterol Hepatol. 2012;9:633-645. 59. Deloose E, Janssen P, Depoortere I, Tack J. The migrating motor complex—control mechanisms and its role in health and disease. Nat Rev Gastroenterol Hepatol. 2012;9:271-285. 60. Vanden Berghe P, et al. Contribution of different triggers to the gastric accommodation reflex in humans. Am J Physiol Gastrointest Liver Physiol. 2009;297(5):G902-G906. 61. Berthoud HR. The vagus nerve, food intake and obesity. Regul Pept. 2008;149(1-3):15-25. 62. Cheng LK. Slow wave conduction patterns in the stomach: from Waller’s foundations to current challenges. Acta Physiol (Oxf). 2015;213(2):384-393. 63. Tack J, et al. Motilin-induced gastric contractions signal hun-ger in man. Gut.


Surgery_Schwartz

Surgery_Schwartz. patterns in the stomach: from Waller’s foundations to current challenges. Acta Physiol (Oxf). 2015;213(2):384-393. 63. Tack J, et al. Motilin-induced gastric contractions signal hun-ger in man. Gut. 2016;65(2):214-224. 64. Marks JM, Ponsky JL. Diagnostic and therapeutic endoscopy of the stomach and small bowel. In: Yeo CJ, et al, eds. Shack-elford’s Surgery of the Alimentary Tract. 6nd ed. Philadelphia: Saunders; 2007. 65. Levine MS, Rubesin SE, Laufer I. Barium studies in modern radiology: do they have a role? Radiology. 2009;250(1):18-22. 66. Furukawa K, Miyahara R, Itoh A, et al. Diagnosis of the inva-sion depth of gastric cancer using MDCT with virtual gastros-copy: comparison with staging with endoscopic ultrasound. AJR Am J Roentgenol. 2011;197:867-875. 67. Chen CY, Hsu JS, Wu DC, et al. Gastric cancer: preopera-tive local staging with 3D multidetector row CT—correlation with surgical and histopathologic results. Radiology. 2007; 242:472-482. 68. Shin KS, Kim SH, Han JK, et al.


Surgery_Schwartz

Surgery_Schwartz. al. Gastric cancer: preopera-tive local staging with 3D multidetector row CT—correlation with surgical and histopathologic results. Radiology. 2007; 242:472-482. 68. Shin KS, Kim SH, Han JK, et al. Three-dimensional MDCT gastrography compared with axial CT for the detection of early gastric cancer. J Comput Assist Tomogr. 2007;31: 741-749. 69. Caddy GR, Chen RY. Current clinical applications of endo-scopic ultrasound. ANZ J Surg. 2007;77:101-111. 70. Power DG, Schattner MA, Gerdes H, et al. Endoscopic ultrasound can improve the selection for laparoscopy in patients with localized gastric cancer. J Am Coll Surg. 2009;208:173-178. 71. Jones DB. Role of endoscopic ultrasound in staging upper gastrointestinal cancers. ANZ J Surg. 2007;77:166-172. 72. Balaji NS, Crookes PF, Banki F, et al. A safe and noninvasive test for vagal integrity revisited. Arch Surg. 2002;137:954-958. 73. Vaira D, Gatta L, Ricci C, Miglioli M. Review article: diagno-sis of Helicobacter pylori infection. Aliment


Surgery_Schwartz

Surgery_Schwartz. A safe and noninvasive test for vagal integrity revisited. Arch Surg. 2002;137:954-958. 73. Vaira D, Gatta L, Ricci C, Miglioli M. Review article: diagno-sis of Helicobacter pylori infection. Aliment Pharmacol Ther. 2002;16:105-113. 74. Walsh JH, Peterson WL. The treatment of Helicobacter pylori infection in the management of peptic ulcer disease. N Engl J Med. 1995;333:984-991. 75. Kao CY, Sheu BS, Wu JJ. Helicobacter pylori infection: an overview of bacterial virulence factors and pathogenesis. Biomed J. 2016;39(1):14-23. 76. Hooi JKY, et al. Global prevalence of Helicobacter pylori infection: systematic review and meta-analysis. Gastroenter-ology. 2017;153(2):420-429. 77. Graham DY. Helicobacter pylori update: gastric cancer, reliable therapy, and possible benefits. Gastroenterology. 2015;148(4):719-731 e3. 78. Noto JM, Peek RM, Jr. The gastric microbiome, its interaction with Helicobacter pylori, and its potential role in the progres-sion to stomach cancer. PLoS Pathog.


Surgery_Schwartz

Surgery_Schwartz. 2015;148(4):719-731 e3. 78. Noto JM, Peek RM, Jr. The gastric microbiome, its interaction with Helicobacter pylori, and its potential role in the progres-sion to stomach cancer. PLoS Pathog. 2017;13(10):e1006573. 79. Blaser MJ, Atherton JC. Helicobacter pylori persistence: biol-ogy and disease. J Clin Invest. 2004;113:321-333. 80. Fox JG, Wang TC. Inflammation, atrophy, and gastric cancer. J Clin Invest. 2007;117(1):60-69. 81. McColl KE. Clinical practice. Helicobacter pylori infection. N Engl J Med. 2010;362:1597-1604. 82. Bedoui S, Kupz A, Wijberg OL, et al. Different bacterial pathogens, different strategies, yet the aim is the same: eva-sion of intestinal dendritic cell recognition. J Immunol. 2010;184:2237-2242. 83. Graham DY, Lew GM, Klein PD, et al. Effect of treatment of Helicobacter pylori infection on the long-term recurrence of gastric or duodenal ulcer: arandomized controlled study. Ann Intern Med. 1992;116:705-708. 84. McColl K, et al. Symptomatic benefit from eradicating


Surgery_Schwartz

Surgery_Schwartz. pylori infection on the long-term recurrence of gastric or duodenal ulcer: arandomized controlled study. Ann Intern Med. 1992;116:705-708. 84. McColl K, et al. Symptomatic benefit from eradicating Heli-cobacter pylori infection in patients with nonulcer dyspepsia. N Engl J Med. 1998;339(26):1869-1874. 85. Atkinson NS, Braden B. Helicobacter pylori infection: diag-nostic strategies in primary diagnosis and after therapy. Dig Dis Sci. 2016;61(1):19-24. 86. Burucoa C, et al. Comparative evaluation of 29 commer-cial Helicobacter pylori serological kits. Helicobacter. 2013;18(3):169-179. 87. Malfertheiner P, et al. Management of Helicobacter pylori infection—the Maastricht V/Florence Consensus Report. Gut. 2017;66(1):6-30.Brunicardi_Ch26_p1099-p1166.indd 116101/03/19 7:13 PM 1162SPECIFIC CONSIDERATIONS PART II 88. Shiota S, et al. Antibiotic resistance of Helicobacter pylori among male United States veterans. Clin Gastroenterol Hepa-tol. 2015;13(9):1616-1624. 89. Holle GE.


Surgery_Schwartz

Surgery_Schwartz. CONSIDERATIONS PART II 88. Shiota S, et al. Antibiotic resistance of Helicobacter pylori among male United States veterans. Clin Gastroenterol Hepa-tol. 2015;13(9):1616-1624. 89. Holle GE. Pathophysiology and modern treatment of ulcer dis-ease. Int J Mol Med. 2010;25(4):483-491. 90. Leong RW. Differences in peptic ulcer between the East and the West. Gastroenterol Clin North Am. 2009;38(2):363-379. 91. Brock J, Sauaia A, Ahnen D, et al. Process of care and out-comes for elderly patients hospitalized with peptic ulcer disease: results from a quality improvement project. JAMA. 286:1985-1993. 92. Yang YR, Richter JE, Dempsey DT. Trends and outcomes of hospitalizations for peptic ulcer disease in the United States 1993-2006. Ann Surg. 2010;251:51-58. 93. Feinstein LB, et al. Trends in hospitalizations for peptic ulcer disease, United States, 1998-2005. Emerg Infect Dis. 2010;16(9):1410-1418. 94. Spechler SJ. Peptic ulcer disease and its complications. In: Feldman M, ed. Sleisinger and


Surgery_Schwartz

Surgery_Schwartz. for peptic ulcer disease, United States, 1998-2005. Emerg Infect Dis. 2010;16(9):1410-1418. 94. Spechler SJ. Peptic ulcer disease and its complications. In: Feldman M, ed. Sleisinger and Fordtran’s Gastrointestinal and Liver Disease. 7nd ed. Philadelphia: Saunders; 2002. 95. Del Valle J, Chey WD, Scheiman JM. Acid peptic disorders. In: Yamada T, et al, eds. Textbook of Gastroenterology. 4nd ed. Philadelphia: Lippincott, Williams & Wilkins; 2003:1321. 96. Fisher WE, Brunicardi FC. Benign gastric ulcer. In: Cameron JL, ed. Current Surgical Therapy. 9nd ed. Philadelphia: Mosby Elsevier; 2008:81. 97. Laine L. Approaches to nonsteroidal anti-inflamma-tory drug use in the high-risk patient. Gastroenterology. 2001;120:594-606. 98. Lanas A. A review of the gastrointestinal safety data—a gastroenterologist’s perspective. Rheumatology. 2010;49: ii3-ii10. 99. Kawasaki K, et al. Low-dose aspirin and non-steroidal anti-inflammatory drugs increase the risk of bleeding in patients with


Surgery_Schwartz

Surgery_Schwartz. gastroenterologist’s perspective. Rheumatology. 2010;49: ii3-ii10. 99. Kawasaki K, et al. Low-dose aspirin and non-steroidal anti-inflammatory drugs increase the risk of bleeding in patients with gastroduodenal ulcer. Dig Dis Sci. 2015;60(4):1010-1015. 100. Mora S, Manson JE. Aspirin for primary prevention of ath-erosclerotic cardiovascular disease: advances in diagnosis and treatment. JAMA Intern Med. 2016;176(8):1195-1204. 101. Vaduganathan M, et al. Proton-pump inhibitors reduce gas-trointestinal events regardless of aspirin dose in patients requiring dual antiplatelet therapy. J Am Coll Cardiol. 2016;67(14):1661-1671. 102. Vaduganathan M, et al. Efficacy and safety of proton-pump inhibitors in high-risk cardiovascular subsets of the COGENT trial. Am J Med. 2016;129(9):1002-1005. 103. Ray WA, et al. Association of proton pump inhibitors with reduced risk of warfarin-related serious upper gastrointestinal bleeding. Gastroenterology. 2016;151(6):1105-1112 e10. 104. Abraham NS, Hlatky


Surgery_Schwartz

Surgery_Schwartz. WA, et al. Association of proton pump inhibitors with reduced risk of warfarin-related serious upper gastrointestinal bleeding. Gastroenterology. 2016;151(6):1105-1112 e10. 104. Abraham NS, Hlatky MA, Antman EM, et al: ACCF/ACG/AHA Expert consensus document on the concomitant use of proton pump inhibitors and thienopyridines: a focused update of the ACCF/ACG/AHA 2008 consensus document on reduc-ing the gastrointestinal risks of antiplatet therapy and NSAID use. Circulation. 2010;122:2619-2633. 105. Chan FK, et al. Similar efficacy of proton-pump inhibitors vs H2-receptor antagonists in reducing risk of upper gastrointes-tinal bleeding or ulcers in high-risk users of low-dose aspirin. Gastroenterology. 2017;152(1):105-110 e1. 106. Hsu CC, et al. Depression and the risk of peptic ulcer disease: a nationwide population-based study. Medicine (Baltimore). 2015;94(51):e2333. 107. Blatchford O, Murray WR. A risk score to predict need for treatment for upper gastrointestinal hemorrhage.


Surgery_Schwartz

Surgery_Schwartz. disease: a nationwide population-based study. Medicine (Baltimore). 2015;94(51):e2333. 107. Blatchford O, Murray WR. A risk score to predict need for treatment for upper gastrointestinal hemorrhage. Lancet. 2000;356:1318-1321. 108. Saltzman JR, et al. A simple risk score accurately predicts in-hospital mortality, length of stay, and cost in acute upper GI bleeding. Gastrointest Endosc. 2011;74(6):1215-1224. 109. Dallal HJ, Palmer KR. ABC of the upper gastrointes-tinal tract: upper gastrointestinal haemorrhage. BMJ. 2001;323:1115-1117. 110. Laine L. Upper gastrointestinal bleeding due to a peptic ulcer. N Engl J Med. 2016;375(12):1197-1198. 111. Cheng DW, et al. A modified Glasgow Blatchford Score improves risk stratification in upper gastrointestinal bleed: a prospective comparison of scoring systems. Aliment Pharma-col Ther. 2012;36(8):782-789. 112. Lo CC, et al. Comparison of hemostatic efficacy for epineph-rine injection alone and injection combined with hemoclip therapy in


Surgery_Schwartz

Surgery_Schwartz. of scoring systems. Aliment Pharma-col Ther. 2012;36(8):782-789. 112. Lo CC, et al. Comparison of hemostatic efficacy for epineph-rine injection alone and injection combined with hemoclip therapy in treating high-risk bleeding ulcers. Gastrointest Endosc. 2006;63(6):767-773. 113. Chey WD, Wong BCY. Practice Parameters Committee of the American College of Gastroenterology. American College of Gastroenterology guideline on the management of Helicobacter pylori infection. Am J Gastroenterol. 2007;102: 1808-1825. 114. Harbison SP, Dempsey DT. Peptic ulcer disease. Curr Probl Surg. 2005;42(6):346-454. 115. Mulholland MW, Debas HT. Chronic duodenal and gastric ulcer. Surg Clin North Am. 1987;67:489-507. 116. Schroder VT, et al. Vagotomy/drainage is superior to local oversew in patients who require emergency surgery for bleed-ing peptic ulcers. Ann Surg. 2014;259(6):1111-1118. 117. Wu SC, et al. Acid-reducing vagotomy is associated with reduced risk of subsequent ischemic heart disease in


Surgery_Schwartz

Surgery_Schwartz. emergency surgery for bleed-ing peptic ulcers. Ann Surg. 2014;259(6):1111-1118. 117. Wu SC, et al. Acid-reducing vagotomy is associated with reduced risk of subsequent ischemic heart disease in com-plicated peptic ulcer: An Asian population study. Medicine (Baltimore). 2016;95(50):e5651. 118. Lagoo J, Pappas TN, Perez A. A relic or still relevant: the nar-rowing role for vagotomy in the treatment of peptic ulcer dis-ease. Am J Surg. 2014;207(1):120-126. 119. Maki T, Shiratoti T, Hatafuku T, et al. Pyrolus-preserving gas-trectomy as an improved operation for gastric ulcer. Surgery. 1967;61:838-842. 120. Morita S, Katai H, Saka T, et al. Outcome of pyrolus-pre-serving gastrectomy for early gastric cancer. Br J Surg. 2008;95:1131-1135. 121. Gilliam AD, Speake WJ, Lobo DN, et al. Current practice of emergency vagotomy and Helicobacter pylori eradication for complicated peptic ulcer in the United Kingdom. Br J Surg. 2003;90:88-90. 122. Reuben BC, Neumayer LA. Variations reported in


Surgery_Schwartz

Surgery_Schwartz. practice of emergency vagotomy and Helicobacter pylori eradication for complicated peptic ulcer in the United Kingdom. Br J Surg. 2003;90:88-90. 122. Reuben BC, Neumayer LA. Variations reported in sur-gical practice for bleeding duodenal ulcers. Am J Surg. 2006;192:e42-e45. 123. Yusuf TE, Brugge WR. Endoscopic therapy of benign pyloric stenosis and gastric outlet obstruction. Curr Opin Gastroen-terol. 2006;22:570-573. 124. Csendes A, Maluenda F, Braghetto I, et al. Prospective ran-domized study comparing three surgical techniques for the treatment of gastric outlet obstruction secondary to duodenal ulcer. Am J Surg. 1993;166:45-49. 125. Lau JYW, Sung JJY, Lee KKC, et al. Effect of intravenous omeprazole on recurrent bleeding after endoscopic treatment of bleeding peptic ulcers. N Engl J Med. 2000;343:310-316. 126. Lau JY, Sung JJ, Lam YH, et al. Endoscopic retreatment com-pared with surgery in patients with recurrent bleeding after initial endoscopic control of bleeding ulcers. N Engl


Surgery_Schwartz

Surgery_Schwartz. 2000;343:310-316. 126. Lau JY, Sung JJ, Lam YH, et al. Endoscopic retreatment com-pared with surgery in patients with recurrent bleeding after initial endoscopic control of bleeding ulcers. N Engl J Med. 1999;340:751-756. 127. Fendrich V, Langer P, Waldmann J, et al. Management of spo-radic and multiple endocrine neoplasia type 1 gastrinomas. Br J Surg. 2007;94:1331-1341. 128. Dolan JP, Norton JA: Zollinger-Ellison Syndrome, in Yeo CJ, et al (eds). Shackelford’s Surgery of the Alimentary Tract, 6th ed. Philadelphia: Saunders/Elsevier, 2007, p. 862. 129. Orlando LA, Lenard L, Orlando RC: Chronic hypergastrinemia: causes and consequences. Dig Dis Sci. 2007;52:2482-2489.Brunicardi_Ch26_p1099-p1166.indd 116201/03/19 7:13 PM 1163STOMACHCHAPTER 26 130. Fraker DL, et al. Surgery in Zollinger-Ellison syndrome alters the natural history of gastrinoma. Ann Surg. 1994;220(3): 320-328; discussion 328-330. 131. Norton JA, et al. Surgery increases survival in patients with gastrinoma. Ann Surg.


Surgery_Schwartz

Surgery_Schwartz. syndrome alters the natural history of gastrinoma. Ann Surg. 1994;220(3): 320-328; discussion 328-330. 131. Norton JA, et al. Surgery increases survival in patients with gastrinoma. Ann Surg. 2006;244(3):410-419. 132. Alhazzani W, Alenezi F, Jaeschke RZ, et al. Proton pump inhibitors versus histamine 2 receptor antagonists for stress ulcer prophylaxis in critically ill patients: a systematic review and meta-analysis. Crit Care Med. 2013;41:693-705. 133. Sasabuchi Y, et al. Risks and benefits of stress ulcer pro-phylaxis for patients with severe sepsis. Crit Care Med. 2016;44(7):e464-e469. 134. Barletta JF, et al. Stress ulcer prophylaxis. Crit Care Med. 2016;44(7):1395-1405. 135. Marik PE, Vasu T, Hirani A, et al. Stress ulcer prophylaxis in the new millennium: a systematic review and meta-analysis. Crit Care Med. 2010;38:2222-2228. 136. Isajevs S, et al. Gastritis staging: interobserver agreement by applying OLGA and OLGIM systems. Virchows Arch. 2014;464(4):403-407. 137. Nam JH, et


Surgery_Schwartz

Surgery_Schwartz. Crit Care Med. 2010;38:2222-2228. 136. Isajevs S, et al. Gastritis staging: interobserver agreement by applying OLGA and OLGIM systems. Virchows Arch. 2014;464(4):403-407. 137. Nam JH, et al. OLGA and OLGIM stage distribution accord-ing to age and Helicobacter pylori status in the Korean popula-tion. Helicobacter. 2014;19(2):81-89. 138. The American Cancer Society. Cancer Facts and Figures 2017; pg 4, Table 1. Cancer.org. https://www.cancer.org/content/dam/cancer-org/research/cancer-facts-and-statistics/annual-cancer-facts-and-figures/2017/cancer-facts-and-figures-2017 .pdf Accessed 1-1-2018. 139. Correa P, Houghton J. Carcinogenesis of Helicobacter pylori. Gastroenterology. 2007;133(2):659-672. 140. McColl KE, Watabe H, Derakhshan MH. Role of gastric atrophy in mediating negative association between Heli-cobacter pylori infection and reflux oesophagitis, Barrett’s oesophagus and oesophageal adenocarcinoma. Gut. 2008;57: 721-723. 141. ZurHausen A, van Rees BP, van Beek J, et al.


Surgery_Schwartz

Surgery_Schwartz. between Heli-cobacter pylori infection and reflux oesophagitis, Barrett’s oesophagus and oesophageal adenocarcinoma. Gut. 2008;57: 721-723. 141. ZurHausen A, van Rees BP, van Beek J, et al. Epstein-Barr virus in gastric carcinomas and gastric stump carci-nomas: alate event in gastric carcinogenesis. J Clin Pathol. 2004;57:487-491. 142. Norton JA, Ham CM, Dam JV, et al. CDH1 truncating muta-tions in the E-cadherin gene: an indication for total gastrec-tomy to treat hereditary diffuse gastric cancer. Ann Surg. 2007;245:873-879. 143. Chiba T, et al. Chronic inflammation and gastric cancer devel-opment (in Japanese). Nihon Rinsho. 2012;70(10):1694-1698. 144. Chiba T, Marusawa H, Ushijima T. Inflammation-associated cancer development in digestive organs: mechanisms and roles for genetic and epigenetic modulation. Gastroenterol-ogy. 2012;143(3):550-563. 145. Park DY, Lauwers GY. Gastric polyps: classification and man-agement. Arch Pathol Lab Med. 2008;132(4):633-640. 146. Shimoyama S, Aoki


Surgery_Schwartz

Surgery_Schwartz. modulation. Gastroenterol-ogy. 2012;143(3):550-563. 145. Park DY, Lauwers GY. Gastric polyps: classification and man-agement. Arch Pathol Lab Med. 2008;132(4):633-640. 146. Shimoyama S, Aoki F, Kawahara M, et al. Early gastric cancer development in a familial adenomatous polyposis patient. Dig Dis Sci. 2004;49(2):260-265. 147. Gylling A, Abdel-Rahman WM, Juhola M, et al. Is gastric cancer part of the tumour spectrum of hereditary non-pol-yposis colorectal cancer? A molecular genetic study. Gut. 2007;56:926-933. 148. Schaefer N, Sinning C, Standop J, et al. Treatment and prog-nosis of gastric stump carcinoma in comparison with primary proximal gastric cancer. Am J Surg. 2007;194:63-67. 149. van der Post RS, et al. Hereditary diffuse gastric cancer: updated clinical guidelines with an emphasis on germline CDH1 mutation carriers. J Med Genet. 2015;52(6):361-374. 150. Ono H. Early gastric cancer: diagnosis, pathology, treatment techniques, and treatment outcomes. Eur J Gastroenterol


Surgery_Schwartz

Surgery_Schwartz. emphasis on germline CDH1 mutation carriers. J Med Genet. 2015;52(6):361-374. 150. Ono H. Early gastric cancer: diagnosis, pathology, treatment techniques, and treatment outcomes. Eur J Gastroenterol Hep-atol. 2006;18:863-866. 151. Pyrhonen S, Kuitunen T, Nyandoto P, Kouri M. Randomised comparison of fluorouracil, epidoxorubicin, and methotrex-ate (FEMTX) plus supportive care with supportive care alone in patients with non-resectable gastric cancer. Br J Cancer. 1995;71:587-591. 152. Bang YJ, Van Cutsem E, Feyereislova A, et al. Transtuzumab in combination with chemotherapy versus chemotherapy alone for treatment of HER2-positive advanced gastric or gas-troesophageal junction cancer (TOGA): a phase 3 open label randomized controlled trial. Lancet. 2010;376:687-697. 153. Begnami MD, Fuduka E, Fregnani JH, et al. Prognostic impli-cations of altered human epidermal growth factor receptors (HERs) in gastric carcinomas: HER2 and HER3 are predictors of poor outcome. J Clin Oncol.


Surgery_Schwartz

Surgery_Schwartz. MD, Fuduka E, Fregnani JH, et al. Prognostic impli-cations of altered human epidermal growth factor receptors (HERs) in gastric carcinomas: HER2 and HER3 are predictors of poor outcome. J Clin Oncol. 2011;29(22):3030-3036. 154. Li HY, Dai J, Xue HB, et al. Application of magnifying endoscopy with narrow band imaging in diagnosing gas-tric lesions: a prospective study. Gastrointestinal Endosc. 2012;76:1124-1132. 155. Chen J, Cheong JH, Yun MJ, et al. Improvement in preopera-tive staging of gastric adenocarcinoma with positron emission tomography. Cancer. 2005;103:2383-2390,2005. 156. Wong J, Coit D. Detection of gastric cancer peritoneal metas-tases by peritoneal lavage: current limitations and future per-spectives. Surgery. 2012;152:1-4. 157. Ikoma N, Blum M, Chiang YJ, et al. Yield of staging lapa-roscopy and lavage cytology for radiologically occult peri-toneal carcinomatosis of gastric cancer. Ann Surg Oncol. 2016;23(13):4332-4337. 158. Sarela AI, Lefkowitz R, Brennan MF, et al.


Surgery_Schwartz

Surgery_Schwartz. staging lapa-roscopy and lavage cytology for radiologically occult peri-toneal carcinomatosis of gastric cancer. Ann Surg Oncol. 2016;23(13):4332-4337. 158. Sarela AI, Lefkowitz R, Brennan MF, et al. Selection of patients with gastric adenocarcinoma for laparoscopic stag-ing. Am J Surg. 2006;191:134-138. 159. Dicken BJ, Bigam DL, Cass C, Mackey JR, Joy AA, Hamilton SM. Gastric adenocarcinoma: review and considerations for future directions. Ann Surg. 2005;241(1):27-39. 160. Squires MH 3rd, Kooby DA, Poultsides GA, et al. Is it time to abandon the 5-cm margin rule during resection of distal gastric adenocarcinoma? A multi-institution study of the U.S. Gastric Cancer Collaborative. Ann Surg Oncol. 2015;22(4):1243-1251. 161. Coburn NG, Swallow CJ Kiss A, Law C. Significant regional variation in adequacy of lymph node assessment and survival in gastric cancer. Cancer. 2006;107(9):2143-2151. 162. Datta J, Lewis RS, Jr, Mamtni R, et al. Implications of inad-equate lymph node staging in


Surgery_Schwartz

Surgery_Schwartz. in adequacy of lymph node assessment and survival in gastric cancer. Cancer. 2006;107(9):2143-2151. 162. Datta J, Lewis RS, Jr, Mamtni R, et al. Implications of inad-equate lymph node staging in resectable gastric cancer: a contemporary analysis using the National Cancer Data Base. Cancer. 2014;120(18):2855-2865. 163. Saidi RF, ReMine SG, Dudrick PS, et al. Is there a role for palliative gastrectomy in patients with stage IV gastric cancer? World J Surg. 2006;30:21-27. 164. Bozzetti F, Marubini E, Bonfantai G, Gennari L. Subtotal versus total gastrectomy for gastric cancer: five-year survival rates in a multicenter randomized Italian trial. Italian Gastroin-testinal Tumor Study Group. Ann Surg. 1999;230(2):170-178. 165. Karanicolas PJ, Graham D, Gönen DM, Strong VE, Ben-nan MF, Coit DG. Quality of life after gastrectomy for adenocarcinoma: a prospective cohort study. Ann Surg. 2013;257(6):1039-1046. 166. Bonenkamp JJ, Hermans J, Sasako M, et al. Extended lymph node dissection for


Surgery_Schwartz

Surgery_Schwartz. Quality of life after gastrectomy for adenocarcinoma: a prospective cohort study. Ann Surg. 2013;257(6):1039-1046. 166. Bonenkamp JJ, Hermans J, Sasako M, et al. Extended lymph node dissection for gastric cancer. N Engl J Med. 1999;340:908-914. 167. Bartlett EK, Roses RE, Kelz RR, Drebin JA, Fraker DL, Karakousis GC. Morbidity and mortality after total gastrec-tomy for gastric malignancy using the American College of Surgeons National Surgical Quality Improvement Program database. Surgery. 2014;156(2):298-304. 168. Cuschieri A, Fayers P, Fielding J, et al. Postoperative morbid-ity and mortality after D1 and D2 resections for gastric can-cer: preliminary results of the MRC randomised controlled Brunicardi_Ch26_p1099-p1166.indd 116301/03/19 7:13 PM 1164SPECIFIC CONSIDERATIONS PART IIsurgical trial. The Surgical Cooperative Group. Lancet. 1996;347:995-999. 169. Degiuli M, Sasako M, Ponti A, et al. Randomized clinical trial comparing survival after D1 or D2 gastrectomy for gastric


Surgery_Schwartz

Surgery_Schwartz. trial. The Surgical Cooperative Group. Lancet. 1996;347:995-999. 169. Degiuli M, Sasako M, Ponti A, et al. Randomized clinical trial comparing survival after D1 or D2 gastrectomy for gastric can-cer. Br J Surg. 2014;101(2):23-31. 170. Songun I, Putter H, Kranenbarg EM, Sasako M, van de Velde CJ. Surgical treatment of gastric cancer: 15-year follow-up results of the randomised nationwide Dutch D1D2 trial. Lan-cet Oncol. 2010;11(5):439-449. 171. GASTRIC (Global Advanced/Adjuvant Stomach Tumor Research International Collaboration) Group; Paoletti X, Oba K, Burzykowski T, et al. Benefit of adjuvant chemo-therapy for resectable gastric cancer: a meta-analysis. JAMA. 2010;303(17):1729-1737. 172. Sasako M, et al. Five-year outcomes of a randomized phase III trial comparing adjuvant chemotherapy with S-1 versus surgery alone in stage II or III gastric cancer. J Clin Oncol. 2011;29:4387-4393. 173. Noh SH, Adjuvant capecitabine plus oxaliplatin for gastric cancer after D2 gastrectomy (CLASSIC):


Surgery_Schwartz

Surgery_Schwartz. S-1 versus surgery alone in stage II or III gastric cancer. J Clin Oncol. 2011;29:4387-4393. 173. Noh SH, Adjuvant capecitabine plus oxaliplatin for gastric cancer after D2 gastrectomy (CLASSIC): 5-year follow-up of an open-label, randomised phase 3 trial. Lancet Oncol. 2014;15(12):1389-1396. 174. Park SH, Sohn TS, Lee J, et al. Phase III trial to compare adjuvant chemotherapy with capecitabine and cisplatin ver-sus concurrent chemoradiotherapy in gastric cancer: final report of the adjuvant chemoradiotherapy in stomach tumors trial, including survival and subset analyses. J Clin Oncol. 2015;33(28):3130-3136. 175. Macdonald JS, Smalley SR, Benedetti J, et al. Chemoradio-therapy after surgery compared with surgery alone for adeno-carcinoma of the stomach or gastroesophageal junction. N Engl J Med. 2001;345:725-730. 176. Cunningham D, Allum WH, Stenning SP, et al. Perioperative chemotherapy versus surgery alone for resectable gastroesoph-ageal cancer. N Engl J Med.


Surgery_Schwartz

Surgery_Schwartz. junction. N Engl J Med. 2001;345:725-730. 176. Cunningham D, Allum WH, Stenning SP, et al. Perioperative chemotherapy versus surgery alone for resectable gastroesoph-ageal cancer. N Engl J Med. 2006;355(1):11-20. 177. Ajani JA, Winter K, Okawara GS, et al. Phase II trial of preoperative chemoradiation in patients with localized gas-tric adenocarcinoma (RTOG 9904): quality of combined modality therapy and pathologic response. J Clin Oncol. 2006;24(24):3953-3958. 178. Sasako M, Sano T, Yamamoto S, et al. D2 lymphadenectomy alone or with para-aortic nodal dissection for gastric cancer. N Engl J Med. 2008;359:453-462. 179. VanCutsem E, Moiseyenko VM, Tjulandin S, et al. Phase III study of docetaxel and cisplatin plus fluorouracil compared with cisplatin and fluorouracil as first-line chemotherapy for advanced gastric cancer: areport of the V325 study group. J Clin Oncol. 2006;24:4991-4997. 180. Cunningham D, Starling N, Rao S, et al. Capecitabine and oxaliplatin for advanced


Surgery_Schwartz

Surgery_Schwartz. chemotherapy for advanced gastric cancer: areport of the V325 study group. J Clin Oncol. 2006;24:4991-4997. 180. Cunningham D, Starling N, Rao S, et al. Capecitabine and oxaliplatin for advanced esophagogastric cancer. N Engl J Med. 2008;358(1):36-46. 181. Gomez-Martin C, Garralda E, Echerri MJ. HER2/neu testing for anti-HER2 based therapies in patients with unresectable and/or metastatic gastric cancer. J Clin Path. 2012;65:751-757. 182. Baptista V, Singh A, Wassef W. Early gastric cancer: an update on endoscopic management. Curr Opin Gastroenterol. 2012;28(6):629-635. 183. Yoon SS, Coit DG, Portlock CS, et al. The diminishing role of surgery in the treatment of gastric lymphoma. Ann Surg. 2004;240:28-37. 184. Farinha P, Gascoyne RD. Helicobacter pylori and MALT lym-phoma. Gastroenterology. 2005;128:1579-1605. 185. Gold JS, DeMatteo RP. Combined surgical and molecular therapy: the gastrointestinal stromal tumor model. Ann Surg. 2006;244(2):176-184. 186. Rubin BP, Heinrich MC,


Surgery_Schwartz

Surgery_Schwartz. 2005;128:1579-1605. 185. Gold JS, DeMatteo RP. Combined surgical and molecular therapy: the gastrointestinal stromal tumor model. Ann Surg. 2006;244(2):176-184. 186. Rubin BP, Heinrich MC, Corless CL. Gastrointestinal stromal tumour. Lancet. 2007;369:1731-1741. 187. Stelow EB, Murad FM, Debol SM, et al. A limited immuno-cytochemical panel for the distinction of subepithelial gastro-intestinal mesenchymal neoplasms sampled by endoscopic ultrasound-guided fine-needle aspiration. Am J Clin Pathol. 2008;129:219-225. 188. Miettinen M, Lasota J. Gastrointestinal stromal tumors: Pathology and prognosis at different sites. Semin Diagn Pathol. 2006;23:70-83. 189. Heinrich MC. Kinase mutations and imatinib response in patients with metastatic gastrointestinal stromal tumor. J Clin Oncol. 2003;21(23):4342-4349. 190. Dematteo RP, Ballman KV, Antonescu CR, et al. Adjuvant imatinib mesylate after resection of localised, primary gas-trointestinal stromal tumour: a randomised, double-blind,


Surgery_Schwartz

Surgery_Schwartz. RP, Ballman KV, Antonescu CR, et al. Adjuvant imatinib mesylate after resection of localised, primary gas-trointestinal stromal tumour: a randomised, double-blind, placebo-controlled trial. Lancet. 2009;373(9669):1097-1104. 191. Joensuu H, Eriksson M, Sunby Hall K, et al. One vs three years of adjuvant imatinib for operable gastrointestinal stromal tumor: a randomized trial. JAMA. 2012;307(12):1265-1272. 192. Balachandran VP, DeMatteo RP. Adjuvant imatinib for GIST: the pie is shrinking. Ann Surg Oncol. 2014;21(11):3365-3366. 193. Raut CP, Kulke MH, Glickman JN, et al. Carcinoid tumors. Curr Probl Surg. 2006;43:383-450. 194. Perren A, Couvelard A, Scoazec JY, et al. ENETS consensus guidelines for the standards of care in neuroendocrine tumors: pathology: diagnosis and prognostic stratification. Neuroendo-crinology. 2017;105(3):196-200. 195. Parkman HP, Hasler WL, Fisher RS. American Gastroen-terological Association technical review on the diagnosis and treatment of gastroparesis.


Surgery_Schwartz

Surgery_Schwartz. Neuroendo-crinology. 2017;105(3):196-200. 195. Parkman HP, Hasler WL, Fisher RS. American Gastroen-terological Association technical review on the diagnosis and treatment of gastroparesis. Gastroenterology. 2004;127: 1592-1622. 196. Yin J, Chen JD. Implantable gastric electrical stimulation: ready for prime time? Gastroenterology. 2008;134:665-667. 197. Zehetner J, Ravari F, Ayazi S, et al. Minimally invasive surgi-cal approach for the treatment of gastroparesis. Surg Endosc. 2013;27(1):61-66. 198. Cappell MS, Friedel D. Initial management of acute upper gas-trointestinal bleeding-from initial evaluation to gastrointestinal endoscopy. Med Clin North Am. 2008;92:491-509. 199. Dempsey DT, Burke DR, Reilly RS, McLean GK, Rosato EF. Angiography in poor-risk patients with massive nonvariceal upper gastrointestinal bleeding. Am J Surg. 1990;159:282-286. 200. Zaman A. Portal hypertension related bleeding-management of difficult cases. Clin Liver Dis. 2006;10:353-370. 201. Coffey RJ,


Surgery_Schwartz

Surgery_Schwartz. upper gastrointestinal bleeding. Am J Surg. 1990;159:282-286. 200. Zaman A. Portal hypertension related bleeding-management of difficult cases. Clin Liver Dis. 2006;10:353-370. 201. Coffey RJ, Washington MK, Corless CL, et al. Ménétrier dis-ease and gastrointestinal stromal tumors: hyperproliferative disorders of the stomach. J Clin Invest. 2007;117:70. 202. Sebastian S, O’Morain CA, Buckley MJ. Current therapeutic options for gastric antral vascular ectasia. Aliment Pharmacol-Ther. 2003;18:157-165. 203. Akhras J, Patel P, Tobi M. Dieulafoy’s lesion-like bleeding: an under-recognized cause of upper gastrointestinal hemor-rhage in patients with advanced liver disease. Dig Dis Sci. 2007;52:722-726. 204. Harbison SP, Dempsey DT. Mallory-Weiss syndrome, in Cam-eron JL, ed. Current Surgical Therapy. 9nd ed. Philadelphia: Mosby; 2008. 205. Schrag SP, Sharma R, Jaik NP, et al. Complications related to percutaneous endoscopic gastrostomy (PEG) tubes. A comprehensive clinical review. J


Surgery_Schwartz

Surgery_Schwartz. Therapy. 9nd ed. Philadelphia: Mosby; 2008. 205. Schrag SP, Sharma R, Jaik NP, et al. Complications related to percutaneous endoscopic gastrostomy (PEG) tubes. A comprehensive clinical review. J Gastrointestin Liver Dis. 2007;16:407-418. 206. McClave SA. Critical care nutrition: getting involved as a gastrointestinal endoscopist. J Clin Gastroenterol. 2006;40:870-890. 207. Dempsey DT. Reoperative gastric surgery and postgastrec-tomy syndromes. In: Zuidema GD, Yeo CJ, eds. Shackelford’s Surgery of the Alimentary Tract. 5nd ed. Vol 2. Philadelphia: Saunders; 2002:161.Brunicardi_Ch26_p1099-p1166.indd 116401/03/19 7:13 PM 1165STOMACHCHAPTER 26 208. Ukleja A. Dumping syndrome: pathophysiology and treat-ment. Nutr Clin Pract. 2005;20:517-525. 209. Cuschieri A. Postvagotomy diarrhea: is there a place for surgi-cal management? Gut. 1990;31:245-246. 210. Forster-Barthell AW, Murr MM, Nitecki S, et al. Near-total completion gastrectomy for severe postvagotomy gastric stasis: analysis of


Surgery_Schwartz

Surgery_Schwartz. a place for surgi-cal management? Gut. 1990;31:245-246. 210. Forster-Barthell AW, Murr MM, Nitecki S, et al. Near-total completion gastrectomy for severe postvagotomy gastric stasis: analysis of early and long-term results in 62 patients. J Gastrointest Surg. 1999;3:15-21. 211. Jones MP, Maganti K. A systematic review of surgical therapy for gastroparesis. Am J Gastroenterol. 2003;98: 2122-2129. 212. Van der Milje HC, Kleibeuker JH, Limburg AJ, et al. Mano-metric and scintigraphic studies of the relation between motility disturbances in the Roux limb and the Roux-en-Y syndrome. Am J Surg. 1993;166:11-17. 213. Farrell TM, Hunter JG. Laparoscopic surgery of the stomach and duodenum. In: Zuidema GD, Yeo CJ, eds. Shackelford’s Surgery of the Alimentary Tract. 5nd ed. Vol 2. Philadelphia: Saunders; 2002:202. 214. Lee J, Kim W. Clinical experience of 528 laparoscopic gas-trectomies on gastric cancer in a single institution. Surgery. 2013;153(5):611-618. 215. Zeng YK, Yang ZL, Peng JS, et


Surgery_Schwartz

Surgery_Schwartz. 2002:202. 214. Lee J, Kim W. Clinical experience of 528 laparoscopic gas-trectomies on gastric cancer in a single institution. Surgery. 2013;153(5):611-618. 215. Zeng YK, Yang ZL, Peng JS, et al. Laparoscopy-assisted ver-sus open distal gastrectomy for early gastric cancer. Ann Surg. 2012;256:39-52. 216. Kim HG, Park JH, Jeong SH, et al. Totally laparoscopic distal gastrectomy after learning curve completion: comparison with laparoscopy-assisted distal gastrectomy. J Gastric Cancer. 2013;13(1):26-33. 217. Moon JS, et al. Lessons learned from a comparative analy-sis of surgical outcomes of and learning curves for lap-aroscopy-assisted distal gastrectomy. J Gastric Cancer. 2015;15(1):29-38. 218. Kim HH, Han SU, Kim MC, et al. Long-term results of laparo-scopic gastrectomy for gastric cancer: a large-scale case-con-trol and case-matched Korean multicenter study. J Clin Oncol. 2014;32(7):627-633. 219. Jung DH, Son SY, Park YS, et al. The learning curve asso-ciated with laparoscopic total


Surgery_Schwartz

Surgery_Schwartz. a large-scale case-con-trol and case-matched Korean multicenter study. J Clin Oncol. 2014;32(7):627-633. 219. Jung DH, Son SY, Park YS, et al. The learning curve asso-ciated with laparoscopic total gastrectomy. Gastric Cancer. 2016;19(1):264-272. 220. Suda K, Uyama I, Kitagawa Y. Technology beats the cur-rent standard: is robotic gastrectomy becoming the standard treatment option for gastric cancer? : “Surgical outcomes after open, laparoscopic, and robotic gastrectomy for gas-tric cancer,” by Kim, Hyuong-Il, et al. Ann Surg Oncol. 2017;24(7):1755-1757.Brunicardi_Ch26_p1099-p1166.indd 116501/03/19 7:13 PM


Surgery_Schwartz

Surgery_Schwartz. Brunicardi_Ch26_p1099-p1166.indd 116601/03/19 7:13 PMThis page intentionally left blank


Surgery_Schwartz

Surgery_Schwartz. The Surgical Management of ObesityAnita P. Courcoulas and Philip R. Schauer 27chapterINTRODUCTIONDespite the global pandemic of obesity, there has been little progress in nonsurgical treatment approaches, especially among patients with severe obesity. In addition, the evidence base for bariatric procedures has grown rapidly over the last 10 years, yielding important shortand long-term data on the safety and efficacy of the surgical treatment for obesity and related metabolic disorders. Therefore, the approach for patients con-sidering bariatric and metabolic surgery has now shifted to a well-informed and shared decision-making process as there are significant tradeoffs between the potential risks and benefits of these procedures.1HistoryDuring the 1950s, operations were first performed to treat severe hyperlipidemia with associated obesity.2 These were ileocolic bypass operations to limit absorption and were associated with severe nutritional complications and liver failure


Surgery_Schwartz

Surgery_Schwartz. to treat severe hyperlipidemia with associated obesity.2 These were ileocolic bypass operations to limit absorption and were associated with severe nutritional complications and liver failure postopera-tively. A more modest jejunoileal bypass was performed next, also a malabsorptive operation, but it bypassed only a portion of the small intestine. Complications after this procedure included severe diarrhea, electrolyte disturbances, protein-calorie malnu-trition, renal stones, and liver failure.In 1969, Mason and Ito performed the first gastric bypass, describing a loop of jejunum connected to a transverse proximal gastric pouch.3 Bile reflux esophagitis was severe postopera-tively, causing Griffin and colleagues to describe the Roux-en-Y modification of the gastric bypass in 1977.4 The gastric pouch was also altered from transverse to vertical using the upper lesser curvature at this time (Fig. 27-1).In 1980, Mason5 first performed the vertical banded gastroplasty (VBG), which was a


Surgery_Schwartz

Surgery_Schwartz. pouch was also altered from transverse to vertical using the upper lesser curvature at this time (Fig. 27-1).In 1980, Mason5 first performed the vertical banded gastroplasty (VBG), which was a restrictive procedure using a stapled proximal gastric pouch of the upper lesser curvature of the stomach with a restrictive band for its outlet to the rest of the stomach. This operation produced excellent initial weight loss (50% of excess weight or more) with low mor-bidity and mortality. It rapidly became the most commonly performed bariatric operation in the United States during the 1980s. However, by the early 1990s, it became clear that patients who underwent VBG modified their diets to high-calorie soft foods and liquids and some regained weight.6 A significant incidence of stenosis at the cuff and staple line Introduction1167History / 1167State of the Field / 1169The Disease of Obesity1169Overview / 1169U.S. Prevalence of Obesity / 1170Causes of Obesity / 1170Concurrent Medical and


Surgery_Schwartz

Surgery_Schwartz. cuff and staple line Introduction1167History / 1167State of the Field / 1169The Disease of Obesity1169Overview / 1169U.S. Prevalence of Obesity / 1170Causes of Obesity / 1170Concurrent Medical and Social Problems / 1170Medical Management of Obesity1171Lifestyle Intervention / 1171Pharmacotherapy / 1172Barriers to Treatment / 1173Candidates for Bariatric Surgery1173Indications / 1173Contraindications / 1173Mechanism of Action of Bariatric and Metabolic Surgery1175Overview / 1175Mechanisms of Bariatric Surgery (Weight Loss) / 1175Mechanisms of Metabolic Surgery (Diabetes Improvement) / 1177Preoperative Issues1177Preoperative Preparation / 1177Anesthesiology Issues / 1179Enhanced Recovery After Surgery / 1179Special Equipment and Infrastructure / 1180Bariatric Surgical Procedures1180Laparoscopic Roux-en-Y Gastric Bypass / 1180Laparoscopic Sleeve Gastrectomy / 1185Laparoscopic Adjustable Gastric Banding / 1187Biliopancreatic Diversion and Duodenal Switch / 1189Investigational


Surgery_Schwartz

Surgery_Schwartz. Roux-en-Y Gastric Bypass / 1180Laparoscopic Sleeve Gastrectomy / 1185Laparoscopic Adjustable Gastric Banding / 1187Biliopancreatic Diversion and Duodenal Switch / 1189Investigational Bariatric Procedures / 1190Follow-Up and Postoperative Care1191Results of Bariatric Surgery1192Short-Term Outcomes / 1192Effectiveness of Bariatric Surgery Compared to Nonsurgical Treatment / 1193Longer-Term Studies / 1193Other Studies / 1198Comparisons Between Procedures / 1199Resolution of Specific Comorbid Conditions / 1199Results of Surgery for Diabetes (Metabolic Surgery) / 1200Complications of Bariatric Surgery1203Surgical Complications / 1203Nonsurgical Complications / 1204Reoperative (Revision and Conversion) Bariatric Surgery1205Introduction / 1205Principles and Preoperative Evaluation / 1205Treatment for Insufficient Weight Loss or Weight Regain / 1206Treatment of Surgical Complications / 1206Special Issues in Bariatric Surgery1207Bariatric Procedures in Adolescents / 1207Cost


Surgery_Schwartz

Surgery_Schwartz. / 1205Treatment for Insufficient Weight Loss or Weight Regain / 1206Treatment of Surgical Complications / 1206Special Issues in Bariatric Surgery1207Bariatric Procedures in Adolescents / 1207Cost Effectiveness / 1207Quality Assurance / 1207Plastic Surgery After Weight Loss / 1208Future Important Questions1209Brunicardi_Ch27_p1167-p1218.indd 116723/02/19 2:20 PM 1168JejunoilealBypassGastricBypassHorizontalGastroplastyAdjustable GastricBandingVertical BandedGastroplastyRoux-en-Y gastricBypassBPD with DuodenalSwitchBiliopancreaticDiversionSleeveGastrectomyMalabsorptiveRestrictiveBoth50s60s70s80s90sdisruptions was also problematic.7 Long-term weight loss was poor,8 and by the 1990s in the United States, Roux-en-Y gastric bypass (RYGB) became the procedure of choice for bariatric surgery.In the meantime, in Italy Scopinaro had developed and pop-ularized the biliopancreatic diversion (BPD) in the early 1980s.9 This procedure was also modified to include duodenal switch (DS),10 the only


Surgery_Schwartz

Surgery_Schwartz. the meantime, in Italy Scopinaro had developed and pop-ularized the biliopancreatic diversion (BPD) in the early 1980s.9 This procedure was also modified to include duodenal switch (DS),10 the only major malabsorptive operation currently in use.The laparoscopic approach to bariatric surgery became available in the 1990s, and Belachew performed the first laparo-scopic adjustable gastric banding (LAGB) operation in 1994.11 Wittgrove and Clark performed the first laparoscopic RYGB the same year.12 LAGB was commonly performed in Europe and Australia during the late 1990s, and in 2001 it was approved for use in the United States. Sleeve gastrectomy (SG) as a primary bariatric operation has grown rapidly in use since 2008.Figure 27-1. History of bariatric surgery. (Reproduced with permission from Arterburn DE, Courcoulas AP: Bariatric surgery for obesity and metabolic condi-tions in adults, BMJ. 2014 Aug 27;349:g3961.)Key Points1 Sixty-five percent of the world’s population live in


Surgery_Schwartz

Surgery_Schwartz. from Arterburn DE, Courcoulas AP: Bariatric surgery for obesity and metabolic condi-tions in adults, BMJ. 2014 Aug 27;349:g3961.)Key Points1 Sixty-five percent of the world’s population live in countries where overweight and obesity are linked to more deaths than underweight and malnutrition. Obesity is the second leading cause of preventable death in adults in the United States.2 There is an ongoing major shift in procedure utilization with the sleeve gastrectomy and Roux-en-Y gastric bypass being the two most common procedures, worldwide.3 The former classification of bariatric operations as either “restrictive” or “malabsorptive” is being replaced by knowl-edge from investigation into the more basic physiologic and metabolic mechanisms responsible for the effects of bariatric surgery.4 Patients who develop a bowel obstruction after laparoscopic gastric bypass require surgical and not conservative therapy due to the high incidence of internal hernias and the potential for bowel


Surgery_Schwartz

Surgery_Schwartz. who develop a bowel obstruction after laparoscopic gastric bypass require surgical and not conservative therapy due to the high incidence of internal hernias and the potential for bowel infarction.5 Malabsorptive operations are highly effective in producing durable weight loss and metabolic improvements but have higher surgical complication rates and considerable nutri-tional side effects. Patients undergoing such procedures require complete follow-up and appropriate nutritional supplements.6 Large, longer-term observational studies of bariatric surgery have shown durable weight loss, diabetes remission, lipid improvements, and improved survival with bariatric surgery. Still unclear are specific preand postoperative predictors of those outcomes, long-term complications, microvascular and macrovascular events, mental health outcomes, and costs.7 High quality data have clearly established that bariatric pro-cedures are more effective than medical or lifestyle interven-tions for inducing


Surgery_Schwartz

Surgery_Schwartz. events, mental health outcomes, and costs.7 High quality data have clearly established that bariatric pro-cedures are more effective than medical or lifestyle interven-tions for inducing weight loss and initial remission of type 2 diabetes, even in less obese patients. Randomized clinical trials showed greater weight loss and type 2 diabetes mellitus remission following bariatric surgery compared with nonsur-gical treatments.8 The incidence of complications after bariatric surgery varies from 4% to over 25% and depends on the duration of follow-up, the definition of complication used, the type of bariatric procedure performed, and individual patient characteristics.9 Emerging areas in bariatric surgery include the use of inter-mediate weight loss devices, adolescent bariatric surgery, and the increase in the need for revision and conversion bar-iatric procedures.Brunicardi_Ch27_p1167-p1218.indd 116823/02/19 2:20 PM 1169THE SURGICAL MANAGEMENT OF OBESITYCHAPTER 2780p <


Surgery_Schwartz

Surgery_Schwartz. surgery, and the increase in the need for revision and conversion bar-iatric procedures.Brunicardi_Ch27_p1167-p1218.indd 116823/02/19 2:20 PM 1169THE SURGICAL MANAGEMENT OF OBESITYCHAPTER 2780p < 0.0017060Relative Procedure Utilization (%)504030201002006200720082009Year of Procedure2010201120122013Adjustable Gastric BandingRoux-en-Y Gastric BypassSleeve GastrectomyDuodenal SwitchFigure 27-2. Changes in bariatric procedure utilization. (Reproduced with permission from Reames BN, Finks JF, Bacal D, et al: Changes in bariatric surgery procedure use in Michigan, 2006-2013, JAMA. 2014 Sep 3;312(9):959-961.)State of the FieldThere has been an ongoing major shift in bariatric procedures both in the United States and worldwide13 with the rapid adop-tion of the laparoscopic sleeve gastrectomy and the simultane-ous decreasing utilization of the laparoscopic adjustable gastric banding procedure (Fig. 27-2). International trends in the utiliza-tion of bariatric surgical procedures have also


Surgery_Schwartz

Surgery_Schwartz. and the simultane-ous decreasing utilization of the laparoscopic adjustable gastric banding procedure (Fig. 27-2). International trends in the utiliza-tion of bariatric surgical procedures have also been published. These show that the total number of bariatric surgical procedures performed in 2014 was 579,517. The three most commonly per-formed procedures in the world were SG at 46%, followed by RYGB (40%), and LAGB (7%). The annual percentage changes from 2013 show an increased utilization of SG and a decreased use of RYGB in the United States, Canada, Europe, and Asia and Pacific countries. In Central and South America, however, the use of SG decreased, and RYGB was most commonly used.14Extension of the indication from bariatric surgery for weight loss to metabolic surgery to treat type 2 diabetes (T2DM) even in patients with less than severe obesity has been another more recent development, driven by the availability of more level 1 data.15,16Also, considerable effort is now being


Surgery_Schwartz

Surgery_Schwartz. 2 diabetes (T2DM) even in patients with less than severe obesity has been another more recent development, driven by the availability of more level 1 data.15,16Also, considerable effort is now being devoted to the study of the basic physiologic mechanisms underlying weight loss and, perhaps more importantly, the resolution of comorbid medical problems associated with obesity. Despite the classic “restric-tive” and “malabsorptive” anatomic conceptualizations of bar-iatric surgical procedures (see Fig. 27-1), there is much ongoing research in animal and human models towards understanding the specific underlying mechanisms of action, which may be more physiologic in nature.17 Some of the potential candidates for the mechanisms of action of bariatric procedures include alterations in ghrelin, leptin, glucagon-like peptide-1 (GLP-1), cholecystokinin, peptide YY (PYY), gut microbiota, and bile acids. In the future, bariatric procedures will not be described by anatomic surgical similarities


Surgery_Schwartz

Surgery_Schwartz. leptin, glucagon-like peptide-1 (GLP-1), cholecystokinin, peptide YY (PYY), gut microbiota, and bile acids. In the future, bariatric procedures will not be described by anatomic surgical similarities but by how they affect key physiological variables, which will provide greater mechanistic insight into how the procedures actually work.THE DISEASE OF OBESITYOverviewWorldwide obesity has more than doubled since 1980. In 2014, 39% of adults age 18 years and over (38% of men and 40% of women) were overweight, and 13% of the world’s adult population (11% of men and 15% of women) were obese. In 2014, an estimated 41 million children under the age of 5 years were overweight or obese.18 Overweight and obesity are now on the rise in lowand middle-income countries, particularly in urban settings. Currently, 65% of the world’s population live in countries where overweight and obesity are linked to more deaths than underweight and malnutrition. Obesity is the second leading cause of preventable


Surgery_Schwartz

Surgery_Schwartz. Currently, 65% of the world’s population live in countries where overweight and obesity are linked to more deaths than underweight and malnutrition. Obesity is the second leading cause of preventable death in adults in the United States, after tobacco use.19The degrees of obesity are defined by body mass index (BMI = weight [kg]/height [m]2), which correlates body weight with height. The World Health Organization international clas-sification of overweight and obesity is shown in Table 27-1. It should be noted that for Asian populations, classifications remain the same as the international classification, but the pub-lic health action points for interventions are set at a lower BMI threshold. For children, age needs to be considered when defin-ing overweight and obesity, so for children age 5 to 19 years, 1Table 27-1The international classification of adult overweight and obesity according to body mass index (BMI)CLASSIFICATIONBMI (kg/m2)PRINCIPAL CUTOFF POINTSADDITIONAL CUTOFF


Surgery_Schwartz

Surgery_Schwartz. age 5 to 19 years, 1Table 27-1The international classification of adult overweight and obesity according to body mass index (BMI)CLASSIFICATIONBMI (kg/m2)PRINCIPAL CUTOFF POINTSADDITIONAL CUTOFF POINTSaNormal range 18.50–24.99 18.50–22.9923.00–24.99Overweight≥25.00≥25.00 Preobese 25.00–29.99 25.00–27.4927.50–29.99 Obese≥30.00≥30.00 Obese class I 30.00–34.99 30.00–32.4932.50–34.99 Obese class II 35.00–39.99 35.00–37.4937.50–39.99 Obese class III≥40.00≥40.00aFor Asian populations, classifications remain the same as the international classification, but public health action points for interventions are set at 23, 27.5, 32.5, and 37.5 kg/m.2Data from WHO, 1995, WHO, 2000 and WHO 2004.Brunicardi_Ch27_p1167-p1218.indd 116923/02/19 2:20 PM 1170SPECIFIC CONSIDERATIONSPART IIoverweight is BMI-for-age greater than 1 standard deviation above the World Health Organization (WHO) growth reference median, and obesity is greater than 2 standard deviations above the WHO growth reference


Surgery_Schwartz

Surgery_Schwartz. is BMI-for-age greater than 1 standard deviation above the World Health Organization (WHO) growth reference median, and obesity is greater than 2 standard deviations above the WHO growth reference median.The fundamental cause of obesity and overweight is an energy imbalance between calories consumed and calories expended. Globally, there has been an increased intake of energy-dense foods that are high in fat and a decrease in physi-cal inactivity due to the increasingly sedentary nature of many forms of work, changing modes of transportation, and increas-ing urbanization. These changes in dietary and physical activ-ity patterns are the result of both societal and environmental changes associated with development. There is also a dearth of supportive policies to counteract these forces in sectors such as health, agriculture, transport, urban planning, environment, food processing, marketing, and education. Obesity as a disease was recognized by the American Medical Association in 2013.


Surgery_Schwartz

Surgery_Schwartz. such as health, agriculture, transport, urban planning, environment, food processing, marketing, and education. Obesity as a disease was recognized by the American Medical Association in 2013. It is multifactorial in its etiology, and the components of the disease likely include a combination of both environmental and genetic factors.U.S. Prevalence of ObesityAccording to the 2013–2014 National Health and Nutrition Examination Survey (NHANES) data, in the United States the overall age-adjusted prevalence of obesity was 37.7% (95% confidence interval [CI], 35.8–39.7%); among men, it was 35.0% (95% CI, 32.8–37.3%); and among women, it was 40.4% (95% CI, 37.6–43.3%). The corresponding prevalence of class III obesity overall was 7.7% (95% CI, 6.2–9.3%); among men, it was 5.5% (95% CI, 4.0–7.2%); and among women, it was 9.9% (95% CI, 7.5–12.3%). Changes over the decade from 2005 through 2014, adjusted for age, race, smoking status, and education, showed significantly increas-ing trends


Surgery_Schwartz

Surgery_Schwartz. and among women, it was 9.9% (95% CI, 7.5–12.3%). Changes over the decade from 2005 through 2014, adjusted for age, race, smoking status, and education, showed significantly increas-ing trends among women for overall obesity and for class III obesity, but not among men.20For children in the United States, obesity is defined as a BMI at or above the sex-specific 95th percentile, and extreme obesity is defined as a BMI at or above 120% of the sexspecific 95th percentile on the U.S. Centers for Disease Control and Prevention (CDC) BMI-for-age growth charts. In the most recent NHANES study of U.S. children and adolescents age 2 to 19 years, the prevalence of obesity from 2011 to 2014 was 17.0%, and extreme obesity was 5.8%.21Causes of ObesityBoth genetic and environmental factors contribute to the devel-opment of obesity. Not everyone exposed to the prevailing envi-ronment becomes obese, suggesting that genetic mechanisms are operating at the individual level. Estimates vary, but twin,


Surgery_Schwartz

Surgery_Schwartz. to the devel-opment of obesity. Not everyone exposed to the prevailing envi-ronment becomes obese, suggesting that genetic mechanisms are operating at the individual level. Estimates vary, but twin, family, and adoption studies show that the rate of heritability of BMI is high, ranging from 40% to 70%.22,23 Eleven rare and monogenic forms of obesity are now recognized, including a deficiency of the leptin and melanocortin-4 receptors, which are expressed in the hypothalamus and are involved in regulating energy homeostasis.24 Heterozygous mutations in the melano-cortin-4 receptor gene are currently the most common cause of monogenic obesity, causative in 2% to 5% of children with severe obesity.Genes and environment interact in a complex process that regulates energy balance and weight. Reducing food intake or increasing physical activity leads to a negative energy bal-ance and a cascade of compensatory adaptive mechanisms that preserve vital functions and are associated with


Surgery_Schwartz

Surgery_Schwartz. Reducing food intake or increasing physical activity leads to a negative energy bal-ance and a cascade of compensatory adaptive mechanisms that preserve vital functions and are associated with reductions in resting energy expenditure, food preoccupation, and many other changes that depend on the amount and duration of caloric restriction. There is also a counterregulatory increase in appetite and food intake that limits the degree of expected weight loss that is associated with interventions such as exercise programs.22Individuals with obesity have excessive adipose cells, both in size and number. The number of such cells often is deter-mined early in life; adult-onset obesity is largely a product of increase in adipose cell size. Weight gain results from increase in both adipose cell size and number. Adipose tissue may be deposited in large quantities in the subcutaneous layer of the abdominal wall or the viscera. Generally, males tend to have central visceral fat distribution,


Surgery_Schwartz

Surgery_Schwartz. size and number. Adipose tissue may be deposited in large quantities in the subcutaneous layer of the abdominal wall or the viscera. Generally, males tend to have central visceral fat distribution, whereas females more often have a peripheral fat distribution. Central or visceral fat distri-bution is associated with metabolic diseases such as diabetes, hypertension, and the metabolic syndrome.Concurrent Medical and Social ProblemsRaised BMI is a major risk factor for diseases such as cardio-vascular disease (mainly heart disease and stroke), which were the leading cause of death in 2012, diabetes, osteoarthritis, some cancers (including endometrial, breast, ovarian, prostate, liver, gallbladder, kidney, and colon).18 The risk for these conditions increases with increases in BMI. Childhood obesity is asso-ciated with a higher chance of obesity, premature death, and disability in adulthood. In addition to increased future risks, children with obesity experience sleep apnea, increased


Surgery_Schwartz

Surgery_Schwartz. obesity is asso-ciated with a higher chance of obesity, premature death, and disability in adulthood. In addition to increased future risks, children with obesity experience sleep apnea, increased risk of fractures, hypertension, early markers of cardiovascular disease, insulin resistance, and psychological effects.The severely obese patient typically presents with multiple chronic and weight-related problems or comorbidities/comorbid conditions. These include degenerative joint disease, low back pain, hypertension, obstructive sleep apnea, gastroesophageal reflux disease (GERD), cholelithiasis, T2DM, dyslipidemia, asthma, hypoventilation syndrome of obesity, right-sided heart failure, migraine headaches, pseudotumor cerebri, venous stasis ulcers, deep venous thrombosis (DVT), fungal skin rashes, skin abscesses, stress urinary incontinence, infertility, dysmenorrhea, depression, and large abdominal wall hernias.There are anatomical, metabolic, and physiological effects of obesity


Surgery_Schwartz

Surgery_Schwartz. skin rashes, skin abscesses, stress urinary incontinence, infertility, dysmenorrhea, depression, and large abdominal wall hernias.There are anatomical, metabolic, and physiological effects of obesity through which this excess adiposity leads to disease risk factors and chronic diseases themselves (Fig. 27-3).22 Subcu-taneous adipose tissue holds most of the stored lipid at a variety of anatomical sites while visceral adipose tissue is a smaller storage compartment with omental and mesenteric fat mechanistically linked to some of the metabolic disturbances and adverse con-sequences outcomes associated with obesity.25,26 Adipose tissue surrounds and compresses the renal parenchyma and may contrib-ute to the hypertension frequently observed in patients who are obese.27 Obesity is frequently accompanied by an increase in pha-ryngeal soft tissues, which can lead to obstructive sleep apnea.28 Excess adiposity also imposes a significant mechanical load on joints, making it a risk factor for


Surgery_Schwartz

Surgery_Schwartz. accompanied by an increase in pha-ryngeal soft tissues, which can lead to obstructive sleep apnea.28 Excess adiposity also imposes a significant mechanical load on joints, making it a risk factor for the development of osteoarthri-tis.29 An increase in intraabdominal pressure likely accounts for the elevated risks of gastroesophageal reflux disease (GERD), Barrett’s esophagus, and esophageal adenocarcinoma among those with obesity.30 Chronic overactivity of the sympathetic ner-vous system is present in some patients with obesity and may contribute to pathophysiological processes, including high blood pressure.27 Obesity is also associated with an increased preva-lence of mood, anxiety, and other psychiatric disorders, especially Brunicardi_Ch27_p1167-p1218.indd 117023/02/19 2:20 PM 1171THE SURGICAL MANAGEMENT OF OBESITYCHAPTER 27ä Adiposity˜ Lipid production˜ Activity ofthe sympatheticnervous system˜ Activity of therenin–angiotensin–aldosterone systemMechanical stress˜ Adipokine


Surgery_Schwartz

Surgery_Schwartz. SURGICAL MANAGEMENT OF OBESITYCHAPTER 27ä Adiposity˜ Lipid production˜ Activity ofthe sympatheticnervous system˜ Activity of therenin–angiotensin–aldosterone systemMechanical stress˜ Adipokine synthesis˜ Adipose tissuemacrophages and otherinflammatory cells˜ Proinflammatorycytokines˜ Pharyngealsoft tissue˜ Mechanicalload on joints˜ Intraabdominalpressure˜ InsulinType 2 diabetesNonalcoholicfatty liver diseaseSteatohepatitisCirrhosisCoronaryartery diseaseObstructivesleep apneaOsteoarthritisGastroesophagealreflux diseaseBarrett’s esophagusEsophagealadenocarcinomaCongestive heart failureStrokeChronic kidney diseaseImpaired insulinsignaling and˜ insulin resistanceLipotoxicityDyslipidemiaSystemic andpulmonaryhypertensionRenalcompressionHydrolysis oftriglyceridesRelease offree fatty acidsFigure 27-3. Pathways through which obesity leads to major risk factors and common chronic diseases. Common chronic diseases are shown in red boxes. The dashed arrows indicate an indirect association.


Surgery_Schwartz

Surgery_Schwartz. 27-3. Pathways through which obesity leads to major risk factors and common chronic diseases. Common chronic diseases are shown in red boxes. The dashed arrows indicate an indirect association. (Reproduced with permission from Heymsfield SB, Wadden TA: Mechanisms, Pathophysiology, and Management of Obesity, N Engl J Med. 2017 Jan 19;376(3):254-266.)among persons with severe obesity and in those seeking bariatric surgery.31-33 Decreased quality of life also results due to severe obesity. Most patients seeking surgical treatment of severe obe-sity do so because of the medical issues they face from comorbid conditions or the decreased quality of life they are experiencing as a result of severe obesity.MEDICAL MANAGEMENT OF OBESITYTreatments should be aligned with the severity of obesity, asso-ciated comorbid conditions, and the individual’s functional limitations. There are guidelines available to evaluate an indi-vidual’s health risks and potential treatment options.34,35 Three main


Surgery_Schwartz

Surgery_Schwartz. asso-ciated comorbid conditions, and the individual’s functional limitations. There are guidelines available to evaluate an indi-vidual’s health risks and potential treatment options.34,35 Three main treatment options exist with sufficient evidence-based support: lifestyle intervention, pharmacotherapy, and bariatric surgery.Lifestyle InterventionLifestyle interventions designed to modify eating behaviors and physical activity are the first option for weight manage-ment, given their low cost and low risk.35 Behavioral therapy, the core of any lifestyle intervention, provides patients with techniques for adopting dietary and activity recommendations. Among these recommendations are regular recording of food intake, physical activity, and weight. Patients review their progress approximately weekly with a trained interventionist Brunicardi_Ch27_p1167-p1218.indd 117123/02/19 2:20 PM 1172SPECIFIC CONSIDERATIONSPART II01020304050Percentage of


Surgery_Schwartz

Surgery_Schwartz. Patients review their progress approximately weekly with a trained interventionist Brunicardi_Ch27_p1167-p1218.indd 117123/02/19 2:20 PM 1172SPECIFIC CONSIDERATIONSPART II01020304050Percentage of Participants6070809010010%5%High-lntensityLifestyleInterventionPharmacotherapyInterventionLook AHEADDPPTeixeira, et aI.PlaceboOrlistatLorcaserinLiraglutidePhentermine-topiramateNaltrexone-bupropionFigure 27-4. 22Percent weight loss at 1 year with intensive lifestyle interventions or pharmacotherapy combined with lower level lifestyle. Shown are the percentages of participants in randomized, controlled trials who had weight loss of at least 5% or at least 10% of their initial weight at 1 year after intensive lifestyle intervention or pharmacotherapy that typically was combined with lower-intensity lifestyle. Percentages shown are cumulative; the percentage of participants who lost at least 5% of their initial weight includes the percentage who lost at least 10%. Additional data on the


Surgery_Schwartz

Surgery_Schwartz. lifestyle. Percentages shown are cumulative; the percentage of participants who lost at least 5% of their initial weight includes the percentage who lost at least 10%. Additional data on the percentage of participants with weight loss at 1 year of at least 15% of their initial weight were available for the Look AHEAD36 study (16%), the DPP39 trial (11%), liraglutide40 (14%), phentermine–topiramate (32%), and naltrexone–bupropion (14%). (Reproduced with permis-sion from Heymsfield SB, Wadden TA: Mechanisms, Pathophysiology, and Management of Obesity, N Engl J Med. 2017 Jan 19;376(3):254-266.)who provides support and encouragement, help setting goals, and problem-solving instructions.35 This type of comprehen-sive program results in a mean weight loss of 5% to 8%, and approximately 60% to 65% of patients lose 5% or more of initial weight. The Look AHEAD study randomized 5145 adults with obesity to either an intensive lifestyle intervention (ILI) or to a diabetes support group and


Surgery_Schwartz

Surgery_Schwartz. to 65% of patients lose 5% or more of initial weight. The Look AHEAD study randomized 5145 adults with obesity to either an intensive lifestyle intervention (ILI) or to a diabetes support group and education group (DSE) to assess the impact on weight loss, T2DM, and cardiovascular outcomes. At 1 year, the intensive intervention group lost an average of 8.6% initial weight compared to 0.7% in the support and educa-tion group. As shown in Fig. 27-4, 68% of participants in the Look AHEAD study lost at least 5% of their initial weight, and 37% of these participants lost at least 10%. Also at 1 year, par-ticipants undergoing the more intensive program experienced improved cardiovascular risk factors and glycemic control.36At 4 years, participants in the intensive intervention group experienced more weight loss (−6.15% ILI compared to −0.88% DSE), better glycemic control, fitness, and an improvement in cardiovascular risk factors.37 Nevertheless, the beneficial clinical effects of the


Surgery_Schwartz

Surgery_Schwartz. more weight loss (−6.15% ILI compared to −0.88% DSE), better glycemic control, fitness, and an improvement in cardiovascular risk factors.37 Nevertheless, the beneficial clinical effects of the improved weight loss achieved with intensive lifestyle intervention did not reduce morbidity and mortality associated with cardiovascular disease after 9.6 years when the Look AHEAD study was stopped due to futility for that primary endpoint.38 Figure 27-4 shows a comparison of several lifestyle intervention trials (Look AHEAD, the Diabetes Prevention Program [DPP] trial,39 and the trial reported by Teixeira et al40) for >5% and >10% weight loss outcomes. These trials, specifically, were selected because they were judged to be good quality by the Guidelines (2013) for the Management of Overweight and Obesity in Adults and because the trial data were reported as categorical weight loss. Categorical weight loss data from the DPP trial were provided by the DPP Research Group to the authors of the


Surgery_Schwartz

Surgery_Schwartz. Obesity in Adults and because the trial data were reported as categorical weight loss. Categorical weight loss data from the DPP trial were provided by the DPP Research Group to the authors of the review.22In summary, multidisciplinary lifestyle intervention and weight-management programs are viable and potentially cost-effective treatment options in overweight or obese patients with or without T2DM. Such approaches, however, often fail to achieve durable weight loss of more than 5% to 10%, so they are not effective enough for the severely obese. Importantly, lifestyle and medical approaches do not appear to improve car-diovascular outcomes in studies so far. Thus, further research is needed to evaluate the role for current medical and lifestyle therapeutic regimens for obesity and T2DM, including compari-sons to surgical interventions. Certainly, and at the very least, these approaches are important adjuncts to bariatric surgery.PharmacotherapyMedications may be considered as an


Surgery_Schwartz

Surgery_Schwartz. including compari-sons to surgical interventions. Certainly, and at the very least, these approaches are important adjuncts to bariatric surgery.PharmacotherapyMedications may be considered as an adjunct to lifestyle modi-fication in adults who have a BMI of 30 or higher or a BMI of 27 to 29 with at least one obesity-related condition.41 Phar-macotherapy and lifestyle intervention together lead to addi-tive weight losses and should be used together and may also be helpful in facilitating the maintenance of reduced weight.34,41,42 Phentermine, the most widely prescribed weight-management medication in the United States, is a sympathomimetic amine that was approved by the FDA in 1959 for short-term use of fewer than 3 months long.41 There are now five newer FDA-approved medications for long-term weight management that include three single drugs and two combination drugs. In 1-year pivotal trials, total weight losses for the three single therapies (orlistat, lorcaserin, and liraglutide),


Surgery_Schwartz

Surgery_Schwartz. weight management that include three single drugs and two combination drugs. In 1-year pivotal trials, total weight losses for the three single therapies (orlistat, lorcaserin, and liraglutide), the effects of which are mediated by different mechanisms, ranged from 5.8% to 8.8% of initial body weight.41,43-45 The two combination medications (phentermine–topiramate and naltrexone–bupropion) include drugs that act on neural weight-loss mechanisms.46,47 In 1-year pivotal trials, total weight loss for these combination drugs ranged from 6.4% to 9.8% of initial body weight.These medications, when prescribed with lifestyle inter-ventions, produce additional weight loss relative to placebo ranging from approximately 3% of initial weight for orlistat and lorcaserin to 9% for the higher-dose phentermine plus topi-ramate–extended release at 1 year. The proportion of patients achieving clinically meaningful (at least 5%) weight loss ranges from 37% to 47% for lorcaserin, 35% to 73% for orlistat,


Surgery_Schwartz

Surgery_Schwartz. plus topi-ramate–extended release at 1 year. The proportion of patients achieving clinically meaningful (at least 5%) weight loss ranges from 37% to 47% for lorcaserin, 35% to 73% for orlistat, and 67% to 70% for higher-dose phentermine plus topiramate–extended release. All three of these medications produce greater improvements in cardiometabolic risk factors than placebo, Brunicardi_Ch27_p1167-p1218.indd 117223/02/19 2:20 PM 1173THE SURGICAL MANAGEMENT OF OBESITYCHAPTER 27but none has been shown to reduce cardiovascular morbid-ity or mortality. There is limited data for the long-term safety and efficacy of these medications, and some of these drugs may increase heart rate43 or attenuate expected blood pressure reductions.47 In addition, completed trials of hard cardiovascular disease outcomes (heart attack and stroke) in patients treated with these medications have yet to be published, except in the case of liraglutide.43 Figure 27-4 shows a comparison of weight loss outcomes