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Surgery_Schwartz. by the world’s leading diabetes organizations. Cleve Clin J Med. 2017;84 (7 suppl 1):S47-S56. 244. Buchwald H, Estok R, Fahrbach K, et al. Weight and type 2 diabetes after bariatric surgery: systematic review and meta-analysis. Am J Med. 2009;122(3):248-256 e245. 245. Sjostrom L, Peltonen M, Jacobson P, et al. Association of bariatric surgery with long-term remission of type 2 diabetes and with microvascular and macrovascular complications. JAMA. 2014;311(22):2297-2304. 246. Schauer PR, Bhatt DL, Kirwan JP, et al. Bariatric surgery versus intensive medical therapy for diabetes—3-year outcomes. N Engl J Med. 2014;370(21):2002-2013. 247. Ikramuddin S, Billington CJ, Lee WJ, et al. Roux-en-Y gastric bypass for diabetes (the Diabetes Surgery Study): 2-year outcomes of a 5-year, randomised, controlled trial. Lancet Diabet Endocrinol. 2015;3(6):413-422. 248. Liang Z, Wu Q, Chen B, Yu P, Zhao H, Ouyang X. Effect of laparoscopic Roux-en-Y gastric bypass surgery on type 2 diabetes mellitus


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Surgery_Schwartz. controlled trial. Lancet Diabet Endocrinol. 2015;3(6):413-422. 248. Liang Z, Wu Q, Chen B, Yu P, Zhao H, Ouyang X. Effect of laparoscopic Roux-en-Y gastric bypass surgery on type 2 diabetes mellitus with hypertension: a randomized controlled trial. Diabet Clin Res Pract. 2013;101(1):50-56. 249. Courcoulas AP, Yanovski SZ, Bonds D, et al. Long-term outcomes of bariatric surgery: a National Institutes of Health symposium. JAMA Surg. 2014;149(12):1323-1329. 250. Wentworth JM, Playfair J, Laurie C, et al. Multidisciplinary diabetes care with and without bariatric surgery in overweight people: a randomised controlled trial. Lancet Diabet Endocrinol. 2014;2(7):545-552. 251. Parikh M, Chung M, Sheth S, et al. Randomized pilot trial of bariatric surgery versus intensive medical weight management on diabetes remission in type 2 diabetic patients who do NOT meet NIH criteria for surgery and the role of soluble RAGE as a novel biomarker of success. Ann Surg. 2014;260(4):617-622; discussion


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Surgery_Schwartz. on diabetes remission in type 2 diabetic patients who do NOT meet NIH criteria for surgery and the role of soluble RAGE as a novel biomarker of success. Ann Surg. 2014;260(4):617-622; discussion 622-614. 252. Schauer PR, Bhatt DL, Kirwan JP, et al. Bariatric surgery versus intensive medical therapy for diabetes—5-year outcomes. N Engl J Med. 2017;376(7):641-651. This is a randomized clinical trial comparing gastric bypass, gastric sleeve, and intensive medical management for the treatment of type 2 diabetes in people with obesity. It is only one of 2 randomized studies with 5 year follow up, at this time. It shows that surgical treatments are superior to intensive medical treatment for glycemic control. 253. Shah SS Todkar J, Phadake U, et al. Gastric bypass vs. medical/lifestyle care for type 2 diabetes in South Asians with BMI 25-40 kg/m2: the COSMID randomized trial Brunicardi_Ch27_p1167-p1218.indd 121623/02/19 2:21 PM 1217THE SURGICAL MANAGEMENT OF OBESITYCHAPTER 27[261-OR].


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Surgery_Schwartz. type 2 diabetes in South Asians with BMI 25-40 kg/m2: the COSMID randomized trial Brunicardi_Ch27_p1167-p1218.indd 121623/02/19 2:21 PM 1217THE SURGICAL MANAGEMENT OF OBESITYCHAPTER 27[261-OR]. Presented at the American Diabetes Association’s 76th Scientific Session; June 10-14, 2016; New Orleans, LA. 254. Encinosa WE, Bernard DM, Du D, Steiner CA. Recent improvements in bariatric surgery outcomes. Med Care. 2009; 47(5):531-535. 255. Birkmeyer NJ, Dimick JB, Share D, et al. Hospital complication rates with bariatric surgery in Michigan. JAMA. 2010;304(4):435-442. 256. Rubino F, Kaplan LM, Schauer PR, Cummings DE. The Diabetes Surgery Summit consensus conference: recommendations for the evaluation and use of gastrointestinal surgery to treat type 2 diabetes mellitus. Ann Surg. 2010;251(3):399-405. 257. Buchwald H, Estok R, Fahrbach K, Banel D, Sledge I. Trends in mortality in bariatric surgery: a systematic review and meta-analysis. Surgery. 2007;142(4):621-632; discussion


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Surgery_Schwartz. 2010;251(3):399-405. 257. Buchwald H, Estok R, Fahrbach K, Banel D, Sledge I. Trends in mortality in bariatric surgery: a systematic review and meta-analysis. Surgery. 2007;142(4):621-632; discussion 632-625. 258. Dimick JB, Nicholas LH, Ryan AM, Thumma JR, Birkmeyer JD. Bariatric surgery complications before vs after implementation of a national policy restricting coverage to centers of excellence. JAMA. 2013;309(8):792-799. 259. DeMaria EJ, Murr M, Byrne TK, et al. Validation of the obesity surgery mortality risk score in a multicenter study proves it stratifies mortality risk in patients undergoing gastric bypass for morbid obesity. Ann Surg. 2007;246(4):578-582; discussion 583-574. 260. DeMaria EJ, Portenier D, Wolfe L. Obesity surgery mortality risk score: proposal for a clinically useful score to predict mortality risk in patients undergoing gastric bypass. Surg Obes Relat Dis. 2007;3(2):134-140. 261. Thomas H, Agrawal S. Systematic review of obesity surgery mortality risk


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Surgery_Schwartz. useful score to predict mortality risk in patients undergoing gastric bypass. Surg Obes Relat Dis. 2007;3(2):134-140. 261. Thomas H, Agrawal S. Systematic review of obesity surgery mortality risk score—preoperative risk stratification in bariatric surgery. Obes Surg. 2012;22(7):1135-1140. 262. O’Brien PE, MacDonald L, Anderson M, Brennan L, Brown WA. Long-term outcomes after bariatric surgery: fifteen-year follow-up of adjustable gastric banding and a systematic review of the bariatric surgical literature. Ann Surg. 2013;257(1):87-94. 263. Rariy CM, Rometo D, Korytkowski M. Post-gastric bypass hypoglycemia. Curr Diabet Rep. 2016;16(2):19. 264. Goldfine AB, Patti ME. How common is hypoglycemia after gastric bypass? Obesity. 2016;24(6):1210-1211. 265. Service GJ, Thompson GB, Service FJ, Andrews JC, Collazo-Clavell ML, Lloyd RV. Hyperinsulinemic hypoglycemia with nesidioblastosis after gastric-bypass surgery. N Engl J Med. 2005;353(3):249-254. 266. Patti ME, Goldfine AB. Hypoglycemia


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Surgery_Schwartz. Andrews JC, Collazo-Clavell ML, Lloyd RV. Hyperinsulinemic hypoglycemia with nesidioblastosis after gastric-bypass surgery. N Engl J Med. 2005;353(3):249-254. 266. Patti ME, Goldfine AB. Hypoglycemia after gastric bypass: the dark side of GLP-1. Gastroenterology. 2014;146(3):605-608. 267. Eisenberg D, Azagury DE, Ghiassi S, Grover BT, Kim JJ. ASMBS position statement on postprandial hyperinsulinemic hypoglycemia after bariatric surgery. Surg Obes Relat Dis. 2017;13(3):371-378. 268. Stephansson O, Johansson K, Naslund I, Neovius M. Bariatric Surgery and Preterm Birth. N Engl J Med. 2016;375(8):805-806. 269. Maluenda F, Csendes A, De Aretxabala X, et al. Alcohol absorption modification after a laparoscopic sleeve gastrectomy due to obesity. Obes Surg. 2010;20(6):744-748. 270. Steffen KJ, Engel SG, Pollert GA, Li C, Mitchell JE. Blood alcohol concentrations rise rapidly and dramatically after Roux-en-Y gastric bypass. Surg Obes Relat Dis. 2013;9(3): 470-473. 271. King WC, Chen JY,


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Surgery_Schwartz. KJ, Engel SG, Pollert GA, Li C, Mitchell JE. Blood alcohol concentrations rise rapidly and dramatically after Roux-en-Y gastric bypass. Surg Obes Relat Dis. 2013;9(3): 470-473. 271. King WC, Chen JY, Mitchell JE, et al. Prevalence of alcohol use disorders before and after bariatric surgery. JAMA. 2012;307(23):2516-2525. 272. King WC, Chen JY, Courcoulas AP, et al. Alcohol and other substance use after bariatric surgery: prospective evidence from a U.S. multicenter cohort study. Surg Obes Relat Dis. 2017;13(8):1392-1402. 273. Peterhansel C, Petroff D, Klinitzke G, Kersting A, Wagner B. Risk of completed suicide after bariatric surgery: a systematic review. Obes Rev. 2013;14(5):369-382. 274. Gribsholt SB, Thomsen RW, Svensson E, Richelsen B. Overall and cause-specific mortality after Roux-en-Y gastric bypass surgery: a nationwide cohort study. Surg Obes Relat Dis. 2017;13(4):581-587. 275. Bhatti JA, Nathens AB, Thiruchelvam D, Grantcharov T, Goldstein BI, Redelmeier DA. Self-harm


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Surgery_Schwartz. Roux-en-Y gastric bypass surgery: a nationwide cohort study. Surg Obes Relat Dis. 2017;13(4):581-587. 275. Bhatti JA, Nathens AB, Thiruchelvam D, Grantcharov T, Goldstein BI, Redelmeier DA. Self-harm emergencies after bariatric surgery: a population-based cohort study. JAMA Surg. 2016;151(3):226-232. 276. Courcoulas A. Who, why, and how? Suicide and harmful behaviors after bariatric surgery. Ann Surg. 2017;265(2): 253-254. 277. Tindle HA, Omalu B, Courcoulas A, Marcus M, Hammers J, Kuller LH. Risk of suicide after long-term follow-up from bariatric surgery. Am J Med. 2010;123(11):1036-1042. 278. Parrott J, Frank L, Rabena R, Craggs-Dino L, Isom KA, Greiman L. American Society for Metabolic and Bariatric Surgery integrated health nutritional guidelines for the surgical weight loss patient 2016 update: micronutrients. Surg Obes Relat Dis. 2017;13(5):727-741. 279. Dogan K, Homan J, Aarts EO, de Boer H, van Laarhoven CJ, Berends FJ. Long-term nutritional status in patients following


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Surgery_Schwartz. 2016 update: micronutrients. Surg Obes Relat Dis. 2017;13(5):727-741. 279. Dogan K, Homan J, Aarts EO, de Boer H, van Laarhoven CJ, Berends FJ. Long-term nutritional status in patients following Roux-en-Y gastric bypass surgery. Clin Nutr. 2018;37(2):612-617. 280. Pellitero S, Martinez E, Puig R, et al. Evaluation of vitamin and trace element requirements after sleeve gastrectomy at long term. Obes Surg. 2017;27(7):1674-1682. 281. Brethauer SA, Kothari S, Sudan R, et al. Systematic review on reoperative bariatric surgery: American Society for Metabolic and Bariatric Surgery Revision Task Force. Surg Obes Relat Dis. 2014;10(5):952-972. 282. Field AE, Camargo CA Jr, Ogino S. The merits of subtyping obesity: one size does not fit all. JAMA. 2013; 310(20):2147-2148. 283. Kellogg TA. Revisional bariatric surgery. Surg Clin North Am. 2011;91(6):1353-1371, x. 284. Moshiri M, Osman S, Robinson TJ, Khandelwal S, Bhargava P, Rohrmann CA. Evolution of bariatric surgery: a historical perspective.


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Surgery_Schwartz. bariatric surgery. Surg Clin North Am. 2011;91(6):1353-1371, x. 284. Moshiri M, Osman S, Robinson TJ, Khandelwal S, Bhargava P, Rohrmann CA. Evolution of bariatric surgery: a historical perspective. AJR Am J Roentgenol. 2013;201(1):W40-W48. 285. Switzer NJ, Karmali S, Gill RS, Sherman V. Revisional bariatric surgery. Surg Clin North Am. 2016;96(4):827-842. 286. Ikramuddin S, Livingston EH. New insights on bariatric surgery outcomes. JAMA. 2013;310(22):2401-2402. 287. Kral JG. Selection of patients for anti-obesity surgery. Int J Obes Relat Metab Disord. 2001;25(suppl 1):S107-S112. 288. Zundel N, Hernandez JD. Revisional surgery after restrictive procedures for morbid obesity. Surg Laparosc Endosc Percutan Tech. 2010;20(5):338-343. 289. Fulton C, Sheppard C, Birch D, Karmali S, de Gara C. A comparison of revisional and primary bariatric surgery. Can J Surg. 2017;60(3):205-211. 290. Hallowell PT, Stellato TA, Yao DA, Robinson A, Schuster MM, Graf KN. Should bariatric revisional


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Surgery_Schwartz. C. A comparison of revisional and primary bariatric surgery. Can J Surg. 2017;60(3):205-211. 290. Hallowell PT, Stellato TA, Yao DA, Robinson A, Schuster MM, Graf KN. Should bariatric revisional surgery be avoided secondary to increased morbidity and mortality? Am J Surg. 2009;197(3):391-396. 291. Sarr MG. Reoperative bariatric surgery. Surg Endosc. 2007;21(11):1909-1913. 292. van Gemert WG, van Wersch MM, Greve JW, Soeters PB. Revisional surgery after failed vertical banded gastroplasty: restoration of vertical banded gastroplasty or conversion to gastric bypass. Obes Surg. 1998;8(1):21-28. 293. Gagne DJ, Dovec E, Urbandt JE. Laparoscopic revision of vertical banded gastroplasty to Roux-en-Y gastric bypass: outcomes of 105 patients. Surg Obes Relat Dis. 2011;7(4):493-499.Brunicardi_Ch27_p1167-p1218.indd 121723/02/19 2:21 PM 1218SPECIFIC CONSIDERATIONSPART II 294. Schouten R, Wiryasaputra DC, van Dielen FM, van Gemert WG, Greve JW. Influence of reoperations on long-term quality


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Surgery_Schwartz. 121723/02/19 2:21 PM 1218SPECIFIC CONSIDERATIONSPART II 294. Schouten R, Wiryasaputra DC, van Dielen FM, van Gemert WG, Greve JW. Influence of reoperations on long-term quality of life after restrictive procedures: a prospective study. Obes Surg. 2011;21(7):871-879. 295. Foletto M, Prevedello L, Bernante P, et al. Sleeve gastrectomy as revisional procedure for failed gastric banding or gastroplasty. Surg Obes Relat Dis. 2010;6(2):146-151. 296. Dapri G, Cadiere GB, Himpens J. Laparoscopic conversion of adjustable gastric banding and vertical banded gastroplasty to duodenal switch. Surg Obes Relat Dis. 2009;5(6):678-683. 297. Coblijn UK, Verveld CJ, van Wagensveld BA, Lagarde SM. Laparoscopic Roux-en-Y gastric bypass or laparoscopic sleeve gastrectomy as revisional procedure after adjustable gastric band--a systematic review. Obes Surg. 2013;23(11):1899-1914. 298. Aarts EO, Dogan K, Koehestanie P, Janssen IM, Berends FJ. What happens after gastric band removal without additional


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Surgery_Schwartz. gastric band--a systematic review. Obes Surg. 2013;23(11):1899-1914. 298. Aarts EO, Dogan K, Koehestanie P, Janssen IM, Berends FJ. What happens after gastric band removal without additional bariatric surgery? Surg Obes Relat Dis. 2014;10(6):1092-1096. 299. Ardestani A, Lautz DB, Tavakkolizadeh A. Band revision versus Roux-en-Y gastric bypass conversion as salvage operation after laparoscopic adjustable gastric banding. Surg Obes Relat Dis. 2011;7(1):33-37. 300. Lanthaler M, Mittermair R, Erne B, Weiss H, Aigner F, Nehoda H. Laparoscopic gastric re-banding versus laparoscopic gastric bypass as a rescue operation for patients with pouch dilatation. Obes Surg. 2006;16(4):484-487. 301. Muller MK, Attigah N, Wildi S, et al. High secondary failure rate of rebanding after failed gastric banding. Surg Endosc. 2008;22(2):448-453. 302. Obeid NR, Schwack BF, Kurian MS, Ren-Fielding CJ, Fielding GA. Single-stage versus 2-stage sleeve gastrectomy as a conversion after failed adjustable gastric


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Surgery_Schwartz. Surg Endosc. 2008;22(2):448-453. 302. Obeid NR, Schwack BF, Kurian MS, Ren-Fielding CJ, Fielding GA. Single-stage versus 2-stage sleeve gastrectomy as a conversion after failed adjustable gastric banding: 30-day outcomes. Surg Endosc. 2014;28(11):3186-3192. 303. Van Nieuwenhove Y, Ceelen W, Van Renterghem K, Van de Putte D, Henckens T, Pattyn P. Conversion from band to bypass in two steps reduces the risk for anastomotic strictures. Obes Surg. 2011;21(4):501-505. 304. Switzer NJ & Karmali S. The sleeve gastrectomy and how and why it can fail? Surg Curr Res 2014;4:180. 2014;4:180. SNKSTsgahawicfSCR. 305. Eid GM, Brethauer S, Mattar SG, Titchner RL, Gourash W, Schauer PR. Laparoscopic sleeve gastrectomy for super obese patients: forty-eight percent excess weight loss after 6 to 8 years with 93% follow-up. Ann Surg. 2012;256(2):262-265. 306. Carmeli I, Golomb I, Sadot E, Kashtan H, Keidar A. Laparoscopic conversion of sleeve gastrectomy to a biliopancreatic diversion with duodenal


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Surgery_Schwartz. with 93% follow-up. Ann Surg. 2012;256(2):262-265. 306. Carmeli I, Golomb I, Sadot E, Kashtan H, Keidar A. Laparoscopic conversion of sleeve gastrectomy to a biliopancreatic diversion with duodenal switch or a Roux-en-Y gastric bypass due to weight loss failure: our algorithm. Surg Obes Relat Dis. 2015;11(1):79-85. 307. Cheung D, Switzer NJ, Gill RS, Shi X, Karmali S. Revisional bariatric surgery following failed primary laparoscopic sleeve gastrectomy: a systematic review. Obes Surg. 2014; 24(10):1757-1763. 308. Nedelcu M, Noel P, Iannelli A, Gagner M. Revised sleeve gastrectomy (re-sleeve). Surg Obes Relat Dis. 2015;11(6): 1282-1288. 309. Dykstra M SN, et al. Roux-en-Y gastric bypass: how and why it fails? Surg Curr Res. 2014;4:165. 310. Tsai WS, Inge TH, Burd RS. Bariatric surgery in adolescents: recent national trends in use and in-hospital outcome. Arch Pediatr Adolesc Med. 2007;161(3):217-221. 311. Zwintscher NP, Azarow KS, Horton JD, Newton CR, Martin MJ. The increasing


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Surgery_Schwartz. in adolescents: recent national trends in use and in-hospital outcome. Arch Pediatr Adolesc Med. 2007;161(3):217-221. 311. Zwintscher NP, Azarow KS, Horton JD, Newton CR, Martin MJ. The increasing incidence of adolescent bariatric surgery. J Pediatr Surg. 2013;48(12):2401-2407. 312. Treadwell JR, Sun F, Schoelles K. Systematic review and meta-analysis of bariatric surgery for pediatric obesity. Ann Surg. 2008;248(5):763-776. 313. Michalsky M, Reichard K, Inge T, et al. ASMBS pediatric committee best practice guidelines. Surg Obes Relat Dis. 2012;8(1):1-7. 314. Inge TH, Zeller M, Harmon C, et al. Teen-Longitudinal Assessment of Bariatric Surgery: methodological features of the first prospective multicenter study of adolescent bariatric surgery. J Pediatr Surg. 2007;42(11):1969-1971. 315. Inge TH, Zeller MH, Jenkins TM, et al. Perioperative outcomes of adolescents undergoing bariatric surgery: the Teen-Longitudinal Assessment of Bariatric Surgery (Teen-LABS) study. JAMA Pediatr.


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Surgery_Schwartz. TH, Zeller MH, Jenkins TM, et al. Perioperative outcomes of adolescents undergoing bariatric surgery: the Teen-Longitudinal Assessment of Bariatric Surgery (Teen-LABS) study. JAMA Pediatr. 2014;168(1):47-53. 316. Bariatric Surgery for Adolescents and Young Adults: A Review of Comparative Clinical Effec-tiveness, Cost-Effectiveness, and Evidence-Based Guidelines [Internet]. Ottawa (ON): Canadian Agency for Drugs and Technologies in Health; 2016 Aug 3. 317. Klebanoff MJ, Chhatwal J, Nudel JD, Corey KE, Kaplan LM, Hur C. Cost-effectiveness of bariatric surgery in adolescents with obesity. JAMA Surg. 2017;152(2):136-141. 318. Sampalis JS, Liberman M, Auger S, Christou NV. The impact of weight reduction surgery on health-care costs in morbidly obese patients. Obes Surg. 2004;14(7):939-947. 319. Cremieux PY, Buchwald H, Shikora SA, Ghosh A, Yang HE, Buessing M. A study on the economic impact of bariatric surgery. Am J Manag Care. 2008;14(9):589-596. 320. Finkelstein EA, Allaire BT,


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Surgery_Schwartz. PY, Buchwald H, Shikora SA, Ghosh A, Yang HE, Buessing M. A study on the economic impact of bariatric surgery. Am J Manag Care. 2008;14(9):589-596. 320. Finkelstein EA, Allaire BT, Burgess SM, Hale BC. Financial implications of coverage for laparoscopic adjustable gastric banding. Surg Obes Relat Dis. 2011;7(3):295-303. 321. Neovius M, Narbro K, Keating C, et al. Health care use during 20 years following bariatric surgery. JAMA. 2012;308(11):1132-1141. 322. Weiner JP, Goodwin SM, Chang HY, et al. Impact of bariatric surgery on health care costs of obese persons: a 6-year follow-up of surgical and comparison cohorts using health plan data. JAMA Surg. 2013;148(6):555-562. 323. Picot J, Jones J, Colquitt JL, et al. The clinical effectiveness and cost-effectiveness of bariatric (weight loss) surgery for obesity: a systematic review and economic evaluation. Health Technol Assess. 2009;13(41):1-190, 215-357, iii-iv. 324. Padwal R, Klarenbach S, Wiebe N, et al. Bariatric surgery: a


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Surgery_Schwartz. loss) surgery for obesity: a systematic review and economic evaluation. Health Technol Assess. 2009;13(41):1-190, 215-357, iii-iv. 324. Padwal R, Klarenbach S, Wiebe N, et al. Bariatric surgery: a systematic review of the clinical and economic evidence. J Gen Intern Med. 2011;26(10):1183-1194. 325. Blondet JJ, Morton JM, Nguyen NT. Hospital accreditation and bariatric surgery: is it important? Adv Surg. 2015;49:123-129. 326. Surgery, A. C. o. S. a. A. S. f. M. a. B. (2016). Standards Manual V2.0: Resources for Optimal Care of the Metabolic and bariatric Surgery patient 2016 (pp. 1-62). https://www.facs.org/quality-programs/mbsaqip: American College of Surgery. 327. Azagury D, Morton JM. Bariatric surgery outcomes in us accredited vs non-accredited centers: a systematic review. J Am Coll Surg. 2016;223(3):469-477. 328. Froylich D, Corcelles R, Daigle CR, et al. Weight loss is higher among patients who undergo body contouring procedures after bariatric surgery. Surg Obes Relat Dis.


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Surgery_Schwartz. Surg. 2016;223(3):469-477. 328. Froylich D, Corcelles R, Daigle CR, et al. Weight loss is higher among patients who undergo body contouring procedures after bariatric surgery. Surg Obes Relat Dis. 2016;12(9):1731-1736. 329. Hurwitz DJ. Body contouring surgery in the bariatric surgical patient. In: Operative Techniques in Plastic Surgery and Reconstructive Surgery. New York: Elsevier; 2002:87. 330. Hurwitz DJ. Single-staged total body lift after massive weight loss. Ann Plast Surg. 2004;52(5):435-441; discussion 441. 331. Balague N, Combescure C, Huber O, Pittet-Cuenod B, Modarressi A. Plastic surgery improves long-term weight control after bariatric surgery. Plast Reconstruct Surg. 2013;132(4):826-833.Brunicardi_Ch27_p1167-p1218.indd 121823/02/19 2:21 PM


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Surgery_Schwartz. Small IntestineAli Tavakkoli, Stanley W. Ashley, and Michael J. Zinner 28chapterINTRODUCTORY COMMENTSThe small intestine is a remarkable and complex organ that is not only the principle site of nutrient digestion and absorption but also contains the body’s largest reservoir of immunologi-cally active and hormone-producing cells. Hence, it can be con-ceptualized as the largest organ of the immune and endocrine systems.1 It achieves this diversity of action through unique anatomical features, which provide it with a massive sur-face area, a diversity of cell types, and a complex neural network to coordinate these functions.Despite the size and importance of the small intestine, diseases of this organ are relatively infrequent and can present diagnostic and therapeutic challenges. Despite introduction of novel imaging techniques such as capsule endoscopy and dou-ble balloon endoscopy, diagnostic tests lack sufficient ability to reliably assess the small bowel. Furthermore, few


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Surgery_Schwartz. Despite introduction of novel imaging techniques such as capsule endoscopy and dou-ble balloon endoscopy, diagnostic tests lack sufficient ability to reliably assess the small bowel. Furthermore, few high-quality, controlled data on the efficacy of surgical therapies for small bowel diseases are available.1Therefore, sound clinical judgment and a thorough under-standing of anatomy, physiology, and pathophysiology remain essential to the care of patients with suspected small bowel disorders.GROSS ANATOMYThe small intestine is a tubular structure that extends from the pylorus to the cecum. The estimated length varies depending on whether radiologic, surgical, or autopsy measurements are made. In the living, it is thought to measure 4 to 6 meters.2 The small intestine consists of three segments lying in series: the duodenum, the jejunum, and the ileum. The duodenum, the most proximal segment, lies in the retroperitoneum immediately adja-cent to the head and inferior border of the body of


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Surgery_Schwartz. lying in series: the duodenum, the jejunum, and the ileum. The duodenum, the most proximal segment, lies in the retroperitoneum immediately adja-cent to the head and inferior border of the body of the pancreas. The duodenum is demarcated from the stomach by the pylorus and from the jejunum by the ligament of Treitz. The jejunum and ileum lie within the peritoneal cavity and are tethered to the Introductory Comments1219Gross Anatomy1219Histology1220Development1221Physiology1222Digestion and Absorption / 1222Barrier and Immune Function / 1225Motility / 1226Endocrine Function / 1227Intestinal Adaptation / 1228Small Bowel Obstruction1228Epidemiology / 1228Pathophysiology / 1229Clinical Presentation / 1229Diagnosis / 1229Therapy / 1231Outcomes / 1232Prevention / 1233Other Causes of Small Bowel Obstruction / 1233Ileus and Other Disorders of Intestinal Motility1233Pathophysiology / 1233Clinical Presentation / 1234Diagnosis / 1234Therapy / 1234Crohn’s Disease1235Pathophysiology /


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Surgery_Schwartz. Small Bowel Obstruction / 1233Ileus and Other Disorders of Intestinal Motility1233Pathophysiology / 1233Clinical Presentation / 1234Diagnosis / 1234Therapy / 1234Crohn’s Disease1235Pathophysiology / 1235Clinical Presentation / 1236Diagnosis / 1237Therapy / 1238Outcomes / 1240Intestinal Fistulas1240Pathophysiology / 1240Clinical Presentation / 1240Diagnosis / 1240Therapy / 1241Outcomes / 1241Small Bowel Neoplasms1241Pathophysiology / 1242Clinical Presentation / 1243Diagnosis / 1243Therapy / 1244Outcomes / 1245Radiation Enteritis1245Pathophysiology / 1245Clinical Presentation / 1245Diagnosis / 1245Therapy / 1246Outcomes / 1246Prevention / 1246Meckel’s Diverticula1246Pathophysiology / 1246Clinical Presentation / 1247Diagnosis / 1247Therapy / 1248Acquired Diverticula1248Pathophysiology / 1249Clinical Presentation / 1250Diagnosis / 1250Therapy / 1250Mesenteric Ischemia1250Miscellaneous Conditions1250Obscure GI Bleeding / 1250Small Bowel Perforation / 1251Chylous Ascites /


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Surgery_Schwartz. / 1249Clinical Presentation / 1250Diagnosis / 1250Therapy / 1250Mesenteric Ischemia1250Miscellaneous Conditions1250Obscure GI Bleeding / 1250Small Bowel Perforation / 1251Chylous Ascites / 1252Intussusception / 1253Pneumatosis Intestinalis / 1253Short Bowel Syndrome1254Pathophysiology / 1254Therapy / 1255Outcomes / 1255Brunicardi_Ch28_p1219-p1258.indd 121923/02/19 2:24 PM 1220JejunumIleumKey Points1 The small intestine performs a diverse set of functions.2 Small bowel obstruction is one of the most common surgical diagnoses.3 Most cases of small bowel obstruction are due to adhe-sions from previous surgery and resolve with conservative management.4 Tumors and malignancies of the small bowel are rare and difficult to diagnose. 5 If following surgical resection less than 200 cm of small bowel remains, patients are at risk of developing short bowel syndrome.retroperitoneum by a broad-based mesentery. No distinct ana-tomical landmark demarcates the jejunum from the ileum; the proximal


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Surgery_Schwartz. bowel remains, patients are at risk of developing short bowel syndrome.retroperitoneum by a broad-based mesentery. No distinct ana-tomical landmark demarcates the jejunum from the ileum; the proximal 40% of the jejunoileal segment is arbitrarily defined as the jejunum and the distal 60% as the ileum. The ileum is demarcated from the cecum by the ileocecal valve.The small intestine contains internal mucosal folds known as plicae circulares or valvulae conniventes that are visible upon gross inspection. These folds are also visible radiographically and help in the distinction between small intestine and colon, which does not contain them, on abdominal radiographs. These folds are more prominent in the proximal intestine than in the distal small intestine. Other features evident on gross inspection that are more characteristic of the proximal than distal small intestine include larger circumference, thicker wall, less fatty mesentery, and longer vasa recta (Fig. 28-1). Gross examination


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Surgery_Schwartz. that are more characteristic of the proximal than distal small intestine include larger circumference, thicker wall, less fatty mesentery, and longer vasa recta (Fig. 28-1). Gross examination of the small-intestinal mucosa also reveals aggregates of lymphoid follicles. Those follicles, located in the ileum, are the most prominent and are designated Peyer’s patches.Most of the duodenum derives its arterial blood from branches of both the celiac and the superior mesenteric arteries. The distal duodenum, the jejunum, and the ileum derive their arterial blood from the superior mesenteric artery. Their venous drainage occurs via the superior mesenteric vein. Lymph drain-age occurs through lymphatic vessels coursing parallel to corre-sponding arteries. This lymph drains through mesenteric lymph nodes to the cisterna chyli, then through the thoracic duct, and ultimately into the left subclavian vein. The parasympathetic and sympathetic innervation of the small intestine is derived from the


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Surgery_Schwartz. nodes to the cisterna chyli, then through the thoracic duct, and ultimately into the left subclavian vein. The parasympathetic and sympathetic innervation of the small intestine is derived from the vagus and splanchnic nerves, respectively.HISTOLOGYThe wall of the small intestine consists of four distinct layers: mucosa, submucosa, muscularis propria, and serosa (Fig. 28-2).The mucosa is the innermost layer and it consists of three layers: epithelium, lamina propria, and muscularis mucosae. The epithelium is exposed to the intestinal lumen and is the surface through which absorption from and secretion into the lumen occurs. The lamina propria is located immediately external to the epithelium and consists of connective tissue and a heterogeneous population of cells. It is demarcated from the more external submucosa by the muscularis mucosae, a thin sheet of smooth muscle cells.The mucosa is organized into villi and crypts (crypts of Lieberkuhn). Villi are finger-like projections of


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Surgery_Schwartz. the more external submucosa by the muscularis mucosae, a thin sheet of smooth muscle cells.The mucosa is organized into villi and crypts (crypts of Lieberkuhn). Villi are finger-like projections of epithelium and underlying lamina propria that contain blood and lymphatic (lacteals) vessels that extend into the intestinal lumen. Intes-tinal, epithelial cellular proliferation is confined to the crypts, each of which carries 250 to 300 cells. All epithelial cells in each crypt are derived from an unknown number of multipotent stem cells located at or near the crypt’s base. Our understanding of these crypt cells is rapidly expanding. It appears that there are two subgroups of intestinal stem cells, with specific cell markers. Bmi1-positive cells are usually quiescent, radiation-resistant cells that are induced by injury, while LGR5-positive cells facilitate homeostatic vs. injury-induced regeneration and are radiation sensitive.3The stem cells can differentiate along one of four path-ways


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Surgery_Schwartz. that are induced by injury, while LGR5-positive cells facilitate homeostatic vs. injury-induced regeneration and are radiation sensitive.3The stem cells can differentiate along one of four path-ways that ultimately yield enterocytes and goblet, enteroendo-crine, and Paneth cells. Except for Paneth cells, these lineages complete their terminal differentiation during an upward migra-tion from each crypt to adjacent villi. The journey from the crypt to the villus tip is completed in 2 to 5 days and terminates with cells being removed by apoptosis and/or exfoliation. Thus, the small-intestinal epithelium undergoes continuous renewal, mak-ing it one of the body’s most dynamic tissues. The high cellular turnover rate contributes to mucosal resiliency but also makes the intestine uniquely susceptible to certain forms of injury such as that induced by radiation and chemotherapy.Figure 28-1. Gross features of jejunum contrasted with those of ileum. Relative to the ileum, the jejunum has a


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Surgery_Schwartz. to certain forms of injury such as that induced by radiation and chemotherapy.Figure 28-1. Gross features of jejunum contrasted with those of ileum. Relative to the ileum, the jejunum has a larger diameter, a thicker wall, more prominent plicae circulares, a less fatty mesentery, and longer vasa recta.Brunicardi_Ch28_p1219-p1258.indd 122023/02/19 2:24 PM 1221SMALL INTESTINECHAPTER 284. MucosaCircular layerLongitudinallayer2. Muscularis propriaSubserous layer1. SerosaVascular network,longisection of villusSimple columnar epitheliumwith mucous cellsLamina propria,smooth muscle cells, blood vesselsCentral lymph capillary (lacteal)Muscularis mucosae3. Submucosa4321Opening of crypts (of Lieberkühn)Figure 28-2. Layers of wall of the small intestine. The individual layers and their prominent features are repre-sented schematically.Enterocytes are the predominant absorptive cell of the intestinal epithelium. Their apical (lumen-facing) cell mem-brane contains specialized digestive


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Surgery_Schwartz. features are repre-sented schematically.Enterocytes are the predominant absorptive cell of the intestinal epithelium. Their apical (lumen-facing) cell mem-brane contains specialized digestive enzymes, transporter mechanisms, and microvilli that are estimated to increase the absorptive surface area of the small intestine by up to 40-fold. Goblet cells produce mucin believed to play a role in mucosal defense against pathogens. Enteroendocrine cells are charac-terized by secretory granules containing regulatory agents and are discussed in greater detail in the “Endocrine Function” section. Paneth cells are located at the base of the crypt and contain secretory granules containing growth factors, diges-tive enzymes, and antimicrobial peptides, through which they control the host-microbe interaction and influence the intestinal microbiome. In addition, the intestinal epithelium contains M cells and intraepithelial lymphocytes. These two components of the immune system are discussed in


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Surgery_Schwartz. and influence the intestinal microbiome. In addition, the intestinal epithelium contains M cells and intraepithelial lymphocytes. These two components of the immune system are discussed in this chapter.The submucosa consists of dense connective tissue and a heterogeneous population of cells, including leukocytes and fibroblasts. The submucosa also contains an extensive network of vascular and lymphatic vessels, nerve fibers, and ganglion cells of the submucosal (Meissner’s) plexus.The muscularis propria consists of an outer, longitudinally-oriented layer and an inner, circularly-oriented layer of smooth muscle fibers. Located at the interface between these two layers are ganglion cells of the myenteric (Auerbach’s) plexus.The serosa consists of a single layer of mesothelial cells and is a component of the visceral peritoneum.DEVELOPMENTThe first recognizable precursor of the small intestine is the embryonic gut tube, formed from the endoderm during the fourth week of gestation. The


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Surgery_Schwartz. a component of the visceral peritoneum.DEVELOPMENTThe first recognizable precursor of the small intestine is the embryonic gut tube, formed from the endoderm during the fourth week of gestation. The gut tube is divided into forgut, midgut, and hindgut. Other than the duodenum, which is a forgut structure, the rest of the small intestine is derived from the midgut. The gut tube initially communicates with the yolk sac; however, the communication between these two struc-tures narrows by the sixth week to form the vitelline duct. The yolk sac and vitelline duct usually undergo obliteration by the end of gestation. Incomplete obliteration of the vitelline duct results in the spectrum of defects associated with Meckel’s diverticuli.Also during the fourth week of gestation, the mesoderm of the embryo splits. The portion of mesoderm that adheres to the endoderm forms the visceral peritoneum, while the portion that adheres to the ectoderm forms the parietal peritoneum. This mesodermal


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Surgery_Schwartz. of the embryo splits. The portion of mesoderm that adheres to the endoderm forms the visceral peritoneum, while the portion that adheres to the ectoderm forms the parietal peritoneum. This mesodermal division results in the formation of a coelomic cav-ity that is the precursor of the peritoneal cavity.At approximately the fifth week of gestation, the bowel begins to lengthen to an extent greater than that which can be accommodated by the developing abdominal cavity, resulting in the extracoelomic herniation of the developing bowel. The bowel continues to lengthen during the subsequent weeks and is retracted back into the abdominal cavity during the tenth week of gestation. Subsequently, the duodenum becomes a retroperitoneal structure. Coincident with extrusion and retraction, the bowel undergoes a 270° counterclockwise rotation relative to the posterior abdominal wall. This rotation accounts for the usual locations of the cecum in the right lower quadrant and the duodenojejunal


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Surgery_Schwartz. undergoes a 270° counterclockwise rotation relative to the posterior abdominal wall. This rotation accounts for the usual locations of the cecum in the right lower quadrant and the duodenojejunal junction to the left of midline (Fig. 28-3).The celiac and superior mesenteric arteries and veins are derived from the vitelline vascular system, which in turn is derived from blood vessels formed within the splanchnopleuric mesoderm during the third week of gestation. Neurons found in the small intestine are derived from neural crest cells that begin to migrate away from the neural tube during the third week of gestation. These neural crest cells enter the mesenchyme of the primitive foregut and subsequently migrate to the remainder of the bowel.During the sixth week of gestation, the lumen of the developing bowel becomes obliterated as bowel epithelial proliferation accelerates. Vacuoles form within the bowel substance during the subsequent weeks and coalesce to form the intestinal lumen by


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Surgery_Schwartz. developing bowel becomes obliterated as bowel epithelial proliferation accelerates. Vacuoles form within the bowel substance during the subsequent weeks and coalesce to form the intestinal lumen by the ninth week of gestation. Errors in this recanalization may account for defects such as intestinal webs and stenoses. Most intestinal atresias, however, are believed to be related to ischemic episodes occurring after organogenesis has been completed rather than to errors in recanalization.During the ninth week of gestation, the intestinal epithe-lium develops intestine-specific features such as crypt-villus architecture. Organogenesis is complete by approximately the twelfth week of gestation.Brunicardi_Ch28_p1219-p1258.indd 122123/02/19 2:24 PM 1222SPECIFIC CONSIDERATIONSPART IIStomachDuodenumProximal limb of prim.intestinal loopVitelline ductDistal limb of prim. intestinal loopSuperiormesentericarteryStomachTransverse colonCecal budVitelline ductAscending colonJejunoileal


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Surgery_Schwartz. limb of prim.intestinal loopVitelline ductDistal limb of prim. intestinal loopSuperiormesentericarteryStomachTransverse colonCecal budVitelline ductAscending colonJejunoileal loopsACDuodenumCecal budTransverse colonSmall intestineHepatic flextureAppendixTransversecolonDescending colonSigmoidcolonCecumBDFigure 28-3. Developmental rotation of the intestine. A. During the fifth week of gestation, the developing intestine herniates out of the coelomic cavity and begins to undergo a counterclockwise rotation about the axis of the superior mesenteric artery. B and C. Intestinal rotation continues, as the developing transverse colon passes anterior to the developing duodenum. D. Final positions of the small intestine and colon resulting from a 270° counterclockwise rotation of the developing intestine and its return into the abdominal cavity.• Oral intake 2000 mL• Saliva 1500 mL• Gastric secretions 2500• Bile 500 mL• Pancreatic secretions 1500 mL• Small intestinal secretions 1000 mL•


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Surgery_Schwartz. intestine and its return into the abdominal cavity.• Oral intake 2000 mL• Saliva 1500 mL• Gastric secretions 2500• Bile 500 mL• Pancreatic secretions 1500 mL• Small intestinal secretions 1000 mL• Small intestinal absorption 7500 mL•1500 mL to colonFigure 28-4. Small intestinal fluid fluxes. Typical quantities (in volume per day) of fluid entering and leaving the small intestinal lumen in a healthy adult are shown.PHYSIOLOGYDigestion and AbsorptionThe intestinal epithelium is the interface through which absorp-tion and secretion occur. It has features characteristic of absorp-tive epithelia in general, including epithelial cells with cellular membranes possessing distinct apical (luminal) and basolateral (serosal) domains demarcated by intercellular tight junctions and an asymmetric distribution of transmembrane transporter mechanisms that promotes vectorial transport of solutes across the epithelium.Solutes can traverse the epithelium by active or passive transport. Passive


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Surgery_Schwartz. distribution of transmembrane transporter mechanisms that promotes vectorial transport of solutes across the epithelium.Solutes can traverse the epithelium by active or passive transport. Passive transport of solutes occurs through diffusion or convection and is driven by existing electrochemical gradi-ents. Active transport is the energy-dependent net transfer of solutes in the absence of or against an electrochemical gradient.Active transport occurs through transcellular pathways (through the cell), whereas passive transport can occur through either transcellular or paracellular pathways (between cells through the tight junctions). Transcellular transport requires solutes to traverse the cell membranes through specialized membrane proteins, such as channels, carriers, and pumps. The molecular characterization of transporter proteins is evolving rapidly, with different transporter families, each containing many individual genes encoding specific transporters, now identified.


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Surgery_Schwartz. The molecular characterization of transporter proteins is evolving rapidly, with different transporter families, each containing many individual genes encoding specific transporters, now identified. Similarly, understanding of the paracellular pathway is evolving. In contrast to what was once believed, it is becoming apparent that paracellular permeability is substrate-specific, dynamic, and subject to regulation by specific tight junction proteins.Water and Electrolyte Absorption and Secretion. Eight to 9 L of fluid enter the small intestine daily. Most of this volume consists of salivary, gastric, biliary, pancreatic, and intestinal secretions. Under normal conditions, the small intestine absorbs over 80 percent of this fluid, leaving approximately 1.5 L that enters the colon (Fig. 28-4). Small-intestinal absorption and secretion are tightly regulated; derangements in water and electrolyte homeostasis characteristic of many of the disorders discussed in this chapter play an


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Surgery_Schwartz. 28-4). Small-intestinal absorption and secretion are tightly regulated; derangements in water and electrolyte homeostasis characteristic of many of the disorders discussed in this chapter play an important role in contributing to their associated clinical features.Gut epithelia have two pathways for water transport: (a) the paracellular route, which involves transport through the spaces between cells, (b) the transcellular route, through apical and the basolateral cell membranes, with most occurring through Brunicardi_Ch28_p1219-p1258.indd 122223/02/19 2:24 PM 1223SMALL INTESTINECHAPTER 28the transcellular pathway.4 The specific transport mechanisms mediating this transcellular transport are not completely char-acterized, and they may involve passive diffusion through the phospholipid bilayer, cotransport with other ions and nutrients, or diffusion through water channels called aquaporins. Many different types of aquaporins have been identified; however, their contribution to


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Surgery_Schwartz. bilayer, cotransport with other ions and nutrients, or diffusion through water channels called aquaporins. Many different types of aquaporins have been identified; however, their contribution to overall intestinal water absorption appears to be relatively minor.5The prevailing model for intestinal epithelial Na+ absorp-tion is shown in Fig. 28-5. Activity of the Na+/K+ ATPase enzyme, which is located in the basolateral membrane and exchanges three intracellular Na+ for every two extracellular K+ in an energy-dependent process, generates the electrochemi-cal gradient that drives the transport of Na+ from the intestinal lumen into the cytoplasm of enterocytes. Na+ ions traverse the apical membrane through several distinct transporter mecha-nisms, including nutrient-coupled sodium transport (e.g., sodium glucose cotransporter-1, SGLT1), sodium channels, and sodium-hydrogen exchangers (NHEs). Absorbed Na+ ions are then extruded from enterocytes through the Na+/K+ ATPase located in the


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Surgery_Schwartz. (e.g., sodium glucose cotransporter-1, SGLT1), sodium channels, and sodium-hydrogen exchangers (NHEs). Absorbed Na+ ions are then extruded from enterocytes through the Na+/K+ ATPase located in the basolateral membrane. Similar mechanistic mod-els that account for the transport of other common ions such as K+ and HCO3also exist.Substantial heterogeneity, with respect to both crypt-villus and craniocaudal axes, exists for intestinal epithelial transport mechanisms. This spatial distribution pattern is consistent with a model in which absorptive function resides primarily in the villus and secretory function in the crypt.Intestinal absorption and secretion are subject to modu-lation under physiologic and pathophysiologic conditions by a wide array of hormonal, neural, and immune regulatory media-tors (Table 28-1).Carbohydrate Digestion and Absorption. Approximately 45% of energy consumption in the average Western diet con-sists of carbohydrates, approximately one-half of which is in the


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Surgery_Schwartz. (Table 28-1).Carbohydrate Digestion and Absorption. Approximately 45% of energy consumption in the average Western diet con-sists of carbohydrates, approximately one-half of which is in the form of starch (linear or branched polymers of glucose) derived from cereals and plants. Other major sources of dietary carbo-hydrates include sugars derived from milk (lactose), fruits and LUMEN –BLOOD +Na+GlucoseNa+K+Na+Na+H+Figure 28-5. Model of transepithelial Na+ absorption. Na+ traverses the apical membrane of enterocytes through a variety mechanisms, including nutrient-coupled Na+ transport, Na+/H+ exchange, and Na+ channels. Activity of the Na+/K+ATPase located on the basolateral membrane generates the electrochemical gradient that provides the driving force for Na+ absorption.Table 28-1Regulation of intestinal absorption and secretionAgents that stimulate absorption or inhibit secretion of


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Surgery_Schwartz. the electrochemical gradient that provides the driving force for Na+ absorption.Table 28-1Regulation of intestinal absorption and secretionAgents that stimulate absorption or inhibit secretion of water Aldosterone Glucocorticoids Angiotensin Norepineprhine Epinephrine Dopamine Somatostatin Neuropeptide Y Peptide YY EnkephalinAgents that simulate secretion or inhibit absorption of water Secretin Bradykinin Prostaglandins Acetylcholine Atrial natriuretic factor Vasopressin Vasoactive intestinal peptide Bombesin Substance P Serotonin Neurotensin Histaminevegetables (fructose, glucose, and sucrose), or purified from sugar cane or beets (sucrose). Processed foods contain a vari-ety of sugars including fructose, oligosaccharides, and polysac-charides. Glycogen derived from meat contributes only a small fraction of dietary carbohydrate.Pancreatic amylase is the major enzyme of starch diges-tion, although salivary amylase initiates the process. The ter-minal products of amylase-mediated


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Surgery_Schwartz. only a small fraction of dietary carbohydrate.Pancreatic amylase is the major enzyme of starch diges-tion, although salivary amylase initiates the process. The ter-minal products of amylase-mediated starch digestion are oligosaccharides, maltotriose, maltose, and alpha-limit dextrins (Fig. 28-6). These products, as well as the major disaccharides in the diet (sucrose and lactose), are unable to undergo absorp-tion in this form. They must first undergo hydrolytic cleavage into their constituent monosaccharides; these hydrolytic reac-tions are catalyzed by specific brush border membrane hydro-lases that are expressed most abundantly in the villi of the duodenum and jejunum. The three major monosaccharides that represent the terminal products of carbohydrate digestion are glucose, galactose, and fructose.Under physiologic conditions, most of these sugars are absorbed through the epithelium via the transcellular route. Glucose and galactose are transported through the enterocyte brush


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Surgery_Schwartz. and fructose.Under physiologic conditions, most of these sugars are absorbed through the epithelium via the transcellular route. Glucose and galactose are transported through the enterocyte brush border membrane via intestinal Na+–glucose cotrans-porter, SGLT1 (Fig. 28-7). Fructose is transported through the brush border membrane by facilitated diffusion via GLUT5 (a member of the facilitative glucose transporter family). All three monosaccharides are extruded through the basolateral membrane by facilitated diffusion using GLUT2 and five trans-porters. Extruded monosaccharides diffuse into venules and ulti-mately enter the portal venous system.There is evidence of overexpression of hexose transport-ers, specifically SGLT1, in disease states such as diabetes.6 Several approaches aimed at downregulation of small intestinal Brunicardi_Ch28_p1219-p1258.indd 122323/02/19 2:24 PM 1224SPECIFIC CONSIDERATIONSPART IIGlucose, galactose, fructoseAbsorptionDietary starchSalivary


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Surgery_Schwartz. aimed at downregulation of small intestinal Brunicardi_Ch28_p1219-p1258.indd 122323/02/19 2:24 PM 1224SPECIFIC CONSIDERATIONSPART IIGlucose, galactose, fructoseAbsorptionDietary starchSalivary amylasePancreatic amylaseBrush-border hydrolasesOligosaccharidesMaltotrioseMaltosea-limit dextransSucrose and lactoseFigure 28-6. Carbohydrate digestion. Dietary carbohydrates, including starch and the disaccharides sucrose and lactose, must undergo hydrolysis into constituent monosaccharides glucose, galactose, and fructose before being absorbed by the intestinal epithelium. These hydrolytic reactions are catalyzed by salivary and pancreatic amylase and by enterocyte brush border hydrolases.LUMENTight junctionTight junctionBLOOD SGLT1GLUT5GLUT5GLUT2FructoseFructoseNa+GlucoseGalactoseGlucoseGalactoseNa+Figure 28-7. Hexose transporters. Glucose and galactose enter the enterocyte through secondary active transport via the sodium-glucose cotransporter (SGLT1) located on the apical (brush


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Surgery_Schwartz. 28-7. Hexose transporters. Glucose and galactose enter the enterocyte through secondary active transport via the sodium-glucose cotransporter (SGLT1) located on the apical (brush border) membrane. Fructose enters through facilitated diffusion via glucose transporter 5 (GLUT5). Glucose and galactose are extruded basolaterally through facilitated diffusion via glucose transporter 2 (GLUT2). Fructose is extruded basolaterally via GLUT5.Dipeptides + Tripeptides + Amino acidsAbsorptionDietary proteinsPolypeptidesAmino acidsTrypsinChymotrypsinElastaseCarboxypeptidase ACarboxypeptidase BOligopeptidesBrush-borderpeptidasesAmino acids++PepsinFigure 28-8. Protein digestion. Dietary proteins must undergo hydrolysis into constituent single amino acids and diand tri-peptides before being absorbed by the intestinal epithelium. These hydrolytic reactions are catalyzed by pancreatic peptidases (e.g., trypsin) and by enterocyte brush border peptidases.glucose transporter are being investigated as a


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Surgery_Schwartz. the intestinal epithelium. These hydrolytic reactions are catalyzed by pancreatic peptidases (e.g., trypsin) and by enterocyte brush border peptidases.glucose transporter are being investigated as a novel therapy for disease states such as diabetes and obesity. In fact, recent con-sensus statements have recognized the small bowel as a thera-peutic target for treatment of diabetes.7Protein Digestion and Absorption. Ten percent to 15% of energy consumption in the average Western diet consists of pro-teins. In addition to dietary proteins, approximately one-half of the protein load that enters the small intestine is derived from endogenous sources, including salivary and gastrointestinal secretions and desquamated intestinal epithelial cells. Protein digestion begins in the stomach with action of pepsins. This is not, however, an essential step because surgical patients who are acholorhydric, or have lost part or all their stomach, are still able to successfully digest proteins.


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Surgery_Schwartz. action of pepsins. This is not, however, an essential step because surgical patients who are acholorhydric, or have lost part or all their stomach, are still able to successfully digest proteins. Digestion continues in the duodenum with the actions of a variety of pancreatic peptidases. These enzymes are secreted as inactive proenzymes. This con-trasts with pancreatic amylase and lipase, which are secreted in their active forms. In response to the presence of bile acids, enterokinase is liberated from the intestinal brush border mem-brane to catalyze the conversion of trypsinogen to active tryp-sin; trypsin in turn activates itself and other proteases. The final products of intraluminal protein digestion consist of neutral and basic amino acids and peptides two to six amino acids in length (Fig. 28-8). Additional digestion occurs through the actions of peptidases that exist in the enterocyte brush border and cyto-plasm. Epithelial absorption occurs for both single amino acids and dior


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Surgery_Schwartz. (Fig. 28-8). Additional digestion occurs through the actions of peptidases that exist in the enterocyte brush border and cyto-plasm. Epithelial absorption occurs for both single amino acids and dior tripeptides via specific membrane-bound transporters. Absorbed amino acids and peptides then enter the portal venous circulation.Of all amino acids, glutamine appears to be a unique, major source of energy for enterocytes. Active glutamine uptake into enterocytes occurs through both apical and basolateral transport mechanisms.Fat Digestion and Absorption. Approximately 40% of the average Western diet consists of fat. Over 95% of dietary fat is in the form of long-chain triglycerides; the remainder includes phospholipids such as lecithin, fatty acids, cholesterol, and Brunicardi_Ch28_p1219-p1258.indd 122423/02/19 2:24 PM 1225SMALL INTESTINECHAPTER 28Dietary long-chaintriglyceridesShort& medium-chaintriglyceridesLong-chain fatty acidsand monoglyceridesTriglyceridesresynthesizedin


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Surgery_Schwartz. 122423/02/19 2:24 PM 1225SMALL INTESTINECHAPTER 28Dietary long-chaintriglyceridesShort& medium-chaintriglyceridesLong-chain fatty acidsand monoglyceridesTriglyceridesresynthesizedin enterocytesGastric lipasePancreatic lipaseChyle (lymphatics)Portal venous bloodAbsorbedAbsorbedFigure 28-9. Fat digestion. Long-chain triglycerides, which constitute the majority of dietary fats, must undergo lipolysis into constituent log-chain fatty acids and monoglycerides before being absorbed by the intestinal epithelium. These reactions are catalyzed by gastric and pancreatic lipases. The products of lipolysis are transported in the form of mixed micelles to enterocytes, where they are resynthesized into triglycerides, which are then packaged in the form of chylomicrons that are secreted into the intestinal lymph (chyle). Triglycerides composed of shortand medium-chain fatty acids are absorbed by the intestinal epithelium directly, without undergoing lipolysis, and are secreted into the portal


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Surgery_Schwartz. lymph (chyle). Triglycerides composed of shortand medium-chain fatty acids are absorbed by the intestinal epithelium directly, without undergoing lipolysis, and are secreted into the portal venous circulation.fat-soluble vitamins. Over 94% of the ingested fats are absorbed in the proximal jejunum.Since fats are normally water insoluble, key to success-ful digestion of ingested fats is solubalization of them into an emulsion by the mechanical actions of mastication and antral peristalsis. Although lipolysis of triglycerides to form fatty acids and monoglyciderides is initiated in the stomach by gastric lipase, its principal site is the proximal intestine, where pancre-atic lipase is the catalyst (Fig. 28-9).Bile acids act as detergents that help in solubalization of the lipolysis by forming mixed micelles. These micelles are polymolecular aggregates with a hydrophobic core of fat and a hydrophillic surface that act as shuttles, delivering the products of lipolysis to the enterocyte


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Surgery_Schwartz. mixed micelles. These micelles are polymolecular aggregates with a hydrophobic core of fat and a hydrophillic surface that act as shuttles, delivering the products of lipolysis to the enterocyte brush border membrane, where they are absorbed. The bile salts, however, remain in the bowel lumen and travel to the terminal ileum, where they are actively resorbed. They enter the portal circulation and are resecreted into bile, thus completing the enterohepatic circulation.Dissociation of lipids from the micelles occurs in a thin layer of water (50 to 500 μm thick) with an acidic microenvi-ronment immediately adjacent to the brush border called the unstirred water layer. Most lipids are absorbed in the proxi-mal jejunum, whereas bile salts are absorbed in the distal ileum through an active process. Fatty acid binding proteins (FABP) are a family of proteins located on the brush border membrane, facilitating diffusion of long-chain fatty acids across the brush border membrane. Cholesterol


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Surgery_Schwartz. Fatty acid binding proteins (FABP) are a family of proteins located on the brush border membrane, facilitating diffusion of long-chain fatty acids across the brush border membrane. Cholesterol crosses the brush border mem-brane through an active process that is yet to be completely characterized. Within the enterocytes, triglycerides are resyn-thesized and incorporated into chylomicrons that are secreted into the intestinal lymphatics and ultimately enter the thoracic duct. In these chylomicrons, lipoproteins serve a detergent-like role similar to that served by bile salts in the mixed micelles.The aforementioned steps are required for the digestion and absorption of triglycerides containing long-chain fatty acids. However, triglycerides containing shortand medium-chain fatty acids are more hydrophilic and are absorbed without undergoing intralumenal hydrolysis, micellular solubilization, mucosal reesterification, and chylomicron formation. Instead, they are directly absorbed and


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Surgery_Schwartz. more hydrophilic and are absorbed without undergoing intralumenal hydrolysis, micellular solubilization, mucosal reesterification, and chylomicron formation. Instead, they are directly absorbed and enter the portal venous circula-tion rather than the lymphatics. This information provides the rationale for administering nutritional supplements containing medium-chain triglycerides to patients with gastrointestinal dis-eases associated with impaired digestion and/or malabsorption of long-chain triglycerides.Vitamin and Mineral Absorption. Vitamin B12 (cobalamin) malabsorption can result from a variety of surgical manipula-tions. The vitamin is initially bound by saliva-derived R protein. In the duodenum, R protein is hydrolyzed by pancreatic enzymes, allowing free cobalamin to bind to gastric parietal cell-derived intrinsic factor. The cobalamin-intrinsic factor complex can escape hydrolysis by pancreatic enzymes, allowing it to reach the terminal ileum, which expresses specific


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Surgery_Schwartz. gastric parietal cell-derived intrinsic factor. The cobalamin-intrinsic factor complex can escape hydrolysis by pancreatic enzymes, allowing it to reach the terminal ileum, which expresses specific receptors for intrin-sic factor. Subsequent events in cobalamin absorption are poorly characterized, but the intact complex probably enters enterocytes through translocation. Because each of these steps is necessary for cobalamin assimilation, gastric resection, gastric bypass, and ileal resection can each result in vitamin B12 insufficiency.Other water-soluble vitamins for which specific carrier-mediated transport processes have been characterized include ascorbic acid, folate, thiamine, riboflavin, pantothenic acid, and biotin. Fat-soluble vitamins A, D, and E appear to be absorbed through passive diffusion. Vitamin K appears to be absorbed through both passive diffusion and carrier-mediated uptake.Calcium is absorbed through both transcellular transport and paracellular diffusion. The


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Surgery_Schwartz. passive diffusion. Vitamin K appears to be absorbed through both passive diffusion and carrier-mediated uptake.Calcium is absorbed through both transcellular transport and paracellular diffusion. The duodenum is the major site for transcellular transport; paracellular transport occurs throughout the small intestine. A key step in transcellular calcium transport is mediated by calbindin, a calcium-binding protein located in the cytoplasm of enterocytes. Regulation of calbindin synthesis is the principle mechanism by which vitamin D regulates intes-tinal calcium absorption. Abnormal calcium levels are increas-ingly seen in surgical patients who have undergone a gastric bypass. Although usual calcium supplementation is often in the form of calcium carbonate, which is cheap, in such patients with low acid exposure, calcium citrate is a better formulation for supplemental therapy.Iron and magnesium are each absorbed through both tran-scellular and paracellular routes. A divalent metal


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Surgery_Schwartz. with low acid exposure, calcium citrate is a better formulation for supplemental therapy.Iron and magnesium are each absorbed through both tran-scellular and paracellular routes. A divalent metal transporter capable of transporting Fe2+, Zn2+, Mn2+, Co2+, Cd2+, Cu2+, Ni2+, and Pb2+ that has been localized to the intestinal brush border may account for at least a portion of the transcellular absorption of these ions.8Barrier and Immune FunctionAlthough the intestinal epithelium allows for the efficient absorption of dietary nutrients, it must discriminate between pathogens and harmless antigens such as food proteins and com-mensal bacteria, and it must resist invasion by pathogens. Fac-tors contributing to epithelial defense include immunoglobulin A (IgA), mucins, and the relative impermeability of the brush border membrane and tight junctions to macromolecules and Brunicardi_Ch28_p1219-p1258.indd 122523/02/19 2:24 PM 1226SPECIFIC CONSIDERATIONSPART IIIntestinal lumenPeyer’s


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Surgery_Schwartz. of the brush border membrane and tight junctions to macromolecules and Brunicardi_Ch28_p1219-p1258.indd 122523/02/19 2:24 PM 1226SPECIFIC CONSIDERATIONSPART IIIntestinal lumenPeyer’s patchLamina propriaFAESEDDCGCIgAPlasmacellM cellBVillusTTbacteria. Other factors likely to play important roles in intesti-nal mucosal defense include antimicrobial peptides such as the defensins.9 The intestinal component of the immune system, known as the gut-associated lymphoid tissue (GALT), contains over 70% of the body’s immune cells.The GALT is conceptually divided into inductive and effector sites.10 Inductive sites include Peyer’s patches, mesenteric lymph nodes, and smaller isolated lymphoid follicles scattered throughout the small intestine (Fig. 28-10). Peyer’s patches are macroscopic aggregates of B-cell follicles and intervening T-cell areas found in the lamina propria of the small intestine, primarily the distal ileum. Overlying Peyer’s patches is a specialized epithelium containing


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Surgery_Schwartz. of B-cell follicles and intervening T-cell areas found in the lamina propria of the small intestine, primarily the distal ileum. Overlying Peyer’s patches is a specialized epithelium containing microfold (M) cells. These cells possess an apical membrane with microfolds rather than microvilli, which is characteristic of most intestinal epithelial cells. Using transepithelial vesicular transport, M cells transfer microbes to underlying professional antigen presenting cells (APCs), such as dendritic cells. Dendritic cells, in addition, may sample luminal antigens directly through their dendrite-like processes that extend through epithelial tight junctions. APCs interact with and prime naive lymphocytes, which then exit through the draining lymphatics to enter the mesenteric lymph nodes, where they undergo differentiation. These lymphocytes then migrate into the systemic circulation via the thoracic duct and ultimately accumulate in the intestinal mucosa at effector sites. Alternative


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Surgery_Schwartz. they undergo differentiation. These lymphocytes then migrate into the systemic circulation via the thoracic duct and ultimately accumulate in the intestinal mucosa at effector sites. Alternative induction mechanisms, such as antigen presentation within mesenteric lymph nodes, are also likely to exist.Effector lymphocytes are distributed into distinct compart-ments. IgA-producing plasma cells are derived from B cells and are located in the lamina propria. CD4+ T cells are also located in the lamina propria. CD8+ T cells migrate preferentially to the epithelium, but they are also found in the lamina propria. These T cells are central to immune regulation; in addition, the CD8+ T cells have potent cytotoxic (CTL) activity. IgA is transported through the intestinal epithelial cells into the lumen, where it exists in the form of a dimer complexed with a secretory component. This configuration renders IgA resistant to proteolysis by diges-tive enzymes. IgA is believed to both help prevent


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Surgery_Schwartz. lumen, where it exists in the form of a dimer complexed with a secretory component. This configuration renders IgA resistant to proteolysis by diges-tive enzymes. IgA is believed to both help prevent the entry of microbes through the epithelium and to promote excretion of anti-gens or microbes that have already penetrated the laminal propria.It has been increasingly recognized that the gastrointestinal tract is colonized with many bacteria that are essential for health. Communication between the microbiota and the host defense allows for protective immune responses against pathogens while preventing adverse inflammatory responses to harmless com-mensal microbes, which could lead to chronic inflammatory dis-orders such as celiac disease and Crohn’s disease.11MotilityMyocytes of the intestinal muscle layers are electrically and mechanically coordinated in the form of syncytia. Contractions of the muscularis propria are responsible for small-intestinal peri-stalsis. Contraction of the


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Surgery_Schwartz. muscle layers are electrically and mechanically coordinated in the form of syncytia. Contractions of the muscularis propria are responsible for small-intestinal peri-stalsis. Contraction of the outer longitudinal muscle layer results in bowel shortening; contraction of the inner circular layer results in luminal narrowing. Contractions of the muscularis mucosa contribute to mucosal or villus motility, but not to peristalsis.Several distinctive patterns of muscularis propria activity have been observed to occur in the small intestine. These patterns include ascending excitation and descending inhibition in which muscular contraction occurs proximal to a stimulus, such as the presence of a bolus of ingested food, and muscular relaxation occurs distal to the stimulus (Fig. 28-11). These two reflexes are present even in the absence of any extrinsic innervation to the small intestine and contribute to peristalsis when they are propagated in a coordinated fashion along the length of the


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Surgery_Schwartz. reflexes are present even in the absence of any extrinsic innervation to the small intestine and contribute to peristalsis when they are propagated in a coordinated fashion along the length of the intestine. The fed or postprandial pattern begins within 10 to 20 minutes of meal ingestion and abates 4 to 6 hours afterwards. Rhythmic segmentations or pressure waves traveling only short distances also are observed. This segmenting pattern is hypothesized to assist in mixing intraluminal contents and in facilitating their contact with the absorptive mucosal surface. The fasting pattern or interdigestive motor cycle (IDMC) consists of three phases. Phase 1 is characterized by motor quiescence, phase 2 by seemingly disorganized pressure waves occurring at submaximal rates, and phase 3 by sustained pressure waves occurring at maximal rates. This pattern is hypothesized to expel residual debris and bacteria from the small intestine. The median duration of the IDMC ranges from 90 to 120


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Surgery_Schwartz. sustained pressure waves occurring at maximal rates. This pattern is hypothesized to expel residual debris and bacteria from the small intestine. The median duration of the IDMC ranges from 90 to 120 minutes. At any given time, different portions of the small intestine can be in different phases of the IDMC.Figure 28-10. Gut-associated lymphoid tissue. Select components of the gut-associated lymphoid tissue (GALT) are schematically represented. Peyer’s patches consist of a specialized follicle-associated epithelium (FAE) containing M cells, a subepithelial dome (SED) rich in dendritic cells (DC), and B-cell follicle containing germinal centers (GC). Plasma cells in the lamina propria produce IgA, which is transported to the intestinal lumen where serves as the first line of defense against pathogens. Other components of the GALT include isolated lymphoid follicles, mesenteric lymph nodes, and regulatory and effector lymphocytes.Brunicardi_Ch28_p1219-p1258.indd 122623/02/19 2:24 PM


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Surgery_Schwartz. pathogens. Other components of the GALT include isolated lymphoid follicles, mesenteric lymph nodes, and regulatory and effector lymphocytes.Brunicardi_Ch28_p1219-p1258.indd 122623/02/19 2:24 PM 1227SMALL INTESTINECHAPTER 28EMNSNIMNProximalDistalFigure 28-11. Ascending excitation and descending inhibition. The presence of a food bolus within the intestinal lumen is sensed by a sensory neuron (SN) that relays signals to (a) excitatory motor neurons (EMN) that have projections to intestinal muscle cells located proximal to the food bolus and (b) inhibitory motor neu-rons (IMN) that have projections to intestinal muscle cells located distal to the food bolus. This stereotypical motor reflex is controlled by the enteric nervous system and occurs in the absence of extra-intestinal innervations. It contributes to peristalsis.The regulatory mechanisms driving small-intestinal motil-ity consist of both pacemakers intrinsic to the small intestine and external neurohumoral modulatory


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Surgery_Schwartz. It contributes to peristalsis.The regulatory mechanisms driving small-intestinal motil-ity consist of both pacemakers intrinsic to the small intestine and external neurohumoral modulatory signals. The interstitial cells of Cajal are pleomorphic mesenchymal cells located within the muscularis propria of the intestine that generate the electrical slow wave (basic electrical rhythm or pacesetter potential) that plays a pacemaker role in setting the fundamental rhythmicity of small-intestinal contractions. The frequency of the slow wave varies along the longitudinal axis of the intestine: it ranges from 12 waves per minute in the duodenum to 7 waves per minute in the distal ileum. Smooth muscle contraction occurs only when an electrical action potential (spike burst) is superimposed on the slow wave. Thus, the slow wave determines the maximum frequency of contractions; however, not every slow wave is associated with a contraction.This intrinsic contractile mechanism is subject to neural


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Surgery_Schwartz. wave. Thus, the slow wave determines the maximum frequency of contractions; however, not every slow wave is associated with a contraction.This intrinsic contractile mechanism is subject to neural and hormonal regulation. The enteric motor system (ENS) pro-vides both inhibitory and excitatory stimuli. The predominant excitatory transmitters are acetylcholine and substance P, and the inhibitory transmitters include nitric oxide, vasoactive intes-tinal peptide, and adenosine triphosphate. In general, the sympa-thetic motor supply is inhibitory to the ENS; therefore, increased sympathetic input into the intestine leads to decreased intestinal smooth muscle activity. The parasympathetic motor supply is more complex, with projections to both inhibitory and excitatory ENS motor neurons. Correspondingly, the effects of parasympa-thetic inputs into intestinal motility are more difficult to predict.Endocrine FunctionEndocrinology as a discipline was born with the discovery of secretin, an


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Surgery_Schwartz. the effects of parasympa-thetic inputs into intestinal motility are more difficult to predict.Endocrine FunctionEndocrinology as a discipline was born with the discovery of secretin, an intestinal regulatory peptide that was the first hormone to be identified. Our improving understanding of the physiology of the small intestine has led to identification of many additional intestinal-derived hormones, which make this the largest hormone-producing organ in the body. Over 30 peptide hormone genes have been identified as being expressed in the gastrointestinal tract. Because of differential posttranscriptional and posttranslational processing, over 100 distinct regulatory peptides are produced. In addition, monoamines, such as histamine and dopamine, and eicosanoids with hormone-like activities are produced in the intestine.“Gut hormones” were previously conceptualized as pep-tides produced by the enteroendocrine cells of the intestinal mucosa that are released into the systemic


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Surgery_Schwartz. activities are produced in the intestine.“Gut hormones” were previously conceptualized as pep-tides produced by the enteroendocrine cells of the intestinal mucosa that are released into the systemic circulation to reach receptors in target sites in the gastrointestinal tract. Now it is clear that “gut hormone” genes are widely expressed through-out the body, not only in endocrine cells but also in central and peripheral neurons. The products of these genes are general intercellular messengers that can act as endocrine, paracrine, autocrine, or neurocrine mediators. Thus, they may act as true blood-borne hormones as well as through local effects.There are notable homology patterns among individual regulatory peptides found in the gastrointestinal tract. Based on these homologies, approximately one-half of the known regulatory peptides can be classified into families.12 For example, the secretin family includes secretin, glucagon, and glucagon-like peptides, glucose-dependent


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Surgery_Schwartz. approximately one-half of the known regulatory peptides can be classified into families.12 For example, the secretin family includes secretin, glucagon, and glucagon-like peptides, glucose-dependent insulinotropic peptide, vasoactive intestinal polypeptide, peptide histidine isoleucine, growth hormone releasing hormone, and pituitary adenylyl cyclase-activating peptide. Other peptide families include those named for insulin, epidermal growth factor, gastrin, pancreatic polypeptide, tachykinin, and somatostatin.Receptor subtype multiplicity and cell-specific expres-sion patterns for these receptor subtypes that are characteristic of these regulatory mediators makes definition of their actions complex. Detailed description of these actions is beyond the scope of this chapter; however, examples of regulatory pep-tides produced by enteroendocrine cells of the small-intestinal epithelium and their most commonly ascribed functions are summarized in Table 28-2. Some of these peptides, or


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Surgery_Schwartz. of regulatory pep-tides produced by enteroendocrine cells of the small-intestinal epithelium and their most commonly ascribed functions are summarized in Table 28-2. Some of these peptides, or their analogues, are used in routine clinical practice. For example, Table 28-2Representative regulatory peptides produced in the small intestineHORMONESOURCEaACTIONSSomatostatinD cellInhibits gastrointestinal secretion, motility, and splanchnic perfusionSecretinS cellStimulates exocrine pancreatic secretion, stimulates intestinal secretionCholecystokininI cellSimulates pancreatic exocrine secretion, simulates gallbladder emptying, inhibits sphincter of Oddi contractionMotilinM cellSimulates intestinal motilityPeptide YYL cellInhibits intestinal motility and secretionGlucagon-like Peptide 2L cellStimulates intestinal epithelial proliferationNeurotensinN cellStimulates pancreatic and biliary secretion, inhibits small bowel motility, stimulates intestinal mucosal growthaThis table indicates which


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Surgery_Schwartz. intestinal epithelial proliferationNeurotensinN cellStimulates pancreatic and biliary secretion, inhibits small bowel motility, stimulates intestinal mucosal growthaThis table indicates which enteroendocrine cell types located in the intestinal epithelium produce these peptides. These peptides are also widely expressed in nonintestinal tissues.Brunicardi_Ch28_p1219-p1258.indd 122723/02/19 2:24 PM 1228SPECIFIC CONSIDERATIONSPART IITable 28-3Small bowel obstruction: common etiologiesAdhesionsNeoplasms Primary small bowel neoplasms Secondary small bowel cancer (e.g., melanomaderived metastasis) Local invasion by intra-abdominal malignancy (e.g., Desmoid tumors) CarcinomatosisHernias External (e.g., inguinal and femoral) Internal (e.g., following Roux-en-Y gastric bypass surgery)Crohn’s diseaseVolvulusIntussusceptionRadiation-induced stricturePostischemic strictureForeign bodyGallstone ileusDiverticulitisMeckel’s diverticulumHematomaCongenital abnormalities (e.g., webs, duplications,


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Surgery_Schwartz. stricturePostischemic strictureForeign bodyGallstone ileusDiverticulitisMeckel’s diverticulumHematomaCongenital abnormalities (e.g., webs, duplications, and malrotation)therapeutic applications of octreotide, a long-acting analogue of somatostatin, include the amelioration of symptoms associ-ated with neuroendocrine tumors (e.g., carcinoid syndrome), postgastrectomy dumping syndrome, enterocutaneous fis-tulas, and the initial treatment of acute hemorrhage due to esophageal varices. The gastrin secretory response to secretin administration forms the basis for the standard test used to establish the diagnosis of Zollinger-Ellison syndrome. Chole-cystokinin is used in evaluations of gallbladder ejection frac-tion, a parameter that may have utility in patients who have symptoms of biliary colic but are not found to have gallstones. Of the peptides listed in Table 28-2, glucagon-like peptide 2 (GLP-2) has been identified as a specific and potent intestino-trophic hormone and is currently


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Surgery_Schwartz. but are not found to have gallstones. Of the peptides listed in Table 28-2, glucagon-like peptide 2 (GLP-2) has been identified as a specific and potent intestino-trophic hormone and is currently under clinical evaluation as an intestinotrophic agent in patients suffering from the short bowel syndrome, as discussed in the “Short Bowel Syndrome” section.Intestinal AdaptationThe small intestine has the capacity to adapt in response to vary-ing demands imposed by physiologic and pathologic conditions. Of relevance to many of the diseases discussed in this chapter is the adaptation that occurs in the remnant intestine following surgical resection of a large portion of the small intestine (mas-sive small bowel resection). Postresection intestinal adaptation has been studied extensively using animal models. Within a few hours after bowel resection, the remnant small intestine displays evidence of epithelial cellular hyperplasia. With additional time, villi lengthen, intestinal absorptive


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Surgery_Schwartz. animal models. Within a few hours after bowel resection, the remnant small intestine displays evidence of epithelial cellular hyperplasia. With additional time, villi lengthen, intestinal absorptive surface area increases, and digestive and absorptive functions improve. Postresection intes-tinal adaptation in human patients is less well studied, but it seems to follow similar steps as that seen in experimental mod-els, and it takes 1 to 2 years to complete.13The mechanisms responsible for inducing postresection intestinal adaptation are under active investigation. Several classes of effectors that stimulate intestinal growth include spe-cific nutrients, peptide hormones and growth factors, pancreatic secretions, and some cytokines. Nutritional components with intestinal growth-stimulating effects include fiber, fatty acids, triglycerides, glutamine, polyamines, and lectins.Postresection adaptation serves to compensate for the function of intestine that has been resected. Jejunal


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Surgery_Schwartz. effects include fiber, fatty acids, triglycerides, glutamine, polyamines, and lectins.Postresection adaptation serves to compensate for the function of intestine that has been resected. Jejunal resection is generally better tolerated, as ileum shows better capacity to compensate. However, the magnitude of this response is limited. If enough small intestine is resected, a devastating condition known as the short bowel syndrome results. This condition is discussed in the “Short Bowel Syndrome” section at the end of this chapter.SMALL BOWEL OBSTRUCTIONEpidemiologyMechanical small bowel obstruction is the most frequently encountered surgical disorder of the small intestine. Although a wide range of etiologies for this condition exist, the obstructing lesion can be conceptualized according to its anatomical relationship to the intestinal wall as:1. intraluminal (e.g., foreign bodies, gallstones, or meconium)2. intramural (e.g., tumors, Crohn’s disease–associated inflam-matory


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Surgery_Schwartz. according to its anatomical relationship to the intestinal wall as:1. intraluminal (e.g., foreign bodies, gallstones, or meconium)2. intramural (e.g., tumors, Crohn’s disease–associated inflam-matory strictures)3. extrinsic (e.g., adhesions, hernias, or carcinomatosis)2Intra-abdominal adhesions related to prior abdominal sur-gery account for up to 75% of cases of small bowel obstruction. Over 300,000 patients are estimated to undergo surgery to treat adhesion-induced small bowel obstruction in the United States annually. A 20-year trend analysis between 1988 and 2007 has documented no decrease in this rate during this period, highlighting the ongoing problem of this “old” disease.14 In fact, small bowel resection and lysis of adhesions account for two of the seven procedures that were responsible for 80% of the emergency surgeries in the United States between 2008 and 2011.15Less prevalent etiologies for small bowel obstruction include hernias, malignant bowel obstruction, and Crohn’s


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Surgery_Schwartz. for 80% of the emergency surgeries in the United States between 2008 and 2011.15Less prevalent etiologies for small bowel obstruction include hernias, malignant bowel obstruction, and Crohn’s dis-ease. The frequency with which obstruction related to these con-ditions is encountered varies according to the patient population and practice setting. Cancer-related small bowel obstructions are commonly due to extrinsic compression or invasion by advanced malignancies arising in organs other than the small bowel; few are due to primary small bowel tumors. The most commonly encountered etiologies of small bowel obstruction are summarized in Table 28-3. Although congenital abnormali-ties capable of causing small bowel obstruction usually become evident during childhood, they sometimes elude detection and are diagnosed for the first time in adult patients presenting with abdominal symptoms. For example, intestinal malrotation and midgut volvulus should not be forgotten when considering the


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Surgery_Schwartz. and are diagnosed for the first time in adult patients presenting with abdominal symptoms. For example, intestinal malrotation and midgut volvulus should not be forgotten when considering the differential diagnosis of adult patients with acute or chronic symptoms of small bowel obstruction, espe-cially those without a history of prior abdominal surgery. A rare etiology of obstruction is the superior mesenteric artery syn-drome, characterized by compression of the third portion of the duodenum by the superior mesenteric artery as it crosses over this portion of the duodenum. This condition should be 34Brunicardi_Ch28_p1219-p1258.indd 122823/02/19 2:24 PM 1229SMALL INTESTINECHAPTER 28considered in young asthenic individuals who have chronic symptoms suggestive of proximal small bowel obstruction.PathophysiologyWith onset of obstruction, gas and fluid accumulate within the intestinal lumen proximal to the site of obstruction. The intestinal activity increases to overcome the


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Surgery_Schwartz. bowel obstruction.PathophysiologyWith onset of obstruction, gas and fluid accumulate within the intestinal lumen proximal to the site of obstruction. The intestinal activity increases to overcome the obstruction, accounting for the colicky pain and the diarrhea that some experience even in the presence of complete bowel obstruction. Most of the gas that accumulates originates from swallowed air, although some is produced within the intestine. The fluid consists of swallowed liquids and gastrointestinal secretions (obstruction stimulates intestinal epithelial water secretion). With ongoing gas and fluid accumulation, the bowel distends and intraluminal and intramural pressures rise. The intestinal motility is eventually reduced with fewer contractions. With obstruction, the luminal flora of the small bowel, which is usually sterile, changes and a variety of organisms have been cultured from the contents. Translocation of these bacteria to regional lymph nodes has been demonstrated,


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Surgery_Schwartz. of the small bowel, which is usually sterile, changes and a variety of organisms have been cultured from the contents. Translocation of these bacteria to regional lymph nodes has been demonstrated, although the significance of this process is not well understood. If the intramural pressure becomes high enough, intestinal microvascular perfusion is impaired leading to intestinal ischemia, and, ultimately, necrosis. This condition is termed strangulated bowel obstruction.With partial small bowel obstruction, only a portion of the intestinal lumen is occluded, allowing passage of some gas and fluid. The progression of pathophysiologic events described previously tends to occur more slowly than with complete small bowel obstruction, and development of strangulation is less likely.A particularly dangerous form of bowel obstruction is closed loop obstruction in which a segment of intestine is obstructed both proximally and distally (e.g., with volvulus). In such cases, the accumulating gas


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Surgery_Schwartz. dangerous form of bowel obstruction is closed loop obstruction in which a segment of intestine is obstructed both proximally and distally (e.g., with volvulus). In such cases, the accumulating gas and fluid cannot escape either proximally or distally from the obstructed segment, lead-ing to a rapid rise in luminal pressure and a rapid progression to strangulation.Clinical PresentationThe symptoms of small bowel obstruction are colicky abdomi-nal pain, nausea, vomiting, and obstipation. Vomiting is a more prominent symptom with proximal obstructions than distal. Character of vomitus is important as with bacterial overgrowth, the vomitus is more feculent, suggesting a more established obstruction. Continued passage of flatus and/or stool beyond 6 to 12 hours after onset of symptoms is characteristic of par-tial rather than complete obstruction. The signs of small bowel obstruction include abdominal distention, which is most pro-nounced if the site of obstruction is in the distal ileum


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Surgery_Schwartz. of par-tial rather than complete obstruction. The signs of small bowel obstruction include abdominal distention, which is most pro-nounced if the site of obstruction is in the distal ileum and may be absent if the site of obstruction is in the proximal small intestine. Bowel sounds may be hyperactive initially, but in late stages of bowel obstruction, minimal bowel sounds may be heard. Laboratory findings reflect intravascular volume deple-tion and consist of hemoconcentration and electrolyte abnor-malities. Mild leukocytosis is common.Features of strangulated obstruction include abdominal pain often disproportionate to the degree of abdominal findings, suggestive of intestinal ischemia. Patients often have tachycar-dia, localized abdominal tenderness, fever, marked leukocyto-sis, and acidosis. Any of these findings should alert the clinician to the possibility of strangulation and the need for early surgical intervention.DiagnosisThe diagnostic evaluation should focus on the


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Surgery_Schwartz. and acidosis. Any of these findings should alert the clinician to the possibility of strangulation and the need for early surgical intervention.DiagnosisThe diagnostic evaluation should focus on the following goals: (a) distinguish mechanical obstruction from ileus, (b) determine the etiology of the obstruction, (c) discriminate partial from complete obstruction, and (d) discriminate simple from stran-gulating obstruction.Important elements to obtain on history include prior abdominal operations (suggesting the presence of adhesions) and the presence of abdominal disorders (e.g., intra-abdominal cancer or inflammatory bowel disease) that may provide insights into the etiology of obstruction. Upon examination, a meticulous search for hernias (particularly in the inguinal and femoral regions) should be conducted.The diagnosis of small bowel obstruction is usually con-firmed with radiographic examination. The abdominal series consists of (a) a radiograph of the abdomen with the patient


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Surgery_Schwartz. should be conducted.The diagnosis of small bowel obstruction is usually con-firmed with radiographic examination. The abdominal series consists of (a) a radiograph of the abdomen with the patient in a supine position, (b) a radiograph of the abdomen with the patient in an upright position, and (c) a radiograph of the chest with the patient in an upright position. The finding most specific for small bowel obstruction is the triad of dilated small bowel loops (>3 cm in diameter), air-fluid levels seen on upright films, and a paucity of air in the colon. The sensitivity of abdominal radiographs in the detection of small bowel obstruction ranges from 70% to 80%. Specificity is low because ileus and colonic obstruction can be associated with findings that mimic those observed with small bowel obstruction. False-negative findings on radiographs can result when the site of obstruction is in the proximal small bowel and when the bowel lumen is filled with fluid but no gas, thereby preventing


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Surgery_Schwartz. obstruction. False-negative findings on radiographs can result when the site of obstruction is in the proximal small bowel and when the bowel lumen is filled with fluid but no gas, thereby preventing visualization of air-fluid levels or bowel distention. The latter situation is associated with closed-loop obstruction. Despite these limitations, abdominal radiographs remain an important study in patients with sus-pected small bowel obstruction because of their widespread availability and low cost (Fig. 28-12).Computed tomographic (CT) scanning is becoming increasingly the imaging test of choice for patients with small bowel obstruction, and it is ideally done with oral contrast. CT is 80% to 90% sensitive and 70% to 90% specific in the detec-tion of small bowel obstruction. The findings of small bowel obstruction include a discrete transition zone with dilation of bowel proximally, decompression of bowel distally, intralumi-nal contrast that does not pass beyond the transition zone,


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Surgery_Schwartz. of small bowel obstruction include a discrete transition zone with dilation of bowel proximally, decompression of bowel distally, intralumi-nal contrast that does not pass beyond the transition zone, and a colon containing little gas or fluid (Figs. 28-13 and 28-14). CT scanning may also provide evidence for the presence of closed-loop obstruction and strangulation. Closed-loop obstruction is suggested by the presence of a U-shaped or C-shaped dilated bowel loop associated with a radial distribution of mesenteric vessels converging toward a torsion point. Strangulation is sug-gested by thickening of the bowel wall, pneumatosis intestinalis (air in the bowel wall), portal venous gas, mesenteric haziness, and poor uptake of intravenous contrast into the wall of the affected bowel (Fig. 28-15). CT scanning also offers a global evaluation of the abdomen and may therefore reveal the etiol-ogy of obstruction. This feature is important in the acute setting when intestinal obstruction


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Surgery_Schwartz. 28-15). CT scanning also offers a global evaluation of the abdomen and may therefore reveal the etiol-ogy of obstruction. This feature is important in the acute setting when intestinal obstruction represents only one of many diag-noses in patients presenting with acute abdominal conditions.The CT scan is usually performed after administration of oral water-soluble contrast or diluted barium. The water-soluble contrast has been shown to have prognostic and therapeutic val-ues too. Several studies and several subsequent meta-analysis have shown that water-soluble contrast could in fact have ther-apeutic and prognostic value. The appearance of the contrast Brunicardi_Ch28_p1219-p1258.indd 122923/02/19 2:24 PM 1230SPECIFIC CONSIDERATIONSPART IIFigure 28-12. Small bowel obstruction. Plain radiographs (A) supine, which show dilated loops of small bowel in the right upper quadrant; (B) erect, which confirm the presence of airfluid level in the loops of small bowel as well as the stomach,


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Surgery_Schwartz. (A) supine, which show dilated loops of small bowel in the right upper quadrant; (B) erect, which confirm the presence of airfluid level in the loops of small bowel as well as the stomach, consistant with small bowel obstruction.Figure 28-13. Small bowel obstruction. A CT scan of a patient presenting with signs and symptoms of bowel obstruction. Image shows grossly dilated loops of small bowel, with decompressed terminal ileum (I) and ascending colon (C), suggesting a complete distal small bowel obstruction. At laparotomy, adhesive bands from a previous surgery were identified and divided.Figure 28-14. Chronic partial small bowel obstruction. This patient presented with a several months history of chronic abdominal pain and intermittent vomiting. The coronal CT image shows grossly dilated loops of proximal small bowel on the left side (wide arrow), with decompressed loops of small bowel on the right side (narrow arrow). The dilated segment shows evidence of feculization of bowel


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Surgery_Schwartz. loops of proximal small bowel on the left side (wide arrow), with decompressed loops of small bowel on the right side (narrow arrow). The dilated segment shows evidence of feculization of bowel contents, consistent with the chronic nature of the obstruction. Patient’s vomitus had characteristic feculent smell and quality. At exploratory laparotomy, adhesive bands were identified and divided.in the colon within 24 hours of administration is predictive of nonsurgical resolution of bowel obstruction with a sensitivity of 92% and a specificity of 93%.16A limitation of CT scanning is its low sensitivity (<50%) in the detection of low-grade or partial small bowel obstruction. A subtle transition zone may be difficult to identify in the axial images obtained during CT scanning. In such cases, contrast examinations of the small bowel, either small bowel series (small bowel follow-through) or enteroclysis, can be helpful. For standard small bowel series, contrast is swallowed or instilled into


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Surgery_Schwartz. examinations of the small bowel, either small bowel series (small bowel follow-through) or enteroclysis, can be helpful. For standard small bowel series, contrast is swallowed or instilled into the stomach through a nasogastric tube. Abdominal radiographs are then taken serially as the contrast travels distally in the intestine. Although barium can be used, water-soluble contrast agents, such as gastrograffin, should be used if the possibility of intestinal perforation exists. These examinations are more labor-intensive and less rapidly performed than CT scanning but may offer greater sensitivity in the detection of luminal and mural etiologies of obstruction, such as primary intestinal tumors. For enteroclysis, 200 to 250 mL of barium followed by 1 to 2 L of a solution of methylcellulose in water is instilled into the proximal jejunum via a long nasoenteric catheter. The double-contrast technique used in enterocolysis Brunicardi_Ch28_p1219-p1258.indd 123023/02/19 2:24 PM


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Surgery_Schwartz. in water is instilled into the proximal jejunum via a long nasoenteric catheter. The double-contrast technique used in enterocolysis Brunicardi_Ch28_p1219-p1258.indd 123023/02/19 2:24 PM 1231SMALL INTESTINECHAPTER 28Figure 28-15. Intestinal pneumatosis. This CT scan shows intestinal pneumatosis (arrow). The cause of this radiological finding was intestinal ischemia. Patient was taken emergently to the operating room and underwent resection of an infarcted segment of small bowel.permits a better assessment of mucosal surface and detection of relatively small lesions, even through overlapping small bowel loops. Enterocolysis is rarely performed in the acute setting but offers greater sensitivity than small bowel series in the detection of lesions that may be causing partial small bowel obstruction. Recently, CT enterocolysis has been used, and it was reported to be superior to plain X-ray small bowel contrast studies.TherapySmall bowel obstruction is usually associated with a marked