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Surgery_Schwartz. for prevention of venous thromboembolism in high-risk abdominal surgery. Br J Surg. 2005;92:1212-1220. 78. Turpie AG, Bauer KA, Caprini JA, et al. Fondaparinux combined with intermittent pneumatic compression versus intermittent pneumatic compression alone for prevention of venous thrombo-embolism after abdominal surgery: a randomized, double-blind comparison. J Thromb Haemost. 2007;5:1854-1861. 79. Rogers FB, Shackford SR, Ricci MA, et al. Routine prophy-lactic vena cava filter insertion in severely injured trauma patients decreases the incidence of pulmonary embolism. J Am Coll Surg. 1995;180:641-647. 80. Rogers FB, Strindberg G, Shackford SR, et al. Five-year follow-up of prophylactic vena cava filters in high-risk trauma patients. Arch Surg. 1998;133:406-411.Brunicardi_Ch24_p0981-p1008.indd 100522/02/19 3:01 PM 1006SPECIFIC CONSIDERATIONSPART II 81. Millward SF, Oliva VL, Bell SD, et al. Gunther tulip retriev-able vena cava filter: results from the Registry of the Canadian


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Surgery_Schwartz. 100522/02/19 3:01 PM 1006SPECIFIC CONSIDERATIONSPART II 81. Millward SF, Oliva VL, Bell SD, et al. Gunther tulip retriev-able vena cava filter: results from the Registry of the Canadian Interventional Radiology Association. J Vasc Intervent Radiol. 2001;12:1053-1058. 82. Allen AW, Megargell JL, Brown DB, et al. Venous thrombosis associated with the placement of peripherally inserted central catheters. J Vasc Intervent Radiol. 2000;11:1309-1314. 83. Chengelis DL, Bendick PJ, Glover JL, et al. Progression of superficial venous thrombosis to deep vein thrombosis. J Vasc Surg. 1996;24:745-749. 84. Lutter KS, Kerr TM, Roedersheimer LR, et al. Superficial thrombophlebitis diagnosed by duplex scanning. Surgery. 1991;110:42-46. 85. Di Nisio M, Wichers IM, Middeldorp S. Treatment for superfi-cial thrombophlebitis of the leg. Cochrane Database Syst Rev. 2013(4):CD004982. 86. Decousus H, Prandoni P, Mismetti P, et al. Fondaparinux for the treatment of superficial-vein thrombosis in the legs.


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Surgery_Schwartz. thrombophlebitis of the leg. Cochrane Database Syst Rev. 2013(4):CD004982. 86. Decousus H, Prandoni P, Mismetti P, et al. Fondaparinux for the treatment of superficial-vein thrombosis in the legs. N Engl J Med. 2010;363(13):1222-1232. 87. Lohr JM, McDevitt DT, Lutter KS, et al. Operative manage-ment of greater saphenous thrombophlebitis involving the saphenofemoral junction. Am J Surg. 1992;164:269-275. 88. Ascer E, Lorensen E, Pollina RM, et al. Preliminary results of a nonoperative approach to saphenofemoral junction thrombo-phlebitis. J Vasc Surg. 1995;22:616-621. 89. Horne MK III, May DJ, Alexander HR, et al. Venographic surveillance of tunneled venous access devices in adult oncol-ogy patients. Ann Surg Oncol. 1995;2:174-178. 90. Landry GL, Liem TK. Endovascular management of Paget-Schroetter syndrome. Vascular. 2007;15:290-296. 91. Rhee RY, Gloviczki P, Jost C, et al. Acute mesenteric venous thrombosis. In: Gloviczki P, Yao JST, eds. Handbook of Venous Disorders. New York:


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Surgery_Schwartz. syndrome. Vascular. 2007;15:290-296. 91. Rhee RY, Gloviczki P, Jost C, et al. Acute mesenteric venous thrombosis. In: Gloviczki P, Yao JST, eds. Handbook of Venous Disorders. New York: Arnold; 2001:244. 92. Morasch MD, Ebaugh JL, Chiou AC, et al. Mesenteric venous thrombosis: a changing clinical entity. J Vasc Surg. 2001;34:680-684. 93. James AW, Rabl C, Westphalen AC, et al. Portomesenteric venous thrombosis after laparoscopic surgery: a systematic literature review. Arch Surg. 2009;144:520-526. 94. Bach AM, Hann LE, Brown KT, et al. Portal vein evaluation with US: comparison to angiography combined with CT arte-rial portography. Radiology. 1996;201:149-154. 95. Burkitt DP. Varicose veins, deep vein thrombosis, and haem-orrhoids: epidemiology and suggested aetiology. Br Med J. 1972;2:556-561. 96. Brand FN, Dannenberg AL, Abbott RD, et al. The epidemiol-ogy of varicose veins: the Framingham Study. Am J Prev Med. 1988;4:96-101. 97. Gibson K, Kabnick L, Varithena 013 Investigator G. A


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Surgery_Schwartz. FN, Dannenberg AL, Abbott RD, et al. The epidemiol-ogy of varicose veins: the Framingham Study. Am J Prev Med. 1988;4:96-101. 97. Gibson K, Kabnick L, Varithena 013 Investigator G. A mul-ticenter, randomized, placebo-controlled study to evaluate the efficacy and safety of Varithena(R) (polidocanol endove-nous microfoam 1%) for symptomatic, visible varicose veins with saphenofemoral junction incompetence. Phlebology. 2017;32(3):185-193. 98. Witte ME, Reijnen MM, de Vries JP, Zeebregts CJ. Mechano-chemical Endovenous Occlusion of Varicose Veins Using the ClariVein(R) Device. Surg Technol Int. 2015;26:219-225. 99. Proebstle TM, Alm J, Dimitri S, et al. The European multi-center cohort study on cyanoacrylate embolization of refluxing great saphenous veins. J Vasc Surg Venous Lymphat Disord. 2015;3(1):2-7. 100. Lurie F, Creton D, Eklof B, et al. Prospective randomized study of endovenous radiofrequency obliteration (closure) versus ligation and vein stripping (EVOLVeS): two-year follow-up.


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Surgery_Schwartz. F, Creton D, Eklof B, et al. Prospective randomized study of endovenous radiofrequency obliteration (closure) versus ligation and vein stripping (EVOLVeS): two-year follow-up. Eur J Vasc Endovasc Surg. 2005;29:67-73. 101. Darwood RJ, Theivacumar N, Dellagrammaticas D, et al. Ran-domized clinical trial comparing endovenous laser ablation with surgery for the treatment of primary great saphenous varicose veins. Br J Surg. 2008;95:294-301. 102. Falanga V. Venous ulceration. J Dermatol Surg Oncol. 1993;19:764-771. 103. Phillips T, Stanton B, Provan A, et al. A study of the impact of leg ulcers on quality of life: financial, social, and psychologic implications. J Am Acad Dermatol. 1994;31:49-53. 104. Skin Substitute Consensus Development Panel. Nonoperative management of venous ulcers: evolving role of skin substi-tutes. Vasc Surg. 1999;33:197. 105. Abenhaim L, Kurz X. The VEINES study (VEnous Insuffi-ciency Epidemiologic and Economic Study): an international cohort study on chronic


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Surgery_Schwartz. role of skin substi-tutes. Vasc Surg. 1999;33:197. 105. Abenhaim L, Kurz X. The VEINES study (VEnous Insuffi-ciency Epidemiologic and Economic Study): an international cohort study on chronic venous disorders of the leg. VEINES Group. Angiology. 1997;48:59-66. 106. Clarke H, Smith SR, Vasdekis SN, et al. Role of venous elasticity in the development of varicose veins. Br J Surg. 1989;76:577-580. 107. Nicolaides AN, Hussein MK, Szendro G, et al. The relation of venous ulceration with ambulatory venous pressure measure-ments. J Vasc Surg. 1993;17:414-419. 108. Christopoulos DG, Nicolaides AN, Szendro G, et al. Air-pleth-ysmography and the effect of elastic compression on venous hemodynamics of the leg. J Vasc Surg. 1987;5:148-159. 109. van Bemmelen PS, Bedford G, Beach K, et al. Quantitative segmental evaluation of venous valvular reflux with duplex ultrasound scanning. J Vasc Surg. 1989;10:425-431. 110. Nehler MR, Porter JM. The lower extremity venous system. Part II: the


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Surgery_Schwartz. Quantitative segmental evaluation of venous valvular reflux with duplex ultrasound scanning. J Vasc Surg. 1989;10:425-431. 110. Nehler MR, Porter JM. The lower extremity venous system. Part II: the pathophysiology of chronic venous insufficiency. Perspect Vasc Surg. 1992;5:81-97. 111. Beidler SK, Douillet CD, Berndt DF, et al. Multiplexed analy-sis of matrix metalloproteinases in leg ulcer tissue of patients with chronic venous insufficiency before and after compres-sion therapy. Wound Repair Regen. 2008;16:642-648. 112. Beidler SK, Douillet CD, Berndt DF, et al. Inflammatory cyto-kine levels in chronic venous insufficiency ulcer tissue before and after compression therapy. J Vasc Surg. 2009;49:1013-1020. 113. Nehler MR, Moneta GL, Woodard DM, et al. Perimalleolar subcutaneous tissue pressure effects of elastic compression stockings. J Vasc Surg. 1993;18:783-788. 114. Dinn E. Treatment of venous ulceration by injection sclero-therapy and compression hosiery: a 5-year study.


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Surgery_Schwartz. pressure effects of elastic compression stockings. J Vasc Surg. 1993;18:783-788. 114. Dinn E. Treatment of venous ulceration by injection sclero-therapy and compression hosiery: a 5-year study. Phlebology. 1992;7:23-26. 115. Mayberry JC, Moneta GL, Taylor LM, Jr, et al. Fifteen-year results of ambulatory compression therapy for chronic venous ulcers. Surgery. 1991;109(5):575-581. This review highlights the impact of compression therapy in venous ulcer therapy. 116. Falanga V, Margolis D, Alvarez O, et al. Rapid healing of venous ulcers and lack of clinical rejection with an allergenic cultured human skin equivalent. Human Skin Equivalent Investigators Group. Arch Dermatol. 1998;134:293-300. 117. Phillips TJ. New skin for old: developments in biological skin substitutes [editorial; comment]. Arch Dermatol. 1998;134:344. 118. Motykie GD, Caprini JA, Arcelus JI, et al. Evaluation of therapeutic compression stockings in the treatment of chronic venous insufficiency. Dermatol Surg.


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Surgery_Schwartz. comment]. Arch Dermatol. 1998;134:344. 118. Motykie GD, Caprini JA, Arcelus JI, et al. Evaluation of therapeutic compression stockings in the treatment of chronic venous insufficiency. Dermatol Surg. 1999;25:116-120. 119. Lippmann HI, Fishman LM, Farrar RH, et al. Edema control in the management of disabling chronic venous insufficiency. Arch Phys Med Rehabil. 1994;75:436-441. 120. Rubin JR, Alexander J, Plecha EJ, et al. Unna’s boot vs. polyurethane foam dressings for the treatment of venous ulceration. A randomized prospective study. Arch Surg. 1990;125:489-490. 121. O’Meara S, Cullum NA, Nelson EA. Compression for venous leg ulcers. Cochrane Database Syst Rev. 2009;1:CD000265. 122. Vernick SH, Shapiro D, Shaw FD. Legging orthosis for venous and lymphatic insufficiency. Arch Phys Med Rehabil. 1987;68:459-461.Brunicardi_Ch24_p0981-p1008.indd 100622/02/19 3:01 PM 1007VENOUS AND LYMPHATIC DISEASECHAPTER 24 123. Sibbald RG. Apligraf living skin equivalent for healing venous and


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Surgery_Schwartz. Rehabil. 1987;68:459-461.Brunicardi_Ch24_p0981-p1008.indd 100622/02/19 3:01 PM 1007VENOUS AND LYMPHATIC DISEASECHAPTER 24 123. Sibbald RG. Apligraf living skin equivalent for healing venous and chronic wounds. J Cutan Med Surg. 1998;3(suppl 1): S1-24-8. 124. Linton R. The communicating veins of the lower leg and the operative technique for their ligation. Ann Surg. 1938;107:582-593. 125. Gloviczki P, Bergan JJ, Rhodes JM, Canton LG, Harmsen S, Ilstrup DM. Mid-term results of endoscopic perforator vein interruption for chronic venous insufficiency: lessons learned from the North American Subfascial Endoscopic Perforator Surgery Registry. The North American Study Group. J Vasc Surg. 1999;29(3):489-502. This study reviews registry outcomes following subfacial endoscopic perforator surgery performed across 17 centers in North America. 126. Vashist MG, Malik V, Singhal N. Role of subfascial endo-scopic perforator surgery (SEPS) in management of perfora-tor incompetence in varicose


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Surgery_Schwartz. performed across 17 centers in North America. 126. Vashist MG, Malik V, Singhal N. Role of subfascial endo-scopic perforator surgery (SEPS) in management of perfora-tor incompetence in varicose veins: a prospective randomized study. India J Surg. 2014;76(2):117-123. 127. van Gent WB, Hop WC, van Praag MC, et al. Conservative versus surgical treatment of venous leg ulcers: a prospective randomized, multicenter trial. J Vasc Surg. 2006;44:563-571. 128. Gohel MS, Barwell JR, Taylor M, et al. Long term results of compression therapy alone versus compression plus surgery in chronic venous ulceration (ESCHAR): randomized controlled trial. BMJ. 2007;335:83. 129. Sottiurai VS. Surgical correction of recurrent venous ulcer. J Cardiovasc Surg. 1991;32:104-109. 130. Raju S, Fredericks R. Valve reconstruction procedures for non-obstructive venous insufficiency: rationale, techniques, and results in 107 procedures with twoto eight-year follow-up. J Vasc Surg. 1988;7:301-310. 131. Raju S, Darcey


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Surgery_Schwartz. procedures for non-obstructive venous insufficiency: rationale, techniques, and results in 107 procedures with twoto eight-year follow-up. J Vasc Surg. 1988;7:301-310. 131. Raju S, Darcey R, Neglen P. Unexpected major role for venous stenting in deep reflux disease. J Vasc Surg. 2010;51:401-408. 132. Masuda EM, Kistner RL. Long-term results of venous valve reconstruction: a fourto twenty-one-year follow-up. J Vasc Surg. 1994;19:391-403. 133. Rockson SG, Miller LT, Senie R, et al. American Cancer Soci-ety Lymphedema Workshop. Workgroup III: diagnosis and management of lymphedema. Cancer. 1998;83:2882-2885. 134. Yasuhara H, Shigematsu H, Muto T. A study of the advan-tages of elastic stockings for leg lymphedema. Int Angiol. 1996;15:272-277. 135. Feldman JL, Stout NL, Wanchai A, et al. Intermittent pneu-matic compression therapy: a systematic review. Lymphology. 2012;45:13-25. 136. Vodder E. Le Drainage Lymphatique, une Novelle Méthode Thérapeutique. Paris: Santé pour tous;


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Surgery_Schwartz. et al. Intermittent pneu-matic compression therapy: a systematic review. Lymphology. 2012;45:13-25. 136. Vodder E. Le Drainage Lymphatique, une Novelle Méthode Thérapeutique. Paris: Santé pour tous; 1936. 137. Ko DS, Lerner R, Klose G, et al. Effective treatment of lymph-edema of the extremities. Arch Surg. 1998;133:452-458. 138. Stevens DL, Bisno AL, Chambers HF, et al. Practice guide-lines for the diagnosis and management of skin and soft tissue infections. Clin Infect Dis. 2005;41:1373-1406. 139. Miller TA, Wyatt LE, Rudkin GH. Staged skin and subcutane-ous excision for lymphedema: a favorable report of long-term results. Plast Reconstr Surg. 1998;102:1486-1501. 140. Baumeister RG, Siuda S. Treatment of lymphedema by micro-surgical lymphatic grafting: what is proved? Plast Reconstr Surg. 1990;85:64-74. 141. Bernas MJ, Witte CL, Witte MH. The diagnosis and treatment of peripheral lymphedema: draft revision of the 1995 Con-sensus Document of the International Society of Lymphology


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Surgery_Schwartz. 1990;85:64-74. 141. Bernas MJ, Witte CL, Witte MH. The diagnosis and treatment of peripheral lymphedema: draft revision of the 1995 Con-sensus Document of the International Society of Lymphology Executive Committee for discussion at the September 3–7, 2001, XVIII International Congress of Lymphology in Genoa, Italy. Lymphology. 2001;34:84-91.Brunicardi_Ch24_p0981-p1008.indd 100722/02/19 3:01 PM


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Surgery_Schwartz. SURGICAL ANATOMYThe esophagus is a muscular tube that starts as the continu-ation of the pharynx and ends as the cardia of the stomach. When the head is in a normal anatomic position, the transi-tion from pharynx to esophagus occurs at the lower border of the sixth cervical vertebra. Topographically this corresponds to the cricoid cartilage anteriorly and the palpable transverse process of the sixth cervical vertebra laterally (Fig. 25-1). The esophagus is firmly attached at its upper end to the cricoid cartilage and at its lower end to the diaphragm; during swal-lowing, the proximal points of fixation move craniad the dis-tance of one cervical vertebral body.The esophagus lies in the midline, with a deviation to the left in the lower portion of the neck and upper portion of the thorax, and returns to the midline in the midportion of the tho-rax near the bifurcation of the trachea (Fig. 25-2). In the lower portion of the thorax, the esophagus again deviates to the left and anteriorly


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Surgery_Schwartz. returns to the midline in the midportion of the tho-rax near the bifurcation of the trachea (Fig. 25-2). In the lower portion of the thorax, the esophagus again deviates to the left and anteriorly to pass through the diaphragmatic hiatus.Esophagus and Diaphragmatic HerniaBlair A. Jobe, John G. Hunter, and David I. Watson 25chapterSurgical Anatomy1009Physiology1015Swallowing Mechanism / 1015Physiologic Reflux / 1017Assessment of Esophageal Function1018Tests to Detect Structural Abnormalities / 1018Tests to Detect Functional Abnormalities / 1019Videoand Cineradiography / 1028Tests to Detect Increased Exposure to Gastric Juice / 1028Tests of Duodenogastric Function / 1030Gastroesophageal Reflux Disease1031The Human Antireflux Mechanism and the Pathophysiology of Gastroesophageal Reflux Disease / 1032Complications Associated With Gastroesophageal Reflux Disease / 1033Metaplastic (Barrett’s Esophagus) and Neoplastic (Adenocarcinoma) Complications / 1035Respiratory Complications /


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Surgery_Schwartz. Disease / 1032Complications Associated With Gastroesophageal Reflux Disease / 1033Metaplastic (Barrett’s Esophagus) and Neoplastic (Adenocarcinoma) Complications / 1035Respiratory Complications / 1035Surgical Therapy for Gastroesophageal Reflux Disease / 1038Primary Antireflux Repairs / 1040Giant Diaphragmatic (Hiatal) Hernias1045Incidence and Etiology / 1045Clinical Manifestations / 1047Diagnosis / 1047Pathophysiology / 1048Treatment / 1048Diaphragmatic Repair / 1048The Short Esophagus and PEH / 1049Results / 1049Schatzki’s Ring1049Scleroderma1050Eosinophilic Esophagitis1051Symptoms / 1051Signs / 1051Pathology / 1051Treatment / 1051Motility Disorders of the Pharynx and Esophagus1052Clinical Manifestations / 1052Motility Disorders of the Pharynx and Upper Esophagus—Transit Dysphagia / 1052Diagnostic Assessment of the Cricopharyngeal Segment / 1052Motility Disorders of the Esophageal Body and Lower Esophageal Sphincter / 1055Operations for Esophageal Motor Disorders and


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Surgery_Schwartz. / 1052Diagnostic Assessment of the Cricopharyngeal Segment / 1052Motility Disorders of the Esophageal Body and Lower Esophageal Sphincter / 1055Operations for Esophageal Motor Disorders and Diverticula1060Long Esophageal Myotomy for Motor Disorders of the Esophageal Body / 1060Myotomy of the Lower Esophageal Sphincter (Heller Myotomy) / 1063Open Esophageal Myotomy / 1065Laparoscopic Cardiomyotomy / 1065Per Oral Endoscopic Myotomy (POEM) / 1065Outcome Assessment of the Therapy for Achalasia / 1065Esophageal Resection for End-Stage Motor Disorders of the Esophagus / 1068Carcinoma of the Esophagus1068Clinical Manifestations / 1068General Approach to Esophageal Cancer / 1069Staging of Esophageal Cancer / 1069Clinical Approach to Carcinoma of the Esophagus and Cardia / 1070Palliation of Esophageal Cancer / 1074Surgical Treatment / 1074Comparative Studies of Esophagectomy Technique / 1077Alternative Therapies / 1077Sarcoma of the Esophagus1078Benign Tumors and Cysts1080Leiomyoma /


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Surgery_Schwartz. of Esophageal Cancer / 1074Surgical Treatment / 1074Comparative Studies of Esophagectomy Technique / 1077Alternative Therapies / 1077Sarcoma of the Esophagus1078Benign Tumors and Cysts1080Leiomyoma / 1081Esophageal Cyst / 1083Esophageal Perforation1083Diagnosis / 1083Management / 1084Mallory-Weiss Syndrome1085Caustic Injury1086Pathology / 1086Clinical Manifestations / 1086Treatment / 1086Acquired Fistula1088Techniques of Esophageal Reconstruction1089Partial Esophageal Resection / 1089Reconstruction After Total Esophagectomy / 1089Composite Reconstruction / 1090Vagal Sparing Esophagectomy With Colon Interposition / 1090Brunicardi_Ch25_p1009-p1098.indd 100901/03/19 6:01 PM 1010abcdeA BKey Points1 Benign esophageal disease is common and is best evaluated with thorough physiologic testing (high resolution esopha-geal motility, 24-hour ambulatory pH measurement, and/or esophageal impedance testing) and anatomic testing (esoph-agoscopy, video esophagography, and/or computed


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Surgery_Schwartz. testing (high resolution esopha-geal motility, 24-hour ambulatory pH measurement, and/or esophageal impedance testing) and anatomic testing (esoph-agoscopy, video esophagography, and/or computed tomog-raphy [CT] scanning).2 Gastroesophageal reflux disease (GERD) is the most com-mon disease of the gastrointestinal tract for which patients seek medical therapy. When GERD symptoms (heartburn, regurgitation, chest pain, and/or supraesophageal symptoms) are troublesome despite adequately dosed PPI, surgical cor-rection may be indicated.3 Barrett’s esophagus is the transformation of the distal esoph-ageal epithelium from squamous to a specialized columnar epithelium capable of further neoplastic progression. The detection of Barrett’s esophagus on endoscopy and biopsy increases the future risk of cancer by >40x compared to indi-viduals without Barrett’s esophagus.4 Giant hiatal hernia, otherwise known as paraesophageal her-nia, should be repaired when symptomatic or associated with iron


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Surgery_Schwartz. of cancer by >40x compared to indi-viduals without Barrett’s esophagus.4 Giant hiatal hernia, otherwise known as paraesophageal her-nia, should be repaired when symptomatic or associated with iron deficiency anemia. Laparoscopic hiatal hernia repair with fundoplication is the most common approach to repair.5 Achalasia is the most common primary esophageal motor disorder. It is characterized by an absence of peristalsis and a hypertensive nonrelaxing lower esophageal sphincter. It is best treated with laparoscopic Heller myotomy and partial fundoplication.6 Most esophageal cancer presents with dysphagia, at which time it has invaded the muscularis of the esophagus and is often associated with lymph node metastases. The preferred treatment at this stage is multimodality therapy with chemo-radiation therapy followed by open or minimally invasive esophagectomy.Figure 25-1. A. Topographic relationships of the cervical esophagus: (a) hyoid bone, (b) thyroid cartilage, (c) cricoid cartilage,


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Surgery_Schwartz. therapy followed by open or minimally invasive esophagectomy.Figure 25-1. A. Topographic relationships of the cervical esophagus: (a) hyoid bone, (b) thyroid cartilage, (c) cricoid cartilage, (d) thyroid gland, (e) sternoclavicular. B. Lateral radio-graphic appearance with landmarks identified as labeled in A. The location of C6 is also included (f). (Reproduced with permission from Shields TW: General Thoracic Surgery, 3rd ed. Philadelphia, PA: Lea & Febiger; 1989.)Three normal areas of esophageal narrowing are evident on the barium esophagogram or during esophagoscopy. The uppermost narrowing is located at the entrance into the esopha-gus and is caused by the cricopharyngeal muscle. Its luminal diameter is 1.5 cm, and it is the narrowest point of the esopha-gus. The middle narrowing is due to an indentation of the ante-rior and left lateral esophageal wall caused by the crossing of the left main stem bronchus and aortic arch. The luminal diameter at this point is 1.6 cm. The


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Surgery_Schwartz. is due to an indentation of the ante-rior and left lateral esophageal wall caused by the crossing of the left main stem bronchus and aortic arch. The luminal diameter at this point is 1.6 cm. The lowermost narrowing is at the hiatus of the diaphragm and is caused by the gastroesophageal sphincter mechanism. The luminal diameter at this point varies somewhat, depending on the distention of the esophagus by the passage of food, but has been measured at 1.6 to 1.9 cm. These normal constrictions tend to hold up swallowed foreign objects, and the overlying mucosa is subject to injury by swallowed corrosive liquids due to their slow passage through these areas.Figure 25-3 shows the average distance in centimeters measured during endoscopic examination between the incisor teeth and the cricopharyngeus, aortic arch, and cardia of the stomach. Manometrically, the length of the esophagus between the lower border of the cricopharyngeus and upper border of the lower sphincter varies according to


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Surgery_Schwartz. aortic arch, and cardia of the stomach. Manometrically, the length of the esophagus between the lower border of the cricopharyngeus and upper border of the lower sphincter varies according to the height of the individual.Brunicardi_Ch25_p1009-p1098.indd 101001/03/19 6:01 PM 1011ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25ABFigure 25-2. Barium esophagogram. A. Posterior-anterior view. White arrow shows deviation to left. Black arrow shows return to midline. B. Lateral view. Black arrow shows anterior deviation. (Reproduced with permission from Shields TW: General Thoracic Surgery, 3rd ed. Philadelphia, PA: Lea & Febiger; 1989.)Pharynx24–26cmUpper sphincter(C6)40cm38cmLower sphincter(T11)15cm14cmAortic arch(T4)25cm 23cmIncisor teethFigure 25-3. Important clinical endoscopic measurements of the esophagus in adults. (Reproduced with permission from Shields TW: General Thoracic Surgery, 3rd ed. Philadelphia, PA: Lea & Febiger; 1989.) Superior pharyngeal constrictor m.Middle pharyngeal


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Surgery_Schwartz. of the esophagus in adults. (Reproduced with permission from Shields TW: General Thoracic Surgery, 3rd ed. Philadelphia, PA: Lea & Febiger; 1989.) Superior pharyngeal constrictor m.Middle pharyngeal constrictor m.Inferior pharyngeal constrictor m.Cricopharyngeus m.EsophagusBAFigure 25-4. External muscles of the pharynx. A. Posterolateral view. B. Posterior view. Dotted line represents usual site of myotomy. (Reproduced with permission from Shields TW: General Thoracic Surgery, 3rd ed. Philadelphia, PA: Lea & Febiger; 1989.)The pharyngeal musculature consists of three broad, flat, overlapping fan-shaped constrictors (Fig. 25-4). The opening of the esophagus is collared by the cricopharyngeal muscle, which arises from both sides of the cricoid cartilage of the lar-ynx and forms a continuous transverse muscle band without an interruption by a median raphe. The fibers of this muscle Brunicardi_Ch25_p1009-p1098.indd 101101/03/19 6:02 PM 1012SPECIFIC CONSIDERATIONSPART IIblend


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Surgery_Schwartz. transverse muscle band without an interruption by a median raphe. The fibers of this muscle Brunicardi_Ch25_p1009-p1098.indd 101101/03/19 6:02 PM 1012SPECIFIC CONSIDERATIONSPART IIblend inseparably with those of the inferior pharyngeal constric-tor above and the inner circular muscle fibers of the esophagus below. Some investigators believe that the cricopharyngeus is part of the inferior constrictor; that is, that the inferior constric-tor has two parts, an upper or retrothyroid portion having diago-nal fibers, and a lower or retrocricoid portion having transverse fibers. Keith in 1910 showed that these two parts of the same muscle serve totally different functions. The retrocricoid portion serves as the upper sphincter of the esophagus and relaxes when the retrothyroid portion contracts, to force the swallowed bolus from the pharynx into the esophagus.The cervical portion of the esophagus is approximately 5 cm long and descends between the trachea and the vertebral column, from


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Surgery_Schwartz. to force the swallowed bolus from the pharynx into the esophagus.The cervical portion of the esophagus is approximately 5 cm long and descends between the trachea and the vertebral column, from the level of the sixth cervical vertebra to the level of the interspace between the first and second thoracic verte-brae posteriorly, or the level of the suprasternal notch anteriorly. The recurrent laryngeal nerves lie in the right and left grooves between the trachea and the esophagus. The left recurrent nerve lies somewhat closer to the esophagus than the right, owing to the slight deviation of the esophagus to the left, and the more lateral course of the right recurrent nerve around the right sub-clavian artery. Laterally, on the left and right sides of the cervi-cal esophagus are the carotid sheaths and the lobes of the thyroid gland.The thoracic portion of the esophagus is approximately 20 cm long. It starts at the thoracic inlet. In the upper portion of the thorax, it is in intimate


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Surgery_Schwartz. sheaths and the lobes of the thyroid gland.The thoracic portion of the esophagus is approximately 20 cm long. It starts at the thoracic inlet. In the upper portion of the thorax, it is in intimate relationship with the posterior wall of the trachea and the prevertebral fascia. Just above the tracheal bifurcation, the esophagus passes to the right of the aorta. This anatomic positioning can cause a notch indentation in its left lateral wall on a barium swallow radiogram. Immediately below this notch, the esophagus crosses both the bifurcation of the trachea and the left main stem bronchus, owing to the slight deviation of the terminal portion of the trachea to the right by the aorta (Fig. 25-5). From there down, the esophagus passes over the posterior surface of the subcarinal lymph nodes (LNs), and then descends over the pericardium of the left atrium to reach the diaphragmatic hiatus (Fig. 25-6). From the bifurcation of the trachea downward, both the vagal nerves and the esophageal


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Surgery_Schwartz. (LNs), and then descends over the pericardium of the left atrium to reach the diaphragmatic hiatus (Fig. 25-6). From the bifurcation of the trachea downward, both the vagal nerves and the esophageal nerve plexus lie on the muscular wall of the esophagus.Dorsally, the thoracic esophagus follows the curvature of the spine and remains in close contact with the vertebral bod-ies. From the eighth thoracic vertebra downward, the esopha-gus moves vertically away from the spine to pass through the hiatus of the diaphragm. The thoracic duct passes through the hiatus of the diaphragm on the anterior surface of the verte-bral column behind the aorta and under the right crus. In the thorax, the thoracic duct lies dorsal to the esophagus between the azygos vein on the right and the descending thoracic aorta on the left.The abdominal portion of the esophagus is approximately 2 cm long and includes a portion of the lower esophageal sphincter (LES). It starts as the esophagus passes through the


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Surgery_Schwartz. aorta on the left.The abdominal portion of the esophagus is approximately 2 cm long and includes a portion of the lower esophageal sphincter (LES). It starts as the esophagus passes through the diaphragmatic hiatus and is surrounded by the phrenoesopha-geal membrane, a fibroelastic ligament arising from the subdia-phragmatic fascia as a continuation of the transversalis fascia lining the abdomen (Fig. 25-7). The upper leaf of the membrane attaches itself in a circumferential fashion around the esopha-gus, about 1 to 2 cm above the level of the hiatus. These fibers blend in with the elastic-containing adventitia of the abdominal esophagus and the cardia of the stomach. This portion of the esophagus is subjected to the positive-pressure environment of the abdomen.The musculature of the esophagus can be divided into an outer longitudinal and an inner circular layer. The upper 2 to 6 cm of the esophagus contains only striated muscle fibers. From then on, smooth muscle fibers gradually


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Surgery_Schwartz. can be divided into an outer longitudinal and an inner circular layer. The upper 2 to 6 cm of the esophagus contains only striated muscle fibers. From then on, smooth muscle fibers gradually become more abundant. Most clinically significant esophageal motility dis-orders involve only the smooth muscle in the lower two-thirds of the esophagus. When a long surgical esophageal myotomy is indicated, the incision needs to extend only this distance.The longitudinal muscle fibers originate from a crico-esophageal tendon arising from the dorsal upper edge of the anteriorly located cricoid cartilage. The two bundles of mus-cle diverge and meet in the midline on the posterior wall of the esophagus about 3 cm below the cricoid (see Fig. 25-4). From this point on, the entire circumference of the esophagus is cAThymusPericardiumSuperior vena cavaTracheal carinaRight main stembronchusEsophagusAscending aortaLeft main stem bronchusBottom of aortic archDescendingaortaIVBaebdFigure 25-5. A.


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Surgery_Schwartz. the esophagus is cAThymusPericardiumSuperior vena cavaTracheal carinaRight main stembronchusEsophagusAscending aortaLeft main stem bronchusBottom of aortic archDescendingaortaIVBaebdFigure 25-5. A. Cross-section of the thorax at the level of the tracheal bifurcation. B. Computed tomographic scan at same level viewed from above: (a) ascending aorta, (b) descending aorta, (c) tracheal carina, (d) esophagus, (e) pulmonary artery. (Reproduced with permission from Shields TW: General Thoracic Surgery, 3rd ed. Philadelphia, PA: Lea & Febiger; 1989.)Brunicardi_Ch25_p1009-p1098.indd 101201/03/19 6:02 PM 1013ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25BAPericardiumRight ventricleRight atriumPericardiumPleuraVIIPleuraAortaEsophagusLeft atriumLeft ventriclefdecabgFigure 25-6. A. Cross-section of the thorax at the midleft atrial level. B. Computed tomographic scan at same level viewed from above: (a) aorta, (b) esophagus, (c) left atrium, (d) right atrium, (e) left ventricle, (f) right


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Surgery_Schwartz. of the thorax at the midleft atrial level. B. Computed tomographic scan at same level viewed from above: (a) aorta, (b) esophagus, (c) left atrium, (d) right atrium, (e) left ventricle, (f) right ventricle, (g) pulmonary vein. (Reproduced with permission from Shields TW: General Thoracic Surgery, 3rd ed. Philadelphia, PA: Lea & Febiger; 1989.)Phreno-esophageal membrane(Ascending leaf)ParietalperitoneumVisceralperitoneumDiaphragmPara-esophageal fat padPhreno-esophageal membrane(Descending leaf)Figure 25-7. Attachments and structure of the phrenoesophageal membrane. Transversalis fascia lies just above the parietal peri-toneum. (Reproduced with permission from Shields TW: General Thoracic Surgery, 3rd ed. Philadelphia, PA: Lea & Febiger; 1989.)covered by a layer of longitudinal muscle fibers. This configura-tion of the longitudinal muscle fibers around the most proximal part of the esophagus leaves a V-shaped area in the posterior wall covered only with circular muscle fibers.


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Surgery_Schwartz. fibers. This configura-tion of the longitudinal muscle fibers around the most proximal part of the esophagus leaves a V-shaped area in the posterior wall covered only with circular muscle fibers. Contraction of the longitudinal muscle fibers shortens the esophagus. The cir-cular muscle layer of the esophagus is thicker than the outer longitudinal layer. In situ, the geometry of the circular muscle is helical and makes the peristalsis of the esophagus assume a wormlike drive, as opposed to segmental and sequential squeez-ing. As a consequence, severe motor abnormalities of the esoph-agus assume a corkscrew-like pattern on the barium swallow radiogram.The cervical portion of the esophagus receives its main blood supply from the inferior thyroid artery. The thoracic por-tion receives its blood supply from the bronchial arteries, with 75% of individuals having one right-sided and two left-sided branches. Two esophageal branches arise directly from the aorta. The abdominal portion of the


Surgery_Schwartz

Surgery_Schwartz. supply from the bronchial arteries, with 75% of individuals having one right-sided and two left-sided branches. Two esophageal branches arise directly from the aorta. The abdominal portion of the esophagus receives its blood supply from the ascending branch of the left gastric artery and from inferior phrenic arteries (Fig. 25-8). On entering the wall of the esophagus, the arteries assume a T-shaped division to form a longitudinal plexus, giving rise to an intramural vascular network in the muscular and submucosal layers. As a conse-quence, the esophagus can be mobilized from the stomach to the level of the aortic arch without fear of devascularization and ischemic necrosis. Caution, however, should be exercised as to the extent of esophageal mobilization in patients who have had a previous thyroidectomy with ligation of the inferior thyroid arteries proximal to the origin of the esophageal branches.Blood from the capillaries of the esophagus flows into a submucosal venous plexus, and


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Surgery_Schwartz. thyroidectomy with ligation of the inferior thyroid arteries proximal to the origin of the esophageal branches.Blood from the capillaries of the esophagus flows into a submucosal venous plexus, and then into a periesophageal Left gastric arteryRight bronchialartery Inferior thyroid arterySuperior leftbronchial arteryInferior leftbronchial arteryAortic esophagealarteriesAscending branches ofleft gastric artery Esophageal branchFigure 25-8. Arterial blood supply of the esophagus. (Reproduced with permission from Shields TW: General Thoracic Surgery, 3rd ed. Philadelphia, PA: Lea & Febiger; 1989.)Brunicardi_Ch25_p1009-p1098.indd 101301/03/19 6:02 PM 1014SPECIFIC CONSIDERATIONSPART IIInferior thyroid veinsAccessory azygous veinHemiazygous veinShort gastric veinsSplenic veinSuperior mesenteric vein Portal vein Coronary vein Azygous vein Figure 25-9. Venous drainage of the esophagus. (Reproduced with permission from Shields TW: General Thoracic


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Surgery_Schwartz. veinSuperior mesenteric vein Portal vein Coronary vein Azygous vein Figure 25-9. Venous drainage of the esophagus. (Reproduced with permission from Shields TW: General Thoracic Surgery, 3rd ed. Philadelphia, PA: Lea & Febiger; 1989.)Left vagus nerveLeft recurrentlaryngeal nerveThoracic chainLeft or anteriorvagal trunkRight or posterior vagal trunkAnterior esophagealplexusRight recurrentlaryngeal nerveRight vagus nerveRecurrent laryngealnervesFigure 25-10. Innervation of the esophagus. (Reproduced with permission from Shields TW: General Thoracic Surgery, 3rd ed. Philadelphia, PA: Lea & Febiger; 1989.)Internal jugularnodesParatrachealnodesSubcarinal nodesInferior paraesophagealnodesParahiatal nodes Splenic arterynodesCeliac artery nodes Hepatic artery nodesLeft gastric artery nodesPulmonary hilarnodesSuperiorparaesophageal nodesFigure 25-11. Lymphatic drainage of the esophagus. (Reproduced with permission from DeMeester TR, Barlow AP. Surgery and cur-rent


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Surgery_Schwartz. gastric artery nodesPulmonary hilarnodesSuperiorparaesophageal nodesFigure 25-11. Lymphatic drainage of the esophagus. (Reproduced with permission from DeMeester TR, Barlow AP. Surgery and cur-rent management for cancer of the esophagus and cardia: Part I, Curr Probl Surg. 1988 Jul;25(7):475-531.)venous plexus from which the esophageal veins originate. In the cervical region, the esophageal veins empty into the inferior thy-roid vein; in the thoracic region, they empty into the bronchial, azygos, or hemiazygos veins; and in the abdominal region, they empty into the coronary vein (Fig. 25-9). The submucosal venous networks of the esophagus and stomach are in continuity with each other, and, in patients with portal venous obstruction, this communication functions as a collateral pathway for portal blood to enter the superior vena cava via the azygos vein.The parasympathetic innervation of the pharynx and esophagus is provided mainly by the vagus nerves. The con-strictor muscles of the


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Surgery_Schwartz. portal blood to enter the superior vena cava via the azygos vein.The parasympathetic innervation of the pharynx and esophagus is provided mainly by the vagus nerves. The con-strictor muscles of the pharynx receive branches from the pharyngeal plexus, which is on the posterior lateral surface of the middle constrictor muscle, and is formed by pharyngeal branches of the vagus nerves with a small contribution from cra-nial nerves IX and XI (Fig. 25-10). The cricopharyngeal sphinc-ter and the cervical portion of the esophagus receive branches from both recurrent laryngeal nerves, which originate from the vagus nerves—the right recurrent nerve at the lower margin of the subclavian artery and the left at the lower margin of the aortic arch. They are slung dorsally around these vessels and ascend in the groove between the esophagus and trachea, giving branches to each. Damage to these nerves interferes not only with the function of the vocal cords but also with the function of the


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Surgery_Schwartz. and ascend in the groove between the esophagus and trachea, giving branches to each. Damage to these nerves interferes not only with the function of the vocal cords but also with the function of the cricopharyngeal sphincter and the motility of the cervical esophagus, predisposing the individual to pulmonary aspiration on swallowing.Afferent visceral sensory pain fibers from the esophagus end without synapse in the first four segments of the thoracic spinal cord, using a combination of sympathetic and vagal path-ways. These pathways are also occupied by afferent visceral sensory fibers from the heart; hence, both organs have similar symptomatology.The lymphatics located in the submucosa of the esopha-gus are so dense and interconnected that they constitute a single plexus (Fig. 25-11). There are more lymph vessels than blood capillaries in the submucosa. Lymph flow in the submucosal plexus runs in a longitudinal direction, and, on injection of a contrast medium, the longitudinal


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Surgery_Schwartz. There are more lymph vessels than blood capillaries in the submucosa. Lymph flow in the submucosal plexus runs in a longitudinal direction, and, on injection of a contrast medium, the longitudinal spread is seen to be about six times that of the transverse spread. In the upper two-thirds of the esophagus, the lymphatic flow is mostly cephalad, and, in the lower third, caudad. In the thoracic portion of the esophagus, Brunicardi_Ch25_p1009-p1098.indd 101401/03/19 6:02 PM 1015ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25the submucosal lymph plexus extends over a long distance in a longitudinal direction before penetrating the muscle layer to enter lymph vessels in the adventitia. As a consequence of this nonsegmental lymph drainage, a primary tumor can extend for a considerable length superiorly or inferiorly in the submucosal plexus. Consequently, free tumor cells can follow the submu-cosal lymphatic plexus in either direction for a long distance before they pass through the


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Surgery_Schwartz. superiorly or inferiorly in the submucosal plexus. Consequently, free tumor cells can follow the submu-cosal lymphatic plexus in either direction for a long distance before they pass through the muscularis and on into the regional LNs. The cervical esophagus has more direct segmental lymph drainage into the regional nodes, and, as a result, lesions in this portion of the esophagus have less submucosal extension and a more regionalized lymphatic spread.The efferent lymphatics from the cervical esophagus drain into the paratracheal and deep cervical LNs, and those from the upper thoracic esophagus empty mainly into the paratracheal LNs. Efferent lymphatics from the lower thoracic esophagus drain into the subcarinal nodes and nodes in the inferior pulmo-nary ligaments. The superior gastric nodes receive lymph not only from the abdominal portion of the esophagus, but also from the adjacent lower thoracic segment.PHYSIOLOGYSwallowing MechanismThe act of alimentation requires the passage of


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Surgery_Schwartz. receive lymph not only from the abdominal portion of the esophagus, but also from the adjacent lower thoracic segment.PHYSIOLOGYSwallowing MechanismThe act of alimentation requires the passage of food and drink from the mouth into the stomach. One-third of this distance con-sists of the mouth and hypopharynx, and two-thirds is made up by the esophagus. To comprehend the mechanics of alimenta-tion, it is useful to visualize the gullet as a mechanical model in which the tongue and pharynx function as a piston pump with three valves, and the body of the esophagus and cardia function as a worm-drive pump with a single valve. The three valves in the pharyngeal cylinder are the soft palate, epiglottis, and cricopharyngeus. The valve of the esophageal pump is the LES. Failure of the valves or the pumps leads to abnormali-ties in swallowing—that is, difficulty in food propulsion from mouth to stomach—or regurgitation of gastric contents into the esophagus or pharynx.Food is taken into the


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Surgery_Schwartz. the pumps leads to abnormali-ties in swallowing—that is, difficulty in food propulsion from mouth to stomach—or regurgitation of gastric contents into the esophagus or pharynx.Food is taken into the mouth in a variety of bite sizes, where it is broken up, mixed with saliva, and lubricated. Once initiated, swallowing is entirely a reflex act. When food is ready for swallowing, the tongue, acting like a piston, moves the bolus into the posterior oropharynx and forces it into the hypopharynx (Fig. 25-12). Concomitantly with the posterior movement of the tongue, the soft palate is elevated, thereby closing the passage between the oropharynx and nasopharynx. This partitioning prevents pressure generated in the oropharynx from being dissipated through the nose. When the soft palate is paralyzed, for example, after a cerebrovascular accident, food is commonly regurgitated into the nasopharynx. During swal-lowing, the hyoid bone moves upward and anteriorly, elevating the larynx and opening


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Surgery_Schwartz. for example, after a cerebrovascular accident, food is commonly regurgitated into the nasopharynx. During swal-lowing, the hyoid bone moves upward and anteriorly, elevating the larynx and opening the retrolaryngeal space, bringing the epiglottis under the tongue (see Fig. 25-12). The backward tilt of the epiglottis covers the opening of the larynx to prevent aspi-ration. The entire pharyngeal part of swallowing occurs within 1.5 seconds.During swallowing, the pressure in the hypopharynx rises abruptly, to at least 60 mmHg, due to the backward movement of the tongue and contraction of the posterior pharyngeal con-strictors. A sizable pressure difference develops between the hypopharyngeal pressure and the less-than-atmospheric mid-esophageal or intrathoracic pressure (Fig. 25-13). This pressure 1. Elevation of tongue2. Posterior movement of tongue3. Elevation of soft palate4. Elevation of hyoid5. Elevation of larynx6. Tilting of epiglottis123456Figure 25-12. Sequence of events during


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Surgery_Schwartz. 1. Elevation of tongue2. Posterior movement of tongue3. Elevation of soft palate4. Elevation of hyoid5. Elevation of larynx6. Tilting of epiglottis123456Figure 25-12. Sequence of events during the oropharyngeal phase of swallowing. (Reproduced with permission from Zuidema GD, Orringer MB: Shackelford’s Surgery of the Alimentary Tract, 3rd ed. Vol 1. Philadelphia, PA: Elsevier/Saunders; 1991.)gradient speeds the movement of food from the hypopharynx into the esophagus when the cricopharyngeus or upper esopha-geal sphincter relaxes. The bolus is both propelled by peristaltic contraction of the posterior pharyngeal constrictors and sucked into the thoracic esophagus. Critical to receiving the bolus is the compliance of the cervical esophagus; when compliance is lost due to muscle pathology, dysphagia can result. The upper esophageal sphincter closes within 0.5 seconds of the initiation of the swallow, with the immediate closing pressure reaching Pressure (mm Hg)% Esophagus


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Surgery_Schwartz. pathology, dysphagia can result. The upper esophageal sphincter closes within 0.5 seconds of the initiation of the swallow, with the immediate closing pressure reaching Pressure (mm Hg)% Esophagus length100–10–505101520253035408060Upright position40200DESGECPAirFigure 25-13. Resting pressure profile of the foregut showing the pressure differential between the atmospheric pharyngeal pressure (P) and the less-than-atmospheric midesophageal pressure (E) and greater-than-atmospheric intragastric pressure (G), with the inter-posed high-pressure zones of the cricopharyngeus (C) and distal esophageal sphincter (DES). The necessity for relaxation of the cri-copharyngeus and DES pressure to move a bolus into the stomach is apparent. Esophageal work occurs when a bolus is pushed from the midesophageal area (E), with a pressure less than atmospheric, into the stomach, which has a pressure greater than atmospheric (G). (Reproduced with permission from Waters PF, DeMeester TR: Foregut motor


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Surgery_Schwartz. area (E), with a pressure less than atmospheric, into the stomach, which has a pressure greater than atmospheric (G). (Reproduced with permission from Waters PF, DeMeester TR: Foregut motor disorders and their surgical managemen, Med Clin North Am. 1981 Nov;65(6):1235-1268.)Brunicardi_Ch25_p1009-p1098.indd 101501/03/19 6:02 PM 1016SPECIFIC CONSIDERATIONSPART II0102030405060mmHgSwallowSeconds01020304050SecondsSeconds01020304050Seconds01020304050Seconds01020304050StomachHigh pressure zoneEsophageal bodyCricopharyngeusPharynxFigure 25-14. Intraluminal esophageal pressures in response to swallowing. (Reproduced with permission from Waters PF, DeMeester TR: Foregut motor disorders and their surgical man-agemen, Med Clin North Am. 1981 Nov;65(6):1235-1268.)approximately twice the resting level of 30 mmHg. The postre-laxation contraction continues down the esophagus as a peri-staltic wave (Fig. 25-14). The high closing pressure and the initiation of the peristaltic wave prevents reflux


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Surgery_Schwartz. of 30 mmHg. The postre-laxation contraction continues down the esophagus as a peri-staltic wave (Fig. 25-14). The high closing pressure and the initiation of the peristaltic wave prevents reflux of the bolus from the esophagus back into the pharynx. After the peristaltic wave has passed farther down the esophagus, the pressure in the upper esophageal sphincter returns to its resting level.Swallowing can be started at will, or it can be reflexively elicited by the stimulation of areas in the mouth and pharynx, among them the anterior and posterior tonsillar pillars or the posterior lateral walls of the hypopharynx. The afferent sen-sory nerves of the pharynx are the glossopharyngeal nerves and the superior laryngeal branches of the vagus nerves. Once aroused by stimuli entering via these nerves, the swallowing center in the medulla coordinates the complete act of swallow-ing by discharging impulses through cranial nerves V, VII, X, XI, and XII, as well as the motor neurons of C1 to C3.


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Surgery_Schwartz. the swallowing center in the medulla coordinates the complete act of swallow-ing by discharging impulses through cranial nerves V, VII, X, XI, and XII, as well as the motor neurons of C1 to C3. Dis-charges through these nerves occur in a rather specific pattern and last for approximately 0.5 seconds. Little is known about the organization of the swallowing center, except that it can trigger swallowing after a variety of different inputs, but the response is always a rigidly ordered pattern of outflow. Following a cere-brovascular accident, this coordinated outflow may be altered, causing mild to severe abnormalities of swallowing. In more severe injury, swallowing can be grossly disrupted, leading to repetitive aspiration.The striated muscles of the cricopharyngeus and the upper one-third of the esophagus are activated by efferent motor fibers distributed through the vagus nerve and its recurrent laryngeal branches. The integrity of innervation is required for the cri-copharyngeus to


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Surgery_Schwartz. of the esophagus are activated by efferent motor fibers distributed through the vagus nerve and its recurrent laryngeal branches. The integrity of innervation is required for the cri-copharyngeus to relax in coordination with the pharyngeal contraction, and resume its resting tone once a bolus has entered the upper esophagus. Operative damage to the innervation can interfere with laryngeal, cricopharyngeal, and upper esophageal function, and predispose the patient to aspiration.The pharyngeal activity in swallowing initiates the esoph-ageal phase. The body of the esophagus functions as a worm-drive propulsive pump due to the helical arrangement of its circular muscles, and it is responsible for transferring a bolus of food into the stomach. The esophageal phases of swallow-ing represent esophageal work done during alimentation, in that food is moved into the stomach from a negative-pressure environment of –6 mmHg intrathoracic pressure, to a positive-pressure environment of 6 mmHg


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Surgery_Schwartz. esophageal work done during alimentation, in that food is moved into the stomach from a negative-pressure environment of –6 mmHg intrathoracic pressure, to a positive-pressure environment of 6 mmHg intra-abdominal pressure, or over a gradient of 12 mmHg (see Fig. 25-13). Effective and coordinated smooth muscle function in the lower one-third of the esophagus is therefore important in pumping the food across this gradient.The peristaltic wave generates an occlusive pressure vary-ing from 30 to 120 mmHg (see Fig. 25-14). The wave rises to a peak in 1 second, lasts at the peak for about 0.5 seconds, and then subsides in about 1.5 seconds. The whole course of the rise and fall of occlusive pressure may occupy one point in the esophagus for 3 to 5 seconds. The peak of a primary peri-staltic contraction initiated by a swallow (primary peristalsis) moves down the esophagus at 2 to 4 cm/s and reaches the distal esophagus about 9 seconds after swallowing starts. Consecutive swallows produce


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Surgery_Schwartz. contraction initiated by a swallow (primary peristalsis) moves down the esophagus at 2 to 4 cm/s and reaches the distal esophagus about 9 seconds after swallowing starts. Consecutive swallows produce similar primary peristaltic waves, but when the act of swallowing is rapidly repeated, the esophagus remains relaxed and the peristaltic wave occurs only after the last move-ment of the pharynx. Progress of the wave in the esophagus is caused by sequential activation of its muscles, initiated by effer-ent vagal nerve fibers arising in the swallowing center.Continuity of the esophageal muscle is not necessary for sequential activation if the nerves are intact. If the muscles, but not the nerves, are cut across, the pressure wave begins dis-tally below the cut as it dies out at the proximal end above the cut. This allows a sleeve resection of the esophagus to be done without destroying its normal function. Afferent impulses from receptors within the esophageal wall are not essential for


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Surgery_Schwartz. end above the cut. This allows a sleeve resection of the esophagus to be done without destroying its normal function. Afferent impulses from receptors within the esophageal wall are not essential for prog-ress of the coordinated wave. Afferent nerves, however, do go to the swallowing center from the esophagus because if the esoph-agus is distended at any point, a contraction wave begins with a forceful closure of the upper esophageal sphincter and sweeps down the esophagus. This secondary contraction occurs without any movements of the mouth or pharynx. Secondary peristalsis can occur as an independent local reflex to clear the esophagus of ingested material left behind after the passage of the primary wave. Current studies suggest that secondary peristalsis is not as common as once thought.Despite the powerful occlusive pressure, the propulsive force of the esophagus is relatively feeble. If a subject attempts to swallow a bolus attached by a string to a counterweight, the maximum


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Surgery_Schwartz. the powerful occlusive pressure, the propulsive force of the esophagus is relatively feeble. If a subject attempts to swallow a bolus attached by a string to a counterweight, the maximum weight that can be overcome is 5 to 10 g. Orderly contractions of the muscular wall and anchoring of the esopha-gus at its inferior end are necessary for efficient aboral propul-sion to occur. Loss of the inferior anchor, as occurs with a large hiatal hernia, can lead to inefficient propulsion.The LES provides a pressure barrier between the esopha-gus and stomach and acts as the valve on the worm-drive pump of the esophageal body. Although an anatomically distinct LES has been difficult to identify, microdissection studies show that, in humans, the sphincter-like function is related to the Brunicardi_Ch25_p1009-p1098.indd 101601/03/19 6:02 PM 1017ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25Gastro-esophagealmuscular ringObliquefibersGreater curvaturewall thicknessLesser curvaturewall


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Surgery_Schwartz. 101601/03/19 6:02 PM 1017ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25Gastro-esophagealmuscular ringObliquefibersGreater curvaturewall thicknessLesser curvaturewall thicknessAnterior wall thicknessPhreno-esophagealmembraneSemi-circularfibers50-0-20--50-0 mm-20-50-0 mm-20Figure 25-15. Wall thickness and orientation of fibers on micro-dissection of the cardia. At the junction of the esophageal tube and gastric pouch, there is an oblique muscular ring composed of an increased muscle mass inside the inner muscular layer. On the lesser curve side of the cardia, the muscle fibers of the inner layer are oriented transversely and form semicircular muscle clasps. On the greater curve side of the cardia, these muscle fibers form oblique loops that encircle the distal end of the cardia and gastric fundus. Both the semicircular muscle clasps and the oblique fibers of the fundus contract in a circular manner to close the cardia. (Reproduced with permission from Glenn WWL: Thoracic and


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Surgery_Schwartz. gastric fundus. Both the semicircular muscle clasps and the oblique fibers of the fundus contract in a circular manner to close the cardia. (Reproduced with permission from Glenn WWL: Thoracic and Cardiovascular Surgery, 4th ed. Norwalk, CT: Appleton-Century-Crofts; 1983.)architecture of the muscle fibers at the junction of the esoph-ageal tube with the gastric pouch (Fig. 25-15). The sphincter actively remains closed to prevent reflux of gastric contents into the esophagus and opens by a relaxation that coincides with a pharyngeal swallow (see Fig. 25-14). The LES pressure returns to its resting level after the peristaltic wave has passed through the esophagus. Consequently, reflux of gastric juice that may occur through the open valve during a swallow is cleared back into the stomach.If the pharyngeal swallow does not initiate a peristaltic con-traction, then the coincident relaxation of the LES is unguarded and reflux of gastric juice can occur. This may be an explanation for the


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Surgery_Schwartz. the pharyngeal swallow does not initiate a peristaltic con-traction, then the coincident relaxation of the LES is unguarded and reflux of gastric juice can occur. This may be an explanation for the observation of spontaneous lower esophageal relaxation, thought by some to be a causative factor in gastroesophageal reflux disease (GERD). The power of the worm-drive pump of the esophageal body is insufficient to force open a valve that does not relax. In dogs, a bilateral cervical parasympathetic blockade abolishes the relaxation of the LES that occurs with pharyngeal swallowing or distention of the esophagus. Conse-quently, vagal function appears to be important in coordinating the relaxation of the LES with esophageal contraction.The antireflux mechanism in human beings is composed of three components: a mechanically effective LES, efficient esophageal clearance, and an adequately functioning gastric reservoir. A defect of any one of these three components can lead to increased


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Surgery_Schwartz. of three components: a mechanically effective LES, efficient esophageal clearance, and an adequately functioning gastric reservoir. A defect of any one of these three components can lead to increased esophageal exposure to gastric juice and the development of mucosal injury.Physiologic RefluxOn 24-hour esophageal pH monitoring, healthy individuals have occasional episodes of gastroesophageal reflux. This physi-ologic reflux is more common when awake and in the upright position than during sleep in the supine position. When reflux of gastric juice occurs, normal subjects rapidly clear the acid gastric juice from the esophagus regardless of their position.There are several explanations for the observation that physiologic reflux in normal subjects is more common when they are awake and in the upright position than during sleep in the supine position. First, reflux episodes occur in healthy vol-unteers primarily during transient losses of the gastroesophageal barrier, which may be due to


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Surgery_Schwartz. upright position than during sleep in the supine position. First, reflux episodes occur in healthy vol-unteers primarily during transient losses of the gastroesophageal barrier, which may be due to a relaxation of the LES or intra-gastric pressure overcoming sphincter pressure. Gastric juice can also reflux when a swallow-induced relaxation of the LES is not protected by an oncoming peristaltic wave. The average frequency of these “unguarded moments” or of transient losses of the gastroesophageal barrier is far less while asleep and in the supine position than while awake and in the upright posi-tion. Consequently, there are fewer opportunities for reflux to occur in the supine position. Second, in the upright position, there is a 12-mmHg pressure gradient between the resting, posi-tive intra-abdominal pressure measured in the stomach and the most negative intrathoracic pressure measured in the esophagus at midthoracic level. This gradient favors the flow of gastric juice up into the


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Surgery_Schwartz. pressure measured in the stomach and the most negative intrathoracic pressure measured in the esophagus at midthoracic level. This gradient favors the flow of gastric juice up into the thoracic esophagus when upright. The gradi-ent diminishes in the supine position. Third, the LES pressure in normal subjects is significantly higher in the supine posi-tion than in the upright position. This is due to the apposition of the hydrostatic pressure of the abdomen to the abdominal portion of the sphincter when supine. In the upright position, the abdominal pressure surrounding the sphincter is negative compared with atmospheric pressure, and, as expected, the abdominal pressure gradually increases the more caudally it is measured. This pressure gradient tends to move the gastric con-tents toward the cardia and encourages the occurrence of reflux into the esophagus when the individual is upright. In contrast, in the supine position, the gastroesophageal pressure gradient diminishes, and the


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Surgery_Schwartz. the cardia and encourages the occurrence of reflux into the esophagus when the individual is upright. In contrast, in the supine position, the gastroesophageal pressure gradient diminishes, and the abdominal hydrostatic pressure under the diaphragm increases, causing an increase in sphincter pressure and a more competent cardia.The LES has intrinsic myogenic tone, which is modu-lated by neural and hormonal mechanisms. α-Adrenergic neu-rotransmitters or β-blockers stimulate the LES, and α-blockers and β-stimulants decrease its pressure. It is not clear to what extent cholinergic nerve activity controls LES pressure. The vagus nerve carries both excitatory and inhibitory fibers to the esophagus and sphincter. The hormones gastrin and motilin have been shown to increase LES pressure; and cholecystokinin, estrogen, glucagon, progesterone, somatostatin, and secretin decrease LES pressure. The peptides bombesin, l-enkephalin, and substance P increase LES pressure; and calcitonin


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Surgery_Schwartz. and cholecystokinin, estrogen, glucagon, progesterone, somatostatin, and secretin decrease LES pressure. The peptides bombesin, l-enkephalin, and substance P increase LES pressure; and calcitonin gene-related peptide, gastric inhibitory peptide, neuropeptide Y, and vasoactive intestinal polypeptide decrease LES pressure. Some pharmacologic agents such as antacids, cholinergics, agonists, domperidone, metoclopramide, and prostaglandin F2 are known to increase LES pressure; and anticholinergics, barbiturates, cal-cium channel blockers, caffeine, diazepam, dopamine, meperi-dine, prostaglandin E1 and E2, and theophylline decrease LES pressure. Peppermint, chocolate, coffee, ethanol, and fat are all associated with decreased LES pressure and may be responsible for esophageal symptoms after a sumptuous meal.Brunicardi_Ch25_p1009-p1098.indd 101701/03/19 6:02 PM 1018SPECIFIC CONSIDERATIONSPART IIASSESSMENT OF ESOPHAGEAL FUNCTIONA thorough understanding of the patient’s underlying anatomic


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Surgery_Schwartz. meal.Brunicardi_Ch25_p1009-p1098.indd 101701/03/19 6:02 PM 1018SPECIFIC CONSIDERATIONSPART IIASSESSMENT OF ESOPHAGEAL FUNCTIONA thorough understanding of the patient’s underlying anatomic and functional deficits before making therapeutic decisions is fundamental to the successful treatment of esophageal disease. The diagnostic tests, as presently used, may be divided into four broad groups: (a) tests to detect structural abnormalities of the esophagus; (b) tests to detect functional abnormalities of the esophagus; (c) tests to detect increased esophageal expo-sure to gastric juice; and (d) tests of duodenogastric function as they relate to esophageal disease.Tests to Detect Structural AbnormalitiesEndoscopic Evaluation. The first diagnostic test in patients with suspected esophageal disease is usually upper gastrointesti-nal endoscopy. This allows assessment and biopsy of the mucosa of the stomach and the esophagus, as well as the diagnosis and assessment of obstructing lesions in


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Surgery_Schwartz. is usually upper gastrointesti-nal endoscopy. This allows assessment and biopsy of the mucosa of the stomach and the esophagus, as well as the diagnosis and assessment of obstructing lesions in the upper gastrointestinal tract. In any patient complaining of dysphagia, esophagoscopy is indicated, even in the face of a normal radiographic study.For the initial endoscopic assessment, the flexible fiber-optic esophagoscope is the instrument of choice because of its technical ease, patient acceptance, and the ability to simultane-ously assess the stomach and duodenum. Rigid endoscopy is now only rarely required, mainly for the disimpaction of diffi-cult foreign bodies impacted in the esophagus, and few individ-uals now have the skill set and experience to use this equipment.When GERD is the suspected diagnosis, particular atten-tion should be paid to detecting the presence of esophagitis and Barrett’s columnar-lined esophagus (CLE). When endoscopic esophagitis is seen, severity and the


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Surgery_Schwartz. suspected diagnosis, particular atten-tion should be paid to detecting the presence of esophagitis and Barrett’s columnar-lined esophagus (CLE). When endoscopic esophagitis is seen, severity and the length of esophagitis involved are recorded. Whilst many different grading systems have been proposed, the commonest system now in use is the Los Angeles (LA) grading system. In this system, mild esopha-gitis is classified LA grade A or B—one or more erosions lim-ited to the mucosal fold(s) and either less than or greater than 5 mm in longitudinal extent respectively (Fig. 25-16). More severe esophagitis is classified LA grade C or D. In grade C, erosions extend over the mucosal folds but over less than three-quarters of the esophageal circumference; in grade D, confluent erosions extend across more than three-quarters of the esopha-geal circumference. In addition to these grades, more severe damage can lead to the formation of a stricture. A stricture’s severity can be assessed by the


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Surgery_Schwartz. more than three-quarters of the esopha-geal circumference. In addition to these grades, more severe damage can lead to the formation of a stricture. A stricture’s severity can be assessed by the ease of passing a standard endo-scope. When a stricture is observed, the severity of the esopha-gitis above it should be recorded. The absence of esophagitis above a stricture suggests the possibility of a chemical-induced injury or a neoplasm as a cause. The latter should always be considered and is ruled out only by evaluation of a tissue biopsy of adequate size. It should be remembered that gastroesophageal reflux is not always associated with visible mucosal abnormali-ties, and patients can experience significant reflux symptoms, despite an apparently normal endoscopy examination.Barrett’s esophagus (BE) is a condition in which the tubu-lar esophagus is lined with columnar epithelium, as opposed to the normal squamous epithelium (see Fig. 25-16). Histologi-cally, it appears as intestinal


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Surgery_Schwartz. (BE) is a condition in which the tubu-lar esophagus is lined with columnar epithelium, as opposed to the normal squamous epithelium (see Fig. 25-16). Histologi-cally, it appears as intestinal metaplasia (IM). It is suspected at endoscopy when there is difficulty in visualizing the squamoco-lumnar junction at its normal location, and by the appearance of a redder, salmon-colored mucosa in the lower esophagus, with a clearly visible line of demarcation at the top of the Barrett’s esophagus segment. Its presence is confirmed by biopsy. Mul-tiple biopsy specimens should be taken in a cephalad direction to confirm the presence of IM, and to evaluate the Barrett’s epi-thelium for dysplastic changes. BE is susceptible to ulceration, bleeding, stricture formation, and, most important, malignant degeneration. The earliest sign of the latter is high grade dys-plasia or intramucosal adenocarcinoma (see Fig. 25-16). These dysplastic changes have a patchy distribution, so a minimum of four biopsy


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Surgery_Schwartz. The earliest sign of the latter is high grade dys-plasia or intramucosal adenocarcinoma (see Fig. 25-16). These dysplastic changes have a patchy distribution, so a minimum of four biopsy samples spaced 2 cm apart should be taken from the Barrett’s-lined portion of the esophagus. Changes seen in one biopsy are significant. Nishimaki has determined that the tumors occur in an area of specialized columnar epithelium near the squamocolumnar junction in 85% of patients, and within 2 cm of the squamocolumnar junction in virtually all patients. Particular attention should be focused on this area in patients suspected of harboring a carcinoma.Abnormalities of the gastroesophageal flap valve can be visualized by retroflexion of the endoscope. Hill has graded the appearance of the gastroesophageal valve from I to IV according to the degree of unfolding or deterioration of the normal valve architecture (Fig. 25-17). The appearance of the valve correlates with the presence of increased esophageal


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Surgery_Schwartz. from I to IV according to the degree of unfolding or deterioration of the normal valve architecture (Fig. 25-17). The appearance of the valve correlates with the presence of increased esophageal acid exposure, occur-ring predominantly in patients with grade III and IV valves.A hiatal hernia is endoscopically confirmed by finding a pouch lined with gastric rugal folds lying 2 cm or more above the margins of the diaphragmatic crura, identified by having the patient sniff. A hernia is best demonstrated with the stomach fully insufflated and the gastroesophageal junction observed with a retroflexed endoscope. A prominent sliding hiatal hernia frequently is associated with increased esophageal exposure to gastric juice. When a paraesophageal hernia (PEH) is observed, particular attention is taken to exclude gastric (Cameron’s) ulcers or gastritis within the pouch. The intragastric retroflex or J maneuver is important in evaluating the full circumference of the mucosal lining of the


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Surgery_Schwartz. is taken to exclude gastric (Cameron’s) ulcers or gastritis within the pouch. The intragastric retroflex or J maneuver is important in evaluating the full circumference of the mucosal lining of the herniated stomach.When an esophageal diverticulum is seen, it should be carefully explored with the flexible endoscope to exclude ulceration or neoplasia. When a submucosal mass is identified, biopsy specimens are usually not performed. At the time of sur-gical resection, a submucosal leiomyoma or reduplication cyst can generally be dissected away from the intact mucosa, but if a biopsy sample is taken, the mucosa may become fixed to the underlying abnormality. This complicates the surgical dissec-tion by increasing the risk of mucosal perforation. Endoscopic ultrasound provides a better method for evaluating these lesions.Radiographic Evaluation. Barium swallow evaluation is under-taken selectively to assess anatomy and motility. The anatomy of large hiatal hernias is more clearly


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Surgery_Schwartz. method for evaluating these lesions.Radiographic Evaluation. Barium swallow evaluation is under-taken selectively to assess anatomy and motility. The anatomy of large hiatal hernias is more clearly demonstrated by contrast radi-ology than endoscopy, and the presence of coordinated esopha-geal peristalsis can be determined by observing several individual swallows of barium traversing the entire length of the organ, with the patient in the horizontal position. Hiatal hernias are best demonstrated with the patient prone because the increased intra-abdominal pressure produced in this position promotes displace-ment of the esophagogastric junction above the diaphragm. To detect lower esophageal narrowing, such as rings and strictures, fully distended views of the esophagogastric region are crucial. The density of the barium used to study the esophagus can poten-tially affect the accuracy of the examination. Esophageal disorders shown clearly by a full-column technique include


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Surgery_Schwartz. are crucial. The density of the barium used to study the esophagus can poten-tially affect the accuracy of the examination. Esophageal disorders shown clearly by a full-column technique include circumferential carcinomas, peptic strictures, large esophageal ulcers, and hia-tal hernias. A small hiatal hernia is usually not associated with significant symptoms or illness, and its presence is an irrelevant finding unless the hiatal hernia is large (Fig. 25-18) or the hernia 1Brunicardi_Ch25_p1009-p1098.indd 101801/03/19 6:02 PM 1019ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25Figure 25-16. Complications of reflux disease as seen on endoscopy. A. Linear erosions of LA grade B esophagitis. B. Uncomplicated Barrett’s mucosa. C. High-grade dysplasia in Barrett’s mucosa. D. Early adenocarcinoma arising in Barrett’s mucosa.is of the paraesophageal variety. Lesions extrinsic but adjacent to the esophagus can be reliably detected by the full-column tech-nique if they contact the distended


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Surgery_Schwartz. arising in Barrett’s mucosa.is of the paraesophageal variety. Lesions extrinsic but adjacent to the esophagus can be reliably detected by the full-column tech-nique if they contact the distended esophageal wall. Conversely, a number of important disorders may go undetected if this is the sole technique used to examine the esophagus. These include small esophageal neoplasms, mild esophagitis, and esophageal varices. Thus, the full-column technique should be supplemented with mucosal relief or double-contrast films to enhance detection of these smaller or more subtle lesions.Motion-recording techniques greatly aid in evaluating functional disorders of the pharyngoesophageal and esophageal phases of swallowing. The technique and indications for cineand videoradiography will be discussed in the section entitled “Videoand Cineradiography,” as they are more useful to evalu-ate function and seldom used to detect structural abnormalities.The radiographic assessment of the esophagus is not


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Surgery_Schwartz. the section entitled “Videoand Cineradiography,” as they are more useful to evalu-ate function and seldom used to detect structural abnormalities.The radiographic assessment of the esophagus is not com-plete unless the entire stomach and duodenum have been examined. A gastric or duodenal ulcer, partially obstructing gastric neoplasm, or scarred duodenum and pylorus may contribute significantly to symptoms otherwise attributable to an esophageal abnormality.When a patient’s complaints include dysphagia and no obstructing lesion is seen on the barium swallow, it is useful to have the patient swallow a barium-impregnated marshmallow, a barium-soaked piece of bread, or a hamburger mixed with bar-ium. This test may bring out a functional disturbance in esopha-geal transport that can be missed when liquid barium is used.Tests to Detect Functional AbnormalitiesIn many patients with symptoms of an esophageal disorder, standard radiographic and endoscopic evaluation fails to dem-onstrate a


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Surgery_Schwartz. when liquid barium is used.Tests to Detect Functional AbnormalitiesIn many patients with symptoms of an esophageal disorder, standard radiographic and endoscopic evaluation fails to dem-onstrate a structural abnormality. In these situations, esophageal function tests are necessary to identify a functional disorder.Esophageal Motility. Esophageal motility is a widely used technique to examine the motor function of the esophagus and ABCDBrunicardi_Ch25_p1009-p1098.indd 101901/03/19 6:02 PM 1020SPECIFIC CONSIDERATIONSPART IIBACFigure 25-17. A. Grade I flap valve appearance. Note the ridge of tissue that is closely approximated to the shaft of the retroflexed endoscope. It extends 3 to 4 cm along the lesser curve. B. Grade II flap valve appearance. The ridge is slightly less well defined than in grade I and it opens rarely with respiration and closes promptly. C. Grade III flap valve appearance. The ridge is barely present, and there is often failure to close around the endoscope. It


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Surgery_Schwartz. than in grade I and it opens rarely with respiration and closes promptly. C. Grade III flap valve appearance. The ridge is barely present, and there is often failure to close around the endoscope. It is nearly always accompanied by a hiatal hernia. D. Grade IV flap valve appearance. There is no muscular ridge at all. The gastroesophageal valve stays open all the time, and squamous epithelium can often be seen from the retroflexed position. A hiatal hernia is always present. (Reproduced with permission from Hill LD, Kozarek RA, Kraemer SJ, et al: The gastroesophageal flap valve: in vitro and in vivo observations, Gastrointest Endosc. 1996 Nov;44(5):541-547.)Brunicardi_Ch25_p1009-p1098.indd 102001/03/19 6:02 PM 1021ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25Figure 25-18. Radiogram of an intrathoracic stomach. This is the end stage of a large hiatal hernia, regardless of its initial classification.RIP = Respiratory inversion pointRIP43424140393837 cmOverall lengthPressure10


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Surgery_Schwartz. of an intrathoracic stomach. This is the end stage of a large hiatal hernia, regardless of its initial classification.RIP = Respiratory inversion pointRIP43424140393837 cmOverall lengthPressure10 secEsophagealbaselinepressureAbdominal lengthGastricbaselinepressureFigure 25-19. Manometric pressure profile of the lower esophageal sphincter. The distances are measured from the nares. (Reproduced with permission from Zaninotto G, DeMeester TR, Schwizer W, et al: The lower esophageal sphincter in health and disease, Am J Surg. 1988 Jan;155(1):104-11.)DFigure 25-17. (Continued )its sphincters. The esophageal motility study (EMS) is indicated whenever a motor abnormality of the esophagus is suspected on the basis of complaints of dysphagia, odynophagia, or noncar-diac chest pain, and the barium swallow or endoscopy does not show a clear structural abnormality. EMS is particularly neces-sary to confirm the diagnosis of specific primary esophageal motility disorders (i.e., achalasia, diffuse


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Surgery_Schwartz. swallow or endoscopy does not show a clear structural abnormality. EMS is particularly neces-sary to confirm the diagnosis of specific primary esophageal motility disorders (i.e., achalasia, diffuse esophageal spasm [DES], nutcracker esophagus, and hypertensive LES). It also identifies nonspecific esophageal motility abnormalities and motility disorders secondary to systemic disease such as sclero-derma, dermatomyositis, polymyositis, or mixed connective tis-sue disease. In patients with symptomatic GERD, manometry of the esophageal body can identify a mechanically defective LES and evaluate the adequacy of esophageal peristalsis and contraction amplitude. EMS has become an essential tool in the preoperative evaluation of patients before antireflux surgery, guiding selection of the appropriate procedure based upon the patient’s underlying esophageal function and excluding patients with achalasia who can be misdiagnosed with gastroesophageal reflux when clinical and endoscopic


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Surgery_Schwartz. appropriate procedure based upon the patient’s underlying esophageal function and excluding patients with achalasia who can be misdiagnosed with gastroesophageal reflux when clinical and endoscopic parameters alone are used for diagnosis.EMS is performed using electronic, pressure-sensitive transducers located within the catheter, or water-perfused cath-eters with lateral side holes attached to transducers outside the body. The traditional water perfused catheter has largely been replaced by high resolution motility (HRM), but knowledge of traditional methods of assessing esophageal motility is helpful for understanding esophageal physiology.As the pressure-sensitive station is brought across the gas-troesophageal junction (GEJ), a rise in pressure above the gas-tric baseline signals the beginning of the LES. The respiratory inversion point is identified when the positive excursions that occur in the abdominal cavity with breathing change to negative deflections in the thorax. The


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Surgery_Schwartz. beginning of the LES. The respiratory inversion point is identified when the positive excursions that occur in the abdominal cavity with breathing change to negative deflections in the thorax. The respiratory inversion point serves as a reference point at which the amplitude of LES pressure and the length of the sphincter exposed to abdominal pressure are measured. As the pressure-sensitive station is withdrawn into the body of the esophagus, the upper border of the LES is identified by the drop in pressure to the esophageal baseline. From these measurements, the pressure, abdominal length, and overall length of the sphincter are determined (Fig. 25-19). To Brunicardi_Ch25_p1009-p1098.indd 102101/03/19 6:02 PM 1022SPECIFIC CONSIDERATIONSPART IILALPLPARPRRA25050Figure 25-20. Radial configuration of the lower esophageal sphincter. A = anterior; L = left; LA = left anterior; LP = left pos-terior; P = posterior; R = right; RA = right anterior; RP = right pos-terior. (Reproduced with


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Surgery_Schwartz. of the lower esophageal sphincter. A = anterior; L = left; LA = left anterior; LP = left pos-terior; P = posterior; R = right; RA = right anterior; RP = right pos-terior. (Reproduced with permission from Winans CS: Manometric asymmetry of the lower-esophageal high-pressure zone, Am J Dig Dis. 1977 Apr;22(4):348-354.)Table 25-1Normal manometric values of the distal esophageal sphincter, n = 50 MEDIAN PERCENTILE2.597.5Pressure (mmHg)135.827.7Overall length (cm)3.62.15.6Abdominal length (cm)20.94.7 MEANMEAN – 2 SDMEAN + 2 SDPressure (mmHg)13.8 ± 4.64.623.0Overall length (cm)3.7 ± 0.82.15.3Abdominal length (cm)2.2 ± 0.80.63.8SD = standard deviation.Reproduced with permission from Moody FG, Carey LC, Jones RS, et al: Surgical Treatment of Digestive Disease. Chicago, IL: Year Book Medical; 1990.account for the asymmetry of the sphincter (Fig. 25-20), the pressure profile is repeated with each of the five radially ori-ented transducers, and the average values for sphincter pressure above


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Surgery_Schwartz. for the asymmetry of the sphincter (Fig. 25-20), the pressure profile is repeated with each of the five radially ori-ented transducers, and the average values for sphincter pressure above gastric baseline, overall sphincter length, and abdominal length of the sphincter are calculated.Table 25-1 shows the values for these parameters in 50 normal volunteers without subjective or objective evidence of a foregut disorder. A mechanically defective sphincter is identified by having one or more of the following characteristics: an average LES pressure of <6 mmHg, an average length exposed to the positive-pressure environment in the abdomen of 1 cm or less, and/or an average overall sphincter length of 2 cm or less.High-Resolution Manometry. Esophageal manometry was introduced into clinical practice in the 1970s and, until recently, has changed little. In 1991, Ray Clouse introduced the concept of improving conventional manometry by increasing the number of recording sites and adding a


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Surgery_Schwartz. practice in the 1970s and, until recently, has changed little. In 1991, Ray Clouse introduced the concept of improving conventional manometry by increasing the number of recording sites and adding a three-dimensional assessment. This “high-resolution manometry” is a variant of the conventional manometry in which multiple, circumferential recording sites are used, in essence creating a “map” of the esophagus and its sphincters. High-resolution catheters contain 36 miniaturized pressure sensors positioned every centimeter along the length of the catheter. The vast amount of data generated by these sensors is then processed and presented in traditional linear plots or as a visually enhanced spatiotemporal video tracing that is readily interpreted. The function of the esophageal body is assessed with 10 to 15 wet swallows. Amplitude, duration, and morphology of contractions following each swallow are visually displayed (Fig. 25-21).The relationship of the esophageal contractions following


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Surgery_Schwartz. with 10 to 15 wet swallows. Amplitude, duration, and morphology of contractions following each swallow are visually displayed (Fig. 25-21).The relationship of the esophageal contractions following a swallow is classified as peristaltic or simultaneous. The data are used to identify motor disorders of the esophagus.The position, length, and function of the lower esopha-geal sphincter (LES) are demonstrated by a high-pressure zone that should relax at the inception of swallowing and contract after the water or solid bolus passes through the LES. Simul-taneous acquisition of data for the upper esophageal sphinc-ter, esophageal body, LES, and gastric pressure minimizes the movement artifacts and study time associated with conven-tional esophageal manometry. This technology significantly enhances esophageal diagnostics, bringing it into the realm of “image”-based studies. High-resolution manometry may allow the identification of focal motor abnormalities previ-ously overlooked. It has


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Surgery_Schwartz. esophageal diagnostics, bringing it into the realm of “image”-based studies. High-resolution manometry may allow the identification of focal motor abnormalities previ-ously overlooked. It has enhanced the ability to predict bolus propagation and increased sensitivity in the measurement of pressure gradients.Esophageal Impedance. Newer technology introduced into the clinical realm a decade ago allows measurement of esophageal function and gastroesophageal reflux in a way that was previously not possible. An intraluminal electrical imped-ance catheter is used to measure GI function. Impedance is the ratio of voltage to current, and is a measure of the electrical conductivity of a hollow organ and its contents. Intraluminal electrical impedance is inversely proportional to the electrical conductivity of the luminal contents and the cross-sectional area of the lumen. Air has a very low electrical conductivity and, therefore, high impedance. Saliva and food cause an imped-ance decrease


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Surgery_Schwartz. conductivity of the luminal contents and the cross-sectional area of the lumen. Air has a very low electrical conductivity and, therefore, high impedance. Saliva and food cause an imped-ance decrease because of their increased conductivity. Luminal dilatation results in a decrease in impedance, whereas luminal contraction yields an impedance increase. Investigators have established the impedance waveform characteristics that define esophageal bolus transport. This allows for the characterization of both esophageal function, via quantification of bolus trans-port, and gastroesophageal reflux (Fig. 25-22). The probe mea-sures impedance between adjacent electrodes, with measuring segments located at 2, 4, 6, 8, 14, and 16 cm from the distal tip. An extremely low electric current of 0.00025 μW is transmitted across the electrodes at a frequency of 1 to 2 kHz and is limited Brunicardi_Ch25_p1009-p1098.indd 102201/03/19 6:02 PM 1023ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25Figure


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Surgery_Schwartz. μW is transmitted across the electrodes at a frequency of 1 to 2 kHz and is limited Brunicardi_Ch25_p1009-p1098.indd 102201/03/19 6:02 PM 1023ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25Figure 25-21A. Normal high-resolution manometry motility study. Pressure measurements are recorded with color coding (red = high; blue = low). LES = lower esophageal sphincter; PIP = pressure inversion point; UES = upper esophageal sphincter.UES19.0LES41.840.343.7Gastric 46.2PIP42.3EsophagusPharynxStomachBrunicardi_Ch25_p1009-p1098.indd 102301/03/19 6:02 PM 1024SPECIFIC CONSIDERATIONSPART IIFigure 25-21B. High-resolution manometry motility study in patient with mechanically defective lower esophageal sphincter. Note the absence of lower esophageal sphincter tone. Pressure measure-ments are recorded with color coding (red = high; blue = low). LES = lower esophageal sphincter; PIP = pressure inversion point; UES = upper esophageal


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Surgery_Schwartz. esophageal sphincter tone. Pressure measure-ments are recorded with color coding (red = high; blue = low). LES = lower esophageal sphincter; PIP = pressure inversion point; UES = upper esophageal sphincter.EsophagusStomachPharynxUES20.8LES41.9PIP41.841.342.7Gastric 50.3Brunicardi_Ch25_p1009-p1098.indd 102401/03/19 6:02 PM 1025ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25Figure 25-21C. High-resolution manometry motility study in patient with deficient esophageal body peristalsis. Note the very weak peristalsis in the lower two-thirds of the esophagus. Pressure measurements are recorded with color coding (red = high; blue = low). LES = lower esophageal sphincter; PIP = pressure inversion point; UES = upper esophageal sphincter.EsophagusPharynxUES18.740.944.6Gastric 47.5LES42.2PIP42.3StomachBrunicardi_Ch25_p1009-p1098.indd 102501/03/19 6:02 PM 1026SPECIFIC CONSIDERATIONSPART IIFigure 25-21D. High-resolution manometry motility study in patient with achalasia. Note the complete


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Surgery_Schwartz. 102501/03/19 6:02 PM 1026SPECIFIC CONSIDERATIONSPART IIFigure 25-21D. High-resolution manometry motility study in patient with achalasia. Note the complete absence of esophageal body peristalsis, and the lack of relaxation of the lower esophageal sphincter. Pressure measurements are recorded with color coding (red = high; blue = low). LES = lower esophageal sphincter; PIP = pressure inversion point; UES = upper esophageal sphincter.EsophagusUES18.0Gastric 48.542.745.7LES43.8PIP44.1StomachPharynxBrunicardi_Ch25_p1009-p1098.indd 102601/03/19 6:03 PM 1027ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25Figure 25-21E. High-resolution manometry motility study in patient with diffuse esophageal spasm. Note the very high amplitude contractions in the esophageal body. Pressure measurements are recorded with color coding (red = high; blue = low). LES = lower esophageal sphincter; PIP = pressure inversion point; UES = upper esophageal sphincter.Gastric


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Surgery_Schwartz. body. Pressure measurements are recorded with color coding (red = high; blue = low). LES = lower esophageal sphincter; PIP = pressure inversion point; UES = upper esophageal sphincter.Gastric 51.745.6PharynxEsophagusLES47.4PIP47.1UES20.349.7StomachBrunicardi_Ch25_p1009-p1098.indd 102701/03/19 6:03 PM 1028SPECIFIC CONSIDERATIONSPART IIpH siteImpedence site17cm15cm9cm7cm5cmDistance above LESDistance above LES5cmLES3cmFigure 25-22. Esophageal impedance probe measures electrical resistance between evenly spaced electrodes. LES = lower esopha-geal sphincter.to 8 μA. This is below the stimulation threshold for nerves and muscles and is three orders of magnitude below the thresh-old of cardiac stimulation. A standard pH electrode is located 5 cm from the distal tip so that the acidic or nonacidic nature of refluxate can be correlated with the number of reflux events.Esophageal impedance has been validated as an appropri-ate method for the evaluation of GI function and is used


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Surgery_Schwartz. or nonacidic nature of refluxate can be correlated with the number of reflux events.Esophageal impedance has been validated as an appropri-ate method for the evaluation of GI function and is used selec-tively for the diagnosis of gastroesophageal reflux. It has been compared to cineradiography showing that impedance waves correspond well with actual bolus transport illustrated by radi-ography. Bolus entry, transit, and exit can be clearly identified by impedance changes in the corresponding measuring seg-ments. Studies comparing standard esophageal manometry with impedance measurements in healthy volunteers have shown that esophageal impedance correlates with peristaltic wave progres-sion and bolus length.Twenty-four-hour pH monitoring, the historical gold stan-dard for diagnosing and quantifying gastroesophageal reflux, has some significant limitations. With 24-hour ambulatory pH testing, reflux is defined as a drop in the pH below 4, which effectively “blinds” the test to reflux


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Surgery_Schwartz. quantifying gastroesophageal reflux, has some significant limitations. With 24-hour ambulatory pH testing, reflux is defined as a drop in the pH below 4, which effectively “blinds” the test to reflux occurring at higher pH values. Furthermore, in patients with persistent symptoms on proton pump inhibitor (PPI) therapy, pH monitoring has lim-ited use as it can only detect abnormal acid reflux (pH <4), the occurrence of which has been altered by the antisecretory medi-cation. Given that PPI antisecretory therapy is highly effective in neutralizing gastric acid, the question of whether persistent symptoms are a result of persistent acid reflux, nonacid reflux, or are not reflux related becomes a key issue in surgical decision making. Until recently, this differentiation could not be made. Detection of both acid and nonacid reflux has potential to define these populations of patients and thus improve patient selection for antireflux surgery. Multichannel intraluminal impedance technology


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Surgery_Schwartz. of both acid and nonacid reflux has potential to define these populations of patients and thus improve patient selection for antireflux surgery. Multichannel intraluminal impedance technology allows the measurement of both acid and nonacid reflux, with potential to enhance diagnostic accuracy.Using this technology, Balaji and colleagues showed that most gastroesophageal reflux remains despite acid suppression. Impedance pH may be particularly useful in evaluating patients with persistent symptoms despite PPI treatment, patients with respiratory symptoms, and postoperative patients who are hav-ing symptoms that are elusive to diagnosis.Esophageal Transit Scintigraphy. The esophageal transit of a 10-mL water bolus containing technetium-99m (99mTc) sulfur colloid can be recorded with a gamma camera. Using this tech-nique, delayed bolus transit has been shown in patients with a variety of esophageal motor disorders, including achalasia, scleroderma, DES, and nutcracker esophagus.Videoand


Surgery_Schwartz

Surgery_Schwartz. camera. Using this tech-nique, delayed bolus transit has been shown in patients with a variety of esophageal motor disorders, including achalasia, scleroderma, DES, and nutcracker esophagus.Videoand CineradiographyHigh-speed cinematic or video recording of radiographic studies allows re-evaluation by reviewing the studies at various speeds. This technique is more useful than manometry in the evaluation of the pharyngeal phase of swallowing. Observations suggesting oropharyngeal or cricopharyngeal dysfunction include misdirec-tion of barium into the trachea or nasopharynx, prominence of the cricopharyngeal muscle, a Zenker’s diverticulum, a narrow pharyngoesophageal segment, and stasis of the contrast medium in the valleculae or hypopharyngeal recesses (Fig. 25-23). These findings are usually not specific, but rather common manifesta-tions of neuromuscular disorders affecting the pharyngoesoph-ageal area. Studies using liquid barium, barium-impregnated solids, or radiopaque pills aid


Surgery_Schwartz

Surgery_Schwartz. not specific, but rather common manifesta-tions of neuromuscular disorders affecting the pharyngoesoph-ageal area. Studies using liquid barium, barium-impregnated solids, or radiopaque pills aid the evaluation of normal and abnormal motility in the esophageal body. Loss of the normal stripping wave or segmentation of the barium column with the patient in the recumbent position correlates with abnormal motility of the esophageal body. In addition, structural abnor-malities such as small diverticula, webs, and minimal extrin-sic impressions of the esophagus may be recognized only with motion-recording techniques. The simultaneous computerized capture of videofluoroscopic images and manometric tracings is now available and is referred to as manofluorography. Mano-fluorographic studies allow precise correlation of the anatomic events, such as opening of the upper esophageal sphincter, with manometric observations, such as sphincter relaxation. Mano-fluorography, although not widely