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Stenosis after colorectal endoscopic submucosal dissection: When to expect, how to manage?
EDITORIAL
Stenosis after colorectal endoscopic submucosal dissection: When to expect, how to manage? Endoscopic submucosal dissection (ESD) was developed in Japan for the en bloc removal of early gastrointestinal tract lesions.1-3 This technique is rapidly extending around the world, and it is now used for the removal of lesions inside the stomach, esophagus, small bowel, and large bowel.4-6 Although ESD has numerous advantages over traditional piecemeal EMR (eg, en bloc removal allows adequate histologic assessment of lateral and deep margins; ESD is associated with a high rate of curative resection and lower recurrence rates), ESD has a higher rate of immediate (bleeding, perforation) and delayed (bleeding, perforations, stenosis) adverse events compared with EMR.7-11 There is a clear consensus in the available literature regarding frequency of stenosis after gastric and esophageal ESD: resection of lesions occupying more than 75% of the esophageal or gastric (cardia, pylorus) circumference has a very high risk (44.4%-100%) of subsequent stricture formation.12-17 However, there is no consensus in the available literature regarding the development of strictures after colorectal ESD. Only 2 previous full-length publications addressed the rate of stenosis after rectal ESD; although the first study18 (69 rectal tumors occupying over 75% of rectal circumference) demonstrated a very high risk of post-ESD rectal strictures (71.4% after total circumferential resection and 43.8% after subtotal [over 90% of circumference] resection), the second study observed rectal stenosis only in 1 (4.2%) clinically asymptomatic patient.19 The study by Hayashi et al20 in the current issue of Gastrointestinal Endoscopy summarized a 12-year (20032015) single-center experience of 822 patients with 912 consecutive colorectal lesions.20 Four (0.49%) of 822 patients developed stenosis after ESD.20 There were no documented strictures where less than 90% of the colorectal circumference was resected.20 Post-ESD stenosis was observed in 11.1% of patients with subtotal resection (more than 90% but less than 100% of circumference) and in 50% of patients with total (100%) circumferential resection.20 All patients were treated successfully with endoscopic dilation, and only 1 patient required additional local administration of steroids.20
What can we learn from this study? First, it appears that the rectum is a more “forgiving” space than the esophagus and stomach; even resection of up to 90% of the rectal circumference did not cause the development of strictures, and resection between 90% and 100% of the circumference had only a modest (11.1%) risk of subsequent stricture formation.20 By contrast, total circumferential resection carries a significant risk (50%) of subsequent rectal stricture.20 The lower rate of rectal post-ESD strictures is most likely due to the larger diameter of the rectum (compared with the esophagus, cardia, or pylorus) and a stronger muscle wall forcing formed stool through the stenotic area.18
What can we learn from this study? First, it appears that the rectum is a more “forgiving” space than the esophagus and stomach; even resection of up to 90% of the rectal circumference did not cause the development of strictures, and resection between 90% and 100% of the circumference had only a modest (11.1%) risk of subsequent stricture formation.
Copyright ª 2017 by the American Society for Gastrointestinal Endoscopy 0016-5107/$36.00 http://dx.doi.org/10.1016/j.gie.2017.04.031
Second, the previously recommended prophylactic use of local (injection of triamcinolone into the ulcer floor and administration of betamethasone suppositories)18,21 and oral (prednisolone in tapered doses)18,22,23 steroids were not needed after large rectal ESD. Third, rectal strictures after ESD rarely caused any clinical symptoms. However, when rectal “self-dilation” by stool failed and patients experienced clinically evident rectal strictures, the rectal lumen was easily restored by endoscopic balloon dilation, and only 1 study patient required additional local steroid suppositories.20 The study definitely has some limitations. It was a retrospective, single-center experience with only a limited number of patients with subtotal (over 90%) and total (100%) circumferential resection. Most of the strictures (3 of 4) discovered in this study were in the rectum, and the exact location of the one encountered colonic stricture was not described. The optimal time for follow-up colonoscopy is still not clear: the authors arranged surveillance colonoscopy 6 months after ESD to “observe the healing progress of the mucosal defect.”20 However, all 4 patients with
370 GASTROINTESTINAL ENDOSCOPY Volume 86, No. 2 : 2017
www.giejournal.org
Kantsevoy
Editorial
post-ESD strictures required “unanticipated” endoscopy based on their clinical symptoms of stenosis not responding to oral “laxatives and lactobacillus preparations.”20 It will probably be more cost effective to perform earlier colonoscopy (3-4 months after ESD) with prophylactic dilation of the developing stenotic area before the first manifestation of clinical symptoms. In conclusion, the interest in the performance of ESD in the United States is growing exponentially, and more gastroenterologists and surgeons are learning and performing colonic ESD. The study by Hayashi et al20 gives us a new, timely insight into the management of a very important delayed adverse event: stricture formation after colorectal ESD. DISCLOSURE Dr Kantsevoy is a consultant for Olympus and Apollo Endosurgery and is a co-founder of, and shareholder in, Apollo Endosurgery. Sergey V. Kantsevoy, MD, PhD Institute for Digestive Health and Liver Diseases Mercy Medical Center University of Maryland School of Medicine Baltimore, Maryland, USA Abbreviation: ESD, endoscopic submucosal dissection.
REFERENCES 1. Larghi A, Waxman I. State of the art on endoscopic mucosal resection and endoscopic submucosal dissection. Gastrointest Endosc Clin N Am 2007;17:441-69; v. 2. Oda I, Suzuki H, Nonaka S, et al. Complications of gastric endoscopic submucosal dissection. Dig Endosc 2013;25:71-8. 3. Ono H, Kondo H, Gotoda T, et al. Endoscopic mucosal resection for treatment of early gastric cancer. Gut 2001;48:225-9. 4. Draganov PV, Gotoda T, Chavalitdhamrong D, et al. Techniques of endoscopic submucosal dissection: application for the Western endoscopist? Gastrointest Endosc 2013;78:677-88. 5. Farhat S, Chaussade S, Ponchon T, et al. Endoscopic submucosal dissection in a European setting: a multi-institutional report of a technique in development. Endoscopy 2011;43:664-70. 6. Uraoka T, Parra-Blanco A, Yahagi N. Colorectal endoscopic submucosal dissection: is it suitable in Western countries? J Gastroenterol Hepatol 2013;28:406-14.
www.giejournal.org
7. Oka S, Tanaka S, Kaneko I, et al. Advantage of endoscopic submucosal dissection compared with EMR for early gastric cancer. Gastrointest Endosc 2006;64:877-83. 8. Oka S, Tanaka S, Kanao H, et al. Current status in the occurrence of postoperative bleeding, perforation and residual/local recurrence during colonoscopic treatment in Japan. Dig Endosc 2010;22:376-80. 9. Fujiya M, Tanaka K, Dokoshi T, et al. Efficacy and adverse events of EMR and endoscopic submucosal dissection for the treatment of colon neoplasms: a meta-analysis of studies comparing EMR and endoscopic submucosal dissection. Gastrointest Endosc 2015;81:583-95. 10. Cao Y, Liao C, Tan A, et al. Meta-analysis of endoscopic submucosal dissection versus endoscopic mucosal resection for tumors of the gastrointestinal tract. Endoscopy 2009;41:751-7. 11. Nakajima T, Saito Y, Tanaka S, et al. Current status of endoscopic resection strategy for large, early colorectal neoplasia in Japan. Surg Endosc 2013;27:3262-70. 12. Katada C, Muto M, Manabe T, et al. Esophageal stenosis after endoscopic mucosal resection of superficial esophageal lesions. Gastrointest Endosc 2003;57:165-9. 13. Mizuta H, Nishimori I, Kuratani Y, et al. Predictive factors for esophageal stenosis after endoscopic submucosal dissection for superficial esophageal cancer. Dis Esophagus 2009;22:626-31. 14. Ono S, Fujishiro M, Niimi K, et al. Predictors of postoperative stricture after esophageal endoscopic submucosal dissection for superficial squamous cell neoplasms. Endoscopy 2009;41:661-5. 15. Coda S, Oda I, Gotoda T, et al. Risk factors for cardiac and pyloric stenosis after endoscopic submucosal dissection, and efficacy of endoscopic balloon dilation treatment. Endoscopy 2009;41:421-6. 16. Iizuka H, Kakizaki S, Sohara N, et al. Stricture after endoscopic submucosal dissection for early gastric cancers and adenomas. Dig Endosc 2010;22:282-8. 17. Shi Q, Ju H, Yao LQ, et al. Risk factors for postoperative stricture after endoscopic submucosal dissection for superficial esophageal carcinoma. Endoscopy 2014;46:640-4. 18. Ohara Y, Toyonaga T, Tanaka S, et al. Risk of stricture after endoscopic submucosal dissection for large rectal neoplasms. Endoscopy 2016;48: 62-70. 19. Abe S, Sakamoto T, Takamaru H, et al. Stenosis rates after endoscopic submucosal dissection of large rectal tumors involving greater than three quarters of the luminal circumference. Surg Endosc 2016;30: 5459-64. 20. Hayashi T, Kudo S-e, Miyachi H, et al. Management and risk factor of stenosis after endoscopic submucosal dissection for colorectal neoplasms. Gastrointest Endosc 2017;86:358-69. 21. Hashimoto S, Kobayashi M, Takeuchi M, et al. The efficacy of endoscopic triamcinolone injection for the prevention of esophageal stricture after endoscopic submucosal dissection. Gastrointest Endosc 2011;74:1389-93. 22. Yamaguchi N, Isomoto H, Nakayama T, et al. Usefulness of oral prednisolone in the treatment of esophageal stricture after endoscopic submucosal dissection for superficial esophageal squamous cell carcinoma. Gastrointest Endosc 2011;73:1115-21. 23. Shoji H, Yamaguchi N, Isomoto H, et al. Oral prednisolone and triamcinolone injection for gastric stricture after endoscopic submucosal dissection. Ann Transl Med 2014;2:22.
Volume 86, No. 2 : 2017 GASTROINTESTINAL ENDOSCOPY 371
Stenosis after colorectal endoscopic submucosal dissection: When to expect, how to manage? Endoscopic submucosal dissection (ESD) was developed in Japan for the en bloc removal of early gastrointestinal tract lesions.1-3 This technique is rapidly extending around the world, and it is now used for the removal of lesions inside the stomach, esophagus, small bowel, and large bowel.4-6 Although ESD has numerous advantages over traditional piecemeal EMR (eg, en bloc removal allows adequate histologic assessment of lateral and deep margins; ESD is associated with a high rate of curative resection and lower recurrence rates), ESD has a higher rate of immediate (bleeding, perforation) and delayed (bleeding, perforations, stenosis) adverse events compared with EMR.7-11 There is a clear consensus in the available literature regarding frequency of stenosis after gastric and esophageal ESD: resection of lesions occupying more than 75% of the esophageal or gastric (cardia, pylorus) circumference has a very high risk (44.4%-100%) of subsequent stricture formation.12-17 However, there is no consensus in the available literature regarding the development of strictures after colorectal ESD. Only 2 previous full-length publications addressed the rate of stenosis after rectal ESD; although the first study18 (69 rectal tumors occupying over 75% of rectal circumference) demonstrated a very high risk of post-ESD rectal strictures (71.4% after total circumferential resection and 43.8% after subtotal [over 90% of circumference] resection), the second study observed rectal stenosis only in 1 (4.2%) clinically asymptomatic patient.19 The study by Hayashi et al20 in the current issue of Gastrointestinal Endoscopy summarized a 12-year (20032015) single-center experience of 822 patients with 912 consecutive colorectal lesions.20 Four (0.49%) of 822 patients developed stenosis after ESD.20 There were no documented strictures where less than 90% of the colorectal circumference was resected.20 Post-ESD stenosis was observed in 11.1% of patients with subtotal resection (more than 90% but less than 100% of circumference) and in 50% of patients with total (100%) circumferential resection.20 All patients were treated successfully with endoscopic dilation, and only 1 patient required additional local administration of steroids.20
What can we learn from this study? First, it appears that the rectum is a more “forgiving” space than the esophagus and stomach; even resection of up to 90% of the rectal circumference did not cause the development of strictures, and resection between 90% and 100% of the circumference had only a modest (11.1%) risk of subsequent stricture formation.20 By contrast, total circumferential resection carries a significant risk (50%) of subsequent rectal stricture.20 The lower rate of rectal post-ESD strictures is most likely due to the larger diameter of the rectum (compared with the esophagus, cardia, or pylorus) and a stronger muscle wall forcing formed stool through the stenotic area.18
What can we learn from this study? First, it appears that the rectum is a more “forgiving” space than the esophagus and stomach; even resection of up to 90% of the rectal circumference did not cause the development of strictures, and resection between 90% and 100% of the circumference had only a modest (11.1%) risk of subsequent stricture formation.
Copyright ª 2017 by the American Society for Gastrointestinal Endoscopy 0016-5107/$36.00 http://dx.doi.org/10.1016/j.gie.2017.04.031
Second, the previously recommended prophylactic use of local (injection of triamcinolone into the ulcer floor and administration of betamethasone suppositories)18,21 and oral (prednisolone in tapered doses)18,22,23 steroids were not needed after large rectal ESD. Third, rectal strictures after ESD rarely caused any clinical symptoms. However, when rectal “self-dilation” by stool failed and patients experienced clinically evident rectal strictures, the rectal lumen was easily restored by endoscopic balloon dilation, and only 1 study patient required additional local steroid suppositories.20 The study definitely has some limitations. It was a retrospective, single-center experience with only a limited number of patients with subtotal (over 90%) and total (100%) circumferential resection. Most of the strictures (3 of 4) discovered in this study were in the rectum, and the exact location of the one encountered colonic stricture was not described. The optimal time for follow-up colonoscopy is still not clear: the authors arranged surveillance colonoscopy 6 months after ESD to “observe the healing progress of the mucosal defect.”20 However, all 4 patients with
370 GASTROINTESTINAL ENDOSCOPY Volume 86, No. 2 : 2017
www.giejournal.org
Kantsevoy
Editorial
post-ESD strictures required “unanticipated” endoscopy based on their clinical symptoms of stenosis not responding to oral “laxatives and lactobacillus preparations.”20 It will probably be more cost effective to perform earlier colonoscopy (3-4 months after ESD) with prophylactic dilation of the developing stenotic area before the first manifestation of clinical symptoms. In conclusion, the interest in the performance of ESD in the United States is growing exponentially, and more gastroenterologists and surgeons are learning and performing colonic ESD. The study by Hayashi et al20 gives us a new, timely insight into the management of a very important delayed adverse event: stricture formation after colorectal ESD. DISCLOSURE Dr Kantsevoy is a consultant for Olympus and Apollo Endosurgery and is a co-founder of, and shareholder in, Apollo Endosurgery. Sergey V. Kantsevoy, MD, PhD Institute for Digestive Health and Liver Diseases Mercy Medical Center University of Maryland School of Medicine Baltimore, Maryland, USA Abbreviation: ESD, endoscopic submucosal dissection.
REFERENCES 1. Larghi A, Waxman I. State of the art on endoscopic mucosal resection and endoscopic submucosal dissection. Gastrointest Endosc Clin N Am 2007;17:441-69; v. 2. Oda I, Suzuki H, Nonaka S, et al. Complications of gastric endoscopic submucosal dissection. Dig Endosc 2013;25:71-8. 3. Ono H, Kondo H, Gotoda T, et al. Endoscopic mucosal resection for treatment of early gastric cancer. Gut 2001;48:225-9. 4. Draganov PV, Gotoda T, Chavalitdhamrong D, et al. Techniques of endoscopic submucosal dissection: application for the Western endoscopist? Gastrointest Endosc 2013;78:677-88. 5. Farhat S, Chaussade S, Ponchon T, et al. Endoscopic submucosal dissection in a European setting: a multi-institutional report of a technique in development. Endoscopy 2011;43:664-70. 6. Uraoka T, Parra-Blanco A, Yahagi N. Colorectal endoscopic submucosal dissection: is it suitable in Western countries? J Gastroenterol Hepatol 2013;28:406-14.
www.giejournal.org
7. Oka S, Tanaka S, Kaneko I, et al. Advantage of endoscopic submucosal dissection compared with EMR for early gastric cancer. Gastrointest Endosc 2006;64:877-83. 8. Oka S, Tanaka S, Kanao H, et al. Current status in the occurrence of postoperative bleeding, perforation and residual/local recurrence during colonoscopic treatment in Japan. Dig Endosc 2010;22:376-80. 9. Fujiya M, Tanaka K, Dokoshi T, et al. Efficacy and adverse events of EMR and endoscopic submucosal dissection for the treatment of colon neoplasms: a meta-analysis of studies comparing EMR and endoscopic submucosal dissection. Gastrointest Endosc 2015;81:583-95. 10. Cao Y, Liao C, Tan A, et al. Meta-analysis of endoscopic submucosal dissection versus endoscopic mucosal resection for tumors of the gastrointestinal tract. Endoscopy 2009;41:751-7. 11. Nakajima T, Saito Y, Tanaka S, et al. Current status of endoscopic resection strategy for large, early colorectal neoplasia in Japan. Surg Endosc 2013;27:3262-70. 12. Katada C, Muto M, Manabe T, et al. Esophageal stenosis after endoscopic mucosal resection of superficial esophageal lesions. Gastrointest Endosc 2003;57:165-9. 13. Mizuta H, Nishimori I, Kuratani Y, et al. Predictive factors for esophageal stenosis after endoscopic submucosal dissection for superficial esophageal cancer. Dis Esophagus 2009;22:626-31. 14. Ono S, Fujishiro M, Niimi K, et al. Predictors of postoperative stricture after esophageal endoscopic submucosal dissection for superficial squamous cell neoplasms. Endoscopy 2009;41:661-5. 15. Coda S, Oda I, Gotoda T, et al. Risk factors for cardiac and pyloric stenosis after endoscopic submucosal dissection, and efficacy of endoscopic balloon dilation treatment. Endoscopy 2009;41:421-6. 16. Iizuka H, Kakizaki S, Sohara N, et al. Stricture after endoscopic submucosal dissection for early gastric cancers and adenomas. Dig Endosc 2010;22:282-8. 17. Shi Q, Ju H, Yao LQ, et al. Risk factors for postoperative stricture after endoscopic submucosal dissection for superficial esophageal carcinoma. Endoscopy 2014;46:640-4. 18. Ohara Y, Toyonaga T, Tanaka S, et al. Risk of stricture after endoscopic submucosal dissection for large rectal neoplasms. Endoscopy 2016;48: 62-70. 19. Abe S, Sakamoto T, Takamaru H, et al. Stenosis rates after endoscopic submucosal dissection of large rectal tumors involving greater than three quarters of the luminal circumference. Surg Endosc 2016;30: 5459-64. 20. Hayashi T, Kudo S-e, Miyachi H, et al. Management and risk factor of stenosis after endoscopic submucosal dissection for colorectal neoplasms. Gastrointest Endosc 2017;86:358-69. 21. Hashimoto S, Kobayashi M, Takeuchi M, et al. The efficacy of endoscopic triamcinolone injection for the prevention of esophageal stricture after endoscopic submucosal dissection. Gastrointest Endosc 2011;74:1389-93. 22. Yamaguchi N, Isomoto H, Nakayama T, et al. Usefulness of oral prednisolone in the treatment of esophageal stricture after endoscopic submucosal dissection for superficial esophageal squamous cell carcinoma. Gastrointest Endosc 2011;73:1115-21. 23. Shoji H, Yamaguchi N, Isomoto H, et al. Oral prednisolone and triamcinolone injection for gastric stricture after endoscopic submucosal dissection. Ann Transl Med 2014;2:22.
Volume 86, No. 2 : 2017 GASTROINTESTINAL ENDOSCOPY 371