Colonoscopic surveillance after polypectomy

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Clinical Practice Guidelines for Surveillance Colonoscopy > Colonoscopic surveillance after polypectomy


Compared with individuals in whom no adenomas are found at colonoscopy, those in whom adenomas have been found and removed are at an increased risk of developing subsequent adenomas. This is the basis for surveillance, with the ultimate goal of reducing colorectal cancer (CRCColorectal cancer)-related mortality.

An overall increase in colonoscopy numbers and quality has resulted in substantially more adenomas being detected and more individuals requiring subsequent surveillance. In the 10 years between 2000–2001 and 2009–2010, the utilisation of Medicare Benefits Schedule items for colonoscopy increased in all Australian states and territories. In per capita terms, there was an 84% increase, from 13.4 per 1000 to 24.6 per 1000 population, between the two periods.[1] The expansion of the National Bowel Cancer Screening Program (NBCSP)An Australian screening program that aims to reduce illness and death from bowel cancer through early detection or prevention of the disease. will further add to the demand for colonoscopies and the associated financial burden.

The cost is not only financial. Although colonoscopy is generally safe,[2] cumulative procedures add risks, and surveillance is increasingly used in the elderly, for whom risks are higher.[3] The ‘burden’ of surveillance colonoscopy on colonoscopy services is also increasingly recognised; there is a major concern that it diverts resources away from others needing colonoscopy (e.g. diagnostic and screening procedures).

To rationalise resource utilisation, surveillance colonoscopy should be directed to those who will benefit most; procedures which are of little, if any, clinical benefit – such as colonoscopies for patients in whom surveillance procedures are less likely to detect significant pathology – should be minimised. In systematic reviews of the overuse of medical care, colonoscopy is consistently featured.[4][5] The screening and surveillance colonoscopy literature also highlights poor compliance with guidelines, with procedures often recommended too frequently overall but with those at high risk often having procedures less frequently than recommended by guidelines.[6][7][8][9]

Given the high quality of contemporary colonoscopy, with a lower risk of missing significant polyps and higher adenoma detection rates at index colonoscopy, recommendations based on data from previous eras of lower quality colonoscopy would result in inappropriately frequent surveillance colonoscopy.[10] New understandings must also be incorporated. In generating the current guidelines, all of these issues have been considered as well as initiatives to ensure Australia’s colonoscopy services are of high quality.[11]Back to top

ColorectalReferring to the large bowel, comprising the colon and rectum. cancer precursors

Two main pathways are recognised in the development of CRCColorectal cancer:

  • the classic adenoma-carcinoma pathway, with conventional tubular, tubulovillous and villous adenoma precursors
  • the serrated pathway, with sessile serrated adenoma (SSA) and traditional serrated adenoma (TSATraditional serrated adenoma) precursors).

The pathway by which CRCColorectal cancer develops in patients with longstanding inflammatory bowel disease (IBDInflammatory bowel disease) is different (see Colonoscopic surveillance and management of dysplasia in IBD)

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Conventional (tubular, tubulovillous and villous) adenomas

Sixty-five to 70% of CRCs originate from adenomas, which are clonal proliferations of colonic epithelial cells with intraepithelial dysplasia or neoplasia.[12] Observational and autopsy studies first suggested adenomas were precursor lesions, [13][14] with a prevalence of 20–53% in adults over 50 years of age and 30% over 35 years of age.[15] The lifetime risk of CRCColorectal cancer is much lower, at 5–6%.[16][17] This means that only a minority of adenomas develop into cancer, highlighting the variable natural history of adenomas, with phases of growth, stability and regression.[18][19] The 10-year cumulative progression from adenoma to carcinoma is less than 10%[20] or 0.25% transition rate per year.[15] Variability in growth and malignant potential are determined by genetic or epigenetic cumulative mutations as well as environmental (diet and lifestyle) interventions.

The main pathways in CRCColorectal cancer carcinogenesis are

  • the chromosomal instability pathway affecting APC, KRASKirsten rat sarcoma and TP53Tumour suppressor p53, characteristic of adenomas in familial adenomatous polyposis
  • the microsatellite instability pathway, which involves mutation of tandem repeats (also known as microsatellites) due to inactivation of the DNADeoxyribonucleic acid mismatch repair (MMRMismatch repair) genes, characteristic of adenomas occurring in Lynch syndrome.

Conventional adenomas may appear macroscopically as elevated, flat or depressed. Elevated lesions may be sessile or pedunculated.[21][22] Classifications of endoscopic appearance of polyps, such as the Paris classification (Figure 1),[23] are useful for standardised polyp description in endoscopy reports.[24][25]

Accumulation of mutations over time leads to a small tubular adenoma increasing in size, the dysplasia becoming high grade and an increasing proportion of villous features. An advanced adenoma (AA) is an adenoma with any one of three features: size ≥10mm, high-grade dysplasia (HGDHigh grade dysplasia) or villosity. The ability to develop angiogenesis and local spread to the lymphatics (found in the submucosal layer in the colon) is associated with progression to a malignant polyp or frank adenocarcinoma. The chance of any single adenoma harbouring a malignant focus is related to size: <1% if <1cm, 5% if 1–2cm and 10–20% if >2cm.[22]

Advanced adenoma features and adenoma multiplicity (≥3 adenomas) are also related to the risk of an individual developing future (metachronous) adenomas.

Figure 1. Paris classification of superficial (Type 0) colonic neoplasia[23]Paris classification.PNG Adapted with permission from Clinical Gastroenterology and Hepatology, Vol 10(9), Holt BA, Bourke MJ, Wide field endoscopic resection for advanced colonic mucosal neoplasia: current status and future directions, 969–979, © 2012 AGAAmerican Gastroenterological Association Institute. Published by Elsevier Ltd.

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Serrated polyps

Over the last 20–25 years, lesions previously labelled as hyperplastic polyps (HPs) have been renamed serrated polyps (SPs), and are characterised by serrated architecture. There are three main sub-groups: true hyperplastic polyps, SSA and TSAs. Whilst the true diminutive distal HP has no significant malignant potential, the malignant potential of the SSA and TSATraditional serrated adenoma has been clearly established and they are thought to be responsible for around 20% of CRCs. Although the natural history of the SSA and TSATraditional serrated adenoma continue to be studied, it is clear some SPs have an indolent course, often remaining benign for many years, but with the potential to then progress rapidly. Factors associated with this malignant transformation are not clear at this stage.

The initiating event for SPs is up-regulation of the MAPK pathwayA chain of proteins in the cell that communicates a signal from a receptor on the surface of the cell to the DNA in the nucleus., usually by mutation of the BRAF oncogene. BRAF mutation is the initiating event in the vast majority of SSAs and two-thirds of TSAs, but is extremely rare in conventional adenomas (which are instead initiated by dysregulation of the Wnt pathway, usually by mutation of the APC tumour suppressor gene). The serrated pathway is thought to progress via DNADeoxyribonucleic acid methylation, which may lead to silencing of MLH1 (and thus microsatellite instability) and other genes, including up-regulation of the Wnt pathway. These additional changes are associated with the development of dysplasia and rapid progression to malignancy.[17][26]

Histologically, SPs are characterised by exaggerated, saw-toothed, luminal serrations. Subtypes, specifically SSAs, show dilation and distortion in the bases of the colonic crypts.[22] SPs from all locations must be assessed by the same reproducible histologic criteria to ensure diagnostic accuracy and consistency, although this may be challenging. Endoscopically, SSAs are often subtle, with indistinct edges and a cloud-like surface. They are more often located in the right colon and covered by a mucous cap. They are characteristically inconspicuous and are easily missed. TSAs are often located more distally and more closely resemble conventional adenomas. The NBI International ColorectalReferring to the large bowel, comprising the colon and rectum. Endoscopic[27] and Workgroup serrAted polypS and Polyposis (WASPWorkgroup serrAted polypS and Polyposis)[28] classifications offer guidance about characterisation of polyps at endoscopy.

Endoscopic and histologic features of higher-risk SPs continue to be described; limitations in this area include the relatively recent recognition and classification of SPs, their relatively low prevalence and variable pathologic definition, particularly the distinction between HPs and SSAs. Size ≥10mm, proximal location and the co-existence of conventional dysplasia have been suggested as important features of higher risk (see First surveillance intervals following removal of high risk conventional adenomas only).

In light of increased understanding of SPs, surveillance recommendations for individuals following the removal of SPs with or without synchronous conventional (tubular, tubulovillous or villous) adenomas are separated from those with conventional adenomas alone.

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Surveillance considerations

Quality of care

Surveillance guidelines are based on the expectation of high-quality care from both endoscopists and pathologists. Endoscopy quality is discussed further in Quality of colonoscopy. Standards for pathology can be found in the section on Pathologic considerations).

Quantifying risk

The exact risk for an individual of developing metachronous neoplasia (MNMetachronous neoplasia) and CRCColorectal cancer-specific mortality must be balanced against the risks of surveillance, taking into consideration the patient’s situation and wishes. Surveillance recommendations require full knowledge of the procedure performed, the findings, pathology results and previous history, since the risk of MNMetachronous neoplasia is variable, with increasing recognition that some post-polypectomy sub-groups are at very low risk of metachronous advanced neoplasia (MANMetachronous advanced neoplasia).

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Limitations of evidence on which to recommend surveillance intervals

Methodological limitations

There are no contemporary high-quality studies comparing outcomes from different surveillance intervals. The main studies on which we have based surveillance intervals to date, have recruited from the late 1980s and 1990s and therefore likely underestimate the efficacy of index colonoscopy as performed today. No randomised controlled trials with a control arm of no colonoscopy/polypectomy or including longer surveillance intervals have been performed. Highly controlled trials[29][30][31][32] which compare surveillance intervals with good surveillance participation and compliance with interval recommendations do not reflect the norm. The generalisability of the results of these studies is questionable, as are those from single centres, from countries not reflective of the Australian population’s demographics and risk factors or even from ‘community’ studies from more westernised countries[33] with other methodologic limitations.

The literature is replete with retrospective cohort studies where surveillance has been performed on a variable proportion, usually less than half, with little information about the reasons for non-participation in surveillance, leading to selection bias. Additionally, there is considerable variation around the recommended surveillance intervals, which often seem to have been determined by default rather than being predetermined. The proportion of patients who are symptomatic varies, as do the background risk factors including personal adenoma history and family history.

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Outcomes reported also vary between studies. Commonly reported outcomes include MNMetachronous neoplasia, metachronous adenoma (MAMetachronous adenoma), metachronous advanced adenoma (MAAMetachronous advanced adenoma), metachronous advanced neoplasia (MANMetachronous advanced neoplasia) and metachronous CRCColorectal cancer. Specific and varying terms such as metachronous low-risk adenomas or high-risk adenomas also make comparison of outcomes difficult.

Quality of colonoscopy and pathology

The greatest difficulty in using the available literature to formulate recommendations about surveillance colonoscopy is the difference in quality between 'historical' and 'modern' colonoscopy. Major technical advances in colonoscopy and greater attention to procedural quality in the past 15 years make it difficult to extrapolate from earlier studies, which failed to mention important quality parameters, such as the quality of bowel preparation, complications, caecal intubation rates and withdrawal times, as well as endoscopist experience and their adenoma detection rates. Additional challenges are variation in pathology, particularly in terms of diagnosis of advanced histologic features and classification of SPs.

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Practice pointA recommendation on a subject that is outside the scope of the search strategy for the systematic review, based on expert opinion and formulated by a consensus process.Question mark transparent.png

Endoscopists and pathologists need to be aware of serrated polyps and be able to recognise and endoscopically manage them.

Practice pointA recommendation on a subject that is outside the scope of the search strategy for the systematic review, based on expert opinion and formulated by a consensus process.Question mark transparent.png

Hyperplastic polyps should be clearly distinguished from sessile serrated adenomas and traditional serrated adenomas. Although hyperplastic polyps are classified amongst serrated polyps, they do not have malignant potential when they are diminutive, confined to the rectosigmoid colon and not associated with proximal serrated polyps.

Practice pointA recommendation on a subject that is outside the scope of the search strategy for the systematic review, based on expert opinion and formulated by a consensus process.Question mark transparent.png

Consistently high quality colonoscopy is imperative for optimal cost-effectiveness and for implementation of uniform surveillance guidelines.

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  1. Department of Health and Ageing. REVIEW OF MBS COLONOSCOPY ITEMS. Canberra, Australia: Department of Health and Ageing; 2011 Available from:$File/FINAL%20colonoscopy%20review%20report%20-FOR%20PUBLIC%20CONSULT.pdf.
  2. Stock C, Ihle P, Sieg A, Schubert I, Hoffmeister M, Brenner H. Adverse events requiring hospitalization within 30 days after outpatient screening and nonscreening colonoscopies. Gastrointest Endosc 2013 Mar;77(3):419-29 Abstract available at
  3. Lieberman DA, Williams JL, Holub JL, Morris CD, Logan JR, Eisen GM, et al. Colonoscopy utilization and outcomes 2000 to 2011. Gastrointest Endosc 2014 Jul;80(1):133-43 Abstract available at
  4. Morgan DJ, Dhruva SS, Wright SM, Korenstein D. 2016 Update on Medical Overuse: A Systematic Review. JAMA Intern Med 2016 Nov 1;176(11):1687-1692 Abstract available at
  5. Brownlee S, Chalkidou K, Doust J, Elshaug AG, Glasziou P, Heath I, et al. Evidence for overuse of medical services around the world. Lancet 2017 Jul 8;390(10090):156-168 Abstract available at
  6. Anderson JC, Baron JA, Ahnen DJ, Barry EL, Bostick RM, Burke CAConventional adenoma, Bresalier RS, Church TR, Cole BF, Cruz-Correa M, Kim AS, Mott LA, Sandler RS, Robertson DJ,. Factors Associated With Shorter Colonoscopy Surveillance Intervals for Patients With Low-risk Colorectal Adenomas and Effects on Outcome. Gastroenterology 2017.
  7. van Heijningen EM, Lansdorp-Vogelaar I, Steyerberg EW, Goede SL, Dekker E, Lesterhuis W, et al. Adherence to surveillance guidelines after removal of colorectal adenomas: a large, community-based study. Gut 2015 Oct;64(10):1584-92 Abstract available at
  8. Schreuders E, Sint Nicolaas J, de Jonge V, van Kooten H, Soo I, Sadowski D, et al. The appropriateness of surveillance colonoscopy intervals after polypectomy. Can J Gastroenterol 2013 Jan;27(1):33-8 Abstract available at
  9. Jover R, Dekker E. Surveillance after colorectal polyp removal. Best Pract Res Clin Gastroenterol 2016 Dec;30(6):937-948 Abstract available at
  10. Rex DK, Schoenfeld PS, Cohen J, Pike IM, Adler DG, Fennerty MB, et al. Quality indicators for colonoscopy. Am J Gastroenterol 2015 Jan;110(1):72-90 Abstract available at
  11. Australian Commission on Safety and Quality in Health Care. Colonoscopy Clinical Care Standard: Consultation draft. Sydney: ACSQHC; 2017.
  12. Fearon ER, Vogelstein B. A genetic model for colorectal tumorigenesis. Cell 1990 Jun 1;61(5):759-67 Abstract available at
  13. Eide TJ. Natural history of adenomas. World J Surg 1991 Jan;15(1):3-6 Abstract available at
  14. Clark JC, Collan Y, Eide TJ, Estève J, Ewen S, Gibbs NM, et al. Prevalence of polyps in an autopsy series from areas with varying incidence of large-bowel cancer. Int J Cancer 1985 Aug 15;36(2):179-86 Abstract available at
  15. 15.015.1 Eide TJ. Risk of colorectal cancer in adenoma-bearing individuals within a defined population. Int J Cancer 1986 Aug 15;38(2):173-6 Abstract available at
  16. Bonnington SN, Rutter MD. Surveillance of colonic polyps: Are we getting it right? World J Gastroenterol 2016 Feb 14;22(6):1925-34 Abstract available at
  17. 17.017.1 Strum WB. Colorectal Adenomas. N Engl J Med 2016 Mar 17;374(11):1065-75 Abstract available at
  18. Loeve F, Boer R, Zauber AG, Van Ballegooijen M, Van Oortmarssen GJ, Winawer SJ, et al. National Polyp Study data: evidence for regression of adenomas. Int J Cancer 2004 Sep 10;111(4):633-9 Abstract available at
  19. Risio M. The natural history of colorectal adenomas and early cancer. Pathologe 2012 Nov;33 Suppl 2:206-10 Abstract available at
  20. Cottet V, Jooste V, Fournel I, Bouvier AM, Faivre J, Bonithon-Kopp C. Long-term risk of colorectal cancer after adenoma removal: a population-based cohort study. Gut 2012 Aug;61(8):1180-6 Abstract available at
  21. Bosman FT, Carneiro F, Hruban R H, Theise N. WHO classification of tumours of the digestive system, fourth edition. France: IARC; 2010 [cited 2018 Jul 10] Available from:
  22. Hornick J, Odze R. Polyps of the large intestine in surgical pathology of the GI tract, liver, biliary tract and pancreas (Second Edition). Saunders, Elsevier; 2009.
  23. 23.023.1 Holt BA, Bourke MJ. Wide field endoscopic resection for advanced colonic mucosal neoplasia: current status and future directions. Clin Gastroenterol Hepatol 2012 Sep;10(9):969-79 Abstract available at
  24. Gupta S. Trouble in Paris (classification): polyp morphology is in the eye of the beholder. Am J Gastroenterol 2015 Jan;110(1):188-91 Abstract available at
  25. The Paris endoscopic classification of superficial neoplastic lesions: esophagus, stomach, and colon: November 30 to December 1, 2002. Gastrointest Endosc 2003 Dec;58(6 Suppl):S3-43 Abstract available at
  26. Bettington M, Walker N, Rosty C, Brown I, Clouston A, McKeone D, et al. Clinicopathological and molecular features of sessile serrated adenomas with dysplasia or carcinoma. Gut 2017 Jan;66(1):97-106 Abstract available at
  27. Hewett DG, Kaltenbach T, Sano Y, Tanaka S, Saunders BP, Ponchon T, et al. Validation of a simple classification system for endoscopic diagnosis of small colorectal polyps using narrow-band imaging. Gastroenterology 2012 Sep;143(3):599-607.e1 Abstract available at
  28. IJspeert JE, Bastiaansen BA, van Leerdam ME, Meijer GA, van Eeden S, Sanduleanu S, et al. Development and validation of the WASP classification system for optical diagnosis of adenomas, hyperplastic polyps and sessile serrated adenomas/polyps. Gut 2016 Jun;65(6):963-70 Abstract available at
  29. Schatzkin A, Lanza E, Freedman LS, Tangrea J, Cooper MR, Marshall JR, et al. The polyp prevention trial I: rationale, design, recruitment, and baseline participant characteristics. Cancer Epidemiol Biomarkers Prev 1996 May;5(5):375-83 Abstract available at
  30. Baron JA, Barry EL, Mott LA, Rees JR, Sandler RS, Snover DC, et al. A Trial of Calcium and Vitamin D for the Prevention of Colorectal Adenomas. N Engl J Med 2015 Oct 15;373(16):1519-30 Abstract available at
  31. Martínez ME, Baron JA, Lieberman DA, Schatzkin A, Lanza E, Winawer SJ, et al. A pooled analysis of advanced colorectal neoplasia diagnoses after colonoscopic polypectomy. Gastroenterology 2009 Mar;136(3):832-41 Abstract available at
  32. Winawer SJ, Zauber AG, O'Brien MJ, Ho MNMetachronous neoplasia, Gottlieb L, Sternberg SS, et al. Randomized comparison of surveillance intervals after colonoscopic removal of newly diagnosed adenomatous polyps. The National Polyp Study Workgroup. N.Engl.J Med. 1993 Apr 1;328(13):901-906.
  33. Viel JF, Studer JM, Ottignon Y, Hirsch JP, Franche-Comté PolypA small growth protruding from a mucous membrane, such as the lining of the bowel. Surveillance Study Group.. Predictors of colorectal polyp recurrence after the first polypectomy in private practice settings: a cohort study. PLoS One 2012;7(12):e50990 Abstract available at

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