British Society of Gastroenterology position statement on serrated polyps in the colon and rectum

Abstract

Serrated polyps have been recognised in the last decade as important premalignant lesions accounting for between 15% and 30% of colorectal cancers. There is therefore a clinical need for guidance on how to manage these lesions; however, the evidence base is limited. A working group was commission by the British Society of Gastroenterology (BSG) Endoscopy section to review the available evidence and develop a position statement to provide clinical guidance until the evidence becomes available to support a formal guideline. The scope of the position statement was wide-ranging and included: evidence that serrated lesions have premalignant potential; detection and resection of serrated lesions; surveillance strategies after detection of serrated lesions; special situations-serrated polyposis syndrome (including surgery) and serrated lesions in colitis; education, audit and benchmarks and research questions. Statements on these issues were proposed where the evidence was deemed sufficient, and re-evaluated modified via a Delphi process until >80% agreement was reached. The Grading of Recommendations, Assessment, Development and Evaluations (GRADE) tool was used to assess the strength of evidence and strength of recommendation for finalised statements. Key recommendation: we suggest that until further evidence on the efficacy or otherwise of surveillance are published, patients with sessile serrated lesions (SSLs) that appear associated with a higher risk of future neoplasia or colorectal cancer (SSLs ≥10 mm or serrated lesions harbouring dysplasia including traditional serrated adenomas) should be offered a one-off colonoscopic surveillance examination at 3 years (weak recommendation, low quality evidence, 90% agreement).

Keywords: COLONIC NEOPLASMS; COLONOSCOPY; COLORECTAL CANCER; HISTOPATHOLOGY; POLYPOSIS.

Figure 1

Considering the spectrum of colorectal cancer (CRC)—conventional adenomas progress by the sequential accumulation of genetic mutations and chromosomal instability causing microsatellite stable (MSS) tumours. Microsatellite instability (MSI) is the result of defective DNA repair through inactivation of mismatch repair genes and is epitomised by the germline mutation of Mis-Match Repair (MMR) genes seen in Lynch syndrome (hereditary non-polyposis coli). The sessile serrated neoplasia pathway is often initiated by genetic mutation of BRAF or KRAS genes but then progresses by methylation of tumour suppressing genes (CpG island methylator phenotype (CIMP)). Both MSS and unstable tumours can result depending on the genes epigenetically silenced as the lesions progress. Comparatively, little is known about the traditional serrated pathway, but evidence is accumulating that this is a distinct molecular subtype. FAP, familial adenomatous polyposis.

Figure 2

Serrated surveillance flow chart.

Figure 3

(A) A 15 mm sessile serrated lesion without dysplasia in the right colon. Note the adherent mucus cap which aids detection. (B) The same lesion after washing and application of indigocarmine dye-spray to clarify lesion boarders and extent. (C) Lesion lifted with dilute methylene blue in lifting solution providing contrasting background to aid precise resection. (D) Postpolypectomy defect after cold snare piecemeal endoscopic mucosal resection.

Figure 4

(A) A microvesicular hyperplastic polyp showing serration within the upper half of the lesion and with none of the characteristic features of a sessile serrated lesion (SSL) (magnification ×100). (B) An SSL showing pronounced serration at the crypt base and horizontal spreading of a crypt, forming a typical ‘L’ or ‘boot’ shape (magnification ×200). (C) An SSL showing a sharp distinction between areas showing no dysplasia and low-grade dysplasia (magnification ×100). (D) A traditional serrated adenoma (TSA) showing a pronounced villous growth pattern, pencillate nuclei, eosinophilic cytoplasm and ectopic crypt foci (magnification ×200). (Reproduced from Bateman and Shepherd, with permission from BMJ Publishing Group.)