Colorectal Polyps

Mucosal protrusions into the bowel lumen, most commonly adenomatous. Adenomatous polyps are precursors of colorectal cancer through the adenoma-carcinoma sequence. Polypectomy at colonoscopy is curative for most.

Key Facts

Adenomatous polyps (70% of polyps): premalignant — tubular (80%), tubulovillous (15%), villous (5%); cancer risk increases with size (>10 mm), villous histology, and high-grade dysplasia Serrated polyps: hyperplastic (benign, most common overall), sessile serrated lesion (SSL — premalignant via serrated pathway), traditional serrated adenoma (rare) Adenoma-carcinoma sequence: ~5-10% of adenomas progress to carcinoma over ~10 years; polypectomy interrupts this sequence BSG post-polypectomy surveillance: risk stratification — low risk (1-2 small adenomas): no surveillance or colonoscopy at 10 years; high risk (≥5 adenomas, ≥20 mm, HGD): colonoscopy at 3 years Familial adenomatous polyposis (FAP): >100 adenomatous polyps; APC gene; near 100% CRC risk by 40 → prophylactic colectomy Large polyps (>20 mm): consider endoscopic mucosal resection (EMR) or endoscopic submucosal dissection (ESD) at specialist centres

Overview

Key Facts

Colorectal polyps are abnormal growths projecting from the colonic or rectal mucosa. They are extremely common, found in ~25-30% of screening colonoscopies. While most are benign, adenomatous and sessile serrated polyps are premalignant and their detection and removal is the basis of colorectal cancer prevention.

Epidemiology

Prevalence increases with age: ~25-30% of adults >50 years have adenomatous polyps. Male predominance (1.5:1). Adenomas are found in ~40% of NHS bowel cancer screening colonoscopies. The transition from adenoma to carcinoma takes approximately 10 years in most cases.

Aetiology

  • Sporadic adenomas: age, obesity, red/processed meat, smoking, alcohol, physical inactivity
  • Hereditary syndromes: FAP (APC gene — AD), attenuated FAP, MUTYH-associated polyposis (AR), Lynch syndrome (MMR genes), Peutz-Jeghers (STK11 — hamartomatous), juvenile polyposis (SMAD4/BMPR1A)
  • Protective factors: aspirin/NSAIDs, calcium, folate, physical activity, high-fibre diet

Pathophysiology

Adenoma-carcinoma sequence (chromosomal instability pathway — ~80% of CRC):

  • APC loss → β-catenin activation → adenoma initiation
  • KRAS activation → adenoma growth
  • SMAD4/DCC loss → advanced adenoma
  • TP53 loss → carcinoma

Serrated neoplasia pathway (~20% of CRC):

  • BRAF mutation → CIMP → MLH1 methylation → MSI-high carcinoma
  • Sessile serrated lesions (flat, right colon) are harder to detect endoscopically
  • Account for many "interval cancers" (cancers arising between surveillance colonoscopies)

Clinical Presentation

Asymptomatic (Most Common)

  • Discovered incidentally at screening or diagnostic colonoscopy
  • FIT-positive on bowel cancer screening

Symptomatic

  • Rectal bleeding (usually occult; rarely overt)
  • Iron deficiency anaemia
  • Change in bowel habit (rare unless large/multiple)
  • Mucous discharge (villous adenomas — may cause hypokalaemia from secretory diarrhoea)
  • Rarely: intussusception (pedunculated polyps), prolapse through anus

Red Flags

  • Large polyp with malignant features (hard, fixed, ulcerated)
  • Multiple polyps (>10 — consider polyposis syndrome)
  • Young patient (<50) with adenomas (hereditary syndrome)
  • Polyp with high-grade dysplasia or invasive cancer on histology

Differential Diagnosis

DiagnosisKey FeaturesInvestigation
Colorectal cancerLarge mass, obstruction, weight lossColonoscopy + biopsy, CT staging
Inflammatory polyps (pseudopolyps)IBD history, multiple, non-neoplasticColonoscopy + biopsy
LipomaSubmucosal, smooth, yellow, pillow signColonoscopy ± EUS
Carcinoid tumourSmall, yellow, submucosalColonoscopy + biopsy, chromogranin A
HaemorrhoidsRectal bleeding, external/internalProctoscopy
Polyposis syndromesMultiple polyps, family history, extra-colonic featuresGenetic testing, colonoscopy

Diagnosis / Investigation

Bedside

  • DRE: may detect low rectal polyps
  • FIT: may be positive (screening or symptomatic investigation)

Bloods

  • FBC: iron deficiency anaemia (occult blood loss)
  • U&Es: hypokalaemia (rare — secretory villous adenoma)

Imaging

  • CT colonography: alternative to colonoscopy; detects polyps >6 mm with >90% sensitivity; polyps found require colonoscopic polypectomy

Special Tests

  • Colonoscopy: gold standard — allows visualisation, biopsy, and polypectomy
    • Assess: number, size, morphology (Paris classification: pedunculated Ip, sessile Is, flat IIa/IIb/IIc)
    • Polypectomy: snare removal with diathermy; EMR for sessile polyps >10 mm; ESD for large flat lesions
  • Histopathology: type (adenoma, serrated, hyperplastic), grade of dysplasia, completeness of excision, presence of invasive cancer
    • Haggitt classification (pedunculated malignant polyps): levels 1-4 invasion
    • Kikuchi classification (sessile malignant polyps): sm1-sm3 submucosal invasion depth
  • Genetic testing: if ≥10 adenomas, or family history suggesting polyposis syndrome; APC, MUTYH, MLH1/MSH2/MSH6/PMS2

Management

Non-pharmacological

  • Polypectomy at colonoscopy: curative for most benign polyps
    • Cold snare: preferred for polyps <10 mm
    • Hot snare: for polyps 10-20 mm
    • EMR: piecemeal or en-bloc for sessile polyps >20 mm
    • ESD: en-bloc resection of large flat/early cancerous lesions at specialist centres
  • Surveillance colonoscopy (BSG 2020 guideline):
    • Low risk (1-2 adenomas, <10 mm, no HGD): no surveillance or colonoscopy at 10 years
    • Intermediate risk (3-4 small adenomas OR ≥1 adenoma 10-19 mm): colonoscopy at 3 years
    • High risk (≥5 adenomas OR ≥1 adenoma ≥20 mm OR HGD): colonoscopy at 3 years; if high risk again, repeat at 3 years; if clear, extend to 5 years
    • Serrated lesions: SSL ≥10 mm or with dysplasia — surveillance at 3 years

Pharmacological

  • Aspirin: chemopreventive evidence (reduces adenoma recurrence and CRC risk); routine use for prevention not currently recommended outside Lynch syndrome
  • Celecoxib: reduces polyp burden in FAP but cardiovascular risk limits use

Surgical/Interventional

  • Surgical resection: for polyps not amenable to endoscopic removal (size, location, suspicion of invasive cancer)
  • Malignant polyp management: if T1 CRC in polyp — assess completeness of excision, invasion depth (sm level), differentiation, LVI; if high-risk features → segmental colectomy
  • Prophylactic colectomy: FAP (typically ileal pouch-anal anastomosis at ~20 years of age)

Referral Criteria

  • Polyposis syndrome suspected (>10 adenomas) → genetics + specialist centre
  • Large complex polyps (>20 mm) → specialist EMR/ESD centre
  • Malignant polyp with high-risk features → CRC MDT
  • Family history meeting criteria for genetic testing

Prognosis

Most adenomatous polyps are cured by polypectomy. Without removal, ~5-10% of adenomas progress to cancer over ~10 years. Cancer risk increases with polyp size (0.3% for <10 mm, 5% for 10-20 mm, ~15% for >20 mm), villous histology, and high-grade dysplasia. FAP without colectomy has near 100% CRC risk by age 40. Surveillance colonoscopy after polypectomy reduces CRC incidence by ~75-90%. Malignant polyps with favourable features (sm1, well-differentiated, no LVI, complete excision) have <3% lymph node metastasis risk — polypectomy alone may be curative.

Other Relevant Information

BSG Post-Polypectomy Surveillance (2020)

Risk CategoryCriteriaSurveillance
Low risk1-2 adenomas, <10 mm, low-gradeNo surveillance or 10 years
Intermediate3-4 small adenomas OR 10-19 mm3 years
High risk≥5 adenomas OR ≥20 mm OR HGD3 years

Hereditary Polyposis Syndromes

SyndromeGeneInheritancePolyp TypeCRC Risk
FAPAPCADAdenomatous (>100)~100% by 40
Attenuated FAPAPCADAdenomatous (10-100)~70%
MUTYH-associatedMUTYHARAdenomatous (10-100)~50-80%
Lynch syndromeMMR genesADFew adenomas (rapid progression)50-80%
Peutz-JeghersSTK11ADHamartomatous~40%
Juvenile polyposisSMAD4/BMPR1AADHamartomatous/juvenile~40%