> Table of Contents > Colonic Polyps
Colonic Polyps
Marcelle Meseeha, MD
Maximos Attia, MD
image BASICS
  • Intraluminal colonic protrusions; most commonly sporadic, or part of polyposis syndromes.
  • Classified according to size:
    • Diminutive ≤5 mm, small 6 to 9 mm, large ≥10 mm (1)
  • Morphologic classification:
    • Depressed, flat, sessile, or pedunculated
  • Clinical significance:
    • >95% of colon adenocarcinoma arise from polyps.
Colorectal polyps are more common in:
  • Western countries
  • Men
  • Non-Caucasian (2)
Incidence increases with age.
  • 15-20% of all adults
  • 30% of U.S. population >50 years
  • 6% of children (2)
  • 12% of children with lower GI bleed (2)
Divided into:
  • Mucosal
    • Neoplastic
      • Adenomatous polyps (tubular >80%, villous 5-15%, tubulovillous 5-15%)
      • Serrated polyps
        • Sessile serrated polyps are common, more in proximal colon, with low malignant potential if with no dysplasia, and significant malignant potential if dysplastic.
        • Traditional serrated adenoma is uncommon, more often noted in distal colon, with significant malignant potential (1).
    • Non-neoplastic polyps (hyperplastic, juvenile polyps, hamartomas, inflammatory pseudopolyps)
      • Hyperplastic polyps are very common, more in distal colon, with very low malignant potential (1).
      • Juvenile polyps are common in childhood, benign hamartomas, more in rectosigmoid, and not premalignant (2).
  • Submucosal (lipomas, lymphoid aggregates, carcinoids)
  • Inactivation of tumor suppressor genes as adenomatous polyposis coli (APC) or mismatch repair genes (MLH1) causes polyps to grow into cancer.
  • Familial adenomatous polyposis (FAP) is autosomal dominant. By age 40, almost all patients develop colorectal cancer (CRC).
  • MUTYH-associated polyposis (MAP) is autosomal recessive caused by biallelic mutations in MUTYH gene.
  • Juvenile polyposis syndrome (JPS) is autosomal dominant. 50-60% of patients have a mutation in the SMAD4 or BMPR1A gene. By age 35, 20% of patients develop CRC (2).
  • Family history of intestinal polyposis, polyps, or CRC
  • Advancing age
  • Male
  • High-fat, low-fiber diet
  • Tobacco use
  • Excessive alcohol intake: >8 drinks a week
  • Inflammatory bowel disease is associated with a decreased prevalence of colon polyps (IBD associated with higher risk of colon cancer).
  • Low-fat, high-fiber diet
  • Avoid smoking.
  • Decrease alcohol intake.
  • Use of NSAIDs and calcium is associated with decreased incidence and recurrence of polyps (3)[A].
  • No lower rates of CRC with azathioprine, 6-mercaptopurine, folate, calcium, multivitamins, or statins
Hereditary polyposis syndromes:
  • Adenomatous
    • Familial adenomatous polyposis (FAP)
      • Classic (CFAP)
      • Attenuated (AFAP)
    • MUTYH-associated polyposis (MAP)
    • FAP variants:
      • Gardner syndrome
      • Turcot syndrome
  • Hamartomatous
    • Peutz-Jeghers syndrome (PJS)
    • Juvenile polyposis syndrome (JPS)
    • Familial juvenile polyposis
    • Cowden syndrome
  • Usually normal
  • Rectal polyps noted as prolapsed or palpated on DRE
  • FOBT by DRE is less effective than FOBT by stool passed spontaneously.
Initial Tests (lab, imaging)
  • CBC; anemia with chronic bleeding
  • Basic metabolic panel; electrolyte disorder with hypersecretory adenomas
  • Fecal occult blood test (FOBT), an insensitive screening test, as small polyps don't usually bleed, includes:
    • Guaiac (gFOBT)—uses a chemical indicator with color change in presence of blood
    • Immunochemical (iFOBT or fecal immunochemical test [FIT])—uses antibodies against human hemoglobin
  • Stool DNA test is more sensitive and less specific than fecal immunochemical test (FIT).
Diagnostic Procedures/Other
  • Colonoscopy is the gold standard test for detection of polyps and polypectomy. Not a perfect screening test, with increased miss rate with right-sided colon polyps, smaller polyp size, low quality of colon prep, less endoscopist experience
  • Computed tomographic colonography (CTC) is less sensitive with flat polyps and requires excellent bowel preparation.
  • Double-contrast barium enema
  • Colon capsule endoscopy
  • Enhanced optical technologies can potentially differentiate between neoplastic and non-neoplastic colonic lesions (4)[A].
  • Enhanced optical technologies include:
    • Narrowed spectrum endoscopy (narrow-band imaging [NBI])
    • Image-enhanced endoscopy (i-scan)
    • Fujinon intelligent chromoendoscopy (FICE)
    • Confocal laser endomicroscopy (CLE)
  • Patients with >10 colorectal adenomas should get genetic testing for APC and MUTYH (5)[C].
Test Interpretation
  • Tubular adenoma
    • Gross: tend to be polypoid
    • Micro: dysplastic epithelium with a tubular architecture
  • Villous adenoma
    • Gross: tend to be sessile
    • Micro: dysplastic epithelium with fine finger-like projections
  • Tubulovillous adenomas have a combination of tubular and villous architecture.
  • Hyperplastic polyps are composed of hyperplastic colonic mucosa.
  • Hamartomatous polyps include muscularis mucosa.
  • Juvenile polyp
    • Gross: pedunculated, smooth, red mass, 1 to 3 cm (2).
  • Colonic polypectomy; diagnostic, therapeutic
  • Techniques are as follows:
    • Snare polypectomy with electrocautery for pedunculated polyps
    • Endoscopic mucosal resection for sessile polyps
    • Endoscopic submucosal dissection
  • P.213

  • Colorectal surgery; prophylactic in FAP and MAP and when there are numerous polyps or persistent bleeding (2,5)[C]:
    • Total colectomy ileorectal anastomosis
    • Proctocolectomy ileal pouch anal anatomosis
  • Chemoprevention: NSAIDs and calcium may reduce incidence and recurrence of polyps in patients with FAP and MAP (3)[A].
Follow-up colonoscopy in:
  • 10 years if no polyps or distal small hyperplastic polyps (<10 mm) (1)[B]
  • 5 to 10 years if 1 to 2 small tubular adenomas (<10 mm) (1)[B]
  • 3 years if 3 to 10 adenomas if any polyp ≥6 mm (1)[B] or if all polyps <6 mm (1)[C]
  • <3 years if >10 adenomas (1)[B]
  • 3 years if one or more adenomas ≥10 mm (1)[A]
  • 3 years if one or more adenomas with villous features of any size or with HGD (1)[B]
  • 5 years if sessile serrated polyp(s) <10 mm with no dysplasia (1)[C]
  • 3 years if sessile serrated polyp(s) ≥10 mm or with dysplasia or traditional serrated adenoma (1)[C]
  • 1 year if serrated polyposis syndrome (1)[B]
Patient Monitoring
  • Colonoscopy for CRC screening starts at age 50 years and earlier for at-risk patients.
  • Stop screening if life expectancy is <10 years.
  • In CFAP and AFAP, screen for extracolonic manifestations: thyroid cancer, desmoid tumors, and gastroduodenal polyposis (every 6 months to 5 years) (5)[C]
  • In families, lifetime screening is indicated in mutation carriers (5)[C]:
    • In CFAP: with sigmoidoscopy or colonoscopy every 1 to 2 years starting at age of 10 to 11 years
    • In AFAP and MAP: with colonoscopy every 1 to 2 years starting at age of 18 to 20 years
  • After colorectal surgery, surveillance of the rectum (every 6 to 12 months) or pouch (every 6 months to 5 years) is indicated (5)[C].
  • First-degree relatives of patients with JPS require screening by colonoscopy and upper endoscopy after age 12 (2)[C].
Low-fat, high-fiber diet has been recommended but with insufficient evidence.
Importance of colonoscopy as a screening tool for reduction of incidence of colorectal cancer
  • Regression or no change in size, more with small hyperplastic polyps and with patients on NSAIDs
  • Recurrence: Juvenile polyps recur in 45% of children with multiple polyps and 17% of children with solitary polyps (2).
  • Increase in size, more with large adenomas
  • Progression to cancer
  • Risk factors for colon cancer (6)[A]:
    • Polyp pathology
      • Adenomatous
      • Serrated
      • With high-grade dysplasia
      • With >25% villous histology
      • Polyp size >1 cm in diameter
      • Polyps located in proximal colon
      • More than three polyps
  • Recurrence rates <10% postpolypectomy
1. Lieberman DA, Rex DK, Winawer SJ, et al. Guidelines for colonoscopy surveillance after screening and polypectomy: a consensus update by the US Multi-Society Task Force on Colorectal Cancer. Gastroenterology. 2012;143(3):844-857.
2. Thakkar K, Fishman DS, Gilger MA. Colorectal polyps in childhood. Curr Opin Pediatr. 2012;24(5):632-637.
3. Johnson CC, Hayes RB, Schoen RE, et al. Nonsteroidal anti-inflammatory drug use and colorectal polyps in the prostate, lung, colorectal, and ovarian cancer screening trial. Am J Gastroenterol. 2010;105(12):2646-2655.
4. Wanders LK, East JE, Uitentuis SE, et al. Diagnostic performance of narrowed spectrum endoscopy, autofluorescence imaging, and confocal laser endomicroscopy for optical diagnosis of colonic polyps: a meta-analysis. Lancet Oncol. 2013;14(13):1337-1347.
5. Stoffel EM, Mangu PB, Limburg PJ. Hereditary colorectal cancer syndromes: American Society of Clinical Oncology clinical practice guideline endorsement of the familial risk-colorectal cancer: European Society for Medical Oncology clinical practice guidelines. J Oncol Pract. 2015;11(3): e437-e441.
6. Gao Q, Tsoi KK, Hirai HW, et al. Serrated polyps and the risk of synchronous colorectal advanced neoplasia: a systematic review and meta-analysis. Am J Gastroenterol. 2015;110(4):501-509.
Additional Reading
  • Ashraf I, Paracha SR, Arif M, et al. Digital rectal examination versus spontaneous passage of stool for fecal occult blood testing. South Med J. 2012;105(7):357-361.
  • Brenner H, Hoffmeister M, Arndt V, et al. Protection from right- and left-sided colorectal neoplasms after colonoscopy: population-based study. J Natl Cancer Inst. 2010;102(2):89-95.
  • Cooper K, Squires H, Carroll C, et al. Chemoprevention of colorectal cancer: systematic review and economic evaluation. Health Technol Assess. 2010;14(32):1-206.
  • Farraye FA, Odze RD, Eaden J, et al. AGA medical position statement on the diagnosis and management of colorectal neoplasia in inflammatory bowel disease. Gastroenterology. 2010;138(2):738-745.
  • Imperiale TF, Ransohoff DF, Itzkowitz SH, et al. Multitarget stool DNA testing for colorectal-cancer screening. N Engl J Med. 2014;370(14):1287-1297.
  • Lee BG, Shin SH, Lee YA, et al. Juvenile polyp and colonoscopic polypectomy in childhood. Pediatr Gastroenterol Hepatol Nutr. 2012;15(4):250-255.
  • Sonnenberg A, Genta RM. Low prevalence of colon polyps in chronic inflammatory conditions of the colon. Am J Gastroenterol. 2015;110(7):1056-1061.
  • Summers RM. Polyp size measurement at CT colonography: what do we know and what do we need to know? Radiology. 2010;255(3):707-720.
See Also
Colorectal Cancer
  • K63.5 Polyp of colon
  • D12.6 Benign neoplasm of colon, unspecified
  • K51.40 Inflammatory polyps of colon without complications
Clinical Pearls
  • Progression from normal mucosa to polyp to carcinoma is a sequence that takes years to develop.
  • Colonoscopy is the gold standard tool for diagnosis of polyps and reduction of CRC incidence.
  • Small hyperplastic polyps should be biopsied to differentiate adenomatous and serrated polyps.
  • Use of NSAIDs and calcium is associated with decreased incidence and recurrence of polyps.