Gastrointestinal tract polyps

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Gastrointestinal tract polyps, also gastrointestinal polyps or GI polyps, are the bread & butter of a GI pathologists workload. Some of 'em are benign... some pre-malignant... some malignant... some weird. Most GI polyps are from the intestine, i.e. intestinal polyps.

Overview - there are four basic types:[1]

  • Hyperplastic - harmless, most common - 90% of all colonic polyps.[2]
  • Hamartomatous - weriod stuff, syndromic things.
  • Inflammatory - think inflammatory bowel disease, AKA pseudopolyps.
  • Adenomatous - premalignant, several types (see below).

Mnemonic: HHI-A.

Basic approach

  1. Sessile (flat) or polypoid (spherical, possibly has a stalk)?
  2. Nuclear features of adenoma & loss of goblets (hyperchromatic nuclei, nuclei round vs. flat, loss of nuclear stratification)?
  3. Inflammation?
  4. Serrated architecture?

A set of decision trees for GI polyps

Decision tree - GI polyps

 
 
 
 
 
 
 
 
GI
polyp
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Polypoid
(Lollipop-like)
 
 
 
 
 
 
 
 
Sessile
(flat)
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Nuclear changes
 
 
 
No nuc. change
 
 
 
Serrated
 
Not serrated
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Polypoid adenoma
(below)
 
Serrated
 
Not serrated
 
SSA vs. HP
 
Normal vs. VA
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
HP
 
See misc.
polyps (below)
 
 
 
 
 
 
 
 

Notes:

  • Polypoid:
    • Stalk visible (lollipop handle visible) or epithelial surface on three sides (or more).
  • Sessile (flat):
    • "Line of muscularis mucosa" visible +/- test tube-like intestinal crypts.
  • Nuclear changes:
    • Nuclear enlargement (elongation), crowding/pseudostratification, hyperchromasia (more blue) - especially at the surface, i.e. adjacent to the lumen (as opposed to the base of the crypt).

Decision tree - polypoid adenoma

 
 
 
 
Polypoid adenoma
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Serrated
 
 
 
 
 
Non-serrated
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
TSA
 
Tubular arch.
 
Tubulovillous arch.
 
Villous arch.
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
TA
 
TVA
 
VA

Notes:[3]

  • TA, tubular component >75%.
  • VA, villous component >50%.


Decision tree - miscellaneous polyps

 
 
 
 
 
 
Misc. polyps
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Inflam.
 
 
 
 
 
No inflam.
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Benign
 
Inflam. p.
 
Hamart.
 
Benign
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
PJP
 
Juvenile
 
Other

Notes:

  • Juvenile polyps may have marked inflammation.


Hamartomatous polyps - basic DDx:

  • Juvenile polyp/Retention polyp -- DIES (dilated glands, incr. LP, eroded surface, stalk).
  • Peutz-Jeghers polyp (PJP) - frond-like with all mucosa components .

Tabular comparison of colonic polyps

Overview in two tables

Common

Type Key feature(s) Details Prevalence / prognosis Other DDx Image
Normal mucosa / no pathology test tube-like morphology small nuclei, abundant goblet cells common / benign moderate inflammation is normal microscopic colitis, colonic spirochetes, microsporidiosis Normal - low mag. (ohio-state.edu)
Hyperplastic polyp serrated at the surface abundant goblet cells, usu. left colon; no features of SSA common / benign may be syndromic sessile serrated adenoma HP (WC)
Traditional adenomas nuclear hyperchromasia & pseudostratification / crowding at the luminal aspect decreased goblet cells, usu. polypoid - on a stalk, usu. left colon common / premalignant tubular adenoma, tubulovillous adenoma, villous adenoma traditional serrated adenoma, reactive changes (inflammation) TA - high mag. (WC), TA - low mag. (WC)

Less common

Type Key feature(s) Details Prevalence / prognosis Other DDx Image
Sessile serrated adenoma (SSA) basal crypt dilation & serration boot-shaped crypts, horizontal crypts, branching crypts uncommon / pre-malignant AKA sessile serrated polyp hyperplastic polyp SSA - low mag. (WC)
Traditional serrated adenoma (TSA) nuclear hyperchromasia & pseudostratification / crowding at the surface, serrated, villous-like architecture decreased goblet cells very rare / premalignant called "traditional" to differentiate from SSA traditional serrated adenoma (esp. villous adenoma) TSA - low mag. (WC), TSA - high mag. (WC)
Juvenile polyp (retention polyp) dilated glands, increased lamina propria eroded surface (due to trauma), stalk (polypoid), inflammation - common uncommon / benign if in isolation may be part of a syndrome inflammatory pseudopolyp Gastric JP - low mag. (WC)
Inflammatory pseudopolyp inflammation, erosion/ulceration adjacent to polyp loss of mucosa adjacent to pseudopolyp uncommon / seen in IBD, increased risk of malignancy only seen in IBD; Dx implies IBD juvenile polyp Image
Peutz-Jeghers polyp (PJP) branching smooth muscle tree-like growth pattern very rare / syndromic; assoc. with cancer PJP not pre-malignant lesion in itself; see Peutz-Jeghers syndrome normal, classically in the small bowel PJP - low mag. (WC)

Common problems

Submucosal invasion

  • This may be difficult to assess histomorphologically.

Poor outcome predictors

Predictors of poor outcome with early submucosal invasion:[4]

  1. Lymphovascular invasion.
  2. High-grade tumour budding.
    • Tumour bud = 1-4 cell(s); "high-grade budding" is >=10 tumour buds in a 250x field[5] - definition suffers from LPFitis.
  3. Extensive submucosal invasion
    • >= 4 mm width or >= 2 mm.

If none of the above factors is present the risk of lymph node metastasis is < 1%. The presence of one risk factor increases the risk to ~20%.

Adenomatous vs. hyperplastic

Adenomatous polyps & hyperplastic polyps - a comparison (adapted from Li and Burgart[6]):

Hyperplastic polyp (HPP) Sessile serrated adenoma (SSA) Traditional serrated adenoma (TSA) Traditional adenoma
-tubular adenoma
-tubulovillous adenoma
-villous adenoma
Classic location rectum/left colon right colon rectum/left colon rectum/left colon
Morphology polypoid flat (sessile) polypoid polypoid
Cytologic atypia
-Cigar nuclei
-Hyperchromasia
-Nuclear crowding		 absent absent present present
Location of worst atypia - - basal luminal
Cytoplasm eosinophilic prominent eosinophilia eosinophilic basophilic
Goblet cells abundant common less common less common
Luminal Serration present common present absent
SSA architecture
-Basal crypt serration
-Basal crypt dilation
-Horizonatal crypts
-Branched crypts		 absent present absent absent
Key feature(s) serrated luminal surf. & goblets abnorm. crypt arch. & sessile nuclear atypia & serrated nuclear atypia (luminal)
Image(s) low mag. low mag, low mag. low mag, very high mag. low mag., high mag.

Normal colonic mucosa:

  • Nuclei - round and basally located.
  • Abundant goblet cells.
  • Moderate inflammation.
  • Paneth cells - present in right colon.
  • Glands - straight, no branching; "test tube" shape.

Notes: Left colon refers to the sigmoid colon, descending colon and the distal half of the transverse colon; right colon refers to the cecum, ascending colon and proximal half of the transverse colon.

Hyperplastic polyp

General

  • Most common colonic polyp (90% of all colonic polyps[2]).

Microscopy

Features:[2]

  • Irregular crypt architecture - tortuosity.
  • Serrated epithelial cells (at the surface of the gland).
    • Serrated appearance = saw-tooth appearance, epithelium has jagged edge.
  • Significant negatives:
    • No nuclear atypia.
    • Goblet cells should be present (as is usual in the colon).

Images:

Inflammatory pseudopolyp

  • AKA inflammatory polyp.

General

  • Not a true polyp.
  • The label inflammatory pseudopolyp = inflammatory bowel disease (IBD).
    • If there is no history of IBD... reconsider the diagnosis.

Microscopic

Features:

  • Polypoid shape.
  • Inflammation - key feature.

Negatives:

  • No nuclear atypia.
  • No dilated glands.

DDx:

Adenomatous polys

Several types of adenomatous polyps are recognized:

  • Traditional adenomas (have three subtypes):
    1. Tubular adenoma - most common, lowest malignant potential.
    2. Tubulovillous adenoma.
    3. Villous adenoma - highest malignant potential.
  • Sessile serrated adenomas:
    • New kid on the block, some people doubt their existance.
  • Traditional serrated adenomas - nuclear features of 'traditional adenoma' + serrated architecture.

Notes:

  • They are all considered pre-malignant, i.e. if you leave 'em in place they often develop into cancer.
  • If multiple... think about familial adenomatous polyposis (FAP).

Management of (adenomatous colonic) polyps

Follow-up interval for polyps (colonoscopy interval):[7]

  • Normal follow-up (includes presence of hyperplastic polyps): ~10 years.
  • 1-2 low risk (adenomatous) polyps: 5-10 years.
  • 3-10 low risk polyps or a high risk polyp: 3 years.
  • >10 low risk polyps: <3 years.
  • Inadequately removed polyps: <6 months.

Classified as high risk (any of the following):[7]

  • Tubulovillous.
  • Villous.
  • High grade dysplasia.
  • Size >= 1 cm.

Mnemonic: GAS = grade (high), architecture (tubulovillous, villous), size (>1 cm).

Traditional adenoma

Microscopic

  1. Nuclear changes at the surface (of the mucosa) - key feature.
    • Cigar-shaped (elongated) nucleus (usu. length:width > 3:1) - key feature.
      • Normal nuclei are round.
    • Nuclear crowding/pseudostratification - key feature.
    • Nuclear hyperchromasia (more blue).
    • +/-Loss of nuclear polarity (nuclei no longer on basement membrane).
  2. Loss/decrease of goblet cells (common).
  3. Cytoplasmic hyperchromasia.

Notes:

  • Nuclear changes deep to the surface are non-neoplastic if normal appearing mucosa (with small round nuclei) is superficial to it; mucosa that is more blue and atypical deep and less blue without nuclear atypia at the surface is said to be "maturing".
    • Classically, adenomatous polyps have "reverse maturation":
      • The surface is more hyperchromatic (more blue).
      • The base is more mature (more globlet cells, no nuclear changes -- less blue).

Typing

Subclassified as:[8]

  • Tubular adenoma (most common), tubular component >75%.
  • Villous adenoma (least common ~= 1% of (traditional) adenomas), villous component >50%.
  • Tubulovillous adenoma (uncommon ~5-10% of (traditional) adenomas), villous component >=25% & <=50%.

In other words:

  • Tubular T/V >75% / <25%; Tubulovillous T/V <=75%-50% / 25%-<50%; Villous T/V <=50% / >50%.

Note 1:[8]

  • Most villous adenomas are sessile, i.e. flat.[9]
  • Tubular adenomas tend to be pedunculated, i.e. have a stalk.
  • Villous adenomas have a worse prognosis and warrant closer follow-up.
  • One needs only to remember the criteria for tubular adenomas and villous adenomas, as tubulovillous adenomas are what is left over.
    • Tubular adenomas >75% tubular, Villous adenoma >=50% villous.
  • There are different definitions for tubular adenoma, tubulovillous adenoma, and villous adenomas.[9]
    • Health Organization (WHO) criteria: villous adenomas >80% villous architecture.

Note 2:

  • The term tubular adenoma is used in different contexts; it should not be confused with Sertoli cell nodule (AKA testicular tubular adenoma).

Grading

Most institutions grade adenomas into:[10]

  • Low grade.
    • Near normal glandular architecture.
    • Goblet cells present.
  • High grade.
    • Have "architectural complexity", i.e. cribriform glands, branching glands.
    • Lamina propria invasion.
    • Sheets of cells -- no longer resemble glands.

NOTE: In the colon, unlike other areas of the GI tract, invasive carcinoma is defined by neoplastic cells through the muscularis mucosae. In all other places, e.g. small bowel, invasive carcinoma is defined by neoplastic cells through the basement membrane.

Micrograph:

Margins

  • Some pathologists believe it is impossible to determine margins in polypectomies.
  • Others comment on what they see and then disclaim based on limitations with something like "... margin clear in plane of section."

The Haggitt classification is margin call taken to the extreme. Surgeons may ask about it 'cause a guy (who probably didn't do a lot of pathology) put it in a widely read surgery textbook. In short:[11][12]

  • 0 - intramucosal carcinoma.
  • 1 - in submucosa but in head of polyp.
  • 2 - neck of polyp.
  • 3 - stalk of polyp.
  • 4 - submucosa of the bowel wall but above muscularis propria.

It is a little scheme that is mostly useless. In the real world surgical pathology most polyps do not have a discernible neck or stalk.

Note:

  • Dr. Haggitt is know for his tragic demise. He was shot by a resident that was about to be fired.[13]

Traditional serrated adenoma

General

  • Very rare.

Microscopic

Features:

  • Serrated.
  • Nuclear atypia (as in tubular adenoma).
  • Villous architecture.

DDx:

  • Villous adenoma.

Images:

Sessile serrated adenoma

  • Often abbreviated SSA.
  • AKA sessile serrated polyp.

General

  • Colonic lesion.
  • More common in the right colon, i.e. ascending colon.

Epidemiology:

  • Thought to lead to colorectal cancer through a different pathway that most tumours in the left colon/rectum.

Microscopic

Features:

  • Serrated.
  • Crypt dilation at base - a key feature - very common.
    • "Boot"-shape or "L"-shaped glands.
  • Crypt branching.
  • Horizontal crypts (crypts that run along the muscular mucosae).

Notes:

  • Typically do not have nuclear atypia, i.e. no nuclear crowding, no nuclear hyperchromasia, no cigar-shaped nuclei.

Micrographs:

Hamartomatous polyps (overview)

Numerous types of hamartomatous polyps exist:

  • Peutz-Jeghers syndrome.
  • Juvenile polyposis syndrome.
  • Cowden's disease.

There are several obscure/very rare types not listed above.

Further reading: Gastrointestinal & Liver Pathology.[14]

Juvenile polyp

General

  • Referred to retension polyps in non-juveniles.

Microscopic

Features:[15][16]

  • Eroded, smooth or lobulated surface.
  • Pedunculated.
  • Increased lamina propria (LP) +/- edema.
  • Cystically dilated gland.
  • Often inflammed.

Mnemonic DIES = dilated glands, increased LP & inflammation of the LP, eroded/smooth surface, stalk.

Notes:

  • Nuclear changes may be like those seen in adenomatous polyps.
  • IHC can be used as an adjunct (p53, Ki-67).
    • p53 mutations in dysplastic epithelium -- negative stain (normal).

Images:

DDx:

  • Inflammatory polyp.

Peutz-Jeghers polyp

General

Epidemiology

Features:[15][16]

Clinical

Features:[17]

  • Melanocytic macules.
    • Lips, buccal mucosa, and digits.
    • Multiple Peutz-Jeghers polyps.

Increased risk of various neoplasms - primarily:

Microscopic

Features:[15][16]

  • Frond-like polyp with all three components of mucosa:
    1. Muscosal epithelium (melanotic mucosa, goblet cells).
    2. Lamina propria.
    3. M. mucosae.

Notes:

  • Frond = leaflike expansion.[20]
    • The key is "thick" smooth muscle bundles - if one is lucky one sees branching.[21]
      • "Thick" ~= thickness of muscularis mucosae.

Images:

Cowden disease

Main article: Cowden syndrome
  • AKA Cowden syndrome.

General

  • Etiology: PTEN gene mutation.

Clinical features:[22]

  • Hamartomatous polyps.
  • Facial trichilemmomas (hair follicle root sheath epithelium tumour).
  • Oral papillomas.
  • Acral keratoses (peripheral keratoses).

Microscopic

Features:

  • Hamartomatous polyp - features non-specific. (???)

Cronkhite-Canada syndrome

  • Abbreviated CCS.

General

Clinical features:[23]

  • Hamartomatous polyps.
  • Ectodermal abnormalities (nail atrophy, skin pigment, alopecia).

Microscopic

Features:

  • Polyps have same morphology as juvenile polyp/retension polyp.
  • Crypt dilation and edema in non-polypoid mucosa[24] - key feature.

See also

References

  1. ↑ Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease (7th ed.). St. Louis, Mo: Elsevier Saunders. pp. 856. ISBN 0-7216-0187-1.
  2. ↑ 2.0 2.1 2.2 Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease (7th ed.). St. Louis, Mo: Elsevier Saunders. pp. 858. ISBN 0-7216-0187-1.
  3. ↑ Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease (7th ed.). St. Louis, Mo: Elsevier Saunders. pp. 860. ISBN 0-7216-0187-1.
  4. ↑ Ueno, H.; Mochizuki, H.; Hashiguchi, Y.; Shimazaki, H.; Aida, S.; Hase, K.; Matsukuma, S.; Kanai, T. et al. (Aug 2004). "Risk factors for an adverse outcome in early invasive colorectal carcinoma.". Gastroenterology 127 (2): 385-94. PMID 15300569.
  5. ↑ Ueno, H.; Murphy, J.; Jass, JR.; Mochizuki, H.; Talbot, IC. (Feb 2002). "Tumour 'budding' as an index to estimate the potential of aggressiveness in rectal cancer.". Histopathology 40 (2): 127-32. PMID 11952856.
  6. ↑ Li SC, Burgart L (March 2007). "Histopathology of serrated adenoma, its variants, and differentiation from conventional adenomatous and hyperplastic polyps". Arch. Pathol. Lab. Med. 131 (3): 440-5. PMID 17516746. http://journals.allenpress.com/jrnlserv/?request=get-abstract&issn=0003-9985&volume=131&page=440.
  7. ↑ 7.0 7.1 Levine JS, Ahnen DJ (December 2006). "Clinical practice. Adenomatous polyps of the colon". N. Engl. J. Med. 355 (24): 2551–7. doi:10.1056/NEJMcp063038. PMID 17167138. http://content.nejm.org/cgi/reprint/355/24/2551.pdf.
  8. ↑ 8.0 8.1 Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease (7th ed.). St. Louis, Mo: Elsevier Saunders. pp. 860. ISBN 0-7216-0187-1.
  9. ↑ 9.0 9.1 http://emedicine.medscape.com/article/170283-overview
  10. ↑ URL: http://www.pathologyoutlines.com/colontumor.html#adenoma. Accessed on: 19 March 2011.
  11. ↑ URL: http://www.ganfyd.org/index.php?title=Haggitt_classification. Accessed on: 19 March 2011.
  12. ↑ Haggitt, RC.; Glotzbach, RE.; Soffer, EE.; Wruble, LD. (Aug 1985). "Prognostic factors in colorectal carcinomas arising in adenomas: implications for lesions removed by endoscopic polypectomy.". Gastroenterology 89 (2): 328-36. PMID 4007423.
  13. ↑ Two die in UW medical school shooting. seattlepi.com. URL: http://www.seattlepi.com/local/pathweb.shtml. Accessed on: April 23, 2009.
  14. ↑ Iacobuzio-Donahue, Christine A.; Montgomery, Elizabeth A. (2005). Gastrointestinal and Liver Pathology: A Volume in the Foundations in Diagnostic Pathology Series (1st ed.). Churchill Livingstone. pp. 345. ISBN 978-0443066573.
  15. ↑ 15.0 15.1 15.2 Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease (7th ed.). St. Louis, Mo: Elsevier Saunders. pp. 859. ISBN 0-7216-0187-1.
  16. ↑ 16.0 16.1 16.2 Bronner, MP. (Apr 2003). "Gastrointestinal inherited polyposis syndromes.". Mod Pathol 16 (4): 359-65. doi:10.1097/01.MP.0000062992.54036.E4. PMID 12692201. http://www.nature.com/modpathol/journal/v16/n4/full/3880773a.html.
  17. ↑ URL: http://www.ncbi.nlm.nih.gov/omim/175200. Accessed on: 13 July 2010.
  18. ↑ Beggs AD, Latchford AR, Vasen HF, et al. (July 2010). "Peutz-Jeghers syndrome: a systematic review and recommendations for management". Gut 59 (7): 975–86. doi:10.1136/gut.2009.198499. PMID 20581245.
  19. ↑ URL: http://www.ncbi.nlm.nih.gov/omim/175200. Accessed on: 22 December 2010.
  20. ↑ URL: http://dictionary.reference.com/browse/frond. Accessed on: 26 July 2011.
  21. ↑ C. Streutker. 26 July 2011.
  22. ↑ Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease (7th ed.). St. Louis, Mo: Elsevier Saunders. pp. 858-9. ISBN 0-7216-0187-1.
  23. ↑ Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease (7th ed.). St. Louis, Mo: Elsevier Saunders. pp. 858-9. ISBN 0-7216-0187-1.
  24. ↑ Mitchell, Richard; Kumar, Vinay; Fausto, Nelson; Abbas, Abul K.; Aster, Jon (2011). Pocket Companion to Robbins & Cotran Pathologic Basis of Disease (8th ed.). Elsevier Saunders. pp. 430. ISBN 978-1416054542.

External links

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