Colon

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The colon and rectum smell like poo... 'cause that's where poo comes from. It commonly comes to pathologists because there is a suspicion of cancer or a known history of inflammatory bowel disease (IBD).

An introduction to gastrointestinal pathology is found in the gastrointestinal pathology article.

Surgery

Introduction to colorectal surgery:

  1. Colonic resection - remove a piece of large bowel.
  2. Total colectomy - leaves rectum and anus.[1]
  3. Subtotal colectomy - part of colon removed --or-- some of the rectum remains.
  4. right hemicolectomy - right colon + distal ileum.
  5. lower anterior resection (LAR) - proximal rectum +/- sigmoid (for proximal rectal malignancies).
  6. abdominoperineal resection (APR) - anus + rectum - results in a permanent stoma (for distal rectal malignancies).

Common clinical problems

Obstruction

Top three (in adults):[2]

  • Neoplasia,
  • Volvulus (cecal, sigmoid),
  • Diverticular disease + stricture formation.

Bleeding

Mnemonic CHAND:[3]

  • Colitis (radiation, infectious, ischemic, IBD (UC >CD), iatrogenic (anticoagulants)),
  • Hemorrhoids,
  • Angiodysplasia,
  • Neoplastic,
  • Diverticular disease.

Infectious colitis with bleeding - causes:

  • Enterohemorrhagic Escherichia coli (EHEC) -- commonly 0157:H7,
  • Campylobacter jejuni,
  • Clostridium difficile,
  • Shigella.

Infectious colitis in the immunosuppressed:

  • Cytomegalovirus (CMV).[4]
    • May afflict patients with IBD and lead to colectomy... as IBD patients are put on immunosuppression.
    • Organ transplant recipients.
    • HIV/AIDS.

Inflammatory bowel disease (IBD)

Exists in two main flavours:

  • Crohn's disease (CD).
  • Ulcerative colitis (UC).

Clinical

  • It is important to differentiate UC and CD as the management is different.
  • UC patients get pouches... CD patients do not.

Epidemiology:

  • NOD2/CARD15 variants are assoc. with stricturing CD, early need for surgery and recurrence.[5]

Microscopic

Features helpful for the diagnosis of IBD - as based on a study:[6]

  • Basal, i.e. crypt base, plasmacytosis with severe chronic inflammation,
  • Crypt architectural abnormalities, and
  • Distal Paneth cell metaplasia.
    • Paneth cells should not be in the left colon[7] - if you see 'em think of IBD and other long-standing injurious processes.
    • Some claim that (friendly right colonic) paneth cells and paneth cell metaplasia look quite different and can be distinguished.[8]

Notes:

  1. Microscopic features can be remembered by mnemonic CPP: Crypts (abnormal), Plasmacytosis, Paneth cells where they don't belong.
  2. If you see architectural distortion (e.g. crypt branching) in the left colon, look for Paneth cells.
  3. The hepatic flexure is considered the divider for normal paneth cells and abnormal paneth cells, i.e. paneth cells proximal to the hepatic flexure are normal; paneth cells distal to the hepatic flexure are abnormal.[9]

Crohn's disease vs. ulcerative colitis

UC features:[10]

  • Mucosal involvement --sometimes submucosa.
  • No skip lesions.
  • Colon/rectum only.
    • UC may have 'ileal backwash' -- mild ileal inflammation due to backwash of inflammatory soup from colon.
  • "No granulomas".
    • Superficial granulomas in the mucosa are non-specific, especially if they are beside an inflammed crypt, i.e. they may be present in UC.[11][12]
      • Deep granulomas are specific for Crohn's disease.

Example of a superficial granuloma that is non-specific, i.e. this could be UC or CD:

Ulcerative colitis

General

  • Often abbreviated as UC.

Epidemiology

Gross

  • Conventionally considered to be contiguous, i.e. no "skip lesions", with rectal involvement being most severe.
  • Dependent on the study one reads... rectal sparing may be seen in 15% of UC patients.[15]

Microscopic

  • Lack of granulomas.
  • No full wall-thickness inflammation.

Crohn's disease

General

  • Often abbreviated as CD.

Gross

Microscopic

Features:[6]

  • Segmental crypt architectural abnormalities,
  • Mucin depletion,
  • Mucin preservation at the active sites, and
  • Focal chronic inflammation without crypt atrophy.

Bowel ischemia

Radiologic correlate

  • Bowel wall thickening.

Gross

Features:[16]

  • Luminal part (mucosa & submucosa) affected.
  • Splenic flexture of colon commonly affected (vascular watershed).

Note:

  • May have pseudomembranes (classically assoc. with C. difficle colitis), i.e. mimics an infectious process.
  • DDx for pseudomembranes:[17]
    • C. difficle induced pseudomembranous colitis,
    • Ischemic colitis,
    • Volvulus,
    • Necrotizing infections,
    • ... anything that causes severe mucosal injury.

Histology of pseudomembranes:[18]

  • Loss of surf. epithelium,
  • PMNs in lamina propria,
  • +/- capillary fibrin thrombi.

NB: Pseudomembranes arise from the crypts.

Image:

Angiodysplasia

General

  • Causes (lower) GI haemorrhage.
  • Generally, not a problem pathologists see.

Location

  • Cecum.

Epidemiology

  • Older people.

Etiology

  • Thought to be caused by the higher wall tension of cecum (due to larger diameter) and result from (intermittent) venous occulsion/focal dilation of vessels.[19]

Melanosis coli

  • AKA Pseudomelanosis coli.[20]
  • Not melanin as the name suggests; it is actually lipofuscin (in macrophages).[21]
  • Endoscopist may see brown pigmentation of mucosa and suspect the diagnosis.

Epidemiology

  • Classically associated with anthracene containing laxative (e.g. Senokot) use and herbal remedies.[21]

Features

  • Brown pigmentation of the mucosa.
  • Typically more prominent in the cecum and proximal colon.[21]

DDx of brown pigment:

  • Lipofuscin - comes with age (can be demonstrated with a Kluver-Barrera stain[22]).
    • Melanosis coli.
  • Old haemorrhage, i.e. hemosiderin-laden macrophages (may be demonstrated with Prussian blue stain[23]).
  • Melanin (from melanocytes) - rare in colon (may be demonstrated with a Fontana-Masson stain[24] -- though not so useful in the GI tract).
  • Foriegn material (e.g. tattoo pigment) - not seen in GI tract.

Images:

Microscopic colitis

General

Definition:

  • As the name suggests, they are microscopic, i.e. endoscopic examination is normal.

Presentation:

  • Chronic diarrhea, non-bloody.[25]

Microscopic colitis - types

  • Lymphocytic colitis (LC).
  • Collagenous colitis (CC).

Some believe that LC and CC are different time points in the same process-- but this is unproven.[25]

Epidemiology

  • Age: a disease of adults - usually 50s.
  • Sex:
    • LC males ~= females,[25]
    • CC females:males = 20:1.[25]
  • Drugs are associated with LC and CC.
    • NSAIDs - posulated association/weak association,
    • SSRIs (used primarily for depression) - moderate association, dependent on specific drug.
  • Associated with autoimmune disorders - celiac disease, diabetes mellitus, thyroid disorders and arthritis.[26]
  • No increased risk of colorectal carcinoma.[26]

Treatment

  • Sometimes just follow-up.
  • Steroids - budesonide -- short-term treatment.[26]

Characteristics

Lymphocytic colitis

  • Lots of intraepithelial lymphocytes (>=20/100 lymphocytes/surface epithelial cells[26]) and
  • lymphocytes in the lamina propria.
  • NEGATIVES:[27]
    • No PMNs.
    • No crypt distortion.

Collagenous colitis

  • Intraepithelial lymphocytes, and
  • lymphocytes in the lamina propria.
  • Collagenous material in the lamina propria (pink on H&E) -- key feature.
    • Can be demonstrated with a trichrome stain -- collagen = green on trichrome.
    • Subepithelial collagen needs to be >= 10 micrometres thick for Dx.[26]
      • 8 micrometres is the diameter of a RBC.
      • The normal thickness of the subepithelial collagen is 3 micrometres.[26]
    • Thickening "follows the crypts from the surface" - useful for differentiating from tangential sections of the basement membrane.[28]
    • Collagen may envelope capillaries - useful to discern from basement membrane.[29]
  • NEGATIVES[27]
    • No PMNs.
    • No crypt distortion.

Notes: CC is typically more prominent in the proximal colon - may reflect concentration gradient of offending causitive agents.[26]

Spirochetes

General

  • Very rare cause of diarrhea.
  • Caused by Serpulina pilosicoli and Brachyspira aalborgi.[30]
  • Tx: metronidazole.[31]

Histology

  • Hyperchromatic fuzz on luminal aspect of epithelial cells; at brush border.

Special stain:

  • Silver stains highlight 'em (e.g. Warthin-Starry stain).

Amebiasis

General

  • Infection with Entamoeba histolytica.[32]
  • May also be spelling amoebiasis.
  • May mimic colon cancer.[33]

May cause:[34]

  • Dysentery (diarrhea containing mucus and/or blood in the feces).
  • Colitis.
  • Liver abscess.

Microscopy

Features:

  • Round/Ovoid eosinophilic bodies ~ 40-60 micrometers in maximal dimension.
  • Found in bowel lumen.
  • Ingest RBCs.

Image:

Polyps

Polyps are the bread & butter of GI pathology. They are very common.

Main types:

  • Hyperplastic (most common)
  • Adenomatous (quite common, pre-malignant)
  • Hamartomatous (rare, weird & wonderful)
  • Inflammatory (associated with IBD)

Most common (images):

Colorectal Tumours

These are very common. The are covered in a separate article entitled colorectal tumours.

Grossing

  • Lymph nodes - should get at least 12.[35]

Quirke method

  • Bowel is not opened.

Standard method

  • Bowel is prep'ed by opening it along the antimesenteric side.
  • Dimensions - length, circumference at both margins.
  • Radial margin/circumferential margin - should be painted.
    • Rectum starts/sigmoid ends @ place where serosa ends on the posterior aspect of the bowel.
      • The proximal, anterior aspect of the rectum has serosa, i.e. it is not painted.

Solitary rectal ulcer

General

  • Clinically may be suspected to a malignancy - biopsied routinuely.
  • Mucosal ulceration.
  • "Three-lies disease":[38]
  1. May not be solitary,
  2. May not be rectal -- can be in left colon,
  3. May not be ulcerating -- non-ulcerated lesions: polypoid and/or erythematous.

Note: Each of the words in solitary rectal ulcer is a lie.

Epidemiology

  • Typically younger patients - average age of presentation ~30 years in one study.[39]
  • Rare.

Clinical

  • Usually presents as BRBPR ~ 85% of cases.[39]
  • Abdominal pain present in approx. 1/3.[39]
    • May be very painful.

Histology

Features:[38]

  • Fibrosis of the lamina propria - should be obliterated.
  • Thickened muscularis mucosa - abnormally extends to the lumen.

Histologic DDx

  • Rectal prolapse. (?)

Treatment

  • Usually conservative, i.e. non-surgical.
  • Resection - may be done for fear of malignancy.

Rectal prolapse

Histopathology

Features:[40]

  • "Fibromuscular hyperplasia":
    • Fibrosis,
    • Muscularis mucosae is "too superficial".
  • Surface ulceration + inflammation (neutrophils).
  • +/-Serration of epithelium at the surface.
  • NEGATIVES:
    • No nuclear atypia.

Mucosal prolapse syndrome

  • Similar to rectal prolapse???

Weird stuff

Kayexalate (sodium polystyrene sulfonate):[41]

  • Used to treat hyperkalemia.
  • Purple blobs on H&E stain - look somewhat like calcium phosphate.
  • Can cause focal necrosis.

Image: Sodium polystyrene crystals - commons.wikimedia.org.

Chronic constipation

This is occasionally an indication for colectomy.

Causes:

  • Tumour.
  • Adhesions - due to previous surgery.
  • Neuropathy.
  • Congenital defect (Hirschsprung's disease).
  • Medications/substance use.
  • Idiopathic.

Work-up if no tumour is identified:[42]

  • Routine H&E.
  • Pan-actin.
  • Gomori trichrome.
  • CD117 - to look for the interstitial cell of Cajal.
  • HU - neuronal marker.[43]

Goblet cell carcinoid

Described in detail in the appendix article.
  • AKA crypt cell carcinoma.
  • Biphasic tumour; features of carcinoid tumour and adenocarcinoma.

See also

References

  1. http://www.allaboutbowelsurgery.com/shared/stoma_care/stoma_surgery/procedures/surgery_colon/subtotal.htm
  2. http://www.emedicine.com/EMERG/topic65.htm
  3. TN 2007 G29.
  4. Golden MP, Hammer SM, Wanke CA, Albrecht MA (September 1994). "Cytomegalovirus vasculitis. Case reports and review of the literature". Medicine (Baltimore) 73 (5): 246–55. PMID 7934809.
  5. Alvarez-Lobos M, Arostegui JI, Sans M, et al. (November 2005). "Crohn's disease patients carrying Nod2/CARD15 gene variants have an increased and early need for first surgery due to stricturing disease and higher rate of surgical recurrence". Ann. Surg. 242 (5): 693–700. PMC 1409853. PMID 16244543. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1409853/.
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  7. Tanaka M, Saito H, Kusumi T, et al (December 2001). "Spatial distribution and histogenesis of colorectal Paneth cell metaplasia in idiopathic inflammatory bowel disease". J. Gastroenterol. Hepatol. 16 (12): 1353–9. PMID 11851832. http://www3.interscience.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0815-9319&date=2001&volume=16&issue=12&spage=1353.
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  40. NEED REF.
  41. Abraham SC, Bhagavan BS, Lee LA, Rashid A, Wu TT (May 2001). "Upper gastrointestinal tract injury in patients receiving kayexalate (sodium polystyrene sulfonate) in sorbitol: clinical, endoscopic, and histopathologic findings". Am. J. Surg. Pathol. 25 (5): 637-44. PMID 11342776. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0147-5185&volume=25&issue=5&spage=637.
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