Ischemic colitis 

– Ischemic colitis (see comment)

COMMENT: The histologic sections show colonic mucosa with hemorrhage and hyalinization within the lamina propria. The crypts demonstrate superficial withering and regenerative changes. The features are those of an ischemic-pattern colitis. While these findings are most common in ischemic colitis, the differential diagnosis is broad and includes mechanical obstruction (e.g. stercoral ulcer), infections (particularly E. coli O157:H7), vasculitis, and medication effect. Clinical correlation is recommended. 

 

Eosinophilic colitis

Although there is no well-established cut-off, >60 Eos/HPF is likely too many:

  – Eosinophil-rich colitis (with up to *** Eosinophils per single high power field) (see comment)

COMMENT: Histologic sections of the *** biopsy show an eosinophilic colitis with up to *** eosinophils per single high-power field. There is also eosinophilic cryptitis, eosinophil degranulation and microabscess formation. This finding is nonspecific and can be seen in association with a variety of other conditions including a food allergy, medication-effect, parasitic infection, Crohn’s disease, and systemic connective tissue diseases. The differential diagnosis also includes an eosinophilic gastroenteritis/colitis, which is a diagnosis of exclusion.  Clinical correlation is recommended.

 

Acute Changes Only 

If there is focal cryptitis, but no evidence of chronicity (i.e., architectural distortion) [NO history of IBD]

 – Focal active colitis (see comment)

COMMENT: Histologic sections show a very focal active colitis with cryptitis and no architectural changes. No viral cytopathic changes or granulomas are present.  This finding is very focal, mild, and nonspecific and can be seen in association with certain medications (particularly NSAIDs), certain infections, ischemia, and even bowel preparation (particularly with sodium phosphate). While an emerging inflammatory bowel disease cannot be entirely excluded, it is not favored. In some patients, it is an incidental finding for which an etiology cannot be determined. Clinical and endoscopic correlation is recommended.

 

History of IBD, there is only very focal cryptitis, but no evidence of chronicity (i.e., architectural distortion):

 – Focal active colitis (see comment)

COMMENT: Histologic sections show a very focal active colitis with extremely focal cryptitis and no architectural changes. No viral cytopathic changes or granulomas are present.  This finding is very focal, mild, and nonspecific.  There is no evidence of dysplasia in any of the biopsies.  Although this could represent extremely limited involvement by their previously diagnosed inflammatory bowel disease, the differential diagnosis also includes certain medications (particularly NSAIDs), certain infections, ischemia, and even bowel preparation (particularly with sodium phosphate). In some patients, it is an incidental finding for which an etiology cannot be determined. Clinical and endoscopic correlation is recommended.

 

If there is diffuse cryptitis and crypt abscess formation, but no evidence of chronicity (i.e., architectural distortion):

– Active colitis (see comment)

COMMENT: Histologic sections show an active colitis with cryptitis and crypt abscess formation. Features of chronicity (such as crypt architectural distortion or a basal lymphoplasmacytosis) are not prominent. No granulomas or viral cytopathic effect is identified. The differential diagnosis includes an infectious colitis (acute self-limited colitis), medication effect (particularly NSAIDs), and an emerging inflammatory bowel disease. Clinical and endoscopic correlation is recommend.

 

Acute and Chronic Changes 

– Chronic active colitis (see comment)

– Chronic active proctitis (see comment) 

Use this for marked chronic changes in chronic active colitis ( i.e. your thinking IBD for sure) :

COMMENT: The histologic sections show an active colitis with cryptitis and crypt abscess formation. There are also features of chronicity including crypt architectural distortion and a basal lymphoplasmacytosis. No granulomas or viral cytopathic effect are identified. There is no evidence of dysplasia.

While these findings may be compatible with inflammatory bowel disease, other etiologies, including medication-effect (particularly NSAIDs) and an infection cannot be excluded histologically. Clinical and endoscopic correlation is recommended.

Or (different last paragraph if they have a history of IBD)

These findings are compatible with the patient’s reported history of inflammatory bowel disease. However, other etiologies, including medication-effect (particularly NSAIDs) and an infection, should be excluded clinically. Clinical and endoscopic correlation is recommended.

 

Use this comment for mostly active colitis that only has mild chronic changes (i.e., it might be IBD, but you’re  not certain)

COMMENT: The histologic sections show an active colitis with cryptitis and crypt abscess formation with only mild architectural changes. The differential diagnosis for these features includes infection, inflammatory bowel disease, drug/medication (particularly NSAIDs)-associated colitis, and segmental colitis secondary to diverticular disease, among other possibilities. No viral cytopathic changes or granulomas are present. Clinical correlation is suggested.

 

Chronic Changes Only 

– Chronic inactive colitis (Quiescent colitis) (see comment)

COMMENT: The histologic sections show architectural changes and Paneth cell metaplasia without active inflammation. No viral cytopathic changes or granulomas are identified. The differential diagnosis includes chronic inactive (quiescent) colitis in the context of inflammatory bowel disease. However, other chronic and resolving forms of injury can appear similar histologically, including certain infections, medication-associated colitides, chronic recurrent ischemia, and radiation colitis. Clinical correlation is needed.

 

  – Paneth cell metaplasia (see comment)

COMMENT: Histologic sections of the  *** colon biopsy (specimen ***) demonstrate focal Paneth cell metaplasia suggestive of previous mucosal injury/inflammation. No active inflammation is identified. Additionally, other features of chronicity (e.g., basal lymphoplasmacytosis and/or architectural changes) are not prominent. There is no evidence of dysplasia in any of the biopsies. Clinical and endoscopic correlation is recommended.

 

Radiation Proctitis/Colitis 

   – Chronic active proctitis, compatible with radiation proctitis

COMMENT: The patient’s history of rectal cancer status post resection and chemoradiation is noted. The rectal fold biopsy demonstrates rectal-type mucosa with active inflammation including numerous intraepithelial neutrophils. There is also architectural distortion consistent with chronic damage. Additionally, the lamina propria contains several telangiectatic blood vessels with mildly atypical endothelial cells and fibroblasts. Overall, these findings are consistent with radiation proctitis given the patient’s history. Clinical and endoscopic correlation is recommended.

 

Microscopic Colitis 

   – Lymphocytic colitis (see comment)

COMMENT: The histologic sections show colorectal-type mucosa with dramatically increased intraepithelial lymphocytes with associated reactive epithelial changes including mucin depletion. There is no significant thickening of the subepithelial collagen table. Although there are scattered intraepithelial neutrophils, this is not the predominant finding. Features of chronicity (including a basal lymphoplasmacytosis) are not prominent.

Overall, these findings are compatible with lymphocytic colitis. However, an expanding list of medications is implicated in lymphocytic-pattern colitis (including NSAIDs, losartan, and ranitidine, among many others). Additionally, some infections can cause a lymphocytic-pattern colitis. As such, clinical and endoscopic correlation is recommended.

 

Looks like lymphocytic colitis, but not quite enough intraepithelial lymphocytes (<20 lymphs/100 epithelial cells):

  – Increased intraepithelial lymphocytes and superficial lymphoplasmacytosis (see comment)

COMMENT: Histologic sections of both the colon biopsies demonstrate colonic-type mucosa with a superficial lymphoplasmacytosis and variably increased intraepithelial lymphocytes. There are associated reactive epithelial changes including mucin depletion. Significant activity (i.e. cryptitis/crypt abscess formation) and chronicity (i.e., crypt architectural distortion) are not identified. There is no significant thickening of the subepithelial collagen layer.

Overall, the findings are most suggestive of mild/emerging lymphocytic colitis. However, an expanding list of medications is implicated in lymphocytic-pattern colitis (including NSAIDs, losartan, and ranitidine, among many others). Additionally, some viruses can cause a lymphocytic-pattern colitis. As such, clinical and endoscopic correlation is recommended.

 

 – Collagenous colitis

COMMENT:  The histologic sections show colorectal-type mucosa with increased intraepithelial lymphocytes. There is also dramatic thickening of the subepithelial collagen layer, with entrapment of inflammatory cells and capillaries. Features of chronicity (including a basal lymphoplasmacytosis) are not prominent.

Overall, these findings are compatible with collagenous colitis. However, an expanding list of medications is implicated in collagenous-pattern colitis (including NSAIDs, losartan, and ranitidine, among many others). Additionally, some infections can cause a collagenous-pattern colitis. As such, clinical and endoscopic correlation is recommended.

 – Microscopic colitis

COMMENT:  The colorectal biopsies demonstrate a superficial lymphoplasmacytosis with variably increased intraepithelial lymphocytes and associated reactive epithelial changes including mucin depletion. There is also somewhat patchy thickening of the subepithelial collagen layer.

These findings are diagnostic of microscopic colitis, with the majority of the biopsies showing an appearance most consistent with lymphocytic colitis, with focal areas suggestive of collagenous colitis.  However, an expanding list of medications is implicated in microscopic colitis (including NSAIDs, losartan, and ranitidine, among many others). Additionally, some infections can cause a microscopic colitis pattern. As such, clinical and endoscopic correlation is recommended.

 

 

Miscellaneous

  – Melanosis coli

COMMENT: Histologic sections of the colorectal biopsies demonstrate variable deposition of brown pigment within lamina propria macrophages consistent with melanosis coli. Melanosis coli is a relatively common, nonspecific finding that is closely related to increased epithelial cell apoptosis. Although it is classically associated with laxative use, it is associated with other medications also, including NSAIDs. Additionally, melanosis is common in the setting of chronic colonic stasis/constipation and colitis. In this case, no significant inflammation is identified within any of the colorectal biopsies. Clinical and endoscopic correlation is recommended.

 


 

Colon – Polyps 

Non-neoplastic

– Prominent lymphoid aggregate

– Juvenile polyp

– Mucosal prolapse-type polyp

– Inflammatory polyp

 

  -Peutz-Jeghers-type polyp (see comment)

COMMENT: Histologic sections show a hamartomatous polyp with a prominent, arborizing smooth muscle core and lobular architecture. These findings are classic for a Peutz-Jeghers polyp. Clinical and endoscopic correlation is recommended to determine if this patient has Peutz-Jeghers syndrome. It has been suggested that even patients with isolated Peutz-Jeghers polyps have an increased risk of malignancy (reference below).

Reference: Burkart AL et al. Do sporadic Peutz-Jeghers polyps exist? Experience of a large teaching hospital. Am J Surg Pathol. 2007 Aug;31(8):1209-14.

 

Neoplastic polyps

– Hyperplastic polyp 

– Sessile serrated adenoma/polyp

 

For When you can’t tell if it an HP or SSP:

 – Serrated polyp (see comment)

COMMENT: The histologic sections show a serrated polyp. Despite multiple deeper histologic findings, no unequivocal deep crypt changes are identified to confirm the diagnosis of a sessile serrated adenoma/polyp. However, the polyp’s right-sided location would favor the diagnosis of a sessile serrated adenoma/polyp. Clinical and endoscopic correlation is recommended.

 

– Tubular adenoma

– Tubulovillous adenoma

– Villous adenoma

 – Traditional serrated adenoma

 

Neoplasia in IBD

-Indefinite for dysplasia

  – Low-grade dysplasia

  – High-grade dysplasia

COMMENT: The biopsy shows ***-grade dysplasia, which could be sporadic or colitis-associated. Regardless, both lesions can be treated similarly. According to the SCENIC consensus, endoscopically visible lesions can be resected and managed endoscopically. Clinical and endoscopic correlation is recommended.

REFERENCE: Laine L et al. SCENIC international consensus statement on surveillance and management of dysplasia in inflammatory bowel disease. Gastroenterology. 2015 Mar;148(3):639-651.

 

  – Serrated epithelial change (see comment)

COMMENT: The *** biopsy shows extensive crypt epithelial serrations with distorted architecture and some crypts that do not reach the crypt base. These findings are diagnostic of so-called “Serrated Epithelial Change” (SEC), a new and evolving entity the full significance of which is unknown. There is no conventional dysplasia in the current biopsy. In some studies, SEC is associated with an increased risk of subsequent or concurrent dysplasia, prompting some to consider close clinical follow-up, similar to the diagnosis of “indefinite for dysplasia.” Clinical and endoscopic correlation is recommended.

REFERENCE:  Parian A et al. Association between serrated epithelial changes and colorectal dysplasia in inflammatory bowel disease. Gastrointest Endosc. 2016 Jul;84(1):87-95.

 

 

Colon Cancer 

Biopsy

– Invasive Adenocarcinoma, *** grade

COMMENT: The histologic sections show an adenocarcinoma of the usual intestinal type. There is *** gland formation consistent with a provisional classification of ***-grade . There is desmoplastic stroma consistent with at least submucosal invasion. No lymphovascular invasion is identified.  Testing for mismatch repair enzymes by immunohistochemical staining has been ordered and will be reported in an addendum.

 

Resection

– Invasive Adenocarcinoma, *** grade, *** cm, excised (see comment)

 – Metastatic carcinoma in *** of *** lymph nodes (***/***)

 

Colon Carcinoma WHO grading

Well-differentiated: >95% of tumor is gland forming (Grade 1, Low grade)

Moderately-differentiated: 50-95% gland formation (Grade 2, Low grade)

Poorly-differentiated: Mostly solid with <50% gland formation (Grade 3, High grade)

 

Mesenchymal polyps/lesions

– Mucosal Schwann cell hamartoma

– Perineurioma

 

 

Last updated: 8/19/2020