Gastrointestinal pathology

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Author: Mikael Häggström, M.D. [note 1]

Contents

Appendix

Gross processing

  • Measure the length of the appendix.[1]
  • ((Note its shape.[1] ))
  • Inspect the serosa (color, congestion, adhesions, hemorrhage, exudate etc)
  • ((Describe and measure the mesoappendix.))
  • Cut off about 1.5 cm from the tip and split it in half long the lumen. Divide the remainder into about 3-5 mm thick transverse slices.[1]
  • ((Note the wall thickness[1]))
  • Look mainly for:[1]
  • Luminal pus or obstruction, including stones.
  • Look for any yellow firm areas at the tip, which may be carcinoids. Carcinoids may hide behind obstructions in the tip. If found grossly, submit entire appendix, and ink the surgical margin and submit separately en face[note 2]
  • Wall defects
  • Exterior coatings. Note if it contains "stones" or fruit kernels.
  • Any tumor. If found:
  • Measure the greatest dimension of the tumor
  • Look for foci of carcinoma or lymph nodes in the mesoappendiceal fat, which may be lymphatic or perineural invasion

Tissue selection

  • At least one half of the tip
  • At least one slice from visually inflamed areas.
  • ((A transverse slice closest to the base, that is, the surgical cut.))
  • ((At least one transverse slice from an intermediate part.))

Particular findings indicating additional sampling include:[1]

  • Wall discoloration
  • External green-gray-yellow coating
  • Suspected wall defects

Submit the entire appendix if:

Excessive mucus.
  • There is excessive amounts of mucus, (including a representative section of any free mucus if the eppendix is perforated).
  • The surgical report mentions perforation but none is found grossly.
  • The surgical report mentions appendicitis but no significant inflammation is found grossly.

Gross report

Example:

((Labeled - appendix. The specimen is received in formalin and consists of a resected)) appendix measuring __ cm in length and __ cm in maximum diameter. The serosa is tan-red {{and
  • hyperemic?
  • smooth / ragged / granular?
  • congested?
  • with a patchy purulent exudate?
  • with adhesions?}}

The attached mesoappendix measures __ cm and appears {{

  • unremarkable?
  • hyperemic?
  • (focally) inflamed?}}

On cut sections, the lumen {{is dilated and contains {{

  • (brown) (semisolid) fecal material?
  • purulent (blood-tinged) exudate?
  • a small amount of blood?
  • a fecalith?}}

No perforation is identified. ((Representative sections are submitted for microscopic examination in __ cassette(s).))

  See also: General notes on gross processing


Microscopic evaluation

Always look for inflammation and malignancy.

Inflammation

Appendix neoplasms by incidence and prognosis.
Main article: Appendicitis

Neutrophilic infiltrates of the wall of the appendix in the correct clinical context confers a diagnosis of appendicitis.

Malignancy

  • Look for cancerous cells (also for specimens with clinical appendicitis).
  • Look in particular for carcinoid tumors of the distal tip.
  • In the presence of mucus, look for any mucinous neoplasm.

Report

  • Description of objective findings.
  • Presence or absence of malignancy.

Example, using image at right:

Histopathology of appendicitis.jpg

Mucosa with ulceration. ((No atypia in residual mucosa.)) Inflammatory cells in the stroma and all muscle layers, as well as on the serosal surface and adherent adipose tissue. No evidence of malignancy. ((Optionally: No perforation))

For cancers, generally include a synoptic report, such as per College of American Pathologists (CAP) protocols at cap.org/protocols-and-guidelines.

  See also: General notes on reporting


Notes

  1. For a full list of contributors, see article history. Creators of images are attributed at the image description pages, seen by clicking on the images. See Patholines:Authorship for details.
  2. En face means that the section is tangential to the region of interest (such as a lesion) of a specimen. Further information: Gross_processing#Cutting

Main page

References

  1. 1.0 1.1 1.2 1.3 1.4 1.5 1.6 Monica Dahlgren, Janne Malina, Anna Måsbäck, Otto Ljungberg (1997-02-13). Lilla utskärningen.
  2. Elkbuli, Adel; Sanchez, Carol; McKenney, Mark; Boneva, Dessy (2019). "Incidental neuro-endocrine tumor of the appendix: Case report and literature review ". Annals of Medicine and Surgery 43: 44–47. doi:10.1016/j.amsu.2019.05.015. ISSN 20490801. 
  3. Hajjar, Roy; Dubé, Pierre; Mitchell, Andrew; Sidéris, Lucas (2019). "Combined Mucinous and Neuroendocrine Tumours of the Appendix Managed with Surgical Cytoreduction and Oxaliplatin-based Hyperthermic Intraperitoneal Chemotherapy ". Cureus. doi:10.7759/cureus.3894. ISSN 2168-8184. 

Image sources


Appendicitis

Gross processing

Standard sections if the appendix appears inflamed and there are no signs of malignancy. Describe abnormal signs including:

Further information: Appendix

Microscopic evaluation

  • Evaluate depth of the inflammation.
  • Look for any perforation of the wall.
  • Look for cancerous cells (which may have caused the appendicitis). Further information: Appendix
  • (Attempt to specify the type of appendicitis as either of the following:)

Types

Classification of acute appendicitis based on gross pathology and light microscopy characteristics[1]
Pattern Gross pathology Light microscopy Image Clinical significance
Acute intraluminal inflammation None visible
  • Only neutrophils in lumen
  • No ulceration or transmural inflammation
Histopathology of acute intraluminal inflammation of the appendix.jpg Probably none
Acute mucosal inflammation None visible
  • Neutrophils within mucosa, and possibly in submucosa
  • Mucosal ulceration
May be secondary to enteritis.
Suppurative acute appendicitis May be inapparent.
  • Dull mucosa
  • Congestion of surface vessels
  • Fibropurulent serosal exudate in late cases
  • Dilation of the appendix
  • Neutrophils in mucosa, submucosa and muscularis propria, potentially transmural.
  • Extensive inflammation
  • Commonly intramural abscesses
  • Possibly vascular thrombosis
Acute suppurative appendicitis with perforation.jpg Can be presumed to be primary cause of symptoms
Gangrenous/necrotizing appendicitis
  • Friable wall
  • Purple, green or black color
  • Transmural inflammation, obliterating normal histological structures
  • Necrotic areas
  • Extensive mucosal ulceration
Histopathology of necrotizing appendicitis, high magnification.jpg Will perforate if untreated
Periappendicitis May be inapparent.
  • Serosa may be congested, dull and exudative
  • Serosal and subserosal inflammation, no further than outer muscularis propria to be called isolated.
Histopathology of periappendicitis.jpg If isolated, probably secondary to other disease
Eosinophilic appendicitis None visible
  • >10 eosinophils/mm2 in muscularis propria.
  • No changes conforming to other types of appendicitis
Possibly parasitic, or eosinophilic enteritis.
Chronic appendicitis[2]
  • Fibrosis
  • Predominantly mononuclear infiltrate rather than neutrophilic.
Should preferably correlate with long-term or recurrent symptoms.

Further workup

(In acute suppurative appendicitis, still look for any periappendicitis. Also look by the lumen for parasites.)

Microscopy report

Should include, if detected:

  • Acute or chronic appendicitis
  • Depth of inflammation
  • Any abscess and\or perforation
  • Necrosis and\or ulceration, at least if transmural

(Classification into one or several types as per table above.)

Example
(Appendix, resection (or appendectomy):)
Acute (suppurative) appendicitis (and periappendicitis) with transmural necrosis and perforation.


Gallbladder

Gross processing

Cholecystectomy grossing

  • Describe the serosa (smooth and intact versus disrupted, adhesions, inflammation, tumor implants, necrosis, porcelain).
  • (Inspect the adventitia (the roughened juxtahepatic surface), where disruptions are generally iatrogenic and optional to report.)
  • Cut off the cystic duct margin and submit
  • Look for any cystic duct lymph node, describe and submit if present
  • Open the gallbladder longitudinally on the serosal surface. Do not open along the adventitia.[note 1]
  • (Estimate the amount of bile.)
  • {{Estimate the number and describe gallstones.}}
  • Describe the mucosa (such as velvety, granular, trabeculated, and/or with cholesterol stippling)
  • Look for any gallbladder polyps or tumors. Tumors will usually be hard.
  • Open the spiral neck, and look for lesions and gallstones therein
  • Cut through the wall, and look for any tumors or Rokitansky-Aschoff sinuses
  • Look for gallstones in the container
Gross report
((Labeled - gallbladder. The specimen is received in formalin and consists of a resected)) {{
  • previously opened?
  • focally disrupted (on the juxtahepatic avdentitial surface only)?
  • edematous?}}

gallbladder measuring __ cm in length and __ cm in maximum diameter. The serosa is

  • {{(mottled) tan / pink / red (generally combinations thereof) and}}
  • smooth {{/ with patchy adhesions}}

Upon opening, the lumen contains ((__ [[volume in cc/cm3]]))

  • green {{/ brown / blood-tinged / yellow-white and chalky / clear colorless
  • viscid / sludge-like / thick}}

bile {{and

  • (approximately) __ (number) / multiple
  • black / brown / green / yellow / tan / white (generally combinations thereof)
  • irregular / multifaceted / spiculated / ovoid / mulberry-like / barrel-like

gallstones measuring up to __ cm in greatest dimension.}} The mucosa is

  • green {{/ tan / yellow-red / brown / pink}}
  • and velvety {{/ granular / trabecular
  • with diffuse cholesterol stippling?}}

The spiral neck is patent {{/ obstructed by one additional similar gallstone measuring __ cm}}. The wall measures up to __ cm in thickness. {{ Rokitansky-Aschoff sinuses are present within the fundus. There is a __ (color) cystic duct lymph node present measuring __ cm in greatest dimension. }} ((Representative sections are submitted for microscopic examination in __ cassette(s). ))

Rifts on the adventitial side that are consistent with surgical trauma need mentioning only in tumor cases.

Carcinoma

Pathology trainees that find an unsuspected tumor should generally notify a senior before continuing.

  • State whether the gallbladder is intact when you received it.
  • Ink the surgical margin (adventitial surface).
  • Ink the cystic duct margin (lightly) and put in a separate cassette. Notify the lab to have it submitted en face[note 2]
  • Look for any cystic duct lymph nodes. If found, bisect and submit.
  • Measure the tumor in greatest dimension and thickness and state where in the gallbladder it is located (fundus, body, etc and whether it is on the peritoneal or hepatic side).
  • Measure the margin to the cystic duct resection
  • State all other abnormalities including stones, Rokitansky-Aschoff sinuses etc.

Take sections from:

  • Cystic duct margin, en face
  • Cystic duct lymph node if present
  • Sections of tumor, full thickness
  • Sections of unaffected gallbladder

Autopsy grossing

Gross pathology of gallbladder carcinoma, with a prominent nodule.

The gallbladder and biliary tract may be cut open from either end:

  • Starting from the gallbladder: Cut the gallbladder open and from there dissect the cystic duct and common bile duct through the ampulla of Vater.
  • Starting from the duodenum: Identify the ampulla of Vater, possibly by bile flow when squeezing the gallbladder. Dissect the common bile duct, cystic duct and thereafter the gallbladder. If the cystic duct is difficult to find, transverse cuts may be performed at its presumed location.
  • In the gallbladder, inspect the contents and the appearance of the wall. Look mainly for signs of carcinoma. Optionally, estimate the volume of bile therein.
  • In the biliary tract, look mainly for stones and stenosis.

Further information: Autopsy

Fixation

Generally 10% neutral buffered formalin.

  See also: General notes on fixation


Microscopic evaluation

Look at least at the epithelial lining, for atypia and inflammation (such as edema and inflammatory cells, Further information: cholecystitis ).

Other findings

Report

Example:

(Gallbladder, resection:)
  • Gallbladder with no significant histopathologic changes

In cholecystitis:

(Gallbladder, cholecystectomy:)
<<Acute and/or chronic>> cholecystitis.
{{Cholelithiasis.}}

For cancers, generally include a synoptic report, such as per College of American Pathologists (CAP) protocols at cap.org/protocols-and-guidelines.


Cholecystitis

Inflammation of the gallbladder:

Gross processing

As per basic Gallbladder.

Microscopic evaluation

Look for signs of acute or chronic cholecystitis. If you find either, keep looking for the other as well, in case it is both acute and chronic.

Findings in acute cholecystisis

Main initial features are edema and hemorrhage.[4]

  • Initially often also congestion and fibrin deposition in and around the muscular layer.[5]
  • Later often necrosis of the mucosa and and deeper layers, with neutrophils.[5]
  • Variable reactive epithelial changes, which may resemble dysplasia.[5]

There may be fresh thrombi within small veins.[5]

Findings in chronic cholecystitis

Rokitansky-Aschoff sinus.

Typical features are:[7]

  • Smooth muscle hypertrophy in the muscularis
  • Mild inflammatory infiltrates
  • Rokitansky-Aschoff sinuses

Other findings favoring the diagnosis are:[7]

  • Granulomas (from ruptured Rokitansky-Aschoff sinuses) strongly favor the diagnosis.
  • Hyalinized collagen
  • Dystrophic calcification
  • Lymphoid aggregates
  • Atrophic and/or ulcerated mucosa
  • Metaplastic changes, such as gastric or intestinal mucosa

For a general gallbladder screening, see gallbladder.

Lymph nodes

Look for reactive lymphadenopathy or metastasis. Further information: Lymph node

Microscopy report

Report:

  • Relevant findings from the evaluation.
  • Any cholelithiasis as per the gross report.
Template

On this resource, the following formatting is used for comprehensiveness:

  • Minimal depth
  • (Moderate depth)
  • ((Comprehensive))
Other legend

<< Decision needed between alternatives separated by / signs >>
{{Common findings / In case of findings}}
[[Comments]]
Link to another page

(Gallbladder, cholecystectomy:)
<<Acute and/or chronic>> cholecystitis.
{{Cholelithiasis.}}


Gallbladder polyp

Fixation

Generally 10% neutral buffered formalin.

Gross processing

Photograph of a 6 mm large hyperplastic polyp of the gallbladder.

As per gallbladder, with addition to submitting the entire polyp unless very large.

Microscopic evaluation

Look for signs of the most common polyp types:


Endoscopic gastrointestinal biopsies

Gross processing

  • Count the number of fragments. They can be classified as “multiple” at over 5 or 6 specimens. Possibly add “Mixed with luminal material”.
  • Preferably stain with eosin if any fragment is smaller than about 0.3 cm
  • Biopsies that are thicker than about 3-4 mm generally need to be bisected.

Microscopic examination

(Read the endoscopy report before evaluating (except for polyp biopsies, where it can be presumed that the purpose is to look for any malignancy).)

Example normal reports

Further information in main articles of each location.

Esophagus
(Middle third esophagus, biopsy:)
Squamous mucosa without significant histopathologic changes.
(Negative for eosinophilic esophagitis.)
Gastroesophageal junction
(GE junction, biopsy:)
Squamous and gastric mucosa without significant histopathologic changes.
(Negative for intestinalized (Barrett's) mucosa.)
Stomach
(Stomach, biopsy:)
Gastric mucosa without significant histopathologic changes.
((Negative for Helicobacter pylori organisms on H&E slide.))
Duodenum
(Small bowel, biopsy:)
Small intestinal mucosa without significant histopathologic changes.
((Negative for celiac disease.))
Terminal ileum
(Small bowel, biopsy:)
Small intestinal mucosa without significant histopathologic changes.
((Negative for ileitis.))
Colon
(Colon, biopsy:)
Colonic mucosa without significant histopathologic changes.
((Negative for colitis.))


Esophagus

Microscopic evaluation

On esophageal biopsies, look at least for esophagitis:

Esophagitis

GE junction with chronic esophagitis, including plasma cells (black arrow), an acute inflammation with neutrophils (white arrow), as well as basal layer hyperplasia (yellow double-headed arrow).

Look for signs of (reflux) esophagitis, mainly:[9]

  • Inflammatory cells, especially when intra-epithelial. Neutrophils confer a diagnosis of acute inflammation, while plasma cells, eosinophils and excess T cells confer a diagnosis of chronic inflammation. In eosinophil-predominant inflammation, also evaluate as suspected eosinophilic esophagitis.
  • Basal cell hyperplasia exceeding 15 - 20% of the epithelial thickness.
  • Stromal papillae reaching upper third of the epithelium.
  • Loss of orientation of superficial epithelial cells.
  • Ballooned squamous cells

Microscopy report

Example normal report for an esophagus biopsy:

(Middle third esophagus, biopsy:)
Squamous mucosa without significant histopathologic changes.
((Negative for eosinophilic esophagitis.))

Example report with signs of reflux:

(Mid esophagus, biopsy:)
Squamous mucosa with reactive changes consistent with reflux.
((Negative for eosinophilic esophagitis.))


Eosinophilic esophagitis

Histopathology of eosinophilic esophagitis, showing multiple intraepithelial eosinophils (bilobed cells with eosinophilic cytoplasm on H&E stain), and edema seen as white clearings.

Microscopic diagnosis

An intra-epithelial eosinophil (characterized by its bilobed nucleus despite scant visible eosinophilic cytoplasm)

It is characterized by a prominent eosinophilic infiltrate in the esophagus. Count in at least one high power field of an intraepithelial area where there may be the highest concentration of eosinophils, and count them. Only count eosinophils where you see the nucleus. If you know your high power field (HPF) is about 0.25 mm2, diagnose it if you see over 15 intra-epithelial eosinophils per HPF.[10] [note 3] If your HPF is significantly different, or if you are not sure, diagnose it at over 60 eosinophils/mm2. Further information: Evaluation

(Also look for other "minor criteria" associated with eosinophilic esophagitis: extreme basal zone hyperplasia with papillary hyperplasia, eosinophils concentrated in the surface epithelium as opposed to the base, eosinophilic microabscesses, eosinophil degranulation, surface desquamation, lamina propria fibrosis.[11])

Further workup

For cases of eosinophilic esophagitis, also look for any fungal organisms.

Report

  • If positive:
  • Presence of eosinophilic esophagitis, or findings consistent thereof
  • Number of eosinophils per HPF
  • (Presence or absence of fungal organisms)

Example in a positive case:

Squamous mucosa with increased intraepithelial eosinophils (up to 80 per high-power field)(, consistent with eosinophilic esophagitis.
Negative for fungal organisms (H&E stained slide). See comment.)

(Comment: Increased numbers of intraepithelial eosinophils in the squamous mucosa can be found in both reflux esophagitis and eosinophilic esophagitis. Although clinical correlation is recommended, some secondary histologic features favor eosinophilic esophagitis.)

In borderline cases, such as an incidental finding of eosinophils at around 15/HPF:

(Esophagus, biopsy:)
Squamous mucosa with increased intraepithelial eosinophils of up to 15/HPF. See comment.
...

Comment: There is no evidence of eosinophilic microabscesses. Although this may represent reflux esophagitis, a diagnosis of eosinophilic esophagitis is considered in the correct clinical setting.


Gastroesophageal junction

Comprehensiveness

On this resource, the following formatting is used for comprehensiveness:

  • Minimal depth
  • (Moderate depth)
  • ((Comprehensive))

Microscopic examination

The main findings to look for are:

Barrett's esophagus

The main diagnostic sign of Barrett's esophagus is the presence of goblet cells. A true goblet cell should have rounded shape, clear to bluish cytoplasmic mucin, and be randomly scattered.[12] The mucin usually indents the nucleus.[12]

Further information: Barrett's esophagus

Esophagitis

GE junction with chronic esophagitis, including plasma cells (black arrow), an acute inflammation with neutrophils (white arrow), as well as basal layer hyperplasia (yellow double-headed arrow).

Look for signs of (reflux) esophagitis, mainly:[9]

  • Inflammatory cells, especially when intra-epithelial. Neutrophils confer a diagnosis of acute inflammation, while plasma cells, eosinophils and excess T cells confer a diagnosis of chronic inflammation. In eosinophil-predominant inflammation, also evaluate as suspected eosinophilic esophagitis.
  • Basal cell hyperplasia exceeding 15 - 20% of the epithelial thickness.
  • Stromal papillae reaching upper third of the epithelium.
  • Loss of orientation of superficial epithelial cells.
  • Ballooned squamous cells

Report

(Document the type of mucosa:

  • If both gastric and squamous mucosa is present in the same fragment, report as "Gastroesophageal junctional mucosa with..."
  • If not, report the presence of squamous and/or gastric mucosa.)

Examples:

(GE junction, biopsy:)
Squamous mucosa without significant histopathologic changes.
(Negative for gastric mucosa or intestinalized (Barrett's) mucosa.)
(GE junction, biopsy:)
Gastroesophageal junctional mucosa with chronic inflammation and reactive changes(, non-specific.
Negative for intestinalized (Barrett's) mucosa.)

In case of multiple signs of reflux esophagitis:

(GE junction, biopsy:)
Gastroesophageal junctional mucosa with changes consistent with reflux esophagitis.
(Negative for intestinalized (Barrett's) mucosa.)


Barrett's esophagus

Microscopic examination

Generally, the main finding to look for in biopsies from the esophagus is intestinalized mucosa (Barret's esophagus), which is defined as the presence of columnar epithelium with goblet cells.[13] A true goblet cell should have rounded shape, clear to bluish cytoplasmic mucin, and be randomly scattered.[14] The mucin usually indents the nucleus.[14]

Further workup of intestinalized mucosa

If intestinalized mucosa (Barret's esophagus) is present, look for dysplasia:

Also perform a screening for esophagitis. Further information: Gastroesophageal junction

Microscopy report

Incomplete Barret's esophagus does not need specific mention:

Histopathology of Barrett's esophagus, annotated.jpg
(GE junction, biopsy:)
Gastroesophageal mucosa with chronic inflammation and intestinal metaplasia, consistent with Barrett's esophagus.
Negative for dysplasia.


Esophageal adenocarcinoma

Mainly present in endoscopic biopsy of the gastroesophageal junction or distal esophagus.

Microscopic evaluation

In biopsies, classify as either low, moderately or high differentiated.

Well differentiated: >95% gland composition Moderately differentiated 50%-95% gland composition, Poor differentiation is <50% gland composition.[15]

Reporting

Esophagus, biopsy:
Invasive adenocarcinoma, moderately differentiated.


Stomach

Microscopic evaluation

Generally screen for:

Microscopy report

Example in case of normal findings:

(Gastric, biopsy:) Gastric (oxyntic/antral) mucosa without significant histopathologic changes.
(Negative for Helicobacter ((pylori{{Comprehensive-end} organisms on H&E slide.)


Gastric polyp

Microscopic evaluation

Relative incidences of gastric polyps. The remaining 4.8% are mainly constituted by lipomas, GIST, xanthomas and inflammatory pseudopolyps.[19]


Fundic gland polyp

Microscopic evaluation

Differential diagnosis

Workup

Dysplasia in fundic gland polyp is mainly seen as nuclear enlargement, hyperchromasia, pseudostratification, and loss of cytoplasmic mucin.[23] However, you don't need to spend much effort in the decision, since these patients have an excellent prognosis whether there is dysplasia or not.

Reporting

Generally, keep it short:

(Stomach, excision:)
Fundic gland polyp

Gastritis

Author: Mikael Häggström [note 5]

Inflammation of the stomach. If biopsy is at the esophagus, evaluate as gastroesophageal junction.

Comprehensiveness

On this resource, the following formatting is used for comprehensiveness:

  • Minimal depth
  • (Moderate depth)
  • ((Comprehensive))

Microscopy evaluation

Mucosal plasma cell infiltrate in mild chronic gastritis.

Look for chronic or acute gastritis. If either is present, still look for the other.

Chronic gastritis

  • Chronic gastritis[24]
  • Presence of plasma cells, lymphocytes, and occasionally lymphoid follicles. Scattered single plasma cells and lymphocytes is normal, and the threshold is subjective, but one definition of chronic gastritis is when seeing chronic inflammation at 4x magnification (as increased dots separating glands)[25] Eosinophils and neutrophils may be present.
  • Reduced mucin in the cytoplasm
  • Enlargement of nuclei and nucleoi
  • Subnuclear vacuolation in antral glands or pits (which is PAS negative)
  • Intestinal metaplasia: with partial replacement of the mucosa of the antrum and body with metaplastic goblet cells of intestinal morphology, absorptive cells and Paneth cells.

When there is at least (mild or) moderate gastritis, especially if relatively superficial, also evaluate as a stomach biopsy for Helicobacter pylori.

Acute gastritis

Histopathology of mild active gastritis, with intraepithelial neutrophils (white arrows) as well as in lamina propria (black arrows).
  • Mild acute gastritis:[16]
  • Modest edema of lamina propria
  • Vascular congestion
  • Scattered neutrophils
  • Mucosal hemorrhage
  • Intact epithelium
  • Moderate to severe acute gastritis:[16]
  • Loss of superficial epithelium above the muscularis mucosa
  • Hemorrhage
  • Variable infiltrate with neutrophils
  • Fibrinopurulent luminal exudate
  • Nearby epithelium may show regenerative changes

Microscopy report

  • Mild and/or chronic gastritis and severity
  • (If present, state if positive or negative for Helicobacter pylori organisms.)

Chronic gastritis without neutrophils is preferably also termed "non-active".

Example:

(Stomach, biopsy:)
  • (Gastric antral/oxyntic mucosa with) mild chronic (non-active) gastritis((, non-specific))
  • (Negative for Helicobacter pylori organisms on H&E slide.)

Notes

  1. If a tumor is found, then the adventitial surface is likely the closest surgical margin, and should therefore be spared during initial opening in order to allow for optimal sections later.
  2. En face means that the section is tangential to the region of interest (such as a lesion) of a specimen. Further information: Gross_processing#Cutting
  3. It has also been described as ≥15 intraepithelial eosinophils in ≥2 hpfs or ≥25 in any single hpf.
    - Parfitt, Jeremy R; Gregor, James C; Suskin, Neville G; Jawa, Hani A; Driman, David K (2005). "Eosinophilic esophagitis in adults: distinguishing features from gastroesophageal reflux disease: a study of 41 patients ". Modern Pathology 19 (1): 90–96. doi:10.1038/modpathol.3800498. ISSN 0893-3952. 
  4. H. pylori is very unlikely without gastritis or reactive changes.
  5. For a full list of contributors, see article history. Creators of images are attributed at the image description pages, seen by clicking on the images. See Patholines:Authorship for details.
  6. The combination of atrophy and gastritis (especially when deeper than submucosal) helps the clinician to potentially make a diagnosis of atrophic gastritis.

Main page

References

  1. Unless otherwise specified in rows, reference is:
    - Carr, Norman J. (2000). "The pathology of acute appendicitis ". Annals of Diagnostic Pathology 4 (1): 46–58. doi:10.1016/S1092-9134(00)90011-X. ISSN 10929134. 
  2. Sierakowski, Kyra; Pattichis, Andrew; Russell, Patrick; Wattchow, David (2016). "Unusual presentation of a familiar pathology: chronic appendicitis ". BMJ Case Reports: bcr2015212485. doi:10.1136/bcr-2015-212485. ISSN 1757-790X. 
  3. Talwar, OP; K.C., Geetika (2014). "Histomorphological changes in gall bladder diseases and its association with helicobacter infection ". Journal of Pathology of Nepal 4 (8): 617–622. doi:10.3126/jpn.v4i8.11607. ISSN 2091-0908. 
    - "Figures - available via license: CC BY 4.0"
  4. Mills, Stacey E; Carter, Darryl; Greenson, Joel K; Reuter, Victor E; Stoler, Mark H (2009). Sternberg's Diagnostic Surgical Pathology (5th ed.). Lippincott Williams & Wilkins. ISBN 978-0781779425. 
  5. 5.0 5.1 5.2 5.3 Hanni Gulwani. Gallbladder & extrahepatic bile ducts - Cholecystitis. Pathology Outlines. Topic Completed: 1 September 2012. Minor changes: 5 September 2019
  6. . Diseases of the Gallbladder. Abdominal Key (2019-09-29).
  7. 7.0 7.1 Hanni Gulwani. Gallbladder - Cholecystitis - Chronic cholecystitis. Topic Completed: 1 September 2012. Revised: 9 January 2020
  8. Pickering, Oliver; Pucher, Philip H.; Toale, Conor; Hand, Fiona; Anand, Easan; Cassidy, Sheena; McEntee, Gerry; Toh, Simon K.C. (2020). "Prevalence and Sonographic Detection of Gallbladder Polyps in a Western European Population ". Journal of Surgical Research 250: 226–231. doi:10.1016/j.jss.2020.01.003. ISSN 00224804. 
  9. 9.0 9.1 Elliot Weisenberg. Esophagus - Esophagitis - Reflux esophagitis / gastroesophageal reflux disease. Pathology Outlines. Topic Completed: 1 October 2012. Minor changes: 8 July 2020
  10. Dellon, Evan S. (2012). "Eosinophilic esophagitis ". Current Opinion in Gastroenterology 28 (4): 382–388. doi:10.1097/MOG.0b013e328352b5ef. ISSN 0267-1379. 
  11. Ryan C. Braunberger, M.D., Joshua A. Hanson, M.D.. Eosinophilic esophagitis. Pathology Outlines. Last staff update: 20 December 2022
  12. 12.0 12.1 Dipti M. Karamchandani. Esophagus - Premalignant - Barrett esophagus. Topic Completed: 19 March 2020, Minor changes: 29 June 2020
  13. . Barrett Esophagus. Stanford University School of Medicine. Retrieved on 2020-09-01.
  14. 14.0 14.1 Dipti M. Karamchandani. Esophagus - Premalignant - Barrett esophagus. Topic Completed: 19 March 2020, Minor changes: 29 June 2020
  15. https://www.sciencedirect.com/science/article/abs/pii/S2590030723000454
  16. 16.0 16.1 16.2 Elliot Weisenberg. Stomach - Gastritis - Acute gastritis. pathologyOutlines. Topic Completed: 1 August 2012. Minor changes: 31 August 2020
  17. Elliot Weisenberg. Stomach - Gastritis - Chronic gastritis. PathologyOutlines. Topic Completed: 1 August 2012. Minor changes: 31 August 2020
  18. Genta, RM. (Nov 2005). "Differential diagnosis of reactive gastropathy. ". Semin Diagn Pathol 22 (4): 273-83. PMID 16939055. 
  19. García-Alonso, Francisco Javier; Martín-Mateos, Rosa María; González-Martín, Juan Ángel; Foruny, José Ramón; Vázquez-Sequeiros, Enrique; Boixeda de Miquel, Daniel (2011). "Gastric polyps: analysis of endoscopic and histological features in our center ". Revista Española de Enfermedades Digestivas 103 (8): 416–420. doi:10.4321/S1130-01082011000800005. ISSN 1130-0108. 
  20. Groisman, Gabriel M.; Depsames, Roman; Ovadia, Baruch; Meir, Alona (2014). "Metastatic Carcinoma Occurring in a Gastric Hyperplastic Polyp Mimicking Primary Gastric Cancer: The First Reported Case ". Case Reports in Pathology 2014: 1–5. doi:10.1155/2014/781318. ISSN 2090-6781. 
    - Attribution 3.0 Unported (CC BY 3.0) license
  21. 21.0 21.1 Naziheh Assarzadegan, M.D., Raul S. Gonzalez, M.D.. Stomach Polyps - Fundic gland polyp. PathologyOutlines. Topic Completed: 1 November 2017. Minor changes: 11 December 2019
  22. Groisman, Gabriel M.; Depsames, Roman; Ovadia, Baruch; Meir, Alona (2014). "Metastatic Carcinoma Occurring in a Gastric Hyperplastic Polyp Mimicking Primary Gastric Cancer: The First Reported Case ". Case Reports in Pathology 2014: 1–5. doi:10.1155/2014/781318. ISSN 2090-6781. 
    - Attribution 3.0 Unported (CC BY 3.0) license
  23. Levy MD, Bhattacharya B (2015). "Sporadic Fundic Gland Polyps With Low-Grade Dysplasia: A Large Case Series Evaluating Pathologic and Immunohistochemical Findings and Clinical Behavior. ". Am J Clin Pathol 144 (4): 592-600. doi:10.1309/AJCPGK8QTYPUQJYL. PMID 26386080. Archived from the original. . 
  24. Elliot Weisenberg. Stomach - Gastritis - Chronic gastritis. PathologyOutlines. Topic Completed: 1 August 2012. Minor changes: 31 August 2020
  25. Lysandra Voltaggio, Johns Hopkins Department of Pathology (2018-10-31). Gastritis: A Pattern Based Approach. Arizona Society of Pathologists.
  26. 26.0 26.1 26.2 26.3 Carrasco G, Corvalan AH (2013). "Helicobacter pylori-Induced Chronic Gastritis and Assessing Risks for Gastric Cancer. ". Gastroenterol Res Pract 2013: 393015. doi:10.1155/2013/393015. PMID 23983680. PMC: 3745848. Archived from the original. . 
    Figures - available via license: Creative Commons Attribution 3.0 Unported

Image sources

Stomach biopsy for Helicobacter pylori

Helicobacter pylori on HE stain, being curved bacteria in the lumen of a gastric foveola.

Microscopic evaluation

Another H&E stain.

Look for:

  • Inflammation, typically a chronic form of gastritis with germinal centers (follicular gastritis), and plasma cells in lamina propria.[1][note 1] There should be at least 3 plasma cells facing each other to make a diagnosis of chronic gastritis.
  • When there is at least (mild or) moderate gastritis, especially if relatively superficial, go to high magnification and look for Helicobacter pylori-like bacteria in the lumen. They are curved, spirochete-like bacteria, generally in the superficial mucus layer and along microvilli of epithelial cells.[1]

Perform immunohistochemistry for H. pylori in cases of moderate to severe chronic gastritis, or even just one neutrophil within the epithelium, where H. pylori is not seen on H&E stains.[2]

Example report

Stomach, biopsy:

Chronic active gastritis.
Positive for helicobacter pylori.

Chronic gastritis without H. pylori-like organisms can be described as non-specific:

Mild chronic gastritis, which is non-specific.

Negative for H. pylori-like organisms on H&E stain.

Stomach tumor

Microscopic evaluation

Stomach cancer types by relative incidence.[3]

In addition to a general screening (Further information: Stomach ), look for atypical or expanded areas, and attempt top classify by at least the most common forms.

Reporting

For cancers, generally include a synoptic report, such as per College of American Pathologists (CAP) protocols at cap.org/protocols-and-guidelines.


Gastric sleeve

Gross processing

  • Measure length and maximum diameter, as well as the length of the staple line.
  • Inspect the serosal surface.
  • Open longitudinally
  • Inspect the mucosa.
  • Measure the maximum wall thickness.

Tissue selection

2 representative sections, in addition to any visible lesions.

Gross report

Example:

((A. Labeled - ___. The specimen is received in formalin and consists of)) a segment of pink-tan stomach measuring __ cm in length and __ cm in maximum diameter. A staple line (surgical margin) is present which measures __ cm in length. The serosal surface is pink-tan and {{focally ragged with scattered transmural defects}}. A minimal amount of soft, yellow perigastric fat is present. Upon opening, the gastric lumen contains a small amount of bloody mucoid material. The mucosa is red-tan with normal rugae and no gross lesions. The wall measures up to ___ cm in thickness. (Representative sections are submitted for microscopic examination in __ cassettes.)

Microscopic examination

Usual stomach screening. Further information: Stomach

Example reports:

Stomach, partial gastrectomy:
Portion of stomach without significant histopathologic findings.
(Negative for helicobacter pylori organisms (H&E stain).)
Gastric body, laparoscopic sleeve gastrectomy:
Mild chronic gastritis, non specific.
(Negative for H. Pylori microorganisms on H&E stained slide.)

Duodenum

Small intestine in celiac disease

Microscopic evaluation

Intraepithelial lymphocytes, in this case still less than <25 IELs/100 enterocytes.
Villous atrophy is another sign of celiac disease. Normal villous:crypt ratio is 3:1. However, this assessment requires proper orientation of biopsies.[4]

The main histologic feature of celiac disease is increased intraepithelial lymphocytes (IELs), with or without villous atrophy of the duodenal mucosa.[5] The number of intraepithelial lymphocytes are classified as follows in the duodenum:[6][7]

  • < 25 IELs/100 enterocytes: Negative for intraepithelial lymphocytosis.
  • 25 to 29 IELs/100 enterocytes: borderline
  • > 30 IEL/100 enterocytes: Pathological "lymphocytosis"

Alternative proposed methods is the presence of over 6-12 IELs per 20 enterocytes at the tips of duodenal villi.[7] In the jejunum, the cutoff is at over 40 IELs per 100 enterocytes.[7]

Suggestive but not specific findings for enterocytes are: decreased height, intracytoplasmic vacuolation and reduction or absence of the brush border.[6]

Differential diagnoses

If findings are suggestive of celiac disease, look for at least the following differential diagnoses:

Microscopy report

Example in an unremarkable specimen:

Small intestine, biopsy:
Duodenal mucosa, negative for significant histopathologic changes.
Negative for celiac disease.

Example in suspected celiac disease:

Histopathology of duodenal intra-epithelial lymphocytes.jpg
Small intestine, biopsy:
Marked villous atrophy with increased intraepithelial lymphocytes, consistent with celiac sprue.
Correlation with serologic testing is recommended.


Colorectal polyp

Gross examination

Further information: Colon

Tissue selection and trimming

There is a separate article for the Grossing of minimally invasive colorectal surgery.

Depending on sample format:[9]

  • Biopsies and polyps of <4 mm are embedded in their entirety. Samples less than 0.3 mm should be stained with eosin to avoid getting lost processing.
  • Polyps 4-8 mm with short stem or without stem: Identify the excision surface and divide the polyp longitudinally through the excision surface.
  • Polyps > 8 mm with a stem long enough to make it possible to take a transverse, whole slice from the stem closest to the excision surface: First, take a transverse slice through the peripheral portion of the stem, encompassing the entire circumference. Then take a 3-4 mm thick slice longitudinally through the polyp and the middle of the stem, after which the two remaining parts on either side are cut into equally thick slices, parallel to the previous slice.
  • Polyps >8 mm with short stem or without stem: Identify the excision surface and cut out a 3-4 mm thick disk that extends longitudinally through the center of the excision surface. Then divide the two remaining portions into equally thick slices, parallel to the previous slice.
  • Polyps that come in parts: Pick out the largest pieces, which are cut as similar as possible to above. Small fragments are sieved and embedded in a separate box.

Gross reporting

  • Polyp and/or fragment sizes
  • Presence or absence of stem of polyps

Example, for a gastrointestinal biopsy:

Labeled: "Sigmoid colon biopsy". The specimen is received in formalin and consists of 4 fragments of pink-tan tissue with a vaguely recognizable mucosal surface, mixed with food-like material. The fragments measure 0.2-0.3 cm in greatest dimension. The entire specimen is submitted for microscopic examination in one cassette.

Microscopic evaluation

Major signs

Look particularly for these, to help sorting into proper diagnosis in next section:

Main types

Consider at least the following conditions:

Incidences and malignancy risks of various types of colorectal polyps.[10]
Colorectal polyps
Type Risk of containing malignant cells Histopathology Image
Hyperplastic polyp 0% No dysplasia.[11]
  • Mucin-rich type: Serrated (“saw tooth”, pictured) appearance, containing glands with star-shaped lumina.[12] Crypts that are elongated but straight, narrow and hyperchromatic at the base. All crypts reach to the muscularis mucosae.[12]
  • Goblet cell-rich type: Elongated, fat crypts and little to no serration. Filled with goblet cells, extending to surface, which commonly has a tufted appearance.[12]
Hyperplastic Polyp of the Rectum (14060044206).jpg
Tubular adenoma 2% at 1.5cm[13] Low to high grade dysplasia[14] Over 75% of volume has tubular appearance.[15] Tubular adenoma of the colon.jpg
Tubulovillous adenoma 20% to 25%[16] 25%-75% villous[15] Histopathology of tubulovillous adenoma.jpg
Villous adenoma 15%[17] to 40%[16] Over 75% villous[15] Villous adenoma of the colorectum (high power view).jpg
Sessile serrated adenoma (SSA)[18]
  • Basal dilation of the crypts
  • Basal crypt serration
  • Crypts that run horizontal to the basement membrane (horizontal crypts)
  • Crypt branching.
Sessile Serrated Adenoma, Transverse Colon, 0.4 cm (3632298679).jpg
Traditional serrated adenoma
  • Protuberant villi with slit-like serrations.[19]
  • Pseudostratified epithelial columnar cells shapes.[19]
  • Eosinophilic cytoplasm and dark, pencil-like nuclei.[19]
  • Golblet cells are present.[19]
Traditional Serrated Adenoma of Colon (5203904731).jpg
Colorectal adenocarcinoma 100%
  • In carcinoma in situ (Tis): cancer cells invading into the lamina propria, and may involve but not penetrate the muscularis mucosae. Can be classified as "high-grade dysplasia", because prognosis and management are essentially the same.[11]
  • Invasive adenocarcinoma: Extending through the muscularis mucosae into the submucosa and beyond.[11]
Adenocarcinoma highly differentiated (rectum) H&E magn 400x.jpg

If you only see normal mucosa but the order/endoscopy says polyp, take additional levels from the paraffin block.

Other benign

Colonic lipoma, a benign polyp, here being submucosal and pedunculated.

If a more specific diagnosis cannot readily be made, clearly non-malignant colorectal polyps may simply be reported as such.

Further information: Evaluation of tumors

Microscopy report

It should include:[20]

  • Size of polyp (from gross examination)
  • Histopathologic type
  • Depth of growth and/or infiltration
  • Whether the resection is radical

Optionally, it can include degree of differentiation and/or dysplasia.

Example:

Micrograph of tubulovillous adenoma.jpg
50 mm large tubulovillous adenoma with up to high grade columnar epithelial dysplasia. No infiltration. Radical excision.

If multiple polyps are submitted in one container, you may count the amount of each polyp type if you can, but if the amount of fragments in microscopy exceeds the amount of fragments purportedly submitted, then you can simply write "fragments of", like the following example:

Fragments of tubular adenoma and hyperplastic polyp.

More details are given in main articles of histopathologic types.

  See also: General notes on reporting


Notes

  1. Plasma cells and lymphocytes are normally found in the lamina propria of the small and large intestine, but is abnormal in the stomach.

Main page

References

  1. 1.0 1.1 Elliot Weisenberg. Stomach - Infections - Helicobacter pylori. Pathology Outlines. Topic Completed: 1 August 2012. Minor changes: 1 September 2020
  2. Hartman DJ, Owens SR (2012). "Are routine ancillary stains required to diagnose Helicobacter infection in gastric biopsy specimens? An institutional quality assurance review. ". Am J Clin Pathol 137 (2): 255-60. doi:10.1309/AJCPD8FFBJ5LSLTE. PMID 22261451. Archived from the original. . 
  3. Parsonnet, Julie; Friedman, Gary D.; Vandersteen, Daniel P.; Chang, Yuan; Vogelman, Joseph H.; Orentreich, Norman; Sibley, Richard K. (1991). "Helicobacter pyloriInfection and the Risk of Gastric Carcinoma ". New England Journal of Medicine 325 (16): 1127–1131. doi:10.1056/NEJM199110173251603. ISSN 0028-4793. 
  4. Juwairiya Arshi, M.B.B.S., Aaron R. Huber, D.O.. Small intestine & ampulla - Malabsorption - Celiac sprue. Last author update: 4 May 2022. Last staff update: 16 September 2022
  5. Brown, Ian S.; Smith, Jason; Rosty, Christophe (2012). "Gastrointestinal Pathology in Celiac Disease ". American Journal of Clinical Pathology 138 (1): 42–49. doi:10.1309/AJCPE89ZPVJTSPWL. ISSN 0002-9173. 
  6. 6.0 6.1 Erdener Özer. Small intestine & ampulla, Malabsorption, Celiac sprue. Pathology Outlines. Topic Completed: 1 June 2017. Minor changes: 4 April 2020.
  7. 7.0 7.1 7.2 . Celiac Disease. Stanford School of Medicine. Retrieved on 2021-03-11.
  8. Hanni Gulwani. Small intestine & ampulla - Infectious disorders - Giardia lamblia. Pathology Outlines. Topic Completed: 1 August 2012. Minor changes: 3 March 2020
  9. Monica Dahlgren, Janne Malina, Anna Måsbäck, Otto Ljungberg (1997-02-13). Lilla utskärningen.
  10. References for pie chart are located at separate image description page.
  11. 11.0 11.1 11.2 Finlay A Macrae. Overview of colon polyps. UpToDate. This topic last updated: Dec 10, 2018.
  12. 12.0 12.1 12.2 Robert V Rouse (2010-01-31). Hyperplastic Polyp of the Colon and Rectum. Stanford University School of Medicine. Last updated 6/2/2015
  13. Minhhuyen Nguyen. Polyps of the Colon and Rectum. MSD Manual. Last full review/revision June 2019
  14. Robert V Rouse. Adenoma of the Colon and Rectum. Original posting/last update : 1/31/10, 1/19/14
  15. 15.0 15.1 15.2 Bosman, F. T. (2010). WHO classification of tumours of the digestive system . Lyon: International Agency for Research on Cancer. ISBN 92-832-2432-9. OCLC 688585784. 
  16. 16.0 16.1 Amersi, Farin; Agustin, Michelle; Ko, Clifford Y (2005). "Colorectal Cancer: Epidemiology, Risk Factors, and Health Services ". Clinics in Colon and Rectal Surgery 18 (03): 133–140. doi:10.1055/s-2005-916274. ISSN 1531-0043. 
  17. Alnoor Ramji. Villous Adenoma Follow-up. Medscape. Updated: Oct 24, 2016
  18. Rosty, C; Hewett, D. G.; Brown, I. S.; Leggett, B. A.; Whitehall, V. L. (2013). "Serrated polyps of the large intestine: Current understanding of diagnosis, pathogenesis, and clinical management ". Journal of Gastroenterology 48 (3): 287–302. doi:10.1007/s00535-012-0720-y. PMID 23208018. 
  19. 19.0 19.1 19.2 19.3 Enoch Kuo, M.D., Raul S. Gonzalez, M.D.. Colon - Polyps - Traditional serrated adenoma. Topic Completed: 1 February 2018. Minor changes: 1 October 2020
  20. Monica Dahlgren, Janne Malina, Anna Måsbäck, Otto Ljungberg. Stora utskärningen. KVAST (Swedish Society of Pathology). Retrieved on 2019-09-26.

Image sources


Hyperplastic polyp

Mucin-rich type.

Commonly presents as a colorectal polyp.

Gross evaluation

Further information: Colon

Tissue selection and trimming

There is a separate article for the Grossing of minimally invasive colorectal surgery.

Depending on sample format:[1]

  • Biopsies and polyps of <4 mm are embedded in their entirety. Samples less than 0.3 mm should be stained with eosin to avoid getting lost processing.
  • Polyps 4-8 mm with short stem or without stem: Identify the excision surface and divide the polyp longitudinally through the excision surface.
  • Polyps > 8 mm with a stem long enough to make it possible to take a transverse, whole slice from the stem closest to the excision surface: First, take a transverse slice through the peripheral portion of the stem, encompassing the entire circumference. Then take a 3-4 mm thick slice longitudinally through the polyp and the middle of the stem, after which the two remaining parts on either side are cut into equally thick slices, parallel to the previous slice.
  • Polyps >8 mm with short stem or without stem: Identify the excision surface and cut out a 3-4 mm thick disk that extends longitudinally through the center of the excision surface. Then divide the two remaining portions into equally thick slices, parallel to the previous slice.
  • Polyps that come in parts: Pick out the largest pieces, which are cut as similar as possible to above. Small fragments are sieved and embedded in a separate box.

Gross reporting

  • Polyp and/or fragment sizes
  • Presence or absence of stem of polyps

Example, for a gastrointestinal biopsy:

Labeled: "Sigmoid colon biopsy". The specimen is received in formalin and consists of 4 fragments of pink-tan tissue with a vaguely recognizable mucosal surface, mixed with food-like material. The fragments measure 0.2-0.3 cm in greatest dimension. The entire specimen is submitted for microscopic examination in one cassette.

Microscopic evaluation

There are two main types of hyperplastic polyps, which have genetic differences, as well as different histologic structure, but no significant differences clinically:[2]

  • A microvesicular mucin-rich type
  • A goblet cell-rich type

Mucin-rich type

(Mucin-rich) hyperplastic polyp.
(Mucin-rich) hyperplastic polyp, with a tangential section, showing serrations peripherally (superficially) and narrow lumina centrally (crypts).

Characteristics:[2]

  • Serrations (“saw tooth appearance”) of the luminal portion.
  • Star-shaped lumina.
  • Crypt elongation but they are straight, narrow and hyperchromatic at the base. All crypts reach to the muscularis mucosae.[2]

The basement membrane is frequently thickened.[2] This is the usual form of hyperplastic polyps, and they do not need to be reported as "mucin-rich".

Histologic structure in goblet cell-rich type

Elongated, fat crypts and little to no serration. Therefore, they may not be obvious without comparing to adjacent normal intestinal wall.[2]

They are filled with goblet cells, extending to surface, which commonly has a tufted appearance.[2]

Epithelial misplacement

Infrequently, the epithelium is misplacement into the submucosa. Such polyps have been termed "inverted hyperplastic polyps". They appear to be restricted to the sigmoid colon and rectum. The misplaced epithelium is mucin-depleted , similar to the basal 1/3 of the polyp. The misplacement is accompanied by the lamina propria, and is continuous with overlying polyp through a gap in the muscularis mucosae. It may require slices at multiple levels to demonstrate microscopically.[2]

In such cases adjacent hemorrhage and hemosiderin deposition is common. Collagen type IV stain will have a strong continuous staining around nests.[2]

Cellular structure

Nuclei are small, regular, round and basal in the luminal half of the crypts, most reliably evaluated near the luminal surface.[2]

There are proliferative changes at the base of crypts, where nuclei are enlarged, the nucleus/cytoplasm ratio is elevated.[2]

Differential diagnoses

The main differential diagnosis for a hyperplastic polyp is adenoma, which generally display:[2]

  • Nuclear stratification
  • Loss of polarity
  • Dysplasia

However, the deep proliferative zones and reactive processes closely mimic changes seen in colorectal adenomas.[2]

Sessile serrated adenoma with minimal deviation dysplasia, wherein architectural changes are subtle, with mild crowding of crypts separated by less lamina propria and showing some degree of disorganization.[3]
Sessile serrated adenoma
  • Size ≥0.5 cm
  • Location in right colon

If both latter findings are present, it is almost always a SSA. Other features causing a suspicion for sessile serrated adenoma are:[2]

  • Dilation of crypts
  • Branching of crypts
  • Horizontal glands at the base
  • Mature mucinous cells at the base of crypts
  • Location in the proximal colon (cecum, ascending, and transverse colon),[4] whereas hyperplastic polyps are most common in the sigmoid colon and rectum. However, both may occur throughout the colon.[5]
Tubular colorectal adenoma
Hyperplastic polyp[6] Tubular adenoma[6]
Nu dysplasia Dysplasia
Proliferative epithelium restricted to base Proliferative epithelium present at the surface
Gland lining cells mature at the surface No surface maturation
Further information: Evaluation of tumors and Tubular colorectal adenoma

Microscopic report

Usually as follows:

(<Sigmoid / Ascending / etc.> colon polyp, polypectomy:) Hyperplastic polyp.

Generally don't report hyperplastic polyp elements of polyps with potential malignant progression (such as tubular and ⁄or villous adenomas), because the patient's clinical management will be based on the more concerning elements.


Tubular and ⁄or villous adenoma

Microscopic evaluation

Criteria

Tubular adenoma with low-grade dysplasia.

Dysplastic changes should involve at least the upper half of the crypts and the luminal surface.[7]

  • Nuclear dysplasia is mandatory to diagnose adenoma. It involves:
  • Nuclear atypia: Enlarged hyperchromatic nuclei (that is, dark purple) that are oval or frequently elongated, and with high nucleus to cytoplasm ratio.[7][8]
  • Other cellular atypia: Often nuclear stratification, nuclear crowding (that is, nuclei are bunched-up) and loss of polarity[7]
  • Always changes in gland architecture, such as:[7]
  • Enlarged crypts
  • Gland budding, or otherwise irregular glands[7]
  • Mucin depletion is often seen, but is not required[7]
  • Goblet cell reduction.

Differential diagnoses

Hyperplastic polyp
Hyperplastic polyp[6] Tubular adenoma[6]
Nu dysplasia Dysplasia
Proliferative epithelium restricted to base Proliferative epithelium present at the surface
Gland lining cells mature at the surface No surface maturation
Colorectal carcinoma
Colorectal adenocarcinoma (in this case, not otherwise specified).

edit
Colorectal carcinoma (mainly adenocarcinoma) is distinguished from an adenoma (mainly tubular and ⁄or villous adenomas) mainly by invasion through the muscularis mucosae.[9]

Also, carcinoma also commonly displays:[10]

  • Varying degrees of gland formation with tall columnar cells
  • Frequenty desmoplasia
  • Dirty necrosis, consisting of extensive central necrosis with granular eosinophilic karyorrhectic debris. Garland of cribriform glands are frequently found in their vicinity.

Low or high grade

In low-grade lesions, the crypts should maintain a resemblance to normal colon.[11]

High-grade dysplasia, in this case seen mainly as loss of cell polarity, as cells become more plump and haphazard than the elongated and parallel nuclei of surrounding low-grade dysplasia.
Typical findings in low-grade versus high-grade tubular and ⁄or villous adenoma
Low-grade[11] High grade[11]
Crowding Pseudo-stratification to early stratification More substantial stratification
Nuclear pleomorphism and atypical mitoses Absent or minimally present Present
Loss of cell polarity Minimal More significant
Crowding, cribriform, or complex architecture No significant Present

High grade lesions also typically have:

  • Cribriform architecture, consisting of juxtaposed gland lumens without stroma in between, with loss of cell polarity. Rarely, they have foci of squamous differentiation (morules). This should be distinguished from cases where piles of well-differentiated mucin-producing cells appear cribriform. In such piles, nuclei show regular polarity with apical mucin, and their nuclei are not markedly enlarged.
  • Increased nucleus to cytoplasm ratio.[11]
  • More "open" appearing nuclei with increasingly prominent nucleoli[11]
  • Back-to-back glands[11]

Tubular or villous

Colorectal adenoma
Type Histopathology Image
Tubular adenoma Over 75% of volume has tubular appearance.[12] Tubular adenoma of the colon.jpg
Tubulovillous adenoma 25%-75% villous[12] Histopathology of tubulovillous adenoma.jpg
Villous adenoma Over 75% villous[12] Villous adenoma of the colorectum (high power view).jpg

Length of villi must be at least twice the depth of the normal mucosal thickness.[7]

Further information: Evaluation of tumors

Further workup

Look for and evaluate any lymph nodes in the tissue specimen, for possible malignancy.

Dissecting pools of mucin at the base of any adenoma should be evaluated for the possibility of mucinous carcinoma.[7]

Report

  • Tubular, tubulovillous or villous adenoma.
  • Any high-grade component (whereas low-grade does not need to be stated in the report as it is presumed otherwise).
  • ((Adenoma size))
  • ((Whether it is radically resected.))

If any lymph nodes are found in the tissue sample, report the presence or absence of malignancy in any of them.

Example:

Sigmoid colon polyp x2, polypectomies:
One tubular adenoma and one tubulovillous adenoma.

Sessile serrated adenoma

Microscopic examination

The characteristics of sessile serrated adenoma are:[13]

  • Sawtooth serrations of the epithelium
  • Abundant mucin, similar to hyperplastic polyps
  • Basal crypt dilation, with mucous retention, and lateral spread of the crypt bases, commonly described as boot shaped or anchor shaped crypts.

Variations

On low magnification, a sessile serrated adenoma may be flat (left) or protuberant (right):[3]


Microscopic report

A brief report is sufficient:

Cecum polyp, polypectomy:
Sessile serrated adenoma.

Differential diagnoses

Regarding location, the diagnosis of a sessile serrated adenoma is supported by a location within the proximal colon (cecum, ascending, and transverse colon), while hyperplastic polyps are most common in the sigmoid colon and rectum. However, both may occur throughout the colon.[16][17]


Traditional serrated adenoma

Microscopic evaluation

This case lacks the typical eosinophilic cytoplasm, but otherwise typical with protuberant villiform growth pattern with slit-like serrations and presence of goblet cells.
  • Protuberant villi with slit-like serrations.[18]
  • Pseudostratified epithelial columnar cells shapes.[18]
  • Eosinophilic cytoplasm and dark, pencil-like nuclei.[18]
  • Golblet cells are present.[18]

Differential diagnosis


Intestine with tumor and colorectal carcinoma are given later in this handbook. If you suspect a colorectal carcinoma at this time, and you are not familiar with the condition, refer the case to a senior.

Notes


Main page

References

  1. Monica Dahlgren, Janne Malina, Anna Måsbäck, Otto Ljungberg (1997-02-13). Lilla utskärningen.
  2. 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 2.12 2.13 Robert V Rouse (2010-01-31). Hyperplastic Polyp of the Colon and Rectum. Stanford University School of Medicine. Last updated 6/2/2015
  3. 3.0 3.1 Liu, Cheng; Walker, Neal I; Leggett, Barbara A; Whitehall, Vicki LJ; Bettington, Mark L; Rosty, Christophe (2017). "Sessile serrated adenomas with dysplasia: morphological patterns and correlations with MLH1 immunohistochemistry ". Modern Pathology 30 (12): 1728–1738. doi:10.1038/modpathol.2017.92. ISSN 0893-3952. 
    - "This work is licensed under a Creative Commons Attribution 4.0 International License."
  4. David Driman, MBChB FRCPC. Sessile serrated adenoma of the colon. MyPathologyReport. Updated July 23, 2021
  5. Author: Adrian C. Bateman, M.B.B.S., M.D.. Colon - Polyps - Hyperplastic polyp. Pathology Outlines. Minor changes: 23 September 2021
  6. 6.0 6.1 6.2 6.3 . Hyperplastic Polyp of the Colon and Rectum - Differential diagnoses. Stanford University School of Medicine. Retrieved on 2019-09-30.
  7. 7.0 7.1 7.2 7.3 7.4 7.5 7.6 7.7 Robert V Rouse. Adenoma of the Colon and Rectum. Stanford University School of Medicine. Original posting/last update : 1/31/10, 1/19/14
  8. Mehran Taherian; Saran Lotfollahzadeh; Parnaz Daneshpajouhnejad; Komal Arora. Tubular Adenoma. National Center for Biotechnology Information. Last Update: May 30, 2020.
  9. Robert V Rouse. Colorectal Adenoma Containing Invasive Adenocarcinoma. Stanford University School of Medicine.
  10. Robert V Rouse. Adenocarcinoma of the Colon and Rectum. Stanford University School of Medicine. Original posting/updates: 1/31/10, 7/15/11, 11/12/11
  11. 11.0 11.1 11.2 11.3 11.4 11.5 David J. Myers; Komal Arora. Villous Adenoma. StatPearls, National Center for Biotechnology Information. Last Update: June 18, 2019.
    -"This book is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/)"
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  16. Author: Adrian C. Bateman, M.B.B.S., M.D.. Colon - Polyps - Hyperplastic polyp. Pathology Outlines. Minor changes: 23 September 2021
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