Esophagus

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Esophagus connects the pharynx to the stomach. It is afflicted by tumours on occasion. For some reason or another, it seems everyone at SMH gets a esophageal biopsy... yet patients at SB don't have esophagi.

Normal

General:

  • Stratified squamous non-keratinized epithelium.

Normal (esophageal) squamous epithelium:

  • Should "mature" to the surface like good stratified squamous epithelium does.
    • No nuclei at luminal surface.
    • Cells should become less hyperchromatic as you go toward the lumen.
    • Mitoses should be rare and should NOT be above the basal layer.
  • Inflammatory cells should be very rare.

Diagnoses

Common

  • Normal.
  • Metaplasia (Barrett's esophagus).
  • Dysplasia.
  • Adenocarcinoma.

Less common

  • Squamous cell carcinoma.
  • Eosinophilic esophagitis.
  • Candidiasis.
  • CMV esophagitis.

Indications

  • Pyrosis = heartburn.[1]

Infection

Main article: Microorganisms

Is a relatively common problem, especially in those that live at the margins (EtOH abusers) and immunosuppressed individuals (HIV/AIDS).

Useful stains

  • PAS.
  • Gram stain.

Candidiasis

Microscopic:

  • Worm-like micro-organisms.

Image: Esophageal candidiasis (WC).

Barrett's esophagus

Definition

  • Metaplastic transformation of stratified squamous epithelium to simple columnar epithelium with goblet cells.

Microscopic

Features:

  • Columnar epithelium.
  • Goblets cells -- key feature.

Significance

  • Increased risk of adenocarcinoma of the esophagus.

Management

  • Long term follow-up/repeat esophagogastroduodenoscopy.

Dysplasia

Classification

  • Low grade.
  • High grade.

Microscopy

Features:

  • Nuclear changes.
    • Nuclear hyperchromatism.
    • Nuclear crowding.
    • Cigar-shaped (ellipical) nuclei.
  • Nuclear changes present at surface (not only in gland crypts).[2]
    • If changes are present at the base but not at the luminal surface -- it "matures" and is not dysplasic.

Notes:

  • Changes similar to those see in colorectal tubular adenomas.
  • Presence of goblet cells is mildly reassuring its not dysplasia.[3]

Management

Low grade dysplasia.

  • Follow-up.

High grade dysplasia.

  • Endoscopic mucosal resection.[4]
  • Surgical resection ???

Eosinophilic esophagitis

General

Clinical:

  • Dyspepsia.
    • Often mimics gastroesophageal reflux (GERD).[5]
  • Dysphagia.[6]

Associations:

  • Atopy.[7]
  • Celiac disease.[8]
  • Oral antigens, i.e. particular foods.[5]
  • Familial association.[5]

Microscopy

Features:[7]

  • Mucosa with "abundant eosinophils".
  • Basal cell hyperplasia.
  • Papillae elongated.

Notes:

  • Criteria for number of eosinophils/area is highly variable; there is a 23X fold variation in published values and only 11% of studies actually define an area (most studies, embarassing, only give the number of eosinophils per "HPF")![9]
    • The group that published the article cited above did another one... [10]
  • The Foundation Series book[7] says: "> 20/HPF"; VL sees this definition as garbage, as "HPF" is not defined (see rant in the basics article).
  • The most commonly reported cut points are 15, 20 and 24 eosinophils/HPF, without defining HPF.[9]
  • Most resident microscopes at the Toronto teaching hospitals have 22 mm eye pieces and have for their highest magnification objective a 40X. De facto, this means most people in Toronto are using the Liacouras et al. definition.[11]

Treatment

  • Avoid exacerbating antigens.
  • Topical corticosteroids, e.g. fluticasone.

Cancer

General

Risks:

  • EtOH.
  • Barrett's esophagus.
  • Smoking.

Adenocarcinoma of the esophagus

General

  • Often a prognosis poor - as diagnosed in a late stage.
  • May be difficult to distinguish from adenocarcinoma of the stomach.

Tx

  • Adenocarcinoma in situ (AIS) - may be treated with endoscopic mucosal resection & follow-up.[4]
  • Surgery - esophagectomy.

IHC

Adenocarcinoma:

  • CK7 +ve, CK20 +ve.

See also

References

  1. ↑ URL: http://dictionary.reference.com/browse/pyrosis. Accessed on: 21 June 2010.
  2. ↑ GAG Jan 2009
  3. ↑ GAG Jan 2009
  4. ↑ 4.0 4.1 Sampliner RE (March 2009). "Endoscopic Therapy for Barrett's Esophagus". Clin. Gastroenterol. Hepatol.. doi:10.1016/j.cgh.2009.03.011. PMID 19306943.
  5. ↑ 5.0 5.1 5.2 PMID 19596009.
  6. ↑ URL: http://www.medicinenet.com/eosinophilic_esophagitis/page2.htm#tocc. Accessed on: 1 December 2009.
  7. ↑ 7.0 7.1 7.2 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. 19. ISBN 978-0443066573.
  8. ↑ Leslie C, Mews C, Charles A, Ravikumara M (April 2010). "Celiac disease and eosinophilic esophagitis: a true association". J. Pediatr. Gastroenterol. Nutr. 50 (4): 397–9. doi:10.1097/MPG.0b013e3181a70af4. PMID 19841598.
  9. ↑ 9.0 9.1 Dellon ES, Aderoju A, Woosley JT, Sandler RS, Shaheen NJ (October 2007). "Variability in diagnostic criteria for eosinophilic esophagitis: a systematic review". Am. J. Gastroenterol. 102 (10): 2300–13. doi:10.1111/j.1572-0241.2007.01396.x. PMID 17617209.
  10. ↑ PMID 19830560.
  11. ↑ Liacouras CA, Spergel JM, Ruchelli E, et al. (December 2005). "Eosinophilic esophagitis: a 10-year experience in 381 children". Clin. Gastroenterol. Hepatol. 3 (12): 1198–206. PMID 16361045.
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