Esophageal stricture pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
It is thought that [[esophageal]] [[stricture]] is the result of lower pressure of [[esophageal sphincter]] in [[gastroesophageal reflux disease]], esophageal motor disorder, [[inflammation]] and [[fibrosis]] in [[neoplasia]]. The most characteristic finding in [[gross pathology]] is thickening of the lower esophageal wall in [[gastroesophageal reflux disease]], pale [[mucosa]] in lymphocytic [[esophagitis]] and [[hemorrhagic]] [[congestion]] in [[caustic]] ingestion. | |||
It is thought that [ | |||
[ | |||
[ | |||
[[Microscopic]] [[histopathological]] characteristic findings of esophageal [[stricture]] is Intraepithelial [[lymphocytes]] and [[basal cell]] [[hyperplasia]] in [[gastroesophageal reflux disease]], [[Infiltration (medical)|infiltration]] T [[lymphocytes]] in [[squamous]] [[mucosa]] in lymphocytic [[esophagitis]] and [[eosinophilic]] [[necrosis]] in [[caustic]] ingestion | |||
==Pathophysiology== | ==Pathophysiology== | ||
===Pathogenesis=== | ===Pathogenesis=== | ||
The normal [[esophageal]] diameter is up to 30 mm. An esophageal [[stricture]] is a narrowing of the [[esophagus]] usually 13 mm or less in diameter that causes [[dysphagia]]. Peptic strictures occur usually at the squamocolumnar junction. <ref name="pmid8338082">{{cite journal |vauthors=Marks RD, Richter JE |title=Peptic strictures of the esophagus |journal=Am. J. Gastroenterol. |volume=88 |issue=8 |pages=1160–73 |year=1993 |pmid=8338082 |doi= |url=}}</ref> | |||
*It is thought that esophageal [[stricture]] is the result of <ref name=":0">{{cite book | last = Holzheimer | first = R | title = Surgical treatment : evidence-based and problem-oriented | publisher = Zuckschwerdt | location = München New York | year = 2001 | isbn = 3-88603-714-2 }}</ref> <ref name="pmid24640761">{{cite journal |vauthors=Belevich VL, Ovchinnikov DV |title=[Treatment of benign esophageal stricture] |language=Russian |journal=Vestn. Khir. Im. I. I. Grek. |volume=172 |issue=5 |pages=111–4 |year=2013 |pmid=24640761 |doi= |url=}}</ref> | |||
*It is thought that [ | **lower pressure of esophageal sphincter in [[gastroesophageal reflux disease]], | ||
*[ | **Esophageal motor disorder, | ||
* | **[[Inflammation]] and [[fibrosis]] due to intrinsic disease of esophagus like [[neoplasia]], | ||
**[[Esophageal]] surgical [[anastomosis]], | |||
* | **[[Esophageal]] compression by other oragans | ||
* | *Most peptic strictures are result of chronic [[reflux esophagitis]] and the process of esophageal [[stricture]] is due to [[mucosal]] [[edema]] and [[Infiltration (medical)|infiltration]] of [[inflammatory cells]] in lamina properia and finally [[collagen]] deposits, [[fibrosis]] and [[scar]] of eshophagus.<ref name="pmid8338082" /> | ||
**[[Lower esophageal sphincter]] (LES) tone is usullay less than 8 mmHg in esophageal [[stricture]] due to [[reflux esophagitis]]. | |||
*[[Radiation therapy]] for thoracic or head and neck [[tumors]] is one of the less common cause of proximal esophageal [[stricture]] by inducing chronic [[ischemia]] and [[fibrosis]].<ref name="pmid89440642">{{cite journal |vauthors=Dhir V, Vege SS, Mohandas KM, Desai DC |title=Dilation of proximal esophageal strictures following therapy for head and neck cancer: experience with Savary Gilliard dilators |journal=J Surg Oncol |volume=63 |issue=3 |pages=187–90 |year=1996 |pmid=8944064 |doi=10.1002/(SICI)1096-9098(199611)63:3<187::AID-JSO10>3.0.CO;2-2 |url=}}</ref> | |||
*[[Liquefactive necrosis]] is the mechanism of esophageal [[stricture]] in [[alkali]] ingestion<ref name="pmid1539568">{{cite journal |vauthors=Zargar SA, Kochhar R, Nagi B, Mehta S, Mehta SK |title=Ingestion of strong corrosive alkalis: spectrum of injury to upper gastrointestinal tract and natural history |journal=Am. J. Gastroenterol. |volume=87 |issue=3 |pages=337–41 |year=1992 |pmid=1539568 |doi= |url=}}</ref> and superficial [[coagulation necrosis]] is the mechanism of esophageal [[stricture]] in [[acid]] ingestion.<ref name="pmid4012549">{{cite journal |vauthors=Fisher RA, Eckhauser ML, Radivoyevitch M |title=Acid ingestion in an experimental model |journal=Surg Gynecol Obstet |volume=161 |issue=1 |pages=91–9 |year=1985 |pmid=4012549 |doi= |url=}}</ref> | |||
**A grading system for esophageal injury due to causric ingestion: | |||
{| class="wikitable" | |||
!Grade | |||
!pathophysiological injury | |||
|- | |||
|0 | |||
|Normal | |||
|- | |||
|1 | |||
|Mucosal [[edema]] and [[hyperemia]] | |||
|- | |||
|2A | |||
|[[Superficial]] ulcers, [[bleeding]], [[exudate]]<nowiki/>s | |||
|- | |||
|2B | |||
|Deep focal or circumferential [[ulcer]]<nowiki/>s | |||
|- | |||
|3A | |||
|Focal [[necrosis]] | |||
|- | |||
|3B | |||
|Extensive [[necrosis]] | |||
|} | |||
==Genetics== | ==Genetics== | ||
Genes involved in the pathogenesis of esophageal stricture due to Dyskeratosis Congenita include:<ref name="pmid20301779">{{cite journal |vauthors=Adam MP, Ardinger HH, Pagon RA, Wallace SE, Bean LJH, Mefford HC, Stephens K, Amemiya A, Ledbetter N, Savage SA |title= |journal= |volume= |issue= |pages= |year= |pmid=20301779 |doi= |url=}}</ref> | |||
*''[[ACD (gene)|ACD]],'' | |||
* | *'' CTC1, '' | ||
*''DKC1, '' | |||
*''NHP2,'' | |||
*'' NOP10,'' | |||
*'' [[PARN]], '' | |||
*''RTEL1, '' | |||
*''TERC, '' | |||
*''[[TERT]], '' | |||
*''[[TINF2]],'' | |||
*''WRAP53 '' | |||
==Associated Conditions== | ==Associated Conditions== | ||
*The most important diseases associated with esophageal [[stricture]] include: | |||
**[[gastroesophageal reflux disease]] | |||
**[[caustic]] ingestion | |||
==Gross Pathology== | ==Gross Pathology== | ||
*On gross pathology, [ | *On [[gross pathology]], circumferential thickening of the lower esophageal wall are characteristic finding of [[esophageal]] [[stricture]] due to [[gastroesophageal reflux disease]].<ref name="YamasakiOzawa2016">{{cite journal|last1=Yamasaki|first1=Yasushi|last2=Ozawa|first2=Soji|last3=Oguma|first3=Junya|last4=Kazuno|first4=Akihito|last5=Ninomiya|first5=Yamato|title=Long peptic strictures of the esophagus due to reflux esophagitis: a case report|journal=Surgical Case Reports|volume=2|issue=1|year=2016|issn=2198-7793|doi=10.1186/s40792-016-0190-1}}</ref> | ||
*Pale [[mucosa]] with white [[exudate]] in lymphocytic esophagitis<ref name="MaejimaUno2016">{{cite journal|last1=Maejima|first1=Ryuhei|last2=Uno|first2=Kaname|last3=Iijima|first3=Katsunori|last4=Fujishima|first4=Fumiyoshi|last5=Noguchi|first5=Tetsuya|last6=Ara|first6=Nobuyuki|last7=Asano|first7=Naoki|last8=Koike|first8=Tomoyuki|last9=Imatani|first9=Akira|last10=Shimosegawa|first10=Tooru|title=A Japanese case of lymphocytic esophagitis|journal=Digestive Endoscopy|volume=28|issue=4|year=2016|pages=476–480|issn=09155635|doi=10.1111/den.12578}}</ref> | |||
*[[swelling]] and [[hemorrhagic]] [[congestion]] in [[caustic]] ingestion <ref name="Contini2013">{{cite journal|last1=Contini|first1=Sandro|title=Caustic injury of the upper gastrointestinal tract: A comprehensive review|journal=World Journal of Gastroenterology|volume=19|issue=25|year=2013|pages=3918|issn=1007-9327|doi=10.3748/wjg.v19.i25.3918}}</ref> | |||
==Microscopic Pathology== | |||
*On microscopic histopathological analysis, characteristic findings of esophageal stricture due to [[gastroesophageal reflux disease]] are:<ref name="urlEsophageal stricture - Libre Pathology">{{cite web |url=https://librepathology.org/wiki/Esophageal_stricture |title=Esophageal stricture - Libre Pathology |format= |work= |accessdate=}}</ref> | |||
**Intraepithelial [[lymphocyte]]<nowiki/>s | |||
**Basal cell [[hyperplasia]] | |||
**[[ulceration]] <ref name="YamasakiOzawa2016" /> | |||
*[[Microscopic]] [[histopathological]] characteristic findings of [[esophageal]] [[stricture]] due to [[Lymphocyte|lymphocytic]] [[esophagitis]] are:<ref name="MaejimaUno2016" /> | |||
* | **[[Infiltration (medical)|Infiltration]] of many [[CD3 (immunology)|CD3+]] /[[CD4+]] / [[CD8+ T cells|CD8+]] [[T lymphocytes]] in [[squamous]] [[mucosa]] in the peripapaillary region without any [[Granulocyte|granulocytes]] | ||
*[[Eosinophilic]] [[necrosis]] in esophageal [[stricture]] due to [[caustic]] ingestion<ref name="Contini2013" /> | |||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
Revision as of 16:31, 25 October 2017
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Esophageal stricture pathophysiology On the Web |
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American Roentgen Ray Society Images of Esophageal stricture pathophysiology |
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Risk calculators and risk factors for Esophageal stricture pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
Overview
It is thought that esophageal stricture is the result of lower pressure of esophageal sphincter in gastroesophageal reflux disease, esophageal motor disorder, inflammation and fibrosis in neoplasia. The most characteristic finding in gross pathology is thickening of the lower esophageal wall in gastroesophageal reflux disease, pale mucosa in lymphocytic esophagitis and hemorrhagic congestion in caustic ingestion.
Microscopic histopathological characteristic findings of esophageal stricture is Intraepithelial lymphocytes and basal cell hyperplasia in gastroesophageal reflux disease, infiltration T lymphocytes in squamous mucosa in lymphocytic esophagitis and eosinophilic necrosis in caustic ingestion
Pathophysiology
Pathogenesis
The normal esophageal diameter is up to 30 mm. An esophageal stricture is a narrowing of the esophagus usually 13 mm or less in diameter that causes dysphagia. Peptic strictures occur usually at the squamocolumnar junction. [1]
- It is thought that esophageal stricture is the result of [2] [3]
- lower pressure of esophageal sphincter in gastroesophageal reflux disease,
- Esophageal motor disorder,
- Inflammation and fibrosis due to intrinsic disease of esophagus like neoplasia,
- Esophageal surgical anastomosis,
- Esophageal compression by other oragans
- Most peptic strictures are result of chronic reflux esophagitis and the process of esophageal stricture is due to mucosal edema and infiltration of inflammatory cells in lamina properia and finally collagen deposits, fibrosis and scar of eshophagus.[1]
- Lower esophageal sphincter (LES) tone is usullay less than 8 mmHg in esophageal stricture due to reflux esophagitis.
- Radiation therapy for thoracic or head and neck tumors is one of the less common cause of proximal esophageal stricture by inducing chronic ischemia and fibrosis.[4]
- Liquefactive necrosis is the mechanism of esophageal stricture in alkali ingestion[5] and superficial coagulation necrosis is the mechanism of esophageal stricture in acid ingestion.[6]
- A grading system for esophageal injury due to causric ingestion:
| Grade | pathophysiological injury |
|---|---|
| 0 | Normal |
| 1 | Mucosal edema and hyperemia |
| 2A | Superficial ulcers, bleeding, exudates |
| 2B | Deep focal or circumferential ulcers |
| 3A | Focal necrosis |
| 3B | Extensive necrosis |
Genetics
Genes involved in the pathogenesis of esophageal stricture due to Dyskeratosis Congenita include:[7]
Associated Conditions
- The most important diseases associated with esophageal stricture include:
- gastroesophageal reflux disease
- caustic ingestion
Gross Pathology
- On gross pathology, circumferential thickening of the lower esophageal wall are characteristic finding of esophageal stricture due to gastroesophageal reflux disease.[8]
- Pale mucosa with white exudate in lymphocytic esophagitis[9]
- swelling and hemorrhagic congestion in caustic ingestion [10]
Microscopic Pathology
- On microscopic histopathological analysis, characteristic findings of esophageal stricture due to gastroesophageal reflux disease are:[11]
- Intraepithelial lymphocytes
- Basal cell hyperplasia
- ulceration [8]
- Microscopic histopathological characteristic findings of esophageal stricture due to lymphocytic esophagitis are:[9]
- Infiltration of many CD3+ /CD4+ / CD8+ T lymphocytes in squamous mucosa in the peripapaillary region without any granulocytes
- Eosinophilic necrosis in esophageal stricture due to caustic ingestion[10]
References
- ↑ 1.0 1.1 Marks RD, Richter JE (1993). "Peptic strictures of the esophagus". Am. J. Gastroenterol. 88 (8): 1160–73. PMID 8338082.
- ↑ Holzheimer, R (2001). Surgical treatment : evidence-based and problem-oriented. München New York: Zuckschwerdt. ISBN 3-88603-714-2.
- ↑ Belevich VL, Ovchinnikov DV (2013). "[Treatment of benign esophageal stricture]". Vestn. Khir. Im. I. I. Grek. (in Russian). 172 (5): 111–4. PMID 24640761.
- ↑ Dhir V, Vege SS, Mohandas KM, Desai DC (1996). "Dilation of proximal esophageal strictures following therapy for head and neck cancer: experience with Savary Gilliard dilators". J Surg Oncol. 63 (3): 187–90. doi:10.1002/(SICI)1096-9098(199611)63:3<187::AID-JSO10>3.0.CO;2-2. PMID 8944064.
- ↑ Zargar SA, Kochhar R, Nagi B, Mehta S, Mehta SK (1992). "Ingestion of strong corrosive alkalis: spectrum of injury to upper gastrointestinal tract and natural history". Am. J. Gastroenterol. 87 (3): 337–41. PMID 1539568.
- ↑ Fisher RA, Eckhauser ML, Radivoyevitch M (1985). "Acid ingestion in an experimental model". Surg Gynecol Obstet. 161 (1): 91–9. PMID 4012549.
- ↑ Adam MP, Ardinger HH, Pagon RA, Wallace SE, Bean L, Mefford HC, Stephens K, Amemiya A, Ledbetter N, Savage SA. PMID 20301779. Vancouver style error: initials (help); Missing or empty
|title=(help) - ↑ 8.0 8.1 Yamasaki, Yasushi; Ozawa, Soji; Oguma, Junya; Kazuno, Akihito; Ninomiya, Yamato (2016). "Long peptic strictures of the esophagus due to reflux esophagitis: a case report". Surgical Case Reports. 2 (1). doi:10.1186/s40792-016-0190-1. ISSN 2198-7793.
- ↑ 9.0 9.1 Maejima, Ryuhei; Uno, Kaname; Iijima, Katsunori; Fujishima, Fumiyoshi; Noguchi, Tetsuya; Ara, Nobuyuki; Asano, Naoki; Koike, Tomoyuki; Imatani, Akira; Shimosegawa, Tooru (2016). "A Japanese case of lymphocytic esophagitis". Digestive Endoscopy. 28 (4): 476–480. doi:10.1111/den.12578. ISSN 0915-5635.
- ↑ 10.0 10.1 Contini, Sandro (2013). "Caustic injury of the upper gastrointestinal tract: A comprehensive review". World Journal of Gastroenterology. 19 (25): 3918. doi:10.3748/wjg.v19.i25.3918. ISSN 1007-9327.
- ↑ "Esophageal stricture - Libre Pathology".