Esophageal web

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Ahmed Younes M.B.B.CH [2]

Overview

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Esophageal web Main page

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Esophageal web from other Diseases

Epidemiology

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

Radiological tests

Other Diagnostic Studies

Treatment

Medical therapy

Surgerical therapy


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Overview

Historical perspective

  • In 1944, esophageal webs were first described by Templeton and it was thought to be a congenital disease because most of the patients were children.
  • In 1953, a series of case reports of patients having dysphagia and radiological signs denoting esophageal narrowing made the diagnosis of esophageal rings not confined to the pediatric population.
  • In 1968, histological examination of specimens from the esophageal rings proved that none of them had muscle involvement.

Classification

Esophageal webs can be classified according to their site and their extent in three categories

Type A

  • Type A esophageal rings describe webs that involve the muscle layer of the esophageal wall and lies in close proximity to the squamocolumnar junction.
  • It is less common than type B esophageal webs.

Type B

  • Type B esophageal rings describe the webs that involve only the mucosa and submucosa of the esophagus.
  • It is often named “Schatzki ring”.
  • It is located exactly at the squamocolumnar junction.

Type C

  • Type C esophageal rings refer to wall invaginations due to pressure from the diaphragm.
  • It is rare with no clinical significance.

Pathophysiology

Pathogenesis

There are multiple theories explaining the origin of esophageal webs

Inflammation

  • Esophageal webs are thought to be due to the chronic damage to the esophageal mucosa.
  • This is supported by the presence of inflammatory cells in the wall of the web.
  • In allergic esophagitis, eosinophils were found while in cases of chronic inflammation as GERD, lymphocytes prevailed.

Congenital theory

  • Esophageal webs are thought to be due to failure of the esophagus to recanalize.
  • Specimens showed that the esophageal webs contained respiratory epithelium supporting this theory.
  • The webs mostly remain asymptomatic for long times and that is why it is not correlated with being congenital.

Iron deficiency

  • The esophageal webs of Plummer-Vinson syndrome have been associated with iron deficiency anemia in many studies.
  • The exact mechanism by which iron deficiency causes esophageal webs is not known, but it was hypothesized that iron deficiency starts a sequence of events in the esophageal epithelium that ends in its damage and formation of a web.
  • Moreover, treatment of iron deficiency in Plummer-Vinson syndrome patients leads to resolution of dysphagia even before the laboratory results become normal.

Gross picture

  • Esophageal webs appear as an eccentric narrowing of the esophageal lumen (while rings cause circumferential narrowing).

Microscopic picture

  • Esophageal webs are covered normally by mucosa and submucosa.
  • It is characterized by the presence of basal cell hyperplasia.
  • The tissue is often heavily infiltrated with chronic inflammatory cells.
  • Eosinophilic esophagitis is characterized by the presence of eosinophils infiltration.

Causes

More common causes

  • Iron deficiency anemia
  • Plummer-Vinson syndrome
  • Celiac sprue
  • Zenker’s diverticulum

Less common causes

  • Epidermolysis bullosa
  • Bullous pemphigoid
  • Graft versus host disease
  • Pemphigus Vulgaris

Differentiating esophageal webs from other diseases

Risk factors

Screening

Acorrding to USPSTF, there are no screening measures recommended for esophageal webs.

Natural history, complications and prognosis

History and symptoms

Physical examination

Lab findings

Radiological tests

Treatment