eMedicine Specialties > Gastroenterology > Esophagus

Esophageal Stricture

Author: Rajeev Vasudeva, MD, FACG, Clinical Professor of Medicine, Consultants in Gastroenterology, University of South Carolina School of Medicine
Contributor Information and Disclosures

Updated: Jun 27, 2006

Introduction

Background

Disease processes that can produce esophageal strictures can be grouped into 3 general categories: (1) intrinsic diseases that narrow the esophageal lumen through inflammation, fibrosis, or neoplasia; (2) extrinsic diseases that compromise the esophageal lumen by direct invasion or lymph node enlargement; and (3) diseases that disrupt esophageal peristalsis and/or lower esophageal sphincter (LES) function by their effects on esophageal smooth muscle and its innervation.

Many diseases can cause esophageal stricture formation. These include acid peptic, autoimmune, infectious, caustic, congenital, iatrogenic, medication-induced, radiation-induced, malignant, and idiopathic disease processes.

The etiology of esophageal stricture can usually be identified using radiologic and endoscopic modalities and can be confirmed by endoscopic visualization and tissue biopsy. Use of manometry can be diagnostic when dysmotility is suspected as the primary process. CT scan and endoscopic ultrasound are valuable aids in the staging of malignant stricture. Fortunately, most benign esophageal strictures are amenable to pharmacological, endoscopic, and/or surgical interventions.

Because peptic strictures account for 70-80% of all cases of esophageal stricture, peptic stricture is the focus of this article. A detailed discussion of possible benign and malignant processes associated with esophageal stricture and its management is beyond the scope of this article.

Pathophysiology

Peptic strictures are sequelae of gastroesophageal reflux–induced esophagitis, and they usually originate from the squamocolumnar junction and average 1-4 cm in length.

  • Two major factors involved in the development of a peptic stricture are as follows:
    • Dysfunctional lower esophageal sphincter: Mean LES pressures are lower in patients with peptic strictures compared with healthy controls or patients with milder degrees of reflux disease. A study by Ahtaridis et al (1979) showed that patients with peptic strictures had a mean LES pressure of 4.9 mm Hg versus 20 mm Hg in control patients. LES pressure of less than 8 mm Hg appeared to correlate significantly with the presence of peptic esophageal stricture without any overlap in controls.
    • Disordered motility resulting in poor esophageal clearance: In the same study, Ahtaridis et al (1979) demonstrated that 64% of patients with strictures had motility disorders compared with 32% of patients without strictures.
  • Other possible associated factors include the following:
    • Presence of a hiatal hernia: Hiatal hernias are found in 10-15% of the general population, 42% of patients with reflux symptoms and no esophagitis, 63% of patients with esophagitis, and 85% of patients with peptic strictures. This suggests that hiatal hernias may play a significant role.
    • Acid and pepsin secretion: This does not appear to be a major factor. Patients with peptic strictures have been demonstrated to have the same acid and pepsin secretion rates as gender-matched and age-matched controls with esophagitis but no stricture formation. In fact, some authors believe that alkaline reflux may play an important role.
    • Gastric emptying: No good evidence suggests that delayed emptying plays a role.

Frequency

United States

Gastroesophageal reflux affects approximately 40% of adults. Strictures are estimated to occur in 7-23% of untreated patients with reflux disease.

Gastroesophageal reflux disease accounts for approximately 70-80% of all cases of esophageal stricture. Postoperative strictures account for about 10%, and corrosive strictures account for less than 5%.

The overall frequency of initial and subsequent dilations for peptic stricture appears to have decreased gradually since the introduction of proton pump inhibitors (PPIs) in the market in 1989. This has been borne out by data at the author's institution and in 2 large community hospitals in Wisconsin. It is also in keeping with the general experience of gastroenterologists in the United States.


Mortality/Morbidity

The mortality rate is not increased unless a procedure-related perforation occurs or the stricture is malignant. However, the morbidity for peptic strictures is significant.

  • Most patients undergo a chronic relapsing course with an increased risk of food impaction and pulmonary aspiration.
  • Frequently, coexistent Barrett esophagus and its attendant complications occur.
  • The need for repeated dilatation potentially increases the risk of perforation.

Race

Peptic strictures are 10-fold more common in whites than African Americans or Asians.

Sex

Peptic strictures are 2- to 3-fold more common in men than in women.

Age

Patients tend to be older, with a longer duration of reflux symptoms.

Clinical

History

  • Patients may present with heartburn, dysphagia, odynophagia, food impaction, weight loss, and chest pain.
  • Progressive dysphagia for solids is the most common presenting symptom. This may progress to include liquids.
  • Atypical presentations include chronic cough and asthma secondary to aspiration of food or acid.
  • The clinician cannot rely on the presence or absence of heartburn to definitely determine whether dysphagia is secondary to a peptic esophageal stricture.
    • Of patients with peptic esophageal strictures, 25% have no previous history of heartburn.
    • Heartburn may resolve with worsening of a peptic stricture.
    • Approximately two thirds of patients with adenocarcinoma in Barrett esophagus have a history of long-standing heartburn.
    • The abnormal esophageal motor activity in achalasia can produce a heartburn sensation.
  • Important points regarding dysphagia
    • The obstruction usually is perceived at a point that is either above or at the level of the lesion.
    • Dysphagia for solids and liquids simultaneously should alert the clinician to the possibility of a motility disorder such as achalasia or collagen vascular disorders.
    • Dysphagia secondary to Schatzki ring usually is intermittent and nonprogressive.
    • Dysphagia for solids and liquids early in the course of disease should alert the clinician to the possibility of achalasia as an etiology.
    • Benign esophageal strictures usually produce dysphagia with slow and insidious progression (ie, months to years) of frequency and severity with minimal weight loss.
    • Malignant esophageal strictures result in a rapid progression (ie, weeks to months) of severity and frequency of dysphagia and are associated frequently with significant weight loss.
  • Determining whether the patient takes any medications known to cause pill esophagitis is important.
  • Determining whether a history of collagen vascular disease or immunosuppression exists may provide clues to the underlying etiology.

Physical

  • Physical examination frequently does not provide clues to the cause of dysphagia.
  • Assessing the patient's nutritional status is important.
  • Patients with collagen vascular diseases may exhibit joint abnormalities, calcinosis, telangiectasias, sclerodactyly, or rashes.
  • The presence of atypical gastroesophageal reflux disease may be suggested by hoarse voice, posterior oropharyngeal erythema, diffuse dental erosions, wheezing, or epigastric tenderness.
  • Patients with adenocarcinoma of the gastroesophageal junction may have left supraclavicular lymphadenopathy (Virchow node).

Causes

  • Proximal or mid esophageal strictures
    • Caustic ingestion (acid or alkali)
    • Malignancy
    • Radiation therapy
    • Infectious esophagitis -Candida, herpes simplex virus (HSV), cytomegalovirus (CMV), HIV
    • AIDS and immunosuppression in patients who have received a transplant
    • Medication-induced stricture (pill esophagitis) - Alendronate, ferrous sulfate, nonsteroidal anti-inflammatory drugs, phenytoin, potassium chloride, quinidine, tetracycline, ascorbic acid
    • Diseases of the skin - Pemphigus vulgaris, benign mucous membrane (cicatricial) pemphigoid, epidermolysis bullosa dystrophica
    • Graft versus host disease
    • Idiopathic eosinophilic esophagitis
    • Extrinsic compression
    • Squamous cell carcinoma
    • Miscellaneous - Trauma to the esophagus from external forces, foreign body, surgical anastomosis/postoperative stricture, congenital esophageal stenosis
  • Distal esophageal strictures
    • Peptic stricture - Gastroesophageal reflux disease, Zollinger-Ellison syndrome
    • Adenocarcinoma
    • Collagen vascular disease - Scleroderma, systemic lupus erythematosus (SLE), rheumatoid arthritis
    • Extrinsic compression
    • Alkaline reflux following gastric resection
    • Sclerotherapy and prolonged nasogastric intubation
    • Crohn disease

More on Esophageal Stricture

Overview: Esophageal Stricture
Differential Diagnoses & Workup: Esophageal Stricture
Treatment & Medication: Esophageal Stricture
Follow-up: Esophageal Stricture
Multimedia: Esophageal Stricture
References
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Further Reading

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Keywords

esophageal stenosis, peptic stenosis, reflux stricture, peptic stricture, postoperative strictures, corrosive strictures, gastroesophageal reflux–induced esophagitis, gastroesophageal reflux disease, dysphagia

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Contributor Information and Disclosures

Author

Rajeev Vasudeva, MD, FACG, Clinical Professor of Medicine, Consultants in Gastroenterology, University of South Carolina School of Medicine
Rajeev Vasudeva, MD, FACG is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy, and South Carolina Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Maurice A Cerulli, MD, FACG, Chief, Division of Gastroenterology and Hepatology, Associate Professor of Clinical Medicine, Department of Internal Medicine, Division of Gastroenterology, New York Methodist Hospital, Cornell University
Maurice A Cerulli, MD, FACG is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, American Medical Association, and American Society for Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Simmy Bank, MD, Chair, Professor, Department of Internal Medicine, Division of Gastroenterology, Long Island Jewish Hospital, Albert Einstein College of Medicine
Disclosure: Nothing to disclose.

CME Editor

Alex J Mechaber, MD, FACP, Assistant Dean for Medical Curriculum, Associate Professor of Medicine, Division of General Internal Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania
Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law Medicine and Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.

 
 
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