Esophageal Stricture

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.