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Dilation of Peptic Esophageal Strictures

Thomas W. Rice
Dilation of Peptic Esophageal Strictures is a topic covered in the Pearson's General Thoracic.

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Key Points

  • Barium esophagography and esophagoscopy with brushing and biopsy must be used to differentiate peptic stricture from other causes of dysphagia.
  • There is no perfect dilator; the most appropriate dilator available must be used.
  • Bougies and balloon dilators are equally effective in the treatment of peptic strictures.
  • Meticulous technique minimizes complications and improves long-term results.
  • Long-term management of GERD and repeat dilation are crucial for successful treatment of peptic esophageal strictures.

A peptic esophageal stricture is the result of excessive and uncontrolled reflux of upper gastrointestinal contents into the esophagus. The amount and composition of refluxed material and the extent of exposure to the esophagus of this material determines the magnitude of damage. Multiple factors control these elements of injury.

Patients with peptic esophageal strictures have very disturbed esophageal physiology. Lower esophageal sphincter (LES) pressures are lowest in patients with peptic esophageal strictures. In one study mean LES pressure was 4.9 mm Hg in patients with peptic strictures, 7.5 mm Hg in patients with uncomplicated gastroesophageal reflux disease (GERD), and 20 mm Hg in control subjects.[1] There was no overlap of LES pressure between patients with peptic strictures and control subjects. Impaired esophageal motility causes inadequate clearance of the refluxed material, which permits prolonged esophageal exposure and heightens injury. Sixty-four percent of patients with peptic strictures had motility disorders compared with only 32% without strictures.[1] Simultaneous or nonpropulsive contractions are most common. In the extreme, aperistalsis has been reported and may be reversible with adequate control of reflux.[2] Abnormal distal gastrointestinal motility may result in excessive intragastric pressures and increased volumes of refluxed material. However, there is only indirect evidence that delayed gastric emptying promotes the development of peptic strictures.[3],[4]

Insufficient esophageal mucosal protection may magnify the injury caused by refluxed material. Although these protective mechanisms are poorly understood, the amount and quality of neutralizing saliva and esophageal secretions may be important in preventing reflux injury. The nature and volume of refluxed material are primary determinates of injury. Undoubtedly, acid is the principal agent. Acid combined with alkaline duodenal contents may cause more injury to the esophageal mucosa than acid alone.[5] Although speculation continues regarding alkaline and enzymatic esophageal injury, some experimental data suggest that nonacid injury alone may play a minimal role in peptic esophagitis.[6],[7]

Hiatal hernia is the main structural defect that facilitates reflux and promotes peptic strictures. Prevalence of hiatal hernia increases with severity of GERD. Hiatal hernias have been reported in 42% of patients with reflux, 63% of patients with esophagitis, and 85% of patients with peptic strictures.[8],[9]

At esophagoscopy peptic mucosal injury is easily visualized and graded, but the damage reaches beyond the mucosa. Usually, peptic stricture is the end-stage finding in any rating of esophagitis; however, changes of peptic injury deep to the mucosa are themselves progressive and can be graded.[10] Early injury is confined to the submucosa and characterized by edema, inflammation, spasm, and the deposition of immature collagen (type III). The resultant grade 1 stricture is “soft” and dilates easily. A grade 2 stricture occurs with maturation of the collagen (type I) in the submucosa, is hard (firm and annular), and requires significant force to dilate. With continued reflux, inflammation and fibrosis advance to involve the entire esophageal wall and periesophageal tissue. This process generally occurs over a substantial length of the esophagus and produces vertical contracture and significant shortening of the esophagus. The result of panmural scarring and cicatricial contracture is a grade 3 peptic stricture.

Dysphagia is the chief complaint of patients with peptic esophageal stricture. However, this symptom is not exclusive to reflux injury. Attempts must be made to exclude all other causes of esophageal stricture. Once confirmed, the mainstay of symptomatic control of peptic esophageal stricture is dilation. Long-term management requires prevention of progressive damage by addressing the multiple factors causing reflux and eliminating further reflux injury. Once reflux is controlled, further dilation is usually needed to treat submucosal, muscular, and periesophageal peptic damage.

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Key Points

  • Barium esophagography and esophagoscopy with brushing and biopsy must be used to differentiate peptic stricture from other causes of dysphagia.
  • There is no perfect dilator; the most appropriate dilator available must be used.
  • Bougies and balloon dilators are equally effective in the treatment of peptic strictures.
  • Meticulous technique minimizes complications and improves long-term results.
  • Long-term management of GERD and repeat dilation are crucial for successful treatment of peptic esophageal strictures.

A peptic esophageal stricture is the result of excessive and uncontrolled reflux of upper gastrointestinal contents into the esophagus. The amount and composition of refluxed material and the extent of exposure to the esophagus of this material determines the magnitude of damage. Multiple factors control these elements of injury.

Patients with peptic esophageal strictures have very disturbed esophageal physiology. Lower esophageal sphincter (LES) pressures are lowest in patients with peptic esophageal strictures. In one study mean LES pressure was 4.9 mm Hg in patients with peptic strictures, 7.5 mm Hg in patients with uncomplicated gastroesophageal reflux disease (GERD), and 20 mm Hg in control subjects.[1] There was no overlap of LES pressure between patients with peptic strictures and control subjects. Impaired esophageal motility causes inadequate clearance of the refluxed material, which permits prolonged esophageal exposure and heightens injury. Sixty-four percent of patients with peptic strictures had motility disorders compared with only 32% without strictures.[1] Simultaneous or nonpropulsive contractions are most common. In the extreme, aperistalsis has been reported and may be reversible with adequate control of reflux.[2] Abnormal distal gastrointestinal motility may result in excessive intragastric pressures and increased volumes of refluxed material. However, there is only indirect evidence that delayed gastric emptying promotes the development of peptic strictures.[3],[4]

Insufficient esophageal mucosal protection may magnify the injury caused by refluxed material. Although these protective mechanisms are poorly understood, the amount and quality of neutralizing saliva and esophageal secretions may be important in preventing reflux injury. The nature and volume of refluxed material are primary determinates of injury. Undoubtedly, acid is the principal agent. Acid combined with alkaline duodenal contents may cause more injury to the esophageal mucosa than acid alone.[5] Although speculation continues regarding alkaline and enzymatic esophageal injury, some experimental data suggest that nonacid injury alone may play a minimal role in peptic esophagitis.[6],[7]

Hiatal hernia is the main structural defect that facilitates reflux and promotes peptic strictures. Prevalence of hiatal hernia increases with severity of GERD. Hiatal hernias have been reported in 42% of patients with reflux, 63% of patients with esophagitis, and 85% of patients with peptic strictures.[8],[9]

At esophagoscopy peptic mucosal injury is easily visualized and graded, but the damage reaches beyond the mucosa. Usually, peptic stricture is the end-stage finding in any rating of esophagitis; however, changes of peptic injury deep to the mucosa are themselves progressive and can be graded.[10] Early injury is confined to the submucosa and characterized by edema, inflammation, spasm, and the deposition of immature collagen (type III). The resultant grade 1 stricture is “soft” and dilates easily. A grade 2 stricture occurs with maturation of the collagen (type I) in the submucosa, is hard (firm and annular), and requires significant force to dilate. With continued reflux, inflammation and fibrosis advance to involve the entire esophageal wall and periesophageal tissue. This process generally occurs over a substantial length of the esophagus and produces vertical contracture and significant shortening of the esophagus. The result of panmural scarring and cicatricial contracture is a grade 3 peptic stricture.

Dysphagia is the chief complaint of patients with peptic esophageal stricture. However, this symptom is not exclusive to reflux injury. Attempts must be made to exclude all other causes of esophageal stricture. Once confirmed, the mainstay of symptomatic control of peptic esophageal stricture is dilation. Long-term management requires prevention of progressive damage by addressing the multiple factors causing reflux and eliminating further reflux injury. Once reflux is controlled, further dilation is usually needed to treat submucosal, muscular, and periesophageal peptic damage.

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Last updated: March 22, 2020