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Complications of Gastroesophageal Reflux Disease


An esophageal peptic stricture is thought to result from fibrosis when inflammation and injury extend below the mucosa as a consequence of chronic Gastroesophageal reflux. Up to 11% of patients with Gastroesophageal reflux disease seem to develop strictures. Factors predisposing to stricture formation include prolonged Gastroesophageal reflux, reflux while supine, nasogastric intubation, duodenal ulcer disease, gastric hypersecretory states, postgastrectomy states, scleroderma, and treated achalasia. Ringlike stricture in the distal esophagus at the E-G junction is called Schatzki’s ring.

  1. Location. Strictures are usually located in the distal third of the esophagus. In the barium esophagogram, they usually have a smooth, tapered appearance and are of variable lengths. In some instances of Barrett’s esophagus, the stricture is located in the middle third or, less commonly, in the proximal third of the esophagus.
  2. Symptoms. Peptic strictures usually produce no symptoms until the esophageal intraluminal diameter is decreased to less than 12 mm. Initially dysphagia is mostly for solids, but with progressive narrowing, swallowing of liquids also becomes a problem. It is not uncommon for the patient to notice improvement in the usual reflux symptoms as dysphagia develops with narrowing of the strictured area. Some patients do not recall even having Gastroesophageal reflux symptoms.
  3. Treatment. After appropriate diagnostic tests (barium esophagram, endoscopy, and biopsies) have been performed to ensure that the stricture is not due to a malignant process, intensive medical therapy is begun for reflux esophagitis. With resolution of edema and inflammation, some patients may have relief of their symptoms. However, most patients require additional therapy in the form of dilatations, surgery, or both.
  4. Dilatation. Progressive dilatations with graded mercury-filled rubber bougies (Maloney or Hurst dilators) have been used in the past for symptomatic relief. Savary dilators passed over a guidewire or inflatable balloon dilators with endoscopic guidance offer safer and more effective means of dilatation.

The major complications of dilatations are perforation and bleeding. Perforations are rare but should be suspected if the patient complains of persistent pain after dilatation. Perforations are identified by a radiologic contrast study. Patients are treated with intravenous nutrition and antibiotics to cover for organisms from the mouth flora. Surgical drainage and repair should be considered early, since mortality associated with large esophageal perforations is high.

Dilatation of the stricture and medical therapy for reflux yield good results in 65% to 85% of patients. The patency of the esophageal lumen is maintained by additional dilatations at intervals of weeks to months.


For the 15% to 40% of patients in whom dilatation and medical therapy fail, surgery is indicated. The preferred surgical approach to strictures is pre- or intraoperative dilatation combined with an anti-reflux operation, such as the Nissen fundoplication. If the stricture cannot be dilated or is too extensive, resection and end-to-end anastomosis or interposition of a segment of colon or small bowel may be used. These may be combined with a Nissen fundoplication to avoid anastomotic leaks or recurrence of the strictures.

Esophageal ulcers and bleeding

A small percentage of patients with Gastroesophageal reflux disease, in addition to severe esophagitis, have deep peptic ulcers penetrating into the muscular layers. These ulcers occasionally perforate or cause massive bleeding.

Most of these ulcers respond to intensive medical therapy, but some require surgery. Often, deep ulcers are found in metaplastic Barrett’s epithelium. These ulcers should be biopsied prior to therapy to rule out the possibility of malignancy.

Pulmonary manifestations

Respiratory problems attributable to Gastroesophageal reflux include laryngitis, hoarseness, chronic cough, asthma, bronchitis, bronchiectasis, aspiration pneumonitis, atelectasis, and hemoptysis. Although most of these patients experience Gastroesophageal reflux symptoms, these symptoms are not always present.

  1. Diagnosis. Documentation of pulmonary aspiration of gastric contents is difficult. Radionuclide scintiscanning of the lungs may be used to document pulmonary aspiration following the placement of technetium 99m-sulfur colloid in the stomach. If a positive result is found, it may be helpful; however, a negative result does not rule out aspiration or absence of a relationship between the pulmonary disease and Gastroesophageal reflux. Prolonged pH monitoring may be helpful in some patients. Numerous studies have demonstrated an increased frequency of reflux in patients with acute and chronic obstructive pulmonary disease. It is accepted that Gastroesophageal reflux with or without aspiration produces an increased airway resistance. Strict antireflux therapy with constant suppression of gastric acid secretion with the use of high-dose proton-pump inhibitors. Fundoplication may be necessary in some patients (e.g., refractory asthma, Gastroesophageal reflux-related apnea, recurrent aspiration pneumonitis).
  2. Treatment. Intensive therapy of Gastroesophageal reflux may be beneficial in these patients. Many of the medications used to treat asthma lower lower esophageal sphincter pressure and increase the chance for Gastroesophageal reflux. Thus, the medications used in these patients should be closely monitored. In addition, patients should be discouraged from smoking. Patients who do not improve with medical therapy with proton-pump inhibitors may require antireflux surgery.

Barrett’s esophagus

In some patients, chronic reflux esophagitis results in replacement of the normal squamous epithelium of the distal esophagus with metaplastic specialized columnar epithelium called Barrett’s epithelium. Depending on the length of the abnormal tissue Barrett’s esophagus may be subclassified as short segment or long segment Barrett’s esophagus. The prevalence of Barrett’s esophagus may be as high as 10% to 20%. Even though Barrett’s esophagus may be seen at any age, most instances come to medical attention after the fourth decade of life.

Barrett’s epithelium consists of a complex mixture of varying cell types, glands, and surface architecture that is normally seen in the small bowel with varying degrees of atrophy.

  1. Complications. Peptic ulceration, strictures, and adenocarcinoma are complications associated with Barrett’s esophagus. Strictures are characteristically found in the mid to lower esophagus with squamous epithelium above and columnar epithelium below the stricture. Dysplasia and adenocarcinoma of the esophagus have been recognized arising in Barrett’s epithelium with a reported prevalence of 3% to 9%. The neoplastic changes may be multifocal and may represent a major pathway in the genesis of adenocarcinoma of the lower esophagus and gastric cardia. The presence of a malignant lesion should be suspected in any patient with mid esophageal narrowing and stricture formation. However, dysplastic and malignant changes may be present in any patient with Barrett’s esophagus. Periodic (e.g., every 1-2 years) multiple endoscopic biopsies and brush cytology should be performed in these patients, especially in patients with histologic dysplasia, to monitor for malignancy.
  2. Treatment. Most patients with Barrett’s esophagus are treated medically for reflux esophagitis with high-dose proton-pump inhibitors. Despite strict intensive medical therapy, regression of this metaplastic change has not been documented. Esophagectomy or mucosal ablation therapy is recommended if severe dysplasia is found. Mucosal ablation may be accomplished by photodynamic therapy followed by laser ablation or by laser or bipolar heater probe cautery. These procedures are still not widely accepted or available except in special tertiary medical center.

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