What is Barrett’s esophagus?
Barrett’s esophagus is a complication of chronic reflux esophagitis where there is change of esophageal mucosa to columnar epithelium. It occurs as an adaptive response to chronic gastro esophageal reflux. This adaptive response involves a mosaic of cell types, probably beginning as a simple columnar epithelium that becomes specialized with time. The hallmark of specialized Barrett’s epithelium is the presence of mucus secreting goblet cells. One of the great mysteries of reflux esophagitis is why some people develop esophagitis and why others develop Barrett’s esophagus, often without significant esophagitis.
What is the magnitude of Barrett’s esophagus problem?
The incidence of Barrett’s esophagus is rising, and it is estimated that it occurs in 10% of individuals with symptomatic reflux esophagitis. Barrett’s esophagus is most common in white males and it typically presents between 40 and 60 years of age. The greatest concern about Barrett esophagus is that it has an increased risk of esophageal cancer. Molecular studies suggest that Barrett epithelium may be more similar to adeno carcinoma than to normal esophageal epithelium. It shows us that Barrett’s esophagus is a pre-malignant condition. A vast majority of esophageal adeno carcinomas are associated with Barrett’s esophagus. But it is also true most individuals with Barrett’s esophagus do not develop esophageal tumors. The risk of cancer probably increases with increasing length of abnormal mucosa. These terms are widely used for describing risk :
- classic Barrett’s (3 cm or more columnar epithelium);
- short-segment Barrett’s (less than 3 cm of columnar epithelium);
- Change to intestinal epithelium at the junction of esophagus and stomach without any macroscopic change at endoscopy.
Symptoms of Barrett’s esophagus
Barrett’s esophagus does not provoke specific symptoms but gastro esophageal reflux disease does. Most patients have a long history of reflux symptoms, such as heartburn and regurgitation. Barrett’s esophagus should be treated with long term proton pump inhibitors once or twice daily to control reflux symptoms. Although these medications do not appear to cause regression of Barrett’s esophagus, they may reduce the risk of cancer. One third of patients report minimal symptoms or no symptoms of reflux esophagitis. This suggests decreased acid sensitivity of Barrett’s epithelium. Indeed, over 90% of individuals with Barrett esophagus in the general population do not seek medical attention.
This requires multiple systematic biopsies to maximize the chance of detecting change of esophageal epithelium to intestinal epithelium and/or dysplasia. Barrett esophagus can only be identified thorough endoscopy and biopsy. Barrett esophagus is suspected at endoscopy from the presence of orange, gastric type epithelium that extends upward from the stomach into the distal tubular esophagus in a tongue like or circumferential fashion. Biopsies obtained at endoscopy confirm the diagnosis. Three types of columnar epithelium may be identified: gastric cardiac, gastric fundic, and changed specialized intestinal epithelium. Only the latter is believed to carry an increased risk of cancer.
In patients known to have Barrett esophagus, surveillance endoscopy every 3 years is recommended to look for low- or high-grade dysplasia or adeno carcinoma. Patients with low-grade dysplasia have 1.5% risk/year of esophageal cancer. Patients with low-grade dysplasia require repeat endoscopic surveillance in 6 months to exclude coexisting high-grade dysplasia or cancer and, if low-grade dysplasia persists, endoscopic surveillance should be repeated yearly.
Approximately 13% of patient with high-grade dysplasia may harbor an unrecognized invasive esophageal cancer. Therefore, patients with high-grade dysplasia should undergo repeat staging endoscopy with mucosal biopsy, resection of visible mucosal nodules, and ultrasonography in order to exclude invasive cancer.
Barium studies are helpful for diagnosing complications like stricture.
Guidelines for cure of Barrett’s esophagus
Neither potent acid suppression nor anti reflux surgery will stop progression or induce regression of Barrett’s esophagus. Treatment is only indicated for symptoms of reflux or complications such as stricture.
Ablation for Barrett’s esophagus
Endoscopic therapies such as argon plasma coagulation, radiofrequency ablation or photodynamic therapy can induce regression but remain experimental.
Regular endoscopic surveillance can detect dysplasia and malignancy at an early stage and may improve survival but, because most Barrett’s esophagus is undetected until cancer develops, surveillance strategies can not influence the overall mortality rate of esophageal cancer. Surveillance is expensive and cost effectiveness studies have been conflicting, but currently it is recommended that patients with Barrett’s esophagus without dysplasia should undergo endoscopy every 2-3 years and those with low grade dysplasia at 6-12-monthly intervals.
Esophagectomy is widely recommended for those with high grade dysplasia, as the cut specimen harbors cancer in up to 40%. This may be an over estimate and recent data suggest that high grade dysplasia, often remains stable and may not progress to cancer, at least in the medium term. A combination of endoscopic mucosal resection (EMR) of any visibly abnormal areas and ablation of the remaining Barrett’s mucosa shows promise as an ‘organ preserving’ alternative to surgery.
Other supportive treatments for complications may include
Iron deficiency anemia occurs as a consequence of chronic, insidious blood loss from long-standing esophagitis. Most patients have a large hiatus hernia and bleeding can occur from small erosions in the neck of the sac (Cameron lesions). Hiatus hernia is very common and other causes of blood loss such as colorectal cancer, must be considered in anemic patients. Even when endoscopy reveals esophagitis and a hiatus hernia.
Benign esophageal stricture
Fibrous strictures develop as a consequence of long-standing esophagitis. Most patients are elderly and have poor esophageal peristaltic activity. They present with difficulty of swallowing which is worse for solids than for liquids. Bolus obstruction following ingestion of meat causes absolute difficulty of swallowing. A history of heartburn is common but not invariable; many elderly patients presenting with strictures have no preceding heartburn.
Diagnosis is by endoscopy, when biopsies of the stricture can be taken to exclude malignancy. Endoscopic balloon dilatation or mechanical bougie is helpful. Long-term therapy with a proton pump inhibitor drug at full dose should be started to reduce the risk of recurrent esophagitis and stricture formation. The patient should be advised to chew food thoroughly, and it is important to ensure adequate dentition.
Occasionally a massive intra thoracic hiatus hernia may twist upon itself, in either the organoaxial or the lateral axis, leading to a gastric volvulus. This leads to complete esophageal or gastric obstruction and the patient presents with severe chest pain, vomiting and dysphagia. Diagnosis is made by chest X-ray (air bubble in the chest) and barium swallow. Most cases spontaneously resolve but tend to recur and surgery is usually advised after nasogastric decompression.