Barrett Esophagus is defined as a metaplastic transformation of esophageal mucosa resulting from chronic GER. Histologically, the metaplastic epithelium must demonstrate intestinal-type metaplasia characterized by the presence of goblet cells. The columnar epithelium of Barrett esophagus may replace the normal squamous epithelium circumferentially, or it may be asymmetric and irregular.
Prevalence. Barrett esophagus is diagnosed in approximately 2% of all patients undergoing esophagoscopy and in 10% to 15% of patients with esophagitis. Autopsy studies suggest that the actual prevalence is much higher because many patients are asymptomatic and remain undiagnosed. Most patients diagnosed with Barrett esophagus are middle-aged white men.
The symptoms of Barrett esophagus arise from longstanding gastric reflux. Approximately 50% of patients with endoscopically proven Barrett have associated heartburn, 75% have dysphagia, and 25% have bleeding (Ann Surg 1983;198:554).
Diagnosis. Barrett esophagus may be suggested on x-ray by the presence of a hiatal hernia (associated with 80% of cases of Barrett esophagus) with esophagitis and an esophageal stricture. Confirmation of the diagnosis requires endoscopy and careful correlation between the endoscopic and histologic appearances.
Esophageal ulceration and stricture are more likely to occur in patients with Barrett esophagus than in those with GER alone. This probably reflects the more severe nature of the GER in patients with Barrett esophagus.
Barrett ulcers are distinctly different from the common erosions seen in esophagitis in that they penetrate the metaplastic columnar epithelium in a manner similar to that seen in gastric ulcers. They occur in up to 50% of patients with Barrett esophagus and, like gastric ulcers, can cause pain, bleed, obstruct, penetrate, and perforate.
A benign stricture occurs in 30% to 50% of patients with Barrett esophagus. The stricture is located at the squamocolumnar junction, which may be found proximal to the GE junction. Strictures secondary to Barrett esophagus are located in the middle or upper esophagus, unlike the routine peptic strictures that usually occur in the distal esophagus.
Dysplasia. The metaplastic columnar epithelium of Barrett esophagus is prone to development of dysplasia that can be detected only by biopsy. Dysplasia is categorized as low or high grade, with high grade being pathologically indistinguishable from carcinoma in situ.
Malignant degeneration from benign to dysplastic to malignant epithelium has been demonstrated in Barrett esophagus. Low-grade dysplasia is present in 5% to 10% of patients with Barrett esophagus and can progress to high-grade dysplasia and malignancy.
Adenocarcinomas that arise within the esophagus above the normal GE junction are characteristic of malignant degeneration in Barrett esophagus. The risk of development of adenocarcinoma in Barrett esophagus is 50 to 100 times that of the general population. In several long-term series, the incidence of malignant degeneration in Barrett esophagus was estimated at between 1 in 50 and 1 in 400 patient-years of follow-up.
Uncomplicated Barrett esophagus in asymptomatic patients requires no specific therapy, but endoscopic surveillance and biopsy should be performed at least annually. Neither medical nor surgical treatment of reflux has been demonstrated to reverse the columnar metaplasia of Barrett esophagus. However, elimination of reflux with an antireflux procedure may halt progression of the disease, heal ulceration, and prevent stricture formation.
Uncomplicated Barrett esophagus in symptomatic patients should be treated using the same principles that apply to patients with GER without Barrett esophagus. In addition, symptomatic patients should have annual surveillance endoscopy with biopsy. After laparoscopic antireflux surgery, patients with Barrett esophagus have symptomatic relief and reduction in medication use equivalent to non-Barrett patients. Absence of progression to high-grade dysplasia or adenocarcinoma suggests that laparoscopic surgery is an effective approach for the management of patients with Barrett esophagus (Am J Surg 2003;186:6).
Barrett ulcers usually heal with medical therapy. Frequently, 8 weeks of treatment with an H2-receptor antagonist or proton-pump inhibitor are necessary to achieve complete healing. Recurrence of ulcers is common after discontinuation of therapy. Ulcers that fail to heal despite 4 months of medical therapy are an indication for rebiopsy and antireflux surgery.
Strictures associated with Barrett esophagus are managed successfully with periodic esophageal dilation combined with medical management. Recurrent or persistent strictures warrant an antireflux operation combined with intraoperative stricture dilation. After surgery, several dilations can be required to maintain patency during the healing phase. Rarely, undilatable strictures require resection.
Dysplasia on biopsy of Barrett esophagus indicates that the patient is at risk for the development of adenocarcinoma.
Low-grade dysplasia requires frequent (every 3 to 6 months) surveillance esophagoscopy and biopsy. Medical therapy for GER is recommended in these patients, even when asymptomatic.
High-grade dysplasia is pathologically indistinguishable from carcinoma in situ and is an indication for esophagectomy. Patients who undergo esophagectomy for high-grade dysplasia have up to a 73% incidence of having a focus of invasive carcinoma present in the resected esophagus. Cure rates of nearly 100% can be expected in patients whose cancer is limited to the mucosa and who undergo esophagectomy (J Thorac Cardiovasc Surg 1994;108:813). Because of the morbidity and mortality associated with esophagectomy, other methods of treatment have been evaluated, such as photodynamic therapy. A recent randomized, phase III trial was performed comparing photodynamic therapy versus omeprazole alone for patients with Barrett and high-grade dysplasia. It showed that photodynamic therapy can reduce the incidence of esophageal adenocarcinoma (Gastrointest Endosc 2005;62:488).
Adenocarcinoma in patients with Barrett esophagus is an indication for esophagogastrectomy. Early detection offers the best opportunity to improve survival after resection, which overall is 20% at 5 years.