10. Barrett’s Esophagus
Definition
Barrett’s esophagus (BE) is a peptic ulcer in the lower esophagus, often associated with stricture, caused by the presence of columnar-lined epithelium. The columnar-lined epithelium may contain functional mucous cells, parietal cells, or chief cells in the esophagus instead of the normal squamous cell epithelium. The presence of specialized intestinal metaplasia (SIM) with goblet cells confirms the diagnosis of BE.
Incidence
The incidence is divided into two subtypes: long-segment Barrett’s esophagus (LSBE) and short-segment Barrett’s esophagus (SSBE). In LSBE, the incidence is reported to be 0.3% to 2% of the entire population, but 8% to 20% in patients with gastroesophageal reflex disease (GERD). In the United States, the incidence is 376:100,000, predominately in Caucasian males. In SSBE, the incidence is reported to be 5% to 30%.
Etiology
BE is a complication of GERD. Patients who develop BE usually have a combination of symptoms. Prolonged esophageal acid fixation produces erosive esophagitis. The pH of the refluxate, combined with the duration of contact with the esophageal mucosa, determines the degree of mucosal injury. Prolonged exposure erodes the esophageal mucosa, promotes inflammatory cellular infiltrates, and can culminate in epithelial necrosis. The damage and necrosis lead to replacement of the damaged tissue with metaplastic columnar cells, the origin of which is not understood. Patients with LSBE generally have longer durations of reflux symptoms, severe combined patterns of reflux (in both supine and erect positions), and low pressure at the lower esophageal sphincter (LES). LSBE patients are less sensitive to direct acid exposure to the esophagus. SSBE patients have a greater sensitivity to direct acid exposure to the esophagus, shorter duration of reflux, and only upright (erect) reflux.
Signs and Symptoms
• Acid regurgitation
• Delayed esophageal acid clearance time
• Duodenogastric reflux
• Dysphagia (occasional)
• Hiatal hernia
• Pyrosis
• Reduced lower esophageal sphincter tone
Medical Management
BE does not warrant a specific therapeutic regimen. Treatment is primarily for the associated GERD, which entails use of histamine (H 2)-receptor antagonists and proton pump inhibitors (PPIs). PPIs may prove more advantageous than the H 2-receptor antagonists because of the relative insensitivity of patients with BE to esophageal acid. Dietary alterations are also part of the treatment regimen, such as elimination of fatty foods, fried foods, chocolate, alcohol, coffee, and citrus fruit or juices. Weight loss and smoking cessation are also of great importance in the treatment of BE. Surgical treatments, such as Nissen fundoplication, do not reverse BE nor do they halt or prevent the progression to development of esophageal cancer. Periodic endoscopic evaluations are needed to monitor the progression of the disease.
Complications
If left unchecked, BE can progress to esophageal cancer. This occurs in approximately 0.5% of cases. When dysplasia is high grade, the standard treatment is surgical esophagectomy. Other complications include esophageal perforation, mediastinitis, and hemorrhage.
Anesthesia Implications
The GERD associated with BE is the primary concern for anesthetists. A rapid sequence induction should be performed. Before anesthesia, the patient should be advised to continue the routine for taking the PPI, especially along with the H 2-receptor he or she has been prescribed.
The use of local anesthetic agents, such as bupivacaine, mepivacaine, and lidocaine should be undertaken with caution because of the increased risk of anesthetic toxicity.
