The esophagus is susceptible to acid damage which can lead to the uncomfortable sensation of acid reflux or gastroesophageal reflux disease (GERD). Over a period of months to years of acid exposure, the esophagus can change to a more acid-resistant type of skin called “specialized intestinal metaplasia” which resembles stomach tissue and can produce protective mucous with “goblet cells”. Finding goblet cells and specialized intestinal metaplasia confirms the changes of the skin are true Barrett’s esophagus and not simple esophageal inflammation or esophagitis. Sometimes the stomach tissue can migrate upward into the esophagus and look like Barrett’s but biopsies will not show characteristic changes.
Your endoscopist/scoping physician will recognize the end of the pale pink esophageal tissue meets a more “salmon pink” skin type. This upper border is called “the squamous-columnar junction” or SCJ. The distance of the Barrett’s segment is then measured from the SCJ to the very top extent of the gastric folds of the stomach. This second landmark is referred to as the “esophagogastric junction” and represents the bottom of the esophagus.
Barrett’s esophagus is sometimes further classified by length.
The overall risk of having Barrett’s esophagus in the general population is 1.6% on studies out of Sweden.
When the skin of the esophagus becomes damaged and changes to Barrett’s epithelium or skin, it can predispose you to cancer.
These cell changes are referred to dysplasia and can be either low grade or high grade depending on the appearance under the microscope. Experts do not always agree on the features that constitute these dysplastic changes, so before considering surgery or other drastic therapy, the slides may be sent out for a second opinion. The type of cancer associated with Barrett’s esophagus is adenocarcinoma of the esophagus. The incidence of this cancer is on the rise likely due to link with GERD.
The risks are not high. The rate is thought to be 0.1-0.3% development per year. The purpose of endoscopic surveillance is to identify cancer and dysplasia at an early stage improving prognosis and likelihood of potential endoscopic vs. surgical cure. If cancer grows to the point of esophageal obstruction the prognosis becomes very grim.
There are no specific symptoms of Barrett’s esophagus—we tend to look for the diagnosis in patients with traditional gastroesophageal reflux symptoms such as:
The only sure was to see if you have the condition is to undergo upper endoscopy and biopsy of suspicious tissue if present. Biopsy of both short and long segments usually involves taking biopsies of any suspicious nodules/lesions and then four quadrant biopsies every two centimeters of length. This collection is termed the Seattle protocol. Newer scopes may have the ability to visualize changes of the skin using optical techniques (narrow band imaging) or we can use special dyes to help identify areas needing biopsy for dysplasia/cancer.
Treatment of the underlying reflux should be your first step:
Barrett’s treatment can require high level acid suppression and so pharmacologic therapy with proton pump inhibitors is important-- especially if dysplasia is present.
Medications such as omeprazole/prilosec, pantoprazole/protonix, lansoprazole/prevacid and esoprazole/Nexium are particularly good at suppressing acid for various intervals. We usually suggest taking these before supper for best effect.
Aspirin 325 mg per day may be helpful as well based on the AspECT trial.
Don’t panic, these do not necessarily mean you have cancer. You need to consult with your gastroenterologist to find out what the next step will be. Sometimes this means higher level acid suppression to twice daily and a endoscopic recheck of Barrett’s in 1-6 months. Dysplasia may mean you need to be referred to a center that does radiofrequency/thermal ablasion of the Barrett’s tissue—burning this away. This treatment does carry some increased risk of strictures and unlikely perforation. Evaluation of lesions with endoscopic ultrasound is sometimes required to evaluate the depth of penetration of a potentially cancerous lesion. Surgery is rarely advocated these days, but may still be appropriate to your situation. This would also depend on your comorbidities, i.e., other illnesses you may have. For patients without dysplasia, repeat endoscopy every 3-5 years is the current standard of care.