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Barrett’s Esophagus

Esophageal Anatomy

The esophagus is the long tube used to transport food from the mouth to the stomach. Typically the esophagus is covered with a pale skin called squamous mucosa—this appears flat and plate-like under the microscope. Normally the squamous mucosa ends where the esophagus ends and meets the harsh acidic environment of the stomach. The skin at the stomach is called “columnar” and is much more resistant to the effects of acid used in the digestion of food. It can secrete a protective layer of mucous.

Acid Exposure Leads to Barrett's Esophagus

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.

How does the doctor see Barrett’s esophagus?

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.

  • Short segment is 1-3 cm, seen in about 10-15% of people scoped for reflux.
  • Long segment is >3.0 cm and carries greater cancer risk—it is seen in about 3-5% of people scoped for GERD.

The overall risk of having Barrett’s esophagus in the general population is 1.6% on studies out of Sweden.

Why should I care if I have Barrett’s esophagus?

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.

What is my risk of developing cancer with my Barrett’s esophagus?

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.

How can I tell if I have Barrett’s esophagus?

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:

  • Sour, burning liquid in your mouth
  • Bloating/gas
  • Sternal burning and pain behind the center of the breastbone.
  • Frequent belching or burning
  • Food getting stuck as you swallow, with vomiting as a result. This is an alarm symptom and should prompt you to see a gastroenterologist as soon as practical.

Obese white males after age 50 are particularly at risk for the development of this condition.

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.

What can I do about my Barrett’s esophagus?

Treatment of the underlying reflux should be your first step:

  • Lifestyle changes such as weight loss, eating smaller and more frequent meals and avoiding meals within 2-3 hours of bedtime.
  • Elevation of the head of the bed 6-8 inches can decrease reflux without drugs.
  • Avoid tobacco and trigger foods such as chocolate, tomato-based foods, peppermints and alcohol.
  • Avoid fatty foods and carbonated drinks.

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.

What if my biopsies show low or high grade dysplasia?

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.

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