New Barrett's Esophagus Guidelines May Be Practice-Changing

This transcript has been edited for clarity.

Hello. I'm Dr David Johnson, professor of medicine and chief of gastroenterology at Eastern Virginia Medical School in Norfolk, Virginia.

Barrett's esophagus is something we all deal with in gastroenterology. Our primary care colleagues often refer patients to us for endoscopic screening. Depending on what we find, it can raise a host of questions about what to do next.

Dr Nicholas Shaheen and his colleagues on the expert consensus group put together the new American College of Gastroenterology (ACG) guidelines on the diagnosis and management of Barrett's esophagus. This is a nearly 30-page tome that is full of evidence-based recommendations, which I suggest you read in full. But for today, I'd like to give you some snapshots of what I consider to be the most impactful, potentially even game-changing, implications of these recommendations upon what we currently do and might need to do going forward.

Making the Diagnosis

The finding of intestinal metaplasia is really the gold standard when it comes to diagnosing Barrett's esophagus. However, the ability to do so using biopsy may be spotty.

So, if you have a patient that you think has Barrett's esophagus but you haven't observed goblet cells, you should consider that they do not have Barrett's esophagus, or you can bring them back again at a later point.

But the diagnosis of intestinal metaplasia requires the presence of goblet cells. This was made evident by an analysis from the University of Chicago. Investigators looked at their data and determined that if you remove the requirement of intestinal metaplasia (the histologic term for this), it would increase the diagnosis of Barrett's esophagus by 147%. That would obviously have a significant impact not only on access but also on costs.

The authors refer to the Prague C & M Criteria — it's not an official recommendation in these updated ACG guidelines but rather a standard recommendation for endoscopic reporting. If you're not familiar with these criteria, you need to be. It uses standardized terminology for both circumferential length (C) and the mucosal extension (M).

One piece of diagnostic advice that really resonated with me was the recommendation to not perform a biopsy in patients with a normal-appearing Z line.

This is based on a couple of studies which looked at patients with short-segment Barrett's esophagus established by intestinal metaplasia who were followed-up for 7-8 years and 6 years, respectively. Investigators found that there was zero risk for development of high-grade dysplasia or cancer in those with an irregular Z line < 1 cm. Interestingly, one of the studies actually found that on repeat evaluation, only 53% still had a diagnosis of intestinal metaplasia.

These results indicate that we probably overdiagnosis this. Please don't biopsy in a normal or irregular Z line. This is something that the authors made as a repeated recommendation.

When considering biopsy from the tubular esophagus, one of the great godfathers to the esophagus, H. Worth Boyce, always made the point about looking at the proximal margin of the gastric folds.

The guideline authors cite a brilliant strategy for not doing this. Instead, they advise to deinsufflate the esophagus before you start to define where the gastroesophageal junction truly is. This is because overdistension sometimes flattens the gastric folds, misleading you to see a hiatal hernia instead of what might otherwise be the tubular esophagus.

The authors also recommend specific endoscopic biopsies that should be done by standard Seattle protocol criteria, which calls for four quadrants every ≤ 2 cm in the absence of dysplasia or visible lesions.

But if you have a shorter segment of Barrett's esophagus (< 3 cm), do at least four biopsies per centimeter of circumferential Barrett's esophagus and one biopsy per centimeter in the tongues of Barrett's esophagus, again using the Prague criteria.

Dealing With Suspected Barrett's Esophagus

If you have a patient whom you suspect of having Barrett's esophagus and who you need to bring back because you didn't find goblet cells, the relative yield for that on repeat examination is only about 25%.

So, if you still think somebody has Barrett's esophagus, based on a longer segment and there's no evidence of goblet cells, bring them back to repeat it once, but recognize that it's not necessarily going to be all that helpful.

Biopsies that show dysplasia should be referred for a second opinion, regardless of where you are in the endoscopic evaluation. This second diagnosis needs to be established by an expert pathologist, which they define as somebody in the region who has a special interest in Barrett's esophagus–related neoplasia and is recognized as an expert by their peers. That second opinion needs to come regardless of whether you're dealing with indeterminate, low-grade, or high-grade dysplasia.

The advice on when to refer for Barrett's esophagus was interesting as well.

The authors used a stratified algorithm looking at relative risk based on three or more criteria, in addition to the chronic gastroesophageal reflux disease symptoms lasting 5 or more years. These risk factors include male gender, age older than 50 years, Caucasian race, tobacco smoking, central obesity, or family history of Barrett's esophagus or esophageal adenocarcinoma. Each of these relative factors increase the prevalence of Barrett's esophagus by approximately 1.2%. So, when you observe three or more of these factors, you'll want to start to consider screening.

It's notable that the authors excluded women, although they clearly can get adenocarcinoma of the esophagus and Barrett's esophagus. However, they did recommend that if you have a woman fulfilling multiple risk factors for Barrett's esophagus, you will want to individualize your approach and potentially prioritize them for endoscopic screening.

If patients have an initial negative endoscopic screening for Barrett's esophagus yet still have ongoing symptoms, the question is when to bring them back for repeat endoscopy.

The guideline authors cite a very extensive study from the Clinical Outcomes Research Initiative database, where they looked at over 24,000 patients undergoing repeat endoscopy. In bringing these patients back, only 2.3% had repeat exams that yielded a diagnosis of Barrett's esophagus.

The exception is in patients who have erosive esophagitis, which may hide Barrett's esophagus. The recommendation here is that patients with erosive esophagitis of Los Angeles grades B or worse should be put on a proton pump inhibitor (PPI). After 8-12 weeks of treatment with PPIs, they can be brought back upon healing and then fully assessed for evidence of Barrett's esophagus.

Surveillance Techniques

Next, the authors delved into the technological advances that we have for surveillance of Barrett's esophagus.

There are chromoendoscopy applications for Barrett's esophagus, such as acetic acid or electronic chromoendoscopy, which can be applied in surveillance. But most of us rely on more standard techniques, like narrow-band imaging, which can highlight the dysplasia-carcinoma–related changes due to an irregular mucosal or vascular pattern.

The Barrett's International Narrow-Band Imaging Group (or BING) has formalized and validated an endoscopic assessment for Barrett's esophagus using narrow-band imaging. You should be evaluating this when you start to look for and report upon Barrett's esophagus in your patients.

But the overarching point is that directed biopsies with chromoendoscopy should not take the place of standard biopsy techniques. Biopsy those areas, but do not use as a substitute for standardized biopsies. I think that was a really resonant point.

The authors also discuss the idea of a structured biopsy protocol. Evidence suggests that only approximately 52% of community-based practices use the Seattle protocol. We need to do better. We need to document how many biopsies we're doing and how the intervals are substantiated as it relates to quality.

Once Diagnosed, How to Manage It

For the management of high- or low-grade dysplasia, the strength of evidence supported additional histologic confirmation by a pathologist with expertise in Barrett's esophagus, followed by endoscopic approach for resection/eradication.

The standard endoscopic intervention was really favored, though certainly not to refer patients for surgery unless there were some other mitigating factors, such as an obvious invasive carcinoma.

I thought the authors provided important recommendations for the management of nondysplastic Barrett's esophagus. This is because they separated the interval on the basis of the length.

For length < 3 cm, it was now recommended to increase the interval; rather than bringing them back in 3 years, you should now bring them back in 5 years. The development of esophageal-related high-grade dysplasia or cancers was nearly fivefold greater for the longer length of Barrett's esophagus. This is something that I think we can also do better at. That's backed up by the fact that this was a strong recommendation based on moderate-quality evidence. So, moving this from 3 to 5 years is something that we can probably take to the bank and start applying going forward.

The authors also recommend extending what we currently do in the colon to Barrett's esophagus: That is essentially saying to stop surveillance when it's no longer appropriate. This is a recommendation based on the relative risk for endoscopic eradication therapies for somebody based on their other comorbidities.

They cite a study of Medicare enrollees, in which investigators looked at a group of men aged 80-84 years and found that 79% of those with a life expectancy of < 5 years still underwent surveillance for Barrett's esophagus. This is crazy. We need to start to rein this in on the basis of age, as we do in the colon. Start to consider cessation of surveillance at age 75 years. And certainly, if there is a relative comorbidity risk, consider stopping long before that.

Regarding PPI therapy, the authors could not make a formal recommendation about combining it with aspirin, as we saw from the AspECT trial a number of years ago. They did recommend using PPIs once a day and twice a day if patients are unable to control symptoms.

The authors do touch on a variety of algorithms for differentiating low- and high-grade dysplasia, but those are a little bit more complicated and beyond the scope of this conversation.

The final recommendation I'd like to discuss, which I think was very important, was about patients who have completed successful endoscopic eradication therapy. They noted that 87% of recurrences of intestinal metaplasia in the tubular esophagus were detected within 5 cm of the distal esophagus. In the area of the esophageal gastric junction, it was absent 60% of the time.

The recommendation here is if you don't see something, you should do at least two biopsies in separate jars: one from the esophageal gastric junction in the fundus and the second from the neosquamous epithelium, particularly in the distal 2-5 cm of the esophagus. Submit them separately, and you may see that there's submucosal evidence of Barrett's esophagus, in particular in the tubular esophagus, but don't forget the esophageal gastric junction.

Hopefully, these recommendations have highlighted a few wake-up calls, things that we can do better at, and things that will change our practice. They're based on what I'd consider moderate, and in some cases, strong evidence. I suggest that you review these guidelines in their entirety, think about them, and put them into practical application.

I'm Dr David Johnson. Thanks for listening.

David A. Johnson, MD, a regular contributor to Medscape, is professor of medicine and chief of gastroenterology at Eastern Virginia Medical School in Norfolk, Virginia, and a past president of the American College of Gastroenterology. His primary focus is the clinical practice of gastroenterology. He has published extensively in the internal medicine/gastroenterology literature, with principal research interests in esophageal and colon disease, and more recently in sleep and microbiome effects on gastrointestinal health and disease.

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