Time Stamps

• 4:12 What is Barrett’s esophagus?
• 8:41 Who do we screen for Barrett’s, and why?
• 13:50 How do we screen for Barrett’s and counsel?
• 18:21 How do we treat and monitor Barrett’s esophagus?
• 21:45 Take Aways
• 23:05 Throwback to trending troponins

Show Notes

Pearl 1: What is Barrett’s esophagus?

• Barrett’s esophagus is metaplasia of the normal squamous epithelium of the esophagus to columnar epithelium.
• Estimated prevalence of Barrett’s in the general population is 5%, and the majority have do not have dysplasia, but if there is high grade dysplasia, there is a 7% annual risk of developing adenocarcinoma, which is what we ultimately want to prevent.

Pearl 2: Who do we screen for Barrett’s, and why?

• According to the American College of Gastroenterology (ACG), we should screen men who have chronic GERD and have at least two risk factors: Caucasian race, age over 50 years, any smoking history, central obesity, or a 1⁰ relative with barrett’s or esophageal adenocarcinoma.

Pearl 3: How do we screen for Barrett’s and counsel if they do have Barrett’s?

• Screening is done with an upper endoscopy (EGD) with 8 biopsies and is specially reviewed by expert pathologists.
• The majority of patients with Barrett’s will have the nondysplastic type. Per Dr. Shaheen, it should be phrased to the patient as, “This is a chronic disease like any other chronic disease, diabetes, hypertension, etc. We check certain parameters to make sure that you’re not having your disease worsen, you should think about this. The overall risk of progression is quite low.” 

Pearl 4: How do we treat and monitor Barrett’s esophagus?

• Patients with Barrett’s esophagus should be on a once daily PPI because of its chemoprotective nature, even in the absence of GERD symptoms.
• Patients with nondysplastic Barrett’s should be reassured that there is low rate of progression, and should have repeat EGD every 3-5 years for surveillance.
• If there is low grade dysplasia, the patient can choice between surveillance with more frequent EGDs or radiofrequency ablation.
• If there is high grade dysplasia, first-line treatment is radiofrequency ablation followed by routine surveillance.

Pearl 5: Throwback to trending troponins

• The delta, or change in between the two values of troponin, can help guide suspicion for ACS in less clear cases.

Transcript

Shreya: I’m really excited to talk about this! At first I thought Barretts was straight forward but as I started reading more, there were nuances that were fascinating, confusing and left me excited to share these nuggets with you all

NICHOLAS SHAHEEN: And unfortunately I think that our specialty has given people even more reason to be confused because as we’ve learned more about the disease, we keep evolving and changing recommendations such that, um, you know, there was a time when patients with Barrett’s were told to get an endoscopy every year. And, if you’ve had Barrett’s for 30 years, you’ve lived through probably four or five iterations of these guidelines and we’re treating you- you haven’t changed. But we keep changing.

Marty: thats Dr. Nicholas J. Shaheen is Professor of Medicine and Epidemiology at UNC and Chief of the Division of Gastroenterology at UNC. He also helped write the American College of Gastroenterology guidelines on Barrett’s esophagus. You’ll hear from him periodically throughout the podcast

Pearl 1: What is Barrett’s esophagus, and should we even care?

Marty: Alright I have my first disclosure to make…

S: What! A disclosure? Marty have you given in to big pharma?

Marty:  Oh, well, no… a different kind of disclosure.  Here is it – I love Sriracha. And Franks. And Wasabi.  And I selfishly sought out this episode to learn more about Barretts because my med school hypochondriasis has finally caught up to me.   

Milna: I feel you, Marty. I also have a confession: I actually am heartburn… personified.!  In fact, I think my heartburn has been giving me heartburn, because I constantly worry: “Is this Barrett’s?”

Shreya: Alright, no more beating around the tamales – time to demystify Dr. Barrett and his legendary Esophagus.  

Vishal: Great call – the history is actually kind of interesting because the man who the condition is named for – Dr. Norman Rupert Barrett – was actually wrong about the pathophysiology.  Barretts is defined by metaplasia, which is when one type of cell is replaced by an entirely different type of cell. In Barrett’s, the normally squamous epithelial lining of the esophagus changes into columnar epithelium.  Dr. Barrett actually thought that the columnar lining of the esophagus – which is usually found in the stomach – represented a “congenital short esophagus”.

Marty: If you’re into the history of the name we’ll link a cool paper from the journal of gastroenterology and hepatology which goes through the story.  

Milna: Barretts usually occurs in the setting of chronic inflammation, most commonly chronic gastroesophageal reflux but as we will see in Pearl 2 this doesn’t always check out!

Shreya: One of the cool things to understand about this change in cell type is how it might play into what a patient might be experiencing!

NICHOLAS SHAHEEN: One of the pearls that primary care docs can take home is that if you have a patient,  if you have a white male fat patient who comes in and says, you know, doc, I don’t know why, but for whatever reason my reflux has gotten spontaneously better and you haven’t changed their medicine, that may not be any cause for joy.

Shreya: I kind of geek out about the pathophys here… thinking about how these of columnar cells – that are usually in the lower down in the GI tract – but now in the esophagus respond to acid? We know these columnar cells are more resistant to acid and so if its in the esophagus, its  gonna be less sensitive  irritation from the acid.

NICHOLAS SHAHEEN: The way these studies were done is, um, they did what’s called Bernstein tests and what a Bernstein test is that you put to tube  somebody’s nose and you drip acid in their discipline esophagus and the the people w/ Barrett’s got less symptoms.

Marty: How much do you guys want to bet that he’s talking about med students… always med students…. Listen the scary part of Barrett’s isn’t necessarily that first transformation from squamous epithelia to columnar, but further changes that are labeled “dysplasia”.  And it’s really those the sum total of these changes increase risk for true cancer.    

Shreya: Exactly, a good analogy here is to think of Barrett’s like we think about pap smears which looking for metaplasia in the cervix.

Milna:  Sorry but the idea of pap smears in my esophagus is not easing my reflux… Alright Vishal break it to me gently, how much time do I have left?

Vishal: Easy Milna!  Only 5% of the overall population end up actually having Barrett’s.  

Milna: 5%!  5% of the U.S. probably represents millions of people.  

Shreya: But I guess the real issue isn’t how many people have Barrett’s; it’s about how many people develop adenocarcinoma.

Vishal:  Right, and risk of progression from Barrett’s to cancer varies significantly based on how abnormal the cellular architecture has become. We call that dysplasia, and we categorize it into low or high grades depending on how abnormal the cells have become.

Milna:  Ok, what’s the chance of Barrett’s converting to adenocarcinoma?

Vishal: For low grade dysplasia, the annual risk of progression is 0.7% per year, but if you find that your patient’s got high grade dysplasia, their risk for developing cancer is about 7% per year.

Marty: Ok so to review the key points from this pearl:   BE is metaplasia of squamous to columnar epithelium – this matters because the estimated prevalence of Barrett’s is 5% in the general population, and of those with high grade dysplasia, there’s about a 7% annual risk of developing adenocarcinoma, which is ultimately what want to try and prevent.

Vishal: The good news here is that we can, and should screen our patients for Barrett’s!  More on this after the chime…

Pearl 2: Screening Population for BE

Milna: Ok so if the prevalence of GERD is increasing in the U.S., with Marty and me contributing to that increasing number, should us GIM doctors be as diligent about Barretts as we are about pap smears?

Marty: This might be a good opportunity to bring in a case.  Mr. Harry T. Burn is a 55 year old overweight white male nonsmoker, with diet-controlled diabetes who is coming in to clinic with a year-long history of intermittent reflux symptoms.

Vishal: Thinking about who to screen is to really about looking for people who would be at highest risk for esophageal cancer

NICHOLAS SHAHEEN: We’re trying to take a relatively high cost screen test, upper endoscopy, apply it to a relatively low risk population. Even in those with Gerd. This cancer’s relatively rare.  So what we need to do is to tailor our screenable population as best we can to the group that’s going to be highest yield.

Shreya: And that’s what the 2016 ACG guidelines focus on just that, better risk stratification of who should get an endoscopy

NICHOLAS SHAHEEN: we know for a long time that gerd was a risk factor for both Barrett’s and cancer, but there are a lot of other risk factors that are actually really useful that we probably don’t make as much use of as we should in primary care.

 Another real, another really simple one, but I don’t think people adequately appreciate his gender. Um, men are much more likely to get both Barrett’s and this cancer. Um, in fact, if you take, if a 60 year old man without gerd drives his 60 year old wife with gerd to the endoscopy center so that she can get her screening endoscopy, the driver is actually at higher risk for Barrett’s than is the patient. And I, I think a lot of people don’t recognize that.

Vishal: Yep and so the new guidelines say we should screen men WITH chronic GERD symptoms for over 5 years and and with 2 or more of the risk factors

Marty: Some other known factors for progression to cancer, includes being Caucasian, age over 50 years, any smoking history. You’ve also got to ask if the patient has any first-degree family members with a history of BE or esophageal adenocancer

NICHOLAS SHAHEEN: One really important one that’s become evident is truncal obesity. If, uh, if people have a lot of intraabdominal fat, they’re clearly at much higher risk for both berets and this cancer

Shreya: What I find fascinating about this screening recommendation being men with chronic GERD sx and 2 RF is the stat that 40% of pts who get esophageal CA NEVER had any symptoms of GERD! So heartburn is not the be all end of all.

NICHOLAS SHAHEEN: And one side effect of doing this, of tailoring our population is that we’re going to lose cases. Um, well we knew that upfront. In a perfect world that would be terrific to be able to screen everybody say over the age of 50. The problem is that the cost effectiveness of that with an expensive screening tests in a rare cancer is so prohibitive that were forced into this situation of trying to really focus in on high risk groups.

Shreya: It’s so interesting what Dr. Shaheen points out here – how population health dilemma goes into these screening guideline. Its limiting the screening pool so that the prevalence of disease is high enough so that the intervention is cost effective.

Milna: And another part I think that can get confusing about the guidelines is what does 5 years of GERD even mean? Do people have to have heartburn for 5 straight years?

Marty: Right – so it’s probably going to be a gestalt thing – we’re looking for either symptoms of GERD for 5 years or the absence of symptoms with PPI for that time period.  

Milna:  Ok guys lets bring it back to our case… so, hes caucasian, male with truncal obesity, but he doesn’t have over 5 years of GERD symptoms, so he’s probably in the clear. See, Marty — you and I have nothing to really worry about!

Marty: I don’t know, Milna. I have this weird feeling that, one day, I’ll be an older Caucasian male with longstanding GERD and central obesity. Long story short, you’re not making me feel any better.

Shreya: Aw, Marty. Maybe you should do a trial of a PPI and see if you can get your heartburn under control! Oh and that gives me flashback to our previous 5 Pearls Segment on PPIs, remember to take that PPI at least 30 minutes before your first meal to get the biggest bang for your buck

Marty: Thanks, Shreya, good point, and props for the hashtag spaced repetition you snuck in there.

Milna: Yeah, Shreya — we see what you did there!

Shreya: Haha, #learningtheory – oh now I’m starting to sound like Marty…

Marty: Fair enough. OK – to summarize.  The American College of Gastroenterology has recommended screening for BE for men with GERD > 5 years and two more risk factors like: Caucasian, age over 50 years, any smoking history, central obesity or family history of barrett’s or esophageal adenocarcinoma.

Vishal:  And despite these guidelines, keep in mind that reflux symptoms are neither sensitive nor specific for Barrett’s esophagus.

Pearl 3: Screening methods for BE / Counseling patients

Shreya: As a primary care doctor, I always wanna give my patients a sense what to expect when I send them to specialists for for testing. So, say our older male did HAVE chronic symptoms, and 2 additional risk factors that we send him to GI, what can i tell them to except:

Milna: So, when you send your patients to GI for an EGD, there’s a catch. Barrett’s tends to occur in a mosaic pattern, so we can easily miss it and the results can be very variable and subjective.  Our past experience has shown limited accuracy if you just grab biopsies willy nilly. GI doctors have to follow a very systematic biopsy protocol, where they grab at least 8 biopsies, and then the path needs to be read by not one but TWO pathologists, with experience in BE pathology.

Shreya: So, two pathologists – that must be to decrease inter-observer variability. Man, screening isn’t a piece of cake, is it?

Marty: Nope, no it isn’t…

JOE KINGSBERRY: a lot of times in the biopsy results you get these indeterminate results and then then requires a base to come back again within six months and then at the end determinant. And again, then you’re basically do an egd every year until, it’s definitely negative word, definitely positive.

Marty: That was Dr. Joe Kingsbury – a current third-year GI fellow at NYU and friend of the pod.  We know Joe from residency where he took home multiple resident and fellow of year awards for his clinical knowledge and excellence in teaching.  

JOE KINGSBERRY: just embarking down that path, like referring to Gi for this specific issue is a, it’s really like the patient thing. Yes, absolutely. No doubt. I want probably multiple procedures, um, just for peace of mind or whatever. But that’s the conversation that can definitely be held, I think before they even see us. Because if they’re like, Oh God, if this is a one and done, then cool. But if I’m going to be going back like a bunch of times a year or every couple of years and I don’t even want to go down that path.

Vishal: So this is where patient-centered decision making comes into play. You and your patient should have a conversation about the risks and benefits of initiating screening. It may not be so cut and dry for every patient.

Shreya: Ah I love these patient convos! This is where the real art of medicine comes in!

Marty: So say we talk to our patient Harry T about whether its even worth heading down that road but he wants some piece of mind and go for their EGD, then what?

Milna: Well the biopsies would come back, and the first branching point would be if there is or isn’t any metaplasia. If negative for metaplasia, he doesn’t have Barrett’s and you stop there.

Vishal: But if the biopsy results indicate metaplasia, then he has Barretts. There are 3 kinds of flavors of positive BE biopsies. You’ll see BE with no dysplasia, BE with low grade dysplasia, and BE with high grade dysplasia.

Milna: And Dr. Shaheen had a good way to think about patients with nondysplastic Barrett’s.

NICHOLAS SHAHEEN:  once they’re told they have Barrett’s and it’s a potentially a precancerous condition, that’s the last thing they  hear.

But your risk of progression is about 3 per 1000 in any patient year. So the nondysplastic barretts, so  over 80% of patients diagnosed with barrett’s will have nondysplastic Barrett’s and the vast majority of those will remain with non dysplastic barrett’s for their entire life. Those patients have very low risk of progression and over 95% chance that they won’t, um, develop esophageal cancer. So with those patients need to hear from you is reassurance.

Marty: That is reassuring, but again there’s definitely an art to how we talk to patients about this

NICHOLAS SHAHEEN: it should be phrased to the patient is this is a chronic disease like any other chronic disease, diabetes, hypertension, etc. We check certain parameters to make sure that you’re not having your disease worsen, you should think about this. Just like that. The overall risk of progression is quite low.

Shreya: But if low-grade or high-grade dysplasia? What are the key thing to talk to our patients about?

Milna: if the path report comes back with dysplasia, you gotta make sure they understand the follow up, more on that in pearl 4

Marty: So let’s review screening procedure for BE.  Screening itself is a endoscopy – but with extra biopsies and specially reviewed by expert pathologists and if the patient has nondysplastic Barrett’s the key really is reasurrance that this a noncancerous condition with low likelihood for progression, and we will continue routine surveillance to make sure it doesn’t.

PEARL 4: So, your patient has BE. Now what? Treatment & Surveillance

Shreya: So, what does the treatment and surveillance look like for our patient has Barrett’s?

Milna: Well, for surveillance, it depends on the grade of dysplasia. If your patient has BE without dysplasia, it’s important they understand they need a repeat EGD every 3-5 years, which sounds like a reasonable time to wait as it takes a long time to progress to dysplasia anyway.

Marty: And ACG now recommends PPI therapy in patients with BE, even in the absence of GERD sx because of its chemoprotective effects

Milna: And we have good data to support chemoprotection. In a recent meta-analysis based on 7 studies with almost 3000 patients, PPI users had a 71% reduced risk of progressing to high grade dysplasia or cancer. The same benefit was not been shown with any of our H2 blockers, like ranitidine, so PPIs rule the day.

Shreya:  Remember there is risk with chronic PPIs  like hypomagnesemia and osteoporosis that we talked about in our previous episode on PPIs. But it sounds the benefits outweigh the risk.

Milna: There you go again with the spaced repetition.

Marty:  Just wait to see how we weasel in a pearl from our contrast induced nephropathy episode…

Shreya: Yep – always looking for an opportunity.  Stay vigilant, Marty.

Marty: Oh I’m on it.

Vishal: Hah alright guys. And what about surveillance for our dysplastic folks?

Milna: If low grade dysplasia, there’s a choice to either get endoscopic treatment, or get annual EGD surveillance.  

Vishal: What about high-grade dysplasia?

Milna:  Right, right, so these are the patient’s we’re trying to find! Well, GI is going to want to treat that bad boy with radiofrequency ablation, which is pretty good at delaying the progression from dysplasia to cancer

Marty: And after ablation, patients need to have a pretty intense surveillance by GI, so at that point it’s our job in primary care to make sure these patients don’t get lost to follow up!

NICHOLAS SHAHEEN: we found that by giving endoscopic treatments to these patients, you can cause the inner lining of the esophagus to change back to squamous from comulmnar. So what you do is you go in with the scope and on the tip of the scope, you either put devices that burn or freeze the tissue and if you destroy the tissue and give the patient rigorous acid suppression, what comes back is not the precancer cells anymore, its squamous lining. And in doing well you can drop their risk of getting cancer by 90%.

Shreya: Thats great and makes me think why dont just ablate everyone with barrett’s?

NICHOLAS SHAHEEN: And the thing is that there are lots and lots of people there. It’s the vast majority has non dysplastic barrett’s and interestingly the complication rate of these ablation procedures, well not real high is 6%. So I’m taking, I’m taking a procedure, um, that has a 6% complication rate to get rid of a condition that has a three per thousand risk of progressing. So you can see the math doesn’t work out. It’s only when you get displayed and the risks go up.

Vishal: So let’s summarize what I am hearing, patients with Barrett’s should be on once daily PPI. If your patient has BE without dysplasia, just screen every 3-5 years, and low-grade you have a choice between screening and treatment – but if high grade dysplasia is found the next step is radiofrequency ablation. In all cases of dysplasia,  ensure that your patients have good follow up with GI for appropriate surveillance.

Take Aways:

Marty: Nice Vishal.  Let’s take it all the way back to pearl 1 and finish this episode off by summing up some of our great clinical pearls on Barrett’s Esophagus.

Shreya: Pearl 1- Most people with Barrett’s actually die of reasons unrelated to Barrett’s, but despite that, we’ve got to keep in mind that patients with high grade dysplasia have an elevated risk for progression to cancer.

Vishal: Pearl 2- Screen males with longstanding GERD if they have more than 2 risk factors, including age older than 50, caucasian race, smoking history, central obesity, or family history. Remember, you should generally avoid screening women, unless they have indications for a diagnostic referral.

Milna: Pearl 3-  When you screen patients, the biopsy confirmation of BE can be super cumbersome, so make sure your institution has experienced professionals so you can make an accurate diagnosis, and be sure sit down with your patients and talk about the risks and benefits of screening before you send them to GI.

Marty- So pearl 4 was all about treatment – all patients with Barrett’s should also be on once daily PPI. Without dysplasia just screen every 3-5 years, and high grade dysplasia is treated with endoscopic ablation. If you have low-grade dysplasia you have a choice between treatment and surveillance.  Follow-up is crucial which was can help with in primary care.

Pearl 5: The troponin trend

Vishal: For our throwback to the troponin podcast, I really liked the discussion about trending troponins

Shreya: Yeah there’s always been dogma to write in your note trend troponin q8hr

Milna: Yeah I’ve heard q8hr, q4hr, q6hr

Marty: What I took away is that the troponin interval should depend on what we’re looking for – if I’m trying to rule out plaque rupture I’d rather not figure that out 8 hours later.   

Shreya: And the important imp thing about this pearl what thinking about the pattern of rise. What can the delta of  change in troponin over time?

Milna: Well, basically, if there is a giant jump in your patient’s troponin from say, 0.06 to 5 within 2-3 hours, then you can be fairly certain you’re dealing with a likely ACS situation, and you should be looping in Cardiology and activating your cath lab.

Vishal: On the flipside, if there is a small delta, say 0.06 to 0.09 in 6 hours, it might just indicate that the heart is stressing because of something else, like when ur resident forces you to walk up 16 flights of stairs on your night shift.

Marty: Do you have something you’re trying to tell me Vishal?

Vishal: You can’t just stress test without asking Marty!

Marty: I do it because I care Vishal.

Shreya: And time to stop. Alright thanks for listening!

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