GERD
Welcome back to the Deep Dive.
Today we're tackling GRD, gastrorosophageal reflux disease.
We've got a whole stack of GI sources, and we're going to build basically the complete roadmap.
That's right.
This isn't just about prescricription.cribing.
We're aiming higher.
We want to give you that board ready walkthrough, a really structured way to think about moving past simple empiric therapy.
Yeah, the goal is mastering the strategy .
Think of it like a mental flow chart, guiding you from that very first patient encounter, the triage, all the way through objective testing and deciding, you know, is this surgical medical or sometimes surprisingly, behavioral.
Exactly.
And it all hinges on getting a couple of key distinctions right .
First, knowing when you actually need to look inside the esophagus..
With an EGD, mean?
Right, an endoscopy.
And second, this is crucial.
Deciding whether you test for reflux while vacation is on medication or after they stop, getting that wrong.
Well, it can lead to years of the wrong treatment.
Okay, let's kick things off with that initial triage.
Patient comes in, Classic Harper, and seems uncomplicated.
Before we even think about a PPI, what's the absolute first hurdle?
The Muskcope rules?
Alarm features?
You have to screen for those first..
If they're present, you skip the whole medication trial, you go straight to EGD.
And what are these non-negotiable red flags?
The big ones are dysphagia trouble swallowing or oophagia, which is painful swallowing?
Unexplained weight loss is another major one?
Things that make you worry about something structural or worse.
Precisely.
Also, any sign of gI bleeding, new iron deficiency, anemia, or interestingly, just being over age 60 with new symptoms, any of those, you need an EG right away to rule out serious stuff before suppressing acid.
Got it.
Now, putting those alarms aside for a moment, there's another group that needs an EG, but it's more for screening, right?
Not necessarily because of active symptoms.
Yeah, that's screening for Barrett's esophagus.
This is for your high risk folks with Chronic GRD, the classic profile, you know, male, white, usually over 50, long history of reflex, often overweight, maybe a smoker.
So even if they feel okay currently , their risk profile warrants a look.
Exactly.
We need to check for Barrett's that specialized intestinal tissue that can develop.
Okay.
So, patient has no red flags, doesn't fit the Barrett screening profile.
Now we're on the standard Empiric PPI trial.
Walk us through how that should ideally go.
It's a process.
You start with a once daily PPI, give it a good four to eight weeks .
And importantly, make sure they're taking it right 30 to 60 minutes before their first meal.
That timing is key.
What if they only get partial relief?
First step isn't always just doubling the dose.
You check timing, you check if they're actually taking it consistently.
If that's all good, then you step up to twice daily dosing before breakfast and before dinner.
Give that another eight weeks.
And lifestyle changes .
We always tell patients about those, but what actually moves the needle?
Well, the list is long, but honestly, only a couple things have really solid evidence. Weight loss is number one, specifically reducing belly fat that directly lowers the pressure pushing stomach contents up.
Makes sense.
What else?
For nighttime symptoms, elevating the head of the bed itself, like putting blocks under the legs six to , that works much better than just stacking pillars.
And yeah, avoiding late meals is standard advice, too.
Okay, let's pause here.
Say the patient does the full optimized BID PPI trial, and they feel great, completely symptom free.
Why would we ever need to do more testing?
Why not just keep him on the PPPI?
That's a really common question.
And the answer , it's a bit nuanced.
Look, if they're older, well-controlled, no major risks, continuing the PPI at the lowest dose that works is often done.
It's common practice.
But there are exceptions.
Definitely.
You need objective testing if you're thinking about long-term therapy in a young person .
You really want proof of the disease before committing them to decades of medicationation.
Or if symptoms keep coming back every time they stop the PPI.
And absolutely, if the patient is considering any kind of anti-flex procedure or surgery..
Right.
If you're going to operate, you absolutely have to prove it GD is the real problem first.
You must.
You need objective evidence of ongoing pathological reflux.
Okay, so let's follow that path.
The patient did the optimized PPI trial, but still has symptoms.
So EGED is the next step.
What's the primary goal of the scope at this stage?
Right.
So here, the EGED is looking for complications like strictures or inflammation, like eophilicosophogitis, EOE, or trying to confirm the GRD diagnosis by looking for a rusivosesophagitis.
And this is where that L.A. Grade trap comes up.
This is exactly where it gets tricky.
The Los Angeles classification, or LA grade for erosive esophagitis, it's graded A through D. Tell us what those grades actually mean in terms of proving GD.
Okay.
LA grades AA and B. You see some small breaks in the ling, maybe to streak here, there.
They're localized, pretty minor.
This is inconclusive evidence.
Inconclusive.
So LAA or B doesn't actually prove GAA.
Correct.
A lot of things can cause minor breaks like that.
Maybe they swallowed a pill that got stuck, maybe just some mild reflux that isn't actually GRD by definition.
So if symptoms persist, A or B alone is not proof.
You need more testing.
Okay, so AB is suggestive, maybe, but not definitive.
What is definitive on AGD?
That would be LA grade C or D. Grade C means the erosions are starting to wrap around the circumference.
Grade D means they're fully circumfntial or large confluent breaks .
That indicates severe undeniable damage from chronic.
So C or D on the scope report means.
Diagnosis secured.
Conclusive GURD.
If you see LA grade CD, GRD is proven anatomically.
You do not need further testing just to prove diagnosis exists.
That's a huge distinction.
CD equals proof, AB doesn't.
I bet a lot of people see AB and just stop there, assume it's G or D. What's the risk?
It's a big risk.
First, you might miss the real cause of their symptoms.
Maybe it's EOE, maybe it's functional.
Second, if you send someone for surgery based only on LA grade A or B, well, the failure rate is much higher because you haven't objectively confirmed reflux is the driver.
So objective testing becomes the safety net.
If you only see A or B or a normal scope.
Absolutely mandatory if symptoms for cyst.
Now, if we do find severe disease on that first scope, LACD, maybe a stricure or Barrett's what's the immediate plan and the crucial follow up..
Right.
So first, you hit it hard with high dose, BDPPI for probably 8 to 12 weeks, let everything heal up, but then the critical step is a repeat EGD.
Why the repeat scope?
You need to confirm healing, make sure the stretcher hasn't worsened, but most importantly, you need to reexamine the area, especially the GE Junction, for any Barrett's esophagus that might have been hidden underneath all that severe inflammation init.
Okay, makes sense.
And just to close the loop on screening, we surveil Barretts, but not just uncomplicated GD itself, right?
Spot on.
Regular GRD doesn't get surveillance endoscopy, but Barrett's without dysplasia NDBE does.
The timing depends on how long the segment is.
Short segment, usually three centimeters or less, maybe every five years, longer segments, over three centimeters. Usually every three years.
All right, this next part feels like where things can really go sideways if you're not careful.
Symptoms persist after the EGD, maybe the scope was normal or just LAB.
Now we're moving to objective refundctionux monitoring.
The big choice, test on PPI or offFPI.
Why is this decision point so critical?
Because it fundamentally changes what question the test is answe .
You basically get one shot with reflux monitoring to answer your most pressing clinical question and whether the patient is taking their PPI determines which question you're asking.
So it defines the purpose of the test.
Exactly.
There are two main scenari.os, two different goals, creating this fork in the road.
Okay, let's take the first path.
The goal is simply to prove GEAC exists.
Right.
This is the OFF PPI test .
You use this when GR is not yet proven.
Think of your patient with persistent symptoms, but a normal EGD or maybe just, or that patient considering surgery.
You need objective proof of pathological acid.
And the test for that?
The standard is usually wireless monitoring the Bravoapsule.
It measures for 48, sometimes up to 96 hours .
But critically, the patient has to be off acid suppression.
Stop PPIs for seven days.
H2 blockers for 48 hours, you need to see their natural acid exposure.
And what's the magic number we're looking for?
It's the acid exposure time, or AET.
That's the percentage of time the pH in the esophagus is below four .
An AET greater than 6% on any day of the study confirms objective GARD, diagnosis made.
And if it's low, say less than 4%.
If AET is consistently low, like under 4%, GRD is effectively ruled out as the cause of ongoing symptoms.
Okay, that's the OFPI patter for proving GRD.
Now, the second path , the on PPI test.
When do we go down this road?
You choose the on MPTI test when GRD is already proven.
Maybe they had that LA grade deesophagitis on a priorcope or they had a previous P study with AT6%.
But they're still having symptoms despite being on optimized twice daily PPI therapy.
So the goal here isn't proving GRE anymore.
It's figuring out why the PPI isn't working for the symptoms.
Precisely.
The goal is to phenotype refractory symptoms.
We use PHMed's testing for this, and the patient stays on their bey PPI.
Imped lets us detect reflux events regardless of whether they're acidic or not.
And this is where we get that crucial separation, the aha, moment you mentioned.
This is it.
This is probably the most strategic point in the whole float chart.
You look at the data while they're supposed to be maximally suppressed , and three main possibilities emerge.
Okay, walk us through them.
Scenario one.
Scenario 1.
True refractory GRD.
This means their AET is still high, maybe over 6%, or they have a very high number of reflux events, even while taking BDPPIs correctly .
The medication is genuinely failing to control the reux.
So what does that mean for treatment?
It means you need to escalate, think procedural options, maybe adjunct medical therapies, but the PPI alone isn't cutting it.
Okay.
What if the PPI is actually working?
Meaning the reflex numbers AET, event counts, look normal on the test?
Right.
If the reflex burden is controlled, now you look at the symptom correlation.
Did the patient push their symptom button during the test and did those symptoms actually line up with a few reflux events that still occurred?
And this leads to the other two scenarios.
Exactly.
This is the split into the functional or sensitivity disorders.
Scenario two, reflux hypersensitivity, R age.
Here, the reflux burden is normal, AET 4%, low event count, but the reported symptoms show a positive correlation with those few remaining reflux events.
Their esophagus is just overly sensitive to even normal amounts of reflux.
They feel something that maybe others wouldn't.
Precisely.
And then scenario 3, functional heartburn, FH.
Again, the reflux burden is normal, but this time there's no correlation between their symptoms and the reflex events .
The symptoms they feel are completely disconnected from any physical re happening.
Wow.
Okay, so RH and FH, the reflux is controlled, but the symptoms persist for different reasons.
This seems like the crucial pivot point for management.
It absolutely is, because for both reflux hypersensitivity and functional heartburn, you do not escalate acid suppression .
Throwing more PPIs at them won't help because excess acid isn't the problem.
So what do you do?
You shift gears completely.
The treatment becomes neuromodulators, things like low dose tricyclic antidepressants or SSRIs, which work on nerve sensitivity and central pain processing, behavioral therapies targeting the gut brain axis are also key.
And what if they originally had proven GRD, like LA grade D, but now test is RH or FH on PPI , do they stop the PPI?
Good question.
Usually, no.
If they had severeesophagit initially, you typically keep them on the PPI for ongoingosal protection, you treats with the neuromod behavioral approach.
It's a functional on underlying G. That makes sense.
Okay, shifting gears slightly.
Let's talk about another test.
High resolution monometry, HRM.
Measures muscle function.
Where does this fit in and what's the common misunderstanding?
Right, HRM, its role is super specific and often misused .
The absolute number one thing, remember, HRM does not diagnose G. That's a classic test trap.
So what is its role?
Why do we do it?
Its primary and really mandatory role is preoperatively.
Before you even consider antiflux surgery like a Nissinund application or implanting a lion X device or even TIF, you must get monometry.
Why mandatory before surgery?
Two main reasons.
Yep.
First, to rule out major motility disorders that can mimic JRD.
The big one is acia, where the lower esophagal sphincter doesn't relax properly and the esophagus doesn't squeeze correctly .
Or something like EGJ outflow obstruction operating on someone with undiagnosedia thinking it's Gard is, well, it's a disaster.
Okay, ruling out mimics.
What's the second reason?
To assess the strength of the esophagus, the parasaltic vigor, if the zes weak, a full 360 degree NISificantallow.
Knowing the motility helps the surgeon choose the right type of cap, maybe a partial one, like a toupe instead.
Got it.
Besides Acholasia, any other key mimics that monometry, maybe with impedance, can help identify?
Yes, one that's increasingly recognized is rumination system. Syndrome.
This can really masquerade as refractory gerity.
That is that present?
It's this effortless regurgitation of recently eaten food, usually not acidic right after meals.
It's often due to an unconscious control of the abdominal muscles, pushing food back up .
Monometry or impedance can actually show that characteristic spike in intrastric or intabdominal pressure just before the regurgitation of it..
And the treatment is totally different.
Completely different.
It's not medication.
It's behavioral therapy, specifically diaphrmatic breathing techniques to control those abdominal contractions.
Okay, let's circle back one last time to the patient with true refractory GD.
We approved it with the on MPPI test, showing AT 6% despite optimized therapy.
We've ruled out mimics withometry.
What are the medical options before considering procedures?
You might try a few adjuncts.
Adding an al like Gav after meals can create a physical barrier .
Sometimes bin is used it can reduce transient relaxations, which are a major mechanism of reflux, especially helpful if regurgitation is a big symptom, maybe a nighttime H2 blocker short term, though evidence is weaker .
But if symptoms are still severe and you've confirmed ongoing objective reflex, procedures are next.
And what are the main procedural categories?
The gold standard has long been a fund application, the Nissin, full, or toup, partial wrap.
Newer options include the LX device, a magnetic ring, usually best for smaller heal heras, less than three centimeters.
TIF is an endoscopic fundlic, less invasive, and importantly, don't forget bariatric surgery.
Bariatric surgery for reflex.
Yes.
Specifically, RU on Y gastric bypass, RYGB.
If the patient also has significant obesity, say, a BMI of 35 or more, RYGB is actually a very effective anti-flux surgery, in addition to being a weight loss procedure.
Interesting.
And across all these procedures, what predicts the best chance of success?
Two things mainly, having that objective proof of Gard, like abnormal AT or LD, and having reg as a dominant symptom, maybe even more so than just heartburn or chest pain , patients primarily bothered volume reux tend to do best surg.
Okay, we have covered a lot of ground there, building that whole GRD diagnostic flow chart.
If you had to boil it down, what are the absolute key takeaways for our listeners?
I think two things really stand out.
First, that EGD finding the LA grade distinction.
Remember, C or D is your conclusive proof of GRD, A or B, or a normal scope , is inconclusive, you need more data symptoms.
And the second.
The testing strategy you'rering the test.
OFPI testing, AT 6% is to prove GD.
On NPPI testing to phenotype refractory symptoms when GRD is already, looking for true refractory GRD versus reux hypersensivity or functional heartburn, where AET 4% on PPI.
That distinction between true refractory and the functional hypersensitive groups seems critical.
It is, and that brings us to maybe the most important trap to avoid in this whole process.
All right, leave for that final provocative thought.
What's the biggest potential misstep?
The single biggest trap is continuing to escalate acid suppression , or worse, sending a patient for anti-reflux surgery, when their objective testing on PPI actually shows reflux hypers sensitiveitivity or functional heartburn.
You've confirmed their reflux is controlled, their AET is low, yet they still hurt.
Pushing more PPIs or doing surgery in that situation is not addressing the real problem.
Which is the gut brain connection, the sensitivity.
Exactly.
The solution lies in neuromodulators, behavioral therapy, addressing that hypersensitivity or functional component .
Recognizing when the problem isn't the acid anymore, even if it started that way, saves patients from ineffective treatments, unnecessary medication exposure, and potentially failed surgeries.
Getting that right, that's the real payoff of navigating this flow chart correctly.
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