Dr GI Joe

Welcome back to the Deep Dive.

Today, we're getting systematic.

We're aiming for a really practical guide to diagnosing and managing some complex esophagitis disorders.

Think of it as taking gastrooneerologyology, fellow resources, and making them really usable.

Exactly.

The goal here is to build up that knowledge base, so it's totally board tight and maybe more importantly, clinic ready for you .

We want those instant recognition patterns right from when the patient walks in, understanding why their complaint dictates our next move.

Okay, love that.

Let's kick off with triage then.

If you could break down those sort of three critical symptoms that should immediately make a suspect esophagitis, that help narrow things down fast.

Absolutely.

Number one, bophagia.

Painful swallowing.

If a patient says it hurts to swallow, that just screamsucal injury.

Your mind should immediately jump to infectious causes,V, CM maybe, you, possibly a severe pill induced ul deep damage something's broken.

Got it.

Pain equals breach.

How does that contrast with just dysphaggia?

Difficulty swallowing?

Well, dysphagia, especially if it's mainly for solids, shifts are thinking.

Now we're considering more mechanical issues or maybe a dense inflammation, things like eosinophilic, esophagitis, COE, or perhaps striptures, or unfortunately, even malignancy.

It's a very different diagnostic patter than pure pain.

Makes sense.

And that third big trigger sign , recurrent food impaction.

Ah, yes, food imp.

If it happens more than once, maybe especially in a younger person, perhaps with some history of allergies or asthma, you absolutely have to think EOE until it's proven otherwise.

That single symptom basically dictates your entire biopsy plan during the EGD.

That distinction alone is huge.

Okay, so we have these triggers , but when do the symptoms become so severe that we need an EGD, like right now or very soon?

We can't scope everyone immediately.

No, you can't.

Urgency comes down down to immediate risk.

So definitely an immediate EGD for an acute food imp that won't pass, or say, a known or suspected caustic ingestion.

Right.

Obvious emergencies.

Exactly.

And severe symptoms in anyone who's immunocompromised that needs a quick look, too .

Beyond those, we really have to respect the alarm features.

Refresh us on those.

Sure.

Weight loss that's unexplained.

Any sign of GI bleeding like documented anemia, dysphia that's clearly getting worse, progressive dysphagia, and then the big risk factors.

Age, usually over 50 or 60, and a significant history of tobacco or alcohol use.

So any of those flags mean you expedite the EGD?

No waiting around?

Precisely.

Get that scope done sooner rather than later.

Perfect foundation.

Okay, let's imagine we're doing the EGD now.

We're looking at reflex damage.

Let's talk LA classification .

How does this ABCD system help grade erosiveosesophagitis?

The L.A System Los Angeles classification is basically our standard language for describingbing those new coal breaks, the erosions we see.

It grades them based on size and crucially whether they connect across newucosal folds.

So grades A and B are the milder end?

Generally, yes.

Grade A means you've got small besikes, five millimeters or less .

Grade B, the brakes are bigger, more than 5 millimeters.

But the key thing for both A and B is that the brakes don't run continuously between the tops of two mucosal folds.

They're kind of isolated erosions.

Okay, isolated.

So C and D are when things get more extensive.

Exactly.

That's the big jump.

Grade C means the brakes are continuous, connecting the tops of two or more mucosal folds, but they still cover less than 75% of the esophal circumference.

Angry D. Grade D is the most severe.

The brakes are continuous and confluent, involving 75% or more of the circumference .

It looks really angry.

And finding C orD, that has immediate treatment implications, doesn't it?

Oh, absolutely.

Finding LA grade CRD is basically considered conclusive evidence of severe GRDD.

You often don't need more diagnostic workup like PH testing at that point.

You move straight to aggressive medical therapy.

Which usually means.

High dose PPIs, typically twice a day BID therapy, you hit it hard.

And hitting it hard leads us to this recurring theme, this follow-up interval.

The 8, 12 week repeat EGD .

Why that specific tomframe?

It pops up a lot.

It It does.

That 8 to 12 week window is generally considered the time needed for the esophagia lining to heal or turnover significantly under effective treatment.

So, whether you're treating that severe LA gradesade CD erosion or later when we talk about EOE, you need that time to see if the therapy actually worked.

So for GAIE, you're checking if the erosion's healed.

Right.

And for EOE, you're checking for histologic remission.

Did the Eacinophil count drop?

If you scope too early, you might not see the full effect.

If you wait too long, well, you're flying blind on whether your treatment is effective.

It's a key decision point.

Makes sense.

Okay Okay, let's pivot to Barrett's esophagus.

Huge topic , all about risk and being precise.

Who even gets screened for Barretts in the first place?

Good question.

Screening isn't for everyone with heartburn.

We target a specific profileile.

Someone with chronic GR symptoms think five years or more, plus several other risk factors.

Which factors are key?

The main ones are age over 50, being male , white race, having central obesity, that abdominal fat and a history of smoking or past.

If you have the chronic GRD and hit three or more of those risk factors, a one-time screening EGD is generally recommended, even without alarm symptoms.

Got it.

So we do the scope, we see that salmon colored lining suggestive of Barrett's.

Now, measurement is critical.

Explain the prog CNM classification.

Right.

Prog CNM.

This is absolutely vital for risk stratification, and it's where people sometimes get confused .

The key is you measure from the top of the gastric folds, which marks the true gastroosophagal junction, not necessarily from the visible Squamacumnar junction, or Z line.

Okay, measure from the gastric folds.

What do C&M stand for?

C is for the circumferential extent.

That's the length of the Barrett's lining that goes all the way around the esophagus.

M is for the maximumimal extent.

That includes the circumferential part, plus any tongues or islands ofret that reach further up.

Why is that distinction C versus M so important?

Give us an example.

Okay, take two patients.

One is CM4, meaning one centimeter circumferential, but a tongue reaches up to four centimeters total .

The other is C44, 4 centimeters all the way around.

Both have M4, so both are are technically long segment barots, right?

Yeah.

Over three centimeters.

Correct.

And if they're both nondislastic, they get the same surveillance interval, EGD every three years.

But that C4M4 patient with the full four centimeter circumference has a significantly higher annual risk of progressing to cancer, maybe two to three times higher, something like 0.30.

0.5% per year compared to maybe a 0.070.2.% for the C1M4 patient.

Wow. Same surveillance interval, but different underlying risk.

Exactly.

And that C44 is also just technically much harder to completely eradicate with ablation if it comes to that, because there's so much more tissue involved.

Okay, so surveillance timing depends purely on the M length.

Less than three centimeters is short segment, EGD every five years.

Three centimeters from more is long segment, AGD every three years, assuming no dis display.

That's the standard for non-isplastic bar, yes.

And how do we biopsy during these surveillance?

The Seattle protocol?

Yep.

The Seattle protocol is the standard.

You take four quadrant biopsies, think 12, 3, six, and nine o'clock positions every two centimeters along the entire length of the Barrett segment.

And if dysplasia is found or there's a history of it..

Then you tighten things up.

You do four quadrant biopsies every one centimeter.

You really increase the sampling density to catch any progression or mist spots.

Okay, now the really high stakes moment.

Yeah.

The biopsy comes back, showing dysplasia, low grade, LGD or high grade, HGD , before any drastic action was the absolute must do step.

This is non-negotiable.

Any finding of LGD or HGD must be confirmed by a second independent pathologist who is an expert in in GI pathology.

Why is that confirmation so critical?

Two main reasons.

First, the management leap is huge.

You go from just watching every few years to actively intervening with eradication therapy.

Second, there's no significant variability between pathologists, even experts in grading dysasia.

It's subjective that second opinion is crucial patient safety check to prevent unnecessary invasive procedures. .

Makes perfect sense.

So, dysplasia confirmed by two experts, what's the standard treatment now?

Endoscopic eradication therapy or E.T?

Yes, E.T. Is the standard of care for confirmed LGD or HGD.

The approach depends on whether there are visible lesions.

Have so?

If you see any nularity or visible les within the barrets, regardless of the biopsyed LGD or HGD, the first step is endoscopic mucosal rection, ER.

You lift and cut out that visible abnormality.

Okay, remove the visible stuff first, then what?

After EMR clears any raised areas or if the dysia was completely flat to begin with, you move to ablation, usually radio frequencyl .

That's used to burn away the remaining flatret Mikosa.

So EMR for bl RFA for flat areas?

Essentially, yes.

That combination aims to completely eradicate the Barrett's epithelium.

Before we leave Barrets, let's address that common trap, the irregular Z line.

Ah, yes, the irregular Z line.

This is crucial.

If you see that salmon colored mucosa extending less than one centimeter above the top of the gastric folds.

Less than one centimeter?

It's not defined as Barret esophagus, even if biopsies from that tiny area show intestinal metapasia, it's just called an irregular line, or short segment intestin metaplasia.

And the implication?

No surveillance needed .

That one centimeter rule means the risk is considered negl and the patient lifelong endoscies for it.

It's a really important cutoff.

Huge distinction.

Okay, shifting gears now to Evoophilic esophagitis, Yo.

What are the specific diagnostic criteria we need to hit?

For EOE, diagnosis hinges on both the endoscopic appearance, maybe rings, furrows, exates, and critically, the biopsies.

You need to take a good number of biopsies, the recommendation is at least six, from at least two different levels in the esophagus, usually proximal and distal.

And what are you looking for on histology?

The magic number is 15.

You need to find 15 or moreophils per high power field, EOf, and at least one of those biopsies to formally diagnose EOE.

15 EO shove from at least six biopsies at two levels.

Got it.

Now, treatment for EOE is interesting there are three equivalent first line options.

That's right, which is a bit unusual.

You can start with high dose PPI therapy, similar to severe GD, often a mezol 20 40 milligram, twice daily.

Or you can use topical steroids that's usually swallowedicone from an inhaler or a binide slurry you mix up.

Or the third option is dietary elimination , typically starting with eliminating the six most common food allergens.

And all three are considered equally valid starting points.

Correct.

The choice often depends on patient preference, potential side effects, insurance coverage, things like that.

And regardless of which one you pick, that 8 to 12 week rule comes back again, doesn't it?

It sure does.

After starting any of those first line therapies, you need to repeat the EGD with biopsies that 8 to 12 weeks.

The goal is to confirm histologic remission did the Eophil count drop below that 15 ESCPF threshold.

And if it didn't?

If you haven't reached histic remission, you know that initial therapy isn't sufficient.

You need to either intensify it, maybe increase the steroidse, or switch to one of the other first line options you didn't try in.

Okay, let's quickly run through infectious asesophagitis.

This often comes up in immunocompromised patients.

It's about pattern recognition on the scope, right?

Exactly.

Quick look, likely diagnosis, start treatment.

If you see those distinct, fluffy white plaques..

Camba.

Think candy..

Treat empiriconol while waiting for confirmation if needed.

If you see more well-ded, punched out ulcers, often multiple.

HSV.

Thinkeslex point here.

Biopsy the ulagnostic yield.

Treat with a cycverver.

In the third main one.

If you see large, often linear, sometimes quite deep ulc, typically more common in theMV.

Suspects CMV, Cygirus.

And for this one, you need to biopsy the base of the ulcer where the virus replicates.

Treatment is val. .

Edge for HV, for CMV.

It matters.

Great distinctions.

Okay, moving from infection to a common mechanical issue.

Yeah.

The Shatky ring, the classic steakhouse syndrome.

Ah., the Shaski ring or B ring.

It's a thin, benign web or diaphragm of Mukosa right at the GE Junction .

Very common, often linked with chronic Gard and hiatal..

And the symptoms are classic, intermittent, solid food dysphagia.

Exactly.

The patient who says, I usually eat fine, but sometimes, especially with bread or meat, it just gets stuck right here.

That's often a shot ski ring.

Management seems straightforward.

Dililation and PPIs.

Pretty much.

You dilate the ring during endoscopy to break it, and because it's often GD related, longterm PPPI therapy is usually recommended to preventur.

Which brings us neatly to dilation safety.

When we're dilating strictures, whether it's a shots ring or something else , what are the key numbers and rules?

Right.

Safety first.

Remember, a normal esophag is wide, maybe 18 to 20 millimeters across.

Symptoms of dysphagia usually start when it narrows down to about 13 millimeters or less.

And real trouble, like food, gets common below 10 millimeters.

So when we're dilating and we start to feel resistance, how do we avoid tearing or perforating?

The guiding principle is the rule of three .

Once you meet resistance with your dilator, you shouldn't try to increase the diameter by more than about three millimeters in that single session.

It's a gradual steps.

Very gradual.

You might start with, say, a 10 millimeter dilator, feel resistance, then go up to 13 millimeter.

Stop there for that session.

Next time you might start at 13 millimeter and go up to 15 or 16 millimeter.

The goal is usually to get them to around 15 to 18 millimeters for good symptom relief, but you do it patiently over potentially multiple sessions to maximize safety .

Don't aggressive.

Excellent practical advice.

Okay, final scenario.

We've done the EGD for dysphagia, maybe even dilated, but the patient still has persistent difficulty swallowing, and maybe the scope looked normal.

Where do we go now?

This feels like a key diagnostic fork.

It is.

It's frustrating for everyone when the EGD is unrevealing, but symptoms persist.

This pushes us beyond just looking towards assessing subtle structure or function .

We have two main tools next bum swallow, and monometry.

When do you choose a standard bum esophogram or swallow?

You'd lean towards the standard bariumesophogram if you still suspect there might be a subtle structural issue the scope could have missed.

Maybe a small esophag web, an incomplete ring, or even extrinsic compression from something outside the esophagus pressing on it.

Barium is great at outlining that fine architecture.

And high resolution monometry.

When is that the go-to?

High resolution monometry is really the gold standard test when you suspect a motility disorder.

Think conditions like echia, esophage spasm, maybe scler affecting the esophagus, you'd strongly consider monometry if the dysphagia is progressive, and importantly, if it affects both solids and liquids .

That pattern really points towards a muscle function problem.

What about the timebarium esophogram, toBE?

Where does that fit?

The TBE is a specialized type of barium study used primarily when you suspect acylasia.

You have the patient swallow barium, and then you take x rays at specific time points, like 1, two, and five minutes, to see how much barium is left standing in the esophagus.

So it quantifies the emptying delay.

Exactly.

It shows delayed emptying, which is characteristic of acylasia.

It's usefulful for assessing severity and also for tracking how well treatment is working later on.

But for the definitive diagnosis of which motility disorder is present, monometry is still the gold standard.

TE is is more of a complementary test for accalasia.

Okay, that clarifies the next steps perfectly.

Wow, we've covered a huge amount of ground from initial triage based on symptoms through LA grading and its implications.

That crucial 8, 12-w follow-up window for checking healing or remission.

To the really detailed rules for Barrett's surveillance and dysplia management, including that vital second pathologists confirmation.

Absolutely.

And I think if there are two take-homes from the Barrett section, it's precision in measurement, getting that prog CN right and the mandatory verification step for dysplasia .

Those points fundamentally alter long-ter management and risk assessment for the patient.

We've learned the protocols, the rules, but maybe let's end of the why.

Why are these protocols, especially around Barrett's dysplasia, so incredibly strict?

It really boils down to the stark difference in absolute risk .

Think about it.

A patient with nondisplastic Barrett, especially short segment, is in a pretty low risk group.

Their annual chance of developing esophual cancer might be, what, maybe a 0.1%?2%? Very low.

Okay.

But if that same patient progresses to high grade dysplasia, that annual risk jumps dramatically.

Now we're talking maybe 5%, even 10% per year.

That's a massive leap.

It's an enormous leap in absolute risk.

So this entire highly structured system, we've discussed the precise measurements, the careful biopsy protocols, insisting on that second pathology read, the specific steps for eradication therapy, it's all designed with one primary goal, to identify and intervene in that small subset of patients before they make that huge jump from low risk dysasia to high risk dysia orasive cancer.

That's the whole game.

Preventing that progression is why adhe meticulously to these rules isn't just best practice.

It's fundamentally protective

Was this transcription useful or not useful?