Peptic Ulcer Disease
Welcome to the Deep Dive.
Today, we're really getting into peptic ulcer disease, or PUD.
Right.
It's super common, usually manageable, but, you know, sometimes it leads to a really dangerous bleed..
Exactly.
So we want to go beyond just the symptoms and really map out the rules, you know, how to figure out the cause, how to handle it, especially when things get serious with bleeding.
Yeah, absolutely.
So PUD, it's fundamentally a break in the lining, a defect, really, in the stomach or the dodenum.
The first part of the small intestine?
Right.
And it goes deep through the protective layers, down to the muscle, layer, the musc is mucose.
Okay.
And when you look at why it happens, there's really this classic triad of causes that kind of drives everything we do.
What are they?
Number one, globally, is helicobactory, you know, HPory.
That's the big one.
The bacterial infection.
Correct.
Then number two, especially in Western countries, is chronic use of NSAIs, those non-steroidal anti-inflammatories and aspirin.
Yeah.
That's definitely on the rise.
And then the third one, it's rare, but you have to keep it in mind, is states where the stomach makes way too much acid, like Zollinger Ellison syndrome.
Gotcha.
Okay, so infection, drugs, and rarely just too much acid.
Pretty much.
So our mission today is clear .
We need to figure out how to tell these ulcers apart based on location, why that even matters, especially for cancer risk.
Crucial point.
Then what's the latest on getting rid of H.
Py Laurie?
I hear the guidelines changed again.
They have.
We'll cover the 2024 approach.
And finally, the big one.
The step-by-step plan for managing a bleeding ulcer, that emergency situation.
A bleeding algorithm, yes.
Okay, so location, location, location .
I find it really interesting that just hearingaring how a patient's pain acts around meals can point you towards either the stomach or the duodenum.
It's often a huge clue.
They're almost mirror images in terms of symptoms.
How so?
Let''s start with duodenal ulcers.
Okay, duadinal ulcers, they're much more common, maybe four times more common than gastric ones.
And the classic story is food makes the pain better.
Initially, anyway.
The food buffers the acid.
Oh, okay.
But then maybe two, three hours later, b, the pain comes back often really intensely.
It's famous for waking people up in the middle of the night, like two or 3 a.m. That late night pain.
Exactly.
And what's really key here , duadal ulcers are overwhelmingly linked to H.
Pyri.
We're talking 90, 95%.
Wow.
Which also means they're almost always benign.
We generally don't worry about cancer there, so routine biopsy isn't standard practice.
Okay, so duatal pain gets better than worse ?
Usually age pyrie, almost never cancer.
Makes sense.
So that leaves the gastric ulcer.
This is the one we worry more about, right?
The cancer risk.
Absolutely.
This is the one that keeps us vigilant.
With gastric ulcers, food typically makes the pain worse.
Opposite of duodal.
Totally opposite.
So patients start to, you know, avoid eating or fuel full really quickly.
They might lose weight.
Yeah, that makes sense.
And while age pilory is still a big factor, maybe 70, 80% , NSADs play a really significant role here, too.
But the absolute must-member rule, the critical difference.
Yeah.
You always biopsy a gastric ulcer.
Always.
They always.
Because gastric cancer can look identical to a benign ulcer on scope.
So you have to take multiple bites, usually from four different spots around the edge to rule out malignancy.
It's nonnegotiable.
Wow, okay.
That's a huge difference in management.
Biopsy versus no biopsy?
Massive.
Quick question about the H py, though.
If it causes both types, why does it seem likealcidid, like?
Yeah, that's a great question.
It has to do with where in the stomach the Hory sets up shop.
Okay.
See, Hilory causesammation, gastritis.
If thatammation is mainly in the lower part, the anm, it actually messes with the feedback loop and ramps up gastron production.
More gasast means more acid, and that extra acid spills over and damages the deoden.
Ah, okay.
So anroinfection leads to high acid, hurting the deodenum.
Exactly.
Yeah.
But if the infection is more widespread, or if it hits the main body, the corpus, where the acid producing cells live, it can actually destroy those cells over time.
Right.
So you end up with lower acid levels, but unfortunately, that environment is more prone to developing atrophy and eventually gastric cancer.
Got it.
So the location of the bug dictates the acid level and the long term risk.
Precisely.
Okay, so we've diagnosed it.
We know where it is.
Now, treatment , for HPri, you mentioned the guidelines shifted.
What's the go-to regimen now in 2024?
Yeah, the big changes we've really moved away from the old standard triple therapies, the ones with chloromycin.
Why is that?
Resistance.omyc resistance rates are just too high in main places now.
Using it first line is often setting yourself up for failure.
Okay, so what do we use?
The preferred first line treatment now is bismuth quadruple therapy.
Bismuth quadruple.
Okay, what's in that?
It's intense.
It's a 14 day course.
You take a PPI that's the acid reducer, twice a day.
Then business, like Pepobismal, essentially, four times a day.
Four times, wow.
Yep .
Plus tetrycling and antibiotic, four times a day, and midroninivisol, another antibiotic, three times a day.
Whoa.
That's a lot of pills.
Yeah.
Four drugs multiple times a day for two weeks straight.
It is.
It's a commitment.
Adherence is definitely the biggest challenge with this regiment.
I can imagine.
How do you even get patients to stick with that?
That sounds really tough.
It takes a lot of upfront education , really explaining why it's crucial to finish every single dose, hammering home that's stopping early just doesn't work and can make the bug resistant.
Right.
Sometimes combination pills can help simplify it a bit, but still a tough course.
And, you know, getting the diagnosis right in the first place is also key.
Ah, yeah, the testing traps.
If you're using the non-invasive test, like the breath test or the stool test, , you can get false negatives, right.
Huge potential trap.
Absolutely huge.
If your patient's taking the PPI or if they've had antibiotics or even bismuth recently.
Like the bismuth and the treatment regimen?
Exactly.
Or even just pepto-ismol over the counter.
Yeah.
These can suppress the bacteria enough to make the test negative, even if the infection's still there, just waiting to flare back up.
So what's the rule for testing?
The golden rule is , stop PPIs for at least two weeks before the test and stop any antibiotics or bismuth products for at least four weeks.
Two weeks for PPIs, four weeks for antibiotics or bismuth?
Correct.
Otherwise, you might tell someone they're cured when they really aren't.
Big pitfall.
Okay, good to know.
Now, switching gears to the other main cause, NSAD, what about people who need to take NSAs or aspirin long term, maybe for arthritis or heart health??
How do you protect their stomach?
Yeah, that's a common scenario.
And the risk is real, maybe up to 15% of chronic users develop an ulcer.
15%.
That's high.
It is.
So if they absolutely must continue the NSAD, you have to add protection.
Usually that means taking a daily PPI along with it.
Okay.
Cotherapy with a PPI.
Right.
Now, if that patient has already had an ulcer bleed in the past because of NSAD, then the safest route, the sort of gold standard, is actually two steps .
Switch from a standard NSA to a CX2 inhibitor, which is theoretically a bit gentler on the stomach.
Okay.
And keep them on the PPI as well.
You need for maximum protection if they have blood before.
You just can't risk another bleed.
All right, let's pivot to the real emergency scenario, the bleeding ulcer.
This is the most common reason PU becomes life-threatening, right?
Vomiting blood, that dark Terry stool.
Comamis and molina, yeah.
Yeah.
This is where things get serious fast.
So patient hits the ER.
They're unstable.
What's the absolute first thing you do?
The sequence?
First things first.
ABC's and resuscitation.
Yeah.
Two large bore IV lines pour in the fluids, get blood products ready, or start transfusing if they need it.
Stabilize, stil, stabilize.
Absolutely.
And right alongside that, you hit them with a high dose IVPPI, usually an 80 milligram bus up front, then a continuous infusion, typically 8 milligrams per hour.
Why the high-dose IVPPI right away?
The goal is to jack up the stomach pH, get it above six quickly.
Why above six?
Because Pepsin, the enzyme that digests protein , also digest blood clots.
But Pepsi gets inactivated when the pH is above 6.
So raising the pH helps stabilize any clot that's formed over the bleeding site.
Ah Ah, okay.
So the PPI buys you time and helps stop the bleeding before you can even scope them.
Exactly.
It stabilizes the clot, reduces the chance of immediate re bleeding, and sets the stage for endoscopy.
Which is the next step, right?
The EGD, the scope?
Correct.
Once they're hemodynamically stable, they go for an EGD, and this is where we use the forest classification.
Okay, the forest classification, what does that tell us?
It's all about predicting the risk of releeding based on what the ulcer looks like during the scope .
It grades the stigmata of recent hemorrhage.
Stigmata, like the visual sign.
Yeah.
So high risstigmata I mean you need to intervene endoscopically..
That includes things like active spurting blood that's forced aia.
Okay.
Obvious bleeding.
Or active oozing blood, which is Ibar.
Also, high risk is a non-bleleeding visible vessel.
You can see that vessel sticking out, even if it's not bleeding right then.
That's IIA.
Right.
Looks like it could go any second.
Exactly.
Or even an adherent clot sitting on the ulcer base, forest dibe, all of those need and discopic therapy because the risk of them rebleleeding is very high, like 50% or more sometimes.
Got it.
So, I, I, Ib, treat endoscopically.
What about low risk?
Low risk are things like just a flat pigmented spot, like an old clot that's IA or a completely clean ulcer base, 3.
Okay.
For those low risk ones, the IVPPI is usually enough.
You typically don't need to do endoscopic therapy, like clipping or burning.
And when you do need that endoscopic therapy for the high risk ones, what's the standard?
Standard of care is dual therapy.
Dual therapy.
Meaning to different methods.
Yes.
We learn the hard way that just injecting epinephrine might stop the bleeding temporarily, but it doesn't last.
Okay.
So you have to combine the epinephrine injection, which helps slow the flow with a second, more permanent method .
That's usually either placing metal clips to pinch the vessel shut or using thermal energy like cauttery to seal it.
Epi+us clips or EB plus heat.
Got it.
Dual therapy, that combination significantly cuts down the rebleing rate compared to just one method alone.
Okay, now here's the tricky part.
The classic board question scenario, right? ?
You do the EGD, you apply dual therapy, Patients seems okay, but then they bleed again.
So you take them back, you do another EGD, you try dual therapy again, and they bleed again..
What now?
You can't just keep scoping them indefinitely.
No, you can't.
There's a very clear escalation ladder here.
After two failed endoscopic attempts.
Two strikes and you're out for endoscopy.
Pretty much.
Yeah.
If they releed after the second successful looking endoscopic treatment, you pivot.
You do not go for a 30D. The next step is interventional radiology or IR.
IR?
For what?
For angiology and embolization.
They go in through the arteries, find the vessel feeding the ulcer, and plug it up.
Ah, okay.
Why IR before surgery?
Isn't surgery the definitive fix?
It used to be the next step, but IR has gotten really good.
It's much less invasive than open surgery, and their success rates for selectively embolizing the bleeding vessel are excellent now, often over 90%.
Less risky than surgery, especially in someone who's already unstable.
Exactly.
Surgery carries significant mort ality and morbidity, especially in an actively bleeding sick patient.
So the modern ladder is clear.
First, EGD with dual therapy, reed.
Sec EGD with dual therapy.
Reed again.
IR embolization.
And surgery is only if IR isn't available or if IR fails.
That's right.
Surgery is now the last resort.
Okay, so we've gotten through the crisis.
The bleeding is stopped .
Now, thinking long term, how long do they need to stay on that PPI?
And what about follow-upopes?
Is it the same for everyone?
No, it's different, and it depends crucially on where the ulcer was, location again.
Okay.
If it was a doden ulcer.
The more common, usually benign one.
Right.
Assuming it wasn't complicated beyond the bleed, the PPI course is typically shorter, usually about four weeks total.
Four weeks.
And do they need another scope to check healing?
Generally, no.
If it was an uncomplicated dinal alter and the H is treated if you don't routinely need to res Okay.
What about gastric ulcers?
Ah, gastric ulcers are different because of that malignancy risk we talked about.
Right, I got to make sure it wasn't cancer hiding.
Exactly.
So for gastric ulcers, the PipI course is longer, typically eight weeks.
Eight weeks.
Double the duad in all time.
Yep.
And critically, a follow-up EGD is mandatory or around six to eight weeks after the initial one.
Mandatory scope for all gastric ulcers after treatment.
Mandatory .
To visually confirm the ulcer has fully healed and to take more biopsies if it hasn't, just to be sure we didn't miss an underlying cancer.
If the ulcer was really big, like over two centimeters, sometimes we even expand the PPI to 12 weeks before that follow-up scope.
Okay, so doinal.
Four weeks PPI, no routine rescope.
Gastric .
Eight weeks PPI, mandatory rescope.
That's clear.
So when does this PPI treatment become like a forever thing?
Who needs to stay on it indefinitely?
It boils down to a simple principle.
Yeah.
If the underlying reason or risk factor for the ulcer is still there, the PPI needs to continue long term, maybe indefinitely.
What kind of risk factors?
The main ones are need to stay on NSIs or aspirin long term or needing other anti-platet drugs, like Klodog .
Also, patients who have had idiopathic ullcers, meaning we couldn't find a cause like H py or NSAides, or those who keep having recurrent ulcers despite treatment.
So if the trigger persists, the protection persists.
Exactly.
But if the cause was H by lori and you successfully eradicate it and the patient isn't taking NSAs or aspirin, then you should absolutely stop the PPI after that initial healing period, whether it was four weeks weeks or eight weeks.
No need for lifelong acid suppression in that case.
Good.
Stop it if you can.
Definitely.
Last question. Circling back to that cancer worry with gastric ulcers .
When the endoscopist is describing the ulcercer, what are the visual buzzwords that scream potential malignancy?
The classic description you worry about is heaped up irregular edges.
Eooped up irregular edges.
Yeah.
A typical benign ulcer looks clean, smooth, almost like it was punched out.
But if the report mentions the edges look thick, raised, nodular, irregular, or heed up , you have to have a high suspicion for cancer until proven otherwise.
That means more biopsies, maybe deeper, and definite follow-up scing to ensure it heals or get a definitive diagnosis.
Got it.
Smooth and punched out is good, heaped up and irregular is bad.
That's a good way to think about it.
Hashtag tag tag out for it.
Oh, okay.
This has been incredibly helpful.
We've got the duadal versus gastric pain patterns, the move to Bismuth Quad for HPory, the whole forest classification guiding bleeding management, and those key differences in PPI duration and follow scopes.
Really practical stuff.
Yeah, hopefully it provides a clear framework for managing these common, but some sometimes tricky situations.
Absolutely.
Any final thoughts or maybe a related pitfall people often encounter?
You know, one thing that comes to mind related to acid suppression is stress ultroproyllaxis in the ICU.
It's often misunderstood.
Ah, giving PPIs or H2 blockers to prevent stress ulcers in critically ill patients.
Exactly.
But the key is , not every patient in the ICU needs it.
It's become almost a reflex for some, but it really should be reserved for patients at genuinely high risk.
Who qualifies as high risk?
The main ones are patients on mechanical ventilation for more than 48 hours, or those with significant coagulopathy, like a low plat count or high INR .
Also, maybe severe burns or major trauma.
Okay, so specific serious conditions.
Right.
If the patient doesn't meet those high- risk criteria, they probably don't need the prophylaxis.
And maybe the most common error is for getting to stop the proflaxis once that risk factor is gone.
Like when they come off the ventilator.
Exactly.
The indication is gone, the drug should be stopped .
Unnecessary acid suppression isn't harmless.
It can have side effects, like increasing monia risk or sea disinfection.
A fantastic point.
Targeted therapy and knowing when to stop is just as vital as knowing when to start.
Precisely.
Well, thank you.
This has been a truly illuminating deep dive into peptic ulcer disease.
Hopefully, everyone listening feels better equipped to navigate these path My pleasure.
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