Dr GI Joe

Welcome back to The Deep Dive.

You know, sometimes you get these complex medical topics and trying to entangle them feels a little impossible.

Today we're tackling one of those big ones, inflammatory bowel disease.

We're aiming to really map out the key differences between Crohn's disease and all sort of colitis, how we diagnose them, finally tell them apart, and crucially how we monitor them long term, giving you that sort of roadm map.

Yeah, that's the core challenge, isn't it?

The symptoms.

They overlap so much.

You've got the chronic diarrhea, fatigue , weight loss, sometimes joint pain, clinically, it's really tough, just based on that.

You really can't just guess based on how someone feels.

Absolutely not.

You need more.

The symptoms help guide us, maybe set our initial suspicion, our pretest probabilities, but they don't give the final answer.

Okay, so let's talk about those initial clues.

What might make you lean towards UC right at the start?

Well, classic UC often presents with bloody diarrhea, urgency is a big one, too.

That feeling of having to go right now and Tenesis feeling like you need to go even when you don't.

And it typically starts down low in the rectum.

Right.

And isn't there that weird thing with smoking?

Ah, yes.

It's strange, but smoking often seems somewhat protective for UC.

Patients might even report their symptoms get better if they smoke, which is obviously not something we'd ever recommend, but it's a clinical quir.

Okay, so that leans you see, what screams crones then?

Anything happening around the Panal area.

So fistulos, abscesses, fissures that just won't heal , that points very strongly towards.

U see just doesn't usually do that kind of damage there.

Makes sense.

What else points to Chn?

Maybe pain after eating, often lower right side of the abdomen, sometimes non-bloody diarrhea, though it can be bloody too.

And the smoking link flips completely.

Smoking definitely makes worse.

So before jumping into, you know, the more invasive stuff, is there a quick check we can do?

Yeah.

Yes, thankfully.

We've got fecal cal protectin and CRP C reactive protein.

These are great non-invasive tests.

If they're high, it basically confirms there's inflammation happening.

So it helps separate actual IBD from something like IBS.

Exactly.

It tells us, okay, this warrants a closer look, likely with endoscopy.

It avoids unnecessary procedures if the inflammation markers are actually low.

All right.

Inflammation confirmed .

Now we need the definitive answer.

UC or Crohn's.

That means scopes and biopsies, right?

That's the gold standard.

You need to look inside with an endoscope and you need tissue samples, biopsies for the pathologists to examine under the microscope.

The combination is key.

What are we looking for visually through this scope?

How do they look different?

UC is typically continuous.

The inflammation starts in the rectum almost always, and spreads upwards in one continuous block , No patches of normal tissue in between.

Okay, continuous starts low. And chs.

Chrome's is patchy.

That's the classic description.

You'll see skip lesions, areas of inflammation, maybe ulcers, right next to a completely normal looking lining.

So it jumps around?

Yeah, I can.

You might also see different kinds of ulcers, like deep linear ones or that cobblestone appearance.

And Crohn's often involves the end of the small bowel, the helium, which you see usually doesn't, and it can sometimes spare the rectum entirely.

But looks can be deceiving sometimes, I guess.

Especially milder cases.

For sure.

That's where the histology, the biopsy results become absolutely critical, especially because those really specific Chn's features that Grant Granuloma aren't always present.

Okay, let's dive into that histology.

What are the buzzwords for UC under the microscope?

For UC, think uniform and superficial.

The pathologist might report chronic Aormalis.

Basically plas cells lin up evenly at the base of the glands.

Okay.

And you see widespread changes in the glandructure, it's generally limited to the mosa, the inner lining, just the layer right beneath it, the superficial subucosa.

It doesn't usually go deep.

So uniform superficial.

That's you see.

Then crones must be patchy and deep.

That's a great way to think about it.

Yeah.

Yeah.

For Chn, you'll hear about focal or patchy chronic changes scients of old inflamm right next door to normal tissue.

And the big one is transmural tendency.

Transmural meaning through the wall.

Exactly.

Through the full thickness of the bowel wall.

That's why Chn causes things like strictures, where the bowel narrows or fistul , where it tunnels through to other organs or the skin, the inflammation goes deeper.

That makes sense why the complications are often so different between the two.

Precisely.

On biopsies, especially deeper ones, or surgical specimens, you might see lymphhoid aggregates deep in the wall, or nerve bundle thickening, things that confirm that deep transmural involvement.

Now, you mentioned diagnostic challenges.

What about this backwash eyatus?

If you see inflammation in the , isn't that game over?

It's?

Not necessarily.

That's a common pit.fall.

Backwash iitis is usually a mild sort of diffuse inflammation you see just in the very end of the ileium, but only when someone has really severe UC affecting the whole colon pancolitis.

Always in it.

Cronhn's then.

Because it's thought to be just that backwash.

Severe inflammation in the colon maybe makes the valve between the colon and a lium a bit leaky, and colonic contents splash back, causing some mild, superficial irritation .

It doesn't have the features of C'sus, no deep ulcers, no transm signs, no grulas, noctures.

Ah, okay.

It's just a side effect of severe.

UC. Doesn't change the diagnosis.

Correct.

And the other tricky one is the granuloma.

We say it's specific for Chn, but there's a catch, a very important one.

Yes, finding a non-caseating epioid granuloma is highly suggestive of Chn's, but only if it's from a ruptured crypt.

Was a ruptured crypt?

Just a damaged gland in the lining.

If the granuloma is right next to that damageage, it could just be the body's reaction to that specific injury, like a little cleanup crew.

It doesn't count .

For it to strongly suggest Crohn, it needs to be sort of isolated, sitting and otherwise okay looking tissue.

Got it.

Okay, so we finally got the diagnosis, UC or Crohn's.

Now the focus shifts, right, to staving it, figuring out severity, and planning treatment.

Absolutely.

And that's where the Montreal classification comes in.

It helps us categorize the disease and guides how we manage it.

Let's start with Crohn.

What's the system there?

It's ALB.

A is for age at diagnosis.

A1 is under 17.

A2 is 17 to 40, A3 is over 40.

Why does age matter so much?

Well, younger patients, A1, often have more aggressive disease, and there's concern about growth, so you might be more aggressive with treatment, like biolog .

Older patients, A3, might have more comorbidity, so you think more about medication safety.

Makes sense.

What's L?

L is location.

L1 is just the ileium.

L2 is just the colon, L3 is bothium and colon.

There's also an L4 for upper GI disease.

Location matters for choos medside, which works best for L1,isease.

And B, you said B was the big one.

B is for behavior.

This is crucial.

B1 is inflammatory, only just inflammation .

B means their stricturing narrowing of the bowel.

B means penetrating diseaseulascesses.

And why is B so important?

Because B2 and B3 tell you the disease is already causing structural damage.

That often means you need to escalate therapy faster, probably to a biologic, and maybe even start thinking about surgery down the line.

B1 might respond well to simpler meds initially.

B behavior really predicts the disease course.

Okay, that's Crohn's ALB.

What about UC?

UC is classified by extent, E, and severity F.tent, how far it spreads.

Exactly.

E1 is proctitis, just the rectum.

E2 is left-sided colitis up to the splinic flexure .

E3 is extensive colit bey flexure, called politis if it involves the whole colon.

And why does extent matter?

It affects treatment options, topical therapies, like suppositories or enemas, work for E1 and maybe E2, but not E3.

And importantly, it determines when you need to start thinking about cancer surveillance, which we'll get to.

Right.

And severity, S. S is about how sick the patient is right now.

S1 is mild, usually defined as like four fewer stools a day, not much blood .

S2 is moderate, maybe four to six stools.

S3 is severe six or more bloody stools a day, plus signs of systemic illness, like fever, rapid heart rate, ania.

And S3 sounds like an emergency.

It is.

An S patient usually needs to be admitted to the hospital for IV steroids, maybe even planning for rescue therapy if steroids don't work quickly.

It dictates immediate action.

Okay, before we jump fully into long-term monitoring imaging, we talked about scopes, but what about things like MRI?

Good point.

MRE magnetic resonance andography is really thought of as a Crohn's.

Why is that?

Because Crohn often involves the small bowel, which the colonoscope can't reach well.

MRE gives us great pictures of the small bowel to look for inflammation, strictures, fistulas.

It's essential for staging Crohn, especially L1 or L3 disease, or if you suspect complications , for UC that's clearly limited to the colon on scope, you don't usually need an MRE routinely.

Okay, Cron.

Got it.

So let's talk long term.

This is where scope timing gets confusing, right?

Management versus surveillance.

Exactly.

People mix these up all the time.

They're two totally different reasons to do a colonoscopy after the initial diagnosis.

So what's a management scope?

That's usually done to check how well treatment is working .

Say you start a patient on a new medication, like a biologic.

You might snope them again, often around six months or so, specifically to see if the lining has healed.

Mucosal healing.

That's the goal.

That's the goal.

It's called Treat to Target, or TT.

Achieving mucosaling predict better longter outcomes, fewer surgeries, fewer hospital stays, so that six-month scope is checking for treatment success.

Okay, that's management.

What about the other reason cancer prevention or displeia surveillance ?

This is the eight-year rule people hear about.

Yes, the famous, or infamous, eight-year rule.

This applies to surveillance fororeal cancer risk, which is higher in people with long-standing, extensive colitis.

So eight years after diagnosis?

Ah, careful.

It's eight years after the onset of symptoms of colonic inflammation, not necessarily eight years after the official diagnosis date.

Oh, that's a key difference.

Huge difference.

Someone might have had symptoms for years, maybe dismissed as IBS, before getting diagnosed .

Their clock started ticking way back then, so it's eight years from when the colitis started.

And does this apply to everyone with IBD?

No.

Only those with significant colonic involvement.

So you see patients with E2, left-sided, or E3 extensive disease, and Crohn's patients with colitis affecting at least one third of their colon.

Who's exempt then?

Patients with just proctitis, UCE1, or Crohn's limited only to the alM L1 without colonic information. Involve .

Their cancer risk isn't considered significantly higher than the general population, so they typically follow standard screening guidelines.

Is there anyone who needs it sooner than eight years?

Like immediately?

Yes.

The major exception is patients who also have primary sclerosing tingitis, or PSC.

What's PSC?

It's a separate liver disease affecting the buct, but it's strongly associated with IBD as especiallyC.

If a patient has both IBD and PSC, their cancer risk is dramatically higher .

They need to start colonoscopy surveillance immediately upon the PSC diagnosis, usually annually, regardless of how long they've had IBD.

Wow.

Okay.

PSC means immediate annual surveillance.

But for others, once they hit that eight year mark, how often do they need scopes?

It becomes risk stratified.

Based on certain factors, the interval will be every one, two, or three years.

What puts someone in the high risk annual scope category?

High risk includes having PSC, finding dysplasia on a previous scope, having a colonic stricture , evidence of severe ongoing inflammation, even if they feel okay, or a strong family history of colorectal cancer, especially if diagnosed under age 50.

Okay.

And intermediate risk every two years.

That might be someone with mild ongoing inflammation, maybe lots of post-in inflammatory polyps.

Those aren't precerous themselves, but indicate past inflammation or family history of cancer, but diagnosed at an older age, say, 50 or older.

And low risk every three years.

That's typically for someone with extensive colitis, but who is in deep, sustained endoscopopic remission, meaning the lining looks great, and they had a high quality previous exam .

But remember, even in remission, the clock keeps ticking, surveillance continues, remission just potentially lengthens the interval.

Now, the technique for these surveillance scopes, it's changed, hasn't it?

We don't just take random biopsies everywhere anymore.

Thankfully, no.

The old way was, like, four biopsies every 10 centimeters throughout the colon.

It was tedious, time consuming, and honestly, not that great at finding the subtle, flat dysplasia we worry about.

So what's the modern standard?

High definition colon.copy, which gives much clearer pictures combined with cremondoscopy.

Chromo, meaning color, like dye.

Exactly.

You can either spray a dye, like indigo carmine onto the lining, or use electronic virtual chromondoscopy features built into modern scopes, like NBI or ICan.

And how does adding color help find dysplasia?

Dysplasia, the precancerous change, often causes subtle alterations in the surface texture and the pattern of tiny blood vessels, the capillaries.

Dye spray or virtual chromo enhances the contrast, making these abnormal patterns pop out visually .

It helps turn previously invisible flat dysasia into a visible target.

So if you can see it better, you don't need random samples.

Pretty much.

With effective chromonondoscopy, the goal shifts to targeted biopsies.

You carefully inspect the entire colon lining using the enhanced imaging, and you only biopsy suspicious areas.

Random biopsies are generally reserved now for specific high risk situations like PSC patients, or if the view is poor due to scarring or poor prep.

What happens if you do find dysplasia on a targeted biopsy?

If it's a visible lesion, like a polyp or a raised area containing low grade or high grade dysasia, the goal is usually to remove it completely endoscopically right then and there.

And then more frequent scopes.

Yes.

After removing visible dysasia, surveillance typically becomes more frequent, often annual, at least for a while, to ens nothing was and nothing new develops.

What's the most worrying finding them?

The trickiest one is finding dysplasia, especially high grade dysasia , on a random biopsy that was taken from Yokosa that looked normal during the scope so called invisible dysia.

Why is that so bad if it looked normal?

Because it implies there could be more advanced, possibly even cancerous, changes elsewhere in the colon that were simply missed because they weren't visible .

If you find invisible high grade dysasia confirmed by an expert pathologist, it often leads to a recommendationation for collectomy.

Removing the whole colon.

Really?

It sounds drastic, but the risk of having an undetected cancer somewhere in that colon is considered very high when invisible high grade displayia is found .

Since you can't see it to remove it endoscopically, removing the colon becomes the safest option to prevent cancer.

So pulling it all together, you can see how managing IBD is this ongoing process.

The colonoscopy isn't just one thing.

Its role changes over the patient's journey.

Diagnosis first, then checking treatment success, and finally shifting into this long term risk-based cancer surveillanceance.

It really is a roadmap.

So the key timing points, Scope it diagnosis to map things out.

Scope again may be six months after starting a major therapy to check for healing.

And then, if there's significant colon involvement, start the eight-year clock for surveillance, adjusting the one, two, or three-year interval based on risk.

That's a great summary.

Unless, of course..

Unless they have PSC, then it's scope immediately and every year.

Got it.

Right.

And just as a final thought, looking ahead , the technology is still evolving.

We're moving beyond just finding dysplasia with things like NBI and chromo.

There's research into field carcinogenesis detection.

Field?

What now?

Field carcinogenesis.

The idea is that widespread molecular changes might happen throughout the colon lining, even in areas that look normal, long before dysplasia develops.

Some researchers hope we could eventually detect these field changes, maybe even just from biopsies of the rectum, which is easy to read..

So a rectal biopsy could predict risk in the whole colon.

Potentially.

It could become like an early warning system telling us who really needs intensive surveillance, maybe even before the eight-year mark and who might be safe with less .

It's still research, but it could fundamentally change how we approach surveillance in the future.

That's fascinating.

Moving from a fixed clock to a truly personalized, biologically driven risk assessment.

Well, this has been incredibly helpful, really clarifying the journey from diagnosis through long-term care and IBD .

Hopefully this gives you a much clearer picture if you're navigating IBD or managing patients.

Thanks for joining us on the Deep Dove and we'll catch you next time.