Dr GI Joe

Welcome to the Deep Dive.

Today, we're tackling a really tough one.

The hostized IBD patient who presents with a severe bloody flare.

We're talking ulcer different colitis or Crohn's disease.

Yeah, and it's high stakes.

Our sources stress having a really systematic framework here.

Exactly.

Not just vague advice, but like actual decision points.

Absolutely.

When someone's that sick, you need clear steps .

What to do first, when to switch gears, when to call surgery.

You can't wing it.

Right.

So that's our plan today.

We'll follow the path right from the ED arrival through r ruling out infections, which is huge..

Then how we figure out severity because you see in are different beasts.

Right.

Totally different metrics.

What happens on day three, if things aren't better?

The big pivot point.

And managing the really scary stuff, like toxic megacolon.

Okay, let's get started.

First steps in the ED.

So this patient often rolls in looking pretty unstable.

What's the absolute must-do list right away?

Okay, first up, stabilize.

Get those vitals, make sure you have two large bore IVs going, start fluids, and get a type and cross just in case.

Standard procedure for selling sick and labs.

Yep.

The full workup.

CBC, CMP, definitely.

Inflammatory markers, CRP, ESR, and co-As. You need the whole picture.

But the number one priority, even before thinking about IBD drugs.

Is infection.

Infection.

You absolutely have to rule it out.

The sources really hammer this point home .

Don't jump to immunosuppression, if it might be an infection mimicking a flare.

Exactly.

That's the classic dangerous mistake.

These patients get infections and C diffI is super common.

It looks just like a flare sometimes, or makes one way worse.

So what tests are we ordering immediately?

Stool studies.

Stat.

You need Ced of PCR and Toxin essay.

Don't forgetool Culture and OMPOva andasites CMV amoeba 2.

And the gold rule then is..

Hold the IBD meds.

Especially the steroids.

Don'tmosuppress you' reasonably sure infection isn't.

Wow.

That feels counterintuitive.

Patients crashing, inflammation's raging, but you're holding back the main treatment.

It feels wrong, but it's crucial.

Imagine giving high dose steroids or starting a biologic on top of untreated seedive?

Disaster.

Or worse, CVitis outmet.

So, the rule is clear .

If any relevant bug pops up on that stool panel, you treat the infection first.

Like Vamy and for diff.

Yep.

Oral Vomycin for C diff.

Glover, if it's CV, treat that, give it a couple of days, maybe 48, 72 hours, then see where the flare stands.

Got it.

Jumping the gun with steroids or biologically is the key error to avoid.

Okay, so let's say we've stabilized them.

Labs are cooking, and infection looks unlikely for now.

Next step, how bad is this flare?

And this is where we can't use the same ruler for UC and Crohn, according to the sources.

Absolutely not.

It's a common pitfall.

UC is new coastal.

It's about the surface lining.

Crohn's is transmural, goes deeper, causes structural problems.

Different diseases need different severity scores.

Okay, let's tackle ulcerative kitis first.

That's where the true love and Wisk criteria come in.

Correct.

That's the classic standard.

It's pretty straightforward.

Yeah.

It's based on stool frequency and signs of systemic toxicity.

So what defines severe UC?

Severe UC is six or more bloody stools per day, plus evidence that the body's really taking a hit.

Systemic toxicity signs like .

Like a fever over 37.8 Celsius., a heart rate over 90, hemoglobin dropping below 10.5 or that classic marker, an ER of 30 or more.

I did see the sources mentioned CRP is often used now, too, maybe more than ESR.

Yes, CRP responds faster, it's more dynamic.

Clinically, a CRP over 30 milligrams per liter is a strong indicator of severe UC activity.

You often look at both, really.

They tell you this isn't just diarrhea.

The patient is systemically unwell.

Okay, clear enough for you, C.

Now let's switch to Cronhn's disease.

If stool count isn't the main thing , what are we looking for?

For Cronhn, you're hunting for complications and systemic illness.

Is there an absst?

Can't pass stool or gas?

Is there an abscess brewing?

Aula,ation, bleing, significant weight loss?

Sounds like imaging becomes way more important here.

Definitely.

If you're worried about any of those structural issues, obstruction, abscess, paronitis, you need a CT scan of the abdomen and pelvis with contrast .

That's often essential early on in in a severe Crohn's fla.

And lab markers for Crohn's severity.

Still ESR.

CRP is really the go-to for Chn's activity.

ESR is less reliable.

A CRP over, say, 45 milligrams per liter.

That's a big red flag, suggests severe disease, maybe complications, poor prognosis if you don't escalate treatment.

So quick recap, you se severity, I'put plus toxicity.

Cron severity equals complicatedlications plus systemic signs, often needing imaging.

You got it.

Two different ways of thinking about severity.

All right, we've stabilized, ruled out infection, assessed severity.

What are the basic inpatient orders before we get to the IBD?

Specific drugs?

Supportive care is key.

Keep up with IV fluids, and correct electrolytes closely.

Often bowel, NPO are clear liquids start.

Okay, makes sense.

But then there's this really tricky one the sources emphasize.

VTyllaxis, blood thinners, while they're having bloody stools.

This is the one that makes everyone pause, but it's critical.

The guidelines are firm.

Pharmacologic VTEyllaxis, usually low molecular weight hep, or hep is mandatory.

Wow, why take that risk?

Because these hospitalized IVD patients are incredibly hypercoagul, Their risk of DVT or PE is like two to three times higher than other hospitalized patients .

That clot risk massively outweighs the risk of slightly increasing rectal bleeding from the heparin.

So unless the bleeding is absolutely catastrophic..

Exactly.

Unless it's truly massive life- threatening hemorrh causing hemodynamic instability, you give the VTE prophyllaxis.

Just seeing blood in the stool is not a reason to hold it.

That is such a key point.

Okay, start the heepurn.

What do we need to stop?

Definitely stop any NSAs the patient might have been taking .

Epiprofen reproxen, out.

And also, stop opioids if possible.

Why stop pain reds?

Narcotics slow the gut, which can worsen things, increase the risk of toxic megolon, and importantly, they can mask serious complications, like perforation or an abscess, especially in cro.

Got it.

Okay, what about looking inside?

Scoping the patient?

Yes, but you have to be about it.

In an acute, severe flare, a full colonoscopy is generally a bad idea .

The risk of perfor is too high.

So what's the approach?

For a severe UC flare, the standard is a flexible sigmoidoscopy, just looking at the lower part within 24 to 48 hours.

No bowel prep needed, usually.

And the goal there.

Confirm how bad the inflammation looks and crucially get biopsies to rule out CMV colitis.

That's vital.

Makes sense.

And for a severe Crohn's flare, scope or no scope.

Generally, you defer endoscopy acutely in severe .

The risk of perforation with that deep transmural inflammation is just too significant and the yield might be limited compared to imaging.

You rely more on that CT or MR you earlier.

Okay, we've done the groundwork.

Infections rolled out, severity assessed, supportive care, and VT propyllaxis started .

Now it's time for the first line IBD treatment.

Right.

For a severe flare, either UC or C's, once infection is reasonably excluded, the first step is high-dose IVorticostids.

Which ones typically?

Usually IV methyl pregnisone, something like 60 milligrams a day as a single dose , or maybe IV hydrocortisone, 100 milligrams every eight hours.

Pretty standard stuff.

Now, the sources highlight a really critical moment, especially for UC patients, the day three check in.

Day three is make or break.

You have to formally assess the response to steroids by day three .

If that patient is still having lots of bloody stools, if they still need blood transfusions, if their CRP isn't coming down, if they're just not improving systemically..

They're a non-resper.

You're a non-resper.

And you cannot afford to wait.

You need to act immediately, either escalate to arcue therapy, or get surgery involved right away.

Waiting until day five or seven is too late.

Okay, so for UC rescue therapy, what are the main options?

The two big ones are inflixomab.

That's an anti-TNF biologic or cyclistrin, an older, potent immunosuppressant.

How do you choose between them quickly?

Generally, inflixomat is preferred these days, especially if the patient hasn't had biologics before, biologically na, and if you're thinking anti-enF therapy might be good for their long term maintenance.cycloss.

Cyclos comes into play more if the patient has already failed antiF therapy.

Or maybe if they have a reason they can't get a biologic like severe heart failure .

It requires careful monitoring, often in an ICU setting.

But regardless of which drug you choose.

You absolutely need a surgical consult at this point. Of steroid non-response.

Even if you start rescue meds, surgery needs to be on the table and aware.

Okay, that's UC.

Now, what about Chrome's disease if it's not responding to steroids ?

The path looks different, no cycosprine.

Absolutely no cycosrine for chhn's.

It just doesn't work well.

Remember, Crohn's is deep transmural inflammation.

Cyclos sprine is better for a superficial mucosal inflammation, like in UC.

So what's the rescue plan for steroid refractory crones?

It's biologic therapy.

Usually, you'd go with inflixomab first line if they're biologically naive.

If they've already had anti TNFs, then you'd pivot to a different mechanism, like Videlazoomab or used toinab.

And we keep coming back to this point about complications.

Always.

If that CT scan showed an abscess or a significificant obstruction in your Chn's patient, you' deal with that before escalating immunosuppression.

Meaning.

Meaning interventional radiology needs to drain that abscess surgery to address the complication before you give a powerful biologic that could make an underlyingfection or mask a perforation, structure first, then drugs.

It's probably worth just touching on mild IBD quickly, because how we treat mild flares also really shows the difference between UC and Crohn's.

It really does.

The approaches are fundamentally different.

For mild ulcerative colitis, the absolute cornerstone drug is missingalamine, also known as 5.

How is that given?

Depends on where the inflammation is.

For disease just in the rectum or s colon, distal disease,ical malamine suppositories or enemas actually better than oral pills .

For more extensive colitis, you' use oral malamine may beedical.

What about sulf fac?

Does that still use?

It can be.

It works for mild UC, but mellamine generally has fewer side effects., so it's preferred.

Sulfacazine might be considered if cost is a major issue, or, interestingly, if the patient also has IBD-related arthritis, because sulfacazine can help both the gut and the joints.

Okay, so five ASA is key for mild UC.

What about mild chomes?

Is 5 ASA useful there?

Nope.

Basically useless for Cones.

Forget the five ASAs.

Really?

So what do you use for mild Cones?

If the inflammation is mild and localized, typically in the Iium and Sium, the Iliosqual region, the go-to is oral binide, usually nine milligrams once a day.

That's a steroid, but different from pregn.

Yeah, it's designeded to have high activity in the gut but get broken down quickly by the liver, so fewer systemic side effects than predisone.

But, and this is a big, but binide is only for short-term use.

How short?

Like induction only.

Maybe up to three months, tops .

It's not for long-term maintance.

If someone needs longer treatment or can't take st, you'd often just jump straight to inducing with a biologic agent like an anti-Nizabab.

Got it.

Big difference.

Five ASA for mild UC, Binide short term, or biologics for mild ?

All right, let's talk about the scariest inpatient scenario.

Toxic megacolon.

Yeah, this is the one you really don't want to miss.

Usually seen more with severe UC, right?

Predominantly, yes, though it can happen in Crohn's colitis 2.

The diagnosis relies on specific criteria.

You need imaging evidence, usually an x, showing the colon is massively dilated.

How dilated?

Typically looking for the transverse colon diameter greater than six centimeters, but that's not enough on its own.

You also need signs of severe systemic toxicity.

Okay, what are those signs?

You need at least three of these .

High fever over 38, fast heart rate, over 120, high white blood cell count, over 10,500 or significant anemia.

So dilated colin plus three toxicity signs.

Plus at least one sign showing how sick they really are, like dehydration, confusion, or altered mental state, low blood pressure, or electrolyte problems.

Once you suspect or diagnosed toxic megacolon, what are the absolute dos?

Okay, critical don'ts.

Stop anything that slows down the gut.

No opioids, no anticolergic drugs, and absolutely do not give them a bowel prep for a colonoscopy.

That could cause a perfor .

Right.

Management then involved.

Get them to an ICU or step down unit immediately..

Strict bowelrest MPO.

Keep giving IV fluids and correct electrolytes and continue the high dose IV steroids we started earlier.

What about antibiotics?

The sources mentioned broad spectrum antibiotics, like sectryacone, plus metronole, or maybe p.

Why antibiotics for inflamm?

This is crucial.

The antibiotics aren't really treating the IBD itself.

They're trying to provvent a catastrophe.

That colon wall is stretched paper thin, incredibly inflamed and fragile.

Bacteria from inside the gut can easily leak across that damaged wall into the bloodstream.ad disepsis.

Exactly.

Massive sepsis or percation.

The broad spectrum antibiotics are given to try and preventerial translocation and potential system infection.

It's life insurance.

And surgery.

Urgent consotiable the suspect .

If the patient doesn't show significant improvement within, say, 48 72 hours of maximum medical therapy, the brest steroids antibiotics, they need surgery.

No waiting around?

No waiting.

Or if they perforate or have uncontrolled bleeding, they go straight to the OR.

The timeline is very tight.

And quickly, are there any newer medical options emerging for these really tough cases?

Yeah, the sources mentioned JAKhibitors specifically to aetinib, as an emerging option for rescue therapy in acute severe UC, particularly in patients who've already failed biologics .

It's another potential tool before resorting toomy.

Hashtagag.

So if you boil it down, the key clinical shortcuts are, for UC severity, think counts plus systemic..

For C's severity, think complications,struction, abscess plus systemic illness, often needing imaging.

And that VThylaxis, even.

Right.

And the biggest takeaway for you, the learner , really seems to be about the sequence.

Don't mess up the order.

That systematic approach stabilize, rule out infection first, then stratify severity, then choose the right initial therapy, and know exactly when to pivot or call for help that seems absolutely critical.

It prevents those key errors, like giving steroids on top of C diffIF or biologics when there's an undrained abscess.

Exactly.

Which leads us to a final provocative thought stemming from the sources discussing Crohn's disease after surgery.

Even when you remove the disease bowel, Crohn's often comes back right where the bowel was reconnected.

Yeah, recurrence rates at the anestomosis are depressingly high.

So the source's stress being proactive, doing a colonoscopy relatively early after surgery, maybe around six months, not necessarily because the patient has symptoms, but to look for early signs of recurrence , and then potentially starting biologics preemptively to prevent it from getting bad again.

Right, shifting from reactive treatment to proactive prevention.

Which raises a bigger question for managing chronic diseases like IBD.

When do we consider the disease truly quiet or in remission?

And when should our interventions be preemptive, treating not just what we see now, but trying to head off the recurrence we know is likely coming down the road, something to definitely think about.