Citywide Conference - Cholangitis
Welcome to the Deep Dive.
Today we're stepping into a really critical clinical scenario, bary infection, specifically colingitis.
Right, and this isn't just, you know, another infection.
Exactly.
It's rapidly escalating, potentially life-threatening.
You've got bilary extraction, bacterial invasion .
It all conspires to drive sepsis and organ failure.
The urgency is key.
Ear recognitionition, timely intervention.
That's everything.
So that's our force for today, navigating this urgent clinical landscape of colingitis, getting a handled on it quickly .
And from here, we'll explore, let's say, three key areas, our trees, if you will, for this deep dive.
Okay.
First up, the path of physiologic roots.
Really digging into what makes b get infected and how the whole system can just spiral.
Understanding the why.
Got it.
Then we'll look at the diagnostic branches.
How do we actually identify colingitis accurately ?
And maybe more importantly, how do we figure out how bad it is, how urgent?
Assessing severity, yeah.
Crucial for guiding what we do next.
And finally, we'll climb into the therapeutic canopy.
What are the strategies for effective management?
Antibiotics, sure, but also that critical piece, Drainage.
Putting it all together for treatment sounds like a plan.
Okay, so let's start at those roots.
Why is colonitis so dangerous?
What's going on, you know, behind the scenes that makes it escalate so incredibly fast?
Well, what's fascinating, and maybe not always appreciated, is that healthy bile is normally sterile.
It's clean.
Right, a closed system.
Exactly.
But when that's steriity gets breached, and maybe even more critically , when the flow of bile is impaired, obstructed, that's when things can go south really, really quickly.
So it's the combination, blockage and bacteria.
Precisely.
And understanding those underlying mechanisms, it helps you anticipate which patients are at higher risk and why the condition just seems to explode sometimes.
So what are the main things that disrupt that flow?
What's the usual suspect?
The most common cause, far and away, is gallstones.
They're implicated in , you know, the majority of cases.
Okay, gall stones makes sense.
But, and this is important, we're seeing an increasing role for malignancies, tumors, especially as our patient population gets older, or you have patients with complex anatomy after surgery, these can cause blockages too.
So not just stones.
Malalignancy is a big one too.
Okay, so once that obstruction happens, stone, tumor, whatever , how does that simple blockage turn into this life-threatening systemic infection?
What's the actual cascade?
It's really a pressure problem, fundamentally.
An obstruction in the biary tree, that stone, or tumor, it causes a significant rise in the pressure inside the duct.
Think of it like water building up a behind a dam.
Press builds up.
And that increased pressure makes the lining of the duct, the epithelium kind of leaky.
Its permeability increases.
Ah So the barrier weakens.
Exactly..
And then bacteria, which are normally just hanging out in the gut nearby, you know, your typical ecole, Clubella, and a recoccus, bactteroids, they can basically seep through that leaky ber.
Through the bile.
Into the bile, yes, and then into the portal system, the liver's blood supply and from there, boom, into the systemic circulation.
That's your sepsis trigger right there.
Wow.
Okay, so what usually stops that?
What are the normal defenses?
Normally, you've got a few things.
The spincter of acts like a one-way valve at the bottom of the bct.
The constant flow of bile itself helps flush things out.
And bile salts actually have some antibacterial properties.
But these can be compromised.
Definitely.
If someone's had a prior procedure, like a sphinterotomy, where that valve is cut or certain types of surgery, those defenses are weakeneded.
Okay.
And to make matters , if there's any foreign material in there, think plastic, sometimes placed to relieve obstructions or even the stones themselves, they act as a perfect and for bacteria to just set up shop and multiply.
A breeding ground.
Exactly.
It creates this protected space for infection to brew.
So thinking about linking this, sometimes see patients say with a new pancreatic mass, they might have painless jaundice, but no infection.
Right, right.
Initially, often sterile, but then maybe we place a stint endyscopically to relieve the jaundice.
And that act of instrumentation.
Can be the very thing that introduces bacteria into that previously sterile obstructed system .
And then they develop colongitis later.
It's a known riskk of the procedure, even though the stinting itself is necessary.
It really highlights that connection between obstruction, instrumentation, and infection risk.
Yeah, that really paints a picture.
It's this vicious cycle, isn't it?
Obstruction leads to pressure, leads to leakiness, lets bacteria in.
Infection takes hold, drives sepsis, organ failure.
It just feeds on itself.
Precisely.
And that explains why it conspirals so fast and why acting quickly is just so critical.
Okay.
That Y is pretty clear, and frankly, a bit scary.
So now the urgent question , how do we spot this?
Especially if it's not always the classic picture.
And just as vital, how do we gauge how bad it is, how far down that spiral the patient already is?
Yeah, that's a really important clinical point because we often can't wait for that perfect, you know, textbook phraseation to show up.
Early recognition and accurate grading are absolutely essential to guide how quickly we need to act.
Time is critical.
And you mentioned the textbook picture isn't always reliable.
Charco's's Triad.
Exactly.
Charco's Triad, that's the fever, right upper quadrant pain, and jaundice.
It's classic, yes, but it's only actually present in maybe half of patients, maybe even less.
This is only the half?
Wow.
Yeah.
And then there's Reynolds Pentad, which is Charcot's plus hypotension and altered mental status .
That usually means severe disease, a real emergency.
But again, probably not seeing that often until things are really bad.
Correct.
And you absolutely have to keep in mind atypical presentations, especially in the elderly, they might just present with confusion or isolated low blood pressure, kind of like how they might present with a UTI sometimes.
Subtle signs.
Very subtle.
Or patients onids, their inflammatory response might be, so they could be quite sick with sym .
The bottom line is, you need a high index of suspicion.
Okay, high suspicion needed.
So if the symptoms could be tricky, how do we actually nail down the diagnosis?
What criteria do we use?
We rely heavily on the Tokyo guidelines.
They're pretty much the global standard .
To make a strong diagnosis, you need evidence from three areas.
Okay, what are they?
First, signs of systemic inflammation.
That means things like fever or looking at the white blood cell t, is it high, maybe even low, or an elevated sea reactive protein, the CRP.
Inflammation markers.
Got it.
Second.
Second is colasis.
Evidence that bile flow is impaired .
Clinically, that's jaundice or labs showing an elevated totalubin, maybe two or more, or other liver enzymes associated with cololis, like alkaline phosphatase or GT being alvated, say, one and half times normal or higher.
Okay, inflammation and colostasis.
And the third?
Third is imaging evidence.
You need imaging that actually shows biliary dilation, the pipes are stretched, or evidenceidence of why it's obstructed, like seeing a stone or a mass causing the blockage.
Right.
You need to see the problem.
And what imaging do we typically reach for?
The go-to initial test is almost always an abdominal ultrasound .
It's easy, it's safe, no radiation, and it's actually very good at seeing if the ducks are dilated and often spots gallstones.
So start with ultrasound.
Yes.
If you see duck dilation or a stone on ultrasound, you often have your answer right there and can move towards treatment.
What if the ultrasound is unclear or you suspect something else?
Then a CT scan can be very helpful.
It's maybe not as great for seeing the stones themselves, but it's excellent for confirming d dilation, which is a key sign and for identifying other causes like masses orcesses.
Okay.
What about MRRCP?
MRCP, or magnetic resonance calandancreatography, is kind of the gold standard for looking at the bucts themselves, especially for things like malignant strictures, but you don't always need it in the acute setting of of colitis itself.
And you mentioned EUS earlier, endoscopic ultrasound?
Yes.
EUS is becoming incredibly valuable, especially in centers with expertise .
It's highly sensitive for ruling out billingsary obstruction, and a key advantage is you can sometimes do it at the bedside for really unstable ICU patients who you can't easily transport for a CT or MRI, helps avoid unnecessary invasive procedures like ERCP if there's no obstruction.
So it's a strategic progression ultrasound first, then CT, MRCP, or maybe U.S., depending on the situation and stability.
Exactly..
Choose the right tool for the question you're asking and the patient in front of you.
Okay, Diagnosis made .
Now, that grading you mentioned, how do we grade the severity and why is that so critical for deciding what to do next?
This is where the Tokyo guidelines become really powerful because the grading directly tells you how urgently you need to intervene specifically with drainage.
Okay, let's break that down.
Grade one.
Grade one is mild .
These patients have colitis, but they show no signs dysfunction.
Their organs are fine.
So what's the approach for mild?
Interestingly, for grade 1, drainage can actually wait.
The initial treatment is medical, antibiotics, IB fluids, pain control.
You observe them closely, they might not even need an intervention if they respond well, and there's no clear obstruction needing removal.
Okay, medical management first for mild.
What about grade two?
Grade 2 is moderate.
These patients don't have organ failure yet, but they have two or more specific warning signs.
Warning signs like what?
Things like a really high fever, being older, say 75 or more, having a very high white blood cell count or a very low one, a significantly elevated Billy Rubin, maybe five or more , or low albumen indicating poor nutritional status or chronic illness.
Okay, multiple flags indicating they're sicker.
What's the urgency here?
For grade two, these patients require early drainage.
The recommendation is typically within 24 to 48 hours, so not immediate panic, but definitely needs to be addressed soon.
Got it.
Early drainage from moderate, which brings us to grade 3..
Grade 3 is severe.
This is the most urgent category.
These patients have evidence of any organ dysfunction or failure linked to the colonitis.
Any organ failure.
So what kind of things are we talking about?
Could be cardiovascular failure, like hypotension, needing vasopressor medications, respiratory failure, needing oxygen, or even mechanical ventilation, acute kidney injury, liver dysfunction, like a high INR indicating clotting problems , altered mental status, confusion, lethargy, or even plat dysfunction, like thrombocopia, any of those bumps them into grade three.
And the management for grade three?
Urgent drainage.
That means ideally the same day or absolutely within 24 hours.
There's no waiting here.
Wow.
So that grading system isn't just like a descriptive label.
It's a direct call to action.
Absolutely.
It dictates the tempo.
And the data is really clear on this.
Getting urgent drainage for grade three patients significantly decreases mortality and shortens their hospital stay.
It makes a huge difference.
And critically, you have to remember, this can change, right?
Someone might start as grade one, but worsen.
Exactly.
It's dynamic, you have to keep reassessing.
A mild case that doesn't improve with medical therapy might quickly become urgent.
Constant vigilance is key.
Okay, that severity grading gives us a clear roadmap for urgency.
Now, let's move into that therapeutic canopy.
We've made the diagnosis, we've graded the severity.
What's the action plan?
What are the immediate moves to stabilize the patient and crucially get control of that source of infection?
Right.
If we think back to the big picture , the main goals are simple but critical. Stabilize the patient and get source control.
You have to address the underlying problem, the blockage and infection.
So the moment you suspect colingitis, what are the absolute first steps?
The non-negotiables?
First, always, always draw blood cultures before before starting ambiotics.
That is absolutely critical for tailoring therapy later on.
Cultures before antibiotics.
Got it.
Then aggressive intravenous fluids, crystalloids like lactated ringers, are often a good choice to support circulation, especially if they're heading to sex.
Start empiric antibiotics, broad .
Don't.
With the hour.
And monitor them a hak.
Close monitoring for any signing function changes in mental status, urine output dropping, blood pressure.
You need to be ready to escal care.
Okay, immediate steps covered.
Let's talk antibiotics.
What's the typical empiric choice and when do you need to maybe call for backup?
For initial empiric treatment, you need broad coverage.
You You're targeting the likely culprits, gram negatives from the gut, and also anerobes.
So what drugs provide that?
Common choices are things like pricillin tezibactum, often con, or sometimes a combination like a third generation cephalisbrin plus metronotol for anaerobic coverage.
Standard broad coverage.
When would you deviate or get help?
Yeah, it's always a good idea to consult infectious diseases, especially if the patient has a complex history , maybe known colonization with resistant bugs like MRSA or VRE, or if they've had prolonged hospital stays or recent antibiotic exposure.
They can help take tailor therapy.
Makes sense.
And then you adjust based on cultures.
Absolutely.
Once those initial blood culture results come back and hopefully they're informative, sometimes biultures can be contaminated, you want to deescalate, nrow the antibiotic spectrum to target the specific organism found.
And how long do you typically treat?
The usual duration is about four to seven days after source control is achieved.
That means after drainage is successful, the patient is stable, fever is gone , American guidelines often lean towards five to seven days in that situation.
Okay, antibiotics sorted.
Now, the big one.
Bill Yerry drainage, that cornerstone you mentioned.
When is it definitively indicated?
Drainage is clearly indicated for all grade two, moderate, and grade three severe cases .
It's also needed for grade 1, mild cases, if they fail to improve with that initial medical therapy within about 24 hours.
And of course, if there's a definite anatomical obstruction on imaging that needs relie..
And the timing, just to recap, is driven by that grade.
Exactly.
Early drainage within 24 to 48 hours for grade two.
Urgent drainage same day, or 24 hours for grade 3..
And if that grade one case fails medical therapy, the urgency bumps up to needing drainage within 24 hours, too.
Right.
And the main way we achieve this drainage is ERCP.
Yes.
ERCP endoscopic retrograde pancreatography is the primary method.
The main goal in hitis is simply to decompress that blocked infected bilary system, get the pus and infected bile flow.
Now, here's a practical point.
During that ERCP , how much do you do?
Do you just drain, or do you try and fix the underlying problem, like remove the stone right then and there?
That's a really key decision point.
And it depends heavily on how sick the patient is.
Okay.
In a stable patient, maybe a grade, who's responding, okay It's generally better to try and treat the underlying cause during the first ECP if you can remove the stone, dilate Stud show this can reduce the need for procedures later and shorten the hospital stay.
Makes sense.
Fix it while you're there if it's safe.
But and this is a big, but in a critically ill patient, say, a grade three patient on press, the priority shifts entirely.
The main goal is just decompression.
Get the pressure down.
Exactly.
So simply placing a plastic stent across the blockage to allow drainage is often the safest and best initial move .
Trying to do aggressive stone removal with baskets and balloons or prolonged manipulation in a very sick patient can actually increase the pressure in the ducts temporarily and potentially make the even sicker, maybe tip them over the edge into worse sepsis.
So less is more in the really sick ones.
Just get the drain in.
Often, yes.
Get the drain in, let the patient stabilize, treat the sepsis, and then you can come back later for definitive stone removal or other treatment when they're more stable.
Okay, that clarifies the ERCP goals.
Right.
What about lithotrisy?
Breaking up stones?
Does that play a role acutely?
Lithiripsies is about breaking up large stones, usually one's bigger than, say, two centimeters.
These are actually only a minority, maybe 10, 15% of buct stones.
Right.
And while there are ways to do it during ERCP, like mechanical bassaskets or electroydraulic shockaves or even older techniques like external shockaves.
The crucial point is lithotsy is very rarely indicated in the acute management of colitis itself.
So it's not for the initial drainage procedure.
Almost never.
It's a secondary step.
You do it after you've secured drainage and the patient is stable .
The immediate goal is always, always decompression, not necessarily getting getting every last bit of stone out right then.
Got it.
Drainage first, definitive treatment later, if needed.
What if URCP doesn't work?
If you can't get into the bileuct or maybe the patient's anatomy is altered from surgery , what are the backup plans?
Yeah, you always need a plan B. And sometimes plan C, ERCP, isn't always technically possible or successful.
So what are the alternatives?
One increasingly used option is ESguided drain, using endoscopic ultrasound to guide a needle puncture directly from the stomach or dodenum into the bi to place a drain.
Okay,S.guided.
What else??
Another major alternative is percutaneous transatic bilary drainage, or PTBD .
This is done by interventional radiology, where they pass a needle through the skin and lired directly into a boduct and place a drain drainage.
PTBD by IR.
Yeah.
Any others.
Surgical drainage is technically an option, but it's really a last resort these days, with modern endoscopic and perccutaneous techniques, open surgery for drainage is very rarely needed for acute colitis.
So ERCPs plan A, but.S.guided drainage and PTBD are strong backup options if needed.
Exactly.
The critical thing is ensuring drainage happens one way or another, according to the urgency dictated by the severity grade.
Okay, so boiling it all down, the therapeutic goal is swift, effective source control.
Get that biary system decompressed, whether it's via ERCP, EUS, or PTBD.
That's what stops the downward spiral and ultimately improves outcomes.
Absolutely.
Stabilize antibiotics, and drain.
That's the mantra.
Well, we've certainly covered a lot of ground here, navigating the complex terrain of colingitis right from its infectious roots through diagnosis and those urgent management decisions.
Yeah, it really highlights just how dynamic this condition is.
And, you know, while our treatments have improved mortality significantly over the decades, it's definitely not zero , especially for that severe grade 3 disease, mortality can still be substantial, maybe 20, 30%, even with prompt ERCP.
It's a serious condition.
Absolutely.
So as you, our listeners, think about applying this.
Remember those key takeaways.
Don't anchor on waiting for the perfect charco triad.
Keep that high index of suspicion.
Right.
And don't underestimate how quickly things can change.
That grade one can become grade 3 fast, reassess constantly.
And practically.
Yeah.
Always get those blood cultures before you give the first dose of antibiotics.
It matters.
Critically important.
And always, always be thinking about source control.
The immediate priority, especially in sick patients, is often just getting that drain in, even if definitively dealing with the underlying stone or stricture, has to wait until things are calmer, stabilized first.
So here's a final thought, Tom all over.
How does truly understanding the why , the path of physiology, the reasons behind the grading empower you when you're faced with that rapidly deteriorating patient, to adapt dynamically?
How does it help you move beyond just following a checklist and make those nuanced, potentially life-saving decisions when the standard path might need a slight detour?
How prepared of you to make that call Thanks for diving deep with us today.
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