April 4, 2023 • 47 mins
Good pals and rising M4s at Northwestern, Nathan Kudlapur and Alek Gorzewski, take the hot seat to discuss a case of upper GI bleed! We are joined by a returning special guest, Dr. Aashish Didwania.
Host: Daniel Matthew
Discussants: Nathan Kudlapur, Alek Gorzewski
Guest: Dr. Aashish Didwania
A&O Team Member: Kevin Grudzinski & Lauren Smith
Produced by: Kevin Grudzinski, Daniel Matthew & Lauren Smith
Alert & Oriented is a medical student-run clinical reasoning podcast dedicated to providing a unique platform for early learners to practice their skills as a team in real-time. Through our podcast, we strive to foster a learning environment where medical students can engage with one another, share knowledge, and gain valuable experience in clinical reasoning. We aim to provide a comprehensive and supportive platform for early learners to develop their clinical reasoning skills, build confidence in their craft, and become the best clinicians they can be.
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Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
(00:00):
This excellent medical student-led podcast is for educational purposes only and not intended
(00:27):
to be used as medical advice under any circumstance.
Alright, welcome back everyone.
It's been a little while.
I'm excited to be back behind the microphone.
We're post-match, so some congratulations are in order to our esteemed Northwestern
host, Dan, who matched at Emory.
Thank you so much, man.
KG, always good to see you, as always.
(00:49):
I'm joined by my OG co-student, Lauren Smith.
Hi everyone.
It's really good to be back.
Really excited to be back post-match and have all of that kind of uncertainty behind us
and excited to have some upcoming M4s with us today.
We were just talking, we've got to expand our podcast to some new locations, so Dan
(01:11):
will be in Atlanta and then I'll be at MGH in Boston, so exciting things coming up.
And then we have a returning guest and huge supporter of the podcast, Dr. Didwania, and
congrats to him too on Northwestern.
I want to get the monitor OG for program director.
The OG program director, this is true.
It's my 11th going on 12th year.
(01:31):
I'm getting close to OG, but it's great to be back.
This is such a fabulous podcast and to work with the two of you, so congrats to both you,
Daniel and Lauren.
And nice to work with the two newbies and rising stars.
Yeah.
KG, I'm not going to lie, it's a little cold outside, but it's getting real toasty in here.
We got two superstar M3s.
We are so excited to have you guys on.
(01:53):
It's going to be such a pleasure to hear your thoughts.
So without further ado, I want our listeners to be introduced to our wonderful M3s.
I'll start off with Nathan.
Go ahead and tell us who you are and we'll go from there.
Hi everyone.
My name is Nathan Kulipur.
I'm a current third year medical student here at Northwestern, really on the tail end of
my third year here, wrapping up my last clerkship, currently on my pediatrics clerkship.
So yeah, originally from southeastern Ohio, went to undergrad at The Ohio State University.
(02:18):
Mixed reaction from the crowd.
Hey everyone.
My name is Alek Ojefsky.
I'm a third year medical student, just finished my third year core clerkships.
And I am from Providence, Rhode Island.
And I went to Hampshire College for undergrad and I was a non-traditional student.
(02:39):
So I ended up going to a post-bac program in Bryn Mawr and here I am now.
So we have a 68 year old man who was in his usual state of health until he suddenly felt
strange, became diaphoretic and then passed out.
He woke up seconds later and vomited up bright red blood.
So obviously there are a couple of different things going on.
What are you guys thinking?
What are your first thoughts?
(03:01):
So I have my initial thoughts.
There's kind of two key presenting symptoms you're going on.
You have the syncope and passing out and you have the hematomasis.
So initial broad buckets I'd be thinking of, central differential would be probably neuro,
cardiac and GI where I'm thinking or trying to connect these.
Yeah.
Right.
So I'm going to go into that.
(03:21):
Okay.
So we have hematomasis as you mentioned.
And what can kind of unify all of those together?
I'm wondering if ETOH is involved.
That's a good point.
Yeah.
If there's either cirrhosis or just esophageal tears from vomiting so much.
Yeah.
With the hematomasis initial thing I'm thinking of, some sort of esophageal rupture or esophageal
(03:42):
tear like Mallory Weiss or something.
I assume, I feel you could have the strange feeling that diaphoresis along with that picture.
I don't think that would be unreasonable.
Yeah.
Yeah, totally.
I'm forgetting right now what's the big kind of, I know that having a prodrome for syncope
is important.
Yeah.
Dividing some or for kind of sifting through the differential does make me think of vasovagal
(04:07):
for sure.
Yeah.
With the prodrome.
Yeah, it's true.
And then other thing in terms of the syncope and like tying in like cardiac being, I think
arrhythmias and the be a driver for syncope.
I don't think I would necessarily explain the hematomasis necessarily.
It would be some sort of MI picture going on.
I've not heard of hematomasis associated with that.
I'd be curious to hear if there's any other symptoms he's also had along with this picture.
(04:31):
Yeah.
Actually, that's a great point.
Why don't we keep going with that?
What other questions would you want to ask this patient?
What are some of that information that you think might be helpful?
Chest pain.
If there's any chest pain, I think that would be helpful.
Getting off of alcohol, you know, what if he's been drinking, what's his sort of substance
use habits?
Also just questions about GI symptoms as well.
If there's, you know, kind of melanoma or something like that.
(04:53):
I also got the sense you were trying to characterize what led up to the syncope a little bit more
to help you focus on how we think about syncope.
Right.
Yeah.
Also wondering how he felt after this episode, you know, because if you think about something
seizures or something, you want to think about what their awareness is and the post post
seizure.
Uh, timeframe.
Yeah.
The fact that he woke just the wording, he woke up seconds later does make me think that
(05:18):
it's probably going to be more syncope, but that's a good point because we don't know
if he's altered.
Right.
Yeah.
I love that you guys are kind of thought through the differential for syncope because it might
be easy to get distracted by this hematomasis, but if you're going to connect the two, how
would you connect the two?
Another thing to think of, of that we didn't mention would be pulmonary embolism.
(05:42):
That's I know a rare cause of syncope, but pulmonary embolism can show up with a bunch
of different things, including cough, including theoretically hemoptysis.
So hematomasis mimic.
Yeah.
That's good.
Keep going.
I'm wondering if he has some kind of esophageal rupture or tear of the esophagus and yet you
lose some of the blood, his blood pressure dropped a lot.
Maybe there'd be some orthostatic type picture going on.
(06:04):
That's a great thought.
So I have that thought too.
And you're making a bunch of different connections between the syncope and hematomasis, maybe
hemoptysis, but some kind of blood loss.
And would that make you mild, medium or hot in terms of your level of worry?
Hot.
Yeah, hot.
Red hot.
What's the hottest flavor you get at Taco Bell Hot Sauce?
(06:26):
Diablo.
That might be this guy.
So right.
Because you often think about when you're seeing a presenting picture of a patient,
your instinct as a physician might not always be what's the diagnosis, but it might be what's
going to potentially kill this person and how to make sure that I'm dying the next couple
of minutes.
And if this is hemorrhage and hemorrhagic shock, you got to act fast.
(06:47):
Nice.
Great work.
I'm just going to touch on a couple of things that you guys mentioned.
Great points.
Number one, identifying if the patient is sick or not sick.
I think that's such a crucial distinction.
And I think you guys nailed it.
This patient is very, very sick.
I also love that you highlighted there's a syncope component and there's this hematoma
system component, both of which need appropriate workup.
And I love the questions that you're trying to ask.
Trying to differentiate why is this happening?
(07:08):
What can be united in these two things?
And where can we go from here?
So how about I get you some more information?
So for the patient's past medical history, the patient has a history of peptic ulcer
disease with a Bill Roth II procedure performed in 1993.
They've got a history of hypertension, cholecystectomy, and an umbilical hernia repair.
In terms of current medications, they're on hydrochlorothiazide, amlodipine, and multivitamins.
For allergies, allergic to iodine.
(07:30):
In terms of a social history, there is no alcohol use.
They do have a one pack per day history of smoking.
They live alone and they are a clerk at a city court.
This patient, in terms of family history, father died of CVA at the age of 67.
Mother has congestive heart failure in her 80s and has a brother who does drink.
So this is a lot of information.
(07:50):
Anything that stands out to you?
I think the no ethanol use is helpful in framing the differential, some of the things we were
thinking about, because some of the Mallory Weiss I believe would be more common in a
patient that consumes a lot of alcohol.
Yeah, in line with that esophageal varices was coming along.
There can be other causes of that associated with total hypertension maybe, but you know,
(08:13):
of course the most common thing we think of is cirrhosis due to ETOH overuse.
Yeah, yeah the key things from the past medical history, peptic ulcer disease.
You can get GI bleeding as a result of peptic ulcers.
So that's something to keep in mind.
I'm not sure what Billy Ross is.
Don't worry, we'll get into that.
I'm going into the 90s.
(08:33):
Yeah, history of hypertension, smoking history, something else we should definitely have been
to be on the differentials, aortic dissection.
So yeah, that's something we do not want to miss.
I really like how you both are thinking about those must not miss diagnoses.
So for example, in this patient we talked about esophageal varices and Alec, I think
(08:53):
it was a great point that you had that we see that this patient doesn't drink alcohol,
but there are other causes for cirrhosis and so that should not immediately necessarily
rule that out.
So we still want to be worried about this patient.
I also feel you guys have kind of honed in on your first kind of differential of causes
of upper GI and Mallory Weiss tear, variceal bleed, peptic ulcer disease.
(09:19):
That's the place to be starting.
But typically peptic ulcers and varices being the two most common causes of upper GI bleed,
at least in the US.
So keep indulging with what else?
The nice thing about GI is it's very anatomic.
And there are mimickers, maybe it's not coming from the South African, maybe it's coming
from the lung and they're coughing it up.
You know, sometimes we think about something that they're swallowing the blood and it's
(09:43):
coming from the nose, the posteriopharynx.
So indulge me a little bit more.
And by the way, nobody has a Bill Roth who's been in med school since 2001.
But I was in med school up until 2001 and I still saw that procedure and I know, Dan
and Lauren, you might get into this.
But I was familiar with that procedure and that procedure was done in the 80s and 90s
(10:03):
as a treatment for peptic ulcer disease because PPIs were still new and they hadn't discovered
one of the biggest drivers of peptic ulcer disease yet.
It was discovered around that time.
I don't know if you're trying to read my mind of what that discovery was.
I'll tell you it's a bacteria.
H. pylori.
H. pylori.
So understanding that there was an infection driving this anatomic thing was new in the
(10:28):
90s and once they figured out how to treat and cure H. pylori, they could give PPIs now
over the counter.
People didn't need procedures, but I suspect our friends here are going to go through a
little bit what that procedure is.
So fantastic job though thinking about the differential property GI bleed.
You know, this is such a great transition.
You know, we're thinking about peptic ulcer disease.
We're thinking about what are some of the ways that we can address this and you know,
(10:49):
I love the thought process about number one, we still have this syncope picture, but we
also have this hematopesis and we're thinking about how does an upper GI bleed fit into
this?
Where anatomically does this all fit in?
So I'd actually do a quick pause and think a little bit more about peptic ulcer disease
specifically.
So from your perception, how would you describe peptic ulcer disease?
Most commonly caused by H. pylori and I think it's sort of an erosion in the mucosa of the
(11:13):
stomach and so I think then you get less acid maybe that secretes.
Yeah, because that erosion.
Well I think there's maybe the baby's acid produced by the H. pylori versus just the
erosion into the stomach mucosa.
Yeah, these are all great points.
One of the reasons I have to just get definitions is just to make it clearer for all of us,
but I agree with one of your points.
(11:34):
So in simple terms, peptic ulcer disease, there if you mentioned, there's some kind
of a defect in the mucosa of either the gastric or duodenal wall.
And as you can imagine, there are a lot of complications that can arise from it.
One of them, you both mentioned hemorrhage.
As you guys mentioned, PUD can often lead to hemorrhage.
Obstruction is another one and of course perforation if the ulcers penetrate through the bowel
wall.
(11:55):
So this is one of the things that we think about, you both mentioned, for this patient
with a history of peptic ulcer disease and this new onset of regi bleeding.
Now this patient had a Delroth II procedure performed.
This is a, definitely something that isn't as routinely done anymore because Dr. Duane
mentioned, we now know that there are these things H. pylori that are contributing to
this.
But I thought we could do a quick overview of what this procedure is and kind of why
(12:17):
it was indicated.
So in this procedure, we have normal anatomy here on the left.
For those of you who are listening, I would encourage you if you can to just, just Google
what the Delroth II procedure looks.
It might be a lot easier than me describing this overhooding.
But basically what we're seeing is we have a resection of the distal end of the stomach
and then we have a duodenal stump that is then closed and there's an anastomosis of
(12:38):
the distal end of the gastrum to the jejunum.
So you had this anastomosis at the gastro-jejunal junction and you have a closure of the stump
of the duodenum.
So we've got a couple of different components going on here, but the goal is to remove the
segment of the stomach that has the suspected peptic ulcer disease.
Does that kind of make sense?
Yeah.
So part of the stomach is still technically still be attached to the proximal duodenum
(13:03):
that's not connected there?
So the proximal duodenum actually is not connected to anything in this case.
Yeah.
Did they just resect the part of the stomach off of that?
Yes, exactly.
Exactly.
Where the ulcer is, they just take it off?
Yes.
Well, I want to add a couple of things.
You can imagine this is a pretty tough surgery.
I mean, they've got to do an open procedure.
You can imagine the complications and postoperatively in bariatric surgery, people didn't suffer
(13:28):
from abdominal pain, malabsorption, diureloscoma.
And if I could comment on a couple of things that have been stated in the discussion, fabulous
discussion is H. pylori is probably causing these ulcers through inflammation and the
infection itself.
Interestingly, H. pylori produces urea, which is an acid buffer.
And so people with H. pylori, when you treat them, might actually be at larger risk for
(13:49):
GERD because the urea is buffering the acid and now you take away the buffer and that
acid can reflux up.
So oddly with H. pylori, acid might be a mitigating factor, but it's not the driver.
It's the infection.
In the bilroth, they often ligate the vagal nerve and the resecting part of the stomach
(14:09):
that are the acid producing cells.
So by taking out the vagal nerve and that section of the stomach, you are dramatically
dropping acid production.
So it's a different mechanism for H. pylori.
You're reducing acid levels and that's going to reduce future ulceration.
So back in the day, they would do this for people that were having severe symptoms from
peptic ulcer disease, complication of peptic ulcer disease and things like Tums, calcium,
(14:35):
those kinds of things that typically buffer the stomach were enough and they would go
to this pretty drastic procedure, but now the PPIs are ubiquitous.
Those are lower acid levels and fixing the things that they were probably fixing autonomically
with this procedure.
But I'll repeat, nobody knows what this procedure is anymore.
I'm very glad you're here, Dr. Zuley.
This is very helpful.
(14:56):
Yeah, thankfully this is not done with T. le anymore because we now have medications
that can help address the underlying peptic ulcer disease.
But just for our patients, nice to know kind of what was going on and what the current
anatomy is.
So you're ready for some labs, some exam findings.
All right, let's let's get into the exam.
All right.
So for this patient's vitals, temperature is 96.3, heart rate of 110, respiratory rate
(15:19):
of 18 and a blood pressure of 81 over 54.
The patient is alert and oriented.
Do you guys do this with every case you have?
Honestly, we should start with a little jiggle after.
Patients pupils are equal round reactive.
(15:39):
The oropharynx was clear.
The lungs are clear to auscultation.
The heart is tachycardic irregular.
The abdomen is non tender, non distended, positive bowel sounds and healed surgical
scars.
The remedies are without edema pulses are one plus and neuro is non vocal.
What are you guys thinking?
The first thing that jumps jumps out to me is the vital signs where this patient's tachycardic
(16:02):
hypotensive I'm really worried about, you know, him being volume deck.
We have the history of, you know, blood and vomit some sort of hemorrhagic shock maybe.
Yeah, yeah, I think the fact that we see the low blood pressure should be very concerning
because if that's all from the blood loss, it means he's lost quite a bit of blood.
Normally you just initially just see the heart rate jump up, but you don't really see the
(16:23):
blood pressure dropping to you lose, I think, 30% of your blood.
So you probably lost quite a bit if we are seeing this hypotension.
Yeah, you're absolutely right.
It's very important to recognize early on that this patient is in shock.
And I think you guys nailed it.
There's a history of hematomasis.
The patient that most likely is in a hemorrhagic shock situation needs to be addressed.
With that being said, what is something?
(16:44):
Well, what are some things that you would want to order urgently?
What is information that you think would help you kind of figure out, OK, what are best
next steps?
Type in screen for sure.
Oh, yeah.
Yeah, type in screen.
Yeah, start placing some large boar IVs.
Yeah, great.
Any imaging studies?
Probably.
You think we should go straight to CT?
Yeah, CT, abdomen and pelvis, but chest as well.
(17:06):
Yeah, right.
The physical exam is there isn't anything super impressive.
There's no tenderness anywhere.
So I don't know if we want to do a fast bedside ultrasound.
That is something we can think about just to see if there's any free fluid anywhere.
Yeah, I think it's reasonable to do that in the interim as well.
Yeah, while we're getting things teed up for CT.
(17:26):
You guys have thrown out varices as a potential cause of upper GI bleed and now we're thinking
a lot about peptic ulcer disease, given this guy's history and given the frequency of it.
What exam findings could help you with either of those?
I think the abdominal exam, non-destended, points away towards some sort of liver pathology
(17:46):
involved.
We don't see any evidence of the side E's.
So that sort of picture, I would say varices is probably less likely.
What are your thoughts, Alec?
One of the things that I am wondering about is that there's no mention of the liver, but
if there's a pattern of megalene, that would make me more concerned that something is happening
in the liver.
(18:07):
That was a physical exam.
What about some other skin findings that you would want to check for?
Thank you for the hint.
Medicine is important.
Exactly.
And jaundice.
Jaundice, yeah.
There you go.
Yeah.
Spider angiomatas.
Yeah.
Gynecomastia.
Yeah.
So I think, I mean, that's exactly right.
(18:28):
You guys threw it out early and it was fantastic that word about alcohol history doesn't maybe
have it.
We're still worried about cirrhosis.
We need some esophageal varices, but also disease probably is not going to have any
telltale physical exam findings, right?
If anything, we talked a lot about H. pylori.
We shouldn't forget NSAIDs and pills.
We looked at it.
We saw his pill list.
Presumably you have an ability to go back and get additional history that he's not down
(18:51):
at NSAIDs either pro-fertiline for the last 10 weeks is another thing.
But looking for signs of cirrhosis in the physical could be very helpful here.
It doesn't always got to be.
Very nice.
Very nice.
All right.
So I think one of the things that I really liked is some of the things that you were
thinking about ordering are really catered to the patient who is in shock.
We talked about a fast anxiety, talked about getting sensitive imaging that will provide
(19:13):
us with as much information as quickly as possible.
I think that's a phenomenal thought process.
We got some different imaging that we'll walk through, but I'd love to get your thoughts
about this.
We have a chest x-ray here.
So we guys think about the left versus right diaphragm.
Which one's typically, it's okay if you're not sure.
Actually you can guess.
It'll be 50, 50 chance.
I believe the right is higher because the liver.
(19:35):
Yeah.
So it's here.
Looks like the side.
Yeah.
So when you thought, when you're seeing the diaphragm does look like it's smashed up,
that might be true.
That might again just be the angle of how the film is taken.
But there's also a little bit of an elevation of that right hemidiaphragm compared to the
left.
Excuse me.
Left hemidiaphragm compared to the right.
I'm going 50, 50.
I'm wondering.
(19:56):
The left is a little bit higher than the right.
And that's a little unusual.
So fluid, what else can push up to one side of a diaphragm, the left side of the diaphragm?
If you can atellectasis the lungs or something, get some negative pressure.
Yeah, that can be true.
Well, we don't really see compressed lung there.
Usually you'd see what could look infiltrator, atellectasis or just consolidation.
(20:18):
Stomach is there.
Spleen is there.
Okay.
So one of the things we talked, you said it was fluid.
Could also be some sort of reflective process going on where maybe the stomach is distended.
That being said on this image, I'm not seeing any sort of air from there.
Okay.
You're in the right organ systems to be thinking about what could push it up.
(20:39):
Yeah, absolutely.
Fantastic work.
I think one of the key things that I wanted to highlight, which you all did wonderfully,
is thinking about anatomically what organs are where and how we can present on a chest
x-ray.
You nailed it.
The liver can tend to push up the right hemidiaphragm.
And in this case, we're seeing the left is a little bit higher.
What does that mean?
Just things to keep in mind, which great.
You guys hit that very well.
Alright, let's get you some labs.
(21:01):
Alright.
Nice.
So in terms of the patient's labs, we have a white blood cell count of 22, a 22% neutrophil,
56% lymphocytes, 19 monocytes and 13, 3% basophils, hemoglobin of 11.1, platelet of
225, sodium of 140, potassium of 3.9, chloride 108, bicarb 25, UN 41, creandin 1.3, mucose
(21:24):
171, lactate 2.1.
We did PT INR, PT is 14, INR is 1, PTT is 36.
And with fluids, the hemoglobin is now shown to be 8, with the white blood cell count of
6,000 and a platelet of 90k.
So a lot of lab, a lot of numbers.
Yeah, wow.
What, what are your thoughts?
What are you, what are you reading?
What are you thinking?
(21:44):
One of the first things that jumps out to me is the PUN being 41 compared to creandin
of 1.3, which is also somewhat elevated, but not as much.
And I have no idea why this is, but I just remember from somewhere in the recesses of
my mind that with peptic ulcer disease, often you have an elevated UN.
(22:05):
Other things, well, I mean, that might make sense.
I guess it was the A-color azeria producing, maybe that could drive up the area.
Oh, nice.
I don't know if that's what happened, but yeah, that's cool.
Yeah, other things I'm thinking.
So I have initial CBC, actually hemoglobin 11, that's better than what I would have anticipated.
I diluted to 8.
(22:25):
Yeah, it makes me wonder if your initial is concentrated and that's why you're seeing
it artificially elevated in terms, the white count 22, that I think is interesting in terms
of differential maybe.
One thing that has made me think of is there's some type of malignancy picture could be going
on because I know H. pylori can be associated with the malt lymphoma.
(22:47):
So that could be maybe something we're thinking about.
In terms of the chemistries, Ni-GAP7.
So yeah.
Right.
Another thing with the hemoglobin of 11.1 down to 8, I think you're right.
There can be a dilutional component of it.
The fact that the white blood cell count went from 22 to 6 though, that's pretty impressive.
(23:09):
Yeah, that's a big difference.
Another thing though is hemoglobin, if it's an acute bleed, you may not see.
Hemoglobin drop.
Yeah, hemoglobin drop as dramatically as you would do it, right?
So maybe there's some of that going on as well.
Yeah.
So I have a question for you both.
We saw this patient's vitals.
You're in the emergency room.
(23:30):
This is your patient.
Are you giving blood?
Yes.
Yes.
Even with the hemoglobin of 8?
What's our usual concentration?
Oh, normally stack less than 6.
Yeah, it's 6.5, 6, something like that.
You're just basing how much blood we have available.
Usually 7.
Okay.
How much shorter than, say, 6.5.
(23:51):
Right.
But we're seeing such-
We're also telling you this person's maybe in hemorrhagic shock, right?
Yeah.
We're seeing such a precipitous decline over not a very long period of time that getting
blood on board sounds a good plan.
I think you're right on track, right?
Clinically, you're worried about this patient.
Even though the hemoglobin isn't at that transfusion threshold, we know that this patient
(24:14):
lost blood.
They were throwing up blood.
So, I think you're thinking about it.
Great.
Exactly right, Lauren.
I mean, guiding these guys, you guys have been on it.
All of the cell lines went down, so there's definitely some chemo concentration, which
adds to the idea that this might be hemorrhage.
He's holding on to whatever fluid he can, but it's not enough from the fluids we're
(24:34):
needed.
But those cell lines look scary to me.
And you threw out a number of 30% before you had 30% blood loss before he was in the emergency
shock.
I remember one of my favorite rules that Tom, tell me gauge how much blood was lost was
10, 20, 30.
10% blood loss makes you tachycardic, 20% makes you work the static, 40% makes you pass
out hypotension.
So, I was happy to hear 20 years after my information, then rule of thumb with 30% still
(25:00):
sticking around.
And that makes you worry that this guy has lost a lot of blood, passed out.
Or that it's going to keep dropping as you add more fluid and maybe he's still bleeding.
I think one of the things that we hit on, I really want to emphasize this because I
think it's such an important point, is treating the patient rather than just treating the
(25:20):
number.
I think you guys picked up on this.
Even if the hemoglobin isn't necessarily below six, we know that the patient is in shock.
And we know that in this case, giving blood may help the patient, especially with the
perfusion status.
We know their lactate is at 2.1.
So, really focusing on how we can help the patient.
I think you hit up on this very well.
So, I'm really glad to see that.
It's great, great work.
So, one of the things I'd love to ask is, based on these, as a based on this information,
(25:44):
how does this affect your differential?
What are you thinking about?
What do you think might be causing this hemorrhagic shock, generally?
One of the things, especially with learning more about the Billy Roth procedure, is could
there be a surgical complication?
I'm thinking a little less of that though, just because of the timeframe.
That's more of an intuition.
From all that we've gotten so far, I would feel, yeah, definitely more narrows towards
(26:07):
thinking some sort of relation to the peptic ulcer disease causing the bleeding.
I think we've talked about esophageal varices, you know, with no history of alcohol use,
pretty much benign abdominal exam, no skin findings.
I think that's less likely.
Also the Mallory Weiss tear.
I think we would expect the mediastide to be a bit more widened on the chest x-ray, and
also less so with alcohol use.
(26:27):
So I think peptic ulcer disease related causes the highest in the differential at this point.
So next steps, are you going to go looking for peptic ulcer disease?
Would you do a scope?
Yeah.
Would you be safe to do that?
That would be my only concern, if I get safe to do that, but I think that would be the
best way to probably visualize it.
Right.
I know outpatient, there's a couple other options with the Rhea Breast Test.
(26:51):
There's two other ones.
Oh, like stool tests.
That would let you know if there's H. pylori, but I don't think it would tell you much about
what's going on inside the stomach mucosa.
So probably upper GI scope, I think is what I would do next.
Yep.
You guys should continue to work together.
When you go into residency, you guys are very effective at working these.
I want to comment on intuition.
(27:12):
Intuition is undersold in medicine.
That's called street smarts.
It's been 30 years since this guy had that procedure.
It would be odd for 30 years to pass, and solidly be a complication of that way you
kind of put it.
Yeah.
And kind of going back to the must not misdiagnoses and everything that's on your differential,
you know, the upper endoscopy would help you to see if there is peptic ulcer disease, but
(27:35):
you know, you don't want to wait around for a urea breast test in the emergency room.
You want to be 100% certain that there are esophageal heresies too.
Right?
So that's a great next step.
So I actually think this is a great point to pause into a quick teaching point.
Just on our approach to upper GI bleeds.
One of our one of the podcasts that we often also ascribe to the clinical problem solvers,
they have a wonderful framework for upper GI bleeds.
(27:57):
You mentioned some of the most common causes of our upper GI bleeds.
We know peptic ulcer disease, esophageal heresies, esophagitis, but just thinking about things
from an anatomic standpoint, Dr. DeWine, you mentioned because the GI system is so easily
anatomically arranged, it's easy just to go proximal to distal and think about, okay,
what is causing upper GI bleed?
As I'm sure you all know, classified upper GI bleeds is anything up to the ligament of
(28:19):
trites.
So we're thinking esophageal, you mentioned this, Mallory Weiss, there's a tumorous camera
lesions, black esophagus, gastric ideologies, gastritis, tumor, oral gastropathy, and small
bowel classically things.
AVMs, tumor, and terioentery fistulas.
A lot of these things are a bit more esoteric and not as commonly seen, but I think the
most common things you guys clearly picked up on.
(28:40):
It's great to just keep in mind.
The important questions that you both asked is number one, is there a history of cirrhosis?
Could that be contributing to these symptoms?
And number two, is there a potential aorta-enteric fistula?
Is there something that is causing this?
Why is there, why are we seeing this constant blood in the upper GI tract?
Great thoughts.
I also love the fact that you picked up on, do we need to do a scope for this patient?
(29:01):
Is there something that we can see that can really help us figure out next steps?
So with that being said, why don't we get to some images.
So we did do an EGD and really to summarize, in the esophagus, there was no evidence of
esophageal varices.
In the stomach, there was a moderate amount of blood.
There were grade two gastric varices in the body of the stomach, none of which appeared
to be actively bleeding.
There weren't enlarged, thickened folds that suggest portal gastropathy.
(29:23):
The anastomoses showed no signs of active evidence of bleeding.
And the scope was introduced into the duodenum that showed no ulcers or masses there as well.
So that's a lot of information.
What are you guys thinking?
So do you think I'm taking it right here?
There's blood in the stomach, but it's not entirely clear where that blood came from.
There's not a huge ulcer listed here.
(29:48):
There are gastric varices, so that's likely the source, but that doesn't get to the question
why does he have gastric varices.
So maybe we can pause here for a moment.
What does portal gastropathy, what does that tell us?
We have a new diagnosis for this patient.
Portal gastropathy.
You don't hear that though.
Yeah.
(30:09):
No.
I think this is the first time I've heard that.
So think of, you've got portal.
You guys are both smart.
I think.
So what could mean?
So I think so the gastric vein, I think, into the portal vein.
So I think this is maybe something where it kind of is portal hypertension, but like it's
shunted towards the gastric veins.
(30:30):
Absolutely.
Yeah.
So maybe I can take a moment and talk about that and then you can fill in.
So I think talking just briefly about portal hypertension here is helpful.
So what happens with portal hypertension is you have increased resistance in portal blood
flow.
And you also get these increase in collaterals, which just makes everything worse and ultimately
(30:51):
can cause hypotension and ascites.
And there are a lot of different reasons why you would have portal hypertension.
Any that you can think of that you may have learned about before.
One classic association.
Right.
So one we talked about was cirrhosis.
I can also think of heart failure.
Yeah, right.
Heart failure.
Yeah.
(31:12):
See that?
Yeah.
So that's a lot of emphasis on the portal vein, malignancy.
Well, you're on the right track for sure.
And I know, Dan, you've got some more teaching points if you want to talk about those causes.
Yeah.
So, you know, I love that you guys are thinking about this anatomically.
I think the easiest way to remember this stuff is to simplify it as much as possible, which
you both are doing.
(31:32):
The way that I think about this and the way, Lauren, you explained it so well.
Just anatomically, we realized that blood drains through the portal vein into the liver
and then ultimately out the hepatic vein and to the right side, right heart for surge circulation.
And as you both mentioned, you can have issues at any of these points.
Prehepatic, intrahepatic, posthepatic.
And just to summarize some of the things that you have already mentioned.
(31:53):
When we're thinking about prehepatic causes, you mentioned, is there an issue with the
portal vein?
Is there perhaps a thrombosis?
Is there an issue in another vein that drains into the portal vein?
When we're thinking about intrahepatic, you guys both mentioned cirrhosis.
Commonly we see potentially schistosomiasis, which is something that I personally never
seen, but apparently the literature can often present with this intrahepatic portal hypertension.
(32:15):
And of course, you both mentioned causes of posthepatic, right heart failure.
Is there a tricuspid valve issue that's just causing blood to just be backed up?
But Chiari, things just to think about.
And I love that you guys are really categorizing this into different systems to help you figure
out, okay, what could be contributing to this?
Based on all of this information, at this point, it's still kind of nebulous as to,
all right, which category are we in?
What are we dealing with?
(32:35):
Is there anything that you think might be helpful to parse out which category this patient
might be experiencing?
LFTs, for one.
LFTs could be useful.
You can echo cardiogram, check the heart function.
You can ultrasound the liver also.
Yeah, some sort of imaging of the abdomen.
What in the abdomen in particular are you looking at?
(32:58):
Portal vein flow.
Portal vein, we talked about the liver.
Anything else you want to look at?
IVC.
IVC.
Okay.
Remember we saw that diaphragm.
What were we concerned about?
Any organs underneath that left side that you think might be?
Scalene.
Great idea.
Very nice, very nice.
And I know you also mentioned earlier on about potentially getting a CT, abdomen, pelvis.
(33:22):
Just some things to think about.
Oh, you know what?
I think we can get to that information.
So we did a liver ultrasound with Doppler that was normal.
We also did a splenic ultrasound with Doppler.
And just to summarize, we are seeing the spleen is diffusely enlarged with a lobulated contour.
It is dilated of quick measurements, 10 centimeters in cradiocardial and 11 centimeters in the
(33:43):
transverse dimension.
Which is big.
Significantly long.
Yeah, yeah, yes.
And we're seeing in the splenic hyaline what looks like a rounded hypoechoic focus that
seems to be within the spleen.
It does not appear to represent a fluid collection, an abscess or a hematoma, because there is
a vessel seen running through this region.
You didn't get to actually examine the patient, but let's hope they felt something.
(34:05):
Yeah, they were.
It's a little bit firmer on that left side.
Uh-huh.
And I think in this particular image, you can see how much the kidney is pushed down
because of how big the spleen is.
Oh, yeah.
You can see how...
Pretty striking.
Exactly, exactly.
So you mentioned something is going on with the spleen.
Yeah.
It's definitely a bit larger than we would expect.
(34:27):
Because I feel we're getting close.
So you got this huge spleen and all these other signs to support you're on the trail
towards getting to this point.
But a normal liver.
Yeah.
What's that about?
I mean, I think everything we learn is, you know, the spleen gets big because of portal
hypertension from cirrhosis, but there's no physical sign of cirrhosis.
(34:48):
The liver looks fine on ultrasound, looks fine on MRI.
Yeah.
I mean, probably some type of type picture going on to cause the gastric portal gastric
bariesis.
Right.
Possibly because of just the complication of the surgery.
Could be that.
I mean, they're moving around a lot of stuff for the Bellaroth procedure.
(35:10):
That's possibly an abnormal vessel connection forms.
But also I'm wondering about the mold lymphoma.
I don't exactly know how that presents, but I know something you can often see malignancy
involving the liver or sorry involving the spleen because the blood cells go and are filtered
there.
So that would be something I would look more into actually.
So just taking a step back, good thoughts.
(35:32):
Let's assume that we also got an echo for this patient and it showed appropriate right
heart function, no signs of tricuspid regurg.
What category do you think you would place this patient in?
Would you think this is a pre-hepatic, intra-hepatic, post-hepatic, particularly if we are seeing
a liver that looks pretty normal on imaging, but a spleen that's just way out of proportion?
But scientifically it's huge.
(35:53):
Yeah.
I would say pre-hepatic.
Yeah, yeah, definitely.
I think it's so important and we both did to realize liver's fine, but something must
be going on distal to this that's causing just a whole host of symptoms.
Any thoughts on what might lead to potential pre-hepatic causes of portal hypertension?
You've actually mentioned a few of these already.
(36:14):
Yeah, tumor, tumor burden.
Sure.
What else can obstruct things?
If you have an abscess perhaps.
How about with the vasculature?
Do you have an aneurysm compressing?
There's some areas on this MRI that are kind of lit up too.
Looks to be in the vascular.
Lossifications.
(36:34):
Potential.
Sometimes maybe things that flow aren't flowing.
Right.
Okay.
Could be embolus as well.
Oh, a blood clot or something.
Could be a clot.
Yeah.
Or it's not from the blood.
Or it's not from the blood.
Yeah.
It's not from the blood.
It's like something must be obstructing the passage of blood.
(36:56):
And so you're having this ballooning of the spleen.
Yeah.
Even with a normal liver appearance.
So with that, let's actually get into the read of the MRI.
So we are seeing complete and chronic thrombosis of the distal portion within a pen proximal
2.5 centimeters of the splenic vein.
So what we are seeing in this case, you both mentioned this, there is some kind of obstruction
for this patient who has a chronic thrombosis of the splenic vein.
(37:20):
As you both mentioned, the splenic vein drains into the portal vein and feeds into the liver
out to the hepatic vein.
And so if you have the blockage at the splenic vein, the spleen is just going to balloon
up and distal to that liver is going to look totally fine.
So I think a good learning point is just to pause and really look into what a splenic
vein thrombosis is all about.
So most common etiologies, classically we think of pancreatitis.
(37:43):
And we know this because the splenic vein actually runs along the posterior surface
of the pancreas.
So when you have this inflammation in pancreatitis, it can lead to thrombosis.
Other things, masses, like you mentioned, the cancer, mecenesis, endoparsenoma, big
things stenosis, posterior gastric ulcers.
I just included this picture here on the side just to kind of show what these various look
for different pathologies.
(38:04):
But one thing I really wanted to highlight is aside from these different etiologies,
patients can be in hypercoagulable state that could lead to these thrombotic episodes.
So I've just summarized a couple of the different hypercoagulable states that we can see.
Most of this is, I'm sure you all know all these.
I won't go too deep into any of these, but inherited causes, common hypercoagulable inherited
(38:26):
causes, factor V laden, protein CNS deficiency, antithrombin 3 deficiency, acquired causes,
different types of cancer, HIT, also PCV, Waldenstrom.
So just things to keep in mind just so we're aware moving forward.
I love when people tell me, I'm sure you know this and then give me the answer.
But there's something that the beautiful part of this case so far is that things are really
(38:47):
adding up.
I mean, we talked a lot about cirrhosis and we talked about esophageal varices.
There were no esophageal varices.
And suddenly the anatomy here explains gastric varices, isolated gastric varices suggest
an issue with the splenic vein.
And it could be as we kind of came to, intravascular clot or something extravascular compressing.
(39:09):
And that could be inflammation, a mass, something bad.
And now we're figuring out why in the heck does this gentleman have a splenic vein for
the gossips.
But everything else is explained now.
It's kind of remarkable.
I mean, you've got to save the guy's life.
But diagnostically, we're down to the central question here is why does this guy have a
clot in his splenic vein?
Yeah.
Oculins, razor.
(39:29):
Yeah.
So let's see what happens.
Let's see what happens to the shuttle.
So he is transfused to maintain hemoglobin, great job.
And surgery is consulted for an urgent splenectomy.
Okay, now, as you're doing this, as the great medical team that you are, you take a look
into his hospital records.
And you see that previous hospital records show a hemoglobin of 20.
(39:51):
And the patient history is notable for erythromyelalgia.
So just to summarize, this is burning, paresthesias, headaches, weakness, dizziness, itching after
a warm bath, hyperhidrosis.
Does this suggest anything to you?
Polycythema varin.
Yeah, exactly.
Sore.
Sore.
(40:12):
Sore in the acu-computer-generated audience of body.
That's exactly right.
Yeah.
It's interesting because when this patient presented, we're seeing a really low hemoglobin
of eight after fluids.
But we're seeing from the history, there's a hemoglobin of 20.
And so you're absolutely right.
The underlying diagnosis for this patient is this polycythemia varia that we're seeing
from especially the patient's history and a lot of the symptoms that he was experiencing.
(40:35):
You know, whenever somebody says something's pathognomonic in modern era, you should worry
that it's not pathognomonic.
But erythromyelgia is pathognomonic for either polycythemia varia and hemoglobins that are
usually over 16, but more likely 18 to 20, or essential thrombocytosis or thrombocytosis
with platelet counts over 400,000.
So it strikes me or concerns me that a hemoglobin of 20 and symptoms of erythromyelgia weren't
(41:02):
on his past medical history and a diagnosis wasn't given to this gentleman earlier.
It just means he probably didn't need a lot of care.
He in the 90s hadn't manifested yet, just part of the disease.
So that's really striking.
It actually makes you terrified of a hemoglobin 8.
You see hemoglobin 8 all the time.
If there's one that passed out from hemoglobin 8, it means they happened really fast or they
(41:22):
started at 20.
Yeah.
You just kind of alluded to that earlier.
Based on the history, you're expecting it to be a lower number.
Yeah.
But to the patient, it was a lower number.
It's just not like the lower what we're used to seeing.
Exactly.
Which is why it's also great that you didn't wait for the hemoglobin to get to that.
Excellent work.
Excellent work.
Yeah, exactly.
And another step pearl, any time a patient on a step exam is itchy after a bath or a
(41:46):
shower.
There it is.
You already know it's polycythemia vera.
Nice.
Great work.
So just a few quick learning points about polycythemia vera.
We touched on a few of these points.
Classically, the hemoglobin is greater than 16.5 or 16.
Patients often have JAK2 mutations.
As I'm sure you know, polycythemia vera, we have a low erythropoietin levels, but we have
an extremely high level of hemoglobin.
(42:08):
And often for these patients there, we do see pretty commonly venous and arterial thrombosis,
which kind of fits what we're seeing for this current patient.
And there's a higher incidence of GI complaints and peptic ulcer disease that can be seen
on endoscopy.
So I'd love to get your opinions on potential treatments for polycythemia vera.
Anything that you can think of that might be helpful for these patients.
I think, I mean, one option would be some sort of adenoforesis or try to take out some
(42:33):
of the blood to reduce hemoglobin.
I don't know what the frequency you'd need to do that and if that's sustainable for the
rest of the patient's life.
That's gonna be one option.
Great.
Yeah, it's fantastic.
So in fact, the treatment that has the best overall survival is in fact phlebotomy.
It has been shown, particularly for patients who have died, it's significant polycythemia
vera.
(42:53):
Phlebotomy is kind of the mainstay, one of the main things that we gotta focus on.
Another therapy that has been shown to be particularly efficacious is hydroxyurea.
It's shown to reduce the risk of thrombosis compared to just phlebotomy by itself.
And of course, for these patients, we also have aspirin, 81 milligrams.
Something that you may remember from step one is with the potential JAK, tyrosine kinase
(43:14):
mutations, there are specific medications, Roxolitinib, I don't know if that rings a
good bell, that specifically target the tyrosine kinase inhibitors.
But really, if for patients, kind of the mainstay therapy, phlebotomy, hydroxyurea, and make
sure they're on aspirin to avoid thrombosis.
Those patients unfortunately phlebotomized himself by hemorrhage.
Right now you don't, or are you gonna forget?
(43:35):
Absolutely.
That would make things worse.
But excellent work, guys.
So honestly, as we kind of take a step back and look over the entire case and kind of
what's been unfolding, you mentioned that initially the patient presented with syncope.
You noted that this is potentially in the setting of hematomasis.
You noted that there are different causes of a potential upper GI bleed, but you really
narrowed it down.
Could this be in the setting of this peptic ulcer disease?
(43:57):
Is there a potential varices?
You worked between different causes of upper GI bleeds.
You narrowed in on a gastric variceal bleed.
You made sure you evaluated all different organ systems.
You found the splenic vein thrombosis, and you had found the polycypheine vera that was
underlying this entire condition.
So round of applause to both of you guys.
Good work, Dallas.
Excellent.
Good job, Nathan.
That was a wild case.
(44:17):
That was incredible.
So many twists and turns.
Seriously.
And then you reflect the journey.
Oh man, I guess, yeah.
Keep on hunting.
Don't stop.
Yeah, because yeah, people just kept on turning over the new leaves, you know, at every step.
(44:38):
And so also, yeah, yeah, just yeah.
How the final destination we got to is, you know, I wasn't necessarily thinking about
ploids at the beginning, but I was definitely.
Well, I'd throw in it that you guys really thought through the acuity of sickopy and
(44:58):
got on this person who was sick and this was being hemorrhage early on, which is essential.
And then the main differential from a learning standpoint is upper GI bleed.
I mean, that's what you really want to take away from how to approach that hematomasis
is what's the source and H. pylori, NSAIDs, varices, malory waste.
That's the differential to really take away.
I say, theemia, we learn about it in med school.
(45:19):
It's rare.
And it's funny that it's common to clot, but they present with bleeding.
So there is trickiness to this case.
Yeah.
And maybe one other pearl that we spent a little bit of time on a different sections
of the case discussion is people that clot in unusual places need a workup versus people
with lower strepia DDTs.
(45:39):
Then you can start to think of that Burkhouse triad and maybe it was immobility or being
bed bound, maybe it was their cancer and they had inflammation.
But if they've got a clot in their splenic vein, they got Bud Chiari, they present with
arterial clots.
You go through the hypercoagulant workup and that differential that you put up there, Daniel
had PCV on it.
(46:00):
So as soon as he's got that clot in an unusual place, you start sniffing around for things.
Great job guys.
Something else that's interesting is this patient had peptic ulcer disease in the nineties.
So PCV usually presents in sixties, this patient's in his late sixties.
So are those things related?
Are they not related?
Was that early symptom or was it just people have peptic ulcer disease and he had both
(46:26):
of those?
I guess we'll never know, but I think it's an interesting thing to think about.
With the bleeding, so when we did the scope, we didn't see any active bleeding from the
varices.
So that's why I'm wondering, how long ago did that bleed?
We're assuming it bled from the varices.
How long ago did the bleeding happen from the varices before I actually saw this?
(46:47):
Great question.
And one of the things that happens when you have a bleeding vessel is if you lose a bunch
of blood, the vessels deflate.
So it fixed itself through a bad means.
So it's not unusual that people hemorrhage from a vessel.
By the time you go look, you don't see any more because they lost that much blood that
the vessel actually decompressed itself.
And then sometimes you just can't see everything.
(47:08):
The gastric bodies got folds in it and they might not easily identify it.
So that's a very great, that's a really good question.
All right.
Thank you Nathan and Al for joining us.
Thanks Dr. D'Onofria for joining us.
Congrats again to Dan and Lauren.
So well deserved.
So happy for both of them.
And thanks everyone for listening.
Thanks everybody.
Yeah, thanks for having us.
It was a blast.
(47:29):
Thanks again for listening.
For some time and place.
See you next time.
This excellent medical student-led podcast is for educational purposes only and not intended
(00:27):
to be used as medical advice under any circumstance.
Alright, welcome back everyone.
It's been a little while.
I'm excited to be back behind the microphone.
We're post-match, so some congratulations are in order to our esteemed Northwestern
host, Dan, who matched at Emory.
Thank you so much, man.
KG, always good to see you, as always.
(00:49):
I'm joined by my OG co-student, Lauren Smith.
Hi everyone.
It's really good to be back.
Really excited to be back post-match and have all of that kind of uncertainty behind us
and excited to have some upcoming M4s with us today.
We were just talking, we've got to expand our podcast to some new locations, so Dan
(01:11):
will be in Atlanta and then I'll be at MGH in Boston, so exciting things coming up.
And then we have a returning guest and huge supporter of the podcast, Dr. Didwania, and
congrats to him too on Northwestern.
I want to get the monitor OG for program director.
The OG program director, this is true.
It's my 11th going on 12th year.
(01:31):
I'm getting close to OG, but it's great to be back.
This is such a fabulous podcast and to work with the two of you, so congrats to both you,
Daniel and Lauren.
And nice to work with the two newbies and rising stars.
Yeah.
KG, I'm not going to lie, it's a little cold outside, but it's getting real toasty in here.
We got two superstar M3s.
We are so excited to have you guys on.
(01:53):
It's going to be such a pleasure to hear your thoughts.
So without further ado, I want our listeners to be introduced to our wonderful M3s.
I'll start off with Nathan.
Go ahead and tell us who you are and we'll go from there.
Hi everyone.
My name is Nathan Kulipur.
I'm a current third year medical student here at Northwestern, really on the tail end of
my third year here, wrapping up my last clerkship, currently on my pediatrics clerkship.
So yeah, originally from southeastern Ohio, went to undergrad at The Ohio State University.
(02:18):
Mixed reaction from the crowd.
Hey everyone.
My name is Alek Ojefsky.
I'm a third year medical student, just finished my third year core clerkships.
And I am from Providence, Rhode Island.
And I went to Hampshire College for undergrad and I was a non-traditional student.
(02:39):
So I ended up going to a post-bac program in Bryn Mawr and here I am now.
So we have a 68 year old man who was in his usual state of health until he suddenly felt
strange, became diaphoretic and then passed out.
He woke up seconds later and vomited up bright red blood.
So obviously there are a couple of different things going on.
What are you guys thinking?
What are your first thoughts?
(03:01):
So I have my initial thoughts.
There's kind of two key presenting symptoms you're going on.
You have the syncope and passing out and you have the hematomasis.
So initial broad buckets I'd be thinking of, central differential would be probably neuro,
cardiac and GI where I'm thinking or trying to connect these.
Yeah.
Right.
So I'm going to go into that.
(03:21):
Okay.
So we have hematomasis as you mentioned.
And what can kind of unify all of those together?
I'm wondering if ETOH is involved.
That's a good point.
Yeah.
If there's either cirrhosis or just esophageal tears from vomiting so much.
Yeah.
With the hematomasis initial thing I'm thinking of, some sort of esophageal rupture or esophageal
(03:42):
tear like Mallory Weiss or something.
I assume, I feel you could have the strange feeling that diaphoresis along with that picture.
I don't think that would be unreasonable.
Yeah.
Yeah, totally.
I'm forgetting right now what's the big kind of, I know that having a prodrome for syncope
is important.
Yeah.
Dividing some or for kind of sifting through the differential does make me think of vasovagal
(04:07):
for sure.
Yeah.
With the prodrome.
Yeah, it's true.
And then other thing in terms of the syncope and like tying in like cardiac being, I think
arrhythmias and the be a driver for syncope.
I don't think I would necessarily explain the hematomasis necessarily.
It would be some sort of MI picture going on.
I've not heard of hematomasis associated with that.
I'd be curious to hear if there's any other symptoms he's also had along with this picture.
(04:31):
Yeah.
Actually, that's a great point.
Why don't we keep going with that?
What other questions would you want to ask this patient?
What are some of that information that you think might be helpful?
Chest pain.
If there's any chest pain, I think that would be helpful.
Getting off of alcohol, you know, what if he's been drinking, what's his sort of substance
use habits?
Also just questions about GI symptoms as well.
If there's, you know, kind of melanoma or something like that.
(04:53):
I also got the sense you were trying to characterize what led up to the syncope a little bit more
to help you focus on how we think about syncope.
Right.
Yeah.
Also wondering how he felt after this episode, you know, because if you think about something
seizures or something, you want to think about what their awareness is and the post post
seizure.
Uh, timeframe.
Yeah.
The fact that he woke just the wording, he woke up seconds later does make me think that
(05:18):
it's probably going to be more syncope, but that's a good point because we don't know
if he's altered.
Right.
Yeah.
I love that you guys are kind of thought through the differential for syncope because it might
be easy to get distracted by this hematomasis, but if you're going to connect the two, how
would you connect the two?
Another thing to think of, of that we didn't mention would be pulmonary embolism.
(05:42):
That's I know a rare cause of syncope, but pulmonary embolism can show up with a bunch
of different things, including cough, including theoretically hemoptysis.
So hematomasis mimic.
Yeah.
That's good.
Keep going.
I'm wondering if he has some kind of esophageal rupture or tear of the esophagus and yet you
lose some of the blood, his blood pressure dropped a lot.
Maybe there'd be some orthostatic type picture going on.
(06:04):
That's a great thought.
So I have that thought too.
And you're making a bunch of different connections between the syncope and hematomasis, maybe
hemoptysis, but some kind of blood loss.
And would that make you mild, medium or hot in terms of your level of worry?
Hot.
Yeah, hot.
Red hot.
What's the hottest flavor you get at Taco Bell Hot Sauce?
(06:26):
Diablo.
That might be this guy.
So right.
Because you often think about when you're seeing a presenting picture of a patient,
your instinct as a physician might not always be what's the diagnosis, but it might be what's
going to potentially kill this person and how to make sure that I'm dying the next couple
of minutes.
And if this is hemorrhage and hemorrhagic shock, you got to act fast.
(06:47):
Nice.
Great work.
I'm just going to touch on a couple of things that you guys mentioned.
Great points.
Number one, identifying if the patient is sick or not sick.
I think that's such a crucial distinction.
And I think you guys nailed it.
This patient is very, very sick.
I also love that you highlighted there's a syncope component and there's this hematoma
system component, both of which need appropriate workup.
And I love the questions that you're trying to ask.
Trying to differentiate why is this happening?
(07:08):
What can be united in these two things?
And where can we go from here?
So how about I get you some more information?
So for the patient's past medical history, the patient has a history of peptic ulcer
disease with a Bill Roth II procedure performed in 1993.
They've got a history of hypertension, cholecystectomy, and an umbilical hernia repair.
In terms of current medications, they're on hydrochlorothiazide, amlodipine, and multivitamins.
For allergies, allergic to iodine.
(07:30):
In terms of a social history, there is no alcohol use.
They do have a one pack per day history of smoking.
They live alone and they are a clerk at a city court.
This patient, in terms of family history, father died of CVA at the age of 67.
Mother has congestive heart failure in her 80s and has a brother who does drink.
So this is a lot of information.
(07:50):
Anything that stands out to you?
I think the no ethanol use is helpful in framing the differential, some of the things we were
thinking about, because some of the Mallory Weiss I believe would be more common in a
patient that consumes a lot of alcohol.
Yeah, in line with that esophageal varices was coming along.
There can be other causes of that associated with total hypertension maybe, but you know,
(08:13):
of course the most common thing we think of is cirrhosis due to ETOH overuse.
Yeah, yeah the key things from the past medical history, peptic ulcer disease.
You can get GI bleeding as a result of peptic ulcers.
So that's something to keep in mind.
I'm not sure what Billy Ross is.
Don't worry, we'll get into that.
I'm going into the 90s.
(08:33):
Yeah, history of hypertension, smoking history, something else we should definitely have been
to be on the differentials, aortic dissection.
So yeah, that's something we do not want to miss.
I really like how you both are thinking about those must not miss diagnoses.
So for example, in this patient we talked about esophageal varices and Alec, I think
(08:53):
it was a great point that you had that we see that this patient doesn't drink alcohol,
but there are other causes for cirrhosis and so that should not immediately necessarily
rule that out.
So we still want to be worried about this patient.
I also feel you guys have kind of honed in on your first kind of differential of causes
of upper GI and Mallory Weiss tear, variceal bleed, peptic ulcer disease.
(09:19):
That's the place to be starting.
But typically peptic ulcers and varices being the two most common causes of upper GI bleed,
at least in the US.
So keep indulging with what else?
The nice thing about GI is it's very anatomic.
And there are mimickers, maybe it's not coming from the South African, maybe it's coming
from the lung and they're coughing it up.
You know, sometimes we think about something that they're swallowing the blood and it's
(09:43):
coming from the nose, the posteriopharynx.
So indulge me a little bit more.
And by the way, nobody has a Bill Roth who's been in med school since 2001.
But I was in med school up until 2001 and I still saw that procedure and I know, Dan
and Lauren, you might get into this.
But I was familiar with that procedure and that procedure was done in the 80s and 90s
(10:03):
as a treatment for peptic ulcer disease because PPIs were still new and they hadn't discovered
one of the biggest drivers of peptic ulcer disease yet.
It was discovered around that time.
I don't know if you're trying to read my mind of what that discovery was.
I'll tell you it's a bacteria.
H. pylori.
H. pylori.
So understanding that there was an infection driving this anatomic thing was new in the
(10:28):
90s and once they figured out how to treat and cure H. pylori, they could give PPIs now
over the counter.
People didn't need procedures, but I suspect our friends here are going to go through a
little bit what that procedure is.
So fantastic job though thinking about the differential property GI bleed.
You know, this is such a great transition.
You know, we're thinking about peptic ulcer disease.
We're thinking about what are some of the ways that we can address this and you know,
(10:49):
I love the thought process about number one, we still have this syncope picture, but we
also have this hematopesis and we're thinking about how does an upper GI bleed fit into
this?
Where anatomically does this all fit in?
So I'd actually do a quick pause and think a little bit more about peptic ulcer disease
specifically.
So from your perception, how would you describe peptic ulcer disease?
Most commonly caused by H. pylori and I think it's sort of an erosion in the mucosa of the
(11:13):
stomach and so I think then you get less acid maybe that secretes.
Yeah, because that erosion.
Well I think there's maybe the baby's acid produced by the H. pylori versus just the
erosion into the stomach mucosa.
Yeah, these are all great points.
One of the reasons I have to just get definitions is just to make it clearer for all of us,
but I agree with one of your points.
(11:34):
So in simple terms, peptic ulcer disease, there if you mentioned, there's some kind
of a defect in the mucosa of either the gastric or duodenal wall.
And as you can imagine, there are a lot of complications that can arise from it.
One of them, you both mentioned hemorrhage.
As you guys mentioned, PUD can often lead to hemorrhage.
Obstruction is another one and of course perforation if the ulcers penetrate through the bowel
wall.
(11:55):
So this is one of the things that we think about, you both mentioned, for this patient
with a history of peptic ulcer disease and this new onset of regi bleeding.
Now this patient had a Delroth II procedure performed.
This is a, definitely something that isn't as routinely done anymore because Dr. Duane
mentioned, we now know that there are these things H. pylori that are contributing to
this.
But I thought we could do a quick overview of what this procedure is and kind of why
(12:17):
it was indicated.
So in this procedure, we have normal anatomy here on the left.
For those of you who are listening, I would encourage you if you can to just, just Google
what the Delroth II procedure looks.
It might be a lot easier than me describing this overhooding.
But basically what we're seeing is we have a resection of the distal end of the stomach
and then we have a duodenal stump that is then closed and there's an anastomosis of
(12:38):
the distal end of the gastrum to the jejunum.
So you had this anastomosis at the gastro-jejunal junction and you have a closure of the stump
of the duodenum.
So we've got a couple of different components going on here, but the goal is to remove the
segment of the stomach that has the suspected peptic ulcer disease.
Does that kind of make sense?
Yeah.
So part of the stomach is still technically still be attached to the proximal duodenum
(13:03):
that's not connected there?
So the proximal duodenum actually is not connected to anything in this case.
Yeah.
Did they just resect the part of the stomach off of that?
Yes, exactly.
Exactly.
Where the ulcer is, they just take it off?
Yes.
Well, I want to add a couple of things.
You can imagine this is a pretty tough surgery.
I mean, they've got to do an open procedure.
You can imagine the complications and postoperatively in bariatric surgery, people didn't suffer
(13:28):
from abdominal pain, malabsorption, diureloscoma.
And if I could comment on a couple of things that have been stated in the discussion, fabulous
discussion is H. pylori is probably causing these ulcers through inflammation and the
infection itself.
Interestingly, H. pylori produces urea, which is an acid buffer.
And so people with H. pylori, when you treat them, might actually be at larger risk for
(13:49):
GERD because the urea is buffering the acid and now you take away the buffer and that
acid can reflux up.
So oddly with H. pylori, acid might be a mitigating factor, but it's not the driver.
It's the infection.
In the bilroth, they often ligate the vagal nerve and the resecting part of the stomach
(14:09):
that are the acid producing cells.
So by taking out the vagal nerve and that section of the stomach, you are dramatically
dropping acid production.
So it's a different mechanism for H. pylori.
You're reducing acid levels and that's going to reduce future ulceration.
So back in the day, they would do this for people that were having severe symptoms from
peptic ulcer disease, complication of peptic ulcer disease and things like Tums, calcium,
(14:35):
those kinds of things that typically buffer the stomach were enough and they would go
to this pretty drastic procedure, but now the PPIs are ubiquitous.
Those are lower acid levels and fixing the things that they were probably fixing autonomically
with this procedure.
But I'll repeat, nobody knows what this procedure is anymore.
I'm very glad you're here, Dr. Zuley.
This is very helpful.
(14:56):
Yeah, thankfully this is not done with T. le anymore because we now have medications
that can help address the underlying peptic ulcer disease.
But just for our patients, nice to know kind of what was going on and what the current
anatomy is.
So you're ready for some labs, some exam findings.
All right, let's let's get into the exam.
All right.
So for this patient's vitals, temperature is 96.3, heart rate of 110, respiratory rate
(15:19):
of 18 and a blood pressure of 81 over 54.
The patient is alert and oriented.
Do you guys do this with every case you have?
Honestly, we should start with a little jiggle after.
Patients pupils are equal round reactive.
(15:39):
The oropharynx was clear.
The lungs are clear to auscultation.
The heart is tachycardic irregular.
The abdomen is non tender, non distended, positive bowel sounds and healed surgical
scars.
The remedies are without edema pulses are one plus and neuro is non vocal.
What are you guys thinking?
The first thing that jumps jumps out to me is the vital signs where this patient's tachycardic
(16:02):
hypotensive I'm really worried about, you know, him being volume deck.
We have the history of, you know, blood and vomit some sort of hemorrhagic shock maybe.
Yeah, yeah, I think the fact that we see the low blood pressure should be very concerning
because if that's all from the blood loss, it means he's lost quite a bit of blood.
Normally you just initially just see the heart rate jump up, but you don't really see the
(16:23):
blood pressure dropping to you lose, I think, 30% of your blood.
So you probably lost quite a bit if we are seeing this hypotension.
Yeah, you're absolutely right.
It's very important to recognize early on that this patient is in shock.
And I think you guys nailed it.
There's a history of hematomasis.
The patient that most likely is in a hemorrhagic shock situation needs to be addressed.
With that being said, what is something?
(16:44):
Well, what are some things that you would want to order urgently?
What is information that you think would help you kind of figure out, OK, what are best
next steps?
Type in screen for sure.
Oh, yeah.
Yeah, type in screen.
Yeah, start placing some large boar IVs.
Yeah, great.
Any imaging studies?
Probably.
You think we should go straight to CT?
Yeah, CT, abdomen and pelvis, but chest as well.
(17:06):
Yeah, right.
The physical exam is there isn't anything super impressive.
There's no tenderness anywhere.
So I don't know if we want to do a fast bedside ultrasound.
That is something we can think about just to see if there's any free fluid anywhere.
Yeah, I think it's reasonable to do that in the interim as well.
Yeah, while we're getting things teed up for CT.
(17:26):
You guys have thrown out varices as a potential cause of upper GI bleed and now we're thinking
a lot about peptic ulcer disease, given this guy's history and given the frequency of it.
What exam findings could help you with either of those?
I think the abdominal exam, non-destended, points away towards some sort of liver pathology
(17:46):
involved.
We don't see any evidence of the side E's.
So that sort of picture, I would say varices is probably less likely.
What are your thoughts, Alec?
One of the things that I am wondering about is that there's no mention of the liver, but
if there's a pattern of megalene, that would make me more concerned that something is happening
in the liver.
(18:07):
That was a physical exam.
What about some other skin findings that you would want to check for?
Thank you for the hint.
Medicine is important.
Exactly.
And jaundice.
Jaundice, yeah.
There you go.
Yeah.
Spider angiomatas.
Yeah.
Gynecomastia.
Yeah.
So I think, I mean, that's exactly right.
(18:28):
You guys threw it out early and it was fantastic that word about alcohol history doesn't maybe
have it.
We're still worried about cirrhosis.
We need some esophageal varices, but also disease probably is not going to have any
telltale physical exam findings, right?
If anything, we talked a lot about H. pylori.
We shouldn't forget NSAIDs and pills.
We looked at it.
We saw his pill list.
Presumably you have an ability to go back and get additional history that he's not down
(18:51):
at NSAIDs either pro-fertiline for the last 10 weeks is another thing.
But looking for signs of cirrhosis in the physical could be very helpful here.
It doesn't always got to be.
Very nice.
Very nice.
All right.
So I think one of the things that I really liked is some of the things that you were
thinking about ordering are really catered to the patient who is in shock.
We talked about a fast anxiety, talked about getting sensitive imaging that will provide
(19:13):
us with as much information as quickly as possible.
I think that's a phenomenal thought process.
We got some different imaging that we'll walk through, but I'd love to get your thoughts
about this.
We have a chest x-ray here.
So we guys think about the left versus right diaphragm.
Which one's typically, it's okay if you're not sure.
Actually you can guess.
It'll be 50, 50 chance.
I believe the right is higher because the liver.
(19:35):
Yeah.
So it's here.
Looks like the side.
Yeah.
So when you thought, when you're seeing the diaphragm does look like it's smashed up,
that might be true.
That might again just be the angle of how the film is taken.
But there's also a little bit of an elevation of that right hemidiaphragm compared to the
left.
Excuse me.
Left hemidiaphragm compared to the right.
I'm going 50, 50.
I'm wondering.
(19:56):
The left is a little bit higher than the right.
And that's a little unusual.
So fluid, what else can push up to one side of a diaphragm, the left side of the diaphragm?
If you can atellectasis the lungs or something, get some negative pressure.
Yeah, that can be true.
Well, we don't really see compressed lung there.
Usually you'd see what could look infiltrator, atellectasis or just consolidation.
(20:18):
Stomach is there.
Spleen is there.
Okay.
So one of the things we talked, you said it was fluid.
Could also be some sort of reflective process going on where maybe the stomach is distended.
That being said on this image, I'm not seeing any sort of air from there.
Okay.
You're in the right organ systems to be thinking about what could push it up.
(20:39):
Yeah, absolutely.
Fantastic work.
I think one of the key things that I wanted to highlight, which you all did wonderfully,
is thinking about anatomically what organs are where and how we can present on a chest
x-ray.
You nailed it.
The liver can tend to push up the right hemidiaphragm.
And in this case, we're seeing the left is a little bit higher.
What does that mean?
Just things to keep in mind, which great.
You guys hit that very well.
Alright, let's get you some labs.
(21:01):
Alright.
Nice.
So in terms of the patient's labs, we have a white blood cell count of 22, a 22% neutrophil,
56% lymphocytes, 19 monocytes and 13, 3% basophils, hemoglobin of 11.1, platelet of
225, sodium of 140, potassium of 3.9, chloride 108, bicarb 25, UN 41, creandin 1.3, mucose
(21:24):
171, lactate 2.1.
We did PT INR, PT is 14, INR is 1, PTT is 36.
And with fluids, the hemoglobin is now shown to be 8, with the white blood cell count of
6,000 and a platelet of 90k.
So a lot of lab, a lot of numbers.
Yeah, wow.
What, what are your thoughts?
What are you, what are you reading?
What are you thinking?
(21:44):
One of the first things that jumps out to me is the PUN being 41 compared to creandin
of 1.3, which is also somewhat elevated, but not as much.
And I have no idea why this is, but I just remember from somewhere in the recesses of
my mind that with peptic ulcer disease, often you have an elevated UN.
(22:05):
Other things, well, I mean, that might make sense.
I guess it was the A-color azeria producing, maybe that could drive up the area.
Oh, nice.
I don't know if that's what happened, but yeah, that's cool.
Yeah, other things I'm thinking.
So I have initial CBC, actually hemoglobin 11, that's better than what I would have anticipated.
I diluted to 8.
(22:25):
Yeah, it makes me wonder if your initial is concentrated and that's why you're seeing
it artificially elevated in terms, the white count 22, that I think is interesting in terms
of differential maybe.
One thing that has made me think of is there's some type of malignancy picture could be going
on because I know H. pylori can be associated with the malt lymphoma.
(22:47):
So that could be maybe something we're thinking about.
In terms of the chemistries, Ni-GAP7.
So yeah.
Right.
Another thing with the hemoglobin of 11.1 down to 8, I think you're right.
There can be a dilutional component of it.
The fact that the white blood cell count went from 22 to 6 though, that's pretty impressive.
(23:09):
Yeah, that's a big difference.
Another thing though is hemoglobin, if it's an acute bleed, you may not see.
Hemoglobin drop.
Yeah, hemoglobin drop as dramatically as you would do it, right?
So maybe there's some of that going on as well.
Yeah.
So I have a question for you both.
We saw this patient's vitals.
You're in the emergency room.
(23:30):
This is your patient.
Are you giving blood?
Yes.
Yes.
Even with the hemoglobin of 8?
What's our usual concentration?
Oh, normally stack less than 6.
Yeah, it's 6.5, 6, something like that.
You're just basing how much blood we have available.
Usually 7.
Okay.
How much shorter than, say, 6.5.
(23:51):
Right.
But we're seeing such-
We're also telling you this person's maybe in hemorrhagic shock, right?
Yeah.
We're seeing such a precipitous decline over not a very long period of time that getting
blood on board sounds a good plan.
I think you're right on track, right?
Clinically, you're worried about this patient.
Even though the hemoglobin isn't at that transfusion threshold, we know that this patient
(24:14):
lost blood.
They were throwing up blood.
So, I think you're thinking about it.
Great.
Exactly right, Lauren.
I mean, guiding these guys, you guys have been on it.
All of the cell lines went down, so there's definitely some chemo concentration, which
adds to the idea that this might be hemorrhage.
He's holding on to whatever fluid he can, but it's not enough from the fluids we're
(24:34):
needed.
But those cell lines look scary to me.
And you threw out a number of 30% before you had 30% blood loss before he was in the emergency
shock.
I remember one of my favorite rules that Tom, tell me gauge how much blood was lost was
10, 20, 30.
10% blood loss makes you tachycardic, 20% makes you work the static, 40% makes you pass
out hypotension.
So, I was happy to hear 20 years after my information, then rule of thumb with 30% still
(25:00):
sticking around.
And that makes you worry that this guy has lost a lot of blood, passed out.
Or that it's going to keep dropping as you add more fluid and maybe he's still bleeding.
I think one of the things that we hit on, I really want to emphasize this because I
think it's such an important point, is treating the patient rather than just treating the
(25:20):
number.
I think you guys picked up on this.
Even if the hemoglobin isn't necessarily below six, we know that the patient is in shock.
And we know that in this case, giving blood may help the patient, especially with the
perfusion status.
We know their lactate is at 2.1.
So, really focusing on how we can help the patient.
I think you hit up on this very well.
So, I'm really glad to see that.
It's great, great work.
So, one of the things I'd love to ask is, based on these, as a based on this information,
(25:44):
how does this affect your differential?
What are you thinking about?
What do you think might be causing this hemorrhagic shock, generally?
One of the things, especially with learning more about the Billy Roth procedure, is could
there be a surgical complication?
I'm thinking a little less of that though, just because of the timeframe.
That's more of an intuition.
From all that we've gotten so far, I would feel, yeah, definitely more narrows towards
(26:07):
thinking some sort of relation to the peptic ulcer disease causing the bleeding.
I think we've talked about esophageal varices, you know, with no history of alcohol use,
pretty much benign abdominal exam, no skin findings.
I think that's less likely.
Also the Mallory Weiss tear.
I think we would expect the mediastide to be a bit more widened on the chest x-ray, and
also less so with alcohol use.
(26:27):
So I think peptic ulcer disease related causes the highest in the differential at this point.
So next steps, are you going to go looking for peptic ulcer disease?
Would you do a scope?
Yeah.
Would you be safe to do that?
That would be my only concern, if I get safe to do that, but I think that would be the
best way to probably visualize it.
Right.
I know outpatient, there's a couple other options with the Rhea Breast Test.
(26:51):
There's two other ones.
Oh, like stool tests.
That would let you know if there's H. pylori, but I don't think it would tell you much about
what's going on inside the stomach mucosa.
So probably upper GI scope, I think is what I would do next.
Yep.
You guys should continue to work together.
When you go into residency, you guys are very effective at working these.
I want to comment on intuition.
(27:12):
Intuition is undersold in medicine.
That's called street smarts.
It's been 30 years since this guy had that procedure.
It would be odd for 30 years to pass, and solidly be a complication of that way you
kind of put it.
Yeah.
And kind of going back to the must not misdiagnoses and everything that's on your differential,
you know, the upper endoscopy would help you to see if there is peptic ulcer disease, but
(27:35):
you know, you don't want to wait around for a urea breast test in the emergency room.
You want to be 100% certain that there are esophageal heresies too.
Right?
So that's a great next step.
So I actually think this is a great point to pause into a quick teaching point.
Just on our approach to upper GI bleeds.
One of our one of the podcasts that we often also ascribe to the clinical problem solvers,
they have a wonderful framework for upper GI bleeds.
(27:57):
You mentioned some of the most common causes of our upper GI bleeds.
We know peptic ulcer disease, esophageal heresies, esophagitis, but just thinking about things
from an anatomic standpoint, Dr. DeWine, you mentioned because the GI system is so easily
anatomically arranged, it's easy just to go proximal to distal and think about, okay,
what is causing upper GI bleed?
As I'm sure you all know, classified upper GI bleeds is anything up to the ligament of
(28:19):
trites.
So we're thinking esophageal, you mentioned this, Mallory Weiss, there's a tumorous camera
lesions, black esophagus, gastric ideologies, gastritis, tumor, oral gastropathy, and small
bowel classically things.
AVMs, tumor, and terioentery fistulas.
A lot of these things are a bit more esoteric and not as commonly seen, but I think the
most common things you guys clearly picked up on.
(28:40):
It's great to just keep in mind.
The important questions that you both asked is number one, is there a history of cirrhosis?
Could that be contributing to these symptoms?
And number two, is there a potential aorta-enteric fistula?
Is there something that is causing this?
Why is there, why are we seeing this constant blood in the upper GI tract?
Great thoughts.
I also love the fact that you picked up on, do we need to do a scope for this patient?
(29:01):
Is there something that we can see that can really help us figure out next steps?
So with that being said, why don't we get to some images.
So we did do an EGD and really to summarize, in the esophagus, there was no evidence of
esophageal varices.
In the stomach, there was a moderate amount of blood.
There were grade two gastric varices in the body of the stomach, none of which appeared
to be actively bleeding.
There weren't enlarged, thickened folds that suggest portal gastropathy.
(29:23):
The anastomoses showed no signs of active evidence of bleeding.
And the scope was introduced into the duodenum that showed no ulcers or masses there as well.
So that's a lot of information.
What are you guys thinking?
So do you think I'm taking it right here?
There's blood in the stomach, but it's not entirely clear where that blood came from.
There's not a huge ulcer listed here.
(29:48):
There are gastric varices, so that's likely the source, but that doesn't get to the question
why does he have gastric varices.
So maybe we can pause here for a moment.
What does portal gastropathy, what does that tell us?
We have a new diagnosis for this patient.
Portal gastropathy.
You don't hear that though.
Yeah.
(30:09):
No.
I think this is the first time I've heard that.
So think of, you've got portal.
You guys are both smart.
I think.
So what could mean?
So I think so the gastric vein, I think, into the portal vein.
So I think this is maybe something where it kind of is portal hypertension, but like it's
shunted towards the gastric veins.
(30:30):
Absolutely.
Yeah.
So maybe I can take a moment and talk about that and then you can fill in.
So I think talking just briefly about portal hypertension here is helpful.
So what happens with portal hypertension is you have increased resistance in portal blood
flow.
And you also get these increase in collaterals, which just makes everything worse and ultimately
(30:51):
can cause hypotension and ascites.
And there are a lot of different reasons why you would have portal hypertension.
Any that you can think of that you may have learned about before.
One classic association.
Right.
So one we talked about was cirrhosis.
I can also think of heart failure.
Yeah, right.
Heart failure.
Yeah.
(31:12):
See that?
Yeah.
So that's a lot of emphasis on the portal vein, malignancy.
Well, you're on the right track for sure.
And I know, Dan, you've got some more teaching points if you want to talk about those causes.
Yeah.
So, you know, I love that you guys are thinking about this anatomically.
I think the easiest way to remember this stuff is to simplify it as much as possible, which
you both are doing.
(31:32):
The way that I think about this and the way, Lauren, you explained it so well.
Just anatomically, we realized that blood drains through the portal vein into the liver
and then ultimately out the hepatic vein and to the right side, right heart for surge circulation.
And as you both mentioned, you can have issues at any of these points.
Prehepatic, intrahepatic, posthepatic.
And just to summarize some of the things that you have already mentioned.
(31:53):
When we're thinking about prehepatic causes, you mentioned, is there an issue with the
portal vein?
Is there perhaps a thrombosis?
Is there an issue in another vein that drains into the portal vein?
When we're thinking about intrahepatic, you guys both mentioned cirrhosis.
Commonly we see potentially schistosomiasis, which is something that I personally never
seen, but apparently the literature can often present with this intrahepatic portal hypertension.
(32:15):
And of course, you both mentioned causes of posthepatic, right heart failure.
Is there a tricuspid valve issue that's just causing blood to just be backed up?
But Chiari, things just to think about.
And I love that you guys are really categorizing this into different systems to help you figure
out, okay, what could be contributing to this?
Based on all of this information, at this point, it's still kind of nebulous as to,
all right, which category are we in?
What are we dealing with?
(32:35):
Is there anything that you think might be helpful to parse out which category this patient
might be experiencing?
LFTs, for one.
LFTs could be useful.
You can echo cardiogram, check the heart function.
You can ultrasound the liver also.
Yeah, some sort of imaging of the abdomen.
What in the abdomen in particular are you looking at?
(32:58):
Portal vein flow.
Portal vein, we talked about the liver.
Anything else you want to look at?
IVC.
IVC.
Okay.
Remember we saw that diaphragm.
What were we concerned about?
Any organs underneath that left side that you think might be?
Scalene.
Great idea.
Very nice, very nice.
And I know you also mentioned earlier on about potentially getting a CT, abdomen, pelvis.
(33:22):
Just some things to think about.
Oh, you know what?
I think we can get to that information.
So we did a liver ultrasound with Doppler that was normal.
We also did a splenic ultrasound with Doppler.
And just to summarize, we are seeing the spleen is diffusely enlarged with a lobulated contour.
It is dilated of quick measurements, 10 centimeters in cradiocardial and 11 centimeters in the
(33:43):
transverse dimension.
Which is big.
Significantly long.
Yeah, yeah, yes.
And we're seeing in the splenic hyaline what looks like a rounded hypoechoic focus that
seems to be within the spleen.
It does not appear to represent a fluid collection, an abscess or a hematoma, because there is
a vessel seen running through this region.
You didn't get to actually examine the patient, but let's hope they felt something.
(34:05):
Yeah, they were.
It's a little bit firmer on that left side.
Uh-huh.
And I think in this particular image, you can see how much the kidney is pushed down
because of how big the spleen is.
Oh, yeah.
You can see how...
Pretty striking.
Exactly, exactly.
So you mentioned something is going on with the spleen.
Yeah.
It's definitely a bit larger than we would expect.
(34:27):
Because I feel we're getting close.
So you got this huge spleen and all these other signs to support you're on the trail
towards getting to this point.
But a normal liver.
Yeah.
What's that about?
I mean, I think everything we learn is, you know, the spleen gets big because of portal
hypertension from cirrhosis, but there's no physical sign of cirrhosis.
(34:48):
The liver looks fine on ultrasound, looks fine on MRI.
Yeah.
I mean, probably some type of type picture going on to cause the gastric portal gastric
bariesis.
Right.
Possibly because of just the complication of the surgery.
Could be that.
I mean, they're moving around a lot of stuff for the Bellaroth procedure.
(35:10):
That's possibly an abnormal vessel connection forms.
But also I'm wondering about the mold lymphoma.
I don't exactly know how that presents, but I know something you can often see malignancy
involving the liver or sorry involving the spleen because the blood cells go and are filtered
there.
So that would be something I would look more into actually.
So just taking a step back, good thoughts.
(35:32):
Let's assume that we also got an echo for this patient and it showed appropriate right
heart function, no signs of tricuspid regurg.
What category do you think you would place this patient in?
Would you think this is a pre-hepatic, intra-hepatic, post-hepatic, particularly if we are seeing
a liver that looks pretty normal on imaging, but a spleen that's just way out of proportion?
But scientifically it's huge.
(35:53):
Yeah.
I would say pre-hepatic.
Yeah, yeah, definitely.
I think it's so important and we both did to realize liver's fine, but something must
be going on distal to this that's causing just a whole host of symptoms.
Any thoughts on what might lead to potential pre-hepatic causes of portal hypertension?
You've actually mentioned a few of these already.
(36:14):
Yeah, tumor, tumor burden.
Sure.
What else can obstruct things?
If you have an abscess perhaps.
How about with the vasculature?
Do you have an aneurysm compressing?
There's some areas on this MRI that are kind of lit up too.
Looks to be in the vascular.
Lossifications.
(36:34):
Potential.
Sometimes maybe things that flow aren't flowing.
Right.
Okay.
Could be embolus as well.
Oh, a blood clot or something.
Could be a clot.
Yeah.
Or it's not from the blood.
Or it's not from the blood.
Yeah.
It's not from the blood.
It's like something must be obstructing the passage of blood.
(36:56):
And so you're having this ballooning of the spleen.
Yeah.
Even with a normal liver appearance.
So with that, let's actually get into the read of the MRI.
So we are seeing complete and chronic thrombosis of the distal portion within a pen proximal
2.5 centimeters of the splenic vein.
So what we are seeing in this case, you both mentioned this, there is some kind of obstruction
for this patient who has a chronic thrombosis of the splenic vein.
(37:20):
As you both mentioned, the splenic vein drains into the portal vein and feeds into the liver
out to the hepatic vein.
And so if you have the blockage at the splenic vein, the spleen is just going to balloon
up and distal to that liver is going to look totally fine.
So I think a good learning point is just to pause and really look into what a splenic
vein thrombosis is all about.
So most common etiologies, classically we think of pancreatitis.
(37:43):
And we know this because the splenic vein actually runs along the posterior surface
of the pancreas.
So when you have this inflammation in pancreatitis, it can lead to thrombosis.
Other things, masses, like you mentioned, the cancer, mecenesis, endoparsenoma, big
things stenosis, posterior gastric ulcers.
I just included this picture here on the side just to kind of show what these various look
for different pathologies.
(38:04):
But one thing I really wanted to highlight is aside from these different etiologies,
patients can be in hypercoagulable state that could lead to these thrombotic episodes.
So I've just summarized a couple of the different hypercoagulable states that we can see.
Most of this is, I'm sure you all know all these.
I won't go too deep into any of these, but inherited causes, common hypercoagulable inherited
(38:26):
causes, factor V laden, protein CNS deficiency, antithrombin 3 deficiency, acquired causes,
different types of cancer, HIT, also PCV, Waldenstrom.
So just things to keep in mind just so we're aware moving forward.
I love when people tell me, I'm sure you know this and then give me the answer.
But there's something that the beautiful part of this case so far is that things are really
(38:47):
adding up.
I mean, we talked a lot about cirrhosis and we talked about esophageal varices.
There were no esophageal varices.
And suddenly the anatomy here explains gastric varices, isolated gastric varices suggest
an issue with the splenic vein.
And it could be as we kind of came to, intravascular clot or something extravascular compressing.
(39:09):
And that could be inflammation, a mass, something bad.
And now we're figuring out why in the heck does this gentleman have a splenic vein for
the gossips.
But everything else is explained now.
It's kind of remarkable.
I mean, you've got to save the guy's life.
But diagnostically, we're down to the central question here is why does this guy have a
clot in his splenic vein?
Yeah.
Oculins, razor.
(39:29):
Yeah.
So let's see what happens.
Let's see what happens to the shuttle.
So he is transfused to maintain hemoglobin, great job.
And surgery is consulted for an urgent splenectomy.
Okay, now, as you're doing this, as the great medical team that you are, you take a look
into his hospital records.
And you see that previous hospital records show a hemoglobin of 20.
(39:51):
And the patient history is notable for erythromyelalgia.
So just to summarize, this is burning, paresthesias, headaches, weakness, dizziness, itching after
a warm bath, hyperhidrosis.
Does this suggest anything to you?
Polycythema varin.
Yeah, exactly.
Sore.
Sore.
(40:12):
Sore in the acu-computer-generated audience of body.
That's exactly right.
Yeah.
It's interesting because when this patient presented, we're seeing a really low hemoglobin
of eight after fluids.
But we're seeing from the history, there's a hemoglobin of 20.
And so you're absolutely right.
The underlying diagnosis for this patient is this polycythemia varia that we're seeing
from especially the patient's history and a lot of the symptoms that he was experiencing.
(40:35):
You know, whenever somebody says something's pathognomonic in modern era, you should worry
that it's not pathognomonic.
But erythromyelgia is pathognomonic for either polycythemia varia and hemoglobins that are
usually over 16, but more likely 18 to 20, or essential thrombocytosis or thrombocytosis
with platelet counts over 400,000.
So it strikes me or concerns me that a hemoglobin of 20 and symptoms of erythromyelgia weren't
(41:02):
on his past medical history and a diagnosis wasn't given to this gentleman earlier.
It just means he probably didn't need a lot of care.
He in the 90s hadn't manifested yet, just part of the disease.
So that's really striking.
It actually makes you terrified of a hemoglobin 8.
You see hemoglobin 8 all the time.
If there's one that passed out from hemoglobin 8, it means they happened really fast or they
(41:22):
started at 20.
Yeah.
You just kind of alluded to that earlier.
Based on the history, you're expecting it to be a lower number.
Yeah.
But to the patient, it was a lower number.
It's just not like the lower what we're used to seeing.
Exactly.
Which is why it's also great that you didn't wait for the hemoglobin to get to that.
Excellent work.
Excellent work.
Yeah, exactly.
And another step pearl, any time a patient on a step exam is itchy after a bath or a
(41:46):
shower.
There it is.
You already know it's polycythemia vera.
Nice.
Great work.
So just a few quick learning points about polycythemia vera.
We touched on a few of these points.
Classically, the hemoglobin is greater than 16.5 or 16.
Patients often have JAK2 mutations.
As I'm sure you know, polycythemia vera, we have a low erythropoietin levels, but we have
an extremely high level of hemoglobin.
(42:08):
And often for these patients there, we do see pretty commonly venous and arterial thrombosis,
which kind of fits what we're seeing for this current patient.
And there's a higher incidence of GI complaints and peptic ulcer disease that can be seen
on endoscopy.
So I'd love to get your opinions on potential treatments for polycythemia vera.
Anything that you can think of that might be helpful for these patients.
I think, I mean, one option would be some sort of adenoforesis or try to take out some
(42:33):
of the blood to reduce hemoglobin.
I don't know what the frequency you'd need to do that and if that's sustainable for the
rest of the patient's life.
That's gonna be one option.
Great.
Yeah, it's fantastic.
So in fact, the treatment that has the best overall survival is in fact phlebotomy.
It has been shown, particularly for patients who have died, it's significant polycythemia
vera.
(42:53):
Phlebotomy is kind of the mainstay, one of the main things that we gotta focus on.
Another therapy that has been shown to be particularly efficacious is hydroxyurea.
It's shown to reduce the risk of thrombosis compared to just phlebotomy by itself.
And of course, for these patients, we also have aspirin, 81 milligrams.
Something that you may remember from step one is with the potential JAK, tyrosine kinase
(43:14):
mutations, there are specific medications, Roxolitinib, I don't know if that rings a
good bell, that specifically target the tyrosine kinase inhibitors.
But really, if for patients, kind of the mainstay therapy, phlebotomy, hydroxyurea, and make
sure they're on aspirin to avoid thrombosis.
Those patients unfortunately phlebotomized himself by hemorrhage.
Right now you don't, or are you gonna forget?
(43:35):
Absolutely.
That would make things worse.
But excellent work, guys.
So honestly, as we kind of take a step back and look over the entire case and kind of
what's been unfolding, you mentioned that initially the patient presented with syncope.
You noted that this is potentially in the setting of hematomasis.
You noted that there are different causes of a potential upper GI bleed, but you really
narrowed it down.
Could this be in the setting of this peptic ulcer disease?
(43:57):
Is there a potential varices?
You worked between different causes of upper GI bleeds.
You narrowed in on a gastric variceal bleed.
You made sure you evaluated all different organ systems.
You found the splenic vein thrombosis, and you had found the polycypheine vera that was
underlying this entire condition.
So round of applause to both of you guys.
Good work, Dallas.
Excellent.
Good job, Nathan.
That was a wild case.
(44:17):
That was incredible.
So many twists and turns.
Seriously.
And then you reflect the journey.
Oh man, I guess, yeah.
Keep on hunting.
Don't stop.
Yeah, because yeah, people just kept on turning over the new leaves, you know, at every step.
(44:38):
And so also, yeah, yeah, just yeah.
How the final destination we got to is, you know, I wasn't necessarily thinking about
ploids at the beginning, but I was definitely.
Well, I'd throw in it that you guys really thought through the acuity of sickopy and
(44:58):
got on this person who was sick and this was being hemorrhage early on, which is essential.
And then the main differential from a learning standpoint is upper GI bleed.
I mean, that's what you really want to take away from how to approach that hematomasis
is what's the source and H. pylori, NSAIDs, varices, malory waste.
That's the differential to really take away.
I say, theemia, we learn about it in med school.
(45:19):
It's rare.
And it's funny that it's common to clot, but they present with bleeding.
So there is trickiness to this case.
Yeah.
And maybe one other pearl that we spent a little bit of time on a different sections
of the case discussion is people that clot in unusual places need a workup versus people
with lower strepia DDTs.
(45:39):
Then you can start to think of that Burkhouse triad and maybe it was immobility or being
bed bound, maybe it was their cancer and they had inflammation.
But if they've got a clot in their splenic vein, they got Bud Chiari, they present with
arterial clots.
You go through the hypercoagulant workup and that differential that you put up there, Daniel
had PCV on it.
(46:00):
So as soon as he's got that clot in an unusual place, you start sniffing around for things.
Great job guys.
Something else that's interesting is this patient had peptic ulcer disease in the nineties.
So PCV usually presents in sixties, this patient's in his late sixties.
So are those things related?
Are they not related?
Was that early symptom or was it just people have peptic ulcer disease and he had both
(46:26):
of those?
I guess we'll never know, but I think it's an interesting thing to think about.
With the bleeding, so when we did the scope, we didn't see any active bleeding from the
varices.
So that's why I'm wondering, how long ago did that bleed?
We're assuming it bled from the varices.
How long ago did the bleeding happen from the varices before I actually saw this?
(46:47):
Great question.
And one of the things that happens when you have a bleeding vessel is if you lose a bunch
of blood, the vessels deflate.
So it fixed itself through a bad means.
So it's not unusual that people hemorrhage from a vessel.
By the time you go look, you don't see any more because they lost that much blood that
the vessel actually decompressed itself.
And then sometimes you just can't see everything.
(47:08):
The gastric bodies got folds in it and they might not easily identify it.
So that's a very great, that's a really good question.
All right.
Thank you Nathan and Al for joining us.
Thanks Dr. D'Onofria for joining us.
Congrats again to Dan and Lauren.
So well deserved.
So happy for both of them.
And thanks everyone for listening.
Thanks everybody.
Yeah, thanks for having us.
It was a blast.
(47:29):
Thanks again for listening.
For some time and place.
See you next time.
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