110. Pulm PEEPs at CHEST 2025 – Widened Airways and Narrowed Differentials

For today’s podcast we have a special episode. We were extremely grateful to be invited to present live at CHEST 2025 this year. Kristina Montemayor, and Pulm PEEPs Associate Editors Luke Hedrick, Tom Di Vitantonio, and Rupali Sood hosted a … Continue reading →

Episode Transcript

(00:16):
Hey, everyone. Thanks for tuning in today.
For today's podcast, we have a special episode
for you. We were lucky enough to be
invited to do a live session at CHEST
twenty twenty five.
Unfortunately, I couldn't make it to the conference,
but Christina held down the fort and hosted
a live session at the conference.
She was joined by associate editors for Poem

(00:37):
Peeps, Luke Hedrick, RuPauli Sud and Tom DiVantonio
And they were joined by an additional guest,
Doreen Adrizo Harris.
The title of this session was widened airways
and narrow differentials.
So you may guess it's a great session
about bronchiectasis
and thinking about the differential of patients who
come in with symptoms or signs of this

(00:58):
wide spectrum of disease.
It sounded like a great session. I've listened
to the audio and watched the video since,
and it's really awesome. And we wanted to
share it with you all. So without further
ado, here's the recording of that episode.
Well, I'm looking at the time. I see
that we are at 08:02,
so we're gonna go ahead and get started.
Good morning, everyone, that is, here live with

(01:20):
us in the room today. I'm Christina Montemayor,
the cofounder and half of the Poem Peeps
and a chess enthusiast.
We're coming to you live from Chicago in
CHESS twenty twenty five. We'd like to thank
CHESS and and specifically doctor Sandy Caruana who
asked us to be here today. And, we
know that we have two other critical care
podcasts that are going on, so ours is

(01:40):
gonna be the great pulmonary focus for you
all. I feel like we all need a
little bit more pulmonary, so that's what we're
bringing for you today. We're here in Chicago,
the headquarters of CHEST,
and I'm really excited to be part of
this ninetieth,
anniversary celebration.
You may you may notice that, I am
missing,
one of my other half, David Ferfarro,
who's currently in Italy with his family, but

(02:02):
he sends his regards. We've been sending notes
to each other about who has the best
pizza.
I was like, we've had deep dish, Dave.
You don't have that in Italy. So,
but he,
he will be excited to hear this podcast.
And as you can see, we have a
fantastic team here today.
If I'm not joined by FIR, very excited
to have our associate editor, Doctor. Luke Hedrick,

(02:24):
who is currently a third year fellow at
Emory, who is here with us today. And
you may recognize his voice from our rapid
bio journal clubs that he does. Welcome Luke.
Hey Christina. Thanks for having me. Maybe just
a little bit. Hey Christina. Happy to join.
I think it's kind of crazy, but I
think this may actually be the first time
we've recorded together in person, which is wild

(02:45):
given how long it feels like, this has
been ongoing, but very happy to be here.
Amazing. And we're excited to have our, a
first time poem peeper to the show,
share a warm welcome to doctor Doreen Idriso
Harris.
Doreen is a professor of medicine at NYU.
She's currently the associate director of clinical and
academic affairs in the division.

(03:08):
In addition to that, she is the director
of the bronchiectasis
and NTM program and also serves as a
program director for the pulmonary and critical care
fellowship. True leader in the field and has
a I know definitely has a special place
here at CHEST,
where in 2023
she served as the eighty fifth CHEST president.
So Doreen, such an honor. Welcome to Poem
Peeps.

(03:28):
Thank you very much. It's, it's a pleasure
to be here today. I'm very excited to
see what this is all about. I know.
I think I know. First first time podcaster,
Doreen.
We I was just asking too. I was
like, Doreen, how many years have you been
the fellowship PD?
And she said twenty five.
So I was like, I'm only 23
behind you.

(03:50):
But a lot to look forward to.
We're also very excited to have two additional
members of our Poem Peeps family. Would like
to send a warm welcome to Tom DiVantonio,
Roopali Sood. You both probably have recognized,
and have been instrumental in our recent asthma
guideline series.
Tom and Roopali are both critical care fellows
at Johns Hopkins, and I have the honor

(04:10):
to have them as my current co chiefs
this year. So welcome, Tom and Mupali.
Good morning, everyone.
Very excited to be joining y'all here from
this awesome CHESS conference,
for this, great podcast.
Yeah. Thank you for having us. We're very
excited to be on stage altogether and in
person,
because even when we're together in the same

(04:32):
place, we're not always in person. So this
is very exciting. So thanks for having us.
Of course.
Alright.
And so then, just as a reminder, this
podcast is not meant to be used for
medical advice. The views we expressed today do
not reflect the opinions or policies of our
respective employers.
The case we're presenting today is HIPAA compliant
and some details may have been changed to

(04:53):
protect the privacy of our patient.
And so without further ado, let's get into
our case. The year is 2010 and we
have a 60 year old father of two
with a history of CLL
in remission after three cycles of chemo who
presents to pulmonary clinic for recurrent infections.
He describes recurrent respiratory infections about one per
year with three hospital admissions for the same.

(05:15):
Most recently he had a right middle lobe
pneumonia.
His PFTs are notable for some airflow limitation
that corrects with bronchodilators,
normal lung volumes, a preserved DLCO and a
pheno of 15.
CT chest imaging isn't available for review at
this first appointment but there is a report
that describes some tree and bud nodularity with
bronchial wall thickening and very mild upper lobe

(05:37):
bronchialectasis.
And I don't know if you guys feel
this way or not, but I feel like
this history sometimes is a pretty tricky one
to take. Ref current respiratory infections are so
common. Like, just ask any parent of a
daycare aged child,
and the vast majority of people in that
setting don't have any underlying issue.
But that being said, for our patient, the

(05:59):
recurrent pneumonias in particular, I feel like perks
my ears up,
especially ones that lead to admission.
And so when I think about a patient
with recurrent pneumonia, I typically try to approach
things geographically,
which is to say, are the infections all
happening in the same particular region of the
lung or not,
which may prompt me to think about an

(06:19):
anatomic problem, some extrinsic compression, an issue with
the airway itself like bronchio bronchiectasis,
excuse me,
or dependent areas where I worry about recurrent
aspiration.
In this case, his infections were diffuse and
kind of scattered throughout the lungs, which leads
to an entirely different set of differentials about
things like underlying systemic issues like cystic fibrosis

(06:40):
or immuno deficiencies like HIV or CVID
or non infectious mimickers like organizing pneumonia or
avasculitis.
And so with our patient,
he, as I said, these were not geographically
restricted and so labs were sent looking for
one of these underlying conditions and he's ultimately
diagnosed with CVID or common variable immunodeficiency.

(07:03):
He started on IVIG with improvement until 2014
when he has a STEMI and develops hemoptysis
with ticagrelor
which leads to a CT chest. Tom, do
you mind just walking us through this picture?
Yeah. Absolutely. So
here we have five,
representative
slices of this gentleman's CT chest from 2014
going from
the apices of the lungs down to the

(07:25):
base. And I think what really jumps out
at me as particularly noticeable is that he
has upper lobe predominant bronchial wall thickening,
and then some mild bronchiectasis.
And if you look, there's some some mucus
impaction
as well in some of those, those airways.
And along with those, I think the other
notable findings
are that there's some scattered central lobular nodules,

(07:49):
and patchy upper lobe predominant opacities. You know,
sometimes the term tree and bud gets thrown
around with these sorts of findings,
and I think it could be applicable here.
Christina, this this term tree and bud, it
it's talked about all the time.
And it's really easy just I think a
lot of us here at tree and bud
equals infection.

(08:10):
Can you talk us through a little bit
more what it means pathophysiologically?
Yes. Absolutely, Tom. Yeah. Right. And I feel
like tree and bud, a little hand wavy.
You're, like, reading it and, like, are like,
a resident will say, I think there's tree
and bud there. Something looks off like, wrong
at the periphery,
but totally right. When I think of tree
and bud, it's gonna be the the small

(08:30):
airway. So really, tree and bud associate with
small airways, really the bronchioles,
for sure. So right, but something is feeling
it, whether it's mucus, pus or something inflammatory.
I definitely, that's what I think of. So
looking on CT,
we can see, right, that the those plugged
little bronchioles look like nodules
connected to branching lines, which I think Luke

(08:53):
is pointing out. I think we're also we're
we're coming live, so we're actually,
show showcasing
some some imaging. But for those that may
be listening after the the conference, we'll definitely
make sure that we, have these images for
you to review.
But like I said, right, it's I would
I don't think of triumvirate as a specific
diagnosis. It's really just pattern. And I think

(09:13):
a lot of what we do in pulmonary
critical care, looking at imaging, is going to
be pattern recognition.
So something is, obstructing
or inflamed in the bronchioles, but that's how
do I think about it. So my mental
model for thinking about tree and bud, you
know, really focus on what etiologies,
you could be thinking about are going to
be really favored on distribution and the chronicity.

(09:35):
So I think if it's diffuse and acute,
right, infection is going to top the list.
So bacterial, viral or mycobacterial.
If we think it's more dependent and basilar,
we're not seeing that in our image today,
but I think most of you here in
the room will also be thinking about chronic
aspiration.
And if it's persistent, if it's nodular and
if it's associated with other findings such as
bronchiectasis,

(09:55):
I know many of you here in the
room will also be thinking of NTM.
So tree and bud, small airways, you know,
bronchioles, bronchiolitis,
pattern recognition.
But the clinical context really matters, right? So
chronic coughs, sputum, weight loss, we're going to
be thinking of infection higher on the differential.
But, you know, recurrent aspiration or structural disease

(10:18):
can also look similar.
Tom, and I, know that I thank you
for pointing that out. I think, you specifically
said, right, the bronchiectasis in our images that
we're seeing primarily in the upper lobes.
You know, Roopali, Tom, I know we've talked
about bronchiectasis
a few times in our fellowship
didactics with our radiology rounds already this year.
But we think of bronchiectasis, it's just not

(10:40):
a it's not just imaging finding. It's more
of a syndrome that we'll think about.
Symptoms,
exacerbations,
but we have to have some type of
CT findings.
Roopali, do you mind walking us through, when
you think of bronchiectasis on CT imaging,
what are you looking for? How are you
gonna classify bronchiectasis?
How are we gonna tell Doreen? Doreen, I
really think this is bronchiectasis.

(11:00):
What How is Doreen gonna tell us? How
is Doreen yes. Exactly.
Yeah. Great question, Monte. I think, when we
think radiographically looking for bronchiectasis, we usually look
for three things. So the first thing we
look for is the bronchoarterial
ratio that's greater than one, and all that's
really saying is that the airway that's paired
next to an artery is greater in diameter
or width than the artery that runs next

(11:21):
to it. Sometimes this is called the signet
ring sign because the paired artery looks like
the ring top and then the airway is
larger and looks like the place where the
finger goes.
The second sign is a lack of normal
tapering of airways. So usually,
airways should narrow as they reach the periphery,
however, if they don't, if the bronchi stay
open or they remain the same caliber throughout,

(11:42):
especially as you go out to the periphery,
that's the second sign to look for radiographically.
The third sign is that airways are sometimes
visible within one sort of centimetre of the
pleura. Usually,
bronchi should tend to disappear before they reach
the end of the long edge, so if
you see open airway way out until the
edge, that's a clue as well. So, those

three signs (12:01):
the bronchial arterial ratio, the lack
of normal tapering, and then the airways being
visible one centimeter from the pleura.
Additionally,
those being the three signs for bronchiectasis
radiographically, but as,
Christina described that this is a clinical syndrome
diagnosis, so it's important to consider whether that
bronchiectasis
pattern that you're seeing, is it focal or

(12:22):
is it diffuse, which can often lead to
whether this is a local process as mentioned
or it's a more systemic process being more
diffuse, are there nodules or trans blood, which
is something we've been talking about to indicate
that there's small active airway disease in addition
to the bronchiectasis, which is a structural change,
And then third, is there mucus impaction or
are there any sort of allergic features which
could help us sort of consider other things

(12:43):
in the differential that have been mentioned
like SCF like process or ABP? We always
talk about bronchiectasis
as location, location, location and so also important
to consider upper lobe, middle lobe, or lower
lobe. I know we have a good Pompey
some demographic
on that as well that we can refer
to.
Amazing. Thank you for walking us through that,
Rapalje. I think,

(13:04):
sometimes taking a step back and reminding myself
what I'm actually looking for instead of just
like the alphabet soup of words that get
put on radiology reports is really helpful for
me keeping some of this straight.
And so for our patient, time advances a
few years.
He's seen in clinic where he describes a
chronic productive cough and night sweats.
Sputum cultures are obtained, which grow MAC or

(13:24):
Mycobacterium
avium complex in three separate samples.
And we've all had patients where the sputum
grows MAC or some M abscessus, and the
big question then becomes, is this real disease,
or is this just colonization?
And so, Doreen, I was hoping you could
walk us through how you think about when
a patient truly meets criteria for having disease.

(13:45):
So based on the guidelines, which we know
came out, in 2020,
you want to have the clinical radiographic
and microbiologic
findings in order to make a definite diagnosis.
But that doesn't always apply to every patient.
I mean, this patient's symptomatic is obviously coughing
and has sputum. That's how we got, got
the MAC. So anybody that we're culturing

(14:06):
MAC on already, we know probably does have
sputum or or cultures. But we can talk
about,
you know, radiographic features, which you've all said
must be present, whether they're,
micro,
nodular disease or cavitary disease,
and then we like them to have,
other symptoms, sometimes fatigue, night sweats, etcetera, to

(14:29):
fit the, the best picture. But there are
patients who are totally asymptomatic,
and may just be picked up with a
cavity or, you know, bronchiectasis
on CT.
They don't think they have symptoms of sputum,
but they say, sure, I cough up some
sputum every morning. So you really have to
ask them. But those patients that are very

(14:49):
asymptomatic,
you know, they don't classically fit the definition.
However, they're not people that you would not
want to follow, particularly if they have a
progressive
CAT scan or cavitary disease. So when, you
know, we say who to treat, who not
to treat. That's the big question and often
the most difficult question.
So

(15:09):
my answer is always, if you decide not
to treat, just make sure that you're following
the patient closely. It will become evident to
you when that time to treat is. If
you're always if you're on the borderline at
the beginning.
Thanks, Doreen, for walking us through that. For
me, you know, I think listening to that,
it's a a huge takeaway is that you
really need all three of these because so

(15:31):
many of all three of these criteria. So
many of our patients are going to come
in with one or two,
but
the decision to treat these people subjects them
to long durations of antibiotics,
some of which have significant side effects, not
always with a chance of cure. So it's
a major decision and it's a big takeaway
for me. And I can see how it
could, if we don't adhere to these guidelines,

(15:53):
it could lead to us overtreating certain patients,
undertreating others.
When as a follow-up question, when you look
at a person's CAT scan, are there any
particular
CT findings that make you more confident that
this is actual disease,
or is that just part of the overall
clinical picture?
Well, your your patient here clearly has

(16:15):
diffuse disease and has disease.
You know, if the patient has bronchiectasis and
bronchiolitis,
they likely have disease.
But again, when to treat, right? And do
you have to treat? We have plenty of
patients who
the progression may be stable for many, many
years until something then actually happens, whether they

(16:36):
have some other comorbidity that occurs or such.
And they may not need treatment for those
ten years. And we know the recurrence and
relapse rate reinfection.
And relapse rate is quite high. In some
studies, up to seventy five percent with reinfection
within two years after treatment is completed.
So these patients often may need to be
treated multiple times. So,

(16:57):
it's not like treatment once is going to,
you know, cure them for the rest of
their lives in in many cases. So you
wanna be sure. I do want to point
out that sometimes on CT scans, you may
not see clear bronchiectasis.
But looking at, first of all, bronchiect mild
bronchiectasis, I think, is missed quite a bit
by our radiologists. Particularly, not to fault them,

(17:19):
but they're looking for the more acute things.
They're doing PE scans,
making sure they don't miss that PE. And
if there's myel bronchiectasis,
well that's not high on the list of
why the patient came into the ED in
the first place. So they may not even
interpret that on the CT. So it's extremely
important, I think, for the pulmonologist to relook
at those CTs and say,

(17:40):
There really is diffuse bronchiectasis
using exactly the criteria you had. Or just
bronchial wall thickening.
We know something must happen before bronchiectasis
occurs. And that's the time we may really
want to do something for prevention.
So bronchio wall thickening and this diagnosis of
PBB, persistent bronchial bronch

(18:00):
persistent,
bacterial bronchitis.
Where patients may be very productive
and may not yet
have bronchiectasis
on CT might be the time where we
really want to intervene.
So look at those CAT scans that you
get on your patients, even if the radiologist
did not call bronchiectasis.
That's so so such such great pearls, Doreen.

(18:23):
Just a second follow-up question, you know, and
kind of going back. You mentioned, right,
you or you may say that this they
they meet criteria, but they don't necessarily,
need treatment yet or,
you know, you're still wanting to flush things
out and have follow-up.
What is your threshold for repeating imaging? How
often do you want to have these patients
come in in clinic for surveillance,

(18:45):
before you actually say that you need to
commit to treatment?
So I think we have to go back
again, because we were all assuming treatment means
pharmacological
treatment, at least I was. And so I
don't we should say all of these patients
need full assessment.
As you brought up earlier, all the different
etiologies that might so
they may not need medications at this point,

(19:06):
but they all need a full diagnostic workup.
And I truly believe that we're not doing
enough. The guidelines only
give us a few items that we should
do on every patient. And that's just because
there's not evidence out there to do more
than that yet. So in a patient who
comes to you like this patient, I think
a full diagnostic workup, we could talk about
what that is later.

(19:28):
And then
most patients who are symptomatic, right, we, most
of us believe that airway clearance, certainly in
the guidelines that came out at ERS recently
and the new ones that will be coming
out from Jess, are gonna support airway clearance
as a mainstay, whether it's exercise
with some component or full, you know, airway
clearance and other modalities

(19:49):
is something that's gonna be treatment Mhmm. But
not pharmacological treatment. Yeah. And then I follow
them, you know, depending on the patient, but
usually every three to six months depending on
them. And
I don't wanna be doing CAT scans in
patients who have minimal symptoms and are doing
very well.
So we will follow
pulmonary function test. We'll follow their sputums if

(20:10):
we see the
they become smear positive or they're starting to
grow other organisms. Right? That will trigger us
to get a CT scan sooner. And those
who are sick, often annual CTs will be
done. And then those in treatment sometimes as
frequently as every six months.
Thank you. Thank you for highlighting,
treatment,
pharmacologic, non pharmacologic. Thank you so much.

(20:33):
Yeah. Thank you. And I I really,
appreciate the reminder that,
there's always more digging to do, which hopefully
we can talk about later. I feel like
one of my big takeaways in fellowship has
been not just stopping at, you know, ARDS
or organizing pneumonia or bronchiectasis,
but trying to figure out why that happened
in the first place because it often really
does affect management.

(20:54):
And so for our patient, he grew the
same MAC three separate times and three separate
specimens,
and I know that pathogenicity
varies a lot by the underlying organism. And
so I'm curious, Doreen, would you mind
helping us think through which bugs you typically
think of as pathogens or which ones you're
less worried about, which you tend to think
of as colonizers?

(21:15):
How do I guess do you approach the
idea of the specific bug that they're growing?
Well, I think you all know the common
bugs.
Mac and it's 12 species, depending on what
gets reported out from your lab. So, AVM
intracellulara
and chimaera are the most common.
But then M abscessus,

(21:35):
M. Zenopi, M. Kensassai,
those are the biggest ones that we'll be
seeing in The United States.
There was a paper that came out on
m gordonae, which we know
is usually a contaminant.
But Chuck Daley and, Mark Petersky along with
others just published it, I think, last year.
Looking at what does it signify.

(21:55):
And it actually
does signify underlying airways disease even though the
gordoni may not be something that you need
to treat. So you should probably be paying
attention to a patient who's growing a different
mycobacterium,
and there are more than a 190
of them in every sputum you send. We
like to say, well, you have to get
two. So I'm waiting for that second one
to come, whether it's a bovis or

(22:17):
a semia or and then I get a
different one every time. And why is that
happening? So maybe there's some underlying,
immunodeficiency
in that patient or some
exposure environmental exposure. So further investigation
is definitely needed. But the common ones are
the ones that I I listed. Yeah. Thank
you.

(22:38):
And then I guess just another teaching point
to call out here is that, as you
mentioned, just because someone meets criteria for NTM
pulmonary disease does not necessarily mean that,
pharmacologic therapy is indicated for them,
in particular the antimicrobials.
These are really long courses
with a high treatment burden.
And it's worth considering how robust your patient

(23:01):
is or how predisposed to toxicity they may
be depending on the agents that you're reaching
for, and then again how virulent the bug
that you're dealing with is.
That begs a question then of what would
be a reasonable first regimen for a patient
with MAC and our patient with MAC.
And in general, I think there's a few
teaching points that I would I try to

(23:21):
remember here. The first is that your susceptibilities
really matter, in particular to macrolides and amikison.
And related to this, it's important that that
testing gets done at an experienced lab. So
as an example, ImbObsessus
needs to have that testing prolonged over fourteen
days because they can have inducible resistance to
macrolides, which clinically is really important for those

(23:43):
patients.
In terms of a standard regimen for macrolide
susceptible mac,
ERA or ethambutol,
rifampin,
and azithromycin
is a typical regimen.
Clarithromycin
or rifamycin
are alternatives, but typically have more side effects
or a little less, more poorly tolerated
and so aren't quite first line.

(24:05):
This regimen then can get adjusted slightly based
on your patient's phenotype. So if someone has
fibro cavitary or, excuse me, nodular bronchiectatic
disease,
ERA with three times per week dosing is
generally appropriate, whereas someone with fibrocavitary
or more advanced disease
may need daily dosing and you should consider
adding an IV immunoglycoside.

(24:25):
It's worth emphasizing here that the macrolide is
the workhorse of this treatment regimen. The other
two agents are mostly existing to try to
prevent
resistance
for that macrolide.
Finally, these people need close monitoring,
while on therapy. They need sputum every few
months. You're typically gonna be treating folks for
about twelve months past when their culture's clear,

(24:46):
and so both monitoring sputum to make sure
that it's responding and they're clearing the cultures
the way that you hope, but also to
keep that clock in your head about how
long things may be going.
They'll need lab work with CBCs and CMPs
at baseline and then every couple months as
well.
Depending on the agents you're using, visual acuity
or audiometry testing can be really important.

(25:07):
And then finally, you'll need to consider how
frequently you're going to be monitoring your imaging,
typically once a year or so or with
big clinical changes.
And so for our patient, he has started
on ERA. He's treated for about a year
with improvement in symptoms and culture clearance.
Unfortunately, about three years later, he begins having
exacerbations again. First with a viral URI triggered

(25:29):
episode and then a few months later, he
grows MSSA and MAC in three separate cultures
again.
Interestingly enough, he's treated with levofloxacin
targeting that MSSA,
and his symptoms resolve entirely.
And so at this point, Doreen, I'm curious
whether you would you know, you mentioned that
sometimes folks need to be treated more than
once. Is this a patient that you think

(25:50):
you would initiate MAC directed therapy again?
So I try not to if his symptoms
are better by treating the easiest to treat
organism like you did, and I would follow
him by making sure his CAT scan is
not progressing.
So at this point, I think I would
just follow
him. Yeah. And and that makes a lot
of sense to me and is similar to
what happened with our patient here. You know,

(26:10):
we don't need to go find another problem
if we take the easy win sometimes.
And so another round of MAC therapy is
opted against, just as you mentioned with his
symptoms resolving with the MSSA treatment, the thought
being that maybe that was the driver and
that the MAC itself wasn't particularly symptomatic.
And so to that point, he gets surveillance
cultures over the next four years that grow

(26:32):
in Masiliency
three times. I'm sure I've butchered the pronunciation
of that particular book.
I was raised by lawyers, so I'm, confidently
wrong a lot.
In any case, all of these different
isolates have different susceptibility patterns, and he actually
has a negative culture in between.

(26:53):
And so kind of corroborating that idea that
maybe the NTM wasn't necessarily the thing that
was driving his symptoms.
Unfortunately, in parallel over that time, his imaging
does slowly progress.
So, Roopali, would you mind helping us think
through this scan?
Yeah. So we'll just take another radiology pause
here. And I think at the beginning when
we discussed we talked about the signs of

(27:14):
bronchiectasis. Right? So I wanna remind you that
we have imaging from 2014, now we're flashing
forward four years, right, 2018. And we're seeing
a slowly progressive process. So you can note
there in the imaging on the top corner,
for those listening, we will post the slides,
but you can see that bronchiectasis
is progressing. You can see again that thickened
enlarged airway, we can see signs of that

(27:34):
signet sign,
down at the bottom there, and there's the
mucus
impaction
that is slowly progressing.
So we see progressive upper lobe predominant
bronchiectasis
with mucus impaction
as well as increasing nodularity.
This patient, I believe, Luke also had some
scans done subsequently after 2018,

(27:56):
2019,
and then following a few years later in
2022,
and they continued to show a slow progressive
story of mild progression of this upper lobe
predominant bronchiectasis,
as well as this waxing and waning nodular
pattern that we're starting to see with very
evident mucus impaction, which you can see here
too with some of the airways actually impacted,

(28:17):
specifically with mucus,
in those settings.
So I'm curious, Doreen, given these findings,
symptoms, the recent cultures that we heard about
with the negative culture and then the positive
cultures,
how confident are you at this point that
what we're seeing right now is NTM and
possibly what we've mentioned before, before, common variable
immunodeficiency
related bronchiectasis,

(28:39):
that we are currently
treating this patient for.
Yeah. So I'm concerned about him. I forget
how old he is, but,
he's progressing. He still has persistent symptoms. I
don't know how many
exacerbations. I'm not too excited about one
M. Abscessus
macilians per year. So I would automatically
be getting sputums on him

(29:00):
several times a month, probably.
Because I want to see what's that pathogen
that's going to be growing the most. And
we haven't really done anything, I don't know
about his airway clearance regimen, if he's compliant
or if he's on anything, but that would
be something I'd wanna make sure we maximize.
Because believe it or not, I can show
you many cases
that you have dramatic improvement in CTs just

(29:23):
after doing.
And I tell my parent patients before
you go for your CAT scan,
I don't care if you haven't done your
airway clearance for six months. The month before
your CAT scan, please make sure you're doing
it regularly.
Because I really do think it makes a
big impact.
And,
so if he is doing airway clearance, let's

(29:44):
assume he's doing it and he's compliant,
then we have to think about anti inflammatory
modulation somewhere here. And
he hasn't been growing Pseudomonas
or repeated staph, it seems like.
So, you know, what about macrolide therapy
for,
anti inflammatory
effects? And the problems we have that in
with him is that he's got the Mac

(30:06):
from before or I I know how recently.
And now
if he actually had a,
a,
M abscessus that was resistant to macrolides, we
could use and no Mac. We could use
azithromycin, because then we wouldn't have to worry
about him becoming resistant. But you have an,
macrolide sensitive m abscessus. So
I would start thinking about if he grows

(30:29):
another, you know, get a few. And if
the mycelians is still growing,
start treatment for myceliancy.
Yeah.
Thank you. That that makes a lot of
sense. I think,
we also shared some questions about, what was
happening to him at the time. He's, just
for reference, in his sixties. We've advanced over
the years now, so kind of in his

(30:50):
mid to late sixties at this point.
He's on a little bit of airway clearance
with some exercise and an aerobica that he
uses, maybe not as often as we've requested,
but he does have one.
So time moves forward. He establishes with a
new pulmonologist in 2022,
and unfortunately his clinical trajectory changes.

(31:11):
He has recurrent exacerbations
over the 2022
and then into early spring twenty twenty three.
So in September, he has hemoptysis while he's
out of state with some stable imaging. He's
given PO antibiotics of some kind. The records
aren't quite available.
In December into January, he gets COVID, then
has purulent sinus drainage. His sputum grows MRSA

(31:33):
this time.
He goes to an urgent care where he's
given doxycycline and prednisone.
In March, he has a recurrent productive cough
with more purulent sinus drainage, worsening fatigue and
dyspnea.
His PFTs now show a new airflow limitation.
Cultures grow MRSA and MAC again.
He's finally started on some 7% saline for

(31:53):
airway clearance and is given amoxicillin clavulanate for
an antimicrobial.
Fortunately, he keeps getting worse and is admitted
at an outside hospital not long after where
he gets a little over a week in
total of a combination of levofloxacin, vancomycin, l
levofloxacin, vancomycin,
lonazolid, and bactrim kind of at various times
in various combinations.

(32:14):
There was a lot of issues with his
insurance improving various antibiotics, and so his outpatient
plan kept changing and then leading to different
regimens. It seemed like every thirty six hours
for him.
And then a week later, his symptoms recur,
and he's directly admitted to the hospital again.
Thanks, Luke. Yeah. I think I think we

(32:34):
could probably all agree, like, the patient is
not thriving, right? Something is not happening. How
can we best,
treat the patient? And I think just show
of hands in the room since we have
this opportunity to do this.
Do we think this is just CVID and
NTM?
Does anyone else in the room think that
maybe something else is going on?

(32:55):
Great. Yeah. So I think at least half
of you are thinking, right, some other process
is going on.
I think some important things that Doreen mentioned,
right, looking at what microorganisms
is a patient growing. You mentioned not Pseudomonas.
We usually think of Pseudomonas with cystic fibrosis,
but, you know, someone growing, you know, MAC,
MRSA, MSSA,
Right? You know, is something else happening? The

(33:16):
patient's now admitted. And I think many of
us here in the room as as trainees
or faculty,
when someone comes in for the inpatient admission,
you get to think of this patient in
a homey way. And I feel like it's
the trainee sometimes that are really like, you
know what? I don't I think something else
is going on, and you're right. So please
continue to think that.
And I think I'm thinking now. Right? He's

(33:37):
admitted,
Luke, what you know, diagnostic pause. We've done
radiology pauses today.
But let's do a diagnostic pause.
Right? Because I think a lot of times,
you know, along the course, it's it's easy
to look back now and just be like,
woah. They're anchoring bias. Someone was like, oh,
this is this is only CVID and NTM.
He's not getting better. We're just giving him
the wrong antibiotics. Maybe he's not doing airway

(33:58):
clearance.
But, Luke, diagnostic pause. What what framework do
you like to to think about when you're
doing a diagnostic pause in a patient? Yeah.
Definitely.
And I will say too, I was, fortunate
to meet Dave very early in my residency,
so I think he actually is the one
who taught me the, like, idea of the
diagnostic time out. And so I have cribbed
some of this from him,

(34:19):
shamelessly since he's not here to claim credit
for himself.
In general, I think my goal when taking
a a time out or a pause like
this is to deliberately work through in a
system one kind of explicit way what the
current diagnosis
is. And so first, I like to name
that working diagnosis, which I call that a

(34:39):
working diagnosis because, again, if we felt really
confident about it and the patient was doing
well, we wouldn't be doing this in the
first place. Right?
And so there's some degree of uncertainty around
whether we've gotten this correct.
Then I like to identify what fits and,
more importantly, what doesn't about our case and
our history with that working diagnosis. Are there
things that are inconsistent with it? What does

(35:02):
seem consistent with it? Hopefully, there's some of
those consistencies that led us to that working
diagnosis in the first place.
Then I try to think about whether this
could just be an atypical presentation of a
common disease, you know, common things being common,
whether the patient has multiple diagnoses, you know,
that kind of inverse of,
Occam's razor that people can have as many

(35:22):
illnesses as they please,
and then whether we've truly ruled out any
can't miss diagnosis. Is there something big and
scary that's kind of lurking in the margin
that either we're worried about or the patient
and their family are worried about? And do
we feel like we've truly
given that a good look?
If I'm still unsure at that point, I
like to load the boat, which that is,
like, ask for help. So either

(35:44):
another attending, a more senior colleague, whether that's
a formal consult to, you know, ID in
a lot of these tricky cases, etcetera.
But I don't like to worry alone.
And then lastly, I just wanna make sure
that I've communicated that uncertainty to the patient
and their family,
just to make sure that they're where everybody
is kind of on the same page about

(36:04):
what exactly it is we're dealing with. And,
you know, I feel like I've I've seen
a couple times where someone feels very blindsided
later when a diagnosis changes, even though ultimately
that is helpful for them clinically and they
improve
this idea that they've kind of had anchored
in their mind for some period of time,
that can be a real shock to folks.
And so just making sure that I'm being
transparent with patients about that.

(36:26):
And so for our patient, some potential considerations
that when I kinda think through things for
him, and please feel free, everyone to add
any others as they occur to you is,
one, whether he just needs IV therapy. Is
oral antibiotics
inadequate for him for some reason?
Whether there's been an incomplete duration of antibiotics,
so his courses were typically somewhere in that
seven to ten day range, and sometimes these

(36:48):
folks just need two weeks.
Whether the staph isn't his major pathogen, you
know, is it that Mac is one of
the various MTMs that he's grown over the
years?
And then finally, I do wonder about whether
there's an underlying process that we're missing.
Yeah. Thanks, Luke. Yeah. And I I think
just maybe a few minor things to add

(37:08):
or as you're thinking about this and how
I would be if I was seeing the
patient for the very first time, in the
hospital, many of you may also be thinking,
you know, what, right, this could be this
could be CBID. We have pulmonary. We have
sinus disease. But I think there's other conditions
that we haven't talked about yet that we
can also think of both pulmonary and sinus
disease,
you know, specifically cystic fibrosis,

(37:30):
primary ciliary dyskinesia.
So thinking about does this patient have a
genetic defect that we should be thinking about?
But also we haven't necessarily talked about are
there allergic or inflammatory etiologies as well, including
ABPA or EGPA?
So I think that this would be an
important time to, like, expand or broaden our
differential.
And I I think as you mentioned too,

(37:51):
right, I do agree with some patients,
I do adult cystic fibrosis. So my typical
duration for patients is about fourteen days of
IV treatment. During for for NTM bronchiectasis,
do you are you usually doing seven to
ten days or do you expand on that?
For bacterial infections, for usually, if it's, depending
on the pathogen, but usually fourteen days. If
it's a very sensitive organism, then we'll reduce

(38:13):
it to seven. Okay. Yeah. So but I
think to your to your point, Luke, are
we treating the right organism and is the
patient getting the right antibiotic?
I would be curious, and I'm sure that
you do have this too, but he's grown
MRSA, MSSA
multiple times. Is he getting some type of
resistance to the typical antibiotics that we think
of as well to consider?
And then one one thing too, I would

(38:35):
also think about at this point, Roopali, you
mentioned earlier, the bronchi bronchiectasis
that we're seeing, you know, you said location,
location, location.
I feel like I'm gonna
Tom and Rupali, we we've had three radiology
conferences so far. When we thought when we
think of location,
and or I'm gonna ask I'm gonna ask
y'all. Thinking about location, how do you how

(38:55):
do you divide it up? What are y'all
thinking?
What should we be thinking about? Yeah. That's
a great question.
This is a I know, an impromptu retention
retention knowledge question. Yeah. So I think of
when we think about location, we're trying to
sort of geographically think about the bronchiectasis in
our mind. Mind. And I think we had
mentioned, right, when we think about lower lobe
predominant bronchiectasis,

(39:16):
right, we're thinking about things that can commonly
affect the lower lobe. So I think aspiration
has been mentioned many times, and that just
logically makes sense to us is where you
would see bronchiectasis
associated with chronic
aspiration.
But CVID has also come up as a
potential etiology, and that can either be more
of a diffuse or in the lower lobes,
sometimes more. Although, I will note in this
patient, we noted upper lobe predominance,

(39:37):
in the first sort of time. And then
I know in the upper lobes, Doctor.
Montemiro is a CF doctor, so we often
talk about genetic defects and how CF can
often be seen in an upper lobes. There
can also be infectious ideologies like HIV,
that can sometimes be seen and then the
great mimicker
of everything. Right? I think we talk about
sarcoidosis
as being the mimic disease that mimics everything,

(39:59):
but can often be seen in sort of
the upper lobes as well.
Tom, you have anything to add? Yeah. I
think the, you know, we've addressed the upper
lobes, we've addressed the middle, the lower lobes.
The only other place to really look is
the, the middle lobe.
And when I think about middle lobe bronchiectasis,
I'm usually, you know, the classic thing that's
gonna jump out as like, NTM disease.

(40:20):
But also if you have the patient with
the right clinical history, you know, whether they
have asthma or they have cystic fibrosis,
maybe they have some very central bronchiectasis,
you're gonna think about things like ABPA.
And if you're studying for the pulmonary boards,
maybe you're gonna come across a Mounier Coon
syndrome or something a little bit more esoteric.

(40:40):
But I think when, you know, when you
are faced with someone with bronchiectasis,
thinking about where is it
is a really good place to start.
Amazing. I feel y'all have been definitely have
been paying attention over our last few conferences,
so appreciate that. Yeah. And I think it
looks like Luke has pulled up a fabulous,
infographic that we can definitely share and we'll

(41:02):
just mention to summarize, right, we said upper
lobes, we had sarcoidosis,
CF, we often think about we've listed radiation
TB here, and the central lobes, we have
AVPA,
some CTDs as mentioned, and then our lower
lobes are aspirate duration. We I think Christina
had mentioned, ciliary dysfunction as well, which we
think about in our lower lobes and then
the immunodeficiencies
like CDID in the lower lobes that we

(41:23):
had mentioned.
Yeah. Thank you for that. That kind of
tore through the lungs. I think,
the way that I remember at least the
lower lobe things, or it's either something that
gravity has dragged down there, like an aspiration
or the ciliary dyskinesia is where you just
can't clear your airways
or there's more perfusion
in the lower lobes. And so that's how
I remember that, you know, IBD and RA,

(41:44):
I'm I'm sure this is not physiologically how
this happens and everywhere rheumatologists
just shuddered hearing me talk about this. But
that's how I remember that the stuff with
positive serologies
often affects the lower lobes.
And so for our patient, here is his
CT from this admission.
He has notably progression of his bronchiectasis
again, his nodularity, and now with pretty extensive

(42:06):
mucus impaction,
pretty impressively here in one of these slices.
And so thinking about what you just shared,
I wonder about
why our patient has bronchiectasis
in the first place. You know, it is
possible that it's from his NTM, but that's
can be a tricky chicken and egg question.
You know, do they have NTM because of

(42:26):
the
or did the NTM give them bronchiectasis?
And in our case, I remember that his
initial CTE did have some upper lobe bronchiectasis,
and so that feels less likely here. Even
though I'm sure it has played a role
in his progression over the years, it maybe
doesn't feel like, you know, the smoking gun
that started things.
He does also have CVID, which could explain

(42:48):
things, but like y'all just discussed, that is
typically either more diffuse or lower lobe predominant,
and so our patient doesn't quite fit that
pattern either.
And so, Doreen, I'm sure you have had
experiences where you need to go back to
the patient and review or rereview a history.
And so I'm curious if there are particular
things that you would ask this patient
to try to target your testing and workup.

(43:10):
Yeah. So I think we sometimes get stuck
in. A patient comes to us already with
a diagnosis of NTM related bronchiectasis,
and then we forget about
really looking at all of the other etiologies,
and they're doing okay. And then this is
what happens. They start to fall off the
cliff, and we're saying, did I I look
back. Oh my god. Did I do that
work up? Did I check for their, you

(43:31):
know,
IGE levels, etcetera, etcetera. So I do think,
you need to go back. Like you said,
take a pause. You talked a lot about
recurrent sinus and,
GI issues. We know that these patients, particularly
those with NTM, have a very high percentage
of esophageal,
dysmotility,
and many of them have aspiration,

(43:52):
that is asymptomatic.
So we pretty much study everybody who comes
in. But there's really almost no lower lobe
disease in this patient, so that's not very
high among those. I like that that CT
with that glove like mucus plugging there is
making me more worried about,
you know, ABPA.
I'm always worried about in patients who aren't

(44:13):
responding,
not having picked up some genetic disorder
for either PCD and even
and I'm not a PCD expert, but even
genetic screening for PCD
misses patients
who have milder disease,
in into their adult life. So
the new guidelines just came out, actually, I
think, two weeks ago with ERS and ATS

(44:33):
together,
showing that you have to use multiple,
exhaled nasal nit
nitric oxide.
You can use genetic testing,
or if,
immunofluorescence,
so spectra spectrometry.
So you have to use multiple things in
order to be able to pick that up.
So it's being at a center where they
can do that is important. And then CFTR

(44:54):
testing is gonna be very important because,
we don't typically do that in our NTM
patients, and we're finding that there are patients
who have CFTR mutations. So I'm though I'm
gonna start thinking about that, making sure I
did my room
basic serologies,
and
unlikely, he has no other symptoms, but to

(45:15):
test that. And you said he's getting IVIG
supplementation?
Yes, ma'am. He's still getting that. So it's
unlikely that we're gonna uncover a bigger,
immunodeficiency
since you've already given him replacement therapy.
So that's where I would start. Yeah. Thank
you. And that's that's all really helpful.
In our case, when you go back to
ask our patient, he shares that while he

(45:36):
does have children, he's a father of two,
they were conceived via sperm aspiration and IVF
as he has a congenital absence of the
vas deferens.
And so history, a nice reminder of how
important it is, in our patients.
And that's so it's really important to think
about too, Luke. Right? Because as I'm seeing
this scan, I'm thinking, right, CF until proven

(45:58):
otherwise. I know I'm coming in with my
own bias, though. But, right, going back to
the patient and just, right, look, not only
physical exam, but really history because, right, as
we all say, the patients are gonna tell
you what's wrong with them.
So but there's a lot of testing to
think about. You know, during and thank you
for kinda going down your review of history.
But then how does that lead us to
think about what type of diagnostics we're gonna

(46:19):
do? Right?
There's so many things that we can, try
to order, and we wanna be, you know,
we wanna be thoughtful, but we also don't
wanna send the entire list of things and
and, charge a great bill if it's not
gonna be clinically relevant for our patients.
So, Rupali, Tom, hoping that you can walk
us through, how you know, it could be
really overwhelming to think about working up bronchiectasis.

(46:41):
What is a good framework that y'all try
to do when when seeing patients in clinic?
Yeah. Definitely. And I think, as Doreen has
mentioned, we have some guidelines and hopefully some
new and upcoming guidelines that can help guide
us. But for what we have right now,
we had do have some available ERS and
BTS guidelines that help serve as an initial
way for us to think about diagnostic work
out through these patients. So when I think

(47:01):
about these patients and I'm seeing that clinical
syndrome of bronchiectasis,
I usually start with a basic workup. And
these are recommended by those ERS BTS bundles.
So the first thing is a CBC with
a DIF. That's to assess for any of
those hematologic abnormalities as well as eosinophilia.
The second thing is a quantitative immunoglobulin
workup, as we've mentioned, that IgA,

(47:21):
IgM, IgG serologies.
That screens for primary or secondary immunodeficiencies,
such as CVID as this patient had initially
had. The third thing to think about is
ABPA testing. So that includes a total IgE
as well as an Aspergillus specific
IgE IgG.
This allows us to test for AVPA as
a treatable cause for what this patient might

(47:43):
have. Next is sputum. I think Nori mentioned
the importance of the sputum. And in terms
of sputum cultures, we can order to stand
out bacterial cultures, special fungal cultures, as well
as AFB stain cultures,
which may take more time, but are helpful
to have at that first visit, if the
patient is able to have, produce that much
sputum, and that's to identify chronic pathogens,

(48:04):
as we mentioned, guide antimicrobial
therapy, as well as detect atypical infections,
such as NTM, which we've been discussing.
And then
the last thing, which hopefully all our patients
have when they're coming to clinic, although in
practice, it doesn't always happen,
PFTs. Right? So we always would like to
establish
baseline what the patient's lung function is. So
that that's something we can clinically follow over

(48:26):
time as well as airflow obstruction can be
helpful in sort of confirming some of those
bronchiectasis,
obstructive like symptoms and allows us to monitor
it over time. And I think starting with
those as a baseline bundle is helpful to
identify any initial treatable causes for bronchiectasis
and reversible things as well that can help
our patients. But, Tom, there are further testing

(48:47):
that we can order. And how can we
think about some of that additional testing that
we can do?
As has been really, I think, appropriately driven
home here, you're going to use your history
to guide your additional testing,
because a shotgun approach sometimes works, but it's
it's better to be targeted and actually think
about what your pretest probability is for a

(49:09):
condition so that you can better interpret what
the test result is when it comes back.
CFTR testing, like Doreen mentioned,
sweat chloride testing is the other way we
test for cystic fibrosis,
particularly
if there's a history of upper lobe predominant,
bronchiectasis,
nasal polyps, chronic rate rhino

(49:29):
sinusitis,
pancreatitis, infertility, malabsorption
problems, all of those are gonna clue us
in that, maybe maybe this is all tied
together with cystic fibrosis.
I think it's important to remember too that,
you know, patients don't like being tested with
needles and needle sticks. Sweat chloride testing does
not involve needles,
but it does require that you have that

(49:50):
test done at a center that is specialized
and familiar with doing this testing.
Other things I think about, again, based on
history, particularly if there's a family history
of liver or lung disease, if there's lots
of emphysema in someone who is a never
smoker,
I'm gonna think about alpha one antitrypsin testing.
In the right context, you'll think about,

(50:11):
primary ciliary dyskinesia
testing.
That could be genetic. It could be nasal
nitric oxide testing,
connective tissue disease serologies.
Doreen mentioned that
aspiration
and GI pathologies are very common and often
missed, so a upper GI evaluation,
particularly when the bronchiectasis
is lower lobe predominant.

(50:33):
And then when you're going down the road
of thinking, does this person have CVID,
often you will see patients get pneumococcal
vaccination antibodies, and then you assess their response
to vaccination,
to help you guide your understanding if it's
if this person indeed does have CVID and
is in need of treatment.

(50:54):
Yeah. That was great. Thanks for walking us
through that. I feel like,
trying to remember
some of the those things, like, why I'm
doing the testing and, like, when to think
about particular conditions helps me keep this, like,
laundry list
of potential orders that could be put into
an order set, but maybe shouldn't be put
into one giant order set straight.
And so on that note, our patient has

(51:16):
a battery of tests sent. His sputum grows
MRSA.
He has a specific, IgE testing done for
aspergillus that is negative. His ANA and rheumatoid
factor are negative and his immunoglobulins
and alpha one antitrypsin testing are unrevealing.
However, on CFTR mutation analysis he is found
to have two pathogenic mutations. He has a

(51:37):
F delta five zero eight and then a,
and I'm gonna probably butcher this so please
don't judge me too hard, Monty, but
the thirty one forty twenty six a greater
than g mutation,
which as I understand it is also pathogenic
for cystic fibrosis.
And so clinically, he gets better with a
fourteen day course of anti MRSA antibiotics.
He's discharged and started on Trikafta and Dornase,

(52:00):
and he's referred to the adult CF clinic
for further care. At follow-up, he has no
constitutional symptoms, very mild ongoing cough, and he's
back in the gym several times per week
with no fevers and night sweats.
Luca, you,
that rolled off the tip of your tongue
like a like a natural CF doctor.
But yeah. So I think I mean, I

(52:21):
think this is really important. Right? We, you
know, we CBID, NTM, patients not getting better,
maybe some anchoring bias along the way, saw
a lot of different positions over over, you
know, five, ten years.
But coming up with with the right diagnosis
for this patient,
I think was really important.
And it's you may be asking, well, starting

(52:41):
Trikafta, for those of you who may not
have heard Trikafta, it's a CFTR modulator, so
a tablet that patients take, three different components
that really help restore the genetic defect in
CF.
But it's pretty remarkable. The, you know, patients
will start this and within a week or
within two weeks, their symptoms, like, almost completely
resolved. Pretty remarkable.
I know that this was,

(53:03):
that this patient had the case, you know,
a few years ago, and, when he started
on Trikafta. There is a new modulator though
now is approved actually between,
Christmas and New Year's of this past year.
So the newest modulator is called the Liftrec.
So a lot of patients may be on
that. So you may be see be seeing
both Trikafta a LiftTrack in CF patients.

(53:24):
A LiftTrack's once a day medication. Trikafta's twice
a day medication.
But I think it's truly is remarkable how
fast and, their symptoms improve, not only subjectively,
but objectively as well.
So I I this is exciting, exciting when
I see patients who,
are on modulators and can and can be
helpful. You're also probably thinking, well, I mean,

(53:46):
this patient 60,
you know, what am I missing CF in
a lot of different patients? But you can
see this is a great example for you
to be thinking about it. You know, we
brought up again, like, is something still not
fitting? But he doesn't have Pseudomonas. But actually
now that the current guidelines within CF, MSSA
is actually, the most common organism now that's

(54:06):
grown in patients with CF followed by Pseudomonas
and then followed by MRSA.
That was another teaching point I just wanted
to make sure that we came to.
But, Luke,
fantastic case. Thank you for bringing this. It
went through so many, I think, different things.
This is our first time about talking about
NTM on Home Peeps, and couldn't be more
excited to have,
the,

(54:27):
OG expert, Doreen,
being able to provide some teaching points today.
I know we usually end with a teaching
point from the case, but since we're at
CHESS,
I thought we could just,
each say CHESS is such a fantastic organization.
I thought we could each, end with what
what are we looking forward to the most
at CHESS and,
how has this conference been for you so

(54:48):
far? So, Luke, I'll start with you. That
may be an unfair question because you just
got here yesterday. But
in your in your the the the twelve
hours that you've been here, what has been
the best thing for you so far? So
I'll take the best part of Chicago so
far and the best part of CHEST maybe
separately. The deep dish pizza we had last
night, truly life changing. I probably don't need
to eat for the rest of the week,

(55:09):
but that's okay.
In terms of CHEST, I think I really
appreciate
the conference's
focus on medical education, both in terms of
education,
both in terms of those in attendance, but
also in the development of people's skills as
educators. There's some really exciting sessions that are
on the docket over the course of the
week, with everything from, like, gamification,
of learning to some of the more practical

(55:31):
logistical steps of building a career as an
educator. So that's, I think, what I'm looking
forward to a lot.
I'll say for me, this is my my
second time attending CHEST in person. And I
really think especially for any trainees in the
room or trainees who might be listening on,
you know, asynchronously
and wondering, hey. Should I go to CHEST
next year?

(55:53):
It's in Arizona,
so it'll be warm this time of year.
But, you know, it CHEST is an incredibly
trainee friendly,
trainee focused
conference.
I'm really grateful to be a member of
the trainee work group, which is part of
the training and transitions committee. And through that
committee, we've had the opportunity to organize a

(56:14):
lot of trainee specific,
excellent programming related to the needs of trainees.
You can come to the trainee lounge,
throughout the week. It's a dedicated space for
trainees to learn.
We go over things like how to study
for the boards,
how to negotiate your first contract, how do
you how do you find your niche, medical
education. The list goes on and on. There's

(56:35):
a lot of really great stuff in there,
and it's also a great opportunity to network.
These are the people that are gonna be
our colleagues,
coming to CHEST, go into national meetings throughout
our career, and CHEST is a great place
to meet people.
Yeah. I totally agree, Tom. It's also my
second time at CHEST this year, and I
wanted was fortunate enough to take advantage of
the CHESS fellows course last year, and it

(56:56):
was a fantastic course for any of our
trainees listening,
really covers a large gamut of things. And,
Christina and, other people have have taught there,
and that's been really excellent. I also wanted
to highlight some of the other awards, trainees
can apply for. I was a fortunate recipient
of a CHESS travel grant this year. That's
a wonderful opportunity for any trainees seeking to
come to the conference. And also wanted to

(57:17):
know that there are a lot of other
opportunities for trainees to be involved. There are
the various networks with, I believe, meetings,
ongoing throughout the week as well as the
matched mentorship program that I'm a part of
this year and really excited, to see where
that takes us. So lots of amazing opportunities,
and I've loved the experience here so far.
I feel like we could probably have a
whole, separate podcast on what Doreen loves about

(57:39):
chess.
But Doreen, any any final words for those
that may be here in the room and
those that may be listening today about what
you love about this organization?
I love everything about CHESTA as you probably
could imagine. But,
I think the best thing is that you
can go up to anybody that you pass.
You may know them. You may have, you
know, read an article and tell them who

(58:01):
you are. Tell them you wanna get involved,
and it will happen. I really do think,
all of the leadership and faculty here are
really willing to help you get started, particularly
if you know the area that you wanna
be in. I wanna highlight, we usually always
have a grant through chest philanthropy on NTM
or bronchiectasis
every year. So, we love to give those

(58:23):
grants to fellows and junior faculty. So please
apply for the grants. They come out,
usually,
announcements around February,
every year.
And, don't forget to go to the chess
challenge.
It's really a great way to meet people
and get to know,
everybody
at chess. So,

(58:44):
yeah. Just, immerse yourself in it for three
days.
Yes. So amazing. I know. And I think
one of my favorite things was was doing
the fellows course. I'm, fortunate to be on
the CHESS t and t committee
as a faculty member, and everything we do
is for trainees. So we do a lot
of programming.
So, again, yeah, definitely,
take take advantage of the trainee,

(59:05):
training lounge. I hear there's free coffee for
you all. So, maybe make your way to
there right after this. And as Doreen said,
chess challenge is gonna be tomorrow night, 05:00
reception,
is gonna be there, and then the challenge
starts at 6PM. So come on come cheer
on. There's three teams. The three finalists are
coming from Marshall University,
University of Buffalo, as well as University of

(59:25):
Colorado.
But great, such a great morning to start
off, Chess on this Monday morning in Chicago.
This, case was edited or was written by
Luke, edited by myself, and our, original music
is, by Eric Rogers.
Have a great day, everyone. And, any any
trainees or fellows on the course as well,
we love we love working with you. So

(59:46):
email myself,
and Dave or come after come up to
me afterwards and love to try to collaborate
with you. Thanks, everyone, for your time.