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okay so today we will be talking about
pulmonary edema on chest x-ray with some
CT correlation so before we jump into
the chest x-ray manifestations that
supposed to talk about how to think
about pulmonary diem and there's some
different ways of doing this so you
could either think about pulmonary edema
as it relates to its pathophysiology or
two specific causes pathophysiology and
for path of physiology we're really
talking about Starling forces so what
are the Starling forces that can allow
fluid to leak out of vessels so the
biggest one here is hydrostatic edema
this is where there's too much pressure
inside the vessels that pressure pushes
fluid out of the vessel into the
interstitial of the lung that's
hydrostatic edema this doesn't have to
be related to hydrostatic pressures
though if the vessels are leaky right so
if they have leaky vessels now fluid can
leak out and as we call permeability
edema and permeability edema we think
about as either being related to diffuse
alveolar damage or without diffuse
alveolar damage the few cellular damage
we typically associate it with a RDS so
permeability edema
with or without a RDS or diffuse
alveolar damage and you can have a mixed
pattern so people with both hydrostatic
and permeability edema it can be kind of
hard to remember which types of causes
fit into each of these specific pathogen
eken isms so I think it's a little bit
more helpful to think about them in
causative so what are the big causes so
the two big causes either parting genic
or non cardiogenic so for Part II
eugenic this is related to congestive
heart failure so this is the biggest
cause under cardiogenic that makes sense
right cardiogenic the three big causes
that we typically see are people that
have too much fluids so they're they're
getting too much fluid or they can't get
rid of the fluid so who can get rid of
fluid people with like renal failure
so fluid overload or aggressive
resuscitation the other type of non-core
tha that demon that we see commonly is a
RDS so this is gonna be your
permeability edema with diffuse alveolar
damage and then some specific clinical
scenarios you just kind of have to
memorize and these are some ones that we
see not uncommonly in clinical practice
so neurogenic edema these are people
with that get your cranial bleeds
massive strokes herniating across
midline this can cause an on cardiogenic
edema pattern within the lungs post
obstructive pulmonary edema this is
someone that has you know really best
writer either from a thyroid or they're
choking on a hotdog or something like
that
and they get intubated the lungs we
expand rapidly against its negative
intrathoracic pressure this can be too
pulmonary oedema reexpansion edema these
are people that have very large pleural
effusions that are you know rapidly
sucked out the lung rapidly re expands
that can cause you need lateral
pulmonary edema on the side of the re
expansion you're drowning heroin and
opioid overdose vacuum caused and we you
know we're really dealing with this
epidemic that's going on right now so
it's not uncommon to see these people
that come in you know with an opioid
overdose that are in non cardiogenic
pulmonary oedema recent lung transplants
we see this as reimplantation edema you
know within 24 to 72 hours they often
have this model degree of a diamond i
typically will resolve over the next
week or so and then lastly is trolly
transfusion related acute lung injury
these are people are receiving blood
products it causes an acute lung injury
pattern along that's a non cardiogenic
type of pulmonary edema
so these are some causative ways to
think about this you just kind of have
to have a bucket list and these are some
examples of some specific clinical
scenarios that can produce non
cardiogenic edema so what about the
imaging appearances so for me the way I
like to think about the imaging
appearance is you know it's bleeding
either to some sort of hydrostatic
process or hydrostatic pulmonary edema
and here we see signs and elevated
venous pressures we're going to talk
about the signs of elevating is elevated
venous pressures that have pushed us
into thinking about you know hydrostatic
from an area edema and then we have
causes that are not related to
hydrostatic pulmonary edema the classic
scenario here is you know permeability
edema with or without diffuse after
they're damaged so people with like a
RDS right so this is non hydrostatic
edema this would be like your opioid
overdose or something like that these
are people that don't have to have
elevated venous pressures and then last
you have the mix pattern and the mix
pattern is really difficult especially
you know for trainees when they first
start out even for you know you know
attendings it could be really difficult
these are people that are in the unit
they have a RDS but they're also getting
resuscitated with fluids and they go
into failure you know there's some fluid
that's translating out to the lungs
that's you know may respond to diuresis
whereas the diffuse alveolar damage
obviously won't right so it's kind of a
mixed mixed bag today for today's
lecture we're really gonna focus on
hydrostatic pulmonary edema and this
concept of elevated venous pressures as
kind of our signpost to say that this
process actually going on so what are
the major causes for hydrostatic edema
so one big cause here is can cardiogenic
pulmonary edema these are people with
tip
left-sided cardiac dysfunction and acute
congestive heart failure so that's them
one of the biggest causes for
hydrostatic edema but you can also get
hydrostatic edema if you just have too
much fluid in your body right so too
much fluid so who gets that people with
kidney injury so whether it's chronic
and they miss dialysis or it's acute and
they can't get rid of the fluid where
they're being aggressively resuscitated
so this is kind of how I think about
hydrostatic pulmonary edema into two big
causes cardiogenic edema volume overload
who gets volume overload chronic people
with some sort of kidney insult the
other brother it's acute or chronic
where people that are being aggressively
resuscitated fluid and the reason why I
like to separate this out is because
hydrostatic pulmonary edema when they
start developing pulmonary edema it
often corresponds the signs correspond
to pulmonary capillary wedge pressure
so normally pulmonary capillary wedge
pressure is on the six to eight
millimeters of mercury range this is
usually acquired with a swan-ganz
catheter when you get to the 12 to 18
millimeters of mercury vein you start to
developing vascular congestion so this
is kind of like the first phase the
first phase of this so you start
developing vascular congestion we're
gonna be 18 to 24 millimeter range this
is when you start developing
interstitial edema now fluid is leaking
out of the vessels into the interstitial
when we're greater than 24 millimeters
this is research developing airspace
edema so this is fluid that's actually
not only in the interstitial but it's
actually leaking into the alveoli going
into the air spaces that belonged okay
so this is kind of the three phases
vascular congestion interstitial edema
and airspace edema and these things look
different radio graphically so let's
first talk about vascular congestion so
what are the signposts for vascular
congestion so we want to look for
widening of the masker pedicle as
against vein distension sound ization
and so to do that what we really want to
do is just blow up the central aspects
of the cardio mediastinum so we really
want to focus on the central aspects of
the chest x-ray because this is where
the signs are most evident let's just
blow up that area so let's talk about
first the vascular pedicle like how do
we actually measure the vascular pedicle
so a normal peak vascular pedicle width
is somewhere between 35 and 50 eight
millimeters in size so let's take a look
at how to do that so here's a
corresponding CT this is a coronal CT
and the coronal CT some relevant Anatomy
is your SVC and this is your aorta and
measure avascular pedicle with here's a
schematic to show you how to do it so
what we do first we have to establish
the right boundary and the left boundary
so for the right boundary the right
boundary is formed where the SVC crosses
the bronchus intermedius so here's your
SVC and this is where it crosses the
bronchus intermedius of this area you
basically just draw a line straight
through that okay so this is the right
boundary
now where's the left boundary the left
boundary is defined as the origin of the
left subclavian artery so here's your
aorta and it's the origin of the left
subclavian artery and that's this vessel
right here so where is that stuff on
chest x-ray and on CT so on CT the SVC
is obviously easy to see it's this area
in here this is all the contrast within
the SVC
over here the SVC and brachiocephalic
means you can see us as density over
here this vague density this is the
outer edge of the SVC and you can see
where the SVC will come down and then
intersect the bronchus intermedius so
it's this dot right here so we're gonna
draw a line through that so let's do
that so that's where it intersects the
bronchus intermedius we drop a line down
so that's gonna be the right edge so
what about the left edge so here's the
left subclavian artery coming off of the
aortic arch there's the luff subclavian
artery where is that radio graphically
can be kind of hard to see but here's
the aorta and you can see how there's a
vessel coming off like right here
there's kind of like nice concavity okay
that represents the origin of the left
subclavian artery so once we find the
origin of that we drop a line straight
down through it and now we have our left
margin so we have a right and left
margin and then we measure the distance
between those two and this represents
your vascular pedicle with okay so
here's a person that's going into
congestive heart failure and so on his
first chest radiograph what do we notice
we could see that the vascular pedicle
whip is actually normal in size so
here's the outer edge of the SVC coming
down through the central Airways here
and so we could see that it's normal in
calibre we also want to look at the
azekah screen so where's the as against
vena
the as I guess mean lives in here it's
nice and small in size typically the as
I guess mean and an upright chest
saturation measure less than one
centimeter and transverse dimension so
you'd see that the as agus Fein is nice
and small and size and kind of tucked
away it's barely visible and then last
we want to look at the basket sure so
here's the vasculature out here so the
vessels are actually in the upper lung
zones are somewhat small and saw
and this can be kind of hard again for
trainees when they first start out what
I typically do is again look at the
vessels in the upper lung zones kind of
look in the lower lung zones it looks
small in size they look smaller than the
vessels in the lower lung zones if they
do I'm okay with it
and so you can see that the vessels in
the upper lung zones look fairly small
in size now he's presenting with acute
shortness of breath and so what are the
changes that we noticed so for one the
agus sorry the SVC we could see it's
just a little bit more prominence off of
midline more than what we saw last time
right so we can see the SVC is all the
way out here now and then we can see
where it intersects the bronchus intra
media so down here so we drop a line we
can measure the width from the origin of
the subclavian artery to the outer edge
of the SVC there and we see that the
vascular pedicle width has increased
it's now measuring 64 millimeters
greater than 60 millimeters so it's
widened in addition if we look at the
osseous being the assets mean is much
more distending than what it was before
I remember was a little small dot it's
barely visible now we have this kind of
greater size the lip storage structure
at the tracheobronchial angle and we
measure it and it measures greater than
1 centimeters there's a sustained
distension in addition if we look at the
vessels the vessels in the upper lung
zones are more prominent than what they
were before and I think again this can
be really hard at first when you're
looking at chest radiographs it's really
helpful if you have a prior imaging
study because if you compare the size of
these vessels to what they look like
before they just look bigger
right so the vessels are becoming more
distended there's vascular
redistribution going on so there's an
example of a sterile redistribution and
then as we progress further in
congestive heart failure we see that
there's increased further increase in
widening of the vascular pedicle and
addition this area is just becoming
denser overall it's filling up with
fluid the azygos vein right is much more
prominent than what we saw initially so
we see this tension of the azygos vein
and then the vessels again you just
compare the vessels here the vessels
over here the mussels are becoming
progressively more distended and backed
up right so this is all examples of
vascular congestion these are all the
signposts of aspirin congestion vascular
pedicle widening as gas main distension
pulmonary vein distension with
redistribution and cephalization so what
about interstitial pulmonary edema so
for interstitial pulmonary edema what
are the signposts that we're looking for
for that so we're looking for curly
lines we're looking for peribronchial
cuffing we're looking for vast
indistinct miss inhaler haze we'll talk
more about that we're also looking for
fish oil thickening so here's an example
of someone that has intersexual edema
let's first recognize that he is
developing hydrostatic edema and we know
that because we see signs of a scar
congestion so for 1.the as a guest vein
right it's just standing out a little
bit too much it's too thick it's too
thick in addition the vessel is right
the muscles are standing up they all
look like they're giving each other
high-fives up here they're just standing
up on end they're too prominent there
just standing out too much so we see
that there is some signs of vascular
redistribution so what are the signs of
interstitial edema that are present on
this radiograph now and I think that can
be really subtle at first when you're
when you first start trying to you know
recognize these signs let's blow up an
area we blow up the area and we blow up
that area we notice that there's all
these little lines right so see these
lines out here lines we also see some
lines more centrally so one of these
lines represent these represent curly a
and curly B lines and once you know that
they're there when it's blown up let's
look at the other side you can start to
notice that you can see them over here
too now so those who are curly being
curly a lines and what does that
represent it represents fluid leaking
out of the vessel into the intercession
of the long and thickening the secondary
pulmonary lobule this what we call in
term lobular septal thickening so as an
example of inter-library septal
thickening both curly a and curly B
lines are the exact same thing
curly B launcher just on the periphery
curly a lines are larger and more
centrally located they both represent
intra lobular thickening so let's blow
up another area here so kind of going a
little bit deeper so I can step in just
a little bit deeper into this
radiographic blow up another area so we
blow up that area what we notice here we
see that there's a vessel and we see
that there's an airway and if you look
at this airway this airway is just again
too thick these airway should be
paper-thin so we'd see that there's
thickening of the airway so this what we
call peribronchial cuffing and why do we
get that and congestive heart failure
it's the same reason why we get
thickening of the interstitial fluid is
leaking out into the intercession of the
lung and one of the interstitials of the
lung is the bronco vascular
interstitials you're gonna get airway
wall thickening right this is like this
one cause bronchial wall thickening can
lead to reason right so there's like the
cardiac wheeze right so you see airway
wall thickening this is at least
is peribronchial cuffing airlie wall
thickening same idea as curly nods in
addition what do we notice is that the
vessel so the artery adjacent to the
airway has increased in size normally
these are around one to one you can see
that this is much larger than one to one
and this is another sign that there's
backing up a fluid and elevated
pulmonary pressure so as we say is an
increased pulmonary artery to bronchus
ratio so let's go on a little bit
further so this is again a person with
congestive heart failure you see the
septal lines out on the periphery
you could also notice that there's
peribronchial thickening so
peribronchial cuffing in addition you
could also see these lines emanating
from the hilum so this is an example
again of interstitial pulmonary edema
curly a curly B and peribronchial
cuffing however there's another sign
that's also present and I think the best
illustrate this we're gonna put up a
normal radiograph adjacent to the
abnormal Renu graph and then what below
of this area in here so we blow up that
area in here we compared to the normal
radiograph if we look in here so see all
the vessels see how nice and sharply
margin ated they are right there really
easy to say but where the vessels on the
other side you just don't see them the
vessels are indistinct and this is what
we call as Tyler Keys or vascular and
distinctness I didn't attending back in
the day they used to say just give him
the Hayes what does that even mean give
him the Hayes what does that even mean
and what he was talking about is it's an
actual sign and it basically means that
there's indistinctness of the central
vasculature we compared the vessels over
here to the vessels over here we just
don't see them well they're all kind of
blurred out this is a sign of
interstitial edema
there's vascular indistinctness from
fluid leaking out around the vessels
it's causing the vessels to be
indistinct so it's an example of Tyler
Hayes another sign of interstitial edema
in addition we can see that there is
thickening of the minor fissure so
here's the minor fish were there this is
we say is fish oil thickening another
sign of intersexual edema flu is leaking
out from the lung interstitial
lymphatics are picking it up and they're
draining it out into the pleural space
so we start to see visceral thickening
so there's a thickening of the minor
fissure another sign of interstitial
edema and this is what this looks like
on CT so on CT what do we see so we see
all these law
and one of these lines represent these
lines represent areas of entry log Euler
septal thickening so interlocutor septal
thickening the short lines out here
represent your curly B lines the larger
lines more essentially represent your
curly a lines as we say is inter lobular
septal thickening in addition we look at
this airway in here this airway is just
way too thick it looks like a cheerio we
can pair this airway to this airway over
here so look at that airway over there
look up nice and thin and smooth that
wall is compared to the airway over here
this airway just way too thick it's the
exact same idea we have flue that's
leaking onto the interstitial and fluid
that's leaking out into the Bronco
vascular intercession that can cause
airway wall thickening this is why they
can weaves or have hair trapping because
the airways are so thickened
so as an example of what interstitial
edema looks like on an axial CA and on a
Colonel CT it's you know it's kind of
nice to see what these curly B lines
look like and so see these lines out
here again these are areas of interlab
Euler septal thickening and these are
all our curly B lines that we initially
saw on a chest radiograph in addition we
also notice that there's wall thickening
again of the Airways right this is your
peribronchial cuffing there's a
peribronchial cuffing in curly B lines
this is an example again of interstitial
edema of what it looks like on CT with
inter-laboratory septal thickening and
air wall thickening all right so let's
now move on to airspace edema so
airspace edema we're talking about a
viola or opacities we're talking about
fluffy stuff within the lung parenchyma
okay now fluid is leaking out from the
intercession and filling up the air
spaces right so this typically is gonna
be symmetric and bilateral sometimes
though it can be diffused or patchy and
it can have a batwing distribution and
the batwing distribution is you know
typically peri hilar okay so Perry high
learned distribution like we see here
however you know a true batting
appearance whereas where we don't see
the vascular congestion where we don't
see the septal lines it's it's fairly
uncommon or represents all about 10 to
15 percent of cases but this a Buehler
edema
tends to be more centrally located and
the reason for that is because the
lymphatics are really robust out on the
periphery of the lung and so they can
have this peripheral clearing it
actually pumps all the fluid out of the
lungs into the pleural space into the
lymphatics and so you can make this
peripheral clearing and because you get
peripheral clearing you have more
central opacity right and so this
central
these fluffy opacities in here it is an
example of that where we see this kind
of fluffy stuff within the long Franklin
and we see that there's other signs of
hydrostatic pulmonary edema going on we
notice that the basket pedicle is too
wide the as against Maine is super
distended we see some subtle pearly
lines on the periphery of the lung
there's vascular and distinctive however
we also note that there's these fluffy
opacities just fluffy opacities peri
Pilar and distribution is an example of
a heavy older and we could see how as
the patient is getting better and is
being diary stand they're gonna have
congestive heart failure under control
how the vascular pedicle is getting
smaller in size the vascular
distinctness is becoming a little bit
more a little bit less you can actually
start seeing some vessels essentially
and then the airspace opacities look a
little bit less evident the patient now
you can see the vascular pedicle is
basically back to normal we can see that
they placed a pacemaker and a swan-ganz
catheter and if we look at the vessels
centrally we could start seeing vessels
right before remember the vessels were
all obscured we couldn't really make out
the vessels right the vessels are
becoming more evident we start to see
them better again that's because the
fluid is being taken off of the
interstitial they're no longer being
obscured and then we can see now that
the vascular pedicle with again it's a
little bit wide it's you know it's but
it's getting back to normal the vessels
look certainly distinct we don't see a
lot of curly B lines but what we do see
is all this haziness down here so see
all this easy
all this haziness this is not pulmonary
edema this is pleural effusions and it's
not uncommon that pleural effusions
develop after or subsequent to the
pulmonary edema clearing and that makes
sense right because we have all this
fluid in her lungs
the body wants to get rid of the fluid
so where does it put the fluid it puts
the fluid in the pleural spaces so you
can actually see improving features of
pulmonary edema but worsening pleural
effusions and this is not uncommon you
see this fairly common in the ICU
setting where they have really bad
congestive heart failure the fluid
starts getting better
it comes off the lungs but goes into the
pleural space you can actually see that
they've developed plural effusion so in
review we really talked about just
hydrostatic pulmonary edema and how its
basic and corresponds to wedge pressures
we go through this characteristic
progression of vascular congestion into
interstitial edema and then finally into
airspace edema and we sell specific
signs for each member for vascular
congestion we talked about
you're pedicle widening as against vein
distension cephalization in vascular
distribution for interstitial edema we
talk curly lines official thickening
peribronchial thickening and hilar haze
for airspace edema we saw these kind of
fluffy peri Hodder opacities more
essentially within the lung now it's
also important to remember that the
heart may be enlarged and that's that
that makes sense people have dilated
cardiomyopathy is but not all the time
not all the time is the heart going to
be enlarged if they're an acute renal
failure or they're gonna aggressively
fluid resuscitated the heart may not be
big in addition if they have an acute
myocardial infarction the heart may not
be enlarged and so the heart does not
have to be enlarged and again don't
forget that polo fusions are very common
in this scenario the body's carrying the
fluid you can put it into the pleural
space they could also be third spacing
accounting for the pleural effusions so
you can see pleural effusions even as
the pulmonary edema is actually getting
better so that concludes this talk if
there's any questions please feel free
to email me
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