All language subtitles for Pulmonary Edema_English (auto-generated)(1)

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