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0:27

We are so excited to welcome back to Noom Conference, Dr.

0:30

Mark Goslin for a lectured entitled Pulmonary Thromboembolic

0:34

Disease, challenging the Conventional Wisdoms and Algorithm.

0:37

Dr. Goslin is the head

0:38

of the cardiopulmonary imaging at Vision Radiology

0:42

and previously he was a diagnostic radiology professor at

0:45

OHSU and the Division Chief of Cardiothoracic Imaging.

0:49

Dr. Goslin started his academic career at the University

0:51

of Utah in 1997.

0:54

At the end of this lecture, please join him in a q

0:56

and a session where he will address questions you

0:58

may have on today's topic.

1:00

And please remember to use that q

1:01

and a feature to submit your questions so we can get to

1:03

as many as we can before our time is up.

1:06

With that, we are ready to begin today's lecture. Dr.

1:09

Goslin, please take it from here.

1:12

Hello everybody. Um, mark,

1:14

and this is gonna be a topic that I hope you enjoy.

1:19

I'm gonna talk a bit about, lemme see here we go

1:23

a bit about, uh, pulmonary emboli.

1:25

So it's gonna be a different approach though.

1:27

There's a lot of things that have been taught, uh,

1:30

through the conventional teaching

1:32

and curriculum that turns out when you kind

1:36

of dive a little deeper, it's only partially true

1:39

or is outright false.

1:41

So we're gonna go through some of this

1:43

and I'm gonna give you a different perspective on it.

1:45

All right, so we're gonna talk a bit about, uh,

1:48

the natural fate of what A DVT does in the legs,

1:51

how it's handled, what's the lungs role

1:54

with pulmonary emboli, with and without therapy.

1:58

And we'll look at a bit about the covid

2:01

and a RDS related emboli versus in situ thrombus.

2:04

I'm using Covid as an example,

2:06

but it applies to a RDS in Gen Diff pular damage.

2:10

And then we're gonna, I'm gonna hit pretty hard, the concept

2:14

of overdiagnosis and false positive exams.

2:18

And as always, I'll do it with some humility

2:22

because the book about

2:23

what we don't know in medicine is much bigger

2:26

than the book that we do know.

2:28

So with that, I'm also gonna share with you this,

2:33

I'm gonna show it to you at the end.

2:34

I love it. Education is the progression from a cocky

2:37

ignorance to a miserable uncertainty.

2:40

Let's see what we can do with you on this one.

2:44

Now, what are my qualifications?

2:45

Well, I'm a cardiopulmonary radiologist.

2:47

I'm not a hematologist. And in fact, um,

2:50

I don't enjoy looking at the coagulation cascade.

2:53

When I do, it's so complicated.

2:55

I tend to kind of retract into the fetal position.

2:58

But I am a curious physician, all right?

3:01

And things that we have seen in imaging, in radiology,

3:05

they don't quite match what the conventional teaching is.

3:09

I mean, that's the privilege about being a

3:12

radiologist, right?

3:13

You get to look inside people and you see things.

3:17

And then if you're observant

3:19

and you're kind of asking questions, you start to notice

3:21

that, gosh, I wasn't really taught this.

3:26

So let's start with an example.

3:28

This was back in my Utah days when

3:30

I was just getting started.

3:32

And one of my residents was 28 years old.

3:35

Um, she's a runner

3:37

and she developed acute onset shortness

3:39

of breath in tachycardia while she was on call.

3:42

Somewhere around like two in the morning, she had an O2 SAT

3:47

of 88%.

3:48

'cause she went to the ER but didn't have any chest pain.

3:51

Then they ordered a CT

3:53

and she had multiple sizable emboli with right heart strain.

3:57

Now, of course, she got up and read her own ct

4:00

'cause she was the radiologist on call.

4:02

They started an IV heparin

4:03

and her shortness of breath resolved within about an hour.

4:07

And her hypoxia was also resolved.

4:09

Heart rate came down

4:11

and she went back to the call room to finish a work

4:14

with an IV pole of heparin.

4:16

Yeah, they, they don't make residents like that anymore.

4:20

So why? Well, people ask me why did she develop that?

4:25

And I thought about it

4:26

and I said, well, I'm not supposed

4:27

to tell you this, but she was pregnant.

4:29

What do you think the response was

4:31

when people who said that?

4:33

Oh yeah, yeah, that makes sense. Now I lied.

4:38

Yeah, I lied, but she was on co oral contraceptive pills.

4:43

Now I lied again. The reason is, is

4:46

because if these had been present,

4:48

that would've been the reason given

4:50

for her developing emboli and were missing something.

4:54

So you gotta dive a little deeper.

4:55

So here are a couple of questions

4:57

that we'll come back to at the end.

5:00

Why did she develop large DVT and pulmonary emboli?

5:04

Why was she hypoxic?

5:08

Why did she improve so quickly in IV heparin?

5:11

All right, I'm gonna come back to those.

5:15

So a lot of what we've learned,

5:17

I call eminent based medicine.

5:20

And when you're in residency

5:21

or in medical school of that ator,

5:23

but residency, you, you've gotta learn so much

5:25

and use so much information you're supposed to get in.

5:28

So you tend to accept what's being taught

5:31

because you don't really have time to kind of think about it

5:34

and dive into it, right?

5:35

Your working memory gets overwhelmed quickly.

5:37

So you just kind of start memorizing.

5:40

And a lot of the stuff that I've found is, you know, a lot

5:44

of people say it and it's partially true

5:47

or you know, maybe it's not true at all.

5:49

Maybe it is true. But when you dive a little deeper,

5:53

you tend to find clinically more relevant information such

5:56

as the sign from Canada, you know, the bridge is out ahead.

6:02

And then you kind of stumble when you go

6:04

to review sites on things like this, which to me are, well,

6:09

I'm not even gonna say, alright, this is

6:11

for me medicine on pulmonary embolus symptoms

6:14

that should provoke a suspicion of pe.

6:17

Must include chest pain, chest ball, tenderness, back pain,

6:19

shoulder pain, upper abdominal pain, syncope, hemoptysis,

6:22

shortness of breath, painful respiration, onset of wheezing.

6:26

What, what? Where are you getting this?

6:28

Any new cardiac arrhythmia

6:29

or any other unexplained symptom referral to the thorax.

6:33

Boy was that helpful? That was so helpful.

6:37

So this brings up Simon,

6:40

a garfunkel's pope, still a man.

6:42

Here's what he wants to hear and disregards the wrist.

6:47

So let's start concept one. Why did we claw?

6:50

Let's think about it. We were all taught about AU triad.

6:54

And by the way, Kel actually didn't describe this,

6:56

it was someone else, but he got credit for it.

6:59

Um, it's a combin combination of endothelial injury, right?

7:04

Which is a little NIUs hypercoagulability

7:06

and abnormal blood flow, specifically slow flow or stasis.

7:10

How many of these do you need?

7:12

Well, actually you really sort of need all three.

7:15

I mean, we can sleep at night and not clot, right?

7:19

Uh, they did a study on dogs

7:20

where they tied off the femoral vein

7:22

and kept the leg still so nothing moves.

7:26

And they waited to see how long it would

7:27

take for a clot to form.

7:29

It actually took 12 hours. So you need all three.

7:34

And the reason that's important is

7:35

because when people say, oh, this patient's had a history

7:38

of DVT, you gotta ask, wait a minute, what, uh,

7:41

what was the circumstance?

7:43

And the response I get is, well, it doesn't matter.

7:47

And it's like, yeah, it does matter.

7:48

If they've had a femoral fracture, it's expected

7:51

because all three are in play.

7:54

But if they were driving a car

7:56

or they're pregnant, okay, wait a minute,

8:00

that's not all three.

8:01

So that tells us there's something else wrong here.

8:04

Probably some sort of thrombophilia

8:06

or hypercoagulable genetic state.

8:09

Okay? So you need at least two,

8:13

but most likely you need all three.

8:17

So if someone says they've had a DVT

8:19

and it was a femoral fracture,

8:20

there's no real increased risk for future events.

8:24

But if they got it from pregnancy

8:25

or say from driving a car,

8:28

yes they are increased for some reason.

8:30

There's something else going on underneath the surface.

8:34

Okay? So concept two, what is the function of the lung?

8:39

This is a study in evolution

8:41

and it's really a remarkable, just a remarkable design.

8:45

So the lungs are essentially a filter, and that is

8:49

because they are one of two organs.

8:52

The liver's the other that are kept alive

8:55

by an arterial supply from the aorta, right?

8:58

The hepatic artery and the bronchial arteries.

9:01

The pulmonary artery you can obstruct, right?

9:04

And the lung doesn't die for the most part.

9:07

Sometimes you see small infarcts

9:09

and that's usually from the small little emboli out in the

9:12

periphery where the collateralization may not

9:14

be quite as robust.

9:16

But what you see here is

9:18

that things don't get past the lung.

9:21

So emboli, metastasis, you know,

9:24

bacteremia, this sort of thing.

9:26

It tends to stop it from going to the other side,

9:28

which is a good thing, right?

9:30

Because if it small clock goes to the brain

9:33

or goes to the finger or goes to, you know, the kidney, the

9:38

or the coronary arteries, right?

9:41

That's when you run into problems

9:42

because now you have obstructed and that induces an infarct.

9:47

And this also goes back

9:49

to medical school when you might have learned about the

9:51

difference between a red infarct and a white infarct.

9:54

And a red infarct is something like the lung or liver

9:57

or sometimes the intestines with its collateral

10:00

because there's persistent blood flow from another source.

10:03

But the white infarct are all the other organs

10:06

where there's just the one arterial supply, it's gone.

10:09

And you develop an infarct.

10:14

This man tried to commit suicide,

10:16

he injected mercury from a thermometer

10:19

into him, no symptoms.

10:23

He's wondering what the hell's going on.

10:24

Well, your lung's A filter, all right?

10:28

It doesn't get past the lung.

10:32

Concept three, and this is a big one, what happens

10:36

to A DVT in the leg?

10:38

How does it get reabsorbed or how does it get broken down?

10:42

Is it fibrotic enzymes? Well that turns out not so much.

10:46

The venous endothelium doesn't tend

10:48

to have a very large component,

10:50

nor does it appear to be

10:52

that important in the um, resolution.

10:56

And there's a study that I'm sure no one read,

10:58

and I've given you the reference

11:00

where they looked at electron microscopy

11:02

of the different stages of the DBT RELU resolution.

11:06

And what they found was it was like wound healing

11:08

as if you cut your skin.

11:10

There's neutrophils and monocytes

11:12

and histamine release and inflammation.

11:15

So that seems to be the major focus, which is why, you know,

11:20

thrombo phlebitis is always present with most DBTs.

11:24

It's just, it's a bell curve.

11:25

And some people have a more, you know,

11:28

aggressive thrombo phlebitis, but it's an inflammation.

11:32

And the pieces that then develop from the clot

11:36

that then go, where do they go?

11:38

Well, they go downstream. And what's waiting for them?

11:41

Well, the lungs, right? The lungs.

11:46

So the lung is a goalie.

11:48

That's essentially what it is for those hockey buffs.

11:50

It's a goalie, right? It stops it.

11:53

And what's in the pulmonary arterial endothelium

11:57

and capillary endothelium.

11:59

Lots and lots of fibrotic enzymes there.

12:01

There is a very large amount. That's what it's designed for.

12:06

It catches the clot and then breaks it down and recycles.

12:10

This seems to be the normal evolution of A DVT.

12:14

Now whether you treat or not, they're going to the lung

12:17

and the lung will stop it and chop it up and recycle it.

12:22

Okay? And that kind of brings me to another point.

12:28

In American medicine, one of the most common

12:31

algorithms I call as the diamond algorithm, an algorithm

12:34

that really results in no change in treatment.

12:39

Alright? So you've got a patient who's got a DVT,

12:43

there it is, it's above the knee, alright?

12:45

They're gonna get treated,

12:46

they're not having any clinical symptoms

12:49

or respiratory symptoms or tachycardia.

12:52

But why order a ct?

12:55

You know, there's some, there's some expected emboli.

12:58

No right? Heart strain doesn't change your management.

13:02

You're still gonna treat, okay? I love this sign.

13:05

How's your week going? It's bad. Have a drink. It's good.

13:08

Have a drink. It's not gonna change.

13:13

One patient I wanna alert you

13:15

to is the renal dialysis patient.

13:16

Now they tend to have thrombus

13:18

and emboli in their lungs relatively commonly.

13:22

Why? Well the origin is usually the fistula.

13:25

When I was a resident we used to

13:27

see these hemodialysis fistulas

13:29

and they would have clots, right?

13:31

Kind of waving in the breeze on the venous side.

13:34

And what the interventionalists would do is go in

13:37

and just kind of rotor ruter it and let it go.

13:40

Well, where'd it go? Well, it went to the lung.

13:43

If we had scanned this patient,

13:46

there would've been a pulmonary embolus.

13:49

This would've instituted some therapy that was not required.

13:53

Okay? So you want to be careful

13:55

with these renal dialysis patients

13:57

because what's the risk

13:58

of therapy versus the risk of withholding therapy?

14:01

To me, if you have something, if a thrombus

14:04

or an embolus in a renal dialysis patient

14:06

probably best just to look in the legs.

14:08

If, um, why? Well, is there anything coming down the road?

14:12

Nope. Don't treat it if they're not having any

14:15

tachycardia or right head strain.

14:17

Don't treat it. If you treat it,

14:19

you can run into some problems.

14:23

Okay? Nice quote here from Alwin Einstein.

14:25

I always thought he was a happy guy,

14:26

but it turns out, eh, those who joyfully march to music

14:31

and rank and file have already earned my contempt.

14:33

They have been given a large brain by mistake since

14:35

for them the spinal cord would suffice.

14:40

So let's move on to this right ventricular strain.

14:45

If you don't take away anything else, take away this.

14:48

When you look at A CTA, the first thing you wanna do,

14:52

look at the heart, what's the right ventricle doing?

14:55

When you have right ventricular strain

14:57

that usually indicates, okay,

14:59

this person's got some symptoms, they got some issues,

15:02

this embolus or this thrombus, whatever it is,

15:05

is not insignificant.

15:06

Even if there's only one segmental

15:09

and you get right heart strain, that means that there is,

15:12

it's causing something to cause the right heart to, to uh,

15:17

to have trouble pumping forward.

15:20

Now it is not related to CLO burden.

15:22

So when people say, oh, I'm worried about the big embolous,

15:26

no, I'm worried about the the CLO burden.

15:29

No, you know, it's not associated with that, okay? It's not.

15:35

Um, it is associated with tachycardia

15:37

unless the patient may be on beta blockers, right?

15:41

PFOS tend to pop open when they have it.

15:44

And the uh, morbidity

15:48

and mortality is more closely related to right heart strain

15:53

as well as pulmonary emboli

15:55

that are in the low bar arteries.

15:57

So the proximal low bar arteries,

15:59

that's another thing you want to take a look at.

16:02

For some reason, these people tend to have more problems

16:06

and tend to develop later in life.

16:08

Pulmonary hypertension, the saddle em bliss,

16:11

which everyone likes to focus on,

16:13

is not associated with right heart strain.

16:15

It is not associated with long-term problems. Okay?

16:19

You might have right heart strain with the saddle,

16:21

but I've seen just as many were you didn't.

16:26

So an example, restaging. Hepatoma, right?

16:30

No symptoms, no right. Heart strain looks good.

16:34

There's an infarct.

16:35

You can tell an infarct

16:36

because there's no air broncho grams a consolidation

16:40

without air broncho Grahams

16:42

does raise the suspicion of an infarct.

16:45

Okay? Consolidation

16:48

with air broncho Grahams is usually not an infarct.

16:55

This patient actually had an incidental sal embolus.

16:59

Again, these patients with widespread tumor

17:01

or metastases do tend to develop d VTS and pulmonary emboli.

17:07

Okay? About one out of 10

17:08

with metastases have incidental emboli.

17:13

So right ventricular strain, when you're looking at it,

17:15

you're looking at the RV ratio to the LV ratio.

17:18

It's usually conventional

17:20

to measure approximately one centimeter distal

17:24

to the tricuspid valve

17:26

and to the mitral valve at the widest segment,

17:30

it sometimes can be a little difficult

17:32

because the heart can kind of rotate.

17:34

But that's gives you, you know, a rule of thumb.

17:38

1.0 kind of suggests it.

17:41

But a better specificity is that like greater than 1.2 ratio

17:46

straightening of the intraventricular septum

17:48

is a very good sign.

17:49

But it does have intra observer variability.

17:52

You really kind of wanna look,

17:53

especially at any concavity, right?

17:58

Or with straightening, especially distally near the apex.

18:03

And I'll show you reflux

18:05

of hyperdense contrast can be helpful.

18:08

And I also use the intra atrial septum

18:11

because that will bow to the left atrium in the setting

18:15

of right heart strain.

18:17

And you can also look for any possible PFO.

18:22

So this would be an example.

18:23

These are low bar, that's already a problem, right?

18:25

Low bar pulmonary emboli.

18:29

You have right heart strain with straightening

18:31

of the intraventricular septum.

18:33

The RV ratio is 1.3.

18:35

You measure about a centimeter in front

18:37

of the tricuspid valve

18:38

and about a centimeter in front of the mitral valve

18:41

there is bowing of the intraatrial septum.

18:45

Okay? Now anything else with this person?

18:48

'cause they presented with chest pain.

18:50

Yeah, there's actually hypo enhancement

18:52

to the left ventricular myocardium.

18:55

So they are developing ischemia or infarction.

18:58

So they must, they have coronary artery disease,

19:01

they have right heart strain.

19:04

This causes the ischemia and infarct.

19:08

So yeah, I don't know.

19:10

Do you all look for areas of hypo enhancement on the CTAs?

19:15

Um, I found them very helpful.

19:18

A lot of times they're known,

19:19

but sometimes the ER doctors are unaware of it.

19:25

Okay, tachycardia, shortness of breath.

19:27

Why is this patient hypoxic?

19:29

Why do you get hypoxia with an embolus?

19:31

Because that's dead space.

19:33

In fact, pulmonary emboli is the poster child

19:36

physiologically for dead space, which tends not

19:39

to give you much for hypoxia.

19:41

It's the shunt that gives you hypoxia.

19:44

Things like ectasis

19:46

or consolidation where you perfuse on ventilated areas

19:50

and the blood returns unoxygenated with the persistent CO2.

19:55

So why with an embolus can you get hypoxia?

19:59

Well, the answer is right there

20:01

when you get right heart strain.

20:02

What is this? This is A PFO.

20:07

And the larger the PFO,

20:08

the more likely you will get hypoxia.

20:11

This is your shunt. The other thing the PFO offers is

20:15

that it bypasses the goalie,

20:18

the the safety function of the lung.

20:21

Remember these emboli want to go, you want them in the lung

20:24

where they can get recycled,

20:26

but now you have a potential bypass

20:28

and that can lead to problems.

20:30

See, when small emboli get going,

20:32

you can get this paradoxical embolus

20:34

and you can get infarcts in other parts of the body.

20:39

Case in point, multiple emboli. Yep. Okay.

20:44

Right. Heart strain. Yep. Intraventricular strain. Yep.

20:47

What's this? There's a PFO. But what's this?

20:53

This isn't, this is an embolus in transit

20:57

through the PFO on the way to the other side,

21:01

which is not where you want it to go.

21:03

Again, the lung is the safety goalie.

21:08

You bypass it, you start to get into problems.

21:12

All right, what are the signs and symptoms?

21:15

Well, if you look in the clinical literature,

21:16

they give you all sorts of things.

21:18

But when you really kind of dive in,

21:20

the most common is acute onset.

21:22

Shortness of breath. Now this is for symptomatic emli.

21:26

Please remember, most of these are asymptomatic.

21:31

Most are, that's the lungs gonna do its function.

21:34

But the ones who have problems,

21:36

maybe they got preexisting cardiopulmonary issues

21:39

or they're having an intense kind of reaction

21:42

and vasoconstriction and right heart strain.

21:45

This will be acute.

21:46

Shortness of breath is usually what they'll present with

21:50

tachycardia, which would often indicate what.

21:53

Right? Heart strain will off also be common, right?

21:57

Unless they're on beta blockers.

21:59

The chest radiograph, is it worth it? Sure. Is it normal?

22:03

Yeah. Shortness of breath. Tachycardia, no wheezing.

22:08

That's key. But you gotta worry about an embolus, then

22:12

that's actually a pretest probability

22:14

that's moderately high.

22:16

All right? And the differential is asthma.

22:20

Small airways disease.

22:21

And again, the wheezing should alert you

22:23

that this is an airway problem,

22:25

not a pulmonary artery problem, but you know, there you go.

22:30

So which radiograph would you pick? All of 'em.

22:33

Acute onset, shortness of breath, tachycardia.

22:39

Which one has an embolus? This?

22:42

No, because infarcts are not very common,

22:45

especially this large.

22:46

This one has air bronchos within it,

22:48

which tells us it's not an infarct.

22:51

That is a strep pneumonia.

22:53

This is a diffused ground glass characteristic

22:56

for non cardiogenic edema.

22:59

Okay, this one is normal.

23:03

And this one had multiple pulmonary emboli.

23:06

And this patient had a glioblastoma

23:09

and that's why they developed emboli.

23:14

All right, what about the mortality?

23:16

Everyone's worried about that. Oh, they could die from it.

23:18

Yeah, that that's true.

23:19

There are some people there do die from an embolus.

23:23

Yeah, but how, what's the actual incident?

23:27

So a lot of the work on teaching of the, you know,

23:30

the death rate and the mortality is based on

23:33

very early work.

23:34

When they looked at retrospectively on inpatients

23:37

and post-surgical patients

23:38

and patients with widespread cancer.

23:41

And the data was skewed.

23:42

And I still hear this quoted at 18 to 35% death rate.

23:47

I'm sorry, what? What are you talking about?

23:51

No, it's not that high.

23:53

Maybe in the ICU it might get up to 18 20%.

23:56

And these are very, very sick people.

23:59

But yeah, you're running the male pulmonary embolus.

24:02

It is not that high.

24:04

Alright, so a lot of this data came kind of skewed

24:08

to these patient populations.

24:11

Okay? Alright.

24:14

So if you look at the actual epidemiology data,

24:17

and this is from 2000, they looked at all pulmonary embol.

24:20

They looked at the pathology data, which found that

24:23

incidental emboli were present in like of,

24:26

of majority of patients.

24:28

They actually came to the conclusion

24:30

that this is the death rate.

24:32

You know, it's a lot lower than what you think.

24:36

And they did find that deaths do tend

24:37

to occur when people had comorbid factors, right?

24:41

Such as preexisting cardiopulmonary problems

24:44

or advanced cancer or the ICU setting.

24:46

So those would be more likely the ones that you might want

24:49

to be a little more careful with the emboli.

24:53

But for everyone else, no tachycardia, no shortness

24:57

of breath, no right heart strain, eh?

25:00

Probably gonna be okay. Okay. All right.

25:04

We're gonna shift gears a little bit.

25:06

It is the mark of an educated mind

25:08

to entertain a thought without having to accept it.

25:12

I'll leave it at that. I'll try to be transparent.

25:15

And I want to talk to you a little bit about this concept.

25:17

This is something that over my years

25:21

I got pretty worried about.

25:22

And I started seeing us do this a lot in radiology

25:26

and not just radiology, other specialties do it too,

25:29

but I ca call it the rolling ball theory.

25:32

And when we read an exam, we are standing up in a hill

25:36

with a ball in inertia.

25:37

Okay? It's, it's it, it's just standing there.

25:42

You call something, you've now pushed that ball in motion

25:46

and once the ball starts rolling,

25:48

it's very difficult to stop.

25:51

So if you think, you know, you wanna pause

25:53

before you push it

25:54

because once you push it, something may happen.

25:58

Now maybe it'll just be a false positive.

25:59

Maybe it, maybe it'll get figured out.

26:01

But I've seen a lot of problems that we initiate

26:07

by calling things and we don't even,

26:09

we're oftentimes may not be aware of it

26:11

because you know, the medical records

26:13

and the other clinicians get involved

26:15

downstream complications and decisions then start to occur.

26:19

So I'm gonna talk to you about the concept of over-diagnosis

26:23

and the false positive CTA.

26:25

So this was an article in 2011.

26:28

Excellent article by the way.

26:29

And there was a paper back in 2008 which said, Hey, let's do

26:33

CTAs on all of these inpatients as they come in.

26:37

And what did they find?

26:38

They found that they've, there was,

26:40

they discovered a lot more emboli.

26:42

And so then they instituted therapy

26:45

and then they looked at the results

26:46

and they said, Hey, the case per fatality

26:49

decreased in these people.

26:51

We need to do more aggressive CTA

26:54

to catch these emboli earlier and give effective treatment.

26:58

Okay, slow down.

27:01

Are there any other conclusions that you could make?

27:04

None were offered in that paper,

27:05

which then instituted this one to come out.

27:08

This is by epidemiologists

27:10

and what they found was mortality really didn't change,

27:14

but the statistics did.

27:16

And they were treating PA most likely patients with emboli

27:20

that were just incidental with the lung doing its job.

27:24

And this was the graft, which I thought was really helpful

27:27

when you institute a screening procedure

27:31

or a treatment procedure or something

27:33

and the apparent incidence increases,

27:36

but you also find the mortality increased.

27:39

That's an indication that there was a true increase in the,

27:43

uh, incidents of this particular disease process.

27:46

You know, brain cancer might be a good one.

27:48

'cause you know, we are seeing it more often.

27:52

This one, you institute a screening or some sort of therapy

27:56

and there's an an apparent increase,

27:59

but the mortality did decrease.

28:00

Now is it cost effective? That's a whole nother thing.

28:03

Well, I won't go into, but that says that, yeah,

28:06

you are catching some things that would result in longer,

28:10

uh, lifespans.

28:13

Now this is over diagnosis.

28:16

You institute this, you get a huge increase in incidents,

28:19

but the mortality state exactly the same.

28:22

But how do you report it?

28:24

Statistics is like a woman's bikini

28:26

or a men's th it's interesting

28:27

what it shows crucial what it hides.

28:32

Fatal PEs per case decreased.

28:38

That's an intellectual way to lie and mislead.

28:41

The mortality did not change.

28:43

You were finding emboli that didn't matter

28:47

and they didn't require treatment.

28:50

That is the example of pulmonary emboli.

28:52

That's also a perfect example of thyroid cancer, by the way,

28:55

if anyone's interested in diving in that topic.

28:58

So ab pelvic ct, this was missed.

29:01

Patient has renal failure and is on dialysis.

29:03

What'd I tell you about dialysis, right?

29:05

They have little emboli. So there's a small embolus here.

29:09

No expansion, right? No, right heart strain.

29:12

So it was missed. So probably good.

29:16

The ball was left in place a couple weeks later they

29:20

developed pulmonary edema.

29:21

This was a CTA, but they had pulmonary edema.

29:26

And this was the dictation. Notice the terminology too.

29:29

Hydrostatic edema, incidental resolving thrombus.

29:32

Don't even say embolous thrombus.

29:33

Columbus symptoms resolved with treatment.

29:36

They did an ultrasound of the lower extremities.

29:38

There was nothing there. They started on me

29:40

anticoagulation anyway.

29:41

And he developed a massive GI bleed.

29:44

You wanna be careful with this because the ball was pushed

29:48

and once it is, that can be a problem.

29:51

Okay? False positive ct.

29:55

How common are they? Pretty common.

29:58

Um, this paper came out in 2015

30:01

and what they found was 26 a quarter of the patients

30:04

that diagnosed with em BLI were found

30:07

to be actually negative based on the three, uh,

30:11

thoracic radiologist evaluation.

30:14

Now that number looks a little high, uh, I have to admit,

30:17

but I find about one out of 10.

30:21

And mostly what I see is that

30:25

it's gonna be smaller emboli.

30:28

And it's usually due to motion artifact or an inci.

30:30

You thrombus or beam hardening artifact,

30:33

sometimes sharp algorithm.

30:35

And what happens is, is that once you call it positive,

30:39

you now push that ball down the hill.

30:42

So let's go over a few, just, just a few of the common ones.

30:46

So in their paper, they found

30:48

that beam hardening artifact was misinterpreted as emboli.

30:52

Now this should never have been called an embolous.

30:55

And if you're not sure, don't, don't call it just,

30:59

it's okay to say determinant or work up some other way.

31:02

But don't, I mean this one is not an embolus.

31:08

How about this? This is called a pulmonary embolus.

31:12

No hedging, just pulmonary emli. Well that's mucus plugging.

31:17

It's mucus plugging the, the artery's right there.

31:20

Mucus plugging. How about this?

31:25

A lot of exams, if you at your institution

31:28

or your practice are doing CTAs with a sharp algorithm,

31:32

you gotta stop it, right?

31:33

You can do it for the lung windows,

31:34

but they need to be a soft algorithm when you are looking at

31:37

the vessels because these artifacts can

31:39

get artificially created.

31:41

Okay? These are not emboli, it's kind

31:44

of was like this laminar flow sharp algorithm artifact.

31:49

This is what can happen. These can be called emboli.

31:52

Now I have seen 'em called emboli.

31:54

Now you go to same patient. This is a soft algorithm.

31:58

It disappears, okay, disappears. Now what about this?

32:04

This one looks a little different. Go to the soft.

32:07

That stayed, that's an embol.

32:10

So you'll see the emli in the soft algorithm,

32:13

but you will avoid this kind of trap

32:16

of the sharp algorithm induced artifacts.

32:18

So soft algorithms for your vascular imaging,

32:21

motion artifact is one of the most common, uh,

32:25

this is called an embolus.

32:26

It's, you can't call an em, don't call it an embolus.

32:30

You know, you if you're not sure you're not sure,

32:33

but don't roll that ball for these.

32:37

What happens to these patients?

32:39

You've read it, you called an embol,

32:41

you went home, did a good job.

32:46

Well now what if it wasn't real?

32:49

Well, this is what you, what happens to these patients?

32:52

Obviously they got a bleeding risk,

32:54

which is estimated about a 7% annual risk if more than three

32:58

months of treatment, which is standard treatment.

33:00

This one big one, medical chart, downstream effects.

33:03

They come into the ER with chest pain.

33:04

They got a history of pe.

33:06

Yeah, you know, they're getting scanned.

33:08

They're getting scanned.

33:09

They're gonna go maybe get workups for thrombophilia,

33:13

they gotta have physician office visits.

33:16

Complications of the wallet are always to be taken

33:19

'cause they can have a great effect on families and people.

33:23

Medical insurance changes,

33:24

potential interactions with other drugs.

33:27

You know, all of these different things can occur

33:29

that we are not aware of.

33:32

So this one was called an embolus. It's motion artifact.

33:36

It's one image called an embolus.

33:39

What happened to this patient?

33:41

Well, they got multiple CTAs, all negative

33:44

and the history given by the er,

33:46

they have a history of pulmonary embolus.

33:49

That's all you need. That's it.

33:51

That downstream complications are now occurring.

33:55

This one, this is an important artifact.

33:58

I can't stress this one enough. I see it all the time.

34:03

It, I don't, I see it called emboli all the time too.

34:06

And it's really distressing.

34:08

Um, this patient comes in, they have covid

34:10

and they did this scan and they have chest pain

34:14

and it was called multiple left lower or low pulmonary emli.

34:19

Look, they're all at the same level. There's no expansion.

34:23

They have a poor cardiac function. How do you know?

34:25

Well, there's no contrast in the left ventricle.

34:28

In fact, there's no contrast in the pulmonary veins.

34:32

So they have a reduced cardiac output

34:35

and reduced forward flow physiologically,

34:38

but they have asymmetry in the flow in the arteries.

34:41

There's a, there's slightly

34:43

faster flow in the right lower lobe pulmonary arteries,

34:46

but you can see how they're enhancing

34:48

and then they gradually just disappear.

34:51

This is non enhancement. Non enhancement, okay?

34:55

Non enhancement. Alright?

34:58

Now what I mean by this is that

35:01

because this was called left lower,

35:03

left mli, what was the history again?

35:05

Chest pain. What about this pericardium?

35:08

It's thickened, it's got indistinct. This in irregularity.

35:11

This patient has pericarditis,

35:13

this patient has a pericarditis.

35:16

Okay? So what happened one week later

35:21

after getting started in anticoagulation?

35:22

They come in with the same symptoms the doc orders the CTA.

35:26

Well I know. So you can see,

35:28

well he had a left lower lobe enhanced this time.

35:30

There was nothing there in the first place, but we knew that

35:32

because it didn't enhance.

35:34

But now they have a hemo pericardium

35:35

from the anticoagulation.

35:37

You shouldn't treat people with pericarditis.

35:39

With anticoagulation. Now this becomes more of an emergency

35:43

downstream complications.

35:47

What about the false negatives?

35:49

Okay, this is, this is a problem

35:51

because basically what we've got here is the

35:56

perception of us missing an embolus.

36:00

We, we get nervous, right?

36:02

Because the opinions are so strong.

36:05

And by the way, these opinions are all cross-referenced.

36:08

There's not really a lot of data,

36:10

it's just cross-referencing that small emboli.

36:14

You know, really honestly, if there's no right heart strain,

36:17

they have a great outcome whether you treat or not.

36:20

And the risks of treatment versus no treatment

36:22

are not considered.

36:24

So once you say you think that's an embolus,

36:27

they're getting treated, the ball is in motion.

36:30

Okay? But we have this perception

36:33

that you do not want to miss them.

36:38

Now I'm gonna tell you, I know this is wordy,

36:42

but it was so well written.

36:44

Uh, it was so well written and you, you can go through it,

36:48

but do you know where all of this came from?

36:50

Anticoagulation gold, you know, standard of care.

36:55

It came from a publication from

36:56

1961 from Barrett and Jordan.

36:59

And that was 19 patients compared to 19 patients.

37:03

All in patients post-surgery, cancer patients.

37:06

There is no real randomization.

37:08

Cochrane library has refuted this being a very good

37:11

paper yet.

37:12

That was it. That was it. And it happened overnight.

37:18

Now this was a time when VQ scans couldn't see small.

37:23

So now we're left with these CT scans

37:27

that unlike the vq, which has more of a probability,

37:29

CT tends to be a more black

37:31

and white even though it's,

37:33

there's a number of indeterminate.

37:35

And this then confined these small emboli

37:39

that were almost certainly present on every

37:41

patient, uh, in this study.

37:43

But you didn't know about it.

37:45

And they said, yeah, it seems remarkable that this one paper

37:51

just one dictated the entire treatment and dogma

37:56

and that new studies were required.

37:58

But who's gonna get it through IRB?

38:00

Because now it's considered standard of care.

38:04

There are studies out there that do support the fact

38:07

of not treating these things.

38:09

And this one in particular was a pretty good one.

38:12

They found that, um, 71 out of 93 was subsegmental.

38:16

So these are small em bli, right?

38:19

Uh, they were treated with anticoagulation or IVC filters.

38:21

IV filters are not a good idea by the way.

38:24

Um, and a quarter of 'em were not treated at all. Okay?

38:29

A quarter were not treated at all.

38:30

They had a similar outcome. Nobody died of an embolus.

38:34

But there were eight hemorrhages that included in that 90,

38:38

uh, 90, 71 patients, okay?

38:41

So there was complications from it.

38:45

Nobody died from the hemorrhage,

38:46

but there were complications.

38:49

So patients diagnosed with isolated subs, segmental mli,

38:52

they have a pretty good favorable outcome.

38:54

Again, if there's no right heart strain

38:58

and the short term prognosis

39:00

and long term actually looks like the risks

39:02

of treatment may be higher than the risks of not treating.

39:07

Again, this is what the literature suggests,

39:10

but that's not the perception that's taught.

39:16

So I wanna take you through this one.

39:17

This one's very problematic

39:19

and you all will be faced with this.

39:22

This is in CTA.

39:23

It's a very nice quality and there is something here.

39:28

One thing not enhancing, okay? What do you do with that?

39:33

Whatcha gonna do?

39:37

It's a young patient, some shortness of breath.

39:40

Call it an artifact. Call it an Inc. Situ thrombus.

39:43

What's the risk if you call that?

39:48

I mean, let's look at it.

39:50

There is no expansion of the vessel.

39:53

No expansion of the vessel. It's single, it's subsegmental.

39:57

There is some mild motion artifact in that area.

40:01

There is no branching to it.

40:04

Still could be a thrombus or an embolus,

40:06

but probably might be best

40:10

for this patient not to call it.

40:13

If you want, you can say,

40:14

why don't you do some lower extremity ultrasounds?

40:16

They'll be negative. Uh,

40:18

this one was called an isolated Subsegmental Emli.

40:22

No, that's it. It's subsegmental. Emli. I'm so sorry.

40:26

There's actually sun here in Portland, Oregon. Um, sorry.

40:33

And uh, let's see if I can I, APO, oh, there we go.

40:36

Okay, now you can see.

40:39

So this was the same patient.

40:43

They got scanned again, same symptoms, some shortness

40:45

of breath and that same subtle little defect is

40:48

there and unchanged.

40:50

So what do you do with this? Do you call it an ems again,

40:53

call it a thrombus.

40:54

What do you think the VQ result would be in this?

40:56

Yeah, it's gonna be negative, right?

40:59

Do you suggest ultrasound?

41:01

Well, based on the literature, it would've been better not

41:03

to call this at all and

41:06

or just recommend some lower

41:07

extremity ultrasound or something.

41:09

Or at least give a differential. So what are the risks?

41:13

What happened to this particular patient?

41:16

She had a full hematology hypercoagulable workup,

41:20

negative money, four more cts the next year,

41:23

two lower extremity ultrasounds.

41:25

I mean this is common. The ball got in motion.

41:31

So another patient,

41:33

this preliminary one was called negative.

41:35

It is some poor enhancement.

41:37

No central emboli, no right heart strain.

41:39

Nothing here to be really concerned about.

41:41

This is clearly an artifact.

41:43

The next day the faculty read it

41:45

as positive for pulmonary embolus.

41:48

Okay? All

41:50

right, you rolled the ball.

41:54

We'll see what happens. We can be absolutely certain only

41:58

about things we do not understand.

42:00

So now I'm gonna take you into another realm.

42:03

I'm betting you didn't learn about this. When is an embolus?

42:07

Not really an embolus, okay, the concept of incite.

42:11

You thrombus these thrombi form within the vessel.

42:16

They didn't come downstream. How often does that happen?

42:20

Hmm, yeah. Relatively commonly. What are they called?

42:25

On every single CT and embolus.

42:29

Okay, here's the problem.

42:32

Patients with A RDS pneumonias can do it too.

42:36

Um, other sort of things can do it,

42:38

but the big one is diffuse ular damage A RDS

42:42

and part of A RDS is

42:44

to develop in situ thrombus within the arterials and venues.

42:47

That's pathologists will tell

42:49

you this, this is not a secret.

42:51

And there was a study here with covid pulmonary pathology

42:55

and they looked at 68 autopsies of these patients

42:57

with diffuse ular damage and 84% of them had microthrombi.

43:01

Yeah, of course, but that's part of the whole thing.

43:04

But they found that about half of them extended

43:08

into larger vessels where we could see them on the CT scan.

43:13

And guess what they're called? They were called emboli.

43:15

The other thing they've noticed, and of course is

43:18

that there is no association of anticoagulation

43:21

or no anticoagulation with the development

43:23

of these in situ thrombus.

43:25

Again, diffuse ular damage is like wound healing.

43:28

You cut the skin, a clot tends to form. Okay?

43:33

This was a paper in 2021

43:35

where they looked at electron microscopy

43:37

and they found that these covid patients,

43:38

but the same with A RDS had widespread in situ you thrombi

43:42

in the veins and arterials, okay?

43:45

This was part of the pathology, it's part

43:48

of the inflammation and wound healing.

43:52

This is a paper back in 1986.

43:55

This is how long we've known this.

43:57

I mean, we've known it before.

43:58

And if you look up any pathology site,

44:00

look at the histology of RES.

44:02

There will be that you will have well-documented fibrin

44:06

thrombosis within the arterials and venues.

44:09

And it doesn't matter the etiology.

44:11

Diffuse ular damage is a, is an injury to the lung

44:15

that results in injury to the alveoli.

44:17

To the interstitial with white,

44:19

with associated in situ thrombus.

44:22

Now what happens if the thrombus

44:23

extends back and you can see it?

44:25

What's it called? It's called an embolus. Why?

44:27

Because we're not teaching this. We're not teaching that.

44:30

This is part of the injury process.

44:33

And then anticoagulation doesn't really have an effect.

44:37

You're just giving them the risks

44:39

and these people are at great risk.

44:43

This is what histology looks like. Okay?

44:46

Widespread thrombus, doesn't matter the cause.

44:49

So this is a patient with coronavirus acute lung injury,

44:52

diffuse ular damage.

44:54

There are some thrombus.

44:56

Is that an embolus or is that thrombus in situ thrombus?

45:00

How can you tell? Well, uh, let's quote the studies.

45:05

There isn't any why we don't know about this.

45:09

We, the pathologists know this,

45:12

but we in the clinical world, we're not aware of it.

45:15

Now as radiologists, we should be aware of it.

45:18

Again, it's our privilege to look

45:20

inside these people and ask questions.

45:23

Yeah, it's, it's relatively common. So this is purely mine.

45:27

Goss is whatever it's worth what it's worth.

45:33

Here are some things that when I look at the pathology data

45:36

and the literature in their description, I try

45:38

to extrapolate, go back

45:40

and see if you have a linear thrombus,

45:44

especially in an area of acute lung injury

45:48

that doesn't branch and doesn't expand,

45:50

that's most likely gonna be an in situ thrombus.

45:53

But recommend bilateral lower extremity ultrasounds anyway

45:56

because if there's nothing there, then

45:59

what are you giving the anticoagulation for?

46:01

Because it's certainly not gonna help that.

46:03

The lung will take care of it as it heals.

46:06

You're just trying to prevent the next one, right?

46:09

How about this? That's clearly an embolus.

46:12

I'll go with that boo.

46:13

This one is not, I think this is an insight to thrombus.

46:17

There's no expansion. It's linear. There's no branching.

46:21

But this one, this one's small. There's a little branching.

46:24

I'm not sure here. I'm not sure. You know, gotta be humble.

46:28

No, there's no real data for this.

46:31

This one has expansion of the vessel.

46:33

That one makes me more nervous.

46:35

I would actually call that an embolus

46:37

because the thrombus shouldn't expand it.

46:40

It's part of the wound healing.

46:41

And their description is it tends to not expand.

46:44

And if anything might constrict when you see expansion

46:48

that suggests it came downstream.

46:50

If you see branching, that suggests it came downstream.

46:54

This one, I called this one

46:56

and I said, look, this is overwhelmingly likely

46:59

in situ you thrombus.

47:00

It's the only one there. It's right in the area.

47:02

It's linear. There's no expansion.

47:04

Do the bilateral lower extremities. They're negative.

47:07

What did they do? They treat 'em anyway.

47:10

They treat 'em with anticoagulation anyway.

47:13

Well, you know, you shouldn't be doing this.

47:16

So casually, what is the rate of complications saying covid?

47:21

Well, the venous thrombosis rate was 4.8%.

47:25

But that was over called

47:26

because a number of these insights you thro

47:28

by were called emboli.

47:30

But that was part of the wound healing.

47:32

Diffuse ular damage histology, normal

47:35

bleeding complications were almost 5%.

47:37

They were the same. 4.8.

47:40

You, you see these

47:41

and they don't, you're not gonna benefit these people

47:44

with insight two thrombus.

47:45

The problem is, is that how do you tell the difference?

47:49

And it can be difficult 'cause there's no real data.

47:52

If you're interested in the topic,

47:53

we published a paper a JR 2023, um, references there.

47:58

We kind of dive into it a bit.

48:01

The greatest optical discovery is not ignorance,

48:04

it's the illusion of knowledge.

48:07

So I'm gonna finish off with a couple of things here.

48:09

Anticoagulation. Oh, anticoagulation.

48:13

People are like snowflakes people, all right?

48:15

Not all thrombi emboli

48:17

or cardiopulmonary status are the same.

48:19

Yet we treat with an algorithmic approach.

48:22

Once you say an embolus, they get the three months.

48:25

And if it was, if it's a recurrence

48:27

or you know, it was non provoked, then might go on for life,

48:32

which may not be a bad idea actually.

48:35

I'm not saying that's a bad thing,

48:37

but, uh, the most important is that,

48:39

is it idiopathic or is it provoked?

48:41

If it's provoked, you know, um, you probably just, you know,

48:45

you do a short term and there's no real

48:47

increased risk later.

48:49

But these are the ones you worry a little bit more about.

48:53

All right. This study, I don't know

48:54

how they got it through IRB.

48:56

This is one of the very, very few studies out there.

48:59

And again, 87 ambulatory, not, you know,

49:01

they're the healthy people, the numbers are eh, uh,

49:04

but this was interesting.

49:06

This was one of the only ones where

49:09

no treatment was started.

49:11

Most of the papers that you'll find treatment

49:14

with anticoagulation was initiated at first

49:16

and then retracted after a short period of time.

49:19

You can't do that. You can't do that

49:22

because once you anticoagulate,

49:24

the body's hemostasis is going

49:26

to activate the coagulation system to maintain balance.

49:29

Now you suddenly take it away and you've got a thrombus.

49:32

Sitis, yeah, it's gonna propagate.

49:35

Yeah, it's gonna propagate.

49:37

But if you don't treat it at

49:38

all, this is what they found.

49:43

There was no difference in clot progression in the DVT.

49:46

There was no difference in DVT regression.

49:49

There was no difference in silent emboli.

49:52

And there was one person who died

49:54

and that was the anticoagulation group.

49:57

Okay? This must be what you know,

50:02

is that, is that correct?

50:04

Well, you know, some people will benefit from

50:06

anticoagulation, but a number of people may not, may not.

50:10

Okay. 30 5-year-old patient jumped off a bridge,

50:14

broke T seven fracture.

50:16

Burst fracture, lots of hematoma. What else is there?

50:18

Well, there's multiple pulmonary bolli with expansion.

50:21

Bilateral, no right heart strain, no symptoms, no hypoxia.

50:26

Do you treat this patient well,

50:29

trauma folks said no.

50:32

How did she do? She did fine. She did fine.

50:35

I don't know why they scanned her 30 days later.

50:37

It made no sense, but they were all gone.

50:42

This is on the number needed to treat website.

50:44

Very interesting website run by kind

50:45

of epidemiologically trained physicians

50:48

and on there anticoagulation for acute venous embolism,

50:51

PE and summary.

50:53

Those who got anticoagulation,

50:54

a hundred percent found no benefit.

50:56

Okay? Is a hundred percent no. In medicine there is no 0%.

51:00

There is no a hundred percent.

51:02

But have you ever even heard anyone say that?

51:06

Have you ever even heard someone mention it?

51:10

It's not a hundred percent

51:11

because there are so few studies out there,

51:15

but the studies that they did find really didn't seem

51:18

anticoagulation, didn't seem to affect them.

51:20

Now I'm sure there are patients, especially some

51:23

of those ICU patients

51:24

who would benefit from anticoagulation.

51:26

I don't know who they would be,

51:28

but I do know that we aggressively treat.

51:31

Now what if the patient has a left ventricular mural

51:34

thrombus or atrial fibrillation clot?

51:37

Those people I would definitely treat with anticoagulation

51:39

because the lung is not be able to protect them.

51:41

It's on the other side, right? It's on the other side.

51:47

Last concept, IV heparin.

51:51

A lot of patients who get IV heparin, they tend

51:54

to improve quickly.

51:56

Not all of them. These are symptomatic pulmonary emboli,

51:59

but they tend to improve quickly.

52:02

Why? Well,

52:04

right heart strain is not related to clock burden.

52:08

So there's gotta be another mechanism at play.

52:11

One that's not taught. And this particular paper was

52:16

extremely interesting.

52:17

They actually did say, you know what embol I do,

52:20

they induce a cascade of pulmonary vasal constriction

52:25

through the vascular bed in a number of patients.

52:28

So the pulmonary vascular resistance is now high.

52:31

The right heart will strain

52:35

and these are the people who have the symptoms.

52:38

You give IV heparin and it turns out IV heparin

52:41

and IV lovenox are pulmonary vasodilators,

52:44

pulmonary artery vasodilators.

52:46

So now they've released the cascade.

52:49

The right heart strain decreases.

52:53

This is fascinating.

52:55

And in the paper they say we've known this

52:57

for about 60 years, but nobody has studied it much.

53:00

There were a few studies on dogs using, um, sildenafil

53:04

and nitrous oxide and stuff, and they had the same results.

53:09

Symptoms improved within about an hour or two.

53:12

Now you might have been told we have

53:14

to bridge Coumadin with heparin.

53:17

Well, why? Oh,

53:18

because Coumadin induces a transient hypercoagulation.

53:22

Okay, wait a minute. I I'm, I'm sorry, you what?

53:26

What paper were you quoting? What's the biochemistry?

53:29

Where's the study on this

53:31

and how does that make things worse?

53:34

You see, Coumadin doesn't dilate the pulmonary arteries.

53:37

And how do you die in embolus is right heart

53:39

strain in arrhythmias.

53:41

And it seems that the most common cause is

53:44

pulmonary vasal constriction.

53:45

So you give IV heparin

53:47

and bridge, you've addressed the reason they die

53:49

and then they go to Coumadin.

53:52

But instead what we'll do is we'll make up a reason.

53:55

We'll just make up a reason.

53:58

So let's go back to our example. The talk is done.

54:02

28-year-old female, my resident.

54:06

All of this information now that we're done,

54:11

let's see how well this stuck.

54:13

Why did she develop large DVT and embolus?

54:17

She was sitting down reading, is that sufficient?

54:21

Cause no, you need all three.

54:23

Turns out she's a marathon trainer,

54:25

was up in the up up in the Wasatch range in um, Utah fell,

54:30

got a big bruise and muscle strain.

54:34

She was sitting and it turned out

54:39

later because she wasn't pregnant

54:40

and all these things that would've

54:42

explained it and not had anyone.

54:43

Look, she is, has a protein C deficiency

54:46

and she has a family history of it.

54:47

So she had all three. If she was

54:50

pregnant, would anyone have looked?

54:52

Probably not. Why did she develop hypoxia?

54:56

Because the emboli blocked it. No, that's dead space.

55:00

She was had right heart strain.

55:01

And on her CT she had a PFO, she had shunt.

55:06

Why did she improve so quickly

55:07

with ivy heparin and then go back to work?

55:10

Because IV heparin, pulmonary artery vasal dilates

55:14

reduces the right heart strain, closes the PFO.

55:21

This is it. It's functional lung, it's a filter.

55:25

It takes care of the emboli.

55:26

Sometimes the emboli can cause adverse effects,

55:30

but for the most part that's what it's style.

55:32

What its job is, watch out for false positives.

55:36

Be careful and just pause before you roll the ball.

55:39

You don't know what the downstream

55:40

complications are for the patient.

55:43

Right? Heart strain and pulmonary artery and lower arteries.

55:46

These are the two factors

55:48

that will increase someone's morbidity and mortality.

55:52

Acute lung injury of any cause will have in situ thrombus.

55:57

These people can also have pulmonary emboli.

55:59

How do you distinguish it too?

56:02

I'm not sure, but at least if you're aware of the concept

56:05

of in situ thrombus

56:06

and it's relatively common,

56:09

maybe at least you can bring it up and pose that question.

56:14

And pulmonary vasoconstriction cascade tends

56:17

to be the reason many people have right heart strain.

56:21

Now, if you gave IV heparin to someone

56:22

with multiple lobar emboli and they didn't improve

56:25

after a few hours, okay, stop.

56:29

That's the patient where the conventional teaching

56:32

of it's a mechanical blockage

56:34

and you should think about going to do thrombolysis.

56:37

That's that patient you gave the IV heparin,

56:40

you've addressed, you've uh,

56:42

addressed the most common cause, pulmonary vasoconstriction.

56:45

It didn't improve it. Now you assume it's a

56:48

mechanical obstruction.

56:51

And as promised,

56:54

education is the progression from a cocky ignorance

56:57

to a miserable uncertainty.

57:00

Thank you so much for listening and I am gonna stay around

57:03

and I'll try to answer some of these questions.

57:06

If you need to go, you can go,

57:09

but I'll see about some of these questions. Um,

57:12

Yeah, thanks so much for your lecture

57:13

and if you do have questions, go ahead and put 'em in that q

57:15

and A feature

57:17

and if you could open Okay, you found him.

57:20

Okay, I'll, I gotta through this first one,

57:23

is there any specific cutoff value

57:24

of D dimer which correlates with the probability of PE

57:28

new I call the D dimer.

57:30

Satan's uh, yeah, I am gonna say it. Satan's a*****e.

57:34

It's a terrible exam because it's way too sensitive.

57:37

It's way too sensitive and there's really no level

57:40

and I don't find it that helpful.

57:43

Um, I mean if it's negative that can be helpful,

57:46

but it's, there are studies

57:48

that have actually said we should increase it.

57:50

So on the ROC curve it's more useful

57:53

and there's both radiology

57:55

and clinical papers that have suggested it yet.

57:58

We still haven't done it.

58:00

Um, if the CTEP is negative

58:04

and there's still a high suspicion of pe, is VQ indicated?

58:06

No, because the VQ scan is more, uh, sensitive,

58:10

but it's not as specific.

58:11

You don't want to be going from the CTE to the vq.

58:15

But if you run into say like the patient who I think

58:19

that's just an artifact

58:21

or an in situ thrombus, if you were to do a VQ scan

58:25

and it was normal, then the OPED study would say,

58:28

this person's fine, but I would've said

58:32

they were fine from the ct.

58:33

But maybe people don't have quite that confidence

58:36

or such, then that could be a potential,

58:39

that could be a potential use.

58:42

Uh, the motion artifact seems

58:44

to produce a Lenin form artifact.

58:47

Hmm. I hadn't noticed that.

58:51

That's a good observation of I will look

58:55

over the next year or so.

58:59

Hmm, I hadn't noticed that. Um, let's see.

59:04

Please review normal appearance

59:06

of int ventricular septum versus

59:07

appearance of right heart strain.

59:09

Okay. Yeah. Intraventricular septum really should be curved

59:12

at gentle curvature to the right ventricle.

59:15

One of the things that happens is first the posterior

59:19

aspect here, lemme get that.

59:20

The posterior aspect of the septum straightens,

59:23

there's still a little curve anteriorly

59:25

and then it'll start to get concave

59:29

and the anterior portion will start

59:32

to flatten when the whole thing is flattened.

59:34

That's usually pretty severe, right?

59:36

Heart strain, some, uh, moderate.

59:39

I found that you still have a little bit

59:41

of curvature anteriorly,

59:43

but there might be straightening or concavity.

59:45

But the first part will be the, the base

59:47

or the posterior aspect of the intraventricular septum.

59:51

Okay. But look at the intraatrial septum too.

59:53

So, you know, if you see the intraatrial septum convex

59:58

into left atrium, that's a pretty good sign

60:00

that there's some heart strain present

60:02

and that's much more, uh, compliant.

60:05

Okay. After pe how often do you see pneumatic seals?

60:11

Never, uh, I do see them with infections,

60:16

but I do not see pneumatic seals with pulmonary bolli

60:21

and even infarcts, infarcts simply melt.

60:26

So when people say infarcts cavitate, no

60:30

infected infarcts cavitate, but not infarcts.

60:35

Okay. How

60:36

to differentiate acute right heart from thrombus, from chronic.

60:39

Oh, good one. Um, that can be tricky.

60:42

I use the right ventricular anterior

60:45

or free wall four millimeters or greater.

60:48

And I tend to say this is more of poor pulmon alley

60:52

or chronic heart strain.

60:55

Okay. Um, if it's really thin, I favor acute,

60:59

but if the pulmonary artery's really large,

61:02

how sure can you be, uh, I favor

61:07

it's probably preexisting.

61:09

It's kind of tough to tell, but that's a great question.

61:12

But if the right ventricular free wall is greater than four

61:15

millimeters and the pulmonary artery is big,

61:18

it's probably preexisting.

61:21

Okay. How can we overcome the flow artifact?

61:25

Oh, um, understand its presence. It's so common.

61:29

It is so common. If you need to repeat, repeat, uh,

61:33

with a longer delay, uh, check the legs

61:37

with doppler ultrasound.

61:38

If you don't wanna scan them again,

61:40

but it, they're all at the same level

61:43

and you will see the gradual opacification

61:47

mixing heterogeneous in, uh, contrast

61:51

and then there's no enhancement

61:54

and the pulmonary veins will probably not enhance either.

61:57

Okay. No expansion all at the same level.

62:01

Um, usually in the setting of, uh, some sort

62:04

of cardiomyopathy or reduced cardiac output.

62:08

It is so common. Please don't call those emboli.

62:12

'cause that, that to me has been one of the most common,

62:14

even more than motion artifact, uh, reasons

62:17

for false positives.

62:20

Okay. Uh, what do we do with subsegmental emboli?

62:25

Do we call them knowing the patient? Yeah.

62:27

Um, welcome to my world.

62:31

Uh, I usually say, uh,

62:36

subsegmental emboli without,

62:38

or subsegmental embolus without right heart strain.

62:43

If treatment is considered, evaluate lower extremity al

62:47

with ultrasound in, um, or these are often incidental

62:52

and in the literature have not been shown to be a problem.

62:55

However, evaluation with lower extremity ultrasound, I'm,

62:58

I'm a big fan of that because if there's something A DVT

63:02

above the knee, I still wouldn't take

63:04

anticoagulation myself.

63:05

But, you know, at least there's a reason, some reason

63:09

to give anticoagulation.

63:11

But if there's nothing in the legs,

63:13

I have no idea what you're treating.

63:15

'cause the emboli will be chopped up

63:17

and recycled in the lung,

63:18

especially without right heart strain.

63:21

The truth is though, when you say it,

63:25

even if you say all those things,

63:26

which I do, they still get treated.

63:30

Um, you just do what you can do.

63:34

Uh, what's the value of detection and reporting?

63:36

Small PE in instigating a workup that

63:41

detects underlying cardio?

63:43

Oh, coagulopathies like factor V and lupus. Um, yeah.

63:47

Uh, I

63:52

don't that to me, I would like

63:57

to know there's a reason for those small mli.

64:00

Um, they've had some recent trauma is a big one.

64:04

Like they're, they're coming off an ankle injury.

64:06

That's the ones I see most often in the younger patients.

64:09

'cause that's who you'd consider this with, right?

64:11

Not so much the older patients.

64:12

You think more cancer for them,

64:14

but younger patients is when you think of these genetic and,

64:17

and autoimmune things.

64:18

And I'd like to have a reason.

64:21

And so if, if there's no, you know, reason

64:24

or provoke, uh, cause then consideration for, you know,

64:29

hematology workup is suggested and they probably will be.

64:33

'cause most young people, once you call

64:34

it, and there's no reason.

64:36

They'll go to hematology and have it worked up.

64:40

Um, that's kind of where I go.

64:41

Just make sure that they are actually emboli

64:44

and if you're not sure, you're not sure.

64:46

Um, let's just kind of make sure they have it. Okay.

64:50

How to differentiate ineffective post MBI area.

64:56

Oh, I don't quite understand that. Abscess. Oh, infective.

65:01

Uh, post mla, uh, cavitation is usually a,

65:05

uh, cavitation.

65:07

Infarcts do not cavitate infarcts do

65:09

not have air broncho grams.

65:10

Infarcts do not cavitate if the cavitate, you consider

65:15

a superimposed infection until proven otherwise.

65:21

That's the word I put until proven otherwise. Okay.

65:26

Oh, thank you. Okay. With a patient with submassive pe

65:29

echo demonstrating right heart strain.

65:31

I don't care what the echo says, I, I don't listen

65:33

to the echo and raised tropen trope

65:36

and borderline hypotension.

65:37

Okay. These, these are sick patients.

65:39

Do you proceed to thrombolysis?

65:41

No, no, that's, no, you don't. Just bear with me.

65:46

You can call 'em, tell 'em, you know,

65:49

maybe come in if they're really

65:51

that borderline, maybe you inject it.

65:53

But I would give a trial of IV heparin or IV lovenox first.

65:58

Okay. Because most of the time they will improve,

66:02

but you'll know within an hour.

66:05

Okay. You'll know within an hour.

66:06

And if they're not improving, absolutely thrombolysis.

66:11

What I find is, uh, the reason I get nervous, I mean

66:16

that patient's really sick.

66:17

So if he did thrombolysis, he did it, it's fine.

66:19

But I, I find it worrisome that there are patients

66:21

who are much more stable with right heart strain,

66:24

where people jump into thrombolysis immediately

66:26

and then they develop these complications

66:28

that are quite severe when you trial of IV heparin.

66:32

If they're stable enough, just give it an hour or two.

66:35

If they don't improve, most will improve.

66:37

But if they don't, those are the patients that would go, uh,

66:41

respond well to thrombolysis.

66:44

Um, boy, that actually sounds pretty unstable.

66:47

So, uh, when is it a role for vq, uh, young patients

66:53

is in order of vq first, if no contradiction better

66:57

to avoid over to Yes.

66:59

On both. Um, yes.

67:02

Useful to repeat in three months.

67:07

I don't know if it's useful. Um, I symptoms persisting.

67:12

Um, maybe, but I like it. Young people go with vq.

67:17

I love it because those tiny subsegmental Yeah,

67:20

you don't have to worry about 'em.

67:21

It's negative. Which it probably will be. That's awesome.

67:25

OpID says they have a great prognosis.

67:27

You avoid the CT artifact dilemma. That is kind of common.

67:32

So your EQ is underutilized in younger patients

67:35

or patients who are older but have normal lungs.

67:39

So Absolutely.

67:41

Is doing peripheral runoff, the lower extremity venography.

67:44

Ooh, no, I, it's been studied.

67:47

I like it, but it's just, that's a lot of radiation.

67:50

That's a lot of imaging. That's a big price.

67:53

Um, and you'd have to do it on everyone.

67:56

'cause you'd have to sort of know right from the start.

67:58

Like I think that's an artifact we should, oh no,

68:00

the patient's already back in the, back in their bed.

68:04

Um, I, I would just probably go with ultrasound.

68:08

Um, but we did it for a while,

68:10

but, woo, that was a lot of imaging too.

68:13

It'll, it'll wear you down with decision making fatigue too.

68:18

Alright. When you measure RV

68:20

and LV to calculate the RVN ratio,

68:22

do you measure your inner wall to the inner wall?

68:25

Yes. Inner wall to inner wall.

68:27

One centimeter from the valve. Both sides. Okay.

68:30

It's just a rule of thumb. Right.

68:32

And it's just kind of giving you an idea, uh,

68:36

PE workup in pregnancy.

68:37

Yeah. I got a whole talk on the myths of, uh,

68:40

pregnancy is a hypercoagulable state.

68:43

I totally don't believe that the,

68:45

the papers are based on surrogate endpoints

68:48

and the coagulation cascade.

68:50

But when you look at the THROMBOELASTOGRAPHY analyzer,

68:53

pregnant and non-pregnant patients are pretty much the same.

68:56

Confidence intervals are basically overlapped.

69:00

Um, I personally think that if you develop a DVT

69:03

or a PE in pregnancy, you probably have

69:07

a preexisting thrombophilia.

69:09

There's a patient, uh, there's a paper by Cunningham

69:12

and all 2010 I think, where they found that two thirds

69:16

of patients who were pregnant in postpartum

69:17

who developed DVT had a known thrombophilia

69:21

and they actually theorized that.

69:23

The other third probably did too.

69:25

It was just a number of things in the coagulation cascade

69:28

that we don't know yet.

69:31

So I do think that that actually is.

69:37

Okay.

69:39

I think you got 'em all. Alright.

69:41

Yeah, if anyone has any questions, this is my email.

69:44

Feel free. Don't mistake my enthusiasm for intimidation.

69:47

Okay.

69:49

Well, thank you so much for sharing your lecture today

69:51

and answering all those questions.

69:52

We love having you on the new conference stage

69:55

and appreciate all that you've done.

69:58

My pleasure. Have a great day everyone.

70:01

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70:03

so much for participating in today's new conference

70:04

and all those awesome questions.

70:06

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70:09

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70:10

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70:13

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70:15

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70:19

Be sure to join us next week on Thursday,

70:21

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70:24

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70:27

A Beginner's Guide to CT

70:29

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70:32

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70:35

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70:38

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