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Hello and welcome to Noon Conference, hosted by Modality

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Noon Conference connects the global radiology community

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through free live educational webinars that are accessible

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for all and is an opportunity

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to learn alongside top radiologists from around the world.

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Today we are honored to welcome Dr.

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Bernardo Tessa for a lecture entitled Intracranial

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Hemorrhage on CT and MRI.

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Dr. Tess completed his radiology training at the State

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University of Rio de Janeiro,

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where he lectured for over a decade.

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He's a neuroradiologist who serves

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as a radiology medical director

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and radiology residency program coordinator at Hospital Bar

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the OR and Rio de Janeiro, professor

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of radiology at Uni Grand Rio,

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and Director of Institutional Relations

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of the Brazilian College of Radiology.

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

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and a session where he will address questions you

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may have on today's topic.

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Please remember to use that q

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

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as many as we can before our time is up.

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

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Tesser, please take it from here.

1:07

Good afternoon everyone,

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and thank you for joining the Modality Noon Conference.

1:10

My name is Bernardo Tesser,

1:12

and today we'll walk through a practical case-based approach

1:15

to intercranial hemorrhage.

1:17

The focus will be on pattern recognition, image includes

1:20

that help determine etiology

1:22

and the pitfalls that radiologists must avoid,

1:24

especially in the emergency setting.

1:28

I have no conflicts of interest related to this presentation

1:31

and the learning objectives.

1:33

By the end of this lecture, it should feel more confident

1:35

in five key areas.

1:37

First, recognizing the main types

1:38

of intracranial hemorrhage, uh, on both CT and MRI.

1:42

Second, differentiation, intraparenchymal, subarachnoid,

1:45

subdural and epidural bleeding.

1:48

Third, understanding the imaging signs that point

1:50

to etiology severity and the hematoma expansion.

1:53

And fourth, identifying septal pitfalls clues that can lead

1:57

to misinterpretation.

1:59

And finally, applying a structured rep reliable approach,

2:02

uh, both in emergency and follow-up exams.

2:08

Uh, and why does mastering hemorrhage imaging matter?

2:11

Intracerebral hemorrhage accounts for about 10 to 15%

2:14

of strokes, and it carries high early mortality imaging,

2:17

especially CT changes management within minutes.

2:21

MRI refined etiology, timing and prognosis.

2:24

Small vessel disease, uh, hypertensive

2:27

or AMY amyloid plays a major role in

2:30

determining hemorrhage location.

2:31

So our ability to distinguish deep from lower

2:33

patterns is essential.

2:36

We start by organizing hemorrhaging

2:38

to anatomical compartments.

2:40

Intact actual, uh, hemorrhage includes intraparenchymal

2:44

and intraventricular blood.

2:46

Extra actual hemorrhage includes subarachnoid,

2:48

subdural epidural collections,

2:50

and cortical superficial cytosis.

2:52

This framework is foundational

2:54

because compartment often suggests etiology In this scheme,

2:57

you can see the mains, so the dura here and the arachnoid

3:01

and all of these hemorrhage will be the epidural, uh,

3:04

above the, the dura subdural, subarachnoid

3:07

and intra parenchymatous.

3:08

Okay, and inter ventricular here.

3:12

Um, so let's begin with a rapid fire case.

3:14

This is a 59-year-old female.

3:17

What three things must be reported in the first 30 seconds

3:20

if the patient's still in the scanner.

3:22

What we see here, this is a ct, this hyperdense, uh, image,

3:27

uh, show that represents blood.

3:30

So this is a hemorrhage.

3:32

It's intra parenchymatous,

3:33

and also it has intravitreal components.

3:36

So it's, uh, going inside the ventricles.

3:39

Also, it has a mass effect.

3:41

It's, uh, pro uh, promoting

3:44

a midline shift to the other side.

3:47

Uh, so the, the three things must,

3:49

must be reported in the first 30 seconds are location

3:52

where the, is it's intraparenchymal

3:55

and it's deep in the brain, uh, in the basal ganglia

3:59

development mass effect, including the midline shift

4:02

and the intraventricular extension,

4:03

because it has a major prognostic impact.

4:06

If you can deliver these three points under pressure,

4:08

you're already helping the clinic,

4:10

the clinical team to make decisions.

4:13

So the CT basics CT is the cornerstone

4:16

of acute hemorrhage imaging.

4:18

It's fast, universally available

4:19

and highly sensitive to acute blood.

4:22

We evaluate presence of blood mass effects

4:25

or herniation hydrocephalus and follow up expansion.

4:29

In terms of density evolution, uh,

4:31

the acutely hyperdense becomes isod dance

4:34

around one to two weeks.

4:36

And in the chronic stage,

4:37

we see encephalomalacia and gliosis.

4:41

Any M-R-I-M-R-I expands our diagnostic ability.

4:45

Gradient and susceptibility weighted imaging are exceptional

4:48

for micro blades, cortical, superficial cytosis,

4:52

small subarachnoid hemorrhage,

4:53

and small intraventricular hemorrhage flare.

4:57

One of the MRI sequences is sensitive to subular blood

5:00

and subarachnoid hemorrhage

5:02

and diffusion imaging is highlight ischemia

5:06

and, uh, hemorrhagic trans transformation.

5:09

If you use galine in the post contrast imaging sequence

5:13

sequences help identify tumors, uh, AVMs, uh,

5:16

arteriovascular malformation and inflammation.

5:21

So here we have the signal characteristics

5:23

of blood evolving, uh, a long time.

5:25

It's very predictable. The hyperacute blood contains oxy

5:29

hemoglobin, which is T two bright.

5:31

So in the hyperacute phase, we had T two bright

5:33

inside the hematoma.

5:35

Uh, in the acute phase that's in one to three days,

5:41

uh, we, we start to lose the oxygen.

5:43

So we have d detox in hemoglobin, and so T two becomes dark.

5:48

Uh, in the early sub acute phase, three to seven days,

5:52

the intercellular met.

5:54

MLO is still one bright,

5:56

and in the late acute, uh, we have extracellular metatag,

6:01

which is both T one

6:02

and T two, right, the chronic phase over a month, uh,

6:08

we have a heid ring ring and it's dark both in gradient

6:11

and suscept susceptibility imaging also.

6:15

So let's take a look at some cases.

6:17

We start by, uh, the intraparenchymal hemorrhage.

6:22

Intraparenchymal hemorrhage has many causes.

6:25

The two most commons are hypertensive, small vessel disease,

6:29

typically deep hypertension related

6:32

and cerebral amyloid angiopathy,

6:34

which is typical, uh, typically lower.

6:37

Other causes include anticoagulation,

6:40

vascular malformations, hemorrhagic tumors, infarct,

6:44

transformation, venous thrombosis, and drug use.

6:48

So location is your first major clue for, for we to start

6:52

here, we have a case

6:54

of a deep hypertensive hemorrhage is a

6:56

classic basal ganglia.

6:57

Hypertensive bleed very large,

6:59

is the one we have seen just a few seconds ago.

7:03

And the key pearls are that the location

7:06

strongly favors hypertensive small vessel disease.

7:10

Okay? We have to estimate the volume using the A, b,

7:14

C divided by two volume, uh, formula.

7:17

How we do that, we take the, the two, uh,

7:21

biggest measures here on the actual plane

7:23

and one measure in the Corona plane, multiply them

7:26

and divide it by by two.

7:28

Then we have a very approximate volume estimation.

7:33

We always evaluate basal cisterns

7:35

and the risk of herniation,

7:36

and we have to consider CTA, um,

7:39

only if the pattern is atypical, meaning unusual age,

7:43

that patient is too young, unusual shape

7:46

or disproportionate iema.

7:48

When we might think of secondary causes, uh,

7:52

I'm gonna show you a, a sequence of cases now

7:55

that reinforce the pattern recognition, not

7:57

how current the the distribution is.

8:01

We have this hemorrhage here in the beal ganglia, actually,

8:06

uh,

8:07

extra external capsule.

8:12

Uh, the next one, we have one close to the alama here,

8:15

talus here, and internal capsule also.

8:17

And the lengthy form, no nuclear thisone.

8:20

The alama is the right tal here,

8:21

and sometimes having the brain stem

8:23

or the bil also, these are deeper perforated territories,

8:27

and hypertension is the dominant cause.

8:31

Uh, this one, we have another one in autonomous

8:34

with ventricular bleeding, uh,

8:37

as you can notice here in the lateral ventricles

8:39

and the third ventricle.

8:43

So when we talk about prognostic imaging markers, we have a,

8:46

a consensus by the American Heart Association

8:48

and in the American Stroke Association, uh,

8:51

and the prognosis depends on fix it and modifiable markers.

8:56

The the fix it ones include the hematoma volume.

9:00

It's one of the strongest predictions of mortality.

9:03

Uh, hematoma is larger than 30 milliliters,

9:05

especially sartorial have worse prognosis.

9:09

Volumes over 60 millimeters are associated

9:11

with very high mortality,

9:13

and so a rapid ES estimation can be performed using the

9:16

formula we just seen A, B, C divided by two.

9:19

Uh, also the location, deep versus lower brain stem

9:24

or CBU location dramatically changed.

9:26

Prognosis, deep intracerebral hemorrhage

9:29

in the basal ganglia.

9:30

Thas, uh, is very common in hypertensive patients.

9:35

Frequently it has intraventricular extension

9:37

and it has an intermediate to poor prognosis.

9:40

We have, uh, an example here

9:42

that we just seen a very large hematoma here

9:45

with intraventricular extension

9:47

and also a, a very, uh, preeminent

9:52

expensive effect here.

9:55

Um, the lower, uh,

9:58

intracerebral hemorrhage is more common in cial

10:01

amyloid angiopathy.

10:03

Uh, it has, of course, a better surgical accessibility

10:07

and has a variable prognosis a little

10:09

better than a hypertensive.

10:12

Here we have an example, a lower hemorrhage,

10:14

actually very large with intraventricular extension here.

10:17

And you can see the patient lost consciousness

10:19

and hit the, the head, you know, on the floor.

10:21

So it has, um, a gyal, uh, hematoma here also.

10:28

And the brainstem hemorrhage, uh, is very complicated.

10:31

Even small volumes can be devastating,

10:34

and it has a very, very high mortality.

10:36

Cellular hemorrhage is also high risk

10:39

because of the, the risk of brainstem compression

10:42

and hydrocephalus.

10:44

The the posterior phospho is very small and,

10:47

and doesn't allow too, too much blood to grow there.

10:50

It often requires early surgical decompression.

10:53

Here we have an example on the right hemisphere of Serbia,

10:56

a hematoma here extending a little bit to the, the vers,

11:01

um, and the modifiable, uh, prognostic imaging markers.

11:06

We have the hematoma expansions, uh, it occurs in up

11:09

to one third of patients.

11:11

Within the first three to 24 hours is associated with use

11:15

of anticoagulants, uncontrolled hypertension,

11:19

and the presence of a presence of a stop sign,

11:21

spot sign on CTA, the ct, an angiography, reducing the risk

11:26

of expansion is a central goal of early management.

11:29

Expansion is one of the most important predictors

11:31

of acute neurological worsening.

11:33

So it had to be pay very close attention to that.

11:35

Okay, I'll show you some cases.

11:38

Uh, here we have an example of an expanding hematoma.

11:41

The patient, um, a male editor, 80 years old male

11:45

who was admitted on the ER

11:46

with these already large hematoma here on the,

11:50

the basal ganglia, uh, on the right.

11:52

And three hours later, he had a, a neurological condition

11:57

worsening very quickly and re had, uh, to repeat the ct.

12:01

What can we notice here?

12:03

A very impressive enlargement of the hematoma.

12:06

It also has some liquid components here.

12:08

There are still not hyper dense, so this means they are,

12:13

they're liquid, they're hyperacute.

12:15

Okay? Um, also,

12:19

the edema per hemal, uh, edema

12:23

progressively increases over the first 48 to 70, 72 hours.

12:27

It's related to inflammation

12:28

and blood toxicity in the brain may contribute

12:32

to delay delayed neurological deterioration

12:35

and more edema means greater mass effect and

12:38

consequently, increased risk of herniation.

12:42

Here we have an example of, uh, uh, hematoma

12:44

and starting to appear here is a lower edema

12:47

that is more prominent on these images, uh,

12:51

below here when the patient repeated the exam.

12:53

So it started to, to have an inflammatory edema

12:56

around the hematoma here, increasing the mass effect

12:59

of the blood and the edem associated.

13:04

Uh, the, also on the modified modifiable prognostic imaging

13:07

markers, we have hydrocephalus

13:09

and may occur due to obstruction of cerebral, uh,

13:13

cerebral spinal flu fluid flow.

13:15

For example, an intraventricular hemorrhage, uh,

13:18

is associated with worse outcomes

13:20

and higher mortality often requires

13:22

external ventricular drainage.

13:24

And acute hydrocephalus increases intracranial pressure

13:28

and leads to rapid deterioration of the,

13:30

the clinical condition of the patient.

13:33

Here we have an example of very large c cbu,

13:37

uh, hematoma here.

13:39

It's obstructing and compressing the fourth

13:41

ventricle and the silver.

13:43

So we have a, a major, uh, impressive hydrocephalus here.

13:48

In a 59-year-old female,

13:50

you could expect ventricles large disease if the patient

13:52

has, I don't know, 120 years.

13:54

So 59 is, is really enlarged.

13:57

These ventricles, they are very enlarged

14:00

and obviously due to the hematoma compression,

14:04

and this will likely require emergent management.

14:07

So never fail to comment the on ventricular size when

14:10

interventricular hemorrhage is present.

14:11

Okay. Also,

14:14

herniation is another modifiable prognostic imaging marker.

14:18

Uh, it's the most extreme sign

14:19

of increased pressure and mass effect.

14:22

Uh, we have some types

14:23

of herniation sub fault sign when it's under the,

14:26

the fox transtentorial, the, the downwards

14:30

and tonsor through the

14:33

magma usually indicates a grave prognosis

14:35

and requires immediate intervention, herniation vehicles,

14:39

compression, vital structures, and imminent risk of death.

14:43

Here we have a case of an 88 years old male.

14:47

He had a CT exam with us one month prior.

14:51

You can see it, it's a normal fall for his age.

14:53

You have some s prominent here, but very, very usual.

14:58

But he came, he comes to the ER in a hospital,

15:01

uh, in a coma.

15:03

And when we perform the ct, what can we see?

15:05

A large hematoma here, okay, with intraventricular, uh,

15:09

extension, actually feeling fulfilling.

15:12

The, the ventricles, the, the th the lateral ventricle,

15:15

the third ventricle and the fourth

15:17

ventricle, I cannot see here.

15:19

And we have a, a huge cerebral edema.

15:21

We cannot see any of the scy that we used to see here.

15:23

They're all, uh, a face because of the edema.

15:28

So we have a, uh, midline shift

15:32

because of the, the hematoma.

15:34

We have effacement of the basal cisterns.

15:36

They're all already raised.

15:38

And this constellation of finances, life threatening,

15:40

it's a diffuse al edema.

15:44

And the spot sign that we have mentioned spot sign is when

15:48

we, we administer, I donated contrast

15:51

and see, uh, extra ization of contrast here.

15:54

It means an active bleeding.

15:56

So this is a 72-year-old male with a large lower hematome

16:00

on CTA, the CT angiography.

16:02

We clearly see one

16:04

or more contrast foci inside the hematoma.

16:07

This is an arterial phase,

16:09

and this is like one minute later a venous phase.

16:12

And this is the classic spot sign where there was some, uh,

16:16

hypodense area here inside the hematoma.

16:19

This means liquid blood yet flowing here.

16:23

When we administered the contrast in a few seconds,

16:26

it's already appearing here and it grows in a minute here.

16:29

So it's a very active bleeding here.

16:33

Uh, this finding is a red flag means the hematoma is

16:36

actively bleeding, which dramatically increases the

16:38

likelihood of expansion.

16:39

So when you see the spot sign, prepare the clinical teams.

16:42

This patient needs aggressive blood pressure

16:44

control and close monitoring.

16:47

So the spot sign predicts expansion is associated

16:51

with a higher mortality

16:52

and is particularly important in anticoagulated patients.

16:55

If you see a spot sign communicated clearly and immediately.

16:59

Okay? Uh,

17:03

so spot sign to summarize indicates active

17:06

contrast extravasation.

17:08

It strongly predicts hematoma expansion expansion.

17:12

It is associated with higher mortality and worse outcomes.

17:16

And it's especially important

17:17

to identify in patients on anticoagulation schemes.

17:20

Okay? In many centers, when we identify, uh, a spot sign,

17:23

it leads to more intensive monitoring,

17:24

sometimes enrolling in, in expansion prevention trials,

17:29

protocols, uh, these other case, a 72-year-old male

17:34

showing, uh, uh, actually the same case.

17:37

Uh, I brought here the revolution of the case.

17:40

30 hours later, what can we see?

17:42

The natural history of the sign.

17:45

The he has massively en large with much mass effect.

17:49

This is a real world consequence of active bleeding.

17:52

Uh, he had to, to go to the,

17:54

or, we have a craniectomy.

17:58

The, the hematoma has been, uh,

18:00

treated here, but it's still bleeding.

18:02

We have a large mass effect here.

18:05

Uh, the, the midline shift is huge. It's very dramatic.

18:10

So recognizing this sign early can change the

18:12

patient's management trajectory.

18:15

Now, let's transition to cerebral amyloid angiopathy,

18:18

a major cause of lower hemorrhage in lot adults.

18:22

Cerebral amyloid angiopathy is characterized by deposition

18:25

of amyloid better in the cortical

18:27

and lepto menal vessels leading to vessel fragility.

18:30

Its imaging signature is unique

18:32

and extremely important for radiologists to recognize.

18:36

We have a 77-year-old female

18:39

with an occi occipital peral lower hematoma,

18:42

and doing the right this distribution is classic

18:46

for amyloid angiopathy, very iCal lower.

18:49

Okay? So remember, in an, in an old pa, older patient,

18:52

without hypertension,

18:53

lower hemorrhage should immediately raise suspicion for

18:57

cerebral on myloid angiopathy.

18:59

Okay, this a ct.

19:01

And here below have an MRI, images, the diffusion

19:04

and a DC map, the susceptibility weighted imaging showing,

19:08

uh, blood here and a flare image.

19:13

Uh, so what imaging clearly supports the cerebral cerebral

19:16

amyloid angiopathy, uh, on susceptibility weighted imaging.

19:22

Look for cortical micro bls, uh, cortical superficial Cy

19:27

Cyderss strongly suggest cerebral amyloid angiopathy,

19:31

and also refer to the Boston Criteria 2.0,

19:34

which we'll we'll discuss shortly.

19:36

Importantly, a lower hematoma is not typical

19:39

for hypertensive hemorrhage.

19:43

So here we have a diagram that summarized the hemorrhagic

19:46

and non hemorrhagic imaging manifestations

19:48

of cerebral amyloid angiopathy.

19:50

We have usually the lower intercerebral hemorrhage,

19:54

the cortical superficial cy theosis,

19:57

which is visible on S-W-S-W-I.

19:59

In hem RI, uh, we might have convex subarachnoid hemorrhage,

20:04

sometimes lower micro bleeds, microbleeds,

20:09

and also non-G markers,

20:11

which include enlarged perivascular spaces.

20:14

White matter hyperintensities,

20:16

which I don't know if you can see here, very small

20:19

and cortical micro inact, they may also appear.

20:25

So the Boston criteria 2.0, uh, are the,

20:28

are the current standard for diagnosing probable ceal angio

20:32

amyloid amyloid angiopathy.

20:35

Uh, they require two or more lower hemorrhagic

20:37

or non hemorrhagic markers on MRI.

20:40

This includes lower, uh, intracerebral hemorrhage,

20:44

microbleeds, cortical osis, convex

20:48

subarachnoid hemorrhage, white matter

20:52

hyperintensity patterns in large paravascular spaces in the

20:55

center of semial and cortical micro infarct.

20:59

Deep hemorrhage, uh,

21:02

are go against ceal amyloid angiopathy

21:05

and extensive cortical superficial cy roses

21:08

strongly supports the, the, the diagnosis

21:10

of cerebral amyloid angiopathy.

21:15

So, uh, here I'll show you.

21:18

This table, uh, shows the, the distinguishing features

21:22

of hypertensive small vessel disease versus

21:24

amyloid angiopathy.

21:26

Hypertensive usually is duplications on basal

21:29

ganglial, spon and serb.

21:31

And also we find deep microbleeds on the SWI

21:35

and cere amyloid angiopathy.

21:37

We have lower or cortical subcortical hematoma,

21:40

cortical microbleeds, and cortico superficial osis.

21:44

This is, uh, uh, a figure from the American Journal

21:47

of Neuro Radiology, which nicely summarized the two main,

21:52

uh, phenotypes, small vessel disease phenotypes, type one

21:55

of which hypertensive, uh, the sclerosis is deep,

21:59

and type two, the ceal amyloid angiopathy is lower.

22:03

If you can master this distinction,

22:04

you'll correctly diagnose most non-traumatic

22:06

interoperable hemorrhage.

22:08

So I'll light you with this image.

22:10

If you can access this article

22:12

later, it's very good to read.

22:16

And here's another lower hemorrhage example.

22:19

Uh, compared this pattern with deep hyper intensive cases

22:21

earlier, it's a very different distribution.

22:24

This is referred lower hematoma.

22:27

Uh, so we have to think on cerebral amyloid angiopathy.

22:31

Okay? Also, it has some, uh, subarachnoid hemorrhage here.

22:36

Uh, it is all already visible. Uh, brain diffuse edema.

22:44

Uh, but not every hemorrhage is hypertensive

22:48

or amyloid related.

22:50

So we have to look for red flags.

22:51

Suggesting secondary causes ages under 55

22:56

of patients with no vascular risk factors.

22:58

Uh, a typical location, disproportionate edema, uh,

23:03

fluid levels strong

23:05

or noal enhancement, large subarachnoid hemorrhages

23:09

that are disproportionate to the, the volume

23:11

of the hematoma, and also venous inact patterns leading to,

23:15

to think on cerebral venous s thrombosis.

23:18

When you see these features broaden your differential.

23:21

Okay, here we have an example.

23:24

A 31-year-old female patient is so is a young female,

23:28

and she's taking oral, oral contraceptives,

23:32

which is an important risk factor for s thrombosis.

23:35

You always have to integrate the clinical context.

23:37

So agent risk, risk factors dramatically affected

23:40

differential diagnosis.

23:42

What we see here, she has a large hematoma also

23:45

with some edema.

23:47

And when we look without contrast,

23:50

we already can see the venous sinus here,

23:54

the superior sagittal sinus is very hyperdense.

23:57

When we administer contrast, it does not enhance.

24:01

So this is a deep venous thrombosis,

24:04

and this is a venous bleeding.

24:06

Okay? Uh,

24:10

so here are situations

24:11

where the secondary causes become more likely.

24:14

Hemorrhagic tumors often have dispropor disproportionate

24:18

edema or mass like effect.

24:20

A typical locations, including the temporal deep,

24:23

the corpus callus, and the central wide matter hit journals,

24:28

uh, hematomas or those with strong enhancement

24:31

after contrast also raise con concern.

24:34

And in young patients without risk factors, of course.

24:37

So when these features appears,

24:39

always consider MRI plus MRA or CTA.

24:42

Okay? Here we have a patient with, uh,

24:46

that has a renal cell carcinoma, which is a tumor

24:50

that frequently metastasized to the brain and can bleed.

24:53

So if a hemorrhagic mass has a strong enhancement like this,

24:57

we see hematoma also very preemt edema.

25:02

And we have noles here at least two, you can see

25:06

that are solid

25:08

and enhanced very heavily when we administer contrast

25:12

with a very impressive edema.

25:15

So this looks like metastasis from the renal,

25:18

uh, cell carcinoma.

25:20

And one of them sadly breed, you have to consider this, uh,

25:24

hemorrhagic metastasis, mainly on patients

25:27

with renal cell carcinoma.

25:29

Oid PO carcinoma can also do that.

25:33

And melanoma, of course, uh, which is this case we see here.

25:36

Melanoma is another highly hemorrhagic tumor.

25:39

The, the melanin itself shortens T one

25:41

and leads to intrinsic hyperintensity.

25:43

So what do we see here?

25:45

Another that's hyper dense on CT

25:47

and enhances with some bleeding.

25:50

Okay? The, this is bleeding prior

25:52

to contrast administration.

25:54

When I looked at the MRI, we can see

25:57

on susceptibility imaging, the blooming here of the,

26:00

and the black signal, the hyper hyperintense signal

26:02

from the, the blood.

26:04

Okay? Uh, when we, we administer contrast,

26:07

you can see the lesion enhancing here,

26:11

and it has some hyper fusion.

26:14

So it was a patient with a melanoma,

26:16

and these were metastasis

26:17

that were bleeding cover.

26:21

Nos are also, another thing to remember.

26:23

This is a 30-year-old male with a caroma.

26:25

We see here without contrast

26:27

and post contrast, they often present with ent,

26:30

small hemorrhages, uh, popcorn appearance

26:33

and blooming on as double eye, which we see here.

26:37

Uh, they can mimic small hypertensive bleeds,

26:40

but tend to be more focal

26:41

and have a characteristic hemo green like this one.

26:45

Okay? So this was a caroma

26:47

and it blood, uh,

26:50

and the hemorrhagic transformation of ischemic stroke.

26:53

Let's shift to that. It's a completely

26:55

different mechanism of bleeding.

26:57

We have two main types, the hemorrhagic infarction,

27:00

which usually is spectacular, and, and no mass effect.

27:04

And the paral hematoma, which has conflict hematoma

27:08

with some mass effect.

27:10

The key point are is not all hyperdensity inside an infect,

27:15

uh, not all hyperness

27:16

inside an infect are equals a catastrophic bleed.

27:19

If they are spec potential, they,

27:21

they might be less dramatic.

27:23

Let's see here with this male, a 70, 80-year-old male,

27:27

he had a ischemic stroke.

27:29

You can see here on the first ct, uh, when he was admitted

27:33

to the er, we have the, a area dense

27:38

spot here inside the, the,

27:40

the median cerebral cerebral artery.

27:42

When we administer contrast in the CTA, you can see the,

27:46

the, the, the flow stopping here.

27:47

So it was a ischemic stroke.

27:50

It was submitted to thrombolysis,

27:52

and unfortunately, he, he pled.

27:54

So what we see here on the, the, the ct, the next day,

28:00

we have now, uh, an edema here, brain edema consequence,

28:03

the, the ischemia, and it has a he

28:06

hemorrhagic transformation.

28:07

We have some spectacular spots here,

28:09

and I also have an hematoma here.

28:11

Okay? Uh, so it's essentially to differentiate,

28:14

differentiate beneath ACH from more dangerous

28:17

parenchymal hematoma.

28:20

Uh, here to the classic, uh, matchings on ct,

28:23

the hyper density inside the infarcted territory.

28:28

And on diffusion weighted imaging,

28:30

you can see the restricted diffusion.

28:32

That is the, the ischemic stroke.

28:35

The infarcted territory,

28:36

which is hypodense on CT is hyperintense on diffusion

28:40

and on flare, uh, we can see the edma due to the che

28:43

and sobi could changes matching the, the infarct core.

28:46

And here we see the, the blood, uh, a little hematoma here,

28:49

and some patag blood appear, the diffusion.

28:54

And here on the, the flare image,

28:59

uh, also patients on anticoagulants

29:02

or with coagulopathy from a unique subgroup form a unique

29:05

subgroup because their hemorrhages behave differently.

29:07

In anticoagulated, patients, hematomas tend

29:10

to be more heterogeneous.

29:11

They may show fluid flu levels

29:12

and have a much higher risk of expansion.

29:15

These patients require early repeat imaging

29:19

and careful multidisciplinary manage management.

29:21

Their eligibility for thrombolysis

29:24

or thrombectomy is also obviously affected.

29:27

Here we have a patient, a 77-year-old female with a history

29:31

of prior stroke and currently on anticoagulation

29:34

because of prior stroke.

29:36

But unfortunately, what we have here are large hematoma.

29:40

And notice the irregular density

29:42

and the complexity of the bleed.

29:44

Uh, this pattern should always make

29:46

you consider coagulopathy.

29:48

It has some hyperdense areas

29:49

and some hyperdense between, uh, inside of the,

29:52

the hematoma also.

29:53

Okay. And obviously you can see here also, uh,

29:58

intraventricular bleeding.

30:01

This is another example, a 72-year-old male, again,

30:04

heterogene hematoma.

30:05

Here we can see with signs that suggest instability.

30:09

anti-D patients can deteriorate quickly.

30:12

And early identification of hematoma behavior is essential.

30:15

You can see a large hematoma here,

30:17

some components of hypo hypodense.

30:18

Here we have interventricular, uh, extension

30:22

of the hematoma, very large bleeding inside the,

30:24

the vent, the ventricles.

30:26

And in a 72-year-old, we can see no psy here.

30:30

So, uh, brain edema also,

30:32

and also have blood in the fourth ventricle.

30:34

Very dramatic situation and micro bleeds.

30:39

Let's move to micro bleed

30:40

and superficial cyros segment,

30:42

which is ex extremely important in understanding

30:45

small vessel disease.

30:47

Uh, SWI is extraordinarily sensitive

30:50

for detecting microbleeds and cyros.

30:53

The key points, uh,

30:54

the deep microbleeds suggests hypertensive

30:57

small vessel disease.

30:58

Okay? And the cortical microbleeds

31:01

and cortico superficial cyto roses, uh, are hallmark,

31:06

hallmark features of cerebral amyloid angiopathy.

31:09

These findings also influence treatment decisions, uh,

31:14

for example, whether to start

31:15

or to avoid antithrombotic therapy.

31:18

Okay, here we have some micro bleeds on SWI,

31:20

and here we have an illustration of osis.

31:23

It'll be this low signal here on the cortical

31:27

S side on.

31:32

And next we turn our attention to subarachnoid hemorrhage,

31:35

which can arise from multiple etiologies.

31:38

Here we have a patient with a dramatic

31:39

subarachnoid hemorrhage.

31:40

We see the blood filling, the, the sci,

31:43

also the fog and the ventricles.

31:46

And as you can see, he, he lost conscious and hit the head.

31:49

So we have sga oma also here.

31:52

The subarachnoid hemorrhage can present

31:55

with distinct patterns, each suggesting a different cause

31:59

and a reasonable subarachnoid hemorrhage.

32:00

Hemorrhage are usually centered in the basal systems

32:04

and the c uh, fist fissures.

32:06

Okay? The per cephalic subarachnoid hemorrhage,

32:10

usually confined as the,

32:13

the name says in the PHA systems,

32:16

usually benign and non.

32:19

Okay. The traumatic subarachnoid hemorrhage obviously have

32:22

the history and predominates over the cortical

32:24

convexity, okay?

32:26

And the spontaneous convexity subarachnoid hemorrhage.

32:29

Uh, you must consider the, as we've seen

32:31

before, the cerebral, uh, amyloid angiopathy.

32:35

Uh, also reversible cerebral vasoconstriction syndrome

32:40

or cerebral vein thrombosis.

32:42

Okay? And now we have a ct,

32:47

no, sorry, the CT may, may show subarachnoid.

32:50

I, when have, when you talk about an reasonable subarachnoid

32:53

hemorrhoids, I'll show you now, is this one.

32:56

You see blood feeling the, the basal CI systems

33:00

and sometimes the serial fisure.

33:03

Um, the CTA may show you an aneurysm on the anterior

33:07

communication, posterior communication,

33:09

or the middle cerebral artery.

33:12

The pearls CT is 95% sensitive in the first six hours.

33:16

So it's the, it is the first line exam, very quick,

33:19

very available, and very sensitive.

33:21

After six hours, the subarachnoid hemorrhage

33:24

may become high dense.

33:26

So MRI FLA is superior to CT if, if available. Okay?

33:31

Always assess also hydrocephalus and VAs risk.

33:35

So the, the case that was showing was a female 44, 44 years

33:38

old with suddenly severe headache.

33:41

What we see here, without contrast,

33:43

we already see blood filling the, the basal sters.

33:46

We see, uh, a little blood lake here.

33:49

And we, when we do the CTA, what do we see?

33:51

And then we popping here, okay, in the,

33:56

the, the medium cerebral artery,

33:58

the left medium cerebral artery.

34:00

So that is a classic presentation

34:02

of an reasonable subarachnoid hemorrage.

34:07

Uh, This example illustrate the evolution of

34:14

He Over time.

34:16

The other phase, the CT ex is extremely sensitive.

34:20

Um, but after see and MRI flare becomes more useful, okay?

34:27

Large s oid hemorrhage here, uh,

34:29

a small aneurysm here popping in the, uh,

34:32

anterior communicating artery.

34:34

And this is a control imaging.

34:35

The next day after he was submitted to a neurosurgery

34:38

to place a, a clip here, okay?

34:43

And this is another patient, a 69, 60 9-year-old female

34:47

with a large hematoma here, the blood oid hemorrhage,

34:50

feeling the base

34:55

of cisterns and

35:01

Had, uh, An a, an eus, it went straight

35:06

to the angiography placed.

35:08

Here. We also have to assess, uh, hydrocephalus

35:13

and vasospasms risk.

35:15

So here we have a patient, a 30-year-old female

35:19

with a hematoma here int parenchymal with intraventricular,

35:22

uh, hematoma here,

35:24

and we can see blood filling the third ventricle,

35:28

the seal, and the fourth ventricle.

35:30

And also this descend here, like it was a myo T and

35:34

after 10 days, she had a, uh,

35:38

decrease in her clinical condition.

35:39

The CT was repeated.

35:41

We can see here that the, this,

35:44

this dense point here is the tip

35:46

of the intra intracranial pressure monitoring,

35:49

but the blood, uh, the, the hematoma is increasing again,

35:53

uh, a little bit is, pardon me, it's not increasing.

35:56

Well, what we see here, she repeated the TC

35:59

and 10 hours later made another tc, a third TC C

36:03

what we see here, comparing these two images,

36:06

an evident brain edema, okay?

36:08

We have also, uh, an imaging on, on the, the base

36:12

of the skull, what we see, the ceil or even normal density.

36:16

And the, the brain is starting to get hypo nas.

36:19

So we have the, the hyperness ceil sign.

36:22

It indicates Ceil cerebral edema. Okay?

36:26

So this patient, uh, develop, uh, diffuse brain edema,

36:31

and eventually we went to brain death, unfortunately.

36:37

Uh, so that was okay.

36:42

Also, uh, hydrocephalus is another risk we see here.

36:46

This patient had a bleeding, uh, that was feeling the, the,

36:50

the, the right ventricle here, the posterior corn.

36:53

Corn, and in a few days

36:55

and day, five, four days later, later, the,

36:58

the ventricles are enlarged here due to, uh, uh,

37:04

to several spine, uh, fluid obstruction.

37:09

The flow obstruction here to due to the,

37:13

the, the blood.

37:15

Another cause I have to remember

37:17

for subarachnoid hemorrhage is trauma.

37:19

Traumatic subarachnoid hemorrhage has a very

37:21

different distribution.

37:22

Uh, the blood usually tracks along the cortical vaccines

37:26

rather than pooling in the basal cisterns.

37:28

And obviously the clinical context is everything.

37:30

You'll know that the patient had a brain, uh, head trauma.

37:35

Here we have an example, uh,

37:37

very large subarachnoid hemorrhage.

37:40

And we can see, uh, against, we can call it a giant

37:44

sub hematoma here.

37:45

The patient fell from a, from a very, very big height here,

37:50

and he hit the head on the floor.

37:53

So he was unconscious.

37:55

And when we performed the ct,

37:56

we had subarachnoid hemorrhage.

37:58

Hemorrhage, and this was obviously traumatic.

38:01

And look for, pay attention to the distribution.

38:04

It is very cortical

38:05

and not in the basal systems permanently.

38:09

Another example here, 3-year-old male,

38:11

a motorcycle accident, he hit a bus.

38:15

And what we can see here,

38:17

we see several implant hemorrhages,

38:20

but also we see cerebral contusion, okay?

38:23

Blood inside the parenchyma due to the impact.

38:26

And this is a high energy mechanism

38:28

with predominant convexity subarachnoid hemorrhage.

38:31

Okay? Again, a pattern that fits the, the clinical scenario.

38:35

Last but not least, this is an actual diffuse lesion.

38:37

A patient with a, a very high deceleration trauma.

38:41

He was in a car accident hitting a, a wall.

38:44

And so you can see many points here of hyperdense points.

38:48

That means, uh, bleeding in,

38:51

in the cortical subcortical transition.

38:54

This, and the patient was in a coma.

38:55

This leads to the diagnosis of, uh,

38:57

actional defusion lesion.

39:00

Another traumatic, uh, lesion

39:03

that was actually after surgery.

39:05

This was a 61-year-old male.

39:07

He developed headache after having a STOs septoplasty

39:11

operating the, the, the nasal septum.

39:15

Uh, and what we see here, we see blood in the base

39:19

of the frontal lobe with some, uh, gas in the middle.

39:24

When we perform the MRI, what we see blood here,

39:26

we can see in the SWI, uh, with some edema around it.

39:31

And so what happened here, uh, accidentally, the, the,

39:36

during the, the procedure, the,

39:39

the frontal lobe was perforated.

39:40

So we have a bleeding here and some blood

39:44

and gas associated.

39:48

One week later, what happened?

39:50

Uh, he developed fever and leukocytosis.

39:55

Uh, and when we repeated the exam, what do we see now?

40:00

We see it starting to form a, an abscess here

40:02

that has hyperintensity on, on diffusion weight imaging

40:07

and a ream of, uh, enhancement here

40:10

when we're administered contrast,

40:12

and also some fluid here, subdural.

40:15

So it's a subdural abscess also. Okay, very complicated.

40:20

And talking about subdural, let's move to subdural hematoma,

40:24

which is another frequent cause of extra actual bleeding.

40:27

Subdural hematoma are usually creasing shape it look like,

40:31

uh, uh, c moon, uh, they cross ERs,

40:36

but do not cross the midline fox.

40:38

When they're acute, acute, they're hyperdense

40:41

and a subacute phases, they turn isod dense and,

40:45

and chronic Phase D move to be hypodense.

40:48

And sometimes with membranes in, in the middle, uh, sub

40:53

subdural hematomas can exert significant mass effect

40:57

even when they are thin.

40:59

So I have to look for that. The pros,

41:01

the coronal ct reformatting is essential.

41:04

Uh, the mass effect may be underestimated on actual only.

41:07

So you have to, to, to make aker reformation.

41:12

And in early patients

41:14

and anticoagulated patients, we have a high reference rate

41:17

of subdural hematoma.

41:19

Here we have an example, a 60-year-old female on a ct.

41:23

What do we see here? A cent shaped, uh, collection,

41:26

a little hypo dense with some membranes in the middle.

41:28

This is a chronic subdural hematoma Look for, look at the,

41:32

at the, the mass effect.

41:33

It has, it push pushes the, the, the, the brain parma here,

41:38

the cel SIR EF face.

41:40

We have a midline shift,

41:41

and the ventricles are diminished here.

41:44

The corona fermentation allows a better visualization

41:47

of the, the shape and the, the volume of the hema tunnel.

41:53

Uh, this other cases

41:55

of subdural hematomas in along the, the time.

41:58

So this is an acute phase. What do we see here?

42:01

And again, a Christian shaped hematoma, very hyper dense.

42:05

So this acute subdural hematoma, look at the mass effect.

42:08

It has the midline shift to the other side.

42:11

The ventricles are very diminishing here.

42:14

So, uh, this can lead to

42:18

intracranial hypertension

42:19

and might be necessary to,

42:21

to have surgery to, to solve this.

42:25

This will be a subacute hematoma.

42:27

Looks how it starts to become dense to,

42:30

to the brain parenchyma.

42:31

Sometimes it, it may be hard to differentiate,

42:33

but you'll see the salsa here.

42:36

And also obviously the, the midline shift to the other side.

42:38

And we, when we administer contrast, we can see the,

42:41

the cortical veins here.

42:44

This would be a more chronical phase, uh,

42:46

subdural hematoma, actually bilateral.

42:49

It looks, look how it becomes very hyperdense.

42:53

And sometimes you can look at hemato fluid level here.

42:57

This, uh, subdural hematoma effect that was chronic,

43:01

but had, uh, recurrent bleeding.

43:03

So now it has a hyperdense com component here,

43:06

and this would be a very chronic, uh,

43:09

hypodense sub hema tunnel.

43:12

Here we, uh, I put together the, some of the case when,

43:15

when we can see the acute very hyperdense,

43:18

the isod dance in the subacute phase,

43:20

becoming very hypodense on the, on the chronic phase.

43:23

Okay, another example here, a patient that had a,

43:26

a major car accident.

43:28

She developed a, a large subdural hematoma here

43:33

that was hemispheric

43:34

and has a, a, a major mass effect compressing the, the, the,

43:39

the brain leading to a, a very big, uh,

43:43

midline shift to the other side.

43:44

Also almost collapsing the, the, the, the lateral ventricle,

43:48

the left lateral ventricle.

43:50

And due to the intracranial hypertension, she had

43:54

to be taken to the or.

43:55

And a c craniectomy was performed to allow the brain

43:58

to have some room here.

43:59

Okay? And now we can see the midline shift very reduced,

44:02

comparing to this first image.

44:07

Uh, another thing to remember about subdural hematomas,

44:10

sometimes they may flow over the tentorium like this.

44:14

And when you look at actual images only, you may be

44:18

caught on a trap and, and miss the, the subdural hematomas.

44:22

So take care of that. Remember to perform the,

44:24

the corneal hema, he fermentation.

44:26

Obviously, this patient has a major, uh,

44:29

intraparenchymal hematoma here,

44:31

but the subdural hematoma can be SubT,

44:33

especially when it goes over the, the tentorium.

44:37

Kay have another case here.

44:39

A 30-year-old female,

44:41

and she had a repetitive support trauma.

44:43

She used to play ball hitting with the head,

44:45

and she had two subdural hematomas here.

44:48

One on the one on the right is chronic,

44:51

so you can see very hypodense.

44:53

And the other one is subacute. You can see isod dance.

44:55

And actually you could, if there, there wasn't, if it wasn't

44:59

for the other side to have sub, uh, a chronic sub hematoma,

45:03

if you look too fast, you could miss the hematoma

45:04

here on the left.

45:06

Okay, obviously the radiologist one miss that,

45:08

but the clinical would miss,

45:10

the clinics would miss this one.

45:12

So this is a chronic hematoma on the right

45:14

and a sub subacute isod dance subdural hematoma on the left.

45:20

And look again, uh,

45:21

a little component here over the tentorium.

45:24

Bring here also on the actual images,

45:26

but much better view on the Corona, uh,

45:30

and epidural hematome.

45:32

It's another important extra actual bleed

45:35

and almost always traumatic.

45:37

Uh, it usually has a, a bicon excellence shape.

45:41

It does not cross sutures, uh, often associated

45:44

with skull fracture.

45:46

Not mandatory, but often does,

45:48

and might have the swirl sign, which means active bleeding.

45:52

I'm gonna show you one of those and has a right his

45:55

of herniation in the temporal lobe,

45:59

and especially when the, when located

46:00

in the, in the temporal lobe.

46:02

Here, we have an example on this. The ct on the bone window.

46:06

We can see a fracture here on the temporal bone associated,

46:09

there is a, a epidural hematoma, if you see the,

46:13

the b convex lens shape.

46:15

And this is a swirl sign.

46:17

Looks like it's moving around inside hematoma.

46:19

This is active bleeding.

46:21

So the, the blood is flowing here

46:22

and, uh, circling around, so makes this swirl sign.

46:27

Okay. Also notice the, the volume effect of this,

46:31

the mass effect it has, it's, it's already starting

46:34

to shift the midline to the other side.

46:37

Another case here is an, uh, 11-year-old kid,

46:40

uh, fell from a hammock.

46:42

Uh, and when we perform the ct, what we see here,

46:45

an epidural hematoma, so the, the back convex shape here,

46:50

and also take a look, he was, uh, allergic

46:53

to, to many things that matter.

46:54

Didn't allow us to, to administrate, uh, alienated contrast.

47:00

But we can see that the hematoma is heterogeneous

47:03

and almost like a scroll sign here.

47:06

So this is very suspect of, uh, an active bleeding.

47:11

And remember in pediatric patients especially,

47:14

to always check carefully for fractures

47:17

and also always make multiplanar reformations.

47:22

And the surface shading format also can help you.

47:27

We have another case. It was, uh, a very dramatic, uh,

47:31

vehicle accident that this patient was involved.

47:34

It, the, the car flipped over many times,

47:37

and we can see a lot of things here in the first image.

47:40

You can check, there is a temporal fracture here.

47:44

Uh, I agree it's not the bone window,

47:45

but you can see the, the fracture also misaligned here

47:48

and associated with it.

47:50

With this one, we have a epidural hematoma on the temporal,

47:54

uh, next to the temporal lobe here, we can see the fracture,

47:58

the fracture a little better, uh, going up a little bit.

48:02

We start to see, uh, cerebral contusions here.

48:06

Okay, parenchymal contusions here.

48:09

And here we start to see another hematoma

48:12

that is extra actual here, a little, uh, epidural.

48:15

We have subdural hematoma on the, the,

48:17

the left frontal associated with subarachnoid hemorrhages.

48:22

We have filling some salsa here, another

48:26

cerebral contusion here,

48:27

and another epidural hematoma here on the left.

48:31

Told this guy actually lost the lottery. Not one.

48:35

He had everything we we could give him.

48:40

So the top five pit falls, uh, we can remember, uh,

48:45

mistaking calcification for hemorrhage.

48:47

Uh, trained radiologist usually won't fall for that.

48:50

But if you're in the very beginning, you,

48:54

you gotta take care of that, okay?

48:56

Missing the subdural hematoma.

48:58

Convexity, especially when there are ance.

49:00

So, uh, and when you, you have a poor window in even the,

49:05

the, the hyperdense,

49:06

acute subdural hematoma might be missed

49:09

when they're very thin.

49:10

So take care of that. Always check the coral imaging.

49:14

Uh, another pitfall is misinterpret interpreting the sub

49:17

arachnoid hemorrhage pattern.

49:19

Uh, and a reasonal versus traumatic.

49:22

So have the, have to to check the history of the patient

49:26

and look for the, the location.

49:28

The aneurysmal usually is in the,

49:31

the basal cis are filled with blood.

49:35

Another pitfall is not investigating unusual

49:37

or a typical hemorrhage.

49:39

And also ignoring micro bleeds

49:41

or superficial cyros in elderly patients.

49:47

Uh, a practical checklist, we can, we can number here.

49:51

Number one, where is the blood, the compartment, you have

49:54

to define is it extra or interal?

49:58

Is it lower? Is it deep? Uh, how much blood do we have?

50:01

The volume, the mass effect it has,

50:04

if it has associated interventricular

50:06

and hemorrhage, where did it spread?

50:09

Do does it go to inside the ventricles?

50:11

Does it fill the systems? Then why did it bleed?

50:14

Do, do the patient has a hypertension. Hypertension.

50:18

Do we have signals of cerebral amyloid angiopathy?

50:21

Do we have a tumor, an arterial venous mal formation,

50:25

a cerebral venous thrombosis,

50:26

or the patient has drug abuse history.

50:29

And last but not least, define what's next.

50:32

Do we have to perform a CTA an MRI follow up ct,

50:35

even a lumbar puncture

50:36

or a vascular workup on the angiography catheter.

50:40

Catheter. Uh, so key, the key take home pearls

50:45

location suggests etiology.

50:47

The shape suggests the compartment.

50:49

It's the interal, actually it's subdural abdu.

50:53

The heterogeneity suggests active, uh, active bleeding.

50:57

So the SW sign

50:58

and the the spot sign also can help you a lot.

51:03

Uh, also MRI may help explain the why, but not the what.

51:06

So first I have to make a ct.

51:09

And the ct an geography is essential when

51:11

the pattern is atypical.

51:13

A typical meaning wrong location,

51:15

the wrong patient and the wrong pattern.

51:17

So consider a CTA

51:19

or even an MRA when the, the patient is young.

51:22

Less than 55. Remember we talked about that.

51:25

When have a low, uh, lower bleeding without al angiopathy,

51:30

uh, markers like cider roses or, or micro bleedings.

51:35

Also, when have d proport, disproportionate edema.

51:38

And we have a typical location, temporal t collosal,

51:41

corpus scone or white matter.

51:44

And so this is the last case, uh,

51:50

a little hematoma here,

51:53

actually very bizarre, large hematoma

51:57

with intraventricular blood filling.

51:59

The third ventricles, the, the, the lateral ventricles.

52:02

Huge mass effect, uh, shifting the, the, the,

52:09

the midline to the other side, promoting effacing

52:12

of the cell side, uh, brain edema.

52:14

It's a very dramatic case here that the, you can tell

52:18

by looking at this, the, the prognosis

52:20

of this patient is extremely poor.

52:23

Hope she had some nice 82 years of life.

52:25

'cause from now on, her chances are very, very small.

52:29

So I'd like to thank you very much for your attention.

52:32

Uh, these are my context.

52:34

Feel free to reach out for discussion collaborations, so,

52:37

or if have interesting cases.

52:38

It has been a pleasure to share

52:40

with you this imaging program.

52:43

Hope you enjoy it. And if we have questions

52:45

and, uh, the, we a session we, let me see here.

52:51

You opening the zoom. I think I can open here.

52:55

Uh, someone asks,

52:57

sometimes I have difficulty telling apart primary hemorrhage

53:01

versus ischemic stroke with hemorrhagic transformation.

53:04

Do you have any suggestions?

53:06

Uh, usually the, the, the history of the, the patient.

53:10

So, uh, patients with ischemic stroke,

53:15

they tend to be more conscious when,

53:18

when they, they come to the er.

53:19

When you perform the, the ct, if it's only ischemic you,

53:24

you'll see the, the, the dark area.

53:26

If it's had some al

53:28

or you won't see a thing, the,

53:29

the brain parenchyma will look normal.

53:31

And if you inject contract, you'll see the,

53:36

the thrombus point where, where it's obstructed.

53:39

And if you perform a CTA, you're gonna find it.

53:42

Uh, and usually the, the hemorrhagic patients,

53:46

the hemorrhagic stroke patients, they are, are, they have a,

53:49

a clinical conscious depression so

53:52

that they're just looking at them.

53:54

The neurologist many times can take a guess.

53:57

That's probably hemorrhagic.

53:59

Uh, also a trans a transformation would need a patient to,

54:04

to have had, uh, thrombosis usually.

54:06

And you have that history, a spontaneous, uh,

54:10

hemorrhagic transformation.

54:12

You, the patient will have to have a lot of hours.

54:15

So it have to be 24, 48 hours to,

54:17

to have a spontaneous transf uh,

54:19

hemorrhagic transformation without having

54:21

performed the thromb.

54:23

And in that case, it's very hard

54:24

that you don't have a prior CT to know that is

54:28

a hemorrhagic transformation and not a primary hemorrhage.

54:32

Uh, also, lemme try to find another question here.

54:38

How to tell if micro bleeds are acute

54:40

or chronic or subacute.

54:42

And you're gonna, uh, the are moving here,

54:46

you're gonna try to, to look in the MRI, the,

54:49

the microbeads appear on the SWI, the susceptibility images

54:53

and, uh, as little dark sun, dark spots, signs.

54:57

And you have to look at T one

54:59

and T two to try to find out if they are near

55:01

or usually they, they have a, a very large

55:05

distribution there, uh, are not very hyperacute.

55:10

Thank you. Another question here.

55:11

As a stroke neurologist, we often only get actuals

55:14

during the stroke alert since

55:16

pictures are sent to our phone.

55:18

So I worry about missing subdural.

55:20

Do worry geologists always get the Coronas

55:22

during stroke alerts?

55:24

Yes. We usually get the Coronas

55:27

or we are in the, the station

55:29

and we, we make the, the, the Corona information.

55:31

So it's our standard to look at the coronal imaging.

55:36

Yeah. But are your tips and tricks for differentiation?

55:41

Relatively small epidural from subdural hematomas?

55:46

Apart from the shape that epidural tend to be bi convex

55:49

and subdural tend to be the, the crescent shape sign.

55:54

Uh, one crosses the, the, the, the sutures

55:58

and the other Don doesn't.

56:00

Okay. Also the epidural usually have that, that, uh,

56:04

wheel sign when it's bleeding.

56:07

Uh, another question here.

56:11

In what cases is it recommended

56:12

to suggest further imaging like CT or MRI?

56:15

Uh, I think what we talked about, a little bit, a bit about

56:19

that in the, the presentation.

56:20

But basically when you're not sure about the radiology,

56:25

if it's hypertensive or,

56:26

or cerebral angiopathy, amyloid angiopathy, if you have

56:31

any suspect of, uh, uh, arterio venous mal formation

56:34

or a brain tumor or anything like that.

56:38

And another one, sometimes theorial is hypertensive, how

56:42

to differentiate from subdural hematoma in case of trauma.

56:46

And usually I have to look at bo the both sides

56:48

and compare when you have a hematoma,

56:50

one side will be thicker, so it will, both

56:53

of them may be hyperdense naturally,

56:56

but the, the one with blood on top

56:58

of it will be a little thicker.

57:01

Uh, what else? Thank you Luka.

57:05

And you have another question here? I guess not.

57:11

I think you got them all.

57:14

Oh, okay. Thank you Ashley.

57:15

Yeah, thank you about the timing.

57:17

Uh, we we're aiming at 60 minutes. We have 58, so yeah,

57:22

Right on the nose.

57:24

Okay. Thank you so much for this presentation

57:26

and for answering all those questions.

57:27

It was a pleasure to have you. Thank

57:29

You so much for the invitation.

57:30

It was my pleasure.

57:31

Awesome. Yeah. And thanks for everyone else

57:33

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57:35

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57:38

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57:47

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57:48

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57:52

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58:02

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