0:01

The final component of a hematoma that we

0:03

talk about is chronic stage hematoma.

0:07

Chronic stage hematoma is dominated by

0:10

a compound called hemosiderin.

0:12

Now, hemosiderin also has proton relaxation enhancement.

0:18

Hemosiderin generally is concentrated within macrophages

0:23

that are eating the blood products.

0:26

At a late stage of the hematoma,

0:29

what happens is that macrophages leave the blood system,

0:33

cross the blood-brain barrier which has been disrupted by

0:36

the hematoma and start to chew away and eat up

0:39

the iron that is present in the hemoglobin.

0:42

It then gets converted to the hemosiderin product.

0:47

Hemosiderin is superparamagnetic, by that it has dramatic

0:52

T2 shortening effects and has dramatic Proton

0:56

Relaxation Enhancement. So proton relaxation enhancement.

1:00

Now one might say, well,

1:02

these macrophages don't they go back into the bloodstream

1:05

and take it to the liver and spleen?

1:08

They do in part.

1:09

But what we say is that the blood-brain barrier gets

1:13

reestablished and these poor macrophages are left behind

1:18

in tissue and therefore lead to tissue hemocytrine

1:22

concentration of the hemocytrine.

1:26

The other thing that may occur in

1:28

the same setting is ferritin.

1:30

Ferritin usually is not within a cell but

1:33

is deposited within the soft tissues.

1:35

And that too has T2 shortening effects.

1:38

So with chronic hematomas, hemocytrine,

1:44

you have dark signal intensity on T2.

1:47

Because of Proton Relaxation Enhancement,

1:49

you have low signal intensity on T1.

1:51

There is no methemoglobin,

1:53

no proton-electron dipole interaction.

1:56

And this is exquisitely well seen on gradient echo

1:59

and susceptibility-weighted imaging.

2:01

It is said that hemosiderin in the tissue

2:04

potentially can last forever.

2:07

You may see a little hemosiderin stain at autopsy on these

2:11

patients who have had trauma as a young adult.

2:14

This is a nice example of something that

2:17

is known as the hemosiderin slit.

2:20

So hemocytrine

2:23

slit in this case,

2:28

the patient had a hypertensive bleed

2:32

within the butamin years ago.

2:36

What you see is dark signal intensity on this T1

2:40

weighted scan as well as hemosiderin staining

2:45

on the T2 weighted scan.

2:48

In addition, you might note that there is volume loss.

2:52

So if we go from the edge of the third ventricle,

2:55

go to the Sylvian Fisher here and we compare

2:58

the distance versus the edge of.

3:00

The third ventricle to the Sylvian fissure on the

3:03

left side, you see that there is loss of volume.

3:06

That's because at one point there was a hematoma here,

3:09

but with the loss of volume,

3:12

as the hematoma has contracted,

3:14

it goes down to a hemosiderin slit.

3:18

You can also demonstrate this by the proximity of the

3:22

hemocytrin to the Sylvian fissure here versus the

3:25

butamin over here that has underlying tissue.

3:28

Before you get to the Sylvian fissure over here,

3:31

hemosiderin dark on T1,

3:34

dark on T2 because of proton relaxation enhancement.

3:39

This is an example of a FLAIR scan

3:44

and a Susceptibility-weighted scan.

3:48

You note that on the FLAIR scan,

3:50

which is a fast bane echo technique with

3:52

multiple 180-degree refocusing pulses,

3:55

there is no evidence of hemorrhage on the FLAIR scan.

3:58

What you see is a little bit of bright signal intensity on

4:01

the FLAIR representing small vessel

4:04

chronic ischemic changes.

4:08

However,

4:09

on the Susceptibility-weighted scan,

4:12

we see lots of little dots of dark signal intensity

4:16

that are not evident on the FLAIR scan.

4:21

At the same level.

4:22

These are dots of hemosiderin from a patient who had

4:28

previous head trauma and had shearing injury.

4:31

At the gray-white junction,

4:34

there is no edema on the FLAIR scan.

4:36

All you see is dark signal intensity,

4:39

proton relaxation enhancement secondary to hemocytrine

4:44

on the Susceptibility-weighted scan.

4:48

This is another example just demonstrating how sensitive

4:53

Susceptibility-weight imaging is compared to

4:56

fast bane echo T2 aid and FLAIR scan,

5:00

T2-weight scan, FLAIR scan,

5:04

susceptibility-weight scan with no evidence of hemorrhage

5:08

that you would report on the MRI scan on T2 or FLAIR.

5:13

And yet multiple areas of hemorrhage demonstrated on

5:18

Susceptibility weight scan. Why do I emphasize this point?

5:22

If you are not including susceptibility weighted

5:25

imaging in your trauma protocol,

5:29

you will miss areas of hemorrhage on your other pulse

5:33

sequences. Be it T2-weighted, be it FLAIR scanning,

5:38

be it diffusion-weighted imaging, please add SWI.

5:42

Sequences or if you do not have susceptibility weight

5:47

scans available, gradient echo scans in order to detect

5:51

subtle areas of hemorrhage that would otherwise be missed.

5:55

A final word about hemorrhage subarachnoid.

6:00

Hemorrhage, as seen on the CT scan to your left,

6:04

is something that is difficult to identify on MRI scanning

6:09

because it resides in the oxygenated cerebrospinal fluid.

6:15

Here we see the subarachnoid hemorrhage in the basal

6:19

synth sterns in the interhemispheric fissure,

6:21

as well as in the Sylvian fissure on this FLAIR scan.

6:25

However,

6:26

we do see bright signal intensity in the Sylvian fissures

6:32

that otherwise would be dark in signal intensity like

6:36

CSF in the cerebrospinal fluid.

6:38

So on a FLAIR scan,

6:40

the PSI should be dark.

6:42

If you are seeing bright signal

6:44

intensity on the FLAIR scan,

6:47

it implies subarachnoid hemorrhage or meningitis or some

6:53

chemical in the CSF or oxygenation that is occurring as

7:00

part of intubation or supplemental oxygen being

7:04

given to the patient. For some reason,

7:06

that supplemental oxygen can dissolve in

7:09

the CSF and turn a FLAIR scan bright.