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Acute Hemorrhage on MRI

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I would be remiss as a University of Pennsylvania

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Neuroradiology fellow graduate if I didn't go through the

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signal intensity characteristics of

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intraparenchymal hematomas on MRI.

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This was work that was done in the late 1980s and

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early 1990s by a series of neuroradiologists,

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including Bob Grossman, John Gamori, Scott Atlas,

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Bob Zimmerman and David Hackney.

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These were my mentors as I was a fellow,

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and they went through the signal intensity characteristics

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of hematoma based on the chemistry.

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I'd like to share that with you.

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The two concepts that you have to understand in order

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to be able to analyze a hematoma on MRI

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are proton relaxation enhancement,

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which we usually refer to as pre, PRE.

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And proton-electron dipole-dipole interaction.

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Proton relaxation enhancement is due to the inhomogeneous

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magnetic field that hematomas cause.

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And this is usually due to T2 shortening effects,

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secondary to concentration of charge within

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a cell versus outside a cell.

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And this will be the major factor

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accounting for T2 shortening,

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which means dark signal on a T2-weighted scan with

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deoxyhemoglobin, that marker of acute hemorrhage,

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and hemosiderin, that marker of chronic hemorrhage.

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This is field strength-dependent, and therefore the dark

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signal intensity on T2-weighted scan will vary depending

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upon whether you're at low field strength.

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For example, 0.15 tesla versus three tesla,

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where it will be very dramatic.

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The second concept I mentioned

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was proton-electron dipole-dipole interaction.

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We use the term "PEDDI" for this.

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PEDDI refers to a T1 shortening effect

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that occurs secondary to

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the methemoglobin molecule's affinity for water.

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The water molecule is able to approach the methemoglobin

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molecule, and it leads to T1 shortening of water

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protons in proximity to the methemoglobin molecule.

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T1 shortening leads to bright signal

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intensity on a T1-weighted scan.

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And this is a field strength-independent property.

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Let's look at the various components of

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hematomas over the course of time.

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The acute hematoma is dominated by deoxyhemoglobin.

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This is an intracellular compound that leads to proton

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relaxation enhancement and T2 shortening.

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It is therefore field strength-dependent and will be very

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dramatic as you go to gradient echo scanning or

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susceptibility-weighted scanning.

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Deoxyhemoglobin,

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because it's a mark of acute hematoma

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is often associated with bright signal intensity

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around the hematoma,

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secondary to the edema in the acute phase.

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So what one has is an intact red blood cell

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that has deoxyhemoglobin within it

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and no deoxyhemoglobin outside the red blood cell,

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which leads to a bar magnet effect

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causing T2 shortening and dark signal on a T2-weighted scan,

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and it usually occurs from 6 hours to three

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days after the initial insult.

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These are pulse sequences and CT scan showing

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acute hematoma and deoxyhemoglobin.

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The acute hematoma is bright on the CT scans,

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hyperdense because of the globin content,

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not the iron content but the globin or hemoglobin content.

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On a T1-weighted scan,

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and I'm showing this

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is a T1-weighted time of flight MRA.

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You see that the signal intensity of the acute hemorrhage

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is isointense to low intensity on T1-weighted scanning.

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This is fast spin echo T2-weighted scanning.

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The fast spin echo scan shows dark signal intensity from

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deoxyhemoglobin and proton relaxation enhancement,

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T2 shortening effect.

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This is the FLAIR scan.

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And this FLAIR scan shows the same thing,

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dark signal intensity, because it has T2 weighting

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within the FLAIR scan.

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This is your DWI scan.

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And the DWI scan also shows dark signal intensity

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because it has T2 weighting.

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This is the ADC map showing dark signal intensity

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but not due to cytotoxic edema,

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but dark due to the presence of hemorrhage.

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This is an SWI scan, a susceptibility-weighted scan.

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As I said,

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susceptibility-weighted imaging shows greater sensitivity

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to blood products than fast spin echo.

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And we could see that by the blooming effect and the size

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of the hematoma between the T2 fast spin echo scan

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versus the susceptibility-weighted scan.

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You could see just how dark this is,

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almost as dark as the bone

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on the susceptibility-weighted image.

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And finally, we have a post-gad T1-weighted scan.

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And as you see,

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the deoxyhemoglobin,

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the acute hemorrhage is somewhat

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low on T1-weighted imaging.

Report

Description

Faculty

David M Yousem, MD, MBA

Professor of Radiology, Vice Chairman and Associate Dean

Johns Hopkins University

Tags

Vascular Imaging

Vascular

Physics and Basic Science

Neuroradiology

MRI

Hematologic

Emergency

CT

Brain

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