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This is a 44-year-old woman with a

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jumping injury, now with ankle pain.

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And I'm going to perform the search pattern

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as if I was sitting by myself in my office.

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And I start out, almost all the time, with the

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sagittal projection because it is comfortable.

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Unless I absolutely know the pathology is not

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going to show up in this view and in another view.

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So this is my expedient way of getting

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through the work during the day,

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and also keeping things interesting and efficient.

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So I start out with my sagittal image

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and I think, "Okay, jumping injury."

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That's usually not a collateral ligament injury.

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In other words, jumping with

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an inversion or eversion, okay.

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Then I would go straight to the axial.

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But just straight jumping up and down, sort of

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a pilon type of component or mechanism,

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I'm thinking about a fracture.

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So I go right to my proton density,

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fat suppression, SPAIR, SPIR, special

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fat sat, whatever you want to call it, and I

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scroll, and I have them linked together.

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Now I do have another sagittal.

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I have a gradient echo, additive gradient

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echo sagittal, also known as adage, merge,

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medic, MFFE, but I don't have it up.

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And there are two reasons why I don't have it up.

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One, I don't have enough spaces on my

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board so that you can see things real clearly.

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But the real reason I don't have it up

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is it's not very good for bone.

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And when I hear an axial load

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force, I'm looking for a fracture.

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And this particular sequence is

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great for osteochondral surfaces,

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with an emphasis on chondral

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and articular, but not for medullary bone.

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So let's keep scrolling the sensitive

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sequence for medullary bone.

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And I'm looking at the calcaneus.

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And I don't have the whole calcaneus on there.

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I'll make it a little smaller just so we get

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it all, where it works somewhat complete.

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And we scroll, and we don't see

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a fracture of the calcaneus.

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Perhaps we see a little periostitis.

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That's not where a fracture would be

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eccentrically like this.

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That's simply periostitis from plantar fasciitis.

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It has absolutely nothing to

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do with the jumping injury.

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And this swelling of the heel pad is a

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common physiologic phenomenon from

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just walking around and weight bearing.

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So I am not going to call this a fracture,

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even though it is a live, actively

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inflamed area, and the patient probably

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had pre-existing plantar fasciitis.

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So where would a fracture be?

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It would be here, in the lower third,

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but medullary, in the middle third,

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or sometimes verticalizing in the upper third.

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And fractures will either have a

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jagged pattern, if they are acute,

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or they'll have a wavy pattern if

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they're overuse or insufficiency related.

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So now that I have done my scrolling and looked

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for medullary edema, one word of caution.

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You can get a pure cortical fracture and have

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virtually no edema in the medullary space.

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So, if you're truly an expert or a master,

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your eye has to trace the cortex going

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both ways, both laterally and medially,

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and the cortices with this exception,

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which we've already outlined, are just fine.

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So what isn't fine?

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Well, if we look very carefully, we see

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that the dome of the talus has this funny,

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ill-defined area of increased water-weighted

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signal and slightly decreased T1 signal.

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Now, you might say, well, is that real?

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We needed another projection to prove it,

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and that is exactly why I have the coronal up.

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And I would have it up in my office

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so I know constantly where I am.

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And I'm expecting either a fracture,

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or an osteochondral injury, or some type

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of subtalar injury due to axial load.

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I know I don't have a subtalar injury,

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because I can see the subtalar space with

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the components of the subtalar space.

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So, my search is really based on the history.

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I'm doing a medullary search, I'm doing

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a cortical search, I'm doing what I call

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a pilon search for axial load forces

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that injure the subtalar space.

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I've got the talocalcaneal interosseous ligament.

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I've got the more centrally positioned

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cervical ligament right here.

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No edema around it.

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And although not really well seen, I have a few

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of the segments of the lateral retinaculum,

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of which there are three, a medial, an intermediate,

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and a lateral, none of which are swollen.

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Our area of swelling that we suspected

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sagittally, now remember we're coming across and

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we could be on the edge, of the talus is real.

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It's right there.

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Let's make it a little bigger for all you

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sports fans out there who like things big.

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The edema is real and what's on top?

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Cartilage.

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And is that cartilage smooth?

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Yes.

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And no.

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The cartilage is roughed and scuffed

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and buffed and impacted and injured.

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So this is an osteochondral injury.

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Now if we keep scrolling sagittally,

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you run into a terrific pitfall.

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Look at that pseudo-defect that looks

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so nasty in the sagittal projection,

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representing the malleolar notch in the talus.

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So you're volume-averaging this

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defect here, which is normal.

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That is not your osteochondral injury.

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That is your osteochondral

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injury, and it's a subtle one.

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Now let's look at our coronal again for a moment.

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I want to draw a little bit.

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And when... Let's pretend we have a defect

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on the other side, or an injury on the other side.

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If the injury goes all the way and involves the

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cortex, so that it leaves no free cortex along

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the edge, we call that a non-shouldered OCD.

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But if, on the other hand, the cortex is spared,

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we see an edge of dark signal around our defect,

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as we do medially, then that is shouldered.

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So, our shouldered superomedial defect has a depth,

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it'll have a length, it'll have a width, and the

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fact that it's shouldered makes it much easier,

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if it ever had to be grafted, to hold the graft

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in place, because we have some cortex to hold it.

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If we had a lesion like this,

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it would be non-shouldered.

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You can also get a good feel, not only for the

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defect, but its size, whoops, let me get out of

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my drawing tool, for its size, and also for the

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presence or absence of loose bodies,

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by scrolling the axial projection.

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Let's do that.

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And as we scroll the axial

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projection, we do see our lesion.

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There it is, right there.

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It's barely visible on the T2.

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It's barely visible on the T1.

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So it's the earliest of bony defects.

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And you might say, well, how do

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you get a cartilage defect,

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but not such a prominent bony defect?

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Well, the cartilage is like a shock absorber.

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So in this case, the cartilage

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absorbed most of the force.

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Sometimes the force, depending

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upon the axis of injury,

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will transmit through the cartilage.

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The cartilage is slightly swollen,

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yet the bone is more heavily affected.

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So it can go either way.

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In this case, I would say the cartilage is

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more affected than the actual underlying bone.

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And we do have an AP dimension,

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a transverse dimension.

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The abnormality is shouldered.

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And now, to complete the examination, I would

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go up and down looking for a potential body,

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not expecting to find one, because I don't have

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a defect. But I would do that just to check.

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I would also look at the collaterals, especially

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the anterior talofibular ligament, which is a

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little bit attritional but present, just to make

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sure I didn't get the wrong history, that the

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patient didn't have an inversion-type injury.

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And then I would just do a general

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check in the axial projection of

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all the tendons and their position.

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Lateral, 2.

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Medial, 1, 2, 3.

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Anterior, 1, 2, 3, 4.

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And one, the achilles in the back, and I

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just do that in general very, very quickly.

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I also get a great look at the

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neurovascular bundle on the medial side,

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I get a great look at the retinaculum.

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These are just routine checks that I

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would go through, not specifically related

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to a drive-down, pylon-type injury.

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And while we're at it, we do see the

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swelling in the plantar fascia that is real

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that preexisted before this patient's injury.

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Now, you'll hear a lot of people talk

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about the grading of stability of OCDs.

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And I think size definitely matters.

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Position also matters.

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You know, eccentricity.

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Ones that are non-shouldered are

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much more likely to dislodge.

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And then you'll also hear that when you have an

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OCD, if that OCD is surrounded by fluid signal

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intensity, so we'll pretend our green is fluid.

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When I say fluid, I mean fluid on the T2.

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Not edema on the PD spur, but

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actual bright fluid like this.

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Water white, super bright, homogeneous,

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fluid signal intensity that communicates

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with the cortex, that does place the

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OCD at higher risk of dislodgement.

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And that's probably as much as you need

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to know about the surrounding signal

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related to your OCD, with one exception.

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If around your OCD you see a lot of small little

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cystic foci, like this, that usually means the

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bony component of your OCD is wiggling around and

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irritating and producing cystic degeneration or

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little atrocious ganglia of the surrounding bone.

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And that usually means that there

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is micro-instability present.

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So in summary, shouldered,

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OCD with chondral scuffing irregularity and

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blistering, size, length, width, and depth given.

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No evidence of loose bodies, small

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effusion, incidental plantar fasciitis and periostitis. Next.