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Microtrabecular Stress Injury and Osteochondral Defect

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Okay, this is a young teenager with pain, possible

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osteochondral defect, possible bone injury,

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possible stress fracture, rule out life itself.

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We have a sagittal T1, a T2,

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and a fat-suppressed PD.

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Let's start scrolling, and I'm going to

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focus primarily on the sagittal, which

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which is my favorite foot and ankle projection.

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And I may pull down one or two

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other projections near to the end.

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And I want you to make some medical, emotional,

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and mental decisions about what types of

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bone injuries or abnormalities you would

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consider in a case like this in a juvenile.

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Well, first, I want to point out to you

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these speckled foci of low signal on T1

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that are scattered throughout the foot, many

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of which are not coalescent, like these.

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They're very delicate.

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They look like somebody

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kind of spray painted them.

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Very gently and focally, these little

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dots across the lower extremity.

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That is a very common scenario in

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juveniles, especially under the age

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of 10, which this person is not.

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And it results from increased bone turnover,

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increased bone metabolism, and hyperemia,

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and you will see this in what I call lower

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extremity abusers, of which all juveniles

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under the age of 10, maybe 12, are guilty.

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That in itself may cause some discomfort,

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but usually does not prompt the

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patient to come in for pain.

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And when I say usually, yes, I do have patients

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that come in, and that's the only finding.

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Somebody looks at it and calls

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it a stress fracture, or RSD.

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That is not a usual manifestation of RSD, also

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known as Complex Regional Pain Syndrome Type 1.

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So, speckling in itself is not an alarm bell.

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And we do have quite a bit of speckling.

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Now let's skip over the T2 for a moment,

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because it is not a marrow-sensitive sequence.

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It's a modifier.

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It helps you decide on age and severity

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and a few other complementary things.

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And let's go over to our water-weighted image.

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And there are some areas that are

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very coalescent, especially in the

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upper calcaneus, where it's brighter.

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There's some linearity to it.

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Let's blow it up, like right here.

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There's linearity along the posterosuperior

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aspect of the calcaneus with more confluent edema.

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What shall we call this?

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A microtrabecular stress injury.

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Now what would be a flat-out stress fracture?

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It'd be a little thicker, it'd be a little

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better defined, and it would have an appearance

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in the bone that looks something like this.

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Almost like atrial fibrillation.

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I may have to do it a little

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bit bigger for you to see.

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Yeah, there we go.

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And I'm going to show you some

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of these in other vignettes.

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So I'm not quite ready to give him a full,

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flat-out, full-blown stress fracture, but I

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am willing to give him a microtrabecular stress

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injury and other areas that are more confluent

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with lesser degrees of stress phenomena.

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In other words, bone marrow edema.

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Now, do notice that the bone marrow edema

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in these other loci, like the talus and the

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navicular and the cuneiforms, is central.

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And the central teaching point of a case like

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this is that in RSD, Complex Regional Pain

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Syndrome Type 1, the edema is subcortical.

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It's in the wrong place for that diagnosis,

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which you should have at least considered.

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So RSD is not going to be a strong

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choice for us radiographically.

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What are we going to do to explain those areas?

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Overuse phenomenon.

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Likely symptomatic, not just

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speckled, but more coalescent.

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So what should we call those?

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Microtrabecular intramedullary bone injuries.

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I'm calling this one a microtrabecular

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overuse fracture, not a full-blown

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stress fracture, but microtrabecular.

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I'm calling these overuse

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microtrabecular injuries.

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Now because this is a young person,

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because every bone is affected, I'm

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a little concerned about possibly an

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underlying metabolic or genetic disorder.

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And the one genetic disorder that I might

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have in the back of my mind, especially if I

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start to see more real stress fractures evolve

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on subsequent imaging, or as I follow this

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patient, is osteogenesis imperfecta tarda.

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This patient doesn't have it, but

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should absolutely be screened for

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this if this process is necessary.

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Let's keep going, shall we, because one of the

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questions asked by the clinician, is there an OCD?

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Let's answer that question,

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and the answer is, absolutely.

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An osteochondral defect, a defect in the

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talar dome, and that's why, as promised,

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I have to call up another projection.

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Another water-weighted projection, and

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here it is, in the coronal plane, and

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there is an osteochondral defect in the

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supramedial aspect of the talar dome.

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The talus was swelling around it.

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Now just a word about osteochondral defects.

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I'll call up the axial to see

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if we can see it as well here.

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There it is.

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I'm going to blow it up and

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make it a little lighter.

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And I'll be brief with this.

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There's a very important teaching point

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here that's separate and distinct from all

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the other things that are causing edema

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in this patient, this juvenile patient.

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And that is the character

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of the osteochondral defect.

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Yes, you can all look up that

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you can measure the defect.

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You can put a ruler on it.

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You can give it a depth, a length, and a width.

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You should look at whether

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there's any loose bodies.

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You should look at the chondral surface to see

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if it's blistered or swollen or there's a defect.

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There's one other really important teaching point.

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And that's not why I'm showing the

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case, but I'll throw it in here since

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we are on an osteochondral defect.

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And that is, is the defect shouldered?

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What I mean by that is, let's

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take the talar dome right here.

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It's a talar dome.

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If my defect is here and I have some

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decent bone to the side of it, like here.

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That means it's shouldered.

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However, if my defect goes all the way up

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to the free edge, out here, and there's

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no shell of bone covering it, now you

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cannot put a bone plug in here or a

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graft that's gonna stay in and be stable.

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So it's important, you tell the clinician whether

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that OCD, which is right here, there it is, I've

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colored it in, is shouldered or unshouldered.

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In this case, it does go up to the free edge,

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even though I don't have the preferred coronal

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T1-weighted image to show you, because that

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is not the main reason I am showing the case.

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So in summary, we've got a lower extremity

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abuser with some speckled areas of high

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turnover, hypervascularity, increased metabolism

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in the skeleton, which we see a lot as a non

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contentious form of lower extremity overuse.

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We've got a microtrabecular fracture in the

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posterosuperior calcaneus, which should heal

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on its own within about two to three weeks.

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We do not have a full blown stress fracture,

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which you'll see a little bit later on.

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We have areas of marrow edema, so-called medullary

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stress or overuse phenomenon in other bones.

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We should make sure the patient doesn't

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have underlying, uh, metabolic bone disease

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or genetic bone disease like OI, imperfecta

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tarda, and the patient does have a clear-cut

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osteochondral defect with a length, with a

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width, with a depth that is non-shouldered

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and goes all the way out to the free cortical

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surface of the supramedial talar dome.

Report

Description

Faculty

Stephen J Pomeranz, MD

Chief Medical Officer, ProScan Imaging. Founder, MRI Online

ProScan Imaging

Tags

Trauma

Musculoskeletal (MSK)

MSK

MRI

Foot & Ankle

Acquired/Developmental

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