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Radiology Review Course – Trailer

Radiology Review Course – Trailer

One of the hallmarks of CPPD is chondrocalcinosis
– calcification within cartilage. It can occur within fibrocartilage. Here it is
within the menisci of the knee. But it can also occur within hyaline cartilage.
Here it is within an elbow joint. You can just see that fine rim –
often very speckled CPPD – speckled calcifications in the hyaline cartilage.
Here it is at the wrist; classic speckled calcifications within the triangular
fibrocartilage. Think of CPPD as an intra-articular phenomenon, within the
joint itself. And that’s why it can lead to joint destruction. Here it is, this
is at the wrist, it classically causes a radiocarpal joint appearance of
osteoarthritis, so joint space narrowing subchondral sclerosis, geode cyst formation. You’ll know that the most common spot for OA
at the wrist is usually this first CMC joint. You can see that looks normal,
so this is atypical for just your standard osteoarthritis – an unusual joint
associated with calcification of the triangular fibrocartilage,
almostcertainly CPPD related. You’ll see that there’s also often
widening of the scapholunate interval and you get proximal migration of the capitate
– likea SLAC wrist – so the differential for this case would probably be post-traumatic.
Has this patient had trauma, scapholunate ligament rupture and then
degeneration secondary to that? Or, more likely, if there’s no trauma
this is probably due to CPPD. So you’ve got a patient whose febrile,
they’re got a cough, they’ve been treated with a few courses of antibiotics, things aren’t
going away on the x-ray as there’s these opacities that kind of come and go and on
the CT you’ve got these peripheral regions of quite geographic
consolidation. You’ve got beautiful air brochograms. It’s a relatively lower
zone distribution and as you are scrolling through you kind of get
fixated on this area and you’re like oooo it’s a bit groundglass in the middle,
it’s a bit consolidation around the outside. You want to call it the atoll sign and
then you said atoll so you want to call it organizing pneumonia and that’s good,
because that’s what it is. But the atoll sign is not at all specific
for organizing pneumonia. It’s the classical description,
it’s the thing that you wanna say, but in fact it occurs in plenty of things,
plenty of pulmonary infections can give you this. That’s not the point.
The point is that you’ve seen these migratory opacities, it’s non
responsive to antibiotics, it’s organizing pneumonia. The important thing to understand
about an abscess is that physiologically it’s a
fundamentally different process to a glioblastoma or a metastasis, where the
enhancement is the pathology in the latter two, whereas in an abscess the
enhancement are the elves – that’s your brain trying to keep the pus contained.
And so it’s a physiological, organized response all the way around the invading horde. So let’s have a look at an abscess. We have a complete sphere of
enhancement and on the middle slices where you’re not getting much partial
voluming, it’s really quite regular. It’ll usually be a bit thicker towards the
cortex where there’s more blood supply, a little bit thinner towards the ventricle,
and eventually it’ll point to the ventricle and discharge into the
ventricle and you get rip-roaring ventriculitis and the patient will die,
usually very quickly. You might get some little pockets
of additional pus that get walled-off. And when you look at T2 weighted imaging,
superimposed on the enhancing margin is a complete T2 low ring and this is due
to cytokines and free radicals released by all those monocytes in that defending border.
And you can see it on SWI as well – susceptibility weighted imaging. It’s
very uniform, there might be tiny little areas of irregularity but it’s a
complete line. Not little segments. Not just blotches. Again, because this is a
organized physiological response. In this case you’ve got again, deep lobe
lesion, not as large, less mass effect on the parapharyngeal fat but clearly
lateral to it. And you can see it’s inseparable to the deep lobe parotid but
it’s very irregular in its shape, it’s multi lobular, it’s not just one oval.
So you go up and again it’s confined in there, it’s well circumscribed throughout
its extent. You look on the T2. Is it T2 very hyperintense? Is it T2 a
little hyperintense? It’s very hyperintense on T2 – very well circumscribed,
solid lesion enhancing. It fits the imaging features most consistent with
a pleomorphic adenoma and that’s what it is. And the pleomorphic adenoma is allowed to be multi lobulated, but it should
always be very bright on T2 and should always be very well circumscribed. In children we’ve got to remember to look at the metaphyses for lucency, because
what we’re looking for here is discontinuity of the cortex, lucency of the underlying bone,
and abnormality of the physis in infection. We can do an MR which will show
widespread edema on both sides of the physis, abnormal physis, lots of inflammatory
change in the soft tissue and in this case non enhancing central component
which on CT we see is a bony sequestrum. When we’ve got infection,
we’re looking for whether or not there are any complications of that. Is there a
subperiosteal collection that the surgeon needs to go in and drain? Is
there a bony sequestrum that they need to go in and drill out. MRI is the best first
test because there’s no radiation involved. But CT is sometimes really
helpful to make the decision about whether there’s a bony sequestrum.

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