 Welcome to Case Crunch rapid case review for the core exam hosted by Medality. In this rapid fire format, faculty will show key images and you'll respond with the most likely diagnosis via the live polling feature. After a quick answer explanation, it's on to the next case. You'll be able to access a recording of today's case review and previous case reviews by creating a free account using the link provided in the chat. Today we are honored to welcome Dr. Navid Faraji for an MSK board prep case review. Dr. Faraji is an MSK radiologist and passionate educator at University hospitals in Cleveland, Ohio. He's the director of medical education in the department of radiology and associate program director of diagnostic radiology residency. As well, he's an assistant professor in the division of MSK radiology and is heavily involved in educating medical students in radiologic anatomy. Questions will be covered at the end if time allows. Please remember to use the Q&A feature to submit your questions. And with that, we are ready to begin today's board review. Dr. Faraji, please take it from here. Thank you for that lovely introduction. Hopefully everybody can hear me okay. I'm gonna share my screen. And so first things first, I'd like to get a gauge of who we have here in the audience to take part in this lovely occasion we are gathered here today. So if you wouldn't mind, yeah, just answering this question. Are you a resident attending just here for the cases or other survey says? All right, 46% residents and some other results. All right, cool. So let's get this party started. As mentioned, I'm Naveed Faraji, MSK Rad here in Case Western slash University hospitals. I have nothing to disclose other than I just ate dinner and hopefully I don't have anything in my teeth. So let's get started. I just wanna preface this is that I made some of these questions somewhat challenging and because it is my impression that this potential upcoming examination that you may or may not have is not tailored to assess whether you are good at memorizing facts but rather can you differentiate pathology, various types of pathology that may look similar and what sort of clues and information can you use to differentiate those things. So we're gonna try to go through that together and yeah, let's have that, have at it. Just a brief distribution of the topics for the ABR guide most recent came out in 2021 that I could find at least. So we got 20 questions today and it's gonna be generally in this distribution to somewhat kind of mirror the examination. Okay, so this is gonna be a multi-image question. I'm gonna give you a moment to take a looksie-loo at this one. Okay, and I can zoom in on things but take a look. Maybe here's a closer view if needed. Here's some more images and if I were you, I'd be asking myself what sequences am I looking at so I can better understand what's happening, right? So every time you take a case, you should be asking yourself what's your sequences you're looking at because various sequences are gonna give you varying pieces of information. We can see fluid is bright on this one, fluid is dark on this one. There's some bright synovial enhancement or hyper intense synovial enhancement so we can infer from that information that this is a T1 fat suppress post-Galilinium image and this is a T2 fat suppress coronal image. Okay, what is the most likely diagnosis? All right, 52% of folks said Milwaukee shoulder. Septic arthritis was close second at 33%. And yeah, I would agree. So this is Milwaukee shoulder and the key is if we go back to these images, septic arthritis could have a very similar appearance but when you couple this with the radiographic appearance of mineralization in the region of the greater tuberosity slash rotator cuff, the best answer is probably Milwaukee shoulder in my view. We can also see that there's loss of particular college, some destruction and flattening of the sub-colonial bone plate loss of sphericity. We also see some associated rotator cuff tearing. I mean, you could see some of those things in septic arthritis, but the mineralization in the region of the rotator cuff would suggest Milwaukee shoulder. Neuropathic arthropathy is a possibility but it tends to be a little bit more destructive and they might give you something that leans you towards some cervical spine disease and suggest a cervical spine MRI. All of those entities could look very similar and they would hopefully on a test have to give you some sort of clue to help you differentiate them. And on this particular question that was the radiographic appearance with mineralization in the rotator cuff. Okay, here's another radiograph. What is the most likely clinical history in this patient? 17 year old weight lifter, 83%. Okay, I guess I made this one too easy. Yeah, well done everybody. So the main imaging finding here is that we have fraying of the distal clavicle. We have resorption, subconjural, resorptive changes, loss of the subconjural bone plate definition. And so here we can see this radiographic appearance with some focal linear hyper density which is our subconjural bone. And we can see that that definition is lost here and we can see this kind of resorpted changes that are isolated to the distal clavicle. It looks like a relatively young patient. So these other questions, other answer choices with 17 year old intermittent fever maybe that would be like a JIA type situation but that should probably involve both sides of the joint rather than one. Hyperureosemia would suggest gout. And again, this is not a classic location for gout and there's no Jason soft tissue prominence. And again, it's not like a juxtarticular erosion but rather it's subconjural. 17 year old weight lifter we can see so distal clavicular osteolysis is the entity here. We can see that there's distal clavicular marrow edema, some loss of the definition of the subconjural bone. And this can be seen in the setting of chronic repetitive microtrauma which is commonly seen in weight lifters, bench pressing, things like that. In addition, someone who had a trauma to the distal clavicular or chromio clavicular joint can have this appearance subsequently in the subacute or chronic phase rather than an acute traumatic like AC joint sprain if it's isolated to the distal clavicle it's most likely to be distal clavicular osteolysis. We're praying some patients can get stress fractures of their ribs or stress reaction, commonly seen in swimmers which we don't see on this image. Okay, next question. Just gonna give you the big pick here and then we'll go to the smaller pick. So what is the most likely associated additional imaging abnormality? Okay, 50% syndesmophytes, 29% MCP erosions and then morale levelly lesion at 14%. So, okay, yeah, this one is, we can see that there's bilateral greater chocantaric merodema which is at the insertion of our gluteal tendons, minimus and medius. Similarly, we just see a little bit of merodema of the acetabulum here on the left and maybe some minimal of the right but the main thing is that these areas of subinsertional merodema is called anthocytus and can be seen in like spondyloarthropathies such as enclosing spondylitis or psoriasis or inflammatory bowel disease related arthropathies. And so you may see them at the ischial tuberosities at the origin of tendons. You can see them at the lesser tropes. You can see them AIIS or anywhere that a tendon is originating or inserting is called anthocytus. And so MCP erosions would most likely be seen in the setting of rheumatoid arthritis is the classic and it's not commonly associated, it's less commonly at least associated with this finding of anthocytus. And syndesmophytes is what we see here where there is our thin linear ossifications between the interfrontable bodies thought to be ossification of the ALL to your longitudinal ligament and slash or annulus fibrosis. They're not big bulky osteophytes like you might see in dish. So multi-level bridging osteophytes is indicative of diffuse adiopathic skeletal hyperostosis. In this case, they're very thin and most indicative of syndesmophytes which is what we might see in ankylosing spondylitis. Morale of allelesion would be more of a post-traumatic thing if we thought this person had a trauma and maybe they had a shearing injury or a de-gloving injury from the across the myofascial plane and of the superficial myofascial plane, you can get fluid collections there. A classic issue of someone gets tossed off of a motorcycle. So that's the various pathologies that might be associated with these answer choices and the best answer choices is syndesmophytes and someone who might have ankylosing spondylitis. Another thing they could show you is some of these patients get other systemic manifestations so ankylosing spond patients can get biapical fibrocystic changes on the chest X-ray, for example. So just be aware of multi-system pathology that can occur in these various patient presentations. Okay, here is another case. I put some arrows there because the imaging findings are somewhat not conspicuous so in order to avoid any confusion the arrows is where I'm suggesting that there is abnormally increased T2 signal. And so arrows aren't here but again, it's here and here. So what is the most likely etiology? Survey says, okay, nice. All right, so relatively even distribution which can mean that this is a terrible question and that the imaging findings aren't great but or it could mean that it's a good difficult question, I hope. But okay, so we see edema here and the infraspinatus region, okay. And in the deltoid, all right. This is subscap, again, supraspinatus, infraspinatus, teres minor. That's how I would separate these. And so this is anterior as opposed to your supraspinatus, infraspinatus, teres minor, subscap, okay. And here's the deltoid which originates from the acromion process and we can see edema. That's relatively diffuse and not feathery, okay. So feathery edema is indicative of muscle strains. So kind of diffuse like edema that doesn't seem to have fluid insinuating between muscle fibers and stuff is most indicative of denervation or subacute denervation change. And so we can have various patterns of denervation in the shoulder that can result from various nerve distribution pathology, right. So let's just take these one by one. Assist in the spinal glenoid notch, okay. Or assist in the supra-scapular notch, okay. So both of these areas is where the supra-scapular nerve goes, all right. So the supra-scapular nerve proximally can be impinged on the supra-scapular notch and then distally in this general area is where the spinal glenoid notch is, okay. And so at the level of the supra-scapular notch because that's proximal, it has not yet innervated the supraspinatus or infraspinatus, okay. So if there was assist there impinging the supra-scapular nerve and the supra-scapular notch, we would expect to see supraspinatus and infraspinatus denervation changes. So that's not the setting here because we only see infraspinatus and deltoid. So spinal glenoid notch, the supraspinatus has already been innervated. So we would expect to see isolated infraspinatus, muscle edema or atrophy. So supra-scapular notch, again it's more proximal, you'd see supra and infraspinial glenoid notch is more deltoid, is more distal on, I'm sorry, it's more distal. So supraspinatus has already been innervated and infraspinatus would have to denervation change. Fibrous bands in the quadrilateral or quadrangular space is in this general area, that's where your axillary nerve is and the axillary nerve innervates the deltoid and the teres minor. But we're saying teres minor is spared here and therefore the best answer is the brachial plexitis which is also known as Parsonage-Turner syndrome which is they're not sure what causes it, it's thought to be post-viral, similar to Bell's palsy where basically you have multi-focal denervation changes that does not match a single nerve distribution. So since we have deltoid and infraspinatus here it doesn't match the nerve distribution and part of the heterogeneity of the answers may be because this is not the best imaging example but that's why I tried to give you the arrows. So hopefully at least going through this process together has provided you with some informative feedback to get this answer right on a future patient or examination. Brachial plexitis. Okay, here's another patient. One clue on the examination is that if they're giving a specific MRI sequence that highlights specific types of tissue the abnormality is likely to be, you know, more indicative of a pathology involving that tissue. But don't let that lead you astray, just look at the pictures and tell me what you think. Survey says Oceus-Middle Subtailor Coalition. Well done, team. Okay, better question. So one, we can see that this is at least the fat-sensitive sequence, probably T1 because we don't see any bright fluid signal intensity within the joint and we can see that this is our talus and this is our calcaneus and that there is continuity of the marrow between the calcaneus and the talus, indicative of a subtaler coalition. Here we can see the sustentatum tali, also continuous with the talus marrow and similarly here. We can see talus and calcaneus with continuity of the marrow there. That is indicative of an Oceus coalition in the subtaler region and then the next part of the question is kind of seeing, do you know the anatomy of the subtaler joint? And this is where the middle facet of the subtaler joint would be, which is the most common area for these coalitions to arise. The posterior facet is a little bit more posterior and not depicted well here. Similarly, the anterior facet is not depicted well here, but on a sagittal plane, it would be in this general or the anterior process of the calcaneuses, which we don't see. So this question is supposed to test whether you can identify continuity of the marrow between two bony structures and then also identify the subtaler anatomy. And subtaler joint is the same thing as saying that talo-calcaneal joint. And here's what this would look like, radiographic appearance. We can see the taler beaking and we can see our C sign, which is continuity of this taler dome and then this region, sustentatum talus. And then we can see that there's continuity here, which usually there is some disruption and lucency in this region, but this is continuous and looks like a backwards C. Okay, next question. Next patient. This is a hip. What is the next best step in management? Contralateral imagine. I had a typo, but I fixed it. So here it is. Yes, contralateral imaging would be the answer choice. We can see here that here's the femur and we can see in the lateral cortex if we trace it down, that there's this cortical bump and you can even hallucinate a little bit of lucency there. If I zoom in, maybe there's a linear lucency and that is indicative of a bisphosphonate associated fracture. And these can be commonly bilateral. So we see here in that same patient that there is bilateral fractures associated with bisphosphonate use. And the key thing here is you don't want to pay, you don't want to fix one side, have the patient walk out of the hospital and fracture through the other side. So we need to suggest this. Usually these will get prophylactically fixed with an intra medullary nail due to the morbidity and mortality associated with femoral fractures in this patient age population. One of these days they are going to ask instead of bisphosphonate, I think they're gonna ask about another drug that can cause this, which is dinosimab. So that is another drug that can cause this. It is used for similar purposes but it can also, yeah, cause the same thing, just a different pathway in causing this abnormality. So dinosimab is another possible answer choice. But they ask you about drugs that can cause this. Okay, this is a wrist. So if you're ever taking case conference at your hospital, your residency program, always start like what views, what is the anatomy, what is the modality? That gives you time to think about what you want to say next, but these are the easiest low hanging fruits and it's actually a good thing to get in the habit of starting with. So you can really, particularly when you get to MR, you can start figuring out what these sequences are showing you. So I highly recommend that. Okay, damage of which structure can result in the given radiographic abnormality? Survey says scaphalunate ligament or lunotracheal ligament. Okay, that is correct. Scaphalunate ligament is the answer. One, we can see widening of the scaphalunate interval, also known as the Terry Thomas sign who was a British comedian, I'm told, although I'd never heard of him until I became a radiology resident. I think more accurately, we should use the at least more modern day, should be the Michael Strahan sign who is the next most popular person I know with a gap tooth in his front tooth. We can see that there's widening of the scaphalunate interval, there's proximal migration of the capitate and it's beginning to insinuate between these two bones and that is called a slack wrist deformity which stands for scaphalunate advance collapse. The lateral view, we can see that there's beginning to have some dorsal tilt of the lunate which is indicative of, so remember this is the lunate, it's half moon shaped, it should be facing straight up but here it's tilted dorsally and that's indicative of dorsal intercalated segmental instability. The scaphalunate angle should be between 30 and 60 and so the thing to know is that the lunate is an innocent bystander in all of this, okay? It does whatever the scaphalunate and lunotriquetral ligaments make it do. Lunotriquetral ligament is rarely torn but it can be torn. So if the scaphalunate ligament is torn here which I agree with you guys if that's the answer then what happens? So the lunotriquetral ligament forces predominate and so we can infer from that information that the lunotriquetral ligament causes dorsal effect on the lunate so it tilts dorsally when the scaphalunate ligament is torn. In contrast to the scaphalunate ligament is intact and the lunotriquetral ligament is torn the lunate starts to tilt volarly because of that traction and that's called volar intercalated segmental instability or viscy. So the biomechanics here is that the lunate just does whatever it's told and whichever of these two is intact is gonna be the predominating force and the other one that's torn is gonna lose its effect and but when everything is intact then it sits neutrally in its upward position like a good lunate. TFCC is a little meniscoid or fibrocarlagin a structure here that cushions the ulna against the carpus so it can be torn sending if ulna positive variants let's say an ulna carpal impaction but not in this particular case. This is one of my favorite cases of all time except for one that I had recently that has a similar pathology but I didn't put on the presentation. Here's the images. Okay, what are the abnormality on the images associated with which structure? Nice, okay. Great, four percent got it right and I feel like this is just a tough question but not a bad question we're gonna talk about, right? So, right, this is the Gaon's canal, right? So where we have the ulnar artery, we have the ulnar nerve and paired veins in that region and in this case we see a P2 hyper intense mass in the region of, I guess it's a little bit distal to Gaon's canal but we see this mass and it has a peripheral low signal intensity rim and the key here to differentiate all of these three structures are in this region. All of these, yeah, the median nerve is in the carpal tunnel so it would not be in this particular area. It's probably right here but sorry for the poor image quality but the key here is that this mass has this artifact going in and out of the plane of the image. We can see it here nicely associated with this mass and here is less conspicuous but the low signal intensity tubular structure going into this mass both on the sagittal and coronal plane also suggests an association with an artery and flow void and then the pulsation artifact really confirms that this is a pulsatile arterial structure and so this is a pseudo aneurysm of the ulnar artery also known as hypophenar hammer syndrome and the clinical history might be a construction worker or someone who works with their hands with like a chronic repetitive traumatic injury to that wrist region can cause an ulnar artery pseudo aneurysm also known as hypophenar hammer. You may say this is an IR case but I saw it as a musculoskeletal radiologist and so do not ignore artifacts that give you information and so if you're having trouble with a question just see if there's any piece of information that you may be missing and it might be artifact that can help you. I just saw a case of there was a patient who had a big femoral hematoma and they were wondering if it was like a neoplasm, hemorrhagic neoplasm, but it happened to be that there was the same pulsatile artifact in there and embedded in the hematoma, there was a pseudo aneurysm resulting from the surgical fixation. So yeah, do not forget about artifacts to help you differentiate various types of mythology and in this case anatomy. Here's what you might see on ultrasound in our Ying-Yang sign and the two and fro flow on spectral Doppler due to turbulent flow within that structure. All right, we're halfway there. Think that's a song. Okay, here's the images. Here's a positive arrow sign in case you can't see the abnormality. I windowed it heavily and I gave an arrow, but don't expect that on the test but hopefully they'd give you a better image. Which examination would be useful for confirmation? Survey says MRI wrist. Agree. So we can see that there's sclerosis of the lunate. Incidentally, or not so incidentally, there's ulnar negative variants which has an association with this particular pathology. Not everybody, most people with ulnar negative variants are not gonna have osteo necrosis of the lunate AKA Keenbox disease, but there is some sort of association between Keenbox and ulnar negative variants. We can see on the MRI, we would expect to see T2 hyper intensity which is non-specific, but it's the relatively confluent loss of T1 signal that is most indicative of osteo necrosis of the lunate. Similar findings, if they give you a scaphoid fracture, for example, the proximal pole, if it had confluent T1 hypo intense signal, that would suggest a vascular necrosis because as we know, the perfusion or the arterial structures that feed the scaphoid go from the distal pole approximately and so if you're a waste fracture, you have loss of the blood flow to the proximal pole and that would lead in a vascular necrosis which would appear similar just on a different bone in a different case. Here's that TFCC we talked about and so MRI would be confirmatory. CT is not gonna add much value, it's just gonna show you its sclerotic guess if it is, it can help, but it's not super sensitive. Bone scan, not super useful in this particular case. Bone age, not particularly useful in this case. Okay, hands. What is the best treatment for this pattern of disease? Survey says 64% NSAZ slash conservative, 24% DMARDS and biologics, 12%, nobody wants to do distal interflames your arthroplasties for some reason, I don't know why, but okay, that is correct. 64% of you got this correct NSAZ, so let's just talk about general diagnosis of hand X-rays when it comes to arthritis. Things you wanna have a systematic approach, my approach is like, what is the distribution, right? Is it distal, is it proximal, is it in the classic distribution for osteoarthritis? And I would say in this case it is a classic distribution for osteoarthritis. One, we can see some triscapion, first carpal and a carpal degenerative change with productive changes, a little bit of sclerosis and joint space narrowing, that's indicative of osteoarthritis. And then we can also see the secondly most involved joints are the DIPs, second, third here and then second, third and fifth here. So distal interflangial and CMC and triscape very commonly involved joints for osteoarthritis. You didn't have to know this here, but we can see that there's central erosions, which is our goal wing deformity here of the fifth DIP, for example, second DIP here shows it quite nicely so that combination of central erosion and peripheral osteophyte formation and productive change is most consistent with erosive osteoarthritis, which is generally treated conservatively or with NSAIDs. Demards and biologics might be given for rheumatoid arthritis or other inflammatory arthropathies. Rheumatoid arthritis we kind of touched on before, but it mostly is the MCPs and other common areas, the ulnar erosions, either the styloid process or of the fovea, for example. So you wanna take a quick look if you're about to call something negative or you're not sure what's going on, take a look at the ulnar, you may see some subtle erosions there. So we talked about distribution is one thing, right? So MCPs would be more proximal diseases, more likely to be rheumatoid. But then the other thing is like, is it predominantly productive? Is it predominantly erosive? Or is it both? Okay, cause that's gonna help. There's a couple of things that can give you a combination of productive and erosive changes. One is this, the other is psoriatic arthritis. Psoriatic arthritis can give you this fuzzy, periostal reaction of the DIPs and it can also give you some erosions and it can be markedly destructive. You can have ankylosis and psoriatic arthritis. I mean, technically anything can happen to anybody, but that is the classic. If the patient reads the books, so the two like mixed productive and erosive ones would be this, erosive arthritis and psoriatic arthritis, but the distribution of psoriatic probably might spare the CMCs and triscapes. You might have this fluffy, periostal reaction. You might see ankylosis and you're not gonna see this gullwing deformity either because the central erosions is classic and erosive, osteoarthritis. But the penicillin cup would be more psoriatic, for example, where there's more like ointee, middle phalanges and cupping of the distal phalanx. Okay, there's a bunch more findings associated with those things. You can look up on the interwebs. Like this case, relatively subtle but real. What is the most likely underlying laboratory abnormality? That is not actually how I say laboratory, but sometimes just like to keep it interesting. Survey says increased serum PTH. Increase SRCRP would be next choice, 19 and 14% decrease serum PTH. So this one would be increased serum PTH. I was going for hyperparathyroidism and we can see here that there is relative lucency of the ischial tuberosities. And fairly they're kind of ragged and indistinct and we don't see like a nice cortical margin. Similarly, the pubic synthesis is not well seen. Similarly, many of you may have perceived that the SI joints were relatively wide and indistinct. There's a little bit of lucency of the femoral heads bilaterally. And then the iliac wings, also relative or crest relatively radiolucent. And so this subinsertional resorptive change or subarticular resorptive change can be seen in subligamentous resorptive change. All those things can be seen in hyperparathyroidism. So increased serum PTH was the answer I was going for. Increased SRCRP is possible if we were just going for like sacroiliitis, but it's unlikely to affect all these various areas if it's inflammatory arthropathy. Increased WBCs would maybe be seen in the setting of like infection, but again, this is multifocal like subconjural, subligamentous subteninous resorptive changes, which can be seen in hyperparathyroidism and decreased serum PTH. The clue here is there's two answers that contradict each other so that likely that one of them is correct. And in this case, it's increased serum PTH. Could be primary, could be secondary, depending on the patient and their clinical situation. I like this case too, actually. Okay, these images are not on the next slide. So really look at them. There's a thing here. There's a thing here. This looks like some sort of ghost cartoon character, but not relevant to the examination. Here, here. Look at everything else too. Maybe there's hidden clues on the image. Here's the next image. This is a radiograph that's a few months later. This is a GRE from the initial MRI. Scout, GRE scout. Conservative management, well done. 70% of you got it correct. And so yeah, so the answer we were going for here is myositis ossificans, okay? So we look at the MRI, which is the way this patient presented initially. We see this T2 hyper intense mass within the anterior hip musculature, let's say. It does kind of have this low signal intensity rim, which is confirmed on this gradient echo scout that there's this peripheral low signal intensity, which can suggest peripheral mineralization. Similarly, the initial radiograph shows this hazy mineralization here in this general area. And we can see subsequently on the followup radiograph that this tends to have trabecular markings, maybe some peripheral cordication, and begins to resemble mature bone. And that's indicative of myositis ossificans. And the alternative diagnosis, which is more sinister would be an extra skeletal osteosarcoma. If you thought this was osteoid matrix, but classically extra skeletal osteosarcoma tends to have central mineralization first, and then peripheral-label mineralized. It shouldn't ossify, it would be more dense without trabecular kind of pattern. And then the other clue here is this patient is an obvious bone former. Sometimes patients who are HO formers, it's kind of like keloids, for example. People or some people are just more predisposed to having HO or MO and being inflammatory bone formers when they're traumatized. We can see this AIIS and rectus femoris tendon have ossified from prior trauma, which can be a clue here in this particular instance. So these things would be radiation, neoadjuvant systemic therapy could be used to treat more sinister neoplastic deologies like extra skeletal osteosarcoma, whereas conservative management for myositis ossificans. You don't wanna biopsy MO because it can look like osteosarcoma histopathologically and you put your pathologist in a tricky situation and it's not unheard of for folks to have had kind of amputations and more aggressive surgeries for MO that was biopsied and thought to be osteosarcoma. So biopsy would not be a good next best step for this particular patient. I think follow-up imaging, if you think it's likely MO would be the next best step. Okay, here we are. The imaging findings are most likely related to chronic renal failure. Love that for you guys. So actually many of these choices are possible answer choices, but the best answer choice is in fact, chronic renal failure. So what we see is large areas of T2 hyperintense signal with maybe some layering hypointensity. We can see on the CT, corresponding CT, that there's these large areas of globular mineralization, periarticular distribution and that's most in keeping with metastatic calcification or tumoral calcinosis. In my quick Google search, there's preferred terminology metastatic calcification is more broad whereas tumoral calcinosis is supposed to primarily be used in patients who have like milk alkali syndrome. But in this case, you're given a CT, coronal CT slice and we can see their kidneys have these multifocal cysts bilaterally, which can suggest end stage renal disease and there's somewhat maybe ash feed. So that's kind of what I was going for is the best answer choice in this instance is chronic renal failure. So I guess the point I want to give you here, even if this question wasn't the most ideal one, is that on the test, if you are in a situation, again, I'm not a ABR exam writer. I'm just a dude who took the boards, whatever, seven years ago or something like that, six years ago. But they're not really always testing facts, okay, fact recognition. They also want to see like, can you think like a radiologist and radiologists are responsible for everything on the image. And if there's multiple correct answer choices to you, I would highly recommend a second look at the image to see if there are any pieces of information that you may be missing. And in this case, it's windowed, it's tricky because it's windowed for the bones, right? But you can still see some solid organs and see if there's any additional information that you may be missing that can help you point to the best answer. And this one, I was gonna go with chronic renal failure. It seems like many of you agree, hopefully for the same reason. Okay, here is an AP in lateral of the knee. What is the most likely diagnosis? This was just a first order question, not second in this case. Nice, okay, what is the most likely diagnosis? 79% of you are gonna correct, which is giant salt tumor bone. A couple of few folks thought maybe congrosarcoma or contrablastoma. And I think those are reasonable. And let's talk about why giant salt tumor bone is the best choice, okay? So similar to hands, I have an approach to these things. And for me, first thing is first is, what is the patient's age? Are they skeletally mature or skeletally immature? Do not expect them to give you that information on a test if you can ascertain it by the image. We can see the ficeal plates are closed. This is a skeletally mature patient. The next thing is it a metaphyseal, diaphyseal or epiphyseal lesion. And we can see on the lateral view that there is involvement of the epiphyseal bone, extends to the articular surface, which is classic for a giant salt tumors of bone. And so we have a radiolucent lesion with marked endosteal scalping and thinning of the cortex. There's no real matrix, right? So the next thing is like, is there matrix? Is it chondroid? Is it osteoid? Or is there no matrix? I guess you could hallucinate and say like there's some curvilinear stuff in here. Maybe that's chondroid matrix. But an m-chondroma generally is not gonna appear like this. They're not usually epiphyseal and don't abut the articular surface are more common in the hands and wrists, but they can be seen in any parts. Usually they're gonna have curvilinear matrix, suggestive chondroid matrix. They can have some endosteal scalping, but usually don't have marked endosteal scalping. The other is a geode. There's not really any osteoarthritis here, maybe some minimal, but so you're not gonna see a random geode the patient doesn't have pronounced osteoarthritis, most likely. Chondroblastoma is usually an epiphyseal lesion in a skeletally immature patient and it can be markedly inflammatory, but this is a skeletally mature patient, so not likely to be chondroblastoma. Chondrosarcoma tends to happen in very old patients, malignant degeneration of an m-chondroma. You might see endosteal scalping, greater than 50% of both lignus cortical breakthrough or soft tissue mass. But this patient doesn't look that old and you don't have any history that suggests that this was previously an end-chondroma, although it's not an unreasonable answer choice. So the best choice here is giant salt tumor of the bone. If you were in person, I would ask you, is it benign or malignant? Hopefully you would say it's benign. I would ask you, can it metastasize though? And it can sometimes rare cases can metastasize to the lungs. So giant salt tumor bone, again, epiphyseal lesions, articular surface extension, middle age, usually 30s, 20s, people who have chlorose growth plates and can be markedly, it's usually well circumscribed and it can really thin the bone and it's generally benign, but it can metastasize. That's the best choice here. Okay, moving on, what is the most likely complication based on the above images did not correct this one? Arthrofibrosis, okay, great. 74% of you got it correct. We can see we are presented with axial T2 fluid sensitive sequence or a T2 fat suppress sequence and we are presented with the sagittal proton density sequence. Why is this not a sagittal T1? We can see a little blip of joint fluid in here, which is not hypo intense. It is actually hyper intense or intermediate signal intensity. We can see that there's an anti-recruciate ligament reconstruction and can in some instances be too far anterior or too far posterior. If it's too far anterior, you can get what's called roof impingement where the ACL graph is impinged upon by the intercondular notch roof. If it's too far posterior, it can result in persistent insufficiency of the anti-recruciate ligament. Here though, we see this big focus of nodular signal in the deep aspect of Hofus badpatter and the intercondular region. On the axials, we see it as this U shaped structure. And if you were putting in an arthroscope here, it might look like an eyeball staring back at you, which is our cyclops lesion or arthrofibrosis patients can present with incomplete ability to extend their knee or pain, loss of ROM after post-op physical therapy and all that. So arthrofibrosis is the question. You can, if the patient is persistently symptomatic, they may go in and resect some of this tissue to allow the patient to extend more fully. Adhesions, it's possible, but nothing in this case to suggest that. What is the most likely diagnosis? Spondyloarthropathy. Okay. All right, so let's talk about it. Secondary hyperparo is a close second. So we do see here that there's chlorosis of the sacroiliac joints. It tends to be on the CT. We can see relatively isolated to the iliac side of the joint. And the sacral side is not as involved here, if at all. We can see a relatively normal peripheral margin of the sacrum, whereas the resorptive change in this case is mostly on the iliac side, okay? Which is one way to differentiate sacralitis versus subconjural resorptive changes or subarticular resorptive changes in that. And similarly or to another case before, this right kidney is looking super atrophic and the left kidney is a little bit atrophic. So these are actually resorptive changes in the setting of secondary hyperparathyroidism. And so that's what I was going for. In this particular case, again, it's more, the two clues are that it's relatively isolated to the iliac side of the bone, which is more indicative of resorptive changes rather than erosions related to sacroiliitis. And then the kidney, the other question I have, there's an axial CT of the kidneys that confirms in a abdominal window that they're small in atrophic, but wanted to make it a little bit more challenging for you. So again, use everything on the image. And then again, that this is isolated to the iliac side is more indicative of secondary hyperparas. Spondylarthropathy could have a similar appearance, but probably not the best answer give for the aforementioned reasons, RA, not really common presentation for RA and insufficiency fractures would be more in the sacrum. We'd see vertically oriented areas of irregularity or sclerosis, which could suggest insufficiency fractures, either bilateral on a nuclear medicine bone scan. You might see your Honda sign, which is focal hypermetabolic activity in the H-shaped distribution. We could suggest insufficiency fractures. Okay, what is the most likely diagnosis? 96%, yeah, that is correct. This is a meniscal flounce. It is just a little bit of hypermobility of lateral meniscal tissue that results in this kind of undulating appearance. It is not pathologic. It is not more prone to tearing. There's no other consequence to this except for knowing that it is a variant that is not pathologic. So you don't want to call this a tear. This is a meniscal flounce. What is the most likely associated serum abnormality? Elevated alkyphos, that is correct. Elevated PTH inviting a decreased vitamin D or the other options that people chose. This is indicative of pageant disease. We can see trabecular coarsening. We can actually partially see in the femur here similar findings, thickening of the cortex. We can see trabecular coarsening as well. And this is most indicative of polyostatic pageant disease which is actually the most common relative to monoostatic pageant disease. And people with pageant disease, the most common abnormality of the serum would be elevated alkaline phosphatase. Elevated PTH could be seen in hyperparathyroidism. Ricketts, decreased vitamin D, deficiency. And then inflammatory atheropathy, elevated DSR, CRP or pretty nonspecific, it can be an infection and other reasons, but this was pageant disease or again, trabecular coarsening, cortical thickening, most indicative of pageant disease of the bone. Here's another manifestation of pageant disease. You can see this kind of blade of grass appearance with a bevel or sharp edge here that can be indicative of pageant disease in the leading edge of the osteolysis. Same patient as we saw on the CT, we can see on the MR, if they wanna be funny and make it somewhat challenging potentially, they can show you these linear trabecular coarsening or cortical thickening on the MRI with preservation of the marrow. Okay, a new question. What imaging finding is not depicted? Survey says sinus tract or invalucrum. Okay, so here the answer is sinus tract. Okay, so we can see in the distal radius, there's this area of lucency which corresponds to this area of fluid signal intensity on this fluid sensitive sequence. We can see that there's a full thickness disruption of the cortex here at the molar aspect of the radius and that's most indicative of a cloaca. A sinus tract would be if the fluid signal extended to the skin surface and that would suggest a sinus tract. Intraseus abscess is present, this is a Brody's abscess and the invalucrum is the like sclerosis and increased cortical bone formation which we can more easily see on the lateral view that there's all this productive cortical change and excess additional bone formation as a reactive change. This sequestrum which was not an answer choice would be if there was a little island of sequestered dead necrotic bone within the center of this invalucrum that would be most indicative of a sequestrum and all of these findings amount to be chronic osteomyelitis this is what you might see in chronic osteomyelitis. Yeah, so we have a Brody's abscess, we have a cloaca, we have a soft tissue, extension of fluid, we do not have a sinus tract, we do have invalucrum which is the success bone formation and then we do have the cloaca. No sequestrum, but that was not an answer choice. Okay, and last but not least on this momentous occasion what is the most likely diagnosis? Sirius says miloryostosis and that is correct. We can see this kind of dripping candle wax appearance of sclerotic bone here. Oh, the second metatarsal, you can even maybe see of the second or the intermediate cuneiform in his most indicative miloryostosis. Alleles and befuchies are like of hands and feet where you get multiple end con dromas. Think in befuchies you can also have associated vascular malformations or vascular lesions and one of these two is more associated with malignant degeneration I think of end con dromas. I don't wanna give you black pearls so I would encourage you to look it up. Multiple familia exhaustosis as if there was multiple osteocondromas which we don't see osteocondromas should have cortical medullary continuity, a cartilage cap. Remember osteocondromas can degenerate into conjo sarcoma, generally an older population and if that cartilage cap is too thick, some literature suggests 15, some literature suggests 20 millimeters. Anyways, here nor there in this particular case but it's factoids to be familiar with for future patient care purposes. So that brings us to the end of this evening and I appreciate everybody's time. Hopefully you found this to be useful even if the cases weren't ideal. Hopefully the thought process and going through things that you should be considering when you're going through these cases in real life and on the test, again we're testing just to see how your thought process is as a radiologist, not necessarily how well you can remember or memorize stuff, a little bit of both probably. So thank you and I'll let the modality team take it home from here. Well, thank you Dr. Ferragi for that awesome case review, that was great. And for everyone else for participating we really appreciate it. Be sure to join us Monday, April 8th for another one of these with Dr. Aaron Gomez. He'll lead us in a rapid review of GU cases. You can register for at the link provided in the chat and follow us on social media for updates on future case reviews. Thank you so much again for learning with us. Good luck on the boards and we hope to see you soon.