Hello, my name is Jiwoo. I'm the chief of MSK Radiology at Beth Israel Deaconess Medical Center in Boston. Minority objectives are to first understand the imaging appearance of cellulitis, ulcer, and sinus tract. And we're going to recognize some imaging pitfalls and mimickers of these conditions through a series of cases. All right, case one. A 60-year-old woman with a recent diagnosis of diabetes and was admitted for fever, cough, and a left lower extremity rash. So on the T1 and weighted image, we can see that there is this reticular pattern to the scufcutaneous tissue on the left side. On the T2, we see that there's quite a bit of edema that's localized just to the superficial top tissue. It does not involve the underlying muscle or the bone. And on the actual images, again, this reticular pattern on the T1, extensive edema on the T2 weighted images. And in post-contrast, we can see that there's quite a bit of an enhancement of the scufcutaneous tissue as well as the skin, but no rim-enhancing collections or involvement of the underlying bone or muscle. So this is a case of cellulitis. So cellulitis is a non-necrotizing bacterial infection of skin, subcutaneous tissue, and superficial fascia, usually due to strep or staph in a high-risk population. They can present with warmth, swelling, tenderness, and usually have signs of infection such as fever or leukocytosis, most commonly in the lower legs like in this case. And one key point is to remember that you do not need imaging to diagnose cellulitis. This is a clinical diagnosis, a visual diagnosis. We do imaging when we're assessing for complications of cellulitis like abscess, polymyositis, or osteomyelitis. So we don't know what's underneath that skin, but we don't actually need imaging to diagnose cellulitis itself. But we see cellulitis all the time on imaging, and it's important to recognize that. MRI is going to be our most important imaging modality. It appears as a reticulated pattern on T1. On T2, we usually see high signal or fluid signal within the subcutaneous soft tissues. And in these areas, it should enhance. Now, this can depend on the vascularity to that body part and also the timing of the image acquisition, but in general, cellulitis should enhance. On ultrasound, you can get this cobblestone appearance on ultrasound. And here's what cobblestone looks like in case you haven't seen this. Case 2, so we have a 40-year-old man with hepatitis C and bilateral calf pain and swelling and mild erythema for five days. So on the T1-weighted image, we can see that there's loss of the subcutaneous fat within the soft tissues bilaterally. And on the T2, we can see that there's extensive amount of edema. And this is not a T1. This kind of looks like a T1 because it looks like there's a lot of subcutaneous fat, but that's actually really edema within the subcutaneous soft tissues. So replacement of the subcutaneous fat on the T1, extensive edema on the T2. And on post-contrast imaging, there's actually no enhancement. So this would not be good for cellulitis. And in this case, this is a case of bland edema, which is excessive tissue fluid in the interstitial spaces. It's usually going to be bilateral and circumferential instead of unilateral and focal like we see with cellulitis. And it's going to be seen in systemic processes like patients with CHF, low albumin, renal disease, and they should not have systemic signs of infection. And also an important finding is that there should not be enhancement in cases of bland edema. And they should obviously also lock the ancillary signs like ulcer, abscess, or sinus tract that we would expect to see in patients with infection. Case three, we have a 44-year-old man with bilateral foot, feet, soft tissue masses. He had a history of Graves' disease, which is treated and now has post-ablative hypothyroidism. So in the T1-weighted images, we can see the skin thickening, these low T1 structures here within the medial feet. And these are high signal on T2 or slightly heterogeneous. Again, low signal on T1, high signal on the both feet on the medial aspects here. And on post-contrast, also no enhancement. So this also would not be good for cellulitis given the no enhancement in these patients. And also given the history of the thyroid disorder, this is very good for thyroid acropathy, which is the term acropathy is thick extremity in ancient Greek. It's a rare extra thyroid manifestation of autoimmune thyroid disease. It's seen in only a small amount of people with Graves' disease, but it is one of the most common extra thyroid manifestations in these processes. And so they present with soft tissue swelling, digital clubbing. They can also have periosteal reaction. The cause of this is unknown, but it's thought to be due to stimulation of the fibrograst by the autoimmune response that leads to production of these masses. On imaging, it's going to look like low T1. Variable on T2, which depends on the content and amount of collagen and the edema in the soft tissue. And there typically should not be enhancement of those structures like we saw in this case. All right, so there's quite a bit of processes that can mimic cellulitis. And these are the disorders here. Some of these are bilateral. Some of these are unilateral. Here's a case of CHF, which is usually going to be bilateral and symmetric. But one of the main issues is that these structures typically will not have enhancement and should not have systemic signs of infection. This is a case of unilateral cellulitis mimicry in a patient with lymphatic obstruction. We can see enlargement of the right lower limb, but it has this reticulated pattern, skin thickening, that we may see with a patient with cellulitis. All right, case four with a 56-year-old man from Puerto Rico who had trauma at a young age to the lower leg and now has a chronic pain within that lower leg. Presents with a three-month history of enlarging mass, which has not improved on antibiotics. On imaging, we can see this very large, fungating, ulcerating mass within the tibia with bony destruction that we can see here on the CT really, really well. On the MRI, we can see that this is a large soft tissue process here that's eroding into the bone with a soft tissue ulceration here on the T1 and T2 and has prominent enhancement within the subcutaneous tissue. All right, so what is this process? Well, this is a case of invasive squamous cell carcinoma, otherwise known as a marginal ulcer. I really wanted to show this case to demonstrate that not all ulcers are due to infection. And so we do want to include that, but there are other processes. So a marginal ulcer, this is due—a squamous cell carcinoma that can occur in an area of traumatized tissue, whether that's skin or subcutaneous tissue or even bone. It's actually the most common malignancy in chronic osteomyelitis, and it's due to irritation of the skin and soft tissue, which leads to exposure to growth hormones, which is thought to lead to the formation of the squamous cell carcinoma. Very poor prognosis and a fairly high metastatic rate. And the treatment is with aggressive surgery. A little bit about ulcers. Remember that ulcer just represents a breach in the skin. It can be limited to the dermis, but it can also extend to the epidermis, dermis, subcutaneous tissue, or even extend deeper into the muscle or into the bone. These are often seen in patients with diabetes or who are immobile. And once you compromise the skin defense, this leads to poor perfusion and creates an ideal environment for infection. MRI can be really helpful for assessing the extent of the infection and for surgical planning. One important thing is that the ulcer should not be seen in people with just Charcot arthropathy, which are not infected. This happens—this is a common scenario. We have a patient with Charcot, and we want to know if it's infected or not. Whether or not there's an ulcer really makes a big difference. In this case, we see that there's edema in the subcutaneous tissue, but the overlying skin is intact. So this is a case with just Charcot, no infection. However, in this case, we see an ulcer. So this patient has cellulitis and osteomyelitis. There's a bunch of ulcer mimickers. These include vascular occlusive disease, vasculitis, tumors like the squamous cell carcinoma that we saw, scleroderma, pyoderma gangrenosum, and a couple of other of these disorders that can mimic infection ulcers. All right, our last case is a 64-year-old man with painful foot mass and skin defect, no history of trauma. Here on the X-ray, pretty unrevealing, so this led to us getting an MRI. On the MRI, we see that there's a skin defect here, and then there's an additional structure that goes a little bit deeper. On the T2, we see that there is a hyper-intense lesion here and a lot of skin, a lot of soft tissue edema. Once we gave contrast, it looks like there was a rib enhancing collection in here. So they wanted us to do an aspiration. And when we did it on the ultrasound, we see this very echogenic structure, and this turned out to be a wood splinter. And so this is a case of a sinus tract with a foreign body granuloma and abscess. And remember that foreign body granulomas, these are inflammatory response to the foreign body. The foreign body often forms an enhancing area of granulation tissue. This is another case of a wood splinter. And these can be associated with an abscess or a sinus tract that extends from the puncture site. So sinus tracts, so these are abnormal channels from the skin to a deep-seated focus of infection. They can contain fluid, granulation tissue, necrotic debris, or pus, and it's best evaluated with MRI. But you really want to give contrast. Because what you're really looking for is that enhancing structure going into the deep abscess. In this case on the T1, very hard to see what's going on in here. We give contrast, we can see the skin defect, and we can see the abscess here in this location. So in summary, cellulitis, ulcer, and sinus tracts are superficial tissue infections best evaluated with a contrast MRI. Imaging is really not necessary for their diagnosis, but that can help identify deeper sites of infection. And there are several non-infectious mimickers of these disorders, and they often are due to underlying systemic diseases. So it's very important to take a really good clinical history. Thank you so much for your attention and time. Good afternoon, everyone. So in this talk, we'll be focusing on necrotizing soft tissue infections, in particular, necrotizing fasciitis. I am Patrick Amoumy, speaking to you from Lausanne in Switzerland. And unfortunately, I could not attend in person this year as expected because I was hit by COVID myself and still recovering from it. The reason why it was more reasonable to turn my camera off. As musculoskeletal radiologists, we are not used to dealing with life-threatening situations or conditions. And necrotizing fasciitis is one of these rare cases. One out of five patients with necrotizing fasciitis will die from it. And out of those surviving, one of five will be amputated. So we're dealing with a serious condition, a rapidly spreading infection with severe systemic signs of sepsis, usually occurring in a patient with predisposing factors such as immunosuppression and so on. This rapid spread is due to the thrombosis of the blood vessels in and around the fascia extending to the deep fascia. Then thrombosis and tissue necrosis will impede the penetration of antibiotics. The reason why this condition requires surgical treatment as illustrated by the adages used by our surgeon colleagues. And these adages also convey a sense of urgency. Indeed, the time to surgery is one of the main prognostic factors that can decrease mortality. So as a rule, imaging should never delay surgery. And the type of surgery we're talking about is a large, deep exploration down to the fascia, looking for pus or necrosis, fasciotomy and large debridement, which can be very impressive, as you can see on those images, all the way to amputation. So a very serious condition. And in practice, the main diagnostic problem will be to differentiate non-necrotizing soft tissue infections, which can be treated medically from necrotizing soft tissue infections, which do require surgical treatment. And among those, the deeper necrotizing soft tissue infections, mainly necrotizing fasciitis, will require emergency life saving surgery. So why is it difficult in practice? Well, first of all, because these infections are rare and physicians are not necessarily used to deal with them. The clinical presentation is also a specific, especially in the early phases of the disease, and biological diagnosis and scores that have been proposed lack sensitivity. So we more often than not perform imaging in those patients which are doubtful. And we as radiologists have to learn how to differentiate non-necrotizing and necrotizing soft tissue infections and localize. And this will be the objective of our talk here. Before we jump in, let's make sure that we're talking about the same thing. And when we're dealing with fascia, we're basically talking about three different types of fascia. The first one is running in the subcontinuous fat, between fat lobules. The second one is around the muscles. And the third one is between the muscles. And if you look at the literature, these structures can be referred to with different terminology. The word superficial and deep can be used to refer to different structures, actually, which can be very confusing. And this talk will try to simplify this and use this adapted terminology. We'll refer to the cutaneous fascia or skin fascia or hypodermis, to the deep peripheral fascia and the deep intermuscular fascia. So the next question is, which imaging modality to perform? And the answer will be basically depending on the clinical and biological context. If you have high suspicion, you don't need any imaging at all, as we already saw. Depending on the sense of urgency, you may need CT, which is fast and available. And this is the modality that has been proposed by the organizer of this session, Dr. Elia, in this consensus paper. But whenever you have the time and possibility, MRI is always better for soft tissue characterization, as we all know. And so this will be the preferred modality in that setting. IV contrast is not required, and more often than not, contraindicated. But if possible, we do use it, especially because it allows better characterization of abscesses and necrosis. And what about ultrasound? Some people have used ultrasound in this setting. And we certainly do not advise the use of ultrasound in this setting. To illustrate it, this is a case which basically was falsely reassuring, and we completely missed those areas of gas. If you put your probe here in these patients which have limited mobility, you may miss all these areas of gas in this setting. And this was a typical case of Fournier gangrene, with the gas extending in the cutaneous fascia as well as the intermuscular fascia. And that is very specific for the diagnostic of necrotizing fasciitis. The presence of soft tissue gas can also be detected by MRI, obviously. You look for areas of absent signal, both on T1, T2, and all your sequences, actually. And this was here associated with extensive signal abnormalities inside the muscles and around the fascia as a typical case of necrotizing fasciitis. However, some theories have reported that the gas is only present in less than 50% of cases. So while a good sign of necrotizing fasciitis, it is not always present. And this was a case of necrotizing fasciitis proven by surgery with obvious involvement of the peripheral fascia. But more importantly, of the intermuscular fascia, which is a sign you need to look for the fat in between the muscles here completely obliterated. And it is associated with areas of lower enhancement of the muscles as signs of necrosis, as confirmed by surgery. On the other hand, if you do have gas, it doesn't necessarily mean that you're dealing with fasciitis, especially if it's localized, as it was the case here in these absences. This was a non-necrotizing soft tissue infection with extensive cellulitis as confirmed by surgery. So the pattern you need to look for is this pattern of gas extending along the fascial planes, as you can see in this cataract case here. This is a case of necrotizing superficial soft tissue infection or cellulitis. You can see the involvement of the skin, the hypodermis, as well as probably the fascia with some areas of lower enhancement. However, important finding the fat in between the muscles here in the posterior compartments is intact, indicating that there might not be fasciitis as confirmed here by surgical exploration. Here, a case of typical necrotizing fasciitis, signal abnormality starting in the skin, going deep down to the peripheral fascia. More importantly, with signal abnormality in between the muscle in the intermuscular fascia, as well as areas of absent enhancement as a sign of necrosis. Another case, which was pretty similar, cellulitis superficially going down to the peripheral fascia, as well as the intermuscular fascia over here. This was diagnosed by the radiologist as necrotizing fasciitis. However, the clinicians found the clinical presentation pretty reassuring, and they decided to treat the patient conservatively and successfully. This was a non-necrotizing soft tissue infection responding to medical treatment. These cases illustrate to you that the diagnosis can be challenging. The presence of gas and the presence of intermuscular involvement are good signs of necrotizing fasciitis, but there's a need to refine these imaging criteria. This has been attempted by several authors in the last 30 years or so. I'm going to summarize for you a few key points from those papers. First, the presence of gas along fascia is specific, but not sensitive for the presence of necrotizing fasciitis. Second, the involvement of the intermuscular fascia is, on the other hand, sensitive, but not specific. If you want to increase your specificity, you need to look for thickened fascia, multi-compartmental involvement, as well as areas of partial enhancement indicating the presence of necrosis. Indeed, if you go back to the two cases I've just shown you, the necrotizing fasciitis did show some thick intermuscular fascia as opposed to thin intermuscular fascia in the case of non-necrotizing infection. Multiple compartments were involved in both cases, but a little bit more so in the necrotizing fasciitis, where partial enhancements were also seen. This could not be assessed on this case because no contrast could be used. Overall, this diagnostic challenge might be overcome by combining the imaging and lab findings, which was shown to slightly improve the diagnostic performance, but this remains a diagnostic challenge in practice. So, a few take-home points. Necrotizing fasciitis does require emergency life-saving surgery, and imaging should never delay surgical treatment. In those doubtful cases, imaging can be performed, and we will be looking for gas along fascial planes, indicating that you're almost certainly dealing with necrotizing fasciitis. On the opposite, if you have no involvement of intermuscular fascia, you're probably not dealing with necrotizing fasciitis. If you have involvement of intermuscular fascia, this is a good sign, quite sensitive for the presence of necrotizing fasciitis, but not specific, so you need to look for thickened fascia and multi-compartment involvement as well as areas of partial enhancement to increase your specificity. Involvement of peripheral fascia only or limited involvement of intermuscular fascia remain of uncertain significance, and for these cases, close collaboration with the clinicians is key, integrating clinical, biological, and imaging data. If you want to go further, you have the references in my talk, including this one by Jacques Malgin, that we published a few years ago. Dr. Malgin was one of my mentors and probably one of the best MSK radiologists I've ever seen. He's also provided me with great material for this talk, and with that, I thank you for your attention. This is Corey Yablon, and I'm going to talk about septic arthritis and its mimics. We'll discuss common presentations and imaging findings of septic arthritis and describe mimics of septic arthritis, including rapidly progressive idiopathic arthritis, rheumatoid arthritis, and the crystalline arthropathy. The delay in diagnosis is the number one cause of poor outcomes in patients with septic arthritis. The mortality is 7% to 18%, and loss of joint function occurs in up to 46% of patients. It occurs most commonly in the knee, and much greater so than in the hip and other joints. Staph aureus is the most common pathogen, occurring in 56% of cases, followed by strep, and then gram-negative rods that also occurs in IV drug users. It's important that we make a quick diagnosis to prevent joint damage. The classic presentation is monoarticular joint pain with erythema, warmth, and swelling, pain on palpation, and pain with ambulation, inability to bear weight. A patient will have fever, elevated white count, sed rate, and CRP. However, the classic presentation doesn't always occur. Patients may present with no fever or a low-grade fever. Patients may present with intermittent pain or a slow presentation of pain. They might not have an elevated white count, and they might even have a lower white count if they are immunocompromised. And ESR and CRP values can be anything from low to high. Causes are hematogenous spread, by far the most common, occurring during transient bacteremia with occult infection or flagrant infection. Also, continuous spread from adjacent infection and direct inoculation of a joint, either iatrogenic or through trauma. 22% of patients have no risk factors, but the most susceptible patients include elderly, IV drug users, immunocompromised, rheumatoid arthritis patients, and those with pre-existing joint damage. This is not an imaging diagnosis, although we always start with an x-ray to get the lay of the land and to assess the joint before any intervention. We consider MRI if there's a non-joint-related process suspected, or to look at alternatives to the diagnosis. Ultrasound is useful to assess for fluid, however, may be unreliable in the hip in patients who are very obese or who have an implant. It can really underestimate the amount of fluid present. Aspiration is the gold standard for diagnosis, and we want to send any aspirate for cell count and differential, gram stain and cultures, and crystals. We want to inject contrast to look for a sinus tract, abscess, or a bursa communicating with the joint. The first case involves a 29-year-old female who is an IV drug user who presents with acute right hip pain. Serum labs are normal white count, elevated sed rate, and CRP. The radiograph shows possible mild osteopenia in the proximal right hip, but really no erosion or overt joint space narrowing. The same-day MRI shows a large joint diffusion distending the joint capsule. Also, pericapsular spread of fluid into the surrounding muscles and along the fascial planes. There's not much in the way of narrow edema. The fluoroguided aspiration yielded 5 cc's of straw-colored fluid. It distended the joint pretty well. There was no bacterial growth. The cell count was on the low side with 87% neutrophils. Synovial aspirate showed uric acid crystals and serum uric acid was elevated. So the patient was discharged home on a prednisone tamper with the diagnosis of gout. However, the same patient, 12 weeks later, came back to the ED. And this time, there's osteolysis of the proximal femur, femoral head, as well as of the acetabulum. There's also soft tissue swelling around the joint with effacement of the normal fat planes. So again, this was a good presentation for septic arthritis. 15 cc's of blood-tinged fluid were aspirated and this grew methicillin-resistant staph aureus. The patient was then sent for irrigation and synovectomy. This contrast injection in this patient shows multiple lobulated filling defects. This appearance is nonspecific, but it is often seen in patients with septic arthritis and any patient who has synovitis. And that can be in autoimmune diseases, inflammatory arthropathy, crystalline arthropathy, et cetera. Any case where the synovium is inflamed. In the second case, we have a 77 year old female with acute left hip pain. She had an intra-articular steroid injection five months before. The aspiration yielded nothing. It was a dry tap. The x-ray taken at that time shows marked osteolysis, bone loss, half the femoral head is gone, and there is bone-on-bone articulation here with small osseous densities, probably some bone fragments within the joint. This is the patient five months prior. She had severe osteoarthritis with joint space narrowing. And that is the reason she got the intra-articular steroid injection to begin with. Given these findings and the absence of a joint effusion, the diagnosis of rapidly progressive idiopathic arthritis was rendered. And this used to be called rapidly progressive OA. It's defined by idiopathic joint space narrowing of greater than two millimeters or greater than half the total joint space within a year. This leads to joint collapse, and we see it in about 7% of patients after an intra-articular steroid injection. It's associated with a higher patient age, greater baseline joint space narrowing, and worse baseline osteoarthritis. The treatment is total hip replacement, and it's important to try to diagnose this condition as early as possible to prevent further loss of bone stock or vascular complications. The third case involves a 61-year-old male with a history of prior septic joints. He had a sudden onset of left hip pain and was unable to bear weight, yet an elevated weight count, elevated ESR and CRP as well. The radiograph shows joint space narrowing with possibly a few erosions in the femoral head. There's also some swelling about the joint and effacement of the normal fat planes. And the same-day MRI shows a bone erosion in femoral head, distension of the joint capsule, as well as extension of pericapsular fluid into the surrounding tissues. Post-contrast shows enhancement of the synovium. So this was a good look for septic arthritis. We aspirated the joint and got 12 cc's of opaque fluid. The cell count was very elevated in the infectious range, 224,000 white cells with 92% neutrophils. So while cultures were cooking, the patient was taken to the operating room for irrigation and debridement. However, subsequently the aspirate and both the intraoperative aspirate and synovial biopsies all came back for negative growth for bacteria. The RF factor, however, was elevated. So in this case, the patient was diagnosed with a rheumatoid flare and the presentation cell counts and imaging findings all mimicked septic arthritis. In the fourth case, we have a patient who has metastatic esophageal cancer, who was receiving chemotherapy and also has a known right rotator cuff tear. He had an acute onset of right shoulder pain and a fever, inability to move his arm. And the initial x-ray shows maybe a faint calcification and a zoomed up view shows again, faint calcification in the region of the subacromial subdeltoid bursa. Subsequent to that, a CT was performed and this showed fluid communicating between the bursa and the joint through the known rotator cuff tear and also several calcifications, both within the bursa and sort of lining the bursa here. SED rate was elevated, CRP elevated, weight count was normal. So the aspiration showed no growth, but did yield calcium pyrophosphate crystals. So this is a case of calcium pyrophosphate deposition or CPPD. The last case is a woman who presented with acute onset of right hip pain. And the radiograph on the left side of the page shows an amorphous calcification. The axial MR stir images show a lot of bone marrow edema in the vicinity of the anterior inferior iliac spine at the origin of the rectus femoris. We also see a low signal calcification at the rectus femoris origin. The sagittal image shows very nicely these calcifications surrounded by a ton of fluid and also some acetaminin bone marrow edema. So this was diagnosed as calcific tendinography. So calcific tendinography is caused by calcium hydroxyapatite deposition. It most commonly occurs in the rotator cuff, but calcium can extend from tendon into the surrounding soft tissues or bursa. The ill-defined calcifications are the most symptomatic and we also see a higher incidence of this in diabetic patients. So septic arthritis is not an imaging, physical or serum lab diagnosis. There's overlap between septic joint and its mimics and joint diffusion is almost always present. Aspiration is the test of choice. We wanna send that for cell count and differential gram stain and culture and to crystals. And radiograph and MRI may be helpful to rule out other causes of acute joint pain. These are some references and I thank you for your attention. So again, everyone, my name is Erin Alea. Today I'm gonna be talking about imaging of acute osteomyelitis. So objectives of my lecture will be to review the characteristic imaging features for acute osteomyelitis. For the purpose of this short 10 minute talk, I'm gonna be focusing on MRI. I'm gonna be talking about important diagnostic pearls and clinical considerations. And then finally, we'll review some common pitfalls in image interpretation. And a lot of the definitions and recommendations that you're gonna be seeing throughout my lecture really were echoed in the recent Society of Skeletal Radiology white paper on MRI nomenclature for musculoskeletal infection. So osteomyelitis is defined as an infection of bone involving the medullary canal. X-ray should always be the primary modality for the diagnosis of osteomyelitis. It's cheap, it's readily available, and as in a case like this where you're seeing multifocal areas of cortical destruction, it easily makes the diagnosis. MRI is gonna be useful for cases in which the radiographs are negative or indeterminate, but there's still a high clinical suspicion, or to further evaluate for soft tissue infection, including abscess. So the radiologists that interpreted these X-rays said, you know, possible cortical destruction along the tuft of the fourth distal phalanx, possible osteomyelitis, and MRI really easily makes that diagnosis. We're seeing confluent T1 marrow replacement within the distal phalanx, and also a portion of the middle phalanx. So to make a diagnosis of osteomyelitis on MRI, you wanna see confluent low signal on the T1-weighted images and concordant matching high signal on the fluid-sensitive images. MRI, by and away, is the best imaging test that we have to offer our patients to make that diagnosis of osteomyelitis. It has a sensitivity as high as 90%, and a specificity from 79 to 82.5%. If you give intravenous contrast, infected bone is gonna show avid post-contrast enhancement, as you're seeing here along the fifth metatarsal. And it's really important to remember, the population that we're seeing in our clinical practice, by and large, are the patients with a diabetic foot infection. In the diabetic foot, osteomyelitis is almost always going to occur, secondary to contiguous spread from an adjacent ulceration or sinus tract. And that's exactly what we're seeing here along the dorsal first digit. We're seeing a thin sinus tract in osteomyelitis of the first metatarsal. So this is the first really important pearl. The ulcer is such an important secondary sign because of that preponderance of contiguous spread. It's really going to improve our diagnostic confidence. And if you can't readily see that ulceration or the sinus tract, I encourage you to open up the clinical note to find the physical exam and see exactly where it's located. Also super important is the T1 signal pattern. This is really essential in making an accurate diagnosis. What you're looking for is a confluent pattern and a medullary distribution, as we're seeing here within the left greater trochanter, or complete marrow replacement of a geographic portion of the medullary canal. And this was first reported by Collins et al. It's another really important pearl. This pattern has a high association with osteomyelitis. But there are other T1 signal patterns that we see, including a reticular pattern, as you're seeing here within the first digit, where you see patchy areas of low T1 signal, but there are interposed areas of normal fatty marrow. Or you could see a subcortical distribution that we're seeing here along the plantar calcaneus, where you have low T1 signal that parallels the cortex, but measures less than three millimeters. So these patterns are gonna have a lower association with osteomyelitis. And often, as you all know in our clinical practice, we have these cases of discordant marrow signal. So we have high signal on the fluid sensitive images, but we don't have that matching confluent low T1 signal. And we're left wondering how to report this to our referring clinicians. When you see discordant marrow signal, you really need to look at the regional soft tissues. And if you look at the dorsal and medial soft tissues overlying the first digit, you're seeing the shallow area of ulceration with adjacent cellulitis. And this is another important pearl. Hyper-intense marrow on fluid sensitive images adjacent to an ulcer, sinus tract, or abscess needs to be interpreted as high likelihood of osteomyelitis, regardless of the pattern that you're seeing on the T1-weighted images. And this is so important. It's one of the major take-home points of the SSR white paper. And that's further echoed in this important study by Durea et al looking at outcomes in patients with diabetic foot ulcers and discordant marrow signal. Most of these cases, 61% with discordant marrow either had an initial histologic diagnosis of osteomyelitis or later progressed to osteomyelitis. And because of the findings of this paper, the SSR panel really recommends that we abandon this confusing term reactive osteitis. It's confusing not only to radiologists, but also to our referring clinicians. And if we think about discordant marrow, you really need to understand how marrow signal alterations occur over time. So remember, most of the patients that we see have a diabetic foot infection. This is going to occur due to contiguous spread. So infection first of the soft tissues, next of the cortex, and then at the later stage, the medullary canal. On MRI, the first finding you're going to see is high signal on the fluid-sensitive images. It takes time for fatty metabolization to occur to get that confluent low signal. That occurs later in the infectious process. So if we capture that patient prior to that confluent, that fatty metabolization development of that confluent low T1 signal, you're gonna be seeing discordant marrow. Yet the patient is still, either has osteomyelitis, or is on the path toward developing osteomyelitis. Also essential is understanding you need an intact vascular supply to produce these marrow signal changes. If you have a patient with avascularity or a hypovascular supply, you're not necessarily going to see the expected marrow signal alterations. And staying on the topic of a vascular supply, you know, I learned this from Dr. Rubin, IV contrast is really a useful triage tool. So as we saw earlier, infected bone should show exuberant enhancement, except when it's devitalized. And here you're seeing a geographic area of non-enhancement within the first distal phalanx tuft. Intravenous antibiotics are never gonna reach this dead bone. So you really need to look for devitalized bone and specifically report it. Also, exposed bone is most likely infected. Remember, the positive probe to bone test has a very high positive predictive value. But exposed bone may not have a vascular supply to produce T1 marrow replacement. So here we see a deep ulceration along the heel, extending to the cortex of the calcaneal tuberosity, where you're seeing a large bone infarct. Osteoclasts are never gonna get into this dead bone and produce the expected marrow signal changes. So when you see a case like this, you should report this as most likely infected, non-viable bone. And then finally, we all struggle with charcot arthropathy and whether or not there's superimposed osteomyelitis. So unfortunately, the uninfected charcot foot has a lot of similar imaging features to the infected charcot foot. For example, we often see cortical destruction, as we're seeing here along the midfoot. We see fluid collections, but this isn't an abscess, it's an adventitial bursa along the plantar aspect of a rocker bottom foot. And if you look at the sub-Q fat around this fluid collection, you can see that it's clean. This is different from what you would see if there was cellulitis adjacent to a soft tissue abscess. Patients with charcot arthropathy also have profound marrow edema, as you also see in osteomyelitis. But in the charcot foot, that marrow edema is gonna be periarticular. And if you go back to the T1-weighted images, it's not going to be confluent low T1 signal. Here you're seeing more of that reticular pattern with interposed areas of fatty marrow. The patient returned four months later and developed a new ulceration overlying the medial cuneiform, as you're seeing here. And then we saw this new confluent T1 marrow replacement within the medial cuneiform. So these new findings were enough to call superimposed osteomyelitis in the setting of charcot arthropathy. So the bottom line is when you see a charcot foot, if you have marrow signal abnormality with adjacent cellulitis, sinus tract, or ulcer, this should be reported as high likelihood of osteomyelitis. And here's another nice case along the plantar midfoot. You're seeing an ulcer, sinus tract, and adjacent osteomyelitis. So the pearls from this lecture that I really hope that you'll remember, the ulcer is such an important secondary sign. It really improves our diagnostic confidence. If you can't readily see the ulcer, find out from the clinical note exactly where it's located. T1 marrow signal in a confluent pattern with a medullary distribution has a high association with osteomyelitis. But hyper-intense marrow signal on fluid-sensitive images adjacent to an ulcer, sinus tract, or abscess needs to be reported as high likelihood of osteomyelitis regardless of the T1 pattern. And finally, IV antibiotics are really unlikely to reach non-enhancing bones. So you really need to point out and let your clinicians know if there's any bony devitalization. So thank you all so much for your attention. Email me if you have any questions. Talking about imaging of chronic osteomyelitis. Hopefully, if there's one thing that you take away from this talk, it's how great a resource this recently in print manuscript is. So thank you, Dr. Alea, again, for leading that effort. The goals of this brief 10-minute session are to clarify this terminology, which sometimes gets a little bit confusing in the later stages of bone infection. We can imagine this longitudinal continuum between acute and chronic sequelae of osteomyelitis. And it's tempting to think about it as this sort of linear march from left to right across the screen. But of course, we can imagine cases where abscesses will progress directly to sequestrum and also to cloaca. So important to stay nimble as we're going here from left to right. Let's start off talking about abscesses. So intraosseous abscesses, as we all know, these are pus-filled cavities with a rim of granulation tissue. We describe a particular variant of subacute chronic osteomyelitis as a Brody abscess that has a predilection for the ends of tubular bones. In general, we're expecting to see high signal on fluid-sensitive sequences, low to intermediate signal on T1-weighted sequences, peripheral enhancement, and if we use diffusion, reduced or restricted diffusion. So here's a nice example of an intraosseous abscess within the calcaneus. We see a nice focus of rim enhancement with this fluid collection within the bone. Notably there, we see a suture anchor. This is a 75-year-old man who had had a prior history of an Achilles repair with a chronic infection of the fiber wire in this area. Now, one thing that was interesting to me as I was trying to identify cases for this particular talk is how often the cases of intraosseous abscess in our case files at UCSF had patients who had a history of prior surgery. So that is a very helpful predictor if you're struggling with imaging findings if things aren't clear. That's a useful secondary sign, almost like the ulcer in the setting of acute osteomyelitis. Here's another case also in a postoperative patient. This patient had a history of an ACL reconstruction. We really don't see that much on the radiograph. Perhaps if we're squinting, we see that there's a little bit of thickening of the periosteum along the medial margin of the distal femur. Maybe I can convince you that there's a little bit of sclerosis here in the distal femur as well. MRI's gonna show things to much better advantage. We see this very striking fluid collection within that distal femur, extensive peripheral enhancement associated directly with the femoral tunnel and the hardware therein, a nice case of an intraosseous abscess. So the Penumbra sign is going to be a helpful sign that we can use to identify the subacute chronic form of osteomyelitis and this represents a rim of vascularized granulation tissue surrounding the abscess. Very key here is the T1 signal with a mildly hyper intense rim. That's gonna distinguish this from other lesions. This is seen in 75% of intraosseous abscesses. It's quite specific but not very sensitive for this diagnosis but helpful to distinguish these infections from neoplasm. So a couple of examples here. This is a younger patient in the proximal tibia. We have a lesion, maybe initially we're not sure if this is infection or neoplasm but again we can nicely see this T1 hyper intense rim along this biloped fluid collection. This is a patient with a staph abscess in the proximal tibia. Another case here, the patient with a much more extensive signal abnormality within the distal femur, so extensive it's almost hard to believe that this could be an infection but again we see the T1 hyper intense signal at the margins of the collection. This is another case of an intraosseous abscess. Another abscess that is important to distinguish from the intraosseous abscess are subperiosteal abscesses and we see these more commonly in the pediatric population. This is thought to be related to the looser adherence of the periosteum to the cortex in these patients. There's a higher association with pathologic fracture thought to be related to compressed periosteal and endosteal vessels that contribute to necrosis and certain subtypes of staph infections are predisposed to this finding. So here's a nice example. This is a 14 year old girl and we see nicely along that left ilium, focal fluid collection extending out into the adjacent muscle with extensive surrounding inflammation and enhancement. A little bit lower down we see another lobe of this collection, so this bilobes subperiosteal abscess in this case associated with extensive myositis and likely some intraosseous fluid as well. So next along our march here from left to right we're gonna consider the sequestrum which is one of the endpoints of an abscess and sequestered bone is a necrotic bone that's separated from the adjacent vehicle bone and it's very important to make this diagnosis because this is gonna be an area of the bone that's protected from circulating antibodies and the only way really for this to resolve is for surgical management. So on CT imaging we're gonna look for a focal area of mineralization that's surrounded by relative lucency and really when we think about all of our other imaging techniques the key finding is the lack of vascular flow. So on nuclear medicine techniques we're gonna see absence of tracer accumulation in these regions. We're gonna have T1, markedly low signal and a lack of contrast enhancement. So here's a nice example of a sequestrum in a patient with a complex history of prior surgery and trauma and we can see this little focus of sclerotic bone centrally there on the coronal image as well consistent with the sequestrum. Here's another example, a patient also had a history of prior traumatic injury and surgery. Again, a little linear sclerotic fragment associated with the surrounding lucency. Nice example of a sequestrum. So moving on as we again move from left to right here we can consider the diagnosis of an involucrum and what that looks like. So an involucrum is a formation of a capsule of viable new bone around an area of sequestered necrotic bone. The inner layer of the structure is gonna be granulation tissue covered by the adjacent biofilm of the infection itself and then the outer layer is gonna be expansile coarse woven bone. I could find no prettier example than what I saw in Dr. Alea's white paper here. A nice example in a young patient, a four year old male with chronic osteomyelitis. So we see here this area of bone that is not enhancing. This is in the proximal tibia in this patient. So clearly that's gonna be our area of necrotic bone, the sequestrum. And then we see this sort of paired area of new bone formation along the margin of that sequestrum. And so that's avidly enhancing. That's our involucrum associated with the sequestrum. So in some instances can sort of point you to the diagnosis of a sequestrum in that you have the presence of necrotic dead bone that needs surgical management. So finally along our march from left to right let's talk about cloaca. And cloaca are openings or ruptures of the bony cortex that overlie an area of osteomyelitis. And they drain granulation tissue, pus, and or necrotic debris to the skin, often associated with sinus tracts. Again, an uncommon complication we can see in this setting is squamous cell carcinoma as Dr. Wu alluded to in his earlier presentation. So here's a nice example. Again, a patient with prior trauma and surgery. And we see this gaping defect within the anterolateral margin of the distal femur, extending out into the adjacent soft tissues but not quite reaching the skin surface. This is a 65-year-old man with a history of acute on chronic osteomyelitis. So finally, before we wrap up, I just wanna highlight an important mimic. So when we're thinking about mimics in the setting of chronic infection in bone, oftentimes we're trying to decide between the presence of an infection like abscess versus tumor. We less often mistake tumor for abscess and more often neglect the possibility of infection in certain situations when the clinical circumstances try to persuade us otherwise. So the classic being here, osteoid osteoma versus Brody abscess. And I'm gonna show an interesting case of just that sort of dilemma. We referred a few months ago, a 14-year-old woman with a history of left leg pain, mostly at night, relieved by ibuprofen. So classic history for an osteoid osteoma. Her basic labs were totally normal. And she was referred by medical and orthopedic oncologists for ablation of presumed osteoid osteoma. And these are clinicians who see these diagnoses fairly frequently, once or twice a month. So here we can see the axial fluid sensitive sequence and the clinicians thought that this was possibly an intramedullary osteoid osteoma. Those do happen rarely. And we see on this particular sequence maybe not the most specific findings. We have the rounded T2 hyper intense focus with the surrounding edema. Hard to say for sure what that is. We see here on the coronal T1 imaging, we're starting to get clues that this is maybe not what our referring clinicians thought we had. And it's a little bit hard to see, sorry, for the size of the abnormality, but there is a mildly T1 hyper intense rim surrounding that lesion in the proximal tibia. Nicely on the T1 FATSAT post contrast images, we see the associated peripheral enhancement that again is more consistent with the presence of an abscess, Brody's abscess, as opposed to an osteoid osteoma. We referred this patient back to our referring orthopedic oncologist who took the patient to surgery and a staph abscess was confirmed. So really important to always have this in the back of our minds no matter the clinical situation. So finally, a few tips. Summarize what we've covered here today. Intra-osteous abscesses typically have reduced diffusion if that's something that you're using at your institutions can be helpful. We're gonna use that penumbra sign, the presence of the T1 hyper intense rim to diagnose the presence of subacute chronic osteomyelitis. With the sequestrum, we're gonna use CT in particular to identify focal mineralization surrounded by relative lucency and recognize that that is likely gonna need surgical management. Squamous cell carcinoma is gonna be an uncommon complication of a cloaca or sinus tract. And finally, always consider infection in the setting of suspected tumor. So thanks very much everyone for your attention.

musculoskeletal infections

imaging techniques

cellulitis

necrotizing fasciitis

osteomyelitis

MRI

diabetes

septic arthritis

diagnosis