 So this topic right now is the last topic for a very exhaustive CME for all of you who have been attending since yesterday. Not only because it's a difficult topic, but because this is not these all these pathologies you kind of read, but don't encounter them frequently in your day to day practice. So it's must have been quite exhaustive. So let's, this is the last topic of the day and of the CME is imaging of the hind foot. The hind foot basically would be a boundary between the ankle and the forefoot forefoot is very nicely covered. Let's move to the hind foot. And this I will also include certain pathologies which will not be included in any hind foot or forefoot as such, but will be commonly seen in day to day practice. So the hind foot basically means there is a presence of heel pain or what we call it in scientific terms as calcaneodinia. Now the causes for these would be either auspicious causes, ligamentous causes, tendinous or other soft tissue structures. Radiographs basically show you acute, auspicious abnormalities like fractures, stress fractures and those kinds of pathologies. But MRI could be beneficial in diagnosis and surgical planning. What are the differential diagnosis for heel pain? A lot of differential diagnosis can be possible. Like arthropathies like gout, rheumatoid arthritis, seronegative arthritis or osteoarthritis. Infections could be diabetic ulcers, diabetic osteomyelitis, other causes of osteomyelitis or superficial lesions in the subcutaneous tissues and skin like plantar warts. Mechanical causes could be plantar or posterior, plantar in the form of plantar fissiitis, heel spurs, bony spurs, calcaneus stress fractures, plantar nerve entrapment, foreign body granulomas or posteriorly like achilles tendinopathy, tears, haglens, deformity or haglens syndrome, retrocalcaneal bursitis, tarsal coalescence, accessory muscles or severs disease in the young age group. It can be neuropathic in the form extending right from the lumbar region like lumbar radiculopathy entrapment of the sciatic nerve somewhere in between along its course. Neuromas which are post-traumatic in the foot, tarsal tunnel syndrome, actual trauma cases, rare cases like ewing sarcoma and neuroma, ewing sarcoma just showed in this lecture or post-traumatic neuromas or nerve sheet tumors and rarely vascular causes. So the main causes that we see in day-to-day practice are those associated with plantar fascia, tendons like achilles, FDL, FHL, those related to the calcaneum and to the bursae around the calcaneum. So first we move to the plantar fascia. Now plantar fascia is basically a thickened deep fascia which extends from the base of the calcaneum anteriorly into the different digits. It has three components, the medial cord, the central cord and the lateral cord. It represents the plantar fascia as such when we mean when we don't say medial central or lateral we mean the thicker central component. So it originates from the medial calcaneum fibrosity and splits into five bands for the five toes. The insertion is at the level of the proximal phallus. They are closely adherent to the flexor digitorum brevis muscles at tendon unit. It should not be more than two to four millimeters in thickness and should be low signal on all sequences. So whenever it is more than four millimeters in thickness, it usually indicates the presence of thickening and ultimately leading to plantar fasciitis or plantar fascia degenerative changes. So it's the commonest cause of heel pain. It is also called as heel pain syndrome or subcalcaneal pain syndrome. There are two causes, either repetitive stress or enthesopathy in the form of seronegative spondyloarthropathy. The repetitive stress leads to, now this is an attachment, so this basically is pulling the calcaneal tuberosity towards the anterior aspect. And this stretched out plantar fascia is very important in maintaining the longitudinal arch of the foot. So because of some changes in the mid foot leading to collapse of the arch or a stress with respect to the attachments to the toe, like overuse of the foot for running or these kinds of similar sports leads to repetitive pulling of the plantar fascia along the calcaneum. So what happens is there is spurring or enthesophied formation in this region and that leads to formation of first a fibrous and later an oscious spur. That is also called as calcaneal spur. By definition a painful calcaneal spur will be bony and on the MR will show marrow edema. Thickening of the plantar fascia at this attachment is called as plantar fasciitis. So this is how a normal plantar fascia would look on the axial images and then this is how it would look in an abnormal situation. So in this patient what you are seeing is abnormal thickening more than 4 millimeters of the posterior portion of the plantar fascia at the calcaneum insertion. There is edema in the underlying calcaneum and you are also seeing in this patient a small spur which is going towards the anterior aspect. So this spur also has presence of marrow edema and there is soft tissue thickening and edema surrounding this area of insertion. So all these findings should be together seen for it to be called as plantar fasciitis. Just the thickening of the plantar fascia or just the presence of a spur without marrow edema will not qualify for plantar fasciitis. Just remember that all these findings should be seen together. This case on the top has thickening again this is significant thickening of the plantar fascia with surrounding soft tissue information. So plantar fascia it is when it is related to spondyloarthropathy is usually bilateral. It is associated with Achilles problems like tendonitis and retrocalcaneum bursitis and is also associated with soft tissue and marrow edema. Next when plantar fascia can be either thickened or plantar fascia can be toned. The tear of the plantar fascia can be because of an acute one episode of trauma or it can be because of multiple related micro stress injuries in which the plantar fascia like Achilles tendon first gets degenerated and this degenerated fascia is not strong enough as compared to a normal fascia and can lead to tear because of micro repetitive micro trauma. Now how it would look on the MR is you will see that there is an acute tear of the plantar fascia at the calcineal attachment. In this patient what you are seeing is this in this patient the plantar fascia is relatively normal and it's just tone. So this is probably an acute post-traumatic event whereas in this patient you are seeing that the tone on the retracted plantar fascia the plantar fascia is also thickened and abnormally hyper intense. So this is probably an already degenerated plantar fascia which is just tone from the calcine because of a relatively minor trauma. So on the coronal images again this is your lateral cord and the central and the medial cord of that of this patient is tone because of a tear of the plantar fascia. Distally the tears can occur but is relatively uncommon distal portion of the plantar fascia it is actually thinner than the posterior portion but because the stress of the single attachment is distributed into the five toes it is relatively uncommon to get tone in its distal portion. Most of the tears you will see in the proximal portion. Next is Achilles tendon. Achilles tendon is basically formed by union of the gastronomies and the soleus muscle tendon units into a solitary tendon which is called as the Achilles tendon. The importance of Achilles tendon is it is a big tendon a big in the sense it's a long tendon and it is relatively avascular over a very long length of the tendon. So that's why it is amenable to not only degenerative changes but also tears. It inserts over the posterior aspect of the calcaneum approximately at the level of the mid portion of the calcaneum when you see it from the top to bottom. This, if you see a bony sparring in this region it's basically anthizophyte but some people call it as posterior calcaneum spurs. It is correctly termed as anthizophyte or posterior calcaneal anthizophyte rather than a spur. It is about one centimetres in EP dimension. It is low signal on all sequences and the anterior boundary of the Achilles tendon should be either straight or it should be posteriorly it should be anteriorly concave. It should never be anteriorly convex. So insertion of Achilles tendonosis is the term given to a tendon which is because of repetitive microdrama or underlying degenerative changes can lead to thickening of that tendon and it is usually affecting the distal most portion of the Achilles tendon. So this is just signal abnormality which is not bright enough on PD-FAT side of fluid sensitive sequences to call it a tear. This is an example of thickening of the Achilles tendon at the insertion in the distal most portion. You are seeing hyper intense signal relative to the muscle and the normal tendon on T1 weighted images which is very very slightly bright on the PD-FAT side or stir sequences. And this is not a tear. This is intra tendinous signal with fusiform thickening of the Achilles and is called as tendinosis. When these tendons or a normal Achilles tendon because of significant trauma gets torn it is called as a tendon tear. It can be either micro tears, interstitial tears along the length or across the length of the tendon, complete tears or partial thickness tears. So this is an example of a signal within the tendon on fluid sensitive sequences which is significantly bright. The tendon itself is normal so there is no underlying tendinosis. You can see this interstitial tear in the axial section as well. So what you need to report is the length of the tear and the percentage of the tendon thickness that it involves. This is kind of less than 10% of the tendon thickness is involved along the deep aspect of the Achilles tendon. Overall length of about 1.5 to 2 cm in length and about 1.5 to 2 cm from the calcineal insertion. So all these things you should report in your written report. Sometimes there is a full thickness tear. This is called as a full thickness or a complete tear. Whenever there is a complete tear usually the proximal tendon segment retracts. Here you are supposed to report whether there is the tear that is a complete tear has been there from the insertion. Or there is a short stump of intact Achilles fibres and then it is 7 cm away from the insertion. That is number one. Second thing is how long or how far the tendon, the torn tendon is retracted. And the third important point that you should address is whether this tendon itself is normal or there is an underlying tendonosis. Now this patient if you see there is the tendon appears slightly heterogeneous on T1 as well as BD5 fat set sequences. So this is probably underlying tendonosis and this is the length of the tendon that is retracted. It should have been here. It is retracted by about 4 cm. And this actually involves the calcaneal insertion side. There is no stump of fibres intact seen at the insertion. So as I said we should call it either interstitial partial thickness or complete percentage of the tendon thickness that is involved tendon gap or retraction. EDMOR hemorrhage within the tendon gap. What it is if it is just EDMOR hemorrhage or some soft tissue abnormality which is seen within the gap distance from the insertion. The size of the stump if there is an intact stump and whether the haculent syndrome is present or not in a case of a partial or interstitial pair. Next we move on to the other two tendons which are involved in posterior or hind foot pain. One is FTL and the second is FHL. So whenever there is fluid along the FHL tendon it is usually normal in most of the patients like this amount of fluid however is abnormal. So there is a normal continuation of the tendon sheet of the FHL with the joint space of the pibiotilar joint. Similar to the popliteus tendon sheet in the knee joint and the tendon sheet along the long head of biceps in the shoulder. The FHL tendon sheet also communicates normally with the ankle joint. However presence of a significant amount of fluid along the FHL tendon is definitely abnormal and this can be termed as tinosinoitis. Especially if there is a presence of a posterior ankle impingement as we saw in the last topic or last lecture. Then this amount of fluid is an indication that there is posterior ankle impingement. Then we have retrocalcaneal bursitis which can lead to heel pain. Retrocalcaneal bursitis is usually almost always associated with a problem either in the calcaneum or in the achilles tendon. In this patient you are seeing that there is a hageland kind of deformity in the posterior superior aspect of the calcaneum. You have fluid in the retrocalcaneal bursa. You have some inflammation in the cages fat pad and you have this signal within the distal portion of the achilles tendon. This tendon, this signal is definitely abnormal. It is slightly higher than what you would expect in a tendonosis and the tendon itself is not swollen. So there is no significant tendonosis but this is a partial thickness or interstitial tear. So what do you see on the x-ray is obniteration of the retrocalcaneal fat. In the MR you will see fluid collection within this bursa along with adjacent soft tissue edema. This is another case of hageland syndrome in which you will see this posterior superior process of the calcaneum. Then fluid in the retrocalcaneal bursa, abnormality in the achilles tendon either in the form of tendinosis or a partial tear and adjacent soft tissue edema as well. All of these together will be called as hageland syndrome. If you see only this projection of the calcaneum and no other inflammatory changes you can call it as hageland's deformity of the calcaneum. Other causes in the calcaneum which can give rise to posterior ankle pain or hind foot pain is this kind of this is relatively common in young patients. This is a stress fracture. The stress young patients or a middle-aged female patient who has just recently started running or marathon running. In these patients you will see that there is significant marrow edema in the calcaneum and you start with first a marrow edema. And eventually you will start seeing this linear hyper-intensities on both the sequences indicating the presence of a stress fracture. This stress fracture if it is ignored can lead to this kind of a proper fracture seen on the radiographs. This has to be correlated in a young in not in young patients but slightly middle-aged female patients to rule out osteomyelitis. This osteomyelitis is also quite common in that age group and usually associated with diabetes. Or marrow contusions and sometimes the marrow edema masks the tumors in the calcaneum which fortunately are not very common but they can be missed. Let's move on to the miscellaneous topics leading to hind foot problems. First is tarsal coalition. Now what is coalition? Coalition is complete or partial union between two or more bones either in the mid-foot or in the hind foot. Basically coalition is union of two bones by either a fibrous tissue, cartilaginous tissue or bonnet tissue. So any kind of union is called as coalition. This is usually developmental. Whatever union between the two bones if it is post-infective or post-inflammation it is called as ankylosis. Whenever it is developmental it is called as coalition. So as I said it can be bony cartilaginous or fibrous. The most common in the foot or hind foot is calcaneunavicular or telocalcane. So this is an example of calcaneunavicular coalition. You have the beak sign that you see on the or the anteater sign that you see on the x-ray. You see that the anterior superior aspect of the calcaneum has come together with the calcaneum. The calcaneum has come together with the navicular bone leading to formation of a pseudoarthrosis. So this is a calcaneunavicular coalition. This is a telocalcaneal coalition in which you see a prominent beak here. And when you trace it in the sag you can see only the beak here in the sag reconstruction of the CT also you can see that. But when you actually see the corona lemma you see that these two bones are completely united. Normally you should have a sustentaculum tali over here and the calcaneum which should be seen separately on the medial aspect. And you have the sinus dorsi on the lateral aspect. But in coalition you see that there is trabecular continuity and this is a complete pony union along the medial aspect or that is of the telocalcaneal joint, telocalcaneal coalition. Basically these coalitions not only present with pain but they usually present initially with flat foot. So whenever there is a flat foot you should have two diagnoses in mind. Either flat foot can be a mobile flat foot or it can be a fixed flat foot. Whenever it is a mobile flat foot it usually indicates a problem in the posterior tibial tendon or malfunction or dysfunction of the tibialis posterior. Either the tibialis posterior has tendinosis or a partial tear or an insertional abnormality. Now this can be taken care of by repairing the posterior tibial tendon. The second variety of flat foot is fixed flat foot. This is a kind of fixed flat foot in which you can't really do anything much on this because you cannot reset this bar and make these bones separate from each other. So this is a fixed flat foot deformity. You have to have in these patients you'll have to have shoe correction and posterior changes in the foot to prevent future arthritis. Whereas the mobile flat foot is something that can be eminently treated surgically as well as by footwear modification. Next of hind foot or the heel pain is osteocondrol lesions. Osteocondrol lesions of the taladome as everybody knows is basically the focal area of damage involving the subcondrol bone plate in the initial stages. Subsequently either involving the articular cartilage which is towards the joint or subcondrol cancellus bone which is away from the joint. So the pathology begins in the subcondrol bone plate. If it extends deeper it extends into the subcondrol bone. If it extends towards the cartilage it can lead to presence of this kind of a defect. Then undermines this portion of the subcondrol bone and then ultimately leading to formation of a loose body. So the Anderson's classification basically says that stage one progresses ultimately to stage four in the form of presence of just marrow edema. Then a proper defect extending as a fluid cleft into the overlying articular cartilage with partial separation and then ultimately complete separation. So this is how it progresses and it's called as osteocondrol lesion of the talas. It predominantly affects the medial portion of the taladome but lateral affection is also known. Sometimes what we see is like this we see the marrow edema. Then you start seeing this thin sliver of the osteocondrol bone. This black area is the cortical bone. Small area beneath that is the subcondrol bone. This is partially separated from the underlying talas leading to formation of a partially loose osteocondrol fragment. Now note that this is on the lateral aspect. So this is a lateral taladome involvement by an osteocondrol lesion. This is the sagittal pain in which you are very well seeing this partially separated osteocondrol bone fragment. This also will lead to hind foot pain. Next is presence of ossicles. As I said, ossicles or accessory ossicles around the ankle are very common. There are different books which give rise to more than 10-15 varieties of ossicles around the ankle joint. Are all of them significant? Well, no, they are not significant. But the significance can be found out if there is a pinpoint tenderness over that ossicle. Either that ossicle has undergone direct trauma or because of the ossicle there are some syndromes like osperonium syndrome or ostrigonum syndrome, posterior ankle impingement. Sometimes these syndromes are associated with accessory ossicles. So typically osperonium is an accessory ossicle at the lateral plantar aspect of the cuboid bone. And this is where your peroneal tendons will come over here from the lateral aspect and cross into the soul of the foot. So if there is this ossicle, then it gives rise to repetitive micro trauma to that tendon through the peroneal tendon. And that can give rise to that rupture or tendonosis within the peroneal tendon. So it starts, the causes can be either an acute or chronic fracture of the ossicle itself or tendon rupture or tear, partial tear or a complete tendon rupture. So this is what you would see on a T1 weighted image. You will see that this tend, this ossicle is very close to or almost within the peroneus longest tendon over here on T1 weighted images. On T2 weighted images, what you're seeing is you're seeing an abnormality or a stern hyper intense signal which is traversing all across this length of this inframalular segment of the peroneal tendon. So this is a partial thickness tear and that is what was leading to pain or posterior, posterior lateral pain in this patient. Next, we move on to a couple of infections that are seen in the foot. The commonest, the most typical infection would be Madhura Mycosis which can be given, which has very dramatic effects and unfortunately is very difficult to treat. The commonest one is diabetes, diabetes related osteomyelitis. So what happens in Madhura Mycosis is the patient presents with a swollen foot with multiple sinus tracts and exuding of dark brown or black material from the sinuses. So the clinical triad is draining sinuses, localized mass like soft tissue swelling of the foot and discharging grains of dark material through it. On the MR, the dot and circle sign is what is very, very typically seen. This is the actual image. Now what you're seeing is multiple foots of the bone, multiple bones of the foot are involved in this patient. You have almost disintegration of the midfoot joints in this patient. Whereas in this patient, there is not much of degenerative changes in the bones, but you see that the soft tissues are involved with this kind of soft tissue involvement. This is a PD-FATSAT image showing this dot and circle sign. What you're seeing is you're seeing a bright circle inside that you're seeing a dark dot. So this dark dot is the fungus and this bright area around that is fluid around that fungus or the reactive granulation tissue. On the post-contest images, you see heterogeneous enhancement. Sometimes you can see the dot and circle in the post-contest images as well. This is difficult to identify on the T1 weighted images. The PD-FATSAT or fluid-sensitive sequences and post-contest are the ones that will pick up the abnormality in Madhura Microsis. So whenever you see this, then you are the first one to give an idea that this could be a Madhura Microsis and not a plain and simple osteomyelitis in this patient. So we have a last couple of slides of diabetes-related osteomyelitis, but before that we'll see a couple of other typical cases in the foot. One is called as the joggers foot and one is called as the Baxter's neuropathy. Now what is joggers foot? Joggers foot is involvement of the medial plantar nerve. So the medial plantar nerve is the one that supplies the medial portion of the sole and the location of the abnormality is basically in the Tarsal Tunnel at the knot of Henry. And this gives rise to impingement or compression of the nerve, the medial plantar nerve, leading to abnormality in the flexor halusis brevis. So this is what you see. This is the entire case. This is the T1 weighted image. This is the PD-FATSAT image. This is a PD-FATSAT and this is a T1. Now what you're seeing in this patient who presented with pain basically in a jogger is you start seeing that the flexor halusis brevis muscle is slightly atrophic on the T1 weighted images and is bright on PD-FATSAT images. This entire muscle is bright on PD-FATSAT and shows mild patchy fatty replacement, especially in the distal portion. This is indicative of a medial plantar nerve involvement leading to changes of denervation atrophy, early atrophy and basically degenerative edema in the flexor halusis brevis muscle. What happens on the lateral aspect is called as Baxter's neuropathy. That is entrapment or compression of the inferior calcaneal nerve, which leads to the same abnormalities as you see on the medial aspect in jogger's foot, the same things you see on the lateral aspect in Baxter neuropathy. And what you see is muscle either early changes will lead to hypertrophy and edema and later it will give rise to atrophic changes and further reduction in the edema. So this is the patient in which you are seeing that this on the medial aspect, this is completely atrophic. In the earlier stages, you have this Baxter neuropathy leading to swollen adductor muscle on the medial aspect, adductor halusis. Sorry, adductor digitaminemia on the lateral aspect and this is the one that is bright in the earlier stages leading to atrophy in the later stages. So this is also seen on the sagittal pain you see this is a great three fatty replacement of the muscle. And in the early stages and the acute stages is quite edematous. Tarsal tunnel syndrome is the syndrome which happens because of compression of the neurovascular bundle in the tarsal tunnel that is a posterior tbl neurovascular bundle. It can be either idiopathic or with respect to the SOL in this region can be due to tinoxinovitis of the same tendons. Or bone deformities or hind foot valgus, bone deformities as well as the impingement abnormalities in the tarsal tunnel as we've seen in the last lecture. In flat foot patients, especially further related to the hind foot valgus and ostrigonal. So what you see is your in the course of the posterior tbl neurovascular bundle happens on the medial aspect of the carcaneum. If you see cystic lesions like this, these are related to the tendon sheets. So these are ganglion cysts related to the tendon sheet leading to compression of the posterior tbl nerve. The nerve itself is showing hyper intense signal and is swollen. And that is leading to the posterior tbl nerve impingement and related pain. Whereas I have a confusing name in the same foot is Sinus Tarsus. Sinus Tarsus syndrome is in the lateral aspect of the telar neck. And that is the region where again you have fat vessels, nerves, and you have small ligaments there. So this is a portion which is called as the Sinus Tarsus. In the Sinus Tarsus you have multiple structures. But basically what you see on the MR is soft tissue edema and fluid collection in the Sinus Tarsus can lead to can be a result of Proma or inflammatory arthritis and can lead to pain in the central portion of the hind foot leading to Sinus Tarsus syndrome. So you have two different syndromes, the Tarsal Tunnel syndrome along the posterior tbl neurovascular bundle and the Sinus Tarsus syndrome which is more centrally and laterally located in the hind foot. What is Mueller v syndrome? The Mueller v syndrome is now commonly seen and is probably going to become more famous as Nadal syndrome rather than Mueller v syndrome because Nadal is suffering from this disease. What you are seeing is a comma shaped navicular. It's because of osteonecrosis of the navicular along its lateral aspect. So it's usually an adult onset osteonecrosis of the navicular. It's usually bilateral and leads to collapse on the lateral aspect. You need to pick up as radiologist Mueller v syndrome in this stage and not in this stage. In this stage it becomes untreatable. In this stage you are able to pick up the abnormality as marrow edema in the navicular which is dark on T1, bright on pdfatsat or stir sequences only in the lateral portion of the navicular. The medial portion of the navicular is relatively normal. You start seeing that from craniocaudally and from lateral medially. The lateral portion is becoming smaller proximal distally as you progressively see it over a few follow-ups and that is going to lead to collapse of the osteonecrotic portion of the lateral aspect of the navicular bone. Plantar fibromatosis has been seen in the previous lecture by Dr. Ajay is basically a fibrous and collagenous nodules in relation to the plantar aponeurosis or the plantar fascia. It can be either a single one or a multiple one, but the most important thing is it is almost similar to the signal intensity of muscle. It gives intense post contrast enhancement and number three it is very closely related to the plantar fascia. You will not find fibromatosis well away from the plantar fascia. If you see this similar lesion which is away from the plantar fascia, it is very unlikely to be a plantar fibromatosis. So what you see here is a small nodular thickening of the plantar fascia here. Sometimes it's slightly larger. It is kind of infiltrating across the plantar fascia into the underlying muscles of the soles of the foot. It is very, very slightly bright on PD-FATSAC sequences and if you give contrast, it will show post contrast enhancement which is usually heterogeneous. So as again told by Ajay, this is usually amenable to ultrasound guided injections and surgical management of this is not recommended because it gives rise to multiple recurrences. The recurrences themselves become more and more there is more and more scarring along the sole of the foot and they keep on recurring because they are fibrous tissue. Ajay has already dealt with shark coats and just giving you two slides in which we have to differentiate between osteomyelitis and active shark coat. So this is active shark coat and there's one more slide in which there is chronic shark coat. You have basically three types of abnormalities in the foot. One is either because of degenerative arthritis like similar to osteoarthritis. You have osteomyelitis because of poorly controlled sugars and diabetes mellitus or you have shark coats disease which is either because of a spinal cause, any neurological cause or basically because of diabetes related neuropathy. So what you actually have to differentiate is whether it is osteomyelitis because if it's osteomyelitis, the treatment is debridement. You have to reduce the bacterial load in that area to be able to make sure that the sinuses as well as the granulation tissue to form and heal. Shark coats on the other hand is basically a progressive disease in which it basically involves non-surgical management with proper footwear adjustments to the foot and weight bearing and everything. Those things are more important in shark coats because it's basically because of peripheral neuropathy which is leading to collapse of the midfoot because of non-weight bearing area in that region. It is not related to infection but these two usually occur together. The third thing is your degenerative arthritis, whether it is osteoarthritis of the foot. Now osteoarthritis of the foot, even if the foot is a weight bearing area, the area of the forefoot and the midfoot usually are not the areas where you have degenerative neuropathy. The degenerative arthritis or osteoarthritis is basically in the region of the ankle. That is the tibio-telar and the subtelar joints is usually does not involve the midfoot and the distal foot. The distal foot is more involved in goutia arthritis and seronegative arthritis and not in osteoarthritis. So osteomyelitis is usually present with ulcers with heart red foot. The weight bearing areas are the ones that are involved in osteomyelitis because those are the ones which initially become avascular and that avascular coupled with increased blood sugars would lead to sinuses and formation of osteomyelitis. So in the metatarsal phylloengyl joints are the heads of the metatarsals and the calcaneum. These are the two weight bearing areas where you will have osteomyelitis. Whereas in the shark ports, in the midfoot you will have in the subarticular portions and this definitely is not the area of weight bearing. So on the MRI you will have marrow edema in the forefoot and hind foot near the ulcer and here you will have in the subconral bone. When you give contrast, there is going to be heterogeneous enhancement because of the necrotic areas not showing any enhancement. The same necrotic areas will be bright on diffusion weighted images. These abnormalities will not be found in active shark ports. In chronic shark ports, unsuperimposed infection, what happens in chronic shark ports? The midfoot eventually gives in and collapses. This collapsed midfoot again will not be associated with any ulcer the patient will not have pain. The x-rays will show that the foot is terribly abnormal in the form of joint deformity, dislocation, rocker bottom foot but the MRI will not show much marrow edema because it is chronic shark ports. In infection, however, you will again start seeing ulcers now in the non-weight bearing portions because this is now become the weight bearing portion and not the calcane and the head of metatarsals. And this on the x-ray again will be associated with joint deformity, dislocation and rocker bottom foot but you will start seeing marrow edema in the cuboid or other weight bearing areas near the ulcer. So this is the shark port with superimposed infection which again will need debridement and not just non-surgical management as you would do in a shark ports. Couple of examples on the MR. This is a patient in which you are seeing a deep ulcer over here. You are seeing marrow edema in the calcane. There is almost complete soft tissue loss in this region with these changes in the calcane. Now this is a weight bearing area. You have the ulcer, you have edematous changes in the rest of the foot. So this is definitely an infection or infective osteomyelitis rather than a shark. So let's move to a few cases. So are you able to see the images? Yes, sir. Okay. So this is the sagittal PD-FATSAT and this is sagittal T1. Now what you are seeing in this patient is you are seeing an achilles tear obviously but what are the findings that you will see in the report? Now this is a full thickness tear from the insertion. There is retraction of the tendon by whatever four or five centimeters. The underlying tendon appears abnormal. It is thickened on T1 as well as PD-FATSAT sequences with heterogeneous signal within. So this is an underlying tendinosis within the retracted tendon. There is no maroedema in the underlying calcaneum. What you are seeing over here is your, this is the enthesopathy that you are seeing. This is the new bone formation along the distal aspect of the achilles tendon. So this is achilles tendon enthesopathy with tendinosis and a full thickness tear with retraction of the torn tendon end. Now this is the next case. In this, what are you seeing? You are seeing that there is maroedema in the region of the calcaneum which is bright on PD-FATSAT sequences. Not appreciated on the T1 weighted sequences. And what is happening to the plantar fascia? Plantar fascia is thickened and shows subtle signal abnormality as it approaches the insertion. So this is, there is also presence of edema in the adjoining soft tissue. So this is plantar fasciitis. In the same patient, what you are seeing is, you are seeing abnormality in the achilles tendon which is slightly bright as compared to what you would see in a normal tendon. This is definitely quite bright. So this is a partial thickness interstitial tear of the achilles tendon in the same patient. And what you are also seeing here is your prominent steada process. So this is the prominent steada process. But as you saw in the other slide, now this is the FHL tendon which is crossing the steada process. And then going here, this is minimal fluid. So this much fluid is okay along the FHL tendon. The amount of fluid that you saw in the other, in the PowerPoint presentation was significantly more. So that is abnormal. This is, that was FHL tinocynometers. This is normal. Now this was a diabetic patient. Now this is in 2016. And in this 2016 patient, what you're seeing is that you're seeing an ulcer over here. There's a focal soft tissue loss on PDFATSAT and T1 weighted images. You see very subtle abnormality in the calcaneum and the cuboid. But you don't see really any floated osteomyelitis in this patient. You're just seeing soft tissue changes in the form of edematous soft tissues, which are dark on T1 and bright on PDFATSAT sequences. So what happens when you follow up the patient? Then in 2018, this is what happens if the diabetes is ignored. You have involvement of the bones here. So you have involvement of the talus, distal end of the TPR, calcaneum, the navicular, the cuboid, even the cuneiforms. All of them show the signal abnormality, just dark on T1, right on PDFATSAT sequences. And what happens when you give contrast in the same patient? You see that there is heterogeneous enhancement. You see some areas which are enhancing, some areas which are not enhancing. So for example, in this portion of the talus, if you're seeing this dark area on T1, it's not showing any enhancement. This central portion is showing enhancement. Some portion is not showing enhancement. So you have the granulation tissue which is showing enhancement and the necrotic portions of the bone which are not showing enhancement. The ulcer is still seen in this patient. So when you give contrast, what you are seeing is this is a case of diabetic osteomyelitis. Eventually what has happened over the two years is there is progression of the soft tissue infection into the bones and there's also presence of early rocker bottom foot. This midfoot and the high foot both are collapsing. So this is an advanced case of diabetic osteomyelitis over the period of two years. So this luckily we got this case in which we could show you what was happening two years back and now what is the current status in 2018. The rest of the cases I've already covered in the presentation. So we are...