 So what is avascular necrosis of the femoral head? Avian is now becoming very common in post-COVID scenario after about a year and a half after the COVID steroids have stopped. We are now seeing a lot of avascular necrosis of the femoral head basically because it has a precarious blood supply. Majority of the blood supply comes from the neck and goes to the head. So there are some retinacular vessels which come from the joint capsule and about 5 or 10% of the blood supply comes from the artery of the ligamentum terris. The majority, about 75% of the blood supply comes from the neck. So what is important is because they are all end arteries, that's why it's steroid as well as other things like alcoholism and substance abuse, obesity and all these conditions lead to thrombosis of the end arteries and that leads to the head avascular necrosis. Secondly, the intra-capsular fractures of the neck of the femur also are very susceptible to avian later on because again this arterial supply is cut off when you have the fracture of the neck of the femur. So that's why we have avian of the femoral head which is the commonest and the most famous avian in the body. So what is your aim of MRI imaging? Firstly, you have to identify the basic gist of the talk today whether it is avian or something else. Once you are sure it is avian, then you have to see the extent of the femoral head involvement that's for prognostication. Second is whether the acetabulum is involved because if the acetabulum is involved then the entire staging changes and the treatment that remains is only hip replacement. You have to accurately stage the avascular necrosis. Any weight-bearing areas are involved or non-weight-bearing areas are involved. That is the central ones and the medial ones are the rarely progressive, the lateral ones are the worst prognosis because they are the most weight. That's why they progress faster and you need to have the total hip replacement at an earlier stage. Is MRI good enough? Avian versus normal. Sensitivity is 97%, specificity is 98%. An MRI to differentiate avian from other pathologies is about 91% sensitive. So still there is a lot of window. That's why we need to really look at the mimics before really calling it as an avian. The sensitivity and specificity of avian is important because if it's 98%, that means you can use it for screening. Now what do you use? How, which sequence will you use for screening? You will use only a T1 coronal. If you have a big population that you want to screen for avian. For example, you have a big chunk of patients who've had a lot of steroids and COVID era. You want to know beforehand whether they have avian before they actually present to you with hip pain. Then you can use only one sequence that is coronal T1 and identify avian because it's very high sensitivity of MR. The hallmark of avian anywhere in the body is the double line sign. So you have to identify this double line sign on a T2 weighted sequence. It shows an inner high signal. The inner high signal is because of a hyperimic or an inflammatory response. Or the body tries to repair the border of the osteo necrotic focus. Now this is the osteo necrotic focus. So the border of the osteo necrotic focus is being repaired by the body. So that inflammatory response or high blood supply in that area gives rise to this high signal. Beyond that you have a low signal or a sclerotic margin. That sclerotic margin is because rest of the body is trying to contain that area of osteo necrosis. It doesn't want the osteo necrosis to spread into rest of the femoral neck. So it creates a sclerotic margin. The central signal of the osteo necrotic focus is not included in the double line sign. Now that varies according to the famous staging which is called as the Mitchell staging. So what happens is first the marrow remains the same. That is it remains the marrow signal right on T1, right on T2. Then it is replaced by hemorrhage. Then it is replaced by reparative tissue and ultimately when nothing happens it is replaced by fibrous tissue. So that we'll see when we see the Mitchell staging. Now do we really need to know this entire staging? Now there are a lot of staging available. There is Fikret and Arlett staging is the most famous but it has been described originally on radiographs. So the latest staging that has come up in 2019 revision is the Arco staging. There is also Mitchell staging. There are hundreds of staging that is basically there on AVN of the femoral head. The important thing is zero. You are not able to see anything. One, you just start picking up. Two and three is the basic borderline. Now two is where your conservative management will still work. Three, everything has failed and three and above it goes for a THR. So your differentiation is between two and three. Now the some stagings have subclassified two as two A and two B. Now two basically represents a crescent sign. Two A and two B have been differentiated in which two A shows less sclerosis and two B shows the crescent sign. And three is crescent sign with a cortical collapse. So now let's understand this. What is happening in the femoral head in the osteo necrotic focus? Now, osteo necrotic focus is blood supply is reduced in the femoral head. There is a borderline area which is the cartilage and the bone has separated by a subchondral bone plate. Now subchondral bone plate is the strongest portion of the femoral head. That is still keeping the foot in spite of the osteo necrotic focus below that. It will keep, it will try to save the femoral head as much as possible. But if the patient undergoes weight bearing or plays or does tracking or whatever he wants, then what happens is that subchondral plate eventually collapses. So when it collapses, it becomes stage three. So when it collapses, the patient goes for THR. Before the collapse, if you do a decompression surgery or ask the patient to be non-weight bearing, don't play sports, don't do excessive exercise and all of that stuff, till stage two we can save the femoral head. So what is your aim as a radiologist is to try to diagnose it up to stage two. Stage three and beyond, MR anyway doesn't help. There are a lot of orthopedic surgeons who send cases to us saying that whether there is an AVN or not in a case of osteoarthrosis. Basically it doesn't matter because osteoarthrosis and a stage three and beyond AVN is eventually going to have a THR. So whether it originally was AVN or not, it really doesn't matter. So now this is how it progresses. This is stage two already because there is an osteo-necrotic focus but you can see that the overline, the subcontinental bone plate black one is intact. There is no subcontinental crescent. Now here you see that this is still on the left side. There is normal osteo-necrotic focus, normal, sorry, now osteo-necrotic focus on a normal subcontinental bone plate area which is black. On the right side you can see that there is a crescent. This is now beyond the crescent, what has happened on the left side, there is collapse. Now the crescent is disappeared and there is collapse on the left side and this ultimately there are collapse progresses. So what will you have when you start imaging? You will first have an osteo-necrotic focus within subcontinental plate which is intact. Beyond that you will have a subcontinental crescent. The plate is still intact. The shape of the femoral head is still normal. Beyond that it collapses, there is flattening but still the osteo-necrotic remains limited to the femoral head. Now beyond the collapse what has happened is the overlying articular cartilage in the initial stages will be normal. Beyond that if the patient continues to bear weight the cartilage also undergoes desiccation and degeneration and tearing or thinning. Then it goes beyond into the acetabulum. When it goes into the acetabulum you have again changes in the acetabular cartilage first, then the subcontinental plate of the acetabulum, then in the subcontinental acetabulum. So when you start seeing marrow edema and subcontinental cysts in the acetabulum the lesion has progressed very significantly and it's gone and crossed the joint. This is the Mitchell staging. So this is very similar to what happens when there is any osteo-necrosis anywhere. So first there'll be a normal maintained signal of the marrow fat that is now replaced by blood because the blood is trying to come and replace the fat and trying to repair it. Beyond that when the blood doesn't repair it becomes fluid that it becomes cystic. Beyond the cystic the water also is taken up by the body and then it becomes fibrous. So it goes from A to D similar to the progress that happens in the osteo-necrotic head from fat to fibrous tissue. Then sometimes you can also have a subcontinental fracture in the, now this is how a subcontinental fracture would look in stage three. So as I said, what is the aim of MR imaging in AVN? Save the femoral head and not replace it. The AVN by and large is bilateral because it is caused by systemic diseases. When it is, when the AVN happens because of a fracture intra-capsular fracture of the neck obviously it is unilateral. But when it happens because of a systemic disease it is usually bilateral. So unilateral AVN you need to think is there any fracture or not? If there is no fracture then think twice is it really AVN? When this marrow edema is there and you see such osteo-necrotic focus the patient usually will present to you with pain. So marrow edema is equal to pain. Whenever marrow edema is there the patient has pain. When there is marrow edema there is absence of marrow edema then the patient does not have pain. That is if you have AVN on both sides and you have marrow edema only on one side then only that side will be painful the other side will not be painful in spite of it being on a higher stage. So marrow edema always correlates with pain. Second thing is marrow edema in the AVN does not go beyond the intertrochanteric line. So if it goes beyond the intertrochanteric line again start thinking of mimics like osteodosteoma stress fractures, infections, osteomyelitis. Then second thing that is almost always associated with AVN is the effusion. You can see that there is more fluid on the left as compared to the right side but that is just an incidental finding. It's a reactive effusion. It does not indicate the presence of inflammatory arthropathy or an infection. So effusion is just because there is some body response to the osteo-necrotic focus. It should not be confused with any other pathology. Now this is a patient on the right side that has undergone a core decompression because originally his AVN at that time was stage two. But you see that in spite of core decompression the subcontral collapse has happened. There is also erosion and destruction of the overlying articular cartilage along the femoral head as well as acetabulum. You have subcontral cystic changes in the acetabulum as well. So these things, even if you don't see very particularly great image of the articular cartilage but you can surely say that the AVN has progressed because you are seeing subcontral cystic changes in the AVN. And secondly you're also seeing larger osteophytes on the lateral margin of the acetabulum on the right side. On the left side it is absolutely normal. Then this is again an AVN with transient marrow edema as well as effusion on the right side as compared to the left side. Note that the marrow edema does not cross the intertrochanteric line.