Radiology Lecture 2 Severts- 0.01 REMS or 10 millirems.

Wont ask you that on an exam (too specific) but it could pop up elsewhere. The sesamoidal axial view is the only view limited by the patient. If the patient has a hallux limitus, if they cant extend their toes, you cant shoot this view. The patient has to extend their toes against the plate and lift their heel. The most common mistake that people make is they dont lift the heel. But the patient ahs to have a ROM, they have to be able to bend the toe against the plate. The lead aprons are put on backwards, protecting them, and the beam is coming in at 90 degrees at the level of the sesamoids. This is the only view we have to totally isolate the sesamoids. Last week we said a transverse fracture, a fracture from side to side, shows up best on a DP view. But any other fracture of the sesamoids will show up best on the sesamoidal axial, but it is limited by the patient. A sesamoid axial isolates the sesamoids. It is also good for looking at hypertrophied condyles of the metatarsals. Also shows structural deformities, such as structurally long met (not a functionally long met though).

3 variations: This is a calcaneal axial view. This is most useful for isolating the Calcaneus.it is shot at 45 degrees, the patient is standing on the XR plate. The beam is coming down, and shooting at about the insertion of the tendoachilles. It is a good view for isolating the Calcaneuscalcaneal fractures and calcaneal

varum/valgum. What if you wanted to look at a posterior heel spur? Doctors will order this but it is a mistake because the plantar and posterior surface of the Calcaneus will overlap. So when we want to look at the posterior Calcaneus we do what is called a modified calcaneal axial, and instead of shooting at 45 degrees, we move the machine all the way up and we shoot straight down at 0, so the patient is standing on the plate, the lead apron is on backwards, and the beam is coming straight down along the back of the leg. When you do it that way, that will show you a posterior heel spur. It is called a Modified Calcaneal Axia, and it will show if it is medial or lateral, and that is about the only value of this view. The third variation of this is your Harris and Beath views. They realized the middle and posterior facets are parallel and in the same plane, so if you see one you should see the other. So they had the patient stand like ski jump view. They had the patient stand on the plate, bend their knees like theyre on skis, and they shot three views: one at 35, one at 45, and one at 55, and they found that in 9/10 people, one of those views would show the facets. You dont have to shoot three views. Shoot a lateral view, draw a lone through the posterior facets, and then draw a horizontal reference- plantar Calcaneus, the plantar head of the fifth met, and whatever angle that forms, if its 47 degrees, youll see the facets. So calcaneal axial 45 degrees- isolate the Calcaneus- fractures, tumors, varum. If you want to see if the Posterior heel spur is medial or lateral, shoot straight down at 0 degrees, modified. If it is an STJ coalition, shoot Harris and Beath view. AP angle anterior posterior- the posterior ankle is touching the plate, the beam is coming in at 90 degrees and you are bisecting the maleoli. Good for looking at the ankle joint, isolating the fibular and the tibial malleoli. The mortise view, they love this view. The fibula is slightly posterior to the tibia. Shot at AP view, youre not looking straight into the ankle joint. So mortise view is internally rotating 15-20 degrees. That is the mortise view- slightly internally rotated, so the tibial and fibular maleolus are in the same plane. That opens up the ankle joint, so if you were looking for intraarticular pathology- intraarticular racture, arthritis, osteochondritis desicans, that would be a good view- a septic joint, shoot that view. Not really good for fractures of the maleoli, this is for looking inter-articular.

Lateral view: remember when we said views are named according to which side of the foot or anatomy is against the plate, but the exceptions are the AP and the lateral. A lateral view of the ankle is shot just like a lateral view of the foot, except the focal spot is going to be on the lateral maleolus. Going back for a second, an AP ankle is good for looking at medial and lateral. A Lateral ankle is good for looking at anterior and posterior- so a lateral ankle would be good for looking at a bony equinus deformity, or if we thought there was a fracture with posterior displacement. With rotational injuries, the fibula often gets posteriorly displaced, like a spiral fracture- that would show up well on a lateral view. Medial oblique ankle. This is important because it is shot so often. In ortho, during the gait cycle, the patient is supinated a lot more than they are pronated, about 82% of the time, so inversion injuries are more common. A medial oblique ankle is the ankle internally rotated 45 degrees. The medial side of the ankle is closest to the plate. The fibula is further away from the plate. Remember whatever is further away from the plate is going to be distorted or enlarged. Good for fibular malleolar fractures because it enlarges the fibula. Ankle trauma, standard ankle view is AP, lateral, and a medial oblique.

Lateral oblique, not commonly shot. 45 degrees externally rotated. Lateral oblique, the fibula totally overlaps the tibia so it is not a good view for looking at the lateral side of the ankle at all. This is a useful view for looking at the medial maleolus, it distorts it. Older patient comes in with pain on the medial side of the ankle and nothing on the lateral, and you are suspicious of Posterior tibial injury near the medial malleolus (Common Posterior tibial injuries in young people are at the insertion).

Angle of base of gait: This is important for biomechanics and surgery. You dont want to supinate or pronate the XR if you are measuring angles. Angle of gait is the deviation from the transverse plane. Normal person is about 7 degrees per foot and about 14 degrees for both. Abducted is about 45 degrees. So if one foot you are doing a DP you tell them to stand up straight and keep weight on both feet. If you have the patient lean back they are going to supinate. So for surgical or biomechanical evaluation, angle of base of gait. Take the patients socks off and make sure they are standing at their actual angle of gait (dont straighten the persons feet out). Watch the way the patients are walking when they come into your office. Accessory bones: all sesamoids are accessory bones, but not all accessory bones are sesamoids. Sesamoids are accessory bones inside the tendon. You have to tell the difference between sesamoids and a fracture. Usually the accessory bone will be smooth and regular, and the fracture will be jagged, but that is not always the case. Know where they are and what they look like. The Os trigonum is a separated posterior process off the talus, and shows up best on the lateral view. Has to be differentiated from a fracture of the posterior process. An enlarged posterior process is called a Staides process. If you plantarflex the foot suddenly you could fracture this, and that is called a Sheppards fracture. Clinically it is easy to diagnose: take the hallux, FHL runs back there, pull it and if the patient screams it is fractured. Radiographically it is not so easy, but look for soft tissue welling on the Lateral view. Os Calcaneus secondarius- accessory bone distal dorsal anterior to the Calcaneus. Exactly the same position that a calcaneal Navicular coalition is found, and at the same site where an avulsion of the bifurcate ligament would occur. That shows up best on a Medial oblique is best because it pronates and opens up the foot. The Os supratalare or os talanavicularis are on the dorsum- they have to be differentiated from osteophytes, part of DJD, hypertrophic and avulsion fractures, they show up best on a lateral view. The Os perineum might be the most common, and it is plantar lateral to the cuboid. That is a sesamoid to the Peroneus longus tendon. That shows up best (because it is plantar lateral) on a medial oblique view. Fractures of the accessory bones are not common. Usually due to direct trauma but not common. Maybe of the Os tibiale, because that is at the insertion of the PT tendon, but the other bones, unless direct trauma, are not common. If the apophysis on the base of the fifth met doesnt fuse is the Os vesalianum. That is distal to the os perineum. Has to be differentiated from an avulsion fracture on the base of the fifth met. The os vesalianum is usually parallel to the long axis of the bone, where a fracture

of the base of the fifth met is more transverse. The os intermetatarsum is an accessory bone that is cylindrically shaped, like a cylinder. That is found between the bases of the metatarsals. It has to be differentiated radiographically from a calcified vessel- the perforating branch of the dorsalis pedis, and it has to be differentiated from a chip fracture off the bone, so history becomes important. There is a difference between an accessory Navicular and an os tibiale. An accessory Navicular is the cartilaginous attachment medial to the Navicular. It is the apophysis. That would show up best medial oblique- its more dorsal, that is not a sesamoid. The os tibiale externum is plantar proximal medial to the Navicular. So that shows up best on a lateral oblique viewplantar medial. That is a sesamoid to the PT tendon and has to be differentiated from an avulsion fracture of the PT tendon.

Colers disease: (in this XR is on the left). Anatomical variant, if we do nothing, it will go away. Osteochondrosis of the Navicular, growth variant, no big deal. Osteochondritities: supposed to be infarcts at a growth center. An osteochondritity is an aseptic necrosis at a growth center. There are3 different categories: 1) anatomical variants, 2) abnormalities in chondrogenesis and osteogenesis, and then there are true infarcts. It is important to differentiate them because they get treated differently. XR of a dead bone- exactly the same. Bone at the time it dies has a normal bone density. At the time it is infracted, it looks normal. After, there is Hyperemiaincreased blood flow because of inflammation. The live bone is going to become demineralizeddecreased bone density. The salts will get blanched out, but the dead bone is dead, so its NOT going to get demineralized like the bone that is still living will. Inflammation and early rheumatoid the live bone is demineralized. The dead bone is still dead, it wont get demineralized. So if you take an XR 2-3 weeks after infracted, and it is still dead, the bone around it will be decreased density, and the

dead bone will have normal density, but therefore the dead bone will appear to have relatively more density. It is not really not dense, it is the live bone is less dense; it is from the dead bone causing an inflammatory reaction. Later on, when granulation tissue, reparative tissue, is lying down around the infracted bone, so now you have the infracted bone, another layer of bone on top of it, itll actually be increased density. So infracted bone at the time of infarct has a normal density. Assuming the patient has a good blood supply and there is an inflammatory reaction around it, in two weeks or so, it would appear relatively more dense, because the live bone around it has been demineralized, and in three months later, after there has been a reparative process, the dead bone will appear more dense, because there are two layers of bone there, and it will stay that way forever. All infarcts (ischemic necrosis of bone) there is an infarct followed by reabsorbtion of the necrotic tissue, revascularization, and remodeling. Four stages, they are important. First infarct- this would happen in sickle cell, this would happen in trauma, this would happen in Casence disease, infarct followed by reabsorbtion due to hyperemia, revascularization and remodeling. If you have an infarct, im going to see changes in the XR, because things are going on. The definition of an osteochondrosis is an infarct at a growth center, and if there is going to be an infarct followed by reabsortion, fragmentation and compression, then we are going to see lots of stuff. In severs disease and colers disease, nothing happens, it does not infarct. If I have an infarct at my growth center and this is going on, and there is going to be fragementation due to compression, how are you going to treat a true infarct? Say a patient has freibergs disease, infarct at the distal epiphyseal area of the second metatarsal, and the second metatarsal head, if she walks on it is going to collapse. Immobilize it until it revascularizes is and she is no longer in danger. So an infarct, an osteochondritity has to be treated with immobilization- prevent the joint from collapsing. If you prevent collapse, it will revascularize and heal. How long? Until it starts to heal. In Perthes disease, the osteochondritity of the femoral epiphysis, the destructive stage lasts for up to two years, so if it lasts for that long, how long will we immobilize for? Two years. They are going to have to get physical therapy because of muscle wasting. But you have to or the joint will collapse. An infarct shows up in bone as a serpentine radiodensity. It is like scarring in the bone. It is a serpentine infarct. For example in sickle cell. Scuba diving- the bends. Normal atmospheric pressure is no big deal. As you go down further, there is more pressure and nitrogen has to dissolve in the blood. Not a problem going down, but a problem coming up. If they come up too quickly, nitrogen comes out of solution too quickly and the blood bubbles, occlude, and cause infarcts. You have to put them in a hyperbaric oxygen chamber. But it causes bilaterally symmetrical large infarcts. Or in casings disease. bilateral large serpentine (zig zag) lesions.

An osteochondrosis is an aseptic (or avascualar) necrosis at a growth plate. All the osteochondritiies have a higher incidence in males than females, with the exception of Freibergs. Young women get this more than men. All of the osteochondirities are more common in Caucasians with the exceptions of Blounts disease, which is an osteochondrosis of the proximal tibia, and that is seen more commonly in black males. Calve- Legg Perthes disease- the whole idea with an aseptic necrosis is collapsing of the head. There is one theory that Freibergs is really a stress fracture in young girls, the weakest part of the metatarsal in an adult is the metaphysis, but the weakest part of the metatarsal in a kid is the epiphyseal plate. Every girls he has seen it in was an athlete. Calve Legg Perthe 6 to 1 males to females, the destructive stage lasts for up to two years, so long time immobilization. Remember infarct, followed by reabsorbtion. Revasculariztion, remodeling. So the end stage of an osteochondosis would be DJD, it causes destruction at the joint. Our rationale is to immobilize it to prevent this. Osgood schlatters disease is not a true infarct. It is a tendonitis of the patellar tendon, with heterotopic new bone formation. It means due to the inflammation, we can get ossification inside the tendon.

Osgood schlaters is the MC etiology of knee pain in young boys (the MC etiology of knee pain in young girls is hydromalacial patella). This is a tendonitis. You treat it with limiting physical activity and mild immobilization. Radiographically, your textbooks are going to say you see a tear drop or fragmented tibial tubercle. If the kid is asymptomatic, this could be normal. This is pain with squatting, pain with physical activity. So if you just look at an XR and someone asks if it is OS or normal, unless they give you a history it is a guess. If the kid is asymptomatic, it is a normal fragmented tibial tubercle. This is a clinical diagnosis, so its OS if he has pain on palpation, etc.

Freibergs- this is the most important one to us as podiatrists. This is the MC osteochondrosis in the foot. it is a true osteochondrosis, it is a true infarct, MC in young girls. Density changes, collapse of head, may see fragmentation and loose bodies. Second met protrusion angle- the second met is longer in these girls usually but the second met is longer in boys too. Clinically it presents just like a stress fracture. It can occur in any of the mets, but it is MC in the second met. Always take an XR to r/o stress fracture. Early on there will be joint space widening and swelling. Look for flattening of the second metatarsal head. With true infarcts like Calve-Leggs Perthes or Friebergs, you will get a triangular radiodensity in the subchondral bone. It is called Cresecents sign, not always, but often. As soon as you realize it is Freidbergs, immobilize. Total immobilization- casts. Treat aggressively to be safe. The end stage of a true osteochondirtiy- the head and neck are going to flatten, it is going to become mushroom shaped, that is what you are trying to prevent. Triangular density and flattening, if you are looking for it you will find it. Some exams will say S-shaped joint. They mean joint widening. Back to Kohlers: aseptic necrosis of the tarsal Navicular, but its not, it is anatomical variant, it is delayed ossification. Radiographically you get a discshaped, sclerotic, fragmented, hazy Navicular. It will heal normally in a couple years. If it was a true infarct, it would hurt. If youre not sure do a nuclear bone scan. If it is an infarct, initially the infarct would be cold, decreased uptake, and then during the healing stage it would be very hot, whereas if it was delayed ossification it would be mildly decreased. So there are ways to do it if youre not sure.

Severs disease- if they are going to claim its an infarct, try and find one case in the literature where the Calcaneus has long term radiographic changes. Severs disease is irregularity, fragmentation, radiolucency, and new bone formation of the calcaneal apophysis. This is the same way a normal calcaneal apophysis looks. As the patients get older the fragmentation will fuse and it will look normal. Iselins disease is another anatomical variant. It is supposed to be an aseptic necrosis of the apophysis on the Styloid process, but we already showed you can have an apophysis and it can be fragmented. What if it is hurting? What is the most lateral part of that girl or boys foot? the Styloid, of course it is going to hurt. Put a pad in it. Treat it with padding or put them in a wider shoe. If it were a true infarct you would have to do more than that. This ossifies in normally. The importance again to understand this is to understand how to treat it.

Blounts disease: it is the only osteochondrosis with a higher incidence in blacks (males over females). It is an abnormality that there is one subcategory. Abnormality and osteogenesis and chondrogenesis. Osgood schlatters and Blounts disease are the only two with abnormalities in osteogenesis AND chondrogenesis. In Blounts disease can cause a tibial varum at the head. If youre looking at an XR, what would be the difference between this an rickets? Rickets will give it to you in the mid shaft. Blounts will give you the varum up top.

Osteochondritis dessicans: most commonly seen in the knee, the lateral aspect of the medial femoral condyle. If you are asked if you, it will be that specific. The lateral aspect of the medial femoral condyle. It occurs commonly in the ankle or the talar dome. It is an osteochondral fragment- an intraarticular fracture. But there is not always a history of trauma. Seen MC in young males in their twenties. Weekend warriors goes out and plays basketball, goes out drinking, wakes up the next day and his ankle is sore. Didnt bang it, doesnt know what happened to it. That is the classic history of osteochondritis dessicans. A localized intraarticular fracture. Button of necrotic bone covered in cartilage, in English that means an intraarticular fracture. Treatment is anti-inflammatories, immobilization, surgical excision of the fragment, or going in and drilling the cartilage to make it more vascular. You would shoot a mortise view to see this, you want to open up the ankle joint.