ICSC03 Transcripts

FICS have not loaded transcripts as PDFs as this restricts students where English is their second language from seeing the transcript in their language. To print the transcript in a different language, follow the steps below. 

1. Select your preferred language first. This will change the transcript into your chosen language.
2. Copy the text
3. Open a word document on your computer
4. Paste the text into your word document and save it to your computer.

If you have any suggestions on how FICS can improve this service, please email us at admin@ficsport.org

If you want the direct download for the English version of the transcript, you can do that from each of the unit modules, which gives you an option at the top of the module to download the PDF.

 

Section 01_ICSC03 
English PDF direct download 01_ICSC03-Section1 IntroModalities

Instructor Dr Chad Warshel
Video Lesson: 01:06:16

Welcome to our FICS module on Diagnostic Imaging in Sports Trauma. My name is Dr Chad Warshel and I will be taking you through the sports imaging module. This is broken into 9 one-hour sections.

A little bit about myself, just so you know who it is that is talking to you. I am a professor at Northeast College of Health Sciences in Upstate, New York, USA. Northeast College of Health Sciences was formerly New York Chiropractic College, you might be more familiar with that name. We made the change earlier this year. I teach in the Chiropractic Program, teaching Chiropractic Students Diagnostic Imaging. I wear a couple of hats here at Northeast, one of the other ones being somewhat of a self-replicating organism. In that, I run our Diagnostic Imaging postgraduate residency. For those who are interested in pursuing a career in Radiology on top of Chiropractic, that is what the residency is there for. Just knowing that we are dealing with an international audience, to familiarize you with some of the terms so DACBR is Diplomate of the American Chiropractic Board of Radiology. Unfortunately, there’s only an American Chiropractic Board of Radiology, we don’t have an international group.

So, folks who have that DACBR designation, are folks who have completed the three-year postgraduate residency to meet the eligibility to sit for the Diplomate examination, and then afterwards have passed the two-part Diplomate examination put on by the American Chiropractic Board of Radiology. The only way to have eligibility is to do a three-year postgraduate residency. I am the director of our program here at Northeast. I have been running the program for a little bit over 10 years now. One of the other hats that I wear is I also have a diagnostic imaging practice that I run through the Chiropractic College here through the College of Health Sciences. I interpret x-ray, MRI, and CT for the box out in the field.

My educational background. How did I get here? Well, I got my chiropractic degree at, what was then Western States Chiropractic College and is now the University of Western States. After completing my DC, I went on and did my three-year residency in Diagnostic Imaging there as well. I got the bug to teach when I was a resident, but I didn’t want to finish residency and then go right into teaching. I wanted to develop some experience. I move down to California in the United States, and I did a split practice. I spend about half my time, treating patients and about half my time reading x-rays, MRIs, and CTs. Did that for 7 years, at which time I transitioned over here to the Northeast. After I had been teaching here for several years, I decided I wanted to pursue an academic degree as well as my professional degree. I did a master’s in Health Professions Education here in New York at the University of Rochester. So that is me in a nutshell. Very important from a lecture standpoint, I have no financial disclosures. I am not going to be selling any products or anything else. I have no agreements with other companies so I have no financial disclosures.

Presentation Placement: 03:40
Breakdown of topics. Section 1 and 2 – first 2 hours. If you are looking at the entire 9-hour module, looking at the sports-med program, the first 2 hours, we are going to be talking about imaging modalities and interpretation. We are going to talk about interpretation first and then imaging modalities, because this is approaching an international audience and there are varying degrees of education in imaging interpretation, imaging orders, owning, and operating radiographic equipment. We will start at the very basics and work our way up from there to make sure that we are all speaking the same language so we all have that commonality of what it is that we are talking about. So those will be our first 2 hours.

Section 3 – We are going to get into trauma to the face and head. It is very common in sporting events to deal with patients being struck in the head. Are there facial fractures? Is there any significant intracranial injury? We will be talking about imaging those things. Then we are going to get into more of our musculoskeletal topics. Section 4 and 5, we will be talking about spine trauma, as well as some other differentials things that we have to be concerned about when we are dealing with the athlete. Not just for traumatic things but also for dealing with pediatric athletes. We need to think about some developmental abnormalities, things like Scheuermann’s disease.

Naturally, we will have to talk about disc herniations. Those can be considered post-traumatic or degenerative phenomena. There are a couple of different pathways there. We will also be talking about spondylolisthesis. Section 6 & 7 we will spend 2 hours talking about the upper extremity, covering everything from the scapula down to the fingertips. Section 8 & 9 the last 2 hours, we will be talking about the lower extremity, going from the hip down to the toe. One of the things that I will try to do during this presentation is as we look at the PowerPoint slides take you through these various imaging injuries, with some live DICOM demonstrations as we move more into a digital imaging world. There are still some folks who run hard copy film, but digital is predominately what’s being done. I want to give you some ideas on how to approach DICOM images and how I deal with them when I get a disc or when I have portal access to my patient’s images.

This is some of the ways I can really make sure that I am interpreting these studies to the best of my ability. I will be honest with you, as somebody who is a radiology educator in the Chiropractic curriculum, regardless of where you are, with an international audience in an incredibly wide array of laws associated with imaging and interpretation. I am a firm believer; you always review all of your own imaging. Whether you are doing your imaging in-house or whether you do your imaging in-house and send it to a radiologist for interpretation or whether you send your patient out to an Imaging Center or if you get your patients to have to bring imaging in if you are not allowed to order imaging, you should always review your own imaging. For a couple of reasons, the first one being, how are you going to get better at this if you don’t practice? I am a big one. Make sure you review all your Imaging-in. It is common in the modern world when we are dealing with these patients coming in with imaging. A lot of times they come with their reports too.

One of my big rules and I reinforce this with my DC students, and I reinforce this with my residents, you never look at their report first. You look at the Imaging, you interpret the imaging, you practice the skill, then you correlate with the report, and you make sure you agree with it. Just because that report was signed off by a radiologist, doesn’t mean that they didn’t miss things. I had a great example just yesterday in practice. So let us work on developing those skills.

One of the things that you need if you are going to be developing these Radiology skills, you need some resources available to you. The internet is all well and good but it is got some limitations so I always like to make sure I cover some of the major texts that I will use in dealing with imaging.

Presentation Placement: 08:15 – References
Because this is a sports module, that primarily we are a little worried about trauma cases. A couple of my big books, are really, my go-to books. Any time I am dealing with trauma cases, the first and original, and one of the most well-recognized textbooks on trauma is Rogers’ Imaging Skeletal Trauma. Rogers’ fantastic speaker. By the way, if you ever get a chance to hear them, really the definitive text. This is where trauma imaging since the 70s and 80s has really been based on Roger’s. Some other texts, Spine Injuries in Athletes by Hecht. This was a great read. It is not an incredibly thick book. It is three-quarters of an inch or so thick, of centimetre and a half. This is a great resource particularly because it is focused on athletic injuries naturally. Not an Imaging book but a clinical book, Essentials of Musculoskeletal Care. What this does is it is great for diagnosing different kinds of musculoskeletal conditions. It also talks a lot about what is the allopathic management of various conditions.

Then, probably the book that I spend more time with than any other these days not necessarily this one specific book but this series of books put out by Elsevier is the diagnostic imaging series. There’s an entire, there’s a huge library of books here, Diagnostic Imaging Brain, Diagnostic Imaging Gastrointestinal, you name it from an MSK standpoint.

The 2 big books, because this is predominately trauma that we are talking about, Diagnostic Imaging, Musculoskeletal Trauma, great book, and the other one kind of its sibling text, is Diagnostic Imaging Musculoskeletal Non-traumatic. So not to surprise you. We are dealing with sports injuries, spend more time with the trauma book. The non-trauma book is great when we are dealing with things like Ankylosing spondylitis, rheumatoid arthritis, or some of the other musculoskeletal conditions that don’t have immediate traumatic incidents. Some general radiology references. One of the things that I get asked a lot, whether I am doing postgraduate seminars or whether I am just talking with colleagues, everybody always wants to learn more about MRI. X-rays are a relatively straightforward, kind of thing. MRI is much more difficult, much more involved. If you graduated more than 15 years ago, it probably wasn’t the core part of anybody’s curriculum.

So, one of the first books that I recommend starting with is in an MRI world is Major’s Musculoskeletal MRI. Wonderful book, light book. It is about a centimetre and a half or so in thickness, and it is a primer. It is the 30,000-foot overview. It talks about how MRI works without getting too deep into the physics because radiology people, we can get pretty deep into the weeds when we start talking about physics. It avoids that. It gives you what you need to know about how MRI works. Then, it breaks down the different musculoskeletal regions with some of your major diagnostics. Great place to start.

Another fantastic book that is relatively new out onto the scene is Pope’s Musculoskeletal Imaging, a wonderful resource up to date in materials. If you want to dig deep and you really want to learn everything, there is to know about musculoskeletal imaging, particularly with an MRI focused, Stoller is the author of the Orthopedics and Sports Medicine series. There’s an extensive multi-volume series of books here, and it covers everything. This is what my residents used when they were talking about internal derangements.  Of course, we cannot talk about Radiology without talking about the big 3 radiology textbooks put out by Chiropractic Radiologists. Dennis Marchiori’s Clinical Imaging, John Taylor’s Skeletal Imaging, and Terry Yochum’s Essentials of Skull Radiology. All three are wonderful textbooks.

We live in an internet age, so, hope you are all well and good, and a lot of these do come in eBooks. But I have some website resources. So big 3. Coming to you from America, one of the resources that I do recommend very heavily is the American College of Radiology (ACR). Their website has an important thing called the appropriateness criteria. A lot of times you are going to have questions; Do I want a CT? Do I want MRI? Is ultrasound the best option? What’s okay? This is my differential; how do I follow up on this?

The appropriateness criteria are a wonderful guideline, and it talks about what imaging might be most appropriate for various conditions, particularly again using a sports medicine lens to look at this. It will talk about applications of the Ottawa criteria for knee and ankle injuries. So, the appropriateness criteria are a fantastic place to start. Regional law being with this, if you are able to order imaging, and you are wondering what the order don’t forget to always just call the radiologist. I would much rather spend 5 minutes on the phone with somebody and get the right study than have nobody get a hold of me, and I write a report that doesn’t tell you what you need to know.

Video Placement: 14:07
Other websites. This one here, www.radiopaedia.org  I have at number 2, but I should put this first on the list. As a radiologist, somebody who practices reading, and imaging every day of my life, and somebody who trains Chiropractic students and radiology residents, Radiopaedia has been the single biggest boon to radiology education in the last 20 years. It is a wiki-style website where you can contribute cases and put in write-ups, it is moderated to make sure that the information put in is cleaned up as much as possible. It is free, which is just amazing to have a reference like this. If you want to see 13 different versions of an aneurysmal bone cyst, it’ll show you 13 different versions. If you want to know, is this what sacroiliac joints are supposed to look like? This is maybe A.S. You are going to see 20 cases of A.S. So wonderful resource. They also do have a lot of other resources available, but 90% of what’s on that website is free. You don’t have to register, but it has really been a wonderful addition to radiology education.

Another good website is www.auntminnie.com . Aunt Minnie is a radiology term, and what it means is, if I walk into a family reunion, I know which one of these people right away is my Aunt Minnie, because I can see her and I recognized her instantly, it is all radiology term. If I see a raindrop skull, I know it is multiple myeloma. If I see a rugger jersey spine, I know it is hyperparathyroidism. Aunt Minnie is just another radiology education website. One of the things that they have that I really enjoy is they have a case in the day that you can sign up for and every day in your email, you will have a new interest in radiology cases. So, just some of those resources that are available to you to help you learn radiology.

Let us start talking about Musculoskeletal Imaging. Before we even get into all the different tools and things that we need to do. How about we just do a quick brief run-through. How do I read imaging the right way? There was a interesting study and unfortunately, I don’t remember the citation off the top of my head. But there was a study that used eye-tracking software, and they watched novice x-ray readers versus experienced radiologists and they tracked eye movements, looking at studies. One of the things they found was a huge disparity between the novice and the expert. Not in all the novices, in between all the novices, they are all over the place. The experts all had a very similar way of approaching imaging and looking at different things in a study. That is one of the things we want to cultivate. We want to cultivate the ability to look at images the same way every time. Why do I want to do this? Because talks there’s this interesting phenomenon in diagnostic imaging called satisfaction of search. It has been very well documented that if you have a patient, looking at imaging on a patient. Let us pick a lumbar spine. We are bringing AP and a lateral view to the lumbar spine. If there is one significant pathology on that x-ray? There’s a good probability as soon as I see that pathology, I stopped reading the film. I found something and that something could correlate with why my patient’s here. I can stop looking at the film. What is interesting is if there are 2 significant pathologies on an x-ray, there’s a ballpark about 30% chance that you are going to miss one of the pathologies. If there are 3 significant pathologies, you have gotten over a 60% probability of missing at least 1 of the 3 because we stop looking when we find an explanation.

We must be careful and aware of that. One of the things that we want is to have a systematic way of approaching radiographs, MRIs, and CTs. So that we do the same thing every time. If we must put less thought into the process, we can put more thought into the diagnostic evaluation. Our eyes can only see what our mind comprehends. We are going to start developing this systematic search pattern. Doctors have a bunch of different ways to do this. Everybody’s got their own little way probably named after themselves. Kind of like Chiropractic techniques. This is one that is fairly generic and widely used so it is an effective system for me from a teaching standpoint. I enjoy watching new students. I get somebody who is new to reading x-ray and as soon as they have x-rays up and their noses right on that x-ray monitor, they are almost leaving nose prints on my screens, and they are trying to find the smallest little minutiae that they possibly can. That is the wrong thing to do. There is an old phrase, one of those idioms, you don’t want to miss the forest for the trees. If you start zooming in really close, you might be able to tell me everything about the bark of one tree, but what does the rest of that forest look like?

Before you ever get into a point-by-point search pattern, particularly we are looking at the x-ray, pull the images up, have them all on the screen and sit back. Just take in the big picture, look everything over, and just let it absorb for a second.  Then, you can get into your search pattern, looking at each individual structure. Things to be aware of and we are going to talk about a search pattern here in a minute. Make sure you look at those things that are the areas that are hard to see. On a lateral cervical, the c-spine is easy to see, the skull, the little bit of the skull we are supposed to see on a c-spine, maybe not so much the CT Junction difficult. You need to be looking outside of that central area, and make sure that you are covering the entire margin of the film. You have to see the entire thing. I used the term film realizing we are looking at digital imaging, but you want to make sure that you look at the whole thing because not surprisingly, as chiropractors, if I take a lumbar spine study, I am going to focus on the lumbar. A lot of times, there might be something in the TL Junction. There might be something in the abdominal soft tissues. We want to make sure that we are paying attention everywhere in the study.

The other thing that you want to do is, that a lot of education is stuck in old-school film and PowerPoint. When we are talking about old-school film, or when we are teaching people using power points, you have got a picture on the screen in front of you. You cannot make it brighter, darker, zoom in, or zoom out. It is the nature of hard copy film, and it is the nature of PowerPoint. That is one of the things that you want to do is you want to use all of those DICOM tools that you have, available to you. This is where we start talking about doing a DICOM demonstration. I have a single view of the thoracic in the lumbar spine study, so again, when I am starting to approach this study, I am going to do a couple of things. The first thing I am going to do is pull up a two-up window. I am going to put the AP in the lateral next to each other, and then I am going to sit back and just take in the whole thing. I did my take on the whole thing and now I am going to focus on the AP. Don’t forget there are DICOM tools. Another one of those big recommendations, get your own DICOM viewer. There are plenty of free where available DICOM viewers. I should clarify DICOM, D-I-C-O-M. Digital Imaging and Communications in Medicine. It is the standardized language of computers for digital imaging. It is a worldwide standard and works really well. What you want to do is if, again, very regional dependent, but if you get patients to come in and they bring imaging from 3 or 4 different imaging centres, you ever notice where are the tools? One of these is built by company A, one of these is built by Company B, and one’s company C, and they are all in different places. How come those cannot be standardized? No. But that is the proprietary nature of things. If you have your own DICOM software and again, there are many freeware versions, or you can get inexpensive DICOM viewers that are fully functional. But that way, you can use your DICOM viewer to open all these studies.

Video Placement: 23:34
The patient brings in a disk, you pop the disc and you open it with your software. You can access somebody’s portal via the Internet, you can download the images, and open them with your viewer. That way, you always have your tools in the right place, and we are going to talk about tools quite a bit here today. So, as I look at this study. you know what, maybe this doesn’t look like it is that large? Well then, all I need to do is I need to enable zooming in. I will zoom in, and then after I zoom in on titled, see, everything. Zoom in and then pan around. Moving the image around is called panning.  I am panning my way through the image, making sure I am accounting for every margin as I am looking at the study. We got really lucky on this particular patient in that, really nice quality radiographs here. This person is pretty homogeneously thick. But what if I got somebody who’s a little chunky, I got somebody who has a little bit extra adipose tissue. You might notice that some areas are overexposed, and some areas are under-exposed. One of the probably single most important tools in digital imaging is the ability to window and level. We can change the brightness and contrast.  In old school films, we could not do that unless we took another x-ray with different factors. PowerPoints you know, we are talking about manipulating jpegs, so not the same thing, and realize jpegs and icons are completely different animals.

When I am looking at this study, let us say this middle portion was nicely exposed, but the pelvis was under-exposed. All I need to do is hit my window and level button. I can change the brightness and I can change the contrast. That will let me highlight different areas. If I really want to get down here into that femur, zoom in on this area on the femur. I am seeing that femur a little bit better when it was a little under-exposed before. But if I look here in the mid-lumbar, well, now there are a little overexposed. One of the other tools, that is really, it is very remarkable in its functionality is the ability to invert images. If you are ever looking at something on an X-ray or an MRI or CT and you are not sure, am I seeing something? Is that really there? I am not 100% convinced. Invert the image. It makes your brain process differently because if this is not what I am used to looking at, so I have to think more about it, and it’ll really help you decide. Is this something real or is this something not? So those are some of our fantastic tools when we start looking at these. We can throw measurements on things if we need to. If I need to measure scoliosis, I can throw a Cobb angle on things, and it’ll calculate the angle for me. There are all kinds of tools available that really make this very functional for us. Make sure you use those DICOM tools.  Then when we start getting into our search pattern, one of the important thing about our search pattern begin with making sure that we have that, doing the same thing every time. We are always doing this the same way, the ABCs. It is in English of course, are the first 3 letters of the alphabet, ABC, and the ABC is kind of how we phrase something like an introductory thing. The first thing we are doing is how to read an x-ray. What are we looking at? We are looking at the alignment /anatomy, bone, cartilage, and soft tissues. So that is our generalized search pattern. We are going to look at those ABCs to try to see what’s going on.

We are going to do this again. I am going to pull up our x-ray that we were just looking at. As I look at this image, alignments, I am going to pull a two up so that we can see both our AP and Lat on this one. Alignment is everything where it is supposed to be? It seems like a basic concept. But again, we are making sure we are starting on a good foundational level. Is everything where it is supposed to be?

I am looking at spinal imaging, on the AP views. Is the spine straight? Is this spine leaning to the side? is the spine curved? I look at the lordosis, is lordosis normal? is it flattened? Is it hyperlordotic? I am looking for all these different alignment things. Some of the other things that we do on a lumbar spine, also pay attention to whether or not your spinal imaging is done upright or recumbent. In the Chiropractic world, we tend to do our spinal imaging upright. In the medical world, they tend to do their spinal imaging recumbent. If it is a recumbent study, you have got no postural information. Always make sure is it upright or recumbent, and obviously, these are labels are upright studies. Getting into the lateral, I am looking at the lateral again from an alignment perspective. This is where I will look at things like the 4 lumbar lines. I look at the anterior body line and see if everything’s lining up. I look at the posture body line, also known as George’s line, a little jog right there. I look at the spinal amateur junction line, and I look at the spinous tip line. As I am perusing alignment in this case, I noticed there was an offset in George’s line, and there is an offset in the spinous processes. That is where I see this alignment abnormality, there’s a spondylolisthesis specifically, an anterolisthesis there be all five.

The night that I would start investigating further and get into the bone and get into the cartilage and we will get there momentarily. If I paid attention to that a-stuff, is everything there? Is everything where it is supposed to be? The other thing we need to do is we need to account for the anatomy, and now this is at the macro level, the gross level.  Count structures, there are five lumbar, and there are 2 emipelviders. There’s 1 sacrum, and there are 2 femurs. I am seeing four sets of paired ribs. I am making sure all the gross structures are there. What I am doing under that a-section, is I am also looking for anomalies in the variance. Extra parts, missing parts, are usually congenital in nature, and realized again, that another one of those interesting phenomena about neural functioning. Extra parts are really easy to see when somebody has more things in that are supposed to the one that jumps out at us that just is not right, but if somebody is missing structures, our eyes tend to fill in missing structures. One of the little catchphrases radiology is the hardest thing to see is the thing that is not there.

We will start doing that from a growth standpoint. From there, we get into the bone. I am going to go to a single up on this one. When we are looking at the bone, again I have got a very systematic way that I do things when I am training people to decrease the probability of missing things and making mistakes. The first thing I assess when I look at imaging pretend, I am focusing on an x-ray right now, I look at the density. Now, the X-ray is a lousy tool for assessing bone density, and it takes big changes. It doesn’t have great threshold discrimination. It is one of those things that it is not great, but I am still going to make sure I assess. How is the bone density? Is the bone density normal? Is it increased? is it decreased? One of the things that we want to get used to doing, is that we also want to quantify things to the extent available. When I see somebody now, this person has good bone density. If this person had decreased bone density, the bones were too loosened, the cortices were thin, and the trabeculae are starting to stand out. If I see that, one of the things I want to get used to doing is quantifying if is this mild, moderate, or severe?

We know that we are not great at this. We are very familiar with the idea that, if you ask 5 different radiologists, you might get 6 different answers. It is what the bone density is, but you want to get used to it, mild, moderate, and severe. Keep life simple. This person has adequate bone density, normal, unremarkable, whatever you want to say. The next thing that we are going to do, and this is one where again, we look at that study, we are watching a radiologist, watching their eyes with tracking software. You can see there’s a very systematic way that things are done. Going to zoom in.  The next thing we want to do is we need to trace every cortical margin of every structure, and then assess the trabecular pattern. I am going to pick on L4 as well, it is easy to do. I traced the cortex of the vertebral body, and then I am going to start running through the posterior elements. Inferior facet, lamina, transverse process, superior facet, pedicle, pedicle, spinous process.

I am going to do that for every structure, from T10, through L5, down the sacrum, looking at the sacral foramina, accounting for the cortical margins in the pelvis. Then after I trace all the cortical margins, I look at the trabeculae and make sure the trabecular pattern is okay. I see normal crosshatch patterning there in the L4 body and L5 and so forth. Then I am going to do here once I get my tools visible. I started looking at the trabecular bone and realized, is that what the super acetabular ilium is supposed to look like? There is always that kind of cross-hatched appearance, and sometimes there’s a little speculating that happens in that trabecular region. When I come down and I get down here into the femur, realizing, what’s normal to the trabecular pattern? There are the primary compressive trabeculae. There are secondary compressive trabeculae. Then there is the primary, tensile trabeculae, and those trabecular patterns create a little triangle called Ward’s triangle. All the cortical margins are intact, and all the trabecular patterns are normal, and basically, when you are doing this, the cool thing is by saying cortical margins are intact and trabecular patterns are normal. You just told me as a radiologist, my patient doesn’t have any fractures and no tumours. You have no fractures; you have no tumours.

Then we look at cartilage. Now we have a little asterisk here. We cannot see cartilage on the x-ray, and keep in mind, that this ABCs approach works with all imaging. When we are dealing with musculoskeletal, you always look at alignment, then bone, cartilage, and soft tissue. Cartilage, I cannot see cartilage on the x-ray. No, I cannot see the cartilage on an X-ray, but what I can see is I can see joint spaces, and I am looking at joint spaces. I am looking at the intervertebral disc spaces if I am looking at the lateral. I know I cannot see the Facet Joint spaces very well when I am looking at a lateral. I even cannot see it on an AP in a lot of cases, but I can also, as a part of that cartilage, I know that, yeah the facet joint is invisible but there’s the articular process. Is it too big? Is it sclerotic? Realize that there are feedback mechanisms. Things that affect joints also influence bones. When somebody decreases disk space with degenerative disc changes, they also get in plate sclerosis and osteophytes, and it kind of goes back and forth. I am looking at those joint spaces. Are they normal? Are they decreased? Are they in very rare instances, increased? Is there ankylosis? Is there any subchondral sclerosis? Is there any osteophyte formation? I am looking at all those joints, making sure I am eyeballing all the joints, and then I get into the soft tissues. The soft tissues are where chiropractors tend to fall down a little bit. This is because we are musculoskeletal specialists, and we really focus on spinal and extremity osseous anatomy, we tend to overlook soft tissues. A lot of times when I get something circled on an x-ray, we are somebody sends me a film and says, “Hey, Chad, what the heck is this?” Turns out to be soft tissue. We are going to make sure we are accounting for the soft tissues that we can see radiographically. On a lumbar spine, there’s a psoas shadow. There’s a psoas shadow, they are roughly symmetric. I can see that. We cannot see the small intestine very well on an X-ray, but we do see the large intestine, and I am following all the way through transverse and then down to the sigmoid, and that all looks good.

Then I am going to start picking out organ structures. There’s a liver. Fantastic, there’s a childney, wonderful. Spleen, most of the time we don’t see the spleen. If we do, there will be a thing tucked up there. If I start seeing the spleen below the ribs that is a problem. We are accounting for all those soft tissue structures. Now outside of the lumbar spine and we might be looking at the lungs, the heart, the trachea, c-spine, and t-spine. In the extremities, we are looking for calcifications and we are looking for swelling. We want to make sure we are looking for all those different kinds of structures as we approach our search pattern. Of course, just as a little satisfaction, we already talked about it. Our patient does have a grade 1 anterolisthesis on L5, and there are some beautiful defects in the parts interarticularis, which is why there’s that step-off in the spinous process between L4 and L5. We are going to move into talking about some of the different imaging modalities and the different things that we are going to have available to us to start assessing our patients that have trauma. There are a lot of choices. Now we know x-ray is kind of the first place we go when we start talking about imaging. When we are dealing with spinal extremity trauma, we tend to start with x-rays and there’s a good reason. X-ray is inexpensive, an x-ray is widely available.  Depending on the laws in your region, you might be able to own and operate X-ray equipment. You might be able to refer directly for imaging to imaging centers and realizing there might be restrictions where you cannot but x-ray tends to be a first-line in diagnostic workup when we are dealing with trauma cases. But what about when do I do an MR? Do I really need it? Is an x-ray going to use be useful here or should I just go to the MR? Maybe a CT would be useful. What do I do? What’s my next step? What’s my tool? Time for a little insight into me. Before I became a chiropractor, I was a mechanic. Technically, I was an Automotive machinist, but it is much more easily explained by saying that I was a mechanic. So, one of the things that as a mechanic I developed early on was a pretty extensive tool collection. I am a huge tool fanatic.

These are 3 of my toolboxes and I have a couple of others because I learned pretty early on, that if all I had was a 10-millimeter wrench, there are only so many jobs that I could do. I also learned that if all I had was a sledgehammer, I wanted to smack everything wet, and that is not great when you are changing out a window. We want to make sure we use the right tool for the job. In order to do that you have to know what the tools are and what their strengths and weaknesses are. Let us talk about some of the different tools that we are going to have available to us as we start dealing with imaging. Let us start off with a regular Run-of-the-Mill X-ray. Technically radiograph. X-rays are the little photons that whizzed by the speed of light. So, you know, even though we colloquially call them x-rays, technically radiographs are a more appropriate term. Radiographs. We are going to keep the physics explanation actually really short. Basically, when we look at the human body, we have 5 general types of tissue, and five different types of materials and those five different tissues absorb different amounts of radiation. This is called differential absorption. The only reason that we can see anything on an X-ray is where we have 2 different tissue densities butted up against each other. When we see two different tissue densities butted up against each other then we can see those things. Our five densities are air, fat, water, bone, and metal. Those are the five things.  Air does not stop radiation very well and of course, we are thinking about this. We must think about this photographically. Light exposes the film. So light, and yet, photons being light, when photons hit film, it makes film dark. Air, like in your lungs, doesn’t stop many radiations that is why the lungs are so dark. Fat absorbs a little radiation but not very much, so it is a light grey. Water absorbs a decent amount, so it is intermediate grey. Bone absorbs, quite a bit so it is pretty white, and then metal stops most photons, so it is very white. Fats are self-explanatory and bones are self-explanatory. I don’t have that much pure water in my body. Why are we talking about water? All of our solid organs are water density, so muscles and solid organs are all water density; liver, pancreas spleen, you name it, those are all water density. Vastus medialis, Vastus lateralis. Those are all water densities. The only reason we see anything on an X-ray is there is an interface between 2 of these densities. Why can I see the bone on this x-ray? Because it is surrounded by water density musculature. Why can I see that there is a change from this musculature right through here? Because there’s some subcutaneous fat, and then outside the skin there’s air. Approaching this from a practical standpoint of looking at an x-ray. As I look at this x-ray, I notice this person was complaining to their doctor about a mass on the outside of the thigh. It was palpated, there’s a palpable mess and I will be, “Is x-ray really the first place I would go for? But it is probably a soft tissue mass?” Well, the answer is probably still yeah.

Even though an x-ray might not be the right tool for it. It is cheap. It is easy. It is quick. It is minimally invasive. Yes, there is no such thing as we are safe, radiation exposure, but it is relatively low on our scale. Take an x-ray and see if we get lucky, if not, then we can always go to something more expensive, more invasive? In this case, we got lucky. What do we see? So, here I am, in the area of Vastus Lateralis. Notice I can tell Lateralis versus Intermedius versus Medialis because they are all water density, butted up against each other. Inside Vastus Lateralis, there is this darker area. It is not as dark as air, but it is not as white as muscle. Well, in between air and water is fat. What we are seeing here is, that this person has a large fatty lesion inside their Vastus Lateralis. Cool. So, we can use that application. Another place.  Another good demonstration of using this application of the 5 radiographic densities. I would like you to take a moment and look at this lateral view of the knee. I will guarantee you, as much as I can because one of the rules of radiology is there are no absolutes. The only absolute in radiology is there are no absolutes. I will guarantee you a 99.99% certainty that this patient has a fracture. I am going to give you about 10 to 15 seconds. I want you to use your search pattern and I want you to find the fracture.

Video Placement: 47:27
Time for a great multiple-choice question. We have got an A, B, C, and D choices. Femur, tib, fib, and patella. There are 4 bones. One of those bones is broken. Think about your answer, and lock in that answer? The answer is E, we cannot tell.  I do not see a fracture on this x-ray. All of the cortical margins are intact. All the trabecular patterns are normal. I do not see a fracture, but I will tell you what the 99.99% certainty that my patient is broken for one simple reason because I see that flat line right there. I want to get rid of that flat line so you can see what I am talking about. But when I look at that flat line. So right there, here’s a flat line. Now above that flat Line, there is this darker area, and then, below the flat line, there is a more opaque area. That little flat line that we are seeing between the arrows here is something called a Light Boheme arthrosis.

This person has broken the bones somewhere inside the joint capsule. While you break a bone, you are going to bleed. So, they are bleeding into the joint capsule. But if they broke in the bone marrow, that liquefied marrow fat is going to escape as well. What’s happened is this marrow fat has floated its way up and it is separated from the blood. A lot like an oil and vinegar salad dressing does, and lipohemarthrosis is a big indicator that this person has an injured captioner fracture. This is a great application of those five densities in my search pattern working on soft tissues and it says, my person’s got a broken bone. I don’t see the fracture, which means I need to look. I need some extra imaging. I even need more x-rays, or I need to think about getting an MRI or a CT, and we will talk more about that a little bit later. 5 radiographic densities, air, fat, water, bone, and metal. We can see a little bit of metal going on with this individual, who obviously had a bad day out on the golf course. As we are looking at this case, it does show us again the density, so air outside the patient. Subcutaneous fat, muscle is water, bones are self-explanatory, and then there’s the metal for this hybrid iron. One of the things that are interesting here is, if you notice in this case that I can see the interface between the deltoid and the bicep and that is because there is a fatty layer in between them. But I cannot tell the difference between bicep and brachialis because there is no fat interposed between the two. The right tool for the right job. To know what tool is right for the job, you must know what that tool is good for. Hammers are good for hitting things. Screwdrivers are good for fitting into a slot and twisting, we don’t want to use screwdrivers as chisels. What is x-ray good for? X-rays are great for looking at bones, especially if I need to count things. If there are extra parts or missing parts, great tool. It is fantastic at looking at fractures if I am looking for broken things. But I do have to realize there are some limitations. Some fractures are notoriously difficult to see, like scaphoid fractures and rib fractures, and that is where I have got to keep that in mind which fractures might be more difficult to see.

It is good at looking at joints. Now realize when we start talking arthritic conditions, whether we are dealing with degenerative or inflammatory conditions, we are not going to see, you know, 5 days after somebody starts getting inflammatory arthritis, we are not going to see them on x-ray. Takes time before those things show up radiographically, but it is a good way of assessing those joints, and not surprisingly, biomechanics. Evaluating a lower dose. Looking for a spondylolisthesis. Is there a Scolio? Those are biomechanical concepts. Things that the x-ray is not good for, and this is a classic example of a patient with metastatic disease. The patient is elderly, has unexplained pain, getting progressively worse, progressive weight loss, and dark stools. Everything that is said that it was a malignancy going on with the patient. One of the students said, “Well, I take an x-ray, and if the x-ray is normal, I would go ahead and start treating the patient.” Well, that is a problem. Because an x-ray is not good for early destruction. Negative x-rays don’t rule out things like metastatic disease. Negative x-rays, say that the structure is relatively normal. But a number that we need to remember is that it takes 30 to 50% destruction before anything shows up on an X-ray, and if I have got somebody who’s got a metastatic disease, it is destroyed 20% of the bony structure, and the vertebrae, that is going to be drastically weaker. But it is still going to look radiographically normal. It is not great for looking for early lytic disease and we cannot use an x-ray to rule out things like metastasis. Similarly, when I look at a generalized bone density, you know, so when we get into bone, the first thing we do is assess bone density. I realized it is got its weaknesses. Can we identify osteoporosis on an X-ray? Absolutely. Is it the best tool? No. But I am still going to look for it.

The other thing to realize is even though soft tissues are part of our search pattern, an x-ray is really not great for looking at soft tissues. If I need to figure out if somebody has a partial thickness supraspinatus there, what’s that going to look like? normal shoulder x-ray. If I am trying to figure out if somebody has an MCL tear in the knee, these were collateral ligaments, am I going to see that? No, probably not. Can I see some other findings? Yes I can. I am realizing that if I am looking for soft tissue problems, an X-ray probably is a great tool you know? I might be starting there, and kind of along the example, of along the lines of our previous example. Let’s talk about metastatic disease. If somebody has breast cancer that spreads to the bone, or prostate cancer that spreads to the bone, it really spreads more to the marrow than it does to the bone itself. Metastatic disease is primarily a marrow pathology, it is a marrow-replacing disease and marrow is soft tissue. X-rays are not great for looking at the marrow. Same thing for things like infections, Osteomyelitis. Osteomyelitis is an infection of bone and myelitis bone marrow. It is more bone marrow than it is bone.

This is not a great tool for those early things. If those are on my differential list, I know that an x-ray is not going to be a rule out. It is just the first part of the diagnostic workup. Now, this applies a little bit more to places where you can own and operate x-ray machines and fewer places, either folks who just send out imaging or if you have to send out Imaging. If you are taking your own x-rays, one of our huge rules in radiology is one view is no view. If we are taking x-rays of any body part, generally we want to have at least two views and sometimes three if the anatomy is more complicated. There are no absolutes in radiology things like an AP pelvis being an exception, one view is no view, and please make sure you are doing standard views. If you want to do made-up views, those are fine. I have made up more than a number of views in my own life.

However, I always start with the minimal series. Standard x-rays and not made-up things. Things that anybody that works in the radiology world will be able to recognize and start with that minimal series. Look at the clear minimal series. The number of places where as soon as it is a neck problem, I am getting seven views. That is a lot of x-rays that you really, probably don’t need. So, clear the minimal series and then decide if you need some extra views.  Now, again is it a little different if you are having to refer patients out? Do I have to send somebody back and forth 15 times? No.  But think about what views I really need. What is really going to change my diagnosis or what’s really going to change how we treat the patient? Talking about some of the extra views, I am jumping to the bottom of the slide and look at some of the extra views in the extremities when we get to those various pathologies. I am talking about Radiohead fractures, about doing the hyper supinated view, things like that. But in the spine, the major extra views that we talked about in the spine are the obliques and the flexion-extension to use. I will be honest with you, as far as obliques go, I am not a fan of obliques, either cervical obliques or lumbar obliques. Because I can see most of what I need to see on an AP and a Lateral. I think obliques are way overdone because they can see what I need to see without the extra radiation exposure.

I will show up some pictures here in a little bit because I would like to get off, I am a picture guy. I don’t like the text slide so much. So that is obliques, we will talk about that in a second and then flexion-extension. If I am worried about ligamentous injury, if I am worried that somebody has too much motion in an area, that is where reflection extensions come into play.When we start talking about cervical obliques the primary thing that we see when we are talking about cervical obliques is, that the cervical obliques are designed to show us the neural foramina, the IVFs. But they are also good for showing us the posterior elements. I can see the pedicle, I can see the articular pillar, and there’s the other pedicle through here, and by looking at a set of obliques, I can evaluate those posture elements. It was concerned that is there a facet fracture there? Is there a laminar fracture? Lumbar obliques, when we look at lumbar obliques, are primarily designed. The number one thing that we see on the lumbar obliques is the pars interarticularis. With that being said, we also see the rest of the posture elements. Superior facet, transverse process, interior facet, lamina, and pedicle, so we can see all those different structures.

Cervical obliques, if I was worried about a posture element fracture or encroachment neural foramen, I do a cervical oblique. Lumbar obliques are designed for looking mostly at that parsed. Now, if we think about this though, the pars. The pars are that thing that we are worried about in patients with the pars interarticularis we saw previously. If I see a part of the effect on the lateral, why would I get a set of obliques? You know, what it is going to tell me, yes confirming what I already saw. If I am not sure, then I think about the obliques. But, what’s the most common level for us to find pars defects? L5. What’s the best way to see the L5 pars? Not the obliques. The best way to see the L5 pars is this view, Ferguson’s view. This is a tilt-up x-ray, so we tilt the X-ray tube up 25 to 30-ish degrees. What this does is it gives us a beautiful frontal view of the lumbosacral junction, and by doing that, I can see the area of the pars interarticularis, just as well, if not better, but I could understand on obliques and I saved a ton of radiation exposure. The other thing that I evaluate, and the other big reason that I ordered this Ferguson’s view also known as an AP Angulated lumbosacral spot. The other reason I do this is when I want to look at the outside ones, beautiful view for looking at the outside.

What else? Flexion-extension views. The big deal with flexion-extension views? We are looking for instability. I have got somebody who’s not getting better. I have got somebody who’s got a clunk. I have somebody who says, I feel unstable. Big deal on the flexion-extension to use? They are not that useful in the acute patient, because I am dealing with somebody who’s got muscles, you know if I ask my patients to do active range of motion, and that is their flexion, and that is their extension. Yeah, I am not going to see any ligament instability on an X-ray. I have got to wait until there is a fuller range of motion before I can assess instability.

Once the muscle spasms are down, if I am worried about instability, then I will think about flexion-extension studies. Not that useful in the occupation. In a case like this, we have somebody who is post-trauma, and on the flexion-extension, the most important thing I see is, wow, there is a big increase in the Atlantodental interval, I am worried about the integrity of this person’s transverse ligament. Another special note from a sporting side of things. When we deal with the special Olympics, one of the things about special Olympics is, when we start dealing with individuals who have down syndrome, folks with down syndrome cannot participate in several of the more contact sports in the Special Olympics. Unless they’ve got flexion-extension cervical spine clearance because there is a frequency of transverse ligament agenesis and insufficiency upwards of 22% in folks that have Down’s. As we are talking about instability, one of the things we must be aware of is the types of instability, and I am focusing on the spine, not so much on the extremities right now. I am going to talk about those as we get to them. When we are dealing with spinal instability, one of the big things about spinal instabilities is 3 kinds, translational, angular, and upper cervical. So, for translational instability, I have got 2 vertebrae here and there’s a little animation. I want you to watch this animation. This is translational motion. We are seeing where one vertebra is shearing on top of the other as it slides back and forth.

We typically cannot watch the motion while it is doing this. So, how am I going to assess this? Well, I do flexion-extension radiographs, and when I do those flexion-extension radiographs, there is the back corner of the vertebrae and there’s the back corner and I would measure that distance. There is the back corner, there’s the back corner, I would measure that distance, and I would know how much total motion is there. The cervical spine is 3.5 millimeters and the lumbar spine is 4.5 millimeters. That is an indicator of instability. Too much motion because of ligamentous damage. Now the other kind of instability is angular instability. Here, we are talking more about that instantaneous axis of rotation. You can see how the upper vertebrae are rotating too much on the lower vertebrae, and what we would do is again we will be looking at flexion-extension radiographs, and there are different ways cervical versus lumbar. I am not going to get too much into this because it is a little beyond the scope of what we are doing. What I do is I would look at the angle created by the end plates, and I would look at the angle created by the end plates, and I would take this angle. Doing this way, I would take this angle and I will take this angle and I would see how much angular motion there is. Again, we have got to find criteria for what is too much. The other instability is upper cervical instability. There’s a slide with a lot of text. Let’s look at pictures. The big idea here is whether we are looking at neutrals or whether we are looking at flexion extensions, there’s a malalignment between C1 and C2. Here we can see where everything lines up the way it should. This is what it is supposed to look like, both on and radiographed and schematically. Well, if I go to this, in this case, I can see where C1 has translated relative to C2. C1 has moved too far while C1 is moved too far forward.

Well, first I need to figure it out because there are 2 things, 2 big things that result in upper cervical instability. It is either a problem with the transverse ligament or it is a problem with the dens. If C1 moves forward as it has in these cases, this can be either transverse ligament or dens, and I want to try to figure that out. The way that I figure that out is I come up here and I look at the Atlantodental interval. We can see here that the ADI is increased. Well, if the ADI is increased, that means the transverse ligament is gone. It is ruptured, it is inadequate. It is insufficient, it is lacking. If the ADI is normal, and again our ADI rule is 3 millimeters or less than on adults, and 5 millimeters or less than on children. If the ADI is normal, well that means that the transverse ligament is still tying the dens to the anterior arch, but it means that the dens are no longer attached to C2, and that is a dens problem. It is either an oxidant odium or a type 2 odontoid fracture. There is the remote possibility of odontoid agenesis, but of course, then you cannot see an ADI. What if C1 moves backward? If C1 moves backward, what we are seeing here schematically, that is a dens problem. Because C1 cannot move back to the dens in the way, that means that if C1 has moved backward, that this person, either has a type 2 odontoid fracture an oxidant odium, or odontoid agenesis which is what we are seeing here. That makes a great place for us to stop our first hour of imaging and sports injuries. In section two we will finish talking about the different choices that we have available to us as far as the tools in imaging.

[END]

Section 02_ICSC03
English Direct Download PDF 02_ICSC03 Section 2_Modalities

Instructor Dr Chad Warshel
Video Lesson: 01:05:03

This second module is going to continue our discussion of various imaging modalities left off after the first or at the first hour, we are talking about x-rays and radiographic procedures and what their strengths and weaknesses are. It is time to get into some of the other diagnostic imaging procedures that we may or may not need to use. What are their strengths; what are their weaknesses; indications, contraindications, and so forth. Going back to my tool reference, we want to know every tool available to us and when we should be using those tools. As we start getting into these different tools, the next thing we would come to which we are not going to spend a lot of time on, but something that is a very interesting modality is fluoroscopy. This is marketed under several different names. You might see something called a digital motion x-ray. You might see video fluoroscopy, but at the end of the day, it is all fluoroscopy. What fluoroscopy is, is a live time motion picture x-ray. When we start thinking about looking at our regular radiographic procedures, standard x-rays, those are snapshots.  It is just like taking a still picture and it is exactly what it is. It is a still picture of that single moment in time. There are times when we want to look and see is their instability.

If we are looking for somebody who had any kind of severe neck injury, we are worried about ligamentous damage.  I was just reading an article about skeletons rider the other day, and their face is only inches away from the ice, traveling at 80 miles an hour. Sounds like a potential neck injury there. Look for ligamentous damage. Well, how do we really assess ligamentous injury? We do that by utilizing flexion-extension radiographs. That is the gold standard. It is what we have always used.

The idea with flexion and extension radiographs is, they are fantastic for looking at the end ranges of motion when the person’s chin is tucked and they are all the way forward. Then when their chin is jutted and they are all the way back. But what if this person has an instability where vertebrae move too much, we talked about the translational and angular types of instability. What if that instability is somewhere in the middle of the arc of motion? When they are fully flexed, they have got enough muscle spasm and guarding that it is pulled everything back to where it is supposed to be. Same thing in extension, they hit that terminal range of extension, and everything guards, and you know, the muscles can help align the bones. That person might look normal on conventional radiographs. What if somewhere in the middle of that arc, between terminal flexion and terminal extension, right about here, that is where the person had a clunk? That is where fluoroscopy comes into play. Fluoroscopy lets us look at the entire range of motion as the person is doing it, to see if there is any mid-range instability. It’ll also show us terminal instability, but it is, what it is really designed for is middle ranges.

Things about fluoroscopy, our big indicator, why do we do it? Looking for instabilities. What are the downsides, why do not we just do fluoroscopy on everybody then? Well, a couple of downsides. One is it is not nearly as readily available. While most imaging centres have C arms that do fluoroscopy and things like that, they do not really do MSK fluoroscopy looking for the instabilities. It is not as widely available. The image quality is quite often very poor. Has it gotten better over the years? Naturally, it has, but when you look at a lot of fluoro images, fluoro images are not necessarily crisp and clean and clear. Because of that, one of the things that you really need is if you are going to have a fluoro study of a patient, you also must have at least a minimal diagnostic series of x-rays. So, I pick on C spine because that is the one that we do most with fluoro. I must have at least my three-view series, AP, AP neutral, lateral, then I do the fluoro. This is something that is above and beyond looking for those motions because it is not great for looking for subtle things, small fractures, things that are difficult to see like that. It is more for growth structures. Because this is something that must be done in addition to a minimal series of x-rays, we are looking at some additional radiation dose. The radiation dose, when we look at a well-done fluoro study for a C spine, is about the same radiation dose as a seven-view cervical conventional radiographic study. The dose is not super high, but keep in mind that you are also doing the minimal series on top of that. There is a dose consideration that must be used, and it really is, is very operator dependent. You have got to be sure you have somebody who is careful with the fluoro unit and sure they are not overdosing. Other downsides, they are only good for small structures. When we start looking at the fluoro that are in use in most chiropractic style settings, they tend to be small office underpowered units. Because of that, they are great for C spines. I can use them for wrists and ankles, looking for some different kind of instability through there. They are not great for the lumbar spine. There are really a couple of reasons that are not great for the lumbar spine. One, they are underpowered for dealing with larger lumbar, and two, your field of view is that large. It is one thing to keep a C spine inside of a circle that large when you are doing flexion-extension, but if you are trying to keep the lumbar spine inside that little field of view as a person’s flexing and extending, a lot of times they are in and out of the field of view. This is where it got its pluses, it got its minuses. The other thing that we run into is one that there is a lot of different laws and rules around fluoro, picking on here in the USA as an example, in California, as a Chiropractor, you can own and operate a fluoro unit. In the state of New York, you cannot own it, you cannot operate it and you cannot even order it. In other countries, there is going to be different laws with fluoro.

Video presentation placement 06:28
Just to show you a fluoro study that is kind of an interesting fluoro study, and before I go further, I am going to apologize right now, even as far as fluoro goes, this one is not great quality. But it does demonstrate a nice example of a concept. You are going to watch the arc of motion through here and what I want you to do is I want you to focus in on the upper cervical spine. So, they just bump the arm up a little bit. Now they have got the person flexing forward and then they have got extending, flexing forward. Hopefully, you notice as this person is flexing and extending there is way too much motion there at C1. So as the person is there in neutral, and as they start to flex, C1 has translated forward, which gives us that dens versus transverse ligament concern. But as this person goes into extension, which you will see here right now, notice that the anterior tubercle landed right on top of the C2 body. Because C1 has translated posterior, that means we know that this is a dens differential, and this is a patient who turns out to have an Osgood-ontodium.

From there, we come into our next imaging modality. As far as things that we as chiropractors look at, we look at a lot of x-rays, the number two thing we look at, MRI.  We look at magnetic resonance imaging a lot because this is really the best tool there is for looking at a lot of soft tissue abnormalities. MRI depends on state country requirements, what you are allowed to do and what you are not allowed to do. This is what we order a lot of, or we are going to end up having patients follow up to get the MRI studies. Now, as we start looking at MRI, magnetic resonance imaging, when you look at your pre-chiropractic education, for those of you who may have had organic chemistry, before you ever went to chiropractic school, sorry for a bad O-chem flashback, but for those of you had O-chem, you remember NMR, nuclear magnetic resonance, you would take a chemical, you put it in a small little very thin glass tube that had fins on it. You drop it in the NMR, spins it up, and then you got a peaked graph that showed you the different chemical compositions of the material. Well, Docs, that is an MRI unit. That is all an MRI is. An MRI is the same thing as the nuclear magnetic resonance that you did in O-chem.

So why is it not called NMR? Well, originally it was called NMR, and then, well, the problem was this became commercially available as an imaging tool in the 80s and nuclear was a bad word in the 80s. So as a marketing thing, they changed it from nuclear magnetic resonance to magnetic resonance imaging. By the way, I am full of useless facts when it comes to radiology. Why MRI? Why is this the second most common imaging modality that we as chiropractors utilize? Because it is great for soft tissues. The thing that MRI does is we are able to distinguish all the different soft tissues of the body. Not only are we looking anatomically, but we are also looking physiologically. We can start assessing not only if there is a tendon, is there oedema in that tendon? Is there oedema around the tendon? Is there fatty atrophy of a muscle belly? We can get anatomic and physiologic information all in one fell swoop, which is really, really nice. We also do not have the restrictions that we have with a conventional x-ray. With an x-ray, we are squeezing a three-dimensional person onto two-dimensional film. Because of that, there are a lot of overlapping structures. One of the terms that you are familiar with from an x-ray standpoint is the mock effect. If you are looking at an AP open mouth radiograph, sometimes you will see the gap between the incisor teeth looks like a vertical fracture of the dens. Well, one of the things with MRI, is we do not have overlapping structures that way because we are taking individual slices of the patient. We get to do these slices and we can image in any plane, we can do axials where we go down and we are just slicing through. We can do coronals, the same way we can do sagittal, we can do any view. If I want to be 22.7 degrees off the axial plane to see something, I can do that. Probably the single biggest benefit of MRI, there is no ionizing radiation. Unlike x-ray, unlike CT, fluoro, and bone scans, there is no ionizing radiation. This is a giant magnetic field. So, because of that, there has never been shown to be any negative consequence to having an MRI, unless there are certain contraindications that we’ll talk about it a little.

That being said, MRI centres tend to be a little bit more cautious about imaging pregnant patients because they do not want to take the risks. What if something were to happen, same thing with infants. Not to mention they move around a lot. So, but, they even do fetal MRI. If they are trying to evaluate, if there is something abnormal about fetal development, fetal MRI is a thing. It is a great tool, and it is a very safe tool. Is it always super comfortable? No, because there are the downsides of a tight little tunnel and the bigger the patient, the harder it is to fit them in. Most regular MRI units can fit somebody up to 250 pounds, maybe 300, if you are pushing it. There are now what are called open bore MRIs. It can get patients up to 500 pounds, these are widely available. If you get somebody who is particularly large, we start getting into the powerlifter category where we are dealing with very large individuals, realize that one of the options available for those athletes, where you get somebody who’s starting to push over 400 pounds, and the table cannot handle them, there are veterinary MRI units. It is something that I have seen done with a 600-pound patient who needed a lumbar spine MRI. They went to the veterinary hospital, and they used the horse MRI on them. There are some interesting availabilities there. The downside of MRI, it is not super readily available everywhere. Here in the US, MRI centres are widely available but outside the US, it might be much more restrictive. It might be more difficult to get your patients in. We run into problems with metal.

Video Placement 13:07
I am going to show you an interesting MRI of somebody who has a knee replacement here in a little bit. Claustrophobics, this is a very tight little tunnel. If you think back to the original picture on this one, actually, let’s just go back to that original picture. That is a small tunnel, and particularly when we are talking about things like brain MRI, on a brain MRI, this is called a head coil. The person’s head goes inside that little cage and then their body goes inside the giant magnet. Claustrophobics can have quite a bit of problem with MRI and that is where open bore MRIs come into play, and that is also where open MRIs are an option, though I’ll be honest with you docs, I try to avoid open MRIs at all possible costs. Is it there? Yes. Is it functional? Yes. Is it great? No, I would much rather have my patient get a closed MRI. The larger the patient, the harder is to get a scan, again, 250, 300 for closed MRI, 500 for bore MRI and open MRI. We will talk about contrast here momentarily. This is a more expensive study. It does cost quite a bit more and trying to get approvals is not always an easy thing to do.

Now the question who can have an MRI and who cannot have an MRI? Going back to my pre-chiropractic background, I was an automotive machinist slash mechanic, and I still do a lot of work for fun using grinders and there is metal in the air. Before I can ever have an MRI, I have to have an x-ray of my skull. That is a requirement. I must get an x-ray on my skull to make sure there is no metal in my orbit because if I have little flakes of metal that are implanted into my cornea, they can move around in an MRI and lacerate my cornea. That is the low end of things but what about the high end of things. What if there is something that is magnetic, like say an aneurysm clip in the circle of Willis?  This is old school. The newer clips are usually MRI-safe, but older MRI clips might move around. Probably a bad thing if the clip holding your aneurysm closed is starting to wiggle around. Pacemakers, now again, these days, there are MRI safe pacemakers. There are pacemakers that can go into the MRI unit and not have a problem. But if a person has a pacer, that is an issue. So before getting an MRI, you are going to have to find out what kind of pacemaker is it and make sure you get approvals. Another really good resource if you are ever questioning this ask yourself, “Is this something that I can do at MRI?” MRIsafety.com is an excellent website and has some great information there.

Video Placement: 15:46
Some relative contraindications or some things that make things a little bit more complicated. Metal in the area. The first rule, if there is a joint replacement, you do not do an MRI of that body part. I am going to show you a knee MRI of a knee replacement here shortly. But what about things like inner body spacers when somebody’s had a fusion or if I have got somebody who has pedicle screws? We can work around those. There are techniques, that decrease metallic artifacts. We can work around those things to the extent possible. Now, what if I have somebody who has a pacemaker and cannot have an MRI? It is not an MRI-safe pacer or maybe they are not sure, then we go to a CT and we’ll work around things that way.

Most imaging centres will have protocols for pregnant patients. I read for an imaging centre that does not image pregnant females, they’ll refer him to a different centre in town. They just do not want to deal with any possible complications there. Claustrophobic patients. With claustrophobic patients and obese patients, the same kind of thing, that is where open MRIs can be useful or open bore MRIs. The ones that can accommodate larger patients also have a bigger tunnel, so it is not quite as claustrophobic, still not fantastic, but it is better. There is also the option of having your patients sedated. They can give the patient medications, anxiolytic medications, and things like Ativan that will help them be able to tolerate the MRI. But again, that is a very patient-dependent circumstance.

The other thing that we need to know about MRI is this is not a class on MRI interpretation, but we need to understand the basics much like we need to understand the basics of x-ray. When we talk about MRI, one of the things that gets thrown around a lot when we are talking about what something looks like on an MRI, is what does it look like on T1? What does it look like on T2? How’s the grading on echo? MRIs come in these things called waiting’s, otherwise known as pulse sequences, and what these are is they are different settings on the MRI that let us highlight different tissues. So, I’ll talk about this here momentarily. Big deal though, you do not need to tell the imaging centre what pulse sequence is to do. The imaging centre has predefined pulse sequences. What they do is they base their study on what it is that you are trying to rule out. So, when your patient is getting this appointment, when you are getting the preauthorization, the big question is, okay, you want to MRI the lumbar spine? Why? What’s the purpose? Because if you say MRI lumbar spine to rule out disc herniation, we are going to look at a disc herniation set of pulse sequences. If I tell the imaging centre that this is an MRI of the lumbar spine to rule out spondylodiscitis, I am going to be looking at different pulse sequences and they are probably going to put contrast on the lumbar.

Video Placement 18:57
So that is where letting the imaging centre know what it is you are looking for is important in this circumstance. What I am going to do on these pulse sequences is I am going to talk you through some of the slides here, but I am also going to do some live demos. You can see some of this MRI from the perspective of the radiologist. Now, main pulse sequences, I could spend hours talking about pulse sequences, A, because I am a nerd, and B, because there are a lot of them, but these are the major pulse sequences that we will see as we look at MRI, T1, T2, proton density, gradient echo, fat suppression, and diffusion. Those are the big sequences and I’ll touch on each of these individually. You will see, there is also a lot of brand-specific names. Hitachi might call a gradient echo one thing, Siemens might call a gradient echo another thing, and Toshiba might use a third name. So those are brand specific, but they are still gradient echos. I am approaching these from the terms of the generic names.

Of the two pulse sequences or of all the pulse sequences, the big two are T1 and T2. Everything else is kind of a hybrid of T1 and T2. Now, without getting too much into physics and without reading repetition times and echo times and things like that, the thing about T1 and T2, everything in the human body has two major compounds in it. There is some water and there is some fat. And when I am trying to evaluate different anatomic structures and pathologies, I might want to see something that is more towards a fat side, more than more towards a water side. Well, T1 is fat, T2 is water. The way to remember that, T2 H2O. So T2 H2O. T2 shows me water. T1 shows me fat. Now, why do I want to look at fat? Well, I am not talking about subcutaneous fat here as a generality. I am talking about marrow fat. I am talking about epidural fat. I am talking about fat pads around joints and around muscles.

Using the spine as an example. How do I know it is a T1? Well, you compared neural structure to CSF neural structure. Myelinated axons have a lot of fat, and CSF is pretty much water. When I say that a pulse sequence is good for something, what I mean is that is going to be bright on the MRI. So, T1 is good for fat. Fat’s going to be bright. T2 is good for water. Water’s going to be bright. As I look at this thing, the myelinated axons are brighter than the CSF because, well, the fat is brighter. As I look over here at the axial, I can see the thecal sac, individual nerve roots in the lateral recesses, surrounded by epidural fat. So, T1 is good for fat. Now, what am I looking for? Epidural fat marrow. T1 is the pulse sequence that we spend the most amount of time looking for marrow pathology. One of our really important things to remember is T1 bright all right. If something is bright on T1, that means it is got a lot of fat and generally, a lot of fat means it is not malignant, particularly when we are looking at the bone marrow.

If something is dark on T1, again, particularly looking at bone marrow, that is a big problem. The other side of the equation is T2. So T1 is good for fat. T2 H2O, T2 is going to show me water bright. I am not looking for pure water. I am looking for CSF. I am looking for joint effusions. I am looking for oedematous changes in soft tissue structures. So, the same patient as before, and now I can see where if I look at the conus medullaris, it is darker than the CSF, or the other way to say it, the CSF is brighter than the conus. It is good for water and what the T2 is really from a spine standpoint, it is designed to look inside the thecal sac so we can see the spinal cord or nerve roots, depending on where we are at. It is good for looking at the hydration of discs, and this is the best sequence to really detect disc herniations because we can see where the disc is displacing the thecal sac. So, good for looking for oedematous changes. Now, something to realize is that T2 pictures are not quite as high-resolution.

In comparison, I am going to do a live demo that’ll make a little more sense for this. Other pulse sequences, proton density, PD. Now with proton density, a proton density is a hybrid of T1 and T2. W

hat that means is it is not great for fat and it is not great for fluid. What it is great for, are tendons ligaments, and fiber cartilage, and it is really high resolution. So where I spend the most amount of time looking at proton densities is really when I am looking at knees or I am looking at wrists and I need to evaluate for meniscal injuries. It is also really great for tendons and ligaments. So and we’ll see that in a little bit, but just as a quick demo, so notice T2 I can see a meniscus, but the resolution isn’t fine. Over on a proton density, now the meniscus is really jumping out at me, but on a proton density, things like an effusion, do not jump out at me because it is not bright. We can see where this patient has a suprapatellar effusion.

What about gradient-echo? Gradient echo, not getting into physics on this, but when we look at gradient echo, what a gradient echo is really strong for is showing a T2 effect with much higher picture quality. So, when I am looking for small structures, I want to look at a gradient echo. So where are gradient echoes really used? Small extremities, and I always want gradient echoes on wrists and ankles and hands and feet. We also see it in the axial cervical spines. So axial C-spines will generally have a gradient echo done because that lets us see those smaller cervical nerve roots.

Another major pulse sequence, fat suppression techniques. There are a couple of different terms that you will hear thrown about when it comes to fat suppression because of one of the problems we run into. So, I am going to back up a few pictures, if we look at this spine. So T1 here, T2 here. We know that T1 is good for looking at fat. T2 is good for looking at water but notice that on both the T1 and the T2, the subcutaneous fat is really bright, again without getting into physics, that is a problem. So sometimes what we want to do is we want to make sure that we kill the signal from fat. And we kill the signal from fat and what that does is it really highlights any kind of oedematous tissue. As we start looking here, we are looking at a T1 and a stir coronal on a knee. This is a patient who has a tibial plateau fracture. Notice we can see the oedema much better here on the coronal stir. Now it is not a high-resolution picture, but I can see it better. Because here’s a thing, I can see this on the T1, why are we so worried about this? Because neurology, one of those things that we understand from a neurologic standpoint of the neurology of visual and visual detection, human eyes are naturally drawn to bright, shiny objects. So our eyes see bright things better than they see dark things. Because of that, these stir sequences really help the oedema jump out at us, even though I can see oedematous change as a darker signal on something like a T1. And it also helps us characterize what kind of tissue something’s made of. Now, we have already seen this patient. We saw this patient in the first hour, they were complaining about a mass in their lateral thigh. An x-ray was done and on the x-ray, there is air, fat, water, bone, and metal. It is a fatty density superimposed on the area, the vastus lateralis. Well, when we go to MRI, so we are looking at an axial T1, and on the axial T1, there is the mass, it is got a lot of fat to it. Then on a coronal fat suppression sequence, we can see where, fantastic it suppresses, it is got a huge amount of adipose content. It is an important thing for this one because what do we think of when we see a fatty lesion? We think lipoma. Well, except there is also liposarcoma and various other soft tissue fatty tumours. Well, the fact that this has so much pure fat too, really helps confirm that I am dealing with a lipoma and not a liposarcoma.

Video Placement: 27:40
It is now time to look at a live DICOM demonstration to show you some of these things live time. I have pulled up a lumbar spine MRI. Recommending that you have your own DICOM viewer for you to pull these things up, and I am not going to get heavily into how to interpret these, but just as a light version thereof. We can see over on the left side, that as we are looking at the MRI, we have got all the different pulse sequences, and this one’s nice enough to label things for us where T2, T1, and so forth. When I start looking at spinal MRI, I only use imaging centres when I am sending patients for spinal MRI. I only send them to centres that will do a stir sequence in the spine because I want to make sure I see that oedematous change. As I am scrolling through, I can see, well, okay, everything’s really dark except for the CSF column and some blood vessels. In this particular case, as I am evaluating this patient, looking at this MRI, one of the things that I can see very nicely, and one of the things that these fluid-sensitive sequences are good for, everything lining up the discs looks okay. Suddenly, right through there, there is some disc material. The stir is specifically designed to look for oedematous change. We are not going to see usually oedema around most disc herniations, but I am looking for fractures and things like that.

Kick over to the T2. Now, you can see it is a lot brighter and on the T2, again, this disc herniation is showing up very nicely. Now, something to be aware of in this particular case is that this person does have a lumbosacral transitional segment. You might have heard the terms, lumbarized or sacralized, we try to get away from those terms, to be honest with you, it is better to describe these as transitional segments. But this person has a disc herniations level above the transitional segment. When we look at T1, T1 is really designed to look at that marrow fat. We can see the epidural fat very nicely as well. And then kicking over to the axials, on the axial T1, do not forget we have to look at all the other structures. We can see kidneys, aorta, vena cava, and so forth. But I am usually looking at the epidural fat. I am looking at the muscular integrity of the paraspinal muscles, fatty infiltration of the multifidi being a very common thing to see. If I am looking for disc herniation, I do not spend a lot of time on that T1, just scanning really quickly. I spend more of the time on the T2. Now, some things to be aware of as we are looking at MRI, pulling a three-up window view here, do not forget to zoom in and zoom out. Remember to move the images around so that they are where you want them to be. Get them into the centre of your window view. Do not forget that you can also window and level these images to make sure that they are not too contrasty, so play with these features. You cannot save changes to the native DICOMs, they are always going to be preserved, but you can save things as layers. So play with the images, and as we are looking at this, we look at the axial of course. The nice thing with digitals is the little line will tell us exactly where we are. It is called a localizer line. We know that we want to spend the most time looking at that L4 L5 disc. So, we get down through here, and we can see there is that protrusion. It is starting to narrow the lateral recess right through here. Fantastic. The other thing that we notice when we are looking at this sagittal, notice that there are some marrow changes as we are looking at the vertebrae, there are some marrow changes.

I’ll talk about this when we get into the spine is this person has something called a modic change. By looking at the T1s and the T2s, I know that this is a type two modic change, which has almost no correlation with symptomatology. It is an incidental finding. But those are our different starter pulse sequences, T1, T2, and stir sagittal axial. Some other pulse sequences, one of the places that we’ll see another important pulse sequence, I am going to pull up a C-spine MRI. As we look at this C-spine MRI, I am going to pull a two view window just so you can see the sagittal. This person has some pretty interesting, gnarly-looking disc herniations plus some congenital stenosis. As we look at the axial on this one, one of the things to realize about this axial is, that this axial is what’s called a gradient echo. Normally we think about T1 and T2, the problem with T2s in the axial plane is they do not give us the resolution we need, but as we look at a gradient echo, and notice it on this gradient echo, I can actually see the dorsal and ventral rootlets that come together to form the cervical nerve root. So, we get a much higher resolution for structures.

We need to see if there is no flow void artifact created. One of the problems with T2s is because CSF moves and T2 is a long pulse exposure. We run into the same problem, we run into with cameras with long shutter speeds is it can blur things out. But in this case, I can see the CSF very effectively. I can see disruptions in the CSF column for this patient and their fairly large disc extrusions. Then again, we can start to see dorsal and ventral rootlets in the lateral recess in the C Spine. So that is gradient echo.

Now, the other major pulse sequence that we are going to talk about is proton density. Now we do not really do proton density in the spine because we do not want that hybridized T1 T2. We are not so worried about the fibre cartilage. We are not so worried about the small ligaments in the spine. We see this more used with the extremities when we are talking about proton density.

As I pull this one over and we look at the knee, I am going to pull up a side-by-side comparison, called a two-up window, T2 is over on the right proton density, fat-suppressed is on the left. So PD, so it is not good for fluid. It is not good for fat. It is great for fiber cartilage and then you fat suppress it and it makes it even better. As we pan through, so we are starting on the lateral side because you can see the fibula and we are scrolling in, and I am looking in the areas of the menisci. I am coming all the way to the medial side, just so we have a normal. When I am looking at this T2, I do not see the menisci really well because the hyaline cartilage and the fiber cartilage have a similar signal. I do see that this person has quite a bit of oedema in their knee, but I can see the menisci over here on the proton density, I can see those menisci very effectively, posterior horn and anterior. Now, as I scroll through, there is the PCL, there is the ACL. As we come out to the lateral side again, I do not see the menisci really well when I am looking at the T2. But as I look at the proton density, I am really not seeing much posterior horn at all. But one thing I do see is I see there is the anterior horn and there is the posterior horn in the anterior compartment of the knee because this patient has something called a flipped bucket handle meniscus.

So those proton densities, we use heavily in the extremities to look at fiber cartilage, tendons, and ligaments, shoulder studies, wrist studies, knees, and ankles. That is where we are going to see a lot of PDs. Generally, we are also going to see quite a few gradient echoes. In this case, there is also a proton density for the axial. To pull a single up, and what this is also letting us do, is it is letting us evaluate the hyaline cartilage. As we look at that patellofemoral joint. So, I am going to close out these other windows and take us back to the PowerPoint. So, that was our live DICOM demonstration. Other things that we need to be aware of when we started talking about MRI is one of the questions that is often asked if your office is scheduling the MRI or, you know, when you are sending off a referral letter for request, do we want contrast? Gadolinium is the contrast agent that is used for MRI and it is a very safe material. The big times that we are going to be ordering contrast, first, we have to realize there are two kinds of contrast. There is intravenous contrast and there is arthrography contrast. So that is a question. When do we do these? Well, we start talking about doing IV contrast if I have three big things on a differential list, tumors, infections, or if I am dealing with someone who’s had back surgery and I am worried about them having a recurrent disc herniation.

Arthrograms are designed to look for cartilage defects, particularly the two big times I ordered an arthrogram shoulder labrum, and the acetabular labrum. Those are my two biggies. We can also do it in the wrist if we are looking for subtle TFC injuries or for some of the small ligaments of the wrist being injured. But the big two are going to be shoulder and hip. I’ll usually order those as arthrograms because it increases my sensitivity drastically. Now, silly little pneumonic, because radiology’s full of them, contrast goes where blood flows. What do we do a contrast for? We are looking for vascularized tissue from an intravenous standpoint.

This is a patient who has had previous back surgery and the person is getting recurrent back pain and ridiculous symptoms. Then the question was, well, did they herniate another disc, or do they have excess scar tissue formation? Well, so when we are looking at contrast, this is the T1 pre-contrast. This is a T1 post-contrast. Notice how all of this is much brighter when we compare it against the pre-con T1 that is because that is all highly vascularized scar tissue. This is a patient that had the unfortunate consequence of developing epidural fibrosis. They got a lot of epidural scars after they had their back surgery. That is where this really comes into play is being able to look for things like that. On tumors and on infections it helps us with the vascularized tissue as the body’s responding to those lesions. Arthrograms, now conventional arthrograms, do not really do conventional arthrograms anymore. Normally, we might still see these pictures because they are using fluoroscopic guidance to make sure they get the contrast into the joint capsule but this is where I am looking at the arthrogram is on the MRI. So, they flooded this person’s shoulder joint with gadolinium and it would let us look at things like the labrum more effectively. So, there is the posterior labrum. This person has a defect in the anterior labrum with a thick rope-like middle glenohumeral ligament. As we start looking at this one, this person has a Buford complex.

It lets us see some cartilage defects much more effectively. Things to realize, we put contrast on board. Contrast, gadolinium is generally considered a very safe agent. However, if somebody has decreased renal clearance, you are not going to get gadolinium. Gadolinium is excreted in the urine and if the person has renal insufficiency, they cannot excrete the gadolinium. It can build up in tissues and in a very small percentage of people, 2.4% of patients that have MRI gadolinium, they can develop something called nephrogenic systemic fibrosis which is a reaction in the body that can result in some pretty drastic consequences. Anybody that has renal clearance issues, they are generally not going to get an MRI contrast. How do we figure that? You get labs. You are going to look at glomerular filtration rates. You will look at creatinine and different imaging centres will have different protocols in place, and they’ll look at those things. We also try to avoid using this on pregnant patients, because again, we are also being careful about what medications are put into pregnant patients. Now, things to be aware of with MRI, do not do an MRI of a joint replacement, and I’ll be honest with you doctor, the number of times I have had one of these things come across my screen where this patient had a total knee replacement and they were having pain afterwards. Then somebody ordered an MRI, and all I can tell is that there is a giant black hole because the titanium doesn’t show up on the MRI. It just creates a large signal void. Again, things like pedicle screws, disc replacements, and interspinous spacers, I can work around all of those. There are pulse sequences. There are artifact-diminishing things that we can do with MRI but we still cannot do an MRI of a replaced joint.

The other thing to be aware of when we are dealing with MRI is, that MRI is very sensitive to motion. The more the person moves, the greater the probability we are going to have a lot of jitteriness in the pictures. So that is something you just got to be aware of and we might have to work around. Now, how about CT? Computed tomography? It used to be called CAT scans. We do not call them CAT scans anymore, mostly because I think the veterinarians got tired of all the CAT scan jokes. So, CT computed tomography, the real reason we do not call it CAT scan is, that the old term was computed axial tomography. While the images can be acquired in the axial plane, they can be reconstructed so it is not just axial anymore. When would we do CT instead of an MRI? Well, why CT versus MRI? One is it is more widely available. MRI centres, and MRI imaging units, are harder to get into., as they are more tightly scheduled, and regulated as far as you know, particularly with their third-party payers. CT is cheaper. It is more readily available. Because of that, it is sometimes easier to get a CT. There are times when a CT and an MRI are pretty much interchangeable, like for a lumbar spine to rule out disc herniation. CT is 95% as good as an MRI.

Video Placement: 42:47
What else? Why else would I get a CT? Beautiful high-resolution for bony structure, particularly difficult to visualize the bony structure, posterior elements of the spine. The pelvis is an amazingly complicated piece of anatomy. It is fantastic for looking at some of those complicated structures. Or if I cannot get an MRI, I got somebody who has a pacemaker. I got somebody who’s claustrophobic. We can get a CT. Now the downside of CT, this is a high dose. When we start looking at a CT versus an x-ray, a CT can be anywhere from 10 to 20 times the radiation dose, or even higher than a comparable x-ray can be. So, that is a problem. We try to avoid that dosing as much as possible. And not as much as in a chiropractic setting, but in an emergency room setting. It has been demonstrated to be grossly overutilized because they got emergency room doctors that just automatically CT everybody, everything. So, because of that, there are some protocols that are put in place to try to diminish CT use. We’ll talk about that when we are dealing with our head trauma section.

Now, there is radiation involved, and this is a relatively high-dose study. We try to be cautious about who we CT and how often we CT. The nice thing is the tunnels are bigger, claustrophobia is not an issue. Obesity is not as much of an issue because it is a very short tunnel. If we were to go back and look at the original picture, you have got a much more open field of view. You do not nearly have the claustrophobia feelings there. Great bony resolution cannot emphasize that one enough. Anytime I am looking for a posterior element fracture, if I have got somebody who’s had an extension injury and they got focal pinpoint tenderness, I know I am going to be getting a CT because the x-ray is great, but it doesn’t have the resolution that CT does.

Let us look at some CTs. So, as we start looking at CT scans, so things to be aware of with CTs, much like MRIs, T1 and T2 waiting’s. CT is CT is CT, but we can change our windows to see things differently. Like right now, as we look at this midsagittal, we are looking at what is called a bone window, but I could change this over and I am going to use abdomen. Now, this creates more of a soft tissue window, so I can see soft tissues a little more effectively. It is not as good at distinguishing soft tissues as an MRI, but it is still a very functional and effective tool. Taking over the bone window on this one, this is a person who had a motor vehicle collision. With that, they had an extension mechanism. They were having focal pinpoint tenderness. The x-rays were equivocal, did not really see anything on the x-ray, but as we look at the CT, we can see right through here, that there is a fracture in the articular pillar. And you can tell that that fracture is so small and subtle. What is the probability we would see that on an x-ray? This is something called a reconstruction. The images are required generally in the axial plane. The axials are of higher resolution. So, we are going through the skull base. We can see sutural changes there getting into the soft tissues. There are the dens coming down into C2. We can see all this bony detail. Do not forget to zoom in. Do not forget the window and level. Now, we can see that fracture extending through the lamina, into the pillar, and then even fracturing through the pedicle. So, something that we would very likely not be able to see on x-ray, but with the degree of pinpoint tenderness on physical exam.

The reconstructions can be done in the coronal plane, the sagittal plane, they can even reconstruct them in the three-dimensional plane. As we start looking at these structures, and again, the sagittal in this case, we can really see very nicely that fracture extending through the articular pillar. I am a big one, anytime I look at CTs, I will not look at just axials. I need axials, coronal’s, and sagittal to make sure I am evaluating things from different planes. So, they acquire it in the axial and then the computer reconstructs things put everything back together and then slices it the other way. So one thing though with CTs, we know it is great for bony resolution, but notice that even if I were to kick over to a soft tissue window, which is the abdomen, in this case, I cannot see discs very well in the C-spine. And it is because there is not much epidural fat up against the discs when we look at a C-spine. But if we look at an L-spine, that is going to be something else altogether.

As I kick us over to a lumbar spine study. Looking at the bone window, as I am scanning through the bone window, looking for fractures, things like that, I noticed this person does have a defect in the area of the pars interarticularis, it has nicely corticated bone, so this is a longstanding pars defect. But one of the things that we can see when we are looking at a CT, particularly the lumbar spine, a lumbar spine CT is as almost 95% as good as an MRI because there is much more epidural fat, which gives us good contrast between tissues. In this case, as I look at this, now it is subtle, but one of the things that I can see is that this person has a very large disc extrusion there at L4 L5. I cannot tell that in the C spine as well, because again, in the C-spine, there is not enough epidural fat to get good contrast. Now, between tissues, but as I am looking at a lumbar spine, it is a great way to be able to evaluate for disc herniations. I can see that as I am looking at this axial soft tissue window, as I am going down through the spine, I am also seeing kidneys and I get down into L4 L5 and right there, I can see that very large herniation that is impinging on the thecal sac.

The other thing that is well seen when we are starting to look at CT again, going into the bony detail. Scanning through the shoulder of this particular patient as we are coming down, I can see the shoulder. I do not see much into the lungs. I can see the thoracic cage. The shoulder itself is looking pretty good. And then as I start getting a little bit lower, we have got a patient who has a rib fracture. They are complaining about shoulder pain, but it is most likely in this case, it is referred pain from those broken ribs. Now, the really nice thing is we can also change our windowing and levelling, and this is a shoulder study, but suddenly, I can kick over here, and I can see the lung tissue and make sure that there is not actually a lung problem that is referring over to the shoulder as well.  That is one of the benefits of CT. Normally, we think about CT as a bony modality, but CT is also the gold standard for evaluating chest and abdomen pathology. You can see the detail that we are able to visualize in the lung field, just by clicking a button. That is CT and MRI. What else does CT is used for? CT is also great for the brain and one of the big questions, so I have seen brain CT and I have seen brain MRI, which one do I want? I am going to talk about that a lot more in our next hour, as we are dealing with imaging of face and head trauma, one of the big concepts, just as a quick preview, less than 48 hours, CT, over 48 hours, MRI. That is kind of our general rule. If I need it fast, if I need it, you know, I am worried somebody’s got a bleed, whether they have had head trauma, whether I am worried about a stroke, anything along those lines, we go to CT. It is a faster acquisition. That is great for acute blood products. On MRI because it takes an hour to get a brain MRI. We do not want to spend an hour if somebody’s got a stroke. So those good strokes go to CT. Once we start getting into the more subacute and chronic brain, that is where we get into MRI. With CT, we can also put contrast on board, and again, just like we saw with MRI contrast goes where blood flows. It is great for evaluating blood vessels, evaluating the vascularity of a lesion. However, we start running into the same problem of it having to clear through the kidneys. If the kidneys are not working, you cannot put IV contrast on board, unless you have got some way to help flush things through, if that person’s on an IV, somebody’s going to have dialysis.

Other things to be aware of when we start talking about CT contrast, is somebody who has a history of an iodine allergy or shellfish allergy, generally, we tend to be very cautious about putting CT contrast on board, because it is an iodine-based contrast agent. Now, this brings us to our next imaging modality and adds ultrasound. I am not going to do any live DICOM demonstrations on ultrasound. Now, normally though, when we think about ultrasound, we usually think of a baby’s blood vessels. One of the things we are seeing is a huge cutting-edge field in musculoskeletal healthcare is musculoskeletal ultrasonography. We are seeing where ultrasound of the musculoskeletal system is fantastic for superficial structures, evaluating rotator cuffs, and looking for medial collateral ligaments in the knee. It is an amazing tool, and we are seeing a huge amount of work being done these days in musculoskeletal ultrasound. One of the problems is, that it is an incredibly steep learning curve. It is hard to learn musculoskeletal ultrasound and be good at it. While you might be ok, it is hard to be really good at it. Make sure that you have got good quality equipment and not something that you bought for 99 dollars off eBay. But this is one where musculoskeletal ultrasound, does not much application in the spine, it is predominantly in the extremities. And this is where working with a centre that has a musculoskeletal ultrasonographer and a musculoskeletal radiologist will really get you the best possible applications. The other place where we see this done a lot, and it is really not so much of an issue here from a sports imaging perspective, it is also cutting-edge in rheumatology. It is one of the things that rheumatologists will use to evaluate pannus formation and rheumatoid arthritis in response to medications.

Video Placement: 53:30
The next imaging tool is scintigraphy. We are talking about something that makes the patient scintillate. They give off little glow little lights. Well, when we talk about scintigraphy otherwise known as nuclear medicine, what we are usually talking about from a musculoskeletal standpoint is the bone scan. I am not a huge fan. I do not order bone scans very often. It is not a common follow-up for me. I do not read bone scans because I am not specialized in nuclear medicine. It is got applications, for me, what I perceive as limited applications. We are talking about this person is injected with a radio-pharmaceutical, most commonly technetium. Sometimes technetium depends on pronunciation and tech goes to osteoblasts and it is a way of assessing metabolic activity and bone. The really nice thing about a bone scan is it is incredibly sensitive. It only takes three to 5% destruction before something shows up on a bone scan. Because of that, it is much more sensitive than an x-ray for things like metastatic disease and infections. It also allows us to visualize the entire skeleton at one time. It is great for, you know, polyostotic diseases like Paget’s disease. If my person has Paget’s and I want to see if is it in one bone or is it in all, you know, how many bones are involved? Great tool for that.

There is the three-phase bone scan. All bone scans go through all three phases, but they are only scanned in certain circumstances. The big-time that the three-phase scan is going to be ordered. Not something that we see as commonly from a sports perspective, complex regional pain syndrome. If I am worried about somebody having CRPS, which used to be known as Sudeck’s atrophy and used to be known as reflex sympathetic dystrophy syndrome. A three-phase bone scan is the diagnostic tool of choice for that because there is a blood component to those a vascular component. Three-phase scans are used for that. Bone scan, what’s our big indicator? High sensitivity, three to 5% bone destruction, whereas it takes 30 to 50% for radiographs. When I am looking for things that can be very subtle, we know that infections have a long radiographic latent period. We know that, is this a tumour? Is this a stress fracture? Those are some of the things that we can be talking about.  I mentioned before the person had a knee replacement who had an MRI of the knee replacement. Well, really, you would’ve been better served to get a bone scan on that one to see if there is loosening in the hardware.

The benefits, are incredibly sensitive. Three to 5% destruction. The downside is having low specificity. It doesn’t generally tell you exactly what something is. It tells you there is something going on and it can have some degree of specificity, but there are still a lot of questions. When do I recommend bone scans? The big time is if I am concerned about metastatic disease. If I see something lytic or I see something blastic in an older individual, you know, 45-50 being my thresholds, I’ll order a bone scan to assess metabolic activity and to see disease burden. Well, in this particular patient, the person was missing a pedicle in their T11. They had pretty much their entire torso x-ray and the only thing wrong was the missing T11 pedicle, but a bone scan that was performed the next day shows that this person actually has 13 sites of osseous metastasis because of that difference in sensitivity between x-ray and bone scan. This is an athletic patient who is complaining about foot pain. In most cases, you know, if we are worried about this being a stress fracture, we get negative x-rays on day one, we treat it as a stress fracture and see, you know, maybe then we can do some follow-up x-rays. This was a high-grade athlete where knowing the diagnosis was really important for return to play. The x-rays were negative on an MRI. It shows that there is focal uptake in a metatarsal neck, consistent with a fatigue fracture. To be honest with you, I would rather get an MRI in a case like that, because with an MRI, it’ll tell me if it is a bone, you know, is there a fatigue fracture, or is this a soft tissue injury? The bone scan wouldn’t give me that information. This is one where this is an application where I would recommend a bone scan. This is an adolescent patient who’s athletic, they have got insidious onset leg pain and it wasn’t responding to care. They ended up taking some x-rays, the pain had been there for several weeks by this point in time. One of the things we see on this one is there is this focal cortical thickening on the posterior aspect of the tibia.

When we are dealing with an adolescent, fatigue fractures slash stress fractures, are very common in adolescent patients. But one of the other things that particularly likes the lower extremity and can have an insidious onset of pain in an adolescent is an osteoid osteoma. This is an incidence where the bone scan was actually very useful in confirming that this was a stress fracture and not actually an osteoid osteoma and there are some applications. Just not something I would order on a regular basis. One thing that we also see with bone scans is kind of the next gen of a basic bone scan is something called a SPECT, single photon emission computed demography. This is a bone scan combined with CT-style imaging. We are getting sectional imaging, and what it does is a SPECT scan is more sensitive for getting into the vertebral structure. If we really need to, I look at a bone scan, I see a bright spot. Is it in the body? Is it in the pedicle? Is it in the facet? That can be a difficult call by going to SPECT scanning, I can section through. For a while, into the 80s, and early 90s, when we were dealing with the adolescent athlete who had back pain, and we worried that they had a fatigue fracture, or stress fracture in the pars interarticularis, the recommendation was for a SPECT scan because a SPECT is 10 to 20 times more sensitive for a fatigue fracture than a bone scan. We do not really do it anymore. We would rather get the MRI because the MRI shows us the same information without the radiation dose. But just to show you what I am talking about, as far as SPECT scanning, you can see where we are looking at bone scan style imaging, but it does have that ability to section through the patient starting very far back, moving more forward, and we can see where the areas of the pars interarticularis are lighting up. I would have much rather got an MRI. We’ll talk about this a bit later, too.

Video Placement: 1:00:30
The last of our imaging modalities that we are going to be covering in this class is the DEXA scan, dual-energy x-ray absorptiometry. What a DEXA scan is if you have had your patients coming, “Oh, I had my bones scanned and they told me I had a bone density of a 20-year-old.” Well, you did not have a bone scan. You add a DEXA scan. A DEXA is a way to quantify bone density and it is accurate and it is reliable, and it is valid and it is a fantastic tool. It is much more accurate and reliable than x-rays. It is still an x-ray tool, but it is hooked up to a computer and it is kind of fancy. When we are looking at this, DEXA is kind of the gold standard for evaluating bone density, and really it should be in the spine and hip because when we start looking at, okay, what kind of things? Why do we test bone density? We are worried about osteoporosis. What are we worried about? What’s the downside of osteoporosis? Spinal fractures, and hip fractures, because they have high morbidity and mortality associated with them. The DEXA scan is what we use to assess bone density. It is a good way of getting fracture risk. There are some other tools, quantitative CT, and quantitative ultrasound, but we do not see those used as widely, DEXA is much more commonly used. It is a very low radiation dose. It is about one-tenth of a chest x-ray, which is really minimal radiation dose.

You may see people who are involved in exercise physiology and that sort of thing, DEXA scans can also assess body mass index. I believe it is more reliable than caliper methods and that sort of. What we are going to get when we order a DEXA is we get some grainy pictures and a graph and more importantly, tables. When we start looking at the tables, the tables give us the numeric values for a person’s bone density score. Notice that we are given two scores. There is T-score and a z-score. What are these different things? One of the ways to remember, T-score and z-score, T-score compares your patient against teenagers. An important thing with DEXA scans, these are always going to be gender and race matched. But the T-score compares your patient against teenagers. The Z-score compares your patient against other patients of the same age. Also, gender and race matched.

Generally, most of the time we are talking about post-menopausal or senile patients and that is where we are concerned about post-menopausal or senile osteoporosis. That is where the T-score is really important because it gives us the fracture risk. We do use the Z score in a very small subset of populations. If we are dealing with younger folks, so men under the age of 50, premenopausal females or kids, and again, one of the places where this can be applied is, we are thinking about the hardcore adolescent athlete where we are starting to see this child is not maturing the way they should. We are getting the female triad of amenorrhea involved with exercise and you know, how is their bone density? We would be using the z-score in that population. Generally, however, the T-score is what we are going to talk about, and the number that we are given is a standard deviation from normal. What we are looking at is, plus one to minus, one is normal because that is a standard deviation concept below minus one we start to deal with diminished bone density, minus 1 to minus 2.5, osteopenia, less than minus 2.5, osteoporosis, less than minus 2.5, with a history of fragility fracture is severe osteoporosis.

These are defined for us by the World Health Organization. The T-score gives us that fracture risk, and as the number goes down, we see an exponential increase in fracture. Minus one, there is twice the risk, if minus two there are four times, if minus three there is eight times the risk. With the younger patients, when we are dealing with the z-scores, so males under 50, children, and premenopausal females, that is where minus 2.0 is our threshold between normal and abnormal.A little bit of a difference there.

That finishes off this second hour in talking about imaging modalities. Next lesson up, we will be talking about head trauma.

[END]

 

Section 03_ICSC03
English Direct Download PDF – 03_ICSC03-Section3-HeadFaceInjuries.doc

Instructor Dr Chad Warshel
Video Lesson: 01:02:49

As we come into the third hour of RFCS sports imaging presentation, this hour is going to be covering head and face injuries and imaging thereof. This is one of my favourite slides to start off with any time I am talking about facial trauma. I like to give you a second, look at this, and see if you can figure out what is going on. Now, quite often, as we look at this one a lot of folks, well, it looks like there is a screwdriver in the face. What we are seeing here is this is one of the circus performers who like to drive things, like tenpenny nails into their nose. So, a friend of mine, had this individual as a patient and the patient said, “Hey, can we see what this looks like on x-ray?” The doctor went ahead and x-rayed the patient with the nail up the nose and the hammer tapping on the nail.

You can see there is quite a bit of space there for that nail to go. When we start dealing with head imaging, we have got patients who have head trauma, or facial trauma, we have to come back to that, what is the right tool for the job? If nothing else, that is my mantra for this series. What is the right tool for the job? Now, when we start dealing with head and face trauma, well, what about conventional radiographs? It is a very common thing that we use when we are dealing with musculoskeletal. Well, what about the face and head injuries? Well, the thing is conventional radiographs really do not have any place when we are talking about head and face imaging.

I mean, there is a very small, dedicated set of things that we’ll use conventional radiographs for. One of the first things that we use conventional radiographs for, and from the standpoint of facial trauma or head trauma is this particular X-ray view, it is called a ‘water view.’ I had alluded to before in the last hour that before I can have an MRI, I have to get an x-ray of my skull. This is the view that would have to be done. Because anybody who has ever used a grinder where they are spending time with little metal fragments flying around the air, there is the possibility that small metal fragments can become embedded into the cornea, and if the person is going in for an MRI, those little pieces of metal can dance around and lacerate the cornea. Prior to getting an MRI for chronic head pain, for a subacute head injury, or anything like that, the person is going to get a water view of the skull. Some of the other very, very soft positive indications for skull and face X-rays are nasal fractures and some subtle face fractures, but there are a couple of things that we need to be honest about, and we are starting to look at nasal imaging and facial imaging.

With small nasal fractures, the X-ray might help confirm that there is a nasal fracture, but it is also a difficult call to make quite frequently, and rarely does it affect management when we are dealing with nasal fractures. When we get into the more complex facial fractures, can we see some of them on an X-ray? But do they give us all the information? Absolutely not. Realistically, when we are dealing with patients that have facial trauma, I am not going to waste time taking X-rays. I know that I am going to go straight to the CT because we are talking about really complicated bony anatomy, and CT is going to give me the best information when I am trying to figure out what is going on as far as facial trauma case. So, can we see some things for sure? Am I ever going to waste time taking X-rays outside of this water view for orbital metal? Never. I am not going to use the wrong tool.

What is the right tool? Our two biggest tools when we start dealing with face and head trauma are CT and MRI. As a general rule, we are going to be looking at non-contrast sequencing. We do not want to put contrast on board when we are dealing with most of these things. Now, from the standpoint of CT versus MRI, now, the quick and dirty. The answer that you usually want to keep in mind is less than 48 hours, CT, over 48 hours, MRI- if we are talking about the brain.

If we are getting into the face, facial imaging is a CT thing. Because again, we are dealing with really complicated bony anatomy there. Some of the great resources that you use, when we are trying to decide what kind of imaging should I be doing for my patient is the American College of Radiology Appropriateness Criteria. I had referenced this at the beginning of the first hour as an excellent resource for what should I do for this? Is this a CT, or is this an MRI? They have great criteria there.

When we start talking about, when am I going to be looking at ordering CT, acute head trauma? My general window here is 48 hours. There are some discussions about what the best cut-off is to go from CT to MRI, you have four hours when we start to see changes in blood product; 48 hours is an excellent window to use there. Acute head and face CT, over 48 hours, MRI. When we are dealing with any kind of concern for intracranial bleeds, with facial trauma, the big thing is that is we are going to CT because we are dealing with really thin bone, really complicated osseous structures, that is where we get our best visualization. Any concern for bleeds, whether it is an ischemic stroke, a haemorrhagic stroke, or epidural hematoma; or subdural hematoma subarachnoid haemorrhage. Any of those were going to go to CT because, particularly when we are dealing with an acute phase, we want to make a diagnosis and get that person into the scanner, scanned, out of the scanner, and treated as fast as humanly possible. Because when we are dealing with these different kinds of bleeds, lost time is lost brain. So, we want to scan them as fast as possible and get that information so that the emergency department can treat things effectively.

Other things we might be looking for. If we see intracranial calcifications that are not where they seem to belong, you know, things that we see very, very commonly like pineal gland calcifications, pretty much everybody over the age of thirty has a pineal gland calcification. Is it in the normal pineal gland location? If it is not, then let’s go to a CT because we’ll be able to see the calcification and localize it very effectively.

Not surprisingly, we start throwing spinal trauma in with the head and face trauma. It is great for visualizing those posterior elements. The temporal bone is one of the single most difficult things to visualize. Temporal bone and skull base. Really complicated anatomy that you need the high resolution of CT. Now, why CT? The big focus here is going to be looking for brain bleeds. When we are dealing with a person who has an ischemic stroke, a person who has a haemorrhagic stroke. We are looking for a subdural, epidural, or subarachnoid haemorrhage. That acute blood product shows up within minutes and what we will see when somebody has acute blood product that is extravasated is we are going to see hyper attenuation.

So, we can see through here that there is this really bright ridge adjacent to the skull for that person that has a hyperacute bleed. As that blood product ages, we know that it goes from haemoglobin to deoxyhemoglobin to methemoglobin, and as it breaks down, we will see where it decreases its attenuation through here. Why a CT instead of an MRI if this is four weeks later? We are following the same person. If there was a change in their mental status, that might be something prompting a different imaging study.

Now MRI. When we start talking about doing MRI, as a generality, we are usually going to be doing this non-contrast. When we are dealing with trauma cases, we do non-con. Contrast is more reserved for chronic head and brain problems where we are searching for tumours, infectious processes, and things like that. So, generally, we are going to be going non-con. Now, if we are concerned about vascular abnormalities, there is the possibility of an MR angiogram which is almost as good as the gold standard of conventional angiography. But again, that is the specific circumstance of looking for vascular occlusions, resulting in ischemia, looking for vascular ruptures, looking for aneurysms. That is where we’ll be doing, talking about angiograms but not in that acute setting because we are worried about lost brain time.

When we start talking about different pulse sequences. If you spend any amount of time looking at neurology literature, if, you are really involved as naturally, sports docs generally are. In head trauma cases and what is the imaging? What is the clearance? How do we deal with it? You will see this is cutting edge as far as imaging goes. Looking at all these different ways to evaluate the brain, and one of the things you will see is there are a million different specialized pulse sequences for evaluating brain tissue.

Just to pick on a couple that usually gets the biggest literature these days, diffusion tensor imaging and functional MR. Realistically, when we start talking about some of these specialized sequences, they are really primarily still in the research phase. If you are working with a world-class research hospital, they might be looking at some of these specialized pulse sequences, but by and large, your average imaging centre is not because they are not that cutting edge. Is it really useful? Have we defined what is positive or negative yet?  We will not see as many of those specialized pulse sequences. Brain MRIs. Still, there are the standard T1s and T2s proton densities, creating echoes. There are some extra pulse sequences that we talked about when we are dealing with the brain, and I am not going to get into doing the live.com demonstrations on the brain as I did with some of the previous material. But there are some special sequences that are standard, something called a ‘flare fluid attenuation inversion recovery.’ Fantastic sequence to look for parenchymal oedema. This is fantastic when we are trying to differentiate against something like multiple sclerosis or vasculitis.

There are also some other sequences, and do not confuse this with diffusion tensor, but there are diffusion-weighted images, DWI, and apparent diffusion coefficients. These are assessing fluid motion within the brain. These are what we are going to be talking about primarily with tumours. Not something so much from the sports side of life. So, MR of the brain, fairly standard pulse sequences. Indications MR without contrast. Ischemic stroke. This is where when we are dealing with that acute patient, where we think they are having a stroke right now, they are going to get a CT. Follow-ups, whether they are looking at using clock buzzing, it must be medications, whether they are looking at doing stent placement, things like that, then they might start getting into MR, but for the acute phase, we are going to be looking at CT.  For the sub-acute to chronic, what is that time window? A big-time doc is 48 hours. We are so worried about things evolving very rapidly in the acute phase, anything less than 48 hours goes to CT. Over 48 hours, we are generally going to go to MR. Then we get into chronic abnormalities. Chronic vascular diseases like atherosclerosis change in our older athletes. In our athletes that might have autoimmune conditions like lupus, they might have chronic vasculitis.

Then we are getting into some unusual conditions. Patients with Marfan’s might have vascular abnormalities, patients that have some of the other different syndromic conditions that have an increased incidence of berry aneurysms in The Circle of Willis. Those are the kind of things we are going to be looking at with an MRI, and a non-contrast could be the first study. When do we put contrast on board when we are talking about the brain? Generally, we are getting into the outside of the sports realm. Here we are talking about a route if I have got a concern for multiple sclerosis. If I have got a concern for vasculitis, I have got a concern for a tumour or infectious process septic emboli, things of that nature, then we will start looking at putting contrast into the brain. Occasionally, you get somebody who has chronic intractable non-responsive headaches. They might decide to put contrast on board, just more like a fishing expedition than anything else. But we do not see that as a standard in sequencing. When we start dealing specifically with trauma to the skull and face, some things are really important in assessing the patient and trying to predict the possibility that our patient is going to have something really significant on that imaging.

When we start looking at traumatic brain injury, there are several things that we consider when we are dealing with the history of the injury and/or the injury unfolding in front of us and how this really affects what we are doing. For anybody who’s very involved in sports work, who’s doing field-side work, particularly with any kind of sport where there is quite a bit of interpersonal contact, the Glasgow Coma Scale is an incredibly important thing in assessing what is the person’s degree of consciousness. This is something, of course that all emergency responders are going to be very familiar with. In the ambulance, they will be asking about it in the emergency department if the person must be transported. Two of the big things that we look at from a severity standpoint are loss of consciousness and post-traumatic amnesia. These are even graded based on how long the person was unconscious. Quite often, when we as chiropractors are dealing with a lot of our patients who have had head injuries, if we are on the field with the team, it is very uncommon to see somebody who is unconscious for over 30 minutes. Most of the loss of consciousness that we tend to deal with is going to be very short-term, a couple of seconds to a couple of minutes, all of which would be categorized as mild post-traumatic amnesia. From the time when the injury was until the person is actually cognizant and can remember things accurately. Depends on the timing there, and that helps describe the severity.

As far as the Glasgow Coma Scale goes, just to refresh your memory, this is a fifteen-point scale, and somebody who is completely alert and oriented times three, we are looking at a 15, where the person will open their eyes spontaneously for a four, they will be oriented times three to verbal command, and they will do what you tell them to do, touch your finger to your nose and so forth. Anybody that has less than that, that is where we start being concerned about those intracranial injuries.

The Mayo Clinic has a head injury classification system. One of the things you discover when you start looking at literature about head and face trauma is there are a bunch of classification schemes. There are different predictive rules, they are all fairly well-researched, and they’ve all got some validity to them. So, it is kind of digging through all of these and looking for commonalities in your jurisdiction. Do they use one versus the other? That is what is going to be an important thing to consider. That is something that you must keep in mind. As far as grading traumatic brain injuries using this Mayo classification. They are fairly easy to see; moderate to severe traumatic brain injuries have a longer-term loss of consciousness and longer-term post-traumatic amnesia. You are looking at imaging and seeing damage to the brain or the skull. Mild traumatic brain injuries, lesser degrees of loss of consciousness and amnesia, and more simple skull fractures. Then the symptomatic traumatic brain injury, and sometimes you will see this described as a minimal TBI, and not surprisingly, this also gets turfed off to the diagnosis of concussion, so no loss of consciousness or anything. Nothing that you can really detect. If somebody loses consciousness for three seconds after they get their bell rung, you are not really going to be able to tell that. They do not have any post-traumatic amnesia, but they have concussive symptomatology where maybe they are confused, they are having some difficulties understanding, then we are dealing with that symptomatic traumatic brain injury, minimal traumatic brain injury, or concussion. Hopefully, by this point in the presentation, you have discovered that I very rarely ever read a slide. I figure that everybody here can read just fine. So, I am not a big fan of reading slides, but every so often, if there is a definition, reading a slide is something that I will do occasionally, and this is one of those cases.

What is a concussion? We throw the term around a lot. What is the definition? The definition, in this case, comes from the American Association of Neurosurgeons. This is a clinical syndrome characterized by immediate and transient alteration of brain function, including mental status and level of consciousness resulting from mechanical force or trauma. Something hits the person’s head, or maybe sometimes it does not necessarily have to hit the head. It can be something like a whiplash injury, where the head itself does not get stuck, but the brain is going to be sloshing around inside the cranium, those kinds of things can result in a concussion. Not surprising, of course.

When we start dealing with patients that have head trauma. The majority of head trauma cases are mild to minimal traumatic brain injuries. Some possible transient loss of consciousness and post-traumatic amnesia to none and just more concussive style symptomatology. The good news when we are dealing with patients that have milder minimal traumatic brain injuries is that it is actually uncommon to find imaging findings on these patients.

Most of what we are dealing with in mild or minimal TBI patients are clinical concerns rather than a hard-and-fast structural abnormality. That being said, talking a little bit about some of the cutting edges in imaging, particularly with things like diffusion tensor imaging or tractography, where they can actually follow neural tracts. You can see disruption in axoplasmic flow in patients with concussion and look at some of these imaging modalities, but in the end, we are still looking for findings, well, not we, I am not involved in this, but the neuroradiologists involved in this research are still working on defining normal. So, it is not something we are going to order on every patient because concussion is something we treat clinically rather than needing to worry about the hard-and-fast imaging findings. We will see disruption and axoplasmic flow in those patients. But that is not what we are considering as a positive structural finding.

What kind of things? I have somebody who has a minimal TBI. They did not lose consciousness, they do not have post-traumatic amnesia, and they are concussed. They have a little confusion; maybe they have slight dizziness and not functioning optimally. What kind of things really increase the predictive value of doing imaging? Is there a structural abnormality? We look at a couple of different things. I already talked about post-traumatic amnesia. I have to probably use headache because everybody who gets their bell rung, everybody who has head trauma is probably going to have a headache, that is very sensitive but poor specificity. Everybody who has head trauma is going to have a headache, but how many headache patients are actually going to have imaging findings? Very remote. One of the things that are actually very consistent through, and I am going to talk about some of the imaging decision rules here, vomiting.

There is a discussion of one-time vomiting versus repetitive vomiting and low-level vomiting versus projectile vomiting. But vomiting is one of the things that we see in all of the different decision rules as an indicator of this is somebody who warrants imaging just to make sure. Not surprisingly, we tend to be much more liberal about imaging older patients, with more things going on. One of the other really major components for older individuals, age-related brain atrophy, gives that much more room for the brain to slop around inside the skull and can create more problems.

Well, poor historian. Well, who is the worst historian there is? The historian that is as altered consciousness due to their favourite recreational substance. Whether somebody has alcohol on board or cannabis or some other thing that creates an altered mental status, you cannot assess them accurately, so you are going to end up having to do imaging in a case like that, which is not surprising. But if you can palpate an offset in the cranium, it is not hard to figure out that this person might have a skull fracture. An interesting note on seizures realize that the immediate post-traumatic seizure is actually a very common thing where the momentary insult to the head just kind of shuts everything off, then when it lights back up, there is a momentary seizure. Is there persistence in the seizure? Are there multiple seizures? Those are things that have to be considered.  What are my imaging choices?  We do not do X-rays. X-ray has no place in acute head trauma. CT, that is our acute patient. When we are dealing with those first 48 hours, I am going to go to CT after 48 hours, I am going to go for MRI.

Some of the different guidelines. These guidelines are all published and validated, and the whole idea is we are trying to figure out who needs a CT and who does not. Because if there is no probability or minimal probability of finding something on the scan, we do not want to do the scan, as we have to keep in mind that CT uses radiation. If we have somebody who’s going to wind up with repetitive CT scans, which really have no possibility of finding anything, we are needlessly imaging somebody, and there is the potential for radiation-induced concerns. Things are as simple as, if you get somebody with repetitive head CTs, it increases the possibility of cataracts because the proteinaceous material in the lens of the eyes is pretty radiation-sensitive. The big three guidelines that are talked about most these days are New Orleans, Canadian CT, and the Nexus Study. New Orleans criteria. I am going to introduce all three of these again. This is one where you might want to find out what your jurisdiction is. If you are doing fieldwork, which one do they ascribe to, and which one do they want you to use to help decide to do we get imaging or not?

Something consistent across all of these, these are all going to be patients that are DCS-15. They are cognizant patients. For New Orleans, we have got somebody who has minimal TBI. loss of consciousness, post-traumatic amnesia, and the coma scale is sitting at a 15. Does this person need imaging? Well, what do they have? Headache, be cautious with headache as an indicator. They are all going to have headaches. It is highly sensitive for this specifically. We already talked about age and intoxication. Anytime we start dealing with a patient who is getting particularly recurrent vomiting, the vomiting is one of my biggest concerns. A single episode of vomiting is common in concussive patients because they are dealing with disorientation as the neurology is working to reset. If they have the spins, it is not uncommon for them to vomit early on. But if there is repetition, then that is a concern. Short-term memory deficit is coming into that post-traumatic amnesia. How long is it lasting, and do we see visible signs of trauma? Which just makes sense.

The Canadian CT Rule. This one is based on exclusion criteria instead of inclusion criteria. You do not want to apply these rules to children because children have their own categories. I am not going to really deal with kid CT rules because, again, there are a bunch of different rules there. I am going to keep more to the adult rules in this case. Minimal injuries. If they have got loss of consciousness and that excludes them from this criteria, or they have got a skull fracture that you can tell, you are not going to be turning down this patient.  We do not CT somebody unless they have one of these things. Their Glasgow Coma Scale is still low, you suspect a skull fracture, suspect a basilar skull fracture, and that might be where somebody’s developing CSF rhinorrhoea as they have leaking CSF out their nose. Vomiting comes in and plays a large role in this one, and you can see here that two or more episodes of vomiting. Age and retrograde amnesia, and dangerous mechanisms where you’ve just got to be concerned based on what happened.

Nexus criteria. So, the third of those rules to help us decide. In this case, head CT is not required if all of these are absent. So, if there is any one of these that is positive, then you CT the patient. In older patients, evidence of skull fracture, skull hematoma, which would imply the concern for an underlying skull fracture, persistence of neuro deficit, GCS alterations, behaviour is inconsistent, and we come back to vomiting. So, what do we do? CT. When we are dealing with the acute head trauma case, this person is going to CT whether it is a minimal, mild, moderate, or severe, they are going to go to CT.  After they’ve had that initial CT, one of the questions is, had this person in the emergency department, how is their neurologic status doing? Well, if we start seeing some delays in recovery, or if we start to see where they are deteriorating, they can go back to CT. There is a possibility here that you can use it in an MR. Generally, however, during that 48-hour window, we are going to start kicking over the MR, and we are not going to be talking about doing any of those specialized imaging modalities. This boils down to the average patient that we will be dealing with, whether you are a field doctor or seeing athletes in the office on Monday after weekend events. We are going to see mostly minimal traumatic brain injury patients, patients with concussions, and those are not folks that are going to need imaging unless we are seeing protracted recovery unless we are seeing where the patient is starting to deteriorate, then we start looking with doing imaging.

Some of the interesting imaging that is coming up; diffusion tensor, tractography, and functional MR, hold a lot of promise, and I think we are going to see a lot of things coming out and imaging these patients over the next ten years, but we are not there yet. I love having a radiologist reading my imaging, usually, it is me, but you should always look over your patient’s imaging. Radiologists have bad days, and can miss things, so it never hurts to look things over.  I already showed you one case where the person had a subdural hematoma, and you saw the hyperattenuating blood on CT. We are going to see some more bleed cases on CT. On MRI, once we start getting into that, persons had some stuff going on for a while. We can age blood products on MRI very effectively, in radiology, we love our mnemonics. We love our little memory tricks or how do I remember things. We can age blood by using this little mnemonic, ‘It bitty-bitty baby doo-doo.’ I realize it sounds goofy as all get out, but that is what we use. What the heck are you talking about it?

Do not memorize the table. I am NOT going to test you on this. What we are talking about is what does the blood product do on T1 and T2 weighted imaging? The first syllable is T1, the second syllable is T2, and we break it down into five stages: hyperacute, subacute, early subacute, late subacute, and chronic. So, ‘It Bi’ means ‘isointense and bright.’ Now when we talk isointense, we are talking isointense to adjacent brain matter. Hyperacute. We are not going to see the hyperacute cases on MR typically because these are gone to CT because of the concern for bleeding. But we occasionally see it on MR, which will be iso and bright. Then once we get past eight hours, we are going to start to see a breakdown in blood products going from oxyhemoglobin to deoxyhemoglobin. because we are getting into that 48-hour range, it is going to be isointense, still on T1 but now on T2, it is going to be dark. After three days, it is going to be bright and dark. As we start getting into one week to four weeks, it will be bright on both. then as we get out past four weeks, it is going to be dark on both. So, we can use that MRI to gauge how old is this blood product and, particularly if we get some patients that have multiple traumas. One of the sports that I like to pick on is a favourite for multiple head injuries, rodeo. When we start dealing with anybody who’s riding a really large, very angry cow, you are going to have somebody who’s going to be getting the head whip around quite a bit, and they might wind up with multiple head traumas. Rodeo clowns in particular.

Video Placement: 33:33
When I was back in clinical practice before I came to the Northeast to teach, I practised in a small town in California called Clovis. The only exciting thing that ever happened in Clovis was the annual Clovis rodeo, and when you get rodeo people, you are used to dealing with a whole lot of polytrauma. We can look at MR, we can also look at CT and again CT for that acute phase. When I am evaluating a head CT as I start looking at that head CT, one of the things that you want to do is you want to make sure that you look at everything possible, everything available to you. This is all done at one time. With MRI, there are different pulse sequences, T1, and T2. And those are different sequences that must be done individually. When we start looking at head CT, there is one sequence that is done. They run from the top of the skull down to the clavicles, and then you change the windowing. You change the brightness and contrast, and it brings out different things. Before I ever even start looking at the meat and potatoes of the CT itself, I start by looking at the skull. It is got that nice X-ray appearance that I am used to looking at. I will look at the skull and see if anything is jumping out of that maze that just is not right. We want to look at a couple of things we want to look at the bone window. The bone window gives us high contrast for bone, and we can distinguish between cortical and trabecular bone.

I am looking for offsets, and make sure that you are aware of sutures; look for symmetry sutures. Sutures tend to be very symmetric, whereas skull fractures tend to not be symmetric. One of your other best clues of, “Hey, you look here.” my patient’s got head trauma. One of the things you want to look at look at the skin, look at the meat, look at the soft tissues outside the cranium. Because if there is one thing that says, “You, look here, it is a scalp hematoma.” So, if you see a large hematoma, make sure you pay attention to that area because that is where the head got hit, and that is where most injuries are going to happen. So first, I look at the bone window, and I evaluate the superficial soft tissues. I will move it to a soft tissue window, and I can evaluate the soft tissue some more, looking for not only soft tissue displacement but also higher attenuation contusion. I am looking at the brain at the same time, and I can see ventricles, there is the septum pellucidum, but notice that I do not have great brain distinction yet, but then I will kick over to a brain window, and on the brain window, I can actually see the distinction of grey matter versus white matter. One of the important things is to trace the outline of the grey matter and make sure there is good grey and white differentiation all the way around.

Start by looking at the outside view, outside in. We start looking for the skull fractures as our first big indicator of “Here’s where a big problem is.” make sure you are looking for those soft tissue findings, and this is working. If you are the one on the field doing the assessment, you will be palpating, and if you feel defects or offsets, that is a good indicator to get some imaging. When we start dealing with skulls, three big kinds of fractures: Linear, the standard longitudinal skull fracture, the depressed skull fracture, where something is impacted and pushed inward, and then something that we typically only see in infants- diastatic fractures, where the sutures are going to separate because the sutures have an interdigitated yet like they do in the adult patient. There is nothing more wonderful than when your CT comes with an arrow. As we look at this person, this is a female post MVA, and we can see a depressed skull fracture through here. That is the bone window. As we look at this on the brain window, we can see some high attenuation blood product immediately adjacent to the fracture site.

Skull fractures are rarely ever symmetric, whereas sutures are. So back through here, we are getting to the top of the lambdoidal suture. Here is where that symmetry is, but here, it is much more sharp and jagged and offset. This patient has dual linear fractures, then if you compare the temporal soft tissues here with the temporal soft tissues here, you can see quite a bit of soft tissue swelling and look at the occipital soft tissues. Quite a bit of hematoma formation that we do not see on the other side. In this patient, I want to ensure I am looking very carefully in those brain windows, looking for parenchymal contusions, and looking for extra-axial blood collections. Relatively straightforward depressed fracture, much more significant depressed fracture, and of course, this is one where very large contusion in the superficial tissues. With that kind of depression, we are going to be very worried about the integrity of brain tissue.

Another one of those interesting phenomena that we tend to see more in children than we see anywhere else but can be seen in older populations is something called ‘leptomeningeal cyst.’ This is somebody who gets a linear skull fracture. One thing that happens is the dura gets trapped in the fracture line. As that dura gets trapped into the fracture line, it can put some pressure on the fracture, and open the fracture, allowing for some progressive herniation of the material through the dura and subjacent CSF through the fracture. We might have somebody who started with a known history of a longitudinal skull fracture, and now when I look at this thing radiographically, I see a geographic lytic lesion. Knowing that this person had a skull fracture, I am very concerned about this being a leptomeningeal cyst. As we look at this on MR, you can see that there is where the skull fracture is. Well, it is an older fracture at this point, and the dura is herniated out past the skull, displacing the scalp and expanding the size of the fracture. The reason that this has such low signal intensity through here is the CSF is flowing through that area and because it is a tight collar, creating some turbulence in the blood flow and decreasing the signal. When we are doing any kind of head imaging post-trauma, one of the really big things that we are looking for is the extra-axial bleeds. There are three major ones and the first one which is the biggest, is subarachnoid, which are the most common of these abnormalities. Subarachnoid hemorrhage tends to be the most common extra-axial hemorrhage. If there is going to be a test, that would be a wonderful test question., it would be “What is the most common extra-axial hemorrhage?” Subarachnoid, most common, then subdural, then epidural.

Let us take these in reverse order. We are working our way from the outside going in. Epidural hematoma. This one has a strong association with fractures, particularly temporal bone fractures. I am going to back up quite a few slides. If I come back here and look at this patient where there is a temporal fracture, I look at this thing under the bone window, and I am going to be concerned. Is there an epidural hematoma? Epidural hematoma. It is between the skull and the dura. This is an important thing for us because it makes it a little easier to diagnose. But one of the downsides of this is these are patients that, they had the head injury, maybe they did not lose consciousness, maybe they do not have post-traumatic amnesia, they have to hiked 15 GCS but then all of a sudden, they crash within a couple of hours because it takes time. Usually, we are seeing a slow bleed where they are slowly bleeding into the space and slowly bleed in space more and more until eventually, they hit a threshold on a mass effect where they compress the brain and create a major negative consequence, and this is where suddenly, they develop a screaming headache, they started vomiting because of the brain pressure.

What are we going to see when we look at these? This has called a lens-shaped lesion. What we are going to see as we think about the dura, the dura adheres to the skull at suture sites. So, wherever the sutures in the skull are, the dura sticks to those areas. The blood is going to be stuck between those sutures, and as it fills in the area, it’ll stop at the sutures, and it creates this elongated pointy, ovoid lens shape. Biconvex or lenticular shape when we are talking about these.

Video Placement: 42:45
Going towards CT in these things, we will see hyper attenuation. In that acute phase, what we are going to see is a bright blood product, and that is what we see here. There is that beautiful lens shape, stopping at the squamosal suture, and stopping at the lambdoid suture in this case. The concern here, as this thing slowly enlarged, eventually they hit the threshold of brain compression, you can see where they’ve completely effaced the lateral ventricle, and that is where these folks can get that, “Why does it take so long?” They must compress the lateral ventricle and once the ventricle is compressed, then they start getting midline herniation, and that is where they are going to start developing those rapidly deteriorating symptoms. So, completely effaced the lateral ventricle on this side. They are also starting to lose their aqueductal pathway.

A much smaller version, but we can see that hyper attenuating biconcave appearance, immediately deep to the calvarium, and it is because of that lens shape, again, stopping at the squamosal suture and the squamosal suture back there on this case as well. But notice the difference in the size of those lateral ventricles and the fact that the septum pellucidum is starting to curve as this patient develops a midline shift, much smaller in this case. I am not familiar with brain imaging, I do not see these things all the time. Is that normal or not? One of my big clues- okay, where am I looking for issues? As I follow the outside and I am following the contours, I look at the soft tissues and notice a very large contusion in the temporal region of this skull. I am now looking in this area very carefully for any kind of abnormalities, and there is that lenticular shape. From the epidural, we go to the subdural. With the subdural hematoma, we are seeing a lesser version of something that can happen inside the pragma of the head. But as the head’s rotating or as the head hit something when the head stops, the brain keeps moving, and there is some inertia there. Because of that continued inertial motion in the brain, that is where we start to see some tearing in the blood vessels between the brain and the dura.

Unfortunately, these have a very high mortality rate, and those that do survive will have persistent deficits neurologically. We are talking about major head trauma here in these cases. The difference between the subdural and the epidural is that because this is deep to the dura, it will not be stopped by the sutures. This is going to be somebody who is going to have bleeding that is deep to the dura, and this is going to take on a crescent shape instead of having that biconvex lens shape. This person is going to have a crescent shape, and that is what lets you know that this one is subdural. It can go across the sutures, and it is going to be hyperattenuating when we are looking at this on CT. We can see this nice crescent-shaped appearance through here on the CT, and this one is also effacing the lateral ventricle of the same side. This is a patient who did survive, and what we are seeing here in the acute phase, there is the hyperattenuating blood, and then as it ages, it loses that hyperattenuating and eventually becomes hypoattenuating. It is also spread out quite a bit more in this case. This person has gone from the acute subdural to the chronic subdural. In this case, what we are looking at here is we are looking at an MR. As we start looking in an MR, can we age what the blood products are as we look at this thing? We cannot on this one because we only have one whole sequence. You must have both a T1 and T2 to effectively age blood product on MR. But as I look at this T1, we are looking at something very high-signal intensity. It is also a very large subdural.

The last of the three bleeds and the most common of the three bleeds is the subarachnoid hemorrhage. The subarachnoid hemorrhage is the one that has that classic. The history is listed on every neuro board exam or every regular board exam with neural questions. When you have a patient with a thunderclap headache, the sudden headache that came on out of nowhere, maybe post-trauma, maybe not, worried about a subarachnoid hemorrhage. What we see with a subarachnoid hemorrhage, we do not see the same kind of displacement we saw in the previous cases. The big thing we find with a subarachnoid hemorrhage is that these patients get something called ‘dirty CSF.’ Because the blood product is in the CSF and it is free to move around in the subarachnoid space, it starts filling up the sulci, it starts filling up fissures, and it is going to be hyperattenuating in the acute phase. As we look at this patient, again, very large scalp contusion. But then what is interesting is that the injury was here, but then I am seeing the dirty CSF as that hyperattenuating blood product is crossing the Sylvian fissure and getting near the insula there. So, dirty CSF, that is our finding for the subarachnoid hemorrhage. This case is probably along the lines of a counter-coup injury where the person was injured. They were hit back here, the brain sloshed, and they bled on the other side. Similar concepts through here. I am starting to look in those external spaces, and we are deep to the Sylvian fissure, and I got up against the insula. We can see that dirty CSF finding.

Video Placement: 49:02
Going to MR, we have somebody, past that 48-hour period when we want to look at the CT, we are now into the MR phase. We can see where this person does have blood product past the Sylvian fissure up against the insula. This would be where we would use ‘it bi itty-bitty baby doo-doo’ to figure out what it is that we are looking at. I am going to look at the T1, and this is technically a flare, but we will treat it as a T2, so it is bright here on T1, and it is bright over here on T2. The combination of those things tells me that I am in the late subacute phase because it is bright on both pole sequences. This person is 1 to 4 weeks post-injury. What else can happen? Rather than having free blood product, as in somebody with a subdural or epidural subarachnoid, we can also see the patient with a parenchymal contusion. So, our previous ones, subarachnoid hemorrhage, epidural hematoma; subdural hematoma, are the blood collections. Contusion, now we are looking at bruising of the brain tissue. This would be something that would show up very nicely on CT when we see that head injury. This can also be one that speaks heavily to the counter-coup style injury, where the head injury comes in on one side, and we might see the parenchymal contusion on the other side. Because as the head is hit, the brain gets bruised from the initial contact, and then as the head moves, the brain keeps going, hitting the calvarium on the other side and bruises there as well. What we are looking at here, is where Isaac Newton is creating some headaches for us. Because we are seeing the initial injury, the bruises on the brain. Then as the brain keeps moving, it gets the parenchymal contusion on the other side.

In the first hour or so, these can be difficult to see. It is an important thing to know how long the head injury to the time of the scan was because if we have a patient, we didn’t scan initially, but there is a deteriorating neurologic picture, then it is time to scan the patient. What are we going to see? Hyperattenuation. Anytime that the person has that parenchymal contusion where they have capillary bleeds into the parenchymal of the brain, there is going to be hyperattenuation on CT, which we will see it in the frontal lobe of this patient. On this patient that we are looking at, bone windows in this case, we can see on the bone window, there is a fracture here, there is a fracture here. This person also happens to have some emphysematous change where they’ve got some air trapping within the skull, which is a concern. If it is in the front, did this person has sinus involvement? Is there a violation of the scalp to where maybe there is air travelling in? Or, on a more posterior aspect, did this person violate the mastoids? They are getting air bleeding from the mastoids into the adjacent space.

On MR, we can start to age blood products using the ‘it bi itty-bitty baby doo-doo’ and knowing in this particular case, this person was hit on this side, we see the parenchymal contusion, and then over here the counter-coup injury as the person’s force was going this direction. What about concussions? The big deal is that we are not doing imaging to look for concussions. We are doing imaging to look for more significant brain injuries. The average run-of-the-mill concussion has no imaging findings, not on standard and brain imaging. When we start looking at the diffusion tensor, we start looking at tractography- yes, there are findings, but it is still experimental. It is one of my pet peeves as somebody who reads brain scans on ambulatory patients. When I have an order that comes across, I am looking at a brain that says, ‘rule out a concussion because I cannot do that. A concussion is a clinical diagnosis, there are no imaging findings associated with it in a standard sequence.

We also have to worry about the post-concussion syndrome, and this is why there are so many different rules and regulations, particularly when we are dealing with pediatric sports about return-to-play issues, to make sure that we are not looking at a second impact syndrome, that we are not dealing with chronic traumatic encephalopathy. Those are more discussions for clinical and return-to-play issues than about imaging perspectives. The other thing that we want to talk about now is facial fractures. I’d like to introduce you to my middle boy, Cody. Luckily, I have got Cody’s permission for this one. So, Cody is my middle son, he is my athlete. He was a three-sport athlete when he was in high school, he did some athletics in college. At one point in time during Cody’s athletic career, he was getting injured on a fairly regular basis. Cody is a keeper in soccer. This picture was taken after he was in the goal and jumping to stop a ball, and somebody jumped to head the ball instead of heading the ball, they headed Cody in the orbit. I was at home; I missed this game and my wife came home to stop at the house before taking him to the emergency room. Cody had walked in with her, and she said, “They didn’t think there was anything going on.” I am looking at Cody’s face and saying, “Well, Cody’s seeing a facial surgeon today.”

Because what can happen here? When we start talking about facial injuries, particularly periorbital injuries, one of the big concerns is tripod fractures and blowout fractures. Those are the two big ones that we are looking at here. A blowout fracture is usually if you get something that hits directly over the globe, and as it does that, it increases the intraconal pressure. Where it likes to break is it wants to break through the thin membranous bone that is right underneath the orbit. So, deep in the face but right along with that, the top part of that orbital ridge there. A thin bone that separates the orbit from the maxillary sinus. What we see with those orbital blowout fractures, one of our biggest findings, anytime we get somebody who’s got facial trauma, one of the big things that we always want to do on those facial trauma patients is you want to make sure you are tracking conjugate gaze. Because in the patient that has the blowout fracture, it is very common as you are doing that conjugate gaze exam, that one eye will stop moving. Mainly when we have somebody who has a blowout fracture, there is herniation of orbital contents and particularly the inferior rectus into the maxillary sinus. The healthy eye goes up, the other eye stays where it is because it is trapped. The inferior rectus is being held, so the person loses conjugate gaze; they get diplopia when that occurs, and what we will see with those blowout fractures is herniation of orbital contents into the maxillary sinus.

Right here, that is the inferior rectus. Here is the thin membranous bone separating the orbit from the maxilla, and you can see where some fatty content has been displaced in this patient. Another relatively common skull or facial fracture is the tripod fracture. This one, rather than the force coming directly over the globe with the eye, comes in more from the side, and it hits the zygomatic arch. This is what happened to Cody. So, the force comes in and hits the zygomatic arch. Now, the zygomatic arch has three major connections: It is got an orbital component, it is got a component that comes back towards the TMJ, and then it is got the maxillary component. When that happens, you will see a fracture of all three components, which is why this is called a ‘tripod injury.’

What we see through here, we are looking at a CT, and this is a bone window. There is the nicely obvious orbital component. You can see the maxillary component coming down here, catching over the posterior compartment, and then there is the fracture of the zygomatic arch. Luckily, there was minimal displacement and cosmetic deformity in this case. The surgeon, in this case, decided, “Let’s go with conservative care.” What is interesting is Cody was able to return to play within two weeks, but he could only return to play with a hard plastic face shield. We had to take him to an orthotist and they used a thermo-moulded plastic to mould to his face, so they had this kind of scary clear face mask that he’d wear when he was back in the goal. This is a different individual. In this case, this is a hockey injury. One of the reasons that helmets are important is that I’d be wearing a face shield if I was playing hockey. Not like I am that pretty, but I still do not want things broken. When we look at this case, this gentleman is playing a pickup game of ice hockey without a helmet. He gets a slap shot on the outside of the orbit and developed the tripod fracture. This one, because of the degree of depression that was involved in that fracture, you can see the surgical repair. This is a fine plastic surgeon that goes in and reduces the fracture and puts in some small plates. The last category of fractures that we have been talking about regarding facial trauma is that I am not going to get into minor nasal fractures because how clinically significant are they? Do they need imaging? It is more of a clinical diagnosis.

The last significant group of fractures is a group of fractures called the ‘Le Fort fractures.’ I have always found this group of fractures to be fascinating. If for no other reason, I remember reading how Le Fort came up with its fracture classification a long time ago during residency. Essentially, he took a baseball bat to some cadaver faces to see what would fracture with different vectors. The Le Fort fractures are broken into three categories: 1, 2, and 3. It is one of the important reasons that anytime we have somebody who’s got facial trauma involved in their injury is, one of the first things to do is glove up, have the person open their mouth, grab their incisors, and gently, of course, first shake their incisors and look to see, does the head move with the teeth? Because one thing that happens with these Le Fort fractures is to varying degrees, they are going to separate the upper dental plate from the rest of the face. To use skull X-rays to illustrate where the fractures are. The Le Fort 1, breaks essentially right through the area where the alveolar plate is in the maxilla. This can damage the roots of the teeth. Quite often, it will be above the roots of the teeth, but you can see where this will separate that maxillary plate from the rest of the skull so that in the incisors, when you grab, they will move independently of the face. Not going to be comfortable for the person, of course.

The Le Fort 2 goes up through the nose. It comes up in an oblique position through the nose. When you grab this person’s teeth, you might notice the nose move slightly. Then the Le Fort 3, the fancy term for a Le Fort 3 is ‘craniofacial dissociation.’ This is where the calvarium and the face are no longer connected. So, if you are grabbing the incisors and moving, you will see the whole face move separately and independently of the calvarium. CT is where we are going to see these best, we can see that fracture right through here, separating out the alveolar ridge from the rest of the face. This person’s bleeding quite a bit on the maxillary sinus. They have got extravasation of air into the adjacent soft tissues, typically coming from the sinus. Le Fort type 2, we see this one coming up across the nasal bridge there.

That takes care of us from the standpoint of craniofacial trauma and imaging thereof. One of the things I like to do during my presentations is, show you some of the different things that radiologists see because if you spend any amount of time around, whether it is a medical radiologist or chiropractic radiologist, we are often accused of seeing things where there is nothing to see. Looking at a brain image in this case and one of the things I noticed is I saw a happy little snowman sitting here in this brain. So, there is the snowman, he has his little sticky arms out, just waiting to give you a big old hug.

Thank you very much. I appreciate you sitting through this particular section. Next imaging lesson, we are going to be talking about spine trauma.

[END]

 

Section 04_ICSC03 – Spinal Injuries Part 1
English Direct Download PDF – 04_ICSC03-Section 4- Spinal Injuries Part1.doc

Instructor Dr Chad Warshel
Video Lesson: 01:08:01

Welcome back. We are going to spend the next two hours talking about imaging spinal injuries. It is broken down into two one-hour sections. As we start dealing with spinal trauma, one of the things that are the major core concepts are the major tenants. When we are dealing with spine trauma, you need to understand two different things.

Number one, mechanism of injury. How does this particular fracture, dislocation, injury happen? That way, if we know what kind of sport the person was playing, how did they injure themselves during that particular sport, those are the things that we can use to try to figure out, “What am I looking for?”

If we see somebody who is playing basketball, they go up for a shot, somebody takes their legs out from under, may land on their neck and shoulders and hyperflexion and rotation. Well, I am going to be thinking about one particular type of injury. If I see somebody who they have a hyperextension, pick on bobsledding, the sled happens to roll and the head goes into hyperextension when the helmet catches the ice, “I am going to be looking for a different set of injuries.”  We look for that mechanism that really helps inform what might be going on with the patient, and of course, sometimes it happens really fast we might not know exactly what is going on.

The second thing that we need to be aware of with all these different injuries is the concept of instability. Is an injury stable or unstable? Now, again, not a big slide reader but definitions, you have to read those. For instability, the injury creates a potential for additional biomechanical or neurologic damage, in particular, we are dealing with spine. What we are concerned about is their cord involved or is their cauda equina involved nerve root and that sort of thing. Knowing which injuries are stable and which injuries are unstable, is a very important concept to make sure that the person is getting managed appropriately because typically, when we are dealing with somebody who has a potentially unstable spinal injury, those are the patients that are going to be back boarded, collared, and transported to the nearest emergency department?

Somebody who has a stable injury, maybe that might be a more casual or urgent at least, referral to a hospital, orthopedic, and so forth. Being aware that the unstable patient is one that does generally need to be transported is a core concept, and when we look at some of these different injuries, some injuries are just by the definition of this person has this injury, picking on burst fractures, chance fractures, things like that, those are by definition unstable so we treat them that way.

The other thing that we have to take into account is, when we look at those are more bony injuries, the fractures, there is the potential for ligamentous injuries. With the ligamentous injuries that we see where there is no associated fracture, particularly things like cervical spine, facet Joint capsule injuries, they tend to let the spine move too much. Not so much in the acute phase where the person is going to damage their cord right then. But more in the okay, as they are healing and there is too much motion, we are going to see accelerated degenerative changes. That is going to create its own problems. There is potential for damaging neurologic structures, again, not so much maybe in the acute phase more in the chronic phase. This is where being able to recognize, are there any findings of ligamentous injury is a very important thing for us because when we are trying to identify that ligamentous injury, what do we look for? C-spine is where we are really talking here. Thoracic spine, ligamentous instability is uncommon, lumbar spine, ligamentous instability is uncommon. It is more of a C-spine finding than anything else. That is where we are looking at neutral radiographs, if you see angular kyphotic deformities, it is always a concern that has this person damage some of that posterior ligamentous complex. Then we will do stress radiographs. Stress radiographs are kind of the core for looking for ligamentous instabilities and that is where we are going to be evaluating for translational or angular motion. This is like I talked about in the first hour of the trauma classes. We will look to see is there a 3.5 mm of translation C-spine, 4.5 mm of translation in the lumbar spine, and then angular motions.

When dealing with spinal injuries, one of the predominant theories that is used currently to assess is an injury stable or is an injury unstable because it answers most of the questions to the best of their ability, is the three-column theory of Dens. With the three-column theory of Dens, it was written for the thoracal lumbar spine but it is since been extrapolated into the lower cervical spine. Of course, it does not work for the C1, C2 complex. Of course, we are dealing with more complicated areas there, but anywhere C3 down essentially is where this is being applied.  We break the spine into three columns. There is the anterior column, which is the anterior two-thirds of the vertebral body. The middle column, which is the posterior one-third of the vertebral body, and then the posterior elements, which of course, is pedicles backwards.

The way that this theory works is when we look at these columns. If somebody has a one-column injury, it is generally a stable injury. If it is two or three columns, it is unstable, and really there are going to be some exceptions to these rules because there are also some things that involve soft tissues that we do not see, we cannot see the soft tissues, but we know the soft tissues are injured. We will talk about those a little bit. One column that is a stable injury, two columns, unstable injury or more, if it is two or three.

Asterisk. One of the first asterisks is that you cannot injure just the middle column. From a physics standpoint in order to enter the middle column, you typically have to break the back or the front as well. If you see what appears to be an isolated middle column injury, it is probably not. There are of course, some more exceptions. One of the big exceptions for that middle column is the traumatic posterior limbus bone that is considered a stable injury, and then if we see anterior column disrupted particularly, when we start looking things like compression fractures, if there is more than 50% loss of anterior body height, that is an indicator that it is probably unstable.

There are things that we need to be aware of when we are interpreting the imaging on these that create some of those subtle nuances. Just like it is possible to have a one-column injury that is unstable, if you look in- and this is where we are getting into the C-spine. When we look at the cervical, a teardrop fracture. Teardrop fracture typically only involves the anterior column. However, because there is so much ligamentous disruption around the other columns, it does create instability. So, let us start working our way from the top down, cervical spine, and we will go on from there.

If we are going to start in the cervical spine, the best place to start is C1. When we look at C1, there are two major fractures in C1. There is the Jefferson fracture and there is the posterior arch fracture.

With the Jefferson fracture this is where mechanism is really an important thing to figure out what is going on with your patient with the Jefferson fracture. The Jefferson fracture is an axial load force, something came down straight through the top of the cranium and it pushed the head down because as that force comes in through the top of the head, what we are going to see, so force is coming down this way. As the force comes down because we are seeing that lateral angulation of the lateral masses, well, as the force comes down and then goes through the occipital condyles, it is going to put a natural force pushing those lateral masses sideways. They don’t go sideways. They are held together by the anterior arch and the posterior arch. What we will see in this case though is the anterior and posterior arch fracture and that allows the lateral masses of C1 to spread out. This is a C1 burst fracture. It is blowing outwards. Now, the problem with most Jefferson fractures is we do not actually see the fracture lines, the anterior and posterior arch fractures can be very difficult to discern radiographically. The most important feature when we are looking at this Jefferson fracture, is if you look at the alignment between the lateral masses of C1 and the lateral edge of C2 is that there’s overhang, and anything more than two millimeters of overhang is an indicator of potential problems, and if whether it is on one side or both sides, because it is possible to have a unilateral Jefferson versus a bilateral Jefferson. If I see that overhang, that is going to be something that I am going to consider is an instability until proven otherwise.  This is a great case where we are going to want to follow up with a CT scan. CT giving us that bony resolution in the axial plane really lets us evaluate the bony C1 ring, and if we are careful about the communicating with RCT technologists, we can also make sure that they angle the Gantry in the CT machine, to make sure that they are in the same plane as C1. There is one of the problems you know, you get someone who is laying on a CT scan. The C1 might be angled like this and because of that, when they’re slicing in a regular axial pattern, we might not be able to see the entire C1 ring at one time. But by angling the Gantry for some specific slices through there, we can really confirm the presence of a Jefferson fracture.

We look for that overhang of the lateral masses, and we can look at the paraodontoid spaces. Now, it is a thing to be aware of. Paraodontoid spaces are highly variable, there’s a symmetry that is a normal development thing, so those are considerations. The thing is, you tend to think that, okay, well, why would I ever see one of these? It is unless I am on the site of the event. What is the probability that I am actually going to see this fracture? Well, one of the interesting things is, this is a classic mechanism that has a classic presentation and that is the positive Rust sign, where the person is holding onto their own head. They are actually creating their own stabilizing collar because well, I hold on to this and it feels better. Anytime we get to any post-trauma come in positive Rust sign, this is on our list of differentials, and I want to find out what was your mechanism of injury.

Video Presentation Placement: 11:13

The other important distinction on this is we talked about the other major fracture of C1 is the posterior arch fracture. That one is a hyperextension mechanism, and with that hyperextension, the posterior arch gets trapped between the occiput and C2 spinous and fractures at off. The nice thing is a posterior arch fracture C1 is considered a stable injury and six to eight weeks of fracture healing time. So big difference, in management when we are looking at somebody with a Jefferson fracture, this person is generally going to be put into a halo and they are going to be in that halo to try to see if this thing heals on its own short of doing a complete C0, C1, C2 fusion.

What else can be damaged when we are looking at the upper cervical spine? There is Jefferson fracture, posterior arch fracture, and now there is the possibility of the transverse ligament rupture. Typically, we tend to see the Dens break more often than the transverse ligament rupture, but transverse ligament rupturing is absolutely a possibility. What are we going to see, remember you can’t see ligament on x-ray, so what is my clue? My big clue is, if the person has anterior translation of C1 with an increase in the atlantodental interval. If I start seeing those things, that is what is going to make me concerned that this person has a transverse ligament rupture. We do know that when we look at an interval, just I am looking at a neutral lateral radiograph and this person has an increased atlantodental interval. There are more than 26 differential possibilities here, could this be rupture, laxity, agenesis, down syndrome, Marfans, Ehlers-Danlos, radical reactive, scleroderma lupus spine angular, rheumatoid arthritis. There are all kinds of possibilities for creating upper cervical instability, but if I have a patient who has a immediately antecedent history of trauma, I have got to consider that this is going to be a transverse ligament rupture until proven otherwise.

There is a little bit of a saving grace on this one. This is an unstable injury because this person is rupture the transverse ligament, the concern is that as C1 translates forward, the posterior arch of C1. So, there’s the spine angular junction. The posterior arch of C1 can trap the cord up against the dens creating something called the guillotine effect. How is it that somebody can have this injury and not have immediate cord injury because of something called Steel’s rule of thirds. If we were to look drawn on the screen, we are looking at the inside diameter of C1, lateral mass, lateral mass. Here’s the dens, and then back here is the spinal cord and I will give it that little ”H”.

When we look at Steel’s rule of thirds, the inside diameter, the ID of C1, 1/3 of that is taken up with dens. One third of that is taken up with cord. One third is taken up with CSF and loose tissue. As a ballpark average, the average dens are about 8mm A to P. The spinal cord at C1 is about 8 mm. That means realistically this person has about eight millimetres of anterior translation that can occur before they generally start to impact the cord, and that is why we can see patients that have this unstable upper cervical complex actually go through and yeah, they have got neck pain and if you look on flexion, they are coming 7 mm forward but they still have not quite hit the cord yet. Steel’s rule of thirds is one of those beneficial things and why folks that have these injuries are able to survive.

Now, looking at this from a radiographically view, here we see a patient. This is a neutral lateral and as I look at this neutral lateral, I look at this person’s atlantodental interval, and we know the rule for the atlantodental interval 3 mm or less on adults 5 mm or less on children. 16 is the age cut-off between child and adult. We look at this one that ADI is definitely increased. One of the things to consider, if you have your own imaging apparatus, you can do the x-rays in your office. I never do flexion extension until I look at the minimal series because I don’t want to do flexion extension if I already know the person is unstable, I am not going to push them into flexion extension if I don’t have to.

Video Presentation Placement: 16:00

Another one, another injury that happens at C1, C2, and this one is very uncommon. This is rare as far as cervical spine injuries go. Atlantoaxial rotary fixation. You’ll also see this going by a couple of different names. One of the less commonly used is Atlantoaxial rotary subluxation. Usually, fixation is the term that if you search the literature and find more of those. What we are seeing here is not surprisingly a traumatic injury, and this one has a rotational component to it. This person was injured when in rotation, and this is a partial dislocation. An orthopaedic subluxation where C1 is fixated and rotational in C2

Most of these are post-traumatic. In little children, when we are dealing with children, there is the potential for this to be post-infectious. You get a child who has an upper respiratory tract infection, and the organisms can see it into the adjacent tissues and the child can present with that same kind of appearance. This does have a very classic clinical appearance called the Cock Robin Appearance and what we are seeing is torticollis. This person is rotated laterally flexed and it is really painful. It is because if it is traumatic, there is this partial dislocation. If it is post-infectious, there is also a partial dislocation quite a bit of spasm involved in both of these cases, this is considered an unstable condition.

What am I going to see when I look at this radiographically? An important thing on this one that helps us distinguish the Atlantoaxial rotary fixation versus the Jefferson fracture. Notice that C1, C2 lineup laterally very nicely but a big deal on this person is look at the asymmetry of the paraodontoid spaces. So, marked asymmetry those paraodontoid spaces, that is one of our indicators particularly with the associated history, and this is when you have got to be cautious,  because one of the things to remember is there are a lot of asymmetry in the paraodontoid spaces as a normal developmental phenomena.  One of the things I look forward to figuring out is this actual rotation between C1, C2 or is this somebody who has got some just developmentally symmetry is to ensure you look at the size of the paraodontoid notches. In this person, the paraodontoid notches are pretty symmetric, and they have about the same side to side, but the paraodontoid notches or a paraodontoid spaces are not, so, we see that asymmetry that says, this is actually a true rotation.

As we are looking at this one, just to show you what this looks like and then to show how much rotation there is, we are looking at a CT of the same patient. As we look at the CT notice, the person’s head is fairly straightforward to backward, but we can see that C1 has pointed in that direction, so there is a substantial degree of rotation in this patient.

Video Presentation Placement: 19:20

The next injury is the Hangman’s fracture. Now, as we look at the Hangman’s fracture, of course, somebody being hung is kind of the classic mechanism for this but that is not really what we are going to see in the modern world. The idea here is to for some of that useless historical information, the radiologists are fairly notorious for, when somebody gets hung, okay? One of the things that happen is there is a shear force that goes between the angle of the mandible and the occiput and that fractures through the pedicles of C2.

Now, when that happens, of course, then the weight of the body pulls down and it distracts the cord and it ends up transecting the cord. There is an extension component when you hit the bottom of the rope, and because we don’t see that many people with this occurring anymore, we see this more of the hyperextension. The person is extending, and now we are not going to get the distraction that we saw previously, so when we get to hyperextension, it fractures through the pedicles of C2.

That fracture through the pedicles of C2, creates an unstable cervical spine because there is complete dissociation between the body and the posterior elements and it typically lacerates the C2, C3 intervertebral disc. Because they lack the distraction component, these patients can be neurologically intact at the presentation again, this is going to be another patient for a positive Rust sign or somebody’s holding onto their own end. The other thing is, that it takes a lot of extensions to fracture those pedicles, so it is very common to see other hyperextension injuries things as posterior arch fractures, which by itself would be a stable injury. We can also see things like extension teardrops.

Video Presentation Placement: 21:05

This is a nice example of the Hangman’s fracture, this is an elderly patient. This particular individual was walking through her bathroom, and she tripped on a rug and she fell on her chin, caught the edge of the sink, hyperextended her neck, and she landed on the floor. She was still alive. She had problems getting up and moving around. She was found by some relatives, a couple of hours later, and the patient, not surprisingly wound up with a fusion. The idea in a case like this because of the instability, they’ll try to reduce the C2 body, will try to reduce the C2 body, and then drive pedicle screws through the posterior elements and hold everything into the vertebral body.

That is a nice little segue into our next injury called a teardrop fracture. Now, teardrop fractures come in two flavors, there are flexion teardrops and there are extension teardrops. They are both unstable. That being said, realize there are even degrees of instability. The extension teardrop is unstable. The flexion teardrop is really, really, really, really unstable. The problem is, when we look at teardrop fractures, they really don’t look like much because a teardrop fracture is a fracture of the anterior inferior body margin, and it is called a teardrop fracture because it looks like a little teardrop fragment.

We see this little teardrop fragment we can see that there’s a small little fragment coming off the corner of the vertebral body. The extension teardrops are usually upper cervical C2, C3, flexion teardrops are usually lower cervical. But the idea being, with the hyperextension in the upper cervical spine, the A.L.L. “Anterior Longitudinal Ligament” transects and ALL also the body corner. Most commonly happens at C2 can happen to C3. You just lost you’reA.L.L. That is a major stabilizing structure in the spine. Not surprising that this is unstable. When we see somebody that has a flexion teardrop which is the lower cervical spine in order to get the flexion teardrop, they tore the nuchal ligament, the supraspinous ligament, the inner spinous ligament, the ligamentum flavum, the joint capsule and the P.L.L. typically also last reading the disc and then taking off the corner. Not surprisingly the flexion teardrop is more unstable because there are more ligamentous injuries, and those patients typically also have concomitant cord injuries where you start seeing anterior cord syndrome.

Video Placement: 23:47
Things that are on your differential for teardrop fractures are limbus bones. Limbus bone is a developmental variant where we see the ring apophysis, never really united in. It’s got smooth all around a corticated margin as opposed to the fracture which is going to be sharp and jagged. The other thing that is on our differential list is an intercalary bone, where we see a small little calcification / ossification of the anterior annular fibers, but it is the annulus, it is outside the normal confines of the vertebral body, it is usually not too difficult to figure. As we work our way down the spine, of course, one of the very unique structures in the spine, is the dens, the structure that allows for so much rotation in our c-spines. Well, it is possible to break the dens and there are three types of odontoid fractures. The type one is an avulsion injury, usually, something is distracting the skull and the alar ligament avulses the tip of the dens.

The Type 2 Dens fracture is one that goes through the base of the dens. Usually, this is a flexion extension style injury and this is seen in a very high incidence in older populations because osteoporosis can contribute to this fracturing, and then type 3 is a fracture that extends down into the C2 vertebral body. Typically also starting to get into the facet. The problem with the literature on these is that they are stable or unstable. I want to know the mechanism; I want to know stability. Well, the problem with stability is its variable and depends on the degree. Type 1 might be stable, might be unstable, and type 3 might be stable might be unstable. Type 2 is always unstable. Well, what is the variable, the force of the trauma? There are a lot of other components to it and that is why when we are dealing with any of these, my safe bet is all of these are going to be treated as unstable injuries and I will let the neurosurgeon make those decisions.

When we start looking at these, type 1 is rare, type 3 is uncommon, and the most common type of odontoid fracture is type 2. What we are going to see in these cases, is it fractures right through the base of the dens or looking on the AP or open mouth radiograph to see it. On the lateral view, the biggest tell is if there’s the displacement of C1 because we know C1 can go forward or backward when we are dealing with somebody who has a dens injury. Those are the big clue. The problem is this is a subtle injury. That is something that is easily overlooked on radiographs like in this particular case, this patient had a seven-view c-spine and the seven-view c-spine is really normal. We couldn’t see any fractures looking at that. But the patient was in really severe pain as was an elderly patient in her 80s, she had fallen down, and she smacked her face on the floor when she fell.

Started off with a seven-view C-spine, and this patient was transported the emergency room. They did a seven-view C-spine, the clinician was really unhappy with how much pain there was, and the negative studies of the patient were sent for a CT. On CT, there is a subtle fracture right through the base of the dens. Interesting on this particular case is they forgot to take the patient’s earrings off for both the X-ray and the CT and one of the problems were the earrings and the earlobes are right at the base of the dens, so they actually obscured things quite a bit and even created some beam hardening artifacts on the CT. It was questioned on the original CT and the patient had to have a second CT to confirm the presence of the dens fracture. The concern with these being they have a very high frequency of non-union. So, because of that, and that creates a relatively permanent instability or possibly permanent instability, these patients will quite often be fused but it depends on the patient and the outcome expected from surgery. In this particular patient’s case, surgery is actually more dangerous than fusing your dens.

Video Placement: 28:03
The type 3 fractures one that extends into the body a little bit more. We can see here there is a Lucent line that is getting further down than just the base of the dens and don’t forget the Mock effect creating problems when we are looking at the base of the dens, sometimes stable, sometimes unstable best to treat all of them is unstable. What else can we see fracture? Let us get into the lower cervical spine and this is where we are going to get into compression fractures. Compression fractures, when we start dealing with spinal fractures, these are incredibly common as far as spinal fractures go. How does it happen, flexion, and or axial load, and it loads the anterior body. In this particular case, this is a motor vehicle accident, so something considers from a maybe a racecar style racing sports standpoint.

This was a regular run-of-the-mill motor vehicle accident. What was interesting in this case is this patient was sent into my office for an outpatient x-ray and had ordered a three-view C-spine, two-view T-spine, two-view L-spine and a three-view fifth finger. The patient was complaining, “I don’t know why I need all these x-rays. The only thing that hurts is my pinkie finger.” So well, the doctor ordered all these. We are either doing all of them or doing none of them. I can’t pick and choose. I have got the entire series on the patient L-spine was fine, and T-spine was fine. When we look at the C-spine, it actually fractured his C5 vertebral body and notice that there is anterior wedging. Loss of anterior vertebral body height compared to posterior vertebral body height. The reason that he wasn’t even really paying attention or wasn’t aware of the fact that he had the cervical spine compression fracture was he’d also fractured the ungual tuft of his fifth finger, and that was incredibly painful. This is something called the confounding injury principle when you have somebody who has multiple injuries, which is one of the paying most attention to. The best explanation I have for this one is the homunculus.

If you remember that from a neurology standpoint, when you look at the sensory cortex and you look at the size distribution of parts compared to what they should be, fingers of course have really heavy innervation, we don’t see as much in the cervical vertebral body. He was paying much more attention to his little finger than he was to the C-spine. The nice thing is this is a stable fracture, with 6-8 weeks of fracture healing time. Generally, patients might be collared for a few weeks to for pain control but you’re usually not worried about neurologic compromise in these patients. Where we are worried about neurologic compromise can be the same mechanism, flexion, and/or axial load, okay, and this is one where we are seeing the cervical spine burst fracture.

Burst fractures. The thing that defines a burst fracture is it involves at least two columns, quite often it involves three columns. This would be easy to write off as just, maybe a compression fracture, where there’s loss of anterior body height or maybe even a traumatic end plate fracture like a schmorl’s node, but one of the single most important things on this particular radiograph, when we look at the posterior cortex in the vertebral bodies, they should be relatively straight or maybe even a little concave. When we look at our patient here and we look at that posterior body, that posterior body has gone convex. That is where when I was talking before about the three column theory of Dens if you see a middle column fracture, it is not, because when we see that middle column fracture one thing that might happen is this retropulsion of fragments and with the retropulsion of fragments, that is the middle column. If all I see is that convex posterior body margin, yeah, it is a middle column fracture, but there’s got to be at least one other column involved in these patients. Not surprisingly, these are unstable fractures with a high degree of neurologic compromise. Will also see a burst fracture with the rack of the lumbar spine, where the degree of neurologic compromise is lower because we are going to the cauda equina region.

As you look at the CT on this patient, you can see they actually vertically split the vertebral body and there’s that convex posterior body margin as they have retropulsion of fragments that are thrown backwards. We worry about that posterior body height with that retropulsion and make sure we are looking at the posterior elements because there can be some associated injuries.

We’ve seen vertebral body fractures. What about the posterior elements? It is absolutely possible to fracture the posterior elements when we are looking at the c-spine. Typically, these posterior element fractures are going to involve hyperextension where the individual is loading the posterior elements. Not surprisingly, if you throw in a little lateral flexion with extension, it loads one side more than the other. Extension and or lateral flexion, we are going to see loading in the posterior elements and typically it will fracture the articular pillar but it can fracture the pedicle, it can fracture the lamina. One of my biggest clues that makes me think this is when I am doing my physical exam on the patient and they’ve got focal pinpoint tenderness because I am palpating the articular pillars now, putting my pressure in through the pillars. I get one pillar that just makes the patient jump up off the table. That is a posterior element fracture until proven otherwise. Because we know that we are dealing with a lot of extension mechanism injuries, there might be diffused neck pain, and really uncomfortable all the way through, but it is that difference of that focal pinpoint you just drove a needle right into the back of my neck.

What are we going to look for? We can see some asymmetry radiographically. We can even see this fracture extending into the lamina. You notice how there’s rotation between those articular pillars. We are looking at a posterior element fracture here, big deal on these, this is where we really want to start looking at a CT. The problem with posterior element fractures is they’re notoriously difficult to see radiographically. Could we do special views like pillars and things like that? Absolutely. I am not a big one for wasting a lot of time if I am really concerned about posterior element fracture. I am going to get my patient’s CT-ed. As we look at some of these posterior element fractures, we can see a fracture here in the pedicle. Here, there’s a fracture through the articular pillar. The nice thing is these posterior element fractures are considered stable. It is one column, it is just a posterior column. Again, this person is generally going to be collared for a little while for some pain control. However, they should heal without any neurologic sequelae and too many ligamentous injuries.

Now, our next injury is the Clay-shoveler’s fracture. Well, it depends on where you live and how much clay you have in your soil. This is one, I am in upstate New York in the United States, and one of the things that we have in upstate New York is we get a lot of snow in the winter and when you watch the snow falling, one of the big questions is always is the light fluffy snow and that is going to be easy to get off the driveway, or is this the heavy wet snow? That is going to be miserable to shovel. Well, one of the things that happen with that, wet heavy snow is very similar to what we see with clays is it is a very heavy material. As you dig and you go to throw the shovel full, well that creates an asymmetric pull on the spinous processes in the cervical thoracic junction. What we are going to see here is with that kind of asymmetric pool, you can fracture off a spinous process in the cervical thoracic junction.

Last time I checked shovelling snow is not an Olympic event so if you live in upstate New York, you kind of think it should be. So how else do we see this? Well, we can see it with any kind of asymmetric throwing event. We can also see this with direct impact. This is one word, let us put a 500-pound barbell across my spinous processes and if athletes aren’t careful, that is potential there. The problem is, that this can be a very subtle injury. When we look at the clay-shoveler’s fracture, this one is pretty blatantly obvious. I can see that fracture through the spinous process. Now, problem is, realize that when so many fractures off a spine are in the CT junction they’re going to tend to spasm. Their traps are going to tend to tighten up. Their levator is going to tighten up and it brings those shoulders up higher when you’re trying to take a lateral cervical spine radiographs.

Video Placement: 36:48
This is one where again if there’s focal pinpoint tenderness right in the midline. Then, I am going to go ahead and make sure I am doing a swim review, my facility is doing the swim view, and I will consider doing obliques. The other thing is to look at the AP view, there’s a subtle finding on the AP view called the double spine sign. As we look at this patient, so, here C6, and there’s the C6 spinous, here C7, there’s the C7s spinous, well, there’s spinous 6.5. That is because that is the tip of the C6 spinous the fractured displaced downward. The spinous is will almost always displace inferiorly when we are looking at them. Because of that, they do have a very high frequency of healing non-union, and one of the things that we always have to distinguish is, is this a new clay-shoveler’s or is this an old clay-shoveler’s fracture? We can see in this case where there is a nicely corticated margin in the intervening space telling me that that is an old clay-shoveler’s fracture.

The other thing that is on your differential diagnosis list for a clay-shoveler’s fracture is a nuchal bone and that is where we see some ossification of the ligament of nuchal and it is a very common degenerative finding to see some little ossifications on the nuchal ligament. There won’t be a matching defect of the spinous process. The nuchal bones tend to run very vertically as opposed to the clay-shoveler’s fracture which matches up with the spinous process.

Video Placement: 38:20
That is taken care of a lot of our fractures in the c-spine, now what about dislocations? The dislocations in the c-spine typically are going to involve the facet joints and they’re both going to involve flexion. The difference is, so there’s a unilateral facet dislocation and a bilateral facet dislocation. The unilateral facet dislocation is flexion or flexion with rotation. The bilateral facet dislocation is just flexion. In either case, we are going to have somebody that has that posterior component pain with a flexion mechanism, which definitely warrants taking some radiographs in a case like this. What is interesting when we look at these, are unstable injuries, there’s a lot of ligamentous damage that occurs with facet dislocations. What is interesting is when they’re particularly the unilateral facet dislocation, while it is dislocated, it actually acts stable because everything is locked. One of the other terms for this is a unilateral facet lock and so it holds everything in place. Once it is reduced because there are so many ligamentous injuries, this person is going to wind up getting a fusion.

One of our big clues that we are starting to look for is the unilateral facet dislocation. There’s the classic, which is described in the Radiology literature, and then there’s the let us be practical and talk about what we actually see. The important thing is, that unilateral facet dislocations will always, 99.9% of the time have an anterolisthesis because it is almost impossible to dislocate a facet without flexion rotation and not have some anterior translation of the vertebral body. That translation is typically less than 50%.  I am going to look for that anterolisthesis. The other thing is, as soon as I see any spondylolisthesis, I always look at the posterior elements to see if there is a cause because most spondylus are driven by the posterior elements. I look at those posterior elements and what things were going to look for is something called the Bowtie sign.

It is worthy, two articular pillars are set off from each other and that is why I’ve got a lovely picture of a nicely actually tied bowtie here. What we are this bowtie sign where it comes from. This segment is neutral, we can see that the articular pillars are superimposed on each other. With a unilateral facet dislocation, it creates an offset of the articular pillars and that offset of the articular pillars creates something that kind of sort of a little bit maybe looks like a bowtie. So that bowtie sign is one of our clues for the unilateral facet dislocation. We can see in this patient as we run George’s line, posterior corner here to posterior corner here, this person is a small anterolisthesis and as I am looking at the posterior elements, I can see and there is some rotations lower segment, which makes this a little confounding, but there’s an articular pillar there. There’s an articular pillar there, draw these in, here’s a pillar, and then here’s a pillar. This pillar is still articulating here. This pillar is no longer articulating, so that is a unilateral facet dislocation.

Our other big clue is steep rotation on the AP view. Notice that the C7 spinous is roughly in midline, and the C6 spinous is deviated way over to the side. That is because to get that unilateral facet dislocation, there will have to be some degree of vertebral rotation. These patients were of course emergency and transported to attempt to reduce the dislocation. The couple that I’ve gotten to see one of them was athletic. One of them was not. The first one was a gymnast, she was doing the Vault and when she did the Vault, she hit the Vault really well but she missed her landing and occasionally landed on her neck and her shoulder in flexion and rotation. The other one was a gentleman who was just jumping into a swimming pool while inebriated and didn’t see a step. His shoulder caught the step of the pool and rammed his head into the side of the pool. But in both cases, they were flexion-rotation mechanisms. The bigger the injuries is the bilateral facet dislocation. This one is a pure flexion mechanism. This is where somebody has thrown forward, and as their head is thrown forward, they tear all the posterior ligaments to structures, not just the facet capsule but also the nuchal ligament and all of those. This person again, our big clinical clue, even if we miss the dislocation component. This person’s going to have at least a 50% anterolisthesis of the involved segment because to get both facets to jump that way requires a large translation, so not surprisingly this tends to lacerate the discs as well as a lot of the other ligamentous structures in the area.

Big anterolisthesis gapping in the inner spinous space which is also our indicators of ligamentous injury and not surprisingly a very high incidence of neurologic deficit because the spinous process will start to approximate the posterior corner of the vertebral body. That is going to transition us from the cervical spine into the thoracic lumbar spine. One of the things that I’d be absolutely remiss is if we didn’t cover disc pathology when we are talking about the thoracal lumbar injuries. Disc injuries also happened in the c-spine, but the single best article and kind of the gold standard for reporting imaging these days is a journal article called Lumbar Disc Nomenclature Version 2.0. This is actually a free article if you just Google Lumbar Disc Nomenclature Version 2.0, this was published in the spine and it was released as a free article because it is basically foundational.

When we start looking at the original article lumbar disc nomenclature, the original was written in 2001. Version 2.0 is the revised version from 2014. This is one where understanding how to classify disc lesions is incredibly important and this is the standardized language that all radiologists should be using. Unfortunately, we see some that are still behind the times on that, but this is the gold standard. When we start looking at disc herniation, and disc lesions, of course, we usually think of those as that generative phenomena, but they can also be post-traumatic. It really applies when we are dealing with traumatic incidents.

I am going to talk about three things relative to disc herniations, well disc pathology. Annular fissures, disc herniation, and modic changes. When we start looking at disc as it either breaks down or there’s the possibility of traumatic, there’s a phenomenon called annular fissuring that can occur. Now, if you’re familiar with the original article, it is written back in 2001, these annular fissures were actually originally called annular tears. The problem with tears is tear implies a traumatic etiology. Because of that, the term was changed away from tear into fissure because yes, these can be traumatic, but more often than not, they’re actually a degenerative breakdown of the annulus. We have got rid of tears and we now call these fissures. When we look in the finding section of a radiology report versus the impressions, one of the things you’ll also see is something called an HIZ or HIZ, the high-intensity zone, that is because it is a bright spot in the annulus on T2.

They do typically happen in the posterior disc that can happen anywhere. Just to posterior disc is the more load-bearing component and there are three types, transverse, concentric, and radial. The radial’s is the ones that we worry the most about. For the transverse tears, I’ve given you a schematic here, so we are looking at a sagittal view of the vertebral body and disc and vertebral body and then an axial view of the disc with the annulus on the outside, the nucleus on the inside. The transverse annular fissure, is right at the edge of the end plate where the annular fibers are inserting via Sharpey’s fibers. We can see there’s this nice bright spot here, so that is very much hugging the end plate, so that is a transverse annular fissure. Typically these don’t allow for much nuclear migration, sometimes we can see similar things on radiographic appearance with a small vacuum cleft which can indicate in a trauma case that this person does have some avulsion of angular fibers. Generally not considered super significant.

The concentric fissure, which is actually the most common of the three types of fissure, is a delamination effect, we are actually seeing. We think about the concentric layering of the annulus much like the steel bands in a radial tire. So we see those alternating bands of ligamentous tissue and sometimes you can get a separation between some of those annular layers and that is a concentric annular fissure. It is going to be vertically oriented on the sagittal and it is going to be not surprisingly, concentric when we look at the axial. We can see that there’s this bright spot in the posterior annulus. It is vertical and then there’s this bright spot that is running around the outside of the circumference.

The radial annular fissure is the more significant of the three because this is the one that allows for nuclear migration to occur. Where we are seeing this fissure cutting across annular layers and not surprisingly the nuclear material can push into that radial region and allow for a disc herniation and this is where we start seeing extrusions in particular and sequestrations. These radial fissures, we don’t really see very well in the axial usually, the bigger tell is on the sagittal. We can see where it is cutting across multiple layers. Well, these are problematic one because they can allow for nuclear migration, but two, they also allow the radial fissure can hit those outer annular layers, where we see the innervation and that can create some pain.

Then we get into herniations.  I realize I am talking to my chiropractic audience, and we are the owners and specialists in spine pathology. I am going to go through this fairly quickly, but just to make sure that we are all using the same language when we are talking about disc herniations. For those of you who have been around a little bit longer like myself, a long white beard kind of help’s out to know I have been here for a while. You remember back when MR was really a new thing and when we started, we could send patients off for MRIs. If I sent the same MRI to three or four different radiologists, the reports would look completely different. Somebody might talk about a bulge, another way to say it is prolapse on the else might say are herniation and that complete disarray in the language is what prompted the American Society of Neuroradiology to create this standardized nomenclature.

This is what everybody should be using and most radiologists really are on board, particularly neuro rads and MSK rads. One of the things to consider is if you are getting your reports from your Imaging center and maybe the body imager was the one that was on duty that day, you might get a non-standard report because the body imagers are more interested in the chest and abdomen. They might not be as conversant with some of the spine terminology which is why I am a stickler for imaging should be read by spine rads or MSK rads. Those are my big preferences there.

When we start looking at the different kinds of discs, what is interesting is if you read the article in 2001 and then you read it in 2014 there not surprisingly, are some changes. One of the big things is in 2001, there were four kinds of disc herniation: bulge, protrusion, extraversion, and sequestration. Well in 2014, Pluto, was not a planet anymore and the bulge is no longer a herniation. Bulges are considered asymptomatic incidental degenerative phenomena of really minimal clinical significance. They are not even qualified as herniations anymore. Protrusions, extrusions, and sequestrations are. Notice that you have got some little brackets here. In protrusions, the annular material is contained or the nuclear materials are contained by the annulus, in the extrusion and the sequestration or sequestered fragment, the nuclear material is not contained by the annulus.

An important thing when we are looking at discs is you have to make sure that you evaluate both the axial and the sagittal when you’re classifying disc pathology. If you look at just one or the other, you might miss some of these findings. Another thing to consider is to remember that you are looking at MRI, different centers will have different protocols, some use thicker slices, some have bigger gaps between slices, and sometimes disc material can hide. That is why we want to make sure we look at both the sagittal in the axial to correlate what it is that we are seeing. Where do I send my patients for imaging if I am sending my patients to a center that does high-quality patient-centered imaging or am I sending my patients to a center that is kind of notorious for, well, we move the meat, okay, one of the colloquial phrases for we get as many patients through per unit of time as possible to maximize profits? Profit is important, but so is good patient care.

Video Placement: 52:10
The disc bulge, again, is not even herniation anymore but when we look at a bulge for seeing the disc material going beyond the vertebral margins, now it has to go more than two millimeters. If we were to draw a line from corner to corner in the vertebral body, the disc material has to go more than two millimeters past that line. When I go corner to corner here, I can see, okay, that disc material is definitely two millimeters beyond. Anything less is just considered normal physiologic bulging has to go more than two millimeters and a disc bulge by definition has to involve greater than 25% of the disc circumference. I will be honest, most disc bulges involve 100%. Because one of the things we see here is the disc desiccates, N plate, N plate with nuclear material in between as that disk desiccates in the end plates approximate, the annulus just starts to bulge all the way around. It is kind of like that middle-aged bulge that happens. When we look at this thing on imaging, we are looking at the T2 Disc material which is going back. There’s some disk off, see if I complex up front, but an important thing is we look at this on the axials. That is axial through the end plate, we are looking at a bone slice in this particular case. Then this is a disc slice and these two images have the same size. When we compare these two images, an important consideration, notice how the circumference of the disc is bigger all the way around than the bone is. Well, that is because that is that annular bulging that is occurring as the N plates approximate, the annulus is starting to bulge out. It is evolving 100% of the circumference. Fantastic.

One of the analogies that I like to use for disc bulges. Not surprisingly, radiologists like food, so, I like to use a food analogy here. If you’ve ever made smores, I don’t know how American of a thing smores are versus an international thing, but if you take two graham crackers and you put a marshmallow in between that you heat it up on the campfire and then you squeeze the graham crackers together, the marshmallow loses all the way around. Well, that is essentially very much like a disc bulge. Now, bulges can be symmetric all the way around and very circumferential and if you have somebody with scoliosis or some side bending, that can create symmetry to the disc bulge. But again, it is more than 25% of the circumference, it is a bulge. What the literature tends to tell us is that bulges are generally asymptomatic incidental findings where lots of people have these and never have pain.

Getting into true herniation is the disc protrusion. Protrusion and extrusion have very similar definitions. They’re similar but actually opposite. When we try to figure out is something a protrusion or is something an extrusion, we look at a couple of things. We look at the depth of the disc material and we look at the width of the disc material. A protrusion should be wider than it is deep. Wider than it is deep, that is what makes a protrusion. Because the protrusion is contained, this is a disc herniation that is contained. If we think about the annular fibers that plug-in corner to corner if the disc material cannot go above or below the level of the end plate. If it goes above or below the level of the end plate, that has to be an uncontained disc.

When you look at this particular case looking at sagittal and axials, so we can see that disc material is coming back here. It is staying between the end plates. Then on the axial, the disc material outlines it here, right there. The disc material is going from here to there, that is the width. It is going from here to there, that is the depth. This disc is wider than it is deep, so we are looking at a protrusion. Now notice, I am really only focusing on the T2s. We don’t really use the T1s to look at this material. I have just included them for completeness’ sake. When we start getting into the literature, one of the things we saw in the ’80s and ’90s when MRI first started being widely available is that there was a massive increase in spinal surgeries in the ’80s and ’90s and it is because of the structural pathology phenomenon. There is a structural problem with the disc. Surgeons were cutting on a lot of discs. Lots of patients with back pain. They did an MRI, they found disc lesion like a protrusion. The person had to diskectomy and then in the late ’90s and early 2000s, all the literature started saying, well there’s a huge amount of failed back surgery, because are these really structurally that important, are they likely to be pain generators?

The epidemiology studies really came out that showed when we look at asymptomatic people, people have never had back pain in life and we look at an MRI their lumbar spine, there’s a huge incidence of disc protrusions. Because of that protrusions are one that could it be an asymptomatic issue? Yes. Is it dislikely? Not so much. That is as diametrically opposed to the extrusion. Extrusions are usually symptomatic because we are dealing with uncontained nuclear material and it creates a host versus foreign reaction. There’s an immune reaction to this. We are looking at extrusions again, we are going to compare the depth of the disc to the width of the disc. We look at how wide it is versus how deep it is. An extrusion is going to be deeper than it is wide because this material’s now, the toothpaste consistency nuclear material has now extruded beyond the margins of the annulus.

This is where we also have to make sure we look at the sagittal and the axials. As we look at both the axial and the sagittal here, this looks like an extrusion on both. It is on the axial, it is wider or steeper than it is wide. On the sagittal, it is dropping down below the end-plate level. But what about something like this? Where okay, the disc material staying between the end plates but on the axial, it looks like an extrusion, well, it is always whichever one you’re considering whichever one’s worse, that is the one it is. So it looks like a protrusion on one and extrusion on another. It is an extrusion. Same thing here, we can see broad-based extrusions. But as soon as it is dropping down below or going up above that end plate, that is extruded material.

We start looking at the imaging on these and here this to me looks like a uvula. Looks like there’s a large uvula of tissue hanging down. It is still connected to the parent disc, which is what makes it an extrusion. If I look at it on the axial, if I were to outline the structure, there’s the disc material there and it is definitely deeper than it is wide. We are looking at an extrusion in this case, and of course, as chiropractors, we know that extrusions tend to do pretty well with conservative care. That is one of my favorite quotes from the literature, I love throwing this one up. 90% of extrusions with radicular symptoms, manage non-operatively with aggressive conservative management have been shown to do well. I always loved the “to do well” part without throwing on some actual qualifiers for that one, but we know that these patients generally do well with conservative care and as we start looking at them, one of the considerations is a lot of times, the pain that we are seeing associated with these is because of an immune system reaction because we are seeing an inflammatory response and that can create its own localized pain.

We can look at some of the axials and if you get poor quality sagittal, or patient the moves. Here, we are looking at a disc slice and I am seeing disc material still a disc slice and disc material. I am getting into the inferior end plate and they’re still disc material. Now I am into the mid-portion of the next body and I am still seeing disc material, so I can tell that that is an extrusion. Bulges, protrusions, extrusions, I see all the time. Sequestered fragments, I don’t see that often as somebody who reads film every day of his life. I only usually see 3-5 sequestration is a year and that is an outside number. Usually, extrusions are much more common than sequester fragments. The idea here is that it is uncontained. The nucleus is broken free of the angles, but an important part is a sequestered fragment, the sequestration doesn’t have a connection to the parent disk anymore.

I use a baby analogy for these. Sequestration is a fetus. It is still got an umbilical connection to the parent. When we look at sequestration, this is a baby’s umbilical cord being cut. It is free and by itself. We are looking at the little baby there that is the sequestered fragment. The same thing that we see with patients that have extrusions, these are going to be generally painful, there’s going to be an immune reaction to this uncontained disc material. Subtle, we don’t see them that often, but as I look at this patient, I can see there’s disc pathology here on the sagittal, but the annulus itself looks intact. When I look at the axial slice the annulus has a normal contour, but then, when I am up here in the mid portion of the vertebral body, there is disc material. So looking at sequestration.

Now, what is interesting. We don’t usually do contrast when we are looking at sequestered discs, but we’ve seen some and it is because we might be looking at a differential of, is this an epidural hematoma is a possibility? Could this be some kind of tumor or lesion because maybe these are fairly large? As we look at this case, we can see that there is this large bolus of material behind the L4 vertebral body. This is a case where the initial read by the radiologist was, is this an epidural hematoma or is this a mass? So they put contrast on board on this one. Now, before I show you the contrast, one thing I will tell you is that this is a very fresh sequestered fragment, because one of the things I notice about this material is, that it is incredibly well hydrated. This is where we really get into that traumatic disc etiology. If I can see, I know that the trauma was within the last two to three weeks and I see how incredibly hydrated that extruded disc material is sequestered disc material, I know that this is tied into that acute trauma. Because one of the first things that happen with these uncontained discs is the hydration is removed from the nuclear material.

We don’t typically put contrast on board because there were differentials of epidural hematoma versus tumor mass like a meningioma or neurofibroma. This one had contrast put on board, and it really illustrates an amazing concept. As far as that immune reaction, we know that one of our terms is contrast goes where blood flows. Well, when we look at this thing post-contrast, so we are looking at T1 fats at post cons, here’s the disc material and notice that there’s a ram of bright white around that disc. We see the same thing over here on the T1 fat set, post-con. Well, contrast goes for blood flows. What we are seeing is we are seeing the immune reaction where there’s increased blood flow in the immune cells is being attracted to that foreign invader material of the nucleus. It really illustrates the concept of chemically mediated pain. Why disc material in an uncontained disc material will resolve itself given time because there’s an immune reaction where the macrophages are actually phagocytizing that nuclear material.

One of the other things that we need to consider with these discs lesions is where are the disc lesions, and we talk about them in a couple of different locations, central, subarticular foraminal, extraforaminal, realizing that most herniations are in the central and subarticular range. Realize that there used to be a different term for subarticular. We also used to use the term paracentral, and I’ll be honest with you, the lumbar discs nomenclatures designed for lumbars and it is been extrapolated in the c-spine. If I am in the lumbar spine, I use the term subarticular because that is consistent with the article. When I am in the c-spine, I will still use the term paracentral because of course the set orientation is different. You will still see some of those terms used, but so central and subarticular most herniations are, it is a very small portion being foraminal or extraforaminal.

Now the last topic for this first hour is Modic Changes. This is something that if you’ve been keeping up with MSK literature, modic changes have seen a lot of press over the course of the last 15 to 20 years. Now, modic changes are in a small percentage of the population that we have no idea who gets them, but in some people, they get a marrow response to disc degeneration. As we look at this marrow response, there are three types: modic 1, 2, and 3, and they happen in order. First, there’s one, there’s two, then there’s three, and they never go backwards. You’ll never see a two turn into a one or a three turn into a two. If you do that, actually means you’re looking probably the spinal infection. But when we look at these modic changes, the first thing that happens, first, there’s almost an inflammatory reaction. There’s a fiber vascular infiltration of the marrow. Then there is a fatty replacement, and then there’s bony sclerosis. And the bony sclerosis is rare. Most people stop the modic two.

The modi type 1, we look at the T1s and the T2s. The modic type 1 because this think about this is an inflammatory process. We are seeing edema on the T2. So bright on T2, dark on T1 and one of the things and if you follow the literature, you know that literature can be all over the place on these motor changes. The predominance of the literature I have seen says the type one modic changes are going to be associated with discogenic pain. So if I see a type one motor change, I can reasonably believe that I am dealing with somebody who has got pain coming from that area.

Now, as that a diva eventually burns itself out, it is going to be replaced with fatty tissue. And when I look at this, what I am really going to see the important part is it is bright on T1, because of fatty materials, bright on T1. On T2, sometimes it is a little bright, sometimes it is a little dark, and sometimes it is the same as the adjacent marrow. The important thing is it is bright on T1. Now, this fatty replacement, this one is not associated with back pain. This is the inflammatory phase is and then as it trickles out, eventually that stops being associated with pain when we see the fatty replacement.

Type 3 modic change is bony sclerosis. This is going to be dark on T1 and dark on T2, and again, it also poorly correlates with symptomatology. That is going to take care of this first hour of spinal trauma, I will see you back for hour two.

[END]

Section 05_ICSC03 – Spinal Injuries Part 2
English Direct Download PDF – 05_ICSC03-Section5-SpinalInjuriesPart2

Instructor Dr Chad Warshel
Video Lesson: 01:08:47

Welcome to Sports Imaging of the Spine Volume 2. We are looking at the second hour here getting into the thoracolumbar and sacral injuries. As we start dealing with these, of course, we left off talking about disc herniation in the thoracolumbar spine. Let us actually start talking about some of those thoracolumbar spine injuries.

Not surprisingly, the most common type of spinal fracture is going to be the compression fracture in the thoracolumbar junction. Thoracolumbar junction being mechanically predisposed towards compression fractures because we are changing from kyphosis to lordosis and that tends to load that into your body plus we are in the stability of the thoracic spine, mobility of the lumbar spine, and those junctional areas we know are very common areas to start to find fractures.

We see this craniocervical junction, cervical thoracic junction, and thoracolumbar junction. Those are where we see the predominance of a lot of our spinal fractures. With the thoracolumbar spine compression fracture, how does this happen? Same thing as we saw on the c-spine flexion and/or axial load. One of those was some of the classic mechanisms: I picked up something too heavy, I bent forward to pick up something too heavy and I felt a pull, heard a pop- instant onset of pain.

The nice thing about the spine compression fracture, I mean, the most common fracture, the good news is It is a stable fracture. When we deal with compression fractures because the middle column in the posterior column is still intact, these are stable fractures. The asterisk on that one is there is that caveat: if somebody loses 50% or more anterior body height that tends to indicate instability even in a compression fracture because there’s probably some degree of ligamentous damage.

One of the other important considerations, when we are dealing with these fractures is once somebody gets a compression fracture where that vertebra takes on an anterior-wedge shape, that vertebra is going to be wedged forever. Then, we start to deal with the issue of, I see wedge-shaped vertebrae. Is this an acute compression fracture? Is this an old compression fracture? What’s going on in this particular case?

When we look at how compression fractures occur, what is really interesting is only about a quarter of compression fractures in the TL spine are from acute trauma. The majority of these are going to be seen in patients that have some degree of lost bone density; whether it is due to post-menopausal or senile osteoporosis, or whether we are looking at secondary osteoporosis from, of course, one of those big culprits being corticosteroid medications.

If I have got somebody there, an athlete, they are dedicated to their life to athletic performance, but they can still have rheumatoid arthritis and maybe they need to take the chronic medications or long-term medications for rheumatoid arthritis. One of the standard meds used very frequently is corticosteroids. Of course, these days I try to wean people off corticosteroids as soon as possible and get them on other medications, but, we can still see where these corticosteroid medications can be a hallmark for the treatment of autoimmune conditions.

The big thing that we need to remember is, if I see a compression fracture, I’m dealing with a young athlete, they have had traumatic incidents. That is not going to be surprising. But I always want to make sure that I do investigate, how does this person’s bone density look? What does their med list look like, to make sure there is nothing that might be diminishing their bone density.

When we start dealing with compression fractures, it is the anterior 2/3 of the vertebral body that is involved, and because of that, what we are seeing up here in the top right image, we are looking at the standard wedge-shaped compression fracture. I know that It is just the anterior 2/3 involved because the posterior vertebral body has maintained a tight. It is still concave and the posterior elements are fine. That is the average run-of-the-mill compression fracture. That is what we see most times. It is possible, particularly in osteoporotic individuals to see the biconcave or fish vertebrae style compression fracture, and this is where is the exact line drawn from the three-column theory of that as well. The nice thing is because they have maintaining posterior body height and it is still concave, most of these are still stable.

The other possibility again, typically, dealing with somebody who’s profoundly osteoporotic or something that raises a concern for other underlying bone diseases, such as multiple myeloma metastatic disease; and that sort of thing is the vertebra plana where the person loses anterior and posterior vertebral body height and that can still happen during a compression mechanism. If it is a minimal mechanism, then we have to be concerned about a pathologic fracture.

Something I alluded to just a moment ago was any time we are looking at a compression fracture, we do run into the problem of that vertebrae going to be wedged, from the day the person gets the fracture until the day they die. Then, we run into this, is this renewer and old compression fracture? Well, one of our first rules in Radiology is, always compare with the previous imaging.

If you have a patient that you know has previous Thoracolumbar Spine Imaging and they come in, they have got a new onset of pain and you see wedge-shaped vertebrae, look at the old studies. That is one of the best things that you can do. Back in the olden days, before the beard turned grey, that was not at most easy to do. Because if the patient had imaging done at another chiropractor’s office, I had to wait and order those in. If they had them done at the hospital, I would definitely have to wait and order those in and comparing those images might take two weeks and that’s a lot of waste of time.

These days with digital health records quite often I can have access to most patients’ imaging within an hour. Comparing against previous imaging is much more user-friendly these days, and that is always something that’s on my list. Have you had previous imaging? I like to pick on my experience having practiced in California. I mentioned that I practiced in a little town called Clovis, where the biggest event was the Annual Clovis Rodeo. Well, do you want to talk about somebody who experiences polytrauma? Rodeo clowns. That is where and quite often a nice thing about rodeo folks, It is they have medical records they bring with them. But comparing new versus old was always an important thing. Let us go into the I do not have previous imaging, not everybody walks around with spine X-rays in their back pocket.

I am going to look to see, does my patient have other findings to tell me if this compression fracture is new or if It is old? When I look at this long list of things, those three: a zone of impaction, paraspinal edema, and step defect. Those are my big three. Those are the things that really help me decide, is this an acute compression fracture? Because if I see any one of those three things, that is an acute compression fracture.

The other things, we got some variability there. We will talk about those in a little bit. Let us look at a patient. So I have given you a very focused close-up on this one. This particular individual, is an electrician and so he does a lot of manual labor. He does a lot of heavy lifting, in a lot of awkward positions, got a past history of spine injuries, and been to several chiropractors throughout his life.

Comes in after doing a recreational weekend of building a concrete patio and he had bent over to pick up an 80-pound bag of concrete: immediate onset of pain. You have got flexion, you have got an axial load, immediate onset pain. This definitely warrants taking some pictures, so, looking in this thoracolumbar junction, there is a wedge-shaped vertebrae, and realize about 10 degrees of wedging can be considered normal too, particularly in the thoracic spine. It is very common to see up to 10 degrees of anterior wedges a normal developmental thing. Here, we are looking at about 25% anterior body height loss.

As I close in on his lateral view, I see a wedge-shaped vertebrae. I have got somebody with heavy manual labor history. Is this new or is this old? Well, one of the first things I noticed when I look at the cortex on these vertebrae, is right there, you are going to take the lines away now. You can see that there is a sharp step defect in the anterior cortex. That is where the fracture line occurred.

I see that sharp step defect and that step defect will typically go away in 6 to 8 weeks. It will start to round off as the body heals.  I can see that sharp step defect, I already know that this is an acute compression fracture. This person also has a second finding. Look at the yellow line I am going to make both things go away. There is a faint white line right behind that step defect and that is known as the zone of impaction. You will also see it described as the zone of condensation.

What is happening there, so if my fingers are trabeculae and the fracture line is right in between, well when that fracture happens, there is an impaction. Now we have twice as much trabecular bone along that fracture line and that creates that sclerotic margin. Again, that goes away in 6 to 8 weeks. I only need one of the three findings to tell me that it is an acute compression fracture. I have got 2 of the 3, so, I am pretty comfortable saying, Tom here has an acute compression fracture, posture body heights maintained, the posture body still concave; posture elements look fine.

There is one thing you got to remember, compression fractures in the thoracolumbar spine, our diagnosis of exclusion/ You have to exclude other things like burst fractures and chance fractures first. What else do I see? The third finding is paraspinal edema. I want you to think back to gross anatomy. If you did cadaver work, or if you did digital work, one of the things that were kind of cool from doing the gross anatomy dissection is, once the ribs were cut and the heart and lungs were dissected out of the thoracic cavity, it was kind of cool to realize that when you look inside the chest, you can see the thoracic spine. But overtop the thoracic spine was a thin membrane of tissue. Part of that is the parietal pleura, part of it is the thoracolumbar fascia. Well, that is the paraspinal soft tissue stripe when we look at a radiograph. Normally that paraspinal stripe should be very close to the vertebral bodies of discs. It is almost like celery skin that is very, very thin. We can see that radiographically quite often.

Video Presentation Placement: 11:41
Less than 2 millimeters is kind of our threshold thickness. Well, not surprisingly, if somebody fractures vertebrae there’s going to be soft tissue swelling in that area. One of the things that we assess is we look at that paraspinal stripe. In this case, we can see where the paraspinal stripe is displaced. Now we get rid of the ink. An important thing is the only place that we can see the paraspinal stripe is T12 and above, and only on an AP thoracic spine. Because that is where we have the patient do a full inhale to get the lungs as long as possible if the diaphragm’s down.

On the lumbar spine, when you have exhaled to get the diaphragms up, it tends to obscure that thoracolumbar junction. So, we are really going to only see this T12 above because you have to have the interface between the lungs and the vertebrae, and generally, only on an AP thoracic. But in this case, I can see that distention of the paraspinal stripe. So that is the swelling that confirms absolutely, I am looking at an acute compression fracture.

What if I do not see those things? Because here is the problem, because there is always a problem. Well, the problem is, if I see a step defect, a zone of impaction, or paraspinal edema, I know it is an acute compression fracture. They are great when they are there, but sometimes, they are not there and it is still an acute fracture. That is where I have to start looking for some other secondary criteria, or I will have to start thinking about some advanced imaging. I will talk about it momentarily. If this patient comes into me and I am looking at this radiograph and I see wedge-shaped vertebrae and I am worried this is an acute compression fracture or not; I am pretty sure this person has an acute compression fracture. Because I am seeing something called abdominal ileus. Well, and what abdominal ileus is? It is a pain reaction. When somebody is in really bad pain, not surprisingly, when we look at the sympathetic versus parasympathetic tone.

When I got somebody who’s in really bad pain, their sympathetic system activates. As your sympathetic system becomes really high tone, your parasympathetic becomes low tone. What happens is peristalsis stops. Digestion is a parasympathetic reaction. Well, if my peristalsis is stopping because I am in so much pain, one of the things we see is all the methanogenic bacteria in the person’s gut have more time to work on the bolus of food and then make more gas.

If you look at this person’s lumbar spine/abdominopelvic radiograph, there is a lot of gas in there. This is somebody that if you were to tap on their abdomen, they will be hyper resonant. They sound like a kettle drum because they have so much gas in there. Is it an indirect finder? Yes, it cannot be one-to-one because it depends on a person’s pain thresholds. It also depends on the person’s diet and it depends on the person’s colonic activities. When we start seeing these things, I am pretty sure that this person has an acute compression fracture. But let us talk about your diet and some of your bowel habits too.

One of the other things to consider and this is one, we always must think about in trauma cases. We tend to focus on the broken bones, not surprising because that is what we see on an X-ray. One of the things that I really try to reinforce in how we think about these fracture cases. We were thinking about fractures. Rather than fracture, think about them as trauma, and one of the things to really focus on is if there is enough force to break a bone, there is going to be soft tissue injury in the adjacent spaces. We should always be considering the soft tissue injuries because realistically bone heals really well. Ligaments, not so much. Discs, not so much.

Always think about what are the associated soft tissue injuries that we might be dealing with in this particular patient. If I have got somebody who is got a traumatic thoracolumbar spine compression fracture, you cannot break vertebrae without injuring at least one of the adjacent discs, if not both. So, one of the other things that I look at to try to help me decide if a wedge-shaped vertebrae is a new compression fracture versus an old compression fracture, is how much degeneration is there in the adjacent intervertebral disc spaces.  In this one, of course, I can see the step defect in the zone of impaction. But there is no degeneration. Pristine-looking disc above, pristine-looking disc below. When I look at this wedge-shaped vertebrae, lots of degenerative changes above and below. If I come down to this disc, it looks pretty pristine. This is an indirect indicator. There are a lot of factors that involve polytrauma age.

If my person is 80 years old is that really going to be that terribly useful if I am dealing with a geriatric athlete? That might be a difficult thing to consider. Again, an indirect indicator might be useful. What if I am still not sure? I do not have old films for comparison. There is no step defect, zone of impaction, paraspinal edema, no real substantial degenerative change around, but it is a young individual. Have they had time? But I am still not sure. They got pinpoint tenderness, their pain scale was 8 out of 10. I am worried that this is an acute fracture but the X-rays are not helping me. It is time to think about 2 advanced imaging options. There are really three, CT, bone scan, and MRI. I will be honest with you that for compression fractures, I am not jumping on the CT for this one. Can it be useful? Yes. But there are some dependent features so, could I? Sure. What about a bone scan? A bone scan is an option. We see in this person, that there’s an L2 biconcave vertebrae.

When somebody has a fracture that is going to increase metabolic activity in that particular bone, so, it will increase the radiopharmaceutical uptake on a bone scan. We can see there is definitely increased uptake in L2. Well, here is the problem, and why a bone scan is not that much of an option for me either. Because a bone scan can be hot for up to two years after a fracture.

Because of the intense remodelling that goes on, because of the accelerated degenerative changes, bone scans will definitely be hot the date the fracture happens. But there is also that concern, this can be hot for up to two years. Bone scan, again, like CT, it is an option but it is not a favorite option. If I really am not sure and I am trying to figure out, is this a new compression fracture or is this an old compression fracture? I would much rather get an MRI.

The MRI is going to be much more definitive, plus I will be able to look for additional things, looking for disc pathology. We can see wedge-shaped vertebrae here at L3 .Let us consider that I do not see the step defect, I do not see the zone of impaction. I am not sure. Is it new or is it old? When I look at the MR I can see the bone marrow edema on the fluid-sensitive sequence, I see the decreased signal on the T1. That goes away 6 to 8 weeks, so, I know that I am dealing with an acute compression fracture. On the outside, the marrow edema might last 12 weeks. So, that is a really more useful modality. The other thing that has to be on my differential list when I find wedge-shaped vertebrae, and this is particularly important if you are going to be dealing with juvenile athletes, is the possibility of Scheuermann’s disease. Now with Scheuermann’s disease, this is osteochondrosis. We are seeing a problem with bone and cartilage and also known as juvenile kyphosis. What we are seeing here is this person essentially gets inflammation of the endplates, and that inflammation of the endplates, there are a couple of major components to this. There is a strong familial incidence of Scheuermann’s disease. But we also see this much more commonly not surprisingly in students with chronic repetitive spinal trauma. If we get children that are getting into heavy-duty powerlifting a little too young, we can see this in gymnasts’ workhorses. They have very mobile agile spines, doing lots of axial loading with floor exercises and that sort of thing. Not to mention just landing from uneven parallel bars and so forth, puts a lot of force through the lower thoracic lumbar spine.

What we will start to see is it creates an inflammation of the endplates and that inflammation of the endplates results in remodelling of the vertebrae, and what we see, the major diagnostic criteria for Scheuermann’s is a bullet point number 1: 3 or more segments with 5 degrees or greater anterior wedging. That is exactly what we are seeing here. Wedge, wedge, wedge, wedge, and there is this hyperkyphosis in this region.

Video Presentation Placement: 20:59
Not surprisingly, because of the endplate component, we will see that the person will have some Scheuermann’s node formation. They can have some endplate irregularities and because of the wedging, there is definitely going to be a hyperkyphosis.

When we see the child that has active Scheuermann’s disease, that might be different than the adult that has the residual deformity from Scheuermann’s disease because that wedging stays forever. It does tend to make the thoracic spine more rigid having experienced several patients with Scheuermann’s disease. This is one where I see that hyperkyphosis in younger individuals through the mid-30s and 40s. It is fairly rigid on palpation. I am thinking, could this be Scheuermann’s? Absolutely, but the other thing on my differential list is Ankylosing spondylitis, enteropathic arthritis, psoriatic arthritis, and reactive arthritis. So those are patients I tend to image to see, is this an inflammatory arthropathy? Is this a developmental abnormality like Scheuermann’s disease, or is this personal hyperkyphotic because they have a single-level compression fracture? Next on my differential list is the burst fracture. With a burst fracture, also flexure or axial load mechanism, same as we have seen previously, the difference being more force, and one of the concerns is when we find these fractures, these are unstable because a burst fracture by definition involves 2 or possibly 3 columns, usually, 3 to be honest with you.

What is interesting is when we look at the burst fracture in the thoracolumbar spine, it has lower incidents of neurologic injury than the cervical spine, and it is because we are getting out of that corded region if we are into the lumbar and learn to cauda equina which tends to be able to shift out of the way. Also, something I am not going to discuss because the likelihood of seeing an acute chance fracture is very low. It is another three-column unstable thoracolumbar spine fracture. But the big idea when we are looking at the thoracolumbar junction is, compression fracture is a diagnosis of exclusion. We make sure that the wedge-shaped vertebra is not a burst fracture or remote possibility of chance fracture before we say that it is a compression fracture.

What do we see? These are going to have anterior wedging, but more importantly, there is going to be middle column involvement. You can see on this MR, where this person has that posterior for tibial bowing. Looks like a compression fracture anterior wedging. Middle column involvement, middle of body height loss or posterior convexity, and then quite often these will involve all three columns, so we are also going to see a vertical fracture on the posterior elements.

One of the things that vertical fracture on the posterior elements can do is spread the pedicles apart. So, we will see an increase in the interpediculate space. Now, chance fractures again. Chance fractures are really rare and not going to address those. They have a horizontal splitting. As we take a moment and look at our two-view thoracolumbar spine radiographs here. When I deal with spinal imaging, I always start on the laterals. The laterals are kind of our high-yield area when we are looking for spinal injuries. As I start running through there, I can see, there is definitely anterior wedging. The person’s actually taken a fragment off, the rest of the body looks okay, posterior body height, still nice and tall. Now, there is a little spondylolisthesis here but it is trauma. Sondylolisthesis can happen with that. But the posterior body is nice and tall; posterior body still concave.

Here on the lateral right now, I am thinking this is a compression fracture in L2. But when I look at this over on the AP view, one of those, I do not pull out rulers very often, I do not do a lot of drawing on my X-rays. But I eyeball the space between the pedicles. As we go down the spine, the space between the pedicles is supposed to get gradually bigger each step. Problem is, when I look at this person from T12 to L1, they got a little wider. L1 to L2 got a lot wider and then L2 to L3, all of a sudden became narrow. That is a problem.

Well, that means that L2 got too wide too fast and that is the spreading of the interpedicular distance that indicates a vertical fracture through the posterior elements. Even though this looks like a compression fracture on the lateral, it is actually a burst fracture. These are unstable spinal fractures, so this is a backboard and transport case. When we look at these burst fractures, the thing that we are most concerned about, when we look at these burst fractures, is this retropulsion of fragments. You can see where the fragments have been blown backward into the spinal canal. But again, because we are dealing in a more cauda region, rather than a corded region, things are able to move out of the way a little bit more, and another slice on the CT on this one shows the vertical fracture through the posterior elements that resulted in the spreading of the pedicles, that this pedicle can actually faintly see a fracture line extending through here. It is not really connected to the body and it is allowing for that lateral displacement of the pedicle in this case.

Not surprising when we are dealing with these burst fractures, if there was any suspicion of a burst fracture, we have it more on field in patients getting altered sensation in the lower extremities. Naturally, this is going to be a backboard in transport for imaging. What is interesting is these patients, because there is a lower incidence of neurologic compromise, there is the possibility of these being ambulatory patients. Maybe they had the athletic event over the weekend, they injure themselves but they delayed going in to see anybody. You know athletes, they can put off a little bit of pain. So, they put off the pain until eventually come in, I will go see the doc on Monday. We might take the imaging, find the injury, and then we’ll have to transport the patient from there.

Other things that can happen in the thoracolumbar junction Schmorl’s nodes. Incredibly common. Now, what we see with the Schmorl’s nodes, is an intra-vertebral disc herniation where the nuclear material breaks through the endplate and herniates into the vertebral body and we will see it contour change the vertebral body. Most Schmorl’s nodes happen during the pubescent growth spurt, you get somebody who is growing really fast or some naturally weak areas at the endplate and allows that to occur in generally, the person never knows it happens. They have no pain. They have no problems. We take X-rays; we see Schmorl’s nodes. It is possible to have the Acute Traumatic Schmorl’s Nodes. This is a very small subset of Schmorl’s nodes.

Unfortunately, I cannot get this X-ray and tell you if these are new or old. Where old imaging might be useful, is you can always compare with previous imaging. Or focal pinpoint tenderness, that spine is really lights-up, the person has an axial load trauma. Could this be an Acute Schmorl’s nodes? I will get an MRI. The MRI will show me bone marrow edema and that will help me figure out that it is a new injury. But again, these are very uncommon and they’re unlikely to change how management is done aside from some rest; I do not know that I’d necessarily go to that degree.

Some of the things that we also have to consider on our differential list when we are dealing with thoracolumbar trauma. If you remember the burst fracture case that we just looked at a minute ago, there was a small triangular fracture fragment that got knocked off the corner of the vertebrae. Well, one of our differentials on some of these cases is something like a limbus bone. These most commonly happened in the thoracolumbar spine. Well, how am I supposed to tell if that is acute fracture or if it is a limbus bone? Well, in my classes here at the College, I teach a mantra of always ask yourself this question, repeat this, repeat it, repeat it, repeat it. Does it have smooth, well-rounded corticated margins? If something has smooth, well-rounded corticated margins, it is been there for a long time. It is not an acute fracture. When I look at this triangular fragment here, it has smooth, well-rounded corticated margins and it is fitting like a puzzle piece. That is a limbus bone.

Video Presentation Placement: 29:31
Limbus bones do come in a couple of different flavors. There is the anterior limbus bone and the lateral limbus bone on the posterior. The anterior, most commonly asymptomatic. Laterals the only place I have ever seen those reliably is on a CT, they’re not common. The one that we worry about is the posterior limbus bone. These can occur traumatically, it is possible to shave off a corner of a vertebral body. When we look at the posterior limbus bone, this is a middle column fracture. This is one of the few exceptions to our three-column theory of Dennis, and what we are seeing is where the person fractures off the posterior body corner. As we deal with these, one of the concerns and we are dealing with the posterior limbus bone is, it doesn’t look like much of a fragment. You can see where this one was from the corner and then displace backwards. This will create some degree of spinal stenosis because of that displacement going backward, it does go into the spinal canal. I will evaluate that patient for stenotic symptomatology and treat them accordingly.

What else can we break in the thoracolumbar spine? The fantastic fracture that occurs with flank trauma, not really fantastic but something occurs very frequently with flank trauma is the transverse process fracture. When we start thinking about thoracolumbar spine transverse process fracture, I want you to reach back, reach behind you, palpate your transverse processes for me. Transverse process, it is a little piece of bone, It is really super thin. What is interesting is, if you have any access to dried specimens, when you look at most dried vertebral specimens, you will notice that a lot of them do not even have transverse processes because they tend to break off really easily when we look at those dry specimens. I think, well it must not be that hard of a thing to fracture. Well, except there is a lot of giving them as living bone and how many of you were actually successful in palpating your TPs? I remember, they told us to help palpate mammillary processes in chiropractic school. So why cannot I palpate my TPs? Because they are covered by 4 to 6 inches of paraspinal muscles. We have 4 to 6 centimeters of paraspinal muscle and soft tissue on top of these. It takes a lot of force to fracture a thoracolumbar TP. So flank trauma is the biggie.

Some of those good mechanisms, how to get flanked trauma like this, the Peloton. If you get a bike that goes down in the Peloton and a whole bunch of bikes starts going over on top of each other. You are going to get people that are the bikes are flipping, they’re landing on their back, that is a flank trauma. One of my favourite sports, this is one that it was a sport that I never really knew about when I was in high school but then my son started to play it Lacrosse.

Lacrosse is a fantastic event when we start talking about flank trauma. Because let us take a bunch of testosterone laid in young men and give them metal poles and tell them to beat on each other with them. Not surprisingly, there is a lot of flank trauma that happens in Lacrosse. So, when we start dealing with this: somebody has flank trauma, something hits the flank region. We can also see this in other things. These can be injuries and hyperflexion, hyperlateral flexion.

We can see them with an event impaction component with extension injury. There are all kinds of mechanisms and flank trauma is the biggie. Let us take some pictures. Obviously, there is a fractured transverse process, fractured TP. One of the other things that should make us worried about this is asking them the right questions. Somebody’s got flank trauma after an event, after an accident. Any problems urinating, are you noticing any discoloration in your urine?

My middle son, Cody, is what I like to pick on a little bit here for sports injuries. Well, Cody played Lacrosse and he was a good player. Not quite as good as he thought he was, but he is a good player. One game, the other team is all on top of him, just wailing on him with a stick. He was complaining a lot about the pain after the game. I was not surprised, and about two hours after the game, there is a blood-curdling scream out of the bathroom and my wife and I run in to see what is going on.

Well, if you look in the toilet, it looked like cherry soda, cherry Kool-Aid, cherry juice, because he was having gross hematuria. They had bruised the dickens out of his kidney. His kidney was really bruised and because of that, he had hematuria. So naturally, we took them off and got Abdo CT, no TP fractures in his case. But what it does illustrate is anything that has the possibility of fracture and transverse process, also has the possibility of damaging the kidney or the ureter, so watch for hematuria. But what is really interesting is when a kidney gets injured, one of the things that can physiologically happen is the ureter clamps down below it, and the person might not actually get gross hematuria.

If I find TP fractures radiographically, I know I am getting an Abdo CT. If I have got a patient with hematuria, I know I am getting an Abdo CT, because they need to evaluate what’s going on in this case. One thing to realize some of these fractures are also small and subtle. So, we can see here that there is a TP fracture of this one It is subacute, there’s some callous around it. The X-ray was completely normal on this case. I never saw the fractures. But one of the things that this does highlight is when and unfortunately, we are looking at a bone window here, not a soft tissue window. Here is psoas, this is the kidney up here, and if there is enough force to go through that thick paraspinal musculature to fracture the TP, that force is probably going to be enough to go forward and hit the kidney. We always worry about renal and ureteral injury when we are looking at TP fracture in the TL junction. Automatically goes to an Abdo CT.

This would not be a complete topic in talking about lumbar spine injuries without also addressing the idea of the spondylolisthesis. As we look at spondylolisthesis, we are seeing those vertebral slippages, remembering there are five major types for spondylolisthesis: Dysplastic, Isthmic, Degenerative, Traumatic, and Pathologic.

I am going to talk about isthmic. Traumatic kind of makes sense. We have already talked about things like unilateral and bilateral dislocations. When I talk about isthmic that is what I am going to focus on here for our next little bit the isthmic spondylolisthesis. This is a problem of the pars interarticularis, which literally translates the part between the facets.

When we look at the pars interarticularis, it is an inherently weak area in the spine. In the thoracolumbar spine between the facets, the bone tends to be fairly thin and what’s really interesting is, there’s actually a large, genetic component to how thick a pars is. We see some populations have a much higher incidence of fractures of their pars than other populations. Not surprisingly, this generally most commonly involves L5, but It is possible to see pars defects at any level in the lumbar spine, and when we start looking at these, what happens to the pars? There are actually three different possibilities of things that happen to the pars.

The first possibility is that there is a fatigue fracture that heals non-union and allows for the slippage to occur. There is an elongated pars and then there is an acute traumatic pars fracture which does not happen that often. These are very common as chiropractors. We all see these pars defects style spondylolisthesis. All the time and practice incredibly common kind of thing. Now what is interesting is it used to be thought that this was a congenital anomaly, you are born with a defective pars. They have never seen this in newborn infants. But the current thought on this one is the type of a fatigue fracture. I will talk about that momentarily. One of the terminology things and this is probably as much of a pet peeve of mine, as anything else, is the number of people who call these pars fractures. The etiology, how does this happen? It happens because of a pars fatigue fracture. But that pars fatigue fracture, typically happens in people between 10 and 15 years of age, and then it heals non-union, and then it is two separate distinct pieces of bone.

The term fracture implies acuity. I prefer to not use the term pars fracture unless I am dealing with an adolescent with an active fatigue fracture. When we are dealing with a 35, 45, 55-year-old individual who’s got a spondylolisthesis, it is better to use the term pars defect rather than pars fracture. When we look at how often this happens, it happens fairly frequently in an athletic population, somewhat sport dependent. I will talk about the different athletic activities here in a little bit. Generally, in the general non-high-grade athlete population, two and a half to 5% of the population has an ethnic spondylolisthesis. When we start looking at athletes, we can see up to a 17% frequency.

For the two to 5% of the general population, a lot of its related to genetic predisposition in the thickness of the pars and how much it can bear load, and when we look at athletes. It is because of higher grade athletes repetitively stress that area. What occurs, how does this happen? What we are looking at is what I like to refer to as a series of unfortunate events. What we are seeing is where we have got an adolescent patient, and again, 10 to 15 is our first standard deviation for where this occurs.

This adolescent patient is doing some type of activity with hyperextension. They are repetitively hyperextending the lumbar spine; and with that repetitive hyperextension, they eventually fatigue fracture the pars interarticularis. Fatigue fracture, stress fracture, interchangeable terms here. They stress fracture that pars interarticularis and then they keep doing their event, and as they keep doing their event while they are not giving that a chance to heal so that fatigue fracture becomes a complete fracture. Then it heals up as two separate bones, and that is what allows the vertebral body to start to slip.

What kind of sports are involving this hyperextension activity? One of the phrases that I like to use for this one is, these are people who participate in “ta-da sports”. Where at some point in time during their thing, they go “ta-da!” and they are hyperextending as a part of the event. Gymnastic floor exercises, gymnastic landing exercises, almost everything involves hyperextension.  When we look at high divers, the best way to get smooth laminar flow into the water with a minimal splash hyperextension of the low back, so you have got that lordosis.

Video Presentation Placements: 41:15
One of the things that is kind of interesting is when I talk about cheerleading as being a major athletic event that has a lot of injuries here in the US. Cheerleading is actually the number one, high school sport and college with significant injuries. Because we are taking people and throwing them high in the air and hoping somebody else can catch them and a lot of repetitive activities.

The whole idea though, is something in this act and this is not an exhaustive list, there are a lot of different sports that involve that lumbar hyperextension. But that repetitive hyperextension, they keep going back, they keep going back, they get that fatigue fracture. Because they are high-grade athletes, they ignore the pain and work through it. That is what allows this thing to heal up, non-union, so what am I supposed to do? I have got this adolescent athlete and they have got back pain and it is focal. When I am palpating and I am going down the articular pillars, I get down over L5 most commonly and they just light up. We need some imaging. We are going to start with an x-ray, but one of the things that you have to remember is stress fractures are hard to see on an x-ray, and there is also a long radiographic latent period, it can take up to three weeks before anything even shows up on the X-ray. There is a long latent period and difficulty in evaluating.

If I have got an athlete who is doing an extension event and they got back pain, I will take the x-rays but I know I am probably going to end up in an advanced imaging tool, and the thing that we really want is we really want MRI. MRI is the preference these days. For a long time, we talked about doing spect, which is a kind of a CT bone scan combination. It is good, spect is okay, but it is a high radiation dose to an adolescent patient so we would much rather get the MR. MR will give us all the same information and a lot more besides, so I would rather get an MRI.

What about things like obliques? I will be honest with you, I am not a huge fan of obliques. Never like them that much. Can they be useful?  But do I like them that much? No, not really. But would oblique show me? Well, if I am really lucky, I might be able to see the pars defect, and of course, that is where we talk about the Scottie dog. It is the collar of the Scottie dog is the area of the pars interarticularis. Normal one is outlined, pathologic one below.

Realize L5 is not always easy to see on the obliques. I will be honest with you. Do I even need the obliques? We will look at the minimal series. If I look into this patient, do I need obliques to figure out that my person has pars defect? No, it is right there. Drive a truck through that thing. What are obliques going to tell me? There is pars defect, clear the minimal series first. I do not do obliques unless I have to.

Is this actually a pars defect or is this an elongation? We are looking more at the type 2B? I am not sure. Could I do obliques? Sure. Do I want to do obliques? Not really. I mean I know there is a spondylolisthesis. I can see that there is a step defect in the spinous processes and in this patient that was actually what prompted the radiographs. This patient is a rock climber, was a cheerleader, was a high diver in high school. Lots of things with chronic recurrent, low back pain. She had like six percent body fat. When you palpate her spine you can actually really palpate her sinuses. She had a big step defect so it prompted taking some radiographs. She’s definitely got a spondylolisthesis there, but I am not sure, is this a 2A, or is this a 2B? So, what I would much rather get rather than a set of obliques is, I would much rather get a Ferguson’s.

Ferguson view, is so much more worthwhile when it comes time to evaluate the pars at L5, and I can see that there is a pars defect there, and there’s a curvilinear pars defect there. In this case where I was questioning, is it a 2A or 2B? The Ferguson view is definitely worthwhile; much better than the obliques. Could I do oblique stir different patients? No reason to do the obliques when I did the Ferguson’s of that one. Realize that L5 part particularly on somebody’s hyper lordotic can be difficult to see. One of my big recommendations from a technique standpoint, if you are doing your own radiographs in these patients, make sure that you do your oblique lumbars P to A instead of A to P. That way you are taking account in the divergence of the ray and help you with lordosis.

What if I am dealing with that adolescent patient? They’ve got focal tenderness, the x-rays were negative, but I am really worried that there’s an active stress fracture going on. Get the MRI and one of my requirements for spinal MR, when I talked to the imaging centers that I utilize for doing spinal MR, I won’t utilize an MR Center, unless when they’re doing my spines. We know that there’s the T1s and the T2’s. One of my requirements is and this is a standard protocol for most places: they have to do a sagittal stir or a sagittal fat sat. I want one of those really fluid sensitive sequences in the sagittal plane.

Because it is what really shows up a lot of pathology with edema, and in this particular case, different patient. In this patient at L4, we are looking at a stir and there is very high signal intensity in that area of the pars and the pedicle and coming down into the inferior facet. This is somebody that has an active fatigue fracture. Their radiographically normal, but there’s bone marrow edema. This is an active fatigue fracture. This is a patient that if I can get this person off activity, get them into a Boston Brace, take out that lordosis so that they’re in an anti lordotic position, give it six to eight weeks to heal. It is probably going to heal so that they won’t have those issues of developing a spondylolisthesis. Because one of my concerns is, you know, is this thing going to progress? Is this thing going to be unstable? Luckily not many spondylosis progress, but the greatest probability progression is within two years of the fracture.  I want to make sure that I am getting this person as young as early on in as possible. Try to keep them from actually even developing the spondylolisthesis.

In the patient that I showed you previously that has a rock-climbing gymnast high diving history. She’s an adult patient. She’s in her mid-20s. One of my concerns on a patient like that is for instability particularly because she has chronic recurrent back pain. Again, instabilities not terribly common when we deal with spondylosis because a lot of times that even though it heals non-union, there’s fibrous connective tissue in the area.  But things that make me concerned for whether or not this might be an unstable spondylolisthesis. If I notice a trapezoidal shape to the L5 vertebral body, where if I look at the anterior body height and I compared it to the posterior, posterior’s, a lot shorter. That makes me a little concerned for whether or not my patient has potential instability.

We can also see this patient has a trapezoidal shape to L5. So anterior, body height, posterior body height, also have a lot of rounding of the lower segment, and one of the things being that, if this vertebrae keeps slipping back and forth, it might be eroding to some degree that lower segment. I am concerned about this person being unstable. I will think about doing flexion-extension radiographs, realizing that it has, this segment is unstable, that celebrates degeneration.

We start to see osteophyte formation and that osteophyte formation creates something called sacral buttressing, and it is where the osteophyte is growing underneath that segment as an attempt to stabilize. The big thing to think about when I am dealing with the spondylolisthesis case, is it stable or is it unstable? We’ll worry about getting flexion-extension radiographs in a point in time.

If you get that patient who keeps doing their repetitive hyperextension event over and over and over, ignoring the pain and pushing through, they are going to get a type 2A where the fatigue fracture becomes complete. The complete fracture heals, non-union, it allows vertebral slippage. What if you get the athlete, who is a little bit more cognizant of using pain as a guide and they do a hyperextension event and then eventually develop pain and then they lay off for about a week or two? But then they go back to their event and then it starts there and then they take a week or two off and they do this repetitive cycle of injure and partially heal and injure and partially heal.

One of the things that that can do is that can create a Wolff’s law, elongation of the pars interarticularis, and allow that vertebrae to slide forward. But the pars are still intact, so on an MRI would show up as a demodus on x-ray, we might not that we would not see anything except some progressive elongation.

That is one of the other causes and then the acute fracture. The pars does not like to have the acute fracture. This does not happen so much, but it takes some kind of massive, hyperextension force. This is where I will pick on American football as opposed to International Football. When we look at American football, if you get somebody who throws a shoulder pad into a low back, that can create a lot of hyperextension injury. A 250-pound linebacker against your lumbar spine, probably not a great choice. But any kind of acute hyperextension, acute onset of pain. The concern here, is this actually an acute pars fracture? Problem is an acute pars fracture, it is hard to see those smooth or undecorticated margins, so going to an MRI or CT is really going to be a good option for that.

What is also interesting is It is possible to get a fatigue fracture on just one side instead of having the spondylol and the other term for that is spondylolysis. Instead of getting it on both sides and allowing the vertebra slip, you can also see it on one side. The vision I put in my head is somebody who’s doing an asymmetric extension exercise. Things like high jumpers, pole vaulters are the kind of pictures that come to my mind for these. That is where they are going to one side for their event. They always go to the same side, not surprisingly. They fatigue fracture that side and it heals up non-union. But the other side still intact. Typically, with a unilateral pars defect, they do not get vertebral slippage. But what we might see when we look at this patient is, we might see a unilateral sclerotic area of the pars and facets.

Video Presentation placement: 52:16
Ferguson’s view would be my preference on this one. On this particular case, I happen to have a set of obliques, I can see there is a pars defect on this side. There is no pars defect on this side, but it is extra sclerotic. Now, this is where we also have to think differentially. If this is our adolescent athlete, we have got somebody who is 15, 16 years old and they are complaining about an insidious onset of back pain. One of the other things that is on my differential, when I look at this really densely, sclerotic pedicle pars area is we have to think about one tumor, in particular, osteoid osteoma. We can also throw osteoid blastoma on our list. If I have got that adolescent patient, who is got this insidious onset, back pain, regardless of sporting event, and then I take an x-ray and I see that there is this one sclerotic pedicle/pars. I know that I am going to an advanced imaging tool. I will be going to either a CT or an MRI. I will be honest with you. This is where I would have a preference for a CT to give me better bony resolution of that area, to see if there is osteoid osteomyelitis or an osteoid blastoma tumor mass to make sure that this is actually a unilateral spondylolysis.

We continue on down, we are now going to get out of the lumbar spine and drop down into the sacrum. As we start looking at sacrococcygeal injuries, a couple of big categories of things. The acute traumatic fractures, vertical sacral fractures, horizontal sacral fractures, sacrococcygeal fractures, sacral stress fractures, very common in athletic populations, also very common in geriatric populations. When we start looking at these sacral fractures, we will go to the traumatic ones and we will talk about the stress fracture. How do you fracture a sacrum? Land on it. We can see a couple of different possibilities: either falling from a height or landing on one foot, landing on one ischial tuberosity puts a vertical shearing through the sacrum. You can see falling directly onto the buttocks and you land on the point of the sacrum/coccyx, and that can create a fracture.

When we start dealing with stability, stress fractures are generally stable. Vertical fractures, potentially unstable horizontal fractures are stable. The stress fracture, we really do break stress fractures into two categories, there is fatigue fracture and insufficiency fracture. A fatigue type stress fracture is healthy bone, abnormal, repetitive stress, the bone fails. Great one for this marathon, any kind of heavy-duty, long-distance running is where we talk about stress/fatigue.

Insufficiency fractures are abnormal bone and normal stress, and as we tend to talk about our geriatric athletes, who have diminished bone density due to menopause or age-related testosterone drop off.  When we are looking at these, and this particular individual had always been a runner and they’ve done some long-distance running most of their life, they jog for fun, decided to do a marathon. Had never done marathon distancing before, and kind of got the bug at the last minute for an open marathon. Really ramped up activity in way too short of a period of time, started to develop sacroiliac pain.

Not surprisingly, because Murphy’s Law being what it was. This is the spouse of a chiropractor and the pain started getting worse and it was SI. Talking to her spouse getting the SI joint adjusted. It is getting, you know how it works, whenever you adjust your spouse and all it seems to get worse. Maybe It is just my spouse. Maybe I am not that good of a chiropractor. This is not like my wife by the way.  The pain is getting worse, so they decided, let us get some x-rays. They take some x-rays, they send the x-rays into meter reading. Everything looks normal. I know the history on this particular case. I know that this person has been ramping up activity, getting ready for an event. There is always a good possibility that you are dealing with stress fracture. We should really get an MRI to see what is going on.

What is interesting? Being this particular patient also worked at an Imaging Center and the MR was backed up. They talked to the radiologist  there and they decided to get a CT instead. On the CT, we can actually see right here in the sacral ala. There is a nice area of sclerosis in the sacral ala, problem is, this is a mid 40s, female with a family history of breast cancer and we are seeing a plastic thing, so that became a concern.  So then got the MRI instead and what we are seeing here. There is edema surrounding that area and this is a classic stress fracture in heavy-duty runners. It is a vertical sacral ala stress fracture because the repetitive heel strike puts a lot of vertical force from the sacrum. This is one of the things that has to be on your differential list for long-distance runners that have SI joint style pain.  In this particular individual, we can see that there is a severe degree of osteoporosis, and with that osteoporosis, we are seeing a kink in the cortex up here at S and the junction between S1 and S2. The concern in this particular casem this was the onset after a kind of a hardcore weekend of gardening, which can be its own sport. So, a hardcore weekend of gardening, this person started getting a lot of SI joint pain. Do not like the shape of the sacrum and when we look at the MRI, we can actually see that there is bone marrow edema in the sacrum where this person has an insufficiency fracture.

It is also something that can happen quite frequently in our geriatric patients. They will actually get a combination of bilateral, vertical, sacral insufficiency fractures and a horizontal fracture, and it creates that H-shaped pattern on bone scan. This is called the Honda sign because it’ll show up taking an egg shape pattern.

The horizontal, sacral fracture again, what do you do? Give you a fall. Maybe you are not even an athlete. Maybe you are just walking between athletic venues for winter sports and there’s an icy sidewalk on your feet, go up and you land on your tush. Well, one of the things that we can see in these patients is a fracture of the distal sacrum or coccyx, and these are horizontal fractures, they are usually below the level of the SI joints. Not a whole lot to do for these. It is the management of most of these horizontal sacral fractures is to sit on a hemorrhoid pillow and try to take some pressure off the sacral apex. The big thing we are looking for here is on the lateral view, look for the offset in the anterior cortex.

Realize sometimes, this is a difficult area to evaluate. So also make sure you look at the space between the sacrum and the rectum, and the rectum should be pretty close to the sacrum. If this fractures though, it will create hematoma and can displace the sacrum or the pre-sacral space forward.

Video Presentation Placement: 59:25
The vertical sacral fracture, usually a higher velocity force landing on either a buttock or landing on your feet, asymmetrically. One of the things that we always want to look very carefully at is. look at those anterior, sacral foramina and as we look at the anterior sacral foramina, here, you will see that there’s a jog it will offset. That is a vertical sacral fracture, and the concern is that can be an unstable pelvic fracture or it can progress to an unstable pelvic fracture. This is one where the person is going to most likely be managed pretty intensively. What is interesting is the coccyx itself does not fracture that often. Well the coccyx cannot fracture. Of course it can, It is a bone, but it tends to move out of the way a little bit and we see more. Sacral coccygeal joint injuries or horizontal, sacral fractures rather than a true coccygeal fracture. I realized this is super blurry and pixelated but there is a little offset in the coccygeal cortex. Person’s going to be sitting on a hemorrhoid pillow.

Realize that some of these sacral fractures, coccygeal injuries. They can hurt for substantial time afterwards, and as an added side on this one, there are stress coccyx views to do. If you got somebody who’s got coccydynia, having fallen down and they have got persistent pain for time afterwards, it is absolutely possible to de-stress radiographs. One is done standing, the others are done sitting, leaning back so you are right on the apex of the coccyx and you are looking to see how much angular motion occurs. It is not that frequent but if you Google it or do a pub med search. You’ll find several articles about coccydynia and hypermobility.

We are going to end off this lecture talking about thoracic cage injuries which we break down into rib fractures versus sternal fractures kind of our big things. A thing to realize about rib fractures, they are incredibly common and also one of the most common radiographically occult fractures in the human body. These can be very difficult to see and one of probably the single, most important thing when we started talking about it.

I have got a patient who has got thoracic cage trauma and they got pinpoint tenderness. Do not rely on a chest x-ray. This is unfortunately what we see a lot of times in an emergency department is to do a chest x-ray, read it, clear and send the patient on their way because there’s nothing that is going to kill the patient.

This is where, if you are really worried about rib pain, make sure you get dedicated rib radiographs. It is not a thoracic spine with an open collimator. It is a dedicated rib study, you are doing a hemithorax. Depending on where you are looking, inspiration, expiration. You are also going to look at your frontals and obliques. Make sure that you are getting dedicated rib studies in patients with rib pain because these are incredibly difficult to see.

One of the most common radiographically occult fractures, and what we do when we are starting to look a rip for ribs., Upper ribs do not fracture that often we can see it in some heavy-duty events. Some of the throwing events, golfing if you’ve ever golfed as badly as I do. Because really, I do not golf, I excavate, I did a lot of holes, you can get a lot of upper rib pain, a lot of sternoclavicular pain. Here we can see that there is some obvious offset in the cortex on the cervical spine radiograph. Again, do dedicated ribs.

The big thing is we are looking at ribs. There are frontals and obliques. Obliques usually show you the entire length of the rib and the important thing is to trace the superior cortex. You trace that Superior cortex by looking for any kind of cortical offset as an indicator of fracture. You do not want to trace the inferior cortex. Because the problem there is, you got the area of the rib flange, really thin bone, and it can be difficult to see. We can see that offset in the cortex here. There is a rib fracture. In this case, there is also a rib fracture there. We are not seeing a quarter gloss set, but notice the change in orientation of the rib. There’s an impaction-style fracture there as well.

We want to look at those really carefully but you also want to look at the soft tissues, and one of the soft tissue findings that can indicate the presence of a rib pathology is something called the extrapleural sign. What I am seeing here is, that I am looking at this half of the thorax. Notice the soft tissue that’s indenting inward. That is called the extrapleural sign. It is soft tissue outside the pleura pushing the pleura in. One of the terms of this is also colloquially called the cat under the rug appearance. Because if you stick a cat under a rug, it has that same kind of humped-up, heaped-up appearance there. I’d be looking really carefully in that area.

Do not forget if you do have your own radiographic equipment, spot views. The number of times that I have had a patient that had rib pain. focal pinpoint rib tenderness and I did this rib series and it was negative. I would then do a follow-up where I would take paper clips, and I tape them above and below the area of maximal tenderness and I would do spot views. That way the paperclip tells me exactly where to look, It is a fantastic way to put markers on the patient to say, hey, pay attention. This is the area of maximum tenderness.

What about sternal fractures? Sternal fractures do not happen too often. If they do It is usually a direct trauma, driving sports, kind of big for this one. If you are thrown against the seat belt, if you are thrown against the steering wheel, but anything where there is blunt force, trauma to the sternum, and typically, this is going to be a transverse fracture. This is very analogous to a sacral fracture. When we look at that lateral view of the sternum, you can see the cortical offset.

The big thing is if there is sternal pain, dedicated sternal radiographs. Do not rely on a T-spine with an open collimator. You actually have to do a right anterior oblique and lateral to see the sternum most effectively. It is possible to damage the manubiosternal joint, the xiphisternal joint. The big thing is breaking the gladius there in the middle.

Not surprisingly, because this thing moves a lot moves 12 to 20 times a minute. Every time the person breathes, there is a decent frequency of non-union healing for the sternal fractures. An important thing on sternal fractures is to make sure you pay attention to the t-spine very carefully because a sternal fracture can actually increase flexion-extension forces on the thoracic spine, and increase the potential for compression fracture. Pay more attention to the sternum because there’s a lot of periosteum involved and It is very painful fracture.

A thing we are worried about any time we deal with patients, who have thoracic cage trauma is what might happen to the organs inside that thoracic cage, and that is what It is there for us to protect them. One of the possibilities, this person’s got a bruised lung. There is a traumatically fractured rib. There is some bruising to the lung underneath that area. Other more significant injuries, of course, require higher velocity diaphragmatic injuries, things like that.

One of the concerns is always, did this person, did they damage the lung when they damage the ribs? We will look for a pneumothorax and that’s when I am dealing with rib series. It is not uncommon to have a chest and a rib series done to look at the soft tissue component with the chest x-ray, and then look at the bony component with the rib x-ray. One of those concerns is pneumothorax. If I have got somebody who, I do not hear breath sounds as well. Maybe they have got hyper resonance on percussion. So let us definitely look at the chest x-ray and with a concern for pneumo, they have got shortness of breath. Make sure we do inspiration expiration x-rays because pneumothoraxes show up better on expiration views.

Patients with rib trauma, we can also see this in patients with underlying conditions like Marfans and Ehlers-Danlos. Barotrauma is a big one for this one, you get pressure changes in the lung. You can damage some of those more superficial blebs or bullae.

It is not as easy to see on this particular one. I am going to give you a clip, the same view, and then a close-up. The big thing we look for is to indicate the presence of a pneumothorax is to notice that the lung vessel markings go all the way out to within one centimeter of the lung periphery, on this side. But on this side, those vessels are stopping dead. Right there. When we look at the close-up, that’s the visceral pleural line. We can actually see the visceral pleura where there’s air trapped between the parietal pleura lining the chest cavity and the visceral pleura lining the lung. General rule and we start looking at these. The question is, does this person need a chest tube? It depends on the size of the pneumothorax.

That takes care of us for the spinal trauma lecture. So next up, we are going to continue on with the extremities. Thank you much.

[END]

Section 06_ICSC03 – Shoulder Upper Extremity
English Direct Download PDF – 06_ICSC03-Section6-ShoulderUpperExtremity.txt

Instructor Dr Chad Warshel
Video Lesson: 01:08:47

Welcome back to our next instalment now we are going to be getting into Upper Extremity Trauma, starting with the shoulder girdle and working our way down.

As we are looking at different shoulder injuries, of course, one of the things before we even get into looking at shoulders, just doing an anatomy overview, this is very important when we start dealing with the shoulder in particular, and we will also see some of the other joints in the lower extremity actually plays a valuable role when we are dealing with a lot of the osseous injuries. But realizing that a lot of the injuries that we see in the lower extremity are well upper extremity, they tend to be soft tissue injuries. It is where we know that we are going to wind up in a lot of these cases having to get advanced imaging tools to help us decide what is the diagnosis and how is this going to affect the prognosis.

One of our other options is we can also start looking at the musculoskeletal ultrasound. With MSK ultrasound, it is an excellent modality for looking at the shoulder structures, realizing again, very operator-dependent, and something that takes a lot of time to learn how to do effectively. I am not going to be getting into the ultrasound side of things, but realize if you do have an imaging centre in your area that utilizes musculoskeletal ultrasound, it is a fantastic modality, as long as you have good operators and good readers. What I would like to start off with is a live DICOM demonstration, looking at an MRI of the shoulder.

I am going to be running it through a shoulder arthrogram. Because this particular study, it is a very high-quality study and shows us a lot of the different structures we need to see. Realize when it comes to imaging the shoulder, most of the time, we are just going to order a standard shoulder MRI, we generally do not need contrast, unless we are looking for tumours or infections. The big question is do we do an arthrogram, where they inject the contrast material into the joint capsule? The answer for that one is if I am looking for labarum pathology, or if I am looking at osteochondral defects, those are the big times that we would be starting to look at putting the arthrogram into the shoulder. What it does highlights the cartilaginous structures more effectively, it also lets us look to see if there any tears in the labarum is their extravasation of material, and so forth. Because we are looking at an arthrogram here, some of the pulse sequences are a little different than we would see on a standard shoulder. Not surprisingly, on a standard shoulder MR, we are going to be looking at T1s and T2s, some cases, proton densities, and then we will be looking at different planes.

One of the things to realize when we start looking at the different planes in the shoulder, the axial plane is the conventional axial plane, there is nothing different or unusual about the axial plane imaging, what is a little bit different, pulling a two-up window and we will use the axial to demonstrate orientation. When we look at the coronal the coronal’s are actually done in an oblique plane. Because we want to make sure that we are in the plane of the scapula. That way we can really effectively evaluate any of the musculoskeletal structures in that region. The same thing for the sagittal oblique, when we look at the sagittal, it is not going to be a pure sagittal. It is going to be about 30 degrees off the sagittal plane because of that way we are getting a tangential slice through the areas of question.

Now Just to do some anatomy review so that we also understand what is the best pulse sequence to see different kinds of structures. The axial, when we start off in the axial coming, it is starting at the top and working our way down. The axial lets us see, we can see acromion and the clavicle AC joint very nicely. It lets us get a good evaluation of infraspinatus and teres minor on the backside through here. It also lets us get an excellent visualization of the subscapularis tendon. We can see the anterior and posterior portions of the glenoid labarum. We want to make sure that we do not confuse the anterior labarum with the middle glenohumeral ligament. This little lighter area through here is very frequently misdiagnosed as a labral tear, but it is just a gap between a ligament and the labarum. We are seeing of course the hyaline cartilage of the humerus and the glenoid. This is an arthrogram, so there is a contrast to standing the joint capsule here.

We can also see the bicipital groove with the long head biceps tendon, and this allows us to evaluate is there Bicipital tendon subluxation or dislocation. Then we continue on them as we will see the various muscles compared to comprising the shoulder region, we will sometimes see a little bit of lung. An important thing to do is when you are evaluating these always make sure you do look for lung pathology. It is a big deal on shoulder x-rays to keep in mind that a lot of things in the chest will refer to the shoulder, so we want to make sure we are evaluating for those.

The coronal oblique, we always run into the first question which is, so where am I? Well, one of the easiest things to do, is when you are trying to figure out where you are, pull up a localizer. Here you see the core code that is in the front. I can always just use the localizer lines. If you are using a single window, and you are trying to figure out where you are, pan through the image until you find something that you know, whether it is from the front or back, there we go, there is the coracoid, so I know I am in the front of the shoulder. There is the coracoclavicular ligament complex. We are seeing shorthead biceps there, as we go backward, we are seeing the subscapularis tendon.

A really important ligament here that is very understated in the shoulder is the coracoacromial ligament here so that coracoacromial ligament can be created as part of the coracoacromial arch, and it can create impingement on the supraspinatus tendon, particularly if a person is developing. In these a fight on the inferior aspect of the acromion, we look at the slope of the acromion. The types of the acromion, we tend to downplay that the type one type two type three, that gets downplayed these days, the literature tends to support that not being as important as it used to be thought, the thing that is believed to be more important from a shoulder impingement syndrome standpoint, is the slope of the acromion. How angled down is it? and how much does it cover the humeral head?

Right through here, we are getting into the humeral head, and we are seeing part of the bicipital groove, and that is the long head biceps tendon, taking the turn from vertical to horizontal. The horizontal component is coming across here, and this is where it ties into the long head biceps anchor, which is associated with the superior portion of the glenoid labarum. The inferior portion of the labarum we also see through here. Now not surprisingly, of all the shoulder muscles, what is the one that is most clinically significant, Supraspinous. When we are dealing with patients with shoulder pain, well, we can see the supraspinatus very nicely in profile, so supraspinatus muscle belly, coming down into the musculotendinous junction and inserting onto the URS, and then as we turn the bend here, we can see that this is Infraspinatus. As I follow this through, here is Infraspinatus, and then there is Supraspinatus.

We can really make our distinctions between the various tendons as we look at that coronal plane, the sagittal plane, we are starting on the outside of the shoulder in the deltoid, seeing the humeral head. As we travel forward, here is the long head, biceps tendon, and you can see where it travels up. One of the big tricks on MRI is if you ever get a chance to sit down with a radiologist, as they are going through a shoulder MRI, one of the things you will notice is we tend to pan back and forth through the entire stack of images continuously. That is because what we are doing is we are following one structure. We look at one structure, we follow that all the way through, then we go to the next structure, follow that all the way through, and that way rather than trying to see what everything is, I want to evaluate every different anatomic structure on this one slice. I follow that one thing, and I can check that for pathology and then all fall, go through and do the next step.

Presentation placement: 09:03
We are coming into the humeral head now. You can see, of course, the Fasil scar where the growth plate used to be epiphysis and metathesis. Now coming through here, we saw that the long head biceps tendon took a turn, and there is the horizontal component. subscapularis, supraspinatus, infraspinatus teres minor, there is a little bone Island and this person’s humerus. As we are getting in, we are coming in towards the anchor, and now we are right at where the long head biceps tendon inserts onto the superior portion of the glenoid.

Coming back the more into scapula at this point, you can see the supraspinatus muscle belly, subscapularis, infraspinatus teres minor, coming down right through here. There is the long head of the triceps origin coming off the inferior aspect of the glenoid and this is an important thing to consider. Because it can be implicated in the end, some shoulder dislocation style injuries, and last lace on through here we can see those coracoclavicular ligaments, which we are going to talk about a little bit when we get into the ac joint injuries. It is possible to see brachial plexus to varying degrees depending on the shoulder study, you are looking at the orientation and the slice thickness, and you can see some brachial plexus.

One of the interesting things right now is that we are seeing a lot of axillary lymphadenopathies, particularly surrounding COVID injections when we are looking at vaccinations. One of the things that a radiologist should be reporting on is how many, are we seeing a lot of lymph nodes in the axilla. That is something that the clinician then has to follow up with, to see if there is a cause for the lymphadenopathy such as a recent immunization. That is our light overview of shoulder MRI, and I am going to be doing several live DICOM demonstrations through the course of the shoulder.

To start getting into some specific injuries, let us start with where does the shoulder kind of join the body? Well, the SC joint. We will start looking at the clavicle and work our way out from there. The sternoclavicular joint, it is uncommon in most sporting events to damage the sternoclavicular joint is something we do see things like motor vehicle accidents, where seat belts can damage the sternoclavicular joint. But in most sporting events it is rare and sprains strains. Sure, but true SC joint injuries are rare. The big thing we look for there is dislocation which has a tendency if it does dislocate the posterior. The problem is it is a difficult area to visualize with an x-ray, so we tend to go to CT or MRI if we need to evaluate the SC joint.

Clavicle fractures are incredibly common. Recognize what are some of the common locations to find those clavicle fractures, and then we will look into AC joint injuries. With clavicle fractures, we break clavicle fractures into three different types. The medial clavicle, the middle clavicle, and the distal or lateral portion of the clavicle. The more proximal portion, the medial part of the clavicle, is incredibly uncommon to fracture just like it is uncommon to see sternoclavicular joint injuries. This does not fracture that often gives it a very protected area, the middle third, a right where we see the S bend in the clavicle, that is a mechanically disadvantaged area. A lot of really complicated force goes through that because of the bend in the clavicle at that point. So that is where we are going to see most fractures.

The distal third of the lateral part of the clavicle, is it possible to fracture course, is it likely, NO.  What will typically happen is, instead of the distal clavicle fracturing, we will see AC joint injuries. That is one we want to be aware of, “Okay, what are some commonalities?” We know that the middle third of the clavicle is the one that is most commonly going to be fractured, and quite often, when you clinically look at the patient, you will know right away that the person has a middle clavicle fracture because there is going to be some clinical offset, you might see some swelling in the area, and that makes it interesting and evaluate.

How do you fracture the clavicle? The two big ways. If at any point in time during the upper extremity lecture, you ask yourself, “What is the mechanism of injury?” and you cannot really remember what it is, just go for the default answer, the person FOOSHED, meaning “Fall on outstretched hand”. That is our classic mechanism for a lot of the things that happened in the upper extremity, and the interesting thing was, if you think about this, in comic book terms, if you are drawing somebody who was falling on an outstretched hand, they will probably have a little bubble around them and went FOOSH, it is the sound that you kind of make when you fall.

Fall on an outstretched hand, will do a lot of things. The other big thing that could damage the clavicle and by extension, also the AC joint is a shoulder pointer. This is where when somebody is falling, and they land right on the point of the shoulder. Think about it from like a gymnastic standpoint. If you are going to do some tumbling, you tuck your shoulder so that you can tumble effectively across your shoulder. We will also see this a lot in martial arts. If you do not get the shoulder tucked in, you land right on the point of the shoulder. That puts a lot of force through that clavicle. That is what I did myself during my little stint in martial arts.

When we start looking at these clavicle fractures, here is a nice example of a proximal middle third clavicle fracture again, very, very uncommon. Here is the big one, this is the middle clavicle fracture. When we start to see that middle clavicle fracture, in this case, this was an equestrian event. We can see in this case, that one of the things that happen quite often when we are dealing with these middle clavicle fractures is the sternocleidomastoid contracts and pulls the proximal portion up, and the weight of the shoulder pulls the distal portion down. Then the pecs traps and rhomboids pull the shoulder a little bit medially. What we see is this finding here called bayonet acquisition, that is where the two parts of the bone offset and overlap, so a bayonet is a knife that you put on the end of a rifle. It is where the handle overlaps the barrel. We are seeing that bayonet acquisition in most of these cases, and that bayonet opposition comes with its own problems in that, try to get this thing to reduce. One of the big questions in orthopaedics is, do they repair clavicles like this? Or do they allow them to heal? There is a big orthopaedic debate on, should these be repaired, or should they be left to heal as is or non-union? It is kind of an interesting phenomenon.

Let us show you what will happen if these are left on their own. This is a friend of mine who is not a sports-related injury. This was a motor vehicle accident. My friend here T-boned somebody at 60 miles an hour, broke 20 ribs and the seatbelt broke his clavicle. You can see where he healed in a malunion pattern. Any person had that persistent bayonet acquisition, and this is where we can see, and this is one of the associated problems that we are concerned about in patients that have this bayonet opposition healing if you can imagine thinking about where his brachial plexus runs. Brachial plexus is running right down through here, and I am not going to draw the cords and divisions and routes and all that kind of stuff. This can impinge on the brachial plexus, and then one of the concerns would be doing this person develops post-traumatic Thoracic Outlet Syndrome?

As we get a little further out into the distal portion of the clavicle and distal clavicle fractures are uncommon. What we are going to see more is we are going to see AC joint injuries. You will see these referred to variously as AC joint separations, AC joint dislocations, there is even always this actually a diastasis rather than a dislocation. I am a big one for calling these AC joint injuries and making my life easy. So, again, FOOSH is not shoulder pointers, a major mechanism for shoulder injuries. There are three big grades when we are looking at AC joint injuries, grades 1, 2, and 3,  I am going to draw this out in a moment. There is a grades 4 or 5 and 6, those are very rare circumstances. It is where there is complete destruction of the AC and coracoclavicular ligaments. Grade 4 dislocates into the trap, grade 5 dislocates higher up into the posterior trap, maybe even under the neck, and grade 6, goes underneath the acromion. Again, very rare circumstances to find those, and those are usually not difficult to diagnose. The important thing is trying to decide, whether we are looking at grade 1, grade 2, or grade 3.

An important thing when we start dealing with a patient who has AC joint injury is we want to evaluate not surprisingly, AC joint x-ray. Now an important thing with AC joint x-ray is we do these with and without weights. We do just stand in neutral and get an AC joint view, and then we have the person hold a weight to distract the shoulder down. Because one of the things that happen with these AC injuries on any of the one-two or three, one of the things that might happen is the person might actually hurt, they are painful, so they tend to contract and guard, and the clavicle will drop back down to a normal position. As we are evaluating AC injuries, there are two structures that we pay a lot of attention to when we start talking about AC joint injuries. We are looking at the ac joint ligaments and the cortical curricular ligaments. We are not going to separate the coracoclavicular into their two components. We are just going to treat these as one group, so AC ligaments and CC ligaments. As we are looking at these two ligamentous complexes in grade 1. A grade 1 AC injury, is generally a normal-looking shoulder because in grade 1 the person mildly sprains the AC joint, but then the coracoclavicular are left intact, and it’ll look pretty normal. Everything generally lines up where it should, maybe there is a little widening of an AC joint.

Presentation placement 20:13
When we start looking at grade 2, so on grade 2, is a complete rupture of the acromioclavicular ligaments, and a spraining of the coracoclavicular ligaments. What you will typically see then is AC joint widening, and also the partial elevation of the distal clavicle?

The big landmarks that I use when I am trying to discern what kind of AC injuries there are. Notice that on the without weights, this joint loads this one up here, this one looks normal. This is the with weights, you will see this as WW with weights, we can see that there is a change, I use three landmarks. When I am looking at AC joints, I use the bottom edge of the clavicle, the top edge, the acromion, and the bottom edge of the acromion. The bottom edge of the clavicle should line up with the bottom edge of the acromion. If the bottom edge of the clavicle is falling in between the top and bottom edge of the acromion, that is generally agreed to, and then if we take this to our next patient, here, we can see where the bottom edge of the clavicle is completely above the top edge of the acromion. So that is going to be a grade 3.

One of the other things which I am a big fan of is using common sense. You can see this clinically, there is this person who is going to have a large step off their shoulder. This is a patient before I inflict the weighted view on them because it is not going to be comfortable. I would clear that minimal that first AC joint x-ray, let us see how this thing looks before I put weights on and cause the person unnecessary pain.

A really interesting thing that can happen when we start dealing with AC joints, is whether the person has a distal clavicle fracture or an AC joint injury for unknown reasons. Sometimes it creates this kind of over-driven inflammatory reaction. The other big thing that we see this with is cumulative trauma where somebody is repetitively injuring their AC joint. In either case, whether it is post-traumatic or whether it is cumulative trauma, the body creates this inflammatory reaction in the distal clavicle. This creates a phenomenon called PTOC, post-traumatic osteolysis of the clavicle. With post-traumatic osteolysis of the clavicle as that inflammatory reaction starts to happen, a big thing to remember from a bone physiology standpoint is when a bone becomes inflamed, it increases osteoclastic activity.

One of the things that will happen in these patients, either, the person who has got the acute trauma, the pain does not die down the way it should, it gets worse because there is inflammation in the distal clavicle. Or if I get a powerlifter, who is starting to complain about AC joint pain, you need to realize bench pressing is incredibly hard on the AC joint, and that horizontal AB duction really stresses the AC, so powerlifting is kind of notorious for this type of injury. They start getting pain in the area, so it is worth taking some imaging to see what is going on.

I am now looking at two different clavicles right going to be normal for comparison. On the normal side, we can see a nice normal AC joint space with a good cortex all the way around. When I look over on this side, this person has an abnormally widened AC joint. But more importantly, we are seeing that there is no cortex on the distal clavicle. This is a case of post-traumatic osteolysis of the clavicle, PTOC. Now, this generally can come on, after an acute injury of two to three weeks, after enough cumulative trauma you can start to now has an insidious onset. The big thing is this inflammatory reaction can last for about six months and it will erode the distal clavicle and it will create instability of the acromioclavicular joint now just to show you what I am talking about again using an MR perspective on what this thing look like when we look at MR.

What I am giving you here, as we look at the MR, is I am focusing on the sagittal oblique and this is a stir sequence and as I scroll in now this is a very poor-quality MR. This is an open magnet, and its stir stirs are always grainy images. One of the things we can see as we are coming in, so is sagittal. We are starting on the outside slicing in, we notice that there is some inflammatory change, but what is interesting is that here is the clavicle, the clavicle is inflamed, but the acromion itself is not. This is a person who has active post-traumatic osteolysis in the clavicle with that bone marrow inflammatory change. I get the self-limiting condition; it does go away on its own and generally about six months and it will have some instability in the AC joint as a generally heals. Now, from there we come into shoulder dislocations, now when we know, I am going to bypass scapular fracture scapular fractures, which is self-explanatory.

Usually, the only way to really break his scapula, the body of the scapula least is through direct trauma, we will see a fracture in the glenoid, and just a little bit. But getting into shoulder dislocations with shoulder dislocations, there are four major directions, and in general here we talked about any kind of joint dislocation. We talked about things and Cardinal planes; does it go anterior? Does it go posterior? Does it go superior? Does it go inferior? Well, when we start looking at the shoulder dislocation, the vast majority of these are going to be anterior. It is because the shoulder is angled anterior, the anterior ligaments are weaker than the posterior ligaments, so anterior dislocations are the most common direction.

Posterior dislocations are a very rare, very small percentage, their big thing is anytime we see a posterior dislocation that means, of course, it could be a foot injury because of its upper extremity. But I always want to see this person have a seizure, seizures are a major cause where the contraction will pull the humerus backward and dislocated, and along those lines, if somebody has an electrical shock, that can induce seizure-style activity, and that can create that posterior dislocation. The inferior and the superior are very rare, and it is not a difficult diagnosis. With the inferior dislocation, the arm is stuck up like this person looks like they are always asking a question in class. This is called Luxatio Erecta (inferior dislocation of the glenohumeral joint trapped underneath the coracoid and glenoid). It is because the person’s arm was AB ducted, and something hit the shoulder and drove it down and it stays up and they cannot put their arm down the superior dislocation to get a true superior dislocation on the shoulder, you have to fracture the spine of the scapula and the acromion. This is not usually a difficult call.

Presentation placement: 27:31
Not surprisingly, radiographs are very important in diagnosing dislocation. We have somebody that has pain in the shoulder, they have limited range of motion after trauma. One of the important considerations, when somebody has an anterior dislocation versus just a simple sprain, is that as the arm is dislocating anterior, it tends to externally rotate a little bit. This person has a little bit of fixation and external rotation, and it is hard for them to internally rotate, because of the way the muscles are going to pull as that shoulder dislocates. We can see the classic subcoracoid location for this shoulder dislocation, not a difficult diagnosis here. The thing that we are worried about them as far as dislocations go, we are worried about fractures that can happen with a dislocation, and we are worried very much about the glenoid labarum. Very common when we see shoulder dislocations that there are going to be labelled pathology. Not surprisingly, once somebody dislocates once, they are more predisposed to having other dislocations, because the ligaments have been damaged. That is why immobilization is one of the keys to treatment to give those ligaments a chance to heal. As we started talking about associated injuries, when we are looking at this when there are three major associated injuries with glenohumeral dislocation, the Hill-Sachs, which is a fracture on the posterior superior portion of the humeral head, where the glenoid impacts the humerus there is the Bankart, which is a fracture of the anterior inferior margin of the glenoid. This can either be direct impaction, or this can be a component of a bulging via the triceps mechanism, and then the flat fracture is where this person evolves as the greater tuberosity with the rotator cuff, the superior rotator cuff tendons.

Other things that we are concerned about, and this is one of the things that must be monitored in somebody with a history of shoulder dislocation. Did they damage the axillary nerve? How is their deltoid doing in the weeks following the dislocation, checking for brachial plexus neuropathy because not surprisingly, again, the brachial plexus is travelling in this direction here? There can be impingement upon the brachial plexus and then damage to the suprascapular nerve as well.

The Hill-Sachs fracture. The thing about the Hill-Sach, is a fracture of the posterior superior portion of the humeral head it is a V-shaped groove, which is exactly what we are seeing here. Because this shoulder dislocated anteriorly, the glenoid acted like a hatchet and rammed into the posterior part of the shoulder, and that is why that Hill-Sachs is also known as a hatchet fracture. That groove is going to be there for the rest of the person’s life, and we will always know that there is a history of dislocation here.

Presentation Placement 30:36

Pulling up a DICOM case, we are now looking at the axial sequence. This is a tee to fat-suppressed as we scroll down, we are in the area of the AC joint, and we are getting down underneath the acromion. Let us see if there is some fluid in this person’s shoulder. This was an equestrian injury and they were holding on to the horses’ reins.  The horse had pulled really forcefully against the reins and dislocated the person’s shoulder, we can see as we are coming down through now that notice that there is bone marrow edema on the posterior aspect of the humerus. We can see there is the V-shaped groove where this person has a Hill-Sachs. That Hill-Sachs fracture is going to be there for the rest of this person’s life because it does create that groove and it is not like it is going to regrow. We will always know that this person has a history of dislocation.

The Bankart fracture, this one is a fracture of the anterior inferior glenoid RAM, you can see a little defect right through there. The big deal about the bank or fracture is if there is a bank card fracture, 99% probability this person’s got labarum pathology because as the shoulder dislocated either the humerus knocked the corner off of the glenoid. Or we can see where the triceps falses, a portion of the glenoid. This is one of those big indicators that if this person’s got persistent shoulder pain, I am going to be thinking about getting an MRI arthrogram, and that is one of my big deals is, that anytime I have a patient with a history of dislocation with persistence or shoulder pain, I am going to consider an arthrogram.

Now, the other dislocation, if we are going to see dislocations, anterior is the most common, it is possible to see posterior. Not surprisingly, a posterior can happen with a Fouche. Because as that arm goes out, and you are landing on it, it is forcing the humerus backward. But again, we can see this with uncontrolled muscular contractions with seizures and electrical shock. This is a very difficult fracture to see or difficult dislocation to see because it does not really move out a plane as we see with the anterior. The anterior dislocation, the humeral, headwinds up down here, with the posterior going straight back, and as it goes straight back, it tends to fix it in internal rotation. This person will lack external rotation from a clinical perspective.

The important thing is, that one of the big x-rays that I am a fan of in the shoulder is something called a grassy view. There is the standard AP, external rotation, and AP internal rotation, but a few that I like to do is I like to rotate my patient 30 degrees, so the scapula is flat against the Bucky. Then I would shoot directly into the glenohumeral joint, and which is called a grassy sheet. Where the grassy, we should see the glenohumeral joint space very nicely. I can see that this is a well-done grassy, there is a nice flat line for the glenoid. But there is an overlap between the humeral head and the glenoid lens because this person has a posterior dislocation, and with that fixation and internal rotation, that is great. Something called the light bulb sign.

The other option you can do is if you are really not sure as humeral head where it is supposed to be doing scapular Y, and looking at the scapular Y,  you can see is their displacement of the head. Not surprisingly, in a posterior dislocation, we can get similar fractures with the anterior dislocation, the reverse Hill-Sachs, and the reverse Bankart. Same thing just on the opposite sides, and of course, labrum pathology.

Presentation placement: 34:22

Now, we really cannot talk about the shoulder unless we also talk about labrum path. When we start looking at labrum injuries, label injuries are very common, and anybody who’s got a history of shoulder dislocation. They are also very common and anybody who’s doing overhead activities. When you are serving in tennis, when you are pitching in baseball, any of the throwing sports really can damage the labrum. In baseball, there is even a question of, can you even really be a good pitcher if you do not have a little labrum tear? When we look at the Labrum, this fiber cartilaginous ring lines the glenoid. Well, we cannot see fiber cartilage when we are looking at an x-ray. If I have any concerns about labrum pathology, I always go to an MRI arthrogram.

Now, what kinds of things make me suspect it? the instability that if the person has any kind of feeling of instability, I am going to be worried about the labrum. If I get somebody who is an overhead sports activity, I am also going to be worried about the labrum and I would think about getting an arthrogram. It is those overhead activities, again, baseball pitchers, we see it in cricket, tennis and Swimmers. With the arm going over the head, painters are notorious for this type of injury and from my world of mechanics, spending a lot of time working over their heads, we look at tears like the labrum. There is a whole bunch of different types of labrum tears. We are going to focus on the most common type called slap tears superior labrum anterior to posterior. With slap tears, there are four major kinds of slap tears, and there is a total of 12 SLAP tears from that. So there are 12 SLAP tears. Types 5 through 12, are academics who are really trying to find something to publish. They are almost all variants of the first four types of SLAP tears.

With four types of SLAP tears, they are categorized as type 1, type 2, type 3, and type 4.

Type 1, this one’s more age-related than anything else with a type 1 SLAP tear. If we think about the glenoid labrum as a ring, and it is got a triangular cross-section to it, then the free margin tends to fray and I am going to show you some schematics here in a little bit. Type 2, this person tears the labrum away from the glenoid, and in doing so, they also ablest the long head biceps anchor, because the long head biceps anchor is very intimately involved with the superior portion of labrum. The type 3 injury is just a bucket handle tear of the labrum but the long head biceps is intact, and then the tight for another bucket handle. But this one splits the biceps tendon.

Schematic for what a normal labrum should look like, we do not use the sagittal that much, I am just giving you the sagittal for representation. When we are talking about superior labrum we see this best on the coronal sequence and glenoid labrum and long head biceps tendon. If you look at this free margin right here, because it is a triangular cross-section, type one is afraid of that free margin. It starts to become indistinct, and this is super subtle, and it takes a lot of time to be able to really evaluate this. The clinical significance of type 1 SLAP is really highly questions can have great pain can it create instability, absolutely. But not to be thought of as likely as with the other types of injuries.

The Type 2 SLAP tear. This is a bucket handle tear, you can see where the labrum is detached along the superior portion of the glenoid, and then there is the labrum there is the long head biceps anchor, and the biceps anchor is no longer attached to the glenoid. That is exactly what we are seeing here, the long head biceps tendon is coming across, and the anchor would be right through there. Here is the triangle for the labrum, and notice that there is this nice line that is going through both of those separating out the labrum and the long head biceps anchor.

Type 3, the long head biceps anchor stays in place. But then the labrum is going to a vault in a bucket handle style. Here is the horizontal component of the long head biceps poking into the superior portion of the labrum or the glenoid rather, and then there is the small triangle for the labrum with a defect through there. Again, these are much easier to visualize and we are looking at arthrograms. The type 4 we see tearing through the labrum and then a longitudinal splitting of the long head biceps tendon. That is what is going on here long head biceps labrum tear goes up, and then there is a longitudinal splitting of that long head biceps tendon. This is sometimes thought to be looking somewhat analogous to an Oreo cookie, where you have got the two chocolate wafers and then the vanilla cream in between. I know shocker, radiologists using food analogies for things.

Presentation Placement 39:58

Now one of the other things we are worried about is when we find patients that have labrum pathology, and the labrum path itself is enough of a problem. But one of the other things that can happen is a phenomenon called a para labrum to assist. This is where the synovial fluid will force its way through that tear, and it will create a cystic lesion outside of the glenohumeral joint capsule. This can happen anywhere along the course of the labrum. The big concern when we are dealing with slap tears is that they can get into an area where there is a nerve, okay? Because if this does tend to go superior or superior little posterior, the two big structures we are worried about are the suprascapular notch and the spinal glenoid notch. Because the suprascapular nerve runs through both of those and if the parallel cyst is in the suprascapular, Notch, this can deactivate the supraspinatus and Infraspinatus. If it is in the spinoglenoid notch can denervate, just the infraspinatus. This is one where we would want to evaluate very carefully as we are looking at that MR.

We are looking at the axial view on this particular shoulder, and as we come down, again, not the highest quality MR, but we can still see what we need to see. One of the things we notice is on this posterior aspect, there is a large fluid-filled cystic structure. One of the things that I can know because this is a non-contrast shoulder, they didn’t put an arthrogram on this one. If I see this cystic structure, I know this person’s got a labrum tear. That is how para-label cysts form. Whether I see it or not, I know that there is a labrum tear.

Because I see this large cyst, and it is right in the area of the spinal glenoid notch, I am going to want to look at the sagittal obliques. When I look at the sagittal obliques, so starting out, so here are the humerus fronts over here and backs over here. As we are scrolling backward, we can see the AC joint. One of the things I am noticing as I am looking at this is there is the supraspinatus as there is a subscapularis, look at the infraspinatus. Notice how the infraspinatus is a much lighter shade of grey than the supraspinatus or the teres minor. That is because this person has acute denervation of that infamous bananas. This large parallel cyst is compressing the suprascapular nerve in the spinal glenoid notch, and it is knocked out the infraspinatus. If this does not get decompressed in a short period of time, this person might be left with a permanent deficit in their infraspinatus.

Presentation Placement: 43:13
Another thing that we can see when we start looking at the shoulders, is pain with a reduction. Is that a Supraspinatus problem? Is that a sub-deltoid subacromial bursa problem? What is it going to look like on x-ray, generally we do not see it? I would take the x-ray to see if there is HADD in the area. But not surprisingly, when we start looking at this, we can see a really nice example of some sub-deltoid subacromial bursitis here. A nice fluid collection that the supraspinatus tendon itself is in good shape. That of course does bring us to the topic of tendinosis. When we start talking about shoulder issues, tendinosis is the big one. We do not use the word tendinitis anymore. Tendinitis implies an inflammatory response. It is a better term to use tendinosis or tendinopathy. When we start looking at tendon pathology, one of the things about tendon pathology is tendinosis happens, sometimes the tendon gets thicker, and sometimes it gets a little thinner. Sometimes you will see some irregular signal inside the tendon from an MRI perspective because we cannot see tendinosis when we look at an x-ray, something that can be very well documented using ultrasound as well.

There is a problem, and one of the problems with MRI is that when we are looking at MR when something is ballparked, around 55 degrees off the long axis, it can create some false high signal on T1s and proton densities, which is where one of those is the pulse sequences that we will use for evaluating tendons and ligaments. That is where we will always compare against the fluid-sensitive sequence like a T2 or a fat surprised to see if it is real or not.

Other things that go wrong with tendons are tenosynovitis, so we can see fluid collections in the synovial sheath surrounding the tendon. That of course is a very common theology. I used an angle here because looking at the tibialis posterior, and flexor helices we get that really nice appearance for the tenosynovitis. Shoulder we do not see tenosynovitis as commonly because there is no synovial sheath for the rotator cuff tendons. We can see it in the long head biceps tendon as it is down in the bicipital groove.

Other things we will see, are tendon tears. If you have looked at MR reports, one of the things you will see is sometimes it seems like there is a conflict, because you will read a report that says there is a full-thickness incomplete tear, and that just does not seem like it makes a lot of sense. Well, when we start looking at tendon tears, there are a couple of different things to keep in mind. It is possible for the tendon to tear longitudinal, and it is called a delaminating tear. Then we talked about completeness and thickness.

One of the things to realize about almost every tendon, tendons are generally not round, tendons are flat. Because they have some flattening to them, will have a longer axis and a shorter axis. The shorter axis is where we talked about thickness, the longer axis is where we talked about completeness. Now a nice example of the longitudinal delamination that is happening through that region, is picked on an Achilles tendon because it is a nice big tendon. This thickness and completeness thing. Tendons are usually flat, they are not usually perfectly round.  They have a short axis, and they have a long axis. The short axis is where we talked about thickness, the long axis is where we talked about completeness.

I like to usually start this explanation by looking at the full thickness, and incomplete tear. Here, we are looking sagely and we are looking along with you, we have the rope, and we are looking along the rope from the side. Here, we are looking down the axis of the rope. If I think about this, as my pen here is a tendon, this is the longitudinal look, and then this is the tangential look. If I drive a nail through a tendon, that nail will go all the way through the tendon from top to bottom, but it won’t split it completely from front to back. Because it is going all the way through that short axis, that is a full thickness. But it is not going all the way front to back in a complete tear. The partial thickness is complete, this is where using a rope as an analogy, if I am taking a knife and I am sawing through a rope, I can saw through it all the way from front to back, and I am getting it partially through. It is a partial thickness it is not all the way on the short axis, but it is all the way on the long axis. So that is complete. A little nick in the tendon is a partial thickness incomplete. And then a full-thickness complete, usually, rather than using the term full-thickness complete, we just say rupture. Let us look at a couple of these on MR to see what they look like.

As I pull up the MRI for this case, I am in the coronal plane. So we are in that frontal plane, we are starting in the front, here is the coracoid, and as we go back, so here is the long head biceps right through here. You see there is some fluid surrounding now and now we are into the area of the supraspinatus standard. Now one of the things I noticed there are tendons are generally supposed to be fairly dark black on MRI, but I noticed as I am looking at this tendon, it is nice and dark black here, but then it starts to become a light, irregular grey, and it is never homogenous in any one shade of grey. There is a lot of streaking and stranding going on through there. A beautiful example of tendinosis. This person has supraspinatus tendinosis, and what are they clinically going to be presenting with probably an impingement style presentation, this person does have that downward-sloping acromion. Because that patient does not have any focal defects, I am not going to call any tears, I am just going to call tendinosis.

For our next patient, I am going to be on the T2 coronal and as I find my coracoid, I know I am starting in the front person has quite a bit of fluid in the bicipital groove, and as I am looking at their supraspinatus tendon, so right here, we are seeing Supraspinous there is a focal defect. So this person has a really nice focal defect. It is on the articular surface. Okay, and then I keep coming through. So, and there is a question on this one, is it actually going all the way through as we are seeing just a hint of fiber there? Could this be a full thickness all the way through? Could this be a partial-thickness involving 80% But it is definitely incomplete because the supraspinatus tendon is starting here? As I am going back the rest of the time That looks good. This person does also happen to have a little sub subacromial slash sub deltoid bursitis.

Coming into the coronal on this one. let us find our front. Here is the core code. We are coming into the supraspinatus tenant. One thing to realize is when we see start to see these little signal changes in the greater tuberosity usually is a good indicator that somebody has some chronic Supraspinous issues. As I am coming in, I am in the tendon, I can see the inferior portion coming all the way across, the superior portion stops, there is a gap, and then it comes through. But it is not all the way in the front. The anterior portion is intact, so this is a partial thickness, incomplete bursal surface tear. Coming into our last patient for rotator cuff pathology, we are on the coronal and I am going to start at the coracoid. As we scroll back, one of the important things to notice is, where is the supraspinatus tendon? I never see it. This person, the humerus is actually articulating with their chromium. This person has a rupture of the supraspinatus tendon with complete retraction.

The question is, how long has it been there? As we look at the sagittal, on this patient, I am going to start off on the humerus, and coracoid on the front side, notice that the supraspinatus has no muscle belly, and there is complete fatty atrophy of this person’s Supraspinatus. We are seeing the same thing on their infraspinatus and on their subscapularis. This person has ruptured three of their four rotator cuff tendons. Teres minor is still intact and this person is why they are still a nice teres minor muscle belly.

Presentation Placement: 52:47
Other things that will be going on in the shoulder. There is an anomaly that can be implicated, so we have a person who’s got, they are doing any of their shoulders, really shoulder-based style events. Racket sports, throwing sports, things of that nature. Well, when we get the person who has pain with AB duction, shoulder impingement rotator cuff tear, I realized that there is an anomaly that predisposes towards impingement. That is something called the Os Acromiale, so this is an opinionated secondary ossification center for the acromion between the scapula and the spine of the scapula and the acromion. The problem here is one of the theories behind how this works is this little junction here is fibrocartilage. As this person’s AB ducts, the deltoid will actually pull down the acromion, instead of here is my acromion. Here is my deltoid. When my deltoid contracts, my arm comes up, and the acromion has a rigid surface. But in this patient, my MCPs, you are going to act like a joint, so as my deltoid can track, it actually pulls that Os Acromiale down to where it can dig into the supraspinatus tendon.

This can be difficult to see on a standard shoulder series, on a standard AP internal rotation, or on external rotation. That is where a scapular wide view can be really useful for a patient like this if I am concerned about it. We can also see it nicely on MR. Just to show you so clavicle acromion, and here is what an Os Acromiale looks like. You can actually see that fibrocartilaginous junction there. If you do have a patient that has chronic impingement, and they have an Os Acromiale, this is a relatively easy orthopedic fix, the orthopedist will drive a screw through the posterior aspect of the acromion and tighten everything up so that it does not have that flexibility.

Something else that is on our list of differentials for a patient that has shoulder pain, whether traumatically induced or chronic long-term is hydroxyapatite deposition disease, and we know that most of the things we see in the shoulder are going to be tendinosis that we will treat conservatively, without even having to get advanced imaging. However, I am pretty liberal about x-ray and shoulders because there are a lot of things that can go onto the shoulders that we can see radiographically and one of those adds hydroxyapatite deposition disease. Technically, realistically, the term for this is technically calcium hydroxyapatite deposition disease. So realistically, this disease should be called CHADD. I am pretty happy that we have dropped the C off of this one so that this is called HADD because I am not really happy about diseases being called CHADD.

Very common to see this in the rotator cuff. It is actually the most common place in the human body to see HADD in the rotator cuff. As we start to look at it, and it is a very characteristic appearance, it is not a difficult thing to call. When I started looking at the shoulder x-ray, I can see that there is a really nice example of calcium in the supraspinatus. I know it is in the supraspinatus because when I compare the external rotation view, with the internal rotation view, I am looking at the greater tuberosity, the first centimeter of the greater tuberosity is the supraspinatus, the second centimeters infraspinatus, and the third centimeter is teres minor. It is pretty easy to figure out which of the tendons is involved when I am looking at a case of HADD. The other thing is how we can see this on advanced imaging, it shows up on MR, and it shows up on ultrasound. In this particular case, I am on the axial. As I scroll down on the axial, I can see that right there in the infraspinatus tendon, there is a huge blob of low signal intensity calcium. This person has HADD of the infraspinatus tendon. This could also involve the bursa we can see this on the subacromial/subdeltoid bursa very commonly.

What about the long head, biceps tendon, and the long head biceps tendon is another one that can very commonly be injured, we can see tendinosis in the long head biceps, and we can see it a vols when we are looking at a slap too, we can see a longitudinal tearing with a slap for. So those are possibilities. One of the other big possibilities is again, I get somebody who does a lot of internal-external rotation as part of their event. We can start to see where I get this snapping in my shoulder every time I internally and externally rotate. Worried about this person having a person having dislocation of the biceps tendon looking at that long head biceps tendon for dislocation.

When I want to evaluate that, we do the orthopedic tests, one of the things that are really interesting to think about is when we look at the long head, the biceps tendon can actually dislocate in two possible directions. It can dislocate superior to the super spear, the subscapularis, if the transverse humeral ligament tears, or it can dislocate deep to the subscapularis if the subscapularis insertion is where the terrorists so pull up our study here.

Now to evaluate, when we start looking at evaluating the biceps tendon, the best way to do the horizontal component we see on the coronal and on the sagittal is, is if I pull this coronal over. Okay, find the coracoid. There, we are in the front, and the long head biceps tendon is going to be coming across here where the biceps anchor is, and to evaluate the vertical component, we use the axial. We are starting at the top and working our way down. As we do, we can see the humerus and there is the bicipital groove. Not surprisingly, the long head and biceps tendon should be located inside the bicipital groove, and in this patient, here is the long head, and biceps tendon, and it never comes anywhere near that groove. What is interesting though, is it is when I follow that tendon, so follow this to here where it is starting to turn and coming over this way. This one is actually deep to the subscapularis tendon. So subscapularis is here, and then the long head, the biceps tendon is here. A good thing to keep in mind.

When we start thinking about the transverse humeral ligament, the subscapularis, actually, if you look histologically, and there is been some interesting anatomic studies, the subscapularis as it comes across, inserts onto the lesser tubercle and onto the floor of the bicipital groove. But it also contributes fibers that make up the transverse humeral ligament. So that is where subscapularis pathology can quite often be intimately related to long head biceps subluxation dislocation, so if this person were to damage the transverse humeral ligament, then that long head biceps tendon will be in front of the subscapularis. But in this case the long head biceps are deep to the subscapular. This person had a partial subscapularis tear at the insertion that let the tendon dislocate deep to the sub scab.

So, those are our various shoulder pathologies, and not surprisingly spent the entire hour on the shoulder because the shoulder is one of the most complicated joints in the body. When we come back as we start getting into Upper Extremity Trauma 2, we are going to focus on the elbow, hand, and wrist, well, all complicated in their very own rights, usually a little bit more straightforward than some of the shoulder pathologies.

Thank you very much for following this lecturer. I will see you back for Upper Extremity Injuries 2

[END]

Section 07_ICSC03 – Upper Extremity Part 2 – Elbow and Hand
English Direct Download PDF – 07_ICSC03-Section7-Elbow Hand Upper Extremity

Instructor Dr Chad Warshel
Video Lesson: 01:09:46

We are going to finish up Upper Extremity, covering the elbow, wrist, and hand. Let us start with the elbow and work our way down.

One of the important things when we are dealing with any kind of musculoskeletal trauma is we also want to make sure we are evaluating the soft tissues. We tend to focus on the bones, and look at the alignment, at the density and the cortices. But unfortunately, we focus so much on the bones, we tend to forget to look at the soft tissues. It is partially probably the fault of how we educate in that X-ray is predominately a bone technique. We want to make sure that we pay attention to the soft tissues because while X-ray is not great for soft tissue resolution, there are some very important clues that can be discerned by evaluating the soft tissues. In the elbow, there is a fantastic thing to do when we are evaluating the elbow. This view is looking at the fat pads. When we start looking at the average run-of-the-mill elbow, one of the things to keep in mind about the elbow is that there are two fat pads that we will see in an elbow. There is an anterior fat pad, and that anterior fat pad is going to be a dark little line that hangs like that. The second fat pad is the posterior fat pad, and we cannot see that fat pad because it is inside the olecranon fossa. What we are seeing is there is a sleeve of the joint capsule that surrounds the elbow joint, holds in the synovial fluid. When somebody has mild, moderate, severe effusion of that elbow joint, it is going to fill the joint capsule up with fluid. As it fills the joint capsule up with fluid, that is where we are going to start to see a displacement of these fat pads. It is one of those things that we always want to pay really close attention to.

When we look at this patient, what I am seeing in this person is the anterior fat pad is displaced outward. That is called the anterior fat pad sign. The other thing that I can see when I look at this patient is, on the back side, there is another dark line. That is called the posterior fat pad sign. So, anterior and posterior fat pads.

What fills up a fat pad or what causes this displacement? The first possibility is synovitis. You have something that is creating an inflammation of the synovial membrane and it is pumping a bunch of fluid into the joint as a simple bland joint effusion. We can see that in things like rheumatoid arthritis. We can see this in patients that have the inflammatory arthropathies. We can see this in some of the other inflammatory arthropathies like gout, CPPD. Some of those things will do it.

Because we are dealing with athletic injuries, not surprisingly we can see this with trauma. One of the things about those elbow fat pads is, when I see those elbow fat pads in a trauma circumstance, that tells me that there might be the possibility of a fracture. I have highlighted those anterior and posterior fat pads so you can see a little bit better. When we look at the fat pads in the elbow, one of the things we always want to think about is Sensitivity and Specificity. Understanding sensitivity and specificity of the fat pads. In order to displace the anterior fat pad, it only takes mild swelling. So, to take that fat pad from down here to out here where we are seeing it, it only takes mild swelling. If the swelling is mild, moderate or severe, it is going to displace that anterior fat pad. By the way, that anterior fat pad is also known as the Sail sign because theoretically it looks like a sailboat’s sail that is full of air. Smile and nod. What that means is the anterior fat pad is very sensitive for an intracapsular fracture because if somebody has a fracture inside the joint capsule, they are going to have at least mild swelling. So, I can use that anterior fat pad and say, there is a possible fracture. It has high sensitivity but it has poor specificity because what if this person has a mild capsular sprain? What if they have got a grade 1 sprain of the radial collateral ligament? That can also cause a mild distention of the joint. If there is fracture, it will have an anterior fat pad. But if there is an anterior fat pad, it does not necessarily mean it is fractured.

The posterior fat pad sign, this one back here, is very specific. If I am in a circumstance of trauma and I see a posterior fat pad, the only way to get that fat pad out of the olecranon fossa where it should be and displace it all the way back to here is if there is severe intracapsular swelling. How do we get that kind of severe? Well, if there is trauma, this person definitely broke their elbow. If I do not see a fracture, it is still broken, and I have to take some more x-rays. I have to think about some other imaging techniques to see what is going on. Posterior fat pad is very specific. Anterior is sensitive, posterior is specific. What are the things that might cause that posterior fat pad? Again, rheumatoid arthritis, gout, septic arthritis. Those are all the other possibilities. But when we are in that circumstance of we are dealing with the post-trauma elbow, I am really careful.

An important thing when we are dealing with an elbow x-ray, you do want to make sure that you get the elbow bent as close to 90 degrees as possible. That is the best way to be able to see those fat pads, realizing the limitations of dealing with the trauma case of how much they can move their elbow without screaming and clearing out the waiting room.

In this particular case, I will give you a second to look it over. I am going to go back up one picture. There is all the arrows and moving things out of the way, look at the X-ray, we know that this person has anterior and posterior fat pad. There is a need for capsular fracture until proven otherwise. See if you can find the fracture in this case. By the way, this is my favourite game. It is “Where is Waldo” of the radiology world? My children never got to play “Where’s Waldo”? My children got to play, “Hey, find the fracture,”.

As we look at this one, we trace the radial cortex around. There is the start of the articular surface, then the articular surface divots down there, and there is the remainder of the radial head. This person has a displaced radial head fracture. It is not always easy to see because there is a lot of overlapping structure there.

Now that we have started the idea, we are going to look at the bones, we will also look at the soft tissues. One of the things that radiology runs on is statistics, understanding what is the most common. We are going to see most common things more often than we are going to see less common things. You always want to keep the zebras in mind. Beyond zebras, there is unicorns. Beyond unicorns, there are pegasi. You want to keep all those things in mind but when I hear hoofbeats, I think horses not zebras.  Do things break around an elbow? Well, the answer to that question depends a lot on the patient. If we are dealing with children, children have elbow trauma and elbow trauma can be direct elbow trauma or it can be a FOOSH. We can see supracondylar fractures most commonly. They will fracture the humerus above the condyles. Then, there are condylar and epicondylar fractures. In the adult, as our bones become more rigid, less plasticity than we see in children. What is the most common mechanism? FOOSH. What is going to happen? When you FOOSH, you load your thenar, thenar loads the carpals, loads the radius, drives the radius into the capitulum.

A really important concept in the physics of fractures is concave versus convex structures. If we look at a radiocapitellar joint, radius comes up. Not the world’s greatest radius, and then the capitulum. I realize this looks like a presynaptic and postsynaptic axon as well. When we look at this, one of our huge concepts in trauma is if there is a longitudinal force across the joint and a concave surface is meeting a convex surface, the convex surface usually wins. There is an inherent strength in convexity. What that means is the capitulum is usually going to be okay, it is the radial head and neck that is going to have the problems. In the adult patient, the most common fracture around the elbow is radial head and neck. We can either see where it splits the radial head like cord wood or it impacts the radial head on to the neck. Otherwise, other things we will see in adults: olecranon fractures, supracondylar fractures, and there is a bunch of forearm fracture dislocation that we need to be aware of.

Starting off with children, the supracondylar fracture. As we look at this patient, it is subtle but there is a posterior fat pad in this case. Right through here, there is a little darkness, that is the posterior fat pad. When I am looking at a pediatric elbow, we know the children are a pain. There are extra growth centers, there is some things that haven’t developed yet. When we are looking at the elbow, there is even a mnemonic as the different growth centers show up at different ages. The mnemonic for remembering that is CRITOE, capitulum, radial epiphysis, and so forth. Do not forget when you are dealing with pediatrics, one of the things you can do when you are dealing with pediatric patients is you can always X-ray the other side. When we are dealing with extremities, we are not worried about radiation exposure to the extremities. There is nothing reproductive or anything damaging in the extremities. So, if I have got a child and I am looking at a right elbow and I am not sure if that is what it is supposed to look like and I do not have a pediatric radiology textbook available, X-ray the left elbow, compare the two sides. I do not do this on every child on every extremity. If I am not sure what is going on, please do not do this.

As I am looking at this child, there are extra missing parts, the AP was unremarkable in this case. One of the things that we will want to do, there is a line and surprisingly, this is a line that has a name that makes sense. This is the anterior humeral line. The anterior humeral line should intersect approximately 50% of the capitulum. As I look at the capitulum in this child, there is the capitulum, it is only getting about 30%, because what happens when we deal with supracondylar fractures, the supracondylar fracture, this is a fracture line through there. Because this typically happens with a FOOSH, as the radius impacts and the ulna impacts under the capitulum and trochlea respectively, it pushes them posterior. So, we are going to see that posterior angulation that occurs in the child that has the supracondylar fracture. This is the very much the average run-of-the-mill supracondylar fracture. Of course, there is always the much more apparent jump-out-and-grab-you fracture.

I do not think I really need to do the anterior humeral line in this particular case. This is a child whose athletic event was jumping off of the top bunk, and in jumping off the top bunk and landing on their outstretched hand, ended up with a very significantly displaced supracondylar fracture. This is the child that you are going to see wearing an elbow cast. They will have the cast from the armpit to the wrist set at 90 degrees as they work on reducing this fracture.

What else can we see broken? I probably should have put the radial head as the next one, but I did not. The next fracture, and this one we tend to see more in adults than we do in peds, which is, of course, why I have thrown up a pediatric case. But there is a nice fracture of the olecranon. How do you fracture the olecranon? Smack it. This is a simple direct trauma. When somebody is falling, if they do not catch themselves on their hand, they catch themselves on the elbow. We can see it with anything where an elbow goes against structure. One of the big clues, typically, when we are dealing with the olecranon fracture is the person is completely unwilling to forcefully hyper-extend their elbow, they are not willing to muscle test into elbow extension because the triceps is pulling against that.

In more severe cases, we can actually see where the fragment will displace and the person loses all triceps mechanism so their arm actually telescopes up and they actually cannot extend their arm because they do not have that extensor mechanism anymore. Quite often, when we start looking at these, these will require open reduction internal fixation, and what they are going to do is drive a screw through the olecranon and into the rest of the ulna.

Video Placement Presentation 14:24

What else can we break? The adult patient who FOOSH is typically going to fracture, and they have elbow pain. Does my shoulder, elbows or wrists hurt? Different fractures. Person FOOSH and they have got radial head tenderness. You start digging in there, they start wincing. Let us get some pictures. An important thing to remember in dealing with the adult that has post-traumatic elbow pain, think about elbows. Elbows are usually a two-view X-ray. There is an AP View and there is a 90-degree lateral view.

When I have the adult patient who has post-traumatic elbow pain, I am going to do three pictures. One more picture that I am going to throw in. The standard AP is done like this. The hand is nicely supinated. I am also going to do a hyper-supinated AP view. Then I am going to rotate the whole patient. I need the rotation to come out of the humerus in this case. What I am doing is I am projecting the radial head free of all the other structures. This is a lateral oblique because the problem is on a straight on AP, there is quite a bit of overlap between the radius and the ulna, and that is usually where the fractures are going to hide.

With these radial fractures, we are going to see generally two fractures. The one that we are seeing in this particular case is right through there. It is where the person has split the head. This is called a chisel fracture because the convex capitulum against the concave radial head, that acts like a chisel and it splits the radial head, again, like cordwood. If you are around anybody who is doing lumberjack style games, splitting like cordwood.

The other possibility when we are dealing with the radial head and neck is the possibility that right at the head-neck junction, you can see an impaction. This where really getting the radius flat is important. I have somebody who has elbow trauma, they do not want to fully extend their arm. I realize you might do two APs, you might do an AP with the humerus on the table and then you will do an AP with a forearm on the table because you are trying to get nice frontal appearances for both sets of bones. Look for that area of impaction where there is a cortical offset. There can also be an extra dense white line right around the zone of impaction. That is the zone of impaction.

What is interesting is if they are not displaced, when we look at the chisel fractures and the impacted neck fractures, they are generally handled conservatively. This person needs to go into a sling and given time to heal, then gradual reintroduction of motion fairly early on because one of the things that can happen in a mobilized elbows is it is possible for the elbow to freeze.

Some of the other elbow fractures that can happen. There is a couple of different possibilities when we start looking at capitular fractures. We can look in this person. We are looking at the AP and the lateral. We can see that there is this irregularity of the articular surface of the capitulum. Three different diagnoses here: osteochondral fracture, osteochondritis dissecans, Panner’s disease.

An osteochondral fracture is a traumatic fracture. Usually, what is happening here is something created a tangential force where the radius is shifting. So radial head has that concave, the capitulum has the convex. Normally, we think about the impaction in that fracture of the radius. The other thing we can see is a tangential force where the radius is sliding against the capitulum, and if that happens, that can shear off a piece of the articular surface. That is an osteochondral fracture. Usually, a single traumatic event.

Possibility two, Osteochondritis dissecans. This is a cumulative repetitive trauma that we typically see in children that are doing any kind of valgus force. Winding up for pitching and then pulling through creates a huge amount of valgus force and that repetitive valgus force in the elbow as it loads the radio capitellar joint can result in mechanical failure. It is very similar in nature to a stress fracture. We are going to talk a lot about stress fractures when we get into lower extremity.

The other possibility is Panner’s disease. This is a true avascular necrosis. It is where the capitulum loses blood supply for whatever reason. It can be a single event; it can be cumulative stress. With avascular necrosis, we start to see sclerosis, flattening, and fragmentation of the articular surface.

There is a continuum here. There is a lot of questions of where do we stop calling osteochondritis dissecans and where do we start calling Panner’s? There is a little bit of an iffy thing here. One of the take-homes on this though, particularly, is we are dealing more with the adult and the osteochondral fracture. Realize that when we are dealing with a lot of osteochondral fractures in the adult patient, one of the questions is surgical versus conservative management. One of the ways that question is asked is by doing an MR arthrogram because the concern is, is the fragment stable or not? If the fragment is unstable, then it is going to have to be surgically pinned in place or removed. If the fragment is stable, it is probably going to heal in-situ. That is a question that is going to be asked depending on what you are allowed to order. If you have a good relationship with your orthopedist and you do a lot of your triaging, you might end up getting that MR arthrogram before they go to the orthopedist.

Other things that can happen in the elbow, getting back into the pediatric elbow. Looking at pediatric pitching sports, baseball. One of the things when we start looking at pediatric baseball in pitchers… one of the things that pitchers are not allowed to do in American Little League, is they are not allowed to throw curve balls because in order to get a curve ball, it requires a really big valgus wind-up and a huge flexion mechanism through the wrist. Between the valgus pull in the elbow and the flexion in the wrist, that can create an avulsion of the medial epicondyle of the humerus. It is common in Little League. It is called Little Leaguers’ elbow. Quite often, this is going to require surgery to reduce this. This will also frequently have associated injury to the ulnar collateral ligament.

Typically, we only see these avulsions in children. Once children hit skeletal maturation, they usually just damage the ulnar collateral and that is where we can start seeing Tommy John Surgeries done. Again, the question does roll in. Where is the trochlea? That olecranon does not look like it is very deep. Is that really supposed to be out there? I am not sure. If you are not sure, X-ray the other elbow. Use it as your normal template, because typically, they are not going to be pitching with both hands. We will be able to look at this and figure out, is this where it is supposed to be?

The other thing that you can have available to you is a good pediatric resource. If you are going to be doing a lot of pediatric athletic events, you have your own X-ray equipment. You are looking at a lot of pediatric X-rays. Having a pediatric radiology textbook is incredibly valuable. Some of the different books that are available. One of the ones that is really designed for the clinician is John Taylor’s Skeletal Imaging: Atlas of the Spine and Extremities. At the beginning of every chapter, it shows you normal pediatric development. If you are hardcore into pediatrics, that is where something like Caffey’s Pediatric Diagnosis, it is a radiology text, is a useful thing to have in your library.  We can see that avulsion and this one has enough displacement where the orthopedist is going to be considering tacking that back into place.

What else can happen to the elbow? Dislocations. This can be a FOOSH injury. This can also be where you get direct elbow trauma into the antecubital fossa because almost always the elbow dislocates posteriorly, of course, named for the distal component. This is a person that has a posterior elbow dislocation and not surprisingly, it tends to lock in this location. It is not one of those ones that will spontaneously reduce. One of the concerns being, if we see this sports field side, we know that we are going to immobilize the patient and get them off to the emergency department.

Maybe two weeks from now, I get this athlete who comes into my office complaining about elbow pain after they had the reduced dislocation. Particularly if you are getting some locking or grinding, one of the questions that I would want to ask at that point is, did this person also fracture their coronoid? It happens with the dislocation. They can fracture off the coronoid, or as it is being reduced, the coronoid can fracture and trap inside the joint. Those are some of the complications that are associated with that.

The other thing we are not surprisingly worried about is neurovascular bundle damage. Could this create some displacement in the brachial artery? If I think about the fact that the ulnar nerve is traveling right through here, if this thing goes posterior, there is a lot of soft tissue injury, and it might have stripped the ulnar nerve out of the cubital tunnel there. I am going to be evaluating this patient very carefully for, the vascular component is usually immediate onset. The neural component might be something where, you have got a little palsy going on. Right afterwards, let us give it a chance and see how it does. Two weeks later, come in to see us. Let us evaluate that ulnar nerve.

We cannot talk about elbows without talking about the possibility of epicondylitis. Should we be calling it epicondylitis? Is there an inflammatory component? No. We should be calling this epicondylosis. That just does not roll off the tongue quite as well. There is both medial epicondylosis and lateral epicondylosis. Medial epicondylosis: Golfer’s elbow in an adult; in a pediatric patient, Little Leaguer’s elbow. Of course, there is all the orthopedic tests. I am not going to get into the orthopedic tests. That is more for the clinical diagnosticians. Then there is lateral epicondylitis, which is a whole heck of a lot more common than medial epicondylitis, and this goes by the colloquial term of Tennis elbow. Anybody who is doing any kind of extension activities with the wrist has the possibility of creating that problem with the elbow.

I am generally not doing imaging for these. Golfer’s elbow and tennis elbow are clinical diagnoses. Little Leaguer’s elbow, I am going to be pretty liberal about X-raying the child to see if there is displacement there. But the adult patient, I am going to treat this clinically. I am going to see how well you do. It is not a difficult diagnosis to make. Poke it, see if it hurts, do some orthopedic testing and some stretching, confirm your diagnosis, and treat the epicondylosis, the tendinosis that goes along with this. We will generally reserve imaging for the patients who do not get better. That is where we start to see the imaging done for patients with epicondylitis/epicondylosis, because one of the concerns, particularly with tennis elbow is, particularly if there is a traumatic component to this, is there a tear? Did they also damage the radial collateral ligament? Then I would start considering doing some imaging. Again, ultrasound is a fantastic tool for this, or I would be more MR centric, so I would tend to go towards MRI.

Looking at an MRI, we are looking at an elbow. This is a patient who had a traumatic injury to the elbow, not responding to the conservative care.  The question then was, is there something more than just a simple tendinosis going on? Now, when we are trying to evaluate tendinosis, for the common extensor tendon, the coronals are where we are going to spend most of our time, and particularly if we have something that is fluid-sensitive, so a T2, a STIR, a gradient echo, and in this case, we are looking at a coronal gradient echo. Now the arm is forearm up, arm down. We are seeing the ulna there, getting into the humerus here, radial head here. We can see through here, there is the ulnar collateral ligament. There is the ulnar collateral, and as I am looking on the radial side, I am seeing a lot of fluid on the radial side for one thing.  I got to dim this down a touch. There is quite a bit of fluid. I am looking at that common extensor tendon. It is not the thick belly tendon that I really expect it to be. I can see there is quite a bit of irregularity, and then deep to the common extensor tendon is the Radial collateral ligament. The Radial collateral ligament in this patient is Grade 2 sprain. This one here is not a complete rupture, but there is a grade 2 sprain of Radial collateral superimposed on that tennis elbow. So those are some of those things, when we start thinking about imaging, the trauma patient that is not responding or we are concerned about internal derangement.

Other things that can happen around the elbow is biceps tendon, which is a big one. This is something that we see in heavy weightlifting activities. It can happen during the concentric phase, but really, most of these tendon injuries happen during the eccentric phase where the person’s extending the elbow against weight, and suddenly, they hear a pop, immediate onset of pain in the elbow, and generally, within 10 minutes, the entire antecubital fossa and leading up into the upper part of the anterior bicep is just turning bright purple as the person is hemorrhaging into that area when that biceps tendon tears. Again, not usually very difficult to diagnose clinically, but one of the reasons that we run imaging on knees is how far is it from the tendon tear to the attachment? Because that might decide is this going to be conservative management with bracing or is this going to be operative management to try to reattach that tendon? This is very athletes specific. What kind of sports are they doing? What level are they at? Can really dictate exactly what is going to be happening when we are dealing with that.  Ultrasound is an option and will show us the biceps tendon, effectively. I tend to be more of an MR person because it is less operator dependent and more universally read, particularly by our orthopedic colleagues when we are doing these things.

Video Placement Presentation: 30:46

Let us look at this elbow MR. I am going to run through a couple of different sequences as we look at this one. Now, when we are dealing with any of these extremity joints, again, we are seeing T1s, T2s, where there may or may not be fat suppression, there may or not be gradient echo sequences. My general rule is anytime I am looking at an MR, I always start on a fluid sensitive sequence because I am looking for something that is angry. I am looking for angry tissue. An angry tissue is usually inflamed tissue. It is going to show up bright when I look at those fluid-sensitive sequences. And on this one, I have got three options for fluid sensitive. There is an axial T2 with fat suppression, there is a coronal proton density with fat suppression, and there is a sagittal proton density with fat suppression. I am going to start with the sagittal PD fat-sat.

I am scrolling in. It is not too hard to figure out whether you are medial or lateral because all you need to do is figure out do I see radius or ulna? I am looking at the radiocapitellar joints, and I am noticing in through here in the region of the antecubital fossa, there is quite a bit of fluid. The stranding that I am seeing here, that is normal blood vessel, but this is soft tissue edema.  Then as I am coming over into the olecranon, there is the triceps. We were talking before about triceps or olecranon fractures can take away the triceps mechanism, especially when the fracture is right through there. There is the coronoid. Nothing else really adenomatous.

I look at the coronal. We are starting in the front and working our way back. There is a substantial degree of soft tissue edema right in through here, and then follow the biceps, that is where the axial is going to play the biggest role. I am going to pull our two up window on this one. I like to start in the humerus and work my way down, because realize there is two different muscle groups we are going to be looking at. We are going to see brachioradialis and we are going to see biceps. The easiest way to figure out which one is which, come down to the elbow, find the ulna, find the tendon that comes into the coronoid process, follow that up. And that tells me that this muscle bundle here is brachialis. This muscle bundle here with this elongated tendon, that is the biceps brachii guy. Here’s the biceps tendon, and it is starting to dip down and we follow that tendon in, and all of a sudden, there is a huge amount of fluid, and we are seeing where there is this continuity through this tendon. So, right in through here, this has become this discontinuous with the radial tuberosity. This person has a biceps insertional rupture. There is no significant retraction. It is very much approximated. That will help the orthopedist with that decision of conservative versus surgical management. One of the big take-homes, always start off on your fluid sensitive sequences, looking for edematous issues. We can see the same thing if we follow that biceps tendon through here. You can see how it got really thick, and then it never really plugs into the radius.

We are finished with the elbow, now we are going to get into the forearm. When we start looking at the forearm, one of the things that we need to keep in mind, and it plays a role in pelvic trauma, it plays a role in leg trauma, and it plays a role in forearm trauma, is something called the Pretzel principle. When we start looking at a hard pretzel, yeah, good Bavarian hard, crispy pretzel. It is hard to break a pretzel in just one place. Where this applies when we are dealing with ring structures because pretzels are ring structure, so you cannot break it in just one place on the ring. Well, the forearm is the same thing. Between the ulna and the radius and the distal radioulnar joint, the proximal radioulnar joint, that makes it ring. One of the things we have to consider is anytime we are in a ring structure and there is a disruption one place in a ring structure, we always have to look for a second disruption or even more.

 

We are not pretzels, it is possible for us to break a ring in one place but always make sure you look carefully around the rest of the ring. This is also known as the Life Saver principle. If you think Life Savers candy, little circular candies, cannot break them in one place.

We start looking at forearm fractures, the first of the forearm fractures is the Nightstick fracture. This one is a direct trauma, something simple and straightforward. Something hits the person on the forearm, and it is very common when we are dealing with martial arts we are looking for blocks and things of that nature. Well, tibia versus ulna. I wonder which one is going to win. We see this with a direct blow, and that direct flow fractures the ulna. This is either known as a Nightstick fracture or as a Parry fracture because you are trying to parry the blow away from you. But I want to make sure I look carefully. I am going to check the radius, the distal radioulnar joint, the proximal radioulnar joint, looking at the elbow, looking at the wrist.

This is a huge, massive rule in radiology. When you are looking at long bone studies, you are looking at a humerus, forearm, femur, leg, you have to make sure you include both joints. If you do not include both joints, that does not meet minimal diagnostic criteria. If I am worried about forearm and it is a midshaft forearm issue, I need the wrist and elbow, otherwise, I am going to be missing things. What I am concerned about is the ulna fracture which jumps out at me. Let us look for some other fractures. In this case, we are seeing that ulna fracture, with the ulnar fracture jumping out at you, note the massive displacement here.

It is not uncommon to see that Bayonet apposition occurring as there is some unopposed muscular action going on, and we might hit satisfaction to search, where? I see that and I stop looking. Well, the problem is when you stop looking you miss the fact that the radius is no longer articulating with the humerus. This is a Nightstick variant, there is a Nightstick fracture of the ulna, but then there is dislocation of the radial head, and that is called a Monteggia via fracture dislocation. A big one for you to be aware of. Sometimes you will see it called fracture, sometimes fracture dislocation. I usually call it Monteggia injury, just to encompass all those different parts.

The concern here is, the ulna fracture is going to heal fine. We reduce the radius, there is going to be ligamentous injury. But keep in mind, how is the interosseous membrane? That is something that is going to be injured quite often when we start dealing with these cases.

This next one, the Galeazzi fracture, also known as a Piedmont fracture. This is one where we are seeing a radial fracture. The radial fracture tends to jump out at us. The problem is on the frontal view, it is subtle. It just looks like the person has a positive ulnar variance, but what they have is a dorsal dislocation of the head of the elbow. The distal radioulnar joint has been dislocated. The fracture is easy to see, the dislocation might be much more subtle, and again, what is the integrity of the distal radioulnar ligaments? How is the triangular fibrocartilage in this person? How is the interosseous membrane? Those are all things that can really be very slow to heal.

Then we come to Essex-Lopresti. With the Essex-Lopresti fracture, notice all these forearm fractures start to sound alike and run together. What we are seeing with an Essex-Lopresti is this is a patient who has a proximal radial fracture and then distal radioulnar dislocation because what happens is with a comminuted radial head neck fracture or an impacted fracture, it shortens the radius. As it is shortening the radius, it creates damage to the distal radioulnar joint. You can see where this person has a post-traumatic positive ulnar variance. This person also has a couple other things going on. Like they have an old die-punch fracture, which I am not going to get into in this class.

Then, we must deal with pediatric fractures. We cannot discuss injuries without talking about pediatric fractures. Children’ bones are plastic. Because children’ bones are plastic, they can get more deformation than they do failure. When we deal with children, there are two major incomplete fractures due to that bone plasticity. The Torus fracture and the Greenstick. This child, was unlucky enough to get both. When we look at this child, probably FOOSH, the most common mechanism, they might have had an angular force come across the forearm. What we see when we look at the radius, notice that there is a fracture that goes about halfway through the bone and then starts to split longitudinally. That is called a Greenstick fracture. It is called Greenstick fracture because if you cut a branch off a living tree, and then you bend it to try to break it, it does not usually break all the way through. It breaks halfway through and then splits longitudinally.

The other fracture that we see right here is called the Torus fracture. The Torus fracture is an impaction injury. The bone is loading, and as that bone is loading, it gets a plastic deformity. We are going to see buckling in the cortex. One of the other names for Torus fracture is a Buckle fracture. This one is not named in a way that makes nearly as much sense unless you are really into Greek architecture. The Torus is the little rounded flare at the top and bottom of pillars, so we are seeing a little rounded flare right there as an indicator of a Torus fracture.

We need to get a little bit further down out of the forearm proper and more in towards the wrist, which is going to bring us to a whole bunch of fractures. One of the things you will notice with the wrist and the hand. There are a bunch of named injuries when we look at the wrist and hand. Because we were just talking about pediatrics, I want to continue our pediatric discussion.

When dealing with pediatric injuries, there are a couple things you should note that is different from  adults: Pediatric injuries have hopes, dreams, and the big one they have growth plates, and growth plates are very susceptible to injury. These injuries are called Salter-Harris injuries. The fracture involves the growth plate, the physis. These are sometimes also called epiphyseal fractures. I am not super fond of them being called epiphyseal because the epiphysis is a specific part of the bone, the physis is the growth plate.

We are looking at these physeal fractures, Salter-Harris classification. There are five different types of Salter-Harris fracture. There is an expanded version of the Salter-Harris fracture classification. We are not going to get into that. That is kind of subtle and rare kind of injuries. Now, with the Salter-Harris classification. There are five Salter-Harris fractures. The fracture involves just the physis. It involves the metaphysis and the physis, the epiphysis and the physis, both metaphysis, epiphysis and physis, and then the crushing injury.

Now the type 1 Salter-Harris fracture. When we are dealing with peds and we are dealing with upper extremity, the type 1 Salter-Harris fracture that we are probably going to see more than anything else is the Gymnast fracture. There is a couple of different manifestations. The first is why is it called a Gymnast fracture? Because they spend a lot of time landing on their hands. Name a sport where people intentionally FOOSH more than gymnastics. So as a combination of just landing on their hands that loads that growth plate. And we can start to see widening of the growth plate, irregularity of the growth plate and a lot of distal radial tenderness. Particularly, you can think about things like handsprings where your hands are going down, but there is a rotational force around the wrist that can shear through the growth plate. And then we can see a growth plate displacement, which is exactly what we are seeing here.

Video Placement Presentation: 44:24

In this case, if you look at the ulna, so metaphysis, physis, epiphysis. We do not see that same relationship in the distal radius because the epiphysis has fallen off the metaphysis. This person fractured right through the growth plate, and then they had posterior displacement. Not surprisingly, we do not see the fracture line because well, the physis is made of cartilage. We do not see the fracture line, but we might see displacement or widening of that physeal plate. Type 1 Salter-Harris fracture, distal radius, that is the gymnast’s fracture. We are going to see another very common type 1 Salter-Harris in the lower extremity when we talk about slipped capital femoral epiphysis.

The type 2 Salter-Harris fracture, as we look at, the pediatric patient, lots and lots of growth plates. But as we are looking at the third digit, notice that there is a fracture through the metaphysis that hits the growth plate. As soon as the growth plate gets hit, that is a Salter-Harris fracture. This one has the metaphyseal component. This is a type 2 Salter-Harris fracture. The type 2 Salter-Harris’s the most common type. This one’s a little bit more subtle. This one is a little bit more overt. See quite a bit of displacement between the metaphysis and the epiphysis. And this person left little metaphyseal corners. Technically, these little corners have a name called Thurstan Holland fragments. We just call these type 2 Salter-Harris fracture to keep life easy.

Type 3, the fracture goes through the epiphysis, and then hits the growth plate. We can see in this case, on only one view, do not see anything on the straight on AP, do not see anything on the lateral. But on the medial oblique, there is a fracture running through the epiphysis that hits the growth plate and is running laterally here and it is separating this fragment. This is a type 3 Salter-Harris fracture.

The type 4 Salter-Harris fracture involves both metaphysis and epiphysis. On the frontal view, we can see the epiphyseal component. Right now, this just looks like a type 3. But then when I look at the lateral, I see that there is a metaphyseal spiral fracture coming down to the growth plate. So that looks like a type 2, and this is one of those interesting instances, where a type 2 plus a type 3 equals type 4. There is a metaphyseal and an epiphyseal component, so that is a type 4 Salter-Harris fracture.

Then the type five is a crushing injury. We look at this child and we know that this child jumped off something landed really hard, and they fractured their calcaneus. We will talk about those in the next section. But this child is having a lot of tenderness along the tibial growth plate. The problem with a type five Salter-Harris, radiographically normal because you cannot see the crush in most cases. You must get the history. They will have tenderness along the epiphyseal plate. One of the clinical rules is if there is tenderness along the epiphyseal plate, it is broken, even if the X-rays are normal, it is broken. And the problem is that crushing injury or any of these growth plate injuries can affect the way that the bone is going to grow.  We want to make sure we keep those Salter-Harris fractures in mind. You realize I have given you a lot of lower extremity examples. Not surprisingly, they are more common than upper extremity.

What else can we injure in the upper extremity? Well, FOOSH injuries. When we start looking at FOOSH, person that goes FOOSH. In this individual, this was not a sporting injury, this was a home-based injury. But this is one where it is not difficult to clinically make a call that this person has a fracture because we are seeing something called a dinner fork deformity, where the arm is bent backwards there at the distal radius. When I see that dinner fork deformity in an adult, I know that I am most likely dealing with a Colles fracture because it is the most common fracture to happen around the wrist in a geriatric population. Little children tend to get Torus fractures, the radius. Anybody from 15 to 40, 50, they tend to fracture the scaphoid. Over 50, that is where we tend to see colles fractures. Typically, because it is due to a change in the bone density. This is the same patient. We can see where there is posterior angulation of the distal radial component with that colles fracture. So colles as opposed to angulation.

There is also something called a reverse Colles, otherwise known as Smith’s. This is where there is volar angulation. This happens in one of two different ways. Possibility one, the person falls on a flexed wrist, or if you fall backwards. The vectoring is such that it creates a volar force, and we are seeing that anterior angulation of the distal radius. Something else to note on this one is this person did also fracture their ulna styloid. Ulna styloid fractures are very common. It is like an add-on. You will see it with colles, Smith’s, Barton’s and all these other fractures that will often fracture the ulnar styloid. If that fractures, then we must worry about the integrity of the triangular fibrocartilage.

Our next fracture is the Barton’s fracture. Not surprisingly, also a FOOSH mechanism. What happens in this case, as the person is landing on that extended wrist, the carpels are going to vector this way. And when they do, they can fracture off the posterior rim. That is what we are seeing right through there. I usually call this Barton’s posterior rim fracture to make life easy. The concern when we see the Barton’s fracture, If the fracture is by itself, it is not that difficult, it is not that big of a deal. The problem is what often happens once Barton’s fracture happens, the carpals dislocate. It is very common to see a posterior dislocation of the carpals in association with a Barton’s fracture.

let us be honest, this is a subtle injury in this case. What would make me concerned that I am looking at somebody that has a fracture? I am seeing distension of the pronator quadratus. Put that together, and it is the quadrator. The pronator quadratus fat stripe is being displaced, which is a good indicator of trauma to the area. I know that this is going to make me sound like a nerd, but realize that every radiologist has a favorite fracture, just like every orthopedist has a favorite fracture. My favorite fracture is the radial styloid fracture, and it goes back to being a car person.  Because if we look at old school vehicles, 1930s, 1940s, realize starters didn’t exist back in the day. In order to start the vehicle, you had to stick a big S-shaped crank into the front of the engine, and you had to manually crank the engine to get it to start. Very much like you see with lawn mowers where you pull start, just a much bigger version.

One of the problems is when you are cranking the engine, sometimes the engine would backfire and it would spin the crankshaft backwards, and when it did that, if that shaft spins backwards, it would come back and hit the person across the radial styloid. That creates what is known by a bunch of different names: Radial Styloid fracture, Chauffeur fracture, because well, hopefully, that is who was starting your car, Backfire fracture, because that is the Backfire mechanism, and then somebody had to throw a name on it, the Hutchinson fracture.

What do we see? We see a Radial Styloid fracture. Realize this is an intra-articular injury, there is going to be damage to the radial articular surface. The person is probably going to have DJD within two years because of that injury. Usually this is conservative management. We touched on this one before, but I am going to touch on it again, the ulnar styloid. This is that same Smith’s fracture patient. When we are looking at these, one of the things about the ulnar styloid, if the ulnar styloid is fractured, you must be worried about the integrity of the triangular fibrocartilage, and it is complex. That is where I am going to be wanting to get an MRI on a patient that has these styloid fractures. We are looking at a coronal on this one, and this is a coronal T2. We are starting on the palm side and working our way back. There is the pisiform. You can see the thumb side over here, and as we come back, there is the triangular fibrocartilage. It is a nice dense fibrocartilaginous disk. I can already tell there is a small tear there. I can see where this person has fractured their ulna styloid. It is not attached, and there is bone marrow edema, and they have damaged the ulnar attachment of that triangular fibrocartilage. We know that the TFC is one of the major stabilizers on the ulnar side of the wrist, so this can create some pain and disability, particularly on that ulna side. When we are looking at the triangular fibrocartilaginous complex, if we are dealing with younger populations, they will dramatically tear their TFC. This being the triangular fibrocartilage here, schematically represented. In older individuals, degenerative cartilage breakdown will occur. Not surprisingly, if somebody has a positive ulnar variance, that tends to impinge the triangular fibrocartilage a little bit more.

We saw a subtle TFC tear previously. Let us look at one that is a little bit more overt. We are on a gradient echo. Now this gradient echo is panning and now we are seeing some good resolution. This person has a negative ulnar variance, and unfortunately, because of that negative ulnar variance, have developed Kienböck’s disease where there is avascular necrosis to carpal lunate. But notice as we are looking at this, I can see some of the triangular fibrocartilage here, but it never makes the connection to the ulnar styloid. I am losing a large portion of it because this person has a complex TFC tear. When we look at it on the coronal T1. Notice there is part of the cartilage. Effectively, it has small attachment on the radius but it is lost most of its radial attachment. There is a large central perforation. The area going to the ulnar styloid has been damaged as well.

Video Presentation Placement: 55:36

What else can we injure? We start looking at the hand and wrist. This is where we start getting into a bunch of named fractures. The Scaphoid fracture, of course, in a younger population, if they FOOSH, they most commonly fracture the scaphoid. This tends to fracture in the mid portion in the waist. These are notoriously difficult to see. One of our rules is if somebody has snuffbox tenderness after a FOOSH injury, if the X-rays are normal, they are going to be put into a brace and re X-rayed in about one to two weeks. After 7 to 10 days, the fracture will show up more clearly. This one is subtle, but you can see the fracture on that oblique view.

The other thing that I do when I am worried about scaphoid fracture is, the standard wrist PA, medial oblique, and lateral. I am going to do a fourth view. I close the thumb in the fist, and then I bend to the ulnar side, and then I take a picture. What that does is help distract fracture fragments and elongate the scaphoid. Big thing on this one is do not confuse the scaphoid tuberosity with a fracture. That is not a problem. That is just where the blood vessel comes in. But with that ulnar deviation view, we can see those fractures more clearly, and the concern is what is the probability of avascular necrosis in these patients.

There is also a high frequency of non-union, which is exactly what we are seeing here. This is somebody who’s developed a SNAC wrist scaphoid, non-union advanced collapse, where we are seeing that there is a nice old fracture here and it is healed non-union with two pieces to the scaphoid. But everything is progressively rotating because there is no ligament to support for that area.  A more advanced case. We are seeing degenerative changes along that pseudarthrosis, and if you have a patient who is developing AVN or non-union, surgical options are going to be explored. AVN, non-union, are the two big concerns. Here is that patient that has the non-union scaphoid fracture. It is gotten nicely corticated margins. Everything is rotating, it is not where it is supposed to be, so that is the diagnostic criteria for a SNAC wrist.

What else can we break? How about a Triquetrum? The Triquetral fracture is usually an avulsion fracture on the dorsum of the Triquetrum, and it is a small little piece. This is one of those ones that has a name that I love as far as the finding goes, because when we look at the scaphoid, we know the scaphoid looks like a rubber ducky, and the Triquetral fracture is right behind the rubber ducky. That is sometimes called the Pooping Duck sign for the Triquetral fracture. You only see this on the lateral. It is a subtle finding.

Hook of the hamate. The hook of the handmade tends to fracture in racquet sports, particularly people who are maybe not great at racquet sports. What we are seeing is where the racquet is really impacting heavily into the hypothenar area. You cannot see these fractures on a standard wrist series. If I have a patient who has either hamate or pisiform tenderness, I do this view, it is the carpal tunnel view. Take the fingers, hyperextend them, shoot down the carpal tunnel, and then we can see the hook of the hamate and the pisiform are far more clearly. Can still be subtle, so we can look at advanced imaging. We can see on this MRI, there is bone marrow edema in the hamate, and there is a fracture line extending through the hook, and that is where it fractures. The hook of the hamate, the hamulus, fractures off.

When this person FOOSH, this person has dislocated their lunate. What happens? Because the extension of the wrist, it spits the lunate anterior. It is like spitting out a watermelon seed. Just spits the lunate right into the carpal tunnel, and because of that one of the symptoms that might present is automatic numbness of those first three digits as it compresses the median nerve. I know that nobody really likes the lateral views of the wrist. You can see this on the frontal view of the wrist, and there is a food sign, and that food sign is called Pie sign because as the lunate dislocates, it rotates, and it starts to look like a piece of pie.

Ligamentous injuries are the other injury that can happen to the wrist.  We know that we cannot see ligaments on X-ray, but one of the things that is beneficial is we can look at relationships. One of the relationships that is really important in the wrist is the scapholunate space. All of the intercarpal spaces should be pretty uniform, but if the scaphoid ligament is injured, then we are going to see an extra gapping in this area, and that extra gapping is called the Terry Thomas sign. That tells me that the scapholunate ligament is injured, and the diagnosis is Scapholunate dissociation. This being Terry Thomas, who is known for having the gap in his front teeth.

As that occurs, we can start to see rotation of the scaphoid-lunate-capitate complex. We can see what is called the Signet ring appearance for the scaphoid. As that scapholunate association progresses, the scaphoid and lunate get further apart from each other, until eventually the capitate can drop into that space, and that is a SLAC wrist, Scapholunate Advanced Collapse. When we are looking at this, this can be cumulative stress, this can be single event traumas. The big thing is this person is losing dexterity and they are losing grip strength because you need a stable carpal row to hold a really tight fist.  They are losing the ability to use their hands as effectively.

One of the other things that can happen as a late term sequela when we start looking at some of these ligamentous injuries in the wrists are things called VISI and DISI, Volar and Dorsal Intercalated Segmental Instability. We look at this on X-ray and we can see it on MR. The important thing is when we start looking at alignment in the wrist… I know that nobody likes the lateral view, but the laterals are important because we are going to look at two axes. We look at the scaphoid axis, then the lunate axis, and take the scapholunate angle. Look at the scapholunate angle, it should be between 30 and 60 degrees. If it is over 60, that is dorsal intercalated segmental instability, and if it is less than 30, that is volar instability. We can see just as a schematic representation how the lunate is going to change its position.

Video Placement Presentation: 1:02:44

In this case, when I look at this lunate, I notice that the lunate is pointing towards the backside of the wrist. It is pointing towards the dorsum. That tells me that this is dorsal intercalated segmental instability, which is usually a scapholunate ligament injury, and in this person, the lunate is tilted towards the palm side, the volar aspect, and that makes that a VISI. We are looking at carpal instability patterns, and these are patients that are generally going to be looking at hand surgeons for reconstructing the integrity of their carpals.

We get down into the hands. Breaking metacarpals and breaking fingers. We start looking at metacarpals. The first metacarpal has a tendency to fracture proximately, and if it is a simple fracture, it is a Bennett. If it is communited fracture, it is Rolando. I am unsure why they had to name these injuries differently. I am assuming two different people need a tenure and had to publish articles. A lot of times these are going to be intra articular fractures, and we are going to start to see quite a bit of DJD happen in that saddle joint of the thumb and create some difficulties.

The distal portions of the second through fourth phalanges. There is a couple of different names through here. Some people are very picky about making distinctions, some are not. But if we start seeing fractures of the distal portions of 2, 3, 4, or 5, how do those most commonly happen? You make a fist, and you punch something. Which metacarpal breaks depends on how you throw the punch. If you are throwing a straight punch, a good martial arts style punch, you are going to be hitting through the second or third metacarpals, and that is where we will see those second and third metacarpal fractures. One of the terms that is applied to this is a Boxer’s fracture, because that is somebody who knows how to throw a punch. Then, you get the person who watches too many action movies and roundhouse punches. With those roundhouse punches, the fourth or the fifth metacarpals impact, and they break. Those are sometimes called Bar Room. You will see both names used. Boxer’s and Bar Room. Just recognize that this is most commonly going to happen because somebody punched something, and one of our concerns when we start dealing with people punching.

This one is not so much of an incident sport because Bare Knuckle boxing is not allowed anymore. But what about hockey? Helmet comes off, throw the gloves down, start wailing on each other, like a good game of hockey. One of the things we see is the possibility of something called a fight bite, because when this person tries to punch their opponent in the mouth, it is a good chance their teeth can impact your knuckles, and if it does, and it breaks the skin, and maybe even violates the joint capsule, there is a concern for developing septic arthritis in the metacarpophalangeal joints because of that fight injury.

Gamekeeper’s thumb is not really so much an athletic sport; however, skiing is. In either case, regardless of which name you want to use, this is a hyper abduction injury of the thumb, and with that abduction injury of the thumb, it creates an injury to the ulnar collateral ligament at the metacarpal phalangeal joint. We can see a couple of things here. It is altogether possible to just tear the ligament. The X-rays can look normal but that is where maybe doing stress radiograph is important. You stress the finger over and take the picture, well thumb over. But the thing that tends to happen more commonly is this person will avulse a piece of bone. You can see the host site right through there, and that is the Gamekeepers or Skier’s thumb. Concern being this does destabilize the thumb. So quite often these are going to need surgical repair.

The other concern is that there is a possibility that this fragment can displace under the palmar aspect, and it can start to scar up some of the palmar tissue there. That is called a Stener lesion. Quite often Gamekeepers lesions are going to wind up getting repaired.

A couple other named fractures, when we start dealing with finger fractures, watch the finger move. How well do the fingers move? Do they flex? Do they extend? Is there smooth motion at all the joints? Well, because one of the things that can happen with flexion or extension injuries is we can see avulsions. In this case, we are looking at a volar plate fracture coming off that middle phalanx. This person might lack the ability to have good flexion at their PIP joints because they hyperextended it and avulsed the tendons. This case, they had to use a pen to extend the person’s finger, and that helped distract the fracture fragments.

The Baseball finger or Mallet finger. Mallet finger because it looks like a hammer, Baseball finger because I am about to catch a baseball and it catches me on the tip of the finger and it hyperflexes me at the DIP joint. What we are going to see is a fracture on the posterior aspect of the distal phalanx. One of the general concepts on management on these, if it involves less than 25% of the articular surface, these are generally conservative management. More than 25%, quite often they are looking at surgical management for those cases. If it is on the dorsal aspect of the DIP, that is a Baseball finger or a Mallet fracture. If on the volar aspect, that is the Jersey finger or Rugby finger. That is where you are grabbing somebody’s jersey as they run and it hyperextends the tip of your finger at the DIP joint and it avulses that flexor tendon. Same rules apply. 25% or less is usually conservative, over 25% of the articular surface looks at surgery.

The last of the finger fractures all the way out at the very tip of the finger is the ungual tuft. That thin spongy bone at the end of the finger is very susceptible to crushing injuries. One of the concerns is quite often you can see nail bed injuries with these because it is a crushing injury, and this person often has just won the purple fingernail award. Now there is a slight increase in infectious rates if somebody has an ungual tuft fracture, and they have a subungual hematoma because that does qualify as an open fracture. That is something that will have to be monitored to make sure that this thing is healing and not starting to develop an inflammatory reaction.

That takes care of Upper Extremity Injuries Part 2. When we come back, we will be getting into Lower Extremity Injuries.

[END]

Section 08_ICSC03 – Lower Extremity Part 1 – Foot and Ankle
English Direct Download PDF – 08_ ICSC03 Section 8 LowerExtremity

Instructor Dr Chad Warshel
Video Lesson: 01:05:59

It is time to work our way down to the lower half of the body and start dealing with the lower extremity. When we did the upper extremity, we started proximal and went distal clavicle, to shoulder, to elbow, to wrist. I am going to do the lower extremity a little differently because the knee is a huge topic, and the knee is such a very large topic, I want to make sure that I devote an entire hour to it. We will cover some general topics, hip, and ankle in the first hour and then I am going to tackle just the knee in the second hour.

Let us start off with a couple of general topics because these can happen anywhere, upper, or lower extremity. There are soft tissue injuries, the first place to go is myositis ossificans. One of the facts about the term myositis ossificans is implies a tissue. Myositis ossificans says to me that this is something that happens in the muscle. Well, it does, but the problem is it also happens in not muscle, because of that, a better term than myositis ossificans is to call this heterotopic ossification, which basically we are saying their bone formation in injured tissue. We will see this, the original descriptions for this were muscular, and we would have somebody who had a deep muscular hematoma. The quads are a notorious location for this to happen. We can also see the glutes, but quads glutes, hams, and we would see a trauma happen to the muscle and a hematoma would form. Hematoma is an actual blood pool, and so there is a cystic pool of blood inside the muscle. For that cystic blood pulled to heal, it starts to heal from the outside and it heals inwards, filling in that blood pool.

In some cases we will see, instead of healing the way it should be creating muscular tissue or by extent ligament, fat, any of these other tissues that it is in, what we see is the tissues undergo a metaplastic process. It is not a neoplastic process. It is a metaplastic process. It is not a cancer, and it is just forming something that is not supposed to. We will see this start to form bone. When we see this bone formation, it forms very much like the hematoma heels. It starts more mature on the outside and then it gradually fills in. One of the problems that we run into, particularly for dealing with under 25-age range patient, is that there is something else that creates bone in the soft tissue. That is something else is an osteosarcoma.

One of the things that is on our differential list when we start dealing with myositis ossificans is, are we looking at myositis ossificans/heterotopic bone, or are we looking at an osteosarcoma? Because there is a drastic difference in management between those two things. Well, we use this thing called the zone phenomenon to help us figure that out because when we look at this heterotopic bone formation, again blood pool, hematoma, so it starts with that blood pool and the more mature bone is on the outside border, and then it heals inward. Then once it is healed, it is solid mature bone, and the solid mature bone really does not look that much like osteosarcoma. Osteosarcoma looks like immature bone, but it starts on the outside and works its way in. Whereas, when we look at an osteosarcoma, an osteosarcoma, you are starting from one cancer cell and then spreading out from there. So, we tend to see more mature bone centrally in an osteosarcoma, and then less mature bone as we move out peripherally.

This can be a difficult call when we are looking at a radiograph unless where it is something like a CT might be useful if we are not sure, is this a heterotopic bone or is this an osteosarcoma? History would also be nice too, but when we are dealing with osteosarcoma, we are dealing with the under 25 age group and really, we are dealing more in the teenage children. We know the teenage children are not always necessarily super reliable in history, and they also tend to get injured a lot if they are athletic teenagers. Otherwise, when we start to see this particularly in adults, it tends to be much more mature in appearance. We can see like in this case, there are some nice bone formation in the soft tissues right in through there. Now, this would be a true myositis ossificans because this one is in the muscular tissue. It does not just form in the muscle. It can form in any soft tissue. One of the places that this is a very common finding outside of the lower extremity is up in the shoulder in somebody who is had an AC separation and AC injury. We can see where this person has had a grade 3 acromioclavicular injury and notice all the bone that is kind of hanging down off the clavicle. Well, that is all heterotopic bone, and it quite often fills itself in along that pathway of the core called clavicular ligaments. So, really interesting phenomena there as that metaplastic process, but it is also fairly easy to identify when we know that there has been trauma. One of the other places that we will see this is and it creates an interesting thing is in the lumbar spine in patients that had transverse process fractures. It is possible to see something called lobs lumbar ossified bridging syndrome where the hematoma that forms in the paraspinals, the QLs and the intertransversarii, can ossify and we will start to see bone bridging between the transverse processes.

The second of the soft tissue lesions, the generic heading is the Morel-Lavallée lesion. With this particular injury, it tends to be something that we see more commonly in the lower extremity, but it can happen in any soft tissue. The concept on this is, we are looking at something called internal degloving. There is a force that shears across the soft tissues, and as it shears across the soft tissues, it separates fascial planes. Quite often, this happens at the junction between subcutaneous fat muscle or inside subcutaneous fat layers. What happens is, when that shear occurs, it creates a pocket, and that pocket fills up with fluid. First as a hematoma and then eventually it becomes blander as the body breaks down the blood products.

If this lesion gets compressed early on, it goes away because the tissue is still raw. If you compress it, it will squeeze the fluid out. It will be resorbed by venous and lymphatic drainage, and then the raw tissue will heal together with some scar tissue, of course. The problem is, if it is left alone, once that fluid-filled cysts starts to form and it stays there eventually develops a fibrous capsule all the way around, and this person is kind of stuck with a water balloon inside in their subcutaneous tissues. If that is something that becomes bothersome, then it is going to have to be surgically removed. Early management on these is an important thing. One of the big clues is when you look at this patient, you will notice superficially, that there is the other can be a soft tissue mass, and it has that very fluidy consistency.

There is a really interesting paper on this but because of copyright issues, I cannot post it in the notes, but if you Google N-E-J-M, New England Journal of Medicine, lumbar, Morel-Lavallée lesion, there is an interesting paper from a chiropractic perspective where I believe the gentleman fallen down. He had sheared the tissue across his lower back and upper sacrum, and he created a Morel Lavallée lesion there. You can see it clinically, so I recommend you take a quick second to Google that paper. As we start looking at these lesions, let us go ahead and look at one of these in live action.  We are looking at a knee in this case. You know how things come in in your office. They usually come you get the same thing three or four in a row. I had the same thing come in three or four times in a row knee Morel-Lavallée lesion, say that three times fast, it rhymes.

Let us look at what is usually happening here. Knee is a great location because if the knee versus a dashboard or falling down, this could be something like sliding into a baseball home plate or something like that, to create that shear. The greater trochanter is another fantastic location to see this. It can sometimes be confused with trochanteric bursitis. So, as I am looking at this one, okay, I know that when I am looking at MRI, I always start on fluid-sensitive sequences because I am looking for that angry tissue. I am always looking for something edematous. Let us start off on the coronal proton-density, fat-suppressed. I am going to start in the front because starting in the back of the knee always drives me nuts. I will start in the front, so superficial skin, and I see the patella.

I am seeing some edematous changes in the superficial tissues through there. They keep going in further, I am getting into the knee. I do not see any internal joint effusion, but I see a small area of bone marrow edema on the posterior aspect there, and then coming out the back side. Then I am going to kick over and we will talk more about knee MRI in that second hour. Now, I am going to kick over to the axial. Here, I am looking at a gradient echo, which is also a fluid-sensitive sequence. We are starting in the femur, and we are working our way down. We are starting to see the quad tendon. If you remember, we did see that there was some soft-tissue edema in the inner medial aspect. As I am looking at this on the axial, yes, there is some fat stranding in the sub-Q fat, but more importantly, there is a fluid-filled pocket here. It is not in a location where I am expecting prepatellar bursitis. It is not in a bursal location. It is separating some layers of fat here. That is what tells me that this is a Morel-Lavallée particularly, this was an auto accident and this person had knee versus dashboard. So, in this case, this one does not have a really thick heavy fibrous capsule to it. There is still a lot of Sub-Q edema. This is a more acute phase lesion and this would be a fantastic time to get this thing detected. Get it compressed. See if we can keep this from becoming a surgical case.

Morel-Lavallée lesion, it is one of my favourites It is a lesion, I had never heard of it, until about 10 years or so ago, then I saw a lot of them coming through my reading practice, and just an interesting phenomenon.

Another thing that I want to talk about is predominantly a lower extremity topic, but it is not isolated to just the lower extremity, and that is stress fractures. When we start looking at stress fractures, it is going to involve the lower extremity more because this is something that we tend to see in those lower extremity, repetitive sporting events, particularly things with running. When we look at stress fractures though, we actually break stress fractures into two categories; fatigue fractures and insufficiency fractures. Usually, we use fatigue fracture and stress fractures synonymously. To give you what is the difference between the two are a stress fracture is an abnormal stress on normal bone that then fails because it is overloaded. This is where we see a lot of repetitive stress injuries particularly, marathons, and running events, fantastic for creating stress fractures. Insufficiency fracture, the definition is actually very similar, just flopped. This is going to be normal stress on abnormal bone resulting in mechanical failure. Now, we did not talk about pathologic fractures through the course of our injuries, but does not that sound like a pathologic fracture? It is normal to stress on abnormal bone resulting in failure. Well, an insufficiency fracture is a pathologic fracture, but not all pathologic fractures are insufficiency because the idea here is normal stress.

Video placement: 13:08

This is one of our classics, grandma, grandpa’s walking down the road steps off a curb and breaks a hip, or compression fractures of vertebrae. That is where we are talking about an insufficiency fracture, as opposed to grandma or grandpa fell, and they are osteoporotic, so they fracture their hip. That would be more of a traumatic pathologic fracture. Now, one of the problems that we have to deal with when we are looking at stress fractures or stress fractures on my differential, I have an athlete, that athlete has really started ramping up their activity to get ready for an event, or to try to push into the next class, and because of that overdoing it, they wind up creating mechanical stress through the bone, and the bone starts to fail.

The problem is, we will not be able to see anything on X-ray for 7-10 days, if it is an extremity; for 21 days if it is in the axial skeleton. That is something that we must be aware of, how long is that pain been there? You know, I really started ramping up my activity. I want to do a want to go from a 5K to a 10K, so I am running a lot more. It has been bothering me for about the last 5 days. What am I going to see on an X-ray? Bones, and it is going to be a fairly normal skeletal structure. That is when we have to be aware of that particular phenomenon, 7 to 10 days in extremities; 21 days in the spines/axial skeleton.

Where does that plays a role is? Pretend I am not a heavily athletic individual, but I decide to go off on a 5-mile hike. If I go off on a 5-mile hike and I am about 4 miles into the woods and I am already getting tired, and I run across a bear, I am going to be turning myself around and running the other way. I am running for miles, and I have not run that far in a lot of years. This is something, that is an abnormal stress on my relatively normal bones, and my bones might fail. If I came into your office the day after running that much with all this pain, what are we going to see radiographically? Nothing.

Now, what do I do for a living? I, either A, talk to my computer teaching webinars or B, I stand in front of a class of chiropractic students teaching them. So, I walk around a little bit, but could I do my job sitting? Sure. In this scenario, we would call that a weekend warrior athlete.

Let us do some conservative management. If we need to, we will re-X-ray in a week. What if we are dealing with a division 1 athlete? Somebody whose scholarship rides on their athletic performance or a professional athlete whose pay check is dependent upon them performing? That is somebody where we are probably going to go above and beyond and really try to make a diagnosis. That is where we have a couple of options. We can look at bone scan, or MRI. A bone scan is not going to be my first option for this. I would much rather get the MRI. It is going to let me know if there is a stress fracture, or whether it is not a stress fracture, but there is a soft tissue injury. I would rather go that direction. Something else that is an important consideration if you are dealing with pediatric athletes. One of the other things to consider in the lower extremity is they can have a very similar presentation. A gradual insidious onset of pain in the lower extremity bone. Osteoid osteoma can have the same presentation. So, that is one of those things that makes it worth imaging to see whether it is consistent with a fatigue fracture? Is this an osteoid osteoma? Do we need to take it to the next level? Some of the common locations where we will see these different kinds of stress fractures, we already talked about the lumbar spine and the pars hyper extension sport creates, we are seeing the stress fracture that heals non-union. But notice when we look at this entire list, lower extremity, lower extremity, lower extremity. Most of these lower extremity because that is where there is repetitive sports come into play.

Is it possible to see the upper extremities?   Coracoid can stress fracture in somebody who is doing repetitive shot gunning so trap shooters, skeet shooter things like that. The hook of the hamate look, we have talked about previously in racket sports. One of the problems with stress fractures, if we leave a stress fracture alone and particularly, we have a heavier duty athlete, who is going to push through the pain and keep doing their event, that stress fracture can eventually become a complete fracture. That is where that gets to be a problem. So, what do we see? If we are in, okay, it has been bothering him for two weeks and now they are finally come in and to see you. What am I going to see? Generally, I will see a faint white line running perpendicular to the long axis of bone, or perpendicular to the axis of force when we see a calcaneus, okay? We might see some periosteum lifting. It compares, we might see some periosteum lifting like we see this is a young ballerina. Periosteum lifting, nice white zone coming across the tibia and realize shin splints are a prestress fracture.

When we start talking about shin splints, shin splints if you keep doing that activity, it eventually becomes a stress fracture. That is where we can start looking at, when do we need to start imaging these? Another great candidate of people forgetting physique rashers, stress fractures, and military recruits. Let us take the average 18-year-old who is been spending a lot of time on Xbox and joined the military. All of a sudden, they are marching and running where they were not expecting to. What do we see? We can see where there is this white line running perpendicular to the long axis of the trabeculae. Remember, when we are dealing with that acute phase, so attendees in extremities, what am I going to see radiographically? Normal bones. Do not forget too, when you have got somebody who is got focal pinpoint tenderness it hurts right here, and that leg is a long, that is a long study. Put something on the X-ray that says, “look, here, this is where the problem is.” Maybe that will help us Identify some more subtle lesions.

Now, in this case, this was followed up with a bone scan. On the bone scan, we can see that at that area of maximum tenderness, there is some increased uptake. So, we do not see on the X-ray; the X-ray is normal. But on the bone scan, we do see that radiopharmaceutical increase for a stress fracture. I introduced this patient to you before. This was the patient who had decided to do a marathon and increase their activity started having sacroiliac pain. X-rays were normal. They got a CT instead of getting an MRI. On the CT, we can see the little sclerotic focus because the thing is with marathoners there kind of notorious for getting a vertical sacral stress fracture. We can see on the MR there is the halo of bone marrow edema on the T-2 that confirms that is a stress fracture.

Watching a couple of live demo DICOMs here. I am starting off with a navicular, and we will be talking about the Ottawa foot and ankle rules here in a little bit. This would be somebody where we would be considering running some imaging. We have a patient who has increase their activity. With that increased activity, they started experiencing quite a bit of foot pain. We are looking at a foot MRI, and I start off on a fluid sensitive. This is a proton-density fat-suppressed. We are in the ankle. You can see there is tibialis anterior. There is Tom Dick and Harry. There is the Peroneal.  As we come down through the ankle mortise, getting down into the foot, all of a sudden, the navicular is lighting up. We are seeing substantial bone marrow edema. The X-rays are normal in this case, but we can see that bone marrow edema with normal X-rays. This is a navicular stress fracture.

This next case, again, I am unfamiliar with the history aside from knowing that this was an athletic individual. The person was having hip pain that was getting progressively worse. They were still doing their activity. It is getting progressively worse. Bone density was adequate, and as we look at the fluid-sensitive sequence, again, we are looking at a coronal stir. What do we see? There is a zone of impaction here on the medial side of the femoral neck and it is surrounded by marrow edema. All of that is very consistent with a stress fracture. Okay. Now, from there we are going to get into the pelvis. Now, as we start looking at the pelvis, realize, when you think back to all the pelvic fractures that you learned in chiropractic school, there was a bunch of things that we learned. I know because I still teach them, but to generally not ambulatory chiropractic patients. If this is something that we are going to happen, if you are a field side doc, this person is going to be in a world of hurt.

This is not somebody where it is going to be coming in and we are going to take an X-ray and find out they have got a malgaigne or a bucket handle, but just to kind of review some of these fractures. So, the malgaigne injury, we are seeing where the person goes through the SI joint, the iliac or the ilium, and then through the same sided superior and inferior pubic rami. The bucket handle goes through the opposite side. Again, we are not going to see these in the acute phase. Again, even if we are sports field side, if somebody were to have this kind of injury, A, I would wondering how they got it, but B, okay, this person is going to be getting transported because they are going to be dealing with some blood loss. The straddle fracture goes through the superior, and inferior pubic rami. The unilateral straddle fracture just goes through one side. The duverney fracture takes off the illiac wing. Pubic diastasis would be abnormal; widening of the pubic symphysis. Then a sprung pelvis would be diastasis plus diastasis of an SI.

Video placement 23:46

I just wanted to cover those just to refresh your name, or refresh your memory on the names, but again, we are not likely to see those. What we are going to see though, hopefully, I will give you a second to look at this X-ray and see if you can identify what pathology is going on with our patient here.

Answer: Hopefully you said, ankylosing spondylitis.

Our patient is working on bilateral sacroiliitis. It is getting closer to the point of SI joint fusion. Just want to throw something else up is a little bit of an eye test. Now, what else can we break in the pelvis? Something that maybe is a little bit more realistic, acetabular fracture. With acetabular fractures, again, motor vehicle accidents are very common for these, but we can also see them in any event. The knee hits something and drives the femur backwards because again, convex femoral head into the concave acetabulum, the acetabulum tends to fail.

There are two major acetabular fractures, the dashboard, which we are more likely to see. The blowout, I am not even going to really cover aside from just the name. The dashboard fracture is a knee versus dashboard or knee versus a mobile object. It drives the femur back and it runs into the acetabulum and breaks the posterior acetabular wall. The blowout fracture is a side-impact style injury. Something hits the greater trochanter and drives it medial and it blows up the pelvis. It is a very unstable pelvic fracture. The dashboard fracture though, this is something that can be ambulatory. That can be coming in a couple of days or a couple of weeks later. Now, with the persistence of hip pain. What we see when we are looking at this person’s radiograph is there is a subtle line running through the posterior acetabular border here. We know that the pelvis is a very complicated piece of anatomy. So, anytime, is that real? Am I making things up? I am not sure. Get a CT.

CT is going to give us that bony definition and here, I can see where this person does have that posterior acetabular border fracture. Very consistent with a dashboard injury. I am also going to be worried about the acetabular labrum in this patient. Any time we see acetabular injuries, the labrum is one of our considerations. Now, other things that can happen as far as pelvic injuries, particularly in getting back to that dealing with pediatric sports up through 16-18 years of age. We can also start to see some avulsion in the pelvis. I like to use ankylosing spondylitis patient here, just as an example. There are three possible avulsion sites. Well, there is a bunch, but there are three big ones. The ASIS, the AIIS and the ischial tuberosity. Those are the big three places where we are going to see avulsion injuries happen.  These avulsions happen in one of two ways, either A, single event. There is one event, pushing person, really pushes and it avulses the bone.

Possibility two, and this one’s a little bit more likely, is chronic repetitive stress. Pull a little bit. Pull a little bit, and then eventually they avulses. When we start looking at these, so the big three, ASIS, AIIS, and initial tuberosity, so, with the ASIS, now, this is one. When we see those fractures occur, they tend to move inferior because the muscle is pulling the piece down. We can see whether this ASIS is displaced inferior, but it is also healed at this point. Go figure, this person might have a change in mechanics with the change in orientation of the sartorius, and they would have a palpable difference in their ASISs.

Pediatric patients, we can see the displacement of the AIIS, and one of the questions that comes on these is, does this need to be surgically repaired? It depends on how much distraction there is. This is a late sequela for the ischial tuberosity. Ischial tuberosity avulsion is due to the hamstrings, and not surprisingly, this is something that we can see in equestrian sports. One of the things that happens with those hamstring avulsions, again, is chronic repetitive stress where it avulses a little, avulses a little. Well, it can elongate over time, and what we are seeing here is we see a normal ischial tuberosity on this side. We can see the overgrowth of the ischial tuberosity on this side. That is something called a rider’s bone. Not surprisingly called a rider’s bone because it is seen in equestrians.

Our next injury up is an interesting one. It goes by a couple of different names. Probably, the more appropriate name is athletic pubalgia. It has been called a sports hernia in the past. Really sports hernia is a term I would probably try to avoid because when we think hernia, we think something poking through something else. There is not really a true herniation in these cases. What we are seeing is we are seeing muscular injury. It is typically in somebody who does a rotation of the torso. They do a rapid deterioration. So, baseball pitchers, American football, quarterbacks, hockey goalies. Really, any hockey players, because when you start looking at slapshots can do this. The big thing that is kind of a close. We have the person that does this twisting event and all of a sudden, they start dropping in performance. They cannot hit the puck as fast as they used to. They cannot hit the 90-mile an hour fastball anymore. It is dropped. They have dropped 10 miles an hour off their fastball.

They are starting to get some pain in the groin. What is happened is they have damaged where some of the small muscles are inserting into the pubic rami. They have damaged the rectus abdominis insertion, the origins of the pectineus, the gemeli and some of adductors, and it takes away a lot of that rotational force. So, when you have that pain in that area, it is down towards the pubic regions and you are starting to lose a lot of your strength. Let us get an MRI to see what is going on. Keep in mind, that this could be an inguinal hernia. It mimics an inguinal hernia, which is where it got its name sports hernia, but they do not actually have a hernia. There is nothing of those. There is no small intestine poking its way through or anything. So, they get checked for a hernia. They do not have a hernia

Then we need to consider that this is actually a muscular tendinitis issue. So, we need to go for an MRI for a case like this. What we are going to see is we evaluate an MRI for this patient. We are going to get a pelvis MRI because that will show us all the pubic region, and there is a possibility of seeing some increased signal in the pubic rami, but much more likely, notice that there is this edematous change in the muscular tissue here immediately adjacent to the superior ramus. Pectineus, gemeli, adductors, rec fem. Rectus femoris reports will be a little bit higher up more in through this area. But we will be looking to see, is there any signal like we are demonstrating here in this case in pectineus? This person is going to end up having to rest and then rehab back with those rotating muscles. One of the other things this brings us to, so as we are working our way down through the pelvis, something else that can create pain in the hip or anything or a region is the acetabular labrum. Now, it would be the whole job of the acetabular labrum is very similar to the glenoid labrum in that it deepens the socket, creates additional stability, and helps guide motion. Now, we can see a couple of different things that will involve the labrum. The first possibility is labral tears. If you get somebody who is in an impinged position flexion and abduction, adduction, internal-external rotation, they can impinge on that anterior acetabular labrum and create labral pathology.

One of the other things that we can see is, okay, does this person just tear their labrum, okay, or do they have femoroacetabular impingement syndrome. Not surprisingly, we start with X-rays and we are trying to figure out why somebody has hip/groin pain to see if there is something going on. Now, I am going to go through the labral path and then we will see the X-ray stuff. So, if I am worried about the acetabular labrum, okay, hockey goalies, are big candidates for this because of all the time spent crouching. Drop it on the ice and move their knees to block pucks, but anybody who is doing a lot of repetitive hip activity like that. If I am worried about the labrum, I know that I am going to go to an arthrogram. That is something where there are, no if’s, no second guessing, no but’s, I am going to get a hip arthrogram because it is going to be up to 60% more sensitive for labral pathology. That is the first thing; I am going to make sure I get the arthrogram.

Video Presentation Placement: 33:07

What would make me suspicious aside from the history? Things that I might see on the radiographs. Some of the things that we will see in radiographically in patients with hip pain, something that for the longest time was just considered an incidental, the finding is Os acetabulum. This is an accessory ossicle that occurs around the acetabular margin. It was okay. You got a nice acetabulum. Yeah, you, got an extra bone. Instead of 206, you got 207. Well, one of the things that have been shown and realised femoral acetabular impingement syndrome is a newer diagnosis. Newer being in the last 20 years. This had shown that you look at epidemiology, patients with an Os acetabulum have an increased incidence of femoroacetabular impingement syndrome.  Make sure that it is not a fracture. It is got smooth all-around a coordinated margin. So, that really lets me know I am not looking at something broken. They can be a little bit harder to discern. This one’s on a more posterior aspect of the hip so it is hiding a little bit. Maybe can even look like an osteochondral fracture, and I would end up having to get some advanced imaging to evaluate that. What that does do is it brings us to femoroacetabular impingement syndrome, FAI. Now, again, newer diagnosis, this is a last 20 years kind of diagnosis. What was been noticed is that the acetabulum or the femoral head/neck can sometimes have variability in appearance. That variability in appearance actually predisposes to damaging the labrum.

There are two kinds of femoroacetabular impingement morphology. Just because you have the shape does not mean you have the FAI, but predisposes. So, the first type is the camp type. What makes the camshaft? Well, it is got an oblong surface to it. That moves the valves in your engine. See? The other kind is the pincer type, a nice crab claws. A good explanation of a pincer. Now, what are we talking about? and now I know what a camshaft looks like and that blue crab claw and when we look at the cam time as we are looking at the AP view, notice that there is a small lump on the lateral aspect of the head/neck junction, and sometimes it might be more on the head. That is the cam type. The problem is that this person is going into flexion and abduction. That little ridge is going to run into the acetabular labrum that lives right here and damage the labrum.

The pincer type is usually an overgrowth of the acetabulum. This can also be something that is acquired as somebody develops DJD of the hip joint. The osteopathic growth can create a problem on Os acetabulum, and can deepen that acetabulum. You can imagine as this person’s going into flexion abduction, that is going to impinge on their femoral neck, and that impingement will potentially damage the labrum. These are patients that have a find camera pincer type, we can always try conservative means, but if I am considering surgery because the pain is not going away or not responding, I will get that MR arthrogram to better evaluates the labrum.

Video Presentation Placement: 36:19

Something else that we as radiologists all of a sudden said was an incidental finding, what they do, pitts, synovial herniation pits. It is really common in the femoral necks to find these little circular loose bits. We always say, “Yes you got pitts pits.” Well, after femoroacetabular impingement syndrome was discovered and people started putting together a couple of different things and discovered, “Oh, we see pit synovial herniation pits much more commonly in patients with femoroacetabular impingement. That is another one of those little subtle clues that if my patients got hip pain, I want to make sure I am checking out that hip very carefully. Then we are coming out of the acetabulum. We are coming into the proximal femur.

Realistically, when we are dealing with most athletic events, hip fractures are not terribly common. Now, as to risk, as we are seeing more extreme sports, we are seeing more significant bone fractures. Femur is the strongest bone in the body. The tibia is the second strongest bone in the body. Well, if you are doing extreme sports, it is more likely to fracture. Typically, when we start thinking about things like hip fractures, usually we are thinking about grandma and grandpa. Yeah, we are thinking about our older patients or elderly patients. That is who typically is going to fracture their hip because it takes a lot of force. In young people, mostly we are dealing really severe forces, big falls from big heights creating these problems. Fatigue fractures are a possibility stress fractures, but generally, we are thinking about the older individual.

Just as a reminder of some of the different locations, when we start talking about these proximal femoral fractures, one of the things we do is divide the fractures which from intracapsular versus extracapsular. This is more for the orthopedist than it is for the conservative care clinician because if there is a fracture in these locations, it helps the surgeon decide on total hip replacement or dynamic hip compression screw. So, the location sub-capital, mid-cervical, basicervical, those are inside the joint capsule. Trochanteric, intertrochanteric, sub trochanteric. As we look at those fractures, there is all of them because it is a nice pretty colourful thing, the one that makes me nervous. Elderly patients, we will see the other hip fractures, the one that makes me really nervous is the lesser trochanter. If the lesser trochanter comes off, that is a huge red flag for pathologic fracture. Whether osteoporosis or metastatic disease or something, malignant, the lesser trochanteric fracture is not a common thing and is not generally good news for the patient.

What are we worried about when we start looking at those fractures? The reason that these tend to be operatively managed is because of avascular necrosis and non-union. Notice, I have not really talked about like midshaft fractures on femurs. I mean, those are straightforward. That is going to orthopedist and they are going to put an intervention and they are nail in. I am not going to worry too much about diagnosing some of those fractures. All that being said, the hip fracture that I do worry about seeing, and this being much more likely is SCFE, slipped capital femoral epiphysis. What we are seeing here is we are dealing with an adolescent patient, and typically, this is an overweight male and they start complaining about knee pain.

As they are complaining about knee pain, they are starting to develop a limp. They usually have a bilateral or they start to develop a trendelenburg gait where they are getting that hip thrust. But what is interesting is they usually complain about knee pain. Well, we start evaluating the knee and we cannot recreate the pain. Time to check out the hip and that lights the patient up. There are a lot of things like pediatric hips, Legg-Calve-Perthes, avascular necrosis. SCFE, slipped capital femoral epiphysis, this is a type 1 Salter-Harris fracture. Septic arthritis is kind of notorious in pediatric hips. I tend to be pretty liberal about X-raying pediatric hips. This is a pretty common disorder. It is the most common hip disorder in adolescence. One of those little factoids that always shows up on board exams. Children are going to have a limited range of motion and have pain when you start evaluating the hip. The big thing is, what we are looking at here, what is an SCFE? It is a type 1 Salter-Harris fracture. The general thought on this is because we are dealing with an overweight child this is almost kind of like a stress injury. Quite often, it is going to be tied in with the pubescent growth spurt when they are growing really quick and the growth plate gets a little weaker. We can see it is predisposed to other conditions. If there are underlying metabolic bone diseases, those children are more likely to get these, but realistically, it is the overweight that is hitting the overweight child, that is hitting their growth spurt. So, what do we see? Really important to us, that when we start looking for pediatric hips and really all hips, make sure we are doing the right X-rays. The number of times that I see somebody default to an AP pelvis on a patient with hip problems, drives me a little nuts. So, you can do a pelvis factual out, but make sure you also get dedicated hip radiographs.

Dedicated hip films include an AP with 15 degrees of internal rotation to take out the inner version. Then the single most important view is the frog-leg because that is where most pathologies really going to show up. What do we see when we are looking at an SCFE case? What am I going to see when I start looking for SCFE? The femoral head starts to get shorter, and so femoral shaft, femoral neck, and femoral epiphysis. That femoral epiphysis rotates in two directions, either posterior or posterior medial. As it does that, if it goes straight posterior, it gets the epiphysis to look shorter. If it goes posterior medial, that is where we start looking at one of those lines. Remember, all those lines that you had to memorize at some point in time, and there is Klein’s line along the lateral aspect of the femoral neck, and it should intersect a decent portion of the femoral head? If it does not, that is one of your big indicators that you are looking at an SCFE.

Video Presentation Placement: 42:47

The big deal is the frog-leg is the more important view because, on the frog-leg, we are going to see that posterior rotation that is very consistent with an SCFE. This child can be taken off weight-bearing because the more they wait-bear, the more the slip is going to occur. The greater the probability of negative consequences, such as avascular necrosis, and severe DJD. These are the kind of children that if you get a child that is got a Legg-Calve-Perthes or SCFE, sometimes these children as well as they become adults, they might be getting hip replacements in their 30s because there is so much degenerative change going on and they are having such difficulty with quality of life. This is what is typically going to be done for SCFE cases is they are going to drive screws through the femoral neck and into the head. The idea being they want to lock this in place. They are not going to try to reduce it because it is difficult to reduce to get it back in a normal position, then screw it into place. So, they leave it slipped and screw where it is, and that is why off weight-bearing, and they are in surgery pretty quick on this. The history of doing SCFE surgery is kind of interesting. Originally, the first surgery they tried to do; they drove one central screw through the femoral neck into the head. One of the things I noticed was that the femoral head could unscrew itself and can create more problems. So, then they started to use three screws, and then, they cause avascular necrosis because they were replacing so much bone marrow. Bone marrow, space on the head. So now, they will usually use either one eccentrically placed screw or two screws and that locks things in place. What is the downside of SCFE? The big, the long and the short are DJD. These patients are set up for premature DJD. Hip replacements in their 30s or 40s are not uncommon in children that have SCFE or Legg-Calve-Perthes, or any of these pediatric hip disorders.

Video Placement Presentation: 44:51

We are going to jump from the hip. We are going to completely skip the knee and we are going to go down into the leg and foot. The second hour is going to cover the knee injuries. Just the list of the things we are going to talk about so that you can see what is coming up. Now, one of the things that is a huge, massive topic when we start dealing with sports injuries is who do we X-ray?

It would be nice to X-ray every part that has a problem, but I know that that is not evidence-based. I know that that is not safe because there is no such thing as safe radiation. There is a problem with too many negative studies that make radiologists miss things. So, some smart people out of Ottawa, particularly a doctor who ran the group, named Dr Ian Steel, started looking at emergency department admissions and they started comparing a whole bunch of physical exam findings with radiographic findings to see what correlates. In doing so, they created something called the Ottawa criteria. There is a foot and ankle. There are also other criteria for the knee. The nice thing is, by looking at Ottawa criteria, if we have a patient who does not meet Ottawa rules if this person has a less than 2.5% chance of having a significant fracture.

We do tend to be cautious and little children, and this is only for acute injuries. It is a very useful tool to help us decide who we imagine. The Ottawa rules are, OR rules, If you look at this from a Boolean logic standpoint. If A or B or C or D or E is positive, then you take a picture. If none of those things is positive, the patient has a less than 2.5% percent chance of having a significant fracture. So, what do we look at, okay? The first part is palpatory. Holcomb, and what you are going to do is you are going to palpate along the posterior Ridge, distal 6 cm of the tibia and the fibula. You are going to go distal 6 centimetres all the way down to the tips. this is one where when I am teaching to an American audience, I usually have to explain to them what 6 cm is? Has a ballpark, it is not 100% accurate because it depends on hand size, but the width of your hand is about 6 centimetres.

Next, I am palpating a distal 6, posterior aspect tip, fib down to the tips. Next squeeze, the fifth metatarsal base, that is the thing that is this most likely to be positive because the fifth metatarsal base fracture is the most common fracture in inversion injuries. Then I squeeze the navicular. We already saw that navicular stress fracture earlier. what else do we do? We do the walking rule, and in the walking role, can the person walk four steps?  four steps are 1,2,3,4, and it is regardless of limping. So, good foot, bad foot, good foot, bad foot. If they are willing to touch the floor and put any weight on it, that is not positive. They have to be unwilling to touch the floor and it is both at the time of trauma and at the time of evaluation. realize, If you are on the field, that is really the same time, but if this is somebody who injured themselves on the weekend and was able to walk in on Monday, that is another story.

what kind of things creates pain and problems down in the lower extremity? this first thing is not actually a fracture. This first thing is a confounder, the Os trigonum. Now, this is an accessory ossicle in the ankle and it is named in a way that makes sense at the junction of three parts; the tibia, the talus, and calcaneus. This extra little piece of bone can be a problem in a couple of categories. Ballet dancers are kind of notorious for being a problem for ballet dancers. Sometimes with sprinters, and then because well, my wife is 4′ 11”, short people. what do ballet dancers, sprinters and short people have in common? They have to stand on their toes a lot. So, with that repetitive plantar flexion, as they go into plantar flexion, the calcaneus comes up and traps that ossicle against the tibia.  Over time that can create a stress reaction. We can see stress fracture of that area, and that is where that becomes Os trigonum syndrome.

try to get a ballet dancer to quit doing dance. Try to get a sprinter to quit doing sprints. Try to get a short person to grow a little bit. So, these are generally going to be an asymptomatic issues, and if they become symptomatic, quite often you are looking at prophylactic removal of that ossicle. We can look at the MR to see if there is a stress reaction. In this case, there is some edema surrounding that ossicle. this next thing is not actually an X-ray diagnosis. There is a clinical diagnosis of Sever’s disease, calcaneal apophysitis. Very common in athletic little children.  Heavy heel strike and it creates inflammation in the calcaneus. normally, when we start talking about apophysitis, if an apophysis is sclerotic or flat fragmented, that means they have apophysitis.

The problem is that calcaneal apophysitis is always sclerotic and usually fragmented. So, we do not diagnose Sever’s disease radiographically. It is a purely clinical diagnosis. Squeeze the calf, the child goes out, they got severs disease. We do not use the X-ray. Anybody that looks at an X-ray and says, “You got Sever’s,” does not know how to read an X-ray. Other injuries that can happen around the foot, mangle the Achilles tendon. We have to look at the foot there. The Achilles tendon is something that is very involved in running. So, runners are very notorious. Fifteen to 20 % percent of runners can have Achilles tendinosis at any one time. The problem is with tendinosis, if you keep using a tendon with tendinosis and overdoing it, eventually it can become a tendon rupture. That is what we are going to look at in this case.

On X-ray, there are findings where you lose the normal Achilles fat stripe. I am not sure that I would really want to rely on losing the Achilles fat stripe to indicate that somebody has an Achilles tendon there. I think I would much rather look at an imaging tool and of course, one of those useful imaging tools. Ultrasound would be good for this. We can also do this on MR, and as we are looking at the sagittal, so we are starting on the lateral side, there is the fibula coming into the talus and calcaneus, and nowhere do we ever see an Achilles tendon. This is a person who is had an Achilles tendon rupture and they have had a proximately 8 centimeters, maybe 10 centimeters of proximal retraction, which is something that the surgeons going to want to look at to help decide. Is this a conservative walking boot case or is this surgical repair?

What is going to be making me check out somebody’s ankle more than anything else? Inversion ankle injuries. The most common ankle injury is an inversion injury. Well, and everybody always, “I twisted my ankle. I need X-rays.” No, because what you most likely did was damaged your ATFL, your anterior talofibular ligament.  Maybe your calk fit, calcaneofibular ligament really remotely, post your tailor fit. Likelihood of fracture, unless you have got positive auto criteria, 2.5% or less. That being said, we get paid people that have ligamentous injuries. Do we need to MR most of these, NO, most of these are conservative rehabilitation? We all we really work on proprioception. We work on strengthening up everything in the area and generally those patients are going to do just fine. One of the things that we know is this somebody is a high-grade athlete. Is it somebody who has to consider a surgical alternative then we can start looking at getting MRs on these patients.

Video Presentation Placement: 53:16

Could ultrasound be done? Absolutely, diagnostic ultrasound can be utilized for this, if you have got somebody in your area who is good at what they do. Absolutely, it is something you should be considering. As we are looking at these. So, the two big ligaments that were most worried about. The two ligaments are most likely damaged, anterior talofibular, calcaneofibular. To see the ATFL the anterior talofibular ligament, we look at the axial and we remember that the ATFL. The ATFL, goes from the anterior talofibular ligament goes from the talus to the fibula. Where do we look for this? Is the ATFL, notice there is a junction where the head or the neck comes up flares into the talar dome right there. That is where we are going to see the insertion of the ATFL. The origin of the ATFL is up on the fibula. Well, in this case, there is no ATFL, and this is somebody who is a higher grade high school athlete soccer football, who had multiple ankle injuries and was starting to have a lot of problems were having difficulty playing even with tape because they just kept injuring their ankles all the time.  Their ATFL was injured and then we start looking for the calcaneofibular ligament in which, again, not surprising, it goes from the calcaneus to the fibula. As I look at the tip of the FIB, there is some ghostly fibers there, but there is no calcaneofibular ligament. That absence of a calcaneofibular, not surprising this person has an unstable ankle, their PTFL, posterior talofibular ligament is still beautifully intact. It is a very dense ligament. It is not injured nearly as often so PTFL looks good in this patient.

Video Placement Presentation: 55:23

What other injuries might we be seeing when we start looking at the lower extremity? The next is the Lisfranc. This one is a game changer. If we get a patient who is got a Lisfranc injury, this person the likelihood of return to sport is really remote because this completely destabilizes the foot.

The LisFranc ligament lives between the first cuneiform and the base of the second metatarsal. It lives right there. There is multiple bands to this ligament, but one of the things to keep in mind, that lisfranc ligament is almost like a keystone. It really controls longitudinal arch. It really controls transverse arch, and what it really does, it holds the tarsometatarsal joined together. That tarsometatarsal joints junction there is called the Lisfranc joint complex. Well, what we see is when somebody is gets into a forced plantar flexion, and quite often, this is somebody as part of an inversion injury. If they landed on top of their foot, and then roll their foot that way, that forced plantar flexion tears the lisfranc ligament. In doing so, it will destabilize the tarsometatarsal joint and you can see what we see here. This person has laterally dislocated all 5 metatarsals, to be honest with you. What will happen a lot of times, the first metatarsal will stay in place and then two through five will displace laterally. Generally, when we are looking at a lisfranc injury, if there is any degree of displacement, this person is probably going to be getting surgery and quite often multiple surgeries in order to repair that region.

Video Placement Presentation: 57:02

From there, let us talk about a few more fractures. This next one, the toddler fracture. Most toddlers are athletes, but you start getting little children. If you are dealing with a pediatric practice, the toddler fracture is generally a small fracture in the tibia, and usually they are very subtle and difficult to see. Little child who is starting to walk. Something that is not subtle, and that is very easy to see is the boot top fracture. Not surprisingly, we see this in skiers, and particularly in skiers whose bindings, do not let go. If the bindings are too tight and the skier ends up ditching it and the legs rotate because of the giant sticks attached to their feet, quite often, we are going to see where this will fracture right through the tib and fib, somewhere near the top of that ski boot.

How about the malleoli? When we start looking at positive Ottawa criteria, this is somebody who is going to have tenderness in the malleoli. In the malleolar fractures are very easily straightforward. This person has a medial malleolus fracture. This person has a bimalleolar fracture. They would have broken both medial and the lateral malleolus. Now thing to keep in mind. When we look at the ring of the ankle mortise, we are back to that pretzel principle, that life saver concept. A disruption one place in a ring is stable. A disruption two or more places is unstable. So, the patient like this first patient over on the left side, this person has a stable ankle fracture. They have just fractured off the medial malleolus. They are probably going to be stable according to what is called the Weber classification. This person with a bimalleolar fracture is going to be unstable.

The other thing that we can see is and one that you must remember is, there is a third malleolus. Well, it limits other medial and lateral and easy because we palpate those and see them, but realize that this is the third malleolus, and it limits us in plantar flexion. So, if an injury involves heavy plantarflexion, it is possible to fracture that posterior malleolus which is exactly what we are seeing through there. This can happen as a combination platter with the medial and lateral and that creates something called the trimalleolar fracture. One thing to realize, if you start, looking at ankle trauma, text, you will notice, man, there is a lot of names. There is duputryen. There is potts, there is a too low, nobody uses those. The problem that we have run into is the definitions of all these different named ankle fractures. They have all crossed over so much and there is so many subtle differences. We do not use those anymore. We just described what we see and stop trying to name things after old orthopedist.

Video Presentation Placement: 59:58

That is a very common injury, is an osteochondral fracture in the elbow. Well, hopeful see osteochondral fractures, in the knee, a little bit. We also see osteochondral fractures in the elbow, and where we saw the capitulate, and then the talar dome is another major site for these injuries. particularly if I get somebody who has an inversion ankle sprain. So, the foot is moving that way. They damage the lateral ligament complex. It is going to allow the tailless to run into the tibia, and then we can see some shearing off the articular surface, so then it can happen on the medial or the lateral side. This is one where when we find these osteochondral fractures, the big question is surgical or non-surgical, and these patients are usually going to wind up with an MRI arthrogram to help decide if the fragment is stable or not.

What else can we break it? Let us break a calcaneus. Well, calcaneus happens to be the most common tarsal fracture. What we see is a comminuted impaction style fracture. Sometimes the fracture itself is hard to see and that is why, not surprisingly, there is another set of lines and that is what creates something called Bohler’s angle. With Bohler’s angle, when Bohler’s angle starts to flatten out, that is an indirect indicator that a person has a calcaneal compression fracture. Those calcaneal compression fractures are often called Don Juan fractures. One of the concerns is, they can be bilateral. They also have an increased incidence of thoracolumbar spine fracture because the person is falling from a height and landing on their feet.

Second most common tarsal to fracture is the talus. We already saw the osteochondral fracture. Other fractures that we can see when we start looking at the talus, this is an equestrian. This is somebody who is a western-style rider, and they were thrown for their horse. Their foot stayed in the stirrup and the horse took off. In doing so, it is hard to tell exactly we can see the foot is not where it is supposed to be, but what this person had is called an aviators fracture. It is a fracture through the neck of the talus. Then she had dislocated her subtalar joint. This is a post-reduction film on this particular case. The concern where we find these aviators fractures is an interrupt to the blood supply to the talar dome, and there is a very high incidence of avascular necrosis, which unfortunately ended up happening in this patient. She developed a vascular necrosis and was having a lot of sequelae as the articular surface started to collapse.

With the orthopedic and radiology circles, if you start getting those folks going, they will start to talk about the differences between Jones fractures and dancer’s fractures. There are different fractures and they are not the same, but what most of the world uses is they use the two terms anonymously. What we are talking about is we are talking about a fracture of the base of the fifth metatarsal. Dancers are more distal; Jones is more proximal. We lump them together. These can be an avulsion by the peroneus brevis. They can be an impaction fracture, and one of the things we see, this is one that basketball is kind of notorious for this one, going up for a jump shot and landing on somebody’s foot rolling the ankle and fracturing the foot. Unfortunately, with these fractures, there is a frequent incident of non-union. So, one of the things that must be considered is, is this athlete’s high grade enough where we actually want to screw that fragment in and be able to get this person to return to play.

The other thing that is on our differential is, in little children, there is a growth plate right there at the 5th metatarsal base. The thing to remember is the fractures – let me use a different color – the fractures are going to run perpendicular to the long axis of the bone. The growth plates are going to run parallel to the long axis of the bone. When we start looking at that 5th metatarsal. If you are dealing with a pediatric patient, trying to figure out is it a Jones or dancers fracture or is it a normal apophysis? Look at the direction. If it lines up with the metatarsal, well, then you are looking at a growth plate.

The last diagnosis for our upper extremity one class is going to be sesamoid fractures. What type of person gets a sesamoid fractures? Anybody who is on their toes on a hard surface. Basketball is  notorious for this type of fracture. Hard court, bad shoes also contribute, runners, sprinters are on the balls of their feet a lot. When I get somebody’s doing that kind of repetitive plantarflexion activity and they start getting pain under the 1st metatarsal head, that is pretty classic for a sesamoid fracture, sesamoid fatigue fracture, sesamoid avascular necrosis, they are lumped together. Definitely we are taking some pictures, and what do we see? We can see here there is some fragmentation of that lateral hallux sesamoid.

The question is, is that a fracture or is that a bipartite sesamoid? Remember the mantra? Smooth, well-rounded coordinated margins. If something has smooth well-rounded coordinated margins, it has been there for a long time. If it is sharp and jagged, like we see, in this case, that is an indicator of an acute fracture. There is also a special sesamoid view. It is very much like doing the sunrise view in the knee. You can have the person do a runner stands on the X-ray cassette and you will shoot down through the sesamoid at the metatarsal head. Notice the sclerosis in this case? Is that avascular necrosis? Is that a healing fracture? It is a difficult call, but we are seeing that sesamoid injury in these patients.

That takes care of lower extremity injuries. We will come back in our last module and we will talk about everything that can happen to the knee.

[END]

Section 09_ICSC03 – Lower Extremity Part 2 – Knee
English Direct Download PDF – 09_ICSC03 Section9-Knee-LowerExtremity

Instructor Dr Chad Warshel
Video Lesson: 01:06:19

I realize that this is a little different than the upper extremity in that we just kind of marched our way down the upper extremity. I reserved the knee for the second hour for the lower extremity just because it is probably the second most complicated joint we deal with in the extremities, the shoulder being the number one, knee being number two. I wanted to give a good focus to this in the second hour.

As we start dealing with the lower extremity, of course, this entire hour is going to be about the knee. Realizing x-ray is a good tool for the knee and we are going to talk about some indications for x-ray and some positive x-ray findings. But one of the things to realize about the knee is, much like the shoulder, a lot of the things that we must deal with in the knee are going to be soft tissue injuries and those soft tissue injuries are going to show up more effectively on MRI. Ultrasound is an option for some of the more superficial tissues. However, MRI is really the gold standard for evaluating the knee anytime we were dealing with soft tissue components.

I want to start off by doing an overview of knee MRI, and a little tour of some of the anatomy of the knee. So, when we start looking at knee MRI, again we are dealing with standard planes on the knees, so it is going to be axial, coronal, and sagittal. There are going to be combinations of T1s, T2s, proton densities. Whenever I am evaluating a knee study, just like I do with any other extremity, I always start with the fluid-sensitive sequence. I am looking for that tissue that is angry, I am looking for fluid, I am looking for edema. I could start on the sagittal or the coronal. I would start on the coronal in this particular case. I just start at the patella and I am working my way back and I can already tell this person has a severe effusion in their knee. I can see that right through there. Then as I am coming backward, evaluating the bone marrow. The bone marrow signal is nice and grey. A little heterogeneity is normal. Remember that the knee is mostly fatty marrow. As we are coming back, again I do not see anything that is hugely aggravated. A little bit of extra fluid in the knee and then I do see that there are a large fluid collection on the posterior medial aspect, very common. What we are seeing there is a Baker’s cyst. But I am not seeing any edematous tissues, I am not seeing anything problematic as I scan through that area.

What else do I evaluate when I am looking at the coronal? The coronal is the fantastic sequence for evaluating the bodies of the menisci. We do not see the anterior and posterior horns as well. We are going to evaluate the bodies of the menisci. I can see the MCL is a beautiful dense, thick band. And usually, I would be able to see the entire MCL in the same coronal slices. The lateral collateral also shows up on the coronal but the problem is we usually have to look at a couple of slices to follow the LCL as it goes from the lateral femoral epicondyle down to the fibular head. And there it is inserted right next to the biceps femoris.

Other things that we are going to see. We already talked about the bodies of the menisci. We can see the popliteus tendon right here, inferior to the LCL. Making sure that you do not confuse the junction between the two for a tear. As we go more anteriorly, we can see the iliotibial band coming down and inserting on Gerdy’s tubercle.

This person does have a severe intracapsular effusion in the knee extending into the lateral recess. We can see the ACL and PCL as we look at the coronal but it is really not the strong sequence for evaluating ACL and PCL injuries. That is where we really want to be looking at the sagittal instead. Now surprisingly, we can see the neurovascular bundles in the back. Not too much usually happens involving the neurovascular structures that we evaluate in the knee.

From there I would go to the sagittal sequence. The first thing I need to figure out is am I medial or am I lateral. Well, if there are no fibula, I am medial. If there are a fibula, I am lateral. So that makes my life pretty easy. I am going to start on the lateral and work my way in. We can see the biceps femoris tendon, we can see the lateral collateral and as we come in now we are seeing the menisci. The sagittal sequence is designed to really show us the anterior and posterior horns of the menisci. We saw the bodies when we were looking at the coronal sequence. As we keep going through, and of course we are evaluating the articular cartilage all of this time, we can see the infrapatellar tendon and Hoffa’s fat pad. We are going to look for edematous changes in the fat pad, scarring in the fat pad, any changes to the tendons. We already talked about how tendinosis looks when we are doing a shoulder review. So, we would be applying the same principles as we look at the tendons through the knee.

I can see the patella. I can see the quad tendon and realize some striations in the quad tendon are a very normal thing to see because while these four tendons coming into one, into that suprapatellar region. And then as I come into the area of the intercondylar notch, I can see the ACL. Now, normally when we start thinking about ligaments, ligaments are usually jet black. The ACL is an exception because it does have some different fiber components to it. It will usually have a little bit more of a striated appearance, a little bit more signal inside. One of the important things on the ACL is sometimes we do not get it sliced perfectly because the ACL does run obliquely through the knee. So, if they do not change their sagittal slicing into that orientation, we might see it on multiple slices. One of the important things is that the ACL should be nice and taut. We can see where this is really super straight, and it is very closely paralleling this cortex of the roof of the intercondylar notch, an area called Blumensaat’s line. That ACL looks good and then I keep going through.  I can see the PCL. This is a sports injury discussion. What does this look like? It looks like a black hockey stick. I can see that black hockey stick for the PCL. Then I start coming out onto the medial side, and again I can see the anterior and posterior horns of the menisci. This person has that large Baker’s cyst. Then here the tendons coming down into the Pes Anserine and part of this Baker’s cyst is actually starting to mimic a pes anserine bursitis in this case.

Video Presentation Placement: 07:00

We have looked at the sagittal, at the coronal, we now need to look at the axial. Starting at the top and working my way down, again lots of edematous change in this particular person. They have got a large intracapsular effusion but the medial retinaculum looks good. The lateral retinaculum looks good. I can see that Baker’s cyst between medial gastroc head and semimembranosus tendon.

As we are coming down, where the axial is really the best for evaluating is the patellofemoral joint. We can see where this person does have irregular signal in their patellofemoral cartilage, patellar cartilage and femoral cartilage, because they do have some chondromalacia changes. We are evaluating tendons, ligaments, and muscles on the posterior aspect. Then we come down and we can see the infrapatellar tendon. We can see some of the menisci occasionally but the axial is really not a great place to evaluate the menisci because our slicing is usually too wide. Then we are coming down into the tibia. Realize this striated appearance. The tibia is very normal. Do not confuse those with fractures. Then we get down into the rest of the leg, and we can see the fibula.

That is our general anatomy overview, as we are looking at the knee. Let us start getting into some specific pathologies. But realistically, before we get into pathologies, one of the things that we need to do is we need to review, probably one of the greatest inventions of the ’90s, from an imaging standpoint at least. One of the big goals in imaging is trying to decide who do we image? It would be nice if we could image everybody with every problem. Going back to a Star Trek reference, if we could have Dr. McCoy’s little magic lipstick canister that we ran to the tricorder to let us know what was wrong, it’d be nice if we could image everybody. But we know that we can, it is just not consistent with an evidence-based practice in health care.

There is a group out of Ottawa, Canada, who came up with some really fantastic decision rules to help us decide when to and when not to do imaging on knees and ankles. These came to be known as the Ottawa Rules or the Ottawa criteria. Now, as we look at these, so the Ottawa Knee Rules. For the Ottawa Knee Rules these are for acute knee trauma cases. What we are trying to do is we are trying to decide who might have a fracture. If we have negative Ottawa criteria, the probability of a fracture is less than 1%, and we are talking significant fracture, not small little avulsive flakes, and things like that. We do want to make sure that we only use this in people that are skeletally mature. The concern being growth plate injuries are an entity in and of themselves. We talked about those growth plate injuries already. We only want to use this in adults.

Video Presentation Placement: 10:03

The Ottawa criteria are what are called “OR” rules. If A or B or C or D is positive then you go ahead and take a picture. If none of them are positive, you do not take a picture because the probability of fracture is less than 1%. First thing, we look at age. If the person is over 55, we x-ray their knee because there are a greater incidence of pathologic processes in elderly patients. We do some fairly simple, fairly straightforward physical exam procedures. We squeeze the proximal fibula. Does the person say ow? You take a picture. We are looking for proximal fibular fractures, where also this will be involved if somebody has a lateral tibial fracture like a bumper or fender fracture. Everything on the exam is negative but the person does have isolated patellar tenderness, we take a picture. Then we are looking primarily for patellar fractures.

The other two parts are more active portions. First is have the person actively flex their knee and this must be active flexion to 90 degrees. If they can’t hit 90 degrees, take a picture. If they can’t hit 60 degrees, it actually increases the probability of fracture. There is the walking rule, is the patient unwilling to take four steps regardless of limping, both at the time of trauma and at the time of evaluation. Of course, if you are on the field that can be a little different than if we are just dealing with being in a clinic. You are evaluating them on the field and 30 seconds afterwards. The idea here is the person that must be willing to touch foot to floor. It is one, two, three, four steps. So, two gait cycles. If they are unwilling to touch foot to floor, that is going to be a positive.

If you have watched football, here in the USA, we call it soccer, a player may torqued the knee and they are on the field, and their teammates will come out, arms around the shoulders and take them off the field. They are not willing to touch their foot to the pitch. But then five minutes later, they are back on the sideline, warming up, getting ready to move around again. That would be somebody who does not pass the walking criteria because they were able to start touching foot to floor. If there is any of these things that are positive, then we can go ahead and start looking at doing some imaging. This is X-ray specific, of course.

Before we even start looking at bony injuries, I want to really reinforce looking at soft tissues. Chiropractors forget to look at soft tissues, they focus on the bones, and they might miss some of these subtle clues. As I look at this lateral view of the knee, I know that this person’s got a fracture. I can see the fractures extending through the tibia and they have even avulsed the tip of the fibula here. So that might be an LCL injury or might be a biceps femoris injury. But let us say I miss those things. We all have bad days. I missed the fracture. I know with 99.9% certainty that my patient has an intracapsular fracture, and I know that they have an intracapsular fracture because one of the things I see as I am looking at this radiograph is I see there is a flat line. I did not draw that very flat, but I am also on third cup of coffee right now. I can see that flat line. Above that flat line, there is a more radiolucent area, a darker area, and below it there is a more radiopaque area. Now what we are looking at in this case, that flat line is called Lipohemarthrosis. It is also known as an FBI sign in your fat blood interface.

Video Presentation Placement: 14:03

What happens when somebody has an intra capsular fracture like we see here? Well, when you break a bone, you bleed. This person is bleeding into their joint capsule. But the other thing that happens is if we think about, well, what is bone full of? Bone is full of bone marrow, and that bone marrow is liquid fat. Well, that liquid fat is going to escape the bone through those fracture lines. The best analogy that I have ever come across for this is oil and vinegar dressing. If we take an oil and vinegar dressing, a nice balsamic or something like that, and we let it sit on the table. The vinegar and the oil are going to separate from each other. The oil is going to float on top. Well, the same thing happens here in the knee. The person’s bleeding and the blood is going to be on the more gravity dependent position, and then the fat is going to be in the more superior position. Then there is going to be a flatline in between the two, just like we see the separation in the oil and vinegar dressing. If I see those, I know that I am dealing with a fracture, no ifs, no ands, no buts. Then I am going to be looking very carefully for some of those fractures.

What kinds of fractures might those be? One of the big ones is a bumper/fender fracture. This one is named because of a common mechanism where somebody is walking across the street and a vehicle comes and hits them on the side of the leg with their bumper. What we are seeing here is this person is going to be experiencing a valgus force, and with that valgus force, what happens is the MCL stays intact and acts like a hinge, and then it drives the lateral femoral condyle into the lateral tibial plateau.

We talked about this before when we covered elbow trauma. When a convex thing meets a concave thing, the concave thing loses. What we are going to see here is this person develops a fracture of the lateral tibial plateau. It can either be here where we see this vertical shearing effect. It could also be something more along the lines of an impaction fracture. But in either case, when we see somebody who has a valgus force, one of our concerns that this person is going to have that fibular tenderness on the Ottawa criteria is that this is a bumper or fender fracture. This was interesting in that this person presented to a chiropractor. This was a motorcycle rider. They were working on a motorcycle, they went to kickstart the bike, their foot slipped off the peg and slammed into the ground, created a valgus force. Immediate onset pain. Knee blew up like the size of a cantaloupe. Went to the chiropractor. This person was hobbling in, but the chiropractor only had upright X-ray facilities, so took an AP upright knee. The person was standing on the good leg and the bad leg was hanging there. But what is interesting is if you look carefully, right up here, you will see that there is a darker area, a little bit more radiolucent area. Well, there is an FBI sign in that suprapatellar pouch, because remember, one of the criteria to be able to see the FBI sign is you have to have the beam to the parallel floor. It has to be horizontally oriented, ao we can see that FBI sign in this case.

Another fracture that happens, and this one much more commonly happens when we are with our classic pivot shift mechanism. Of course, we know pivot shift is one of those ones that always makes us nervous because the pivot shift mechanism is classic for an ACL injury. With that pivot shift, one of the other injuries that might happen is that the IT band comes down here and inserts onto Gerdy’s tubercle and this person might avulse Gerdy’s tubercle. That little avulsive fracture is called a Segond fracture. Now, because this is a pivot shift mechanism, not surprisingly, this person also has an incredibly high frequency of ACL tears and meniscal tears. The main portion of the lateral collateral ligament is generally going to be intact, because realize the lateral collateral ligament is the most boring of the knee ligaments. Nothing ever happens there. We are going to see the LCL stay intact. In these patients, it is usually an ACL or meniscus. But this is one of those injuries that when I see this, as soon as I see that little fracture, I know I am getting an MRI on this patient’s knee because I am concerned about the internal derangement.

What else can we break? Well, let us look at fracturing the patella. Ottawa criteria, our patient has isolated patella tenderness, and it is because of a direct patellar trauma. Something smacked the person in front of the knee. When that occurs, realize the patella is actually pretty easy to fracture because particularly if the knee is flexed, that is putting a lot of tension on the patella, and if you tank the patella just the right way it is going to split much like a diamond would. And because of that one of the most common types of patellar fracture is the transverse fracture. Looking at a schematic of a patella, we can see transverse fracture is going to run straight across, and there might be little bits of comminution, it might be a little bit more top or a little bit more bottom but it is going to be short and running straight transverse. Not surprisingly, there is varying degrees of this. If they also tear the retinacular tissue and the paratenon from the quad and the infrapatellar tendon, there are going to be substantial separation between those fragments. If all the soft tissue is still intact, and you just broke the patella, a lot of times that can go conservative.

Higher velocity trauma usually results in a stellate fracture. This is where we are going to see significant comminution. Quite often these patients are going to be looking at having their patella removed because the problem here is, it is hard to put Humpy Dumpy back together again. The patella is in so many pieces, and they are guaranteed such a bad case of patellofemoral DJD that quite often the patella is going to be removed.

The vertical patellar fracture, usually against direct trauma, but this one has a vertical orientation to it. I have seen three of these and all three are people who fell on a curb and they landed straight up and down on their patella on the curb. Now we are looking at an axial view of the patella. The other kind of injury we will think we will talk about is the osteochondral fracture and we will talk about osteochondral fractures in general.

Video Presentation Placement: 20:53

Something else that is on our differential list for this is the bipartite patella, which is an anomaly that occurs during development. I would show you a case here in a little bit.

As we are looking at this person, this person has a horizontal or transverse patellar fracture. Is it a touch oblique? Yeah. Is it comminuted?  However, it is predominantly a transverse patellar fracture. We can see that there is distraction between those fracture fragments. We know that the articular surface is involved. This is a person who needed surgery to put the patella back together. You can see where some wires were put in place and then some figure eights mechanic’s wire, for lack of a better term, pulling the patella back together.

The thing about all these patellar fractures is they all involve the articular surface. They all guarantee a certain degree of degenerative joint disease within a couple of years. The vertical patellar fracture is the one that is most difficult to see and this one requires a sunrise view. Believe me people who have a vertical patellar fracture are not fond of having a sunrise view done where the knee is flexed and they are holding the cassette so that we can get that tangential view of the patella. Sunrise view, tangential patella, Merchant’s view, they are all different names for the same thing. But as we look at this, we can see that vertical fracture running right through the patella. Our distinction is, vertical patellar fracture here, well that looks like a fracture too. This one is a bipartite patella and we can see where this does have smooth well-rounded coordinated margins consistent with a long-standing abnormality like a bipartite.

The other patellar fracture is the osteochondral fracture. Now this is a patient when I look at the alignment, we know, when we look at radiographs, we can do the alignment/anatomy, bone, cartilage, soft tissue search pattern. This patella is not sitting in the patellar groove the way it should. And when we are looking at a sunrise view, realize this person’s knee is flexed. That is going to pull that patella into the trochlear groove of the femur. Well, why is this person’s displaced? Because they have a medial retinaculum tear. I do not see the medial retinaculum but I know based on the alignment, the medium retinaculum is no longer intact. This person had dislocated their patella and in doing so they had fractured the articular surface. We can see a divot through here. There is a little debris down through here where that person has an osteochondral fracture.

Now on our differential list for patellar fractures is the bipartite patella, and what we are looking at here is an extra ossification center, and it never unites in. One of our big clues is the most common location for these is on the superior lateral border of the patella. It is incredibly uncommon to see a fracture right through there. Unless you get somebody who smacks you with a hammer and chisel right on that superolateral aspect, that’d be uncommon. Plus, it is got some of the undecorticated margins. What is interesting when we start looking at these bipartite patella is generally these are incidental findings. We want to make sure we do not confuse them with fractures. If you are not sure, X-ray the other side. These things are bilateral 80% of the time. But one of the things that is interesting about a bipartite patella from an athletic standpoint is that these can become symptomatic in athletes who are doing repetitive heavy quad work. We can see this in runners. We can see this in weightlifters that are doing squats and dead’s, anybody who is doing repetitive quad work because if we think about it, the quad is coming in and inserting across the superior part of the patella. This portion is connected by fibrocartilage. And if the lateral components of the quad are pulling repetitively, they can injure that fibrocartilage.

This is a great segue to look at an MRI on a patient that has a symptomatic bipartite patella. I have somebody who has got patellofemoral pain, chronic, insidious onset, chronic pain, and they come in. Ottawa criteria do not apply. I takes her some radiographs to see what is going on, then I see a bipartite patella. But now this person is symptomatic, the pain is very focal, and it is right around the area of that bipartite. I know that I am going to go to my fluid sensitive sequences. We are here in the knee, if we can tell, here is the lateral side. Now this is a STIR, so it is a little grainy and it is a poor-quality MRI because it is an open MRI. But as we come forward into the patella, so right in through here, we are starting to see the patella, and then over here in the patella there is a huge amount of edematous change. This is a symptomatic bipartite patella. The bony fragment itself is edematous, the fibrocartilaginous junction is edematous. We are looking at Bipartite Patella Syndrome, and of course what is the best treatment for this? Rest, take it easy, give it a chance to heal. Things should be okay. If it has a repetitive recurrent issue, then it can be removed, and the quads can be reattached.

Video Placement Presentation: 26:26

Something else that is on our differential when we start looking at knee is the potential for a Nursemaid’s knee. So again, patellofemoral pain, one of the questions is what else might be causing Patellofemoral Pain aside from the patellofemoral joint, chondromalacia, and things like that? Well, one of the other things that is on that differential list is Nursemaid’s knee. This would be somebody who spends quite a bit of time on their knees as part of their event. I cannot say specifically that I know that this is a frequent thing. But one of the assumptions that I would make is that this might be something I would tend to see in somebody who’s involved in curling. The person who is sliding the rock is involved on their knees quite a bit.

As I look at a knee MRI, pulling up the sagittal and looking at a fluid sensitive, we are on a T2 sagittal, what do I see in this person’s knee? Here is the patella, and there is the prepatellar bursa, full of fluid. When you palpate these, you can palpate there is a fluid feel to them. It feels like there is a little water balloon deep to the skin. We can see that prepatellar bursa and of course checking for any recent skin abrasions or lacerations and to make sure it is not a septic bursitis. But otherwise, a simple prepatellar bursitis.

On our differential for this, something we talked about in the first hour of lower extremity, is the Morel-Lavallée lesion. Making sure you know is this a bursitis versus had this person had a shearing force across their patella, and now we are seeing that fluid collection from the hematoma starting to encapsulate as a Morel-Lavallée. I already touched on patellar dislocation but wanted to revisit this one as we start looking at some patellofemoral issues. One of the great candidates for developing patellar dislocation, we see this in bicyclists. It is also fantastic for any other running sports where there are lots of pivoting and shifting going on. I have seen this in soccer/football. I have seen this in rugby. There is a interesting YouTube video of a female rugby player who dislocated her patella while she was on the field. She just laid down, she smacked her patella back into place, got up and started running again.

We can see with that patellar dislocation, one of the important things for this person is disruption of the medial retinaculum. Sometimes retinaculum is a difficult thing to assess. There is a lot of edema. Did they tear the retinaculum? Is this new or is this old? But one of the other things I see, the patella almost always dislocates laterally, and when that patella dislocates laterally, the medial patellar facet is going to ram into the lateral femoral epicondyle, and we are going to see what are called kissing contusions as a great indicator that this person has had a patellofemoral dislocation. I am going to make sure I watch very carefully for in this patient is to see whether or not there is an osteochondral injury, osteochondral fractures being very common in these patients.

Another big, relatively common cause of pain in athletes because this is a relatively frequent finding is a remnant embryologic fold inside the knee called a plica. There are four different players. But the medial plica is the one that is most likely to be symptomatic. It is a band of fibrous tissue that goes from the joint capsule to portions of the fat pad. We can see there are that nice plica right through there. This is implicated in patients that have clicking, snapping knees. We can see some transient locking in patients that have plagued. Definitely worthwhile getting imaging to see what is going on, and then help to make those decisions. Does this person need surgery to release that plica or not?

From there, we get into osteochondral injuries of the knee. Already touched a little bit on the patellar osteochondral fractures, but really, that one is not the more common. The more common involves the medial femoral condyle. This is quite often as a component of an ACL injury. We can see some shearing forces happening inside the knee and the tibial spines can impact the femur and shear off a piece of the articular surface. A big area, lateral aspect of the medial femoral condyle. Other location is going to be that patellar location with a dislocation. This is one where generally this person is going to have positive Ottawa criteria and more the walking rules than anything else or possibly the flexion rule, depending on how stable or unstable the fragment is.

Looking at the straight on AP and lateral, this one is subtle on the AP view. But right through here, we can see where there is an articular surface defect. It is on the lateral aspect of the medial femoral condyle. It is very subtle, but we can see a curvilinear change through here. Just as a side note, make sure we do not confuse this with an abnormality. What we are looking at there is an os fabella, which is a very common anomaly where there is an extra piece of bone located in the lateral gastroc tendon.

The thing about these osteochondral fractures in the knee, single traumatic events or cumulative stress can do these as well. Sometimes they are hard to evaluate, and one of the best additional views to do is, using a tunnel view. This is a flexed view of the knee and you are angling the X-ray tube, and you can see that articular surface defect more effectively. Plus, it is also great to see if there are displacement of the fragments into the intercondylar notch because that notch is one of the locations that osteochondral bodies like to hideout.

Already touched on the patellar osteochondral fracture. With a patellar osteochondral fracture, lateral patellar dislocation. As the patellar service is going out of the trochlear groove, it will fracture off a piece of the articular surface. One of the things that we end up seeing done in patients with osteochondral fractures is these patients will usually end up getting MR arthrograms because evaluating the stability of the fracture fragment is an important thing for conservative versus operative management. This will be injected with a contrast to try to figure out stable versus unstable fragments. It is also possible to not have an osteochondral injury, but to just have a chondral injury, where cartilage is usually fairly squishy, but if you hit it hard enough, it becomes more and more solid and it is more possible for that cartilage to fracture or tear. What we will see when we look at an MR, we will see a defect in the articular surface. The tibial articular surface is nicely maintained. The femoral surface comes across, stops, restarts over here. This person has a chondral injury. This one is an older injury, because in the acute chondral injury, we will usually see some adjacent bone marrow edema that we do not see in this case.

Video Presentation Placement: 34:08

As we continue on our journey through the knee, we have done quite a few fractures, it is also time to think about some of those soft tissue injuries. In this particular patient, this is more of a middle-aged gentleman. You can tell there are some degenerative changes in the knee. He was doing that most classic of all middle-aged athletic events, mowing the lawn. If you’ve been in some suburban areas, you know that there are a lot of competitiveness here. I think it qualifies as an athletic event. He was mowing the lawn, on a hill. An overweight gentleman, lots of force going through his leg. And while he was working on cutting the grass on this hill, suddenly, his leg collapsed out from under him. As we are looking at this, he had positive Ottawa criteria that he could nott bear weight. But what is interesting is as you palpate the leg, the patellar wasn’t tender, the fib wasn’t tender. He was able to flex his knee, but he had problems with extending his knee. And when you look at his knee, just even before doing all this, you can see that there is a large sulcus, there are a big divot above his patella. The fact that he had lost his extension capabilities, was unable to walk on the leg, it was a pretty good call that what we are seeing here, if you notice that divot in the superior soft tissues, this gentleman had detached his quad. It is a rupture of his quadriceps tendon. Typically, that happens right near the base of the patella. Then as the quad comes off the patella, the patella tends to shift downward, and we see that this does have a patella baja appearance to it. It is subtle but there is a little redundancy to the infrapatellar tendon. This one typically requires surgery and it did in this case.

What else can involve the structures around the patella? Well, one of the things that we see in the infrapatellar tendon, Sinding-Larsen-Johansson otherwise known as jumper’s knee, which is usually a more common colloquial term for it. Who do we see this in? Hurlers, people that like to do hurdles, fantastic candidates for seeing this particular thing. It is usually in their leading leg because with the leading leg, there are a heavy quad pull to kick the leg up to get over the hurdle, and what we are seeing is either tearing of the infrapatellar tendon at the patellar apex or we can see bony fragmentation at the apex of the patella like we are seeing here. We see this a little bit more commonly in children than we do in adults, but it can absolutely happen in adults as well if they are doing the heavy, repetitive quad work.

Video Placement 37:08

This is one where I want to kick over to a live demo on a case of Sinding-Larsen-Johansson. This is an athletic 19-year-old female complaining about she’d been doing quite a bit of quad work as a runner, was developing progressively worsening pain at the apex of the patella. Originally, had been written off as a chondromalacia patella or patellofemoral pain, but then it started to get worse and really started to localize. I am going to kick over to the sagittal on this case, and as we pan in, so we are starting on the lateral aspect, you can see the menisci. And as we are coming into the patella, watch the patellar tendon. We can see that patellar tendon, infrapatellar tendon. And as we come in towards the apex of the patella, suddenly it gets really wide, and we are still seeing some intact superficial fibers. But the deep fibers are really being disrupted and there are some edema in the apex of the patella. We can see this nicely on this T2 where there is the infrapatellar tendon, all of a sudden, it loses that integrity right through here. There are still some superficial fibers which is why the quads hadn’t let go or the infrapatellar tendon hadn’t let go and retracted the patella superior. But this is a beautiful example of a Sinding-Larsen-Johansson, jumper’s knee.

Video Placement Presentation: 38:36

Now Osgood-Schlatter, you must read the docs. This is one that is not a radiographic diagnosis. Osgood-Schlatter is a pediatric patient. Again, a running sport. Pick your favorite running sport with little children and well it is very common to see this condition. They start developing a lot of pain at the insertion of the infrapatellar tendon. This is not a radiographic diagnosis, rather a clinical diagnosis. You got a runner, they got pain, it is tibial tuberosity, they got Osgood-Schlatter. If we do X-ray these patients to rule out other things, what we are going to see is fragmentation of the tibial tuberosity. It is an easy diagnosis, and typically addressing biomechanics and putting the child into a Cho-Pat brace. Most of the children will not take the time off the sport for this to heal up on its own until they get in between sports. You can see that there are also some thickening of the infrapatellar tendon. So, we deal with the chronic issue in this one and then eventually get the child to rest for a while and it will usually resolve.

What  else can create some pain in the leg? Iliotibial band syndrome. Typically when we talk about IT band syndrome, we think about it down towards the knee but realize IT band syndrome can hurt all the way up to the hip. Again, clinical diagnosis, typically there are focal pinpoint tenderness over the iliotibial band. Sometimes you can sense some edema as your palpating. Not usually something we need advanced imaging for. If we do get advanced imaging, we can see in this case, this person does have a mild intracapsular fusion. But they have also got edema, deep to the iliotibial band more approximately. So not surprising that would go along with an iliotibial band syndrome.

This is a classic history. This is one that is really, common as far as conditions go. The history is incredibly classic. Something we see a lot in tennis players. Tennis players a lot of times will complain about, “I was pivoting around the court and all of a sudden, it feels like somebody just hit me in the calf with a tennis ball.” They tore their plantaris. The plantaris tends to tear at the musculotendinous junction, which is going to be up closer to the knee. It can tear down further in towards the Achilles. But usually that is going to be accompanied by an Achilles tear. So usually, it is going to be much more up towards that musculotendinous junction.

I would pull this one up. This is a 16-year-old tennis athlete and had a really sharp stabbing pain in the backside of the calf.  I always go to the fluid sensitive sequences. I am going to coronal STIR. I am going to start in the front and work my way back. Window this little bit just to make it easier to see. So there are the patella, there are a mild intracapsular effusion. We go back, the menisci look fine, the iliotibial band looks good. And then right here, on this lateral aspect of the leg, in between the gastroc heads, I can see a substantial degree of edema. I can see that same thing if I were to kick over to the axial. I can see there are a substantial degree of edema there on that lateral aspect. Well, that is where the plantaris muscle comes in. This person has torn the muscular tendinous junction. and there are some edema and hemorrhage along the pathway of that plantaris. Generally, this is the left-alone kind of lesion, not typically surgically repaired because it is not a major contributor to function in the lower extremity.

Video Presentation Placement: 42:42

The last of the fractures that I want to talk about before we get into ligamentous injuries, because of course, with the knee, ligaments, and menisci, those are our big deals. This is a patient who has an ankle injury. But one of the rules that we always want to keep in mind anytime we are dealing with joint injuries is when somebody has a joint injury, we always check out the joints above and below just to see how things are doing. This is somebody who is complaining about an ankle injury. They had twisted their ankle, and in twisting their ankle, it is subtle, but they fractured their medial malleolus, and with that medial.

There is an ankle injury. One of the things that is possible is we are looking at a neutral, but part of the damage is did they damaged the interosseous membrane? Did they have a high ankle sprain? Well, when that medial malleolus goes, then maybe the talus rotates and shoves the fibula laterally. They are focusing on this because they can feel a lot of pain, very superficial structure, lots of swelling. But as you start palpating up this person’s leg, the tib feels fine. You are starting to come up the fibula. Then suddenly, there is a proximal fibula fracture. That means that this is something called a Maisonneuve fracture. One of the ways to think about a Maisonneuve fracture is like a wishbone injury. We take the wishbone of the turkey, grab the parts, spread it apart. Same thing is happening here. As this injury occurs, this person is damaging the interosseous membrane. The tib and the fib are separating from each other distally until eventually there are enough of an anchoring point that holds the fibula in place, and then the fibula is going to fracture. That is why we always want to make sure we check out the joints above and below, and in this case, we can see that Maisonneuve injury.

That is going to bring us into the ligamentous injuries of the leg. Not surprisingly, when we are dealing with knee injuries, the vast majority of the injuries are going to be soft tissue. The fractures are all well and good, they are easy to see radiographically. The positive Ottawa criteria are wonderful. But what are the ligaments like? What are the menisci like? Let us make sure we are paying attention to soft tissues. And we know that this is predominantly going to be an MRI diagnosis. We can use ultrasound for some of the more superficial ones. But again, lots of user dependency on that. We are seeing more and more use of ultrasound. Particularly, every major sporting team generally has ultrasound on the sideline to make sure that they are… You know, we are dealing with fairly expensive players here. They are going to make sure they try to get the best management possible.

Video Placement Presentation: 45:36

When we start dealing with patients that have ligament injuries, the two big ligaments that are going to be injured are the ACL and the MCL. The anterior cruciate ligament and the medial collateral ligament. The PCL tears occasionally, the LCL is a boring ligament. Nothing much ever happens with the LCL. So not too terribly worried about lateral collateral ligament injuries. ACL and MCL are going to be the vast majority of all of these. One of the things that they are, is they are a part of this thing called O’Donoghues terrible triad, or O’Donoghue,  It goes by a couple of different names. I am unhappy. If my ACL and my MCL are gone, I am probably a little more than unhappy. That is pretty terrible for my athletic career.

How do these injuries happen? Well, for the ACL, it is a pivot shift. Plant the foot and rotate. With that planting the foot and rotating, hear a pop, hit the ground because the ACL is gone. Now, what is interesting, when we start talking about these, as a part of that injury, there are also a typically a transient subluxation of the knee. That can result in meniscal injuries, that can result in MCL injuries, and that is O’Donoghue unhappy triad, O’Donoghue terrible triad. ACL, MCL, and meniscus. Typically, the posterior horn of the medial is the classic codon to use. O’Donoghue has really been extrapolated out to be all meniscal injuries, just posterior horn of the medial is the most common. It is also possible to see other things. Osteochondral fractures can happen when we start to see those ligamentous instabilities. Well, one of the things that might happen is the ACL might be intact and the person evolves their tibial spine instead.

Already talked about Segond fractures as well. If I do a pivot shift, and I hit the floor, because I heard a pop, an immediate onset of knee pain. I am hoping this is me right now because what we are seeing in this particular case, this person, their ACL is actually intact. What they did is they avulsed the anterior tibial spine. I would much rather have an avulsed anterior tibial spine than an ACL tear because this is an easy surgical procedure. Arthroscopically, the surgeon can go in, drive a screw in, and that thing is going to be beautifully intact because the ACL is still there, just the anterior tibial spine is not attached. But the bone will heal really nicely. So that is where we are going to wind up going into an MRI though, because what is going to happen more commonly as the ACL goes?

What is interesting is how the thought process on the ACL has changed over the years. It used to be conventional wisdom that there was no such thing as a partial thickness ACL tear. One of the goofy little phrases was when an ACL goes, an ACL blows. It blows up. But now there are something mysterious about it, the ACL is two different ligaments. There are two different bundles of ligamentous tissue inside an ACL. There are an anteromedial bundle and there is a posterolateral bundle. Depending on whether the knee is an extension, or flexion, it is possible to tear just one of the bundles and get partial ACL tears.

Video Presentation Placement: 49:13

We want to start looking at the MRIs to evaluate what is going on. It is difficult to distinguish the anteromedial versus the posterolateral. History is kind of important, and the orthopedist can tell when they scope it. We can tell that there is partial tearing, though. What are we going to see? Well, let us look at some diagrams and see what we can see. Now I am going to start off with the ACL rupture. I am going to go in reverse order from what I have here on the slide. What I am looking for is the ACL. I am paying attention to the sagittal. I showed you an ACL at the very beginning of the hour, where the ACL is a dense taut band that follows the Blumensaat’s line. As we scroll in on the knee on this person, and we are starting on the medial side, I can already see that there are a lot of fluid in this knee. This is an unhappy knee. There are the PCL. Now the PCL we see on a couple of slices, but it is intact. It is redundant, it looks fine. But then when I try to get into the area of the ACL from the anterior tibial spine, coming into the medial aspect of the lateral femoral condyle, I never see a ligament. Well, all I see is a little bit of dandelion fluff floating around in the wind. That is an ACL rupture. This person has a completely ruptured their ACL. One of the things that happened with that as we pan out through the lateral aspect, notice that there is bone marrow edema in the anterior aspect of the lateral femoral condyle and the posterior aspect of the lateral tibial plateau. When an ACL tears with that pivot shift mechanism, what happens is there are a transient subluxation. The tibia is going forward, the femur is going back, and this portion of the femur slammed into this portion of the tibia. We are seeing that kissing contusions concept that we saw previously. So even if I overlooked the ACL tear, I see those kissing contusions. That should be one of my big clues that I am looking at a ruptured ACL. So that is the rupture. Now let us look at what a partial thickness tear looks like.

Video Presentation Placement 51:22

We are going to go to the sagittal again. As I look at the sagittal on a fluid sensitive sequence I am coming in from the medial side. There are the PCL a little redundancy in the PCL is a very normal finding. But then as I come in through here, the ACL is still present. Now, this is a lower field strength magnus, so the ACL is not jumping out. Let me kick over to thin slice ACLs. This one, they slice in the orientation of the ACL. As I look at this one, notice how the ACL is curved, and then there are a thin band here and there are a defect here. When I see that curving to the ACL, when it is not in a straight line following the Blumensaat’s line up here on the roof of the intercondylar notch, that is a partial thickness tear. In this case, because I can see where the defect is and I can see where the intact fibers are, this is somebody that has a partial thickness tear of the anteromedial bundle. That anteromedial bundle is what is torn in this individual. There is a partial thickness there. That is a discussion then to have with the orthopedist, does this person need reconstruction or do we go with conservative means and start making an informed decision there?

What about the PCL. When we look at the PCL, PCL tears do not happen that often. How do they happen? Easy. Well, let us back up. How do I assess for a PCL tear? Posterior drawer. Well, you know how you tear a PCL, you traumatically posterior drawer somebody. Big thing is here, somebody lands on their knees, something hits the tibial tuberosity, drives the tibia back, tensions that PCL. If I want to see a PCL tear in this individual, this was not an athletic event. This was somebody who had fallen from a moving vehicle and landed on their knees. As we scroll in, we are on the medial side. Lots of fluid in the knee. When somebody has an internal derangement, there are going to be intracapsular effusion. If there are no intracapsular effusion, there are no internal derangement, or it is a chronic old case. As we come in, here is the ACL looking really nice following Blumensaat’s line. Here is the PCL. Now remember, the PCL is generally a dense black hockey stick in the backside of the knee. But in this case, there are a lot of high signal intensity contained within that ligament, demonstrating that this gentleman does have a PCL tear. The nice thing in this case, this is a partial PCL tear, there are still some intact fibers, and because the PCL is not super contributory to the knee, this one was managed without surgery.

Video Presentation Placement: 54:39

What about the MCL? The medial collateral ligament of the knee can also tear. This one is going to involve a valgus stress, like we saw previously in the patient that had the bumper fracture, but in this case, well we are going to see where the MCL goes instead of the tibia. One of the things is when we grade these ligament injuries, it is possible to grade ligament injuries. There are different grading schemes. I am kind of fond of one, two and three, mild, moderate and severe. So mild, some mild disruption of the fibers, some superficial edema. Moderate, we are seeing some more edematous changes, more disruption. And complete, the grade 3, would be a rupture.

Let us look at some MCL injuries. Starting in the front, lots of edema, and as we come backwards, we are in the area of the MCL. Notice that superficial to the MCL, there is this higher signal, that fluid signal in this MRI. The MCL itself looks grossly intact. That means that we are looking at a grade 1 MCL injury. When we start looking at the more significant MCL injuries, coming in through the anterior side here. I can see some MCL fibers, but then there is loss of integrity up here at the femoral epicondyle. This person has a grade 3 ACL injury. They are superficial and deep edema, and the fibers are never intact. We are looking at an MCL rupture in that patient.

Something else that can happen when we start looking at the medial collateral, somebody who has chronic valgus injuries to the knee, it is possible to see where over time that MCL can develop some ossification, and there are a question. Is this hydroxyapatite deposition disease? Or is this a myositis ossificans? But in either case, we have a diagnosis for this called Pellegrini-Stieda. That is a good indicator of chronic MCL injury.

Video Presentation Placement 57:17

Then we are going to finish off our time today talking about meniscal injuries. We know that ligaments are very commonly injured. Now we will get into the menisci. We know that when we are dealing with menisci, there are a medial meniscus and a lateral meniscus. The posterior horn of the medial meniscus is the high traffic zone. That is what bears the most weight. That is what gets the most damage. The posterior horn of the medial meniscus, most common injury. Can the lateral meniscus tear? Of course. Anterior horns are much less likely. Can they? Of course. But the poster horns are really where we pay the most attention. The other thing that meniscus does is as the athlete ages, we are also going to see where the center part of the meniscus tends to break down. I mean something called a myxoid or mucoid degeneration depending on which author you read, where the fibrocartilage breaks down. There is a little bit more of a gelatinous central nature to it. To make sure that that is not a tear, it should never communicate with the articular surface. It will be located just centrally within the meniscus.

One of the big questions for meniscal tear management is, where is the tear? If the tear is more peripheral like we see in this case, peripheral tears are a good thing because peripheral tears are in what is called the red zone where there is still blood supply to the meniscus. That blood supply is going to allow this to heal. Once we get out into the white zone, which is more towards the more central margin, the meniscus, those are less likely to heal on their own.

A couple of different kinds of meniscal tears. I am going to give you some schematics and then I am going to pull up some diagrams. The horizontal or the horizontal oblique. We can see a tear that runs straight horizontally. Much more commonly, they run obliquely, and they almost always communicate with the tibial articular surface. We see this best when we are looking at our coronals and sagittals. We generally do not see that axial view. I just threw the axial in for completeness sake. The bucket handle tear is a vertical tear, and it separates the free margin from the more peripheral portion. One of the problems with the bucket handle is that piece can flip over. That creates a finding called the Flipped bucket handle meniscus. There are some radiology signs that are great for multiple choice tests like the double PCL sign and the double Delta sign. There is the radial tear. Radial tear just goes out from the radius of the circle, and what we typically see is a truncated appearance, where we lose the very tip of that free miniscule edge.

Then the parrot beak is a combination of a radial and a bucket handle. This one is much more difficult to diagnose.  let us take a peek at some of these different tears. We know that when we are evaluating meniscal injuries, we are going to spend the most of our time on the coronals and on the sagittals. The coronals are good for seeing the bodies of the menisci. I know that most injuries involve the posterior horn, so I am going to spend most of my time on the sagittal. From an MRI perspective, we want to look at the proton densities. A proton density is the sequence or T1 that is great for evaluating fiber cartilage. As we come into this knee, we are starting on the medial side. There are the pes anserine tendons. We can see right away that this person has a massive horizontal tear in the area of that posterior horn. As we come in, there are that horizontal tear. It is communicating down here towards the tibial articular surface. Good news for this patient is it is going all the way through, so it is hitting that red zone. This is one that might experience healing on its own without needing surgical debridement or suturing. But again, that is an informed consent decision to make with the athlete and their orthopedist.

So we come into our next patient. I am going to want to be on the sagittals for this. This one is a proton density without fat suppression. We can see there is this higher signal intensity contained in the posterior horn. It is communicating with a tubular surface. It is coming out in the peripheral edge, so it is catching redzone. Just to illustrate the concept, this is why we want to use the proton density. Notice that it is not nearly as easy to see when we look at the T2.

Coming to a different patient. This time we are starting on the lateral side of the knee, you can see the fibula. Nice example of the anterior and posterior horns. One thing you want to be careful of is there is a small ligament that goes off the front side, the anterior intermeniscal ligament, do not confuse that with a tear. As we come out to the other side, in this person, I do not see the posterior horn really well. There are some complicated tearing going on there.  I am not even really seeing the anterior horn. Well, that is because as I come more into the intercondylar notch area, there are the PCL, and it looks like there are a second PCL. Well, that is because this person has a flipped bucket handle meniscus, where that meniscus flipped over and is now residing in the intercondylar notch.

The radial meniscal tear is much more difficult to see. With the radial tear, I am going to start on the coronal proton density. We are starting in the front, working our way back. I can see the dense triangle for the meniscus. Fantastic. But then notice on this one, as I am looking at the coronal, this person has two radial tears. On the posterior horn, there are a very small defect there. That is a radial tear. Then notice that the meniscus kind of goes away and then comes back. That is because we are in the same plane as a radial tear in that case. This person has a couple of radial tears, and they are much more subtle. There is part of the radial tire there, and we go from sharp and point, to blunted, to sharp and pointy. There is a second radial tear.

Now, the last topic for today before we finish off with our imaging of lower extremity trauma and finish off with all of our traumatic sports injury all together is the discoid meniscus. Not a trauma thing, but something that we see very commonly in athletes as a pain generator, is the discoid meniscus. This is a congenital anomaly. It is where we see instead of having a circular structure for their meniscus, this person has a flat plate of cartilage completely interposed between the femur and the tibia, typically on the lateral side of the knee. This does occur in about 3% of the population. This is pretty frequent.

An important finding for that discoid meniscus. What are we going to see? When I look at the coronal, I am starting on the backside, there are the posterior horns, and follow the medial and notice that the medial comes into a pointy triangle, and then we see the anterior component. But when I am looking at the lateral component, there is always a thick black bar interposed in between the femur and the tibia, and that is a discoid meniscus. This discoid meniscus has been implicated as a pain generator even if it is not torn.

Now one thing we should see when we look at knees, as we come into the meniscus, we should see what are called 2 bow ties. So we are on the medial side, there are a bow tie, thicker on the two ends than in the middle. There are a bowtie and then there are separation between the anterior and posterior horns. When we start on the lateral side, bow tie, bow tie, bow tie, bow tie all the way across. So that is that thick cartilaginous plate for the discoid meniscus, and again, it can be a pain generator in and of itself, and it is of course more susceptible to tear.

That takes care of us as far as our imaging of sports injuries goes. I hope you have enjoyed these 9 hours and it was informative for you.

 

 

Thank you very much for allowing me to help with your education on imaging of sports injuries.

To contact Dr Warshel reach out to admin@ffirscport.org

[END]