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CME Infectious Disease

Diagnosis, Classification, Treatment of Osteomyelitis

Richard Weiner, DPM

Richard Weiner, DPM presents the principles of management for osteomyelitis for the podiatric physician. Dr Weiner reviews the basic observations and lab tests to aid in diagnosis of the disease and reviews different classification systems and treatment options. Along with citing relevant literature, he adds pearls of wisdom to better understand the rationale behind treatment choices.

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Goals and Objectives
  1. Discuss the epidemiology of osteomyelitis (OM).
  2. Understand the principles of managing osteomyelitis (OM)
  3. Identify the steps to treating OM
  4. Describe the various diagnostic modalities for identifying OM
  5. Understand the rationale behind treatments for OM
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  • CPME (Credits: 0.5)

    PRESENT eLearning Systems, LLC is approved by the Council on Podiatric Medical Education as a provider of continuing education in podiatric medicine.

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    Release Date: 03/16/2018 Expiration Date: 12/31/2018

  • Author
  • Richard Weiner, DPM

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  • Lecture Transcript
  • Robert Frykberg: Now, we’re going to have a talk on osteomyelitis. Our next speaker is a good friend of mine. We’ve traveled to Greece together. We’ve traveled to Russia together, to the Kurgan Illizarov Institute. Dr. Rick Weiner is a residency director of a very large and good program, the Grant Hospital in Columbus, a good friend. He’s recently published a paper within the last year, dealing with this particular topic, which is why I asked him to come and speak. Let’s welcome Dr. Rick Weiner.

    [Applause]

    Rick Weiner: Thank you Dr. Frykberg for those kind words. We’re going to talk about diagnosis and classification. What I hope to get by the end of the 15-minute break is when, you, residents go back, have an eye open, what are you doing, why are you doing it? Not saying what you’re doing is right or wrong, but you guys are supposed to be based on the literature. You’re supposed to be based on what does the evidence show, not what, us, old guys did in our program, so automatically, you’re doing in yours. That’s how you’re being taught. The purpose of this today, I want to get you to think why are you doing it, what are you doing it, and how do you diagnose the different things? So, what are the problems? Okay. We know that there’s 300 million worldwide with diabetes. Of those, we also know that if 25% of them are going to have an ulceration some time in their life. And of that, 10 to another 60% will be complicated by diabetes. Somewhere, complicated by osteo, 25 to 38 million ulcers have osteomyelitis worldwide. That’s an astonishing number. So, how do you diagnose osteo? That’s the question. Is there a right way to diagnose it? Okay. We know a couple basic tenements and everything else goes off of this, one, depth of your wound. Size of the wound doesn’t matter. Fleischer out right here in Chicago, a couple of years ago, publishes, wounds greater depth than 3 millimeters have 10 times full of osteo present. Each of these main topics, these five headlines, we’re going to talk about in depth. Lab analysis, we all know about the ESRs, CRPs, WBC, but do they actually mean anything. Micro, how many of you are taking cultures on your patients that are either on antibiotics or recently off antibiotics? The literature is clear, remnants of antibiotics are being found in tissue up to two weeks after the last dose of antibiotic, depending on the half-life of the antibiotic. Are they valid cultures you’re taking? We’re going to talk about pathology and both in complements of Dr. Frykberg. I’m going to a little bit more into imaging that he shows. Let’s talk about each one of these things and what do they do. Lab analysis on the immunocompromised patient we all know is difficult to assess. Why? You know that part, but what’s happening. We know these patients have a systemic inability or they’re compromised to being able to mount an immune response to phagocytosis, to chemotaxis, to intracellular bacteria killing. Does this provide your laboratory analysis suspect? The purpose of diagnosing osteo, and later on, you’re going to hear about the treatment, but you first have to get an accurate diagnosis. What I want to get you guys to think about is not straight off a paper. You need to use heart. You need to use your brains and your eyes to get a feel, is this osteo or isn’t it? Calcitonin, how many of you are using them? And if you’re not, what is it? We know it’s a precursor to calcitonin, and I don’t have time to go into it now, but pull your emergency medicine article. Pull these literatures and see, is it more sensitive than CRP? Why aren’t we using it? It’s a good tracer of effectiveness of antibiotics. It should be being used. Okay, CRP. We know that if the CRP and the ESR are of normal values, then everybody says, “Gee, you don’t need to keep going on for osteo.” But look in the pediatric literature. Last year, it got published, that just because those are normal, did not correlate with evidence of osteo in the pediatric patients.

    [04:58]

    Again, some of these things that we know, does the pediatric literature then translate into our diabetic literature? We know that CRP has a sensitivity of 91%, specificity of 86%. The ESRs are a similar, okay. But, that information, is it foot specific? The only literature out there that specifically talks about correlating this with osteo has an ESR of 70. Some of the literature says it’s 60. But, this article will talk about, if you’re greater then 70%, sensitivity is almost 90%, but you have 100% specificity. That’s an amazing number. What happens is your WBC does not correlate to evidence of osteo. We know there are studies out there that show, diabetics who have a Wagner level 3 wound, 50% of them did not mount a leukocytosis and had normal temperature. Okay, bone biopsies. What do you do with your bone? Do you send it to path or do you send it to micro? Why? What are you doing in your programs and why are you doing it? Not because that’s what you do in your program, but what’s the rationale behind it? That’s what this slide, I really want to hit home on. Last year, we published, “Do you go to micro? Do you go to path?” It doesn’t matter. Statistically, it did not matter in the diagnoses of osteo, what you’re doing with your cultures, but there’s more to it than just that. Okay. We know when you send it down to histology, what are they looking for, acute osteo? They’re looking for neutrophils. Chronic osteo, we’re looking for plasma cells and lymphocytes. That part is easy, but this gets to be the literal part I hope you raise your eyebrows on now. First of all, how many are just taking one culture? I’m not talking about maybe just a digit, but back in the midfoot, the hind foot, when we get up into the leg. This is coming out of, you know, from the hip and the knee surgery. You need to be taking multiple site cultures. Why micro? Beside the diagnosis, we’ve proven there’s no statistical difference between micro and path, but the micro will also aid you in your treatment of the antibiotic. Now, this is something here. When you send them down to path, pathology is sensitive at 75%, but the specificity of it is only 42%. So, we have a positive predictive value of 77% and a negative predictive value of 39%. What happens when you go down to pathology? The specimen gets down there, and especially those of smaller community hospitals, I hope this one hits home with you. Literature in the pathology field, hold this up and look, when they show that same slide, only 1/3 of the pathologists looking at that slide agreed on the diagnosis of osteomyelitis. Here, we know what our sensitivity or specificity is, but now, we’re taking only 1/3 are in agreement, and we are making treatment decisions off of, is it or isn’t it. Again, each one of these should be added on to each other modality of your diagnosis. Please, don’t make your diagnosis just off of one specific piece of paper. Frozen sections, what do you do with the frozen sections? Hopefully, a lot of you are using the frozen sections, alright. We know that we’re looking at the number of neutrophils in the high-powered field. But again, it’s got to be multiple sites. So, what’s happening is we need 10 or more neutrophils on a minimum of five different fields for the diagnosis of osteo. If you’re only using five neutrophils on your high-powered field, you have a likelihood of the false positives. Frozen sections, the difference is your sensitivity is only at 25%, but your specificity jumps up to 98 or 100% on the field. So, we have a positive predictive value of 100, but a negative predictive value of anywhere from 73 o 95%. What will happen is because of this, more people are using this as a negative predictive indicator more so than a positive predictive. Okay, imaging. We all do imaging. What happens? X-ray, first line of defense. It’s quick. It’s easy. We can see cortical destruction. We can see disuse atrophy and all these wonderful things. But what’s the problem with the x-rays? We have a delay, three, four, five-week delay before we’re going to see a radiographic changes.

    [10:03]

    CT, we have the same problem as x-rays. CT cannot pick up and differentiate the difference between purulence, between phlegmon, between granulation tissue. Sure, it does show our gas, but here, this specific clock is on osteo. CT’s only sensitive as is the radiograph. You’ll notice a sensitivity and the specificity are both very similar. We jump down to the MR, and notice the difference on what will happen. Our sensitivity will jump up to 90%, but specificity is at 82%. Nuclear medicine is where we’re heading. The nuclear medicine is the key here. The fallacy with this is it’s only good if our blood flow provides enough flow to get our isotopes down to the affected area that we need. But our sensitivity, at 91%, specificity is at 54%. We’re going to come back and we’re going match all of these together in a second. So, we go to Indium-111 scans. Sensitivity 79% with a specificity similar. What’s the problem within Indium-111? We know and we’ve been able to track that the label gluco cyto shows up a noninfected neurotrophic bone. We can get that in the noninfected Charcot. Why? Because we have hemopoietically active marrow, and it will allow that to take up. So, what do we do with that? That’s why you need to get your sole for colloid study. When you’re doing your scans, you need to be getting both the bone scan. Why are we getting our tech scan? The tech is the most anatomically sensitive test of the three exams. So, you’re able to get your anatomy and isolate that more on the tech 99. Your Indium will be sensitive for leukocytes, but the sulfur colloid will push out, is it a marrow issue or not. You need to layer your three different nuclear scans to be able to get the diagnosis. When you’re dong it, make sure when you order your Indium-111 that you’re getting both four-hour and 24-hour pictures. This is important. When you combine Indium with your sulfur colloid scans, look at what happens. There’s level three evidence. All of a sudden now, sensitivity jumps to 100% and specificity at 94%, giving you 96% accuracy. There’s really no good reliable agents on the gallium. I don’t have a lot of experience with PET scanning. At our institution, it’s still pretty much a preview of the tumor board. But certainly, last year, there was a nice article that came out about PET for diagnosis here. I think we’ll seeing more and more as the volume increases, and certainly, the cost comes down. How do we classify osteo? If we made the diagnosis of it, what do we do and classify? How many of you are treating osteo of the ankle? You have to know Cierny-Mader’s classification for this. This is specific to adult osteomyelitis. It directly not only talks about what will happen with the treatment ability, the success of the treatment of the patient, but it matches a treatment with outcomes. Going quickly, we have four types of the anatomic location of it. You guys pull these articles. Remember, there’s the original article. A couple of years later, they’ve revised the article. There’s a second edition. You need to pull both articles. We have four types identifying medullary, superficial, localized, and diffused osteo. The second part of it talks about the physiologic component of it, the host. What’s happening with the host? Type A is a good immune and the ability to deliver treatment to that patient. A B host is compromised both locally or systematically. Then, a C host is sometimes the treatment is worse than the disease. We leave them alone, whether to the suppressive antibiotics, but they’re not a surgical candidate. You need to be pulling these articles. When you’re talking to people, one of the biggest things I try to get my residents to do when they’re talking to me and they’re trying to describe a wound, guys, you will cut 10 minutes of conversation talking to your attending if you just classify your conversations. If you call me on the phone, when you’re doing a check out and tell me you have an osteo of the ankle, “It’s a Cierny type 2, host B,” you don’t have to tell me anything else.

    [15:07]

    I understand what that means, and now, you’re talking medicine, and then go on and you just saved yourself time. So please, whatever you’re talking, these are important classifications that the literature has shown are prognostic on what’s going to occur on the outcome of it. Alright, we’re going to pass this. But when talk about the treatment of it, we know and it was mentioned earlier here today, if you let your R1s do these resections, for those of you that are R3s out here and you know amputating is beneath you. But if they’re not paying attention, half these patients are going to back for revisional surgery. This is an important concept here. Why are we treating these patients for six weeks of antibiotics? The purpose of this is to get you guys to be asking questions, where is that coming from, why is the sweet spot six weeks? Somebody find the literature that shows that. There is no literature. I understand that’s what we do, but we need to track down and see where that is coming from. There’s new literature now that talks about MRSA should be eight weeks, alright. You guys, you’re the generation who should be understanding why you’re doing way what we’re doing. Cement, and I’ll just talk real briefly about cement real quickly. We know it’s been around for 30, 40 years, okay. We know we have high concentration of it. But the question I always ask students and residents, how does cement work? You guys are putting antibiotics in it. You’re putting it in our wounds, but why? You need to go to literature and you need to understand where the solution is coming from and how the principles of it is happening. When we take this antibiotic, what is polymethyl methacrylate? Well, we know it’s a liquid monomer and it’s a powered polymer. So, we’re going to making it, and now, you guys are going to pour in antibiotic. My question is, what antibiotic are you using? The antibiotic has to be thermal stable. It has to be hydrophilic. Then, my question to you is to going to be, what cement are you using? How many of you have used this in your OR? What brand of cement are you using? There are different brands of cement. If you don’t know the brand of cement you’re using, how can you know the principles behind it? We know it hardens by an exothermic reaction, but how many of you know the temperature of that reaction? This is what you guys need to be doing as a resident is this is the type of thing you need to be looking for. The temperature range, depending on the brand of cement, is anywhere from 94 to 165 degrees. So, why does that matter? Because too often, I see my residents taking the cement, weighing till it gets putty-like, and then they’re putting it in their wounds. Well, there’s a wonderful thing to do to our infected osteo patient, that we just cut out all the dead bone. I’ve got good bone, and now, you put my cement in there that gets up to 165 degrees and kill my good bone. Each step that we’re doing needs to be understood on why it works. Where is the antibiotic coming from? Is it coming from the shape of our PPMA? Is it coming from the cracks in it? Is it eluding right from the polymers itself? Nobody really knows. Everybody thinks it’s probably a combination of the three things. We do know what happens, highest concentration in the first three days, and then it kind of evens out afterwards. We’ll pass through a little bit, how much antibiotic do we pour in? Everybody’s going to take the 1 gram or the 2 gram. But where is this coming from? There is no literature that says how much antibiotic you should put in. There is literature that talks about, don’t use more than 8 grams per 40 grams of PPMA. That part we do know, alright. The advantage of using the bone cement, you all know this part, will deliver localize without our cytotoxic concerns. It can be a real nice thing to do. Again, which antibiotic, how come no one’s using more? You want more clindamycin. We want to be specific about what part of this are we trying to treat? Here’s the advantage of having done your frozen sections. Where did you take the specimen from?

    [20:00]

    Where did the tissue come from? Was it the tissue surrounding my bone? Was it in my joint? Was it on my hardware? Because different antibiotics have higher concentrations in our seromas, in granulation tissue and in bone, so we want to be able to narrow down and identify what we’re trying to do and where the best antibiotic to be able to do this. The allusion, I mentioned briefly about. It’s a passive type of a content. Alright, let’s go through this real quick. Alright, it doesn’t matter if we’re trying to use the joint spacers or if you’re trying to use rods. You can make it. Burns had a great article, how he gets his cement on. We just use test tubes with a wire right up. You should just make your own and you can put it right up. It doesn’t really matter where you’re trying to do. Alright, real quickly, the last part of this is the reamer irrigator aspirator. Hopefully, you’re all using this, again, for your hind foot and your tibial osteos. You need to be reading. If you’re not familiar with this, Hyer had a great article on this, French [indecipherable] [21:15] came out in the ortho trauma literature last year with it. The advantage of this is it’s a two-tube system. You’re able to take it up. Assuming you’re going to be using an IM rod, the first one rims it. You’re going to be able to irrigate it, but then you’re also going to be able to obtain the stock from the tibia, and that collects in a separate bowl that you’re able to use for bone graph. We no longer have to be opening the hips or using any other type of a product. We can get it from the same patient. The Masquelet technique, why are we using the antibiotic? Because of this concept, alright. When we put in the antibiotics, we know the membrane that’s going to develop is up to 2, 3 millimeters in thick. We know the cells that are on the inside of it, the growth factors, we know it will help protect our bone from further destruction. When we put in the cement, the part where you want to careful, trying to get the membrane to come over, the trick here is don’t allow your cement to go posterior, anterior or outside your bone cavity that you wanted to be. You want it to fit snug right up to all four of the cortices within the bone. You can leave it in for as long as you want, cut it out, and then go ahead and however you choose to repair it. Alright, hopefully, if you have questions or you need the literature, feel free to email us. We have everything cited and we’ll be happy to get you the articles. Thank you very much.

    [Applause]