Guido LaPorta, DPM, FACFAS, MS discusses the diagnosis and treatment of osteomyelitis. Dr LaPorta reviews tools and methods of diagnosis and the advantages and disadvantages of specific antibiotics used with or without surgical intervention for treatment. He outlines literature and experience that support both conservative and/or surgical interventions.
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Gran: Diabetic foot osteomyelitis is indeed a surgical disease, so Dr. Port [Phonetic].
Dr. Port: Thanks, Gran [Phonetic]. We’re actually going to have to reevaluate our friendship. First, I get to talk I know nothing about. Secondly, I have to counterpoint Dr. Jeff Kirk [Phonetic]. Thank you very much. I guess there’s an old adage, “If all.” I’m going to come to it from a surgeon standpoint. Quite frankly, what I just heard is very much you own is a hammer, everything looks like a nail commonsensical to me and seems to be something that we should all consider. But I would suggest to you that medical treatment of osteomyelitis may be a very effective alternative when one is talking about osteomyelitis in the digits and possibly even the metatarsal heads. But I would also suggest that as one moves more proximal into the midfoot, talus, calcaneus, even tibia, that that may not be a good alternative as a primary interdiction. It may be. The answer may lie in what we diagnose as osteomyelitis and what type of osteomyelitis that we have. Suppose this patient comes in, who’s had a diabetic patient, who’s had a previous ankle fusion with an intramedullary nail. The nail is now migrating. It is toggling within the tibia. If you look closely enough around the margins of the nail, there’s a radiolucency suggesting at the very least loosening, possibly even infection. He arrives at your clinic with this Ceretec white blood cell scan and presents like this. This is osteomyelitis in a diabetic patient. What I’m trying to point out is that, can it be treated medically? I think it depends on your definition of osteomyelitis and maybe even the geographic location of what in fact you’re treating. In this particular case, we elected not to treat it medically, at least medically alone. We elected to treat it with a combination of surgery and antibiotics. We use the antibiotics in one of two ways, not just parenterally but also locally in the form of antibiotic beads and antibiotic nail. This patient had a nail. We removed it. You can see an antibiotic nail used in its place to treat intramedullary osteomyelitis, antibiotic beads over a drain and this is very difficult patient, this was a 50-year-old. This was Ohanda [Phonetic], I think I heard before. This was a 50-year-old patient with diabetes, alcoholic problem and certainly a very non-adherent patient. Yet, in this particular case, it took us seven months. But we got to a point where not only did we remove all infected bone but we’re able to affect the solid fusion, and the leg lengthening. If you were to ask me, could that be achieved in this particular patient pre-op, I would have basically said no. What about the type of osteomyelitis? Well, Cierny-Mader classification tells us a number of things that we should be familiar with. I would suggest that if we have a superficial, even a localized osteomyelitis that medical treatment may in fact be very effective and should be tried first. But once it becomes medullary or once it becomes diffused, at least in my clinical setting, I would be expected to attack that surgically and with antibiotics. The first thing that I would have to do as a clinician is make a diagnosis and I can do that in any one of a number of ways. The gold standard, of course, is the bone biopsy which can be done at the time of debridement.
But many times, we have to make a clinical decision prior to doing that. How many of you have had on service when you’re co-managing a diabetic patient, have somebody order a triphasic bone scan to help you out? I’m sure a number of you had, right? It basically is a totally useless test other than to tell you that something is wrong, okay. How do we make a diagnosis? What are things we have to be familiar with? Well, we can do it clinically. We can do it with lab analysis. We can do it with microbiology, pathology and imaging modalities. How about our bone biopsy? Is there a difference between histology and microbiology? The literature would suggest that it pretty much gives you the same amount of useful information. If you look at the pathology, pathology has a sensitivity of about 75% and specificity or 42% with a positive predictive value of 77, a negative predictive value of 39. Its reliability is about 33%. Well, why would that be? Well, it depends on how your lab handles the pathology. The only really good studies about pathologic benefit or in periprosthetic infections, there are very few studies in the patient population we’re talking about. But one of the things you can go down is ask your pathologist what their criteria is for diagnosing infections. Are they looking for 5 or 10 neutrophils per high power field? How about frozen sections? How do you feel about that? How many do frozen sections at the time of debridement? Frozen section has the sensitivity of 25 to 28% but a specificity of 98 to 100%. It has a positive predictive value of 100% and a negative predictive value of somewhere between 70 and 90%. It adds time to your operative procedure but it gives you good information. You may want to consider that with your bone biopsy to see if in fact you have done an adequate debridement. What about imaging modalities? Well, x-ray and CT scan are pretty much similar. They have a sensitivity of 75, specificity of 74. But it’s difficult and there is no differentiation between osteo versus Charcot. And that’s my toughest clinical problem when I’m dealing with these types of patients. MRI has the sensitivity of 90% and a specificity of 82%. They’re better than bone scans. Most people say, if no Charcot or hardware, but my experience clinically is that the MRI is as good as the person reading it. Unless you have a musculoskeletally trained radiologist, you can give confusing readings from your MRI. I’m going to get an MRI and say suggest bone scan based on the results where you get a bone scan and suggest MRI. Well, I think it’s difficult to rely on one test to make that particular diagnosis. In fact, I think MRIs tend to over read most things. How about nuclear medicine studies? As I mentioned before, the triphasic bone scan is in fact, in my mind, a waste of time with respect to trying to differentiate between osteomyelitis especially in Charcot disease. All of our medical colleagues ordered this and it makes for good arguments and food fights and things like that in cafeteria. But it gives us very little information. The literature would suggest that indium has a sensitivity of 79, specificity of 78. But an interesting phenomena occurs when you combine indium and/or Ceretec with sulfur colloid scans. You’ll notice that it has an accuracy up in the 90s as far as being able to differentiate osteo from Charcot. The terminology is concordance. If you have a positive Ceretec and a positive sulfur colloid, you probably do not have an infection. If in fact you have a positive Ceretec and a negative sulfur colloid, you probably do have an osteomyelitis.
If you have a negative Ceretec, your job is done. You don’t have to go any further. Gallium is not used too much anymore, it’s pretty much shown to be non-reliable. Of course, everybody is chomping it a bit to utilize PET scans in order to make this particular diagnosis. Now, I noticed that some of the articles that were quoted previously, I’m also going to quote. It’s observations made about antibiotic treatments. Senneville said there was a 36% failure when treated non-operatively. Indecipherable] [10:43] said there was a 44% failure with deep infection when treated non-operatively. Kowalski, 44% failure when surgical resection left a positive margin. And 44% need a more proximal AMP when a positive margin was left behind. Therefore, I think there is good evidence for the local use of antibiotic cement. Buchholz and Engelbrecht in ‘70 were the ones to show that if you had high concentrations of antibiotic locally, that it would elute into the local tissues. Stevens agreed and noted that there was a lack of systemic risks. It needs the antibiotic that you use, needs to be thermostable and hydrophilic. Palacos itself, in antibiotic-impregnated PMMA was shown to be bioactive levels of above the minimal inhibitory concentration at 80 days. The typical antibiotics that that are used are gent, tobra, vanco and cephalosporins. The dosage is debatable but most people would agree that you should not go above 8 grams per 40 grams of PMMA. Setting properties will vary with humidity. The setting properties in northeastern Pennsylvania where I’m at are different than they would say be in Atlanta where Ciranni [Phonetic] practiced for much of his career. How about the illusion characteristics? Clindamycin is definitely the best. It has high seromic concentration and granulation tissue and bone. Tobra and vanco are both considered to be good. Tobra has high seroma and granulation tissue but poor bone. Vanco has poor seroma but high granulation tissue and bone. But you noticed they’re used together a lot. There’s a reason for that. The reason is that the tobra elutes quicker. Because of that, studies have shown that as it elutes quicker, it makes the PMMA beads more porous and allows for more elution of the vancomycin. You noticed in the studies that vanco eluted at a higher rate when it was combined with tobra. One of the reasons they’re used together is for that particular effect. It’s also been shown that if you add a soluble such as dextran to the beads that you can get a higher elution of antibiotics into the soft tissue. Because of the phenomena of intracellular Staph aureus which I have become enamored with over the last half year, we are now routinely adding rifampin to the beads. But Warren [Phonetic] told me, “Why do that? Why not just give it orally and have a potentially same effect when treating this?” I think that’s something we should be paying more attention to. There is a phenomena with intracellular Staph that Staph aureus can invade the osteoblast. As soon as it does, it becomes less effective and the antibiotic can’t reach it. The osteoblast dies. It’s a double whammy, if you will. It’s protected from antibiotics to some extent. The osteoblast can’t function like an osteoblast. Consequently, I think it’s important you realize that and also to realize that one of the medications that can effectively address the intracellular Staph is rifampin. There are other tricks. You can use a RIA device. This is a reamer, irrigator and aspirator, especially when you’re dealing with tibial osteomyelitis.
You can irrigate the canal if the IM nail is infected. You can ream to the proximal tibia so you can actually recruit good bone graft and get autogenous bone graft. You can also use the concept of induced membranes, known as Masquelet technique. Membranes one to two millimeters thick or form, they’re rich with growth factors. What you do is place in an antibiotic spacer. That spacer needs to cover both ends of the bones. It’s removed in about four to eight weeks. Instead of curetting that nice membrane out, you take advantage of the fact that it is full of growth factors and you pack it with cancellous bone. There is a reported 8% failure rate, so this really should be used only in defects that are within two to four centimeters. If you have a larger defect, the Masquelet technique is proved to be ineffective. Let me answer the same question. Can medical treatment of osteomyelitis be effective? My answer is yes, and no. I think it depends on the quality of the osteomyelitis, how it affects the bone, and the geographic location. I would not hesitate to use medical treatment as the primary approach in digital and metatarsal head osteomyelitis. I would be very hesitant to depend on it alone in more proximal forms of osteomyelitis, specifically those which are diffused and/or intramedullary. The end. Thank you.