Lessons in Orthopaedic Leadership: An AOA Podcast
Lessons in Orthopaedic Leadership: An AOA Podcast
Revolutionizing Fracture Care: The Future of Orthopaedic Trauma with William T. Obremskey, MD, FAOA
Douglas W. Lundy, MD, MBA, FACS, FAOA, discussed the future of orthopaedic trauma with William T. Obremskey, MD, FAOA, Director of Orthopaedic Trauma at Vanderbilt University Medical Center. Dr. Obremskey shares his vision for the future of orthopaedic trauma surgery, focusing on reducing complications through advanced technologies and improved practices.
Perhaps most thought-provoking is Dr. Obremskey's perspective that some of the most impactful advances may not come from fancy technology at all—but from addressing underlying patient factors like smoking cessation and blood sugar control that dramatically affect healing outcomes. The future of trauma care involves both cutting-edge science and fundamental public health initiatives working in tandem.
Welcome to the AOA Future in Orthopedic Surgery podcast series. This AOA podcast series will focus on the future in orthopedic surgery and the impact on leaders in our profession. These podcasts will focus on the vast spectrum of change that will occur as the future reveals itself. We will consider changes as they occur in the domains of culture, employment, technology, scope of practice, compensation and other areas. My name is Doug Lundy, host of this podcast series.
Speaker 2:Joining us today is Dr Bill Abramski is the Director of the Division of Orthopedic Trauma and the Fellowship Director for Orthopedic Trauma Research at Vanderbilt University Medical Center in Nashville, Tennessee. Bill also serves as a lead investigator for the Major Extremity Trauma Research Consortium, also known as METRIC, which is a large clinical research network aimed at defining treatment guidelines for injuries throughout the world and specifically combat injuries. Dr Obremski did his doctor of medicine at Duke University and then also did his master of public health at the University of North Carolina. At Chapel Hill he did his residency at the University of Washington Medical Center, then his fellowship at the AO Research Institute in Davos, Switzerland. Not only after that, he also did his management in healthcare master's degree at Vanderbilt University, where he's currently, of course, on faculty. So, Dr Abramski, my friend, welcome to the podcast series, sir.
Speaker 3:Doug, thank you. It's a pleasure and an honor to be here.
Speaker 2:Thank you, bill. Thank you very much. We appreciate you being on and, as I was saying before, so I've known Bill for quite a while. In full disclosure, I did my trauma fellowship at Vanderbilt University and Bill and I have overlapped in many places over our careers. But Bill and I were also on the question writing task force for the American board of orthopedic surgery and it became very clear to me that I didn't know anybody who knew the orthopedic literature he's embarrassed me saying this, but I'm going to say it anyway better than Bill did, and so I don't think there's anybody I would rather talk to about the future in orthopedic trauma than you, sir. So when we look at where our specialty in orthopedic trauma than you, sir. So when we look at where our specialty in orthopedic trauma surgery is headed over the next 10, 15, 20, whatever you feel comfortable, going out to years, where do you see us heading in the future within the United States and North America about trauma surgery?
Speaker 3:Sure, I think our advances will be more in identifying and preventing complications, in that it's truly amazing that the human body heals the vast majority of times, sometimes in spite of us, and in orthopedic trauma we have maybe one of the highest complication rates in general if you look at infection and non-union compared to any other specialty.
Speaker 3:The total joint doctors are up in arms about an infection rate of 0.5% and there's been more literature on that and ACLs and stiffness, the number of NIH grants go into those things. But we truly, in 2024, have infection rates of 20% to 30% in some pretty common injuries open tibia fractures and peel on some plateaus, and non-union rates of you know, even in one of the most common surgeries of, you know, clavicle fractures of still 5%. So I think a lot of our future will be hopefully decreasing the complications and maybe helping us predict who is at risk for those complications and even significant complications like DVT or infection as well from biomarkers. So I think that's the general area we will be heading to try to decrease some of those problems, and I guess I could talk about some of the specifics of those.
Speaker 2:So I know that you've been involved in some pretty extensively high level collaborative research on preventing and diagnosing infection and orthopedic trauma. Can you tell us briefly about what your consortium has been working on and what that consortium is?
Speaker 3:Sure, I have worked with the well.
Speaker 3:I think it probably came from working on the OTA evidence-based medicine committee and when I was lucky enough to chair that for the task force and then the committee for a total of about 10 years.
Speaker 3:But we did some work on infection prevention with open fractures and developing some guidelines. And somewhat because of that work the AO group was looking to incorporate more of a collaborative and international group of people and asked me to, as the OTA representative from the Evidence-Based Medicine Committee, to participate on a group, the AO Anti-Infection Task Force as it was called at the time, and that group looked at the literature and tried to develop a consensus evidence-based medicine guidelines and consensus recommendations with several members of the OTA and then the AO as well as several international groups from around the world to participate in that. And I think we tried to look very critically at the world's literature to try to make management or treatment decisions for prevention and management. And also around the same time the Parvizi group had expanded their infection prevention to all specialties and we had a summer meeting in there and I helped lead that group and one of my goals was to try to make all these consistent so there weren't conflicting guidelines across different specialties.
Speaker 2:So some people could accuse us of being knuckle draggers, because in many ways, I think we probably are, because I know many orthopedic trauma surgeons who are still using the antibiotics that still on Anderson recommended in 1976 for crying out loud. So what are your thoughts in terms of what should we be doing currently to reduce infection in 2024? And you talked about biomarkers and other forms of technology. Can you tell us what's been being worked on that's going to propel us into the future?
Speaker 3:Sure, looking at infection prevention, maybe open fractures are a reasonable model for that and, as you said, we are still in 2024, not a hundred percent sure what the right dose and duration of antibiotics are to prevent.
Speaker 3:The metric group has a proposal in to try to work on this in a large-scale fashion. But the current recommendations so far for type 1 and type 2 and possibly even type 3 open fracture is that you need a first-generation cephalosporin primarily and that for those that are at higher risk for gram-negative, which are type 3A contaminated fractures and or 3B, that we increase the spectrum to have gram-negative coverage. And historically those were often gentamicin. I think both of those the guidelines and the Parvizi infection ICM guidelines both caution people on using gentamicin in that we don't always know people's renal function when they hit the door and that that can potentially cause some renal or nephrotoxicity and so. But some gram negative coverage has indicated the exact type. Whether it's genomycin or fluoroquinolone or tobramycin is not completely clear or whether you just need a third-generation cephalosporin, septazidime or some type of broader coverage for those. There's a little bit of data that indicates that type 3 contaminated fractures. That extension beyond 24 hours is helpful, up to 72 hours.
Speaker 2:So tell us about these biomarkers you were discussing and what technology is being used in the future to reduce infection rates.
Speaker 3:Yeah. So I'm not sure that the biomarkers will help us reduce them initially, but there does seem to be some evidence from micro RNA and that the those who are at risk for non-union and infection is evident very early in their serum. One thing Vanderbilt is very you know, I guess, lucky to have is that we have been gathering patient serum for 15 years and there's hundreds of thousands of patients that are in a database and I am working with the AO Institute to attempt to look at people who have and have not had non-unions or infections and look at the early microRNA that are present when they are early postoperatively to see if some of those hypotheses or what micro RNA you know may help predict those who are going to have a non-union or be at risk for infection. It may not be 100% but it might raise our you know, level of concern or earlier intervention in those at risk.
Speaker 2:What about implants? You could obviously we can coat implants with bone healing chemicals versus antibiotics, versus both. How do you see the implants being changed that will help mitigate our two, you could argue. Our two biggest complications on the fracture side are non-unions and infections. Of course, we have the whole DVT thing to deal with as well, but how do you see the implants helping with that?
Speaker 3:How do you see the implants helping with that? Yeah, so there's only one coated implant on the market currently is a genomycin coated nail and been released about 10 years in Europe, but there's surprisingly little data on that. Does it really decrease infection rate? I think there have been other nails that have been electrically charged to see if that electrical charge tries to decrease infection rate. And a nail like that is also available internationally, but not in the US, with a gold palladium coating which creates a charge, electrical charge that may help repel bacteria to prevent them from sticking to the implant. And Christina was right 60 years ago. You know it's all about the race for the surface. And how do you prevent that? With a local antibiotic, with the centering or some sort of modulation of the surface of the implant to make it more amenable for eukaryotic cells as opposed to prokaryotic cells. So I think all those things may develop over time either antibiotic coating or electrical coating or some sort of a sintering of the implant to make it more amenable, to prevent or to make it more unlikely that bacteria prokaryotes will adhere to the implants. The other thing that in terms of infection is not just the implants but maybe local use. You know the metric group has done the Banco trial looking at use of local antibiotics, and have the infection rate of gram positive from 7% to 3% with use of vancomycin in use in pylons and plateau fractures. The problem is it's still 3% and it didn't affect the gram negatives and powder goes away fairly quickly. And I think there will be other substances such as hydrogels and or a macromolecule polymer that often has a combination of PDLA, lipid and then drug of some sort that can be applied and protect the race for the surface longer, and that how long that is exactly? But it's probably in the three to seven day range. And if you look at when cells migrate onto implants and so we can have some substance like that that can be put in the wound at the time or in the canal at the time of implant fixation, a bone fixation with implants that they can help protect the implants, that that will probably be the next phase. I think eventually we will probably have implants that are made of peak or some substance like that that will eventually dissolve or slowly dissolve and eliminate.
Speaker 3:You know what no surgeon looks good doing the hardware removal phenomena. That's right. It's one of the most common procedures for orthopedic surgeons applying for their boards and it's a huge healthcare cost for hardware removal. And I in clinic this morning I signed up two you know people who they're tired of their olecranon plate or tired of their screws on their anterior medial tibia from a nail and, and some people just want their hardware out. And if we have slowly dissolvable plates or nails that modulate and change their, you know, change their elasticity as they dissolve and that that may help, you know, eliminate that complication of you know, change their elasticity as they dissolve and that may help, you know, eliminate that complication of, you know, hardware removal. Whether you've got a complication expectation, it may be a, you know, purely parsing your words, but it's a huge healthcare cost and a risk cost. You know there's nothing you can't make worse than an operation.
Speaker 2:Right. How about non-unions, both from a implant standpoint, in terms of improving our implants?
Speaker 3:the freshness to heal better and also the biologics.
Speaker 3:Yeah, I hope one thing we can do is educate people to stop things or control do a better job of controlling things that put them at risk for non-unions, such as their hemoglobin A1C, or stopping smoking and help their own biology. I do think that we will eventually have either coating on the implant but it's probably more appropriate to have it at the fracture site a implantable and biologics that occur in the right sequence. You know, right now we have BMP2, you know which recombinant BMP2, which is just a foghorn, a huge super physiologic blast, and what you need is a symphony of, you know, bmp7 and BMP2. And then you know PDGF and some sort of up and down regulation at the fracture site, and we will probably figure that out someday and have some sort of coating or implant or goes in like toothpaste and sets up like concrete and provides additional stimulation but also has, you know, the correct biologic transformation and release of bone healing substances in the right sequence and the right dose.
Speaker 2:Very interesting, very, very good. So what about deep vein thrombosis and pulmonary emboli? You and I treat injuries that set folks up for those, yeah, proximal femurs, pelvis. We've probably way over-treated people.
Speaker 3:We've probably way over-treated people. We have probably way over-treated some people and way under-treated some people. And you know, I think we were both part of this large 12,000 patient prospector randomized trial of multi-trauma patients looking at aspirin versus Lovenox and I think what we all knew and the total joint docs knew before is that lovinox causes bleeding in some people and it can be a problem and increase their risk of reoperation and infection because of the blood that's in the in the area of the injury and bacteria like blood. Ever heard of blood auger? That's what they grow it on. So it's a huge risk for patients having, you know, excess bleeding at a fracture, at a fracture site or injury site.
Speaker 3:And there are probably people who are clotters that may clot no matter what you do. And there are those who are non-clotters and this is also where I think the biologic, genetic makeup or understanding those who are really at risk for clotting and you probably only need to prophylax those who are really at low risk for clotting for a very short period of time until they are up and mobile and then those who may need it for a much longer time and need one or two substances that maybe help prevent their coagulation cascade at a couple points. Right now we have found that platelets blocking platelets which are the beginning of a clot with aspirin is as good in terms of DVT prophylaxis, preventing PEs, preventing DVTs, preventing all-cause death as Lovenox has been. That we have been done and we are beginning to make that transition.
Speaker 3:That was a New England Journal article. I think we can probably be even more specific, more patient specific, based on their gene pool. We just haven't figured out what that gene pool is, but I envision the day where you come in, you're a multi-trauma, we draw your gene pool. Come in, you're multi-trauma, they. We draw your gene pool, we run it through the, through the, the match.
Speaker 2:We, we know that you're at a 10 or 20 or a 50 risk for dvd prophylaxis and that you will respond to platelet blockers or cascade blockers or both, depending upon your risk profile that's funny seeing that I'm looking at that vanderbilt health sign behind you as you're doing this and I always my youngest, my oldest son was born while we were at Vanderbilt and I always thought that someday he's going to look at what I do and go well, bless his heart. Dad thought he was doing the right thing, but we all know it's this thing now. But things are going to change so dramatically between the time that and you have. You have a daughter who's a physician, don't you?
Speaker 3:dramatically between the time that and you have, you have a daughter who's a physician, don't you? I have a son and a daughter that are both smart like their mother, and pediatricians.
Speaker 2:Ah, okay, all right, let's step out of the clinical. We'll directly clinical run for a minute and start looking at some of the healthcare practice and stuff like that. Like everything else in the world, orthopedic trauma surgery is heading into the outpatient arena. Where do you see that headed?
Speaker 3:I mean that's a train that's already headed that way and you know our entire department is planning on moving offsite and having an offsite. You know 24-hour surgery and ASC and that'll probably just continue, except for multi-trauma. You know complex spine, complex joints, tumor cases and that's probably better. I think every time it's been studied that it's done more efficiently with greater patient satisfaction, with lower complication rates in those outpatient or you know systems where that's what they do at that surgery center is they do pylons, they do plateaus, we do. You know outpatient fracture fixation and you can increase productivity.
Speaker 3:The patients drive up, they get in their car, they drive away. I mean every day today in clinic, every patient. I apologized for the parking, the transport. You know we're under construction and it's just impossible and they walk, they walk, they walk farther to come see me than I probably do from our parking lot to the clinic and but that's that's just part of it. I think can you do it safely with patients and our we think we'll rely on our anesthesia team to identify those patients that can safely have outpatient or 24-hour surgery in a different setting than a main hospital.
Speaker 2:You kind of tapped around the edge of it, but I found regional blocks, especially with the bupivacaine sorry, the liposomal bupivacaine to really help out. Have you stepped into that part?
Speaker 3:Oh, yeah, I like to say I am the greatest utilizer of the block team in the entire hospital. I just, I mean it, we've studied it works right, you know, I mean, some people hate to get stuck with the, you know, stuck with the needle before and I think it takes communication and we have developed a protocol with our anesthesia team that you know. These are the things that you can block and we want you to block them and please block them pre-op and if there's any questions, or we put in a note saying you know, we need to check the radial nerve post-op. So don't, you know, don't block it before. But blocks, you know, decreases anesthetic intra-op. Decreases delirium post-op. Decreases narcotics post-op. Improves patient satisfaction. What's the problem? Right, I? Uh, and yeah, you have to have a system so they're not delaying your time by 30 to 40 minutes by doing that. But I, I think we will continue to use different blocks. You kidding me when, when you and I were in training, you gave everybody intramuscular demerol, right, you know, we kept total knees in the hospital for five days, immobilized their knee and gave them Demerol for three or four days and zonked them. And you know, now you're getting non-union operation as an outpatient. So yeah, we will continue to make advancements in regional block.
Speaker 3:And not just that, but multi modal medication. And you know, now we use multi. You knowontin, tramadol, toradol, you know a variety of medicines and we know they work better together and the ota wrote some great clinical practice guidelines for that. And it's not just the medications. And you know joe shoe. Joe shoe has been great at promoting multi-therapy. You know, using aromatherapy or sound therapy, electrical, you know 10 unit therapy. There are lots of different modalities that just work. Every time we've studied them in prospective randomized trial. They work better than monotherapy. And just given and I was guilty, I gave everybody Oxycontin, you know, and we create a lot of addicts based on false data and we were guilty, so we got, so we were part of the problem. We need to be part of the solution and read our literature and change our practices to try to decrease the problems which we have created and with better pain control with patients.
Speaker 2:Now, how many orthopedic surgeons do y'all make every year? Were there in Nashville Four or five. I know it was five when.
Speaker 3:I was. Our residency program has five, just going to six last year.
Speaker 2:I think there was four when I was there, I can't remember, I was only there for my fellowship. But so y'all are making five a year. You're fixing to make six a year. Those are very expensive people to make orthopedic surgeons. You and I both know that. So in the future, let's, let's crown you as a secretary of health and human services.
Speaker 2:Okay, so now you're doing that. How do you see the scope of practice in terms of developing what the nation needs in the future for orthopedic trauma surgeons? Are orthopedic trauma surgeons doing all the fresh work? Do we have other people doing the ankles and the other stuff like that and we are doing the high energy stuff? What's the best utilization, as we go forward, for the workforce?
Speaker 3:Yeah, I don't know the answer to this. I do know that, in general, 90% of fractures are cared for in this country by non-fellowship trauma trained individuals, by non-fellowship trauma trained individuals, and so we cannot we being the Orthopedic Trauma Association generate enough orthopedic surgeons to do all the fracture work Right, and so routine fracture care has got to continue to be part of the general orthopedic knowledge, so that ankles, wrists, hips, you know, femoral neck fractures, can all be cared for by people who are well-trained in general orthopedics. That that should probably maintain, and so and they can stay close to their home for care and to just help make sure that people continue to be competent and patients could get care with that, and so I don't think that will or should change. I mean to continue to provide excellent educational opportunity to help them with the fine points, to identify, maybe, what's not routine and to transfer patient, transfer care that they're not comfortable with. And I do see, though, that complex fracture work is expanding into the level twos. You know, when you and I do see, though, that complex fracture work is expanding into the level twos, you know, when you and I were training, it was almost all level ones. Everything got shipped there.
Speaker 3:The reality is that you know we have been fortunate enough to train enough orthopedic trauma surgeons that now the primary place that our graduates are going on the fellowship committee are going to level two centers. Personally, I think that's a good thing, I think they're, and I think it's good for patients, it's probably good for local orthopedic surgeons and and hopefully it's good for the our trainees that are going there and they're a resource in their community that can do the harder fractures or those that you know that maybe need a little more experience. And and also so that the everybody, the total joint surgeon or the sports surgeon don't feel compelled to start that tibia nail at seven o'clock at night after their you know their last elective case went and you know they're tired, the team's tired. I mean, even at Vanderbilt we are one of the busiest trauma centers in the world. It's got to be really bad for me to be there doing it after 7pm, because I am not much good by myself and and and when I say give me a what's it and I get a who's it in my hand and and they are. They look at me and say I don't know what you're talking about.
Speaker 3:I mean, even at a busy place like ours, our personnel are just not skilled enough and and there are many things you just need the A game team and you know we have been fortunate to go through that transition to make trauma more semi-elective. I mean sure there's things that we're going to have to get up middle of middle of the night and do Dirty, dirty compartment syndrome, bad infections, bleeding to death but the routine stuff I can and hope should be semi-elective and that systems will have OR capacity and personnel trained available in terms of x-ray techs, scrub techs, first assistants, to make it a much more sustainable life and career. I feel fortunate we've been able to build that at Vanderbilt and you've been our guest speaker and you've seen our system and I tell our fellows when they leave that you're going to miss us a little bit, the faculty. You're really going to miss our techs, our cast techs, our system that we've built around it with APPs to help us run a fairly efficient high volume system.
Speaker 2:I barely recognized that. I was there 98 to 99. And when I was up there it was like, wow, this place has exploded and it was great when I was there and it's unbelievable now. Trauma. Now, obviously you and I are highly biased on this, so I can hear everybody rolling their eyes and that's okay.
Speaker 2:But trauma is the number one killer of Americans between the age of six months and 45 years of age, and so our disease process that we treat is crippling the American economy, the North American economy, the world economy. When I work in Africa, it causes a massive amount of problems there for the economic driving force of the societies that people are injured in. So, as you and I also know, a significant amount of funding is directed toward cancer, cardiac disease, hiv you name it as opposed to what you and I also believe is something that, if more money and attention was applied to it, we could really make societal changes for a disease process that massively affects a significant amount of the economic driver and the of important workforce folks in our country. Once again, your secretary of hhs, how do you fix this? Heck, I'll make you president us. How do you fix this problem? What? What do you think in the future. What's the right thing to do to try to mitigate this? This? However, you want to finance trauma care, trauma prevention, whatever.
Speaker 3:Yeah, so you know, I was a undergraduate econ major and, as you said, I did a business degree a while ago, and so in my view it's it's about value and and what's the cost per quality adjusted life year and that's cost per quality in the econ world and I hope we get to the point where that society at least looks at where you're going to put your investment. I mean, the amount of need is infinite in terms of problems of the human condition and every government you know needs to put resources towards what I would hope would be those where they get the greatest bang for their buck. And for I don't know 20 years I have been saying you know, bring it in terms of orthopedics in general or particularly orthopedic trauma. You know, right now total joints get all the credit for having one of the lowest you know costs per quality. But the reality is that I would say, compare that to a femur fracture. All right, you know. I mean the average age of a person with a total joint is 60 something. Average patient with femur fracture is 40 something, this 40 year old. If they don't get this done, 60% don't go back to work. This is why Switzerland invested in femoral nailing and why the Swiss government funded the AO Research Institute in the 50s 60s, because they realized they had a workforce and they had a universal coverage and so people would go back to work. And so the cost just think of the cost per quality of those two things Total joints are more expensive than a femoral nail. Their patients don't live as long, they're not working anymore, they're not paying taxes, assuming they're retired and this 40-year-old's got another 20 to 30 years of work life in them. And so if you want to run that economic analysis, bring it.
Speaker 3:And so in a world where value matters and maybe worlds or governments have to make decisions, I would hope that you and I, or our specialties, could make that argument that this is worth investing in in preventing disability death. You know the deaths come from motor vehicle collisions and that's maybe. You know we the rare, our patients don't usually die. They do occasionally they get infection at around or you know. But the prevention comes on the car manufacturers on the driving on.
Speaker 3:You know, preventing drinking and driving and drinking and motor scootering in Nashville, taxpaying people to requiring government assisted often, and investing in those people to prevent disability, to return them to the working force, I think could be the ROI on that. I mean, you're the business guy, you've been the leader of huge groups and chairman of the department and you understand ROI. If you're going to put your where's your, where are you going to put your investment? Your return on investment would be much greater in that population of people who are going to return to work to avoid complications of infection, non-union DVT or death or amputation. You prevent those four things or amputation. You prevent those four things and you have greatly improved the quality of life with a fairly low cost per quality adjusted life year.
Speaker 2:That's funny. You were saying something I thought. We did a tour of the Porsche museum in Stuttgart and there was a little plaque that if you weren't looking you'd miss it. But they said that deaths from motor vehicle collisions have decreased substantially and of course they patted themselves on their back for their vehicular safety. But they did acknowledge that trauma care had improved dramatically over that time.
Speaker 2:But thinking out of the box I think you touched on this, I know you touched on this earlier and I think this may be the disruptive way of looking at it. Tell me what you think of this. In many ways, if we want to really reduce the complications of fractures, many things outside of the things that you and I focus on on a daily basis specifically eradicating smoking and doing something to help with these horrible HbA1c's that we see all the time would materially probably do more than many other things we do. Unlike the joint surgeons, we don't have the opportunity many times to tee our patients up. We do in a non-union setting, but prior to that we don't. It's kind of interesting to think that maybe in trauma surgery, if we could hit a magic wand and get rid of smoking and get rid of crazy HPA1Cs. We may do more to affect the outcome of our care than almost anything else. What do you think of that?
Speaker 3:Oh, I know, we know that's true, you know orthopedics and the consequences are public health diseases and crises. And you know, I think it's pretty common knowledge that smoking increases non-union infection rate. What's not really been known is that hyperglycemia, perioperatively is also raises infection rates. And and I mean we have looked at this retrospectively, prospectively, in isolated orthopedic and in multi-trauma patients and published it. All the above and every time that the odds ratio of infection with hyperglycemia in non-diabetic patients raises the risk about three times equal to an open fracture of having a perioperative infection, a fracture-related infection. So this perioperative hyperglycemia is huge, even in the non-diabetics. So in the diabetics it's even greater. And you're 100 right. That's where those who are at risk is, where we ought to put as much or as as of our effort as we can it's almost funny that the best thing made me to come out is none of the cool sexy technology driven stuff.
Speaker 2:Have it's. Just quit smoking and get your diabetes under control and we, materially, would do more yeah yeah.
Speaker 3:And the chronic inflammatory state of obesity is a problem as well for fracture healing and the hormonal imbalance of that. That's more of a data-free opinion, but I think that it's true.
Speaker 2:Funny that that would be the thing that would really help the most. So where do you see the future as it relies or relates to the management and or the prevention of fracture-related infection?
Speaker 3:Yeah, we talked a little bit about prevention in terms of the patient-coded implants or local antibiotics. But one thing that is feasible and I think in almost every systems is the fix and flap philosophy which the Oxford group in Europe has really promoted. And I think they're right. And I think Paul Tornetta recently put together a four 400 plus tibia fractures and the greatest predictor was doing the fixation with doing the flap coverage within 48 hours of definitive fixation. And we have a patient like that this week that came in he's got a 3B tibia. My partner did IND damage control plate, did another debridement yesterday and then I'm going to do a debridement and put a nail in it tomorrow and then on Friday morning the patient is scheduled for their free flap and to try to minimize that time from a system standpoint in trading off who's taking care of the patient and then providing definitive coverage, you know to try to decrease the time to race to the surface and get that patient covered is within 48 hours. So that's one thing we're trying to do for prevention, the management future.
Speaker 3:I think we've come a long way but we still have so far to go and I think part of it is this once bacteria become established. They're really hard to get rid of. I just it's like a worthy adversary. And you know, I was a Duke guy. I spent undergrad med school at Duke and I sort of think of his Duke Carolina basketball games and Coach K and in 40 years he was 50-50. He only won half the games. That's just a great rivalry, and in our fight with bacteria we won't always win but we should do better. And because, you know, staff in particular goes up the canaliculi of our bone trabeculae, they form micro abscesses, they form biofilm, become senescent and in none of those I mean even our white blood cells can't get up into the canoleculi. They can't get in the micro abscess, nor can they get in the biofilm. And so we have got to develop some ways to try to help eradicate infection once it's established. And I think some of those on the bacteria and also in the bone and some of those ways that I think that we might make progress in the future, because our recurrence is embarrassingly high. When we look at infected non-unions, the management of those, we fail one out of five about the reality is when you look at large series, it's about a 20% failure rate, and so we need to do better in that.
Speaker 3:And so what are the things we can do in the face of infection to help eradicate the bacteria? Even if you remove the implant, you still have trouble with the bacteria there. But I think there will be solutions that are biobusting biobusters that can really penetrate the mechanism and what holds biofilm together and cause it to dissolve, and that may help us eradicate the biofilm in some ways. Other things that can remove biofilm from implants that are in place and maybe you don't want to do. You get an infection at three weeks from a bicon or plateau that you smoosh together. Do you really want to take all that hardware out? You know we've proven that you can treat them to union. You know, with just debridement and antibiotics 80% of the time, but you're still not winning 20% of the time. And so when something that might improve that is using electrical current and I see as potentially electrifying the implants and that that being effective at sloughing off or killing the bacteria that are in the biofilm and and I think that may be something that will help us Other solutions that may sit for a while. You know there's all this in the total joint of Experian or dilute betadine and more in the prevention world, but I think that some of that will translate into the infection management world to try to help with these micro abscesses, these bacteria up the canaliculi that need to sit for a while before the bacteria can be killed from those areas.
Speaker 3:And the other thing that I think we will develop is the use of phages. Phages are the natural hunter killers of bacteria. They were all the rage of the forties, fifties until penicillin got invented and then all that phage data and just sort of went away. But now with multi-drug resistance returning that phage therapy in terms of ability to maintain an implant, because phages are so small that they come in and they can go into the biofilm, they can go up the canaliculi and they can even penetrate a micro abscess and then they go in, they attach themselves to bacteria and then they enter the bacteria, they take over the mechanism of the bacteria and then they make morphages and then they disrupt, that cell dies and they go away and they look for more and they hunt and kill and then they go away when all the bacteria are dead. What a great natural hunter killer of bacteria to use that in combination with either total joints or implants. We want to keep in place.
Speaker 3:The standard mechanisms of doing that, I think, are challenging and we don't know those yet, but I see phages as in our armamentarium in the future. Until then, I think we will get more use of local antibiotics as well, which can sit in high dose locally where there may not be great blood flow because of a perfascial disease or the damage to that area, but either with right now one of the best carriers is calcium sulfate, and I use far more than I ever used to because it all dissolves and it just takes several weeks, but it can be effective in the management of a chronic infection in terms of letting high dose local that doesn't have has very little systemic effects on patients or kidneys. And so that combination of local antibiotics with either a hydrogel or a calcium sulfate, having bio busters some, or electricity to eliminate or solutions to eliminate the biologic biofilm, are some of the things that we can. We can do in the future to try to help maintain hardware and do it better than we are in terms of allowing, you know, fractures to heal without having to take it out.
Speaker 3:And then the other trend which is coming is the PO antibiotics. I've been on that train for 30 years, you know we have finished our metric study on acute FRA where it's represented, at the OTA a couple of years ago and that has been submitted to JAMA surgery and hopefully it'll come back positive accepted. But we're in the middle of enrolling patients in PO versus IV antibiotics in infected non-unions and I expect the data will be the same. There's some data out of Europe that says it is the same already. So those were. I think we're going in terms of management of acute and of of infections associated with fractures with or without a non union.
Speaker 2:Wow, this has been an absolute pleasure talking with my friend and colleague, dr Bill Labrowski, who is well-recognized as an international leader in orthopedic trauma surgery, on the future in orthopedic trauma. Dr Abramski, sir, thank you for being on the podcast.
Speaker 3:Doug, my honor and pleasure. It's been an honor to be your friend and colleague and I look forward to following in your footsteps as the president of the Orthopedic Trauma Association.
Speaker 2:You're very generous, sir. Thank you and I look forward to seeing you in Montreal and, for the rest of y'all, stay tuned for more in this series on the future in orthopedic surgery, on this AOA podcast channel. Thank you.