Episode Transcript
[00:00:03] Speaker A: Welcome to your Cases on Hold, a JBJS podcast hosted by Antonia Chen and Andrew Stonefield.
[00:00:10] Speaker B: Here we discuss the science of each issue of JBJS with an additional dose of entertainment and pop culture.
[00:00:17] Speaker A: Take us with you in the gym, on the commute, or most certainly whenever your case is on.
[00:00:27] Speaker B: Welcome Back to episode 94 of your Cases on Hold. It's dropping on November 18th for a November 19th episode.
Best part about this and we're going to keep you in suspense till we tell you what's coming next at jbjs.
Without further ado, I am Antonia Chen, Executive Editor at jbjs, and I have.
[00:00:49] Speaker A: Here I'm Andrew Schoenfeld, Associate Editor for Methods.
[00:00:55] Speaker B: And we just want you to know that these opinions are our own. They don't represent JB JS editorial board. They don't represent JBGS board. These are strictly our own views. But one of our views is that this next episode or next issue of JVDS is pretty cool. So check it out, look at the print version. For those of you who don't do a print, pick one up, take a look at it. It's a new sleek look to JBGS and touches on a topic that's near and dear to my heart of infection.
So I'm super excited to be presenting this one on your Cases on hold. You haven't grabbed an issue of JBGS in a long time. Go pick it up, take a look at it. If you're an AOA member, you get it as well too. It's a new look themed issue and lots of global perspectives.
So lots to see there. So pick it up and definitely read. Read it more. We're going to go over to the top of the pile and tell you what's in there, but there's a lot digging deep in this issue of jbjs. So beyond words moving from ideas to action now. This is the brainchild of Mo Bindari, who is the JBGS Editor in Chief.
And it's really cool to understand where this came from, what the idea was and the impetus behind this to really make this a global branded project with regards to orthopedic publications.
Bryce Attack et al. It's what's new in musculoskeletal infection. This is permanently free mandated patient reported outcome measures Driving reimbursement for arthroplasty is a disturbing new reality for orthopedic surgeons. This is by Adam Rana. He's in charge of the Aukis Advocacy committee.
Really good information there about patient reported outcomes coming your way. Objective ignorance A flaw in our ability to predict patient outcomes by Mattson A second trauma Navigating infection after Orthopedic Surgery by Marvel et al. And it's also permanently free.
Faux ongoing. I like the drama behind that one by Dr. Yates. And this is permanently free, so definitely go check that out. World Report A snapshot of Orthopedic surgery in the Netherlands by Pullman et al. Getting a really nice global perspective and understanding what else is going on in the world of orthopedics throughout the world.
If you want to learn even more about that Global Perspectives on the Management of Periprosthetic Joint Infection by Piusi et al. Also an Executive editor at JBJS and an all star cast of individuals contributing their global view of infection throughout the world.
About a holiday in two stage exchange for periprosthetic joint infection A scoping review by Fravol et al. And it's 30 days free and there's a commentary on it.
International Consensus Meeting on infection top 10 evidence based recommendations and Insights by Ed Kitari et al. And there's a commentary times two. So when you'll think you'll see about this new issue of JBJS is there's more commentaries and more thought processes so you don't have to take our word on it. You can hear it from other people as well too and then make your opinions on it and see if you agree with us or not.
So kicking us off with the headlines, Dr. Schoenfeld will be talking about the diagnostic utility of a rapid myeloperoxidase test in synovial fluid for chronic periprosthetic joint infection by Akita et al. And there's a commentary and a visual summary.
[00:04:10] Speaker A: Yes. Okay, thanks for that introduction. This is a study that was looking to apply myeloperoxidase, an enzyme with microbiocidal properties, through the catalysis of hypochlorous acid production and as a promising biomarker.
Now they say that alpha defensin the premise for this, the motivating statement alpha defensin is an excellent biomarker, included as a minor criterion in the second ICM International Consensus Meeting for PJI diagnostic criteria. However, they say it's high cost and that limits its accessibility at many general medical facilities. Is that your experience?
[00:04:55] Speaker B: It's actually interesting. The cost is a perspective of it, but typically actually you can put it as a lab test outside of it cost. It's actually more access and what happened with our lab is that they wanted to do the labs all through our labs if you wanted to get it. It wasn't necessarily the cost aspect, but it was actually the logistic aspect. And running the rest of the test through our lab.
[00:05:19] Speaker A: Do you have any experience using myeloperoxidase?
[00:05:22] Speaker B: I've never used my leproxidase except in a laboratory setting, not a clinical setting.
[00:05:26] Speaker A: Well, these are both ELISA tests. So it's, you know, something that has to be done intentionally using enzyme linked immunosorbent assay. I guess in this case the, you know, they don't really say ever really how, how much less expensive The MPO is versus the alpha defensin. But they included 23 patients with PJI and 23 with aseptic failure.
Both MPO and alpha defensin exhibited a strong correlation and at the optimal cutoff, both tests demonstrated the exact same sensitivity and specificity, 0.96. Essentially, the myeloperoxidase produced results in 10 minutes. In the formulation that they are using, they say that the MPO ELISA demonstrated high diagnostic accuracy for PJI equivalent to that of the alpha defensin test. And they render this level two evidence.
They support their inclusion of 23 patients, which I thought was quite low through a power analysis.
It's important to keep in mind that this is not an rct. This is a diagnostic study. And we talked about the necessary parameters of diagnostic studies which are well defined. This is not like my opinion, this is not my own custom pet hypothesis around what should be the gold standard approaches for a diagnostic study.
This is accepted scientifically. And to those who maybe didn't listen to the last episode, definitely go back and listen to it because it's on a different study. But just to spell it out here it's everyone should have the same test or tests. The test should be compared to a gold standard, which is done here, I guess, using the ICM PGI criteria.
The important thing is that there has to be sufficient numbers across the spectrum of disease to replicate testing in the entire universe of patients with sufficient clinical representation. And that's what's lacking here. They had 23 patients with PGI and 23 patients with aseptic failure. That's just 46 patients.
It's just not enough. And they are trying to immunize themselves strategically by saying, well, we did a power calculation. But power calculations are not about clinical representation, they're about defining a difference.
It's not showing the performance of the test, it's just showing that you can detect a difference.
In this case, I don't think that the power calculation really adds anything. It helps them justify this number to reviewers and maybe the erstwhile reader. But the real concern here is across the full spectrum of disease, from basically clinically asymptomatic to fulminant, how is this test going to perform? And this study cannot tell you that.
That is the fundamental crux on which my determination hangs.
So, yes, it's showing that basically in this very limited sample, MPO did as well as alpha defensin. But let's just say that this sample is really like the pgi. Patients really have pgi. Like, it's really bad pgi. So maybe in that context it does really well, but it isn't calibrated. Maybe alpha defensin can detect it in the patient that no one thought they had a pgi, but they ended up having a pgi.
And MPO doesn't perform that well in that context.
So those are the important matters that need to be discussed. You know, calibration.
Does it perform equally well across the full spectrum of disease, regardless of the disease severity, or are there certain things that it doesn't detect especially well?
[00:09:34] Speaker B: And that's the hardest part with these laboratory tests. I will say every single one of the laboratory tests wants to be the holy grail of what the best way to diagnose, like you one test, and that's going to tell you they're infected and it doesn't exist.
So it is one of those things where it adds the compendium of things.
[00:09:52] Speaker A: And again, if I, if I'm not wrong, and correct me here, these tests are really only coming into play when there's a clinical conundrum. In any case, like if there's gross pus in the joint, you don't need the alpha defense and test to tell you that it's infected.
And so this is only a very certain small subset of patients you can get. There are all sorts of. I'm not fully up on the ICM PJI criteria. I know their primary and secondary criteria And I know Dr. Parvizi has done a lot of work in this context, but there's a lot of ways to get at the diagnosis, right? It's like some from column A and some from column B sort of thing, right?
[00:10:32] Speaker B: It is. And that's the thing with these diagnostic criterias. It's that you get ICM1 is you get certain number of points for whatever criteria you have. And the, the interesting thing is alpha defensin is equal to white blood cell, which is equal to. Yes. Which is we get the White blood cell self count. And that is one of the. And leukocyte esterase. Right. Which are all parameters of that similar vein of basically body reaction from a white blood cell perspective to an organism or an infection.
So, you know this performs as well as alpha defensin, which is on par with leukocyte esterase. Right. So it wouldn't add more necessarily to the current diagnostic criteria. Yet another different test. And ELISA's are still hard to do. You know, there is a point of care alpha defense and test, which is nice, but you do it in the lab, you don't do it at the bedside, but you can do them bedside if you need to. It's supposed to be done in the lab anyway. So it adds to the repertoire but doesn't become the one that you go to, if that makes sense.
[00:11:27] Speaker A: Yeah, no, definitely.
[00:11:29] Speaker B: There you go. All right, so I'm going to talk about something a little bit different. I'm going to talk about chemical disinfection of an accidentally contaminated and irreplaceable inorganic element during orthopedic surgery is a safe option by Korbez et al. There's a commentary and it's permanently free.
Have you heard the phrase oops, I did it again?
The idea here is that you could say, oops, I dropped it again. And what happens is when we're in surgery, sometimes you can drop an instrument during surgery. We've all been there. And most of the time you can just open up a new one. Typically the problem is if you drop something and you don't have anything else to open you. To fully sterilize instruments, it can take three to four hours, which you're not just going to sit there and wait with an open patient at that time frame, or 30 minutes for flashing, which is highly discouraged in hospitals, of course.
So how often are instruments dropped? Conodel reported 39 falls of objects across 120 surgical procedure, with seven of the falls involving an implant. Those sound like slippery fingers to me.
When considering autographs, 25% of orthopedic surgeons admit to having confronted at least one once with the problem of an accidental contamination, with the rate rising to 70% among plastic surgeons. For grafts, chemical disinfection is typically used to avoid a second graft. Harvest, especially autograft, of course, is a problem. Even allograft, though, is very expensive and hard to obtain. And recent studies have found that there are relatively low rates of contamination. 0.8 to 3% if you use chlorhexidine, permitting the implantation of graft even after dropping.
That said, these studies have mostly looked at organic material, because that's really irreplaceable. If you take someone's hamstring autographed and then you drop it, and then what do you do? What about inorganic materials? What if you can't just open up a new one or it's not cost effective to open up a new one? So this is a basic science study that evaluates how to disinfect a contaminated or dropped instrument without going through the entire re sterilization process.
So they did lose these disks and these three different discs. There were three sets of 30 discs with three types of materials. They used ones that are commonly used in orthopedics. Cobalt, chromium, titanium and polyethylene were used for testing. The discs were sterilized by steam sterilization at 121 degrees Celsius for 20 minutes and packed in a sterile manner. The discs were used a maximum of four times each, and they were cleaned and sterilized before each use. After the use, they were dipped into an instrument cleaning agent, diluted at 2% for 15 minutes, then swept and left in tap water until they were ready to be sterilized again.
To do the right concentration of bacteria, they took these different discs and contaminated with them. Staph epidermidis. They purposely chose staph epidermators and no other organisms because they wanted to keep it consistent across all the different planes. It's a very commonly found organism in orthopedic infections. They incubated at 37 degrees Celsius for at least two days, and the number of CFU were counted.
So they found the number that 10 to the 7 was the magic number. So for the first part of the study, they had these disks soaked in bacteria for 10 minutes and then dried for 20 minutes to really soak it in. And they were treated with three different solutions. These were the treating solutions. One was 2% chlorhexidine in 70% isopropyl alcohol, 0.9 povidone iodine in 46% isopropanyl alcohol or 70% ethanol, and a control group that got no disinfection after they were disinfected, or the control group, they were rinsed in 20 ML of sterile water to remove the residual disinfectant left on the discs. And the remaining bacteria were counted by CFU or colony forming units. This was repeated 10 times.
For the second group, they wanted to pretend that you were in an operating room, and they dropped the discs on the floor. They were left on the floor for 30 seconds and then collected before undergoing the exact same procedure as in part one.
They didn't in fact even think that they just were able to clean them and they wanted to test them. The results were the average of CFUs observed across the 10 or 8 iterations.
For the statistical analysis, an unpaired student T test was used to calculate the P values. A P value of less than 0.5 was considered significant.
What did the results say? Remember, 10 to the 7 was the magic number and it contaminated disk at a rate of approximately 150 to 500 colony forming units per disc. In part one, all three alcohol based disinfection procedures showed high efficacy. There was no growth on these discs and compared to the control group it was basically with nothing. So it was statistically different.
In the control group, polyethylene had the highest mean concentration of contamination. Cobalt chromium had the middle amount and titanium had the least number of CFUs. And we're talking about 157 on the poly to 58 CFUs on the titanium. So interestingly enough, polyethylene has a high affinity for it versus titanium or cobalt chromium.
Part two showed no growth after alcohol based disinfection.
So what's the magic solution here? It's probably the alcohol. So in the control group no growth was observed in 26 of 30 experiments. So even though there's no growth from the alcohol based disinfection, know that most of them didn't grow anything. So dropping on the ground for 30 seconds, you know, you talk about the five second rule, probably doesn't make a difference in terms of bacterial growth. Now you're not going to take it off the ground and then just stick it back into the wound and use it. You're probably going to disinfect it at this point in time, but it really didn't grow much. One to eight CFUs are observed in the remaining four experiments. They found Staphydipodentus, Staphylococcus wanari, Staphylococcus hominis, Staphylococcus borealis, Cocoura palustis, Cornebacterium aforementis, and cornea bacterium, tuberculosterone, basically contaminants.
So most of them were not infected, but they did grow some of the stuff. Again, just like the group 1 part, polyethylene seems to be the most prone to contamination. However, the level of contamination was low for all materials.
If you were to accidentally drop something that's irreplaceable or think of yourself in a place where it's not affordable to go ahead and reprocess them, soak it in alcohol based disinfectant for two minutes and then rinse it with sterile saline afterwards. As long as it contains alcohol then it doesn't matter what solution you use. So ultimately the old adage of the solution to pollution is dilution. Then you just need to add with alcohol and then your inorganic materials good to use.
[00:17:55] Speaker A: This is now called the Steve Urkel paradigm. But I don't know if that's going to make, that's not going to make sense to people who are children of the 80s, I think.
Yeah, I mean I don't like are you going to have like in an op note, you know, the case was performed in usual manner. The polyethylene implant was dropped on the floor.
We just soaked it in alcohol for two minutes and rinsed it with normal saline and then put it in there.
I don't know.
[00:18:21] Speaker B: Now that begs a whole separate question here, but do you tell the patient why?
[00:18:28] Speaker A: I think you, you know, it's interesting.
[00:18:31] Speaker B: I will tell you. I've, you know I've heard of people who will say if they drop their graft and they've soaked it, they will tail the patient and they say this is 100% supported by literature and it should be totally safe and stuff like that. But it's interesting, it brings up a separate ethical question.
[00:18:46] Speaker A: Yeah, just don't drop stuff on the floor.
[00:18:48] Speaker B: Just don't drop it.
[00:18:49] Speaker A: Right, Easy.
[00:18:50] Speaker B: Just easy. Don't drop it.
[00:18:52] Speaker A: No, no. We want, we want, you know, first team wide receivers everywhere around the OR table. No, no butterfingers around in the OR table.
[00:19:03] Speaker B: Exactly. Perfect way to put it.
All right, switching to something very different. Are your cases on hold? Featurette infection and non union rates and open fractures. Description of 6042 fractures from the flow and prep it trials. This is by Natoli et al. There's a commentary, there's an infographic and it's permanently free. So you have no excuse not to read this.
Infection and nonunions commonly happen after open fractures.
Studies have shown that the infection rates range from 2 to 52% which is a huge range. And the non union rates range from 12 to 17%.
The purpose of this study was to describe the rates of surgical site infection and delayed union nonunion following open fractures based on the fracture location using the OTAAO fracture classification and severity using the Castillo Anderson classification system. They use the three largest RCTs in orthopedic trauma, the flow study and the prep it trials. The prep it trials included the aqueous prep and the prepare open studies.
The data from these studies were qualitatively compared with historical controls from large series of open fractures. Now these studies were all published in the last 10 years and included multiple international trauma teams and shared definitions for surgical site infections, most being focused on the CDC definition with delayed union being less than six months and non union which means non union, a lot of outcomes to be pooled for descriptive analysis. Delayed union and non union rates were stratified by the fresh fracture classification and the Castillo Anderson open fracture classification that reported by the treating surgeon. Gunshot injuries were included if the surgeon felt that the formal open fracture irrigation debridement were warranted. Amputations were also recorded. Once an amputation occurred, the fracture no longer contributed SSI or delayed union or non union estimates. All acute amputations however were excluded and patients were followed for one year after enrollment.
The patients so the authors eliminated any subgroups with less than 10 fractures in that classification. Kaplan minor estimators were utilized to obtain point estimates and the log log transformation approach was used to calculate 95% confidence intervals for outcome rates. So what do the results show?
There's a total of 5753 patients with 6042 open fractures. As the title stated, a total of 41 centers participated in the FLOW trial, 14 in the Aqueous PREP trial and and 22 in the PREPARE open trial with 69 unique centers. Fractures were grouped according to upper extremity, femur and patella, tibia and foot and ankle. So what were the cumulative surgical site rates at 12 months? For Casteel Anderson type 1 it was 5.1%, type 2 is 9.7%, type 3A was almost 14%, type 3B was almost 29% which was the worst one and then type 3C was 26.2% when it came to delayed union and non union when combined at 12 months for type 1 it was 3%, type 2 was about 5%, type 3A was 8%, type 3B was 14% and type 3C was the worst one at 17%.
So utilizing the OTAO class fracture classification to increase the point estimate granularity, the estimated 12 month SSI and delayed union and non union rates and 156 Castile Anderson type 3B open tibial shaft fractures were almost 35% and 18% otherwise so that's almost 35% surgical site infection and then 18% of delayed unions. Non Unions compared to historical data though how did they do? The results were similar with regards to cervical site infection, delayed union and nonunion rates. Of note, the authors created a companion website with with surgical site infection and delayed union and non union rates to supplement this article in case you want more information.
HTTPs Nathan O' Hara GitHub IO Shiny SSI I don't know what the title is from, but if you want to check out more it is there.
So in conclusion, the results of the study show that despite current treatment approaches, the rates of SSI and delayed union and union following treatment of open fractures remain high at one year and haven't really changed a lot from historical rates spann spanning several decades now. Of course, the authors conclude there's opportunities for improvement in these outcomes and how we treat these open fractures. It's good that you can use these Level 1 studies. You can aggregate these studies just from a research methodology perspective. It does encourage researchers to obtain similar outcomes for analyses so data can be combined to find more generalizable outcomes over different patient populations.
Love to know your hot takes on this.
[00:23:49] Speaker A: Yeah, so the first thing is that I don't they gave this level one evidence. I don't understand how this is level one evidence.
Level one evidence is derived from a specific study question relative to randomized controlled trials. They use data from randomized controlled trials. So as you could certainly argue that this was a, you know, basically secondary use of prospective data for prognostic purposes, I would say it's level two.
So I don't see how you can make the claim that this is level one data. It's probably the highest quality data in terms of eyes on these patients who are followed prospectively with minimal loss to follow up and things like that. But it's also as somebody who is a student of history and in their heart of hearts, as a historian.
[00:24:40] Speaker B: I.
[00:24:41] Speaker A: Think they're using the term like in history very, very loosely here because, you know, it's a very short time frame that they're sort of considering history.
If we consider how these fractures have behaved over the course of the last 2,000 years or the last 200 years, you know, say, go back to the founding of this country. So since 1776, for the majority of that time window, open fractures were probably, if not uniformly fatal, very close to that.
And if they weren't fatal, they were profoundly disabling.
A lot of the classic surgical intervention of the American Civil War is the amputation. And what they were essentially amputating, by and large, were open for fractures. I mean that's, that was, that's what they were doing, you know, open injuries from either ballistic missile or blast cannon.
So, you know, if we take the longer view here and we consider the infection rates and the non union or even the mortality rates of the. We're doing great.
The fact that in the last, whatever it may be, 20 years or 30 years, whenever the sort of, that the maximum of the, you know, the eight surgical intervention in eight hours for the open fracture, so to speak, was implemented, I think we're really seeing a flattening of the curve or a ceiling effect in terms of when you're Talking about certainly 3B and 3C injuries, these are devastating injuries to the soft tissue envelope, to the muscular structures and even the nerve structures and vascularity being at risk as well. And 3A injuries are also not, you know, clinically insignificant.
So the fact that it's like, well, in the last 30 years, things haven't gotten better.
Well, the passage of time alone does not potentiate improvement. Friends, what has changed in the way we treat? You know, you and I, I'm a little bit older than you, but you know, we trained at the beginning of this century or were in medical school and training at the beginning of this century. And when I look at what our trauma colleagues are doing now, I don't really see anything all that, that's, it's very recognizable to what I was looking at in the year 2000.
And yes, there, you know, there's the potential, there's some different types of implants or you could be a little bit more minimally invasive and there's better understanding and some things that might marginally prevent infection. But again, these are within the context of randomized controlled trials and what they were trying to do in the context of those controlled trials, the narrative is like, oh, it's not better than what happened 30 years ago. But my question is, why do you think it should be better than it was 30 years ago? What's changed?
I think we made the steep part of the curve was probably between the end of World War II and, you know, the 50 year spanning 1945 to 1995. From 1995 on, there's just marginal changes. And that's why you have this, these findings.
Yeah, I mean, I think this is interesting information.
I think it's good for benchmarking.
They made a curious statement to me that where, I don't know, they said something about this is going to affect health policy. Oh, data are useful for informing policy.
I don't know how this would inform Health care policy. Really?
[00:28:36] Speaker B: It's going to get better, huh? The policy is not going to get better. So should we just not treat them because it's not going to get any better?
[00:28:44] Speaker A: Well, that's what I'm saying. I think that the narrative is unnecessarily, like, pessimistic because they're using a very, very narrow lens when they're considering history.
[00:28:55] Speaker B: Great.
[00:28:56] Speaker A: Like history. The history of orthopedic surgery didn't start in 1990.
[00:29:03] Speaker B: It. Did it?
[00:29:05] Speaker A: No, it didn't.
[00:29:06] Speaker B: Amazing.
[00:29:08] Speaker A: It started in 1981.
[00:29:13] Speaker B: Really? When everything started. Let's be honest. I'm just kidding.
[00:29:15] Speaker A: For some. For some people on this podcast, it.
[00:29:18] Speaker B: Did start some time. You're correct. So keeps it interesting. But, yeah, it is hard to see these studies kind of say, all right, I mean, I guess we get better. But how? And it doesn't point to how.
[00:29:29] Speaker A: Well, I mean, these are. These are devastating injuries, and that's the reality. And we're trying to modify those to the. The extent that we can.
And nothing is. Is never. Like, you're not going to get to zero here. I think we're looking at, you know, 14 infection for 3A.
Would you like it to be lower?
Of course you would.
[00:29:56] Speaker B: Of course.
[00:29:57] Speaker A: Is it. Is there the potential to get it lower? I'm not sure.
[00:30:01] Speaker B: That's the hard part. What does it take to get there?
[00:30:03] Speaker A: Right. Yeah.
Like, what can you do differently?
[00:30:07] Speaker B: Exactly.
[00:30:08] Speaker A: If we're gonna do like they have in Star wars, where they come with, like, the pod that they, you know, put people in right. At the point of, like, their injury, and it has the. The back to fluid to, you know, magically heal them, but it doesn't heal Darth Vader. So I don't know how. Well, it works. Right.
There's a ceiling effect for that as well.
[00:30:29] Speaker B: Darth Vader get infected, though. I mean, come on. Just kidding.
[00:30:32] Speaker A: No, because, like, the wounds were cauterized by the lava.
[00:30:35] Speaker B: Exactly. Now we're talking.
All right, going on to some fun honorable mentions. The first one being timing of debridement, antibiotics and implant retention for early periprosthetic joint infection. Data from the Finnish Arthroplasty Register by Chemo et al. That's free for 30 days. The authors assess the success of DARE, which is debridement, antibiotics and implant retention performed during different time intervals after primary total hip arthroplasty and total knee arthroplasty using data from the Finnish Arthroplasty Register.
Because the large country registry, there were 178,498 primary operations from May 2014 to April 2022 and the total HIP group the failure rate was 15% was when DARE was performed within 42 days, 10% when performed in 43 to 84 days and 31.4% when performed at 85 to 180 days after primary total hyperthoplasty. In the total knee group the failure rate was 8.9% when dare was performed within 42 days, almost 17% were performed from 43 to 84 days, 9% when dare was performed within 42days and then 17% were performed from 43 to84 days and then 10% were performed from 85 to 180 days after primary total knee arthroplasty. So the authors concluded that later DARE was not associated with an increased re revision risk for total hip or total knee. So if the failure rate may not increase as much as previously thought if performed greater than six weeks after a primary Trojan arthroplasty I think the one thing I would caution with this article is the fact that if the patient came in with symptoms greater than six weeks after the primary joint arthroplasty, they may have gone to a two stage. So maybe it was really really healthy patients or really really selective patients that ended up with a dare. I don't think it was all commerce. So caution words to the wise that just because you do a do a DARE late doesn't mean they're going to have a good outcome. The last honorable mention is Synovial fluid Microrna biomarkers enable accurate diagnostics of hip and knee peripreception joint infections by Frank et al. There's a commentary and it's permanently free. Diagnosing hip and knee periprosthetic joint infections is challenging, necessitating sensitive and specific biomarkers for accurate diagnosis. Small RNA next generation sequencing was used to screen mirnas in the discovery samples with reverse transcriptate quantitative polymerase chain reaction used to confirm the NGA's finding and to validate results. In independent larger cohort of 133 samples. There were 132 Mirnas with significant differences between septic and aseptic synovial fluid samples. Of these, 18 were further analyzed with MIR223.3P and MIR3.385P showing the highest increases in septic synovial fluid, a log two fold change of greater than 4 and the other ones had the most reductions were MIR151A 3P and MIR2143P. I'm going to test you on this later, by the way, which indicates immune selectivity in the joint.
These mirna offer sensitive specific pathogen independent biomarkers with potential clinical applications in the diagnosis of hip and knee pgi. But unlike mpo, MPO is way more studied and way more used than any of these mirnas. But is there a genetic component? If the bacteria is dead but there's still genetic material present and you can test for it, maybe it's useful in that manner, but otherwise this is an interesting exploratory study that maybe there's more to come, maybe there's not. We'll see. Thanks for joining us on this brand new issue of jbjs. Again, get it in your hands, feel it, touch it, smell it, look at it. It's a beautiful episode or issue.
[00:34:20] Speaker A: Yep. And hopefully your cases are ready to go. But even though we have a whole new horizon in terms of the look of the content of the journal here in this podcast, the cases are still on hold.
