William Tettelbach, MD, CWS discusses the essentials of wound care. Dr Tettelbach reviews the microbiology of diabetic foot infections and the team approach to healing. He examines treatments including antibiotics and topical wound treatments.
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TAPE STARTS – [00:00]
Male Speaker: Our next talk is going to be by someone new to our group, I believe, Dr. William Tettelbach who’s going to be speaking on wound bed management and dealing with infections and beyond, just like we all have to deal with on a regular basis. Dr. Tettelbach was initially training in Tennessee and received training in infectious diseases as well internal medicine and now, I believe you’re in Utah now, Intermountain Medical Health from Utah. And he is the director of fellowship in Undersea Hyperbaric Medicine, I believe. Correct? Has a great deal of experience in wound care so let’s welcome Dr. Tettelbach.
William Tettelbach: Well, good morning. Thank you for coming out so early. So today we’re going to talk about wound bed management. Most of this is, you know, dealing with infection and then other things that help heal wounds or you can get closure with, say, with protease activity and biofilm. I think you’ve had other lectures on that, but we’ll touch on it from sort of an infectious disease, sort of bent.
I do my disclosures on PI on a DFU trial with my medics and advisory board with facility. And some of the objectives we’re going to get today again are, you know, understanding the microbiology of diabetic foot ulcers, you know, the course of colonization. We were going to touch on that with burn, but I took that out because you guys really don’t see many burns. In the outpatient setting, I think we don’t see much either, but we do on the inpatient side. And then we’ll get into biofilms and then a protease activity as we’ve mentioned.
Now, I'm going to touch on my background a little bit. Over the years since I've come to Intermountain in Utah, we brought in this hyperbaric fellowship. But at the same, time we folded the podiatry residency program into our clinic. So now in our clinic, we have wound care specialists, we have podiatrists. The program director is actually located in the third year podiatry clinic is in that clinic. And we have the second years rotate with the ID folks, two weeks inpatient, two weeks outpatient. So they get, you know, ideas on how to manage their patients from an ID perspective and they get comfortable with that.
One of the things over the years being involved in these studies and doing photo adjudication and actually working with the residents, it’s interesting because at least in our program, the first year residents were actually told not to culture any wounds because they’re afraid they’re going to over treat because of these cultures. But, you know, we teach them the exact opposite, is that you really need culturing wounds when you suspect anything so you can target, you know, your therapy. And actually if you do ahead of time and they get in trouble later and, say, in the weekend or at night, you know exactly what you need to start.
The other thing I kind of came across is the degree of debridement that needs to be done. And that’s one thing in our field across the board and wound care especially in the outpatient setting is that we are not aggressive enough on our initial debridement.
So this is an example of someone who had fallen from a bike. The anterior shin got caught in the sprocket or the spoke, you know, in the teeth of the gear. And this was a month out after someone in their notes who’s saying they had debrided this. But, you know, this person, when they came in, went from this to this and there was actually a hidden sinus tract in there and this patient went on to heal in less than a month once this was cleaned up.
This is an example of a heel abscess that was sent to us that had been sitting for almost two months. The day he showed up, we did this in the outpatient setting to this, and this is a case I'm going to show you real quick at the end.
The bottom line is we aren’t debriding enough. So when you get plantar ulcers that have a lot of callus build-up, the funny thing is you can clean the middle of those out but folks aren’t debriding the calluses off and they’re causing delayed healing because of their shearing forces with that. So I just wanted to touch on that to begin with.
And so one of the things that we deal within and put on a lot is negative pressure. But what I wanted to mention is that negative pressure, you need to think of negative pressure not just as pulling off fluid and managing drainage, but it also has the ability to, you know, remove infectious material. While it’s pulling off that drainage, it’s actually reducing the bioburden of those wounds.
But what happens when you put on negative pressure, it creates a zone of hypoxia down here. And that zone of hypoxia stimulates endothelial growth factor and capillary bed density growth. So you actually stimulate hormonal release of growth factors below the bed and increase blood flow and oxygenation which actually delivers your antibiotics better, which actually allows white cells to come in or neutrophils to come in and fight infection.
So this is a key component that we really don’t think about is really this hormonal cytokine and chemokine up regulation when we deal with this. So sometimes you can just -- if you have a hypoxic-looking or, say, like a yellow granulation bed, think of not just managing your drainage because the drainage may not be that bad, but think about transforming that wound bed in getting ready for closure by transforming your granulation tissue. This is sort of prepping the bed mentality.
So these are sorts of the callus that I was talking about. These were folks, we saw a lot of these in this last study I was involved with, the folks would come, they would get this area cleaned out and that’s it. They would have this macerated wet area that would never get touched, but you really need to take those down. You will actually make the wound larger when you do that, but don’t be afraid of that. You need to offload it. And if you do that, you can get these to close much more quickly, so just a note on it being a little more aggressive on you initial debridements.
So on diabetic foot ulcers, this actually has heavy impact on healthcare. There are billions of dollars a year on wounds associated with diabetic foot ulcers, venous leg ulcers that costs the healthcare industry. And these are numbers that, you know, a lot of you know like the annual incidents of diabetic foot ulcers and diabetics is up to 3.4%. The most common one is lifetime incidence of diabetic foot ulcers maybe as high as 25%.
But actually with the new paper that came out with Armstrong and Andrew Bolton in a New England journal this summer, the estimates actually go up even higher now. And so that’s the burden is even higher on us to treat these. Because the problem is after 30 days, the likelihood of someone getting infected is almost five times or 4.7 times higher than someone who has a diabetic foot ulcer that is not chronic under that 30-day monitor.
And the other thing is the 5-year mortality rate. Once you get a below the knee amputation, it’s as high as 70%. So it’s almost like putting a death sentence on some of these folks when we do BKA. This is not for minor amputations, below the knee.
And so this kind of points that out. And when you put the 5-year mortality of all these cancers, breast cancer, bladder, colorectal, it’s about 5-year mortality is about 32%. This is 50% to 70%, which is much higher. So this is kind of an ignored area when we think about just, you know, when I work with orthopedist, their first thing is to go, in the past at least, in our system, is to go to a BKA. But that’s why our clinic now is so embedded with a podiatrist because the podiatry folks that we work with were more and have been more about limb salvage and realizing that once you do this, you really have a struggle to keep people from becoming depressed and then eventually maybe passing away from the complications of this.
So predictive factors for amputation, you know, previous ulcer, neuropathy, foot deformity, peripheral artery disease, you know, we need to be innovative in our area of wound care because reimbursement is going down and we’re looking ways to manage these. And so with the neuropathy being a big part of this, we’re actually working with a company that has these thermogram devices that people stand on and then a Wi-Fi enabled. And we will be embedding this into our support centers. We’re going to doing a one-year study with looking at this where people who have previously had ulcers, 40% of these folks typically re-occur. So in that three years, 60% or more re-occur.
So we will able to monitor these deviations and hotspots under feet and actually call them up in a proactive manner to say, “Hey, you need to ice that foot.” These thermal wands that have been around a while but they just haven’t been adopted. They don’t get paid for. So we’re looking to do study that actually would be taking to the insurance companies to get these paid for your patients and you can setup a system where they could monitor these proactively.
And this would be something that almost anyone can do especially you could set it up where you had someone in your clinic who had the alerts coming on their phone. And you can monitor your patients that way. So those are kind of future state.
You also have to think about re-occurring ulcers has been more being in remission than being healed. We put in our notes, wound resolved but the thing is these re-occur like I said so commonly in these folks. They are eventually going to come back. So that’s why we have to think to be proactive with these folks all the time.
The microbiology of a diabetic foot ulcer. We’ve kind of learned that gram negatives are a big part of this, polymicrobial, multiple bugs are involved. But really for acute – so someone comes in who has a wound that’s less than 30 days or is not chronic, you’re really more concerned about the gram positives, Staph and Strep. And Staph aureus is your big player and then you also have strep like group B strep.
And depending on where you live, when you think about Staph, you have to be worried about methicillin-resistant staph or MRSA. So in Salt Lake, our community prevalence is maybe about 35% to 40%, but when I was working in Memphis, it was as high as 70%. So the minute you thought Staph, you had to put something on that would cover MRSA. And Bactrims are great choice and doxycycline is also a good choice, minocycline has a little better activity against Staph than doxycycline does. But you have to remember strep is a big player in this as well. So Bactrim or Septra has terrible, terrible strep coverage. It has very low MICs against that. So if you have someone coming in and you start Bactrim, and they have an area of redness that’s maybe spreading and after three to four days are starting to stink, maybe this is actually a streptococcal infection and it’s now becoming early cellulitis. You need to switch those folks over to something that’s going to cover that as well.
So you may want to go with dual therapy. You could keep Bactrim going and then add Augmentin or Keflex or clinda on that but just be aware of that. Bactrim tends to be a go-to drug but you can act there’s some holes with it. And then your anaerobes are definitely just not a big player especially in more acute versus chronic wounds.
Now, if you get the classic, you know, penetration of a sharp object through a tennis shoe or a boot, then you need to think, you know, pseudomonas or aeromonas, these are water based bugs or there’s an injury that occurred and you have an open wound and they put some sort of occlusive dressing themselves over it and they have a heavy lymphedema or a edema and draining and that’s been sitting there for weeks on in, then you should consider a polymicrobial situation or at least a gram-negative situation where you have E. coli and pseudomonas kind of in the forefront of your mind.
Now, with osteo, it switches a little bit. The big players that you need to think of are still are Staph and MRSA. But MRSE and Staphylococcus epidermis are actually big players as well and that’s why when you are trying to figure out or get a culture of these, it’s preferable to get a bone culture. But you also have to remember, if you get a swab or a deep swab, of course, always culture after you have debrided that wound aggressively, basically taking off the biofilm and you’re kind of doing a Levine method where you’re pushing hard down on the wound and squeezing things out of these micro sinus tracts.
There are already been studies that shown that 80% to 90 % of the time those surface cultures do not correlate. So if you have a wound and you suspect osteo underneath that probes bone or close the bone and you get it and you say it grows out three or four bugs, and it wasn’t staph. I would still add staph onto that versus the other – you are basically going to be treating a soft tissue localized infection but you also need to figure out or at least cover what the probabilities would be for that deep tissue infection. So that’s just kind of a take home on that. So sometimes with the residents when I’m teaching they are like, “Oh, we are going to start IVs because this patient really can’t take orals compliantly but we are going to put vanc on top of this ceftriaxone or Rocephin.” And they are like, “Why?" Because, you know, they just grew out E. coli. And then I said, “Well, we didn’t get it, we haven’t had a good sample of this and there’s a high likelihood that Staph is still a major player on this.” I’ve been burned too many times on this.
Again, when you probe the bone, you hear about this, this is for the diabetic foot also. The study that was done with Grayson in the past was with diabetic foot is using it like a metal rod or a stiff rod. We do not use the wooden end of the cotton tip applicators anymore because actually wooden shards can come off of that and actually complicate the infection or the healing rates or what’s going on when you have foreign objects being placed into those wounds. So if you do have those, I will replace those with the plastic tip applicators. I mean the Q-tips with the plastic stems.
But if you can’t probe the bone, clinically that will be osteomyelitis. Now, a lot of times you will get an MRI and that’s the sort of a gold standard but if you can probe the bone and it is somewhat early, you may not see like a deep marrow enhancement or cortical enhancement or degradation or it may be just an early periosteal infection and you still have to sort of consider that especially if the bed is open and there is no tissue coming over the top of that. There’s not good delivery of antibiotics since it’s on the periosteal surfaces. It’s very poor blood flow on the periosteal surface. So you typically want a treat as if it is and then you want to debride that area back to try to – once, you get heavy colonization and biofilm on that, you won’t get it a good encroachment over the top of that periosteal layer. You really have to either in the outpatient or the OR clean that up to get closure on that. And we do a lot of closure on things in the outpatient setting versus having to take them to the OR.
If the x-rays are great, you almost have to have like 40% to 50 % demineralization of the bone to actually see any in that, changes for osteo on that. So be aware of that. You can have a perfectly normal x-ray, that’s great for figuring out foreign bodies but it’s not really good for determining osteomyelitis.
And these are things that you should all be doing with treating the diabetic foot ulcers or lower extremity ulcers. Offloading is key, that’s a key component with this. Nutrition optimization, we have dieticians in our clinics that we set-up our new patients with. And we get an ABI or sensolates on all our patients to determine what the vascular flow. Without good vascular flow, that’s it why is it at the top of the list , you can’t really get healing.
And these are things that will be the slides you can look at. If you are going to use any kind of skin substitute or sort of these more expensive tissues to close, you need to really think about doing all of these steps to ensure that your final products going to work. The thing that we had a consensus, there’s actually, I think in September in New England journal, another lower extreme management paper that came out with Kirschner and then another paper this September came out on chronic wound management. And the consensus with these is if you are having trouble with closing these wounds, don’t be afraid to start over again. So if you have done all of these, you’ve offload, you’ve done vascular, you’ve used all the compression techniques for edema, start over again, consider maybe an angiogram instead of your ABI is not your end-all in determining if there is a vascular blockage on that. I’ve been burned many times where we finally get an interventionist to do an angiogram and there’s clearly something that can be turned around.
And then also think about biopsy in vasculitis and Pyoderma. Marjolin’s is a -- squamous cell is something that sneaks up on us all the time that can be changed with just turn around with simple surgery in excision.
So things that you have, I mean to be successful in this, and we’ve done this over the years, is really developing a network. Wound care, there’s no one person who gets trained well enough to do everything that needs to be done for wound care. And so that’s why you need this type of network. So surgery is definitely one of the basis of this. You could actually put any one of these in the middle of this but you need this network.
The things that we have improved our outcomes is actually building relationships with our supply chain and being able to have decision rights and what we need to have in our clinics, at least on an institutional level.
We’ve actually had administrative support by developing service lines and we have created a service line in our Mountain, which means that we sit at the table when we say, “Oh, we need to expand, we will make our own budget for putting new clinics in and having an assay in how we bring new FTEs and so on. So, it's a big part of being successful.
The new part is actually telehealth. We actually have established telehealth in four of our regions, going all the way from St. George up to Logan. And we now support all our rural hospitals in the system and we have started doing home care visits and offloading, how often these patients have to come in for visits, so we can see newer patients. And this has been really enlightening in the sense of how many patients we were even just missing that were out there that had, say, a wound VAC on their foot for like 8 months and no one was following them, except for this nurse.
And so we did a home care visit. We’re like, well, just take that off. He said, “Well, I never could get an order for that.” We took it off and within a month, they healed. So… because when you’re trying to get a wound to epithelialize, a VAC isn’t necessarily what you need on a wound. You need to go back to just a moist dressing.
It’s amazing how many patients are out there that home care is doing a great job. They’re doing as well as they can. But they don’t have the expertise that you all have to just look at it and make an ordinary decision that you would make in your office. But the fact is a lot of these folks are homebound. They can’t even get out, it’s very hard for them.
So when you’re seeing patients… this is one thing that also is you need to know. It’s really inpatient versus outpatient. And if you have critical limb ischemia or systemic toxicity or necrotizing tissue that is progressing like signs of fasciitis, these folks would go in. But I tell you, we offload the EDs a lot. We now will either direct admit our patients to the hospital services.
And one of the tricks I like to use is, say, call one of our podiatrist and say, “Hey. This person really needs to go to surgery. We’re not going to be able to save the forefoot.” And they go, “Fine, I can go see them right away.” And I said, “Great, I’m going to call the medicine team now.” And then I’ll call the medicine team and say, “Look, I have a diabetic. His white count is up. He’s got elevated glucose. He needs to be tuned up. Surgery already wants to take him to surgery. Could you manage the medicine? The surgeon’s going to be in tonight.” And they’re like, “Oh, wow. You already have the plan together. Sure.” A lot of times if I call and say I have this patient who’s sick and needs to be admitted, they’re like, “Oh, that’s a surgical case. Let's surgery take care of that.”
But that’s just a way that maybe you can think about getting folks in. Because I was sitting down with one of our podiatrist last night, he had a case that he tried to admit himself, and the medicine team refused that but it ended up, he got blood cultures. The patient ended up being bacteremic, had cardiac issues and he was just sitting there, sort of floundering. Got ID involved and they helped. But it’s best when we work like that network, we work as a team, get the medicine folks taking care of the medicine, complicated medicine issues and having the surgeons do what they do best, like you guys, it’s to get rid of the source of infection or reconstruct and save quality of life.
And so these are kind of the drugs that we have the ability to use. Augmentin is a great drug. As we mentioned, minocycline has a little better Staph activity. The thing is it causes more nausea than this. So in the elderly population, I generally will go with the doxycycline over the minocycline. It’s less nauseous.
IVs, I just want to mention on this, we use a lot of ertapenem. But Ertapenem, all the carbapenems, like imipenem, carbapenem, they are nice, they’re once a day, but they have terrible bone penetration for osteo. So you will do much better if you feel like you don’t have like pseudomonas, and even ertapenem doesn’t cover pseudomonas that well at all. But the cephalosporins have much better bone penetration, so that would be sort of my initial go to if you were going to do like vanc and rocephin versus vanc and ertapenem as an outpatient treatment with a PICC line.
Remember, if folks have prior exposure to antibiotics, they are actually at risk for MRSA as well as gram negative. So if someone comes in and says, “Oh, yeah, I’ve been taking three or four drugs before I showed up to you.” That is a time where you want to think about covering multiple organisms.
And then actually like, you know, questions like so I say do a minimal resection and there’s still – it looked clean, but there may be some tissue involvement with the infection. Well, at that point, you really want to go if there’s residual infected soft tissue but not bone.
Two weeks, two to four weeks, typically two weeks would be that. But if you are limited on what you can take off and there is still some infected bone, even though the surgery has been done, you’d probably want to go out another six weeks. If everything was, you know, like if you did a BKA and then it was a toe infection, you’re done. You shouldn’t need more from that point.
Also, consider hyperbaric oxygen. Hyperbaric oxygen is very beneficial. It actually not so much reduces but increases the effectiveness of white cells. A lot of wounds and areas that are infected are hypoxic and white cells need 30 mm of oxygen tension to do their oxidative burst to create hydrogen peroxide and then hypochlorous acid to kill bacteria. Without that, they’re really ineffective. It actually helps antibiotics go across the bacterial membranes through the AT process when there’s actually oxygen. It’s oxygen dependent.
So a lot of these folks with Wagner 3s, with chronic osteo or if you admit a patient and do surgery, the old studies have shown that, let’s say, post-transmetatarsal amputation, the need to take those patients back for further revision and the outcomes are actually better when you involve hyperbaric oxygen when it’s available.
So I’m going to skip ahead real quick. One thing, this is interesting as well. There’s future state – there’s actually these photodynamic therapies were actually specific wavelengths can actually increase the balance of electrons and oxygen. And they become reactive and actually will kill bacteria. They’ll kill fungi, parasites. They actually have this technology in Foley catheters now, there’s a light at the tip and it actually creates an environment that this reactive oxygen states are available to kill bacteria and reduce UTIs related to catheter infections.
I think there will be the day when you will have dressings that will work the same way with a substrate and like methylene blue or, you know, a porphyrin-type base.
One thing I wanted to mention on Medihoney, we always ask, “Why is it active?” Well, one of the reasons is it actually can create hydrogen peroxide through a glucose oxidase in that. It’s also the high osmolarity that does that, but it’s a great topical. We use it a lot. It’s cheap. And I, you know, support using that. There’s others that will actually can have hemostasis. So when you have debridements, you put these on, the dressings on the wound and the bleeding will stop.
One other thing I wanted to mention and we’ll have this is hypochlorous acid. One of the things that we have done that changed post-debridement problems in our wound beds is actually soaking every wound with hypochlorous acid or you can use a sodium hypochlorite. We have antidotally almost had no complicating cellulitis under a wrap or under occlusive dressings if we soak our wounds 10 to 5 minutes with this post-debridement. We have 10 clinics across the system and we use all, that’s standard now across the system is soaking after you debride these wounds. And this is actually, I think, in a consensus meeting, this is now becoming a sort of a standard and taught in wound care is post-debridement treatment with hypochlorous.
So I was going to get in to some other things. I’m running out of time. You can look at the slides. The one other thing is looking at protease activity. So if you don’t have any bacteria or thoughts of bacteria and your wound isn’t closing, then think about protease activity. And that’s another reason why we need to be good debriders because you actually will remove biofilm and you actually release natural chemicals into the wound bed, secreted by the cells in that wound bed to inhibit, you know, MMPs. And so you can – there’s plenty -- collagen is great, you know, if you’re not using collagen, collagen products suppress collagenase. Alginase will suppress elastase. And so these are things you have to think about when you’re treating.
And I’ll just give one – we’ll do one case study. So this is an interesting case study. So this was an orthopedist who called me on a Friday. And he said, “I’m going out of town. I’d probably have to do a partial calicectomy on this. But can you see this patient?” We saw this patient the following Monday. He had stepped on an object and sat on this for almost three months. He had a purulent material coming out of this. There was evidence of superficial like periosteal, you know, or superficial inflammation. Came into the Wound Clinic. We debrided this. He has no sensation. We took this all the way down right to the level right above the bone or the calcaneus.
The one thing we do have in our clinic are these mechanical negative pressure devices. These are deep debridements and we feel we’re going to lose ground like especially when you get into adipose tissue. We put these on right away. And so we put it on right away. And basically five days later, you can see what we went, how it contracted down. He was on oral antibiotics. He was very compliant. So that’s unusual. He used a knee scooter and basically went on to where we got a great wound bed. We put on a skin substitute and he went on to heal. And that’s a great save.
And so that’s where we are on that and I really appreciate it. Thank you.
TAPE ENDS - [30:48]