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Preparing to Repair in Wound Care
Welcome to Podiatry Today Podcasts where we bring you the latest in foot and ankle medicine and surgery from leaders in the field. I'm Dr. Jennifer Spector, the assistant editorial director for Podiatry Today. We're excited to bring you a two-part series here from Matthew Regulski, DPM on a comprehensive paradigm to wound care that he's developed. He will discuss with us in these two episodes how a clinician can go about properly preparing to repair a wound. Dr. Regulski has multiple certifications in wound healing and lectures nationally and internationally. We are so grateful that he's agreed to share the details of this paradigm with us today. You've shared with us an observation about how clinicians approach wound healing that resulted in your developing an interesting teaching algorithm. Can you tell us briefly about that problem that you identified?
Matthew Regulski, DPM:
The problem is that clinicians and physicians in this space always talk about advanced therapies, things they're putting on. But unfortunately, you can't get to that step of putting skin on, doing skin grafting, all these new advanced things, until you have prepared the wound to repair itself. And thus the genesis of prepare to repair was in teaching residents and other physicians to do all of these good evidence-based medicine things that you have to do each and every time you see a wound patient. That you have to follow this paradigm in order to prepare, to repair, to move it on through a proliferative healing phase, and even utilizing more advanced therapies such as skin substitutes or skin grafting. And that is the genesis of prepare to repair.
Jennifer Spector, DPM:
Next, could you tell us about the basic framework of a prepare to repair approach to wound healing?
Matthew Regulski, DPM:
The basic framework is to think about what you are trying to accomplish and what you are trying to make better within that chronic wound. There's no particular order for those until you get to the last one, but at this point, these are all good things that you have to think about, that you have to correct or that you have to fix in order for the wound to move into a repaired phase and be acceptable to a healing paradigm. Or to accepting a more advanced tissue substitute or skin grafting itself. So thus, the framework was to develop these different things that you have to think about in no particular order, but just that you cover each and every time that you see your wound patient so that you don't forget something or miss something that could be detrimental to your patient.
Jennifer Spector, DPM:
Before we get into the individual steps, is there any particular order or way in which clinicians should undertake such an algorithm?
Matthew Regulski, DPM:
I do not think that I put this in particular order, except for the last one. When you think about after four weeks, if you've done all of these steps and you don't see that significant healing, then you move on to these advanced therapies. But this is just a good algorithm for people to remember to go through all of these things and cover all of these things. Because of all the thousands of patients that I treat, and especially once that come on consultation, something in this paradigm has been missed. They forget to prepare the wound to repair itself.
Jennifer Spector, DPM:
So let's take each of these steps and briefly talk a little more about them. So the first one we've got on our list is biofilm, chronic infection management and assessment.
Matthew Regulski, DPM:
Well, t's very important to understand that every chronic wound will have significant bioburden contained in it. When we talk about biofilm, that 90% of all bacteria naturally produce biofilm. 80 to 90% of all in infections, chronic infections, are due to biofilm. That's right from your NIH. Now, if you were to cut me and leave it open for two days and run a swab across it, you're going to grow ... I'm going to grow bacteria. You have a billion bacteria per square centimeter on your body. This needs to be addressed from day one of any chronic wound. And you can't see biofilm. Now, the slough that you see in a chronic wound is the sequelae of the chronic inflammatory destructive process that is going on. But you need scanning electro microscopy or confocal laser microscopy in order to see biofilm. So in a chronic wound, that slough you see is the sequelae of the destruction.
But that needs to be managed from day one because that not only is a main component of keeping the wounds stuck in the inflammatory phase, because the biofilm, bacteria, toxins that they make, different proteases and they have different things on their surface that stimulate your own white blood cells to come down and try to destroy that biofilm and that bioburden. But unfortunately, your immune system can't get through a biofilm. Antibiotics, oral antibiotics, can't get through a biofilm. It can't get the flow rates high enough out of the plasma without blowing somebody's kidneys out. So that constant stimulation by the biofilm stimulating your white blood cells ... So your white blood cells are secreting different hydrolytic enzymes and reactive oxygen species, trying to break through the biofilm. Well, that bounces off and destroys the matrix. And then your white blood cells become senescent themselves.
They don't apoptose because they are programmed to apoptose and neutrophils have an eight-hour half-life. So when they become senescent, they become apoptotic resistant but still highly metabolically active in a very prone, inflammatory way. So that's the continued circle of vicious inflammation that is going on. And of course then all chronic wounds become hypoxic because they're absorbing the oxygen out of the bed. But at the same time, that is one of the reasons that it has to be managed from day one. And yes, you can go in there and debride it and it's one of the great ways to rip apart the biofilm is good debridement. But then you need things to keep that and protect that debridement because biofilm can start to reform in five minutes and be fully mature in five hours.
So you have to avail yourselves of things that are able to prevent that reformation. Because otherwise, like I said, with a billion bacteria per square centimeter on your body and the reforming of the biofilm begins in five minutes, after a good debridement, that's why we need to put things on there to protect that. But it has to be treated from day one. You have to think of your chronic wound being chronically infected. You may not see the acute signs per IDSA guidelines of an acute infection that may warrant an antibiotic, but chronic infection, chronic wounds, do not, most of the time, 95% of the time, require an antibiotic unless you see the acute signs of that. They're going to be chronically infected. There're always going to be some bacteria in there.
If you don't believe me, take a swab and then you'll see what grows out of it. But remember, when is the last time that you got an anaerobic bacteria on a culture swab because they can't detect biofilm bacteria because they're in a quiescent phase, they're dormant, they're asleep, so to speak, and they're protected by the biofilm. You need real PCR or some type of 16S ribosomal RNA to detect biofilm bacteria and their DNA. But it's real. It's present. It is there and it needs to be treated from day one and continue to think about that process as you are going forward with other treatments. Because a chronic wound is a multifactorial problem. It requires multimodal therapy.
Jennifer Spector, DPM:
So our next one is offloading. Why don't we delve into that?
Matthew Regulski, DPM:
Offloading, in the diabetic foot ulceration, is key. And when you look at total contact casting, it has over five RCTs that have level one evidence to show it has an 89% healing rate on average. So you think about just putting somebody into a total contact cast, you can have a 90% healing rate, but why is it only used in two to 4% of all diabetic foot ulcerations? There is multiple clinical trials to show its value and its need. I try to put everybody into a total contact cast, and I know there's some instances when they can't. Perhaps it's their driving foot, they live alone, they have to go places and do things. I've had some people be claustrophobic or some people couldn't tolerate it.
It hurt their back. I understand that and I get that. And then there are other devices that you can use. I put in prepare to repair the foot defender's an excellent offloading boot to use. And even sometimes there's possibilities that you're not able to even get them into a boot because of their biomechanics or something of that nature. But it's important that you have to think about that each and every time. Because again, in this prepare to repair paradigm, we can put all kinds of different things onto the wound, but if we don't take off the pressure that keeps the friction, the shearing, the stress, to negate the negative pull of their equinus deformity, if we do not get the pressure off, you're going to have a very, very difficult time, if at all, healing a chronic diabetic plantar foot ulceration.
But at the same time, I used total contact casting for heel ulcers, for dorsal foot ulcers, for even ankle wounds to immobilize the joint. And it also works very great for hallux and/or phalangeal joint ulcerations to take that pressure off. We have got to get the pressure off. You need to follow the evidence, level one evidence showing total contact cast has a 90% healing rate. If you can't do that, then move them into a foot defender or a Cam Walker diabetic boot. Something to get the pressure off. You have to do that each and every time that you see somebody with a chronic diabetic foot ulceration is you have to get the pressure off.
Jennifer Spector, DPM:
So what about moving on to vascular assessment?
Matthew Regulski, DPM:
Vascular is incredibly important because, like I said, every chronic wound is hypoxic. Because they're hypoxic, you don't have collagen synthesis, angiogenesis, resistance to infection and epithelialization. And I know that as occurring in the microvasculature but you have to look at the macro vasculature. Diabetes and vascular disease go hand in hand. Diabetes makes plaque. That's why 80-90% of diabetics will die from heart attack and stroke. But they also embolize and they also get severe PVD. Diabetes makes vascular disease. I can't tell you how many times I've seen somebody with a chronic wound that's never had a vascular study, arterial or even venous. People with venous leg ulcerations, never had a venous reflux study, which baffles me. Because you need to know what is going on into the supply of oxygen to those wounds. As I said, diabetes makes vascular disease. Chronic venous ulcerations usually have a significant venous reflux component or there is some type of perforator disease and varicosities that can easily be fixed with ablations.
And ablations are critical in the healing of a venous leg ulceration. Because if you don't ablate that and stop that venous reflux and venous hypertension, your healing rates are about 20% and your recurrence rates are over 80% in three months if you're lucky enough to get that wound healed. So it always baffled me how people that have chronic wounds, I've seen people out to two and three years, never had a vascular study to assess their arterial flow. And these are people with significant risk factors. Diabetes, smoker, rheumatoid arthritis, lupus, scleroderma, because the autoimmune diseases and also connective tissue diseases engender because of chronic inflammation. Vascular disease, that's in the literature of showing rheumatoid patients and psoriasis and lupus and scleroderma, they all have increased risk of vascular disease because of the chronic inflammatory pathway that is occurring in their body. But it's just amazing to me that people aren't thinking of that first and foremost when somebody has a chronic ulceration because all chronic wounds are hypoxic.
Jennifer Spector, DPM:
What about inflammation management?
Matthew Regulski, DPM:
Well, you may say that inflammation is part of the biofilm, the bioburden, the chronicity of the wound, and that is true. But at the same time, we want to use things that we can put in the wound to mitigate inflammation, to absorb MMPs. And everybody's familiar with MMPs. There's 28 different types of MMPs. But only your immune cells are producing MMPs. Bacteria does not produce MMPs. Yes, they have toxins and they have proteases that they make, but they don't ... The matrix metalloproteinases are more reserved for your human cells. So they're very destructive. They're being produced in there to try to break down bacteria and biofilm.
But so we need things to put in there to bind them, to absorb them, to mitigate their potentiality as a destructive process. And so we use a lot of collagen and as I teach my residents about that, to utilize that in the wound, because collagen can sacrifice itself to the inflammation in helping to bind and use up those MMPs. And at the same time, collagen connect as a scaffolding to enhance cellular migration. But when I talk about that inflammatory component, those are the things that I'm talking about, utilizing dressings or things that we can put in there to mitigate and modify the inflammatory response.
Jennifer Spector, DPM:
Next, we have moisture balance.
Matthew Regulski, DPM:
It's always interesting to me, and it's still happening, is that I get patients that they've seen other physicians and they or other ... they've listened to other people that said, "Leave it open to air, let it breathe, let it dry out." Now we've known since 1958 that we do not leave wounds open to air. That's when some of the first blister studies were done showing you that proper moisture balance is critical to facilitate cell migration. You're 90% water. If your things dry out and they scab up or they get these dry eschar cells can't burrow across that. They have to try to burrow underneath that and that is not going to happen. So we don't want to leave wounds open to air, but at the same time, we don't want things soaking wet. And I've seen people that were told to take showers and get soap on it.
Can you imagine taking a shower if you had a big venous leg ulceration or diabetic foot ulceration? And all that bacteria and all that gunk is being washed off your body and it's coming down in there and your foot is underneath this cesspool of fluid macerating tissue, seeding more bacteria into there because of the open wound. And when things are soaking wet and macerated, they will smell, there'll be odor, it'll break down the surrounding tissue, and things can't heal as well. So that's why it's a very fine moisture balance as you, as the clinician, you have to foster that appropriate moisture balance that facilitates cell migration. So we don't leave things open to air, but at the same time, we don't want things soaking wet. You have to be able to balance that and absorb that inflammatory exudate that comes out of there by maintaining proper moisture balance.
Jennifer Spector, DPM:
You do have exudate management listed next. Is there more to expand on there?
Matthew Regulski, DPM:
Well, the exudate management is, because again, I think from all the experience of teaching residents and other physicians, they always have questions about, "What do I put on there to absorb the drainage?" Well, the drainage is highly inflammatory. That exudate that comes out of there is full of inflammatory mediators, protein as well. And if we allow that to sit on the wound, then it's going to break down that tissue, macerate the tissue, you could get redness and you're going to get a lot of odor. And then people are going to think that they're some type of super infection and they've got to be in the hospital, but we're not managing the edema.
Even when you look at a wound, for instance, a diabetic foot ulcer, when people are walking on that, they are going to push fluid out simply by the pressure of walking. After I take people have a total contact cast and we have Drawtex or heavy absorptive stuff on there, you will see a lot of fluid that is pushed out onto that. And that has to be managed, that has to be wicked off and taken off the skin and locked into the bandage to keep that away. Because if not, the exit is highly inflammatory. It's going to break down your tissue, macerate, cause erythema and cause a lot of odor and can lead to an acute infection. So that has to be managed appropriately each and every time you see that wound.
Jennifer Spector, DPM:
So what about edema control?
Matthew Regulski, DPM:
Edema is really interesting. When you look at what happens when somebody swells or any type of edema, it pulls the arterials farther apart in the skin, and that means the greater distance that oxygen has to go to diffuse to get to that wound. Edema is quite pathologic, particularly not only in venous wounds, but you'll see that in diabetic foot ulcers and other lower extremity wounds is we have to manage that edema. Because we want to bring those arterials closer together, so shorter distance that oxygen has to diffuse to get to the wound. And that's why a lot of things where you look at multi-layer compression bandaging for venous leg ulcer, it has a lot of level one evidence.
Yes, there's a lot of biochemical things that are going on because of the multi-layer compression, but the underlying theme is to manage that edema, remove that pathologic edema so that we can allow more oxygen to get to the wound and stop the backflow of venous hypertension, which then creates a lot of inflammation itself. Causes a lot of leaking, because when you swell, that fluid's got to go somewhere and it's going to come out the break in the skin, which is your ulceration. And that fluid, again, because of the exudate management, is highly inflammatory. So edema has to be looked at, it has to be treated and is, particularly in venous wounds or even in your diabetic foot ulcer patients that could have a concomitant venous reflux or lymphedema, the edema has to be managed as part of the prepare to repair scenario. Because it will improve oxygenation when we reduce that pathologic edema.
Jennifer Spector, DPM:
Next, we have debridement and wound bed preparation.
Matthew Regulski, DPM:
I mean, debridement is essential, as we talked about, particularly in the biofilm application. It is necessary for us to debride, to rip open biofilms, to remove a lot of the sloughy garbage tissue that you see within the wound that acts as an impediment to the wound healing process and acts as a nidus for bacterial growth. Debridement is one of the simplest things that we can do to help prepare a wound to enter into a repair phase. It's simple, it's easy, a nice little blade, very inexpensive. Or if you use a curette, I like blades because they're more fine, it's less pressure that you have to put on. A nice 15 blade has a defined area that will cut so you can monitor how you're doing. But you have to have some type of wound bed preparation. I get it. You want to get your dopplers done and make sure their blood flow is okay. I understand that.
But at the same time, you need to debride that tissue that's slough. Look at your wound edge. We don't want wound edges coming in in that cliff-like appearance. We want our skin edge to come in a nice 45 degree angle or nice end level to facilitate proper healing. You have to debride away all of those thickened wound edges, obviously once you know how the arterial flow is. But you can still do some light debridement upon these wounds to help remove that slough. And by doing that, this is one of the most easiest, inexpensive ways to do. But again, there are different types of debridement. Obviously autolytic debridement, mechanical debridement, hydrosurgery, Versajet, ultrasonic debridement, people use. But we have to think about debridement as a very easy and inexpensive way to help these wounds to prepare to repair. It's one of the hallmarks of treatment of a chronic wound is we have to debride the tissue.
Jennifer Spector, DPM:
There's so much more to learn from Dr. Regulski's paradigm in our next episode, so make sure to tune in to that and other episodes of Podiatry Today Podcasts on podiatrytoday.com. SoundCloud, Apple Podcasts, Spotify, or your favorite podcast platforms.