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Male Speaker: Okay. So back to ABSCESS which -- and actually this -- this is very helpful for my students or somebody that’s trying to think their way through wounds. Did you do something about this? What are we doing about this? When they come to me and they present a patient, et cetera, what are you going to do? What do you want to do? You know, they don't know where to start. I said, “Well, start with A. Tell me what you would do in A category. Tell me what you would do in B. What would you do in C? We have choices there.” And then we get around to the last one which we’ll talk about at the very end is like what do you do for the skin? What are we doing for the periwound? The wound heals on the outside in, and the inside out, and underneath-up. So it’s healing from everywhere, so everything has to be healthy.

Okay. So that’s our system. Oh, and the people out there, these are -- whenever I do stuff, I always have students on every paper that we ever do. And that’s because they need to get published so they can get residency programs. And they all get published by doing cool stuff with us, and they really like wound care. It’s interesting. Podiatry is a very surgical specialty. I’ll just tell the story because it’s kind of cute. And they put a survey out. The surgeons put a survey out to find out what part of surgery was what the students really wanted to learn. So they said, “What’s your favorite part of podiatric medicine?” Thinking that, you know, it’ll be one of their surgical things. And everybody said wound care. So we are making some headway for those of you that don’t think we’re treating podiatrist effectively.

Okay. So this is kind of cool. I mean this is the part about wound care that like -- we’re just going to go like Star Trek for a little bit then we’ll come back to life. This is a Hoxworth study. If you look at this, this is 2009. It’s not that far -- you know, it’s a while ago. It’s like old.

[2:00]

And what they identified were these markers, if you found those in a wound with a genetic test, a PCR or a DNA analysis, that wound was healing, and it would go on to heal. These were traumatic battle wounds and they were trying to predict what wounds are going to close, and wounds aren’t. So like in intervening on wounds that were going to become, you know, going to break down and dehisce. These guys dehisced and they’re all inflammatory markers, and these are all the markers of healing.

So if you look at this as a -- what kind of paper or biomarkers, it’s very detailed. But they broke them into metabolite markers, enzymatic markers and bacterial markers. But then there were -- oh, and I have this in here because that right there, you know, you think you’re like either have trouble figuring out what bandages to use. That right there is a bandage that gives you read out like that. That’s your future bandage. You’re going to plug the bandage into the computer and it’s going to tell you what’s on the wound and what levels. And then you’re going to make dressing choices based on that. Isn’t that cool? I mean that’s the coolest thing ever. That little sampling dressing picks up everything in a surface, and it tells the computer what biomarkers are there, you know. That’s cool.

So this is the wound fluid analysis, and this is what you get if you do a wound fluid assessment. This is a serum analysis to look for blood serum markers that tell you whether they are in inflammatory or healing phase. And then this is a study that was done on -- is this the M1 -- yeah, M1, M2 biomarkers. This was potential biomarkers that delayed wound healing, increased protease levels, we know those. Gene expression analysis, cytokine levels, all these things are possible -- most of them are in wound fluid.

[04:03]

And what we have is that dipstick thing that just tells us very little when what we really need is to be able to just aspirate the wound fluid out and just find out what’s in it. It’s not there yet. This is a really simple test. So some of my friends at Hammond University were studying M1 and M2 biomarkers. And they developed a spot PCR assessment for M1 and M2 phenotype. They basically put a little wound fluid in there and they -- or wound tissue in it, and they just run it real quick in a machine and told them right way, and it told them percent 1 or percent M2 biomarkers.

Wounds that had majority, like 50% or higher M2 biomarkers all healed. All wounds that’s stalled, that it was 90% predictive, had predominance of M1 biomarkers. I mean that’s such a simple thing. It’s either inflammatory or not. And you know what that would tell you, I want to put a thousand dollar tissue graft on somebody. I think it’s a great idea because that wound looks like it’s ready and I think it’s ready. You don’t know. If you see those pictures like -- is there a biofilm in this wound. You don’t know. You can’t see it. It’s sort of there, eventually, it gets to be this sloughy mass, but it’s not when it first start.

So this was -- I want to put a thousand dollar thing down, what’s your M2 marker say? Says M1, no. You’re going to wait, you need to get the wound a little healthier, and then you’re going to use it when you hit 50% or greater. And then it will take off, like when you put it on, you’re not going waste a single one of them. They will all take. That’s what I think is cool about cellular markers.

This is looking at some of these expensive things we put on people. This is actually cellular therapy when you do mesenchymal stem cell stuff and all that, you’re like doing cellular therapy to the wound, you’re adding things to the wound that help -- and you get closure rates.

[6:01]

You know, this is looking at a particular live stem cell tissue product, the study that showed complete wound closure at 12 weeks, 85%, 67%, venous leg. This is the kind of numbers you get with studies like this. This is a little bigger one looking at live placental versus human fibroblast versus bilayer CTPs, and look at the pivotal studies on healed versus control, 62%, 30%, 56%. That one is not too hot but, you know, it’s better than a lot of wounds we see.

This is like a comparison of studies between -- and there are -- there are comparison studies, you know, Apligraf versus Theraskin, Oasis versus Dermagraft, Oasis versus Regranex, Apligraf versus the non-adherent. These are comparing them to dressings to see what the percent heals are -- healing is at 12 weeks, 49%, 57%, 70%, 77%. This tells you what kind of potential healing you might get with these various tissues, but they are potent tissues you want to apply to a wound at a receptive moment.

That’s what I’m trying to get across is that you put it out every week. You’re supposed to put it out every week for 12 weeks, and that’s how you get the best results. Not necessarily. You have to look at the wound, you have to decide whether it’s receptive to what you’re putting on, and apply it intelligently.

I'm not an automaton. I don’t like to do things 12 weeks in a row the minute I get because I can make money on it. That always bugs me. I want to make money. I need to make money. My clinic’s going to go under if I don’t make money. But I also don’t want to make money at the expense of patients in the system that much. I want to try to keep costs down and do the right thing.

This is some more studies on this, looking at Apligraf versus Theraskin, Oasis. This is Oasis versus Regranex, again, looking at some of the percent healing across the board. So there’s a lot of that. So that’s another thing that we have.

You saw there’s a new product out that’s taking your patient’s blood.

[8:01]

I'm particularly fascinated by anything that uses you to heal you. I don’t want to buy this stuff. I want to whip it up in my own clinic and put it on. I mean, that part is neat. They have a microtome now that just takes little tiny skin samples and puts it on the wound, leaves no scar behind. It’s gorgeous. They have one now where they take -- you can take a 2-centimeter like incision or biopsy off the upper leg or somewhere, and they homogenize it and turn it into a product paste. They send it back to you in the mail and you spread it on the wound like butter two days later, and you have a human -- live human skin cells that have been cultured into this paste that you’re going to put on. That’s amazing. And it’s all stuff that, you know, probably cost a fortune, so you don’t want to do it on the wrong wound.

When do you biopsy a wound? This is a really good friend of mine who pulled up his pants -- a podiatrist, pulled up his pants and said, “Do you think I need to check this out?”

That’s a basal cell carcinoma that had already started to metastasize. I mean, they don’t -- they’re usually kind of in site, too, and they don’t go anywhere, but that one actually had started to get aggressive and you really need to have that out.

So when do you biopsy wounds? When you do need to do a cellular assessment on wounds? And it’s basically when the wound fails, it falls into -- out of a typical behavioral pattern and becomes atypical. It should be biopsied.

My friend asked me the other day, “Do you think I should biopsy this?” I said, “You already answered your own question.” So if you’re asking me, you have a reasonable suspicion that it should be biopsied, then just take a piece. You get paid to do a biopsy and it’s the right thing to do, so take a biopsy. And half the time where I take a biopsy, the area where I biopsied, it heals better than the rest of the wound.

If there’s any clinical suspicion of a skin cancer, raised border, crusting, and it changes in shape or color, look at that, and it’s still spreading away from the wound, previous history of skin problems or family history, wound isn’t responding through traditional things, or if it’s gone too long and re-biopsy of the wound continues to languish.

[10:11]

And what’s languishing is -- this is the O’Donnell guideline, Management of Venous Leg Ulcers Wound Biopsy Guideline. Recommend a wound biopsy for leg ulcers, and you know, you could do this to any ulcer, if it fails to enter wound and compression to every -- for four to six weeks of treatment for all ulcers with atypical features.

So, they’re saying every six or eight weeks or so, if it’s like not going anywhere and it’s not behaving in a typical manner, we kind of look at stuff. And if it’s two months, if it’s at least two months old and they present with something that’s unusual and it’s something that we just doesn’t have a right -- or a new ulcer that’s been around a long time, we tend to biopsy in at least a couple of places on each wound, one from the bed, one from the margin. They usually say three or four are good things to do.

So, that’s the abscess acronym. This is the last one, skin, effects of aging. We already heard a lot about this. The epidermis gets thin, dermis and subcutaneous layers thin out, epidermal turnover decreases, compromise barrier to the skin. It’s not -- it gets infected easier than it used to. It gets irritated more easily.

Delayed chemical clearance, when you put things on the skin, it doesn’t go away. Reduced sensory perception, patients don’t feel stuff so they get further along before it bothers them and then it bothers them a lot. And then, decreasing immune function, they don’t respond to things that are on the surface the way they should.

Thermal regulation is down. They have infections that get out of control, particularly diabetics before their temperature goes up.

I had a guy with a 32,000 white count who is a DIC, who is in my clinic and said he felt fine and he didn’t see any reason why he needed to go to the hospital. He actually died the next morning because he was in DIC and he popped a blood vessel in his brain.

[12:01]

And he died because they happened to be in the basement of the brain.

Decreased immune function of vascular response. Glycosylation. Diabetics, it doesn’t just affect, you know, their skin. It affects everything. Loss of elasticity. Every single one of them has an Achilles Tendon tightness. So they all should be stretching. Like stretch and posterior muscle group out. They should be doing stretching exercises because it increases forefoot pressures. It causes digital gripping to add to the problem, and it increase their risk of having ulcers on the toes.

Then they go to plantar fat pad and stiffening of the plantar fat pad, which means they have more shearing. They have less ability to handle stress on the forefoot and they get ulcers faster. Stiffening of the plantar fat pad.

Loss of connective tissue. Loss of protective sensation and diminished healing response. So they’re – everything is going down in the presence of glycosylation. So blood sugar control is important. Getting it under control is important. But recognizing that – and when it’s there, once you find it, it’s already done damaged. I always try to figure out, why do we use the 5.07 monofilament. Because it tells us we have what? Loss of protective sensation. Why don’t we use the 4.01 monofilament which tells you, you are losing sensation, but you haven’t lost it yet.

I’d rather have a marker that tells me, “I see smoke, your house may burn,” than one that comes up and says, “Oh, look at the flames.” That sucker is gone now. Yeah. Should have done something when we smelled smoke. When you smell smoke is when you start to do things. Moisture-associated skin damage. Wound exudates that drains out. Remember that has to do with bandages, dressings. We’re going to hear about that. Incontinence, f-word from stoma, perspiration.

[14:00]

Principles of skincare, this is no Wiki. Best practice skincare management, this is a really nice little graphic that kind of takes you through good skincare.

Pressure offloading, last thing, I’ll stop with this. We’ll stop with this slide, which is the offloading continuum and the idea that you don’t -- the International Working Group on the Diabetic Foot says the best thing for a diabetic foot ulcer is a non-removable knee-high device. TCC is the best. You get paid for it if you use it, if you bill for it. Or a cast walker that’s locked on so it won’t come off. They have an 80-plus healing rate at 12 weeks. Anything that is removable is 50% or less.

So when you do this -- this was a little bit of a guideline for types of ulcers, and these are patients that are -- if you can -- anything removable, they have to be in a compliant patient. And you start here, and you progress to this kind of slowly over time. You don’t just take the TCC off and hop -- pop them in there and never go back to their old shoe. Whatever it was that gave them an ulcer, they should never wear again. They have to go back to something else and you should be the prescriber for that.

So I’ll stop there. And there’s a couple more. That’s the guideline. These are the words of the guideline, but I basically told you what it says. Gold standard.

Heel ulcers, I hate. There’s nothing that you can really ambulate in that protects the heel ulcer well. And everybody tries to walk on them and then they die in beds. I don’t treat patients with bed sores very often or decubituses or pressure injuries. But keep in mind that when people are immobile for long periods of time, they need pressure reduction devices.


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