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Male Speaker: Okay. So now weâre going to look at this ABSCESS thing. And there is this TIME, DIME, and MEASURE. Those were all three different systems for looking at wounds. That hasnât changed in the last few minutes anyway.
And these are the objectives. Weâre going to look at the components of that and weâre going to see how they affect wound management. And weâre going to look A and B on the word ABCESS and then weâre going to look at C, E, and S in the second part. This is the longer part. This is the part that I probably wonât make 25 minutes if Iâm going to do my best. This is the old TIME and DIME, you know, tissue infection or inflammation, moisture balance, and edge of wound.
And, you know, weâve used this ad infinitum. Companies have used this over and over and, you know, itâs kind of the background for like when their products are ready and how to use their products. And it always -- it just seemed a little restricting to me with todayâs wound management and everything youâve seen already and what you all see -- continue to see in all the products and everything that are available on wounds. And we need something that had a bigger spread to it.
And I started writing the components of wound management and I tried to come -- I was on an airplane. I had five hours to kind of look at words and try to come up with a word and I come up with ABCESS which seemed to work and it was that you start out with a vascular assessment that you do, you know, like in podiatry, the first thing we look at is arterial assessment or like whatâs the patientâs circulation like. And Iâve always heard that, you know, like do they have enough blood, do they have enough oxygen, or are theyâre going to heal.
So I started with arterial, and then that led to making it arterial venous and then I started working with women who were extremely -- I havenât worked with too many men in the field yet. But in trying to influence the podiatry profession, to think about lymphedema has been, you know, like moving an elephant.
But the lymphatic system and the importance of the lymphatic system to the whole -- all of wound care is much more important. So we added in there that you would normalize these, that you would consider vascular surgery, compression, signal compression, manual lymph drainage, completed decongested therapy, that all these things are always a consideration that you maximize a vascular inflow and outflow. Viable wound management, this is looking at the wound surface itself and deciding what weâre going to do about whatâs happening with the cellular structure, physically what are we going to do, debridement, removing necrotic material from the wound, trying to restore the wound to an acute phase, controlling bioload and bacteria on the wound, sometimes the dressing choices are related to bacterial load.
Most of the time when you talk about dressings, and Iâm not going to about E at all. Lynâs going to do that very effectively, but that exudate is dressings, and itâs our choices of what weâre going to put on the wound to manage the fluid thatâs coming from that wound, and a lot of the stuff thatâs out there with biofilm, and managing biofilm, and thereâs new things coming out in the biofilm arena almost every day, new topicals, new substances, new ways to manage to wound biofilm and just keep bacterial load on the surface down.
Cellular activity, we already touched on a little bit, but thereâs like, you know, spot of care wound fluid analysis thatâs kind of there but not really, we donât really utilize it as much as I think they thought we would, PCR DNA analysis for culturing. Instead of culturing, we are looking at PCR DNA sequencing to see what our bacteria are showing us and thatâs fascinating. Wound biopsy or tissue biopsy, growth factors, autographs, you saw there are like, thereâs two new blood products out now.
Whole blood products, thereâs a new PRP, like a new product for like turning PRP into a suturable wound covering. Exudates, systemic disease we went through, and then skin protection and treatment, which is not just the wound edge.
Itâs periwound skin and itâs the entire area, the entire geography of the wound, and how do we keep pressure up and prevent it from being injured, or that we get an injury associated to this, so we look at just some of the components of the assessment.
You know, the symptoms of arterial claudication or pain, or arterial insufficiency, claudication, reproducible exertional muscle pain. I try and tell my students, itâs like people with arterial problems are very consistent. They canât very walks so far, they have to sit down and re-vascularize. They have no -- every time they elevate their feet for a while, they have to put them down. When they lay down, to go to sleep at night, they donât have enough blood flow to lower extremity, so they kind of have to dangle their legs or walk around a little bit, then they can get to back to sleep.
Venous ulcer patients do the opposite, they can -- as they walk around and do things during the day, they very slowly get more and more uncomfortable with standing or sitting for long periods of time with their knees down, and their legs will begin to like ache and just kind of generally donât feel good. And they get to the point where something -- where they just have to do something to elevate. And when they elevate, instead of getting worse, they actually start to get better and their legs feel a little better.
The problem is that when you get increasing venous outflow abnormalities, youâll start to see sometimes some claudicatory muscl, like discomfort. And they can only walk so far at the end of the day, they need to sit down to rest. Then theyâre actually claudicating within a venous condition, which is complicating.
Rest pain is when theyâre really far -- really far along, or numbness when theyâre actually reducing the circulation to the nerves so much that it starts to go numb. Ulceration and gangrene, obviously, when weâre to the point where things are things are really bad.
Physical signs, absent pulses. Put your fingers down, look for pulses, see what you can feel. Make sure you know where they are so that when you look for them, you could find the DP artery, you can find the PT artery. And when you canât find the DP, look for a perforating peroneal, which is a little tiny -- the auxiliary artery thatâs just to the left -- to the left or to the right of the DP. And itâs -- sometimes it actually provides most of the circulation to the dorsal aspect to the foot. And itâs not a loss of dorsal circulation, itâs just that the DP pulse is not palpable where the perforating peroneal is.
The dependent rubor coolness, we went through all that. Absence of hair, dry skin. Donât forget this, they tell me they donât smoke. âHow are you doing today? Oh, yes you do.â And then any history of prior amputation.
They have a distal distribution, which we went through. Deep sharp edges, punched out dry, necrotic fibrous eschar type bases. They may or may not be painful depending on the state of the patientâs neuropathy. They may not hurt in a diabetic neuropathic. They will, eventually, because it begins to affect kind of the deeper structures, and they start to have pain. But initially, in the skin, they might not feel some of the changes, like that little distal ulceration in the toe, until that actually starts to affect them a little more with edema, that starts to affect the smaller muscles of the foot, and then at night, they start to hurt.
Now, the base of diagnostic test, weâre going to -- one of the little lab things we do is how to do an ABI, or ankle-brachial index. Itâs sort of looking at the ankle pressure and the arm pressure, and they should be one to one.
If theyâre not, youâll see a decrease in flow to the lower extremity, and youâll see some of these symptoms that we talked about.
Paulâs fine recordings are a little more formal way of looking at pressures in the limb. And looking for places where pressure drops or changes across a particular area or zone, indicating that there might be a blockage or a reduced flow across that area.
Toe pressures are very valuable in diabetic patients because they often don't have a very readable ABI, but the TBI is very, very telling. You might be lucky enough to have a skin perfusion pressure. Skin perfusion pressure uses a laser Doppler around the skin, in the area that you want to able to evaluate. So it would be your arterial zone and -- or aorta zone, or whatever you want to call it, where it looks at, as you -- when you include the limb, so thereâs no flow, the laser Doppler is looking for the first moving cap or RBC in a capillary. Itâs very sensitive to pressure, and as you begin to release the cuff, it will look for the first time they see RBC slide on the capillary, and that tells you thatâs the pressure.
Ultrasonic Doppler or wave forms, for venous conditions and venous insufficiency, transcendence oximetry, everybody is doing that if you have a hyperbaric chamber, or you work at a hyperbaric unit. Thatâs sort of the mandated test, but itâs slow, itâs tedious. It only looks at a small area of the foot at a time. And thereâs nowhere near as, I think, as helpful as skin perfusion pressure. Thatâs never caught on as sort of a major or vascular assessment.
And then, thereâs near infrared photography, which may find a way to replace, as it gets more sensitive, to replace Tcombs in looking at oxygenation in various areas in the foot. Whether or not there was good O2 concentration, whether itâs deoxygenated, is it the area the wound where youâre working? We started working with those cameras and it was kind of fun to take pictures of the wound.
And you could see oxygenation, deoxygenation, you could debride it and show that you had returned oxygenation to the entire surface. So what youâve done is remove the barrier to reading the blood flow underneath and kind of get a feel for where -- what the state of the wound is.
Just so you know, itâs -- not everybody uses exact same numbers. This is the ankle-brachial index for the ADA guidelines that we would go by 0.9 to 1.3, 0.7 and all, et cetera, for the different levels of ischemia. And then you already saw the WIfI classification which kind of breaks it down in a little different classification, but not that much. Itâs very similar.
And thatâs how you calculate an ABI. Take an arm pressure with the Doppler, you take an ankle pressure with the Doppler, and ideally, you should do resting and relaxing, you know, not sitting in a chair. And they should be -- you should do left arm, right arm, left leg, right leg, take the best pressure in each site and average those out to determine whatâs your actual ABI is. And not just do one site. Thatâs what your non-invasive vascular testing looks like. And you look for places where the flow decreases, which would be in the popliteal area in this particular limb.
Different findings. These are poor healing indicators. The systolic pressure, less than 60. But if youâre a diabetic, less than 90 because diabetics tend to have more atherosclerosis, calcification of the vessels, lower flow. ABI, less than 0.05. Toe systolic pressure is less than 35 or 50 in diabetic. TBI is a 0.4 or less. TCPO2s, TcPO2s, less than 20. And skin perfusion pressure, Laser Doppler is less than 30. Theyâre all indicative of, you know, severe limb ischemia or critical limb ischemia.
Venous ulcers. Good guideline, this is American Venous Forum guidelines, the -- and the Society for Vascular Surgery are all, you know, good places to go. I just have this in here, if you want to find it, the reference is down there, itâs Kimmel and Robin and it was -- I forgot what year it was. I donât know, I canât read it, maybe Pamela Kim, Kimmel and Robin. And it look -- itâs an algorithm for treating a venous leg ulcer.
So what I go through with the students, we do a complete medical history, detailed physical exam looking at all the things weâve already talked about. Test for venous disease if necessary, to send out -- send them out for a duplex to look at the veins.
Typically, if they have an ulcer on the leg, and theyâve never had any kind of venous assessment, itâs not a bad idea to get one. Make sure youâre not dealing with an arterial problem at the same time. Because sometimes you get -- you get, you know monolithic, you know. I see the ulcer, I know itâs a venous disease. They always look like this. Weâre just going to treat this with compression, and it looks like they have -- they are rubor, so it looks like they have pretty good circulation in the digits.
You do the old, classic, like, you know, like a capillary refill on a patient whoâs sitting there with their legs dangling down and touch them and all. It fills right back up again, they got plenty of flow. No, they donât. Get him up, elevate them, do a capillary refill test the right way and see what they really have.
And then if you have an abnormal arterial exam, refer to vascular diseases. Thereâs anything that could be done to improve the vascularity of the limb, and donât use multilayer compression on people less than -- with ABIs less than 0.7. If you do this -- and you canât use any compression, you got to be very careful using pressures when the ABIs are low. You donât want to cause any injuries from what youâre doing.
Compression is the gold standard. Failure to get closure, and this was what I talked about, in this particular guideline, I was looking at the Cochrane data.
And what Cochrane did at the time was -- the only thing they had really good data on was bilateral skin -- artificial skin or skin equivalent, which was the old apograph at that time.
Donât forget to walk your venous patients. A lot of them are very heavy that they very often donât walk much. They donât like to walk, itâs difficult for them to walk, they sit around a lot. But we forget that probably one of the main things that moves venous fluid out of our limbs is exercise. So even if youâre getting them -- my wife just completed -- she is a Tai Chi mistress or masteress. Sheâs a Tai Chi master now. Sheâs an instructor in Tai Chi. Iâm very proud of her. She stuck out -- there she had to get in front of 30 people, do her lower -- I said, is that a Kata? She says, âNo, itâs a set.â She said she has to do her set.
But what sheâs found is -- she works with geriatric rehab all the time, and she has got these people out there, doing these little Tai Chi moves, and just kind of moving through this format of movement, which is extremely helpful in just getting patients to use their muscles.
Youâd be amazed. If youâve never put a Doppler on anybodyâs ankle, or even up on their leg, and then squeeze the foot, youâd be amazed at how much fluid comes shooting up out of the foot every time you step down. So what do we do with venous leg ulcer patients? We put metatarsal pads in their shoes. When they step down, they get like a bump that kind of pushes up in the middle of the foot. A little soft, gentle. It doesnât have to be really hard. It can be kind of soft, and it just gives them that extra lift of fluid up into the leg.
Then when theyâre working in the leg, theyâre going to get this nice muscle pump activity, especially if they have appropriate out external compression. They have external compression, you have some long stretch effect, which is kind of squeezing the edema down when theyâre not moving at all. Or they have a short stretch bandage on, which is most effective on people who are moving or moving around.
Weâre going to see a very effective short stretch bandage today, which is the one that we use a lot.
Non-stretch elastic, short stretch, long stretch, these are all our compression choices, and they all have some value. A lot of people will say to not use segmental compression or intermittent compression with lymphatic patients. There is some evidence out there that some types of compression can be adjunctive to a lot of the other stuff, but you canât substitute this for a complete decongestive therapy. Like, thatâs what people tried to do lots of times. âOh, itâs a pump. Itâs easier. Iâll just do that.â Sometimes itâs access. With fluid, itâs access to people that can actually do complete drainage on patients.
So the other circulatory systems, the lymphatic system, weâve heard a lot of. These are your primaries, melaroids, praecox, and tarda, and we deal mostly with secondary edema. And even though these are all causes of secondary lymphedema, the most common one is this one. And this is that slide that goes around and does them all, so rather than have -- I should have it on pop-on. But phlebolymphedema, which is secondary lymphedema associated with long-standing venous insufficiency that is sort of unmanaged.
Some of you might have heard me today, I was talking about having, you know, varicose veins in my leg. And I just have been wearing compression stockings since I was like, 25 years old. As soon as I finished PT school, I started putting them on. So I donât have any of these secondary problems associated with -- but I could, if I just ignored them.
Stages, you know, Heather kind of went through the stages a little bit, so I donât need to do that. This is the B part. These are the classic wound types. We know that thereâs now a ton more out there.
When youâre looking at -- doing a complete wound assessment, I have kind of taken this out for a time but Pamela put it back in. She said, âNo, you should really talk about that one thing thatâs on that slide.â
Because we forget, you see all these other things on here. Do we do mechanical imbalance? Do we actually look at their foot and say, they have a huge, big bunny, and they got hammertoes, like absolutely flat now at the mid foot. Theyâre standing on their navicular, their cuboid is touching the ground all the time. You know, theyâre really, really knock-kneed. And then they just put all these pressure on the medial foot, and thatâs where theyâre breaking down all the time. So thatâs why thatâs in there is to pay attention to that.
This is a new Wound Infection Continuum. It is contamination, colonization, what used to be here. Remember critical colonization, it is no more. Now, itâs local infection to spreading, to systemic. And you can look down here, now the picture kind of moves along, but itâs -- it has -- people are making, basically making decisions on topical antimicrobials and other things based on the state at which the patientâs in at that time. This is following, kind of, like following more the IDSA guidelines, which is when you intervene with various, you know, therapies.
If you think about biofilms on the wound, itâs platonic, early biofilm formation, mature biofilm formation, and then seeding in that biofilm where it actually starts to break off and go to other places in the area or within the body via the lymphatic system, essentially.
Who do you culture? You do not culture on infected wounds unless you have to for your facility. I think Iâm good with this, sometimes I think that decision, particularly, is made just because we have lawyers in the world. Just because we have lawyers in the world.
Mild infection, no culture. Just start empiric -- these are the IDSA recommendations. And then we can talk a little bit about reality if you want.
But modern -- moderate infection, culture then start empiric therapy. Yeah, I mean, if you really think -- this is -- this is one there in that IDSA, that PEDIS classification 3 -- PEDIS classification 4 is severe infection, theyâre going to the hospital. Three is they might -- it might be a good idea to send them to the hospital but they might be able to manage it at home. And you have to look at other criteria to decide. Donât use topical antimicrobials on clinically unaffected wounds.
But if you put Neosporin and everything, you shouldnât do that. Donât use -- especially, donât use gentamicin cream on everything. Gentamicinâs an antibiotic that you might need someday, and you donât want to develop a gent allergy, or a gent resistant showing up in the -- in our microbiome. If you culture an infected wound, make sure you stay in your chart, it is for a surveillance purposes only. Just from a legal stand point.
Why did you culture it? You must have thought it was infected. Look at that, you put down on there. What's the word they always look for? You wrote âpurulenceâ down. Whatâs that mean, buddy?
I have a student -- students that love to -- they just -- everything looks like purulence to them. Itâs all puss. It all stinks. So they write -- they put âpurulenceâ down every time, and I take it out immediately. I said, âThatâs a lawyer trigger word. I donât even use it.â It has to be oozing out puss and I have to be taking a culture for them to put down âpurulenceâ. I just donât like the word. I'm not triggering any of these things.
Do get a culture from almost all infected wounds. Cleanse and debride the wound before you get that culture. Do not culture yucky spots. You donât go under edges. You donât go down holes. You donât go into dumps within the wound. You clean it with saline. You go to a nice, clean spot on that wound, and you use the Levine technique or you aspirate fluid from what you think might be sort of an abscess area. And you properly send specimens in as soon as possible.
That is always the one that bothers me because it takes forever for the thing to get to the lab. And if you look at the ideas, say, guidelines, youâre supposed to be cultured within two hours of the culture time, and then nobody is.
Donât culture on infected wounds. Obtain the specimen -- do not cleanse the wound and get a specimen by just swabbing it. Donât do that.
How to culture? You can either do a deep tissue biopsy or scraping, which is better. Needle aspiration, if you think you have a fluid collection that you can take it from. And if you have to do a swab culture, use whatâs called the Levine technique, which is to clean the wound. Youâre not swabbing it, you clean the wound aggressively, go to a nice, clean place, take that culture at, and drive it into the wound base to where you get subcutaneous fluid on it. I spin it until they bleed a little, and then I put it in the tube.
Donât just do this, donât just touch it, donât do that. Actually, get some of the subcutaneous fluid in there. Youâre most likely going to pick up the proper -- yeah, right around there, 1 centimeter or smaller. Where would you swab that? This has been cleaned with saline and weâre ready to go. Youâre going to take your culture from right there.
I know. I want to be the one that does that. Pamela made this slide for me. But right there, thatâs your spot, not down that hole. Thatâs where you want to go. Thatâs where every student wants to stick every swab, or they want to go up under some lip.
If youâre doing DNA culturing or DNA sequencing, you can scrape the whole surface and send it all in to look for everything thatâs there. Just remember, with DNA sequencing, you find any DNA signature on the wound surface. So, it finds dead ones and live ones.
So if youâve been using an antiseptic on the surface, you may have a lot of dead bacteria around. Itâll pick them up and itâll tell you whatâs been there. Things that are dead actually show up.
This is just the new kind of -- this is the guidelines for this. Itâs covert and overt. Just look for covert signs or secondary signs of infection, friable granulation tissue, delayed healing, and then overt signs, which is they -- whatâs Sybilâs thing, their time, era -- yeah, Stone Age and, you know, whatever. He likes those.
And then, this is looking at spreading infection or systemic infection and how to deal with that.
These are secondary signs of biofoam or infection. Increased exudates, discoloration of wound bed, friable granulation tissue, pocketing, odor, delayed healing. Thatâs what you look for. When you see that in a wound, you think the bugs are taking over the surface, you know. Primarily bugs.
Now, I have this on here because I wanted to have -- I found it while you guys were lecturing us, playing around, looking. And yes, I was on the internet. Playing around, looking at Google for a huge picture of a swamp. And one of the picture where you looked over the monstrous swamp and way in the distance was like this beautiful mountain. And itâs -- thatâs the distance from eschar to granulation tissue in wounds, which is thereâs nothing that tells you anything about the middle. We just call everything thatâs yellow, slough. And somewhere it goes from black to brownish to that, you know, those definitions of eschar.
But at some point, it crosses from eschar to slough, then from slough to granulation with something in the middle. And we came up with this -- I like these words. Theyâre very descriptive. Students can -- they come to me and they tell me what it is. Thereâs a couple that are harder. If you start with necro slough, start with the necrotic tissue of an eschar, you basically end up with the eschar coming off.
You soften the eschar. And now youâve got this dead tissue. And what is it? Itâs actually anatomical structure thatâs now necrotic. And itâs slowly dissolving. And it becomes this sloughy material on the wound. And thatâs why we refer to it as necro slough, itâs like a step down from eschar, itâs on the way to being replaced with fibrous tissue and granulation tissue.
Sometimes thereâs over producing of fibrous tissue and theyâll end up with a fibrousy like wound bed, but itâs actually in the middle there somewhere. If itâs covered with a lot of white blood cells, so theyâre soft. And the difference between those is how theyâre debrided. And this necro slough is you need fairly aggressive surgical appear -- like you have to do surgical debridement in stages.
And then in between surgical debridement, you may be doing enzymatic debridement to remove whatâs left on there to soften it up and help you get rid of it.
Once you get to fibrous slough, now you probably all -- you might be still doing a little debridement on that material, but itâs also autolytic and enzymatic. Leuko slough is soft, itâs white blood -- accumulation of white blood cells. It kind of easily comes off. If you take a wound and just kind of peel it off, itâs more likely -- more an accumulation of WBCs on the wound thatâs resulting in these easily removed soft slough thatâs on the wound.
And then bile slough is when it starts to turn black and stinky and nasty, and itâs becoming the luco slough, that kind of condition thatâs sort of in this area, is giving way to an overgrowth of bacteria in the wound or bile slough.
I just think -- I think theyâre interesting terms to help you negotiate the field of slough.
Debridement, you have macro and micro. Every time you do macro, you can think micro. You donât have to stop with a scalpel and put a dress again. You could follow-up with auto-levican and endomatic. Or if you like bile surgery, thatâs really somewhere in the middle. We have a lot thatâs free in Philly. There should be a C in there, I didnât notice, surgial. And they are larva, theyâre flies.
I have a partner who hates bugs. I have some crazy students. I really -- I actually have a Japanese student who is now an entomologist turned podiatrist, and she loves bugs. And I have this thing where I do with the students, I said things they say are like weird, itâs a weird meter. So she was telling us she likes bugs and I was there, laughing. And I said -- and then she said she collects them. And she has living bugs in cages that -- because she likes them.
And then I said, âDo you eat these things?â Yes, she toasts them and -- some, yes. So here they are, and this is, you know, necro slough. Treatment is primarily aggressive surgical debridement followed by fiber slough, accumulated collagen and fiber. And this is where it starts to build up healthy, but then it goes backwards. Thatâs he wound thatâs -- boy, itâs starting to get better now. Itâs not. Itâs getting better, itâs not. Itâs the typical chronic wound. It builds the stuff up on the surface.
The luco part of it is easily pulled away, but then thereâs the stuff behind it that you have to scrape away, you have to take a scalpel to. Thatâs that fiber slough material. And when it becomes overwhelmed by bugs, itâs bile slough.
Debride non-viable tissue, where you kind of beat this to death, but itâs - there is a guideline for it, in the Hoff guideline. Make sure you have adequate circulation before you take a scalpel to any ischemic spot, because youâll just make it worse.
Once it starts to loosen, itâs a different story.
So this is overall management strategy, abscess, aggressive frequent debridement, good dressing selection, which Winâs going to talk about, and then anti-biofilm or biofilm disruptor therapies. And a good anti-biofilm strategy is changing up what you do. So every day, you change, so the anti-microbial, you add a little debridement, you change the dressings a little, you change the environment for bacteria so theyâre not too happy landing where they land.
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Male Speaker: Okay. So back to ABSCESS which -- and actually this -- this is very helpful for my students or somebody thatâs 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, âWell, 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.â And then we get around to the last one which weâll 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 itâs healing from everywhere, so everything has to be healthy.
Okay. So thatâs 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 thatâs 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. Itâs interesting. Podiatry is a very surgical specialty. Iâll just tell the story because itâs 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, âWhatâs your favorite part of podiatric medicine?â Thinking that, you know, itâll be one of their surgical things. And everybody said wound care. So we are making some headway for those of you that donât think weâre treating podiatrist effectively.
Okay. So this is kind of cool. I mean this is the part about wound care that like -- weâre just going to go like Star Trek for a little bit then weâll come back to life. This is a Hoxworth study. If you look at this, this is 2009. Itâs not that far -- you know, itâs a while ago. Itâs like old.
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 arenât. So like in intervening on wounds that were going to become, you know, going to break down and dehisce. These guys dehisced and theyâre 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, itâs 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 youâre like either have trouble figuring out what bandages to use. That right there is a bandage that gives you read out like that. Thatâs your future bandage. Youâre going to plug the bandage into the computer and itâs going to tell you whatâs on the wound and what levels. And then youâre going to make dressing choices based on that. Isnât that cool? I mean thatâs 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. Thatâs 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.
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 whatâs in it. Itâs 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 thatâs stalled, that it was 90% predictive, had predominance of M1 biomarkers. I mean thatâs such a simple thing. Itâs 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 itâs a great idea because that wound looks like itâs ready and I think itâs ready. You donât know. If you see those pictures like -- is there a biofilm in this wound. You donât know. You canât see it. Itâs sort of there, eventually, it gets to be this sloughy mass, but itâs not when it first start.
So this was -- I want to put a thousand dollar thing down, whatâs your M2 marker say? Says M1, no. Youâre going to wait, you need to get the wound a little healthier, and then youâre going to use it when you hit 50% or greater. And then it will take off, like when you put it on, youâre not going waste a single one of them. They will all take. Thatâs 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, youâre like doing cellular therapy to the wound, youâre adding things to the wound that help -- and you get closure rates.
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, itâs 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.
Thatâs what Iâm trying to get across is that you put it out every week. Youâre supposed to put it out every week for 12 weeks, and thatâs how you get the best results. Not necessarily. You have to look at the wound, you have to decide whether itâs receptive to what youâre putting on, and apply it intelligently.
I'm not an automaton. I donât 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 clinicâs going to go under if I donât make money. But I also donât 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 thereâs a lot of that. So thatâs another thing that we have.
You saw thereâs a new product out thatâs taking your patientâs blood.
I'm particularly fascinated by anything that uses you to heal you. I donât 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. Itâs 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 youâre going to put on. Thatâs amazing. And itâs all stuff that, you know, probably cost a fortune, so you donât 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, âDo you think I need to check this out?â
Thatâs a basal cell carcinoma that had already started to metastasize. I mean, they donât -- theyâre usually kind of in site, too, and they donât 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 itâs 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, âDo you think I should biopsy this?â I said, âYou already answered your own question.â So if youâre 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 itâs 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 thereâs any clinical suspicion of a skin cancer, raised border, crusting, and it changes in shape or color, look at that, and itâs still spreading away from the wound, previous history of skin problems or family history, wound isnât responding through traditional things, or if itâs gone too long and re-biopsy of the wound continues to languish.
And whatâs languishing is -- this is the OâDonnell 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, theyâre saying every six or eight weeks or so, if itâs like not going anywhere and itâs not behaving in a typical manner, we kind of look at stuff. And if itâs two months, if itâs at least two months old and they present with something thatâs unusual and itâs something that we just doesnât have a right -- or a new ulcer thatâs 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, thatâs 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. Itâs 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 doesnât go away. Reduced sensory perception, patients donât feel stuff so they get further along before it bothers them and then it bothers them a lot. And then, decreasing immune function, they donât 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 didnât 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.
And he died because they happened to be in the basement of the brain.
Decreased immune function of vascular response. Glycosylation. Diabetics, it doesnât 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 theyâre â everything is going down in the presence of glycosylation. So blood sugar control is important. Getting it under control is important. But recognizing that â and when itâs there, once you find it, itâs 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 donât we use the 4.01 monofilament which tells you, you are losing sensation, but you havenât lost it yet.
Iâd rather have a marker that tells me, âI see smoke, your house may burn,â than one that comes up and says, âOh, look at the flames.â 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. Weâre going to hear about that. Incontinence, f-word from stoma, perspiration.
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, Iâll stop with this. Weâll stop with this slide, which is the offloading continuum and the idea that you donât -- 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 thatâs locked on so it wonât 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 donât 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 Iâll stop there. And thereâs a couple more. Thatâs the guideline. These are the words of the guideline, but I basically told you what it says. Gold standard.
Heel ulcers, I hate. Thereâs 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 donât 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.