Section: CME Category: Wound Care

Why are My Wounds not Healing?

Anthony Iorio, DPM, MPH, C Ped

Anthony R Iorio, DPM, MPH reviews the pathophysiology of both healing and non-healing wounds. Dr Iorio discusses basic and advanced wound care for diabetic wounds as well as appropriate dressing selection to aid in wound healing.

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Goals and Objectives
  1. Understand the difference between good and advanced wound healing
  2. Review epidemiology and economic burden of diabetes and its complications
  3. Establish prevalence and impact of lower extremity diabetic neuropathic ulcers
  4. Review normal and chronic wound pathophysiology
  5. Discuss the management of bio burden and proteases in the chronic wound
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  • CPME (Credits: 0.5)

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    Release Date: 03/16/2018 Expiration Date: 12/31/2020

  • Author
  • Anthony Iorio, DPM, MPH, C Ped

    Assistant Dean for Continuing Education
    Chairman, Department of Community Health and Medicine
    New York College of Podiatric Medicine
    New York, NY

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    Anthony Iorio has nothing to disclose.

  • Lecture Transcript
  • Male Speaker: I want to now bring up another Italian, Dr. Anthony Iorio who is going to be speaking about Why Wounds Don’t Heal. Dr. Iorio is an associate professor and the chair of the Department of Community Health and Medicine and also the assistant dean for Continuing Medical Education at the New York College of Podiatric Medicine. Please help me welcome Dr. Iorio.


    Anthony Iorio: Thank you. Good morning and I want to thank present for the opportunity of doing my first Superbones Superwounds conference and I welcome our international Irish, Canadian and other faculty who have been so nice in joining us and having them present this year. They have been our newest affiliate and our newest allies. But then I welcome our Irish and English contingency too to this convention as well. I am going to do in the next 20 minutes discuss with you why our wounds are not going to heal. As we all know, there is not going to be one wound product that’s going to heal all wounds at all times. If we start with our basics in wound care, wound bed preparation that perhaps will make us look a little bit more understanding of when and why and how we need to use products and where to use them as well. As a disclosure, I am a consultant for MyMedics as well as for Smith & Nephew, which I sit on their advisory board as well. Some of the objectives today that we like to get a point across is to appreciate the difference with good wound care as well as advanced wound care. Always, a good lecture starts off with the economic burden with diabetes as well as the epidemiological factors that add into this picture. Also, we’re going to look at the prevalence of the whole extremity diabetic, diabetic ulcerations and how it’s going to affect the wound pathophysiology and how we clinically look at a wound particularly during the clinical stages. We will discuss some of the management of bioburdens and when and where it is appropriate to treat a wound, either in the acute phase or in the chronic wound phase as well and then we’re going to review maybe one or two cases just to get our point across and put everything together. Let’s start off our conversation with what happens in one day in the United States. Well, in the United States in one day, and this comes from literature in 2014 which was published 5,000 new diagnoses of diabetes is mentioned. We also know that in one day, we spend over $670 million spent with 20 lives that are lost on a daily basis and of course, 200 limbs are amputated. The epidemic of diabetic foot infections, we know already by speaking that somewhere in the world, a leg is lost to diabetes every 30 seconds. We also translate that into 85% of the diabetic-related lower extremity amputations are preceded by a diabetic ulceration and that it is estimated that up to 85% of all amputations due to diabetes can be prevented and this is what we as podiatric physicians do their best and that’s in prevention. As our colleagues in the audience have mentioned earlier with some of the information that was published in the Journal of Ankle Surgery, we know that the prevalence of diabetes is on the rise. Back in 2009, we know that we had 4 million people and then in the next 20 years or so, it’s going to increase by 7 million people. We know that there is no shortage of having this epidemic or pandemic rise. Harold Brem for those who follow him out of Columbia at that mention mentioned that 82,000 amputations a year of which 80% are preceded by an ulcer, very similar to those in which we had forecast in the Journal of Foot Surgery. Also, the risk of lower extremity amputation is about 30 to 40 times higher in the diabetic versus the nondiabetic population. When we look at those who had it, 50% who’ve had one amputation within five years will have another on the same level of the contralateral limb. The mortality rate is approximately 54% but 39% being the lowest, 68% being the high. So you know when you look at the five-year mortality rate and some of those preventative cancers that you see, the prostate and breast to mention a few, still do not add up to the magnificent number of what a diabetic foot be an ischemic ulcer or a neuropathic ulcer can do. But yet there is little, if any, awareness not only on our part but also on the part of the public that addresses this problem. Let us take a look and see why we are so important in making sure that we give good ulcer care. When we look at a wound and if I can just have you put own protocol together and you debride the fibrotic and necrotic tissue, we already have heard this morning several ways of doing that. We know that the gold standard is sharp debridement but there are multiple other forms of debriding a wound. Obviously, not only is debriding the wound good for fibrotic tissue but it also facilitates drainage and it also stimulates healing.


    During that time of debridement, you are exposing newer growth factors into the area. The second point I want to consider is infection control. Infection control, we had a lecture earlier of talking about bioburden. We also need to understand the stable bacterial balance as well and we’re going to briefly discuss that as well. Not to mention all floating which is the gold standard for which we need to do some type of a pressure or plantar pressure release and that can be done, of course, in combination with a lot of, let’s say, improved blood flow. Blood flow is obviously something which we need to look at too. If we take a look at all three of those things including increase in the blood flow then why does 49% of the wounds continue to fail to heal. Despite the fact that we are doing this good wound care, we still have about 50% of the wounds not healing. In adapting some type of a cost-effective practice to help decrease the amount of lower extremity amputations and speeding healing is vitally important. How do we do that? But before we do that, we wanted to discuss that after four weeks and I’m going throw this point at you, we know that even though a wound, after four weeks, needs to be assessed, still 50% of the wound of a diabetic ulcer must be closed and that of 30% must be closed. If not, we need to begin to look at alternative care. What is our approach to wound care? Well, some of the things in which we look for and this is the paradigm which we use is blood flow. We make sure that we address the blood flow from an arterial, as well as a vascular point of view. We look at a sharp debridement, be that sharp debridement in the operatory suite or any sharp debridement or type of debridement that can be used on the wound. We address the bioburden and the biofilm. We also look at the edema and we make sure that the edema is also under control. Of course, we use moisture balance dressing. Moisture wound balance dressing is probably the best and then of course we move on into advanced modalities if needed. Just taking a step through the advance in wound healing not to bore you but just to inform you that we have several parts of the healing phase which are important. The first phase is the hemostatic phase which we have the clouding and the vascular response. Then we move on into the inflammatory phase where this is the phase which actually can occur early but stay late. It is at this point that the end of the inflammatory state that if a wound is not going to heal, it begins to stall in this area. Inflammation is a key in predicting the future of that wound. Looking on into a proliferative or reparative stage, we need to make sure we have modalities which we use to jump from the inflammatory state into the reparative state or the proliferative state and then finally the contracture state. There are different products and modalities that work during each phase of that wound cycle. If we address the problem at that phase, we will be go on to continue to have successful healing. Let’s take a look at some of the wound pathophysiology and in this cascade, for those who follow Schultz at the University of Miami, his theories, obviously the tissue that’s going to have a repetitive trauma, injury and ischemia which that is going to cause prolonged, elevated inflammation. That’s where we get the increase and the unstableness of our neutrophils, our macrophages and our mast cells. Not to mention the imbalanced proteases and the inhibitors that continue to go on and that’s where the MMPs and the TIMPs, the good ones and the bad ones are under imbalance. Finally, there's a destruction of the growth factors, the destruction of the extracellular matrix and also the decrease in cellular migration. All these things enter into what we call the reciprocity process for which this wound probably will not heal. How do we address that? Well, from a clinical point of view, let’s take a look at the pathophysiology of the wound. In a nonhealing wound, we know we have increased bioburden at the early phases of the healing cycle. We know that we have imbalanced proteases at the end of the inflammatory state going into reparative state. We know that our extracellular matrix is damaged. What do you think we need to do? Well, one of the things in which we need to do is we need to break that chronicity cycle and how do we do that? Well, let’s take a look. We have this nonhealing wound, so that one of the easiest things to do early on is to manage the bioburden. As we all mentioned earlier, there is ways in which we can handle a bioburden and once we handle a bioburden, everything else will be managed. Once the bioburden is managed, the protease balances can be restored. The extracellular matrix won’t be damaged and our wound is going to progress to closure.


    Let’s take a look at the scale for which we look at the bacterial bioburden and how and where we need to begin looking. In this particular slide, we’re looking at wounds that are contaminated for which we can then apply a certain product. When they are contaminated, we can look at signs of probably some types of some local collagen that can be applied to the area to help stimulate that. But when we look into the colonized and the pretty good colonized, this is where we begin to look for other things. We look into our bacteriostatic, our bactericidal dressings for which play a huge role in controlling the abnormal colonization and others. It’s not until we get to the infection that we begin to understand that this is going to kill a bacteria that’s going to require more than just a bactericidal dressing that we also, at the same time, need to consider parenteral antibiotics or I.V. antibiotics. Let’s take a look at this chronicity and we see a wound and how we manage it. Well, if we have managed bioburden, we need to use an appropriate dressing. If we have excess proteases, we need to use a collagen and I’ll go through why we use a collagen in a second. Then when we have supplements to that extracellular matrix, we look at it. Keep in mind one other concept that not all MMPs are bad. Actually, we know that the word MMP is going to drag us down but sometimes controlled MMPs are necessary and are good and we need them because they participate in a lot of different types of activities. The first activity you see is remove some of denatured matrix. It also helps in degrading the capillary basement memory. For angiogenesis to occur, it also helps in the contraction of the extracellular matrix and also involving of the scar and migration of epithelial cells. These is where it’s good. Where it is not good is in the areas which I’ll show you. But remember, when we have these controlled levels of MMP, we need to do that because that’s what’s going to make the wound heal. But we need to have those MMPs at the right place, at the right time, at the right amounts. One of the things in which they actually occur, well if you know the extracellular matrix, if you see that extracellular matrix is being sacrificed or is being eaten up in the wound, you know that there’s a lot of proteases. I wanted to take you to two extracellular matrixes, at how can it occur. If you look at the two types of MMPs, we have the collagenases which are considered our MMP1 and MMP8. If you look at our gelatinases, which are our MMPs 2 and MMP9, you will see that the 1s and 8s will be cleaved from the cartilage. In a wound that has a high exudate of high MMPs, you will see that wound being full of MMPs 1 and 8. What happens that matrix then becomes cut and the gelatinases, the 2 and the 9s come into play and further cut that cleaved collagen. Having that cleaved, collagen is going to prohibit the wound from progressing out of the proliferative stage. When we have the MMPs, remember, it degrades the extracellular matrix and also it increases the inflammatory and it delays wound healing. At this point of the game, what you want to do early on in the late inflammatory or the early proliferative stage is to use a collagen. A collagen-based dressing which will absorb the excess amount of exudate containing those MMPs, they will sacrifice themselves in closing the wound. Instead of using advanced therapy later on, you can use simple therapy of collagen or collagen-based dressings that can absorb those extra MMPs. How do you know that will work? We’ll show you some slides that can do that. We know what it looks like with bioburden but do we know what a wound looks like when it has elevated MMPs. This is what a wound looks like when you have elevated MMPs. This is an area for which I feel very comfortable in putting on say a collagen dressing or collagen-based dressing and it could be a number of things that you can use but one of the first things in which I would consider would be to use something very simple, a simple collagen that will work very nicely on that and it will obviously take it apart. You will see some of these in some of the cases for which I am going to present right now. This is a 60-year-old female who had everything done who was referred to us and have this wound for which we had done all kinds of studies. Remember the algorithm that we have much recommended and suggested that this patient needed to be revascularized. After doing a comprehensive vascular examination, we found that the wound needed to be further controlled for which we did.


    After the point in time which we had the patient revascularized in the dorsalis pedis and the posterior tibial pulses were good, we then went on and use an enzymatic debriding agent. We use enzymatic debriding agents in addition to sharp debridement because both modalities are great. Of course, hyperbaric oxygen et al. was also use and confirmed. Keep it in mind that after this went on, we went on to begin to use a growth factor. As you know, sometimes, you can use a simple growth factor, PDGF is good and because you can use it from day one and that wound will actually be absorbed and it will also help in that wound progressing to the next stage. Here, we are beginning to introduce growth factors to a point where obviously, beginning to see good, clean granular tissue. That good, clean granular tissue in conjunction with hyperbaric oxygen, in this particular case, have the wound to close within a reasonable time. This wound close within, I would say, about 12 weeks. Now, moving on to another incident which we had a split thickness skin graft we applied but of course here, we knew that the wound, instead of eating the split thickness skin graft, we put on collagen and a collagen-based dressing because the collagen-based dressing was going to absorb the extra MMPs. We know that we can control the MMP increased activity by just doing that alone. At week 24, we begin to see closure. Not all times do we do that, but you also put on some type of dehydrated human amniotic chorion membranes for which we at that point can also consider. This is a patient that had that too and in addition to that, we also put on some of that graft as well. You can see here that at different times, we use different products so to that these products be at the early stage of the inflammatory stage or the latter stage of the proliferative stage, both those parts of the wound cycle which are under control will help keep the wound clean and healed. This is a schematic that’s going to show us that, of course, every patient is going to be different. But this is a type of wound in which we look at the first line. If you want to put these all together in your mind’s eye, we want to look at debridement, we want to make sure that we use sharp and other types of debridement. We want to look at appropriate offloading, be it a total contact cast or others. We want to make sure that our dressing, be it contains collagen or not and of course vascularization is very important. Moving on forward, we look into the biologics where we look for our PDGF which is also great to be used from day one because it will release upon debridement and it will release some of the growth factors which can also enhance the wound. Of course some of the bioengineered skin substitutes as well as the dehydrated human amniotic chorion layer. Now, this is adjunct therapy I’m going to say because this is an area for which we are going up in cost. As you can see, our first line of approach is so inexpensive but as we go up higher, we are beginning to see the cost factor go up to and that’s where our pressure therapy, our hyperbaric, our ultrasounds, stem cells come into play and finally, revascularization and then amputation being the most expensive. If you look at this continuum, we see that wound healing does occur, can occur earlier and wounds can heal early and in so doing, it will help us in our changing healthcare environment. Because where we’re going now is we’re looking for the best treatment while the cost being cost effective. We also focus on global management and just not regular charges. Of course, we look at the protocol to avoid the extra visits and also save our system some money. We’re going to incentivize and get our patients heal quickly and we are going try to prevent the wound from occurring again. In conclusion, all wounds will not heal. Wounds will not heal in the presence as we know of inadequate circulation in bone infection. All those things needs to be attended to first. In some instances, dressings may not be enough. In addition to the dressings that I’ve mentioned, you may need other types of adjunct therapy, being the growth factors and/or surgical procedures. If a wound is not reduced by 50% the first month, I think what we need to do is we need to stop. We need to reevaluate and we need to understand what is going on and to see where we’re going from there. Okay, with that, I want to thank you very much for your attention and I just want to welcome the Irish once again and thank you very much for your understanding. Thank you.