James McGuire DPM, PT, CPed discusses the ABCESS principles of wound management, reviews the elements of the predictive model for wound healing, as well as describes the wound, ischemia, and foot infection classification.
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James McGuire, DPM, PT, LPed
Leonard Abrams Center for Advanced Wound Healing
Department of Podiatric Medicine and Orthopedics
Temple University School of Podiatric Medicine
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Speaker: Alright, so this is the purpose of the program. There we are moving on. So this is who I talk with or for at different times that sort of changes every year depending on whatever research we are doing at the school or whatever project we are like playing with, materials that we use and different things that we get pulled into working with and for. We are going to look at something called abscess, which is a new mnemonic for both wound assessment and also wound management. We will have fun with that, know the elements of predictive model for wound healing, the FUs, VLUs and PUs and understand the Society for Vascular Surgery and the WIFI classification and how that applies. This is abscess. I have tried to do this talk. It's like when we talk about abscess, you're all day just doing everything that has to do with this. And the reason we came up with this is to replace time and dime and we are going to talk about this in detail later. So we are going to move on from that but it's basically from arterial venous and lymphatic to wound bed and bio-load, cellular activity, which is a new thing like really doing the biomarker analysis on wounds, exudate systemic disease and then periwound skin offloading and everything associated with that. So we are going to talk about -- actually, we zip into the S because this first part of the topic, which is kind of figuring out whether your patient is going to heal and how well they are going to do and where they are is important. This is the wild world of wound care and I had another slide up there which just showed the four basic wound types, venous, you know like diabetic foot, venous ulcer, arterial ulcer, pressure ulcer. And then if you look at Caroline Fife's new one where she broke it down, it's ulcers to amputation, arterial ulcers, chronic ulcers, diabetic foot, flap or graft, pressure, the heel. Interesting that they did heels and non-heels and then pressures ulcers, surgical wound, traumatic wound, venous ulcer and then there is sort of mixed another category in there.
It's interesting. She just published another paper and she said the most prominent wound we see is the unclassifiable wound, which isn't really any one type. They are like multiple types. They are mixed ulcers. My students always ask me what's the classification of that ulcer. The patient is diabetic. They have venous disease and they have connective tissue disease and it's mixed as everything. Everything we see is a mixed ulcer. This is Caroline Fife. She did a predictive model for diabetic foot ulcer and I think it's interesting for what it doesn't have on it, which is there are the things that led to people not healing in the group. Patients have these characteristics and really she was saying, you should develop your questionnaire for patients around this, which is how old is the wound, how big is the wound, how many other wounds they have somewhere else on their body, evidence of bio-burden infection, age, Wagner grade, not whether they are ambulatory or non-ambulatory, whether the patient can actually move, whether they are renal dialysis, renal transplant patient, whether they have PVD and then patient hospitalization for any reason, what is glaringly missing on a diabetic foot ulcer reasons for why they don't heal. Neuropathy, it's like that didn't play a factor. The presence or absence of neuropathy and degree of neuropathy wasn’t in a predictive model. I thought that was very interesting but also very telling about the things that actually are the complicating factors for diabetic. It's not necessarily just the neuropathy. Although neuropathy is a main reason they get it, it's not the main factor why they don't heal. There is a little questionnaire that they develop if you have the slide and print out this later and you can get that. Pamela will help you with that color PDF. She will ship to you if you wish to have any of these slides.
Me, personally, I don't have any complaints about anybody. My stuff is your stuff, anytime. My slides, my pictures, anything you want, you just say McGuire gave me permission to use these and yes, you may. I want people to talk and do things and get this information around, so. Nothing I have is mine. I stole it from everybody anyway. So basically based on that thing, this is a great questionnaire. So what I tell my students to go through when they ask a patient. Hey, how are you? You know like blah-blah-blah. How old is your wound? Let's measure and see how big it is that kind of thing. This was pressure ulcers. Pressures ulcer size, pressure ulcer age, number of concurrent wounds of any etiology, looks very similar. What stage is it, which is really the depth. Evidence of bio-burden infection, patient age, whether they are non-ambulatory, renal transplant, whether they have paralysis, malnutrition or they have been hospitalized for any other reason. That's what slows down your pressure ulcer patient. These are the things you look for that are going to tell you -- remember that there was a really old term, which we use, which was difficult-to-heal wounds, difficult-to-heal patients. Those are the ones that when they come to you, you don't have to wait for them to become chronic. They are going to be chronic. They walk in the door chronic. They come to you with an ulcer that's one day old and you better treat it like it was a chronic wound because it's going to go chronic if you don't. They are the patients that are predictably difficult to heal. This is Margolis. Again, venous leg ulcers. 20,000 patients, wounds that are in the 10 cm. If they are less than 10 cm, they do great. If they are over that, they do horribly. Wounds older than 12 months obviously. These are the well-established chronic patterns. Wounds that are bigger than 10, they have a terrible time and they have 78% chance of not healing.
Venous leg ulcers in the presence of PAD and wound beds with lot of fibrous tissue in them. This is the WIFI classification. It's a tissue loss dominant, infection dominant and ischemia dominant system that uses these characteristics. I actually think WIFI is pretty good. When it first came out, I wasn't sure. That's another gimmicky key mnemonic for remembering things and then I developed gimmicky mnemonic, so I can't yell about that. But tissue loss dominant wound, is there no ulcers to zero and I noticed recently that the Texas classification, they just changed and they went to use the same kind of depth that are sort of on here except for they changed a little bit. They changed their categories a little and I thought it was very interesting. I don't know if I have it in here or not. It was pretty new. No ulcer, shallow ulcer, and these are no gangrenous areas or areas that are questionable. Deeper ulcer with exposed bone or shallow heel ulcer, no calcaneal involvement. I really liked the system because it says whether or not they was calcaneal involvement with heel ulcers. Very different that deep, deep heel ulcer. I hate them. I can't offload them and I can't get blood to them and I really have a hard time getting better. And then extensive deep ulcer that involves that calcaneus and that's in the same category as extensive gangrene forefoot or equal midfoot. ABI with ischemia dominant section where ABI is greater than 0.8, you don't want it to be any less than that or you start to have trouble. And then pressure is greater than 100 mmHg at the ankle, toe pressures or TCPO2 greater than or equal to 60. ABIs in the 0.6 to 8 range, being to see some problems and the reason there is other numbers in here is ABIs is sort of terrible marker for diabetics that they don't read right.
If they have calcification of the arteries, you take an ABI. It can look great. It doesn't have to be 1.0, 1.2, 1.3. What if they have calcification and they're reading like one to one but they may actually have enough calcification that they don't have kind of circulation that they should. Even though the ABI is really normal, they may actually have a problem because they have a lot of sclerosis and calcification and maybe narrowing of the system and a lot of small vessel disease associated with it. And then ABI is less than 0.3. They are just not going to heal very well at all. And then infection dominant, they use the IDSA/PEDIS system, which we will look at a little bit. No symptoms or signs of infection, local infection, skin and subcutaneous, local infection with -- it should say kind of less than 2 cm of erythema. And then it goes, well, now this is greater than, less than it's really but number one and then local infection with signs of SIRS or systemic disease is 3. So two or more of that SIRs is two or more of increased temperature, heart rate, respiration or white blood cell. And that's a severe infection obviously. What they did from that is went on to estimating amputation risk and they came up with categories of very low, low, moderate and high and what's the risk of these patients. This is a vascular classification, so what's the risks of these people getting any amputation and looking at wound depth as the depth increases and as the levels of ischemia increase across the top and then this is categories of infection within those little groupings, the risk of the amputation gets higher and higher and higher. Same thing down here. This is estimated likelihood of the benefit of revascularization in those patients. How much is revascularization is going to actually help them and again as you march over to lower right hand column, things get worse and worse and worse.
Vascular assessment should look at regional flow, local perfusion and micro environment and that sounds nice. That's kind of big to little. We are getting proximal to distal, big to little and then put that up there to make sure you don't forget that this isn't -- you can't pump blood into the foot at a regular rate and not have it come out and have a system that works. You are going to have all your arteries open to be banging away and if nothing is coming out of that leg because there is massive amount of venous leg congestion and the lymphatic system is overloaded then limbs has got tremendous amount of edema pressure in it. It's going to prevent anything from getting to the skin or the outer tissue is just going to run in the big arteries. It's going to get to the big veins and get out the system as fast as possible and the limb is not going to be well perfused. So we have to think of all the system and that we balance in order for the patient to get better. This is a weird afternoon because it's everything in wound care. And this is a massive field and it's why I got fascinated by wound care years ago, why I kind of stayed in wounds. I mean what's the podiatrist doing in wounds, which is really lot of what we do but everybody [indecipherable] [11:17] interested in doing a bunionectomy and an ankle fusion and everything else and I am down here yelling wounds, it's a lot of fun. This is the half guideline and the only thing I want to put on here if patient s have strong DP and PT pulses, they don't need any vascular referral. Also they are probably going to heal. More than likely, those patients are going to heal. So put your hands on them and feel pulses. My kids are always pulling out of Doppler. I said, yeah, but could you palpate anything? What do you feel when you try to palpate them? And then use standard palpation technique. For optimal tissue perfusion, all factors affecting inflow and outflow must be eliminated or minimized to the maximum extent that you can and oxygen patients that have decent oxygen delivery to the tissues are more than likely go on to heal.
These are looking at the risk factors for PAD. Man do worse than women, older people do worse than younger, sorry Pam we are -- she is like Pamela and I am just -- I am kind of short name kind of a guy. I can't remember names at all. Whether you are old, whether you have diabetes, whether you are smoking or not, hypertension, dyslipidemia, homocysteinemia. What your races has a factor and then whether there is a lot of inflammatory markers in your system, CRP and whether you have any kind of renal disease or renal insufficiency or all peripheral arterial disease markers but there are also markers for healing. All of those things or many of those things were elements within the evaluations that you saw by Fife that showed that healing is a significantly impaired if they are present. Systemic factors affecting wound care. I put up there nutrition and hydration at the tippy top because we don't think of that enough. What are they eating, how well are they -- how much are they drinking. I mean half of my patients don't seem to drink anything. They drink a lot of coffee in the morning and then they just sit around and -- they are not mobile, so they don't go get a drink. They are sitting in the chair, watching TV all day and they don't drink until nighttime when somebody gives them a glass of water. They are chronically dehydrated. They are diabetic, smokers, so they are already in the state of hypercoagulability and their arteries are just ready to clot up. All they need is one reason to clog up and they just go -- they just close right down. Whether or not they are on some of these medications that interfere with healing, some of them help but some of them also tend to hinder; steroids, aspirin, anticoagulants. Just actually always been asking patients about these, particularly if we got to take scalpel to them.
I always forget I want to cut everything and I don't worry too much about bleeding, but I just have to put a check on myself just before I touch them and just say, are you taking any kind of anticoagulant, maybe I should slow down. Presence of infection, incontinence and immobility, particularly with pressure ulcers and the old bed sore thing but now they are injuries. I heard a nice talk on that the other day as it has this name is they come out and state that these, the name of this is now going to be pressure injury when every lawyer in the country, all they wanted to hear was that you injured the patient somewhat. What a word. I think it's going to come back to bite them, but that's interesting. Let's go back. I went too fast. And then comorbid disease, states of diabetes and COPD and sickle cell. All these things have major contributing factors whether or not this patient is going to be able to heal and things that you are going to need to be looking for, particularly any history of past radiation and radiation is terrible. Really, really significantly interferes with the skin's ability to generate new tissue. Common systemic things affecting wound chronicity. All of the endocrine disease do, all the hematological conditions -- look for anemia, lack of iron you know like anemia in the tissues. Look at that. I could borrow those today. Anemia in the tissues. It has significant effect that whether or no oxygen is available to the tissue in these patients. Cardiopulmonary problems, are the getting enough -- are they breathing, do they have congestive heart failure or are they causing backups in the limb associated with lack of fluid movement or fluid overload in the system? Whether or not they can actually absorb the things you are asking them to eat. You know, okay, you need to eat more protein.
Can they actually absorb that protein that you are giving them? Are they getting it in a form that's good for them? Is it loaded with fat or is it good healthy lean protein that they are getting? And then with the [indecipherable] [00:16:10] autoimmune disorders and how many of our patients have some underlying like significant inflammation and I think we all walk around with some level of inflammation. Even those of us that are reasonably healthy have some level of inflammation and almost all of us will benefit from reducing the amount of endovascular inflammation in our system. So we are not injuring our small vessels and causing them to repair themselves and end up producing plaques and laying down all kinds of things that interfere with circulation. Workup for patients; CBC to look for leukocytosis or anemia, thrombocytopenia, analysis of the basic metabolic profile to look for renal insufficiency and electrolyte imbalances. Look at their serum protein, albumin, prealbumin, transferrin levels to assess the patient's nutritional status. Do coagulation studies if you are worried about their coagulability or if they have a coagulopathy. And then tissue cultures of the wound to determine appropriate wound healing therapy if you need to do biopsy on tissues. That one is down there, for me in my mind, that's the future. The future is going to be that you are going to be -- all that stuff that we scrape off the wound now and we throw it away. Everything you scape off one day be useable. You will be able to send it in, find out what cells are on the wound, what state are the cells in. We are really close. It's going to be so much fun. You will be able to know if the dressing you put on last week changed the M1 configuration of the macrophagias. Are they M1 or M2? Did that make a difference in the wound? Did the inflammation go down? Did what you do reduce the bio-load on the wound? What happened to the bacteria on the wound? Do we have friendly bacteria there that are proliferating versus non-friendly bacteria? It's kind of exciting. I mean we may be able to take bacteria that we put on the wound that compete with the staph, MRSA and all these other things that are negative on the wound and out-compete them so the wound stay healthy.
This is a lab workup and they sent this in one time as a slide and they said, you don't recommend at all that for a wound care patient, are you? And actually almost all of that will be somewhat helpful to know in a wound care patient. The ones that are in red are the ones that I said, alright, these are sort of basic blood work, particularly on a diabetic patients that we really want to know what their protein levels are, whether they are absorbing protein, they have enough protein to heal, what their electrolytes and glucose and hemoglobin A are like, particularly their A1c value. It's a lot more telling than what their daily blood glucoses are. I usually tell patients two things. I ask them two questions. I say, do you know your glucose and they say, well, I don't take it everyday. That tells me that they are not a very complaint patient. They have been told to and they are just not doing it. Then I ask them, do you know what your A1c is? If they don't know that number, I know they have a doctor that never sits down with them and talks to them about the importance of diabetes because every doctor that's a decent doctor always tells the patients to pay attention to that number. They know A1c. They have had it done a million times. They had doctors tell them they have to change their life based on the A1c, so they are working with somebody that's conscientious. If they don't know that number, I don't know who they are going to. If you are a diabetic and you don't know your A1c number, who do you see. Probably, podiatrist. Actually, a podiatrist probably would know it. I don't know where they go. Complete blood count and differential, you are looking at your white blood cell count. Nobody is waving five fingers at me yet. Sedimentation rates, CRP. That's your inflammatory markers, basic inflammatory markers. There are plenty of other ones. PT, PTT, just to know what their blood supply is. Any of these other ones if you suspect things can be added in but that's sort of your basic. It's nice to know what your liver is doing and what your lipids are and all that. They all contribute.
Albumin. Why do you want to know that? Condition associated with high levels of albumin or dehydration, low levels of ascites, burns, glomerular nephritis, liver disease, malabsorption syndromes and malnutrition, which is the major one as they are not getting in enough food that we see. I see a lot of ambulatory patients. They walk in. They are kind of home, eating their regular food, but whether that regular food in our particular population in Center City, Philadelphia, I don't know whether they are eating the right kinds of food, whether they get a good protein balance in their diet, whether they are getting the right fruits and vegetables and all that stuff. Prealbumin. Normal prealbumin is 15 to 35. Between 11 and 15 indicate kind of a high risk and warrant weekly measurement of your albumin levels and this is when patients really get -- they are like more immobile and you are watching them more closely. And if they are below 11, they need aggressive nutrition therapy. That's my fingers. She gives me the fingers. Fine. I will try to stay on task. This is just looking at the iron binding capacity and why it's important and these are the different types of anemia associated with iron levels, iron deficiency, hemochromatosis, sideroblastic anemia, etc and looking at whether they are low or high and then the percent transferrin and ferritin levels in the wound to give you an idea what's happening in those various conditions. So you have an idea of what kind of patient you are dealing with. Electrolytes. Basically, we are looking for kidney function and whether or not the kidney function is appropriate and whether the patient is going to be at risk for healing associated with small vessel disease related to renal insufficiency. Nutritional assessment. This is just -- we can zip through this.
But you are looking at suspect malnutrition in patient with any kind of chronic illness, inadequate societal support, that's my group, multi-systemic trauma. Obviously, they are severely challenged. GI or neurologic problems where they have had -- we have had a lot of patients that have stomach stapling and everything to try to lose weight and they are sort of taking organs out of their system in order to get thinner, which is not the way to do it. Anything that can get in the way of oral intake and protein deficiency occurs in approximately 25% of all the hospitalized patients that are out there. So it actually exists in the population that are higher rate than you think. Serum prealbumin is sensitive for relatively acute malnutrition because its half life is just a couple of days. So you take a look at that and you have an idea what's happening within the short term, within the last few days. Vitamin A reduces fibronectin on the wound surface, cell chemotaxis, cell adhesion. All these little vitamins are important. I mean l like telling patients that take a multi to try to do a probiotic to keep things up in there GI system. All they are trying to heal, to eat a good balanced diet and eat protein and take vitamin C, zinc and all these other things. We have a whole array of natural products that we recommend for patients. For neuropathy, it seems to help a great deal, vitamin array that we use. Imaging studies when you have a wound that comes in, plain radiography but you also have ultrasonography. You have got scans that you can do. We are going to go through a lot of these as we go ahead. Bone scanning may be necessary. We are going to review that in a little while and how it affects, how it goes into looking an osteomyelitis. Everything from regular photography to plain photography. I have hyperspectral imaging in here because I think that may actually provide some significant information test in the future.
We were just laughing at this at breakfast this morning. Why don't they just make a scanner like they have it on Star Trek, which is you go up to the the wound, you hold your phone up to the wound, the phone does infrared analysis on the wound, looks for oxy and deoxyhemoglobin in the margins, takes a picture, measures the wound, takes the depth measurement of the wound, which they can do now with the hand-held camera like your phone and then it measures that all out for you, tells exactly what's going on. It can look at tissue composition and then tells you everything you need to know. It's all the technologies out there, individual companies and they are all this big. We just need to get them down where they are smaller and we actually get this information quickly. That's an ultrasound image of a hair follicle. You can actually see this skin. You can look below the skin. That's a DTI, deep tissue injury under an ulceration with the scan and then bone scans and MRI and everything else. And I am done.
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