Section: CME Category: Wound Care

ABCESS System of Wound Management - Part 1

James McGuire, DPM, PT, LPed

James McGuire, DPM, PT, CPed discusses the ABCESS system for wound management, helps recognize essential elements of arterial, venous and lymphatic assessments, as well as help formulate the basics of wound bed management and bioload assessment.

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Goals and Objectives
  1. List the components of the vascular & wound bed and bioload sections of the ABCESS System for wound management
  2. Recognize essential elements of arterial, venous, and lymphatic assessments
  3. Formulate the basics of wound bed management and bioload assessment management techniques to optimize wound healing outcomes
  4. Describe the elements of the TUSPM McGuire/Nassar Slough classification system and hot it aids in decision making in debridement choices in the chronic wound
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    PRESENT e-Learning Systems is approved by the Council on Podiatric Medical Education as a provider of continuing education in podiatric medicine. PRESENT e-Learning Systems has approved this activity for a maximum of 0.75 continuing education contact hours

    Release Date: 12/04/2018 Expiration Date: 12/31/2020

  • Author
  • James McGuire, DPM, PT, LPed

    Leonard Abrams Center for Advanced Wound Healing
    Clinical Professor
    Department of Podiatric Medicine and Orthopedics
    Temple University School of Podiatric Medicine
    Philadelphia, PA

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  • Lecture Transcript
  • TAPE STARTS – [00:00]

    Male Speaker: Okay. So now we’re 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 hasn’t changed in the last few minutes anyway.

    And these are the objectives. We’re going to look at the components of that and we’re going to see how they affect wound management. And we’re going to look A and B on the word ABCESS and then we’re going to look at C, E, and S in the second part. This is the longer part. This is the part that I probably won’t make 25 minutes if I’m 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, we’ve used this ad infinitum. Companies have used this over and over and, you know, it’s 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 today’s wound management and everything you’ve 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 what’s the patient’s circulation like. And I’ve always heard that, you know, like do they have enough blood, do they have enough oxygen, or are they’re 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 haven’t 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 we’re going to do about what’s 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 I’m not going to about E at all. Lyn’s going to do that very effectively, but that exudate is dressings, and it’s our choices of what we’re going to put on the wound to manage the fluid that’s coming from that wound, and a lot of the stuff that’s out there with biofilm, and managing biofilm, and there’s 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 there’s like, you know, spot of care wound fluid analysis that’s kind of there but not really, we don’t 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 that’s fascinating. Wound biopsy or tissue biopsy, growth factors, autographs, you saw there are like, there’s two new blood products out now.


    Whole blood products, there’s 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.

    It’s periwound skin and it’s 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, it’s like people with arterial problems are very consistent. They can’t 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 don’t 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 don’t 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, you’ll 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 they’re actually claudicating within a venous condition, which is complicating.


    Rest pain is when they’re really far -- really far along, or numbness when they’re actually reducing the circulation to the nerves so much that it starts to go numb. Ulceration and gangrene, obviously, when we’re 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 can’t find the DP, look for a perforating peroneal, which is a little tiny -- the auxiliary artery that’s just to the left -- to the left or to the right of the DP. And it’s -- sometimes it actually provides most of the circulation to the dorsal aspect to the foot. And it’s not a loss of dorsal circulation, it’s 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. Don’t forget this, they tell me they don’t smoke. “How are you doing today? Oh, yes you do.” 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 patient’s 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, we’re going to -- one of the little lab things we do is how to do an ABI, or ankle-brachial index. It’s sort of looking at the ankle pressure and the arm pressure, and they should be one to one.


    If they’re not, you’ll see a decrease in flow to the lower extremity, and you’ll see some of these symptoms that we talked about.

    Paul’s 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 there’s no flow, the laser Doppler is looking for the first moving cap or RBC in a capillary. It’s 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 that’s 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. That’s sort of the mandated test, but it’s slow, it’s tedious. It only looks at a small area of the foot at a time. And there’s nowhere near as, I think, as helpful as skin perfusion pressure. That’s never caught on as sort of a major or vascular assessment.

    And then, there’s 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 it’s deoxygenated, is it the area the wound where you’re 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 you’ve 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, it’s -- 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. It’s very similar.

    And that’s 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 what’s your actual ABI is. And not just do one site. That’s 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 you’re 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. They’re 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, it’s Kimmel and Robin and it was -- I forgot what year it was. I don’t know, I can’t read it, maybe Pamela Kim, Kimmel and Robin. And it look -- it’s 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 we’ve 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 they’ve never had any kind of venous assessment, it’s not a bad idea to get one. Make sure you’re 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 it’s a venous disease. They always look like this. We’re 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 who’s 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 don’t. 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. There’s anything that could be done to improve the vascularity of the limb, and don’t use multilayer compression on people less than -- with ABIs less than 0.7. If you do this -- and you can’t use any compression, you got to be very careful using pressures when the ABIs are low. You don’t want to cause any injuries from what you’re 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.

    Don’t forget to walk your venous patients. A lot of them are very heavy that they very often don’t walk much. They don’t like to walk, it’s 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 you’re getting them -- my wife just completed -- she is a Tai Chi mistress or masteress. She’s a Tai Chi master now. She’s an instructor in Tai Chi. I’m 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, “No, it’s a set.” She said she has to do her set.

    But what she’s 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.

    You’d be amazed. If you’ve never put a Doppler on anybody’s ankle, or even up on their leg, and then squeeze the foot, you’d 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 doesn’t 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 they’re working in the leg, they’re 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 they’re not moving at all. Or they have a short stretch bandage on, which is most effective on people who are moving or moving around.


    We’re 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 can’t substitute this for a complete decongestive therapy. Like, that’s what people tried to do lots of times. “Oh, it’s a pump. It’s easier. I’ll just do that.” Sometimes it’s access. With fluid, it’s access to people that can actually do complete drainage on patients.

    So the other circulatory systems, the lymphatic system, we’ve 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 don’t 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 don’t need to do that. This is the B part. These are the classic wound types. We know that there’s now a ton more out there.

    When you’re 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, “No, you should really talk about that one thing that’s on that slide.”


    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. They’re standing on their navicular, their cuboid is touching the ground all the time. You know, they’re really, really knock-kneed. And then they just put all these pressure on the medial foot, and that’s where they’re breaking down all the time. So that’s why that’s 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, it’s local infection to spreading, to systemic. And you can look down here, now the picture kind of moves along, but it’s -- it has -- people are making, basically making decisions on topical antimicrobials and other things based on the state at which the patient’s 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, it’s 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 I’m 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, they’re 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. Don’t use topical antimicrobials on clinically unaffected wounds.

    But if you put Neosporin and everything, you shouldn’t do that. Don’t use -- especially, don’t use gentamicin cream on everything. Gentamicin’s an antibiotic that you might need someday, and you don’t 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 “purulence” down. What’s that mean, buddy?

    I have a student -- students that love to -- they just -- everything looks like purulence to them. It’s all puss. It all stinks. So they write -- they put “purulence” down every time, and I take it out immediately. I said, “That’s a lawyer trigger word. I don’t even use it.” It has to be oozing out puss and I have to be taking a culture for them to put down “purulence”. I just don’t 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 don’t go under edges. You don’t go down holes. You don’t 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, you’re supposed to be cultured within two hours of the culture time, and then nobody is.

    Don’t culture on infected wounds. Obtain the specimen -- do not cleanse the wound and get a specimen by just swabbing it. Don’t 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 what’s called the Levine technique, which is to clean the wound. You’re 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.

    Don’t just do this, don’t just touch it, don’t do that. Actually, get some of the subcutaneous fluid in there. You’re 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 we’re ready to go. You’re 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, that’s your spot, not down that hole. That’s where you want to go. That’s where every student wants to stick every swab, or they want to go up under some lip.

    If you’re doing DNA culturing or DNA sequencing, you can scrape the whole surface and send it all in to look for everything that’s 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 you’ve been using an antiseptic on the surface, you may have a lot of dead bacteria around. It’ll pick them up and it’ll tell you what’s been there. Things that are dead actually show up.

    This is just the new kind of -- this is the guidelines for this. It’s 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 -- what’s Sybil’s 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. That’s 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 it’s -- that’s the distance from eschar to granulation tissue in wounds, which is there’s nothing that tells you anything about the middle. We just call everything that’s 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. They’re very descriptive. Students can -- they come to me and they tell me what it is. There’s 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 you’ve got this dead tissue. And what is it? It’s actually anatomical structure that’s now necrotic. And it’s slowly dissolving. And it becomes this sloughy material on the wound. And that’s why we refer to it as necro slough, it’s like a step down from eschar, it’s on the way to being replaced with fibrous tissue and granulation tissue.

    Sometimes there’s over producing of fibrous tissue and they’ll end up with a fibrousy like wound bed, but it’s actually in the middle there somewhere. If it’s covered with a lot of white blood cells, so they’re soft. And the difference between those is how they’re 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 what’s 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 it’s also autolytic and enzymatic. Leuko slough is soft, it’s 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, it’s more likely -- more an accumulation of WBCs on the wound that’s resulting in these easily removed soft slough that’s on the wound.

    And then bile slough is when it starts to turn black and stinky and nasty, and it’s becoming the luco slough, that kind of condition that’s sort of in this area, is giving way to an overgrowth of bacteria in the wound or bile slough.

    I just think -- I think they’re 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 don’t 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, that’s really somewhere in the middle. We have a lot that’s free in Philly. There should be a C in there, I didn’t notice, surgial. And they are larva, they’re 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, it’s 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, “Do you eat these things?” 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. That’s he wound that’s -- boy, it’s starting to get better now. It’s not. It’s getting better, it’s not. It’s the typical chronic wound. It builds the stuff up on the surface.

    The luco part of it is easily pulled away, but then there’s the stuff behind it that you have to scrape away, you have to take a scalpel to. That’s that fiber slough material. And when it becomes overwhelmed by bugs, it’s bile slough.

    Debride non-viable tissue, where you kind of beat this to death, but it’s - 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 you’ll just make it worse.


    Once it starts to loosen, it’s a different story.

    So this is overall management strategy, abscess, aggressive frequent debridement, good dressing selection, which Win’s 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 they’re not too happy landing where they land.

    TAPE ENDS [0:30:37]