Thank you so much, guys. So I'm an acute care surgeon, surgical critical care intensivist at Rush, and I also do all of the wound care. And it really has become my passion to involve skin in ICU rounds. Skin is our largest organ, and it can tell us a lot about the patient and has special ramifications for the patient as well. Good deal, we can't advance. Thank God for audio-visual aid. No. and chronic skin failure actually already exists in the palliative care literature. So we're gonna be drawing on that a lot. So here are the objectives of the entire plenary session. And we will get to my specific objectives here, which is where we're gonna examine skin as an organ system that can fail and describe what acute and chronic skin failure in other hospital setting means. We're gonna also talk about how to assess and protect the skin on daily ICU rounds. How do you engage your residents and how do you also get the knowledge that you need to be able to teach appropriately at the bedside? So let's think about the epidermis, probably my favorite thing. So it protects us from water loss. It provides a mechanical barrier. It protects from sheer friction and toxic irritants. And it's also acidic. So that acidic environment helps to also keep things in a bacteriostatic way and also suppresses growth. So it really is a physical barrier. It's a chemical barrier that maintains moisture and maintains this acid mantle. It's an immunologic barrier with your cells of Longerhans, your B and T lymphocytes, your complement system. It's a microbiome. So much in the same way that we think of the gut flora as a microbiome, we're really starting to think of skin and wounds as containing a microbiome. So it's not so much about eradicating bacteria as it is about making sure that none of those bacteria start utilizing host resources and start replicating greater than they should in their microbiome environment. And then it also acts as thermoregulation. Osmoregulation, it has significant endocrine functions, which if you do any burn, you realize that is the skin is really the way that we feel emotion. So socialization and reproduction. And also helps with our blood pressure. So this slide, I really just want you to take away that there is the epidermis and the dermis and all of regeneration happens from the basement membrane. It comes from these reedy ridges that run along the basement membrane and they actually project into the dermis and they are mitotically active. You can see them here as they project into the skin. So dermal appendages are where all wounds regranulate from. So hair follicles, sebaceous and sweat glands, they're all lined with epithelial cell islands. And this is very clear when you see a wound that's not fully full thickness. So when you have a partial thickness wound, you will see that skin will actually start to regrow in the center because of those dermal buds that are present because they're still part of the gland or the follicle intact that's lined with these epithelial cells. I love this because it's probably the first graph I ever saw at how a post-injury goes. And the extracellular matrix is a really, really unique substance. You know, when I was a medical student, I used to think about this as if it were some kind of rigid road work or road map. But really what it is is more of this primordial ooze that your body is constantly secreting with these fibroblasts, keratinocytes, GAGs, and proteoglycans. And then your MMPs, your matrix metalloproteases, come and take this away, breaking it down via proteolytic reactions. And then your body starts the whole process again. This is important because in chronic wounds, especially ones which we see in the ICU when they become chronic, those MMPs will actually build up to an inappropriate concentration and cause senescence in the wound. And there are things that need to be done there. So here are some intrinsic and extrinsic factors that your patient may bring into the ICU with you. And you have to think of all of these things as they affect the skin. So their age, their BMI, what systemic illnesses do they have, do they have CHF? And they have poor tissue perfusion on a chronic basis. You know, do they have COPD? Do they just have poor oxygen perfusion due to PAD or end-stage renal disease? And then what baggage is the patient bringing to the table? What lifestyle do they live? In what circumstances do they live? Are there other bacterial pathogens exposed to them? Do they smoke, et cetera, et cetera? So skin failure has been proposed to be this thing that has risk factors like these acute and chronic skin conditions, these age-related changes, structural impairment, medications that you may be on. Then you add the pathophysiology in the ICU of hypoperfusion, hypoxia, inflammation, vascular permeability as our capillaries dilate to try to get healing cells where they need to go, and edema, then you add to that a barrier disruption, what happens all the time, right? We constantly find patients lying on caps, you know, from the IVs, they are getting stuck all the time, you know, they're getting washed and they scratch themselves, all these things happen, and so that creates a barrier disruption, and now you have these risk factors combined with your pathophysiology, combined with this disruption, which all leads to skin failure. So it's a big topic of conversation because we're trying to understand how it affects our acute patient population, not just our dying patients in palliative care. So we know that it occurs with critical illness, and then we know that chronic skin failures occur with chronic disease states. I'm also the wound director of an LTAC, and so this is actually something that comes up quite a bit, and you may or may not know this, but in palliative care, once somebody has been described to have acute or chronic skin failure within an LTAC, then they no longer can be, that can no longer be held against them. They say that it is non-reversible and it could not have been prevented. It was non-preventable. So this actually means a lot to us because what if we in the ICU could identify wounds that were actually non-preventable? What would that mean to our practice kind of overall? Hypoperfusion is what we think the primary cause is. The other question is do other acute skin failure causes like SJS or EM or pemphigus, does that contribute? And if we have the CMS billing in 2010 that declares this an entity of unavoidable PI, is that something that we can bring into the ICU for our patients as well? So from the clinician and the resident standpoint, how do we start assessing a wound, right? So you wanna look at temperature, color, hyper or hypopigmentation, you know, is it venous stasis? And so it's got that hyperpigmentation around it from the hemocytogen deposition. Is it macerated or is it dry, which would help you think that you maybe need to change your dressing. The main way to measure these is to pick the longest length and then bisect perpendicularly at the longest width. And those are the measurements that you would use for any billing. So wounds are billed if you debrided them, if you performed wound care, it's billed every 20 square centimeters and there is a zero day global. And so if you're doing these at bedside, it is something that you can write for and bill. And then you wanna know about odor. I always say the nose knows. It freaks my residents out when I wipe every wound and then hold it up to my nose, but it's a necessity. So you also wanna look at the peri-wound. Is there a piboli? So a piboli is this entity that a lot of people don't know about, but it's basically, I think of it as an impacted wisdom tooth. It's when the skin starts growing around and you'll see undermining and you'll see that the wound has not actually sealed to the skin or to the wound underneath. And that is because of that a piboli. It has been so denatured by those MMPs that it actually has to be surgically removed or it will never grow and it will never heal. You wanna describe if there are any exposed structures. Pictures with rulers for scale are always helpful. And then you wanna describe the wound bed. Do you see granulation? Do you see eschar? Do you see slough? Do you see epithelium or open wound? And do you see tissue necrosis? For the residents, it's sometimes hard for them to tell the difference between an open wound and new epithelium. So I always tell them that if you shine a light on it, epithelium is matte and wound is shiny. And if you squirt a little thing of saline on it, then if it is epithelium, it'll just run down like water off a duck's back. But if it's a wound, it will hit it and then soak in. So those are just some hints that you can use. Then you wanna assess and talk about your exudate. So if it was changed about a week ago, it's small. If it was changed an hour ago, it's really large. You wanna discuss the character of the fluid that's coming out. And you need to understand what's on there because this bottom right picture, there was silver placed on the wound. And so if you didn't realize that, you might look at this dressing and think that there was eschar or infection or something else, but this is really just what you put on. And don't mistake liquefactive necrosis or fibrinolysis as purulence because they can look very similar, but they are not the same. I always tell people open wounds are kind of like if you pulled the scab off your own wound when you're a kid, you would see all that nasty stuff under there. That's the normal liquefactive necrosis and ECM production that's supposed to happen. And so that's why I always say you have to trust your nose. So let's talk a little bit about etiology. And I'm just gonna touch briefly on these because each person who comes up after me is gonna focus. But basically we have pressure injuries, which you wanna think of on pressure points. Do they blanch? Are they partial or full thickness? What structure is exposed, if any? Just a quick note for arterial ulcers, they tend to be on the distal areas or the pressure areas of the heels, malleoli, and shins. They're well circumscribed and demarcated. They're very painful. And as of 2016, any patient who was greater than 50 years of age with any of those risk factors is supposed to get at least an annual ABI. Then obviously there's surgical wounds. We deal with a lot of surgical wounds. And these I'll say that we usually leave it up to the co-management that we have with our surgeons. And then there are also the primary skin diseases, which we actually get a fair amount of. I think every year I treat at least two or three purpurofulminans in the MICU. And then we get things like SJs and 10s. And then don't forget that dermatology always plays a great role in this as they perform the biopsies that usually help us to understand what exactly is going on. Something I've started doing in the ICU when patients have venous insufficiency or lymphedema is I'll actually wrap their arms and legs for six hours on, six hours off. It helps to return their fluid intravascular where it belongs and gives them that 500 cc bolus that a straight leg graze would. And it helps a lot with helping the skin not to form bullae and break down. You also wanna do venous insufficiency ultrasounds. So you don't just wanna order a venous duplex because that would just look for DVTs. You wanna get the insufficiency one. And there's very clear evidence that compression is superior to no compression with actually seven RCTs. Multicomponent systems are more effective than single component. So if you combine a short stretch like a co-man with a long stretch like an ACE, which can be very easily done in the ICU with your patients. And then don't forget the pathologic diseases like calciflaxis and pyoderma, which actually need to be kept very, very well protected and managed medically. Just a quick note on some disinfectants. So, you know, saline is always available. If you're gonna use a cleanser, please watch for compatibility and cytotoxicity because many of them do not work well with Santol. So I just identified in my hospital that we were using a dermal cleanser on wounds that nullified Santol by 100% and then we were putting Santol on top. So we were using very expensive Vaseline. Dakin's, you wanna limit to two weeks. Betadine, you wanna allow to dry for two to three minutes. That's actually when it starts working. Wet Betadine is just a pool for bacteria. And then we recently got approved for hypochlorous acid in our hospital, which I'm very pleased with, as it is 100 times more effective than Dakin's and you can drink it, which I've done for some of my patients who didn't believe me. Don't forget about collagenase. We talked about it. Some other easy things that you might have available in your ICU are honey-based, any antibacterial like Polymyxin and Bacitracin, or just your plain old hydrogels, which I think of as hydrogel and an alginate as the new wet to dry, right? Wet to dry should go away. Then secondary dressings, we have all these things, negative pressure, hydrocolloids, pigmented foams, and then silicone and other dressings. The mepelexes that we put on patients can actually be left in place for five days or 75% saturation and they're made to work that way. They form a seal all the way around the wound that creates a scab. So what I tell nurses is peel it back every shift to look at it, but then put the same one back on because those things are $12 a piece. And then as far as the pigmented foams, they're impregnated with gentian violet and methylene blue. They're very, very cheap. They're six bucks for a six by six square and you can also leave them on for five days in the hospital. Of note, my hair is colored with gentian violet, so I really am a wound surgeon. And then last but not least, I want to go through the didn't heal monomics. When you're trying to figure out why something didn't heal, think about these steps. So diabetes, infection, drugs, nutritional problems. Basically all my patients in the ICU who are there for a long amount of time get put on multivitamins, something like Juven, vitamins A, C, and zinc, and we check labs on a monthly basis. And then tissue necrosis that needs to be debrided. Do your blood glucose control, control your infection, monitor your drugs, add your nutritional multivitamins, and do sharp debridement when necessary. Infection, I just want to make a point that there is a difference between contamination colonization, critical colonization, and infection, and you don't actually need systemic antibiotics until that last stage. And I think that's important for antibiotic stewardship. If you are going to culture, you want to pick after you've cleansed it with saline, the cleanest area using Levine's technique. And again, a quick note for nutrition. Remember that these patients, if they have a large stage three or stage four, usually need up to 4.5 grams per kilogram of protein per day, and up to 45 grams per kilogram of calories per day. So just remember that they need a lot of things that we don't necessarily give them. All right, I think I made it just under the wire. Thank you so much for your time. I think questions will be at the end. Thank you.

acute care surgeon

skin

ICU rounds

wound assessment

wound healing