Good morning. Good morning. Thank you all for being here. My apologies up front. I am almost a month now into this cold. It is not COVID. I've checked twice, but I can't seem to shake it. Keeps coming and going. Hopefully my voice won't give out during this. For the purposes of this talk, I have no financial conflicts to disclose, but I would like to disclose that I have no expertise whatsoever in dermatology. I have been a surgical intensivist for greater than 25 years, so had to deal with dermatologic insults for a bit of time. And what I really hope to do is just provide sort of a framework for the diagnosis and treatment of ICU dermatologic disorders. So first, let me define what I mean by an ICU dermatologic disorder, at least for the purposes of this talk. Really, problems involving the skin in which, because of their magnitude, need for treatment, or the fact that they may indicate a severe underlying medical condition, need a medical diagnosis. That's a big, broad group of conditions. You know, they're actually pretty common in the ICU. If you look at all patients, depending on just how sensitive your diagnosis is, anywhere from 10 to 40 percent of patients in the ICU will be reported to have some dermatologic disorder during their stay, and the differentials are quite broad. And as Dr. Lee mentioned, they can be quite confusing and sometimes overwhelming, at least for me when I'm trying to approach them. You know, one of the earliest ways to think about them for me would be related to their ICU admission. So there are four ways to, or four classes, if you're thinking about them in that way. The next two speakers really are addressing predominantly conditions that are the reason for ICU admission, although dermatologic conditions really aren't that commonly the reason for ICU admissions. Less than 1% of all ICU admissions are caused by dermatologic disease, specifically. My talk really focuses on two and three associated with or reflecting an underlying disease or developing as a factor, really, of our treatment. The final one is conditions that just sort of coexist with our ICU admission. Occasionally they're important because you can get confused by them, or sometimes this first time somebody has noticed this and trying to separate that from ongoing disease processes can be important. So we'll focus on two and three for my portion of the talk. These are just examples that fall into those four categories. As you can see, things like Stevens-Johnson syndrome are the reason for ICU admission. Again, we'll focus on two and three. All the different drug reactions fall under number three. That's probably one of the most common things that we have to deal with as an intensivist in the ICU. So, you know, if you look at something and you look in a dermatologic book, there are all these terms that all apply to the same thing sometimes. And most of the terms describe something in which the physiology has nothing to do with something that's named very similarly to it. It's, you know, why is that? So my theory on that is, you know, this skin disease has been around for a really long time, and humans have been describing skin diseases for a really long time. So that naming them started a long time ago. You can see in this, in the mummy here, had a scalp skin disorder, leprosy, been around for a really long time, scabies, and other things that had to be described. And so, but dermatologists still really use this same sort of method of, hey, what does a lesion appear to be, rather than a pathophysiologic cause, which is more, I think, what most intensivists probably use in the way they approach things. So I did want to start with just throwing out some of the terms that you see. It's like, well, where's that term come from? You'll see the term exanthem used in part or all of a name frequently, and it really just means breaking out easily. That's used just to describe a macular papular rash, which frequently is also the term mebilliform used, which literally means measles-like. Measles been around for a long time. Urticaria comes from the stinging nettle, because it creates that angioedema in wheels. Erythema, just red. Pemphis, used in a lot of names describing things, just means blister or bubble. Eczema really comes from a Greek term describing a particular pustule, which is a ulcerative pyoderma caused by bacteria. Purpura really was the term for the purple dye, and so purpura in skin discoloration is a frequently used term. And finally, miliary really means millet, really small, fine, usually sort of small crested lesions. There's just pictures of some of those, not my pictures. I stole these because I don't typically take pictures in the ICU, but just some examples of each of those terms to see. So as I mentioned, I'm not, you know, dermatologists are very helpful in this, but they they come at this process from very differently than I probably do. From my standpoint, I have to think about it probably as either the break it down into more of a pathophysiology. First would sort of be the origin of insult. Is it from external, or is it likely from internal? You know, external processes come to the skin from the outside, and so usually they're localized, although obviously as they progress they may get, create systemic symptoms, but usually it's localized to the area of contact. Things like bacteria, fungi, allergens, toxins, all create a local reaction, although then it can become systemic if that becomes a severe infection from outside to in a severe process. Internal processes are much more likely to be symmetrically distributed across the body. They're more likely to have diffuse involvement. They are commonly associated with systemic symptoms, much more commonly than an external source. Examples, immune reactions, bacterial, viral, fungal infections, perfusions, nutrients, all that are examples of internal sources of skin disorders. And then there's, I break them down probably into six common physiologic causes, which is sort of the mechanism of insult. Probably the most common that we have to deal with is an immunologic hypersensitivity type reaction, but there's also vasculitides. Those two can overlap substantially in their pathophysiology and be caused by the same thing, but they are sort of classified separately. You can have infectious etiologies, systemic toxins, direct injury, obviously, and then nutritional deficiencies mentioned at the end. Because hypersensitivity is such a common problem in this for, in this talk for dermatologic disorders, I want to just spend a minute on this. It's not surprising that the skin manifests a lot of hypersensitivity. The skin's loaded with immune cells. Just the classification of hypersensitivity reactions, remember there's type 1 through 4. 1 and 2 really are, represent urticaria. They're preformed antibodies. IgE is type 1. IgG and M is type 2. Type 3, there's probably some of that in the ICU, but it's not very well characterized. SLA is an example of a type 3 reaction. Most of the things that we probably see in the ICU are type 4 delayed hypersensitivity reactions. Remember delayed hypersensitivity usually doesn't manifest for somewhere between 5 and 14 days after the exposure. Although if you have a pre-exposure, it could manifest some much more quickly. But in looking for the offending agent, you have to look back fairly far to discover what might be causing a type 4 reaction. And the eximitus reactions and erythematous reactions and bullous reactions all are type 4 type delayed hypersensitivity pathophysiology. It's important to sort of think, hey, are there symptoms of this particular skin disorder that might mean that this is going to be a severe problem? Some in the literature call them alarm symptoms. And I think it's important to sort of consider whether they're present or not. Clearly, if they're the reason for the ICU admission, that's a severe problem. The conditions, if they have new onset fever or rash at the time of the presentation, acute blistering, any mucus or ocular involvement can indicate severity. Generalized erythema over 90% of your body is a substantial problem. Painful purpura or clearly some of the drugs that are high risk, if those have been started recently, ought to raise a red flag because of their potential progression to a severe problem. This, I found, you probably can't see it from where you are, but the reference is there if it's helpful. This little thing about, hey, when should you get a dermatologist? Now that you know everything's remote, finding a dermatologist may be difficult and they can do a lot remotely by just looking at what you're saying. But sometimes they have to be present. So are the alarm symptoms present? Yes. You ought to involve Durham quickly. And most of the things that we're talking about, hey, did they develop while they're in the ICU is here. And then if it's generalized or not, if it's not generalized, it's typically not a big issue. It's all the generalized stuff that may progress to more severe that ought to involve Durham to help you figure out what the offending agents are or the diagnosis so you can appropriately treat the condition. This is an algorithm that is similar to something I'll show in the next slide that our local dermatologist who's been doing it for years, she's about to retire. I don't know that there'll be anybody else will do it after that. But it's just an algorithm that you walk down a series of questions of, hey, you know, is the condition, is it blisters? If it's yes, are they fluid filled? Are they solid? And you walk down this and it tells you sort of what the disease conditions are and then what diagnoses can cause those disease conditions. If they're not blistering, are they inflammatory? There are not many ICU conditions that are important that are non-inflammatory. These are usually things that they come in with, but the inflammatory things come into the vasculopathies and all that are more important for us to understand. So this type of process can be helpful in trying to figure out, hey, what is this condition? If you don't have that, this is very similar. You can just go to your app and type in dermatologist in your pocket. This is $5 and it's a very similar process. It goes through a series of questions. The nice thing about this, they've got a great library of pictures in there for early and late and progression of the skin processes. So if you're motivated, you can download this onto your phone and use it. So I guess for me, I wanted to put sort of how I think about these probably. There's really, in my simplified approach to both diagnosis and treatment, in the diagnosis, you know, what is most common in the ICU? Cutaneous infections are very common in the ICU, though those are not generalized. Drug reactions are probably equally as common, and if it's a diffuse dermatologic disorder, it's likely to be a drug reaction because they cause more than 50% of them, right? So just by probabilities, a drug is your problem. Positioning vasculitis and contact dermatitis are much less common, but occur with some significant frequency. Then for me, I go through a series of questions of, okay, how long has this been there? What's the timing of it? Is it related in timing to other conditions and other symptoms? Is it localized or diffuse? Are there febrile? Do they have other symptoms that would point us in the right direction? Then what are the morphologic characteristics of what I'm saying? Frequently, cultures are helpful, whether that's culture of the lesion or systemic cultures, and then biopsies for a number of conditions will help confirm the diagnosis, and for a few are probably fairly mandatory to establish a clear, absolute diagnosis. That's usually a biopsy. A dermatologist can actually talk you through it. Almost all of them are at the leading edge of lesions so that you get some healthy and involved skin, and then skin that's not progressed to necrosis. So there are two areas of sort of treatment, but you know, hey, if it's infectious, that's a pretty easy, easy problem to think about treating. We just need to directly treat the infectious problem, but for the hypersensitivity immune reactions, you know, most of those, again, because it's an immune reaction, steroids are indicated for most, although in some of the more severe ones, other immunosuppressants may be indicated, you know, in the erythema multiforme and multiforme agalosum, which really, Stevens-Johnson, may be indicated, urticaria, H1 and H2 blockers. Most importantly, though, is identifying the stimulus and removing it so that it doesn't continue to drive the process. Vasculitides are a similar thing. Got to figure out what you think is driving this vasculopathy. Can be immunologic. It certainly can be infectious, and those two actually can cross over into each other, and it could be driven by certain toxins, can do it as well. So figuring out what that is, sometimes not straightforward. They mentioned calciflaxis, which is a big problem. Unfortunately, we don't see it too terribly much. It's commonly a problem of end-stage renal disease, and particularly patients who progress to hyperparathyroidism. It's a problem of micro-vesicle calcification and occlusion that propagates really through the subcutaneous adipose tissue, and you'll see it early on. It looks almost like a fishnet stocking, a red fishnet stocking in early presentation, but will progress to necrotic ulcers, and you can see this big necrotic area. Really, to confirm it, it's a biopsy on this leading edge. It can be very difficult to treat. You got to get the calcium regulation and process in control. There are phosphate binders, but for many patients it means you need to get a parathyroidectomy done and try and get their calcium deposition under control. Finally, the last group is actually very easy to treat, but frequently you don't really think about them. Probably the most common deficiencies are vitamin A, C, and zinc. There can be some other vitamin B deficiencies, but usually most of the patients in our ICUs have been either not that deficient or already treated that would give them the vitamin B that they need. All of these will cause some form of impaired wound healing, and occasionally you'll see wounds heal, and then, you know, if you have a skin graft, they're healing, and they just sort of start disappearing before your eyes. You're trying to figure out what the heck is going on. So patients who are at risk, prolonged TPN, anybody with malabsorption, inflammatory bowel disease, patients with alcoholism, and any really chronic, critically ill patient that is been having trouble with a lot of nutrition and stuff could be at risk. It's so easy to treat. It's just a course of vitamins typically resolves it, and it's almost like magic. If you gave them that, and that's what it was, healing just goes back the other way very quickly. So just wanted to mention that so that you keep that in your differential at the end. So with that, I'll hand this over to others. Thank you very much.

dermatologic disorders

ICU

diagnosis

treatment

hypersensitivity reactions