Dr. Olushola Vaughn, she works at MCW with me, and she is such a blessing because she's really an expert with vulvar concerns. And so her interests include vulvar dermatoses and skin of color, transgender skin concerns, and global health. She's the director of Frederick's Mucosal Skin Specialty Clinic for oral and anal genital skin disorders. She's also the dermatologist for Frederick's Inclusion Health Clinic, the medical home for Milwaukee's LGBTQIA population. She has completed two medical mission trips to Vietnam in collaboration with health volunteers overseas. And really, she's just like such a wealth of knowledge. I'm very excited for her to be here. Oh, and somebody left a stylus somewhere. So if you're missing one, feel free to find me. Hi, everybody. Look at us. We're starting early, even. Let me just get myself situated here. OK, great. Ah. Oh. Thank you. Let me see if I can make sure I know how this works. Let's see. Next. Back. OK, great. I think I'm going to try and do it with the, I think I can do it with this. Well, hi, everybody. I'm Shiloh LaVaughn. I want to thank Carissa for having me. It's a real pleasure to be here this morning, especially as you all finish breakfast. I feel like people who are eating are always happy. So hopefully, I won't put you off your breakfast with all these vulva pictures that you're about to see. But it's a necessary evil. So I have no disclosures. Our objectives for today will be reviewing vulvar anatomy from a dermatologic perspective, understand how to approach vulvar dermatosis using an algorithm for categorizing symptoms and clinical findings. And then we'll talk about the first line therapies for the most common vulvar skin conditions. I know we have people in the room at different stages of comfort with vulva. So I will start with a brief review of anatomy. Especially important, because one pearl that I'd like to leave you with is to be very specific in your PATH reports. I get patients a lot of times who have had a biopsy. And they come back four years later. And they can't really remember which side it was on. They healed really well. They can't find the site anymore. And if you're trying to follow a DVIN or a precancerous lesion, that can be dangerous. And so very important that you're specific when you enter those biopsy reports. Don't just say vulva. Say exactly where the anatomy was. I know that a lot of times people will use o'clock. But I think that we could maybe even do better than that. The vulva is composed of the labia majora, labia minora. The singular of those is actually labium magus and labium minus. If you're a real vulva nerd like me, then you use those words. The vestibule and the clitoris. I love the vulva vagina, because all three is the only place in the body where all three embryonic layers are represented. So the keratinized skin and its appendages are ectodermal. The vulvar vestibule is endodermal. And the vagina is mesodermal. The labia majora originate from the mons pubis anteriorly and merge with the perineal body posteriorly. And they are separated from the inner thighs by the genitocrural folds. That's kind of like that fold right after the pubic hair on the majora ends before you get to the thigh. It's one of my favorite words. The labia minora anteriorly unite to form the clitoral hood and posteriorly form the forchette. And when someone has a cosmetic labiaplasty, this is generally the structure that is targeted. Don't get me started on cosmetic labiaplasty, by the way. They should lay down flat against the majora. Otherwise, that is a sign of edema in the tissue. So here's a picture of normal, healthy labia minora. As you can see, if you press them down against the majora, they should stay there. But then here's a picture of very edematous minora. And you can see that they kind of want to rise up like a ship's sail. If you push them down, they kind of come back up. That's a sign of unhealthy or edematous labia minora in this patient with allergic contact dermatitis. The vestibule is made up of, well, it extends to the clitoris and the forchette, and then laterally to the labia minora. The perimeter of it is called Hartzline. That doesn't have too much clinical relevance in dermatology. And it contains the openings of the vagina, the urethra, vestibular, and periurethral, or Skeen's glands, the Bartholin ducts, not the glands, and the hymen. And I know this is kind of getting into more of your wheelhouse, so that should all be pretty familiar. And then the clitoris, of course, is homologous to the male penis. The prepuce, or clitoral hood, is homologous to the male foreskin. And if you ever have patients who are wondering if their clitoris is a normal size, someone actually studied this and came up with a formula for it, which you can go down a rabbit hole and enjoy. But the average adult clitoris is 19.1 millimeters in length and 5.5 millimeters in width. It is important to say in your exam whether that clitoral hood is retractable, because just like if a foreskin has phimosis, this can be an early sign of lichen sclerosis. And this is an excellent example of that. Not my photo, not my patient, but same patient, same day. And you can see on the left, if you didn't really try to retract that skin, it could almost look like normal clitoral hood. But when you actually try to retract it, you can see that the glands is not visualizable at all. This is complete phimosis of the clitoral hood. So that is kind of a brief review of the anatomy. And I carry a printout of this in my pocket, and then I have many printouts that I hand to patients. And I would encourage you to do the same. You can find pictures like this on the internet and print them out. And I just have a really quick spiel that I give people, which is I kind of whip out the piece of paper, and I say, this is you laying on the table. Here's your pubic hair up top. These are your big lips or your labia minora. These are little lips, your labia minora. Here's the clitoris, or the love button. Here's the urethra, where urine comes out. Here's the anus, where poop comes out. And then here's the vagina, where a tampon or a penis might go in. And so it's like a, how long was that, 10 seconds? A 10-second spiel. And I'm always shocked how many patients are like, really? They had no idea that there was three holes down there and not two. And I have to say, I do remember learning that myself when I was whatever, 10 years old, and being like, mind blown. And some people, they haven't learned that yet. So really good to just review that anatomy with your patients, and also to show them where they should be applying their medicine. Next, I'd like to talk about a little bit of normal variation. Since we're talking about anatomy, let's talk about what's normal. Normal to have asymmetry. So this is a picture of a woman who has three labia minora on the right, or a triphid minus on the right, and then one labia minus on the left. Totally normal. Some women don't have any. That makes it sometimes difficult when we're evaluating for something like lichen sclerosis, where we expect the minora to be changed. I often rely on them to tell me, did you feel like your lips were getting smaller? Did you ever have bigger lips? Did you ever have lips at all? Because some women just don't have any. The color can be dark sometimes. Darker patients, like patients with skin of color, pregnant patients, people on hormones, they may have hyperpigmentation of the labia minora and perianal skin. Totally normal. Texture is often irregular, kind of rough, bumpy. Those things are OK. And then these cream-colored spots that are often on the medial minora and around the introitus, they are normal glands, sebaceous glands. They're called four-dye spots. In patients with vestibulodynia, they are never the problem. Please don't biopsy them to prove it, because then you'll actually cause problems. These are normal. Just patients sometimes need a lot of reassurance. I've had patients who sometimes one gland or another will get inflamed, and they're wondering about having them removed. I tell them just to leave them alone. I've seen so many times this caused way more problems when people try to mess with them. So leave these alone. And then vulvar papillomatosis, this is similar to pearly penile papules. They are totally normal. They should be symmetric and discrete. And they are often confused, of course, with genital warts. And the way to tell the difference, as you can see on the left here, condyloma or genital warts are non-symmetric, and they have the same base for many polyps. So they have that papillomatous or verrucous surface, whereas papillomatosis is symmetric, and every papilla has its own separate base. Angiokeratomas, a lot of patients are concerned about these. Sometimes they can bleed. Even younger patients can have these bleed in the shower or are traumatized with shaving or waxing. But they're totally normal. The homologue of these is on the scrotum of older men. We often see these, super common. They are harmless. They're just nectasia of vasculature, and we leave these alone. If they are constantly bleeding, constantly symptomatic, then we can hyphrocate them, kind of hot needle them. But if they are not causing any problems, we leave these be. And then we have a new normal, which is our transgender population, and lots of neo-vulvas that we're seeing. I included just a couple of examples of abnormal new normal, which is two patients with vulvar dermatosis in transgender skin. And this is a 52-year-old male to female transgender woman who had contact dermatitis to a topical antibiotic, something we see really commonly in both neo-vulvas and native vulvas. And then this is a 50s male to female transgender woman who had lichen sclerosis, a really curious case from literature, because she had involvement of the labia majora, which were built from scrotal skin. And it's almost unheard of to see lichen sclerosis affect the scrotum of a male. So it tells us that our new normal vulvas are going to have some things that present differently. All right, with all of that as context, now we can actually get into the algorithm of how I think about vulvar dermatosis, how I approach these conditions. When I started my vulva clinic many years ago now, it was a little overwhelming, because everything that can happen on skin can happen on the vulva. It's got mucosal. It's got keratinized. And in fact, there's more things that can happen there sometimes because of the milieu of periods and urine and all these things. And dermatology, our two textbooks are huge, and all those things happen on the vulva. So it helped me to just think about categories and be able to at least look at a patient and say, OK, what category am I in, so I can have an idea of how to start treating them. So for me, I simplified into these five categories, and we're going to go through these five today. Of course, there's more things than these five, congenital anomalies and such. But to me, most of what I see falls into one of these five categories. Some things like hydrodinitis operativa may overlap into a couple. But for simplification, I love this algorithm. I find it really serves me well. Those five categories are inflammatory, infectious, neoplastic, hormonal, and nerve and muscle. This is where I spend most of my time in the inflammatory dermatoses. So that's where I'm going to focus today. And this category is either the red vulva, the white vulva, things that erode. And for each of those, I have an hour-long talk that I give on each of those topics, and that doesn't even cover them comprehensively. So we're just going to kind of scratch the surface a little bit today, and I'm going to really hit the high yield. The red vulva, to start. The red vulva has a wide differential, but some of the most common that we see, dermatitis, psoriasis, chronic candidiasis, and extra mammary pageants. Again, this is where I spend most of my time. Dermatitis is by far the most in a vulva clinic, so I'm going to really drill down there. Dermatitis can be either a true dermatitis or a mimicker. And in the true dermatitis, we can either have inside jobs or outside jobs. The true endogenous inside jobs are atopic dermatitis and seborrheic dermatitis. And then the outside jobs, the exogenous dermatitis, are irritant contact and allergic contact. And then we have things that look like dermatitis. Sometimes they fool us, but they're not true dermatitis, which includes candida, estrogen hypersensitive vulvovaginitis, and steroid-induced or periorificial dermatitis. As far as the true dermatitis goes, they have unifying features. Dermatitis is always itchy. Of course, if the patient has some kind of sensory abnormality or do not feel their vulva as well, then they might not be itchy. But as a rule, dermatitis is itchy. If the mucosal surface gets involved, then they will start to report burning. And if they have excoriations or fissures, breaks in the skin, then they'll report pain, and sometimes pain with sex or dyspareunia. Always worse at, usually worse at night, interferes with sleep, and then worse with things like heat, sweat, and friction. On exam, you'll see a poorly defined erythema with the caveat that irritant contact dermatitis is sometimes a little bit more sharp. But in general, it's a poorly defined erythema. And you can contrast that with psoriasis that you can see on the bottom right photo, how sharp that is. And it extends onto the mons pubis and the inner thighs often, kind of just this messy, ill-defined rash. If it's chronic, then you can get lichenification. So that's when the red vulva, if left untreated long enough, can become a white vulva. And that's what's happening on the lower right-hand picture, a photograph of lichen simplex chronicus, where that patient, it was left untreated for so long that now it appears white. That is just lichenification. The vagina is almost always spared. And there's no true discharge here. Patients may be reporting discharge. That's usually because they have noticed increased desquamation, so they're noticing a residue on the skin. That's actually just all the inflammation is causing increased cellular turnover. So they're seeing that keratinocyte debris in their underwear. On path, you'll see spongiosis, which just means edema of the epidermal layer. And they all have this in common. So when you get that path result back and it says spongiosis, that is usually telling you that it is a dermatitis. And then how we treat these after a thorough HPI and physical exam, we really are kind of a one-trick pony, which is we throw steroids on this. That is what works best for dermatitis. And so that is always our go-to. But the thing that makes it challenging to treat is that a lot of times there's overlap. People who have atopic dermatitis because their skin barrier has not been working well, they are at much higher risk for having allergic contact dermatitis. And then they start trying to put things on, and they're using all these medicines. And now they have an allergic contact dermatitis and an irritant contact dermatitis. So many of these patients will have two, three, or even more vulvar dermatosis at the same time. And then in addition, if that wasn't complicated enough, sometimes they also get a super infection because that skin barrier is not working well. If they have staph or group A strep, then like strep pyogenes, that should be treated, of course. But if they have group B strep, that should not be treated. They found that in patients who have dermatitis and group B strep, when they treated the group B strep, the dermatitis didn't get any better. As opposed to Canada on bacterial swab, Canada will grow on a bacterial swab. And if you have Canada that grows, you should treat that because oftentimes that will allow the patient to get better. Historically, when they've looked at those patients, they have gotten about half of them have improved. Half of them, you treat the Canada, it still doesn't get any better. The dermatitis doesn't get any better. So atopic dermatitis and seborrheic dermatitis are a little easier to diagnose because they'll usually have sequelae somewhere else. So atopic dermatitis, you'll see rash in the antecubital fossa or popliteal fossa. Seborrheic dermatitis, you'll see dandruff on the scalp, dandruffy stuff on the face. So those are generally a little easier to detect. Whereas irritant contact and allergic contact require a little bit of detective work. And so I'm going to focus in a little bit more on those. Irritant contact dermatitis is a persistent low-grade dermatitis. It affects the labia majora and perineum classically, but can also affect minora that protrude past the majora. And often, if you dig deep enough, there is an identifiable irritant, including constant use of over-the-counter antifungals. And this is an example that I thought you might all enjoy. This is a 60-year-old woman who was being worked up by GI for a persistent cough. And as you can imagine, every time she coughed, she peed a little bit, so now she's wearing a pad. And her dermatitis is in the exact shape of the pad. And so the way to fix this, of course, is to fix the underlying issue with the urinary tract. The causes of irritant contact dermatitis. I talk so much about how vulva is just exposed to so much stuff. There's so much stuff going on down there. It's amazing that skin is so resilient. Things like blood, sweat, urine, feces, wipes, tight pants, lubricants, pads. I mean, so many things. And so the way that we approach irritant dermatitis in terms of treatment is often just to put a barrier on that skin. My favorite is Vaseline. Vaseline is like a perfect substance. Nobody gets allergic to it. It doesn't cause any rashes. It's not the molecules are not small enough to really penetrate into the skin. It just gives them a nice barrier. And then, of course, eliminate the underlying issue, like any urinary issues, if you can. Allergic contact dermatitis is a little trickier. It's a type 4 hypersensitivity reaction. And up to 54% of women who come to vulva derm clinic have either allergic or irritant contact dermatitis. So this is, by far and away, the most common skin problem of the vulva. And the most common culprit in allergic contact dermatitis is actually our medications and the things over the counter that people are buying to try to treat their skin problems. And that is part of the reason why this condition is so resistant to treatment, is because no matter what we're doing, no matter how well we're fixing the problem, if the culprit is still there every day, if they're being exposed to that thing, we can't overcome that. And in addition, with allergies, because it's a type 4 hypersensitivity, these rashes take about three weeks to come in and three weeks to wash out. And I think if I asked any of you, without looking at your phones, what did you put on your skin three weeks ago? Was there anything special that happened three weeks ago today? You'd have no idea, right? I asked you what you ate for breakfast two days ago. You might be like, huh, let me think about that. So patients will come in, and they'll be like, well, I know it wasn't my soap, because I stopped the soap. Well, they stopped the soap for a couple of weeks. The rash didn't get better. So they started using the soap again. That gives you no information. That tells you absolutely nothing. You stop the soap for a month, then you might be able to say, OK, that's not the culprit. So that is another reason why patients come in, and they have no idea what the problem was. And we have to really do the detective work to figure out, okay, what things have you been using for a long time? What are the time courses of these? And that is why the allergic contact is so resistant to treatment. And then also another clue to look for is involvement of the fingers and eyelids. Usually they're putting that antifungal or their topical hydrocortisone cream that they bought over the counter, they're putting that on with their hands and then they're touching their face and if they're allergic to it, it'll spread to those areas too. The way to test for allergic contact hermenditis is patch testing. This is different than the PRIC testing that allergists do, like the allergy and immunology doctors do PRIC testing and that's testing to things like dander and mold and dust and tomatoes. Whereas patch testing is testing to things that might come in contact with the skin, so things like fragrances, preservatives, nickel, things that are often put into cosmetic products. And it's kind of an extensive process. It's a three day process. They come in on Monday and we put all these patches on. They keep them dry all day Tuesday. On Wednesday, a nurse takes all the patches off and sees if anything reacted. And then on Thursday, they meet with a patch testing expert at our institution, it's Dr. Carrie Chaney. And she kind of like rereads everything, looks at all the products which people bring in sometimes in a wheeled extra large suitcase. I encourage people just to take pictures of the labels and bring them in on their phone. But a lot of times people bring in their whole products. And then she creates a safe list that tells you what things you can use. And then you also get a series of codes so that in the future, if all of a sudden you wanna start using a different deodorant and you're like, I don't know what deodorants are safe and the labels, I can't even read them anymore. My eyes are so bad, that print is so small. And they can put that into, put their codes into this database and look for their products and then they can find out what's safe for them to use. The true test is kind of like the poor man's version of it. It's FDA approved, but it's only 40 patches. And it's kind of like anyone can slap that on even if they're not really trained in doing patch test reading. But at our institution, at most academic institutions, it's gonna be a specialized FDA non-approved, but 80 patches of testing. The number one thing for vulvar and anal dermatitis is fragrance. Fragrance sneaks into everything. A lot of times it's kind of hidden on labels and people wouldn't really know. So I usually ask them, if they name some product that I don't know, I'll just say, does it smell good? Does it smell like flowers or summer rain? And that will help us know. And if they're like, well no, it doesn't really have a smell, that's a good sign. And what I really strongly encourage people to pay attention to is the wording on these labels because unscented or dermatology approved or natural does not mean that there's not fragrance in there. That means that they put extra chemicals in to cover up the chemical smell to make it unscented. That's literally what it means. So they have to look for those words, fragrance free, to make sure that it is safe for them. Again, this term natural is not safe. And my other line that I always say is poison ivy is natural, but you wouldn't rub it all over your vulva. People think that because they went to like, you know, some natural website and it was all essential oils that it's totally, this can't be harmful. Absolutely not. Balsam of Peru is a common thing that's in essential oils that is essentially a fragrance derivative. Essential oils can have just truly fragrance added to them or colophony, which is another common offender. And then parthenolide, which is a sesquiterpene lactone is, you know, is in chrysanthemums. It's like all these flower things. Lavender is a really common offender. A lot of times people are allergic to these botanicals. And so if they're, you know, using any kind of like body freshener or even their soaps, that can cause a lot of allergic contact dermatitis. And then sadly, we do this to patients a lot with our medicines. A lot of times when someone has a dermatitis, a non-dermatologist might not be quite sure. And sometimes us too, if it's dermatitis or a fungal infection. And so they'll kind of hedge their bets by using Nystatin plus triamcinolone or beta methasone plus clotrimazole. The issue is that sometimes when they give it in a cream that it has all these allergens and here, my eyes again, but this one has parabens in it. And I think propylene glycol, those are two really common allergens. Patch test positives on those are very common. Instead, just use the ointment. Then it's really in just that petrolatum base. And if they are allergic to this, then they are truly allergic to one of the ingredients. People can be allergic to triamcinolone. They can be allergic to different classes of steroids. But this is just much safer. Dermatologists always prefer the ointment. So in summary, for management of dermatitis, we're looking at avoidance of the irritants and allergens, treatment of any super infection, and then topical steroids or steroid-sparing medicines like Protopic or, sorry, Tacrolimus. But what is really important, I think, and which I'm kind of proselytizing all the time now, is fighting the steroid phobia that patients have. They have been told, yes, they have been told, sometimes they've been told by another provider that steroids will cause thinning of the skin. And that sounds really frightening. I'm gonna thin out my vagina? That's awful. And also, when they go to the pharmacy, the pharmacist will often tell them the same thing. Don't use this for more than two weeks. You will thin the skin. And that is just blatantly untrue. What I tell patients is, oh, and then the third thing that they get is use a pea-sized amount. And I always say, they don't know how big your vulva is. You need to put on as much medicine as it takes. For some people, that is a pea-sized amount. But it's different when you have someone who's maybe just treating the clitoral hood or the labia minora, versus someone who has rash everywhere. A pea-sized amount isn't gonna cut it. What they're really doing is just spreading their vaginal secretions around and thinking that they're applying medicine so that they don't get better. So I tell them, it doesn't have to be frosted on like a cake but apply the medicine to these areas. And I show them on the chart where to apply it. But also I tell them, the women who have trouble, and this has been my experience, the women who have trouble are the ones who we tell them to put this on twice a day. And then we give them instructions to taper it and they don't taper it. And then they don't come back for their follow-up. Maybe I canceled it, maybe they canceled it. But their follow-up gets pushed out. And so they come back after a year and they say, I've been using this twice a day. Well, then we have problems. So when I prescribe this, I always give them a taper. Right now, my kind of standard taper is that I tell them to apply it twice a day for one month, once a day for one month, and then every other day until I see you again. Or sometimes it's Monday through Friday, take the weekends off until I see you again. And then I'm hopeful that I'll be able to see them somewhere in the six-ish month range. But even just taking that break just to every other day or weekends off is usually enough to spare them from having the sequelae of striae or thinning of the skin. I've been doing this for many years now and I've never had anyone who came back who followed the instructions, who had any thinning of the skin. The ones I've had come back with problems were the ones, like I said, who some other provider gave them the steroid and didn't give them a taper, or they didn't understand the taper that I gave them. And that's on me to be really clear with my instructions. But the ones who follow the instructions, we don't get atrophy. So I think it's helpful to have some go-tos. My go-tos are clobetazole if I need something very strong. That used to be really expensive. The price has come down a lot because people were kind of outraged at the prices. So always in an ointment, clobetazole for when I need something really strong. The workhorse of dermatology is Triam.1 ointment that is very hypoallergenic. A lot of people, you know, some people get allergic to clobetazole. It's the sorbitol that's in it. And whereas Triamcinolone is, people generally don't get allergic to it, but some people do. And then we have to go to desoxymetazone. And then if we need something that is not all that strong, like I'm not even, you know, it's kind of like a placebo almost, then I'll give them hydrocortisone 2.5% ointment, which is just a little bit stronger than the 1% that's available over the counter. Oh, that was all red vulva. Okay, now we're moving on to the white vulva. So actually, just kidding, because I'm gonna be talking about the white vulva in my next talk, stay tuned for this, vulvar dermatologic skin condition, or conditions in skin of color. I'm gonna be talking a lot about the white vulva. So I'm gonna leave you with a little bit of a cliffhanger on that one. And then we're gonna come back to that. And then we'll move on to erosive conditions. Here is a list of some things that erode, lichen planus, graft-versus-host disease, DIV and PCV, disquamative inflammatory vulvovaginitis, and plasma cell vulvitis, formerly known as Zunes vulvitis, aphthous ulcers, Crohn's, and autoimmune bullous or blistering diseases. These are all things that erode. We're gonna focus on lichen planus and DIV PCV in the interest of time. Vulvar lichen planus is actually relatively rare. About 0.5 to 2% of the population is affected less than lichen sclerosis. But women who have oral lichen planus, those women have much higher rates. That's like over 50% of those women will have vulvar lichen planus. So really important that those patients get checked. I have a lot of patients come to me and they're like, I've had oral lichen planus for 10 years. No one ever looked down there. And then they have scarring. So the incidence is not the same. They will report burning, soreness, plus or minus itch because the most common type of vulvar lichen planus is erosive lichen planus. And so because of the erosion, it's gonna hurt. It's a T cell related TH1 specific cytokine response. And that does open up some new pathways for treatment, which I'll talk about. On exam, you'll see painless white streaks, which we call Wickham's striae. And those are the areas that should be biopsied. That gives you the best chance to get a positive result on the slide. Whereas the erosions, which is where most people kind of wanna go because that looks the most impressive, those are actually the worst to biopsy. That gives you the least chance of getting the result. When someone has vulvar lichen planus, that condition can spread to other mucosal surfaces. So very important that they are getting the vagina checked with a speculum exam. Check their oral mucosa and then also the esophagus. They can have scarring there. Our treatments, we usually start when it's, when we think it's limited to the vulva, we'll usually start with topicals. But a lot of times these patients do progress to needing systemic treatment. And sadly, our systemic treatments for vulvar vaginal lichen planus are not that great. This was a study that just came out last year that looked at oral lichen planus. And they looked at mycophenolate, mofetil, methotrexate, azathioprine, and hydroxychloroquine. And complete remission was less than 15% after six months. And oral, I think that vulva vaginal is about the same as oral. So you can see that our medicines are just not doing that well. Luckily, we do have some things on the horizon. Jack inhibitors are gonna start to be used a lot more for vulvar lichen planus. And the one that has been kind of published the most at this point is upatacitinib. And it's been having some pretty good results. There are some companies that are working on some topical jack inhibitors for lichen planus and lichen sclerosis. So we should see those coming out hopefully soon. I also wanna talk about DIV and PCV. I feel like these are poorly understood conditions even by the vulvar people and certainly by patients. This diagnosis is generally made clinically. You'll see this red orange skin change. So it's a little distinctive, but almost always gets biopsied. And so most of the time what we see is that someone has gotten this on a PATH report and they're like, oh boy, I don't know what to do about this. What's interesting is that we're starting to think of these two disorders as more on the spectrum, as more kind of like one kind of process in the skin. And this was a paper that kind of looked at a bunch of specimens and found that these two disorders had more in common than differences. And that was things like symptoms, signs, and what they looked like histopathologically, very similar disorders. And so they kind of postulated that they represent kind of one of many stereotypical reaction patterns that the vulva might have. What this means is that the vulva doesn't have a broad language to say something's wrong. Like it really, even symptom-wise, it has like itch, pain, annoyed. Like that's pretty much all the vulva can say. And on the slide, it's the same thing. We have this spectrum, hemorrhagic things, lichenoid, granulomatous, acantholytic, and then I would add spongiotic to that. And that's about like, the vulva doesn't have many things to show. And so this is one kind of reaction pattern. So it's a sign that something's wrong, but we don't quite know why this hemorrhagic reaction pattern is happening. So that's kind of a new framework to think about it. Our treatments have kind of been pretty similar over time. Our treatment for plasma cell vulvitis, this is a little bit newer approach, which is just to alternate intravaginal hydrocortisone and estrogen, and that has been working well. And then for DIV, historically, we've done intravaginal clindamycin and topical steroid. I usually do triamcinolone. And that also, I've had good luck in my patients who have DIV PCV with using those regimens. When one doesn't work, I go to the other. All right, moving on to infectious things. We'll start with things that ulcerate. And I'm gonna move a little bit faster. I think I'm right up against my time, actually. So I'm gonna move a little bit faster. Things that ulcerate include herpes, syphilis, HIV. And I wanted to share this case. This is a woman, of course, someone biopsied this, because when you see this, you'd be worried that it was a huge squamous cell cancer. But it was actually herpes. This is called pseudotumoral herpes. And this is a patient who also had HIV. That tends to be who we see this condition in, people who have concomitant HIV and HSV. And so a lot of those patients, they're already on valicyclovir or acyclovir, and they still get this. And so our treatment for this is actually intralesional sudofovir. It's an unpleasant treatment, but you have to do it once a week. And then in between, you can compound topical sudofovir for them to put on top of this. And we have good luck with that. A couple of the patients who have had with this, they are lost to follow-up. You know, this is a high-risk population, people living with HIV. And so a lot of times, they don't come back. But when they come back, we have been able to clear this up. And then non-ulcerative things, looking at candida. So just a couple quick pearls. A post-menopausal woman who does not use exogenous estrogen should be assumed to not have candida, unless proven otherwise. Candida needs estrogen. It eats estrogen. So if there's not estrogen there, then very unlikely that the candida is the culprit. It probably is just there. And then candida is a vaginal problem. Remember, candida is supposed to be in the vagina. And a lot of times, when the vulva is irritated as a result of the candida overgrowth, it is a hypersensitivity. And so you can actually treat that with topical steroid and beware of irritant contact dermatitis when people are using topical antifungals. That almost never works. And then this is a case report that looked at 200, sorry, a case series that looked at 200 chronic vaginitis patients. And you can see that only about a fifth of them actually had candida. Even more had contact dermatitis. And about a fifth of them had two or more problems going on at the same time. And then let's talk quickly about tinea, a common fungal infection, but a really uncommon vulvar infection. Tinea, I always think of as a little bit more refined than candida. It doesn't like to go on the scrotum. It just is like, I don't like balls. It's not going there. And similarly, it does not like to go on the labia majora. It does like the genitocleral folds. It likes the inguinal folds. But it really doesn't come on to the majora often. When it does, then they must be treated with an antifungal, because it is most likely in the hair follicles, so with an oral antifungal, so diflucan or fluconazole. And then if they really do have any groin tinea, make sure that you treat their feet, because what they're usually doing is pulling their underwear up past these onychomycosis fungal toenails. They're bringing it to the groin. And so even if you treat this area, they're still going to keep inoculating it up to the groin, because their feet have so much fungus. So make sure that you treat that at the same time. OK, neoplastic things. Ooh, I'm going to go like two minutes late. Neoplastic things. Really quickly, benign vulvar serengomas, we see that a lot. Usually, they also will have them on the eyelids. Sadly, antihistamines and topical steroids do not alleviate the itch. The best thing that we have right now is CO2 laser. Not every institution has that, so that's sometimes hard to find. In the past, I tried topical atropine, because it's a sweat gland overactivity. And so by using atropine, you can kind of shut down that sweat gland production. It's been really messy when you just get the normal atropine. You have to especially compound it. And some patients do have relief with that. And then I wanted to share this case of vulvar melanosis. So that was a benign thing. Now, this is a neoplastic malignant thing. This is vulvar melanosis and lichen sclerosis, a well-characterized entity. We know that people with lichen sclerosis have vulvar melanosis. And this patient was biopsied, saw lichen sclerosis on the slide, and vulvar melanosis, it was called. And so we were monitoring that for a long time. And it turns out that this was actually miscalled at the time. This was melanoma. It was slowly getting worse. And so rebiopsied, it was looked back at the original slide, and it had been melanoma at the time as well. And so just a warning to have a very low threshold in those lichen sclerosis patients who have hyperpigmentation, to watch it with photographs and have a very low threshold to biopsy if you think that is changing. And then hormonal things, I know that you're all kind of expert in that. So I leave that to the endocrinologist and the gynecologist. And I'll talk very quickly about nerve and muscle. I heard that yesterday we had lots of discussion of pelvic floor PT. I'm just going to share two cases that I have. On the left, a 72-year-old woman who had squamous cell cancer. Status post, you know, vulvectomy on the right. Radiation, it was complicated with irritant and allergic contact dermatitis. And then on the right, a 36-year-old woman who came to see me for clitoral pain, but really normal exam. And so, of course, both of these patients are so different and have different reasons for pain, but they both have the same diagnosis, which is vulvodynia. I know Cara King, I think, is talking about vulvodynia. So I think I'm going to let her do that. The only thing I want to say, shout out to Beth Barkowitz in the audience today. I love pelvic floor PT. It is my favorite thing. I send tons of patients there. This is a website where you can find a pelvic floor PT near you. And for these two patients, the one on the left, the pelvic floor PT was helping a little bit, but we had a lot of other work to do. Radiation dermatitis is very notoriously difficult to treat. Whereas the one on the right went to pelvic floor PT, and I never saw her again. Her mother is also a patient of mine and reported that she was doing very well and trying to get pregnant. So happy ending to that story. So that's it. That is my algorithm. I hope that this is helpful to just give you a thank you. I am. That is, I'm done. Thank you.

vulvar dermatoses

pathology reports

vulvar anatomy

lichen planus

steroid use

multidisciplinary approach

emerging treatments