Wounds Caused by Disease Process/Burns

Speaker A: 00:00:10

So we've talked about wounds caused by pressure, by moisture, by friction.

We've talked about lower extremity wounds that can be caused by arterial disease, venous disease, lymphedema, and we talked about atypical leg ulcers. Now we're going to talk about wounds that are caused by specific disease processes. So here's our objectives.

To discuss the pathology, clinical presentation and appropriate management of wounds caused by bacterial, fungal and viral infections. Those are very common.

To identify options for systemic and topical management of patients with bullous lesions, describe classification and principles of management for burn injuries to include criteria for transfer to a burn center to identify management goals and options for the patient with a fungating tumor complicated by malodorous drainage or bleeding. To describe measures for prevention and management of radiodermatitis and discuss assessment and management for extravasation injuries.

So there's a lot, and we've got it divided into two sections. If you're interested in background reading, it's chapters 27 through 30. So it's a lot.

So you might want to pick the ones that are most relevant to your practice. In part one, we're going to talk about wounds due to infectious processes, wounds due to spider bites and bullous lesions.

Now, going back to our basic concepts of wound care, you should have this locked into your head by now. So we always start by identifying and correcting etiologic factors.

Then we move on to systemic support, topical therapy and ongoing monitoring with modifications as indicated. So most of the wounds that we see are caused by the common factors.

They're caused by pressure and moisture and friction and arterial disease and venous disease and neuropathy. They're the horses, but there's occasional zebras that come in.

So you might have in a lower extremity wound that's not caused by vascular issues, that's not caused by neuropathy. It's probably one of those atypical. You might have a trunk wound that doesn't fit into the major categories.

So you always have to recognize, hey, this wound doesn't look like any of the usual types of wounds that I take care of. I've got to think outside the box in terms of identifying the etiology. And most of the time, patient history is a major contributing factor.

So let's start talking about wounds that are caused by infectious processes. You've all seen patients with herpetic lesions. You've seen patients with viral lesions.

You've probably all had patients with cellulitis and with necrotizing fasciitis.

All of those of course, are infectious wounds, and a critical element of effective management is to identify them appropriately and then to treat them with the right antimicrobial, with an antibacterial, with an antifungal, with an antiviral. We're going to start with viral lesions. So, you know, there's two major types of herpetic lesions we can have. Herpes simplex.

If you look at the third or fourth bullet point, those herpes simplex causes oral lesions, perioral lesions, and perianal lesions. Those are the most common sites of herpes simplex. Herpes zoster, remember, is a reactivation of the varicella zoster infection.

In other words, a reactivation of the chickenpox virus. That virus lurks along dermatomes and stays dormant until the immune system is compromised, and then it becomes active.

But the active infection of herpes zoster always follows the nerve pathway, always follows the dermatome, is always unilateral. Both herpes zoster lesions and herpes simplex lesions are painful vesicles. So it starts out as this rash.

It's kind of a red rash, erythematous rash, with distinct little blisters scattered throughout the rash. And then the blisters open to form discrete individual lesions, typically with a pink, yellow base. When do we typically see herpes lesions?

Usually in our immunosuppressed patients, because we know that herpes organisms are everywhere. When you have a fever blister, what do you have? You have herpes simplex. When do you typically get a fever blister? When you're stressed.

So, yes, all of us come in contact with herpes virus all the time. As long as our immune system functions normally, we typically do not get open wounds.

But if our immune system is compromised, that's a perfect open door for the herpes virus to move in and to cause problems so very common in our oncology population. You might see it in older individuals. They're high risk for zoster, and that's why we now see the zoster vaccine.

How do you diagnose lesions caused by herpes virus? Well, primarily by clinical assessment.

So we observe the location, we observe the fact that we have clusters of these clear, fluid filled blisters or vesicles, and that they open to create very superficial wounds with a pink, yellow base. We note that they are acutely painful. With Zoster, we note that it follows a dermatome.

The only way to definitively diagnose herpetic lesions is to get a viral culture of a wet lesion. So if the lesions have already unroofed and dried, you're not going to get a valid culture.

So you have to have exudate in the wound bed and you have to follow the guidelines for a viral culture in your agency. Most of the time we don't even need a definitive diagnosis. Most of the time we treat empirically.

So we give antiviral agents, systemic antiviral agents, then we provide topical therapy.

The goal of topical therapy is to provide protection of the nerve endings, to reduce the pain, to absorb any exudate, to maintain a moist ring surface, and to prevent trauma. If you go back to no matter what caused the wound, the healing pathway is the same. The principles of moist wound healing are essentially the same.

What are some good choices?

If you have trunk wounds, which is what you typically have when it follows the dermatome, your silicone adhesive foams are a great choice because they provide very gentle removal. They effectively absorb exudate, they maintain a moist surface, and they have, you can get them with antimicrobial effects.

You could also use a glycerin based gel. It offers a lot of the same advantages. If you have perianal lesions, you're going to want to use a zinc oxide based preparation.

And for oral lesions, we typically use a topical antiviral. Okay, so we've talked about viral infections. What about fungal infections?

We just talked about fungal infections in some previous discussions because it's so common, so many times we have patients who have candidiasis, a yeast rash. We know that this is a maculopapular rash.

It's typically solid in the center, it thins at the periphery, so that you have distinct satellite or border lesions. Many times patients say, oh, it's so itchy, but when I scratch, or even when I rub, it's so tender. So itching, tenderness, pain are very common.

The color varies. So in people with light skin and medium tone skin, it's going to be bright red.

It's going to be bright red in the center, thinning at the periphery with those solid little lesions. But in someone with dark skin, it's going to start out lighter than the surrounding skin.

The distribution will be the same, solid in the center, patch formation in the center, distinct little maculopapular lesions at the periphery. Now, as it heals, this is what happens in somebody with light skin or medium tone skin.

It goes from bright red to dull red, to brown red and sloughs off. And somebody with dark skin.

It goes from being lighter than the surrounding skin to being darker than the surrounding skin, it goes from being kind of wet to dry and flakes off. Who's at risk? Anybody who has areas where moisture is trapped.

So we see this a lot under body folds, we see it under the pandas, we see it under large, pendulous breasts. We can see it in the inguinal area, you can see it in the perineal area.

Any place that's wet is a perfect breeding ground for fungal organisms, antibiotics, because when you knock out the bacteria, the fungal organisms go wild, and people who are immunosuppressed, because what normally keeps fungal organisms under control? Your immune system. What about diagnosis? Just like with viral lesions, diagnosis of yeast infections. Fungal infections is primarily empiric.

That means we say it looks like a yeast rash. This patient's high risk for a yeast rash.

I'm going to treat it with an antifungal, and if it improves, I am going to conclude that it was a yeast rash.

So typically, based on clinical findings, a definitive diagnosis requires you to take a little stick, get skin scrapings, stain them with potassium hydroxide, look at it under the microscope, and then you can see the hyphae of the yeast organisms. Treatment is obviously going to be antifungal. It's usually empiric, as we've already said. So we start out and we usually treat topically.

Your two big options are your azole products, like myconazole or nystatin. Nystatin is prescription. Azole products are over the counter. Interestingly, over the counter, your azole products have a wider antifungal spectrum.

So they're usually more effective as well as being less expensive. So typically we go with our azole products. They come in creams, they come in ointments, they come in powders.

Now, if I was treating under a body fold, I definitely would not want an ointment because that's just going to trap more moisture. So I would either use a cream, massage it in really well, and then use an absorptive product on top or a wicking product.

So if you have inter dry ag, you could put your inter dry ag into the body fold. You could also do powder. But remember what happens with powder and moisture at clumps.

So if you do powder, you want to do a very thin layer and you still need to tuck something in the body fold to wick the moisture. So your intra dry ag, your AbD pads, something. If I'm dealing with perineal fungal rash, then I'm almost always dealing with incontinence.

And so I'm probably going to use an antifungal ointment. So I get the antifungal, get the antifungal and the benefit of a moisture barrier product that repels urine and stool.

So you have to use powder very, very selectively. You can use cream, but you have to massage it in and then manage the moisture in the perineal area. The ointment is usually the best choice.

Now, if you have a female and she has perianal perineal yeast and there's labial involvement, she's probably got yeast vaginitis, and you need to treat intravaginally as well as topically. And then finally, if you have people and they're like, this is driving me crazy, you can use burrow solution.

You can do intermittent burrow solution soaks because it's an astringent and an antipuritic. So you can almost always get an order for that. When would you move to systemic antifungals?

Only if you have multiple areas of infection or if you have refractory infections. So if you had somebody with thrush in the mouth, yeast in the axillary areas, yeast under the breast, yeast in the inguinal folds, yes.

You may need to treat systemically, or if you have had them on topical treatment and they're just not responding. And if you're treating systemically, it's going to come down to ketoconazole or fluconazole. Now, there's another type of fungal infection.

These are caused by dermatophytes rather than yeast. So these are your tinea lesions. Like ringworm is a classic, jock itch is a classic. The big difference in tinea lesions and candidiasis?

Candidiasis is intense in the center, thins at the periphery. Tinea infections are intense at the periphery and thin toward the center.

So think about ringworm, its classic intense at the periphery, thinning toward the center. So again, the diagnosis is typically made based on clinpre clinical presentation.

You could use skin scrapings to verify, and you're definitely going to use azole treatment, I mean, azole products, because nystatin is not effective against tinea lesions. So in most agencies, what we stock are azole products.

So things like myconazole, 2%, those products can be used for both candidiasis and for tinea lesions like joc itch or ringworm or whatever. So we've talked about viral, we've talked about fungal. What about bacterial?

So you think about your skin and you think about the number of staph and strep organisms on your skin. It's not surprising that bacterial skin and soft tissue infections are pretty common. They vary tremendously in severity.

They can be as minor as one or two pimples caused by folliculitis, or they can be as severe as necrotizing fasciitis that causes major tissue loss. So we're going to start with simple and move toward severe. Folliculitis is a very simple and very common skin infection as caused by staph.

And what happens is you get some damage to that pilosabaceous unit, the hair follicle, and the oil producing gland. And once you damage the hair follicle and the oil producing gland, then it's very easy to get bacterial migration and infection.

So you think about all the things that can cause damage to the hair follicle. If we take tape off aggressively and rip the hair out, we can damage the hair follicle.

If we're doing aggressive shaving, we can cause damage to the hair follicle. And then what do you end up with? Many times you end up with pustular lesions, where you can see bacteria penetrated and caused a localized infection.

It can also contribute to obstruction of the oil producing gland, which then further contributes to the infectious process. So how do we prevent it? How do we treat it? We want to provide atraumatic hair removal.

We want to be very careful when we're removing adhesive products so we don't damage the hair follicle. Once we have evidence of folliculitis, we want to clean gently with an antimicrobial soap.

We may need to use topical antibiotics, but many times we can just do cleansing with an antimicrobial, monitor it, and wait it out. If we do use topical antimicrobials, the best one is mupirosin, because it covers staph and MRSA cellulitis, much more significant than folliculitis.

So with cellulitis, of course, you have invasive infection of the soft tissue. So it affects the dermis and the subcutaneous tissue. It can be caused by staph or strep.

If you have an open wound and you get infection around the open wound, it's usually staph if you've got a red hot leg, but you can't really see what caused the infection. There's really no open wound. It's probably a strep infection. Now, the signs and symptoms are classic. You recognize them, you get pain, you get edema.

Sometimes the edema is intense. So many times when you have acute cellulitis, you have intense erythema, acute edema to the point of large blister and bulla formation.

So it's very common to see blistering and bulla formation. When the edema is severe, you'll have induration, so the tissues will be harder to touch. Many times there will be lymph node enlargement.

So if you've got a hot leg, you might have enlargement of the inguinal nodes. If your arm is infected, it's going to involve axillary notes, but very commonly is the lower extremity.

We see this a lot in the lower extremity, so they come in typically to the emergency room, red hot leg, a lot of pain, swelling. Their white count might be up. Their lymph nodes might be enlarged. We end up admitting them. We put them on systemic antibiotic therapy.

Typically, topical therapy just involves moist wound healing. But you're frequently asked to determine whether or not you should un roof the blisters. So it goes back to size and how tense they are.

If you've got small blisters and they're not tense, let the fluid resorb. You might choose to cover the area with an antimicrobial porous foam and then just wrap the leg or the arm.

If you have large tense bully, then typically you do open that bulla so that the fluid can drain out. You can create a little window and drain the fluid out. You would definitely then need to dress with something like a porous antimicrobial foam.

Then abds and rap calls Camrsa. So this was something we hadn't heard that much about until about 15 years ago.

And all of a sudden, we were seeing community acquired MRSA everywhere. So we have to realize that community acquired MRSA is very different than hospital acquired MRSA. It's genetically different.

It causes different types of infection. It is, unfortunately, very contagious and very easily spread. So you see it a lot in areas where you have groups in close proximity.

You see it in prisons, you see it in daycare centers. You see it spreading among sports teams when they share locker rooms and they share equipment like helmets and things like that.

So we have to just be aware that if anybody develops community acquired MRSA, we need to look at who they've been in contact with because it's likely to spread. It can cause pneumonia, it can cause sepsis.

Typically, it causes relatively localized soft tissue infections, but it can make people really ill, so we just have to be aware of that. Now, how do you identify community acquired MRSA?

Well, many people think they're dealing with a spider bite because it's usually a single, solitary, localized lesion. It's typically very erythematous, very indurated with a purulent center that may be a different color. It might be kind of purple in color.

And so a lot of times people think, oh, I got a spider bite.

But when we first started seeing a lot of CAMRSA, epidemiologists were reporting that if you look at all of the reports that come in from all of the agencies across the country, that we were reporting more spider bites than spiders. In other words, they know what the population of spiders is in different geographic locations.

And the numbers of reported Cam RSA or the numbers of reported spider bites exceeded the spider population. So unless they had developed a sudden aggressive streak and they were running out and attacking people, we were misdiagnosing.

So if you look at a lesion and you think spider bite, think again. It's probably community acquired MRSA. How do you prevent CAMRSA? Well, first of all, just being very careful with antibiotic utilization.

So we don't use antibiotics unless truly indicated.

Making sure that people in community settings like prisons, like daycare centers, like sports teams, making sure that people are washing their hands, using alcohol based hand sanitizers, taking hot showers, not sharing equipment, those things make a big difference. And then how do we treat? Well, if you have a fluctuant purulent fluid collection, typically we will do incision and drainage.

So when the patient comes into the emergency room, they have a wound that looks like the one on top. They're typically going to open and drain that wound. Most patients will require antibiotics.

Sometimes, once you drain the wound, it resolves pretty quickly without antibiotics, but very common to see antibiotics prescribed. The most commonly effective antibiotics for community acquired MRSA are actually a little bit different. So Bactrim is number one.

Doxycycline is frequently used, sometimes vancomycin, sometimes linezolid. So back to room number one.

Whereas for hospital acquired MRSA, vancomycin is number one, with community acquired, vancomycin is down the list and not used nearly as often, which is actually good because vancomycin is primarily given iv and Bactrim's given po. So it makes it much easier to manage these people in the community.

When you're dressing these wounds, remember how infectious the staph organism is, so you want to secure your dressings on all four sides so you're not aerosolizing the staph organism. This is a very rare condition. Staphylococcus cold and skin syndrome. I'll mention it briefly. It's pretty much limited to children and infants.

You rarely see it in anyone over five years of age. The organism that causes staphylococcus, called a skin syndrome, secretes a toxin that causes the skin to slough. So it looks terrible.

You have a vesicular rashidae. It progresses to bulla formation. Then the skin starts to slough, and they can get major sloughing.

Treatment is with antibiotic therapy to get the infection under control, stop toxin production. Sometimes they will use topical antimicrobials as well, but primarily siv antibiotics.

They want you to come in and tell them, how do we manage this baby, this child who's sloughing their skin? So you're going to use non adherent dressings. You can use any of your silicone based products.

So we talked about silicone adhesive contact layers, like meputel or versatile.

We talked about silicone based foam dressings, and in this case, you would probably use your porous foam dressings that have very gentle adhesive and cover the open areas to prevent further infection. But here's the good thing. As awful as it looks, it usually heals in less than a week. Hepetitiga contagiosum, not serious, miserable, and common.

So it can cause be caused by strep a or by staph aureus. You get these little blisters, and it's usually around the nose and mouth. They rupture to form red wounds with kind of a yellow, crusty base.

You don't see it as much in adults unless they have young children, because it usually starts with children, involves the face and typically the upper body. If you have a child in daycare who develops impetigo, you know how generous kids are and how they're willing to share.

Well, they share these organisms very readily, so you can see it spread very, very quickly. But the good thing is it's relatively self limiting, and treatment is simple and pretty benign.

So it's basically hygienic and infection control measures. So keep the areas clean. Make sure that all family members are showering with an antimicrobial soap.

They should be using mupirosin intranasally, and they can apply mupiracin to the open wounds as well, because that's effective against staph and strep. And that's typically all you need to do. Just take care of everybody in the vicinity, keep the lesions clean, and use mupirocin hydradinidosupertiva.

Not terribly common, but we're definitely seeing it more than we did in the past, maybe harshly, because we know how to recognize it. So this is a chronic, infectious and inflammatory process that involves the apocrine sweat glands and the associated hair follicles.

It's a very difficult condition because it primarily affects the axillary area, the perianal area, sometimes the breast. It's recurrent, and it forms very painful lesions with malodorous drainage. So this is a miserable condition.

Eventually, they tend to outgrow it, but it takes a long time.

So risk factors, if you have somebody in your family who had this, they might not know the name of it, but they're like, yes, my aunt had the same thing under her arms and in the crotch area, and sometimes she had it on her breast.

More common in individuals who are obese, much more common in women than in men, though I have had men as well, more common in African Americans, but I've had Caucasians as well. Smoking is considered a risk factor, and there's some question as to whether fragranced antiperspirants can contribute. We all hope not. Right.

The other big risk factor is if you do have a patient with hyperhidrosis, where they overproduce sweat, that is considered to be a risk factor as well. Important to recognize this when you see it, because it's managed differently than, just, say, a pimple or a folliculitis.

So what you start out with are tender nodules. It's very different. So you have areas that are very tender to the touch? Very definitely.

Nodules, frequently erythematous, they open, they have malodorous drainage.

Then what happens is they close at the surface, but the infection tends to tunnel underneath, and you'll have another lesion that pops up here and another lesion that pops up here.

And then you get significant scarring because it does extend into the deep dermis and the subcutaneous, so painful, nodular draining lesions, tracking in the underlying tissue, extensive scarring. What can we do? How do we treat?

Well, typically when they come in, they have an acute, very tender draining nodule, and many times, incision and drainage is warranted, as well as aggressive antibiotic therapy to get the infection under control.

Wound care, typically, you're going to be using porous antimicrobial gentle foam dressings because you need something that absorbs drainage, something that kills bacteria, something that's conformable and soft.

For difficult areas like the axillary area or the inguinal area, pain management is important because these lesions are painful and smoking cessation also, we recommend loose clothing, because look at where these lesions are, axillary, perineal, and you want good circulation of air, you don't want to be trapping moisture here. Now, I've already said the major problem is that these wounds, these lesions tend to be recurrent, they tend to result in excessive scarring.

So if you do have a patient with significant refractory recurrent disease, they're going to want to know what else can be done. And you look at the patient on bottom, look at all that disease, what can be done?

So what they can do is they can do surgical excision all the way through the dermis, remove the affected glands, remove those apocrine glands, remove the hair follicles. So you're doing full thickness skin excision, and then you're going to have to do skin grafting.

So surgical intervention is only undertaken when there's very significant, very extensive disease. And the most complicated wound that we see related to an infectious process, of course, is necrotizing fasciitis.

And the newer term is necrotizing soft tissue infection. We still call it NF, but they're starting to call it NSTI in the literature.

So you know that necrotizing fasciitis is an infectious process that spreads very rapidly along the fascial planes. So you're down below the sub q, you're at the fascia muscle layer, and that's where the infection spreads. It can spread as quickly as 2.5 cm an hour.

Now this can be very beneficial in differential diagnosis, because if a patient comes into urgent care in the emergency department, they have something going on. We're not quite sure what it is. It could possibly be necrotizing fasciitis.

You can take a Sharpie and literally mark along the perimeter of the involved area. And if it is at f, is going to rapidly extend beyond your marks. So very rapidly spreading, it causes massive tissue destruction.

You tend to lose tissue above the fascia muscle layer. Typically you retain the muscle and organs.

Anything below that point, high mortality rate although the mortality rate is declining as emergency department staff have become much more aware and much more able to do an early diagnosis and to initiate early intervention, here are the predictors of poor outcomes.

So mortality rates are higher in people over age 50, higher among those who are immunosuppressive, higher among those who rapidly deteriorate and develop shock symptoms. What are the risk factors? Who gets this? Well, the scary thing is that about half of the cases there is no known risk factor.

So the answer is we don't totally know, but we have been able, with all of the studies that have been done, these have been identified as risk factors. Older age, but many people are young, definitely more common in the diabetic population. A lot of our patients are diabetic.

Many of them are immunosuppressed. They're either on immunosuppressive medications or they have some kind of immunosuppressive condition.

But diabetes, if you look at what we see clinically, diabetes very commonly involved obesity. Also, many, many of our patients are obese. And then if there's any break in the skin, you can get bacterial penetration and rapid proliferation.

Some patients develop necrotizing fasciitis as a result of iv drug abuse. Now, there are three types. The first type is polymicrobial and synergistic. So it usually involves both aerobes and anaerobes.

Very commonly involves the trunk or perineum. A lot of times there is a break in the skin that you can identify. Many times it does involve a vulnerable patient, like an obese diabetic patient.

This is the most common type.

And I should just mention that if you have necrotizing fasciitis or necrotizing soft tissue infection involving the groin and the perineum, it's usually labeled Fournier's gangrene. So you may see that diagnosis. Type two is very different. It's caused by group a. Beta hemolytic strep most commonly involves head and neck.

50% of the patients with type two are young and healthy. A lot of them were out hiking two days, and they're like, I don't know what happened. Many times there is no identifiable break in the skin.

And the only real risk factor that's been identified is use of non steroidal anti inflammatories in kids with varicella. So we no longer do that.

But like we said, many young adults who develop necrotizing fasciitis, the people you read about in the paper see on the news, who lose part or all of a limb or who may have massive head involvement. It's usually type two. Type three is much less common. It's single organism, usually either it's a saltwater source or a soil source.

So either oibrio or aeromonas. The pathology in type one, it's aerobes and anaerobes working together.

So aerobes deplete oxygen levels, and then that is just great for the anaerobes. They're like, thank you so much. Now I can grow.

And then the anaerobes cause massive tissue breakdown that provides nutritional support for the aerobes. So it's the very worst kind of, you scratch my back and I'll scratch yours. Group a, beta hemolytic strep. This is type two.

You get massive tissue breakdown caused by the bacterial enzymes and toxins. The surface proteins actually protect the organisms against phagocytosis.

So this is a very scary organism, causes major tissue damage and is very capable of self protection. In addition, the toxins that are produced cause release of inflammatory cytokines and inactivate your t cell receptors.

So it's like a complete package. Massive tissue destruction, self protection, inactivation of your immune system. Clinically, how do they present?

Stage one is where we really want to catch this, but it's hard because it's kind of non specific. You have erythema, you have edema, you have induration. Biggest indicator is pain that is totally out of proportion to the injury.

So you see this area, this injury? Yes, you do see erythema and induration. That suggests maybe you have a cellulitis, but the patient's telling you that they have off the charts pain.

And the patient's having is febrile and frequently presents with chills. So you're like, okay, this doesn't quite go together. That's your first indication. Everything doesn't match. So you should start thinking right then.

Could this be necrotizing fasciitis? Stage two. Now the disease process has progressed, now you have patchy blisters, you can have bullet formation, you can get discoloration of the skin.

Now the margins become much less distinct, the patient becomes much sicker, and many times they develop altered mental status. Now your chance of recovery is deteriorating.

Once you get to stage three, the chances of recovery are increasingly limited because now you've got escort like skin plaques, the wounds may become numb, so the pain levels diminish. That's because of nerve destruction. You might feel gas in the underlying tissue, crepitus.

Many times they have hemorrhagic bulla, and at this point, they frequently are developing shock like symptoms. Diagnosis all depends on high index of suspicion.

So when I look at this wound, if I just think, oh, cellulitis, I don't know why they're having so much pain. Probably they just have low pain tolerance. I'm going to miss it.

If I look at a wound and I'm like, well, I would think cellulitis, except the patient's reporting such high levels of pain. I'm going to mark the perimeter, I'm going to get labs, I'm going to watch this patient very carefully.

Labs do give you some indications you'll have rapid onset of leukocytosis and also their sodium levels start to drop. You can do a CT or an MRI stat, and you will see gas pockets and extensive infection and necrosis.

Typically, these patients end up in surgery very quickly, within hours of presentation to the emergency room. And at surgery, what they find is a positive fingertip, meaning that they can literally poke their finger through the tissue.

You shouldn't be able to push your finger through the soft tissue. You should get major resistance.

So when you open up the area with necrotizing fasciitis, you're going to see this gray, non bleeding tissue, very friable tissue that you literally can put your finger through at the time of surgery. They're going to get cultures and they're going to do a wide trying to capture all of the involved tissue and to interrupt the process.

So that's step one in effective treatment, early aggressive surgical debridement. Treat it like a tumor, wide margins. Then of course you're going to do aggressive antibiotic therapy.

If it's type one, you've got to cover gram positive and gram negative aerobes and anaerobes.

If it's type two, clindamycin is a really good option for group a strep because it helps to inhibit production of those toxins that cause bacterial adherence and tissue damage.

And sometimes they send these patients for hyperbaric oxygen therapy because remember that hyperbaric oxygen therapy is synergistic or has a synergistic effect on antibiotic therapy.

So if you put me in the chamber and give me antibiotics, you're going to drive more antibiotics into the tissues, you're going to kill a lot more bacteria. Also, remember, white blood cells use oxygen to kill, okay? So goal number one, get the infection under control.

Once you get the infection under control, you've done wide excision, you've done a aggressive antibiotic therapy, you might have done hyperbaric oxygen therapy. And now we have a clean wound bed. There's no longer any extension of the disease process, no new necrosis.

Once we have a stable, viable wound bed, most of the time we do negative pressure wound therapy to promote rapid granulation. Sometimes it's almost impossible to do negative pressure wound therapy because of the extent of the wounds and the location of the wounds.

If you cannot do negative pressure wound therapy, you'll do topical therapy, moist wound healing, typically with antimicrobial dressings, like an antimicrobial alginate, an antimicrobial hydrofiber, then dry galls. And sometimes we secure the dressings just with mesh briefs.

Once we get a healthy bed of granulation tissue, typically flaps and grafts are used to provide final closure of the wound. Now, notice in italics, it says, iv immunoglobulin for group a strep.

This is sometimes used to help neutralize the antigens, but it is considered off label use, so we won't ask you about that. I would not expect you to see it on certification.

Okay, so remember when we talked about community acquired MRSA and we said that those lesions were commonly mistaken for spider bites and that a lot of times people would report, I had a spider bite that got infected, and maybe it was cam or sa, but there are indeed some wounds caused by spider bites, much less common than reported, but they definitely do occur, and they're always caused, of course, by poisonous spiders. So brown recluse being the most common offender, especially in this country. So what are the characteristics of these wounds?

Well, they are full thickness wounds. They do progress to necrosis. You typically have a necrotic center, an intense erythematous halo, or sometimes it's a bluish halo.

So either a red or blue halo around a necrotic center, they're very painful. Some patients also have itching, but all of them have pain. Very common for them to have systemic indicators as well, like fever, like nausea.

Some of them develop thrombocytopenia. So that's the effect of the toxins systemically. What can we do?

Well, the damage has already occurred, so all we can do is implement moist wound healing. We're going to initiate measures to eliminate the necrotic tissue, to manage the exudate, to keep the wound bed moist.

But sometimes anti inflammatory agents can be beneficial in limiting tissue damage and reducing some of the pain. So we'll be doing moist wound tilling, but they may get systemic anti inflammatory agents to help with generalized tissue response and with pain.

We're going to talk briefly about bullous lesions. Depending on your care setting will dictate how often you see this.

So there's many different pathways, pathways to the same kind of clinical picture where you have formation of large blisters, also known as bully, with very minor trauma. Now, what's happening at a cellular level is that you've gotten.

You're getting damage to the anchoring fibrils between skin cells or between skin layers. Once you break down those little anchoring filaments, then very minor trauma can cause one skin layer to peel off of another skin layer.

It can cause skin to slough spontaneously. So we see blistering with minor trauma, and sometimes we say, see spontaneous skin loss.

On a positive note, these are usually partial thickness, so we expect them to heal without scarring. But if they continue to get recurrence, because sometimes this is chronic, if they get recurrent lesions, they can end up with scarring.

If these lesions get infected, they can end up with scarring. So yes, most of the time they heal without scarring, but scarring can be seen.

You can also get hyperpigmentation, an overreaction of the melanocytes to recurrent trauma in the area. Now, what are the specific causative factors for bullous lesions?

Well, in the pediatric population, it's usually epidermalysis bullosa, and that is a congenital absence or very weak anchoring fibrils. So these babies can actually be born with lesions, and you find that you just touch them and you can cause a lesion. Again, the severity varies.

So some infants have scattered lesions, other infants have massive skin loss. It can also be the result of an autoimmune condition that attainden attacks, the anchoring fibril.

So if you have a patient with bullous pemphigoid or pemphigus vulgaris, those are autoimmune conditions, and that's what you see in the center. And finally, it could be an allergic reaction. If you have a severe allergic reaction, it can target the anchoring fibril.

So a lot of you have taken care of patients who had Stevens Johnson syndrome or toxic epidermal necrolysis, where they formed blisters and bully over the entire surface. Minor trauma would cause the skin to slough. Whether it is congenital, autoimmune or an allergic reaction, you're going to get variable severity.

If it's mild, it will just be blister formation in response to minority trauma. If it's major, you can see massive skin loss. Also, if you have severe forms of this process, you can get mucosal lesions as well.

So sometimes we see patients that are sloughing their skin, they have bloody crusty drainage all the way around their mouth, and they have difficulty swallowing. So nutrition becomes an issue. So variable severity, you need to be aware of that. Now, how do you manage these patients?

Well, it's going to depend on what the underlying condition is. I want you to focus on the top because that's what we're responsible for.

So regardless of whether this is congenital or autoimmune or an allergic reaction, I want to minimize damage to the skin. So I'm going to put them on a low friction, low shear support surface so that when they move, it doesn't drag the skin off of their body.

And we're going to use non adherent dressings so that when we remove the dressing, we don't cause more trauma. So typically we use our contact layer dressings, either silicone based or petrolatum based contact layer dressings, so we can put them down.

Then we can cover with galls like abdsen, and we can wrap extremities, we can wrap the trunk. Sometimes, if they have major areas of skin loss, they end up looking almost like a mummy.

Now, if the underlying pathology is an autoimmune process or an allergic reaction, the patient's going to be receiving anti inflammatory agents like steroids or biologics to interrupt that process, and they may go for plasmapheresis because remember, plasmapheresis can remove antigen antibody complexes from the bloodstream. Those therapies will not work for the infant or child with a congenital absence or weakening of the anchoring fibers.

They're looking into gene therapy. Can we correct this through gene therapy?

If there are areas of frequent recurrence, they may treat that with bilayer skin and tissue substitutes with apligraph, because then you're replacing the damaged skin with a much more normal, much more functional substitute. And because it is congenital, genetic counseling is frequently used, indicated for the parents as well as for the child later in life.

So we're going to summarize this section.

If you have a disease or if you have wounds caused by an infectious process, the challenge is to recognize it as an infectious process, to identify and treat the causative organism correctly. Beyond that is systemic support for healing, your standard topical therapy. So your fungal organisms, pretty easy to recognize, identify and treat.

Viral organisms, pretty easy to recognize and treat. Your bacterial infections can cause a wide range, so it can be as mild as folliculitis, as severe as necrotizing fasciitis.

At this point in time, most of us have seen every one of these conditions often enough that we're much more likely to identify it correctly. Spider bites, rare. You're not going to see many of those, but if you do, you're going to manage them with moist wound healing.

Bullous lesions can be caused by congenital absence of anchoring fibrils, by autoimmune attacks on anchoring fibrils, or by an acute allergic reaction reaction. The medical surgical team is going to treat the underlying condition.

We're going to make sure they're on a no shear or low shear, low friction surface, and we're going to use non adherent contact layers to manage the wounds. Okay, in just a minute, in the next class, we'll move on to other wounds caused by disease processes. Can I just move on? Okay. Okay.

So in part two, we're going to talk about wounds due to oncologic disease processes, either to the cancer itself or to the related therapy. And we're going to talk about burn injuries. Now, typically, wound care nurses do not have primary responsibility for burn care.

Most major burns go to a burn treatment center. But many times we do end up caring for patients with minor burns. And we definitely need to know when to refer to a burn center.

So that will be our focus. So let's start with wounds that are caused either by cancer or by cancer treatment.

One of the most distressing wounds you'll take care of are cutaneous malignant lesions. So these are solid tumors that invade the skin. It can be kaposis sarcoma in an AIDS patient, it can be breast cancer. It can be head and neck cancer.

And what happens is the tumor cells literally invade the skin and create a new tumor on the surface of the skin.

Now, usually when we see solid tumors invading the skin surface, it usually means the patient has very advanced disease, but we should still do a metastatic workup if the patient is open to treatment of the underlying disease process. Sometimes they didn't even know they had cancer. So when we tell them what's going on, they're like, well, what can be done?

Those patients are open to surgical intervention, chemo, radiation. So we would do the workup so that we know exactly what we're dealing with. Other patients might say, I just want you to help me manage the odor.

I just want you to stop the bleeding. Help me with the drainage. Here are the major management issues for patients with fungating tumors involving the skin surface.

The number one is necrosis and odor. And what patients were control of is odor. Definitely, we need to manage exudate. Some of these bleed very readily because the tissue is so friable.

So we would definitely need to control bleeding. Patients frequently worry about infection, but that's not the most common issue with these wounds. Body image and appearance is huge.

So if we can come up with something that manages the drainage, reduces or contains the odor, conceals the wound, then we have done a lot to improve this person's quality of life. We not might not impact on the overall outcome of their disease process, but we can definitely improve their quality of life.

We're going to start out with odor control because it's the number one concern for the majority of these patients, and you can imagine the impact on quality of life. Where can you go if you have a very malodorous wound? It impacts on everyone. It impacts on your family, on your friends.

Your family has a hard time being in the room with you. Your friends don't want to come. You feel so isolated. So you're going to do absolutely everything you can to get under odor under control.

And the number one agent in terms of effectiveness is topical metronidazole, flagyl. Why? Because it's an anaerobic antibiotic.

So you think about the type of organisms that grow very well on a necrotic wound surface where there's low oxygen levels, anaerobes. So if you can use topical metronidazole, you can kill the anaerobes that are producing the very malodorous drainage.

So there's several different forms of topical metronidazole. If you have a relatively dry wound.

Now, most of these are wet, but some of them are relatively dry, you could use topical metronidazole gel, or you could ask the pharmacy to reconstitute metronidazole into a 1% solution solution. You could saturate gauze and then pack it over the tumor, conforming it to the tumor.

If you have a wet tumor, and most of them are, you can get metronidazole tablets and you can crush them, and you can sprinkle the crushed tablets over the surface of the tumor. Then cover with something like vaseline galls.

And the vaseline galls holds the crushed metronidazole in place and also is somewhat occlusive, so helps to trap odor. Then you can cover with dry gauze and secure it with cling or whatever. So let's say I have a breast wound and it's wet.

So I'm going to do my crushed flagal. I'm going to do my Vaseline gauze.

I'm going to do an ABD, and then I might secure with a surgical bra, or I could secure with plastic wrap, like glad wrap, press and seal. It would seal all the way around the wound. It would be non adhesive, and it gives a very effective odor barrier.

Remember, plastic wrap will seal odors in, so you can use that as an alternative to adhesive and sealing your dressing around a very malodorous wound. Sometimes we'll use dacon soaked galls. Sometimes we'll use odor proof ostomy pouches.

If it's a localized wound, we can use other measures, like room deodorizers, coffee grounds, that kind of thing. But your number one approach is to try to eliminate the odor either with top topical metronidazole or with deconcepticols.

Now, one thing I should mention is that use of topical metronidazole for odor control and for management of fungating tumors, that is off label. So you might have to talk to the pharmacist about it, but it is discussed in your core curriculum, so you can take that with you.

They just want to see that this is evidence based practice, even if the evidence is primarily anecdotal in nature. So top two, flagyl or daikins, exudate management.

You're typically going to use your antimicrobial absorptive dressings, like your silver based alginate antimicrobial foam, then dry galls. Again, you have to think, how am I going to conceal this?

So if it's head and neck, maybe I'm going to cover with a porous conformable foam and then either wrap with a roll gauze or take some of the stretch net to hold it in place. What if I have a very friable tumor and bleeding is a major concern? If I can identify the surface bleeders, I can use silver nitrate.

I can always use hemostatic dressings like surgacel, surgacel, snow, or calcium alginates, and critical to use non adherence so that I don't cause recurrent bleeding. So remember having a lady who came in, she had advanced breast cancer. She didn't want any treatment. She wanted help with bleeding.

And she said, I asked her what she was doing at that time. She said, well, I don't want to look at it. So she's like, I get in the shower, I get out, she's like, I pat dry.

I don't look, I pat dry with paper towels. Then I put paper towels over it and I put on my bra.

Well, then what was happening, of course, was the paper towels were becoming adherent and causing bleeding when she took them off. So all we had to do was substitute non adherent dressings. I think we just used Vaseline galls for her. That's all she needed.

That's all she wanted at that point in her life. Patients worry about infection. That's typically not an issue.

But, yes, we do always monitor for evidence of cellulitis, and we spend time and effort and creativity in coming up with an effective way to conceal the tumor. So if we can manage the odor and conceal the tumor, we make things better for that patient.

Your conformable foam dressings very, very helpful in doing this. What about radiodermatitis? Radiation induced skin damage?

So, you know, we use radiation therapy to kill malignant cells, and we know that it works by damaging the DNA. And if you significantly damage the DNA of a cell, you render it incapable of reproduction. So you basically take it out.

You might not kill it outright, but if you damage the DNA, you keep it from reproducing. Then you start to get that tumor under control. The bad thing about radiation is that it can damage the good cells in the radiation treatment area.

Now go back to the fact that about 10% of the cells in that basement membrane layer of the epidermis divide daily. So let's take the radiation treatment area.

And you're like, okay, about 10% of the cells in this area, the good cells in this area, will be dividing daily. Any cell that is dividing at the time of radiation therapy is at risk.

So as you get further into the treatment protocol, you've got more and more cells that have potentially been impacted by radiation, and the level of skin damage starts to increase. So you give me treatment number, 110 percent of my cells are at risk. Some of the cells will be killed outright, they're gone.

Some cells will be damaged and they will shed at a faster rate because of the damage sustained with the radiation. A third group of cells will have damage to the DNA, but it's minor enough that they can recover. The problem is you can't reproduce.

If you're a cell, you cannot reproduce until you fix your DNA strands. So instead of reproducing on schedule, the cells over there in the corner redoing this DNA strand, fixing this DNA, and they're like, hey, you.

You're supposed to be over here reproducing. Can't do it right now. Have to fix my DNA. So you get progressive thinning of the epidermis in the treatment area.

Some cells are lost, some cells are shedding an accelerated rate. And the cells that are scheduled to reproduce are less able to do so because of the damage to the DNA. Clinically, what do we see?

We see hyperpigmentation. That's the skin's attempt to protect itself.

So the melanocytes produce extra pigment to try to protect the skin against irradiation because some of the cells are damaged and they're going to shed at a faster rate. You see what we call dry desquamation.

So that dry, flaky, shedding skin, if you get enough skin cells killed, shed and unable to reproduce, you can get open areas, areas of skin loss. And this is called wet desquamation. Now, there's a staging system for radiodermatitis. We're not going to ask you this.

So this is reference material, but it's good to know because you'll see that this is frequently used by your radiation oncologist. So a stage one radiodermatitis.

You have inflammation, so you've got some erythema, you might have some edema, you'll have some tenderness, and you'll have that dry desquamation. So you've got flaky, dry skin and some tenderness. Stage two now is bright red.

You have patchy areas of skin loss, most commonly in body folds, because wherever you have folds, there's increased friction and moisture. And if you add that to the underlying damage, then you get skin loss. Stage three, you have extensive moist esquimation, major areas of skin loss.

And then stage four, you've got deep dermal damage. It results in a full thickness. You get loss of hair follicles, sweat glands, sebaceous glands. You may get necrotic tissue.

So stage one, dry, flaky skin. Stage two, patchy areas of skin loss. Stage three, extensive skin loss. In stage four, extension into the deeper tissues.

Now, anyone who's getting radiation is at risk for radiodermatitis, but we've learned a lot about radiation therapy, and radiation oncologists work very hard to minimize the damage to good skin. These are the risk factors, and it helps you predict who's going to have issues with radiodermatitis. So first of all, how big is the treatment area?

The larger the treatment area, the higher the total radiation dose, the more likely that this person is going to have skin issues. Also superficial lesions.

So if you're doing radiation therapy for breast cancer, you're trying to treat skin cells or cancer cells and the skin and tissue layers that are very close to the surface. And it's very hard to adequately shield the skin when you're targeting the tissues right beneath the skin.

So when you have breast cancer, when you're treating breast cancer, radiodermatitis is more common.

We also see it when you're treating patients who have squamous cell cancer of the anus, and they're treating superficially much more likely to get skin damage.

Also, if the treatment area involves skin folds or bony prominence, and if you're giving the patient chemo at the same time that they're being exposed to radiation, then that's two cytotoxic therapies affecting reproducing cells in that area. So what can we do to minimize the incidence and severity of radiodermatitis. And then what can we do to manage?

Well, interestingly, we have seen recommendations change for a long time. They told patients, don't do anything with that skin. Don't shower, don't bathe, don't wash your hair. Now, some people did it anyway.

And now their recommendations are, do carry out daily hygiene so that you minimize bacterial loads at the skin surface. Patients are much happier because they can do daily bathing. Yes, they want to be gentle, but they can bathe daily. They can wash their hair.

The goal is keep the skin clean. We want them to minimize trauma to the area. So avoid very hot water, avoid very cold water. Avoid the sun.

Don't dress in rough or constrictive clothes. Clothing. Don't use aggressive cloths for bathing. Use soft cloths for bathing. Don't shave. Avoid tape to the area.

If you have to use tape to the area, put down a thin hydrocolloid as a base or use a silicone base tape. We should be recommending routine use of approved emollients, and approved emollients include aquaphor, lubriderm and usurin.

So you can always check with the radiation oncologist in your agency, but most approve of any of those. So you can tell the patient, yes, we want you to shower daily. Warm water, mild soap, soft cloths. We want you to routinely use moisturizers.

This is the ones we recommend to.

Now, in some settings, they use topical steroids to the area of radiation because there are some very limited studies that show that topical steroids can reduce the inflammatory response of the good cells in the area and reduce the incidence of skin loss. Again, you're going to have to talk to your radiation oncologist to see what their protocol is in terms of management.

If it's dry desquamation, you're going to do everything we've talked about. Daily bathing, mild soap, moisturizers, emollients to keep the skin as soft as possible, as moist, as supple as possible.

Avoid trauma, possibly topical steroids, especially if they're experiencing itching and burning. Most often we get consulted because there are areas of wet desquamation, skin loss, and you go back to, well, the pathway to healing is the same.

I'm going to do moist wound healing. So you want to manage the extra day. You want to keep the surface itself moist. You definitely want to provide a traumatic removal.

You have to think, how wet is it? So how much absorption do I need? Here's the other thing you have to think about. If they're still getting radiation.

If they're still in the middle of their treatment protocol, some radiation oncologists remove all dressings for treatments. Others will leave very thin dressings in place.

So again, very helpful to talk to the people in your radiation oncology department to know what their guidelines are and what their practice is. Do you want dressings routinely removed? Then I've got to select a dressing that can be removed without trauma to the underlying wound bed.

It has to be non adherent. So good options. Foam dressings are almost always a good choice. You can use either non adherence foams or silicone adhesive foams.

They're soft, they're conformable, they absorb, they maintain a moist wound surface, they provide a traumatic removal. Now, some foams are silver based. A lot of radiation oncologists require removal of any dressing that has any metallic components.

So if you had a choice of a non silver based foam and a silver based foam, use the one without silver. In that case, sometimes the radiation oncologist decides to leave the dressing in place.

You could use hydrocolloids, but only if they're through with their therapy. Or the radiation oncologist says, that's very thin, you can leave it in place. You could use solid gels, like your glycerin.

Gels are very easy to use, very soothing. So you can put them on, you can take them off, you can put them back on.

So again, determine where the wound is, how wet the wound is, where the patient's two, and their therapy program, what the radiation oncologist wants to do with dressings, and then you can pick the best one. Patients who get radiation therapy for management of cancer are at risk for osteo radionecrosis.

This is a long term injury, so it's not what you see immediately. This is down the road. And some radiation oncologists will tell you radiation keeps on giving, unfortunately, in a very bad way.

So what's the mechanism of injury? Underlying osteo radionecrosis?

Radiation can damage the cells lining the blood vessels, the endothelial cells, and so you can get progressive damage to the blood vessels and the fibroblast in the affected areas. The end result is chronic ischemia, even though it's a trunk wound, even though it's a breast wound. So you get chronic ischemia.

You get fibrotic changes in the soft tissues, like the dermis, and you get high risk for failure to heal because of the combination of ischemia and damage to the fibroblast. That means any patient who has an area that has been radiated for the rest of their life. Needs to be provide very gentle care to that skin.

They need to avoid trauma. They need to avoid sun exposure. They need to keep the skin clean, soft and supple.

It also means that if a wound develops in an area that was previously treated with radiation. It's very likely to be non healing. And right now we don't have great options for managing these wounds. We could try hyperbaric oxygen therapy.

Because ischemia is one element contributing to failure to heal. And we know that hyperbaric oxygen therapy. Will help to correct localized ischemia. Since the tissue is perfused.

The other thing that could be done is you could rotate healthy tissue in to cover the defect. You could do a surgical flap. So you would take non radiated tissue. And rotate it to cover the area of injury.

But obviously, that's going to depend on what's going on with the patient. What's their long term prognosis? Is this a reasonable thing to do? Sometimes we end up with long term wounds. That just don't heal.

And we just manage them. If they're small, we may just end up managing them long term. Just a couple more things related to oncology, to cancer care.

You might have patients who come in with graft versus host disease. When does that happen? So if you have a patient who has an allogeneic blood or bone marrow transplant. They are at risk.

Allogeneic means you got that bone marrow. You got that blood from someone else. In contrast, if you have an autologous bone marrow transplant. You're not at risk.

So let's just walk through this. Patients who have malignancies. That do not involve the bloodstream or the bone marrow. So let's say I have refractory breast cancer.

Then what they might do is they might have me donate my own blood. Donate my own bone marrow. Because there's nothing wrong with my bone marrow. So they have me self donate.

Then they give me high dose chemo and radiation. To try to eradicate the cancer. And then they rescue me with my own bone marrow.

Because the problem is sometimes it's very difficult to eradicate cancer. Without killing off the bone marrow. And you can't live without your bone marrow. So this is a way to get around that.

So if you have a tumor that does not involve the bone marrow. You can be your own donor. Donate the marrow, get the treatment, rescue yourself. But what if your cancer is a lymphoma.

Or a leukemia involving the bone marrow itself? Then you're dependent on donated bone marrow or donated stem cells.

So what they do with allogeneic is they first of all, identify a donor who hopefully has good tissue mapping, has your same blood type, very comparable tissue types. So I have my donor. Now I'm going to undergo high dose radiation and chemotherapy to try to eradicate the, the leukemia or the lymphoma.

Then you're going to give me that bone marrow or stem cell transplant from that donor. If I get bone marrow, stem cells, blood from a donor, I'm at risk for graft versus host disease.

Okay, now, there are definite phases when you talk about bone marrow transplant. There's the conditioning phase. The conditioning phase is the high level chemo and radiation.

It's the very intensive treatment phase designed to eliminate the malignancy. Then you provide the transplant, usually just intravenously. Then you have to wait for those cells to begin working.

So pre engraftment is the time frame when you're waiting for the donated red blood cells, white blood cells, platelets to begin reproducing, to begin protecting the host. Engraftment is when the cells begin to work. So they're constantly monitoring blood counts.

And until the blood cells start to work, they're covering that patient who is very vulnerable with antivirals, antifungals, antimicrobials, antibacterial agents. They may be providing platelets via infusion to control bleeding. Now, who's most at risk for graft versus host disease?

Anytime there's a mismatch between my tissue and my donor tissue. So the greater the discrepancy, the closer the match, the better, the more different we are, the higher my risk. How old am I?

Well, now, if you're over 40, your risk goes up. If you have a history of blood transfusions, your risk goes up. Also, you have to look at how aggressive the conditioning regimen was.

How much did you lose, how much damage was sustained from the chemo and the radiation? And how effective is your prophylaxis protocol, your antivirals, antifungals and antibacterials? So here's the pathology of graft versus host disease.

So you've destroyed your own bone marrow, and now you've gotten someone else's bone marrow. And the risk is that your immune system system will identify that donated marrow as foreign, that it will basically say, what is that doing here?

That's not us, it doesn't belong here. And that the t lymphocytes will actually attack the donated cells and tissues.

Now, there are three organ systems that are most commonly involved in graft versus host disease.

When the donated marrow or stem cells actually trigger a reaction, the skin is the most commonly involved, and it's usually a progressive rash that begins on the palm, spreads to the upper body, and then can lead to generalized skin loss or desquamation. The liver can be affected, the GI tract can be affected. They can end up with severe diarrhea, but most commonly it's the skin.

Graft versus host can be acute or chronic. So if it occurs during the first 100 days post transplant, is considered to be acute.

If it occurs more than 100 days post transplant, is considered to be chronic. So with acugraph versus host disease, what do you typically see? Well, you see this moist desquamation, you see skin loss.

You have large areas of partial thickness injury. You're going to treat systemically with immunosuppressants to try to shut down that immune response, right?

You don't want the donated marrow attacking you. So they're going to give, typically steroids, they're going to give other anti rejection meds, things to interrupt the immune response.

What do they want from you? They want you to help with topical therapy. So you go right back to, I've got skin that's very vulnerable. I have open areas.

I'm going to put the patient in a low shear, low friction support surface. I'm going to use non adherent dressings that will maintain a moist surface that will absorb any exudate, that will provide antimicrobial effects.

And I want to be sure that when I take it off, I'm not going to cause any more trauma. You can also get chronic graft versus host disease, which is very frustrating for the patient because of all of the clinical manifestations.

So if you get chronic graft versus host, now you get this very dry, flaky skin. You get sclerotic changes in the soft tissues, so you lose the normal softness, suppleness of your skin and tissues.

You get patchy or diffuse erythema. You can get ulcers, especially in areas subjected to any trauma. So once again, you do a biopsy to determine, is this a rejection phenomenon?

Is that what's going on? Are we dealing with graft versus host? And then we try to shut that response down with our anti inflammatories, our systemic agents.

Again, we're responsible for topical therapy, daily bathing to keep bacterial counts low, constant use of high level emollients to keep the skin soft dressings for open wounds. If you have a lot of edema and lower extremities, you may need to use compression wraps or stockings. So all of our management is symptomatic.

Systemic therapy is always focused on interrupting that rejection. Phenomenal phenomenon, shutting down the immune system.

The last thing we're going to talk about under oncology related lesions is extravasation injuries.

So extravasation injuries can occur when we're giving chemotherapeutic drugs, if the angiocath actually penetrates the vessel wall and allows that chemotherapeutic agent to leak out into the tissues. Now we talk about this under oncology because chemo drugs are the most common vesicants.

Vesicants cause active tissue damage, but we should be aware that vasopressors can also cause significant damage. So everything we're saying here would be relevant also if you had extravasation of a vasoconstrictive agent.

So your initial management is not you, it's the staff they're going to recognize. I've got an infiltration. They're going to discontinue the infusion.

Most protocols call for the nurse to aspirate any medication that can be aspirated. So you discontinue the infusion, pull back on the angiocath to see what you can pull, pull out of the tissues.

Many times they recommend an antidote, so you instill the antidote at multiple points around. The extravasation injury most commonly is hyaluronidase. But if you have extravasation of a vasopressive agent, you would typically use phantolomy.

That's not your responsibility. Your responsibility is wound care. So they want you to come in, look at the area, decide what needs to be done.

You go right back to the pathway to healing is the same. The principles of moist healing or moist wound healing are the same.

So you're going to use moisture retentive dressings, you're going to use a traumatic dressing, you're going to manage any exudate. If it involves joints, you're going to splint the area to prevent any kind of contracture formation.

But many times you'll need to do a plastic surgery consult.

If there's tendon exposure, if there's joint involvement, bone involvement, then you definitely want plastic surgery to come look at that patient with you to determine, is that patient a candidate for excision? Does that area need to be surgically excised? Will they need a skin graft? What else needs to be done? Your focus, moist wound healing.

But many times you'll bring in plastic surgery. The last type of wound that we're going to talk about that is due to a specific disease process or a specific type of injury is your burn wounds.

And remember that burn wounds that are significant are usually cared for in a burn center. But you might be asked to help manage minor burns, or you might help manage patients post burn down the road when they're in rehabilitative care.

So key considerations when a assessing burns includes the depth of the burn, and you may have questions on classification and staging of burn depth. You should be aware that the depth is not always clear initially. So if you do an initial assessment, day one, post burn, you need to follow up.

Day two, day three, post burn, because it's very common for burnt and burn injuries to progress over the first few days following injury. You should also be aware that you will have zones of injury. So the central zone is the area of most intense injury.

That's where you typically have devitalized tissue. It's also sometimes called the zone of coagulation. The stasis zone is right outside the central zone zone.

That zone may survive as long as you maintain tissue hydration. You provide aggressive fluid resuscitation, you prevent infection. So the central zone is the dead tissue.

That's the most intense injury, the most severe injury. Then you've got a zone of less severe injury that may or may not survive. And then the outermost zone is the hyperemia zone, and that is red.

But there's no active tissue death, and that zone will definitely survive. It's autologous or analogous, rather, to a first degree burn. So you don't worry about the hyperemia zone, you worry a lot about the stasis zone.

That's the zone you can rescue. Central zone, you can't undo the damage this done. Okay, let's talk about the way they currently stage burn wounds, because it has changed a lot.

So instead of talking about stage one, stage two, stage three, stage four, now we talk about epidermal superficial partial thickness, deep partial thickness, and full thickness. So epidermal burns, there is no skin loss. They're red, they're hot, they're painful. It's like a sunburn.

They will heal in three to four days, typically with no skin loss, and you do not include epidermal burns. When you're calculating total burn surface area. Partial thickness burns are going to involve skin loss. They can be either superficial or deep.

Superficial partial thickness burns. Again, very painful. You have blanchable erythema. You do have blistering. They typically heal in two weeks as long as you manage them correctly.

Now, a common question is, what should I do about those blisters? Should I open those blisters? Should I leave them alone? Here's the guidelines. If you have small blisters, you leave them alone.

You allow the fluid to reabsorb, but if the blisters are larger than 2 cm in diameter, you need to open them. One reason for opening them is that a lot of times burn fluid has high levels of inflammatory mediators, so you want to drain that out.

But also when you have large blisters, you could have a deeper wound underneath. And so one of the reasons for opening large blisters is to accurately assess the depth of the burn.

If you have a deep partial thickness burn, is going to extend deeper into the dermis. The wound is going to look pale and dry and non blancible.

Now, these wounds usually do heal within three to four weeks, as long as we provide moist wound healing, as long as we prevent infection, as long as we manage blisters appropriately.

But even after they heal, they'll be very prone to recurrent blistering for a number of months post burn because it takes time for that epidermodermal attachment to be reestablished.

And if you have a deep partial thickness burn that is very slow to heal, if it hasn't healed, let's say four to six weeks, then a lot of times they'll go ahead and excise it and graft it. Full thickness burns, by definition, extend all the way through the dermis.

They involve at least the fat, they may involve muscle, they might involve bone. So these are very serious burns. The surface of the burn usually appears dry, waxy and white, sometimes black.

So if it's a thermal burn, it's usually dry, waxy and white. You can get brown, dry and leathery, and other burns. No matter which you see waxy, dry, white, okay, brown, black, gray.

The burns that are covered with eschar are usually relatively insensate because you have burned past the nerve endings. But many times the patient will still report pain. And this is why many times you have a combination of deep burns and shallow burns.

So right in this area, I have full thickness, I have ascalonic, but right adjacent to that, I might have partial thickness. And partial thickness burns are very painful.

So we look at full thickness burns, we see Eschar, we're like, okay, well, that's not going to be a painful burn. You always talk to the patient, they'll tell you whether it's painful or not. They may have partial thickness, very close.

One very important thing to think about is that if you have a circumferential burn. With eschar formation, you're at risk for circulatory compromise because the eschar compresses and acts as a tourniquet to the underlying tissues.

So early burn care may involve an escherotomy, cutting through the eschar to maintain profusion of the underlying tissue. So many times you'll see Esther Otomie done. And typically with full thickness burns, they're going to do early excision and grafting.

That helps to prevent complications like infection, like contracture formation related to hypertrophic scarring. So partial thickness, the superficial partial thickness, we manage with moisture. Deep partial thickness.

Initially, we start with moist wound tilling, but if they don't heal pretty quickly, then they may excise them and graft them. Full thickness. Always you are going to excise and graft three phases of management. You know this.

During the emergent phase, you're just trying to save the patient's life. You're doing fluid resuscitation. You can do early wound management, clean, assess unroof large blisters, do escarotomy as indicated.

Then you move into phase two, which is acute wound management. Now, we've stabilized the patient. Our major focus is on burn care. So this is where you do thorough debridement.

So you excise the dead tissue, you graft, and you provide support for healing. And then you move into the rehabilitation phase. And now you're trying to maximize function and maximize psychosocial adaptation.

Also during this phase, you're probably using pressure dressings to minimize hypertrophic scarring. You might be using silicone sheeting to help reduce hypertrophic scarring.

Now, one thing that you'll read a lot about when you talk about burn wounds, one of the critical factors in determining whether or not this patient should go to the burn center is the total burn surface area. It's a critical assessment parameter. It correlates significantly with mortality. And as we've said, with the need for transfer.

There's many formulas used to calculate, calculate total burn surface area. There's the Lund router, there's the rule of nines, and then there's the hand method. You're not usually doing that.

That's usually done in the emergency department, and they usually have charts up in the emergency department that reflect whichever system is being used. Other things to think about and to assess in determining whether or not the patient should be transferred to a burn center. Where is the burn located?

Facial burns, hand burns, burns over feet and joints. Perineal burns are very high risk. For infection or for loss of function? Almost all of those patients should go to a burn center. What about age?

So infants, children, elderly should go to a burn center. What about concurrent trauma? What else happens? You sustained a burn. Do you have other injuries? Do you have pulmonary injuries?

Do you have inhalation injuries? What other comorbid conditions do you have? So the primary indications for transfer to a burn center are significant total burn surface areas.

So again, do you need to memorize this?

No, but you need to be able to reference it and notice that the indications for transfer to burn center are different for children and for adults over 50 years of age. So smaller burn area in children, smaller burn area.

And adults over 50 mandates transfer full thickness burns if it's over 5% total burn surface area.

If you have electrical burns or chemical burns or inhalation injury, again, joint involvement, genitalia involvement, or a lot of comorbid conditions. In managing burn wounds, think what your goals are. Always we're trying to prevent infection and manage pain.

We want to prevent any underlying progression, so we don't want a partial thickness burn to progress to a full thickness burn. How do we keep that from happening? Partly through hydration, partly by preventing infection, partly by maintaining a moist room surface.

Long term, we want to optimize functional and cosmetic results. So when you look at your principles of management, remember you're going to drain large blisters and you're going to debride necrotic tissue.

That's an early goal of therapy. You're going to do escherotomy to prevent any circumferential compromise of the underlying tissue.

Anytime you have circumferential burns, you're going to use antimicrobial dressings typically to prevent infection.

So you know that we've used silvadine for many years, and silvadine is appropriate for both partial thickness and full thickness burns because it does not cause pain and it kills a wide spectrum of bacteria. Sulfomylon you could use only for full thickness burns because it causes a lot of pain, so you'd never use it for partial thickness burns.

And of course, you can use your sustained release silver dressings. That's what we use a lot. You want to always maintain a moist wound surface. You want to absorb your exudate.

So some of the more advanced dressings that you might see used, you might see biologics used, you might see skin substitutes used for selected burns. Most of the time, decisions about biologics and about skin substitutes are made by the burn team.

Typically, we're not making those decisions, but very helpful to be aware of dressings that might be used and how they are used. And again, this is discussed in great detail in the chapter on burn wound management in your core curriculum.

The burns that we manage were typically using our sustained release silver dressings or our non adherent contact layer dressings.

If you're helping to care for a burn over a joint, remember you have to have that splinted at all times to prevent contractures and loss of joint function. And then long term, you're providing protection from trauma, you're providing protection from contamination. You're managing itching.

Itching is a common long term issue. So they're going to be on antihistamines long term. They're going to be on pressure dressings.

They might be on silicone sheet dressings long term to help reduce scarring. They may require. They may require an excision of scar and then use of silicone sheets and pressure dressings.

We want to remind them because it's very frustrating when your burn finally healed and then a week later you've got open areas that increased fragility and increased tendency to blister formation is a common issue for up to two years. So it means you have to protect that area. A lot of times we'll use non adherent protective dressings. We might use solid glycerin based gel dressings.

We might use silicone adhesive dressings, silicone contact layer dressings that just act as a second skin. So if we summarize, this part has all about, has been all about wounds due to oncology processes or oncology treatments.

So we talked about managing cutaneous malignancies. We talked about radiodermatitis, extravasation injuries, graft versus host disease.

And then we talked about thermal trauma to include assessment and staging guidelines, overall management guidelines, and general principles of topical therapy.