Topical Therapy: Infection, Epibole, Hypergranulation, and Wound Pain

Speaker A: 00:00:09

Okay, we're moving on to the second portion of principles of topical therapy.

In this section, we're going to talk about management of infected wounds, management of closed wound edges, also known as epiply, management of hypergranulation tissue, and management of wound related pain. So let's talk about management of infected wounds. Now, we know that all open wounds are contaminated by bacteria.

So sometimes you'll hear people say, why aren't you using sterile technique to take care of that open wound? Because that open wound is not sterile. Any open wound is contaminated by bacteria because we have bacteria on all skin surfaces.

And interestingly, studies have shown that low levels of bacteria can actually contribute to stimulation of the repair process. So low levels of bacteria are not a problem. You want to know the difference between the terms contamination colonization and critical colonization.

You also want to know what constitutes invasive infection. So, contamination means that there are bacteria present on the wound surface, but they're not actively reproducing.

They're causing absolutely no interference to repair and no interventions required. Colonization means that you have bacteria on the wound surface. They are reproducing at a fairly slow rate of.

But the numbers are low enough that they're not really competing with the fibroblasts. They're not interfering with the repair process. And again, intervention is not required.

Critical colonization means that the numbers of bacteria on the wound surface have risen to a level where they are interfering with repair. Now, there's so many bacteria at the level of the wound surface that they're competing with fibroblasts for nutrients and for oxygen.

They're starting to break down newly formed collagen fibers. They're starting to degrade growth factors.

Once the level of bacteria on the wound surface rises to a level that interferes with repair, you have to intervene. Now, as long as the bacteria are confined to the wound surface and there's no evidence of invasive infection, you can treat topically.

You can treat with antimicrobial dressings. But if it progresses to invasive infection, you have to treat systemically. What's invasive infection?

With invasive infection, you have bacteria that are migrating out into the periwound tissues. It's triggering a systemic response. So you're starting to see erythema in duration fluctuance. The level of exudate is increasing.

You might have elevated white count. You might have fever.

At this point, you have to provide systemic antibiotic therapy because you have to reach the bacteria out in the soft tissue around the wound. So we know that very high levels of bacteria interfere with repair.

We know that bacteria out in the surrounding tissue trigger a host response and require treatment. So here are the implications for management.

As we've said, if there's no interference to repair, if your wound is doing well, it's progressing normally, it's continuing to granulate. You don't need to worry about the bacteria.

But once you start to see a plateau or if you see any sudden deterioration, you have to intervene with antimicrobial agents. If you see evidence of invasive infection, erythema in duration, you intervene with systemic antibiotic therapy.

Now, surgical site infections are one of the patient safety issues that are gathering a lot of attention, and so our goal across the country is to minimize the incidence of surgical site infections. And some guidelines have been published by CDC and by the World Health Organization for Prevention of surgical site infections.

You'll hear the terms superficial, deep and organ space infections. What does that mean? Superficial infections are the ones we see all the time. So you're looking at the incision.

There's an area where you've got periwound erythema. Maybe you're starting to see some drainage. The surgeon comes, removes sutures, removes staples.

Now it opens up and it extends into the dermis or possibly into the fat, but there's no deep involvement. A deep surgical site infection extends beyond the fat to the fascia, to the muscle.

So this is where the wound opens up and goes all the way down to fascia level. Organ space infection is where it involves the abdominal cavity, the sternal, the mediastinal cavity, or involves specific organs.

So most surgical site infections are superficial. Some are deep. A few involve organs or spaces.

When you look at the current guidelines for prevention of surgical site infections, they focus very heavily on preoperative measures and intraoperative measures. So preoperatively, we want to encourage patients to eliminate smoking for the weeks prior to surgery.

We want to make sure they're eating a protein rich diet during the weeks prior to surgery, that they're maintaining glycemic control intraoperatively. A lot of recommendations, there's very specific guidelines about when antibiotics should be administered to have maximum benefit.

A lot of guidelines are about appropriate use of iv fluids to maintain adequate perfusion oxygenation guidelines and the importance of keeping patients warm during surgery.

There's very little focus on postoperative management because the recognition is that it's really improving the patient's resistance before they come in, and everything we do to minimize the risk of bacterial introduction and invasion during the surgical procedure, the recognition is that once the surgical site has been closed, it's probably not the post op dressing that makes the difference. So heavy focus on pre op and intraop prevention.

As wound care clinicians, of course, we want to be very alert to early signs of surgical site infections. We want to report them and we may very well be involved in topical therapy for management of superficial and deep infections.

Now let's talk about wound infections involving chronic wounds. And again, we're going to talk about different levels of infections.

When you're managing a chronic wound, what infectious complications do you have to worry about?

The infection could involve the bone, so you might have osteomyelitis, you could have infection that involves the soft tissue around the wound cellulitis, or you might have an infection confined to the wound surface. The clinical presentation will be different for each of those. Diagnostic tests will be different and management will be different.

So we're going to talk about each one of those. Let's start about start with the most serious osteomyelitis, infection involving the bone.

Now the wounds that are highest risk for bone infection are foot wounds because each foot, each of your feet has 26 bones. So any foot ulcer is very close to a bone.

Anytime you have a foot ulcer that has any degree of tunneling or undermining, there's major risk that bone will be involved and bone will be infected. Even if the wound looks relatively shallow and you don't identify a tunnel.

If that wound is not healing normal normally, you have to be concerned that it may be tracking to bone and you may need to recommend an MRI. The other area where osteo is common is in deepen trunk wound.

So if you have stage four pressure injuries involving the sacrum, the coccyx, the ischial tuberosities, if there is any tunneling, if you can see bone or you can palpate bone, osteo is a very common complication of those wounds. So you have a very high index of suspicion with any foot ulcer and with deep trunk wounds or tunneling trunk wounds.

The two major indicators, a non healing tunnel, visible or palpable bone. How do you diagnose osteo?

So even though we know that probably 90% of wounds with visible or palpable bone have osteomyelitis, you can't diagnose osteo simply by seeing or touching bone. You have to get an MRI, a bone scan or a bone biopsy. You can do labs and they can point toward osteo like elevated sedimentation rates.

But the definitive diagnosis is either MRI, bone scan or bone biopsy. So let's say you recommend an MRI. They do an MRI, or you recommend a bone scan because the patient's not a candidate for an MRI, they do it.

The report comes back either presumptively positive for osteo or conclusive for osteo. Now what, what we know is until that osteo is eliminated, until that bone infection is resolved, the wound will not heal.

If the goal for that wound is healing, then you've got to involve infectious disease or orthopedics to establish an effective management plan, which typically involves long term antibiotic therapy. In some situations, if you have exposed bone, they might need to excise some of the infected bone, so surgical intervention may be required.

You should also be aware that some patients will require hyperbaric oxygen therapy. Very hard to eradicate infection involving the bone because bone is very poorly profuse.

So it's hard to get high levels of antibiotics at the level of the bone. The advantage of hyperbaric oxygen therapy is it has a synergistic effect with antibiotics.

So if you give antibiotics and provide hyperbaric oxygen therapy, you make the antibiotics much more effective and you're more likely to resolve the underlying osteo. But osteo is tough and even with long term treatment, you may not eradicate it or it may recur.

The second type of infection that we see a lot with chronic wounds is infection involving the soft tissue around the wound, also known as cellulitis. Now, you're very familiar with this, you've seen this many times.

So you know that the classic indicators of soft tissue infection are erythema that extends at least 2 cm circumferentially from the wound edge heat. So when you palpate the tissue around the wound, it feels warm. There's edema, there's frequently induration.

It feels hard to touch, sometimes it's fluctuant. You might have a patient who has fever. There might be an elevated white count. How do you diagnose cellulitis?

Well, actually, it's typically a clinical diagnosis. I look, I see those classic indicators. I know we have soft tissue infection. Do I have to do a wound culture to diagnose that infection? No.

Look at the wound on the bottom. There might not even be an open wound.

But you know that you have cellulitis, the wound on top, you need a bigger picture that shows more of the peri wound.

But I saw that wound and the erythema extended 2.5 cm from the wound edge, and it was circumferential and it was associated with heat tenderness, edema and induration. We know, just from our clinical assessment, that both of those wounds are complicated by soft tissue infection. Cellulitis.

Current guidelines say, if possible, if there's viable tissue in the wound bed, you should obtain a culture, but the culture is not to diagnose the cellulitis. The culture is to direct your antibiotic therapy. So it's a clinical diagnosis? Yes.

You try to get a wound culture so you know what the infecting organism is, and you know which antibiotics are going to be most effective in managing that infection. Should you do blood cultures? If the patient is afebrile, you do not need blood cultures.

But if the patient is febrile, blood cultures are recommended. Treatment always involves systemic antibiotics. In some patients with good perfusion, you can use oral antibiotics.

In other patients where the wound is not as well perfused or where they're critically ill at baseline or they're spiking temps and their white count is up. Typically, we begin with iv antibiotics.

One thing to be aware of is that if your patient is immunosuppressed or if the wound is ischemic, you will not see this bright red erythema. You'll see a faint halo of erythema, slight induration. Underlying process is the same.

You just don't get such a brisk vascular response because of diminished perfusion or because of immunosuppression. So let's talk about wound cultures. We've all done wound cultures, and many times we've done them incorrectly. So we already said what the purpose is.

We want to identify the infecting organism, and we want to determine which antibiotics are going to be effective for treatment.

Now, the gold standard, according to current evidence based guidelines, is a wound biopsy, also known as a punch culture, where you literally use a dermal punch, you clean the skin, you use a dermal punch, you literally retrieve tissue, send it to the lab. The lab basically pulverizes or grinds the tissue, mixes it with diluent, and then they can do both a quantitative and a qualitative culture.

That's gold standard.

But in many settings, either the lab is not prepared to process that type of culture, or you don't have anyone readily available who's covered to do that type of culture.

So swab cultures are still done very commonly, and there's a specific type of swab culture that gives the most accurate results and the results that most closely align to those obtained by punch biopsy, and that is schwab culture using the levene technique. It's a very simple technique. You are going to flush the wound with normal saline to remove contaminants.

You're going to moisten the swab with normal saline. You're going to select a 1 cm² area of viable tissue. You're going to swab forcefully for about 5 seconds until you moisten the swab with exudate.

You do not swaben slough, eschar or purulent drainage, which is very commonly done. So how many of you were taught to go for the goo? Look at that purulent drainage. Dip your swab in that, get it saturated with that pus.

That's where the good stuff is. No, pus is dead white blood cells, dead bacteria and wound fluid. It does not tell you what's infecting the viable tissue.

So you want to teach your staff, don't swab this purulent drainage. Don't go for pus. Don't go for slough. Don't go for Eschar. Swab 1 viable tissue.

Now let's talk about the type of information that you get back from your cultures. First of all, standard wound cultures are aerobic.

So you're going to, you know, you're going to recover aerobes, your staff, your pseudomonas, that kind of thing. Common culprits. And if you have an open wound, aerobic is what you need.

If you have a deep tunneled wound with very malodorous drainage, you need an anaerobic culture. So you should call the lab to ask them about the technique for obtaining an anaerobic culture in your setting.

In terms of results, you're going to get qualitative results with both swabs and punch biopsies. Punch biopsies will also give you quantitative results. So what's the difference?

Well, qualitative tells you what the organisms are and what antibiotics will be effective against those organisms. So qualitative results, direct therapy, punch biopsy also gives you quantitative results.

It gives you colony counts, so it tells you not only what you've got, but how many. And punch biopsies can be used as a diagnostic tool.

So if your punch biopsy shows that your colony counts are 100,000 organisms per milliliter or more, that's considered independently diagnostic of soft tissue infection. If your colony counts are less than 100,000 organisms per milliliter and you have clinical signs of impaired healing, it suggests surface infection.

But this is important to know. Any level of beta hemolytic strep indicates infection in an acute wound.

In a chronic wound, if you have betahemolytic strep with colony counts greater than ten to the third, that's considered indicative of infection. So I want to summarize, because in most settings, your primary approach to culture is swab cultures.

Swab cultures will give you valid qualitative results as long as they're done correctly. If you have access to punch biopsies, yes, it can be beneficial because it gives you additional data. It gives you that quantitative data.

But routinely, in clinical practice, that's not what you get. Okay. The last type of wound infection is wounds. With surface infection, this is critical colonization.

This is when the levels of reproducing bacteria on the surface of the wound rise to a level that interferes with wound repair. High levels of bacteria interfere with wound repair because they compete with fibroblasts for oxygen and nutrients.

They attack newly formed collagen fibers and break them down. They degrade growth factors, so they interfere with repair in multiple ways. Now, how do I know that I have critical colonization?

How do I know that I have surface level wound infection? I see sudden deterioration in the quantity or quality of granulation tissue, or I have a sudden plateau.

The wound had been progressing, but it stops progressing all of a sudden. It just hits this plateau and is not going anywhere. I probably will have persistent high volumes of exudate.

The patient may complain of increasing pain. There may be persistent odor. I may get recurrent formation of a slimy film on the wound surface like you see in the wound on bottom.

So I'm going to tell you briefly about these two wounds. The wound on top had been doing very well. One week prior to this photo, the wound had been filling very well with granulation tissue.

The tendon was covered. The periwound scan had no erythema, no breakdown, no irritation.

There was minimal to moderate amounts of drainage, and the patient reported pain as being one out of ten. One week later, we come back and the nurses are like, I don't know what's wrong, but that wound looks so much worse. We take off the dressing.

We've had marked reduction in the volume of granulation tissue, re exposure of the tendon, increase in pain, increase in exudate.

When you look at the peri wounds, you see all that erythema, patchy areas of skin loss on the inferior aspect where the drainage was getting trapped against the skin. So multiple indicators that there are high levels of bacteria at the wound surface. The wound on bottom is a venous ulcer.

And you see that you've got this recurrent yellow tissue in the wound bed, a classic indication of what is sometimes labeled biofilm. How are we going to. Well, let me back up. So it is a clinical diagnosis? It's based on our assessment. Is there a laboratory diagnosis at present?

Can you send anything to the lab to rule out critical colonization? Not unless you have access to punch biopsy. If you have access to punch biopsy, yes, you could send a sample to the lab from the wound bede.

And if it came back that you had elevated bacterial counts, less than 100,000, but more than 10,000, that, coupled with your clinical indicators at this point in time, would constitute a diagnosis of surface infection. Most of the time, we base our diagnosis simply on clinical findings. So now how do we treat it?

Well, we want to do aggressive cleansing to reduce the levels of bacteria on the wound surface. If we have evidence of this recurrent film, we want to disrupt the film.

We can disrupt the film by use of a blunt curette, by use of a debriding swab or mitt with galls moistened with saline. You use what you have to disrupt that film and reduce bacterial counts on the wound surface, and then you're going to use an antimicrobial dressing.

Now, one thing you have to think about with surface infection is that wounds that have surface infection are at risk for biofilm formation. So what is biofilm? It's a community of bacteria that are protected by a slimy film.

And that slimy film repels white blood cells, repels antibiotics, and repels most of our antis, most of our antiseptics. Dental plaque is the original biofilm. So you think, how do you clean your teeth when they feel furry? You scrub them.

You mechanically disrupt that biofilm. And that's because it's very difficult to penetrate biofilm with any kind of antiseptic agent.

What we know, pseudomonas and staph are bacterial agents that are commonly associated with biofilm formation. And we also know a little bit about how biofilm forms.

So as bacterial counts on the wound surface rise, bacteria begin to communicate with each other through a process known as quorum sensing.

But I have a cartoon brain, so in my head, what happens is, as the bacterial counts rise, they start talking to each other, they start alerting each other to what they perceive as threats.

So think about sending out a text to all your fellow bacteria that says, increased number of white blood cells patrolling the area, talk of dacons and possibly antibiotics. We have to work together to protect ourselves. Meet at Starbucks at seven. Well, then what happens is they band together to produce this slimy film.

They hide behind that film, and that film repels the white blood cells repels the antibiotics and repels most antiseptics, so they're literally protected. In the meantime, the level of inflammation in the wound rises because the increasing bacterial counts trigger white blood cell migration.

But when the white blood cells get there, they can't get through, they can't do anything. So in the end, you end up with this gated community that protects the white blood cells. You end up with persistent inflammation.

How do we diagnose biofilm? At present, no diagnostic test. It's a clinical diagnosis.

It's failure to heal, sudden plateau, sudden deterioration, and possibly that recurrent film on the surface of the wound. How do you manage these wounds?

We've already talked about mechanically disrupting any recurrent film using blunt curette, your debriding sponge, wet gauze, break it up, irrigate it thoroughly, and then use your antimicrobial dressing. So when you see the term planktonic bacteria, planktonic bacteria are free floating. They're no longer protected by the slime.

So you have disrupted the slime. Now all the bacteria are running for cover. That's where they're vulnerable.

So now we use antimicrobial agents on the surface of the wound to kill the bacteria and hopefully to prevent recurrent biofilm formation. A lot of research going on at present to determine if there are antiseptic agents that are available to us that will penetrate biofilm.

And here's what we've learned so far. Cadeximuriodine, also known as iotosorb or iodoflex, can penetrate biofilm, at least in the lab. So this is the way it works.

It's iodine suspended in a starch base. So as it absorbs exudate, it releases iodine in its. It's an exchange program. Absorb, release, absorb, release, absorb, release.

And in the lab, it can penetrate biofilm. So if you have access to cadex, myriadine, and you're concerned about biofilm, you think you have biofilm formation.

That would be a very good choice, so long as the patient has no iodine allergies and it's not a very large wound.

There are some new surfactant gels on the market that act on biofilm very much like soap acts on grease, so helps to break down the biofilm, penetrate the biofilm with the surfactant gels. They usually have to be applied daily. So you have to think, is that going to work with this wound and with this care situation?

We are going to learn a lot more about biofilm. We're just beginning to learn. It's an area of intense.

So when you go to conference and there's a presentation on surface infection, biofilm, go, you pick up your journal, there's an article, read it. We are going to end up with multiple options for managing biofilm. We're just not there yet.

So if we put it all together and we talk about managing infected wounds, if there's a any necrotic tissue we want to debride, if there's biofilm, we want to break it up, we want to use forceful irrigation for cleansing, and then we want to use topical therapy for surface infections.

So some combination of antiseptics or antimicrobial dressings, and we want to use systemic antibiotics for soft tissue infections where we have invasion into the surrounding tissue, definitely systemic antibiotics for any infections involving bump.

So the last thing we're going to mention about wound infection is the topical agents that are available to us that allow us to reduce bacterial counts at the level of the wound surface. Antiseptics are frequently preferable to antibiotics because antiseptics have very broad spectrum effects.

They essentially kill all bacteria, and many of them are selective. So they kill bacteria while protecting the good cells. Some antiseptics kill bacteria but also kill good cells.

So we have to know for each agent, how does it work? What impact does it have on bacteria? What impact does it have on good cells, fibroblasts, keratinocytes?

Can I use it in a wound that is in the proliferative phase, or should I limit use to wounds in the inflammatory phase? So what about dacin, sodium hypochlorite, or a comparable dilute bleach solution?

In general, you're gonna limit use of that type of antiseptic agent to wounds in the inflammatory phase. You're going to discontinue that once the wound moves into the proliferative phase. What about povidone, iodine, betadine solution?

You're going to limit use to wounds in the inflammatory phase. You're going to discontinue use when the wound moves into the proliferative phase. What about acetic acid? Quarter percent vinegar? Essentially.

That can be very effective against pseudomonas. But again, once you establish a clean wound bed, once you get the pseudomonas under control, you want to discontinue use.

What about antimicrobial dressings? The advantage of antimicrobial dressings, again, they're broad spectrum, so you don't have to use, you don't have to do a wound culture.

You can use them for any wound with surface infection, and they're non cytotoxic to good cells. So you can use these dressings for any wound where you're concerned about high bacterial loads at the wound surface.

And you don't have to wait for a culture. Codeximar iodine we've already discussed sustained release iodine. Very effective with exudative wounds, not effective with dry wounds.

Has the advantage of penetrating biofilm, at least in the lab. But you do have to consider the size of the wound.

You don't want to run the risk of iodine toxicity, and you have to make sure the patient does not have iodine allergy or shellfish allergy. What about sustained release silver? We have many, many silver dressings.

So we have silver gel, silver alginate, silver hydrofiber, silver foam, silver hydrocolloids. You name the type of dressing, we have it with silver. That means that we can select a silver dressing that matches the characteristics of the wound.

If we need an absorbing agent, we can pick a silver dressing that absorbs. If we need a hydrating agent, we can pick a silver dressing that hydrates.

Now there is a wide variety of silver dressings, so some of them donate silver to the wound bed and kill bacteria at the wound surface, and others absorb exudate into the dressing and kill within the dressing. So we'll talk a little bit more about that as we move into dressing selection.

Whenever you're talking to your vendors about their formulary and products, they have a good question to ask them is how does this silver dressing work?

Now there have been major concerns about bacterial resistance to silver because we've used silver extensively in wound care, and we certainly know that with use of antibiotics, bacterial resistance has been an issue. But our evidence to date shows very little indications of bacterial resistance to silver.

And that's probably, probably because as a category, silver and other antiseptics have multiple mechanisms of action for killing. So while an organism is trying to develop resistance to one killing pathway, another killing pathway takes them out.

So, so far, silver has been shown to be safe, non cytotoxic to good cells, generally effective against a wide range of bacteria and low risk for resistance. What about your methylene blue and crystal violet polyvinyl alcohol foams?

You can get the methylene blue, crystal violet polyvinyl alcohol combination, or you can get methylene blue, crystal violet and polyurethane pump. These are your hydrofuryl blue hydrofiroblue ready hydrofuryl blue transfer and your RtD dressings.

This combination of antimicrobial agents in the lab has shown to be very effective against a broad range of bacteria also have anti inflammatory effects. Right now, they're available as flat foam dressing and as tunnel dressings. Some do have to be pre moistened.

So they're a major tool in your toolkit for managing bacteria within open wounds. If that's an option you have, it's going to help you to manage these wounds. What are the other things that are out there?

There's AMD dressings that stands for antimicrobial dressing. It comes in roll galls and in strip galls. The active agent is phmb polyhexamethylene bi guanide. Again, a broad spectrum antiseptic agent.

There are manuka honey based dressings. Now, honey is a very effective debriding agent. It works for autolytic debridement because honey is hypertonic.

So it's going to attract fluid, the surface, that's going to enable white blood cell migration. It's the white blood cells that do the debridement. But manuka honey also has weak antimicrobial effects.

So if you're using a manuka honey based dressing to promote autolytic debridement, you're also getting some antimicrobial effects. And the newest entry into the antimicrobial dressing arena is your DAC dressings, dialkyl carbamoyl chloride dressings.

And they look just like a very simple mesh type dressing, but they are hydrophilic. So they attract bacteria to the wound surface, and then the bacteria binds to the wound surface or to the dressing surface.

I'm sorry, it attracts the bacteria to the surface of the dressing, binds the bacteria to the dressing, and when you remove the dressing, you remove the bacteria. So we need a lot more data. But what I want you to recognize is that we have increasing options in our war against surface bacteria.

Whenever you're talking to a vendor, you want to know what options they provide, what data they can supply in regards to their agent.

So to summarize, infected wounds, and we're almost through here, you have to intervene when you have invasive infection involving the soft tissue or the bone. You have to intervene when surface bacteria rise to a level that interferes with healing.

The last things we're going to review, we've talked about one of these already, and that is management of wounds with closed wound edges and management of wounds with hypergranulation tissue.

We've talked already in the class on wound healing about the fact that if your wound edges close prematurely, they will prevent epithelial resurfacing. So when your wound is fully granulating and approaching skin level.

You have to look very closely at your wound edges, and if they have closed, you have to intervene to create open wound edges that permit keratinocyte migration and resurfacing. At this point in time, we have two options.

We can cauterize with silver nitrate, so we can take a silver nitrate stick, wet it with water, and go right along the base of the wound edge so that we're burning off the epidermal cells at the womb surface.

It's going to take more than one treatment, because remember that the epidermis is about 15 to 20 cell layers thick, and each treatment will burn off only two to three cell layers. So most of the time, it's going to take five to six treatments. So you treat, you will see the skin change color. It will turn gray.

Once that gray layer sloughs off, you can retreat. Now, many times, the wound edges are insensate so you can do cauterization, and it causes absolutely no discomfort.

In some patients, the wound edges are sensitive. If there's any sensitivity, you can use topical lidocaine to numb the wound edges before you treat.

If cauterization is ineffective, the other option is to take a sharp curette and literally to pair the wound edges. Advanced practice nurses are covered to do that. Physicians are covered to do that. So if you can't do it, you want to see who on your wound team can.

What about hypergranulation tissue? We see a lot of that in chronic wounds. We know that if there's hypergranular tissue, it literally causes a mountain effect in the wound bed.

That makes it very hard for your keratinocytes to resurface, because now they're just not moving across the wound surface. They're having to climb up and over.

So whenever you see hypergranulation tissue, you want to treat it, you want to flatten it out, and you want to keep it from reforming. So it would be really helpful to know what causes it. And unfortunately, we're not sure.

The theories are that if there's high levels of moisture at the wound surface, that that might promote hypergranulation, tissue formation or that heavy bacterial loads might promote hypergranulation, tissue formation. So we are not sure what causes it, but we do know how to treat it. We know that you can take silver nitrate, roll it across the wound surface.

It will burn off the top layer of granulation tissue and flatten out the wound surface. It will also inhibit bacterial reproduction, so it will help to establish low bacterial loads at the wound surface.

Then you can cover with an antimicrobial foam to keep bacterial counts low and to reduce level of moisture at the womb surface. So cauterize and use an antimicrobial foam. The last thing what about wound related pain?

So important because even though it's the last thing we're talking about for many patients is their number one concern. So you never want to forget this. So you always ask your patients how much wound related pain they're having, what's the severity?

When do they have the pain? Only when they're getting wound care. Or is it around the clock? If it's persistent pain, around the clock analgesics will be required.

You may have to refer them to a pain center so that you get a pain specialist involved. If it's procedural pain, you can premedicate. You can use topical lidocaine, allow time for that to take effect.

So most of us use 2% lidocaine gel and wait ten to 15 minutes. You also want to be sure you're using very gentle technique in providing wound care. You don't want to snatch dressings off. You want to peel them off.

You want to use gentle technique when cleansing wounds and you want to put the patient in control.

Allow them to call timeouts, allow them to take off their own dressing, anything that makes it easier for them, and that reduces the level of pain associated with wound care. So in summary, if you have infected wounds, your first goal is to determine, well, what structures are involved in the infection.

If there's evidence of bone infection, you want to treat with long term antibiotics, you will have to involve infectious disease. Hyperbaric oxygen therapy may be beneficial.

If you have cellulitis, soft tissue infection, you should be using culture directed, culture based antibiotic therapy. It could be oral if the wound is well profused. It could be iv if you have severe infection or a poorly perfused wound.

If you have surface infection, you want to disrupt any biofilm and you want to use topical agents, antimicrobial dressings, closed wound edges, epipyly, you're going to cauterize with silver nitrate or you're going to use a sharp curette to excise that wound edge hypergranulation tissue. You're going to use silver nitrate in an antimicrobial foam and never, ever forget to assess and manage wound related pain.

In our next class, we're going to focus on dressing selection. So don't think we forgot that we didn't. We're just going to come back to that. Thanks.