Description

Wound management can present a variety of challenges for the whole veterinary team, with various reasons for why a wound may not progress through the normal stages of healing. Biofilms are established as a serious complication in human health care, leading to chronic wounds, but how concerned should we be about biofilms in veterinary practice? This webinar aims to discuss how these complex colonies of bacteria can lead to delays in wound healing and how we can effectively manage and prevent biofilms. The webinar also explains what exudate is, the benefits of exudate, causes of excessive exudate and what impact this has on the wound and how to manage exudate effectively.

Transcription

Welcome to this talk on managing exudate in wounds in small animal practise. My name is Elisa. I'm an advanced practitioner in small animal surgery, and I work mainly in the field of soft tissue surgery.
Learning objectives exudate, how it's formed, the benefits and negative impacts on wounds, causes of excessive and decreased exudate, and also how to manage exudate. Exudate explained. So what is wound exudate?
The fluid that leaks from capillaries during the wound healing process is normally what we would classify as exudate. It occurs as part of the inflammatory phase of wound healing. When an injury occurs, neutrophils will migrate into the wound during the 1st 3 days, and they release a compound called nitric oxide, which helps to kill bacteria.
This compound is also a potent vasodilator, which will then increase blood vessel permeability, and this causes a protein-rich fluid to leak into the tissues. Combination of the protein-rich fluid, cells, and inflammatory mediators will make up what we call wound exudate. If an animal becomes hypoxic or hypothermic during a surgical procedure, this may affect the neutrophil function and therefore local immunity to infection.
Wound exudate is mainly water, but also contains electrolytes, nutrients, proteins, inflammatory mediators, protein digesting enzymes, or as we like to call them, MMPs or matrix metalloproteinases, growth factors and waste products, and various types of cells, neutrophils, macrophages, and platelets. MMPs are very crucial in all stages of wound healing, as they will modify the wound matrix and allow for cell migration and tissue remodelling. Some types of wounds that we would classify as being in the inflammatory phase, from left to right.
So this particular wound here was an avulsion and you can see that the skin has been torn away from the underlying tissue. The wound in the middle is an RTA, so a road traffic accident where an animal has been dragged along the tar and caused severe abrasions, and the wound on the right is a surgical wound breakdown over an implant on a tibia, . And you can see that the metal of this implant is now exposed.
Examples of wounds in the proliferative phase, from left to right, a dog with a post-surgical skin loss after tarsal arthrodesis. This wound was managed with moist wound healing dressings, and eventually a flap local flap of skin was used to close the wound. The following two wounds have got a very nice example of granulation tissue.
Both of these have been treated with negative pressure wound therapy, which we will talk about later, which does produce an incredibly even nice bed of granulation tissue. Characterised wounds in in the proliferative phase all have this lovely granulation bed. What are the benefits of exudate?
So exidate is a natural normal thing. It is there for a purpose. Purpose number one is that it stops the wound bed drying out.
2, it aids migration of tissue repairing cells, so they move more easily in this fluid. Number 3, it provides essential nutrients for cell metabolism. Number 4, it enables diffusion of immune and growth factors.
And number 5 assists in separation of dead or damaged tissue or pholicis. So it basically helps to clean up the wound as well as helping the cells that are required to migrate across. Unfortunately, wound exudate also has negative impacts.
If wounds are not healing as expected in chronic wounds, The exudate that is present often contains very high levels of inflammatory mediators and activated MMPs. Although these are essential in wound healing, high levels of them can delay wound healing. The other problem is that excessive exudate can also contaminate the periwound skin, which may lead to maceration or damage.
It can also contaminate bandages and the environment. This is an example of a wound that has become macerated. You can see that we have a wound on the ventral aspect of the animal near the anus.
We have a sutures placed around it, which indicates we had a tie over dressing on and you can see that the skin around the wound has changed colour. There is also some white ointment, which is a barrier cream that has been used to try and prevent maceration of this wound. Causes of excessive exudate.
The most common reason we see excessive exudate is that the wound has become what we would call stuck in the inflammatory phase, which means it has not moved past phase one into the proliferative phase. Causes in dogs and cats usually correlate with factors that would affect or delay wound healing, and most commonly these are local factors. Infection is one presence of dead and revitalised tissue, excessive dead space, so that means a big gap in the wound, wounds in high motion areas, and certain types of wounds, for example, bones, will produce a lot of exudate.
Metabolic or systemic factors are of much lower importance in domestic animals. So generally, if a wound isn't healing and there's a lot of exudate, we need to look locally and try and work out what the cause of this might be. This is an example of an infected wound.
This is the bottom of a cat, the anus is off to the right hand side, and you can see that the wound has got the sort of horrible sticky exudate, and this wound was in fact infected. This wound is an abrasion stroke degloving wound in a cat that suffered a road traffic accident, so you can see there are some defects in the skin, but additionally quite a lot of bruising and damage and devitalized tissue which is going to go on probably to necros, and because of that we've got a huge amount of exudate and this wound is definitely in the inflammatory phase. This is a wound with excessive dead space, so what we mean is that the skin here, you can see has been pulled away from the underlying tissue, leaving a big pocket or gap.
And when there is a big pocket or gap, the body will try and fill that with fluid, and this is why we end up with exudate when we have lots and lots of dead space. This is a dog that jumped over a fence and became impaled on us. You can see two nice wounds either side of the groyne.
This is a classic high motion area, so the, the bit where the hind legs meet the body, the other place we would find that is the axilla or the armpits on the front legs. So anywhere where there is a lot of movement, we can expect wound healing to be delayed and we can expect excessive exudate to form. Burn wounds.
Both of these are iatrogenic heat mat burns that have occurred on the dorsum of an animal. You can see the one on the left, we have quite a thick air char, sort of a big piece of dead necrotic tissue, and in the one on the right hand side, the necrotic tissue has been removed and we're left with the wound as it is to now go on to heal. Classifying exudate.
Colour, consistency, odour, and volume can all give us clues as to the underlying issues affecting our healing. Please be aware that some hydrocoloid dressings will produce a really malodorous exudate, and this is not to be mistaken for infection. Once you see healthy granulation tissue, i.e., the wound has moved into the proliferative phase, any bacteria in surface exudate is of no clinical importance.
Very common for people to swab wounds that have granulation tissue, culture all sorts of nasty bacteria, and then try and hit them with systemic antibiotics. This should not be necessary as granulation tissue provides a complete barrier to infection. And therefore, all you're doing is creating resistance by giving antibiotics to these animals.
Most important thing with classifying exudate is that we document all the characteristics of the exudate at each dressing change, especially important if you're not the only person dealing with that particular wound. It's best to write in text and clinical notes and describe, but also taking photographs if possible. This will really help the next person who comes along and even yourself to remind you what the wound looked like last time so that you can see if it's progressing in the right direction and if you need to change anything, then you can do it early.
Causes of reduced exudate. Very uncommon problem in domestic animals. We don't have the factors in in in humans that that cause a problem in humans, it's normally down to ischemia and dehydration.
It normally in small animal practise indicates that the wound is progressing and healing. And normally it's because we've applied a dressing that is maybe inappropriate for that particular wound, so a wound that a dressing that's too absorbent for the actual exoate level of that particular wound. Managing exudate.
We need to manage exudate effectively because it does have positive effects on the wound. However, as we've seen, too much of it will delay wound healing and potentially also cause problems with the skin around the wound. Usually manage exudate by using dressings, and there's lots and lots of them out there with different levels of absorption, which we're going to talk about next.
But also bear in mind that there are newer technologies out there such as negative pressure wound therapy or VAC therapy, which is very, very handy in keeping wounds at their optimum moisture levels. It's very important to record the characteristics of the wound at each dressing change so that we can make sure that we're progressing the wound in the right direction. And in the fact that now everybody has good mobile phone cameras, this has never been easier to do, and there's really no excuse for not doing it.
Managing exudate. At each dressing, exudate should be evaluated, and there are 3 possible things that we can do. So we either need to increase the amount of wound moisture, and for that we would use a dressing type to conserve or donate moisture to the wound.
We would potentially use a thinner or less absorbent type of the same dressing, or we would decrease the frequency with which we're changing the dressings. If we need to maintain the moisture level, we will continue on the current dressing regime, and if we feel we need to reduce the amount of moisture, we would use a thicker, more absorbent version of the current dressing. We would change to a dressing that has greater fluid handling capacity.
We would potentially increase the frequency of the dressing changes, or we would go to something completely different like negative pressure wound therapy. When do we change the dressing? Well, any sign of strike through, any leakage of exudate, and any signs of the skin becoming macerated.
Better to change too frequently than not frequently enough. When changing the dressing, really important to note any changes and whether we need a more absorbent contact layer or whether the frequency of dressing changes needs to be increased. So talking a little bit about negative pressure wound therapy, as it's a very handy, useful management tool in wound management, particularly when we have high levels of exudate.
Negative pressure wound therapy or back assisted closure involves application of sub-atmospheric pressure to a wound via a foam dressing that is sealed with a film. Benefits of it are that it removes excessive exudate. Because of this, it also decreases the interstitial pressure in the tissues and reduces wound edoema.
And because of this, we get better oxygenation to the tissues, which will stimulate healing, also causes an ingrowth of blood flow and new capillary, so promotes angiogenesis, which is why we get such lovely granulation tissue forming. And it also removes all this exudate which is going to slow down wound healing. And of course, because it's a completely sealed system, the exudate cannot contaminate the periwound skin or cause any sort of maceration.
This is an example of a wound prior to negative pressure wound therapy. There's excessive exudate in this wound. It was dead space and it's in a very high motion area.
This was in the groyne of a dog that had another dog that had impaled itself on a fence, and you can see that the tissue does not look particularly healthy. This is the negative pressure wound therapy applied. You can see it's sort of the inside thigh groyne area of this dog.
And here the dog is carrying the pump around on its own, so we've strapped it to the dog's harness. And this is post negative pressure wound therapy. This is two cycles of 48 hours each, and you can see a dramatic change in the quality and consistency of that wound.
So this is now a healthy wound that's ready to close. And here we have clothes that we've literally just pulled the skin together, put in a closed suction drain, and this wound went on to heal very nicely. So in summary, exudate is a normal part of the wound healing process and important in facilitating moist wound healing.
Excessive exudate can have a deleterious effect on wound healing. And is effectively managed using appropriate dressings and technologies. Accurate record keeping is vital when managing wounds and can be aided by taking photographs of the wound at each dressing change.
Thank you for listening. Hello everybody, and thank you for joining us, for this webinar. We're going to be discussing in this part, about wound biofilms and infections in small animal wound care.
I'm Amanda. So some of our learning points for tonight should hopefully be for us to be able to identify infection versus inflammation and the different signs and symptoms we may see between the two of those. We're then also gonna be looking at bacterial loads and contamination as an overall in our wounds.
And also then looking at an overview of what biofilms are, how we can prevent them, how we can detect them, and also some management potential as well. And we're also gonna be looking at the prevention management of infected wounds overall too. So looking at what infection versus inflammation is, we kind of really need to start by looking at maybe what separates these two things, and it can be quite difficult and quite challenging at times.
Our inflammatory phase will typically start, usually on day 0, so as the wound initially is created and can last up until about day 6. Inflammation is a natural stage of our wound healing, and there are certain characteristics that we would expect to see during these early stages, and these typically can include exudate. So this can be clear or erro sanguinous in colour.
Usually the amount of it should be only mild to moderate, but again, that's going to depend on the size of your wound and how it's been caused, and we should be seeing kind of minimal to, to no odour really. We may get a certain amount of redness, a certain amount of erythema that can be kind of generally localised to around the wound bed. We're also going to get an extent of localised swelling, so we're going to see some edoema in again that surrounding tissue.
And we're also going to see as well some, non-viable tissue. So we may see some necrosis, or some really green fluffy vitalized tissue. That can be pretty standard.
But in our infected wounds, we may see some of these signs, but generally they will be more exasperated. So we may see a disproportionate. Amount of these normal signs of information to the size of our wounds.
So if you've got a relatively small wound that's actually showing quite a lot of signs of inflammation, I may be sort of looking to assess that a little bit further. Have we got changes in our ex date between dressings, the level of it, the colour, odour, or can help us point to whether we've got infection or inflammation going on? Are we seeing increases in pain in devitalized tissue, is that going up instead of down as we would typically expect it to as we move through the inflammatory phase?
Is there spreading erythema? Is the redness and is there spreading edoema? Is there spreading out further into our surrounding tissue?
Are we starting to see pocketing? Is our granulation bed changing as we move through the inflammatory phase, we should start seeing our granulation bed. Move on to being quite nice and pink and typically that kind of strawberry jam colour that we're looking for, it shouldn't be pale or sensitive and it shouldn't be easily haemorrhaging.
So sometimes it's a little bit easier for us to be able to compare these signs and symptoms side by side. So we've got two wounds here. Both have been surgically repaired.
One has both, both of them have moved through their inflammatory phase or should have been moving progressively well through their inflammatory phase. The one side we've got a post-op wound adhesence of a mast cell tumour removal, and the other side we've got a traumatic injury, and aetiology and a cat leg. And again, this one on this side may have been closed a little bit too soon.
It tends to be moving through the standard phases of inflammatory signs, which we can see here. So we've got some localised swelling. We've got minimal exudate.
It's fairly clear as well. We've got some erythma coming around the edges of these wounds, and we've got some devitalized necrotic tissue as we would expect. But Lynn, comparing to this side on this wound, We've actually got a pale, really kind of not healthy looking granulation bed there.
You can't really see it on the photo, but we actually had quite a lot of pocketing going further underneath this wound. We've got erysema that's starting to spread out. The devitalized and nec carottic tissue is also spreading and it exudate was quite thick and perulent and fairly odorous.
So again, it's just looking at these signs and going, what's normal and what's not for our inflammatory phase. So now we're gonna talk a little bit about bacterial loads and contamination. So as a standard, our main aims of wound management should be moving and progressing through the inflammatory phase into our prolative phase, getting it through and facilitating the natural healing process.
We're not looking to speed this up, but we're looking to really make the environment as optimal as possible for us to be able to progress our wounds through to healing. We should consider that all wounds that are presented to us, especially probably in the veterinary field, are going to be contaminated. Any kind of break in the skin, bacteria can move in.
So it's a good little thing to live by. And also in our chronic wounds. We don't see chronic wounds quite the same as, they do on human medicine side.
But again, if we're starting to see a wound that's not really progressing as normal, we should be considering that maybe there's a bit of a fire burden going on in that wound. So what do we need to consider? How are we going to decide this wounds infected, it's not moving on as it should be.
There are a couple of things that we can Look for in some factors that may affect this. So the aetiology of our wounds, how it occurred, bite wounds are more than likely going to be more susceptible to having a higher level of bio burden maybe than some other wounds are. But we also see a lot of traumatic wounds where there's going to be a high amount of debris or road traffic accidents, these kind of wounds, they'll tend to come in and be, to be fairly full of foreign material.
And also it can come down to the pathogenicity of what's in our wound or the virulence of our microorganisms that are present as well. And we should be considering that. Any wound that could have the potential to be infected, we'll be looking at what level that bacteria reaches, and we'll go through now some of the different levels of bacterial load.
So, as you said, all wounds that present should really be considered to be contaminated. There's a break in that skin barrier. So there is going to be some compromise in the defence mechanisms and it's going to lead and Allow bacteria to start proliferating, especially if we don't initiate some wound management.
But generally in this initial stages of contamination, this should be fairly easy for us to remove using good debridement and lava techniques. This shouldn't really impede our healing. Then we move on to where you've got some more bacterial pro proliferation, so colonisation, that bacteria is starting to replicate a little bit more rapidly, and we're gonna start seeing increases in our bio burden.
And also the bacteria is going to start adhering and binding to our wound bed. So it's not quite penetrating deeper tissue. It is still on the surface, but we are going to see some of that bacteria starting to stick, and this is where our biofilms are going to start coming in and they're going to be starting to become a little bit more virulent.
But again, through good wound management, we should hopefully have no impeding of our healing. We should be able to look at using techniques that we'll discuss a little bit later that should help us to minimise and hopefully remove this colonisation. So then we move on to our, our more critical colonisation then.
This can also be referred to as a more localised infection. So we're starting to see the host immune system be a bit overwhelmed. They're not going to be managing that by a burden as well.
This shouldn't still again be a deeper invasion of tissue. And not as much of the surrounding tissue is involved as with further colonisation, but, we'll still start to see those signs of infection, kind of ramping up. There's quite a nice mnemonics that you can use, which is, nerds.
So is our wound non-healing. Is there changes in our ex date? Are we seeing red friable tissue?
Is there debris, so an increase in devital necrotic tissue, has the odour changed the smell? And 3 or more of these are gonna kind of point us along that we've maybe got a bit of critical colonisation going on. And these can actually cause a prolonged inflammatory response.
Then we move on to our localised invasive infections. So this is where our bio burden's really getting embedded and starting to invade that deeper tissue. We're going to see a lot more of our surrounding tissue involved.
And again, I say that deeper tissue is going to start to become infected. Our granulation bed isn't going to be forming like it should be. The host immune system's going to be pretty much overwhelmed at this point, and it's not going to be managing it on its own.
So again, we're going to see some changes in potentially the size of our wound. We may see temperature changes around the surrounding skin may feel warm. There may be bone involvement.
Again, we're not going to be seeing healing. We're not gonna be moving out of that inflammatory phase, and we're not going to be moving on to our proliferate phase like we should be naturally. We're going to see changes in exudate.
Further edoema, and again, that smell of that wound, so odours and things are gonna change. So all of these things, again, 3 or more of these kind of things together, we should be maybe thinking actually if we got a bit of a deeper, more invasive problem. And then finally I'm not going to cover this too much.
It's probably not as common to see systemic infection in animals, . Typically, we do tend to kind of intervene and their bodies do tend to kind of cope quite well, but it can happen and it is something to be very aware of, especially when you're dealing with kind of implants, open fractures, all these kinds of things. There's going to be a higher risk of us seeing bacteria rema.
So we're going to see that surrounding tissue becoming involved. We're going to start seeing signs of Sepsis says, I'm gonna start seeing signs of more systemic infection going on. So we're going to move on to talking about kind of what actually biofilms are, how they form and, and how we can make maybe manage these and how maybe these are becoming a bit more relevant in veterinary medicine now.
Biofilms have been quite known through human medicine for a number of years now, and there is more research going into it. So these are basic microbial communities. So as we said, our wounds are contaminated generally as soon as they happen.
So you'll have planktonic bacteria or other microbes that are sitting planktonically just on your wound bed. So they're in a single state at this point. But what can happen, if these are left to proliferate and carry on growing, they can actually then become communities.
So they'll form these communities, they'll be embedded in a matrix, which basically allows them to grow and adhere to our wound bed. And this is what can cause us problems. Because once they start to adhere to our wound bed, they're actually very difficult to get rid of.
They can also, due to this extracellular matrix that they embed themselves in, they can actually be less susceptible to our topical and biocidal agents, and also our impregnated dressings and systemic antibiotics. So they can be really, really difficult to actually manage once they've become mature and once they've actually formed and adhered to that bed. There is a little bit of a mess that you could potentially see a mature biofilm.
You may read some studies that suggest that it can cause and create a kind of viscous, almost shiny film over the top of the wound bed. But actually this is a little bit of a mess. If you're seeing a biofilm, it means it's in the really, really late stages, .
And management has not been initiated for quite a prolonged period of time. So, more than likely, most of the biofilms that we're going to be dealing with in practise, we're not actually going to be able to see. And again, visualisation alone isn't adequate.
If you've got a wound that is not progressing as you would expect, more than likely just assume that you've maybe got some sort of biofilm or critical colonisation going on in that wound. So what are the stages of our biofilm cycle? So as we said, so stage one, we're looking at the wound occurs, our wound becomes contaminated, and we've got bacteria sitting there in this planktonic state.
So the planktonic microbes will actually kind of begin to aggregate, so they start to join together, and this can happen fairly quickly. And it's still reversible at this stage, even when they start to kind of form together to start looking like they're going to create a colony. The body's innate immune response should be able to deal with this, and it should be able to actually reduce that by a burden again, if we're initiating general kind of wound management, as well.
Stage 2 is the kind of critical stage really. And this is where you start to get your colonisation and permanent attachment occurs. So these actually occur quite quickly.
It can be within 2 to 4, up to kind of 6 hours really, that this happens, and this is where these colonies start to form and they become irreversibly attached to our womb beds. It just makes them a lot more difficult to remove. The bacteria actually starts communicating with each other, and their behaviours can start to, to change.
So they do something which is known as quorum sensing. So when they form these colonies, they can actually start to change gene expressions. It can alter the patterns in their behaviour, and they can actually start to communicate and share between different types of, microbes as well.
They can actually start to share different, Different qualities with each other. Then we're moving on to stage 3 of the biofilm. So again, this is where it's going to start to be further, proliferation of that polymicrobial, bacterial colony.
Typically they are polymicrobial. You can see some biofilms that may just be singular species, but a lot of the time they are actually full of a couple of different types of species together. This further kind of viscous, shiny film known as the extracellular, extracellular polymeric, actually starts to grow further at this point and this actually feeds all of the microbes inside of it.
So it contains lots of nutrients. It also contains the bacterial. DNA and proteins.
And this really does help to further develop and it also deprives all of our, our natural healing cells of oxygen and nutrients as well, because it'll start to soak those up. And again, we're going to start seeing further resistance to, topical and systemic biocides at this point. Stage 4 to stage 5.
This is where we're going to see the biofilm really maturing, So typically these colonies at this point, again, they're full of these different types of single species of bacteria that are all now floating around and sharing their quorum senses so that they're sharing lots of different, characteristics between each other. And they're just a lot, a lot more difficult to remove at this stage. They'll start to also then form almost a mushroom shape.
They'll start to protrude out of the wound bed ready to move on to stage 5, which is where they will then disperse bacteria back into a planktonic state. This bacteria then hits our wound bed in different places, and further, colonies of biofilms will start to form. So as we slightly discussed during the cycle of the biofilm, they do have a lot of characteristics that really work together to impede our healing.
So they share nutrients in that EPS. That EPS also acts as a, as a barrier, so it can prevent our biocides, our antibiotics, and our antimicrobials penetrating and actually dealing with that bacteria. It increases our inflammatory response, basically by increasing a macrophage response, but this then also increases their cell death.
They can help to release endotoxins and exotoxins, which really alters our wound bed, and it can really impede healing. They do this through a lot of different, processes. There can be a lot of systemic factors.
We can see it through ischemia, movement, malnutrition. Patient interference, all of these can contribute to delays in healing and also increase the risk of biofilm development. Most studies are suggesting to us that it's this prolonged prolonged inflammatory response that's actually causing the problem and that actually allows the biofilm to progress.
So our growth factors are going to be destroyed. Our membrane receptor proteins are going to be degraded, and excelling matrix proteins again, they're going to be destroyed and all of these things which usually work together. To actually help and heal our wounds and progress it out of the inflammatory phase.
But instead the biofilm is actually gonna start affecting and creating rises in proteasers. Most commonly it's the neutrophilastase and our, matrix metatala proteases, so our MMPs, and these are what contribute to actually reducing all of our, they basically, they accidentally destroy all of our essential proteins that we need for healing. And again, during this pro-inflammatory phase, we may see increases in cytokines which contribute, we know through studies contribute to, chronic wound healing.
So how are we going to detect these biofilms? Unfortunately, diagnosis of biofilms is pretty difficult. There's no really effective way that we can do this in in practise.
Most current methods rely on, kind of more identifying. And localization of the actual pathogens that are involved. There are no real optional tests at the moment.
There are some in development, but I'm not really going to go into all of those that can look at quantitative, numbers of bacteria that are in our wounds. Most of the time our superficial wound swabs are going to be pretty inadequate. They may give us an idea of what's in there, but they aren't actually going to tell us if there's a biofilm.
And the same with tissue biopsies. Even if we're using these to look at deeper tissue infections, they're still not going to isolate whether there is actually a biofilm present or not. The only actual test at the moment, for biofilms is using certain specialised, microscopy techniques, in the form of confocal laser scanning microscopy.
So really trying to diagnose these even at bedside is going to be really, really difficult. So it's more than likely we're just going to be looking for all of those indicators of a prolonged, prolonged inflammatory response or those signs of infection. And if you've got a wound that isn't progressing as you would expect it to progress, just probably assume that there may be a biofilm involved.
So we're gonna talk a little bit about the prevention and management of biofilms. So if these do become established in our wound bed and we are seeing prolonged and issues of healing, what are we gonna do about it? So really the main aims of biofilm management and prevention are firstly to identify, do we have signs of infection?
Do we have just signs of inflammation. So using our different signs and symptoms to determine what's actually going on in that wound bed. If we've decided that we may have biofilm involvement, we're then looking to try and reduce and disperse that biofilm.
So what we want to do is to move it out of its sess our state. So we want to move it out of that colony and back into a plantonic state. And then we're looking to prevent recontamination.
So there are a lot of things that go into our wound management, that can really affect how well and how effective our wound management plans are. And it's really important to maybe establish a good wound management plan from the beginning of presentation, whether this is in a form of a checklist that you can run through with the client, establish all of the information that you need, and ensure that actually we've managed that wound as effectively as possible from the beginning. And there are a lot of things that go into this.
We're going to be dealing with client expectations. It's all going to depend on our wound, position, size, the aetiology of that wound, how much debris is actually present? Are we going to be surgically intervening, or are we going to be looking at just second intention healing, animal temperament, do we need to consider sedation?
We're gonna then need to take the age of the animal, animal history including any underlying diseases, current medi medication. And nutritional status and a whole host of things. So there's a lot that we're looking and and having to use together to try and create a really good wound management plan from the start.
And hopefully this is one of those things that actually could work to prevent a biofilm from forming. If you have a wound that's presented and you know that you've performed lavage fairly early on, you know, hopefully you're stopping that irreversible attachment of the bacteria before, it has time to form colonies. So some of our methods of wound management, so initially, we're gonna be looking at clipping, We really want to make sure that we're We're optimising from the very first point that we're touching that wound.
So we need to make sure that our, our clippers and our clipper handles are all cleaned before use. Hair acts as a contaminant, so we want to look at doing a wide clip as possible so we can really also see what's going on in that surrounding tissue. Ideally, we should be applying a sterile wound prep prior to clipping.
This can be in the form of sort of your KY jellies, your hydrogels or equivalent. You can get these single-use sterile sachets now, so you know that nobody's been dipping into your KY, and more than likely we want to reduce micro abrasions as well. So using an appropriate clipper size and also making sure that blade is nice and sharp.
So again, we're not causing trauma to the surrounding tissue. Lavage, generally, we're going to be looking at more volume of our lavage and how we do it rather than what we do it with. More than likely in clinic, you're going to be using your isotonic crystalline solutions, whether that's your Hartman's, your saline, our compound la sodium lactate, all of these are going to be absolutely fine in the initial stages of flushing with your wound.
Iodine and chlorhexidine, if you're concerned that you do have a high bio burden, you could potentially use these, but being careful in our wounds that are progressing through because sometimes they can impede and interfere with some of our wound proteins and they can actually damage them. . There are also then are polyhexametamine, by gluonides, so your PHMBs.
These are probably more relatively new in, veterinary medicine, but they are actually, biofilm aidal, so they do help to actually disperse and break down, those biofilms so they can be a good option if you've got a wound again, that's not progressing as you're expecting. It can actually just maybe be a little bit of an extra kick on top of your standard solutions that you may use. But we're going to be looking at our volume.
Ideally, we're going to be looking to use any kind of these kind of volumes really, 550 to 100 mL per centimetre laceration, or 150 to 100 mL per centimetre of wound, or as a general, about 150 to 200 mil at a minimum. But your larger wounds, you could be even looking up to using a litre or so. Pressure then we want to make sure that we're getting the correct pressure into these wounds.
What we don't want to be doing is using too high a pressure and driving that bacteria deeper into our wound bed. It also then can loosen fascial planes, and we can look at actually impairing our wound defences, so we may actually interrupt what the wound bed is doing. And obviously if we're not using an adequate enough pressure, it may be that we're actually not even removing that debris and bacteria.
We've then got our mechanical or non-surgical options. So we have these debridement pads. These are generally consist of a looped monofilament fibre.
So these ones here actually have two sides. So there's the white side, which is a little bit for more gentle, debridement. So the monophyllum 5, so a little bit looser, and then the blue side for a little bit deeper debridement.
So these are a little bit more abrasive. These are more selective than other forms of mechanical debridement. Little skill is required, so these can be performed by nurses at triage, quicker than some other forms, so they're quicker than our autoholytic debridement because it actually lifts and removes that sort of devitalized tissue, and they should actually scruff against the wound bed to disperse that bacteria and prevent it from becoming attached.
They tend to be painless, but obviously most wounds are going to be a little bit uncomfortable, so we should be making sure we've got adequate analgesia on board with these animals anyway. They're fairly cost effective, but they may be a little bit less effective for really thick, dry s or really, really thick, heavy necrotic tissue. But in most of our kind of initial wounds, as you can see here, where you've got, Sorry.
These may be a little bit more effective for our kind of very superficial wounds as you see here. We've got some sort of nice, really necrosseed vitalized tissue up in here, and these pads can actually get in there just to really remove that while being fairly gentle on the actual surrounding tissue. And then again, just to try and reduce this chance of this bio burden, forming a colony and moving on to form a biofilm, we're going to be looking at imploring our moist wound management.
So we're going to be looking at maybe dressing these if it's not a case of that we need to close that wound immediately, are we going to be doing a little bit of delayed primary primary healing or second intention healing? So we're going to be looking at trying to use some moist wound management and, and once we've debrided and lavaged and we're happy that we've done that effectively, we're then going to be getting our antimicrobial agents involved and trying to prevent that bacterial contamination from reforming. There is a chance once you actually disperse.
A film, if you, that's not just the end of it. That's not it gone. There is the potential that within 24 hours, if we're not managing that wound effectively, there is a chance that those biofilms can actually reform within 24 hours.
So it is really important that we're actually looking at Covering these wounds and keeping that wound bed as protected as possible to help it move through and out of this inflammatory state. So just to sum up, so as you know, our biofilms are these complex and communities, they can be full of singular or more commonly poly microbial bacterial communities, and these cause a prolonged inflammatory response, which is going to lead to delays in our normal healing process. So if we're in the inflammatory stage, we're not going to move and it's the wound is not gonna heal.
We need to move it on to that second, that third stage of healing into our stage, so we can start seeing that granular, patient bed start to develop and we can start to see epithelialization. If we allow biofilms to get into a mature state, they build a really high tolerance systemic antibiotics. Our biocides, and most of our topical antimicrobials as well are not going to be able to penetrate that matrix that they're contained in.
Identification of biofilms could be pretty challenging. Visualisation alone is not adequate. We could just assume if your wound is not moving on through the normal stages of healing, you may have a biofilm there.
The most effective management of a biofilm is this disruption. So we need to actually use divide and lava to temporarily make. This biofilm back into a planktonic state, which is going to make it susceptible to our conventional microbials, and we can move on to use our moist wound management and using our topical antimicrobials that are hopefully then going to prevent that reformation.
And again, just to drive home that prevention really is the best option with these wound biofilms. They are so difficult to remove and can cause so much problems with healing that really the thorough preparation and handling of a wound in the initial stages can really help us prevent these from forming. And again, in viewing a nice wound management plan from the start, again can really link in with that and help reduce any complications later on.
Hello everyone, my name is Charlotte Wood, and I am the veterinary key account manager for SAT. Today I will be talking through some of SAT's advanced wound care products. We will start by looking at the Q toed sil tech range of foam dressings for extra date management.
Heat mesil tech foam dressings are designed to offer dynamic ed state management for a variety of wound types. These dressings are a traumatic yet reliable and are quick and easy to apply. The layers of the dressing integrate perfectly to provide the ideal dressing for treating chronic wounds.
The upper layer branded cutammed siltec is highly breathable, given a dynamic moisture vapour transmission rate. The middle layer is made up of a highly absorbent open porous polyetthane foam core for excellent fluid absorbency. Attached to the foam core is super absorbent strips for additional absorption and retention capacity.
The wound contact layer of the dressing is a perforated silicon layer with either a low tack in the case of cutammed siltec, which you can see here, or a soft tack with a self-adhesive border in the case of Cutammed siltec B. Ketamed siltec B is a foam dressing with a silicon-coated adhesive border, offering reliable but gentle adhesion, resulting in less pain and trauma at dressing changes. The dressings can be cut to size if required.
Super absorbent technology offers excellent ed state retention even under pressure. The foam core vertically absorbs extradate to prevent maturation, and meaning the dressing copes well with all types of extraate, even very viscous extradate. With dynamic breathability, the rate of MVTR adapts to changing extate levels present within the wound.
Cutamed Siltec Sawback is a foam dressing with a sawback technology wound contact layer. Sawback technology is capable of binding bacteria in a moist wound environment. Therefore, combining the benefits of both infection and X-shape management in this product, we will look at the sawback technology in more detail further into the presentation.
Putyed siltte dressings easily absorb extradate vertically, transporting it to the super absorbent fibres in the adhesive above the foam. These fibres expand and form a gel which safely retains fluid. The polyurethane top film is dynamically breathable and is able to adapt to the rate of MVTR to the saturation level of the dressing.
The transparency of the top film allows visibility of the saturation level to help determine the ideal time for a dressing change. Even the most viscous exudate can be managed by this dressing due to the silicon wound contact layer and large pores in the foam core. Vertical absorption also draws out state away from the wound edges, distributing it evenly inside the foam while minimising the risk of maceration and preserving an optimal moist wound environment.
The silicone wound contact layer seals around the wound margins, helping to protect the wound edges against contact with extradate. The silicon wound contact layer allows easy passage of fluid while forming an effective barrier against tissue ingrowth into the foam. The silicon wound contact layer adheres gently to dry skin but never a moist wound bed, protecting the fragile newly formed tissue while offering pain-free and a traumatic dressing changes.
Cediltech B has a secure adhesive border which can reduce the need for additional bandages, therefore saving time and money. The adhesive border secures the dressing in place which supports the wound healing process, allows for easy and quick dressing changes, and prevents movement of the dressing, therefore helping to create an optimal moist wound healing environment. That rounds up a summary of the Q to meil tech range of foam dressings for Xtate management.
Next we will take a look at cutimed sorbian S's range of super absorbent dressings. Ketamed absorbian dressings offer hydration response technology. The dressing core is made up of a fibre matrix and gel forming polymers which offer excellent absorption and retention of exudate.
The polymers expand towards the womb bed as they fill with exudate, ensuring close contact with the womb bed at all times. The edges of the dressing are sealed by ultrasound, which means the dressing has a high tear strength even when saturated. Cutamed sorbian also offers some wound bed preparation in its ability to provide gentle and soft debridement by removing slough and toxins during dressing changes.
The dressing also reduces the concentration of MMPs in the wound to kickstart the healing process and immobilises microorganisms, therefore reducing the risk of cross contamination by locking in detrimental substances transported in wound exudate. Cutamed sorbian sachets for moderate to high tate levels is suitable for many wound types. The product effectively manages moderate to high levels of extradate, retains its extradate even under pressure, and removes slough and maintains a moist wound environment.
Using utamed sorbian in wounds with a high level of extradate helps to reduce dressing changes. Cutamed sorbian sachet border is a self-adherent super absorbent dressing which is ideal for when a fast and easy dressing application is required. The advantage of this dressing is secondary fixation is not required.
That rounds up an overview of cutimed sorbian Estes range of super absorbent dressings. Now we will take a look at the Cimed and leuammed sorbat range. Sawback technology combines unique surface characteristics to bind and remove bacteria and fungi.
Sawback dressings display hydrophobic properties enabling them to irreversibly bind bacteria and fungi in a moist wound bed. There are no chemical agents in this technology which could cause side effects through the release of endotoxins. Sorback technology is unique.
It has no known side effects. It's suitable for all types of wounds, including chronic or acute wounds. It's safe and effective to aid in infection management and suitable for prolonged treatment duration without the risk of any bacterial or fungal resistance developing.
Here are some variants of the cuteed saw-backed range. We have the cuteed saw-backed swab, which is an acetate primary wound contact layer which can be used in all types of wounds. We have the cuteed sawback dressing pad, which has a slightly absorbent core for use on shallow wounds with low to moderate levels of extradate, and we have the cutamed sawback ribbon, which is a cotton ribbon for use in deep or cavity wounds, also suitable for use between digits or in skin folds where fungal infections may be a problem.
We look again here at the Cimed Siltec sacked, a combination of the sawback technology and the Cimmed Siltec foam dressing. The sawbacked wound contact layer is capable of binding bacteria and fungi in a moist wound environment, therefore helping to manage or prevent infection in the wound. Leucamed sorbbat combines the Soback technology with a sterile and waterproof film dressing.
The dressing is highly breathable and conformable and capable of binding bacteria at the wound site, an ideal dressing of choice for surgical wounds that you believe may be at risk of becoming infected. We will look at the leucommed range of dressings further on in this presentation. That rounds up the ketamed and leucamed sorbba range.
And now we will look at the leucommed range of post-op film dressings in more detail. Here are the dressings we have within the leucamed range of post-op film dressings. Leucamed tea and T+ are sterile, water and bacteria-proof transparent film dressings, which can reliably secure cannula and protect dry wounds.
Leucamed T+ also incorporates a dressing pad. Leucamed sawbba, as we have already discussed, is an innovative post-op dressing which protects a wound from external contamination with its sawback technology coated microbial binding wound contact there. Leucomed control combines highly innovative hydropolymer technology with a transparent film dressing for continuous wound inspection.
The benefits of the leucamed range include safe and skin friendly dressings which protect the wound from bacteria and viruses while being highly permeable, which reduces the risk of maceration and bacteria pooling at the wound site. The dressings offer excellent skin adherence using a full adhesive coating while maintaining a high moisture vapour transmission rate. Premium in their quality and appearance, matte and ultra thin, the dressings have a statin touch and are not noticeable on the skin.
The dressings are easy to apply using the unique red strip technology. They are comfortable and offer low friction dressings for lasting adherence. Good moisture per mobility is important to prevent maceration and help prevent microbial proliferation and migration, prevent moisture pooling at the wound site and create the ideal conditions for wound healing.
Leucamed control is a completely transparent dressing which is ultra thin and conformable. Leucamed control also has a thin absorbent hydropolymer wound pad which is capable of absorbing a low level of extradate. The image shows the use of leucomed control post orthopaedic surgery on a dog.
The dressing allows full wound visibility while avoiding external contamination and creating an optimum healing environment. The dressings offer strong but gentle adhesion. Here we will quickly recap Leucommed Sorbact.
Leucommed Sorback combines the sawback technology with a sterile and waterproof film dressing. The sawback technology is capable of binding bacteria in a moist wounded environment and the dressing is highly breathable and conformable. In summary, the Leucommed range of post-doc film dressings includes leucamed tea and T+, sterile water and bacteria-proof transparent film dressings, where Leucamed T+ incorporates a dressing pad.
Leucamed Soback, a combination of the sawback technology and a waterproof but breathable film dressing, and Lucamed control, a film dressing that offers full wound visibility. That rounds up a summary of the Luucomed postdoc film dressings from SCT. Finally, we will take a look at the new Cutimed debris clean, a debridement tool that offers fast and effective wound cleansing.
Heimer debris cleaner is made up of a foam layer to support absorption and rinsing during use. This also aids with the cleansing efficiency of the pad. A perforated adhesive layer attaches the foam to the debridement surface, which is made up of both white looped monofilament fibres for gentle debridement and blue or abrasive fibres for strong debridement where required.
The pad has a hand loop for easy, comfortable, and accurate use. The hard blister pack can be used for both moistening the pad with a wound rinsing solution and disposal of the pad after use. The white gently abrasive monofilaments are designed to remove and retain slough, biofilms and microorganisms.
The more abrasive blue looped fibres break up firm slough and remove it from the wound. Tests show cuteed debri clean is effective at binding to wound microorganisms, therefore reducing the wounds bio burden after use. In summary, Cutimed debris clean offers strong cleaning efficiency.
It can effectively bind bacteria and can remove more than 99% of a biofilm from a wound. That concludes this short presentation on some of ST's advanced room care products. Thank you for listening.

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