We have touched on wound aetiology previously, however in this episode we dive deeper into how wound types interface with mechanism of injury and dilemas faced when there are multiple causes - what actually is a mixed wound?. We canvass all the major hard to heal wound types including incontinence associated dermatitis, pressure injury, skin tears, moisture lesions, chronic oedema, venous, arterial and more. How does this all relate to management of these wounds? We're sure our discussions in this episode will raise a few clinical conundrums and questions for you. Indeed, you may start to see more of these in your own practice and become more aware of these prickly challenges. The simple isn't always so simple.

Timestamps:

00:00 Introduction

01:12 Mechanism of injury versus aetiology

02:30 The value of clinical audit and quality indicators

03:20 Misdiagnosis of Incontinence-Associated Dermatitis (IAD)

03:56 Intertriginous dermatitis misdiagnosed as IAD

05:29 The challenges of addressing gaps in clinical guidelines

06:03 Be confident to be unconfident

06:20 What is the mechanism of injury for skin loss in IAD?

07:21 When experts conclude that the simple ain’t that simple

08:45 When clinicians are approached by academics to fit a square peg into a round hole

10:36 Tips for researchers undertaking research in venous leg ulcers

11:52 When wound education is siloed and does not replicate clinical reality

13:35 Making clinical hunches and not always on the first visit/assessment and that’s OK

13:50 Current wound documentation does not support multiple aetiologies and impediments to healing

14:00 Challenge of teaching clinical realities to students when they are taught in siloes

14:33 Figuring out what is the predominant aetiology

14:50 How do we define and teach simple versus complex wound

15:13 Mixed aetiologies presenting above and below the groin

15:56 Prioritising which aetiology to treat / manage

16:57 Post operative wound dehiscence and lymphoedema

17:48 Capacity building in lymphoedema

19:27 The need for clinicians working in Hospital in the Home to understand lymphoedema

19:43 The challenge of diagnosing inflammatory conditions such as IAD and intertriginous dermatitis of the pelvic girdle

20:30 Influence of climate on dressing performance and skin injuries

21:00 Mixed aetiologies of the pelvic girdle

22:20 Is IAD avoidable and how easy is it to categorise, manage and report

24:00 Continue reevaluating aetiology

24:12 It is OK change or add to aetiology if clinical rationale can be provided

24:57 Call it what it is. A vascular assessment includes arteries, veins and lymphatics, not just the arteries

25:21 Venous disease plus a wound on the same leg does not necessarily mean the wound is of venous aetiology

26:57 Mechanism of injury v aetiology v impediments to healing. Simple v complex

28:40 Opportunities to improve accuracy of wound data reporting and quality improvement

30:27 When is a stage 1 Pressure Injury of the foot, a “Diabetic Foot Ulcer”

Resources mentioned:

• GlobIAD Incontinence Associated Dermatitis - Tools https://www.skintghent.be/en/onderzoek/tools/2/incontinence-associated-dermatitis-iad
• Australian Aged Care Quality and Safety Commission - Incontinence associated dermatitis and pressure injury https://www.agedcarequality.gov.au/news-publications/clinical-alerts/incontinence-associated-dermatitis-and-pressure-injury

If you enjoyed this episode please like, subscribe, leave a comment or share with your colleagues.

Connect with us at:

Email [email protected]

TikTok https://www.tiktok.com/@twoechidnae

Connect with Donna's resources and sign up for the Woundy Wisdom's newsletter at https://goodwoundcare.carrd.co/

Disclaimer:

The views expressed in this podcast are our own. This podcast is intended specifically for healthcare professionals. Always follow your organisation's policies and procedures. Please consult your own healthcare provider for individual wound advice.

Welcome to the 2Echidney podcast.

You're with Mon and Don, two advanced.

Practice nurses with decades of experience in hard to heal wounds burrowing into prickly conversations.

Welcome to the TUA Kidney Podcast with Monica Samalik and Donna Nyah.

I try and change it up a bit.

Today's topic, close to many wound clinicians, hearts and brains, is wound etiology.

Something, you know, I talk about.

Well, we talk about the dressings as the full stop at the end of the sentence.

This is the big capital letter at the beginning of the paragraph.

Wound etiology.

Love it.

And wound definitions and wound etiology versus or v mechanism of injury.

So that's the intro.

Don and I, you go to town.

Great.

Well, I can give the intro as to what perhaps brought us to have this topic to start with, but I really love from the outset how you've brought in the mechanism of injury.

It's something I find in my clinical practice is not understood well.

And I said probably because, you know, my cohort two, I'm seeing a lot of wounds that have been around for a while, 2, 3, 4 months, 2, 3, 4 years.

And the mechanism of injury is not the, is not the current etiology and may not be what is causing it to fail to progress and heal.

So, you know, the burns and the traumas and the skin tears that may have happened six months ago are currently not what the wound is that I'm looking at, but they're still called that by the clinicians and on the wound chart and is the reason for referral.

So that's really important.

But sometimes the original mechanism of injury is the wound.

So I've had a clinical conundrum the last couple of months and I raised it with you the other day because I just wanted to hash it out a little bit.

I think I'm almost there with it.

But, you know, as all good wound clinicians do, they discuss things with their colleagues and benchmark.

I have been assisting some facilities with residential aged care facilities with quality indicators, and we know that incontinence associated dermatitis has been added on to their mandatory quarterly quality indicators.

So I do some significant chart reviews and assist with data capture in some places that I go to, which is fantastic because I think there's a lot of quality improvement that can be done in interpretation of results, not just counting the numbers.

But how is that trending and what's that telling us about practice and then informing interventions, not just let's blatantly educate people on a topic we think they need.

Let's be a little bit more strategic with it.

So that's all very positive.

And it's not about blaming staff for a certain amount of injuries.

But what I've noticed is, since the IAD indicators have come along, is they either haven't picked up anything at all and they've gone to all of us, they've swung the other way and picked up so many.

And then, of course, you know, there's the staging, sorry, the classifications that need some refinement.

But I'm finding a lot more IADs being ruled in now and I need to rule it out.

They're kind of seeing everything that's red across the pelvic girdle.

They know it's not a pressure injury, but it's being called iad, even a little bit of redness.

And where I had found there were a number of residents who I was clinically challenged with.

Yes, we get challenged all the time and we go back to those really important definitions to.

Because that, you know, that's your, your, your point of truth, I guess I'm.

I'm finding, you know, a lot of residents with intergluteal, you know, redness, much like I might describe as intertragnus dermatitis.

It's not.

Definitely not pressure injury.

They definitely are incontinent.

So it fits the, you know, the criteria of being assessed for iad, but it's been called iad, but it doesn't fit the pattern of iad.

And yet they're incontinence.

I have this, you know, which came first, the chicken or the egg?

Would they have this if they didn't have incontinence increases the humidity in the area, but it doesn't.

It's not typically iad.

And, you know, I've gone back to the globiad categories and definitions and even supporting pictures that are there.

And this is the challenge, isn't it, when I don't know if you've had this.

I've just thought of this one.

You know, I've had a number of times, you know, quality managers come to me and say, we want to put some pictures up of the pressure injury stages to help people stage either on their lanyards or attach it to vims, the riskman quality management systems.

But, you know, a stage three might look so different across many things.

I've gone back to the globe yet IAD photos and definitions, and it's not giving me any resolve.

So I end up ruling it in or out and I give a clinical rationale, but I find that if that's complex for me.

Gee, that must be complex for the floor staff on the ground.

So no wonder.

And that's okay.

And I'm gonna quote you, if you don't mind, because I think we've used it a number of times over the last couple of.

We've been benchmarking between ourselves.

We are really unconfident with some things, but we can be confident to be unconfident.

Please quote Monica Samolin.

It's really, really gold.

And that's okay.

It's okay to question.

And certainly that's what we're doing here on this podcast.

So I brought it up with you.

And then we were talking about, well, is the skin loss in IAD more to do with sheer.

Does it.

Does a category where there's some damage without skin loss make it more susceptible?

And is shear more of a factor or friction?

Friction.

Friction, absolutely.

And then we started talking about friction on the feet, and we were reviewing our own understandings and definitions of friction and how we respectively teach the difference between pressure, friction and shear when it comes to pressure injuries, but also wounds on the foot.

Oh, boy.

So it's a massive competence.

So, yeah.

So where would you like to head first with that?

I think for me, yes, definitely being confident to be unconfident.

But the reason why we got here, you were involved.

You're one of the founders of a social media page in wound management.

Way back when we were in our.

In our.

In the.

Yeah, in that regional role.

And.

And we spent many hours as a group, and there were nine of us trying to format the questions to be put up on Facebook.

And we learned very quickly, we thought, oh, no, let's do some.

Put up some complex questions and some simple questions, but always have standards, you know, good quality evidence to back it up.

Bamboo, first mistake.

Well, first of all, we thought the simple.

We thought the simple would be easy.

But what we realized amongst the nine of us, that we all still had very different interpretations of the literature or very different, you know, there was not much evidence out there, so we did things very differently, or we assumed there was evidence out there because we thought so damn basic when there wasn't.

And, you know, we started talking about what's an etiology?

You know, so then we start talking, you know, it extrapolated to what's an etiology?

What's the mechanism of injury?

And I'll never forget someone coming to us.

And you'll remember this coming.

So it was an academic who approached us, and they were doing research on venous Leg ulcers.

Yes, I do recall and I looked at this person and they wanted us to recruit people into that, into that study and that you know, fair request.

It was a data set as well something.

But I one thing I said to this person that was many years ago, sorry but we don't see people just with Venus etiology.

And little did I know then that what I assumed was Venus ideology in fact wasn't.

But that's for another time.

And I'm saying we often see mixed disease and so because this person wanted someone with purely with venous disease and venous disease that was related to the wounding.

And we now know there's no such thing as a venous leg.

I'll say it's now phlebolymphoedema or.

And that's why it's another thing.

We'll talk about language later and even the.

We'll get onto that.

Even the lymphoedema is controversial.

Oh yeah, yeah.

Versus chronic oedema.

But keep going with vlu.

So but I didn't know that at the time.

I was just thinking what I was seeing in clinical reality.

Often people with arterial disease, venous disease, diabetes, neuropathy, skin cancers, lymphedema, the whole works.

And so little did I know that that methodology years ago and this is prickly.

I suggest to anyone who's currently doing research on venous leg ulcers, stop or change it up maybe.

Can I just be cut to the chase there and say definitely go and do a lymphedema course.

Yeah, yeah.

Don't do venous leg ulcer research without having a background in lymphedema, please.

And I'm giving you a heads up what's going to be coming out there.

And that's one of the intents of these episodes.

But boy oh boy.

And even in our journal we keep seeing the topic venous leg ulcer stop.

You're going down the wrong rabbit.

Going down the wrong echidna hole.

And so there's not just one area of wound aetiology.

This is across all areas.

And I struggle in education when and this probably segues from or leverages rather off the last episode we've done on wound education and the topics of wound education.

How often do we piecemeal education.

I know I've mentioned before pressure injury, skin tear might be venous arterial lymphatic, diabetic foot iad, a whole host of other moisture related lesions, et cetera, et cetera list goes on.

They're the big common etiologies that most people are going to be familiar with.

How often in clinical practice do we see routine garden variety isolated to one of those.

There's always confounding.

There's always multiple things going on at once and that's how we teach.

But we're not sending that other message that you're going to see these things and are more mixed.

So, you know, I was originally taught arterial venous mixed.

Yes, it was below the knee.

Okay.

Yes.

You also had diabetic neuro.

Ischemic.

That's another topic for another day.

Diabetic, neuro, ischaemic and those, those terms.

But mixed.

I reckon every leg ulcer now is mixed if I'm going by that type of thinking and definition.

And so I'm going to prompt you here.

So do you want to talk to how you were saying that if we're going to teach that uni and whatever year level it's at.

I knew you're going to ask me something really hard to answer.

No, no, no, It's a good question.

So I'm preempting your question.

Keep going.

Yeah, yeah, but do you want to talk?

No.

But you had.

I think you had a solution.

If we're going to teach it in silos, which you probably still have to teach the pathophysiology in silos, but you really have to preface it talk to what the clinical reality is out there in the clinical setting is that I'm taking your.

It does.

This is your.

Sometimes we make a hunch ourselves and we go, okay, we.

From the data that we've gathered, our clinical assessment, and that might not all be on the first visit.

It's okay to say, I'm not sure yet.

That's a hard one.

Our documentation doesn't support that really well either because people are ticking boxes on a wound chart.

So when we were talking absolutely.

About wound education, as we were, as you've said, it's a challenge for us to get that across to undergraduate students.

Yeah, but I think what I'm.

Cause this is what I was trying to prompt you on is I remember you saying the other day that, yeah, teach in silos, but say this doesn't happen in clinical reality, you often have mixed disease.

So maybe err on the caution on the side that you will have mixed disease and not just one or two, but three or four different etiologies.

And sometimes it's a real struggle to work out which is the predominant factor and you know, what's the.

You know.

And do we have to do that.

So, so I think that, you know, that's what you were talking to and I was going to say something else.

Anyway, go on.

It lends itself.

I'm going back to the other episode, aren't we, when it was talking about simple versus complex wounds.

So how do we define if we're saying that most of these wounds have multiple issues going on and we're struggling to identify which might be the cause and it may or may not change what our management is.

How do we teach simple versus chronic wounds?

And what is that definition?

Yeah, and we've been focusing on a lot on the, on the lower limbs, but you know, even lymphedema of the pannis and of the pelvic girdle.

Again.

Tabitha Rando, a nurse practitioner from South Australia, she presented on lymphedema of the pelvic girdle in conferences a few couple of years back, but I've really not heard more about that.

And pressure injury and lymphoedema of the pelvic girdle.

Hmm.

I think that's often not considered the poor tissue tolerance of people who have lymphoedema.

So if you've got lymphoedema and arterial disease, does that mean.

And significant arterial disease?

And I'm talking you've only got your perineal artery perfusing and that may have even poor flow, but you've got a really woody oedema, fibrotic oedema.

First of all, that's lympho arterial disease.

Which do you treat?

I mean, of course the arteries trump anything, but do you really try to protect the arteries over the lymphatics?

You know, so I think that, I think it's really important to consider etiologies, mixed etiologies, right up the body, not just the legs.

And of course diabetes is another, you know, systemic disease that impacts healing anywhere.

And so then, you know, how many times do we see abdominal dehiscence from post surgical wounds or hips or knees and edemas?

The Tyrannosaurus.

I have to think of something bigger than a Tyrannosaurus rex.

I don't know.

Yeah, elephant doesn't.

The Grand Canyon anyway.

But we've got to think of something.

It's huge.

It's huge.

So people working in that abdominal space, if you've got someone with a dis.

His wound, bet your bottom dollar that that person has got coexisting lymphoedema.

And then begs the question, what are we doing about it?

How are we.

Well, going back this is why I'm so thankful that now there are some services out there in regional Victoria who've got lymphoedema practitioners in their district nursing services.

There's one service that.

In the last.

Very most recent history had a fellow who was.

This feeds into the weight inclusive approach as well, who was 230 kilos and decongesting his pannus lymphedema.

He said to me when he was 180 kilos and he's now 175, but when he was 180 kilos he said, oh, Monica, I.

There's nothing that I've done different.

I haven't put anything more or less into my, my mouth.

But now that I've been able to, the swelling's gone down so much I can walk a little bit.

That's amazing.

That is incredible.

From some conservative lymphedema.

Yeah.

And so.

But these nurses were these lymphedema nurses in the community setting have managed his lymphedema with some pretty sophisticated garments and managed that.

So there's huge capacity out there to upskill people in lymphoedema and really change the referral pathways.

Ah.

We will talk about cellulitis at some point and hi.

Hi.

People working in HI need to do a lymphoedema course as well.

Big time.

Huge time.

Oh.

Not only nurses, anyone working in the heath environment.

So.

Yep.

I've really talked a lot about.

So going back to wound etiologies and going back to your iad, I was thinking when you raised that issue with me, I went, oh, I never even thought of that about IAD not actually being iad, that they may be incontinent, they may be doubly incontinent.

But does that mean that.

Yeah.

But is that irritant actually in contact with skin or is it providing the humidity and depending on heat and heat.

And is that more reliant on the.

Determined by the ambient humidity?

You know, whether you live in Queensland or whether you live in Tasmania.

It could be anywhere at the moment it's humid, but yeah, and so what?

Oh, here we go.

The climate impacts of.

There you go.

Climate impacts of dressing capacity and moisture vapor transfer.

I think that would be a very interesting study because, you know, I certainly get a lot more into trigonous dermatitis from my long term clients around the warmer months.

So how does that impact on other moisture humid type skin injuries.

And the other thing is too.

So especially with injuries around the pelvic girdle, we know that iad, pressure injury and skin tears coexist, especially around the pelvic girdle.

But even those things, maybe the skin tear is actually a friction injury, maybe the pressure injury is actually a friction injury.

Maybe it's the lymphedema, that's the pelvic girdle lymphedema, that's really the problem here.

That is another risk factor for all those injuries.

So again, going back to what we started talking about, be confident, to be unconfident.

Like I'm just telling you now, the audience that Donna's just raised this clinical.

We always raise clinical conundrums but this one really has resonated with me.

I've gone, no, that's so true.

I've actually been seeing those things and yet I've probably said, oh, incontinence, associated dermatitis,.

Throw another spanner in.

In some of these clients there were elements of inappropriate self care and behavioural issues and, and I was doing the, you know, as I'm tossing it over in my brain and I'm doing the analogy to pressure injuries, is it, oh no, we don't have this language around iad.

Is it avoidable or not?

So, you know, I'd often look at iad, we should be able to resolve it, but when it's there for a longer period of time, that was also my challenge because they were there for a longer period of time and I don't believe necessarily had secondary infective issues like fungal or bacterial concerns going on.

So looked at all the topical management over the preceding months, but when it hangs around for a while, that was also my clinical conundrum.

It affected my decision making around what is it?

And it could have been, it could have been IAD initially, I don't know.

And then maybe there's a residual interdigenous dermatitis.

And how do we manage that from a staging and reporting standpoint?

What box do we tick on the.

Wound management challenges and what does it mean?

How does it get interpreted?

How does that then affect floor staff when we're looking at quality improvement?

Yeah, all of those things.

So that's why it's important.

I guess that's why I'm raising it.

It's why it's important to and continually review an aetiology.

Because what might have been, it's a good example actually.

Something a couple of months ago, has it changed?

And at what point do we, I don't think we have good guidance as to what point do we call something, something else and a floor Stuff is the generalist really.

Are we empowering them enough to.

Or saying it's okay to change?

I will tell people, change the wound chart.

Go ahead, change it.

If it's really not this anymore, we should be able to give a clinical rationale as to why something's become something else.

But I think people are really scared to do that.

I'm fine.

That doesn't happen a lot.

I'll come along and do it.

But I want other people to feel confident, to be unconfident and call it.

I've got the privilege to be in a space where we're doing a lot of vascular sonography on people and vascular as in arterial and venous.

I don't mean vascular as in arterial.

Yeah, arterial or peripheral vascular disease, which is peripheral arterial disease.

Please stop using the word vascular, everyone.

Everyone stop using that word vascular.

If you don't mean arteries and veins.

And then including lymphatics, another top.

But.

What.

I've identified and I is that many times where I thought someone had venous disease, they've got a wound on them, you know, above the medial malleolus or on the gait region, either medially or laterally, and they've had coexisting venous disease.

Not that I've guessed or screened, but observed by a vascular sonographer or a radiologist.

Just because they've got a wound and they've got coexisting venous disease, the wound may not be as a consequence of poor drainage because of the venous system.

Just because.

So you can have two things, and I can tell you now that most of my wound management colleagues out there do that.

And I find we're often guilty of the things that we're saying we don't do anymore.

You know, it's not as if we're saying these things about ourselves quite often as well.

Oh, well, I've been doing that for years.

It's just that I've learned this and I want to share this with people.

But.

So mechanism of injury, for example, skin tear, pressure.

So skin tear, say on the leg, or pressure injury on the heel, skin tear.

The mechanism of skin tear may be the actual blunt trauma to the leg.

And we know that if it's less than four weeks old, it's classed as simple skin tear.

So that's one.

One framework that defines what a simple tear is.

And again, you can contest that because if you have a skin tear and you've got coexisting arterial disease or venous disease.

So anyway, going back, so a skin tear that's the initial mechanism of injury.

But then you've got to look at what's stopping the wound from progressing, if that's the case.

And that's where your mixed diseases can come in.

And so you may very well know that you've got a complex wound from the outset.

So, you know, it may be defined as simple wound for academic learning, but in fact a skin tear may be considered simple.

But in fact, if there's underlying coexisting.

If they're underlying.

Yeah.

From the moment of injury, at what.

Point do we identify that?

Yeah.

And so a pressure injury can occur for many reasons, but in the context of arterial disease.

Well, the mechanism of injury is pressure shear, but the reason why it's failing to heal is because of the unstable diabetes or all the arterial disease could be factitious wounding.

I think there's a lot of that.

Yeah.

What we call.

Look, I used to have a saying where I used to work monitors.

It's reminding me of this now that, you know, not everything that looks and smells like a pressure injury is a pressure injury.

Go you.

I know where you're going.

And that's again, I'm just coming back to the reasons why this conversation is really, really important.

Because in, at an organisation I was at, in thoroughly drilling down to definitions, critiquing, staging, critiquing, mechanisms of injury and aetiologies and all of that data was significantly changed at a benchmarking level, not by educating staff, just by making sure the data was correct that's, you know, recorded in the systems and that those systems were talking to each other.

I'm talking about the difference between, you know, coding and vims and clinical documentation that don't necessarily talk all the time well and marry up.

When you put them side by side, you can have a significant outcome in quality improvement.

So there's so many things that affect our figures and I just.

A lot of that comes down to definitions and working definitions.

I've been at facilities that have not been using the most up to date definitions in our clinical practice guidelines that we would consider as a benchmarking guidelines to follow that form part of national standards, et cetera, et cetera.

And just by updating our definitions, we completely change the data outcomes.

So, yeah, look, that's.

They're the backstories in healthcare that I don't think general public understand at all.

Of course they don't, but.

And I want to do this teaser because it's really something that I think is going to be a point of difference for us.

Is.

When is a stage one pressure injury?

And when do you have.

A DFU diabetic Fudula.

That's another podcast.

I think we need to.

That is.

And we need a.

We need some guest speakers for that.

I think so, but differing opinions.

Yeah.

And I even spoke to Professor Fran Game.

She's the chief endocrinologist of the British.

I know the name Diabetes Society.

My apologies, Fran, but Diabetes uk.

And she actually agreed that there's ambiguity and confusion and.

And it's still.

Evidence is unclear.

And I'd really like to have the opportunity leading up to that podcast.

And this is a teaser.

I know we're closing up, but just another teaser that we have another good opportunity to look at the literature and see where it's at.

Because there've been in the last four years some publications out there that have only added to my confusion about it rather than cleared things up.

And as we say, if we're having problems, what's the.

You know, a person not even in, who has not any formal wound management experience in an aged care facility, absolutely charged with working out what that etiology is, what the mechanism of injury is.

I think really, hopefully these podcasts will give clinicians the confidence to be curious as well and ask many more questions and not put those unrealistic expectations on them that they should know.

I couldn't agree more.

I can't add to that.

Okay.

I really can't add to that.

Well, you can finish off.

Yeah, let's.

Let's do that.

So we're getting into some really deep burrows and scratching around with all four claws.

So thank you for that.

That one.

It's been good.

I felt this has been a really illuminating episode.

I hope so.

Force.

So we're happy for any feedback.

We know it's controversial, so thank you for listening to these will cover aetiologies and a lot of those ones we've mentioned in future episodes, no doubt.

So we'll catch you in the next one.

Yes.

Thanks, fellow echidnas.

Yeah, thanks for listening.

We are so grateful to have this opportunity to share our learnings and challenges with you today.

Hopefully it has inspired you to be more curious in your clinical practice and burrow down to issues that bug you.

If you liked today's episode, follow and subscribe on Spotify, YouTube and TikTok.

Ooakidnae if we were too prickly, we'd also like to know.

All our contact details and links we've mentioned are in the show notes below.

You can also help us by leaving a review and sharing this with your colleagues.

We will see you in the next episode.

And in the meantime, go forth, be curious and burrow into some ant nests.

To cover you.

But what you do.