Chapter 28: Integumentary Function & Skin Care in Aging

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Welcome back to the Deep Dive.

Today we are, we're shaking things up a little bit.

Usually we take a whole range of articles and try to synthesize them, but today we're going into what we like to call steady bunker mode.

I like that, locking the door.

Exactly.

We are locking the doors and settling in for a focused last minute lecture session.

So if you're a nursing student or you know just someone fascinated by how the human body weathers the storm of time, consider this your survival guide.

We are tackling chapter 28 of gerontologic nursing,

integumentary function.

I love these sessions.

It's about taking that really dense textbook material and turning it into something you can actually use on the floor.

It's all about translation.

Exactly.

And if you're a student, you're probably thinking, okay, skin, I see it every day.

It's simple.

But we are here to tell you that chapter 28 is one of the most

underestimated chapters in the book.

Underestimated is the perfect word.

I think students often gloss over the skin because it's on the outside.

You know, we assume that because it's visible, it's straightforward.

Right.

But when you're dealing with older adults, the skin is, well, it's arguably the most critical indicator of systemic health.

It's like the dashboard for the rest of the body.

And the stakes are just incredibly high.

Yeah.

We're not just talking about wrinkles and gray hair here.

Absolutely not.

In gerontology, skin failure is not a cosmetic issue.

It leads to high morbidity and mortality.

We're talking about severe burns from reduced sensation, pressure ulcers that can lead to sepsis, and infections that their immune system just can't fight off.

The skin is the body's first line of defense.

It handles immunity, fluid balance,

thermoregulation.

If that system crashes, the patient is in serious, serious trouble.

So our mission today is to decode the largest organ of the body.

We're going to break down exactly how the skin changes with age, how to assess it correctly, especially across different skin tones, which is, I mean, that's a huge gap in a lot of traditional education.

And how to complex wounds that older adults face.

We have a lot of ground to cover.

I mean, from the microscopic level all the way to the bedside assessment.

We do.

So let's unpack this systematically.

I feel like we have to start with the anatomy.

You have to.

And every nursing textbook, you kind of skip the anatomy section to get to the diseases.

But here, the anatomy is the disease in a way.

The normal aging process just sets the stage for everything else.

It does.

You absolutely have to understand the baseline to recognize the pathology.

So let's look at the integumentary system as a whole, you know, skin, hair, nails, and glands.

Okay.

Its job is protection, fluid retention, vitamin D synthesis, and sensation.

But as we age, every single layer changes structurally.

It's a complete renovation and not really for the better.

Let's go layer by layer them elevator style, starting at the top floor,

the epidermis.

So the biggest change here is the placement rate.

The stratum corneum, that outer layer of skin cells, its turnover rate declines by about 50%.

50%.

That is a massive drop.

So you're basically walking around with older skin cells on the surface for much longer.

That's exactly right.

And just think about the implications of that for a second.

The most obvious result is slower healing.

Of course.

If an older adult gets a simple scratch, it takes twice as long to clear up as it would for a 20 year old.

Okay.

But it also impacts pharmacology.

It means delayed drug absorption for topical medications.

You apply a patch or a cream and it's just not getting through that barrier as efficiently because the cell turnover is so sluggish.

That's a key clinical nugget right there.

But looking at the notes, it seems the most clinically relevant change in the epidermis is actually structural.

Something about the connection to the dermis.

This is the concept you really need to visualize.

It's the

dermis.

The layer below it is wavy.

They interlock kind of like puzzle pieces.

We call those reed ridges.

Like Velcro.

Ideally, yes.

Like Velcro.

Locked tight.

Those ridges create surface area and grip.

But as we age, those ridges flatten out.

The boundary becomes smooth.

I can see where this is going.

If it's smooth, there's no grip.

Precisely.

They just slide over each other way too easily.

This is the physiological reason behind skin tears.

You might be doing something completely harmless like removing a piece of surgical tape or just sliding a patient up in bed.

And the epidermis literally shears off from the dermis.

That is a terrifying thought for a student nurse.

You're trying to help and suddenly you've caused a tear.

It happens and it's not necessarily because you were rough.

It's because of that structural flattening.

It's why we have to be so incredibly gentle with tape, with friction, with everything.

So what about pigmentation?

We also see changes there in the epidermis.

The number of melanocytes, the pigment cells, decreases overall.

Which explains why skin gets paler and protects less against UV rays.

Right.

But the melanocytes that do remain tend to clump together.

They cluster.

And that's what gives us those age spots or lentigines.

It's this uneven pigmentation distribution.

It's not just about losing color.

It's about the color becoming disorganized.

Okay.

Moving down a level to the infrastructure layer.

Yeah.

The dermis thins by about 20%.

But the quality of the tissue changes too.

Collagen, which gives skin its tensile strength, it becomes stiff and less soluble.

Like an old rubber band.

Exactly like an old rubber band.

It loses its snap.

And this leads to sagging and decreased elasticity.

Is this also where the blood supply issues come in?

Yes.

The number of blood vessels declines significantly.

That contributes to the paler we see in older adults.

They look paler because there is literally less blood flowing near the surface.

Okay.

But critically, the nerve endings also decrease.

So the sensory input is dampened.

Significantly.

Reduced pain and touch sensation.

And that is a massive safety risk.

Can you imagine?

A younger person feels a pebble in their shoe or tight sock immediately.

An older adult might not feel a blister forming until it's a full blown wound.

They lose that early warning system.

And then the basement level.

Subcutaneous fat.

I feel like this is the one that impacts day to day comfort the most.

It really, really does.

Aging causes subcutaneous fat to thin out and redistribute.

It leaves the face and hands and it moves to the visceral area, the abdomen and thighs.

The classic shift to the apple shape.

Exactly.

But the so what here is vital for care.

That fat was insulation.

Right.

Without it, older adults lose body heat rapidly.

They are at high risk for hypothermia.

You know how older patients are always asking for a sweater even when it's 75 degrees in the room?

Yeah.

I always just assumed that was a circulation thing.

Circulation is part of it for sure.

But mostly they have lost their natural winter coat.

They just have no insulation left.

And I assume that loss of fat also means loss of cushioning.

Precisely.

You lose the cushion over bony prominences.

The sacrum, the heels, the hips.

And that immediately skyrockets the risk for pressure ulcers, which we're going to do a deep dive on later.

It's literally bone pressing against skin with no buffer.

Let's quickly touch on the appendages, hair, nails, glands before we get to the diseases.

What's happening with the sweat glands?

Both eccrine and apocrine glands decrease in number and function.

So, less body odor.

That sounds like a win, socially speaking.

It is but physiologically, it's really dangerous.

How so?

Less sweat means a compromised cooling mechanism.

Older adults are at a very high risk for heat stroke because they just can't sweat effectively to cool down their core temperature.

They can overheat very, very rapidly in environments that wouldn't bother a younger person.

That is a great point.

And what about oil?

The sebaceous glands?

This one is a paradox.

The glands actually get bigger, physically larger, but they produce less sebum.

A larger factory with lower output.

That's strange.

It is.

And sebum is the body's natural moisturizer.

So less sebum leads to xerosis or dry skin, which is the single most common skin complaint in the elderly.

And it's not just annoying, right?

It leads to other things.

It leads to itching, scratching, and eventually infection.

And hair.

I feel like there is a cruel joke in nature regarding hair and aging.

There definitely is.

It thins on the scalp.

But due to hormonal shifts, women might start growing coarser facial hair on the chin or lip.

And men.

Men start growing thick wire -like hair in their ears and nose.

Which sounds like a cosmetic annoyance, but the text mentioned it can actually impact function.

It absolutely can.

Thick ear hair acts like a net.

It traps cerumen earwax.

This leads to impaction and can cause significant inductive hearing loss.

It's a small detail, but if your patient is ignoring you or seems confused, check their ears.

It might just be wax trapped by hair.

Okay, finally, nails.

They become thick, brittle, and dull.

You'll see these longitudinal ridges.

And they are much harder to cut, which can lead to self -neglective foot care because the patient physically can't trim them.

They just can't squeeze the clippers hard enough.

So that's the normal aging process.

But as nurses, we have to assess this changing landscape.

And this brings us to a really important section.

Cultural education is still playing catch -up.

Standard textbooks have historically described skin conditions based on how they look on white skin.

Redness,

pallor, blue lips.

If you rely solely on those color -based descriptors, you will miss critical signs in patients with darker skin tones.

So let's break down the big ones.

How do we spot cyanosis, that blue tint, indicating low oxygen in a patient with dark skin?

You absolutely cannot rely on the skin surface color.

If the melanin is dark enough, you won't see the blue.

So what do you do?

You have to play detective.

First, look at the clinical picture.

Level of consciousness, respiratory rate.

Are they struggling to breathe?

Right, context first.

Then for the physical check, you look at the conjunctiva of the eyes or the tongue.

But, and this is important, be aware that some people of Mediterranean descent have a normal blue tint around the lips.

It's just their baseline.

That is a great watch out to avoid a false alarm.

What about jaundice, the yellowing from liver tissues?

Okay, the classic teaching is to check the sclera, the whites of the eyes.

But in darkly pigmented patients, you often see subconjunctival fatty deposits.

And those look yellow.

They look like little yellow spots in the corners of the eyes.

That is normal.

That is not jaundice.

So if the eyes are unreliable, where do we look?

The palate, the roof of the mouth.

Even in very dark skinned individuals, the hard palate will show that yellow bilirubin stain.

It's much more accurate than the eyes in this population.

It works under any light.

It's your best bet.

That's a pro tip right there.

What about power?

When someone is anemic or in shock, white skin turns ghostly white.

What does brown or black skin look like?

Brown skin will appear sort of yellow brown.

Black skin will appear ashen or gray.

Okay.

And again, you have to look at the mucous membranes, pull down the lower lip and the nail beds, and always look for the other signs of shock rapid pulse.

Restlessness.

Don't just trust the face.

And finally, erythema, redness, inflammation.

If I have a patient with very dark skin, I might not see a big red patch.

You likely won't.

You have to use your hands.

You palpate for warmth.

Inflammation is hot.

You feel for tautness, edema, or hardness, what we call induration.

If one area is hot and hard compared to the surrounding skin, that's your erythema, even if the color hasn't changed much.

Your hands are as important as your eyes.

I like that.

Okay, let's move into section three.

Common skin conditions.

Let's categorize these into benign, don't panic, and inflammatory do something.

Sounds good.

First up, benign.

You're doing a skin assessment and you see these bright red tiny little dots on the patient's trunk.

What are those?

Cherry engemas.

Totally normal.

They start appearing after age 30.

They're benign.

Don't panic.

Okay, they look like little drops of blood, but they're contained.

Exactly.

What about the ones that look scary?

The crumbly, waxy, brown, or black, stuck -on lesions.

These are the ones that freak students out because they can be pitch black and irregular.

They look like they could be melanoma.

But the key is that stuck -on appearance.

It looks like someone took a piece of dirty wax and just stuck it to the skin.

So they sit on top of this skin rather than growing out of it.

Exactly.

And they're usually waxy or rough to the touch.

They are benign.

But if we aren't sure.

If you aren't sure, you refer.

Always.

But generally, once you've seen a few seborrheic keratosis, you'll recognize them.

And then you also see skin tags, which are just tiny stalks of flesh usually on the neck or in the armpit.

Purely cosmetic.

Now the inflammatory issues.

Let's talk about the cradle cap of the elderly.

Seborrheic dermatitis.

It presents as a yellow or white scale with a red base.

Common on the scalp, eyebrows, and the sides of the nose.

Interestingly, we see it a lot in patients with Parkinson's disease or after a stroke.

It's linked to sebum overproduction in those specific areas.

And the treatment isn't rocket science, is it?

No, not at all.

Selenium sulfide shampoo and topical steroids.

It's just simple maintenance.

What about inner trigo?

I feel like this is when every nurse sees constant.

Oh, constantly.

This is inflammation in the skin folds, under the breasts, in the groin, abdominal folds.

It's caused by friction plus moisture.

Very common in obesity and diabetes.

It's red, it's angry, and it hurts.

And the nursing priority here is essentially keep it dry, isn't it?

It is.

But you have to be careful how you keep it dry.

Do not use cornstarch.

Wait, really?

That's an old home remedy I've heard a million times.

Why not cornstarch?

Because cornstarch is a carbohydrate.

When it gets wet, it clumps into this gritty pace that actually increases friction.

Oh, wow.

But worse, because it's a carb, it ferments.

It actually feeds fungal growth.

That's like a buffet for yeast.

You are basically baking bread in the patient's skin folds.

Wow.

OK, striking that from the list immediately.

That is a horrifying visual.

Right.

Use proper antifungal powders or creams, or you can separate the skin folds with dry gauze or cotton fabric just to absorb the moisture.

Good to know.

Let's talk about the itch, pruritus.

The itch is miserable.

And in older adults, it's usually caused by that xerosis, the dry skin we talked about earlier.

It creates this vicious cycle.

You itch, so you scratch.

You scratch, so you break the skin barrier.

You break the skin, you get an infection or inflammation, which then makes it itch more.

So how do we break the cycle?

We have to rehydrate the skin.

And this goes against what a lot of people think about hygiene.

Older adults should not

That feels counterintuitive.

I know.

But daily bathing, especially with hot water, strips those few remaining natural oils from their skin.

OK.

Bathing every other day, or even less in the winter, is better.

Use tepid water, not hot.

And the most important rule, apply emollients lotions immediately after bathing.

While they are still wet?

While the skin is still damp.

You want to trap that water in the skin.

If you dry off completely and wait minutes, the water has already evaporated.

You missed the window.

The dry cell is a dead cell.

Exactly.

You want to lock the moisture in.

That leads us right into section four.

Infectious and viral conditions.

Because if you have moisture and friction like with intertrigo, you often invite a guest.

Candida.

Yeast.

Candidiasis.

It loves warm, dark, moist places.

How do we spot it versus just regular irritation?

What's the giveaway?

Look for the satellite

You'll see a main rash that is fire red.

It's a bright, angry red.

But then, spreading out from the edges, you'll see these little isolated red dots.

Those are the satellites.

That is the hallmark of Candida.

And it loves sugar as much as it loves moisture.

It does.

If you have a diabetic patient who keeps getting yeast infections under their breasts or in their groin, you have to check their blood sugar.

Uncontrolled hyperglycemia feeds yeast.

The sugar is literally coming out in their sweat and urine, just feeding the fungus.

Moving to a viral condition that strikes fear into the hearts of many.

Herpes zoster shingles.

This is the reactivation of the chicken pox virus, varicella.

It basically hides in the dorsal root ganglia, the nerve roots, for decades, just sleeping.

And then it just wakes up.

It wakes up when your immune system takes a dip due to age, stress, or another illness.

And it travels down the nerve, right?

Exactly.

It travels down the nerve fiber to the skin.

This is why the pattern is so specific.

It follows the dermatome.

The dermatome being the specific area of skin supplied by that single nerve.

Right.

And the key diagnostic sign, the thing you have to remember, is that it never crosses the midline.

Never.

It will be on the left side of the chest or the right side of the face, but it stops dead at the center.

If a rash crosses the spine or the sternum, it's probably shingles.

And it's incredibly painful.

It hurts before you even see the rash.

That's the prodromal phase.

Burning, tingling, shooting pain.

Then the blisters appear.

The big complication we worry about is percipedic neuralgia.

What that?

The rash goes away, but the pain stays.

It can last for months or years because the nerve itself has been damaged.

Is it contagious?

This is a common question for students.

It is infectious to anyone who hasn't had chicken pox or the vaccine.

You can't shingles from someone, but you can catch chicken pox from their shingles blisters.

So if you're a student nurse and you've never had chicken pox and you've never been vaccinated, you shouldn't be caring for a shingles patient.

Period.

Okay.

Let's get serious for a moment.

Section five,

skin cancer.

As nurses, we're often the first ones to see a patient's back or feet during a bath.

We need to know what to look for.

We do.

And you can start with the pre -malignant stuff.

Actinic keratosis.

These are rough scaly patches from sun damage.

The text mentioned they feel like sandpaper.

Yes.

That's a perfect description.

You can often feel them better than you can see them.

They are potentially precancerous.

If left alone, they can turn into squamous cell carcinoma.

So we treat them early, usually by freezing them off.

Then we have the big three malignancies.

Can you walk us through them?

Sure.

First, basal cell carcinoma or BCC.

This is the most common form of skin cancer.

Okay.

It usually looks like a pearly papule.

It's shiny, almost like a little pearl, often with a depressed center.

Like a donut.

A tiny flesh colored donut.

It rarely metastasizes, so it doesn't usually spread to other organs, but it is locally invasive.

It will just dig deep and destroy the tissue right where it sits.

Next up.

Squamous cell carcinoma.

SCC.

These look different.

They are firm, scaly, and often ulcerated.

They look like a sore that won't heal.

And these can spread.

These can metastasize.

You often see them on the lower lip or the tops of the ears.

High sun exposure areas.

And the big one.

Melanoma.

The killer.

It has a high mortality.

If it's not caught early, you just need to memorize the ABCDE rule.

Okay.

Let's hear it.

A is for asymmetry.

One half doesn't match the other.

B is for border irregularity.

The edges are ragged.

C is for color variation.

It's not all one shade of brown.

It has red, white, blue, or black mixed in.

So multiple colors is a bad sign.

A very bad sign.

D is for diameter greater than 6 millimeters, which is roughly the size of a pencil eraser.

And E is for evolution.

It's changing over time.

You mentioned earlier that assessment in dark skin is different.

Does that apply to melanoma?

Absolutely.

African Americans, Asians, and dark skin whites are at lower risk for melanoma overall, but when they do get it, the mortality is higher.

Why is that?

Because it's caught late.

It's often a specific type called acrolyntigenous melanoma.

And this type appears where you might not think to look.

The palms of the hands, the soles of the feet, and under the nail beds.

So for a dark skinned patient, checking the bottom of the feet is a life -saving assessment.

It is absolutely mandatory.

If you aren't checking the soles of the feet, you aren't doing a complete skin assessment on a dark skinned patient.

Check the feet seems to be a recurring theme in nursing, which brings us perfectly to sections 6.

Lower extremity ulcers.

I feel like students get these mixed up constantly because they all result in a sore on the leg, but the causes are totally different.

They are, and if you treat them the wrong way, you can make them so much worse.

Let's build a mental table to differentiate the three main types.

Arterial, diabetic, and venous.

Okay, column 1.

Arterial ulcers.

Think ischemia.

The problem is blood can't get to the foot.

It's a supply issue.

Arteriosclerosis blocks the flow.

What does the leg look like?

The skin is pale, shiny, and hairless because the hair follicles are starving for nutrients.

The toenails are thick in yellow.

The whole leg feels cool to the touch.

And the ulcer itself, what's its appearance?

It's usually on the toes or the top of the foot.

It looks punched out, very defined edges, and it is so painful.

Painful because the tissue is dying.

Yes,

especially at rest or at night.

Gravity helps get blood down there, so these patients often sleep in a recliner with a leg dangling.

If you elevate their legs, it hurts more because you're fighting gravity, making it even harder for blood to reach the toes.

Okay, column 2.

Diabetic or neuropathic ulcers.

The driver here is sensation, or really the lack thereof.

They have neuropathy.

They can't feel trauma.

So they don't know they're hurt.

Exactly.

So they walk on a pebble or wear a tight shoe or get a callus, and they just keep walking on it until it breaks down.

Location.

Pressure points.

The plantar surface, the bottom of the foot, or under the metatarsal heads, basically anywhere they step.

And the appearance?

It's deep, circular, and often surrounded by a callus.

And it's usually painless, which is the real danger.

They don't know it's there.

So the assessment tool here is the monofilament test.

Right.

You poke the foot with a calibrated plastic wire to see if they can feel it.

If they can't, they are at extremely high risk.

And column 3.

Venous ulcers.

This is the most common one.

By far.

The problem here is congestion.

Blood gets down to the leg fine, but the veins are where the valves are shot, so it can't get back up to the heart.

Venous hypertension.

Exactly.

The blood pools, fluid leaks out, and it creates this boggy, edematous mess.

What does that look like?

It looks wet.

Lots of edema.

You see this brown discoloration hemocytorin staining around the ankles.

It almost looks like they're wearing brown socks.

And the ulcers.

They're usually on the medial aspect of the leg near the ankle bone.

They have irregular borders and they just weep fluid constantly.

So to recap, arterial is dry,

pale, and painful.

Venous is wet, brown, and swollen.

Correct.

And the management is the complete opposite.

For arterial, you want to improve flow to the leg so you don't compress it tightly.

For venous, you need compression.

You have to squeeze that fluid back up.

Exactly.

You have to squeeze that fluid back up to the heart.

And this is critical.

You have to check pulses first.

Never, ever, ever compress a leg if you suspect arterial disease.

If the arteries are blocked and you wrap that leg tight, you will cut off the little blood flow they have left and kill the leg.

Wow.

Always check the ankle brachial index, or at the very least, the pulses, before applying compression.

That is a massive safety tip.

All right.

Take a deep breath.

We are arriving at section seven.

This is the core nursing skill of this chapter.

Pressure ulcers.

This is where nurses make the biggest difference.

Pressure ulcers, or pressure injuries, as they're now called, are caused by pressure over bony prominences plus time.

It creates ischemia tissue death.

The text distinguishes between friction and shear.

I think people use these interchangeably, but they're different.

Can we clarify that?

Yes.

And it's a critical difference.

Friction is surface damage.

Think sheet burn.

You rub the skin against the sheets.

It hurts.

It's red, but it's superficial.

Shear is much more dangerous.

How does shear happen?

Shear happens when gravity pulls the skeleton down, like when a patient slides down in a hospital bed, but the skin stays stuck to the sheet.

The bone moves down.

The skin stays put.

So the layers are sliding against each other deep inside.

Exactly.

And what happens is the blood vessels deep inside connecting the skin to the underlying tissue, they get kinked, stretched, and torn.

Oh, wow.

It cuts off the blood supply from the inside out.

So you get deep tissue ischemia before you even see a mark on the skin.

Shear is a major cause of deep stage three and four wounds.

So we use the Braden scale to assess risk.

What's the magic number?

A score of 18 or less indicates at risk.

The scale goes from six to 23.

The lower the number, the higher the risk.

It looks at sensory perception, moisture, activity, mobility, nutrition, and friction share.

I always found it interesting that sensory perception is rated so highly.

It's the alarm system.

If you can't feel discomfort, you won't shift your weight.

And if you don't move, you get an ulcer.

It's that simple.

Let's visualize the staging system.

This is classic exam material.

Okay.

First suspected deep tissue injury or DTI.

The skin is intact, but it's purple or maroon.

It looks like a deep bruise.

This is usually from shear.

The damage is deep.

Then stage one intact skin,

non -blanchable erythema.

You press on the red spot over a bone and it stays red.

It doesn't turn white.

That means the microcirculation is already compromised.

And we recall our cultural competence lesson in dark skin.

You won't see the red.

You feel for heat or hardness.

Exactly.

Stage two.

This is partial thickness loss.

The skin is broken.

It looks like a popped blister or a shallow abrasion.

It involves the epidermis and maybe the top of the dermis.

Stage three.

Full thickness skin loss.

You've gone through the dermis.

You can see subcutaneous fat.

It looks like a deep crater.

And stage four.

Full thickness tissue loss.

You are seeing the architecture.

Bone muscle or tendon is visible.

This is a massive life -threatening wound.

And finally, unstageable.

What's that about?

This is when the wound bed is covered in slew, that yellow stringy goo or escher,

that thick black leathery crust.

So you can't see the bottom.

You can't see the bottom of the wound because of the junk covering it.

So you can't tell if it's a stage three or four.

It is unstageable until you clean it out.

But there is one major exception regarding escher, right?

The heels.

Yes.

This is a do not touch zone.

If you see stable, dry, black escher on the heels, do not remove it.

It acts as a natural biological band -aid.

Why?

The heels have really poor blood flow.

If you peel that scab off, you open the door to infection in area that cannot heal.

If it's dry and stable, leave it alone.

Okay, prevention.

This is a bread and butter.

Turning the patient.

Standard of care is turning every two hours.

But notice the position.

We use the 30 degree lateral position.

Why not just roll them on their side?

90 degrees.

If you put them 90 degrees on their side, you are putting all their body weight directly on the trochanter, the hip bone.

You will just cause a sore there instead of the sacrum.

30 degrees is a tilt, using pillows to support the back.

It distributes pressure much better across the soft tissue of

And nutrition.

You can turn them all day, but if they aren't eating.

You can't build a house without bricks.

You need protein to build tissue.

We watch the albumin levels.

If albumin is less than 3 .5 grams per deciliter, that's a huge red flag for malnutrition.

They need high protein supplements to heal.

Now management.

Let's talk about putting things on the wound.

The text had a major warning about antiseptics that surprised me.

This surprises a lot of people.

Do not use betadine, pavadone, iodine, or hydrogen peroxide on a healthy, granulating wound.

But aren't those for cleaning wounds?

I see peroxide on cuts at home.

They are cytotoxic.

That means they kill cells.

They kill bacteria, yes, but they also kill the good cells, the fibroblasts and epithelial cells that are trying to knit the wound back together.

So you're killing the healing process.

You are essentially scrubbing away the healing process.

You only use those for infected wounds and only for a short time.

For a clean, pink, healing wound, just use normal saline.

So we are back to, a dry cell is a dead cell.

That's the mantra for dressings.

Right.

You want a moist wound environment, not soaking wet, not desert dry.

Moist.

It just speeds up epithelialization.

Can we do a quick rapid fire on the dressing types?

Sure.

Match the dressing to the wound.

First, transparent film, like Tegaderm.

Think plastic wrap.

Right.

It keeps moisture in bacteria out.

Yeah.

Good for stage one or just for protection against friction.

Okay.

Hydrocolloids, like duoderm.

These are wafers that melt into a gel.

They're occlusive.

Yeah.

Good for stage two or third.

Got it.

Alginates.

These are cool.

They're made from seaweed.

They're super absorbent.

You use these for wounds with heavy exudate, really wet wounds.

They soak it all up.

That last one.

Hydrogels.

This is basically water in a tube.

You use this to add moisture to a dry wound.

So if it's wet, you absorb it with an alginate.

If it's dry, you hydrate it with a hydrogel.

Exactly.

It's all about balancing the moisture.

Wow.

We have covered a massive amount of ground, from the cellular level of the epidermis all the way to staging deep tissue injuries.

It is a lot, but if you boil it down, the take home message is this.

The skin reflects the overall health of the older adult.

It's not just a wrapper.

And our role as nurses.

We are the detectives.

We are turning the patient at 2 a .m.

We are the ones spotting the redness on the heel before it breaks open.

We are the ones noticing the patient isn't eating their protein.

So it's all prevention.

Prevention is the most powerful tool we have.

By the time a stage four ulcer forms, the system has already failed.

That is a powerful perspective.

It really highlights how critical this basic care actually is.

And one final thought for the road, if I can.

Please.

Consider the emotional impact.

Imagine having a wound that smells bad or a rash that itches constantly or a lesion you fear is cancer.

Skin issues lead to isolation.

They affect body image.

Absolutely.

So when you treat the wound, remember you are treating a person who might be embarrassed or afraid or just miserable.

Treat the person, not just the sore.

I love that.

All right, learners, that wraps up our deep dive into Chapter 28.

Take these nuggets, review your mental tables for those leg ulcers, and remember, look at the palette for jaundice.

Good luck on the exam and in your clinical rotations.

You've got this.

Thanks for listening to the deep dive.

Catch you next time.