Welcome to the bed. We'll go ahead and give you
the story. This is all going to happen super
fast. Welcome to the emergency room. 45 minutes
of CPR. We can stop CPR. Welcome back to The
Deep Dive. We are shifting gears today. A little
bit of a different focus. Yeah, exactly. Usually
when we talk about emergency medicine or, you
know, critical care and pediatrics, everyone
wants to talk about the high drama organs. The
heart, the lungs, the brain. Oh, absolutely,
the glamorous stuff. The glamorous stuff that
beeps on the monitor. They certainly get all
the glory in the textbooks. Everyone wants to
interpret the ECG or manage the ventilator. So,
so lately. But today, we are focusing on the
unsung hero, the body's largest organ, the skin.
And honestly, for a lot of nursing students and
even experienced nurses, the skin is, well, it's
an afterthought. It's seen as just the wrapper.
It's just the wrapper, right, until it isn't.
I've heard it described as the check engine light
of pediatric nursing. That is a perfect analogy,
but I'd take it a step further. It's not just
a light. It's the entire dashboard. The dashboard.
I like that. In pediatrics, the skin is often
your first clue, sometimes your only clue, that
there is a systemic issue, a raging infection,
or a severe trauma occurring. If you ignore the
check engine light, the car breaks down. And
if you ignore the skin findings in a child, the
child crashes. It's that simple. So here is the
setup for today. We are treating this deep dive
as a specialized exam cram session. But I don't
want the superficial flash card version. I really
want the why. The deep mechanics of it. Yes.
We are imagining our listener is stepping into
the shoes of a nursing student right before finals
or a nurse prepping for their pediatric certification.
We need to be rigorous. And we are going to cut
through the noise. We're going to look at Chapter
23, integumentary disorders and the drug protocols.
But we aren't just reading the list. We are applying
the Pareto principle, the 80 -20 rule. Which
means we are identifying the 20 % of skin concepts
that show up on 80 % of exams and are critical
for safety. I'll play the role of the ambitious
student who wants the cheat codes but also demands
to understand the mechanics. I'm not just going
to nod along. I want to know why the physiology
works the way it does. and I will play the clinical
educator. My job is to filter the list, focus
on safety, assessment priorities, and explain
the path of physiology so you don't have to memorize
it by rote. OK, let's dive in. Section A, the
master 80 -20 map. When you look at the integumentary
system in kids, it can feel like a laundry list
of weird Latin names, teneavus, dermatitis, that.
How do we organize this into big buckets so we
don't lose our minds? You have to categorize
them or you will get overwhelmed. In the source
material we have today, everything really falls
into four distinct patterns. If you can recognize
the pattern, you can predict the test question
and the clinical intervention. Okay, lay out
the four buckets for me. Bucket one is infectious
patterns. This is your biological warfare section,
bacteria versus fungus. Think impetigo versus
ringworm. The exam priority here is almost always
contagion control. How do I stop this from spreading?
And of course, identifying the rash by its visual
description. Contagion and description. Got it.
Bucket two. Inflammatory and allergic patterns.
This is where the body attacks itself or overreacts
to the environment. Eczema and dioper dermatitis
are the big ones here. And the priority there
isn't so much life or death. Not in the immediate
sense, no. It's symptom management, comfort,
and a huge amount of parent education. Right.
Okay, what's bucket three? Hormonal and developmental
patterns. This is primarily acne vulgaris. Now,
you might roll your eyes and think acne is low
stakes, but the exam priority here is the psychosocial
impact on the adolescent and medication safety.
Medication. Specifically, there are some very
dangerous drugs used for severe acne that show
up on exams constantly. We have to know them
inside and out. And the fourth bucket. I'm guessing
this is the scary one. This is the scary one.
Trauma and emergency patterns. This is burns.
This is the highest stakes bucket. This is where
skin issues become life -threatening airway and
circulation issues. So if I'm looking at this
stack of papers and I'm panicking because my
exam is tomorrow, what is the can't miss list?
What absolutely must I know to be safe? OK, cut
to the chase. If you remember nothing else from
today, you must master the management of burns,
specifically the prioritization of airway and
fluid volume, and you must master the safety
protocols for severe acne medication, specifically
isotrenilin or acucaine. Burns and acutane. Those
are the two areas where a wrong answer or a missed
assessment leads to significant harm or death.
Full stop. OK. Burns and Accutane are the heavy
hitters. We will definitely spend a significant
amount of time on those. But let's start with
the stuff that you see every single day in the
clinic. Let's go to that first bucket, infectious
pattern. Let's do it. Topic one, Empedigo. Even
the name sounds unpleasant. It sounds like something
a goblin would have. It is unpleasant. It's the
classic bacterial skin infection in kids. It's
incredibly common. Give me the one -liner, the
thing I should immediately think of when I see
the word Empedigo. The honey -crusted contagion.
Okay. Honey -crusted. That's the visual cue.
Let's unpack the pathet here. I don't want just
the visual yet. What is happening at the cellular
level? So you're usually dealing with Staphylococcus
aureus or Streptococcus pyogenes. These are bacteria
that naturally colonize our skin. They hang out
on the surface and cause zero problems. They're
just part of the normal flora. Exactly. They're
fine. Until there's a breach. The breach being
the key. We aren't just talking about a massive
cut, right? This isn't from falling off a bike.
No, and that's the exam trap. The breach is microscopic.
It's a mosquito bite the kid scratched. It's
a runny nose where the tissue got raw from constant
wiping. It's a little patch of eczema. The bacteria
finds that opening, dives into the epidermis,
and releases toxins. And those toxins are what
caused the blistering. Is that the mechanism?
That's it, exactly. The toxins break down the
proteins that hold skin cells together, specifically
the desmosomes. So the skin literally starts
to separate. Fluid leaks out. That's your vesicle.
And when that vesicle pops, the serum dries up.
Ah, so that's the honey. That dried serum is
what gives you that classic golden honey -colored
crust. Okay, that makes the honey description
surprisingly grosser when you know it's dried
serum. But distinguishing this on an exam, is
it always crested or are there different types
I need to watch for? Great question. because
you can get tripped up here. There are two types,
non -bullis and bullis. The honey crust is the
non -bullis type. That's the most common, maybe
70 % of cases. OK, so what is bullis and pedigo?
Bullis is exactly what it sounds like. Big, fluid
-filled, glisters bully. These don't always crust
immediately. They look like shiny, raw, red circles
after they pop. It's often caused by specific
toxin -producing staph. I feel like that's a
critical distinction, because if a student is
only hunting for the keyword crust, they might
miss a case study describing a shiny, denuded
red area on an infant. Precisely. If you see
bulo, or varnish -like crust, you still need
to be thinking in pedigo. It's the same family
of infection, just a different presentation.
And where do we usually see this? Anatomically?
Off and around the nose and mouth. Think about
toddlers. They're constantly wiping their noses,
touching their faces. They create little micro
abrasions. The bacteria gets in, and boom, honey
crusts. So what's the need to know treatment?
How do we fix this? If it's mild and localized,
just a few spots. We use a topical bacterial
ointment. like muperosin. We just put the medicine
right on the lesions. But before you apply it,
there is a nursing step that people often forget.
Oh, this sounds like a good test question. What
is it? You have to remove the crust. Really?
You have to pick it off? You do. The crust is
a barrier. It's like a shield. If you put ointment
on top of a hard scab, it doesn't get to the
bacteria underneath. You need to soak it with
warm water and gently scrub it off. Gently being
the operative word, you're not trying to make
it bleed. No, not at all. Just soften and de
-bride that superficial layer so the medication
can penetrate. OK, so that's for mild cases.
What if it's severe, like it's all over their
body? If it's widespread, or if there is fever
and lymphadenopathy, swollen lymph nodes, we
move to oral antibiotics, usually a syphilis
warren or a moxacillin clavulinate, something
that gives good staph and strep coverage. And
for the parents? Because I imagine they freak
out when they see this scabbing all over their
kid's face. What's the key education point? The
biggest parent education point is hygiene. This
is highly contagious. If that kid touches the
crust and then touches another kid or touches
a toy that another kid touches, it spreads. What's
that term for when they spread it on themselves?
Auto -inoculation. They scratch their nose, then
scratch their arm, and suddenly they have a new
spot on their arm. Right. So hand washing is
paramount. Keep the child's fingernail short
so they can't scratch and spread it. They need
to stay home from daycare or school for the first
24 hours after starting antibiotics. Is there
any good news for the parents? Something to calm
them down? Yes. A common fear is scarring. Parents
see these nasty scabs on their beautiful baby's
face and worry it's permanent. You can reassure
them. Empedigo is superficial. It sits in the
epidermis. It tends to heal without scarring.
It looks worse than it is. That's a huge relief
for them, I'm sure. Okay, let's move from bacteria
to fungus. Topic two. Fungal skin infections.
The tiniest. We call them the tiniest. It's a
fungus among us, differentiated by location.
I feel like ringworm is the term everyone knows,
but it's kind of a misnomer, right? It's not
a worm. Completely. There is no worm. It's a
dermatophyto, a fungus that feeds on keratin.
Keratin is the protein in your hair, skin, and
nails. So it's literally eating the skin. It
is, and it grows in a circle, expanding outward
as it eats the keratin in your skin. The center
clears up because the fungus has moved on to
fresher pastures at the edge, creating that classic
ring. That is disturbingly evocative, fresher
pastures. Let's run down the anatomy lesson because
the Latin names tell you exactly where it is.
Right, so if you see tinea caddis on an exam.
Epitetus means head, so scalp. Correct, tinea
cruus. Cruus. Sounds like crutch, groin, jock
itch. Exactly, tinea pedis. Pedis is foot, athlete's
foot. Easy enough. Tinea corporis. Corporis means
body, so arms, legs, trunk. Yes, that's your
classic ringworm presentation, the circular patch
on the arm. And then tinea versicolor is specifically
on the trunk and extremities, often looking like
discolored patches, either lighter or darker
than the surrounding skin. Okay, let's talk treatment.
This seems straightforward. Is it just put cream
on it for all of them? This is the exam trap,
and it's a big one. For most tinea, you know,
like tinea corporeis on the arm or tinea pedis
on the foot, yes, you use a topical anti -fungal
cream like clitrimazole or miconazole. And there's
a specific way to apply it, right? Yes, you apply
it an inch past the border to catch the spreading
fungus. You're trying to create a firewall. Why?
I hear a butt coming. But tinea capitis on the
head is different. Think about the anatomy. The
fungus isn't just on the skin, it's down inside
the hair follicle. Oh, so a topical cream isn't
going to reach it? It can't get down that deep?
Correct. Creams can't penetrate deep enough into
the follicle bulb. So if a child has tinea capitis,
we usually need oral systemic medication. Grizzle
fulvin is the gold standard here. Oral meds for
a scalp rash? That's a massive distinction. So
if you pick topical nystatin for tinnacupitis
on an exam, you are wrong. You are wrong, and
the patient won't get better. And clinically,
tinnacupapetus can cause permanent hair loss
if it causes a carrion. a big, boggy inflamed
abscess. So we treat it aggressively from the
inside out. Okay, that's a huge clinical pearl.
Oral meds for the head, topical for the body.
And sometimes we add a special shampoo, like
selenium sulfide shampoo, to help decrease the
fungal load on the scalp. But the shampoo alone
is not enough. It's an adjunct to the oral therapy.
Got it. Okay, moving on to Book It 2. Inflammatory
patterns. Topic 3 is a big one. Eczema. Or atopic
dermatitis. The itch that rashes. Wait, don't
you mean the rash that itches? No. And that's
a crucial distinction in pediatrics. We call
it the itch that rashes, because the itching
often comes first. The child feels this intense,
pruritus itching, and they scratch. The scratching
damages the skin barrier, and then the rash flares
up. It's an allergic cycle. Scratching leads
to rash, which leads to more itching. That's
a paradigm shift for me. So the itching is the
cause, not the symptom. In many ways, yes. The
primary sensation is the pruritus. Let's talk
about the atopic triad. I see this term everywhere.
What is it and why does it matter? This is essential
for history taking. Eczema rarely travels alone.
It travels with two friends, asthma and allergic
rhinitis or hay fever. If a kid comes in with
severe eczema, you could be asking about breathing
issues and allergies. So if you see one, you
should be looking for the others. You should
have a high index of suspicion. It's all the
same underlying hypersensitivity. an overactive
immune system. Pathologically, what is wrong
with their skin? Why is it so dry? It's often
a genetic defect in a protein called filigrin.
Filigrin? Imagine your skin cells are bricks.
Filigrin is the mortar that holds them together
and keeps moisture in. In eczema, the mortar
is crumbly. Water evaporates out. We call that
transepidermal water loss. Yeah. And allergens
get in. So the skin is literally leaky? The barrier
is compromised from birth. Yes. It's dry, cracked,
and defenseless against the environment. So what
is our priority intervention? If the problem
is dry, itchy skin, how do we fix it? What's
the 80 -20 here? Hydration and moisture preservation.
That is the number one goal. We have to seal
the barrier. How do we do that? The source material
explicitly names some products here. Yes, it
mentions aquaphor and Cetaphil. We need heavy,
thick emollients. We are not talking about watery
lotions that smell like vanilla. Why not? Lotions
seem like a good idea. Lotions have high water
content and can actually dry the skin more as
they evaporate. It's counterintuitive. We need
ointments, grease, petroleum -based products
that create an occlusive barrier. So grease them
up. Grease them up. Especially right after a
bath, when the skin is still damp. We call it
the soak and seal method. A short, lukewarm bath,
pat dry, and then immediately slather on the
ointment to trap that moisture. What about medications?
If the moisturizing isn't enough? We attack the
two problems. The inflammation and the itch.
For inflammation, we use topical steroids during
flare -ups. Now, parents are often terrified
of steroids, steroid phobia. They think it will
stump the kid's growth or thin their skin instantly.
How do you counsel them? And that's a valid concern
is misused. But as the nurse, you educate. We
use the lowest potency that works only on the
affected areas and only for short bursts like
one to two weeks. We don't slather high -dose
steroids on the face for months. It's about appropriate
use. So low and slow. And there's a mention of
immunomodulators like tacrolimus. What's their
role? Right. Those are non -steroidal options.
We use them specifically for sensitive areas
like the face or eyelids where you want to avoid
long -term steroid use. Or we use them for maintenance
to prevent flares. And what about the itch? How
do we stop that cycle we talked about? Antihistamines.
Especially at night. Something like diffenhydramine
or hydroxazine can help break the cycle by reducing
the itch and helping the child sleep. I want
to pause on the developmental impact here. Because
eczema sounds annoying, but is it really a developmental
issue? Hugely. Imagine you were a two -year -old.
Your main job is to sleep and grow. But your
skin feels like it's on fire. You itch constantly.
You can't sleep. And if you don't sleep? If you
don't sleep, you don't... release growth hormone
properly. You are irritable. You aren't playing.
You aren't learning. Severe eczema can be a major
disruptor to infant and toddler development,
strictly due to sleep hygiene and chronic discomfort.
It affects the whole family dynamic. That puts
it in perspective. It's not just dry skin. quality
of life issue that has real developmental consequences.
Exactly. Let's slide down to the other inflammatory
issue. Diaper dermatitis versus candidiasis.
This is the battle of the diaper rashes. The
common versus the east. Every parent deals with
this at some point. How do I tell them apart
visually? What's the key finding? Standard diaper
dermatitis is usually erythema redness on the
convex surfaces. Convex, so the parts that stick
out. Exactly. The parts of the butt that touch
the diaper. The cheeks. It spares the folds.
Wait, it spares the folds? That seems odd. Usually,
yes, because it's caused by friction and irritation
from urine and stool. The folds are tucked away
and protected from that direct contact. OK, so
redness on the cheeks, but the creases look fine.
And the treatment? Varioidments. We need to put
a wall between the skin and the diaper. Zinc
oxide, vitamin A, D, E, petrolatum. You slather
it on like frosting on a cupcake. I like that
visual. And you don't wipe it all off. You don't
scrub it off fully with every change. You just
clean the soiled part and add more frosting.
Protect that barrier at all costs. Air time is
also great. Let them run around without a diaper
for a bit. OK, what about candidiasis, the yeast?
How does that look different? Candidiasis loves
the folds. It loves warm, dark, moist places.
So if the redness is deep in the inguinal folds,
you should suspect yeast. So it's the opposite
of the standard rash. Exactly. And what's the
hallmark visual finding? This sounds like a test
question. It is. Satellite lesions. This is the
buzzword. You have the main beefy red rash and
then a little red dot scattered outside the main
border. Like satellites orbiting a planet. If
you see satellite lesions, it's yeast. And barrier
cream won't fix yeast. Correct. You're just trapping
the yeast under a layer of ointment. You need
an antifungal. Neustatin or Clotrimazole. The
source explicitly separates these because the
treatment path is totally different. If you treat
yeast with zinc oxide, it won't go away and the
parents will be back in two days. Got it. Okay,
let's graduate from babies to teenagers. Bucket
three, hormonal patterns. Topic five, acne vulgaris.
The adolescent rite of passage. The source material
emphasizes that this is exclusively discussed
in the context of adolescence. Which makes sense
physiologically. Puberty hits, androgens, the
male hormones, surge in both boys and girls.
Those androgens tell the sebaceous glands to
go into overdrive and you get acne. And developmentally,
this is massive. This isn't just a cosmetic issue.
It is absolutely not. Adolescence is all about
identity formation, body image, and peer acceptance.
Acne strikes right at the center of their vulnerability.
A bad breakout can lead to social withdrawal,
depression, anxiety. It's never just a pimple
to a teenager. So how do we treat it? I see a
treatment ladder here in the outline. Think of
it as steps. We start mild and get heavier. Step
one is hygiene. Gentle cleansing. Twice a day.
The text says mild cleanser. Why not scrub it?
I feel like the instinct is to scrub the grease
off. That's the wrong instinct and it's a common
mistake. Scrubbing irritates the skin, causes
more inflammation, and can actually stimulate
more oil production as a rebound effect. We want
gentle cleansing to remove the surface oil without
destroying the skin's natural barrier. Okay,
so no harsh scrubs. Step two on the ladder. Topicals.
We use retinoids like tretinoin to help turn
over skin cells so pores don't clog, or benzoyl
peroxide, which is an antibacterial agent, to
kill the P. acnes bacteria that contributes to
inflammation. So you're unclogging and killing
bacteria at the same time. Ideally, yes. Sometimes
we use them in combination. Step three. What
if the topicals don't work? If topicals don't
work, we add systemic antibiotics, the sourceless
tetracycline. This is an oral pill to fight the
infection and inflammation from the inside out.
And if all that fails, the kid is still miserable,
they're getting scars, we bring in the big guns.
Isotretinoin. Brand name Accutane, though there
are many generics now. This is reserved for severe,
nodulacistic acne that is scarring and resistant
to everything else. Alright, let's climb the
ladder to the top rung. We've tried the special
soaps, we've tried the creams, we've even done
the oral antibiotics. The kid is still suffering.
We bring in the nuclear option. Isotretinoin
is a miracle drug for acne. I mean, it really
can be life -changing. But it is the highest
maintenance drug in dermatology. The source material
highlights box 23 .2 for Accutane. Whenever a
textbook puts a black box around something, I
pay attention. What is the absolute red flag
do not pass go risk here? Teratogenicity. Meaning
birth defects. Severe life altering birth defects.
If a female patient takes this drug while pregnant
or becomes pregnant while on it, the fetal outcomes
are catastrophic. Craniofacial abnormalities,
heart defects, brain malformations, it is incompatible
with a healthy pregnancy. Which leads to the
IPLGG's program. I remember this being a huge
logistical hurdle in the clinic. Can you explain
what that is? It is, but it's necessary. You
cannot just write a script. The patient, the
provider who prescribes it, and the pharmacist
who dispenses it all have to be registered in
a federal database. Everyone has to be in the
system. Yes. And clinically, what does that look
like for the nurse? You aren't just asking, are
you pregnant? No, I imagine it's more involved.
Much more. You need proof. two negative pregnancy
tests before you even start the first dose, a
negative test every single month before a refill
can be dispensed, and usually a requirement for
two simultaneous forms of birth control. Two
forms. So the pill plus condoms or an IUD plus
condoms. Exactly. Redundancy is key. And here
is where the art of nursing comes in. You are
having this conversation with a 16 year old girl,
maybe with her mom in the room. It can be awkward.
Extremely. How do you navigate that? You have
to be fearless and non -judgmental. You have
to advocate for that safety protocol because
the alternative is tragic. You explain the risks
clearly, you assess their understanding, and
you document everything. Is there a mental health
component, too? I feel like I've heard about
mood changes. There is. It's controversial in
the data. Some studies show a link, some don't.
But the protocols are clear. Monitor for depression
and suicidal ideation. But isn't the acne itself
causing depression? It is. That's the confounding
variable. Does the drug cause depression or does
the drug fail to relieve the depression caused
by the acne fast enough? Regardless, our job
is to monitor. So you are monitoring the skin,
the womb, and the brain. Wow. It's a heavy -duty
medication. It absolutely is. All right. We have
arrived at the final bucket, the most critical
section of this entire deep dive. If you are
listening to this on your commute, turn the volume
up. Bucket four. Trauma, specifically burns.
This is the section where skin issues stop being
dermatology and start being critical care. A
severe burn is a full body insult. You called
it systemic trauma earlier. But a burn is on
the skin, why is it systemic? What's the mechanism?
Because the skin does so much for us. It keeps
fluids in, it keeps heat in, it keeps bacteria
out. When you burn a large percentage of a child's
body, all those systems fail at once. You lose
fluid, you lose heat, you invite infection. But
there's more to it than that, right? Much more.
The burn releases a storm of inflammatory mediators,
cytokines, that cause blood vessels all over
the body to dilate and leak. So even if the burn
is just on the legs? the blood vessels in the
lungs or the arms might start leaking. Exactly.
It's a systemic inflammatory response syndrome,
or SIRS. The whole body is on fire, metaphorically.
The outline gives us a very specific need -to
-know list for emergency assessment priorities.
It's the ABCs, but tailored for burns. Let's
walk through them in order, because the order
matters for the exam. Airway is always king.
Always. But in burns, the threat is insidious.
What do you mean by insidious? It's not obvious.
Well, if a kid breaks their leg, The leg is broken,
you can see it. In a burn, specifically with
smoke inhalation, the damage is internal. You
might look at the child and they seem fine, they
were talking to you. But five minutes later,
their airway has swollen shut due to edema from
the heat and soot. That is terrifying. So what
are the clues? If I can't see the swelling yet,
what am I looking for? What are the red flags
for airway involvement? You are looking for the
evidence of the fire on the face, singed nasal
hairs, soot around the mouth or in the sputum,
burns on the neck or face, and listen to their
voice. Any hoarseness is a major red flag. And
if I see those, what's the move? You assume the
airway is compromised until proven otherwise.
You don't wait for them to start gasping or for
their oxygen saturation to drop. We often intubate
these kids prophylactically early. Better to
intubate early than try to shove a tube through
a swollen throat later. 100%. Once that airway
swells, it can be impossible to get a tube in.
So secure the airway. That's priority number
one. Now once the airway is secure, we move to
the other silent killer. Priority two, fluid
volume. Hypovolemic shock. Right. And this is
pure physics. The skin holds our water in. You
burn the skin, the water evaporates. But it's
worse than that. We talked about those leaky
capillaries. Fluid rushes out of the blood vessels
and into the tissue. We call this third spacing.
So the patient looks puffy and swollen, but their
blood vessels are empty. Exactly. It's a paradox.
Yeah. They are demidus, but their blood pressure
is tanking because the tank is empty. The heart
has nothing to pump. This is burn shock. And
kids are at higher risk for this than adults,
right? Why is that? Yes. Kids have a larger body
surface area relative to their weight. Think
of a baby's head. It's huge compared to its body.
They have more skin per pound, so they lose fluid
much, much faster. This brings us to the Parkland
formula. I know we aren't doing math on a podcast,
but conceptually, what is the goal here? The
goal is aggressive replacement. using lactated
ringers. We are pouring fluids in to keep up
with the leak. The formula gives you a target
volume to infuse over 24 hours, with half of
it going in during the first eight hours. But,
and here's the pediatric nuance, you can't just
open the fire hose. You absolutely cannot. Kids
have tiny hearts and a fixed stroke volume. If
you flood them with fluid too fast, you send
them into pulmonary edema, you drown their lungs,
it is a tightrope walk. So how do you know if
you're giving the right amount? You titrate the
fluids based on urine output. Urine output is
the speedometer. Exactly. If they're making adequate
urine, which for a child is about one milliliter
per kilogram per hour, then the kidneys are happy.
If the kidneys are happy, it means they're getting
enough blood flow, which means the heart is pumping
effectively. It's our best real -time indicator
of organ perfusion. Okay. Airway, then fluids.
Priority three. Hypothermia. Again, skin keeps
us warm. A burned child has no insulation. They
lose heat rapidly to the environment. And getting
cold is bad for more than just comfort. It's
deadly. If they get cold, their clotting factors
stop working and they can start bleeding. Their
metabolism crashes. You have to keep them warm.
Crank the room heat. Use warm IV fluids. Use
warming blankets. Priority four. Infection. The
barrier is gone. Sepsis is a huge risk, but it's
usually a later complication, not an immediate
one. Right. This is why we use sterile technique
for dressing changes and monitor for signs of
infection down the line. And finally, the last
two pieces. Pain management and nutrition. Pain
is obvious. Burns are excruciating. We use IV
opioids. Never IM injections in a burn patient.
Why no IM shots? Because absorption is totally
unpredictable in that edematous third spaced
tissue. You might give a shot and it just sits
there. Then suddenly it all gets absorbed at
once. FOIVI is the only safe way. And nutrition.
A major burn puts the body into a hyper metabolic
state. The body is burning calories like crazy
trying to heal and stay warm. They need massive
nutritional support. high protein, high calorie,
to rebuild that tissue. If you don't feed them,
they won't heal. So for the exam, airway first,
always, check for certs, singed hair, then fluids
using the Parkland formula and watching urine
output, then temperature, then later, infection,
pain, and nutrition. That is your roadmap. Yeah.
If a question asks what is the nurse's priority
action for a child with facial burns, the answer
is assess airway, not start an IV. Airway first.
Got it. Okay, let's move into section C, the
medication module. We've touched on some of these,
but let's do a rapid fire review of the specific
drugs mentioned in the source material. I want
the Pearls, the specific nursing considerations.
Let's do it. Category one, acne management. We
talked about retinoids like tretinoin. What's
the Pearl? The Pearl is photosensitivity and
time. These take four to six weeks to work and
they make the skin burn easily. Parent teaching.
Wear sunscreen and don't give up after week one.
It might get worse before it gets better. It
bleaches everything. It bleaches towels, pillowcases,
shirts. Tell the teen, use an old white towel,
or your mom's gonna kill you for ruining the
fancy linens. It's a real world tip that improves
compliance. Used for resistant acne. The pearl
here for pediatrics, and this is a general rule,
is to be careful with age. Petrocyclins can stain
developing teeth gray or yellow. Permanently.
Permanently. So we usually reserve them for children
over eight or nine years old, once the permanent
teeth are fully calcified. OK, category two.
Eczema management. Topical immunomodulators like
Tacolimus. The plural is that it is a non -steroidal
option. Great for faces. But it can burn or sting
when first applied. You have to warn the parents
so they don't think the child is having an allergic
reaction to the medicine and stop using it. Topical
steroids. Potency matters. Avoid the face and
diaper area if possible, or use very low potency.
Thin skin absorbs too much. The side effect to
watch for long term is skin atrophy, which is
thinning, and striae, or stretch marks. Antihistamines,
like diphenhydramine or hydroxazine. Crucial
distinction. Antihistamines treat the symptom,
which is the itch, not the rash itself. They
help the child sleep and break that itch scratch
cycle. Side effect in kids. Sedation is common,
but watch out for the paradoxical effect. Where
they get hyper instead of sleeping. Exactly.
Instead of calming down, they're bouncing off
the walls. You need to warn parents that this
can happen. Category three. Anti -infectives.
Grizzofilvin. Oral antifungal for tinea capitis.
The pearl is absorption. It is insoluble in water.
It needs fat to be absorbed. So take it with
what? A fatty meal. Whole milk. ice cream, peanut
butter. If you give it with water or juice on
an empty stomach, it won't work. The patient
won't get better. That's a great tip. Take your
medicine with ice cream. I bet compliance goes
way up with that instruction. It definitely helps.
And one other thing, you need to monitor liver
enzymes, the LFTs, if they are on it for a long
time, as it can be hepatotoxic. Good to know.
OK, we are in the home stretch, section D, cross
-linking and synthesis. Let's connect some dots
here, bring it all together. The biggest connection
I want listeners to make is the scratch infection
cycle. Walk me through it. Connect the dots for
me between the different buckets. OK, so we talked
about eczema. That's an inflammatory condition.
It itches, the child scratches. Now you have
an open wound, a breach in the barrier, what
lives on the skin? Staff bacteria. Staff bacteria.
The staff gets in the open wound, and now you
have impetigo, an infectious condition, on top
of eczema. This is called a secondary infection.
So treating the itch isn't just about comfort,
it's about infection prevention. Exactly. Giving
that antihistamine for the eczema prevents the
scratch, which prevents the impetigo. It's all
connected. You're treating the inflammation to
prevent the infection. Another theme I'm seeing
is the barrier theme. It keeps coming up. It's
the central theme of pediatric dermatology. Whether
it's dipodermatitis, where we use zinc oxide,
or eczema, where we use aquaphor, or burns, where
we use dressings, the nursing goal is always
restoring the skin barrier. The skin is the castle
wall. If the wall is breached, the enemy gets
in. Our job is to patch the wall. And finally,
let's talk about the adolescent compliance piece.
This seems to cross over from acne to other things
too. It's huge for acne. The treatments retinoids,
antibiotics, require long -term daily compliance.
But adolescents are developmentally notorious
for poor compliance. They want instant results.
And these things don't work instantly. Not at
all. When the cream doesn't fix their face in
two days, they stop using it. Or they get frustrated
and use way too much and burn their face, and
then they stop using it. So nursing care involves
a lot of expectation management. It's more coaching
than just giving instructions. Exactly. You have
to say, this will take six weeks to see a difference.
It might look worse before it looks better. You
have to keep doing it every single day, even
when you don't see results yet. Coaching the
teen is just as important as writing the prescription.
You have to treat them like a partner in their
own care, not a child you're ordering around.
This has been a fantastic run -through. Let's
do the final tally. If you could only remember
a few things from today for an exam, what are
the big takeaways? Okay, the rapid -fire summary.
Visuals. If you see Honeycrest, think in pedigo.
If you see satellite lesions, think yeast. If
you see a ring with a clear center, think Tina.
Got it. Emergencies. If you see burns, think
airway. Looking for singed hair or soot. And
fluids. Thinking Quarklin formula and urine output.
Those come first, before anything else. And meds.
The big one. If you see Accutane or Isotretinoin,
think safety. Think pregnancy prevention. And
think mental health monitoring. Short, sweet,
and saves lives. I want to leave the listeners
with a final provocative thought. Something to
chew on. Okay. We spend a lot of time looking
at the surface. rashes, burns, pimples. But in
pediatrics, the skin is just the messenger. My
thought for you is specifically on burns. We
treat the skin but the killer is often what we
can't see. The insidious part you mentioned earlier?
Exactly. It's the airway swelling shut inside
the throat. It's the fluid leaking out of the
vessels inside the body, causing shock. In pediatric
burns, you must look past the surface immediately.
Don't get distracted by the gore of the bulk
itself. Focus on the invisible physiology that
keeps them alive. That's where you'll save a
life. That is a powerful place to end. Whether
you are walking into an exam tomorrow or walking
onto the unit, keep your eyes open, check that
check engine light, and trust your assessment.
Thanks for diving in with us. Good luck out there.
It was a pleasure. See you next time.