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. Welcome
back to the deep dive. We are jumping straight
into the fire today. We're tackling a topic that
Honestly, I think strikes more genuine fear into
the hearts of nursing students. And let's be
real, new grads and even seasoned nurses than
almost anything else. Oh, for sure. We're looking
at pediatric respiratory disorders. It's the
absolute high stakes arena of pediatrics. It
really is the great equalizer. You can have a
nurse with 10 years of adult ICU experience.
I mean, rock solid scene at all. But. you put
a six month old in respiratory distress in front
of them, the heart rate in the room just goes
up, it changes everything. Because children are
not just small adults, right? That's the cliche
we hear on day one of nursing school. But it's
just so fundamentally true. It is the truth of
the field. And absolutely nowhere is that truth
more critical, more life and death than in the
airway. In pediatrics, the maxim is simple. Airway
is king. If you lose the airway, you lose the
child. And it happens fast. The margins for error
are just razor thin. Well, to keep you from hyperventilating
along with your future patients, we do have a
very specific mission for this deep dive. We've
combed through a massive stack of sources here.
A huge stack. We're talking ATI pediatric nursing
materials, the heavy -hitting Wolters Kluwer
textbooks, lecture slides, clinical charts, the
works. And our goal is to boil this ocean. We
are going for the Pareto principle today, the
80 -20 rule. Exactly. We want to find the 20
% of the content. that is going to answer 80
% of the exam questions you'll face, and vastly,
more importantly, handle 80 % of the safety scenarios
you will actually see at the bedside. Yeah, we're
bypassing the fluff. We are not here to memorize
obscure statistics that nobody actually uses.
No. We're going to focus on safety, pathophysiology,
and that critical thinking, that NCLEX -style
judgment that separates a rookie from a really
safe practitioner. So let's crack the code on
this. We're dividing this deep dive into three
distinct sections. Section A is the map. the
big patterns that dictate everything in PEDS
respiratory. Section B is the meat, the specific
diseases, system by system, and then Section
C is the cross -reference where we're gonna link
it all together so you don't get tricked. Sounds
like a solid plan. Let's get to work. Okay, Section
A, the master 80 -20 map. Before we even talk
about asthma or croup or anything specific, you've
identified some patterns. in the source material.
These are like the recurring themes that seem
to dictate the rules of the game. They really
are. They're the foundational principles. And
the first one is catchy. You call it, anatomy
is destiny. Or as I like to call it, the case
of the four millimeter straw. Unpack that for
me. This stat, I mean, it really blew my mind
when I read the notes. So if you look at the
source images, specifically from the ATI and
Walter's Clure anatomy comparisons, there's this
really stark visual. An adult trachea, the windpipe.
is about 20 millimeters wide. Okay, that's a
pretty generous size, almost like a garden hose.
You can move a lot of air through that. It is
a generous size, yeah. Now, look at an infant's
trachea. It's approximately four millimeters
wide. Four. That is roughly the width of a standard
plastic drinking straw. That is tiny. that is
terrifyingly small. It is. Now here's the math
that appears in almost every major pediatric
respiratory text, and it's a favorite concept
for exam writers because it involves physics,
right? If you have one millimeter of swelling
edema in that 20 millimeter adult trachea. So
20 millimeters goes down to 19. No big deal.
Right. It's maybe a five to 20 % reduction in
the cross -sectional area. You might clear your
throat, feel a little scratchy, you carry on
with your day. It's an annoyance. Right. But
if you take that infant with the four millimeter
straw and you add one millimeter of edema all
the way around. You've practically closed it.
You have reduced the airway diameter by 50%.
Wow. One single millimeter equals a 50 % loss
of airway. Yes. And here's the kicker. The resistance
to airflow. So how hard that baby has to work
to pull air in increases by a factor of 16. 16.
16 times harder to breathe. 16 times the work.
So a little bit of swelling in a baby is a catastrophic
event compared to an adult. That is why we panic
over a stuffy nose in an infant. And speaking
of stuffy noses, the sources mention that infants
are preferential nose breathers. What does that
actually mean in practice? It means until about
for maybe six weeks of age, they don't have the
neurological reflex to automatically open their
mouth and breathe if their nose is plugged. They
don't know how. They're just hardwired to breathe
through their nose. It's to facilitate breastfeeding,
right? You latch on, you breathe through your
nose. So if a newborn has a stuffy nose, whether
it's from mucus or a condition like coanal atresia,
they aren't just uncomfortable. They're in actual
distress. They are in respiratory distress. They
are, for all intents and purposes, suffocating.
That is a massive exam tip right there. If the
question says newborn with copious nasal secretions,
it is not a hygiene issue. Not at all. That's
an airway issue. Correct. Your nursing diagnosis
isn't impaired comfort. It's ineffective airway
clearance, and it's your number one priority.
And there's one more anatomical nugget from the
sources regarding the lungs themselves, the alveoli.
Ah, yeah, the little air sacs where all the magic
happens. The gas exchange. So adults have about
300 million of them. A huge surface area, like
a tennis court spread out inside your chest.
And infants. They're born with only about 150
million. Half. So half the engine room. Half
the surface area means less room to trade oxygen
for carbon dioxide. So when they get sick, when
they have inflammation or fluid, they get hypoxic
much, much faster. They just have less reserve.
They run out of gas quicker. An adult can tread
water for a while. An infant just sinks. OK,
so pattern one is small airway, big danger. That
is crystal clear. Let's move to pattern two,
the assessment hierarchy. How do we spot trouble
before the code bell rings? Because looking at
the sources, there seems to be a major trap here
that catches a lot of students. There is. And
the sources all highlight a very specific progression
of signs, and the trap is waiting for the wrong
sign. It's the wrong sign. Cyanosis. Turning
blue. Turning blue, yes. But blue means... Lack
of oxygen. Shouldn't that be what we're looking
for? If they're blue, you're late. I mean, you
are profoundly late to the party. If they are
blue, you are practically performing CPR. Cyanosis
is a late ominous pre -terminal sign. If you
wait for the baby to turn blue, you have failed
the assessment. OK, so what is the first sign
then? If I'm on top of my game, what am I actually
seeing? The sources all emphasize that the very
first sign of respiratory distress and hypoxia
is behavioral. It's the brain screaming, hey,
any more oxygen down here. Behavioral, like crying.
Oh, not just crying, it's restlessness. irritability,
agitation. Think about it. If I put a pillow
over your face, what's the first thing you're
going to do? I'm going to slash around. I'm going
to get anxious. I'm going to fight. Exactly.
The baby can't use words. They can't tell you,
I can't breathe. So they get restless. They get
agitated. They get tachycardia, a fast heart
rate, and tachypnea, fast breathing. Their body
is compensating. So exam tip. The child is described
as fussy and cannot be consoled. breathing fast.
That is hypoxia until proven otherwise. Bingo!
Don't just assume they're hungry. Don't assume
it's a wet diaper. Assume airway first. Always.
Okay, so after that initial restlessness, what
are we looking at? The sources have great diagrams
on retractions. Right. Retractions are the muscles
sucking in between the bones, because the body
is working so hard to pull air through that tiny,
swollen straw we talked about. And there is a
hierarchy here, too, right? The location tells
you how bad things are. Yes, absolutely. It's
a progression. It usually starts low on the body.
OK. You'll see subcostal. That's right below
the ribs, or substernal, right below the sternum.
As the distress gets worse, the recruitment of
muscles moves up the body. Moves up. Yes. Next,
you'll start to see intercostal retractions.
That's when the muscles between the ribs get
sucked in. Then when things are really bad, you'll
see super sternal, that little notch above the
sternum, and finally super clavicular, which
is above the collarbone. So if I see a kid with
muscles sucking in way up by their neck. That
is severe obstruction. The higher the retraction,
generally speaking, the worse the struggle. If
you see super clavicular retractions, that child
is using Every single accessory muscle they have,
just to move a tiny bit of air, they are getting
exhausted. And there's a specific terrifying
concept mentioned in the asthma sources that
fits here. It's called the silent chest. The
silent danger. This is a classic NCLEX trap and
honestly a real life horror story. Set the scene
for me. OK, imagine you are listening to a child
with a severe asthma attack. They are wheezing
like a freight train. It's loud. It's scary.
You can hear it from the doorway without a stethoscope.
OK, I can picture that. You give a breathing
treatment, or maybe you don't have time, and
suddenly the wheezing stops. The room goes quiet.
And the novice nurse thinks, oh, thank goodness
they're better. The wheezing is gone. And the
expert nurse calls the rapid response team. Because
wheezing is the sound of air moving through a
tight tube. If the wheezing stops, but that child
still looks like they're struggling, they're
retracting, they're sitting bolt upright, maybe
turning pale, it means they aren't moving enough
air to even make a noise anymore. That's total
obstruction. That is impending respiratory arrest.
Silence is not always golden. In pediatric respiratory
distress, silence can be deadly. That's a chilling
point. No lie. And it brings us perfectly to
pattern three. The noise dictates the location.
I love this because it really simplifies things.
The sound tells you where the problem is. It's
like a diagnostic map for your ears. There are
three main sounds you absolutely need to master.
Stridor. wheezing, and crackles. OK, bring them
down for me. Let's start with stridor. Stridor
is a high -pitched, inspiratory sound. It happens
when they breathe in. It sounds like a seal barking
or a high -pitched gasp. And where is that coming
from? It comes from the upper airway, the neck
area, the larynx or trachea. So think croup,
think epiglottitis, or think a foreign body caught
in the throat. OK, stridor equals upper. Neck
issues. Got it. What about wheezing? Wheezing
is usually expiratory when they breathe out,
and it's a musical sound, a high -pitched whistle.
It comes from lower airway constriction. The
bronchi and the bronchioles are squeezed tight.
So we should be thinking. Think asthma, think
bronchiolitis or RSV. Wheezing equals lower,
the squeeze. Okay, last one, crackles. Crackles,
sometimes you'll see them called rails. That
sounds like Velcro being pulled apart or like
rubbing hair between your fingers right next
to your ear. What does that mean? That is fluid
in the alveoli, the very bottom of the lungs.
So for crackles, you should immediately think
pneumonia. Crackles equals fluid deep down. If
you can just memorize that map stridor is up,
wheezes down the squeeze, and crackles are fluid,
you can answer half the scenario questions before
you even read the vital signs. That is the 80
-20 right there. Okay, we have our map. We know
the anatomy is dangerous. We know to look for
restlessness first, not blueness. And we know
what the noises mean. Now we can apply it to
the specific diseases. Let's do it. Let's move
to section B, the system -by -system lecture.
We're going to cross -reference the ATI and Voulter's
Clure materials to give you the absolute need
to know for each major condition. Let's start
at the top of the airway and work our way down.
Perfect. Up first, the sore throat spectrum,
tonsillitis and pharyngitis. Right. So clinically,
this is simply inflammation of the lymph tissue,
the tonsils, or the pharynx, which is the back
of the throat. Give me the one -liner on the
patho. What's going on here? It can be viral,
and most of the time it is, which is self -limiting.
You just need supportive care. But the big bad
wolf here, the one we really care about, is Gabby
HS. Group A beta -hemolytic streptococcus. Or
just strep throat to you and me. And the reason
we care so much about strep isn't just because
of the sore throat. The sources are very, very
clear on this. Why do we care so much, then?
If you don't treat Gabby HS with antibiotics,
it can trigger a delayed post -infectious autoimmune
response in the body. an autoimmune response
from a sore throat. Yes. The body creates antibodies
to fight the strep bacteria, but those antibodies
can then mistakenly attack the body's own tissues.
Specifically, they can lead to rheumatic fever,
which attacks and scars the heart valves, or
acute glomerulonephritis, which damages and can
shut down the kidneys. So just to be clear, the
antibiotics aren't just for the pain. They're
to save the heart and the kidneys down the line.
Precisely. That's the why behind the prescription.
You aren't just treating the throat. You're preventing
potentially permanent organ damage. It's a huge
public health concept. That makes so much sense.
Now, sometimes the tonsils are just chronically
inflamed and they have to come out. Let's talk
about the surgical fix, the tonsillectomy. This
is huge on exams. There's a specific can't -miss
complication. Bleeding. Post -op hemorrhage.
The tonsils are extremely vascular. When you
cut them out, you leave a raw open bed of tissue
that has to scab over. And when is the risk for
that bleeding the highest? There are two distinct
windows you have to know. The first is obvious.
It's the first 24 hours post -op immediate bleeding.
That makes sense to everyone. But the second
window is the trap. It's seven to ten days later.
Wait, seven to ten days... After the surgery,
why the delay? That's when the scabs, the escher,
start to slog off and fall off. If the tissue
underneath isn't fully healed, or if the kid
eats something rough and scrapes it like a parkeia
chip or a piece of toast, they can start bleeding
again, sometimes heavily. So what does the nurse
look for? Because a four -year -old isn't going
to walk up to you and say, excuse me, I believe
I am hemorrhaging from my tonsillar fossa. No,
they're not. And what's worse is they just swallow
the blood. Blood tastes metallic and salty, and
it just trickles down the back of their throat.
So the number one most frequent early sign of
post -op bleeding is frequent swallowing. Frequent
swallowing. If you see a child after a tonsillectomy
who is constantly gulping, swallowing, clearing
their throat, you need to get a pen light and
look in the back of that throat. They are very
likely swallowing blood. And eventually that
blood is going to hit the stomach. And they will
vomit. It might be coffee ground emesis if it's
old blood or it could be Frank bright red blood.
Which brings up a very practical exam tip in
clinical rule. No red colored fluids post -op.
No red popsicles, no cherry jello, no fruit punch.
Absolutely not. Because if they vomit red fluid,
you can't tell if it's Gatorade or blood. You
want clear differentiation. It removes all ambiguity.
That makes total sense. Now let's talk about
the developmental angle here. You've got a toddler
who just had major throat surgery. Their throat
hurts like crazy. They don't want to drink. Dehydration
is the other massive risk. So really, pain management
is actually dehydration management. What do you
mean by that? If you don't adequately control
their pain, they will refuse to drink. A toddler
in pain will not swallow. So staying on top of
the pain with round the clock Tylenol, acetaminophen,
or whatever is ordered is absolutely key. So
they will take those fluids. A dehydrated toddler
is a toddler who ends up right back in the hospital
on an IV. OK, that's a great connection. Let's
move down the airway. Next up, croup syndromes.
Specifically, the classic one, acute laryngotracheal
bronchitis, or LTB. This is the classic. You
will hear this sound in the grocery store in
November, and you'll know exactly what it is.
The barking seal. Exactly. It's almost always
viral. Perinfluenza is a common culprit. And
as the name says, it affects the larynx, the
trachea, and the bronchi. Because of that swelling,
remember our four millimeter straw, the subglottic
area gets very tight. And what's the typical
presentation for croup? Usually a toddler, say
three months to three years old, it's often a
gradual onset and it's classically worse at night.
They might have had a little cold during the
day, they go to bed and they wake up at 2 a .m.
with that characteristic barky seal -like cough
and inspiratory stridor. That phrase, worse at
night, is all over the source material. It is.
It's a key feature. So for the need to know interventions,
if it's mild and that means no stridor when they're
resting, only when they get upset and cry, the
first line treatment is Cool Mist. Why Cool Mist?
What's the science there? It causes vasoconstriction.
The cool, humidified air constricts the tiny
blood vessels in the swollen tissue, which helps
to reduce the edema just enough to open the airway
a little. The old school trick is to take the
kid outside into the cool night air or even just
stand in front of an open freezer door. It often
works surprisingly well. Okay, but what if it's
severe? What if they have stridor while they're
just sitting there quietly watching TV? Then
we bring out the big guns. That's an indication
for nebulized racemic epinephrine. Epinephrine.
Like an EpiPen for allergies. Similar concept,
but it's a specific formulation that's nebulized
and inhaled directly onto the vocal cords. It
is a powerful, rapid -acting vasoconstrictor.
It shrinks that swelling almost immediately,
but... And here's the major safety alert you
have to know. It wears off very quickly. You're
talking about the rebound effect. Exactly. The
medication might wear off in about two hours,
and the swelling can come right back, sometimes
even worse than it was before. So you can't just
treat and street them? Absolutely not. You cannot
send a child home immediately after getting racemic
epi. They have to be observed in the ER or admitted
for at least two to four hours to ensure they
don't rebound and lose their airway on the car
ride home. That is a critical safety point. Don't
discharge the croup kid immediately after the
breathing treatment. Correct. We also give corticosteroids
usually a single dose of dexamethasone, either
oral or IM, to help with the inflammation long
term over the next few days. Now, croup has a
scary and thankfully much rarer cousin, the true
emergency, epiglottitis. This is the nightmare
scenario. Croup sounds worse than it looks. Epiglottitis
looks worse than it sounds until it stops sounding
like anything at all. Give me the one -liner
on the path though. It's bacterial, almost always
haemophilus influenza type B or Hib. The epiglottis,
that little flap of cartilage that covers your
windpipe when you swallow, gets infected and
swells up like a giant inflamed cherry red cherry.
And if it swells too much, it just acts like
a cork in a bottle. It completely occludes the
airway. Total obstruction. Game over. This is
a can't miss, drop everything emergency. So how
do we spot this? The sources consistently list
the four Ds. Yes. Dysphonia, a muffled, quiet
voice, often described as a hot potato voice,
like they're trying to talk with a hot potato
in their mouth. Dysphagia, they have severe pain
on swallowing, so they can't swallow at all,
which leads to the third D, drooling, because
they can't swallow their own spit. It just runs
out of their mouth. And the fourth D is distress.
Respiratory distractor. At the posture, there's
a classic look, right? The tripod position. You
will never forget it if you see it. They are
sitting bolt upright, hands on their knees or
the bed, leaning forward and jetting their jaw
out. They're physically trying to pull their
airway open using gravity and muscle. They look
terrified. Okay, here is arguably the most important
single rule in this entire deep dive. If you
suspect epiglottitis, there is one thing you
must never... Never, under any circumstances,
put a tongue blade, a throat swab, or any kind
of instrument into that child's mouth. Do not
try to visualize the throat. Do not ask them
to say, ah. Why not? I mean, assessment is usually
good, right? Getting a look is important. Not
here. The stimulation of the gag reflex or even
just touching that inflamed epiglottis can trigger
a complete laryngospasm. The airway will slam
shut. And because it's so swollen and didymidous,
you cannot bag mask, ventilate them. You cannot
easily intubate them. You have just lost the
airway completely. So if the exam question asks,
the nurse suspects epiglottitis, what is the
priority action? The answer is almost always
something like, do nothing to upset the child
or keep the child calm and prepare for emergency
airway management. You do not inspect the throat.
You keep them with their parents. You let them
stay in their position of comfort. You call for
help, anesthesia and ENT and you get them to
the operating room for a controlled intubation.
And thankfully we see less of this now than we
used to. Yes. This is one of the great victories
of modern medicine. The Hive vaccine, which starts
at two months, has made bacterial epiglottitis
incredibly rare in vaccinated populations. But
you still see it, so you have to know it. Developmentally,
if you have a child in that tripod position,
drooling, looking toxic. You do not leave their
side. Your job is to be the calm in the storm.
You keep the parents there to keep the child
calm. Crying makes the swelling and the obstruction
worse. Your entire job is to be the zen master
until that airway is secure. Okay, wow. Moving
down from the throat into the chest. Bronchiolitis.
AKA RSV. Ah, respiratory syncytial virus. This
is the scourge of every pediatric unit in the
winter. So what's actually happening inside the
lungs here? This is a lower airway problem. Right.
This attacks the bronchioles, the tiniest little
airways that lead to the alveoli. It causes inflammation,
sure, but the main problem is that it causes
the production of tons and tons of thick, sticky
mucus. And it also causes sloughing of the dead
epithelial cells from the airway lining. So the
airways are getting clogged with all this debris.
Exactly. It's like trying to breathe through
a straw filled with rubber cement. And because
babies have those tiny airways to begin with,
they get air trapping. They can get air in past
the mucus, but they can't get it back out. hyperinflated
and they have to work incredibly hard to breathe.
And who gets this the worst? It's most severe
in infants under two years of age and especially
in premature babies or those with underlying
heart or lung disease. So what is the need -to
-know assessment? What does an RSV baby look
like? It's a wet messy disease. First, Reineria,
a runny nose like you wouldn't believe, just
copious, thick nasal secretions. Then you'll
hear wheezing, a horrible hacking cough. And
because they're working so hard, you'll see tachypnea
and retractions. And the sources all mention
a specific risk related to feeding. Yes, this
is critical. Remember, infants are nose breathers,
and they have to coordinate that complex suck
-swallow -breath pattern. If they're touch -and
-nake breathing 60, 70, even 80 times a minute,
and their nose is completely full of snot, they
cannot safely eat. They'll aspirate. They'll
aspirate, or they'll just get too tired and give
up. So dehydration is a major, major secondary
issue. So what's the number one priority intervention
then? Suction. The snot sucker. The nasopharyngeal
suctioning. Before they eat, before they sleep,
and anytime they look like they're in distress,
you have to clear the path for air. It's often
more effective than oxygen. What about medications?
Do we give antibiotics? No. It's a virus. Antibiotics
will do absolutely nothing. It's a common mistake,
but it's incorrect. OK. What about bronchodilators,
like albuterol? We use that for wheezing in asthma.
This is controversial. The official sources and
guidelines say it's not generally recommended,
but you will sometimes see a trial dose given.
The reason it's often ineffective is that the
problem in RSV isn't primarily bronchoconstriction,
a muscle spasm. The problem is obstruction from
mucus and debris. So relaxing the muscle doesn't
clear the mucus plug. So it's really just supportive
care. Oxygen, suction, and hydration. That's
the core of it. And isolation. RSV is incredibly
contagious and spreads like wildfire on a pediatric
floor. It requires contact and droplet precautions.
That means gown, gloves, and a mask. And it's
nice to know. There is a way to prevent this
in high -risk kids, right? Yes. There's a medication
called Pellivizumab, brand name Sinages, or the
newer Nursivamab. These are monoclonal antibodies.
They are given as monthly injections to preemies
or babies with significant heart or lung disease
during RSV season to give them passive immunity
and prevent severe infection. It's not a vaccine
in the traditional sense, but it's very effective.
OK, let's move on to pneumonia. Right. The definition
here is inflammation of the lung parenchyma.
Basically, the alveoli, those little air sacs,
fill up with fluid or pus. And this can be viral
or bacterial? It can be either, and the presentation
can vary. In younger kids, it's often viral and
follows a cold. In older kids and teens, we start
to see more bacterial causes, like mycoplasma,
the walking pneumonia, or strep pneumo. What's
the classic assessment for pneumonia? A high
fever, a cough, which can be productive with
colored or just dry and hacking, to chipnia is
a big one. Sometimes chest pain, especially with
breathing. And remember our sound map from before,
crackles, or what we call dullness on percussion.
Tapping on the chest over the affected area will
sound dull because you're tapping over fluid,
not air. And what are the key interventions?
It depends on the severity. Oxygen for hypoxemia,
for sure. Antibiotics, if it's bacterial. Antipyretics
like Tylenol for the fever. And fluids, fluids,
fluids to thin the secretions. And positioning
is also important. The sources mention splinting.
What is that? If a child has chest pain from
the coughing or pleural irritation, having them
hug a pillow or a stuffed animal tightly against
their chest when they cough, that's splinting.
It helps to brace the chest wall and manage the
pain so they can take a deeper, more effective
cough to clear secretions. OK, that's a great
practical tip. Let's talk about a huge chronic
one. Asthma. The most common chronic disease
of childhood. You will see this everywhere. The
sources define it as a chronic inflammatory disorder
with reversible airway obstruction. And that
word reversible is the absolute key. It sets
it apart from things like CF or anatomical defects.
It comes and goes. The airway can be completely
normal between attacks, but it's always hyper
responsive to triggers. And the patho involves
three things. The asthma triad. Yes, you have
to know these three. Inflammation. The airway
lining is always chronically swollen and angry.
You have mucus production thick, tenacious mucus.
And you have bronchoconstriction. The smooth
muscle wrapped around the airway spasms and squeezes
them shut. So how do we treat this three -headed
monster? The sources outline a tiered system
of medications. This is the absolute bread and
butter of asthma management. You have rescue
meds and you have maintenance meds and you must
know the difference. It's a huge safety issue.
Let's start with the rescue meds. These are the
short -acting beta agonists, the SAPAs. Albuterol
is the prototype. This is your in case of fire
break glass medication. It works within minutes
to relax that squeezed smooth muscle and open
the airway. What are the side effects parents
should know about? It revs you up. It can cause
tachycardia, jitters, a feeling of anxiety, even
hyperactivity in some kids. Parents need to know
this is a normal and expected side effect. Otherwise,
they get scared and might not give a medication
that their child desperately needs. OK. And the
maintenance meds? The controllers? These are
the meds that prevent the fire from starting
in the first place. They treat the underlying
inflammation. The cornerstone of this is inhaled
corticosteroids, like fluticasone. Or you might
see leukotriene modifiers, like Montelucast brand
name Singulair. And what's the most important
teaching point for those inhaled steroids? Rinse
the mouth out with water after every single use.
If the steroid medication sits on the tongue
and oral mucosa, it can suppress the normal flora
and lead to thrush a painful oral fungal yeast
infection. So just to be crystal clear, do you
ever use a control or medication for an acute
attack? Never. Absolutely not. It's a common
and dangerous mistake. It won't work fast enough.
If a kid is gasping for air, you give them albuterol,
not fluticasone. Let's talk about the equipment.
Spacers. The sources all have pictures of a metered
dose inhaler, an MDI, with a spacer chamber attached.
Why is that so important? A spacer is non -negotiable
for kids. Honestly, it should be for most adults,
too. Without it, the medicine, which comes out
of the MDI at about 60 miles per hour, just hits
the back of the tongue and gets swallowed. So
it doesn't even get to the lungs. Barely. With
a spacer, it holds the aerosolized mist in the
chamber, allowing the child to take a slow, deep
breath and inhale it deep down into the small
airways where it needs to go. It increases the
drug delivery efficiency by a huge margin. In
the peak flow meter. This is like a traffic light
system for their breathing. It is. It's an objective
measure of how open their airways are. Green
zone is 80 to 100 percent of their personal best
number. They're good to go. Okay. Yellow zone
is 50 to 79 percent. This is a caution sign.
The airway is tightening. The asthma action plan
will say to use the rescue inhaler, albuterol.
And red zone. That's below 50 percent of their
personal best. This is a medical alert. Danger.
The plan will say to use the rescue inhaler immediately
and call the doctor or go straight to the emergency
department. This sounds like a Harry Potter spell,
but it's really bad. It means the asthma attack
isn't breaking. It's refractory to treatment.
They've had multiple doses of albuterol and they're
still in severe distress. This is a medical emergency
that requires IV magnesium sulfate to help relax
that smooth muscle as well as continuous nebulizers
and high dose systemic steroids. Developmentally.
How does chronic asthma impact a kid's life?
It has a huge impact. It's a leading cause of
school absenteeism. It can lead to exclusion
from sports if it's not well managed, though
with a good plan they absolutely should play
sports, just pre -medicate before exercise. And
there's a concern about growth. Long -term, high
-dose systemic steroid use can slow bone growth,
so we have to monitor their height carefully.
Okay, we have to shift gears to a genetic heavyweight.
Cystic fibrosis or CF. This is a multi -system
disorder. It's so much more than just the lungs.
And it's autosomal recessive. Meaning both parents
must be carriers of the faulty gene. And if they
are, there's a 25 % chance with each and every
pregnancy that the child will have CF. The patho
is fascinating. It's a defect in a chloride channel.
Right, the CFTR protein. In very simple terms,
the cells can't move chloride, which is a component
of salt, and by extension water, properly across
the cell membrane. The result is that mucus secretions
everywhere in the lungs, the pancreas, the gut,
the reproductive tract, become incredibly thick,
sticky, and dehydrated. It's like trying to move
cement. How is it diagnosed? The gold standard
is the sweat chloride test. Because the sweat
glands can't reabsorb the chloride, their sweat
is incredibly salty. Parents will often be the
first to notice, saying, when I kiss my baby,
he tastes like salt. Let's break down the management
of this. It's intense. Let's start with the respiratory
side. They need aggressive pulmonary toilet,
a daily routine to clean out the lungs. The cornerstone
of this is chest physiotherapy, or CPT. This
can be done with cupped hands, percussing on
the chest wall, or more commonly now with a high
frequency chest wall oscillation vest. The shaker
vest? The shaker vest. It vibrates at a high
frequency to loosen that thick mucus from the
airway walls. And how often do they have to do
this? Every single day. Often twice a day for
20 to 30 minutes each time. When they get sick,
it can be up to four times a day. It's a huge
burden of care. And the sequence of medications
and treatments matters here, doesn't it? Critically.
You give the bronchodilator, like albuterol,
first to open up the airways as much as possible.
Then you might give an inhaled mucolytic, like
door nose alpha, which is an enzyme that acts
like molecular scissors to chop up the thick
mucus. Then you do the CPT to shake it all loose.
And finally, you have them do huff coughing to
get it up and out. Wow. Now, the GI side, this
is where the exams love to test because it's
so unique to CF. The same thick muphous that
clogs the lungs also clogs the tiny ducts of
the pancreas. So the digestive enzymes that the
pancreas makes, the ones needed to break down
fat, protein, and carbs, can't get to the food
in the intestine. So the child eats, but they
can't digest or absorb the nutrients, resulting
in... Two things. First, statorrhea, which is
fatty, frothy, foul -smelling, floating stools.
And second, failure to thrive. They are literally
starving despite having a ravenous appetite.
So the key intervention is replacing those missing
enzymes. Yes. They must take pancreatic enzymes
in capsule form with every single meal and every
single snack. Every single snack. They eat one
cracker. If they eat one cracker, they take enzymes.
If they have a glass of milk, they take enzymes.
Otherwise, they don't absorb the nutrients. For
babies and young children, you can open the capsule
and sprinkle the little beads on a non -alkaline
food like applesauce, but you must teach parents
not to let them chew the beads because they are
enteric -coated and can burn the mouth. On the
diet itself, usually for chronic diseases, we
think low fat, low salt. CF is the complete opposite.
They need a high calorie, high protein, unrestricted
fat diet, and they need extra salt. Because they
lose so much salt in their sweat, they are at
constant risk for hyponatremia, especially when
it's hot or they have a fever. That is such a
crucial counterintuitive fact that makes for
a perfect exam question. It really does. Also,
they need supplemental fat -soluble vitamins
A, D, E, and K. Since they don't absorb fat well,
they can't absorb these vitamins from food, so
they need to take special water -soluble forms
of them to prevent deficiencies. One last specific
need to know on CF. sign in a newborn. Meconium
ileus. This is when the baby doesn't pass that
first sticky black stool, the meconium, within
the first 24 to 48 hours. It's because the meconium
is even thicker and stickier than usual and it
gets stuck, causing an intestinal blockage. About
10 to 20 percent of babies with CF will present
with this at birth. That is heavy stuff. Let's
do a quick hit on a couple of acute issues. First,
foreign body aspiration. Toddlers put everything
in their mouths. It's a developmental stage.
If they inhale something small like a peanut,
a piece of a hot dog or a toy part, where does
it most likely go? It goes to the right bronchus.
Correct. The anatomy dictates this. The right
main stem bronchus is shorter, wider, and straighter
than the left. So gravity and momentum favor
the right side. So you'll often hear diminished
breath sounds or localized wheeze on the right
side specifically. And epistaxis, the simple
nosebleed. A classic playground injury. And the
old Old advice from our grandparents was, tilt
your head back. Which is wrong. Very wrong. And
potentially dangerous. That just makes all the
blood run down the back of their throat, which
can cause nausea, vomiting, and a risk for aspiration.
The correct position is to have them sit up and
lean forward. Lean forward. Yes. And pinch the
soft, fleshy part of the nose. Not the bony bridge,
but the soft cartilage below it. And hold continuous
pressure for 10 solid minutes. No peeking. OK.
We have covered the systems. This is great. Let's
move to section C, crosslinking and comparisons.
This is where we synthesize and make sure we
don't get these conditions confused. Let's compare
croup versus epiglottitis again just to hammer
it home because they both present with stridor
and confusing them is dangerous. Okay, lay it
out for me. Croup. Croup? It has that loud barking
cough. The patient sounds way worse than they
actually look. The treatment is supportive with
cool mist and, if needed, racemic epi and steroids.
Yeah, epiglottitis. Epiglottitis. There is no
cough. The room is quiet. The patient looks toxic.
They're in the tripod position. They're grueling.
The treatment is protecting the airway and IV
antibiotics. Perfect. Next pair. Asthma versus
bronchiolitis. Both have wheezing. They do. But
asthma is usually related to an allergic or chronic
trigger. The cough is often dry. And the treatment
is with bronchodilators and steroids. It responds
well to albuterol. And bronchiolitis. Bronchiolitis
is viral and seasonal. You see it in the winter.
It's a very wet disease with tons of secretions.
And the treatment is primarily supportive. suction,
and hydration. It often doesn't respond well
to the albuterol. And finally, let's compare
the logic of the tent versus the vest. Right.
We use humidity, like a mist tent or a cool mist
humidifier for upper airway swelling, like in
croup. The goal is to soothe the inflamed mucosa.
OK. We use percussion, the vest, or manual CPT
for lower airway mucus plugging, like in CF or
pneumonia. The goal is to physically shake the
mucus loose. so it can be coughed out. You would
generally not do CTT on a kid with Croof. It
would just agitate them and make the stridor
much worse. That is excellent clinical judgment
right there. One last link. Development. We've
touched on it throughout, but it's important
to remember that any hospitalization for a serious
respiratory illness can cause regression in kids.
You mean the toddler who is perfectly potty trained
suddenly starts wetting the bed again. Totally
normal. It's a stress response. Don't shame them
and support the parents in understanding that
and for the teenager with CF or asthma The developmental
task is all about identity and peer acceptance.
It's all about compliance and body image They
don't want to be different. They don't want to
take pills or do an inhaler in front of their
friends That's where the nurse has to become
a negotiator and an educator, not just a task
doer. Incredible. We have mapped the airway,
we've dissected the diseases, and we've linked
it all back to safety and development. We've
covered the four millimeter straw, the frequent
swallowing after tonsillectomy, the danger of
the silent chest, and the importance of salty
sweat. So as we wrap up this incredible deep
dive, what is the one provocative thought you
want to leave our listeners with to mull over?
It's the concept of work of breathing versus
oxygen saturation. New nurses and even experienced
ones can get fixated on the monitor. They look
up and say, oh, his O2 sat is 95%. He's fine.
Right. The number looks good. But you have to
look at the child. Is he retracting? Is he using
his neck muscles? Is he grunting with every breath?
Is his respiratory rate 60 times a minute? A
child has a tremendous physiological reserve.
They can maintain a normal O2 sat by, working
incredibly, incredibly hard. right up until the
moment they run out of energy. And then they
crash. They don't drift down gently. They fall
off a physiological cliff. They go from compensating
to coding in a matter of minutes. So treat the
patient, not the monitor. Exactly. If the work
of breathing is high, that child is in danger.
No matter what the number on the pulse oximeter
says, your assessment of their work is a better
predictor of their stability than that number
is. That is a powerful and essential thought.
Thank you for that deep dive. Listeners, go find
that four millimeter straw and protect it. We'll
see you on the next one. Stay safe out there.