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 today. Today is a big one.
I'm sitting here looking at this. stack of materials
we've uploaded. It's a mountain. It really is.
We've got textbook chapters on cellular regulation
that seem to go on forever, drug monographs that
look like they were written in ancient Greek,
nursing care guides, lecture notes. Honestly,
it's intimidating. It is. We are diving headfirst
into pediatric hematology and oncology. And it's
a massive topic. I won't sugarcoat it. It's one
of those areas in nursing school and in practice
where the stakes feel incredibly high. We're
dealing with children, often very sick children,
and the biology is complex. Yeah. But, you know,
despite the volume of information you're looking
at, there is a very clear structure to it. OK.
if you know how to read them out. And that is
exactly our mission today. We are going to take
this mountain of medical literature, and we are
going to apply the Pareto principle. We are hunting
for the 20 % of the information that answers
80 % of the exam questions and, more importantly,
keeps these kids safe when you're actually at
the bedside. That's the goal. And I want to frame
this entire deep dive from the perspective of
an exam coach. OK, I like that. I'm not just
going to read the textbook definitions to you.
That's useless. We're going to deconstruct why
exam writers test certain things, what the specific
safety traps are, and how to spot the patterns
that repeat over and over again. I love that
approach, because when I was reading through
the notes on leukemia or sickle cell, I found
myself just getting lost in the weeds of cell
counts and protocol. It's so easy to do. So.
We need a roadmap. You're saying we're going
to start with what you call the master 80 -20
map to find the big patterns. Exactly. Find the
patterns first. Then we'll go system by system
anemia, bleeding disorders, and then the big
one, cancer. And we have a dedicated segment
on pharmacology called The Chemo Man, which I'm
actually really curious about. Oh, yeah. We'll
get to him. And then we'll wrap up with oncologic
emergencies. And throughout all of this, we have
to keep one thread running through every single
topic, development. You cannot treat a child
like a small adult. The sources are so emphatic
about this. The disease impacts the child's development,
and where the child developmentally impacts how
we treat the disease. So let's unpack this. Before
we get into the nitty gritty of specific diseases,
you mentioned there are four mega patterns or
buckets that pretty much everything in this stack
fits into. Right. If I'm a student walking onto
the unit, What are these buckets? OK, so if you
step back from the hundreds of pages, you're
really only looking at four fundamental problems.
The first pattern is the something is low pattern.
This is anemia. OK. Red blood cells or hemoglobin
are down. Simple enough. On the surface, yes.
But the exam decision point, the thing the test
wants you to figure out, is why is it low? OK.
Is it a production problem? Is the bone marrow
factory just not making enough? That's your iron
deficiency or your plastic anemia. Right. Or
is it a destruction problem? Is the body making
them but then, you know, chewing them up? That's
sickle cell or thalassemia. And clinically, if
I walk into a room, what is the first thing I'm
going to notice in a kid with this something
is low pattern? Crackicardia. That is your priority
assessment. The heart rate. The heart is the
engine. If the blood can't carry enough oxygen,
the heart has to pump faster and harder to compensate.
It's working overtime. Okay, so that's the first
vital sign I'm looking at. Absolutely. You'll
probably also hear a murmur because the blood
is thin and turbulent. The kid will be exhausted,
pale. But tachycardia is the body's primary distress
signal. Got it. Pattern number two. The bleeding
pattern. This covers all your clotting disorders.
The basic mechanism to stop bleeding is broken.
And the decision point for the exam. The decision
point here is distinguishing which part of the
mechanism failed. Is it the platelets? You know,
the little first responder cells? That's usually
ITP. If it's platelets, you see superficial bleeding,
petechiae, those little red pinpoints, or purpura.
Okay, so skin level stuff. Exactly. Or is it
the clotting factors? The proteins that build
the strong clot? That's hemophilia. And does
that look different to the naked eye? Oh, completely
different. Factor issues cause deep bleeding.
We're talking bleeding into the joints, into
muscles, deep tissues. It's internal. You might
not see anything on the skin at first. Oh. And
the safety can't miss rule for this entire bucket
is simple. Do not traumatize the child. Meaning
what exactly? No rectal temperatures ever. No
IM injections unless it's an absolute life or
death emergency. And strict fall precautions,
padded bed rails, grippy socks, the whole nine
yards. OK. Pattern three involves the starey
stuff, the C word. Yes. The mass or cellular
chaos pattern, neoplasms, uncontrolled growth.
And the first signs are subtle. So subtle. The
priority cues are often things that could be
anything else. Weight loss, pallor, maybe some
swollen lymph nodes that don't hurt, or the silent
abdominal mass. And the safety rule here, and
I cannot stress this enough, it was everywhere
in the notes, relates to a specific tumor called
Wilms tumor. I saw that in the notes in all caps.
Do not palpate. Exactly. We'll get into the why
later, but if you palpate that abdomen, you could
kill the child. It is a never event. Wow. Okay.
And the fourth and final pattern. The neutropenic
pattern. This is immunosuppression, whether it's
from the leukemia itself crowding out the good
white blood cells or the chemo just wiking them
out. Right. The decision point is that fever
in a cancer kid is not Just a fever. It's an
emergency. It is a full -blown medical emergency.
You have to treat it like sepsis until proven
otherwise. We have a specific number for the
danger zone, right? We do. An absolute neutrophil
count, or ANC, of less than 500. 500. That is
the definition of severe neutropenia. If you
see that number on a lab report, your radar needs
to be on high alert. OK, so we have our four
pillars. Anemia, bleeding, mass, and neutropenia.
That actually makes it feel manageable. It's
the framework for everything. So let's zoom in
on pattern one, anemia. And I want to start with
a concept that I found fascinating because it
sounds so innocent, but it's actually dangerous.
The milk baby. Ah, the milk baby. This is a classic,
classic presentation for iron deficiency anemia
or IDA. So paint the picture for me. What does
this kid look like? The paradox here is that
the child, usually a poddler, looks chubby. They
look well -fed. They might even be in a higher
weight percentile. So they look healthy. They
look like the picture of health. But they are
pale, almost porcelain -like, and completely
exhausted. Listless. They don't want to play.
It feels counterintuitive, though. We're raised
to think milk does a body good. You see a chubby,
bouncing toddler, you think, that's a healthy
kid. Why is that chubby appearance actually a
warning sign here? It is the classic deception.
And this is where you had to think like a nurse
and separate calories from nutrients. OK. Cow's
milk is high in calories and fat, which is why
they bulk up. But it is virtually devoid of bioavailable
iron. So you have a child who is calorically
replete, but nutritionally starving for one specific
critical nutrient. They're full, but they're
running on empty. Exactly. And there's a mechanical
issue here too. Think about a toddler's stomach.
It's small, right? It's the size of their fist.
Tiny. So if you fill that tank with 30, 40, even
50 ounces of milk a day, which is so easy to
do with a sippy cup they carry around like a
security blanket. There is physically no room
for broccoli or steak or iron -fortified cereal.
So it's a displacement issue. The milk is pushing
the iron right off the plate. That's factor one.
But factor two is where the exam writers will
trap you. It's not just that they aren't eating
iron. Wait. They're actively losing blood. Wait.
From the milk. How? Yes. And this is distinct
to cow's milk in young intestines. The proteins
in cow's milk can actually irritate the lining
of a toddler's gut. It causes a low -grade chronic
inflammatory response. Chronic allergy. You can
think of it like that, yeah. A condition called
allergic colitis. It's not a massive hemorrhage
where you see bright red blood in the diaper
every time. It's microscopic, occult bleeding.
So the gut is just weeping blood. And slowly,
drip by drip, day after day, you're losing hemoglobin
and iron in the stool. and it's invisible to
the naked eye. So you have zero intake plus active
loss. That is why these kits crash so hard and
so fast. That makes so much more sense now. So
let's talk about the path, though, in plain language.
Why does iron matter so much? I know it's for
blood, but what is it actually doing? Think of
iron as the magnet or the glue. It's the core
component of the hemoglobin molecule that physically
binds to oxygen. So it's the seat on the bus
where oxygen sits. Perfect analogy. Without iron,
you can make the bus the red blood cell, but
there are no seats. The factory still works,
but the cells it produces are useless. On a lab
report, they're described as microcytic, meaning
small, and hypochromic, meaning pale. Little
pale cells. They can't carry the payload. It's
like sending out a fleet of delivery trucks with
no cargo space. And this change is based on age,
right? A newborn usually has iron. They don't
come out anemic. Correct. A full -term newborn
has the maternal iron stores that they packed
away in the third trimester. Those last about
four to six months. And for a preemie. They miss
that third trimester packing party. So their
stores are not much faster, maybe around two
months. That's why the age of presentation for
IDA is usually later infancy or toddlerhood,
once those stores are gone and the diet transitions
to cow's milk. So for the need to know the 80
-20 core for the exam, what are we looking for?
What are the top findings? Top findings, tachycardia
and power, obviously. But look for the weird
stuff, the things that make you go, huh, spoon
-shaped fingernails. The medical term is koala
nikia. The nail becomes concave. And pica craving
and eating non -food items. Like what? Ice is
a classic one. But also dirt, clay, paint chips,
laundry starch. If a parent says their toddler
is eating the potted plant soil, your first thought
should be to check a hemoglobin. And the priority
intervention is not a blood transfusion right
away, is it? Not usually. You fix the underlying
problem. So diet first. You have to educate the
parents. Limit that milk to 24 ounces a day.
That is a hard number you need to know for your
exams. 24 ounces. Got it. Introduce iron fortified
cereals, pureed red meats, beans, spinach. But
usually, diet alone isn't enough to replete their
stores. They need oral iron supplements. And
I notice in the drug guides, there are some very
specific kind of fussy rules for giving oral
iron. It is fussy, but it's all about chemistry.
And exam writers love this stuff. So what are
the rules? Rule one. Give it with vitamin C.
a little bit of orange juice or some citrus fruit.
An acidic environment converts the iron into
a form that is much easier for the gut to absorb.
Okay, so OJ with the iron drops, what's rule
two? Rule two. Do not give it with milk or antacids.
Calcium is the enemy of iron absorption. It binds
to it and blocks it. Which is so ironic given
the cause is often milk. Exactly. You have to
separate them by at least an hour or two. And
you have to warn the parents about the side effects,
or they will stop giving it within a week. What
are they? It causes GI upset nausea, constipation.
It can stain teeth. So you teach them to give
it through a straw or a syringe and at the back
of the cheek. And the big one, it turns the stool
a tarry green or black color. That's the good
side effect, right? You want to see that. It
is. If the poop is black, it means the iron is
being absorbed and processed. If the parents
call into panic saying there's blood in the stool,
your first question is, what color is it? Black
and terry is expected with iron. Bright red is
not. Before we move on, let's circle back to
development. How does this affect a growing brain?
Oh, it's huge. The brain is the most oxygen -hungry
organ in the body. Chronic hypoxia in a rapidly
developing brain leads to measurable cognitive
delays and behavioral changes. For how long?
Is it permanent? There are studies showing long
-term impacts on math scores, reading comprehension,
and even attention span if severe idea isn't
caught and treated early. And then there's the
physical aspect, the fatigue. Right. If a toddler
is too tired to pull to stand to cruise to run
and explore their environment, their gross motor
development just stalls. They don't play. They
don't learn from their environment. It has a
domino effect. Wow. Okay, let's shift gears from
a production problem to a destruction problem.
Sickle cell disease. This feels like one of the
absolute pillars of pediatric nursing exams.
It's a major topic for sure. Sickle cell disease
or SCD is an autosomal recessive genetic disorder.
Meaning both parents must be carriers. Right.
Both parents carry the trait and there's a 25
% chance with each pregnancy that the child will
have the full disease. And the one -liner here,
the core concept is the traffic jam. That's the
perfect visual. Normal hemoglobin, hemoglobin
A, is in a red blood cell that's round, squishy,
and flexible. It can squeeze through the tiniest
capillaries with no problem. Like a water balloon.
Exactly. In SCD, the person has hemoglobin S.
And under certain conditions of stress, when
oxygen levels drop, HGVS polymerizes. It forms
these long, rigid rods inside the cell. And that's
what stretches the cell into that classic sickle
or crescent shape. Right. And a rigid, pointy,
crescent -shaped cell doesn't flow. It's sticky.
It hooks onto other sickled cells. They clump,
and they create a log jam that blocks the blood
vessels. This is vaso -occlusion. I want to pause
on the word crisis, because in medical textbooks,
we use that word a lot. Hypertensive crisis,
thyrotoxic crisis. But in sickle cell, vaso -occlusive
crisis feels like a sanitized, almost sterile
way of describing something horrific. It is.
What is actually happening inside the body to
cause that level of pain? It's a traffic jam.
But that metaphor is almost too soft. Imagine
your blood vessels are a highway, and suddenly
the road is blocked. Not with cars. but with
concrete barriers. The blood flow stops completely.
The tissue beyond that roadblock, whether it's
bone marrow, muscle, or organ tissue, starts
to starve for oxygen. It's ischemia. The cells
are screaming for oxygen, and they start to die.
Ischemia is tissue death. Essentially. It's the
exact same mechanism as a heart attack, but it's
happening in your femur, or your spine, or your
spleen. The pain isn't a simple ouch. It is bone
crushing. Patients describe it as deeper and
more intense than almost any other pain imaginable.
Which explains why our notes emphasize pain management
so heavily. I was struck by the dosage recommendations
here. We're not talking about Tylenol. No. And
this is a major advocacy point for nurses. There
is, unfortunately, a stigma with sickle cell
patients seeking opioid medications. You hear
about drug seeking. Right. And you have to throw
that out the window. You have to understand,
this child is having a heart attack in their
skeleton. We are talking high dose IV opioids,
morphine. Hydromorphone, which is deloaded, usually
via a PCA, a patient -controlled analgesia pump.
The absolute key for the exam and for real life
is the schedule. You don't wait for them to ask.
Never. Never. If you see an order that says PRN
as needed for a sickle cell crisis, you need
to question that order. You are always chasing
the pain. You need to be ahead of it. Scheduled
around the clock dosing is the standard of care.
What about the triggers? The exam usually asks
what happened right before the crisis? What pushes
them over the edge? We call them stressors. If
it's anything that increases the body's demand
for oxygen or alters their fluid status, epoxy
is the obvious one. Dehydration is a massive
one. Why dehydration? Because it makes the blood
more viscous. It gets sludgy. It's thicker, which
makes it even easier for those sticky cells to
jam up. Fever or any kind of infection is a huge
trigger. And cold? Yes. Cold temperatures are
a big one because cold causes vasoconstriction,
which narrows the vessels and creates a bottleneck.
So for the 8020 core, We have a kid who comes
into the ER in a vaso occlusive crisis. They
are screaming in pain. What are our priority
assessments? Pain score is vital, of course,
but you need to assess their respiratory status
immediately. Why? We are terrified of a complication
called acute chest syndrome. OK. It looks just
like pneumonia. They get chest pain, fever, a
cough. They become hypoxic. It's sickling in
the vasculature of the lungs, and it is the leading
cause of death and sickle cell disease. Wow.
What else are you assessing? You also need to
palpate the abdomen, specifically over the spleen
in the left upper quadrant. The spleen. Splenic
sequestration. This is another emergency. The
sickled cells can get trapped in the spleen causing
it to swell up rapidly like a sponge. And that's
bad. Because it pulls a huge volume of blood
out of the general circulation. The child can
go into hypovolemic shock in a matter of minutes.
So if you feel a massive hard spleen and the
kid is hypotensive with a high heart rate, that's
a surgical emergency. Let's talk interventions.
There's an acronym here in the notes, HOP. HOP.
It stands for hydration, oxygen, and pain management.
Some people teach HOK to it. OK, so hydration
first. Hydration is absolutely critical. We run
IV fluids at one and a half to two times the
normal maintenance rate. We need to dilute the
blood, make it less viscous, and help flush those
sickled cells through the logjam. What about
oxygen? Only if they are hypoxic. If their oxygen
saturation is low, then yes, oxygen helps to
reverse the sickling process. But giving oxygen
to a kid who isn't hypoxic doesn't really help
and isn't the priority. Hydration and pain control
are the drivers. And there is a specific drug
warning here in the notes regarding pain, a big
do not use E. Yes, no meparidine. The brand name
is Demerol. Do not give it. It has a toxic metabolite
called Normapyridine that can build up, especially
with repeated doses. It's a neurotoxin. It lowers
the seizure threshold and can cause tremors and
seizures. And kids with SED are already at risk
for strokes. Exactly. So we never use a medication
that could further destabilize their central
nervous system. Speaking of CNS issues, let's
talk about stroke. That's a huge complication.
It's a devastating complication. The sickled
cells block the blood flow to the brain, causing
an ischemic stroke. This is why we do routine
transcranial Doppler, or TCD, ultrasound screening
annually for kids with SED, usually from ages
2 to 16. And what are you looking for with that?
We're looking for high velocity blood flow in
the cerebral arteries. If the blood is moving
really fast through a certain area, it means
that vessel is probably narrowed. That's a high
-risk sign. And those kids might be started on
chronic blood transfusion therapy to prevent
a stroke. And developmentally, how does a lifetime
of this impact a child? It disrupts everything.
We have delayed physical growth and delayed sexual
maturation because of the chronic anemia and
poor oxygenation. And socially? Socially, it's
incredibly isolating. These kids have frequent
painful hospitalizations. They miss school. They
miss birthday parties. It's hard to form and
maintain peer relationships. Is there an early
developmental sign we should look for in babies?
Yes. In infants, the first sign of SED is often
dactylitis, also called Hanfoot syndrome. What's
that? It's a vaso -occlusive crisis in the small
bones of the hands and feet. They get symmetrically
swollen, red, and are incredibly painful. An
infant who should be learning to grasp or crawl
suddenly won't use their hands or bear weight
on their feet. It hinders those early motor milestones
right from the start. Okay, moving to our second
pattern, bleeding. Let's start with hemophilia.
The missing factor disorder. The classic genetics
are X -linked recessive. So the mom is the carrier
and the son has the disease. That's the textbook
exam scenario. Yeah. Hemophilia A is a deficiency
of factor 8. and that accounts for about 80 %
of cases. Haemophilia B, which is sometimes called
Christmas disease, is a deficiency of factor
9. Can you explain the why briefly? Why does
missing just one of these dozens of factors cause
such a profound problem? Think of the clotting
cascade as a line of dominoes. To form a stable,
strong, fibrin clot, you need every single domino
to knock over the next one in the correct sequence.
Okay. If factor 8 is missing, the dominoes stop
falling right in the middle of the chain. You
might form a weak little platelet plug, which
is why they might stop bleeding from a tiny paper
cut. But it's not enough for a real injury. Not
at all. You can't form the strong fiber mesh
that's needed to seal the vessel and stop deep
bleeding. So that explains the clinical picture.
It's not usually superficial cuts. It's deep
tissue bleeding. Exactly. The hallmark finding
of hemophilia is hemarthrosis bleeding into the
joint cavities. The big joints are the most common
targets. knees, elbows, and ankles. And the priority
action when a kid comes in with a swollen, hot,
painful knee. RICE. That's the acronym you need
to remember. Rest, ice, compression, and elevation.
Okay, RICE. Now here is the trick question I
saw in the notes. Do you perform passive range
of motion or ROM exercises during an active bleed?
My gut says no. If I move it, I feel like I might
break whatever weak clot is trying to form. Your
gut is 100 % right. Absolutely not. Why? If you
move a joint that is actively bleeding, you stretch
the joint capsule, which increases the space
for blood to pool and can dislodge any fragile
clot. You immobilize it during the acute phase.
ROM comes later, after the bleeding has completely
stopped, to prevent long -term joint damage and
contractures. And the medical management is just
giving them what they're missing. Right. Factor
8 or factor 9 replacement given intravenously.
The key exam tip here is to always administer
the factor before any invasive procedure, even
a routine dental cleaning. Prophylactically.
Yes. And for mild hemophilia A, there's a drug
called DDAVP or desmopressin, which can be given.
It works by stimulating the body to release its
own stored factor 8 from the lining of blood
vessels. Safety and education seem huge here.
This is a lifestyle diagnosis. It is. A huge
part of the nurse's role is education. No contact
sports, so no football, no hockey, no wrestling.
What can they do? We encourage sports that build
muscle without high impact. Swimming is perfect.
Golf, jogging, tennis are usually okay. They
need to use a soft bristled toothbrush to prevent
gum bleeding and they must wear a medical alert
bracelet. And there's a big medication class
to avoid. Yes, absolutely. Avoid NSAIDs and aspirin.
So no Ibuprofen, no Naproxen. Why? because those
drugs inhibit platelet function. The kid already
has a factor problem. The last thing you want
to do is give them a drug that creates a platelet
problem on top of it. Acetaminophen or Tylenol
is the pain reliever of choice. Developmentally,
this must be so tough for toddlers. It's a nightmare
for parents of toddlers. Toddlers fall. That's
their job description. So you see these little
kids wearing soft helmets and knee pads just
to play in their own living room. It's about
creating a safe environment. And for teens. For
the school -aged kid and the teen, it's all about
the struggle between autonomy and safety. Teaching
them how to perform their own venipuncture and
self -administer their 5V factor is a huge developmental
milestone. It gives them control back over their
bodies and their lives. Okay, let's contrast
that with our other bleeding disorder, ITP, idiopathic
thrombocytopenic purpura. Or immune thrombocytopenic
purpura. Or immune thrombocytopenic purpura.
This is the viral aftermath. What's the story
here? The story is almost always the same. A
perfectly healthy kid gets a cold or some other
common virus, they get better. And then about
two to three weeks later, they suddenly wake
up covered in bruises and little red spots. What's
the mechanism? Why does that happen? It's a case
of mistaken identity by the immune system. The
immune system ramped up to fight the virus. But
after the virus is gone, it gets confused and
starts producing antibodies that attack the body's
own platelets. It marks them for destruction
by the spleen. So the platelet count just plummets.
Yeah. It crashes. We're talking below 20 ,000.
Remember, normal is 150 ,000 to 400 ,000. And
you see the classic signs, petechiae, which are
the little pinpoint spots, and purpura, the larger
purplish spots. But how is this different from,
say, leukemia, which also causes low platelets?
This is a key distinguishing point for exams.
In ITP, the child looks well. They're not acting
sick. They're happy, running around playing,
but they're covered in bruises. A child with
leukemia is usually pale, febrile, lethargic,
and has bone pain. They look sick. And the treatment
for ITP? For many kids, we just watch and wait.
It's often self -resolving. If the platelets
are critically low or there's active significant
bleeding, we might give IVG intravenous immunoglobulin
to basically distract the immune system. Or we
give steroids to calm it down. And you avoid
platelet transfusion. We try to. Because the
spleen is primed to destroy platelets, if you
give a transfusion, the spleen will just eat
those new platelets immediately. It's like pouring
water into a bucket with a hole in it. We only
do it for a life -threatening hemorrhage, like
an intracranial bleed. It's all about trauma
precautions. No contact sports. quiet activities.
But you don't need seizure precautions like you
write with other conditions. It's strictly about
not letting them bang into things until their
platelet count recovers. Great. Let's move to
patterns three and four combined. This is the
heavy hitter leukemia, specifically AICIO and
AML. This is the most common form of childhood
cancer. We absolutely need to spend some quality
time here. I feel like leukemia is a word everyone
knows, but very few people really understand
the mechanics of it. It's cancer of the blood,
but what does that actually mean? The one liner
you need to remember is bone marrow failure.
That's the core concept. OK, explain that. The
bone marrow is the factory for all of our blood
cells, red cells, white cells, platelets. In
leukemia, one specific cell line, usually a lymphoid
or myeloid precursor, mutates and starts producing
blast cells. Blast cells. Blasts are immature,
baby white blood cells. completely useless. They
can't fight infection. They can't do anything.
But they have one terrifying superpower. They
replicate incredibly fast. I call them bully
cells. My bully cells. Because they don't just
sit there. They take over the factory. They grow
so fast and in such numbers that they physically
crowd out all the normal healthy cell production
lines. So the symptoms we see aren't from the
cancer cells themselves, but from what the cancer
pushes out of the way. Precisely. This connects
right back to our master map. The blasts crowd
out the red blood cell production line, and what
do you get? Anemia. So pallor, fatigue. Right.
They crowd out the platelet production line,
and you get? Thrombocytopenia. Bruising, bleeding,
petechia. And paradoxically, they crowd out the
production of mature, functional white blood
cells. So you get? Neutropenia. High risk of
infection. So even if the lab report comes back
and says the total WBC count is 50 ,000, which
is huge, that kid is profoundly immunocompromised.
Because it's 49 ,000 useless blast cells. Exactly.
Yeah. They are cardboard cutouts of soldiers.
They look the part on the roster, but they can't
fight. How do we confirm the diagnosis? The gold
standard, the definitive test, is the bone marrow
aspiration and biopsy. Where is that done? Usually
from the posterior iliac crest, the back of the
hip bone. We're looking for the percentage of
blasts in the marrow. A normal, healthy marrow
has less than 5 % blasts. Leukemia is defined
as greater than 25 % blasts. That sounds incredibly
painful. It is uncomfortable, for sure. Conscious
sedation is standard practice for kids. The nurse's
role is critical in positioning the child, providing
comfort, and then monitoring the site for bleeding
afterwards. And there's another diagnostic procedure
that's critical, the lumbar puncture or LP? Yes,
the LP is vital. Why do we tap the spine for
a blood cancer? Two crucial reasons. One, to
check if the cancer has metastasized to the central
nervous system, the CNS. We look for blast cells
in the spinal fluid. And the second reason? To
inject chemotherapy directly into the spinal
fluid. This is called intrathecal chemotherapy.
Why not just give all the chemo through an IV?
Because of the blood -brain barrier, a protective
layer that keeps toxins out of the brain, which
is normally a very good thing. But it also blocks
most IV chemo from getting in. So the CNS becomes
what we call a sanctuary site. Leukemia cells
can hide out there, survive the IV chemo that's
treating the rest of the body, and then reemerge
later to cause a relapse. We have to go in and
treat the sanctuary directly. Okay. Let's talk
about the treatment journey. It's not just take
a pill for a few weeks. It's broken into phases.
It is a marathon, not a sprint. Phase one is
induction. The goal is absolute obliteration
of the cancer. We hit them with a very intense
multi -drug chemotherapy regimen to get the blast
count in the marrow down to zero. This is when
they are at their sickest, most vulnerable, and
most neutropenic. If they achieve remission,
then what? Phase two. Phase two is consolidation,
sometimes called intensification. This is designed
to clean up any microscopic residual disease
that might be left behind. And finally, you have
maintenance, which is a less intense off an outpatient
chemo regimen that can last for two to three
years to keep the cancer from coming back. I
want to talk about the side effects from all
this chemo. We mentioned moon face earlier from
steroids. Yes, that's from high dose steroids
like prednisone or dexamethasone. They are a
key part of the chemo protocol, but they have
major side effects. It changes their appearance,
the chubby cheeks, weight gain, a buffalo hump
on their back. For a teenager, this body image
alteration is just devastating. And it affects
their mood too, right? Oh, absolutely. It causes
irritability, mood swings, insomnia, and a voracious
appetite. They call it roid rage for a reason.
And infection control is the absolute number
one need to know priority intervention. Without
a doubt. Neutropenic precautions. This is the
bubble boy concept, but modernized for the hospital.
What does that entail? No fresh flowers or plants
in the room. The stagnant water and soil can
harbor fungus. No raw fruits or vegetables that
can't be peeled. Everyone who enters the room
must wear a mask and practice meticulous hand
washing. And going back to our patterns, fever
is an emergency. Fever is an emergency. If a
neutropenic kid spikes a temp, usually defined
as a single temp greater than 38 .3C or a sustained
temp of 38 .0C for an hour, you assume it is
life -threatening sepsis until proven otherwise.
What's the protocol? You move fast. You get blood
cultures from all their central line lumens and
a peripheral site. You get a urine culture, chest
x -ray. You pan culture them to find the source.
And you start broad spectrum IV antibiotics immediately.
You don't wait for the culture results to come
back. You do not wait. Time is tissue. Time is
life. You have a golden hour to get those antibiotics
on board. You treat first and you ask questions
later. Okay, that leads us perfectly into our
pharmacology section. We call this the chemo
man. This is a memory tool, right? A way to link
drugs to their main side effects. Yes. The chemo
man is a way to visually map the specific high
-yield toxicities of common chemo drugs to different
body parts. The uploaded drug guides give us
four of five heavy hitters we absolutely need
to know for exams. Let's start at the bottom
with the bladder. Cyclophosphamide, brand name
Cytoxin. The target organ here is the bladder.
The exam trap is hemorrhagic cystitis. Bleeding
from the bladder, what causes it? This drug breaks
down in the body into a toxic metabolite called
acrolein. This acrolein sits in the bladder waiting
to be excreted and it chemically burns the bladder
lining. It causes it to bleed. How do we prevent
it? Prevention is key. Number one is aggressive
hydration to constantly flush the bladder out.
But the specific rescue drug, the antidote, is
mesna. M -E -S -N -A. Mesna. It binds to that
toxic acolyte metabolite in the bladder and detoxifies
it, rendering it harmless. So on an exam, if
you see cyclophosphamide, you should be looking
for answers that include mesna and encouraging
frequent voiding. OK. Moving to the nerves. Finchristine.
This is a mitotic inhibitor. To understand its
side effects, you have to understand how it works.
Okay. I remember mitosis from biology class cell
division. How does stopping cell division lead
to nerve damage? This is actually fascinating.
Vincristine works by freezing the skeleton of
the cell, the microtubules. It prevents them
from pulling the chromosomes apart so the cell
can't divide. It stops the cancer from multiplying.
Okay, that's great for killing cancer. It is.
But guess what other system in your body relies
entirely on those same microtudial tracts? Your
nervous system. Ah. Your nerves use those same
tracts as a railway system to send signals and
transport nutrients from your spine all the way
down to your toes. So the drug can't tell the
difference between a dividing cancer cell and
a functioning nerve cell. Precisely. It gums
up the tracts. And that's why the signature side
effect of incristine is peripheral neuropathy.
It attacks the longest nerves first, the ones
reaching down to the feet. And that's why we
see foot drop. Yes. That's a classic sign. The
nerve signal just doesn't get to the muscles
in the foot. The kid tries to lift their toes
to take a step, and they can't. They might start
tripping a lot. They might complain of numbness,
tingling, or burning pain. And there's a GI component,
too. Yes, for the same reason. It causes a paralytic
alias, severe constipation. The nerves that control
gut motility stop firing. These kids need a proactive
bowel regimen from day one. And there's a massive
safety alert in the notes about this drug. A
huge one. Vincristine is a vesicant, so you have
to watch that IV line carefully for infiltration.
But more importantly, it is fatal if given intrathecly.
So it can never go in the spine. It is for IV
use only. If you accidentally inject Vincristine
into the spinal fluid, it causes ascending paralysis
and destroys the central nervous system. It is
an agonizing and irreversible death. Hospitals
have multiple safety checks in place to prevent
this. Wow. Okay. Noting that in big red letters.
Moving up to the heart. Doxorubicin, often called
Adriamycin. The red devil. The target organ is
the heart. The toxicity is... Cardiotoxicity.
How does it damage the heart? It generates free
radicals that damage the cardiac muscle cells.
This damage is cumulative over a lifetime. So
we track the total lifetime dose a patient receives.
It can lead to cardiomyopathy and congestive
heart failure, sometimes years after treatment
has ended. So we're monitoring for signs of heart
failure. Exactly. Edema, shortness of breath,
crackles in the lungs, regular echocardiograms
are part of the surveillance. And it changes
the color of body fluids. It does. It turns urine
and sweat, a bright ruby red or orange color,
for a day or two after infusion. This is not
bleeding, it's just the dye from the drug being
excreted. You have to warn the parents and the
child so they don't panic thinking they're peeing
blood. Okay, last one on the chemoman. Methotrexate.
A real workhorse drug in pediatric oncology.
The primary targets are the kidneys and the reproductive
system. How does it work? It's an anti -folate.
It starves the rapidly dividing cancer cells
of folic acid, which they need to make new DNA.
And there's a rescue drug for this one too. Yes.
Leucovorin, which is a form of flenic acid. We
give high dose methotrexate to kill the cancer.
And then we rescue the normal healthy cells by
giving them leucovorin a few hours later. It's
a very precisely timed dance. And for nursing
interventions, what's the priority? Kidney protection.
Intense Favi hydration is critical, and we have
to alkalinize the urine, usually with sodium
bicarbonate in the IV fluids. Why do we want
alkaline urine? We need the urine pH to be greater
than 7 .0. If the urine is acidic, methotrexate
will crystallize in the retal tubules. It literally
forms tiny sharp crystals like shards of glass
and causes acute renal failure. So we're constantly
checking urine pH. That is a solid pharmacology
review. Let's move to section D. Solid tumors.
We need to distinguish between two abdominal
tumors that often get confused on exams, Wilms
tumor and neuroblastoma. Yes, let's set up a
comparison table in our minds. First, Wilms tumor,
also called nephroblastoma. So a kidney tumor.
Right, it's a tumor of the kidney. The peak age
is around two to five years old. And critically,
it is typically unilateral. It arises in one
kidney and usually does not cross the midline
of the abdomen. And the non -negotiable safety
rule we mentioned at the very beginning. Do not
palpate the abdomen. You put a sign on the bed.
You put it in the chart. You tell every single
person who comes near that child, do not palpate.
Let's really break down the why. Is it because
it's painful? It's not primarily about pain.
It's about containment. This tumor is encapsulated.
It's enclosed in a thin, fragile sac. If you
push on it, You can rupture that capsule. And
what happens then? You seed cancer cells all
over the abdominal cavity. You take a stage one
easily treatable tumor and you instantly turn
it into a stage three or stage four disaster
that requires much more aggressive chemo and
radiation. You can worsen their prognosis with
one push. Now contrast that with neuroblastoma.
Neuroblastoma arises from primitive cells of
the sympathetic nervous system. Most commonly,
it starts in the adrenal medulla, which is that
little gland that sits on top of the kidney.
And this one is different because? Because it
is a silent tumor. It's often called that because
by the time it's diagnosed, it is usually already
metastasized. It's a much more aggressive cancer
than Wilms. How does it look different on physical
exam? The abdominal mass itself often crosses
the midline. Wilms tumor usually respects the
midline because it's confined to one kidney.
Neuroblastoma is more diffuse and grows across
the belly. And because it's metastatic, you see
signs elsewhere. Exactly. You see the classic
raccoon eyes, period orbital eczemosis, which
is bruising around the eyes from orbital metastasis.
You might also see bone pain from bone mets.
And the lab test is different. Yes. The key diagnostic
lab is a urine test for catecholamines, specifically
VMA and HVA. Because this is a tumor of the adrenal
sympathetic system, it often pumps out massive
amounts of stress hormones. You'll need to do
a 24 -hour urine collection to catch these metabolites.
Moving up to the eye, retinoblastoma. The eye
tumor. The key assessment cue you need to know
is the cat's eye reflex. The medical term is
leukocoria. What does that mean? Normally when
you shine a light in a pupil like for a photograph
with a flash, you see the red reflex. In retinoblastoma,
the tumor is growing in the back of the eye and
it reflects the light back as a white or yellowish
glow. And the exam trap here. The trap is thinking
that blindness or a painful red eye is an early
sign. Those are late signs. The white glow, the
leukocoria, is the early sign. Parents are often
the first to notice it when looking at photos
of their child. One eye is red, the other is
white. OK, let's briefly touch on the two main
bone tumors, osteosarcoma versus Ewing's sarcoma.
Osteosarcoma is the most common. It typically
occurs in the long bones, especially during the
adolescent growth spurt. The most common site
is the distal femur, right near the knee. On
an x -ray, it has a classic sunburst appearance.
And the treatment is pretty drastic. It often
is. The tragic part is that it frequently requires
amputation of the limb or a complex limb salvage
surgery. Dealing with amputation in an adolescent...
That's a massive developmental and psychosocial
crisis. Huge. Body image is everything to a teenager.
Your nursing care has to focus on that. You have
to educate them about phantom limb pain, that
it's real, it's not in their head, the severed
nerves are still firing. And getting them connected
with other teen amputee survivors is absolutely
critical for their coping. And Ewing's sarcoma,
how is it different? Ewing's sarcoma is a tumor
of the marrow space within the bone. It can be
in long bones but also flat bones like the pelvis
or ribs. On x -ray it has an onion skin appearance.
The key difference is that Ewing's is very sensitive
to radiation, so limb salvage is often more feasible
than with osteosarcoma. We're in the home stretch.
Section E oncologic emergencies. You missed this
they die list. Let's start with tumor lysis syndrome
or TLS. This is a metabolic emergency that happens
when we start chemotherapy, especially for fast
growing, bulky cancers like leukemia or Burkitt's
lymphoma. The chemo works too well, too fast.
It kills a massive number of cancer cells all
at once. So the cells burst open. They burst
open, they lies and everything that was inside
those millions of cells dumps into the bloodstream
simultaneously. What's in this chemical soup
that gets dumped out? Three main things you have
to worry about. First, potassium. Cells are basically
little bags of potassium. When they burst, you
get sudden, severe hyperkalemia, which can cause
fatal cardiac arrhythmias and cardiac arrest.
OK, that's number one. What's two? The breakdown
of the cell's DNA releases uric acid. So you
get hyperuricemia. This uric acid crystallizes
in the kidneys, just like with methotrexate,
and causes acute renal failure. And number three?
Phosphate. Cells are also full of phosphate.
You get hyperphostatemia. And because phosphate
and calcium exist on a seesaw in the blood? Exactly.
When phosphate goes way UP, it binds with calcium
and pulls it way down in. So you get profound
hypocalcemia. And what does low calcium look
like? Titany. Muscle cramps, twitching, positive
Schwastik's or Trousseau's sign. And if it's
severe, seizures. The intervention. What do we
do? We anticipate it and... Try to prevent it.
Aggressive hyperhydration to flush the kidneys
out. And we give a drug called allopurinol, which
blocks the formation of uric acid. We're on strict
INOs and monitoring those electrolytes every
few hours. We've already mentioned sepsis in
the neutropenic child, but it bears repeating
here. Fever plus cancer equals antibiotics and
no W. That is the mantra. Do not pass code. Do
not wait for a full workup. If their ANC is low,
they have no defense system. A simple bacteria
can kill them in hours. Just a couple of quick
add -ins from the sources before we wrap up.
Lead poisoning. I saw this tucked into the hematology
section. Why? Yes, because lead causes a type
of anemia. It interferes with hemoglobin synthesis
and blocks iron absorption. But the real danger
of lead is neurological. It's a potent neurotoxin
that causes irreversible damage to a developing
brain. Main sources we need to know. Paint in
houses built before 1978 is the big one. Also
contaminated soil, some imported pottery or toys,
and the treatment, chelation therapy. A drug
like succimer is given, which binds to the lead
in the blood so it can be excreted in the urine.
But you have to monitor kidney function closely.
because the chelating agents themselves can be
tough on the kidneys. And finally, testicular
cancer. This is a cancer of young men. The peak
age is 15 to 35. This is why a key part of adolescent
health teaching is the testicular self -exam,
or TSE. What's the teaching point? We teach them
to do it once a month, usually in the shower.
The warm water relaxes the scrotum, making it
easier to feel for any hard lumps, nodules, or
changes in size. Early detection is key. We have
covered a marathon of content. From the milk
baby to the chemo man. If we had to summarize
the survival hierarchy for these exams, the things
you absolutely cannot miss, what does that look
like? It looks like this in this order of immediacy.
One, oxygen and hydration for the sickle cell
crisis. That's an immediate life threat. Okay.
Two, safety and bleeding precautions for hemophilia
and ITP prevent the injury. Three, infection
control for the neutropenic and leukemia child.
Protect them from the outside world. And four.
And four. Kidney protection. That means knowing
your chemotoxicities and, for Wilms, do not palpate.
And bringing it all back to the human element,
to the child in the bed. What's the final thought?
The final provocative thought is the concept
of normalcy. We fill these kids with powerful
drugs. We isolate them in rooms. We poke and
prod them constantly. But the nurse's biggest
and maybe most important developmental job is
finding a way for that child to just be a child.
How do you do that? Play. is the work of childhood.
It's how they learn and cope. So if they're too
sick to run around, we find quiet play they can
do in bed. If they're isolated, we use technology
to connect them with their friends and family.
We decorate their room. We maintain routines.
We cannot let the disease and the treatments
steal their childhood along with their health.
That's our job. That is the perfect place to
leave it. To our listeners, take these patterns,
visualize the chemo man, and go crush those practice
questions. We'll see you on the next Deep Dive.
Stay curious.