So let’s focus on iron deficiency anemia
and I want to do that because
this is so common in children.
This is more common in periods of rapid
growth, when kids need their iron the most.
Also, it’s more common on strict vegetarians
because iron is repleted in meat.
Most commonly, we see it in
infants who drink lots of milk.
I’ve had many patients
come in and mom says,
“Oh, that’s the only thing he’ll
eat and I want him to grow
and so I give him 4 glasses
of 8 ounces of milk a day.”
Those children are going
to present with anemia.
Occasionally, iron deficiency
can also be seen in blood loss
because when you lose blood,
you’re essentially losing iron
if you don’t replete
the iron in your diet.
So patient’s with inflammatory bowel
disease, GI bleeds or parasites,
celiac disease or even
patients with excessive menses
are all at risk for
Well in adolescent girls, even
girls with normal menstrual issues
can have blood loss and
resulting iron deficiency
if they are not having
enough iron in their diet.
So for iron deficiency, the CBC
will show a microcytic anemia
and they will typically have
a low erythrocyte count.
You might want to get iron studies.
Sometimes, I get confused about the iron
studies so let’s go through them carefully.
So, the ferritin reflects
your total body stores.
This is the best single
test for iron deficiency
and it usually is low in iron deficiency
because this is reflecting
your body stores of iron.
The challenge with ferritin is
it's also an acute phase reactant.
So if I get a pneumonia, I’m
going to have a high ferritin.
I may have iron deficiency and
have a falsely high ferritin
and miss the diagnosis if ferritin
is the only thing I’m getting.
Another iron study you might
get in your iron panel
is the total iron-binding capacity.
This represents how many free transferrin
sites there are in a patient.
So if there are lot of free
spaces for iron to bind,
that means your iron is low, they
should be bound, they are not,
so you may have a total iron
binding capacity this high.
If I have a patient who has
inflammation and a normal ferritin
and a high iron binding capacity,
I may have a patient
with iron deficiency,
oh yes, and their ferritin is high
because they have a pneumonia.
The serum iron is not really
a particularly useful test.
It comes along with that often.
I don’t use it very often.
So how do we manage
iron deficiency anemia?
It seems pretty obvious we
have to give them iron.
Usually, we provide iron as a medication,
a dose of around 4-6 mEq/kg/day.
We’re going to restrict milk
consumption in these children
because that is such a common cause.
Sometimes kids don’t want
to go along with that plan
and you have to spend some time
encouraging the families to teach
them how to say no to their
child who wants more milk.
Additionally, we will hopefully
increase iron-containing foods.
You can look that up on the internet,
involves foods like meat and legumes.
We often supplement vitamin C because this
facilitates iron absorption in the gut.
Also, if a patient has become tachycardic,
we’re going to need to
transfuse that patient.
Typically, this is at
hemoglobin of around 7.
We don’t usually use the hemoglobin number
itself for when we need to transfuse,
we usually use when
However, you may use it
in certain circumstances.
An example would be if a
patient has a brisk GI bleed
and was 9 and then was 7
and still is tachycardic,
I’m probably going to transfuse that
child because next time I look,
the child will be 5.
Okay, vitamin B12 and folate deficiency.
This is much more common
in adults than children
because B12 and folate are
fairly ubiquitous in the diet.
We typically think of this as a
problem in adult alcoholics.
It could happen in a very
severe teen alcoholic,
but whatever the case may be deficiency
of these two nutritional elements
cause a macrocytic megaloblastic anemia.
B12 is absorbed in the ileum,
so we also see this problem in
patients with ileal inflammation.
The classic example would
be a Crohn’s patient.
like I said is rare.
We will treat these patients
with IM vitamin B12.
Folate disease is very,
very rare in children
and generally associated with
a generalized malnutrition.
We use oral supplementation of
folate and that will be fine.
So both of these are erythrocyte aplasias.
of childhood is a disease
that sometimes pops up on exams and
you should probably be familiar with.
of childhood or TEC
shows up around six months
to four years of age.
I usually think of it about a
year older or two-year-old.
This is a transient phenomenon,
but by transient, I mean several
months not just for a few minutes.
It’s a normocytic anemia because these
patients are transiently incapable
of making red blood cells and it’s
usually preceded by a viral illness.
Often that virus is parvovirus B19,
but it might be another
virus as well.
In fact, parvovirus is only
implicated in the minority of cases.
There is no known cure to this,
but the good news is it always
gets better on its own.
So typically these children will be
fine, gradually become more pale,
begin getting lethargy and that progression
of signs and symptoms that we discussed
at the beginning of this lecture and the
parent will bring them in for evaluation.
You get a CBC and you notice they
have a pure erythrocyte aplasia.
We will now watch these
patients for a period of time,
sometimes they require transfusions and
then over a few months, they get better.
Flipside is when a child never develops
those red cells in the first place.
They start off with red blood cells
because they have fetal hemoglobin,
but then they’re incapable
of making any further.
This is a congenital erythrocyte aplasia.
It presents soon after birth
with a rapid onset anemia.
And there is a predisposition to cancer in
these patients even after they’re anemic.
One-third of cases will
remit in the first decade,
but many of these patients
after multiple transfusions
simply go on to a bone
Bone marrow transplant
is obviously not benign,
so we want to approach this with care,
but that is really the only cure for these
patients who have persistent disease.