In this lecture, we’re going
to discuss 2 major causes of
acute hypercoagulability in
an otherwise normal child.
One is DIC or disseminated
and the other is ITP or immune
Let’s start with DIC.
So DIC is a systemic body wide
activation of the coagulation cascade.
This can cause both microemboli
but also an overall overconsumption
of clotting factors,
which then results
It can either be low grade or chronic
or it can be acute and very severe.
So there are many causes of DIC.
It could just be surgery.
It could be a traumatic event.
It could be an overwhelming bacterial
infection or it could be cancer.
The idea here is that it’s something
that’s activating the clotting cascade.
One unusual cause of DIC that’s specific
to children is Kasabach-Merritt syndrome.
All these infants you can see on this slide
have hemangiomas and this can be large.
And in these infants, all of these infants,
they develop Kasabach-Merritt syndrome.
Kasabach-Merritt is when there’s a
consumption of these coagulable products
inside the hemangioma.
Sometimes, these hemangiomas
are on the outside of the body
and sometimes they are on
the inside of the body
and it can be hard to figure out
and very challenging to treat.
Another unusual specific to
children is snake bites.
Of course adults get snake bites too,
but the majority of snake
victims are actually children
who don’t know better than to
avoid handling poisonous snakes.
Snake bites can cause a DIC picture
and that’s typically the pit vipers
rather than something like the coral
snake which is more of a neurotoxin.
Also, patients may simply develop sepsis
and we do see DIC sometimes
especially in neonatal sepsis.
What are the signs and symptoms of DIC?
These patients will typically
have acute and severe bleeding
from the nose, from the
mouth, from the orifices.
They will develop bruising and, body wide,
they may have purpura and petechiae.
The blood may be oozing from
IV sites or surgical sites
and may be coming
from the rectum.
They may start coughing up blood
and have a pulmonary bleed
or they may develop a stroke
and have a CNS hemorrhage.
The bleeds may happen really anywhere
and result in end-organ dysfunction.
This is a very severe disease.
So how do we make the diagnosis?
There are several labs that can
key us in to a diagnosis of DIC.
Patient should have
a prolonged PT/PTT
because they are having consumption
of their clotting cascades,
both intrinsic and extrinsic.
They may have decreased fibrinogen
which is used to create clots,
because in those areas where
those clots are forming,
the rest of the blood
has less of it.
Likewise, they will have
increased fibrin split products,
a side effect of having clotting
happening elsewhere in the body.
The D-dimer is very likely
to be elevated in DIC.
In fact, it’s ubiquitous.
So what’s interesting about the
D-dimer is if that’s normal,
it’s almost convincing that
your patient does not have DIC.
That said, there is a lot
of false positive D-dimers.
The patient could simply have a
bad viral illness, for example,
and have an elevated D-dimer,
but a D-dimer that’s normal
assures you that this is not DIC.
In the CBC, we will notice low platelets
as a result of consumption in those
areas where there are clots.
How do we manage it?
Well, first we need to treat
the underlying cause.
If it’s an infection, we
need to give the antibiotics
that are necessary to treat the infection,
because otherwise this is
just going to keep burning.
Next, we’re going to
replace consumed products.
In particular, these patients
may require platelets.
They may require fresh frozen plasma
and they may require cryoprecipitate.
Basically, they need those factors
back in their clotting cascade.