Our next topic, all part of what's known us our thrombotic microangiopathies, right?
All part of thrombotics.
So far we'll get two, or the TTP and HUS.
Here we'll take a look at DIC now.
DIC is rather interesting.
The ideologies are quite enigmatic actually.
Sepsis, especially E. coli or maybe Neisseria meningitidis.
Maybe malignancies such as acute promyelocytic leukemia.
What is acute promyelocytic leukemia?
Do you remember?
What kind of leukemia is that?
Acute type, is it ALL or AML?
AML, very good.
And on the FAB classification, which M type is it?
So M3 is your acute promyelocytic leukemia,
could be a possible trigger for DIC or maybe even obstetric complications in which remember
if you're a pregnant lady during delivery is undergoing eclampsia.
What does that mean to you?
Unfortunately, she has developed seizures, hasn't she?
When the seizure's taking place there's every possibility that now
that there's mixing of the epithelial cells of the fetus, the placenta,
the squamous cells then entering or the squames entering the maternal circulation
and there's every possibility with that happening may then develop amniotic fluid emboli.
All these could be a possible trigger of DIC as well.
So we have interesting ideologies here in terms of DIC.
Now, take a look at the name.
Within a blood vessel, very quickly now we'll be focusing on acute.
Acute is the one in which this patient based on that type of history
is going to be bleeding from every single orifice.
You may find bleeding from the mucosal membranes.
There might be nose bleeding.
There's internal bleeding taking place everywhere,
so therefore, every single platelet count "Oh, excuse me!" the plate count is diminished
because there's drastic drop in platelet, therefore, the bleeding time will be elevated greater than 7 minutes.
Rapidly, both the intrinsic and extrinsic branches of the coagulation pathway
are being stimulated acutely and rapidly,
therefore causing'well, if it's intrinsic it'd be PTT to be elevated,
if it's the extrinsic it'd be the PT to be elevated.
So now we have an increase in BT, PTT and PT.
And then finally, as quickly, you also having destruction in dissolution of your thrombi.
So you find an elevated in D-dimer.
The only lab test to be decreased in DIC will be the platelet count.
Welcome to DIC.
No other condition would give you such an extensive lab workout.
Trauma, snake bites and maybe even cancers might be other triggers that we talked about.
With DIC, widespread activation of all coagulation system like we talked about.
So now we have once again formation of thrombi.
So what happens to RBCs please?
We have massive thrombi hypoxia.
Number two, consumption clotting factors we talked about and platelets,
therefore, increasing BT, PT, PTT.
And just as rapidly, you're breaking them down and increase in D-dimers.
Lab findings like we talked about, elevated PT, PTT, decrease in platelet count.
Remember those RBCs with all those thrombi formation, what's happening?
Boom, boom, boom!
I am now forming schistocytes, yet another cause of microangiopathic hemolytic anemia.
And the D-dimers, obviously, will be elevated.
Two differentials that you should be thinking about with elevated D-dimers,
DIC with the rest of these couldn't be anything else except for DIC.
But obviously, if the patient had a DVT and you find an elevated D-dimer?
uh-oh, that patient may have now developed what?
PE, right, pulmonary emboli. What does it look like?
Bleeding everywhere. Acute, acute, acute.
There's no specific treatment, however, if there's a bleeding taking place what would you like to do?
Wouldn't you like to then stop the bleeding?
You may do this by giving what?
Fresh frozen plasma.
And always make sure if you can, once the bleeding has been stopped,
to quickly go back and take a look at the underlying issue.
Was it the snake bite? Was it the cancer? Was it the sepsis?
And so on and so forth but poor prognosis if your patient goes into DIC.