Hi this is Dr. K from iMedicalSchool and today we are going to talk about heparin induced
thrombocytopenia otherwise known as HIT.
So the first question to ask is want is thrombocytopenia?
Thrombocytopenia is a fancy term that means low platelet count.
Platelets are fragments of a larger cells found in the bone marrow called megakaryocytes.
The function of platelets is to help form clots to stop bleeding.
Now heparin induced thrombocytopenia is when heparin, an anticoagulant agent used commonly
in the hospital, leads to a drop in a patient's platelets.
Now ther are two type of heparin induced thrombocytopenia.
Type 1 heparin induced thrombocytopenia is a non-immune mediated process.
In some people heparin causes platelet activation leading to a partial consumption of platelets.
If you continue heparin the platelet count returns to normal within a day or two.
Now type heparin induced thrombocytopenia type 2 is immune mediated and will be our
focus for the rest of this discussion.
type 2 HIT involves the formation of heparin-platelet factor 4 complex antibodies.
We will discuss how these antbodies play a role in the development of immune mediated
thrombocytopenia a little bit later.
Keep in mind HIT type 2 is a rare disorder and can lead to thrombi including arterial
thrombi that are platelet rich.
Of all the patients you see only 5 % are likely to develop hit who have had a prolonged exposure
to heparin.
An important point to note is that your patients on unfractionated heparin have a higher risk
of developing HIT than if they are on low molecular weight heparin.
Risk factors for immune mediated heparin induced thrombocytopenia include long duration of
exposure to heparin exposure to unfractionated heparin,being female, and history of recent
surgery.
So lets discuss the physiology of HIT.
Platelets have a receptor called platelet factor 4 bound to their outer surfaces.
When heparin is introduced into the blood stream the heparin binds the platelet factor
4 receptor.
Generally if a patient had a previous exposure to heparin they may have developed an anti
heparin platelet factor complex antibody.
This antibody binds the heparin platelet factor complex.
The anti-Hep-PFR antibody when bound to its target can activate platelets.
The activation of platelets can lead to thrombi or clot formation and consumption, as well
as, removal of activated platelets by the spleen.
Now that we have gone over the physiology lets talk about how to diagnose heparin induced
thrombocytopenia type 2.
If a patient with a current exposure to heparin has a 50% drop in their platelets after 5
to 10 days of exposure.
Now keep in mind this time frame may be shorter if they had previous known exposure to heparin.
Other important findings that are indicative of HIT is if your patient develops a reaction
to heparin.
These reactions to heparin include necrotic skin lesions, tachycardia, dyspnea or difficulty
breathing, chills, and fevers.
Remember that patients with HIT are hypercoaguable so thrombi can develop.
Thrombi include DVTs, PEs (otherwise known as pulmonary embolisms), limb gangrene due
to arterial thrombi, and finally cerebral sinus thrombosis.
So what labs are used to diagnose hit?
Well lets first talk about the serotonin release assay.
The serotonin release assay is the gold standard for diagnosis of HIT type 2.
The way the serotonin release assay works is that you take your patients serum who you
suspect has HIT and mix it with platelets that have a radiolabeled 14-C. When these
platelets are activated they release the serotonin 14 carbon.
The radiolabeled platelets are mixed with you patient's serum then the combination is
exposed to heparin.
If your patient has HIT the heparin will lead to activation of platelets and release of
14-C serotonin.
If the radiolabeled 14- carbon serotonin is detected than you ahve a positive serotonin
assay for HIT type 2.
Another test used to detect HIT type 2 is the platelet aggregation assay.
In this assay we take normal platelets and mix them with them with the serum of your
patient with suspected HIT.
We then introduce different doses of heparin into 3 samples.
If the patient has HIT then at low levels and at therapeutic levels there will be low
aggregation and high aggregation respectively.
At high doses no aggregation occurs as the heparin-PF4 antibodies become overwhelmed.
Now that we have discussed how to diagnose HIT type 2 we will discuss treatment.
If you suspect a patient has HIT stop all heparin injections and products.
Keep in mind certain devices may be line with heparin so just stopping their roaring injection
may not be enough.
Given these patients are hypercoaguable they need to be started on a direct thrombin inhibitor
like argatroban or bivalrudin.
Argatroban has the ability of being able to use it in renal insufficiency and hepatic
insufficiency, while bivalrudin generally can be use in hepatic insufficiency.
Do not start warfarin or low molecular weight heparin for anticoagulation.
Once a patient has a confirmed HIT study then you can bridge them with a direct thrombin
inhibitor to Coumadin.
INR goal is 2 to 3 with duration of therapy being 2 to 3 months in patients with HIT but
no thrombus or 5 to 6 months in patients with HIT and thrombus.
All right that was a review of heparin induced thrombocytopenia.
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down below to discuss in a future video.
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This is Dr K and I will see you next time.