Fourth year pharmacy students Shanna & Sierra are sharing with you their handout and few words below about the topic:
Anticoagulating patients can seem like an already daunting task. Taking indication, renal function, hepatic function, and bleed risk into account, selecting an appropriate agent can be challenging.
What happens when you run into trouble? Heparin Induced thrombocytopenia (HIT) is a rare complication that patients can present with after receiving heparin. While heparin does not normally cause any major change in platelets, HIT causes a profound platelet drop. There are two types: HIT I and HIT II.
HIT I (non-immune mediated) generally has a quicker onset and causes a milder platelet count decrease. HIT II occurs when the body interprets heparin as a foreign substance and subsequently forms anti-heparin antibodies. These antibodies activate Platelet-Factor 4 (PF4). Activated platelets put the patient at a more hypercoagulable state. PF4 complexes with the heparin-platelet molecule and the immune system sends macrophages to destroy the ‘foreign’ complex, further dropping the platelet count.
The first course of action should be stopping heparin and starting an anticoagulant to prevent DVT, PE, or MI by combatting the hypercoagulable state. There are several different options for HIT management with IV and oral direct thrombin inhibitors, SQ and oral Xa inhibitors, and the old faithful oral vitamin K antagonist, warfarin. Each of these have their place in therapy and knowing how to utilize each properly is essential.
When using warfarin, it is important to wait until the platelet count rises above 150×109/L3, so this is typically not the initial treatment option. Bridging is still required when initiating warfarin and the bridging technique can change depending on what injectable agent is being used. Bridging from argatroban to warfarin is unique because argatroban also affects the INR. Close INR monitoring while warfarin is being initiated and after the argatroban has been stopped is important.
There are studies showing the efficacy of DOACs as an IV to PO switch choice or even initial treatment agents for HIT II, simplifying the treatment process and risks. Additionally, newer agents do not require the same rigorous monitoring as warfarin. This is a greater convenience for patients.
Duration of anticoagulation after the onset of HIT differs among patients depending on if they have evidence of developing thrombus or not. It could be as short as 4 weeks, could extend to 3 months, or it could be indefinitely. More and more of the DOACs are being studied for HIT, so practices may change and these could become more commonly used.
-Shanna & Sierra, PharmD Candidates, March 2020