HIT occurs in 5 % of patients exposed, regardless of the dose, schedule, or route of administration.
HIT is caused by an autoantibody directed against platelet factor 4 (PF4) in complex with heparin. HIT antibodies activate platelets and can cause catastrophic arterial and venous thrombosis.
HIT can cause arterial thrombosis which leads to vital organs not getting perfused and this is worse than DVT or venous thrombosis.
Presumptive diagnosis of HIT. Confirmatory HIT antibody test will take several days to come back. You have to act with only a presumptive diagnosis of HIT.
HIT requires 50% drop in platelets in say 5-10 days.
HIT antibodies need to be tested.
Pretest probability of heparin-induced thrombocytopenia (4-T’s score)
Tx:
-Consult Hematologist early.
-Argatroban: Use non-heparin anticoagulants such as argatroban, which is a direct thrombin inhibitor.
–D/C Warfarin if the patient was being bridged when the HIT occurred. In addition to D/C Warfarin, give Vitamin K (if Warfarin has already raised the INR, even if it’s not reached therapeutic range yet).
Don’t use LMWH (e.g. Enoxaparin, dalteparin, etc.) – they also cause HIT, even though not as much as heparin.
“In patients who develop HIT while on warfarin therapy, there is an even greater risk of associated thrombosis because of the continued thrombin generation (as a result of HIT), and also because of the depletion of protein C anticoagulant resulting from warfarin therapy. Therefore, it is recommended that warfarin not be used in patients with HIT, at least until the platelet count has normalized (SOR B). If the patient was already on warfarin at the time HIT was discovered or suspected, it should be discontinued and reversed with vitamin K.” The ABFM