Formerly called type 2 HIT

Epidemiology


Etiology


Tip

Heparin treatment, especially with unfractionated heparin (UFH), often causes thrombocytopenia. For this reason, a baseline check and regular monitoring of platelet counts are required.

Pathophysiology


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  • Heparin and platelet factor 4 (PF4) form a complex → production of IgG antibodies against the heparin/PF4 complex → IgG antibody-heparin/PF4 immunocomplex binds on platelet surface → platelet activation and aggregation → consumption of platelets (thrombocytopenia) and arterial/venous thrombosis
  • Thrombocytopenia also occurs due to phagocytosis of IgG antibody-heparin/PF4 immunocomplex-bound platelets by macrophages in the spleen, liver, and bone marrow.

Clinical features


  • HIT is primarily a prothrombotic disorder, with venous and/or arterial thrombosis developing in 25–50% of affected patients.
  • Venous thrombosis occurs most frequently; manifestations include:
    • Calf swelling and pain from lower extremity DVT
  • Arterial thrombosis occurs less commonly
  • Localized skin necrosis at heparin injection sites

Tip

HIT more commonly manifests with symptoms of thrombosis than with bleeding

Diagnostics

Differential diagnostics


  • Nonimmune heparin-associated thrombocytopenia (formerly called type 1 HIT)
    • A transient and clinically insignificant mild to moderate thrombocytopenia, usually occurring within 5 days of heparin initiation
    • Caused by a direct effect of heparin on platelet activation
    • Not associated with an increased risk of thrombosis

Treatment


Empirical management of HIT

  • Stop all heparin exposure immediately (including heparin flushes and heparin-coated catheters).
  • Patients on vitamin K antagonists (e.g., warfarin): Stop the medication and consider reversal with vitamin K.
  • Initiate nonheparin anticoagulation