What is HIT, including its pathophysiology?
HIT, which usually develops after a patient has been on heparin for 5 or more days, may develop sooner if there has been previous heparin exposure (see Figure 1).[3,14] Heparin binds to platelet factor 4 (PF4), forming a highly reactive antigenic complex on the surface of platelets and on endothelial cell surfaces, thereby increasing the number of targets for heparin-dependent antibodies.[3,14] Susceptible patients then develop an antibody (IgG) to the heparin-PF4 antigenic complex. Once produced, immunoglobulins, usually IgG, bind to the heparin-PF4 immune complex on the platelet surface. The Fc portion of the IgG then activates the platelets by binding to platelet Fc receptors.[3,14] Thrombocytopenia develops as the reticuloendothelial system consumes activated platelets, platelet microaggregates, and IgG-coated platelets.[3,14] Most devastating, however, is the thrombotic state that develops as a result of platelet activation and the generation of procoagulant microparticles, and an
