Keywords
Heparin, Thrombocytopenia, Autoimmune, Hypersensitivity, Spleen, Thrombosis
Abstract
Heparin induced thrombocytopenia (HIT) is a complicated disease that arises from an autoimmune attack against platelets. Heparin that is administered in a patient with HIT forms a complex with Platelet factor-4 (PF4), which is found on the surface of platelets. This complex leads to a Type III Hypersensitivity reaction where IgG antibodies bind to the Heparin/PF4 complex. The platelet-IgG complex subsequently becomes a target for destruction by the spleen. Platelet destruction eventually results in thrombocytopenia five to ten days following heparin exposure. The severity of the resultant thrombocytopenia can range from bruise-like discoloration of the skin all the way to hemorrhagic stroke in the most severe cases. Fragments of the destroyed platelets can further induce the activation of additional platelets, which lead to a thrombotic state. As a result of the recurrent thromboses, patients can develop a deep venous thrombosis (DVT) which can progress into a pulmonary embolism in severe cases. Full understanding of this phenomenon is essential in management of patients who develop this condition.
Citation
Gergis R, Soliman I, Gad M, Long L, Josephs M, et al. (2021) Managing Heparin induced Thrombocytopenia in patients who are undergoing Left Ventricular Device Placement procedure and ultimately Heart transplant. SM J Hematol Oncol 4: 4.