Heparin-induced thrombocytopenia (HIT): Review of incidence, diagnosis, and management

Abstract

Heparin-induced thrombocytopenia (HIT) is a life and limb-threatening complication of heparin exposure. Here, we review the pathogenesis, incidence, diagnosis, and management of HIT. The first step in thwarting devastating complications from this entity is to maintain a high index of clinical suspicion, followed by an accurate clinical scoring assessment using the 4Ts. Next, appropriate stepwise laboratory testing must be undertaken in order to rule out HIT or establish the diagnosis. In the interim, all heparin must be stopped immediately, and the patient administered alternative anticoagulation. Here we review alternative anticoagulation choice, therapy alternatives in the difficult-to-manage patient with HIT, and the problem of overdiagnosis.

Thrombocytopenia and Intracranial Venous Sinus Thrombosis after “COVID-19 Vaccine AstraZeneca” Exposure

“…The consumption of platelets, thrombocytopenia, and disseminated intravascular coagulation ensue. This pathomechanism has similarities with heparin-induced thrombocytopenia (HIT) [26]. COVID-19 has been described as a possible predisposing factor for HIT [27].…”

Limb ischemia and pulmonary artery thrombosis after the ChAdOx1 nCoV-19 (Oxford–AstraZeneca) vaccine: a case of vaccine-induced immune thrombotic thrombocytopenia

“…[2][3][4][5][6][7] It closely resembles HIT, in which antibodies, typically immunoglobulin G (IgG), are produced against circulating complexes of PF4 and endogenous heparin. [8][9][10] and regulate hemostasis by releasing PF4, a 70-amino acid protein that binds heparin. In HIT, the IgG antibody that is bound to the PF4-heparin complex also binds to platelet Fcγ receptors, triggering platelet activation and promoting thrombosis.…”

“…In HIT, the IgG antibody that is bound to the PF4-heparin complex also binds to platelet Fcγ receptors, triggering platelet activation and promoting thrombosis. 10 In VITT, the vaccine is believed to lead to development of an IgG that targets PF4 (as opposed to the PF4-heparin complex), also binding platelet Fcγ receptors and activating platelets. 7 Although IgG does not require heparin to activate platelets in VITT, heparin may aggravate VITT because circulating PF4-heparin complexes may also bind IgG from VITT as from HIT.…”

Ischémie d’un membre et thrombose de l’artère pulmonaire après l’administration du vaccin ChAdOx1 nCoV-19 (Oxford–AstraZeneca) : un cas de thrombocytopénie thrombotique immunitaire induite par le vaccin

“…La TTIV est un syndrome qui a été signalé pour la première fois en avril 2021 chez des patients qui avaient récemment obtenu le vaccin ChAdOx1 nCoV-19 2 – 7 . Elle ressemble fortement à la TIH, chez laquelle des anticorps, typiquement l’immunoglobuline G (IgG), sont produits contre les complexes formés du facteur plaquettaire 4 circulants et de l’héparine endogène 8 – 10 . Les plaquettes neutralisent l’héparine endogène et régulent l’hémostase en libérant le facteur plaquettaire 4, une protéine à 70 acides aminés qui se lie à l’héparine.…”