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Review
. 2024 Aug 9;13(16):4686.
doi: 10.3390/jcm13164686.

Management of Heparin-Induced Thrombocytopenia: A Contemporary Review

Jun Yen Ng  1 , Melanie D'Souza  1 , Felanita Hutani  1 , Philip Choi  1
Affiliations
Review

Management of Heparin-Induced Thrombocytopenia: A Contemporary Review

Jun Yen Ng et al. J Clin Med. .

Abstract

Heparin-induced thrombocytopenia (HIT) is a life- and limb-threatening immune-mediated emergency classically associated with heparin therapy. This review focuses on type II HIT, characterized by the development of antibodies against platelet-factor 4 (PF4) bound to heparin after exposure, causing life-threatening thrombocytopenia, arterial thrombosis, and/or venous thrombosis. The high morbidity and mortality rates emphasize the need for early recognition and urgent intervention with discontinuation of heparin and initiation of non-heparin anticoagulation. We discuss the management of HIT with an emphasis on recent developments: (i) incorporating the phases of HIT (i.e., suspected, acute, subacute A and B, and remote) into its management, categorized according to platelet count, immunoassay, and functional assay results and (ii) direct-acting oral anticoagulants (DOACs), which are increasingly used in appropriate cases of acute HIT (off-label). In comparison to parenteral options (e.g., bivalirudin and danaparoid), they are easier to administer, are more cost-effective, and obviate the need for transition to an oral anticoagulant after platelet recovery. We also identify the knowledge gaps and suggest areas for future research.

Keywords: antibody-mediated; heparin; thrombocytopenia; thrombosis.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
Pathogenesis of heparin-induced thrombocytopenia. Heparin exposure leads to the production of immunoglobulin G (IgG) antibodies against PF4 bound to heparin. These antibodies bind to and activate platelets causing thrombosis and thrombocytopenia. They also bind to endothelium, monocytes, and neutrophils leading to thrombin generation, which promotes thrombosis and further activation of platelets. Created with BioRender.com. PF4: platelet factor 4, IgG: immunoglobulin G.
Figure 2
Figure 2
Key management steps in each phase of heparin-induced thrombocytopenia. HIT: heparin-induced thrombocytopenia, ICU: intensive care unit, VTE: venous thromboembolism.
See this image and copyright information in PMC

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