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Postgraduate Education Corner: CONTEMPORARY REVIEWS IN CRITICAL CARE MEDICINE |

Heparin-Induced Thrombocytopenia: A Contemporary Clinical Approach to Diagnosis and Management

Eduard Shantsila, MD; Gregory Y. H. Lip, MD; Beng H. Chong, MD
Author and Funding Information

*From the Haemostasis Thrombosis and Vascular Biology Unit (Drs. Shantsila and Lip), University Department of Medicine, City Hospital, Birmingham, UK; and the Department of Haematology (Dr. Chong), St. George Hospital, Kogarah, NSW, Australia; and SGCS (Dr. Chong), University of New South Wales, Kensington, NSW, Australia.

Correspondence to: Eduard Shantsila, MD, University Department of Medicine, City Hospital, Birmingham, B18 7QH, UK; e-mail: shantsila@yandex.ru


The authors have reported to the ACCP that no significant conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/site/misc/reprints.xhtml).


© 2009 American College of Chest Physicians


Chest. 2009;135(6):1651-1664. doi:10.1378/chest.08-2830
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Thrombocytopenia following heparin administration can be associated with an immune reaction, now referred to as heparin-induced thrombocytopenia (HIT). HIT is essentially a prothrombotic disorder mediated by an IgG antiplatelet factor 4/heparin antibody, which induces platelet, endothelial cell, monocyte, and other cellular activation, leading to thrombin generation and thrombotic complications. Indeed, HIT can also be regarded as a serious adverse drug effect. Importantly, HIT can be a life-threatening and limb-threatening condition frequently associated with characteristically severe and extensive thromboembolism (both venous and arterial) rather than with bleeding. This article provides an overview of HIT, with an emphasis on the clinical diagnosis and management.


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