Eduard Shantsila, MD*, Gregory Y. H. Lip, MD and Beng H. Chong, MD
CHEST June 2009 vol. 135 no. 6 1651-1664
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.
Heparin-induced thrombocytopenia (HIT) is a prothrombotic disorder initiated by heparin administration and is related to antibody-mediated platelet activation causing thrombin generation and thrombotic complications. Essentially, HIT can be regarded as a very severe adverse drug reaction resulting from multicellular immune activation.1
The administration of heparin is often associated with a reduction in platelet count. In the majority of cases, this phenomenon is independent of any immune reaction, and thrombocytopenia is mild (platelet count, > 100 × 109 cells/L), not progressive, and is not associated with bleeding or thrombosis.2 Such nonimmune heparin-associated thrombocytopenia (previously called HIT type I) can occur during the first few days of heparin administration (Table 1). Direct platelet membrane binding of heparin has been suggested as a potential mechanism of the condition.3–5 Other factors unrelated to heparin administration, such as sepsis, platelet-reactive autoantibodies, drug reactions, transfusion reactions, and foreign-body reactions (endograft), can also provoke thrombocytopenia.6 Nonimmune heparin-associated thrombocytopenia gradually resolves without heparin treatment interruption, and platelets gradually rise to pretreatment levels within a few days with no special treatment required.7–10 Nonetheless, thrombocytopenia following heparin administration may also be associated with an immune heparin-related response, now referred to as HIT (formerly called HIT type II). HIT can be a life-threatening and limb-threatening prothrombotic complication, which can lead to a systemic thrombotic response (both venous and arterial) rather than to bleeding.3,11 This article provides an overview of HIT, with an emphasis on the clinical diagnosis and management.
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