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Heparin‐induced thrombocytopenia: pathogenesis and management

Heparin-induced thrombocytopenia (HIT) is a transient prothrombotic disorder initiated by heparin. Its central feature is thrombocytopenia caused by antibody-mediated platelet activation. HIT can be viewed as an acquired hypercoagulability disorder, with increased thrombin generation in vivo, and increased risk for arterial and, especially, venous thrombosis. The pathogenic HIT antibodies are directed against neoepitopes on a ‘self’ protein, platelet factor 4 (PF4), that are expressed when PF4 is bound to heparin or certain other polyanions. This review focuses on studies published since 1990, and summarizes the pathogenesis, laboratory testing, frequency and clinical picture of HIT. Two treatment situations are reviewed critically: management of thrombosis complicating HIT and treatment of ‘isolated HIT’ (HIT recognized because of thrombocytopenia alone). There is potential for medicolegal risk, particularly if inappropriate therapy contributes to patient harm.