Heparin-induced thrombocytopenia: clinical manifestations and management strategies

Thrombocytopenia is a relatively frequent and usually benign clinical complication of heparin therapy. However, some patients receiving heparin and heparin-based products experience an immune-mediated reaction due to the development of heparin-induced antibodies. This reaction leads to a highly specific and paradoxical form of thrombocytopenia, known as type II heparin-induced thrombocytopenia (HIT). Unlike other types of drug-induced thrombocytopenia, HIT promotes thrombosis rather than bleeding; therefore HIT should be suspected in patients who experience thrombotic events despite adequate anticoagulation therapy. Early identification and treatment of HIT can prevent more serious complications associated with this disorder (e.g., exacerbation of venous thromboembolism, limb gangrene, and skin necrosis). Both arterial and venous thrombosis can arise from a single episode of HIT. Routine assessment of platelet counts is necessary with heparin therapy, as a decreased platelet level is usually the only indication of HIT. Although compared with unfractionated heparin, low-molecular-weight heparin therapy is less likely to result in HIT, the use of these agents is contraindicated in HIT patients. Concomitant warfarin therapy is not contraindicated in such patients but must be carefully monitored. Treatment with a direct thrombin inhibitor, such as lepirudin or argatroban, is an effective strategy in reversing the thrombocytopenia associated with HIT and reducing its complications. This article discusses the clinical syndrome of HIT, including pathophysiology, diagnostic criteria, clinical presentations, and current available management strategies in the context of 2 case studies.