Etiology and assessment of hypercoagulability with lessons from heparin-induced thrombocytopenia.

Hypercoagulability, or thrombophilia, is a condition associated with an abnormally increased tendency toward blood clotting. Affected individuals are prone to developing venous or arterial thrombosis and often require thromboprophylaxis. Hypercoagulability can be generally classified as either an inherited or acquired condition. Patients with an inherited thrombophilia have genetic variances that alter the quality or quantity of proteins involved with hemostasis. Hypercoagulability may also be acquired and develop as an exaggeration of normal physiologic responses to major tissue injury, or an abnormal response to various prothrombotic clinical factors. Careful assessment for hypercoagulability is important because effective management strategies, often involving anticoagulation, may be available. Heparin-induced thrombocytopenia is an example of an acquired hypercoagulable state that has been well studied and, when recognized, responds to appropriate therapy. In this article, we review the etiology, risks, and assessment of thrombophilia, with emphasis on the clinical lessons learned from heparin-induced thrombocytopenia.

Emergency department awareness of heparin-induced thrombocytopenia: how frequently is risk assessment documented in patients with thrombosis?

Evidence-based guidelines recommend that heparin-induced thrombocytopenia (HIT) should be suspected whenever a patient develops thrombosis or thrombocytopenia 5 to 14 days after heparin initiation. The authors determined how frequently emergency department (ED) physicians document HIT risk assessment in patients presenting with thrombosis. Relevant data were extracted from the ED charts of 134 patients with venous or arterial thrombosis. Documentation (ie, notation of positive or negative findings) existed for recent heparin exposure in 7 (5.2%) of 134 charts, recent hospitalization in 33 (24.6%), history of thrombocytopenia in 0 (0%), and history of thrombosis in 62 (45.5%). Of 35 patients administered heparin in the ED, the preheparin platelet count was available for 19 (54.3%) and old records for 5 (14.3%). Thus, HIT risk assessment frequently remains undocumented for ED patients with thrombosis, including those administered heparin. Approaches to increase HIT awareness and facilitate HIT risk assessment and documentation in the ED may be needed.

Direct thrombin inhibition during percutaneous coronary intervention in patients with heparin-induced thrombocytopenia.

Patients with or at risk of heparin-induced thrombocytopenia (HIT) who are undergoing percutaneous coronary intervention (PCI) are at particular risk of thrombosis due to the prothrombotic nature of HIT and the endovascular disruption from PCI. Patients require aggressive anticoagulation during PCI, and alternative, nonheparin anticoagulation is recommended over heparin in patients with acute or previous HIT. Argatroban, bivalirudin, and lepirudin are nonheparin, fast-acting, parenteral direct thrombin inhibitors (DTIs). Multicenter, prospective studies have demonstrated that argatroban and lepirudin each reduce thrombosis in HIT and that argatroban and bivalirudin each provide adequate anticoagulation during PCI in patients with or at risk of HIT. We review current therapeutic practices with direct thrombin inhibitors in patients with or at risk of HIT during PCI, including individuals requiring periprocedural anticoagulation, and the factors influencing the choice of DTI in this setting.