ABSTRACT
Heparin-induced thrombocytopenia (HIT) is an immune-mediated syndrome characterized by thrombocytopenia, which can be isolated or associated with thrombotic events (see Chaps. 1-4). Complications ofHIT span a spectrum of venous and arterial thromboembolic events, including deep venous thrombosis, pulmonary embolism, myocardial infarction, thrombotic stroke, and limb artery occlusion requiring amputation (Warkentin, 2003). The elimination of all heparin sources and the initiation of alternate anticoagulation are recommended for treating patients with HIT (Hirsh et aI., 2001). Not infrequently, thrombosis is the first manifestation of HIT. Even among patients with isolated thrombocytopenia who are managed by heparin cessation alone, approximately 25-50% develop new thrombosis (Warkentin and Kelton, 1996; Wallis et aI., 1999; Lewis et aI., 2003). Furthermore, many patients with HIT require ongoing anticoagulation for underlying medical conditions.
