ABSTRACT
Skin necrosis is a rare complication of heparin therapy. Strong evidence suggests an immune-mediated mechanism in which heparin-antibody complexes bind to platelets, resulting in platelet aggregation, thromboembolism, and ischemic necrosis. Heparin-induced thrombocytopenia (HIT) may also occur in response to immune-mediated platelet aggregation. The presence, of heparin-dependent antibodies can be confirmed by platelet aggregometry, (14)C-serotonin release assay (SRA), or enzyme-linked immunosorbent assay (ELISA). Clinical suspicion, early detection and immediate cessation of heparin therapy are important in preventing the potentially severe complications of heparin-induced platelet aggregation. Potential therapeutic approaches include plasmapheresis and alternative forms of anticoagulation such as warfarin, aspirin, dipyridamole, or other novel investigational agents.
