Dieser Beitrag enthält keine Schlüsselwörter
Critical care, Thrombocytopenia, Heparin
Dieser Beitrag enthält keine Zusammenfassung
ummary: Heparin binds to platelets dependent on its molecular weight and the negative charges. This causes platelet activation. In case of concomitant diseases associated with preactivated platelets (i.e. peripheral arterial disease), this effect may cause a transient decrease of platelet count. The clinical course of these non-immunologic interactions of heparin and platelets is benign. More important are immunologic effects of heparin on platelets. After 5 – 8 days of heparin treatment some patients form antibodies against complexes of platelet factor 4 (PF4) and heparin. These antibodies lead to platelet and endothelial cell activation, which results in thrombocytopenia, thrombin generation, and new thrombotic events. The clinical diagnosis can be verified by demonstration of HIT antibodies either by a sensitive functional assay (i.e. HIPA test) or by a PF4/heparin ELISA. Affected patients do need further parenteral anticoagulation. Danaparoid sodium (Orgaran®) and the recombinant hirudin Lepirudin (Refludan®) are the most important options for further parenteral anticoagulation of HIT patients. The clinical impact of HIT antibodies without clinical manifestation (i.e. decrease of platelet count > 50%, new thromboembolic events, skin necrosis) is currently unknown. A general screening for HIT antibodies is not justified. However, it must be recommended to monitor platelet count every alternate day between day 5 and 20 of heparin treatment.