decades, heparins have been used successfully for prophylaxis and treatment of thromboembolic complications. although heparin-induced thrombocytopenia (HIT Type II) is a well-known adverse effect of heparin therapy, thromboembolic complications during heparin therapy are rarely diagnosed exactly to be related to HIT. An immunologic cause of HIT by generation of multimodal immune complexes against a neo antigen of heparin and platelet factor 4 is equivocally accepted as the decisive pathophysiological mechanism. The incidence of HIT seems to be related to the type of heparin (unfractioned/low molecular weight) or other underlying risks such as peripheral occlusive vessel disease. Mortality on complications resulting from HIT is reported to be about 20 – 30%. For diagnosis of HIT Type II, clinical observation and simultaneous laboratory testing are essential. Discontinuation of any heparin therapy is necessary, and other well controllable anticoagulation regimens have to be continued. The heparinoid danaparoid-sodium and the thrombin inhibitor recombinant hirudin have been used successfully world-wide for treatment in many patients with HIT Type II including cardiopulmonary bypass surgery or renal replacement procedures. Furthermore, other therapeutical alternatives (e.g. immunoglobu- lins, prostaglandins) exist. Randomised controlled studies have to evaluate which drug has to be preferred in the future including risk/benefit ratio. The need of supplementary procedures (e.g. embolectomy) depends on the individual clinical status. The patients have to be informed in detail about their underlying disease and further deleterious consequences of re-exposition with heparin. HIT should be recorded in an emergency certificate and the national Committee on Drugs should be informed about this severe side effect of heparin thera

        Key words: heparin – thrombocytopenia – thrombosis – danaparoid-sodium – recombinant hirudin