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Updated: Aug 23, 2026

A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia
Published on: August 18, 2015
Pathophysiology, epidemiology, diagnosis and treatment of heparin-induced thrombocytopenia (HIT)
Susanne M Picker1, Birgit S Gathof
1Transfusion Medicine, University of Cologne, Germany. susanne.picker@medizin.uni-koeln.de
Due to the widespread use of unfractionated (UFH) and low molecular weight heparins (LWH) for prophylaxis and treatment of thrombosis, heparin-induced thrombocytopenia is considered to be the most frequent (and potentially the most devastating) drug-induced thrombocytopenia. Induced by an immune response, excessive activation of platelets and endothelium cells causes massive thrombin generation and, as a result, life-threatening venous and arterial thrombotic vessel occlusion. The rate of mortality and amputation in HIT II is estimated to be 30% and 20%, respectively. The clinical course of HIT II depends highly on early therapeutic intervention consisting of immediate interruption of heparin application and, most important, of compatible thrombin inhibition. All measures implying a potentially procoagulant risk such as begin of oral anticoagulation or platelet substitution may result in disastrous side effects.
Due to the widespread use of unfractionated (UFH) and low molecular weight heparins (LWH) for prophylaxis and treatment of thrombosis, heparin-induced thrombocytopenia is considered to be the most frequent (and potentially the most devastating) drug-induced thrombocytopenia. Induced by an immune response, excessive activation of platelets and endothelium cells causes massive thrombin generation and, as a result, life-threatening venous and arterial thrombotic vessel occlusion. The rate of mortality and amputation in HIT II is estimated to be 30% and 20%, respectively. The clinical course of HIT II depends highly on early therapeutic intervention consisting of immediate interruption of heparin application and, most important, of compatible thrombin inhibition. All measures implying a potentially procoagulant risk such as begin of oral anticoagulation or platelet substitution may result in disastrous side effects.
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