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[Heparin induced thrombocytopenia. A frequently unrecognised complication after major orthopedic surgery]
1Transfusionsmedizin der Universität zu Köln. susanne.picker@medizin.uni-koeln.de
The application of unfractioned (UFH) and low molecular weight heparins (LMH) has reduced the incidence of thromboembolic events. However, the frequency of heparin-induced thrombocytopenia (HIT II) in orthopedic patients, particularly susceptible for both thromboembolic complications and HIT II with potentially life threatening complications, is about 0.5% for LMW and 3% UFH. Induced by an immune response, the excessive activation of platelets and endothelial cells causes massive thrombin generation and, as a result, thrombotic vessel occlusion. The rates of mortality and amputation in HIT II are estimated to be 30% and 20%, respectively. The clinical course is highly dependent on early therapeutic intervention, consisting of compatible and adequately dosed anticoagulation drugs. Vitamin K antagonists as well as platelet substitution may lead to disastrous sequelae. We summarize the current state of the pathophysiology, diagnosis and therapy of HIT II and illustrate therapeutic mistakes in a case report.
The application of unfractioned (UFH) and low molecular weight heparins (LMH) has reduced the incidence of thromboembolic events. However, the frequency of heparin-induced thrombocytopenia (HIT II) in orthopedic patients, particularly susceptible for both thromboembolic complications and HIT II with potentially life threatening complications, is about 0.5% for LMW and 3% UFH. Induced by an immune response, the excessive activation of platelets and endothelial cells causes massive thrombin generation and, as a result, thrombotic vessel occlusion. The rates of mortality and amputation in HIT II are estimated to be 30% and 20%, respectively. The clinical course is highly dependent on early therapeutic intervention, consisting of compatible and adequately dosed anticoagulation drugs. Vitamin K antagonists as well as platelet substitution may lead to disastrous sequelae. We summarize the current state of the pathophysiology, diagnosis and therapy of HIT II and illustrate therapeutic mistakes in a case report.
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