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Published on: January 4, 2019
[Heparin-Induced Thrombocytopenia after Total Knee Replacement]
M Salášek1, J Šlechtová, T Pavelk
1Klinika ortopedie a traumatologie pohybového ústrojí Lékařské fakulty Univerzity Karlovy a Fakultní nemocnice Plzeň.
Heparin-induced thrombocytopenia is a rare complication of treatment with both unfractionated heparin (UFH) and low molecular weight heparin (LMWH). Antibodies against the complex heparin-platelet factor 4 are the main cause of pathogenesis, resulting in the activation of thrombocytes, coagulation, endothelium, monocytes, neutrophils and subsequent highly prothrombotic state. The prothrombotic state can result not only in venous but also in arterial thrombosis at different locations (which is manifested apart from venous thromboembolic disease also by acute limb ischemia, acute myocardial infarction, ischemic stroke, skin necrotizing lesion exanthema). If HIT is not adequately treated, it may be fatal in up to 10% of patients. For early diagnosis, a combination of 4T scores and diagnostic lab tests for HIT is required. Immediate discontinuation of heparin therapy (UFH, LMWH) and switching to non-heparin anticoagulants (fondaparinux, bivalirudin, argatroban or in some situations DOACs) are essential in HIT treatment. The case report describes the patient after primary knee replacement, complicated by the development of HIT with no evidence of venous thromboembolic disease. Preoperatively, the patient was administrated nadroparin due to paroxysmal atrial fibrillation, after the development of HIT, anticoagulation was modified to fondaparinux and subsequently to warfarin after the platelet count normalization. Key words: unfractioned heparin, low molecular weight heparin, thrombocytopenia, total knee replacement.
Heparin-induced thrombocytopenia is a rare complication of treatment with both unfractionated heparin (UFH) and low molecular weight heparin (LMWH). Antibodies against the complex heparin-platelet factor 4 are the main cause of pathogenesis, resulting in the activation of thrombocytes, coagulation, endothelium, monocytes, neutrophils and subsequent highly prothrombotic state. The prothrombotic state can result not only in venous but also in arterial thrombosis at different locations (which is manifested apart from venous thromboembolic disease also by acute limb ischemia, acute myocardial infarction, ischemic stroke, skin necrotizing lesion exanthema). If HIT is not adequately treated, it may be fatal in up to 10% of patients. For early diagnosis, a combination of 4T scores and diagnostic lab tests for HIT is required. Immediate discontinuation of heparin therapy (UFH, LMWH) and switching to non-heparin anticoagulants (fondaparinux, bivalirudin, argatroban or in some situations DOACs) are essential in HIT treatment. The case report describes the patient after primary knee replacement, complicated by the development of HIT with no evidence of venous thromboembolic disease. Preoperatively, the patient was administrated nadroparin due to paroxysmal atrial fibrillation, after the development of HIT, anticoagulation was modified to fondaparinux and subsequently to warfarin after the platelet count normalization. Key words: unfractioned heparin, low molecular weight heparin, thrombocytopenia, total knee replacement.
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