Management of Vascular Thrombosis in Patients with Thrombocytopenia

Abstract

Platelets play critical roles in hemostasis and thrombosis. While low platelet counts increase the risk of bleeding, antithrombotic drugs, including anticoagulants and antiplatelet agents, are used to treat thromboembolic events. Thus, the management of thrombosis in patients with low platelet counts is challenging with hardly any evidence available to guide treatment. Recognition of the underlying cause of thrombocytopenia is essential for assessing the bleeding risk and tailoring therapeutic options. A typical clinical scenario is the occurrence of venous thromboembolism (VTE) in cancer patients experiencing transient thrombocytopenia during myelosuppressive chemotherapy. In such patients, the severity of thrombocytopenia, thrombus burden, clinical symptoms, and the timing of VTE relative to thrombocytopenia must be considered. In clinical practice, distinct hematological disorders characterized by low platelet counts and a thrombogenic state require specific diagnostics and treatment. These include the antiphospholipid syndrome, heparin-induced thrombocytopenia (HIT) and (spontaneous) HIT syndromes, disseminated intravascular coagulation, and paroxysmal nocturnal hemoglobinuria.

Expert Report on Immune Thrombocytopenia: Current Diagnostics and Treatment – Recommendations from an Expert Group from Austria, Germany, and Switzerland

“…On the other hand, anticoagulants are usually contraindicated in thrombocytopenia. Therefore, Table 22 and Table 23 are based on the recommendations for oncology patients with thrombocytopenia who require anticoagulation [137,138].…”

Real-World Electronic Medical Records Data Identify Risk Factors for Myelofibrosis and Can Be Used to Validate Established Prognostic Scores

“…The data from the present study suggest that the risk of thrombosis increases with IPSS scores. Interestingly, both hemorrhage and thrombosis risks were higher for patients with thrombocytopenia, further suggesting an increase in platelet consumption due to disease-induced hemostatic dysregulation as a pathophysiological mechanism [30,38]. Further research is necessary to assess the pathophysiological mechanism explaining this divergence and to assess the drivers of thrombosis risk in myelofibrosis in order to identify patients potentially benefiting from antithrombotic prophylaxis.…”