![]() Several studies have evaluated the prevalence of VTE in SCD patients and provide some insight into the burden of this complication in adult SCD patients. ![]() However, VTE affects nearly one-quarter of adult patients and appears to be a risk factor for death in SCD therefore, management by anticoagulation experts is an essential part of care for the SCD population. In addition, risk of VTE in SCD patients is influenced by factors outside the disease itself such as hospitalization and catheter use. Thrombotic complications such as stroke in pediatric SCD patients have been more robustly characterized, in part, because VTE is primarily a complication of adults and has only been recently recognized with advances in therapies and increased survival of SCD patients. ĭespite the known association between hypercoagulability and SCD, venous thromboembolism (VTE) is often overlooked as a major complication of SCD. In fact, every aspect of Virchow’s triad-increased coagulability, endothelial dysfunction, and impaired blood flow-is present in patients with SCD and results in a highly thrombogenic environment. In addition, vaso-occlusion of sickled RBCs contributes to decreased blood flow and local vascular ischemic injury. Circulating free hemoglobin in the setting of hemolysis also causes nitric oxide depletion, which leads to chronic vasoconstriction and platelet activation. ![]() These perturbations are partly due to alterations in sickled RBC structure leading to intravascular hemolysis and externalization of highly procoagulant phosphatidylserines on the RBC membrane. The mechanisms of hypercoagulability in SCD are vast, including enhanced platelet function, activation of the coagulation cascade, and impaired fibrinolysis. While historically the pathophysiology of the clinical complications of SCD was attributed solely to direct entrapment of deformed RBCs in the microcirculation, it is now recognized that various complex mechanisms, and importantly hypercoagulability, contribute considerably to disease pathology. Sickle cell disease (SCD) is an inherited disorder resulting in the production of abnormal hemoglobin (hgb S) that polymerizes in hypoxic conditions to form sickle-shaped red blood cells (RBCs).
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