Platelet phenotype and function in the absence of splenic sequestration (Review)

The spleen, in addition to its role in immunity, plays key roles in erythrocyte maintenance and platelet sequestration. Loss of the spleen via splenectomy occurs in approximately 6.4 to 7.1 per 100 000 people per year globally, commonly as a life-saving emergency procedure in trauma and a therapeutic procedure in hematological and hematological malignant conditions. It is associated with increased risk of life-threatening infection and thromboembolism, presumably via loss of splenic function, but the underlying mechanisms behind post-splenectomy thromboembolism are unclear. The splenectomized individual has a two-fold risk of thromboembolism as compared to non-splenectomized individuals and the risk of thromboembolism is elevated both post-operatively and in the longer term. Although those splenectomized for hematological conditions or hematological malignant conditions are at highest risk for thromboembolism, an increase in thromboembolic outcomes is also observed amongst individuals splenectomized for trauma, suggesting underlying disease state is only a partial factor. Although the physiological role of the splenic platelet pool on platelets is unclear, platelet changes after splenectomy suggest that the spleen may play a role in maintaining platelet quality and function. In hypersplenic conditions, sequestration can increase to sequester up to 72% of the total platelet mass. Following splenectomy, a thrombocytosis is commonly seen secondary to the loss of the ability to sequester platelets. Abnormal platelet quality and function have been observed as a consequence of splenectomy. These platelet defects seen after splenectomy may likely contribute to the increase in post-splenectomy thromboembolism. Here we draw upon the literature to characterize the post-splenectomy platelet and its potential role in post-splenectomy thromboembolism.