Sepsis remains a leading cause of critical illness with substantial mortality, and sepsis-associated thrombocytopenia (SAT) markedly elevates the risk of death and signals poor prognosis. Although platelets are central to the inflammation–coagulation–immunity axis, the literature has predominantly focused on platelet counts rather than functional heterogeneity or regulatory mechanisms, which constrains biomarker discovery and targeted therapy development.
This assessment highlights the dual roles of platelets in sepsis: they serve in host defense by recognizing pathogens via pattern recognition receptors and contributing to anti-infective responses; conversely, excessive platelet activation can drive endothelial injury and microvascular thrombus formation through multiple signaling pathways and mediator release. The synthesis emphasizes the need to integrate platelet quantity with functional phenotypes and regulatory mechanisms to better characterize sepsis pathophysiology.
Where data are provided, platelets’ quantitative and qualitative aspects are linked to outcomes, suggesting potential avenues for diagnostics and precision approaches. If any aspects remain uncertain in the source, acknowledge these gaps briefly to avoid overinterpretation.
Overall, the framework connects platelet numbers, function, and mechanism to inform future diagnostic and targeted treatment strategies in sepsis.