Platelets in Hemostasis, Thrombosis, and Inflammation After Major Trauma

Abstract

Trauma currently accounts for 10% of the total global burden of disease and over 5 million deaths per year, making it a leading cause of morbidity and mortality worldwide. Although recent advances in early resuscitation have improved early survival from critical injury, the mortality rate in patients with major hemorrhage approaches 50% even in mature trauma systems. A major determinant of clinical outcomes from a major injury is a complex, dynamic hemostatic landscape. Critically injured patients frequently present to the emergency department with an acute traumatic coagulopathy that increases mortality from bleeding, yet, within 48 to 72 hours after injury will switch from a hypocoagulable to a hypercoagulable state with increased risk of venous thromboembolism and multiple organ dysfunction. This review will focus on the role of platelets in these processes. As effectors of hemostasis and thrombosis, they are central to each phase of recovery from injury, and our understanding of postinjury platelet biology has dramatically advanced over the past decade. This review describes our current knowledge of the changes in platelet behavior that occur following major trauma, the mechanisms by which these changes develop, and the implications for clinical outcomes. Importantly, supported by research in other disease settings, this review also reflects the emerging role of thromboinflammation in trauma including cross talk between platelets, innate immune cells, and coagulation. We also address the unresolved questions and significant knowledge gaps that remain, and finally highlight areas that with the further study will help deliver further improvements in trauma care.

Prognostic value of the systemic immune-inflammation index in critically ill elderly patients with hip fracture: evidence from MIMIC (2008–2019)

“…The underlying mechanisms likely include a sequence of inflammatory cytokines and chemokines, which stem from the dysfunction of lymphocytes within the immune reaction, resulting in the accumulation of neutrophils and macrophages ( 40 , 41 ). Also, injury, infection, or ischemia can trigger a defensive inflammatory response, leading to an increase in platelets ( 42 ). The nature of reduced physiological reserve in elderly patients makes them more vulnerable to post-injury release of aggressive cytokines (TNF-a, IL-6, and IL-1β, etc.…”