The systemic inflammatory response syndrome (SIRS) after severe injury can lead to distant organ injury, multi-organ failure, and complications during recovery. Post-injury SIRS is driven by the activation of innate immune cells and release of pro-inflammatory cytokines that drives this inflammation response. In addition, the coagulation cascade and complement system is altered, resulting in a widespread inflammatory response. Importantly, these different components of SIRS are interrelated and propagate further alterations in thrombosis and inflammation. Efforts to mitigate the acute changes in coagulation and inflammation and its complex interactions following injury could provide novel strategies for resuscitation and management of complications of trauma-induced coagulopathy, SIRS, and multiple organ failure. In this review, we review the pathophysiology of post-traumatic SIRS and highlight current approaches to mitigate innate immune cell activation, thromboinflammation, and associated clinical complications.
Level of Evidence
IV, Review article