TABLE 2.

The Systemic Inflammatory Response to Injury: What You Need to Know

Key Points: • The host response to injury results in a widespread and interrelated SIRS. • SIRS includes activation of innate and adaptive immune cells, cellular and noncellular coagulation cascades, and complement systems. • There is a simultaneous increase in genes related to innate immunity and suppression of genes related to adaptive immunity within 12 hours of injury. • Inflammatory mediators activate coagulation by promoting the expression of TF on endothelial cells and monocytes and alters the normal ratio of procoagulation and anticoagulation effects. • SIRS leads to endothelial cell, platelet, and leukocyte activation that result in appropriate and inappropriate thrombus formation, thrombolysis, and exhaustion of clotting cycle components. • Fibrinogen and fibrin play multifaceted roles influencing both thrombosis and inflammation, with effects that extend beyond serving as a passive substrate for clot formation by activating immune cells and promoting leukocyte adhesion and migration. • Early increases in activated protein C levels after injury increase coagulopathy, decrease clot strength, and increase fibrinolysis. • Endothelial dysfunction after injury is associated with shedding of the proteoglycan layer and loss of barrier function and promotes thrombus formation. • Activation of the complement system promotes inflammation by recruiting immune cells and enhancing vascular permeability and interacts with the coagulation system to contribute to coagulopathy.