In traumatic shock, soft tissue and bony injury leads to the activation of inflammatory cells and the release of cir- culating factors, such as cytokines and intracellular molecules that modulate the immune response. Recent investigations have revealed that the inflammatory mediators released in response to tissue injury (damage-associated molecular patterns [DAMPs]) are recognized by many of the same cellular receptors (pat- tern recognition receptors [PRRs]) and activate similar signal- ing pathways as do bacterial products elaborated in sepsis (pathogen-associated molecular patterns), such as lipopolysac- charide. 5 These effects of tissue injury are combined with the effects of hemorrhage, creating a more complex and amplified deviation from homeostasis.