SEVERE DEPRESSION OF HOST IMMUNE FUNCTIONS FOLLOWING CLOSED-BONE FRACTURE, SOFT-TISSUE TRAUMA, AND HEMORRHAGIC-SHOCK

Objective: To determine the contribution of soft-tissue trauma plus he morrhage, bone fracture and hemorrhage, as well as the contribution of bone fracture, soft-tissue trauma and hemorrhage on host immune funct ion. Subjects: Adult male mice (n = 6/group). Design: Prospective, ran domized, controlled study. Setting: Animal laboratory at a university- affiliate hospital. Interventions: Closed-bone fracture (right lower l eg; external fixation) and/or soft-tissue trauma (2.5-cm midline lapar otomy, closed in two layers) were induced before hemorrhagic shock (me an arterial blood pressure of 35 +/- 5 (SEM) mm Hg for 90 mins, follow ed by fluid resuscitation) in male C3H/HeN mice and the animals were k illed at 72 hrs after initiation of the experiment. Measurements and M ain Results: Splenocyte interleukin (IL)-2 and IL-3 release capacity, as well as splenic and peritoneal macrophage IL-l and IL-6 release cap acity were determined. Different traumatic insults, i.e., bone fractur e or soft-tissue trauma in conjunction with hemorrhage, produced compa rable immune depression. More significant depression of splenocyte IL- 2 and IL-3 release capacity as well as macrophage IL-l and IL-6 releas e capacity occurred with the combined insult (i.e., bone fracture/soft -tissue injury and hemorrhage) than after bone injury or tissue trauma alone with hemorrhage. Conclusions: The combination of closed-bone fr acture and soft-tissue trauma before hemorrhage leads to even more com promised immunity than either soft-tissue trauma or closed-bone fractu re along with hemorrhage. The markedly depressed immune function follo wing bone injury, soft-tissue trauma, and hemorrhagic shock may contri bute to the increased susceptibility of severely injured patients to s epsis and the ensuing multiple organ failure in the clinical situation .