Trauma: Damage recognition and response

Abstract

Introduction: Patient outcome after trauma is influenced by their immune response to injury. How trauma activates the immune system and why this affects recovery is unclear. This investigation examined three aspects of the immune response after trauma: cytokine production, alarmin release and the innate immune cell populations. Methodology: Timed blood samples were drawn from trauma patients recruited to a prospective observational cohort study at a London Major Trauma Centre. The first sample was drawn at admission, within 2h of injury and prior to intervention in order to capture early inflammation events. Patients were observed until death or discharge for clinical outcomes. Results: Inflammation after traumatic tissue damage can be described in isolation. If haemorrhagic shock is also present, the inflammatory effects cannot be separated using the seven cytokines examined in this investigation. Within 2h of injury, isolated tissue damage is associated with systemic release of intracellular nuclear molecules. Tissue damage combined with shock, is associated with release of different nuclear materials. Low numbers of lymphocytes at 48h from injury are associated with poor clinical outcome. Patients who develop infections and multiple organ dysfunction syndrome during recovery, have high numbers of cytotoxic lymphocytes in their peripheral blood at admission. Conclusion: Inflammation is activated prior to arrival at hospital. Haemorrhagic shock augments the inflammatory response after isolated tissue damage. Tissue damage and blood loss may lead to the release of different alarmin substances. Lymphocytes are implicated in the pathogenesis of poor outcome. The molecular events which lead to poor clinical outcome are activated before hospital admission and prior to intervention. Greater understanding of the activation mechanism(s) may result in development of therapeutics for early delivery, in order to improve patient recovery.