Accelerated Biologic Aging, Chronic Stress, and Risk for Sepsis and Organ Failure Following Trauma

Chronic stress and accelerated aging have been shown to impact the inflammatory response and related outcomes like sepsis and organ failure, but data are lacking in the trauma literature. The purpose of this study was to investigate potential relationships between pretrauma stress and posttrauma outcomes. The hypothesis was that pretrauma chronic stress accelerates aging, which increases susceptibility to posttrauma sepsis and organ failure. In this prospective, correlational study, chronic stress and accelerated biologic aging were compared to the occurrence of systemic inflammatory response syndrome, sepsis, and organ failure in trauma patients aged 18-44 years. Results supported the hypothesis with significant overall associations between susceptibility to sepsis and accelerated biologic aging (n = 142). There were also significant negative associations between mean cytokine levels and chronic stress. The strongest association was found between mean interleukin-1β (IL-1β) and human telomerase reverse transcriptase (hTERT), r(101) = -0.28), p =.004. Significant negative associations were found between mean cytokine levels, IL-12p70, r(108) = -0.20, p =.034; and tumor necrosis factor- (TNF-), r(108) = -0.20, p =.033, and positive life events via the behavioral measure of chronic stress. Results may help identify individuals at increased risk for poor outcomes of trauma and inform interventions that may reduce the risk for sepsis and organ failure.