Background: Inflammatory responses to trauma, especially if exaggerated, drive mortality and morbidities including infectious complications. Geriatric patients are particularly susceptible to profound inflammation. Age-related declines in inflammatory and immune systems are known to occur. Geriatric patients display dampened inflammatory responses to non-critical disease processes. Specific inflammatory responses in critically ill geriatric trauma patients, and how the inflammatory profile associated with subsequent infections or mortality, remain unknown.

Methods: Geriatric (≥65 y) and young (18-50 y old) critically ill blunt trauma intensive care unit (ICU) patients were enrolled prospectively. Blood was drawn within 36 h of presentation to measure circulating cytokines including interleukin (IL)-6 (pg/mL), IL-10 (pg/mL), and tumor necrosis factor (TNF)-α (pg/mL) levels. Age, gender, Acute Physiology and Chronic Health Evaluation (APACHE II) score and outcomes were reviewed.

Results: Twenty-one young and 29 geriatric critically ill patients were recruited. Groups were comparable in male gender and age-adjusted APACHE II score, but geriatric patients had higher mortality (38% versus 9.5%; p=0.04). Within geriatric trauma patients, the development of a secondary infection was associated with significantly lower presenting IL-6 and IL-10 levels and no difference in TNF-α levels. Furthermore, geriatric patients who died had elevated IL-6 and IL-10 and decreased TNF-α levels compared with geriatric patients who lived. Compared with the young cohort, IL-6 and IL-10 levels were similar between geriatric patients who died and young patients who lived. However, geriatric patients who lived, compared with young patients who lived, had significantly lower IL-6 and IL-10. There was no such relation noted with TNF-α.

Conclusions: A lowered inflammatory response in geriatric patients is associated with the development of a subsequent infection. However, geriatric patients exhibiting inflammatory responses as robust as their younger counterparts have increased mortality. Redefining our understanding of an appropriate geriatric inflammatory response to trauma will help future therapy, thereby improving morbidity and mortality.