Association between systemic immune-inflammation index dynamics and time to pressure injury onset in intensive care units: A retrospective cohort study

Pressure injuries constitute a significant burden in intensive care units due to increased morbidity and healthcare costs. Since systemic inflammation is a key driver of tissue breakdown, this study evaluated the association of dynamic changes in the neutrophil-to-lymphocyte ratio, systemic immune-inflammation index, and platelet-to-lymphocyte ratio with the onset of pressure injuries in individuals with severe acute conditions. This retrospective observational analysis was carried out across the critical care departments of a regional referral center between January 2023 and June 2024. The analytical cohort was restricted solely to 51 adult critical care patients who acquired pressure injuries during their hospitalization. Baseline clinical profiles, including comorbid conditions and hematological data, were documented. The inflammatory indices were computed both upon critical care entry and concurrently with injury identification. Furthermore, the magnitude of biomarker reduction (admission-to-onset fold-decrease) was analyzed for potential correlations with the precise timeline of pressure injury formation. The analytical cohort comprised 52.9% females with an average age of 77.6 ± 9.1 years. Pressure injuries emerged, on average, at 19.4 ± 13.0 days after intensive care admission. Longitudinal tracking revealed a pronounced reduction in median inflammatory index values (all p < 0.001). Markedly, the proportional declines in the neutrophil-to-lymphocyte ratio and systemic immune-inflammation index demonstrated a strong positive correlation with the precise onset interval of pressure injuries (p = 0.011 and p = 0.047, respectively); however, this statistical link was absent for the platelet-to-lymphocyte ratio (p = 0.549). Dynamic decreases in neutrophil-to-lymphocyte ratio and systemic immune-inflammation index were associated with a longer time to pressure injury onset, suggesting that sustained systemic inflammation may accelerate tissue breakdown. Given the absence of a non-injury comparator group, these findings specifically reflect associations with the timing of onset rather than the absolute risk of occurrence. These markers may serve as useful indicators for monitoring the inflammatory trajectory in patients prone to pressure injuries.