V. E. Polcz1, E. L. Barrios1, M. C. Cox1, M. Alves1, I. L. Rocha1, M. Liang2, E. C. Navarro1, G. Ghita2, R. B. Hawkins1, D. Darden1, J. C. Rincon1, R. Ungaro1, M. L. Dirain1, S. D. Larson1, R. T. Mankowski3, A. M. Mohr1, F. A. Moore1, P. A. Efron1, L. L. Moldawer1, S. C. Brakenridge4, T. J. Loftus1 1University of Florida, Surgery, Gainesville, FLORIDA, USA 2University of Florida, Biostatistics, Gainesville, FLORIDA, USA 3University of Florida, Physiology And Aging, Gainesville, FLORIDA, USA 4University of Washington, Surgery, Seattle, WA, USA
Introduction: Sarcopenia is a known risk factor for adverse outcomes across multiple disease states, including severe trauma. Factors such as age, hyper-inflammation, prolonged immobilization, and critical illness may not only exacerbate progression of this disease but also contribute to the development of “acute sarcopenia”. Our study explores the effects of severe traumatic injury on changes in skeletal muscle mass in older patients, its functional implications on clinical frailty, physical performance, and health-related quality of life (HRQOL), and associations between sarcopenia and clinical and functional outcomes.
Methods: We conducted a prospective, longitudinal cohort study of critically ill, older (≥45 years) patients presenting after severe blunt trauma utilizing abdominal CT on admission to determine baseline skeletal muscle index (SMI). Serial measures of frailty and HRQOL were obtained in addition to serum biomarker levels (IL-6, IL-8, IL-10, TNFα, irisin, myostatin/GDF8, osteonectin) and interval CT imaging (3 and 6 months post-injury) to assess changes in SMI post-injury. Outcomes included hospital length of stay (LOS), development of chronic critical illness (CCI), unfavorable discharge disposition, 180-day readmissions and mortality, and changes in clinical frailty (as measured by Rockwood Clinical Frailty Score), HRQOL and performance measures.
Results: Among 47 patients enrolled, 17 (36%) had baseline sarcopenia. Severe injury was associated with significant decreases in SMI over time, and increased incidence of acute sarcopenia (baseline: 36%, 3 months: 63%, 6 months: 60%, p<0.05). Severe trauma was also associated with an increase in frailty and worse HRQOL, with a return to baseline by six months post-injury. Distinct temporal alterations in the myokine/chemokine profile were noted, irrespective of pre-existing or acute sarcopenia. Early IL-10 levels were the only biomarker lower in patients with acute sarcopenia (p<0.05), and acute sarcopenia was also associated with smaller changes in IL-10 over six months (p<0.05). Both early and two-week IL-10 concentrations were associated with persistent clinical frailty at six months (p<0.05). Multivariate analysis revealed several low magnitude, but significant correlations between remaining myokine/chemokine levels at day 14 and six-month change in SMI.
Conclusion: Severe blunt trauma is associated with distinct temporal changes in myokine and chemokine levels, induced frailty, and development of acute sarcopenia in older patients. A better understanding of early proteomic responses after severe trauma is essential to allow for more accurate prognostication and targeted intervention for patients at increased risk for adverse functional outcomes.
