Stephen S Cai1, Brandon W Bonds, Peter F Hu, Deborah M Stein. 1. From the R Adams Cowley Shock Trauma Center (B.W.B., P.F.H., D.M.S.), Baltimore, Maryland; and University of Maryland School of Medicine (S.S.C., P.F.H., D.M.S.), Baltimore, Maryland.
Abstract
BACKGROUND: Cardiac dysfunction is frequently observed after severe traumatic brain injury (sTBI); however, its significance is poorly understood. Our study sought to elucidate the association of cardiac troponin I (cTnI) elevation with all-cause in-hospital mortality following isolated sTBI (brain Abbreviated Injury Scale score ≥3 and admission Glasgow Coma Scale score ≤8, no Abbreviated Injury Scale score ≥3 to any other bodily regions). METHODS: We retrospectively reviewed all adult patients (aged ≥18 years) with isolated sTBI admitted to a Level I trauma center between June 2007 and January 2014. Patients must have cTnI values within 24 hours of admission. Mortality risks were examined by Cox proportional hazard model. RESULTS: Of 580 patients identified, 30.9% had detectable cTnI in 24 hours of admission. The median survival time was 4.19 days (interquartile range, 1.27-11.69). When adjusted for potential confounders, patients in the highest cTnI category (≥0.21 ng/mL) had a significantly higher risk of in-hospital mortality (hazard ratio, 1.39; 95% confidence interval, 1.04-1.88) compared with patients with undetectable cTnI. Mortality risk increased with higher troponin levels (p < 0.0001). This association was more pronounced in patients aged 65 years or younger (hazard ratio, 2.28; 95% confidence interval, 1.53-3.40; p < 0.0001) while, interestingly, insignificant in those older than 65 years (p = 0.0826). CONCLUSION: Among patients with sTBI, cTnI elevation is associated with all-cause in-hospital mortality via a nonlinear positive trend. Age modified the effect of cTnI on mortality. LEVEL OF EVIDENCE: Prognostic and epidemiologic study, level III.
BACKGROUND:Cardiac dysfunction is frequently observed after severe traumatic brain injury (sTBI); however, its significance is poorly understood. Our study sought to elucidate the association of cardiac troponin I (cTnI) elevation with all-cause in-hospital mortality following isolated sTBI (brain Abbreviated Injury Scale score ≥3 and admission Glasgow Coma Scale score ≤8, no Abbreviated Injury Scale score ≥3 to any other bodily regions). METHODS: We retrospectively reviewed all adult patients (aged ≥18 years) with isolated sTBI admitted to a Level I trauma center between June 2007 and January 2014. Patients must have cTnI values within 24 hours of admission. Mortality risks were examined by Cox proportional hazard model. RESULTS: Of 580 patients identified, 30.9% had detectable cTnI in 24 hours of admission. The median survival time was 4.19 days (interquartile range, 1.27-11.69). When adjusted for potential confounders, patients in the highest cTnI category (≥0.21 ng/mL) had a significantly higher risk of in-hospital mortality (hazard ratio, 1.39; 95% confidence interval, 1.04-1.88) compared with patients with undetectable cTnI. Mortality risk increased with higher troponin levels (p < 0.0001). This association was more pronounced in patients aged 65 years or younger (hazard ratio, 2.28; 95% confidence interval, 1.53-3.40; p < 0.0001) while, interestingly, insignificant in those older than 65 years (p = 0.0826). CONCLUSION: Among patients with sTBI, cTnI elevation is associated with all-cause in-hospital mortality via a nonlinear positive trend. Age modified the effect of cTnI on mortality. LEVEL OF EVIDENCE: Prognostic and epidemiologic study, level III.
Authors: Anne C Mosenthal; Robert F Lavery; Michael Addis; Sanjeev Kaul; Steven Ross; Robert Marburger; Edwin A Deitch; David H Livingston Journal: J Trauma Date: 2002-05
Authors: Bryan A Cotton; Kimberly B Snodgrass; Sloan B Fleming; Robert O Carpenter; Clinton D Kemp; Patrick G Arbogast; John A Morris Journal: J Trauma Date: 2007-01