Key result
Early cardiac troponin I elevation in severe TBI is linked to ~39% higher in-hospital mortality.
Why the study?
Does elevated cardiac troponin I predict all-cause in-hospital mortality in adult patients with isolated severe traumatic brain injury?
Cohort (n=580)
No
Does elevated cardiac troponin I predict all-cause in-hospital mortality in adult patients with isolated severe traumatic brain injury?
Effect estimate: HR 1.39 (95% CI 1.04-1.88)
p-value: p=<0.0001
Elevated cardiac troponin I within 24 hours of admission is associated with increased all-cause in-hospital mortality in patients with isolated severe traumatic brain injury, particularly in those aged 65 years or younger.
May aid early risk stratification in isolated severe TBI; leaves open prospective validation before changing practice.
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.
No takes yet. Share an insight, caveat, or question.
Cai et al. (2015) conducted a cohort in isolated severe traumatic brain injury (n=580). Cardiac troponin I (cTnI) elevation (≥0.21 ng/mL) vs. Undetectable cTnI was evaluated on All-cause in-hospital mortality (HR 1.39, 95% CI 1.04-1.88, p=<0.0001). Cardiac troponin I elevation ≥0.21 ng/mL within 24 hours of admission for isolated severe traumatic brain injury was associated with increased in-hospital mortality (HR 1.39; 95% CI 1.04-1.88).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: