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 AIS ≥ 3 and admission GCS ≤ 8, no AIS ≥3 to any other bodily regions).
Patients and methods: After approval of this study from local ethical committee, and obtaining written informed consent from relatives, head trauma patients will be enrolled in this observational prospective study. study was conducted in the 10-bed trauma-surgical ICU in Sohag university hospital , Fifty patients with isolated TBI , were consecutively included between January 2015 and February 2017.
Results: our study validated cTnI as a novel biomarker and independent predictor of all cause in-hospital mortality in patients with TBI. these findings have several implications. First, cTnI assay should be considered in patients with sTBI even in absence high suspicion of cardiac injury. Second, cTnI is a sufficiently prognostic biomarker of mortality in patients with sTBI. Third, cTnI elevation in patients with sTBI must be treated with caution.
Conclusion: cTnI level was a significant indicator for stress cardiomyopathy , severity of trauma calculated by RTS had no relation with incidence of stress cardiomyopath . Our study provided important insights to the heart-brain interactions following TBI and possible schemes for subsequent optimization of management of these patients.