J. Murry1, D. Hoang1, G. Barmparas1, D. Lee1, M. Bukur1, M. Bloom1, K. Inaba1, D. Margulies1, A. Salim1, E. J. Ley1 1Cedars-Sinai Medical Center,Los Angeles, CA, USA
Introduction: Beta adrenergic receptor blockade may improve outcomes after traumatic brain injury (TBI) by modulating the subsequent cascade of immune and inflammatory changes, but its early use is not routine in part due to concern for bradycardia and hypotension. We hypothesize that judicious early propranolol after TBI (EPAT) does not alter bradycardia and hypotensive events.
Methods: We conducted a prospective, observational study on all patients who presented with moderate to severe TBI from March 2010 to August 2013. The first 10 patients enrolled did not receive propranolol at SICU admission (CONTROL). Subsequent patients received propranolol at 1mg IV every 6 hours starting within 12 hours of SICU admission (EPAT) for a minimum of 48 hours. Propranolol was held for heart rate <60bpm (bradycardia), blood pressure <90mmHg (hypotension), SICU transfer, or patient deterioration. Bradycardia and hypotensive events were recorded hourly for the first 72 hours after SICU admission.
Results: Thirty-eight patients met enrollment criteria; 10 CONTROL and 28 EPAT. EPAT patients received 6.6±3.9 (mean±sd) doses of propranolol. The two cohorts were similar when compared by age>65 years, male gender, ED SBP< 90mmhg, head AIS≥4, ISS≥16 and hospital mortality (table). ED GCS≤8 was higher in CONTROL (100% v. 35.7%, p<0.01). Mean number of hypotensive events per patient, mean heart rate per bradycardia event, and mean blood pressure per hypotensive event were similar. The mean number of bradycardia events per patient was higher in CONTROL (mean 5.8 v. 1.6, p = 0.047).
Conclusion: While bradycardia and hypotensive events occur early after TBI, low dose intravenous propranolol does not increase their number or severity. Early use of propranolol after TBI appears to be safe. Additional enrollment continues to determine if EPAT improves outcomes.
