Using propranolol in traumatic brain injury to reduce sympathetic storm phenomenon: A prospective randomized clinical trial.

Background: Traumatic brain injury (TBI) correlated with increased sympathetic activity on the expense of parasympathetic system due to loss of cortical control after brain injury. Manifestations of sympathetic storm include tachycardia, hypertension, tachypnea, and hyperthermia. The neuroprotective effects via reducing cerebral metabolism and lowering O and glucose consumption are the targets early after trauma. Beta-blockers reduce sympathetic activity.

Objectives: We suppose that using propranolol blunts the sympathetic storming phenomenon as it is a nonselective β inhibitor and has a lipophilic property to steadily penetrate blood-brain barrier.

Patients And Methods: Sixty patients allocated randomly into two groups, each consisting of 30 patients. Group A started propranolol and Group B received placebo within first 24 h. Primary outcome was catecholamine levels on day 7, and the secondary outcomes were physiological measures (heart rate [HR], respiratory rate [RR], mean arterial blood pressure [MABP], temperature, random blood sugar, and follow-up Glasgow coma score [GCS] and sedation score).

Results: Analysis of outcomes demonstrated that Group A tended to have lower catecholamine levels in comparison to Group B in day 7 (norepinephrine 206.87 ± 44.44 vs. 529.33 ± 42.99 pg/ml, = <0.001), epinephrine level (69.00 ± 8.66 vs. 190.73 ± 16.48 pg/ml, < 0.001), and dopamine level (32.90 ± 4.57 vs. 78.00 ± 3.48 pg/ml < 0.001). GCS of the patients in Group A improved and was statistically significant compared to Group B in day 7 (13 vs. 10, = 0.006), with percent change interquartile range (20.0 vs. 8.33, = 0.006). Regarding hemodynamic parameters between the two groups MABP, HR, RR, and temperature, there was no statistically significant difference on day 1, while on day 7, there is high statistical significance and significant percent change ( < 0.001).

Conclusion: Early usage of propranolol after TBI controls hemodynamics and blood sugar with decreased catecholamine levels correlated with the improvement of GCS.