(1767) Effect of Propranolol on Hyperpyrexia in Patients With TBI and Paroxysmal Sympathetic Hyperactivity

Introduction:

Introduction: Patients with traumatic brain injury (TBI) may develop paroxysmal sympathetic hyperactivity (PSH), a syndrome manifesting as cyclic increases in heart rate (HR), blood pressure (MAP), respiratory rate, and temperature. Propranolol mitigates sympathetic symptoms associated with PSH, but few studies assess its effect on temperature. The primary objective of this study was to determine if propranolol attenuates hyperpyrexia secondary to PSH in patients with TBI.

Methods:

Methods: This retrospective study evaluated patients ≥16 years old, admitted to the trauma service, febrile (≥38.0°C), and initiated on propranolol. The primary outcome was any difference in intra-patient temperature before and after propranolol initiation, and other vitals including HR and MAP were evaluated secondarily. Vitals were collected 24 hr before (Day -1), on the day of (Day 0), and for 72 hr after (Days 1, 2, 3) propranolol initiation. Outcomes were evaluated using repeated measures ANOVA to identify any difference among days of therapy. Post-hoc Tukey’s tests for all significant variables identified any between-day differences if they existed.

Results:

Results: Fifty-nine patients were included. The majority were male (76.5%), experienced blunt trauma (78%), and had severe TBI with GCS ≤8 (78%). Average temperature (TAvg) was significantly different over the 5 days assessed (P=0.03) and trended downward by Day 3. Maximum temperature (TMax) also trended downward and approached significance (P=0.05). However, post-hoc Tukey’s tests failed to show any significant pairwise differences in TAvg and TMax on any day assessed. Maximum HR (P < 0.001) and average HR (P < 0.001) were also significantly different across Days -1 to 3, and demonstrated significantly lower values on Day 3 after propranolol initiation versus Day 0 (117.12.5 vs 131.52.4, P< 0.001 and 98.21.8 vs 107.21.9, P=0.01, respectively). Changes in MAP were not significant.

Conclusions:

Conclusion: While TAvg and TMax trended down after propranolol initiation, magnitude of change was small, and post-hoc analysis showed no significant between day differences. Propranolol expectedly lowered maximum and average HR by day 3 of therapy. Larger studies are needed to definitively characterize the effect of propranolol on vital signs in patients with PSH.