Use of beta blocker in severely head injured patients receiving mechanical ventilation in trauma intensive care: A prospective randomized double-blind study

Traumatic brain injury (TBI) is defined as functional brain disturbance or pathological sign of blunt or severe head injury. Neurological dysfunction following TBI depends on the extent and volume of tissue injury. This depends on the primary brain injury, which results from mechanical trauma at the time of initial insult, and secondary brain injury, which refers to the further tissue and cellular damage evolving over a period of time (from hours to days) following the initial primary insult.  Catecholamine surge that occurs following TBI is one of the reasons of secondary brain injury as its levels increase in proportion to the severity of TBI. This increase in catecholamines has a significant impact on long-term outcomes, both on morbidity and mortality. The systemic consequences of elevated catecholamine levels following both generalized trauma and traumatic/non-traumatic brain injury have been documented concerning the cardiac, pulmonary, endocrine, and immune systems, though their effects on the brain remain less well-understood. Propranolol is among the frequently employed beta blockers in this context as it is hypothesized that the neuroprotective benefits of propranolol results from enhanced cerebral perfusion pressures, reduced cerebral hypoxia, and the decreased catabolism and oxygen consumption during adrenergic crisis. We have thus planned this study with the aim of evaluating the effect of beta blocker therapy on cerebral hemodynamics following TBI using transcranial doppler. We hypothesize that improved function outcome seen following beta-blockers in patients with severe TBI is due to improved cerebral perfusion pressure by reduced action of catecholamine.