Adrenergic Suppression Modalities in Acute Traumatic Brain Injury

The relationship between catecholamine surge and acute traumatic brain injury (TBI) has been shown in the literature.[1] [2] [3] [4] The catecholamines released during acute TBI lead to a higher metabolic rate, increased systemic blood pressure blood flow, and hyperemia in the brain. The brain autoregulation is linear due to TBI,[5] this leads to uncontrolled perfusion and hence cerebral edema. Also, this pathophysiological process is directly related to a significant and potentially life-threatening increase in intracranial pressure (ICP). In patients with TBI, multiple pharmacological tools are used to prevent and treat high ICP. These include nonselective beta-blockers for suppression of hypertensive response, beta-blockers to suppress adrenergic surge, hypertonic saline, osmotic diuresis with mannitol, and sedative agents including midazolam, lorazepam, propofol, pentobarbital, and inhaled anesthesia. In the more extreme cases, an induced coma is introduced with pentobarbital or inhaled anesthesia. This is to decrease cerebral metabolic rate and sometimes even to the point of complete loss of brain activity.