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.

The adrenergic stimulation during TBI causes inhibition of thick lymphatic removal of cellular debris and toxins, thus worsening cellular injury and cerebral edema (Hussain). In addition to this adrenergic suppression may then improve the glim flattish drainage and removal of these toxins from the brain, thus reducing injury and cellular damage. This indirectly impacts high ICP ([Fig. 1]).

Beta-blocker therapy in acute TBI can decrease the physiological effects of the hyperadrenergic state. This effect should be in context with maintained cardiac index and hence continue stable cerebral perfusion. Sedated agents with a central effect like propofol, dexmedetomidine, and benzodiazepines can reduce systemic hypertensive response with reduced adrenergic outflow. Pentobarbital interferes with the impact of plasma catecholamines on physiological factors.[6] [7] The increased sympathetic outflow and surge after TBI is abutted which can impact TBI outcome. This adrenergic inhibition has been shown to improve ICP by interfering with the sympathetic surge that occurs after TBI. A single dose of pentobarbital in patients who present with low Glasgow Coma Scale and TBI with evidence of hyperemia and swelling on the initial computed tomography scan seems to break the cycle of the sympathetic surge. This effect of pentobarbital has a multipronged effect by interfering with the sympathetic outflow cascade.

The development of a hyperadrenergic state in patients with TBI is a major pathophysiological process.[8] [9] This elevation of blood levels of catecholamines and the action of adrenergic lead to pathophysiological changes including tachycardia, hypertension, tachypnea, hyperemia, peripheral vasoconstriction, rise in lactic acid, hypercarbia, hypoxemia, increased ICP, and agitation. The elevation of catecholamines is associated with a hypermetabolic state, hence reduced outcomes. Proper use of therapeutic modalities including beta-blockers, propofol, dexmedetomidine, and pentobarbital will impact ICP and TBI outcomes. Further studies are required where this impact is confirmed with cardiopulmonary dynamics monitoring.

Article published online:
04 June 2024

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