Patients with traumatic brain injury (TBI) may require some type of sedation during their stay in intensive care. The sedation and analgesia of the neurocritical patient represent a cornerstone for management. The administration of sedative agents in a protocolized way facilitates the management, acute treatment, and follow-up of patients with TBI1). In a young patient, pain and agitation are seen with moderate TBI. Severe TBI patients have other injuries, and most of these are intubated and have high intracranial pressure2).
In neurotrauma patients, each class has both good and negative consequences. There are few research on how the brain's metabolism acts on physiological thresholds. Neurocritical phycisions must use data judiciously3). Understanding the effects on brain metabolism and intracranial compliance should guide agent selection. The optimal drug boosts cerebral blood flow and volume, increases cerebral blood pressure, without lowering the mean arterial pressure4). Inhaled halogenates impair brain hemodynamics via vasodilation. Thus, intravenous sedatives are preferred5).
It is in this subsection of moderate TBI patients where adequate sedation and pain control will help to follow these patients with serial neurological examinations. In contrast to propofol6), dexmedetomidine is a tool to use to get cooperation from the patient for continued close neurological monitoring in intensive care7).
Dexmedetomidine is an alpha-2 adrenergic agonist used in intensive care practice for sedation. One of the pain control mechanisms at the central level is constituted by the activation of alpha-2-adrenergic receptors8). This class of receptors is located in the gelatinous substance of the human dorsal horn. This agent does not suppress ventilation, and its hemodynamic impact is less aggressive8) This is in contrast to Midazolam, which is used to achieve ventilator compliance and reduce the use of muscle relaxants9). The effect of dexmedetomidine is attained within 15 minutes (peak plasma concentration ≈ 1 hr)10). The combined effect of controlled ventilation, pain-controlling impact, and sedation will help with neurointensive care. A protocol can be used in neurointensive care for moderate TBI patients to have this agent available for the staff to use. The scores to help with initiation and titration include the Glasgow coma scale and the Richmond agitation and sedation scale11). We suggest that this should be a standard protocol in neurointensive care.
In conclusion, cooperative sedation is a useful approach for patients with moderate TBI presentation. Control of agitation and pain without masking ventilation and neurological examination is important. Dexmedetomidine is a safe agent to use. A protocolized approach is recommended.
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