Traumatic brain injury (TBI) is the leading cause of death and disability around the world. Every year, about 1.7 million people in the United States suffer head injuries, leading to 275,000 hospitalizations and 52,000 deaths (Curry, Viernes & Sharma, 2011). According to the Centres for Disease Control and Prevention (CDC) (2015), falls among children and elderly are the leading cause of TBI, accounting for 40% of all TBI in the United States, whereas young adult males in motor vehicle accidents and alcohol-related trauma comprise the second leading cause of TBI. Dinsmore (2013) mentions that the World Health Organization forecasted that TBI related to motor vehicle-traffic injury “will be the third greatest cause of disease and injury worldwide
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The primary brain injury is produced by an initial direct mechanical impact to the skull and brain tissue due to acceleration-deceleration forces, resulting in skull fractures and intracranial lesions (Curry, Viernes & Sharma, 2011). The intracranial lesions are the result of focal brain injury or diffuse brain injury. Focal brain damage is produced by contact injury resulting in contusion, laceration, intracranial hemorrhage and hematoma, whereas diffuse brain damage is produced by acceleration-deceleration injury resulting in diffuse axonal injury and brain swelling (Werner & Engelhard, 2007). The primary insult further progresses to an inflammatory process, brain edema, and bleeding leading to an increase in intracranial pressure (ICP) and decrease in cerebral perfusion pressure (CPP). The secondary brain injury is the consequence of further physiological damage to the brain that develops within minutes, hours, or days after the initial brain injury (Curry et al., 2011). Yao et al. (2012) offer some examples of the physiological processes that contribute to the secondary brain injury, such as alterations in the balance between cerebral blood flow and metabolism, disruption of cerebral autoregulation, loss of cerebral vascular reactivity to carbon dioxide, and cytotoxic vasogenic fluid accumulation. Cerebral ischemia, intracranial hypertension, hypoxemia, hypotension, hypercapnia or hypocapnia, hyperglycemia or hypoglycemia are all of the factors that increase the severity of the secondary insult to the brain (Dinsmore, 2013). Preventing and minimizing the effect of these secondary insults, especially hypoxemia and hypotension, is the cornerstone of TBI management. A single episode of intraoperative hypotension in the TBI patient has a three-fold increase in morbidity and mortality compared to a normotensive patient (Curry et al., 2011). Thus,
The primary brain injury is produced by an initial direct mechanical impact to the skull and brain tissue due to acceleration-deceleration forces, resulting in skull fractures and intracranial lesions (Curry, Viernes & Sharma, 2011). The intracranial lesions are the result of focal brain injury or diffuse brain injury. Focal brain damage is produced by contact injury resulting in contusion, laceration, intracranial hemorrhage and hematoma, whereas diffuse brain damage is produced by acceleration-deceleration injury resulting in diffuse axonal injury and brain swelling (Werner & Engelhard, 2007). The primary insult further progresses to an inflammatory process, brain edema, and bleeding leading to an increase in intracranial pressure (ICP) and decrease in cerebral perfusion pressure (CPP). The secondary brain injury is the consequence of further physiological damage to the brain that develops within minutes, hours, or days after the initial brain injury (Curry et al., 2011). Yao et al. (2012) offer some examples of the physiological processes that contribute to the secondary brain injury, such as alterations in the balance between cerebral blood flow and metabolism, disruption of cerebral autoregulation, loss of cerebral vascular reactivity to carbon dioxide, and cytotoxic vasogenic fluid accumulation. Cerebral ischemia, intracranial hypertension, hypoxemia, hypotension, hypercapnia or hypocapnia, hyperglycemia or hypoglycemia are all of the factors that increase the severity of the secondary insult to the brain (Dinsmore, 2013). Preventing and minimizing the effect of these secondary insults, especially hypoxemia and hypotension, is the cornerstone of TBI management. A single episode of intraoperative hypotension in the TBI patient has a three-fold increase in morbidity and mortality compared to a normotensive patient (Curry et al., 2011). Thus,