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INTRODUCTION AND EPIDEMIOLOGY
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Traumatic brain injury is brain function impairment that results from external force.1 The clinical manifestations represent a broad constellation of symptoms from brief confusion to coma, severe disability, and/or death. The underlying pathology ranges from temporary shifts in cellular ionic concentrations to permanent structural damage.
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Traumatic brain injury (TBI) is classified as mild, moderate, and severe based on the Glasgow Coma Scale (GCS) score. Over 80% of TBI is defined as mild (GCS 14 to 15) (mTBI) and is often called "concussion."2 The label of mild, however, is a misnomer. mTBI may lead to significant, debilitating short- and long-term sequelae. Moderate TBI (GCS 9 to 13) accounts for approximately 10% of head injuries. Mortality rates for patients with isolated moderate TBI are <20%, but long-term disability can be higher. Overall, 40% of patients with moderate TBI have an abnormal finding on CT scan, and 8% will require neurosurgical intervention. In severe TBI (GCS 3 to 8), mortality rate approaches 40%, with most deaths occurring in the first 48 hours after injury. Fewer than 10% of patients with severe TBI experience good recovery.2,3
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The prevalence of TBI is twice as high in males as in females. Distribution of age at injury is trimodal, with peaks at 0 to 4 years, 15 to 24 years, and >75 years of age. Mortality rate increases with age at time of injury.4,5 Motor vehicle collisions are the primary cause of blunt head injury in young adults and children, and falls are more common in the elderly.2 TBI has been called the "signature injury" of the conflicts in Iraq and Afghanistan.6
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Autoregulation, cerebral perfusion pressure (CPP), mean arterial pressure (MAP), and intracranial pressure (ICP) are interrelated factors that affect cerebral blood flow (Table 257–1). Under normal circumstances, autoregulation regulates local cerebral blood flow to maintain equilibrium between oxygen delivery and metabolism.7 Other systemic factors, such as hypertension, hypocarbia, and alkalosis, can affect cerebral blood flow by causing vasoconstriction.
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Under normal situations, autoregulation can adjust to CPPs from 50 to 150 mm Hg to maintain local cellular oxygen demands and regional cerebral blood flow. In brain injury, autoregulation is often impaired, so even modest drops in blood pressure can decrease brain perfusion and result in cellular hypoxia. A CPP <60 mm Hg is considered the lower limit of autoregulation in ...