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KEY CONCEPTS

KEY CONCEPTS

  • Image not available. Cerebral ischemia is the key pathophysiologic event triggering secondary neuronal injury following severe traumatic brain injury (TBI). Intracellular accumulation of calcium is postulated to be a central pathophysiologic process in amplifying and perpetuating secondary neuronal injury via inhibition of cellular respiration and enzyme activation.

  • Image not available. Guidelines for the Management of Severe Brain Injury, published by the Brain Trauma Foundation (BTF)/American Association of Neurological Surgeons (AANS), serve as the foundation on which clinical decisions in managing adult neurotrauma patients are based; comparable guidelines for infants, children, and adolescents have also been published.

  • Image not available. Correcting and preventing early hypotension (systolic blood pressure [SBP] less than 90 mm Hg) and hypoxemia (PaO2 less than 60 mm Hg [8.0 kPa]) are primary goals during the initial resuscitative and intensive care of severe TBI patients.

  • Image not available. Nonpharmacologic treatment in the management of intracranial hypertension includes raising the head of the bed 30°, short-term mild hyperventilation (PaCO2 30-35 mm Hg [4.0-4.7 kPa]), ventricular drainage if a ventriculostomy is present, and decompressive surgery.

  • Image not available. The principal monitoring parameter for severe TBI patients within the intensive care environment is intracranial pressure (ICP). Cerebral perfusion pressure (CPP) is also a critical monitoring parameter and should be maintained between 50 and 70 mm Hg (6.7 and 9.3 kPa) (greater than 40 mm Hg [5.3 kPa] in pediatric patients) through the use of fluids, vasopressors, and/or ICP normalization therapy.

  • Image not available. Nonspecific pharmacologic treatment in the management of intracranial hypertension should include analgesics, sedatives, antipyretics, and paralytics under selected circumstances.

  • Image not available. Specific pharmacologic treatment in the management of intracranial hypertension includes mannitol, hypertonic saline, furosemide, and high-dose pentobarbital. Neither routine use of corticosteroids nor aggressive hyperventilation (ie, PaCO2 less than 25 mm Hg [3.3 kPa]) should be used in the management of intracranial hypertension.

  • Image not available. Use of phenytoin for the prophylaxis of posttraumatic seizures usually should be discontinued after 7 days if no seizures are observed.

  • Image not available. Numerous investigational strategies targeted at limiting injury and/or stimulating axonal repair following severe TBI have been employed, but no proven therapeutic benefits have been identified.

Traumatic brain injury (TBI) is currently the leading cause of death and disability among children and young adults in the industrialized world.1 A focus on TBI prevention, improved acute care, and rehabilitation must remain national priorities. This chapter summarizes TBI epidemiology and pathophysiology, and highlights the major guidelines and systematic reviews of the literature pertaining to the management of severe TBI patients.

EPIDEMIOLOGY

It is estimated that approximately 1.7 million persons sustain a TBI each year in the United States equating to a TBI every 15 seconds.1 Among these individuals, 275,000 require hospital admission, and 53,000 die annually.1 Importantly, an estimated 5.3 million Americans currently live with disabilities as a result of their TBI, highlighting the enormous physical and emotional toll of this health care problem.2 The economic effects of acute neurotrauma are also enormous, with ...

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