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  • 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/American Association of Neurological Surgeons, 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 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. The principal monitoring parameter for severe TBI patients within the intensive care environment is intracranial pressure (ICP). Cerebral perfusion pressure is also a critical monitoring parameter and should be maintained between 50 and 70 mm Hg (greater than 40 mm Hg 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, furosemide, and high-dose pentobarbital. Neither routine use of corticosteroids nor aggressive hyperventilation (i.e., Paco2 less than 25 mm Hg) should be used in the management of intracranial hypertension.
  • Image not available.Phenytoin (or alternatively carbamazepine) should be used to prevent seizures in TBI patients at high risk for the first 7 days after injury. 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 (e.g., calcium antagonists, glutamate antagonists, antioxidants, free-radical scavengers, and progesterone) targeted at interrupting the pathophysiologic cascade of events occurring following severe TBI have been employed, but no proven therapeutic benefits have been identified.

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Upon completion of the chapter, the reader will be able to:

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  • 1. Describe the most common causes of severe traumatic brain injury (TBI) and the typical age distribution for patients sustaining such injuries.
  • 2. Differentiate between primary and secondary brain injury.
  • 3. Explain the central role of ischemia in triggering secondary neuronal injury following severe TBI.
  • 4. Compare and contrast the process of cellular necrosis and apotosis along the spectrum of secondary neuronal injury.
  • 5. Discuss the cascade of biochemical events proposed to occur following a severe TBI.
  • 6. Evaluate the neurological state of a severe brain injury patient using the Glasgow Coma Scale (GCS) and factors that may affect the GCS in addition to TBI.
  • 7. Summarize the impact of the Brain Trauma Foundation Guidelines for the Management of Severe Brain Injury on the consistency of care for severe TBI patients.
  • 8. Outline several general short-term treatment goals in the acute management of the TBI patient.
  • 9. Formulate a general treatment plan for a severe TBI patient during ...

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