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KEY CONCEPTS

KEY CONCEPTS

  • image 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 Guidelines for the Management of Severe Brain Injury, 4th edition, 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 Correcting and preventing early hypotension (systolic blood pressure [SBP] less than 100 to 110 mm Hg depending on age) with an SBP goal of 120 to 140 mm Hg and reversal of hypoxemia are primary goals during the initial resuscitative and intensive care of patients with severe TBI.

  • image Nonpharmacologic management of intracranial hypertension includes raising the head of the bed 30°, and ventricular drainage if an extraventricular drain (EVD) is present.

  • image The principal monitoring parameter for patients with severe TBI within the intensive care environment is increased intracranial pressure (ICP). Cerebral perfusion pressure (CPP) is also a critical monitoring parameter and should be maintained between 60 and 70 mm Hg (8.0 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 Nonspecific pharmacologic management of intracranial hypertension should include analgesics, sedatives, and antipyretics; paralytics may be advantageous under selected circumstances.

  • image Specific pharmacologic 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 Numerous investigational strategies targeted at limiting injury and/or stimulating axonal repair following severe TBI have been employed; however, no proven therapeutic benefits have been identified.

  • image Use of phenytoin (alternatively levetiracetam) for the prophylaxis of posttraumatic seizures generally should be discontinued after 7 days if no seizures are observed.

PRECLASS ACTIVITY

Preclass Engaged Learning Activity

Watch the video entitled “Overview of Traumatic Brain Injury (TBI)” (https://www.youtube.com/watch?v=T0WBMM7WKL4) which is a presentation delivered by Dr. Christopher Wolf and moderated by Brent Ghan at the University of Missouri School of the Health Professions. This 7.5 minute video provides a general overview of human brain anatomy and physiology. Thereafter, TBI pathophysiology is briefly outlined including cerebral contusions, diffuse axonal injury, secondary brain injury, in addition to TBI recovery. This video provides a succinct introduction to the more detailed pathophysiology outlined in the chapter and a context for understanding TBI pharmacologic and nonpharmacologic management.

INTRODUCTION

Traumatic brain injury (TBI) is one of the leading causes of death and disability among children and young adults in the industrialized world and is often referred to as the “silent epidemic.”1 A ...

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