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KEY POINTS

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  • Primary injury occurs at the moment of trauma and is the result of direct damage to brain tissue. All subsequent preventable brain injuries are termed secondary injuries.

  • Head trauma is associated with cervical spine injury and stabilization of the spine (eg, cervical collar, log rolling) is maintained until the spine is cleared.

  • Hypoxemia, hypotension, and raised intracranial pressure (ICP) are the leading causes of death in severe traumatic brain injury (TBI) and are related to the severity of the brain injury as well as the systemic complications.

  • Critical care of the TBI patient is centered on airway control, favoring early intubation, resuscitation, maintenance of homeostasis, early detection of neurosurgically treated complications, and interpretation of information from bedside monitors to minimize disruption of cerebral perfusion, (oxygenation and nutrient supply) in order to prevent or limit secondary injury.

  • Level II evidence supports a minimum systolic blood pressure of 90 mm Hg. An SBP of <90 mm Hg must be avoided if possible, or rapidly corrected.

  • Currently there is no evidence from controlled clinical trials to indicate an optimal CPP goal in terms of reducing secondary ischemic injury or improving the neurological outcome; however, published guidelines state as a level III recommendation that the treatment range for CPP should be 50 to 70 mm Hg. Maintaining CPP >70 mm Hg has been associated with the development of acute respiratory distress syndrome (ARDS).

  • TBI is the second highest risk factor for the development of venous thromboembolism (VTE), second only to acute spinal cord injury and the incidence of deep venous thrombosis (DVT) 7 to 10 days after TBI is as high as 31.6% even with mechanical prophylaxis.

  • Antiseizure prophylaxis with phenytoin is recommended for the prevention of early posttraumatic seizures, that is, within 7 days of the TBI. Routine prophylaxis later than 1 week following TBI is not recommended

  • Recent studies have not demonstrated an overall beneficial effect of steroids on outcome and there is level I evidence that high-dose methylprednisolone increases mortality after moderate to severe TBI.

  • After TBI, persistent ICP >20 is associated with poor outcome and there are limited data—class III and II level evidence—that patients responding to ICP lowering treatments have a lower mortality and better outcome.

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INTRODUCTION

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Traumatic brain injury (TBI) is a major cause of morbidity and mortality worldwide and in the United States. TBI is caused by a blunt force or penetrating injury to the head that causes brain dysfunction. The severity of TBI may be evident immediately or may initially appear to be mild, only to deteriorate later and often rapidly. Symptoms of traumatic brain dysfunction include unconsciousness, amnesia, focal deficits, and cardiorespiratory instability due to brain stem dysfunction. TBI may be isolated but is often accompanied by additional injuries.

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Of an estimated 1.7 million people in the United States that sustain TBI each year, about 52,000 die before reaching the hospital and 275,000 are hospitalized.1 TBI accounts for one-third of trauma-related mortality.1 Children less than ...

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