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Source: Boucher BA, Wood GC. Acute management of the brain injury patient. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM, eds. Pharmacotherapy: A Pathophysiologic Approach. 10th ed. New York, NY: McGraw-Hill; 2017. Accessed February 23, 2019.


  • Traumatic brain injury (TBI)


  • Neurologic sequelae of brain trauma can occur as a result of primary or secondary injuries.

    • Primary injuries

      • Contact related (ie, blunt-object blow, penetrating-missile injuries) resulting in skull fractures, brain contusion, hemorrhages

      • Acceleration/deceleration

        • Instantaneous brain movements following motor vehicle accidents

      • Injuries defined as focal (eg, contusions, hematomas) or diffuse

        • Major factor as to which of the secondary injury mechanisms discussed below will predominate following a TBI

    • Secondary neuronal injuries

      • Energy-dependent cellular necrosis due to membrane cell lysis, edema, inflammation, or apoptosis leading to cell shrinkage and cell membrane dissolution


  • TBI is the leading cause of death and disability among children and young adults.

  • 1.7 million persons sustain a TBI each year in the United States equating to TBI every 15 s.

  • Among these, 275,000 require hospital admission and 53,000 die annually.

  • 5.3 million persons currently live with disabilities as a result of their TBI.

  • Direct and indirect spending on TBI patients requiring hospitalization of $76.5 billion in the United States in 2010.


  • General

    • Level of consciousness on admission ranges from awake and alert to completely unresponsive (ie, Glasgow coma scale [GCS] 15–3, respectively)

    • GCS to grade arousal and functional capacity of cerebral cortex

      • Defines level of consciousness according to eye opening, motor response, and verbal response

  • GCS scores (Table 1)

    • GCS 15: Normal

    • GCS 3–8: Severe

    • GCS 9–12: Moderate

    • GCS 13–15: Mild or minor brain injuries

  • Agents to avoid until initial examination is complete because they affect neurologic examination

    • Opiates, sedatives, neuromuscular blockers

  • Rapidly attainable clinical variables predictive of poor outcomes

    • Patient’s age

    • Presence of hypotension

    • Increased intracranial pressure (ICP)

    • Decreased GCS score (especially motor score)

    • Pupillary reactivity

    • Computed tomography (CT) scan (+) for hematoma, subarachnoid hemorrhage, midline shift, and compression of ventricular cisterns

  • Signs and symptoms

    • Symptoms: Posttraumatic amnesia (>1 hour), dizziness, moderate to severe headache, nausea/vomiting, limb weakness, paresthesia

    • Signs: Cerebrospinal fluid (CSF) otorrhea or rhinorrhea, seizures, unequal or unreactive pupils indicating more severe injury, rapid deterioration in mental status indicating expansion of lesion within the skull, alteration/unstable vital signs, Cheyne-strokes respiration, tachypnea, hypertension, bradycardia

TABLE 1Glasgow Coma Scale

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