Shiber: Updates in Traumatic Brain Injury

Today we are fortunate to again welcome Joseph R. Shiber MD. Dr. Shiber is an Associate Professor of the Departments of Emergency Medicine and Surgical Critical Care; is the Co-Director of the Neuroscience ICU; and acts as a regular Intensivist in the SICU/TICU at the University of Florida College of Medicine. Today Dr. Shiber has been generous enough to travel all the way up to Baltimore in order to share just a taste of his immense knowledge on the devastating topic of traumatic brain injuries. This is a topic that you cannot miss if you ever plan to take care of critically injured patients!!

Clinical Pearls

(Summary assistance provided by Dr. Negar Naderi) 


  • Traumatic brain injuries (TBIs) are a leading cause of morbidity and mortality in trauma
  • Bimodal age distribution of 15-24 year olds and >75 year olds

Types of Injury

  • Extra-Axial
    • Epidural Hematomas
      • Usually middle meningeal arterial bleed (or bony bleeding in younger pts)
      • Convex lens shaped on head CT with dura adhering to the skull
      • 2/3 no significant brain damage
    • Subdural Hemorrhage (SDH)
      • Bridging veins and venous sinus bleeds
      • Crescent shaped on T and bound by falx
      • No midline crossing
      • Isodense bleeding, often difficult to see with subacute bleeds or anemia
    • Intra-Axial
      • Subarachnoid Hemorrhage (SAH)
        • Most common cause of bleed in TBIs
        • Blood is in CSF spaces and in cisterns or sulci
        • Important to distinguish between traumatic and spontaneous SAH
      • Intracerebral Hematoma (ICH)
        • Contusion of brain parenchyma usually in frontal, temporal or occipital poles
        • Look for coup and contra coup injuries
      • Diffuse Axonal Injury (DAI)
        • Deceleration or rotational injury causing sheer injury to deep white mater causing axonal injury with diffuse tissue loss
        • Usually diagnosed on MRI, can have normal CT
        • Graded 1-3 with grade 3 leading to severe brain damage and poor prognosis
      • Goal of treatment: Limit secondary injuries (hypoxia, hypotension, hyperthermia, hypo/hyperglycemia, edema, infection, hyponatremia)

Monitoring and Treatment

  • Pressure Basics
    • Intracranial volume can be expanded by 100 ml before an exponential rise in intracranial pressure
    • Normal ICP is <10, sustained ICP>20 needs to be treated and ICP>40 is life-threatening
    • Cerebral perfusion pressure (CPP)>60 is associated with decreased mortality
  • Diagnosis and Treatment
    • Cardiopulmonary resuscitation: single episode of hypotension increases mortality from 27 to 50%
    • Beware of treating GCS as patients can start with GCS of 15 and rapidly decline and other factors i.e. alcohol can lower GCS in absence of TBI
    • CT head in those with trauma + LOC or trauma + GCS of <14 for evaluation of blood/edema/air
    • Management:
      • Elevate HOB 15-30 degrees, neck straight, 1-week seizure prophylaxis for ICH or SDH
      • Maintain normocarbia, MAP >75-80 (with pressors and fluids), PaO2>80, Hgb>8, PaO2>80, PbtO2>20 (Licox), Jugular ScVO2>60%
      • Avoid hypoglycemia, hypotonic fluids, hyperthermia, heparin/LMWH
      • EVD placement is the most accurate for ICP monitoring and can be therapeutic for draining CSF
      • If ICP is elevated: mannitol, hypertonic saline or CSF drainage via EVD, consider sedatives and paralytics if hyperosmolar therapy fails
        • Watch for dehydration s/p mannitol use
        • Only hyperventilate (PaCO2<30) during emergencies and for short periods, as hyperventilation can cause secondary injury
      • Decompressive craniotomy: large space occupying lesions, depressed skull fractures, GSW
      • For severe ICP elevations unresponsive to therapy: can decompress the downstream pressure gradient (laparotomy, thoracotomy) to lower ICP or induce a barbiturate coma to decrease metabolism
    • Recent data for treatment modalities
      • Hypothermia: mixed data, no benefit of any cooling below normothermia
      • Progesterone: based on gender disparity to outcomes with TBI
        • No difference in mortality or neurological outcomes, though may be time dependent benefit
      • EPO: no improvement in neuro outcomes; mild improvement in mortality (p=0.07) though possibly thrombogenic
      • >200 Clinical trials- no neuroprotective agents found
        • Simvastatin, sulfonulureas, etc.
      • Currently looking for a lab markers: S-100B, GFAP, MBP all correlate with TBI severity
      • APRV used less analgesia/sedation than conventional MV
      • Vasopressin gtt for CV support may induce DI due to hypothalamic suppression
        • Wean slowly and watch UO!


Suggested Reading

  1. Andrews PJ, Sinclair HL, Rodriguez A, Harris BA, Battison CG, Rhodes JK, Murray GD; Eurotherm3235 Trial Collaborators. Hypothermia for Intracranial Hypertension after Traumatic Brain Injury. N Engl J Med. 2015 Dec 17;373(25):2403-12.[PubMed Link]
  2. Joseph B, Haider A, Rhee P. Traumatic brain injury advancements. Curr Opin Crit Care. 2015 Dec;21(6):506-11.[PubMed Link]
About the Author

Jim Lantry

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Just your average critical care doc: Wandering the ED and ICUs for the USAF down in the San Antonio Military Medical Center, traveling the globe to cannulate for ECLS wherever the need arises, and trying to keep up with great minds of today. E:

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