Shiber: Updates in Traumatic Brain Injury

Clinical Pearls

(Summary assistance provided by Dr. Negar Naderi) 

Epidemiology:

• 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!