NEW CONCEPTS IN THE MANAGEMENT OF SEVERE TRAUMATIC BRAIN INJURY

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NEW CONCEPTS IN THE MANAGEMENT OF SEVERE
TRAUMATIC BRAIN INJURY

• FIA MEDICINE IN MOTOR SPORT SUMMIT 2010
• Stephen E. Olvey M.D.
• Associate Professor of Clinical
  Neurology/Neurosurgery
• Director Neuroscience Intensive Care Unit
• University of Miami-Miller School of Medicine
• Fellow FIA Institute for Motor Sport Safety

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HISTORY

• The most common cause of death in motor sports
  has always been severe brain injury
• Drivers that survived a major head injury were
  often left severely disabled.

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HISTORY

• Through the 1970s, approximately 1 out of 7
  drivers died each year in all major forms of
  motor sports
• Death was nearly always due to fire and/or severe
  brain injury
• During the period 1978 1980, both Formula 1 and
  Indy Car developed expert traveling medical and
  safety response teams (Watkins/Olvey)

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HISTORY

• Mortality and morbidity among drivers has
  steadily declined since the institution of these
  rapid response teams
• In Indy Car, from 1996 thru 2006 there have been
  57 recorded head injuries with 6 fatalities, 45
  concussions, 8 classified as severe with diffuse
  axonal injury.
• All 8 of these drivers were able to return to
  competition. Some are still competing and none
  have developed late onset seizures.

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HISTORY

• These excellent results are thought due to the
  fact that none of the drivers were allowed to
  become severely hypoxic or hypotensive.
• A literature review reveals an expected mortality
  rate of from 27 68 with these injuries and a
  severe disability score at 6mos. of from 44
  88.
• These are great results yet there were still 6
  fatalities, not all racing is on a protected
  closed course with rapid response.
• Can anything else be done?????

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• Actual and experimental neuro-protective agents
  do exist, but for these agents to have their
  greatest effect they must be administered very
  early post injury in order to avoid the secondary
  chemical cascade responsible for severe and often
  fatal outcomes

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AVAILABLE NOW

• HYPOTHERMIA
• HYPERTONIC SALINE

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HYPOTHERMIAGOOD RESULTS SHOWN WITH ANIMAL STUDIES

• Clifton, 1991- Hypothermia to 33C in a percussion
  rat model showed a significant reduction in
  mortality as well as improved neurological
  deficits post injury (beam walking, balance)
• Dietrich, 1994- Hypothermia to 30C initiated 5
  min after percussion type injury reduced overall
  contusion volume by 40 improving survival of
  overlying cortical neurons

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HYPOTHERMIA

• Cooling patients post cardiac arrest has now
  become the accepted standard of care.
• - Two common methods are used
• Surface cooling
• Intravascular cooling
• - Both require in-patient locations

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HYPOTHERMIA

• Research over the last decade has supported the
  use of iced saline in post cardiac arrest
  resuscitation
• Difficulty with storage and availability of
  suitable solutions outside of the hospital

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FIELD USE IS AVAILABLE

• Cold intravenous infusions (1 to 4 C)
• - 2.3 liters of cold solution over 50 min.
• can cool a 70Kg male from 36.9 C to
• 32.9 C in 60 minutes.-
• - No adverse effect seen on BP, HR, CVP,
• ABG, WBC, Plts., glucose or electrolytes
• -Crit Care
  Medicine, 2000, vol 28, No. 9

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TECHNIQUES

• NOW, A common cooler with ice packs can store up
  to 3-4 liters of saline at 4C for gt 20 hours-
  Kampmeyer, M. Pre- Hosp. Emerg. Care, 2009
• FUTURE, Argonnes Energy Technology Division
  Developing ice slurry, now used in industry, for
  human use in partnership with the University of
  Chicago (micro ice slivers for injection)-
  University of Chicago Emergency Resuscitation
  Center

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HYPERTONIC SALINE

• THE BRAIN NEEDS TWO THINGS
• TO FUNCTION NORMALLY
• 1. Oxygen
• 2. Glucose

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HYPERTONIC SALINE

• Appropriate treatment of cerebral edema and
  elevated ICP improves cerebral perfusion and
  reduces mechanical damage caused by compartmental
  shifts and local compression of brain tissue.
• (Fishman et.al. NEJM, 1975)

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HYPERTONIC SALINE WILL

• Improve intravascular volume and cardiac
  performance
• Improve intracranial elastance, and regional
  cerebral blood flow by reducing the size of
  ischemic, swollen endothelial cells.
• Stabilize ion concentrations of sodium and
  chloride thus maintaining resting membrane
  potentials.
• Reduce adhesion of polymorphonuclear cells to
  intravascular membranes thought important in
  reducing the secondary inflammatory insults
  following TBI.
• Reduce ICP !!!!!
• (Qureshi, et. al. Crit. Care Medicine
  2000)

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AVAILABLE SOLUTIONS

• 3 Saline A continuous drip of from 20 -40
  cc/hr. may work better than mannitol to remove
  cerebral edema fluid with less side effects while
  helping to maintain ICP.
• 7.5 Saline Boluses of 250 ccs can
• reduce ICP and enhance systemic BP
• in hemorrhagic shock with TBI.-Neurosurgery,
  Aug/2005
• 23.4 Saline Boluses of 30-60 cc over 5 minutes
  will drastically reduce ICP and can prevent
  herniation syndrome!!!! Can be given in
  peripheral vein -Brain over Vein

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POTENTIAL SIDE EFFECTS

• All side effects are related to a rise in
• serum sodium.
• - Decreased consciousness
• - Seizures
• - Central Pontine Myelinolysis
• - CNS Hemorrhage
• - Rebound cerebral edema
• None of these have been seen in our
• experience. Serum sodium is checked
• frequently and kept lt 160

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SUGGESTED PRE-HOSPITAL THERAPY FOR SEVERE TBI

• In severe TBI
• - ABCs (O2 at 100, SBP gt100)
• - Hyperventilate patient (15 to 20 bpm)
• - 3 Iced saline IV (1-2 liters at 4C)
• - Blown pupil/pupils 23.4 saline
• (30 to 60 cc boluses IV over 5
• min, may repeat x 3) unproven but looks
  good
• - Rapid transport, continue above in
• ER and in the OR, or also use 7.5 in 250
• cc boluses to control ICP once
• monitored especially with multiple trauma
  and shock

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THANK YOU