NEW CONCEPTS IN THE MANAGEMENT OF SEVERE TRAUMATIC BRAIN INJURY

1. 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

3. 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.

4. HISTORY • Through the 1970’s, 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)

5. 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.

6. 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?????

7. 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

9. AVAILABLE NOW • HYPOTHERMIA • HYPERTONIC SALINE

10. 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

12. 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

13. 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

14. 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

15. TECHNIQUES • NOW, A common cooler with ice packs can store up to 3-4 liters of saline at 4C for > 20 hours- Kampmeyer, M. Pre- Hosp. Emerg. Care, 2009 • FUTURE, Argonne’s Energy Technology Division: Developing iceslurry, 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

16. HYPERTONIC SALINE THE BRAIN NEEDS TWO THINGS TO FUNCTION NORMALLY 1. Oxygen 2. Glucose

17. 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)

18. 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)

19. 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 cc’s 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

20. 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 < 160

21. SUGGESTED PRE-HOSPITAL THERAPY FOR SEVERE TBI In severe TBI: - ABC’s (O2 at 100%, SBP >100) - 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

22. THANK YOU