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Written by: Rebecca L. Smith, John C. Lin, David Adelson, Patrick M. Kochanek, Erica L. Fink, Stephen R. Wisniewski, Huelya Bayir, Elizabeth C. Tyler-Kabra,

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Presentation on theme: "Written by: Rebecca L. Smith, John C. Lin, David Adelson, Patrick M. Kochanek, Erica L. Fink, Stephen R. Wisniewski, Huelya Bayir, Elizabeth C. Tyler-Kabra,"— Presentation transcript:

1 Written by: Rebecca L. Smith, John C. Lin, David Adelson, Patrick M. Kochanek, Erica L. Fink, Stephen R. Wisniewski, Huelya Bayir, Elizabeth C. Tyler-Kabra, Robert S. B. Clark, S. Danielle Brown, Michael J. Bell Presented by: Lucan Sanchez

2  Over 300,000 concussions are diagnosed, in athletes, annually  50,000 deaths a year due to TBI’s  2% of the US’ population lives with neurological disabilities resulting from TBI’s

3  The series of steps that follow a TBI in the brain  1. Calcium and Potassium ion imbalance in the brain  2. Ion pumps work overtime in order to restore balance, require large amounts of glucose  3. Impaired blood flow to brain limits amount of glucose available, massive energy crisis  4. Brain begins anaerobic respiration, produces lactic acid which further damages the brain

4  An excess of glucose in the brain  Why is it bad?  No definitive answer yet, all scientists have are theories  One theory is that the excess glucose in the brain produces oxygen free radicals that then attack the brain cells

5  Traumatic Brain Injury(TBI)- any impact to the head that can cause physical damage and long- term complications  Dextrose- a simple plant based monosaccharide used as a fluid and nutrient replenisher  Hypoglycemia- a shortage of glucose in the brain

6  Glasgow Coma Score- A scale from 3-15 that measures the severity of the TBI  Lactate- the lactic acid production by the brain during anaerobic respiration  NG, MHG, SHG

7  Yung M, Wilkins B, Norton L, et al; Glucose control, organ failure, and mortality in pediatric intensive care Pediatr Crit Care Med 2008; 9:147-152  Hirshberg E, Larsen G, Van Duker H: Alterations in glucose homeostasis in the pediatric intensive care unit: Hyperglycemia and glucose variability are associated with increased mortality and morbidity Pediatr Crit Care Med 2008; 9:361-366

8  Michaud LJ, Rivara FP, Longstreth WT Jr, et al: Elevated initial blood glucose levels and poor outcome following severe brain injuries in children. J Trauma 1991; 31:1356-1362

9  To determine the relationship between hyperglycemia and outcome in infants and children after severe TBI

10  All Children admitted with a TBI and Glasgow Coma score <8 were eligible for the study  A subset of these kids were also enrolled in a trial in which they tested hypothermia as a nueroprotectant

11  Glucose administration avoided for 48 hours post-TBI  Glucose timing and insulin administration was at discretion of team  48 hours post injury 5% dextrose IV drip

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13 Early NG Late NG 64% Late MHG 18% Late SHG 18% Early MHG Late NG 46%Late MHG 27%Late SHG 27% Early SHG Late NG 26%Late MHG 40%Late SHG 34%

14  Insulin administration was a potential source of error  Hypothermia and the re-warming process could have skewed results  More regulated glucose administration after 48 hours may yield different results

15  Hyperglycemia beyond 48 hours(Delayed hyperglycemia) post-injury results in poor outcome  This study found no association between early hyperglycemia and outcome  More research must be done in order to discover the optimal approach to treating kids with a TBI

16  Ms. Gleason  My family  Fellow Science Research Students

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