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Case Study: Traumatic Brain Injury

Case Study: Traumatic Brain Injury. By Barbara Amsler , Miranda Bryan, Emmilia Smith, Jessica Stern and Joy Yagi. Background. Acute traumatic brain injury leads to: 1 st stage of injury: mechanical/direct tissue damage and ischemia.

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Case Study: Traumatic Brain Injury

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  1. Case Study: Traumatic Brain Injury By Barbara Amsler, Miranda Bryan, Emmilia Smith, Jessica Stern and Joy Yagi

  2. Background • Acute traumatic brain injury leads to: • 1ststage of injury: mechanical/direct tissue damage and ischemia. • 2ndstage: related consequences to 1st stage, such as: • Loss of membrane/blood-brain barrier function • ion flux • excessive excitatory neurotransmitter release • Mitochondrial dysfunction • Loss of ATP • Generation of ROS • Anaerobic glycolysis  acidosis • Necrosis and apoptosis

  3. Etiology • Trauma leads to activation of sympathetic nervous system, which induces a hormonal stress response and a release of: • Catecholamines (dopamine, epinephrine, norepinephrine) • Glucagon • Cortisol • Elevated hormones stimulate: • Energy mobilization • Amino acid availability • Goal: Provide energy and building blocks to cells repairing and regenerating damaged tissue • Result  hypermetabolismand hyperglycemia

  4. Hormones • Normal scenario: • Insulin and glucagon counter-regulate each other during fed/fast states • Balance prevents hyperglycemia or hypoglycemia • Insulin promotes: • Energy storage through glycogenesis and lipogenesis and protein synthesis • Glucagon • Energy mobilization through gluconeogenesis, glycogenolysis, lipolysis

  5. Hormones • Stress response scenario: • Release of catecholamines and cortisol prevent normal balance of insulin and glucagon • Catecholamines increase the release of glucagon and inhibit the release of insulin even in conditions of high glucose levels • Outcome: • Increased catabolism and gluconeogenesis • Hyperglycemia

  6. Metabolic Alterations • Pancreas: • Suppression of insulin release • Promotion of glucagon release • Origin of hyperglycemia • Liver: • Increased glycogenolysisand gluconeogenesis resulting in increased hepatic glucose output.

  7. Metabolic Alterations • Adipose: • Activation of hormone sensitive lipase • Increased lipolysis • Release of glycerol to blood  Liver for gluconeogenesis • Release of free fatty acids • To peripheral tissue for beta oxidation • To liver for beta oxidation and/or ketogenesis

  8. Metabolic Alterations • Muscle • Increased proteolysis from cortisol stimulation • Release of amino acids for gluconeogenesis and protein synthesis for the repair process. • Increased glycogenolysis and glycolysis providing alanine and lactate to blood for gluconeogenesis in liver.

  9. Metabolic Alterations • Brain: • Area of tissue damage will have altered metabolism because of ischemia, mitochondrial dysfunction, acidosis from anaerobic glycolysis • Remaining tissue: • Glucose uptake is not insulin-dependent (GLUT 1, 3) • Oxidative stress  impaired glucose utilization? • Available KB utilized during stress period • KB potential neuroprotective effects

  10. Prognosis • Evaluation of injury: • Type and severity • Pre-injury health • Individual variability • Methods: • Glasgow Coma Scale used to evaluate neurological function • Hyperglycemia – very high blood glucose levels and persistence past 48 hours  poor outcomes

  11. Treatment • Adding to hyperglycemia should be avoided – no glucose, glucagon, cortisol • Controlling blood glucose with insulin? • Conservative vs. intensive insulin therapy • Risk for hypoglcyemia poor outcomes • No consensus on use for IIT, some research indicates very narrow room for error • High blood glucose resolved within 48 hours may be physiologically advantageous • Suggestion: Treat persistent hyperglycemia with insulin to maintain blood glucose in 120-150 mg/dL range

  12. Question for Class • Why do we see an increased release of alanine and lactate from skeletal muscles during TBI-induced stress?

  13. Answer for Class • Epinephrine stimulating glycogenolysis and glycolysis in skeletal muscle • However, ATP demand is low in a brain-injured patient • Therefore, Acetyl CoA accumulates and inhibits Pyruvate dehydrogenase complex  increase in pyruvate levels • Pyruvate then diverts to alternative pathways • Alanine aminotransaminase • Lactate dehydrogenase

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