1 / 15

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.

dinos
Télécharger la présentation

Case Study: Traumatic Brain Injury

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  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

More Related