Download
traumatic brain injury n.
Skip this Video
Loading SlideShow in 5 Seconds..
Traumatic Brain Injury PowerPoint Presentation
Download Presentation
Traumatic Brain Injury

Traumatic Brain Injury

155 Views Download Presentation
Download Presentation

Traumatic Brain Injury

- - - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript

  1. Traumatic Brain Injury • 1.6 million head injuries in US annually • 250,000 hospital admissions • 60,000 deaths • 70,000 - 90,000 permanent neurologic disabilities • Causes • Motor vehicle accidents • Falls

  2. Primary Survey • Stabilize the spine • Establish adequate airway • Ensure adequate ventilation • IV access to initiate volume resuscitation • Avoid secondary insults to brain Hypoxia Hypotension • Determine level of consciousness examine pupils

  3. Secondary Survey • Once relatively stable • Includes a complete neurologic examination • Severity of the head injury is classified clinically by GCS • 13 to 15 mild • 9 to 12 moderate • 8 or less severe • Assess strength, sensation

  4. Overall goal with neurologic injury • Presume injury until proven otherwise • Identify early • Allow injured tissue the best chance to repair itself • Adequate delivery of oxygen and glucose • Avoid infection • Preserve residual nervous tissue

  5. Primary Brain Injury • Trauma: concussion, contusion, diffuse axonal injury • Ischemia: global, regional • Inflammation • Direct Injury: hemorrhage, penetrating injury • Compression: tumor, edema, Hematoma • Metabolic insults • Excitatory toxicity: seizures, illicit drugs, severe hyperthermia

  6. Secondary Brain Injury • Hypoperfusion: hypotension, high intracranial pressure, vasospasm • Single episode SBP <90 mm Hg increases morbidity & doubles mortality* • Hypoxemia* ** • pO2 ≤ 60 mm Hg increases poor outcome from 28% to 71% * • Increases mortality • 50% from 14.3% ** • Harmful mediators: reperfusion, inflammation • Electrolyte changes *Chestnut RM, et al. J Trauma 1993;34:216-222 **Jones PA, J NeurosurgAnesth 1994;6:4-14

  7. Basic Premises: • 1. Monro-Kellie hypothesis • 3 compartments: brain, blood, & CSF • Increase in one must be compensated by • decrease in others or the ICP will increase • 2. Compliance • volume to pressure relationship

  8. Basic Premises: • Monro-Kellie hypothesis • 2. Compliance • 3. Cerebral autoregulation

  9. Intact autoregulation Lang et al JNNP 2003;74:1053-1059

  10. Intact autoregulation

  11. Intact autoregulation Lang et al JNNP 2003;74:1053-1059

  12. Defective autoregulation

  13. Basic Premises: Monro-Kellie hypothesis 2. Compliance 3. Cerebral autoregulation 4. CPP = MAP – ICP

  14. Optimal cerebral perfusion pressure (CPP) in patients with acute traumatic brain injury by current guidelines is: A. Maintaining a mean arterial pressure of greater than 90 mm Hg. B. 50-70 mm Hg. C. greater than 70 mm Hg. D. determined without an ICP monitor. E. not important, ICP is the parameter to follow

  15. Cerebral perfusion pressure • CPP = MAP - ICP • Normal is 70-100 mm Hg • Adequate 50-60 mm Hg • Ischemia 30-40 mm Hg

  16. High MAP • WARNING ! ↑ in BP may be a sign of ↑ICP DO NOT TREAT/OVERTREAT BP alone CPP = MAP - ICP 70 = 75 - 5 70 mm Hg = ↑ ← ↑ 70 = 110 - 40 35 = 75 - 40

  17. Cerebral perfusion pressure • CPP=MAP-ICP • Current AANS guidelines specify ICP <20 & CPP of 50-70 mmHg • Lower CPP : poorer outcome (ischemic) • Higher CPP: more ARDS J Neurotrauma. 2007; 24:S59-64

  18. Initial Management – Pre-hospital • A B C D • Intubate early if GCS <8 • Systolic BP of < 110 requires fluid resuscitation • Rapid transport to trauma center • Avoid sedation if possible to preserve neuro exam

  19. Early Hospital Management • Intubate if GCS <8 • Rapid sequence preferred • Avoid increased ICP with placement of ETT • Preferred drugs • Etomidate – rapid acting, short duration, min BP effect • Rocuronium- short duration, no BP effect, no increased ICP • 100% O2 until transferred to ICU • Initial target PCO2 should be 35 to 40 mm Hg • MAP goal 90 • Use only LR or NS – NO HYPOTONIC FLUID

  20. Maintain Oxygenation! • Hypoxemia ≤ 60 mm Hg increases poor outcome from 28% to 71% (trauma)

  21. CT head – non contrast • All patients at risk • GCS <15 • Depressed skull or evidence of basilar skull fracture • Focal neuro deficits • GCS 15, +LOC • Neurosurgical consultation • Surgical evacuation • all acute traumatic extra-axial hematoma >1 cm • subdural or epidural hematoma > 5 mm with an equivalent midline shift and GCS<8 • depressed, open, and compound skull fractures • recommended if hematoma > 20 ml with mass effect

  22. ICU Management • Serial neurologic exams • ICP monitor recommended in patients with a GCS score < 8 • intracranial HTN > 60% • No RCT’s to support improved outcomes with ICP monitor • Studies demonstrate outcome is inversely proportional to max ICP reading and time spent >20

  23. ICP Monitoring • Different sites 1) Intraventricular- Gold standard 2) Intraparenchymal 3) Subarachnoid 4) Subdural 5) Epidural • Different modalities 1) Fiberoptic 2) Fluid-coupled

  24. Jugular Venous Oximetry • Continuous SjVO2 • Blood Draws for CvO2 Value Normal Ischemia SjVO2 > 60% <50% (10 min.)

  25. Tissue PO2 Monitoring:Pbto2 Licox- Integra • Direct measurement of tissue oxygen tension (?) • Local measurement • Part of ICP-bolt system • Experimental use in Europe since 1992 • Approved for use in Europe, Canada, and US

  26. Management of Intracranial HTN • 3 targets • Intracranial blood volume reduction • CSF drainage • Brain parenchyma reduction

  27. Decrease Elevate head to 30 degrees Midline position of head Sedation Muscle relaxation Decrease airway pressure Increase Ischemia Acidosis Hypercapnia Increased venous pressure Hyperthermia Cerebral blood volume

  28. Hyperventilation • Begins almost immediately • Peak effect in 30 minutes • Lowers ICP by 25-30% in most patients • May decrease cerebral blood flow: • No lower than pCO2 of 30mm Hg • Normalize within hours

  29. Ventilation: Hyperventilation • PaCO2 of 25-30 mm Hg can cause significant vasoconstriction and reduction in cerebral blood flow Coles JP, Crit Care Med 2002;30:1950-1959 Diringer MN. J Neurosurg 2002;96:103-108 Imberti R. J Neurosurg 2002;96:97-102 Muizelaar J Neurosurg 1991;75:731-739 Cold. ActaNeurochir 1989;96:100-106 Raichle, et al. Stroke 1972;3:566-575

  30. Hyperventilation • Hyperventilation lowers CBF, and therefore ICP, by raising the extracellular pH in the CNS • CO2 is not the direct mediator of this response • Hyperventilation does not ‘stop working;’ however, The choroid plexus exports bicarbonate to lower the pH • 6 hour time course • The cause of the ICP elevation is usually progressive • Further attempts at hyperventilation will raise intrathoracic pressure, decreasing jugular venous return and thereby raising ICP

  31. Hemodynamic • CBF is independent of MAP between 50-150 • Autoregulation • With injury 50% pts lose autoregulation ability • GOAL – Normal MAP or MAP >90 • Treat hypotension with thoughts of cause • Treat HTN with B-blockers, nicardipine • Use vasodilators with caution

  32. Cerebral autoregulation in normal subjects and patients with chronic hypertension Marik, P. E. et al. Chest 2002;122:699-711

  33. Osmotic Agents: Mannitol • Acts within 20-30 minutes • Dosage: 0.25-1 g/kg bolus • Filtered needles! • Actions: 1) osmotic gradient 2) may increase cardiac preload, output and elevate MAP 3) improves rheology of red blood cells 4) decreases CSF production 5) free radical scavenger

  34. Osmotic Agents: Mannitol • Serum osmolality <320 mOsm/L vsosmolar gap <10 • Measured osmoles – (2Na +glu/18+BUN/2.8) • Watch for osmotic diuresis: Dehydration and hypotension • MAINTAIN EUVOLEMIA

  35. Hypertonic Saline • 3% saline 250cc bolus (run in as fast as possible) • 7% saline bolus • 23.4% saline 30cc bolus

  36. Fever • Each increase in 1degree Celsius increases cerebral metabolic rate by 7% • One study w/ exercise: 1.5º C increased CMRO2 by 23% increase in CMRO2 Vasodilation CBV ICP • Increases O2 requirements • Increases CO2 production (may need to adjust ventilator minute ventilation!!!) NunnelySA et al. J ApplPhysiol 2002;92:846-851.

  37. McIntyre L et al JAMA 2003

  38. Pentobarbital coma may result in: A. hyperthermia. B. hypertension. C. increased respiratory drive. D. unreactive large pupils. E. increased electrographic activity