1 / 64

Traumatic Brain Injury

Explore the prevalence, causes, and management of traumatic brain injury in pediatric intensive care units. Learn about primary and secondary injury mechanisms, cerebral metabolism, blood flow, and autoregulation. Discover clinical signs of increased intracranial pressure and how to interpret pupils for diagnostic insights.

jday
Download Presentation

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. Traumatic Brain Injury Pediatric Intensive Care Unit

  2. Epidemiology of TBI • An estimated 5.3 million Americans - a little more than 2% of the U.S. population - currently live with disabilities resulting from brain injury • Each year, in the United States: • ~1 million people are treated for TBI and released from hospital emergency rooms • 80,000 Americans experience the onset of long-term disability • More than 50,000 people die • Vehicle crashes are the leading cause of brain injury • Risk of TBI is highest among adolescents, young adults and those older than 75

  3. Pediatric TBI • At least 185 - 334 cases per 100,000 • Precise causes and distributions vary by locale • Boys more often injured; girls more often injured fatally • Head injury is more common in younger children, but severe injury more common in the older children • Suspicion of abuse raises likelihood of serious injury Berney, Child's Nerv Syst (1994) 10:509

  4. Pediatric TBI – cont. • Kennard Principle • “The age of animals affect both the rate of recovery and degree of deficit. Young and immature animals recover more quickly and extensively than adults” • “Talk and Die” • Head injured children often exhibit rapid neurologic deterioration and high mortality after an initial lucid period • Edema around a contusion

  5. Glascow Coma Scale • Best Eye Response (4) • 4.      Spontaneous • 3.      To verbal command • 2.      To pain • 1.      No response • Best Verbal Response (5) • 5.      Orientated • 4.      Confused • 3.      Inappropriate words • 2.      Sounds • 1.      No response • Best Motor Response (6) • 6.      Obeys commands • 5.      Localizes pain • 4.      Withdraws to pain • 3.      Flexion to pain • 2.      Extension to pain • 1.      No response

  6. Primary Injury • Direct mechanical injury • Disruption of vascular or neuronal elements • Initiation of cytotoxic cascades

  7. Hemorrhage – Subdural or Epidural?

  8. Secondary Brain Injury • Systemic: hypoxia (PaO2 < 60), hypotension (SBP< 90), hyperthermia, hypoglycemia, anemia, SIRS • Cerebral: edema, vasospasm, seizures, infection, ischemia • Cellular: excitotoxicity, membrane transport failure, fluid shifts, free-radical oxidation injury, apoptosis

  9. Secondary Damage following TBI Kochanek et al. Pediatric Critical Care Medicine. 1(1):4-19, July 2000

  10. Cerebral Metabolism • High metabolic demands • Aerobic metabolism • Glucose, oxygen used to generate ATP • Substrate delivery affected by acid/base balance and temperature • Matching of cerebral blood flow (CBF) with cerebral metabolic rate of oxygen (CMRO2) • Under normal conditions, rate of oxygen consumption not limited by supply • Uncoupling of CBF from CMRO2 can result in either ischemia or hyperemia

  11. Cerebral Blood Flow • Normal CBF: 45 - 60ml/100g/min • Reductions in CBF result in time-dependent neuronal events • Loss of consciousness, EEG slowing (20ml/100g/min) • Disruption of ionic homeostasis and conversion to anaerobic metabolism (18ml/100g/min) • Loss of membrane integrity, massive calcium influx -> irreversible damage (10ml/100g/min) • Tissue infarction (5ml/100g/min)

  12. Cerebral Blood Flow and Ischemia/Infarct http://www.fac.org.ar/scvc/llave/stroke/heiss/heissi.htm

  13. Cerebral Blood Flow in TBI Patients • CBF falls precipitously in first 24 h • < 20-30 mL/100g tissue/min • In survivors, CBF then increases for three days • No fundamental difference between children and adults • Previously thought that cerebral hyperemia occurs in children • High ICP is associated with low CBF • CMRO2 is highest initially, then falls • Systemic hypotension linked to poorer outcomes in head-injured patients

  14. CBF and Outcome in Head-Injured Children • CBF measured by XeCT in 30 children • 18 boys, 12 girls, mean age 2.2y range 0.10-8.0y • Early CBF = 25.1 ± 7.7 cc/100g/min • “Good” outcome mean 43.9 ± 11 (n=12) • “Bad” outcome mean 9.9 ± 5.9 (n=18) • CBF < 20 at any time = bad outcome • p = 0.0006, sensitivity 63%, specificity 100%, positive predictive value 100% Adelson, et. al., Pediatr Neurosurg 1997;26:200-207

  15. Cerebral Autoregulation • Consistent perfusion with MAP’s 60 – 150 mm Hg • Cerebral autoregulatory triggers include pressure, viscosity, O2 delivery, and CO2 • Autoregulation is impaired in injury

  16. Monroe-Kelly Doctrine Vtotal = Vtissue + Vblood + Vcsf

  17. Intracranial Pressure

  18. Early vomiting headache mental status changes acute neurologic deterioration respiratory irregularities Late Cushing’s Reflex III or IV palsy motor posturing pupillary dilation papilledema Clinical Signs of Increased Intracranial Pressure

  19. Pupils: Window on the Brainstem • If normally reactive, problems are in the hemispheres • If not, problems are in the brainstem Hypothalamus  small, reactive Dorsal midbrain  slightly large, non-reactive Central midbrain  fixed, midpoint Pontine  pinpoint

  20. Brain Herniation • Herniation types • 1. Subfalcine • 2. Uncal • 3. Caudal • 4. Tonsillar • Risk of herniation increases with intracranial hypertension

  21. Cerebral Edema • Vasogenic • Accumulation of water in interstitial CNS spaces due to increased vascular permeability • Cytotoxic • Accumulation of water in injured cells

  22. Sequelae of Neurologic Injury: Cardiac • ECG changes seen in nearly all patients • Cerebrally induced arrhythmias seen in ~50% • Related to autonomic dysfunction • Rate, rhythm or repolarization aberration • Peaked P’s, shortened PR’s, inverted T’s, ST changes, large U waves, prolonged QTc, deep Q’s • Asystole is rare • Abnormalities resolve in 10 days to 2 weeks (or with brain death) • No direct correlation between type of injury and specific changes

  23. Sequelae of Neurologic Injury: Pulmonary • Acute neurogenic pulmonary edema • Seen with large injury or acute ICP rise • May be secondary to hypertension • Brainstem injury usually present • Acute respiratory distress syndrome (ARDS) • Aspiration pneumonitis

  24. Sequelae of Neurologic Injury: GI • “Cushing’s ulcer” • Related to hyperacidity + ischemia • Seen most often with hypothalamic injury • 40% of bleeds start in first 48 hours • Steroid ulcer • Stress gastritis

  25. Sequelae of Neurologic Injury: Fluid & Electrolytes • Minor to moderate injury  SIADH • Urine scant and concentrated • Serum sodium low • Seizures • Severe injury Diabetes insipidus • Urine copious and dilute • Serum sodium high and rising • Unpredictable  Cerebral salt wasting

  26. Sequelae of Neurologic Injury: Metabolic • Hyperglycemia • Commonly seen in pediatric head injury • Serum glucose correlates with severity of injury • Worse outcome with higher levels • May be marker or part of pathophysiology • Temperature instability • Hyper- or hypo-thermia • Associated with neuroendocrine failure

  27. Sequelae of Neurologic Injury: Hematologic • Anemia • Thrombocytopenia • Disseminated Intravascular Coagulation

  28. Management of TBI • Minimize secondary damage • Beginning in the 1970’s, use of intensive management protocols resulted in significant reductions in morbidity and mortality • Mortality rate: 50% -> 36% • Objective of intensive monitoring: • maintain cerebral perfusion/oxygenation and avoid medical/surgical complications while the brain recovers

  29. Early Management • ABC’s • Secure the airway if GCS < 8 • Use of appropriate induction agents • Restore perfusion using isotonic fluids (NS) colloid, and pressors • Induction agents • Etomidate, propofol, thiopental • Ketamine? • Muscle relaxant • Rocuronium • Succinylcholine?

  30. Early Management – cont. • ATLS evaluation • C-spine, associated injuries • Emergent non-contrast head CT • Pursue surgical remedies • Decompressive craniectomy • Clot evacuation • Minimize ED and intra-hospital transport time

  31. General Management • Maintain BP with balance of isotonic fluid (euvolemia) and pressors • Maintain normal physiologic parameters • PaO2100, PCO2 30-35, T 37, [glucose] 80-110, HCT 30 • Head of Bed 30°, in midline • Minimize noxious stimulation • Sedation/analgesia

  32. Specific Therapies for TBI • ICP/CPP directed therapy • Hyperventilation* • Osmotherapy • Barbiturates • Anticonvulsants • Steroids * • Hypothermia *

  33. ICP Monitoring • Intracranial hypertension associated with poor neurologic outcome • ICP monitoring and aggressive treatment of intracranial hypertension associated with best reported clinical outcomes • Ventricular pressure measurement • “Gold standard” • Therapeutic CSF drainage • Parenchymal catheter tip pressure transducer devices • Easy of placement • Cannot be recalibrated in-situ • Potential for drift • Clinically significant infections or hemorrhage are rare

  34. Types of ICP Monitors • Intraventricular devices • Parenchymal catheter tip pressure transducer devices • Subdural devices • Subarachnoid fluid coupled device with an external strain gauge • Epidural devices

  35. ICP Monitoring: Assessment of Disease Severity • Patients with GCS≤8 at highest risk for intracranial hypertension • Marmarou et al. (1991) Analysis of 428 severely head-injured patients from Traumatic Coma Data Bank (TCDB) • Strongest predictor of outcome was percentage of time ICP exceeded 20 mmHg • Class II

  36. How Does ICP Monitoring Change Management? • Objectively guide: • ICP-lowering interventions • CPP-driven treatment strategies • Early detection of developing brain swelling or mass lesions in the sedated/paralyzed patient • Deleterious side effects of ICP control therapies • Hyperventilation • Mannitol • Sedation and paralysis • Decompressive craniotomy • Potential elimination of unnecessary interventions • Outcome prediction

  37. Evidence for ICP Monitoring • Eisenberg et al. (1988) Prospective study of 73 patients with severe head injury and elevated ICP refractory to standard measures • Patients randomized to receive high-dose pentobarbital or similar treatment without pentobarbital • All decisions relative to therapy were based on ICP data • Patients whose ICP was controlled with pentobarbital had much better outcome • Class I evidence

  38. Cerebral Perfusion Pressure (CPP) • CPP = MAP – ICP • Low CPP (<40mmHg) and hypotension have both been associated with worsened clinical outcomes • Studies have shown that increasing blood pressure does not significantly increase ICP • Suggested critical adult threshold: 70 – 80 mmHg • Optimal pediatric threshold may be lower (50 – 65 mmHg)

  39. CPP-Directed Therapy • M. Rosner, Journal of Trauma, 1990 • Autoregulation not defective, but autoregulatory curve shifted to the right • CPP below lower limit of autoregulation -> decreased ICP, but risk for ischemia • CPP exceeds lower limit of autoregulation -> decreased ICP via vasoconstriction-induced reduction in intracranial blood volume

  40. Vasodilatory Cascade ↓SBP hypovolemia, cardiogenic, loss of sympathetic tone ↓ CPP ↓ CBF ↑ICP Vasodilatation ↑ Edema ↑ CSF ↑ CBV Rosner et. al. J. Neurosurg 1995; 83:949-62

  41. Reversing the Vasodilatory Cascade Rosner MJ. Introduction to Cerebral Perfusion Pressure Management. Neurosurgery Clinics of North America 1995;6(4):761-773

  42. CPP Monitoring – Clinical Outcomes • Rosner et al, 1990: Prospective study of 34 TBI patients managed by keeping CPP above 70 mm Hg • Mortality rate 21%; good recovery rate 68% • Robertson et al, 1998: Randomized clinical trial of 189 TBI patients comparing ICP with CBF-targeted therapy • No significant difference in outcome • Increased rate of ARDS in CBF group • No pediatric studies demonstrating that active maintenance of CPP above any threshold is responsible for improved morbidity or mortality • Potential hazards • Intentional hypertension  raised ICP via pressure or leak

  43. Lund Model Max ΔPoncotic Min DPhydrostatic ↓ capillary pressure ↓diffusion distances ↓capillary obstruction ↓ capillary leak ↓ edema Eker et. al. Crit Care Med 1998; 26:1881-6

  44. ICP-directed No specified CPP Keep ICP < 20 mmHg Keep BP normal, treat hypertension CPP-directed (Rosner) Maintain CPP > 70 mmHg Volume expansion Vasopressors Lund therapy Maintain CPP > 50 mmHg Aggressively treat hypertension Maintain low venous pressures

  45. Hyperventilation • Decreased pCO2 -> cerebral vasoconstriction -> decreased ICP • Decreases regional cerebral blood flow CT Baseline PET Hyperventilation PET Coles, et. al., Crit Care Med 2002; 30(9):1950-1959

  46. Hyperventilation in TBI • ICP decreased in only 15 of 31 head-injured patients • J Neurosurg 51:292, 1979 • ICP actually increased in 4/14 patients • Br Med J 4:634, 1973 • Hyperventilation -> ischemia • J Neurosurg 61:241, 1984 • Brain Trauma Foundation Recommendations: • Avoid pCO2 < 25 torr • Avoid entirely, if possible (esp. day 1) • Use during acute deterioration or refractory ICP > 20

  47. Osmotherapy • Osmotic Agents are solutions containing simple, LMW solutes; hyperosmolar relative to plasma • Examples: mannitol, glycerol, dextrose, sorbitol, sucrose, sodium chloride

  48. A Few Important Concepts • Molarity vs. Tonicity • Molarity is function of the number of osmotically active particles per unit volume of solution • Tonicity depends on membrane properties as well as respective molarities • Uniqueness of Blood-Brain Barrier • Impermeable to small particles such as mannitol, sodium ions, and chloride • For any given change in plasma concentration of LMW impermeants, there is much greater osmotic force favoring movement of water out of the brain in comparison with other tissues

  49. Mannitol • Hexahydric alcohol related to mannose; isomeric with sorbitol • C(6)H(14)O(6) • Mannitol is not metabolized, but has a short elimination half-life of 30-60 minutes because of rapid renal clearance • In the presence of intact renal function, the accumulation of mannitol within tissues is unlikely – “autodilution effect” • Dose: 0.25 – 1 gm/kg IV over 30 minutes • Co-administration of Furosemide

  50. Hypertonic Saline • Several concentrations used, including 3%, 7.5%, and 23%; no evidence that one more effective than others in reducing brain water volume • Effect of HS on the cardiovascular system is transient, lasting between 15 – 75 minutes • Action augmented by addition of a colloid such as hydroxyethyl starch or dextran Qureshi et al., Crit Care Med, 2000

More Related