Management of Traumatic Brain Injury (TBI)

  1. Prehospital management:
    1. Keep SBP >90 mmHg, PaO2 >60 mm Hg – fluids (NS preferred, albumin associated with increased mortality)
    2. Early intubation is controversial
    3. Assume spinal fracture
    4. Prehospital assessment of GCS (helps triage)
  2. ED
    1. Follow ATLS protocol
    2. VS: HR, BP, RR (pulse oxymetry, capnography), T
    3. Complete neuro exam ASAP, determine clinical severity
      1. GCS 8 or less = severe TBI
    4. Assess for other systemic trauma
    5. Labs: CBC, BMP, glucose, coags, ETOH level, urine tox
      1. If INR elevated, reverse coagulopathy immediately
    6. Evaluate and manage ICP
      1. Impending herniation (unilat / bilat fixed dilated pupils, decorticate or decerebrate, bradycardia, HTN and/or resp depression)
      2. Elevate HOB
  • Osmotic therapy (mannitol 1G/Kg IV)
  1. Neuroimaging – CT ASAP
    1. Current guidelines recommend head CT in all TBI patients with GCS 14 or lower
    2. Follow-up CT with any clinical deterioration
  • Routine follow-up imaging??
  1. Parenchymal contrast extravasation or spontaneous ICH = higher risk of hemorrhage progression
    1. EDH –
      1. > 30ml regardless of GCS
      2. Acute EDH and coma with anisocoria
    2. SDH
      1. Acute SDH >10mm thickness or with MLS >5mm on CT regardless of GCS
      2. GCS </= 8 or if decreased by 2 points from time of injury to hospital admission
      3. Asymmetric or fixed and dilated pupils
      4. ICP >20mm Hg
  • ICH
    1. Traumatic ICH in posterior fossa with mass effect (distortion, dislocation, obliteration of IV, compression of basal cisterns, obstructive HCP)
    2. ICH in cerebral hemispheres – not clearly defined
      1. >50 cm3
      2. GCS 6-8 in frontal or temporal hemorrhage >20cm3 with MLS >5mm and/or cisternal compression
    3. Penetrating injury
      1. Superficial debridement + dural closure to prevent leak
      2. Simple closure for small entry wounds
      3. Routine prophylactic BSA (cephalosporin)
    4. Depressed skull fracture
      1. Elevation and debridement if depressed greater than thickness of cranium or if dural penetration, significant hematoma, frontal sinus involvement, cosmetic deformity, wound infection / contamination or pneumocephalus
    5. Decompressive craniectomy – technique still controversial, efficacy uncertain; decreased ICP and shorter ICU stays, but worse GOS at 6 months (flawed study?)
  1. ICU management
    1. Principal focus is to limit secondary brain injury
    2. Maintain SBP >90mm Hg and PaO2 >60mm Hg
      1. Normal saline, maintain euvolemia; albumin higher mortality vs NS (33% vs 20%) especially in severe TBI (42% vs 22%)
      2. Correct electrolytes
    3. DVT prophylaxis
      1. Mechanical prophylaxis using IPC stockings
      2. Risk of hemorrhagic expansion greatest in first 24-48h; use and timing of antithrombotic agents must be individualized
    4. Nutritional support – should be fed to full caloric replacement by day 7 post-injury
    5. ICP
      1. elevate HOB to 30 degrees, neck in neutral position, loosen neck braces if too tight
      2. monitor CVP, avoid excessive hypervolemia
  • indications for ICP monitoring
    1. GCS 8 or less
    2. Abnormal CT with evidence of ME from hematomas, contusions, swelling
    3. If 2 or more are present: >40y/o, posturing, SBP , 90 mm Hg
  1. Ventricular catheter connected to strain gauge transducer most accurate and cost effective
  2. ICP monitoring has not been supported by large RCTS
  3. Initiate treatment if ICP rises above 20 mm Hg (VOHSBID)
    1. Ventricular drainage first
      1. Remove CSF at 1-2ml/min x 2-3 minutes every 2-3 minutes, until ICP <20mm Hg or CSF no longer easily obtained
      2. Alternative: passive gravitational drainage
    2. Osmotic therapy
      1. Mannitol bolus 0.25-1G/Kg q4-6h PRN, check POsm (<320 mMol/L), fluid balance, crea, electrolytes
      2. Hypertonic saline
    3. Hyperventilation
      1. Mechanical ventilation to prevent inc intrathoracic pressure that elevates CVP and impair venous drainage,
      2. Low PaCO2 leads to cerebral vasoconstriction, resulting in decreased cerebral bf and ICP
      3. May also cause secondary ischemia and worsen outcoes; inc lactate and glutamate levels lead to secondary injury
      4. Guidelines recommend avoid hyperventilation, esp first 24-48h following TBI
      5. May consider mild to moderate hyperventilation at later stages, but avoid PaCO2 <30mm Hg
    4. Sedation – can also cause hypotension and cerebral vasodilation
      1. Propofol preferred, short duration of action, reduces ICP, neuroprotective; but potentially fatal propofol infusion syndrome (severe metabolic acidosis, rhabdomyolysis, hyperkalemia, renal failure, cardiovascular collapse); do not exceed 4mg/Kg/h, monitor EKG changes, lactic acidosis, elevated creatinine kinase and myoglobin
    5. Barbiturate coma – little clinical data
      1. Pentobarbital did not improve 30d mortality, high doses may cause hypotension, remains a treatment option if refractory, load 5-20mg/Kg as bolut then 1-4 mg/Kg/hr; continuous EEG monitoring, titrate to burst-suppression pattern
      2. Other agents: benzos or opiates (midazolam, morphine, fentanyl); high dose opiates found to cause transient increases in ICP
    6. Induced hypothermia
    7. Decompressive craniectomy
  • Cerebral perfusion pressure
    1. Normal cerebral vasculature maintains CBF across a wide range of MAP (50-150mm Hg)
    2. Cerebral autoregulation disrupted in 1/3 of severe TBI à “pressure-passive”
    3. Rise in MAP leads to inc ICP, drops in MAP associated with hypoperfusion and ischemia
    4. CPP = MAP-ICP, low CPP or low MAP or inc ICP associated with secondary brain injury
    5. Induced hypertension to target CPP >70mmHg – volume expansion and vasopressor agents à initial studies appeared to reduce M&M, but subsequent studies does not confirm and noted risks of ARDS
    6. 2007 guidelines recommend CPP target 60mm Hg, avoid below 50 and above 70 mm Hg
  • AEDs
    1. Incidence of early post-traumatic seizures (first 2 weeks) 6-10% (30% in severe TBI)
    2. 15-25% of coma and severe TBI will have nonconvulsive seizures on continuous EEG
    3. AEDs reduce incidence of early seizures, but does not prevent later development of epilepsy
      1. Early seizures risk status epilepticus; recurrent seizures increases cerebral blood flow and increases ICP; seizures place metabolic demand on damaged brain tissue
    4. Approach to seizure management in TBI:
      1. 7-day course of prophylactic phenytoin or valproic acid, no long term AEDs
      2. Consider EEG and/or EEG monitoring in coma
      3. Treat both clinical and EEG-only seizures with AED
    5. Temp management
      1. Maintain normothermia – antipyretic, surface cooling devices, endovascular temperature management catheters
      2. Mild to mod hypothermia (32-35C) small but significant decrease in risk of death (RR 0.76) or poor neuro outcome (RR0.69); increases risk for pneumonia
      3. Therapeutic hypothermia should be limited to clinical trials or patients with elevated ICP refractory to other therapies
    6. Glucose management
      1. Glu >/=170mg/dL at ICU admission is an independent predictor of poor GCS score 5d later
      2. Target 140mg/dL to 180mg/dL
    7. Hemostatic therapy
      1. 1/3 of severe TBI develop coagulopathy à TBI systemic release of tissue factor and brain phospholipids into circulation leading to inappropriate intravascular coagulation and consumptive coagulopathy
      2. Treat Coumadin coagulopathy
      3. Thrombocytopenia – maintain platelet count >75,000 with plt transfusion if necessary; platelet transfusion in patients on antiplatets unknown
      4. Other categories: when coaguopathy identified, use FFP, PCC and/or Vit K as for warfarin-reversal; arbitrary target of INR <1.4
      5. There is no evidence that hemostatic therapy benefits noncogulopathic patients with severe TBI
    8. Glucocorticoid – methylprednisolone harmful (increased mortality at 2 weeks, 21% vs 18%) and at 6 months 26% vs 22%)
    9. Neuroprotective treatment
      1. To date, no neuroprotective agents have been shown to improve outcomes
      2. IV progesterone, magnesium, hyperbaric oxygen, cyclosporine, citicoline
  • EPO postulated to have neuroprotective effects, requires validation
  1. Advanced neuromonitoring
    1. Jugular venous oximetry: retrograde cannulation of internal jugular, measure O2 sats; normal SjVO2 (jugular venous O2 sats) ~60%; <50% x 10 mins considered ischemic desaturation
    2. Brain tissue oxygen tension (PbtO2) monitoring: intraparenchymal O2 electrode, measures PbtO2 in WM, Normal is >20 mmHg; >25 associated with better outcomes, <15 mmHg associated with worse outcome
    3. Cerebral microdialysis: intraparenchymal probe measures glucose, lactate, pyruvate, glutamate; lactate:pyruvate ratio >40 suggestive of anaerobic metabolism (exacerbate secondary brain injury)
    4. Thermal diffusion flowmetry: measure CBF in WM (very preliminary
  2. Prognosis in TBI
    1. Negative outcome predictors: GCS at presentation, esp motor score; CT abnormalities (SAH, cisternal effacement, MLS), papillary function, age, associated injuries and complications, hypotension, hypoxemia, pyrexia, elevated ICP, reduced CPP, bleeding diathesis (low plt, coagulopathy)
    2. Other potential biomarkers: s-100B protein, neuron-specific enolase, a-synuclein in blood or CSF
    3. Except in the most extreme cases, a trial of early aggressive neurosurgical and neurocritical care management should be undertaken
    4. Severe TBI = 30% risk of death
    5. Only 25% achieve long term functional independence, 5-15% of severe TBI discharged from acute care in vegetative state; only half regain consciousness in 1 year and virtually all remain severely disabled
  3. Amantadine
    1. Antagonizes NMDA and/or indirect agonist of dopamine
    2. 100mg BID
    3. Associated with accelerated recovery during 4week active treatment phase
    4. Further study needed


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