Diffuse Axonal Injury


Background
  1. Cause of prolonged traumatic coma when NO mass lesions or ischemia are present
  2. Most common CT finding after trauma
  3. Account for about 50% of primary brain injuries
  4. Has classically been considered a primary injury

Pathophysiology

  • Extensive, generalized damage to brain white matter
    • Caused by shear forces on brain
      • Strains tentorium and falx
  • Acceleration-deceleration impact applies rotational force to brain
    • Injury greatest where tissue density differences is greatest
    • 2/3 of DIA lesions are at gray-white matter junction
  • Axonal trauma
    • Damage to axonal membrane
      • Axons can be partially torn
      • Axons can be disconnected from their distal segments
        • Disconnection develops over several hours
      • Axoplasmic leakage and edema
        • Worst during first 2 weeks after injury
      • Axon splits in two
      • Eventually forms "retraction bulb"
        • Pathognomonic for DAI
        • Visible by MRI
  • Injury Grading
    • Stage 1
      • Axonal injury mainly in parasagittal white matter of the cerebral hemispheres
        • Frontal lobes, periventricular temporal lobes
        • Parietal and occipital lobes
        • Internal and external capsules
        • Cerebellum
    • Stage 2
      • Stage 1 plus lesions in the corpus callosum
        • Most common: splenium and posterior body
        • Usually unilateral, can be bilateral
        • Can be hemorrhagic
        • Poorer prognosis
    • Stage 3
      • Stage 2, plus involvement of brainstem
        • Superior cerebellar peduncles
        • Medial lemnisci
        • Corticospinal tracts

Diagnosis

  • Suspect in any patient with Sx out of proportion to CT findings
  • Indicated by prolonged traumatic coma
  • Traditionally, coma from time of injury for > 6 hrs
    • Some patients may recover briefly, then go into prolonged coma
  • Imaging
    • X-rays cannot demonstrate this lesion
    • CT scan findings (moderately sensitive)
      • NO mass lesions
      • NO ischemia
      • NO acute focal lesions on CT scan
      • Sometimes see small petechial hemorrhages
        • Near third ventricle
        • In white matter of corpus callosum
        • In internal capsule
    • MRI (best imaging)
      • Get T-1 and T-2 weighted images
      • See bright T-2 weighted signal
        • At white matter in temporal or parietal cortico-medullary junctions
  • Severity determined by clinical course
    • Mild DAI: coma for 6-24 hrs
      • 1/3 show decorticate posturing
      • Are following commands within 24 hrs
      • Most have no/ minor disabilities
    • Moderate DAI: coma for > 24 hrs
      • Most common clinical picture
      • Most have transient decorticate or decerebrate posturing
      • Most have moderate/ severe cognitive defects after awakening
    • Severe DAI
      • Almost always caused by vehicle crashes
      • Remain in coma for prolonged periods
      • Usually show persistent dysfunction
        • Posturing (brainstem dysfunction)
        • Autonomic (hypertension/ hyperpyrexia)
      • Usually see diffuse edema and increased ICP
      • 90% never awaken (persistent vegetative state)
      • Few who awaken
        • Severely disabled

Treatment

  1. ABCs
  2. Intubation (presume elevated ICP)
    • Pretreatment (2-3 minutes before intubating)
      • Lidocaine: 1.5 mg/kg IV
        • To prevent incr ICP
      • Vecuronium; 0.01 mg/kg IV
      • Fentanyl: 3 mcg/kg IV (over 1 min)
    • Induction / Paralysis
      • Etomidate: 0.3 mg/kg IV
      • Succinylcholine: 1.5 mg/kg IV
    • See RSI Calculator
  3. Fluid resuscitation to treat shock
  4. Spine precautions
  5. Survey for additional injuries
    • Chest, abdomen
    • Spine, extremities
  6. Treatment is supportive
    • Treat elevated ICP
    • Treat seizures
      • Acute seizures:
        • Lorazepam: 1 to 2 mg IV q 5 min up (max :4 mg)
        • Diazepam (0.1 mg/kg IV (up to 5 mg) q 5 minutes (max: 20 mg)
      • Long-term or prophylactic Tx:
        • Phenytoin: Load: 15-20 mg/kg IV (give at < 50 mg/min)
        • May follow with 100-150 mg after 30 min
  7. Further treatment
    • Optimize cerebral perfusion
      • Treat systemic shock
      • Treat hypoxia
    • Good general medical care
    • Monitor ICP and arterial pressure
      • Keep ICP < 20
      • Keep CPP  < 70
    • Repeat head CT as needed

Disposition

  1. ICU admission
  2. Neurosurgery and trauma consults