Neurosurgery notes/Trauma/Secondary head injury/Cerebral ischaemia

Cerebral ischaemia

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Secondary head injury
  • In normal physiology
    • AVDO2 remains relatively constant
    • CBF changes in accordance to CMRO2 / CMRG.
  • Ischaemic injury consists of
    • Infarct core
      • Undergoes hypoxia- induced loss of cellular homeostasis and necrosis, .
    • Penumbra
      • Apoptotic processes can be targeted for therapeutic intervention
  • Cerebral ischaemia occurs when CBF does not meet cerebral metabolic demands (e.g. low CBF and high AVDO2).
  • Ways to measure
    • Jugular bulb oximetry
    • Transcranial doppler
    • PET
      • Demonstrated that previous definitions of hyperaemia and ischaemia based on CBF and oxygen are inaccurate,
      • Maintaining oxygen delivery may not be sufficient to prevent secondary injury.
        • Due to Mitochondrial dysfunction see above
        • Head injury → mitochondrial dysfunction → decreases oxygen demand + transition to hyperglycolysis → lactate accumulation.
        • Here a dec. In CBF can be misinterpreted as ischaemia
  • Ischaemia is often seen in
    • Acute SDH
    • Diffuse cerebral swelling
  • Inadequate metabolic supply to the brain after TBI is predictive of high morbidity and disability.
  • In head injury
    • Autoregulation is lost in TBI
      • The ability of CBF to meet metabolic demands is impaired,
      • AVDO2 may increase to improve O2 extraction in the cerebral circulation.
        • AVDO2 is capable of increasing from baseline value 6.7 ml/ 100 ml to a maximum 13 ml/ 100 ml.
        • The normal CBF threshold at which AVDO2 compensation occurs is 18 ml/ 100 g/ min, and can rise to 20 ml/ 100 g/ min following TBI due to decreased oxidative metabolism.
    • 15 O PET shows that diffusion barrier ischaemia (increased oxygen diffusion gradient from vasculature to interstitium) is due to microvascular disturbances such a perivascular oedema surrounding traumatic lesions → decreased partial pressure of oxygen in brain tissue (PbO2).
    • Neuronal death
      • Mech
        • Caspases and other proteins directly causing neuronal death,
        • 3 distinct mitogen- activated protein kinase (MAPK) inflammatory pathways contribute to ischaemic injury:
          • Extracellular signal- regulated kinase (ERK) pathway,
          • c- Jun- N- terminal protein kinase (JNK) pathway,
          • p38 pathway.
    • Biomarkers used in the assessment of neuronal, glial, and axonal damage.
      • Neuron- specific enolase
        • Is a glycolytic enzyme predominantly in neurons.
      • S100B
        • A calcium binding protein predominantly in astroglia.
      • Myelin basic protein
        • Located in white matter
        • A marker for axonal damage.