Neurosurgery notes/Trauma/Management of trauma/Neuromonitoring/Cerebral oxygenation monitoring

Cerebral oxygenation monitoring

View Details
logo
Parent item
Neuromonitoring

Jugular venous oxygen monitoring (SjVO)

  • Indications
    • The need for augmented hyperventilation (pCO2 = 20–25) to control ICP.
  • Parameters related to oxygen content of the blood in the jugular veins are global in nature and are insensitive to focal pathology.
  • Requires retrograde placement of catheter near to the origin of the internal jugular vein at the base of the skull.
  • Parameters that can be measured:
    • Jugular venous oxygen saturation (SjVO2):
      • Measured continuously with special fibreoptic catheter.
      • Normal SjVO2: ≥ 60%.
      • Desaturations to <50% suggest ischemia.
        • Multiple desaturations (< 50%) or sustained (≥ 10 minutes) or profound desaturation episodes are associated with poor outcome.
        • Sustained desaturations should prompt an evaluation for correctable aetiologies:
          • Kinking of jugular vein
          • Anaemia
          • Increased ICP
          • Poor catheter position
          • CPP< 60mm Hg
          • Vasospasm
          • Surgical lesion
          • PaCO2 <28mm Hg
      • High SjVO2 >75% may indicate hyperemia or infarcted tissue and is also associated with poor outcome
    • Jugular vein oxygen content (CVO2).
      • Requires intermittent sampling of blood
    • Arterial-jugular venous oxygen content difference (AVdO2):
      • AVdO2 >9 ml/dl (vol%) probably indicates global cerebral ischemia,
      • AVdO2 < 4 ml/dl indicate cerebral hyperemia (“luxury perfusion” in excess of the brain’s metabolic requirement)

Brain tissue oxygen tension monitoring (PbtO2)

  • General
    • ‘Gold standard’ bedside monitor of cerebral oxygenation
    • A biomarker of cellular function rather than simply a monitor of hypoxia/ ischaemia.
    • PbtO2 is affected by
      • Systemic blood pressure
      • PaO2
      • PaCO2
      • Haemoglobin concentration
  • Indications
    • The need for augmented hyperventilation (pCO2 = 20–25) to control ICP.
  • Monitored e.g. with Licox® probe.
  • Poor outcome (death)
    • Longer times of brain tissue oxygen tension (pBtO2) <15mm Hg
    • A brief drop of PbtO2 < 6.
    • Initial pBtO2 < 10mm Hg for >30 minutes
  • Probe placement:
    • TBI:
      • Placed in tissue immediately surrounding a hematoma or contusion to monitor ‘at risk’ brain regions
    • SAH: placed in vascular distributions at greatest risk of vasospasm
      • ACA (with ACA or a-comm aneurysm):
        • Standard frontal placement (≈ 2–3cm off midline on appropriate side)
      • MCA (with ICA or MCA aneurysm):
        • 4.5–5.5cm off midline
      • ACA-MCA watershed area:
        • 3cm lateral to midline
    • ICH: usually placed near the site of the hemorrhage
  • Effect of pBtO2 monitoring/intervention on outcome: no randomized studies
    • Normal:
      • 2.7 and 4.7 kPa (20– 35 mmHg),
    • Ischaemic threshold
      • 1.33– 2.0 kPa (10– 15 mmHg).
    • In TBI:
      • Goal was to maintain pBtO2 > 25mm Hg.
      • Adding pBtO2 monitoring resulted in improved outcome.
      • May have been result of increased attentiveness (“Hawthorne effect”)
    • In SAH:
      • A moving correlation coefficient (ORx) between CPP and pBtO2 was used to label high Orx (brain tissue oxygen pressure reactivity) as disturbed autoregulation, and this value on post SAH days 5 & 6 had predictive value for delayed infarction
  • Management suggestions for pBtO2 < 15–20mm Hg:
    • Consider jugular venous O2 saturation monitor or lactate microdialysis monitor for confirmation
    • Consider CBF study to determine generalizability of pBtO2 monitor reading
    • Treatment: proceed to each tier as needed
      • Tier 1
        • Keep body temperature < 37.5 C
        • Increase CPP to > 60mm Hg (use fluids preferentially to pressors until CVP>8cm H2O, then use pressors)
      • Tier 2
        • Increase FiO2 to 60%
        • Increase paCO2 to 45–50mm Hg
        • Transfuse PRBCs until Hgb> 10 g/dl
      • Tier 3
        • Increase FiO2 to 100%
        • Consider increasing PEEP to increase PaO2 if FiO2 is at 100%
        • Decrease ICP to <10mm Hg (drain CSF, mannitol, sedation…)
  • Evidence
    • Brain Tissue Oxygen Monitoring in Traumatic Brain Injury (BOOST2) study:
        • ICP + PBtO2 monitoring is superior than ICP monitoring in terms of GOS-E at 6 months
        • Awaiting BOOST 3 results
        ㅤ
        ICP < 20
        ICP ≥ 20
        pBtO₂ ≥ 20
        Type A
        No interventions directed at pBtO₂ or ICP needed
        Type B
        Interventions directed at lowering ICP
        pBtO₂ < 20
        Type C
        Interventions directed at increasing pBtO₂
        Type D
        Interventions directed at lowering ICP and increasing pBtO₂

Near infrared spectroscopy (NIRS)

  • Near infrared spectroscopy- based cerebral oximetry
  • Differential absorption and scatter of near-infrared light allow assessment of changes in the chromophores
    • Oxyhemoglobin (HbO2),
    • Deoxyhemoglobin (Hb),
    • Cytochrome oxidase.
  • Provides regional
    • Cerebral hemoglobin oxygen saturation,
    • Cerebral blood volume (CBV),
    • Cerebrovascular responses to therapeutic interventions
  • Advantage
    • Provides continuous and non- invasive monitoring of regional cerebral oxygen saturation (rScO2)
    • High temporal and spatial resolution,
    • The possibility simultaneous measurement over multiple regions of interest.
  • The ‘normal’ range of rScO2
    • 60– 75%
  • Disadvantage
    • Substantial intra- and interindividual variability,
    • rScO2 values are best used as a trend monitor.
    • There has been limited investigation of the utility of NIRS after TBI where its application is confounded by the optical complexity of the injured brain (Ghosh et al., 2012).