Neurosurgery notes/Trauma/Management of trauma/Non surgical/PaO2 and PbtO2

PaO2 and PbtO2

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Non surgical

General

  • Monitor oxygenation and avoid hypoxia (PaO2 < 60mm Hg or O2 saturation < 90%)
  • Hypoxia (apnea or cyanosis in the field, or PaO2 < 60mm Hg on ABG) also increases mortality
  • Hypoxia + Hypotension triples mortality

Hypoxaemia

  • McHugh et al., 2007: A single episode of hypoxaemia (PaO2 <8 kPa or SpO2 <90%) or hypotension (systolic BP <90 mmHg) is strongly associated with poorer outcomes after severe TBI, and the combination of the two is more deleterious than either insult alone
  • Therapeutic hyperoxia
    • Is associated with adverse effects, including
      • Free radical formation
      • Pulmonary injury,
    • Normobaric hyperoxia does not result in clinically significant improvements in brain oxygen metabolism
    • Some evidence that hyperbaric oxygen reduces mortality, there is little evidence of improved functional outcome in survivors (Bennett et al., 2012).

Why can we not give all patient high FiO2=1.0 O2

  • Hyperoxia
    • Is known to induce cerebral vasoconstriction
    • Potentially increase free radical production
    • Associated with worse outcome in other brain ischaemic injuries.

Evidence

  • BOOTS 3 trial still awaiting
  • BOOST 2 trial (is not designed to test for clinical outcomes but 2ndary results showed there is mortality and GOS-E benefits to allow for a phase 3 trial.
      • Primary outcome:
        • Tiered management for episodes of PbtO2<20mmHg resulted in significantly less brain tissue hypoxia in the ICP+PbtO2 group than the ICP group.
      • Secondary outcome:
       
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  • OXY-TC n= 318 ICP vs ICP + PbtO2 for adults with non penetrating severe head injury
    • ICP + PbtO2 did not reduce the proportion of patients with GOSE score 1–4
      • ICP + PbtO2=51%
      • ICP = 52%
    • ICP + PbtO2 had greater complications
      • ICP + PbtO2 = 4%
      • ICP = 0%
    • No difference in mortality rate in both 24% at 12 months
    • Critique by Chestnut
      • We have not select patients that truly require brain oxygen monitoring so the beneficial effects of brain oxygen monitoring is loss as the percentage that requires it very small

SIBICC 2

See Chesnut 2020
This matrix provides the schema for the 4 clinical conditions encountered in patients with both ICP and brain oxygen monitors in situ. Type A reflects normal values for both monitors and does not require treatment. Type B involves ICP elevation but normal brain oxygen values; we propose a distinct treatment algorithm for such patients than in those with ICP elevation and unknown PbtO2 values. Type C patients have hypoxic brains but normal ICP and Type D patients have both brain hypoxia and ICP elevation. An ICP of 22 mmHg discriminates normal (lower) and abnormal (higher) values while PbtO2 values of 20 mmHg discriminates normal (higher) and abnormal (lower) values. ICP intracranial pressure, PbtO2 partial pressure of brain oxygen
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I have evolved to PbtO2 focused care

  • It is usually the last monitor to optimized
  • A better surrogate measure of brain health than ICP (in my opinion)
  • Encouraging preliminary data (BOOST II)
  • Brain hypoxia drives ICP elevation
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