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Protocolized Brain Oxygen Optimization in Subarachnoid Hemorrhage.

Verena Rass1, Daria Solari2, Bogdan Ianosi1,3

  • 1Neurological Intensive Care Unit, Department of Neurology, Medical University of Innsbruck, Anichstrasse 35, 6020, Innsbruck, Austria.

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|June 21, 2019
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Summary
This summary is machine-generated.

Brain tissue hypoxia remains common in poor-grade subarachnoid hemorrhage (SAH) patients despite targeted therapy. Further optimization is needed to improve outcomes in these critical cases.

Keywords:
Aneurysmal subarachnoid hemorrhageBrainCritical careNeurology

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Area of Science:

  • Neuroscience
  • Critical Care Medicine
  • Neurology

Background:

  • Brain tissue hypoxia (PbtO2 < 20 mmHg) is frequent after subarachnoid hemorrhage (SAH) and linked to poor patient outcomes.
  • Previous studies in traumatic brain injury suggest brain oxygen optimization is feasible.
  • This study aimed to quantify brain tissue hypoxia in SAH patients despite a protocolized treatment approach.

Purpose of the Study:

  • To assess the incidence of brain tissue hypoxia in poor-grade SAH patients managed with a PbtO2-targeted protocol.
  • To identify concurrent pathological physiological values during hypoxic episodes.
  • To evaluate the effectiveness of a multimodal monitoring and treatment protocol.

Main Methods:

  • A bi-centric observational cohort study of 100 poor-grade SAH patients.
  • Multimodal brain monitoring including continuous PbtO2, cerebral perfusion pressure (CPP), and temperature.
  • Management involved a PbtO2-targeted protocol aiming for CPP ≥ 70 mmHg, normocapnia, normoxemia, normothermia, and adequate hemoglobin levels.
  • Data from blood gas analysis and cerebral microdialysis (CMD) were analyzed over the first 11 days.

Main Results:

  • Overall incidence of brain tissue hypoxia was 25% in poor-grade SAH patients.
  • Hypoxic episodes frequently coincided with low CPP (27%), hypocapnia (19%), low PaO2 (14%), low hemoglobin (11%), metabolic crisis (7%), and hyperthermia (4%).
  • No significant difference in hypoxia incidence was observed between the two centers despite treatment variations.

Conclusions:

  • Brain tissue hypoxia persists in a significant portion of poor-grade SAH patients even with a PbtO2-targeted therapy protocol.
  • The findings suggest that current therapeutic strategies for optimizing brain oxygenation in SAH may require further refinement.
  • Concurrent physiological derangements highlight the complexity of managing these critically ill patients.