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Cerebral Autoregulation in the Prediction of Delayed Cerebral Ischemia and Clinical Outcome in Poor-Grade Aneurysmal Subarachnoid Hemorrhage Patients*

Gaasch, Max, MD1; Schiefecker, Alois J., MD, PhD1; Kofler, Mario, MD1; Beer, Ronny, MD1; Rass, Verena, MD1; Pfausler, Bettina, MD1; Thomé, Claudius, MD2; Schmutzhard, Erich, MD1; Helbok, Raimund, MD1

doi: 10.1097/CCM.0000000000003016
Neurologic Critical Care
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SDC

Objectives: Pressure reactivity index and oxygen reactivity index are used to assess cerebral autoregulation after acute brain injury. The value of autoregulation indices in the prediction of delayed cerebral ischemia and outcome in patients with subarachnoid hemorrhage is still inconclusive. In this study, we aimed to focus on the predictive value of the first 72 hours commonly referred to as “early brain injury” in comparison to the overall monitoring period.

Design: Retrospective observational cohort study.

Setting: Neurocritical care unit at a tertiary academic medical center.

Patients: Forty-three consecutive poor-grade patients with nontraumatic subarachnoid hemorrhage admitted between 2012 and 2016 undergoing continuous high-frequency monitoring.

Interventions: High-frequency monitoring includes arterial blood pressure, intracranial pressure, and brain tissue oxygen tension. Pressure reactivity index and oxygen reactivity index were evaluated as moving correlation coefficient between mean arterial pressure/intracranial pressure and cerebral perfusion pressure/brain tissue oxygen tension, respectively.

Measurements and Main Results: Median autoregulation monitoring time was 188 ± 91 hours per patient. Initial pressure reactivity index was 0.31 ± 0.02 and decreased significantly to 0.01 ± 0.01 (p < 0.001) 3 days after admission with a second peak 10 days after admission (0.18 ± 0.14; p = 0.001). Admission oxygen reactivity index was high, 0.25 ± 0.03, and decreased to a minimum of 0.11 ± 0.02 eight days after admission (p = 0.008). Patients with delayed cerebral ischemia had significantly higher overall mean pressure reactivity index values (p < 0.04), which were more pronounced during the first 72 hours, reflecting early brain injury (p < 0.02). High pressure reactivity index during the first 72 hours was associated with poor functional outcome (p < 0.001). No association between oxygen reactivity index and delayed cerebral ischemia or clinical outcome was observed (p = 0.8/0.78).

Conclusions: High initial pressure reactivity index, presumably reflecting early brain injury, but not oxygen reactivity index, was associated with delayed cerebral ischemia and worse clinical outcome in poor-grade subarachnoid hemorrhage patients. Our data indicate that autoregulation indices should be interpreted cautiously when used in these patients and that timing is crucial when autoregulation indices are evaluated as predictor for delayed cerebral ischemia and outcome.

1Neuro-Intensive Care Unit, Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria.

2Department of Neurosurgery, Medical University of Innsbruck, Innsbruck, Austria.

*See also p. 828.

Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal’s website (http://journals.lww.com/ccmjournal).

Supported, in part, by grants from Austrian Science Fund (FWF) under project number KLI375 (Austrian National Research and Planning Institute for Health Care/Federal Ministry of Health) (to Dr. Beer).

Drs. Gaasch, Beer, and Helbok received support for article research from the Austrian Science Fund (FWF). Dr. Beer’s institution received funding from FWF, and he received funding from Austrian National Research and Planning Institute for Health Care/Federal Ministry of Health. Dr. Thomé’s institution received funding from medical device companies unrelated to the work presented (DepuySynthes, Medtronic, Signus Medizintechnik, Tissue Engeneering Technologies AG, Intrinsic Therapeutics, and Edge Therapeutics), and he received funding from consultant and speakers honoraria from medical device companies unrelated to the work presented (Aesculap, AOSpine, DepuySynthes, Iconic, Medtronic, Signus Medizintechnik, TETEC, Intrinsic Therapeutics, Edge Therapeutics). The remaining authors have disclosed that they do not have any potential conflicts of interest.

For information regarding this article, E-mail: raimund.helbok@tirol-kliniken.at; raimund.helbok@i-med.ac.at

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