Abstract

BackgroundCerebral hypoperfusion may aggravate neurological damage after cardiac arrest. Near-infrared spectroscopy (NIRS) provides information on cerebral oxygenation but its relevance during post-resuscitation care is undefined. We investigated whether cerebral oxygen saturation (rSO2) measured with NIRS correlates with the serum concentration of neuron-specific enolase (NSE), a marker of neurological injury, and with clinical outcome in out-of-hospital cardiac arrest (OHCA) patients.MethodsWe performed a post hoc analysis of a randomised clinical trial (COMACARE, NCT02698917) comparing two different levels of carbon dioxide, oxygen and arterial pressure after resuscitation from OHCA with ventricular fibrillation as the initial rhythm. We measured rSO2 in 118 OHCA patients with NIRS during the first 36 h of intensive care. We determined the NSE concentrations from serum samples at 48 h after cardiac arrest and assessed neurological outcome with the Cerebral Performance Category (CPC) scale at 6 months. We evaluated the association between rSO2 and serum NSE concentrations and the association between rSO2 and good (CPC 1–2) and poor (CPC 3–5) neurological outcome.ResultsThe median (inter-quartile range (IQR)) NSE concentration at 48 h was 17.5 (13.4–25.0) μg/l in patients with good neurological outcome and 35.2 (22.6–95.8) μg/l in those with poor outcome, p < 0.001. We found no significant correlation between median rSO2 and NSE at 48 h, rs = − 0.08, p = 0.392. The median (IQR) rSO2 during the first 36 h of intensive care was 70.0% (63.5–77.0%) in patients with good outcome and 71.8% (63.3–74.0%) in patients with poor outcome, p = 0.943. There was no significant association between rSO2 over time and neurological outcome. In a binary logistic regression model, rSO2 was not a statistically significant predictor of good neurological outcome (odds ratio 0.99, 95% confidence interval 0.94–1.04, p = 0.635).ConclusionsWe found no association between cerebral oxygenation measured with NIRS and NSE concentrations or outcome in patients resuscitated from OHCA.Trial registrationClinicalTrials.gov, NCT02698917. Registered on 26 January 2016.

Highlights

  • Cerebral hypoperfusion may aggravate neurological damage after cardiac arrest

  • 123 unconscious, mechanically ventilated patients resuscitated from witnessed of-hospital cardiac arrest (OHCA) with ventricular fibrillation (VF) or ventricular tachycardia (VT) as the initial rhythm were randomly assigned to one of eight arms with each arm having a different combination of targets for Arterial carbon dioxide tension (PaCO2), Arterial oxygen tension (PaO2) and mean arterial pressure (MAP)

  • We found no statistically significant correlation between median Regional cerebral oxygen saturation (rSO2) during the first 36 h in the intensive care unit (ICU) and serum neuron-specific enolase (NSE) concentration at 48 h after cardiac arrest (CA), rs = − 0.08, p = 0.392 (Fig. 2)

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Summary

Introduction

Cerebral hypoperfusion may aggravate neurological damage after cardiac arrest. Near-infrared spectroscopy (NIRS) provides information on cerebral oxygenation but its relevance during post-resuscitation care is undefined. We investigated whether cerebral oxygen saturation (rSO2) measured with NIRS correlates with the serum concentration of neuron-specific enolase (NSE), a marker of neurological injury, and with clinical outcome in out-of-hospital cardiac arrest (OHCA) patients. Cerebral hypoperfusion may lead to diminished cerebral oxygenation after initially successful resuscitation from cardiac arrest (CA). Near-infrared spectroscopy (NIRS) provides a non-invasive technique to assess cerebral oxygenation [2], and the changes in regional cerebral oxygen saturation (rSO2) are considered to reflect changes in the relationship between oxygen delivery and consumption in the brain [3]. An increasing body of evidence suggests that optimised cerebral oxygenation is associated with favourable neurologic outcome in a variety of perioperative settings [4]. The clinical relevance of NIRS during post-resuscitation care remains undefined

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