Abstract
BackgroundThe aim of this study was to elucidate the possible role of cerebral saturation monitoring in the post-cardiac arrest setting.MethodsCerebral tissue saturation (SctO2) was measured in 107 successfully resuscitated out-of-hospital cardiac arrest patients for 48 hours between 2011 and 2015. All patients were treated with targeted temperature management, 24 hours at 33 °C and rewarming at 0.3 °C per hour. A threshold analysis was performed as well as a linear mixed models analysis for continuous SctO2 data to compare the relation between SctO2 and favorable (cerebral performance category (CPC) 1–2) and unfavorable outcome (CPC 3–4–5) at 180 days post-cardiac arrest in OHCA patients.ResultsOf the 107 patients, 50 (47 %) had a favorable neurological outcome at 180 days post-cardiac arrest. Mean SctO2 over 48 hours was 68 % ± 4 in patients with a favorable outcome compared to 66 % ± 5 for patients with an unfavorable outcome (p = 0.035). No reliable SctO2 threshold was able to predict favorable neurological outcome. A significant different course of SctO2 was observed, represented by a logarithmic and linear course of SctO2 in patients with favorable outcome and unfavorable outcome, respectively (p < 0.001). During the rewarming phase, significant higher SctO2 values were observed in patients with a favorable neurological outcome (p = 0.046).ConclusionsThis study represents the largest post-resuscitation cohort evaluated using NIRS technology, including a sizeable cohort of balloon-assisted patients. Although a significant difference was observed in the overall course of SctO2 between OHCA patients with a favorable and unfavorable outcome, the margin was too small to likely represent functional outcome differentiation based on SctO2 alone. As such, these results given such methodology as performed in this study suggest that NIRS is insufficient by itself to serve in outcome prognostication, but there may remain benefit when incorporated into a multi-neuromonitoring bedside assessment algorithm.
Highlights
The aim of this study was to elucidate the possible role of cerebral saturation monitoring in the post-cardiac arrest setting
This may be explained by the fact that the brain of an of-hospital cardiac arrest (OHCA) patient is subjected to a sequence of pathophysiological changes during the arrest itself, and during the return of spontaneous circulation (ROSC) and in the post-resuscitation phase
One hundred and seven consecutive OHCA patients were included in this study
Summary
The aim of this study was to elucidate the possible role of cerebral saturation monitoring in the post-cardiac arrest setting. Almost 70 % of patients who die during their hospital stay after out-of-hospital cardiac arrest (OHCA) decease due to post-anoxic neurological injury [1]. After ROSC is achieved a post-CA syndrome develops, which is characterized by a short-lasting cerebral hyperemia followed by an increase in cerebrovascular resistance resulting in a decrease in cerebral blood flow (CBF) [2]. During this post-CA phase, there is an imbalance between oxygen delivery relative to oxygen requirements, which can last for several hours to days. Far, targeted temperature management (TTM) is the only treatment with proven efficacy on neurological outcome after OHCA [3, 4]
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