Abstract
This study aimed to determine the prognostic ability of serial neuron-specific enolase (NSE) and lactate in cardiac arrest survivors treated with targeted temperature management (TTM) and to investigate whether a combination of NSE and lactate could increase prognostic information. This observational, retrospective, cohort study was conducted between January 2013 and December 2018; data were extracted from an out-of-hospital cardiac arrest registry. We collected serial serum NSE and lactate levels during TTM. The primary endpoint was poor neurological outcome at 28 days from cardiac arrest. Of all 160 included patients, 98 (61.3%) had poor neurological outcomes. Areas under the curves (AUCs) for NSE were 0.797, 0.871, and 0.843 at 24, 48, and 72 h, respectively (all p < 0.05). AUCs for lactate were 0.669, 0.578, 0.634, and 0.620 at 0, 24, 48, and 72 h, respectively (all p < 0.05). Although the combination of initial lactate and NSE at 48 h yielded the highest discovered AUC (0.877) it was not statistically different from that for the 48 h NSE alone (p = 0.692). During the TTM, NSE at 48 h from cardiac arrest was the most robust prognostic marker in comatose cardiac arrest survivors. However, a combination of the 48 h NSE with lactate did not increase the prognostic information.
Highlights
Prediction of neurological outcomes after cardiac arrest is critical since we have to distinguish late awakening from irreversible brain damage
Data were extracted from the out-of-hospital cardiac arrest (OHCA) registry, which prospectively collected data for consecutive, comatose survivors of non-traumatic OHCA, who were treated with temperature management (TTM) between January 2013 and December 2018
The univariate analysis for the prediction of 28-day poor neurological outcomes associated with each optimal cut-off value was OR 121.8 for a 48 h neuron-specific enolase (NSE) of 83 ng/ml; OR 3.1 for an initial lactate value of 10 mmol/L; and OR 127.8 for a 48 h NSE + an initial lactate value of 94
Summary
Prediction of neurological outcomes after cardiac arrest is critical since we have to distinguish late awakening from irreversible brain damage. In the era of targeted temperature management (TTM), we should carefully assess the potential for improved neurological outcomes. There is no single test to reliably predict an outcome; a multimodal diagnostic approach is currently used to minimize prognostic uncertainty [1]. To predict a neurological outcome, various tests have been conducted in cardiac arrest survivors. Neurological examinations, imaging tests, neurophysiologic studies, and specific biomarkers such as neuron-specific enolase (NSE) or lactate have been used [2,3,4]. As biomarkers are relatively applied and are not affected by post-cardiac arrest care such as TTM, their importance has increased
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