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This study aimed to investigate the efficacy of the combination of neuron-specific enolase (NSE) measurement and initial neurological examination in predicting the neurological outcomes of patients with cardiac arrest (CA) by retrospectively analyzing data from the Korean Hypothermia Network prospective registry. NSE levels were recorded at 48 and 72 h after CA. The initial Full Outline of UnResponsiveness (FOUR) and Glasgow Coma Scale (GCS) scores were recorded. These variables were categorized using the scorecard method. The primary endpoint was poor neurological outcomes at 6 months. Of the 475 patients, 171 (36%) had good neurological outcomes at 6 months. The areas under the curve (AUCs) of the categorized NSE levels at 72 h, GCS score, and FOUR score were 0.889, 0.722, and 0.779, respectively. The AUCs of the combinations of categorized NSE levels at 72 h with categorized GCS scores and FOUR score were 0.910 and 0.912, respectively. Each combination was significantly higher than the AUC value of the categorized NSE level at 72 h alone (with GCS: p = 0.015; with FOUR: p = 0.026). Combining NSE measurement and initial neurological examination improved the prediction of neurological outcomes.

Background Measurement of serum neuron-specific enolase (NSE) for neuro-prognostication post out-of-hospital cardiac arrest (OHCA) is recommended by international guidelines. There is, however, a lack of consensus regarding the cut-offs and time points to use. In addition, NSE is particularly susceptible to haemolysis interference. This study aimed to define the optimum NSE testing strategy to support the intensive care unit (ICU). Methods Patients admitted to ICU post-OHCA over 16 months had NSE measured. The outcome was survival to ICU discharge. NSE at 0 h, 24 h, 48 h, 72 h and change in NSE (ΔNSE) were assessed for prognostic accuracy using receiver operator characteristic curve analysis. The magnitude of haemolysis interference was quantified by spiking haemolysate into paired serum. Results There is a consistent linear increase in NSE with increasing haemolysis, independent of baseline NSE concentration. A haemolysis index acceptance threshold was defined as 20. There were 142 patients, and 82 survived to ICU discharge. The NSE parameter with best predictive performance was ΔNSE at 48 h, which had an area under the receiver operator characteristic curve of 0.91. A cut-off of >0 μg/L at this time point had sensitivity of 80% and specificity of 97% for predicting death on ICU. When patients who died of non-neurological causes were removed, the sensitivity increased to 91%. Conclusions Application of a stringent haemolysis interference threshold and measurement of NSE at two time points enabled us to achieve excellent discrimination. Increasing NSE over the first 48 h, suggestive of an ongoing reperfusion injury to the brain, is a strong predictor of poor outcome.

As a specific biomarker in neonatal hypoxic-ischemic encephalopathy (HIE), the measurement of neuron-specific enolase (NSE) has been advocated as a predictor of outcome in neurological injury. However, the measured levels of NSE may be influenced by hemolysis. In the current study, the change in the concentration of NSE in serum was measured by chemiluminescence prior to and following the addition of individual frozen and thawed red blood cells from 86 neonates that were collected within 24 h of birth. The changes in the concentration of NSE were compared with the changes in the concentration of hemoglobin (Hb), measured by the hemoglobin cyanide (HiCN) method, to establish a correction formula. The performance of the correction formula was evaluated by comparing the corrected concentration of NSE using the individual constants and the correction formula. The average individual constant of NSE from the 86 hemolyzed neonatal serum samples was 25.15±3.94 mg/g Hb. The concentration variation between NSE and Hb in neonatal sera could be described by the equation ΔNSEserum=1.8594+24.0670 xΔHbHiCN (r2=0.8045, P