To characterize the pattern of serum biochemical markers of central nervous system injury (neuron-specific enolase [NSE], S-100B, plasminogen activator inhibitor-1 [PAI-1]) after pediatric cardiac arrest and determine whether there is an association between biomarker concentrations and neurologic outcome.
Prospective, observational study.
Urban, tertiary care children's hospital.
Cardiac arrest survivors, n = 35.
Serial blood sampling, pediatric cerebral performance category, and standardized neurologic examination.
Serial serum NSE and S-100B concentrations over 96 hrs and PAI-1 at 24 hrs were measured in children (age <18 yrs) who had return of spontaneous circulation following cardiac arrest. Neurologic outcome was prospectively categorized as poor if the change in pre- to postarrest pediatric cerebral performance category was ≥2. Biomarker concentrations were compared between outcome groups and between survival groups using longitudinal analysis correcting for multiple comparisons. Median levels (25th, 75th percentiles) are reported. Receiver operating characteristic analyses were performed at all time points. Biomarker concentrations showed statistically significant differences. Of the 35 patients, neurologic outcomes were poor in 19, with 15 deaths. Median NSE concentrations differed by outcome when measured at ≥48 hrs, and by survival at ≥24 hrs. S-100B concentrations were not significantly associated with neurologic outcome. S-100B levels were associated with survival outcome at ≥48 hrs. PAI-1 levels were not significantly associated with either neurologic or survival outcomes.
The timing, intensity, and duration of serum NSE and S-100B biomarker concentration patterns are associated with neurologic and survival outcomes following pediatric cardiac arrest. Serum NSE concentrations at ≥48 hrs are associated with neurologic outcome, whereas serum S-100B levels at ≥48 hrs are associated with survival. Prospective analysis of these markers may help to predict outcomes and guide postresuscitative therapies.
From the Departments of Anesthesiology and Critical Care Medicine (AAT, RL, MAH, VN), and Neurology (RI), The Children's Hospital of Philadelphia, Philadelphia, PA; Department of Pediatrics (MCM), The Children's Hospital of New York-Presbyterian, New York, NY; Clinical Laboratory (HD), The Children's Hospital of Philadelphia, Philadelphia, PA; and Department of Pediatrics (CRB), The Center of Excellence for Sexual Health, Morehouse School of Medicine, Atlanta, GA.
Supported, in part, by Endowed Chair of Pediatric Critical Care Medicine and CTRC grant MO1-RR00240.
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