Article Text
Abstract
Background: More than 50% of patients initially resuscitated from out-of-hospital cardiac arrest die in hospital.
Objective: To investigate the prognostic value of serum protein S-100 and neuron-specific enolase (NSE) concentrations for predicting (a) memory impairment at discharge; (b) in-hospital death, after resuscitation from out-of-hospital cardiac arrest.
Methods: In a prospective study of 143 consecutive survivors of out-of-hospital cardiac arrest, serum samples were obtained within 12, 24–48 and 72–96 hours after the event. S-100 and NSE concentrations were measured. Pre-discharge cognitive assessment of patients (n = 49) was obtained by the Rivermead Behavioural Memory Test (RBMT). The relationship between biochemical brain marker concentrations and RBMT scores, and between marker concentrations and the risk of in-hospital death was examined.
Results: A moderate negative relationship was found between S-100 concentration and memory test score, at all time points. The relationship between NSE and memory test scores was weaker. An S-100 concentration >0.29 μg/l at time B predicted moderate to severe memory impairment with absolute specificity (42.8% sensitivity). S-100 remained an independent predictor of memory function after adjustment for clinical variables and cardiac arrest timing indices. NSE and S-100 concentrations were greater in patients who died than in those who survived, at all time points. Both NSE and S-100 remained predictors of in-hospital death after adjustment for clinical variables and cardiac arrest timing indices. The threshold concentrations yielding 100% specificity for in-hospital death were S-100: 1.20 μg/l (sensitivity 44.8%); NSE 71.0 μg/l (sensitivity 14.0%).
Conclusions: Estimation of serum S-100 concentration after out-of-hospital cardiac arrest can be used to identify patients at risk of significant cognitive impairment at discharge. Serum S-100 and NSE concentrations measured 24–48 hours after cardiac arrest provide useful additional information.
- cardiac arrest
- hypoxia–ischaemia (brain)
- cognitive function