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Published on: November 21, 2017
Neuron-Specific Enolase Predicts Poor Outcome After Cardiac Arrest and Targeted Temperature Management: A Multicenter
Kaspar Josche Streitberger1, Christoph Leithner, Michael Wattenberg
11Department of Neurology, Charité Universitätsmedizin Berlin, Berlin, Germany.2Department of Anesthesia, Surgical and Internal Intensive Care, Emergency Medical Services, Klinikum Links der Weser, Bremen, Germany.3Division of Intensive Care and Emergency Medicine, Department of Internal Medicine, Medical University, Innsbruck, Austria.4Department of Anesthesia, Intensive Care and Emergency Medical Service, Santa Maria degli Angeli Hospital, Pordenone, Italy.5Department of Anesthesia and Intensive and Emergency Care, Evangelisches Waldkrankenhaus, Bonn, Germany.6Department for Biostatistics, Coordination Center for Clinical Trials, Charité Universitätsmedizin Berlin, Berlin, Germany.7Department of Nephrology and Intensive Care Medicine, Charité Universitätsmedizin Berlin, Berlin, Germany.
Objective:
Outcome prediction after cardiac arrest is important to decide on continuation or withdrawal of intensive care. Neuron-specific enolase is an easily available, observer-independent prognostic biomarker. Recent studies have yielded conflicting results on its prognostic value after targeted temperature management.
Design, Setting, And Patients:
We analyzed neuron-specific enolase serum concentrations 3 days after nontraumatic in-hospital cardiac arrest and out-of-hospital cardiac arrest and outcome of patients from five hospitals in Germany, Austria, and Italy. Patients were treated at 33°C for 24 hours. Cerebral Performance Category was evaluated upon ICU discharge. We performed case reviews of good outcome patients with neuron-specific enolase greater than 90 μg/L and poor outcome patients with neuron-specific enolase less than or equal to 17 μg/L (upper limit of normal).
Measurements And Main Results:
A neuron-specific enolase serum concentration greater than 90 μg/L predicted Cerebral Performance Category 4-5 with a positive predictive value of 99%, false positive rate of 0.5%, and a sensitivity of 48%. All three patients with neuron-specific enolase greater than 90 μg/L and Cerebral Performance Category 1-2 had confounders for neuron-specific enolase elevation. An neuron-specific enolase serum concentration less than or equal to 17 μg/L excluded Cerebral Performance Category 4-5 with a negative predictive value of 92%. The majority of 14 patients with neuron-specific enolase less than or equal to 17 μg/L who died had a cause of death other than hypoxic-ischemic encephalopathy. Specificity and sensitivity for prediction of poor outcome were independent of age, sex, and initial rhythm but higher for out-of-hospital cardiac arrest than for in-hospital cardiac arrest patients.
Conclusion:
High neuron-specific enolase serum concentrations reliably predicted poor outcome at ICU discharge. Prediction accuracy differed and was better for out-of-hospital cardiac arrest than for in-hospital cardiac arrest patients. Our "in-the-field" data indicate 90 μg/L as a threshold associated with almost no false positives at acceptable sensitivity. Confounders of neuron-specific enolase elevation should be actively considered: neuron-specific enolase-producing tumors, acute brain diseases, and hemolysis. We strongly recommend routine hemolysis quantification. Neuron-specific enolase serum concentrations less than or equal to 17 μg/L argue against hypoxic-ischemic encephalopathy incompatible with reawakening.
