Postanoxic electrographic status epilepticus and serum biomarkers of brain injury. (January 2021)

• Record Type: Journal Article
• Authors: Lybeck, Anna; Friberg, Hans; Nielsen, Niklas; Rundgren, Malin; Ullén, Susann; Zetterberg, Henrik; Blennow, Kaj; Cronberg, Tobias; Westhall, Erik
• Is Part Of: Resuscitation. Volume 158(2021)
• Page Start: 253
• Page End: 257
• Publication Date: 2021-01
• Subjects: CPC cerebral performance category -- EEG electroencephalography -- cEEG continuous electroencephalography monitoring -- GCS Glascow coma scale -- GFAP glial fibrillary acidic protein -- ICU intensive care unit -- NfL neurofilament light chain -- NSE neuron-specific enolase -- ROSC return of spontaneous circulation -- SSEP somatosensory evoked potentials -- TTM Target Temperature Management -- WLST withdrawal of life-sustaining treatments; Cardiac arrest -- EEG -- Seizures -- Electrographic status epilepticus -- Biomarkers; Resuscitation -- Periodicals; Resuscitation -- Periodicals; Réanimation -- Périodiques; Electronic journals; 616.025
• DOI: 10.1016/j.resuscitation.2020.10.027
• Languages: English
• ISSNs: 0300-9572

Abstract

Abstract: Aim: To explore if electrographic status epilepticus (ESE) after cardiac arrest causes additional secondary brain injury reflected by serum levels of two novel biomarkers of brain injury: neurofilament light chain (NfL) originating from neurons and glial fibrillary acidic protein (GFAP) from glial cells. Methods: Simplified continuous EEG (cEEG) and serum levels of NfL and GFAP, sampled at 24, 48 and 72 h after cardiac arrest, were collected during the Target Temperature Management (TTM)-trial. Two statistical methods were used: multivariable regresssion analysis; and a matched control group of patients without ESE matched for early predictors of poor neurological outcome. Results: 128 patients had available biomarkers and cEEG. Twenty-six (20%) patients developed ESE, the majority (69%) within 24 h. ESE was an independent predictor of elevated serum NfL (p < 0.001) but not of serum GFAP (p = 0.16) at 72 h after cardiac arrest. Compared to a control group matched for early predictors of poor neurological outcome, patients who developed ESE had higher levels of serum NfL (p = 0.03) and GFAP (p = 0.04) at 72 h after cardiac arrest. Conclusion: ESE after cardiac arrest is associated with higher levels of serum NfL which may suggest increased secondary neuronal injury compared to matched patients without ESE but similar initial brain injury. Associations with GFAP reflecting glial injury are less clear. The study design cannot exclude imperfect matching or other mechanisms of secondary brain injury contributing to the higher levels of biomarkers of brain injury seen in the patients with ESE.