Clinical PaperThe frequency and timing of epileptiform activity on continuous electroencephalogram in comatose post-cardiac arrest syndrome patients treated with therapeutic hypothermia☆,☆☆
Introduction
Cardiac arrest results in a high rate of mortality and neurologic morbidity. Historically, mortality for comatose, post-cardiac arrest syndrome (PCAS) patients has ranged from 30% to 69%1 and a substantial proportion regaining consciousness have significant neurologic deficits.1, 2, 3 Therapeutic hypothermia (TH) is the only intervention demonstrated to significantly improve neurologic morbidity and mortality in comatose ventricular fibrillation (VF) patients, and is now considered standard of care.1, 4
Seizures are common after cardiac arrest. It remains unclear whether they contribute to poor neurologic outcomes or are simply a marker of an irreversibly damaged brain. Acute seizures occur in between 15% and 44% of post-arrest patients.3 They often occur as status epilepticus, which is frequently nonconvulsive, difficult to control, and associated with higher rates of morbidity and mortality.5 An American Academy of Neurology practice parameter examining pre-TH data reached the conclusion that the clinical diagnosis of myoclonus status epilepticus (MSE) during the first 24 h post-arrest is a predictor of poor outcome with a very low false positive rate.6
Recent studies examining electrographic seizures in PCAS patients treated with TH have yielded similar results.7 However, cases of recovery after MSE have been documented.8, 9 Continuous-EEG (cEEG) monitoring has been recommended for comatose PCAS patients treated with TH.10 However, cEEG-monitoring is resource-demanding and is not available at all institutions performing TH. Identification of the timing of seizures and other epileptiform patterns and associated outcomes might help optimize cEEG use. We hypothesized that a substantial number of comatose PCAS patients treated with TH have epileptiform cEEG patterns (i.e. seizure patterns or interictal epileptiform discharges) in the first 24 h post-arrest and that these cEEG findings are associated with poor outcomes. Our objectives were to determine the incidence and timing of epileptiform activity and electrographic seizures and demonstrate their association with poor short-term neurologic outcomes.
Section snippets
Methods
After obtaining IRB approval, we utilized a pre-existing cardiac arrest database to identify consecutive, comatose, adult (>18-years-old), PCAS patients treated with TH and monitored with cEEG or frequent routine EEGs, between 5/1/2005 and 1/1/2009 at the Hospital of the University of Pennsylvania (HUP) in Philadelphia, PA. Therapeutic hypothermia was induced with infusion of two liters of 4 °C normal saline solution via peripheral intravenous (IV) catheters, ice bags, and water-filled surface
Results
Between 5/1/2005 and 1//1/2009, 41 consecutive comatose PCAS patients were treated with TH at our hospital. Thirty-six patients had cEEG monitoring and two patients had frequent routine EEGs. In three patients only one routine EEG was obtained and they were excluded from further analysis. Therefore, a cohort of 38 patients was included in the analysis.
Discussion
In a cohort of 38 consecutive comatose PCAS patients treated with TH and monitored with cEEG or frequent routine EEGs, we found that interictal and ictal epileptiform activity are fairly common (17/38 [45%] and 9/38 [23%] respectively). Nearly all of the epileptiform activity had onset detected within 24 h post-arrest. Interictal epileptiform discharges are associated with evolution to electrographic seizures, and the majority of the electrographic seizures have onsets resembling generalized
Conclusion
In this preliminary study, electrographic seizures and epileptiform activity were common cEEG findings in comatose, PCAS patients treated with TH. Onset of these patterns was, in general, during the first 24–48 h post-arrest for patients monitored with cEEG for 2–3 days. Most seizures had onset prior to rewarming, were associated with prior interictal epileptiform activity, manifest as status epilepticus, and were associated with short-term mortality and poor neurologic outcome despite multiple
Conflict of interest statement
None.
Acknowledgements
The authors thank the HUP EEG technologists for acquiring EEG data and extend special thanks to Ben Ninan for preparing the EEG data. The authors also thank Lawrence J. Hirsch (New York, NY) for his constructive feedback regarding early drafts of the manuscript.
References (16)
- et al.
EEG should be performed during induced hypothermia
Resuscitation
(2006) - et al.
Therapeutic hypothermia after cardiac arrest in clinical practice: review and compilation of recent experiences
Crit Care Med
(2009) - et al.
Therapeutic hypothermia after cardiac arrest: an advisory statement by the advanced life support task force of the International Liaison Committee on Resuscitation
Circulation
(2003) - et al.
Long-term neurological complications after hypoxic-ischemic encephalopathy
Semin Neurol
(2006) - et al.
Outcome, timing and adverse events in therapeutic hypothermia after out-of-hospital cardiac arrest
Acta Anaesthesiol Scand
(2009) - et al.
Outcome from coma after cardiopulmonary resuscitation: relation to seizures and myoclonus
Neurology
(1988) - et al.
Practice parameter: prediction of outcome in comatose survivors after cardiopulmonary resuscitation (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology
Neurology
(2006) - et al.
Electroencephalographic monitoring during hypothermia after pediatric cardiac arrest
Neurology
(2009)
Cited by (118)
Neuroprognostication in the Post Cardiac Arrest Patient: A Canadian Cardiovascular Society Position Statement
2023, Canadian Journal of CardiologyEpileptiform patterns predicting unfavorable outcome in postanoxic patients: A matter of time?
2023, Neurophysiologie CliniqueElectrographic Seizures in the Critically Ill
2022, Neurologic ClinicsEEG patterns and their correlations with short- and long-term mortality in patients with hypoxic encephalopathy
2021, Clinical Neurophysiology
- ☆
A Spanish translated version of the abstract of this article appears as Appendix in the final online version at doi:10.1016/j.resuscitation.2012.02.015.
- ☆☆
Study funding: This study was funded by training grant NRSA T32 NS061779-01 (RM).