Elsevier

Resuscitation

Volume 83, Issue 7, July 2012, Pages 840-847
Resuscitation

Clinical Paper
The frequency and timing of epileptiform activity on continuous electroencephalogram in comatose post-cardiac arrest syndrome patients treated with therapeutic hypothermia,☆☆

https://doi.org/10.1016/j.resuscitation.2012.02.015Get rights and content

Abstract

Aim

The incidence and timing of electrographic seizures and epileptiform activity in comatose, adult, post-cardiac arrest syndrome (PCAS) patients treated with therapeutic hypothermia (TH) have not been extensively investigated. We hypothesized that onset most frequently occurs within the first 24 h post-arrest and is associated with poor neurologic outcome.

Methods

Single-center, retrospective analysis of a cohort of 38 comatose PCAS patients treated with TH and continuous-EEG-monitoring (cEEG), initiated as soon as possible after ICU admission. All raw cEEG waveform records were cleared of annotations and clinical information and classified by two fellowship-trained electroencephalographers.

Results

Twenty-three percent (9/38) of patients had electrographic seizures (median onset 19 h post-arrest); 5/9 (56%) had seizure-onset prior to rewarming; 7/9 (78%) had status epilepticus. Forty-five percent (17/38) had evidence of epileptiform activity (electrographic seizures or interictal epileptiform discharges), typically occurring during first 24 h post-arrest. Interictal epileptiform activity was highly associated with later detection of electrographic seizures (6/14, 43%, p = 0.001). Ninety-four percent (16/17) of patients with epileptiform activity had poor neurologic outcome or death at discharge (Cerebral Performance Category scale 3–5; p = 0.002) as did all (9/9) patients with electrographic seizures (p = 0.034).

Conclusions

Electrographic seizures and epileptiform activity are common cEEG findings in comatose, PCAS patients treated with TH. In this preliminary study, most seizures were status epilepticus, had onset prior to rewarming, evolved from prior interictal epileptiform activity, and were associated with short-term mortality and poor neurologic outcome. Larger, prospective studies are needed to further characterize seizure activity in comatose post-arrest patients.

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)

  • A. Hovland et al.

    EEG should be performed during induced hypothermia

    Resuscitation

    (2006)
  • E. Sagalyn et al.

    Therapeutic hypothermia after cardiac arrest in clinical practice: review and compilation of recent experiences

    Crit Care Med

    (2009)
  • J.P. Nolan 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)
  • S. Khot et al.

    Long-term neurological complications after hypoxic-ischemic encephalopathy

    Semin Neurol

    (2006)
  • N. Nielsen et al.

    Outcome, timing and adverse events in therapeutic hypothermia after out-of-hospital cardiac arrest

    Acta Anaesthesiol Scand

    (2009)
  • A. Krumholz et al.

    Outcome from coma after cardiopulmonary resuscitation: relation to seizures and myoclonus

    Neurology

    (1988)
  • E.F. Wijdicks 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)
  • N.S. Abend et al.

    Electroencephalographic monitoring during hypothermia after pediatric cardiac arrest

    Neurology

    (2009)
There are more references available in the full text version of this article.

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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).

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