Neurocrit Care (2015) 22:165–172 DOI 10.1007/s12028-014-0018-4
REVIEW ARTICLE
Electroencephalography in Survivors of Cardiac Arrest: Comparing Pre- and Post-therapeutic Hypothermia Eras Amy Z. Crepeau • Jeffrey W. Britton • Jennifer E. Fugate • Alejandro A. Rabinstein Eelco F. Wijdicks
•
Published online: 17 July 2014 Ó Springer Science+Business Media New York 2014
Abstract Electroencephalography in the setting of hypothermia and anoxia has been studied in humans since the 1950s. Specific patterns after cardiac arrest have been associated with prognosis since the 1960s, with several prognostic rating scales developed in the second half of the twentieth century. In 2002, two pivotal clinical trials were published, demonstrating improved neurologic outcomes in patients treated with therapeutic hypothermia (TH) after cardiac arrest of shockable rhythms. In the following years, TH became the standard of care in these patients. During the same time period, the use of continuous EEG monitoring in critically ill patients increased, which led to the recognition of subclinical seizures occurring in patients after cardiac arrest. As a result of these changes, greater amounts of EEG data are being collected, and the significance of specific patterns is being re-explored. We review the current role of EEG for the identification of seizures and the estimation of prognosis after cardiac resuscitation.
A. Z. Crepeau (&) Division of Epilepsy, Department of Neurology, Mayo Clinic Arizona, 5777 East Mayo Boulevard, Phoenix, AZ 85054, USA e-mail: [email protected] J. W. Britton J. E. Fugate A. A. Rabinstein E. F. Wijdicks Department of Neurology, Mayo Clinic, 200 First Street SW, Rochester, MN 55901, USA J. W. Britton Division of Epilepsy, Mayo Clinic, 200 First Street SW, Rochester, MN 55901, USA J. E. Fugate A. A. Rabinstein E. F. Wijdicks Division of Neurocritical Care, Mayo Clinic, 200 First Street SW, Rochester, MN 55901, USA
Keywords Cardiac arrest Therapeutic hypothermia Prognosis EEG Clinical neurophysiology
Introduction Sudden cardiac arrest is a common condition with an incidence between 0.04 and 0.13 % of the population in industrialized countries [1, 2]. Mortality is extremely high, with an estimated mortality assessed by EMS response of approximately 94 % [3]. Of those patients that are successfully resuscitated, in-hospital mortality remains high at 60 % [4]. For patients who remain comatose after cardiopulmonary resuscitation, physicians—and in particular neurologists and neurointensivists—use a number of tools to prognosticate. Outcome after out-of hospital cardiac arrest is generally poor but not in survivors and there is an obligation to identify patients who may have a ‘‘fighting chance’’, patients with ‘‘no hope for recovery’’ and to best narrow down the category of patients with a clinical course that is too difficult to predict. Since the 1950s—before the era of modern neuroimaging—EEG has provided valuable data to predict neurologic outcome. When the earlier literature was thoroughly reviewed, some flaws in predictive ability became apparent, but these studies are the foundation upon which much has been learned regarding EEG after cardiac arrest [5, 6]. The utility of EEG in post-arrest coma was challenged after the emergence of better clinical data and neuroimaging. In parallel, the number of publications on the value of EEG dropped precipitously. Additional modalities, including imaging, evoked potentials, and serum markers of neuronal injury, showed value in providing prognostic information, in addition to EEG. However, in recent years,
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there has been renewed interest in EEG findings after cardiac arrest, largely due to increased utilization of prolonged EEG monitoring in the ICU. As more data emerge, it is challenging to determine how these findings fit with earlier findings, before regular use of therapeutic hypothermia (TH) and early, continuous EEG monitoring (cEEG).
First Descriptions of EEG After Cardiac Arrest Experimental studies demonstrating the effect of anoxia on EEG patterns in animals date back to the late 1930s. However, data regarding the application of EEG to the study of patients with anoxic encephalopathy did not appear in the literature until the 1950s. Early descriptions of EEG in cardiac arrest emerged from surgeries with intraoperative circulatory arrest and patients that were successfully resuscitated after cardiac arrest. Consistent EEG changes with anoxia were described by Pampiglione in 1960 based on EEG findings observed during intraoperative cardioplegia and following spontaneous cardiac arrest. In these studies, Pampiglione described diffuse slowing followed by suppression and return of cerebral activity upon restoration of cerebral circulation [7]. These findings were confirmed and expanded upon by his contemporary physiologists. Electrographic seizures and epileptiform activity after anoxia were recognized early on. Action myoclonus after cardiac arrest was reported by Lance and Adams in 1963. They described action or intention myoclonus after cardiac arrest, which could occur with or without EEG correlate [8]. In 1970, Madison and Niedermeyer described a series of patients after cardiac arrest with myoclonic and tonic-clonic seizures and consistently associated seizure discharges [9]. These early studies showed that patients were at high risk for seizures after cardiac arrest. As EEG was used more frequently, certain characteristically abnormal patterns were recognized. In 1975, an EEG background of ‘‘alpha-like rhythm’’ was described in 12 comatose patients after cardiac arrest [10]. Westmoreland et al. [11] described 5 patients with anoxic injury with this ‘alpha coma’, all of whom had poor outcomes, suggesting this pattern was a poor prognostic sign. Sorensen subsequently compared two groups of patients in coma after cardiac arrest: patients with the alpha coma EEG pattern and those without. There was no difference in outcomes between the two groups, though both groups overall did poorly [12]. From early on, it was appreciated that anoxia fundamentally changed the EEG and cerebral electrical activity.
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Neurocrit Care (2015) 22:165–172
Hypothermia and Its Effect on EEG Descriptions of EEG findings during hypothermia eventually emerged following the inception of use of hypothermia and cardiac by-pass in cardiac surgery. Human data largely have been gathered in the context of surgery with circulatory arrest and varying degrees of induced hypothermia. Large series of intraoperative studies go back to the 1950s. Pearcy and Virtue described 108 patients undergoing cardiac surgery with hypothermia in 1959. With induction of hypothermia, they noted a decrease in the amplitude and frequency of the EEG. These patients also underwent occlusion of cerebral circulation as part of surgery, and interestingly, those patients with lower core temperatures (
REVIEW ARTICLE
Electroencephalography in Survivors of Cardiac Arrest: Comparing Pre- and Post-therapeutic Hypothermia Eras Amy Z. Crepeau • Jeffrey W. Britton • Jennifer E. Fugate • Alejandro A. Rabinstein Eelco F. Wijdicks
•
Published online: 17 July 2014 Ó Springer Science+Business Media New York 2014
Abstract Electroencephalography in the setting of hypothermia and anoxia has been studied in humans since the 1950s. Specific patterns after cardiac arrest have been associated with prognosis since the 1960s, with several prognostic rating scales developed in the second half of the twentieth century. In 2002, two pivotal clinical trials were published, demonstrating improved neurologic outcomes in patients treated with therapeutic hypothermia (TH) after cardiac arrest of shockable rhythms. In the following years, TH became the standard of care in these patients. During the same time period, the use of continuous EEG monitoring in critically ill patients increased, which led to the recognition of subclinical seizures occurring in patients after cardiac arrest. As a result of these changes, greater amounts of EEG data are being collected, and the significance of specific patterns is being re-explored. We review the current role of EEG for the identification of seizures and the estimation of prognosis after cardiac resuscitation.
A. Z. Crepeau (&) Division of Epilepsy, Department of Neurology, Mayo Clinic Arizona, 5777 East Mayo Boulevard, Phoenix, AZ 85054, USA e-mail: [email protected] J. W. Britton J. E. Fugate A. A. Rabinstein E. F. Wijdicks Department of Neurology, Mayo Clinic, 200 First Street SW, Rochester, MN 55901, USA J. W. Britton Division of Epilepsy, Mayo Clinic, 200 First Street SW, Rochester, MN 55901, USA J. E. Fugate A. A. Rabinstein E. F. Wijdicks Division of Neurocritical Care, Mayo Clinic, 200 First Street SW, Rochester, MN 55901, USA
Keywords Cardiac arrest Therapeutic hypothermia Prognosis EEG Clinical neurophysiology
Introduction Sudden cardiac arrest is a common condition with an incidence between 0.04 and 0.13 % of the population in industrialized countries [1, 2]. Mortality is extremely high, with an estimated mortality assessed by EMS response of approximately 94 % [3]. Of those patients that are successfully resuscitated, in-hospital mortality remains high at 60 % [4]. For patients who remain comatose after cardiopulmonary resuscitation, physicians—and in particular neurologists and neurointensivists—use a number of tools to prognosticate. Outcome after out-of hospital cardiac arrest is generally poor but not in survivors and there is an obligation to identify patients who may have a ‘‘fighting chance’’, patients with ‘‘no hope for recovery’’ and to best narrow down the category of patients with a clinical course that is too difficult to predict. Since the 1950s—before the era of modern neuroimaging—EEG has provided valuable data to predict neurologic outcome. When the earlier literature was thoroughly reviewed, some flaws in predictive ability became apparent, but these studies are the foundation upon which much has been learned regarding EEG after cardiac arrest [5, 6]. The utility of EEG in post-arrest coma was challenged after the emergence of better clinical data and neuroimaging. In parallel, the number of publications on the value of EEG dropped precipitously. Additional modalities, including imaging, evoked potentials, and serum markers of neuronal injury, showed value in providing prognostic information, in addition to EEG. However, in recent years,
123
166
there has been renewed interest in EEG findings after cardiac arrest, largely due to increased utilization of prolonged EEG monitoring in the ICU. As more data emerge, it is challenging to determine how these findings fit with earlier findings, before regular use of therapeutic hypothermia (TH) and early, continuous EEG monitoring (cEEG).
First Descriptions of EEG After Cardiac Arrest Experimental studies demonstrating the effect of anoxia on EEG patterns in animals date back to the late 1930s. However, data regarding the application of EEG to the study of patients with anoxic encephalopathy did not appear in the literature until the 1950s. Early descriptions of EEG in cardiac arrest emerged from surgeries with intraoperative circulatory arrest and patients that were successfully resuscitated after cardiac arrest. Consistent EEG changes with anoxia were described by Pampiglione in 1960 based on EEG findings observed during intraoperative cardioplegia and following spontaneous cardiac arrest. In these studies, Pampiglione described diffuse slowing followed by suppression and return of cerebral activity upon restoration of cerebral circulation [7]. These findings were confirmed and expanded upon by his contemporary physiologists. Electrographic seizures and epileptiform activity after anoxia were recognized early on. Action myoclonus after cardiac arrest was reported by Lance and Adams in 1963. They described action or intention myoclonus after cardiac arrest, which could occur with or without EEG correlate [8]. In 1970, Madison and Niedermeyer described a series of patients after cardiac arrest with myoclonic and tonic-clonic seizures and consistently associated seizure discharges [9]. These early studies showed that patients were at high risk for seizures after cardiac arrest. As EEG was used more frequently, certain characteristically abnormal patterns were recognized. In 1975, an EEG background of ‘‘alpha-like rhythm’’ was described in 12 comatose patients after cardiac arrest [10]. Westmoreland et al. [11] described 5 patients with anoxic injury with this ‘alpha coma’, all of whom had poor outcomes, suggesting this pattern was a poor prognostic sign. Sorensen subsequently compared two groups of patients in coma after cardiac arrest: patients with the alpha coma EEG pattern and those without. There was no difference in outcomes between the two groups, though both groups overall did poorly [12]. From early on, it was appreciated that anoxia fundamentally changed the EEG and cerebral electrical activity.
123
Neurocrit Care (2015) 22:165–172
Hypothermia and Its Effect on EEG Descriptions of EEG findings during hypothermia eventually emerged following the inception of use of hypothermia and cardiac by-pass in cardiac surgery. Human data largely have been gathered in the context of surgery with circulatory arrest and varying degrees of induced hypothermia. Large series of intraoperative studies go back to the 1950s. Pearcy and Virtue described 108 patients undergoing cardiac surgery with hypothermia in 1959. With induction of hypothermia, they noted a decrease in the amplitude and frequency of the EEG. These patients also underwent occlusion of cerebral circulation as part of surgery, and interestingly, those patients with lower core temperatures (
