Protocol-driven neurological prognostication and withdrawal of life-sustaining therapy after cardiac arrest and targeted temperature management

Dragancea, Irina; Wise, Matthew Peter; Al-Subaie, Nawaf; Cranshaw, Julius; Friberg, Hans; Glover, Guy; Pellis, Tommaso; Rylance, Rebecca; Walden, Andrew; Nielsen, Niklas; Cronberg, Tobias

doi:10.1016/j.resuscitation.2017.05.014

Cited by 97 publications

(69 citation statements)

References 32 publications

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“…[6][7][8][9] Nevertheless, our findings and the proposed mechanism offer some immediate potential implications for patients in prolonged post-cardiac arrest coma and lack of overwhelming cortical injury on MRI or CT. As discussed earlier, prolonged BSP may be linked to impaired metabolism in posthypoxic neurons; therefore, maintaining caloric intake and hydration during recovery may be important in post-cardiac arrest patients with these clinical features. As decisions to limit both hydration and gastrostomy feeding often arise coincident with early observational periods, 36,46,47,55 these patients may benefit from maintaining available metabolic substrates during an extended observation period. In addition, as done for Patient 1, institution of a time-limited trial of pharmacologic activation, such as amantadine, should be considered to drive anterior forebrain activity.…”

Section: Discussionmentioning

confidence: 99%

Independent Functional Outcomes after Prolonged Coma following Cardiac Arrest: A Mechanistic Hypothesis

Forgács

Devinsky

Schiff

2020

Annals of Neurology

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Objective Survivors of prolonged (>2 weeks) post–cardiac arrest (CA) coma are expected to remain permanently disabled. We aimed to investigate 3 outlier patients who ultimately achieved independent functional outcomes after prolonged post‐CA coma to identify electroencephalographic (EEG) markers of their recovery potential. For validation purposes, we also aimed to evaluate these markers in an independent cohort of post‐CA patients. Methods We identified 3 patients with late recovery from coma (17–37 days) following CA who recovered to functionally independent behavioral levels. We performed spectral power analyses of available EEGs during prominent burst suppression patterns (BSP) present in all 3 patients. Using identical methods, we also assessed the relationship of intraburst spectral power and outcomes in a prospectively enrolled cohort of post‐CA patients. We performed chart reviews of common clinical, imaging, and EEG prognostic variables and clinical outcomes for all patients. Results All 3 patients with late recovery from coma lacked evidence of overwhelming cortical injury but demonstrated prominent BSP on EEG. Spectral analyses revealed a prominent theta (~4–7Hz) feature dominating the bursts during BSP in these patients. In the prospective cohort, similar intraburst theta spectral features were evident in patients with favorable outcomes; patients with BSP and unfavorable outcomes showed either no features, transient burst features, or decreasing intraburst frequencies with time. Interpretation BSP with theta (~4–7Hz) peak intraburst spectral power after CA may index a recovery potential. We discuss our results in the context of optimizing metabolic substrate availability and stimulating the corticothalamic system during recovery from prolonged post‐CA coma. ANN NEUROL 2020;87:618–632

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Section: Discussionmentioning

confidence: 99%

Independent Functional Outcomes after Prolonged Coma following Cardiac Arrest: A Mechanistic Hypothesis

Forgács

Devinsky

Schiff

2020

Annals of Neurology

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“…The intensity and duration of treatment of postanoxic RSE are highly controversial issues. 23,24 No evidence is currently available on whether a more aggressive treatment would substantially affect the final neurologic outcome in refractory postanoxic status epilepticus.…”

Section: Discussionmentioning

confidence: 99%

Neurologic outcome of postanoxic refractory status epilepticus after aggressive treatment

et al. 2018

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ObjectiveTo investigate neurologic outcome of patients with cardiac arrest with refractory status epilepticus (RSE) treated with a standardized aggressive protocol with antiepileptic drugs and anesthetics compared to patients with other EEG patterns.MethodsIn the prospective cohort study, 166 consecutive patients with cardiac arrest in coma were stratified according to 4 independent EEG patterns (benign, RSE, generalized periodic discharges [GPDs], malignant nonepileptiform) and multimodal prognostic indicators. Primary outcomes were survival and cerebral performance category (CPC) at 6 months.ResultsRSE occurred in 36 patients (21.7%) and was treated with an aggressive standardized protocol as long as multimodal prognostic indicators were not unfavorable. RSE started after 3 ± 2.3 days after cardiac arrest and lasted 4.7 ± 4.3 days. A benign EEG pattern was recorded in 76 patients (45.8%); a periodic pattern (GPDs) was seen in 13 patients (7.8%); and a malignant nonepileptiform EEG pattern was recorded in 41 patients (24.7%). The 4 EEG patterns were highly associated with different prognostic indicators (low-flow time, clinical motor seizures, N20 responses, neuron-specific enolase, neuroimaging). Survival and good neurologic outcome (CPC 1 or 2) at 6 months were 72.4% and 71.1% for benign EEG pattern, 54.3% and 44.4% for RSE, 15.4% and 0% for GPDs, and 2.4% and 0% for malignant nonepileptiform EEG pattern, respectively.ConclusionsAggressive and prolonged treatment of RSE may be justified in patients with cardiac arrest with favorable multimodal prognostic indicators.

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“…This suggests that even in people with good prognosis after cardiac arrest there may be an initial transient release of tau, which does not reflect irreversible neurological injury or poor outcome. An alternative explanation is that people who die very soon after cardiac arrest (during the first 2–3 days) are more likely to die from cardiac causes or multiorgan failure (which may not correlate directly with high tau), whereas people who die later are more likely to die from causes related to their brain injury 20, 27. There may also be a pathophysiological delay until a significant amount of tau has been released from injured neurons and axons, which make the later samples more reliable to measure brain injury.…”

Section: Discussionmentioning

confidence: 99%

Serum tau and neurological outcome in cardiac arrest

Mattsson

Zetterberg

Nielsen

et al. 2017

Annals of Neurology

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ObjectiveTo test serum tau as a predictor of neurological outcome after cardiac arrest.MethodsWe measured the neuronal protein tau in serum at 24, 48, and 72 hours after cardiac arrest in 689 patients in the prospective international Target Temperature Management trial. The main outcome was poor neurological outcome, defined as Cerebral Performance Categories 3–5 at 6 months.ResultsIncreased tau was associated with poor outcome at 6 months after cardiac arrest (median = 38.5, interquartile range [IQR] = 5.7–245ng/l in poor vs median = 1.5, IQR = 0.7–2.4ng/l in good outcome, for tau at 72 hours, p < 0.0001). Tau improved prediction of poor outcome compared to using clinical information (p < 0.0001). Tau cutoffs had low false‐positive rates (FPRs) for good outcome while retaining high sensitivity for poor outcome. For example, tau at 72 hours had FPR = 2% (95% CI = 1–4%) with sensitivity = 66% (95% CI = 61–70%). Tau had higher accuracy than serum neuron‐specific enolase (NSE; the area under the receiver operating characteristic curve was 0.91 for tau vs 0.86 for NSE at 72 hours, p = 0.00024). During follow‐up (up to 956 days), tau was significantly associated with overall survival. The accuracy in predicting outcome by serum tau was equally high for patients randomized to 33 °C and 36 °C targeted temperature after cardiac arrest.InterpretationSerum tau is a promising novel biomarker for prediction of neurological outcome in patients with cardiac arrest. It may be significantly better than serum NSE, which is recommended in guidelines and currently used in clinical practice in several countries to predict outcome after cardiac arrest. Ann Neurol 2017;82:665–675

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Protocol-driven neurological prognostication and withdrawal of life-sustaining therapy after cardiac arrest and targeted temperature management

Cited by 97 publications

References 32 publications

Independent Functional Outcomes after Prolonged Coma following Cardiac Arrest: A Mechanistic Hypothesis

Independent Functional Outcomes after Prolonged Coma following Cardiac Arrest: A Mechanistic Hypothesis

Neurologic outcome of postanoxic refractory status epilepticus after aggressive treatment

Serum tau and neurological outcome in cardiac arrest

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