Late awakening, prognostic factors and long-term outcome in out-of-hospital cardiac arrest - results of the prospective Norwegian Cardio-Respiratory Arrest Study (NORCAST).

Cerebral performance category EEG Glasgow coma scale Neuron-specific enolase Out-of-hospital cardiac arrest Prognostication SSEP Sedation Targeted temperature management Withdrawal of life-sustaining therapy

Journal

Resuscitation
ISSN: 1873-1570
Titre abrégé: Resuscitation
Pays: Ireland
ID NLM: 0332173

Informations de publication

Date de publication:
04 2020
Historique:
received: 13 09 2019
revised: 24 11 2019
accepted: 04 12 2019
pubmed: 12 1 2020
medline: 22 6 2021
entrez: 12 1 2020
Statut: ppublish

Résumé

Outcome prediction after out-of-hospital cardiac arrest (OHCA) may lead to withdrawal of life-sustaining therapy if the prognosis is perceived negative. Single use of uncertain prognostic tools may lead to self-fulfilling prophecies and death. We evaluated prognostic tests, blinded to clinicians and without calls for hasty outcome prediction, in a prospective study. Comatose, sedated TTM 33-treated OHCA patients of all causes were included. Clinical-neurological/-neurophysiological/-biochemical predictors were registered. Patients were dichotomized into good/poor outcome using cerebral performance category (CPC) six months and > four years post-arrest. Prognostic tools were evaluated using false positive rates (FPR). We included 259 patients; 49 % and 42 % had good outcome (CPC 1-2) after median six months and 5.1 years. Unwitnessed arrest, non-shockable rhythms, and no-bystander-CPR predicted poor outcome with FPR (CI) 0.05 (0.02-0.10), 0.13 (0.08-0.21), and 0.13 (0.07-0.20), respectively. Time to awakening was median 6 (0-25) days in good outcome patients. Among patients alive with sedation withdrawal >72 h, 49 % were unconscious, of whom 32 % still obtained good outcome. Only absence of pupillary light reflexes (PLR) -and N20-responses in somato-sensory evoked potentials (SSEP), as well as increased neuron-specific enolase (NSE) later than 24 h to >80 μg/L, had FPR 0. Malignant EEG (burst suppression/epileptic activity/flat) differentiated poor/good outcome with FPR 0.05 (0.01-0.15). Time to awakening was over six days in good outcome patients. Most clinical parameters had too high FPRs for prognostication, except for absent PLR and SSEP-responses >72 h after sedation withdrawal, and increased NSE later than 24 h to >80 μg/L.

Sections du résumé

BACKGROUND
Outcome prediction after out-of-hospital cardiac arrest (OHCA) may lead to withdrawal of life-sustaining therapy if the prognosis is perceived negative. Single use of uncertain prognostic tools may lead to self-fulfilling prophecies and death. We evaluated prognostic tests, blinded to clinicians and without calls for hasty outcome prediction, in a prospective study.
METHODS
Comatose, sedated TTM 33-treated OHCA patients of all causes were included. Clinical-neurological/-neurophysiological/-biochemical predictors were registered. Patients were dichotomized into good/poor outcome using cerebral performance category (CPC) six months and > four years post-arrest. Prognostic tools were evaluated using false positive rates (FPR).
RESULTS
We included 259 patients; 49 % and 42 % had good outcome (CPC 1-2) after median six months and 5.1 years. Unwitnessed arrest, non-shockable rhythms, and no-bystander-CPR predicted poor outcome with FPR (CI) 0.05 (0.02-0.10), 0.13 (0.08-0.21), and 0.13 (0.07-0.20), respectively. Time to awakening was median 6 (0-25) days in good outcome patients. Among patients alive with sedation withdrawal >72 h, 49 % were unconscious, of whom 32 % still obtained good outcome. Only absence of pupillary light reflexes (PLR) -and N20-responses in somato-sensory evoked potentials (SSEP), as well as increased neuron-specific enolase (NSE) later than 24 h to >80 μg/L, had FPR 0. Malignant EEG (burst suppression/epileptic activity/flat) differentiated poor/good outcome with FPR 0.05 (0.01-0.15).
CONCLUSION
Time to awakening was over six days in good outcome patients. Most clinical parameters had too high FPRs for prognostication, except for absent PLR and SSEP-responses >72 h after sedation withdrawal, and increased NSE later than 24 h to >80 μg/L.

Identifiants

pubmed: 31926258
pii: S0300-9572(20)30011-3
doi: 10.1016/j.resuscitation.2019.12.031
pii:
doi:

Substances chimiques

Phosphopyruvate Hydratase EC 4.2.1.11

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

170-179

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2020 Elsevier B.V. All rights reserved.

Auteurs

Espen R Nakstad (ER)

Department of Acute Medicine, Oslo University Hospital, Ullevål, Postboks 4956 Nydalen, N-0424 Oslo, Norway. Electronic address: uxnaes@ous-hf.no.

Henrik Stær-Jensen (H)

Department of Anaesthesiology, Oslo University Hospital, Ullevål, Postboks 4956 Nydalen, N-0424 Oslo, Norway.

Henning Wimmer (H)

Department of Acute Medicine, Oslo University Hospital, Ullevål, Postboks 4956 Nydalen, N-0424 Oslo, Norway.

Julia Henriksen (J)

Department of Neurology, Oslo University Hospital, Ullevål, Postboks 4956 Nydalen, N-0424 Oslo, Norway.

Lars H Alteheld (LH)

Department of Neurology, Oslo University Hospital, Ullevål, Postboks 4956 Nydalen, N-0424 Oslo, Norway.

Antje Reichenbach (A)

Department of Neurology, Akershus University Hospital, Postboks 1000, N-1478 Lørenskog, Norway.

Tomas Drægni (T)

Department of Research and Development, Oslo University Hospital, Ullevål, Postboks 4956 Nydalen, N-0424 Oslo, Norway.

Jūratė Šaltytė-Benth (J)

Institute of Clinical Medicine, Campus Akershus University Hospital, University of Oslo, Institute of Clinical Medicine, PB 1171 Blindern, N-0318 Oslo, Norway; Health Services Research Unit, Akershus University Hospital, Postboks 1000, N-1478 Lørenskog, Norway.

John Aage Wilson (JA)

National Centre for Epilepsy, Oslo University Hospital, Postboks 4950 Nydalen, N-0424 Oslo, Norway.

Lars Etholm (L)

Department of Neurophysiology, Oslo University Hospital, Ullevål, Postboks 4950 Nydalen, N-0424 Oslo, Norway.

Miriam Øijordsbakken (M)

Department of Biochemistry, Norwegian Radium Hospital, Oslo University Hospital, Postboks 4953 Nydalen, N-0424 Oslo, Norway.

Jan Eritsland (J)

Department of Cardiology, Oslo University Hospital, Ullevål, Postboks 4956 Nydalen, N-0424 Oslo, Norway.

Ingebjørg Seljeflot (I)

Department of Cardiology, Oslo University Hospital, Ullevål, Postboks 4956 Nydalen, N-0424 Oslo, Norway; Institute of Clinical Medicine, University of Oslo, Institute of Clinical Medicine, PB 1171 Blindern, N-0318 Oslo, Norway.

Dag Jacobsen (D)

Department of Acute Medicine, Oslo University Hospital, Ullevål, Postboks 4956 Nydalen, N-0424 Oslo, Norway; Institute of Clinical Medicine, University of Oslo, Institute of Clinical Medicine, PB 1171 Blindern, N-0318 Oslo, Norway.

Geir Ø Andersen (GØ)

Department of Cardiology, Oslo University Hospital, Ullevål, Postboks 4956 Nydalen, N-0424 Oslo, Norway.

Christofer Lundqvist (C)

Health Services Research Unit, Akershus University Hospital, Postboks 1000, N-1478 Lørenskog, Norway; Department of Neurology, Akershus University Hospital, Postboks 1000, N-1478 Lørenskog, Norway; Institute of Clinical Medicine, University of Oslo, Institute of Clinical Medicine, PB 1171 Blindern, N-0318 Oslo, Norway.

Kjetil Sunde (K)

Department of Anaesthesiology, Oslo University Hospital, Ullevål, Postboks 4956 Nydalen, N-0424 Oslo, Norway; Institute of Clinical Medicine, University of Oslo, Institute of Clinical Medicine, PB 1171 Blindern, N-0318 Oslo, Norway.

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