Espen R Nakstad1, Henrik Stær-Jensen2, Henning Wimmer3, Julia Henriksen4, Lars H Alteheld4, Antje Reichenbach5, Tomas Drægni6, Jūratė Šaltytė-Benth7, John Aage Wilson8, Lars Etholm9, Miriam Øijordsbakken10, Jan Eritsland11, Ingebjørg Seljeflot12, Dag Jacobsen13, Geir Ø Andersen11, Christofer Lundqvist14, Kjetil Sunde15. 1. Department of Acute Medicine, Oslo University Hospital, Ullevål, Postboks 4956 Nydalen, N-0424 Oslo, Norway. Electronic address: uxnaes@ous-hf.no. 2. Department of Anaesthesiology, Oslo University Hospital, Ullevål, Postboks 4956 Nydalen, N-0424 Oslo, Norway. 3. Department of Acute Medicine, Oslo University Hospital, Ullevål, Postboks 4956 Nydalen, N-0424 Oslo, Norway. 4. Department of Neurology, Oslo University Hospital, Ullevål, Postboks 4956 Nydalen, N-0424 Oslo, Norway. 5. Department of Neurology, Akershus University Hospital, Postboks 1000, N-1478 Lørenskog, Norway. 6. Department of Research and Development, Oslo University Hospital, Ullevål, Postboks 4956 Nydalen, N-0424 Oslo, Norway. 7. 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. 8. National Centre for Epilepsy, Oslo University Hospital, Postboks 4950 Nydalen, N-0424 Oslo, Norway. 9. Department of Neurophysiology, Oslo University Hospital, Ullevål, Postboks 4950 Nydalen, N-0424 Oslo, Norway. 10. Department of Biochemistry, Norwegian Radium Hospital, Oslo University Hospital, Postboks 4953 Nydalen, N-0424 Oslo, Norway. 11. Department of Cardiology, Oslo University Hospital, Ullevål, Postboks 4956 Nydalen, N-0424 Oslo, Norway. 12. 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. 13. 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. 14. 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. 15. 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.
Abstract
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.
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.
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