Cornelia Genbrugge1, Cathy De Deyne2, Ward Eertmans3, Kurt Anseeuw4, Dirk Voet5, Ilse Mertens6, Marc Sabbe7, Jan Stroobants8, Liesbeth Bruckers9, Dieter Mesotten10, Frank Jans11, Willem Boer12, Jo Dens13. 1. Department of Medicine and Life Sciences, Hasselt University, Diepenbeek, Belgium; Department of Anaesthesiology, Intensive Care, Emergency Medicine and Pain Therapy, Ziekenhuis Oost-Limburg, Genk, Belgium; Schiepse Bos 6, 3600, Genk, Belgium. Electronic address: cornelia.genbrugge@uhasselt.be. 2. Department of Medicine and Life Sciences, Hasselt University, Diepenbeek, Belgium; Department of Anaesthesiology, Intensive Care, Emergency Medicine and Pain Therapy, Ziekenhuis Oost-Limburg, Genk, Belgium; Schiepse Bos 6, 3600, Genk, Belgium. Electronic address: cathy.dedeyne@zol.be. 3. Department of Medicine and Life Sciences, Hasselt University, Diepenbeek, Belgium; Department of Anaesthesiology, Intensive Care, Emergency Medicine and Pain Therapy, Ziekenhuis Oost-Limburg, Genk, Belgium; Schiepse Bos 6, 3600, Genk, Belgium. Electronic address: ward.eertmans@uhasselt.be. 4. Emergency Department, Ziekenhuis Netwerk Antwerpen, Campus Stuivenberg, Lange Beeldekensstraat 267, 2060, Antwerpen, Belgium. Electronic address: Kurt.anseeuw@zna.be. 5. Emergency Department, Gasthuiszusters Antwerpen, Campus Sint-Vincentius, Sint-Vincentiusstraat 20, 2018, Antwerpen, Belgium. Electronic address: Dirk.voet@gza.be. 6. Emergency Department, Algemeen Ziekenhuis Turnhout, Campus Sint-Elisabeth, Rubensstraat 166, 2300, Turnhout, Belgium. Electronic address: ilse.mertens@azturnhout.be. 7. Emergency Department, University Hospitals Leuven, Leuven, Belgium. Electronic address: Marc.sabbe@uzleuven.be. 8. Emergency Department, Ziekenhuis Netwerk Antwerpen, Campus Middelheim, Lindendreef 1, 2020, Antwerpen, Belgium. Electronic address: Jan.stroobants@zna.be. 9. I-Biostat (CenStat), Hasselt University, Agoralaan gebouw D, 3590, Diepenbeek, Belgium. Electronic address: Liesbeth.bruckers@uhasselt.be. 10. Department of Anaesthesiology, Intensive Care, Emergency Medicine and Pain Therapy, Ziekenhuis Oost-Limburg, Genk, Belgium. Electronic address: Dieter.mesotten@zol.be. 11. Department of Medicine and Life Sciences, Hasselt University, Diepenbeek, Belgium; Department of Anaesthesiology, Intensive Care, Emergency Medicine and Pain Therapy, Ziekenhuis Oost-Limburg, Genk, Belgium; Schiepse Bos 6, 3600, Genk, Belgium. Electronic address: frank.jans@zol.be. 12. Department of Anaesthesiology, Intensive Care, Emergency Medicine and Pain Therapy, Ziekenhuis Oost-Limburg, Genk, Belgium; Schiepse Bos 6, 3600, Genk, Belgium. Electronic address: willem.boer@zol.be. 13. Department of Medicine and Life Sciences, Hasselt University, Diepenbeek, Belgium; Schiepse Bos 6, 3600, Genk, Belgium; Department of Cardiology, Ziekenhuis Oost-Limburg, Genk, Belgium. Electronic address: jo.dens@zol.be.
Abstract
AIM: To date, monitoring options during pre-hospital advanced life support (ALS) are limited. Regional cerebral saturation (rSO2) may provide more information concerning the brain during ALS. We hypothesized that an increase in rSO2 during ALS in out-of hospital cardiac arrest (OHCA) patients is associated with return of spontaneous circulation (ROSC). METHODS: A prospective, non-randomized multicenter study was conducted in the pre-hospital setting of six hospitals in Belgium. Cerebral saturation was measured during pre-hospital ALS by a medical emergency team in OHCA patients. Cerebral saturation was continuously measured until ALS efforts were terminated or until the patient with sustained ROSC (>20 min) arrived at the emergency department. To take the longitudinal nature of the data into account, a linear mixed model was used. The correlation between the repeated measures of a patient was handled by means of a random intercept and a random slope. Our primary analysis tested the association of rSO2 with ROSC. RESULTS: Of the 329 patients 110 (33%) achieved ROSC. First measured rSO2 was 30% ± 18 in the ROSC group and 24% ± 15 in the no-ROSC group (p = .004; mean ± SD). Higher mean rSO2 values were observed in the ROSC group compared to the no-ROSC group (41% ± 13 versus 33% ± 13 respectively; p < 0.001). The median increase in rSO2, measured from start until two minutes before ROSC, was higher in the ROSC group (ROSC group 17% (IQR 6-29)) than in the no-ROSC group (8% (IQR 2-13); p < 0.001). An increase in rSO2 above 15% was associated with ROSC (OR 4.5; 95%CI 2.747-7.415; p < 0.001). CONCLUSION: Regional cerebral saturation measurements can be used during pre-hospital ALS as an additional marker to predict ROSC. An increase of at least 15% in rSO2 during ALS is associated with a higher probability of ROSC.
AIM: To date, monitoring options during pre-hospital advanced life support (ALS) are limited. Regional cerebral saturation (rSO2) may provide more information concerning the brain during ALS. We hypothesized that an increase in rSO2 during ALS in out-of hospital cardiac arrest (OHCA) patients is associated with return of spontaneous circulation (ROSC). METHODS: A prospective, non-randomized multicenter study was conducted in the pre-hospital setting of six hospitals in Belgium. Cerebral saturation was measured during pre-hospital ALS by a medical emergency team in OHCA patients. Cerebral saturation was continuously measured until ALS efforts were terminated or until the patient with sustained ROSC (>20 min) arrived at the emergency department. To take the longitudinal nature of the data into account, a linear mixed model was used. The correlation between the repeated measures of a patient was handled by means of a random intercept and a random slope. Our primary analysis tested the association of rSO2 with ROSC. RESULTS: Of the 329 patients 110 (33%) achieved ROSC. First measured rSO2 was 30% ± 18 in the ROSC group and 24% ± 15 in the no-ROSC group (p = .004; mean ± SD). Higher mean rSO2 values were observed in the ROSC group compared to the no-ROSC group (41% ± 13 versus 33% ± 13 respectively; p < 0.001). The median increase in rSO2, measured from start until two minutes before ROSC, was higher in the ROSC group (ROSC group 17% (IQR 6-29)) than in the no-ROSC group (8% (IQR 2-13); p < 0.001). An increase in rSO2 above 15% was associated with ROSC (OR 4.5; 95%CI 2.747-7.415; p < 0.001). CONCLUSION: Regional cerebral saturation measurements can be used during pre-hospital ALS as an additional marker to predict ROSC. An increase of at least 15% in rSO2 during ALS is associated with a higher probability of ROSC.
Authors: Hasan Ayaz; Wesley B Baker; Giles Blaney; David A Boas; Heather Bortfeld; Kenneth Brady; Joshua Brake; Sabrina Brigadoi; Erin M Buckley; Stefan A Carp; Robert J Cooper; Kyle R Cowdrick; Joseph P Culver; Ippeita Dan; Hamid Dehghani; Anna Devor; Turgut Durduran; Adam T Eggebrecht; Lauren L Emberson; Qianqian Fang; Sergio Fantini; Maria Angela Franceschini; Jonas B Fischer; Judit Gervain; Joy Hirsch; Keum-Shik Hong; Roarke Horstmeyer; Jana M Kainerstorfer; Tiffany S Ko; Daniel J Licht; Adam Liebert; Robert Luke; Jennifer M Lynch; Jaume Mesquida; Rickson C Mesquita; Noman Naseer; Sergio L Novi; Felipe Orihuela-Espina; Thomas D O'Sullivan; Darcy S Peterka; Antonio Pifferi; Luca Pollonini; Angelo Sassaroli; João Ricardo Sato; Felix Scholkmann; Lorenzo Spinelli; Vivek J Srinivasan; Keith St Lawrence; Ilias Tachtsidis; Yunjie Tong; Alessandro Torricelli; Tara Urner; Heidrun Wabnitz; Martin Wolf; Ursula Wolf; Shiqi Xu; Changhuei Yang; Arjun G Yodh; Meryem A Yücel; Wenjun Zhou Journal: Neurophotonics Date: 2022-08-30 Impact factor: 4.212
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