Abstract
Purpose: Severe traumatic brain injury is a leading cause of mortality and morbidity, and these patients are frequently intubated in the prehospital setting. Cerebral perfusion and intracranial pressure are influenced by the arterial partial pressure of CO 2 and derangements might induce further brain damage. We investigated which lower and upper limits of prehospital end-tidal CO 2 levels are associated with increased mortality in patients with severe traumatic brain injury. Methods: The BRAIN-PROTECT study is an observational multicenter study. Patients with severe traumatic brain injury, treated by Dutch Helicopter Emergency Medical Services between February 2012 and December 2017, were included. Follow-up continued for 1 year after inclusion. End-tidal CO 2 levels were measured during prehospital care and their association with 30-day mortality was analyzed with multivariable logistic regression. Results: A total of 1776 patients were eligible for analysis. An L-shaped association between end-tidal CO 2 levels and 30-day mortality was observed (p = 0.01), with a sharp increase in mortality with values below 35 mmHg. End-tidal CO 2 values between 35 and 45 mmHg were associated with better survival rates compared to < 35 mmHg. No association between hypercapnia and mortality was observed. The odds ratio for the association between hypocapnia (< 35 mmHg) and mortality was 1.89 (95% CI 1.53–2.34, p < 0.001) and for hypercapnia (≥ 45 mmHg) 0.83 (0.62–1.11, p = 0.212). Conclusion: A safe zone of 35–45 mmHg for end-tidal CO 2 guidance seems reasonable during prehospital care. Particularly, end-tidal partial pressures of less than 35 mmHg were associated with a significantly increased mortality.
Original language | English |
---|---|
Pages (from-to) | 491-504 |
Number of pages | 14 |
Journal | Intensive care medicine |
Volume | 49 |
Issue number | 5 |
Early online date | 2023 |
DOIs | |
Publication status | Published - May 2023 |
Keywords
- Carbon dioxide
- Critical care
- Endotracheal intubation
- Traumatic brain injury
- Ventilation
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In: Intensive care medicine, Vol. 49, No. 5, 05.2023, p. 491-504.
Research output: Contribution to journal › Article › Academic › peer-review
TY - JOUR
T1 - Association between prehospital end-tidal carbon dioxide levels and mortality in patients with suspected severe traumatic brain injury
AU - Bossers, Sebastiaan M.
AU - Mansvelder, Floor
AU - Loer, Stephan A.
AU - Boer, Christa
AU - Bloemers, Frank W.
AU - van Lieshout, Esther M. M.
AU - den Hartog, Dennis
AU - Hoogerwerf, Nico
AU - van der Naalt, Joukje
AU - Absalom, Anthony R.
AU - Schwarte, Lothar A.
AU - Twisk, Jos W. R.
AU - Schober, Patrick
AU - the BRAIN-PROTECT Collaborators
AU - de Boer, Anne
AU - Goslings, Johannes C.
AU - van Helden, Sven H.
AU - Hesselink, Danique
AU - van Aken, Gijs
AU - Beishuizen, Albertus
AU - Egberink, Rolf E.
AU - ter Bogt, Nancy
AU - de Jongh, Mariska A. C.
AU - Lansink, Koen
AU - Lansink, Koen
AU - Roks, Gerwin
AU - Joosse, Pieter
AU - Ponsen, Kees J.
AU - van Spengler, Lukas L.
AU - Asper, Stasja
AU - Peerdeman, Saskia M.
AU - Houmes, Robert J.
AU - van Ditshuizen, Jan
AU - van Voorden, Tea
AU - Edwards, Michael J. R.
AU - Dercksen, Bert
AU - Spanjersberg, Rob
AU - Venema, Lieneke
AU - Weelink, Ellen
AU - Reininga, Inge H. F.
AU - Innemee, Gerard
AU - de Visser, Matthijs
AU - de Leeuw, Marcel A.
AU - Kooij, Fabian O.
N1 - Funding Information: This work was supported by the Dutch Brain Foundation (“Hersenstichting”) under Grant F2010(1)-14, and Achmea Healthcare Foundation (“Stichting Achmea Gezondheidszorg”) under Grant Z644. The funding sources did not have a role in the design or execution of this study and did not have any role during analysis and interpretation of the data, or in the decision to submit results. Funding Information: SMB reported receiving grants from Achmea Healthcare Foundation during the conduct of the study. ARA reported receiving grants and personal fees from Becton Dickson and The Medicines Company; grants from Draeger; sponsor-initiated and funded phase 1 research from Rigel; and personal fees from PAION, Janssen Pharma, Ever Pharma, and Philips outside the submitted work. PS reported receiving grants from Dutch Brain Foundation and Achmea Healthcare Foundation during the conduct of the study. No other disclosures were reported. Funding Information: BRAIN-PROTECT collaborators: Anne Boer, de: MSc. SpoedZorgNet, Amsterdam, The Netherlands, Site facilitation. Johannes C. Goslings: MD, PhD, OLVG, Amsterdam, The Netherlands, Site facilitation. Sven H. Helden, van: MD, PhD, Isala Zwolle, The Netherlands, Site facilitation. Danique Hesselink: MSc, Netwerk Acute Zorg Zwolle, Zwolle, The Netherlands, Site facilitation. Gijs Aken, van: Netwerk Acute Zorg Zwolle, Zwolle, The Netherlands,Site facilitation. Albertus Beishuizen: MD, PhD, Medisch Spectrum Twente, Enschede, The Netherlands, Site facilitation. Rolf E. Egberink: MSc, Acute Zorg Euregio, Enschede, the Netherlands, Site facilitation. Nancy Bogt, ter: PhD, Acute Zorg Euregio, Enschede, The Netherlands, Site facilitation. Mariska A.C. Jongh, de: PhD, Netwerk Acute Zorg Brabant, Tilburg, The Netherlands, Site facilitation. Koen Lansink: MD, PhD, Elisabeth-TweeSteden ziekenhuis, Tilburg, The Netherlands, Site facilitation. Gerwin Roks: MD, PhD, Elisabeth-TweeSteden ziekenhuis, Tilburg, The Netherlands, Site facilitation. Pieter Joosse: MD, PhD, Noordwest Ziekenhuisgroep, Alkmaar, The Netherlands, Site facilitation: Kees J. Ponsen: MD, PhD, Noordwest Ziekenhuisgroep, Alkmaar, The Netherlands, Site facilitation. Lukas L. van Spengler: MSc, Traumazorgnetwerk Midden-Nederland, Utrecht, The Netherlands, Site facilitation. Stasja Aspers: Traumazorgnetwerk Midden-Nederland, Utrecht, The Netherlands, Site facilitation. Saskia M. Peerdeman: MD, PhD, AUMC, Amsterdam, The Netherlands, Study design, Steering Committee member. Robert J. Houmes: MD, PhD, Erasmus MC, Rotterdam, The Netherlands, Site facilitation. Jan Ditshuizen, van: MSc. Traumacentrum Zuidwest-Nederland, Rotterdam, The Netherlands, Site facilitation.Tea Voorden, van: MSc, Traumacentrum Zuidwest-Nederland, Rotterdam, The Netherlands, Site facilitation. Michael J.R. Edwards: MD, PhD, Radboudumc, Nijmegen, The Netherlands, Site facilitation. Bert Dercksen: MD, UMCG, Groningen, The Netherlands, Site facilitation. Rob Spanjersberg: UMCG, Groningen, The Netherlands, Site facilitation. Lieneke Venema: MD, UMCG, Groningen, The Netherlands, Site facilitation. Ellen Weelink: MD. UMCG, Groningen, The Netherlands, Site facilitation. Inge H. F. Reininga: PhD, Acute Zorgnetwerk Noord Nederland, Groningen, The Netherlands, Site facilitation. Gerard Innemee: MD, PhD, RAV Gooi & Vechtstreek, Hilversum, The Netherlands, Study design, Steering Committee member. Matthijs Visser, de: MSc, RAV Hollands Midden, Leiden, The Netherlands, Study design,Steering Committee member. Marcel A. Leeuw, de: MD, PhD, AUMC & Lifeliner 1, Amsterdam, The Netherlands, Study design. Fabian O Kooij: MD, PhD, AUMC & Lifeliner 1, Amsterdam, The Netherlands, Site facilitation. Publisher Copyright: © 2023, The Author(s).
PY - 2023/5
Y1 - 2023/5
N2 - Purpose: Severe traumatic brain injury is a leading cause of mortality and morbidity, and these patients are frequently intubated in the prehospital setting. Cerebral perfusion and intracranial pressure are influenced by the arterial partial pressure of CO 2 and derangements might induce further brain damage. We investigated which lower and upper limits of prehospital end-tidal CO 2 levels are associated with increased mortality in patients with severe traumatic brain injury. Methods: The BRAIN-PROTECT study is an observational multicenter study. Patients with severe traumatic brain injury, treated by Dutch Helicopter Emergency Medical Services between February 2012 and December 2017, were included. Follow-up continued for 1 year after inclusion. End-tidal CO 2 levels were measured during prehospital care and their association with 30-day mortality was analyzed with multivariable logistic regression. Results: A total of 1776 patients were eligible for analysis. An L-shaped association between end-tidal CO 2 levels and 30-day mortality was observed (p = 0.01), with a sharp increase in mortality with values below 35 mmHg. End-tidal CO 2 values between 35 and 45 mmHg were associated with better survival rates compared to < 35 mmHg. No association between hypercapnia and mortality was observed. The odds ratio for the association between hypocapnia (< 35 mmHg) and mortality was 1.89 (95% CI 1.53–2.34, p < 0.001) and for hypercapnia (≥ 45 mmHg) 0.83 (0.62–1.11, p = 0.212). Conclusion: A safe zone of 35–45 mmHg for end-tidal CO 2 guidance seems reasonable during prehospital care. Particularly, end-tidal partial pressures of less than 35 mmHg were associated with a significantly increased mortality.
AB - Purpose: Severe traumatic brain injury is a leading cause of mortality and morbidity, and these patients are frequently intubated in the prehospital setting. Cerebral perfusion and intracranial pressure are influenced by the arterial partial pressure of CO 2 and derangements might induce further brain damage. We investigated which lower and upper limits of prehospital end-tidal CO 2 levels are associated with increased mortality in patients with severe traumatic brain injury. Methods: The BRAIN-PROTECT study is an observational multicenter study. Patients with severe traumatic brain injury, treated by Dutch Helicopter Emergency Medical Services between February 2012 and December 2017, were included. Follow-up continued for 1 year after inclusion. End-tidal CO 2 levels were measured during prehospital care and their association with 30-day mortality was analyzed with multivariable logistic regression. Results: A total of 1776 patients were eligible for analysis. An L-shaped association between end-tidal CO 2 levels and 30-day mortality was observed (p = 0.01), with a sharp increase in mortality with values below 35 mmHg. End-tidal CO 2 values between 35 and 45 mmHg were associated with better survival rates compared to < 35 mmHg. No association between hypercapnia and mortality was observed. The odds ratio for the association between hypocapnia (< 35 mmHg) and mortality was 1.89 (95% CI 1.53–2.34, p < 0.001) and for hypercapnia (≥ 45 mmHg) 0.83 (0.62–1.11, p = 0.212). Conclusion: A safe zone of 35–45 mmHg for end-tidal CO 2 guidance seems reasonable during prehospital care. Particularly, end-tidal partial pressures of less than 35 mmHg were associated with a significantly increased mortality.
KW - Carbon dioxide
KW - Critical care
KW - Endotracheal intubation
KW - Traumatic brain injury
KW - Ventilation
UR - http://www.scopus.com/inward/record.url?scp=85152357172&partnerID=8YFLogxK
U2 - https://doi.org/10.1007/s00134-023-07012-z
DO - https://doi.org/10.1007/s00134-023-07012-z
M3 - Article
C2 - 37074395
SN - 0342-4642
VL - 49
SP - 491
EP - 504
JO - Intensive care medicine
JF - Intensive care medicine
IS - 5
ER -