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.
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 - 10.1007/s00134-023-07012-z
DO - 10.1007/s00134-023-07012-z
M3 - Article
C2 - 37074395
SN - 0342-4642
VL - 49
JO - Intensive Care Medicine
JF - Intensive Care Medicine
IS - 5
ER -