Association between prehospital end-tidal carbon dioxide levels and mortality in patients with suspected severe traumatic brain injury

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. Supplementary Information The online version contains supplementary material available at 10.1007/s00134-023-07012-z.

Clinical practice and effect of carbon dioxide on outcomes in mechanically ventilated acute brain-injured patients: a secondary analysis of the ENIO study

“…Interestingly, in the above-mentioned CENTER-TBI study, centers where profound hyperventilation was used did not present worsened outcomes [ 4 ]. On the other hand, a recent study from the BRAIN-PROTECT group [ 26 ], including a cohort of 1776 TBI patients with end-tidal (ET) CO 2 levels measured during prehospital care, found a L-shaped association between ETCO 2 levels and 30-day mortality, with important increase in mortality for values below 35 mmHg. However, this study presents important limitations, as it refers only to a limited timeframe setting (prehospital) and does not totally take in account confounding physiological factors which can have influenced decreases in ETCO 2 .…”

Hyperoxaemia in Acute Trauma is Common and Associated with a Longer Hospital Stay – a Multicentre Retrospective Cohort Study

“…Our ndings regarding oxygenation do not parallel those related to decarboxylation. Previous research has shown that mortality follows a U-shaped curve concerning PaCO 2 in trauma patients, particularly in patients with traumatic brain injury (18)(19)(20). In this study a similar curve for PaO 2 was not observed.…”

PaCO2 Association with Traumatic Brain Injury Patients Outcomes at High Altitude: A Prospective Single-Center Cohort Study.

“…The median (IQR) for AISh was 3 (2)(3)(4). In terms of the overall severity of trauma, the median (IQR) of ISS was 24 (13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32), among which 72% (58/81) had major trauma (ISS > 15). Structural severity of head trauma was determined through the Marshall CT classi cation, where 31% (24/81) of cases fell into diffuse injury I, 36% (31/81) diffuse injury II, 8% (6/80) diffuse injury III, 20% (16/81) evacuated mass lesion V, 4% (3/81) non-evacuated mass lesion VI, and 1% (1/81) diffuse injury IV.…”

“…Hypercapnia causes blood vessels to dilate due to cerebrospinal uid acidosis and the direct effect of extracellular H + on vascular smooth muscle (11), while hypocapnia constricts them via alkalosis, in uencing intracranial pressure and adjusting brain tissue perfusion in response to the environment (12). Maintaining optimal partial pressure of carbon dioxide (PaCO2) levels is crucial in cases of brain injury, as hypoperfusion and hypoxemia are closely linked to secondary brain injury and long-term consequences, impacting disability and survival rates (13,14). Guidelines recommend maintaining a target PCO2 range between 35-45 mm Hg to prevent cerebral ischemia in the case of low PaCO2 or hyperemia that could lead to elevated intracranial pressure if PaCO2 is high (15).…”