Pre-hospital endotracheal intubation in severe traumatic brain injury: ventilation targets and mortality-a retrospective analysis of 308 patients.

BACKGROUND: Traumatic brain injury (TBI) remains one of the main causes of mortality and long-term disability worldwide. Maintaining physiology of brain tissue to the greatest extent possible through optimal management of blood pressure, airway, ventilation, and oxygenation, improves patient outcome. We studied the quality of prehospital care in severe TBI patients by analyzing adherence to recommended target ranges for ventilation and blood pressure, prehospital time expenditure, and their effect on mortality, as well as quality of prehospital ventilation assessed by arterial partial pressure of CO2 (PaCO2) at hospital admission. METHODS: This is a retrospective cohort study of all TBI patients requiring tracheal intubation on scene who were transported to one of two major level 1 trauma centers in Switzerland between January 2014 and December 2019 by Swiss Air Rescue (Rega). We assessed systolic blood pressure (SBP), end-tidal partial pressure of CO2 (PetCO2), and PaCO2 at hospital admission as well as prehospital and on-scene time. Quality markers of prehospital care (PetCO2, SBP, prehospital times) and prehospital ventilation (PaCO2) are presented as descriptive analysis. Effect on mortality was calculated by multivariable regression analysis and a logistic general additive model. RESULTS: Of 557 patients after exclusions, 308 were analyzed. Adherence to blood pressure recommendations was 89%. According to PetCO2, 45% were normoventilated, and 29% had a SBP ≥ 90 mm Hg and were normoventilated. Due to the poor correlation between PaCO2 and PetCO2, only 33% were normocapnic at hospital admission. Normocapnia at hospital admission was strongly associated with reduced probability of mortality. Prehospital and on-scene times had no impact on mortality. CONCLUSIONS: PaCO2 at hospital admission is strongly associated with mortality risk, but normocapnia is achieved only in a minority of patients. Therefore, the time required for placement of an arterial cannula and prehospital blood gas analysis may be warranted in severe TBI patients requiring on-scene tracheal intubation.

End-tidal to arterial carbon dioxide gradient is associated with increased mortality in patients with traumatic brain injury: a retrospective observational study.

Early definitive airway protection and normoventilation are key principles in the treatment of severe traumatic brain injury. These are currently guided by end tidal CO2 as a proxy for PaCO2. We assessed whether the difference between end tidal CO2 and PaCO2 at hospital admission is associated with in-hospital mortality. We conducted a retrospective observational cohort study of consecutive patients with traumatic brain injury who were intubated and transported by Helicopter Emergency Medical Services to a Level 1 trauma center between January 2014 and December 2019. We assessed the association between the CO2 gap-defined as the difference between end tidal CO2 and PaCO2-and in-hospital mortality using multivariate logistic regression models. 105 patients were included in this study. The mean ± SD CO2 gap at admission was 1.64 ± 1.09 kPa and significantly greater in non-survivors than survivors (2.26 ± 1.30 kPa vs. 1.42 ± 0.92 kPa, p < .001). The correlation between EtCO2 and PaCO2 at admission was low (Pearson's r = .287). The mean CO2 gap after 24 h was only 0.64 ± 0.82 kPa, and no longer significantly different between non-survivors and survivors. The multivariate logistic regression model showed that the CO2 gap was independently associated with increased mortality in this cohort and associated with a 2.7-fold increased mortality for every 1 kPa increase in the CO2 gap (OR 2.692, 95% CI 1.293 to 5.646, p = .009). This study demonstrates that the difference between EtCO2 and PaCO2 is significantly associated with in-hospital mortality in patients with traumatic brain injury. EtCO2 was significantly lower than PaCO2, making it an unreliable proxy for PaCO2 when aiming for normocapnic ventilation. The CO2 gap can lead to iatrogenic hypoventilation when normocapnic ventilation is aimed and might thereby increase in-hospital mortality.