Key result
Every 1 kPa increase in the CO2 gap at hospital admission was independently associated with a 2.7-fold increased odds of in-hospital mortality (OR 2.692) in patients with traumatic brain injury.
Why the study?
Severe traumatic brain injury management relies on end-tidal CO2 as a proxy for PaCO2 to guide normoventilation, but whether the difference between them at admission relates to in-hospital mortality was unclear.
Does the CO2 gap at hospital admission predict in-hospital mortality in patients with traumatic brain injury?
Cohort (n=105)
No
Does the CO2 gap at hospital admission predict in-hospital mortality in patients with traumatic brain injury?
Odds Ratio: 2.692 (95% CI 1.293–5.646)
p-value: p=0.009
The difference between end-tidal and arterial CO2 is significantly associated with in-hospital mortality in TBI patients, suggesting end-tidal CO2 is an unreliable proxy for PaCO2 that may lead to iatrogenic hypoventilation.
Larger admission CO2 gap was associated with higher TBI mortality; leaves open whether EtCO2 reliably guides prehospital normoventilation.
Background 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.Method 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.Results 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 hours 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).Conclusions 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 higher-than-expected CO2 gap will lead to iatrogenic hypoventilation when normocapnic ventilation is aimed at, and might thereby increase in-hospital mortality.
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Doppmann et al. (2021) conducted a cohort in Traumatic brain injury (n=105). CO2 gap (difference between end-tidal CO2 and PaCO2) vs. Lower CO2 gap was evaluated on In-hospital mortality (OR 2.692, 95% CI 1.293-5.646, p=0.009). Every 1 kPa increase in the CO2 gap at hospital admission was independently associated with a 2.7-fold increased odds of in-hospital mortality (OR 2.692) in patients with traumatic brain injury.
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