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Carbon Dioxide Reactivity of Brain Tissue Oxygenation after Pediatric Traumatic Brain Injury
Damla Hanalioglu1, Ann Oh2, M'Hamed Temkit1
1Barrow Neurological Institute at Phoenix Children's Hospital, Phoenix, AZ 85016, USA.
Insights
In pediatric traumatic brain injury (TBI), brain tissue oxygenation (PbtO2) CO2 reactivity varies. Some patients show intact reactivity, while others have impaired reactivity, impacting outcomes.
Area of Science:
- Neuroscience
- Critical Care Medicine
- Pediatric Neurology
Background:
- Traumatic brain injury (TBI) in children can significantly affect brain physiology.
- Understanding the relationship between carbon dioxide levels and brain oxygenation is crucial for managing TBI.
Purpose of the Study:
- To investigate the association between partial pressure of brain tissue oxygenation (PbtO2) and end-tidal carbon dioxide (EtCO2) in pediatric TBI patients.
- To determine the prevalence of intact versus impaired CO2 reactivity in this population.
Main Methods:
- Dynamic structural equation modeling (DSEM) was employed to analyze the relationship between EtCO2 and PbtO2.
- Sub-analyses explored associations of PbtO2 with intracranial pressure (ICP), arterial blood pressure (ABP), and cerebral regional oximetry (rSO2).
Main Results:
- A positive association between PbtO2 and EtCO2 (indicating intact CO2 reactivity) was observed in the cohort.
- Nine out of 14 patients demonstrated intact CO2 reactivity, while 5 showed impaired reactivity.
- Impaired CO2 reactivity was associated with increased ICP, lower PbtO2, and higher PRx values.
Conclusions:
- CO2 reactivity of PbtO2 in pediatric TBI is heterogeneous.
- Further research is needed to identify factors contributing to impaired CO2 reactivity and guide clinical management.
Abstract:
Background: We investigated how changes in partial pressure of brain tissue oxygenation (PbtO2) relate to end-tidal carbon dioxide (EtCO2) after pediatric traumatic brain injury (TBI). Methods: Dynamic structural equation modeling (DSEM) was used to investigate associations between EtCO2 and PbtO2, with positive associations indicating intact CO2 reactivity of PbtO2, and negative associations indicating impaired reactivity. Sub-analyses were performed to investigate associations of PbtO2 to intracranial pressure (ICP), arterial blood pressure (ABP) and cerebral regional oximetry (rSO2). Results: Among 14 patients, a positive association between PbtO2 and EtCO2 was demonstrated (SRC 0.05, 95% CI [0.04, 0.06]), with 9 patients demonstrating intact CO2 reactivity and 5 patients demonstrating impaired reactivity. Patients demonstrating intact CO2 reactivity had positive associations between PbtO2 and ICP (0.22 [0.21, 0.23]), whereas patients with impaired reactivity had negative associations (−0.28 [−0.29, −0.28]). Patients demonstrating intact CO2 reactivity had negative associations between PbtO2 and rSO2 (−0.08 [−0.09, −0.08]), whereas patients with impaired reactivity had positive associations (−0.15 [0.14, 0.16]). Compared to patients with intact CO2 reactivity, those with impaired reactivity had increased ICP (p < 0.0000), lower PbtO2 (p < 0.0000) and higher PRx (p = 0.0134). Conclusion: After TBI, CO2 reactivity of PbtO2 can be heterogenous, necessitating further work investigating factors contributing toward impaired reactivity.
