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.
Highlights
Traumatic brain injury (TBI) is the most common cause of death and disability among children and young adults worldwide [1,2]
Researchers reported that hyperventilation to induce cerebral vasoconstriction and reduce cerebral blood flow (CBF), intracranial pressure (ICP), and cerebral blood volume may unintentionally lead to brain tissue hypoxia after traumatic brain injury (TBI)
We aimed to identify times series associations between end-tidal carbon dioxide content (EtCO2) and partial pressure of brain tissue oxygenation (PbtO2) as well as their relationships with intracranial pressure (ICP), arterial blood pressure (ABP) and cerebral regional oxygen saturation
Summary
Traumatic brain injury (TBI) is the most common cause of death and disability among children and young adults worldwide [1,2]. Existing management strategies focus on the prevention of secondary brain insults that may contribute toward worsened outcomes, including but not limited to maintenance of adequate cerebral blood flow (CBF) and oxygenation. The mechanisms to optimize brain tissue oxygenation and avoid hypoxia include maintenance of appropriate cerebral perfusion and adjustment of ventilation to influence arterial content of partial pressure of carbon dioxide (PaCO2) [6]. Since carbon dioxide (CO2) affects cerebrovascular resistance, deliberate changes in CO2 partial pressure have been considered as useful to manipulate CBF regulation in an environment of impaired autoregulation and disrupted blood brain barrier (BBB) [8]. 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). Conclusion: After TBI, CO2 reactivity of PbtO2 can be heterogenous, necessitating further work investigating factors contributing toward impaired reactivity
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