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Carbon Dioxide Reactivity of Brain Tissue Oxygenation after Pediatric Traumatic Brain Injury.

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.

SUBMITTER: Hanalioglu D

PROVIDER: S-EPMC8947728 | biostudies-literature | 2022 Mar

REPOSITORIES: biostudies-literature

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Carbon Dioxide Reactivity of Brain Tissue Oxygenation after Pediatric Traumatic Brain Injury.

Hanalioglu Damla D Oh Ann A Temkit M'Hamed M Adelson P David PD Appavu Brian B

Children (Basel, Switzerland) 20220314 3

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 intr ...[more]

PMID: 35327781

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Project description:BackgroundThe aim of this study was to describe the utilization patterns of brain tissue oxygen (PbtO2) monitoring following severe traumatic brain injury (TBI) and determine associations with mortality, health care use, and pulmonary toxicity.MethodsWe conducted a retrospective cohort study of patients from United States trauma centers participating in the American College of Surgeons National Trauma Databank between 2008 and 2016. We examined patients with severe TBI (defined by admission Glasgow Coma Scale score ≤ 8) over the age of 18 years who survived more than 24 h from admission and required intracranial pressure (ICP) monitoring. The primary exposure was PbtO2 monitor placement. The primary outcome was hospital mortality, defined as death during the hospitalization or discharge to hospice. Secondary outcomes were examined to determine the association of PbtO2 monitoring with health care use and pulmonary toxicity and included the following: (1) intensive care unit length of stay, (2) hospital length of stay, and (3) development of acute respiratory distress syndrome (ARDS). Regression analysis was used to assess differences in outcomes between patients exposed to PbtO2 monitor placement and those without exposure by using propensity weighting to address selection bias due to the nonrandom allocation of treatment groups and patient dropout.ResultsA total of 35,501 patients underwent placement of an ICP monitor. There were 1,346 (3.8%) patients who also underwent PbtO2 monitor placement, with significant variation regarding calendar year and hospital. Patients who underwent placement of a PbtO2 monitor had a crude in-hospital mortality of 31.1%, compared with 33.5% in patients who only underwent placement of an ICP monitor (adjusted risk ratio 0.84, 95% confidence interval 0.76-0.93). The development of the ARDS was comparable between patients who underwent placement of a PbtO2 monitor and patients who only underwent placement of an ICP monitor (9.2% vs. 9.8%, adjusted risk ratio 0.89, 95% confidence interval 0.73-1.09).ConclusionsPbtO2 monitor utilization varied widely throughout the study period by calendar year and hospital. PbtO2 monitoring in addition to ICP monitoring, compared with ICP monitoring alone, was associated with a decreased in-hospital mortality, a longer length of stay, and a similar risk of ARDS. These findings provide further guidance for clinicians caring for patients with severe TBI while awaiting completion of further randomized controlled trials.

Project description:ImportanceAlterations in the partial pressure of carbon dioxide, arterial (Paco2) can affect cerebral perfusion after traumatic brain injury. End-tidal carbon dioxide (EtCO2) monitoring is a noninvasive tool used to estimate Paco2 values.ObjectiveTo examine the agreement between Paco2 and EtCO2 and associated factors in children with traumatic brain injury.Design, setting, and participantsA secondary analysis was conducted using data from a prospective cohort study of 137 patients younger than 18 years with traumatic brain injury who were admitted to the pediatric intensive care unit of a level I trauma center between May 1, 2011, and July 31, 2017. Analysis was performed from December 17, 2018, to January 10, 2019.Main outcomes and measuresThe closest EtCO2 value obtained within 30 minutes of a Paco2 value and the closest systolic blood pressure value obtained within 60 minutes prior to a Paco2 value during the first 24 hours after admission were recorded. The main outcome of Paco2-EtCO2 agreement was defined as Paco2 between 0 and 5 mm Hg greater than the paired EtCO2 value, and it was determined using Bland-Altman analysis, Passing and Bablok regression, and the Pearson correlation coefficient. Multivariable regression models determined which factors were associated with agreement.ResultsThe analysis included 137 patients (34 girls and 103 boys; mean [SD] age, 10.0 [6.3] years) and 445 paired Paco2-EtCO2 data points. On average, Paco2 was 2.7 mm Hg (95% limits of agreement, -11.3 to 16.7) higher than EtCO2. Overall, 187 of all Paco2-EtCO2 pairs (42.0%) agreed. There was larger variation in the Paco2-EtCO2 difference during the first 8 hours compared with 9 to 24 hours after admission to the pediatric intensive care unit. Development of pediatric acute respiratory distress syndrome within 24 hours of admission was associated with a lower likelihood of Paco2-EtCO2 agreement (adjusted odds ratio, 0.20; 95% CI, 0.08-0.51) compared with no development of pediatric acute respiratory distress syndrome. A diagnosis of pediatric acute respiratory distress syndrome 1 to 7 days after admission was associated with a larger first-day Paco2-EtCO2 difference compared with those who never developed pediatric acute respiratory distress syndrome (mean [SD] difference, 4.48 [3.70] vs 0.46 [5.50] mm Hg).Conclusions and relevanceIn this study of pediatric traumatic brain injury, Paco2-EtCO2 agreement was low, especially among patients with pediatric acute respiratory distress syndrome. Low Paco2-EtCO2 agreement early in hospitalization may be associated with future development of pediatric acute respiratory distress syndrome. Data on EtCO2 should not be substituted for data on Paco2 during the first 24 hours.

Project description:Pressure reactivity index (PRx) and brain tissue oxygen (PbtO2) are associated with outcome in traumatic brain injury (TBI). This study explores the relationship between PRx and PbtO2 in adult moderate/severe TBI. Using the Collaborative European NeuroTrauma Effectiveness Research in Traumatic Brain Injury (CENTER-TBI) high resolution intensive care unit (ICU) sub-study cohort, we evaluated those patients with archived high-frequency digital intraparenchymal intracranial pressure (ICP) and PbtO2 monitoring data of, a minimum of 6 h in duration, and the presence of a 6 month Glasgow Outcome Scale -Extended (GOSE) score. Digital physiological signals were processed for ICP, PbtO2, and PRx, with the % time above/below defined thresholds determined. The duration of ICP, PbtO2, and PRx derangements was characterized. Associations with dichotomized 6-month GOSE (alive/dead, and favorable/unfavorable outcome; ≤ 4 = unfavorable), were assessed. A total of 43 patients were included. Severely impaired cerebrovascular reactivity was seen during elevated ICP and low PbtO2 episodes. However, most of the acute ICU physiological derangements were impaired cerebrovascular reactivity, not ICP elevations or low PbtO2 episodes. Low PbtO2 without PRx impairment was rarely seen. % time spent above PRx threshold was associated with mortality at 6 months for thresholds of 0 (area under the curve [AUC] 0.734, p = 0.003), > +0.25 (AUC 0.747, p = 0.002) and > +0.35 (AUC 0.745, p = 0.002). Similar relationships were not seen for % time with ICP >20 mm Hg, and PbtO2 < 20 mm Hg in this cohort. Extreme impairment in cerebrovascular reactivity is seen during concurrent episodes of elevated ICP and low PbtO2. However, the majority of the deranged cerebral physiology seen during the acute ICU phase is impairment in cerebrovascular reactivity, with most impairment occurring in the presence of normal PbtO2 levels. Measures of cerebrovascular reactivity appear to display the most consistent associations with global outcome in TBI, compared with ICP and PbtO2.

Project description:BackgroundBrain tissue hypoxia is an independent risk factor for unfavorable outcomes in traumatic brain injury (TBI); however, systemic hyperoxemia encountered in the prevention and/or response to brain tissue hypoxia may also impact risk of mortality. We aimed to identify temporal patterns of partial pressure of oxygen in brain tissue (PbtO2), partial pressure of arterial oxygen (PaO2), and PbtO2/PaO2 ratio associated with mortality in children with severe TBI.MethodsData were extracted from the electronic medical record of a quaternary care children's hospital with a level I trauma center for patients ≤ 18 years old with severe TBI and the presence of PbtO2 and/or intracranial pressure monitors. Temporal analyses were performed for the first 5 days of hospitalization by using locally estimated scatterplot smoothing for less than 1,000 observations and generalized additive models with integrated smoothness estimation for more than 1,000 observations.ResultsA total of 138 intracranial pressure-monitored patients with TBI (median 5.0 [1.9-12.8] years; 65% boys; admission Glasgow Coma Scale score 4 [3-7]; mortality 18%), 71 with PbtO2 monitors and 67 without PbtO2 monitors were included. Distinct patterns in PbtO2, PaO2, and PbtO2/PaO2 were evident between survivors and nonsurvivors over the first 5 days of hospitalization. Time-series analyses showed lower PbtO2 values on day 1 and days 3-5 and lower PbtO2/PaO2 ratios on days 1, 2, and 5 among patients who died. Analysis of receiver operating characteristics curves using Youden's index identified a PbtO2 of 30 mm Hg and a PbtO2/PaO2 ratio of 0.12 as the cut points for discriminating between survivors and nonsurvivors. Univariate logistic regression identified PbtO2 < 30 mm Hg, hyperoxemia (PaO2 ≥ 300 mm Hg), and PbtO2/PaO2 ratio < 0.12 to be independently associated with mortality.ConclusionsLower PbtO2, higher PaO2, and lower PbtO2/PaO2 ratio, consistent with impaired oxygen diffusion into brain tissue, were associated with mortality in this cohort of children with severe TBI. These results corroborate our prior work that suggests targeting a higher PbtO2 threshold than recommended in current guidelines and highlight the potential use of the PbtO2/PaO2 ratio in the management of severe pediatric TBI.

Project description:BackgroundLow-normal levels of arterial carbon dioxide (PaCO2) are recommended in the acute phase of traumatic brain injury (TBI) to optimize oxygen and CO2 tension, and to maintain cerebral perfusion. End-tidal CO2 (ETCO2) may be used as a surrogate for PaCO2 when arterial sampling is less readily available. ETCO2 may not be an adequate proxy to guide ventilation and the effects on concomitant injury, time, and the impact of ventilatory strategies on the PaCO2-ETCO2 gradient are not well understood. The primary objective of this study was to describe the correlation and agreement between PaCO2 and ETCO2 in intubated adult trauma patients with TBI.MethodsThis study was a retrospective analysis of prospectively-collected data of intubated adult major trauma patients with serious TBI, admitted to the East of England regional major trauma centre; 2015-2019. Linear regression and Welch's test were performed on each cohort to assess correlation between paired PaCO2 and ETCO2 at 24-hour epochs for 120 hours after admission. Bland-Altman plots were constructed at 24-hour epochs to assess the PaCO2-ETCO2 agreement.Results695 patients were included, with 3812 paired PaCO2 and ETCO2 data points. The median PaCO2-ETCO2 gradient on admission was 0.8 [0.4-1.4] kPa, Bland Altman Bias of 0.96, upper (+2.93) and lower (-1.00), and correlation R2 0.149. The gradient was significantly greater in patients with TBI plus concomitant injury, compared to those with isolated TBI (0.9 [0.4-1.5] kPa vs. 0.7 [0.3-1.1] kPa, p<0.05). Across all groups the gradient reduced over time. Patients who died within 30 days had a larger gradient on admission compared to those who survived; 1.2 [0.7-1.9] kPa and 0.7 [0.3-1.2] kPa, p<0.005.ConclusionsAmongst adult patients with TBI, the PaCO2-ETCO2 gradient was greater than previously reported values, particularly early in the patient journey, and when associated with concomitant chest injury. An increased PaCO2-ETCO2 gradient on admission was associated with increased mortality.

Dataset Information

Carbon Dioxide Reactivity of Brain Tissue Oxygenation after Pediatric Traumatic Brain Injury.

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Carbon Dioxide Reactivity of Brain Tissue Oxygenation after Pediatric Traumatic Brain Injury.

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