Jaskaran Rakkar1,2, Justin Azar1,2,3, Jonathan H Pelletier1,2, Alicia K Au1,2,4,5, Michael J Bell6, Dennis W Simon1,2,4,5, Patrick M Kochanek1,2,4, Robert S B Clark1,2,4,5, Christopher M Horvat7,8,9,10,11. 1. Department of Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA. 2. Safar Center for Resuscitation Research, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA. 3. Pediatric Critical Care, Geisinger Medical Center, Danville, PA, USA. 4. Department of Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA. 5. Brain Care Institute, UPMC Children's Hospital of Pittsburgh, Pittsburgh, PA, USA. 6. Division of Critical Care Medicine, Children's National Hospital, Washington, DC, USA. 7. Department of Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA. christopher.horvat@chp.edu. 8. Safar Center for Resuscitation Research, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA. christopher.horvat@chp.edu. 9. Department of Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA. christopher.horvat@chp.edu. 10. Brain Care Institute, UPMC Children's Hospital of Pittsburgh, Pittsburgh, PA, USA. christopher.horvat@chp.edu. 11. Department of Pediatrics, Division of Health Informatics, UPMC Children's Hospital of Pittsburgh, Pittsburgh, PA, USA. christopher.horvat@chp.edu.
Abstract
BACKGROUND: Brain 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. METHODS: Data 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. RESULTS: A 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. CONCLUSIONS: Lower 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.
BACKGROUND: Brain 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. METHODS: Data 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. RESULTS: A 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. CONCLUSIONS: Lower 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.
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