Given pulse oximetry is increasingly substituting for arterial blood gas monitoring, noninvasive surrogate markers for lung disease severity are needed to stratify pediatric risk. We sought to validate prospectively the comparability of SpO2/Fio2 to PaO2/Fio2 and oxygen saturation index to oxygenation index in children. We also sought to derive a noninvasive lung injury score.
Prospective, multicentered observational study in six pediatric intensive care units.
One hundred thirty-seven mechanically ventilated children with SpO2 80% to 97% and an indwelling arterial catheter.
Simultaneous blood gas, pulse oximetry, and ventilator settings were collected. Derivation and validation data sets were generated, and linear mixed modeling was used to derive predictive equations. Model performance and fit were evaluated using the validation data set.
One thousand one hundred ninety blood gas, SpO2, and ventilator settings from 137 patients were included. Oxygen saturation index had a strong linear association with oxygenation index in both derivation and validation data sets, given by the equation oxygen saturation index = 2.76 1 0.547*oxygenation index (derivation). 1/SpO2/Fio2 had a strong linear association with 1/PaO2/Fio2 in both derivation and validation data sets given by the equation 1/SpO2/Fio2 = 0.00232 1 0.443/PaO2/Fio2 (derivation). SpO2/Fio2 criteria for acute respiratory distress syndrome and acute lung injury were 221 (95% confidence interval 215–226) and 264 (95% confidence interval 259–269). Multivariate models demonstrated that oxygenation index, serum pH, and Paco2 were associated with oxygen saturation index (p < .05); and 1/PaO2/Fio2, mean airway pressure, serum pH, and Paco2 were associated with 1/SpO2/Fio2 (p < .05). There was strong concordance between the derived noninvasive lung injury score and the original pediatric modification of lung injury score with a mean difference of 20.0361 α0.264 sd.
Lung injury severity markers, which use SpO2, are adequate surrogate markers for those that use PaO2 in children with respiratory failure for SpO2 between 80% and 97%. They should be used in clinical practice to characterize risk, to increase enrollment in clinical trials, and to determine disease prevalence. (Crit Care Med 2012; 40:–1316)
From the Children’s Hospital Los Angeles (RGK, PAR, CJLN), University of Southern California Keck School of Medicine, Los Angeles, CA; Penn State Children’s Hospital (NJT), Pennsylvania State University College of Medicine, Hershey, PA; the University of Virginia Children’s Hospital (VV, DFW), University of Virginia School of Medicine, Charlottesville, VA; Nationwide Children’s Hospital (JPS, MWH), The Ohio State University College of Medicine, Columbus, OH; Monroe Carell Children’s Hospital (TB), Vanderbilt University School of Medicine, Nashville, TN; and Cohen Children’s Medical Center of New York (JBS), North Shore Long Island Jewish Health System, New Hyde Park, NY.
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*See also p. 1386.
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Dr. Khemani received funding from the National Institutes of Health/National Library of Medicine 1RC1LM010639-01 and a fellowship from the Whittier Foundation. Dr. Willson received support from Pneuma Pharmaceuticals (50% salary support plus support for a research nurse). Dr. Thomas received support from the Food and Drug Administration 1R01FD003410-01A1. Dr. Thomas is a paid consultant and a member of the Scientific Advisory Board for Discovery Laboratories. Dr. Newth received funding from the National Institutes of Health/National Institute of Child Health and Human Development 2U10HD050012-06, National Institutes of Health/National Heart, Lung and Blood Institute 1U01HL094345-01, and a pharmacokinetics study from Hospira on dexmedetomidine in infants and children. The remaining authors have not disclosed any potential conflicts of interest.