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PaCO2 in Surfactant, Positive Pressure, and Oxygenation Randomised Trial (SUPPORT)
  1. Namasivayam Ambalavanan1,
  2. Waldemar A Carlo1,
  3. Lisa A Wrage2,
  4. Abhik Das3,
  5. Matthew Laughon4,
  6. C Michael Cotten5,
  7. Kathleen A Kennedy6,
  8. Abbot R Laptook7,
  9. Seetha Shankaran8,
  10. Michele C Walsh9,
  11. Rosemary D Higgins10
  12. For the SUPPORT Study Group of the NICHD Neonatal Research Network
  1. 1Department of Pediatrics, University of Alabama at Birmingham, Birmingham, Alabama, USA
  2. 2Social, Statistical and Environmental Sciences Unit, RTI International, Research Triangle Park, North Carolina, USA
  3. 3Social, Statistical and Environmental Sciences Unit, RTI International, Rockville, Maryland, USA
  4. 4Department of Pediatrics, University of North Carolina, Chapel Hill, North Carolina, USA
  5. 5Department of Pediatrics, Duke University, Durham, North Carolina, USA
  6. 6Department of Pediatrics, University of Texas Medical School at Houston, Houston, Texas, USA
  7. 7Department of Pediatrics, Women and Infants Hospital, Providence, Rhode Island, USA
  8. 8Department of Pediatrics, Wayne State University, Detroit, Michigan, USA
  9. 9Department of Pediatrics, Rainbow Babies & Children's Hospital, Case Western Reserve University, Cleveland, Ohio, USA
  10. 10Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, USA
  1. Correspondence to Dr Namasivayam Ambalavanan, University of Alabama at Birmingham, 176F Suite 9380, Women and Infants Center, 619 South 20th St., Birmingham, AL 35249, USA; ambal{at}uab.edu

Abstract

Objective To determine the association of arterial partial pressure of carbon dioxide PaCO2 with severe intraventricular haemorrhage (sIVH), bronchopulmonary dysplasia (BPD), and neurodevelopmental impairment (NDI) at 18–22 months in premature infants.

Design Secondary exploratory data analysis of Surfactant, Positive Pressure, and Oxygenation Randomised Trial (SUPPORT).

Setting Multiple referral neonatal intensive care units.

Patients 1316 infants 24 0/7 to 27 6/7 weeks gestation randomised to different oxygenation (SpO2 target 85–89% vs 91–95%) and ventilation strategies.

Main outcome measures Blood gases from postnatal day 0 to day14 were analysed. Five PaCO2 variables were defined: minimum (Min), maximum (Max), SD, average (time-weighted), and a four level categorical variable (hypercapnic (highest quartile of Max PaCO2), hypocapnic (lowest quartile of Min PaCO2), fluctuators (hypercapnia and hypocapnia), and normocapnic (middle two quartiles of Max and Min PaCO2)). PaCO2 variables were compared for infants with and without sIVH, BPD and NDI (±death). Multivariable logistic regression models were developed for adjusted results.

Results sIVH, BPD and NDI (±death) were associated with hypercapnic infants and fluctuators. Association of Max PaCO2 and outcomes persisted after adjustment (per 10 mm Hg increase: sIVH/death: OR 1.27 (1.13 to 1.41); BPD/death: OR 1.27 (1.12 to 1.44); NDI/death: OR 1.23 (1.10 to 1.38), death: OR 1.27 (1.12 to 1.44), all p<0.001). No interaction was found between PaCO2 category and SpO2 treatment group for sIVH/death, NDI/death or death. Max PaCO2 was positively correlated with maximum FiO2 (rs0.55, p<0.0001) and ventilator days (rs0.61, p<0.0001).

Conclusions Higher PaCO2 was an independent predictor of sIVH/death, BPD/death and NDI/death. Further trials are needed to evaluate optimal PaCO2 targets for high-risk infants.

  • Neonatology
  • Respiratory
  • Neurodisability
  • Mortality
  • Intensive Care

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