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Apnoea-triggered increase in fraction of inspired oxygen in preterm infants: a randomised cross-over study
  1. Andrew Marshall1,
  2. Oliver J Ladlow2,
  3. Charlotte Bannink2,
  4. Kathleen Lim3,
  5. Sanoj K M Ali4,
  6. Timothy J Gale1,
  7. Peter A Dargaville3,4
  1. 1 School of Engineering, College of Sciences and Engineering, University of Tasmania, Hobart, Tasmania, Australia
  2. 2 School of Medicine, College of Health and Medicine, University of Tasmania, Hobart, Tasmania, Australia
  3. 3 Menzies Institute for Medical Research, College of Health and Medicine, University of Tasmania, Hobart, Tasmania, Australia
  4. 4 Department of Paediatrics, Royal Hobart Hospital, Hobart, Tasmania, Australia
  1. Correspondence to Andrew Marshall, School of Engineering, University of Tasmania College of Sciences and Engineering, Hobart, Tasmania, Australia; andrew.marshall{at}


Objectives To investigate the impact of a pre-emptive apnoea triggered oxygen response on oxygen saturation (SpO2) targeting following central apnoea in preterm infants.

Design Interventional crossover study of a 12-hour period of automated oxygen control with an apnoea response (AR) module, nested within a crossover study of a 24-hour period of automated oxygen control compared with aggregated data from two flanking 12-hour periods of manual control.

Setting Neonatal intensive care unit

Patients Preterm infants receiving non-invasive respiratory support and supplemental oxygen; median (IQR) birth gestation 27 (26–28) weeks, postnatal age 17 (12–23) days.

Intervention Automated oxygen titration with an automated control algorithm modified to include an AR module. Alterations to inspired oxygen concentration (FiO2) were actuated by a motorised blender. Desired SpO2 range was 90–94%. Apnoea detection was by capsule pneumography.

Main outcome measures Duration, magnitude and area under the curve (AUC) of SpO2 deviations following apnoea; frequency and duration of apnoeic events. Comparisons between periods of manual, automated and automated control with AR module.

Results In 60 studies in 35 infants, inclusion of the AR module significantly reduced AUC for SpO2 deviations below baseline compared with both automated and manual control (manual: 87.1%±107.6% s, automated: 84.6%±102.8% s, AR module: 79.4%±102.7% s). However, there was a coincident increase in SpO2 overshoot (AUC (SpO2>SpO2(onset)); manual: 44.3±99.9% s, automated: 54.7%±103.4% s, AR module: 65.7%±126.2% s).

Conclusion Automated control with a pre-emptive apnoea-triggered FiO2 boost resulted in a modest reduction in post-apnoea hypoxaemia, but was followed by a greater SpO2 overshoot.

Trial registration number ACTRN12616000300471.

  • Neonatology
  • Respiratory Medicine
  • Intensive Care Units, Neonatal
  • Technology

Data availability statement

No data are available.

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  • Contributors AM conceived and developed the algorithm and study equipment, assisted in conducting the study, compiled and analysed the data, wrote the first draft of the manuscript and approved the final version. OJL, CB, and SKMA enrolled eligible infants, reviewed and edited the manuscript and approved the final version. KL compiled and analysed the data, edited the manuscript and approved the final version. TJG conceived the study (with PAD), oversaw its conduct, reviewed and edited the manuscript and approved the final version. PAD conceived the study (with TJG), oversaw its conduct, oversaw data analysis and interpretation, reviewed and edited the manuscript and approved the final version. All authors approved the final manuscript as submitted and agree to be accountable for all aspects of the work. PAD is the guarantor.

  • Funding Supported by grants from the Royal Hobart Hospital Research Foundation, Hobart, Australia (12-019 and 15-203).

  • Competing interests The University of Tasmania and Royal Hobart Hospital have jointly lodged a patent application concerning automated control of inspired oxygen concentration in the newborn infant. TJG and PAD are named inventors. The authors have no other conflicts of interest relevant to this article to disclose.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.