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A Swine Model of Neonatal Asphyxia
Published on: October 11, 2011
Apnoea-triggered increase in fraction of inspired oxygen in preterm infants: a randomised cross-over study
Andrew Marshall1, Oliver J Ladlow2, Charlotte Bannink2
1School of Engineering, College of Sciences and Engineering, University of Tasmania, Hobart, Tasmania, Australia andrew.marshall@utas.edu.au.
Insights
Automated oxygen control with an apnoea response module modestly reduced hypoxemia in preterm infants. However, this intervention also led to increased oxygen saturation (SpO2) overshoot following apnoea.
Area of Science:
- Neonatal medicine
- Respiratory physiology
- Medical technology
Background:
- Preterm infants often experience central apnoea, leading to potentially harmful fluctuations in oxygen saturation (SpO2).
- Automated oxygen control systems aim to maintain target SpO2 levels, but their efficacy during apnoeic events requires further investigation.
Purpose of the Study:
- To evaluate the impact of a pre-emptive apnoea-triggered oxygen response on SpO2 targeting in preterm infants experiencing central apnoea.
- To compare the effectiveness of automated oxygen control with and without an apnoea response (AR) module against manual control.
Main Methods:
- An interventional crossover study involving preterm infants receiving non-invasive respiratory support and supplemental oxygen.
- Automated oxygen titration using a motorized blender, with an AR module designed to detect apnoea via capsule pneumography and adjust inspired oxygen concentration (FiO2).
- SpO2 deviations, apnoea frequency, and duration were measured and compared across manual, automated, and automated with AR module control periods.
Main Results:
- The AR module significantly reduced the area under the curve (AUC) of SpO2 deviations below baseline compared to both automated and manual control.
- Despite reducing hypoxemia, the AR module was associated with a notable increase in SpO2 overshoot (AUC of SpO2 > SpO2(onset)).
Conclusions:
- A pre-emptive, apnoea-triggered FiO2 boost in automated oxygen control offers a modest benefit in reducing post-apnoea hypoxemia in preterm infants.
- The observed increase in SpO2 overshoot necessitates careful consideration of the overall impact and potential risks of this intervention.
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.
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