RESPIRATORY CONDITIONS
A practical guide for paediatric registrars · Immature respiratory control in the preterm infant
The brainstem respiratory centres and chemoreceptor responses are immature. The core mechanism.
Immature CO₂ responses; in preterm infants, hypoxia can depress rather than stimulate breathing.
Poor pharyngeal tone leads to obstructive and mixed events.
Reflexes such as the laryngeal chemoreflex can provoke apnoea.
Sepsis, NEC, IVH, hypoglycaemia, anaemia, reflux and temperature all cause apnoea and must be excluded.
Why there's no "chest X-ray" panel here: AOP is a clinical diagnosis of exclusion, not an imaging one - the chest film is normal. Imaging and a septic/metabolic workup are used to rule out other causes of apnoea (sepsis, NEC, aspiration, IVH), not to confirm AOP.
Exclude the dangerous mimics first, then treat the immature control with caffeine and, where needed, airway support.
How do you distinguish apnoea of prematurity from apnoea due to another cause - and what makes you investigate?
What is the evidence base (CAP trial) for caffeine, and what are its benefits beyond apnoea?
Why does CPAP help obstructive and mixed apnoea?
When is it safe to stop caffeine and discharge?
Take-home message: Apnoea of prematurity is recurrent pauses (>20s, or shorter with bradycardia/desaturation) from immature respiratory control, appearing after the first day in preterm infants and resolving by ~34-37 weeks. It is a diagnosis of exclusion - new or worsening apnoea should prompt a search for sepsis, NEC, IVH or a metabolic cause. Treat with caffeine (first-line, with neurodevelopmental benefits per the CAP trial) and CPAP/high-flow for obstructive events, after excluding and treating other causes.
For educational purposes only. Always align management to current ANZCOR/NRP guidelines and your local SCN/NICU or NETS protocols.