PHYSIOLOGICAL-STUDIES OF GASTROESOPHAGEAL REFLUX AND AIRWAY PROTECTIVE RESPONSES IN THE YOUNG ANIMAL AND HUMAN INFANT

1. The mechanisms that underlie the Sudden Infant Death Syndrome (SIDS) must explain its two unique features; age at death and death during apparent sleep. 2. The occurrence of gastro-oesophageal reflux (GOR) during active sleep in infants presenting with apparent life threatening episodes (ALTE) and their similar age distribution to SIDS infants, suggested that reflux could be a cause of asphyxia. 3. Sleep related GOR was found to be a physiological and not a pathological event in normal, healthy term infants. 4. In healthy term infants, those infants that were formulated (who have a higher incidence of SIDS) had significantly longer oesophageal clearance times for acid reflux and significantly more active sleep compared with breast fed infants. 5. In very preterm infants (who are at increased risk for SIDS), both the frequency and duration of reflux during active sleep was significantly less at term equivalent age compared with healthy term infants, suggesting additional factors must operate to promote an ALTE. 6. One mechanism which may explain the pathogenesis of GOR could be that the reflux reaches the level of the pharynx and this, in turn, stimulates laryngeal receptors to produce apnoea. 7. Simulated reflux to the level of the pharynx in the sleeping piglet evoked airway protective responses, namely swallow, arousal and occasionally expectoration, but neither apnoea nor oxygen desaturation. 8. in the same piglets treated with pentobarbitone sodium, swallowing was impaired and arousal depressed. Simulated reflux to the pharynx produced significant apnoea and oxygen desaturation and death in two of five piglets. 9. In the infant, the co-existence of reflux to the level of the pharynx during sleep, together with impaired swallowing, depressed arousal or both, is one mechanism that may lead to an age-limited, sudden and fatal apnoea.