Gut 51:475-479 doi:10.1136/gut.51.4.475
  • Gastro-oesophageal reflux

Mechanisms of gastro-oesophageal reflux in preterm and term infants with reflux disease

  1. T I Omari1,
  2. C P Barnett2,
  3. M A Benninga3,
  4. R Lontis2,
  5. L Goodchild2,
  6. R R Haslam2,
  7. J Dent4,
  8. G P Davidson1
  1. 1Centre for Paediatric and Adolescent Gastroenterology, Women’s and Children’s Hospital and Department of Paediatrics, University of Adelaide, Australia
  2. 2Neonatal Medicine Unit, Women’s and Children’s Hospital, North Adelaide, Australia
  3. 3Academic Medical Centre, Amsterdam, the Netherlands
  4. 4Gastrointestinal Medicine, Royal Adelaide Hospital, Adelaide, Australia.
  1. Correspondence to:
    Dr T I Omari, Centre for Paediatric and Adolescent Gastroenterology, Women’s and Children’s Hospital, North Adelaide, Australia 5006;
  • Accepted 6 February 2002


Background: Transient lower oesophageal sphincter relaxation (TLOSR) is the predominant mechanism of gastro-oesophageal reflux (GOR) in healthy infants but the mechanisms of GOR in infants with GOR disease (GORD) are poorly understood.

Aims: To measure the occurrence of TLOSR, GOR, and gastric emptying (GE) rate in preterm and term infants with GORD.

Patients: Thirty six infants were studied and grouped as normals or GORD based on a routine clinical assessment and confirmation of an assessment of GORD by reflux symptom charts and oesophageal pH monitoring.

Methods: A micromanometric assembly incorporating a micro pH electrode recorded oesophageal motility and pH. GE rate was determined using the 13C-octanoic acid breath test.

Results: TLOSR was the predominant mechanism of GOR, triggering 50–100% of GOR episodes (median 91.5%). Abdominothoracic straining significantly increased the occurrence of GOR in association with TLOSR. In infants with GORD, the number of TLOSRs overall was similar to normals but the proportion of TLOSRs accompanied by acid GOR was significantly higher than in normals (16.5% v 5.7%, respectively; p<0.001). Infants with GORD had a similar GE rate to normals.

Conclusions: In infant GORD, acid reflux associated TLOSRs are abnormally common and likely to be a major contributing factor to the pathophysiology of GORD. Infants with GORD do not have delayed GE.