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Published on: April 17, 2020
Strain induced augmentation of upper oesophageal sphincter pressure in children
J Willing1, Y Furukawa, G P Davidson
1Gastroenterology Unit, Adelaide Children's Hospital, South Australia.
Insights
Gastroesophageal reflux in children is not caused by a defective upper esophageal sphincter response to straining. Instead, a failure to augment upper esophageal sphincter tone during strain may be a secondary factor in developing reflux.
Area of Science:
- Pediatric Gastroenterology
- Physiology
- Reflux Disorders
Background:
- Gastroesophageal reflux (GER) is a common concern in infants and children.
- Oesophagopharyngeal reflux (OPR) is a specific type of reflux involving the pharynx and esophagus.
- The role of the upper oesophageal sphincter (UES) in OPR during straining is not fully understood.
Purpose of the Study:
- To investigate the hypothesis that troublesome oesophagopharyngeal reflux arises from defective upper oesophageal sphincter response to straining in children.
- To analyze the pressure dynamics of the pharynx, UES, oesophageal body, and gastric pressures during spontaneous straining events in children with suspected GER.
Main Methods:
- Study included 53 children (2-81 months) referred for suspected GER.
- Analysis of spontaneously occurring pharyngeal, UES, oesophageal body, and gastric pressures after feeding.
- Identification and analysis of inspiratory strain and sustained strain episodes.
Main Results:
- During inspiratory strain, UES pressure significantly increased (5 to 27 mm Hg, p < 0.01).
- Sustained strains also augmented UES pressure (39 to 60 mm Hg, p < 0.01).
- No significant difference in UES response patterns to straining was observed between children with and without OPR.
Conclusions:
- The study suggests that a defective UES response to straining is unlikely to be the primary cause of OPR in children.
- Failure of UES tone augmentation during strain-induced increases in oesophageal pressure may be a secondary factor in OPR development.
- Further research is needed to elucidate the precise mechanisms of OPR in pediatric populations.
Abstract:
The hypothesis that troublesome oesophagopharyngeal reflux arises from defective upper oesophageal sphincter response to straining has been evaluated in 53 children aged two to 81 months (median 13) referred with symptoms thought to be related to gastro-oesophageal reflux. Spontaneously occurring pharyngeal, upper oesophageal sphincter, oesophageal body, and gastric pressures were analysed after feeding. Inspiratory strain was the most common spontaneously occurring strain (172 episodes), defined as an oesophageal body inspiratory negative pressure dip at least twice the size of the normal inspiratory wave. Overall, during inspiratory strain, upper oesophageal sphincter pressure was significantly higher than before straining (p < 0.01) (5 v 27 mm Hg, p < 0.01). Sustained strains defined as increases in gastric and oesophageal body pressure for two to 20 seconds were also common (149 episodes) and when compared with just before straining, also augmented upper oesophageal sphincter pressure (60 v 39 mm Hg, p < 0.01). The vigour of straining, estimated as increase of gastric pressure, correlated significantly with the degree of augmentation of upper oesophageal sphincter pressure (p < 0.05). Children with and without evidence of troublesome oesophagopharyngeal reflux showed no difference in upper oesophageal sphincter response patterns to straining. Failure of augmentation of upper oesophageal sphincter tone in the face of strain induced increases of oesophageal body pressure is probably a secondary factor in the production of oesophagopharyngeal reflux in children.
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