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DOI 10.1016/j.jpedsurg.2013.07.024

Медицинская библиотека · Journal of pediatric surgery · 2013

Evaluation of gastroesophageal function and mechanisms underlying gastroesophageal reflux in infants and adults born with esophageal atresia.

van Wijk Michiel, Knüppe Fransje, Omari Taher, de Jong Justin, Benninga Marc

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Аннотация

PURPOSE: To evaluate the mechanisms underlying gastroesophageal reflux (GER) following esophageal atresia (EA) repair and gastroesophageal function in infants and adults born with EA.

METHODS

Ten consecutive infants born with EA as well as 10 randomly selected adult EA patients were studied during their first postoperative follow-up visit and a purposely planned visit, respectively. A (13)C-octanoate breath test and esophageal pH-impedance-manometry study were performed. Mechanisms underlying GER and esophageal function were evaluated.

RESULTS

Transient lower esophageal sphincter relaxation (TLESR) was the most common mechanism underlying GER in infants and adults (66% and 62%, respectively). In 66% of all GER episodes, no clearing mechanism was initiated. On EFT, normal motility patterns were seen in six patients (four infants, two adults). One of these adults had normal motility overall (>80% of swallows). Most swallows (78.8%) were accompanied by abnormal motility patterns. Despite this observation, impedance showed normal bolus transit in 40.9% of swallows. Gastric emptying was delayed in 57.1% of infants and 22.2% of adults.

CONCLUSIONS

TLESR is the main mechanism underlying GER events in patients with EA. Most infants and adults have impaired motility, delayed bolus clearance, and delayed gastric emptying. However, normal motility patterns were seen in a minority of patients.

Для цитирования: van Wijk Michiel, Knüppe Fransje, Omari Taher, de Jong Justin, Benninga Marc. Evaluation of gastroesophageal function and mechanisms underlying gastroesophageal reflux in infants and adults born with esophageal atresia.. Journal of pediatric surgery. 2013. DOI: 10.1016/j.jpedsurg.2013.07.024.

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