Abnormal preoperative and postoperative esophageal peristalsis in gastroesophageal reflux

Insights

Nissen fundoplication effectively cures pediatric gastroesophageal reflux (GER) and normalizes pH monitoring. While lower esophageal sphincter length improves, abnormal esophageal peristalsis persists, suggesting it contributes to GER symptoms.

Area of Science:

  • Pediatric Gastroenterology
  • Gastrointestinal Surgery
  • Esophageal Motility Disorders

Background:

  • Gastroesophageal reflux (GER) in children can cause esophagitis and symptoms due to impaired antireflux mechanisms.
  • Nissen fundoplication is a surgical option for severe, symptomatic GER.
  • Understanding the impact of surgery on esophageal function is crucial for managing GER.

Purpose of the Study:

  • To evaluate the long-term effects of Nissen fundoplication on esophageal function in children with symptomatic GER.
  • To assess the correlation between esophageal peristalsis and clinical outcomes after surgery.
  • To investigate the role of different antireflux mechanisms in GER pathogenesis.

Main Methods:

  • Prospective study involving 14 children with symptomatic GER and esophagitis.
  • Pre- and post-operative (6 months) 24-hour pH monitoring and esophageal manometry.
  • Assessment of lower esophageal sphincter pressure (LESP), lower esophageal sphincter length (LESL), and esophageal wave patterns.

Main Results:

  • All patients achieved clinical cure of GER with normalized pH monitoring parameters post-surgery.
  • Lower esophageal sphincter length (LESL) significantly increased, but LESP remained unchanged.
  • Abnormal esophageal peristalsis (tertiary waves) persisted postoperatively, indicating persistent motility issues.

Conclusions:

  • Nissen fundoplication effectively corrects GER by creating a competent antireflux barrier, even with impaired esophageal peristalsis.
  • Persistent abnormal peristalsis suggests a dual failure of the antireflux mechanism (LES and esophageal pump) in severe GER.
  • Surgical restoration of the LES barrier alone can compensate for esophageal motility deficits, leading to clinical improvement.

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