OBJECTIVE: To determine the local prevalence and optimal therapy for children with Barrett's esophagus (BE), the authors studied children with esophageal strictures or gastroesophageal reflux (GER), or both, to diagnose BE and to follow after therapy. SUMMARY BACKGROUND DATA: Barrett's esophagus is seldom reported in children and therapeutic recommendations are unclear. Barrett's esophagus usually develops during the mucosal reparative process after acid-reflux injury to the esophageal mucosa. Risk factors for BE include conditions that are associated with GER such as mental retardation, esophageal stricture, esophageal atresia, and reversed gastric tube esophagoplasty. Barrett's syndrome increases the risk of esophageal adenocarcinoma by 30 to 40 times. METHODS: All children with the risk factors had repeated esophagoscopy and multiple mucosal biopsies before and after therapy. RESULTS: Eleven children have been documented with BE. The initial diagnoses were: GER, 5; esophageal atresia, 4; nasogastric intubation, 1; lye ingestion, 1. A gastric tube esophagoplasty had been performed in three patients with BE in the esophagus proximal to the anastomosis. Three children with mid-esophageal strictures and long segments of BE had total resection with colic interposition. An additional two patients with tight stricture were treated with colic-patch esophagoplasty without resection. The final three patients were treated with fundoplication alone. CONCLUSIONS: Barrett's esophagus can be caused by acid from gastric tubes but responds to H2 blockers and diet. Resection eliminates BE; esophagoplasty only controls the stricture and must be accompanied by fundoplication. Barrett's esophagus persists in patients with fundoplication alone if reflux control is incomplete. The authors conclude that acid reflux must be controlled to treat BE successfully or the involved segment must be resected. Esophagogastrostomy apparently predisposes to BE.
OBJECTIVE: To determine the local prevalence and optimal therapy for children with Barrett's esophagus (BE), the authors studied children with esophageal strictures or gastroesophageal reflux (GER), or both, to diagnose BE and to follow after therapy. SUMMARY BACKGROUND DATA: Barrett's esophagus is seldom reported in children and therapeutic recommendations are unclear. Barrett's esophagus usually develops during the mucosal reparative process after acid-reflux injury to the esophageal mucosa. Risk factors for BE include conditions that are associated with GER such as mental retardation, esophageal stricture, esophageal atresia, and reversed gastric tube esophagoplasty. Barrett's syndrome increases the risk of esophageal adenocarcinoma by 30 to 40 times. METHODS: All children with the risk factors had repeated esophagoscopy and multiple mucosal biopsies before and after therapy. RESULTS: Eleven children have been documented with BE. The initial diagnoses were: GER, 5; esophageal atresia, 4; nasogastric intubation, 1; lye ingestion, 1. A gastric tube esophagoplasty had been performed in three patients with BE in the esophagus proximal to the anastomosis. Three children with mid-esophageal strictures and long segments of BE had total resection with colic interposition. An additional two patients with tight stricture were treated with colic-patch esophagoplasty without resection. The final three patients were treated with fundoplication alone. CONCLUSIONS: Barrett's esophagus can be caused by acid from gastric tubes but responds to H2 blockers and diet. Resection eliminates BE; esophagoplasty only controls the stricture and must be accompanied by fundoplication. Barrett's esophagus persists in patients with fundoplication alone if reflux control is incomplete. The authors conclude that acid reflux must be controlled to treat BE successfully or the involved segment must be resected. Esophagogastrostomy apparently predisposes to BE.