Chang Gung medical journal · 2006
Gastric outlet obstruction in pediatric patients.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
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Yen Ju-Bei, Kong Man-Shan
Аннотация
BACKGROUND: This study reports the etiologies, management and outcome of children with gastric outlet obstruction (GOO) in a children's hospital.
METHODS: The medical records of 11 children with GOO not associated with idiopathic hypertrophic pyloric stenosis (IHPS) were reviewed. They were categorized into one group of anatomic abnormality (AA group) and one group of peptic ulcer disease (PD group). One case underwent episodes of GOO caused by anatomic abnormality and peptic ulcer disease, respectively.
RESULTS: Six cases belonged to the AA group. Mean age was 58 months with a male to female ratio of two to four. Underlying etiologies were prepyloric mass (2), web (2) and gastric volvulus (2). Four patients underwent surgery. One patient was lost to follow-up. GOO did not recur in the follow-up period (mean duration 24 months) in the remaining cases. One case in the AA group and the remaining five patients composed the PD Group. Mean age was 49 months and all were male. Underlying causes were gastric ulcers (4) and chronic duodenal ulcers (2). Two of the five patients had Helicobacter pylori infection found by rapid urease test. Four patients recovered after medical management and another two, with normal serum gastrin levels, underwent surgery because of poor response to medical treatment. One case was lost to follow-up. No recurrence of GOO was noted in the follow-up period (mean duration 27 months) in the remaining cases.
CONCLUSIONS: In our study, peptic ulcer disease was as important as anatomic abnormalities as the etiology for GOO not associated with IHPS, and medical management could release GOO caused by it. Compared to adult patients, H. pylori infection played a less important etiologic role in pediatric patients with GOO.
METHODS: The medical records of 11 children with GOO not associated with idiopathic hypertrophic pyloric stenosis (IHPS) were reviewed. They were categorized into one group of anatomic abnormality (AA group) and one group of peptic ulcer disease (PD group). One case underwent episodes of GOO caused by anatomic abnormality and peptic ulcer disease, respectively.
RESULTS: Six cases belonged to the AA group. Mean age was 58 months with a male to female ratio of two to four. Underlying etiologies were prepyloric mass (2), web (2) and gastric volvulus (2). Four patients underwent surgery. One patient was lost to follow-up. GOO did not recur in the follow-up period (mean duration 24 months) in the remaining cases. One case in the AA group and the remaining five patients composed the PD Group. Mean age was 49 months and all were male. Underlying causes were gastric ulcers (4) and chronic duodenal ulcers (2). Two of the five patients had Helicobacter pylori infection found by rapid urease test. Four patients recovered after medical management and another two, with normal serum gastrin levels, underwent surgery because of poor response to medical treatment. One case was lost to follow-up. No recurrence of GOO was noted in the follow-up period (mean duration 27 months) in the remaining cases.
CONCLUSIONS: In our study, peptic ulcer disease was as important as anatomic abnormalities as the etiology for GOO not associated with IHPS, and medical management could release GOO caused by it. Compared to adult patients, H. pylori infection played a less important etiologic role in pediatric patients with GOO.