Department of Pediatric Surgery, Hacettepe University Faculty of Medicine, Ankara 06100, Turkey.
J Pediatr Surg. 2010 Sep;45(9):1777-83. doi: 10.1016/j.jpedsurg.2010.04.014.
Gastric outlet obstruction (GOO) may be caused by various congenital and acquired conditions in children. The authors report 11 cases of GOO caused by muscular hypertrophy of the pylorus, which was proven histologically in 7. They describe this entity as "late-onset hypertrophic pyloric stenosis (HPS)," define the diagnostic criteria of the disease, and produce an algorithm for its management.
The medical records of patients with GOO treated from 1999 and 2009 were retrospectively reviewed. Patients with infantile HPS and GOO secondary to corrosive ingestion or neoplasm were not included. Age, sex, family history, presenting symptoms and signs, radiologic methods and findings, type of management, histopathologic features, and outcome were noted for each patient.
Eleven patients (4 male, 7 female) ranging in age from 2 to 8 years (mean, 3.6 years) were included in the study. The symptoms were nonbilious vomiting (n = 11), abdominal pain (n = 4), and weight loss (n = 2). Abdominal ultrasound (n = 6) and upper gastrointestinal contrast studies were obtained (n = 11). Gastroscopy revealed complete (n = 6) or partial (n = 5) obstruction of the pylorus. Balloon dilatation of the pylorus was performed in 5 cases and repeated in 3 cases. Conservative treatment was initially attempted in 11 patients. Two patients with chronic gastritis and Helicobacter pylori (n = 2) were treated with amoxicillin-clavulanic acid, clarithromycin, and lansoprazole. A Billroth I procedure was performed in 7 cases. Hypertrophied pyloric muscle was noted in 7 patients and chronic gastritis in 2. The postoperative course was uneventful.
Hypertrophic pyloric stenosis is rarely seen after infancy. Analysis of our results and review of the literature prompted us to redescribe this entity as "late-onset HPS" and define the diagnostic criteria. Late-onset HPS is probably an acquired disease of unknown etiology. The management of late-onset HPS has been summarized in an algorithm, which will also be useful in the treatment of GOO in children caused by etiologies other than classical infantile HPS.
胃出口梗阻(GOO)可由儿童的各种先天性和获得性疾病引起。作者报告了 11 例由幽门肌肥大引起的 GOO,其中 7 例经组织学证实。他们将这种实体描述为“迟发性肥厚性幽门狭窄(HPS)”,定义了该疾病的诊断标准,并提出了其管理算法。
回顾性分析了 1999 年至 2009 年治疗的 GOO 患者的病历。未包括婴儿型 HPS 和腐蚀性摄入或肿瘤引起的 GOO 患者。记录每位患者的年龄、性别、家族史、临床表现和体征、影像学方法和结果、治疗类型、组织病理学特征和结局。
研究纳入了 11 例年龄 2 至 8 岁(平均 3.6 岁)的患者(4 例男性,7 例女性)。症状为非胆汁性呕吐(n = 11)、腹痛(n = 4)和体重减轻(n = 2)。6 例行腹部超声检查,11 例行上消化道造影检查。胃镜检查显示幽门完全(n = 6)或部分(n = 5)梗阻。5 例行球囊扩张,3 例重复扩张。11 例患者最初尝试保守治疗。2 例慢性胃炎和幽门螺杆菌感染患者(n = 2)接受阿莫西林-克拉维酸、克拉霉素和兰索拉唑治疗。7 例行 Billroth I 手术。7 例患者发现肥厚性幽门肌,2 例患者发现慢性胃炎。术后过程顺利。
婴儿期后肥厚性幽门狭窄很少见。对我们的结果进行分析并复习文献后,我们将该实体重新描述为“迟发性 HPS”并定义了诊断标准。迟发性 HPS 可能是一种病因不明的获得性疾病。我们总结了迟发性 HPS 的治疗方案,该方案也将有助于治疗非经典婴儿型 HPS 引起的儿童 GOO。