Patients with gastric outlet obstruction caused by caustic ingestion usually require surgical intervention [5]. However, in our study, 41% of cases did not need surgery, possibly due to early diagnosis and management within 3 weeks from ingestion and before the occurrence of scarring in the pylorus. In contrast to post-caustic oesophageal injury, limited series reporting the sequel of acid ingestion on the stomach have been published [6,7,8,9,10]. Although rare, a high index of suspicion must be maintained for acquired NHGOO, in the differential diagnosis of children with nonbilious vomiting and failure to thrive especially with metabolic alkalosis [3, 4]. Following diagnostic workup, appropriate management should be initiated [1]. Gastric outlet obstruction should be treated with EBD [1, 11, 12] of the pylorus or with surgery. The success of EBD is related to the timing after injury. All successful EBD in our series were done within 3 weeks from the injury. This might be related to the fact these cases were less affected to start with or due to the fibrosis not yet being severe enough to preclude successful EBD. The later explanation makes EBD intervention time sensitive. Whenever possible, EBD should be attempted within 3 weeks from injury to maximise the chances of successful nonoperative treatment. In our case series, the earliest EBD was attempted 9 days after injury.

Surgery remains the mainstay of management for GOO in late-presenting cases (usually after 3 weeks) or when nonoperative treatment fails. Surgical procedures used are multiple and include GJS, HMP and GDS [1, 3, 5, 13, 14]. The choice of surgical technique depends on the findings at laparotomy [5, 6], such as the extent of fibrosis in the pylorus or past surgeries in the same anatomical region, in addition to the surgeon’s preference and experience (in our case series, four surgeons were involved). When choosing surgical technique, the surgeon should consider the possibility of formation of adhesions and the need for reoperation and the possible complications of each procedure. We usually recommend attempting preservation of normal anatomical passage of enteric contents (HMP) over bypass procedures (GDS or GJS), which other authors agree with [5, 7, 8]. If the fibrosis at the level of the pylorus is limited to the mucosa, then pyloroplasty can be considered; otherwise, some form of bypass surgery is required [5].

A case of complete obstruction of the gastric outlet due to an unusual and previously undescribed cause is documented in our series: a high dose of NSAID (ibuprofen). The child presented within less than 24 h of taking the drug with a history of severe hematemesis and was admitted to the intensive care unit and required blood transfusion. The child was discharged 9 days after admission in a reasonable condition but presented 4 days later with progressive, postprandial non-bilious vomiting. The child had supportive treatment for 12 days. An early upper gastroduodenal endoscopy was not performed due to parental refusal. The patient was subsequently transferred to the surgical department and eventually had upper gastroduodenal endoscopy 25 days following ingestion. By that time, the child was severely malnourished, and the pylorus showed signs of ulceration and scarring leading to GOO. The pylorus would not even admit a wire to permit dilatation, and the child ended up having surgery.

Accidental caustic material ingestion by children still occurs in some developing countries [15]. Acquired GOO is a significant complication of caustic acid ingestion [16]. Most cases leading to pyloric stenosis in our study are related to SAI. The chemical is a colourless fluid, like water, and is used in the manufacturing of some large batteries. The incidence of SAI seems to have increased in northwest of Syria due to the widespread use of batteries in houses where main electrical supply is patchy and often non-existent. The fluid is commonly stored in inappropriate containers (sometimes water cans) and kept within households so it can be used to top-up battery fluid. This made it within the reach of young children, which led to the increase in ingestion cases [17].

No cases in our series had significant oesophageal injury, despite the severity of pyloric lesions. This suggests that the caustic effect on the pylorus is related to the stagnation that occurs at the level of the antrum, while the oesophagus is spared due to the rapid transit through it. It is generally thought that “acid licks the oesophagus and bites the pyloric antrum” [18]. These patients might benefit from delayed emptying of the stomach with an NGT, which is not generally recommended with other caustic material ingestions. This, however, needs clinical confirmation with prospective trials.

Two cases in our series were treated as peptic ulcers following an initial endoscopy, with an initial decision to repeat the endoscopy after few weeks. This might have resulted in missing the opportunity to treat pyloric strictures endoscopically. One case had delayed treatment due to parental refusal. Quite few cases reached us severely malnourished and/or dehydrated. There is clearly a room for improving awareness of this condition in the community and within medical practitioners. This will hopefully lead to improvement in storage conditions and earlier establishment of diagnosis and initiation of appropriate treatment.