Non-hypertrophic gastric outlet obstruction in the paediatric population: a case series with focus on management

Elhalaby E.A., Halawa N.A., Elhalaby I.E., Shawky D., Hassan H., Almetaher H.A.

Gastric outlet obstruction (GOO) may follow acid corrosive ingestion. Several surgical techniques have been reported after the failure of endoscopic dilatation. The aim of this study was to evaluate the feasibility and safety of Heinecke-Mikulicz pyloroplasty (HMP) through a circum-umbilical skin incision in children with pyloric stricture after accidental acid corrosive ingestion. Seven patients were males and 4 were females, their ages ranged from 17 months to 6 years at the time of definitive treatment. The surgery was completed successfully in all patients through the circum-umbilical incision. Vertical extension of skin incision was needed in one patient. The pylorus was grossly affected in 9 patients. Both pylorus and gastric antrum were involved in 2 patients. Nine patients had an excellent postoperative course with the cessation of vomiting and progressive weight gain. One patient developed postoperative recurrent stricture treated by gastrojejunostomy. Another patient with associated esophageal stricture responded to repeated endoscopic dilatation for the esophageal stricture and pyloroplasty for the pyloric stricture. No surgical site infection or wound dehiscence occurred in any patient. Heinecke-Mikulicz pyloroplasty through a circum-umbilical approach is both feasible and safe in the majority of children with post-acid corrosive GOO. It is associated with satisfactory wound healing and excellent cosmetic outcome. Different techniques are recommended in cases of severe pyloric stricture associated with significant proximal gastric antral scarring.

Lone Y.A., Hushain D., Chana R.S., Khan R.A., Sachdeva S., Mushtaq E.

Idiopathic hypertrophic pyloric stenosis is by far the most common cause of gastric outlet obstruction (GOO) in young infants, with more than 90% of cases presenting between 3 and 10 weeks after birth. While cases of late onset pyloric stenosis beyond infancy have been reported, the etiology is poorly understood. We report our experience of 5 cases, describing the similarities and differences in management of our patient population which happens to be the second largest reported in literature.From July 2014 to June 2018 (4 years) a total of five patients of primary acquired GOO were encountered at our center.The age range was 3 to 6 years and only one of them was a female. All presented with characteristic nonbilious vomiting that was recurrent and episodic. Upper GI (gastrointestinal) contrast study series revealed a dilated stomach and delayed gastric emptying. Upper GI endoscopy also demonstrated a dilated stomach without any intraluminal polyp, ulcer or any other pathology. Intraoperatively the pylorus had no evidence of scarring, inflammation, external compression or any mass in and around the pylorus. A retrocolic gastrojejunostomy was curative in all patients.Though rare, one must maintain a high index of suspicion for primary acquired GOO in the differential diagnosis of older children with nonbilious vomiting and failure to thrive. Following appropriate diagnostic workup, surgical interventions should be performed expeditiously because adequate nutrition is key to proper physical and mental development of the child. Further research will hopefully elucidate the underlying pathophysiology in order to guide clinical options for both prevention and treatment.Retrospective single center study.Level 4.

El-Asmar K.M., Allam A.M.

The purpose of this study was to report surgical management and outcome of corrosive-induced gastric injuries in children at our institute over the last decade.Medical records of patients admitted for corrosive-induced gastric injury at the Pediatric Surgery Department of Ain Shams University between January 2007 and January 2017 were retrospectively reviewed.Twenty six cases (17 boys and 9 girls) were enrolled. Mean age was 3.61±1.29. Ingested agent was acid in all the patients. Main presenting symptom was gastric output obstruction in 22 cases. The interval between corrosive ingestion and presentation ranged from one to 135days (mean=43.9±34). Surgical procedure included total gastrectomy (n=2), partial gastrectomy (n=2), augmentation gastroplasty (n=1), Billroth I (n=2), antrectomy (n=2), antroplasty (n=3), gastrojejunostomy (n=2), Heineke-Mikulicz pyloroplasty (n=9), Finney pyloroplasty (n=5), and feeding jejunostomy (n=4). Anastomotic stricture requiring a second operation developed in one patient. There were three mortalities related to the associated esophageal strictures. The mean follow-up period is 3.5years. All patients are free of symptoms and gained adequate weight.Surgery is the mainstay of management for corrosive-induced gastric injuries with good long-term results. Surgical procedure should be tailored according to the patient's general condition and extent of gastric injury.This is a case series with no comparison group (level IV).

Chao H.

Endoscopic balloon dilatation (EBD) and surgical intervention are two most common and effective treatments for gastric outlet obstruction. Correction of gastric outlet obstruction without the need for surgery is an issue that has been tried to be resolved in these decades; this management has developed with EBD, advanced treatments like local steroid injection, electrocauterization, and stent have been added recently. The most common causes of pediatric gastric outlet obstruction are idiopathic hypertrophic pyloric stenosis, peptic ulcer disease followed by the ingestion of caustic substances, stenosis secondary to surgical anastomosis; antral web, duplication cyst, ectopic pancreas, and other rare conditions. A complete clinical, radiological and endoscopic evaluation of the patient is required to make the diagnosis, with complimentary histopathologic studies. EBD are used in exceptional cases, some with advantages over surgical intervention depending on each patient in particular and on the characteristics and etiology of the gastric outlet obstruction. Local steroid injection and electrocauterization can augment the effect of EBD. The future of endoscopic treatment seems to be aimed at the use of endoscopic electrocauterization and balloon dilatations.

Andrade M., Sawamura R., Cupo P., Lopes Del Ciampo I.R., Fernandes M.I.

Accidental corrosive ingestion is not rare in pediatric patients in developing countries. We report a case of gastric outlet obstruction after the accidental ingestion of an acidic substance by a child who was successfully treated with endoscopic balloon dilatation.

Urganci N., Usta M., Kalyoncu D., Demirel E.

To evaluate children who ingested corrosive substances, in terms of demographic features, nature of ingested substances, clinical findings, management and complications. A total of 1709 cases aged between 0 and 16 y who ingested corrosive substance were analyzed retrospectively by evaluating the medical records of the patients. The mean age of the cases was 35.23 ± 30.65 mo and male:female ratio was 1.45. Forty one percent of corrosive substances causing intoxication contained NaOH. Thirty percent of the families consisted of 5 or more members. Fourteen percent of the mothers were illiterate. Stricture formation was observed in 29 (1.69 %) of the cases during follow-up. In 79.31 % of those cases alkaline substance ingestion was responsible for stricture development. It was found that stricture formation occurred more frequently among cases who were older than 5 y of age and this finding was statistically significant (p = 0.001). The cases older than 5 y of age with the diagnosis of grade 2b esophagitis must be followed up closely for the stricture formation. In order to protect children from corrosive ingestion, importance must be given to preventive measures such as education of families, keeping and storing these agents out of the reach of children and providing safety caps for these products.

Contini S.

Prevention has a paramount role in reducing the incidence of corrosive ingestion especially in children, yet this goal is far from being reached in developing countries, where such injuries are largely unreported and their true prevalence simply cannot be extrapolated from random articles or personal experience. The specific pathophysiologic mechanisms are becoming better understood and may have a role in the future management and prevention of long-term consequences, such as esophageal strictures. Whereas the mainstay of diagnosis is considered upper gastrointestinal endoscopy, computed tomography and ultrasound are gaining a more significant role, especially in addressing the need for emergency surgery, whose morbidity and mortality remains high even in the best hands. The need to perform emergency surgery has a persistent long-term negative impact both on survival and functional outcome. Medical or endoscopic prevention of stricture is debatable, yet esophageal stents, absorbable or not, show promising data. Dilatation is the first therapeutic option for strictures and bougies should be considered especially for long, multiple and tortuous narrowing. It is crucial to avoid malnutrition, especially in developing countries where management strategies are influenced by malnutrition and poor clinical conditions. Late reconstructive surgery, mainly using colon transposition, offers the best results in referral centers, either in children or adults, but such a difficult surgical procedure is often unavailable in developing countries. Possible late development of esophageal cancer, though probably overemphasized, entails careful and long-term endoscopic screening.

Otjen J.P., Iyer R.S., Phillips G.S., Parisi M.T.

Gastric outlet obstruction in children encompasses a spectrum of disorders that extends beyond hypertrophic pyloric stenosis. Each condition can result in the clinical syndrome of persistent nonbilious vomiting, which can progress to dehydration and electrolyte imbalances. This paper reviews the spectrum of both the common and uncommon entities that cause partial or complete gastric outlet obstruction and their imaging appearances. The correct diagnosis of those with gastric outlet obstruction can be achieved by combining clinical presentation with appropriate imaging, leading to optimal and timely patient management.

Özokutan B.H., Ceylan H., Ertaşkın İ., Yapıcı S.

Corrosive substance ingestion is still a major medical and social problem for children. Gastric injury after corrosive ingestion is relatively uncommon as compared with esophageal injury. Gastric outlet obstruction (GOO) is a significant complication of corrosive ingestion. Medical records of 20 consecutive patients with GOO due to corrosive ingestion during an 8-year period between 2002 and 2009 were retrospectively reviewed. There were 10 boys and 10 girls with a mean age of 5.1 years (1.5–15 years). Ingested material was acid in all the patients. Two patients had associated esophageal stricture. The mean time between the ingestion and the development of GOO was 27.8 days (range 21–45 days) and all the patients presented with postprandial epigastric distension, nonbilious vomiting and weight loss. Surgical treatment included gastroduodenostomy (n = 8), Billroth I (n = 7), pyloroplasty (n = 5), and gastrojejunostomy (n = 2) procedures for GOO. Anastomotic stricture requiring a second operation developed in two patients. There was no surgical mortality. The mean follow-up is 3.3 years and all patients are free of symptoms. GOO is one of the most common gastric complications of corrosive ingestion that may require surgical treatment. Prevention of corrosive ingestion has great importance to avoid such complications.

Chan K.L., Saing H.

In the past 3 years, three children (ages 2, 4, and 8 years) suffering from peptic pyloric stenosis and repeated vomiting were treated in our department with balloon dilatation followed by H2-receptor antagonist therapy. After the dilatation, all three patients could take solid food without vomiting. There were no complications as a result of the procedures. During a mean follow-up of 17 months (range, 5-30) there was no recurrence of symptoms. The method of dilatation is described, and we recommend it as an option for the initial nonoperative treatment of pediatric peptic pyloric stenosis. The long-term results of balloon dilatation of peptic pyloric stenosis will, however, require further evaluation.

Özcan C., Ergün O., Şen T., Mutaf O.

Gastric outlet obstruction (GOO) is a well-known complication of acid ingestion. However, most reports deal with adults. In this report, the authors present their experience with the treatment of acid-induced GOO in children.The records of patients admitted for unintentional ingestion of corrosive agents between 1980 and 2002 were reviewed retrospectively. Data concerning age at ingestion, type of ingested substance, time between ingestion and the first signs of GOO, weight loss, treatment, complications, duration of hospital stay, and long-term follow-up were reviewed.GOO was not observed in any of the children admitted for alkaline ingestion, whereas GOO developed in 8 of 98 children (8.2%) in a mean period of 26.7 +/- 10 days after the ingestion of acid substances. Presenting symptoms were frequent nonbilious vomiting and marked weight loss. All had pyloric obstructions in the upper gastrointestinal series and required surgical intervention. Gastrojejunostomy was the operation of choice for all patients. Oral feedings were started on the third postoperative day. The complications were wound infection in 1 and upper gastrointestinal bleeding in another in the early postoperative period. Mean follow-up is 8.33 +/- 4.45 (4.8-18.7) years. No late complications such as marginal ulcus or stricture at the anastomosis site were observed in the series.Treatment of GOO with gastrojejunostomy gives good long-term results in children. This procedure is safe and causes minimal morbidity particularly in patients without extensive gastric damage.

Tekant G., Eroğlu E., Erdoğan E., Yeşildağ E., Emir H., Büyükünal C., Yeker D.

During the last 5 years, 61 children were admitted to the authors' hospital because of corrosive substance ingestion, and among them 6 patients were seen with gastric outlet obstruction. Two of them had ingested acid substances, and the other 4 had ingested alkali corrosives. The mean age was 2.9 years (range, 1.5 to 3). Their common complaint was postprandial vomiting, which had begun 3 weeks after the event (range, 1 week to 10 weeks). Endoscopic evaluation and barium contrast radiographies were performed at admission. Four patients had a pyloric stricture, 1 had an antral stricture, and another had an antropyloric stricture. Balloon dilatation of the pylorus (in 1 patient), pyloroplasty (in 3 patients), and Billroth I procedures (in 2 patients) were performed. The mean follow-up period was 22 months (range, 6 weeks to 48 months). One patient, who had undergone a Billroth I procedure, underwent reoperation because of intestinal obstruction 3 months later. On follow-up they are all free of symptoms.The treatment of gastric outlet obstruction caused by corrosive ingestion should be treated surgically. Although endoscopic and radiologic evaluation helps to determine the time and necessity, once the diagnosis is confirmed, early definitive surgical intervention should be performed, and the type of the surgery depends mostly on the findings of the surgeon at laparotomy. Endoscopic balloon dilatation of the pylorus maybe attempted in suitable cases. Special care should be given to prevent children from accidental corrosive ingestion.

Ciftci A.O., Şenocak M.E., Büyükpamukç N., Hiçsönmez A.

A retrospective clinical study was performed to determine the incidence, management, and outcome of gastric outlet obstruction (GOO) caused by caustic ingestion in children. Of 220 patients who sustained caustic substance ingestion and were treated at our unit between 1976 and 1996, 168 ingested alkaline substances; of these, 9 children (5.3%) developed GOO in addition to esophageal strictures. The remaining 52 patients ingested acid agents, and 2 of them (3.8%) presented with GOO without esophageal strictures. The overall incidence of corrosive GOO was 5% (n = 11). The mean age of the patients with GOO was 5.7 ± 2.8 years (range 2–14) with a female:male ratio of 6:5. Sodium hydroxide (n = 6), potassium hydroxide (n = 3), and hydrochloric acid (n = 2) were the ingested caustic agents. The patients were subdivided into two groups according to serial endoscopic and radiologic findings: group I: moderate (dense superficial and spotty ulcerations with intact mucosa) mucosal injury with partial pyloric obstruction; and group II: severe (deep ulcerations, extreme hemorrhagic erosions, eschar formation with white plaques) mucosal injury with complete pyloric obstruction. Group I consisted of 5 patients who ingested alkali agents while group II included 6 who presented with ingestion of alkaline (n = 4) and acid (n = 2) agents. Surgical treatment included Billroth I (n = 6) operations performed in group II and Finney (n = 3) and Heineke-Mikulicz (n = 2) pyloroplasty procedures done in group I. All patients are alive without any complaints. Fiberoptic endoscopy should be the preferred method of evaluating a patient with ingestion of a corrosive agent. It determines the presence of injury and assesses the extent of damage, establishing the diagnosis and allowing therapy to be instituted immediately. Our experience revealed that substantial damage has occurred early after ingestion, and early surgical intervention has decreased the morbidity and mortality. The extent of the mucosal injury and status of the pylorus and antrum determined the type of surgical treatment. A Billroth I procedure recommended for severely injured mucosa with complete pyloric obstruction, and pyloroplasty for moderate mucosal injury associated with partially obstructed but still viable pylorus. In contrast to the current belief, alkali ingestion also has a high risk of corrosive gastric injury causing GOO, which should be considered during assessment of the injury. We emphasize that a detailed evaluation of radiologic and especially endoscopic findings is very important for determining the timing, necessity, and type of appropriate surgical treatment.

Gillis D.A., Higgins G., Kennedy R.

Acid ingestion occurs relatively rarely and produces a spectrum of injury that is markedly different from the more commonly encountered alkaline burns of the oropharynx and esophagus. Gastric damage results from pylorospasm with pooling of the ingested caustic in a dependent location. Symptoms may be delayed for days or weeks. Perforation and/or strictures may require extensive gastric surgery. Early fiberoptic endoscopy is essential.

Marks I.N., Bank S., Werbeloff L., Farman J., Louw J.H.

Case reports of 5 patients with corrosive gastritis are presented. The corrosive was ingested accidentally in one, without the patient's knowledge in another, and with suicidal intent in 3. Hydrochloric acid in the form of cleaning fluid was the offending substance in 4 and potassium hydroxide in 1. The natural history of the disease is outlined. The dramatic onset of dyspepsia, the liability to hemorrhage, and the relentless progression to pyloric stenosis is stressed, and the tendency of the pyloric gland area to be selectively involved is confirmed. The entire stomach was stenosed in one, and associated involvement of the esophagus was present in 2 of the patients. The radiological and clinical points of similarity between corrosive gastritis and carcinomatous infiltration of the antrum are mentioned. The danger of gastroscopy in the condition is discussed. Attention is drawn to the finding of low serum albumin values in patients with corrosive gastritis. It is tentatively suggested that the latter may constitute another cause of protein-losing gastropathy. The treatment of the condition is briefly considered.