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Gastric outlet obstruction due to corrosive ingestion: incidence and outcome
A O Ciftci1, M E Senocak, N Büyükpamukçu
1Department of Pediatric Surgery, Hacettepe University Medical Faculty, 06100 Ankara, Turkey.
Insights
Caustic ingestion in children can cause gastric outlet obstruction (GOO). Early diagnosis via endoscopy and prompt surgical intervention are crucial for successful outcomes in pediatric corrosive injury management.
Area of Science:
- Pediatric Gastroenterology
- Surgical Gastroenterology
- Toxicology
Background:
- Caustic ingestion is a significant cause of upper gastrointestinal injury in children.
- Gastric outlet obstruction (GOO) is a potential complication of corrosive substance ingestion.
- Understanding the incidence and management of corrosive GOO in pediatric populations is essential.
Purpose of the Study:
- To determine the incidence, management strategies, and outcomes of gastric outlet obstruction (GOO) resulting from caustic ingestion in children.
- To analyze the types of caustic agents involved and their correlation with injury severity and obstruction.
- To evaluate the effectiveness of different surgical interventions for corrosive GOO in pediatric patients.
Main Methods:
- Retrospective clinical study of 220 pediatric patients treated for caustic substance ingestion between 1976 and 1996.
- Classification of patients into two groups based on endoscopic and radiologic findings of mucosal injury and obstruction (moderate vs. severe).
- Analysis of surgical treatments performed, including Billroth I and pyloroplasty procedures.
Main Results:
- An overall incidence of 5% for corrosive GOO was observed in pediatric patients.
- Alkaline substances were more frequently ingested (168/220), with 5.3% developing GOO.
- Severe mucosal injury with complete obstruction (Group II) was treated with Billroth I, while moderate injury with partial obstruction (Group I) underwent pyloroplasty; all patients survived.
- Fiberoptic endoscopy proved effective in diagnosing and assessing the extent of corrosive injury.
Conclusions:
- Caustic ingestion poses a significant risk of GOO in children, with both acidic and alkaline agents capable of causing severe gastric injury.
- Early endoscopic evaluation is critical for timely diagnosis and management of corrosive GOO.
- Surgical intervention, tailored to the severity of mucosal injury and obstruction, leads to favorable outcomes and reduced morbidity/mortality.
Abstract:
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.