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Published on: April 17, 2020
Oesophageal replacement in the management of corrosive strictures: when is surgery indicated?
E Panieri1, H Rode, A J Millar
1Department of Paediatric Surgery, University of Cape Town, Institute of Child Health, Red Cross War Memorial Children's Hospital, 7700 Rondebosch, Cape Town, South Africa.
Insights
Accidental ingestion of corrosive agents causes esophageal strictures in children. Early identification of predictive factors can help avoid ineffective dilatations and complications, guiding surgical intervention.
Area of Science:
- Pediatric Surgery
- Gastroenterology
- Otolaryngology
Background:
- Accidental corrosive ingestion is a leading cause of pediatric esophageal strictures.
- Current primary treatment involves repeated dilatations, but many children require esophageal bypass.
Purpose of the Study:
- To review outcomes of esophageal stricture treatment in children.
- To identify early predictors of failed dilatation therapy.
Main Methods:
- Retrospective review of pediatric cases managed at University of Cape Town teaching hospitals (1976-1994).
- Analysis of treatment success rates, morbidity, and factors predicting dilatation failure.
Main Results:
- Dilatation therapy alone succeeded in only 41% (14/39) of patients.
- Failed dilatation led to prolonged hospital admissions, numerous dilatations, and 18% esophageal perforation rate.
- Predictive factors for failure included delayed presentation (>1 month), severe burns needing tracheostomy, perforation, and stricture length >5 cm.
Conclusions:
- Specific early clinical and radiological criteria can predict failure of conservative dilatation therapy.
- Early surgical intervention in high-risk cases may prevent complications and unnecessary dilatations.
Abstract:
The accidental ingestion of corrosive agents is a major cause of oesophageal strictures in children. The mainstay of treatment is repeated dilatations. Despite this, a significant number of patients eventually require oesophageal bypass. We reviewed the records of all cases managed with this condition at the University of Cape Town teaching hospitals between 1976 and 1994. Dilatation therapy alone was successful in 14 out of 39 patients (41%). Morbidity of failed dilatation therapy included repeated hospital admissions over an average 11.5 months and 17 dilatations each. Oesophageal perforations occurred in 7 cases (18%). Early factors predictive of failure of conservative treatment were: delay in presentation of more than 1 month; severe pharyngo-oesophageal burns requiring a tracheostomy; oesophageal perforation; and a stricture longer than 5 cm on radiological assessment. The size of dilators accepted during early bougienage also correlated with eventual outcome. These criteria may be useful in predicting which patients will not respond to repeated dilatations. Early surgical intervention in such cases will prevent fruitless dilatations and related complications.
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