Published online Feb 21, 2019. doi: 10.3748/wjg.v25.i7.870
Peer-review started: November 14, 2018
First decision: January 6, 2019
Revised: January 17, 2019
Accepted: January 26, 2019
Article in press: January 26, 2019
Published online: February 21, 2019
Processing time: 100 Days and 11.6 Hours
Caustic ingestion continues to be a major health hazard in developed and developing countries despite continuing educational programs and legislation limiting the strength and availability of corrosive substances. It has been reported that the accidental corrosive substance ingestion is seen mostly among children younger than 5 year of age. Corrosive strictures are usually managed by endoscopic dilatation. The target is to dilate oesophageal strictures to a level that allows patients to tolerate a regular diet without dysphagia. The research in paediatric age group was very deficient so we are concerning about the histopathological changes in post corrosive oesophageal stricture in paediatric age and safety of endoscopic dilatation.
Dysplasia has been postulated to be a precancerous lesion of the oesophagus, which in turn is considered to be preceded by chronic oesophagitis. Patients with corrosive induced oesophageal strictures have more than a 1000-fold risk of developing carcinoma of the oesophagus. The incidence of cancer in corrosive strictures has been estimated to be 2.3% to 6.2%, and a history of caustic ingestion was present in 1% to 4% of patients with oesophageal cancer. Risk factors of oesophageal dysplasia in post corrosive stricture were chronic irritation at the site of the scar, local chronic inflammatory responses in the oesophageal mucosa, long latency period from the corrosive ingestion and genetics playing a minor role. The diagnosis of corrosion cancer should be suspected in patients with corrosive ingestion if after a latent period of negligible symptoms there is development of dysphagia, poor response to dilatation, or if respiratory symptoms develop in an otherwise stable patient of oesophageal stenosis. The significance of this study was to set strategy provide early detection of dysplastic changes of oesophageal mucosa in post corrosive stricture. The determination of oesophageal dysplasia which is the pre-neoplastic lesion for oesophageal squamous cell carcinoma provides the possibility of screening not just for early stage oesophageal squamous cell carcinoma, but also to screen for and treat the pre-neoplastic lesion itself.
The main objectives were to detect the possibility of oesophageal mucosal dysplasia after prolonged dilatation of post corrosive oesophageal stricture and to assess the relationship between duration since the corrosive ingestion and number of oesophageal dilatation sessions with degree of oesophageal mucosal dysplasia.
The work was carried out at the Paediatric Endoscopy Unit in Cairo University Children’s Hospital, from March 2015 to September 2016. The study included the patients older than 2 years of age who had established diagnosis of post corrosive oesophageal stricture on repeated endoscopic dilatation sessions for more than of six-month duration; of both sexes. Infants below 2 year and other causes of oesophageal stricture were excluded. Data included: history taking; age of onset of ingestion of corrosion, type of corrosion, age at the time of enrollment in the study, number of dilation sessions. Clinical examination included Anthropometric measures. All patients were evaluated on the 21st post ingestion day with a barium swallow. Upper gastrointestinal endoscopic dilatation of oesophageal stricture was done for all patients with biopsy from the stricture site after at least six-month duration of regular endoscopic dilatation. Histopathological examination of oesophageal mucosal biopsy was performed for detection of chronic oesophagitis, inflammatory cellular infiltration and dysplasia. As regard the patients who had early grade dysplasia, we rebiopsied them after period of time ranged from 6 months to one year from the initial pathological assessment but with the use of the chromoendoscopy by Lugol's iodine.
This study included 100 patients, and males represented 63% of the patients. The mean age of the patients was 5.9 ± 2.6 years. The mean age at the time of corrosive ingestion was 21 ± 1.1 years. The general examination of the patients revealed that the median and range of weight and height by Z-score were -1.20 (-10.81-1.91) and -2.11 (-5.82-0.61), respectively. The majority (90%) of our patients ingested an alkaline substance (potash); 6% of them ingested a neutral substance (chlorine); and only 4% of them ingested an acidic substance (H2SO4). The total number of endoscopic dilatation sessions were ranging from 16 to 100 with mean number of sessions was 37.2 ± 14.9. Biopsy specimens were obtained from the oesophageal stricture site at the time of endoscopic examination before the dilatation using biopsy forceps after at least six-month duration of regular endoscopic dilatation. According to the histopathological findings of specimens from the upper gastrointestinal endoscopy, group A: eighty-five patients (85%) had evidence of chronic oesophagitis, group B: thirteen patients (13%) had evidence of reactive epithelial atypia/indefinite for dysplasia, group C: only two patients (2%) had low-grade squamous dysplasia. The pathological follow up of two patients with low grade squamous dysplasia revealed the same grade of dysplasia. The patients with dysplasia should be followed up every year to evaluate the degree of deterioration as well as the group of patients with reactive atypia.
This observational study is a single centre vast experience in which huge number of young children with post corrosive oesophageal stricture was screened for histopathological changes in oesophageal mucosa after long period of endoscopic dilatation. Oesophageal squamous dysplasia could be occurred in that young age. It has been reported that the accidental corrosive substance ingestion is seen mostly among children younger than 5 years of age. Corrosive ingestion in children may cause clinical manifestations varying from no injury to fatal outcome, including the risk for squamous cell carcinoma of the oesophagus. The endoscopic dilatation is considered the safest method for management of paediatric post corrosive stricture. Chronic oesophagitis is the most common histopatholgical findings in post corrosive patients. Dysplasia is one of the complications of post corrosive oesophageal stricture. The development of dysplasia had several risk factors but the number of dilatation session and duration since ingestion of corrosive substance didn't show statistically significant relation with development of dysplasia. Immense the awareness of patients with corrosive ingestion to report if after a latent period of negligible symptoms, there is development of dysphagia, or poor response to dilatation. This needs prompt medical consultation. Aim was to allow the early dignosis of dysplasia or cancer. We reported cases had low grade of dysplasia in spite of young age of patients included in the study. Long term follow up of the patients who had early grade dysplasia is mandatory for the future following years. To screen who became deteriorated to high grade dysplasia or carcinoma in situ with prompt treatment plan.
High attention should be taken from the parents to avoid the availability of the corrosive substances in reachable areas for their kids. Chemical substances should not be stored in food containers. Implementation of preventive programme is very crucial to limit the use of corrosive materials. The use of other methods in future research to detect the oesophageal dysplasia as narrow band imaging technique in endoscopy.