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Brief Reports

Indian Pediatrics 2000;37: 1111-1114

Endoscopic and Histologic Evaluation of Reflux Esophagitis


S.K. Dadhich
S.K. Yachha
A. Srivastava
S.S. Sikora*
R. Pandey**

From the Departments of Gastroenterology (Pediatric GE Division), Surgical Gastroenterology* and Pathology**, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow 226 014, India.

Reprint requests: Dr. S.K. Yachha, Associate Professor, Department of Gastroenterology (Pediatric GE Division), Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow 226 014, UP, India.

E-mail : [email protected]

Manuscript Received: August 25, 1999;
Initial review completed: September 29, 1999;
Revision Accepted: April 13, 2000

Reflux esophagitis (RE) in infants and children has been recognized as an important cause of morbidity which can be effectively managed by medical and/or surgical therapy. Largely RE stands ignored in our country. There is paucity of data on this subject from India(1). We therefore subjected all the children who presented to us with symptoms suggestive of gastroesophageal reflux disease (GERD) to endoscopic and histologic examination of esophagus.

 Subject and Methods

All consecutive children (less than 13 y) who presented to Pediatric Gastroenterology Clinic at our Institute with symptoms suggestive of GERD were studied. Children with symptoms of recurrent vomiting or regurgitaion, epigastric pain, heartburn, failure to thrive or respiratory symptoms (persistent or recurrent symptoms of cough, pneumonia or wheezing) either in isolation or in combinations were evaluated. Referral notes of these children revealed that GERD was not suspected and they had received prokinetics without any symptomatic benefit. Drugs were stopped 2 weeks before evaluation. Patients presenting with dysphagia were subjected to barium swallow study prior to endoscopy.

All such children were subjected to eso-phagogastroduedenoscopic (EGD) exami-nation. Esophageal mucosal abnormalities of erosions, ulcertaion, Barrett's, strictures and hiatus hernia were noted(2). We did not consider endoscopic changes of hyperemia, friability or edema as evidence of RE. The endoscopic examination was peformed by one examiner using Olympus PQ20 fibroscope. Esophageal biopsies were obtained, 5 cm proximal to gastroesophageal (GE) junction in all the children. On histopathological examination presence of basal zone thickness >15% of total thickness of epithelium, papillae extending >2/3 of distance to the surface (mild esophagitis) and neutrophilic or eosinophilic infiltration (severe esophagitis) were taken as diagnostic of reflux esophagitis(3). Reflux esophagitis was diagnosed by (a) demonstrating endoscopic and histopathologic changes or (b) normal endoscopy and changes of RE on biopsy.

 Results

From January 1993 to July 1999, out of 33 children who presented with symptoms suggestive of GERD, reflux esophagitis was diagnosed in 26. The median age of the children with reflux esophagitis was 7.6 yr (range 6 mo to 13 yr; 21 boys). Median duration of symptoms was 24.3 (range 1-36) months. Among the symptoms recurrent vomiting was the commonest (Table I). The associated disorders were seen in seven cases (nephrotic syndrome-2, celiac disease-1, obesity-2, cerebral palsy-1, angioneurotic edema-1). Associated H. pylori infection was diagnosed in two cases.

Table I - Symptoms of Children with Gastro-esophageal Reflux Disorder (n = 26)

Symptoms n %
Recurrent vomiting* 18 69.2
Epigastric pain 10 38.4
Heartburn 2 7.6
Failure to thrive 3 11.5
Hematemesis 1 3.8
Respiratory symptoms# 2 7.6
Dysphagia 1 3.8
* 2 had regurgitation; # recurrent cough, dyspnea and wheeze

Of the 26 cases of reflux esophagitis, abnormalities on endoscopy were observed in 7 (27%) cases (ulceration in 4 cases, erosions in 2, Barrett's esophagus with stricture in one). Nineteen children had normal esophageal mucosa on EGD; however, on histology all of them had changes of reflux esophagitis (endoscopy negative reflux disease). Histo-logically 95% of children had mild esophagitis.

Twenty five children were treated with H2 blockers or proton pump inhibitors for 3 months and prokinetics for 6 months. Over a mean follow up period of 28 (9-56) months in 23 children, 2 cases developed recurrence of symptoms. Other two children have been recently started on medical antireflux treatment. One child with recurrence of symptoms was treated successfully with medical therapy. Other child who presented with hematemesis was a case of cerebral palsy. He developed severe hemetemesis on follow up and was subjected to antireflux surgery.

One child who presented with dysphagia had stricture at the lower end of esophagus with Barrett’s mucosa. Successful endoscopic dilata-tion of the stricture was done and antireflux medical therapy was instituted. On follow up surveillance biopsies were negative for dysplasia but he developed recurrence of the stricture and growth failure.

 Discussion

Gastroesophageal reflux (GER) is characterized by the effortless passage of gastric contents into the lower esophagus. Reflux can be classified either as physiologic or pathologic (gastresophageal reflux disease (GERD). Physiologic reflux often occurs in infants who remain free of clinical sequelae. In GERD, infants and children develop gastrointestinal, pulmonary or neuropsychiatric complications and are associated with intraesophageal acidification. Esophagitis is a histological term used to describe ischemic, infectious, chemical, degenerative or mechanical abnormalities. GER is a frequent cause of morbidity in childhood. It occurs due to hypotonia or inappropriate relaxation of lower esophageal sphincter, impaired clearance of refluxed material from the esophagus, increased intragastric pressure or abnormal tissue resistance of esophageal mucosa(4). Of all infants with GER, 65% become symptom free by two years of age, 30% develop prolonged symptoms that last beyond 4 years of age and 5% may develop esophageal stricture(5).

In our series we had only one infant who presented with regurgitation and failure to thrive. The small number of infants in our series could be because of referral bias and lack of awareness among pediatricians about the disease and referral to specialized centers. Older children with GERD have symptoms that are more or less similar to those of adults(6). However, in our series children >1 year of age had symptoms of vomiting more often than heartburn as seen in adults.

In our series one child with cerebral palsy presented with hematemesis and failed to respond to medical therapy. Surgical correction (Nissen's fundoplication) resulted in complete asymptomatic state in this child. Children with neurologic disease appear to be at particular risk for reflux esophagitis (65-76%)(7). Although, the pathogenesis underlying this association remains unknown, low LES pressure, chronic supine positioning, abdominal muscle spasticity, scoliosis, seizures, medication, abnormal esophageal motility and perhaps chronic nasogastric intubation contribute to the high prevalence of reflux in this population(8). These children often have significant GER and may suffer from serious sequelae. Recurrent pneumonia, blood loss from erosive esophagitis or association with anatomic problems such as large hiatus hernia are common. They are more likely to require aggressive or definitive therapy such as surgical fundoplication to reduce complications of esophagitis with bleeding, aspiration pneumonia or both.

A recent recommendation suggests that minor endoscopic mucosal changes (erythema, edema, friability) attributable to reflux disease are unrealiable to diagnose reflux esophagitis. These changes are not recognized to an acceptable level of reproducibility, either by individual observer or between observers. Therefore, any patient who is considered to have such changes should be defined as having endoscopy negative reflux disease (ENRD). Endoscopic esophageal mucosal breaks (erosions or ulcerations) are absent in more than 50% of individuals who have had heartburn two or more times a week for six months(9). We found endoscopic changes of RE in 27% cases (mild changes in 6/7 cases). Endoscopic evidence of esophagitis in GERD patients varies from 40% to 76%(10). Large majority of RE in childhood are known to be mild (erosions, ulcertions) on endoscopy(3). One of our patient had Barrett's esophagus which is severe form of GERD. Barrett's esophagus may be complicated by ulcerations, stricture, bleeding or neoplastic transformation.

In our study 33 children who presented with GERD, 26(78.7%) cases had esophagitis on histology. Esophagitis has been reported in 60%-80% infants and children with GERD(11). In 73% of our cases with GERD, endoscopy was normal however on histology all these had evidence of esophagitis (ENRD).

In summary reflux esophagitis should be suspected in infants and children in a setting of persistent vomiting/regurgitation, epigastric pain and failure to thrive. Majority of children have mild RE. Endoscopy and histology are useful diagnostic tools.

Contributors: SKY coordinated and designed the study; he will act as the guarantor for the paper. SKD and AS compiled and analyzed the data. SSS performed the surgery and gave his surgical inputs during the study. RP did histologic evaluation.

Funding: None.
Competing interests:
None stated.

Key Messages

  • Reflux esophagitis should be suspected in infants and children in a setting of persistent vomiting/regurgitation, epigastric pain and failure to thrive.

  • The median age of the children with reflux esophagitis was 7.6 yr (range 6 mo to 13 yr).

  • Abnormalities on endoscopy occurred in 27% cases.

  • Histologically 95% of children had mild esophagitis.

  References
  1. Channa RS, Singhania RU, Bansal A. Gastroesophageal reflux in infants and children. Indian Pediatr 1989; 26: 139-143.

  2. Boyce HW. Hiatal hernia and peptic disease of the esophagus. In: Gasroenterologic Endoscopy. Ed. Sivak MV. Philadelphia, W.B. Saunders Company, 1987; pp 409-410.

  3. Vandenplas Y. Reflux esophagitis in infants and children: A report from the working group on gastroesophageal reflux disease of the European society of Pediatric Gastroenterology and Nutrition. J Pediatr Gastroenterol Nutr 1994; 18: 413-422.

  4. Kahrilas PJ. Gastroesophageal reflux disease and its complications. In: Gastrointestinal and Liver Disease. Philadelphia. Feldman M, Sleisenger MH, Scharschmidt BF. W.B. Saunders Company, 1998; pp 500-504.

  5. Carre IJ. Management of gastroesophageal reflux. Arch Dis Child 1985; 60: 71-75.

  6. Tolaymat N, Chapman DM. Gastroesophageal reflux disease in children older than 2 years of age. W V Med J 1998; 94: 22-25.

  7. Bohmer CJ, Niezen-deBoer MC, Klinkenberg-knol EC, Deville WL, Nadorp JH, Meuwissen SG. The prevalence of gastroesophageal reflux disease in institutionalized intellectually disabled individuals. Am J Gastroenterol 1999; 94: 804-810.

  8. Glassman MS, Dozor AJ, Newmann LJ. Gastroesophageal reflux in neurologically impaired children in perioperative evaluation and management. South Med J 1992; 85: 289-292.

  9. Dent J, Brun J, Feendrick Am, Fennerty MB, Janssens J, Kahrilas PJ et al. An evidence based appraisal of reflux disease management - Geneva Workshop Report. Gut 1999; 44: S5.

  10. Eriksen CA, Cuschieria A. Diagnostic tests for gastroesophageal reflux disease. In: Reflux Esophagitis. Edn. Henessy TP, Cuschieria A, Bennett JR London. Butterworth, 1989; p 63.

  11. Glassman M, George D, Grill B. Gastro-esophageal reflux in children: Clinical mani-festation, diagnosis and therapy. Gastroenterol Clin North Am 1995; 24: 71-98.

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