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Brief Reports

Indian Pediatrics 2001; 38: 766-770  

Gastroesophageal Reflux Disease in Children with Cerebral Palsy


Ashutosh Gangil,
A.K. Patwari, Promila Bajaj* ,Ravi Kashyap**, V.K. Anand

From the Division of Pediatric Gastroenterology and Nutrition, Department of Pediatrics, Kalawati Saran Children’s Hospital, New Delhi 110 001, India; *Department of Pathology, Lady Hardinge Medical College, New Delhi 110 001, India; and **Department of Nuclear Medicine, Institute of Nuclear Medicine and Allied Sciences, Delhi, India.
Correspondence to: Dr. A.K. Patwari, Flat No. 4, Lady Hardinge Medical College Campus, New Delhi 110 001, India.

Manuscript received: March 29, 2000; Initial review completed: May 22, 2000;
Revision accepted: January 24, 2001.

Gastroesophageal reflux occurs in up to 70-75% of children with cerebral palsy (CP)(1,2) and can occur even without overt vomiting(1). Children with gastroesophageal reflux disease (GERD) may present with feeding difficulties, recurrent vomiting and recurrent chest infection associated with poor growth and nutrition, reactive airway disease particularly nocturnal asthma, choking attacks, anemia and wheezing(1,2,4,5). Onset of symptoms of GERD occur relatively late in neurodevelopmentally retarded children in comparison to children of normal develop-ment(6). Sometimes symptoms of Oral Motor Dysfunction (OMD) and abnormalities of pharyngeal coordination may mask or can be confused with GERD. Apart from delay in diagnosis, problems are also encountered in the management of these children due to persistent abnormal posture(7) and various feeding problems(1). This study was con-ducted to find out prevalence of GERD in CP patients and its relationship with gender, chronological age, nutritional status, feeding skills and type and severity of cerebral palsy.

Subjects and Methods

The study was carried out from April 1998 to April 1999 and children of either sex less than 12 years of age with CP were randomly enrolled. All the patients with clinical features suggestive of GERD (failure to thrive, recurrent vomiting, recurrent chest infection, anemia and wheezing) as well as those without obvious symptoms of GERD were subjected to endoscopy, esophageal biopsy and gastroeso-phageal scintiscan. Upper Gastrointestinal endoscopy was performed by pediatric fiber-optic endoscope (GIF type PQ 20 Model Olympus) after written consent from the parents and desired preparation and mild sedation. Endoscopy was performed to (i) identify any gross abnormalities, mucosal erythema, linear ulceration, exudate, bleeding and stricture in the esophagus, and to (ii) take multiple biopsies (at least 3 biopsies) from 4-5 centimeters above the identified gastroeso-phageal junction and area of gross pathology. Samples were preserved in 10% formaline and sent for histopathological examination. Biopsies were stained with hematoxyline and eosin to study histological changes and type of inflammation. Histological criteria used for making a diagnosis of GERD was based on evidence of reflux esophagitis(8) which is graded as: Grade 0 (no changes), Grade I (basal zone hyperplasia with >20% of the epithelial thickness, and elongation of papillae), Grade 2 (Grade 1 + ingrowth of vessels in the papilllae), Grade 3 (Grade 2 + 1-19 eosinophils and/or neutrophils on the most involved high power field), Grade 4 (Grade 3 + >20 eosinophils and/or neutrophils on the most involved high power field), Grade 4 (Grade 3 + >20 eosinophils and/or neutrophils on the most involved high power field) and Grade 5 (mucosal erosions and/or ulcerations).

Gastroesophageal scintiscanning was undertaken whenever possible and was done at Institute of Nuclear Medicine and Allied Sciences, Delhi. Written consent was taken from parents before the scan. In the scanning 500 micro-curi of Technetium 99 m labeled sulfur colloid mixed with patient’s routine milk of formula feed was administered orally or by feeding tube which was later removed, before taking the images. Serial thoracoabdominal images for 30 minutes at a frame rate of 30 seconds per frame were obtained using gamma camera. The data were also collected in an online computer. The digital and analog processing was done to determine the presence of gastroesophageal relux.

Feeding skill assessment was based on Gisel and Patrick’s feeding behavior skill score(9). A score of 4 or less was regarded as normal, score of 5-8 was defined as marginal and 9 or more as inadequate feeding skills. Nutritional status was determined by measure-ment of weight, skinfold thickness and midarm circumference. Weight was measured by electronic weighing machine to the nearest 10 g. Skinfold thickness was measured at biceps, triceps, suprailial region and subscapsular by a vernier caliper. Midarm circumference was measured by nonstrechable measuring tape graded in centimeters. A detailed history and thorough clinical examination of the case was performed to assess the type of cerebral palsy. Clinical classification of CP included spastic, hypotonic athetoid, ataxic and mixed while severity was graded as mild, moderate and severe.

All the cases with mild GERD were initially managed by nonpharmacological therapy for 2 weeks. Children with moderate and severe GERD and those with mild GERD who did not respond to nonpharmacological therapy in 2 weeks were treated with antacids and cisapride. Ranitidine was added if 2 weeks therapy with antacids and cisapride did not result in satisfactory results. Non-pharmaco-logical therapy included thickening of feeds, small feeding volume, avoiding over feeding, feeding after episodes of vomiting, burping technique, upright position during waking hours and elevation of head while sleeping. Decision for undertaking surgical therapy was considered whenever indicated.

All enrolled patients were followed up in the Pediatric Gastroenterology and nutrition Follow-up Clinic of the hospital every week or fortnight, depending upon the nature of feeding problem and response to nutritional and therapeutic interventions. In the follow up, decrease/disappearance of symptoms of GERD, and improvement in nutrition was noted.

Statistical methods included Pearson Chi square test, Student ‘t’ test and z test.

Results

Eighty children diagnosed as CP with mean chronological age of 2.5 years (range 1 to 9 years) were studied and included more boys (75%) than girls (25%). Most (78.7%) of them had spastic quadriplegic cerebral palsy (SQCP). Mean developmental age was 7.6 month (range 1 to 36 month). All of them belonged to severe CP group.

Symptoms suggestive of GERD were present in 72 (90%) cases. Failure to thrive with feeding difficulties was the commonest presenting symptom (53.7%) in the enrolled cases of CP, followed by recurrent chest infection (15%), vomiting, with or without recurrent chest infection (15%) and anemia (6.3%). Eight (10%) cases did not have any symptoms of GERD Endoscopic examination and multiple biopsies were taken from the lower end of the esophagus in all the cases but gastroesophageal scintiscan was performed in only 65 cases. GERD was diagnosed in 25 children, using the histological criteria of reflux esophagitis, and of these, endoscopic examination suggested esophagitis in 18 (72%) and scintigraphy suggested GERD in 20 (80%) cases. In 10 cases scintigraphy was suggestive of GERD but histology was normal.

Out of 25 cases diagnosed to have GERD, 24 (96%) presented with symptoms suggestive of GERD and 1 (4%) did not have any obvious symptoms related to GER. Mean age of children with GERD was 1.8 ± 1.04 year. GERD was significantly common in females (p <0.001). Presence of GERD was signifi-cantly higher in hypotonic group when compared with other, (p <0.0001) (Table 1). GERD was diagnosed in significantly higher proportion of children with inadequate feeding, skill score (p <0.001) (Table II). Thirty five cases (43.7%) had associated seizures. Eight out of 14 cases (57.1 %) with generalized tonic clonic seizures had GERD in comparison to 5/21 (23.5%) cases with myo-clonic seizures. The difference was statistically significant (p <0.001). Cases with GERD had significantly poor nutritional status in compari-son to cases with no GERD (p <0.001) (Table III). Gastroesophageal scintiscan suggested GERD in only 80% and had a specificity of 75%.

Follow up of patients ranged from 3 months to 9 months. Four children (16%) with GERD showed complete improvement and in 6 (24%) there was some improvement in their symptoms. However, 15 (60%) children did not show any significant improvement with treatment. Of these 15 cases, 3 had severe GERD and 6 had inadequate feeding skill score.

Discussion

Gastroesophageal reflux occurs in up to 70-75% of children with cerebral palsy(1,2), but considering a strict diagnostic criteria of GERD, a more accurate estimate of the prevalence is around 30-35%(3). In our study, it was diagnosed in 31.3% of cases. Out of 25 cases diagnosed to have GERD by histological evidence of reflux esophagitis, 96% presented with symptoms suggestive of GERD and 4% did not have any obvious symptoms suggestive of GERD. Reflux was detected more often in 1-2 years age group (p <0.001) and in females (p <0.001) in our cases though no association was detected with chronological age and GERD by other workers.

Table I - Relationship Between Type of Cerebral Palsy and GERD

Type of cerebral palsy
Total cases (n = 80)
Cases with GERD (n = 25)
 
Number
%age
Spastic quadriplegia
63
19
30.1
Hypotonic
7
4
57.1
Diplegia
6
1
16.6
Hemiparesis

4

1
25.0

 

Table II - Relationship Between Oral Motor Dysfunction and GERD

Feeding skill score Total cases(n = 80)
Cases with GER(n = 25)
   
Number
%age
Normal
18
10
55.5
Marginal
54
9
16.6
Inadequate

8

6

75.0

Table III - Relationship Between Nutritional status* and GERD

Nutritional status
GERD positive (n = 25)
GERD negative (n = 55)
 
Number
%age
Number
%age
Normal
12
21.8
Malnourished
Grade I

2

8

12

21.8

Grade II
3
12
17
30.9
Grade III
12
48
9
16.4
Grade IV
8
32
5
9.1

*Grading as per recommendations of IAP.

Severe feeding difficulties, failure to thrive, anemia, and recurrent chest infection have been reported as the commonest pre-senting symptoms of GERD(2) whereas others have reported vomiting to be the main symptom(6,7). In our study, failure to thrive with feeding difficulties was the commonest symptom (53.7%) followed by recurrent chest infection (15%), vomiting with or without recurrent chest infection (15%) and anemia (6.3%). GERD was observed to be signifi-cantly higher in hypotonic group (p <0.001) in comparison to other groups. However, some workers observed spasticity in 73% of their patients with GERD(6), while others did not document any significant difference between reflux and type of CP(2). Similarly, positivity of GERD was significantly higher in our children with inadequate feeding, skill score (p <0.001) and children with generalized tonic clonic seizure (p <0.001). Children with hypotonic CP also had inadequate feeding skill score which could partly explain GERD in higher proportion of children in this subgroup. Persistent supine position, reduced basal lower esophageal sphincter pressure(6), abdominal compression resulting from scoliosis or spasticity of abdominal muscles thereby increasing intragastric pressure(10) delayed gastric emptying(11) and impaired esophageal motor function(12) predispose to GERD in CP patients. Poor nutritional status is a common feature in children with CP and is a conglo-meration of several factors including oral motor dysfunction. However, presence of GERD appears to be an important factor because higher proportion of children with GERD had poor nutritional status.

In the follow up, only 40% children showed some/complete improvement but majority (60%) did not respond, highlighting the extent of treatment failures in CP children who have GERD, particularly those with oral motor dysfunction. For those who improved, a combination of pharmacologic and non-pharmacologic therapy was found to be effective.

Our results suggest that GERD is present in a high proportion of cases of CP and these children should be assessed for gastro-esophageal reflux and nutritional status early in the course of the disease. It will not only help in starting appropriate therapy to improve their nutritional intake but will also help to prevent complications related to GERD.

Contributors: AG participated in collection of data, analysis and drafting of paper. AKP co-ordinated the study (design and analysis) and drafted the paper. PB conducted the histopathological examination of the biopsies. RK conducted the gastroesophageal scan-ning of the cases. VKA participated in endoscopic procedures and data collection. AKP will act as guarantor for the paper.

Funding: None.
Competing interets: None stated.

Key Messages

  • Gastroesophageal reflux diseases (GERD) is common in children with cerebral palsy.

  • Early recognition and appropriate treatment of GERD can be helpful in achieving desired rehabilitation of children with Cerebal palsy.

  • GERD can influence the nutritional status of a child with cerebral palsy.

 

 References


1. Couriel JM, Bisset R, Miller R, Thomas A, Clarke M. Assessment of feeding problems in neurodevelopmental handicap: A team approach. Arch Dis Child 1993; 69: 609-613.

2. Reyes AL, Cash AT, Green SH, Booth IW. Gastroesophageal reflux in children with cerebral palsy. Child Care. Hlth Dev 1993; 19: 109-118.

3. Sochaniwskyj AE, Koheil RM, Bablich K, Kenny DJ. Oral motor functioning, frequency of swallowing and drooling, in normal children and children with cerebral palsy. Phy Med Rehab 1986; 67: 861-874.

4. Berquest WF, Rachelefsky GS, Kadden M, Siegel SC, Katz RM, Fonkalsrud EW, et al. Gastroesophageal reflux-associated recurrent pneumonia and chronic asthma in children. Pediatrics 1981; 68: 29-35.

5. Orenstein SR, Orenstein DM. Gastroeso-phageal reflux and respiratory disease in children. J Pediatr 1988; 112: 847-857.

6. Sondheimer JM, Morris BA. Gastroesophageal reflux among severely retarded children. J Pediatr 1979, 94: 710-714.

7. Cadman D, Richards J, Faidman W. Gastro-esophageal reflux in severely retarded child-ren. Dev Med Child Neurol l 978; 20: 95-98.

8. Simeone D, Caria MC. Miele E, Staiano A. Treatment of Childhood Peptic Psophagitis: A double- blind dacebo controlled trial with Nizatidine. J Pediatr Gastroenterol Nutr 1997: 25: 51-55.

9. Gisel E.G. Patrick J. Identification of children with cerebral palsy unable to maintain a normal nutritional status. Lancet 1988; 1: 283-285.

10. Kassem NY, Groen JJ, Fracnkel M. Spinal deformities and esophageal hiatus hernia. Lancet 1965; i: 887.

11. Delgiudice E. Cerebral palsy and gut func-tions. J Pediatr Gastroenterol Nutr 1997; 25: 522-523.

12. Staiano A, Cacchiara S, Del Giudi CC, Andreotti MR, Mihella R. Disorder of esopha-geal motility in children with Psychomotor retardation and gastroesophageal reflux. Eur J Pediatr 1991; 150: 638-641.

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