Gastroesophageal Reflux

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134 PEDIATRICS Vol. 68 No. 1 July 1981

be infrequent, and may not occur during a period of

monitoring. Gastric scintiscans have been used to

demonstrate GER, and if the nucleotide is detected

in the thorax, it is good presumptive evidence of

reflux and aspiration.25’26 The finding of lipid-laden

macrophages in tracheal aspirates has also been

used as evidence that aspiratiort of gastric contents

has occurred.4 The challenge for the future is the

development of easily available and reliable tests to

document GER, to detect those patients whose

pulmonary symptoms are caused by reflux, and to

predict their response to different medical or

sur-gical therapy.

JOHN J. HERBST, MD

Department of Pediatrics

University of Utah Medical Center

Salt Lake City

toring of the distal esophagus. Surgery 84:16, 1978 17. Kennedy JH: “Silent” gastroesophageal reflux: An important

but little known cause of pulmonary complications. Dis Chest 42:42, 1962

18. Sondheimer JM, Morris BA: Gastroesophageal reflux among

severely retarded children. J Pediatr 94:710, 1979

19. Mansfield LE, Stein MR: Gastroesophgeal reflux and

asthma: A possible reflex mechanism. Ann Allergy 41:224, 1978

20. Jolley SG, Herbst JJ, Johnson DG, et al: Patterns of

postci-bal gastroesophageal reflux in symptomatic infants. Am J Surg 138:946, 1979

21. Hillemeier AC, Lang ER, McCallum R, et al: Delayed gastric emptying in infants with gastroesophageal reflux. J Pediatr

98:190,1981

22. Euler AR: Use of bethanechol for the treatment of gastro-esophageal reflux. J Pediatr 96:321, 1980

23. Drugs for esophageal reflux. Med Lett 22:26, 1980

24. Jolley SG, Herbst JJ, Johnson DG, et al: Mean duration of gastroesophageal reflux identifies children -with

reflux-in-duced respiratory symptoms. Gastroenterology 78:1189, 1980

25. Heyman S, Kirkpatrick JA, Winter HS, et al: An improved

radionuclide method for the diagnosis of gastroesophageal reflux and aspiration in children. Radiology 131:483, 1979

26. Rudd TG, Christie DL: Demonstration of gastroesophageal

reflux in children by radionuclide gastroesophagography. Radiology 131:483, 1979

REFERENCES

1. Euler AR, Byrne WJ, Ament ME, et al: Recurrent pulmo-nary disease in children: A complication of gastroesophageal reflux. Pediatrics 63:47, 1979

2. Jolley SG, Herbst JJ, Johnson DG, et al: Surgery in children

with gastroesophageal reflux and respiratory symptoms. J Pediatr 96:194, 1980

3. Danus 0, Casar C, Larrain A, et al: Esophageal reflux-an unrecognized cause of recurrent obstructive bronchitis in children. J Pediatr 89:220, 1976

4. Wagener JS, Taussig LM: Chronic aspiration pneumonitis. Ariz Med 37:400, 1980

5. Shapiro GG, Christie DL: Gastroesophageal reflux in

steroid-dependent asthmatic youths. Pediatrics 63:207, 1979 6. Berquist WE, Rachelefsky GS, Kadden M, et al:

Gastro-esophageal reflux-associated recurrent pneumonia and chronic asthma in children. Pediatrics 68:29, 1981

7. Carre IJ: Pulmonary infections in children with a partial

thoracic stomach (‘hiatus hernia’). Arch Dis Child 35:481,

1960

8. Christie DL, O’Grady LR, Mack DV: Incompetent lower

esophageal sphincter and gastroesophageal reflux in recur-rent acute pulmonary disease of infancy and childhood. J Pediatr 93:23, 1978

9. Herbst JJ, Minton SD, Book LS: Gastroesophageal reflux causing respiratory distress and apnea in newborn infants. J Pediatr 95:763, 1979

10. Parker, AF, Christie DL, Cahill JL: Incidence and

signifi-cance of gastroesophageal reflux following repair of esopha-geal atresia and tracheoesophageal fistula and the need for antireflux procedures. J Pediatr Surg 14:5, 1979

1 1. Fonkaisrud EW: Gastroesophageal fundoplication for reflux

following repair of esophageal atresia: Experience with nine patients. Arch Surg 114:48, 1979

12. Behar J, Biancani P, Sheahan DG: Evaluation of esophageal

tests in the diagnosis of reflux esophagitis. Gastroenterology

71:9, 1976

13. Arasu TS, Wyllie R, Fitzgerald JF, et al: Gastroesophageal

reflux in infants and children-comparative accuracy of

di-agnostic methods. J Pediatr 96:798, 1980

14. Roberts, CC, Herbst JJ, Jolley SG, et al: Tests for gastro-esophageal reflux in patients operated on for tracheoesoph-ageal fistula. J Pediatr Res 14:509, 1980

15. Demeester TR, Johnson LF, Jaseper GJ, et a!: Patterns of gastroesophageal reflux in health and disease. Ann Surg 184:

459, 1976

16. Jolley SG, Johnson DG, Herbst JJ, et al: An assessment of

gastroesophageal reflux in children by extended pH

mom-Gastroesophageal

Reflux

In this issue of Pediatrics (p 29), Berquist and

colleagues present a detailed study of the

associa-tion between chronic pulmonary disease and

gastro-esophageal reflux. Of 283 children referred for

pos-sible gastroesophageal reflux, 82 patients had

chronic asthma, or recurrent pneumonia, or both.

These patients were divided into subgroups based

on their presenting symptoms. Group 1 consisted of

patients with recurrent pneumonia, and group 2

consisted of patients with chronic asthma. The

pa-tients in group 1 were further subdivided into those

with only pulmonary symptoms and those with

both pulmonary symptoms and symptoms of

gas-troesophageal reflux. The patients in group 2 were

similarly subdivided: those with asthma only; those

with asthma and pneumonia; those with asthma

and symptoms of acid reflux; and those with all

three symptoms. Patients were evaluated using

multiple esophageal function tests. Unfortunately,

because we do not know what percentage of all

asthma/recurrent pneumonia patients are

repre-sented by the 82 referred patients, it is impossible

to estimate the overall prevalence of associated

gastroesophageal reflux and pulmonary disease.

The present study does demonstrate an association

between acid reflux and pulmonary disease, but like

others, does not establish a causal relationship.

American Academy of Pediatrics.

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COMMENTARIES 135

Many attempts have been made to define the

pathophysiologic relationship between acid reflux

and pulmonary disease. Possibilities include

aspi-ration,’ bronchospasm due to autonomic reflex

be-tween the esophagus and bronchial smooth

mus-culature following acid reflux,2 or hypersensitivity

to specific antigens resulting in concomitant

bron-chospasm and acid reflux.

The diagnostic approach used to define presence

of acid reflux in children has not been critically

standardized. Because there is no single test that

definitely documents pathologic reflux, the authors’

criteria consist of a minimum of any of two

abnor-mal tests among the following: barium swallow,

Tuttle test, esophageal manometry, esophagoscopy,

or esophageal biopsy. Equal diagnostic significance

was assigned to each. It is important to know

whether a child with only reflux shown on x-ray

and a low sphincter pressure is in the same category

of pathologic reflux as a child with esophagitis and

an abnormal endoscopy. Do the children with

esophagitis and presumably more severe reflux have

more pulmonary symptoms than the children

with-out esophagitis? It would be important to ascertain

if there is any relationship between the degree of

acid reflux and the severity of pulmonary disease.

Since the completion of this study, overnight pH

monitoring has become an important tool in

assess-ing pathologic acid reflux.35 A comparison of Tuttle

tests and pH monitoring (18 to 24 hours) in children

has recently been published,6 and observations

sug-gest that acid reflux within a single hour following

probe placement may not reflect true pathologic

reflux. The authors made a conscientious effort to

define pathologic reflux accurately, and the

meth-odology cannot be faulted. However, as newer more

sensitive techniques become available, a

standard-ized method for determining pathologic reflux may

become available.

In this study, pulmonary involvement was

as-sessed radiographically and clinically using

de-creased steroid or bronchodilator requirements;

number of fewer emergency room visits and

hospi-talizations; school time missed; and severity and/or

frequency of pneumonia as evaluated by chest

x-ray only. Because of the age group of the patients,

rigorous documentation by pulmonary function

testing was not reported. An optimal patient

pop-ulation would allow collection of pulmonary

func-tion data before and after medical or surgical

treat-ment. This would permit objective documentation

of pulmonary improvement following intervention.

A key factor in the development of esophagitis, one

of the sequelae of acid reflux, appears to be the

rapidity of acid clearance, and the percentage of

time during which the esophageal pH is less than 4.

Continuous intraesophageal pH monitoring is

use-ful in assessing these aspects. Perhaps evaluation of

such factors and correlation with the degree of

pulmonary function will provide clues to the link

between reflux and asthma.

Finally, the authors state that the mean age of

patients who became asymptomatic after

fundopli-cation was 1.5 years as compared to 6.7 years in the

group who improved but were not free of symptoms

following fundoplication. This discrepancy is

trou-blesome. Do younger children respond because

their airways are still reactive and can return to

normal compliance after reflux has decreased? Do

some of the infants have transient pulmonary

hy-persensitivity which resolves after infancy? Do

im-munologic or infectious mechanisms play a

tempo-rary role in their improvement independent of the

reflux? As recently suggested by Hfflemeier et al,7

do some infants have delayed gastric emptying

which results in prolonged esophageal acid reflux?

Is the excellent clinical response of younger children

following fundoplication due to therapeutic

inter-vention or maturation?

Berquist and colleagues are to be congratulated

for their precise reporting of data and for raising

the question of the association between

gastro-esophageal acid reflux and pulmonary disease. It is

clear that some children require surgical

interven-tion for control of gastroesophageal reflux, and

chil-then with severe pulmonary disease deserve to be

evaluated for reflux.8 If severe esophagitis at any

age is unresponsive to medical therapy or if

esoph-ageal stricture is found, clearly, an antireflux

oper-ation should be considered. It is possible that

changes in pulmonary compliance may be

deter-mined by the effects of intraesophageal acid. This

is, at present, not feasible to assess in younger

children. Until we are able to discriminate among

various etiologies, the decision to control acid reflux

surgically remains a clinical one with few objective

guidelines.

HARLAND S. WINTER, MD

RICHARD J. GRAND, MD

Division of Gastroenterology and Nutrition

Children’s Hospital Medical Center

Boston

REFERENCES

1. Wynne JW, Modell JA: Respiratory aspiration of stomach contents. Ann Intern Med 87:466, 1977

2. Mansfield LE, Stein MR: Gastroesophageal reflux and asthma: A possible reflex mechanism. Ann Allergy 41:224,

1978

3. Winter HS, Madara J, Stafford R, et al: Functional and morphological assessment of acid reflux in children. Gastro-enterology 78:1293, 1980

4. Johnson LF, Demeester TR: Twenty-four-hour pH

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American Academy of Pediatrics. Reprints will not be available.

136 PEDIATRICS Vol. 68 No. 1 July 1981

ing of the distal esophagus. Am J Gastroenterol 62:325, 1974 5. Boix-Ochoa J, Lafuente JM, Gil-Vernet JM:

Twenty-four-hour esophageal pH monitoring in gastroesophageal reflux.

J Pediatr Surg 15:74, 1980

6. Euler AR, Byrne WJ: Twenty-four-hour esophageal

intra-luminal pH probe testing: A comparative analysis. Gastro-enterology 80:957, 1979

7. Hillemeier AC, Lange, R, McCallum R, et a!: Delayed gastric emptying in gastroesophageal reflux. J Pediatr 98:190, 1981

8. Krantman HJ, Rachelefsky GS, Lipson MH, et al: Recurrent

pulmonary infiltrates, digital clubbing, and failure to thrive in a 4-year old boy. JAllergy Clin Immunol 61:403, 1978

Spina

Bifida:

A New

Disease

The paper by Wald entitled “Biofeedback in the

Treatment of Fecal Incontinence in Patients with

Myelomeningocele” (Pediatrics 68:45, 1981)

repre-sents an additional small, but significant step in

the management of children with spina bifida.

In the 195Os most children with spina bifida were

left to die. In the 1960s most were vigorously

treated. In the early 1970s Dr John Lorber

pre-sented a retrospective analysis of his results, and

published his criteria for selection.’ Over these three

decades the approach to the newborn with spina

bifida has swung like a pendulum. More recent

series2’3 demonstrate that with early treatment

more than 80% of children survive; in our experience

more than 95% survive. Thus, the English mortality

has not been replicated in this country, nor has the

English morbidity.

Along with an increase in survival have come

increasing awareness and attention to the multiple

problems faced by these children and the

develop-ment of new approaches to minimizing their

hand-icap. It should be remembered that there is a

dis-tinction between impairment and handicap.

Im-pairment is the amount of fixed deficit. Handicap is

the disability superimposed on that deficit by

soci-ety. What are the deficits, and what progress has

been made in minimizing the handicap?

MOTOR IMPAIRMENT

The level of paralysis is relatively fixed at birth.

Yet virtually all children are able to stand in braces

and platforms by 1 to 2 years of age. Most children,

even those with high lesions, can be taught to

“walk” with braces and crutches.4 This promotes

independence and a positive attitude which may be

critical in later life, even for those who end up in

wheelchairs as adolescents. For all of these children,

but particularly for those with high lesions, careful

attention to the kyphosis and scoliosis with

appro-priate bracing and later fusion may make a major

difference in the severity of spinal deformity.

HYDROCEPHALUS

Of all children with spina bifida, 70% to 90% will

develop hydrocephalus. Major advances in shunt

technology allow most of these children to grow to

adulthood with normal intellect.5 Close attention to

shunt blockage and repeated computed tomography

(CT) scans (or ultrasound in infancy) can detect

subtle hydrocephalus before intellect is impaired.6

New approaches utilizing medication to avoid the

problem ofshunting may be on the horizon.7

Which-ever approach is taken, it is clear that careful

man-agement of the hydrocephalus has decreased

mor-tality and presumably has decreased the medical

and intellectual morbidity of hydrocephalus.

INTELLIGENCE

Children with spina bifida have a normal

distri-bution of intelligence, but there is a slightly

in-creased incidence of mildly retarded individuals.

Few are moderately or severely retarded.2 Close

attention to shunt function and prevention and

vigorous management of central nervous system

infections avoid added intellectual impairment.

Most children can attend regular schools. Many

have visual and perceptual disabilities which should

not be mistaken for retardation and which should

be detected and remediated during the early school

years.

Mainstreaming these children avoids the effects

of educational deprivation and teaches them to

cope with the “normal” society that most will

even-tually have to enter.

URINARY INCONTINENCE

A life of urinary incontinence, in diapers, has

added considerable handicap to the child with spina

bifida. Smelly, wet, and different, these

.

children

were clearly socially undesirable. Reflux,

hydrone-phrosis, and smoldering infection often led to renal

parenchymal damage and early death. Ileal loop

diversions have provided continence and ureteral

drainage, but added a new set of problems. These

procedures should no longer be performed for

con-tinence alone. Dramatic changes in the

manage-ment of urinary incontinence over the past decade

now allow most children to be dry and free of reflux

and infection. Reimplantation of ureters minimizes

reflux, and appropriate medication suppresses

in-fection. Use of medication to alter bladder and

sphincter tone,8’9 and the use of nonstenile

cathe-terization by parent or child’#{176}” have been a

signifi-cant advance in providing continence. Artificial

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1981;68;134

Pediatrics

Harland S. Winter and Richard J. Grand