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OESO©2015
 
Volume: The Esophageal Mucosa
Chapter: Newborn and children
 

When does the maturation process really occur?

S.R. Orenstein (Pittsburgh)

The question of when maturation occurs with regard to reflux in infants may be approached from several directions. Symptomatic clinical maturation can be examined, or the maturation of mechanisms underlying reflux can be evaluated.

Symptoms of reflux: changes during development

As noted in the section on physiologic vs. pathologic reflux, infants manifest more reflux than adults when evaluated by any of several methods, including simple observation for regurgitation, fluoroscopic monitoring and pH probe monitoring. However, pH probe studies of normal infants and adults clearly show that this decrease in acid gastroesophageal reflux during infancy is much less than one might anticipate from the decrease in observable regurgitation during this period of maturation.

Infants are usually not symptomatic with reflux disease at birth, but develop symptoms during the first month or two of life [1]. The symptoms tend to peak by 4-6 months and usually decline thereafter, disappearing between 8 and 18 months of age [2]. Symptoms persistent beyond 24 months are far less likely to resolve. In this respect, they are similar to symptoms in older children and adults [3].

Mechanisms of reflux: changes during development

Mechanisms contributing to the occurrence of reflux episodes include: 1) hypotonia of the lower esophageal sphincter (LES); 2) transient relaxations of the LES; and 3) increases in intragastric pressure or volume, the latter often due to delayed gastric emptying [4-6]. Factors contributing to the damage done by reflux episodes include: 1) impaired esophageal clearance and neutralization; and 2) increased noxiousness of gastric contents. The presence of other abnormalities, such as a propensity to laryngospasm, aspiration, or bronchospasm, may make reflux more likely to produce disease; these abnormalities, too, may change during development.

The LES tone (and length) has been found to increase during the first months of life in normals [7], although others have found a higher tone in infants than in older children [8].

Esophagitis probably lowers LES tone in both infants and adults. The frequency of transient LES relaxations in adults is debated, ranging up to seven per hour in normals [9-13]; the frequency in infants has not been completely described. We have identified transient increases in intra-abdominal pressure as probable precipitants of regurgitant reflux [14] and similar findings have been reported in rare adults with regurgitation, but the frequency of those events and their modification during development are unknown.

The average esophageal clearance time in normal infants and adults can be calculated from data from several authors [15-18]. The data suggest that the average reflux episode is 2 to 3 min in normal infants and perhaps minimally less in the adult, although differences in techniques may explain these small differences. Similarly, normal infants have peristaltic amplitudes which should produce effective esophageal clearance [19,20]. Decreased peristaltic amplitude and impaired clearance are present in adults and infants with reflux disease, and are probably secondary phenomena like LES hypotonia, due to esophagitis [17,19,20]. The noxious gastric contents probably actually increases during development, as gastric, biliary and pancreatic secretion mature and as the frequency of neutral liquid meals decreases.

There are probably not important maturational changes between young infancy and adulthood in most of the above-noted reflux mechanisms.

The most important maturational change is the marked decrease in regurgitant reflux during the first 12 months - the cause for this change is unknown and requires further study. Since nonregurgitant acid reflux does not change much during development, the other mechanisms for reflux probably do not change much either. Auxiliary mechanisms, however, may be important. These include the unclear developmental phenomena which allow apnea to occur as a response to reflux or to other stresses prior to about 6 months of age. Other manifestations of reflux disease, particularly esophagitis and its sequelae (Barrett's esophagus and stricture), actually increase during maturation, but this increase is due to the cumulative total duration of esophageal exposure to refluxate rather than to a maturational change in reflux mechanisms.

References

I Orenstein SR, Cohn JF, Shabby TM, Kartan R. Reliability and validity of an infant gastroesophageal reflux questionnaire Clin Pediatr 1993;32(8):472-484.

2. Carre IJ. The natural history of the partial thoracic stomach (hiatus hernia) in children. Arch Dis Child 1959:34:344-353.

3. Treem W, Davis P, Hyams J. Gastroesophageal reflux in the older child: presentation, response to treatment and long-term follow-up. Clin Pediatr 1991;30(7):435-440.

4. Cucchiara C, Staiano A, DiLorenzo C, DeLuca G, dellaRocca A, Auricchio S. Pathophysiology of gastroesophageal reflux and distal esophageal motility in children with gastroesophageal reflux disease. J Pediatr Gastroenterol Nutr 1988:7(6): 830-836.

5. Werlin SL, Dodds WJ, Hogan WJ, Arndorfer RC. Mechanisms of gastroesophageal reflux in children. J Pediatr 1980,97(2): 244-249.

6. Hillemeier AC, Lange R, McCallum RW, Seashore J, Gryboski J. Delayed gastric emptying in infants with gastroesophageal reflux. J Pediatr 1981;98(2):190-193.

7. Boix-Ochoa J, Canals J. Maturation of the lower esophagus. J Pediatr Surg 1976;11 (5):748-756.

8. Moroz S, Espinoza J, Gumming W et al. Lower esophageal sphincter function in children with and without gastroesophageal reflux. Gastroenterology 1976;71(2):235-241.

9. Mittal RK, McCallum RW. Characteristics of transient lower esophageal sphincter relaxation in humans. Am J Physiol 1987;252(Gastrointest Liver Physiol 15):G636-G641.

10. Mittal RK, Stewart W, Schirmer B. Effect of a catheter in the pharynx on the frequency of transient lower esophageal sphincter relaxations. Gastroenterology 1992;103(4);1236-1240.

11. Holloway RH, Kocyan P, Dent J. Provocation of transient lower esophageal sphincter relaxations by meals in patients with symptomatic gastroesophageal reflux. Dig Dis Sci 1991;36(8):1034-1039.

12. Freidin N, Ren J, Sluss J, McCallum RW. The effect of large meal on the frequency and quality of transient LES relaxations (TLESR). Gastroenterology 1989;96(5,Pt2):A159.

13. Freidin N, Fisher M, Boyd D, Taylor W, Sluss J, McCallum RW, Mittal RK. Pattern of sleep and acid reflux in normal subjects and gastroesophageal reflux patients Gastroenterology 1989:96(5):A158.

14. Orenstein SR, Deneault LG, Lutz JW, Wessel HB, Dent J. Regurgitant reflux, in contrast to non-regurgitant reflux, is associated with rectus abdominus contraction in infants. Gastroenterology 1991;100:A135.

15. Johnson LF, DeMeester TR. Twenty-four-hour pH monitoring of the distal esophagus: a quantitative measure of gastroesophageal reflux. Am J Gastroenterol 1974;62;325-332.

16. Orenstein SR. Gastroesophageal reflux. In: Stockman J, Winter R (eds) Current Problems in Pediatrics Chicago: Mosby Year Book Medical Publishers, 1991:193-241.

17. Sondheimer JM. Clearance of spontaneous gastroesophageal reflux in awake and sleeping infants. Gastroenterology 1989;97(4):821-826.

18. Vandenplas Y, Sacre SL. Continuous 24-h esophageal pH monitoring in 285 asymptomatic infants 0-15 months old. J Pediatr Gastroenterol Nutr 1987;6(2):220-224.

19. Hillemeier AC, Grill BB, McCallum RW, Gryboski J. Esophageal and gastric motor abnormalities in gastroesophageal reflux during infancy. Gastroenterology 1983;84(4):741-746.

20. Kahrilas PJ, Dodds WJ, Hogan WJ. Effect of peristaltic dysfunction on esophageal volume clearance. Gastroenterology 1988;94(1):73-80.


Publication date: May 1994 OESO©2015