Pediatric Gastroesophageal Reflux 

  • Author: Steven M Schwarz, MD, FAAP, FACN, AGAF; Chief Editor: Carmen Cuffari, MD   more...
 
Updated: Jan 13, 2010
 

Background

Gastroesophageal reflux (GER) represents the most common gastroenterological disorder that leads to referral to a pediatric gastroenterologist during infancy. It refers to immaturity of lower esophageal sphincter (LES) function, manifested by frequent transient lower esophageal relaxations (tLESRs) that results in retrograde flow of gastric contents into the esophagus.

Although minor degrees of gastroesophageal reflux are noted in both children and adults, the degree and severity of reflux episodes are increased during infancy. Thus, gastroesophageal reflux represents a common physiological phenomenon in the first year of life. As many as 60-70% of infants experience emesis during at least one feeding per 24-hour period by age 3-4 months. The distinction between this "physiologic" gastroesophageal reflux and "pathologic" gastroesophageal reflux in infancy and childhood is determined, not merely by the number and severity of reflux episodes (when assessed by intraesophageal pH monitoring), but is most importantly determined by the presence of reflux-related complications, including failure to thrive, erosive esophagitis, esophageal stricture formation, and chronic respiratory disease.

Other complications noted in adults with gastroesophageal reflux, including Barrett esophagus and esophageal mucosal dysplasia, are uncommon in childhood.

Gastroesophageal reflux is classified as follows:

  • Physiologic (or functional) gastroesophageal reflux: These patients have no underlying predisposing factors or conditions. Growth and development are normal, and pharmacologic treatment is typically not necessary.
  • Pathologic gastroesophageal reflux or gastroesophageal reflux disease (GERD): Patients frequently experience complications noted above, requiring careful evaluation and treatment.[1]
  • Secondary gastroesophageal reflux: This refers to a case in which an underlying condition may predispose to gastroesophageal reflux. Examples include asthma (a condition which may also be, in part, caused by or exacerbated by reflux) and gastric outlet obstruction.
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Pathophysiology

Similarities between adults and infants

  • For many years, gastroesophageal reflux during infancy and childhood was thought to be a consequence of absent or diminished LES tone. However, studies have shown that baseline LES pressures are normal in pediatric patients, even in preterm infants.
  • The major mechanism in infants and children has now been demonstrated to involve increases in tLESRs. Factors that may promote gastroesophageal reflux during tLESRs include increased intragastric liquid volume and supine and "slumped" seated positioning.
  • Likely because of reduced viscosity and increased gastric volumes, the fluid diet of the infant facilitates the process of regurgitation compared with solid meals ingested by older children and adults.
  • Esophageal clearance is similar in infants and adults, although evidence of reduced peristaltic activity in preterm infants has been reported.

Differences between adults and infants

  • The volume ratio of meal-stomach-esophagus differs. Necessary amounts of infant caloric requirements easily overwhelm gastric capacity. Reflux occurs when esophageal capacity is exceeded by refluxate.
  • Decreased gastric compliance is believed to lead to LES relaxation at lower intragastric volumes in infants. This aspect, in conjunction with abdominal wall muscle contraction (if it occurs during periods of LES relaxation) propels refluxate into the esophagus with subsequent regurgitation.
  • An association between gastroesophageal reflux and delayed gastric emptying is recognized. This is more common in premature infants.

Gastroesophageal reflux and respiratory symptoms in infants and children

  • Gastroesophageal reflux has been associated with significant respiratory symptoms in infants and children.
  • The infant's proximal airway and esophagus are lined with receptors that are activated by water, acid, or distension. Activation of these receptors can increase airway resistance, leading to development of reactive airway disease.[2]
  • In 1892, Osler first postulated a relationship between asthma and gastroesophageal reflux, manifested by a bidirectional cause and effect presentation. Accordingly, although gastroesophageal reflux may be involved in both the etiology and progression of reactive airway disease, the asthmatic condition (in addition to antiasthmatic medications) may play a role in exacerbation of gastroesophageal reflux.
  • One postulated mechanism for gastroesophageal reflux–mediated airway disease involves microaspiration of gastric contents that leads to inflammation and bronchospasm. However, experimental evidence also supports the involvement of esophageal acid–induced reflex bronchospasm, in the absence of frank aspiration. In such cases, gastroesophageal reflux therapy using either histamine 2 (H2) blockers or proton pump inhibitors has been shown to benefit patients with steroid-dependent asthma, nocturnal cough and reflux symptoms.

Gastroesophageal reflux and other conditions in infants and children

  • Two major areas of controversy surround the relationship between gastroesophageal reflux and both apnea and otolaryngologic disease. Although early studies appeared to demonstrate a link between gastroesophageal reflux and obstructive apnea (including an association with apparent life-threatening events [ALTE]), recent work suggests a weak relationship between these disorders.[3]
  • Laryngeal tissues are exquisitely sensitive to the noxious effect of acid, and recent studies support a significant relationship between laryngeal inflammatory disease (manifested by hoarseness, stridor, or both) and gastroesophageal reflux.
  • Conversely, no conclusive clinical evidence supports a link between gastroesophageal reflux and other supraesophageal problems, including otalgia, recurrent otitis media, and chronic sinusitis.
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Epidemiology

Frequency

United States

  • Symptoms of gastroesophageal reflux are most often directly related either to the consequences of emesis (eg, poor weight gain) or a result of exposure of the esophageal epithelium to gastric contents.
  • Approximately 85% of infants vomit during the first week of life, and 60-70% manifest clinical gastroesophageal reflux at age 3-4 months.
  • Symptoms abate without treatment in 60% of infants by age 6 months, when these infants begin to assume an upright position and eat solid foods. Resolution of symptoms occurs in approximately 90% of infants by age 8-10 months.
  • Symptoms that persist after age 18 months suggest a higher likelihood of chronic gastroesophageal reflux.[4]

Age

  • Gastroesophageal reflux is most commonly seen in infancy, with a peak at age 1-4 months. However, it can be seen in children of all ages, even healthy teenagers.
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Contributor Information and Disclosures
Author

Steven M Schwarz, MD, FAAP, FACN, AGAF  Professor of Pediatrics, Children's Hospital at Downstate, SUNY-Downstate Medical Center

Steven M Schwarz, MD, FAAP, FACN, AGAF is a member of the following medical societies: American Academy of Pediatrics, American College of Nutrition, American College of Physician Executives, American Gastroenterological Association, American Pediatric Society, Gastroenterology Research Group, New York Academy of Medicine, North American Society for Pediatric Gastroenterology and Nutrition, and Society for Pediatric Research

Disclosure: Curemark, LLC Consulting fee Board membership; Centocor, Inc. Grant/research funds Independent contractor; Johnson & Johnson, Inc. Grant/research funds Independent contractor

Coauthor(s)

Andre Hebra, MD  Chief, Division of Pediatric Surgery, Professor of Surgery and Pediatrics, Medical University of South Carolina College of Medicine

Andre Hebra, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American College of Surgeons, American Medical Association, American Pediatric Surgical Association, Children's Oncology Group, Florida Medical Association, International Pediatric Endosurgery Group, Society of American Gastrointestinal and Endoscopic Surgeons, Society of Laparoendoscopic Surgeons, South Carolina Medical Association, Southeastern Surgical Congress, and Southern Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Jayant Deodhar, MD  Associate Professor in Pediatrics, BJ Medical College, India; Honorary Consultant, Departments of Pediatrics and Neonatology, King Edward Memorial Hospital, India

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Pharmacy Editor, eMedicine

Disclosure: Nothing to disclose.

B UK Li, MD  Professor of Pediatrics, Division of Gastroenterology, Hepatology and Nutrition, Director, Pediatric Fellowships and Gastroenterology Fellowship, Medical Director, Functional Gastrointestinal Disorders and Cyclic Vomiting Program, Medical College of Wisconsin; Attending Gastroenterologist, Children's Hospital of Wisconsin

B UK Li, MD is a member of the following medical societies: Alpha Omega Alpha, American Gastroenterological Association, and North American Society for Pediatric Gastroenterology and Nutrition

Disclosure: Nothing to disclose.

Steven M Schwarz, MD, FAAP, FACN, AGAF  Professor of Pediatrics, Children's Hospital at Downstate, SUNY-Downstate Medical Center

Steven M Schwarz, MD, FAAP, FACN, AGAF is a member of the following medical societies: American Academy of Pediatrics, American College of Nutrition, American College of Physician Executives, American Gastroenterological Association, American Pediatric Society, Gastroenterology Research Group, New York Academy of Medicine, North American Society for Pediatric Gastroenterology and Nutrition, and Society for Pediatric Research

Disclosure: Curemark, LLC Consulting fee Board membership; Centocor, Inc. Grant/research funds Independent contractor; Johnson & Johnson, Inc. Grant/research funds Independent contractor

Chief Editor

Carmen Cuffari, MD  Associate Professor, Department of Pediatrics, Division of Gastroenterology/Nutrition, Johns Hopkins University School of Medicine

Carmen Cuffari, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, North American Society for Pediatric Gastroenterology, Hepatology and Nutrition, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

References
  1. Bhatia J, Parish A. GERD or not GERD: the fussy infant. J Perinatol. May 2009;29 Suppl 2:S7-11. [Medline].

  2. Rudolph CD. Supraesophageal complications of gastroesophageal reflux in children: challenges in diagnosis and treatment. Am J Med. Aug 18 2003;115 Suppl 3A:150S-156S. [Medline].

  3. Mousa H, Woodley FW, Metheney M and Hayes J. Testing the association between gastroesophageal reflux and apnea in infants. J Pediatr Gastroenterol Nutr. 2005;41:169-177. [Medline].

  4. Gold BD. Gastroesophageal reflux disease: could intervention in childhood reduce the risk of later complications?. Am J Med. Sep 6 2004;117 Suppl 5A:23S-29S. [Medline].

  5. Chao HC, Vandenplas Y. Effect of cereal-thickened formula and upright positioning on regurgitation, gastric emptying, and weight gain in infants with regurgitation. Nutrition. 2007;23:23-28. [Medline].

  6. [Best Evidence] Horvath A, Dziechciarz P, Szajewska H. The effect of thickened-feed interventions on gastroesophageal reflux in infants: systematic review and meta-analysis of randomized, controlled trials. Pediatrics. Dec 2008;122(6):e1268-77. [Medline].

  7. Diaz DM, Winter HS, Colletti RB, et al. Knowledge, attitudes and practice styles of North American pediatricians regarding gastroesophageal reflux disease. J Pediatr Gastroenterol Nutr. 2007;45:56-64. [Medline].

  8. [Guideline] Rudolph CD, Mazur LJ, Liptak JS et al. Guidelines for evaluation and treatment of gastroesophageal reflux in infants and children: recommendations of the North American Society for Pediatric Gastroenterology and Nutrition. J Pediatr Gastroenterol Nutr. 2001;32:S1-S22. [Medline].

  9. Hassall E. Decisions in diagnosing and managing chronic gastroesophageal reflux disease in children. J Pediatr. Mar 2005;146(3 Suppl):S3-12. [Medline].

  10. Diaz DM, Gibbons TE, Heiss K et al. Antireflux surgery outcomes in pediatric gastroesophageal reflux disease. Am J Gastroenterol. 2005;100:1844-1852. [Medline].

  11. Rabinowitz SS, Piecuch S, Jibali R, Goldsmith A and Schwarz SM. Optimizing the diagnosis of gastroesophageal reflux in children with otolaryngologic symptoms. Int J Pediatr Otorhinolaryngol. 2003;167:621-626. [Medline].

  12. Rosen R, Lord C and Nurko S. The sensitivity of multichannel intraluminal impedance and the pH probe in the evaluation of gastroesophageal reflux in children. Clin Gastroenterol Hepatol. 2006;4:167-172. [Medline].

  13. Orenstein SR. Management of supraesophageal complications of gastroesophageal reflux disease in infants and children. Am J Med. 2000;108 (4A):139S-143S. [Medline].

  14. Gold BD. Outcomes of pediatric gastroesophageal reflux disease: in the first year of life, in childhood, and in adults. J Pediatr Gastroenterol Nutr. 2003. 2003;37:S33-S39. [Medline].

  15. Nelson SP, Chen EH, Syniar GM, Christoffel KK. Prevalence of symptoms of gastroesophageal reflux during childhood: a pediatric practice-based survey. Pediatric Practice Research Group. Arch Pediatr Adolesc Med. Feb 2000;154(2):150-4. [Medline].

  16. Salvatore S, Hauser B, Vandemaele K. Gastroesophageal reflux disease in infants: how much is predictable with questionnaires, pH-metry, endoscopy and histology?. Journal of Pediatric Gastroenterology and Nutrition. 2005;40:210-5. [Medline].

  17. Ton M, Suwandhi E and Schwarz SM. Gastroesophageal Reflux. Pediatr Ann. 2006;35:259-266. [Medline].

  18. Vandenplas Y. Gastroesophageal Reflux : Medical treatment. J Pediatr Gastroenterol Nutr. 2005;41:S41-S42. [Medline].

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The image is a representation of concomitant intraesophageal pH and esophageal electrical impedance measurements. The vertical solid arrow indicates commencement of a nonacid gastroesophageal reflux (GER) episode (diagonal arrow). The vertical dashed arrow indicates the onset of a normal swallow.
Algorithm for evaluation and "step-up" management of gastroesophageal reflux (GER).
Diagram illustrating the Nissen fundoplication. Note how the stomach is wrapped around the esophagus (360-degree wrap).
 
 
 
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