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| AuthorsRichard Martin, MDAnna Maria Hibbs, MD, MSCE | Section EditorSteven A Abrams, MD | Deputy EditorMelanie S Kim, MD |
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INTRODUCTION
Gastroesophageal reflux (GER), the passage of gastric contents into the esophagus, occurs commonly in newborn infants, especially those born prematurely. Physiologic GER typically is a developmental process that resolves with maturation. GER generally resolves on its own by one year of age. In infants who remain asymptomatic, no further evaluation or intervention is typically required.
In contrast, GER disease (GERD), as defined by the North American Society for Pediatric Gastroenterology and Nutrition, is clinically significant GER that causes morbidity [1]. Putative morbidities of GERD in preterm infants include frequent vomiting, aspiration pneumonia, irritability, failure to thrive, and exacerbation of respiratory symptoms, including chronic lung disease.
Gastroesophageal reflux (GER) in preterm infants will be reviewed here. GER in infants, children, and adolescents are discussed separately. (See "Gastroesophageal reflux in infants" and "Clinical manifestations and diagnosis of gastroesophageal reflux disease in children and adolescents" and "Management of gastroesophageal reflux disease in children and adolescents".)
MECHANISMS
Gastroesophageal reflux (GER) is extremely common in healthy infants in whom gastric fluids reflux into the esophagus 30 or more times daily. It appears that GER is more common in healthy preterm compared to term infants. The pathogenesis of GER in preterm infants appears to be multifactorial due in part to immature or impaired anatomic and physiologic factors that typically limit reflux.
Relaxation of lower esophageal sphincter — The most important mechanism of GER in preterm infants (similar to older infants and adults) is transient relaxation of the lower esophageal sphincter (LES) [2,3]. The LES is comprised of intrinsic smooth muscle of the esophagus and skeletal muscle of the crural diaphragm [4].
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