Gastroesophageal Reflux Disease
Kandace Kichler
Many parents report that their infant will spit up or develop emesis of milk after feedings. This is usually inconsequential and considered normal, and infants often outgrow postprandial regurgitation by 2 years of age.
Pathologic gastroesophageal reflux (GER), or gastroesophageal reflux disease (GERD), can be associated with failure to thrive, apnea, extreme irritability, and aspiration of gastric contents.
RELEVANT ANATOMY
The esophagus has cervical, thoracic, and intra-abdominal segments that arise from the embryonic foregut.
The esophagus travels through the esophageal hiatus in the diaphragm and is enveloped by the diaphragmatic crura on each side. Once inside the abdomen, the esophagus makes an acute angle (the angle of His) and enters the stomach.
The lower esophageal sphincter (LES), not a true muscular sphincter, is located in the intra-abdominal esophagus adjacent to the body of the stomach. This is a physiologic high-pressure zone that, when diminished, can result in GER (Figure 17.1).
Other anatomic contributors to GER include a shortened intra-abdominal esophagus, presence of hiatal or paraesophageal hernia, widened angle of His, and both functional and neurologic issues with esophageal and/or stomach motility.
EPIDEMIOLOGY AND ETIOLOGY
Incidence: Approximately 1 in 300 to 1000 children has excessive, passive reflux with an incompetent LES and requires medical or surgical therapy.1
Etiology: Many theories as to the exact etiology exist, but it is likely multifactorial.
Children with neurologic impairments are more likely to be affected by GER as well as delayed gastric emptying.1
Prolonged exposure of squamous esophageal mucosa to gastric acid and refluxed contents results in the symptoms.
 Figure 17.1 Esophagus (terminal part), stomach, and proximal duodenum. A, Parts of stomach. B, Internal surface of stomach. C, Radiograph of stomach and duodenum after barium ingestion (arrows, peristaltic wave). D, Coronal section of region of esophagogastric junction. D, diaphragm; E, esophagus; ST, stomach; Z, esophagogastric junction (Z-line). (Reprinted with permission from Moore KL, Agur AMR, Dalley AF. Essential Clinical Anatomy. 5th ed. Philadelphia, PA: Wolters Kluwer Health; 2015.) |
 Figure 17.1—cont’d |
CLINICAL PRESENTATION
Classic presentation: A mother will complain that her infant has recurrent, severe postprandial regurgitation of milk and irritability.
Patients with GERD also vomit with coughing, exertion, and crying.
It is paramount to distinguish this from infants with bilious emesis, which can suggest a multitude of other pathologies that will be discussed in other chapters.
Patients with GERD typically have either respiratory or esophageal symptoms. Infants usually present with
respiratory complications, whereas very young children will present with esophageal symptoms.
Respiratory symptoms occur from aspiration of gastric acidic contents and include bronchospasm, laryngospasm, hoarseness, pneumonia, apnea, and choking spells.1 This aspiration is usually right-sided and worsened at night or when the patient is in recumbent positions.
Esophageal symptoms include irritability, heartburn, and esophagitis. Endoscopy can disclose columnar metaplasia in the distal esophagus secondary to prolonged GERD. Esophagitis can result in hematemesis, heme-positive stools, and chronic iron anemia.
Malnutrition can be seen with prolonged GERD, as well as growth delays.
DIAGNOSIS
Laboratory Finding
If a patient presents with signs or symptoms of dehydration or failure to thrive, it is essential to obtain intravenous access and check basic electrolytes.
Patients with significant vomiting and regurgitation could potentially have a hypokalemic, hypochloremic, metabolic alkalosis.
Imaging Findings
Imaging modality of choice for the diagnosis is an upper GI series with barium.
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