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Gastroesophageal Reflux

Michael A. Davis, MD

Gastroesophageal reflux is defined as passive retrograde movement of gastric contents into the esophagus. GER often presents as frequent "spitting up" after meals, and it is a normal physiologic event for most infants.

Fifty to 65% of normal 2 month old infants regurgitate 3 or more times a day. By 3 months of age, only 4% are still regurgitating this amount. Two-thirds of these infants improve by 18 months of age, as the diet becomes more solid. By four years of age, symptoms resolve in most children with persistent GER. Severe GER can cause esophagitis, anemia, failure to thrive, and recurrent respiratory disease.

Physiology and Pathophysiology of GER

Two physiologic phenomena contribute to GER--transient lower esophageal sphincter (LES) relaxations and persistent or recurrent intraabdominal pressure increases. In infants with functional GER--which is what most babies have--transient LES relaxations are asynchronous with swallowing and last 5 seconds. Gastric distention due to delayed emptying, overfeeding, or gastric hypersecretion can provoke these inappropriate relaxations. Sustained increases in intraabdominal pressure can occur with excessive coughing, straining, or crying.

Gastroesophageal reflux is a physiologic phenomenon up to a certain point, beyond which it becomes pathologic. Even healthy persons have reflux, but it becomes a disease if the reflux causes symptoms and complications.

Physiologic reflux presents in infants as regurgitation in the first few months of life and resolves by 6-18 months of age.

Functional GER refers to reflux that is more frequent than physiologic GER, but which does not cause complications.

Pathologic GER consists of GER that is associated with complications. The most common pathologic presentation is failure to thrive.

Gastroesophageal reflux may cause vagal stimulation leading to bradycardia, with or without apnea and apparent life-threatening events.

Otalgia, recurrent abdominal pain, and Barrett's esophagus (glandular metaplasia of the distal esophagus) are complications of prolonged gastroesophageal reflux.

Diagnostic Approach to Gastroesophageal Reflux

Regurgitant GER must be differentiated from disorders such as gastric outlet obstruction (especially pyloric stenosis), acid-peptic disease, food allergies or intolerances, malrotation, cyclic vomiting, and CNS lesions. Infants with intractable vomiting should also be evaluated for immunologic, metabolic, renal, and infectious disorders.

The physical examination should include observation of the infant during and after feeding. Examination of the stool for occult blood is mandatory.

Vomiting in an infant younger than 2 months of age suggests possible anatomic abnormalities of the GI tract or metabolic disease. In an older infant, effortless regurgitation is a common manifestation of GER. No invasive evaluation is needed in an otherwise thriving infant.

Laboratory Evaluation

In a patient with significant vomiting, a complete blood cell count, electrolytes, blood urea nitrogen, urinalysis, and urine culture should be obtained.

Esophageal pH monitoring is the procedure of choice to evaluate infants with GER. Flexible probes are used to determine esophageal pH over a period of 18-24 hours.

Barium contrast radiography. In a patient with regurgitant reflux, this test can exclude causes such as structural abnormalities, strictures, malrotation, and suspected motility disorders that may present with similar symptoms. This study, which has a high incidence of false-positive and false-negative results, is not an accurate modality for detecting GER.

Scintigraphy is helpful in evaluating gastric emptying, non-acidic reflux, and pulmonary aspiration, but not GER. Scintigraphic findings do not correlate with the diagnosis of pathologic GER by pH monitoring.

Upper GI tract endoscopy should be the first test done in older children if the predominant symptom is vomiting with bleeding. This provides direct visualization of the esophageal mucosa, and immediate biopsy specimens can be taken. Endoscopy can detect esophagitis, hiatal hernia, and peptic ulcer disease. A negative endoscopic examination, however, does not exclude GER unless biopsy findings are also normal.

Conservative Therapy

Since the natural history of GER in pediatric patients is generally favorable, initial management should be conservative. Most infants and children with GER respond to conservative management.

Observing the parents feeding the infant, to be sure the infant is properly positioned and frequently burped, will eliminate the possibility of improperly held or propped bottles.

Dietary Measures. The parents should avoid overfeeding the child, and smaller, more frequent meals will decrease intragastric distention. Thickening agents (rice cereal) may deter some reflux; however, recent studies have discounted this effect in non-regurgitant occult reflux, possibly because of an adverse effect on gastric emptying.

Postural therapy for GER. Some evidence suggests that the prone position may reduce GER, but because of its association with sudden infant death syndrome, it is not routinely recommended. Keeping the baby upright after feeding may help.

Pharmacologic therapy

Patients who do not respond to conservative measures can be treated with prokinetic agents and acid-suppressing therapy. Prokinetic agents are the initial drug therapy for GER in infants. If complications arise, acid-suppressing medication is added.

Cisapride ( Propulsid). This agent promotes GI motility and increases antroduodenal coordination. Cisapride lowers the frequency and duration of prolonged GER episodes, reduces esophageal acid exposure, and decreases the frequency of vomiting.

The recommended dosage is 0.25-0.30 mg/kg, 15-30 minutes before meals, 3-4 times a day. It is available in suspension form.

Abdominal cramps, diarrhea and headaches are common side effects. Cisapride has been associated with arrhythmias when used with erythromycin-based antibiotics or ketoconazole.

Histamine-2-receptor antagonists may be used in infants and children with esophagitis or with colic due to GER-related feeding refusal. Some commonly used H2-receptor blockers include ranitidine ( Zantac), 2.0 mg/kg bid, and famotidine ( Pepcid), 0.6 mg/kg bid. Liquid preparations are available.

Omeprazole ( Prilosec), a proton-pump inhibitor, is effective treatment for neurologically impaired children with severe esophagitis, and it can be used as a second-line acid suppressant in neurologically normal children. Omeprazole can be difficult to administer because no liquid preparation is available and its granules should not be chewed or crushed.

Surgery

Patients who do not respond adequately to dietary modifications, postural changes, and pharmacologic management or who develop complications are candidates for surgical intervention. GER patients with neurologic disorders, such as cerebral palsy and Down syndrome, often require surgery.

The procedure of choice is the Nissen fundoplication, in which the gastric fundus is wrapped around the lower 2-3 cm of the esophagus. This procedure is well tolerated and is effective. Its efficacy rate ranges from 60-90%. §