Gastroesophageal Reflux Disease in Infants and Children

Tracy Sandritter, PharmD

Disclosures

J Pediatr Health Care. 2003;17(4) 

In This Article

Treatment Options

Therapy for GER/GERD should follow a stepwise approach; however, some of these steps may occur simultaneously. The steps are lifestyle modifications, pharmacologic therapy, and surgical procedures (Boyle, et al., 2001). The goals of therapy include decreasing symptoms, frequency, and duration of reflux episodes; healing the injured mucosa; and preventing complications (DeVault, 1999; Williams & Welage, 1997).

For infants, lifestyle modifications might include a variety of feeding adjustments. This might include administering smaller amounts of formula at more frequent intervals, observing the infant during feeding to minimize air swallowing, thickening the formula, using a formula with mostly medium-chain triglycerides instead of long-chain fatty acids, and selecting a hypoallergenic formula. In addition, avoidance of the seated position after feeding, elevation of the head of the bed, and prone positioning while awake are beneficial. During sleep, prone positioning, under the right circumstances (no fluffy bedding), should only be considered for very unusual and select cases. Other options might include continuous intragastric feeding via a nasogastric or gastrostomy tube. Lifestyle changes for children and adolescents include dietary changes, weight loss, loose clothing, adjustment of sleeping position, and smoking cessation (first and second hand). Dietary adjustments should include avoidance of caffeine, chocolate, spicy foods, cigarette smoking, and alcohol (Rudolph, et al., 2001; DeVault, 1999; Glassman, et al., 1995; Orenstein, Zadnia, & Khan, 1999).

Pharmaceutical therapies are aimed at the various steps in the pathophysiology of GER(D). Unfortunately, there is not a therapy that directly targets the primary mechanism of GER. The agents most frequently used as first line therapy work by protecting the esophageal mucosa from acidic refluxate or by decreasing gastric acidity. Other medications work by increasing LES pressure, esophageal clearance, or gastric emptying (Rudolph, et al., 2001; Williams & Welage, 1997).

Acid suppressants work by protecting the esophagus from acidic refluxate. Agents in this group of medications include antacids, histamine-2-receptor antagonists (H2-blockers), and proton pump inhibitors (PPI). Agents in this family of medications are typically used as first line pharmacotherapy in the treatment of GER(D) (Rudolph, et al., 2001; DeVault, 1999). Antacids work by neutralizing gastric acid. H2-blockers and PPIs work by decreasing the secretion of gastric acid. More specifically, H2-blockers work by inhibiting the histamine receptor, one of three receptors on the parietal cells that affect acid production. PPIs are antagonists of the proton pump itself; thereby effectively inhibiting acid production (Shamburek & Schubert, 1992). Use of antacids has fallen out favor because of concern for aluminum toxicity in infants and the increased efficacy and convenience of H2-blockers. However, antacids provide quick, short-term relief of intermittent symptoms in older children (Rudolph, et al., 2001). Gaviscon, an over-the-counter antacid preparation of alginic acid, does not contain aluminum and may be of some benefit in infants (dose of 0.5 ml/kg between feedings) (Glassman, et al., 1995). H2-blockers are typically more effective in the treatment of milder forms of GER(D) (Rudolph, et al., 2001). PPIs have only recently been used in pediatric patients with GER(D). The benefits of PPIs include increased reduction of acid secretion and longer duration of action when compared to H2-blockers. Maximal benefit is achieved with the PPIs when they are administered half an hour before meals. Also, these agents should not be administered in addition to H2-blockers because concomitant use of these agents inhibits the effectiveness of the PPIs. Because of limited experience with the use of these agents in children, PPIs are usually used after a therapeutic failure of H2-blockers (Rudolph, et al., 2001; DeVault, 1999; Gold & Freston, 2002). However, in adult reflux guidelines, a step-down approach is recommended, during which a PPI is started to gain control and is then stepped down to a H2-blocker for maintenance (Dent, Brun, & Fendrick, 1999).

Prokinetic agents are those medications that work by increasing the movement of materials through the GI tract. Motility of the GI tract is mediated via smooth muscle cell response to neurotransmitters. Reflux of gastric material into the esophagus involves movement of gastric contents in the wrong direction through the GI tract. Therefore, medications that aid in the correct flow of gastric materials through the GI tract should decrease GER(D). There are three pathways through which GI motility is mediated: cholinergic, dopaminergic, and noncholinergic nonadrenergic compounds (e.g., motilin) (Reynolds & Putnam, 1992).

Prokinetic medications include beth-anechol, cisapride, metoclopramide, domperidone, and erythromycin. Beth-anechol and cisapride work by increasing LES pressure and esophageal clearance. Cisapride also works by increasing gastric emptying (Williams & Welage, 1997). Due to concerns of cardiac arrhythmias, cisapride is not readily available, but it may be used if the patient is enrolled in a limited access protocol through the pharmaceutical company. Unfortunately, cisapride has thus far been the only prokinetic agent that has shown some benefit in pediatric GER(D) clinical trials (Boyle, et al., 2001). Because this agent is no longer readily available on the United States market, it will not be further discussed. While metoclopramide's mechanisms of action include increased LES pressure and gastric emptying, it has not shown clear efficacy data in clinical trials. Concern over central nervous system adverse effects such as Parkinsonian reactions and tardive dyskinesia limit its prolonged use. Domperidone has been studied in children; however, its use is limited because it is currently not approved by the U.S. Food and Drug Administration (Rudolph, et al., 2001). Erythromycin is believed to work via its action as a motilin receptor agonist and possibly by increasing LES pressure (Glassman, et al., 1995).

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