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Sandifer Syndrome Medication

  • Author: Pegeen Eslami, MD; Chief Editor: Carmen Cuffari, MD  more...
Updated: Nov 11, 2015

Medication Summary

Therapeutic response for the treatment of gastroesophageal reflux disease may take several weeks. If treatment is successful, the frequency of posturing and apparent distress will decrease.



Prokinetic agents

Class Summary

These agents are used to augment cholinergic activity. As such, they can improve contractility of the lower esophagus, increase lower esophageal sphincter pressure and augment the rate of gastric emptying.  However these agents have a limited role in this age group as the risk of adverse side effects generally outweighs benefit. Current guidelines do not support the routine use of prokinetic agents for the treatment of GERD in infants or older children.[12, 17] Use of PPIs should be considered only in specific situation with thorough consideration of risks and benefit.

Metoclopramide (Reglan)


Dopaminergic antagonist that works by increasing LES tone and gastric emptying. Stimulates muscular activity, leading to decrease in reflux.



Class Summary

These agents have traditionally been used as a diagnostic tool, providing symptomatic relief in infants. However, although they may confer short term relief, they are not recommended for long-term use due to the risk of associated aluminum toxicity and/or milk-alkali syndrome.[20]   They are not currently recommended for the treatment of GERD in infants and children.[14, 20]

Aluminum hydroxide (ALternaGEL, Amphojel)


Increases gastric pH above 4 and inhibits proteolytic activity of pepsin, reducing acid indigestion. Antacids can initially be used in mild cases. No effect on frequency of reflux but decreases its acidity.

Magnesium hydroxide (Phillips Milk of Magnesia)


Causes osmotic retention of fluid, which distends colon and increases peristaltic activity. Forms magnesium chloride in vivo after reacting with stomach hydrochloric acid.


H2 receptor antagonists

Class Summary

Like antacids, these agents do not reduce the frequency of reflux, but they are very effective in decreasing the amount of acid in the refluxate through inhibition of acid production by blocking the histamine H2 receptors on gastric parietal cells. All are equipotent when used in equivalent doses. Long- term use is limited by the development of tachyphylaxis  or tolerance. These medications are very useful for short term trial of acid suppression.

Ranitidine (Zantac)


Inhibits histamine stimulation of the H2 receptor in gastric parietal cells, which reduces gastric acid secretion, gastric volume, and hydrogen ion concentrations.

Famotidine (Pepcid)


Competitively inhibits histamine at H2 receptor of gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and hydrogen ion concentrations.

Nizatidine (Axid)


Nizatidine is approved by the FDA for use in adolescents aged 12-18 y. Off-label use in children younger than 12 y has been described.


Proton pump inhibitors

Class Summary

Proton pump inhibitors (PPIs) decrease acid secretion by irreversibly binding to and inhibiting the H+-K+-ATPase pump on the gastric parietal cell surface. They are more effective at increasing gastric pH, and for a longer duration, compared with H2 receptor antagonists (H2RA). Additionally, they do not cause the tolerance seen after several weeks use of the H2RAs. As a result, PPIs contribute to more rapid healing of erosive esophagitis.[21] There is mixed evidence as to their efficacy in reducing irritability in infants.[15, 22]  Concerns exist regarding overuse and over prescribing of PPIs, and the long-term adverse effects (eg, increased in respiratory infections in infants, headache, nausea, diarrhea and constipation in older children and adults).[12, 20]  

Omeprazole, lansoprazole, pantoprazole and esomeprazole have all been studied in infants and young children. Currently, the only PPI approved by the FDA for use in infants aged 1-12 months is esomeprazole.

Omeprazole (Prilosec)


Decreases gastric acid secretion by inhibiting the parietal cell H+-K+-ATP pump.

Lansoprazole (Prevacid, Prevacid 24HR, Prevacid Solu Tab)


Suppresses gastric acid secretion by specific inhibition of the (H+, K+)-ATPase enzyme system (ie, proton pump) at the secretory surface of the gastric parietal cell. It blocks the final step of acid production. The effect is dose-related and inhibits both basal and stimulated gastric acid secretion, thus increasing gastric pH.

Esomeprazole magnesium (Nexium)


S-isomer of omeprazole. Inhibits gastric acid secretion by inhibiting H+-K+-ATPase enzyme system at secretory surface of gastric parietal cells.

Contributor Information and Disclosures

Pegeen Eslami, MD Associate Professor of Pediatrics, Division of Pediatric Emergency Medicine, UMass Memorial Medical Center

Pegeen Eslami, MD is a member of the following medical societies: Academic Pediatric Association, American Academy of Pediatrics, American College of Emergency Physicians, Massachusetts Medical Society

Disclosure: Nothing to disclose.


Raj D Sheth, MD Chief, Division of Pediatric Neurology, Nemours Children's Clinic; Professor of Neurology, Mayo College of Medicine; Professor of Pediatrics, University of Florida College of Medicine

Raj D Sheth, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Pediatrics, American Epilepsy Society, American Neurological Association, Child Neurology Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

David A Piccoli, MD Chief of Pediatric Gastroenterology, Hepatology and Nutrition, The Children's Hospital of Philadelphia; Professor, University of Pennsylvania School of Medicine

David A Piccoli, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American Gastroenterological Association, North American Society for Pediatric Gastroenterology, Hepatology and Nutrition

Disclosure: Nothing to disclose.

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, Royal College of Physicians and Surgeons of Canada

Disclosure: Received honoraria from Prometheus Laboratories for speaking and teaching; Received honoraria from Abbott Nutritionals for speaking and teaching.

Additional Contributors

Jorge H Vargas, MD Professor of Pediatrics and Clinical Professor of Pediatric Gastroenterology, University of California, Los Angeles, David Geffen School of Medicine; Consulting Physician, Department of Pediatrics, University of California at Los Angeles Health System

Jorge H Vargas, MD is a member of the following medical societies: American Liver Foundation, Latin American Society of Pediatric Gastroenterology, Hepatology & Nutrition, American Society for Gastrointestinal Endoscopy, American Society for Parenteral and Enteral Nutrition, North American Society for Pediatric Gastroenterology, Hepatology and Nutrition

Disclosure: Nothing to disclose.

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Diagram illustrating the Nissen fundoplication. Note how the stomach is wrapped around the esophagus (360º wrap).
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