Medscape is available in 5 Language Editions – Choose your Edition here.


Pediatric Esophagitis Treatment & Management

  • Author: Gayle H Diamond, MD; Chief Editor: Carmen Cuffari, MD  more...
Updated: Dec 11, 2015

Approach Considerations

Specific treatment for esophagitis varies with the etiology. Symptomatic treatment may include antacids for mild reflux esophagitis or viral esophagitis in the immunocompetent host. Hospitalization is required if patients have significant bleeding, hemodynamic compromise, obstruction, perforation, or respiratory distress or are unable to feed themselves. In particular, be certain to have a low threshold for admitting a child to the hospital after any caustic ingestion.


Treatment of Reflux (Peptic) Esophagitis

For mild gastroesophageal reflux (GER), prone and elevated head positioning, feeding recommendations (eg, thickening formula, providing smaller and more frequent feedings, fasting for at least 2 h before sleeping in older children), and other conservative reflux measures (eg, eliminating tobacco smoke exposure) may be used.

Although gastroesophageal reflux disease (GERD) may be initially treated with histamine-2 (H2)–receptor antagonists, tachyphylaxis quickly develops. Proton pump inhibitors (PPIs) should be used when reflux esophagitis is diagnosed because the effect of PPIs is more sustained and powerful.[28] A study of healthy children found that erosive esophagitis treated with adequate doses of PPIs for 3 months has a low relapse rate and does not require maintenance with PPIs or H2 -blocker therapy.[29, 30]  Emerging research has shown associations of long-term use of acid blocking medications with adverse events in children including increased incidence of necrotizing enterocolitis in preterm infants and increased risk of infections. These infections include clostridium difficile colitis, candida esophagitis, and community-acquired pneumonia. Clearly, risks and benefits of these medications need to be considered alongside the decision to prescribe.[31, 32, 33]

In severe cases of reflux esophagitis that are unresponsive to aggressive medical management, consider surgical referral for Nissen fundoplication. With the availability of PPIs, this surgical indication is now restricted to less than 1% of all cases. Patients with associated delay in gastric emptying may require a pyloroplasty. A gastrostomy or jejunostomy tube may be placed to assist with feeding.


Treatment of Corrosive (Caustic) Esophagitis

For corrosive esophagitis with alkalis or acids, any continued exposure to the eye, mouth, and skin should be ceased and the area flushed with water. Airway, breathing, circulation, and the overall cardiorespiratory status should be addressed following any possible ingestion. Endotracheal intubation or tracheostomy may be required if severe upper airway edema is present.

Although large quantities of fluid (eg, water, milk) have often been given to dilute the corrosive agent, be aware that if perforation has occurred, these fluids may extravasate, leading to mediastinitis. Large volumes of fluid may also induce vomiting, but a small amount of water or milk may wash away any residual agent from the mucosal surface.

If alkaline or acidic fluids are given, an exothermic reaction can occur. Induced emesis or gastric lavage for GI decontamination is contraindicated and may exacerbate esophageal injury or lead to aspiration. Charcoal is not recommended.

Most children who have ingested a caustic substance need to be admitted at least for observation to keep them on nothing by mouth (NPO) status, provide intravenous hydration until endoscopy, and monitor vital signs and respiratory distress.

If no mucosal burns are detected, a patient may be discharged home after tolerating a normal diet. For patients with first-degree burns only, observe for at least 48-96 hours and until tolerating a normal diet. Patients with second- and third-degree burns require prolonged hospitalization.

Broad-spectrum antibiotics may be used in severe cases to prevent secondary infection. The use of systemic corticosteroids is controversial, but they may be used in an attempt to decrease stricture formation. Surgical management of perforations and revisions may be required. 


Treatment of Infectious Esophagitis

Infectious esophagitis requires the appropriate antiviral, antifungal, or antibiotic therapy based on the causative organism. For bacterial esophagitis, drainage of a paraesophageal abscess may be required.


Treatment of Eosinophilic Esophagitis

The treatment of eosinophilic esophagitis is still widely debated.[4] Patch testing in combination with skin prick testing can help determine the causative food allergen (most commonly, milk, eggs, wheat, beef, soy, chicken).[34]

Selective elimination of implicated foods based on allergy testing or, in certain cases, initiation of elemental diet is required. For 1-3 months, patients are placed on an exclusion diet or an elemental diet, and repeat endoscopies with biopsies are often necessary to determine both improvement and the time to start progressive reintroduction of foods. Elemental diet has a higher success rate than testing-based elimination diet.[35, 36]

Other treatments, such as anti-inflammatory medications, mast cell stabilizers, and leukotriene receptor antagonists, have also been used. Oral corticosteroids were demonstrated to be effective in treating symptoms and normalizing the histology, but the disease recurs when these agents are discontinued.

Since 1998, multiple studies have demonstrated the effectiveness of swallowed topical corticosteroids delivered from a metered dose inhaler (fluticasone) or oral viscous budesonide in treating clinical symptoms and abnormal histology associated with eosinophilic esophagitis.[37, 38, 39] When using swallowed fluticasone, patients should be instructed to administer the metered dose inhaler without using a spacer. The inhaler should be inserted into the mouth and sprayed with the lips sealed around the device; the powder should then be swallowed and not rinsed. The patient should not eat or drink for at least 30 minutes. When using oral viscous budesonide, the patient should not eat or drink for at least 30 minutes after taking the medication.

The course of treatment with topical corticosteroids should be 4-12 weeks. However, similar to the effect seen with oral steroid treatment, the disease generally recurs upon discontinuation of treatment.[40]

The use of a topical steroid for maintenance treatment has not been studied. The adverse effects with this form of treatment are thought to be significantly less than those with oral steroid therapy because of the much smaller dose and the rapid metabolism by the liver with first-pass effect.

Oral cromolyn sodium and other mast cell stabilizers have not been shown to be effective. Studies have demonstrated benefits from leukotriene-receptor antagonists in adults, and studies of monoclonal antibodies directed against interleukin (IL)–5 are ongoing.[41, 42]



Dietary Measures

No dietary changes are required once proper medical treatment is successfully initiated. However, foods that exacerbate reflux or delay gastric emptying (eg, fats, fried foods, tomatoes, caffeine) should be restricted.


Prevention of Esophagitis

Prevention of accidental ingestion is critical, because of the potentially high associated morbidity and mortality. Corrosive agents should be locked up and kept out of reach of young children and maintained in their closed original containers.



Consult a gastroenterologist, especially if endoscopy or biopsy is required for definitive diagnosis.[43]

For corrosive ingestions, always notify a local Poison Control Center. Their staff can help identify problematic active ingredients and provide immediate management and monitoring guidelines. A gastroenterologist and, possibly, a surgeon need to be consulted. A significant number of patients have esophageal burns without oral burns.


Long-Term Monitoring

Close monitoring with the primary physician after caustic ingestion is important in the early detection and intervention of stricture formation. Among patients who develop strictures, 50% develop them in 1 month, 80% develop them in 2 months, and all patients develop them by 8 months. Late esophageal squamous carcinoma is rare.

Contributor Information and Disclosures

Gayle H Diamond, MD Assistant Professor, Department of Pediatrics, Children’s Hospital of Philadelphia

Disclosure: Nothing to disclose.


Maria Rebello Mascarenhas, MBBS Associate Professor of Pediatrics, University of Pennsylvania School of Medicine; Section Chief of Nutrition, Division of Gastroenterology and Nutrition, Director, Nutrition Support Service, Children's Hospital of Philadelphia

Maria Rebello Mascarenhas, MBBS is a member of the following medical societies: American Gastroenterological Association, American Society for Parenteral and Enteral Nutrition, North American Society for Pediatric Gastroenterology, Hepatology and Nutrition

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.

Stefano Guandalini, MD Founder and Medical Director, Celiac Disease Center, Chief, Section of Pediatric Gastroenterology, Hepatology and Nutrition, Department of Pediatrics, University of Chicago Medical Center; Professor, Department of Pediatrics, Section of Gastroenterology, Hepatology and Nutrition, University of Chicago Division of the Biological Sciences, The Pritzker School of Medicine

Stefano Guandalini, MD is a member of the following medical societies: American Gastroenterological Association, North American Society for Pediatric Gastroenterology, Hepatology and Nutrition, European Society for Paediatric Gastroenterology, Hepatology & Nutrition, North American Society for the Study of Celiac Disease

Disclosure: Received consulting fee from AbbVie for consulting.

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. for: Abbott Nutritional, Abbvie, speakers' bureau.

Additional Contributors

Marianne V Augustine, MD Fellow, Division of Pediatric Gastroenterology, Hepatology, and Nutrition, The Children's Hospital of Philadelphia

Marianne V Augustine, MD is a member of the following medical societies: American Academy of Pediatrics, American Association for the Study of Liver Diseases, American Gastroenterological Association, North American Society for Pediatric Gastroenterology, Hepatology and Nutrition

Disclosure: Nothing to disclose.


Andrew S Chu, MD Medical Director, CHOP Connection at Grand View Hospital, Children's Hospital of Philadelphia; Clinical Assistant Professor, Division of General Pediatrics, Department of Pediatrics, University of Pennsylvania School of Medicine

Andrew S Chu, MD is a member of the following medical societies: American Academy of Pediatrics and Society of Hospital Medicine

Disclosure: Nothing to disclose.

Vera De Matos, MD Fellow in Pediatric Gastroenterology, The Children's Hospital of Philadelphia, University of Pennsylvania School of Medicine

Vera De Matos is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, and North American Society for Pediatric Gastroenterology and Nutrition

Disclosure: Nothing to disclose.

Jayant Deodhar, MD Associate Professor in Pediatrics, BJ Medical College, India; Honorary Consultant, Departments of Pediatrics and Neonatology, King Edward Memorial Hospital, India

Disclosure: Nothing to disclose.

Jessica Wen, MD Clinical Fellow, Department of Pediatric Gastroenterology, Hepatology and Nutrition, Children's Hospital of Philadelphia

Jessica Wen, MD is a member of the following medical societies: American Academy of Pediatrics, American Association for the Study of Liver Diseases, American Medical Association, and North American Society for Pediatric Gastroenterology, Hepatology and Nutrition

Disclosure: Nothing to disclose.

  1. Jensen ET, Kappelman MD, Kim HP, Ringel-Kulka T, Dellon ES. Early Life Exposures as Risk Factors Forpediatric Eosinophilic Esophagitis: A Pilot and Feasibility Study. J Pediatr Gastroenterol Nutr. 2013 Mar 19. [Medline].

  2. Homan M, Orel R, Liacouras C. Caustic ingestion: a possible cause of eosinophilic esophagitis?. Pediatrics. 2013 Apr. 131(4):e1284-7. [Medline].

  3. Al-Hussaini A, Al-Idressi E, Al-Zahrani M. The role of allergy evaluation in children with eosinophilic esophagitis. J Gastroenterol. 2013 Jan 11. [Medline].

  4. [Guideline] Furuta GT, Liacouras CA, Collins MH, et al. Eosinophilic esophagitis in children and adults: a systematic review and consensus recommendations for diagnosis and treatment. Gastroenterology. 2007 Oct. 133(4):1342-63. [Medline].

  5. Liacouras CA, Ruchelli E. Eosinophilic esophagitis. Curr Opin Pediatr. 2004 Oct. 16(5):560-6. [Medline].

  6. Noel RJ, Tipnis NA. Eosinophilic esophagitis -- a mimic of GERD. Int J Pediatr Otorhinolaryngol. 2006 Jul. 70(7):1147-53. [Medline].

  7. Freedberg DE, Lamousé-Smith ES, Lightdale JR, Jin Z, Yang YX, Abrams JA. Use of Acid Suppression Medication is Associated With Risk for C. difficile Infection in Infants and Children: A Population-based Study. Clin Infect Dis. 2015 Sep 15. 61 (6):912-7. [Medline].

  8. Cohen S, Bueno de Mesquita M, Mimouni FB. Adverse effects reported in the use of gastroesophageal reflux disease treatments in children: a 10 years literature review. Br J Clin Pharmacol. 2015 Aug. 80 (2):200-8. [Medline].

  9. Terrin G, Passariello A, De Curtis M, Manguso F, Salvia G, Lega L, et al. Ranitidine is associated with infections, necrotizing enterocolitis, and fatal outcome in newborns. Pediatrics. 2012 Jan. 129 (1):e40-5. [Medline].

  10. Spergel JM, Brown-Whitehorn TF, Cianferoni A, Shuker M, Wang ML, Verma R, et al. Identification of causative foods in children with eosinophilic esophagitis treated with an elimination diet. J Allergy Clin Immunol. 2012 Aug. 130 (2):461-7.e5. [Medline].

  11. Esophageal reflux. Walker WA, Goulet O, Kleinman RE, et al, eds. Pediatric Gastrointestinal Disease. 4th ed. Lewiston, NY: BC Decker; 2004. 400-24.

  12. Ruchelli ED, Liacouras CA. Esophageal disorders in childhood. Russo P, Ruchelli E, Piccoli DA, eds. Pathology of Pediatric Gastrointestinal and Liver Disease. New York, NY: Springer-Verlag; 2004. 37-46.

  13. Committee on Infectious Diseases. Candidiasis. 2006 Red Book: Report of the Committee on Infectious Diseases. American Academy of Pediatrics; 2006. 242-6.

  14. Committee on Infectious Diseases. Cytomegalovirus infection. 2006 Red Book: Report of the Committee on Infectious Diseases. 27th ed. American Academy of Pediatrics; 2006. 273-7.

  15. Committee on Infectious Diseases. Antifungal drugs for systemic fungal infection. 2006 Red Book: Report of the Committee on Infectious Diseases. 27th ed. American Academy of Pediatrics; 2006. 774-6.

  16. Committee on Infectious Diseases. Antiviral drugs for non-human immunodeficiency virus infections. 2006 Red Book: Report of the Committee on Infectious Diseases. 27th ed. American Academy of Pediatrics; 2006. 785-9.

  17. Committee on Infectious Diseases. Herpes simplex. In: 2006 Red Book: Report of the Committee on Infectious Diseases. 27th ed. American Academy of Pediatrics; 2006. 361-71.

  18. Rodrigues F, Brandao N, Duque V, et al. Herpes simplex virus esophagitis in immunocompetent children. J Pediatr Gastroenterol Nutr. 2004 Nov. 39(5):560-3. [Medline].

  19. Henderson CJ, Abonia JP, King EC, Putnam PE, Collins MH, Franciosi JP, et al. Comparative dietary therapy effectiveness in remission of pediatric eosinophilic esophagitis. J Allergy Clin Immunol. 2012 Jun. 129 (6):1570-8. [Medline].

  20. Assa'ad AH, Gupta SK, Collins MH, Thomson M, Heath AT, Smith DA, et al. An antibody against IL-5 reduces numbers of esophageal intraepithelial eosinophils in children with eosinophilic esophagitis. Gastroenterology. 2011 Nov. 141 (5):1593-604. [Medline].

  21. Xinias I, Maris T, Mavroudi A, Panteliadis C, Vandenplas Y. Helicobacter pylori infection has no impact on manometric and pH-metric findings in adolescents and young adults with gastroesophageal reflux and antral gastritis: eradication results to no significant clinical improvement. Pediatr Rep. 2013 Feb 5. 5(1):e3. [Medline].

  22. Ramakrishnan JB. The role of food allergy in otolaryngology disorders. Curr Opin Otolaryngol Head Neck Surg. 2010 Feb 17. [Medline].

  23. Papadopoulou A, Koletzko S, Heuschkel R, et al. Management guidelines of eosinophilic esophagitis in childhood. J Pediatr Gastroenterol Nutr. 2014 Jan. 58 (1):107-18. [Medline].

  24. Straumann A, Conus S, Degen L, Felder S, Kummer M, Engel H, et al. Budesonide is effective in adolescent and adult patients with active eosinophilic esophagitis. Gastroenterology. 2010 Nov. 139 (5):1526-37, 1537.e1. [Medline].

  25. Rodrigues M, D'Amico MF, Patiño FR, Barbieri D, Damião AO, Sipahy AM. Clinical manifestations, treatment, and outcomes of children and adolescents with eosinophilic esophagitis. J Pediatr (Rio J). 2013 Mar-Apr. 89(2):197-203. [Medline].

  26. Haddad I, Kierkus J, Tron E, Ulmer A, Hu P, Silber S, et al. Maintenance of efficacy and safety of rabeprazole in children with endoscopically proven GERD. J Pediatr Gastroenterol Nutr. 2014 Apr. 58 (4):510-7. [Medline].

  27. Vandenplas Y, Badriul H, Verghote M, Hauser B, Kaufman L. Oesophageal pH monitoring and reflux oesophagitis in irritable infants. Eur J Pediatr. 2004 Jun. 163(6):300-4. [Medline].

  28. Gold BD. Gastroesophageal reflux disease: could intervention in childhood reduce the risk of later complications?. Am J Med. 2004 Sep 6. 117 Suppl 5A:23S-29S. [Medline].

  29. Boccia G, Manguso F, Miele E et el. Maintenance therapy for erosive esophagitis in children after healing by Omeprazole: is it advisable?. Am J Gastroenterol. Jun 2007. 102(6):1291-7. [Medline].

  30. Dellon ES. Epidemiology of eosinophilic esophagitis. Gastroenterol Clin North Am. 2014 Jun. 43 (2):201-18. [Medline].

  31. Cianferoni A, Spergel J. Eosinophilic Esophagitis: A Comprehensive Review. Clin Rev Allergy Immunol. 2015 Jul 22. [Medline].

  32. Kim KY, Jang JY, Kim JW, Shim JJ, Lee CK, Dong SH, et al. Acid suppression therapy as a risk factor for Candida esophagitis. Dig Dis Sci. 2013 May. 58 (5):1282-6. [Medline].

  33. Daniell HW. Acid suppressing therapy as a risk factor for Candida esophagitis. Dis Esophagus. 2015 Apr 1. [Medline].

  34. Gupta SK, Vitanza JM, Collins MH. Efficacy and safety of oral budesonide suspension in pediatric patients with eosinophilic esophagitis. Clin Gastroenterol Hepatol. 2015 Jan. 13 (1):66-76.e3. [Medline].

  35. Spergel JM. Eosinophilic esophagitis in adults and children: evidence for a food allergy component in many patients. Curr Opin Allergy Clin Immunol. June 2007. 7(3):274-8. [Medline].

  36. Dutt P, Shukla JS, Ventateshaiah SU, Mariswamy SJ, Mattner J, Shukla A, et al. Allergen-induced interleukin-18 promotes experimental eosinophilic oesophagitis in mice. Immunol Cell Biol. 2015 Nov. 93 (10):914. [Medline].

  37. Liacouras CA, Wenner WJ, Brown K, Ruchelli E. Primary eosinophilic esophagitis in children: successful treatment with oral corticosteroids. J Pediatr Gastroenterol Nutr. 1998 Apr. 26(4):380-5. [Medline].

  38. Blanchard C. Molecular pathogenesis of eosinophilic esophagitis. Curr Opin Gastroenterol. 2015 Jul. 31 (4):321-7. [Medline].

  39. Zhang S, Wu X, Yu S. Prostaglandin D2 receptor D-type prostanoid receptor 2 mediates eosinophil trafficking into the esophagus. Dis Esophagus. 2014 Aug. 27 (6):601-6. [Medline].

  40. Mavi P, Niranjan R, Dutt P, Zaidi A, Shukla JS, Korfhagen T, et al. Allergen-induced resistin-like molecule-α promotes esophageal epithelial cell hyperplasia in eosinophilic esophagitis. Am J Physiol Gastrointest Liver Physiol. 2014 Sep 1. 307 (5):G499-507. [Medline].

  41. Noel RJ, Rothenberg ME. Eosinophilic esophagitis. Curr Opin Pediatr. Dec 2005. 17(6):690-4. [Medline].

  42. Dellon ES, Kim HP, Sperry SL, Rybnicek DA, Woosley JT, Shaheen NJ. A phenotypic analysis shows that eosinophilic esophagitis is a progressive fibrostenotic disease. Gastrointest Endosc. 2014 Apr. 79 (4):577-85.e4. [Medline].

  43. Chan SK, Mahmoudi M. Eosinophilic esophagitis. Compr Ther. 2009 Fall-Winter. 35(3-4):160-6. [Medline].

Location of fungal and viral infections in ulcers.
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.