Pediatric Esophagitis 

  • Author: Jayant Deodhar, MD; Chief Editor: Carmen Cuffari, MD   more...
 
Updated: Mar 29, 2011
 

Background

Esophagitis (inflammation of the squamous esophageal epithelium) may result from various causes, including acid and nonacid gastroesophageal reflux (GER), food allergies, dysmotility due to various causes, infections, trauma, and iatrogenic causes. In the pediatric population, gastroesophageal reflux disease (GERD), infection, eosinophilic esophagitis, and corrosive ingestions account for most cases. (See Pathophysiology and Etiology.)

The clinical presentation depends on the etiology. Bleeding or upper airway obstruction with hemodynamic compromise and perforation of the esophagus or stomach are the most significant immediate complications. Over the long term, all types of esophagitis can be complicated by the development of strictures. (See Clinical Presentation.)

In infants, GER may be difficult to differentiate from colic. Treatment often includes therapy for excessive gas or changing of formulas, especially because parents may note pain and crying, pulling up of legs, and abdominal distention. (See Diagnosis.)

Few laboratory studies are helpful for the diagnosis of esophagitis. Esophagogastroduodenoscopy (EGD) is performed to allow more definitive visualization of the esophageal mucosa. Biopsy samples are always obtained to look for histologic confirmation. An upper gastrointestinal (GI) study should be considered in all patients with persistent emesis and in whom esophagitis is suspected. (See Workup.)

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. (See Treatment and Management, as well as Medication.)

Go to Esophagitis for more complete information on this topic.

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Pathophysiology

The pathophysiology of esophagitis can be categorized according to the etiologic type. These types include chemical esophagitis (ie, esophagitis resulting from gastroesophageal reflux [GER] or from the ingestion of corrosive substances such as certain medications or caustic cleaning products), eosinophilic esophagitis, infectious esophagitis, and radiation esophagitis.

Reflux (peptic) esophagitis

Distal esophageal inflammation results when gastric and duodenal fluids, including gastric acid, pepsin, trypsin, and bile, are regurgitated into the esophagus. A decrease in the lower esophageal sphincter (LES) tone and altered motility increase esophageal clearance time and cause GER. Esophageal inflammation can further induce both mechanisms, creating a vicious circle.

Although decreased LES tone occurs in infantile GER and gastroesophageal reflux disease (GERD) and in dysmotility disorders, the single factor currently regarded as the most important in the pathogenesis of GERD is the repeated occurrence of inappropriate transient LES relaxations (TLESRs). Factors that increase esophageal clearance time include posture-gravity interactions, size and content of a meal, abnormal gastric emptying, and abnormal esophageal peristalsis.

Mild, early changes may include irritation of the esophageal mucosa with basal cell hyperplasia and thickening of the papillae. This progresses along a spectrum of severity that can lead to infiltration of inflammatory cells, ulcerations, scarring, and fibrosis with stenosis. Cellular metaplasia to columnar epithelium, known as Barrett esophagus, can also occur. Barrett esophagus is rare in the pediatric population; within the pediatric population, this condition is more frequent in adolescents than in younger children.

Corrosive (caustic) esophagitis

Depending on the type, concentration, and volume of the ingested substance, varying degrees of chemical burns that involve different layers of the esophagus may occur. Superficial mucosal injury (first degree), transmural mucosal injury with possible muscularis involvement (second degree), or full-thickness injury (third degree) can result. The condition can extend into periesophageal or perigastric tissues, resulting in perforation, peritonitis, or mediastinitis. The volume of the substance ingested does not necessarily correlate with the degree of tissue injury.

Household and garden materials are alkalis. Crystalline forms of these agents may cause linear burns, whereas liquid forms may lead to circular burns. Lesions vary from mild oral lesions to severe deep liquefaction necrosis with fat and protein digestion that affects all layers of the esophagus.

Acids are less frequently encountered and typically lead to a more superficial coagulation necrosis with eschar formation, which is usually limited to the mucosa and superficial muscle layers. Perforation is less likely to occur.

A pill trapped in the esophagus may cause ulceration and esophageal perforation 24-48 hours after ingestion (so-called pill esophagitis). Corrosive esophagitis induced by direct contact of the mucosa with a medication is seen mainly in patients who have abnormal esophageal motility. Drugs implicated include the following:

  • Doxycycline
  • Clindamycin
  • Tetracycline
  • Ferrous sulphate
  • Potassium chloride
  • Quinidine
  • Anti-inflammatory agents

Eosinophilic esophagitis

The exact pathophysiology of eosinophilic esophagitis is unknown. However, contact of the allergen with the esophageal or intestinal mucosa is thought to be the initiating event.

In contrast to GERD, eosinophilic esophagitis involves the mucosa, the submucosa, and, possibly, the muscularis. Multiple food antigens (eg, eggs, nuts, beef, wheat, fish, shellfish, corn, soy) can induce eosinophilic esophagitis; cow’s-milk protein is the most common precipitant.

In recent years, animal models of oral and respiratory eosinophil-associated gastrointestinal (GI) disorders have been developed. In these models, oral antigens induced the recruitment of eosinophils to the GI tract, including the esophagus and Peyer patches, and promoted GI inflammation and motility dysfunction. Interleukin-5 (IL-5), interleukin-13 (IL-13), and eotaxin-1, a chemokine specific to eosinophils, play a major role in eosinophil recruitment and T-cell proliferation and polarization in the tissues.[1, 2, 3]

Radiation esophagitis

The histologic changes characteristic of radiation esophagitis start within 2 weeks of the radiation dose and consist of epithelial damage, sloughing, and necrosis, which can extend to the deeper layers. Resolution and healing occur within 3-4 weeks of the last radiation dose.

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Etiology

Gastroesophageal reflux

GER is the most common cause of esophagitis among infants and children. Although a significant proportion of infants have symptoms of GER, only a minority develop GERD and esophagitis. Conversely, infants can have peptic esophagitis without GER (silent GERD). Mild GER is common, with symptoms peaking in infants younger than 6 months.[4, 5]

Spontaneous resolution occurs by age 1 year in 70-80% of patients and by age 2 years in 80-90% of patients. A small minority of patients continues to experience reflux symptoms, with a variable time to resolution. The resolution in infants correlates with solid food intake, slowing caloric intake, growth, upright positioning, and increased truncal tone.

Systemic disorders that cause delayed gastric emptying and poor esophageal motility can induce GER and esophagitis. These disorders include cystic fibrosis, severe combined immunodeficiency, cerebral palsy, increased intracranial pressure, and celiac disease. Esophagitis can be a manifestation of Crohn disease, scleroderma, glycogen-storage disease type 1b, and chronic granulomatous disease. Neurologic impairment, medications, and certain diseases, including those that cause musculoskeletal abnormalities, may exacerbate GER.

Factors that decrease the tone of the LES include a diet rich in fat, caffeine, chocolate, and alcohol. Increased intra-abdominal pressure in obesity and pregnancy, hormonal changes during pregnancy, and smoking also promote acid GER.

Exposure to corrosive substances

Corrosive (caustic) esophagitis may follow the ingestion of various household cleaning products. Of such ingestions, 95% occur inside in the home, usually in the kitchen or bathroom. Nearly 73% occur while a product is in use, and 24% occur while a product is in storage. Almost 50% of ingested products were transferred out of their original containers.

Alkalis account for approximately 70% of corrosive ingestions; lye (sodium hydroxide) ingestions are the most common. Potassium hydroxide and ammonium hydroxide are also observed. Drain pipe cleaners, oven cleaners, powdered laundry detergents, and dishwasher detergents all include an alkali. The concentrations of base vary from liquid agents (10-25%) to industrial-strength agents (30-35%) to granular agents (50-95%). Alkalis have no taste; thus, a child may ingest a larger amount.

Acid ingestions account for approximately 20% of corrosive ingestions and include hydrochloric, sulfuric, oxalic, and nitric acids. Toilet bowl cleaners, drain cleaners, and rust and stain removers are some of the products that contain acids, ranging in concentration from 8-65%. Liquid chlorine bleaches contain a less concentrated hydrochloric acid. Acids tend to taste bitter, which usually limits the amount a child will ingest.

Although alkalis and acids are encountered most commonly, corrosive esophagitis can also be caused by detergents, disc batteries, and overheated food, milk, or formula.

Infection

Infectious esophagitis occurs most often in those who are immunocompromised (eg, as a result of malignancies, acquired immunodeficiency syndrome [AIDS], long-term steroid or immunosuppressive use, diabetes, congenital immunodeficiencies). However, it can also occur in immunocompetent patients, especially those with preexisting esophageal damage due to chemical or physical causes.

Infectious esophagitis may be viral, fungal, protozoal, or bacterial. Overall, Candida organisms and herpes simplex virus (HSV) are the most commonly encountered agents.[6, 7, 8, 9, 10, 11]

HSV and cytomegalovirus (CMV) are the most common viral pathogens, while varicella-zoster virus and enterovirus are rarely encountered. HSV is the only viral pathogen also commonly found in the immunocompetent host.[7, 10, 11]

CMV is observed more commonly in patients with AIDS and in recipients of bone marrow or solid organ transplants. Esophagitis and enterocolitis are the most common CMV GI infections. Consider CMV in the newborn with physical findings consistent with congenital infection and symptoms of esophagitis (a rare complication). Go to Cytomegalovirus Esophagitis for more complete information on this topic.

Papillomavirus infection can develop in neonates born to mothers with the infection.

Candida albicans is the most common infective agent in immunocompromised or immunocompetent patients; it can be associated with inhaled steroid therapy.[6]

Rare pathogens may include Aspergillus species, Candida glabrata, and Cryptosporidium species in patients with AIDS. Megaesophagus may be a late complication of Chagas disease caused by Trypanosoma cruzi.

Various gram-negative bacilli and gram-positive cocci may be pathogens. This is usually secondary to an extension from a retroesophageal, retropharyngeal, or paravertebral abscess; spinal osteomyelitis; pleuritis; mediastinal lymphadenitis; pericarditis; or diphtheria. Iatrogenic trauma and perforation from procedures may contribute. Pill adherence to the esophagus may result in an ulcer and secondary bacterial infection.

Helicobacter pylori, usually found in gastric mucosa, has been observed in the metaplastic changes with Barrett epithelium of the esophagus.

Radiation

Radiation esophagitis is not a common occurrence, because the esophagus is relatively resistant to radiation injury compared with the rest of the GI tract. However, radiation doses higher than 30 Gy may result in retrosternal burning, dysphagia, and esophagitis. Doses of 50 Gy cause severe esophagitis, and doses of 60 Gy cause esophageal strictures, fistulas, or both.

Other causes

Traumatic esophagitis can occur after nasogastric tube placement or after esophageal or gastric suctioning. This was found to be the first cause of esophagitis in newborns who had undergone vigorous nasopharyngeal aspiration.

Ingestion of foreign bodies such as zinc-containing coins, toys, sharp objects, and disc batteries can cause pressure sores or chemical lesions.

Food allergies and eosinophilic esophagitis can cause esophagitis.[12]

Systemic diseases such as Crohn disease, chronic granulomatous disease, scleroderma, polyarteritis nodosa, graft versus host disease, Behçet disease, and glycogen-storage disease type 1 can cause esophagitis.

Chemotherapy-induced (doxorubicin) esophagitis and esophagitis secondary to epidermolysis bullosa are very rarely encountered in the pediatric population.

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Epidemiology

Gastroesophageal reflux is the most common esophageal disorder. In infancy, the typical onset is during the second month of life, with a peak in the fourth month. However, some studies report the occurrence of GERD and peptic esophagitis throughout childhood.

Approximately 50% of infants aged 2-3 months and 67% of infants aged 4 months have daily regurgitations (thus, GER but not GERD). Approximately 8% of infants have an abnormal quantity of acid GER on pH probe findings that results in signs or symptoms (ie, GERD). Histologic esophagitis can be observed in 61-83% of infants with clinically significant esophagitis.

Corrosive ingestions (ie, alkalis, acids, bleaches) account for 3-5% of reported accidental ingestions, or approximately 5,000-10,000 cases per year in the United States. Corrosive esophagitis from unintentional ingestions usually occur in children younger than 5 years, whereas nonaccidental ingestions in adolescents may suggest a suicide attempt.

The exact incidence of eosinophilic esophagitis is unknown, although the prevalence appears to be increasing in recent years in both the pediatric and adult population. Whether the apparent increase in prevalence is due to recognition and surveillance bias is unknown. A boy-to-girl ratio of 2-3:1 is observed in eosinophilic esophagitis.

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Patient Education

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Contributor Information and Disclosures
Author

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.

Coauthor(s)

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.

Maria Rebello Mascarenhas, MBBS  Associate Professor of Pediatrics, University of Pennsylvania School of Medicine; Section Chief 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, and North American Society for Pediatric Gastroenterology and Nutrition

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.

Specialty Editor Board

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Pharmacy Editor, eMedicine

Disclosure: Nothing to disclose.

Stefano Guandalini, MD  Director, University of Chicago Celiac Disease Program, Section Chief of Gastroenterology, Hepatology and Nutrition; Professor, Department of Pediatrics, University of Chicago Comer Children's Hospital

Stefano Guandalini, MD is a member of the following medical societies: American Gastroenterological Association, European Society for Paediatric Gastroenterology, Hepatology & Nutrition, and North American Society for Pediatric Gastroenterology 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, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

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

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

  10. 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.

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

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

  15. 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].

  16. 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].

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

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

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