Pediatric Esophagitis

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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.

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.

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 affect 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 affect 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.

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/nonsteroidal anti-inflammatory drugs (NSAIDs)

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. ^{[1, 2, 3]}

In contrast to GERD, eosinophilic esophagitis involves the mucosa, the submucosa, and, possibly, the muscularis. Multiple food antigens (eg, milk, eggs, nuts, beef, wheat, fish, shellfish, corn, peanut, soy, chicken) 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. 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. ^{[4, 5, 6]} In addition, activated mast cells may act through prostaglandin D2 (PGD2) to attract eosinophils to the esophagus. ^[7] Animal models have shown a role for interleukin-18 (IL-18) overexpression in the induction of eosinophil active cytokines IL-5, IL-13, and intercellular adhesion molecule (ICAM)/vascular cell adhesion molecule (VCAM). ^[8] Lastly, tissue fibrosis is important in the long-term effects of active eosinophilic esophagitis. Tissue growth factor beta 1 (TGF-β1) is an important cytokine in tissue remodeling and fibrosis in the esophagus of patients with eosinophilic esophagitis. Mouse models suggest a role for resistinlike molecule (Relm)-α in epithelial cell hyperplasia and basal layer thickness in eosinophilic esophagitis. ^{[7, 8, 9, 10]}

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.

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 clinical symptoms of GER (silent GERD). Mild GER is common, with symptoms peaking in infants younger than 6 months. ^{[11, 12]}

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.

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 or button batteries, and overheated food, milk, or formula.

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, long-term proton pump inhibitor (PPI) 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. ^{[13, 14, 15, 16, 17, 18]}

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. ^{[14, 17, 18]}

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 and long-term PPI use. ^{[13, 19, 20]}

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. ^[21]

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.

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. ^[22]

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.

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.

According to more recent studies, the prevalence of eosinophilic esophagitis is 0.5-1 cases per 1000 persons, and the incidence is 10 cases per 10,000 cases per year. A boy-to-girl ratio of 3:1 is observed in eosinophilic esophagitis. ^{[23, 24]}  A retrospective study of 558 children with eosinophilic esophagitis found that 22.8% of children with new diagnoses were younger than 5 years. ^[25]

For patient education information, see eMedicine’s Heartburn/GERD/Reflux Center, Esophagus, Stomach, and Intestine Center, and Yeast and Fungal Infections Center, as well as Reflux Disease (GERD), Heartburn, and Candidiasis (Yeast Infection).

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Gayle H Diamond, MD Assistant Professor of Pediatrics, Perelman School of Medicine, University of Pennsylvania; Attending Physician, Division of Gastroenterology, Hepatology, and Nutrition, The Children’s Hospital of Philadelphia

Disclosure: Nothing to disclose.

Maria Rebello Mascarenhas, MBBS Professor of Pediatrics, Perelman School of Medicine at the University of Pennsylvania; Section Chief of Nutrition, Division of Gastroenterology and Nutrition, Director, Nutrition Support Service, Medical Director, Integrative Health Program, Children’s Hospital of Philadelphia

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

Disclosure: Received research grant from: Kabi Fesinius<br/>Faculty member, DIGEST and member DSMB for: Cystic Fibrosis Foundation.

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, European Society for Paediatric Gastroenterology, Hepatology & Nutrition, North American Society for Pediatric Gastroenterology, Hepatology and Nutrition, North American Society for the Study of Celiac Disease

Disclosure: Nothing to disclose.

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.

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.

Pediatric Esophagitis

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