eMedicine Specialties > Pediatrics: General Medicine > Gastroenterology

Esophagitis

Author: Jessica Wen, MD, Clinical Fellow, Department of Pediatric Gastroenterology, Hepatology and Nutrition, Children's Hospital of Philadelphia
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; Maria Rebello Mascarenhas, MBBS, Associate Professor of Pediatrics, University of Pennsylvania School of Medicine; Section Chief, Division of Gastroenterology and Nutrition, Director, Nutrition Support Service, Children's Hospital of Philadelphia; Vera De Matos, MD, Fellow in Pediatric Gastroenterology, The Children's Hospital of Philadelphia, University of Pennsylvania
Contributor Information and Disclosures

Updated: Mar 5, 2008

Introduction

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. The clinical presentation, diagnostic evaluation, and management principles depend on the etiology; however, in the pediatric population, gastroesophageal reflux disease (GERD), infection, eosinophilic esophagitis, and corrosive ingestions account for most cases.

Pathophysiology

The pathophysiology of esophagitis can be categorized according to the etiology.

• Chemical esophagitis: Chemical esophagitis can result from GER or from the ingestion of corrosive substances such as certain medications or dishwasher cleaner.
• 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 cycle. Although decreased LES tone occurs in infantile GER and 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 lower esophageal sphincter 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.
  • Household and garden materials are alkalis and cause a deep liquefaction necrosis with fat and protein digestion. Acids are less frequently encountered and typically lead to a more superficial coagulation necrosis with eschar formation.
  • Corrosive esophagitis induced by direct contact of the mucosa with a drug is mainly seen in cases that involve abnormal esophageal motility. Drugs implicated include doxycycline, clindamycin, tetracycline, ferrous sulphate, potassium chloride, quinidine, and anti-inflammatory agents. A pill trapped in the esophagus may cause ulceration and esophageal perforation 24-48 hours after ingestion.
• Eosinophilic esophagitis
  • Eosinophilic esophagitis can occur at any age.
  • In infants and young children, eosinophilic esophagitis presents with symptoms similar to those of GERD but fails to respond to conventional acid blockade therapy.
  • Dysphagia and food impaction can occur in older children and adolescents. Eosinophilic esophagitis is often seen in patients with atopy who have asthma, eczema, or chronic rhinitis or in those who have a family history of atopic disease.
  • Endoscopy may reveal a ringed appearance or linear furrows. Standard biopsy findings reveal severe eosinophilic infiltration; more than 15-20 eosinophils per high-magnification microscopic field are necessary for diagnosis.
  • In contrast to GERD, eosinophilic esophagitis involves the mucosa, 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.
  • Eosinophilic esophagitis is currently diagnosed based solely on endoscopy findings. Standardized skin-prick testing and radioallergosorbent testing (RAST) are helpful only in immunoglobulin E (IgE)–mediated disorders, including urticaria and anaphylaxis. These tests and IgE levels or serum eosinophil counts are not useful in the diagnosis of eosinophilic esophagitis, though about two thirds of children with EE have an increased peripheral eosinophilic count.
  • The exact pathophysiology of eosinophilic esophagitis is unknown, but contact of the allergen with the esophageal or intestinal mucosa is thought to be the initiating event. In recent years, animal models of oral and respiratory eosinophil-associated 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.
• Infectious esophagitis
  • This type of esophagitis develops most often in immunocompromised patients. Up to 10% of liver or kidney transplant recipients have herpes simplex virus (HSV) or cytomegalovirus (CMV) esophagitis.
  • HSV, CMV, and Candida species are the most frequent agents that cause esophagitis in immunocompromised patients. Occasionally, varicella-zoster virus causes esophagitis. In acute human immunodeficiency virus (HIV) infection, esophagitis can be seen as well.
• Radiation esophagitis
  • 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 of greater 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.
  • Histologic changes 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.

Frequency

United States

GER is the most common esophageal disorder. 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 (GERD). Histological 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. 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 increased diagnosis is due to recognition and surveillance bias is unknown.

Mortality/Morbidity

All types of esophagitis can be complicated by the development of strictures. GERD can be complicated by Barrett esophagus and, subsequently, by adenocarcinoma, although these 2 conditions are rare in the pediatric population. Enamel and dentine erosions can complicate GERD. Caustic esophagitis can result in perforation and life-threatening mediastinitis. Infectious esophagitis can result in ulcerations, fistula formation, and sepsis. After radiation therapy, strictures can occur within 1-10 years after the initial radiation treatment.

Race

No racial predilection is known.

Sex

A boy-to-girl ratio of 2:1 to 3:1 is observed in eosinophilic esophagitis.

Age

Reflux esophagitis occurs in all age groups. 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. With corrosive esophagitis, unintentional ingestions usually occur in children younger than 5 years, whereas nonaccidental ingestions in adolescents may suggest a suicide attempt.

Clinical

History

• Reflux esophagitis
  • Emesis is typically effortless and is accompanied by frequent regurgitation in infants. However, less commonly, emesis may be forceful and projectile. Hematemesis may also be observed. Hiccoughs that last a long time and hard swallows are subtle signs of gastroesophageal reflux disease (GERD) in infants and young children.
  • Nonspecific signs such as crying, irritability, sleep or feeding problems, arching of the back, and colic may suggest esophageal pain in infants.
  • Infants may also demonstrate head tilting that can mimic torticollis, neck cocking, and opisthotonic posturing with arching of the back (Sandifer syndrome) or other neurobehavioral manifestations.
  • Apnea, chronic respiratory illnesses (pneumonia, wheezing, stridor), and asthma exacerbation may be associated with chronic GERD. Food aversion and failure to thrive or weight loss are frequent manifestations. Anemia due to iron deficiency may result from occult blood loss.
  • Abdominal pain, dysphagia, heartburn, and chest or epigastric pain may occur in older children and adolescents.
• Corrosive esophagitis
  • Coughing, crying, and vomiting following ingestion may be initial symptoms.
  • Dysphagia, refusal to drink, and mouth or chest pain with drooling and salivation may follow. Respiratory distress and stridor can result from airway obstruction and glottic edema.
  • To help determine the potential for morbidity, always try to obtain the original container or exact product name of the caustic substance ingested.
  • Dysphagia and chest pain may occur after ingestion of pill forms of antibiotics or any of the medications mentioned above.
• Eosinophilic esophagitis
  • Consider eosinophilic esophagitis when GERD symptoms, including regurgitation, irritability, food refusal, and failure to thrive in infants, do not respond to aggressive anti-reflux therapy.
  • Dysphagia, food impaction, and chest pain may occur in older children and adolescents.
• Radiation esophagitis
  • Retrosternal chest pain and dysphagia occur.
  • Strictures that present with dysphagia can occur up to 10 years after the treatment.
• Infectious esophagitis
  • Mouth ulcers, thrush, fever blisters, or skin lesions (viral) may be the presenting concerns.
  • Odynodysphagia, refusal to drink, and dysphagia may occur, especially with viral and fungal esophagitis.
  • Fever, dyspnea, or atypical chest pain may also occur.
  • In immunocompetent patients, HSV infection can present with fever, odynodysphagia, and acute-onset retrosternal pain. Oropharyngeal lesions are usually absent. Rarely, HSV, CMV, and HIV can cause an asymptomatic esophagitis.

Physical

• Assess vital signs because a patient may exhibit tachypnea, increased work of breathing, tachycardia, fever, or hypoxia, especially following caustic ingestions.
• Carefully examine the oropharynx for thrush (suggestive of candidal esophagitis), dental enamel and dentine erosions (suggestive of acid gastroesophageal reflux [GER]), burns, erythema, plaques, and ulcerations; however, oral findings may not be present, even with more severe esophageal or gastric burns.
• Examination of the skin may reveal eczema. The respiratory examination may reveal signs of asthma or reactive airway disease.
• In newborns who have esophagitis as a complication of congenital infections, intrauterine growth retardation, lymphadenopathy, hepatitis, organomegaly, and CNS abnormalities can be observed.
• Check stools for heme positivity in any child with possible esophagitis.

Causes

• Reflux or peptic esophagitis
  • 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. 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 lower esophageal sphincter 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.
• Infectious esophagitis: Infectious esophagitis occurs most often in those who are immunocompromised (eg, malignancies, acquired immunodeficiency syndrome [AIDS], long-term steroid or immunosuppressive use, diabetes, congenital immunodeficiencies). It can also occur in immunocompetent patients and is often associated with a preexistent esophageal damage due to chemical or physical causes. Overall, Candida organisms and HSV are the most commonly encountered agents. HSV and CMV are the most common viral pathogens, while varicella-zoster virus and enterovirus are rarely encountered.
  • Viral
    • HSV is the only viral pathogen also commonly found in the immunocompetent host. Usually, no oropharyngeal lesions are present, and the diagnosis can be delayed because of an atypical presentation. In the immunosuppressed patient, vesicular lesions are observed, but, more commonly, ulcers with a characteristic raised yellow border are observed via endoscopy. The mucosa may also appear normal.
    • 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).
    • Papillomavirus infection can develop in neonates born to mothers with the infection.
  • Fungal, protozoal
    • Candida albicans is the most common infective agent in immunocompromised or immunocompetent patients; it can be associated with inhaled steroid therapy. Oral candidiasis is not predictive of esophageal involvement, except in the immunocompromised child. The lesions can be localized or can involve the entire esophagus. In immunocompromised patients, extensive esophagitis may be present without oral candidiasis. The typical finding on endoscopy is a raised, white, adherent lesion with erythematous borders that cannot be washed out or brushed off.
    • Rare pathogens may include Aspergillus species, Torulopsis glabrata, and Cryptosporidium species in patients with AIDS. Megaesophagus may be a late complication of Chagas disease caused by Trypanosoma cruzi.
  • Bacterial
    • 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.
• Corrosive esophagitis: This condition 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. The volume of the product ingested does not necessarily correlate with the degree of tissue injury. Although alkalis and acids are encountered most commonly, detergents; disc batteries; and overheated food, milk, or formula can also cause corrosive esophagitis.
  • Alkalis
    • 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. Alkalis have no taste; thus, a child may ingest a larger amount.
    • The concentrations of base vary from liquid agents (10-25%) to industrial strength (30-35%) to granular agents (50-95%). Crystalline forms may cause linear burns, whereas liquid may lead to circular burns. Lesions vary from mild oral lesions to severe deep liquefaction necrosis that affects all layers of the esophagus.
  • Acids
    • Acid ingestions account for approximately 20% of corrosive ingestions and include hydrochloric, sulfuric, oxalic, and nitric acids. Acids tend to taste bitter, which usually limits the amount ingested.
    • 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.
    • Coagulation necrosis and thick eschar formation are usually limited to the mucosa and superficial muscle layers; perforation is less likely to occur.
• Miscellaneous 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.
  • Radiation- and chemotherapy-induced (doxorubicin) esophagitis and esophagitis secondary to epidermolysis bullosa are very rarely encountered in the pediatric population.
  • Food allergies and eosinophilic esophagitis can cause esophagitis.
  • Systemic diseases such as Crohn disease, chronic granulomatous disease, scleroderma, polyarteritis nodosa, graft-versus-host disease, Behcet and glycogen-storage disease type 1 can cause esophagitis.

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