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Pediatric Esophagitis Clinical Presentation

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

History

Reflux (peptic) esophagitis

Typically, emesis is effortless and is accompanied by frequent regurgitation in infants. Less commonly, however, 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 (caustic) esophagitis

Coughing, crying, and vomiting following ingestion may be initial symptoms of corrosive esophagitis. 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. Do not be falsely reassured by the quantity of the ingestion. Significant burns have followed minimal exposures, such as licking the bottle cap of a container that holds an alkali and eating from an unwashed spoon that had been used to measure liquid lye.

Dysphagia and chest pain may occur after ingestion of pill forms of antibiotics (eg, doxycycline, clindamycin, tetracycline) or medications including ferrous sulphate, potassium chloride, quinidine, and anti-inflammatory agents.

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, herpes simplex virus (HSV) infection can present as fever, odynodysphagia, and acute-onset retrosternal pain. Oropharyngeal lesions are usually absent. Rarely, HSV, cytomegalovirus (CMV), and HIV can cause an asymptomatic esophagitis.

Eosinophilic esophagitis

Eosinophilic esophagitis can occur at any age. In infants and young children, eosinophilic esophagitis presents with symptoms similar to those of GERD (including regurgitation, irritability, food refusal, and failure to thrive in infants) but fails to respond to aggressive antireflux therapy. Dysphagia, food impaction, and chest pain may 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.[25]

Radiation esophagitis

Retrosternal chest pain and dysphagia occur. Strictures that present as dysphagia can occur up to 10 years after the treatment.

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Physical Examination

Assess vital signs. Patients 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. Oral candidiasis is not predictive of esophageal involvement, except in the immunocompromised child. Nevertheless, extensive esophagitis may be present without oral candidiasis in immunocompromised patients.[13]

Immunosuppressed patients with infectious esophagitis caused by herpes simplex (HSV) typically have vesicular lesions in the oropharynx. However, immunocompetent patients with esophagitis from HSV—the only viral pathogen that commonly causes esophagitis in immunocompetent hosts—usually have no oropharyngeal lesions.

Oral findings may also be absent in corrosive esophagitis, even in patients with more severe esophageal or gastric burns. In one study of patients with a history of caustic ingestion, almost 50% of patients with no oral lesions had esophageal burns, whereas only slightly more than 50% of patients with oral lesions also had esophageal lesions.

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 central nervous system abnormalities can be observed.

Check stools for heme positivity in any child with possible esophagitis.

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Complications of Esophagitis

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. After radiation therapy, strictures can occur within 1-10 years after the initial treatment.

Apnea, chronic respiratory illnesses (including asthma), and failure to thrive are not rare complications of reflux esophagitis. 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.

The long-term complications of corrosive esophagitis include perforation, secondary bacterial infections (aspiration pneumonia, peritonitis, mediastinitis, sepsis), altered motility, and obstruction with stricture formation.

Complications of infectious esophagitis include abnormal motility, obstruction, ulceration, perforation, fistula formation, secondary bacterial infections, and hemorrhage.

Long-term complications of eosinophilic esophagitis include progressive fibrostenotic disease. This can in turn lead to food impactions and may necessitate the need for endoscopic dilatation, which puts patients at risk for perforation and mediastinitis.[24, 26]

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Contributor Information and Disclosures
Author

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

Disclosure: Nothing to disclose.

Coauthor(s)

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.

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.

Acknowledgements

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.

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