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Pediatric Esophagitis Workup

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

Approach Considerations

In the patient who is immunocompromised (eg, secondary to cancer, immunodeficiencies, immunomodulating medications), esophagitis may have multiple etiologies. Clinically, noninfectious and infectious causes may be difficult to distinguish. Consequently, antireflux, antifungal, antiviral, and antibiotic therapies are often instituted. Although fungal and viral causes are usually considered first, chemotherapy, radiation therapy, emesis, acid reflux, and bacterial colonization may be contributors to mucosal injury.

In certain cases, esophagogastroduodenoscopy (EGD) with biopsy may assist in the management of infectious esophagitis. The absolute neutrophil count (ANC) or presence of oropharyngeal colonization does not necessarily predict the cause of the esophagitis.

Endoscopy is the only study used in the diagnosis of eosinophilic esophagitis. Standardized skin-prick testing and radioallergosorbent testing (RAST) are helpful only in immunoglobulin E (IgE)–mediated disorders, including urticaria and anaphylaxis. These tests, patch tests, and IgE levels or serum eosinophil counts are less useful in the diagnosis of eosinophilic esophagitis, though about two thirds of children with eosinophilic esophagitis have an increased peripheral eosinophilic count.

Infiltration of eosinophils in the esophageal epithelium is not pathognomonic for allergic esophagitis, as eosinophilic infiltration is also observed in reflux esophagitis. The severity of the eosinophilic infiltration, the presence of other signs and symptoms suggestive of an allergic etiology (eg, eczema), and the lack of response to aggressive antireflux therapy assist in making the correct diagnosis.

Go to Imaging in Infectious Esophagitis for more complete information on this topic.

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Blood Studies

Few laboratory studies are helpful for the diagnosis of esophagitis. A complete blood count may reveal anemia (usually iron deficiency with blood loss) or a nonspecific leukocytosis. A peripheral eosinophilia may be observed in patients with eosinophilic esophagitis. Enzyme-linked immunosorbent assays (ELISAs), acute/convalescent titers, and polymerase chain reaction (PCR) for viral etiologies may be of benefit, although often not in the acute management. Serum albumin levels may be decreased in patients with corrosive esophagitis or cytomegalovirus (CMV) infection.

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Esophagogastroduodenoscopy

EGD allows more definitive visualization of the esophageal mucosa. Biopsy samples at different levels of the esophagus should always obtained to look for histologic confirmation; in fact, the lower esophageal tract is well known as an area in which discrepancies between endoscopic and histologic findings are often found. If needed, brushings and cultures can be obtained. Therapeutic procedures such as dilatation of esophageal strictures can also be performed.

Characteristics of corrosive esophagitis

Following a corrosive ingestion, endoscopy should usually be performed within 24-48 hours in all patients. This helps to determine the degree of mucosal burns and ulcerations and the risk of complications of the esophagus, stomach, and duodenum (including possible perforation). Circumferential ulcers and mucosal sloughing indicate greater severity.

Late-forming ulcers and fibrin deposits may not be observed if endoscopy is performed in the first 12 hours. A string can be placed through the endoscope into the esophagus and can be left in place to help with subsequent dilatations by the surgeons.

Characteristics of infectious esophagitis

With infectious esophagitis in immunocompromised patients, EGD with biopsy may be a valuable tool. Biopsy is the most sensitive and accurate method in diagnosing fungal esophagitis. With Candida esophagitis, the typical finding on endoscopy is a raised, white, adherent lesion with erythematous borders that cannot be washed out or brushed off. The lesions can be localized or can involve the entire esophagus.

In the immunosuppressed patient with herpes esophagitis, ulcers with a characteristic raised yellow border may be observed. The mucosa may also appear normal.

Fungal and viral infections in ulcers tend to occur in particular locations (see the image below).

Location of fungal and viral infections in ulcers. Location of fungal and viral infections in ulcers.

Characteristics of eosinophilic esophagitis

In eosinophilic esophagitis, various patterns of morphological alterations may be seen on endoscopy, including furrowing of the mucosa, presence of white plaques, and mucosal rings. Typically, the gastric mucosa and duodenal mucosa are normal in appearance. Standard biopsy findings reveal severe eosinophilic infiltration; more than 15-20 eosinophils per high-magnification microscopic field are necessary for diagnosis.

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Barium Studies

An upper gastrointestinal (GI) study should be considered in all patients with persistent emesis and in whom esophagitis is suspected. An upper GI study is helpful in defining any anatomic abnormalities such as esophageal strictures, gastric outlet obstruction, pyloric stenosis, or intestinal malrotation. Esophageal motility abnormalities can be revealed with this examination. Additionally, a barium swallow test can be performed to demonstrate swallowing abnormalities. These studies are not helpful in diagnosing gastroesophageal reflux (GER).

In older compliant children, a double-contrast upper GI study may be performed and may be more sensitive. Mucosal irregularities, ulcers, nodules, plaques, and cobblestoning may be observed. Following a caustic ingestion, mucosal edema, dilatation, atony, or strictures are visualized.

An upper GI study may produce normal results even with underlying pathology. In addition, lack of patient cooperation can lead to the performance of a suboptimal study.

Go to Imaging in Infectious Esophagitis for more complete information on this topic.

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Chest Radiography

An increased retrotracheal space may appear on lateral chest radiography with paraesophageal infections or abscesses. Chest radiography may reveal evidence of aspiration pneumonia following a corrosive ingestion.

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Computed Tomography

Computed tomography (CT) may be useful for visualizing paraesophageal abscesses that may extend into the esophagus. CT scanning is also useful in evaluating perforations.

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Esophageal pH Probe Monitoring

Esophageal pH probe monitoring can be used to document the severity of acid GER on the day of the study. However, the presence of reflux does not necessarily indicate that esophagitis is present.[27]

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Intraluminal Impedance Monitoring

Findings from this intraluminal impedance monitoring document nonacid GER that would otherwise be missed with esophageal pH probe monitoring.

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Gastroesophageal Scintigraphy

Gastroesophageal scintigraphy (milk scan) can be useful in revealing the gastric-emptying rate and GER that leads to pulmonary aspiration but is not specific for esophagitis.

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Esophageal Manometry

Esophageal manometry study can help clarify a differential diagnosis. It is not usually performed in the evaluation of esophagitis, however.

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Histologic Findings

Reflux esophagitis

The following 3 types of histologic changes occur in reflux esophagitis:

  • Intraepithelial infiltration of inflammatory cells (small number of eosinophils, lymphocytes and neutrophils, and squiggle cells)
  • Epithelial alterations (basal cell hyperplasia, basal cell spongiosis, abnormal nuclei and increased mitosis, balloon cells)
  • Changes in the lamina propria (elongation and increased number of papillae and vascular dilatation of papillae)

Metaplasia of squamous epithelium to columnar epithelium or Barrett esophagus can occur. This pathology is rare in the pediatric population compared with adult populations.

Corrosive esophagitis

Biopsy in corrosive esophagitis may reveal polymorphonuclear cell infiltration, vessel thrombosis, bacterial invasion, and granulation tissue following second- and third-degree burns. Fibrous tissue, collagen deposition, and stricture formation may occur after 2 weeks.

Infectious esophagitis

In candidal esophagitis, erythema, friability, and adherent white plaques that cover the mucosa are seen macroscopically. The plaques are composed of acute inflammatory exudate mixed with necrotic debris, pseudohyphae, and budding yeast. Because Candida species can often be found in the esophagus without clinical significance, diagnosis of candidal esophagitis depends on the presence of squamous epithelium with invading hyphal forms. Invasive candidiasis can produce transmural inflammation, necrosis, and possible perforation.[13]

In herpes simplex virus (HSV) esophagitis, shallow ulcers are the typical lesions. An acute, nonspecific inflammatory exudate covers the ulcer. Biopsy samples collected from around the ulcer may reveal a viral cytopathic effect in the squamous epithelium (nuclei with clear appearance and condensed chromatin at the periphery) or aggregates of macrophages around herpetic ulcers.

In CMV esophagitis, the viral cytopathic effect is seen in the stromal elements, endothelium, and submucosal glandular epithelium rather than in the squamous epithelium. Therefore, biopsy samples taken from the base of the ulcer can be more informative than those taken from around the ulcer.

Allergic or eosinophilic esophagitis

Histologic changes in allergic or eosinophilic esophagitis are similar to those seen in reflux esophagitis, but the eosinophilia is more severe, with 20 or more eosinophils per high-magnification microscopic field. In some cases, small microabscesses of eosinophils are present, and the inflammatory lesions can extend into the muscular layer of the esophagus.

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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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Location of fungal and viral infections in ulcers.
 
 
 
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