Overview
Definition:
Eosinophilic gastroenteritis (EG) is a rare, heterogeneous group of disorders characterized by eosinophilic infiltration of the gastrointestinal tract in the absence of other identifiable causes of eosinophilia
It can affect any part of the GI tract from the esophagus to the rectum, with varying clinical presentations and degrees of mural involvement.
Epidemiology:
EG is considered a manifestation of a systemic allergic disorder, often associated with other atopic conditions like asthma, eczema, and allergic rhinitis
Prevalence data is scarce but it is believed to be increasing, particularly in developed countries
It can occur at any age but is more commonly diagnosed in children and young adults
The exact incidence is unknown due to diagnostic challenges and underreporting.
Clinical Significance:
Prompt diagnosis and appropriate management of EG are crucial to prevent long-term complications such as growth failure, strictures, obstruction, and malnutrition
It is a significant cause of chronic abdominal pain, vomiting, and diarrhea in children, often mimicking other common gastrointestinal disorders, making differential diagnosis challenging
Understanding its pathogenesis and treatment is vital for pediatric residents preparing for DNB and NEET SS examinations.
Clinical Presentation
Symptoms:
Presentation varies based on the layer of the GI tract involved and the extent of eosinophilic infiltration
Common symptoms include: Abdominal pain, often colicky and crampy
Nausea and vomiting, which can be severe
Diarrhea, which may be watery or bloody
Failure to thrive or weight loss in infants and children
Early satiety and anorexia
Symptoms may be intermittent or chronic
In some cases, intestinal obstruction or intussusception can occur.
Signs:
Physical examination findings are often non-specific and can include: Abdominal distension
Tenderness on palpation
Signs of dehydration
Poor growth parameters (short stature, low weight)
Palpable abdominal mass in cases of intussusception or thickened bowel loops
Peripheral eosinophilia may be present but is not always observed.
Diagnostic Criteria:
Diagnosis of EG relies on a combination of clinical suspicion, exclusion of other causes of eosinophilia, and characteristic histopathological findings
The core diagnostic criteria include: 1
Clinical symptoms suggestive of GI disease
2
Eosinophilic infiltration of the GI tract (usually >15-20 eosinophils per high-power field in biopsies)
3
Exclusion of other causes of eosinophilic infiltration (e.g., parasitic infections, drug reactions, other systemic diseases)
Specific criteria for subtypes (mucosal, muscularis, serosal) exist but are often not strictly applied in routine practice.
Diagnostic Approach
History Taking:
A detailed history is paramount, focusing on: Onset, duration, and character of gastrointestinal symptoms
Associated symptoms (fever, rash, wheezing)
History of atopy (eczema, asthma, allergic rhinitis) in the patient and family
Dietary history, including introduction of new foods and potential food triggers
History of recent infections or travel
Use of medications known to cause eosinophilia or GI symptoms
Red flags include: persistent vomiting, significant weight loss, abdominal pain suggestive of obstruction, and family history of allergic diseases.
Physical Examination:
A thorough physical examination should include: Assessment of growth parameters (height, weight, BMI)
Detailed abdominal examination to detect distension, masses, tenderness, or organomegaly
Examination for signs of atopy (eczema, urticaria) and respiratory distress (wheezing)
Assessment for signs of dehydration.
Investigations:
Laboratory investigations may include: Complete blood count (CBC) to assess for peripheral eosinophilia (often >5% or absolute count >500/ยตL), though normal counts can be seen
Serum IgE levels (may be elevated)
Stool examination for ova and parasites to rule out parasitic infections
Allergy testing (skin prick tests or specific IgE antibodies) for suspected food allergens
Endoscopy with biopsies is the gold standard for diagnosis: Upper endoscopy for esophageal, gastric, and duodenal biopsies
Colonoscopy with biopsies for colonic and terminal ileal involvement
Biopsies should be examined for the degree and location of eosinophilic infiltration
Imaging may include abdominal ultrasound (to detect intussusception or thickened bowel walls) or contrast studies.
Differential Diagnosis:
Differential diagnosis for EG is broad and includes: Food protein-induced enterocolitis syndrome (FPIES) - typically presents acutely after ingestion of a specific food
Allergic eosinophilic esophagitis (EoE) - primarily affects the esophagus
Inflammatory bowel disease (IBD) - Crohn's disease and ulcerative colitis
Celiac disease
Infectious enteritis
Malabsorption syndromes
Irritable bowel syndrome
Gastrointestinal malignancies (rare in children).
Management
Initial Management:
Management focuses on symptom relief and reducing eosinophilic inflammation
For severe presentations like obstruction or dehydration, initial management may involve: Hospitalization
Fluid and electrolyte correction
Nasogastric decompression if obstruction is suspected
Discontinuation of suspect offending foods if identified.
Medical Management:
The cornerstone of medical management is dietary intervention and pharmacotherapy
Dietary therapy: Elimination diets are highly effective, especially in children
A stepwise approach is often used: 1
Elemental diet (using amino acid-based formula) is the most effective but least palatable
2
Amino acid-based formula or hydrolyzed casein/whey formulas
3
Six-food elimination diet (SFED): excludes milk, egg, soy, wheat, peanuts, and fish
Reintroduction of foods is done systematically to identify triggers
Pharmacotherapy: Topical or systemic corticosteroids are used to reduce eosinophilic inflammation
Oral corticosteroids (e.g., prednisone) are typically used for more severe disease, with doses tapered as symptoms improve
Topical steroids (e.g., swallowed fluticasone propionate for esophageal involvement) may be an option for milder disease
Other agents like montelukast, cromolyn sodium, or biologics (e.g., anti-IL-5 antibodies) are used in refractory cases but are less common in routine pediatric practice.
Surgical Management:
Surgery is reserved for complications of EG and is not a primary treatment
Indications include: Intestinal obstruction or intussusception
Stricture formation
Perforation
Abscess formation
Surgical procedures may involve adhesiolysis, bowel resection and anastomosis, or stricturoplasty.
Supportive Care:
Supportive care is essential and includes: Nutritional support to ensure adequate growth and prevent malnutrition, especially if strict dietary restrictions are required
Monitoring of growth parameters
Close follow-up to assess treatment response and monitor for complications.
Complications
Early Complications:
Acute complications can include: Intestinal obstruction due to luminal narrowing from eosinophilic infiltration or edema
Intussusception, particularly ileo-ileal or ileocolic
Dehydration and electrolyte imbalances
Severe abdominal pain and vomiting.
Late Complications:
Long-term complications may arise if EG is not effectively managed: Chronic malnutrition and failure to thrive
Bowel strictures leading to recurrent obstruction
Malabsorption
Growth retardation
In rare cases, perforation or fistula formation.
Prevention Strategies:
Prevention strategies focus on early recognition and prompt, effective management: Strict adherence to elimination diets and timely reintroduction of foods
Judicious use of corticosteroids, aiming for the lowest effective dose
Regular monitoring of growth and nutritional status
Patient and family education on recognizing symptoms of relapse or complications.
Prognosis
Factors Affecting Prognosis:
Prognosis is generally good with appropriate management, especially in children
Factors influencing prognosis include: Extent and depth of eosinophilic infiltration
Presence of complications like strictures or obstruction
Response to dietary therapy and corticosteroids
Co-existing atopic conditions.
Outcomes:
Most children respond well to dietary elimination and/or corticosteroid therapy, leading to symptom resolution and normalization of GI histology
Many achieve remission, although some may experience relapses
Long-term outcomes are usually favorable, with catch-up growth possible in those who experienced initial growth failure
Patients with severe disease or complications may have a less favorable prognosis.
Follow Up:
Regular follow-up is crucial for patients with EG
This involves: Monitoring for symptom recurrence or relapse
Serial assessment of growth parameters
Periodic re-evaluation of dietary triggers and adherence
Assessment for development of complications
Endoscopic surveillance may be considered in select cases, especially those with severe disease or strictures.
Key Points
Exam Focus:
EG is a rare GI disorder of eosinophilic infiltration
Diagnosis requires biopsy showing eosinophils (>15-20/HPF) and exclusion of other causes
Dietary elimination (elemental or SFED) is the mainstay of treatment
Corticosteroids are used for severe/refractory cases
Complications include obstruction, strictures, and failure to thrive
Remember to exclude parasitic infections
Differential diagnosis is broad, including FPIES, EoE, and IBD.
Clinical Pearls:
Consider EG in children with chronic, unexplained abdominal pain, vomiting, or diarrhea, especially those with atopic history
Peripheral eosinophilia is common but not universal
Always biopsy multiple segments of the GI tract when suspecting EG
Dietary therapy is often successful and can minimize the need for long-term steroids
Careful reintroduction of foods is key to long-term management.
Common Mistakes:
Mistaking EG for common gastroenteritis or functional abdominal pain without adequate investigation
Failing to biopsy all affected segments of the GI tract
Overreliance on peripheral eosinophilia for diagnosis or exclusion
Inadequate dietary history or poorly executed elimination diets
Delaying corticosteroid therapy in severe cases or not tapering appropriately.