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.