Eosinophilic oesophagitis versus paediatric GERD in practice

Distinguishing eosinophilic oesophagitis (EoE) from gastro-oesophageal reflux disease remains one of the more frequent diagnostic puzzles in paediatric gastroenterology. Both conditions cause vomiting, feeding aversion, and heartburn-like discomfort, yet their underlying biology and the treatments that follow diverge sharply. A child labelled with reflux who actually has EoE will often cycle through acid-suppressing medications without meaningful improvement, while the underlying T-helper-2 driven inflammation continues to remodel the oesophageal wall.

In Australia, where food allergy and atopic disease sit among the highest documented rates worldwide, the index of suspicion for EoE tends to be higher than in many other regions. Frontline clinicians in general practice, paediatrics, and emergency departments are usually the first to weigh the two diagnoses against each other.

When reflux symptoms are not what they seem

GERD reflects a mechanical and chemical problem: a relaxed lower oesophageal sphincter allows gastric contents to reflux upwards, irritating the squamous mucosa. The resulting inflammation is typically modest and non-specific. Acid suppression, feed thickeners, and positional measures address the upstream cause.

EoE is a chronic immune-mediated disorder. Food and aero-allergens trigger a Th2-dominant response, with eosinophils, mast cells, and basophils infiltrating the oesophageal epithelium. Cytokines such as IL-5 and IL-13 sustain the inflammation, leading over time to tissue remodelling, fibrosis, and strictures. The two conditions can coexist, and a subset of children with EoE shows a partial response to proton pump inhibitors (so-called PPI-responsive oesophageal eosinophilia), which historically blurred the boundary between them.

Listening to the child: clues from history

A careful feeding and symptom history often raises suspicion before any scope is booked. Children with EoE commonly describe dysphagia, food impaction, and learned adaptations such as slow eating, excessive chewing, or drinking large volumes of fluid to wash food down. They may avoid textured foods, refuse meat or bread, or present with growth faltering. A personal or family history of atopy, including eczema, asthma, allergic rhinitis, or IgE-mediated food allergy, strengthens the case considerably.

Children with uncomplicated reflux more often present with regurgitation, effortless vomiting in infancy, and irritability after feeds. They respond to upright positioning and smaller, more frequent feeds. Odynophagia and food bolus obstruction are red flags that should steer thinking away from isolated reflux and toward endoscopic assessment.

Red flags that warrant prompt endoscopy

• Dysphagia or a sensation of food sticking
• Food bolus obstruction requiring emergency care
• Failure to thrive or dropping across growth centiles
• Persistent vomiting despite an adequate PPI trial

What endoscopy and biopsies reveal

Upper endoscopy is the decisive step. The Endoscopic Reference Score captures the visible features of EoE: oedema with loss of vascular pattern, fixed or transient concentric rings (the so-called trachealisation of the oesophagus), white exudates, linear furrows, and strictures. Many children, however, have a macroscopically normal oesophagus, which makes biopsies essential.

Histologically, EoE is defined by 15 or more eosinophils per high-power field in at least one biopsy, after exclusion of other causes. Reflux may also show scattered eosinophils, but counts usually remain below five per high-power field, and the inflammation is accompanied by typical reflux changes such as basal cell hyperplasia and elongation of the rete pegs. Sampling from both proximal and distal oesophagus improves diagnostic yield.

Putting the picture together

The contrast between the two conditions can be summarised before moving to therapy. The table below draws on current consensus guidelines and reflects the patterns seen in Australian paediatric cohorts.

PPI-responsive eosinophilia blurs these categories, and clinicians should remain alert to the possibility that a child initially labelled with reflux may have an evolving eosinophilic phenotype requiring biopsy confirmation.

Australian realities for paediatric care

Specialist endoscopy is concentrated in tertiary children's hospitals such as the Royal Children's Hospital Melbourne, the Children's Hospital at Westmead in Sydney, Perth Children's Hospital, and the Queensland Children's Hospital in Brisbane. Waiting lists can be long, and paediatric gastroenterology remains one of the more constrained subspecialties in the public system. General paediatricians often begin empirical PPI trials and basic allergy workup before referral, which is reasonable when endoscopy is delayed.

The Australasian Society of Clinical Immunology and Allergy (ASCIA) provides widely used guidelines on allergy-focused history taking and elimination diets, which integrate smoothly with EoE management. Children with suspected food triggers are usually referred to a paediatric allergist for skin-prick testing or specific IgE measurement, followed by supervised empiric elimination of the most common culprits.

Practical considerations for Australian families

• Long travel distances to a tertiary centre are common; MBS-funded telehealth follow-up has become a routine part of paediatric subspecialty care since the COVID-19 era.
• The Royal Flying Doctor Service occasionally retrieves children from very remote locations for urgent endoscopy after a food bolus obstruction.
• The Pharmaceutical Benefits Scheme subsidises most PPIs and several swallowed steroid formulations used off-label for EoE; biologic therapies such as dupilumab are PBS-listed for specific paediatric indications.
• Dietitians with paediatric allergy experience help families maintain adequate nutrition across diverse food cultures and during elimination trials.

Therapy, monitoring, and shared care

A positive response to therapy is itself a diagnostic clue. Children with true reflux settle quickly on acid suppression, while children with EoE may show partial improvement on PPIs but usually relapse unless anti-inflammatory treatment is added: swallowed fluticasone or budesonide, an elimination diet, or both. Repeat endoscopy at 8 to 12 weeks confirms histological remission, and emerging tools such as the oesophageal string test and the EoE Histology Scoring System are starting to refine follow-up.

Long-term, untreated EoE leads to strictures and persistent food impaction, with knock-on effects for nutrition, school attendance, and quality of life. A shared-care arrangement between the family, GP, paediatrician, and tertiary centre tends to produce the best outcomes and keeps travel and costs to a minimum.

The next concrete step for any clinician managing a child with refractory reflux symptoms is to book an upper endoscopy with multiple oesophageal biopsies rather than escalating acid suppression indefinitely. Six biopsies taken from proximal and distal oesophagus will usually resolve the diagnostic question and direct the family toward the correct treatment pathway.