Epidemiology & Risk Factors

Physiologic GER: Immaturity of the esophageal sphincter mechanism in the first 6 weeks of life. Peak incidence at 4 months; resolves spontaneously by 12–18 months in >90% of infants due to elongation of esophagus and upright posture.
Pathologic GERD: Persistent reflux causing symptoms or complications.
Risk Factors:
- Prematurity.
- Neurological impairment (e.g., Cerebral Palsy).
- Hiatal hernia.
- Congenital esophageal anomalies (e.g., repaired esophageal atresia).
- Chronic lung disease (e.g., Bronchopulmonary Dysplasia).

Clinical Features

Physiologic GER (the “Happy Spitter”):
- Effortless, non-bilious, postprandial spit-up.
- Normal weight gain and development.
- No distress, respiratory symptoms, or feeding difficulties.
Pathologic GERD:
- Failure to thrive (FTT) or poor weight gain.
- Feeding refusal, irritability, and crying during/after feeds.
- Sandifer syndrome: Paroxysmal dystonic posturing (arched back, head turning) during feeds that mimics seizures.
- Respiratory symptoms: Chronic cough, wheezing, hoarseness, recurrent aspiration pneumonia.

Physiologic GER: Clinical diagnosis based on history and PE. No diagnostic testing required.
Pathologic GERD:
- Initial Assessment: Detailed feeding history and growth chart monitoring.
- Key Labs: Usually normal; BMP if severe vomiting to rule out metabolic alkalosis.
- Diagnostic Trial: 2-to-4-week trial of acid suppression (PPI) in older children with typical symptoms.
- Upper GI Series (Barium Swallow): NOT used to diagnose reflux; used to rule out anatomic abnormalities (e.g., malrotation, hiatal hernia, pyloric stenosis).
- Confirmatory/Gold Standard (if atypical or refractory):
  - 24-hour pH/Impedance Probe Monitoring: Quantifies acid/non-acid reflux frequency and correlates with symptoms.
  - Esophagogastroduodenoscopy (EGD) with biopsy: Evaluates for reflux esophagitis, strictures, or Eosinophilic Esophagitis (EoE).

Pyloric Stenosis:
- Diff: Presents at 3–6 weeks of age with progressive, projectile, non-bilious vomiting, hypokalemic hypochloremic metabolic alkalosis, and an “olive-shaped” abdominal mass. Diagnosis confirmed by abdominal US.
Malrotation with Midgut Volvulus:
- Diff: Presents with bilious vomiting and acute abdomen. Diagnosis confirmed by Upper GI series showing “corkscrew” duodenum.
Eosinophilic Esophagitis (EoE):
- Diff: Pt with history of atopy/allergies presenting with dysphagia or feeding refusal. EGD biopsy shows ≥15 eosinophils/HPF and esophageal trachealization (concentric rings).
Cow’s Milk Protein Allergy (CMPA):
- Diff: Presents with vomiting, poor weight gain, and painless hematochezia (blood-streaked stools) or eczema. Diagnosed clinically via maternal dietary elimination (if breastfed) or switching to hydrolyzed formula.

Physiologic GER (“Happy Spitter”):
- First-line: Reassurance and education.
- Conservative measures:
  - Avoid overfeeding (smaller, more frequent feeds). c
  - Keep infant upright for 20–30 minutes post-feed.
  - Thicken feeds with oatmeal cereal (1 tbsp per oz of formula).
Pathologic GERD:
- First-line (Infants):
  - Two-week trial of hypoallergenic formula (extensively hydrolyzed) or maternal dairy elimination to rule out CMPA.
  - If no improvement, initiate medical therapy.
- First-line (Older Children / Refractory Infants):
  - Acid suppression: Proton Pump Inhibitors (PPIs) (e.g., omeprazole) or H2 Receptor Antagonists (H2RAs) (e.g., famotidine) for a 4–8 week trial.
- Refractory/Severe Cases:
  - Surgical intervention: Nissen fundoplication reserved for pts with severe GERD refractory to medical therapy, life-threatening complications (e.g., recurrent apnea, severe aspiration), or severe neurologic impairment.

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