**Background:** Gastroesophageal reflux (GER) — the involuntary passage of gastric contents into the esophagus — is very common in children and often physiological. In contrast, gastroesophageal reflux disease (GERD) is a less common pathologic process causing troublesome symptoms that affect daily functioning or lead to clinical complications. The review aims to provide up-to-date information on the pathogenesis, diagnostic evaluation, and management of GERD in children.
**Methods:** This is a narrative review. The authors synthesize evidence from published literature, including guidelines from ESPGHAN and NASPGHAN, systematic reviews, prospective studies, and clinical trials. No formal systematic search strategy or meta-analytic methods are described.
**Key Results:** The pooled prevalence of GERD symptoms from four cross-sectional studies was 26.9% (95% CI 20.1–33.7, I²: 6.83). In infants, prevalence decreases with age: from 25.5% at 1 month and 26.5% at 6 weeks to 7.7% at 3 months, 2.6–2.9% at 6 months, and 1.1–1.6% at 12 months. Prevalence in Asia (8.7%) is comparable to the US (8.9%) and Europe (8.3%–32.0%). High-risk groups include children with corrected esophageal atresia (GERD prevalence up to 47.1% by impedance-pH and 64.7% by histopathology), neurological impairment, prematurity, and cow’s milk protein allergy. The main pathogenesis is abnormal transient lower esophageal sphincter relaxation (TLESR), with contributing factors including anatomical defects (hiatal hernia, immature antireflux barrier in infants), impaired esophageal and gastric motility, and compromised esophageal mucosal defense. Diagnostic tools include ultrasound (sensitivity 76%–100%, specificity 50%–100% compared to pH studies), endoscopy with histopathology, pH-monitoring, combined multichannel intraluminal impedance-pH (MII-pH) monitoring, esophageal manometry, and electrogastrography. No single gold standard exists. Management includes non-pharmacological measures (head and body positioning, dietary modification with extensively hydrolyzed formula or amino acid formulas, thickened formula), pharmacological treatments (proton pump inhibitors, prokinetics such as domperidone, metoclopramide, erythromycin, and baclofen, alginate antacids, esophageal mucosal protectants including sucralfate and Esoxx™, and probiotics), and surgical options (transpyloric feeding, fundoplication, transoral incisionless fundoplication) for severe cases.
**Clinical Implications:** Clinicians must differentiate GERD from physiological GER and from mimics such as eosinophilic esophagitis, cow’s milk protein allergy, and anatomical abnormalities. A therapeutic trial of PPI for up to 8 weeks may be considered in older children with typical symptoms, but investigations are warranted if there is no response or if alarm features are present. The updated Cow's Milk Symptom Score (CoMiSS), with a threshold of >10 (previously >12), may help evaluate infants for cow's milk protein allergy. Management should target the underlying aetiopathogenesis. PPIs remain the gold standard for acid suppression but may not be effective for non-acid reflux and carry risks of respiratory and gastrointestinal infections with prolonged use. Probiotics, particularly Lactobacillus reuteri DSM 17938, have shown efficacy in reducing regurgitation but strong evidence for GERD is lacking. Surgery is reserved for severe, treatment-refractory cases, with transpyloric feeding emerging as a viable alternative to fundoplication even in high-risk patients.