Sarcouncil Journal of Medical Series

Abstract: Background: Adenoid hypertrophy is often involved in the pathophysiology of chronic rhinosinusitis (CRS) in children, but its exact role in disease severity, microbiology, and treatment is not fully described. This paper set out to assess the importance of adenoid hypertrophy measured by the adenoid-nasopharynx ratio (ANR) in clinical presentation and management of CRS in children. Methods: A prospective cohort study design was used to study 102 pediatric patients (aged 314 years) diagnosed with CRS based on EPOS 2020 criteria. The participants were thoroughly assessed with nasal endoscopy, low-dose paranasal sinus CT, middle meatus microbiological samples, and validated quality-of-life scales (SNOT-20, PedsQL). Eadenoid hypertrophy (ANR ≥0.70; n=67) and non-hypertrophy (ANR <0.70; n=35) were used to stratify patients. They all were given 12 weeks of maximum medical treatment; those who were refractory in the hypertrophy group were given an adenoidectomy. Clinical success at 12 weeks was the primary outcome; secondary outcomes were changes in symptom scores, recurrence rates, and predictors of treatment failure. Results: The adenoid hypertrophy group was significantly younger (7.2 vs. 9.1 years; p<0.001), had longer symptom duration, higher Lund-Mackay CT scores (14.1±4.8 vs. 9.2±4.6; p<0.001), and worse baseline SNOT-20 scores (46.7±11.4 vs. 33.9±11.6; p<0.001). The hypertrophy group had a greater prevalence of biofilm formation (56.7% vs. 25.7; p=0.003). The success rate of medical therapy alone was 32.0% in hypertrophy and 62.9 in non-hypertrophy (p<0.001). Adenoidectomy in the cases of refractory hypertrophy showed an 83.3% success rate with significant changes in SNOT-20 (mean of 28.5±9.1 points) and PedsQL. A multivariate analysis revealed that both adenoid hypertrophy (adjusted OR 2.87, 95% CI 1.21682; p=0.017) and biofilm presence (adjusted OR 3.24, 95% CI 1.38761; p=0.007) were independent predictors of treatment failure. Conclusion: Adenoid hypertrophy is a major, disease-independent disease contributor with stronger disease severity and refractoriness to therapy in pediatric CRS.