The impact of adenoid hypertrophy on obstructive sleep apnea in children with allergic rhinitis: a retrospective analysis of ventilation function and treatment outcomes

Introduction

Obstructive sleep apnea (OSA) and allergic rhinitis are prevalent pediatric respiratory conditions that can significantly impact children’s health and well-being. OSA is characterized by recurrent upper airway obstruction during sleep, leading to intermittent hypoxia, fragmented sleep, and a spectrum of related symptoms (1,2). Allergic rhinitis, on the other hand, is a common inflammatory condition of the nasal mucosa that manifests as nasal congestion, rhinorrhea, sneezing, and nasal itching and often contributes to impaired quality of life and sleep disturbances in affected children (3,4). Coexisting allergic rhinitis and OSA pose a unique clinical challenge, with upper airway pathology and allergic inflammation potentially synergizing to exacerbate respiratory disturbances and sleep-related symptoms in affected pediatric patients (5,6).

Adenoid hypertrophy, characterized by the enlargement of nasopharyngeal lymphoid tissue, is a well-documented contributor to upper airway obstruction and OSA in children (7,8). Adenoids play a crucial role in the immune response to inhaled antigens, particularly during childhood, and can become hypertrophied in the context of chronic upper airway inflammation, including allergic rhinitis (9-11). The presence of adenoid hypertrophy in children with allergic rhinitis-related OSA may introduce additional complexities in the pathophysiology, clinical presentation, and management of these interconnected respiratory conditions (12,13). However, the specific impact of adenoid hypertrophy on ventilation function, allergic rhinitis symptoms, and treatment outcomes in children with coexisting allergic rhinitis and OSA has not been extensively characterized (13-15).

This retrospective analysis aimed to delineate the impact of adenoid hypertrophy on ventilation function and treatment outcomes in children with allergic rhinitis-related OSA. By retrospectively analyzing clinical data from pediatric patients with confirmed OSA and allergic rhinitis, we sought to elucidate the interplay between adenoid hypertrophy, upper airway function, allergic rhinitis symptoms, and response to intervention. Understanding the multifaceted interactions among these factors is essential for guiding tailored management strategies and improving outcomes in children with coexisting allergic rhinitis and OSA. We present this article in accordance with the STROBE reporting checklist (available at https://tp.amegroups.com/article/view/10.21037/tp-2025-163/rc).

Methods

Research subjects

This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. This study was approved by the Wuming Hospital Affiliated to Guangxi Medical University Institutional Review Board (approval No. Lunshen WM-2025[105]). Informed consent was waived for this retrospective study because of the exclusive use of deidentified patient data, which posed no potential harm or impact on patient care. This waiver was approved by our institutional review board and ethics committee in accordance with regulatory and ethical guidelines pertaining to retrospective research studies.

This study retrospectively analyzed clinical data from patients with allergic rhinitis-related OSA admitted to Wuming Hospital Affiliated to Guangxi Medical University from January 2022 to December 2023; 52 patients without adenoid hypertrophy and 53 patients with adenoid hypertrophy were included. During the study period, 112 consecutive children with allergic rhinitis-related OSA were identified. Seven patients (6.3%) with discordant adenoid assessments were excluded.

Inclusion and exclusion criteria

The inclusion criteria for children were as follows: aged 2–12 years with confirmed allergic rhinitis [diagnosed according to the Allergic Rhinitis and its Impact on Asthma guidelines (16) with typical symptoms, including nasal congestion, rhinorrhea, sneezing, and/or nasal itching, supported by a positive skin prick test or serum-specific IgE], OSA [defined as an obstructive apnea index (OAI) ≥1 event/h or an apnea-hypopnea index (AHI) ≥5 events/h (17)], complete clinical data, no history of adenoidectomy, and symptoms such as nasal congestion, snoring, and mouth breathing.

The exclusion criteria for children were as follows: respiratory difficulties due to pulmonary diseases; concomitant measles, influenza, or infectious mononucleosis; recurrent tonsillitis; herpetic pharyngitis; and primary diseases affecting the liver, kidneys, or hematopoietic system.

Adenoid examination methods

The adenoids of the children were evaluated via nasal endoscopy and lateral X-ray imaging of the nasopharynx. Nasal endoscopy was performed via a 70° nasal endoscope and a television imaging system produced by the American company Stryker, with observation under general anesthesia. The degree of adenoid hypertrophy was classified into four grades on the basis of the extent of nasal obstruction: grade I for <25%, grade II for 25–50%, grade III for >50–75%, and grade IV for >75–100%. Lateral X-ray images of the nasopharynx were obtained during the inspiratory phase via the New Eastern-1000 digital imaging system. Imaging was performed with the child in a standing position, the chin was slightly elevated, and the machine’s focus was adjusted to 110 cm. The tube voltage ranged from 50 to 60 kV with a current of 20 to 25 mAs. The airway-to-nasopharynx (A/N) ratio was measured. Children with nasal endoscopy findings of grade I or II and an A/N ratio ≤0.60 on lateral X-ray imaging were categorized into the no-adenoid hypertrophy group, whereas those with nasal endoscopy findings of grade III or IV and an A/N ratio >0.60 on lateral X-ray imaging were classified into the adenoid hypertrophy group. Children with discordant findings between endoscopy and radiography (e.g., grade I/II endoscopy + A/N ratio >0.60 or grade III/IV endoscopy + A/N ratio ≤0.60) were excluded to ensure group homogeneity. This affected 7 patients (6.7% of initially screened patients), who were not included in the final cohort.

Measurement methods

Polysomnography (PSG)

The sleep graph (SG) monitoring method was employed to assess the sleep parameters of the pediatric patients. The children spent two consecutive nights in the laboratory, with the first night for acclimatization to the environment and the second night for the official recording. The monitoring equipment and recordings were placed in a separate room with the temperature maintained between 18 and 26 ℃, allowing the children to set their own sleep and wake times. Overnight-attended PSG was performed following the American Academy of Sleep Medicine (AASM) guidelines (18). Central apnea was defined as a ≥90% drop in airflow for ≥20 seconds or ≥2 missed breaths (in children) with no respiratory effort throughout the entire event. Sighs/postsigh central hypopneas were not scored as central apnea per AASM Rule III.A.2 (18). The children spent two consecutive nights in the laboratory, with the first night for acclimatization and the second night for official recording. The PSG system (Sleep Fairy-A7, Hunan Wanmai Medical Technology Co., Ltd., Shaoyang, China) recorded oxygen saturation at a 1 Hz sampling frequency (1 sample/second) via finger pulse oximetry. The mean oxygen saturation during sleep was calculated as the average of all valid measurements during the total sleep time (excluding movement artifacts and wake periods). Sleep staging and respiratory event scoring followed the AASM pediatric criteria. The PSG system (Sleep Fairy-A7, Hunan Wanmai Medical Technology Co., Ltd.) was used for the assessment, with 1 cm diameter silver-plated disc electrodes, including four leads: two for electrooculography (EOG) placed 1 cm down (or up) and 1 cm toward the outer canthus of the left eye (or right eye), with a reference electrode placed on the earlobe; one for chin electromyography (EMG) positioned 1.5 cm lateral to the midline; and the remaining lead for electroencephalography (C3-A2). The input signals were amplified and recorded via a multichannel physiological recorder, with a time constant of 0.3 seconds, high-frequency filtering at 30 Hz, a gain of 1, and a calibration voltage of 50 mV. Follow-up PSG for treatment response assessment was performed via identical protocols and equipment.

Nasal cavity index detection

The children underwent nasal acoustic rhinometry in a quiet examination room, with the temperature maintained between 23 and 24 ℃ and the humidity between 69% and 71%. Prior to the examination with a Rhinomanometer (NR6, GM Instruments Ltd., Irvine, UK), the subjects remained seated quietly for 20 minutes in the examination room, and then, while maintaining a seated position, a suitable-sized nasal cavity probe with a sealing adhesive was used for the assessment. The subjects held their breath and emitted a sound wave for 10–12 seconds, which was repeated three times, from which the most stable area-distance curve was selected. After the instillation of a vasoconstrictor (ephedrine) into both nasal cavities, the same procedure was repeated 15 minutes later to complete the nasal acoustic rhinometry examination. The nasal resistance, peak inspiratory nasal flow, nasal inspiratory flow velocity, and nasal expiratory flow velocity indices were obtained by processing the nasal acoustic rhinometry results via computer software.

Satisfaction survey

Nursing satisfaction survey questionnaire scores were collected for all patients before and after the intervention, covering aspects such as nursing methods, nursing techniques, nurse-patient communication, and nursing effectiveness. The total score was 100 points, with scores ≥90 indicating satisfaction, scores between 80 and 89 indicating a moderate level of satisfaction, and scores <80 indicating dissatisfaction. The overall satisfaction rate was calculated as the percentage of satisfied and moderately satisfied cases out of the total number of cases.

Data collection

General information about the children [age, sex, body mass index (BMI), duration of allergic rhinitis, family history of OSA], nasal parameters (nasal resistance, nasal peak inspiratory flow, nasal inspiratory flow velocity, nasal expiratory flow velocity), PSG comparisons (AHI, sleep oxygen saturation, mean sleep efficiency, OAI, central apnea index), allergic rhinitis symptoms (nasal congestion, rhinorrhea, sneezing, itchy nose, and olfactory function), and treatment outcomes (improvement in OSA severity, reduction in allergy symptoms, decrease in medication use, parental satisfaction with treatment) were obtained from the medical records system. Improvement in OSA severity was defined as ≥50% reduction in the AHI from baseline on follow-up PSG performed 3 months posttreatment via protocols identical to those used for the baseline assessment. Symptom severity for nasal congestion, rhinorrhea, and itchy nose was assessed via a 10-cm visual analog scale (VAS), where parents marked intensity (0= no symptoms, 10= worst imaginable symptoms), with measurements recorded in cm from the left anchor. Sneezing frequency was recorded as daily episodes. Olfactory function was evaluated via the Sniffin’ Sticks odor identification test (Burghart Messtechnik, Holm, Germany), with the percentage of correctly identified odors recorded. The duration of allergic rhinitis was calculated from the date of the first physician-diagnosed AR symptoms (documented in medical records) to the date of PSG. A family history of OSA requires formal diagnosis confirmation in first-degree relatives (e.g., PSG reports in medical records or physician-documented OSA diagnosis with treatment history). All the data were collected by the same experienced physician.

Statistical analysis

The data were analyzed via Statistical Package for the Social Sciences (SPSS) 25.0 statistical software (SPSS Inc., Chicago, IL, USA). For categorical data, [n (%)] was used for representation. The Chi-squared test was applied with the basic formula when the sample size was ≥40 and the expected frequency (E) was ≥5, with the test statistic represented by χ². When the sample size was ≥40 but the expected frequency was 1≤ E <5, the Chi-squared test was adjusted via the correction formula. In cases where the sample size was <40 or the expected frequency was E <1, statistical analysis was conducted via Fisher’s exact probability method. For normally distributed continuous data, the format [mean ± standard deviation (SD)] was employed, and between-group comparisons were analyzed via independent t-tests (reported as t values). Nonnormally distributed data were analyzed via the Wilcoxon rank-sum test. P<0.05 was considered statistically significant.

Results

Demographic information

A total of 112 children were initially enrolled. After excluding 7 patients (6.3%) (4 with grade I/II endoscopy but A/N ratio >0.60; 3 with grade III/IV endoscopy but A/N ratio ≤0.60) with discordant adenoid assessments, 105 children (52 without adenoid hypertrophy and 53 with adenoid hypertrophy) were analyzed. No missing data occurred for demographic variables. Within our study cohort, we found no significant differences in age, sex distribution, BMI, duration of allergic rhinitis, or the presence of a family history of OSA between the nonadenoid hypertrophy group and the adenoid hypertrophy group (Table 1). The t tests and P values for these parameters were 0.761 and 0.45 for age, 0.008 and 0.93 for sex, 1.383 and 0.17 for BMI, 0.711 and 0.48 for duration of allergic rhinitis, and 0.555 and 0.46 for family history of OSA, respectively.

Nasal ventilation function parameters

Comparative analysis of nasal ventilation parameters revealed significant differences between the groups (Figure 1). Specifically, nasal resistance was greater in the adenoid hypertrophy group (0.42±0.08 cmH₂O/L/s) than in the nonadenoid hypertrophy group (0.39±0.07 cmH₂O/L/s; P=0.03). Similarly, the nasal expiratory flow velocity was greater in the adenoid hypertrophy group (0.92±0.15 m/s) than in the nonadenoid hypertrophy group (0.85±0.11 m/s; P=0.01). In contrast, no significant differences were observed for nasal peak inspiratory flow (P=0.19) or nasal inspiratory flow velocity (P=0.35). All measurements were complete for 105 patients.

Figure 1 Comparison of nasal ventilation function parameters between the adenoid hypertrophy group and the no-adenoid hypertrophy group. (A) Nasal inspiratory flow velocity (m/s); (B) nasal expiratory flow velocity (m/s); (C) nasal peak inspiratory flow (L/min); (D) nasal resistance (cmH₂O/L/s). Box plots within violin plots show median and interquartile ranges, with individual data points represented as dots.

PSG findings

Compared with the nonadenoid hypertrophy group, the adenoid hypertrophy group presented a significantly greater AHI (5.18±2.16 vs. 4.31±1.54 events/h; P=0.02) and lower mean oxygen saturation during sleep (93.25%±2.33% vs. 94.81%±1.78%; P<0.001) (Table 2). Both the OAI (P<0.001) and central apnea index (P<0.001) were significantly elevated in the adenoid hypertrophy group. PSG data were available for all 105 patients.

Allergic rhinitis symptoms

Significant differences in nasal congestion (3.21±0.53 vs. 2.98±0.47 cm; P=0.02) and rhinorrhea (2.78±0.62 vs. 2.45±0.56 cm; P=0.006) were detected between the adenoid hypertrophy and nonadenoid hypertrophy groups (Table 3). No significant differences were found in sneezing frequency (P=0.13), itchy nose sensation (P=0.33), or olfactory function (P=0.21). All symptom assessments were completed for all participants.

Treatment outcomes

Improvements in OSA severity (80.77% vs. 56.60%; P=0.01) and parental satisfaction (84.62% vs. 58.49%; P=0.006) were significantly greater in the nonadenoid hypertrophy group (Table 4). A nonsignificant trend favored allergy symptom reduction in the nonadenoid hypertrophy group (69.23% vs. 50.94%; P=0.09), whereas there was no intergroup difference in medication use reduction (P=0.50). All outcome data were fully documented.

Discussion

In this retrospective analysis, we investigated the impact of adenoid hypertrophy on OSA in children with allergic rhinitis. The findings shed light on the interplay between adenoid hypertrophy, ventilation function, allergic rhinitis symptoms, and treatment outcomes.

The assessment of nasal ventilation function parameters revealed significant differences between the no-adenoid hypertrophy group and the adenoid hypertrophy group. Nasal resistance and nasal expiratory flow velocity were significantly greater in the adenoid hypertrophy group than in the control group. These findings suggest that adenoid hypertrophy contributes to increased upper airway resistance and altered airflow dynamics during respiration. This finding aligns with previous studies highlighting the mechanical obstruction caused by adenoid hypertrophy, which can lead to nasal congestion, mouth breathing, and altered respiratory patterns, thus predisposing children to OSA (19,20). Adenoid hypertrophy leads to mechanical obstruction of the nasopharyngeal airway, which can significantly compromise ventilation function in affected children (21). Enlarged adenoids can physically obstruct the airway, leading to increased nasal resistance and altered airflow dynamics during respiration (22). This mechanical obstruction can contribute to nasal congestion, snoring, and mouth breathing, which are common symptoms observed in children with adenoid hypertrophy-related OSA (12,23,24). Additionally, increased nasal resistance and altered airflow patterns can disrupt normal ventilation function, leading to impaired nasal inspiratory and expiratory flow velocities, as demonstrated in the study findings. The impact of adenoid hypertrophy on ventilation function underscores the importance of addressing upper airway obstruction in the evaluation and management of pediatric OSA in the context of allergic rhinitis.

The PSG findings in this study demonstrated a significant effect of adenoid hypertrophy on OSA severity in children with allergic rhinitis. Compared with the nonadenoid hypertrophy group, the adenoid hypertrophy group presented a greater AHI, lower oxygen saturation during sleep, and greater obstructive and central apnea indices. These findings are consistent with the literature, which suggests that adenoid hypertrophy contributes to the pathophysiology of pediatric OSA by causing upper airway obstruction and subsequent respiratory disturbances during sleep (25). The substantial impact of adenoid hypertrophy on OSA severity highlights the need for comprehensive assessment and management of upper airway anatomy in children with allergic rhinitis and OSA (26,27).

Furthermore, our analysis revealed a significant association between adenoid hypertrophy and specific allergic rhinitis symptoms. Compared with those without adenoid hypertrophy, children with adenoid hypertrophy presented greater nasal congestion and rhinorrhea. While the mechanisms underlying this association warrant further investigation, it is plausible that the mechanical obstruction caused by adenoid hypertrophy contributes to nasal obstruction and exacerbates allergic rhinitis symptoms in affected children. Adenoid hypertrophy has been associated with alterations in local inflammatory pathways, which may contribute to the exacerbation of allergic rhinitis symptoms in affected children (28-30). The enlarged adenoids can serve as reservoirs for inflammatory cells and mediators, leading to chronic inflammation within the nasopharyngeal mucosa (31,32). This persistent inflammation can exacerbate nasal congestion, rhinorrhea, and other allergic rhinitis symptoms, thereby amplifying the impact of allergic rhinitis on upper airway patency and ventilation (33). The presence of adenoid hypertrophy may thus amplify the effects of allergic rhinitis, leading to a more pronounced clinical presentation of nasal congestion and rhinorrhea, as observed in the present study. The latent inflammatory pathways underlying the association between adenoid hypertrophy and allergic rhinitis symptoms highlight the complex interaction between upper airway pathology and allergic manifestations in pediatric patients.

The treatment outcomes of this study demonstrated the impact of adenoid hypertrophy on the response to intervention in children with allergic rhinitis and OSA. Compared with the adenoid hypertrophy group, the nonadenoid hypertrophy group presented greater rates of improvement in OSA severity and parental satisfaction with treatment. While there was a trend toward a reduction in allergy symptoms in the nonadenoid hypertrophy group, the difference did not reach statistical significance. These findings underscore the need for individualized treatment approaches that consider the presence of adenoid hypertrophy in pediatric patients with allergic rhinitis and OSA. Addressing adenoid hypertrophy as part of a comprehensive management plan can potentially improve treatment outcomes and parental satisfaction.

The clinical implications of our findings extend to the evaluation and management of pediatric patients with coexisting allergic rhinitis and OSA. This study highlights the multifactorial nature of OSA in the context of allergic rhinitis, emphasizing the role of upper airway pathology in contributing to OSA severity, ventilation function, and treatment response. These findings underscore the importance of comprehensive clinical assessment encompassing nasal ventilation function testing, adenoid evaluation, and PSG in children with allergic rhinitis and suspected OSA. By identifying and addressing factors such as adenoid hypertrophy, healthcare providers can optimize treatment strategies and improve outcomes for pediatric patients with coexisting allergic rhinitis and OSA.

The research implications of this study include the need for further investigations to elucidate the mechanisms underlying the associations among adenoid hypertrophy, allergic rhinitis, and OSA in pediatric patients. Prospective studies incorporating longitudinal assessments of ventilation function, allergy symptoms, and treatment outcomes can provide valuable insights into the dynamic interactions among these factors over time. Additionally, studies focusing on the impact of adenoidectomy and its timing on OSA severity and allergic rhinitis outcomes could contribute to the development of evidence-based guidelines for the management of pediatric patients with coexisting upper airway pathology and allergic rhinitis-related OSA.

Limitations of this retrospective analysis should be considered when interpreting the findings. The study design inherently limits causal inference and the establishment of temporal relationships between adenoid hypertrophy, allergic rhinitis symptoms, and OSA severity. Additionally, the retrospective nature of the study introduces potential selection bias and limited control over confounding variables. Prospective studies incorporating comprehensive assessments and longer follow-up periods are warranted to further elucidate the relationships identified in this analysis. Furthermore, we excluded 7 patients (6.3% of initially enrolled patients) due to discordant adenoid assessments to ensure diagnostic consistency. While this approach enhances internal validity, it may limit generalizability. All analyzed variables had complete data with no missing values.

Conclusions

In conclusion, this retrospective analysis provides valuable insights into the impact of adenoid hypertrophy on ventilation function, allergic rhinitis symptoms, and treatment outcomes in children with allergic rhinitis-related OSA. These findings underscore the multifaceted nature of OSA in the context of allergic rhinitis, emphasizing the need for comprehensive clinical assessment and individualized management strategies. Addressing adenoid hypertrophy as part of the management plan for pediatric patients with coexisting allergic rhinitis and OSA can potentially improve outcomes and increase patient satisfaction. Future research endeavors to elucidate the underlying mechanisms and optimize treatment approaches for this patient population are warranted to advance the fields of pediatric sleep medicine and otolaryngology.

Acknowledgments

The authors are grateful to all participants in the present study.

Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://tp.amegroups.com/article/view/10.21037/tp-2025-163/rc

Data Sharing Statement: Available at https://tp.amegroups.com/article/view/10.21037/tp-2025-163/dss

Peer Review File: Available at https://tp.amegroups.com/article/view/10.21037/tp-2025-163/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://tp.amegroups.com/article/view/10.21037/tp-2025-163/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. This study was approved by the Wuming Hospital Affiliated to Guangxi Medical University Institutional Review Board (approval No. Lunshen WM-2025[105]). Informed consent was waived for this retrospective study because of the exclusive use of deidentified patient data, which posed no potential harm or impact on patient care. This waiver was approved by our institutional review board and ethics committee in accordance with regulatory and ethical guidelines pertaining to retrospective research studies.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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