Abstract
Study Objectives:
(1) To assess adenotonsillectomy (AT) outcomes in adolescents with obesity and with obstructive sleep apnea (OSA); (2) To identify clinical factors predicting OSA in adolescents following AT.
Methods:
Adolescents 12 to 18 years old with obesity who underwent AT for OSA were included. Subjects had pre-AT and post-AT polysomnogram. Nonobese adolescents with OSA that underwent AT were included as a comparison.
Results:
Seventy adolescents with obesity with a mean age of 14.2 years and a mean body mass index of 38.0 kg/m2 were included. Patients in the nonobese group (n = 32) were similar demographically to the obese group, with the exception of body mass index. The majority of adolescents with obesity (74%) had severe OSA (apnea-hypopnea index [AHI] ≥ 10 events/h) with a mean baseline AHI of 33.9 events/h (standard deviation 28.5). The obese and control groups experienced clinically meaningful improvements in AHI following AT, with median change scores of 18.3 (95% confidence interval −29.2, −11.2, P < .001) and 14.6 (95% confidence interval −25.5, −8.5, P < .001), respectively. In the adolescents with obesity, 48% had an AHI < 5 events/h on postoperative PSG. However, adolescents with obesity were 7 times more likely (odds ratio = 7.1, 95% confidence interval [2.24, 22.48], P = .001) to have moderate or severe persistent OSA (AHI > 5 events/h) after AT compared with patients who were not obese. The need for post-AT positive airway pressure therapy was significantly higher in adolescents with obesity, with 37.1% of participants requiring this therapy (odds ratio = 8.3, 95% confidence interval 1.8, 37.6, P < .001).
Conclusions:
AT results in improvement in polysomnogram parameters in adolescents with obesity and OSA. However, patients with obesity are at high risk for persistent OSA. Future research should include prospective trials to compare outcomes between AT and positive airway pressure therapy for adolescents with obesity.
Citation:
Kearney TC, Vazifedan T, Baldassari CM. Adenotonsillectomy outcomes in obese adolescents with obstructive sleep apnea. J Clin Sleep Med. 2022;18(12):2855–2860.
Keywords: adenotonsillectomy, obesity, adolescent, obstructive sleep apnea
BRIEF SUMMARY
Current Knowledge/Study Rationale: The current gold standard treatment for obstructive sleep apnea in the pediatric population is adenotonsillectomy. In adults, it is continuous positive airway pressure. Little data exists exploring the surgical outcomes of the adolescent population.
Study Impact: This study will help establish an evidence-based treatment protocol for adolescents with obstructive sleep apnea.
INTRODUCTION
Obstructive sleep apnea (OSA) is a sleep-related breathing disorder characterized by intermittent episodes of upper airway collapse during sleep. In the pediatric population, adenotonsillar hyperplasia is one of the most common causes of upper airway obstruction.1 Obesity, which has been rising among young patients, is another risk factor for OSA. The obesity rate among children and adolescents in the United States has increased dramatically in the last few decades; over 20% of young people now meet the clinical criteria for obesity.2 Compared to children of normal weight, those with obesity have a 5-fold increase in the likelihood of developing OSA.3 The pathophysiology of OSA in young people with obesity is still being investigated; it is postulated that pharyngeal narrowing due to adipose tissue plays a role in addition to external compression of airway by subcutaneous neck fat.2,3
The gold standard for diagnosis of OSA is full-night polysomnogram (PSG). OSA has been linked to metabolic changes and cardiovascular sequelae.1,3 Furthermore, there is a growing body of literature demonstrating the negative impact of OSA on quality of life (QOL) and cognitive function in children.4 OSA has been associated with behavior problems, poor attention, memory and cognitive deficits, and poor school performance. Thus, this disease can have a significant impact on the health and wellbeing of affected children and adolescents.
The primary treatment for OSA in children is adenotonsillectomy (AT). AT has been shown to improve PSG parameters, QOL, and behavior in children of normal weight. Recent studies have shown that while children with obesity do experience improvement in AHI with surgery, they are at increased risk for persistent sleep apnea following AT. In adults with obesity, the primary treatment for OSA is continuous positive airway pressure (PAP) therapy. Controversy exists regarding the optimal treatment for adolescents with obesity and OSA. Little data have been published regarding surgical outcomes in this group of patients. While PAP therapy is effective in treating OSA in adolescents with obesity, these patients often struggle with compliance. Further research is needed to assess the efficacy of AT in the treatment of adolescents with obesity and to establish evidence-based treatment protocols for this group of patients. Thus, our primary objective was to examine changes in PSG parameters, including the apnea-hypopnea index (AHI) and nadir oxygen saturation, in adolescents with obesity undergoing AT for OSA. We hypothesized that OSA severity would improve following surgery, but many patients would have persistent disease. We also sought to compare AT outcomes between adolescents with obesity and those without and to determine whether there were any factors that predicated persistent obstruction following AT.
METHODS
Approval from the Eastern Virginia Medical School Institutional Review Board was obtained. A retrospective chart review was conducted at the Children’s Hospital of The King’s Daughters, a tertiary, free-standing children’s hospital in Norfolk, Virginia over a 10-year period (2009 to 2019). Current Procedural Terminology codes were utilized to identify children who underwent AT (42821 and 42826) and PSG (95810 and 95811). Patients were eligible for inclusion if they were between 12 and 18 years of age at the time they underwent AT for the indication of OSA (AHI > 1 events/h). All adolescents included in the study had an overnight PSG pre-AT and post-AT to assess OSA severity. Children who had undergone previous tonsil or adenoid surgery and those with a history of significant medical comorbidities such as neuromuscular disorders or Down syndrome were excluded. Subjects were excluded if they underwent additional procedures as the time of AT such as pharyngoplasty or turbinate reduction.
PSGs were performed in accredited pediatric sleep laboratories at our institution in accordance with the American Academy of Sleep Medicine guidelines. Similarly, pediatric sleep medicine specialists scored and interpreted all PSGs according to the American Academy of Sleep Medicine guidelines. Standard PSG recordings included oronasal airflow, respiratory effort (chest and abdomen), oxygen saturation and end-tidal carbon dioxide levels, submental electromyography, electrocardiography, electroencephalography, extremity muscle activity, and body position. The obstructive AHI was calculated as the number of obstructive and mixed apneas and hypopneas divided by the total sleep time; central apneas were excluded from this calculated value. Baseline OSA severity was categorized according to AHI as mild (AHI ≥ 1 events/h and < 5 events/h), moderate (AHI ≥ 5 events/h and < 10 events/h), or severe (AHI ≥ 10 events/h) based on the most commonly used pediatric OSA classification.5 Classifying OSA severity in adolescents remains controversial as dedicated classification and scoring systems for this population are lacking. At our institution, pediatric sleep medicine specialists score studies utilizing pediatric criteria for patients 18 years of age and younger. Post-AT PSGs are recommended for all adolescents with continued obstructive symptoms following AT and for those that have severe baseline OSA (regardless of postsurgical symptomatology). Post-AT PSGs are typically performed 3 to 6 months following surgery. Adolescents that had PSGs greater than 6 months following AT were excluded.
Body mass index (BMI) and BMI percentiles were calculated according to the Centers for Disease Control and Prevention guidelines.6 Obesity was defined as a BMI percentile ≥ 95%. All healthy adolescents with a BMI < 95% who underwent AT for OSA during the study period and had both presurgical and postsurgical PSG were included in our analysis as a “control group.” Like our study group, patients were excluded from the control group if they had any significant comorbidities, such as neuromuscular disease or Down syndrome. As this was a retrospective study, we did not match adolescents with obesity and those without by clinical factors such as race and age. Electrocautery was used to for tonsillectomy, while adenoidectomies were performed using a combination of electrocautery and microdebrider.
Demographic information, such as age and race, and PSG parameters, such as AHI and nadir oxygen saturation, were documented for both adolescents with obesity and those without. Tonsil size was graded based on the system developed by Brodsky.7 When available, pre-AT and post-AT OSA-18 QOL scores were recorded. The OSA-18 is a validated, disease-specific QOL survey that is widely utilized to assess the impact of OSA on children and adolescent’s health and wellbeing.8 Need for additional intervention for OSA following AT for both adolescents with obesity and those without was recorded. At our institution, adolescents with an AHI greater than 5 events/h and less than 10 events/h on post-AT PSG are considered to have moderate persistent OSA and are typically treated with observation, medication, or positive airway pressure (PAP) therapy; those with an AHI 10 are offered continuous PAP for their severe disease. Adolescents with an AHI less than 5 events/h are considered to have disease resolution and no further intervention is prescribed.
Continuous variables were described as mean, standard deviation median, and interquartile range. Categorical variables were described as proportions. Two-sided t-test and Mann–Whitney U test were used to analyze the differences in continuous variables between control and obese groups. Chi-square test and Fisher’s exact test were used to analyze the association between categorical variables and control/obese group. Multiple logistic regression model was conducted to test the adjusted effect of control and obese groups, along with adjusted effect of other related risk factors, on categorical outcomes. Adjusted odds ratio and 95% confidence intervals were computed using logistic regression model. All statistical analyses were performed using SPSS (Chicago, IL). Statistical tests were 2 sided, and P < .05 was considered statistically significant.
RESULTS
Ninety-eight adolescents with obesity and OSA underwent an AT during the study period. Twenty-eight patients were excluded due to the following: (1) lack of postoperative PSG (n = 10); (2) additional airway surgical procedures performed at time of AT such as pharyngoplasty (n = 12); or (3) the presence of significant medical comorbidities (n = 5). Thus, data from 70 obese patients was included in the analysis. Thirty-two adolescents who were not obese and who underwent AT for OSA were included for comparison. Table 1 depicts the baseline demographic data of patients with and without obesity. The mean age of all adolescents was 14.5 years (standard deviation 2.1). Twenty-seven of the patients with obesity (38.6%) had morbid obesity, defined as a BMI percentage greater than the 99th. The majority of patients (n = 44, 62.9%) in the obese group were Black. The obese and nonobese groups were similar in terms of age (P = .51), race (P = .07), sex (P = .20), and tonsil size (P = .12).
Table 1.
Baseline patient demographic data.
| Obese (n = 70) | Nonobese (n = 32) | P | |
|---|---|---|---|
| Age (years), mean ± SD | 14.5 ± 1.9 | 14.2 ± 2.4 | .51 |
| Female | 32 (45.7%) | 19 (59.4%) | .20 |
| BMI mean ± SD | 38.0 ± 7.2 | 21.9 ± 3.6 | |
| BMI percentile median [IQR] | 99.0 [99.0, 99.8] | 75.0 [44.7, 89.0] | |
| Race | |||
| Caucasian | 23 (32.9%) | 18 (56.3%) | .07 |
| African American | 44 (62.9%) | 13 (40.6%) | |
| Hispanic/Latino | 2 (2.9%) | 0 (0.0%) | |
| Asian | 1 (1.4%) | 1 (3.1%) | |
| BMI Category | |||
| < 95% | 0 | 32 (100%) | |
| 95–99% | 43 (61.4%) | 0 | |
| > 99% | 27 (38.6%) | 0 | |
| Tonsil Size | |||
| 1 | 2 (3.3%) | 4 (13.8%) | .12 |
| 2 | 8 (13.3%) | 7 (24.1%) | |
| 3 | 27 (45.0%) | 11 (37.9%) | |
| 4 | 23 (38.3%1) | 7 (24.1%) |
BMI = body mass index, IQR = interquartile range, SD = standard deviation.
The mean baseline AHI of the adolescents was 31.8 events/h (standard deviation 28.4). The majority (n = 75, 75.0%) of adolescents with and without obesity had severe baseline OSA with an AHI greater than 10. Table 2 depicts the baseline and post-AT PSG parameters for both groups. Prior to AT, the AHI was similar (P = .16) between patients with and without obesity. There were also no differences between the groups in terms of arousal index (P = .49) and peak CO2 levels (P = .92). The nadir oxygen saturation was significantly lower (P = .001) in patients with obesity compared to those without at baseline.
Table 2.
Pre-AT and Post-AT PSG Parameters for obese and normal weight adolescents.
| Non-Obese Adolescents (BMI < 95%) | Obese Adolescents (BMI ≥ 95%) | Total Group (All Adolescents) | P | ||
|---|---|---|---|---|---|
| AHI (pre-AT) | Mean (SD) | 26.8 (28.0) | 33.9 (28.5) | 31.8 (28.4) | .16 |
| Median [IQR] | 18.4 [10.2, 29.8] | 27.5 [9.2, 51.1] | 23.9 [9.7, 46.1] | ||
| AHI (post-AT) | Mean (SD) | 2.5 (2.8) | 9.9 (16.3) | 7.6 (14.1) | < .001 |
| Median [IQR] | 1.8 [0.5, 3.6] | 5.3 [1.8, 10.8] | 3.5 [1.3, 8.8] | ||
| Nadir O2 (pre-AT) | Mean (SD) | 87.4 (7.9) | 84.4 (7.0) | 85.3 (7.4) | .001 |
| Median [IQR] | 89.5 [87.0, 91.0] | 86.0 [82.0, 89.0] | 87.0 [83.0, 90.0] | ||
| Nadir O2 (post-AT) | Mean (SD) | 92.3 (4.8) | 89.1 (5.4) | 90.1 (5.4) | .001 |
| Median [IQR] | 92.5 [91.0, 95.0] | 89.0 [86.0, 93.0] | 91.0 [87.0, 94.0] | ||
| Arousal index (pre-AT) | Mean (SD) | 27.0 (23.6) | 28.3 (19.0) | 27.9 (20.3) | .49 |
| Median [IQR] | 18.2 [14.0, 33.0] | 24.1 [12.0, 34.0] | 22.0 [13.5, 34.0] | ||
| Arousal index (post-AT) | Mean (SD) | 9.8 (5.5) | 14.2 (9.6) | 12.8 (8.8) | .011 |
| Median [IQR] | 9.0 [6.3, 11.0] | 11.5 [8.5, 16.8] | 10.7 [8.0, 15.0] | ||
| Peak CO2 (pre-AT) | Mean (SD) | 48.9 (8.8) | 50.5 (14.0) | 50.0 (12.7) | .92 |
| Median [IQR] | 49.0 [43.0, 52.0] | 47.0 [44.0, 51.0] | 47.0 [43.0, 52.0] | ||
| Peak CO2 (post-AT) | Mean (SD) | 54.4 (20.5) | 51.3 (15.4) | 52.2 (17.1) | .70 |
| Median [IQR] | 47.0 [40.0, 50.0] | 47.0 [42.5, 52.0] | 47.0 [42.0, 52.0] | ||
AHI = apnea-hypopnea index, AT = adenotonsillectomy, P < .05 = significant; P values are comparing obese and nonobese groups.
Following AT, both the obese and control groups experienced significant improvements in PSG parameters (Table 2). Patients with obesity experienced a clinically meaningful improvement in AHI following AT with a median change score of 25 events/h (95% confidence interval −31.2, −18.8, P < .001). Similarly, adolescents without obesity also had an average improvement in their AHI of 23.1 events/h (95% confidence interval [−33.8, −12.7, P < .001). Fifty-two percent of adolescents with obesity had an AHI < 5 events/h on postoperative PSG. However post-AT, children with obesity had a higher AHI (P < .001) and arousal index (P = .011) when compared to the nonobese group. Nineteen patients with obesity (27.5%) still had evidence of severe OSA (AHI > 10 events/h) on their postsurgical PSG compared to only 1 event/h (3.3%) in adolescents without obesity (Table 3). Furthermore, adolescents with obesity were 7 times more likely (odds ratio = 7.1, 95% confidence interval [2.24, 22.48], P = .001) to have moderate or severe persistent disease (AHI > 5 events/h) following surgery compared with counterparts without obesity. We conducted a regression analysis to assess for patient factors that predicted moderate or severe persistent OSA (AHI > 5 events/h) following AT (Table 4). Baseline AHI, nadir oxygen saturation, or age did not impact likelihood of persistent OSA; obesity was the only predictor of persistent obstruction following AT.
Table 3.
Pre-AT and post-AT OSA severity.
| Obese Adolescents (n = 70) | Nonobese Adolescents (n = 30) | P | |
|---|---|---|---|
| Baseline Severity | n (%) | n (%) | |
| Mild OSA | 8 (11.4) | 3 (10.0) | .97 |
| Moderate OSA | 10 (14.3) | 4 (13.3) | |
| Severe OSA | 52 (74.3) | 23 (46.7) | |
| Post-AT Severity | |||
| AHI < 1 events/h | 6 (8.7) | 9 (30.0) | n/a |
| Mild OSA | 27 (39.1) | 17 (56.7) | .014 |
| Moderate OSA | 17 (24.6) | 3 (10.0) | < .001 |
| Severe OSA | 19 (27.52) | 1 (3.3) | .003 |
AHI = apnea-hypopnea index, Mild OSA = AHI > 1 events/h and < 5 events/h, Moderate OSA = AHI ≥ 5 events/h and < 10 events/h, OSA = obstructive sleep apnea, Severe OSA = AHI ≥ 10 events/h.
Table 4.
Regression analysis; predictors of residual OSA following AT.
| aOR | 95% CI | P | |
|---|---|---|---|
| Obese group | 6.44 | (2.0, 21.09) | .002 |
| AHI | 1.01 | (0.99, 1.02) | .44 |
| Nadir | 0.96 | (0.89, 1.04) | .32 |
| Age | 1.07 | (0.86, 1.35) | .54 |
AHI = apnea-hypopnea index, aOR = adjusted odds ratio, AT = adenotonsillectomy, CI = confidence interval.
Twelve patients with obesity had pre-AT and post-AT OSA-18 scores. At the baseline, the median (interquartile range) OSA-18 QOL score was 66.0 (46.0, 81.0), indicating a moderate impact of sleep disturbance on QOL. Following AT, QOL scores improved to a median of 28.0 (21.5, 33.5). Only 5 adolescents without obesity had complete pre-AT and post-AT QOL scores. Similar to the children with obesity, their scores improved from a median of 83.0 (40.0, 86.0) to 27.0 (23.0, 57.0) following surgery.
Twenty-six adolescents with (37.1%) were recommended to have post-AT PAP therapy due to persistent obstruction. This contrasts with only 6.77% (n = 2) of patients without obesity.
DISCUSSION
AT remains the primary treatment for children with obesity with OSA. A recent meta-analysis that included 5 articles, however, highlighted that pediatric patients with obesity are at increased risk for persistent obstruction. While the majority of patients with obesity included in the analysis did experience clinically significant improvements in AHI, between 33% and 76% of obese children had residual OSA following AT compared to only 15%–37% of normal weight children.4 The data were limited by the focus on AT outcomes for children with obesity with no studies identified in the analysis that focused exclusively on adolescents. Com et al reviewed OSA outcomes for older (median age of 12), children with severe obesity (median z-score of 2.8) and adolescents and found that AT resulted in resolution of OSA (AHI < 5 events/h on postoperative PSG) in 55% of patients.9 These findings are comparable to our study where we noted that the majority of patients (80%) had improvement in post-AT AHI, with 48% of patients with obesity having a AHI < 5 events/h following AT. However, adolescents with obesity in our study were at 6-fold-increased risk for persistent moderate or severe OSA following AT compared to their nonobese peers. Lennon et al in 201610 described an inverse linear relationship between preoperative BMI and change in AHI following AT in children with obesity with a mean age of 11 years. The authors concluded that patients with a BMI z-score greater than 3 did not derive benefit from AT due to high rates of persistent OSA.10
In nonobese children, prior studies have demonstrated improvement in additional sleep parameters beyond the AHI following AT. Such changes included higher oxygen saturation, decreased arousals, and greater sleep efficiency. Less is known about the impact of AT on sleep parameters in obese children and adolescents. Lee et al11 found that improvement in the minimum oxygen saturation following AT was greater for the children without obesity compared to those with obesity. Similarly, in our study, adolescents with obesity had lower nadir oxygen saturation and higher arousal index on post-AT PSG compared to adolescents without obesity. Despite this discrepancy, children with obesity still experienced clinically meaningful improvements in PSG parameters such as a mean decrease of 14 in the arousal index. Thus, although adolescents with obesity are at risk for persistent obstruction, AT likely still leads to improvement in several sleep parameters that result in better sleep quality. Further research is needed to confirm this hypothesis.
OSA can have a significant impact on the overall health and wellbeing of children. Despite the finding that many children with obesity have residual disease following AT, this population has been shown to experience significant improvement in QOL following surgery. Mitchell et al12 found that OSA-18 QOL scores improved from a mean total of 78.2 (severe impairment of QOL) to 39.8 (mild impairment of QOL) following AT in children with obesity. Again, there is a lack of data examining QOL and symptom data in adolescents with obesity that are managed surgically with AT. In the small subset of our patients who completed pre-AT and post-AT OSA-18 QOL assessment, there was improvement noted in QOL scores. Future research should include the use of validated QOL, symptomatology, and behavioral assessments at baseline and follow-up to allow for better understanding of AT outcomes in this population of patients.
To improve treatment outcomes for adolescents with obesity and OSA, researchers need to identify factors that predict persistent disease. A recent study13 showed that abdominal fat distribution (which was clinically assessed by measuring waist circumference) negatively correlated with a curative response following AT in young adolescents with OSA. Waist circumference also predicted the percentage of improvement in AHI after AT. In another review of surgical outcomes,9 children and adolescents with obesity and with mild to moderate baseline disease and those with tonsil hypertrophy were more likely to be cured of their obstruction following AT. In our study, adolescents with obesity with more severe baseline disease (AHI greater than 10 events/h) had an increased risk of persistent obstruction following AT. Other factors such as presence of additional comorbidities and morbid obesity did not predict AT outcomes.
While AT is the main treatment for OSA in children, PAP therapy and weight loss are the primary management options in adults with obesity and OSA. Controversy remains as to whether adolescents with obesity should be managed as children or adults when it comes to approaching OSA treatment. An interesting study by Schwab et al14 sought to determine the primary structural cause of OSA in adolescents with obesity. The authors hypothesized that soft tissue components such as tongue base enlargement were more likely to play a role in obstruction in adolescents with obesity than lymphoid tissue. However, after assessing adolescents with obesity with and without OSA by magnetic resonance imaging, adenotonsillar hypertrophy was identified as the primary anatomic risk factor for OSA, not tongue base enlargement. These results lend support to consideration of AT as the initial treatment for OSA in adolescents with obesity and adenotonsillar hypertrophy.
The role for nonsurgical treatment for adolescents with obesity and OSA, including PAP therapy and weight loss, merits further study. Problems with patient compliance for these treatments have limited their utility as management strategies. Indeed, in a recent study examining treatment outcomes in children and adolescents with obesity and OSA,9 50% of patients that were recommended to have PAP therapy as their primary treatment were lost to follow-up after 2 years. Another systematic review5 that focused on OSA outcomes in children and adolescents with obesity noted that the mean nightly PAP usage for the majority of patients was less than 4 hours. Conflicting results have been reported regarding the impact of weight loss on pediatric and adolescent OSA resolution. Some studies report improvement in the severity of OSA following weight loss,14,15 while others note no significant impact due to patients being unable to achieve weight loss.9 We did not assess the impact of weight loss on OSA outcomes in this study. At our institution, there is a dedicated pediatric multidisciplinary weight management clinic to which we frequently refer patients with obesity and OSA. Unfortunately, nonadherence and lack of engagement are common among the adolescents with obesity that we refer. With increasing acceptance and use of bariatric surgery for childhood obesity, it will be interesting to see whether weight loss plays a more prominent role in the management of adolescent OSA. Indeed, in a recent review by Alqahtani et al16 of 226 children with obesity undergoing laparoscopic sleeve gastrectomy, the rate of OSA symptoms improved from 43% preoperatively to 18% 6 months postoperatively. Data on the amount of weight loss required to achieve resolution of OSA is lacking; this topic should be the focus of future studies that examine outcomes in children and adolescents with obesity.
The strengths of the current study include availability of pre-AT and post-AT PSG data for both obese and nonobese patient groups for analysis. In addition, this is the first paper to focus exclusively on AT outcomes for adolescents with obesity and OSA. Limitations of the study include retrospective design, which did not allow for subject matching, and relatively small sample size. In addition, our sleep laboratory does not typically report the oxygen desaturation index, so we are unable to comment on the impact of AT on this outcome. In addition, there was a higher percentage of children with obesity that were Black. Our study is underpowered to draw any definitive conclusions regarding race on surgical outcomes. Previous studies have suggested that Black children may be at risk for poorer surgical outcomes so future research is needed to investigate the complex relationship between obesity, race, and OSA treatment outcomes.17,18 Finally, we did not have follow-up data regarding the patients’ weight so we cannot comment on whether weight loss impacted outcomes. However, in our clinical experience most adolescents are not able to achieve significant weight loss.
CONCLUSIONS
The management of OSA in adolescents with obesity is challenging. While persistent disease is common following surgery, AT does result in clinically meaningful improvement in PSG parameters such as the AHI. AT is an effective treatment option for adolescents with obesity and OSA and should be strongly considered as adherence is often poor with other management strategies such as PAP therapy and weight loss. Further studies are needed to definitively identify which factors put obese adolescents at risk for persistent obstruction. In the meantime, it is essential that clinicians counsel adolescents with obesity and families regarding the importance of follow-up after surgical intervention and the potential need for additional treatment. Future research is needed to determine how to improve treatment outcomes in adolescents with obesity and OSA. Prior studies on pediatric drug-induced sleep endoscopy have shown that children with severe OSA have multiple levels of collapse. Data are lacking on drug-induced sleep endoscopy findings in adolescents with obesity and OSA. In upcoming studies, our research team plans to assess whether surgically addressing additional sites of obstruction noted on drug-induced sleep endoscopy at the time of AT in adolescents with obesity and severe OSA such as performing a pharyngoplasty will lead to improvement in OSA outcomes.
DISCLOSURE STATEMENT
All authors have seen and approved this manuscript. The authors report no conflicts of interest.
ABBREVIATIONS
- AT
adenotonsillectomy
- AHI
apnea-hypopnea index (AHI)
- OSA
obstructive sleep apnea
- PSG
polysomnogram
- PAP
positive airway pressure
- QOL
quality of life
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